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CR2 > Stroke > Flashcards

Stroke Flashcards

1
Q

What is stroke a consequence of?

A

cerebrovascular disease interrupting blood flow to part of the brain causing ischemia and hypoxia

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2
Q

What is ischemia?

A

inadequate blood flow

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3
Q

What might cause blood flow to be interrupted?

A

Infarction - artery blockage

haemorrhage - aneurysm rupture

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4
Q

What are the types of haemorrhage stroke?

A

parenchymal - into brain tissue

subarachnoid - into subarachnoid space

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5
Q

What are some stroke symptoms?

A 
All symptoms happen suddenly:
FAST
face loss of tone or facial muscle weakness, cannot raise both arms equally, changes in speech - slurring and slow
numbness/weakness on one side of body
confusion and trouble speaking
trouble seeing
dizziness/loss of balance and co-ordination
severe headache
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6
Q

Why is time important in a stroke?

A

quicker person receives help more brain function can be preserved

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7
Q

What are the types of strokes?

A

TIA
thrombotic
embolic
haemorrhagic

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8
Q

What is an ischemic stroke?

A
  • thrombotic and embolic strokes
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9
Q

What is a TIA?

A

Transient Ischemic Attack - sudden neurological deficit with symptoms typically lasting less than one hour but never more than 24 hours, confined to one area of brain/eye perfused by a specific artery

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10
Q

What is a TIA a result of?

A

release of small emboli from a thrombus which temporarily block downstream vessel but then dissolves quickly so blow flow resumes

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11
Q

How is stroke diagnosed?

A

Physical exam - neurological signs/symptoms, blood pressure, ophthalmoscope
blood tests - cholesterol, C reactive protein
CT - haemorrhage, tumour can be seen
MRI - detect brain tissue damage by ischemic stroke and brain haemorrhages
extra - carotid ultrasound (plaques and blood flow in carotid arteries), cerebral angiogram, echocardiogram

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12
Q

How does thrombotic stroke occur?

A

formation of blood clot in a cerebral artery normally at site of atherosclerotic plaque, plaque surface breaks open collage and tissue factor is exposed producing a thrombus which blocks blood supply to local tissue

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13
Q

What is the significance of obstructive sleep apnea?

A

caused by obstructions In upper airway due to soft tissue in throat collapsing and blocking it
triggers a sudden a rise in blood pressure rupturing plaque surface so a lot of thrombotic strokes develop during sleep

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14
Q

What are slow onset thrombotic strokes?

A

Develop over several hours to a few days, initial neurological deficits then no deterioration then more symptoms/signs, may be as several plaques in different vessels forming thrombi

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15
Q

What are most thrombotic strokes due to?

A

atherosclerosis in cerebral artery

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16
Q

How does embolic stroke occur

A

blood clot (or other foreign substance) broke free from thrombus and lodged in other part of circulation, can be mass of bacteria, neurological signs develop rapidly is cerebral and don’t progress, usually during activity, remain conscious

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17
Q

What are some heart diseases which lead to emboli production?

A

Source of embolism is always on LHS so:

- AF, MI, defective/artificial heart valves (mitral especially)

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18
Q

What are the most common types of stroke?

A

thrombotic and embolic make up 85%

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19
Q

How does a haemorrhagic stroke occur?

A

intracerebral haemorrhage develops sudden neurological symptoms, severe headache, may cause stupor/coma that may progress, hypertensive patients in some cases but not all the time as aneurysms and arteriovenous malformations may bleed spontaneously

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20
Q

What is a lacunar stroke?

A

occlusion of one of the arteries providing blood to brain’s deep structures as opposed to the cerebral cortex

21
Q

What are some deep structures of the brain?

A

basal ganglia, cerebral white matter, thalamus, pons, cerebellum

22
Q

What are the forms of lacunar stroke?

A
  • motor hemiparesis with dysarthria: most common, infarct in posterior limb of internal capsule
  • ataxia & hemiparesis: 2nd most common, infarct in posterior limb of internal capsule
  • dysarthria & clumsy hand: infarct in anterior limb of internal capsule
23
Q

How does lacunar stoke present?

A

Well defined deficits

Absent Cortical infarct signs - aphasia, neglect, visual field defects

24
Q

What are the most important risk factors for stroke?

A

hypertension, AF, diabetes, hyperlipidaemia

25
Q

How beneficial can reducing blood pressure be for stroke risk?

A

reduction of 10/5 reduces risk by 40%
lowering can prevent ischemic and haemorrhagic strokes
secondary prevention as RF for atherosclerosis

26
Q

How beneficial can blood sugar control be for stroke risk?

A

reduces neuropathy and retinopathy

does not reduce stroke

27
Q

How can smoking increase stroke risk?

A

general inflammation in blood vessels, atheroma formation, hypertension

28
Q

What are some less significant risk factors for stroke?

A
  • diet low in potassium and hypokalaemia (increase risk of hypertension and stroke)
  • thiazides and loop diuretics (block sodium and water reabsorption upstream from DCT promoting increased secretion of potassium = hypokalaemia, solution is to provide potassium supplements)
29
Q

Why are cerebral arteries prone to aneurysms and stroke?

A

Have lots of twists and turns (tortuous)

30
Q

What is the role of the sodium pump in nerve cells?

A

Maintains nerve cell size and shape
Removes sodium from cells so water follows meaning cells don’t swell
Maintains membrane potential

31
Q

How do sodium pumps in nerve cells differ from those in other cells?

A

Work at very high levels as have a large surface-volume ratio so more sodium leakage occurs. Also allow sodium in during AP when it must be pumped out, high ATP usage

32
Q

How much extracellular fluid is there in the brain?

A

20%

33
Q

What happens to the extracellular space in the brain in hypoxia?

A

Sodium pump stops working so sodium leaks into cells, cells swell, brain contained in rigid cranial cavity so swelling exerts pressure on each other and EC space = 5%, cells press against each other and intracranial pressure rises, compresses cerebral veins so blood flow loss and worsening hypoxia

34
Q

What is coning/tonsillar herniation?

A

intracranial pressure rise causes cerebellum to extrude through foramen magnum, cerebellar tonsils move downward through magnum, lower brainstem compression and upper cervical spinal cord

35
Q

What are common signs of coning/tonsillar herniation?

A

Intractable headache, head tilt, neck stiffness, consciousness loss, flaccid paralysis

36
Q

What happens to potassium in a hypoxic brain?

A

Potassium in EC space not removed by glial cells so depolarises adjacent cells = excess neurotransmitter release, transporters reuptake neurotransmitters using ATP, low ATP so not taken up and remain in synaptic cleft/EC space = excitotoxicity

37
Q

What is excitotoxicity?

A

excess release of excitatory neurotransmitter

38
Q

What is the main excitatory transmitter in the brain? What does it do?

A

Glutamate- acts on several different receptors in brain (NMDA and AMPA), NMDA excess stimulation = excess influx of calcium ions into nerve cells as too early excitotoxicity, AMPA excess stimulation slow delayed excitotoxicity

39
Q

How does an excitotoxic loop occur?

A

Hypoxia - ATP levels drop - failed reuptake of glutamate by glial cells and axon terminal - NMDA post synaptic glutamate receptor overstimulated - calcium influx - excitotoxic loop

40
Q

What is the excitotoxic loop?

A

Increased influx of calcium increases cell’s metabolic demand and more oxygen used = free radicals form triggering cell death/apoptosis

41
Q

What are the area of a stroke focus?

A

centre - cells face inevitable death
middle - penumbra, hypoxic/damaged region but survival possible
outer - cells survive

42
Q

What are the 3 main stroke treatment strategies?

A
  • restore blood flow
  • combat excitotoxicity
  • combat free radical damage
43
Q

What is the main goal of current stroke treatment?

A

max survival of neurones in the penumbra region

44
Q

What does stroke outcome post-treatment depend on?

A
  • how quickly treatment started = early/better
45
Q

What stroke treatment helps to restore blood flow?

A
  • tissue plasminogen activators allow thrombolysis

efficacy depends on how soon it is administered (3-4hrs best)

46
Q

What stroke treatment helps combat excitotoxicity?

A
  • NMDA antagonists, blocks fast excitotoxicity, serious side effects
  • AMP antagonists, reduce slow excitotoxicity
  • newer drugs prevent delayed triggering of apoptotic pathways
47
Q

What stroke treatment helps reduce free radical damage?

A
  • antioxidants (vitamin C and E)
  • free radical scavenging enzymes (superoxide dismutase)
  • cool down brain (reduces oxygen demand, allows neurones in penumbra to survive with small O2 supply from collateral vessels)
48
Q

How do you reduce primary stroke risk?

A
  • treat hypertension
  • treat AF: aspirin for healthy patients <65, warfarin for patients >65 or have other RF
  • statins to those with vascular disease

CR2 (35 decks)

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