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1901 Cards in this Set

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Examples of Localization - can be localized to? (7)

- brain


- spinal cord


- nerve root


- anterior horn cell


- peripheral nerve


- NMJ


- muscle




* localize based on history and neuro exam

UMN Findings - pattern of weakness? reflexes? babinski is? also see (2)




*diseases affect?

- spasticity


- hyperreflexia


- pyramidal pattern of weakness (extensors in lower, flexors in upper limbs)


- upgoing toes = positive Babinski


- clonus




**diseases affect CCS tract

LMN Findings - atrophy of? tone is? muscle may? reflexes?


- diseases affect? (3)

- muscle atrophy


- fasciculations


- flaccid tone


- hyporelfxiea


- areflexia




** diseases affect nerve roots, anterior horn cells, peripheral nerves

Vascular vs Inflammatory Events


- vascular involve? typically?


- Inflamm in? onset? evolve over?

V = involving the nervous system are typically abrupt onset




I = in nervous system, typically gradual onset and evolve over hours to days

Localization in Brain - would see if right sided?


- weakness? loss of? on?


- reflexes? positive?



- left sided weakness in pyramidal pattern


- left hemi-sensory loss


- left arm and leg hyper-reflexia


- positive left babinski

For left lumbosacral nerve root lesion, would expect?


- lower back?


- weakness in?


- sensory loss in?


- loss of?


- muscle?

- lower back and radiating left leg pain


- weakness in myotomal pattern


- sensory loss in dermatomal paterrn


- loss of deep tendom reflexes = L4 or S1


- uscle atrophy in left leg if chronic

For thoracic spinal cord lesion, expect


- weakness of? sensory loss of?


- symptoms seen in?


- in legs see?

- bilateral lower limb weakness (spared arms)


- bilateral lowrr limb sensory loss 9spared arms)


- sensory level on torso


- bowel and bladder symptoms


- UMN findings in legs

EMG - reduced sensory amplitudes


- consistent with? can diagnose?

- consistent with diffuse, axonal, length-dependant sensory peripheral neuropathy


- can diagnose idiopathic peripheral neuropathy

In diffuse length-dependent sensor peripheral neuropathy, expect?


- bilateral? (2)


- reflexes?

- bilateral distal limb weakness


- bilateral distal limb sensory loss


- reduced or absent distal reflexes

See bilateral eyelid ptosis, bilateral weakness of eye closure, reduced reflexes and diffuse limb weakness, expect?


- think of? such as?

- pre-synaptic NMJ transmission defect, such as botulism

Disorders of NMJ, expect? (6) = P/D/B/Diffuse? Symptoms of? Weakness that?

- ptosis


- diplopia


- bulbar symptoms


- diffuse limb weakness


- resp symptoms


- weakness fluctuates

When to use electromyogrpahy and nerve conduction symptoms? (5)

- peripheral neuropathy


- radiculopathies


- anterior horn cell disease


- myopathy


- disorders of NMJ

All causes of left foot weakness?


- brain? could be? from? spinal cord? idiopathic? NMJ of?

- right hemisphere lesion = Hematoma, stroke


- left L5 radiculpathy = disk herniation


- spinal cord lesion = thoracic cord compression


- peripheral neuropathy = idiopathic


- NMJ = botulism

When to suspect increased Intracranial pressure when lesion is in the brain


- see? (5) due to?


- see focal? and related?

- see headache, N, V, papilledema, diplopia due to 6th nerve palsies


- see focal neuro symptoms


- see related seizures

SC Syndromes - Brown Sequard


- is a lateral?


- below level, see ipsilateral? (2)


- contralateral?


- no? **

is a lateral hemisection syndrome, see:


= ipsilateral UMN signs below level


= ipsilateral loss of prop and vibration sense


= contraL loss of pain and temp below level of lesion


= no bladder symptoms**

SC Syndromes - AC Syndrome


- syndrome of?


- can see changes of?


- bilateral?


- symptoms of?


- normal? **** as this is found in?

- is a ventral cord syndrome, see:


= weakness, reflex chnages


= bilateral loss of pain and temp


= urinary incontinence


= normal tacitle, position and vibration sense (in dorsal columns)

SC - Posterior Cord Syndrome


- is a syndrome of?


- weakness presents as? A vs C?


- loss of?


- may have both? (2)**

- is dorsal cord syndrome, see:


= weakness, if acute (muscle flaccid, hyporeflexia), if chronic (hypertonia, hyperreflexia)


= loss of tactile, position and vibration


= +/- upgoing plantar


= +/- urinary incont

SC CENTRAL CORD SYNDROME


- loss of? in the? at?


- presents as a? *


- normal?


- alsp normal?


- some? if?

- loss of pain and temp in dermaotmes at site of SC lesions **suspended sensory level**


- normal pain and temp above and below


- normal vibration and proprio


- see some weakness and reflex loss with larger lesion

DDx for Polyneuropathy - (7)

- diabetes


- HIV infection


- Amyloidosis


- Hypothyroidism


- B12 defic


- lyme


- Malignancy

Signs and Symptoms of brain Lesions


- signs of? pattern?


- general?


- focal? aphasia of?


- dysfunction of?

- UMN signs, pyramidal pattern


- general = headache, seizure, nausea, vomiting,syncope


- focal = weakness, sensory loss, aphasia if dominant side (apraxia if non-dom)


- visual spatial dysfunction

Signs of SC Lesions


- big hint is?


- signs of? weakness in?


- if localized?

- bilateral motor and sensory signs is big hint


- UMN signs and pattern of weakness


- if localized, symptoms in muscle groups innervated below that level, normal abovw

Cauda Equian Syndrome


- pain that is?


- weakness of?


- dysfunction of?

- assymetric multiradicular pain, leg weakness and sensory loss, bladder dysfunction

Segmental Transection Syndrome


- loss of all?


- weakness found?


- see dysfunction of?



- loss of all sensory modalities, weakness below affected level, bladder dysfunction

Nerve Root Signs and Symptoms


- signs? (3)


- weakness in? sensory loss in? (patterns)


- diff mainly by?


- damage due to?


- hallmark?

- LMN signs and weakness with hyporeflexia, muscle atrophy, fasciculations


- weakness in myotomal pattern, sensory loss in dermatomal pattern


- diff. mainly by sensory loss symptoms


- damage often due to compression, results in hallmark symptom of pain

LS Radiculos - S1 vs L5 vs L4 vs L3


Cervical Radulos - C5 vs C6 vs C7 vs C8



Anterior horn Cell Signs and Symptoms


- signs of? see??


- difficulty?


- no***


- vs peripheral nerve, see?

- LMN signs, see muscle atrophy, difficulty performing or doing things do to weakness


- no sensory deficits ******


- vs peripheral nerve, see some sensory defs

Periphral Nerve signs and symptoms


- can be either?


- sensory with?


- motor with? resulting in? likely affected?

- can be mono or pomy neuropathy


- see sensory with burning, tingling, numbness


- motor, see weakness to muscles supplied by peripheral nerve, muscle cramps, longest nerves with largest diameter fibres more likely of disruption

NMJ signs - P/D/B such as?


- intermittent?


- resp?


- no?


- key is**

- ptosis


- diplopia


- bulbar symptoms = dysphagia, dysarthria


- intermittent, limb weakness,


- resp symptoms


- no sensory deficits


- key is fluctuation of symptoms **

Lhermitte Signs


- transient? described as? after?


- seen mostly in? but also? (3)

- transient sensory symptoms described as electric shock radiating down spine into limbs most often after flexion of the neck


- seen in MS mostly but also lesions of cervical cord, tumours, cervical disk hernaition

Uhthoffs Phenom - worsening of?


- condition of? when body?


- result of? seen in?


- see?

- worsening of neuro symptoms in MS


- demyelinating condition when body gets overheated from hot weather, showering, etc


- result of conduction block developing in central pathways


- see black spots when exercising, have hot shower

GBS Lumbar Puncture


- LP reveals? elevated? normal?


- abnormal?

- LP reeals elevated CSF protein when normal CSF WBC count


- elevated WBC count is abnormal

NMJ - see a? fluctuating?

- pure motor syndrome with fluctuating ptosis, diplopia, bulbar symptoms, limb weakness

Acquired Myasthenia Gravis - is? prevalence of?


- found in all?


- onset?


- women, more common in? men?

- AI disorder of NMJ, prevalence of 20/ 100, 000


- all age groups


- bimodal onset


= more common in women when onset <40


= more common in men when onset > 50

Clinical Features of MG - P/O


- weakness of? (2)


- neck?


- limb?


- also see?




*mainly can tell by?

- ptosis


- opthalmoparesis


- faical muscle weakness


- bulbar weakness


- neck flexor and extensor eakness


- limb weakness


- dyspnea




* see fluctuating and fatig. weakness, betters with rest****

Pathophys of MG


- antibody that? at?


- results in? to?

- Antibody destroying Acetycholine receptors of post-synaptic junction


- results in decreased ability of Ach to eleicit response

Diagnostic Testing to make MG diagnosis -3 steps


- bedside?


- then do? which can show?


- serological then?

1) Bedside test = tensilon test




2) Electrodiagnostic Test = Repetitive Nerve Stimulation (RNS) and Single Fiber EMG (SFEMG)


- RNs shows decrease power with repetition




3) serological tests = Acetylcholine receptor Abs

MG Disease Management


- symptomatic? = (3)


- DMT = (3)


- surgery?

1) Symptomatic Therapy


= Mestinon, Plasma Exchnage, IVIG




2) Disease Modifying Therapy


= Corticosteroids, Azathioprine, Cyclosporine, Myco Mofetil




3) Disease Mod Surgeyr = thymectomy?

MG Disease Prognosis


- disease has become?

- before modern day therapy, see 33% remission, 33% active disease and 33% died


- with today's therapy, see disease well controlled in most, mortality less than 5%

Myopathy Signs ****


- pure? proximal? lower?

- pure motor syndrome with proximal upper and lower extremity weakness ***

See myopathy in? (2)


investigations should include? (5)


- should perform?


- do MRI of? for?

- Hyperthyroidism and Graves disease


- should investigate CK levels, TSH, ESR and CRP and ANA


- should perform EMG and nerve conduction studies, MRI of proximal muscle for myositis, muscle biopsy and genetic testing

DD of Muscle Diseases - MD/CM/ MM/ MM/ ERM/ Med induced? Inflamm?

- muscular dystrophy


- congenital myopathy


- mitochondiral myopathy


- metabolic myopathy


- endocrine related myopathy


- medication-induced/ toxic myopathy


- inflamm myopathy

Diffuse Motor Neuron Disorder presents as? *****


- a progressive? mixed? seen in?

- a progressive pure motor syndrome involving mixed upper and lower motor neuron findings in bulbar and limb muscles

Motor Neuron Disease = subtypes?


- upper and lower include?


- could also be just? or just?


- incidence of ALS is?


- peak incidence?


- mean survival after?

- subtypes include:


= upper and lower motor neurons= ALS


= upper motor neurons


= lower motor neurons


- incidence of ALS is 1-2/ 100,000


- peak incidence is age 50-75


- mean survival after diagnosis = 3 yeras

Amyotrophic Lateral Sclerosis (ALS)


- progressive disorder of?


- pathophys is poorly?


- pyramidal cells in?


- sparing of?

- progressive disorder of upper and lower motor neurons:


- pyramidal cells in motor cortex = layer 5


- alpha motor neurons of brainstem and spinal cord


- sparing of oculomotor motor nuclei and nucleus of Onufrowicz




* pathophys poorly undestood

Clinical Features of ALS


1) Spinal? %? upper vs lower?


- distal? typically? gradual?


2) Bulbar? affects? presents as? is typically?




* key feature

1) Spinal Onset ALS = 80%


= upper limb onset > lower limb


= distal focal limb weakness and atrophy


= typically unilateral


= gradual spread to other regions




2) Bulbar Onset ALS


= cranial nerves 7,9 and 10


= dysarthria and dysphagia


= aggressive disease with typically rapid progression




* key feature is Upper and Lower motor neurons findings in involved region

Diagnosis of ALS requires progressive?


- supportive?


- no evidence of?

- progressive pure disorder of upper and lower motor neurons


- supportive EMG studies


- no electrophysiologic, neuroradiological or neuropathological evidence of another condition to explain findings

Pathophys of ALS - poorly? major focus on? (2)


- additional theories include? (4)

- poorly understood


- excitotoxicity and oxidant stress are current major areas of focus


- additional theories include = genetic predisposition, toxin exposure, mito dysfunction and viral etiology

Natural History of ALS - relentless? results in?


- ultimately causes?

- relentless progressive disease


- quadraplegia


- respiratory muscle involvement and ult. resp. failure



treating ALS - primarily? Riluzole is? only gives?

- treatment are primarily supportive


- Riluzole often prescibed but effect in minimal


- 3 month average increase in survival

A pure motor syndrome with fluctuating ocular, bulbar and limb weakness makes you think?

NMJ

A pure motor syndrome with proximal upper and lower extremity weakness makes you think?

- myopathy

A progressive pure motor syndrome involving upper an dlower motor neuron findings in bulbar and limb muscles makes you think?

- diffuse motor neuron disorder

Peripheral Nervous System


- originates in? ends in?


- includes both? as well as?

- analogous to the wiring of the NS


- originates and ends in SC and end organs


- motor and sensory systems involved in involuntary reflex arc as well as volutnary control/awareness

General Localizations in PNS - (7)

- myopathy


- NMJ


- mononeuropathy


- plexopathy


- radiculopthy


- motor/sensory neuronopathy


- polyneuropathy

Components of Peripheral Neurons - Motor


- cell body in? then? then? then? at?

- cell body located in anterior horn of SC


- nerve root


- axon/ myelin sheath


- NMJ


- muslce

Components of Peripheral Neurons - Sensory


- sensory end organs are?


- cell body is?


- axon terminal in?

- sensory end organs = receptors


- axon/ myelin sheath


- sensory ganglion = cell body


- nerve root


- axon terminal located in dorsal horn of SC

Principles of Nerve Conduction


- propagation of impulses occurs?


- depol is?


- transmission depends on?

- propagation of nerve impulses occurs analogously to transmission in CNS


- depol/ hyperpolariation dependent balance between sodium influx and K efflux from cells


- strength and speef of transmission depends on type of nerve fibre = motor, sensory, autonomic

Saltatory Conduction


- nerves contain? acts as? prevents? enhances? via?


conduction ranges from?


- autonomic conduct? due to?

- motor and sensory nerves contain myelin sheaths = neuronal insulation


- myelin sheath prevents currents "leak" and enhances neuronal transmission via saltatory conduction (current skipping)


- nerve conduction ranges from 40-60 meters/ second depending on location (upper and lower extremity) and modality (motor vs sensory)


- autonomic nerves conduct much slower due to lack of myelin

Mechanisms of Nerve Injury


- disrupted? is most?


- also can be due to? (2)


- or?

- disrupted axonal transport = most common


- nerve infarction


- nerve inflammation


- compression / direct trauma

Axonal Transport


- see transportation along?


- anterograde used for?


- retrograde used for?


- highest chance of disruption in?

- building blocks are transported from the cell body throughout the length of the axon


- anterograde transport is responsible for bringing essential nutrients to the neuron


- retrograde transport returns debris to cell body for recycling


- longest nerves (toes) and largest diameter fibers (sensory) have the highest chance of having disruption in this system

Polyneuropathy - most common type of?


- has a? affects first? then reaches? then seen in?


- is dependent on?

- most common type of peripheral neuropathy


- "length dependent" pattern:


= affects sensation in the toes first


= once symptoms reach the level of the knees, fingertips begin to be affected




** length dependent = related to deficiency in axonal transport

Clinical Features of Polyneuropathy


- Sensory = ?


- tingling of? also see?


- motor see? (2)

- Sensory:


= itching, burning, freezing = +, small fiber


= tingling = +, large fiber


= numbness (-)




- Motor:


= muscle cramps (+)


= weakness (-)




* leads to gait difficulties, falls, self-injury

Polyneuropathy - Clinical Features - Autonomic - can cause? HR? increased? bowel? dysfunction of? blurring of?

- syncope/ presyncope


- arrythmia = tachy, brady


- increased + or decrease perspiration (-)


- diarrhea + or constipation +


- bladder dysfunction


- visual blurring


- sexual dysfunction

Etiologies of Polyneuropathy - can be either?

- can be hereditary or acquired

Acquired - Distal Symmetric Polyneuropathies - Main Categories


- metabolic includes?


- defic in?


- toxic?


- also caused by? (3)

- metabolic neuropathy = endocrinopthies, organ dysfunction


- nutritional deficiencies


- toxic neuropathy = enviro, medications


- infectious causes


- cancer assoc.


- connective tissue diseases

Acquired - Distal Symmetric Polyneuropathies = Common Specific Etiologies (10)

- idiopathic


- diabetic neuropathy = impaired glucose tolerance


- B12 defic


- thyroid disease


- paraproteinemia = monoclonal gammopathy, malignant


- alcohol


- renal disease


- syphilis/ HIV

Acquired - Medications Causing Neuropathy


- chemo =? anti? cardiac? also with?(4)

= chemo = cisplatin, taxol, Vincristine


= anti-infectious = Isoniazid, metro, colchicine, Ethambutol, HIV meds


- phenytoin


- cardiac meds = amiodarone, hydralazine


- pyridoxine


- Cimetidine


- Disulfiram


- Chloroquine

Acquired Neuropathy - developing world #1 cause? developed?

- in developing world = #1 cause of neuropathy is leprosy


- in developed world = #1 cause is Diabetes

Hereditary Neuropathy - ISP - often without?


- abnorms of? such as?


- usually focused?


- most common hered is? **

1) Insidious Symmetric Progression = often without pain or positive sensory or motor symptoms, often severe weakness and sensory loss without much disability


2) Bony and Cutaneous Abnorms = pes cavus = high arched feet and hammer toes


3) Usually a focused FH




* most common type of hereditary neuro is Charcot-Marie-Tooth = CMT

NCS/EMG uses


- evaluates the?


- able to provide info on? (4) - if and when? extent? duraiton? type?



- test evaluating the electrophys of the peripheral nervous system




- able to provide info on:


= if and when there is signif damage


= extent of injury


= duration of dysfunction


= type of damage (axonal vs demyelinating)




** does not tell us about:


= etiology


= central or non-neuro disorders

NCS relies on? from/ on?


- evaluates? in?

- relies on responses obtained from recording electrodes following a delivery of current to the skin


- evaluates certain motor and sensory nerves in the distal arm and leg

EMG uses a? inserted into?


- in order to?


- can tell us? in?

- uses a micro-electrode inserted IN the muscle itself, in order to study the properties of the muscle and indirectly the nerve


- can tell us about the nerve and muscle lesions in any accessible muscle

Distal Symmetric Polyneuropathy - Lab Tests


- (4)


- comprehensive? including?

- CBC


- ESR


- comprehensive metabolic panel = blood glucose, renal function, liver function, thyroid function tests


- serum B12


- serum protein immunofixation electrophoresis

Lab and Testing for Distal Symmetric Polyneuropathy


- screening should be considered for?


- highest yield is? with?


- perform a?

- screening lab tests may be considered for all patients with polyneuropathy


- highest yield = serum B12 with metabolites and serum protein immunofixation electrophoresis


- 2 hour glucose tolerance test may be considered if fasting blood sugar, hemoglobin A1c normal

Patterns of Peripheral Nerve Dysfunction


- PN/P/R/MN/ MNM

1) Polyneuropathy


2) Plexopathy


3) Radiculopathy


4) Mononeuropathies = CTS, Ulnar Neuropathy, Peroneal Neuropathy, Cranial Neuropathy


5) Mononeuropathy Multiplex

Atypical Features = Red Flags


early?


- involvement of?


- rapid?


- pure?


- involvement of?


- asoc of?

= early simultaneous upper limb symptoms


= cranial nerve involvement


= rapid progression


= focality/ multifocality


= pure motor involvement


= bower or bladder involvement


= assoc symptoms = rash, weight loss, organ involvement

Axonal, Length Dependent Polyneuropathy vs Demyelinating Neuropathy


- seen in? (2)


- GB, CIDP

Polyradiculopathy vs Mononeuropathy Multiplex



Etiologies of Atypical Neuropathy


- radiculos = C/I/I - examples


- MNM - includes (3 - V/A/M)


- demyel - can be? (3)

1) Radiculopathy


= compressive = spinal stenosis


= inflammatory = GBS, CIDP


= infiltrative = Leukemia




2) Mononeuropathy Multiplex


= Vasculitis, Amyloidosis, Mimics (Leprosy, Diabetes)




3) Demyelinating = CMT, CIDP, GBS

Disease Dependent treatment


- B12 - give?


- if toxic?


- if diabetes?


- if infectious?

- B12 related = replacement


- Toxic = removal of toxic agent / drug


- Diabetes = diabetic control


- Infectious = anti-microbial treatment

Polyneuropathy Treatment


- no general?


- treatment directed at?


- mainstay of treatment?

- no general disease modifying treatments available for polyneuropathy


- specific treatment should be directed at underlying causes


- symptomatic treatment is mainstay of management

Polyneuropathy Symptoms


- main symptoms of? (4)


- affects? (3)

- main symptoms = pain, cramps, autonomic, anesthesia


- affects sleep, mood, QOL

Neuropathic Pain Symptomatic Treatment


- Pain = N/PG/AT/D/CC/T/O

1) Pain


- neurontin/ pregabalin


- amytriptyline


- duloxetine


- Capsaicin Cream


- tramadol


- Opioids


- non-steroidal anti-inflammatory




2) Anti-Epileptics


= dilantin


= carbemazepine

Muscle Cramps Symptomatic Treatment


- give? tell to?


- supplement?


- give?


- also can give?


- meds for? (3) = D/C/L

- stretching/ hydration


- Vitamin B supplementation


- Calcium channel blockers


- Quinine sulphate


- Baclofen


- Anti-epileptic meds = dilantin, Carbemazapine, Leveteracitam

Conclusions of Peripheral Neuropathy


- most common type of periph nerve is?


- pathophys is?


- length dependent patterns affect?

- most common type of peripheral nerve dysfunction is a distal, length dependent sensorimotor polyneuropathy


- pathophys behind polyneuropathy is disrupted axonal transport causing a length dependent pattern of injury


- length dependent patterns affects distal sensation in the legs feet initially

Conclusion of Peripheral Neuropathy


- screening tests should include?


-non-length dependent pattern should prompt? (3)***


- treatment should include?

- screening tests for PN include fasting blood glucose, 2-hour glucose tolerance test, Hb A1c, TSH, B12, CBC, metabolic profile, serum protein electrophoresis, ESR


- non-length dependent pattern should prompt consideration of alternate etiologies (Mononeuro Multiplex, Radiculopathy, Demyelinating Neuro)


- treatment of peripheral neuropathy should include global approach

Headache - why care - most common?


- 1/3 of?


- most are not?


- most expensive?

- most common medical disorder


- 1/3 of patients in doctors offices have headaches


- most headaches are not serious


- WHO deems headache the most expensive brain disorder


- 100 billion dollars lost annually due to headaches

Primary Headaches - DD


- migraine - can include? (3) C/E/M


- TGA = includes? (3)


- Tension? Or?

1) Migraine:


= episodic = with or without aura


= chronic


= menstrual




2) Trigeminal autonomic :


= cluster, SUNCT,Hemicranias




3) Tension type headaches


4) Other

Headache History


- when? how? F? dur? also see?


- factors that?


- strategies that?


- history of?


- factors of?

- when and how did a headache first present


- frequency


- duration


- pain location, quality, severity


- assoc. features


- exac. or attenuating factors = positional? triggered by exertion?


- curent and past treatment strategies, over the counter med use, alternative treatment


- history of head, neck injury or MVA


- lifestyle factors


- adverse childhood events, FH of headaches

Classification of primary headaches


= three most useful clinical features include?


F / AFs / dur?

= three most useful clinical features:




1) Frequency - chronic vs episodic




2) Assoc. Features - migrainous (worse with exertion), sympathetic, paraS




3) Duration - 4 hours? seconds vs minutes?

Classification of Primary headaches - recurrent


- time? types? (3)


- of time of? types? seen with? (4)


- other includes? (2)

1) Recurrent, >4 hours duration


= migraine, tension type, Hemicrania Continua




2) Recurrent HAs < 4 hours


= trigeminal autonomic Cephalagias (V1 pain, ipsi autonomic features, cluster)


= cough, exertion, sexual, hypnic HA


= other = trigeminal neuralgia, primary stabbing headache

Differentiating Trigeminal Autonomic Cephalalgias (TACs)


- attack frequency/ duration/ pain quality/ pain intensity/ circadian



Definition of Migraine without Aura


- 5 or more?


- 2 or more - qualities include? (4) loc/puls/intens/agg?


- at least 1 of? = (4)

- 5 or more attacks lasting 4-72 hours


- 2 or more of the following characteristics = unilateral location, pulsating quality, moderate to severe intensity, aggravation by routine


- at least 1 of the following assoc. symptoms = N/V, photophobia and phonophobia

Prevalence of Migraines in Adolescents


- see increase in? then?


- in females, see?

- see increase in prevalence until 11 or 12, then decline


- rise again in females at 15

Childhood Migraine Equivalents


- cyclical? recurrent?


- in sleep? sickness of?


- abdos?


- infant?


- alternating?

- cyclical vomiting


- recurrent abdo pain


- sleep walking


- motion sickness


- abdo migraine


- infant colic


- alternating hemiplegia of childhood


- vestibular migraine


- benign paroxysmal torticollis

Treatment of Young Migraineurs


- mods of? including?


- acute treatment - mild? severe?


- preventative - done if?

- behaviour and lifestyle mods = protein, hydration, sleep hygiene, exercise, supplements such as B2, Magnesium Citrate


- acute treatment = mild (NSAIDs), mod and severe (triptans)


- preventative treatments = done if HAs more frequents than 1/week

Treatment of Young Migraineurs - Acute Treatment - NSAIDs


-superior one is?


- dose?


- can slo give?

- NSAIDs


= ibuprofen demonstrated to be superior to placebo or acetaminophen in children and adolescents


= 7.5-10 mg/kg per dose


= +/- anti-emetics

Treatment of Young Migraineurs - Acute Treatment - Triptans


- agonist of (2)


- in Canada, there are?

- agonist of serotinin 1B and 1D receptors


- 7 are available in Canada = Sumatriptan, Zolmitriptan, Rizatriptan, Almotriptan, Eletriptan, Frovatriptan, Naratriptan

Migraine with Aura - 1 and 2


- need at least 2?


- aura consists of? (3) all are? no?

1) At least 2 attacks fulfilling criteria 2-4


2) Aura consisting of at least 1 of the following, but no motor weakness


= fully reversible visual symptoms


= fully reversible sensory symptoms


= fully reversible dysphasic speech disturbance





Migraine with Aura - 3 and 4


- at least 2 of? VS/ SS


- >1 aura symptom of? or different?


- each symptom is?


- HA fulfilling? migraine without aura - begins? and then follows?

3) At least 2 of the following:


= homonymous visual symptoms and or unilateral sensory symptoms


= 1> aura symptom over >5 minutes and or different aura symptoms in succession over >5 minutes


= each symptom >5 and <60 minutes




4) headache fulfilling criteria B through D for migraine without aura begins during the aura and follows aura within 60 minutes

Clinical Features of Migraine


- attacks have a? then?


- duration of attack? in children?


- unilateral vs bilateral?


- pain can be? 50% have?

- attacks have a gradual onset and a peak, and then subside


- the duration of an attack ranges from 4 to 72 hours in adults and 2 to 48 hours in children


- the location is unilateral in 60% of indivs and bilateral in 40% of indivs


- the pain can be moderate to severe in intensity, pulsating in 50% of individuals and feeling tight or exerting pressure in 50%

Clinical Features of Migraines


- increased incidence of?


- exac during?


- reduced during?


- from?


- increased after?


- caused by certain?



- increased incidence on weekends and holidays


- menstrual and ovulatory exarcerbations


- educed frequency in 1st trimester of pregnancy


- stress


- fasting, missing meals, sleep disruption


- certain foods, ex/ MSG, alcohol, cheese


- changes in weather = drops in barometric pressure




* see hormonal modulation of migraine - low estrogen, after migraine see high estrogen


* see hormone - related to pain free at 2hours and 24 hour relapse after 4 hours pain free

Pathophys of Aura


- is a transient? which then?


- seen in?


- mechanism is?

- transient focal visual, sensory, or motor symptoms which develop gradually


- 30% of migrainers experience aura


- mechanism is Cortical Spreading Depression:



Cortical Spreading Depression Mechanism


- slowly prog? assoc with? massive?


- correlates with?


- vascular correlate is a?


- migrainers have?

= slowly propagating wave of neuronal depol assoc. with cessation of spontaneous or evoked synaptic activity, massive glutamate and K release


= correlates with prop. of neurological symptoms rates of 3 mm/min


= vascular correlate is a focal wave of hyperemia followed by oligemia


= migrainers have reduced thresholds for cortical excitability

Stroke Risk in Migrainers


- migraine without aura doesnt?


- yet in women under 45, with aura?


- MWA and hormonal creates?


- women - MWA and smoke?

- migraine without aura does not confer increased stroke risk


- in women under 45 migraine with aura confers a 2x increased stroke risk


- migraine with aura and hormonal therapy confers a higher increased risk, further 2x increase


- risk in women with migraine with aura who smoke very high, estimate RR of 4

Treatment of Migraine - Acute


- mild - use? short acting? long?


- severe - use? or combine?

1) Mild to Moderate = NSAID


= short acting = Naproxen


= long acting = nabutone




2) Moderate to Severe


= Triptan


= NSAID


= Triptan + NSAID

Proper Use of Triptans

- take first dose as early as possible


- second dose can be taken after 2-4 hours if response is suboptimal or if headache recurs


- dose can be front loaded but should not exceed 2 in 24 hours


- consider wafers, subcut, nasal formulations in patients with very rapid onset or delayed gastric emptying


- maximum per month = my rule of thumb is NO MORE THAN 8x per month



Selecting a Triptan - formulation? T1/2?


- adverse effects? (6)

- adverse effects = nausea, dry mouth, paresthesia, dizziness, somnolence, pain/pressure

- adverse effects = nausea, dry mouth, paresthesia, dizziness, somnolence, pain/pressure

Selecting a Triptan - if wakens with severe HA - use? such as?


- if ident onset, such as? use? such as? (A/E/R)


- if has N/V - use? with?


- if slow onset - use? (N/F) - same for?

1) Wakens with severe headache


= fast acting = Sumatriptan injectable or nasal spray




2) Identifiable Onset, develops over 30-60 mins


= fast acting = Almotriptan, Eletriptan, Rizatriptan




3) Rapidly develops N/V


= nasal spray or oral triptan + anti emetic




4) Slow onset


= Naratriptan or Frovatriptan




5) Predictable Menstrual Migraine


= Naratriptan or Frovatriptan



Cintraindications to Triptans


- if have? (4)


- type of migraine? (3)


- relative - use of? or use of?

- ischemic heart disease, uncontrolled hypertension, PVD, stroke


- basilar, hemiplegic migraine or ophthalmoplegic migraine


- relative = use of SSRIS and SNRIs or use with MAO inhibitors

Prevention of Migraines - Triptans


- reduces (3)


- may prevent?


- using both? to help decrease?

- reduces frequency, severity and duration


- may prevent chronification of HA


- using both acute and preventative rx results in decline in office visits, ER visits, CT and MRI scans and acute med costs

Preventing Migraines - behav and lifestyle


- keep? document? (7)

= keep diary **


= sleep routine


= diet


= hydration


= walking/exercising


= stress management


= mindfulness


= psych support


= PT

Pharm Prevention of Migraines


- Approved = T/ D/ T/ P - strong = (2)


- off label = (4)


- herbal = (3)

1) Approved


= topiramate = strong rec for use


= Divalproex = often CI due to teratogen


= Timolol


= Propranolol =strong rec for use




2) Off label


= nadolol, metoprolol, candesartan, gabapentin all strong rec, some SSRIs




3) Herbal = Mg Citrate, Riboflvin, Butterbur, Q-10 - strong rec for use

Prophylactic Drug Choice in Migraine Prevention


- should be based on? (3)


- most commonly used?


- if have depression? if have anxiety?


- start? then go? better?

- should be based on efficacy, SEs, clinical features and other disorders


- most commonly used in Topiramate, if have depression use SSRIs, if anxiety use Gaba, etc


- start low, go slow = evtter efficacy at lower doses with fewer AE

DD of Chronic Headaches


- CM


- Chronic TT = present as? intensity? not?

1) chronic migraine




2) chronic TT headache


= bilateral, pressing, mild to mod, not agrr. by PA



DD of Chronic Headaches


- new persistent - defined by? (3) diagnosis of?


- HC =? is seen on? often is? and lasts?


- moderate with? features such as? (3) P/L/R

3) new persistent daily HA


= defined by new onset, persistent, diagnose of exclusion




4) hemicrania Continua


= unilateral, daily, continuous, moderate with exacerbations, has trigeminal features such as ptosis, lacrimation, rhinorrhea

Definition of Chronic Migraine


- duration? with ? with or without?


- typical patient is? has?


- as HAs become more frequent?

- >15 days HA per month with current or prior diagnosis of migraine with or without medication overuse


- typical patient is female, has migraines without aura


- as headaches become more frequent, migrainous features become less prominent

Chronification of Migraine


- at first? then as prolongs? becomes?


- can lead to? (3)

- see episodic at first, then as prolongs, HA symptoms do no return to baseline, becoming chronic


- leads to depression, anxiety, sleep disorders

Structural Chnages in Chronic Migraine


- MRI shows? in? such as? (5)

- MRI shows gray matter volume reductions in pain modulating structures


= bilateral insula, motor/premotor, prefrontal cingulate cortex, right posterior parietal cortex and orbitofrontal cortex

RFs for Chronic Migraine


- freq?


- treatment?


- chronic?


- weight? low? stress?


- things like?

- attack frequency - or 8, 10-14d


- treatment patterns - or 4-5 acute meds >10ds


- chronic back pain


- obesity


- low SES


- stressful life events = ACE/PTSD


- head injury, snoring, caffeine, psychiatric illness


- allodynia

Medication Overuse HA (MOH) - interaction between?


- prevalence is?


- seen with? of?


- using increased? with?


- when off meds?


- incomplete?


- patients begin to fear?

- MOH is an interaction between a therapeutic agent and susceptible patient


- prevalence = 10-20% of referrals, in US up to 80%


- seen with analgesic use > 2-3 days of a week


- escalating doses with decreased effectiveness


- withdrawal symptoms when off medication


- incomplete relief with re-dosing


- patients fear next attack = anxiety

MOH Thresholds


- number of days/ month?


- triptans used? length?


- analgesics? opioids?


combo?

- HA on >15 d per month and:


= triptans > 10 d per month for > 3 months


= analgesics > 15 d per month for 3 months


= opioids > 10 days/mo for 3 months


= combo of above > 10 days/ m for 3 months

MOH Treatment


- essential is?


- led to decrease in?



- Essential is detox from over-used medications


- see 73# decrease in HA frequency and 70% returned to episodic HAs when continued med overuse

Adverse Childhood Events and Migraine


- dysfunctional? witnessed? death of?


- strong assoc of?



- storng assoc with depression, anxiety, abuse, assoc of ACE, migraine and inflammatory markers

- storng assoc with depression, anxiety, abuse, assoc of ACE, migraine and inflammatory markers

Managing Migraine in Pregnancy


- lifestyle mods = (8)

Managing Migraine in Pregnancy


- acute include? (3)


- preventative include mainly? (4)


- can also try? (3)

Acute Stroke - sudden loss of? due to? loss of?


- 2 main types? caused by? %?

- sudden loss of brain function


- interruption of blood flow


- loss of oxygen and glucose supply to a part of the brain


- 2 major types:


1) Ischemic stroke = lack of blood flow due to clot (85%)


2) Intracerebral hemorrhage = bleeding in brain due to vessel rupture (15%)

Transient Ischemic Attack (TIA)


- self limited?


- temporary? not assoc with?

= self-limited episode of neurologic dysfunction


= temporary focal cerebral ischemia not assoc. with cerebral infarction

Impact of Stroke - for developed countries, is the?

- for developed countries = 3rd most common cause of death, leading cause of disability


- in Canada, 1 stroke / 10 mins, costs 2.7 billion annually

Stroke and Aging Population


- age is the? each decade see?


- M vs F?


- growth of pop vs interventons - means?

- age is the single most important non-modifiable risk factor for stroke


- stroke rates double each decade after 55 got both men and women


- incidence is 1.25x higher in men than women


- growth of population over 65 years will continue at the same rate but impact of interventions will reach plateua


- decrease in stroke hosp. is projected to flatten out, may increase in future

Key Stroke Points - important cause of?


- have long term?


- aging will? as ages?

- strokes are important cause of morb affecting 1% of Canadians chronically, use 3% of health care dollars


- have long term and wide ranging impacts on people


- effect of aging on population have been countered by inteventions to prevent strokes


- as pop ages, impact of interventions expected to plateua, may see increase in stroke rates

Arterial Territories and Stroke Localization - 4 major? each with?

- 4 major arterial territories, each with own symptom signature

Cerebral Vascular Anatomy - Extracranial


- aortic arch is the?


- EC circulation includes? (2)


- VAs arise from? (2)

- aortic arch is the origin of all cerebral blood supply


- extracranial cerebral circulation includes internal carotid arteries and vertebral arteries


- vertebral arteries arise from common carotid arteries and subclavian arteries

Cerebral Vascular Anatomy - Intracranial


- includes the? location?


- connects?

- intracranial circulation includes circle of willis:


= circle of anastomoses at the base of the brain, connecting the right, left, anterior and posterior circulations

Cerebral Vascular Territories - Main - Brainstem


- supplied by? (2)

- supplied by basilar and vertebral arteries penetrating brances

Cerebral Vascular Territories - Main - Cerebellum


- supplied by? (3) P/A/S

- supplied by:


= PICA = posterior inferior cerebellar arteries


= AICA = anterior inferior cerebellar arteries


= SCA = superior cerebellar artery

Cerebral Vascular Territories - Main Cerebral Arteries? (#) = A/M/P

= ACA = anterior cerebral


= MCA = middle cerebral


= PCA = posterior cerebral arteries

Cerebral Vascular Territories - ACA mainly?


- MCA mainly? PCA mainly?



Cerebral Vascular Territories - Deep Brain Structures


- includes? perfused by? (2)


- Thal - perfused by top of? and the?

= BG = largely perfused by MCA and perforating arteries


= Thalamus = perfused by the top of the basilar and proximal perforating arteries

ACA - Supplied and Syndrome


- supplies medial?


- ischemia leads to CL? leg vs arm and face?

- ACA supplies the medial portion of the frontal and parietal lobes


- ACA ischemia leads to:


= contralateral hemianesthesia and hemiparesis


= leg affected more than the arm or face

MCA Supply - supplies lateral? superior?

- MCA supplies the lateral frontal and parietal lobes and superior temporal lobes

MCA Syndrome - ischemia results in?


- CL? face vs leg?


- eyes?


- neglect?


- gaze deviation? due to?

- MCA ischemia results in:


= CL hemianesthesia and hemiparesis, (face, arm > leg)


= CL homonymous hemianopsia


= CL hemineglect and ipsilateral gaze deviation (due to loss of attention-related frontal lobe functions)

MCA Syndrome and Language


- language affected if?


- can have expressive if? lobes? as affect?


- can have receptive if? lobes? as affect?

- language impairment occurs if the dominant hemisphere is involved


- expressive aphasia = lesions in the left posterior-inferior frontal love = Broca's area


- receptive aphasia = lesions in the left posterior-superior temporal lobe = Wernicke's area

PCA Supplies the inferior? and the? as well as?

- supplies the inferior temporal love and occipital lobe as well as the thalamus



PCA ischemia - results in mainly?

- CL homonymous hemianopsia

Brainstem Syndromes - Basilar Artery territory


- supplies the? (2)


- brainstem contains both?


- tracts carry? side?


- nuclei supply? side?

- supplies the pons and midbrain


- brainstem contains both tracts and nuclei


- tracts carry signal to/from CL body


- nuclei supply ipsilateral head/face structures (except for trochlear nuclei)

Brainstem Ischemia


- lesions involving both tracts and nuclei result in? ips vs CL?


- commonly result in? (4)

- lesions involving both tracts and nuclei result in ** crossed face-body deficits


- see ipsilateral face and contralateral body weakness and/or sensory loss


- commonly results in:


= eye movement abnormalities and nystagmus


= diplopia


= dysphagia


= N/V

Cerebellar Syndromes


- if affects vermis? (2)


- if affect cerebellar henispheres - see ipsi? (2), also? (3)

1) lesions to the vermis = gait ataxia and truncal instability




2) lesions to the cerebellar hemispheres:


= ipsilateral limb ataxia and nystagmus


= vertigo, N, V

Small Penetrating Arteries


- come off of? perfuse?


- affect the? including (CR/IC/DGN)

- small penetrating arteries of the ACA, MCA and PCA or basilar artery territories perfuse deeper structures of the brain


= white matter tracts - corona radiata and internal capsule and deep grey nuclei



Small vessel Ischemia


- result in? causing?


- commonly results in dense? without**

- results in small discrete lesions causing classic syndromes


- commonly results in dense deficits in one modality, **without language or visual impairment

Lacunar Syndromes


- small infarcts in? (5)


- can result in? (3)


- ataxix? which is?


- or clumsy?

- small infarcts in corona radiata, internal capsule, BG, thalamus or pons can result in:


= pure hemi-motor stroke


=pure hemi-sensory stroke


= hemi-sensorimotor stroe


= ataxic hemiparesis = weakness and incoord. of limbs on one side of the body


= dysarthria-clumsy hand syndrome

Top of Basilar Perforators = Thalamic Lesions


- CL loss of? may lead to?


- Dejerine-Roussy Syndrome sees initial? then?

= CL sensory loss is most common, may lead to chronic painful condition


= Dejerine-Roussy Syndrome = initial CL loss of sensation, weeks to months later numbness can develop into severe and chronic pain

Key Points for Vasc Territories and Stroke Localization


- cerebral circulation includes?


- EC vessels from? are? (3)


- IC vessels forms? include (3)


- main three? ac tto?

- cerebral circulation consists of EC vessels in neck and IC vessels


- EC vessels from aortic arch = common carotids, internal carotids, subclavian arteries


- IC vessels anastomose to form Circle of Willis = IC internal carotid arteries, vertebral arteries, basilar arteries


- ACA, MCA and PCA emerge from Circle of Willis to perfuse hemispheres

Key Points for Vasc Territories and Stroke Localization


- vertebral and basilar role?-


- ACA role?


- MCA role?


- PCA role?


- stroke results from?

- vertebral arteries and basilar artery perfuse brainstem and cerebellum


- ACAs perfuse medial frontal and parietal lobes


- MCAs perfuse lateral frontal, parietal, temporal lobes


- PCAs perfuse the occipital lobes and medial and inferior temporal lobes


- stroke results from loss of blood flow to an area of the brain causing a neurological lesion that is confined to a vascular territory

Key patterns of Stroke Localization


- ACA sees combo of? seen more in?


- MCA seen combo of? side? also includes? (3) some dysfunction of? if?


- PCA - CL? no? if thalamus, get?

1) ACA = combo of CL hemiparesis and hemianesthesia, leg> face, arm




2) MCA = combo of CL hemiparesis, hemianesthesia (face, arm> leg), CL hemianopsia and gaze deviation, CL hemineglect and language dysfuction (left hemisphere)




3) PCA strokes = CL hemianopsia without motor or sensory deficit, hemisensory loss if thalamus is involved

Braimstem Strokes - due to? (2)


- combo of?


- CS/ eye? dys? N/V?

- due to basilar and vertebral arteries


- combo of:


= crossed symptoms


= eye movement abnorms and nystagmus


= dysphagia


= N/V

Cerebellar Strokes - combo of?


- G/TI/ Ipsi?


- also see? (3)

- combo of:


= gait ataxia, truncal instability


= ipsilateral limb ataxia


= nystagmus, vertigo


= N/V

Lacunar Strokes


- result from?


- pure HM? HS? SM?


- Ataxic? or?

- result from small infarcts in deep brain structures


- pure hemi-motor stroke


- pure hemi-sensory stroke


- hemi-sensorimotor stroke


- ataxic hemiparesis


- dysarthria = clumsy hand

Mechanisms of Ischemia


- common pathway is?


- main etiologies = (4)

- common pathway = insufficient blood flow to perfuse cerebral tissue leading to irr. neuronal damage


- main etiologies:


= thrombosis


= embolism


= hemorrhage


= systemic hypoperfusion

Thrombosis


- formation of a? in an? causing?


- triggered by?


- from? inherently?


- plaques can? or? to expose?


- leading to?

- formation if clot or thrombus in an artery persisting long enough to cause ischemic insult to cerebral tissue it supplies


- triggered by local pathology in endothelium:


= atherosclerotic plaques - inherently pro thrombotic


= plaques can rupture or ulcerate exposing contents with highly thrombogenic properties = leads to in situ thrombosis at site of ulceration

Internal Carotid Artery and Atherosclerosis


- ICA is a? due to buildup of? leading to?

- ICA common sites of Athero related to strokes


- plaque buildup at common carotid junction and ICA leads to reduced blood flow to brain

Embolism


-formation of? which then? lodging in?


- common sources (A/C)


- causes of those (1/ 3)

- formation of clot/thrombus in an other area of circulation, which then travels to cerebral circulation lodging itself in a smaller vessel and occluding it


- common sources of embolism:


= artery to artery = from athero plaque


= cardiac to artery = atrial fibrillation, valvular disease (mech, infection, masses), poor cardiac function

Intracerebral Hemorrhage


- common cause?


- Amylood Angiopathy is a? that? leads to?


- results in loss of?

- hypertension is a common cause


- Amyloid Angiopathy = vasculopathy that weakens vessel walls leading to spont rupture and large lobar hemorrhages


- results in loss of perfusion of territories distal to ruptured vessel

Systemic Hypoperfusion


- generalized? leading to?


- commonly due to?


- leads to global?

- generalized loss of arterial pressure leads to systemic HP that includes the brain


- commonly due to cardiac arrest


- leads to global brain hypoperfusion and brain anoxia

Key Points of Stroke Etiology


- caused by?


- related to either?


- results if? both related to?


- athero? cardiac?


- 30% are?

- caused by blood flow interruption, leading to ischemia and brain dmamage


- related to blockage (ischemic strokes) or rupture (hemorrhage) of a vessel


- result if presence of a clot that formed locally or came from another area, both related to stroke RFs due to:


= athero changes in large and small arteries of brain


= abnormal cardiac function = Afib, abnormal valves or abnormal wall movement from MI




**30% cryptogenic strokes = no cause identified

Ischemic stroke Etiologies


- 45% are? due to?


- 20% are? due to a?

- 45% are atherosclerotic = small or large vessel disease, due to athero thrombotic or embolic events


- 20% due to cardiogenic = cardio-embolic event

Stroke RFs - Modifiable = (8)


- related to both?

- related to arteries (AS RFs) and heart (cardiac sources)

- related to arteries (AS RFs) and heart (cardiac sources)

Stroke RFs - non-mod = (4)



Hypertension


- is the most important?


- risk of stroke increase with?


- for each 10 mmHg reduction? until?

- single most important modifiable risk factor for stroke


- risk of stroke increases linearly with increases in systolic or diastolic BP


- 30% reduction in stroke risk for each 10 mm Hg of sbP or 5 or dBP


- effect maintained down to BPs of 115/75

Hypertension and Stroke


-lowering BP helps to?


- greatest drop with?


- optimal targets havent? want?


- combo = use of? (P/I_

- lowering BP reduces stroke risk in both hypertensive and normotensive patients = PROGRESS trial - see greatest drop with combo therapy


- optimal targets have not been formally defined through RCTs, want > 140/90 or 130/80 for diabetics


- *** combo = use of Perindopril and Indapamide

Lowering BP should be considered for? (2)


- good for both?

- considered for patients with history of stroke or TIA, irrespective of baseline bp


- lowering BP reduces stroke risk across all ages in both hyper and normotensive patients

Diabetes - poorly controlled leads to? such as?


- bad for?


- high risk of? both?


- tied to?


- target?

- poorly controlled glycemia leads to microvascular and macrovascular complications as elevated blood glucose bad for vascular endothelium


- diabetics have high risk of vascular events, both cerebrovascular and cadiovascular


- risk in diabetes tied with hypertension, have strict target of <130/80


- target fir glycemic control is HbA1c < 7%




* negative effect of hypertension is compounded in diabetes

Dyslipidemia


- strong relationship between?


- fibrates act to? yet no effect on?


- more effective? which lower?

- strong relationship between dyslipidemia and atherosclerosis


- fibrates reduce cholesterol but have not shown a beneficial effect on stroke, pref. effect on reduction of triglycerides, do reduce CV risk


- statins most effective at reducing stroke risk, via reducing LDL

Statin Therapy and Dyslipidemia


- statins resulted in? via?


- each 10% decrease in? saw?

- statins results in 25% reduction in vascular events, Heart Protection Study


- each 10% reduction in LDL reduces stroke risk by 13%


- risk reduction increases with increases doses, seen via Treating New Targets Study and SPARCL study

Targets for Stroke Prevention


- stroke prevention guided by?


- for high risk, LDL <? TC:HDL <?


- secondary, want LDL? TC:HDL? LDL reduction of?

- primary stroke prevention guided by Framingham, for high risk LDL <2.0, TC:HDL< 4.0


- secondary stroke prevention, want LDL <2.0, TC:HDL< 4.0 and 50% LDL reduction

Dyslipidemia Key Points


- strong relationship between?


- statins are the only? % decrease?


- most beneficial in?


- effect is?

- strong relationship between dyslipidemia and atherosclerosis


- statins are the only lipid lowering therapy that reduces stroke risk


- statins result in reduction of 25% across all levels of risk, most beneficial in high risk patients and for secondary prevention but will also benefit lower risk patients, in primary prevention


- statins have dose dependent effect, higher doses more effective

Lifestyle Modifications


- essential part of? often?


- includes? (5)

- essential part of approach to lowering risk of first or recurrent stroke, often underestimated


- include:


= smoking cessation


= diet = low Na, low fats, high fiber, limit alcohol


= weight loss


= exercise


= obstructive sleep apnea assessment

Heart - Atrial Fibrillation


- common? %? over age?


- causes? forms in?


- results in more? higher?


- most common cause of? age?

- common arrhythmia present in 14% of patients over 75 years of age


- causes stroke via embolization of thrombus forming in left atrium


- results in more severe strokes with higher morbidity and mortality


- most common cause of stroke in population > 80 yo

Benefits of Anticoagulation


- reduces risk in?


- superior is? yet increased risk of?


- dosing of warfairn must?


- requires? many?

- reduces stroke risk in Afib


- warfarin superior to ASA, 68% reduction with warfarin compared to 19% of ASA, yet see increased risk of major bleeds


- dosing of warfarin adjusted to maintain an INR between 2-3


- requires regular blood tests, see many interacitons with meds and food

Alternatives to Warfarin


- includes = D/A/R - ban


- shown to be?


- lower?


- are easier? no? less? require good?

- include dabigatran, Apixaban, Rivaroxaban


- as effective or superior to warfarin


- lower risk of bleeding complications


- these are easier to use, no INR to monitor, standard dosing, require good renal function

Afib key points


- major? especially in?


- assoc with?


- once diagnosed, should be?


- screening?

- major stroke RF in elderly


- assoc. with more severe strokes and higher stroke mortality


- once diagnosed, should be treated with oral anticoags


- patients over 80 presenting with stroke should be screened for Afib

TIA definition


- self-limited? resulting from? no?


- symptoms can be? high ris of?


- treat as strong?

- self-limited episode of neurologic dysfunction resulting from focal temporary cerebral ischemia without infarction


- symptoms can be of variable duration, high risk for stroke within next 90 days


- treat as strong risk of stroke after TIA

Approach to Stroke Prevention


- manage? such as?


- treat? such as?

1) manage RFs = atherosclerotic and cardiac


2) Treat established problems = antipt medications, carotid artery disease

Managing Modifiable RFs


- treat? start? aiming for?


- screen for? target?


- for Afib?


- discuss?

- treat hypertension


- start a statin aiming for 50% reduction in LDL and LDL <20, TC:HDL <4.0


- screen for diabetes and treat target of HbA1c <7%


- anticoag for Afib


- discuss and encourage lifestyle modifications

Treating Established problems


- atherosclerotic plaques have? can be a?


- Antipts are used to reduce?


- common site? can?

- atherosclerotic plaques have thrombogenic properties and can be focal source of thrombus formation


- Antipts are used to reduce stroke risk by reducing the potential for thrombus formation on atherosclerotic plaques


- internal carotid arteries are a common site of atherosclerosis - severe narrowing assoc. with high risk of stroke, can be treated surgically

Benefits of ASA - reduced? saw small?


- absolute benefit is? but good as? (3)


- dose should be? standard is?

- ASA reduced risk of recurrent stroke and ICH risk only slight increased


- absolute benefit small but:


= widely available intervention


= low cost


= minimal adverse events




* at any dose over 30 mg, equally effective in preventing vascular events after stroke, lower doses have fewer bleeding events


- standard therapy is 81 mg PO daily

Newer Antipts = Aggrenox = ?


- slighlt better than? but caused?

= Dipyramidole + ASA


- slightly better than ASA, but more discontinuation due to HA


- ESPS and ESPRIT trials

Newer Antipts = Plavix - also known as?


- better than? no benefit of adding?

= Clopidogrel


- slightly better than ASA, equiv to Aggrenox


- no added benefit of adding ASA

First Line Antipt therapy


- ASA/Plavix/ Aggrenox = at?


- generally start? in? more?

- ASA 81 mg daily, Plavix 75 mg daily, Aggrenox 1 tab bid


- generally start ASA in antipt naive patients, most cost-effective

Second Line Antip Therapy


- plavix ar? or?


- generally used when?


- considered a?

- plavix 75 mg daily or Aggrenox 1 tab BID


- generally used when patients on ASA present with stroke or TIA


- considered failure of ASA, these agents slightly superior

AntiPt Key points


- ASA at? prevents? small? but good as?


- Plavix and Aggrenox are better? but need to?


- start ASA after? in? switch once?


- not recommended to have?

- ASA 81 mg prevents recurrent strokes, small absolute effect but widely available, low cost, minimal SEs


- plavis and Aggrenox are better than ASA but need to consider cost and SEs


- start ASA after stroke or TIA, in patients not on any antipt therapy


- switch to Plavix or Aggrenox after stroke or TIA, for paitnets who have event on ASA




* long term dual antipt therapy not recommended

Carotid Disease Management


- can be done via? (CS/CE)


- CE reduces? yet benefir?


- should do following? goal to?


- if younger than 70?

- via carotid endarterectomy and carotid stenting


- CE reduces risk of recurrent stroke, yet benefit of surgery decreases with time


- should do following TIA, goal should be to operate within 14 days


- up to 70, no diff between stenting and endarterectomy, over 70 slight CE benefit

Carotid Revasc Key Points


- all patients with >50% symptomatic carotid stenosis should?


- benefit depends on?


- over 70%?


- 50-69%?

- all patients with >50% symptomatic carotid stenosis should be considered for CE or stenting


- benefit from CE depends on degree of stenosis, delay to surgery afetr events


- patients with symptomatic stenosis over 70% benefit most from surgery, revasc and should be referred


- paitents with 50-69% stenosis should be assessed


- ideally patients treated within 2 weeks of stroke symptoms

Key Points of Stroke, TIA management


- treat? start? revasc at? give? for?


- lower?


- add?


- screen and treat?

- treat early


- start antipt agent


- revasc ICA stenosis of 70%


- anticoag Afib


- lower bp (<140/90)


- add a statin (50% LDL reduction)


- screen for and treat diabetes (HbA1c <7%)

Acute Management of Major Ischemic Strokes - Thrombolysis


- most signif? had 6?


- TPA =? known as a?


- time window is?

- most signif advance in stroke care, 6 landmark RCTS (Atlantis)


- TPA = tissue plasminogen activator = clot busting drug


- ** time window for benefit of tPa is within 4.5 hours of stroke onset

Risks of TPA


- risk of? =? increases with?


- odds of dying werent?


- requires?

- ICH risk of 5%, risk of ICH assoc. with increasing age


- overall odds of dying were not increased however


- requires careful selection of patients

Key Pints for Thrombolysis


- tpA can be used within? try to?


- restoring? to improve?


- non-neg?

- tPa can be used within 4.5 hours of stroke onset to try to reverse a clot and restore blood flow to brain


- restoring blood flow limits extent of ischemic damage to brain and improves outcomes


- non-neg risk of significant bleed

Endovascular Therapy = ? also known as a?


- extraction of? from? with?


- need to? time from onset?

= Embolectomy = catheter cerebral angiogram

- extraction of a clot from larger proximal vessels of anterior circulation in addition to tPa


- need to carefully select paitents, up to 6 hours from symptom onset

Key Points for Embolectomy


- time with tpA? to?


- time without tpA?


- improves? leading to?


- requires careful?

- used within 4.5 hours of stroke onset in combo with tpA to restore blood flow to brain


- used within 6 hours of stroke onset without tPA, extending treatment window


- improves rates of early recanalization leading to improved outcomes


- requires careful selection of patient = based on clinical and radiological criteria

Practical Guide to CNS Tumours


- if it is CNS - ask whether it is? (3)


- if intra-axial - ask if it is?


- if within parenchyma - is it? is it even a?

- if it is in CNS = is it intra axial? (within brain parenchyma), extra-axial? or intraventricular?


- if intra-axial - is it above the tentorium or below it?


- if within brain parenchyma - is this a primary tumor or met? is it a tumour?

CNS Mass Lesions in Adults


- tumour =?


- vascular = (3)


- infectious = (3)


- inflammatory = (2)

- tumour = primary, met


- vascular = AVM, cavernous malformaiton, aneurysm


- infectious = bacterial or fungal abscess, tuberculoma, parasite


- inflammatory = MS, vasculitis

Where Can lesions Be?


- Extra axial = (3) = M/ HP/ Mets


- Intra axal = G/Me


- IntraVent = CPT / M / Me?

1) Extra axial = Meningioma, Hemangiopericytoma, Mets


2) Intra-axial = glioma, mets


3) Intra-ventricular = choroid plexus tumour, meningioma, mets

Posterior Fossa Tumours in Children


- Intra axial = Pil Astro? Ependy? Medullo?


- Intravent = CPP? CPC?

1) intra axial = Pilocytic Astrocytoma, Ependymoma, Medulloblastoma




2) Intraventricular = choroid plexus papilloma, choroid plexus carcinoma

Piloctic Astrocytoma - commonly occurs in?


- manifests as? (2)


- in children, common in? can also be in?


- Grade 1 = ?


- imaging - see? may have strong?

- most commonly occurs in children and manifests as hydrocephalus or cerebellar dysfunction


- in children, most commonly occurs in posterior fossa, but may occur in brainstem or along optic tract/nerve


- WHO Grade 1 Astrocytoma = non-infiltrative


- Imaging = cystic lesion with mural nodule - may have strong contrast enhancement**



Pilocytic Astrocytoma


- pathology is? with compact? fibers?


- goals of therapy?


- outcomes - 5 year?

- pathology is biphasic appearance with compact fascicles of bipolar cells, loose mesh interspersed, Rosenthal fibers


- goals of therapy = if safe, surgery


- outcomes = 90% 5 year progression-free survival

Glioma Grades



Pediatric/Posterior fossa Tumour Guidelines


- #1 = pediatric tumours occur in?


- #2 = Posterior fossa tumour present with? (2)


- #3 = WHO Grade 1 tumours are? curable via?

#1 - Pediatric tumours occur in the posterior fossa


#2 - Posterior Fossa tumours present with cerebellar signs or hydrocephalus


#3 - WHO Grade I tumours are non-infiltrative and surgically curable



Oligodendroglioma


- most commonly present with?


- typically arise within? opposed to?


- WHO Grade II = ? surgery isnt?


- imaging - on CT see? on T1? on T2?

- most commonly present with seizure (50-80%)


- typically arise within the cortex as opposed to subcortical white matter


- WHO Grade II tumour = infiltrative, surgery not curative


- imaging = calcification of CT, dark on T1, bright on T2, does not enhance

Oligodendroglioma


- pathology = appear? vasculature?


- defined by presence of? loss of?


- goals of therapy are? maintain?


- outcome of survival is? with (3)

- pathology = fried egg appearing cells, chicken-wire vasculature


- defined by presence of IDH mutation and loss of 1p and 19q chromosomes


- goals of therapy = prolongation of disease remission and maintenance of neuro function


- outcomes = overally survival 8-16 years with surgery, radiation and chemo




** inevitably undergo malignant degen



IDH1 Mutation - IDH1 is foind in?


- mutation seen in? mutations result in decreased ability to? loss of? leads to?


- assoc. with dysregulation of?


-thought to be?

- IDH1 = isocitrate dehydrogenase 1, found in cytoplasm


- mutation seen in Oligoden, mutations results in:


= decreased ability to produce NAPDH, loss of substrate leads to DNA hypermethylation




*IDH mutations assoc. with dysregulation of glial differentiation and global histone methylation


*thought to be one initial hit in gliomagenesis

Tumours Guidelines


#4 = if infiltrative, are?


#5 = low grade tumours present with? rather than?


#6 = appearance on CT? T1? T2?


#7 = low-grade tumours dont? on CT have?

#4 = infiltrative gliomas (WHO grade II-IV) are incurable


#5 = low grade tumours present with seizure rather than neuro deficits


#6 = tumours are hypodense on CT, hypodense on T1 MRI and hyperintense on T2 MRI


#7 = low-grade tumours do not enhance and have calcification on CT

Secondary Glioblastoma


- accounts for %?


- may present with? (4) H/ND/S/raised?


- Grade? are? not?


- imaging - present as?

- accounts for 20-30% of all glioblastomas


- may present with HA, neuro deifcits, seizure or raised ICP


- WHO grade IV tumour - infiltrative, not curative surgery


- imaging = heterogenous enhancing mass

Secondary Glioblastoma


- pathology - see areas of? with pockets of?


- goals of therapy are?


- outcome include survival of?

- pathology = areas of low-grade tumours with pockets/sheets of malignant degeneration


- goals of therapy = achievement of disease control and maint neuro function


- outcomes = overall survival 12-14 months

Glioblastoma


- by definition is?


- treatment includes? with daily (2)

- by definition is an infiltrating cancer


- treatment - Stupp Protocol, with TMZ daily and RT

Glioblastoma and MGMT Methylation


- MGMT is located on?


- encodes a?


- target site for?

- MGMT = located on chromosome 10q26


- encodes a DNA-repair protein that removes alkyl group from O position of guanine = target site for chemo-induced DNA alkylation

Tumours Guidelines


- #8 = low grade gliomas will?


- #9 = if malignant?


-#10 - rapid symptom progression assoc. with?

#8 = low-grade gliomas will invariably progress to glioblastoma


#9 = malignant tumours enhance


#10 = rapid progression of symptoms is assoc. with increased malignancy

Tumour Summary

Tumour Summary

Epilepsy Epi


- active prevalence is?


- active means?


- 5% of people by?

- active prevalence is 4-7/100 (active = getting treatment or seizures within 5 years)


- 5% by age 80, increases past 60

Epileptic Seizure is? Epilepsy is?


- ES is transient? due to abnormal?


- epilepsy is disorder of? generate?


- must have had?

- ES is transient occurrence of signs and symptoms due to abnormal excessive synchronous neuronal brain activity


- epilepsy is a disorder of the brain with an enduring predisp, to generate epileptic seizures


- in a patient who has had at least one seizure

Focal Seizures


- conceptualized as? limited to?


- there may be discretely? or more?

- conceptualized as originating within networks limited to one hemisphere


- these may be discretely localized or more widely distributed

Generalized Seizures


- originating at some point within?


- both?


- can include both? but not necc?

- conceptualized as originating at some point within, and rapidly engaging, bilaterallly distributed networks


- can include cortical and subcortical structures, but not necessarily include the entire cortex

Seizure Classification


- focal = (2)


- generalized means?


- unknown means?

1) Focal = motor vs non-motor


2) Generalized = motor vs absence


3) Unknown Onset = motor vs non-motor

Childhood Absence Epilepsy


- is known as?


- seen in? may have?


- ages? peak?


- prior hx of?


- frequent daily? usually? can be provoked by?



- genetic generalized epilepsy


- cognitive normal children - may have ADD or learning difficulty


- ages 2-12 (peak 5-6 years)


- prior hx febrile seizures


- frequent daily absence seizures, usually brief <10 seconds, can be provoked by hyperventilation


- GTCs may occur, usually later after adolescence


- imaging = normal

Juvenile Myoclonic Epillepsy


- onset at? occasionally evolve from?


- normal?


- 5% have?

- onset 8-25 years of age, occasionally evolve from CAE


- normal cognition and development


- febrile seizures = 5%



Seizures of Juvenile Myoclonic Epilepsy


- myoclonic seizures are a? often occur within?


- generalized? seen in? often preceded by?


- absence seizures seen in? time? less frequent than?

1) Myoclonic Seizures


= mandatory feature of syndrome, often occur within 30-60 minutes of awakening




2) Generalized Convulsive Seizures


= 90% of patients, often preceded by myoclonic seizures




3) Absence Seizures


= 1/3 of patients, briefer (3s) and less frequent than in CAE or JAE

Epilepsy with Generalized Tonic-Clonic Seizures- known as?


- genetic?


- normal?


- infrequent? at age? occur within?


- often provoked by?


- require?



- "Grand Mal Seizures on Awakening"


- genetic generalized epilepsy


- normal cognition and development


- infrequent generalized convulsions starting 11-20 yo, predom. these occur within 1-2h of awakening


- often provoked by sleep deprivation, fatigue, alcohol


- require lifelong therapy

DD for Spells


- S/ C/ M/ S/ Dec/ Movement/ Psych?

- seizure


- cardiac = syncope, cardiac arrythmia, PE


- migraine


- stroke/ TIA


- decerebration


- movement disroder = paroxysmal kinesigenic/nonkin choreo


- psychogenic nonepileptic event

Epilepsy historical Interview


- warning? any? such as? or any?


- precips = S/A/W/ chnage in? lack of?


- ask about health at?

- Warning with seizure - presyncopal sensation? olfactory or epigastric or deja vu aura? hallucinations?


- Precipitating factors - sleep deprivation? alcohol consumption? withdrawal? positional change? dehydration? painful?


- Health at seizure onset? febrile, confused? HA?

Patient History


- positive = S/J/S/A/ deviation of?


- any post-ictal? (3)

- Positive Phenomenology - shaking? jerking? stiffening? flashing light auras? head deviation? automatic behaviour?


- Post-ictal confusion? tongue-biting? urination?



Patient history - Predisp. Factors for Remote Sympt Seizures include?


- insult of? type of seizure? previous? traumatic? FH of?

- predisp. factors for remote symptomatic seizures:


= birth insult


= febrile seizures


= meningitis/enceph


= traumatic brain injury


= FH or epilepsy

Prior history of Seizures?


- ask about time? if any? spells where? lose? become? act as? awaken with?


- about 50% of patients with first seizure have?

- frequency - times a month?


- experience of auras?


- spells where space out? lose awareness? become confused? are lost?


- awaken with tongue-biting? urinary incontinence? pillows on floor?




** about 50% of patients present with first seizure have evidence of having had a prior seizure that was unrecognized as such

Potential Causes


- acute intoxication - due to? (6)


- remote symptomatic, such as?

- Acute precipitants = drug intoxication, drug withdrawal, metabolic derangement, meningitis, brain abscess, ICH/SAH/ Venous sinus


- Remote symptomatic = sequelae of stroke, ICH, SAH, enceph, febrile seizures, tumour, focal cortical dysplasia

Investigations for Solitary Seizure


- general?


- labwork = (8)


- EKG - look for?


- also perform?

- general system and neuro exam


- labwork = CBC, lytes, MG, Ca, glucose, urea, Cr, tox screen, LP


- EKG = long QT syndromes, Brugada, Holter, Echo, Cardio


- EEG


- Neuroimaging

EEG - Diagnosis- helps with?


- look for presence of? to confirm?


- type? can help?

- helps with diagnosis:


- presence of epileptiform abnorm will confirm suspicion of epileptic events if clinically consistent with seizures


- type of epileptiform abnorms can help classify the epilepsy syndrome

EEG - Prognostification


- if negative, 27% risk of?


- if positive, 50% risk of?

- if negative, 27% risk of recurrent seizures in the next 5 years after a 1st isolated seizure


- if positive, 50% risk of recurrent seizures in the next 5 years after 1st isolated seizure

Sensitivity of Interictal Epileptiform Discharges (IEDs) for Epilepsy


- Initial EEG - IED seen in?


- repeat EEG - IEDs seen in?




** negative EEG doesnt?

- Initial EEG = IEDs seen in 29-55% of patients


- Repeat EEG = IEDs ultimately seen in 80-90% of patients




* negative EEG does not rule out epilepsy

Neuroimaging and Epilepsy


- imaging abnorm found in?


- should get an? unless?


-do for?

- CT/MRI signif abnorm found in about 10% of paitents


- should get MRI unless you know its primary generalized epilepsy syndrome


- do for brain tumours, vascular malforms, neurocyst, mesial temporal sclerosis

Predictors for Recurrent Seizures


- look for epileptiform abnorms on?


- look for prior? such as?


- post-ictal?


- prior seizure risk is?


- multiple seizures in first 24 hours?

- epileptiform abnormalities on EEG


- known etiology, remote symptomatic = prior head injury, prior stroke, mental retardation, CP, tmour


- post-ictal Todd's paresis


- prior seizure = after 2nd sz, recurrence risk is 70%


- multiple seizures in first 24 hours are not predictive of recurrence

JME made worse by? (3)


- myoclonus can be exac by?

- can be made worse with CBZ, OCX, GBP


- myoclonus can sometimes be exacerbated by use of LTG

Initiation and Dosing



Phenytoin Dosing


- for emergencies, give? IV


- otherwise give? may need?


- pharmaco is? small dosing changes can? may need to?

- for emergencies = 20 mg/kg load oral or IV - max of 50 mg/minute


- otherwise = 300 mg po daily, may need titrating upwards or downwards to get levels into therapeutic range


- phenytoin exhibits non-linear pharmso a certain point, small change in dosing can result in dramatic chnages in levels, may need to change doses in small increments

Phenytoin Adverse Effects


- CNS - see N/A/D? little effect on? enceph with? can cause?


- in GI - should give?

- CNS = nystagmus, ataxia, drowsiness, modest to little effect on cognition, encephalopathy with toxic range doses, movement disorders (dyskinesia, choreoathetosis)


- GI = helped with admin with meals

Phenytoin Chronic Adverse Effects


- dysfunction of?


- periph?


- cosmetic? 20% of? results in?

- cerebellar dysfunction - may be rare complication of PHT intox


- peripheral neuropathy


- cosmetic - gingival hyperplasia - 20% of pts, hirsutism, coarsening of facial features

Phenytoin Idiosyncratic Reactions - can cause? (6)

- rash, fever, leukopenia, lymphadenopathy, SJ syndrome, hepatitis, SLE

Contraindications to Phenytoin


- hypersens to?


- ULD?


- acute?


- heart = (2 - SBC/AVB)

- hypersensitivity to hydantoin drugs


- Unverricht-Lundbord Disease


- Acute intemittent porphyria


- sinus bradycardia, AV block, Stokes-Adams Syndrome

Carbamazepine Dosing


- stating dose of? usual adult dose is?


- titration time is?


- start with? then give? then increase by? for day #?


- get to?

- starting dose of 200 mg/day


- usual adult dose of 600-1600 mg/day


- titration time to maintenance = usually 7-14 days


- regular and CR formulations


- SO:


= start with 100 mg po bid x 3 days


= then 100 mg po tid x 3 days


= then increase by 100 mg each 3 days until


= 200 mg po tid * initial target dose

Carbamazepine


- good efficacy against? (2) POS/GTCS


- ineffective against? (A/M)


- dont use in?


- not really useful in? like?

- good efficacy against partial onset seizures and generalized tonic-clonic seizures


- ineffective against absence seizures and myoclonic seizures


- dont use in Juvenile Myoclonic Epilepsy


- not really useful in symptomatic generalized epilepsies like Lennox-Gastaut syndrome or West Syndrome

Carbamazepine SEs - are often?


- GI - causes?


- neurotoxic effect is? (5) - fewer cognitive effects than?

- dose-related SEs


= nausea, Gi discomfort


= neurotoxic effect = dizziness, diplopia/blurred vision, sedation, HA, ataxia, incoordination, fewer cognitive effects than phenobarb or phenytoin

Carb Idiosyncratic reactions


- R/AG/H/H

- hypersensitivity rash


- agranulocystosis/aplasitc anemia


- hepatitis


- hyponatremia

VPA Dosing


- emergencies - can be loaded?


- usually will want to?


- start at?


- increase by? time?


- goal to reach?

- emergencies - can be loaded IV 20 mg.kg IV or even higher


- usually will want to gradually titrate the dose upwards for tolerability


- start at 250 mg po bid


- increased by 250 mg/day each week


- goal in newly diagnosed epilepsy of 750-1500 mg/day

VPA SEs


- hematologic = thromb? abnormal? BMF?


- bone?


- can cause?

- haematologic = thrombocytopenia, abnormal pt function, bone marrow failure, myelodysplasia


- osteopenia, osteoporosis


- hypersens rash


- tertogenicity

Levetiracetam


- can be started at?


- rapid? within?


- push doses to? returns?

- can be started at an initial therapeutic dose


- 500 mg po bid


- rapid onset o faction within first 1-3 days of use


- can push doses u pto 1500 mg po bid, although diminishing returns in seizure control by this point

Levetiracetam Adverse Effects


- somn? D?


- chanhes in? S?


- rare?

- somnolence, dizziness


- behav/ mood disturbs = seen in 13% of patients, suicidal ideation


- hypersens/ SJ reactions rare

Juvenile Myoclonic Epilepsy


- is a triad of? (A/GC/M)


- high rate of? on?


- commited to?


- historical drug choice is? now use?

- triad of absence seizures, generalixed convulsions, and myoclonic seizures


- high rate of seizure freedom on AED


- committed to life long therapy


- historical drug of choice is Valproate


- Lamotrigine is the recommended alternative

Issues in Women with Epilepsy - Teratogenicity


- major fetal malform rate is? increased with many? such as? (3)


- VPA is bery?


- also really bad to use?


- attmept to mitigate with?

- major fetal malform rate in general pop is 2%


- increased risk of malforms 4-6% with many major anticonvulsants = Phenytoin, Carb, Pheno


- VPA very teratogenic, see 10% risk of major malforms


- polytherapy (multiple drugs) also bad 15%


- attempt to mitigate with folic acid 1-5 mg daily

Medications with High Risk for reducing the efficacy of OCP


- P/P/P/C/X/T

- phenobarb, primidone, phenytoin, carbamazepine, Oxcarbazepine, Topiramate

Meds for Epilepsy for Women in OCT - can use depot? L? or copper?


- possibly can use?


- dont use combine? (3)

- can use depot MPA, levonorgestrel, or Copper IUD


- possibly can use combined injectables, Levo/Etonogestel implants


- dont use combined OCP, Prog. only OCP or transdermal patch

Status Epilepticus - definition includes:


= time? of?


- or 2 or more?

- operational definition:


= 5 minutes or longer of continuous seizure


= or 2 or more discrete seizures without complete recovery of consciousness

Classifications of SE


- generalized?


- nonconvulsie = (2)


- focal motor = EPC?


- status?

- generalized tonic-clonic status


- nonconvulsive status = absence status, complex partial status


- focal motor status = epilepsia partialis continua


- myoclonic status

Mortality of Status Epilepticus =?


- variable depending on?


- best predictor?


- age effect?

- mortality for 17-23%


- variable depending on etiology, duration (best predictor of mortality), age (worse if older) and treatment adequacy

Morbidity of Status Epilepticus


- leads to delay of?


- if febrile status, can cause?


- left with?


- changes in?

- neurodevelopmental delay in 34% of children with prolonged status epilepticus


- speech deifcits in children with febrile status epilepticus


- 10-23% of patients with SE left with disabling neuro deficits


- hippocampal chnages seen following SE

Difficulty of Therapy with Time


- in rats, dizaepm good for? but not?


- delays in treat make SE?


- important for?

- rat models = easy to use diazepam to stop sz < 5 min, but not longer seizures


- delays in therapy may make status epilepticus more likely to be refracotry to treatment


- therefore early therapy important to prevent the development of refractory status epilepticus

epilepsy Management Pathway


- manage? perform a?


- check? (2)


- meds?


- diagnose and treat?

- Manage ABCs = O2, IV Access, EKG, labs


- check serum glucose, thiamine if admin glucose


- anticonvulsant meds


- diagnose and treat underlying cause

Anticonvulsant Meds


- timing - once?


- at 6-10 minutes, use? (3)


- at 10-20 minutes? (2)

- timing = once seizure has been established for 5 minutes or more


- Benzos = 6-10 minutes = Ativan, Diastat, Midazolam


- Next line = 10-20 minutes = Phenytoin, Fosphenytoin

Next Line = ICU needed


- give continous? (3 = M/P/P)


- then IV?

1) Contiuous IV Midazolam


2) Cont. IV Propfol


3) Continuous Phenobarb


4) IV VPA

Establishment of Underlying cause


- determine if caused by? (M/Acute? Symptomatic)

- medication reduction/change/ noncompliance in the context of longstanding epilepsy


- acute brain injury = trauma, hem, stroke, sinus thrombosis, mening, enceph, tumour


- symptomatic = metabolic (hypon, hypogly), anoxia, hypertensive enceph, drug, EtOH, EtOH withdrawal

What to Do if First Drug Fails


- consider if have? titrate? try to minimize?


- goal is no? (2)


- you can either? or try to?

- consider if have right diagnosis


- titrate upward as tolerated, minimizing or avoiding SEs


- goal is no seizures, no SEs


- you can either introduce a secoond drug as adjunct, or switch from first drug to second drug

Refractory Epilepsy


- definition is not well controlled after? at?


- 20-40% end up?

- epilepsy not well controlled after 2 appropr. first-line drugs at max tolerated doses


- 20-40% end up being difficult to control on meds alone

Kwan and Brodie Take Home


- should be referred if?


- seizures will continue to be?


- most likely need?

- patients who continue to have seizures after you have tried them on adequate doses of two approp. chosen drugs should be referred on for subspec. care


- their seizures will be difficult to control with med manip alone and their situation needs to be re-eval


- patients in this situation likely need an eval. in an Epilepsy Monitoring Unit (EMU) to confirm diagnosis and to evaluate poss. epilepsy surgery

Epilepsy Surgery


- concept that partial epilepsies may be from?


- surgery to resect? may?


- epileptogenic zone is the minimal?

- concept - partial epilepsies may be the rsult of specific dysfunctional regions of brain that are sites for onset of seizures


- epilepsy surgery to resect these regions of brain may potentiall cure seizures


- epileptogenic zone = minimal amount of cortex needed to be resected to effect a surgical cure of epilepsy

Value of Epilepsy Surgery- chance of seizure freedom is?


- decreased?


- improvement in?

- seizure freedom chance of up to 70-80%


- decreased mortality = standardized mortality is probably 2-5


- improvement in QOL = regaining driver's license and independent, employment, depression scales improve

Getting Referred for Epilepsy Surgery


- is the? average duratino to get to?


- should be refeered to if?

- common perception that surgery is last resort


- patients at times specific. advised against surgery and given dissuasive info aobut surgery, espec. if have serious neuro complications


- average duration of havign surgery before patients have surgery = 20 years


- should be referred to spec. centre if seizure not control not achieved within 9 months by the general neuro

Epilepsy Take Home Points

New Paradigm Shift in Dementia


- new?


- pathology believed to be?


- role of?

- new criteria


- specific distribution of pathology


- pathology present years before clinical signs


- investigation


- treatment

Dementia Criteria


- type of symptoms? that ?


- decline? not explained by?

- cognitive and behavioral symptoms that:


= interfere with work or usual social activities


= represent a decline from prior levels of functioning


= not explained by delirium nor major psych disorder



Dementia Criteria


- cognitive impairment involves at least two of? (4)

- cognitive impairment is detected and diagnosed, involves at least two:


= impaired ability to acquire and remember new info


= impaired reasoning and handling of complex tasks, poor judgement


= impaired visual spatial and abilities


= impaired language functions


= chnages in personality/ usual character




** not a diagnosis

Dementia - seen in? (8)

- seen in Alzheimers, Parkinsons, Frontotemporal Dementia, Primary Progressive Aphasia, Vascular disease, Lewy Body Disease, Huntingtons Disease, Creutzfeld Jacob Disease

Primari Neurodegenrative Diseases include? (6) = A/LB/P/FTD/PS/CB

- Alzheimers Disease


- Lewy Body Disease


- Parksinsons Disease Dementia


- Frontotemporal Dementia (bvFTD, svPPA)


- Progressive Supranuclear Palsy


- Cortciobasal Syndrome

Alzheimer's Disease - on history, see?


- most common presentation? impairment in?


- non-amnestic means?


- AD is the?

- cognitive deficits are evident on history and exam


1) Amnestic Presentation = most common syndromic presentation of AD dementia, see impairment in learning and recall, see cog dysfunction


2) Non-Amnestic Presentation = language, visual and executive dysfunction




** most common cause of dementia

Lewy Body Dementia - see diffuse?


- have dementia, plis 2 of? (3)

- see diffuse atrophy, normal hippocampi


- dementia + 2 of:


= fluctuation


= visual hallucinations


= Parkinsonism

Parksinson's Disease Dementia


- dementia with? two parts are?

= Parkinson's disease (tremor, rigidity) + Dementia

Vascular Dementia - Probable VaD


- have? evidence of?


- clear relationship between?


- severity of CI related to?



= cognitive impairment and imaging evidence of CVD


= clear temporal relationship b/w vascular events and onset of CI


= relationship b/w severity and pattern of CI and presence of diffuse, subcortical CVD


= no evidence for other neurodeg. disorder

Vascular Dementia - Possible VaD


-have? with evidence of?


- no clear?


- insuff? as no?


- may have? however cant test?


- some evidence of?

= cognitive impairment and imaging evidence of CVD but no clear temporal relationship b/w vascular event and onset of CI


= insuff. evidence for dx of VaD because no imaging evidence


= severe aphasia so cannot test but normal before


= evidence for other neurodeg. disorder

Frontotemporal Lobar Degeneration - is a?


- includes? (3) = Beh? Sem? Non-fluent?

- family of syndromes, including:


= behavioral variant FTD


= semantic variant Primary Progressive Aphasia (svPPA)


= non-fluent variant PPA

Behavioral Variant FTD - syndrome of? see change in?


- need three of six? = BD/A/loss of? Com? changes in? also chnage in?

= behav. syndrome, see change in personality


= possible if three of six:


= early behav. disinhibiton


= early apathy or inertia


= early loss of emotional reactivity


= perservative/stereotyped or compulsive


= Hyperorality and dietary changes


= FTD neuropsych profile = executive

Behav Variant FTD - Probable


- on MRI, see?


- presence of?

1) Frontal and/or anterior temporal atrophy on MRI


2) Presence of known mutation

Behav. Variant FTD


- most common of?


- gender?


- onset?


- progress?


- high relationship to?


- assoc. with?

- most common of 3 clinical syndromes (56% of all FTD)


- M:F = 2:1


- earliest age of onset, 58 yo


- progresses most rapidly (3-4 y)


- highest genetic susceptibility


- strongly assoc. with ALS/MND

Primary Progressive Aphasia


- syndrome involving?


- 3 different? = ?

- clinical syndrome that involves language impairments selectively or primarily early on


- 3 syndromes = 2 FTLD syndromes, 1 AD syndrome

Semantic Variant PPA


- presentation determined by?


- if left sided, see? lose?


- right sided, see? altered? loss of?

- hemisphere affected determines presentation


- left-sided atrophy = loss of meaning for words, objects and emotions


- right sided atrophy = behav. syndrome, alterations on social conduct, loss of person-based semantic knowledge, loss of empathy/ability to recognize emotions

Semantic Variant PPA


- %?


- onset age?


- progression?

- <20% of all FTD cases


- shares earlier age of onset with bvFTD


- slowest progression (5.2 yrs from diagnosis to death)

Nonfluent Variant PPA


- disorder of?


- primary sign is? also see? PP/SA


- preserve?


- often develops into?

- disorder of expressive language/speech production


- nonfluent speech + agrammatism, phonemic paraphasias and speech apraxia


- behaviour/ insight preserved early on


- often develops into PSP or CBS

Nonfluent Variant PPA


- %?


- progression?


- intermediate rate of?

-25% of FTD


- intermediate rate of progression (4.3 years from diagnosis)


- intermediate rate of genetic cause

Extending Term FTLD


- originally? which includes (2)


- those added inclide? (MND, CBS, PSP)

- originally FTD = bvFTD,svPPA and nfvPPA


- added to the fold:


= FTD-with motor neuron disease (FTD-MND)


= Corticobasal Syndrome (CBS)


= Progressive Supranuclear Palsy (PSP)

Aiding Dementia Diagnosis


- test? looking for (2) - sens and spec? for?


- amyloid increases with?


- in AD trials, see?

- CSF = A-beta, Tau


- Sens = 91%, Spec = 85%, accuracy 90% for neuritic plaque


- presence of amyloid increases with cognitive decline


** most clinical trials in Alzheimers disease require biomarker positivity before can enroll

Misdiagnosis


- AD is often? yet 11%


- gender role?

- studies showing that AD often misdiagnosed


1) 78% have correct diagnosis, 11% of patients diagnosed with AD did not have it, 11% had it and didnt get diagnosed with it


2) Men more likely to get misdiagnosed because present with behav, language or other non-memory symptoms

Disease Onset Before Clinical Symptoms - seen in both?

- seen in both AD and FTD

Mild Cognitive Impairment - concern regarding?


- impairment seen in? below mean of?


- yet have preservation of?


- not?**

1) Concern regarding a change in cognition


2) Impairment in one or more cognitive domains below the mean for their age and education matched peers on culturally approp. norm data


3) Preservation of independence in functional abilities


4) Not demented

Top Ten DD for Cognition/Behaviour



1) Alzheimer Disease


2) vascular Disease


3) Drugs, Depression, Delirium


4) Ethanol


5) Medical/ Metabolic


6) Endocrine


7) Neurologic


8) Tumor, Toxin, Trauma


9) Infection, Idiopathic, Immunologic


10) Amnesia, AI, Apnea

Goals of Treatment for Cognitive Impairments


- interfere with?


- remove?

- interfere with formation and accumulation of toxic substances


- remove toxic substances

Pharm for Dementia


- no meds to? but meds for?


- make sure to treat, such as?


- review all?

- no meds available to cure or delay signif progression of any dementia, but meds available for symptomatic relief


- treat concomitant medical conditions including infections, parkinsonian symptoms, seizures, pain and improve nut status


- review all meds = incl. alternative

Pharms for Alzheimers Disease


- first give? main one? (A/E)


- then can give antag of? E?


- antideps?


- low doses of?



1. Acetylcholinesterase Inhibitors (AChEIs) = Aricept, Exelon


2. NMDA-receptor antag = Ebixa


3. SSRIs = antideps = Citalopram, Effexor


4. Atypical Antipsychotics =low doses of atypical antipsychotics such as quetiapine, olanzepine or risperidone for agitation, aggression


5. Others = Trazadone, VPA




* many anti-amyloid treatments in clinical trials for Abx and Ace-inhibs

Frontotemporal Dementia


- no? can try to give? or low dose?


- in future?

- no treatments available


- antidepressants


- low dose antipsychotics


- future = protein specific treatments for Tau, Progranulin, and FUS

Parkinson's Disease Dementia and Lewy Body Disease


- give a? such a?


- can also try (ACEI)? (ex/) or?

- dopamine agent, ex/ Sinemet


- anticholinesterase inhibitor, ex/ Aricept, Exelon


- Antidepressant

Vascular Dementia - must control?


- ex/ (3)


- tell to?


- may use?

- control vascular RFs


- ex/ BP, sugars, lipids


- exercise


- +/- Aricept

Dementia Risk is Reducible


- S/ D/ HTN/ edi/ D/ O/ decreased by?


- lots of evidence that?

- diabetes heightened risk by 50%


- smoking heightened risk by 50%


- HTN in midlife increased risk of vascular dementia by 60%


- education lowered risk by 40%


- depression and obesity also increased risk


- PA and cognitive stimulation decreased it




*lots of evidence that dementia risk is reducible

Role of Lifestyle in Dementia


- moderate? assoc with?


- independent of? (6)

- moderate PA, ie more strenuous than walking, assoc. with better cognition in a 25 year follow up


- assoc. with better cognition in old age


- independent of midlife hypertension, smoking, education level, sex, obesity, binge drinking

Dementia and Cognitive Reserve


- role of occupation?


- growing evidence that?

- people who had more complex jobs, remained socially active and avoided depression were also more resilient to Alzheimers




* growing evidence that incidence of dementia has decreased

Diagnosis of Dementia


- begins during?


- patient's?


- informants?

- exam begins during history


- patient's CC, education, work history - attention, speech and language, orientation and insight


- informant's chief complaint and social interaction

1st Symptoms in Dementia


- first symptoms include?


- required for? which is then ndded for?


- important to elicit?

- first symptoms - clue to anatomy and neurophysiology


- anatomy and neurophys clue to diagnosis


- diagnosis required for treatment and prognosis


- eliciting detailed and accurate history is paramount for adequate exam

AD 1st Symptom - is?


- seen with? (4)

- 1st symptom is memory


- missing appointments, losing keys, repeating stories, asking repetitive questions, getting lost

Frontotemporal Dementia - begins in? (3) = AC,I, VPC


- 1st symptom is?


- chnage in? lack of?


- loss of?

- FTD begins in anterior cingulate, insular and ventral prefrontal cortex


- 1sy symptoms in FTD are:


= disinhibition, personality chnage, lack of concern for others, apathy, overeating, executive difficulty- cannot plan/organize, poor judgment

Dementia with Lewy Bodies


- progressive? changes in?


- also see? (VH/P)


- fluctuation?


- affects?

- progressive dementia = Attention, V-S


- visual hallucinations


- parkinsonism


- day to day fluctuation


- REM sleep behav. disorder


- neuroleptic sensitivity

1st Symptoms


- AD =?


- FTD = ?


- DLB =? visual? fluctuations of?

AD - memory, language, executive, spatial


FTD - behavioural


DLB - movement, visual hallucinations, fluctuations, REM motor behaviour

How to Assess Dementia - global? M/L/VS/ EF/ M

- global cognition


- memory


- language


- visual-spatial function


- executive function


- mood/personality

Summary of Dementia


- first symptoms provide?


- pattern of? assoc with?


- need for?

- first symptoms provide clues to underlying neuropathology


- pattern of cognitive deficits are assoc. with specific anatomy and neurodegen. diseases


- accurate diagnosis required for treatment

Approach to CBC - review? (4)


- also look at?


- think about? whether it is?

- review Hb, mcv, WBC coutn and differential


- review pt count


- bone marrow problem?


- production vs destruction? decide?



CBC Abnormalities


- if multiple cell lines affected? such as?


- if single line affected, think? such as?

- if multiple cell lines affected, thick about bone marrow problem, ex/ chemotherapy


- if single cell line affected, think about missing building block or something causing a peripheral destruction of that cell line ex/ iron deficiency

Signs and Symptoms of Anemia


- F/H/L/N/CP/S/T/HF/H

- fatigue


- HA


- lightheadedness


- nausea


- chest pain = ischemia


- SOB


- tachycardia = fast heart rate


- heart failure


- hypotension


- death




* rate of development very important

Approach to Anemia - 2 Key Pieces of Info


- size of? helps to?


- count of? if low? if high?

1) Red cell size = MCV = helps narrow diff.


2) Reticulocyte Count - underproduction (low retics) vs destruction/loss (high retics)

Role of Retics


- retics are? if able to make?


- on blood film, retics present as? (3)


- still contain?

- retics are brand new RBCs


- if able to make retics, means production is okay


- retics on a blood film have increased colour, decreased central pallor and larger size


- retics still contain RNA so we can stain for this to help us count them = Retic count

Exam of CBC = MCV < 80 - means?


- often related to? measure? (2)


- if low? suspect?


- if normal?


- if high ferritin, suspect?

- microcytic anemia, often related to iron, measure ferritin and serum iron


- if low ferritin (<15), low serum iron and high TIBC, suspect iron defic.


- if normal = thalassemia


- if high ferritin (>100), low serum iron and low TIBC, suspect anemia of chronic disease

If MCV 80-100? - called? look at?


- if <2%, may mean? seen in? (2) L/AA


- if >2%? due to? (2)

- normocytic anemia, look at reticulocyte count


- if <2% = hypoproliferative = leukemia, aplastic anemia, pure red cell aplasia


- if >2% = hyperprolif = hemorrhage, hemolytic anemia

Causes of Microcytic Anemia = TAILS = means?

= thalassemia


= anemia of chronic disease = anemia of inflammation


= iron defic - most common cause worldwide


= lead poisoning = rare


= sideroblastic anemia = rare

Iron Indices - ferritin is? reflects?


- Tf is synth in? acts as? known as?


- uptake from? via?


- TIBC is then? used to?

- ferritin is primary iron storage protein and reflects total body iron stores


- transferrin (Tf) is synth in liver, acts as iron transporter = TIBC


- uptake from transferrin is via transferrin receptors


- serum iron/transferrin (or TIBC) = % transferrin saturation used to assess iron overload

Diagnosis of Iron Defic.


- low ferritin diagnostic of? start with?


- decreased MCV usually is?


- would then find decreased? (2)


- increased?

- low ferritin is diagnostic of iron defic = start with ferritin if low, no further testing needed


- decreased MCV usually - MCV falls before Hb but sometimes will fall together, ex/ pregnancy


- dont need to measure but would find decreased retics, decreased serum iron and increased serum transferrin (TIBC)

Diagnosing Iron Defic.


- iron defic warrants?


- ask about? (3)


- ferritin of less than 50 with normal Hb assoc with?


- always treat? even if?


- iron nec. for?

- in males and non-menstruating females, iron defic. always warrants search for blood loss from GI tract


- ask about diet, GI bleeding and GU bleeding


- although most labs report 20-200 normal, ferritin of less than 50 with normal Hb assoc. with fatigue


- treat iron defic. even if not anemic esp. in women of child bearing age


- iron is nec. for normal fetal development

Iron Defic.


- WHO defines iron defc as?


- most common?


- found in?


- result of increased? or?

- WHO defines iron defic. as ferritin < 15 in adults and <12 in children younger than 5 years


- is the most common and widespread nutritional disorder in the world


- 20-25% of humans are iron defic.


- result of increased demand, limited supply and increased blood loss


- disease of women and children

Presentation of iron Defic


- increased? decreased? (2)


- changes in?


- in women of childbearing?

- increased fatigue (ferritin <50)


- decreased physical performace


- decreased cognitive abilities


- irritability and mood chnages


- 40% women of childbearing age have iron defic. (ferritin <30) and 4% IDA

How Does Iron Defic. Affect the Brain?


- decreased, leading to less?


- altered? important in?


- glucose utilization is?


- decreased functioning of?

- decreased arborization of dendrites, decreases interneuronal connections


- altered neurochem and monoaminergic pathway, important in motor control, sleep cycles, learning and memory


- altered bioenergetics - glucose utilization in the brain is highly iron dependent


- decreased functioning of oligos and decreased myelin - effect is not reversible

Treatment of Iron Defic.


- can be given?


- start with? go? try to minimize by?


- if not tolerating?


- IV is?

- iron supplementation can be given po or IV


- start with oral iron, go slow, take iron at bed to try and minimize symptoms and take with source of vitamin C to increase absorption


- try different preparations if trouble tolerating - N/bloating, const. common


- IV iron well tolerated offer to patients if urgent treatment needed or can not tolerate oral iron

Transfuse RBC rule?


- do not? for? without?


- IV or oral iron for?

- dont transfuse RBCs for iron defic. without hemodynamic instability


- preop and patients with chronic iron defic. without hemodynamic instability should be given oral or IV iron

Microcytic Anemia - Anemia of Chronic Disease


- is anemia secondary to?


- most commonly due to? (5)


- can be either?


- caused by? increased? leading to reduced?

- anemia secondary to acute or chronic inflammatory state


- most commonly = chronic infections, IBD, rheum disorders, malignancy, renal disease


- can be microcytic or normocytic


- caused by cytokines that increase hepcidin leading to:


= reduced RBC survival, reduced response to EPO, reduced iron utilization

Anemia of Inflammation Investigations


- if see increased ferritin?


- may also see decreased? (3)


- reduced?

- see increased ferritin = retics will be inapprop. low for the anemia


- decreased serum iron, decreased TIBC, and decreased % transferrin saturation


- soluble transferrin receptor - normal in anemia of inflammation but increased in IDA


- inapprop. reduced EPO level

Treatment of Anemia of Inflammation


- treat the?


- give EPO at?


- may need?


often difficult?

- treat underlying disorder


- EPO = 150-200 IU/kg 3x week, or 40,000 once/week


- may need po/ IV iron also


- often difficult to treat


- Hepcidin inhibitors in development

Thalassemia is abnormal?

- abnormal production of Hemoglobin

Macrocytic Anemia Approach - MCV is?


- check to see if? (2) on?


- if present? means? either?


- if not present? (4) - A/MDS/LV/CBM

- MCV < 100


- check to see megalocytes and segmented neutrophils on peripheral smears


- if present = megaloblastic = Vit. B12, folate defic or drug-induced


- if absent = alcohol abuse, myelodysplastic syndrome, liver disease, congenital bone marrow failure

Macrocytic - Check to see if?


- looking for?


- if nonmegalo, see?

- check to see if megaloblastic blood film - look for oval macrocytes and hypersegmented neutrophils


- nonmegalo blood film= round or oval macrocytes

Megaloblastic Anemia


- characteristic?


- cells cannot? due to?


- cause mainly by? (2)

- characteristic bone marrow morphology of open chromatin


- cells can not mature due to defective purine and pyrimidine production


- caused by B12 defic, folate defic, cytotoxic drugs, rare genetic disorders

B12 (Cobalamin) Defic


- B12 found in? absorbed by?


-body stores?


- assoc with abnorms of? (3)


- see? (MA/P)


- on blood film?

- found in animal products, also synth by microorgs


- absorbed via intrinsic factor


- body stores last for 3-4 years


- assoc. with psychiatric, neuro and hematologic abnorms = macrocytic anemia and panctyopenia


- oval macrocytosis and hypersegmented neutrophils on blood film

Causes of B12 defic


- strict?


- unable to? seen in?


- no? called? or have had?


- infections of?

- strict vegan


- unable to absorb = terminal ileum disease


- no IF - pernicious anemia or gastric surgery


- GI infections - tapeworm, bacterial overgrowth

Pernicious Anemia


- lack of? due to?


- not? classicaly described as?


- measure?(2)


- before a?


- treat with?


- may see no improvement of?

- lack of intrinsic factor due to autoantibodies


- uncommon


- classically described as lemon yellow


- measure B12 (10% falsely normal) and IF antibodies


- OGD and biopsy


- trat with high dose IM or po B12


- psychiatric symptoms may not improve

Non-Megaloblastic Causes of Macroytic Anemia


- other (4)

- myelodysplastic syndrome


- possibly retics = bleeding or hemolysis


- liver disease


- hypothyroidism - uncommon

Destruction of RBCs - if destroyed too soon?


- if enough retics made, see? therefore can be?

- destroyed to soon = hemolysis


- if enough retics made, can see increased MCV - can be macrocytic or normocytic

Approach to Normocytic Anemia - Need?


- if low, cant? =? such as?


- or secondary =?


- make diagnosis with?

- need retics


- if low retics = cant make new RBC effic.


= primary bone marrow failure = aplastic anemia


= secondary bone marrow failure = HIV infection



*diagnosis made via bone marrow aspriate and biopsy



If have low retics, may have low? secondary to?


- need to determine?

- may also have low EPO secondary to renal failure


- diagnosis = need EPO levels

Hemolysis - Extra vs Intra


- extravascular means? destoryed by?


- intravascular means?


- when hemolysis occurs?

- Extravascular = RBCs dont make it to 120 days, destoryed by reticuloendothelial system


- Intravascular = abnormal process leading to red cells being destroyed within Bvs




*when hemolysis occurs, red cell contents spill out

Investigations for hemolysis


- destruction of RBCs leads to increase? (3)


- decreased?

- destruction of RBCs leads to:


= increeased retics, increased bilirubin, increased LDH and decreased haptoglobin (protein that binds free Hb)



To determine EV vs IV


- perform a? EV if see? IV if see?


- also can perform? looking for?

1) Blood film - Sperocytes (EV) vs Schistocytes (IV)




2) DAT direct Antiglobulin test - look for complement and Ab on RBC surface

What Causes Red Cell Hemolysis - Internal


-Hb? enzymes? cyto?

- intrinsic red cell problems:


1) Hb = Sickle Cell


2) RBC enzymes = G6PG defic.


3) RBC cytoskeleton = hered. spherocytosis

What Causes Red Cell Hemolysis - External


- D/I/ Abs/ struct/ dissem/ MAHA - decreased?

- drugs


- infections


- Abs against red cell antigens - ABO incompatible


- Struc. problems - defective valves


- disseminated intravasc. coagulation


- Microangiopathic Hemolytic Anemia (MAHA) or MA = decresed Hb and pts

Internal IV Hemolysis Investigation - see free? fragments of?

= free Hgb, schist fragments

Extravasc. Hemoylsis = Investigations - see? +? iron is?

- spherocytes


- DAT +


- iron recycled

Investigation of Erythrocytosis - look for increased? decreased?


- relative erythro = decrease? due to?

- increased red cell mass vs decreased plasma volume


- relative erythrocytosis = decreased plasma volume, often due to reduction in plasma volume (diuretics, smokers)

Investigation of Erythrocytosis - Increased red cell mass


- meassure? if low, means? if high?


- EPO released due to?



- measure EPO level


- low EPO means red cell production independent of EPO


- high EPO means inapprop EPO driving red cell production




*hypoxia = causes Epo secretion

Primary Erythrocytosis


- increased RBC mass with low EPO caused by?


- is a? due to?


- mutation in?

- increased RBC mass but low EPO caused by:


= polycythemia vera (PV) which is a bone marrow myeloprolif disorder = JAK-2 tyrosine kinase mutation


= mutation of EPO receptor gene

Secondary Erythrocytosis - increased? driven by?


- main cause is? from? (3)


- EPO can also be increased by? (5)

- increased red cell mass driven by high EPO


1) Hypoxia = heart/lung disease, high altitude living, abnormal Hbs


2) Increased EPO = cancer, uterine fibroids, renal cysts, renal artery stenosis, EPO doping

Increased Red Cell Mass Symptoms


- (5)

- symptoms include HA, plethora, shortness of breath, numbness and tingling in hands and feets, blood cots

Treatment of Increased Red Cell Mass - Polycyhtemia Vera


-is a? increased progression to?


- key issues are?


- perform?


- can give? to prevent?



= this is a pyeloprolif disorder increased risk of progression to leukemia


- key issues are preventing thrombosis and managing symptoms


- phlebotomy or chemo to keep hematocrit below 0.45 for men and 0.42 for women


- give Anticoags to prevent thrombosis


- use JAK2 inhibitors

Treatment of Increased Red Cell Mass - EPO Mutation? Secondary Erythrocytosis


- mutation in? maintain? via?


- or manage the?

1) EPO Mutation = maintain hematocrit with plhebotomy




2) Secondary Erythrocytosis = manage underlying cause

WBC Terminology


- too few WBCs? too many? too few Ns? too many? too few lymphs? too many?

- leukopenia = too few WBCs


- leukocytosis = too many WBCs


- neutropenia = too few neutrophils


- neutrophilia = too many neutrophils


- lymphopenia = too few lymphocytes


- lymphocytosis = too many lymphocytes

Leukopenia - Ethnic Variations - normal depends on?


- CBC only assess?


- lower normals in?


- need diff to?

- normal depends on controls


- CBC only assesses the circulating WBC pool


- lower normal range in South African blacks, Arab Jordanians, Yemenite Jews


- normal response to infection - need differential to see which WBCs are low

Causes of Neutropenia


- decreased? seen with? (4)


- increases? due to?


- may be? seen with?




* can lead to?

1) decreased production = drugs (chemo), bone marrow disorders, benign cyclic neutropenia, congen. neutropenia syndromes




2) increased destruction = AI or alloimmune


3) dilution/sequestration = Felty's syndrome






* can lead to fatal bacterial infection if ANC < 0.5

Febrile Neutropenia


- seen in? if ANC?


- must monitor for?


- if develop? must?


- Neuopgen is? sometimes used to?

- patients receiving chemotherapy at risk if ANC <0.5


- patients must monitor for signs of infection


- if develop temp >38.3, must use broad spectrum Abx immed.


- G-CSF (Neupogen) sometimes used to stimulate granulocyte prolif, accelerate recovery

Causes of Neutrophilia


- demarg means? dues to?


- reactive sees? often due to?


- or due to a?

1) Demargination = from endothelium into circ. blood = exercise, pain, infection, steroids


2) Reactive = left shift, immature WBCs move out of marrow, due to infection or inflammation


3) Bone Marrow Malignancy

Causes of Lymphopenia


- I/D/CID/ mild?

1) Infection = bacterial, viral, parasitic, fungal


2) Chemotherapy/Drugs


3) Congenital Immunodefic. disorders


4) Mild lymphopenia on very CBC common

Causes of Lymphocytosis


- reactive = such as? also due to? (2)


- malig?

1) Reactive = viral infections (infectious mono), stress (MI), smoking


2) Lymphoid Malignancy

Approach to Lymphocytosis


- need to? to?


- also determine if it is? via?

- cant guess if reactive or malignant need to investigate further if not clear


- is it polyclonal or monoclonal = morphology, immunophenotype, molecular studies

Eosinophilia - seen with? (A/P/M)

- allergic reactions = enviro, medication


- parasitic infections = strongyloides, schistosomiasis


- malignancy

Monocytosis - seen with chronic? such as?


- also diseases like? (2)

- chronic infections - TB, syphilis


- Chronic Inflamm Diseases = IBD, RA


- malignancy = Acute and chronic leukemias

Platelet Conditions - too few? too many?

- too few = thrombocytopenia


- too many = thrombocytosis

Approach to Thrombocytopenia - is it true? take?


- is it? or are other?

- is it true thrombocytopenia = take a bleeding hisotory, review blood film


- is it isolated TC or are other cell lines affected = review blood film

Pseudothrombocytopenia - due to? pts get?


- machine cant?



- due to platelet clumping, pts get activated during collection


- machine cant count them, lab should report pt clumping on blood flilm


- platelet satellitism = in vitro phenomena

Thrombocytopenia


- disorder of? often presents as?


- no smyptoms until?


- presence of? which are?


- worry when?

- disorder of primary hemostasis, see mucous membrane bleeding


- usually no symptoms until pts <30


- presence of petechiae - non blanching non-palpable or mucosal bleeding - pts below 10 = worry

Approach to Thrombocytopenia


- decreased? inceased? or stuck?

- decreased platelet production


- increased platelt destruction


- sequestration = pts suck in spleen/liver

Thrombocytopenia - History and PE


- bleeding? recent? B? ask aobut? such as? past?


- history of?


- bruising of?


- exams?

- bleeding hisotry


- recent infection - HIV and Hepatitis


- systemic symptoms = fever, night sweats, weight loss


- AI disease = thyroid disease


- past medical, surgical transfusion history


- Meds, FH, alcohol and smoking history


- petechiae bruising - look inside mouth


- exam = LNs, hepatosplenomegaly

Bleeding and Thrombocytopenia


- if < 10? need?


- 10-30, are? will then?


- 30-50 - mild? dont?


- higher than 50?

- pts < 10 = risk of spont bleeding = need treatment


- pts 10-30 = symptomatic, usually treat (chidlren <50)


- pts 30-50 = mild or no symptoms, dont need treatment unless surgery or pregnant


- pts >50= do not need treatment

Thrombocytopenia and Decreased production


- often due to a? such as? (5)


- toxin of? from?


- infection such as?


- or defic of?


- iron defic will?

- primary bone marrow disorder = aplastic anemia, leukemia, myelodysplastic syndrome, congenital thromboytopenia


- marrow toxin = alcoho, drugs


- infection - viral, bacterial, malaria


- B12 or folate defic = not iron defic as it usually increases pts

Thrombocytopenia and Increased Destruction - Immune Causes


- Primary =? is a?


- Secondary includes? (4) post? use of?

Primary - Immune Thrombocytopenia = ITP = diagnosis of exclusion




Secondary = viral, collagen vasc disease (SLE), lymphoprolif disorder, drugs (esp. heparin), post-transfusion

Immune Thrombocytopenia ITP


- in children, most are? then?


- in adults are? onset?


- no standard? always are?


- must rule out? important to?

- in children, >80% cases are acute, follow viral illness and resolve spontaneously


- in adults, usually chronic, insidious onset


- no gold standard test for ITP, always looking for other causes


- must rule out HIV, hep B and C- important to investigate in women on childbearing age as Ab can cross to baby = cause neonatal thrombocyto

Primary ITP - is immune mediated? live less than?


- inapprop repsonse of?


- treat includes? imm. vs longterm?


- TPO increase cia?

- immune mediated early destruction, live less than 7 days


- inapprop. TPO response = like anemia of chronic disease for pts


- treatment = steroids immediate, longterm do splenectomy or immune suppression


- can also increase TP = receptor agonist

Heparin Induced Thrombocytopenia


- should ask if?


- usually occurs after?


- patient will? dont?

- should ask in any patient on heparin and see sudden fall in pts


- much more common with UFH and usually occurs 5-10 days after starting heparin


- patients clot, dont bleed

HIT


- caused by? which causes?


- patient develops? leads to? not?


- patients die of? need to stop? and start?

- caused by an antibody to heparin and PF4


- antibody activates pts


- patients develop low pts but lead to thrombosis not bleeding


- patients die of thrombosis if heparin not stopped and another non-heparin anticoag is not started

treatment of HIT


- stop all? must use? no?


- so use?


- warfarin may?

- stop all hepatin


- must use alternative non-heparin and non-warfarin anticoag even if no thrombosis


- use Fondaparinux or Argatroban


- warfarin may cause massive thrombosis

Thrombocytopenia and Increased Destruction - Non Immune Causes


- D/D/S/M/PE


- MAHA - see low? due to?


- worry if on film?

- drugs, DIC/sepsis/ mech destruction, TTP/HUS or pre-eclampsia


- MAHA - see low pts and red cell fragments due to fibrin activation causes RBC frag




** if see thrombocytopenia and red cell fragments on film, worry!

Thrombotic Thrombocytopenic Purpura TTP - caused by lack of? which can be?


- many symptoms = (2)


- also see? (3)

- caused by lack of ADAMTS13, which can be congenital (very rare) or autoimmune


- symptoms = anemia (schists), low pts


- also see fever, renal failure, neuro symptoms

TTP - Thrombotic Thrombocytopenic Purpura


- untreated mortality?


- fibrin? leads to? pts are?


- patients both?


- treatment is urgent? to replace?

- untreated mortality is >80%


- fibrin clots in small blood vessels from uncontrolled VWF, leads to red cell fragents, pts activation, fever, renal failure, neuro symptoms


- patients bleed and clot


- treamtent is urgent infusion of plasma (to replace VWF) followed by plasmapheresis

In TTP, see uncontrolled? plus uncontrolled? due to?

- uncontrolled vWF release + uncontrolled plt activation due to loss of ADAMTS13

Thrombocytosis


- reactive = I/I/B/ Defic of/ or?


- bone marrow? known as?


- redis = ?

1) Reactive = infection, inflamm, bleeding, iron defic, cancer, bone marrow infiltration


2) Bone marrow premalig or malig = myeloprolif disorders = essential thrombocytosis


3) Redistributive = post splenectomy

Categories of Bone Marrow Disorders


- failure = not enough? seen in (2)


- myeloprolif =? seen with? (3)

1) Bone Marrow Failure = not enough blood = aplastic anemia, myelodysplastic syndrome




2) Myeloprolif Neoplasms = too much blood = polycythemia vera, essential thrombocythemia, primary myelofibrosis



Aplastic Anemia - destruction of?


- have empty? leads to severe?


- if untreated?

- destruction of HSCs


- empty bone marrow = bone marrow failure


- severe pancytopenia


- untreated, severe aplastic anemia leads to rapidly to death

Presentation and Diagnosis of Aplastic Anemia


- presents over? F/I/ B/B - from?


- diagnose using? (2)

P = pancytopenia, progressive over weeks-months, anemia (fatigue), leukopenia (recurrent infection), thrombocytopenia (bruising, bleeding)


D = bone marrow aspiration and biopsy

Treatment of Aplastic Anaemia


- regen - via?


- best in patients that are?


- remission?

1) Regenerate Stem Cells


= immunosuppressive therapy = ATG


= best for patients > 40 years


= long term remission in 60%

Treatment of Aplastic Anaemia


- replace - via?


- best for patients that are?


- cure rate?



2) Replace Stem Cells


= allogeneic stem cell transplantation


= best for patients <40 years


= cure in >80%

Myelodysplastic Syndrome (MDS)


- disorder of?


- affected stem cell then?


- progeny are? with?


- leads to?

- clonal stem cell disorder


- affected stem cell takes over the marrow


- progeny of affected stem cell are defective = abnormal morphology, function, apoptosis


- cytopenias

Presentation and Diagnosis of MDS


- progresses over? seen? most commonly see?


- diagnose using? can also perform? look at (3)

P = cytopenias, slowly progressing over months-years, most commonly anemia


D = blood film, bone marrow aspirate and biopsy (blast count, cytogenetics, iron stains)

MDS Treatment - Must first?


- as some become? others?

- risk stratification = heterogenous disease, some transform rapidly to AML, some are stable and chronic



MDS Treatment


- lower risk - fix? to help? give (E/L/A)


- if high risk, want to delay? to extend? - perform? or give?

- lower risk = fix cytopenias to ameliorate symptoms = ESAs, Lenalidomide, ATG




- higher risk = delay or prevent AML to extend lifespan = Azacytidine or Allogeneic stem cell transplantation

Aplastic Anemia Summary


- very? seen in? BM is? due to either?


causes? two treatments?

- very rare


- younger patients


- bone marrow empty


- AI or toxic


- pancytopenia


- immunosuppressive treatment or BMT

MDS Summary


- patients are? bone marrow is? disorder of? cells are? leads to? treatment based on?

- older patients


- bone marrow full


- clonal disorder


- dysplastic cells


- cytopenias


- variety of treatment according to risk stratification

Myeloproliferative Neoplasms


- disroder of?


- see overproduction of?


- may eventually enter?


- can transform to?


- 97% have a?

- clonal stem cell disorders


- overproduction of one or more cell lineage


- may eventually enter a fibrotic phase


- can transform to acute leukemia (rarely)


- in 97%, activating mutation of JAK2 or MPL or CALR

Three Types of MPN - PV/ ET/ PMF

1) Polycythemia Vera


2) Essential Thrombocythemia


3) Primary myelofibrosis

Polycythemia Vera - overproduction of? blood is? leads to symptoms like? (5)


- red seen with?


- develop?


- risk of?

- overproduction of RBC


- thick blood leads to symptoms = HA, visual distrbs, bleeding, pruritis


- red = plethora, bloodshot eyes, erythromelalgia


- splenomegaly


- thrombosis**

EPO and JAK2 V617F


- present in %? activates? which then?


- EPO is?

- JAK2 V617F present in 97% of PV, activates JAK-STAT which activates EPO receptor, allows EPO receptor to fire without EPO, EPO is unrestrained

Diagnosis of Polycythemia Vera


- D must exclude? such as? (2)


- other features include?

D = exclude other causes = Spurious polycythemia (dehydration), secondary polycythemia (hypoxia, EPO)


- other features of MPN (splenomegaly), JAK2 mutation (97%)

Treatment of Polycythemia Vera


- reduce? via? or oral?


- ASA to reduce? inhibitors of?


- is a? AML? LE is?

- reduce RBCs = phlebotomy, oral chemo (hydroxyurea)


- ASA = reduce thrombosis


- JAK2 inhibitors = Ruxolitinib




* chronic disease, AML develops in <5%, life expectancy = decades

Essential Thrombocythemia


- overproduction of?


- usually/


- sometimes causes?


- develop? risk of?

- overproduction of pts


- usually asymptomatic


- sometimes bleeding


- splenomegaly


- thrombosis

Mutations seen in ET - 65% have? 15% have? 5% have?

1) JAK2 = 65%


2) MPL = 5%


3) CALR = 15%

Essential Thrombocythemia Diagnosis


- must exclude? check for? (4)


- check for?


- disease is? AML?


- LE?

- exclude reactive thrombocytosis - infection, inflammation, malignancy, iron deficiency


- JAK2 mutation (in 65%)


- chronic disease, AML in <1%


- life expectancy same as healthy person

Treatment of Essential Thrombocythemia


- if asymptomatic? even if?


- if thrombosis? give? (2)


- if bleeding?

- if asymptomatic = observation = even if pt count is very high


- if thrombosis = ASA, hydroxyurea


- if bleeding = hydroxyurea

Primary Myelofibrosis


- marrow replaced by? see abnormal? that then?


- leads to? blood made in? so they are?


- early see increased? then later?

- marrow is replaced by fibrosis, see abnormal megakaryocytes that stimulate collagen deposition


- leads to extramedullary haematopoiesis, as blood is produced in liver and spleen, which are hugely enlarged


- early = see increased blood counts


- later = counts fall

Diagnosis and Life of Primary Myelofibrosis


- beware? look at both?


- mutations?


- AML in? chronic? with?


- survival?


- dependent?


- see symptoms of? (2)

- marrow and blood = beware "dry tap"


- JAK2 mutation in 70%


- CALR mutation in 25%


- AML in 8-23%


- chronic disease with steady deterioration


- survival is 2-15 years


- transfusion dependency


- see const symptoms and symptoms from splenomegaly



Treatment of Primary Myelofibrosis


- mainly do? risky to perform?


- can transplant?


- inhibitors of?

- transfusions


- splenectomy = very risky


- stem cell transplantation can be curative - very risky


- JAK2 inhibitors (ruxolitinib) can be used

Summary of Myeloproliferative Neoplasms


- overproduction of?


- in 97%, see?


- for PV and ET, LE is? main issue is?


- for PMF, see? problems with? LE?

- overproduction of one or more lineages


- in 97%, JAK2 or MPL or CALR activated by mutation


- PV and ET:


= life expectancy is long, thrombosis is most signif issue, has complex pathogenesis


- PMF: progressive course, problems from splenomegaly, cytopenias, LE shorter

Defenses Against Bleeding


- primary hemostasis is? with? (2)


- secondary is the? phases of? pathways? end result?

1) Primary Hemostasis = cellular defense = pts and VWF


2) Secondary Hemostasis = coagulation cascade = new initiation and propagation phases, old extrinsic and intrinsic pathway, end result of thrombin and fibrin clot

Defenses Against Bleeding


- clot stab via? and?


- last step is? includes activation of?

3) Clot stabilization = Factor 13 and Thrombn Activatable Fibrinolysis Inhibitor (TAFI)




4) Healing = delayed activation of fibrinolytic cascade (starts with coagulation)

Common Pathway - starts with? activated by? which then activates? known as?


- this activates? known as? which forms?


- prothrombinase complex is?

- factor 10, activated by 5, activates factor 2 (Prothrombin)


- Thrombin activates Factor 1, Fibrinogen, which forms insoluble fibrin clot




* Prothrombinase Complex = 10 + 5

Extrinsic Pathway of Coagulation


- Factor? activated by? which is activated by?

- Factor 7, activated by TF, which is activated by vascular injury

Intrinsic Pathway - starts with? then? then? with faxtor 8, activates?


- starts overall with (2) = H//PK

- HMWK and Prekallikrein, activates Factor 12, which activates Factor 11, which activates Factor 9


- Factor 9, with Factor 8, activates Factor 10

Contact factors


- PK =? HMWK =? lead to?


- generally not needed to?

- Prekallikrein (PK)


- High molecular weight kininogen (HMWK)


- Factor 12




* PK and HMWK help activate Factor 12




* not needed to control bleeding

Coagulation Cascade

Natural Anticoagulants


- proteins? (2) act to degrade?


- the rest inhibited by? which acts on?

1) Protein C and S = proteolytically degrade Factors 5 and 8


2) Anti-thrombin inhibits the rest, mostly 2a and 10a

Basic Clot based tests


- PT =? use?


- or use? means?


- end result?

1) Prothrombin = PT, use INR = International Normalized Ratio


2) Activated Partial Thromboplastin Time (PTT)




*end result = clot formation

INR = equation? ^?


ISI is the? indicates? assessed by?

= (PT in seconds / Geometric mean of normal range) ^ ISI




* ISI = International Sens. Index = indicates reagent sensitivity to vitamin K dependent factors assessed by PT


- designed for Warfarin

Coagulation Factors


- no-enzymatic? (3)


- zymogens are mostly? include (4) - undergo?

1) Non-Enzymatic Cofactors = F-V, F-VIII and TF


2) Zymogens = mostly serine proteases = F2, 7, 9 and 10 undergo vitamin K dependent gamma carboxylation (charged groups allow these factors to bind membranes via calcium bridge)

Vitamin K Dependent Factors - include? (4)


- are?

= enzymes and substrates of Xase and Prothrombinase

= enzymes and substrates of Xase and Prothrombinase



Coag. Cascade



Where are Coagulation Proteins Made


- all made in? except (3)?

- all are made in the liver, except:


1) tPA = activator of fibrinolysis


2) VMF


3) Thrombomodulin = important endothelial substance that triggers activation of the natural anticoagulants




*Factor 8 is also made by the endothelium

Half Lives of Coagulation
- shortest? and?

- shortest = Factor 7 and Factors 5 + 8

Common Disorders of Hemostasis - Primary Hemostasis


- inherited =?


- acquired = (3)

1) Inherited = VWD




2) Acquired = drugs, thrombocytopenia, uremia

Common Disorders of Hemostasis - Secondary Hemostasis


- inherited =? defic in? or defic in?


- acquired = ? (4)

1) Inherited = Hemophilia (Factor VIII or IX defic), Factor XI defic.




2) Acquired = drugs, liver disease, DIC, Vitamin K defic.

Standardized Bleeding Assessment


- most important predictor is? BATs are?


- improves?


- informs? allows?

- bleeding history is the most important predictor of the presence of a bleeding disorder


- validated bleeding Assessment Tools = BAT's


- improves post test probability of lab tests, facilitates exploration of variability in bleeding severity


- informs treatment decisions


- allows effective communication

vin Willebrand Factor


- made by? (2)


- stored in? (2)


- role in (2)


- chaperones? t 1/2 with and without VWF?

- synthesized by endothelial cells and megakaryocytes


- stored in Weibel-Palade bodies (endothelial cells) and alpha granules (pts)


- role in platelet adhesion and aggregation


- chaperones = F - VIII


* t1/2 = 12h with VWF


* t1/2 = 2h without VWF

von Willebrand Disease - published prev? symptomatic?


- inheritance? gender?



- published prevalence in 1 in 100, symptomatic prevalence is 1 in 1000


- autosomal inheritance = M=F


- females diagnosed 2-3:1

Diagnosis of VW Disease - 3 Clinical Components (3)

1) Bleeding Symptoms


2) FH


3) Laboratory results

Bleeding Symptoms - MC vs MSK


- in MC, see? excessive? from minor? in the? (2) also after?


- MSK, such as?

1) Mucocutaneous = menorrhagia, epistaxis, bruising, excessive bleeding from minor wounds, GI bleeding, oral cavity, post-op, post-partum




2) Muskuloskeletal = hemarthrosis, soft tissue, muscle hematomas

Family History - look for? as it is?


- asking more about? pre test?

- positive FH helpful


- autosomal inheritance


- low VWF > bleeding


- pre-test probability 50%

ISTH VWD Classification


- Type 1 means? %?


- Type 2 means? %?


- dominant are? (3) recessive?


- Type 3 =? 1 per?

- Type 1 = mild/ mod quant. trait = 80%


- Type 2 = qualitative trait = 20%


= 2A, 2B, 2M = dominant


= 2N = recessive




-Type 3 = severe quantitative trait = 1 per million



VW Disease Lab Tests


- normal are? (3)


- decreased? (3)

- CBC, INR, PTT often normal


- VWF Antigen = decreased


- VWF Ristocetin Cofactor Activity = decreased


- Factor VIII activity = decreased

Treatment of VW Disease - Medical


- can give?


- transfusion based?


- women to use?


- agent of?

- DDAVP/Desmopressin


- Transfusion based - VWF:FV-III concentrate


- Combined OCP


- topical agents


- Anti-fibrinolytic agents

Treatment of VW Disease - Gynecology


- give? ablation of? or perform?

- hormonally coated IUD = Mirena


- endometrial ablation


- hysterectomy

Hemophilias - X linked


- intrinsic complex =?


- Hem B is? seen in?


- Hem A is? seen in?


- FH in?

- factor 9 and factor 8 = intrinsic complex


- Hem B = Factor 9 defic = 1 in 30,000 males


- Hem A = Factor 8 defic = 1 in 5,000 males




* 3200 in Canada, no FH in 30% of cases

Clinical Manifestations of Hemophilia - Bleeding Severity a Factor Levels


- mild sees > then? %? present as?


- moderate is? %? provoked by?


- severe is? %? often see?

1) Mild > 0.05 U/mL = 5%


- mild symptoms, can be asymptomatic aside from trauma or surgery


2) Moderate 0.01-0.05 U/mL = 1-5%


- provoked by minor trauma, serious with trauma or surgery


3) Severe < 0.01 U/mL = <1%


- frequent, spontaneous, life-threatening with trauma or surgery

Clinical Manifestations


- MSK? (3)


- mouth?


- brain?


- bleeding with?


- women may have? may mean?

- MSK bleeding = hemathrosis, intra-muscular hematoma


- mouth bleeding, epistaxis


- intracranial bleeding


- bleeding with trauma, procedures, surgery


- menorrhagia = symptomatic carriers

Principle of Bleed Management ****

- treat first, investigate later

Categories of treatment Products


- specific? such as? role of DDAVP?


- topical agents to promote?


- stabilize clot with?


- ancillary?

- specific replacement of FV III or F IX = concentrate (F VIII or F IX) or DDAVP (recruitment of endogenous F VIII)


- topical agents to promote fibrin clot formation


- stabilization of clot with anti-fibrinolytic agents


- ancillary strategies = rest, cold, anti-inflamms

Factor XI Defic = Hemophilia C


- transmission? seen is?


- very important to determine?


- PTT vs PT? diagnostic assay?


- bleeding pheno is?


- no correlation of?


- treatment = (4)

- autosomal recessive


- gene freq - 4.3% in Ash Jews


- patient and FH of bleeding very important


- PTT very long, PT (INR) normal, Factor XI assay diagnostic


- bleeding phenotype is variable


- degree of factor defic. does not correlate with bleeding severity


- may bleed with trauma and surgery


- treatment = DDAVP, anti-fibrinolytics, frozen plasma, Factor XI concentrates

Liver Disease and Hemostasis


- liver disease can cause? such as? (3)


- bleeding with?


- less common to see?


- risk of both?

- patients with severe liver disease can suffer life-threatening bleeding problems - see esoph and GI varices, gastritis, ulcers


- bleeding can occur with trauma, biopsies, surgery


- mucosal and soft tissue bleeding - less common


- coagulopathy is complex because of multiple hemostatic problems - risk of bleeding and thrombosis

Liver Disease and Hemostasis



Liver Disease and Hemostasis



Liver Disease - Common Lab Findings


- prolonged?


- decreased?


- decreased?


- evidence of?

- thrombocytopenia


- prolonged PT/INR, APTT


- decreased factors except Factor VIII


- fibrinogen assay = decreased


- evidence of DIC = increased FDPs, D-dimers

Treating Liver Disease and Hemostasis


- first treat?


- Vit K not?


- if bleeding, consider? (3)

- treat liver disease if able to at this stage


- Vit K usually not effective


- bleeding or major surgery consider = DDAVP, anti-fibrinolytic agents, replacement therapy

Dissem. Intravascular Coagulation (DIC)


- acquired? with?


- overwhelms?


- may result in? or? depending on?

- an acquired syndrome wit widespread systemic activation of coagulation


- overwhelms to natural antithrombotic control mechanisms


- may result in systemic bleeding and/or clotting depending on the balance of prothrombotic and antithrombotic forces

Pathophys of DIC - activation of? uncontrolled generation of?


- leads to:


- formation of? consumption of? concomitant activation of? generation of?

- activation of the coagulation system results in the ongoing uncontrolled generation of both** thrombin and plasmin


- leads to:


= intravasc. formation of fibrin


= consumption of all hemostasis components


= concomitant activation of fibrinolysis


= gen. of coagulation by products = FDPs, D-dimers

Clinical Conditions Assoc. with DIC


- all assoc with release of?


- S/T/C/O/VD/ID/ T

- all assoc. with excessive TF release


= sepsis


= trauma


= cancer


= obstetrical


= vasc. disorders


= immunological disorders


= toxins drugs


= liver disease

Diagnosis of DIC - no single?


- combo of?


- tests need to? to?


- most helpful to watch?

- no single test will acc. diagnose DIC


- diagnosis of DIC made by combination of:


= clinical disorder assoc. with DIC
= abnormal hemostatic screening tests




- tests need to be repeated to monitor progress and severity of DIC


- monitoring fibrinogen levels often most helpful

Screening Tests for DIC


- blood = (3)


- pts?


- prolonged? due to?

- blood fil - frag RBCs, low pts, MAHA




- pt count - pt consumption is low




- prolonged PT/INR - consumption of multiple factors



Screening Tests for DIC


- prolonged? due to?


- decrease? due to?


- increased? (2) due to?

- prolonged APTT = consumption of multiple factors (incl. 8)


- decreased fibrinogen = consumption of fibrinogen


- increased FDPs, D-dimers = formation and lysis of fibrin




*indicative of thrombin and plasmin action

Treatment of DIC


- treat the underlyic?


- early - use? (2)

- treat underlying cause = protein C and antithrombin concentrates have been shown to help if used early in overhwhelming DIC

Vit K Deficiency


- VK facilitates? dependent factors include (4), anticoags (2)


- defic results in? if level below?

- Vitamin K facilitates carboxylation of 6 coagulation factors, coverts them to functional forms


- Vitamin K dependent factors = procoagulants (factors 2,7,9,10), anticoagulants (protein C, protein S)


- Vitamin K defic. will result in signif bleeding if factor level activity falls below 10-15%

causes of Vitamin K Defic.


- warfarin is an?


- poor?


- some?


- GI?


- newborn?

- Vit. K Antags = Warfarin


- Nutritional deficiency / poor oral intake


- antibiotics


- biliary obstruction/ malabsoprtion


- hemorrhagic disease of the newborn

Vit K Defic Labs and Treatment


- see prolonged (2)


- reduced?


- treat via?

- labs:


= prolonged PT/INR


= prolonged APTT in more severe cases


= reduced factors 2,7,9,10




- treatment:


= oral or IV vitamin K

Differential Diagnosis: Isolated Prolonged APTT (normal PT)


- defic of a? likely?


- if factor 12? if HMWk or PK?


- uncommon is?


- acquired includes (3) inhibit? or specific?

1) Single Factor defic = inherited


- defic of factors 8,9, or 11


- defic of 12 = no bleeding history


- defic. of HMWK or Prekallikrein = no bleeding history


2) VW disease = uncommon, inherited


3) Inhibitors = acquired


- drugs = heparin, direct thrombin inhibitors


- non-spec = antiphospholipid antibody


- specific = factor inhibitor (most comm. to factor 8)

Differential Diagnosis: Isolated Prolonged PT/INR (and normal APTT)


- inherited?


- acquired? seen with (4)

1) Inherited Factor 7 defic.


2) Acquired Factor 7 defic


= Vitamin K Antagonist


= Vitamin K defic


= early liver disease


= specific inhibitors to factor 7 (rare)

DD of Prolonged APTT and PT/INR - Inherited


- inherited defic of? such as? (4)


- abnormal?

- inherited defic. of common pathway factors = 10,5,2, fibrinogen


- inherited dysfibrinogenemia = abnormal fibrinogen

DD of Prolonged APTT and PT/INR - Acquired


- non specific inhibitors of? such as?


- specific inhibitors of?


- severe?


- severe?


-seen in?


- massive?


- dilution?

- non-specific inhibitors = drugs, heparin, direct thrombin inhibitors, direct Xa inhibitors, antiphospholipid antibodies


- specific inhibitors to common pathway fator


- severe vitamin K defic.


- supratherapeutic warfarin


- severe liver disease


- DIC


- isolated factor X defic. associated with amyloidosis


- severe depletion of fibrinogen - massive hemorrhage or fibrinolysis


- hemodilution - post-op sample, massive transfusion

Most Common Bleeding Disorders


#1? then? then? finally defic of?

1) VW DIsease


2) Platelet Function Disroder


3) Hemophilia A and B


4) Factor XI Defic.

aPTT =?

- activated partial thromboplastin time

Platelet-Fibrin Thrombus is mix of? leads to?


- RBCs are trapped in?

- mix of fibrin, platelets and RBCs in BV, leading to a thrombus


- see RBCs trapped in a fibrin mesh

Venous Thromboembolism = VTE = types? (2)

1) Deep Vein Thrombosis = DVT




2) Pulmonar Embolism = PE

Deep Vein Thrombosis - thrombus in?


- legs vs arm?


- other sites?

- thrombus in one or more deep veins


- legs >>> arms


- other sites include abdo, cerebral,etc

Proximal DVT


- likely in? then? then?


- behind?


- leads to 90% of?

- popliteal -> femoral -> iliac veins -> IVC


- behind the knee, up to the heart


- leads to >90% of PE

Distal or Calf DVT


- are found distal to?


- most calf are?


- rarely lead to?

- distal to the popliteal vein, below knee


- most calf DVT asymptomatic


- rarely lead to PE

Superficial Thrombosis


- not? doesnt lead to?

- not DVT, doesnt lead to PE

Potentiation of Calf DVT


- 90% of calf? 10-20% become?


- >50% of proximal lead to? can caus?


- calf rarely?

- 80-90% of Calf DVT resolves spontaneously


- 10-20% becomes proximal DVT


- >50% proximal DVT leads to PE, possibly death




*rare that Calf DVT causes death

How Common is VTE?


- occurs in? 2- vs 80?


- is commonly a? yet causes?

- VTE occurs in 1 per 1000 pop/year


- age <20 = 1/10,000


- age >80 = 1/100




- VTE is a common preventable cause of hospital death (5-10% of in-hospital deaths)

Risk Factors for VTE - Virchows Triad =?


** all contribute?

- Virchow's Triad:


1) Activation of coagulation


2) venous stasis


3) Injury to the BV wall




* all contribute to thrombosis

RFs for VTE - major? T?C?Imm? acute? inflamm? use of?



RFs for VTE - previous? FH? inherited? age? body weight?



Important RFs for VTE - increases with?


- largely acquired in?


- high risk for? (4)


- mod risk for (3)


- risk if no? risk duration?

- increases with age


- largely hospital-acquired (60% of all VTE in the pop)


- 5,000 hospital-acquire VTE in Ontario every year


- different risk:


= high risk = SC injury, major trauma, THR, TKR


= mod risk = gen surg, gyne/urol, neurosurg




*no prophylaxis + routine screening for asympt DVT


* risk of VTE after surgery is prolonged

VTE is common in Cancer - RR?


- 20% will?


- is occasionally the?

- VTE is 25x more common in cancer patients than people without cancer


- 20% of cancer patients will develop VTE


- VTE is occasionally the 1st manifestation of cancer

VTE Risk Factors in Cancer patients - Related To


- type? patients? treatment?

1) Cancer = specific type, advanced stage, location


2) Patient = increased age, previous VTE, immobility


3) Treatment = surgery, radiotherapy, hosp, chemotherapy, hormonal therapy, central venous lines

Estrogen, Pregnancy and VTE


- OCT causes?


- risk depends on?


- HRT also?


- pregnancy risk? PP period?

- OCT (combined estrogen-prog) causes 4x increased risk of VT


- risk depends on dose of estrogen, specific progestogen, patient age and other RFs (smoking, obesity)


- HRT also increases risk 4x


- pregnancy carries 4x risk, postpartum period has 8x increased risk

Thrombophilia


- deficiency of?


- % in population? in VTE is?



- see factor V Leiden, Prothrombin, deficiency of AT, PRc and PRs and Antiphos. Ab


- thrombophilia in general pop is 10%, in unprovoked VTE is 30%


- only test if results will affect management = almost never do

Multifactorial VTE - based on? (3)


- consider? (6)

- genetic


- acquired


- provoking and triggering factors




*consider, age, tamoxifen use, FH, coag abnorms, triggering surgery

Deep Vein Thrombosis Signs


- (4)


- yet many are?

- leg swelling


- leg pain


- warmth


- purple-blue colour


- many are asymptomatic

PE Signs - (7) **

- SOB


- chest pain - pleuritic


- desaturation


- tachycardia


- unexplained fever


- blood in sputum


- feeling faint, collapse


- cardiac arrest


- many are asymptomatic

Investigating Suspected VTE


- assess? (3) - forms?


- look at?


- if suspect DVT perform?


- if suspect PE perform?

- risk factors + PE + history = pretest probability


- D- dimer


- if suspect DVT = Doppler US


- if suspect PE = CT pulmonary angiogram

D-Dimer - formed by effect of? increased in? as plasmin causes?


- also increased after? there normal?


- if positive?


- never done on? as?

- is formed by effect of plasmin on fibrin


- increased in acute VTE as plasmin causes more FDPs made


- also increased after surgery, trauma, cance, infection, liver disease, pregnancy, elderly


- normal D-dimer rules out acute VTE


- positive D-dimer not helpful, may mislead




*never done on inpatients or patients at high risk of having a positive result

Doppler US


- very accurate for? do over? looking for?

- very accurate for proximal DVT, do over femoral vein in which dont see compression, still has large gap

Diagnostic Tests for PE - CTPA is the?


- sometimes look for?


- VQ - can rule out? most are?


- only VQ if? with normal?

1) CT Pulmonary Angiography (CTPA) = test of choice for most patients


2) Sometimes look for DVT = DUS


3) Vent/Perfusion Scan = rules out PE if perfusion scan normal, but 60% are non-diagnostic




*only use VQ if young patient with normal CXR, renal failure, and allergic to contrast

CTPA - very accurate for?


- if normal, no?


- may be too?


- requires? therefore must consider? alot of?

- very accurate for PE (normal = no PE)


- too sensitive? (uncertain about small defects)


- requires contrast dye = think kidneys


- alot of radiation

Treatment of VTE - IV heparin


- advantage is good? rapidly?


-DAs = need? frequent? can lead to?

Advans = good control of cascade, rapidly reversed when discontinued


Disads = IV, frequent lab tests (aPTT), heparin-induced thrombocytopenia (HIT)

Treatment of VTE - SC Low Molecular Weight Heparin


- examples = (D/E)


- As = given? can be? effect is? better for?


- DAs - need? if renal failure? more?

- LMWH = Dalteparin, Enoxaparin


- Advans = SC (outpateint, predictable effect, no lab, safe in preg, best cancer option)


- Disads = SC needles, accumulates in renal failure, most costly

Treatment of VTE - Oral Warfarin -


- As - no renal? able to? $?


- DAs - effect may be? see variation in? regular? affected by?

- Advats = >6% experience, no renal elim, antidotes (vit. K), cheap


- Disads = unpredictable effect, 50x varition in dose, affected by foods, meds, regular lab monitoring (INR)

Treatment of VTE - Direct Oral Anticoaga (DOACs)


- Ads = effect is? few? fixed? dont need any?


- DAs = may acc in? cant use with? problem of?

- Ads = predictable, few interactions, fixed dose, no lab monitoring


- Disads = accumulates in renal dysfunction, not with mech. heart valves, cost

Treatment of VTE Mechs - 4 anticoagulants


- Hep acts on? (4)


- LMWH - acts on (2)


- Warfarn - acts on (4)


- DOACS on? (2)

1) IV Hep = Factors 12, 11, 9, 10 and 2


2) LMWH = Factors 10 and 2


3) Warfarin = 7,9, 10 and 2


4) DOACS = Oral Xa inhbis and Oral IIa inhibs

Treatment of VTE - immediate? stop? if doesnt? then?

- immediate anticoagulation


- stops the acute thrombotoc process


- does not dissolve the thrombus = 3 options

3 Options for Treating DVT/PE


- use? for? with? maintain?


- for 28 days give? done for? high risk of?


- DOACs? - three ones are?

1) LMWH injections once a day for 7 days with warfarin = INR of 2.0-3.0


2) LMWH injections for 28 days = pregnancy = ost VTE assoc. with cancer, high bleeding risk


3) DOAC use = rivaroxaban, apixaban, dabigatran

Length of VTE Treatment - if provoked? for? means?


- if unprovoked - means? length is?


- if continued risk, then?

- if provoked = surgery, trauma, pregnancy, acute illness = transient, reversed risk = anticoagulation done for 3 months




- if unprovoked = active cancer, ongoing RF, high risk thrombophilia, male, residual DVT = indefinite length


- if continued risk = unresolved cancer = indefinite

For most patients with unprovoked CTE


- risks of bleeding are?


- therefore should continue? msut?

- risks of bleeding (<1%/year), lifestyle impact, costs, labs are outweighed by risks of recurrence (5-10%/year) and security of being protected



- therefore continue with anticoagulation


* must reassess with new RFs, new knowledge and patient preference

Natural History of VTE/ PE


- most improve with? however can lead to?


- PEs over time?


- yet is? see? 50% develop? 3% develop?

- most improve over time, like iceberg melting


- however can lead to chronic venous insufficiency with recanalization


- most PEs also resolve over time


-is a chronic disease however, with recurrent VTE (30% over 5 years), post-thrombotic syndrome (50% 5 YEARS) and chronic TE pulmonary hypertension (3% PE patients)

Prevention of VTE = Thromboprophylaxis


- 60% VTE is? most are? therefore need?

- 60% of all VTE in population is hospital-acquired


- most are preventable - TP is standard of care for most hosp. patients

Thromboprophylaxis Summary



VTE Summary - common are? Rfs are? investigate with?


- treat with? then? then?


- duration is? indef for?


- TP is mostly?

- DVT and PE are common, often multi-causal


- RFs = genetic, acquired, triggering


- Investigate via Doopler US and CTPA


- treat with DOAC, LMWH then warfarin then LMWH alone (preg,cancer)


- Duration is 3 months (provoked), indef (unprovoked)


- TP is LMWH for most in patients

Multiple Myeloma Diagnostic Pitfalls


- can present with? main two are? (2)


- myeloma can present without?


- disease is?


- median age? more common in?

- can present with non-specific symptoms = low back pain, anemia


- myeloma can present without symptoms = 30-35% present with lab abnorms


- disease is rare = <1% of malignancies




*median age in 65, most common in black than white males

Multiple Myeloma pathophys


- cancer that forms in?


- plasma cell helps by?


- MM causes? crowd out?


- can lead to (3) **

- a cancer that forms in plasma cell


- Plasma cells help you fight infections by making antibodies that recognize and attack germs


- Multiple myeloma causes cancer cells to accumulate in the bone marrow, where they crowd out healthy blood cells


- can lead to neuropathy, infections and renal failure

Renal Failure in MM


- due to? called?


- also deposition of? causes?


- pre-renal failure see?


- production of?


- also see ? (A)

- tubular deposition = cast nephropathy


- light chain deposition disease


- volume depletion


- hypercalcemia = pre-renal failure


- nephrotoxins = NSAIDs for bone pain


- Amyloidosis

Myeloma Features - CRAB ***

- Calcium elevation


- renal disease


- anemia


- bone disease




* CRAB

Presenting Symptoms of Myeloma - most common is? then F/A/RI/C/S/F/NP

- Back pain/ bone pain - most common


- fatigue


- anorexia


- recurrent infection


- constipation


- somulence


- fracture


- neuropathy

Presenting Signs of Myeloma


- also can have? hyper? renal? lytic?

- anemia/pancytopenia


- hypercalcemia


- renal infsuff


- lytic lesions/ osteoporosis


- monoclonal proteins


- organomegaly


- hypogammaglobulinemia

Initial Diagnostic MM Workup


- main symptoms suggesting MM = (6)


- investigations include? (8)

- symptoms suggesting MM = fatigue, back pain, anemia, renal failure, infections, periph neuropathy


= CRB, Creat/Lytes, Calcium, Albumin, SPEP, immunofix, immunoglob quant, urine bence jones

SPEP = Serum protein electrophoresis


- investigate?


- in normal, see?


- in MM, see? (2)



- investigate globulins


- in normal, see polyclonal smeart


- however in M, see high Albumin peak and high M-spike




( in immunofix, see IgA kappa)

Bence Jones Testing = 24 hr hour


- 20% myelomas assoc with? only see?


- light chains wil then? when? called?

- 20% myelona assoc. with light chain production = only kappa or lambda


- light chains precip when urine is heated to 40C, unlike albumin = BJ testing



Full Diag. Workup for MM - many things include?


- also do biopsy of? looking for?



- do BM biopsy, look for clonal plasma cells

- do BM biopsy, look for clonal plasma cells

MM Features - have? M protein? clonal plasma cells?


- is smoldering MM if?

- CRAB +


1) M-protein = often > 30g/l in serum


2) Clonal plasma cells = often >10% in BM




** smoldering MM if have two features but no CRAB features

MGUS = Monoclonal Gammopathy of Undetermined Signficance


- prevalence increases as? at 70 yo?


- 1% risk of?

- prevalence increase with age, 5% at 70 yo


- on average, 1% risk per year of progression to MM or Lymphoma

MGUS Diagnostic Criteria


- serum M protein is?


- marrow plasma cells are? no?


- later becomes? with? no? then symptomatic with?

- serum M-protein <3.0 g/L


- marrow plasma cells <10%


- no related organ damage




* later becomes asymptomatic MM (has lab targets but no organ involvement) and then symptomatic (lab values + CRAB or events)

Summary of Myeloma


- can present with? or no?


- problem as delay?


- consider workup in? (5)


- prognosis is?

- can present with non-specific symptoms or no symptoms at all


- delays in diagnosis can be devastating


- consider workup in anemia, renal failure, bone pain, fatigue and infections


- prognosis is improving

Lympadenopathy Epi


- defied as nodes that are?


- occurs in? % malignant?

- seen when nodes are greater than 1 cm in size


- 0.6% annual incidence of unexplained adenopathy in general population = 10% referred, 3.2% had biopsy, 1.1% malignant

When to Worry about Lymphadenopathy


- A/ chars/ loc / clinical?

1) Age


2) Node characteristics


3) Location of node


4) Clinical setting assoc.

Age and Lymphadenopathy


- in children, more likely to?


- patients <30 - %?


- >50, %?

- children/young adults - more likely to respond to minor stimuli with lymphoid hyperplasia


- LNs in patients <30 are clinically benign in 80% of cases


- whereas in patients >50, only 40% are benign

Characteristics/ Locations of LA


- look at? duration? location?


- common is? size? often?


- if supraclav? older than 40?


- other locations? (2)

- consistency, <2 weeks, cervical nodes (50% young adults have)


- inguinal is common - 1-2cm in size, often benign reactive


- supraclav = high risk of malig - 90% in patients older than 40


- paraumbilical


- epithrochlear

LA History


- cause of? symptoms that suggest?


- sites = (4)


- symptoms of?


- clues related to?


- meds?

- identifying cause = localizing symptoms or signs to suggest infection/neoplasm at particular site = sinusitis, pharyngitis, periodontal disease, conjuct insect bites


- const symptoms


- epi clues = occupation, animal, travel, high-risk behav.


- medications - serum-sickness syndrome

PE of LA


- full? consider?


- size of?


- localized?



Causes of Generalzied LA


- M/I/ AI/ D/ rare?

1) Malignancy = lymph, leuk,mets


2) Infections


3) AI - Seropositive Spondyl


4) Drugs


5) Rare = sarcoid, amyloid, lipid, hyperthyroid, Kawasakis, Rosai

Treatment of LA - wait? then?


-no indication for?


- glucos can be? may?

- wait 4 weeks and re-examine


- no indication for empiric Abx


- glucos can be harmful, can delay diagnosis

Options for LNs


- FNA - 1/3 will? other need?


- perform a? as sees?


- gold standard?

1) FNA = 1/3 complete diagnoses, 2/3 require addit. biopsy


2) Core needle biopsy - see arch


3) Excisional LN biopsy = gold standard

Lymphoma - cancer of?


- fifth most?


- lifetime prob of leukemia?


- in young adults?


- many?

- cancer of IS cells


- lymphoma is fifth most common cancer in NA


- 3.8% lifeitme prob. of developing leukemia or lymphoma


- 2nd leading cause of cancer death in young adults


- many years lost

Classifying Lymphomas


- main WHO classes are? (F/D/C)


- more reasonable classes = A/I/H/Z - %?

- main WHO ones = follicular, Diffuse large B cell, Composite, etc


- more reasonable = Aggressive (46%), Indolent (38%), Hodgkins (10%) and Zebras (6%)

Aggressive vs Indolent Non-Hodgkins Lymphoma


- growth? symptoms? survival? cure? often classified as?

1)Aggressive = rapid growth, symptomatic, fatal in months if untreated, potential for cure, * diffuse Large B cell lymphma




2) Indolent = slow growth, asymptomatic, fatal in years, incurable, ** follicular lymphoma

Hodgkin Lymphoma - look for?

- see Reed-Sternberg Cells

Symptoms of Lymphoma - enlarged? low?


- general? (5)


- less than 20% have?

- enlarged LNs


- low blood cell counts


- general = weight loss, fever, night sweats, fatigue, itching


- less than 20% of patients have general symptoms at onset

Staging of Lymphoma


- Stage I at? II at? III both? no? IV - involvement of?


- A - means absence of?


- B - see? (3)

A = absence of B symptoms
B = fever, night sweats, weight loss

III = above and below diaphragm, no liver

A = absence of B symptoms


B = fever, night sweats, weight loss




III = above and below diaphragm, no liver

Diagnosis and Staging of Lymphoma


- perform? (2)


- labs = (3)


- then finally?

1) Biopsy = LN biopsy, bone marrow


2) labs = CBC, LDH, viral serologies (HIV, hep B, C)


3) imaging = CT

Treating Lymphoma - can do?


- CD20 is a? as expressed on? not?


- use? which is?

- can do chemo and radiation


- CD20 is a good target, as expressed on ?90% of B cells NHL, not shed or internalized = use of Rituximab = anti-CD20

Leukaemia - arises in?


- takes over? prevents?

- clonal disease arising in a single haematopoitic cell


- takes over the bone marrow, prevents normal blood cell production

Acute Leuks


- AML = ? blasts have chars of? reminiscent of?


- ALL = ? blasts have chars of? reminiscent of?


- without? will be?

1) AML = myelogenous - blasts have residual characteristics of myeloid cells, reminiscent of neutrophils or monocytes


2) ALL = lymphoblastic = blasts have residual chars of lymphoid cells, reminiscent of B cells or T cells




* without treatment, fatal in weeks

Haem Stem Cell vs Leuk Stem Cell


- in leuk, gets? no?

- in leuk, get formation of blasts, no blood

- in leuk, get formation of blasts, no blood

Why Leuk Makes you sick


- start with?


- as LSC, get decreased? and appears?


- by end, have?


- hard to tell**

- start with nice, blood cell forming bone marrow


- as get LSC, see blood cell production decrease and leukaemia appears clinically


- by end, have useless, leuk filled bone marrow




*hard to tell AML and ALL blasts apart

Acute Leuk Epi


- AML is mostly? vs ALL?

- AML is mostly a disease of older adults


- ALL is mostly a disease of young children

Presentation of Acute Leuk (AML or ALL)


- developed over? see manifestations of?


- A =?


- L = ?


- thrombo = ?


- LA = ?

- develop over a period of weeks, see manifestations of bone marrow failure:


= anemia = pallor, breathlessness, chest pain


= leukopenia = infection


= thrombocytopenia = bruises, bleeding


= lymphadenopathy = mostly ALL

Treatment of Acute Leuk


- still the same?


- Phase 1 is the? via? not a?


- Phase 2 -post?


- in ALL - do? below?

- standard of care for ALL, AML same as 1979


- Phase 1 = Induction of remission via chemotherapy after Leuk appers ***not cure, can relapse


- Pase 2 = Post-remission therapy chemo = cure




* in ALL = do intrathecal chemo, below L3

Tissue Infiltration in AML


- favourite spot? known as?


- seen in? with?

- the gums are a favourite spot = gingival infiltration


- especi. with AML with monocytic characteristics

Leukostasis


- develop? known as? occurs when?


- blasts then? can lead to? (3)

- myeloid leukaemias = sticky blasts


- occurs when blast count > 100


- blasts sludge the microvasculature, can lead to retinal hemorrhage, stroke, resp. failure

Acute Promyelocytic Leukemia


- abnormal? called?


- characterized by? involving?


- known for its? give? (2)


- CR rate is? 2 year?

- APL, there is an abnormal accumulation of immature granulocytes called promyelocytes. The disease is characterized by a chromosomal translocation involving the retinoic acid receptor alpha


- known for its responsiveness to all-trans retinoic acid = ATRA + arsenic


- CR rate 100%, 2 year DFS 97%

Chronic Leukaemias


- CML =? prolif of? (3) and?


- CLL =? just prolif?


- mostly affect?


- more common is? CLL starts?

1) CML = myeloid = see prolif of granulocytes (Ns/Es/Bs) and precursors


2) CLL - lymphocytic = see prolif of B cells




* CML and CLL mostly affect older adults, CLL is much more common than CML and CLL starts much further down Haem Line

CML Presentation


- incidental findings on? such as? also see? (2)


- usually?


- may have?

- incidental finding on routine CBC = leukocytosis, extended left shift, basophilia, thrombocytosis


- usually asymptomatic


- splenomegaly - may be massive

CLL Presentation - finding on CBC is?


- on slide see?


- usually is?


- later in disease, see?

- incidental finding on CBC = lymphocytosis


- see smudge cells


- usually asymptomatic


- nodes and spleen come later in disease

CML Natural History - starts with? then? crisis of?


- median survival?



CLL Natural history?


- starts with?


- develop? then?


- then on CBC get?


- median survival? many never?



CML treatment


- treatment starts?


- use? such as? (5)


- block function of?


- STKIs do no? but help to?

 - STKIs do not cure CML, keep in remission

- STKIs do not cure CML, keep in remission

CLL Treatment


- treatment started only?


- use? such as? (F/CPP)


- give?


- or Bruton's kinase inhibitor =?


- need successive?


- over time see?

- successive rounds of treatment provide control
- chemo has diminishing returns with time

- successive rounds of treatment provide control


- chemo has diminishing returns with time

AML Summary


- treatment is? presentation is?


- alot of? many?


- treatment?



ALL Summary


- treatment is? presentation is?


- so many? many? including?


- treatment?

CML Summary


- is only? presentation? spleen in?


- blasts are?


- genetics?



CLL Summary


- urgency? idea that?


- no? look for?


- treatment is?

Child Presenting with lower back pain, pallor and fatigue - DD?


- ortho =? (2)


- rheum =?


- infectious = ? (2)


- malig = ? (3)

1) ortho = trauma, spondylolysis


2) Rheum = arthritis


3) infectious = viral, discitis


4) Malignant = bone tumour, tumour on cord, leukemia/lymphoma

Most Common Childhood Maligs


- most common at 0-14?


- most common at 15-19?

Childhood Cancer


- % total cancer? third largest?


- most childhood cancers are?


- 2/3 survivors are? 1/3 have?


- are relatively? must be?

-1-2% of total cancers, the leading cause of disease-related death among children beyond infancy


- third largest contributor to PYLL/G after breast and lung cancer


- see 1500 children with new cancer diagnosis per year in Canada, most ALL, 90% survival


- 2/3 survivors have one more more chronic condition, 1/3 have severe complication


- relat rare, diagnoses and outcomes differ, must be suspicious

Leukemia


- is clonal? from both?


- myelos? lymphos?


- acute leukemias %? ALL vs AML %?


- chronic leuks only?

- a clonal proliferation of blood cell precursors, from myeloid stem cells and lymphoid stem cells


- myeloblast = granulocytes


- lymphoblasts = NK, T and B cells


- acute leukemias = 95% of childhood, ALL is approx 80%, AML is approx 15%


- chronic leuks = 5% in childhood

ALL - most common?


- %?


- gender? race?


- peak age?


- 5 year survival?

- most common paeds malignancy


- 25-30% of paeds cancer


- M > F, white > black


- peak age = 2-5 years


- 90% 5 year survival

Making ALL Diagnosis


- look at both? (2)


- perform a? with?


- do a?


- also perform a?


**diagnose leukemia if?

- blood counts and periph smears


- BM aspirat and +/- biopsy


- lumbar puncture for CSF exam


- testicular exam




* leuk diagnosed if there are >25% blasts in BM

ALL Peripheral Blood Caveat


- WBCs may be?


- HbG or plts may be?


- 20% of ALL pts will not?

- white cell counts may be low, normal or high


- HgB or pts may be low or normal


- 20% of ALL patients will not have circulating blasts at diagnosis

Bone Marrow/Periph Blood testing


- morphology - AML - see?


- imm - look for?


- cytogens - use? identify?


- molecular - look at?

- morphology - Auer rods only in AML


- immunophen = use antigen to distinguish


- cytochem - less specific


- cytogenetics - FISh and kary to identify known and unknown leuk clone


- molecular - PCR to look for transcripts

RFs for Childhood Cancer


- genetic? enviro? infection?


- in most?

1) Genetic - in utero, polymorphs, genetic conditions such as T21, fragility syndromes, cancer predisp syndromes


2) Enviro - radiation, in utero, chemical? dietary?


3) infection - rare immune response to common virus




* most- dont know why develops, complex, always take FH, address guilt up front

Children with Down Syndrome and Cancer


- x risk?


- lower risk to develop?


- inferior? as more?


- better outcomes with?

- 10-20x increase risk of leuemia


- lower risk to develop solid tumours


- inferior outcomes for ALL due to more severe toxicities


- better outcomes for AML with less therapy

Clinical Presentation of Childhood Cancers


- often have non? yet need to maintain?


- lack normal?


- presence of?


- often related to? main ones** (2)

- non spec signs and symptoms, maintain high suspicion, consider:


- lack of normal BM output


- presence of leukemic blasts


- related to extramed disease = CNS disease, testicular disease, other

Lack of Normal BM Output preseents as - Hb/ WBC/pt

1) Hb = pallor, fatigue, irritability


2) WBCs = fever, sepsis


3) pts = bruising, bleeding, petechiae

Leukemic Blasts Symptoms


- bone? organs? LA? presentation of? sludging due to?

1) Bone pain = Xray changes, path features


2) Hepatosplenomegaly


3) Lymphadenopathy


4) Lymphomatous Presentation


5) Hyperleukocytosis = WBC >50-100 = can cause sludging

Extramedullary Disease - affects? % in?


- most are? yet some present with? such as? if paenchymal involvement?


- in testicular - see? %?

1) CNS = 1.5-1% at diagnosis


- most asymptomatic, may present with increased ICP symptoms such as HA, V, CN VI palsy


- may show parenchymal involvement = seizure, CN palsies




2) Testicular = 2% at diagnosis = painless enlargment

First 24 Hours - What can Harm patient


- HL =?


- lysis?


- mass? or? (2)

- hypeleukocytosis = sludging


- tumour lysis syndrome


- mediastinal mass


- infection


- bleeding

Further Lab Work for Children - chemistries?


- perform a?


- if fever?


- also improtant to do?


- check?

- chemistries = K, CA, PO4, uric acid, LDH


- CXR


- blood cultures if fever, start Abx


- type and screen


- varicella serology


- INR/PTT

Tumour Lysis Syndrome (TLS)


- occurs at? or soon after?


- cell lysis when? leads to? (3) K/Ur/Ph = cause ???

- at presentation or after tratment initiation


- metabolic derangement resulting from cell lysis with tumour kills, leads to:


1) increased K = arrhythmias


2) increased urate = renal failure


3) Increased phos/decrease calcium = tetany/seizure

Approach to TLS - frequent? no IV? for?


- forced?


- medical?


- give allupurinol to?


- worst case?

- frequent bloodwork


- hyperhydration - no IV additives


- forced diuresis


- medical man. of electrolytes


- allupurinol or rasburicase to prevent, manage hyperuricemia


- worst case = dialysis

Reason for CXR?


- check for? risk of?


- think about? (3)

- mediastinal mass


- anaesthesia risk


- think about:


= SVC compression, airway compression, cardiac tamponade, right ventricular outflow tract obstruction

Other Issues after Diagnosis - infection


- due to? counts dont?


- start? if fever?

- Infection due to dysregulated immune status, WBC and neuts counts dont matter


- start Abx and do blood culture stat if fever or unwell



Other Issues after Diagnosis - Transfusions


- pt transfusuons for? for coag, use?


- RBC transfusion will increase? only do if? use?

1) pts transfusions = for bleeding and procedures, use frozen plasma for coag




2) RBC transfusion = will increase viscosity, only transfuse if symptomatic, use small aliquots due to hyperleukocytosis

Treatment for ALL - chemo phases = (4)


- duration?


- intensity based on?


- includes ?

- chemo phases = induction, consolidation, re-intensification, maintenance


- is a 2-3 year duration


- intensity based on risk group


- includes CNS prophylaxis/treatment

Prognostic Factors for Risk Assessment


- age at? initial?


- presence of?


- immuno?


- response to?


- best indicator?

- age at diagnosis


- initial WBC at diagnosis


- CNS or testicular disease


- immunophenoytpe = B vs T


- cytogenetics


- initial response to therapy*** - best


- pharmacogenetics

Response to Initial Therapy is the most?


- measured by?


- performed following?


- remission defined by?


- MRD able to?

- most important prognostic variable


- measured b minimal residual disease = MRD


- performed following 1st phase = induction


- bone marrow morphology defines remission if blast count <5%'


- but MRD can identify even less cells

Chemo in ALL - use combo of? at?


- now using? such as? (3)

- use combo of non-cross resistant chemo agents at maximum dose intesnity


- designer approach to Therapy, now use targeted therapies such as Ritizumab, Car T-cells or Blinatumomab

Late Effects of Therapy


- depends on?


- can lead to? (6)


- most common cause of death?

- depend on therapy recieved and complications arising during therapy


- obesity, bone health, endocrine dysregulation, neurotox, cardiotox, secondary neoplasms, psychosocial effects




* most common cause of death is relapse

Whole Blood Collection


- plasma contains? (3)


- buffy coat =?


- then finally?

1) plasma = cryosupernatant, crytoprecipitate and fractionated products (PCCs, Albumin, IVIG)


2) Buffy coat = WBCs and Pts


3) RBCs

Old Female - Anemic- Why? (3)


- consider?

- menorrhagia


- blood loss


- iron defic anemia




* consider iron supps

Manifestations of Anemia - RBCS needed to?


- no accurate way to determine? surrogate marker is?


- symptoms = (4)

- RBCs are transfused to increase oxygen delivery to tissues


- no accurate way to determine if oxygen deliv. in inadequate so use symptoms of anemia (non-spec) and Hb level as surrogate markers


- symptoms = fatigue, chest pain, SOB, lightheadedness

Whats in a unit of RBC?


- volume? RBC/ plasma/ anticoag/ and finally?


- one unit raises Hb by? pt isnt?

- volume of RBC unit = 280 ml = 160 ml RBCs, 20 ml plasma, 100 ml of anticoagulant (citrate) and SAG-M additive (sodium, chloride, adenine, dextrose, mannitol)


- one RBC unit raises Hb by 10 g/ L in non-bleeding patient

When Should we Transfuse RBcs


- HB > 90? 70-90 - do if? <70? if younger?

1) Hb > 90g/L = likely inappropriate


2) Hb 70-90 = depends on patient = in CAD, elderly, closer to 80 g/L


3) Hb < 70 = likely approp, younger patients may tolerate Hb <60

TRICC Trail - transfused 1 unit as? mortality higher in?

- transfused 1 unit at restrictive Hb <70 or liberal Hb <100


- mortality higher in liberal group




*similar to FOCUS trial

Acute UGI Bleeding


- higher survival in?


- note increase?

- transfused 1 unit at restrictive Hb <70 or liberal Hb <100


- higher survival in restrictive group, saw more adverse events and bleeding in liberal group




*noted increased portal pressure gradient in liberal group

Acute Coronary Syndrome and HB


- rule to? re-assess as?


- consider closer?

- RCTs - conflicting as CRIT found restrictive did better and MINT, liberal did better


- transfuse a unit at a time and re-assess clinically




**remember CAD, consider transfusion closer to 80 g/l

How to transfuse RBCs


- transfuse one unit over? not more than?


- consider slower rate? if? also consider?


- outcome is? check before?

- transfuse one unit at a time over 2 hours, not more than 4 hours


- consider slower rate and furosemide for patients with suspected impaired cardiac function


- assess the outcome = clinical Hb level, before transfusing further

Writing a RBC Transfusion Order


- order? then?


- max time? longer if?


- always include

1) Order one unit at a time - then reassess patient and HgB between


2) Max is 3.5 hours per unit, longer if at risk for cardiac overload


3) Always include indication for transfusion

Why My Patient be thrombocytopenic


- likely? on film? suggests?

- likely bone marrow failure because there are blasts on blood film, suggests leukemia

Caution when ordering Pt transfusion in? as may? these include (3)


- if immune thrombocytopenia, more effective to?

- thrombotic thrombocytopenic syndromes as may add fuel to the fire:


= TTP, HIT, APLA syndrome




- immune thrombocytopenias, as other therapies such as prednisone more effective

Manifestation of Low Pts


- plts mediate? therefore symptoms include?


- in mouth?


- GU? GI?


- plt transfusion used to?

-pts mediate primary hemostasis, bleedign due to low pts typically seen as:


= petechiae, ecchymoses


= mucosal bleeding = epistaxis, gum bleeding, blood blisters in mouth, GU (hematuria, menorrhagia) and GI (melena, hematochexia)




- pt transfusion used to prevent or treat bleeding

What's in a dose ot Pts?


- 1 adult dose contrain 1 pool of? made from?


- volume? increases count by?

- 1 adult dose of pts:


= 1 buddy coat pool of pts (made from 4 whole blood donations


= 1 apheresis pt = volume 250-300 ml, will increase pt count by 15-50 x 10^9

When Should We transfuse Pts


- when plts less than? treating? prevent?


- when pts less than? to prevent?

- when pts < 50 x 10^9, to treat major bleeding and to prevent bleeding with major procedures


- when Pts < 10 x 10^9, to prevent spontaneous bleeding (except ITP)

When Should We Transfuse Pts


- at any pt count when? such as?


- pts <100 - to treat? prevent?

- Any pt count = to treat severe bleeding in setting of pt dysfunction = antipt agents, post CPB)




- pts < 100 X 10^9 = to treat bleeding in sancutary sites (CNS, eyes), to prevent bleeding in sanc sites

Therefore transfuse for major bleeding if? for minor bleeding

- major bleeding = pts 50-75




- minor bleeding and minor procedures - pts between 50 and 10

How to Transfuse Pts


- transfuse over? max?


- slower rate if? also can give?


- assess outcome via? before?

- transfuse each dose over 1-2 hours (max 4 hours)


- consider slower rate and furosemide for patients with suspected impaired cardiac function


- assess outcome = clinical, pt count, before transfusing further

How to Write a Pt Transfusion Order


- transfuse at? max?


- always include?

-transfuse at 1 hour, longer if at risk for cardiac overload, max is 3.5 hours per unit


- always include indication for transfusion

Manifestations of Elevated INR


- plasma contains? for?


- bleeding due to? results in? (3) E/H/GI


- need plasma to?


- hemostasis needs?

- plasma contains all clotting factors required in secondary hemostasis


- bleeding due to clotting factor deficiency = Echhymoses, hematoma (intramuscular, intra-articular), GI bleeding


- plasma transfusion used to treat bleeding


- require levels of 30-50% for hemostasis

What is in a unit of Frozen Plasma- volume?


- contains all?


- t1/2 is? in?


- dose =? increases?

- volume of 1 unit of FP is 250 ml


- contains all nec. clotting factors for hemostasis = T1/2 is 6-8 hours in non-bleeding patient


- dose = 15 mL/kg (3-4 units) which increases clotting factors by 20%

When Should We Transfuse Plasma - when need?


- for major? when INR is? not really for?


- cant wait for labs for? (2)

** multiple clotting factor defics where a more specific concentrate is not available, and :


1) Major bleeding, procedure with INR >1.5 (most minor procedures such as line placement, paracentesis done safely any INR)


2) Microvasc bleeding, massive transfusion and cannot wait for labs

Frozen Plasma Practical Info


- needs to be?


- must be?


- universal plasma is?

- FP needs to be thawed for 30 minutes


- must be ABO compatible


- universal plasma is AB plasma

How to Write Plasma Transfusion order


- max time? longer if?


- always indicate? have high?

- max is 3.5 hours/unit, longer if cardiac overload risk


- always include indication for transfusion - high INR and why?

Warfarin and Increased INR


- causes defic. in?


- these include? (6) pro/anti

- warfarin causes defic. if Vit. K dependent factors = ,9,10, 7, and 2 and Protein C and S which stop cascade

Prothrombin Complex Concentrates


- contains the? = ?


- are? and made sure to be?


- used for emergent? (2)


- typical dose?


- effect only lasts?

= contains Vit K dependent factors = II, VII, IX, X and Protein C and S


- pooled, virally inactivated products, indicated for urgent or emergent reversal of warfarin or Vit K defic


- typical dose in 1000 units (40 mL) but depends on INR elevation


- effect lasts only 6 hours

PCC Practical Info - infuse volume? over?


- form? therefore is?


- for prolonged reversal, need?


- for emerg bleeding - give? works in?


- for nonemerg bleeding - give?

- infuse 100 units PCC IV over 15 minutes - in powder form so quickly available


- Vit K required for prolonged reversal:


- Therapeutic INR and emergency bleeding/procedure = vitamin K 10 mg IV (works in 6 hours)


- Supratherapuetic INR and not bleeding = may require small dose vit K PO alone (works in 24 hours)



Low fibrinogen - seen in?


- assoc with? can complicate?

- seen in obstetrical hemorrhage


- assoc. with microvascular bleeding and can complicate massive hemorhhage

What is in a Unit of Cryoprecipitate


- 1 unit volume? contains? also (4)


- typical dose units?


- increases fibrinogen by? per?

- volume of 1 unit = 15 ml


- contains fibrinogen = also factor VII, VWF, XIII,fibronectin


- typical dose = 10 units


- increases fibrinogen by 0.5 g/L per 10 units

When Should you Order Cryoppt?


- if fibrinogen <1.5 ? <1?

- fibrinogen <1.5-2 - to treat life-threatening hemorrhage


- fibrinogen < 1g/L - to treat microvasc. bleeding

Summary - Approach to prescribing blood transfusion


- must consider? as well as the?

- what is mech of abnormality


- potential manifestations


- management of the problem

Informed Consent for Blood Transfusion


- obtained by? always is? except?


- must discuss? and then?


- afterwards?

- obtained by treating physician


- mandatory except if patient's life at immediate risk and neither patient nor SDM able to conset


- benefits, risks, alternatives discussed


- discussion documented in chart


- afterwards, advise patient of what was recieved

Risks of Transfusion - from RBCs (2)? from pts? from volume? or?


- viral infection is?

- main ones:


= red cell sensitization and hemoltyic transfusion reaction


= febrile reaction from pts


= circulatory overload


= minor allergic reaction




*viral infection = less than one in a million

Risks fo Transfusion - most common? (3)


- serious = (4)

- common things = fever, hives, Taco


- serious = TRALI, sepsis, anaphylaxis, wrong blood

Acute Transfusion reactions - occur?


= (4) F/U/D/H

- symptoms occurring during or shortly after transfusion:


= fever


= urticaria


= dyspnea


= hypotension

fever def and DD - defined as? up to? may present with?


- DD = (4) A/B/F/U

- >1C rise in temp and temp >38C during or up to 4 hour post-transfusion, may present with chills/rigors


- DDx:


= acute hemolytic transfusion reaction = AHTR


= bacterial contamination = BaCon


= febrile non hemolytic transfusion reaction = FNHTR


= fever due to underlying illness

Acute Hemolytic Transfusion Reaction = AHTR


- mech is due to? less common due to?


- manifests as? (6) F/C/H/P/H/N/V/D

- mechanism: due to ABO incompatibility, less common due to other minor blood group


- manifests as fever, chiils, hemoglobinuria, pain, hypotension, N, V, dyspnea, renal failure, DIC

Managing AHTR - stop? check for? compare?


- notify? send?


- send samples to?


- send labs to look for?


- give?

- stop transfusion


- check for clerical error = amr band vs blood label


- notify blood bank, send bag bank


- send samples to recheck ABO group


- send labs to look of rhemolysis - CBC, LDH, bili, haptoglobin, creatinine, INR, PTT, fibrinogen


- support care

BACTERIAL CONTAMINATION (BaCon)


- blood components can be? from? (3)


- most often occur in? due to?

- blood components can be contam by normal skin flora from donor, bacteremia in donor, contam in handling (rare)


- most often occur with pts due to room temp storage

BaCon Manifestation and Management


- manifests as? (6)


- manage by stopping? notfiy? quarantine? culture? start?

- Manifests = fever, rigors, tachy, hypotension, N, V, dyspnea, DIC


- Management = stop transfusion, notify blood bank and quarantine other blood components from same donor, culture patient and start broad-spectrum Abx immed.

Febrile Non-Hemo Transfusion Reaction (FNHTR)


- mech = in product there are? such as?


- leads to?


- diagnosis of?

- Mech = cytokines in transfused product, recipient Abs (to WBCs or pts) in transfused product


- Manifests as fever, chills, rigors, N,V, hypotension


- is a diagnosis of exclusion

FNHTR Management - pause? give? if fever resolves?

- pause transfusion


- give acetaminophen


- if fever resolves and no serious symptoms, then restart transfusion

Managing fever Patient during Transfusion



If Have Fever and Serious Symptoms

Urticaria Def and DD


- defined as? assoc with? may present with? FE/AE/D/W/HT


- DD = major? minor? cause?

- urticaria = hives = assoc with allergic reaction, may present with facial edema, airway edema, dyspnea, wheezing, hypotension, or shock


- Ddx:


= anaphylaxis/ major allergic reaction


= urticaria / minor allergic reaction


= urticaria from another cause = drug/food

Anaphylaxis Mechs - mostly?


- recip has?


- transfusion of?


- passive?

- most unexplained, potential mechs:


= recip has IgG against missing protein


= transfusion of allergen to sens patient


= passive transfer of IgE from donor



Anaphylaxis Manifestation and Management


- main manifestation is? (3), some resp as?


- CV as?


- management to? give?


- if anaphylaxis, give? then? then? (2 - E/C/V)

- Manifests as cutaneous reaction such as rash, pruritus, angioedema, some resp such as wheezing, stridor, dyspnea and some CV such as hypotension, chest pain and tachy


- Management = stop transfusion, admin diphenhydramine


- if anaphylaxis, give DPH then epinephrine, corticos and vasopressors

Urticaria and minor Allergic Reaction


- very? mech is something?


- manifests with no?


- management is to? give? then restart if?

- very common (1 in 100)


- mechanism - something in plasma


- manifests with no serious symptoms


- management = pause transfusion, give DPH 25-50 mg po/iv and restart if urticaria < 2/3 of body and no serious symptoms

Managing Hives



Hives and Serious Symptoms



Dyspnea Def and DD = ? assoc with?


- TACO =?


= TRALI =?


- major? or not?

- dyspnea = SOB, may be assoc. with drop in O2 sat


- DDx:


= transfusion assoc. circulatory overload = TACO
= transfusion related acute lung injury = TRALI


= major allergic transfusion reaction


= dyspnea not related to transfusion

TACO - mechanism is?


- RFs = (3)


- manifests as? O/C/TC/HT/ increased?


- CXR can fine?



- mech = volume overload


- RFs = CHF, elderly, renal dysfunction


- manifests as orthopnea, cyanosis, increased HR, increased BP*** and increased JVP


- CXR finds volume overload


- NT-proBNP from normal to elevated after transfusion

Taco Mangement


- stop? CXR to? support via?


- key is?

- stop transfusion


- CX to discern other causes


- support = oxygen and diuretics




* prevention is key

TACO Prevention - transfuse one?


- do over? for?


- consider use of? particularly for pts with? age?

- transfuse one unit at a time for prophylactic transfusion

- transfuse slowly over 3.5 hours for prophylactic transfusion


- consider use of furosemide in patients >60 years or hx of CHF

TRALI - also known as?


- defined by onset of?


- see new? on CXR see?


- no evidence of? no pre-existing?

- non-cardiogenic pulmonary edema


- definition = onset during or within 6 hours of transfusion


- see new acute lung injury, bilateral infiltrates on CXR


- no evidence of circulatory overload and no pre-existing acute lung injury

TRALI Mechanism- Ab hypothesis includes? sbstances then cause?


- two event hypothesis has underlying? then see?

1) Ab Hypothesis


- donor Abs lead to release of substances that cause pulmonary endothelial damage and cap leak




2) Two Event Hypothesis


= underlying condition = 1st event


= transfusion of BRM or Abs = 2nd event

TRALI - Manifests and Management


- manifests as? (4) D/H/F/HT


- manage by stopping? assess? quarantine?


- do a?


- provide?

- Manifestations = dyspnea, hypoxia, fever, hypotension


- Management - stop transfusion and assess patient, inform transfusion lab and quarantine other products with dangerous Abs, CXR and supportive care = oxygen, fluids, mech vent in 75%

Managing Patient with Dyspnea During Transfusion

Hypotension Def and DDx


- >? in?


- csn be due to? (6)

- >30 mmHg drop in SBP or DBP


- DDx:


= AHTR


= BaCon


= TRALI


= Anaphylaxis


= Severe FNHTR


= Bradykinin Mediated Hypotension

Mech and Manifestation of Hypotension


- mediated by? often occurs with? also often involves?


- manifests as? (4)

Mech = Bradkinin-mediated, often occurs with pt transfusion and often involves ACE inhibitors




Manifestation = assoc. with dyspnea, urticaria, nausea, vomiting

Management of Hypotension - stop? provide? rule out other? such as?


- check?


- culture?


- look for symptoms of?


- look for signs of?

-stop transfusion


- supportive care = fluids


- rule out other transfusion reactions such as:


= AHTR = check bag for clerical errors


= BaCOn = culture bag and patient


= Look for symptoms of dyspnea and CXR = TRALI


- look for skin and allergic symptoms = Anaphylaxis

Delayed Reactions in Transfusions = (4)

= DHTR
= TTI


= PTP


= TaGVHD

Delayed Hemolytic Transfusion Reaction - results from formation of? in response to?


- occurs after?


- leads to? decreased? increased? (3)


- need to identify? give?


- notify?

- results from formation of Abs in recipient to transfused RBC that was not initially detected


- occurs 3 days-2 weeks after transfusion


- see hemolysis = decreased Hb, increased retics, increased bili, increased LDH, decreased hapto and + DAT


- need to identify Ab and give Ag neg. blood for future transusion


- notify patient that they have Abs

Transfusion Transmitted Infections = TTIs


- use questionnare to? these include?


- test all? for? (6)


- risk is?


- may be? that?

- all volunteer donors


- donor screening questionnaire to screen for diseases not captured = malaria, CJD


- donor testing = HIV, Hep C,B, HTLV, West Nile, Syphilis, Chagas


- risk is negligible but not zero


- potential pathogens we dont yet know about

Function of Skeleton - (4)



- locomotion and function


- protection of soft tissue and viscera


- environment for marrow


- mineral depot

Long Bone Anatomy - at end? between that and middle?


- metaphyses is where?

- epiphysis at end of bone, metaphysis between epiphysis and diaphysis (middle of bone)


- metaphysis is where bone flares

Bone Organic vs Inorganic - %?


- organic includes? has both? contains? minerals are laid down on?


- inorganic has deposition of? is seen on?

1) organic = 30%


- collagen type I scaffold "osteod", osteoblasts, osteoclasts, periosteam, BVs and nerves


- minerals laid down on collagen scaffold




2) Inorganic = 70%


- calcium phosphate salt deposition, hydroxylapatite, seen on xray

Bone Types - L vs W?


- majority of bone is? tubes arranged?


- woven bone seen in? seen in? is more?


- cortical more on?


- both cortical and cancellous are?

- lamellar bone and woven bone - majority of bone in body is lamellar bone, tubes arranged parallel to lines of stress


- woven bone seen in immature bones - in kids and at fracture sites, more flexible


- cortical bone and cancellous bone - both have lamellar bone


- cortical makes up wall of diaphysis, cortical more on edges

Bone Mechanics - mineral component for?


- stiff so? strong so? brittleness so?


- organic component for? is?

1) compression load = mineral component


- stiff = deforms very little under laod


- strong = high load before failure


- brittleness = breaks with veyr little deformation


- collagen component makes it flexible




2) Tension sheer load = organic component


- elastic



Fracture - is an?


- trauma increase? stress decreases? pathology decreases?

- interruption in the continuity of bone


- trauma = increased force against normal bone


- stress = low force that is repeated, overwhelms normal bone and healing response


- pathologic = less force against abnormal bone

Stress Fractures


- due to? happens in? as? transfer?


- see acute chnages in?


- risks? (4)

- do to overuse/fatigue, happens in areas not used to seeing force, muscles are overwhelmed and transfer abnormal force to the bone


- see acute change in amount/intensity of activity


- risks:


= lower extremity


= tennis/ track/ distance/ basketball


= female


= delayed Xray, CT, MRI

Pathological Fracture


- bone is?


- two most common causes?


- can be due to?


- seen in?


- most common at?


- on xray see?

- bone and its biomechanical properties are weakneded


- two most common causes are metastatic disease and hematologic malignancies such as multiple myeloma


- can be due to metastatic tumour


- seen in older age group (>50)


- also seen in breast,lung,renal, prostate, thyroid, hema MM - mets often comes from paired structures


- axial sites are most common


- xray - see osteolysis


- see osteoclast activation via RANK

Pathological Fractures - osteomalacia vs osteoporosis - decreases?

1) Osteomalacia = less organic matrix = then less decreased inorganic




2) Osteoporosis = decreased inorganic


- see fragility fractures

Pathological Fracture - Biphosphate Paradox


- biphos can cause? that?


- bone is? but also is? not good for?


- increased risk of?

- biphos can cause paadoxial chnages in bone, can predispose to fractures as alter mineralization


- bone is stronger but more rigid, not good against shearing or bending forces


- see reduced incidence of fragility fractures


- see increased risk of femur fractures

Traumatic Fracture Appearance


- detemrined by?


- cimminuted?


- displacement determined by? (3)

- pattern determined by mechanism of injury and direction of force


- ex/ simple vs comminuted = comminuted = multiple fragments**


- displacement determined by:


= integrity of perisoteum


= direction of force


= pull of unopposed attachments




*displacement described according to position of distal component relative to proximal

Communication Traumatic Pattern


- closed reduction is reversing?

- closed reduction = reverse the deformity by reversing mechanism and displacement

Tensile or Distracting Force - Trauma Pattern


- type of fracture?


- fracture line is?


- often from?

- see transverse fractures


- fracture line perpendicular to long axis (+/- 30 degrees)


- often high energy



Compressive Force - Trauma Patterns


- type of fracture?


- fracture line is?


- from?

- oblique fractures


- fracture line 30-60 degrees greater than perpendicular to long axis


- high energy

Spiral Fractures - Trauma Patterns


- fracture line is?


- energy? type of froce?

- fracture line greater than 60 degrees to perpendicular to long axis of bone


- low energy


- rotational force

fracture Displacement - consider (7)


- fractures most oftne lead to?

- translational


- direction = AP, Med, Lat


- quantity % of diameter


- length


- impaction/shortening


- distraction/ lengthening


- quantify


- fratures most often lead to shortening, may get lengthening if soft tissue is interposed

Fracture Displacement - angle described as?


- angle described by direction?

- angle described by direction of displaced distal fragment


- angle described by direction of apex of created angle: varus vs valgus

Valgus vs Varus - apex is?

- Valgus = apex medial




- Varus = apex lateral, distal medial

Xray interpretation Checklist - intro? pattern? location? displacmernt? exceptions?

- introduction = views, site, patient


- pattern = simple vs comminuted, transverse, oblique, spira


- location = name bone, rule of 1/3s, epiphysis, metaphysis, diaphysis, intra-articular


- displacement = translation, length, angle, rotation, distal relative to proximal


- exceptions - fractures of humeral head and femoral head and neck

Pediatric Fractures - Salter-Harris Classification - S/A/B/T/C


- have thicker? fractures less likely to?


- msot bone is? more?


- most fractures occur at?

= Straight


= Above


= Below


= Through


= Crushed




*have thicker periosteum, makes fractures less likely to displae


- most bone is woven, more elastic and not rigid = angulated breaks, less likely to be complete with rotation or angulation componenet


- most fractures occur at growth plates where there is more woven immature bone

Pediatric Fractures - Type 1 through 5


type 2 invovles? 3 goes through?


- 4 - from? into?


5 - is a full?

-Type I: transverse across growth plate


-Type II: across growth plate and involvesproximal metaphysis


-Type III: across growth plate and goesthrough physis


-Type IV: goes from metaphysis into the physis


- Type V: compression fracture of growthplate

Healing Response


- three phases?


- overlap of? process take around?


- fracture does not?

= inflammation phase, reparative phase, remodelling phase


= overlap of phases, process takes months or years


- fracture does not regain full strength untul about 2 years

Hematoma Phase (inflammation phase)


- sourrounding fracture is?


- have assoc.


- see necrosis of?


- time course?

- hematoma surrounds fracture


- assoc. intramedullary hemorrhage


- necrosis of bone ends


- inflamm. mediators


- time course is days or weeks

Proliferative Phase (Reparative phase)


- new? such as?


- response from?


- time course?

- new bone forms:


= periosteum, endosteum, cortex, pluripotential mesenchymal cells


= response primarily from periosteum


- time course = weeks and months

Remodelling Phase


- first bone is? process is?


- bone hypertrophies accoridng to?


- signal for maturation is?

- initial bone is "woven"


- remodelling an ongoing process


- bone hypertrophies according to Wolf's law


- trabecular formation and realignment


- signal for maturation is application of stress

Timing of Healing and Strength


- Hema? inflamm? soft callus? hard callus? remod takes?


- beginnign of woven bone is?


- hematoma and inflammation one pahse

- soft callus os beginning of org of woven bone, hard callus when well established

Fracture Healing - Timing


- on palpation feel?


- pain on?


- xray not normal for?

- tenderness on palpation


- pain on fracture stress = angulation, weight bearing


- xray not normal for months - can see fracture lines


- think of activity type

History of Fractures - ask about?


- events? function? assess?

- allergies


- meds


- PMH


- last meal


- events = mechanism, energy high vs low


- function = occupation, handedness, ADL independent, sports/interests


- assessment = multifocal MSK, head, thorax, abdo, spine, neurovasc

Fracture Examination


- around? also check?


- look for? E/S/T - ROM NV? screen?

- skin/wounds around wound/trauma, also check remainder of limb


- deforms, position of limb


- ecchymosis


- swelling


- tenderness


- ROM = pain, decreased, crepitus


- neurovasc status


- MSK screen


- most common assoc. injury is neurovascular, need to do distal vascular exam

Radiograph Rules


- rue of 2s = (3)

- rules of 2s


= 2 orthogonal views


= 2 joints above and below


= 2 sides PRN = pediatric

Goals of Fracture Treatment - save? (3)


- restore? while?

- saves lives, save limbs, save joints


- restore function, prevent complications

Main Three Principles of Fracture care - R/I/R

1) Reduction


2) Immobilization


3) Rehabilitation

Reduction and Immob. Immediate


- gross? not triyng? simply?


- prevent? minimize? relief?

- gross realignment - not trying to get displacement perfect, simply re-align limb grossly


- prevent further injury


- minimize blood loss


- pain relief


- transport


- temporize for consultation

Closed Reduction Definitive - Correction of Deformity


- no reduction needed if? or if?

- no reduction needed if initial position acceptable


- no reduction if displacement is zero or acceptable, can move onto immobilization

Closed vs Open Reduction


- closed is no? indirect? non?


- open means? direct?

Closed = no visualization, indirect manipulation, non-operative




Open = means surgical, direct visualization, direct manipulation, operative

Reduction means? to?


- must be? to?

- surgical procedure to restore a fracture or dislocation to the correct alignment


- For the fractured bone to heal without any deformity the bony fragments must be re-aligned to their normal anatomical position

Closed vs Open Reduction

- Open reduction is where the fracture fragments are exposed surgically by dissecting the tissue




- Closed reduction is the manipulation of the bone fragments without surgical exposure of the fragments

Closed Reduction Step 1 - Analgesia - for? helps to?


- muscles are in? need to?

- comfort


- relaxes voluntary and involuntary displacing forces


- muscles are in spasm and are contracting, need to neutralize this

Closed Reduction Steps


- then provide? which? heps to?


- finally? by applying? using?

Step 2 = traction - try to tire out muscle, may end up reducing displacement as well


Step 3 = Reverse deformity - apply forces opposite to displacing force as splint or cast must maintain reduction forces

Closed - Post Reduction must?


- can do?


- ensure?

- must re-examine neurovascular exam/status


- xray - acceptable


- need to ensure new position is accetable

Casting Immobilization


- see adequate?


- during acute injury crescendo - use? as?


- plateua - use? as?


- want frequent?


- need to account for?

- see adequate padding = Gypsum plaster and molding


- acute injury swelling crescendo = non circumferential split - therefore start with


- subacute injury swelling plateau = circumferential cast to increase stability


- maintenance of reduction reliability = frequent Xray followup


- need to account for continued swelling


- can apply circumferential cast for definitive mgmt after swelling has subsided

What's an Acceptable Reduction - Fracture Factors


- avoidance of? return? avoid?

- evidence based criteria range


- union rate


- avoidance of deformity


- return to function


- avoidance of complications




*criteria different for each bone

What's an Acceptable Reduction - Patient Factors - consider? (3)


- crtieria is?


- if not satisfactory?

- age


- functional demand/goals


- comorbidity




*criteria different for each patient, functional demands of patient have impact on displacement management


- if unsatisifactory reduction radius, try closed reduction again or proceed t open reduction

Open Reduction Advantages - more?


- early?


- aovids?


- implant will?

- accurate reduction


- reliable maintenance of reduction


- early mobilization - patient, limb


- avoids prolonged time in external immobilizers (internal fixation)


- implant will hold fracture in desired position

Open Reduction Indications


- inability to?

- inability to obtain or maintain an acceptable reduction by closed mean

Open Reduction Special Scenarios


- strict? as need to?


- when there is? such as? (3)


- or if there are? as may develop?

- strict acceptable criteria - need to preserve blood flow


= high risk of AVN
= femoral neck


= talus neck


= scaphoid waist


= intra-articular fractures = may go on to develop OA with articular damage, want no displacement in this case


= Salter Harris III or IV

Open Reduction Indications - compromise of? (2)


- pathology of? as it prevents?


- if cannot?


- for both (2)


-

- vascular compromise


- neurological compromise


- metastic pathological features as tumour prevents bone from healing (even if no displacement)


- do if closed reduction unacceptable


- for hip and femoral shaft fractures




* need to document neurovasc status

Open Reduction Risks


- do for? or for?


- complications from? - (4)

- use OR if result from closed reduction is unacceptable for type of fracture = hip, femur, polytrauma, even undisplaced,


- complications from long term immobilization:


- DVT/PE


- pressure ulcers


- pneumonia


- pain


- nursing care

Open Reduction - Open Fracture


- infection due to? can lead to?


- problem as?


- deformiton may?

- infection due Staph, Strep, Clostridium, life-threatening sepsis, limb threatening amputation


- due to communication with external enviro


- deformation may push bone outside muscular envelop, open would chnages management

Open Fracture IV Antibiotics


- risk of amputaiton when wound < 1cm? when > 10cm?


- increase amputation risk with? (4) - treatment time? defect in? injury to?


- strong bearing on?


- high risk = level 3 = risk of amputation is 25%

- has strong bearing on prognosis

Open Fracture Approach - must consider (6)


- compromise prognosis when?

- tetanus status


- emergent OR - 6 hours


- when/where, ABCs


- wound size


- contamination


- soft tissue defect




* prognosis compormised when outside 6 window, open fractures always high energy, ATLS is trauma protocol

Open Fracture treatment - give IV? also give?


- then steps = (4)


- need to?


- most limb threatening infection?


- do? to reduce?

- IV antibiotics


- tetanus


- irrigation and debridement, ORIF, wound cover




* need to close wound so fracture no longer exposed


* Clostridium tetani is most limb threatening infection


- see irrigation, debridement, stabilization with hardware to reduce risk of infection and amputation then close wound

Open Fracture IV Antibiotics


- start with? such as?


- if wound > 10 cm?


- if soft tissue defect or gross contam?

- start with Gram + = Ancef


- then move to Gram - if the wound >10cm = Gentamycin


- if soft tissue defect or gross contamination = anaerobes = Flagyl

Complications Approach Fractures - Early


- local (3)


- systemic? **

local = infection, neurovascular, compartment sx




systemic = fat embolism syndrome





Complications Approach Fractures - Late (5) early? systemic?

local - stiffness, malunion, nonunion, AVN, osteoarthritis




- systemic - none

Early Local Vascular Injury


- is a? essential to get?


- can be both?


- always assess? and make sure to?

- surgical emergency


- early diagnosis and treatment essential


- limb and life threatening


- assoc. with displaced and/or open fractures


- always assess and record vascular status, even in closed fractures

Early Local Neuro Injury


- always assess? assoc with? assess?


- laceraiton assoc with?


- explore?


- closed injuries - observe for? even if?


- nerve may be? is the most?

- always assess and record distal function


- assoc. with specific fractures


- assess both pattern and severity of loss


- laceration assoc. with open injuries


- explore open injuries


- observe closed injuries for 3 months


- explore closed injuries at three months if recovery has not occurred


- nerve may be overstretched, causing dysfunction - most common cause of injury is overstretching

Early Local Compartment Syndrome


- compartments defined by? with?


- pressure normally is? yet in CS?


- signs when? in the?


- >6 hours?

- compartments defined by fascial envelop, muscles, nerves BV in compartment


- pressure in normally higher in vascular bed then tissues around it, see reversal in CS where pressure in interstitium is higher


- see signs and symptoms caused when the intracompartmental pressure exceeds perfusion pressure in an anatomic compartment


- see irreversible muscle necrosis at >6 hours contracture

Causes of Early Local Compartment Syndrome


- intracompartmental = (5)


- extra = ***** - may get?

- Intra compartmental = fracture, crush injury, coagulopathy, vascular reperfusion, pus/tumour




- extra compartmental = cast, cast, cast, cast, burn eschar


- may get edema and compartment syndrome after reperfusion

Clinical Diagnosis of ELCS


- presents as? with? seen as?


- discuss?


- determine via?


- RF is?

- ++++ pain, pain with passive stretch, tense comp = pain out of proportion


- discuss pain scale, pain evolution, pain setting, use of analgesics over time


- determine via pressure measurement


- RF for CS in high energy injury

Unreliable Pain Perception in?


(7)

- paediatric


- elderly


- head injury


- intoxication


- intubated


- nerve injury spine/peripheal


- distracting injru

Early Local Compartment Syndrome treatment


- release? then? re-eval every?


- no role for?


- need urgert? to release?


- will then need?

- release circumferential constraints


- elevate limb


- re-eval every 15 minutes


- no role for pressure measurements


- need urgent fasciotomy within 6 hours, release fascia longitudinally along length of whole compartment


- will need skin graphs after compartment pressure is released

Early Systemic Fat Embolism Syndrome


marrow contents? common after?


- blood clots will not?


- deposition of lipids in skin?


- see? (4)


- mortality?

- marrow contents spill into venous system, most common after long bone fracture


- blood clots will not cross from R to L side, fat/oil in this case can pass to L side


- deposition of lipids in skin give petechial rash pattern


- see hypoxia, pulmonary edema, petechial rash, CNS depression


- mortality at 15%


- need early ventilatory support, early fracture stabilization

Late Local Complication - Stiffness - most?


- due to? (5)


- most chnages are?

- stiffness is most common complication


chnages:


= inflammatory infiltrate


= fibrotic reaction


= prolonged cast immbolization


= callus adhesions


= inadequate rehab




- most changes that occur are reversible with physiotherapy

Late Local Complications - Stiffness


- can see? (HO) formation of?


- can cause? needs to be?

- can see heterotopic ossification, which is formation of bone outside of the skeleton and soft tissues


- see overexuberant bone formation


- this can cause stiffness, needs to be excised

Late Local Complications - Malunion healed frature is?


- not obtained? not?


- need to have?



- healed fracture position outside of acceptable range


- not obtained = missed fracture


- not maintained = follow up/compliance


- have osteotomy/ open reduction/ internal fixation


- may have cosmetic or functional deficits

Late Local Complications - Nonunion - Hypertrophic


- adequate? inadequate?


- often due to?


- can occur when?


- need to have?


- can have? yet still see?


- hypertrphic nonunion occurs when?



- adequate biology, inadequate stability


- poor casting


- non compliance


- return to activity too soon


- have open reduction and internal fixation


- can have abundant callous but patient still has pain


- hyertrophic nonunion - fracture environment not stable enough for hematoma to progress to woven then lameller bone

Late Local Complications - Nonunion - Atrophic


- suboptimal?


- location often (2)


- can be due to? (7)


- no evidence of?


- cant give? as they?

- suboptimal biology/ vascularity


- location = tibia, femoral neck


- fracture personality


- smoking, meds, NSAIDs, malnutrition, diabetes, open fractures and infection


- no evidence of formation of fracture callous


- no anti-inflamm can be given as they block inflammatory healing phase

Late local Complications - OA, AVN - can happen with?


- AVN often occurs at? (3) FN/TN,SW


- can islands of? develop?


- also may lead to?

- can happen with intraarticular fractures


- AVN = femoral neck, talus neck, scaphoid waist - get weakened bone as have islands of subchondrial bone and no support, can develop osteochondral flaps on femur head


- AVN may also cause compression fractures, abnormal mechanics leading to OA

Non-Accidental Trauma


- unroecgnized %? abuse is?

- unrecognized = 25% risk of serious injury, 5% risk of death within one year


- abuse is second leading cause of mortality in infants and children


- 1-1.5% incidence

RFs for Non-Accidental Trauma


- young? infant age? the first? if child is? parents are?


- fmailes that are?



Red Flags to Watch for in Non-Accidental Trauma


- history of? different? multiple?


- different? delay in?

- history of multiple fractures


- different stages of healing for fractures


- multiple hospital visits


- multiple care givers


- different stories given from different caregivers


- delay in seeking medical attention


- mechanism of injury does not fit fracture/injury pattern

Non-Accidental Trauma - Full Physical Exam


- child must be?


- signs = (4)


- head - look for?


- also look at? (3)

* child must be fully undressed and examined


- sign = bruises, abrasions, burns, cigarettes


- head = examine for skulltrauma, palpate fontanelles if open, optho exam


- trunk = palpate rib cage, abdo


- extremities = palpate every bone


- genitalia

Suspicious Fractures


- MCF? <1 yo? <3 yo? sternal? posterior?

- metaphyseal corner fracture


- femur fracture < 1 yo


- humeral shaft < 3 yo


- sternal fractures


- posterior rib fractures


- spinous process fractures

Suspicious Fracture Workup


- consult?


- make sure to?**


- eplain?



Developmental Hp Dysplasia (DDH)


- is abnormal?


- subluxatable? dislocatable? subluxated? dislocated? or finally?


- more likely to occur in?

- hip dysplasia = abnormal developmental of femoral head and/or acetabulum


- spectrum of instability:


= subluxatable = partial displacement, lies in socket at rest


= dislocatable = can be moved completely out of socket


= subluxated = reducible, outside of socket at rest but can be put back in


= dislocated = reducible


= irreducible




- teratologic hip dislocation = syndromes = Arthrogryposis


- first child more likely to have hip dysplasia

Epi and Etiology of DDH


- incidence is? true incidence


- RFs = (4)


- - uterius problems such as?


- also seen more in?

- incidence of hip instability at birth is 1/100


- true incidence of DDH = 1/1000


- RFs


= breech


= positive FH = 7x increase


= female = 80% cases


= 1st born = primigravida uterus = prolonged periods of abnormal positioning, limited hip motion, tight package, left side more commonly adducted against sacrum


= cultures where babies are swaddled

DDH RFs - Absolute Risk gender? positive? presentation? if held?

1) all newborns = 11.5/1000 = girls = 19/1000, boys = 4.1/1000


2) positive FH = girls 32/1000, boys = 6.4/1000


3) Breech Presentation = 133/1000, boys = 29/1000


4) Swaddling = high risk when hips are held adducted and extended

Natural History of DDH - first seen with?


- can have? get ipsilateral? leads to?


- pain in? then degen?

- leg length inequality - if unilateral


- scoliosis


- ipsilateral knee pain and deformity


- gait abnormality


- low back pain due to hyperlordosis (if bilateral)


- disabling degen. arthritis


- degen. arthritis related to severity of dysplasia

DDH Clinical Screening


1 - look for assymetric?


2 - barlow = perform - move hips? see hips? is a?

1) Asymmetric Abduction of hips




2) Barlow's Sign = Clunk of Dislocation


= hip is in at rest, hip slips out when adducted and a posterior force applied, provocative test



DDH Clinical Screening


- Ortolani sign is?


- Galeazzis sign is?

3) Ortolani Sign = Clunk of Reduction = hip is out at rest, reduces with a clunk when hip is abducted and an upward force applied




4) Galeazzi Sign = shorter thigh segment

DDH Clinical Findings in Older Child (> 3 months)


- absent?


- limited? seen with?


- discrep?


=- painless?


- can do? before 6m? after?

- signs of instability are absent (usually)


- limited ROM = asymmetric abduction


- leg length discrepancy


- painless limp = Trendelenberg gait


- imaging studies = US up to 6 months, radiographs after 6 months of age

Imaging Studies


- do a? on?


- indications? (2)


- radiographs after?

- dynamic US


- coronal and transverse plane


- indications = high risk baby, equivocal PE


- radiographs after 6 months of age, when ossific nucleus has developed

AAP Clinical Practice Guidelines


- do for all?


- check with?


- if positive Barlow or Ortolani?


- imaging?


DDH Management - Pavlik Harness - is the? used for?


- age? length of time?


- use US to?


- abandon if? used during?


- complications (2)


- effective in?

- initial management - Pavlik Harness = guided reduction


- up to 6m old


- full time use for 6 weeks


- U/S to confirm reduction


- abandon if not reduced within 3 weeks


- night time for 6 weeks


- complications = AVN, femoral nerve palsy


- effective in majority of cases (>85%)


- double/triple diapers are ineffective



DDH Management - Closed reduction with spica cast


- done after? age?


- usually done by?


- use imaging to?


- use for?

- done with failure of Pavlik harness


- older than 6 months


- usually accomp. by adductor tenotomy


- CT or MRI scan to confirm reduction in the cast


- Spica cast for 6 to 12 weeks followed by abduction brace

DDH Surgical Management - is a?


- after 18 months, add?


- older child add?


- main risk?

- open reduction and capsulorraphy


- add inominate (pelvic) osteotomy after 18 months


- add femoral shortening osteotomy in older child


- risk of AVN

Clubfoot - Congenital Talipes Equino Varus


- is? seen in? gender? often?


- prenatal diagnosis?


- FH?


- see variability in?

- congenital, 1 in 1000 birth, M:F = 2:1, 50% bilateral


- pre-natal diagnosis by US


- FH = 2nd child has 2-5% chance (20 to 30x baseline rate)


- see variable severity and stiffness

Congenital Talipes Equino Varus Idiopathic Etiology


- mech? neuromusc? arrested? inherited?



= mech factors = unlikely in isolation


= neuromusc defect = subclinical


= arrested fetal development


= inherited (polygenic multifact. trait)



Congenital Talipes Equino Varus Syndromic and Neuromusc. Causes


- seen in? (4)

- spina bifida


- Arthrogryposis


- Cerebral palsy


- Polio

Talipes Equino (Cavo) Varus - known as?


- see deep?


- empty?


- hindfoot varus is? midfoot cavus is?


- see? lateral border?

- hindfoot equinus = hell looks rounded and soft


- deep posterior crease


- empty (soft) heel


- hindfoot varus = apex lateral


- midfoot cavus = deep medial crease


- see forefoot adducted, lateral border is convex



Calcaneovalgus Foot - not? is a? corrects?

- not clubfoot


- is a positional deformity


- correct spontaneously

Treatment Goals - be?


- no? normal? close to?

- plantigrade = flat on ground


- flexible


- painless


- normal shoe wear


- functional


- close to normal appearance

Standard Treatment of Clubfoot - early?


- 80% require? in?


- release of?


- AFO to?


- recurrence?


- long term? (3)

- early serial casting


- 80% required surgery = 3 to 9 months


- postero-medial or complete subtalar release


- AFO to maintain correction


- 20% recurrence rate = reoperation


- long term = stiff feet, weak, painful

Clubfoot Ponseti treatment


- manip?


- serial casting means? average?


- CAVE correction?

- manipulation prior to each casting


- serial casting = weekly changes, above knee onset, average 6 sets


- sequential correction = CAVE = Cavus, Adductus, Varus, Equinus

Clubfoot Ponseti Treatment


- residual? percutaneus?


- cast for?


- full time for?


- until age 4?

- residual equinus = percutaneus tenotomy of achilles tendon


- cast for additional 3 weeks


- foot abduction Orthosis (Boots + Denis-Browne Bar) to maintain


= full time for 3 months


= night and nap times until age 4

Update on Clubfeet


- clubfoot surgery has been?


- use? is easy?


- start?


- essential treatment?

- Ponseti method of casting has virtually eliminated clubfoot surgery


- Ponseti method is easy to learn and implement


- start casting early = 1st month


- night time foot abduction orthosis (DBB) is essential part of treatment package

Ponseti Method Recurrences


- reported up to? poor?


- repeat?


- resume?

- reported up to 20%, assoc. with poor compliance with food abduction orthosis wear


- repeat serial casting, repeat tenotomy as needed


- resume bracing

Ponseti Method Late Recurrence


- foot see? weight bearing?


- perform a?

= supinated foot, weight bearing on outer border of foot


= tibialis anterior tendon transfer to 3rd cuneiform + Tendo Achilles lengthening if equinus present


= posterior release as needed

Surgical Management - Posteromedial Release - Inidcations


- limited?


- failed? late?


- recurrent?

- limited indications:


= failed non-operative management, late referrals (neglected or older clubfoot), recurrent clubfeet (post-surgical), revision surgery





Surgical Management - Posteromedial Release - contains? pinning to? Brace for?

- posteromedial/circumferential release:


= tendons, joint capsule, ligaments


= pinning to maintain position


= Brace for 1 or 2 years

Malalignment - Bowed Legs - Consequences


- problem as?


- disturbance of?


- joint?


- abnormal?


- see? (3)

- cosmetic


- growth disturbance


- joint laxity


- joint instability = patellofemoral, knee


- abnormal gait


- OA


- pain


- functional problems

Bow Leg Deformities - DD (8)


- metabolic =?


- skeletal?

- physiologic Genu varum


- Blount's disease


- Metabolic bone disease = Rickets, Renal disease, X-linked hypophosphatemia


- Skeletal dysplasias = Achondroplasia, MED


- post-traumatic


- post-infectious


- tumour = multiple hereditary exostoses

History of Bowed Leg


- ask about?


- history of?


- also?

- history - when noticed, progression, any symptoms


- pregnancy and birth history = gestation, presentation, mode of delivery, complications


- developmental history


- nutritional history


- history of immunization


- PMH - infection, trauma


- ROS


- FH

Alignment in Frontal Plane


- all babies have?


- neural at? by 7, are?


- at birth, normal to?

- 15 degree varus at birth = all babies have bowed legs at birth


- neutral at 18 months


- 10-12 valgus = 3 to 4 years


- 5-7 valgus by 7 years


- bowed legs are normal from birth to walking age

PE of Bowed Legs


- cna be due to? general?


- assess via satic? dynamic?


- supine? prone?


- main RFs? (20

- body habitus = height, weight


- general = dysmorphic features


- static assessment = standing alignment, frontal/sagittal/transverse


- dynamic assessment = walking: look for varus thrust, foot progression angle, knee progression angle


- supine: ROM and joint stability


- prone = torsional profile


- RFs - heavy, early walking

Physiologic Genu Varum


- seen in? if have?


- often is?


- have bowed?


- no joint?


- MD angle of?


- resolves by?

- early walker


- FH
- bilateral


- femur and tibia bowed


- no joint laxity


- normal physes


- MD angle < 11 angle


- resolves by 2-3 years

Infantile Blount's Disease


- onset?


- is the abnormal?


- decrease?


- leads to deform of?


- inceases?


- causes?

- early onset as a toddlet - is the abnormal or asymmetric growth in proximal tibia


- decreased medial physeal growth


- deformity of proximal tibia


- increasing genu varum


- internal tibial torsion = in-toeing


- varus thrust



Infantile Blount's Disease


- is comon to have?


- gender?


- assoc with?


- more common in?

- commonly bilateral > 50%


- females > males


- assoc. with obesity


- more common in blacks


- in children <2 years, difficult to distinguish from physiologic genu varum

Infantile Blount's Disease - Management Strategies


- if not improving?


- done before?


- role for?


- little evidence to support?

- early osteotomy if the bowing is not improving spontaneously


- ideally before 4 years


- over correct


- role for guided growth (temporary hemiepiphyseodesis)


- very little evidence to support bracing

Late Onset Blount's Disease


- ages? common cause?


- different as common to only?


- have assoc.?


-assess?

- juvenile = 5 to 10 years


- adolescent = 11 years and older


- obesity common


- commonly unilateral tibia vara


- often multiplanar deformity


- assoc. knee pain


- assess femoral alignment = Valgus (1/3), Varus (1/3), normal alignment (1/3)

Late Onset Blount's Disease - Management


- restore? via?


- guided grwoth via? (HE)


- want to minimize? via early? over?

- restore mechanical axis


= acute correction


= gradual correction with external fixator (monolateral, circular)


= hemiepiphyseodesis = guided growth, staple, screw




* want to minimize risk of recurrence = early intervention, overcorrection, complete epiphyseodesis


*consider limb lengths

Features of Rickets


- impaired? failure of?


- impact on growth?


- often are?


- have iregular?


- looser's lines =?


- bowed?

- impaired mineralization


- failure of osteoid to calcify


- growth retardation


- skeletal deformity


- osteopenia = thin cortices, small trabeculae


- irregular widened physes


- flared, cupping metaphysis


- Looser's lines = milkman's pseudofractures


- Bowed diaphyses

Rickets/Metabolic DIsease - ask about? (3)


- perform? give?


- surgical treatment?

- nutritional history


- prolonged breast feeding without supplementation


- limited exposure to sunlight = North


- skeletal survey


- lab tests


- Med treatment = Vit. D


- surgical treatment = residual deformity

Summary = Age consider? Etiology consider?



Peds Orthopedics - Spectrum of Disorders



Clinical Features of Bone Tumours


- 4 ways of presentation (4)

- typically present in one of 4 ways:


= pain


= mass/swelling


= pathological fracture


= incidental finding on xray

Pain Features of Bone Tumours


- most malignant have?


- get pain when? usually from?


- pain at?

- Where:


= location, most malignant tumours are painful and have pain related to lesion




- When:


= with activity/weight-bearing - usually destructive lesion and bone is mech compromised


= night pain = typical of malignant tumors

Pain Features of Bone Tumours


- quantity - malig vs benign


- quality - malig is usually? burning if?

- Quantity:


= severity, pain from malignancy usually severe, requiring narcotics whereas benign not severe




- Quality:


= nature of pain, pain due to malignancy is usually constant, deep seated ache


- may be burning pain if adjacent to nerve

Pain Features of Bone Tumours


- allev by? or by?


- aggrav by?

- Alleviating Factors


= typically analgesics, sitting down or taking weight off leg




- Aggravating Factors


= typically weight bearing

Soft Tissue Mass


- impotant to determine whether? if it is?


-most benign?


- soft tissue tumours usually?

- important to ascertain whether the mass is fixed to bone, then it is likely a primary bone malignancy


- most benign bone tumours do not have soft tissue masses


- soft tissue tumors are usually mobile over bone

Other features of Malignancy on Clinical Assessment


- const symptoms? history of cancer? history of radiation or pagets?

- may have const. symptoms = Ewing's Sarcoma


- may have history of cancer elsewhere = bone mets


- may have history of radiation or Paget's disease = Osteosarcoma

Clinical presentation of Bone Tumours - (4)

= pain


= mass


= pathologic fracture


= incidental finding on xray

Radiographic Features of Bone Tumors - (4)

= bone destruction


= periosteal reaction


= soft tissue mass


= matrix

Bone Destruction on Xray - bone appears?


- due to?

- aka lysis


- bone appears darker on xray


- tumour cells activate osteoclasts in the bone that stimulate resorption


- feature of benign aggressive or malignant lesion

Periosteal Reaction on Xray


- reaciton of? as it is?


- hallmarks of?


- malignant appears? have?


- if benign, has?

- reaction of periosteum as it is lifted off the bone by growing tumour


- some are hallmarks of malignant lesions, others of benign


- malignant - onion-skinning, sunburst, Codman's traingle


- Benign - Periosteal neocortex

Osteosarcoma and Periosteal Reaction = Sunburst


- also known as?


- see spicules?

- "sunburst" or "hair on end " typical features


- spicules of bone emanating at right angles to the bone

Periosteal Reaction - Codman's Triangle


- angle of new bone that? as?


- is a?

- an angle of new bone that is formed along the cortex as the periosteum is lifted up by the tumor


- feature of malignant tumors

Periosteal Reaction - Ewing Sarcoma


- see multiple? as?


- feature

- see multiple lamellae of new bone laid down as tumor elevates the periosteum


- feature of malignancy and Ewing Sarcoma

Periosteal Reaction - Periosteal Neocortex


- thin? made by? after?


- feature of?

- thin "eggshell" of new bone formed by periosteum after the cortex is destroyed by tumor


- features of benign aggressive tumors

Periosteal Reaction - in benign tumors see?

- well-ordered new bone without onion-skinning, sunburst or Codman's triangle



Soft Tissue Mass - Xray - typically seen with?


- mass grown through? presents with?

- typically a feature of primary malignant bone tumours


- mass growth through Haversian BV system, presenting with mass outside bone with bone intact

Tissue in MSK Tumours


- MSK tumours can make?


- if bone? if cartilage? if fibrous tissue?

- 3 types of tissue typically manufactured by MSK tumours


= bone = osteoid = Osteosarcoma


= cartilage = chondroid = Chondrosarcoma


= fibrous tissue = fibrous dysplasia

Osteioid Matrix - looks like? in? called?

- looks like clouds of bone that have been formed in medullary canal or soft tissue


- Osteosarcoma

Chondroid Matrix - called?


feature of? (2) B vs M

- cause "punctate" or "popcorn" calcification


- can be feature of benign (enchondroma) or malignant (chondrosarcoma) tumours

Fibrous Matrix - also called?


- loss of? but not? appears?


- found in?

- AKA = ground glass


- loss of normal bone trabeculae but not completely lytic, there is a hazy matrix present


- found in benign lesions = ex/ fibrous dysplasia, non-ossifying fibroma

Summary of Radiographic Features - Malignant


- often?


- periosteal reaction includes? (3)


- mass?


- make?

- often destroy bone


- periosteal reaction including onion-skinning, sunburst or Codman's triangle


- soft tissue mass


- produce matrix

Summary of Radiographic Features - Benign


- don? periosteal? no? may or may not?

- usually don't destroy bone = exception is giant cell tumour


-periosteal neocortex


- no soft tissue mass


- may or may not have matrix

Enchondroma - benign? also called?

- definition = benign hyaline cartilage neoplasm of medullary bone


- synonyms = central chondroma

Enchondroma - Epi % of benign?


- age? seen in? failure of?


- can be present in?


% malignant?

- Solitary


= 10-25% of benign bone tumours


= all age groups, predominate in 2nd-4th decades


- Enchondromatosis


= Ollier's disease and Maffucci's syndrome = developmental disorder caused by failure of enchondral ossification


= present in first two decades if life


= malignant transformation in 25%



Enchondroma


- sites of involvement? small? long?


- see tenderness over? no? normal?


- gross - size? appears? frequently?

- Sites of Involvement:


= small bones of hands, feer = 50%


= long tubular bones (proximal humerus, femur)


= enchondromatosis = any part of skeleton


- see tenderness over proximal humerus, normal ROM, no soft tissue mass




Gross:


= small, often <3cm, white-grey, translucent, gritty


= frequently multi-nodular

Enchondroma - Microscopic - closely rsembles?


- lacks? dont see?


- on xray, see? erosion of? no?

- hypocellular tumiur closely resembling normal hyaline cartilage


- lacks invasion of surrounding tissues


- dont see multiple nuclei


- radiographic = lesions similar in hand and shoulder, erosion of cortex, punctate calcification (suggests cartilage), no soft tissue mass or periosteal reaction

Enchondroma - Pathogenesis - poorly?


- gene affected?


- abnorms?

- poorly understood


- diploid or near-diploid with simple structural abnormalities, particularly involving chromosomes 6 and 12


- HMGA2 gene frequently rearranged


- A mutant PTHR1 has been ident in subset if patients with enchondromatosis

Chondrosarcoma - defined as?


- synonyms?

- definiton= malignant neoplasm composed of hyaline cartilage


- synonyms = NA

Chondrosarcoma - Epidemiology


- accounts for?


- age? gender?

- accounts for 20% of malignant bone tumours


- adults and elderly


0 M > F (slight)

Chondrosarcoma - Sites of Involvement, Gross


- sites mainly? (2)


- gross appears as? size? is?

- Sites:


= pelvis (partic. iliac)


= long tubular bones (proximal femur and humerus(, ribs




- Gross:


= large, blue-grey, translucent, gritty, soupy


= destructive

Chondrosarcoma - Microscopic - invades?


- see?

- hypercellular tumour that invades bone trabeculae and surrounding tissue


- pleomoprhism, mitotic activity

Chondrosarcoma - Genetics - poorly?


- most have?

- poorly understood


- complex and hetero structural abnorms, particularly involving many


- most have isocitrate dehydrogenase mutations

Management of Enchondroma - are? typically do not?


- assoc with? espec in?


- treat with?


- if repeated fractures? then?

- benign and non-progressive, do not typically require treatment


- can be assoc. with pathologic fracture, esp. in hands and feet


- treat with cast and fracture will heal


- with repeated fractures, scrape tumour out of bone (curettage) and fill with bone graft, cement or synthetic bone substitute

Management of Chondrosarcoma - image? to?


- often not?


- standard is?


- resection is?


- then? via?

- staging= CT of chest and bone scan


- not responsive to chemotherapy or radiation therapy


- surgical management is standard


- wide resection - removal of tumour with a margin of normal tissue around it


- reconstruction of defect - prosthesis or bone graft

Ewing Family Tumours


- defined as? origin? one of?


- % of bone tuours?


- age? gender? more in?

- definition = primitive small cell neoplasm, with neuroectodermal differentiation, one of small round blue cell tumours


- synonyms = Ewing Sarcoma, Askin tumour, Primitive Neuroectodermal tumour


- epi = 6-8% of primary malignant bone tumours, second most common sarcoma of bone and soft tissue in children, majority < 20 years, M>F, more common in Caucasians

Ewing Family Tumours - Sites of Involvement - Osseous


- main site is? of?


- common at?


- rarely in? (5)

= mainly diaphysis or metaphyseal-diaphyseal portion of long bones


= pelvis and ribs = common locations


= rarely skull, vertebra, scapula, hands and feet




-

Ewing Family Tumours - Extra- Osseous - ST/M/V

- soft tissue


- mucosa


- viscera

Ewing Family Tumours - Gross -texture? colour? often are?

- soft and/or friable


- tan-grey


- necrotic and/or hemorrhagic

Ewing Family Tumours - Microscopic - cell is? arranged in? cytoplasm?

- small round cell tumour


- cells arranged in sheets, occasionally rosettes


- cytoplasm contains abundant glycogen

Ewing Family Tumours - Immunohistochemical Stains - stain for?

- + CD00, FLI-1


- (+/-) Neuron Specific Enolase, Synaptophysin

Ewing Family Tumours - Pathogenesis


- origin is? may be?


- translocaton of?


- common to do?

- cell of origin remains unknown, may be mesenchymal stem cell


- characteristic translocation partners EWS with an ETS transcription factor family (FLI-1, ERG)


- karyotype showing the most common rearrangement


- arrowheads indicate breakpoint

Management of Ewing Sarcoma


- first do? to? apsirate?


- responsive to?


- surgery to?


- sometimes need?

- staging = CT of chest, bone, bone marrow aspirate


- very responsive to chemo = referral to medical oncologist


- surgical removal of tumour and reconstruction using prosthesis or bone graft


- sometimes needs radiation if response to chemotherapy is poor or if margins are close

Giant Cell Tumour of Bone


- defined as? but is locally? componsed of?


- also known as?


- 20% of all?


- age? gender?

- definition = benign, locally aggressive neoplasm composed of sheets of neoplastic mononuclear cells interspersed with reactive osteoclast-type giant cells


- synonyms = Osteoclastoma


- epi = 20% of all benign bone tumous, peak between 20-45 years (rarely in immature skeleton)


- F > M

Giant Cell Tumour of Bone - Sites of Involvement


- often at the? of? espec is? (4)


- occassionly seen in?


- xray will shown? cortex is? margin?


- is? so see?

- metaphysis of long bones = esp. distal femur, proximal tibia, distal radius, proximal humerus


- occasionally flat bones and spine


-radiographic = location at end of done, cortex eroded, geographic margin (easy to tell where stops/starts), has neocortex with thin new bone around lesion


- is hemorrhagic, see large cavities

Giant Cell Tumour of Bone - Gross - texture? colour? may have?

- friable, hemorrhagic, red-brown


- may have cortical destruction and extension into soft tissue



Giant Cell Tumour of Bone- Microscopic


- sheets of? nuclei? cells?

- sheets of polygonal mononuclear cells


- osteoclast-type giant cells = 50-100 nuclei


- multinulceat giant cells

Giant Cell Tumour of Bone - Pathogenesis


- poorly? may be from?


- cells express? which increases?

- poorly understood


- cells of origin unknown, possibly derived from osteoblasts


- mononuclear tumour cells express RANKL, which stimulate formation and maturation of osteoclasts from monocyte precursors


- cytogenetically contain telomeric associations representing end-to-end fusions of chromosomes

Giant Cell Tumour of Bone - Management


- mainly? includes? and then?


- high?


- may want to?

- surgical resection - scraping tumour out of bone and filling defect with bone graft or bone cement


- may require use of adjuvant such as liquid nitrogen or phenol as the recurrence rate of the tumour is very high (approx 15%)


- if bone is expendable, it can be resected (proximal fibula, distal ulna)

Osteosarcoma


- defined as? cells make?


- many different?

- definition = conventional osteosarcoma is an intermed. high grade malignant tumour in which neoplastic cells produce osteoid


- other variants = telangiectatic, small cell, low grade central, parosteal, periodteal, high grade surface

Epi of Osteosarcoma - is the most common?


- is? age?


- gender?


- predisposing = (3)

- most common non-haem malingant tumour of bone


- bimodal; 60% < 25 years of age


- M > F = 3:2


- predisposing conditions = Paget disease, prior radiation, genetics

Osteosarcoma Sites of Involvement


- long bones of? (3) site?


- on xray, is? see extensive? immature?


- cortex is?


- MRIs show?

- long bones of distal femur, proximal tibia, proximal humerus


- metaphysis


- radiographic = poorly defined, dense bone formation, extensive soft tissue mass, periosteal reacton with immature new bone formation (sunburn appearance), cortex is intact


- MRI shows tumour inside and outside bone

Osteosarcoma - Gross - size? texture? colour? appears?


- produces a? as it?


- on xray is poorly? no?

- large, fleshy or hard


- gray-white, necrotic


- granular or densely sclerotic (depending on amount of mineralization)


- frequently transgresses cortex, producing a soft tissue mass


- radiographic = lytic lesion, poorly defined, erosion of cortex, no signfic soft tissue mass, no periosteal reaction

Osteosarcoma - Microscopic


- sheets of? that? osteoid is?


- osteoblastics vs condroblastic vs fibroblastic

- sheets of pleomorphic cells producing osteoid


- osteoid is dense, pink, extracellular material


- conventional OS has several subtypes based on extracellular matrix


= osteoblastic = 50% = osteoid matrix


= chondroblastic = 25% = osteoid and chondroid matrix


= fibroblastic = 25% = spindle cells with minimal matrix

Osteosarcoma - Pathogenesis - poorly?


see genetic?


- RB is resp for? if hered, see increase in?


- p53 causes?

- poorly understood


- aneuploidy and complex chromosomal aberrations


- genetic susceptibility:


1) RB = 30-40% of sporadic cases, hered RB causes 1000x risk of osteosarcoma


2) P53 - 35% of cases, increased in Li-Fraumeni syndrome

Management of Osteosarcoma


- historically?



- historically extremity was amputated


- 95% of patients had amputation


- 90% of patients died from mets

Current Management of Osteosarcoma


- staging bia?


- referred to?-


- resections of? with?


** no role for?


- currently?



-

-

Mets- Definition and Epi


- defined as? is the third?


- age?


- often deposits from?

- Defs = neoplasm, usually malignant, originating at another site to involve bone




- Epi = third most common site (after lung, liver)


= majority 40-60 years


= breast, lung, prostate, kidney and thyroid represent over 90% of deposits



Mets - Gross and Microscopic


- appears as? feels?


- tumours attempt to appear like?

Gross:


= occassionaly sclerotic


= friable, tan-haemorrhagic




Microscopic:


= tumours attempt to recapitulate primary


= may not be able to identify by morphology or immunohistochemistry

Mets - Pathogenesis - usually result of? rarely via?

- usually result of haeomatologic spread


- rarely via direct tumour extension

Investigation of Met Carcinoma


- search for? likeky sites? (5)


- do CT of?


- manage?


-treat?

- search for primary - lung, kidney, breast, thyroid and prostate most likely sites


- CT scan of chest/abdo, mammogram, thyroid US, prostate exam


- management of metabolic abnorms esp. hyperclacemia


- treatment of primary with chemotherapy

Investigation of Met arcinoma


- first treatment?


- surgery for?


- treatment almsot always?

- radiotherapy usually first treatment for bone mets


- surgery for mechanically compromised bone to prevent fracture - scrape tumour out of bone, fill with cement, plate, nail or prosthesis


- treatment is almost always palliative

Summary of Investigations for Patient with Bone Tumours


- if malignant features on clinical exam - do? (4)

- if there are malignant features on clinical exam and xray:


= MRI, bone scan, CT chest, biopsy - can be done by radiologist (needle biopsy) or ortho onco (surgical biopsy)

ACL Anatomy


- maintains?


- runs from?


- blood supply?


- AM tight in? PM tight in?


- also has?

- anatomy and function still debated, maintains stability of the kee


- runs from femur to tibia


- patellar fat pad provides blood supply from front


- anteromedial (AM) and posterolateral (PL)


- bundles:


= AM = tight in flexion, an anterior restraint


= PL = tight in extension, rotatory restraint


- blood: middle geniculate artery and trough patella fat pad


- has mechanoreceptor fibres = proprio

ACL Injuries


- more in? due to? resulting from?


- when have injury, see? hear?


- associated? acute vs medial?

- more in females = smaller notch and ligaments, more laxity, different landing biomechanics (greater total valgus knee loading)


-result from noncontact pivoting injuries


- audile pop and immediate hemarthrosis


- assoc. meniscal injuries


- more lateral meniscus tear with acute ACL tear


- more medial meniscal tear with chronic ACL tear


- usually not an isolated injury

ACL: Exam


- Lachman test is? Anterior Drawer? Pivot shift?

- Lachman = pull tibia forward at 30 degress flexion


- Anterior Drawer = pull tibia forward at 90 degree flexion


- Pivot Shift = thigh internal rotation + knee valgus, bring knee from extension to flexion (sudden anterior tibial thrust)

ACL: Imaging - XR generally?


- do a? to confirm need a?


- Segon sign is?

- XR will generally be normal, may see Segon sign


- lack of ACL on Sagittal T2 confirms injury


- Lateral capsule (Segond) sign: small lateral tibial avlsion


- MRI : to confirm diagnosis - Sagittal T2


- can scope as remnant stays with tibia



*lateral bone bruise (trab microfracture) in >50% in acute injury

Treatment Options for ACL


- (3)

1) physiotherapy


2) Custom ACL brace


3) Reconstruction

ACL Treatment

- Factors = activity level, instablity, assoc. injuries and medical condition




- Initial treatment = physiotherapy and mobilization (avoid immob.)




- Isolated ACL tear and competitive sport = reconstruction




* dont treat based on age



ACL Treatment - reconstruct if? may be non-op if?


- in elderly or arthritis?

- Isolated ACL and strenuous activity = reconstruction




- Isolated ACL and recreational and light activity = recon or non-operative




- ACL tear in elderly or arthritis = non-operative

ACL Reconstruction


- not recommended to do?


- instead do a? often from?

- primary repair not recommended = myofibroblasts "coat" at stump end


- graft selection:


1) Bone Tendon Bone = faster healing, earlier return to sport, higher rate of anterior knee pain and arthritis


2) Hamstring Tendon Autograft


3) Single bundle ACL vs double bundle ACL - no signif clinical difference




* use hamstring for most cases


- others = quadriceps tendon, allograft

Reconstruction Options


- options?


- no?

- Bone tendon bone


- single vs double bundle


*no clinically significant difference between single and double bundle repair

ACL Surgical Complications


- suboptimal? causes limited?


- stiff knee known as? seen in?


- BTB = leads to?

1) Suboptimal tunnel placement = too anterior femoral tunnel causes limited flexion, vertical graft causes rotational instability


2) Arthrofibrosis (stiff knee) = occurs in acute reconstruction


3) BTB: anterior knee pain, kneeing discomfoty, extension loss, poor Q-ceps recovery

ACL Surgical Complications


- higher rates of?


- use allograft if?


- main two also?

4) Hamstring = knee flexion and internal rotation weakness, saphenous nerve injury


5) Allograft = higher re-tear in active patients, higher infection (clostridium, HIV), generally used for revision surgery


6) Infection


7) DVT

ACL Post-Op Protocol


- early? (2)


- want some?


- for 6 weeks avoid?


- generally dont need?

- early motion (extension) and early weight bearing


- closed-chain and compressive loading (co-contraction of muscles)


- open-chain extension should be avoided for 6 weeks


- generally dont need a brace post-op



ACL Post-Op Protocol


- no diff. between?


- post op brace proved?


- want early?

- no diff. between accelerated vs non-accelerated rehab


- post op brace proved to be beneficial only in downhill skier


- early progressive eccentric exercise improve quadriceps and gluteal bulk and function

Meniscus: Anatomy - shape? medial vs lateral?


- only 30% is? to?


- stability via?


- not completely?

- crescent-shaped, triangular in cross section


- medial = C shape, lateral = O shape


- fibrocartilage, type I collagen


- only 30% of peripheral are vascularized = genicular arteries


- stability = deepen tibial plateau


- not completely fixed, only part of periphery has blood supply

Meniscus Role - acts as? role in?


- can move?


- lateral is more?


- problematic if?

- shock absorber, role in joint nutrition


- move anteriorly with extension and posteriorly with flexion


- lateral meniscus more mobile (x2) than medial meniscus


- longitudinal tears very problematic

Meniscus tear Classification based on? (4)

- blood supply


- position


- appearance


- orientation

Meniscal Tear


- MM tear is more?


- lateral more with?


- high rate of OA with?

= MM tear = more common = 3x


= LM tear = more common with ACL tear


= high rate of OA after both meniscal tear and meniscectomy



Types of Meniscal Tears


- traumatic - to? often are?


- degen - with? onset?


- periph - has highest?

1) Traumatic tears = young patient, sport related - get surggical repair


2) Degen. tear = older patient with insidious onset - do not do surgical repair


3) Peripheral third tear = highest potential for healing

Meniscal Tear Exam


- Apley?


- McMurray?


- tests?


- can image using? see?

- Apley = prone-flexion compression


- McMurray = IR and ER of tibia from deep flexion to extension - best test


- tests = squat test, McMurray test (ER and IR of knee)




* can see tear on MRI - see white ligaments indicating tear or inflammation

Treatment of Meniscus Tear = Conservative


- no? such as?


- tear is?


- partial?

- no mechanical symptoms = swelling, catching, locking, giving way


- tear is degenerative type


- partial-thickness teat = <5-10mm in length, <1-2 mm displacement



Treatment of Meniscus Tear = Operative - seen in? symptoms of? cant?

- younger patient with acute tear


- mechanical symptoms


- failure of conservative managment

Partial Meniscectomy


- most tears not?


- higher risk of? with?

- most tears not amenable to repair: complex, central, radial, degenerative, unstable flip


- arthroscopic minimal resection to stable rim


- higher risk of arthritis with a more severe meniscal injury

Meniscal Repair - done in? such as?


- able to?

- in peripheral tears = especially in young and in conjunction with ACL tear


- can repair if tear is peripheral

Meniscal Repair Results


- depends on? in acute perihperal? if ACL intact? ACL defic knee?

- depends on location, type of tear, chronicity


- 90% success in acute peripheral tear in young with concurrent ACL recon.


- 60% success rate when ACL is intact


- 30% success rate in ACL defic. knee

Meniscal Cyst


- seen with?


- treated with? (2)



- with lateral meniscal horizontal cleavage tear


- Rx = partial meniscectomy and decompression through it


- Popliteal(Baker) cyst = related to meniscal pathology

Discoid Menisci - can be?


- may develop? hear?


- can be?

- can be complete or partial


- may develop mech symptoms or popping with extension


- can be a congenital deformity



Discoid Menisci - Xray see? widening?


- treat with? if no tear?

- Xray = squaring of lateral femoral condyle, cupping of lateral tibial plateau, widening of joint space


- Rx = partial menisectomy for tear, simple observation if no tear

Rotator Cuff Tear/Impingement Pathology


- acts as a? from? to?


- in athletes, often to?

- a continuum = mild impairment, partial tear, full tear, massive and irreparable tear to cuff tear arthropathy


- tear in chronic management impingment: bursal surface or within tendon substance


- tear in young athlete = articular surface


- deltoid not able to perform its functions without these muscles




*likelihood of full tear increases with age

Rotator Cuff tear - History


- pain? ask about? partial tear can be?


- onset?

- pain = activity related vs rest/night pain


- weakness


- partial tear can be asymptomatic and age related


- gradual onset, or sudden pain after a traumatic event


- acute on chronic tear


- diff. from neck referring pain

Sizes of Rotator Cuff Tears


- small? medium? large? massive?

- small < 1cm


- medium = 1-3 cm


- large = 3-5 cm


- massive > 5cm (>one tendon)

Rotator Cuff Tests


- impngement?


- SS - able to? test?


- IS amd TM - do?


- ER - asssess?


- Xxray see? US? mri?

- impingement tests = Hawkins, Neer


- SS = empty can test, drop arm test


- IS and TM = external rotation tests


- subscapularis = liftoff test, belly press test


- external rotation test assesses infraspinatus and teres minor


- Xray = usually no findings, appears normal


- US - normal


- MRI - white tendon indicates tear or inflammation



Muscles to consider in Rotator Cuff tear - four muscles (4)


- tear - can see? do ?

- SS = supraspinatus


- IS = infraspinatus


- SP = subscapularis


- TM = teres minor


- Tear Arthroplasty - see with proximal humral head migration = indicates loss of SS and IS with proximal humeral head

Rotator Cuff Tear Treatment


- conservative managemen tfor? (5)


- Arthroplasty fr?

- conservative management for:


= impingement syndrome or partial tear


= small full thickness tear


= chronic cuff tear


= noncompliant patient


= medical contraindications


= RC arthropathy = massive irreparable tear with joint arthritic chnages

Conservative Management for RCT


- modify? best exercise?


- PT via?


- meds?


- try conservative for?

- activity modification, best exercise is external rotation


- physiotherapy = RC strengthening, scapular stabilization exercises


- NSAIDs, modalities, steroid or PRP injection


- want to try conservative for 4-6 months

Surgery for RCT


- done if?


- Rx is?

- in chronic impingement non-response to 6 months of conservative manageent


- Rx = Arthroscopic subacromial decompression = bursectomy and acromioplasty

RC Repair - done for? (2)


- can be? (3)


- healing time?

- done for non-responders and large tears


- can be open, mini-open and all arthroscopic


- biologic healing time = minimum 8-12 weeks

RC Repair - Acute full thickness tear for?

- for acute thickness tear = early repair (rapid progress)


- partial tear = debridement vs repair

Large and Massive Cuff tear


- higher? tissue?


- infiltration of?


- treatment? (3)

= higher failure rate = tissue fails


= fatty atrophy and fatty infiltration


= treatment = graft augmentation, tendon transfer, arthroplasty

Signif if Hip Fractures


- incidence? ris doubles?


- large?

- 2.5x incidence in women, see incidence increasing in future


- risk doubles/ 10 years > 50


- 20% require LTC admission


- 50% independent ambulation


- 25% mortality within 1 year


- big burden

Anatomy of Hip - Intracapsular Zone


- is insie? have a?


- therefore is a? risk of? damage to?

- is inside hip capsule, have ring of vessels that come off of femoral artery, travel upwards


- femoral neck base = head


- vulnerable blood supply


- femoral head AVN risk is proportional to displacement of head fragment


- fracture sees damage to periosteum, compromising blood supply to femoral head


- dispalcement surrogate for AVN risk

Anatomy of Hip - Extracapsular Zone


- includes? no risk of? as?

- intertrochanteric and subtrochanteric zones


- no risk of AVN


- multiple blood source

Normal Pelvis Xray


- three? large vs small?


- most common spot of fracture? look for?


- Shenton's line is? want to see?

- three bony rings:


= large = levic brim


= small = obturator rings




-pelvic fracture needs to be on Ddx, most common place for these is in rami, want to make sure intact


- Shenton's line = line along the inner margin of the femoral neck and extending the superior margin of the obturator foramin, want to see smooth continuous arc


- Neck Shaft Angle = 130


- with reduced neck shaft angle, see apex more aaway from midline

Types of Hip Fracture


- intracasp disrupts? closer to? increasing?


- or can be? (2)

- Intracapsular fractures - see disrupted Shenton's line (not smooth, cont), see closer to 90 degrees = increased varus


- Intertrochanteric fractures


- Subtrochanteric fractures

Hip Fracture RFs - big 4? often with?

- age, osteoporosis, female, falls




*often seen with polypharmacy and comorbidities



Hip Fracture Presentation - leg is? (4)


- do a?


- shortens due to?

- shortened


- externally rotated


- unable to weight bear


- guarding/ minimal ROM


- MSK fragility screen


- in intracapsular = abductors and ERs will pull leg out, iliopsoas accounts for shortening

Treatment Plan- Surgery


- unacceptable to?


- always do for?


- risks like? (3)

- closed reduction and immobilization unacceptable


- do if hip and femoral shaft fractures, polytrauma - unacceptable


- unacceptable if mortality near 100%


- see risks like DVT/PE, pressure ulcers and pneumonia


- consider pain, nursing care

Preop Phase - consider? (4)


- proph of? (2), give?


- time to OR is?

- admit to hospital, preop investigations, anesth and med optimize comorbs and stratify risk


- DVT proph, Abx proph preop, analgesics, operative plan, consent


- time to OR < 48 hour

Operative Plan - if Extracapsular Zone - no? perform? with?

- intertroch/ subtroch


- no risk of AVN




*perform open reduction internal fixation

Operative Plan - INTRACAPSULAR Zone - seen in? risk of?


- choice between? (2)

- seen in femoral neck fracture


- risk of AVN


- choice of:


1) open reduction internal fixation


2) hemiarthroplasty prosthetic replacement




*risk of AVN related to displacement at fracture site

AVN Risk - if undisplaced? includes?


- garden 1 - see? garden 2 - is?


- if displaced? includes?


- G3 has increase?


- G4 is a?

1) Undisplaced = low risk of AVN = 10-30%


= Garden 1 (increased valgus, increased angle)


= Garden 2 = still 130 degrees, undisplaced




2) Displaced = high risk of AVN = 50%+


= Garden 3 = increased varus


= Garden 4 = complete, angle close to 90%

Operative Plan - Intracapsular - Non-definitive = Open Reduction Internal Fixation (ORIF)


- risk of? (2)


- may require?


- long term? spare?


- great?



- risk of AVN, non union


- may require revision surgery


- long term definitive


- femoral head spared


- revision surgery unlikely


- great definitive outlook with ORID if short term risks avoided

Operative Plan - Intracapsular - Definitive - Hemiarthroplasty Prostethic Replacement


- no risk of? unlikely to need?


- long term? as?

- no risk of AVN, nonunion


- revision surgery unlikely


- long term nondefinitive


- prosthesis life span 8-10 years


- revision surgery depends

Operative Plan - Old, low AVN risk - do? as unlikely to?

- do hemiarthroplasty, unlikely to wear out joint

Operative Plan - Young, displaced - opt for? likely to? chance of getting?


- want to aovid?

- opt for ORIF, reason is because they are likely to burn through the prosthesis, also chnace they may not get AVN, better outcomes if ORIF is replaced with THR layer


- avoid years of wear on prosthesis if ORIF is done

Operative Plan


Operative Plan - high AVN risk, displaced and old - can do?

- ORIF or total hip

Complications of Hip Fracture Surgery - Early

Local = infection, neurovascular




Systemic = mortality, transfusion, cardiac, medical, DVT/PE, pneumonia, pressure sores




*early = same risks for ORIF and hemiathroplasty

Complications of Hip Fracture Surgery - Late


- local? systemic?


- in ORIF?


- in HA?

Local = revision surgery, AVN/ nonunion, osteoarthritis, prosthesis failure




Systemic = N/A




ORIF - late = AVN, nonunion, OA, need for revision surgery


- HA - late = prosthetic failure, need for revision surgery

Post Operative Hip Fracture Surgery


- goal is for?


- critical factor?


- MDs invovled?

- goal = immediate mobilization and weight bearing, time to get into OR critical factor in mortality


- MD care = nursing, diet, hospitalist, neuropsych, endocrine, PT, occ. therapy, social work, discharge planner, CCAC

Post Operative QBP Bench Marks


- inpatient for?


- inpatient rehab for?


-

- mean acute inpatient LOS of 7 days


- 90% of all hip fracture patients discharged from acute care within 7 days of admission


- mean inpatient rehab LOS of 28 days


- 90% of all hip fracture patients discharged from inpatient rehab within 28 days of admission




- dont need to know

Post Operative QBP


- 25%?

- 25% mortality within 1 year


- 12.5% mortality in ON


- 2.5x incidence in women


- risk doubles/ 10 years women > 50


- 20% require LTC admission


- 50% indep. ambulation

Trauma Overview


- deaths worldwide?


- more affects?


- gender?


- from 10-24, accounts for?

- worldwide, >5 million deaths/year


- 14,000 injuries/day, every six seconds


- low and middle income countries affected even more


- males > females


- trauma is a disease of the young, leading cause of death in Western world between ages 1 and 44


- >50% death in males 10-24


- fourth leading cause of death in all age groups, 2/3 unintentional

Trauma Oeverview


- is a major?


- third most commn?


- many are?


- important factor?

- major cause of morbidity, with third most common cause of years lived with disability, large $ burden


- many are preventable, alcohol and drugs are major players


- speed is an important factor

Mechanisms of Trauma - Blunt vs Penetrating


- blunt seen in?


- penetrating with?

- Blunt = MVCs, pedestrians hit, falls, assaults




- Penetrating = firearms, knives, variety of sharp objects

Mechanisms of Trauma - also can consider? especially for?

- high vs low energy


- seen especially for firearms

Injury Severity - AIS - is an? based on?


- each region gets? 1 = ? 6 =?

= Abbreviated Injury Score = AIS = an anatomic scoring system that divided body into six regions


= each region gets a score from 1-6, with:


=1= mild injury


= 6 = nonsurvivable injury

Injury Severity Score = SS - is the sum of?

= the sum of the squares of the 3 (of the 6) body regions with the highest AIS

AIS



Injury Severity Score -



Injury Severity - ISS correlates with?


- minor trauma defined as? major? severe?

- ISS correlates with length of hospital stay, morbidity and mortality


- minor injury defined as ISS < 9


- major trauma defined as ISS > 15


- severe trauma defined as ISS > 25

Deaths from Trauma - Time Distribution


- if seconds to minutes - must?


- golden hour is? need?


- if days, consider?

1) Seconds to Minutes = prevention key = trauma


2) Golden hour = minutes to hours = appropriate and timely care is key


3) Days - Weeks = sepsis, MOSF

Early Deaths - often due to massive? from?


- or injury of? affecting? (3)

1) Massive Hemorrhage = large vessel injury




2) Catastrophic Neurologic Injury = high spinal cord, brainstem, brain

Advanced Trauma Life Support (ATLS)


- organized? focus on? and determine?


- TEAM = ? for?

- organized approach to trauma pt, focus on initial assessment and management and determination of need for transfer for definitive treatment


- PHTLS = Pre-hospital


- ATCH = Advanced Trauma Care for Nurses


- TEAM = Trauma Eval and mangement = for med students

Approach to Any** Acutely Ill Patient


- need rapid? consider? (5)

- rapid, simultaneous assessment and management of life-threatening conditions


= A = airway


= B = breathing


= C = circulation


= D = disability


= E = exposure

ABCDE - airway is it? protect from?


- breathing consider?


- circulation consider? (3)


- disability - look at? such as?


- E - means? prevent?

A = airway = patency? protection for aspiration


B = breathing = oxygenation, ventilation (CO2)


C = circulation = shock - BP, HR, C.O.


D = disability = neurologic assessment = GCS/pupils


= E = exposure - undress but prevent hypothermia

History of Trauma - AMPLE - ?

- A = allergies


- M = meds


- P = PMH


- L = last meal


- E = events leading to trauma

Approach to Trauma Patient - ATLS - Primary Survey


- airway also includes? B? C? and? D? E?


- deal with each? do not need a?

= A = airway (and C spine protection)


= B = breathing


= C = circulation (and hemorrhage control)


= D = disability


= E = exposure (and enviro control)




* deal with each category before moving on to the next


* do not nec. nee a defintiive diagnosis before going to the OR

Approach to Trauma Patient - ATLS - Secondary Survery


- goal of 2 survey is to detect? perform? start?


- do not go to until? discuss?

- goal of 2 survey is to:


= detect non-life threatening injuies


= head to toe assessment


= radiologic investigations = XRays, CTs




*do not go to 2 survey untilfinished 1 survey


* discuss definitive care = OR, ICU, specialized centre, etc

ATLS Full Approach

Field Traige - Where to Take patient



Field Traige - Where to Take patient

Trauma Management in Toronto - Team - usually has a? with?


- also need?


- non MDs?

- Team = MDs


=Trauma Team Leader (surgery, emerg, Anesthesia, occasionally ortho),


= Anesthesia, gen surg and orthopedic residents,others as needed




= non - MDs = RNs, RTs, Xray techs, USWs, etc

Summary of Trauma


- can become?


- need a?


- not always crucial to?


- key to get?

Best Way to Elicit ABCs? - ask patient?


- if give approp response? from?


- failure to respond/

- ask patient for their name and what happened


- appropriate response suggests no major airway complications (able to speak clearly), breathing not severely compromised (ability to generate air movement to permit speech) and there is no major decrease in consciousness (alert enough to describe)


**failure to respond suggests A,B, or C abnormality

Airway Maintenance - have to protect? make sure dont?

**protect and immobilize neck and spinal cord
* make sure dont rotate head when assessing airway

**protect and immobilize neck and spinal cord


* make sure dont rotate head when assessing airway

Breathing Assessment


- expose? assess?


- listen for?


- inspection of? identify?



Circulation Assessment


- predom cause? eliminate?


- consider?


- look at? (3)



Disability and Neuro Assessment


- rapid? includes? (50


- perform the?

Enviro Control and Exposure


- patent should be? remove? make sure doesnt?

Priorities in Trauma Patient - 1 and 2 Survey


- 1 = assess and manage?


- 2 - perform a? search for?

1 = assessment and management of life-threatening injuries, prioritize




2 = head to toe examination, search for non life-threatening injuries

A and B in 1 Survey


- top priority are? as patient must have?


- no point in having normal?

- A and B = top priority, as patient must have patent airway and adequate ventilation


- no point in having a normal BP if not getting any oxygen in

Airway Management Questions


- is the airway? if not?


- in trauma, first goal is to?

- is the airway patent? - if no, must establish patency


- in trauma patient, first goal*** of A is to ensure C-spine maintained in neutral position

Normal Airway - look at? (4)

= mouth/nose


= orophharynx/ nasopharynx


= larynx/glottis = vocal cords


= trachea

Normal Patient Airway - see intact?


- normal?


- tissues arent?


- in airway, no? (4)

- intact anatomy = bones and cartilage


- normal airway muscle tone


- no swelling of tissues


- no foreign bodies, blood, vomit, teeth in airway

3 possibilities of airway patency?

1 = unobstructed


2 - partial


3 = complete

Recnognizing Airway Obstruction


- if talking? if noisy breathing? no breathing? could be due to?

1 = Talking = normal, patent for now


2 = noisy breathing = snoring/gurglng = partial


3 = no breathing = not breathing due to drugs, secondary injury or complete obsutction

Airway Obstruction - Hoarseness


- means that? likely a?


- these injuries often? have to be aware that?

- means vocal cords affected, likely laryngeal injury or burn


- these injuries can worsen rapdily so beware, airway may be patent now but mat be completely obstructed a short time later due to swelling and//or bleeding

Recognizing Airway Obstruction


- look for? (5)


- listen for? (2)


- feel for? (3)

1) Look - respiratory effort, chest rising, indrawing (trachea, intercostals), paradoxical breathing (chest/abdo) for FBs, vomit, secretions in mouth


2) Listen - noisy breathing, voice (hoarseness)


3) Feel - air via mouth/nose, face, neck (for trachea, subcut emphysema)

Establishing Airway Patency


- remove? via?


- perform the? which then?


- Oro airway? LMA?

1) Suction = remove debris = blood/vomit/secretions


2) Jaw Thrust/Chin Lift = pulls mandible and tongue forward


3) Oroph/Nasoph Airway = pushes and keeps tongue forward


4) Layngeal mask airway

Laryngeal Mask Airway - do if?


- often provides?


- does not however? not a?


- yet can be used as?

- do if other maneuvers dont work


- often provide patnet airway when other maneuvers fail


- does not protect from aspiration = not a definitive airway


- lifesaving piece of equipment

Once Youve Established Airway Patency


- 1st goal to? must also ensure?


- need to be?


- definitive means?

- 1st goal is to establish patency, but: not enough just to establish


- must also ensure airway is protected from aspiration


- needs a definitive airway for this


** definitive airway = tube with a cuff in trachea = with cuff inflated

ETT - means? goes through?

= endotracheal tube, goes through mouth and oropharynx into trachea

Definitive Airway provides? (3) **

= patent airway


= protection from aspiration = vomit, blood


= able to deliver gas by pressure to the lungs

Choosing a Definitive Airway - can be inserted?


- from above? = ?


- from below? through? = (2) C/T

1) From above vocal cords = mouth/nose = endotracheal intubation (oral/nasal)




2) Below vocal cords = go through neck:


= cricothroidotomy = via crico membrane


= tracheostomy = via trachea

Indications for Definitive Airway


- P/P/O/V/P


- almost always give?

1) Patency


2) Protection from aspiration


3) Oxygenation (improves p02/o2)


4) Ventilation (improve pCO2)


5) Pulmonary (suctioning of secretions, rarely sole indication)




*almost always an oral ETT

Indications for Definitive Airway - often oral ETT - 4 Ps**


- patients often have?

= patency


= protection


= positive pressure ventilation**


= pulmonary toilet




*patients often have several of these issues

Airway Management in Elective Surgical Patients


- anatomy often? stomach is? normal? no (2) **

- normal anatomy


- fasted = empty stomach


- normal BP/BV


- no head injury


- no limitation of C-spine mobility

Airway Management in Elective Surgical Patients


- put in? apply? get it? have?


- meds for? ventilate via?


- confirm?

- put in an IV


- appliy monitors


- sniffing position = C spine flexion, head extension


- 100 O2


- anaesthetic meds = hypnosis, paralysis


- ventilate = jaw thrust, oral a/w if required


- intubate


- confirm correct placement of ETT in trachea

Confirming Definitive Airway is in the Trachea


- visualize? exhaling? is the***


- look for?


- equal?


- on tube, see?


- cna perform?

- visualizing tube going in


- exhaled CO2 = gold standard, should be sustained


- chest rising


- equal A/E - listen in axillae


- condensation on tube


- bronchoscopy = look thorugh tube with scope to see if tube is in trachea

Confirming Definitive Airway is in the Trachea


- perform a? does not confirm? as could be in?


- also useful to look at?

- Chest Xray = single view AP CXR


- does not confirm ETT is in trachea, could be in esophagus


- CXR useful for seeing the position of the ETT in the trachea once you have confirmed it is actually in trachea


- also useful for looking at thorax, lungs and rubs





Airway in Trauma Patient


- is? altered? often?


- risk of?


- possible ?


- other injuries of?


- decrease?


- laso (2)

- is emergent and urgent


- altered LOC or uncooperative = HI/intoxicated


- full stomach = vomiting/aspiration


- possible C-spine injury***


- facial #s, neck hematoma, airway injury


- hypovolemic, decreased BP


- hypoxemic

Managing the Airway in Trauma


- presume a? therefore need to?


- importance of putting into? while?


- as it helps to?

- presume C-spine injury**


- C spine immobilization needed = keep in neutral position at all times




- importane of putting into sniffing position while intubating, can do without but does make it more difficult and increases the chances you wont get a good view of the cords so have to be prepared


*sniffing position increases good view of the cords

Breathing - patent airway doesnt always mean?


- patient may be? (3)

- patent airway does not mean adequate ventilation/breathing


- patent may be:


= breathing adeqautely, not breathing at all, breathing but not adequantely (taking small tidal volume breaths or breathing just injuries are decreases O2 and increasing CO2)

Assessing Breathing -2 aspects


- act of? including getting?


- then the? into?

1) Act/Mechanics of breathing = taking normal VT breath, getting O2 into alveoli


2) Diffusion of O2 from alveoli into pulmonary capillaries (and CO2 from capps to alveoli)

Assessing Breathing


- look for? (3)


- feel? assess for? (3)


- listen for (3)

1) Look = resp rate/ distess, adequate TV, chest rising symmetrically


2) Feel =chest wall = tenderness, rib #s, subcutaneous emphysema)


3) Listen = to patient = speaking, pain, SOB, to lungs

Assessment Breathing - Measure (if inad ventilation)


- (2)


- perform a? to look for?


- also do (2)

- oxygen saturation


- ABG


- CXR = PTX, HTX, aspirations, rib numbers


- CT scan of chest


- ultrasounds

Management of Breathing - if breathing adequately


- apply? start with?


- also apply?


*** to all trauma patients?

- apply oxygen mask = start with 100% O2


- apply an oxygen saturation monitor


- monitor for deterioration




*note: apply oxygen to all trauma patient on arrival

Management of Breathing - If not breathing at all (apnea)


- ensure? then? with?


- determine?

- ensure airway is actually patent


- ventilate patient - can be with rescuscitation bag or a ventilator


- determine etiology of apnea

Management of Breathing - If not breathing Adequately


- ventilate? intubate if?


- then?

- ventilate patient if inadequate VTs


- intubate patient if inadequate O2 sat/pO2 despite high FI02


- determine etiology of inad. ventilation

Inadequate Ventilation


- think about?


- affected could be? (4)


- look for?


- poor ventilation could be due to?

- think about neuro control and mechanics of normal breathing and diffusion


- brainstem, SC, phrenic nerve and intercostal nerves, respiratory muscles (diaphragm, intercostal muscles), a breath, O2 into lungs, blood stream, exhale, CO2 eliminated


** injury anywhere can lead to poor ventilation

Brainstem to Lungs


- brainstem affected by? (3)


- spinal cord?


- check wall mainly?


- pleural space? (2)


- lungs (2)

1)Brainstem = injury, drugs, meds


2) Spinal cord = injury


3) Chest wall = chest wall injury = ribs = can affect resp mechanics and cause pain


4) pleural space = PTX, HTX
5) lungs = contusions, aspirations

Airway and Breathing Summary


- must ensure? must have?


-patent airway doesnt?


- lack of breathing due to?


- must consider?


- use adjuncts to? =?

- ensure adequate delivery of oxygenated blood, must have patent airway and adequate breathing


- patent airway doesnt ensure ventilation


- lack of breathing could be due to either airway or breathing


- must take into accoutn trauma issues = CSI, aspiration risk, airway anatomy


- use adjuncts to supplement = ETCO2, oxygen sat, CXR

Common Thoracic Injuries


- (6)

- rib fractures


- flail chest


- pulmonary contusions


- PTX, HTX


- pericardial tamponade


- traumatic aortic injury



Assessing Ventilation - look for? (6)


- auscultate for?


- palpate for (2)


- ancillar =? (5)

1) Look = resp distress, resp rate, TV, chest rising symmetrically, chest wall bruising/open wounds, cyanosis


2) Auscultaiton = ait entry


3) Palpation = chest well = rib fractures, subcut, emphysema


4) Ancillary = Oxygen saturation, ABG, CXR, CT scan, US

Rib Fractures - are the most important due to? (2)


- markers of? as need?

- most important because ofL


1) Assoc. injuries = pulmonary contusion, PTX, HTX


2) Pain - pain management




*rib fractures are markers of more severe concomitant injuries, as signif force required to fracture a rib

Rib Fractures


- 1st and 2nd ribs need?


- with lower ribs, see?


- fractures increase? each rib sees?

- especially large amount of force required to fracture 1st and 2nd rubs


- spleen and liver injuries with lower ribs = 9th to 12


- rib fractures increase morbid,mortal, especially in elderly (each rib increases 20%, 27% increase in pneumonia)

Flail Chest - defined as? fractures in?


- leads to??


- problems related to? (3)

- defined as 3 consecutive ribs, each fractures in 2 places


- leads to free-floating segments


- causes problems related to:


= pain


= paradoxical movement


= injury to underlying lung = pulmonary contusion

Treating Flail Chest


- manage?


- give?


- can?


- surgery to?

= pain management = oral and/or IV, or epidural


= oxygen


= intubation and mechanical ventilation prn


= surgical stabilization of rib fractures

Pulmonary Contusions - defined as? due to?


- may only be seen on?


- over time?


- worsen with?


- usually peak by? resolve within?

- bruising of lungs = microhemorrhages and alveolar hemorrhages


- may only be seen on CT scan initially


- evolve over time***


- worsen with + fluids


- usually peak by 72 hours


- resolve with 5-7 days

Pulmonary Contusions


- may develop?


usually occur with?


- Rx =? give if?

- may develop ARDS if severe


- usually also have rib fractures but can occur without, esp. in children


- Rx = analgesia, PPV (NIPPV or intubation) as needed for hypoxemia and/or hypercarbia

Pneumothorax - air between?


- can be get in from?


- types = 5?

- air between visceral and parietal pleura


- air can get in from outside or from lungs


- types:


= closed vs open


= simple, tension, occult

Closed vs Open PTX - gets into pleural space from? air in due to?



- closed = no connection to outside, air gets into pleural space from inside (alveoli, bronchi)




- open = hole in chest wall and parietal pleura, air gets sucked into pleual space from outside on inspiration due to negative intra-thoracic pressure

Open PTX - air then unable to? leads to? forcing?

- if these is a ball-valve effect, air can be sucked into pleural space and unable to escape, can lead to tension PTX if enough air trapped, forces lung to shrink

Simple vs tension PTX


- defined by?


- simple has no affect on? no shift in?


- tension has? leads to shift in? increasing? leading to?

= defined by affect on BP


= simple = no affect on BP or shift of mediastinum


= tension = air in pleural space, leads to shift of mediastinum, increase in intrathoracic pressure, decrease in venous return, leading to decreased BP

Clinical Signs of Tension Pneumothorax


- signs of? plus?


- on side of TPTHX, see? (2)


- trachea? JVP?

- all of the signs of resp distress discussed, plus:


= hypotension


= decreased air entry on side of TPTX


= hyperresonance on side of TPTX


= deviation of trachea to opposite side


= elevated JVP if pt not hypovolemic

Note for PTX - simple PTC can be from? same with?


- air can access?



- a simple PTX can result from either a closed or open PTX mechanism


- same for tension PTX




*air can access pleural space from either the inside (lung/bronchus) or outside

Occult PTX


- not visible on? only?


- some will?


- treatment?

- not visible on CXRm only on CT scan


- some (25%) will progress to tension PTX


- treatment = observation vs chest tube

Treatment of Pneumothorax


- provide?


- drain?


- in simple use?


- in tension need? given at?


- follow needle with?

1) oxygen


2) drain air from pleural space:


= simple PTX = chest tube


= tension = needle decompensation (2nd ICS MidClav line - above rib) *always follow needle with chest tube



Hemothorax - blood is in?


- bleeding may be? (6)

- is blood in the pleural space


- bleeding may be from:


= lung parenchyma = low pressure


= pulm vessels = low pressure


= intercostal artery = arterial pressure


= internal mammary artery = arterial pressure


= aorta (traumatic aortic injury) = L HTX


= abdo = rare




*detected by CXR, US, CT

Hemothorax


- Rx with? size?


- occasionally use?


- indications for thoracotomy include? (2) >*


- most important factor?


- also indicated if it is?

- most rxd with chest tube - large = 32F, 36F, 40F


- occassionaly require thoracotomy, indications:


= 1 = > 1500 cc initial drainage


= 2 = > 250 cc/hr x 4 hours


* clinical status is most important factor


= 3 = retained hemothorax, can lead to empyema fibrothorax - consider thorascopy vs thoracotomy

Pericardial Tamponade


- blood is in the?


- pericardium has limited?


- accumualtes slow vs fast?

- blood in the pericardial space


- pericardium has limited ability to stretch, if accumulates slowly it can accomodate but if rapidly, cannot


- restricts filling of the heart, decreasing BP

Pericardial Tamponade


- need pressure gradient of?


- tamponade sees? leads to ? that then?

- need pressure gradient from SVC/IVC to right atrium to fill RA


- tamponade = increase pressure in all 4 chambers of heart


= increased RA pressure decreases venous return to RA, decreases BP

Pericardial Tamponade Diagnosis


- Beck's Triad = (3)


- may see?

= Beck's Traid:


= hypotension


= muffled heart sounds


= elevated JVP




* may see pulsus paradoxus (accentuated drop in SBP on inspiration)


* look at US

Treatment of Pericardial Tamponade


- if time to go to OR, do?


- if emergent? seen by? perform?

- if time to get to OR = surgery = sternotomy


- if emergent = severe decreased BP = emergent thoracotomy and pericadiocentesis (only if no other option)

Traumatic Aortic Injuries (TAI)


- blunt injury to? classic location?


- varies in?


- 85%?

- blunt injury to thoracic aorta


- classic location of injury is descending aorta at level of aortic isthmus (ligamentum arteriosum)


- severity of injury varies from intimal flap to complete transection


- 85% die at scene (transection), 5% make it to hospital hemod unstable (MR > 90%)

TAI Mechanism of Injury - classic is? means shearing of? immobile?


- also due to? (3)

- classic = decelaration injury = shearing of mobile heart and proximal aorta vs immobile descending aorta (junction at ligamentum arteriosum)


- also due to lateral impact, thoracic compression and abrupt increased BP

Diagnosis of TAI - problematic as not?


- suspect in any?


- on CXR, see? such as?


- yet can see with?


- 10%

- problematic because no classic physical findings


- suspect in any patient with high energy trauma


- CXR = numerous signs, none specific


- wide mediastium = 2' to mediastinal hematoma


- however any condition with mediastinal hematoma can cause a wide mediastinum


*** 10% TAI pts do not have wide mediastinum

TIA Dx - other CXR findings


- loss of? deviations of?


- depression of?


- left?


- fractures of?

- loss of aortic knob


- NG deviation to R


- tracheal deviation to R


- depression of L mainstem bronchus


- opacification of aorto-pulmonary window


- apical cap


- L HTX


- 1st and 2nd rib fractures


- sternal fracture, T spine fracture

TAI - Other Dx modalities


- A = is the prveious?


- currently use? as very? can diagnose also?


- TEE = ? for those? yet can miss?

1) Aortography - previous gold standard, sensitive and specific, only 10% pts with wide mediastinum will have aortic injury


2) CT = current, very sens and specific, can diagnoise other thoracic injuries,


3) Transesoph Echocardiography = TEE = for patients too unstable for CT, can miss injuries in aortic arch

TAI Treamtent - BP control is?


- control the? *** chnage?


-want BP to be?

- BP control is crucial while awaiting defin treatment


- control shear stress*** against aorta - change in pressue vs time


- exact level of BP unclear but as low as possible while still having adequate perfusion to major organs = SBP of 100

TAI Treatment - traditionally was? yet had?


- therefore now? until?


- use now?

- traditionally was surgery but high morbidity


- therefore delayed surgery advised until stable, esp resp, CV, coagulation, neuro


- endovascular therapy (stents) now replaced open surgery

Thoracic Trauma Summary - high? accounts for?


- most trated with? yet can?


- can be?

- high morbidity, accounts for 25% of all trauma deaths


- most treated without surgery


- can lead to problems with oxygenation and/or ventilation


-can be life--threatening, must be recognized and dealt with emergently

Definitions - Hypotension vs Shock


- hypotensuon is? doesnt use?


- shock means? not?


- hypoxemia vs hypoxia?

1) hypotension = low blood pressure, dont use a specific number


2) Shock = inadequate oxygen delivery to tissues = cant meet metabolic demands


3) Hypoxemia = decreased oxygen in blood


4) Hypoxia = decreased oxygen in tissues

Physiologic Concepts of BP


- flow = ?


- pressure?


- BP = ?


- CO = ?


- SV considers?


- CO of 70/minute =?

-flow = pressure / R


- pressure = R x flow


- BP = CO x MAP


- CO = HR x SV


- SV = preload, contractility, afterload


- CO = 70/minute = 70 xx = 5000 cc/min

Assessment of Circulation - BP - use?


- can also feel? carotid vs femoral vs radial?


- pulse pressure =?

- BP - use cuff, can also estimate SBP by feeling pulses


- if only carotid pulse present - SBP = 60


- if femoral also present = SBP = 70


- if radial pulse also present = SBP > 80




*pulse pressure = SBP-DBP

Assessment of Circulation - also loo at? its?


- assess? via? (3)

2) pulse - rate, strength (gives assessment of BP)




3) Organ perfusion:


= skin = colour (pale), temp (cool), sweaty


= other organs = mental status, urine output

Classes of Shock


- Class II HR?


- CLASS II BP sees?


- Class IV sees?


(loss, HR, BP, PP)



Approach to Trauma Patent with Hypotension


- must do both? look at?


- determine then?


- could be?


- A/R/C

- assessment and management must occur simultaneously


- A, B, C, D, and E


- determines causes of low BP and correct them = hemorrhagic, non-hem


- assess severity of blood loss


- resuscitate


- constant assessment of resuc efforts

Assessing Trauma Patient with Low BP


- determine? assess?

= determine causes of decreased BP


- assessment of severity of blood loss

Management of Trauma Patient with Low BP


- correct? determine if?


- then?


- then?

= correct causes of low BP = non hem vs hemm (source control)


= resuscitate (volume)


= assess response to resusc efforts

Causes of Decreased BP (Physio Approach)


- H/ O/ D/ C - do to?


* in trauma, decreased BP is? until



- hypovolemic


- obstructive = obstruction of VR to RA


- distributive = vasodilation


- cardiogenic




* in trauma, decreased BP is due to hypovolemia until proven otherwise

Causes of Decreased BP in Trauma


- HV from? Obstructive seen in? (2)


- dis seen with? (3)


- CARDIO FROM?

1) Hypovolemic = blood loss


2) Obstructive = TPTX, pericardial tamponade


3) Distributive = vasodilation (spinal cord, sepsis, anaphylaxis)


4) Cardiogenic = cardiac causes (rare in trama)

Causes of Decreased BP in Trauma - SHOCK stands for?

S - spinal cord, sepsis


H - hemorrhage


O - obstructive - TPTX/HPTX, tamponade


C - cardiogenic - pericardial, myocaridal, endocardial


K - anaphylaksis

DDx of Hemorhhage/ Decreased BP in Trauma


- E/C/A/P/LBs


- dont need?

1 = External


2 = Chest


3 = Abdo = Peritoneum, Retroperit


4 = Pelvis


5 = Long bones = femurs




*dont need defin diagnosis to go to OR for surgry

Clinical Approach of Decreased BP in Trauma Patient


- for spinal cord, do?


- consider?


- for obstructive, look for? (2) perform?


- if tamponade, look for? = (3)



1) Spinal cord = PE, radiology


2) Hemorrhage


3) Obstructive:


= TPTHX/HPTX = exam = decreased A/E, increased JVP, CXR


= Tamponade = exam = Beck's triad = decreaed BP, increased JVP, muffled heart sounds


4) Cardio = exam, US, echo




*dont see increased JVP if pt is hypovolemic

Hemorrhage Clinical Approach in Trauma Patient-


- external? chest? abdo? pelvis? long bones?




*assoc with?

1) External = hx, PE


2) Chest = PE, CXR, CT scan


3) Abdo = PE, US, CT


4) Pelvis = exam, XR, CT, angio


5) Long bones = exam, xray




*hem assoc with low JVP

Treatment of Trauma Patient with low bp depends on?


- determine if? then do?

- non hem. causes


- hemorrhagic causes = source control

Treatment of Reversible Non-Hem Causes in Decreased BP Trauma


- for TPTX? for tamponade?

- needle and/or chest tube for TPTX


- surgery/EC thoractomy, pericardiocentesis for PC tamponade

Treatment of Hemorrhage in Decreased BP Trauma Patient


- stop? usually via? then do?


- prevent? ** - must stop? (2) as they?

1) Stop the bleeding - usually surgery, occas/ inteventional radiology


2) Volume resusciatation




*prevent coagulopathy/hypothermia/acidosis (latter two wrosen the first)

Volume Resuscitation - use?


- need 2? size? to?


- usually done it? such as the?


- best if IVs have? are?


- want? for btter?

- IV access:


= Need 2 large IVs (14g, 16g) to give fluids rapidly


= usually in upper extremities - antecubital fossae usually


= peripheral IVs best = large, short cannulae




*flow = P/R = want large diamter and short length IV cannulae

Intraosseus Access - is an alternative when?


- as BM is?


- vasc is?


- highly vasc BM is? need to infuse under?

- an alternative when IV access unsuccessful


- bone marrow is highly vascular


- vasculature is non-collapsable even when hypovolemic


- highly vasc. bone marrow connected to central vascular system via nutrient and emissary veins


- need to infuse under pressure = use pressure bags

Volume Resucs - Traditional Approach


- start with? make sure they are?


- 3:1 rule?


- after 3L cryst? or if?


- in severely injured patients?

- start with crystalloid (ringers or saline), **warm fluids


- 3:1 rule = need to give 3-4 mls/1ml blood loss


- switch to blood after 3L crystalloid (40 cc per kg) or earlier if severely decreased BP


- in severely injured patients - approach assoc. with worse coagulopathy and outcome

Damage Control Resucs (DCR)


- an approach to? consists of? rapidly? and then?


- goal to? stop? (2)


- main aspect is? with? rather than?

- an approach to resuscs, consisting of a number of aspects/goals with aims to rapidly stop bleeding and prevent further bleeding until bleeding is stopped


- goal to correctminimize coagulopathy, hypothermia and acidosis


- main aspect is early and aggressive resusc with blood products (RBCs, coag products) rather than crystalloids to prevent worsening coag.

Damage Control Resuscitation Steps


- identify? perimissive? minimize? early? use of? (3), give? minimize? (2)

1) Identify and stop bleeding


2) permissive hypotension


3) Minimize crystalloids


4) Early PRBCs


5) Early and aggressive use of coagulation products = FFP, pts, fibrinogen


6) Tranexamic Acid


7) Minimize Hypothermia and Acidosis

Hypotensive Resuscitation (permissive Hypotension)


- aggressive resusc with? could dislodge? lead to? increase?


- suggested to only? until?


- mostly for? to? not for?

- aggressive resusc. with normalizaiton of BP could dislodge clots and dilute coagulation factors, leading to increased bleeding


- suggested to resusc. only to SBP 80-90 (or less) until definitive surgical control of bleeding


- mostly for stab wounds to trunk (chest and abdo), not for pts with head injuries

Damage Control Resuscitation


- start with?


- aggressive use of?


- provide? (3)


- pharm agents =? attenuates?

- start with RBCs rather than crystalloids


- aggressive use of coagulation products


= plasma (FFP), fibrinogen (cryoprecipiate) and pts


- pharmacologic agents:


= antifibrinolytics (TXA) = attenuates hyperfibrinolysis assoc. with severe trauma

Role of Transexamic Acid


- used largely in?


- dose?


- decreases?


- no decrease in

- largely in developing country


- 1g/10 mins then 1gm/8 hours vs placebo


- decreased all-cause mortality (if given within 3 hours of injury)


- decreased deaths due to bleeding


- no decrease in blood transfer between groups

RBCs in Volume Resusciation


- fully? need type?


- uncrossmatched use? in females of childbearing age?


- temp?


- also give? to prvent?

- fully crossmatched (Xm) blood


- type-specific blood


- uncrossmatched blood = O+ in most, O- in females of childbearing age


- give warm blood to avoid hypothermia


- give plasma, pts, cryprecipirate to prevent coagulopathy

Blood in Volume Resuscitation (Fully Xm blood)


- identify?


- screen for?


- ensure?


- time?

- identify pts blood type (ABO and Rh)


- screen for any Abs in pats serum


- ensure donor blood fully* compatible with pts (no antigens in donor blood that pt has antibodies to)


- takes about 45 minutes

Blood in Volume Resuscitation - Type-Specific


- identify?


- release? that is? hasnt been?


- lab will continue to?


- time?

- identify pts ABO and Rh blood type


- release donor blood that is compatible with pts ABO/Rh blood type


- but: hasnt been tested to see if fully compatible


- lab will continue to do full crossmatch


- takes about 10 minutes

Blood in Volume Resuscitation - Uncrossmatched Blood


- need? give? as it is?


- therefore give?


- O- for? O+ for?

- need blood imeediately


- type O blood is universal donor


- therefore give type O blood


- O- for women of child-bearing age


- O+ for everyone else

Response of Blood Pressure to Fluids


- normalized?


- transient?


- no/min reponse? leads to?

1) normalized = volume loss replaced, no ongoing bleeding




2) transient = volume loss replaced, ongoing bleeding, need to stop bleeding




3)No/min response = volume loss not replaced and ongoing bleeding; impending death if not treated




* Need definitive treatment to stop bleeding*

Trauma Induced Coagulopathy (TIC)


- traditional causes are? (6 = B/C/D/H/A/H)

- traditional causes of coagulopathy have been:


= bleeding (loss of blood - RBC, plasma, pts)


= consumption


= dilution


= hypothermia


= acidosis


= hypocalcemia

The Lethal Triad/ Vicious Cycle - bleeding leads to? which further?

- bleeding leads to acidosis and hypothermia, all three contribute further to coagulopathy

Trauma Induced Coagulopathy (TIC)


- now known that?


- 1/3 patients are? with increased?

- now known that there is an endogenous coagulopathy that occurs in some trauma patients (acute coagulopathy of Trauma)


- recent evidence has shown that 1/4-1/3 of trauma pts are coagulopathic (increased INR) at time of presentation/scene




*occurring long before traditional causes of TIC have had time to occur

Acute Coagulopathy of Trauma (ACT)


- requires both? not just?


- seen in ISS of?

- severe tissue trauma** and hypoperfusion** (shock) BOTH appear to be required for development of ACT


- not either alone


- in study of ACT, the worst coagulopathies were seen in pts with ISS > 35 and** base deficit less than -12 mEq/L

Clinical Importance of ACT


- see increased? (4)

in ACT, we see:


= increased transfusion requirements


= increased mortality


= increased morbidity in survivors


= increased multi-organ failure, infection, time on mechanical ventilation, hospital LOS

ACT Mechanisms - normally, see?


- coagulation includes? (3)


- anticoag includes? (2)

- normal hemostasis is a balance between coagulation and anticoagulation


- coagulation:


= endothelium, platelets, coagulation factors


- anticoagulation:


= anticoagulant factors (Protein C,S), fibrinolysis

ACT Mechanisms - The Procoagulant Side


- vascular?


-plts are? dont usually?


- see low?

1) Vascular Endothelium = glycocalyx disrupted




2) Platelets = plts counts are mildly reduced in trauma, dont usually decline to levels expected to contribute significantly to coagulopathy, probable that functional impairment occurs




3) Factors = fibrinogen levels low in many ACT patients, factor 5 levels low in ACT

ACT Mechanisms - Anticoagulant Side


- Fibrin? Protein C is? leads to?


- PAI-1 leads to?

1) Fibrinolysis = Hyperfibrinolysis when it occurs, high mortality


2) Protein C = gets activated by trauma and shock, leads to inhibition of thrombin, inactivation of F5 and F8, consumes PAI-1




*PAI-1 leads to release of tPA and causes hyperfibrinolysis

Assessing and Managing Patient


- A?B?C?


- assess? such as?


- manage via?

A = ensure ETT in good position


B = ensure chest clear and good A/E


C = assess and manage simultaneously


- assess = BP, pulse, skin, urine output, cause of decreased BP: shock pneumonic, clinical exam and xrays


- manage = treat non-hem causes, 2 large bore IVs and fluid warmer, fluids (blood, RBCs, plasma, FBG), transexamic acid, hem. control

Abdominal Trauma


- if patient has? goal to?


- perform laparotomy if? (2)


- do CT scan if? but no?

- if patient has decreased BP, goal to determine cause


- if decreased blood pressure + intra-abdominal bleeding = laparotomy (dont need to determine exact organ injured)


- if intra-abdominal bleeding + no decreased BP = further investigations (usually CT scan)

Abdominal Trauma - Diagnostic Options


- exam of? is?


- need further?

- clinical exam of abdomen in trauma is notoriously inaccurate


- false + and false -s


- need further investigations

Abdominal Trauma - Investigations


- FAST is? also can do? (4) C/L/A/WE

- US = FAST = focused assessment with Sonograph in Trauma


- CT scan


- Laparoscopy


- Angiography


- Wound Exploration = stab wounds

US (FAST) - assess for?


- not for? 4 regions include?


- E-FAST for?

- assesses for free fluid (blood)


- not for organ injury


- 4 regions:


= RUQ (liver/kidney/Morrison's pouch)


= LUQ (spleen/kidney)


= Bladder (cul-de-sac)


= Pericardium




- E-FAST = Extended = also looks for PTX

US (FAST) + means? appears? needs to be?


- indications are?


- advantages (4) - highly?

- FAST +ve means (blood = black), need 400 cc to be positive


- indications are decreased BP


- advantages = noninvasive, portable, can repeat, high spec (95+)



CT Scan - only for? need?


- good for? and entire? such as?


- may also see? indicates? called?

- only for stable patients, need IV contrast


- good for: Dx for solid organ injury (liver, spleen) and entire abdomen (including retroperitoneum)


- may also see extravasation of contrast (indicates active bleeding) = is called "blush"



Disads of CT SCAN - misses? also misses?

= misses hollow organ injuries (bowel)


= misses diaphragm injuries

Disads of US (FAST) - not useful in? cant be used in?


- does not?

= early


= subsequent emphysema, obese


= insensitive (80%)


= does not assess retroperitoneum

Indications for Laparotomy in Blunt Abdo Trauma


- HI? with either (2)


- P?


- DI?

1) Hemodynamic Instability


= with intra-abdo blood (on FAST)


= with intra-abdo injury




2) Peritonitis


3) Diaphragmatic Injury

Abdo Trauma - Nonoperative Management of Solid Organ Injuries


- solid? must be?


- go to OR if?

= solid organ injuries (spleen, liver)


= must be hemodynamically stable


= if develop decreased BP or require blood, go to OR

Abdo Trauma - Management is?


- if stable, can?


- if unstable?


- unstable means? (4)

- is surgery


- if patient is hemod. stable, can take time in the OR to perform definitive surgery


- if unstable, must be quick




*unstable = hemodynamically, coagulopathic, acidotic, hypothermic

Damage Control Surgery - prevent? (4)


- deal with? pack to?


- go to ICU to? return to? to?


- very beneficial in reducing? yet new problem of?

- prevent/minimize: hypothermia/coagulopathy/ acidosis, death


- deal with life-threatening problems only (Hem, Bowel perfusions) in most expeditious way, packs to tamponade bleeding


- go to ICU to resuscitate, return to OR in 24-48h to remove packs and definitive surgery




*very beneficial in reducing lethal triad and acute mortality, yet new problem of Abdo. Compartment Syndrome (ACS)

Intraabdo Pressure and Intraabdo Hypertension


- normal IAP?


- elevated if?

- normal IAP = 0 to 5 mmHg


- IAH = elevation of IAP above "normal" defined > 12 mmHg

Abdominal Compartment Syndrome (ACS)


- abdo cavity can only?


- if over certain point?


- seen in? (5)


- anything that decreases? will also?

- abdo cavity can only hold so much volume


- if volume increases over certain point, pressure inside abdo increases


- blood, ascites, bowel edema, ileus, and packing all increase intra-abdominal volume


- anything that decreases compliance of abdo wall will also increase IAP (edema, burns)




*increased IAP can cause adverse physiologic effects

ACS - increased? + end organ?


- in CV, see decreased? (2)


- in resp, see decreased? (3)


- renal, see?


- neuro - see?



- ACS = increased IAP (>20) + end-organ dysfunction


- CV = decreased venous return, increased afterload, decreased BP and C.O.


- Resp = decreased compliance, decreased FCR, atelectasis/collapse, decreased O2


- Renal = low urine output; acute renal failure


- Neuro = increased intracranial pressure

3 Parts of ACS **


- improvement with?


- organ systems?

1) Organ dysfunction


2) Resulting from elevated IAP


3) Improvement with abdo decompression




- organ systems = splanchnic, CVS, pulm, renal, CNS (intracranial)

IAH and ACS acts as?


- acts as a? IAH is a? can lead to?


- key to monitor?

- acts on a continuum


- IAH is an earlier phenom that when uncorrected leads to ACS


- key to monitor and Tx of IAH to prevent ACS

Diagnosis of ACS - measurement of?


- direct?


- indirect? **

- involves measurement of IAP


- direct = intraperitoneal


- indirect = gastric, IVC, bladder**

Measurement of IAP = Bladder Pressure - is the? correlation with? acts as a?


- use a? inset? see change with?


- can use?

- is the gold standard, high correlation with IAP


- bladder acts as a passive conduit


- use foley catheter, insert 25 cc (max) NS into bladder, connect to transducer and see respiratory variation


- can use intermittent or continuous monitoring

ACS Treatment


- only defin treatment is?


- must open?


- temporizing measure include? (2)


- have temp?

- only definitive Tx is to open the abdomen


- must open fascia and skin


- temporizing measures = paralyze patient, paracentesis (drainage of any fluid, ie ascites, collections)


- have temp closure = protective covering over top with room to expand*

Pelvic Fractures


- can lead to?


- patients often are?


- PF must be in DD of?


- require? so often?


- need to determine if?

- can lead to massive bleeding


- patients with hemodynamic instability from pelvic fractures have high MR


- must be in the DD of hypotensive trauma pt


- requires a lot of force, have other injuries


- high incidence of concomitant intra-abdo injury


- need to determine if decreased BP is from pelvis/abdo/both

Diagnosis of Pelvic Fractures


- clinical exam is?


- CT scan for?

- clinical exam = pain, mechanical instability


-plain X rays


- CT scan (if stable) = can see fractures and contrast blush

Pelvic Fractures and Bleeding


- bleeding from?


- major vessels run along?


- see colalterals between?


- bleeding is mostly from?

- bleeding occurs from bones, veins (90%), arteries (10%)


- major vessels in pelvis run along posterior aspect of pelvis


- ++ collaterals between R and L sides


- arterial bleeding is mostly from internal iliac artery or branches of it

Management of Pelvic Fractures


- must?


-options include? wrap?


- perform? give?


- or do a? with?

- must stop the bleeding, options include:


= stabilize pelvis = wrap with sheet, pelvic binder, external fixator


= surgery = pre-peritoneal packing


= angiography + embolization

Surgery - Pre-Peritoneal Packing - Packing ExtraPerit. Space


- incision? location?


- open? not? called?



- midline incision 8 cm in length just above the pubis extending toward the umbilicus


- skin and subcut. tissue is opened in the midline, as is the fascia (not peritoneum) = Space of Retzius

Surgery - Pre-Peritoneal Packing - Packing Retroperit. Space


- bladder is then? use? and place?


- then? time?

- bladder retracted away from the fracture, blunt dissection with hands and three laparotomy pads placed in the RP space on each side toward the iliac vessels


- fascia and skin are closed


- takes about 20 minutes

Pelvic Fractures - Angiography and Embolization


- indicated in?** especially if?


- use in patients with? (2) after trying?


- do ahead of packing if?

- indicated in pts with contrast blush on CT, esp. if decreased BP


- pts with pelvic fractures and decreased BP (no other cause) despite above measures (binder, preperitoneal packing)


- can also be used ahead of packing if angio suite and personnel immed. available

Definitive Pelvic Fracture Treatment


- (2)

- external fixator


- open reduction internal fixation (ORIF)

Approach to Pt with Pelvic Fracture and Decreased BP


- rule out? such as?


- in trauma room?


- if FAST +?


- last option is?

- rule out/ in additional sources of decreased BP and Tx accordingly, esp. intra-abdo bleeding


- pelvic binder (or sheet) in Trauma room


- if FAST + = OR for laparotomy and preperit. packing for pelvis


- if still decreased BP from pelvis after this, do angio

Approach to Pt with Pelvic Fracture and Decreased BP - If FAST negative


- apply?

- pelvic binder applied



Approach to Pt with Pelvic Fracture and Decreased BP - If BP improves with + resusc.


- to? if contrast blush? if external fixator?

- to CT


- to angio if contrast blush seen on CT


- to OR for external fixator

Approach to Pt with Pelvic Fracture and Decreased BP - If BP doesnt improve?


- give? or go to?

- pre-perit. packing or angio suite


- if BP still doesnt improve: Angio suite or pre-perit packing

Summary of Abdo Trauma


- exam is? need?


- never go to CT with?


- surgery for?


- need to determine?


- key to good outcome is?



- abdo exam unreliable in diagnosing intra-abdo trauma


- need imaging = US, CT


- never go to CT scan with decreased BP patient


- decreased BP + Intra-Abdo blood = surgery


- pelvic fractures bleed like crazy ,need to determine whether from pelvis or other sites as well (abdo)


- rapid management is key to good outcome in pts with pelvic fractures (dx and tx of bleeding + resuc)

Before Sending Patient to Radiology Department, need?


- patient needs to be?


- stab. devices include? (2)


- deadly if?

- patient needs to be hemo stable


- stabilising devices = neck brace (C-spine), spinal board (lumbar spine)


- facial and C-spine fractures can be deadly if neck flxed during CT scan

Trauma Imaging



Types of Imaging


- plain films for?


- US for?


- CT for?


- Angio for?


- MRI for?

- Plain films = CXR, fractures, long bones


- US = abdo injury, fluid (assessing hemoperitoneum)


- CT = organ injury


- Angio = bleeding requiring embolization


- MRI = neuroassessment, espec. SC

CT Scan for Fractures


- important for? such as?


- better at? shows?


- can do?

- important for complex fractures:


= facial, spinal, pelvic fractures


= defines fractures better


= shows assoc. complication


= useful for surgeon




* can do 3D reconstruction of CT images - can be used to plan type of surgery

MRI used for?


- to assess?


- done in? assess for?

- used mostly for CNS trauma, to assess cord and brain injury, surgery planning, assess prognosis


- done in hemodynamically stable patient


- can assess for cervical spine fractures

Two Types of Angiography


- conventional is? punctures? after do?


- CT is? only? after?

1) Conventional


= invasive, artery punctures, can embolize sites of bleeding, do xray after




2) CT Angiography


- not invasive, only antecubital vein punctures, CT scan done after

Types of Trauma - either?


- types of injury include?

1) Organ Specific


= multiple organ involvement = MHC, etc


= localized organ invovlement = abdo, chest, head injury




2) Type of Injury


= penetrating


= blunt trauma

Multi Organ Trauma - requires? best if CT is?


- look for lacerations of? appear?


- shock bowel appears as?

- requires aggressive imaging


- best if CT located in emergency room


- head,chest and Abdo CTs can be done quickly




* look for liver or renal laceration ( more hypodense due to blood)


* shock bowel = hyper enhancing bowel wall, adrenal gland can look bright



Single Organ Trauma


- careful? need more?


- can become? look for?


- may need?

- careful clinical analysis before imaging as usually stable


- more selectively imaging


- can become unstable quickly, ex/ delayed rupture of organs (ex/spleen), look for splenic hematoma


- may need spec. care = complex pelvic, C-spine fractures

Type of Injury - Penetrating


- can be? if penetrating?


- imaging? do not perform**?

- can be life threatening, instrument best left in patient


- imaging:


= plain film, CT scan to assess internal organ damage


= MRI cannot be performed

Fall From height - type of injury?


- see fractures of? (3)


- must see?

** type of injury determines tests


- see fractures of:


= Calcaneus


= Pelvis


= Lumbar spine, see compression fractures




* must xray many areas

Lateral Cervical Spine X-ray - ABCs


- A/B/C and then?


- alignment - should see?


- bones - look for?


- also want?

= Alignment - 4 lines - should be straight (\), last should be curved


= Bones = Vertebral Bodies = 7


= Cartilage (Disc)


= Soft Tissue




*also want open mouth (odontoid) view

Adequacy of Cervical Spine X-Ray


- must visualize? from? to?


- C1 is? see separate?


- C2 is? up to?


- inadequate film if?

- must visualize the entire cervical spine, from skull base to the cervico-thoracid junction


- C1 is small, separate between spinous process and vertebral body


- C2 is large, up to C7


- film that does not show the upper border of T1 is inadequate**



Cartilage and Soft Tissue


- cartilage should be?


- soft tissue, look for?


- at #4 size? #6 size?

- cartilage - should be symmetrical between vertebral bodies


- soft tissue: look for misalignmentt


= 4-7 mm = 1/2 vertebral body at #4


= 16-20 mm = full vertebral body at #6

Spinous Process Fracture of C7 called?

- Clay-Shoveler Fracture

Open Mouth (Odontoid) View


- C1 appear? look at? should be?


- can assess? when not?

- see C1 on each side of C2


- look at open mouth view, should be symmetrical


- can assess for fracture of C1 when not aligned on sides of mouth

Hangman Fracture - fracture of? seen in?

- fracture of C2 posterior element


- seen in those trying to hang themself

Heads - Types of Bleeds - 4 types?

= epidural hem


= subdural hem


= subarachnoid hem


= intracerebral hem

Epidural Hemorrhage - occurs between?


- dura is? adherent to?


- hemorrhages appear? seen more commonly in? with?

- occur between the dura and bone = dura in thick, dense and closely adherent to inner surface of bone


- are lenticular and biconvex**, more commonly seen in young patients (with trauma, assoc. bleeding)

Epidural hemm looks like?



Subdural Hemm - occurs between?


- appears? shape?


- seen in more? due to movement of?


- if hypodense? hyperdense? also see?

- occurs between dura and arachnoid


- appears crestentic, concave inner margin


- seen in older patients, due to movement of smaller, atrophic brain leading to bleeds in bridging veins


- if hypodense - chronic


- if hyperdense - more acute


** also see midline shifts

Subarachnoid Hemm - appear? are both inter? bright in?

- subtle, diffuse, inter-hemispheric, inter-ventricular


- bright in sub-arachnoid spaces

Intra-cerebral Hemorrhage - appear?


- can be either?


- also can see?

- hyperdense areas inside parenchyma


- can be hemorrhagic or non-hemorhhagic


- can see intra-ventricular extensions

Chest - Consider? (4) A/F/L/PI


- lung injury includes? pleural injury includes?

- aortic injuries


- fractures


- lung injury = contusions, lacerations


- pleural injury = PTX, HTX

Imaging Assessment in Trauma


- CXR is usually? CT then for? Angio is becoming?

1) CXR = usual method of inital screening in trauma




2) CT = often needs CT for assessment of other regions (abdo, head)




3) Angiography = becoming uncommonly used for aortic injury (CT is most common)

Life Threatening Events of Chest (4) T/F/HT/AD

= TPTH


= flail chest


= large hemothorax


- aortic dissection/ rupture

CXR Findings in Aortic Injury - is? but not?


- should first do?


- signs of hematoma? (5) *** M/I/A/D/ increased?

- CXR sensitive but not specific for aortic injury


- normal CXR should preclude further assessment for aortic injury


- CXR findings = signs of Hematoma


= Mediastinal widening


= Indistinct aorta


= Apical cap (darkening at lung top)


= Displacement of NG tube


= Increased density behind heart

CT Findings in Aortic Injury


- indirect =?


- direct = signs of? such as? look for?

1) Indirect Signs


= mediastinal hematoma


2) Direct Signs


= sign of aortic injury = pseudoaneurysm = hyperdense, circular inside organ




*look for trachea movement to side

In hemothorax, see complete? shift of?


- CT, see? can also see?

- complete opacification of right hemi thorax


- shift of mediastinum, trachea to one side


- CT see completely dense area


- can also see rib fractures

Flail Chest- definition? ribs then? leads to?

- see three continuous ribs, breaks in two more spots


- ribs completely independent of rib cage, area will be inefficient in breathing

Diaphragmatic Rupture - rise of? displaced? ***


- PTX appears as?

- diaphragm rises


- see displaced NG tube


- see distended stomach in chest***




**PTX appears as dark top of lung

Multiple Trauma Patient - Organ Specific Injuries - often to (4)


- injury appears are? fat? blood?

- liver


- spleen


- kidneys


- bladder




*hypodense in organs likely from injury, fat appears dark, lighter for blood

Traumatic Solid Organ Injury - Clinical Findings - commonly seen in?


- clinical findings = (3) ** signs of?

- commonly injured in blunt trauma


- clinical findings


= often non-specific


= peritoneal irritation


= signs/symptoms of acute hemorrhage

Solid Organ Injury Imaging - do not use?


- US for? modality of choice is?


- angio for?

- plain film not useful


- US = hemoperitoneum


= contrast- enhanced CT is modality of choice


- angio = therapeutic embolization

Types of Solid organ injuries - (3)

= hematomas


= lacerations


= infarctions

For hematomas, do?


- high density shows?


- with IV - no?


- with time? can become?

- CT is best imaging


- on plain CT = high density shows blood


- with IV = no enhancement


- density of hematoma decreases with time, can become hypodense

Laceration and CT - spleen? kidney?


- defects are often?


- if hyperdense?


- if hypodense?

- can see peri spleen, kidney fluid


- low density linear defects within the organs (usually from lateral border towards hilium)


- if hyperdense, may be pseudoaneurysm


- hypodense shows lacerations

Lacerations


- mechanism is often? torn by?


- clinically see? (3)


- can affect? and the?


- imaging to use? delayed images to diff between?

- Mech = blunt trauma, laceration by lower ribs, torn by rapid accel/decel


- clinically see back pain, hematuria, hemo unstable


- can affect renal parnechyma, vessels, collecting system


- US is limited


- CT is study of choice - important of delayed images to diff. between hematoma (hypodense) and leakage from collecting system (appear hyperdense)

Lacerations Transecting Collecting System - best?


- absence of? due to?


- around kidney see?


- abrupt?

- CT is best, see:


= absence of contrast enhancement due to no flow


= hematoma around kidney


= abrupt cut off of contrast filled renal artery

Pelvic Fractures with Active Bleeding - do? see?


- to stop bleeding?

- do contrast extravasation to see active bleeding, fracture locations, can use catheter and coil or gelfoam to stop bleeding

Traumatic Brain Injuries Epi


- one of the leading?


- importance of? assesses? (2)

- one of leading causes of trauma-related deaths, huge amount of disability and cost to society


- importance of D = GCS, pupils (size, response to light)

Glasgow Coma Scale - Eyes - out of? scoring?



Glasgow Coma Scale - Verbal - out of? scoring?



Glasgow Coma Scale - Motor Response - out of? scoring?

GCS - devised for assessing? in?


- useful to follow? for?


- categories? min? max?

- devised for assessing LOC in pts with TBI


- useful for following pts progress and for communication with MDs


- 3 categories = eyes, verbal, motor


- min score = 3


- max score 15

Classification of TBI


- mild? moderate? severe?

= Mild Head Injury = GCS 13-15


= Moderate Head Injury = 9-12


= Severe Head Injury = GCS < 8

Classification of TBI - CT Scan Findings in TBI


- look for? (4)


- may be?

- normal


- epidural hematoma


- subdural hematoma


- intracerebral contusions


- diffuse axonal injury




*may be more than one of these on CT

Subdural Hematoma - see shift in? compressed?

- see shift in midline


- compressed lateral ventricles

Intracerebral Contusions - see? usually?

- see contusions inside parenchyma


- usually >1cm in diameter

Diffuse Axonal Injury - see? in?

- see blood in lateral ventricles, basal cistern, petechial hemorrhages

Assessment and Management of TBI - Mild Head Injury


- defined as? with? GCS?


- CT?


- discharged if? must have?


- generally admit if?

= defined as witness LOC, amnesia, witnessed disoreintation with GCS of 13-15


= usually normal CT


= discharged home if GCS = 15 = must not be intoxicated and must have a reliable caregiver, be able to return


= generally admit for observation if 13 or 14

Canadian CT Head Rule - High Risk


- only required for?

 = only required for patients with minor head injuries with any one of following:

= only required for patients with minor head injuries with any one of following:

Canadian CT Head Rule - Medium Risk



Moderate Head Injury - GCS of?


- do? and then?


- intervention as?


- if deteriorates?

- GCS of 9-12


- do CT head and admit for observation


- intervention as appropriate based on CT and clinical status


- if deteriorates: repeat CT head and treat as appropriate

Severe TBIs are?

- GCS equal to or less than 8

Severe TBI - Management - crucial? look for?

- A, B, Cs are crucial


- TBI + Hypoxemia +/or Hypotension increase mortality

Severe TBI - Goal is to? maintain? equation?


- maintained mainly by?


- ** goal to prevent? (3)

- prevent secondary injury


- maintain cerebral perfusion pressure (CPP)


- CPP = MAP - ICP, primarily by reducing intracranial pressure (ICP)


- prevent/treat hyperthermia


- prevent/treat seizures


- prevent/treat hyperglycemia

Severe TBI - ICP Management - doctrine?


- skull is?


- able to? compensatory as?


- after limits?

= Monroe-Kellie Doctrine:


- skull is rigid, contains brain (cells + ISF), blood, CSF


- can accommodate some increase in volume


- compensation occurs by displacing CSF/venous blood


- after limits of compensations, ICP will increase ++

ICP Increase - in compensated? see decrease in? (2) as?


- inuncomp, ICP is? see very little?


- after decomp?

- in compensated state, ICP is normal, see decrease in venous volume and CSF as mass increase


- in uncompensated state, ICP elevated as mass increases more, see very little venous volume and CSF


- after point of decompensation, see ICP increase steeply until herniation

Upon high ICP, look for? occurs as?

-fixed, dilated pupils can be sign of very high ICP and hernation as 3rd cranial nerve gets compressed

ICP Management - increased ICP leads to? leads to?


- assoc. with? treatment towards?

- increased ICP leads to compression of small arteries, leading to brain ischemia


- increased ICP assoc. with worse outcomes


- therefore, treatment targeted towards reduced ICP



Monitoring ICP- normal ICP at? to measure?


- monitor ICP if? look for?


- EVD is?

- normal ICP at 10 mmHg, various devices to measure ICP are invasive


- monitor ICP if GCS <8 and abnormal CT scan


- monitor via External Ventricular Device (EVD), can use intraparenchymal probe and epidural transducer

Goal of CPP - want to maintain? to prevent? (3)


- CPP is?


- number?

- want to maintain CPP to prevent hyperthermia, seizures and hyperglycemia


- CPP = MAP - ICP




* want to maintain ICP < 20-25 so CPP > 60

ICP Management - 1st Line Options/Measures - Hematoma and CSF - do?

- think of contents of skull:


= hematoma = evacuate = craniotomy


= CSF = drain (if ventricular drain in place)



ICP Management - 1st Line Options/Measures - ICF/ISF and Blood


- for ICF- use? these include (2) - act to?


- for blood, venous want to? by?


- if arterial? which decreases? then?

= ICF/ISF:


= hyperosmotic agents = mannitol, hypertonic saline, pull water out of ISF and ICF spaces




= blood:


= venous = encourage venous drainage from brain (elevate head)


= arterial = hyperventilation (mild) - decreases paCO2 leads to cerebral v/c leading to decreased CBF and CBV



paCO2 and Cerebral Blood Flow - as increase paC02? causes?

- as increase PaCO2, see MAP increase and CBF increases


- high enough PaCO2 eventually causes CBF to plateua

ICP Management - 2nd/3rd Line Options


- propofol to? decreases?


- temp? to decrease?


- or can perform? to?

= barbiturates or Propofol = lower cerebral metabolism = decreases CBV to decrease ICP


= hypothermia = decreases CBV by lowering metabolism


= decompressive craniectomy = removal of skulls to allow brain to swell to reduce ICP

CPP Management - want to keep CPP at?


- done via?


- if CPP < 60 and? use? such as?

- want to keep CPP 50-70 mmHg


- generally accomplished with ICP management


- if CPP < 60 with maximal ICP control, use meds to raise MAP = Norepinephrine

Severe TBI - Other NB issues- things that increase? act to? and therefore?


- prevent? (3)

- things that increase cerebral metab = fever, seizures = increase CBF and CBV to increase ICP


- therefore prevent:


= hyperthermia**


= seizures = look for non-convulsive seizures on EEG


= hyperglycemia = worse outcomes

Severe TBI and Sodium


- NA affects?


- HyperNa causes?


- HypoNa causes?



Summary of Brain Injuries


- cant chnage? focus on?


- act to? understand?

- cant change primary injury, focus on preventing 2nd injury


- optimize ABCs, understand determinants of ICP and CPP and management

C-Spine Injuries - Incidence


- in blunta trauma? most common level of injury?


- 2nd most common?


- not uncommon to have?

- in blunt trauma - 2-3%, 1% in low energy and 10% high energy


- C2 most common level of injury (25% of all fractures)


- C6 and C7 2nd most common = 40%


- not uncommon to have more than one fracture, can also have ligament disruption

CSI and head Injuries - with GCS <8, see?


- 7% have? therefore increased incidence of?


- often have?

- % CSIs increasing with GCS <8, accounts for most, 10% of CSIs


- 6-7% CSI have facial injuries


- therefore injuries above clavicles have increased incidence of CSI


- often have other injuries = 25-50% of patients with CSI have head injury (HI)

Missed CSIs and Deterioration - Causes for Missing CSIs


- injuries? (3) need for?


- poor? miss?

- head injury


- intoxication


- distracting injuries


- need for urgent ETT


- poor quality of imaging/missed on imaging


- neurol symptoms missed or attributed to other causes (periph injuries/anxiety)

if Missed CSIs - often leads to? more likely to?


- include?


- can occur with?

- often leads to failure to immobilize, more likely to suffer primary or secondary spinal cord injury


- include of neurologic deterioration (after reaching hospital) = 2-10%


- can occur with airway management/ halo application/ surgery/ sepsis, still can occur with appropriate mgmt

C Spine Immbilization


- must assume?


- always remember to?


- immobilize with?

- must assume every blunt trauma patient has a C-spine injury until proven otherwise**


- remember = A = airway + C spine protection


- immobilize = hard collar + sandbards + tape log roll when turning patient


-

C- Spine Immobilizaiton - must keep? until?


- make sure to? if?

- must keep spine imm. at all times until injury ruled out


- in-line immob./stab/ whenever performing maneuvers that could cause neck movement (airway maneuvers, etc)

Clearing the C-Spine - ruling out? must also rule out?


- can clear?


- can not?


- often need?

- ruling out a significant injury in the vertebral column (bones and/or ligaments)


- must R/O bony and ligamentous injury


- can clear clinically without xrays


- can not clear with xray without clinical exam


- often need neurosurgical or orthopedic opinion

Clearing C Spine - ClinicalClearance


- no (4)??


- painless?

1) No sensorium = no alcohol, drugs, TBI


2) No midline spine pain/tenderness


3) No neuro signs/ symptoms


4) No distracting injuries


5) Painless ROM of C-spine (after above 4 criteria are met)

Clearing C Spine - Must perform radiologic evaluation, if?


- if do not meet? do ?

- if any of these 4 not met:


1) No sensorium


2) no midline spine pain/tenderness


3) no neurologic signs/ symptoms


4) no distracting injuries




* do CT scan with 3-d reconstructions

Ruling Out Clinically - can not? without?


- must still?


- after CT, still make sure? (3)


- if not?

- can not clear with xrays, without clinical exam


- must still clear clinically as well (still possibility of ligament injury), therefore after a normal CT, must make sure:


= No pain/ tenderness


= No neurologic symptoms/ signs


= able to move head/neck without pain




*if not, keep immobilized and get NSx/Ortho consult

Clearing C-Spine - Severely Head Injured Patient Special Situation


- may not? for?


- options - leave?


- take off?


- MRI isnt?

- may not be able to clear clinically for days/wks/ever


- options:


= leave collar on until wakes up (sometimes done)


= take collar off and re-apply if wakes up with pain or symptoms (most common approach)


= dynamic flex/ext views - not done


= MRI = not routine, done at some centres

Spinal Cord Injuries - Complete vs Incomplete SCI


- motor and sensory?


- reflexes?


- incomplete if?

1) Complete = no* motor or sensory function below level of injury, reflexes often hyperactive


(motor function will not improve with time)




2) Incomplete = some* motor and/or sensory function below lesion (may improve with time)


- any preserved motor or sensation (may only be sacral sparing/perianal sensation) makes the SCI incomplete

Spinal Cord Injuries - Spinal vs Neurogenic Shock


- spinal shock sees? patient will have? lasts?


- nero sees? loss of? at?

1) Spinal Shock = complete loss of all spinal cord function below level of injury


- Pts will have no motor, sensory or reflxes below


- lasts days-weeks




2) Neurogenic Shock = decreased BP occurring secondary to SCI, occurs secondary to loss of sympathetic innervation (T1-L2)


- higher lesions = most sympathetics lost

SCI Goals - prevent? (2)

- prevent secondary injury


- prevent/ treat complications

SCI and Preventing Secondary Injury - cant? focus on?


- even 1?

- cant affect injury thats already occured, focus to prevent worsening


- even 1 level worsening could be signif


= ex/ C6 to C5 level

Ways to Prevent Secondary Injury - imm? maintain? via? avoid? (2)



- immobilization


- maintain Spinal Cord Perfusion Pressure


= MAP - CSF pressure


- avoid hyperglycemia and hyperthermia


- early surgical intervention?

SCI - Complications - RESP - remember**


- loss of?


- decreased?


- look for?


- think about? (2)

= C345, keeps diaphragm alive


= loss of intercostals, abdo muscles


= decreased FEV, FVC, cough


= atelectasis/collapse


= pneumonia


= prolonged ventilation


= tracheostomy = secondary to prolonged ventilation

SCI - Complications - CVS - decreased? worsens with?


- cant? see?


- problem of? due to?


- increased BP due to?

= decreased BP = worsens with decreased VR (such as PPV)


= hypothermia = cant vasoconstrict


= DVT = from immob and hypercoag


= Autonomic dysreflexia = increased BP with certain stim. below SCI level

Other Spinal Cord Injuries - GI? skin?

- GI = gastric atony/ileus, Gi ulcers


- Skin = decubitus ulcers

Myotomes - Assessing Motor Level


- C5 to L5?

- C5 = deltoid


- C6 = elbow flexion


- C7 = elbow extension


- C8 = finger flexor


- T1 = small finger abductors


- L2 - hip flexor


- L3 = knee extension


- L4 = ankle dorsiflexor


- L5 = 1st toe extensor


- S1 = plantar flexor

Grading Motor Power - scale? may add?



Fluids - Dont give PO (by mouth) and use IV route if? - need to give?


- cant tolerate? due to?

- need to give large volume or complex solution


- patient cant tolerate p.o. due to GI problem or depressed level of consciousness

Goals of Fluid Therapy - rapidly? restores? avoid? especially?

- rapidly expand intravascular volume to restore blood pressure and therefore perfusion of vital organs


- avoid change in cell size, especially of brain cells

Choice of Fluids = Normal Saline (NS) - is?


- NaCl is?


- % means?


- 154 is? close to?


- giving NS means?

- normal saline = 0.9%


- NaCl = 154 mmol/ L NaCl


- % means g solute / 100 cc of water


- 154 pretty close to 140, very close to plasma water Na of 151


- giving NS means plasma Na will change only a little as direct effect of giving the fluid

Body Fluid Compartments


- ICF is? ECF is? separated by? - sizes

- ICF = 2/3 = small amount is water in RBCs




- ECF = 1/3


= 3/4 ISF, 1/4 plasma

What is Tonicity - this is?


- an effective osmole is one that?


-not effective osmoles? (2)

- this is effective osmoles


- an effective osmoles is one which when added to the ECF stays there (does not enter cells); eg Na


- urea and ethanol are not effective osmoles, since they enter cells and achieve the same concentration in ICF and ECF

Where Does the Water Not go


- if ICF tonicity < ECF?


- if ECF < ICF?


- if NS doesnt chnage? then?

- water crosses into the cell if the tonicity of the ICF exceeds that of the ECF


- water comes out of the cell if the tonicity of the ECF exceeds that of the ICF


- if the NS does not change the [Na] and therefore doesnt change the tonicity, then the cell size does not change

What fraction of admin NS stays in circulation?


- as add water with NaCl? force for?


- majority of NS? only?

- as add water with NaCl, the capillary hydrostatic pressure rises and the capillary albumin concentration falls, leading to a force for water to exit capillaries


- majority (2/3-3/4) of admin NS enters interstitial space, so only 1/3-1/4 stays in plasma

How Much NS to Give- standard bolus? over?


- may give?


- often follow this with? about?


- maintenance rule?

- standard bolus is 10-20 cc/kg over 30-60 minutes, may give faster or slower depending on severity of clinical situation


- often follow this with an infusion of fluid, about 50 ml/h above maintenance


- maintenance from 4-2-1 rule

4-2-1 Rule - is?

- first 10 kg = need 4 cc/kg/h


- next 10 kg = need 2 cc/kg/h


- remaining kgs = 1 cc/kg/h

60 kg patient gets?

- (4x10) + (2x10) + (60-20)x10




= 40 + 20 + 40 = 100 cc/h

Problems with NS - if give too much NS? can lead to?


- give a large volume of? can lead to?

- give too much NS with too little clinical monitoring, espc. with an older patient and/or one with heart disease = CHF


- give a large volume of NS leading to dilution of HCO3 = dilutional acidosis

Ringers - Lactate - nearly? contains? regens?

= nearly isotonic alternative to NS


= contains lactate as it is metabolized in the liver and regenerates HCO3

Fluids - What are We not Using - C? shown to?

- colloids


- eg/ Albumin, Pentaspan


- dont work, except with advanced liver disease

Route of Admin for Fluids (6)

- peripheral IV line


- central IV line


- intra-osseous


- subcutaneous


- oral


- G tube or NG tube

What is Free Water - water without?


- consider a litre of? which is equivalent to?

- water without isotonic Na


- consider a litre of "half-normal" (0.45%) NaCL iv fluid


- equivalent to:


= 0.5 L of NS


= 0.5 L of just water = free water

Patient - Why Hypernatremic - received? losing? that is?


- defic of? leads to? often during?


- leads to failure to?

- received isotonic fluid


- losing large volumes if dilute urine full of free water


- free water urine loss often due to acute deficity of ADH = due to hypothalamic injury peri-op


- leads to failure to reabsorb free water from renal tubule

If hypernatreamic, need ? Na?


- options include? (3) **

- need an IV fluid that has free water in it = [Na] < 140


- options:


= 5% dextrose = D5W = glucose - H20


= 0.45% NaCl = 1/2 normal saline


= 3.3% dextrose and 0.3% NaCl = 2/3 and 1/3

Why Cant We Give IV Water - at end of cannula, see? as?


- need a? that?

- hemolysis at the end of the IV cannula because the RBCs are suddenly bathed in hypotonic fluid, they osmotically suck up the water and they burst


- need a particle that stays in plasma (glucose, NaCl) to prevent the administered water entering RBC

Where in Body Does Administered Free Water Go?


- initially added?


- 2-3 goes into? like?


- added? to? meaning?


- 2/3 of added free water goes?

- initially added free water is in plasma


- 2-3 of it goes into ISF, just like NS


- added free water reduces the tonicity of ECF fluid below tonicity of ICF, meaning a proportion of added water will enter cells


- recall: 2/3 of TBW is inside cells as thats where 2/3 particles are, therefore 2/3 of added free water enters cells ***

How Much Free Water to Give?


- calculate with?


- TBW x current plasma = ?


- 70 kg man TBW is?

- calculate free water deficit using C1V1 = C2V2


- TBW (now) x current plasma [Na] = TBW (normal) x 140


- recall TBW man = 60% of body weight


- patient is 70 kg, so TBW = 42 L



How Much Free Water to Give?


- 42 x 155 =?


- deficit = ?

- 42 L x 155 = TBW (normal) x 140


- TBW (normal) = 42 L x 155 / 140 = 46.5 L


- deficit = TBW (normal) - TBW (now)


- deficit = 46.5 - 42 = 4.5 L

How Quickly Should We Give this?


- if chronic hypernatremia? avoid?


- safe limit? correct over?


- free water? or?

- chronic hypernatremia should be corrected slowly to avoid causing cerebral edema


- safe limit = 8 mmol/L/day, so with a patient whose plasma [Na] = 155, correct here over 2 days


- 4.5 L of free water / 48 h = 100 cc/h of free water


= 5% dextrose at 100 cc/hour


= 0.45% NaCl at 200 cc/hour

If have acute hypernatremia - can be corrected?

- can be corrected more quickly

Ongoing Losses - need to remember there will be? must either?

- need to remember there will be ongoing losses


- must either correct the cause of the losses (here, give exogenous ADH = DDAVP) and/or keep up with ongoing losses

Considerations for IV fluid - losses during? =?


= stress of surgery causes? so if give free water? leads to? risk of?

- losses of fluid during surgery = blood, isotonic fluid into surgical field (third-spacing)


- release of ADH by stress of surgery = if give her free water, she will retain it and she will develop hyponatremia and risk of brain cell swelling

Types of Deficits - deficit in? indicated by?


(3)


- free water deficit indicated by?



- isotonic fluid deficit, as indicated by physical exam = flat JVP, dry mouth, low level of consciousness


- free water deficit as indicated by hypernatremia (Plasma Na of 155)


- K+ Deficit as indicated by hypokalemia

If need isotonic fluid and free water and have K+ deficit?


- can give? to?


- can start? to?


- add? to?


- or give?

1)


= can give NS bolus to raise BP


= can start infusion of D5W to correct hypernatremia


= add KCl (10-20 mmol/L) to D5W




2)


= 0.45% NaCl plus KCl

Why Hyponatremic?


- diuretic can lead to? resulting in?


- causes include increases? or release?

- ECF volume depletion from diuretic can result in hyponatremia


- causes:


= thirst with increased fluid intake = add free water


= volume-mediated ADH release = fail to excrete free water

Why Hyponatremia - free water? tends to?


- over time?

- free water gain dilutes plasma [Na], tending to cause brain cell swelling


- over time, brain adapts by exporting particles

What if Hyponatremic and give lots of NS?


- sudden? drop in? increase in?


- rise in? shrinkage of? can cause?

- sudden correction of ECF volume depletion


- sudden drop in ADH levels


- sudden increase in urinary excretion of free water


- sudden rise in plasma [Na]


- sudden shrinkage of brain cells with risk of devastating demyelination

Take Home Points


- if hyovolemic and hypotensive?


- if hypernatermic? also should?


- post op patients release? if give free water?

1) Hypovolemic, hypotensive patients should get NS or Ringer's lactate


2) Hypernatremic patients need free water (D5W 2/3 & 1/3, 0.45% NaCl) but also treat underlying cause of free water deficit


3) Post-op patients release ADH and will get hyponatremic if given free water, so use NS

Take Home Points


- NaCl is used for?


- if hyponatremic, dont give? as can?


- IV fluids require?

4. 0.45% NaCl is useful fluid for hypernatremic, volume-depleted patients


5. Dont give large volumes of NS to hyponatremic patients due to risk of overly-rapid correction with devastating CNS outcomes


6. IV fluids require careful reassessment to avoid complications

Percentages of Body Weight that is Water


- 2/3 is? 1/3? plasma vs ISF?


- newborns have higher? elders have?

ICF = 2/3
ECF = 1/3 = 25% plasma, ISF 75%
- newborns have higher fraction, elderly have lower fraction, obese is lower

ICF = 2/3


ECF = 1/3 = 25% plasma, ISF 75%


- newborns have higher fraction, elderly have lower fraction, obese is lower

Movement of Water



Calculate Effective osmolarity - calculated as?


- if add Kcl to body?

= 2 x ( Na + K )




* if add Kcl to body, plasma Na > 140, cell size < normal

Effects of Hypotonic, Isotonic and Hypetonic Solutions on Cell Size


- if gain fluid? if lose fluid?

- free water refers to waterin a solution in addition to isotonic protein

- free water refers to waterin a solution in addition to isotonic protein

Sites of Blood Loss = (5)


- causes reduction in? leads to?

- GI bleeding, uterine bleeding, urinary bleeding, trauma and surgery bleeding


- causes reduction in intravascular volume and leads to translocation of ISF into bloodstream

Isotonic Fluid Losses - from (4)


- causes loss of? % - from? no change in?


- third space losses assoc. with? (5)

- from skin, urine, gut, or third space losses


- cause loss of ECF volume = 25% of loss from plasma, 75% from ISF, see no change in ICF volume


- third space losses = pancreatitis, peritonitis, crush injury or major fracture, DVT, post-op fluid losses


Loss of Fluid from Plasma



If have 12 litres, with 3 L in plasma and 9 L in ISF and lose 4 litres, end up with?


- from plasma lose? ISF?

- lose 1L from plasma and 3 from ISF


- results in 2 L in plasma, 6L in ISF, end with 8 litres

Pure of Free Water Loss - happensvia?


- lost from? form ICF? from ECF?


- therefore if lose 3L from ECF? see?


- overall then?

- happens via skin or occasionally in the urine


- lost from TBW = 2/3 from ICF and 1/3 from ECF


- of ECF loss, 1/4 from plasma and three quarters from ISF space


- therefore if lose 3 L from ECF, 2 litres of water moves from ICF to ECF


- overall lose 2L from ICF and 1 litre from ECF




**free water loss always 2/3 from ICF and 1/3 from ECF

Introduction to Burns


- high?


- centers have improved?


- survival now? depends on?

- approx 500,000 burns per year in US, approx 10% require transfer to birn centre


- high morbidity and LOS


- burn centres have improved morbid/mortal


- survival from burns now >94%, but depends on availability of expertise, resources


- see mortality at extreme ages

Etiology of Burns - occur from contact with?


- majority from?


- degree of injury determined by (2) also?

- burns occur from contact with heat, chemical agents, radiation


- will be focusing on thermal burns


- majority of burns are from fire, scalds, and contact with hot objects


- degree of injury determined primarily by temp, duration of contact, also by thickness of skin

Classification of Burns - Etiology


- flame from? scald from? contact from? chem? electricity?


- most common?

- flame = damage from superheated oxidized air


- scald = damage from contact with hot liquids


- contact = damage from contact with hot solidmaterials


- chemicals = contact with noxious chemicals


- electricity = conduction of electrical current through tissues




*flame and scalds are most common causes

Classification of Burns - Depth


- 1st degree? 2nd degree? through?


- supericial 2nd - to?


- deep 2nd - into?

- 1st degree = injury localized to the epidermis


- 2nd degree = partial thickness = thru epidermis and into dermis


= Superficial 2nd = injury to epidermis and supericial dermis


= Deep 2nd = injury through epidermis and into deep dermis

Classification of Burns - Depth


- 3rd degree =? through? into?


- 4th degree - through? into?

-3rd degree = full thickness = injury through the epidermis and entire dermis and into subcut. fat




-4th degree = injury through skin and subcut. fat into underlying muscle or bone

Degrees of Burns



Classification of Burns - Depth

- most burns are not uniform and have areas of varying depth


- depth often continues to evolve after presentation

Thermal Injury Zones - 1) Zone of coagulation


- necrosis of? irreversible?

= necrosis of epidermis and underlying tissue, area of necrosis and irreversible damage



Thermal Injury Zones - 2) Zone of stasis/ ischemia


- immed?


- assoc with? decreased?


- area can? go on to?

- immed. surrounding the zone of coagulation


- assoc. with vascular damage, decreased tissue perfusion (also vessel leakage)


- this area can survive or go on to coagulative necrosis

Thermal Injury Zones - 3) Zone of Hyperemia


- VD from? tissue is? not at risk for?

- VD from inflammation


- tissue is viable and not at risk for further necrosis, often includes dermis

1st Degree and 2nd Degree Burns



3rd and 4th degree burns



Assessment of Burn Size: Percentage of Body Surface Area - must assess? with?


- rule?


-- 1% BSA is?

- must assess % BSA with 2nd and 3rd degree burns


- rules of nines


- palm of patient's hand and fingers = 1% BSA

Rule of Nines - front of trunk? back? legs? arms? head? perineum?

- front of trunk = 18% = thorax 9%, abdo 9%


- back of trunk = 18% (^^)


- legs = 18% each (front 9%, back 9%)


- arms = 9% each (front 4.5%, back 4.5%)


- head = 9%


- perineum = 1%

Rule of Nines



Classification of Burn Severity in Adults


- mild? moderate? severe?

- mild: <10% BSA


- moderate: 10-20% BSA


-severe: >20% BSA




*also considered severe: >5% full thickness burns, signif burns to eyes, face, ears, genitals or joints, assoc. trauma and high voltage injury




- pts with severe injuries should be transferred to burn centre

Criteria for Transfer to Burn Centre


- BSA? burns on?


- >5%? burns injury of? burns from?


- complicating factors?

- >20% TBSA


- burns on face, hands, feet, perineum, joints


- >5% full thickness burns


- electrical, chemical burns


- inhalation injury


- complicating factors = patient with special medical needs

Inhalation Injuries - inhalation of?


- causes injury to?


- causes edema of?


- can lead to?


- also a concern of?

- inhalation of steam (heat) or toxic compounds from burning can cause injury to upper and lower airways


- cause edema of upper airway (lips, vocal cords), can occur rapidly


- edema and inflammation of lower airways and parenchyma leads to pulmonary infiltrates


- CO toxicity also a concern

Management of Pt with Thermal Injuries - 4 Phases



1) Initial evaluation and resuscitation


2) Initial Wound Management


3) Definitive Wound Closue


4) Rehab

Thermal Injuries Management Overview


- remove?


- then?


- remember?


- may need? due to?


- first? next most important?


- pts wil be?

- remove pt from source and stop burning process


- A,B,C,D,E


- remember poss. of traumatic injuries


- may need early defin. airway due to rapid upper airway edema


- after stabilization of A and B, volume resuc. is most important


- patients with signif burns will be suffic. volume depleted

Thermal Burns - Airway Special Aspects of management


- early? esp. if?


- can progress to?


- injury of? to?


- compounded by? (2)



- early airway management is essential esp if signs of airway obstruction (stridor/hoarseness)


- can progress to airway obstruction rapidly


- inhalation injury can lead to signif upper airway edema


- this is compounded by generalized vascular permeability and massive fluid resusc.

Airway Management


- if have facial burn? also if fire in?


- also possibly?


- ideally?

- suspect airway injury in pts with facial burns or carb. sputum; fire within a closed space; also possibly if singed nasal hairs or tachypneic


- however these are not sens or specific; therefore, ideally fiberoptic laryngoscopy recommended (if not, use above signs)

Thermal - Airway Management


- all inhalation injury pts?


- those who should be intubated? (3)

- intubate pts with inhalation injury early (progression)


- also intubate early:


= pts with burns > 40% TBSA


= resp. distress


= usual criteria for intubation

Thermal - Special Aspects of Breathing Management


- hypoxemia, hypercarbia may occur due to? (5)

- hypoxemia and/or hypercarbia may occur b/o:


= airway obstruction


= thoracic trauma


= eschars and edema of chest and/or abdo wall


= CO poisoning


= abdo compartment syndrome (ACS) - can also occur with massive fluid resusc

Thermal - Special Aspects of Circulation Management


- pts will be? mainly from?


- could also be?


- in first few days?


- can also develop? with?

- pts with signif burns will ultimately be hypotensive


- mainly because of volume loss from vascular perm (so will be very edematous)


- could also be hypotensive from trauma


- also can get myocardial depression for first few days


- can also develop ACS with large amounts of fluid (>250 mls/kg fluid)


- may need to insert IVs through burnt tissue

Thermal - Special Aspects of Fluid Resuscitation = Parkland Formula


- amount? type of burn?


- in first 8 hours, give? then?


- use? monitor?

= 4 mls/kg/% BSA burned = 2nd and 3rd degree


- give 1/2 over first 8 hours (from time of burn) and give 1/2 over next 16 hours


- use Ringers


- monitor organ perfusion, U.O and adjust fluids

70 kg pt with 35% BSA burns need?

= 4 mls x 70 xs 35 = 9800 mls = 9.8 L

Thermal - Special Aspects of D and E


- all usual?


- think about?


- loss of skin could cause?

- all usual causes of altered level of consciousness, but:


- also could be from CO poisoning


- loss of skin = loss of heat = hypothermia

Inhalation Injury - Three Processes


- upper? subglottic? chemical? from?

1) Upper airway injury = lips to larynx


2) Subglottic Injury (subglottic airway and pulm parenchyma)


3) Chemical Asphyxia (CO)

Inhalation Injury Mechanisms


- in upper airway?


- inhale also? leads to injury of? causing?


- CO causes?

1. Inhlalation of hot gases leads to edema of upper airway


2. Inhalation of toxic gases and particulate matter, leads to injury to airways and pulmonary parenchyma, small airway obstruction and pulmonary inflammation and edema, leading to bronchospasm and airspace disease


3. Inhalation of CO = chemical asphyxia

Carbon Monoxide


- produced by? have in body from?


- binds to? forms?


- CO vs O2 affinity?


- COHb means?

- CO = produced by oxidation of carbon, have CO in body from breakdown of heme


- CO binds to Hb, forms COHb


- CO's affinity for Hb = 240x > 02


- COHb means less O2Hb = results in tissue hypoxia

Role of Carbon Monoxide


- leads to loading? doesnt?


- O2 decreases?


- without vs with O2? yet with hyperbaric?

- COHb also leads to loading (left) shift of 02 Hb curve


- doesnt affect pO2


- O2 decreases half life of CO:


= 4-6 hrs without O2 (room air)


= 1 hour with 100% O2


= 20 mins with hyperbaric O2

Diagnosis of CO Poisoning - diagnosed? via? (3)


- no single?

- diagnosed clinically via:


= Hx of suspected/exposure to CO


= Symptoms of CO poisoning


= Increased COHb level in blood




* note = no single symptom is either sens or spec for dx

CO Symptoms - (8)


- symptoms do not?


- main problem is?


- most common symptom?

- headache, confusion, dizziness, LOC, N, V, SOB, chest pain


- symptoms do not correlate with COHb levels


- main problem form CO is long term cognitive sequelae




*HA most common symptoms

CO Hb levels for Diagnosis


- smoker baseline? abnormal? non vs smokes


- levels must be measured by?

- smokers have baseline 3-5%. abnormal is >3% in non smoers, 10% in smokers


- levels must be measured by co-oximetry, will get falsely elevated O2Hb on pulse oximetry


- COHb is misread on SaO2 probe as O2Hb

COHb levels for CO Diagnosis - CPHb only used to? dont necc? dont predict?


- major outcome?



CO Poisoning Treatment


- goal to prevent? treatment is? competes for?


- accelerates?


- give? to decrease?


- therefore should?

- goal to prevent long term deficits


- treatment is O2, competes for Hb binding


- accelerates elimination of CO


- half life of COHb decreased with 100% O2


- therefore give 100% for anyone with suspected CO poisoning



CO Poisoning Treatment


- recommended to? requires?


- evidence showed?

- hyperbaric oxygen (HbO2) therapy recommended for CO poisoning


- HbO2 therapy requires trasnfer to proper facilities


- evidence showed pts with 3x HBO2 treatment within 24 hours had half rate of cognitive problems at 6 weeks, 6 months, etc

Suggested Indications for HBO2 - (3)


- signic? COHb?

- LOC, neuro deficits, ischemic cardiac chnages


- signif metabolic acidosis


- COHb level >25%

Burn Summary - burns have?


- all but mild burns are?


- hypothermia is?


- most burns from?


- must assess?


- early?


- if severly burned, then?


- need aggressive?


- consider?


- major concern?

- hypothermia is major concern, keep warm
- consider CO poisoning so admin 100% O2 to everyone

- hypothermia is major concern, keep warm


- consider CO poisoning so admin 100% O2 to everyone

Vaccines and GBS


- believed that?


- vaccine effect?


- imms shown to?

- believed that immune stimulation plays a role in pathogenesis of BGS


- vaccines have effect on IS


- immunizations such as H1N1 or meningococcal have been shown to increase risk of contracting GBS

GBS is a?


- presents as? provoked by?


- immune response? because of?

- acute immune-mediated polyneuropathy, presenting as acute paralyzing illness provoked by preceding infection


- immune response cross-reacts with peripheral nerve components because of molecular mimicry and attacks myelin or axons

Clinical features of GBS


- progressive? absent?


- weakness starts in? can?


- weakness in?


- pain in?


- also see?

- progressive, fairly symmetric uscle weakness with absent or depressed deep tendon reflxes


- weakness usually starts in legs, can lead to respiratory weakness


- see facial, oropharyngeal and oculomotor weakness


- pain typically in back and extremities


- dysautonoia

Diagnosis of GBS


- LP reveals? seen in?


- use? believed to?

- LP often reveals elevated CSP protein with normal CSF


- seen in >75 patients after third week


- use IMIG, believed to create anti-idiotypic Abs that interfere with complement and cytokine production

Dementia DDX (10)

- Alzheimers


- Mild cognitive impairment


- vascular dementia


- mixed dementia


- dementia with lewy body


- Parksinsons disease


- frontotemporal dementia = FTD


- CJD


- normal pressure hydrocephalus


- huntingtons


- Wernice- Korsakoff Syndrome

Complications of Hip Fractures - seen more in?


- (5)

- seen more in femoral neck fractures


- infection


- thromboembolism


- AVN, nonunion


- chronic pain


- dislocation



5 Is of Falls = ?

- intellectual impairment


- instability


- immobility


- incontinence


- iatrogenic = polypharm

Why is leg shortened and externally rotated - due to? with some?


- axis of?


- iliopsoas causes?

- due to irritation and spasming of the iliopsoas muscle, with some contribution from lateral rotators of the hip


- axis of femoral head is altered


- when liopsoas contracts, leads to shortening as well as external rotation

Garden 1 - is a? not? typically? orientation?

= impaction fracture, is undisplaced and typically impacted with a valgus and retroverted orientation

Garden 2 - is? but is also? less? no shift in?

= undisplaced, complete fracture. Less common, have break in trabeculations but no shift in bone alignment

Garden 3 - involves? is? not completely?

= Involves varus displacement of the femoral head, shaft however is not completely displaced

Graden 4 - complete loss? between? shaft often?

involves comples loss of continuity between fragments, shaft translates proximally

Long bone fractures - more likely to see?

- higher rate of fat embolization

NPO Guideleines - goal to minimize?


- at 8 hours? 6 hours? 4 hours? 2 hours?

- goal to minimize gastric volume at time of surgery to prevent pulmonary aspiration


- 8 hours - stop fried or fatty food, or meat


- 6 hours - stop nonhuman milk, formula, light meal


- 4 hours - stop breast milk


- 2 hours - clear liquids, chewing gum (if not swallowed)

3 Antipt meds - A/ C/ Di / Ti - MOA?

- Aspirin = inhibits COX to decrease T-A2 production


- Clopidogrel = inhibits ADP-dependent plt aggregation


- Dipyridamole = inhibits AD and phospho, accumulates cyclic AMP to inhibit plt aggregation


- Ticlopidine = MOA similar to Clopidogrel




**these stop primary hemostasis

3 Anticoag meds - D/R/A - inhibitor of? prevents?


- all affect?

- Dabigatran = direct thrombin inibitor, prevent it from cleaving fibrinogen to fibrin


- Rivaroxaban = direct factor Xa inhibitor, prevent cleaving prothrombin to thrombin


- Apixaban = direct factor Xa inhibitor, prevent it from cleaving prothrombin to thrombin




* affect secondary hemostais


* still not as good as warfarin as reversible

Advantages of LMWH over heparin - greater? longer? better? lower risk of?

- greater BA


- longer duration of anticoag effect


- better correlation between dose and response


- lower risk of HIP


- lower risk of osteoporosis



Disads of LMWH - delayed? less easily? prolonged?

- delayed onset of action


- less easily inactivated


- prolonged half life in renal failure patients

Open Reduction Internal Fixation


- open eduction means?


- internal fixation refers to? used to?

- open reduction = surgery needed to realign bone fracture to normal position


- internal fixation = refers to steel rods, screwes, plates used to stabilize fracture to heal right way

Joint Resurfacing - preserves? uses?


- metal? usused to?


- now has?

- preserves femoral enck and uses metal prosthesis to replace femoral head


- metal acetabular component used to create a metal on metal bearing surface


- fallen out of faven

Hemiarthroplasty - replacing? leaves?

= replacing femoral head and neck while leaving acetabulum intact

Total Hip Athrplasty - used in those? signif?


- most common?


- some more?

- used in those who have failed to responed to nonpharm and pharm management, significant decrease in QOL


- most common defin surgical procedure for OA


- some more serious adverse events

Cough


- is a common? may be?


- different types?

- is a common presenting symptom, may be very distressing symptom for the patient


- acute < 3 weeks


- subacute = 3-8 weeks


- chronic > 8 weeks

Function of Cough


- clear? inhaled?


- protect?

- clear mucuous and inhaled substances


- protect airway from inhalation of foreign substances

Cough Receptors


- 5 locations?


- all act on? via? also receives?

- larynx and supralaryngeal area


- trachea and bronchi


- ear canal and eardrums


- pleura, pericardium and diaphargm


- esophagus and stomach




** all act via vagus to cough centre (medulla, mucleus tractus and solitarus)


** also recieves from CNS cortical modulation

Cough Centre Acts on? (3) which include? (SM/P/V)

- spinal motor = expiratory muscles, pelvic sphincters


- phrenic = diaphargm


- vagus = larynx, trachea, bronchi

Physiology of Cough


- Inspiratory? Compressive? Expuls?

1) Inspiratory phase = wide open larynx, diaphragm contracts for rapid, deep inspriation


2) Compressuve phase = larynx closes and expiratory muscles contract, generating positive intrathoracic pressure


3) Expulsive phase = larynx open widely, with sudden outflow of air

Causes of Chronic Cough


- if healthy, then? which?

- generally healthy person - if have chronic cough


- the big 3 = accounts for 90%

Big 3 of Chronic Cough **

1) Upper Airway Cough Syndrome = Post Nasal Drip


2) Asthma


3) GERD

Upper Airway Cough Syndrome


- secretions in?


- symptoms ? (ND/T/S)


- causes? (3)


- sometimes can be?

- secretions in the upper airway stimulate cough receptors in the laryngeal mucosa


- symptoms = nasal discharge, throat clearing, sensation of dripping in back of throat


- causes - allergic rhinitis, vasomotor rhinitis, sinusitis


- sometime difficult to diagnose = empiric therapy may be best test

Treatment - Upper Airway Cough Syndrome


- may respond to? but dont want to?


- may also use? or?

- may respond to antihistamines and decongestants (pseudoephedrine), but may not want to use these longer term


- may also use topical nasal steroids (esp. if allergic component) or ipatropium bromide (if vasomotor rhinitis)

Asthma - Symptoms - main four? (4)


- cough may only be?

- cough, wheezing, chest tightness and dyspnea


- cough may be only manifestation of asthma

Asthma - Diagnosis and History


- often history of?


- diagnosis may be? or do a?


- cough usually responds to?

- often a history of atopy or a FM of asthma


- diagnosis may be confirmed on spirometry or bronchoprovocation (methacholine challenge) testing


- cough usually responds to treatment of asthma (inhaled steroids, bronchodilators)

GERD


- acid from? that then?


- may have? such as?


- cough may ?

- acid from stomach acting on esophagus, laryngopharyx, stimulating cough receptors


- may have symptoms of heartburn = burning retrosternal chest discomfort, worse after meals and lying down, acid taste in mouth


- cough may be only manifestation

GERD - Diagnosis and treatment


- done with?


- often give? such as? (2)

- diagnoses made on 24 hour esophageal pH monitoring, empiric therapy is often instituted instead


- can be treated with H2 antags, PPIs

The others


- responsible for?


- include? (70

- responsible for 10% of chronic cough


- Resp tract infection


- ACE inhibitors


- chronic bronchitis


- bronchiectasis


- lung cancer


- intersttial lung disease


- recurrent aspiration

Resp Tract Infection


- caused by? may lead to?


- may have history of? see?


- other elements?

- viral URTI may lead to prolonged cough


- may have had a history of other URTIs ymptoms at onset of cough =runny nose, sore throat, fever and myalgias


- etiolgoy of cough has some element of upper airway cough syndrome from nsasal secretions, airway inflammation from infection, airway hyperresponsiveness from underlying asthma

RTI - mostly caused by?


- most do not?


- post viral cough often?


- consider?

- chronic cough is mostly caused by viral infections


- most do not benefit from Abx therapy


- post viral cough may respond to inhaled ipatropium bromide


- consider specific infections in certain cases = Bordatella pertussi, Myco tb

Bordatella pertussis Infection


- sometimes referred to as?


- can also be seen in?


- is highly? but usually?


- caused by?

- sometimes referred to as whooping cough


- commonly regardas as childhood illness, can be seen in adults


- highly contagious but vaccination usually effective at preventing severe cases in childhood


- caused by gram neg coccobacillus

Bordatella Pertusiss - Whooping Cough


- see? following?


- % present?


- mean cough duration? referred to as??

- inspiratory, stridorous sound following paroxysms of coughing


- only 20 to 40% of adults present with whooping


- may have post-tussive vomiting


- mean duration of cough in adults is 36 to 48 days but sometimes referred to as "100 day cough"

Diagnosis of Bordatella


- can be a? made with? or by?


- highest sens in?


- if presenting after 4 weeks?

- can be a tricky diagnosis


- can be made with nasopharyngeal swab, by PCR or by culture


- highest sensitivity within first few weeks of symptoms


- if presenting after 4 weeks, can consider doing serology for IgG titres if not vaccinated within 2 years

Treatment of Bordatella Pertussis


- treatment may reduce?


- many patients do no?


- treat if?


- treat with either?

- treatment may reduce the severity of illness and reduce inectivity if admin early


- many patients do no present early enough


- treat if within 3 to 4 weeks of symptoms


- consider treatment if persistent symptoms after 4 weeks


- macrolide Ab = Azithro at 500 mg x 1 day, then 250 mg for 4 days or Clarith 500 mg 7 days

Mycobacterium Tb


- consider if? such as?


- present with (3)

- consider TB especially if patient is from a higher risk group = immigrant from endemic region, first nations, immunocomp


- may present with hemoptysis, weight loss and night swetas

ACE Inhibitors


- commonly used to?


- % that develop?


- thought to be due to? which?

- commonly used to treat hypertension and heart disease


- up to 15% of patients devleop cough


- thought to be due to accumulation of bradykinins, which stimulate cough receptors

ACE Inhibitor Cough


- usually occurs? but can?


- may have?


- improves with?


- usually recurs with?

- usually occurs within 1 week of initiation, but can present after even 6 months


- may have itchy or scratchy sensation in throat


- improves with stopping therapy but may take up to 4 weeks


- usually recurs with re-challenge

Chronic bronchitis


- major RF?


- diagnosis confirmed?


- cough may improve with?

- majorRF is smoking


- diagnosis confirmed by pulmonary function testing


- cough may improved with inhaled bronchodilators and steroids, smoking cessation

Bronchiectasis


- inflammation that?


- leads to? poor? and then?

- inflammation causes small airway damage


- leads to airway dilatation and scarring, poor secretion clearance, and chronic recurrent infection

Some Causes of Bronchiectases (7)

- postinfectious


- primary immune disorders


- CF


- alpha-1-antitrypsin disease


- inflammatory disorders and connective tissue diseases


- airway obstruction


- allergic bronchopulmonary aspergillosis

Imaging of bronchiectasis - on CXR, look for?

- features can be noted on chest xray but best seen on high-resolution CT scan


- dilated, thickened airways

Treatment of Bronchiectasis


- exacs treated with? to?


- base Abx choice on?


- candidates for? think about?


- enhance sputum clearance with?


- surgery may be?

- treat exacerbations of bronchiectasis with Abx to prevent worsening of bronciectasis


- may base antibiotic choice on sputum culture


- patents (esp CF) may be candidates for chronic inhaled Abx, chest physiotherapy and inhaled agents (mucolytics) to enhance sputum clearance


- surgery is occasionally considered for very localized bronchiectasis or for recurrent hemoptysis

Lung Cancer


- may present with? (3)


- key is?

- may present with chronic cough, hemoptysis, weight loss


- imaging is key to the diagnosis

Interstitial Lung Disease


- cough is? (2)

- cough from ILD is usually persistent and non-productive

Recurrent Aspiration


- seen in?


- RFs = (4)


- ask whether?

- patients with swallowing difficulty (dysphagia) may be prone to recurrent episodes of aspiration


- RFs = neurologic dysfunction, esophageal disease, NG feeding tubes, prolonged recumbency


- ask whether coughing is often temporally related to eating or drinking

Cough Algorithm - do? consider? tihnk of?



Big Three - Investigation? Treatment?



After the Big Three - do? imaging of?


- also perform? (3)



Resp General Principles


- goal should be? and then?


- monitor?


- often multiple?

- goal should be to elucidate the causes of the cough and use directed therapy


- monitor response to therapy and compliance


- there are often multiple causes of cough, mainly partially effective treatments



Cough - If All else falls


- consider? can use?


- non opioids?


- or use?

- consdier central acting anti-tussive agents


- opioids such as codeine


- non-opioids such as dextromethorphan


- Gabapentin

Asthma Definition


- is a? char. by?


- defined by? (3) vary over?


- has variable?

- heterogenous disease, usually characterized by chronic airway inflammation


- defined by history of respiratory symptoms such as wheeze, SOB, chest tightness and cough that vary over time and in intensity


- has variable expiratory airflow limitation

Symptoms of Asthma


- vary over? usuallt?


- wheeze is a? seen on?

- vary over time and severity, usually multiple:


= SO, wheeze, coughing, chest tightness


- wheeze = a continuous whistling sound associated most commonly with expiration due to collapse of intrathoracic airways



Symptoms of Asthma


- worsen ? provoked?


- seen with? worse with?

- occur or worsen at night


- provoked by exposures, either specific allergens or nonspecific irritants


- recurrent or prolonged chest infections (>2 weeks), actually asthma exacerbations

Epidemiology of Asthma


- high? prev? 15%


- most?

- high burden of disease around the world


- 10% prevalence of asthma


- 15% if children have had asthmatic symptoms


- most cases allergic/atopy related


- occupational exposures

Causes of Wheeze


(9)

- allergic rhinosinusitis


- post-infectious cough


- GERD


-COPD


- acute bronchitis


- heart failure


- foreign body


- obstructing lesion


- vocal cord dysfunction

Diagnosis of Asthma - demonstration of?


- increased? after?


- variability in? (2)


- response to?


- positive?



- demonstration of reversible airflow obstruction is key


- increased FEV1 > 12% and >200 cc after bronchodilator (+/- norm. of FEV1/FVC)


- variability in FEV1 over time


- variability in Peak Flow over time


- response to trial of therapy


- positive challenge test (Methacholine, Exercise) with fall in FEV1 by >20%

Spirometry in Asthma


- pattern = (2)


- see positive

- the pattern of asthma on spirometry is:


= reduced FEV1/ FVC ratio


= positive bronchodilator response






* see positive methacholine challenge

Pathophys of Asthma


- inducers? (3)


- inflammation leads to?


- triggers = (4)


- symptoms (4)

- inducers = allergens, chemical sensitizers, air pollutants, virus infections


- inflammation leads to airway hyperresponsiveness and airflow limitation


- triggers = allergens, exercise, cold air, particulates


- symptoms = cough, wheeze, ches ttightness, dyspnea

Therapies for Asthma


- avoid?


- bronchodilation via? (2)


- anti-inflamm? (2)

- allergen/ trigger avoidance


- bronchodilation = B2 agonists, anticholinergics


- anti-inflammation = stewards, leukotriene, receptor antagonists

Therapy and Allergen Avoidance


- avoid? often is?


- crucial to?


- 25% is?

- avoidance of identified triggers in allergic asthma is beneficial but often difficult


- occupational allergens are crucial to identify and avoid


- up to 25% of asthma is work related with up to 10-15% of cases caused by occuptational allergen

Therapy - Bronchodilation - generally used for?


- good for?


- B2 agonists - reduced? target?


- dont use antichols when?


- comes as either?

- BDs are generally relievers or rescue medications


- have immediate effect with relief of symptoms**


- B2 agonists = B2 vs B1 = reduced cardiac SEs, target smooth muscle cells


- anticholinergic drugs exist, but not used as commonly for asthma when stable


- comes as short acting or long acting

Short Acting Bronchodilators


- colour? types? S/T

- Salbutamol


- Terbutaline


= "blue" puffer

Long Acting B2 Agonists


- better for? then?


- dont use as?


- types = S/F

- provide improved and prolonged bronchodilation compared to short-acting drugs


- but when used as monotherapy, resulted in increased mortality


= Salmeterol and Formoterol

Therapy - Corticosteroids


- need to treat? which is?


- used as both?


- see improvement over?


- delivered by? prefer? oral when?

- treat the underlying pathophys of asthma - inflammation


- mainstay treatment of asthma = maintenance or preventer


- improvements over days


- can be delivers by inhaled route = much preferred, action at target organ with reduced SEs


- oral route is systemic, see large inflammation reduction, use during severe exacerbations but has alot of SEs

Inhaled Corticos - Safety


- local = 2 - C/D 0 are?


- systemic are? including (4)

- local = risk modifiable = candidiasis, dysphonia


- systemic, rare, risk modifiable:


= adrenal suppresion (very rare)


= growth inhibition in children (1 cm)


= osteoporosis


= cataracts, glaucoma

Inhaled Coticos - colour? examples (3 - T/M/B)

= orange/red/brown puffer


= Takeda, Mometasone, Budesonide

Asthma Combination Therapy - better to?


- reduced? (2) better (3)

- LABA combined with ICS was better than doubling the dose of ICS


- reduced symptoms


- better nocturnal control


- better QOL
- better lung function


- reduced exacerbations

Combination Therapy - such as? (2)


- S/FP


- B/F

=Salmeterol/ Fluticasone Propionate


= Budesonide/ Formoterol


- many others

Asthma Therapy - Leukotriene Receptor Antags


- leukotrienes are made by?


- promote? increase? cause?


- LTRAs block?

- leukotrienes produced by the action of the arachidonate 5-lipoxygenase enzyme


- promote bronchoconstriction, increase mucous secretion and cause inflammation


- LTRAs block action of leukotrienes on target cells such as bronchial smooth muscle cells

Leukotriene Receptor Antagonist


- med used for?


- is good for?


- used largely in?


- inferior to?


- only avail?

- a maintenance/preventer medication


- non steroidal, oral medication


- used largely in children


- inferior to ICS in adults as controlling medication


- Singulair = only one available in Canada

Escalation Therapy of Asthma

- maintenance = ICS

- maintenance = ICS

Managing Asthma - Control means? daytime? night time? during PA? exacs? absence? need for?

- uncontrolled if any char. is out of range

- uncontrolled if any char. is out of range

Asthma Control - if not controlled, means?


- good control means?


- see athletes?

- patients who are not controlled have decreased QOL, increased risk of exacerbations


- good control = means essentially normal activity with no symptoms


- 5-10% of Olympic athletes have asthma

Acute Exac of Asthma


- acute loss of control assoc. with? (3)


- admission based on?


- useful to get?

- acute loss of control is often assoc. with triggers = infection, enviro, allergen


- admission to hospital can be predicted based on response to bronchodilator and ER therapies


- serial peak flow of FEV1 is useful,quant measure of response to therapy

Acute Exacerbations of Asthma - Acute Treatment


- BD = (2)


- oral - such as?


- monitor?


- Abx?

- bronchodilators = B agonists and anticholiners = lots


- oral steroids = 4o to 60 mg of prednisone


- monitor peak flow/ spirometry


- Abx not usually indicated

Acute Exacerbations of Asthma - Ward - (3)


- monitor? training? role in?

- asthma education


- inhaler technique training


- monitor peak flow/ spirometry

Testing to investigate asthma symptoms


- in office, can? start on? give?

- spirometry can be done in office


- start on low dose inhaled ICS (Budesonide) and reassess symptoms


- give rescue med = Salbutamol inhaler



Adjusting Meds in Uncontrolled Asthma Patient


- increase to? review?

- increase to combination inhaler (Salmeterol/Fluticasone) and review inhaler technique

Definition COPD


- slowly? involving?


- characterized by?


- caused mainly through?

- slowly progressive disease involving the airways or pulmonary parenchyma (or both) that is characterized by persistent airflow limitation


- caused mainly through exposure to tobacoo smoke, but can also be attrib. to other inhaled irritants like biomass fuels and occupational exposures

Chronic Bronchitis


- known as?


- see? (6) no? frequent? excess?

- known as blue bloater


= chronic cough


= wheeze


= excess mucus from goblet cells in airway


= frequent bronchitis


= no air hunger


= hypercapnic, hypoxic

Emphysema - known as?


- are? see? abnormal? destruction of?


- blood is?

- known as pink puffer


= breathless


= wheeze


= abnormal enlargement of alveolar spaces


= destruction of the alveolar walls and diffusing membranes


= normocapnic, mildly hypoxic

Most COPD is a bit of both?

- a bit of both emphysema and chronic bronchitis

DD - Breathlessness - main one? airways vs parenchymal (1) vs vessels (2) vs muscles (1)


- also from? (3) CD/A/D

1) Pulmonary Disease


= airways = asthma, bronchiectasis


= parenchyma = ILDs


= vessels = PH, PE


= muscles = neuromusc. disease


2) Cardiac disease


3) Anemia


4) Deconditioning / Obesity

DD - Chronic Cough


- main one? airways (2) vs parenchyma? (2)


- also consider? (3) S/R/M

1) Pulmonary DIsease


= airways = asthma, bronchoiectasis


= parenchyma = ILDs, infection


2) Sinus disease


3) Reflux


4) Medication = ACEi

Epi of Cough - is the 4th leading?


- only cause of death that?


- prevalence?

= 4th leading cause of death


= only major cause of death that has increased in recent years


= prevalence = 5% of Canadians >35 yo, % of women and 4% of men

Causes of COPD


- most prev?


- occupational?


- biomass?


- defic?


- long standing?

- smoking = most prevalent, easily rec. "noxious" fume


- occupational = organic, inorganic dust exposures


- biomass fuels = wood, animal dung, coal, crop residues, women who cook in developing nations


- a1 - antitrypsin deficiency


- long standing/ untreated asthma


- air pollution

Smoking and COPD


- rates in smokers? continuous smoker risk?


- see contnued?


- cessation therapy is?

- rates of COPD in smokers varies considerably in studies, but it is not 100%


- continuous smokers have an estimated lifetime risk of COPD of 25-50%


- see continued effect of smoking, leading to disability and death


- smoking cessation is 1 of only 2 therapies that reduces mortality

Diagnosis of COPD


- clinical suspicion when? (4), with?


- key to diagnosis?


- do not accept?

- clinical suspicion in patients with dyspnea, wheeze, chronic cough and/or sputum production with an exposure history (most commonly smoking)


- spirometric confirmation is key to the diagnosis**


- do not accept a clinical diagnosis unless the patient is unable to perform spirometry

COPD Pulmonary Function tests


- obstruction defined by?


- reduced? shows?


- elevated? shows?


- emphysema sees low?

- obstruction defined by low FEV1/FVC


- reduced FEV1 shows severity of airflow obstruction


- elevated TLC shows hyperinflation


- low diffusion capacity consistent with emphysema

Spirometry - FEV1/FVC Ratio of COPD


- hard cutoff at? overdiagnosis of? underdiagnosis of?

- hard cutoff of <0.70


- overdiagnosis of the elderly where the FEV1/ FVC naturally falls bellow 0.070


- underdiagnosis of the young where the FEV1/FVC naturally falls above 0.070



Pathophys of COPD


- inflammation plays? pattern is?


- amplifie? resulting in?

- inflammation plays central role in development of COPD, but the pattern is different from asthma


- amplified response to noxious stimuli resulting in inflammatory mediators, oxidative stress, protease-antiprotease imbalance

Pathophys of COPD


- increase? leading to?


- decreased? leads to?


- gas exchange?

1 = Mucus hypersecretion = increased cough


2 = Airflow limitation from decreased airway luminal diameter = results in dypsnea


3 = gas exchange abnorms from destruction of alveoli = hypoxia, hypercapnia and dyspnea

COPD - Hyperinflation


- limitation of? trouble with?


- less air is? leading to?


- with high RV, see? makes? gives?


- leads to?

- airflow limitation = >> trouble with exhalation


- with each breath, less air is expelled versus amount inhaled = "Breath Stacking"


- with high RV, the lung is now at a mechanical disadvantage, making respiratory efforts inefficient = sensation of dyspnea


- high RV due to obstruction, build up gas in lung

Therapies fo COPD


- broncho - use?


- give? for?


- rehab for?


- try both? (2)

- bronchodilation = B2 agonists, anticholinergics


- anti-inflammation = steroids


- physical conditioning and education = pulmonary rehab


- oxygen


- vaccinations

Therapy for COPD = Bronchodilation


- lack of?


- reduces? (2)


- can use?


- or use?

- although lack of bronchodilator response on spirometry, clinical response recognized


- reduces dynamic hyperinflation


- may reduces exacerbations


- can use anticholinergics = short and long acting


- B2 agonists = short and long acting

Therapy - Anticholinergics


- prefer? in?


- better? reduced?


- examples = (3)

- prefer long-acting agents in patients with persistent symptoms


- better bronchodilation


- reduced exacerbations




= Tiotropium, Umeclidinium, Aclidinium

Therapy - Long Acting B2 Agonists


- can use? unlike in?


- use? (3) = S/F/I

- unlike asthma, monotherapy with LABA is acceptable


= use Salmeterol, Formoterol, Indacaterol

COPD Combination Therapy


- now have a? in COPD use?


- such as?

- cones in a now wide assortment


- dual bronchodilators indicator in COPD only


- Umeclidinium/ Vilanterol, Aclidinium/Formoterol, etc

Therapy - Inhaled Corticos


- unlike asthma as use? as?


- decreases? improves?


- cant use a? must?

- unlike in asthma, where corticos are the mainstay, in COPD, ICS is an adjunct therapy


- decreases frequency of exacerbations, improved QOL< indicated in more severe disease for symptoms of breathlessness


- not a monotherapy option in COPD = always with long acting bronchodilators

COPD Therapy - Pulmonary Rehab


- focused?


- reduces? increases? improved?

- focused exercise and educational program geared to patients with a chronic resp. illness


= reduces dyspnea


= increased exercise capacity


=improved QOL


= reduced risk of exacerbations and mortality after exacerbations

COPD Therapy - Oxygen


- one therapy that?


- titrate to?


- excessive?

- one of the few therapies in COPD that actually reduces mortality from the disease


- titrate to target SpO2 = 88-92%


- excessive oxygen (often during acute exacerbation) can be detrimental



Problem of Excessive Oxygen


- careful in? increased?


- loss of? worsening? change in?



- in patients who are CO2 retainers, excessive O2 will result in increased hypercapnia which may be fatal


- loss of hypoxic drive to breathe, worsening V/Q mismatch, chnage in carrying capacity of HgB for CO2

COPD Therapy - Imms


- weak evidence for? but minimal?


- annual?


- should also get?

- weak evidence for benefit in preventing exacerbations, but minimal harm/risk


- influenza annually


- pneumococcal variation:


= Prevnar 13 x 1


= Pneumovas x1 with 1 repeat booster after 10 years

COPD Escalation Therapy



COPD Acute Exacerbations


- worsening of? often?


- see? (3)


- as progresses?


- will likely?

- worsening of resp. symptoms beyond day to day variation, often triggered by infections


- see dyspnea, cough and sputum chnage


- as COPD progresses, exacerbations become more frequent


- an exacerbator will likely continue to have frequent exacerbations

AE COPD Impacts - more rapid?


- reduced?


- loss of?

- more rapid decline of lung function = FEV1


- reduced QOL


- reduced exercise tolerance


- loss of income/ health care expenditure


- increased mortality

AE COPD Management


- use?


- give? at?


- oxygen with?


- consider?

- bronchodialtors = alot and often


- systemic steroids = 40 mg prednisone x 5


- oxygen with careful titration


- Abx


- ICU care if needed

AE COPD and Abx


- 50% caused by? may relate to?

- bact. infections cause 50% of exacs


- may relate to increased bacterial burden when chronically colonized


- strongest evidence for use in purulent exacerbations, mod to severe COPD and AE needing ICU


- reduces treatment failure, mortality and symptoms

Diagnosis of COPD


- use? then?

- pulmonary funtion test and Xray to loo for hyperinflation

Approp Therapy for COPD


- stop?


- give? as needed?


- also give?

- smoking cessation


- long acting anticholinergic = Tiotropium


- use as needed = Salbutamol inhaler


- have inhaler teaching

AE COPD Therapy


- oral?


- if purulent?


- then give?


- consider?

- oral steroids = prednisone


- purulent = Abx


- Salbutamol and Ipratropium every 2 to 4 hours




* consider hypercapnia due to retaining oxygen

Breathing Discomfort caused by? (4)


- inability to?


- heavy?

- air hunger


- chest tightness


- heavy breathing effort


- inability to get a deep breath

Mechanisms of Dyspnea


- increased? decreased? also?


- increased? leads to?


- heavy? from? that then?

- increased PCO2, decreased PO2 and acidosis leads to air hunger


- increased J receptors and airway irritant receptors leads to bronchoconstriction and chest tightness


- brain causing heavy breathing = increases work of breathing

Approach to Dyspnea - Mechanisms


- CHF leads to? that then?


- increased? then causes?


- anemia then? leads to?

= CHF leads to increased interstitial fluid = increases J receptor stimulation


= Poor fitness increases anaerobic metabolism = acidosis


= Anemia decreases oxygen delivery = leads to acidosis

Approach to Dyspnea - Acute Causes - (5)

- upper airway


- pulmonary


- cardiac


- toxic/metabolic


- misc

Pulmonary Causes of Dyspnea - causes (6)

- PE


- COPD/asthma


- pneumothorax


- chest trauma


- infection


- pulm hemorrhage

Approach to Acute Dyspnea - establish? provide? assess?


- screening for? (4)


- initial treatment = (3) D/B/VS

1) Establish stability of the patient = provide O2, assess vitals, IV access, monitoring, airway assessment


2) Screening exam = pneumothorax, tamponade, foreign body, bronchospasm


3) Initial treatment = decompression, bronchodilator, ventilatory support

Approach to Acute Dyspnea


- initial?


- then do?


- treatment? (4)


- further investigations =? (5)

- initial investigations = Xray, ECG, bloodwork


- history and physical


- further treatment - steroids, bronchodilators, Abx, diuretics for CHF


- further investigations = CT chest, spiromtery, echo, ABG, BNP level

Dyspnea Signs of Severe Resp. Distresss


- (6)



- tachypnea


- indrawing and accessory muscle use


- inability to lie down


- inability to speak in sentences


- agitation


- cyanosis, diaphoresis

Signs of Impending Resp. Failure - reduced? inability to? rising?

- reduced level of consicousness


-inability to maintain resp. efforts


- rising PCO2 and acidosis

Pulmonary Causes of Chronic Dyspnea


- (5) A/R/PV/P/P

- airway disease


- restrictive disease


- pulmonary vascular disease


- parenchymal disease


- pleural disease

Approach to Dyspnea - Chronic - History - ask about? (6)

- onset and duration


- quantify severity


- exacerbating/ alleviating factors


- associated symptoms


- general medical and FH


- social history

Dyspnea - Medical Research Council Dyspnea Scale


- Grade 1? 2? 3? 4? 5?

- Grade 1 = breathless with strenous exercise


- Grade 2 = SOB when hurrying on the level or walking up hill


- Grade 3 = walks slower than people of same age


- Grade 4 = stops for breath after waling 100 years


- Grade 5 = too breathless to leave the house or breathless when dressing

Dyspnea - Chronic - PE - perform?


- look for? (3)

- respiratory


- CV


- general = thyroid disease, anemia, clubbing

Dyspnea - Chronic Tests - (7) Investigations

- chest Xray


- blood tests


- PFTs


- CT scan


- ABG


- echo


- exercise testing

Dyspnea Test - Chest Xray


- may show? or other?


- may not show? (2)

- may show interstitial disease, other parenchymal disease, pleural disease


- may not show airways disease, pulmonary vascular disease

Dyspnea test - Blood Tests - main two? (2)


- look at? for?

- Hemoglobin may show anemia or polycythemia (2 to chronic hypoxemia)


- TSH may show evidence of thyroid disease

Dyspnea - PFTs - obstructive causes (2)


- restrictive = (3)


- low diffusion = see? (4)

- obstructive = asthma, COPD


- restrictive = ILD, chest wall, neuromuscular


- low diffusion = anemia, ILD, emphysema, pulmonary vascular

Approach to Dyspnea ask? yes?


- if no - it is?


- if yes - ask? yes or no?

- Is FEV1/ FVC low? (<70%)


- Yes = is FVC low (<80% pred):


= if no = obstructive


= if yes = is TLC low? (


= if no = obstructive


= if yes = mixed

Approach to Dyspnea - ask?


- if no - ask?


- no?


- yes - ask? yes?

- Is FEV1/ FVC low? (<70%)


- No = is FVC low? (<80%)


= No = normal


= Yes = Is TLC low (<80%) = yes = restriction

PFT Algorithm


- first check? then ask? then ask?



PFT Causes and Diagnosis - Obstructive


- if normal DLCO? low?


- asthma if post bronchodilator?

- obstructive + normal DLCO = asthma or chronic bronchitis


- obstructive + low DLCO = emphysema




* increase in FEV1 of >12% and >200 cc post bronchodilator = asthma

PFT Causes and Diagnosis - Restrictive


- normal DLCO? (2) low?

- restrictive + normal DLCO = chest wall, neuro-muscular


- restrictive + low DLCO = ILD

PFT - If normal and low DLCO? (2)

- anemia


- pulm. vascular

Tests of Chronic Dyspnea - CT and ABG


- CT - better for? see?


- ABG - look at? if? from (2)

- CT = better definition of parenchymal interstital disease, pleural disease, contrast evaluation for thromboembolism




- ABG = PCO2 if suspect hypoventilation (chest wall, neuromuscular)

tests of Chronic Dyspnea - Echo, Exercise Testing


- echo to assess? (3)


- exercse - evaluate?

- Echo = cardiac function, valvular disease, shunt, pulmonary hypertension


- Exercise = evaluate functional capacity, prognosticate and evaluate response to therapy, diff. causes of exervise

Asthma when? triggers?


- have?


- CXR?


- on PFT?

- episodic dyspnea, triggered by cold air, viral infections


- wheezing


- normal CXR


- obstruction on PFT when bronchodilator response



- Interstitial Lung Disease when? on?


- hear?


- on CXR? on PFT?


- do? (2)

- slowly progressive dyspnea on exertion, cough


- crackles, clubbing


- increased interstitial markings on CXR


- restriction with low DLCO on PFT




* do CT chest = 6MWT


* do echo to assess cardiac function and pulm.pressures

- consider COPD or CHF, when? (4)


- do? to then?

- history of CHF, smoker, dyspnea


- elevated JVP


- hyperinflation on CXR


- moderate obstruction on PFT




* do cardiopulmonary exercise test to distinguish cause of exercise limitation

Dyspnea when?

Restrictive Lung Disease Definition


- disease that? defined as?


- main three causes? (3) - PR/CW/NM ***

- disease that reduces the size of the lungs (TLC)


- defined as TLC <80% predicted


- several possible causes:


= interstitial lung disease = parenchymal restriction


= chest wall restriction


= neuromuscular disease

ILD - Parenchymal Restriction


- diseases that?


- thickened alveolar membrane causes? (2) increased/decreased? leading to?

- diseases which increase the thickness of the alveolar membrane


- thickened alveolar membrane causes:


= increased stiffness of the lungs (less compliance, more work to inflate lungs)


= reduced diffusion across the alveolar membrane, leads to hypoxemia

Making ILD Diagnosis - CXR for? PFT for?


- retics seen as? nodes as?

- CXR will show interstitial changes


- PFT will show parenchymal restriction




* reticulation shown as lines


* nodularity shown as dots

ILD and Parenchymal Restriction on PFT


- restrictive causes? also see?


- causes prop?


- therefore both?


- normal?

- restrictive = TLC goes down


- Measures like FVC go down with TLC


- cause a proportional reduction in FEV1 and FVC


- both FEV1 and FVC are reduced by similar amount


- see normal FEV1/FVC ratio = >0.7

Spirometry of Normal vs Obstructed vs Restricted

Fick-s Law - Diffusion of gas influenced by? (5)


- in ILD, see?

- SA for diffusion


- gradient across the membrane


- solubility of the gas diffusing


- thickness of the membrane the gas must cross**** ILD = more thick


- molecular weight of the gas

ILD Causes


- on CXR? seen as?


- reduced?


- reduction in? ratio?


- low?


- spiro shows?

- an interstitial pattern on CXR = lines, dots or both


- reduced lung volumes = low TLC


- proportional reduction in FEV1 and FVC (ratio > 0.7)


- low diffusing capacity and hypoxemia


- spirometry shows upward loop

Diagnostic Approach to Restrictive Lung Disease


- restrictive, see?


- parenchymal restriction shown by?


- results in?


- if normal DLCO?

- low TLC = restrictive lung disease


- low DLCO = parenchymal restriction




* creates ILD




- if normal DLCO = extra-parenchymal restriction



Chest wall restriction due to?


- low TLC due to?


- possible causes? (3)

- low TLC due to squeezing from the outside


- possible causes include obesity, bony abnorms, pleural disease

Bony Abnorms - Chest Wall Restriction - (3)

- pectus excavatum


- pectus carinatum


- Ankylosing Spondylitis



Cobb Angle - used to measure


- lung restriction at?


- if >100? due to?

- Kyphoscoliosis severity is measured using Cobb angle


- Cobb angle > 60 degree assoc. with lung restriction


- Angle >100 can lead to hypercapneic resp. failure due to diaphragm dysfunction

Chest Wall Restriction - Pleural Disease - look at?


- see? also see?

- look at ray, see large pleural effusion, calcified pleural plaques secondary to asbestos exposure

Chest Wall Restriction - PFT Summary


- shown? means that?


- reduction in?


- prop.?


- diffusion is? no?

- PFTs show extra-parenchymal restriction = caused by something outside the lung = extra-parenchymal


- reduction in TLC < 80%


- proportional reduction in FEV1 / FVC


- diffusion capacity is normal because gas exchange at the level of the alveolus is normal (**no thickening of the membrane like in ILD)

ILD - Neuromuscular Disease - results in? problems in?


- due to?

- results in muscle weakness, causing problems with active expansion of the lung


- due to problems along the path from brain to diaphargm



Neuromuscular Disease causes - C ? causes


- P = (3)

1) C Spine = C3,C4,C5


= mechanical, ischemic, inflammatory




2) Phrenic nerve


= mechanical, ischemic, idiopathic



Neuromuscular Disease causes


- N? pre vs post?


- D? from? (2_

3) Neuromuscular Junction


= pre-synaptic (Lambert Eaton), post-synaptic (MG)




4) Diaphargmatic Muscle Disease


= muscular dystrophies, inflammatory myositis

Making NM Disease Diagnosis - History


- common? episodes of?


- may have? previous? FH?

- dyspnea and orthopnea are common


- episodes of hypercapneic resp. failure


- may have weakness in other groups


- previous trauma or thoracic surgery


- FH of myopathy

Making NM Disease Diagnosis - Physical Exam


- use of?


- in neck? decreased? abdo? means?

- use of accessory muscles on quite respiration


- hypertrophy of access muscles in neck


- decreased diaphragmatic excursion (percussion)


- abdo paradox(moves inward) on inspiration

Neuromuscular Disease (Muscle Weakness) - PFT show? similar to?


- low? prop. reduciton in?


- diffusion?


- to diff from chest wall problems?

- PFTs show extra-parenchymal restriction


= similar to PFTs in mech chest wall disease


= low TLC, proportional reduction in FEV1/ FVC


= diffusion capacity is normal




* diff muscle problems from chest wall problems with tests assessing muscle strength

Tests of Resp. Muscle Strength - MIPs/ MEPs - stand for? muscle weakness when?

- maximum inspiratory and expiratory pressures


- MIPs or MEPS < 50% of predicted suggests muscle weakness



Tests of Resp. Muscle Strength - Positional Forced Vital Capacity


- when lie supine, see?


- therefore takes?


- if have muscle weakness? defined as?

- when lie supine, gravity pushes abdo contents into chest


- so it takes more diaphragmatic strength to take a breath when supine


- patients with muscle weakness have a smaller FVC when supine


- drop in FVC of >20% from sitting to supine = muscle weakness

Diagnostic Approach to Restrictive Lung Disease


- extra-parenchymal if?


- if normal muscle strength - DDx?


-NMD if?

- low TLC and normal DLCO = extra-parenchymal


- normal muscle strength = DDx of chest wall and pleural disease


- abnormal MIPS/MEPS or positional VC = DDx of neuromusc. disease

Diagnostic Approach to Restrictive Lung Disease


- parenchymal restriction - see?


- ILD can be either?

- low TLC and low DLCO = parenchymal restriction


- ILD = upper lobe disease or lower lobe disease

Diagnostic Approach to Restrictive Lung Disease



Upper Lobe Interstitial Disease = FASST


- stand for?

= Farmer's Lung = Hypersens. Peumonitis


= Akylosing Spondilitis


= Silicosis


= Sardoidosis


= TB

Pathogenesis of Hypersens. Pneumonitis


- repeated? can cause?


- debated mech?


- onset can be?

- repeated inhalational exposure to some antigens can cause pulmonary sensitization


- debated mech = Type 3 or 4 hypersens reaction


- latency of onset = sens. can be weeks or years after exposure, requires ongoing exposure to cause symptoms



Causes of Hypersens Pneumonitis


- organisms include? (3)

- Microbial organisms:


= Farmers lung = Thermophillic actinomyces in hay


= Tobaccos long = Asperigullus


= Hot tub lung = Mycobact in water

Causes of Hypersens Pneumonitis - Other Causes


- (3)

- animal proteins -bird feathers, feathers of pillows or duvets


- low mol. weight chemicals - isocyantes


- meds

Clinical Presentation of Hypersens Pneum - can be? should have?


- resp see? also see? (5)

- can be non-specific = should have temporal relationship to exposure


- resp. symptoms are variable = cough, sputum, dyspnea, wheeze


- const symptoms = fevers, chills, sweats, weight loss



Hypersens Pneum - Variable Latency


- acute? subacute? chronic?

= acute HP = symptoms 4-6 hours after exposure


= subacute HP = intermittent exposure and fluc Sx


= chronic HP = long term exposure with progressive lung fibrosis

Diagnosis of Hypersens Pneum


- determine?


- ask about? worsening?


- PFT?

- determine exposure to HP antigen = history, serology


- clinical syndrome and HP = resp and const. symptoms, worsening symptoms when exposred to Ag


- PFT abnorms = obstruction, restriction or combo of both with low DLCO

Diagnosis of Hypersens Pneum


- radiographic? see? (2)


- cytology?

- radiographic abnorms = upper lobe nodules, reticulation, fibrosis


- supportive cytology/pathology = lymphocytosis on BALF (>20% lymphocytes), poorly-formed non-nec. granulomatous inflammation on lung biopsy

Treatment of Hypersens Pneum


- avoid?


- can give? that then?

- Antigen avoidance


= remove, prevent leaks, workplace design (ventilation, moisture)


- Immunosuppression


= accelerates recovery, reserved for more severe cases, prednisone 1.0 mg/kg over weeks,

Upper Lobe Interstitial Disease - Silicosis


- almost always?


- symptoms are?

- almost always occupational exposure = mining, quarrying, etc


- symptoms variable = may be asymptomatic with CXR, PFT abnorms, may have severe resp. symptoms with progressive massive fibrosis


- PFT - parenchymal restriction with low DLCO

Silicosis


- imaging - see? (3) of?


- develop a?


- treatment involves?

- imaging = upper lobe nodules and fibrosis, calcified LNs


- inflammatory reaction to inhaled silica particles, pathology shows silicotic (dust) nodules within lung tissue


- treatment involves reducing exposure to solica dust

Sarcoidosis


- is a? of non?


- cause is?


- inflamm can be?


- occurs more often in?


- lungs often?

- inflammatory reaction of non-caseating granulomatous inflammation


- cause unknown = probably due to an undetermined exposure


- inflammation can occur anywhere in body


- occurs more often in people <50 and of African descent


- lungs are invovled in 90% of cases, often other organs involved

Sarcoidosis Different presentations - Stage?


- incidental? resp? Loffgrens? may have?

- incidental finding = Stage 1 / 2


- resp. symptoms = Stage 2, 3, 4


- Loffgren's Syndrome = Subgroup of Stage 1


- extra-pulm symptoms

Stage 1 and 2 Sarcoidosis


- Stage 1 finding? is?


- 2 = combo of? may have some?

-Stage 1:


= incidental finding of bilateral hilar adenopathy, asymptomatic


= asymptomatic


- Stage 2:


= combination of hilar adenopathy and upper lobe ILD (nodules)


= may have some resp. symptoms

stage 3 and 4 Sarcoidosis


- Stage 3 = fibrosis of? common to have?


- Stage 4 = end? signfic?

- Stage 3


= upper lobe ILD with fibrosis (no adenopahy)


= resp. symptoms are common




- Stage 4


= end stage fibrosis of the upper lobes


= signif resp. symptoms

Sarcoidosis Chances of Spont. Remisson in 2-3 years


- each stage?

- Stage I = 70-90%


- Stage II = 50-70%


- Stage III = 10-30%


- Stage IV = 0%

Upper Lobe Interstital Disease = Sarcoidosis - Loffgren's Syndrome


- subgroup of? on CXR see? also have?


- pathology of?


- commonly with? use? to?

- subgroup of Stage 1 sarcoidosis with:


= bilateral hilar adenopathy on CXR


= fever


= migratory polyarthralgias / arthritis


= Erythema nodosum = Leukcytoclastic vasc. on pathology - non-spec


- common presentation - resolves spont, use NSAIDs to help with skin and joints

Sarcoidosis Extrapulm Disease


- often have? can be?


- ocular?


- calcium is then? due to? leads to symptoms of?


- also have?

- skin lesions common (up to 20%), rash to disfiguring lupus pernio


- ocular symptoms - Uveitis is most common ocular Sx


- Calcium met due to activated Vitamin D, increases calcium absorption


- symptoms of hypercalcemia and kidney stones can result


- cardiac involvement- granulomas = arrhythmias, sudden death

Making Sarcoidosis Diagnosis


- CXR shows? patients may? either?


- PFTs may be?


- pathology?

- CXR shows different abnorms = usually 1st symptoms (Stage 1-4)


- patients may or may not have symptoms = pulm or extra-pulm


- PFTs - may be normal or have obstruction or restriction with low DLCO


- pathology - non-nec. granulomatous inflammation without identified cause

Sarcoidosis treatment - many pts dont?


- Stage 1 and 2 often?


- Stage 3 and 4 use?


- extra-pulm?

- many patients do not require treatment


- Stage 1 and 2 = often resolves spontaneously without treatment


- Stage 3 and 4 = treat with prednisone if severe/progression


- Extra-pulomary disease = immunosupp therapy differs by organ, treat if severe/progressive

Lower Lobe interstitial Disease = RAAIDS

= rheumatoid arthritis


= Asbestosis


= Aspiration = recurrent


= idiopathic Pulmonary Fibrosis


= Drugs = Amiodarone, Nitrofurantoin, others


= Scleroderma

Lower Love Interstiital Disease - Connective Tissue Disease = CTD-ILD


- common for? is the?


- in RA? in Sclero?


- lung symptoms can? should screen?

- most rheum conditions can cause ILD, leading cause of death if present in CTD


- RA common CTD-ILD = uncommon manifestations of common disease


- Scleroderma is common CTD-ILD = common manifestation of rare disease


- lung symptoms can come before or after joints - must screen all ILD patients for occult CTD

Connective TIssue Disease - ILD


- if have ILD, need?


- look for? (5)


- investigations?


- treated with?

- patients with ILD need careful history, PE


= joint pains, Raynauds, skin rashes, examine for active joints, nail and skin changes


- basic serology should be done = ANA, RF, anti CCP, ENA


- progressive CTD-ILD can be treated with immunosupp. therapy

Asbestosis


- is a? used for? now is?


- significant exposure defined by?

- naturally occurring fiber, primarily excavated in Russia, China, Canada


- many desirable properties for use in insulation, now mostly banned yet still see disease


- significant exposure - working with, not just living in space

Manifestations of Asbestosis


- lower? appearance of? can also cause? (3)

- lower lobe ILD


- pleural plaques = often calcified


- pleural effusions


- lung cancer


- mesothelioma = pleural malignancy

Diagnosis and Treatment of Asbestosis


- diagnosis based on? with?


- treatment?

- diagnosis based on history with compatible disease, +/- fibers seen on pathology


- treatment = no specific except avoidance, patient report to WSIB



Idiopathic Pulm Fibrosis (IPF) - most common?


- cause? must?


- pathogenesis is? without?


- survival?

- IPF is most common ILD in patients aged >50


- idiopathic = due to unknown cause, must rule out other ILD causes, importance of PE and history


- pathogenesis appears wound healing and fibrogenesis without signif inflammation (others ILDs due to inflammation)


- mean survival is 3-5 years after diagnosis

IPF


- prognosis is?


- disease is?


- patients may?


- most patients die from?

- prognosis is worse than all cancerrs except lung, pancreatic


- disease course in unpredictable


- patients may progress slwoly, step-wise or wuickly


- most patients die from hypoxic resp. failure`

Making IPF Diagnosis


- need to rule out? do?


- CT for? (4) ** signs

- rule out all other causes of ILD via history and PE, do blood work for CTD serology


- CT scan shows usual interstitlal pneumonia pattern:


= reticulation (lines) as predom abnormality


= subpleural and basal predom. distribution


= honeycombing cysts with/wo traction bronchiectasis


= absence of features that are inconsistent with UIP

IPF Lung Biopsy


- pathology shows?


- distribution is? see some areas?


- should be little?

- pathology shows fibrosis with fibroblastic foci


- distribution is heterogenous with areas of relatively normal lung and areas of severe fibrosis


- there should be minmal active inflammation (not inflamm disease)

Treatment of IPF


- do not treat with?


- very different?


- consider using? caused?

- treatmen with prednisone, immunosupps shown to increase mortality


- very different than other forms of ILD


- new class of drugs = anti-fibrotics = slow fibrosis


= Pirfenidone in Canada, Nintedanib

Diagnostic Approach to Restrictive Lung Disease



ILD History


- resp symptoms = (3)


- CTD - consider? (4)


- also consider?

- respiratory symptoms - cough, sputum, wheezing


- connective tissue diseases - GERD, dysphagia, aspriation, Raynauds


- toxins, exposures, RFs (smoking, FH)

ILD Physical Exam


- resp = look for? (5)


- CV = (3)


- rheum - look for?

- resp = cyanosis, muscle use, clubbing, muscle weakness, fine crackles


- cardiac = pulm hypetension, right sided heart failure, cor pulmonale


- rheum = active joints, skin rashes, findings in fingers and nails

ILD Investigations


- PFTs - do? NMD for?


- CXR - look for? (3)


- CT - look for?


- if suspect sarcoidosis?

- PFTs = MIPS/MEPS, positions VC for NMD


- CXR = nodules, reticulation, distribution


- CT = UIP pattern


- Bllod work, serology, ANA, Abx for hypersens, calcium and ECG if susepct saroidosisI

ILD - Treatment


- diseases by? then?


- systemic = (3) - treat?


- immunosupp is?


- consider?



- diseases by agents = Hypersens, silicosis, asbestos = avoid


- diseases with systemic component = Sarcoid, RA, Slceroderma = treat extra-pulm manifestations


- immunosuppression - helpful in many, **harmful in IPF


- consider new anti-fibrotics = IPF

What is Pulmonary Hypertension (PH)?


- elevation of?


- mPAP sees?


- caused by?

- elevation of mean pulmonary artery pressure (mPAP)


- right heart catheterization showing mPAP > 25 mmHg


- caused by problems anywhere in pulmonary circulation

What is Pulmonary Arterial Hypertension (PAH)


- narrowing of?


- leads to? causing?


- right side vs left side?

- narrowing of the small pulmonary arteries and arterioles


- leads to progressively increasing vascular resistance = causes right heart failure and death


- right heart catheterization shows mPAP > 25 mmHg and normal left sided heart pressures (wedge pressure < 15 mmHg)

Mean PAP (mPAP) - measured at?

- measured at the pulmonary artery

Causes of Pulm. Hypertension


- at pulm artery? at pulmonary arteriole? at capillary? (2)

1) Pulmonary Artery = acute and chronic pulmonary embolism


2) Pulmonary arteriole = PAH


3) Pulm Capillary


= chronic lung disease (destruction of capillary bed)


= hypoxic lung disease = vasoconstriction of capillary bed

Causes of Pulm. Hypertension - at PV? at left heart?

4) Pulmonary veins = veno-occlusive disease (PVOD)


5) Left heart = backflow from problems in left heart

Pulmonary Hypertension Nice Classification


- Group 1 through 5?

- Group 1 = PAH and PVOD


- Group 2 = left heart disease


- Group 3 = respiratory diseases


- Group 4 = Pulmonary Artery


- Group 5 - Miscellanous

Causes of Group 1 (PAH) - is? genetic? (2)


- acts as a?


- can be induced by?


- associated with? (5)

- idiopathic


- genetic = BMPR2, ALK-1


- veno-occlusive disease


- drug and toxin induced = Fenfluramine, Amphetamine, SSRIs


- associated with underlying:


= CTD, HIV, portal hypertension, congenital heart disease, Schistosomiasis

causes of Group 2, 3 PH


- Group 2 from?due to? (2)


- Group 3 is from? due to? seen in those with?

- Group 2 = Left heart Disease


= LV dysfunction, Valvular (MR, MS, AI, AS)




- Group 3 = Resp. Disease


= destruction of lung (COPD, IPF, bronchiectasis)


= chronic hypoxia = hypovent, OSA

Causes of Group 4, Group 5


- 4 from? 5 is ? includes (2)

- Group 4 = Pulmonary Artery


= chronic thromboembolic disease




- Group 5 = misc


= sarcoidosis, hemolytic anemia

Group 1 = PAH


- is a? cases? less common than?


- gender?


- age of diagnosis?


- usually have symptoms for? if untreated?

- rare disease = 1-2 cases per million = PAH is much less common than group 2 disease (left-sided heart disease)


- F:M


- generally diagnosed in 4th decade of life


- time from symptoms to diagnosis = 2.5 years


- survival 2.5 years from diagnosis if untreated

Pulmonary Hypertension - History and PE


- see?


- RFs? (6)


- group 2 through 5?

- resp and cardiac symptoms = dyspnea, chest pain, syncope, leg swelling


- RFs for PAH = group 1 = FH, toxic drugs, CTD, HIV, liver disease, travel history


- RFs:


= Group 2 = extensive cardiac history


= Group 3 = extensive resp. history


= Group 4 = thrombosis history


= Group 5 = hemoglobin, other diseases



PE of PH


- heave? loud?


- extra?


- increased?


- positive? liver is? also see? (2)

- parasternal heave


- loud S2


- right sided S3/S4


- elevated JVP


- positive abdo jugular reflex


- pulsatile liver


- ascites, edema

PH investigations


- look for? by doing? (4)


- also look for?


- perform? (2)


- measures?

- look for resp disease = PFT, CXR, ABG, sleep study


- look for underlying conditions that predispose PAH = lab testing, HIV, liver enzymes


- look for cardiac disease (ECG), thromboembolic disease (CT, V/Q scan)


- measures pulmonary pressures = echo, right heart catheterization

Pulmonary Hypertension Treatment


- treat the?


- give? for?


- oxygen for?


- in select cases?

- treat underlying disease = cardiac, respiratory


- diuretics for right sided CHF


- oxygen for hypoxemia


- lung or heart transplantation in selected cases



Pulmonary Hypertension - Specific Vasodilatory Therapy


- entags of? include? (3)


- inhibitors of? fils? (2)


- cyclins?

= endothelin antags = Bosentan, Ambrisentan, Macisentan


= Phos 5 inhibitors = Sildenafil, Tadalafil


= Prostacyclines = Epoprostonol

Groups of PH - 1 through 5?



Lung Cancer Epi


- 2nd highest?


- gender? increased chance of?


- trends?

- 2nd highest incidence in males and females


- more common in males, higher chance of developing lung cancer and dying from lung cancer in men than women


- decreasing in males, increasing in females

Smoking and Lung Cancer


- leading cause?


- change in RR?

- cigarette smoking is the leading cause of lung cancer


- 90% of lung cancer cases are caused by cigarette smoking


- compared to never-smokers, current smokers have 20x increase in lung cancer risk

Risk of Lung Cancer and smoking


- risk increases with? decreases with? use of?


- also assoc with?

- risk of lung cancer increases with number of cigarettes smoked per day and duration of smoking


- risk of lung cancer decreases with time since quitting smoking, use of filtered cigarettes and lower tar yield


- cigar and pipe smoking are also assoc. with increased lung cancer risk, not as high as cigarettes

Second Hand Smoke


- spouses of? have a?


- up to 35% of LC in never smokers is?

- non-smoking spouses of smokers have an approx 30 increased risk of developing lung cancer


- about 15 to 35% of lung cancer cases in never smokers have been attrib to second hand smoke exposure

Other Environmental Risks


- (4)

-tar and soot = benzopyrene


- metals = arsenic, chromium, nickel


- asbestos


- radiation = radion, radiation

Classification of Lung Cancer


- primary? (6)


= SCC/SCC/AC/LCC/CT/ carc of?

- primary malignant epithelial tumours of lung:


= squamous cell carcinoma


= small cell carcinoma


= Adenocarcinoma = Bronchioalveolar carcinoma


= large cell carcinoma


= carcinoid tumour = typical, atypical


= carcinomas of salivary gland type

Practical Classification of Lung Tumours - mainly?

- non small cell lung cancer


- small cell lung cancer

Why the Practical Classification - two groups separated based on? (3)


- greater need to?

- two groups are separated based on:

= clinical behaviour, likelihood of mets, molecular genetics, response to currently available therapies


- with increasing awareness of molecular genetics, greater need to properly subclassify non-small cell carcinomas

Primary vs Secondary Lung Cancers


- primary has? must rule out? as this?


- if multiple lesions?

- lung is the site of numerous met lesions that must be ruled out


- changes tumour behaviour, prognosis and therapy


- multiple lesions, especially bilateral, favour mets over primary lung cancer

Incidence of Different Histologic Types of Lung Cancer


- men highest? then?


- women highest? then?



Squamous Cell Carcicoma


- tumur of? showing? may have?


- usually have? with possible? (2 - C/BO)

- malignant epithelial tumour of squamous cells, showing kerat and/or intercellular bridges


- usually have central (hilar) lesions with


- +/- cavitation


- +/- bronchial obstruction

Precursor to SCC


- see? dyspslasia of?

- squamous metaplasia and dysplasia of bronchial epithelium

Adenocarcinoma of Lung


- malignant? with diff of?


- usually is?


- not as strong assoc. with?

- malignant epithelial tumour with glandular diff. +/- mucin


- usually peripheral lesion


- not as strongly assoc. with smoking as squamous or small cell carcinoma (75% of lung adenocarcinomas occur in smokers vs 98%)

Incidence of AC of Lung


- incidence is? yet?

- incidence has increased significantly in last two decades


- rise in incidence is unclear



Precursor Lesions to AC of Lung


- atypical? also?

- atypical adenomatous hyperplasia


- bronchioalveolar carcinoma

Bronchioloalveolar Carcinoma


- specific? that may?


- tumour cells grow along?


- is at first? but then may?


- no present?

- specific in-situ form of adenocarcinoma which may precede development of invasion


- tumor cells grow along intact alveolar architecture


- non-invasive but may spread aerogenousl throughout lungs




** no destructive tissue invasion present

Small Cell Carcinoma of Lung


- origin?


- composed of? cytoplasm? cell borders? nucleus? (3)


- mitoses are?


- behaviour?

- malignant tumor of neuroendocrine origin


- composed of small cells with scant cytoplasm, ill-defined cell borders, round to oval nuclei with nuclear molding and inconspicious nucleoli


- mitoses are numerous and necrosis common


- extremely aggressive behaviour

Small Cell Carcinoma of Lung


- arise from? along?


- NE markers = (S/C)


- central vs periph?


- ability to? leads to?

- arise from neuroendocrine cells present along bronchial epithelium


= Neuroendocrine markers = synaptophysin, chromogranin


- typically central lesion


- ability to secrete polypeptide hormones = paraneoplastic syndromes

Small Cell - cells appear? (4)


- see areas of?

- small cells with scant cytoplasm, irregular nuclei, nulcear molding and frequent mitoses


- see areas of necrosis

Large Cell Carcinoma of Lung


- an undiff? lacks features of?


- cytoplasm?


- may represent? that?


- small subset show?

- an undiff malignant epithelial tumour that lack squamous and glandular features and the cytologic appearance of small cell carcinoma


- may represent squamous cell carcinomas or ACs that are too poorly diff to recognize


- subset of large cell carcinomas show neuro-endocrine differentiation

Carcinoid Tumours of Lung - type of tumours?


- T vs AT vs LC vs SC?

- neuroendocrine tumours of lung:


= typical carcinoid tumour


= atypical carcinoid tumour


= large cell neuroendocrine carcinoma


= small cell carcinoma

Carcinoid Tumours of Lung - % of tumours?


- low grade are either?


- typical patient? gender?


- located in either?

- represent 1-5% of lung tumours


- low-grade malignant neuroendocrine tumours = typical vs atypical


- usually occur in patients <40 yo (M=F)


- may be located centrally or in the periphery of the lung

Carcinoid Tumours of Lung - Typical


- composed of? with?


- mitotic count? no?

- typical carcinoids are composed of nests of uniform, regular cells with round nuclei


- mitotic count < 2 mitoses/10 HPF


- no necrosis

Carcinoid Tumours - Atypical


- mitotic count? or see?


- often see?

- mitotic count 2-10 mitoses/ 10 HPR or focal necrosis


- often show increased cellular atypia

Small Cell Carcinoma - Molecular Genetics


- mutated genes include? (4) M/R/p/B


- see overexpression of?


- see increased?

- dominant genes mutated include Myc, Rb, p53, and BCL-2


- overexpression of c-kit


- increased expression of telomerase

Non-Small Cell Molecular Genetics


- mutated genes include? (4) p/p/E/K


- AC - primarily see? (2)


- squamous and AC - see?


- increased?

- dominant genes mutated include EGFR, K-ras, p53 and p16


- EGFR and K-ras occur primarily in AC
- p53, p16 mutations have same frequency in squamous and AC


- see increased expression of telomerase

Targeting Genetic Therapies


- if EGFR mutations, see? therapy?


- K-ras - see?


- K-ras causes?

- patients with EGFR mutations have improved survival with upfront EGFR inhibitor therapy = gefitinib


- mutations in K-ras correlate with worse outcome and resistance to EGFR inhibition


- constitutive activation of K-ras bypasses EGFR, leads to downstream activation

Grading of Lung Cancer


- if non-small cell?


- high grade when?

- non-small cell carcinomas should be graded according to histo features


- small cell carcinoma and large cell carcinoma = high grade

Clinical Manifestations of Lung Cancer


- (8)

- cough, hemoptysis


- dysphagia, chest pain, dyspnea


- hoarseness, Horner's, SVC obstrcution

Hoarseness - is a disruption of? often from? (2)


- results in?

- disruption of recurrent laryngeal nerve (esp. left) from tumour or mediastinal adenpathy


- results in unilateral vocal cord paralysis

Horner's Syndrome


- weakness of? PD/LP = (2) called? (M/P)


- lack of? called?


- apical tumour can?

- weakness of pupillary dilators = miosis


- weakness of levator palpebrae = ptosis


- lack of sweating = anhydrosis


- apical tumour invades superior sulcus, impinging on sympathetic chain

Climical Symptoms of Mets


- liver? bone? adrenal? brain? (6)

- liver = asmpt or increased liver enzymes


- bone = pain, increased alk phos, increased calcium


- adrenal = suaully asymptomatic


- brain = HA, vomiting, visual changes, focal weakness, CN deficits, seizures

Paraneoplastic Syndromes with Lung Cancer - results in/


- HC/ S/ H/ HO/ DM/ CS/ N

- hypercalcemia


- SIADH secretion


- hematologic


- hypertrophic osteoarthropathy


- dermamyositis


- Cushing's syndrome


- neurologic

Hypertrophic Osteoathroplasty


- also known as?


- may be? symptom?


- may invovles? (4)


- new? in?


- assoc with?

- clubbing


- may have symmetrical, painful polyarhtopathy involving ankles, kness, wrists, elbows


- periosteal new bone formation in long bones


- most commonly with AC

Diagnosis of LC - CXR


- see increased? do? looking for?

- see increased opacity


- can do CT to look for nodules

Diagnosis of LC - Percutaneous Transthoracic Lung Biopsy


- performed by?


- best for?


- localized using? (2)


- insertion of? to?


- done under?

- performed by interventional radiologist


- best for peripheral lung lesions


- localized using US, CT


- insertion of needle into lesion with aspiration or core biopsy


- done under local anesthetic

Percut. TT Lung Biopsy


- sens and spec?


- complications? (4) - main one?

- sens and spec both around 90%


- complications include:


= pneumothorax = 20%


= pneumothorax requiring chest drain = 3%


= hemothorax = 1.5%


= hemoptysis = 5%

SVC Obstruction


- means that?


- venous drainage from upper body is? leads to?


- over time, see? appears as?

- SVC becomes occluded by the tumour/clot


- venous drainage fro the upper body is impaired, leading to upper extremity and facial edema


- over time, collaterals form, see dilated veins over chest

Bronchoscopy


- best for lesions with?


- perfomed by?


- to oropharynx, apply? also to? reducing?

- best for lesions with endobronchial component


- performed by respirologist or thoracic surgeon


- conscious sedation


- local anesthetic applied to oropharynx, also injected through the scope onto vocal cords and airways, to reduce coughing

Samples via Bronchoscopy


- use forceps to?


- cytology brush to?


- to aspirate cells, use?



- biopsy forceps to take chunks of tissue


- cytology brush to scrape cells onto a slide


- transbronchial needle to aspirate cells onto a slide, may be done with endobronchial US


- saline lavage to wash cells off and spin down

DD for Solitary Pulmonary Nodule - Malignant


- (3)

- lung cancer


- metastatic cancer


- carcinoid

DD for Solitary Pulmonary Nodule - Benign


- infection =? (2)


- benign?


- vascular?


- congen?


- inflamm? (3)

- infectious granuloma = TB, fungal infection


- other infections


- benign neoplasms = hematoma, lipoma


- vascular malformations


- congenital abnorms = bronchogenic cyst


- inflammatory = Wegeners, granulo, rheumatoid

Probability of malignancy based?


- age? Rfs? (3)

- patient factors


= age - older = more likely


= RFs = smoking, occupation, FH

Borders


- benign if? (2)


- malignant if?

- if smooth or lobulated = suggest benign


- if irregular or spiculated = suggest malignants

Role of Size - more likely to be malignant if?

- larger lesions more likely to be malignant

Calcification and Malignancy


- benign suggested by? (4) C/D/P/L


- malig suggested by? (2) S/E

- if diffuse, central, popcorn shaped or laminated, suggests benign


- if stippled or eccentric, suggests malignancy

Growth and Malignancy


- if doubles in volume, results in?


- malignancy considered if?


- if less than? or greater than? means that benign nodule likely?

- doubling in volume, results in about a 26% increase in diameter


- doubling time between 20 and 400 days is consistent with malignancy


- a nodule that grows very rapidly or very slowly is more likely to be benign

Making Lung Cancer Diagnosis - after Solitary Nodule Algorithm



FDG - Positron Emission Tomography (PET) Scan


- measures?


- patient is administered? that is tagged with?


- taken up by?


- very? but not? as other lesions may?

- measures the metabolic activity of lesion


- patient is administered glucose tagged with positron emitting isotope of fluorine = FDG


- metabolically active cells such as malignant cells take up FDG more avidly


- very sensitive but not very specific (infectious and inflammatory lesions may also be positve)

Staging - Non-Small Cell


- depends on? presence or absence of? distant?

- staging depends on cell type of cancer (non-small cell versus small cell)


- depends on the size and location of tumour, presence or absence of involved LNs, and distant metastases

Determining LN Involvement


- radiographic staging using?


- bronchoscopic staging using? (TBNA) with?


- surgical staging with?

- radiographic staging using CT and PET scanning


- bronchoscopic staging using transbronchial needle aspiration with endobronchial US


- surgical staging with mediastinography

Simplified Staging of Non-Small Cell Lung Cancer - TNM


- stage 1 and 2 - size? no?


- stage 3 - size? or involvement or? (3)


- stage 4 = any? (2)

- Stage 1, 2 Cancers

= tumour size < 7cm and no mediastinal or contralateral nodes


- Stage 3 Cancer


= tumour size >7cm or invading important structures and/or mediasitnal or contralateral nodes


- Stage 4 Cancer


= any pleural involvement or distant metastases

Treatment of Non-Small Cell Lung Cancer


- treatment of stage 1 and 2?


- generally involves? either by?


- proximal tumours require?

- treatment of choice for Stage I and II tumours is surgical resection


- this generally involves performing a lobectomy, either using VATS or open thoracotomy


- more proximal tumours may require pneumonectomy

Treatment of Non-Small Cell Lung Cancer


- patients with lung cancer often have?


- for resection, must? to help predict?


- to tolerate surgery, must have post-op est?


- may also need?

- patients with lung cancer frequently have comorbs including underlying lung disease such as COPD and cardiac disease


- suitability for resection must first be determined by evaluating pulmonary function to predict remaining function after surgery


- post-op estimated FEV1 and DLCO must be at least 40% of predicted to tolerate surgery


- patients may also require cardiac evaluation

Treatment of Non-Small Cell lung Cancer


- if cannot tolerate surgery?


- Stage II also get?

- patients with Stage I and II tumours who cannot tolerate surgery may be given radiation


- adjuvant chemotherapy (after surgery) may be given in patients with Stage II disease

Treatment of Non-Small Cell Lung Cancer


- Stage III treated with? (3)


- Stage IV not? given? (2)

- patients with Stage III tumours are often treated with a multi-modality approach, involving chemotherapy, radiation therapy, and sometimes surgical resection


- Stage IV tumours are not surgically resectable and are generally managed with chemotherapy and sometimes radiation therapy

Small Cell Lung Cancer


- if limited, means that it is? treated with?


- if extensive, means? outside? treated with?


- not an option?


- small cell is sens to? yet able to?

- limited = confined to ipsilateral hemithorax and 1 radiation port (30 to 40%), usually treated with chemotherapy and sometimes radiation therapy


- extensive = metastatic disease outside the ipsilateral hemithorax (60 to 70%), usually treated with chemotherapy alone


- surgery not an option


- small cell lung cancer is very sensitive to chemo and radiation therapy but the cancer recurs quickly

Prognosis of Small Cell Lung Cancer - median survival and 5 year survival rate - limited stage vs extensive stage



Pleural Effusion - Normal Anatomy and Fluid


- visceral pleura has? drain into? pushes into?


- parietal pleura has? drain into? pushes into?

- visceral pleura has bronchial lymphatics, bronchial microvessels that drain into pulmonary veins, pushes into lungs


- parietal pleura has intercostal microvessels that drain into systemic circulation and lymphatic lacunae that pushes into chest wall

Pleural Effusion and Abnormal Fluid Accumulation


- steady state means?


- fluid accumulation when? (2)


- see decreased absorption if? can also lead to?


- seen in?

- fluid absorption = fluid formation = steady state

- if have decreased absoprtion or increased formation, see fluid accumulation


- decreased absoprtion due to lymphatic drainage


- also see pleural membrane disruption and increased micro vessel pressure


- ex/ see in CHF

CHF = Transudate


- seen during? PVH


- fluid pushed from/to?


- systemic venous hypertension sees fluid pushed from?

- see pulmonary venous hypertension push fluid from visceral pleura into pleural space, from higher to lower pressure


- see systemic venous hypertension push fluid from parietal pleura to pleural space, from higher to lower pressure

Inflammation = Exudate


- occurs when inflammation? fluid moves from? also causes fluid from?

- inflammation disrupts pleural membrane, see movement of fluid from visceral pleura to pleural space


- inflammation also causes movement of fluid into pleural space from parietal pleura

Malignancy = Exudate


- decreased? disrupting? increased?


- fluid then? yet protein?

- decreases lymphatic drainage, disrupts pleural membrane and increases microvessel pressure


- cytokines from malignancy, causes movement of fluid into pleural space, protein out of lymphatic lacuna into parietal pleura

Causes of Transudate Pleural Effusions (3)****** C/H/N

- CHF


- Hepatic hydrothorax


- Nephrotic syndrome

Causes of Exudate Pleural Effusions


- infection -? (4)


- malignancy? (4)


- inflamm?(5)


- other? (2)

- infection = bacterial, TB, viral, fungal


- malignancy = carcinoma, lymphoma, mesothelioma, chylothorax, myeloma


- inflammatory = connective tissue disease, pancreaittis, benign asbestos, ARDS, post cardiac injury


- other- drug induced, hypothyroidism

Chest Xray and Pleural Effusion - AP Xray


- see blunting of?


- increased?


- silhouetting of? diaphragm?

- see blunting of costophrenic angles


- increased opacity at base


- so silhouetting of heart border


- can see hemidiaphragm

Lateral Chest Xray


- look for? (2)


- look in the? as can see?

= look for pleural effusions and hemidiaphragm


= look in lateral decubitus, can see pleural fluid

Thoracentesis


- is a sampling of?


- use of? fluid level is localized by?


- can be done under?


- needle inserted above? to?


- complications (3)

- is a sampling of pleural fluid


- use local anesthetic, fluid level localized by percussion/aucultation


- can also be done with US guidance


- needle inserted above the rib to avoid neurovasc bundle


- complications = infection, bleeding, pneumothorax

Light's Criteria


- fluid is an exudate if?


1) pleural fluid protein: serum?


2) P and serum LDH?


3) pleural fluid LDH? upper limit is?

- fluid is an exudate if any one of the following is present:


= pleural fluid protein : serum protein > 0.5


= pleural fluid LDH = serum LDH > 0.6


= pleural fluid LDH > 2/3 upper limit of normal for serum LDH (about 200 IU/L)

Pleural Fluid Analysis


- LDH - high in? (3)


- protein - high in? (2)


- pH - normally about? low in? (5)


- glucose - low in? (5)

1) LDH = high in emphysema, rheumatoid, malignancy


2) Protein = high in TB, myeloma


3) pH = normally about 7.6, very low in emphysema, TB, rheumatoid, malignancy, esophageal rupture


4) Glucose = low (fluid to serum ratio <0.5) in emphysema, TB, rheumatoid, malignancy, esophageal rupture

Pleural Fluid Analysis


- cell count - see high neuts in? lymphs in (2)? eosino in? (3)


- cytology to see?


- stains - such as?

5) Cell Count and Diff = neutrophil's predominant: bacterial infections, lymphocyte predom in malignancy and TB, eosinophilia in pneumothorax, hemothorax, parasites


6) Cytology = may show malignant cells


7) Stains and Cultures = gran stain and bacterial culture, AFB stain and mycobacterial culture

Video Assisted Thoracoscopy


- can be used to identify? then used to?

- thoracentesis can sometimes identify an exudate


- VATS can be used to remove fluid and biopsy abnormal areas of pleura

Chest Xray of Pleural effusion


- see?

- see bilateral ppleural effusions

Transudative Effusion


- most likely diagnosis?


- if new onset pleural effusions, should?


- transudates more likely to be?

- most likely diagnosis = CHF


- most new-onset pleural effusions require thoracentesis for diagnosis but this is one situation in which one might not perform thoracentesis unless effusions fail to resolve with therapy for heart failure


- in general, transudates are more likely to be bilateral than exudates

Management of Transudate


- if CHF, treat with? manage?


- in general, primary treatment is to?

- treat for congestive heart failure with diuretics and afterload reduction, management of angina


- in general, primary treatment of transudative effusions is to treat the underlying condition

Exudative Effusion


- may be due to? also due to?


- first? then due?


- most likely?

- may be due to underlying primary lung carcinoma but metastatic disease to pleura from an extrapulmonary site is also possible


- after drainage of effusion, repeat imaging showed an underlying lung mass, likely AC of lung with mets to pleura

Management of Malignant Effusion - Repeated Thoracentesis


- is done for? requires?

- for slowly re-accumulating effusions in patients with shift life expectancy


- requires repeated instrumentation

Management of Malignant Effusion - Pigtail Catheter Insertion


- more complete?


- not meant for?


- effusion likely?

- more complete drainage of effusion


- not meant for long term fluid management


- effusion likely to recur after removal

Management of Malignant Effusion - Pleurodesis


- is a more?


- requires? with a?


- success rate?


- dine via?

- more definitive management


- requires hosp, chest tube, complete fluid removal and sclerosing agent (talc, doxycycline)


- success rate 80-90%


- can be done surgically using VATS

Management of Malignant Effusion - Indwelling Pleural Catheter


- tunneled under?


- can be done?


- patient able to?

- tunneled under skin to prevent accidental removal and reduce risk of infection


- outpatient insertion


- patient can intermittently connect self to drainage system

Purulent Fluid likely?


- high? low? (2)


- is most likely? from?

- exudate with very high LDH, low glucose and low pH


- aspiration consistent with empyema probably secondary to bacterial pneumonia

Uncompliated Effusion - see decreased? increased?


Complicated effusion means?


Can lead to?

- uncomplicated can lead to bacterial invasion = decreased pH, increased LDH


- complicated effuision means pH < 7.20


- can lead to empyema = pus or bacterial growth

Management of Empyema in Pleural Effusion


- commonly has?


- pH <7.20 means?


- give? with?


- if chest tube fails?

- bacteria common in empyema as there may be anaerobes


- pH < 7.20 predicts poor response to Abx


- in addition to broad spectrum Abx, requires chest tube drainage of fluid


- if chest tube fails to clear fluid, surgery may be required = VATS or open thoracotomy

Pneumothorax and Tension Pneumothorax


- PTX leads to?


- decreases? (2)


- leads to?

- PTX leads to mediastinal shift


- decreases venous return


- decreases BP


- leads to tension pneumothorax

Pathophys of PTH


- in traumatic PTX, communication with either? or?


- in spont PTX, see comm. with?


- results in the? and subsequent?


- if one way valve mech, leads to? (4)

- communication with pleural space can develop on chest wall side, alveolar side, or both in traumatic pneumothorax


- communication is on the alveolar side in spont. PTX


- results in accumulation of air within the pleural space and collapse of the lung


- if there is one way valve mechanism, this can lead to progressive ipsilateral hyperinflation, mediastinal shift, hemodynamic compromise and death

Causes of Primary Spont PTX


- no?


- see in? (4)

- no lung disease


- see smoker, male, FH, Marfan's

Causes of Secondary Spont PTX


- have?


- see in? (4)

- have lung disease


- COPD, CF, pneuocystis jiroveci infection, TB

PTX Clinical Presentation - History


- sudden onset? (2)


- onset usually at? or after?


- may have underlying?

- sudden onset dyspnea and pleuritic chest pain


- onset usually while at rest (spontaneous) or history of chest trauma


- may have history of underlying lung disease (secondary)

PTX PE Findings


- see? (3)


- on affected side, reduced?


- percussion?


- trachea?


- if tension PTX - see?

- respiratory distess, tachypnea, tachycardia


- reduced chest excursion on affected side


- reduced breath sounds on affected side


- hyper-resonance on percussion of affected side


- tracheal shfit away from PTX


- subcut. emphysema


- if tension = hypotension

Management of Primary Spont PTX - Stable Patient


- look first at?


- then if?


- if minimal symptoms? if symptomatic? unsuccessful?

- if unsuccesful, chest tube

- if unsuccesful, chest tube

Management of Primary Spont PTX - Unstable


- put in a? if successful? unsuccessful?

Management of Secondary Spont PTX - Stable


- first look at?


- symptoms vs no symptoms?



Management of Secodnary Spont PTX - Unstable


- first do? if unsuccessful?

Microbio of TB


- belongs to? caused by?


- have a special? resistant to? leading to?

- belongs to genus Mycobact which includes the NTM such as MAC


- TB caused by members of M.tuberculosis complex


- special cell envelope around mycobact is resistant to destaining by acid alcohol leading to the term acid fast bacillus (AFB)

Microbio of TB


- to detect, use?


- growth is? to culture, can take?


- treatment minimum of?


- see red?

- use Zhiel-Neelsen or Kinyoun stain to detect them


- M. tuberculosis is very slow growing, it can take up to 7 weeks to culture and treatment takes a minimum of 6 months or more


- see red TB bacillus on ZN stain

Transmission


- appear as?


- people then? get to?


- no infection occurs if?

- patients with pulmonary or laryngeal TB aerosolize the TB bacilli in droplet nuclei


- contact person inhales the TB bacilli which they may get to the alveoli


- if the local defenses can destroy the TB bacilli, no infection occurs

Transmission TB


- if TB bacilli gets to alveoli? get encased in?


- then considered?


- about 10% of people will? time?

- if TB bacilli gets to alveoli in large numbers in normal immunity, cell mediated immunity eventually responds in several weeks to encase the TB in granuloma


- then considered latent TB infection


- about 10% of people with latent TB infection will develop active TB in their lifetime, half of those cases will occur within the first 2 years after infection

Active and latent TB


- if primary infection is unchecked?


- within 2 years, see?


- majority of active TB is?

- if the primary infection is unchecked, progressive primary TB disease can occur


- see active disease development within 2 years of initial infection


- majority of active TB in the world is usually reactivation TB from latent TB infection

Latent vs Active TB


- 1/3 of worlds population is?

- 1/3 of the worlds population is infected with M TB



Diagnosis of TB Infection - Latent - perform a? also do a?

- tuberculin skin test


- interferon gamma release assays (IGRAS)

Diagnosis of Active TB Disease


- perform a?


- pathology - look for? presence? positive?


- also have?

- acid fast bacilli (AFB) and TB cultures from a particular site (sputum, LN, etc)


- patohology consistent with necrotizing granulomas and presence of AFB and positive TB cultures


- clinical presentation

TST Tuberculin Skin Test


- is a? from?


- patients infected with MTB - see delayed?


- give? to the?


- read at?


- measure the?

- glycerol extract of tubercle bacillus


- in patients infected with MTB causes a delayed hypersens type of reaction


- 5 tuberculin units of purified protein derivative (PPD-S) given intradermally on the volar aspect of the arm


- read at 48 to 72 hours later


- ** measure only the transverse diameter of induration - record in mm

LTBI = latent TB infection


- goal is to identify?


- two accepted tests? (2)


- IGRA measures? as WBC from infected patient will?

- goal is to identify indivs at increased risk for development of active TB


- two accepted tests for identification of LTBI = the TST and the interferon gamma release assay (IGRA)


- IGRA measures person's immune reactivity to M. tuberculosis, as WBCs from infected patient will release IFN-g, when mixed with antigens derived from M. tuberculosis

LTBI vs IGRA


- IGRAs are more specific than?


- both IGRA or TST cant separate?

- IGRAs are more specific than TST if previous vaccination with Bacille Calmette-Guerin (BCG), especially if BCG is given after infancy or multiple times


- neither can separate LTBI from TB disease and therefore have no value for active TB detection


- IGRAs also more specific for M.TB infection vs non-tuberculous mycobact

Interpretation of TST


- considered according to? (3)

- TST should be considered according to three dimensions:


1. size of induration


2. positive predictive value


3. risk of disease if the person is truly infected

TST Size


- negative? positive? >10 mm when?

- less than 4 mm = negative


- greater than 5 mm = positive


- certain conditions, greater than >10 mm

TST PPV


- probability that?


- dependent on?


- confounded by? (2)

- probability that a positive TST represent true presence of TB infection


- dependent on age, incidence of TB in the population and is confounded by:


= previous BCG vaccination


= previous NTM exposure

PPV and BCG Effect


if received BCG <1 yo, then 1% haad?


- if BCG from 1-5 yo, then positive TST is?


- BCG after 6?



- BCG received <1 years old, 1% had a TST result of >10 mm if tested > 10 years later


- BCG received between ages of 1 to 5 years old = positive TST seen in 10-15% up to 25 years later


- BCG recieved >6: 40% had persistent positive reactions

PPV and BCG


- therefore if BCG receieved after 1?


- espec if person is?

- therefore if BCG was received after age 1, it can cause false - positive TSTs, espec. if the population from which the person is from has a low prevalence of LTBI

Non-tuberculous Mycobacterium


- found in? people may be?


- in Canada, doesnt normally?


- this is why?

- found in soil and water in warm, temperate climates so people may be exposed and sensitized


- in Canada, sens is less common and does not usually cause a TST reaction greater than 10 mm


- this is why 10 mm remains the standard cut-point to determine whether TB infection is present

TB - Risk of Development of Active TB - high risk (8)



TB - Risk of Development - Increased Risk and Low risk



Interpretation of Positive TST


- calc risk based on?

- by utilizing the info from TST size, PPV of a positive TST (espec. if the person had a BCG) and risk of development of active TB, one can calculate risk of developing active TB

Positive TB Skin test - what to do - first rule out?


- perform a?


- sputum if?



- rule out active TB:


= history and PE


= CXR to rule abnorms


= Sputum if symptoms or abnormal CXR + referral to a TB clinic


= if CXR normal and no symptoms

Who should get treatment of latent TB Infection


- all convertors have? then rest of lives?


- offer to? of those who?


- also to those that are?


- and those with increased? (3)

- all convertors = 5% chnace of reactivating in first 2 years after conversion and then 5% for rest of their lives


- offer to new immigrants, less than 5 years in Canada


- offer to HIV+ and immunosuppressed


- offer to those with increased risk of reaactivation = renal failure, diabetes, abnormal CXR

LTBI Treatment - given in?


- for 9 months? 4 months?

- in immunocompetent or immunocompromised:


1) INH 9 months


2) Rifampin 4 months

What are the Major SEs of Isoniazid


- max dose?


- <1% chance of?


- SEs?


- treat for? also give?

- 5 mg/g to max 300 mg/day


- <1% chance of hepatotoxicity if excluding alcoholics and those with chronic active hepatitis


- see rash, GI upset


- treat for 9 months, give vitamin B6 25 mg per day to decrease neuropathies

Repeating TST


- in someone who is already positive, repetitive TB skin tests?


- once positive? do not?

- repetitive TB skin tests in someone who is already positive will continue to increase the size of reaction (Booster effect)


- once positive will always be positive, even after treatment, do not repeat TST if already positive once

When Do I Suspect Active TB - common symptoms of active pulm TB


- prolonged?


- other symptoms (5)

= prolonged cough (>3 weeks) and sputum


- fevers, chills, night sweats


- weight loss


- fatigue, loss of appetite


- hemoptysis


- other = LN swelling

RFs for Active TB


(4)


- consider immunosuppression in? (5)

- Aboriginal population


- previous history of TB or contact with active TB


- marginalized population


- immunosuppresion = HIV transplants, chronic steroid use, cancer, renal failure, diabetes

What Do I DO if I think someone has active TB?


- first do? investigation?


- analysis of? via? (3)


- TBST - still see? do not use?

- isolation precautions


- CXR


- respiratory secretion analysis:


= spont. early morning sputum x 3


= induced sputum


= bronchoscopy samples




* TBST = 20-30% false negative in active TB, therefore do not use TST if suspect active disease

Active TB


- most active cases are missed as?


- high resistance due to? therefore use? different from latent as?


- must consider?

- most active TB cases are missed because diagnosis is not considered ***


- since number if organisms are much higher, chance of resistance to a single treatment agent is high, therfore multi-drug regimen is needed for treatment in contrast to latent TB where only one agent is effective


- must consider resp. isolation and testing and treating the contact cases as well***

Extrapulm Disease (8)

- LN TB


- pleural TB


- CNS = mening, tuberculoma


- pericardial TB


- MSK TB


- peritoneal


- genitourinary


- dissem TB

Suspected Active TB Patient Algorithm

 

Pulmonary vs Extrapulm Source - Flow

If Positive for Active TB?


- give? discuss? then start?

- give education in patients own language


- transmission, med SEs, action plan for SEs, role of public health


- then start therapy

Active TB - steps


- monthly? await? adjust?


- follow up for?

- monthly clinical follow up and drug supply


- await final sensitivities, adjust meds as needed


- follow for sputum conversion

DOT therapy?


- stands for?


- do if TB is?


- or if? (5)



- if TB drug-resistant, language barrier, prolonged positive sputum, non-compliant, homeless, Hx of substance abuse, consider:


= Direct Observed Therapy = Public Health = DOT

Managing Active TB

- always start 4 drugs until sensitivities are known (>4% 1 drug resistance)


= INH = isoniazide = 5 mg/kg


= RIF = rifampin = 10 mg/kg


- PZA = pyrazinamide = 20-25 mg/kg


- EMB = ethambutol = 15-20 mg/kg


- Vit B6

Effect of Drugs on Various Bacillary Populations


- INH kills? acts?


- RMP kills? is the?


- PZA used to? therefore?

- INH kills dividing bacteria = first exponential


- RMP kills bacterial with spurts of metabolism = second exponential


= PZA kills dormant organisms = second exponential

Differential Diagnosis of Wheezing


- 9

- asthma


- congenital anomalies with airway impingement = vascular rings, tracheobronchial obstruction, mediastinal mass


- bronchopulmonary dysplasia


- cystic fiboris


- GERD
- aspiration


- FB aspiration


- heart failure


- sinusitis and allergic rhinitis


- bronchiolitis


- pertusiss


- TB


- immune system disorders



Potential RFs for wheezing - Host


- G/A/AH/G/R

- genetics


- atopy


- airway hyperresponsivenes


- gender


- race/ethnicity



Potential RFs for Wheezing - Environ


- (10)

- indoor allergens, outdoor allegens, occupational sensitizer


- tobacoo smoke, air pollution, resp infections, SE status, family size, diet and drugs, obesity

Operations Diagnostic Criteria for Asthma in Children One to Five years of Age


- documented?


- see? improves with?


- no?

1) Documentation of airflow obstruction - documented wheezing


2) Documentation of reversibility of airflow obstruction - improvement with SABA, oral corts


3) No clinical evidence of an alternative diagnosis

Diagnosis of Asthma - Pulm Function Criteria


- reduced? increase in? after?


- is less than the?


- after BD challenge?

- reduced FEV1/FVC and increase in FEV1 after bronchodilator or therapy


- less than lower limit based on age, etc reduced FEV1/FVC


- >12% increase after bronchodilator challenege

Asthma Management - start with? mainstay? if worse?



Asthma Control Chractarized as?


- daytime? nighttime? PA? exacs? need for?

 - see much more not controlled than thought

- see much more not controlled than thought

Key Diffs between Peds and Adult Asthma Management - Meds


- most children controlled on? if 6 to 11?


- if 12 and over - add? in form of?


- high doses ICS assoc with?


- less than 12 - dont use?

- most children control on low dose ICS


- if not adeaquate:


- children 6 to 11 = increase ICS to moderate dose


- 12 and over = add LABA to low dose ICS in form of combination inhlaer


- high doses ICS assoc with many SEs


- use of single inhaler therapy combo of budesonide and formoterol not approved in children less than 12 years old


- most children 6 years and over should be able to use a holding chamber with mouthpiece

Key Diffs between Peds and Adult Asthma Management - Monitoring


- start with? given to?


- in children, monitor?


- see increase in exacs in?


- lower dose in?

- education given to parent - child triad for young children, shift to child as age


- carefullly monitor growth (H/W) in childen each visit, fall needs to be prompt referral


- see increase in exacs in Sept/OCt yea rround


- lower dose - see better growth velocity

ICS vs Anti-Leuks


- moe effective? at?

-ICS more effective at decreasing asthma exacs than anti-leuks agents

Cystic Fibrosis


- is a? caused by?


- see abnormal? median survival?

- AR genetic disease affecting more than 70,000 people worldwide


- caused by CFTR mutation


- see abnormal transport of chloride and sodium across the epithelium leading to thick secretions


- median survival is 51.8 years

of 2000 CFTR Mutations


- CF disease caused by? classified into?


- all rest mutations cause? classified into?

- 242 become CF disease, classified ito pancreatic insufficient or pancreatic sufficient


- all the rest are benign polymorphs or CFTR related disorders


- mutation classified from 1 through 6

CFTR Mutation Classes


- Class I - see?


- Class III - see?


- Class 6?

- Class I = no functional protein due to absent functional CFTR


- Class 3 = Defective channel regulation


- Class 6 = decreased CFTR stability

Pan Insuff vs Pan suff


- 85% are? 15% are?


- change due to? (3)

- idea of genotypoe vs phenotype


- 85% are pancreatic insufficient, 15% are pancreatic sufficient


- change due to genetic modification, environment and passage of time

CF Related Lung Disease ad Damage


- abnormal CFTR leads to? impaired? cycle of?


- in turn leads to? (4)


= SD/B/PI/RF

- abnormal CFTR leads to reduced airway surface liquid and impaired mucociliary clearance


- leads to cycle of infection and inflammation


- in turn leads to:


= structural damage


= bronchiectasis


= pulmonary insufficiency


= respiratory failure

Prevalence of Resp Infections


- up to 25, most common?


- above 25?

- in younger patients, up to 25, S. aureus is the most common


- above 25, P aeruginosa is most common cause of infection

Sinopulmonary Manifestations


- 90% of?


- B/A/C/S/NP/P/H/A

= 90% of the M % M


= bronchiectasis


= asthma like phenotype


= clubbing


= sinusitis


= nasal polyps


= pneumothorx


= hemoptysis


= ABPA

In Pulmonary Disease, - during exacerbations - see?


- increased? (3)


- decreased?


- loss of? missed? PE? decreased? new?

- increased cough


= increased sputum production


= decreased exercise tolerane


= increased dyspnea


= weight loss


= missed school


= PE findings = crackles


= decreased FEV1 10%


= new CXR findings

In Pulmonary Disease - Pulm Function - see?


- decline starts?


- increased? due to?


- worsening?


- decreased?

= decline starts early in life


- air trapping = increased RV/TLV


= worsening airway obstruction:


= decreased FEV1, FVC, FEF 25-75


= FEV1 drops once signif disease

Primary CFTR Dysfunction


- see? (10) P/MI/D/C/NC/S/C/I/H

= pancreatic insufficiency


= CFRD


= pancreatitis


= meconium ileus


= DIOS
= constipation


= neonatal cholestasis


= steatosis


= cirrhosis


= infertility


= heat protration

Secondary CFTR Dysfunction


= G/O/ rectal? defic in?

= GERD


= OP


= rectal prolapse


= vitamin ADEK deficiency


= zinc defic


= FTT

Lab Evidence of CFTR Dysfunction


- positive? (2)


- want to see two?

- positive sweat test


- positive nasal PD


- two disease-causing mutations in CFTR

Clinical Features Compatible with CF


- sinopulm? abnorms in? snndromes related to ?


- relative?

- sinopulm disease


- GI and nutritonal abnorms


- salt loss syndromes


- obstructive azoospermia


- or CF history in sibling or positive newborn screening

Newborn Screening for CF


- started in? checking?


- if? then do? looking for?


- perform sweat chloride if? or if?

- stated in 2008, checks immunoreactive trypsinogen (IRT) on bloodspot


- if elevated (top 4%) DNA testing performed for top 35 mutations


- sweat chloride is performed if 1 or 2 mutations are found or if IRT is top 99th percentile

Sweat Test


- developed in? give? to?


- in CF. see increased? due to?


- positive? intemediate?


- lower sweats in? (2)


- if less than 3 months, positive in?


- if intermediate?

- developed in 1959, stimulate sweating with pilocarpine


- in CF, see increased Cl in sweat due to obstructed CFTR


- sweat Cl > 60 mmol/L is positive


- sweat Cl 40-60 mmol/L is intermediate


- pancreatic sufficient have lower mean sweats


- infants how lower sweats


** <3 months of age = positive is > 30 mmol/L




* cant exclude diagnosis of CF if intermediate if clinical symptoms

Algorithm to CF


- first have?


- three options of mutations =?


= 2? 1? O?



CF Algorithm


- first have?


- if 2 mutations? follow in?


- if 1 mutation do? check if?


- if 0 mutations? then?

- see increased immunoreactive trypsinogen, then do DNA analysis:


= 2 mutations = CF diagnosis = follow in CF clinic


= 1 mutations = sweat test = if above >60mmol/L, CF


= 0 mutation = do IRT again = if still increased, do sweat test and if not, discharge

Nasal Potential Difference Measurement


- assesses?


- in CF airway, see? leads to?

- assessment of CFTR function in nasal mucosa using NPD


- in CF airway epithelium, see water can only go into epithelium and not out, leading to decreased potential

Treatment of CF - Pulmonary Manifestations


- give a chest?


- mucolytics?


- Abx?


- anti?


- give supplemental?

- chest PT


- mucolytics = dornase alfa, hypertonic saline


- Abx = inhaled, oral, IV


- bronchodilators


- anti-inflamms = inhaled, oral


- supplemental oxygen


- BiPAP


- lung transplant

Treatment of Cystic Fibrosis - Extrapulmom Manifefestations


- replace? also give?


- diet?


- consider transplants of?


- ursodiol if? insulin if?

- enzyme replacement


- ADEK vitamins


- high calorie,high fat diet


- Ursodiol if CFLD


- Insulin if CFRD


- liver transplant


- pancreas transplant

CFTR Modulators - Potentiators


are?


- increase? name?

- orally bioavailable drugs


- potentiator = Ivacaftor = increases opening of CFTR channel


CFTR Modulators - Correctors


- are? increase? name?

- BA drugs


= Lumicaftor = increase number and function of CFTR channels at the cell surface

Primary Ciliary Dyskinesia


- is a? prevalence?


- often is a?


- abnormal?


- impaired?

- AR recessive disease


- prevalence is 1 in 10-40 000


- late diagnosis


- abnormal ciliary structure and function


- impaired mucociliary clearance

Signs of PCD


- recurrent?


- neonatal?


- serous?


- loss of?


- in males?


- also see?

- recurrent pulmonary infections


- neonatal respiratory distress


- sinusitis


- serous otitis media


- hearing loss


- bronchiectasis


- male infertility


- laterality disorders in 50%

Diagnosis of PCD - Screening


- no? **


- look at? NO produced throughout?


- level in PCD? however not?

*** no perfect test


= Nasal Nitric Oxide


- NO produced throughout airways but more abundant in paranasal sinuses


- low in PCD patients


- but not diagnostic because reported to be normal in subset of PCD patients

Diagnosis of PCD - Diagnostic


- try?


- EM for? yet is?


- genetics as?

- high speed video microscopy


- electron microscopy = normal in 20% PCD


- immunofluorescence


- genetics = >30 genes and identify 60% of cases

CF vs PCD - CF


- no? (2)


- FTT if?


- male?


- low?


- on PFT?

- no neonatal resp distress


- no increased incidence of ear infections


- FTT if pancreatic insufficient CFRD


- male infertility


- airway obstruction on PFTs


- low NO

CF vs PCD - PCD


- see? prominent feature?


- no assoc?


- on PFT?


- low?


- not all wheeze is?

- neonatal resp distress


- prominent feature is recurrent otitis media


- no assoc GI disease


- male infertility


- airway obstruction of PFTs


- low NO




*no all wheeze is athma

If obstructive pulm. graph and normal DLCO? Asthma if?


- can be either?


- asthma if?

- can be chronic bronchitis or asthma


- if increase in FEV1 is >12% and >200 cc post bronchodilator, is asthma


- sub-optimal control if have persistent symptoms

Asthma Treatment


- patient needs? (3)


- 1st line?


- 2nd line is? should not?

- patient needs:


= environmental control, rescue bronchodilator, controller medication


= 1st line = inhaled steroid


= 2nd line is long acting beta agonist = should not be sed as controller monotherapy

Algorithm of Chronic Cough


- if have cause? then? if inadequate?


- if smoking? then if inadequate?



Red flags of cough **

- hemoptysis


- weight loss


- abnormal CXR

Big Three Causes of Cough and Treatment


# 1 is? give? (3)


# 2 is? do? give? then?


# 3 is? give or do?

1) Upper Airway Cough Syndrome = antihistamines, decongestants, nasal steroids


2) Asthma - do spirometry with methacholine challenge = inhaled steroids then bronchodilators


3) GERD = PPI, lifestyle mods

COPD treatment ladder


- start with?


- then give? then? if that doesnt work?

COPD - Mild vs Mod vs Severe Treatment


- always do?


- always start with? then?


- last resort?


- to reduce exacs

- theophylinne last resort
- smoking cessation no brainer
- SA and LA BDs are approp. with pulm rehab to reduce exacs

- theophylinne last resort


- smoking cessation no brainer


- SA and LA BDs are approp. with pulm rehab to reduce exacs

COPD Treatments


- ICS used to?


- theophyilline only used if?

- inhaled cortcs (ICS) reduce frequency of exacerbations but shouldnt be used as monotherapy


- theophylline may be used if having persistent symptoms despite all other treatments

Acute Exacs of COPD


- systemic steroids to?


- Abx used in?


- oxygen for?


- SABDs vs LABDs?

- systemic steroids can reduce duration of hospitalizations and increase time to next exacerbation


- Abx are indicated in exacerbations with sputum purulence


- oxygen is indicated if patient is hypoxemic


- SABDs are appropriate, LABDs can be continued but likely not helpful for acute relief

If restrictive and low DLCO - think of?


- hallmarks are? (3)


= low? (2)


= normal?

- think of ILD


- hallmarks of restriction on pulmonary function testing are:


= low FVC


= normal FEV1/FVC


= low TLC



ILD and Idiopathic Pulmonary Fibrosis


- on PE, see?


- on walk test? on CT chest?


- patients with ILD do not?

- crackles and clubbing consistent with IPF


- see desaturation on walk test and honeycombing pattern on CT chest


- patients with ILD do not usully have hemoptysis, unless other problem also **

Most likely etiology of hoarseness when have lung cancer?


- recurrent?

- recurrent laryngeal nerve involvement of lung tumour

Hoarseness caused by disruption of? from? (2)


- see unilateral?

- disruption of recurrent laryngeal nerve (esp. left) from tumour or mediastinal adenopathy


- unilateral vocal cord paralysis

Most likely cell type in lung cancer of non-smoker?


- smoking history in AC or other cell types?

- adenocarcinoma


- smoking history in 75% of ACs vs 98% of other cell types

Nodules and Risk of malignancy


- age?


- popcorn means? stippled or eccentric?


- smooth or lobulated borders? irregular or spiculated borders?


- diameter?


- nodule growth?

- older patients have higher risk of malig


- popcorn calcification suggests benign etiology


- most patterns of calc suggest benign except stippled or eccentric


- smooth or lobulated borders suggests benign


- irregular or spiculated suggest malignant


- diameter > 1cm (large lesions) increases risk of malignancy


- nodule that grows very quickly and have doubling <20 days, or very slowly (> 400 days) are more likely to be beinign

Light's Criteria - fluid is an exudate if?


- protein?


- LDH?


- pleural fluid LDH > then? usually?

- if any one of the following present:


= pleural fluid protein: serum protein > 0.5


= pleural fluid LDH: serum LDH > 0.6


= pleural fluid LDH > 2/3 upper limit of normal for serum LDH (200 IU/L)

Pleural Effusions - Causes - Transduate - main causes? (3)

- CHF


- hepatic hydrothorax


- nephrotic syndrome

Pleural Effusions - Causes - Exudate


- I/ M/ I/ other

- Infection = bacteria, TB, viral, fungal, parasitic


- Malignancy = Carc, Lymphoma, Meso, Chylo, Myeloma


- Inflammatory - CTD, pancreatitis, asbestos, PE, ARDS


- Other = iatrogenic, drug-induced, hypothyroid

Types of Pain


- nociceptive can be? neuropathic can be?

- nociceptive = somatic vs visceral = more dull


- neuropathic = central vs peripheral = more burning


- mixed

Pain Vs Suffering


- nociception is the?


- pain is the?


- suffering is the?

- nociception = is the physiologic formation of pain signal


- pain = perception or feeling or sensation


- suffering = reception or response to feeling

Pain Mechanisms


- gate theory sees ascending? before? used in?


- biomech theory - response affected by


- pro noci signals = (3)


- anti noci signals are? (3)

1) gate Theory = ascending pain signals blocked at spinal cord, before thalamus, theory behind TENS


2) Biomechanical Theory = response to pain stimulus affected by intra-neuronal neurotransmitters


- pro-nociceptive = glutamate, aspartate, substance P


- anti-nociceptive = GABA, serotonin, ACh


3) Chronic Pain Theory

Pain and Signal Processing


- transduction? transmission? modulation? perception?

1) Transduction = receptor activation = energy converted into nerve impulses


2) Transmission = information is transferred from primary afferent fibres to SC dorsal horn and onto brain stem


3) Modulation


4) Perception = begins with activation of sensory cortex

Nociceptive Pain


- fibers that respond to damaged tissue?


- goes through? then? then?

- primary afferent fibers = A-delta, C = respond to damaged tissue


- cell bodies = DRG or cranial nerve ganglia


- spinal columns


- brain

- Pain Subtypes - Nociceptive, Somatic


- quality?


- location is?


- ex/? (2)

- quality = sharp, stabbing, throbbing


- well localized


- ex/ meniscal tear, laceration

- Pain Subtypes - Nociceptive, Visceral


- quality?


- location is?


- seen in? (2)

- quality = deep, dull, cramping


- poorly localized


- cholecystitis, endometriosis



- Pain Subtypes - Neuropathic


- quality?


- location?


- seen in? (2)

- quality = burning, tingling, numb


- localized or generalized


- radiculopathy, polyneuropathy

Acute Pain


- usually a response to? stimulus can be?


- causes? time?


- treatment aimed at?


- seen in?

- usually a response to noxious = mechanical, thermal, chemical stimulus


- causes depolarization of nociceptors


- time-limited


- treatment aimed at removing underlying pathologic process


- ex/ wrist fracture

Chronic Pain


- may not be assoc. with?


- have a? that correlates less with?


- additional?


- sleep? function?


- seen in?


- higher costs than?


- seen more in? (3)

- may not be associated with noxious event/ pathologic process


- underlying pathology correlates less with reported level of pain


- additional psychologic and behavioural mechs


- often poor sleep and decrease in function


- 2-55%, 70% in primary disability


- higher costs than cancer, depression, hypertension


- seen in elderly, disabled, terminal conditions

Complications of Chronic Pain


- physical?


- psychological?


- societal?

1) Physical = decreased ROM, myofascial pain, muscle weakness, tolerane, substance use disorder, drug dependency


2) Psychological = depression, spouse distress, family distress, insomnia


3) Societal = lost wages, social support systems

Chronic Pain Mood Symptoms


- depression leads to higher? greater? life interference related to?


- pain related? leading to higher? more? behaviours?

1) Depression in Chronic Pain = higher lvels of pain, less active, report greater disability and life interference related to pain


2) Pain related Anxiety = higher severity, great disability, pain behaviours (fear avoiding)

Assessing Chronic Pain


- perception?


- cognition?


- attention?


- emotion?


- learning and memory?


- motivation?

- perception - altered perception


- cognition - deficits in performance


- attention - hypervigilance


- emotion - depression, anxiety, suicide


- learning and memory - deficits, fear learning


- motivation - decreased, centered value

Chronic Pain Biopsychosocial Assessment


- history to characterize? via?


- investigations if?


- assessment of? (4) - good for?

1) Pain history = OPQRST = characterize as somatic, visceral, neuropathic to guide mngmt




2) Red flag symptoms = warrant investigations




3) Functional Assessment = IADLS, BADLs, Vocational, PA = context pain, goal-setting

Chronic Pain Biopsychosocial Assessment


- screening for? if untreated can?


- ask about? feeling?


- if untreated, can?



4) Mood Screening = depression, anxiety = untreated can amplify pain




5) Sleep screening = OSA, non-restor sleep = untreated, amplifies pain, with opioids can increase risk of overdose




6) PE




*pain is subjective, acknowledge pain

Normal Sensation after damage?


- nociception leads to?


- low-threshold mechs lead to?

- is pain from nociception


- low-threshold mechanoceptors lead to touch

If have central sensitization


- nociception can lead to?


- low threshold mechs lead to?

- can lead to hyperalgesia from nociception


- low-threshold mechanoceptors leads to allodynia

Chronic Pain - Brain Morph Chnages


- see decreased?


- in CBP - affects? PFC/T


- IBS? I and CG


- fibromyalgia? N


- tension HAs? N


- treatment able to? normalizes?

- see decreased gray matter


1) Chronic Back Pain = prefrontal cortex, thalamus


2) IBS = insulate and cingulate gyrus


3) Fibromyalgia = numerous


4) Tension Headaches = numerous




*see treatment can reverse abnormal brain anatomy and function, normalizes brain activity

Chronic Pain - Variability in Perception


see different? in? (CG/I)

- variable correlation between stimulus and ratings for the 16 subjects


- activity in cingulate gyrus and insula statistically different between stimulus and perception

Addiction vs Dependence vs Tolerance - Addiction


- considered impaired? use is? continued despite?

- Addiction = impaired control over drug use, compulsive use, continued use despite harm and craving


Addiction vs Dependence vs Tolerance - Dependence


- pattern marked by?


- see? made by? or decreased?

- Dependence = maladaptive pattern of drug use marked by tolerance and a drug class-specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreased blood levels of drug or admin of an antag

Addiction vs Dependence vs Tolerance - Tolerance


- state of? drug induces changes that?

- state of adaptation in which exposure to a drug induces changes that result in diminution of one or more of the drug's effects over time

Chronic Pain Management and Assessment


- pain best managed using?


- assess (4) = P/M/FI/C - via?

- pain is best managed using biopsych assessment and approach


- assess via:


= pain = OPQRST


= mood = anxiety, depression, anger = DSM-5


= functional interference = vocational, IADLs, BADLs


= coping and beliefs

Chronic Pain Management - six parts


- AM/ RP/ PM/ IP/ PI/ S


- forms a?

= activity modification


= rehabilitation program


= pharmacological management


= interventional procedures


= psychiatric interventions


= surgery




*forms comprehensive pain program

Chronic Pain Non-Pharm Management (8)

- MCEs


- taichi


- yoga


- progressive relxation


- EMG


- CBT


- mutlidisc rehab


- acupuncture


- etc

Chronic Pain Pharm Management (10)

- acetaminophen


- NSAIDs


- gabapentinoids


- Tricyclic Antidepressants


- Opiods


- SNRIs


- SSRIS


- ketamine


- lidocaine


- cannabinoids

Chronic Pain - Pharm Management Peripherally, Centrally


- peripherally at receptor - use? (4)


- peripherally along nerve? (2)


- centrally =? use (4)

1) Peripherally at nociceptor = cannabinoids, NSAIDs, opioids, tramadol


2) Peripherally = along nociceptive nerve = local anesthetics, anticonvulsants


3) Centrally = various parts of the brain = acetaminophen, anticonvulsants, tramadol, opioids

Chronic Pain - Pharm Management - Descending Inhibitory Pathway, Dorsal Horn


- DIP = (4)


- Horn = (5)

4) Desc Inhibitory Pathway in SC = cannabinoids, opiods, TCA, SNRIs




5) Dorsal horn of SC = anticonvulsants, cannabinoids, gabapentin, NMDA antags, opioids

Interventional Pain Management


-blocks? (2)


- injections (2)


- soft tissue?


- RF ablations to? (2)

1)Diagnostic nerve blocks = medial branch, lateral femoral cutaneous


2) Intra-articular injections = glenohumeral, sacroiliac


3) Soft tissue injections - bursas, trigger points


4) Radiofreq ablations - suprascapular, medial branch

Chronic pain Management - 6 parts **


- also want to normalize?

- CBT, relaxation strategies, mindfulness based stress reduction
- TFESI to decrease pain
- want to normalize sleep

- CBT, relaxation strategies, mindfulness based stress reduction


- TFESI to decrease pain


- want to normalize sleep

Pain Clinical Points


- always examine? make sure to?


- pain wont? is a?


- do not? especially? unless?

- always examine patient


- always acknowledge the patient's suffering from pain


- pain does not show up on imaging, subjective experience


- do not order imaging, especially MRIs, unless it will def chnage management

Allodynia? Hyperalgesia?


- A = stimulus?


- HA - increased?

- pain caused by stimulus that does not normally provoke pain


- HA = increased response to a stimulus that is normally painful

Nociception vs Pain

Why Treat Pain with Medication?


- patients want? doctors want?


- expect?


- practice?


- non-drug?


- anecdotes?


- goal is not only?

- patient want relief, doctors want to help


- societal expectation


- practice models/ insurance coverage


- non-drug measures are hard


- anecdotes of success


- goal is not simply pain relief but to afford benefit > harm

Acetaminophen


- #1?


- major uses? mechanism?


- adult dose? peds dose?


- dont give reflexively for?

- #1 analgesic worldwide


- major uses for pain, fever


- mechanism is decreased prostaglandin synthesis in CNS


- adults dose is 1000 mg 3-4x/day


- peds dose is 10-15/kg 3-4 times/day


- dont not give reflexively for fever


- better for acute pain ? chronic

Acetaminophen for Back Pain and OA


-shown to be?

- ineffective, minimal short term benefit for people with OA



Acetaminophen Toxicity


- produces? which is?


- dose dependent?


- therefore if go over? see increase in?

- produces NAPQI, which is toxic to the liver


- hepatotoxicity is dose-dependent


- therefore if go over regular amount use, see increase in liver enzymes due to damage as NAC enzyme cannot handle

APAP-Warfarin Interaction


- warfarin blocks? therefore warfarin reduces?


- NAPQI acts to?


- together put?

- warfarin blocks enzyme that recycles vitamin K


- therefore patients on warfarin have depleted Factors 2,7,9 and 10


- NAPQI = acetmainophen metabolite, also decrease y-carboxylase activity


- two put patient into grossly anticoagulated state

Role of NSAIDs


- inhibit?


- COX1 has? inhibited by? (2)


- COX2 has? inhibited by? (3)

- inhibit COX


- COX-1 has cytoprotective PGS = inhibited by NSAIDs and Aspriin


- COX-2 has inflammatory PGs = inhibited by COX-2 inhibs, NSAIDs, Aspirin`

Different Role of Different NSAIDs


- ASA is? acts to? isnt?


- Nonselective means? include? (4)


- COX-2 inhib =?

1) ASA = Aspirin = platelet inhibition = irreversible




2) Nonselective (COX-1, COX-2) = ibuprofen, naproxen, indomethacin, ketorolac




3) COX-2 Inhibitor = celecoxib

NSAID Gastropathy


- prevent by?


- injury at?


- consider?


- consider use of? in those? (5)

- prevention via limiting dose and durarion


- injury to GI tract happens at 7-14 days


- consider H.pylori eradicaiton


- use PPi in high risk:


= age > 60, steroids, dyspepsia, concurrent ASA, previous ulcers

NSAIDs and Kidney - act to? therefore reduce?

- NSAIDs constrict afferent arteriole, also reduce glomerular perfusion

Different Opioids (7)

- heroin, morphine, hydromorphine, oxycodone, fentanyl, methadone, tramadol

Mechanism of Opioids


- stimulate?


- presynaptic binding acts to?

- stimulate opioid receptors in PNS/ CNS = mu, kappa, delta


- presynaptic mu binding decrease release of other NTs

Evolution of Opioids


- 70s, 80s - limited?


- but in 90s, see? due to?


- in 2002, see?

- 70s, 80s - limited prescribed just for acute and cancer pain


- 90s - see better treatment for all pain, due to toxicities and limited effectiveness of other drugs


- 2002- WHO Analgesic Ladder - still a problem as oxycodone shouldnt be considered a weak opioid = industry influence

WHO Analgesic Ladder


- 1 = known as (3)


- 2 = known as (3)


- 3 = known as(6)


** problem as?



Role of Oxycodone


- see prescribing?


- problem with codeine?


- after 2000, sales?

- bought into use of oxycodone, see prescribing of oxycodone increase after induction of long-acting oxycodone


- codeine becomes unknown amount of morphine, do not give as dont know how much is being converted


- see sales of oxycodone significantly increase after 2000, differs based on region, highest in ontario

Evidence for Opioids


- is? no studies that?


- typical RCTs (3) - easy to show?

- terrible - no study of opioid therapy versus no therapy evaluated >1 year outcomes elated to pain, QOL, function


- typical RCTs are 12 weeks long, exclude high risk patients, measure pain scores compared to placebo, easy to show it doesnt hurt in small time

Problems in Over prescribing


- large? see rapid increase in?


- also increase in?

- large harm, see rapid increase in commonly prescribed opioids and synthetic opioids and has been steadily increasing since 2001

Side Effects of Opioids


- C/D/F/SA/ decreaed/ OIH/ PD/D/S

- constipation


- delirium


- falls and consequences


- sleep apnea, altered sleep architecture


- reduced testosterone


- hyperalgesia (OIH)


- physical dependence


- depression


- suicide


- see increase risk of road trauma

Important of First Prescription


- if first round supply is less days? if more?

- if supplied less days in first supply of first opioid prescription, see less likely to continue use


- if have increased days in first opioid prescription, more likely to continue use

Physical Dependence


- response that is? not?


- defined by? under?


- results in? (5)


- dependence within?

- expected, adaptive response = not addiction


- defined by withdrawal under sudden decrease in dose


- results in symptoms = fatigue, headaches, nightmares, numbess, anxiety, etc


- dependence happens within 24 hours



Opioid Induced Hyperalgesia


- features increased? known as?


- pain often? and is?


- mechanism is?

- features:


= increase sensitivity to noxious stimuli, allodynia, pain often generalized and ill-defined


- mechanism:


= excessive activation of NMDA receptors



What to Do about OIH


- recognize?


- can give? such as? (3)


- must do?

- recognize +/- opioid rotation


- NMDA antagonist = Ketamine/ DM/ methadone


- slow taper

Patients not Addicts


- patients using?


- genuine? less likely as ?


- illusory?

- patients using opioids daily to control pain


- genuine benefit >harm = less likely as daily dose increase


- illusory benefit = physical dependence/ withdrawal

Key Points of Opioids Prescribing


- used as? start with?


- keep dose less than? can accept?


- encourage?


- avoid in? (2)

- opioids effectively last resort for chronic pain, sensible to start with morphine


- keep dose <50 mg morphine or equivalent, 90 for patients willing to accept increased risk


- encourage slow taper for legacy patients


- avoid in patients with active SUD


- avoid co-prescribing with Benzos

Problems of Opioids


- deaths at?


- increased risk of? in?


- twin crises of?

- see deaths at higher doses


- see increase risk of overdose in those with concurrent use of BZDs


- twin crises of addiction and of flawed pain management

Cervical Axial Pain Epi


- prevalence?


- chronic pain in? severe in?


- workers under? over 45?

- prevalence = 9-18%


- traumatic pain = chronic in 40%, severe in 8-10%


- workers under 30 - 30%


- workers 45+ = 50%

Radicular Pain Epi


- under 30? 45+


- history of? or preceding?

- annual incidence is 83/ 100 000


- under 30 = 5-10%


- 45+ = 25-40%


- history of trauma or preceding physical exertion in only 15%

Cervical Spine Anatomy


- vertebrae? roots?


- most axial rotation? most flexion? most lateral flexion?

- 7 vertebrae and 8 roots


- most axial rotation at C1-C2


- most flexion at C4/5 and C5/6


- most lateral flexion = C3/C4 an C4/C5



Cervical Spine Anatomy - ZPP facet joints for? connect?


- Luschka joints =? prevent?


- Intervertebral discs are found between? act to?

- Zygapophyseal Facte joints allow motion within C-spine and connect vertebral segments




- Uncovertebral Joints = Luschka = C3-C7 = prevent lateral translation




- Intervertebral Discs = between bodies f C2-C7 and dissipate axial forces

Cervical Intervertebral Disc


- inner = is? %? throughout life?


- outer = ? are? withstand?


- main function?


- axial load pushes on? acts to?


- if AF break?

- inner nucleus Pulposus = gelatinous, 90% water at birth, dessicates throughout life


- Outer Annulus Fibrosis = concentric fibrous layers to help withstand strains


- main function is shock absoprtion


- Axial load pushes on nucleus and stretch annulus fibers


- If annulus fibers break, have herniated NP

Mechanical Axial Pain


- cervical? (2)


- herniated?


- FJMP?


- cervical?

- cervical sprain


- cervical strain


- herniated Nucleus Pulposus


- Facet Joint-Mediated Pain


- Cervical Stenosis/ Myelopathy

Axial Pain Rheumatologic (8)

- Ankylosing Spondylitis


- Reiter Syndrome


- Psoriatic Arthritis


- Enteropathic Arthritis


- Rheumatoid Arthritis


- Diffuse Idiopathic Skeletal Hyperostosis


- PMR


- Fibromyalgia

Other Causes of Axial Pain - Endo = (5)


- also consider? (2)

- Endocrinologic


= Osteoporosis = compression fracture


= Osteomalacia


= Parathyroid Disease


= Paget Disease


= Pituatary Disease




- Infections


- Tumours

Cervical Sprains and Strains


- sprain means? from?


- strain is a?


- account for?


- mechanism = M/W/A

- ptrain = MSKtendinous injury produced from overload


- Strain = ligamentous overstretching or tearing


- account for 85% neck pain


- mechanisms:


= MVA = accel/decel


= Workplace = postural (thoracic kyphosis)


= Athletes = trauma, repetition

Symptoms and Signs of Cerivcal Sprain and Strains


- symptoms = (4)


- aggravated by?


- signs = decreased? palp of? normal?


- no painless?

- Symptoms: neck pain, stiffness, fatigue, HAs, aggravated by passive or active neck motion


- Signs: decreased cervical ROM, palpation of area uncomfortable or mod painful (upper trap, SMC), normal neuro exam and motor exam shows no painless weakness

Investigations of Cervical S/S


- indicated for?


- do?


- most common cause = ? from?

- indictaed for neurologic or motor abnorms


- do flexion/extension Xrays


- most common = straightening of lordosis from muscle spamsTrea

Treatment of Cervical S/S


- control? to allow?


- meds (2)


- modalities? (4)


- gradual return to?


- exercise program with?

- control pain and inflammation to facilitate active rehab


- meds = NSAID, acetaminophen


- modalities = massage, heat, TENS, soft cervical collar


- gradual return to activities 2-4 weeks post injury


- exercise program = incorporate proprioceptive retraining, balance, postural conditioning

Herniated Nucleus Pulposus


- NP migrates through? release of?


- most common at?


- often at? then? then?

- NP migrates through annular fibers, see release of inflamm mediators


- most common at 30-40 years of age


- L4/5-L5/S1 > C5/C6

Etiolgy of Hrniated NP


- (4)

= spontaneous


= lifting activities


= coughing/ sneezing


= bending / twisting

Symptoms of Herniated Nucleus Pulposus


- acute? interscap?


- if no nerve root impingement?


- if NR impingement?


- or can be?


- aggrav by?


- allev by?

- acute cervical or back pain, interscapular pain


- may cause:


= axial pain if no nerve root impingement (radiculo)


= radiating pain down the arm or leg if NR impingement


= both


- aggrav. by coughing, lifting


- allev by lying supine with head support

Signs of Herniated Np


- must exclude?


- restrictions?


- tender to? over?

- must exclude myelopathy and radiculopathy


- suble range of motion restrictions


- tender to palpation over the cervical spinous processes



Imaging of Herniated NP


- MRI isnt useful?


- look for?



- MRI not useful in detecting symptomatic cervical disks


- look for red flags


- cervical provocation discography

Treating Herniated NP


- control?


- modalities?


- meds? (2) sparingly?


- staiblize?


- interventional?-


- surgery?

- control pain and inflammation


- modalities = heat, traction (CI in myelopathy), TENS, cervical collar (<72 hours)


- Meds = NSAIDs, TCAs, sparingly opiates


- Cervical Spine Stabilization


- Interventional = Epidural Steroid Injections


- Surgery = Fusion

Cervical Radiculopathy - Common Causes


- #1 is? due to? #2 is cervical? or? due to?

#1 = cervical herniated NP = structural compression and peri-neural inflammation


#2 = cervical spondylosis (Osteoarthritis) = zygophophyseal hypertrophy or uncovertebral hypertropy

Symptoms of Cervical Radiculopathy


- axial? followed by?


- gradual? that is?


- deep?


- aggrav by?


- allev by? as relieves?

- axial cervical pain followed by explosive onset of upper limb pain


- spondylotic, gradual onset of pain


- deep,dull ache or sharp/ lancinating


- aggravating by coughing, sneezing


- allev by elevating humerus = abduction relief manuever

Signs of Cervical Radiculopathy


- (4)


- no?

- muscle wasting/ atrophy


- motor weakness


- decreased or absent reflex in affected myotome


- decrease sensation (light tough, pinprick, vibration) in affected dermatome


- no UMN signs = Hoffmans, Babinksi

Cervical Radiculpathy - C5 through T1 - nerve and Muscle ??


- nerve is? muscle?


- C5/6 is? 7/8? C8/T1 is?

C5/6 - biceps, BR
C7/8 - triceps
C8/T1 - finger flexors

C5/6 - biceps, BR


C7/8 - triceps


C8/T1 - finger flexors

UMN Syndrome


not?


- hyper?


- gait?


- also see?

- not radiculopathy


- positive Hoffmans


- hyperreflexia


- gait ataxia


- spasticity


- clonus

Investigations of Cervical Radiculopathy


- mRI to see if?


- NCS to test? assess?


- Nerve root block has?

1) MRI to see structual compression at nerve root




2) Nerve Conduction, EMG - test 6 peripheral nerves and parapsinal, assess for other neuropathies such as CTS - high detection for CRs




3) Fluroscopically Selective Nerve Root Block - high spec

Treatment of Cervical Radiculopathy


- patient?


- modification of? avoid?


- pain relief via?


- stab via?


- interventional? surgery?

- patient educaiton


- activity modification - avoid heavy lifting, repetitive C-spine extension/rotiation


- pain relief via nonpharm (TENS) and pharm (NSAIDs, TCA, MRelx, Opiates in acute)


- Stabilization via posture, strengthing


- Interventional = neve root injectiosn


- Surgical Discectomy

Facet Joint- Mediated Pain - Cervical


- mostly seen at?


- prevalence is?


- at same level?



- C2/3 > C5/6 > C6/7


- chronic, traumatic cervical facet pain prev is 64%


- usually have symptomatic disc at same level


- 53# patients after whiplash injury

Symptoms of Facet Joint- Mediated Pain


- no? to?


- more likely facet pain if source is?

- no pathognomonic findings to distinguish form other sources of axial neck pain


- unilateral paramidline more likely facet than disc

Signs of Facet Joint-Mediated Pain - Cervical


- neuro exam?


- tenderness? low?


- imaging role?

- neuro exam normal


- may have focal tenderness to palpation over facet joint


- low spec




* image via Xray/Ct/MRI - hard to discriminate

Treatment of Facet Joint-Mediated Pain - Cervical


- analgesia via?


- therapy to? strengthen?


- interventional is?

1) Analgesia = ice, mobilization, massage colage <72 hours, NSAIDs, opiates




2) Therapy = normalize ROM, soft tissue length, strengthen spine, proprioception




3) Intervention = MBB, RFA, Intra-articular

Diagnostic Zygaphophyseal Joint Blocks for FJMP


- block of ? as it?


- if positive?

- is a medial branch block with local anesthetic to medial branches that supply facet joint


- if positive, then candidate for long-term radiofrequency denervation (median 9 months relief)

Cervical Stenosis/ Myelopathy


- injury to?


- age of onset?


- caused by? (6)

- injury to cervical spina cord


- average age of onset = 50


- caused by OA, motor neuron disease, MS, nasculitis, syringomyelia, spinal tumours

Symptoms of Cervical Stenosis - gait? changes in? overall? dysfunction of?

- gait ataxia


- weakness


- sensory changes


- bowel dysfunction


- bladder dysfunction

Signs of Cervical Stenosis/ Myelopathy


- hyper?


- also see? (2)


- positive signs? are? (3)

- hyperreflexia


- clonus


- spasticity


- L'Hermittes Sign


- Hoffmans Sign - flick patients extended middle finger and monitor for twitching of thumb


- Babinski sign

PE for Myelopathy vs Radiculopathy



Red Flags and Condition


- gait ataxia =?


- bladder dysfunction = ?


- night pain?


- fevers?

1) Gait Ataxia/ UMN changes = myelopathy


2) Bowel/bladder/Sexua dysfunction = Cauda Equina Syndrome


3) Night pain/ weight loss = tumour


4) Fevers/ chills = infection

Masqueraders of Cervical Radiculopathy


- majority of patients have?


- most common MSK?

- 69% of patients referred for radiculo with normal studies had MSK disorder


- 29% of patients with NCS/EMG confirmed radiculo had an MSK disorder


- most common MSK disorder = myofasical pain syndrome

Causes of Upper Extremity "radicular pain"


- true = (2)


- also see? (6)

- true radiculopathy - herniated NP, lateral stenosis


- tendinopaties = RC, etc


- OA, Inflamm Arthritis


- muscle pain syndromes


- ligament injuries - MCL


- neurologic - CTS, ulnar neuropathy


- vascular

Regional Pain Syndromes - Myofasical Pain Syndrome


- characterized by? caused by?


- MtrPs are? with? taut band of? compression causes?

- a regional pain syndrome characterized by muscle pain caused by myofascial trigger points (MTrPs)


- MtrPs are:


= circumscribed split in muscle with pain or tenderness


= taut band of skeletal muscle fibres


= compression can cause referred pain

Myofasical Pain Syndromes - muscles affected? (4) I/T/S/B

- see:


= infraspinatus


= trapezius


= scalenes


= brachialis

Etiology of Myofascial Pain Syndrome


- usually secondary to? (4)


= muscular? chronic? Poor? systemic?

- usually secondary to:


= NMDs = strains, sprains, arthritis


= chronic repetitive minor muscle strains


= poor posture


= systemic disease

Symptoms and Signs of Myofascial Pain Syndrome


- main symptom is? can be?


- sign is tender? referral?

- symptoms = pain = can be nociceptive, neuropathic, axial or appendicular


- signs = tender taut band, possible referral of pain with palpation of taut band

Imaging of Myofascial Pain Syndrome


- EM see? LM see? US see? MR see?


- not seen on?

- EM = taut bands and contraction knots


- LM = contracrtion knots


- US = hypoechoic


- MR elastography




* not seen on routine imaging

Microdialysis Needle


- used to measure?


- looking for? (5)


- bchs assoc. with?

- use to measure biochem responses of soft tissue to pain


- look for CRGP, bradykinin, TNFa, IL-6 and IL-8


- biochemicals assoc. with pain eleveated in soft tissue near TPI

Myofascial Pain Syndrome Treatment


- treat the underlying?


- PT for?


- home exercise with?


- focus on the? to suppress? with?

- treat underlying lesions (tear)


- PT = stretching, manual release, modalities


- home exercise program = stretching, focal massage, heating


- trigger point injections = suppression of local nociceptors with needle in trigger point

Fibromyalgia Pathophys


- lower? due to dysfunction of?


- all nociceptors are? seen in?


- muscles only vs widespread called?

- lower pain threshold related to dysfunction of descending anti-nociceptive system


- all nociceptors in the body are hyperirritable


- muscles, tendons, ligaments, fat (myofasical = muscles only)


- widespread/ whole body pain (myofascial = regional)

Triggers of Fibromyalgia - PA/PI/ sleep? or?

- physical activity


- physical inactivity


- sleep disturbance


- emotional stress

Symptoms and Diagnosis of Fibromyalgia main three are? (3)


- all rated from?

- fatigue


- waking unrefreshed


- cognitive symptoms




* all rated from 0 to 3


- many other symptoms

Unique Approach to Fibromyalgia


- accurate? accept? role of?


- encourage patient to?


- importance of?

- accurate diagnosis based on Am. Coll. of Rheum


- accept diagnosis = both patient and physician


- patent and family education


- encourage patient to take an acitve role in self-care


- psychologic and psychiatric counselling


- rehab programs (PT, OT)

Management of Fibromyalgia Syndrome inAdults (11)

- self-management strategies


- psychological interventions


- exercise


- complementary and alternative medications


- tylenol


- NSAIDs


- Opioids


- Cannabinoids


- Antidepressants


- Anticonvulsants

Shoulder Pathology


- always examine? these incloude?


- muscle? bursa? referred?

- always examine the joint above and below for referred patterns of pain


- joints = glenohumeral, Acromioclavicular, Sternoclavicular


- Muscle = rotator cuff strain, bicipital tenosynovitis


- Bursa = subacromial subdeltoid bursitis


- Referred = neck, elbow, myofascial pain syndrome

Glenohumeral Osteoarthritis


- OA leads to? in the?


- symptoms mainly? relieved by? may be at?


- signs = limitation in? **


also tenderness to?

- OA leads to destruction of the articular cartilage of the joint space


- symptoms = pain with activity, may be nocturnal, may be relieved by rest


- signs = **limitation in AROM and PROM****, tenderness to palpation of the anterior and posterior shoulder

Imaging for Glenohumeral Osteoarthritis


- xrays see (6)


- irreg? narrow? sclerosis? OP? flattened?

- xrays see:


= irregular joint surfaces


= joint space narrowing


= subacromial sclerosis


= osteophytosis


= flattened glenoid


= cystic changes of humeral head

Treatment of Glenohumeral Osteoarthritis


- goal is to decrease? start? modify?


- rehab can include? (2)


- meds?


- interventional?


- surgical?



- goal is to decrease pain and inflammation, start rehab program


- activity modification


- rehab = ROM, rotator cuff strengthening


- medications = Tylenol, NSAID


- interventional = US or Fluroscopic-guided injections


- Surgical = total shoulder arthroplasty, Arthrodesis

Rotator Cuff Syndromes - Tendinopathy


- tendons become more? leads to? (2)


- symptoms? (2)


- signs include? positive (2)


- investigate with?


- treatment starts with? then? then do? with?

- tendons become swollen and hypercellular, collagen disorganization, weakness in tendon, can become calcified


- symptoms = pain with overhead activity, night pain


- signs = tenderness to supraspinatus tendon, painful arc, positive Neers and hawkins


- investigation with US, RI


- Treatment starts with activity modification, NSAID, US, then do rehab, GH stability, muscular strengthening

Rotator Cuff Tear


- any? most commonly?


- see pain with resisted? signs and symptoms?


- investigations?


- tratment starts with? then? then do with?

- any rotator cuff muscle, most commonly Supraspinatus


- see pain with resisted testing of other muscles, same signs and symptoms as tendinopathy


- investigations = US, MRI


- treatment same as tendinopathy, consider surgery for full tear

Subacromial Subdeltoid Bursitis

Rotator Cuff Impingement



Lumbar Axial Pain


- pain between?


- 10% develop from?

- pain between costal margins and gluteal folds


- lifetime prevalence up to 84%


- 80-90% of health care and social costs of back pain are for the 10% who develop from acute to chronic

Lumbar Anatomy


- 2 roles of spine?


- 3 joint complex with?


- 5?

- dichotomous role of spine = support and protection, flexibility as allows limbs to move


- 3 joint complex = intervetebral disc with vertebral endplates, 2 zygapophyseal (facet joints)


- 5 lumbar vertebrae (rarely 6)

Lumbar IV Disc


- inner is? 90%? throughout life? outer is? withstands?


- main function?


- axial load pushes one? stretches?

- inner NP = gelatinous, 90% water at birth, desiccates throughout life


- outer annulus fibrosis = concentric fibrous layers to help withstand strains


- main function = shock absoprtion


- axial load pushes on nucleus and stretches annulus fibers, if AF break, see herniated NP

Main Common Causes of Axial Lumbar Pain


- herniated? pathology at? (2)


- MFPS?

- herniated NP


- Zygophophyseal Joint Parhology


- Sacroiliac Joint Pathology


- Myofasical Pain Syndrome = Paraspina/ Gluteal Muscles

Less Common and not to be missed causes of axial lumbar pain



Approach to Mechanical Lumbar Axial Pain


- pattern guides? anatomic guides?

1) Pattern Bases Approach


= guides initial management




2) Anatomic Apporach


= guides late stage management

Pattern based Approach to Lumbar Back Pain


- evidence with?


- tools for?


- supporting?

- evidence review with expert opinion for areas with lack of evidence


- 2 page tool = history, physical, initial management, referrals


- supporting amterial of opioid risk tool, StarT back screening


- endorsed by Spine Society, Fam Phys of Canada

Classifying Mech LBP


- four different?


- 1 and 2 are? 3 and 4 are?

- four different patterns of mech LBP with anatomical correlates


- patterns 1,2 = back dominant symptoms


- pattens 3,4 = leg dominant symptoms

Patterns 1-4 - ask if? rule out? what increases typical pain? **

Red Flags of Back Pain - prform?


- neuro?


- infection?


- fracture?


- tumour?


- inflammation?

1) Neuro = motor or sensory loss, neuro deficits, CE syndrome = urgent MRI


2) Infection = fever, IV drug use, immune supprssed = XR and MRI


3) Fracture = trauma, OP, frgility fracture = Xray and CT


4) Tumour = hx of cancer, severe fatigue, weight loss = Xray and MRI


5) Inflammation = chronic pain, <45 yo, morning stiffness, better with exercise = rheum

Yellow Flags - are? questions include? (4)

- are psychosocial RFs for developing chronicity

- are psychosocial RFs for developing chronicity



Why Assess yellow Flags - 30-40% also develop?


- persistent pain causes? higher risk of?


- LBP x3 more likely?


- see beliefs of? relucatance to?

- 30-40% of patients with chronic back pain also hae depression


- persistent pain leads to depression, and those have a higher risk of developing neck and back pain


- LBP patients 3x more likely to have low physical and emotional function


- see fear avoidance beliefs = relucatance to engage in active rehab, must treat fear avoidance to reduce disability

Inflammatory BLP


- age? onset? pain when? improves with? morning stiffness? elevated?

- <40 year old


- insidious onset, 3 months +


- back pain in 2nd half of night


- improves with exercise


- moderate morning stiffness, 30-45 mins


- elevated inflamm markers

Mech LBP


- any? variable?


- with rest? morning sitffness? markers?

- any age, variable onset and features


- improves with rest


- short-lived morning stiffness


- normal inflamm markers

Ankylosing Spondylitis


- chronic? of the? affects?


- onset? gender? race?


- onset? lngth?


- AM see? improves with?


- 16+?

- chronic inflammation disorder of axial skeleton affecting spine and SI joint


- onset in late adolescence, early adulthood, M>F, more in whites


- symptoms:


= insidious onset of back pain at SI joint for 3x mnths


= AM stiffness, improves with exercise


= cervical ankylosis in those with AS for 16+ years

Ankylosing Spondylitis

- manifests as? (6)


- decreased? +


- serology?


- tests? (4)

- Manifestations = fatigue, weight loss, fever, iritis, aortitis, pulm fibrosis, CE syndrome


- Signs = + Schober's test, decreased chest expansion


- Serolgy = HLAB27 +, increased ESR, CRP, RF + , ANA negative



Ankylosing Spondylitis Imaging and Management


- imaging do? see? (6) bone? spine look?


- management - refer? give? (2)

I = Xrays = SI pseudowidening, scleorsis, bone resoprtion, bamboo spine, syndesmophytes, osteopenia


M = refer to rheum = education, PT, NSADIS, DMADS, ICS

Painful Spinal Structures = innervated structures


- bone? joints? disk? ligs? all?


- means they cause?

= bone = vertebrae


= joints = ZPP


= disk = only external annulus


- ligaments = ALL, PLL, interspinous


- muscles and fascia


- nerve root




**cause pain, can be targeted

Noninnervated Structures of Spine - Do not cause pain


- LF? IA? of disk?

- ligamentum flavum


- internal annulus


- disk = nucleus pulposus

Mechanical Lumbar Pain Syndromes



Herniated Nucleus Pulposus


- similar assess and management as? therapy is based on?


- if no nerve root? if NR impingement?

- similar A/M as cervical - usually extension based therapy program


- axial pain if no nerve root impingement


radicular and leg pain if NR impingement



Anatomical Diff between C and L Spine


- C - disk and nerve#? if hits C6/7


- L - hits nerve that is? if hits L4/5

- C = disc # = nerve # = ex/ C6/7 disc hits C6




- L usually hits nerve below disc level = ex/ L4/5 disc hits L5 traversing nerve root, not exiting L4

Diagnostic Testing for LBP - frequrntly?


- lab testing for?


- imaging based on?

- frequently unnecessary


- lab testing = as indictaed for infections, malignancies, other testable conditions


- imaging = based on disease, modality, availability, recomms

Indications for Imaging - Xryas


- done for ages? Hx (2)


- recent?


- progressive? prolonged?

- age <15 or >50 yo


- Hx of malignancy or unexplained weight loss


- Hx of fever, IC state of IVDU


- recent trauma (aside from low energy lifiting)


- progressive neurologic deficitis


- prologne durations of S/S

Indiciations for Imaging - CT, MRI


- for vertebral fractures, superior? all other soft tissue?


- LBP almost never see? as in MRIs?

- CT superior to MRI for vertebral fracture


- MRI superior for all other soft tissue pathologies




* 90% of MRIs for LBP are abnorma and only <2% of CTs for HA are abnormal making value of a negative test is nearly non-existent for LBP

MRI and Lumbar Spine


- is the?


- yet common to find? espec in?


- poor correlation with?


- hard to determine?

- modality of choice in evaluation of most spinal disorders


- incidental abnormal findings common within asymptomatic individuals (57-80% abnorms for those over 60 yo)


- poor correlation with symptoms, therapeutics, patient outcome


- hard to determine candidacy for spinal surgery

Imaging Recomms


- uncomplicated LMP?


- low velocity trauma, osteopor?


- cancer, IS =?


- radiculo = ?


- past lumbar surgery?


- CE syndrome?

- uncomplicated LBP = any


- low velocity trauma, OP = MRI without constrast


- Cancer, ImmunoSupp = MRI without contrast


- Radiculopathy = MRI without contrast


- Past Lumbar Surgery = MRI +/- contrast


- CE Syndrome = MRI without contrast

Lumbar Root Lesions - Root - Muscle - Reflex


- L2? L3? see? L4? see? L5? S1 is? see?



Role of EMG

- Nerve Conduction Studies = motor, sensory


- Electromyography


- H and F


- Structure vs Function

Herniated Nucleus Pulposis Treatment


- control?


- modalities? dont use in?


- rehab for? via? (3)


- meds (3)


intervention is for? give? or perform?

- control pain and inflammation


- modalities = heat, traction (CI in myelopathy), TENS


- rehab for spine stab = education, stretching, core strength (extension)


- Meds = NSAIDs, TCAs, Opiates


- Interventions = Steroid injections for leg dominant pain, decompression surgery

Etiology of Facet Joint- Meidated Pain


- O/ C/ Im/ Sp?

- overload


- capsular tears/ injury


- Synovial impingement


- Spondylosis



Symptoms and Signs of Facet Joint- Meidated Pain


- pain exac by? or by?


- signs is localized? no?


- pain can be?

- Symptoms = pain exacerbated by lumbar extension, rotation


- Signs = localized tenderness over facet joints, no neuro deficits




* pain can be referred in non-dermatomal distribution

Imaging and Treatment of Facet Joint- Meidated Pain


- imaging via?


- treatment = (3)


rehab with? interventions with? (2)

- Imaging = XR, bone scan, CT, MRI


- Treatment:


= acitivity mod


= pain management


= rehab program - flexion based exercises


= interventions = medial branch block = RF ablation

Spondylolysthesis is slippage of? relaitve to?


- spondylosis is?


- spondylolysis is?


-

- Spondylosis = OA of spine (facet)


- Spondylolysis = fracture of pars intercularis


- Spondylolisthesis = slippage of vertebral body relative to vertebral body below it

Spondylolysthesis Etiologies D/I/D/T/P/P

- dysplastic


- isthmic


- degenerative


- traumatic


- pathological


- post-surgical

Spondylolysthesis Symptoms and Imaging


- main symptom is? with?


- imaging (4)


- non-operative for?


- surgery for?

- Symptoms = low back pain +/- radicular pain


- Imaging = Xrays, bone scan, CT, MRI


- Tx - non-operative Grades 1-2, asymptomatic grade 3


- Tx - surgery for Grades 4,5, symptomatic Grade 3

Spinal Stenosis - Central - narrow? due to?


- hypertrophic? leads to?


- can affect? cause?

- narrowed vertebral canal


- because of facet arthritis, hypertrophied ligamentum flavum, disc encroachment, SL


- can affect spinal cord (possible neural ischemia)

Spinal Stenosis - Lateral


- narrowed? away from?


- can affect? via? (2)

- narrowed lateral elements (away from SC)


- can affect nerve roots (structural impingement, inflammation)

CSS and LSS Symptoms


- CSS symptoms is? can have?


- LSS syptom is? with possible?

- CSS Symptoms = Back Pain +/- neurogenic claudication


- LSS Symptoms = Back pain +/- radiculopathy

Neurogenic Claudication


- pain in? (3)


- relieved with? sign of?

- pain in buttock, thigh or calf


- relieved with sitting or leaning forward = shopping cart sign

Neurogenic Claudication vs Vascular - pain/location, exac riding bike? downhill? walking uphill? remission? assoc factors?

Vascular Claudication

- pain, location, exac, riding bike, downhill walking, uphill, remission, assoc. factors

- pain, location, exac, riding bike, downhill walking, uphill, remission, assoc. factors

Scoliosis - curvature of? symptoms? imaging? obtain?

- lateral and/or rotatory curvature of anywhere in C/T/L spine


- symptoms = back pain


- imaging - Xrays to obtain Cobb Angle

Causes of Scoliosis


- idiopathic?


- congenital? due to?


- neuromusc?

1) Idiopathic = most common = infantile, juvenile, adolescent




2) Congenital = due to embryologic deficit = myelomeningocoele




3) Neurmusc = DMD, assoc pulmonary, SC complications

Treatment of Scoliosis


- need to decide? depends on? (3)


- assessed by?

- surgical vs non-surgical


- depends on Cobb Angle, etiology, rate of progression


- shpuld be assessed by spine specialist

Cauda Euqina Syndrome Anatomy and Pathophys


- SC ends at? becomes? that still?


- pathophys is injury to?

- A = SC ends at L1-L2, becomes a horse tail below this level that still innervates lumbar and sacral segments


- Pathophys = injury of nerve roots forming the Cauda Equina

Etiology of CES


- (4)

- lumbar + sacral fractures


- pelvic ring fracture


- spondylosis


- large disc herniation

Symptoms of CES


- flaccid? sensory loss in?


- pain in? (3)


- dysfunction of? (3)


- saddle?

- flaccid paralysis in affected nerves


- dermatomal sensory loss


- pain = lumbar, buttock, perianal


- Bowel and Bladder dysfunction - retention, freq, incontinence ***


- sexual dysfunction


- saddle anesthesia

Signs of Cauda Equina Syndrome


- LMN? high post void?


- hypo? absent?


- emergency as need to?

- LMN weakness


- high post-void residual = urinary retention


- hyporelfexia


- absent bulbocavernosis reflex




** Manage by ER for surgical decompression

Vertebral Body Compression fracture Etiology (5)

- trauma


- OP, OM


- medicated related = coticos


- neoplasms

Vertebral Body Compression Fractures Symptoms


- have sudden?


- exacerbated by? (4)


- imaging?

- have sudden onset thoracolumbar pain


- exacerbated by Valsalva, turning in bed, coughing, incidental trauma (step oof curb)


- imaging = xrays, bone scan, CT, MRI

Vertebral Body Compression Fracture Treatment - restrict? manage? rehab for? consider?


- surgery sees? can lead to?

- acitvity restriction


- pain management


- rehab program - hyperextension


- bracing


- vertebroplasty in some acute


- surgery = 50% loss of vertebral height, instability, neurologic compromise

Sacroiliac Joint Pain Etiology


- (4)

- hyper or hypomotility


- repetive overload


- trauma


- capsular tears

SI Joint Pain Symptoms


- pain can be either? in (4)


- referred to?


- signs include? no?


- imaging?

- acute or gradual back, buttock, leg or joint pain


- painc an be referred in non-dermatomal distribution


- signs = localized tenderness over SI joint, no neuro signs, SI joint special tests


- imaging = xrays, bone scan, CT, mri

Treatment of SI Joint Pain


- mod of? manage? rehab on?


- interventional include (3)


- surgery for?

-activity mod


- pain management


- rehab program - core and hip girlde strengthening


- Intervention = articular injections, branch block, RF denervation


- surgical fusion

Causes of Lower Extremity Radicular Pain - True Radiculo


- main two?


- central vs lateral - see?

- disc herniation


- spinal stenosis:


= central = neurogenic claud


= lateral = radiculopathy

Masqueraders of Lower Extremity Radicular Pain (7)



Hip Pain - must consider?


- OA seen with? rathe than?


- always assess if? for? in (3)


- AN - most commonly from?

1) OA = most often groin rather than lateral thigh or buttock pain


2) Hip fractures = always assess if trauma, OP or elderly


3) Avasc Nec = most common from steroid use or alcohol use

Greater Trochanteric Pain Syndromes Symptoms and Signs


- pain of? (2) aggrav by? (2)


- signs = pain with? (2) positive?


- investigate with? MRI for? (2)

- Symptoms = nociceptive lateal thigh or psoterior gluteal pain, aggrav by activity, lying on affected side


- Signs = pain with restricted hip abductor testing, pain with palpation of peritrochanteric tissues (GT, abductor insertions, bursas, tenor fascia), positive FABER test


- investigate with US, MRI for tendinosis or tendinitis

Treatment of Greater Trochanteric Pain Syndromes


- Stage 1 = (4)


- Stage 2 = eccentric? focus on?


- interventional uses? for?

- Stage 1 = activity modification, NSAIDS, US, glycerul trin


- Stage 2 - rehab,, hip girdle stability, eccentric strengthening, lumbopelvic biomech


- Interventional = US guided injections for trohcnateric bursitis or intralesional injections

Take Home Points


- always screen for?


- most conditions treated with? (3) not?


- myofascial pain syndrome is a? cannot be??

- always screen for non mech sources of axial/lumbar pain


- most conditions treated with activity modificaiton, pain management and an active rather than passive rehab program


- myofascial pain syndrome is commin masquerader of radiculopathy and cannot be diagnosied on routine imaging



Take Home Points


- look for? as the can?


- red flags must be?


- always examine**

- lumbar pain yellow flags can identify patients who may have poorer outcomes for same condition


- lumbar pain red flags must be considered on every assessment


- alwaus****** examine patient with axial pain

Epidemiology of Immobility - hours sedentary - men? women? boy? girl? 4 of 5 Canadians dont?

- Men = 9.6 hours/day sedentary


- Women = 9.8 hours/ day sedentary


- boy = 8.5 hours


- girls = 8.7 hours




*4/5 Canadians do not meet the Canadian Physical Activity Guidelines

PA is bodily movement made by?


- measured in?


- exercise is a? has a?

- bodily movement produced by the contraction of skeletal muscle that increases energy expenditure above the basal level


- measured in metabolic equivalents (METs) = metabolic activity


- exercise = a form of PA that is planned, structured, repetitive, and purposeful with a main objective of improvement or maintenance of one or more components of physical fitness

Difference in Mets



Exercise Physiology


- focuses on?


- at rest? with exercise - burn?


- need?

- Energy Expenditure of a human


= @ rest = 1.2 kcal/ min


= intense exercise = 18-30 kcal/min = 15-25x


- ADP to ATP to allow exercise to continue

3 Pathways to Produce ATP


- for quick energy? for minutes? are?


- aerobic limited by?

1) Creatine Phosphate = 25-30 seconds (anaerobic) = spirting


2) Rapid glycolysis = 0.5-2 minutes (anaerobic) = weightlifting


3) Aerobic Oxidation = limited only by fuel (carbs, fat, protein) and oxygen (aerobic)

Muscle Physiology - Type 1


- speed? high in? innerv. by?


- rich? for low/long? slower?

= Slow Twitch


- high in oxidative enzymes


- innervated by slow motor units


- rich capillary supply


- for low intensity, long-duration exercise


- slower peak tension and relaxation

Muscle Physiology - Type 2 - speed?


- large? innerv by?


- for more? rapid?

= fast twitch

- large fiber diameter


- innervated by large, fast motor neurons


- for high intensity, short-duration exercise


- rapid peak tension and relaxation

Cardioresp. Physiology


- HR? SV? CO - change with exercise?

1) Heart Rate = resting (60-80 bpm), increases with relative workload, max HR decreases with age


2) Stroke Volume = reaches max at 50% of aerobic capacity then plateaus, higher in supine/ prone position, decreased in upright position


3) Cardiac Output = resting = 4-5 L/min, 20L with exercise

Cardioresp Phys - blood flow/ venous return/ BP / pulm vent - with exercise?

4) Blood flow = rest is 20% of CO, exercise is 90%


5) VR = contracting skeletal muscle as pump, diaphragm contraction lowers intra-thoracic pressure


6) BP = SBP increases with work intensity, can monitor inotropy of heart


7) Pulm Ventiliation = 15-25x in exercise > rest, increase in tidal volume then resp. rate

Benefits of Exercise - Physiological


- decreases? increases?


- increases in muscle?


- hypertrophy of? improved?

- reduction of BP in hypertensive patients


- increase in HDL, decrease in LDL, decrease in TG


- decrease in TBW


- increase in muscle glycogen


- hypertrophy of fast and slow twitch fibers


- improved capacity of ATP-Creatine phosphate system


- improved VO max

Benefits of Exercise - Specific Populations


- for renal? for schiz? for pain? for breast cancer? for anxiety?

1) Renal failure = lowers BP


2) Schizo = cognitive enhancement


3) Chronic pain = improves pain severity, QOL


4) Breast cancer = alleviates radiation fatigue


5) Anxiety = decreases anxiety




*at least 30 chronic diseases

Definitions - Forms of Activity


- PA is? sedentary is? moderate is? vigorous is?


- CSEP guidelines want?

PA = movement increasing heart rate and breathing


Sedentary = postures or activities that require very little movement


Moderate = 5-6/10 on personal capacity scale, can talk but not sing during activity


Vigorous = 7-8/10 on personal capacity scale, cant say more than a few words


- CSEP guideline - aim for moderate to vigorous acitvity = MVPA



CSEP Activity - want for toddlers? children? youth? adults?

- toddlers and preschoolers should get 180 minutes


- children 5-11 should get 60 minutes


- youth aged 12-17 should get 60 minutes


- adults should get 150 minutes

Canadian Association of Sport and Exercise Med Statement


- benefits of exercise are?


- NNT is? vs smoking cessation?

- beenfits of exercise = reduced BP, glycosylated hemoglobin, reduced risk of depression, improved cognition with dementia


- NNT = 12 to meet rec. guidelines, 4x lower than smoking cessation


- exercise prescription could save 2.1 billion $/year if adopted at population

CASEM Position Statement


- can be given like a?


- good for?


- tools?


- need to try to avoid?

- if healthy, progression to MVPA is safe and can be self-admin, like an OTC medication


- stable asymptomatic CV, metabolic, renal disease


- tools = step counts, texts, exergames


- exercise profs = avoid barriers to integration of daily PA, MDs should feel enabled to prescribe PA

Par-Q Pre-Participation Screen



Major Symptoms suggestive of Cardiopulm Disease



Exercise Prescription - FITT (P) - ASS


- FITT stands for?

1) Frequency = # of exercise session per day/week


2) Intensity = physiologic difficulty of exercise


3) Timing = length of exercise session


4) type = particular form of exercise


5) progression = increase in activity over time

FITT(P) - ASS Types of Exercise - ASS = types?

- aerobic


- strengthening


- stretching = flexibility

Exercise Prescription Aerobic ACSM


- FITT?

- frequency = 3-5x / week


- intensity = perceived exertion 13-16 "somewhat hard to hard"


- timing = 1 or more sessions of 10+ minutes, at least 150min/ week or 30 min/day


- type = large muscle groups engaged in rhythmic aerobic activity = walking, jogging, cycling, rowing, stair climbing, water exercise

Exercise Prescription - Strength ACSM - FITT?

- frequency = at least 2 days per week


- intensity = one set of 8-12 repetitions resulting in volitional fatigue for each exercise


- timing = the entire program should last no more than 1 hour (grater than 1 hr have higher dropout rate)


- type = perform a minimum of 8-10 exercises that train the major muscle groyps

Exercise Prescription - Stretching ACSM - FITT?

- frequency = at least 2-3 days per week


- intensity = mild degree of tightness without discomfort


- timing - stretches held for 15-60 seconds


- type = static, dynamic and PNF stretching of major muscle groups including the low back and posterior thigh

PARmed-X for Pregnancy - benefits include improved? promotion of? facilitaiton of? may prevent?


- want? attempt? no?

- benefits:


= improved aerobic and muscular fitness


= promotion of appropriate weight gain


= facilitation of labour


= may prevent glucose intolerance


= may prevent pregnancy-induced hypertension




* 3 times/week, attempt 15 minutes, not weight-bearing

Exercise SMART Goals - stand for?


-ex/

- specific, measurable, achievable, relevant, timed




ex/ I am going to be walking on the treadmill 3x a week for 40 minutes at a hard intensity by our follow up in 4 weeks

Summary of CSEP, CASEM and ACSM - Aerobic, Resistance and Stretching of F/I/T/T

- individualize via SMART goals

- individualize via SMART goals

Extreme Conditioning Programs (ECP) - includes?


- no high quality?


- benefits?


- case reports see?


- need further?

- crossfit, insanity, Gym Jones, P90x


- no high quality lit comparing to traditional


- benefits = muscle strength, endurance, aerobic fitness


- case reports see rhabdomyolysis and carotid artery dissection


- further high-quality studies needed

Immbolity - Muscle


- by day, decreases? by 9 days?


- plateua at?


- decrease endurance by decreasing? and?

- decreases strength by 1.0-1.5%/day


- as much as 30% with 9 days of bedrest


- plateau at 25-40% of original strength


- decreases muscular endurance by decreasing Type 1 fiber diameter and oxidative enzymes

Immobility on Bone and Joints


- OP due to? HC due to?


- decreased? from?


ligaments have less? increased?

- Osteopenia = lack of stress and tension on bone


- Hypercalcemia = excreted in urine = atrophy, fractures


- Decreased joint extensibility = cartilage deterioration from less nutrition


- Ligaments = decreased strength, increased compliance, increased collagen degradation

Immobility on Cardiac Function


- reduction in? postural?


- increased? decreased CV?


- increased risk of? from? (2)

- reduction in blood and plasma volumes


- postural hypotension = venous blood pooling


- increased resting HR, decreased SV = decreased CV efficiency, HR up by 0.5 beats/min/day, immob. tachy, see SV down


- increased risk of thromboembolism = decreased BV, increased coag.

Immobility on Other Organ Systems


- pulmonary? GI? GU?


- also see? (2)

- Pulmonary = decreased CE, diaphragmatic movement, reduced cough, bronchial ciliary activity, reduction in TV


- GI = constipation and loss of appetite


- GU = urinary stasis, increased risk of urolithiasis


- Integumentary = skin atrophy, pressure ulcers

Take Home Points of Exercise and Immobility


- exercise is? good for?


- can use tools for?


- importance of?

- exercise is medicine for everyone


- exercise is beneficial and encouraged in pregnancy with approp precuaitons


- pre-participation screening should be performed with approp. tools


- individualize patient's exercise program


- immob. negatively affects multiple systems

Physiatry is?


- focus shifts from?


- not just a?


- time limited?

- inpatient rehab here focus shifts from acute care to getting back to life


- not just a discharge destination


- time limited therapy with specific goals (like a Rx)


- not approp. for eveyone

Good Candidate fo SCI/ABI inpatient rehab?


- new loss of? patient is? also is?


- demonstrates ability to?


- requires at least?


- want to have?

- new loss of functional chnage


- motivated/interested in participating


- medically stable


- demonstrates ability to learn and retain skills


- requires at least two allied health services


- functional goals can be sustained in community

Elements of a Rehab Prescription


- physical = treating? used in?


- cognitive used in? includes?

1) Physical = TBI and SCI


= treating spasticity, mobility, pain, pressure ulcers, bowel/bladder function




2) Cognitive = TBI


= cognitive retraining, adaptation, aids

Elements of a Rehab Prescription


- behav- used in? uses? (3)


- functioning - used in? includes ideas like?

3) Behav/ Psychiatric (TBI and SCI)


= counselling, Mx, behavioural strategies, supports




4) Functioning/Community/Social Integration (TBI and SCI)


= transition from patient to person, redefining self, redefining roles, involving family, learning self-advocacy

SCI and TBI means?

SCI = spina cord injury


TBI = traumatic brain injury

Rehab Focus on? relearning? directing?


- examples? (5)

- functional goals as an inpatient and outpatient

- relearning ADL/IADLS or directing your care


- examples = self-feeding, walking, accessible enviro, accessible transporation, attendant care services, vocational, avocational goals, parenting, injury preventon, sexuality

Why is SCI and TBI rehab important - can affect?


- common causes? (4)


- are potentially?

- these injuries can affect anyone


- common causes of a SCI or TBI include:


= MVA


= falls


= medical


= violence


- potentially preventable


- annual cost = 3.6 billoon

SCI - causes of death? TBI is more common than?

- pressure ulcer cause of death in SCI


- TBI more common than AD and MS combined

Tetraplegia - impairment or loss of? in the?


- affects?

- impairment or loss of motor and/or sensory function in the cervical segments of the SC


- arms, trunk, legs and pelvic organs affected

Paraplegia - impairment or loss of? in the? (3)


- spared?


- affected? includes?

- impairment or loss of motor and/or sensory function in the thoracic, lumbar or sacral segments of SC


- arms spared


- trunk, legs, pelvic organs may be affected


- includes conus medullaris and cauda equina injuries

Skeletal Level vs Neurologic Level - Skeletal


- on xray can see? yet on neuro exam?


- skeletel level is level at which

- can see C5 burst fracture n Xray and C6 appearance on neuro exam


- skeletal level = level at which, by radiographic exam, the greatest vertebral damage is found

Skeletal vs Neuro - Neuro Level


- the most? with? on both?



- the most caudal segment of the SC with normal sensory and motor function on both sides of the body


- 4 segments identified

Importance of knowing the Neuro Level Post SCI - if C5 neuro level, cant? if C6 neuro level, cant?


Importance of Knowing Neuro Level Post SCI - ADLs - C5 vs C6 neuro level



Common Complications in SCI Rehab


- physical - main one? seen if SCI is?


- neurogenc? (2)


- PUs? pain that is? also see dysfunction of? bones?

1) Physical


= autonomic dysreflexia (SCI T6 or above)


= neurogenic bowel


= neurogenic bladder


= pressure ulcer


= neuropathic and nociceptive pain


= spasticity


= osteopenia/ osteoporosis


= sexual dysfunction




2) Psych/Psych = life adjustment, depression

TBI definitions - head injury may or may not?


- mild vs mod vs severe TBI = GCS of? can have? LOC?

= traumatic brain injury - head injury may or may not have brain injury


= mild TBI = concussion, GCS 13-15, LOC < 15 min


= mod TBI = GCS 9-12, LOC 15 min-6 hours


= severe TBI = incl. coma, GCS <9, LOC > 6 hours

Common Complication in TBI Rehab


- physical = (5)


- cognitive - main ones? (2)

1) Physical


= seizures, hemiplegia/spasticity, diplopia, hormonal complications, vertigo, fatigue, sleep distubs, HA/pain




2) Cognitive


= impaired arousal and attention**, learning and memory**, language and communication, executive function

Common Complication in TBI Rehab


- psych - main ones? (2)


- behav = (4)

3) Psych/Psychiatric


= depression**, anxiety, delirium**, psychosis, life adjustment




4) Behav


= apathy, agitation, disorganization, sexual dysfunction

- Unique concern in SCI


- is? is a? unique to? if it is at?


- risk of? (3)

- autonomic dysreflexia = is a medical emergency


- unique to SCI if it is at T6 or above


- risk of cardiac arrest, stroke, death

Autonomic Dysreflexia Symptoms


- occurs at?


- two main symptoms?


- PSNS symptoms seen? include? (4)


- SNS seen? include? (2)

- occurs at SCI at or above T6


- two main symptoms = 20-30 mmHg rise in SBP and pounding headache**


- see PSNS symptoms above SCI level = nasal congestion, sweating, chest tightness, flushing


- see SNS symptoms below SCI level = cold/clammy skin and goosebumps

Triggers of Autonomic Dysreflexia


- any potential?


- most common? then? other? (3)

- any potentially painful stimulus below SCI level


- bladder distention = 75-85%


- bowel distention = 13-19%


- other = DVT, menstrual period, cholelithiasis

Pathophys of Autonomic Dysreflexia


- potent? response? caused? increases? reduced - due to? get descending? that are only?

1) Potent painful stimulus below SCI


2) Sympathetic response


3) Generalized VC including splanchnic vasculature bed which is located below T6 = SNS


4) Increased BP = SNS


5) Carotid Baros reduce HR = PSNS


6) Get descending PSNS inhibitory signal that are only effective above SCI level

Treatment of Autonomic Dysreflexia


- sit? remove? monitor? every?


- BP >150 - give? such as?


- dont use? if?

- sit patient up as blood pools in legs


- remove the cause = bladder/bowel distention


- monitor BP every 2-5 minutes until symptms resolve


- if systolic BP > 150, give fasting acting antihypertensive (Nitropaste, Captopril) to reduce SBP <150


- * do not use nitrates if PDT-5 inhibis (slidenafil) used within 24 hours or vice versa

SCI - Neurogenic Bowel Routine


- diet? give? digital?

- diet = fibre and fluids


- laxatives and suppositories


- digital stimulation

SCI - Neurogenic Bladder Routine


- have intermittent? or use a?

- intermittent catheterization (every 4 hours or based on fluid intake)


- condom catheter

SCI and Pressure Ulcers


- need a? shift every/when? turn every/when?

- need skin pressure relieving routine:


= shift every 15 minutes when seated


= turn every 2 hours when lying in bed

Common Causes for Cognitive Decline post TBI


- main there = C/D/M - due to?


- must then?

= cerebral complication = seizures, hydrocephalus


= delirium = new enviro factors, new medications (sleep,pain) , new medical condition (UTI, hyponatremia)


= mood disorder




* do H/PE/rule out medical illness via lab and talk to family (see if fluct.)

Common Cognitive Impairments post TBI


- impairments in? (4)

- impairments in:


= arousal and attention


= learning and memory


= language and communication


= executive function

Dealing with Changes in Cognitive Function


- Remediation includes?


- compensation includes?

1) Remediation = manageable sub-tasks, cueing and redirection, overlearning


2) Compensation = electronic reminder system, work modification, pacing, safety dogs, engagement of family

Common Behavioural Impairments due to TBI - A/A/D/MI


- often are mislabelled as?

- apathy


- agitation


- disinhibition


- mental inflexibility/preservation


- often mislabelled as lazy, rude, stubborn, argumentative

Behavioural Strategies for Behavioural Impairments from TBI


- use simple? avoid? repeat? redirect?


- avoid (2)

- use simple directions


- avoid scolding


- repeat instruction


- redirect attention


- avoid environmental overstimulation


- avoid restraints = consider sitters, bed alarms, transponders (wrist alarm), locked units

Post-TBI Depression


- seen in about? RF for?


- may be confused with?


- predisposed by? such as? (3)

- depression = 25-60% in 8 years


- RF for poor recovery


- may be confused with cognitive deficits


- premorbid conditions may predispose = poor supports, coping strategies, PMHx

Causes of Post-TBI Depression


- chnages in? reduction in?


- see chnages in?


- increased TB severity doesnt?

- neurochemical/structural changes = see reduction in serotonin over time


- see changes in life situation


- *** Increased severity of TBI does not increase risk of depression

Time Course of Cognitive and Depressive Complaints Post TBI


- as time from TBI goes on, decrease in? increase in?

- as time goes on from TBI:


= see decrease in cognitive impairments from TBI


= see increase in depression causing cognitive complaints

SC and TBI Take Home Points


- after SCI - rehab based on? not?


- AD is a? also is?


- cognitive impairment post TBI can be?


- depression is?

1) After an SCI, rehab goals are based on the neurological level, not the skeletal level


2) Autonomic Dysreflexia is a potentially life threatening but treatable condition post SCI


3) Numerous factors can worsen cognitive impairment post TBI


4) Depression is common post TBI

What is Arthroplasty?


- refers to?


- in total? see that pelvic and femoral?

- refers to replacement of a joint with a prosthetic implant


- total joint arthroplasty = entire joint replaced


- sometimes interested in replacing bone leading up to the joint


- in total, pelvic and femoral sides not linked



What is Hemiarthroplasty


- only replacing? capped with? no?

- only replacing one side of the joint


- capped with a second larger head, need to add this second head to size mathc with the acetabulum


- no pelvic component

Total hip vs total knee replacement


- TH - dont need to? forces are?


- TK - need? to?

- TH = dont need cement or grout becuase the forces are mostly compression so they promote fusion


- TK = shear component on the parts, need cement as well to lock everything in

Athroplasty Technique Template


- done to detemine? first step is?


- match?

- done to determine the size of femoral and tibial prosthesis to optomize fit and fill on AP and Lay


- first phase is preoperative phase


- match the best components to each patient, use software to help with this but dont make custom components

Arthrplasty Surgical Technique


- need to? cut through?


- shape?


- have trial?

- need to expose knee joint, need to cut through quadriceps tendon


- shape distal femur to match back of femoral component


- have trial components during surgery

Conditions for Arthroplasty - (8) - #1?

- osteoarthritis = #1


- rheumatoid arthritis


- psoriatic arthritis


- AVN = hip, shoulder, knee


- post-trauamtic arthritis


- fractures


- bone tumours


- paget's disease

OA - most common? most disalbing? 95% of?

- most common arthritis with 3/4 of people with arthritis have OA


- 1 in 3 by 2040


- knee OA most disabling


- most joint replacements for OA = 95%

OA Indications for Athroplasty


- pain for? do?


- have to make sure?

- pain arising from OA


- history, PE, history


- need to make sure pain is in fact from OA


- may have psitive Xray findings but no symptoms

Knee OA history - pain is? may?


- agrav by? relieved by? no? onset?

- pain localized over knee


- may radiate to hip or shin


- aggrav. by prolonged activity


- relieaved by rest


- limitation of activity


- no neuro sympotms


- often insidious in onsent


- can cause radicular pain - vague pain radiating down leg

Hip OA History


- pain in? that may?


- aggrav by? releive by? no? onset?

- groin pain that may radiate to buttock, thigh, knee


- aggravated by prolonged activity


- relieved by rest


- limitation of activity


- no neuro symptoms


- often insidious onset


- pain radiating below knee may be due to neuro cause

PE in Knee OA


- look for? (6)


- reduced?


- typically dont see?

-mal-alignment


- varus/valgus


- antalgic gait


- joint line tenderness


- bony enlargement


- crepitus


- reduced ROM = extension


flexion contracture


- inflammation typically not present = no redness, swelling

PE in Hip OA - gait? lean to?


- legs? first lose? limited?

- tredelenberg gait - lean to affected side


- leg length discrepancy


- contracture


- first lose internatal rotation


- able to ext rotate, flex, abduct


- limited ROM

Diagnosis OA on Xray


- (4)

- see joint space narrowing


- see marginal osteophytes


- see subchondral scleorsis = response to arthritic friction


- may also see subchondral cysts

Varus vs Valgus - if lateral affected, alignment is? medial?

- if lateral component affected, get valgus malalignment


- if medial, get varus

OA Indications - if it is? effect on? night? failure of?

- if it is significant and disabling pain


- negative effect on QOL


- affecting sleep


- pain at rest and activity


- failure of med management

Nonop OA Mngmt - non pharm = (3), pharm = (5)

- non pharm = weight loss, activity modification, cane, physio


- pharm = acetaminophen, NSIADs, narcotics, topical, CS injections

OA Indiciations - Function - ask how? need to? dificulty in?

- walking distance = aks how far they can walk


- need for cane/crutch


- difficulty climbing stairs


- difficulty with shoes/ socks


- difficult foot hygiene


- work, hobbies, sport

OA Contraindications - ongoing? as can? is an?


- too?


poor?


- relative include?


- not candidate if?

- ongoing infections = absolute - infeciton elsewhere can seed prosthesis


- too young and active


- poor skin coverage around hip, knee


- paralyzed qaudriceps or abductor msucles


- NMD = relative


- severe mental dysfunction = relative


- serious physical disease


- extreme obesity, cardiopulm disease


- not candidate if they cannot do physio

OA Indications (4)

- patient choice


- subjective pain


- magnitude of quality of life compromise


- balance of benefit and risk

Athroplasty Benefits


- success rate of hip vs knee?


- benefit defined as?

- hip athroplasty = 95% success rate


- knee arthroplasty = 80% success rate




*benefit defined as a pain improvement after surgery to the extent that the patient says they would go through the same operation again

Complications/Risks of Arthroplasty - Early


- local (3) systemic (5)

- local = infection, neruvasc, hip dislocation


- systemic - mortality, transfusion, cardiac, stroke, DVT, pneumonia

Complications of Arthroplasty - Late - mainly?

- local = prothesis failure, revision surgery

Infeciton - occurs in? give?


- if infeciton, need to do a?

- approx 1% incidence of deep infection in primary THA and TKA


- approx 4% in revision TJA


- proph Abx have been critical to infection reduction


- see two stage revision - put in spacer filled with Abx, close wound, put on IV Abx for 6 weeks then need to be readmitted and have another knee replacement

Neurovasc Injuries


- injury to? most improve by?

- nerve injury


- primary 1-2%, revision 3-4%


- neuropaxia = 90% improve by 12 weeks


- vascular injury = 0.003%

Complications - Dislocation


- incidene related to?


- prine because of?


- also prone due to?

- incidence inversely prop. to surgical experience


- shallow cup for femoral head with an arthroplasty is prone to dislocation


- soft tissue (capsule, ligaments) restrains also removed during operation, also makes it prone to dislocation


- >50 THA / yr = 1.5% at 90 days


- <5 THA/yr = 4.2% at 90 days

Complications - Lossening and Wear


- life spaan of hip? knee? therefore if 50 years old?


- wear from?

- hip arthroplasty life span is about 15 years


- knee arthroplasty life span is 20 years


- 50 year old = 75% lifetime risk of revision


- 75 year old = 25% lifetime risk of revision




* excessive use can cause loosening, wear, as do more revision, see complications go up and success rate lowers