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1 - PBS2 > 41 - Stroke > Flashcards

41 - Stroke Flashcards

1
Q

Definition of stroke

A

Development of a focal or global neurologic deficit related to a vascular event
Can be transient (transient ischaemic attack)
Can be ‘silent’ (not immediately apparent, EG cerebellar infarct manifesting as brief dizzy spells)

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2
Q

Pathologic processes involved in stroke
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A

•INFARCTION— 75%
•(Death of tissue due to inadequate blood supply)
•HAEMORRHAGE— 20%
•(tissue injury due to escape of blood from vessel/s)
•SUBARACHNOID HAEMORRHAGE— 5%
(Escape of blood primarily into the subarachnoid space. Not related to trauma)

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3
Q

Number of Australian deaths attributable to stroke

A

~10% of all deaths.
Third leading cause of death.
Significant morbidity in survivors

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4
Q

Risk factors for cerebral infarction

1 - 8

A
  • AGING
  • HYPERTENSION
  • CARDIAC DISEASE [eg atrial fibrillation]
  • HYPERLIPIDAEMIA
  • DIABETES MELLITUS
  • HYPERCOAGULABLE STATES eg antiphospholipid antibody syndrome
  • SMOKING
  • OBESITY
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5
Q

Most common cause of cerebral infarction

A

Arterial obstruction.

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6
Q

Ways in which cerebral vessels can narrow

A

Atherosclerosis
Thrombosis
Hypertensive vessel thickening, diabetes,
Amyloid angiopathy (small vessel disease, can cause either obstruction or rupture)

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7
Q

Most common cause of cerebral arterial blockage

A

Embolus

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8
Q

Main source of emboli for anterior cerebral arteries

A

Cardiac emboli

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9
Q

Main source of emboli for posterior cerebral arteries

A

In situ emboli

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10
Q

Pathology state where cardiac emboli can be generated

A

Valve vegetations in bacterial or non-bacterial thrombotic endocarditis

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11
Q

Structural defect in heart that can increase risk of cardiac emboli

A

Probe-patent interatrial septum.
Increases risk of an embolus passing from right to left atrium during raised right atrial pressure (EG: a thrombus formed in legs, EG DVT).
In ~1/3 people.

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12
Q

Common sites of atherosclerosis in the Circle of Willis

A

Internal carotids.
Vertebral arteries.
Basilar artery.

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13
Q

Surgery for removing atheroscleroses

A

Endarterectomy

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14
Q

Why does the brain swell after infarction?

A 
Cytotoxic oedema (main source of oedema) 
Vasogenic oedema (where there is still a blood supply).
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15
Q

Appearance of a 36-hour brain infarction

A

No difference in gross and microscopic appearance of cerebral tissue.
Swelling (can lead to subfalcine, tentorial herniations)

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16
Q

Appearance of a brain infarct after days-weeks

A

Macrophages, etc infiltrate tissue, begin phagocytosing dead tissue
Process of liquefaction
Swelling decreases a lot.

17
Q

Appearance of a brain infarct after months-years

A

Gliosis (not fibrosis).

Hole where the necrosis was

18
Q

What often happens with embolic cerebral infarcts?

A

Become haemorrhagic

Can also occur with venous obstruction.

19
Q

Pathology of small cerebral vessels that can lead to thrombosis, aneurysm, bursting.

A

Hyaline arteriolosclerosis

20
Q

Type of aneurysm caused by hyaline arteriolosclerosis

A

Microaneurysms deep within brain

21
Q

Lacunar infarctions

A

Small infarctions in brain, often from small-vessel blockage

22
Q 
Causes of death in people with cerebral infarction 
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A
  • Involvement of vital centres
  • Cerebral swelling
  • Pneumonia (from being immobilised, EG from damage to motor centres)
  • Cardiovascular disease
  • Pulmonary thromboembolism
23
Q

False localising sign

A

Where there is swelling in one area (EG from subfalcine, transtentorial herniations), and because this compresses the contralateral part of the brain, can make it appear that both parts of brain have been lesioned.

24
Q 
Causes of intracranial haemorrhage
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A
  • Hypertensive small vessel disease
  • Amyloid angiopathy
  • Blood disorders
  • Tumour
  • Vasculitis
  • Vascular malformation
  • Drugs
25
Q

Characteristic of hypertensive haemorrhage (cerebral)

A

Small vessel disease (hyaline arteriolosclerosis)

26
Q

Why is acute cerebellar hypertensive haemorrhage an acute surgical emergency?

A

Can put pressure on 4th ventricle, close it, and dramatically increase ICP

27
Q 
Particular sites of hypertensive cerebral haemorrhage 
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A

Basal ganglia/thalamus
Lobar white matter
Cerebellum
Pons

28
Q

Cerebral amyloid angiopathy
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A

1) Deposition of amyloid beta in walls of superficial supratentorial blood vessels
2) Associated with superficial haemorrhages, often multiple (as more likely to survive more superficial haemorrhages)
3) Association with Alzheimer’s disease

29
Q

Disease affecting deep blood vessels in brain

A

Hypertension

30
Q

Disease affecting superficial blood vessels in brain

A

Cerebral amyloid angiopathy

31
Q

Histological appearance of amyloid angiopathy

A

Looks very similar to hyaline arteriolosclerosis with H/E stain.
Will be located superficially, whereas hyaline is deeper.
Need to stain for amyloid.

32
Q

Causes of non-traumatic sub-arachnoid haemorrhage
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A

1) Rupture of saccular (Berry) aneurysm (most common cause)
2) Rupture of other types of aneurysm (mycotic (infective), atherosclerotic)
3) Extension of intracerebral haemorrhage

33
Q 
Risk factors for saccular aneurysms
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A

1) Female
2) Increased age
3) Polycystic kidney disaese
4) Coarctation of aorta
5) Hypertension

34
Q

Where do saccular aneurysms occur?

A

Sites of congenital weakness at arterial bifurcations.

In anterior circulation much more than posterior

35
Q

Three common sites of saccular aneurysm

A

1) Middle cerebral artery bifurcation/trifurcation
2) Junction of internal carotid and anterior communicating arteries
3) Distal anterior communicating artery complex

36
Q 
Complications of aneurysm rupture 
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A

1) Subarachnoid haemorrhage
2) Cerebral oedema, increased ICP
3) Vasospasm leading to infarction
4) Ventricular obstruction leading to hydrocephalus

37
Q

What leads to vasospasm, leading to infarction?

A

Bursting of aneurysm leads to vasospasm

1 - PBS2 (96 decks)

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