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stroke Flashcards

1
Q

what is stroke?

A

consequence of an interruption to blood flow to part of the brain –> hypoxia and ischaemia

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2
Q

what may cause interruption of blood flow to the brain?

A

o Infarction – blockage of an artery

o Haemorrhage – rupture of an aneurysm

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3
Q

what is haemorragic stroke subdivided into?

A

o Parenchymal – into brain tissue

o Subarachnoid – into the subarachnoid space

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4
Q

what are symptoms of stroke?

A
  • Numbness or weakness of face, arm or leg, especially on one side of the body
  • Confusion, trouble understanding or speaking
  • Trouble seeing in one or both eyes
  • Dizziness, loss of balance or coordination
  • Severe headache with no known cause
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5
Q

what does FAST stand for?

A

o Face: is loss or tone or weakness in any facial muscles
o Arms: can they raise both their arms equally?
o Speech: any changes e.g. slurring, slowness
o Time: the quicker the person receives help, the more brain function can be preserved

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6
Q

what is transient ischaemic attack?

A

• Sudden, focal neurologic deficit with clinical symptoms lasting less than an hour but always lasting less than 24 hours, confined to an area of the brain/eye perfused by a specific artery

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7
Q

what causes a TIA?

A

Result of the release of a small embolus from a thrombus. Blocks a downstream vessel but then quickly dissolves, allowing blood flow to resume

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8
Q

what is a TIA a sign of?

A

an impending stroke

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9
Q

how long do TIAs last for?

A

seconds to 10 minutes

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10
Q

what physical exams are used to diagnose stroke?

A

neurological signs/symptoms; blood pressure; opthalmoscope exam

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11
Q

what blood tests are used to diagnose stroke?

A

cholesterol, C-reactive protein

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12
Q

what does a CT scan show?

A

shows a haemorrhage, tumour, stroke and other conditions

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13
Q

what can an mri detect?

A

can detect brain tissue damaged by an ischaemic stroke and brain haemorrhages

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14
Q

what extra tests can you do for stroke?

A
  • Carotid ultrasound. This test shows presence of plaques and blood flow in your carotid arteries.
  • Cerebral angiogram.
  • Echocardiogram.
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15
Q

what is cerebral thrombosis?

A

formation of a blood clot in a cerebral artery, normally at the site of an atherosclerotic plaque

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16
Q

what happens if a plaque breaks open?

A

collagen and TF are exposed – produces a thrombus that blocks blood supply to the local tissue

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17
Q

why do 60% of thrombotic strokes develop during sleep?

A

obstructive sleep apnea triggers a sudden rise in BP that ruptures the surface of a plaque

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18
Q

what causes obstructive sleep apnea

A

caused by obstruction in the upper airway, usually due to soft tissue in the throat collapsing and blocking the airway

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19
Q

how do slow onset strokes present?

A

20% of thrombotic strokes develop stepwise over several hours/days. Initial neurological deficits appear, followed by a period without further deterioration

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20
Q

define arteriosclerosis

A

Thickening, hardening and loss of elasticity of the walls of arteries

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21
Q

define arteriolarsclerosis

A

Thickening, hardening and loss of elasticity of the walls of arterioles

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22
Q

define atherosclerosis

A

when the inside of an artery narrows due to the build-up of plaque

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23
Q

where do most thrombotic strokes that arent caused by emboli occur?

A

occur at sites of atherosclerosis or arteriosclerosis in the brain

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24
Q

define embolism

A

foreign substance that occludes a blood vessel
o Most are blood clots that broke free from a thrombus
o Can also be a mass of bacteria

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25
Q

how do signs develop in cerebral embolisms?

A

• Neurological signs develop quickly w cerebral embolisms and usually don’t progress

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26
Q

where is the source of the embolism in an embolic stroke?

A

Source of embolism is almost always the L side of the heart

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27
Q

what heart diseases produce embolisms?

A

AF, MI, and defective or artificial heart valves, esp the mitral valve

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28
Q

what % of strokes are made up by thrombotic and embolic strokes?

A

85%

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29
Q

how do neurological symptoms present in intracerebral haemorrhage?

A

sudden onset (mins to hours)

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30
Q

why is haemorrhagic stroke frequently associated with severe headache?

A

Possibly due to stretch of the vessel before rupture

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31
Q

what is the cause of haemorrhagic stroke?

A

often caused by a ruptured aneurysm

32
Q

what are indicators of haemorrhagic stroke?

A

nausea, vomiting, intolerance of noise or light
o These patients are usually hypertensive but not always
o Aneurysms and arteriovenous malformations can bleed spontaneously under normal pressure

33
Q

what are lacunar strokes?

A

• Type of stroke where there’s occlusion of one of the arteries that provides blood to the brain’s deep structures as opposed to the cerebral cortex e.g. basal ganglia, cerebral white matter, thalamus, pons and cerebellum

34
Q

what signs are always absent in lacunar strokes?

A

Cortical infarct signs (aphasia, neglect, and visual field defects) are always absent

35
Q

what % of ischaemic strokes do lacunar strokes make up?

A

15-20%

36
Q

what are common forms of lacunar strokes?

A

o Motor hemiparesis with dysarthria: most common (33-50%): infarct in posterior limb of internal capsule
o Ataxia & hemiparesis: infarct also in posterior limb of internal capsule
o Dysarthria & clumsy hand: infarct in anterior limb of internal capsule

37
Q

what are the most important risk factors for stroke?

A

hypertension, atrial fibrillation, smoking, diabetes and hyperlipidaemia

38
Q

what is the main cause of all haemorrhagic strokes?

A

hypertension

39
Q

how does reducing BP by 10mmHg reduce the risk of stroke?

A

reduces risk by 40%

40
Q

what is a major risk factor of atherosclerosis?

A

hypertension

41
Q

what drugs are useful for atrial fibrillation?

A

Anticoagulation with meds such as warfarin, aspirin or other anticoagulants is useful for prevention

42
Q

how does diabetes mellitus affect the risk of stroke?

A

increases risk of stroke by 2 to 3 times

43
Q

how does controlling blood sugar levels affect microvascular and macrovascular complications?

A

• Intensive control of blood sugar has been shown to reduce microvascular complications e.g. nephropathy and retinopathy – hasn’t been shown to reduce macrovascular complications e.g. stroke

44
Q

how do statins help stroke risk in those with hyperlipidemia?

A

Statins reduce the risk of stroke by about 15-20% in those with high LDL cholesterol.

45
Q

how does smoking contribute to stroke risk?

A

causes general inflammation in blood vessels, increases formation of atheromas, causes hypertension etc.

46
Q

name lesser risk factors of stroke

A
  • low K+ diet and low K+ blood

- sickle cell disease

47
Q

name foods high in potassium

A

nuts, potatoes, chocolate, bananas, orange juice etc

48
Q

why does sickle cell disease increase the risk of stroke?

A

increased risk of clotting bc of increased fragility of RBCs

49
Q

how much extracellular space does the brain?

A

20%

50
Q

what organ uses the most ATP and why?

A

brain - needs it to fuel the Na+ pumps in the membrane

51
Q

why is sodium important in nerve cells?

A

• Na+ important in nerve cells to keep the membrane potential intact and to maintain nerve cell size and shape

52
Q

why are nerve cells so sensitive to swelling?

A
  • Neurons have a high SA:V ratio – small Na+ per unit area = lots of Na+ enters
  • When Na+ enters, water follows
  • If Na+ pump breaks – nerve cell swells
53
Q

how does hypoxia lead to an increase in intracranial pressure?

A
  • Hypoxia can cause Na+ pumps to stop working  swelling
  • Brain is contained in the rigid cranial cavity – swelling cells exert pressure on each other and the amount of extracellular space decreases
  • Eventually reduced so much that the cells press against each other – produces a rise in intracranial pressure (ICP)
54
Q

what is a major sign of cerebral hypoxia

A

raised ICP

55
Q

how does a high ICP worsen hypoxia?

A

High ICP will compress cerebral capillaries and veins, leading to a loss of blood flow –> worsens hypoxia

56
Q

what is cerebral blood flow determined by?

A

cerebral perfusion pressure

57
Q

what is cerebral perfusion pressure?

A

difference between mean arterial pressure and ICP

58
Q

what is coning/tonsillar herniation?

A

ICP rise can cause cerebellum to extrude through foramen magnum
Cerebral tonsils move downwards through FM causing compression of the lower brainstem and upper cervical spinal cord

59
Q

what are common signs of coning?

A

intractable headache, head tilt, and neck stiffness

Level of consciousness may decrease – gives rise to flaccid paralysis

60
Q

what happens to potassium released into the ECS by APs in a healthy brain?

A

removed by glial cells which maintain the homeostasis of the brain environment

61
Q

how does hypoxia affect the amount of NTS in the synaptic cleft and how?

A

K+ isn’t removed. Increased extracellular potassium depolarises adjacent cells and leads to excess NTS release
• NTS are normally taken back up into nerve cells by pumps which use ATP.
o Low ATP means that NTS isn’t taken up and remains in the synaptic cleft

62
Q

what is excitotoxicity?

A

effects of excess excitatory NTS

63
Q

what is glutamate?

A

a dicarboxylic amino acid; main excitatory NTS in the brain

o Acts on NMDA rand AMPA receptor

64
Q

how does fast excitotoxicity occur?

A

Excess stimulation of the NMDA receptor after 3-5mins of anoxia leads to excess influx or Ca2+ ions into nerve cells –> fast excitotoxicity

65
Q

how does slow excitotoxicity occur?

A

Excess stimulation of AMPA receptors over several hours leads to slow (delayed) excitotoxicity

66
Q

explain the excitotoxic loop

A
  • Increased influx of Ca2+ increases metabolic demand on the cell and uses more O2
  • High metabolic demand in the absence of oxygen leads to the formation of free radicals which trigger cell death or apoptosis
67
Q

what are the 3 regions of the brain around a stroke focus?

A
  • area where cells face inevitable death
  • penumbra
  • area where cells survive
68
Q

what is the penumbra region?

A

neurons are hypoxic and/or damaged but survival is possible

69
Q

what is the main goal of stroke treatment?

A

max survival of neurones in the penumbra region

70
Q

what is the median time to presentation of a stroke?

A

• 13 hours after onset of symptoms is the median time to presentation

71
Q

what are the main treatment strategies of stroke?

A

o Restore blood flow
o Combat excitotoxicity
o Combat free radical damage

72
Q

how can you restore blood flow after a stroke?

A

• Use of IV tissue plasminogen activators improves outcome after stroke

73
Q

when should IV tissue plasminogen be used?

A

until CT has ruled out a brain haemorrhage

74
Q

what does the efficacy or tissue plasminogen activators depend on?

A

• Efficacy of treatment depends on how critically soon it’s administered – within 3-4 hours for maximum benefit

75
Q

how can we combat excitotoxicity and how do these methods work?

A
  • NMDA antagonists e.g. Cerestat – block NMDA receptors and fast excitotoxicity – hasn’t been successful in practice bc it may have been administered late and also has serious side-effects
  • AMP antagonists e.g. NBQX – reduces slow excitotoxicity. More hope bc AMPA effects are delayed and drug treatment after 1 hour may be beneficial
  • Newer drugs to prevent delayed triggering of apoptotic pathways- ‘programmed cell death’. (e.g. Lithium,)
76
Q

how can we reduce free radical damage?

A

• Antioxidants e.g. vitamin C and E given intravenously
o Dietary supplements shown to reduce risk of stroke in vulnerable groups.
• Free radical scavenging enzymes – superoxide dismutase is low in stroke patients
• Cool down the brain – reducing body temp reduces O2 demand and may allow neurones in the penumbra to survive if there’s small O2 supply from collateral BVs

77
Q

how can we reduce primary risk?

A
  • Treat hypertension – diuretics, ACE inhibitors, AR antagonists, change diet
  • Treat AF – give aspirin to healthy patients <65 years. Give warfarin for patients >65 years or having other stroke risk factors.
  • Give statins to patients with vascular disease

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