hypoxia, ischemia, and stroke Flashcards

1
Q

HIE

A

hypoxic-ischemic encephalopathy
basically hypoxia of whole brain
initially a grey matter process

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2
Q

steps of energy crisis

A

energy failure -> depolarization -> glutamate discharge -> opening of NMDA, AMPA Rs -> Ca influx -> apoptosis

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3
Q

reperfusion injury

A

free radiacal damage, lactic acid damage, cerebral edema

monocytes to area

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4
Q

first damage

A

cell membranes compromised, metabolism ceases, neurons die (grey more then white)

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5
Q

after 4-5 min of ischemia

A

irrecersible hippocampal, neocortical, striatal, and prukinje cell death

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6
Q

> 5 min of ischemia

A

thalamic and brain stem damage

spinal cord resistant to hypoxia

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7
Q

red neurons

A

appears w/in hour os reperfusion

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8
Q

which cells of hippocampus die first?

A

CA1

most likely explanation is that these cells produce more glutamate

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9
Q

which layers of neocortex die first?

A

3
5
6
most likely explanation is that these cells produce more glutamate

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10
Q

cerebral infarction

A

focal brain necrosis d/t complete and prolonged ischemia focally affecting all tissue elecments, neurons, glia, and vessels

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11
Q

penumbra

A

area of brain that has not yet become necrotic d/t ischemia, if O2 is delivered in time neurons can be saved

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12
Q

hemorrhagic infarct

A

NOT an actual hemorrhage

is lesion d/t to reperfusion injury

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13
Q

bland infarct

A

no reperfussion just swelling and disintegration

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14
Q

thalmus blood supply>

A

thalamoperforator aa from PCA

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15
Q

caudate nucleus blood supply

A

lenticulstriate aa (from MCA)

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16
Q

globus pallidus blood supply

A

anterior choroidal aa

17
Q

putamen blood supply

A

brr of ACA

18
Q

man in barrel syndrome

A

d/t death of watershed areas

produces proximal arm and leg weakness

19
Q

watershed regions

A

ACA-MCA
MCA-PCA
zones, can occur with severe hypovolemia

20
Q

ischemic stroke gross

A

48hrs- edema and loss of gray-white matter jnx
2-10 days- gelantinous and friable w/distinct necrotic borders
3wks- liqufaction and cyst formation

21
Q

ischemia stroke microscopic

A
24hrs- red neurons
48hrs- neutrophils
1-2 wks- gliosis by astocytes
2-3wks- microglial cells predominate and neovascularization with granulation tissue 
months- cyst cavity w/gliotic lining
22
Q

10% of ischemic stokes

A

have hemorrhagic conversion/evolution

maybe d/t restored luminal patency of occluded vessel or reperfusion injury

23
Q

lateral medullary syndrome

A

aka PICA or wallenberg syndrome
loss of pain and temp sensation on c/l side of body and i/l side of face (this is Dx for condition)
ataxia
horner syndrome
nystagmus and vertigo
nausea and vomiting (fatal gastroenteritis syndrome)

24
Q

TIA

A

clinical presentation <10min

emergency- full work up

25
what are the major causes of hemorrhagic strokes?
HTN, anticoagulants, bleeding disorders, cerebreal amyloid depostion, ruputured aneurysms, AV malformations, trauma
26
pure motor stroke
contralateral pons or internal capsule lacune
27
pure sensory stroke
contralateral thalamus lacune
28
MCA syndrome
``` hemiparesis (face & arms >> legs) aphasia sensory loss hemianopia eye deviation ```
29
ACA syndrome
lower extremity weakness sensory loss incontinence
30
PCA syndrome
homonymous hemianopia | sensory loss
31
PICA syndrome
ataxia horner syndrome ipsilateral loss of face sensation contralateral loss of pain and temp sensation
32
arterial aneurysms
``` aka saccular or berry aneurysms subarachnoid (high pressure) hemorrhage majority in circle of wilisi at first bifurcation of MCA W>M risk factors: smoking, alcohol ```
33
berry aneurysms associated with
polycystic kidney disease marfans and other CT diseases coarctation of aorta NFI
34
sturge weber syndrome
rare sporadic neurocutaneous sydrome meningeal and ipsilateral cutaneous angiomatosis port wine stain on face if severe enough will see calcifications of vessels
35
symptoms of sturge-weber
``` seizures developmental delay TIAs hemiparesis HAs glaucoma ```
36
HTN encephalopathy
``` severe HA nausea, vomiting papilledema visual disturbances seizures confusion coma ```
37
cerebral amyloid angiopathy
almost all pts with alzheimers have some degree of amyloid deposition stains with congo red usually deposition is in small vessles rarely d/t neoplasm, but usually idiopathic can cause ischemic or hemorrhagic lesions cause dementia it is associated with ApoE phenotypes