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Cardiorespiratory 2 > Stroke > Flashcards

Stroke Flashcards

1
Q

what is the definition of stroke

A
  • The consequence of an interruption to blood flow to part of the brain, cuasing ischemia (inadequate blood flow) and hypoxia
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2
Q

why might interruption of flow happen to the brain

A
  • infarction (blockage of an artery)

- haemorrhage (e.g. rupture fo an aneurysm)

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3
Q

what are the 2 types of haemorrhage stroke

A
  • Parenchymal – into brain tissue

- Subarachnoid- into the subarachnoid space

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4
Q

what is the 3rd most common cause of death after cancer and heart disease

A
  • Stroke is the third most common cause of death in the UK after heart disease and cancer
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5
Q

what are the 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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6
Q

all symptoms happen….

A

suddenly

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7
Q

describe the parts of FAST

A
  • Face – is their loss of tone or weakness in any facial muscles
  • Arms – can they raise both arms equally
  • Speech – is there any changes e.g. slurring and slowness
  • Time – the quicker the person receives help, the more brain function can be preserved
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8
Q

name the types of stroke

A
  1. (TIA)
  2. Thrombotic
  3. Embolic
  4. Haemorrhagic
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9
Q

what are the types of ischeamic stroke

A

Thrombotic and Embolic strokes are forms of ischaemic stroke

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10
Q

what percentage of strokes are ischaemic strokes

A

75% of all strokes

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11
Q

what is a distinguiable trait between a TIA and stroke

A
  • If the symptoms go away within the day then it is a TIA and not a stroke, usually confined to one functional part of the brain
  • typically last 1 hour but always last less than 24 hours
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12
Q

what is a TIA caused by

A
  • The cause is assumed to be an embolise, that is small enough to be dissolved by the tissue lysing agents
  • Most TIAs dissolve quickly, therefore the symptoms are only shorter
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13
Q

what is the TIA a sign of

A

it is a sign that a thrombotic stroke is about to happen

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14
Q

name the tests you would use to diagnose stroke

A
  • physical examination
  • blood tests
  • CT scan
  • MRI
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15
Q

describe the tests you would use to diagnose stroke

A

Physical examination.

  • Neurological signs/ symptoms
  • Blood pressure, ophthalmoscope exam

Blood tests.
- Cholesterol, C-reactive protein

CT scan. Really important part of the diagnosis
- A CT scan can show a hemorrhage, tumor, stroke and other conditions. (computerized tomography angiography). CT most important imaging.

MRI
- MRI can detect brain tissue damaged by an ischemic stroke and brain hemorrhages.

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16
Q

what is the most important test for the diagnosis of stroke

A

CT scan
- this Is because it can tell the difference between an haemorrigic stroke and an infract which is important for treatment

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17
Q

what other tests can you perform on someone who you suspect to have a stroke

A
  • Carotid ultrasound. This test shows presence of plaques and blood flow in your carotid arteries.
  • Cerebral angiogram.
  • Echocardiogram
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18
Q

what is the percentage of thrombotic strokes that develop during sleep

A
  • About 60% of thrombotic strokes develop during sleep
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19
Q

why do thrombotic strokes tend to develop during sleep

A
  • unsure
  • but one theory is that obstructive sleep apnea where the airway gets blocked during sleep can cause the blood pressure to shoot up and this can cause the rupture of the surface off a plaque
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20
Q

what is cerebral thrombosis

A
  • Cerebral thrombosis is the formation of a blood clot in a cerebral artery, normally at the site of an atherosclerotic plaque
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21
Q

how can a thrombus cause a stroke

A

. If the surface of the plaque breaks open collagen and tissue factor are exposed which produce a thrombus that blocks blood supply to the local tissue (much like an AMI blocks blood supply to part of the heart).

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22
Q

describe how slow onset strokes develop

A
  • About 20% of thrombotic strokes develop stepwise over a several hours to a few days.
  • In these situations initial neurological deficits appear, followed by a period without further deterioration.
  • Another period of deterioration is heralded by expansion of the neurological signs
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23
Q

why do slow onset strokes develop

A

This may be due to several plaques in different vessels forming thrombi.

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24
Q

what is arteriosclerosis

A
  • This is the thickening hardening and loss of elasticity of the walls of the arteries due to fibrotic deposition, the elastin is converted to collagen and they lose their elasticity, this happens naturally in ageing but can be accelerated by smoking and other chemicals in the blood
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25
Q

what is atherosclerosis

A
  • this is when there is a plaque that comes on after there has been some arteriosclerosis, this causes the artery to narrow
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26
Q

is atherosclerosis or aterioscloersis associated with nearly half of all strokes

A

atherosclerosis is associated with nearly half of all strokes

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27
Q

what are the blood vessels like in the brain

A
  • They are much more tortuous than in other structures, they twist and turn in a convoluted way
  • This is different to the normal arteries in the body
  • This twist and turn can make it much more vulnerable to thrombi formation because thrombi form where there is reduced or stagnant blood or due to a vortex effect
  • therefore the intrinsic pathway is triggered and it is strongly correlated with clots forming
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28
Q

why is AF a risk factor for stroke

A

AF is a major risk factor for stroke, because if the atria is in fibrillation and not contracting properly the blood can be stagnant in the auricles which triggers the intrinsic pathway and this causes clot formation
- When the sympathetic nervous system starts making the heart beat faster the clots can get dislodged and they pass up the vertebral arteries and you can get an embolic stroke

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29
Q

how is damage to the heart valves a risk factor that can cause an embolic stroke

A
  • Damage to the heart valves can induce turbulence, this is a risk factor in increasing spontaneous thrombi form
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30
Q

what is an embolism

A
  • An embolism is a foreign substance that occludes a blood vessel
    .
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31
Q

what are most embolism made out of and what can some embolisms be made out

A
  • Many embolisms are blood clots that broke free from a thrombus and lodged in a remote part of the circulation.
  • Embolism can also be a mass of bacteria.
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32
Q

neurological signs develop rapidly with …

A

Neurological signs develop rapidly with cerebral embolisms and usually do not progress

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33
Q

what stroke is rarely preceded by a TIAs

A

embolic stroke

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34
Q

where is the source of the embolism from embolic strokes usually for

A
  • The source of the embolism is almost always the left side of the heart. Heart diseases that lead to the production of emboli include atrial fbrillation, myocardial infarct, and defective or artificial heart valves, particularly the mitral valve
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35
Q

what percentage of strokes do thrombotic and embolic strokes make up

A
  • Thrombotic & embolic strokes make up ~ 85% of all strokes
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36
Q

what is haemorrhage stroke associated with

A
  • Intracerebral haemorrhage is associated with the sudden onset (minutes to hours) of neurological symptoms.
  • It is frequently associated with severe headache. (Possible due to stretch of the vessel before rupture).
  • Nausea and vomiting, intolerance of noise or light
  • can be associated with hypertension but sometimes bleeds happen under normal pressure
37
Q

what is haemorrgic stroke often caused by

A

Often caused by a ruptured aneurysm.

38
Q

is consuiness preserved in haemorrhage stroke

A
  • Unlike the occlusive strokes, in which consciousness is preserved, intracerebral haemorrhage may cause stupor or coma that may progress with time.
39
Q

what is a lacunar stroke

A
  • Lacunar stroke is a type of stroke where there is occlusion of one of the arteries that provides blood to the brain’s deep structures as opposed to the cerebral cortex
40
Q

what are the deep structures of the brain

A 
basal ganglia, 
cerebral white matter, 
thalamus
 pons
cerebellum.
41
Q

what are the signs of lacunar strokes

A
  • Well defined deficits are present but cortical infarct signs (such as aphasia, neglect, and visual field defects) are always absent
42
Q

what percentage of lacunar strokes count for ischemci strokes

A

. Lacunar stroke accounts for 15 – 20% of ischemic strokes

43
Q

what are the common forms of lacunar stroke

A
  • Motor hemiparesis with dysarthria(difficult articulation of speech): the most common lacunar syndrome: (33-50%): infarct in posterior limb of internal capsule
  • Ataxia(lack of muscle coordination) & hemiparesis(weakness of one half of the body) : the second most common form of lacunar stroke ; infarct also in posterior limb of internal capsule
  • Dysarthria & clumsy hand : infarct in anterior limb of internal capsule
44
Q

what are the 5 main risk factors for stroke

A
  1. Hypertension
  2. Atrial fibrillation
  3. Smoking
  4. Diabetes
  5. Hyperlipidaemia
45
Q

what percentage of risk does hypertension cause for stroke

A

Hypertension accounts for 35-50% of stroke risk

46
Q

what can lowering blood pressure prevent

A

Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes

47
Q

what is the risk of stroke caused by AF

A

Those with atrial fibrillation have a 5% a year risk of stroke, and this risk is higher in those with valvular atrial fibrillation.

48
Q

what is a useful prevention for reducing risk of stroke caused by atrial fibrillation

A

anticoagulation with medications such as warfarin or aspirin or other anticoagulants is useful for prevention

49
Q

how much does diabetes increase your risk of stroke

A
  • Diabetes mellitus increases the risk of stroke by 2 to 3 times
50
Q

how can diabetes cause stroke

A
  • Dameges the endothelium, reduces NO therefore increases vasoconstriction and causes hypertension
51
Q

how much does statins reduce the risk of stroke by

A
  • Statins reduce the risk of stroke by about 15-20% in those with high LDL cholesterol
52
Q

how does smoking increase the risk of stroke

A
  • Causes general inflammation in blood vessels, increases formation of atheromas, causes hypertension
53
Q

how much does obstructive sleep apnea increase stroke risk in

A
  • Increases stroke risk by up to 3x especially in men
54
Q

what are the other factors that can cause stroke

A
  • diet low in potassium and low blood potassium (hypokalaemia)
  • sickle cell disease
55
Q

how does a die low in potassium and low blood potassium cause stroke

A
  • they may cause hypokalaemia

- and can therefore increase the risk of stroke and hypertension

56
Q

how does sickle cell disease cause stroke

A
  • Increased risk of clotting due to increased fragility of red cells, don’t bend so easily so when they go through capillaries they tend to break open and this releases haemoglobin and once the haemoglobin is out of the red cell it can act to produce clotting
57
Q

why is ATP so important in the sodium pump

A
  • most of ATP is used to fuel the sodium pump in the brain cells
  • in nerve cells the sodium pump does not just keep the membrane potential intact but has a role in maintaining nerve cell size and shape
  • when sodium enters water follows
58
Q

what happens if the sodium pumps stop working in cells

A
  • if the sodium pump stops working or works at a reduced rate this means that too much water can enter and this can cause the nerve cells to swell as the sodium is not being pumped out
59
Q

how long does it take for a brain cell to die

A
  • After 2-3 minutes of hypoxia nerve cell starts to die
60
Q

why is swelling so bad in the brain

A
  • In most cells of the body swelling doesn’t matter but in the brain it is serious because if the neurones swell there is no where for them to swell to except against each other as the brain is a bony box and the amount of extracellular space decreases
  • The intracranial pressure arises as cant remove fluid
61
Q

how much extracellular space is there in a normal brain

A
  • In a normal brain there is 20% extracellular space, this is where the CSF seeps through the space and drains
62
Q

what is a raised ICP a major sign of

A
  • A raised icp is a major sign of cerebral hypoxia
63
Q

what is the cerebral perfusion pressure

A
  • The cerebral perfusion pressure (CPP) is the difference between mean arterial pressure and ICP
64
Q

what is cerebral blood flow determined by

A

cerebral perfusion pressure

65
Q

what is the extracellular space in a hypoxic brain

A

In a hypoxic brain the extracellular space is 5%

66
Q

what happens in tonsillar herniation

A
  • Rise in ICP can cause the cerebellum to extrude through the foramen magnum
  • This is called coning or tonsillar herniation
  • The cerebellar tonsils move downward through the foramen magnum causing compression of the lower brainstem and upper cervical spinal cord
67
Q

what are the most common signs of tonsillar herniation

A
  • intractable headache
  • head tilt
  • neck stiffness
  • The level of consciousness may decrease and also give rise to flaccid paralysis
68
Q

what do glial cells do

A

In a healthy brain the potassium released in to the ECS space in the brain by action potentials is removed by glial cells.
- The glial cells maintain the homoeostasis of the brain environment

69
Q

what happens in an seizure

A
  • Neurones in a particular part release potassium ions, the diffusion of the potassium may be comprised
  • The membrane potential is caused by the ratio of potassium inside and outside, if the outside potassium goes up the ratio gets smaller and the membrane potential is less
  • This is what happens during seizure – lot of neurones simultaneously release potassium, which makes them more active so release more potassium, this only stops when they cant release anymore potassium as they are so depolarised
70
Q

what do glial cells need to work

A
  • Potassium rise is normally controlled by glial cells but the glial cells need ATP to do this but if hypoxic cant do this
71
Q

what does a build up of potassium cause to be released

A
  • A build up of potassium in the extraceullar space, which causes glutmate to be released
72
Q

what happens in a hypoxic brain when the potassium is not removed

A
  • In a hypoxic brain the potassium is not removed; the increased extracellular potassium depolarizes adjacent cells and leads to excess (excitatory) neurotransmitter release.
  • After release from synaptic endings, neurotransmitters are normally taken back up into nerve cells by uptake pumps or ‘transporters’. These transporters use ATP. When ATP levels are low, the neurotransmitters are not taken up, but remain in the synaptic cleft or extracellular space.
  • Glutmate diffuses around, high levels of glutmate cause excitotoxicity
73
Q

what does high amounts of glutamate cause

A
  • excitotoxicity
74
Q

what receptors does glutamate act on

A

NMDA

AMPA

75
Q

what does excess stimulation of the NMDA receptor do

A

Excess stimulation of the NMDA receptor after 3-5 minutes anoxia leads to excess influx of calcium ions into nerve cells and this is cause of fast (early) excitotoxicity.

76
Q

what does excess stimulation of AMPA do

A

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

77
Q

what is the difference between slow and fast excitotoxcity

A

slow is due to excess stimulation of AMPA receptors

fast is due to excess stimulation of NMDA receptors

78
Q

what is the basic excitotoxic loop

A
  • The increased influx of calcium increases the metabolic demand on the cell and uses more oxygen.
  • The high metabolic demand in the absence of oxygen leads to the formation of free radicals which trigger cell death or apoptosis
  • this is the main reason why cells die
79
Q

what are the 3 regions of the brain that focus around a stroke and what happens to the cells there

A
  • The centre – cells here face inventible death
  • The penumbra region – neurones are hypoxic and/or damaged but survival is possible
  • At a distance there are cells supplied by other arterial arteries or there is enough oxygen that pass through which keeps them alive
80
Q

what are the three main treatment strategies for stroke

A
  1. Restore blood flow
  2. Combat excitotoxicity
  3. Combat free radical damage
81
Q

how do you restore blood flow

A
  • Use of i.v. tissue plasminogen activators (thrombolysis) improves outcome after stroke (thrombotic stroke). However, fibrinolytic agents should be withheld until CT has ruled out a brain hemorrhage.
    = ONLY FOR ISCHEMIC STROKE
82
Q

when is the best time frame to use tissue plasminogen activators as a treatment of stroke

A
  • Efficacy of treatment depends critically on how soon it is administered: within 3-4 hours at most for significant benefit
83
Q

Describe how quickly IV fibrinolytic therapy can be given and how effective they are

A
  • within the first 3 hours of ischemic stroke onset offers substantial net benefits .
  • within 3-4.5 hours offers moderate net benefits .
  • in the 3-6 hour window offers moderate net benefits
  • After 3 hours it is progressive decline, after 6 hours not so good
84
Q

how to we treat excitotoxicty

A

NMDA antagonists

AMP antagonist

Newer drugs to prevent delayed triggering of apoptotic pathways- ‘programmed cell death’. (e.g. Lithium,)

85
Q

How do NMDA antagonists work

A

block NMDA receptors & fast excitotoxicity

86
Q

how do AMP antagonists work

A

to reduce slow excitotoxicity.

  • (Appear to hold out more hope as AMPA effects are delayed and drug treatment after one hour may be beneficial)
87
Q

How can we reduce free radical damage

A
  1. Antioxidants such as vitamin C and E have been administered i.v. to boost brain’s antioxidant defenses.
  2. Free radical scavenging enzymes such as superoxide dismutase have been found to be low in stroke patients. Clinical trials with SOD are showing hopeful results.
  3. Cool Down the Brain. Reducing body temperature reduces oxygen demand, and may allow neurones in the penumbra to survive if there is a small oxygen supply from collateral blood vessels
88
Q

how to you treat hypertension thus lowering the risk of stroke

A

Diuretics, ACE inhibitors, AR antagonists. Change diet

89
Q

how do you treat atrial fibrillation thus lowering the risk of stroke

A

Give Aspirin for healthy patients < 65 years

Give Warfarin for patients > 65 years or having other stroke risk factors

Cardiorespiratory 2 (43 decks)

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