Stroke Flashcards

1
Q

Define a stroke

A

Stroke is the ‘umbrella’ term used to describe an event where the blood supply to part of the brain is disrupted.

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2
Q

Explain the two types of stroke.

A

Ischaemia (infarction)- where the blood supply to part of the brain is cut off due to a clot.

Haemorrhage - where the blood supply is disrupted in the brain due to a weakened blood vessel bursting.

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3
Q

What type of stroke is more common?

A

85% of strokes are ischaemic
10% are due to primary haemorrhage (IntraCerebral Haemorrhage)
5% due to subarachnoid haemorrhage

Ischaemic strokes are 7-8 times more common

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4
Q

In relation to ischaemic strokes, will all patients experience the same symptoms?

A

No, patient symptoms due to ischemia result as a consequence of the blood vessels in a particular area of the brain that is affected.
Therefore Doctors can use their understanding of arterial anatomy and the brain territories supplied by the cerebral arteries to predict the blood vessels that have been affected and the consequence that this will have on the patient.

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5
Q

When do stroke symptoms occur?

A

When the oxygen and nutrient supply to the brain is cut off.

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6
Q

State the three arteries that supply each of the cerebral hemispheres.

A

Anterior cerebral artery - ACA
Middle cerebral artery - MCA
Posterior cerebral artery - PCA

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7
Q

Describe where the anterior cerebral artery supplies.

A

Supplies the medial portion of the frontal and parietal lobes and anterior portion of the basal ganglia.

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8
Q

Describe where the middle cerebral artery supplies.

A

Supplies the lateral portions of the frontal and parietal lobes and the lateral portions of the temporal lobes.

It is the dominant source of vascular supply to the hemispheres.

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9
Q

Describe where the posterior cerebral artery supplies.

A

Supplies the thalamus, brainstem, posterior and medial, temporal and occipital lobes.

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10
Q

Which side of the brain controls movement on each side of the body?

A

The nerves that originate in the right hemisphere are responsible for the motor control of the left side of the body.

The nerves originating in the left hemisphere are responsible for the motor control of the right side of the body.

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11
Q

State the four different areas of the cerebrum and what are they responsible for?

A

For each cerebral hemisphere there are different areas which control planned movement (on that correlated side of the body), thinking, feelings, emotions, memory

The fourdifferent areas are:
Frontal lobe
Parietal lobe
Temporal lobe
Occipital lobe

Each lobe is responsible for different skills.

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12
Q

What are some of the functions of the frontal lobe?

A

Speaking
Planning
Problem solving
Starting some movements
Processing emotions
Part of your personality and character

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13
Q

What are some of the functions of the parietal lobe?

A

Touch
Temperature
Pressure
Pain
Reception and evaluation
Object recognition

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14
Q

What are some of the functions of the temporal lobe?

A

Evaluating auditory (processing language)
Olfactory input
Important role in memory, thought and judgement

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15
Q

What are some of the functions of the occipital lobe?

A

Reception and integration of visual input (colour, shape and distance)

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16
Q

Describe what is an transient ischaemic attack.

A

The acute loss of focal cerebral or ocular function with symptoms (neurological deficit) lasting less than 24 hours’.

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17
Q

When do the symptoms associated with a TIA resolve?

A

Usually resolve within minutes or a few hours at most

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18
Q

Why should TIAs still be treated as a medical emergency?

A

Often a warning sign that you are at risk of having a full stroke in the near future .

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19
Q

Describe the risk of having a full stroke after a TIA?

A

Very high risk within one month and up to a year afterwards

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20
Q

What happens during a primary haemorrhagic stroke?

A

When a blood vessel bleeds into the deep
cerebral tissue of the brain, this is known as a Intracerebral Haemorrhage

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21
Q

What happens during a subarachnoid haemorrhage?

A

Occurs when a blood vessel on the surface of the brain ruptures and bleeds into the subarachnoid space

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22
Q

Under what circumstances does a haemorrhagic stroke occur?

A

Occurs when there is weakened or abnormal blood vessels.
May also be caused when the blood vessels are under pressure due to brain tumours, inflammation or after trauma.

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23
Q

Is stroke a leading cause of death?

A

It is the second leading cause of death worldwide.

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24
Q

Is it a leading cause of death in the UK?

A

Fourth leading cause in the UK

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25
Q

How many strokes occur each year in the UK?

A

There are more than 100,000 strokes in the UK each year

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26
Q

What is the prevalence of strokes in the UK?

A

Around 1 in 6 men and 1 in 5 women will have a stroke in their lifetime

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27
Q

Does risk of stroke increase with age?

A

Incidence of stroke increases with age, although people are having strokes at earlier ages than in the past

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28
Q

What is the relationship between ethnicity and stroke in the UK?

A

Black people are almost twice as likely to have a stroke as white
people.
Over the past 20 years, stroke incidence has decreased by 40% for white people in London but has not decreased for black people

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29
Q

Which ethnicities are more prone to having strokes earlier in their lifetimes and why?

A

On average, people of black African, black Caribbean and South Asian descent in the UK have strokes earlier in their lives – potentially due to increased risk of hypertension and diabetes.

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30
Q

What are two of the most common consequences of having a stroke? How many people suffer from them?

A

1/3 of people suffer depression after having a stroke
2/3 of stroke survivors leave hospital with some form of disability

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31
Q

How many stroke survivors are there in the UK?

A

1.3 million

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32
Q

What is the cost of strokes on society?

A

£26 million a year

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33
Q

What is the prevalence of TIAs?

A

50 per 100,000 people experience a TIA for the first time each year

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34
Q

What is the prevalence of the subarachinoid haemorrhages?

A

6-12 people per 100, 000 of population per year

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35
Q

What are the risk factors of developing an ischaemic stroke?

A

Family history of a stroke/TIA
Previous stroke or TIA
Hypertension
Diabetes
Smoking
Excess alcohol
Illicit drug use
Inactivity
Migraine
Increased age
Males
Cardiac disease
Dysplipidemia
Ethnicity
Hypercoagulabel status
Carotid artery stenosis

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36
Q

What are the cardiac diseases that are a risk factor for ischaemic strokes?

A

Atrial fibrillation
valvular disease
Heart failure
Mitral stenosis
Structural abnormalities
Atrial and ventricular enlargement

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37
Q

What are some of the risk factors for haemorrhagic strokes?

A

Hypertension
Males
Smoking
Excessive alcohol/illicit drug use
Diabetes
Head injury
Use of anticoagulants

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38
Q

State the known causes of Ischaemic strokes

A

Atherosclerosis
Arterial stenosis
Cardiac or carotid emboli
Hypercoagulabel status
Arterial dissections
Vasoconstriction associated with substance misuse

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39
Q

What are the causes of an intracerebral haemorrhage?

A

High blood pressure
Vessel abnormalities
Bleeding disorders
Vasculitis
Amyloid angiopathy
Arteriovenous malformations

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40
Q

What are the causes of a subarachinoid haemorrhage?

A

Arteriovenous malformations
Aneurysm (congenital or due to chronic high BP)

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41
Q

Explain what type of stroke is associated with atrial fibrillation?

A

Ischaemic stroke, specifically ischaemic strokes caused by the formation of arterial emboli.
Arterial emboli ischaemic strokes are defined by blood clots (thrombus) that accumulate away from the brain. The thrombus or a fragment of the thrombus becomes dislodged and travels to the brain causing a blood clot.

When the thrombus formation originates in the heart and then this or part of it travels to the brain, this is known as a cardioembolic stroke. Atrial fibrillation is a heart condition known to cause cardioembolic strokes.

(formation of thrombus in the heart)

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42
Q

What percentage of people presenting with a stroke are in atrial fibrillation?

A

25%

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43
Q

Describe how atrial fibrillation leads to increased risk of stroke.

A

Atrial fibrillation is the most common sustained cardiac arrhythmia resulting in haphazard (generally rapid) atrial contraction.
In a normal heart beat the atria
communicate with the ventricles (via the atrioventricular node) to ensure
subsequent, sequential contraction to eject blood from the heart. However, in AF only a few of the pulses pass through to the ventricles leading to irregular and incomplete (varied force) contraction.

Both Turbulent flow and blood stasis in the heart increases the risk of emboli formation which increase the risk of stroke.

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44
Q

If a stroke is caused by atrial fibrillation what type of stroke can it be caused?

A

Cardioembolic stroke

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45
Q

Aside from atrial fibrillation which other cardiac complication is associated with strokes?

A

Atherosclerosis which also leads to thrombi formation.

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46
Q

What are the two pathophysiological causes of an ischaemic stroke?

A

Arterial thrombi
Arterial emboli

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47
Q

What is the differences between arterial thrombi and arterial emboli?

A

Arterial thrombi - occurs when a thrombi forms in one of the vessels supplying the brain with oxygen and nutrients, this often occurs due to a ruptured atherosclerotic plaque which initiates the clot formation.

Arterial emboli- This type of stroke occurs when a thrombus or other debris forms/accumulates at a site away from the brain. Part of the thrombus can become dislodged and it can travel up to the brain.

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48
Q

Where is the extra and intra cranial vasculature in the brain?

A

Extra cranial blood vessels are outside of the skull
Intracranial blood vessels are within the skull or are at the base of the skull

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49
Q

Do clots occur in the extra or intra cranial vasculature and what is the outcome?

A

Both and in both cases parts of the brain are starved of oxygen and nutrients causing the central core cells to die.

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50
Q

Define infarct.

A

A small localized area of dead tissue resulting from failure of blood supply

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51
Q

What is the clinical significance of the penumbra in treatment of a stroke?

A

Penumbra is the area surrounding an ischemic event such as thrombotic or embolic stroke. Immediately following the stroke, blood flow and therefore oxygen transport is reduced locally, leading to hypoxia of the cells near the location of the original insult. This can lead to hypoxic cell death (infarction) and amplify the original damage from the ischemia; however, the penumbra area may remain viable for several hours after an ischemic event due to the collateral arteries that supply the penumbral zone.

Therefore as the penumbra is reversibly injured brain tissue- trying to restore blood flow and hence supply of oxygen throughout the brain, attempts to restore as much of the tissue as possible.

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52
Q

What happens within the ischaemic area during a stroke?

A

As blood flow in the brain is restricted hypoxia occurs and leads to neuronal damage.
There is a fall in ATP with release of glutamate, which opens calcium channels with release of free radicals.
These alterations lead to inflammatory damage, necrosis and apoptotic cell death

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53
Q

Describe the relationship between the size of the emboli and the blood vessels affected?

A

Larger emboli will occlude larger blood vessels which are responsible for carrying a supply of blood and hence oxygen and nutrients to a larger proportion of the brain and therefore will have larger consequences on brain function as a larger portion of the brain is being starved of oxygen.

Smaller emboli will occlude smaller blood vessels and therefore have a smaller impact on portion of brain starved of oxygen, resulting in a smaller impact on brain function.

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54
Q

Is it possible with a small emboli to have minimal effects on brain function?

A

Yes, especially if the emboli blocks a blood vessel but there are other blood vessels also serving that area (collateral circulation) , meaning that some supply is still achieved.

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55
Q

How do patients experience different effects from having a stroke?

A

The position of the thrombus or eventual position of the embolus will dictate the
types of brain functions that are affected - essentially which blood vessel in the brain are blocked serving which areas of the brain and the functions those areas are responsible for.

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56
Q

What complication is likely to arise following a ischaemic stroke?

A

Up to 6% of ischaemic stroke patients will sustain a symptomatic haemorrhagic transformation (will also suffer a brain haemorrhage) and more will have asymptomatic bleeding.

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57
Q

What types of stroke are more commonly associated with haemorrhagic transformation?

A

Following a cardioemolic stroke or those with a larger infarct size (area of dead tissue following failure of blood supply)

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58
Q

How does the pathophysiology of a TIA compare with ischemic stroke?

A

Same process but resolves quickly meaning that infarction does not occur

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59
Q

How is flow restored in TIA?

A

Autolysis (self-digestion)

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60
Q

What does the severity of clinical neurological impairment after arterial occlusion depend on?

A

The degree of obstruction
Area and function of tissue supplied
Time the thrombus obstructs the vessel
The ability of the collateral circulation

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61
Q

Explain the pathophysiology of intracerebral haemorrhage.

A

Weakened arteries burst and release blood into the surrounding brain tissue.
This increases the pressure in that area of the brain and causes the release of
excitatory amino acids and the infiltration of immune cells.

In addition to the effect of the released blood on the brain tissue, the usual area
served by the damaged vessel has its blood supply compromised leading to
increased damage to brain tissue.

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62
Q

What are some of the complications associated with an intracerebral haemorrhage?

A

Haemotoma formation
Increase intracranial pressure (ICP),
Hydrocephalus
Compression – can damage the surrounding brain area

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63
Q

Explain the pathophysiology of subarachinoid haemorrhage.

A

An artery on or near the surface of the brain bursts and releases blood into the
subarachnoid space between the brain and the skull.
SAH results in elevated intracranial pressure and impairs cerebral
autoregulation. These effects can occur in combination with acute
vasoconstriction, microvascular platelet aggregation and loss of microvascular
perfusion, resulting in a reduction in blood flow and cerebral ischaemia

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64
Q

What are some of the complications arising from a subarachinoid haemorrhage?

A

Haematoma formation
Hydrocephalus
Compression

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65
Q

What do the clinical features arising from a stroke depend on?

A

Location of disrupted blood flow (which blood vessels in which area of the brain)
Extent of damage
Patient’s underlying health

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66
Q

What does HANDBAG stand for in recognising focal ischaemic stroke symptoms?

A

Hemisensory deficit- loss of sensation on one side of the body
Ataxia- – failure of muscular coordination or irregularity of muscular action
Nystagmus – rhythmic oscillating motions of the eyes more usually horizontal
Dysarthria – difficulty in articulating words due to difficulty in coordinating
the muscles used in speech
Blindness either monocular or binocular blindness - affecting the sight in one or both eyes
Aphasia – partial or total loss of the ability to communicate verbally or using
written words
Gazing – looking steadily in one direction for a period of time

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67
Q

Aside from HANDBAG what are the other focal symptoms of an ischaemic stroke?

A

Weakness or paresis
Unilateral facial droop
Blurred vision
Vertigo
Double vision
Dysphagia
Decreased consciousness
Confusion
Severe headache

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68
Q

Where does weakness or paresis occur?

A

Can affect a single extremity (monoparesis), one half of the body (hemiparesis) or (rarely) all four extremities (quadraparesis)

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69
Q

What are some of the complications associated with aphasia?

A

People may experience difficulty in reading, writing and speaking, recognising objects or understanding. People may use the wrong word or struggle stringing a sentence together, wrong sounds in a word.

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70
Q

What symptoms are suggestive of an increase in intracranial pressure?

A

Nausea, vomiting, sudden onset headache and altered level of consciousness

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71
Q

If symptoms of an increase in intracranial pressure did occur what type of stroke are they likely to be experiencing?

A

Large ischaemic stroke or haemorrhagic stroke

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72
Q

Do seizures commonly occur alongside strokes?

A

Seizures are more common in haemorrhagic stroke occurring in up to 28% of patients either at the onset or within 24 hours of the event.

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73
Q

From the symptoms alone can you determine a haemorrhagic or ischaemic stroke?

A

No, not from the symptoms alone

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74
Q

What are some of the symptoms that suggest a disturbance of the physiological homeostasis?

A

Increase in temperature
Increase in blood pressure
Increase in blood glucose
Hypoxia

Larger the infarction, the greater the extent

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75
Q

What is the purpose of FAST?

A

Provides a memorable way of identifying the most common signs of a stroke and emphasises the importance of acting quickly by calling 999 and is the tool of choice for pre-hospital clinicians such as GP and paramedics.

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76
Q

What does FAST stand for?

A

Face weakness: Can the person smile? Has their mouth or eye drooped?
Arm weakness: Can the person raise both arms?
Speech problems: Can the person speak clearly and understand what you say?
Time to call 999: if you see any of these signs.

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77
Q

What are the limitations of FAST?

A

Doesn’t cover all of the stroke symptoms are therefore a stroke can’t be ruled out if patients not defined as having those symptoms but others that do align with a stroke (visual disturbances).

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78
Q

A patient has a positive FAST or negative FAST but a stroke is strongly suspected what should you do?

A

Transfer to a a hospital with a specialist acute stroke unit. As there is strong evidence to suggest that a specialist unit to deliver effective acute treatment that
reduces long term brain damage and disability if given within a few hours (better patient outcomes).

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79
Q

What is a CRUCIAL intervention that must be made regarding the administration of a stroke patient’s medication?

A

Patient must be assumed NIL BY MOUTH
This means that:
No fluid, food or medication should be given orally until this has occurred

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80
Q

When is the swallowing status of a stroke patient determined?

A

The screening of a patient’s swallow is made within 4 hours of arrival usually by a Speech and Language team. This is known as having a SALT assessment.

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81
Q

Until a safe swallowing method is established what pharmaceutical interventions should be considered?

A

Feeding by a nasogastric tube within 24 hours
Considered for alternative fluids (intracranial pressure considerations- reduced fluids)
Referred to a dietician for assessment, advice and monitoring
Have a comprehensive specialist assessment of their swallow
Receive hydration, nutrition and medication by alternative means
Be referred to a pharmacist to review the formulation and administration of
medicines.

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82
Q

What are some of the scans used with a suspected stroke and what is the purpose of the scan?

A

Brain imaging must be done via CT scan

CT scans are the most cost-effective strategy and imaging enables
identification of the presence of a haemorrhage or ischaemic infarct, the extent of the cerebral damage (core and penumbra) and aetiology as this will dictate
the treatment.

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83
Q

Are these scans limited to stroke patients?

A

No these scans should be completed for anybody presenting with an acute onset of neurological syndrome with persisting
symptoms requires a full diagnosis to differentiate between an acute
cerebrovascular cause and other causes.

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84
Q

When should a CT scan be done for a suspected stroke patient?

A

Within 1 hour of arrival at hospital as it dictates treatment.

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85
Q

What is the Carotid doppler?

A

This is a non-invasive test using sound waves to measure the flow of blood
through the carotid arteries which supply blood to the brain. It is used to identify
narrowing of these arteries.

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86
Q

State the additional tests that are completed with a suspected stroke patient and the purpose of them?

A

Blood glucose
Clotting
ECG
Fasting lipids
Blood culture
Full blood count
Urea and electrolytes

Helps to determine, exclude and diagnose strokes.

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87
Q

What is the purpose of taking a patient’s blood glucose?

A

Determine whether symptoms are related to a hypoglycaemic episode as they can be similar

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88
Q

What is the purpose of taking a patient’s clotting factors?

A

Clotting factors such as APTT, PT and INR determine whether there is any underlying bleed risk which may be a causative factor in the presentation or dictate
treatment.

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89
Q

What is the purpose of taking a patient’s ECG?

A

Detect any cardiac arrythmia which may have been causative of the stroke

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90
Q

What is the purpose of taking a patient’s fasting lipids?

A

Determine the likelihood of atherosclerotic plaque rupture

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91
Q

What is the purpose of taking a patient’s full blood culture?

A

Determine an infective causative agent

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92
Q

What is the purpose of taking a patient’s full blood count?

A

May reveal a cause for the stroke, (i.e. thrombocytosis, polycythaemia, leukaemia, thrombocytopenia).

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93
Q

What is the purpose of taking a patient’s urea and electrolytes?

A

Baseline study to determine whether there are any other likely causes of the symptoms (i.e. hyponatraemia) or evidence of
concurrent illness (i.e. renal impairment).

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94
Q

What scale is used to determine a patient’s level of consciousness?

A

Glasgow Coma scale

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95
Q

What is the purpose of the physical examinations in a suspected stroke patient?

A

To determine the area of the brain affected and the extent of damage

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96
Q

What are some of the physical examinations that should be completed?

A

Cranial nerve examination
Motor function examination
Sensory function
Cerebellar function
Gait
Deep tendon reflex
Language (expressive and receptive capabilities)
Lumbar puncture

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97
Q

What is the purpose of completing a lumbar puncture in a potential stroke patient?

A

To rule out meningitis or subarachnoid haemorrhage

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98
Q

When is a CT scan used in suspected TIA patients?

A

Only when there is clinical suspicion that it may not be a TIA (such as symptoms or history does not align).

-Area of the brain affected is unknown
-Cause of the symptoms is unknown (atypical presentation)
-Detect haemorrhage
-Or if these factors influence treatment (such as if treatment is dependent on the area affected).

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99
Q

When may it be likely that a patient has experienced a haemorrhage?

A

If they are on anti-coagulation and therefore should be scanned immediately to locate the site of bleeding

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100
Q

What is the purpose of acute treatment of a stroke?

A

To maintain/improve vascular perfusion of the brain

To prevent further deterioration of neurological symptoms by
preventing the advancement of the penumbra

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101
Q

What is the duration of the acute phase care?

A

This is the immediate care of the patient from the symptom onset and up to 7 days depending on the severity of the disease; for most people this phase lasts 3 days

102
Q

What does the initial management of the stroke depend on?

A

The diagnosis (either TIA or stroke)
Severity

103
Q

What is the NIHSS?

A

It is the National Institutes of Health Stroke Scale and is used to assess the severity of impairment caused by the stroke in areas such as:
Consciousness, vision, sensation, movement, speech and language. The result is out of 42 points

104
Q

What are the different scales of the NIHSS, depending on the points?

A

0 : no stroke
1 - 4 : minor stroke
5 – 15: moderate stroke
16 – 20 :moderate/severe stroke
21 – 42: Severe stroke

105
Q

What is the initial management of suspected TIA patients?

A

Initial management of suspected TIA (symptoms resolved) – in patients
that do NOT have AF, who have presented within 24 hours of onset:

Aspirin 300mg OD immediately - unless contra-indicated

106
Q

What is the initial management of TIA patients and those who have suffered a minor stroke regarding referral?

A

This is for patients that do NOT have AF:

Refer to a specialist investigation/assessment within 24 hours of symptom onset

For those whose symptoms occurred more than a week ago should be assessed by a
specialist physician as soon as possible but within 7 days

107
Q

When is the risk the highest for patients who have suffered a TIA or minor stroke of then experiencing an additional stroke?

A

Soon after experiencing a minor stroke or TIA, risk is less with patients who experienced symptoms more than a week ago

Increased risk with:
AF
Anticoagulants
Recurrent attacks

108
Q

Once a TIA or minor stroke diagnosis is confirmed by imaging what pharmacological intervention should be made?

A

Within 24 hour onset & confirmed diagnosis:

Dual antiplatelet therapy:
▪ Clopidogrel 300mg STAT, followed by 75mg once daily, with aspirin 300mg STAT,
followed by 75mg for 21 days.

▪ Then, clopidogrel 75mg once daily monotherapy (long-term antithrombotic).

Or
▪ Ticagrelor 180mg STAT, followed by 90mg twice daily, with aspirin 300mg STAT, followed
by 75mg for 30 days.

▪ Then, ticagrelor 90mg BD or clopidogrel 75mg OD (prescribers’ discretion), (longterm antithrombotic).

109
Q

What is the criteria for a patient not being applicable for dual anti-coagulation therapy?

A

Patients presenting outside of the 24 hour onset

110
Q

If not appropriate for dual-anticoagulation what should be given?

A

Clopidogrel 300mg STAT followed by 75mg once daily

111
Q

Aside from dual-anticoagulants, what other drug may need to be co-prescribed?

A

PPIs to reduce the risk of GI bleeding associated with both Clopidogrel and Aspirin.

Esomeprazole and Omeprazole should not be prescribed as they reduce the efficacy of Clopidogrel.

112
Q

Aside from the acute phase care medicines - such as the dual anticoagulants what interventions should be made for secondary prevention?

A

High intensity statin therapy - Atorvastatin 80mg
Antithrombotic, in the form of an antiplatelet,
Hypertension control (if indicated)
Lifestyle management

113
Q

What is the initial management of patients with suspected TIA (symptoms resolved) , minor stroke with AF?

A

Firstly patients must be scanned (CT scan) to exclude intracranial bleed.

Then in patients with non-disabling ischaemic stroke or TIA, who are in atrial fibrillation,
should be anticoagulated with a rapid onset anticoagulant, provided there are no
contraindications.

114
Q

When should secondary prevention interventions be made?

A

As soon as diagnosis is confirmed

115
Q

What are some of the secondary prevention interventions should be made following suspected TIA, minor stroke with AF?

A

Hypertension control (if indicated),
High intensity statin therapy (atorvastatin 80mg),
Discussion of individual risk factor management – lifestyle

116
Q

What is carotid artery stenosis?

A

Carotid artery stenosis is narrowing of the carotid arteries. These arteries deliver oxygenated blood from the heart to the brain and can be the cause of strokes.

Patients with TIA or stroke will be assessed to see if this is present.

117
Q

If carotid artery stenosis is present what are some of the interventions that may be made?

A

Ultimately this will result in the patient undergoing surgery known carotid endarterectomy.

This will be followed by optimum medical treatment (blood pressure control, antiplatelets, cholesterol reduction and lifestyle advice).

118
Q

A patient has reached diagnosis of an ischaemic stroke following brain imaging what is the treatment option?

A

Treatment aims to break up the blood clot

Thrombolysis – use of drugs, such as alteplase or Tenecteplase

Patients must have been imaged before to confirm ischaemic rather than haemorrhage stroke

119
Q

What blood pressure should be achieved before thrombolysis treatment is given?

A

Reduced to below 185/100 mmHg

120
Q

When is thrombolysis therapy considered in ischaemic stroke patients?

A

Patients with acute ischaemic stroke, regardless of age or stroke severity,
in whom treatment can be started within 4.5 hours of known onset,
should be considered for thrombolysis with alteplase or tenecteplase.

If it was more than 4.5 hours, alteplase can be considered in patients if:
- The treatment can be started between 4.5 and 9 hours of known onset or within 9 hours from the midpoint of sleep when they have woken up with symptoms.
AND
- Scan shows the potential to salvage brain tissue

121
Q

After a patient has received alteplase or tenecteplase, what should they then receive within the next 24 hours?

A

Antiplatelet therapy once significant haemorrhage has been excluded and unless contraindicated

122
Q

What are the contra-indications of use of Alteplase in acute ischaemic stroke?

A
  • Symptoms of ischaemic attack beginning more than 4.5 hours prior to infusion start or symptoms for which the onset time is unknown and could potentially be more than 4.5 hours ago (see section 5.1)
  • Minor neurological deficit or symptoms rapidly improving before start of infusion
  • Severe stroke as assessed clinically (e.g. NIHSS>25) and/or by appropriate imaging techniques
  • Seizure at onset of stroke
  • evidence of intracranial haemorrhage on the CT-scan
  • Symptoms suggestive of subarachnoid haemorrhage, even if CT-scan is normal
  • Administration of heparin within the previous 48 hours and a thromboplastin time exceeding the upper limit of normal for laboratory
  • Patients with any history of prior stroke and concomitant diabetes
  • Prior stroke within the last 3 months
  • platelet count of below 100,000/mm3
  • Blood pressure above 185/110 mmHg or aggressive management (intravenous pharmacotherapy) necessary to reduce BP to these limits
  • blood glucose < 50 mg/dl or > 400 mg/dl (< 2.8mM or > 22.2mM)
123
Q

What are some of the side effects of Alteplase?

A

Very common (occurs in more than 1 in 10)
* heart failure
* bleeding in the brain (cerebral haemorrhage) after the treatment of an acute ischaemic stroke

Common (occurs in less than 1 in 10)
* bleeding in the brain (cerebral haemorrhage) after the treatment of heart attacks (myocardial infarction)
* cessation of heartbeat (cardiac arrest)
* shock (a very low blood pressure) due to heart failure

Uncommon (occurs in less than 1 in 100)
* lung-related bleeding, such as blood stained phlegm (haemoptysis) or bleeding in the respiratory tract
* damage to the heart valves (mitral regurgitation)
or to the wall dividing the heart chambers
(ventricular septal defect)

124
Q

What are some of the contra-indications for Tenecteplase?

A
  • History of haemorrhagic stroke or stroke of unknown origin
  • Known history of ischaemic stroke or transient ischaemic attack in the preceding 6 months
    -Peptic ulceration
    -Significant bleeding disorder either at present or within the past 6 months
  • Patients receiving effective oral anticoagulant treatment, e.g. warfarin sodium (INR > 1.3)
  • Any history of central nervous system damage (i.e. neoplasm, aneurysm, intracranial or spinal surgery)
  • Known haemorrhagic diathesis
  • Severe uncontrolled hypertension
    -Hepatic dysfunction
    -Acute pericarditis
    -Acute pancreatitis
125
Q

What are some of the side effects of Tenecteplase?

A

Very common (more than 1 in 10 people):
- Bleeding

Common (may affect up to 1 in 10 people):
- Bleeding at the injection or puncture site
- Nosebleeds
- Genitourinary bleeding (you may notice
blood in your urine)
- Bruising
- Gastro-intestinal bleeding (e.g. bleeding
from the stomach or bowel)

Uncommon (may affect up to 1 in
100 people):
- Irregular heart beat (reperfusion
arrhythmias), sometimes leading to
cardiac arrest.
- Internal bleeding in the abdomen
(retroperitoneal bleeding)
- Cerebral haemorrhage
- Eye haemorrhage

126
Q

What is a thrombectomy?

A

The mechanical removal of a blood clot

127
Q

What is the eligibility for patients to receive a thrombectomy?

A

Area of the brain affected and position of the occlusion
Neurological deficit
Consideration of life before the stroke and the time since known onset

128
Q

Is a thromboectomy given as a solo intervention?

A

Often given alongside thrombolysis unless contra-indicated

129
Q

Following the treatment of an disabling acute ischaemic stroke, when and which anti-platelet treatments should be given?

A

Aspirin 300mg OD for up to 2 weeks.

▪ For patients that have been thrombolysed, the aspirin should be
started 24 hours after alteplase or tenecteplase treatment unless
contraindicated.

▪ For patients that have NOT been thrombolysed, aspirin should be
started ASAP, but within 24 hours.

130
Q

What must be ruled out before aspirin is administered?

A

CT brain imaging must be completed to rule out haemorrhage

131
Q

What formulation considerations should be made regarding aspirin?

A

Aspirin should be given orally if the patient is not dysphagic and swallow has
been assessed or rectally/via NG tube if the patient is dysphagic

132
Q

When should long term anti-thrombotic therapy start?

A

2 weeks following a stroke

133
Q

How does long-term treatment differ for patients with and without AF?

A

For patients without AF- if they are discharged less than 2 weeks, long-term treatment can be started at the point of discharge

For patients with AF- anticoagulation, in the form of a DOAC or vitamin-K antagonist, should be started as the long-term antithrombotic

134
Q

When should a proton pump inhibitor be started alongside aspirin?

A

If a patient has reported dyspepsia with prior use of aspirin

135
Q

If a patient is allergic or intolerant to aspirin, which alternative should be given?

A

Clopidogrel

136
Q

What is the appropriate management of lipid therapy following a stroke?

A

Consider starting lipid therapy (high intensity Atorvastatin 80mg) 48 hours after an acute stroke and not immediately

In patients already on a statin therapy, they can continue

137
Q

Why is it important not to start statin therapy immediately?

A

This is due to some evidence associating the early use of statin with haemorrhagic transformation

138
Q

When should a patient receive supplemental oxygen therapy in treatment of an acute stroke?

A

Stroke patients should only receive supplemental oxygen if their oxygen saturation drops below 95%

139
Q

What blood glucose should you aim for a patient to be in?

A

Between 5-15 mmol/L

140
Q

Why might an excessive control or reduction in blood pressure not be beneficial?

A

Has been linked to compromised cerebral blood flow and lead to development of the penumbra (i.e. death of brain tissue).

141
Q

What is the clinical consequences of short-term hypertension and long-term hypertension following an ischaemic attack?

A

Hypertension following an ischaemic injury is common and this will actually resolve by itself after 4-10 days, so needs minimal clinical intervention.

However continued or excessive blood pressure is associated with development of oedema, haemorrhage and future stroke.

142
Q

That being said when is hypertensive intervention required following an ischaemic stroke?

A

Only recommended if there is a ‘hypertensive emergency’ with one or more of the following medical issues:
▪ Hypertensive encephalopathy
▪ Hypertensive nephropathy
▪ Hypertensive cardiac failure/MI
▪ Aortic dissection
▪ Intracerebral haemorrhage with systolic blood pressure over 200mmHg
▪ Pre-eclampsia/eclampsia

May also need it before receiving thrombosis

143
Q

What administration considerations should be made for administration of anti-hypertensives?

A

Oral only if the patient has received a safe swallow assessment or parental tube

144
Q

What are some anti-hypertensives that are safe for parental administration?

A

Calcium channel blockers, e.g. amlodipine (safe for administration down NG
tubes, always check reference sources)
▪ Parenteral beta blocker, e.g. Labetolol

145
Q

Why to some extent is slight hypertension beneficial in the first few days following a stroke?

A

To ensure adequate perfusion

146
Q

What interventions should be made if a stroke patient is already taking anti-hypertensives?

A

Those admitted already taking antihypertensive therapy - treatment can be
safely withheld until patients are medically and neurologically stable and
have suitable oral or enteral intake

147
Q

What are some complications of hemiplegic strokes?

A

DVT and PE

148
Q

What DVT prophylaxis should stroke patients receive whilst in hospital?

A

Should be offered intermittent pneumatic
compression (on the legs), within 3 days of admission for the prevention of deep vein
thrombosis.

They should not be offered:
Low molecular weight heparins due to risk of intracerebral haemorrhages
Graduated compression stockings as they are ineffective in stroke patients

149
Q

What is the risk of a vascular event in a stroke or TIA patient?

A

The greatest risk of a vascular event is highest after a TIA or stroke and may
be as high as 25% in the first 3-months, half of which are within the first 4-
days

This risk is about the same for other vascular events such as a myocardial infarction.

150
Q

What should be devised regarding the secondary prevention of a vascular event?

A

A comprehensive and personalised strategy for vascular prevention including medication and lifestyle factors and this should be implemented when appropriate to do so.

151
Q

What percentage of strokes is linked to hypertension?

A

50%

152
Q

Why do treatment recommendations regarding blood pressure differ in acute and long-term treatment?

A

Sudden changes to blood pressure in the acute treatment of a stroke correlate to changes in cerebral pressure and alter the extent of brain damage as it changes perfusion. Therefore may be reluctant to intervene unless it is a hypertensive emergency

However modification of blood pressure long-term does reduce risk of stroke.

153
Q

What did the progress study conclude about the benefits of controlled blood pressure and incidence of stroke?

A

That blood pressure reduction after stroke
or TIA (using two different anti-hypertensives) prevented further vascular events.

It showed that even in normotensive patients, a reduction in blood pressure (of
12/5mmHg) resulted in a 42% reduction in recurrent stroke and 35% fewer major
coronary events

154
Q

Is stroke reduction risk related to magnitude of reduction or the baseline level?

A

Risk is correlated to the magnitude of reduction rather than the systolic baseline level.
Overall, a 10 mmHg reduction in
systolic BP reduced the risk of cardiovascular disease by 20% and stroke by 27%.

155
Q

What is the blood pressure target for patients after a TIA or stroke?

A

Should aim for a systolic blood pressure below 130 mmHg

156
Q

What is the blood pressure target for patients with bilateral carotid stenosis?

A

140-150mmHg

157
Q

When should anti-hypertensive medication be started for stroke or TIA patients?

A

Upon discharge or at 2 weeks, whatever is earliest.

If the patient stabilises but BP remains high, treatment may be initiated sooner.

158
Q

How frequently should the monitoring occur for blood pressure in patients following a stroke?

A

Close monitoring to try and stabilise the patient quickly and then this should be done annually at least.

159
Q

Does the blood pressure recommendations differ for stroke patients?

A

No same as the NICE guidance for the age, ethnicity and diabetes status.

160
Q

What is the relative risk reduction of initiating Atorvastatin 80mg OD in stroke patients after 6 months?

A

A relative risk reduction of 15% in stroke and 35% in major coronary events

161
Q

What is the risk reduction of lowering LDL by 1mmol/L?

A

Reduces the relative risk of major vascular events by 21%, total mortality by 9% and stroke by 15% irrespective of baseline cholesterol or gender.

Therefore the decision to initiate is based on reducing CVD risk rather than cholesterol level.

162
Q

What did the Treat Stroke to Target Trial show?

A

In patients with evidence of
atherosclerosis, had a lower risk of cardiovascular events with a target-LDL
below 1.8 mmol/L

163
Q

What is the associated risk of starting statins in the acute setting?

A

Increased risk of haemorrhagic stroke/ transformation - so avoid in the first 48 hours

164
Q

What are the pharmaceutical interventions therefore regarding statin therapy in stroke patients?

A

Patients should be offered advice on lifestyle factors that may modify lipid
levels (diet, physical activity, weight, alcohol and smoking).
▪ Patients who have had a stroke should be offered treatment with a statin
unless contraindicated/
▪ Begin with a high intensity statin such as atorvastatin 80mg, change
to an alternative statin at maximum tolerated dose if a high intensity
statin is unsuitable or not tolerated.
▪ Those with evidence of atherosclerosis, should aim to reduce fasting LDLcholesterol to below 1.8 mmol/L.
▪ If this is not achieved by 4-6 weeks – discuss adherence/tolerability,
optimise diet and lifestyle, optimise dose, consider adding ezetimibe
10mg OD

165
Q

What does studies show regarding anti-platelet therapy in patients with ischaemic stroke or TIA without AF?

A

Aspirin plus modified release dipyridomole and clopidogrel monotherapy are equally effective and both SUPERIOR to aspirin
monotherapy

166
Q

Therefore which drug is the first line choice for long term treatment following a stroke?

A

Clopidogrel 75mg once daily

If contra-indicated or intolerated then Aspirin 75mg once daily

167
Q

When should long-term antiplatelet therapy be started?

A

Following a minor stroke or TIA - this should be started following completion of dual-antiplatelet therapy

Following a disabling stroke- this will start 2 weeks after the onset of symptoms (following on from the aspirin 300 mg, which will be stopped), or at the point of discharge if this is sooner

168
Q

Is aspirin plus clopidogrel more beneficial?

A

Not been shown to be more beneficial than clopidogrel monotherapy and has more side effects.

Reminder patients with dyspepsia should be on a PPI

169
Q

What long term therapy is recommended in patients with a stroke/TIA with AF?

A

For a cardioembolic stroke, particularly AF, anti-coagulation therapy should be initiated.

In a non-cardioembolic stroke, anti-coagulants were not seen to be more beneficial than anti-platelets and carries a greater risk of bleeding.

170
Q

What is the attributable risk of recurrent stroke per year associated with
permanent AF ?

A

12%, therefore most patients perceive anticoagulation therapy to be beneficial

171
Q

When should anticoagulation not be given?

A

Severe haemorrhage identified on screening
Severe hypertension above 180/120 mmHg

172
Q

What is the purpose of CHA2 DS2-VASc assessment tool?

A

Used to identify the stroke risk in patients with AF, usually who have not had a
stroke or TIA, to determine the future CVA risk and therefore whether
anticoagulation should be started.

173
Q

What are the different components of the CHA2 DS2-VASc?

A

C Congestive heart failure
H Hypertension
A2 Age >75 (2 points)
D Diabetes mellitus
S2 Prior stroke or TIA (2 points)
V Vascular disease
A Age >65
Sc Sex (female 1 point)

174
Q

Using the CHA2 DS2-VASc tool how many points should initiate the patient on anti-coagulation therapy?

A

1 for a man , 2 for a women

175
Q

What is the ORBIT assessment tool?

A

Used in conjunction with the CHA2 DS2-VASc tool to estimate the risk of bleeding for patients on anticoagulation for AF.
Dependent upon the number of points awarded the risk of bleeds per year can
be estimated. This helps guide the decision on whether anticoagulation should
be started.

176
Q

What are the different components of the ORBIT assessment tool?

A

Hb <13g/dL male <12g/dl female (2 pts)
Age >74 (1 point)
Bleeding history GI/intracranial/haem stroke (2 points)
Renal function eGFR<60ml/min/1.73m2
(1 point)
Antiplatelet treatment (1 point)

177
Q

What ORBIT values should be used to guide the decision of whether anticoagulants should be initiated?

A

Unlike CHA2 DS2-VASc there is no threshold values that should be used to guide the clinical decision making.

However,
An ORBIT score of 0-2 is considered low risk, 3 medium risk and 4-7 high risk of bleeding

178
Q

What is an additional benefit of using the ORBIT assessment tool?

A

Address modifiable risk factors for bleeding and therefore reduce the risk of bleeding.

179
Q

Is aspirin a suitable alternative if the risk remains high for bleeding?

A

No it is not considered to be a safe alternative

180
Q

What factors are you trying to weigh up before starting anticoagulation therapy?

A

The decision based on the risk of haemorrhagic transformation and the risk of further infarcts as a result of the
AF.

181
Q

When is haemorrhagic transformation most commonly seen?

A

Increased size of the infarct and occurs in around 6% of patients

182
Q

In TIA patients which anticoagulant should be initiated and when?

A

Anticoagulation with a DOAC (or low molecular weight heparin
and vitamin-K antagonist for those with valvular AF) – should be started
immediately after diagnosis and brain haemorrhage has been excluded by
brain imaging

183
Q

In minor stroke patients which anticoagulant should be initiated and when?

A

Anticoagulation should be considered earlier than 5 days, if the prescriber considers the benefits to outweigh the risk of early intracranial haemorrhage. In the meantime, as discussed above, aspirin
300mg OD should be used (this will be stopped upon initiation of the
anticoagulant).

184
Q

In moderate to severe stroke patients which anticoagulant should be initiated and when?

A

Anticoagulants should be considered 5-14 days from the onset
Wherever possible these patients should be
offered participation in a trial of the timing of anticoagulation after stroke to
gain data around optimal start time. In the meantime, as discussed above,
aspirin 300mg OD should be used (this will be stopped upon initiation of the
anticoagulant).

185
Q

What are the cautions for Warfarin use?

A

Bacterial endocarditis (use only if warfarin otherwise indicated);
Conditions in which risk of bleeding is increased;
History of gastrointestinal bleeding; Hyperthyroidism;
Hypothyroidism;
Peptic ulcer;
Recent ischaemic stroke;
Recent surgery;
Uncontrolled hypertension

186
Q

What are the contra-indications for Warfarin use?

A

Avoid use within 48 hours postpartum; Haemorrhagic stroke;
Significant bleeding

187
Q

What are some of the side effects of Warfarin?

A

Common/ very common:
Haemorrhage

Rare:
Alopecia
Nausea
Vomiting

Frequency unknown:
Blue toe syndrome;
CNS haemorrhage;
Diarrhoea;
Fever;
Haemothorax;
Jaundice;
Pancreatitis;
Skin necrosis (increased risk in patients with protein C or protein S deficiency);
Skin reactions

188
Q

What is the monitoring required for Warfarin?

A

The base-line prothrombin time should be determined but the initial dose should not be delayed whilst awaiting the result.

It is essential that the INR be determined daily or on alternate days in early days of treatment, then at longer intervals (depending on response), then up to every 12 weeks.

189
Q

When may the frequency of Warfarin be increased?

A

Change in the patient’s clinical condition may increase monitoring frequency associated with liver disease
Intercurrent illness
Drug administration

190
Q

What do DOACs inhibit?

A

DOACs known as direct oral anti-coagulant inhibit Factor Xa or are direct thrombin inhibitors

191
Q

What are the cautions for use of DOACs?

A

Elderly
Low body weight
Risk of bleeding
Anaesthesia with postoperative indwelling epidural catheter

192
Q

What are the contra-indications of DOACs?

A

Active, clinically significant bleeding; antiphospholipid syndrome (increased risk of recurrent thrombotic events);
Prosthetic heart valve (efficacy not established);
Significant risk of major bleeding;
Use with any other anticoagulant

193
Q

What are some of the side effects of DOACs?

A

Anaemia;
Haemorrhage;
Nausea;
Skin reactions

Uncommon:
CNS haemorrhage; hypotension; post procedural haematoma; thrombocytopenia; wound complications

194
Q

What is the monitoring that is required for DOACs?

A

Patients should be monitored for signs of bleeding or anaemia; treatment should be stopped if severe bleeding occurs.

No routine anticoagulant monitoring required (INR tests are unreliable).

195
Q

When are the DOACs considered first line for the secondary prevention of a stroke in patients with AF?

A

Patients with non-valvular AF

(Warfarin is second line)

196
Q

When is Warfarin considered first line for the secondary prevention of a stroke in patients with AF?

A

DOACs are contra-indicated, not tolerated or not suitable

It would be used in patients with mechanical heart valves, valvular or rheumatic AF

197
Q

Which specific DOAC is most effective?

A

Limited data to determine efficiency of each individual one therefore assessment of the drug profile is required.

198
Q

What are the advantages of Warfarin therapy?

A

Been used for many years -
experience
Antidote available
Requires regular INR monitoring –
efficacy/compliance monitoring

199
Q

What are the disadvantages of Warfarin?

A

Many food and drug interactions
Requires loading to be therapeutic
Requires INR monitoring – time and
resource consuming

200
Q

What are the advantages of DOAC therapy?

A

Rapid onset – no loading required
Coagulation monitoring not required
Predictable anticoagulant effect
Fewer interactions with drugs and no
known food interactions compared to
warfarin
Fixed dosing

201
Q

What are the disadvantages of DOACs?

A

Other antidotes in trials.
Increased cost
Long term adverse effects unknown
Relatively new to the market
Unable to monitor efficacy and compliance
Short half life means that missed doses could leave the patient unprotected
Only suitable for patients with a creatinine clearance above 30mL/min
Idarucizumab antidote for dabigatran
– limited use
Andexanet antidote for apixaban,
edoxaban, rivaroxaban

202
Q

What did the RE-LY study demonstrate regarding effectiveness of DOAC vs Warfarin?

A

The benefit of dabigatran over warfarin was greatly reduced in patients
where the quality of anticoagulation control was high.
‘Quality’ of warfarin
anticoagulation is determined by the ‘time in therapeutic range’ (TTR)
, i.e. the time that a patient on warfarin is maintained at the desired therapeutic range; the average for UK centres was documented as 72%

203
Q

What is INR?

A

International normalised ratio and it is a measure of the time taken for blood to
clot (expressed as a ratio against population data), the higher the number the
greater time blood will take to clot/
INR of 2.5, it takes someone on Warfarin 2.5 times longer for their blood to clot compared to a normal patient.

204
Q

What is the associated risk between smoking and strokes?

A

Smokers have up to 3 times the risk of stroke and double the risk of recurrent stroke compared to non-smokers

But if they stop the risk decreases significantly and is at the level of a non-smokers by around 5 years.

205
Q

What is the UK statistics for smoking adults and hospital admissions?

A

Around 1 in 5 adults in the UK smoke with an estimated 454,700 hospital admissions being attributable to smoking.

206
Q

What percentage of stroke patients smoke?

A

1 in 4

207
Q

What intervention should be made for smoking stroke of TIA patients?

A

Smoking cessation immediately

208
Q

What exercise advice should be given to patients following a stroke?

A

Same as healthy lifestyle advice
Patients should aim for 150 minutes of exercise a week, active every day, minimise sitting for long periods.
Adults should aim to complete strengthening exercises at least 3 times a week.
Older people at risk of falls should
activities which incorporate balance and coordination, patients should be
active every day and minimise the amount of time sitting for long periods.

209
Q

Do cardioprotective diets prevent stroke reoccurrence?

A

Limited evidence to show that cardioprotective diets prevent stroke reoccurrence

210
Q

What diet recommendations should be made following a stroke?

A

5 or more portions of fruit and vegetables/day
Two portions of oily fish/week
Replace saturated fats with poly- and mono- unsaturated fats
Overweight/obese patients should be offered advice and support to aid weight loss
Reduce their salt intake
Reduce alcohol intake to a maximum of 14 unit/week

211
Q

What are some of the rehabilitation services available to support patients following a stroke?

A

Complete and relevant information transfer from secondary care back to
primary care
▪ Early supported discharge to deliver stroke specialist rehabilitation at home
or in a care home,
▪ Services in outpatient and community settings in liaison with inpatient
services to continue rehabilitation,
▪ Specialist follow-up at 6-months and annually after a stroke (including a
review and monitoring of risk factors),
▪ Further therapies if goals for specific function and activities are identified and
a change is likely,
▪ Practical and emotional support (i.e. housing and employment),
▪ GP support,
▪ Social services.

212
Q

What should patients be screened for regarding their mental health?

A

To identify mood disturbances and cognitive impairment

213
Q

How many patients receive end of life care?

A

1 in 20 stroke patients within 72 hours of onset and 1 in 7 will die in hospital

214
Q

What are some of the side effects of strokes which high quality end of life care should attempt to minimise?

A

Pain
Distress
Confusion
Agitation
Issues relating to nutrition and hydration

215
Q

What is haemostasis?

A

The arrest of blood loss from damaged blood vessels

216
Q

What happens when there is damage to blood vessels?

A

It causes vasoconstriction plus adhesion and activation of platelets to form a plug and formation of fibrin (reinforcing network) to stop the bleeding.

217
Q

What is thrombus?

A

The formation of a haemostatic plug in the vasculature without the presence of bleeding (it is situated in the wrong place)

218
Q

What does arterial thrombus consist of?

A

Mainly of platelets

219
Q

What does arterial thrombus result from?

A

Atherosclerotic plaque rupture

220
Q

What does venous thrombus consist of?

A

Small white head (platelets) and a large red tail (red blood cells).

221
Q

What is an embolus?

A

When part of the thrombus breaks away and travels to a secondary site.

222
Q

Where do venous emboli and arterial emboli become dislodged?

A

Venous emboli become dislodged in the lungs whereas arterial emboli travels to other organs such as the heart or the lungs.

223
Q

What factors influence blood coagulation?

A

Clotting factors
Vessel endothelium
Blood components such as platelets

224
Q

What are the main components of the coagulation cascade?

A

Each components are known as factors and they are found in the blood as inactive precursors of proteolytic enzymes and co-factors. Each factor in tern activates another
down the cascade (starting at the top of the page) and amplifies the downstream
effects.

225
Q

What are the two mechanisms that lead to the downstream effects of fibrin formation and coagulation?

A

Extrinsic (as some of the components come from outside the blood vessels) and intrinsic (as all components are present within the blood vessel wall) pathways.
In vivo the whole system functions as a single pathway.

225
Q

When do the intrinsic and extrinsic pathways converge?

A

Activation of factor X, and have a shared final course ending with the last enzyme thrombin, derived from prothrombin (II),
which converts soluble fibrinogen to an insoluble meshwork of fibrin in which cells
and platelets become trapped.

226
Q

What happens when an atherosclerotic plaque ruptures?

A

Culminates in the formation of a thrombus.
Adhered and activated platelets
provide co-factors and expose phospholipids important in activating the clotting cascade. Pro-thrombotic factors are synthesised and stored in the endothelium,
for example, tissue factor is also responsible for activating the cascade.

227
Q

State the six reactions that occur as a result of platelet activation.

A

Adhesion
Shape change
Secretion
Biosynthesis
Aggregation
Phospholipid exposure

228
Q

Describe where the adhesion that occurs as a result of platelet activation.

A

To areas of vascular damage via the glycoprotein 1b receptors on the
platelets

229
Q

What is the shape change that occurs after platelet activation?

A

Smooth disc changes to spiny spheres to enable entrapment within the fibrin mesh

230
Q

What is secreted after platelet activation?

A

Platelet agonists (i.e. ADP) and coagulation factors to further activate other platelets and the clotting cascade

231
Q

What is biosynthesised after platelet activation?

A

Factors such as TXA2 and platelet-activating factor responsible for platelet aggregation and vasoconstriction.

232
Q

What aggregates after platelet activation?

A

Aggregation agonists lead to expression of GPIIb/IIIa receptors that bind fibrinogen linking adjacent platelets.

233
Q

What does phospholipid exposure do?

A

Promote thrombin formation

234
Q

What is an example of an inappropriate activation of this pathway?

A

Artery wall is deceased such as atherosclerosis

235
Q

Describe what happens in the fibrinolytic system.

A

Endogenous plasminogen activators, for example, tissue plasminogen activator (t-PA) is released and diffuses into a thrombus where plasminogen is deposited on the fibrin strands.
The t-PA activates plasminogen to form active plasmin which cleaves fibrin and
a number of clotting factors. It acts locally to lyse the thrombus and halt further
clotting action

235
Q

What is an inhibitor/reversal of the coagulation pathway?

A

The fibrinolytic system

236
Q

What type of drug is alteplase?

A

Thrombolytic, recombinant t-Pa

237
Q

What is the mechanism of aspirin?

A

Irreversible inhibition of COX-I in
platelets preventing the formation of Thromboxane A2 (TXA2) preventing the
downstream steps needed for platelet aggregation

238
Q

What is the mechanism of Clopidogrel?

A

P2Yqw receptor antagonist on platelets
responsible for promoting aggregation

239
Q

What is the mechanism of Warfarin?

A

Certain factors within the coagulation cascade rely on the presence of Vitamin K specifically in the reduced form.
Warfarin inhibits the enzyme Vitamin K reductase allowing formation of the active form of Vitamin K and therefore reducing formation of certain clotting factors and their downstream factors.

240
Q

What type of drug is Rivaroxaban and Apixaban?

A

Direct factor Xa inhibitor

241
Q

What type of drug is Dabigatran etexilate?

A

Is a prodrug which is converted to dabigatran by hydrolysis
in the plasma and liver. In this form it is a potent, competitive, reversible direct
thrombin inhibitor.

242
Q

What type of drug is Edoxaban?

A

Direct and reversible inhibitor of factor Xa

243
Q

What are some of the observations and monitoring requirements for a patient following a stroke?

A

Blood glucose – should be maintained between 5 and 15 mmol/L19
Blood pressure
▪ Oxygenation – supplemental oxygen should be given if saturation drops
to below 95%
▪ Nourishment and hydration – food and fluid chart completion
▪ Temperature
▪ Early mobilisation and positioning – sitting will help maintain oxygen saturation and reduce the risk of pneumonia. Patients should be helped to sit up and mobilised as soon as their condition permits.

244
Q

List the multidisciplinary team involved in the care of a stroke patient?

A

Registrars
Consultants
Senior and Junior doctors
Pharmacists
Nurses
Dieticians
Speech and Language therapists
Support workers
GPs
Occupational therapists
Physiotherapists
Psychologists

245
Q

What is the most common type of feeding tube used in patients with dysphagia?

A

Nasogastric tube

246
Q

How and where is a NG tube positioned?

A

Lubricate the end of the nasogastric tube. Gently insert the tip of the tube into the nose and slide along the floor of the nasal cavity. Aim back then down to stay below the nasal turbinate. Expect to feel mild resistance as the tube passes through the posterior nasopharynx.

247
Q

What are the different types of nasogastric tube?

A

Two types of NG tubes are in common use—the single-lumen tubes (Levin) and the double-lumen sump (Salem’s sump) tubes. The single-lumen tubes are best for decompression, and the double-lumen sump tube is best for continuous lavage or irrigation of the stomach.

248
Q

What are the pharmaceutical care issues associated with the administration of
medication via an NG tube?

A

May not be appropriate to deliver liquid medicines this way
Some medicines may not be suitable to be given this way as they may block or bind to the tube
Cleaning of the tube and infection risk

249
Q

Which factors should you consider before giving medicines via the enteral tube?

A

Tube size
Tube material
Site of tube (and associated site of medicine absorption)
Tube Function
Feed timing – feeds may interact with medicines to reduce bioavailability.
Administration Route – other administration routes to consider include intravenous, transdermal, buccal, etc.
The critical nature of the medicine, e.g. antiseizure medication, etc.
Formulation – modified release tablets should not be given via a feeding tube. More viscous liquids e.g. syrups may clog tubes, as may larger medicine particles

250
Q
A