Cerebrovascular Pathology Flashcards
Ischemia
Infarction
Hypoxia
Inadqueate blood flow
Ischemia thats gone on too long and cant be undone
INadequate oygenation
CBF
Constant steady flow is autoregulation
If it drops below 40 mmHG, will lose this and get ischemia
Local ischemia cause of small and large
Small - lacunar
- caused by thrombus
Major
- caused by embolus
Source is heart (AF), bifurcation points
- always serious
Lacunar infarcts risks
HTN
Atheroscleorsis
Mostly thrombi
Typically medial
Global hypoxia/ischemia causes and what’s affected
Drop in BP (shock)
Increase in ICP (edema, hemorrhagfe)
Watershed regions
Typically bilatetral
Causes of hypoxic hypoxia-ischemia
CO poisoning
Near dorwning/suffocation
Resp arrest
Seizure
Vulnerability of hypoxic type
1st - hippocampus
2 - neocortical pyramidal neurons
3 - cerebellar purkinje neurons
Acute lesions gross and micro
1-4 days
Blurring of grey-white matter, duskiness of grey, slight softening
Dead red, neuropil vacuolation, neutrophils
Subacute
5-30 days
More prominant acute changes, cerebral edema, cracking (separatiion of gray rom white)
Macrophages, microvascular proliferation, reactive gliosis and microglia
Chronci
Weeks to year
Liquefactive necrossi leds to cavitation
Then get cystic cavity lined by firm wall
Few macrophages, abundant gliosis
Penumbra physiology
Tissue acidosis leads to failure of Na, K, ATPase pump (cytotoxic edema), glutamate rlewase (excitotoxicty), mito dysfuntion, free rads
Cerberal edema
Failiure of K, Na, ATPase pumps - cytotoxic edema
Interstitial
Can lead to hernaition (transforaminal will kill)
What herniates in subflaacine
Transtentorial
Transoforaminal
Cingulate gyrus
Medial temporal lobe
Tonsil
uncal hernation
Trnastentorial
COmpresses CN3 (blown pupil)
Compresses PCA - cortical blindness
Aneurysms
Saccular are most
Anterio circulation most
Most silent
Can get SAH
