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MD2 Neuro > Stroke and TIA > Flashcards

Stroke and TIA Flashcards

1
Q

What % of stroke/TIA survivors go on to have a further stroke in less than 5 years?

A

20%

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2
Q

What is the global burden of stroke?

A

20 million/year

2nd leading cause of death

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3
Q

Describe the “FAST” system for approach to stroke recognition

A

F: facial weakness

A: arm weakness

S: speech difficulty

T: time to act fast

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4
Q

Associated features of stroke

A

Weakness, numbness or paralysis of face or limbs

Difficulty speaking or understanding

Dizziness and loss of balance

Loss of vision

Headache (may be severe and abrupt)

Difficulty swallowing

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5
Q

What are the 3 assessments to make in the Cincinnati pre-hospital stroke scale?

A

Facial droop: smile

Arm drift: close eyes and hold out arms

Speech: say “you can’t teach an old dog new tricks” or similar familiar saying

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6
Q

Define stroke

A

Brief episodes

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7
Q

Define TIA

A

Brief neurological episodes (usually less than 24 hours) without damage on imaging

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8
Q

63 year old Mrs Faul with PHx of smoking and untreated HTN experiences sudden onset speech difficulties and R sided weakness with confusion

O/E (90 mins after onset of Sx): alert, BP 170/100, irregular pulse, expressive dysphasia, moderate R hemiparesis, appears frustrated

What should be done next?

A

Code stroke:

1) Urgent triage and high priority for stroke patient
2) Mobilise stroke team
3) Establish IV access and test glucose, routine biochem, FBE
4) ECG
5) Accurate clinical Dx (exclude mimics)
6) Urgent CT

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9
Q

List 11 recognised stroke mimics

A

Seizure

Sepsis

Toxic/metabolic

Space-occupying lesion

Syncope/presyncope

Acute confusional state

Vestibular dysfunction

Acute mononeuropathy

Dementia

Migraine

Spinal cord lesion

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10
Q

List 4 clinical features which suggest stroke over some other mimic

A

Exact time of onset

Patient could recall exactly what they were doing at symptom onset

Well in the last week

Definite focal symptoms or signs, worse NIHSS

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11
Q

List 5 clinical features which suggest stroke mimic over a stroke

A
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12
Q

What is the NIHSS and what does it assess?

A

National Institute of Health Stroke Scale

Assesses 11 aspects and provides a score from 0-42 (stratifies as no stroke Sx, minor stroke, moderate, moderate to severe, severe stroke)

Assesses level of consciousness, horizontal eye movement, visual field test, facial palsy, motor (UL, LL), limb ataxia, sensory function, language, speech, extinction and inattention

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13
Q

What is shown on this DWI MRI?

A

Lightbulb sign

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14
Q

What does this CT show?

A

Early (4.5 hours) ischaemic changes in a R MCA infarct

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15
Q

What does this scan show?

A

Deep putamenal ICH

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16
Q

What are the 3 major stroke types?

A

Ischaemic stroke (cerebral infarction)

Intracerebral haemorrhage (ICH)

Subarachnoid haemorhage (SAH)

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17
Q

What are the 3 main causes of ischaemic stroke?

A

Large artery thromboembolism

Cardiogenic embolism

Small vessel (lacunar) infarct

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18
Q

What are the most common sites for intracerebral haemorrhage?

A

Deep HTNive location

Lobar

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19
Q

What are the most common causes of SAH?

A

Ruptured aneurysm

AVM

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20
Q

What is the most common underlying cardiac cause of a cardiogenic embolism?

A

AF

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21
Q

What cerebral region is affected in a lacunar infarct?

A

Subcortical

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22
Q

List 4 rarer causes of ischaemic stroke

A

Arterial dissection

Drugs

Vasculitis

Rarer arteriopathies (e.g. Moyamoya disease)

23
Q

What is the most lethal subtype of stroke?

A

ICH: mortality is 30-40%, patients have worse functional outcomes

24
Q

How is ICH classified? What sites are affected in each and what is the typical offending pathology?

A

Deep: affects putamen, thalamus, brainstem, cerebellum, and usually due to HTN and rupture of deep penetrating arteries

Lobar: superficial, often secondary to amyloid angiopathy, tumour, AVM, aneurysm

25
Q

What is the aim of therapies for ischaemic stroke and ICH?

A

Limiting stroke growth (rescuing the penumbra)

26
Q

Mx for ischaemic stroke

A

Thrombolysis: IV tPA

Admission to stroke unit

Ix for underlying cause (e.g. AF, large artery stenosis)

27
Q

Why are TIA and ischaemic stroke patients considered high-risk?

A

5-10% of TIA patients have a stroke at 1/52, 10-20% at 3/12

Even higher recurrence rate if DWI performed

Probably similar for ischaemic stroke

Patients with CVD are at high risk of CHD and vascular death

28
Q

List 5 non-modifiable RFs for ischaemic stroke

A

Age

Gender

FHx

Ethnicity

Contraceptive use

29
Q

List 9 established modifiable RFs for stroke

A

HTN

DM

Smoking

AF/heart disease

Hyperlipidaemia

EtOH consumption

Prothrombotic factors

Prior TIA

Prior stroke

30
Q

List 9 possible modifiable RFs for stroke

A

Physical inactivity

Obesity

Dietary factors

Oral

Lack of HRT

Infection

Stress

Sleep apnoea

SES

31
Q

What are the main modifiable RFs for stroke and how can these be managed?

A

RFs: smoking, HTN, DM, obesity

Mx: smoking cessation, weight loss, increased physical activity, healthy diet, anti-HTN, in high risk of CVD consider aspirin (but no clear indication for antiplatelet treatment in low risk or intermediate risk - i.e. uncomplicated DM, HTN, hyperlipidaemia - of stroke)

32
Q

By what % do anti-HTN drugs reduce risk of primary stroke?

A

Up to 40%

33
Q

Give 3 examples of NOACs and their mechanisms of action

A

Direct thrombin inhibitors: dabigatran

Factor Xa inhibitors: rivaroxaban, apixaban

34
Q
A
35
Q

When are NOACs indicated in stroke prevention?

A

Prevention of stroke (or systemic embolism) in non-valvular AF in a patient with one or more RFs for developing stroke

36
Q

What is the risk of haemorrhage with oral anticoagulation?

A

1-1.5% per annum (greater if over 80 years old)

37
Q

CHADS2

A

Cardiac failure

HTN

Age >75

DM

Previous Stroke or TIA (2 points)

If 1 or more, recommend oral anticoagulant

If 0, undertake a more comprehensive risk assessment (e.g. VASc)

38
Q

By what % do oral antiocoagulants reduce the risk of stroke in people with AF?

A

Risk of stroke reduced by 60%

39
Q

What is the recurrent stroke risk after a first stroke?

A

4% per annum

40
Q

ABCD^2 score

A

AGE: 60 or above - 1

BP: SBP 140 or above, DBP 90 or above - 1

CLINICAL: focal weakness - 2, speech impairment without focal weakness - 1

DURATION: 60 min or more - 2, 10-59 min - 1

DM - 1

Low risk = 0-3, moderate risk = 4-5, high risk = 6-7

41
Q

What are the principles of secondary prevention in stroke?

A

BP lowering

Cholesterol lowering and statins

Antiplatelet therapy

AF and anticoagulation

Carotid revascularisation (endarterectomy and stenting)

42
Q

At what level should BP and cholesterol lowering medications be initiated post-stroke?

A

ANY level; any reduction is beneficial

43
Q

What is the polypill and what is its expected impact on CVD rates?

A

Statin, 3 BP drugs (e.g. thiazide, B blocker, ACEI), aspirin, folic acid

44
Q

What is the effect of aspirin on risk of subsequent stroke and all vascular events?

A

Reduces risk of subsequent stroke by ~13%

Reduces risk of all vascular events by 20%

45
Q

When is dipyridamole + aspirin indicated over aspirin alone?

A

If patient at moderate to severe absolute risk, or in cases of recurrent stroke

SE of headache common

46
Q

When is clopidogrel recommended post-stroke over aspirin?

A

Modestly more effective than aspirin in prevention of serious high risk vascular events so prescribed in these contexts

47
Q

When might there be a role for aspirin + clopidogrel post-stroke?

A

In first 90 days after stroke or TIA

48
Q

List 4 complications of CEA

A

Death or stroke

Cranial nerve palsy

Wound complications

CVS complications

49
Q

What are some of the limitations of CEA?

A

Only marginal benefits on annual rates of ipsilateral stroke for patients with asymptomatic or moderate lesions; dramatic benefit is only seen for high-grade (above 70%) symptomatic stenoses

Benefits are time-linked to last symptomatic event (best within 30 days)

Risk of complications

50
Q

What is more effective at reducing risk of ipsilateral stroke and perioperative death in patients with advanced symptomatic carotid artery disease: CEA or medical therapy?

A

CEA

51
Q

Mrs Faul has had an ischaemic stroke secondary to carotid artery thromboembolism, managed with thrombolysis (to which she had a good response)

Post-stroke Mx for Mrs Faul?

A

Lifestyle issues: smoking cessation, regular exercise, weight reduction and maintenance

BP: reduce to 120/80

Statin

CEA or stenting

Long-term anticoagulation with dabigatran or other NOAC

52
Q

Summarise important principles of secondary prevention for stroke

A

High-risk patients benefit from BP and cholesterol reduction regardless of baseline

Antiplatelet therapy is routine if patient not anticoagulated

Warfarin for AF may be replaced by NOAC

CEA proven therapy for carotid artery stenosis, but carotid stenting may be equivalent for patients less than 70 years old

53
Q

Dipyridamole

A

Inhibits PDE which normally breaks down cAMP (increasing cellular cAMP levels and blocking the platelet aggregation response to ADP), and/or cGMP (resulting in added benefit when given together with nitric oxide or statins)

Inhibits cellular reuptake of adenosine into platelets, RBCs and endothelial cells leading to increased extracellular concentrations of adenosine

MD2 Neuro (9 decks)

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