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118 Cards in this Set
- Front
- Back
two main structural divisions of the nervous system
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central nervous system
peripheral nervous system |
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what are the two main divisions of the peripheral nervous system
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afferent - to brain from periphery
efferent -= to periphery from brain |
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what are the two main divisions of the efferent nervous system?
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autonomic - automatic
and somatic - voluntary |
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what are the two main divisions of the autonomic nervous system
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parasympathetic - cholinergic/rest & digest
sympathetic - adrenergic/fight or flight |
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what are the protective structures of the CNS?
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cerebrospinal fluid
bony structures meninges |
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what are the meninges and their purposes?
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dura mater: outmost, tough and thick layer
arachnoid space: not true space = potential space - only if pathology does space become evident pia mater: attached to brain, conforms to every sulcus/gyrus |
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where is the favored place for csf samling?
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from the large subarachnoid cistern at the end of the spinal cord at L1, L2
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what structure produces CSF?
How much CSF is produced every day? |
choroid plexus
500 mL/day |
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describe the arterial blood supply to the cns
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2 pairs of arteries
• Internal carotids (anterior circulation) • Vertebral arteries (posterior circulation |
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describe Production of CSF
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production independent of BP or intraventricular pressure
Will continue to produce even when circulation/absorption blocked -↑CSF with pathology=hydrocephalus |
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Which cells line the BBB? Which molecules get through
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*Cells that line CSF spaces: very tight, difficult to penetrate = **Blood Brain Barrier (BBB): astrocytes maintain integrity by extending “feet” to capillaries
Lipid-soluble molecules pass easier than water-soluble ones. Polar/charged molecules do not pass |
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General functions of:
• Cerebrum • |
Example: frontal lobe, motor cortex responsible for complex thought, behavior, morality
o Example: limbic structures: memory, emotion Broca/Wernicke’s Area: language Basal ganglia: coordination of movement • Parkinson’s disease pathology happens here |
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General functions of:
• • Cerebellum • |
Execution of movement, moment-to-moment adjustments (proprioception)
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General functions of:
• • Diencephalon • |
Thalamus, hypothalamus, pineal gland, hypothalamic extension to pituitary
• Hypothalamic extension: responsible for ANS functions (sleep, temperature, appetite, sex drive, regulation of BP, somolarity, blood O2 & CO2, pH, temperature |
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general functions of the brainstem
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“Stalk” between upper spinal cord and diencephalon
• Vital centers for respiratory/CV function |
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what is the vagus nerve significance. Which cranial nerve is it.
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Cranial nerve X (VAGUS NERVE) is critical to CV, resp, GI function
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afferent neurons lead from:
efferent neurons take information from to?: |
to brain from periphery
information away from CNS to periphery Muscles, glands, postganglionic |
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autonomic nervous sytem does what in general
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mediate autonomic or involuntary processes
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nicotinic receptors are part of which division of the nervous system and are located where?
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the somatic nervous system
skeletal muscle |
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nicotinic receptors receive what neurotransmitter and are excitatory or suppressor in effect?
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Ach - excitatory
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muscarinic receptors are part of which divition of the nervous system, and are located where?
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the parasympathetic ns
the autonomic organs |
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muscarinic receptors receive what nt's and are excitatory or suppressor in effect?
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Ach - suppressor
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differentiate between neurons and glial cells
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Neurons: generate + transmit impulses
• Glial Cells: supportive, don’t transmit impulses |
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what generates membrane potential in the neuron?
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K+ greater in ICF
• Na+ greater in ECF o K+ moves to ECF in concentration gradient, generates Membrane potential (-70mV); |
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what stimulates release of nt's
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Open voltage-gated Ca+2 channels simulate release of neurotransmitters…they move to next synapse, Na+ then rushes in, impulse moves down dendrite
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what enzymes break down Ach
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Acetylcholinesterase (AchE): quickly degrades Ach after release into synapse to limit duration of action. After degradation, immediately resynthesized
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what enzymes break down dopamine?
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Degraded by catechol-O-methyltransferase (COMT)
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what does dopamine affect?
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the CNS muscle regulation
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what is an example of abnormal dopamine metabolism
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parkinson's, schizophrenia
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what is NE degraded by?
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Degraded by catechol-O-methyltransferase (COMT)
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if a amine neutotransmitter is not broken down in ECF, can be broken down in presynaptic nerve by
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monoamine oxidase (MAO)
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List the amine neurotransmitters
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Dopamine (DA): CNS muscle regulation
Degraded by catechol-O-methyltransferase (COMT) Abnormal DA metabolism=pathology • Example: Parkinson’s, Schizophrenia o Norepinepherine (NE) Degraded by catechol-O-methyltransferase (COMT) o Epinepherine o Serotonin (5-hydroxytryptamine, 5-HT) Sleep, mood, pain control o Histamine o Endorphins |
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Ca++ channels allow:
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NT into the synaptic cleft
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define ischemia
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occurs when the delivery of oxygenated blood is below the level needed to meet the metabolic demands of the tissue "inadequate blood flow"
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define hypoxia
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a reduction in oxygen at the cellular level
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which comes first, ischemia or hypoxia?
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ischemia leads to hypoxia
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why is neuronal tissue especially susceptible to hypoxic damage?
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Has a limited capacity for anaerobic metabolism
during ischemia Uses 20% of total body O2 consumption Is dependent on glucose for ATP production Has little glycogen for storage |
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what is the mechanism of cellular damage from ischemia?
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ischemia leads to cell hypoxia. O2 is needed to accept electrons in the TCA/Krebs Cycle. with reduced ATP production and glycolysis running out, H+ accumulates and acidosis occurs. Also, mitochondria fail leading to impaired Ca++ pumps, cuasing Ca++ overload, leading to free radical production and cell death
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define CVA
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The onset and persistence of neurological
dysfunction lasting longer than 24 hours and resulting from disruption of blood supply to the brain |
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define hemorrhagic stroke
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Leakage of blood or blood vessel and hemorrhage into brain
tissue, which causes edema, compression of brain tissue, and spasm of adjacent blood vessels Can occur outside the dura, beneath the dura ( subdural), in 12 , ), the subarachnoid space, or within the brain substance itself (intracerebral) |
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define ischemic stroke
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Partial or complete occlusion of the cerebral blood
flow to an area of the brain |
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what are the two possible causes of ischemic strokes?
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Thrombus, most common, generally due to an
10 atherosclerotic plaque in a cerebral artery usually at a point of bifurcation, occurs over several days Embolic, a moving clot of cardiac origin, frequently from a-fib that travels quickly to the brain and lodges in a small artery, occur suddenly, immediate and maximum deficits |
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which kind of stroke is associated with a greater morbidity and what is it almost always caused by?
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hemorrhagic
caused by Hypertension |
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clinical manifestations of CVAs
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Severe HA, paresthesia, weakness, loss of motor
ability on one side of the body, difficulty in swallowing, aphasia (expressive, receptive, global), visual difficulties, loss of half of a visual field, double vision, altered cognitive abilities |
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what is the treatment goal for strokes?
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save the penumbra (the area of eschemia in which cells are still viable and have the potential to be saved via reperfusion (initiate RX within 3 hours)
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what is the significance of the optic nerve in a stroke?
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↑ICP leads to: HA, vomiting, altered LOC, blurry vision, papilledema (optic disc swelling that is caused by increased intracranial pressure), pupil responsiveness
to light |
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what is the cushing reflex
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last ditch effort of the body to maintain cerebral perfusion through clamped vessels = extreme somatic nervous sytem response which causes systolic blood pressure to rise above 200 mmHg
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Define TIA
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A transient ischemic attack (TIA) is an acute episode of
temporary and focal loss of cerebral function of vascular (occlusive) origin. TIAs are rapid in onset; symptoms reach their maximal manifestation in fewer than 5 minutes (usually <1 min). M if i f i bl d i d i ll l 2 15 27 Manifestations are of variable duration and typically last 2-minutes (rarely as long as 24 h). Most TIA durations are less than 1 hour; median duration is 14 minutes in the carotid distribution and 8 minutes in vertebrobasilar ischemia. Temporary reduction or cessation of cerebral blood flow adversely affects neuronal function in cortical, subcortical, and nuclear regions of the CNS. |
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what makes a TIA different than a CVA?
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Death does not occur directly from a single
episode of TIA. A TIA may be considered a sign of generalized atherosclerotic disease Blood flow is re established before infarction 28 re-takes place, “brain angina” TIAs are important warning signs of a potential impending stroke |
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what is meningitis?
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Meningitis is an infection of the linings of the
brain and ventricles. Can be fungal, viral, bacterial |
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what is the mechanism of infection in the meninges?
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Usually the brain is protected naturally from the
immune system by a barrier created by the meninges, the blood brain barrier Evolutionarily, this was seen as an advantage, since the barrier prevents the body from attacking itself b h h h f d h 30 However, bacteria or other organisms that have found their way into the brain are isolated from the immune system and can spread quickly. Once the body recognizes that there is an infection, as it tries to fight the infection, the blood vessels become leaky, and allow fluid, white blood cells, and other infection fighting particles to enter the meninges and the brain, causing swelling, decreased blood flow to parts of the brain, and worsening symptoms of infection |
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what are the routes of infection in meningitis
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Hematogenous spread
Nose and throat Localized extension otitis media sinusitis mastoiditis 31 extension, media, sinusitis, Bone fracture, head or neck surgery, penetrating bone injury, skull fracture |
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what is the triad of symptoms in meningitis?
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Meningitis develops quickly with a classic triad:
1. fever 2. headache 3. stiff neck developing over several hours to one to two days |
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what are other symptoms of meningits?
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Other symptoms include nausea, vomiting,
photophobia, mental status change, sleepiness Petichial, purpuric rash esp with N. menindititis Two classic signs: Kernig, Brudzinski |
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describe kernig and brudzinski
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Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip
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what cells would you see increases in a lumbar puncture lab result?
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↑Neutrophils, ↑protein,(decreased glucose)
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The principal damage from bacterial meningitis
is caused by the _____________ and not the ___________________ |
inflammatory reaction
pathogen |
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define parkinson's
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Parkinson’s disease is a progressive neurodegenerative
disorder associated with loss of dopamine neurons Named after James Parkinson, English physician who first described the shaking palsy in 1817 41 The underlying etiology is unclear, possible virus possible genetic susceptibility, possible toxicity from pesticides, repeated head injury or other unknown cause Idopathic vs. acquired (infection, intoxification, trauma) |
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Two pathways exist within the basal ganglia circuit, one
stimulatory the other inhibitory, which NTs are which? |
Stimulatory: Ach
Inhibitory: DA |
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what area of the brain is affected in Parkinsons'
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the cerebral cortex
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signs and symptoms of Parkinson's
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Tremor
the tremor he is noticed in the hands, feet, head, face, lips The most noticeable tremor he is pill rolling Rigidity This is the resistance to movement of both flexor and extents muscles through full range of motion jerky, ratchet like movement of the joints Bradykinesia slowness in the initiating or performing of conscious movements 45 Shuffling gait, no swinging of the arms with walking The face lacks emotional expression, poor link reflects Tongue, palate, and throat muscles become rigid, frequent drooling, speech becomes slow and poorly articulated Autonomic problems Orthostatic hypotension Excessive sweating, sebaceous gland secretions, salivation Swallowing delayed: aspiration risk Dementia |
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how is Alzheimer Disease diagnosed?
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R i hi l i l fi i l d
48 Requires histological confirmation, only done postmortem, but diagnosis can be made with high certainty based upon a progressive cognitive decline that is expressed in loss of memory, language skills, and activities of daily living |
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describe the pathophysiology of AD
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The classic neuropathological findings include
amyloid plaque neurofibrillary tangles 51 Tangles~ tau protein/neural thread protein Normally neural thread proteins bind/stablize microtubules-- essential for axon growth and development. In AD, tau twists into paired helical filaments called neurofibrillary tangles synaptic and neuronal cell death. Brain in AD=ATROPY Changes in Cholinergic System choline acetylesterase Ach synthesis |
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what are the changes you see in the cholinergic system of someone with AD?
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choline acetylesterase
Ach synthesis |
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describe the amyloid plaques in AD
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Beta amyloid protein
thought to cause O id i f li id 53 Oxidation of lipids Activation of apoptotic genes Disruption of cell membranes Forms insoluble plaques |
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describe the neurofibrillary tangles
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Neurofibrillary tangles are
deposited in neurons located in the hippocampus, temporal lobe, frontal lobe, leading to cell death |
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signs and symptoms of AD
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AD is a progressive dementia with memory loss as a major
clinical manifestation Language disturbance searching for words when naming objects is common and evolves into communication breakdown as the patient struggles with a very limited b l i l h i d d f t i l h i 56 vocabulary, nominal aphasia, and defects in language comprehension Behavioral problems are common throughout the disease process Early-stage disease shows disturbances of mood such as depression, anxiety Late stage and manifest as delusions, hallucinations, psychosis, aggression, and inappropriate sexual behavior End-stage disease has the patient in a vegetative like state, as cognitive activity ceases |
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cause of death in AD is usually from:
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accident/infection
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differentiate btw concussion and contusion
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Concussion
A sudden trauma induced alteration of the alert state No brain damage Contusion 59 damage the cerebral cortex by bruising CT will show necrosis, laceration, bruising Cerebral contusions tend to occur at the tip of the frontal and temporal lobes where they bang up against interior of the skull or the deep white matter can suffer diffuse axonal injury, which can stretch, tear the axonal connection |
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discuss coup and contracoup
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Contusion from direct
trauma Brain shifts side to side Shockwaves are sent to the brain matter Even though the skull may 60 not be penetrated or fractured, the forces imparted to the brain can cause the brain to collide against the inside of the skull, coup, and against the opposite area of the brain =countercoup. Both areas of the brain will be contused and subject to hemorrhage |
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define DAI
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or the deep white matter can suffer diffuse axonal injury,
which can stretch, tear the axonal connection Diffuse Axonal Injury (DAI) occurs more towards the center of the brain, where axons are subjected to maximal stretching, best example is a whiplash injury |
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describe whiplash and its relationship to shaken baby syndrom
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Whiplash, DAI
The brain consists of billions of nerve cells that communicate by way of axons 62 In a whiplash injury, stretching, twisting, and tearing of these axons and their connections can occur Shaken baby syndrome is the equivalent |
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define epidural hematoma
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EDH is a collection of blood which
occurs below the skull but above the dura This area of the brain is basically fluid and acts as a shock absorber The veins that feed and drain the brain which move through this area can be EDH area, torn, resulting in a bleed |
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s/s and tx of epidural hematoma
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These patients have a lucid interval
Patient is struck in the head, short period of unconsciousness, followed by wakefulness and seeming normality, then rapid deterioration This is from the gradual accumulation of blood in this area which presses on the brain over time, creating a mass effect Surgery is done to relieve the pressure, if the person has progressed to coma with GCS <9 |
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define subdural hematoma
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Between dura and outer
arachnoid membrane The source of the bleeding can b f d h b i SDH 68 be from damage to the brain itself, damage to a vein, More common in elderly patients after a fall The presence of blood directly under the brain tissue is thought to be an irritant to the brain, frequently causing a seizure |
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discuss the skull characteristics that make compensation difficult
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Skull is a closed system
Finite ability to compensate Brain parenchyma has little ability to volume CSF can shunt to venous system via arachnoid villi Blood vessels can vasoconstrict |
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what the ranges of ICP
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Normal = 0-15mmHg
> 20 abnormal >40 = neurological impairment ( decreased level of consciousness, problems with breathing, pupil dilation, compression of bringing on MRI, abnormal EEG >60 = fatal |
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what does high ICP cause?
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High ICP will
deform the brain and push tissue in such a way as to cause herniation, or a shifting of the brain tissue under pressure, which is tearing and stretching neurons |
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what is herniation in TBI
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Complication of ↑ICP
Protrusion through opening in dura mater |
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Glasgow coma scale ranges
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GCS =
Eye+Motor+Verbal 15 = WNL Mild head injury = 13-15 76 pp p 2 incomprehensible sounds 1 no response Moderate head injury = 9-12 <8 severe head injury |
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which is worse decorticate posturing or decerebrate?
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decerebrate
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what is the common denominator with all migraine headaches
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Common denominator is meningeal instability/hyperexcitability that releases
several neurotransmitters: Dopamine Serotonin Histamine Prostaglandin All of these mediate the inflammatory response and cause vascular dilation |
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signs and symptoms of migraines
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85% of migraineurs have HA without aura
Pulsatile, unilateral (but can be bilat), throbbing, lasts 1-2 days, inc pain with physical activity, +n/v from pain, photophobia, inc sound sensitivity 15% f i i h HA i h a ra 79 of migraineurs have with aura All of the above symptoms plus aura Spots, flashing lights, zig-zag/wavy lines cutting across visual field Aura lasts < 1 hour |
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what is the significance of vasodilation in migraine?
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Vasodilation causes more meingeal irritation trigeminal
instability NT release vasodilation… and a vicious cycle is born which causes a self-sustaining HA that can go on for days So, a migraine is a neuro-vascular disorder at heart and is treated as such |
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define multiple sclerosis
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Primary demyelinating disease, acquired,
recurrent, multifocal often presents with optic neuritis but can present with any neurologic abnormality 82 any white matter can be involved, usually periventricular, brainstem, optic nerve (optic neuritis onset at any age, peak 20-50, females 2x times more likely to get than males |
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3 s/s
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3 major symptoms: nystagmus, intention tremor,
scanning speech (monotonous or slurred speech |
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describe optic neuritis in MS
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optic neuritis - papillitis acutely - central scotoma, decreased
visual acuity, Marcus-Gunn pupil, unilateral papilledem |
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what is the significance of placques in MS
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MRI is diagnostic, looking for placques in the white matter on CNS
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seizures are
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Transient neurological events
Excessive cortical electrical discharges Skeletal motor Fx Sensation Autonomic visceral Fx Behavior Consciousness Idiopathic, or with a known cause Environmental/physiologic/psychosocial |
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define epileptogenic focus
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Neurons form an epileptogenic focus
Area in brain where seizure begins Functions autonomously, emitting ↑↑discharges Can recruit neurons from opposite hemisphere Partial=focal; part of brain surface affected Generalized=entire brain surface affected |
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what happens if seizure is not treated in status epilepticus
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Continued seizures without recovery period
Can be life threatening! If not treated for 30-40 minutes Ischemic brain damage |
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#1 nursing intervention in seizures
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#1 PROTECT AIRWAY
#2 Protect from injury |
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significance of aura/prodrome in seizures
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Aura/Prodrome associated with seizures
Subjective sense of impending seizure Prodromal period: HA, myoclonic jerking, lethargy, mood change, palpitations, epigastric sensations Can last several hours Aura: odd sensory experience before seizure Patient remembers this after recovery |
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what are the psycotic illnesses
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schizophrenia
delusional disorder depression bipolar disorder |
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what are the non-psycotic illnesses
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anxiety disorders (panic d.o, ocd)
personality d.o.'s eating disorders |
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NT comprimised in Schizophrenia
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dopamine
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definition of Schizophrenia
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Disturbance/deterioration of cognitive, social, emotional functioning
More of a syndrome than a single illness |
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Pathophys of schizoprenia
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Exact cause unknown. Probably presynaptic dysregulation of DA in D1 and D2 receptors. Excessive DA D2 receptor activity produces more noticeable symptoms
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s/s of schizophrenia
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Disorganized thinking, unusual speech (invented words), odd behavior, delusions, hallucinations
Delusion=systematic fixed false beliefs. Can be religious, grandiose, and persecutory Neologisms=invented words with invented special, private meanings Hallucinations: breakdown of perceptual selectivity, can affect 5 senses anhedonia absence of pleasure, interest Self-identity disturbance= lack of identity; cannot tell self from others Autism=profound detatchment |
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NT comprimised in Delusional D.O.
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dopamine
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definition of delusional d.o.
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Similar to schizophrenia. Systematic false beliefs. Persist despite evidence demonstrating otherwise. Can dramatically reshape personality and character. Person’s life shapes the delusion; life then confirms the delusion. A defense mechanism?
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s/s of delusional d.o.
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Systematic delusions/not bizarre
Impaired reality testing |
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NT comprimised in depression
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serotonin (5-HT)
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definition of depression
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A multi-faceted disorder characterized by: Low energy, inability to experience joy, difficulty initiating tasks, reduced decision-making ability, difficulty sleeping, poor appetite, weight loss, and decreased libido. Thoughts may focus on guilt, futility, emptiness, hopelessness, helplessness, and suicide
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pathophysiology of depression
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Low CNS 5-HT transmission: brain serotonin activity via excessive pre-synaptic uptake. OR, could be through stress-related down regulation of post-synaptic receptors
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s/s of depression
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Sleep disturbance (melatonin from Pineal Gland)
Depressed mood; loss of interest (anhedonia), fatigue not relieved by rest, restless/irritable/agitated/pacing, impaired concentration, low self-esteem, negative thinking, vegetative state, appetite disturbance, psychosis |
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difference btw minor and major depression
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Minor depression: symptoms usually resolve in 1-2 years. Also known as dysthymia
Major depression: symptoms last for 2+ years |
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NT comprimised in Bipolar d.o.
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Serotonin, Norepi (NE), Dopamine
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definition of bipolar d.o.
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Depression and/or elation (mania), often mistaken as schizophrenia. A mood disorder connected to diencephalon dysfunction.
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pathophysiology of bipoloar d.o.
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Neurotransmitter deficit~depression
Neurotransmitter overactive~mania |
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s/s of bipolar
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Mania, or hypomania. Depression, or euphoria
Seemingly limitless energy level, impervious to fatigue Speech disturbances, hallucinations/delusions, impulsive action, impaired judgment, sleep disturbance, hypersexuality. Appetite decreased because they are too distracted to eat |
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NT comprimised in anxiety do's
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5HT primarily
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s/s of anxiety do's
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Panic 5HT Physical (resp. distress, palpitations, choking); Fearful; exaggerated startle response
Generalized GABA, NE, 5HT Muscle tension, sweating, palpitations, Uncontrollable worry OCD 5HT, DA Compulsions (repetitive rituals), Obsessions (uncontrollable) |
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NT compromised in personality do's
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HPA axis, 5HT
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s/s of personality do's
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borderline = Combination of psychosis/neurosis, alienation, impulsiveness; Manipulation, self-harm, Devalues others (splitting)
Antisocial = “psychopath”, “sociopath”, disregard for others |
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NT compromised in Eating do's
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NE, 5HT, DA
Related to depression |
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s/s of anorexia
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Severe ritualistic restriction of caloric intake, binging/purging, body dysmorphia; cardiac arrhythmias, K+
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s/s of bulimia
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Binging/purging
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