Cerebrovascular Diseases Flashcards

1
Q

What regions of the brain are supplied by:

  • PCA
  • MCA
  • ACA
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Circle of Willis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is hypoxia?

A

Deprivation of O2 in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 mechanisms of hypoxia?

What are some examples?

A
  • Low level of O2 in blood
    • Respiratory arrest, near drowning, severe anemia, CO poisoning
  • Low blood flow to tissue (ischemia)
    • Cardiac arrest, vessel obstruction, increased intracranial pressure
  • O2 utilization by tissue is impaired
    • Cyanide poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which statement is true?

  1. Ischemia causes more damage than hypoxia.
  2. Hypoxia causes more damage than ischemia.
A

Ischemia causes more damage than hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is global ischemia?

A
  • Systolic pressure <50 mmHg
  • Generalized reduction in cerebral perfusion, usually due to cardiac arrest, shock or severe hypotension
  • Clinical outcome dependent upon severity & duration of ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

With global ischemia, where is the damage most severe? What can this cause?

A
  • Brain damage is most severe in watershed/borderzone territories
  • If ischemia is severe, widespread neuronal death may result in:
    • Persistent vegetative state
    • Brain death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Borderline infarcts occur in watershed areas between……

A

Anterior cerebral & middle cerebral arteries
Middle & posterior cerebral arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Focal Ischemia

Definition

Causes

A
  • Infarction from obstruction of local blood supply (stroke)
  • Results from arterial stenosis and/or thrombosis, atheroemboli or thromboemboli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is selective vulnerability?

A

Certain brain cells & regions are more susceptible to hypoxia/ischemia than others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 3 most vulnerable cells of the brain?

(in decreasing order)

A
  • Neurons
  • Oligodendrocytes
  • Astrocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 most vulnerable regions of the brain?

(in decreasing order)

A
  • Hippocampus (CA1 sector – Sommer sector)
  • Lamina 3 & 5 of cerebral cortex (laminar necrosis)
  • Purkinje cells in cerebellum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What determines selective vulnerability?

A
  • Variable O2/energy requirements of different neurons & neuronal populations
  • Glutamate receptor densities
    • Glutamate is neurotoxic when present in excess, as occurs in hypoxic/ischemic brain damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do acutely hypoxic/ischemic neurons look like microscopically?

A
  • “Red is dead”
  • Pyknotic cell w/ shrunken & dark nucleus, no nucleolus visible
  • Red cytoplasm (no Nissl substance visible)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is severe global ischemia?

A
  • Severe ischemia –> widespread neuronal death irrespective of regional vulnerability
  • Corresponds to brain death
  • Non-perfused brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical signs & symptoms of severe global ischemia?

A
  • Persistent vegetative state
    • Unconscious, but w/ retention of sleep-wake cycles, primitive orienting responses, brainstem & diencephalon reflexes
  • Brain death
    • Diffuse irreversible cortical injury w/ brainstem injury (absent reflexes & respiratory drive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does severe global ischemia look like….

Grossly?

Microscopically?

A
  • Gross
    • Swollen brain
    • Slit-like ventricles
    • Often herniation
  • Microscopic
    • Pallor
    • Vacuolation of parenchyma
    • Sparse eosinophilic neurons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 3 most common causes of focal ischemia?

A
  • Thrombosis
  • Emboli
  • Lacunar infarcts/slit hemorrhages
19
Q

How does thrombosis cause focal ischemia?

A
  • Atherosclerosis
  • Most common sites
    • Carotid bifurcation
    • Origin of middle cerebral artery
    • Origin or end of basilar artery
20
Q

How do emboli cause focal ischemia?

Cardiac vs. non-cardiac sources?

A
  • Infarcts are most likely hemorrhagic
  • Cardiac source
    • Mural thrombus
      • L atrium or L ventricle
      • Predisposing factors: MI, valve disease, atrial fibrillation, paradoxical embolism
    • Endocarditis
      • Bacterial or marantic
  • Non-cardiac source
    • Atheroma (plaques in carotid arteries)
    • Fat, neoplasm, air
21
Q

______ is the most frequent vessel affected by emboli.

A

MCA

22
Q

How do lacunar infarcts/slit hemorrhages cause focal ischemia?

A
  • Hyaline arteriolosclerosis (HTN & DM)
  • Lacunes
    • Small strokes (<1-1.5cm) in subcortical brain structures
    • Basal ganglia, internal capsule, thalamus, white matter, pons
    • May be hemorrhagic
23
Q

What are some less common causes of infarction? (6)

A
  • Vasculitis
    • Non-infectious causes
    • Infectious causes
  • Arterial dissection of carotid arteries
  • Coagulation disorders
  • Microvasculopathy
    • Arteriosclerotic Leukoencephalopathy
    • CADASIL
  • Amyloid angiopathy
  • Drug abuse
24
Q

What is primary angiitis (vasculitis) of the CNS?

What is it characterized by?

Histology?

A
  • Involves multiple small/medium sized meningeal & parenchymal vessels
  • Characterized by
    • Chronic inflammation
    • Fibrinoid necrosis
    • Multinucleated giant cells
    • Wall destruction
  • Histology: fibrinoid necrosis of vessel wall w/ inflammation
25
Q

**Gross Morphology of Infarct **

  • Acute
  • Subacute
  • Chronic
A
  • Acute
    • Up to 48 hrs
    • Soft, swollen
    • Gray-white distinction blurred
  • Subacute
    • Up to 2-3 wks
    • Liquefactive necrosis
  • Chronic
    • Several months
    • Cavitated, all dead tissue removed
26
Q

Microscopic Morphology of Infarct

  • Acute
  • Subacute
  • Chronic
A
  • Acute
    • 8-12 hrs: red neurons, pallor
    • Up to 48 hrs: neutrophils (not always)
  • Subacute
    • 48 hrs to 3 wks
    • MΦ, necrotic tissue, reactive astrocytes, vascular proliferation
  • Chronic
    • Several months: cavity w/ glial scar
27
Q

What does an acute infarct look like microscopically?

A
  • Pallor, neutrophils
  • Preservation of small area around vessel
  • Red neurons
28
Q

Subacute infarct

Histology

Imaging

A
  • Days to wks
  • Histology
    • Liquefactive necrosis
    • Many MΦ, reactive astrocytes, vascular proliferation, necrotic tissue
  • Imaging
    • Maximum swelling
    • Shifting of midline structures
    • Compression of uninfarcted areas
29
Q

Chronic Infarct

Gross/Histology

Imaging

A
  • Gross/Histology: cavity w/ fibrillary astrocytic scar
  • Imaging: large cavity, scar tissue
30
Q

Vascular Dementia

Definition

Patterns of damage

A
  • Clinical S/S: stepwise progression
  • Patterns of damage
    • Small areas of infarction – multiple lacunar infarcts
    • Diffuse white matter disease – Binzwanger disease & CADASIL
    • Strategic infarcts – areas important for cognition/memory
      • Hippocampus, dorsomedial thalamus, frontal cortex, cingulate cortex
  • Many individuals will have multiple strokes & some changes of Alzheimer’s disease (mixed dementia)
31
Q

Cerebral Venous Thrombosis

Definition

Causes

A
  • Hemorrhagic infarcts
  • Superior sagittal sinus or lateral sinuses
    • Parasagittal hemorrhagic infarcts
    • Causes
      • Infection, injury, neoplasm, surgery
      • Pregnancy, oral contraceptives, hematologic abnormalities, dehydration, malignancy
32
Q

What are the 3 major causes of Intracerebral Hemorrhage?

A
  • HTN
  • Vascular Malformations
  • Amyloid angiopathy
33
Q

How does HTN cause intracerebral hemorrhage?

A
  • Most common cause of primary ICH
  • Peak occurrence in 60s
  • Abrupt onset of severe neurologic dysfunction when hematoma is large
  • Putamen, thalamus, pons, cerebellum
  • Hyaline arteriolosclerosis
34
Q

What does hypertensive intracerebral hemorrhage look like….

Grossly?

Histologically?

A
  • Gross
    • Extravasation of blood, compression of adjacent brain
  • Histology
    • Hyaline arteriolosclerosis
    • Weakens arteriole & predisposes rupture
    • Charcot-Bouchard microaneurysm
35
Q

What are the 2 types of vascular malformations that cause intracerebral hemorrhage?

A
  • Arteriovenous malformations
  • Cavernous angioma
36
Q

Arteriovenous Malformation

Definition

Epidemiology

Clinical Presentation

A
  • Most common
  • M > F
  • 10-30 YO
  • MCA distribution
  • Can present w/ bleeding
  • Often presents as:
    • Seizures
    • Headaches
    • Focal deficits
37
Q

Arteriovenous Malformation

Gross

Histology

A
  • Gross
    • Tangled network of vessels w/ arteriovenous shunt
  • Histology
    • Greatly enlarged blood vessels separated by gliotic tissue (evidence of prior hemorrhage)
38
Q

What is a cavernous angioma?

A
  • Cerebellum, pons, white matter
  • No intervening brain tissue
  • _Evidence of prior bleeding _
39
Q

What is amyloid angiopathy?

A
  • Deposition of β-amyloid into the vessel wall
  • Elderly, Alzheimer’s disease
  • Histology: Congo red stain, β-amyloid immunostain
40
Q

What are 5 common causes of lobar hemorrhage?

A
  • Neoplasms
  • Drug abuse
  • Vasculitis
  • Hemorrhagic diathesis
  • Amyloid angiopathy
41
Q

What are the 2 common causes of subarachnoid hemorrhage?

A
  • Trauma
  • Aneurysms
42
Q

What types of aneurysms can cause a subarachnoid hemorrhage? (3)

A
  • Saccular (berry)
  • Mycotic (fungus)
  • Fusiform, atherosclerotic
43
Q

Saccular “Berry” Aneurysm

Definition

Clinical Presentation

Histology

A
  • “The worse headache I’ve ever had!”
  • Increased risk w/ HTN, smoking, AVM, etc.
  • Increasing risk of rupture as size increases
  • Not present at birth, but defect in media is congenital & aneurysm develops over time
  • Occurs at branch points, 90% in anterior circulation
  • Histology
    • Fibrous wall
    • Defect in elastic & media (elastic stain)