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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
histological features at 24-48 hours
microscopy - increasing neutrophils, extravasation of red blood cells (haemorrhagic conversion) and activation of astrocytes ad microglial
26
histological features at 2-14 days
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
27
histological features after several months
macroscopy - increasing liquification apparent. eventual formation of cavity lined by dark grey tissue microscopy - ongoing phagocytosis brings increasing cavitation and surrouding gliotic scar formation
28
risk factors for ischaemic stroke (name 10)
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
29
criteria for a TAC
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)
30
TACs affect which part of the circulation
entire anterior circulation supplying one side of the brain
31
criteria for a PAC
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)
32
PACs affect which part of the circulation
part of the anterior circulation supplying one side of the brain
33
criteria for a LAC
Affect 2 any two of face arm and leg | pure motor or pure sensory stroke or an ataxic hemiparesis
34
LACs affect which part of the circulation
occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery
35
criteria for a POC
ipsilateral cranial nerve palsy with contralateral motor and/or sensory deficit Bilateral motor and/or sensory deficit Cerebellar dysfunction Isolated homonymous visual field defect
36
POCs affect which part of the circulation
affecting the posteriorcirculation supplying one side of the brain.
37
strokes involving the anterior cerebral artery affects...
motor and sensory cortices of the contralateral lower limbs
38
strokes involving frontal eye fields causes...
eyes to look towards lesion
39
strokes involving dominant middle cerebral artery involves...
motor and sensory cortices controlling contralateral upper limb and face
40
what is FAST?
``` allows for FAST recognition of symptoms Facial drooping Arm weakness Speech difficulties Time to call emergency services. ```
41
Rosier scores suggest
>0 stroke is likely | =0 have low possibility of stroke (not completely excluded)
42
what brain imaging should be done in ischaemic stroke
CT/MRI | CT contrast
43
what additional investigations should be done in ischaemic stroke
blood glucose, full lipid profile, BO, carotid scan, ECG, ECHO
44
what will T1 weighted imaging show in ischaemic stroke
hypotense
45
what will T2 weighted imaging show in ischaemic stroke
hypertense
46
what should first e excluded before commencing aspirin
haemorrhagic stroke
47
what is the management of ischaemic stroke
thrombolysis | Aspirin 300mg for 2 weeks (after 24 hours of trhombolysis)
48
what is thrombolysis
intravenous recombinant tissue plasminogen activator (alteplase)
49
what is the time window for thromoblysis
4.5hrs
50
additional aspects of stroke management
swallowing assessment, nutrition ad hydration, DVT prophylaxis
51
what secondary prevention measures can be used
anti-thrombotic therapy | BP, cholestrol, diabetes, smoking cessation, statins, lifestyle, carotid surgery, rehab and recovery.
52
types of spontaneous spontaneous haemorrhagic stroke
intracerebral, subarachnoid, haemorrhagic infarct
53
types of trauma haemorrhagic stroke
extradural haematoma, subdural haematoma, contusion, intracerebral haemorrhage, subarachnoid haemorrhage
54
what are the primary causes of a intracerebral haemorrhage
idiopathic, anticoagulation
55
what are the secondary causes of intracerebral haemorrhages
``` identifiable vascular malformation, medical or neurological diseases that impair coagulation or promote vascular rupture hypertensive ICH (charcot bouchard microaneurysms, basal ganglia haematoma) ```
56
Risk factors for intracerebral haemorrhages
hypertension, advanced age, male sex, asian, black or hispanic, family history, smoking, diabetes, alcohol, sympathomimetic drugs, NSAIDs
57
Medical conditions associated with intracerebral haemorrhage
haemophilia, cerebral amyloid angiopathy, moyamoya disease, leukaemia, cerebral vasculitiis, thrombocytopenia, hereditary haemorrhagic telangiectasia, autosomal dominant mutations in the COL4A1, KRIT1, CCM2, PDCD10 genes
58
morphology of the brain after intracerebral haemorrhage
asymmetrically distortion, various shifts and herniation are common, well demarcated intra-parencyhmal haematomas, softening of adjacent tissue, surrounding oedema
59
symptoms of ICH
``` 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
investigations for an ICH
non infused CT/MRI chemistry panel to rule out stroke mimics FBC, clotting tests, ECG, CT angiography
61
which cranial nerve do haemorrhagic strokes often compress?
3rd nerve palsy - ptosis, restriction of movement, pain in eye dilated pupil
62
differentials for strokes
``` hypoglycaemia and hyperglycaemia complicated migraine sepsis seizures metabolic abnormalities drug overdose other intracranial lesions ```
63
management of ICH
consider hemicranectomy (within 48 hours) surgical evacuation of haematoma +/- treatment of underlying abnormality stop anti platelet and anticoagulant medications
64
what is a subarachnoid haemorrhage
blood in the subarachnoid space between the pia and arachnoid membrane. Consequently reduces blood flow downstream
65
what is a cerebral vasospasm
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
how does subarachnoid haemorrhages cause hydrocephalus
blood irritates meninges, causes scarring effecting re absorption
67
how does subarachnoid haemorrhages cause meningitis
blood irritates meninges
68
most common cause of subarachnoid haemorrhage
aneurysms
69
most common causes of subarachnoid haemorrhage
aneurysms and trauma
70
where are aneurysms most commonly located
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
features of bifurcations that make them susceptible too aneurysm
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
what features of aneurysms increase risk of rupture
size - high if >25mm location - posterior circulation > anterior family histiry hypertension co-morbidity - smoking, connective tissue disease
73
risk factors for subarachnoid haemorrhages
previous spontaneous SAH, female, increasing age, family history, smoking, alcohol, drugs, hypertension, connective tissue disorders (Ehlers-Danlos, polycystic kidney disease)
74
symptoms of a subarachnoid haemorrhage
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
how to diagnose a subarachnoid haemorrhage
CT | small change of false negative - lumbar puncture
76
what does CSF in subarachnoid haemorrhage look like?
xanthochromic - broken down bilirubin
77
what is the gold standard diagnosis of SH
digital subtraction angiogram
78
Initial management of SH
investigations, refer, obs, control BP <160mmHg, surgery within 72 hrs, nimodipine 60mg/4hours PO for 21 days,
79
surgical management of SH
endovascualr coiling or surgical clipping | also balloon remodelling or flow diversion
80
How can you prevent vasospasm in SH
calcium channel blockers
81
how does SH cause hyponatraemia
SIADH or cerebral salt wasting
82
what is a interventricular haemorrhage
• occurs with rupture of a subarachnoid or intracerebral bleed into a ventricle
83
what are the causes of an interventricular haemorrhage
Trauma | Stroke = any combination of subarachnoid, intracerebral and intraventricular haemorrhage can occur
84
Symptoms of interventricular haem
similar to intracerebral haemorrhages
85
diagnosis of interventricular haemorrhage
xanthochromia CSF
86
how does hypertension affect the brain
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
consequences of hypertension on brain
lacunar infarcts multi-infarct dementia ruptured aneurysms hypertensive encephalopathy
88
what is a AVM
arteriovenous malformations, tangle of blood vessels, arterio-venous shunts
89
AVM treatment
surgery, endovascular embolisation, stereotactic radiotherapy, conservative
90
what is the fisher grading system
scale calculating risk of delayed vasospasm based on blood seen in CT

Neurology (18 decks)

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