Cerebrovascular Disease Flashcards

1
Q

What are the two classes of cerebrovascular disease?

A

Ischemic (85%)

Hemorrhagic (15%)

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2
Q

What are the major etiologies of global cerebral ischemia?

A

Low perfusion (ie atherosclerosis)

Acute decrease in blood flow (ie cardiogenic shock)

Chronic hypoxia (ie anemia)

Repeated episodes of hypoglycemia (ie insulinoma)

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3
Q

Clinical features of mild global ischemia?

A

Transient confusion with prompy recovery

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4
Q

Clinical features of severe global ischemia

A

Diffuse necrosis

Survival leads to “vegetative state”

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5
Q

What are 3 highly vulnerable structures in moderate global ischemia?

A

Pyramidal neurons of the cerebral cortex

Pyramidal neurons of the hippocampus

Purkinje layer of the cerebellum

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6
Q

What is the effects of damage to the pyramidal neurons of the cerebral cortex?

A

Laminar necrosis

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7
Q

What is the effect of damage to the pyramidal neurons of the hippocampus?

A

Damage to long term memory

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8
Q

What is the role of the Purkinje layer of the cerebellum?

A

Integrate sensory perception with motor control

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9
Q

What is an ischemic stroke?

A

Regional ischemia to the brain that results in focal neurologic deficits lasting > 24 hours

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10
Q

What is a regional ischemia to the brain with symptoms that last for less than 24 hours?

A

Transient ischemic attack

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11
Q

What are the subtypes of strokes?

A

Thrombotic stroke

Embolic stroke

Lacunar stroke

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12
Q

Thrombotic stroke is due to _____________

A

rupture of an atherosclerotic plaque

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13
Q

Where does atherosclerosis usually develop?

A

Usually develops at branch points (ie bifurcation of internal carotid and middle cerebral artery in the circle of Willis)

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14
Q

Does a thrombotic stroke result in a pale or hemorrhagic infarct?

A

Pale infarct

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15
Q

Where is the most common source of an emboli causing an embolic stroke?

A

emboli from the left side of the heart

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16
Q

Which artery is usually involved in an embolic stroke?

A

Middle cerebral artery

17
Q

Does an embolic stroke result in a hemorrhagic infarct or pale infarct?

A

Hemorrhagic infarct

18
Q

Lacunar strokes are usually secondary to __________

A

Hyaline arterolosclerosis

19
Q

Lacunar strokes usually involve what vessels?

A

Lenticulostriate vessels

20
Q

How do the lacunar strokes involving the lenticulostriate vessels grossly present?

A

Small cystic areas of infarction

21
Q

What are the results of lacunar strokes afecting the internal capsule?

A

Pure motor stroke

22
Q

What is hte result of lacunar strokes affecting the thalamus?

A

Pure sensory stroke

23
Q

Ischemic strokes result in what kind of necrosis?

A

Liquefactive necrosis

24
Q

How does liquefactive necrosis progress from the time of initial necrosis to end result?

A

Eosionophilic change in the cytoplasm of neurons (red neurons) 12 hours after infarction

Coagulative necrosis 24 hours after infarction

Infilitration by neutrophils (days 1-3)

Microglial cell infiltration (days 4-7)

Granulation tissue (weeks 2-3)

Results in fluid filled cystic space surrounded by gliosis

Remember as:

Red neurons (hrs) –> Neutrophils and microglial cells (days) –> granulation tissue (weeks) –> gliotic cyst (months)

25
Intracerebral hemorrhage is classically due to \_\_\_\_\_\_\_\_
Rupture of Charcot-Bouchard microaneurysms of the lenticulostriate vessels
26
Rupture of Charcot-Bouchard microaneurysms of the lenticulostriate vessels is a complication of what condition?
HTN
27
What site is most commonly affected by intracerebral hemorrhage?
Basal ganglia
28
Presentation of intracerebral hemorrhage
Severe headache Nausea Vomiting Eventual coma
29
How does subarachnoid hemorrhage present?
Sudden headache ("worst headache of my life") with nuchal rigidity
30
What does a lumbar puncture show in subarachnoid hemorrhage?
Xanthochormia (yellow CSF due to bilirubin breakdown)
31
MCC of subarachnoid hemorrhage
Rupture of berry aneurysm (85%)
32
What are berry aneurysms?
Thin walled sacular outpouchings that **lack a media layer **
33
What is the MC location of berry aneurysms?
Anterior circle of Willis at branch points of the anterior communicating artery (branch points often missing media layer)