Neuro 70: Pathology of cerebral vasc disease Flashcards

1
Q

How does the healing of a cerebral infarct differ from an infarct that occurs elsewhere in the body?

A
  • cerebral infacts do not result in collagenous scars
  • instead the necrotic issue is removed –> cavity is left behind
  • the cavity is surrounded by gliosis
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2
Q

What is the most common dirrect cause of death following a stroke?

A
  • herniation of the brainstem
  • during the first several days after an infarct there is swelling due to edema that can cause compression or herniation of important structures
  • *so initial tx of stroke is to reduce this swelling!
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3
Q

What are 4 factors that can contribute to a pt having an infarction?

A
  1. decreased oxygen of the blood - Hbopathy, hypoxia
  2. decreased perfusion - hypotension, stasis, increased intracranial P
    - could also be from carotid stenosis –> dont need total occlusion to get and infarct!
  3. hypercoaguable state - pregnancy, oral contraceptives, antiphospholipid antibody syndrome
  4. HTN
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4
Q

Histology of an acute cerebral infarct

A
  • nuclei will have ground glass appearence
  • cytoplasm shrinks
  • cell becomes esinophilic
  • nackground becomes vacuole-ated & fluffy looking = edema
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5
Q

Histology of the early organization following an acute infarct

A
  • see lots of macrophages that come in from the peripheral blood
  • see endothelial cells begin to grow in the damaged areas
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6
Q

What is seen 4 days after a cerebellar infarct

A
  • the affected area is well demarcated

- the defective area is swollen and fragile –> begins to fall appart and crack

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7
Q

What is see 2-3 weeks histologically after an acute cerebellar infarct

A
  • sea of macriohages that fill up the area where the brain tissue was previously
  • see neovascularization and capillaries
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8
Q

What is seen in the early cavitation stage of healing from an acute infarct?

A
  • about 2 mnths after the infarct
  • macrophages begin to leave
  • the infarcted area begins to collapse, leaving behind the neovascularzation –> see lots of tiny vessels
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9
Q

What is left 3 weeks after an acute infarct has been healing?

A
  • there is a cavity with thin-walled blood vessels within it
  • trabecular looking
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10
Q

3 most common locations for primary thrombosic occlusions to occur?

A
  1. Basilar a.
  2. Vertebral a.
  3. Internal carotid a.
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11
Q

3 most common locations for embolic occlusions?

A
  1. Middle cerebral artery –> sort of like a continuation of the internal carotid, so thats why a lot of emboli will end up here!
  2. Anterior cerebral artery
  3. Posterior cerebral artery
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12
Q

What makes the lenticulostriate arteries more vulnerabel to infarcts?

A

-b/c they are skinny vessels that come off at right angles !

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13
Q

Lacunar infarcts

A
  • typcially seen in pts with HTN
  • the compensation to normotension will cause distal areas to become ischemic –> causes tiny infarcts
  • there can be early swelling around these lesions that causes the compression and dysfunction of the surrounding tissue –> so the sx can be more severe than expeted
  • recovery is uaully good and the sx often go away after 3mnths when the swelling reduces
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14
Q

Granular atrophy

A
  • secondary to multiple small infarcts that are the result of poor profusion to distal vasculature
  • seen in pts with poor control of their HTN
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15
Q

Leukoaraiosis

A
  • areas in the white matter of decreased density
  • shows up on CT as an UBO (unidentified bright object)
  • associated HTN
  • can cause cognitive impairment
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16
Q

HTN

A
  • most important cause of both infarction and spontaneous hemorrhage
  • causes both atherosclerosis and changes in smaller vessels of the brain
17
Q

MIliary microaneurysms

A
  • AKA Charcot-Bouchard aneurysms
  • microscopic swellings of the small perforating arteries in the brain
  • usually seen in HTN pts –> but occassionally in normotensive elderly pts
  • the rupture of these small vessels can cause HTN intracerebral hemorrhages
  • most commonly seen in lenticulostirate arteries
  • the hemorrhages are seen (in decreaseing order) in the deep grey matter –> pons –> cerebellum –> and a few in the cerebral hemispheres
18
Q

Infarct v. hemorrhage: TIA hx

A
  • Infarct = hx of TIA

- hemorrhage = NO hx of TIA

19
Q

Onset of infarct v. hemorrhage

A
  • infarct = onset @ rest

- hemorrhage = onset during activity

20
Q

Pain w/ infarct v. hemorrhage?

A
  • infarct = minimal discomfort

- hemorrhage = headache (often severe)

21
Q

Deficits w/ infarct v. hemorrhage?

A
  • infarct = sudden onset of focal deficit w/out change in consciousness or mental status
  • hemorrhage = rapidly evolving neurological deficit w/ altered mental status/conciousness
22
Q

HTN and infarct v. hemorrhage?

A
  • infarct = moderate HTN (occasionally normotensive)

- hemorrhage = severe HTN (occasionally moderate)

23
Q

CSF in infarct v. hemorrhage?

A
  • infarct = clear

- hemorrhage = bloody

24
Q

Amyloid angiopathy

A
  • amyloid deposits in the walls of the vessels in the CNS

- use congo red stain or polarized light to see the amyloid material

25
Q

Duret Hemorrhages

A
  • hemorrhages in the ventral and paramediam portions of the midbrain and the pons
  • associated with brainstem herniation & raised ICP
  • can be caused by acute hematoma
26
Q

Where are berry aneurysms typically seen? + what do they typically have associated with them?

A
  • in the branch points of arteries
  • usually in the anterior portion of the circulation
  • AKA saccular or congenital aneurysms
  • polycystic kidney is usually associated!!!
27
Q

What is the most common cause of spontaneous (non-traumatic) subarachnoid hemorrhage?

A

-rupture of a berry aneurysm