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Medical Studies 2A > 1.10 Acute Insults to the CNS: Stroke/TIA > Flashcards

1.10 Acute Insults to the CNS: Stroke/TIA Flashcards

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USMLE® Step 1 flashcards
1
Q

How long does neurological dysfunction have to persist to be considered a stroke?

A

At least 24 hours

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2
Q

List some non-modifiable risk factors for stroke

A
  • Age
  • Race
  • Gender
  • History of TIA/other conditions
  • Genetics
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3
Q

List some modifiable risk factors for stroke

A
  • Things that cause clots (diabetes, heart disease like AF, hypertension)
  • Lifestyle factors (diet, exercise, alcohol, smoking)
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4
Q

Which is more common: haemorrhagic or ischaemic stroke?

A

Ischaemic (~85%)

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5
Q

What are the two kinds of ischaemic stroke?

A

Thrombotic and embolic

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6
Q

Where in blood vessels is it most common for atherosclerotic plaques to form that cause strokes?

A

Branches and curves in circulation

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7
Q

What is the most common cause of cerebral infarction?

A

Cerebral atherosclerosis

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8
Q

What are some common upstream causes of embolic stroke?

A
  • Atrial fibrillation
  • Infective endocarditis
  • Recent MI
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9
Q

Which tends to have faster onset: thrombotic or embolic stroke?

A

Embolic

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10
Q

Compare and contrast large vessel disease and small vessel disease

A
  • Usually multiple sites of infarction in SVD
  • SVD occurs in smaller vessels (“end of the road”)
  • SVD entails much smaller infarct(s)
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11
Q

What structures is small vessel disease most likely to affect?

A

Deep non-cortical structures: internal capsule, basal ganglia, brain stem

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12
Q

What is the most common risk factor for lacunar strokes in small vessel disease?

A

Chronic hypertension

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13
Q

Why are the resulting infarctions from small vessel disease called “lacunar” infarctions?

A

Because the process of healing results in small lake-like cavities

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14
Q

What syndromes can small vessel disease cause?

A

Think about the origin:
- Pure motor hemiplegia
- Pure sensory hemiplegia
- Dysarthria

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15
Q

What are some factors that influence the size of a cerebral infarction?

A
  • Availability of collateral circulation
  • Duration of ischaemia
  • Magnitude of reduction in cerebral blood flow
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16
Q

Describe red infarcts. What causes them, and are they haemorrhagic or ischaemic?

A
  • Often caused by embolic events (ischaemic, not haemorrhagic)
  • After tissue is reperfused, tiny amounts of blood leak out of damaged vessels, resulting in petechial pattern
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17
Q

Describe pale infarcts. What underlying events are they usually associated with?

A
  • Usually associated with thrombosis (non-haemorrhagic)
  • Typical thrombosis -> loss of oxygen to tissue -> infarction
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18
Q

True or false: penumbra tissue can survive for many hours using collateral blood supply

A

True

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19
Q

Under what circumstances would it not be useful to reperfuse brain tissue with thrombolysis/thrombectomy?

A

If there is no penumbra, then reperfusion injury may cause more harm than good.

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20
Q

List some factors that can cause secondary injury following stroke

A
  • Inflammation
  • Excitotoxicity
  • Loss of ion homeostasis
  • Mitochondrial damage
  • Disruption of blood brain barrier
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21
Q

Give two examples of conditions where reperfusion injury is more likely to occur?

A
  • Embolic stroke
  • Long-lasting ischaemic event
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22
Q

Describe the mechanism of reperfusion injury following embolic stroke

A
  • During embolic stroke, the endothelial lining of the vessels may be damaged
  • Upon reperfusion, this causes leakage of blood components into brain parenchyma (red infarct)
  • Damaged endothelial cells release inflammatory mediators and generate free radicals, both of which lead to increased neuronal death
23
Q

What is the typical duration of a TIA?

A

Less than 1hr

24
Q

In terms of types of tissue damage, what is occurring in a TIA?

A

Penumbra without infarction

25
Q

What pathologies can TIAs mimic?

A
  • Migraine
  • Hypoglycaemia
  • Brain tumours
  • Multiple Sclerosis (demyelinating)
26
Q

Describe the basic difference in pathology between TIA and stroke

A

Same mechanism, different duration of arterial occlusion

27
Q

Describe haemorrhagic transformation of ischaemic stroke

A
  • Re-delivery of blood into ischaemic tissue
  • Vessels damaged/leaky from ischaemia
  • Blood moves into brain parenchyma
28
Q

What is the most common underlying cause of intracerebral haemorrhage? What about non-spontaneous causes?

A

Most common: Long-standing hypertension
Non spontaneous: traumatic brain injury

29
Q

Describe cerebral amyloid angiopathy and its role in haemorrhagic stroke

A
  • Amyloid (protein) deposition in walls of arterioles
  • Leads to weakening of walls and potential haemorrhage
30
Q

Where doe intracerebral haemorrhages occur (be specific)?

A

Arterioles. Typically in deep non-cortical structures

31
Q

Describe charcot-bouchard aneurysms

A

Deposition of lipid-hyaline into walls of small branching arterioles, weakening vessel wall, leading to aneurysms

32
Q

Aside from typical clinical signs (e.g. hemiparesis/hemiplegia) of stroke, what are some clinical features specific to haemorrhagic strokes?

A
  • Severe headache
  • Vomiting
  • Rapid loss of consciousness
33
Q

What is the most common cause of subarachnoid haemorrhage?

A

Berry aneurysms

34
Q

What causes berry aneurysms, and where do they occur?

A
  • They occur at branch points in the circle of Willis
  • Developmental defects in elastic lamina causes decreased elasticity, leading to aneurysm
35
Q

How can hypertension worsen berry aneurysms?

A

By exacerbating deficits in arterial elastic laminae, increasing chance of rupture (like a bursting balloon)

36
Q

What is the most common consequence of a ruptured berry aneurysm? What is a less common consequence?

A

Most common: Subarachnoid Haemorrhage
Less common: Intracerebral haemorrhage

37
Q

What percentage of patients die immediately after a ruptured berry aneurysm?

A

30%

38
Q

What are some common clinical features of subarachnoid haemorrhage (SAH)?

A
  • Sudden onset of severe headache (nociceptors in meninges)
  • Nausea and vomiting (increased ICP)
  • Stiff neck (meningeal irritation)
  • Photophobia
  • Loss of consciousness
39
Q

What factors influence the outcome of subarachnoid haemorrhage?

A
  • Haeomorrhage severity
  • Age
  • Gender
  • Time to treatment
40
Q

Describe 2 mechanisms by which SAH causes hydrocephalus

A
  • Scarring of arachnoid granulations
  • Blocking flow of CSF
41
Q

How is hydrocephalus treated?

A

Extraventricular drain

42
Q

True or false: vasospasm occurs most commonly immediately after a SAH

A
  • False
  • Takes 4-14 days, most commonly 7 days
43
Q

Describe the mechanism of vasospasm post SAH

A
  • Blood products released due to haemorrhage
  • These products are toxic to the brain, causing them to constrict
  • Decreased blood flow to distal parts of brain
44
Q

List three common complications of haemorrhagic stroke

A
  • Hydrocephalus
  • Peri-haematomal oedema
  • Vasospasm
45
Q

Why is it better to administer antithrombolytics (e.g. alteplase) sooner in a stroke patient? (2 reasons)

A
  • Faster medication leads to higher rates of clot removal (and therefore reperfusion)
  • As time passes, the clot becomes more resistant to fibrinolysis
46
Q

True or false: endovascular thrombectomy works when tPA cannot

A

True; results in improved patient outcomes

47
Q

What investigations are used to make the diagnosis of stroke?

A
  • CT scan
  • MRI
48
Q

Describe the acute treatment of ICH

A
  • Reduce BP to around 140
  • Reverse coagulopathy
49
Q

What is a hemicraniectomy?

A

Removal of a part of the skull to allow the brain to bulge out, thus reducing some pressure.

50
Q

Describe a subacute ischaemic stroke CT presentation

A
  • Hypodensity (darkness) around vascualr territory
  • Oedema
  • Common haemorrhagic transformation
51
Q

What characterises chronic brain infarct on CT?

A

Encephalomalacia (liquefactive necrosis)

Greek word “Malakos” = “soft” ≈ “malaka”

52
Q

Risk factors for venous sinus thrombosis

A
  • Female
  • Hormonal factors (pregnancy, steroids, hyperthyroidism)
  • Infection
  • Trauma
53
Q
A

Medical Studies 2A (110 decks)

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