Cerebrovascular Diseases Flashcards

(43 cards)

1
Q

What regions of the brain are supplied by:

  • PCA
  • MCA
  • ACA
A
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2
Q

Circle of Willis

A
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3
Q

What is hypoxia?

A

Deprivation of O2 in the brain

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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
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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.

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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
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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
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8
Q

Borderline infarcts occur in watershed areas between……

A

Anterior cerebral & middle cerebral arteries
Middle & posterior cerebral arteries

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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
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10
Q

What is selective vulnerability?

A

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

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11
Q

What are the 3 most vulnerable cells of the brain?

(in decreasing order)

A
  • Neurons
  • Oligodendrocytes
  • Astrocytes
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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
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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
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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)
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15
Q

What is severe global ischemia?

A
  • Severe ischemia –> widespread neuronal death irrespective of regional vulnerability
  • Corresponds to brain death
  • Non-perfused brain
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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)
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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
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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.

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
**Gross Morphology of Infarct ** * Acute * Subacute * Chronic
* **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
**Microscopic Morphology of Infarct** * Acute * Subacute * Chronic
* **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
What does an **acute infarct** look like microscopically?
* Pallor, neutrophils * Preservation of small area around vessel * Red neurons
28
**Subacute infarct** Histology Imaging
* 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
**Chronic Infarct** Gross/Histology Imaging
* Gross/Histology: cavity w/ fibrillary astrocytic scar * Imaging: large cavity, scar tissue
30
**Vascular Dementia** Definition Patterns of damage
* 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
**Cerebral Venous Thrombosis** Definition Causes
* **Hemorrhagic infarcts** * **Superior sagittal sinus or lateral sinuses** * Parasagittal hemorrhagic infarcts * Causes * Infection, injury, neoplasm, surgery * Pregnancy, oral contraceptives, hematologic abnormalities, dehydration, malignancy
32
What are the 3 major causes of **Intracerebral Hemorrhage**?
* HTN * Vascular Malformations * Amyloid angiopathy
33
How does **HTN** cause intracerebral hemorrhage?
* 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
What does **hypertensive** intracerebral hemorrhage look like.... Grossly? Histologically?
* Gross * Extravasation of blood, compression of adjacent brain * Histology * **Hyaline arteriolosclerosis** * Weakens arteriole & predisposes rupture * Charcot-Bouchard microaneurysm
35
What are the 2 types of **vascular malformations** that cause intracerebral hemorrhage?
* Arteriovenous malformations * Cavernous angioma
36
**Arteriovenous Malformation** Definition Epidemiology Clinical Presentation
* Most common * M \> F * 10-30 YO * MCA distribution * Can present w/ bleeding * Often presents as: * **Seizures** * **Headaches** * **Focal deficits**
37
**Arteriovenous Malformation** Gross Histology
* Gross * Tangled network of vessels w/ arteriovenous shunt * Histology * Greatly enlarged blood vessels separated by **gliotic tissue** (evidence of prior hemorrhage)
38
What is a **cavernous angioma**?
* Cerebellum, pons, white matter * No intervening brain tissue * _Evidence of prior bleeding _
39
What is **amyloid angiopathy**?
* **Deposition of β-amyloid into the vessel wall** * Elderly, Alzheimer’s disease * Histology: Congo red stain, β-amyloid immunostain
40
What are 5 common causes of **lobar hemorrhage**?
* Neoplasms * Drug abuse * Vasculitis * Hemorrhagic diathesis * Amyloid angiopathy
41
What are the 2 common causes of **subarachnoid hemorrhage**?
* Trauma * Aneurysms
42
What types of _aneurysms_ can cause a subarachnoid hemorrhage? (3)
* Saccular (berry) * Mycotic (fungus) * Fusiform, atherosclerotic
43
**Saccular "Berry" Aneurysm** Definition Clinical Presentation Histology
* **“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)