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Neruo 1 - Test 3 > Ischemic CVA -Lecture 11 > Flashcards

Ischemic CVA -Lecture 11 Flashcards

1
Q

ischemic CVA are

A

most common type of CVA

80%

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2
Q

what is an ischemic CVA

A

complete loss of blood flow to the cerebral tissue

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3
Q

what do ischemic strokes result in

A

decreased O2 and metabolites (glucose)

results in neuronal dysfunction and cell death

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4
Q

energy requirements for the brain

A

high

25% of all O2 supply

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5
Q

the brain has almost no

A

metabolic reserves

dependent on rich supply of O2 and glucose to fxn

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6
Q

what triggers the onset of neurologic deficits

A

stores of O2 and glucose are used quickly

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7
Q

what happens w/o blood flow

A

there is a toxic build up of metabolic waste –> additional damage

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8
Q

secondary damage

A

occurs in the aftermath of the acute infarct

damaged or dying neurons release excessive amounts of glutamate

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9
Q

what occurs to cells that normally take up glutamate

A

compromised

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10
Q

what occurs d/t the compromising of the cells that take up glutamate

A

inability to produce ATP

facilitates entry of Ca2+ into cells

area of apoptosis and tissue death beyond the infarction usually w/in 3-4 hours

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11
Q

facilitates entry of Ca2+ into cells

A

activates catabolic enzymes that further degrade neural structures

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12
Q

mechanisms of injury that occur in ischemia CVA

A

local hypoxia

local hypoglycemia

build-up of toxic metabolic waste

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13
Q

medical intervention

A

ischemia is reversible if it lasts for less than first 3 hrs

meds

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14
Q

meds

A

remove embolus

prevent secondary neuronal death

ex: t-PA

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15
Q

most common cause

A

thrombic and embolic occlusion of major vessels

80%

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16
Q

damage can be

A

cerebral infarction involving

–>all NS cells in a wide area

–>selective neuronal necrosis

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17
Q

selective neuronal necrosis

A

refers to structures that are most susceptible to ischemia

neurologic symptoms due to thrombic ischemia may be seen in these regions first

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18
Q

ischemic penumbra

A

transitional area surrounding the core

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19
Q

in the core zone of the ischemic penumbra

A

decrease of O2 and glucose –> rapid depletion of energy stores

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20
Q

severe ischemia –>

A

necrosis of neurons and supporting cellular elements (glial cells)

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21
Q

how long may the penumbra remain viable

A

several hours

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22
Q

how does the penumbra remain viable

A

collateral arteries anastomosing w/ branches of the occluded vascular tree

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23
Q

when is ischemic CVA fatal

A

rarely

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24
Q

ischemic cascade is

A

potentially fatal

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25
Q

ischemic cascade

A

decreased vascular perfusion into the brain

osmolarity increased during ischemia

influx of fluid into the brain to restore normal osmotic pressure

edema

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26
Q

when does ischemic cascade begin

A

minutes after occlusion

peaks in 3-4 days

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27
Q

what can ischemic cascade cause

A

increased ICP

severe secondary structural damage

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28
Q

what is the most frequent cause of death seen in large infarcts involving MCA and ICA

A

ischemic cascade

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29
Q

thrombic ischemia

A

development or existence of a blood clot within the cerebral vascular system

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30
Q

most common type of all CVAs

A

thrombic

40%

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31
Q

where does thrombic ischemia occur

A

already partially occluded vessel

partially occluded by atherosclerosis

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32
Q

where do thombic occlusions occur

A

at sites of turbulent flow

bifurcations and curvatures

33
Q

thrombic occlusions are most common in

A

internal carotid and vertebral a

basilar a and middle cerebral a

34
Q

atherosclerosis

A

most common form of vascular dz

35
Q

what is atherosclerosis associated with

A

accumulation of lipids, fibrous tissue and calcium deposits on arterial walls

36
Q

what do the accumulations on the arterial walls form

A

plaques

narrow the lumen

37
Q

what aggregte around the plaques

A

platelets

produce clots

38
Q

onset of thrombic CVA

A

slow or fast

frequently preceded by several TIAs

often manifests as a focal neurologic deficit that evolves over several hours or days

39
Q

thrombus in evolution

A

symptoms occur over days

40
Q

when do thrombic CVA occur

A

in sleep

41
Q

what are thrombic CVA associated w/

A

atherosclerotic vessel dz

DM

HTN

42
Q

deterioration from thrombic CVA

A

may continue first 2 days secondary to cerebral edema

43
Q

prognosis –> thrombic CVA

A

poorer compared to emobolic

44
Q

embolism

A

obstruction of blood secondary to a blood clot that is not inherent to the cerebral vascular system

45
Q

most common form of cerebral emboli

A

fragments from a thrombus within the heart can dislodge and enter the cerebral circulation

75% of cardiac emboli lodge in the brain

someone w/ cardiac dz is 2-5x more likely to sustain a CVA

46
Q

most common origins of emboli

A

a-fib

MI

47
Q

a-fib

A

blood flow is stagnant in the L atrium

48
Q

MI

A

damaged myocardium

49
Q

other origins of emboli

A

intra-arterial thrombus

dislodged plaque

50
Q

where is the progression of an emboli halted

A

bifurcation

where the lumen is narrowed and the ischemic infarction occurs

51
Q

focal deficits correspond to

A

anatomic region supplied by the occluded vessel

52
Q

what may there be during the onset of embolic CVA

A

“stuttering” onset of symptoms appearing & clearing as the emoblism moves along the blood stream

53
Q

what are embolic CVA more frequently associated w/

A

TIA

54
Q

what are embolic CVA associated w/

A

seizures

precipitating headache

transient confusion and/or loss of conciousness

55
Q

where to emboli tend to terminally lodge in

A

smaller vesserls

producing more discrete, focal deficits

56
Q

systemic cause of ischemic CVA

A

low systemic perfusion secondary to cardiac failure or significant blood loss

widespread hypoperfusion and ischemia

neurological deficits are global and bilateral in nature

57
Q

anoxic brain injuries

A

ischemia can cause a hypoxic or an anoxic event within minutes of oxygen deprivation to the brain

58
Q

areas most prone to anoxic brain injury

A

hippocampus –> memory deficits

purkinje fibers of the cerebellum –> ataxia

basal gangila –> increased muscle tone

59
Q

what could lead to cerebral hypoperfusion

A

systemic hypertension

60
Q

anoxic brain injuries can lead to

A

watershed lesions

61
Q

watershed lesions

A

certain areas of the brain do not get sufficient blood supply

62
Q

anterior watershed zone

A

ACA meets MCA

often causes bilateral UE weakness

63
Q

posterior watershed zone

A

PCA meets MCA

often causes cortical blindness and aphasia

64
Q

trombic/embolic CVA syndromes focal deficits

A

dictated by the location of the blockage of the cerebral vasculature

65
Q

syndromes may be

A

partial or complete

66
Q

where are more hypoxic damages found

A

proximal

67
Q

greater collateral circulation results in

A

less extensive damage

less complete syndromes

circle of willis

68
Q

what occurs with cerebellar edema

A

death from brainstem compression or herniation

69
Q

medical treatment of ischemic CVA

A

blood pressure management

anticoagulation therapy

thrombolytic agents

nimodepine

corticosteroids

70
Q

blood pressure management

A

pt is kept horizontal for the 1st few days post CVA

limited to bedside PROM

71
Q

anticoagulation therapy

A

coumadin –> those w/ a-fib

used acutely with ischemic stroke to decrease occurrence

risk of conversion –> turning an ischemic stroke into a hemorrhagic CVA

prothombin time are –> closely monitored

72
Q

thrombolytic agents

A

t-PA

given within 3-6 hours to break up thrombus to restore normal circulation

73
Q

could you use t-PA for hemorrhagic strokes

A

no

74
Q

t-pa gives

A

a chance of recovery and minimize disability

75
Q

nimodepine

A

ca2+ channel antagonist

76
Q

corticosteroids

A

decreased cerebral edema or in extreme cases

77
Q

surgical management

A

carotid endarterectomy

posterior fossa decompression

78
Q

carotid endarterectomy

A

removing the atherosclerotic deposits from the lining of the carotid artery

can dislodge a clot and cause more sx**

79
Q

posterior fossa decompression

A

performed for potentially fatal brainstem compression

can be life saving**

Neruo 1 - Test 3 (12 decks)

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