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OMS - 2 Neuro Final > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

Global cerebral ischemia (diffuse hypoxic ischemic encephalopathy) occurs when there is a _____.

A

generalized reduction of cerebral perfusion

(due to blood lost due to trauma, surgery or shock)

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2
Q

Morphologic findings of global cerebral ischemia (3)

A
  1. Watershed (Border Zone) infarcts and laminar necrosis
  2. Necrosis of purkinje cells in the cerebellum OR of pyramidal neurons in the Sommer sector of the hippocampus
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3
Q

3 ways that a cell (neuron) can exhibit selective vulnerability for necrosis?

A
  1. They have a higher metabolic demand
  2. They release excessive amount of AA NT which can be toxic to post-synaptic neuron
  3. excitotoxicity
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4
Q

Global cerebral ischemia can lead to

A

Widespread neuronal death→ clinical brain death

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5
Q

Watershed (Border Zone) infarct occurs in the _____ (location)

A

Far end of the distribution of the anterior and middle cerebral arteries (it is poorly perfused where they meet)

(this leaves it likely to undergo infarction if it demands too much metabolically)

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6
Q

Define laminar necrosis

A

Necrosis that occurs in a lamina and spreads along the cerebral cortex

(these are affected first when there is a decrease in blood flow to the brain)

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7
Q

What is it?

Location of brain?

A
  1. Watershed or Border Zone infarct in a patient with global cerebral ischemia
  2. Parasagittal region of the hemisphere

(most common area for watershed infarct)

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8
Q
A
  • Histological side of the cerebral cortex
  • Arrows point to an area of laminar necrosis
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9
Q

Where is this most likely located?

A

This is likely a deeper area of the brain

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10
Q

Focal cerebral ischemia is an occlusion of the

A

Local blood supply (infarction)

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11
Q

Causes of focal cerebral ischemia

A
  1. Atherosclerosis
  2. Vasculitis
  3. Emboli
  4. Thrombus (especially patients with a hypercoagulable state)
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12
Q

What is the difference between nonhemorrhagic or hemorrhagic infarcts?

A
  1. Nonhemorrhagic (anemic) infarcts occur when due to an atherosclertic block→ occludes artery
  2. Hemorrhagic (red) infarct occurs when an embolus suddenly excludes the artery and lyses→ collateral vessels pre-perfuse→hemmorhage

(it is important to make the distinction between the two for medication)

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13
Q

Why is it important to make a distinction between a non hemorrhagic and a hemorrhagic infarct?

A

Thrombolytic medications = contraindicated in hemorrhagic infarcts

(we can make this distinction with an MRI)

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14
Q

Early on an infarcted area of focal cerebral ischemia is described as ____.

A

Soft and edematous

(encephalomalacia; malacia=softening)

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15
Q

Later on and infarct is phagocytized and a _____ is left.

A

cystic cavity is surrounded by gliosis

(there are no fibroblasts in the area to fill it in)

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16
Q
A

Hemorrhagic infarct in the temporal lobe

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17
Q
A

Non hemorrhagic infarct in the temporal lobe (oval)

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18
Q
A

Acute cerebral infarction

(note the red-neuron changes: pykanosis of nuclei and eosinophilic)

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19
Q
A
  1. Infarct at about 10 days exhibiting necrotic debris with infiltration by macrophages and surrounding reactive gliosis.
  2. Reactive gliosis can be seen in the lower right corner
  3. Brain tissue is liquefying
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20
Q
A

Small old infarct consisting of small cystic space accompanied by some surrounding gliosis

(8 weeks-years old)

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21
Q

Hypertensive cerebrovascular disease leading to dementia: pathophysiology

A

Increase blood pressure → athero and arteriosclerosis→ vascular multi infarct dementia

22
Q

Binswanger disease

A

When infarcts mainly involve subcortical white matter

23
Q

Symptoms of vascular (multi-infarct) dementia:

A
  1. Dementia
  2. Gait disturbance
  3. Pseudobulbar signs
24
Q

Hypertensive cerebrovascular disease leading to lacunar infarcts: pathophysiology

A

Increase blood pressure → arteriolosclerosis deep penetrating vessels (small muscular arteries and arterioles in the cerebral hemispheres and brainstem)→ end up being empty cystic spaces

(internal capsule, basil ganglia and ponds or common sites)

25
Q
A

Lacunar infarct in the caudate and putamen

26
Q

Where are these typically found?

A
  1. Internal capsule
  2. Basal ganglia
  3. White matter
  4. Thalamus
  5. Pons

(typically seen in patients with hypertension)

27
Q

Lacunar infarcts of the ______ will lead to significant motor deficits

A

internal capsule

(typically seen in patients w/HTN)

28
Q

Intraparenchymal hemorrhage is also known as _____.

A

Intracerebral hemorrhage

29
Q

Intraparenchymal hemorrhage

A

Spontaneous & non-traumatic hemorrhage

30
Q

MCC of intraparenchymal hemorrhage

A

Hypertension

31
Q

MCC of intracerebral hemorrhage in patients with hypertension?

A

Charcot Bouchard microaneurysms

(involves small muscular arteries and arterioles. They also have ganglionic hemorrhages)

32
Q

Second most common cause of intraparenchymal hemorrhage?

A

Cerebral amyloid angiopathy

(Aβ40 deposited in vessel walls & Lobar hemorrhages)

33
Q

What are other causes of spontaneous intraparenchymal Hemorrhage?

A
  1. Hemorrhagic diathesis (deficient in coagulation factor or platelet dysfunction)
  2. Vasculitis
  3. Tumors

(most commonly occurs in the lobes of the cerebral hemispheres)

34
Q

Early on an intraprarenchymal hemorrhage is ______.

A

Extravasated blood compresses brain parenchyma

35
Q

Later on, an intraparenchymal hemorrhage leaves a _____.

A

Cavity surrounded by rim of hemiosiderin-laden macrophages & gliosis

(there are no fibroblasts in the brain to fill in this hole)

36
Q
A

Spontaneous intracerebral hemorrhage

37
Q

ganglionic hemorrhages are typically located in the

A

Basal ganglia or thalamus

(common in patients w/HTN)

38
Q
A

Cerebral amyloid angiopathy

(these usually give rise to lobar hemorrhages)

39
Q

______ usually gives rise to lobar hemorrhages, whereas _______most commonly gives rise to ganglionic hemorrhages.

A
  • Cerebral amyloid angiopathy
  • hypertension
40
Q
A
  • Histologic section of small arteriole of cerebral cortex
  • Cerebral amyloid angiopathy
  • Amyloid (Aß40) is the yellow part in the arteriole

(stained with Congo red)

41
Q

Subarachnoid hemorrhage most common cause

A

Saccular (berry) aneurysm

(occur in 2% of ppl)

42
Q

Saccular aneurysms occur in or near

A

The Circle of Willis

43
Q

Cause of saccular aneurysm

A

Congenital attenuation or absence of the media of arteries (typically where they come to join together)

44
Q

Once a saccular (Berry) aneurysm becomes bigger than 10 mm in diameter, there is a _____ risk of rupture per year. Mortality rate?

A
  • 50%
  • 35% (higher if they bleed again)
45
Q

What are the typical locations of Saccular (Berry) aneurysms

A
  • 30% internal carotid complex
  • 30% anterior communicating artery
  • 30% trifurcation (one of the middle cerebral arteries)

(20 to 30% of cases have multiple aneurysm sites)

46
Q

MCC of Intraparenchymal and/or subarachnoid hemorrhage

A

Arteriovenous malformation (AVM)

47
Q

Define arteriovenous malformation (AVM)

A

Composed of a tangled network of dilated blood vessels

48
Q

Arteriovenous malformations are caused by

A

Focal congenital absence of capillary bed in the brain→ arteries will then directly communicate with arteries→ veins can’t handle the pressure→ rupture

49
Q

Patients with arteriovenous malformation typically present with _____ (2).

A
  • Seizures
  • Hemorrhage (intraparenchymal or subarachnoid)
50
Q
A

Arteriovenous malformation

(“bag of worms”)

51
Q

Arteriovenous malformation ratio male to female

A

2/1

52
Q

What is the most common cause of a lobar hemorrhage in an elderly patient?

A

Cerebral amyloid angiopathy

OMS - 2 Neuro Final (36 decks)

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