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36 Cards in this Set
- Front
- Back
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afferent |
from periphery. sensing |
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nociceptive pain |
pain resulting from stimulation of periphery nerve fibers nociceptors detect pain, cell body in dorsal root ganglia three types: thermal, pressure, chemical (capsaisin) two types of fibers: a delta fibers (fast, myelinated, low threshold) (thermal and mechanical stimuli), c fibers (slow, non myelinated high threshold (thermal, mechanical, chemical) (higher threshold) CRPU1- heat TRPM8- cold TRPA1- laceration/ puncture prostaglandins and histamines lead to release of substance p and signal to nerves. other neurotransmitters later are released to reduce signal propagation (gaba, enkaphilins) |
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acute pain |
protective mechanism. seconds to three months duration, intense onset and then decrease because of endorphins or enkaphalins that dampen it. anxiety and fear can affect it signs: tachycardia, hypotension, tachypnea, dilated pupils |
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neuropathies |
damage to pain pathways mononeuropathies- singular, one nerve or nerve bundle is injured from trauma, compression, injury. carpel tunnel nerve bundle from overuse, pain, sensory loss, weakness. |
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mononeuritis multiplex |
simultaneous involvement of several nerve trunks leading to loss of function of some nerves. asymetric (can occur in different body parts) can become more symmetrical. aching pain, deep, worse at night, lower back, hips, legs. diabetes, lyme, hiv, jelly fish stings |
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polyneuropathy |
damage to vasanervorum- arteries that supply blood to peripheral nerves diabetes sustained elevation in blood glucose levels leading to glucose binding to nerve proteins and activation of enzymes involved in vasoconstriction or oxidative stress that damages blood vessels and nerves. nerve death exedes ability to repair them. decreasing sensation to feet and lower extremities, balance problems, like walking on nails treatment: glucose control |
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dementia |
loss of global cognitive ability, static (one time event- from TBI) or progressive (alzheimer's) decrease in memory/ learning, depression, lack of feelings, inappropriate feelings, fixed dementia (from TBI, stroke, Wernicke's encephalopathy from thymine deficiency seen in alcoholism (thymine is important for myelin)) Wernicke's-ataxia, nystagmis (shaking of eyes), dementia (short term memory), fabrication- make up stories/ things |
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slow progressive dementia |
neurodegenerative, alzheimers, onset after 65 normally, slow, sporadic, genetic causes (0.1%), pathophysiology: protein misfolding (of APP- amyloid precursor protein)( which is important for growth and survival of neurons) (broken down into smaller amyloid proteins called beta amyloid which accumulates into plaques which induces apoptosis of neurons), Tau is also involved (microtubules of cytoskeleton)(bind to other proteins leading to tau tangles making nerve non functional) hippocampus (cingulate gyrus), frontal cortex are most effective inability to learn, cognitive decline, inability to express emotion, |
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dementia with lewy bodies |
neurodegenerative alpha synuclein protein is involved- clumps of this protein form- function of protein is unknown as is why they accumulate loss of neurons that produce acetylcholine and dopamine is the result leads to acute onset of dementia, parkinson's disease, fluctuating cognition (good days and bad days), blank expression, gate issues, reduplicative paramnesia (location has been duplicated, think that there is another hospital with the same people doing the same thing occurring at the same time) cause: sporadic, some genetic link to Park 11, poorly understood |
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creutzfeldt-jakob disease |
acquired, prion proteins, amyloids form-inappropriately folded fibrous proteins that form from otherwise normal proteins- disrupt tissue structure creating holes and spongy architecture. rapidly developing dementia, hallucinations, ataxia, myoclonus, no tests, treatment or cure |
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parkinson's |
degenerative disorder of substantia nigra (neuromelanin creates black pigment), produces dopamine, death of dopaminergic neurons, idiopathic (don't know the cause of most cases), 15% are genetically linked, mutations lead to lewy bodies, affects lots of areas in motor, memory, language, thought, limbic dopamine inhibits abnormal movements so without it there is a shaking tremor change in balance of dopamine (inhibitory) and acetylcholine (excitatory) signs: ataxia, tremor at rest, pill rolling (looks like rolling pill between first finger and thumb), bradykinesia, rigidity, cog wheel rigidity, postural instability (hypotension when standing leading to fall risk), neuropsychiatric- loss of emotion, inappropriate emotion, dementia, loss of memory history and physical exam to diagnose CT and MRI may play a role but not normally. |
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huntington's disease |
autosomal dominant of huntingtin gene, encodes for huntingtin protein which is important for signaling and protection of apoptisis, gene mutation leads to triplet of CAG which normally stabilizes protein. if greater than 35, huntington might ensue. mutated gene leads to abnormal protein which forms bonds with itself and other proteins to form protein aggregates which ccan be cleaved by enzymes to form neuronal intranuclear inclusions which are protective and help to disperse large aggregates, but reach saturation and leads to decrease in neuronal activity and death, mutated protein also affects chaperone protein which help to fold normal proteins and help to remove abnormally folded proteins. overproduction of glutamate leading to excitotoxicity and cell death. interaction with antiapoptic protein (Kreb) (delays programmed cell death) making it unavailable leading to early neuronal death s/s: after 35, personality changes, jerky random movements, abnormal facial expressions, chewing and swallowing problems, cognitive problems, depression treatment is symptomatic, walking aids, speech and swallow therapy, depression, help with movement problems no cure |
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myasthenia gravis |
autoimmune, neuromuscular, antibodies produced against nicotinic acetylcholine receptors involved in muscular contraction, also against MUSK- muscle specific kinase muscle fatigue, worse with activity, better with rest, droopy eyelids, generalized including diaphragm and respiratory failure, diplopia (double vision), dysphagia, upper and lower extremity weakness, thymoma- tumor of thymus gland diagnosis: history and physical exam, electrophoresis measurement of acetylcholine and MUSK antibodies (high level), electromyography where they try to induce muscular contraction, chest exray of thymoma, ice test* (eyelid drooping, ice over the eye normalizes the drooping) treatment: acetylcholine esterase inhibitors, immunosuppressants, remove antibody through plasma phoresis, IV Ig (immunoglobulin that binds to abnormal antibodies), surgery of thymoma |
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guillan-barre syndrome |
FDR might have had it. acute polyneuropathy, autoimmune, t and b cells respond to antigen that is mistargeted towards nervous tissue (molecular mimicry- foreign antigen and self peptide are very similar so t and b attack normal peptide), gangliocides are targeted (modulate and interpret cell signals) (look similar to actual antigen) (destroyed) infection is common predisposing factor food poisoning, influenza, influenza vaccine demyelinate neuron by attacking gangliocides- produces accending myloparalesis leads to respiratory paralysis treatment: supportive, mechanical ventillation, administer Ig IV against antibodies, plasmaphoresis to filter out antibody 80% recover within a year 5-10% have a permanent paralysis |
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multiple sclerosis |
inflammatory, autoimmune, myelin sheaths damaged, more common in females, onset in young adults in 20's, lesions and plaques that deposit into areas of myelin, ventricles, cerebellum, brain stem, basal ganglia, pathophys: destruction of oligodendrocytes that form myelin sheaths, disrupt myelin deposition, decrase conduction, overproduction of inflammatory modulator called interleukin 12 which transforms naive t cells into proinflammatory t cells process of remyelination early on which compensates and eventually this can't keep up and manifestation of symptoms reoccur disruption of blood brain barrier and t cells can enter- activates metaloproteases which attack proteins, inflammatory cytokines, activation of macrophages. cause is unclear, environmental (vitamin B deficiency), not genetic cerebrospinal fluid from lumbar puncture MRI to look for lesions that are enhanced s/s: parastigia (numbness/ tingling in extremities, muscle weakness, ataxia, dysarthria, speech, dysphagia, optic neuritis (transient, visual loss), uhtffsos (markedly worse symptoms with fever because of decrease in conduction of nerves as temperature increases) treatment: no cure, inhibitors of inflammatory and immune system (interferons), monoclonal antibody against disruptive antigens, symptomatic |
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mcdonald criteria |
helps to stage and quanitfy likelihood of multiple sclerosis |
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subarachnoid hemorhage |
secondary to head trauma or aneurysm, arterial bleeding in circle of willis, can live asymptomatically for a while until it ruptures (hypertension, catecholamine surge, sexual intercourse, cocaine, scary experience, sudden increase in pressure (lifting something heavy)) blood is under arachnoid layer so direct contact with brain tissue thunderclap headache worst headache of life pulsatile or steady occipital lobe is common place nausea/ vomitting, seizures, dilated pupil, hypertensive 85% are aneurysmal and normally in circle of willis barry aneurysm close head injuries diagnosis: CT imaging, less sensitive as time goes by, if they come by six hours after onset, lumbar puncture can be done to obtain cerebral spinal fluid to see RBC or hemochromatosis for breakdown of RBC (yellowish billirubin) treatment: recussitative, blood pressure decrease, seizure prophylaxis (prevents seizures), calcium channel blocker (for vascular spasm which can cut more blood off to surrounding areas) endovascular coiling- induces blood clot craneotomy- place clips to cut off damaged area of brain |
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platinum coils |
wire that is irritant to cuase blood clots to seal off aneurysm
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clipping |
cut into brain and put a clip in to snag off aneurysm |
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subdural hematoma |
traumatic- head injury disruption of bridging veins between meninges and dura no contact of blood with brain not immediately symptomatic (can be acute, subacute, or chronic)- irritation is less because not directly on brain acute is often the most lethal (acceleration/ decelleration injuries) (falls, motor accidents) 60-80% death rate, acumulates pocket of blood and pushes on brain surfaces chronic- takes days, weeks, or months, to develop because slow bleeding (minor trauma) (bump to head)- people prone to this have some space to bleed due to atrophy from age, alcoholism- decrease in consciousness, headaches, vertigo if in cerebellum, amnesia to the trauma, weakness, ataxia, asymptomatic clinical suspicion due to elderly who has fallen and has cognitive decline etc. CT scan to diagnose, when blood is white it is fresh, darker or black is subacute or chronic. treatment: chraneotomy and evacuation of clot if needed or observe patients who will reabsorb the blood |
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epidural hematoma |
pushes in one side of the brain accumulation between dura and skull or spinal cord secondary to trauma- coup contracoup injuries acceleration/ deceleration, direct blows especially to temporal bone (middle meningial artery) arterial bleeding in brain, spinal cord is normally due to procedure during epidural anesthesia, lumbar punctures (in spinal cord it is normally venous) cauda equina- bleeding expands to spinal nerves leading to weakness of legs, loss of bowel/ bladder control how does it progress: direct head injury, loss of consciousness, followed by lucid period, headache, relapse into coma may see fixed dilated pupil on injury side contralateral weakness on side opposite of injury severe- herniated brain- kushing's triad, very high blood pressure, bradycardic, kushmall's respirations (deep breathing pattern) CT imaging resuccitation efforts, hyperventilation if herniation is there, craneotomy (burning hole and draining off blood) |
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intraparenchymal hemorrhage |
bleeding within brain tissue, pathology: chronic hypertension leading to rupture of blood vessels, tumors leading to angiogenesis of new blood vessels, anticoagulant long term use, rupture of AVM (arteriovenous malformation- abnormal connection between vein and artery), RAS opathy (RAS is protein that controls signal transduction, mutations lead to disruption of growth and division leading to connection between artery and vein) s/s depend on area of the bleed: hypertension, change in mental status, abnormal dilated/ fixed pupil, nystagymus, aphasia, dysphasia, hemiparesis diagnosis through CT imaging resucitation, managing blood pressure, vitamin K and plasma to return clotting factors if called from anticoagulant |
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transient ischemic attack/ stroke |
TIA is a stroke like syndrome with no evidence of MRI damage to brain parenchyma (could last a minute or 24 hours) stroke is further defined as either from blood clot, hemorrhagic decrease in blood flow due to preexisting atherosclerosis embolic event thrombus- development of clot in local area hypotension- atherosclerosis is bad and decrease in blood leads to stroke |
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risk factors for embolic stroke |
hypertension, atherosclerosis, hyperlipidemia, diabetes, birth control pills, smoking s/s depend on area of brain: spinothalamic stroke leads to decrease in ability to receive and interpret pain, temperature touch brainstem leads to ataxia, nystagmus, ptosis, diplopia, cortex: aphasia, dysarthria, hemineglect relates to area of brain pronater drift- have put arms up and watch for one arm to fall ask them to smile, repeat simple sentence to look for dysarthria and aphasia, diagnose: CT imaging which won't show early stroke or TIA, but excludes hemorrhage. can pick up older strokes MRI with or without contrast to show change in tissue. resuscitation, TPA, breaks up clots, aspirin, antihyperlipidemics (statin), blood pressure decrease, weight loss, management of diabetes, smoking cessation |
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schizophrenia |
splitting of the mind breakdown of thought processes anterior cingulate cortex- involved in rational cognitive functions- abnormal shape and size can be genetic damage to oligodendrocytes dopamine theory treatment: dopamine antagonist haldol, abilify |
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stroop effect/ test |
say color of word rather than word itself, say how many words are in each box, excessive stimulation that alters perception (visual optical illusion making wheels spin), triangle without an actual triangle
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a delta fibers |
detect nociceptive pain very fast, well myelinated low threshold |
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c fibers |
slow, nonmyelinated, high threshold |
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what pain is protective in nature |
acute pain |
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somatic pain |
superficial, well localized, sharp, throbbing sprained ankle, fracture |
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visceral pain |
poorly localized, sharp, dull, stabbing, aching difficult to localize |
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referred pain |
pain signal that shares same spinal nerve segment as a different section of the body |
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kehrs sign |
irritation of the diaphragm which shares same signaling pathway as shoulder referred pain sign of MI |
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wegener's granulomatosis |
type of mononeuritis multiplex inflammation of blood vessels in granulomas and neutrophils antibodies may be responsible for inflammation arthritis, glomerulonephritis, conjunctivitis, pulmonary nodules damage vasculature that supply nerve bundles autoimmune disease recurrent respiratory infections wounds |
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reduplicative paramnesia |
belief that the place has been duplicated, existing in two or more places simultaneously |
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pronater drift |
have patient put arms up and watch if one arm begins to fall could mean embolic stroke |
