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Neuro + special senses > Stroke medicine > Flashcards

Stroke medicine Flashcards

1
Q

Define stroke + its pathophysiology

A

Syndrome of rapid onset focal neurological deficit lasting >24h or leading to death

Hypoperfusion (O2+glucose) to endothelial lumen - depletes ATP - impaired membrane transport - AP not generated - stroke symptoms

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2
Q

What is a stroke syndrome?

A

Neurological disturbance that evolves suddenly (AP cessation), is focal (only affects neurovascular units in the concerned territory) of predominantly negative symptoms that fit into a vascular territory

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3
Q

What are the typical features of a stroke syndrome?

A
  • Sudden onset i.e. <2s wish
  • Focal
  • Predominantly negative sx i.e. loss of a function
  • Hypoperfusion to a vascular territory can explain the symptoms
  • Symptoms don’t migrate
  • Episodes do not usually stereotype (a repeat stroke would usually be in a different part of the vessel)
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4
Q

What is stereotyping and does it occur in strokes?

A

Episodic recurrence of neuro disturbance with complete resolution between, e.g. migrainous aura or focal seizure. Not typical of strokes as a repeat stroke would affect a different area

however

capsular warning syndromes + intracranial stenosis causing global hypo perfusion (e.g. postural hypotension) are both examples of when it may be part of a stroke syndrome

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5
Q

Define TIA

A

Rapid onset of symptoms that usually recovers within seconds-minutes, recovery is complete, and no infarction occurs

Usually due to microemboli from a carotid thrombus or atheromatous plaque

Is a retrospective diagnosis but a notice of an impending stroke/MI

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6
Q

How may a TIA present based on where the ischaemia occurs?

A
  • Anterior circulation-carotids: motor weakness/heaviness, hemisensory deficit (numb, aphasia, monocular blindness, amaurosis fugax, hemianopia)
  • Posterior circ-vertebrobasilar: vertigo, diplopia, ataxia, amnesia, hemisensory loss, hemianopic/bilateral vision loss, paresis, LoC (rare), transient global amnesia
  • Limb-shaking TIA -severe carotid stenosis
  • Source of emboli: carotid artery bruit, valvular heart disease, AF, recent MI
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7
Q

What are the risk factors for stroke events?

A
  • Modifiable: smoking, HTN, DM, obesity, inactivity, dyslipidaemia, carotid artery stenosis, post-TIA, AF (responsible for 25% of strokes)
  • Non-modifiable: black+Asian populations, age, genetics (e.g. SCD), being male, family history
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8
Q

Outline stroke primary prevention (preventing a first episode)

A
  • Risk assessment tools like QRISK2, ETHRISK
  • Lifestyle - less fat, more fish, exercise moderate intensity 30m 5xweek (or whatever they safely can do), WL if fat, limit alcohol max 14U and avoid binges, STOP SMOKING
  • Hypertension-NICE therapy guidance if raised
  • Anti-thrombotic therapy if have had MI/other RF
  • Aspirin low dose if benefits>risk (but no net effect on stroke, shouldn’t be used for stroke prevention cos bleeding but obv used for other things)
  • Statin: if 20% 10y risk of stroke
  • Manage AF with anticoagulant if needed
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9
Q

How do you manage the risk of stroke in pt with atrial fibrillation?

A

CHADVASc - 1y risk of thrombotic event in a non-anticoagulated pt with AF. If score 0 (men) or 1 (female-only RF is female) don’t need anticoagulation

HAS-BLED - risk of major bleeding (ie needing hosp or Hb drop of 20) for a pt on anticoagulation. Point score translates to % risk

If score raised need warfarin or a DOAC (aspirin is less effective than anticoagulants and risk of bleeding means shouldn’t really be used for stroke prevention; used for MI prevention)

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10
Q

What investigations are done in a stroke/TIA clinic and why?

A
  • Bloods - FBC (plts), clotting, thrombophilia screen, U+E (general, renal function for drugs), LFT (general, needed for statins), CRP, lipid profile, HbA1c, ANCA (vasculitis)
  • 24h ECG - see AF
  • Echocardiogram - vegetations, valve incompetence, ASD/VSD
  • Imaging with CT/MRI brain - evidence of infarcts, SOL. MRI better but limited by cost so only certain pt have
  • Carotid artery doppler
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11
Q

What are your differentials for a suspected TIA?

A
  • Mass lesions
  • Focal epilepsy - usually recognised by LoC
  • Cerebral amyloid angiopathy - seen on imaging, anti-plt contraindicated
  • Migraine with aura - esp when no headache, differentiate as positive visual aura not seen in TIA, slower onset + evolution, limb weakness is uncommon
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12
Q

What is the prognosis like for TIAs?

A
  • 30% have a stroke in 5y post-TIA
  • 15% have an MI 5y post-TIA
  • Anterior circulation TIAs have a worse prognosis

ABCD2 score - used to use to rial-stratify but now not used

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13
Q

Outline the pathophysiology of ischaemic stroke

A

Hypoperfusion –> ischaemia + neuronal injury

Osmotic activity –> oedema –> can cause subfalcine/tentorial herniation

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14
Q

What causes ischaemic stroke?

A
  • Thrombosis e.g. atherosclerotic plaque rupture, usually secondary to HTN
  • Embolism in a cerebral vessel - cardiac source (from AF thrombosis in LA, mural thrombosis post-MI, infective vegetations), athero-emboli from the ICA/CCA/aortic arch (bruits), paradoxical embolism (when a DVT enters the left heart instead of lungs via an ASD [quite common to have asymptomatic] or PFO)
  • Small vessel disease - HTN or DM - LACS/gradual diffuse changes
  • Rarer causes - systemic hypo perfusion (e.g. post cardiac arrest), vasculitis like GCA or APS, carotid/vertebral artery dissections (higher risk in Marfan syndrome; CF include neck/face pain + Horner syndrome + lower CN palsies; blood goes between wall layers causing emboli), venous sinus thrombosis (higher risk in pregnancy + thrombotic disorders)
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15
Q

What are the features of a MCA ischaemic stroke?

A
  • c/l hemiplegia (UL>LL)
  • hemisensory loss
  • neglect syndromes (esp if non-dominant side-usually right)
  • aphasia (esp dominant side-usually left)
  • eye deviation to affected side, hemianopia
  • coning

Branch occlusions less severe than full occlusions

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16
Q

What are the features of an ACA ischaemic stroke?

A
  • C/L hemiparesis LL>UL
  • Minimal sensory loss, LL>UL
  • May have frontal lobe deficits - apathy, apraxia, aphasia, urinary incontinence, dysarthria
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17
Q

What are the features of a PCA ischaemic stroke?

A
  • Homonymous hemianopia + macular sparing (u/l)
  • Cortical blindness (b/l)
  • C/L hemisensory loss in the DCML modalities
  • Memory deficits
  • Vertigo, nausea
  • Prosopagnosia (right-‘face blindness’)
  • Visual agnosia (left-not recognising)
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18
Q

What are the features of brainstem infarction?

A

It depends on the location irt CN nuclei, tracts + brainstem connections

  • Hemi/tetraparesis - affecting CSTs
  • Sensory loss - affecting sensory tracts, CN V nucleus etc
  • Facial weakness - CN VII nuclei
  • Dysphagia/dysarthria - CN IX + X nuclei
  • Nystagmus/vertigo - vestibular connections
  • Horner syndrome - sympathetic fibres
  • Altered consciousness - reticular formation
  • Dysarthria, ataxia, hiccups, vomiting - cerebellar connections
  • Locked in syndrome - basilar artery, paralysis of all voluntary muscles except eyelid+eye movement
  • Lateral medullary syndrome - PICA/vertebral artery occlusion - ipsilateral Horner’s, CN X palsy, facial sensory loss, ataxia, c/l STT sensory loss, vertigo, dysphasia
  • Medial medullary syndrome - ipsilateral loss of CN XII + c/l hemiparesis
  • Vertebrobasilar artery - ipsilateral CN deficits, vertigo, tinnitus, hiccups, dysarthria, dysphasia, visual problems, ataxia, crossed paraesthesias, crossed hemiplegia
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19
Q

What are the features of a cerebellar infarction?

A
  • DANISH
  • No hemiparesis, unless part of a brainstem syndrome
  • Swelling - brainstem compression/coma/obstructive hydrocephalus
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20
Q

What are the features of a thalamic infarction?

A
  • C/l hemiparesis + hemisensory loss
  • Miotic unresponsive pupils
  • Eyes deviate away from lesion

Thalamus involved in sensory system, consciousness + sleep. Supply by branches of PCA

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21
Q

How may strokes of the extra cranial arteries present?

A
  • ICA: neck/face pain, ipsilateral Horner’s, lower CN palsies, ipsilateral amaurosis fugax, signs of MCA stroke but collaterals often reduce infarct sign
  • CCA: Horner’s, CN XII paralysis, signs of MCA infarct
  • Vertebral artery: Wallenberg (lateral medullary) syndrome, neck pain, signs of PCA infarct
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22
Q

What are watershed infarcts?

A

When there is infarct in the border zones between areas supplied by the ACA, MCA + PCA, due to severe cerebral hypo perfusion e.g. post-cardiac arrest

CF: complex visual loss patterns, memory loss, intellectual impairment, motor deficits, bilateral, signs of systemic hypo perfusion e.g. low BP

Comps: PVS, MCS

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23
Q

Where do lacunar strokes arise?

A

Deep penetrating arteries in the white matter - affect basal ganglia, capsule, thalamus + pons

E.g. lenticulostriate artery occlusion

RF - HTN

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24
Q

What are the CF of lacunar strokes?

A
  • Lack of cortical signs like aphasia, agnosia
  • Pure motor most common –> C/L hemiparesis
  • Pure sensory –> C/L numbness/paraesthesia, usually thalamic
  • Sensori-motor –> C/L hemiparesis + sensory sx
  • Ataxic hemiparesis (2nd most common) –> C/L impaired coordination + weakness, LL>UL (mix of cerebellar + pyramidal)
  • Dysarthria clumsy hand syndrome –> dysarthria, dysphagia, C/L face+hand weakness
  • Hemiballismus –> infarct in sub thalamic nucleus causing c/l involuntary large flinging movements of arm/leg
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25
Q

What is multi-infarct dementia?

A

Multiple lacunar infarcts –> generalised intellectual loss with dementia, pseudo bulbar palsy + shuffling gait

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26
Q

What imaging is done in suspected stroke?

A
  • MRI more sensitive for underlying causes

* CT rapid, do non-contrast CT urgently to rule out haemorrhage, but ischaemic changes often not seen for 24-48h

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27
Q

What abnormalities may be seen on a non-contrast CT in stroke?

A
  • Haemorrhage-bright white
  • Early infarction: hyper dense artery (clot), early parenchymal changes (hypodense grey matter, loss of GM/WM differentiation cos of oedema from fluid/electrolyte shifts, effacement of sulci), increased attenuation
  • 12-24h - hypodense
  • After days - hyperdense

Can also be used to see a cause –> cardiac emboli, small indicates lacunar, watershed ischaemia (indicates carotid disease or intracranial stenosis), deep bleeds in BG/cerebellum (often HTN)

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28
Q

What are the rare causes of stroke?

A

Polycythaemia, hyper viscosity syndromes, antiphospholipid syndrome, low dose oestrogen-containing contraceptives, migraine, vasculitis (SLE, GCA), amyloidosis (cerebral haemorrhage), hyperhomocysteinaemia (thrombotic), neurosyphilis, mitochondrial diseases, sympathomimetic drugs e.g. cocaine

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29
Q

What is amaurosis fugax?

A

Sudden transient LoV in one eye, may be able to see the embolus if in retinal arteries

May occur in TIA - indicates ICA and is a warning of an impending ICA stroke

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30
Q

What is the ischaemic penumbra?

A

An area surrounding the infarct that is swollen + ischaemic so non-functioning but still structurally intact, so can regain function with revascularisation

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31
Q

Use Virchow’s triad to explain why strokes occur

A
  • Stasis - AF
  • Altered blood components - dehydration, pregnancy, cancer, syndromes like APS
  • Damaged vessel wall - atherosclerosis, GCA, dissection
32
Q

What are the types of dysphasia?

A

Broca (expressive) - lesion to inferior frontal gyrus (superior MCA)
Wernicke (receptive) - lesion to superior temporal gyrus (inferior MCA)
Conduction aphasia - lesion to arcuate fasciculus, fluent speech but abnormal comprehension + poor repetition (whereas Broca + Wernicke’s repetition is good)
Transcortical sensory aphasia-lesion to temporo-occipital region

33
Q

Left MCA stroke

A

Right hemiplegia with face+arms>legs, dysphasia

34
Q

Right MCA stroke

A

Left hemiplegia with face+arms > legs, visual/sensory neglect, denial of disability

35
Q

Vascular basis + clinical features of TACS

A

Hemiparesis/hemisensory deficit of face arm + leg
AND
homonymous hemianopia
AND
higher cerebral dysfunction (dysphasia, visuospatial disorder)

Proximal MCA or ICA occlusion, large stroke affecting areas supplied by both the MCA+ACA

36
Q

Vascular basis + clinical features of PACS (partial anterior circ stroke)

A

Two of hemiparesis, higher cortical dysfunction or hemianopia; or isolated higher cortical dysfunction

Branch of MCA occluded-only part of anterior circulation compromised

37
Q

Vascular basis + clinical features of POCS (posterior circ stroke)

A
  • CN palsy AND c/l motor/sensory deficit
  • B/l motor/sensory deficit
  • Conjugate eye movement disorder e.g. horizontal gaze palsy
  • Cerebellar dysfunction
  • Isolated homonymous hemianopia (PCA)

Vertebral, basilar, cerebellar or posterior cerebral vessels

38
Q

Vascular basis + clinical features of LACS (lacunar syndrome)

A

Pure motor/pure sensory/sensorimotor/ataxic hemiparesis

  • unilateral
  • motor weakness may affect face/arm/leg or all of them

Due to lenticulostriate branches of the MCA, supply to the brainstem or deep WM supply

39
Q

What is the TOAST classification for stroke?

A

Another way to classify ischaemic stroke, based on the cause e.g. large artery atherosclerosis, cardio-embolic, small vessel disease or undetermined/multiple causes

40
Q

Outline the pathophysiology of haemorrhagic stroke

A

Blood breaks parenchyma - WM fibres split - neurones don’t function - blood expands causing more damage/trans-tentorial coning

Cerebellar haematomas can cause obstructive hydrocephalus or coma from brainstem compression

41
Q

What causes haemorrhage strokes?

A
  • Intracerebral haemorrhage
    1. Chronic HTN causing ruptured micro aneurysms (Charcot-Bouchard aneurysms) + degeneration small deep arteries, usually causes a massive haemorrhage
    2. Cerebral amyloid angiopathy (elderly): lobar ICH, esp posterior, a/w particular ApoE subtypes
    3. Secondary causes: AV malformations (commonest cause in children), aneurysms, dural venous thrombosis, CNS infection, stimulant drugs, anticoagulant drugs, thrombolysis, haemorrhagic transformation of a large ischaemic infarct
  • Subarachnoid haemorrhage (5%, can also be caused by trauma but this wouldn’t be a stroke)
    1. Ruptured berry aneurysm at branching points in CoW, round saccular aneurysms
    2. Ruptured AVM
    3. Other: cortical thrombosis, neoplasm, infection
42
Q

How would you differentiate ischaemic from haemorrhagic strokes if you didn’t have a CT scanner?

A
  • No reliable CF to distinguish
  • ICH more often causes severe headache, coma or meningism
  • On anticoagulants - ICH until proven otherwise
  • SAH: sudden thunderclap headache, occipital, vomiting, neck stiffness, papilloedema, subhyaloid haemorrhage (on fundoscopy)
  • Berry aneurysms: may have h/o sentinel headaches from small bleeds, may LoC, may have h/o ADPKD/NF1/Marfans etc
43
Q

What findings are seen on imaging after haemorrhagic stroke?

A

CT: seen immediately, intraparenchymal/intraventricular/subarachnoid bleed.

  • Hypodense lesion in hyper acute phase
  • Hyperdense lesion + hypodense oedema in acute phase
  • May show midline shift

Later - MRI + MRA to look for aneurysms or AVM

LP - for suspected SAH, do after 12h to see xanthochromia (rather than blood from trauma of LP)

44
Q

Outline the management of haemorrhagic stroke

A
  • Non-contrast CT to confirm haemorrhage
  • Medical (stroke unit or ICU): reverse anticoagulation (e.g. warfarin -give IV vit K+prothrombin complex concentrate/FFP), control HTN, reduce ICP, in SAH you give IV CCB for 3w (nifedipine, reduces vasospasm as this can induce ischaemic stroke)
  • Surgical: cerebellar needs urgent craniotomy + clot evacuation; for others depends on neurosurgery opinion. Hydrocephalus may have ventricular drain/serial LPs/VP shunt, SAH aneurysms may have clipping/endovascular coiling to prevent re-bleeding
45
Q

What are stroke mimics and when would you suspect them?

A

Conditions that resemble an acute stroke

May suspect if can’t fit symptoms into a presentation or the syndrome is gradual, non-focal, mostly positive and shows evolution of symptoms or stereotyping

Some are recognised on imaging easily e.g. MS/SDH, some diagnosed clinically e.g. TIA/vestibular disorders/syncope, others are more subtle and need specialist assessment e.g. complex migraine with aura/functional syndromes

46
Q

Give examples of stroke mimics

A 
*HEMI most common:
Hypoglycaemia
Epilepsy e.g. Todd's palsy (post-ictal paresis) or focal seizures that stereotype
Migraine (cortical spreading depression)
Intracranial infection/tumour

*Others: syncope, sepsis, peripheral vestibular disorder, EDH/SDH, drugs/alcohol, transient global amnesia, functional syndromes, apparent neurological deficit

47
Q

What are stroke chameleons?

A

Conditions where presentation suggest another cause, but it is actually a stroke!

48
Q

Give some examples of stroke chameleons

A
  • Venous infarct - gradual onset, may have seizure
  • Small cortical strokes - may present as peripheral nerve lesions
  • Limb shaking TIA - may look like a movement disorder/seizure
  • Occipital stroke - if predominant feature is confusion/delirium
  • Stroke amnestic syndromes
  • Stroke that mimics vestibular dysfunction
49
Q

What investigations are done in suspected stroke?

A
  • CT brain non-contrast
  • Bloods-FBC for plt/polycythaemia, ESR (GCA), glucose, lipids, U+E + LFT
  • ECG - rule out AF
  • Carotid doppler studies in anterior circ strokes to identify stenosis needing surgery
  • Others done if young.no cause: CT/MR angiography, prolonged cardiac monitoring, echo, carotid USS, vasculitis screen, APS antibodies, thrombophilia screen
  • MRI brain - good for underlying causes, mimics like demyelination
  • LP - definitive test in SAH if CT inconclusive. Xanthochromia, high opening pressure, high RBC, normal glucose
50
Q

What is the cause of deep vs lobar bleeds?

A

Deep - HTN

Lobar - secondary causes e.g. mass lesions

51
Q

What is apparent neurological deficit?

A

Area of damaged brain - residual scar tissue (gliosis) forms new connections that can function normally if physiology is optimal, but if something offsets it e.g. infection/hypotension/hypoglycaemia a stroke picture can damage

52
Q

What do you look for on the immediate CT head done in suspected stroke?

A

Pipes, parenchyma, perfusion + penumbra

ASPECTS score: different areas of MCA given a score based on if normal or not, out of 10 where 10/10=normal and 0/10=extensive ischaemia (1 point deducted for each abnormal area)

53
Q

What immediate management is done once haemorrhagic stroke is confirmed?

A
  • Do not give drugs that affect clotting
  • Control BP, control clotting, may evacuate haematoma/insert drains - as they cause RICP
  • Anticipate + prevent comps
  • Neurosurgery discussion - balance between stability _ accessibility e.g. thalamus isn’t accessible
54
Q

What is the purpose of thrombolysis and how is it done?

A

Reduction of infarct size to reduce disability - activate plasminogen to form plasmin - degrades fibrin - breaks up thrombi

Indicated where there is an acute ischaemic stroke + persisting neuro deficit + well-established timing of onset

IV alteplase given within 4.5h (preferably 3h) of sx, bolus over 1min then over 1h

55
Q

What are the contraindications to thrombolysis?

A
  • Historical: stroke/head trauma in past 3m, prev ICH, major surgery in past 14d, GI/GU bleeding in last 21d, arterial puncture at non-compressible site/LP in past 7d
  • Clinical: rapidly improving sx, minor/isolated neuro signs, persistent HTN, pregnancy, active bleeding, active #
  • Lab: plt <100, high/low glucose, INR>1.7, on warfarin, elevated PTT if on heparin
56
Q

What outcomes are there after thrombolysis?

A

1/3 improve
1/10 make a complete recovery
1/20 get a symptomatic haemorrhage

57
Q

What are the complications of thrombolysis?

A
  • Extracerebral haemorrhage-thin thready pulse, low BP, melaena/haematemesis, distended abdomen
  • Intracerebral haemorrhage-neuro decline, new headache, rising BP, N+V
  • Anaphylaxis
58
Q

What management is done for ischaemic strokes not eligible for thrombolysis?

A
  • Aspirin 300mg per day for 2w then switch to clopidogrel
  • Mechanical thrombectomy
  • Decompressive hemicraniectomy
59
Q

Mechanical thrombectomy

A

Emerging, plans to make this future of care similar to PCI for MI but currently only done in specialist centres –> used if large vessel occlusion within 6h of sx

60
Q

What is the role of the NIHSS score?

A

Used to grade severity of stroke-related neurological deficit

Used in assessment + prediction of prognosis + charting recovery

61
Q

Decompressive hemicraniectomy

A

Do within 48h to manage malignant oedema in younger/fitter patients in large MCA strokes to prevent coning

Can preserve life, but balance with significant dependency

62
Q

What management is undertaken in the stroke unit?

A
  • Plan discharge early on-shouldn’t be kept longer than necessary, need proactive plan for rehab
  • Antiplatelets
  • Anticoagulants
  • Treat BP e.g. enalapril if high or midodrine if low (permissive hypertension to ensure adequate perfusion) – aim for <130/90
  • Lipid control total cholesterol <4, LDL <2
  • Glycaemic control HbA1c < 7
  • Carotid endarterectomy
  • MDT: asses swallow, VTE prophylaxis, treat medical complications or causes like AF, investigate RF, begin PT/OT input, secondary stroke prevention, early mobilisation, pt education + support, nutritional support if unsafe swallow with NG/PEG
63
Q

Antiplatelets after ischaemic stroke

A

300mg aspirin

  • Immediately in suspected TIA or on confirmation of ischaemic stroke
  • 24h post-thrombolysis
  • Aspirin for 2w, then switch to clopidogrel
64
Q

Anti-Thrombotic + anticoagulant therapy after ischamic stroke

A

Aspirin initially then switch to clopidogrel after 2w for antiplatelets

Anticoagulant:

  • Assess if needed using CHADVASC + HASBLEd
  • Started immediately in TIA, after a few days for small strokes or after 2w for large strokes
  • Wait 2w in large strokes as infarcted area at higher risk of bleeding
  • If AC contraindicated but have AF can refer for left atrial appendage closure
65
Q

Carotid endarterectomy after stroke

A

Do within 2w for symptomatic disease with >50% occlusion of lumen

Reduce recurrent stroke by BP control + statins + dual anti platelet therapy

Can also try to stabilise the plaque if surgery not suitable, as it is an embolic source

66
Q

Outline the process of stroke rehabilitation

A
  • Specialised unit e.g. community hospital, or in community
  • In hospital sort out transfers, positioning, swallowing, orientation, pressure areas, continence, communication, nutrition, hydration
  • Vision: functional task practice for neglect, orthoptics, eye movement therapy for hemianopia
  • Memory: consistent environment + routines, aids like medication alarms
  • Emotional: opportunity to talk, support + educate, manage depression/anxiety
  • Swallowing: screen for dysphagia, mouth care to reduce aspiration, nutrition support
  • Communication: SALT, minimise environmental barriers, appreciate their frustration
  • Motor: strength + balance training, walking practice, use of walking aids, splints for high tone
  • Self-care: OT assess ADLs, equipment, home adaptations
  • Management of return to wider participation in society
  • Monitor for comps - mood, bowel + urine, progress of stroke impairments, DVT, blood results
  • Impact on pt + family: education + support to understand impact + extent of deficits, recognising these vary over time/setting, help train communication e.g. using props
67
Q

Outline secondary stroke prevention

A

Begin within a week of the stroke

  • Lifestyle
  • Review RF
  • Stroke register - annual FU
  • Lifelong anti-thrombotic therapy with clopidogrel or if CI dipyridamole+/- aspirin (preferred if have also had MI)
  • Anti-lipid unless CI usually simvastatin
  • Carotid artery endarterectomy or stenting
  • Anti-hypertensive: lower BP slowly
68
Q

When can you drive after a stroke or TIA?

A

1m - normal driving
1y - HGV

Inform DVLA if there are persisting deficits (don’t need to inform if no residual neuro deficit)

69
Q

What aspects of palliative care apply to stroke?

A

Pain control, mouth + skin care, agitation, airway secretions, communication w families

Usually feed orally + accept risk of aspiration as less invasive

70
Q

What is the Modified Rankin Scale?

A

A measure of global disability to assess baseline function + evaluate outcomes.
0-no sx
1-some sx but can do everything
2-slight disability, can look after own ADLs but not all previous activities
3-moderate disability, needs some help but can walk unassisted
4-moderate to severe, can’t attend to own bodily needs without assistance, needs help to walk
5-severe disability, constant nursing care, bedridden, incontinent
6-death

71
Q

What is the Rosier scale?

A

A tool used to recognise stoke in the emergency department, for initial differentiation of acute stroke from stroke mimics

72
Q

How is the stroke prognosis determined?

A
  • Tools like NIHSS, OCSP class
  • Pattern + number of complications
  • Recovery trajectory: indicates neuroplasticity @ site of damage, continues until pt reaches their plateau.

Generally TIA/minor stroke early high functioning plateau, TACS - early low functioning plateau, or most moderate strokes medium functioning plateau reached after a delay

73
Q

What is the ABCD2 prognostic score?

A

Used to be used for TIA, was in workbook but now NICE don’t recommend it. If score is 4 high risk of a stroke so have aspirin 300mg daily + specialist assessment

  • Age 60+ (1)
  • BP >140/90 (1)
  • Clinical features: 2 for u/l weakness, 1 if speech disturbance
  • Duration: 2 for >1h, 1 for 10-59min
  • Diabetes (1)
74
Q

List the early complications of stroke

A
  • Death - if affects brainstem or causes RICP
  • RICP -haematoma expansion, malignant oedema, haemorrhagic transformation, hydrocephalus
  • Recurrent stroke due to unaddressed RF, or suboptimal physiology causing loss of ischaemic penumbra
  • Infections: aspiration pneumonia, UTI (poor hydration or incomplete emptying from constipation/supine)
  • Immobility: VTE, constipation, pressure ulcers
  • Visual impairment
  • Bladder/bowel problems
  • Swallow impairment-dehydration, malnutrition, aspiration
  • Seizure
  • Vasospasm 5-7d after haemorrhagic can lead to ischaemic
  • SIADH
75
Q

List the long-term complications of stroke

A
  • Death
  • cognitive dysfunction-concentration, memory, spatial awareness, apraxia, executive function e.g. planning
  • mood changes - mood disorders, disturbed social interaction, disinhibition, aggression
  • bladder, bowel or sexual dysfunction
  • inability to complete ADLs
  • vascular dementia
  • MSK: spasticity, balance/tone/movement/sensation
  • secondary epilepsy
  • post stroke pain + fatigue: multifactorial like the spasticity, injury sustained from stroke, neuropathic pain, fatigue from pain/pain from fatigue, poor sleep, meds, brain cell damage
76
Q

Outline the provision for stroke services in the NHS

A
  • Rapid access TIA clinics
  • Hyperacute stroke units with access to neurosurgical + interventional radiology services
  • Acute stroke wards
  • Inpatient rehab
  • Outpatient rehab inc early supported discharge services
  • Outpatient stroke clinics
77
Q

How would you treat a clinically suspected TIA?

A

300mg aspirin immediately for clinically suspected TIA (+ gastroprotection if indicated) - unless bleeding disorder/on anticoagulant/already on low dose aspirin

Refer for specialist review within 24h if has happened within the last week, or if happened >1w ago then refer within 7d

Don’t drive until have been seen

After specialist is usually clopidogrel daily (or aspirin + dipyridamole 2nd line), carotid endarterectomy if had TIA in carotid territory and stenosis >70%

Neuro + special senses (5 decks)

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