Strokes Flashcards

1
Q

risk factors for TIAs

A
Prior TIA or stroke
Hypertension
AF
Diabetes
History of Ischaemic heart disease
Smoking
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2
Q

visual syndrome from TIA

A

amaurosis fugax - embolism of retinal artery, painless loss of vision in one eye, curtain coming down

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3
Q

clinical features of TIA

A

similar to stroke
cortical symptoms - facial or limb weakness
speech abnormalities - dysphagia or dysarthria
visual disturbance - visual field defect or amarousis fugax
cranial nerve involvement
memory disturbance

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4
Q

general investigations for TIAs

A

FBC, renal function, glucse, ESR, ECG

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5
Q

specific investigations for TIAs

A

MRI, carotid doppler

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6
Q

what does the ABCD2 score stand for

A

age, blood pressure, clinical features, duration, diabetes

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7
Q

how quickly should patients who score >4 in ABCD2 be seen

A

assessed within 24hrs

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8
Q

what is the medication management of TIAs

A

aspirin 300mg daily for 2 weeks, then 75mg of clopidogrel for life

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9
Q

what is the management of TIAs in those already on anti platelet therapy

A

dipyridamole

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10
Q

what are the indications for warfarin in TIA treatment?

A

if cause is a cardio-embolism and the risk factors (chronic non-valvular AF, metallic prosthetic cardiac valves and acute left ventricular wall motion impairment)

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11
Q

Definition of a stroke

A

rapidly developing clinical symptoms and/or signs of focal, and at times global, loss of brain function, with symptoms lasting more than 24 hours of leading to death with no apparent cause other than that of vascular origin

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12
Q

2 types of stroke

A

ischaemic and hemorrhagic

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13
Q

ischaemic stroke pathophysiologically can be classified into

A

primary vascular pathologies
cardiac pathologies
haematological pathologies

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14
Q

examples of primary vascular pathologies are

A

atherosclerosis, aortic arch atherosclerosis, arterial dissection, migraine or vasculitis

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15
Q

examples of cardiac pathologies

A

AF, MI, patent foramen ovale

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16
Q

examples of haematological pathologies

A

prothrombic hypercoagulable or hyperaggregable states

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17
Q

what is global hypoxic ischaemia

A

damage is when the systemic compromise to circulation cannot be compensated for by CNS auto-regulatory mechanisms – generalised reduction in blood flow
occurs in cardiac arrest, severe hypotension e.g. hypovolemic shock
Occurs when BP is below 50mmHg
Severe ischemia leads to pan-necrosis

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18
Q

what is focal hypoxic ischaemia

A

involves restriction of blood flow to a localised area of the brain)
typically due to vascular obstruction

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19
Q

What are watershed areas?

A

Watershed areas sensitive – zone between two arterial territories so furthest from heart and least well supplied

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20
Q

what are the sensitivities of different brain cell types

A

Neurons more sensitive than glial cells, and some neurons are more sensitive than others: Neocortex and hippocampus, Purkinje cells

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21
Q

what are the different types of thrombus ischaemic strokes and what is the thrombus made from

A

cardioembolic (fibrin)

atheroembolic (platelet)

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22
Q

which vessels are most commonly affected by thrombotic stroke?

A

branching points of the internal carotid and the middle cerebral artery

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23
Q

histological features at 0-12 hours

A

macroscopy - little visible

microscopy - little visible

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24
Q

histological features at 12-24 hours

A

macroscopy - pale soft and swollen with ill defined margin between injured and normal brain
microscopy - red neuron, oedema (cytotoxic and vasogenic) with generalised cell swelling

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25
Q

histological features at 24-48 hours

A

microscopy - increasing neutrophils, extravasation of red blood cells (haemorrhagic conversion) and activation of astrocytes ad microglial

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26
Q

histological features at 2-14 days

A

macroscopy - brain becomes gelatinous and friable. A reduction in the surrounding tissue oedema demarcates the lesion
Microscopy - microglia become predominant cell type, myelin breakdown. Reactive gliosis begins from as early as 1 week

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27
Q

histological features after several months

A

macroscopy - increasing liquification apparent. eventual formation of cavity lined by dark grey tissue
microscopy - ongoing phagocytosis brings increasing cavitation and surrouding gliotic scar formation

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28
Q

risk factors for ischaemic stroke (name 10)

A

older age, family history of stroke, history of ischaemic stroke, hypertension, smoking, diabetes mellitus, atrial fibrillation, comorbid cardiac conditions, carotid artery stenosis, sickle cell disease, dyslipidaemia, people with lower levels of education, African-American or Hispanic ancestry, poor diet and nutrition, physical inactivity, obesity, alcohol abuse, oestrogen-containing therapy, illicit drug use, migraine, hyperhomocysteinaemia, elevated lipoprotein(a), hypercoagulable states, elevated C-reactive protein, aortic arch plaques

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29
Q

criteria for a TAC

A

all three of:
Higher cerebral dysfunction (e.g. dysphasia).
Homonymous visual field defect
Ipsilateral motor and/or sensory deficit of at least two areas (out of face, arm and leg)

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30
Q

TACs affect which part of the circulation

A

entire anterior circulation supplying one side of the brain

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31
Q

criteria for a PAC

A

2 out of 3 features present in a TACS or;
Isolated Cortical Dysfunction such as dysphasia or;
Pure motor/sensory signs less severe than in lacunar syndromes (eg monoparesis)

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32
Q

PACs affect which part of the circulation

A

part of the anterior circulation supplying one side of the brain

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33
Q

criteria for a LAC

A

Affect 2 any two of face arm and leg

pure motor or pure sensory stroke or an ataxic hemiparesis

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34
Q

LACs affect which part of the circulation

A

occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery

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35
Q

criteria for a POC

A

ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit
Bilateral motor and/or sensory deficit
Cerebellar dysfunction
Isolated homonymous visual field defect

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36
Q

POCs affect which part of the circulation

A

affecting the posteriorcirculation supplying one side of the brain.

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37
Q

strokes involving the anterior cerebral artery affects…

A

motor and sensory cortices of the contralateral lower limbs

38
Q

strokes involving frontal eye fields causes…

A

eyes to look towards lesion

39
Q

strokes involving dominant middle cerebral artery involves…

A

motor and sensory cortices controlling contralateral upper limb and face

40
Q

what is FAST?

A
allows for FAST recognition of symptoms
Facial drooping
Arm weakness
Speech difficulties
Time to call emergency services.
41
Q

Rosier scores suggest

A

> 0 stroke is likely

=0 have low possibility of stroke (not completely excluded)

42
Q

what brain imaging should be done in ischaemic stroke

A

CT/MRI

CT contrast

43
Q

what additional investigations should be done in ischaemic stroke

A

blood glucose, full lipid profile, BO, carotid scan, ECG, ECHO

44
Q

what will T1 weighted imaging show in ischaemic stroke

A

hypotense

45
Q

what will T2 weighted imaging show in ischaemic stroke

A

hypertense

46
Q

what should first e excluded before commencing aspirin

A

haemorrhagic stroke

47
Q

what is the management of ischaemic stroke

A

thrombolysis

Aspirin 300mg for 2 weeks (after 24 hours of trhombolysis)

48
Q

what is thrombolysis

A

intravenous recombinant tissue plasminogen activator (alteplase)

49
Q

what is the time window for thromoblysis

A

4.5hrs

50
Q

additional aspects of stroke management

A

swallowing assessment, nutrition ad hydration, DVT prophylaxis

51
Q

what secondary prevention measures can be used

A

anti-thrombotic therapy

BP, cholestrol, diabetes, smoking cessation, statins, lifestyle, carotid surgery, rehab and recovery.

52
Q

types of spontaneous spontaneous haemorrhagic stroke

A

intracerebral, subarachnoid, haemorrhagic infarct

53
Q

types of trauma haemorrhagic stroke

A

extradural haematoma, subdural haematoma, contusion, intracerebral haemorrhage, subarachnoid haemorrhage

54
Q

what are the primary causes of a intracerebral haemorrhage

A

idiopathic, anticoagulation

55
Q

what are the secondary causes of intracerebral haemorrhages

A
identifiable vascular malformation, medical or neurological diseases that impair coagulation or promote vascular rupture
hypertensive ICH (charcot bouchard microaneurysms, basal ganglia haematoma)
56
Q

Risk factors for intracerebral haemorrhages

A

hypertension, advanced age, male sex, asian, black or hispanic, family history, smoking, diabetes, alcohol, sympathomimetic drugs, NSAIDs

57
Q

Medical conditions associated with intracerebral haemorrhage

A

haemophilia, cerebral amyloid angiopathy, moyamoya disease, leukaemia, cerebral vasculitiis, thrombocytopenia, hereditary haemorrhagic telangiectasia, autosomal dominant mutations in the COL4A1, KRIT1, CCM2, PDCD10 genes

58
Q

morphology of the brain after intracerebral haemorrhage

A

asymmetrically distortion, various shifts and herniation are common, well demarcated intra-parencyhmal haematomas, softening of adjacent tissue, surrounding oedema

59
Q

symptoms of ICH

A
acute onset headache
reduced/loss of consciousness
pressure effects
focal neurological deficit
hemoparesis, hemisensory loss and homonyous hemiopia, ataxia, dysarthria, nystagmus, vertigo, vomiting, hydrocephalus, quadraplea, respiratory problems, pinpoint pupils, dysconguate eye movements, 6th nerve palsy
60
Q

investigations for an ICH

A

non infused CT/MRI
chemistry panel to rule out stroke mimics
FBC, clotting tests, ECG, CT angiography

61
Q

which cranial nerve do haemorrhagic strokes often compress?

A

3rd nerve palsy - ptosis, restriction of movement, pain in eye dilated pupil

62
Q

differentials for strokes

A
hypoglycaemia and hyperglycaemia
complicated migraine
sepsis
seizures
metabolic abnormalities
drug overdose
other intracranial lesions
63
Q

management of ICH

A

consider hemicranectomy (within 48 hours)
surgical evacuation of haematoma +/- treatment of underlying abnormality
stop anti platelet and anticoagulant medications

64
Q

what is a subarachnoid haemorrhage

A

blood in the subarachnoid space between the pia and arachnoid membrane. Consequently reduces blood flow downstream

65
Q

what is a cerebral vasospasm

A

occurs 5-7th day after aneurysm event
blood products released stimulates tyrosine kinase pathway causing the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of cerebral arteries.
Oxyhaemoglobin in cerebrospinal fluid (CSF) causes vasoconstriction by increasing free radicals, endothelin-1, prostaglandin and reducing the level of nitric oxide and prostacyclin.
autonomic nervous system innervating cerebral arteries

66
Q

how does subarachnoid haemorrhages cause hydrocephalus

A

blood irritates meninges, causes scarring effecting re absorption

67
Q

how does subarachnoid haemorrhages cause meningitis

A

blood irritates meninges

68
Q

most common cause of subarachnoid haemorrhage

A

aneurysms

69
Q

most common causes of subarachnoid haemorrhage

A

aneurysms and trauma

70
Q

where are aneurysms most commonly located

A

berry aneurysms are bifurcations of major arteries that form circle of willis
majority located anterior communicating/anterior cerebral artery junction, and distal internal carotid artery/posterior communicating artery junction

71
Q

features of bifurcations that make them susceptible too aneurysm

A

greater pressures at the apexes of arterial bifurcation
pulsatile flow patterns
(due to blood flow at these branching points hits the wall at continual high pressure and previous weakness predisposition of wall

72
Q

what features of aneurysms increase risk of rupture

A

size - high if >25mm
location - posterior circulation > anterior
family histiry
hypertension
co-morbidity - smoking, connective tissue disease

73
Q

risk factors for subarachnoid haemorrhages

A

previous spontaneous SAH, female, increasing age, family history, smoking, alcohol, drugs, hypertension, connective tissue disorders (Ehlers-Danlos, polycystic kidney disease)

74
Q

symptoms of a subarachnoid haemorrhage

A

sudden onset severe headache, vomiting, seizures, collapse, coma/drowsiness can last for days after, signs neck stiffness, Kernig’s sign (flex hip and knee, when you go to extend knee patients resists), 3rd nerve palsy

75
Q

how to diagnose a subarachnoid haemorrhage

A

CT

small change of false negative - lumbar puncture

76
Q

what does CSF in subarachnoid haemorrhage look like?

A

xanthochromic - broken down bilirubin

77
Q

what is the gold standard diagnosis of SH

A

digital subtraction angiogram

78
Q

Initial management of SH

A

investigations, refer, obs, control BP <160mmHg, surgery within 72 hrs, nimodipine 60mg/4hours PO for 21 days,

79
Q

surgical management of SH

A

endovascualr coiling or surgical clipping

also balloon remodelling or flow diversion

80
Q

How can you prevent vasospasm in SH

A

calcium channel blockers

81
Q

how does SH cause hyponatraemia

A

SIADH or cerebral salt wasting

82
Q

what is a interventricular haemorrhage

A

• occurs with rupture of a subarachnoid or intracerebral bleed into a ventricle

83
Q

what are the causes of an interventricular haemorrhage

A

Trauma

Stroke = any combination of subarachnoid, intracerebral and intraventricular haemorrhage can occur

84
Q

Symptoms of interventricular haem

A

similar to intracerebral haemorrhages

85
Q

diagnosis of interventricular haemorrhage

A

xanthochromia CSF

86
Q

how does hypertension affect the brain

A

Increased atherosclerosis contributes to thromboembolism from extra or intracranial arteries
Hyaline arteriolosclerosis = weakening of small vessel walls
Stiffer arteries require a higher blood pressure for perfusion
Chronic hypertension = micro-aneurysms (Charcot-Bouchard)

87
Q

consequences of hypertension on brain

A

lacunar infarcts
multi-infarct dementia
ruptured aneurysms
hypertensive encephalopathy

88
Q

what is a AVM

A

arteriovenous malformations, tangle of blood vessels, arterio-venous shunts

89
Q

AVM treatment

A

surgery, endovascular embolisation, stereotactic radiotherapy, conservative

90
Q

what is the fisher grading system

A

scale calculating risk of delayed vasospasm based on blood seen in CT