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Neuro II Exam 1 > Hypoxia and Stroke - Fremont-Smith > Flashcards

Hypoxia and Stroke - Fremont-Smith Flashcards

1
Q

initial HIE

A

grey matter process

first cortical matter
then white matter
then SC

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2
Q

astrocyte

A

brief storage of glycogen

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3
Q

HIE

A

hypoxia of whole brain

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4
Q

energy crisis

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

lead to cell injury

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5
Q

reperfusion

A

leads to cerebral edema and increased ICP

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

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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

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7
Q

red neuron formation

A

requires reperfusion

ischemia >4 minutes

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8
Q

papilledema

A

edematous optic papillae protrudes into vitreous chamber

-edema of optic nerve

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9
Q

astrocyte scar

A

gliosis

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10
Q

hepatic encephalopathy

A

get type II alzheimer cells

due to hyperammonia

large clear nuclei on H and E

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11
Q

brain death

A

terminal clinical state
loss of cerebral and brainstem function

electrical silence of brain

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12
Q

selective loss of sensitive neurons

A

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

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13
Q

persistant vegetative state

A

loss of cognitive fxn and emotion

preserve sleep-wake cycle, autonomics, and breathing

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14
Q

duration of brain insult effects

A

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

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15
Q

susceptible to hypoxia

A

neurons with lots of glutamate

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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)
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17
Q

hippocampal sclerosis

A

B/L neuron loss and gliosis

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18
Q

vascular to hippocampus

A

anterior temporal branch of posterior cerebral artery

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19
Q

anterior cerebral artery

A

covers middle section of brain

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20
Q

middle cerebral artery

A

covers frontal/temporal cerebral cortex

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21
Q

posterior cerebral artery

A

anterior and posterior branch

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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

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23
Q

selective neuronal necrosis to total tissue necrosis

A

key factor - lactic acidosis

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24
Q

cerebral infarction

A

focal brain necrosis

affects all tissue elements

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25
Q

compartments of infarct

A

core and penumbra

penumbra - moderate ischemia and delayed infarct

this is what you want to save - penumbra

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26
Q

2 types of stroke

A

ischemic

hemorrhagic

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27
Q

most dangerous period of large cerebral infarct

A

3-4 days - get edema - and herniations

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28
Q

bland infarc

A

swelling and early disintergration of infarcted area

29
Q

hemorrhagic infarct

A

usually disintegration of lesion followed by reperfusion

-blood gets to affected area

30
Q

most common cause of cerebral infarct

A

atherosclerosis - atherothrombosis and emboli of thrombus from atherosclerotic plaque

small vessel disease

embolism

31
Q

hypercoagulability

A

factor V deficiency (leiden)
protein C and S deficiency
antiphospholipid Ab syndrome
prothrombin 20210A mutation

32
Q

patient with diabetes

A

get small vessel disease

33
Q

lacunar infarct

A

often near basal ganglia

34
Q

neovascularization

A

peaks at 2 weeks

-endothelial proliferation around infarct

35
Q

glial scar

A

from astrocytes

-by 2 months

36
Q

thrombolytic therapy

A

may convert bland to hemorrhagic infarct

37
Q

lacunar infarct

A

with HTN and diabetes - with associated small vessel disease

38
Q

small vessel disease

A

hyaline arteriolosclerosis
-in HTN and diabetes

narrow lumen - more distance for blood to diffuse
-ischemia results

39
Q

congo red

A

for amyloid

-can also be in small vessel disease

40
Q

small vessel disease and lacunar infarct

A

lenticulostriate arteries

41
Q

anterior choroidal artery

A

supplies medial globus pallidus, posterior limb internal capsule, and tail of caudate, optic tract

42
Q

medial striate artery

A

also important

43
Q

watershed infarct

A

ACA/MCA - man in barrel - trunk and proximal limbs

MCA/PCA

with acute episode of hypovolemia

44
Q

time of ischemic stroke - gross

A

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
Q

time of ischemic stroke - micro

A 
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
Q

hemorrhagic conversion

A

within first week - ischemic stroke has hemorrhage to area of infarct

47
Q

lateral medullary syndrome

A

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
Q

fatal gastroenteritis syndrome

A

with lateral medullary syndrome

-nausea and vomiting - due to damage to deiter nucleus and other vestibular nuclei

49
Q

massive burn

A

fat embolism to brain

-see black dots all over brain

50
Q

TIA

A

last < 10 minutes

> 1 hour - leaves small infarct

important warning sign**
-need to admit and work up

51
Q

hypertensive intracerebral hemorrhage

A

rupture small penetrating arteries

  • HTN - small vessel disease - fragile
  • often bleed to basal ganglia/thalamus
52
Q

hemorrhagic stroke

A

weakened vessel rupture

  • often with lenticulostriate arteries
  • to caudate/putamen (striatum)
53
Q

basal ganglia in and out

A

input - striatum

output - internal segment globus pallidus and substantia nigra pars reticulata

54
Q

PCA syndrome

A

homonymous hemianopia

sensory loss

55
Q

ACA syndrome

A

lower-extremity weakness
sensory loss
incontinence

56
Q

MCA syndrome

A 
hemiparesis (face and arm)
aphasia
sensory loss
hemianopia
eye deviation
57
Q

pure sensory stroke

A

C/L thalamus lacunae

58
Q

pure motor stroke

A

C/L pons or internal capsule lacunae

59
Q

lacunae

A

empty space

60
Q

MRI

A

mores sensitive in diagnosis of small ischemic areas - but not fast and available

61
Q

intracranial aneurysms

A

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
Q

risk fx of intracranial aneurysms

A

smoking
alcohol
coarctation of aorta
polycystic kidney disease

63
Q

terrible headache and visual changes

A

berry aneurysm rupture

64
Q

duret hemorrhage

A

with herniation

-bleed in pons and brainstem

65
Q

arteriovenous malformation

A

consist of arteries and veins
-seizure, neuro deficit, bleeds

tissue not oxygenated

66
Q

sturge weber syndrome

A

ophthalmic division of trigeminal n face lesion
also cerebral atrophy and calcification

abnormal vessels in SA space

67
Q

HTN encephalopathy

A

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
Q

cerebral amyloid angiopathy

A

almost always with alzheimers

beta-amyloid deposition in small vessels - congo red positive

can cause ischemic and hemorrhagic lesions
-can obliterate vessel lumen

Neuro II Exam 1 (14 decks)

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