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EOY4 > Stroke > Flashcards

Stroke Flashcards

1
Q

What are the relative contraindications to thrombolysis? (5)

A

Already on anticoagulants

Known coagulopathy

Active diabetic haemorrhagic retinopathy

Suspected intracardiac thrombus

Major surgery / trauma in the preceding 2 weeks

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2
Q

What are the absolute contraindications to thrombolysis that relate to bleeding? (7 - quite a few)

A

Active bleeding

Suspected SAH

Previous intracranial bleed

GI bleed in the last 3 weeks

LP in past 7 days

Uncontrolled HTN I.e. above 200 systolic

Oesophageal varices

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3
Q

What are the absolute contraindications to thrombolysis that DO NOT relate to bleeding? (4)

A

Pregnancy

Intracranial neoplasm

Stroke/ traumatic brain injury in past 3 months

Seizure at onset of stroke

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4
Q

What are the time frames for thrombolysis and thrombectomy following a stroke?

A

Thrombolysis = within 4 hours

Thrombectomy = 4-6 hours

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5
Q

What is the definition of a stroke?

A

The sudden onset of focal symptoms that are mainly negative and can be explained by hypo perfusion to a specific vascular territory

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6
Q

How do ischaemic and haemorrhagic strokes lead to hypo perfusion?

A

I = blocked artery

H = Bleeding

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7
Q

What is the TOAST classification?

A

5 Types of ischaemic stroke

1) Large artery atherosclerosis (embolus or thrombus)
2) Cardioembolism (high or med risk)
3) Small vessel occlusion
4) Stroke of other aetiology
5) Stroke of undetermined origion

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8
Q

What is the NIHSS?

A

Way to quantify severity of stroke

Higher score = more severe BUT the dominant side can give a higher score for the same amount of neuronal death

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9
Q

What is the CHADSVASC?

A

Way of assessing embolic stroke risk. Score of 2 = 2.2% risk

Congestive Cardiac Failure (1)
HTN (1)
A2 = Age 65-74 or 75 (1)
Diabetes (1)
S2 = Stroke/TIA/VTE (2)
V
Ascular disease (1)
Sex
Category Female (1)
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10
Q

What is the HASBLED?

A

Way to assess risk of bleeding when anti coagulated (all score 1 each)

HTN
A3 - abnormal LFTs, renal failure, alcohol use (1 each)
Stroke
Bleeding
Labile INR
Elderly >65
Diabetes
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11
Q

Where does the anterior cerebral artery supply? How would an ACA infarct present?

A

Medial hemispheres = lower limbs and genitals

Contralateral motor deficit - initial flaccidity that becomes spastic

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12
Q

Where does the middle cerebral artery supply? How would an MCA infarct present?

A

Lateral hemispheres = face and upper limbs

Contralateral motor and sensory deficits

internal capsule affected

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13
Q

Where does the posterior cerebral artery supply? How would a PCA infarct present?

A

Occipital lobe = vision

Visual defects - contralateral homonymous hemianopia with macular sparing as macula is supplied by the MCA

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14
Q

Define a Transient Ischaemic Attack

A

An ischaemic neurological event with similar symptoms to a stroke i.e. relate to a particular vascular territory but symptoms resolve within 24 hours (in real life it is quicker so usually 1-2 hours)

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15
Q

What is the ABCD2?

A

A method of stratifying risk of a stroke following a TIA (I don’t think it is actually used any more)

Age >60 (1)
BP >140 (1)
Clinical Features (unilateral weakness (1), speech disturbance (1))
Duration >1 hour (2), 10-59 mins (1). Diabetes (1)

> 4 = high risk

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16
Q

What is now used instead of ABCD2?

A

Anyone in past week is high risk

Low risk is >1 week

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17
Q

Which bed and blood tests should be done if someone presents with a TIA?

A

Bed = BP (baseline obs)

Blood = Lipids, glucose, U&E, FBC, VBG

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18
Q

What imaging should be done in TIA clinic?

A

ECG - AF?

DWI MRI - shows acute changes or areas of ischaemia and is sensitive for up to 2 WEEKS

CT - shows older changes i.e. after 4 hours and rules out bleeding

CUSS - >50% occlusion = carotid endartectomy?

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19
Q

What is the conservative management of a TIA?

A

Urgent referral to TIA clinic as risk of recurrent stroke is 10%

No driving for 4 weeks!!!!

Lifestyle - weight loss, stop smoking

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20
Q

What is the primary medical management of a TIA?

A

Aspirin 300mg for 2 weeks (+PPI if needed)

Switch to Clopidogrel 75mg PO

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21
Q

What is the secondary medical management of a TIA?

A

Manage HTN

Statin

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22
Q

What is the surgical management of a TIA?

A

Carotid endarterectomy if >50% stenosed and are of an acceptable surgical risk

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23
Q

What are the main 6 clinical features of a stroke/TIA?

A

Focal

Sudden Onset

Mainly -ve symptoms

Relates to a vascular territory

Symptoms don’t migrate

Stereotyping is not usual

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24
Q

Give 4 general clinical features of a stroke/TIA

A

Confusion
Headache
Dizzy/vertigo/Syncope
Nausea and vomiting

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25
Q

Give 5 neurological features of a stroke/TIA

A 
Sensory loss/parasthesia
Initial hypotonia that becomes hypertonic
Cranial nerve deficits
Homonymous hemianopia
Speech - dysarthria, aphasia, dysphasia
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26
Q

Which blood vessel is associated with total anterior circulation syndrome (TACS)?

A

Proximal MCA

ICA (which leads to MCA anyway)

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27
Q

What are the clinical features of a TACS?

A

Hemiparesis

Higher cortical dysfunction e.g. dysphasia AND homonymous hemianopia

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28
Q

Which blood vessel is associated with partial anterior circulation syndrome (PACS)?

A

MCA +/- branches

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29
Q

What are the clinical features of a PACS?

A

Isolated higher cortical dysfunction

OR

Higher cortical dysfunction, 2x hemiparesis, hemianopia

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30
Q

Which blood vessel is associated with posterior circulation syndrome (POCS)?

A

Posterior circulation (surprisingly)

PCA, basilar, vertebral, cerebellar arteries

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31
Q

What are the clinical features of a POCS?

A

Isolated hemianopia OR

Brainstem/cerebellar symptoms

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32
Q

Which blood vessel is associated with Lacunar syndrome (LACS)?

A

Lenticulostriate arteries (branch of MCA)

OR

Small penetrating artery occlusion

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33
Q

What are the clinical features of a LACS?

A

Isolated motor OR

Isolated Sensory OR

Sensorimotor OR

Ataxic hemiparesis OR

Clumsy hand dysarthria

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34
Q

Define stereotyping

A

Episodic recurrence of symptoms in the same way each time e.g. capsular warning syndrome or intracranial stenosis

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35
Q

What is capsular warning syndrome?

A

Intermittent reduction in MCA perfusion so reduced flow to the lenticulostriate arteries

Get intermittent symptoms rather than a complete resolution

Usually LACS

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36
Q

What is intracranial stenosis?

A

Seen when there is another cause of generalised hypo perfusion so get that kind of symptoms e.g. dizziness, pallor

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37
Q

What are the 3 types of stroke mimics?

A

Can be identified with imaging e.g. tumour, MS

Have secure features that distinguish from stroke e.g. BPPV, syncope, transient global amnesia

Can be distinguished if all info is available e.g. migraine + aura, focal seizures

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38
Q

What is the mechanism of action of Warfarin?

A

Acts on Vit K dependent clotting factors (IX, X, VII and Prothrombin)

Inhibits reductase that regenerates active vitamin K = factors don’t forms

SO acts on intrinsic and extrinsic pathways = prevents initiation and amplification of the cascade

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39
Q

What are 4 important things to remember when prescribing warfarin?

A

Requires 3 days to start working so have to cover wit LMWH during this time as become pro-thrombotic

Target INR is 2-3

CYP450 metabolised

Teratogenic

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40
Q

What is the mechanism of action of Heparin?

A

LMWH = Acts on Factor Xa, accumulates in renal failure

Unfractionated = Acts on Antithrombin III. Needs protamine sulphate to reverse + risks heparin induced thombocytopenia

41
Q

What is the mechanism of action of DOACs?

A

Dabigatran = acts on Thrombin

Rivaroxaban, Apixaban etc = Acts on Factor Xa

42
Q

What are the positives and negatives of DOACs?

A

+ves = more reliable and equally effective as Wardarin, don’t require regular monitoring, lower risk of intracranial haemorrhage [than warfarin]a

-ves = Higher risk of GI bleeding, CI if renal impairment or pregnant

43
Q

What are the non-modifiable risk factors for stroke?

A

Age

Thrombophilia

Migraine + Aura + COCP (younger pt)

44
Q

What are the modifiable risk factors for stroke?

A

HTN

Cardiovascular disease

AF

Smoking

T2DM

45
Q

Define aphasia

A

A selective impairment of language or the cognitive processes that underlie language

46
Q

What is Broca’s aphasia? Which bit of the brain is damaged?

A

Non-fluent, poorly articulated, and agrammatic speech output (in both spontaneous speech and repetition) with relatively spared word comprehension.

Can understand what you’re saying but can’t communicate coherently back

left posterior inferior frontal cortex, in the distribution of the SUPERIOR division of the left middle cerebral artery (MCA).

47
Q

What is Wernicke’s aphasia? Which bit of the brain is damaged?

A

Fluent but meaningless speech output and repetition, with poor word and sentence comprehension.

Don’t understand what you’ve said and just say randomish words

Posterior superior temporal cortex, in the distribution of the INFERIOR division of the left MCA.

48
Q

Give 4 differential diagnoses for a stroke

A

Hypoglycaemia/DKA

Hemiplegic migraine

Post-ictal (could still be a stroke esp if haemorrhagic)

Previous cerebrovascular accident + systemic illness

49
Q

What are the targets for blood pressure control, acutely and long term?

A

Acute = <180 if ischaemic, <140 if haemorrhagic

Long term = <130/80

50
Q

What is the definition of malignant MCA syndrome?

A

Rapid neurological deterioration due to the effects of space occupying cerebral oedema or haemorrhagic transformation following a middle cerebral artery (MCA) territory stroke

51
Q

How would a malignant MCA present? (4)

A

Acute onset of left sided hemiplegia.

No loss of conscience,

Patient is agitated and anxious.

CVS risk factors

52
Q

What are the 3 layers of meninges from out to in?

A

Outermost = Dura mater - tough and fibrous

Middle = Arachnoid mater - Contains CSF in subarachnoid space

Innermost = Pia mater - protection from chemicals/infections as adheres closely to brain and spinal cord

53
Q

What are the 2 layers of dura?

A

Periosteal and meningeal

They separate to contain the dural venous sinuses

54
Q

What is the function of the arachnoid mater?

A

Buffer layer and allows the brain to be weightless

55
Q

Define an aneurysm

A

A sac formed by the localised dilation of an arterial wall/vein due to wall weakness

56
Q

How does a true aneurysm differ from a false?

A

True = at least one arterial layer is unbroken. Most associated with atherosclerosis

False = usually caused by trauma + wall rupture - blood escapes to form a clot

57
Q

What is a berry aneurysm?

A

An aneurysm within the cerebral blood system

Usually occurs where the cerebral arteries leave the circle of willis

More likely to rupture if posterior

58
Q

Define a haemorrhage (in brain terms)

A

Abnormal escape of blood from an artery (subarachnoid, extradural, subdural)

59
Q

Define a subarachnoid haemorrhage

A

Bleeding into the subarachnoid space (between Pia and arachnoid mater)

60
Q

What are 5 symptoms of a subarachnoid haemorrhage?

A

Thunderclap headache!!!! (sudden onset, worst pain ever, occipital)

N&V

Reduced GCS/drowsy

61
Q

Give 3 signs of a subarachnoid haemorrhage

A

Neck stiffness after 6 hours

Focal neurology @ presentation

Terson’s Syndrome if more severe

62
Q

What is Terson’s syndrome

A

Increase in intraocular pressure due to intraocular haemorrhage

Subhyaloid haemorrhage
Vitreous haemorrhage

63
Q

What are 5 non-modifiable risk factors for SAH?

A

FHx (3-5x risk)
Coagulopathy
Past Hx

Other medical conditions: Polycystic Kidney Disease, Ehlers Danlos

64
Q

What are 3 modifiable risk factors for SAH?

A

Smoking
HTN
Alcohol Misuse

65
Q

What are 2 investigations for SAH?

A

Urgent CT

Lumbar puncture (if CT is -ve but strong S&S)

66
Q

What is important to remember about doing a lumbar puncture to investigate a SAH?

A

Have to wait 12hr after 1st presentation as RBCs need to break down

If yellow due to bilirubin = old blood from a SAH

67
Q

What is the very initial management of a SAH?

A

A to E!!!!
Neurosurgery referral!!!!
HDU admissioN!!!

68
Q

What is the conservative management of a SAH?

A

Regular reexamining of the CNS

Hydration to maintain BP and cerebral perfusion

69
Q

What is the medical management of a SAH?

A

Treats actual condition - Nimodepine (Ca channel antagonist) to reduce vasospasm therefore maintaining cerebral perfusion

Treats symptoms - opiate analgesia + laxative, anti-emetic, NO NSAIDS OR ANTICOAGULANTS

70
Q

What is the surgical management of a SAH?

A

Coil/clip the aneurysm

External ventricular drain

71
Q

What are the causes of a SAH?

A

Trauma

Berry aneurysm e.g. at MCA bifurcation

72
Q

What are the early complications of a. SAH?

A

Rebleeding

Hydrocephalus (ventricles block so CSF can’t drain)

Stroke

Hyponatraemia

73
Q

What are the late complications of a SAH?

A

Seizures epilepsy

SIADH and hyponatraemia

Coil prolapse

74
Q

Define a subdural haemorrhage

A

A collection of blood/bleeding into the subdural space (between dura and arachnoid mater)

75
Q

What is the aetiology of a subdural haemorrhage?

A

Rupture of bridging veins as they cross from the subdural space into dural sinuses e.g. due to shearing forces from trauma

76
Q

What are the symptoms of a subdural haemorrhage?

A

Fluctuating levels of consciousness

Pupillary changes

Headache

‘within the setting of head trauma’

77
Q

What are the signs of a subdural haemorrhage?

A

Raised ICP

Seizures

78
Q

What are the changes of a SDH seen on CT? (4)

A

Colour = Acute (<3 days) = bright, white blood. Chronic (>3 weeks) = black blood

Usually unilateral - fall cerebri prevents movement

Crescent shaped

+/- midline shift

79
Q

What is the conservative and medical management of a subdural haemorrhage?

A

C - A to E

M - none really

80
Q

What is the surgical management of a subdural haemorrhage?

A

Acute = Relieve ICP via immediate neurosurgery (do a craniotomy)

Can do burr holes for subacute or chronic

81
Q

Define an extradural haemorrhage

A

Bleeding between the periosteal layer of the dura mater and the inner surface of the skull

82
Q

What are the symptoms of an extradural haemorrhage?

A

LOS at time of initial injury

Lucid interval - transient recover +/- ongoing headache

Reduced consciousness, vomiting, seizures

Coma, CN palsies, pupillary changes

83
Q

What is the aetiology of an extradural haemorrhage?

A

Secondary to trauma/fracture of temporal or parietal bone e.g. at pterion

Severs the middle meningeal artery

Or, can be venous if tearing of dural venous sinus

84
Q

Can an extradural haemorrhage cross the midline?

A

Yes!

Can cross the sutures as the periosteal layer travels though the suture line
Size is still limited as dura is strongly adhered to the bone at certain points

85
Q

What are the investigations for an extradural haemorrhage?

A

CT - acute = blood is white

Biconx/round
Well demarcated
+/- midline shift

86
Q

What is the management of an extradural haemorrhage?

A

C - A to E
M -
S - urgent neurosurgery referral + craniotomy + clot removal + ligation of blleding

87
Q

What are the acute and chronic complications of an extradural haemorrhage?

A

A = death + seizures

C = permanent brain damage, AV fistula, pseudo aneurysm, seizures

88
Q

Define cerebral venous thrombosis

A

Occlusion of venous channels in the cranial cavity including IVT, DVT

89
Q

What is the cause of a cerebral venous thrombosis

A

Thrombus in dural venous sinuses = prevention of venous return in sinuses

Increased deoxygenated blood in parenchyma
+ Increased CSG as also can’t drain through arachnoid granulations

90
Q

What is the clinical presentation of a cerebral venous thrombosis?

A

Depends where it is:

Sagittal - headache, vomitign, seizures, papilloedema

Transverse - Headache -/+ mastoid pain, papilloedema

Sigmoid - cerebellar signs

Inferior petrosal - CN V and CN VI palsy

Cavernous - Eye signs - chemosis, proptosis, pain on movement

91
Q

What are the modifiable risk factors for a cerebral venous thrombosis?

A

Hormones - COCP, pregnancy, steroids

Infection - mastoiditis, folliculitis

Malignancy

Trauma

Dehydration

92
Q

What are the non-modifiable risk factors for a cerebral venous thrombosis?

A

Congenital mainly e.g. skull abnormality, connective tissue disorders, coagulopathy

93
Q

What are the investigations for a cerebral venous thrombosis?

A

Digital subtraction angiography is gold standard but hard to do in practice

CT to exlude SAH or meningitis

94
Q

What is the management of a CVT?

A

C = A to E

M = LMWH, ?thrombolyse

S = Thrombectomy - not if large

95
Q

What are the acute complications of CVT?

A

Venous infarction +/- haemorrhage

Hydrocephalus

AV fistula

96
Q

What are the Long term complications of CVT?

A

Dependency

Death

97
Q

What is lateral medullary syndrome?

A

Infarct of the posterior inferior cerebellar artery (PICA)

Presentation

ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss

98
Q

Does a patient still need to be anti coagulated following a catheter ablation e.g. for AF

A

yes please continue to take medications

99
Q

What is Weber’s syndrome and what are the clinical findings?

A

Infarction of the arteries supplying the midbrain

ipsilateral III palsy
contralateral weakness

EOY4 (22 decks)

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