hypoxia, ischemia, and stroke Flashcards
HIE
hypoxic-ischemic encephalopathy
basically hypoxia of whole brain
initially a grey matter process
steps of energy crisis
energy failure -> depolarization -> glutamate discharge -> opening of NMDA, AMPA Rs -> Ca influx -> apoptosis
reperfusion injury
free radiacal damage, lactic acid damage, cerebral edema
monocytes to area
first damage
cell membranes compromised, metabolism ceases, neurons die (grey more then white)
after 4-5 min of ischemia
irrecersible hippocampal, neocortical, striatal, and prukinje cell death
> 5 min of ischemia
thalamic and brain stem damage
spinal cord resistant to hypoxia
red neurons
appears w/in hour os reperfusion
which cells of hippocampus die first?
CA1
most likely explanation is that these cells produce more glutamate
which layers of neocortex die first?
3
5
6
most likely explanation is that these cells produce more glutamate
cerebral infarction
focal brain necrosis d/t complete and prolonged ischemia focally affecting all tissue elecments, neurons, glia, and vessels
penumbra
area of brain that has not yet become necrotic d/t ischemia, if O2 is delivered in time neurons can be saved
hemorrhagic infarct
NOT an actual hemorrhage
is lesion d/t to reperfusion injury
bland infarct
no reperfussion just swelling and disintegration
thalmus blood supply>
thalamoperforator aa from PCA
caudate nucleus blood supply
lenticulstriate aa (from MCA)
globus pallidus blood supply
anterior choroidal aa
putamen blood supply
brr of ACA
man in barrel syndrome
d/t death of watershed areas
produces proximal arm and leg weakness
watershed regions
ACA-MCA
MCA-PCA
zones, can occur with severe hypovolemia
ischemic stroke gross
48hrs- edema and loss of gray-white matter jnx
2-10 days- gelantinous and friable w/distinct necrotic borders
3wks- liqufaction and cyst formation
ischemia stroke microscopic
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
10% of ischemic stokes
have hemorrhagic conversion/evolution
maybe d/t restored luminal patency of occluded vessel or reperfusion injury
lateral medullary syndrome
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)
TIA
clinical presentation <10min
emergency- full work up
what are the major causes of hemorrhagic strokes?
HTN, anticoagulants, bleeding disorders, cerebreal amyloid depostion, ruputured aneurysms, AV malformations, trauma
pure motor stroke
contralateral pons or internal capsule lacune
pure sensory stroke
contralateral thalamus lacune
MCA syndrome
hemiparesis (face & arms >> legs) aphasia sensory loss hemianopia eye deviation
ACA syndrome
lower extremity weakness
sensory loss
incontinence
PCA syndrome
homonymous hemianopia
sensory loss
PICA syndrome
ataxia
horner syndrome
ipsilateral loss of face sensation
contralateral loss of pain and temp sensation
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
berry aneurysms associated with
polycystic kidney disease
marfans and other CT diseases
coarctation of aorta
NFI
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
symptoms of sturge-weber
seizures developmental delay TIAs hemiparesis HAs glaucoma
HTN encephalopathy
severe HA nausea, vomiting papilledema visual disturbances seizures confusion coma
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
