Hypoxia and Stroke - Fremont-Smith Flashcards

1
Q

initial HIE

A

grey matter process

first cortical matter
then white matter
then SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

astrocyte

A

brief storage of glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HIE

A

hypoxia of whole brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

energy crisis

A
depolarization
glutamate discharge**
NMDA/AMPA receptor
calcium influx
NO production and catabolic enzyme formation

lead to cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

reperfusion

A

leads to cerebral edema and increased ICP

intracellular edema, vascular injury, insterstitial edema, release of vasoactive metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

4-5 minutes

A

long enough for irreversible damage
-hippocampus, neocortical cells, striatal cells, purkinje cells

> 5 minutes - thalamic and brain stem damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

red neuron formation

A

requires reperfusion

ischemia >4 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

papilledema

A

edematous optic papillae protrudes into vitreous chamber

-edema of optic nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

astrocyte scar

A

gliosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hepatic encephalopathy

A

get type II alzheimer cells

due to hyperammonia

large clear nuclei on H and E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

brain death

A

terminal clinical state
loss of cerebral and brainstem function

electrical silence of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

selective loss of sensitive neurons

A

CA1 of hippocampus
layer 3,5,6 of neocortex
purkinje cells
striatal neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

persistant vegetative state

A

loss of cognitive fxn and emotion

preserve sleep-wake cycle, autonomics, and breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

duration of brain insult effects

A

selective loss of neurons
> vegetative state / dementia
> brain death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

susceptible to hypoxia

A

neurons with lots of glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

korsakoffs amnesia

A

B/L hippocampal injury

  • loss of CA1 neurons in hippocampus
  • anterograde amnesia
  • less severe defect of retrograde amnesia (old memories)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hippocampal sclerosis

A

B/L neuron loss and gliosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

vascular to hippocampus

A

anterior temporal branch of posterior cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

anterior cerebral artery

A

covers middle section of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

middle cerebral artery

A

covers frontal/temporal cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

posterior cerebral artery

A

anterior and posterior branch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

respirator brain

A

severe HIE damage to cortex, deep nuclei, brainstem

  • put on respirator - autodigestion and liquefaction occurs
  • aka - non-perfused brain

no inflammation, macros, or gliosis - only autolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

selective neuronal necrosis to total tissue necrosis

A

key factor - lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

cerebral infarction

A

focal brain necrosis

affects all tissue elements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
compartments of infarct
core and penumbra penumbra - moderate ischemia and delayed infarct this is what you want to save - penumbra
26
2 types of stroke
ischemic | hemorrhagic
27
most dangerous period of large cerebral infarct
3-4 days - get edema - and herniations
28
bland infarc
swelling and early disintergration of infarcted area
29
hemorrhagic infarct
usually disintegration of lesion followed by reperfusion | -blood gets to affected area
30
most common cause of cerebral infarct
atherosclerosis - atherothrombosis and emboli of thrombus from atherosclerotic plaque small vessel disease embolism
31
hypercoagulability
factor V deficiency (leiden) protein C and S deficiency antiphospholipid Ab syndrome prothrombin 20210A mutation
32
patient with diabetes
get small vessel disease
33
lacunar infarct
often near basal ganglia
34
neovascularization
peaks at 2 weeks | -endothelial proliferation around infarct
35
glial scar
from astrocytes | -by 2 months
36
thrombolytic therapy
may convert bland to hemorrhagic infarct
37
lacunar infarct
with HTN and diabetes - with associated small vessel disease
38
small vessel disease
hyaline arteriolosclerosis -in HTN and diabetes narrow lumen - more distance for blood to diffuse -ischemia results
39
congo red
for amyloid | -can also be in small vessel disease
40
small vessel disease and lacunar infarct
lenticulostriate arteries
41
anterior choroidal artery
supplies medial globus pallidus, posterior limb internal capsule, and tail of caudate, optic tract
42
medial striate artery
also important
43
watershed infarct
ACA/MCA - man in barrel - trunk and proximal limbs MCA/PCA with acute episode of hypovolemia
44
time of ischemic stroke - gross
48 hours - edema and loss of gray-white junction 2-10 days - gel and friable with border of necrosis 3 weeks - liquefaction and cyst (lacunar)
45
time of ischemic stroke - micro
``` 24 hours - red neurons 48 hours - neutrophils 1-2 weeks - astrocytes 2-3 weeks - microglial cell - gliosis - and neovascularization months -cyst cavity with gliotic lining ```
46
hemorrhagic conversion
within first week - ischemic stroke has hemorrhage to area of infarct
47
lateral medullary syndrome
posterior inferior cerebellar artery syndrome wallenberg syndrome - acute onset with severe vertigo - deiter nucleus - also nausea/vomiting - spinothalamic tract damage - loss of pain/temp C/L body - ataxia - cerebellar damage - horner syndrome sx - hypothalamospinal fiber injury
48
fatal gastroenteritis syndrome
with lateral medullary syndrome | -nausea and vomiting - due to damage to deiter nucleus and other vestibular nuclei
49
massive burn
fat embolism to brain | -see black dots all over brain
50
TIA
last < 10 minutes >1 hour - leaves small infarct important warning sign** -need to admit and work up
51
hypertensive intracerebral hemorrhage
rupture small penetrating arteries - HTN - small vessel disease - fragile - often bleed to basal ganglia/thalamus
52
hemorrhagic stroke
weakened vessel rupture - often with lenticulostriate arteries - to caudate/putamen (striatum)
53
basal ganglia in and out
input - striatum | output - internal segment globus pallidus and substantia nigra pars reticulata
54
PCA syndrome
homonymous hemianopia | sensory loss
55
ACA syndrome
lower-extremity weakness sensory loss incontinence
56
MCA syndrome
``` hemiparesis (face and arm) aphasia sensory loss hemianopia eye deviation ```
57
pure sensory stroke
C/L thalamus lacunae
58
pure motor stroke
C/L pons or internal capsule lacunae
59
lacunae
empty space
60
MRI
mores sensitive in diagnosis of small ischemic areas - but not fast and available
61
intracranial aneurysms
saccular or berry - develop at branching points major cerebral arteries - majority - circle of willis - first bifurcation of middle cerebral artery defect in vessel wall - present at birth -develop later in adulthood
62
risk fx of intracranial aneurysms
smoking alcohol coarctation of aorta polycystic kidney disease
63
terrible headache and visual changes
berry aneurysm rupture
64
duret hemorrhage
with herniation | -bleed in pons and brainstem
65
arteriovenous malformation
consist of arteries and veins -seizure, neuro deficit, bleeds tissue not oxygenated
66
sturge weber syndrome
ophthalmic division of trigeminal n face lesion also cerebral atrophy and calcification abnormal vessels in SA space
67
HTN encephalopathy
severe HA, nausea/vomiting, papilledema, visual distubrance, seizure, confusion, even coma malignant HTN with retinopathy and nephropathy culmination of severe chronic HTN fibrinoid necrosis of small arteries
68
cerebral amyloid angiopathy
almost always with alzheimers beta-amyloid deposition in small vessels - congo red positive can cause ischemic and hemorrhagic lesions -can obliterate vessel lumen