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17 CNS Pathology > 17.4 Cerebrovascular disease > Flashcards

17.4 Cerebrovascular disease Flashcards

1
Q

Berry aneurysms

  • describe how they are formed
  • most common location
A
  • they occur at branch points of vessels because that is where they lack a media layer (between intima and adventitia)
  • anteior circle of willis, at branch points of the anterior communicating artery
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2
Q

cerebrovascular disease:

  • divide into what categories?
  • what %
A
  1. ischemia–85%
    a. focal
    b. global (GCI–global cerebral ischemia)
  2. hemorrhage–15%
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3
Q

Global cerebral ischemia (GCI)

  • major etiologies (4)
  • give mech and example for each
A
  1. low blood perfusion (atherosclerosis)
  2. acute decrease in blood flow (shock)
  3. chronic hypoxia (anemia)
  4. hypoglycemia (insulinoma)
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3
Q

Lacunar stroke:

-involvement of what brain part leads to a pure motor stroke?

A

Internal capsule

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4
Q

Intracerebral hemorrhage

  • classic cause
  • most common location
A
  1. rupture of charcot-bouchard microaneurysms of lenticulostriate vessels. (caused by chronic HTN)
  2. basal ganglia
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4
Q

Pt with Marfan’s

-what to worry most about in the brain?

A

-berry aneurysms leading to SubA hemorrhage

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5
Q

What is the final gross appearance/state of brain tissue involved with ischemic stroke?

A

After a month, there is a glial cyst (cyst lined with astrocytes)

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6
Q

Lacunar stroke

  • mech
  • common locations and their effects (2)
  • gross appearance
A
  • hyaline arteriolosclerosis (from benign HTN or diabetes) affects smaller vessels, most commonly the Lenticulostriate vessels.
  • causes small cystic ‘Lake’ infarcts.

locations near base of brain:

  1. thalamus–leads to pure sensory stroke
  2. internal capsule–leads to pure motor stroke
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7
Q

Cortical lamellar necrosis

A

-damage to pyramidal neurons of layers 3,5,6 due to Global cerebral ischemia, moderate

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9
Q

Global cerebral ischemia (GCI)

  • divided into what severities?
  • describe them
A
  1. mild–transient confusion, prompt recovery (classic ex is insulinoma with tx)
  2. moderate–infarcts in watershed aeas, with damage to vulnerable regions
  3. severe–diffuse necrosis, survival leads to vegetative state
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10
Q

Intracerebral hemorrhage

  • how to best prevent
  • presentation
A
  • Tx chronic HTN (which causes the charcot-bouchard microaneurysms)
  • HA, nausea, vomiting, eventual coma.
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10
Q

Pt presents with ‘worst headache of his life’ and has a stiff neck..

Think what?

A

Think subarachnoid hemorrhage.

-meningitis can present similarly, but ‘worst HA’ reserved for SubA hemorrhage.

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11
Q

Ischemic stroke:

-what is the earliest sign of cellular change? histologically

A

Red neurons, appear at 12hours

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13
Q

How does an insulinoma classically affect the brain?

A

Global cerebral ischemia, mild.

High insulin means transient hypoglycemia, which causes ischemia to brain. This, when treated with glucose, resolves quickly (mild GCI)

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13
Q

TIA vs stroke

A

TIA is

Focal neurologic defects from regional ischemia

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15
Q

Lacunar stroke:

-infarct of what brain area leads to pure sensory stroke?

A

Thalamus

16
Q

Subarachnoid hemorrhage

  • classic clinical symptoms
  • what do you see on LP?
A
  • ‘worst headache of life’ with nuchal rigidity
  • lumbar puncture: see xanthochromia (yellow hue due to bilirubin breakdown of blood)
17
Q

Subarachnoid hemorrhage

-assoc with what disorders? (2)

A
  1. Marfan’s
  2. ADPKD–auto dominant polycystic kidney disease
18
Q

Pt has family history of people dying of hemorrhagic strokes.

Think what?

A

ADPKD

  • auto dom polycystic kidney disease
  • increased risk of berry aneurysms
19
Q

Subarachnoid hemorrhage

  • most common cause
  • other causes include (2)
A
  • rupture of berry aneurysm
    1. AV (arteriovenous) malformation
    2. anticoagulated state
20
Q

Embolic stroke

  • mech
  • where does embolism usu come from?
  • where does embolism usu lodge?
  • gross appearance
A
  • Embolism (usu from heart, left side from A Fib), usu lodges in MCA. After the body lyses it, there is a hemorrhagic infarct.
  • Hemorrhagic infarct
21
Q

Ischemic stroke, in general

-what are the pathological changes over time? (5)

what timeframe?

A

Think: 1 day, 1 week, 1 month

  1. Red neurons–12 hours

—-1 day—-

  1. neutrophils–day 1-3
  2. macrophages (microglial cells)–days 4-7

—-1 week—-

  1. granulation tissue, healing

—-1 month—-

  1. gliosis–gliotic cysts (cysts lined by astrocytes)
22
Q

Global cerebral ischemia, moderate

-what are highly vulnerable regions, vulnerable to damage? (3)

A
  1. pyramidal neurons of cerebral cortex (layers 3,5,6)–Cortical Lamellar Necrosis
  2. pyramidal neurons of hippocampus (temp lobe)–long term memory
  3. Cerebellum, purkinje layer. (integrate sensory perception with motor control)
23
Q

How can Global cerebral ischemia affect cerebellum?

A

Moderate GCI can damage vulnerable Purkinje layer of cerebellum.

(integrates sensory perception with motor control)

25
Q

Thrombotic stroke

  • mech
  • typical location
  • gross appearance of infarct
A
  • rupture of atherosclerotic plaque causes clotting. Even though body tries to lyse the clot, the presence of the ruptured plaque will make clot regrow. Thus, no blood will reach past the clot, resulting in Pale infarct.
  • atherosclerosis usu occurs at branch points (eg bifurcation of internal carotid and MCA in circle of willis)
  • Pale infarct
26
Q

what are microglial cells and their role in stroke

A

-they are the macrophages of the brain.

appear days 4-7 after ischemic stroke

27
Q

You do a lumbar puncture and it has a yellow hue.

Think what?

A

Xanthochromia, from bilirubin breakdown. Must be bleeding into CSF

-Think subarachnoid hemorrhage

28
Q

Ischemic stroke

  • divided into what types (3)
  • what is characteristic type of damage?
A
  1. thrombotic–Pale infarct
  2. embolic–hemorrhagic infarct
  3. lacunar–Lacunar infarcts

17 CNS Pathology (8 decks)

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