Cerebrovascular Disease and CNS Trauma 1 Flashcards

1
Q

What is a TIA

A

TIAs are transient ischaemic attacks - short-lived loss of blood supply to a certain area of the brain. TIA’s are reversible and can last froma a few minutes to 24 hours.
You may not know that you’re having a TIA while it is happening.

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2
Q

Relationship between TIA and stroke, and why?

A

Risk of stroke is highest 24-72h after a TIA.

This is due to the same mechanisms and risk factors applying to both TIA and stroke - vessel narrowing, small infarcts, hypertension.

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3
Q

What are the 4 groups of things that increase risk of stroke/CVD?

A
  • Things that increase chance of HTN
  • Things that increase chance of atherosclerosis
  • Things that increase change of thrombosis/thromboembolism
  • Diseases that weaken cerebral vessel walls (aneurysm, amyloid angiopathy)
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4
Q

List some specific risk factors for stroke

A

Hypertension

Hyperlipidaemia

Obesity

Diabetes

Smoking

Atrial fibrillation (causes 11% of stroke deaths)

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5
Q

Difference and causes of hypoxia vs ischaemia in the brain

A

Hypoxia can be caused by low oxygenation (high altitudes, lung disease) or impaired carrying capacity (carbon monoxide poisoning)

Ischaemia refers to lack of blood supply. Can be focal ischaemia (single vessel, stroke) or multifocal (rare)

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6
Q

What global condition can hypoxia lead to ?

A

Hypoxia can lead to global neuronal dysfunction - leads to ischaemia and death.

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7
Q

What are the 3 stages of morphological changes in cerebral ischaemia. What do they involve?

A
  1. Early (<24h)
    * Red neurons - swell up, become red and develop microvacuoles
  2. Subacute (24h-2wk)
  • Liquefactive tissue necrosis (no structure in brain)
  • Reactive gliosis
  • Neutrophil infiltration
  1. Repair
  • Removal of necrotic tissue
  • Further gliosis
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8
Q

What is selective vulnerability in ischaemia?

What cells are sensitive?

A

Some parts of the brain are more vulnerable to ischaemia than others:

  • Neurons are more sensitive than glial cells
  • Pyramidal cells of hippocampus and Purkinje cells of cerebellum are most sensitive
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9
Q

What is selective vulnerability in ischaemia?

What cells are sensitive?

A

Some parts of the brain are more vulnerable to ischaemia than others:

  • Neurons are more sensitive than glial cells
  • Pyramidal cells of hippocampus and Purkinje cells of cerebellum are most sensitive
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10
Q

What is ‘global cerebral ischaemia’?

How can it happen

A

Lack of supply of blood to all aras of the brain. Can occur if systolic BP < 50mmHg

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11
Q

Pathology of a severe global cerebral ischaemia case

A
  • Brain becomes oedematous and swollen, widening gyri and narrowing sulci
    • Neuronal loss and gliosis are uneven, producing a pattern called pseudolaminar necrosis
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11
Q

Pathology of a severe global cerebral ischaemia case

A
  • Brain becomes oedematous and swollen, widening gyri and narrowing sulci
    • Neuronal loss and gliosis are uneven, producing a pattern called pseudolaminar necrosis
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12
Q

What are the three different mechanisms behind focal cerebral ischaemi?

A

FCI, a.k.a. stroke, can occur from:

  • Blockage of blood supply (e.g. thromboembolus, atherosclerosis, compression of vessel)
  • Disruption of blood supply (haemorrhage - aneurysm)
  • Reduction in blood supply (decreased perfusion, reduction in cardiac output)
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13
Q

Two mechanisms of stroke

A

Haemorrhagic stroke - red

Ischaemic stroke - pale

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14
Q

What is the most common outcome of stroke

A

Localised loss of neuroglial tissue

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15
Q

Describe the pathophysiology of stroke - starting with the first change that results in oedema

A

Ischaemia causes cellular hypoxia, and depletion of ATP.

Cells then can’t maintain ionic gradient. Sodium, calcium influx into cell brings in water, causing oedema.

Cell death and inflammation worsens the oedema.

16
Q

What are the sequelae of haemorrhagic stroke not seen in ischaemic stroke?

A

Extravascular red cells break down, causing inflammation.

Blood creates haematoma, which furrther compresses brain mesenchyme.

17
Q

Sensory presentation of strokew

A

Diplopia

Visual field deficit

Vertigo

18
Q

Motor presentation of stroke

A

Hemiparesis/monoparesis

Dysarthria

Facial droop

Ataxia

19
Q

What are the roles of CT and MRI in the management of stroke?

A

CT + CT angiogram/perfusion studies are useful early to identify bleeds and oedema.

MRI is more useful in established lesions.

20
Q

Is thrombolysis always beneficial in strokes?

A

It may be beneficial (e.g. Aspirin + thrombolytic agents) in early management.

However, haemorrhagic strokes will not benefit.

21
Q

Differences in mortality and recovery in ischaemic vs haemorrhagic stroke

A

Ischaemic stroke - 10% die <1 month

Haemorrhagic stroke - 50% die <1 month

Ischaemic stroke - up to 2 years of recovery

Haemorrhagic stroke - up to 6 months of recovery

22
Q

What demographic of people are most likely to have a stroke?

A

Previous stroke patients.

23
Q

What is involved in stroke healing?

A

Removal of damaged tissue and reactive gliosis.

This slows down, leaving meshwork of glial fibres with new capillaries.

I.e. leaves a meshed cavity with some glial tissue

24
Q

What is a lacunar stroke and its cuase?

A

Lacunar strokes are occlusion of small brnahces of cerebral arteries, deep in grey/white matter and pons.

Result in small cavity (lacuna = empty space)

Always caused by HTN + ischaemic

25
Q

What are border zone strokes and what are they caused by?

A

Area of ischaemia localised to border zones between arterial territories.

Always caused by global hypoperfusion