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WI18 Neuro > Cerebrovascular Dz > Flashcards

Cerebrovascular Dz Flashcards

1
Q

anterior circulation

A

anterior and middle cerebral arteries

arise from internal carotid

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2
Q

posterior circulation

A

vertebral a. –> basilar a. –> posterior cerebral a.

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3
Q

posterior circulation supplies

A

thalamus, brainstem, cerebellum

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4
Q

stroke

A

acute loss of brain function due to disturbance in blood supply to brain/brain region

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5
Q

potential causes of strokes (6)

A 
arterial thrombus
arterial dissection 
embolism 
systemic 
hypoperfusion 
hemorrhage
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6
Q

stroke due to embolism/thrombus

type

A

CVA

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7
Q

stroke due to hemorrhage type of stroke

A 
intercerebral hemorrhage (ICH)
subarachnoid hemorrhage (SAH)
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8
Q

ischemic stroke etiologies

A

include embolism, thrombus, systemic hypo perfusion (shocK)

80% of strokes

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9
Q

hemorrhagic stroke

A

bleeding of brain causing decreased perfusion downstream from bleed + mass effect of blood and irritation of tissue

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10
Q

TIA

A

focal, ischemic neurological event without infection visible on imaging (typically lasts 1 hr)

reversible ischemia, <24hrs

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11
Q

TIA is a risk…

A

pts with TIA have an increased risk of CVA

esp. in first 48 hrs**

can be a sign to adjust some risk factors, or come in ASAP next time

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12
Q

important to ID TIA bc

A

can mimic an evolving CVA

CVA and TIA both have relapsing/remitting presentations

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13
Q

differential ddx of TIA

A 
focal seizure
Todd's paralysis 
cerebral tumor 
complex migraine
hypoglycemia 
syncope
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14
Q

Todd’s paralysis

A

transient neurological defect that follows a seizure

typically weakness of hand, arm, leg

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15
Q

TIA management (as a PCP)

A

most TIA patients should go to the hospital

To determine management: ABCD2 algorithm to predict CVA in 48hrs following TIA

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16
Q

ABCD2 score recommendation

A

hospital eval if >3

Outpatient eval 0-2 (if can be done in 48hrs)

hospitalize if thought other dz causing

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17
Q

TIA workup

A
  1. EKG/Echo (looking for AFib)
  2. Lab evaluation (CBC, PT/INR, PTT, Chem Panel, glucose)
  3. Neuroimaging
  4. Neurovascular studies
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18
Q

cardiac rhythm evaluation TIA

A

12 lead EKG and possible 2D echo

looks for L atrial thrombus

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19
Q

neuroimaging TIA

A

MRI NON CONTRAST ***

CT w/IV contrast can be done

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20
Q

TIA management (following work up)

A

ER admission for 1 day (outpatient management 48hrs)

no etiology determined = secondary prevention

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21
Q

CVA epidemiology

A

highest risk in BLACKS, OLDER, MEN

2nd MC cause of death worldwide, 3rd MC cause of disability

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22
Q

non modifiable risk factors for Ischemic TIA

A

older age
race (black) sex male

Fibromuscular dysplasia, Sickle Cell, Migraine

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23
Q

modifiable risk factors for Ischemic TIA

A

HTN, DM, cardiac DZ, dyslipidemia, elevated homocysteine levels, OCs

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24
Q

neurovascular studies TIA

A

anterior: carotid ultrasound, CTA
posterior: MRA

this is a SCREENING procedure

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25
Q

risk factors for thrombosis ischemic stroke

A

cardiovascular risk factors (I.e. HTN, DM, age, smoking)

rupture clot and get in situ thrombosis of cerebral arteries

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26
Q

common etiologies of embolic TIA/CVA + source/cause (4)

A

cardiac emboli (AF, mural thrombus, endocarditis)

peripheral emboli (DVT + atrial septal defect)

arterial emboli (carotid a. stenosis)

fat emboli (break long bone)

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27
Q

uncommon TIA/CVA causes

A

blood vessel disorders (inflammation, vasospasm, compression, dissection)

hematologic causes (sickle cell, hyper coagulable, polycythemia vera)

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28
Q

CVA patho

A

interruption of blood flow - decreased supply of oxygen and glucose to the neurons

  1. Swelling of neuron (ion channels fail causing edema) causes release of free radicals that degrade neighboring cells
  2. Extracellular edema (decreased fluid removal from space) = vasogenic edema
  3. liquefaction necrosis and breakdown of affected tissue = parenchymal brain tissue loss
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29
Q

s/s of ANTERIOR loss (carotid)

A

weakness/numbness/paresthesia of contralateral extremities or face

aphasia

dysphagia

vision loss ipsilateral

flaccid weakness, hyperreflexia

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30
Q

vertebrobasilar CVA s/s

A

POSTERIOR

vertigo

diplopia

perioral numbness/paresthesia

dysarthria

ataxia

drop attacks

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31
Q

Broca’s aphasia

A

expressive aphasia

inability to communicate in full sentences/FORM fluent speech

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32
Q

wernicke’s aphasia

A

receptive aphasia

inability to comprehend speech

speech will have no relationship to consent of conversation

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33
Q

ataxia

A

loss of voluntary coordination of muscle movements

cerebellar strokes

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34
Q

apraxia

A

inability to execute learned purposeful movements

not due to sensory loss, incoordination, or weakness

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35
Q

dysmetria

A

type of ataxia characterized by lack of coordinated movement (I.e. overshoot/undershoot)

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36
Q

homonymous hemianopsia

A

unilateral field of vision loss

same field on same side in both eyes

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37
Q

lacunar infarction + areas commonly affected

A

infection of small arteries that come off the MCA (penetrate deep into brain)

most commonly affects basal ganglia, subcortical white matter, pons

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38
Q

lacunar infarction associated with + where affected

A

poorly controlled HTN + DMN

MC affects basal ganglia, subcortical white matter, pons

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39
Q

MC types of Lacunar infarctions

A
  1. pure motor hemiparesis
  2. pure sensory
  3. sensorimotor
  4. ataxic hemiparesis
  5. dysarthria-clumsy hand syndrome
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40
Q

ataxic hemiparesis

A

ipsilateral weakness and gait ataxia out of proportion to motor deficit

type of lacunar infarction

41
Q

dysarthria-clumsy hand syndrome

A

type of lacunar infarction

facial weakness, dysarthria/dysphagia and weakness/clumsiness of the hand

42
Q

signs of cerebral stroke

A

cranial nerve deficit
aphasia
dysarthria

unilateral weakness/paresthiesia/snesory loss

43
Q

signs cerebellar stroke

A

dysdiadochokinesia
imbalance
tremor
coordination difficulties

44
Q

infarct of corticospinal tract

A

from cerebral hemisphere

deficit will be on contralateral side

45
Q

anterior cerebral artery

A

frontal lobes

disinhibition
AMS
impaired judgement
urinary incontinence

weaknesss and sensory loss in CONTRALATERAL leg&raquo_space; arm>face

46
Q

middle cerebral artery infarct

A

dominant source of blood supply for cerebral hemisphere

Contralateral arm/face>>>> leg 
Homonymus hemianopsia 
Aphasia
Neglect 
Gaze preference to side of lesion
47
Q

posterior cerebral artery infarct

A

Diplopia
Dizziness
Dysphagia
Dysarthria

+thalamic syndrome

48
Q

thalamic syndrome

A

contralateral hemisensory disturbance and development of spontaneous pain and hyperpathia

49
Q

cerebellar signs

A

infarct of vertebral/baslar a. and cerebellar a.

dizziness, diplopia, ataxia vertigo, nystagmus

50
Q

hallmark finding of cerebellar stroke

A

crossed findings

IPSILATERAL cranial n. deficits and CONTRALATERAL motor deficit

51
Q

TIA/CVA standardization assessment

A

NIHSS

allows you to quantify neuroimpariment/localization of stroke

lower number = less severe

does NOT measure posterior infarct

52
Q

neuroimaging of TIA/CVA

A

CT Non Contrast in ER

diagnostic: MRI non contrast

+ carotid US, CTA, 2 D echo

53
Q

why do we CT first? TIA/CVA

A

rules out hemorrhage, tumor, and really large stroke

DOES NOT show changes in early stroke

54
Q

first decision to make with a stroke pt

A

thrombolytic therapy?

55
Q

goal of TIA/CVA management

A

rapidly restore blood flow to ischemic areas not yet infarcted

best thing we can do is move quickly

56
Q

IV thrombolytics TIA/CVA + risk

A

approved to restore blood flow BUT

risk of hemorrhagic transformation = more morality and worsen outcomes

57
Q

IV thrombolytic used in stroke + risk/reward

A

tPA/Alteplase

6% risk of conversion, but 50% no disability 3 months post stroke

58
Q

time line for IV thrombolytic therapy

A

must be within 3-4.5 hrs of stroke ONSET (after realization, trip to ER, diagnosis)

59
Q

inclusion criteria for IV thrombolytic tx

A
  1. clinical stroke diagnosis
  2. age > 18
  3. time < 4.5 hrs
60
Q

exclusion criteria for IV thrombolytic tx (8)

A
  1. stroke/head trauma <3 months
  2. any hx of hemorrhage
  3. intracranial neoplasm, AVM, aneurysm
  4. recent intracranial/intraspinal sx
  5. hypoglycemia, HTN >185/110
  6. active internal diathesis
  7. recent heparin use
  8. Coumadin use (INR >1.7)
61
Q

mechanical thrombectomy

A

surgical intervention

grasp and aspirate clot or deliver clot lysis and restore blood flow

62
Q

anti platelet options TIA/CVA

A

ASA
Clopidigrel (Plavix)

Dipyridamole/ASA (Aggrenox)

63
Q

ASA TIA/CVA

A

decrease mortality, repeat stroke risk, and death

325 mg po or 300 mg rectal ASAP

64
Q

Clopidigrel (Plavix)

A

just as effective as ASA in secondary prevention

pro-drug (must be metabolized)

75mg/day

65
Q

Anticoagulant options TIA/CVA

A

given if cardioembolic source

Warfarin (INR 2-3, AVR 2.5-3.5)
Dabigitran (pradaxa)
Apixiban (eliquis)
Rivaroxaban (Xarelto)

66
Q

anti platelet options TIA/CVA

A

ASA
Clopidigrel (Plavix)

Dipyridamole/ASA (Aggrenox)

67
Q

ASA TIA/CVA

A

decrease mortality, repeat stroke risk, and death

325 mg po or 300 mg rectal ASAP

68
Q

Clopidigrel (Plavix)

A

just as effective as ASA in secondary prevention

pro-drug (must be metabolized)

75mg/day

69
Q

Anticoagulant options TIA/CVA

A

given if cardioembolic source

Warfarin (INR 2-3, AVR 2.5-3.5)
Dabigitran (pradaxa)
Apixiban (eliquis)
Rivaroxaban (Xarelto)

70
Q

HTN management TIA/CVA

not using tPA

A

keep BP where it is

carotid auto regulation has adjusted to this BP

sudden correction will cause worsening of stroke due to hypo perfusion

71
Q

HTN goal no tPA TIA/CVA

A

170-220/100-120

72
Q

tPA BP goal

A

<185/105

73
Q

how is HTN urgency managed

A

sodium nitroprusside drip

74
Q

when do we correct the HTN?

A

permissive HTN for 2-3 days, lower BP to goal (130/80)

ACE I/TZD

75
Q

additional CVA care

A

increased risk of DVT = LMWH/UFH

DM care (A1c 7% - >9%= insulin)

evaluate swallowing

early mobilization Pt/OT

disposition discussion

statin

sleep apnea

76
Q

how to ID cerebral edema in TIA/CVA

A

mass effect in initial imaging

increased ICP = neuron checks q 2hrs

will show postural change, chyene stokes respiration

77
Q

how is cerebral edema treated?

A

IV steroid (decahedron), mannitol, hyperventilation, neurosurgical decompression

78
Q

additional CVA care

A

increased risk of DVT = LMWH/UFH

79
Q

lipid lowering therapy

A

high intensity statin REGARDLESS of cholesterol level (anti-inflammatory)

80
Q

what drugs are given for HTN management

Cardiac Dz
DM
CKD
CHF

A

cardiac dz: BB

dm: ACE/ARB

CKD: ACE/ARB

CHF: ACE/ARB + BB

81
Q

long term stroke management

A

majority of stroke related deaths occur from complications (PNA, MI, sepsis)

counsel about risk factors (smoking cessation)

82
Q

secondary CVA prevention

small vessel dz/cryptogenic

A

ASA 81 mg OR 75 mg Plavix/Clopidogrel daily lifelong

83
Q

secondary CVA prevention

large vessel arteriosclerotic dz

A

DAPT with ASA and clopidigrel x 90 days

then single anti-platelet therapy

84
Q

secondary CVA prevention

cardioembolic source

A

large or hemorrhage transformation: ASA mg daily 7-14 days, then anticoagulation

NO: anticoagulation

85
Q

secondary CVA prevention

carotid dz

A

CEA or CAS

86
Q

secondary CVA prevention CEA

A

DAPT before then ASA 81 mg after

87
Q

secondary CVA prevention CAS

A

DAPT with ASA 81 mg and clopidigrel 75 mg daily prior to and 90+ days after stent

long term single agent

88
Q

anticoagulation, who gets what agent?

A

CKD: warfarin/apixaban

AF due to Mitral dz: warfarin

AF mural thrombusL warfarin only

OR watchman define

use CHADS2VAS to determine

89
Q

paroxysmal AF tx?

A

anti-platelet therapy until AFib is able to be diagnosed

then start anticoagulation

these patients have SAME risk as regular AF

90
Q

statin dosages

A

given to every

LDL < 100 (<70 if at risk)

Atorvastatin (Lipitor) 40-80 mg
Rosuvastatin (crestor) 20-40 mg

91
Q

primary stroke prevention

A

counsel how to recognize a stroke

FAST (face, arm, speech = time to go!)

stop smoking, control HTN/DM/lipid

daily ASA if only at stroke risk

92
Q

CHADS2VAS criteria

A 
CHF 
HTN 
Age > 75
DM 
Stroke/TIA + 2 
Vascular dz
Age >65
Sex- female
93
Q

CHADS2VAS interpretation

A

0-1: ASA only
2: anti-coagulant OR ASA (AC preferred)
>3: anti-coagulate

94
Q

carotid stenosis and CVA

A

> 75% occlusion is at a high risk of stroke, typically have other CV risk factors

evaluated with carotid US or CTA

95
Q

carotid stenosis CVA values

> 70%

A

refer to vascular surgeon for CEA or CAS

life expectancy > 5 yrs

IF 100% = do nothing :)

96
Q

carotid stenosis CVA values

60-70%

A

consider referral

anti-platelet therapy and pts will need monitoring

97
Q

carotid stenosis CVA values

<60%

A

anti platelet therapy and semi annual repeat study

98
Q

amaurosis fugax

A

infarction of renal artery (unilateral)

transient, typically present to eye doc

“shade pulled over eye”

same work up

WI18 Neuro (16 decks)

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