Stroke Flashcards

1
Q

Define stroke

A

Clinical term

Development of focal/global neurological deficit related to vascular event

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2
Q

Can transient clinical events occur due to vascular events?

A

Yes

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3
Q

Can vascular events go undetected clinically?

A

Yes

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4
Q

What are the pathological processes involved in stroke?

A

Infarction
Haemorrhage
Subarachnoid haemorrhage

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5
Q

What percentage of strokes are caused by infarction?

A

75%

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6
Q

What is an infarction?

A

Death of tissue due to inadequate blood supply

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7
Q

What percentage of strokes are caused by haemorrhage?

A

20%

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8
Q

What is a haemorrhage?

A

Tissue injury due to escape of blood from vessels

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9
Q

What percentage of strokes are caused by subarachnoid haemorrhage?

A

5%

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10
Q

What is a subarachnoid haemorrhage?

A

Escape of blood primarily into subarachnoid space

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11
Q

What is the third leading cause of death?

A

Stroke

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12
Q

What are the risk factors for cerebral infarction?

A
Ageing
Hypertension
Cardiac disease; eg: atrial fibrillation
Hyperlipidaemia
Diabetes
Hypercoagulable states
Smoking
Obesity
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13
Q

What happens in a cerebral infarct?

A

Necrosis of cerebral tissue in particular vascular distribution
Due to vessel occlusion/severe hypoperfusion

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14
Q

What is cerebral infarction usually related to?

A

Arterial obstruction

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15
Q

Where can the primary problem causing a cerebral infarct be?

A

Arterioles
Veins
Heart

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16
Q

What are the possible mechanisms of infarction?

A
Inadequate supply of blood due to pump failure
Inadequate supply of blood due to narrowed vessel lumen
- Atherosclerosis
- Thrombosis
- Hypertensive vessel thickening
- Diabetes
- Amyloid angiopathy
Vessel occlusion by embolus
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17
Q

Why is haemorrhage more likely than infarction if you have an amyloid angiopathy?

A

Wall thickens > weakens

Lumen narrowed

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18
Q

What can cause a large artery occlusion?

A

Thrombosis

Embolus

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19
Q

What can cause a small vessel occlusion?

A

Thrombosis

Embolus

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20
Q

What can cause a venous occlusion?

A

Thrombosis

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21
Q

How can infective endocarditis cause a cerebral infarction?

A

Mycotic embolus blocks vessel

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22
Q

What percentage of people have a probe-patent interatrial septum?

A

30%

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23
Q

What is a probe-patent interatrial septum?

A

Flap that can be open

24
Q

How can a probe-patent interatrial septum contribute to a cerebral infarct?

A

If right heart pressure increased > embolus crosses into left atrium from right > travels up into cerebral vessel > occlusion

25
Q

What are the common sites of atherosclerosis in the circle of Willis?

A

Anterior circulation at bifurcation
Vertebral artery
Basilar artery
Internal carotid artery

26
Q

How do thrombi form in atherosclerotic vessels?

A

Narrowing of vessel lumen
Irregularities in intima
Lend themselves to thrombus formation

27
Q

Where is an embolus more common?

A

In aortic and internal carotid branches than vertebro-basilar system

28
Q

What does the brain look like within one hour of a cerebral infarct?

A

Relatively normal

29
Q

How does cerebral oedema form?

A

Cells swell because of cytotoxic oedema

Vasogenic oedema in vascularised edges

30
Q

What does cerebral oedema cause?

A

Raised intracranial pressure

31
Q

What happens to the gyri and sulci around the swelling tissue?

A

Gyri expand

Sulci are obliterated

32
Q

What does the brain look like macroscopically in the days/weeks after a cerebral infarct?

A

Clear interface between dead and normal tissue

Liquefactive necrosis

33
Q

What does liquefactive necrosis look like microscopically?

A

Massive influx of macrophages
More and more cavitation
Some surviving blood vessels with a little new growth
Neurons don’t regenerate

34
Q

What does the brain look like in the months/years after a cerebral infarct?

A

Infarcted area replaced by cavity

35
Q

What are most cerebral infarcts caused by: thrombus or embolus?

A

Embolus

36
Q

How does a haemorrhagic infarct happen?

A

Embolus lodges > tissue necrosis, damage to blood vessels > embolus removed, naturally/iatrogenically > reperfusion into necrotic area > weakened blood vessels rupture > haemorrhage over necrosis

37
Q

Why must blood be restored before complete necrosis?

A

Avoid haemorrhagic infarction

38
Q

What is hyaline arteriolosclerosis?

A

Small vessel disease associated with hypertension

39
Q

What causes lacunar infarcts?

A

Hyaline arteriolosclerosis

40
Q

In which areas do lacunar infarcts usually occur?

A

Basal ganglia

Internal capsule

41
Q

Why do people with cerebral infarction die?

A
Most people
- Pneumonia
- Cardiovascular disease
- Pulmonary thromboembolism
Involvement of vital centres
Cerebral swelling
42
Q

What are the effects of raised intracranial pressure?

A

Transtentorial herniation

Brainstem haemorrhages

43
Q

What are the two most common causes of intracerebral haemorrhage?

A

Hypertensive small vessel disease

Congophilic/amyloid angiopathy

44
Q

Which demographic is amyloid angiopathy most common in?

A

Older people

45
Q

What are the causes of intracerebral haemorrhage?

A
Hypertensive small vessel disease
Amyloid angiopathy
Blood disorders
Tumour
Vasculitis
Vascular malformation
Drugs
46
Q

What is a hypertensive haemorrhage?

A

Presence of small vessel disease like hyaline arteriolosclerosis

47
Q

In which sites is hypertensive haemorrhage likely to occur?

A
Basal ganglia
Thalamus
Lobar white matter
Cerebellum
Pons
48
Q

What is amyloid angiopathy?

A

Deposition of beta amyloid in walls of superficial supratentorial blood vessels

49
Q

What type of haemorrhage is amyloid angiopathy associated with?

A

Superficial haemorrhages

Often multiple and of varying age

50
Q

Which neurodegenerative disease is amyloid angiopathy associated with?

A

Alzheimer’s disease

51
Q

What are the non-traumatic causes of subarachnoid haemorrhage?

A
Rupture of saccular/berry aneurysm in circle of Willis and its branches
Rupture of other aneurysms
- Mycotic
- Atherosclerotic
Extension of intracerebral haemorrhage
52
Q

What does it mean by a congenital berry aneurysm?

A

Aneurysm develops at sites of congenital weakness

Aneurysm develops with ageing

53
Q

What are the risk factors for developing a saccular aneurysm?

A
Age
Polycystic kidney disease
Coarctation of aorta
Type III collagen deficiency
Hypertension
Smoking/alcohol
54
Q

Where do 90% of aneurysms form?

A

In anterior circulation of circle of Willis

55
Q

Where are sites of congenital weakness in the circle of Willis?

A

Arterial bifucations

56
Q

What are the most common sites of berry aneurysm formation?

A

Bi/trifurcation of middle cerebral artery
Junction of internal carotid artery and posterior communicating artery
Anterior communicating artery

57
Q

What are the complications of an aneurysm rupture?

A

Subarachnoid haemorrhage
Cerebral oedema and raised intracranial pressure
Vasospasm and infarction
Ventricular obstruction > hydrocephalus