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24 Cards in this Set

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defn stroke
cerebrovascular accident (CVA)
sudden death of barin cells when O2 supply is removed
what are 2 main problems that can cause stroke?
hemorrhagic event(20%)
ischemic infarction(80%)-thrombus, clot
what is the difference between embolism and thrombus?
embolism-clot from elsewhere
thrombus-locally formed clot
risk factors for stroke
HTN, diabetes, hypercholesterolemia, smoking, cardiac disease, family history
large vessel strokes
major aa on surface (MCA)
usually embolism
(worst headache of my life)
sudden onset
maximal deficit
small vessel stroke
penetrating vessels
"lacunar infarcts"
assoc with chronic HTN
5 major signs of stroke
SUDDEN:
1. numbness/weakness-onesided
2. confusion, trouble speaking
3.trouble seeing
4.trouble walking
5. sever headaches
when can we use tPA to treat stroke? what is the risk? what is another option?
within first 3 hours of stroke
NOT due to hemorrhage
dissolves clot
risk of hemorrhage
also, heparin
2 methods of imaging for stroke
CT- faster, more sensitive for blood
can see bones
MRI-higher resolution
DWI=diffusion weighted imaging; BEST for acute ischemic stroke; looks at water flow
what is the penumbra?
region surrounding infarcted, necrotic area in stroke
region we are trying to save to prevent spread of necrosis
where will we see necrosis?
in the region of the infarct
rapid, passive
swelling of cells
leak contents
toxic
irreversible
occurs with high excitotoxicity
where will we see apoptosis?
penumbra
prolonged, programmed (Ca2+ influx)
loss cell vol (blebbing)
less toxic
potentially reversible
occurs at low levels of excitotoxicity
what is the main way we could reverse or limit apoptosis in the penumbra?
with drugs that block NMDA receptors
what is the majoy mxn causing cell death in ischemia?
glutamate excitotoxicity
hwo does the NMDA receptor normally fxn?
voltage-gated AND ligand-gated
norm, glutamate binds non-NMDA receptors, opening Na+ channels, allowing the cell the depolarize
glutamate also binds NMDA receptors but these do not open until after the cell has depolarized. the positive interior of the cell displaces a Mg2+ ion that is blocking the channel. once, the Mg2+ ion is repelled out, the channel allows Ca2+ to enter the cell further depolarizing it
so why is the NMDA receptor important in stroke?
ischemic cells are unable to fxn properly; some release contents including glutamate;
XS glutamate cant be removed and activates too many NMDA receptors, causing too much Ca2+ to enter the cell. this destablizes the cell interior and uncouples the ETC which kills the neuron
how is XS glutamate normally removed from the synapse?
EATT transporters on glial cells (astrocytes)
so why is the NMDA receptor important normally?
strengthens synapses
imp for memory, learning, altering gene expression; also, involved in chronic pain
how does an infarct appear on a CT?
hypodensity (black) due to cell death
how does a hypertensive hemorrhage usually present?
acute
immediate collapse if lg
focal mass effect;seizures, headache, nausea, vomiting
bleeding self-limited
bleeding may dissect into ventricular system-> hydrocephalus from obstruction
what is the prognosis for htn hemorrhage?
if survive initial bleed and mass effect, recovery is better than for stroke
presentation in subarachnoid hemorrhage
abrupt onset
worst headache of my life
may/may not lose consciousness
no focal sx (hemiplegia)
drowsy, confused
nuchal rigidity
diagnosis of subarachnoid hemorrhage (SAH)
lg SAH: CT
small SAH may not be visible on CT
LP-look for RBCs and xanthochromia (yellow color in centrifuged CSF)
definitive diagnosis-angiography
sites of subarachnoid hemorrhages
berry aneuysm at bifurcation of vessel
90-90% in circle of willis (Ant comm a, post comm a, MCA bifurcation, bifurcation of internal carotid into MCA and ACA