Week 1 Day 2

Front 1

Different causes of hypoxia

Back 1

Low level of oxygen of blood (CO poisoning, drowning)
Low blood flow (aka ischemia)
Oxygen utilization by tissue is impaired (cyanide poisoning)

Front 2

Low blood flow

Back 2

Ischemia; causes more damage than hypoxia; no outflow of metabolites

Front 3

Global ischemia is defined as?
Where is brain damage most severe?

Back 3

systolic pressure <50 mmHg (d/t shock, heart attack, shock)

Brain damage is most severe in watershed areas; if severe enough vegetative state or brain death may occur

Front 4

Focal ischemia is typically d/t?

Back 4

arterial stenosis, thrombosis, atheroemboli, or thromboemboli

Front 5

Where are the watershed areas?

Back 5

Between ACA and MCA
Between MCA and PCA

Front 6

What are the selective vulnerable regions Cells and regions?

Back 6

Cells: Neurons>Oligodendroytes>astrocytes
Regions: Hippocampus (CA1 sector)>lamina 3 and 5 of cortex>Purkinje cells in cerebellum

Front 7

What determines the selective vulnerability?

Back 7

Variable oxygen/energy requirements of different neurons and neuronal populations

Glutamate receptor densities-->glutamate is neurotoxic when present in excess, as occurs in hypoxic/ischemic brain damage

Front 8

Acutely hypoxic/ischemic neurons histological appearance?

Back 8

"red is dead"
shrunked and dark nucleus, no nucleolus visible
Red cytoplasm (no Nissl substance)

Front 9

Pathology?

Back 9

Hippocampal infarct; loss of neurons in the CA1 sector of the hippocampus d/t selective vulnerability

Front 10

Most common sites of thrombosis (atherosclerosis)

Back 10

Carotid bifurcation
Origin of MCA
origin or end of basilar artery

Front 11

Common sources of Emboli?

Back 11

Cardiac: Mural thrombus-->left atrium or ventricle (d/t afib, MI, valve disease)
Non-Cardiac Source-->Atheroma (plaques in carotid aa.) Fat, neoplasm, air

Front 12

What is the most frequent vessel affected by emboli?

Back 12

Middle cerebral artery is most frequent vessel affected by emboli

Front 13

Hyaline arhteriolosclerosis caused by hypertension and diabetes mellitus?

Back 13

Lacunar infarcts/slit hemorrhages

Front 14

Chronic inflammation, fibrinoid necrosis of the wall; multinucleated giant cells and wall destruction

Back 14

Primary angiitis (vasculitis) of CNS

Front 15

Acute, subacute, and chronic gross morphology of infarct

Back 15

Actue-->up to 48 hours: soft, swollen, gray white distinction blurred
Subacute: up to 2-3 weeks: liquefactive necrosis
Chronic: several months: CAVITATED, all dead tissue removed

Front 16

Acute, subacute, and chronic microscopic morphology of infarct

Back 16

Acute: red neurons pallor, up to 48 hours-->neutrophils
Subacute: macrophages, necrotic tissue, reactive astrocytes, vascular proliferation (picture)
Chronic: several months: cavity with GLIAL SCAR

Front 17

Pathology?

Back 17

Chronic infarct

Front 18

Typical locations of venous thrombosis?
D/t?

Back 18

Usually superior sagittal sinus or lateral sinuses
Results in parasaggital hemorrhagic infarct

Infection, injury, neoplasm, surgery
Pregnancy, oral contraceptives, hematologic abnormalities, dehydration and malignancy

Front 19

Most common cause of intracerebral hemorrhage (ICH)
Common locations?

Back 19

Hypertension

Putamen, thalamus, pons, cerebellum

Front 20

Weakens the arteriole and predisposes to rupture?

Back 20

Hyaline arteriolosclerosis

Front 21

What age group presents with arteriovenous malformations? (Tangled network of vessels with arteriovenous shunt)

Back 21

M>F
Presentation between 10-30 years
Most often distribution of MCA

Front 22

Capillary telangectasia: location? bleed? Intervening brain tissue?

Back 22

Pons
DONT usually bleed
Capillary telangiectasia

Front 23

Cavernous angioma: location? bleed? Intervening brain tissue?

Back 23

Cerebellum, pons, white matter
Evidence of prior bleeding (greatly enlarged blood vessels are evidence of prior hemorrhage)
NO intervening brain tissue

Front 24

Lobar hemorrhage causes (closer to the surface of the brain)

Back 24

Neoplasms, drug abuse, vasculitis, hemorrhagic diathesis, amyloid angiopathy

Front 25

The work headache ever!

Back 25

Saccular (Berry) aneurysims-->subarachnoid hemorrhage; mosly by the ACA/ant comm artery

Increased risk with HTN, smoking, AVM
DEFECT in media is CONGENITAL

Front 26

Strokes that are in large vessels or at the end branches

Back 26

"pump" Cardioembolism stroke

Front 27

Hypoperfusion if no flow?
Low flow?

Back 27

NO flow=cortical laminar necrosis
Low flow=watershed injury

Front 28

Sites for lacunes and hemorrhages

Back 28

Basal Ganglia, pons, thalamus, cerebellum