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NPS Lectures > AP: Cerebral Hypoxia, Stroke and Cerebral Haemorrhage > Flashcards

AP: Cerebral Hypoxia, Stroke and Cerebral Haemorrhage Flashcards

1
Q

What is the difference between hypoxia and ischaemia?

A
  • Hypoxia is reduced oxygen supply.
    • Doesn’t necessarily cause damage to nerve tissue.
  • Ischaemia is reduction in blood supply.
    • A reduction in oxygen itself will not affect the brain unless it goes long enough for the heartbeat to be affected.
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2
Q

What is the mechanism in hypoxemia? (6 points)

A
  • Mechanisms to maintain oxygenation and cerebral metabolic rate
  • Hyperventilation increases tidal volume
  • Brain takes more oxygen out of blood
  • Cerebral blood flow increases
  • Erythropoietin production
  • Neovascularisation of the brain
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3
Q

What is anaemic hypoxia?

A

Low blood haemoglobin (because of anaemia) causes decreased oxygen carrying capacity.

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4
Q
  • What is histotoxic hypoxia?
  • What two toxins does it involve?
A
  • Inability of the tissue to utilise oxygen - exogenous or endogenous.
  • Involves environmental toxins such as cyanide and sulfide.
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5
Q

What is the affinity of CO for Hb compared to Oxygen?

A

200x

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6
Q

Explain the process of carbon monoxide poisoning

A
  1. Effect is similar to anaemic hypoxia
  2. Permanent until new red blood cells are produced
  3. CO binds to receptors in the brain rich in haem iron (directly, causing necrosis)
    1. globus pallidus
    2. pars reticulata of the substantia nigra
  4. CO is cardiotoxic and hypotension results
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7
Q

What are the 2 different types of pathology in hypoxia?

A
  1. Selective neuronal necrosis - only the neurones are affected as they are the most vulnerable cells
  2. Pan-necrosis - all the tissue elements undergo death: neurones, glia and vessels
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8
Q

What are the 5 kinds of asphyxia?

A
  1. Environmental - insufficienct oxygen in air e.g. child in refrigerator
  2. Toxic - competiting for oxygen e.g. CO
  3. Mechanical - airways are blocked in an unnatural fashion - e.g. postural asphyxia
  4. Pathological - respiratory diseases
  5. Iatrogenic - divers, anaesthesia
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9
Q
  • The hippocampus and the cerebellum are two regions of the brain most affected in asphyxia. What region/area/cells are first affected in these areas?
  • What are the other three areas most affected in asphyxia?
A
  • Hippocampus - CA1 region first affected.
  • Cerebellum - Purkinje cells first affected (need 4-6 hour survival time post injury for changes to be seen).
  • Thalamus.
  • Basal ganglia.
  • Brainstem.
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10
Q

Why distinguish clinically between hypoxia and ischaemia?

A
  • To predict the clinical outcome of a global insult and coma.
  • Hypoxic coma can be followed by a complete recovery; non-perfused brain results in brain death.
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11
Q

What is a subarachnoid haemorrhage?

A

Bleeding occuring in the sub-arachnoid space.

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12
Q

What are 3 causes of non-traumatic subarachnoid haemorrhage?

A
  • Rupture of a saccular (berry) aneurysm:
    • small thin walled protrusion from arteries of Circle of Willis and major branches
  • Arteriovenous malformations:
    • Abnormal development of vessels - 5% have saccular aneurysm on feeding vessels
  • Other aneurysms:
    • Fusiform: atherosclerotic
    • Mycotic: infectious - septic embolus weakens vessel wall there it lodges
    • Traumatic - old traumatic injury that ruptures later
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13
Q

What are the presentations of a subarachnoid haemorrhage?

  • Is it accepted as a sudden cause of death?
  • What symptoms?
A
  • Not accepted as sudden cause of death.
  • May present with warning symptoms.
  • Severe headache few days to weeks before rupture.
  • Ruptures when physically active/stressed/hypertension.
  • Severe generalised headache.
  • Vomiting.
  • Rapid LOC or similar but lucid interval.
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14
Q

Astrocytes, oligodendrocytes, vascular cells, and neurons are all affected in ischaemic stroke. What is the order that these cells are affected?

A
  • Neurons.
  • Oligodendrocytes.
  • Astrocytes.
  • Vascular cells.
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15
Q

What are the 2 kinds of ischaemic strokes?

A
  • Focal cerebral ischaemia.
  • Global cerebral ischaemia.
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16
Q

What is a focal cerebral ischaemia?

A
  • Outcomes of focal arterial occlusions.
  • Depends on the artery that is blocked, site of the occlusion, and the blood supply (collaterals?)
17
Q
  • What are the hallmarks of transient ischaemic attack?
  • Are there visible brain changes?
A
  • No changes visible in the brain.
  • Impaired regional blood flow - abrupt neurological deficit <24 hours.
18
Q
  • What is a lacunar stroke?
  • Clinical outcomes?
  • Where is it most frequently found?
A
  • Small occlusions (5-10mm) in small penetrating branches.
  • No clinical effect or severe effect depending on the site.
  • Frequent in the pons.
19
Q

Thrombotic strokes.

  • Most common cause?
  • What causes complete vessel occlusion?
  • Describe the pathology of thrombotic strokes.
  • Treatment plan?
A
  • Atherosclerosis
    • Plaques form at branches and curves of arteries.
    • Atheromatous plaques narrow the lumen.
  • Superimposed thrombus occludes vessel completely.
  • Initially, neurons become pink and die → Macrophages come in → Eventually a scar or cavity forms → Eventual cavitation, tissue loss, gliosis.
  • Treat with streptolysin.
20
Q

What is the Penumbra zone of focal cerebral ischaemia?

A

The central core of necrotic tissue surrounded by area of low tissue perfusion, where blood flow is critically reduced.

21
Q

How do TIAs resolve?

A

Recanalisation

22
Q
  • What are the macroscopic features of ischaemic stroke?
  • The necrotic tissue is ____ upon palpation.
A
  • Hard to see.
  • Necrotic tissue is soft on palpation.
23
Q

What are the microscopic changes of ischaemic stroke at the following time intervals?

  • 1 hour.
  • 4-12 hours.
  • 15-24 hours.
  • 2 days.
  • 3-5 days.
  • 5-7 days.
A
  • 1 hour: Microvacules visible in neurones
  • 4-12 hours: Pyknotic nuclei, cytoplasm hypereosinophilia
  • 15-24 hours: Neutrophil infiltrate
  • 2 days: Macrophages
  • 3-5 days: Astrocyte proliferation
  • 5-7 days: Capillaries start to proliferate
24
Q
  • What is an embolic stroke?
    • Where does it occur?
    • Where does it usually originate + what cause?
A
  • A cerebral embolism.
  • Usually originates from thrombus in the heart.
25
Q

What is a haemorrhagic stroke?

A

A non-traumatic (spontaneous) intracerebral haemorrhage

26
Q

What are the four most common causes of haemorrhagic stroke?

A
  • Hypertensives
  • Anticoagulants
  • Amyloid angiopathy
  • Illicit drugs
27
Q
  • What are hypertensive haemorrhages?
  • How common are they?
  • Where do they generally occur? (5 places)
A
  • Chronic hypertensive changes in the vessels (very common).
  • Generally occur:
    • Putamen
    • Internal capsule
    • Thalamus
    • Cerebellar hemisphere
    • Pons
28
Q

Explain how vascular malformations can cause haemorrhagic stroke? (2 ways)

A
  • Arterial veinous malformations - tangle of dilated vessels of abnomal arteries and veins.
  • Cavernous haemangioma - dilated thin walled channels with minimal intervening brain.
29
Q

What are other causes of cerebral haemorrhage?

A
  • Anticoagulant therapy - warfarin patients, complication of thrombolytic treatment of stroke
  • Cerebral amyloid angiopathy (CAA) - Beta amyloid deposition on vessel walls causes weakness
30
Q

What are THE three main stroke mechanisms?

A
  • Thrombus.
  • Haemorrhage.
  • Embolus.
31
Q

*HARD*

What is the standard cerebral blood flow level in mmHg?

(Idk if this is the actual typical range it’s just what I wrote down from her lecture lol)

A

69-153 mmHg.

32
Q

Describe a pure hypoxic coma?

  • How are the heart and organ affected?
  • How long can you be ventilated for before recovery?
A
  • Reduction in oxygen → can be ventilated for two weeks → recovery.
  • Heart not affected, no change in blood supply.
33
Q

The brain can be deprived of oxygen by two different mechanisms. What are they? Give examples/describe these mechanisms.

A
  • Functional hypoxia.
    • Decreased to oxygen in environment.
    • Low partial pressure of oxygen → high altitude.
    • Impaired oxygen carrying capacity (carbon monoxide).
    • Toxins that interfere with oxygen (cyanide poisoning).
  • Ischaemia.
    • Decrease in the blood supply.
    • Tissue hypoperfusion.
    • Transient or permanent.
    • Hypotension or vascular obstruction or both.
    • Decreased blood supply fails to provide the required nutrients but the removal of damaging metabolites is also impaired.

NPS Lectures (36 decks)

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