Hypoxia and Stroke - Fremont-Smith Flashcards
initial HIE
grey matter process
first cortical matter
then white matter
then SC
astrocyte
brief storage of glycogen
HIE
hypoxia of whole brain
energy crisis
depolarization glutamate discharge** NMDA/AMPA receptor calcium influx NO production and catabolic enzyme formation
lead to cell injury
reperfusion
leads to cerebral edema and increased ICP
intracellular edema, vascular injury, insterstitial edema, release of vasoactive metabolites
4-5 minutes
long enough for irreversible damage
-hippocampus, neocortical cells, striatal cells, purkinje cells
> 5 minutes - thalamic and brain stem damage
red neuron formation
requires reperfusion
ischemia >4 minutes
papilledema
edematous optic papillae protrudes into vitreous chamber
-edema of optic nerve
astrocyte scar
gliosis
hepatic encephalopathy
get type II alzheimer cells
due to hyperammonia
large clear nuclei on H and E
brain death
terminal clinical state
loss of cerebral and brainstem function
electrical silence of brain
selective loss of sensitive neurons
CA1 of hippocampus
layer 3,5,6 of neocortex
purkinje cells
striatal neurons
persistant vegetative state
loss of cognitive fxn and emotion
preserve sleep-wake cycle, autonomics, and breathing
duration of brain insult effects
selective loss of neurons
> vegetative state / dementia
> brain death
susceptible to hypoxia
neurons with lots of glutamate
korsakoffs amnesia
B/L hippocampal injury
- loss of CA1 neurons in hippocampus
- anterograde amnesia
- less severe defect of retrograde amnesia (old memories)
hippocampal sclerosis
B/L neuron loss and gliosis
vascular to hippocampus
anterior temporal branch of posterior cerebral artery
anterior cerebral artery
covers middle section of brain
middle cerebral artery
covers frontal/temporal cerebral cortex
posterior cerebral artery
anterior and posterior branch
respirator brain
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
selective neuronal necrosis to total tissue necrosis
key factor - lactic acidosis
cerebral infarction
focal brain necrosis
affects all tissue elements
compartments of infarct
core and penumbra
penumbra - moderate ischemia and delayed infarct
this is what you want to save - penumbra
2 types of stroke
ischemic
hemorrhagic
most dangerous period of large cerebral infarct
3-4 days - get edema - and herniations
bland infarc
swelling and early disintergration of infarcted area
hemorrhagic infarct
usually disintegration of lesion followed by reperfusion
-blood gets to affected area
most common cause of cerebral infarct
atherosclerosis - atherothrombosis and emboli of thrombus from atherosclerotic plaque
small vessel disease
embolism
hypercoagulability
factor V deficiency (leiden)
protein C and S deficiency
antiphospholipid Ab syndrome
prothrombin 20210A mutation
patient with diabetes
get small vessel disease
lacunar infarct
often near basal ganglia
neovascularization
peaks at 2 weeks
-endothelial proliferation around infarct
glial scar
from astrocytes
-by 2 months
thrombolytic therapy
may convert bland to hemorrhagic infarct
lacunar infarct
with HTN and diabetes - with associated small vessel disease
small vessel disease
hyaline arteriolosclerosis
-in HTN and diabetes
narrow lumen - more distance for blood to diffuse
-ischemia results
congo red
for amyloid
-can also be in small vessel disease
small vessel disease and lacunar infarct
lenticulostriate arteries
anterior choroidal artery
supplies medial globus pallidus, posterior limb internal capsule, and tail of caudate, optic tract
medial striate artery
also important
watershed infarct
ACA/MCA - man in barrel - trunk and proximal limbs
MCA/PCA
with acute episode of hypovolemia
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)
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
hemorrhagic conversion
within first week - ischemic stroke has hemorrhage to area of infarct
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
fatal gastroenteritis syndrome
with lateral medullary syndrome
-nausea and vomiting - due to damage to deiter nucleus and other vestibular nuclei
massive burn
fat embolism to brain
-see black dots all over brain
TIA
last < 10 minutes
> 1 hour - leaves small infarct
important warning sign**
-need to admit and work up
hypertensive intracerebral hemorrhage
rupture small penetrating arteries
- HTN - small vessel disease - fragile
- often bleed to basal ganglia/thalamus
hemorrhagic stroke
weakened vessel rupture
- often with lenticulostriate arteries
- to caudate/putamen (striatum)
basal ganglia in and out
input - striatum
output - internal segment globus pallidus and substantia nigra pars reticulata
PCA syndrome
homonymous hemianopia
sensory loss
ACA syndrome
lower-extremity weakness
sensory loss
incontinence
MCA syndrome
hemiparesis (face and arm) aphasia sensory loss hemianopia eye deviation
pure sensory stroke
C/L thalamus lacunae
pure motor stroke
C/L pons or internal capsule lacunae
lacunae
empty space
MRI
mores sensitive in diagnosis of small ischemic areas - but not fast and available
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
risk fx of intracranial aneurysms
smoking
alcohol
coarctation of aorta
polycystic kidney disease
terrible headache and visual changes
berry aneurysm rupture
duret hemorrhage
with herniation
-bleed in pons and brainstem
arteriovenous malformation
consist of arteries and veins
-seizure, neuro deficit, bleeds
tissue not oxygenated
sturge weber syndrome
ophthalmic division of trigeminal n face lesion
also cerebral atrophy and calcification
abnormal vessels in SA space
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
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
