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
Q

what are the major causes of hemorrhagic strokes?

A

HTN, anticoagulants, bleeding disorders, cerebreal amyloid depostion, ruputured aneurysms, AV malformations, trauma

26
Q

pure motor stroke

A

contralateral pons or internal capsule lacune

27
Q

pure sensory stroke

A

contralateral thalamus lacune

28
Q

MCA syndrome

A
hemiparesis (face & arms >> legs)
aphasia
sensory loss
hemianopia
eye deviation
29
Q

ACA syndrome

A

lower extremity weakness
sensory loss
incontinence

30
Q

PCA syndrome

A

homonymous hemianopia

sensory loss

31
Q

PICA syndrome

A

ataxia
horner syndrome
ipsilateral loss of face sensation
contralateral loss of pain and temp sensation

32
Q

arterial aneurysms

A
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
Q

berry aneurysms associated with

A

polycystic kidney disease
marfans and other CT diseases
coarctation of aorta
NFI

34
Q

sturge weber syndrome

A

rare sporadic neurocutaneous sydrome
meningeal and ipsilateral cutaneous angiomatosis
port wine stain on face
if severe enough will see calcifications of vessels

35
Q

symptoms of sturge-weber

A
seizures
developmental delay
TIAs
hemiparesis
HAs
glaucoma
36
Q

HTN encephalopathy

A
severe HA
nausea, vomiting
papilledema
visual disturbances
seizures
confusion
coma
37
Q

cerebral amyloid angiopathy

A

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