Term
| what is cerebrovascular disease? |
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Definition
| any abnormality of the brain resulting from a pathologic abnormality of the blood vessels or their contents. |
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Term
| what is a cerebrovascular accident (CVA)? |
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Definition
| the same as a stroke; a sudden neurologic deficit resulting from cerebrovascular disease |
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Term
| how do strokes differ from heart disease? |
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Definition
| heart disease, if not immediately fatal and survived does not usually incur lasting damage - whereas a stroke often will. |
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Term
| what are the 2 primary mechanisms of a stroke? |
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Definition
| ischemic (large artery thrombosis, cardiogenic embolism, small artery thrombosis, concurrent etiologies, idiopathic) and hemorrhagic (15% of strokes) |
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Term
| what are the 2 vascular systems supplying the brain? |
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Definition
| carotid: internal carotid covers 2/3 of the anterior brain (external carotid can provide some retrograde flow if internal is occluded). vertebrobasilar: more posterior, supplies brainstem and terminates at the posterior cerebral artery (which supplies the posterior portion of the cerebral hemispheres). |
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Term
| how does the state of the circle of willis affect stroke risk? |
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Definition
| if the pt has a more patent circle of willis, they are less likely to experience a stroke (loss of blood flow to the cortical area of the brain). most people have a patent anterior communicating artery = why anterior brain strokes are less common. |
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Term
| how does increased pCO2 (hypoventilation) affect cerebral vasculature? |
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Definition
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Term
| how does decreased pCO2 (hyperventilation) affect cerebral vasculature? |
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Definition
| vasoconstriction (this mechanism may be used to treat elevated ICP) |
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Term
| how does decreased systolic blood pressure affect cerebral vasculature? |
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Definition
| vasodilation. this is problematic for elderly pts w/atherosclerosis whose vasculature cannot dilate - which is problematic b/c HTN often causes strokes, but lowering BP can also cause a stroke. |
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Term
| what are the risk factors for strokes? |
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Definition
| HTN, cardiac disease (particularly a fib), hyperlipidemia, carotid stenosis, prior stroke, obstructive sleep apnea, smoking, alcohol abuse, physical inactivity, and fam hx. |
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Term
| what is the pre-motor cortex? |
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Definition
| the homunculus, which starts w/the toes in the longitudinal fissure, goes from the hip to the trunk, to the shoulder to the fingertips+thumb, to the face and larynx. |
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Term
| what is anterior cerebral artery syndrome? |
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Definition
| the anterior cerebral artery supplies the medial portion of the hemispheres, therefore a stroke here causes contralateral hemiparesis and hemisensory deficits in the leg and sometimes arm. |
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Term
| what is middle cerebral artery syndrome? |
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Definition
| the MCA supplies the lateral portion of the hemispheres and therefore a stroke in this area = contralateral hemiparesis and hemisensory deficits involving the face, arm and sometimes the leg. aphasia may result if the dominant hemisphere is affected. |
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Term
| what occurs with a stroke involving the posterior cerebral artery? |
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Definition
| the posterior cerebral artery supplies the occipital and posterior temporal lobes, therefore a stroke involving it may result in: contralateral homonymous hemianopia and/or receptive aphasia (if dominant hemisphere). |
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Term
| what may be seen w/a stroke involving the vertebrobasilar artery? |
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Definition
| b/c the basilar artery supplies the brainstem, pons, midbrain and occipital lobe (via the PCA), a stroke here = dizziness, diplopia, dysarthria, and locked in syndrome (large infarct in pons: reticular activating system which controls consciousness, but all descending motor pathways are dead - can move eyes) |
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Term
| what is a transient ischemic attack (TIA)? what imaging is used to dx? |
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Definition
| symptoms due to a stroke lasting < 1 hour and *no infarct on imaging. MRI is preferred. TSI = transient symptoms associated w/infarction. CITS = cerebral infarction w/transient symptoms. |
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Term
| how does the ocular syndrome associated w/a carotid TIA present? |
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Definition
| ocular syndrome: transient monocular blindness involving the R eye (graying of vision) if the R carotid artery is involved. since the R carotid also supplies the R MCA/ACA, they may also experience L-sided weakness and numbness. |
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Term
| how does a vertebrobasilar TIA present? |
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Definition
| 4 D's: dizziness (vertigo), diplopia (double vision), dysarthria (difficulty w/speech articulation), and dysphagia (difficulty swallowing). |
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Term
| what is the natural hx of TIAs? |
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Definition
| 1/3 of pts have a stroke w/in 5 yrs, 1/3 of pts have continuing TIAs, and 1/3 have no further TIAs. |
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Term
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Definition
| a scoring system for TIA risk. A: over 60 = 1 pt. B: BP > 140/90 = 1 pt. C: clinical features; unilateral weakness = 2 pts. and speech impairment w/out weakness = 1 pt. D: duration; > 60 min = 2 pts. and 10-59 min = 1 pt. D: diabetes = 1 pt. pts w/a score of 6-7 need to go to the hospital (8% risk of another stroke in 48 hrs). pts w/a score of 4-5 have a 4% chance = go to hospital. pts w/a score of 0-3 have a 1% chance = go home. if a small stroke is visible on MRI or TSI/CITS is apparent = 16% chance. *bottom line: if there is an event w/in 72 hrs and ABCD2 great than 3, then you need to bring the pt into the hospital.* |
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Term
| what is the hemodynamic pathophysiology of a carotid TIA? |
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Definition
| this requires a *residual carotid lumen of < 2 mm (normal: 1 cm), is often associated w/carotid bruit and requires an *impairment in collateral circulation. it is suggested by spells which are *short lived and *stereotyped (each successive spell is relatively similar in its anatomic distribution to the last). |
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Term
| what is the embolic pathophysiology of a TIA? |
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Definition
| emboli may arise from an ulcerated plaque and cause a carotid TIA. this is suggested by longer lasting spells (persistence of fragments) which may be more heterogenous (emboli may travel to different locations) |
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Term
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Definition
| antiplatelet agents: ASA (proved 48% reduction in stroke+death in men, some benefit in women), ticlopidine, clopidogrel, and aggrenox (aspirin and extended release dipyridamole). anticoagulants: heparin, coumadin, and dabigatran. |
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Term
| what is primary stroke prevention? secondary? |
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Definition
| primary: giving ASA to pts w/risk factors but no hx of TIA/strokes. secondary: giving ASA to pts who have had a TIA/stroke, which really isn't too effective in men, but may be in women. |
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Term
| what characterizes ticlopidine? |
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Definition
| a reasonably effective antiplatelet rx but has ADRs: neutropenia and pancytopenia |
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Term
| what characterizes clopidogrel (plavix)? |
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Definition
| this antiplatelet rx is the 2nd most common rx in the US as it reduces mortality from all causes of vascular disease (stroke, MI, PVD). it is taken 1x daily. |
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Term
| what characterizes ER dipyridamole + ASA (aggrenox)? |
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Definition
| this will reduce stroke incidence but can cause headaches. taken 2x/daily. |
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Term
| what is the summary of antiplatelet therapy rx efficacy? |
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Definition
| ASA is still good, but plavix and aggrenox provide a modest advantage. plavix/clopidogrel is the best as it has less bleeding, is taken 1x/day and is not associated w/headaches. ASA + plavix is not recommended for stroke prevention due to increased bleeding risk. |
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Term
| what is the only clear indication for anticoagulants in TIA? |
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Definition
| strokes from cardiogenic emboli (*A fib). anticoagulants may also be used in crescendo TIA (like unstable angina in brain) and/or antiplatelet failure. |
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Term
| what is carotid endarterectomy? |
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Definition
| cleaning out of carotid plaques. stroke risk is actually increased in the subsequent 24 hrs. |
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Term
| who is carotid endarterectomy indicated vs just ASA therapy? |
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Definition
| sx is superior to ASA in pts w/a hx of carotid TIAs/minor stroke and 70% stenosis of the ipsilateral carotid artery (pts w/less stenosis and TIA will benefit less and difference takes a few years to become apparent). |
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Term
| how does carotid stenting compare to endarterectomy? |
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Definition
| carotid stenting: higher risk of perioperative stroke, lower MI rate. endarterectomy: higher rate of perioperative MI, lower stroke rate and better for elderly pts (stent harder to put in more tortuous vessels). |
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Term
| what is the etiology of cerebral thrombosis? presentation? |
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Definition
| cerebral thrombosis is related to atherosclerosis of large and medium sized arteries and presents as a stroke preceded by TIA OR stepwise development of a stroke OR abrupt development w/fluctuating course. |
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Term
| what is a watershed infarction? |
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Definition
| a possible complication of a stroke due to cerebral thrombosis = hemodynamic hypoperfusion *w/o occlusion. ischemia may occur at the MCA-ACA border zone or the MCA-PCA border zone (fragile areas in terms of blood supply). |
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Term
| what is ischemic penumbra? |
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Definition
| the area of brain tissue which may temporarily be non-functional due to lack of perfusion but w/appropriate tx may recoverable. |
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Term
| what is acute ischemic stroke tx? |
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Definition
| BP management: BP often returns to baseline w/in several days w/out additional therapy and this is called permissive HTN. BP should not be acutely lowered unless systolic is about 200. aggressive tx of hyperglycemia and hyperthermia: both may increase metabolic demands of ischemic areas = expanded areas of cell death. *determine if pt is a candidate for thrombolysis. |
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Term
| what is the etiology for embolic infarctions? |
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Definition
| most common: cardiac due to A fib. also: acute MI (mural thrombus), severe CHF (mural thrombus), valvular disease (prosthetic, infectious, MVP), congenital heart disease, and artery-artery embolus. |
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Term
| what characterizes the presentation of an embolic infarction? |
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Definition
| a sudden deficit of onset (tend to be large clots which block large proximal vessels), other warning signs = uncommon. |
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Term
| what % of embolic infarctions will re-embolize w/in 2 weeks? |
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Definition
| 20% - which is why anticoagulant therapy is used |
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Term
| what is tx for embolic infarction? |
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Definition
| anticoagulation to reduce risk of re-embolization, then determine if pt is a candidate for thrombolysis (INR < 1.7). on CT if there is no blood/significant infarct, put the pt on heparin then long term coumadin. if there is blood on CT and a large infarct - wait 7-10 days (preventing the next stroke, large infarcts become more hemorrhagic w/anticoagulants) then put them on long term coumadin. |
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Term
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Definition
| this recently approved drug is superior to warfarin (fewer strokes, less bleeding) in prevention of strokes due to non-valvular A fib by direct inhibition of thrombin. it has no significant drug/good interactions and works quickly (12-24 hrs). |
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Term
| what is a lacunar infarction? |
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Definition
| a stroke due to occlusion of small deep penetrating arteries (arteriolar sclerosis or lipohyalinosis). this is one of the most common asymptomatic strokes and HTN/DM are risk factors. |
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Term
| what is the clinical presentation of a lacunar infarction? |
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Definition
| the most common type of lacunar infarction to be clinically evident affects the internal capsule = pure motor hemiparesis (no sensory deficits). that affecting the thalamus may cause a pure hemisensory deficit. if a lacunar infarction affects the basis pontis = clumsy hand dysarthria/ataxia hemiparesis. |
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Term
| what is the tx for a lacunar infarction? |
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Definition
| determine if the pt is a candidate for thrombolysis, and if not: antiplatelet therapy and aggressive control of BP after acute phase |
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Term
| what are the inclusion therapy for thrombolytic therapy? |
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Definition
| ischemic stroke, tx w/in 4.5 hours of symptom onset (very important to determine the last time the pt was normal: onset of symptoms), no hemorrhage on CT, and age > 18 y/o |
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Term
| what are contraindications for thrombolytic therapy? |
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Definition
| intracranial injury w/in 3 mos, any hx of intracranial hemorrhage, pericarditis, sx w/in 2 wks, GI/GU hemorrhage w/in 3 wks, bx w/in 1 wk, seizure w/stroke (not absolute), minor or improving symptoms (NIH score < 4), uncontrolled HTN (systolic > 180), stupor/coma/large deficit (NIH score > 22), coagulopathy (only if INR > 1.7), and glucose < 50 or > 400. |
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Term
| what is the risk/benefit ratio for tPA? |
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Definition
| if tPA is administered the pt has a 1/8 chance of being significantly improved and a 1/4 chance of some benefit - however there is a 1/18 chance of causing significant harm. after 4.5 hours from the onset of symptoms, any benefits from tPA are no longer available. |
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Term
| what are the AHA guidelines for prevention of a 2nd stroke? |
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Definition
| antihypertensive tx beyond hyperacute period (effective even in non-hypertensives), DM management, smoking cessation/avoidance of environmental smoke, reduce EtOH to 2 in men/1 in women, BMI to 18.5-25, 30 min of moderate intensity exercise on most days, if A fib: warfarin w/INR of 2-3, antiplatelet therapy (ASA, ASA+dipyridamole, clopidogrel), and statins (regardless of CHD/hyperlipidemia if not contraindicated). |
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Term
| what is the LDL target for stroke reduction/prevention? |
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Definition
| LDL: less than 70 or half of what it currently is |
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Term
| what is the 3rd leading cause of death and the number 1 cause of disability? |
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Definition
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Term
| look over scribe notes for stroke coordinator's stuff |
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Definition
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Term
| what is the leading killer in stroke pts? |
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Definition
| aspiration pneumonia (reason for dysphagia screening), followed by systemic infection then DVT/PE |
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Term
| what is tested in the NIH stroke scale? |
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Definition
| 1) level of consciousness/questions/commands. 2) best gaze. 3) visual fields. 4) facial weakness. 5) motor UE. 6) motor LE. (test bilaterally) 7) limb ataxia (judging a degree of ataxia that is unexpected for the degree of motor weakness). 8) sensory. 9) best language. 10) dysarthria. 11) extinction/inattention. this all adds up 0-30. |
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Term
| what are some misc causes of stroke? |
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Definition
| patent foramen ovale, vasculitis, carotid artery dissection, migraine w/aura, hematologic disease, and OCPs |
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Term
| what is the first thing which needs to be determined when presented w/a stroke pt? what are the next 2 necessary determinations? |
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Definition
| first determine: when onset of symptoms started (determines urgency and if tPA is on the table). next, determine mechanism via CT: ischemic (thrombotic/embolic/lacune) or hemorrhagic (ICH, MCA). then determine location/vascular territory: carotid (ACA/MCA) and vertebrobasilar (PCA, brainstem) |
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