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Path II > Cerebrovascular > Flashcards

Cerebrovascular Flashcards

1
Q

What causes CVAs?

A

Vascular occlusion, cardiovascular collapse, hemorrhage

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2
Q

What is the most important in degree of injury for a ischemic stroke?

A

TIME

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3
Q

How do CNS hemorrhages occur?

A

Traumatic or Non traumatic

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4
Q

What causes non traumatic hemorrhage strokes?

A

Hypertension or atypical vessles

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5
Q

What are signs of a CVA?

A

Sudden onset

Neuro deficit

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6
Q

What are watershed zones?

A

Between MCA, ACA

Penetrating arteries of MCA

Hippocampus

Purkinje cells of Cerebellum

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7
Q

What are watershed zones?

A

Between MCA, ACA

Penetrating arteries of MCA

Hippocampus

Purkinje cells of Cerebellum

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8
Q

What are common causes of infarct?

A

Atherosclerosis (carotid/cerebral arteries)

Cardiac Valvular disease

Cardiac mural thrombi

Vasculitis

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9
Q

What type of necrosis is caused by a infarct?

A

Coagulation necrosis but BOARDS is Liquefactive

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10
Q

The location of infarct affects where the injury occurs, what are these injuries?

A

Total MCA occlusion both internal structures and outer

Partial thrombus over lenticulate arteries only affects internal structures

Partial thrombus past the lenticulate arteries only affects cortex

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11
Q

What type of infarcts are in the brain?

A

Non-hemorrhagic: No reperfusion injury after due to thrombus formation

Hemorrhagic: Reperfusion injury, weaker vessels
-usually due to embolus

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12
Q

What are the stages of cerebral infartcion?

A

Acute (week or less)

Subacute: 1-4 weeks

Remote: Months to Years

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13
Q

What are the stages of acute infarct?

A

Coagulation necrosis (RED neurons)

Axonal degen (spheroid bodies)

Cerebral Edema (might need to do craniomty to relieve pressure)

Vascular proliferation

Neutrophil response (not as many as in MI)

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14
Q

What are changes in the subacute stage?

A

Macrophages

Reactive Gliosis (gemistocytes)

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15
Q

What are changes in the subacute stage?

A

Macrophages (FOAMY)

Reactive Gliosis (gemistocytes, Small nuclei pushed to the side)

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16
Q

What are changes in the remote stage?

A

Cyst Formation

Glial Scarring

17
Q

What happens in perinatal asphyxia in premature infants?

A

Germinal matrix hemorrhage

Intraventricular hemorrhage

18
Q

What happens to term infants that experience perinatal asphyxia?

A

Oligos are vunerable

Periventricular leukomalacia

Multicystic encephalopathy (basket brain)

19
Q

What causes cerebral palsy?

A

Survivors of perinatal asphyxia

20
Q

What causes spontaneous hemorrhage?

A

Hypertension

Ruptured aneurysm

Vascular malformation

Other: amyloid, vasculitis

21
Q

What is the most common sites of HTN hemorrhage?

A

BG (65%), Pons 15%, Cerebellum 10%

22
Q

Where do saccular berry aneurysms occur?

A

They arise at branch points

Result in subarachnoid hemorrhage (WHOL)

Might rupture into ventricles to split the brain

23
Q

What is the main cause of saccular berry aneurysms?

A

Abnormality of internal elastica

24
Q

Where is the most common site of saccular aneurysms?

A

Anterior communicating/anterior cerebral junction (40%)

Posterior communicating and MCA junction

25
Q

What are some types of vascular malformations?

A

Arteriorvenous malformations (AVMs)

Cavernous angioma

Telangiectasia

26
Q

What causes AVMs?

A

hemorrhage, seizure, local ischemic injury

27
Q

What are some characteristics of amyloid angiopathy?

A

Deposits of amyloid (from APP) close relation to Alz D

Familial: APP (dutch)
-Icelandic (cystatin C mutation)

28
Q

Where do amyloid deposit hemorrhage usually occur?

A

Within the lobar interparenchyma (White matter)

-HTN usually hits gray matter

29
Q

What are some genetic Cerebrovascular diseases?

A

CADASIL: cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
-NOTCH-3 mutations

MELAS: mitochondrial encephalopahty Lactic acidosis stroke like episodes
-MITO dna mutations

Path II (11 decks)

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