stroke Flashcards

1
Q

stroke

A

“acute focal neurological deficit resulting from cerebrovascular disease and lasting more than 24hrs or causing earlier death”

Death of brain tissue from hypoxia

  • No local cerebral blood flow
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2
Q

3 types of stroke

A
  • Ischaemic stroke (like MI)
  • Haemorrhagic stroke (bleed into brain tissue)
    • pressure = damage
  • TEMPORARY ischaemia
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3
Q

TIA

A

transient ischaemic attack)

  • Rapid loss of function, but regains all neurological components which were lost (within 24hrs)
  • Issues in blood vessels
    • suggestive of a ‘proper’ stroke in future
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4
Q

accronym to spot a stroke

A

FAST

Facial drooping

Arm weakness

Speech difficulty

Time

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5
Q

TIA

incidence and effect

A

Incidence 25% that of stroke

Localised loss of brain function

  • Ischaemic event – not haemorrhage

FULL recovery within 24hrs

  • Most recover in 30mins

Thought to happen as platelet emboli (from vessels in neck) block blood to brain but are rapidly removed, so blood flow restored before permanent damage incurred

Higher risk of ‘proper’ stroke over 5 years

  • 12% in 1yr
  • 29% in 5yrs
  • 2.4% risk of myocardial infarction
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6
Q

risks for stroke (6)

A
  • HYPERTENSION
  • SMOKING
  • Alcohol
  • ISCHAEMIC HEART DISEASE
  • Atrial Fibrillation
  • Diabetes Mellitus
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7
Q

diastolic for risk of stroke

A

if DIASTOLIC >110mm Hg then a x15 risk compared to diastolic <80mm Hg

  • Even borderline hypertension has risk
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8
Q

atrial fibrilation linked to stroke

A

Association with emboli from abnormally contracting atria passing through ventricle into cerebral circulation

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9
Q

% death due to stroke

A

12%

Infarction 85%

Haemorrhage 10%

Subarachnoid Haemorrhage 5%

Venous thrombosis <1%

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10
Q

commonest cause of adult disability

A

stroke

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11
Q

incidence and risk of stroke

A
  • Lifetime risk of 1 in 6
  • Incidence 2 in 1000 pop/year
  • Male > female
  • Increasing incidence with age
    • 0.5/1000 pop age 50
    • 15/1000 pop age 80
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12
Q

causes of ischaemic stroke

A
  • uncertain
    • Most of time due to narrowing of vessels and plaques forming – alike MI
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13
Q

causes of haemorrhagic stroke

A
  • Intracranial Bleed
    • Aneurysm rupture – weak point which eventually fail
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14
Q

causes of embolic stroke

A
  • Embolism from left side of heart
    • Atrial fibrillation
    • Heart valve disease
    • Recent MI
  • Atheroma of cerebral vessels -> changes
    • Carotid bifurcation
    • Internal carotid artery
    • Vertebral artery
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15
Q

how to identift a haemorhhagic stroke on imaging

A

CT – brain extends to bone around the outside

Radio-opaque mass – blood

  • Passed out from blood vessel
  • Accumulate in brain

Digital subtraction angiogram

  • Small buds (berry aneurysms)
    • Weak points for rupture

Can be familial - ask

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16
Q

how to identify an infarction strok on imaging

A

Harder to see

CT scan – hard to see lesions early after onset

MRI – can see inflammatory taking place around the bleed

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17
Q

3 less common causes of stroke

A
  • Venous thrombosis
    • OCP use
    • Polycythaemia – high haemoglobin level
    • Thrombophilia
  • ‘borderzone’ infarction
    • Severe hypotension
    • Cardiac arrest
  • Vasculitis
    • Narrow blood vessels into brain, so limitation of oxygen delivery into brain -> strok

e

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18
Q

5 preventative strategies of stroke management

A
  • Reduce risk factors
    • Smoking
    • Diabetes control
    • Control hypertension
  • Antiplatelet action
  • Anticoagulants

SURGICAL

  • Carotid Endarterectomy
  • Preventative neurosurgery
    • Aneurysm clips, AV malformation correction
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19
Q

antiplatelet drugs for stroke prevention

A

Aspirin

Dipyridamole

Clopidogrel

secondary prevention only

20
Q

anticoagulant drug for stroke prevention

A

embolic risk – AF, LV thrombus occasionally

  • warfarin,
  • apixaban
21
Q

surgical prevention for strokes

A

carotid endarterectomy

preventative neurosurgey

22
Q

cartoid endartectomy

A
  • Severe stenosis
  • Previous TIAs
  • <85 years of age
  • But 7.5% mortality from surgery

esp when carotid artery involved

  • Large amount of atherosclerosis around carotid furcation
    • Either excise (collateral blood supply brain relied on) or remove plaque
23
Q

important 1st stage in stroke intevestigation

A

Need to differentiate

  • INFARCT
  • BLEED
  • Subarachnoid Haemorrhage

EARLY information needed to assess treatment options

  • Most effective treatment if started early on – minimise tissue loss
24
Q

imaging options for stroke (3)

A

CT scan

MRI scan

Digital subtraction angiography (DSA)

25
Q

CT scan

A
  • rapid, easy access
  • good for haemorrhagic
  • poor for ischaemic stroke (most common)
26
Q

MRI Scan

with MR angiography

A
  • Good for both types of stroke
  • Difficult to obtain quickly
    • Not as easily available in majority of hospitals esp out of hours
  • Better at visualising early changes of damage

MRA (MR angiography) is the best investigation for visualising the brain circulation

27
Q

digital subtraction angiography DSA

A
  • Blood flow in brain
  • If MRA not available
28
Q

MR angiography

A
  • Can see both BV and their location in 3D
29
Q

subtraction angiography

A
  • Brain tissue removed
  • Only see changes in BV
30
Q

assessing risk factors in stroke investigation

A
  • Carotid ultrasound
    • Evidence of carotid sclerosis in carotid artery
  • Cardiac ultrasound
    • LV thrombus
  • ECG changes/abnormalities
    • Arrhythmias
    • Atrial fibrillation
  • Blood pressure
  • Diabetes screen
  • Thrombophilia screen (young patients)
    • higher tendency to form clots
31
Q

effects of stroke

3 main

A
  • loss of functional brain tissue
  • gradual or rapid loss of function
  • inflammation in tissue surrounding the infarct/bleed
    • not able to determine extent for a few days

Like CVD depend on the size of loss and location of loss

32
Q

loss of functional tissue due to stroke

A

Like CVD depend on the size of loss and location of loss

  • immediate nerve cell death
  • Nerve cell ischaemia in penumbra around infarction
    • Will die if not protected – dependent on treatment instituted
      • Acute stroke units have evolved (like acute coronary care)
        • Specialist treatment familiar with the condition then better outcome more likely
33
Q

how can a stroke ‘evolve’

A

Gradual or rapid loss of function

  • Stroke may ‘evolve’ over minutes or hours

Inflammation in tissue surrounding the infarct/bleed not able to determine extent for few days

  • Recovery of some function with time
34
Q

3 main complication categories from stroke

A
  • motor function loss
  • sensory loss
  • cognitive impairment
35
Q

motor function loss

due to stroke

A
  • Cranial nerve or somatic (opposite side!)
  • Autonomic in brainstem lesions
    • Dysphonia
    • Swallowing
      • Aspiration of food & saliva

Pneumonia and death

36
Q

sensory loss due to stroke

A
  • Cranial nerve or somatic (opposite side!)
    • Body perception
      • Neglect
        • Do not feel it is part of their body
      • Phantom limbs

May take while to present all

37
Q

cognitive impairment in stroke

A
  • Appreciation – special sensation
  • Processing
    • understanding of information
    • Speech and language
      • Dysphasia, dyslexia, dysgraphia & dyscalculia
  • Memory impairment
  • Emotional lability and depression
    • Distressing

may take a while to present all

38
Q

2 phases of stroke management

A

acute phase

chronic phase

39
Q

2 aims of acute phase stroke management

A
  • Limit damage
    • Manage penumbra effectively
  • Reduce future risk
40
Q

2 aims of chronic phase stroke management

A
  • Rehabilitation
  • Reduce future risk
41
Q

acute phase stroke treatment

A
  • Reduce damage
  • Normoglycaemia - hyper/hypo harmful
  • Remove haematoma
    • Subarachnoid haemorrhage only, or ongoing issues of intra-cranial bleeds
  • Prevent future risk
42
Q

acute phase stroke management techniques to reduce damage

A

Penumbra region – survivable ischaemia

  • Calcium channel blockers (Nimodipine)

Improve blood flow/oxygenation

  • Thrombolysis possible within 3hrs (alteplase)
    • When ischaemic stroke – requires MRI rapidly after admission
  • Maintain perfusion pressure to brain tissue
43
Q

importance of normoglycaemia in acute phase stroke management

A

Brain solely dependent on glucose for its energy stores

  • If not available pt will have exaggerated damage

Hyper/hypo = harmful

44
Q

acute phase stroke management - preventing future strokes

A

Aspirin 300mg daily

Anticoagulation if indicated (delay 2 weeks)

  • Atrial Fibrillation
  • Left ventricular thrombus
45
Q

chronic phase stroke treatment

A
  • Nursing and Rehabilitation
    • Immobility support
      • Prevention of bed sores
      • Physiotherapy to prevent contractures
  • Speech and language therapy
    • Communications
    • Swallowing and eating
  • Occupational therapy
46
Q

dental aspects of stroke (6)

A
  • Impaired mobility & dexterity
    • Attendance
    • Oral Hygiene
  • Communication difficulties
    • Dysphonia, dysarthria processing words and language
    • cognitive difficulties
  • Risk of Cardiac Emergencies
    • MI
    • Further stroke
  • Loss of protective reflexes
    • Aspiration
    • Managing saliva
      • anticholinergic drugs help - block parasym innervation of salivary glands
  • Loss of sensory information
    • Difficulty in adaption to new oral environment
      e. g. new dentures
  • ‘Stroke pain’
    • CNS generated pain perception – reported by pt but not due to any peripheral stimulation