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Pathophysiology - Neurology > Pathology of Cerebrovascular Disease > Flashcards

Pathology of Cerebrovascular Disease Flashcards

1
Q

What is the most important predisposing factor to cerebrovascular disease and is it worse in intracranial or extracranial vessels?

A

Atherosclerosis
- could be worse in either, not necessarily occurring together

  • intracranial vessels i.e. circle of willis
  • extracranial vessels i.e. vertebral artery, internal carotid artery
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2
Q

Other than atherosclerosis, what are some other vascular disorders which can cause damage to the brain?

A

Arteriolosclerosis - i.e. hyaline, due to chronic HTN or diabetes
Aneurysms - saccular, mycotic
Cerebral amyloid angiopathy - Abeta amyloid
Vasculitidies
Clotting disorders
Nonthrombotic emboli

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3
Q

What gives rise to the anterior and posterior circulation of the brain?

A

Anterior - internal carotid arteries. Includes anterior and middle cerebral arteries

Posterior - vertebral arteries. Combine to form basilar and splits to form posterior cerebral arteries.

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4
Q

Give the arteries travelled around one trip of the circle of Willis, starting at basilar artery

A

Top of basilar artery -> P1 segment of PCA -> PCA junction -> posterior communicating artery -> MCA/ICA junction -> A1 segment of ACA -> anterior communicating artery -> A1 segment of ACA -> MCA/ICA junction -> posterior communicating artery -> PCA junction -> P1 segment of PCA -> top of basilar artery.

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5
Q

What are the main arteries supplying the basal ganglia and thalamus?

A

Basal ganglia - lenticulostriate arteries - arise from M1 segment of MCA

Thalamus - branches of the posterior cerebral artery

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6
Q

What artery supplies the medial convexity of the brain? The lateral surface?

A

Medial convexity - primarily the ACA, back to the occipital lobe, then it’s he PCA

Lateral surface - supplied by MCA

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7
Q

What makes cutting off blood supply to the brain so problematic and which zones are most susceptible?

A

There is no collateral circulation. Watershed zones (border zones) are susceptible to decreased flow and oxygen delivery

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8
Q

What is the definition of stroke? TIA?

A

Acute neurologic dysfunction developing over minutes / hours which rapidly progresses, due to parenchymal damage due to a vascular process. Continues for more than 24 hours

TIA will have symptoms resolve in less than 24 hours (no lasting damage)

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9
Q

What is diffuse hypoxic ischemic injury?

A

Injury reflecting global brain insult such as systemic hypotension or hypoxia

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10
Q

What is the pathology of a brain infarct known as?

A

Encephalomalacia - brain softening

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11
Q

What is the timeline of histological changes which occur in ischemic stroke?

A

12 hours: Red dead neurons - eosinophilic cytoplasm with pyknosis
24-72 hours: Necrosis + neutrophilic acute inflammation
3-5 days: Microglial infiltration + liquefaction, inflammatory edema peaks
1-2 weeks: Gliosis with increased astrocytes / progressive liquefaction and removal of necrotic debris
Weeks later: Fluild-filled cystic cavitation surrounded by gliosis

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12
Q

What neurons in the brain are most susceptible to ischemic infarct during diffuse ischemic injury?

A
  1. Pyramidal neurons of cortex in layers 3, 5, and 6
  2. Pyramidal neurons of hippocampus in Sommer’s sector (CA1)
  3. Cerebellar Purkinje cells
  4. Watershed zones
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13
Q

What is the most likely cause of death in a patient with stroke?

A

Increased ICP due to inflammatory edema which occurs a few days after stroke (influx of neutrophils and microglial cells with brain swelling due to vasogenic / cytotoxic edema)

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14
Q

When is development of a secondary hemorrhagic infarct common?

A

Embolic (rather than thrombotic, superimposed on vessel) stroke, where the embolus is broken up by the body so the organ is reperfused.

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15
Q

What is a lacunar stroke and why do they generally occur?

A

A small infarct (<1cm) which occurs due to small vessel occlusion.

Commonly due to hyaline arteriolosclerosis secondary to chronic hypertension

-> occurs in lenticulostriate arteries most commonly

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16
Q

What secondary changes occur in the brain following infarct?

A

Wallerian degeneration of affected fiber pathway

Atrophy of involved adjacent structures (orthograde or retrograde degeneration)

Hydrocephalus ex vacuo may occur

17
Q

What are the causes of diffuse hypoxic / ischemic injury in the brain (global stroke)?

A
  1. Global ischemia -> failure of systemic circulation (i.e. cardiogenic shock, atherosclerosis)
  2. Systemic hypoxia -> anemia, CO poisoning, or respiratory issue
  3. Hypoglycemia -> systemic, i.e. due to insulinoma (brain needs glucose)
18
Q

What are the mediators of neural injury in ischemia?

A
  1. O2 deprivation
  2. Metabolic disruption: calcium influx, lactate buildup, free radical damage due to reperfusion
  3. Release of excitotoxins during injury (glutamate, aspartate) -> more calcium influx
19
Q

How long does it take for ischemic injury to set in for neurons?

A

About 5 minutes. Cessation of function occurs in just 10 seconds though.

20
Q

How does glucose affect cellular damage in stroke? How does temperature?

A

Hyperglycemia - promotes damage dude to overproduction of lactate, slight hypoglycemia may be protective

Temperature - hypothermia (under 30 degrees C) permits longer period of ischemic cell survival

21
Q

What happens in mild, moderate, and severe diffuse hypoxic/ischemic injury? What condition does this cause varying degrees of?

A

These are varying degrees of diffuse encephalopathy:

Mild - Transient post-ischemic confusion with recovery
Moderate - damage to most susceptible areas -> permanent deficits in memory / learning, ataxia, etc
Severe - diffuse necrosis = persistent vegetative state -> if some autonomic / brainstem functions are spared

22
Q

What is it called when you have necrosis of cerebral cortex layers 3, 5, and 6?

A

Laminar necrosis -> affecting only certain laminae

23
Q

How do brain death and respirator brain occur?

A

Ultra-severe diffuse encephalopathy

-> prolonged ischemic affects even brainstem
Braindeath: cessation of electrical activity and cerebral blood flow

Respirator brain: autolytic change from failure of perfusion following diffuse brain swelling

24
Q

What are the most common types of nontraumatic and traumatic intracranial hemorrhages?

A

Nontraumatic - intraparenchymal hemorrhage and subarachnoid hemorrhage

Traumatic - epidural and subdural hematoma (but can be any compartment)

25
Q

What are the two types of intraparenchymal hemorrhage? Where do they each occur?

A
  1. Ganglionic - “deep” - occurs in basal ganglia (lenticulostriate arteries), thalamus, pons, or deep cerebral hemisphere
  2. Lobar - superficial in cerebral lobes, not as severe
26
Q

What are the causes of each type of intraparenchymal hemorrhage?

A

Ganglionic - typically secondary to chronic hypertension -> arteriosclerosis of small vessels with formation of Charcot-Bouchard aneurysms -> massive rupture / bleed

Lobar - May also be secondary to hypertension, but often due to cerebral amyloid angiopathy, vascular malformations, coagulopathies, or vasculitis

27
Q

What is the clinical presentation of intraparenchymal hemorrhage?

A

Massive headache, nausea, vomiting, and rapid loss of consciousness due to increased ICP

Ganglionic - more severe, usually causes massive hemorrhage which is lethal

Lobar - variable clinic outcome depending on severity

28
Q

If one is to ultimately survive intraparenchymal hemorrhage, what does the pathology look like?

A

Hematoma is resorbed from periphery, and cavity is ultimately formed with gliotic hemosiderin-stained brain surrounding it

29
Q

Where in the brain does subarachnoid hemorrhage usually occur and what are two important causes?

A

Usually occurs at the base of the brain where the Circle of Willis lies

  1. Saccular “berry” aneurysm
  2. Congenital arteriovenous malformation
30
Q

What conditions predispose to berry aneurysms and where do they often occur? How do they predispose?

A
  1. Autosomal dominant polycystic kidney disease
  2. Marfan syndrome

Often occur at branch points in the circle of willis:

  1. Anterior communicating/ACA junction
  2. Posterior communicating / MCA junction
  3. MCA/lenticulostriate junction
31
Q

How do the associated syndromes of berry aneurysm predispose to forming them and what is the #1 factor for their progression?

A

Congenital loss of the tunica media at the branch points

-> #1 factor for progression is hypertension

32
Q

What is the clinical presentation of subarachnoid hemorrhage? What will lumbar puncture show?

A

Acute onset of “most severe headache of my life” due to stretching of blood vessels
-> rapid deterioration of neurologic function and increasing ICP

Lumbar puncture shows xanthochromia (yellow) or blood depending on how soon after the event it’s taken

33
Q

What are the acute and chronic complications of subarachnoid hemorrhage and what drug can be used to reduce this?

A

Acute - arterial vasospasm leading to ischemia / infarction of structures supplied by vessels (secondary ischemic stroke)
-> prevented by nimodipine

Chronic - Breakdown of hematoma with scarring which may cause a communicating hydrocephalus (damage to granulations)

34
Q

What is the most common location for lacunar infarcts secondary to hypertension?

A

Basal ganglia and internal capsule (deep cerebral white matter)

35
Q

Other that Charcot-Bouchard aneurysms and lacunar infarcts, what is one important brain pathology finding that chronic hypertension can cause?

A

Etat crible - loss of tissue density around small arteries without any infarction

“perivascular vacuolization”

  • frequently occurs in basal ganglia or white matter
36
Q

What brain syndrome does chronic hypertension cause?

A

Chronic hypertensive encephalopathy - progressive vascular dementia, gait abnormlaities, loss of reflex inhibition (pseudobulbar signs), and focal deficits

37
Q

What does malignant hypertension cause in the brain and clinically?

A

Acute hypertensive encephalopathy

Increased ICP, confusion, headache, brain edema, petechial hemorrhages, and fibrinoid necrosis of arterioles

Pathophysiology - Neurology (21 decks)

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