Stroke Pathology Flashcards

1
Q

define stroke

A

development of a focal or global neurological deficit due to a vascular events.

warnings signs:
transient clinical events may also occur due to a vascular event.
Silent vascular events may occur.

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2
Q

what is the most common pathological event behind a stroke? second most? third most?

A

Infarction (75%)

Haemorrhage (25%)

Subarachnoid haemorrhage (5%) 
-more related to pathology large vessels in subarachnoid space, rather than trauam
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3
Q

prevalence of stroke related mortality?

A

third leading cause of death. 10% of all deaths attributable to stroke.

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4
Q

Risk factors for cerebral infarction?

A

aging, hypertension, cardiac disease (atrial fibrillation), hyperlipidaemia, diabetes mellitus, hypercoagulable states (antiphospholipid antibody syndrome), obesity, smoking

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5
Q

what is a cerebral infarction?

A

necrosis of cerebral tissue in a particular vascular distribution in response to vessel occlusion or severe hypo-perfusion.
–>usually related to arterial obstruction, but may also be at level of arterioles, veins, and heart.

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6
Q

mechanisms of infarction?

A
  • inadequate supply of blood to tissues due to pump failure.
  • inadequate supply of blood due to narrowed vessel lumen (due to atherosclerosis, thrombosis, hypertensive vessel thickening, diabetes, amyloid angiopathy).
  • vessel occlusion by embolus (most common)
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7
Q

what is the most common cause of infarction? and thus stroke?

A

vessel occlusion by embolus

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8
Q

cardiac cause of cerebral infarction?

A

from thrombi built up in valves or recent infarct site in myocardium

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9
Q

T/F - in pathogenesis of cerebral infarction, the most common cause of large and small vessel occlusion is thrombosis (not emboli).

A

TRUE. Thrombosis is much more common. Except in the posterior circulation, where emboli are more commonly the cause of occlusion.

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10
Q

T/F thrombosis is the most common cause of venous occlusion leading to cerebral infarction?

A

TRUE.

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11
Q

how might a probe-patent interatrial septum result in thrombosis potentially causing cerebral infarct?

A

this is a congenital condition where valve flaps have not fully fused, leaving a potential opening. 1/3 of people have this.
clot thrombotic material could pass from Rt atrium to Lt atrium in situation where right atrial pressure is raised
–>right sided thrombi could develop in the legs
—–>more likely in younger patients than older.

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12
Q

what are most common sites of athersclerosis in the cerebral circulation?

A

circle of willis and associated vessels:

  • basilar artery
  • junction of vertebral arteries
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13
Q

3 risks of atherosclerosis?

A

hypoperfusion
stenosis
thrombosis

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14
Q

what gross/histological features would be present 36hrs after cerebral infarction?

A

loss of definition b/w gray and white matter; ventricles have narrowed with midline shift at falx cerebri, sulci obliteration.

nerve cell and glial nuclei would appear shrunken, pyknotic.

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15
Q

what gross/histological features would be present days/weeks after cerebral infarction?

A

liquefactive necrosis

-lots of neutrophils and cellular debris

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16
Q

what gross/histological features would be present months/years after cerebral infarction?

A

crater in the brain left behind, with gliosis (scarring) in the margins

17
Q

how are cerebral micro aneurysms caused?

A

hyaline arteriosclerosis of tiny vessels deep in the brain substance.
-diabetes (and other conditions) may cause these vessels to thicken, allowing thrombus to develop and causing either burst or stricture.

18
Q

what causes death following cerebral infarction?

A
infarction of brain stem (and adversely affected vital areas), 
cerebral swelling,
pneumonia,
cardiovascular disease, 
pulmonary thromboembolism
19
Q

what are possible effects of raised intracranial pressure?

A

transtentorial herniation; brainstem hemorrhages

20
Q

most common cause of intracerebral haemorrhage?

A

hypertensive small vessel disease

21
Q

what are the causes of intracerebral haemorrhage?

A
hypertensive small vessel disease, 
congophilic (amyloid) angiopathy, 
blood disorder,
tumour,
vasculitis,
vascular malformation, 
drugs
22
Q

which regions of the cerebrum are most susceptible to hypertensive haemorrhage ?

A
  • basal ganglia/thalamus,
  • lobar white matter,
  • cerebellum,
  • pons

NB: characterized by presence of small vessel disease! (hyaline arteriosclerosis)

23
Q

What are the causes of non-traumatic subarachnoid hemorrhage?

A

-Rupture of sacculur aneuryms (Berry Aneurysm)**most common

  • Rupture of mycotic/atherosclerotic aneurysm
  • extension of intracerebral hemorrhage (going into ventricular system and out into subdural space)
24
Q

what are the risk factors for developing a saccular/berry aneurysm

A
  • being female
  • aging
  • polycystic kidney disease
  • Type III collagen deficiency
  • coarctatation of aorta
  • hypertension
  • smoking/alcohol
25
Q

where are saccular aneurysms most likely to occur?

A
  • sites of congenital weakness at arterial bifurcations
  • more likely anterior than posterior circulation

especially at:

  • bifurcation of middle cerebral artery
  • junction of ICA and posterior communicating artery
  • anterior communicating artery
26
Q

complications of ruptured aneurysm?

A
  • subarachnoid haemorrhage (+/- intraparanchymal)
  • cerebral oedema and raised ICP
  • vasospasm and infarction (vessels in circle of willis)
  • ventricular obstruction
  • hydrocephalus