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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
ischemic cascade
decreased vascular perfusion into the brain osmolarity increased during ischemia influx of fluid into the brain to restore normal osmotic pressure edema
26
when does ischemic cascade begin
minutes after occlusion peaks in 3-4 days
27
what can ischemic cascade cause
increased ICP severe secondary structural damage
28
what is the most frequent cause of death seen in large infarcts involving MCA and ICA
ischemic cascade
29
thrombic ischemia
development or existence of a blood clot within the cerebral vascular system
30
most common type of all CVAs
thrombic 40%
31
where does thrombic ischemia occur
already partially occluded vessel partially occluded by atherosclerosis
32
where do thombic occlusions occur
at sites of turbulent flow bifurcations and curvatures
33
thrombic occlusions are most common in
internal carotid and vertebral a basilar a and middle cerebral a
34
atherosclerosis
most common form of vascular dz
35
what is atherosclerosis associated with
accumulation of lipids, fibrous tissue and calcium deposits on arterial walls
36
what do the accumulations on the arterial walls form
plaques narrow the lumen
37
what aggregte around the plaques
platelets produce clots
38
onset of thrombic CVA
slow or fast frequently preceded by several TIAs often manifests as a focal neurologic deficit that evolves over several hours or days
39
thrombus in evolution
symptoms occur over days
40
when do thrombic CVA occur
in sleep
41
what are thrombic CVA associated w/
atherosclerotic vessel dz DM HTN
42
deterioration from thrombic CVA
may continue first 2 days secondary to cerebral edema
43
prognosis --> thrombic CVA
poorer compared to emobolic
44
embolism
obstruction of blood secondary to a blood clot that is not inherent to the cerebral vascular system
45
most common form of cerebral emboli
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
most common origins of emboli
a-fib MI
47
a-fib
blood flow is stagnant in the L atrium
48
MI
damaged myocardium
49
other origins of emboli
intra-arterial thrombus dislodged plaque
50
where is the progression of an emboli halted
bifurcation where the lumen is narrowed and the ischemic infarction occurs
51
focal deficits correspond to
anatomic region supplied by the occluded vessel
52
what may there be during the onset of embolic CVA
"stuttering" onset of symptoms appearing & clearing as the emoblism moves along the blood stream
53
what are embolic CVA more frequently associated w/
TIA
54
what are embolic CVA associated w/
seizures precipitating headache transient confusion and/or loss of conciousness
55
where to emboli tend to terminally lodge in
smaller vesserls producing more discrete, focal deficits
56
systemic cause of ischemic CVA
low systemic perfusion secondary to cardiac failure or significant blood loss widespread hypoperfusion and ischemia neurological deficits are global and bilateral in nature
57
anoxic brain injuries
ischemia can cause a hypoxic or an anoxic event within minutes of oxygen deprivation to the brain
58
areas most prone to anoxic brain injury
hippocampus --> memory deficits purkinje fibers of the cerebellum --> ataxia basal gangila --> increased muscle tone
59
what could lead to cerebral hypoperfusion
systemic hypertension
60
anoxic brain injuries can lead to
watershed lesions
61
watershed lesions
certain areas of the brain do not get sufficient blood supply
62
anterior watershed zone
ACA meets MCA often causes bilateral UE weakness
63
posterior watershed zone
PCA meets MCA often causes cortical blindness and aphasia
64
trombic/embolic CVA syndromes focal deficits
dictated by the location of the blockage of the cerebral vasculature
65
syndromes may be
partial or complete
66
where are more hypoxic damages found
proximal
67
greater collateral circulation results in
less extensive damage less complete syndromes *circle of willis*
68
what occurs with cerebellar edema
death from brainstem compression or herniation
69
medical treatment of ischemic CVA
blood pressure management anticoagulation therapy thrombolytic agents nimodepine corticosteroids
70
blood pressure management
pt is kept horizontal for the 1st few days post CVA limited to bedside PROM
71
anticoagulation therapy
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
thrombolytic agents
t-PA given within 3-6 hours to break up thrombus to restore normal circulation
73
could you use t-PA for hemorrhagic strokes
no
74
t-pa gives
a chance of recovery and minimize disability
75
nimodepine
ca2+ channel antagonist
76
corticosteroids
decreased cerebral edema or in extreme cases
77
surgical management
carotid endarterectomy posterior fossa decompression
78
carotid endarterectomy
removing the atherosclerotic deposits from the lining of the carotid artery can dislodge a clot and cause more sx**
79
posterior fossa decompression
performed for potentially fatal brainstem compression can be life saving**

Neruo 1 - Test 3 (12 decks)

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