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Y3 Oxford Cases > Blackout > Flashcards

Blackout Flashcards

1
Q

What are the divisions of syncopal causes of blackout

A

Reflex
Cardiac (reduced CO in arrhythmia, outlet obstruction)
Orthostatic
Cerebrovascular

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2
Q

What is reflex syncope

A

“primitive reflex”. HR and BP drops temporarily, reducing cerebral perfusion and leading to syncope. Some have a low threshold for activating this reflex in specific situations e.g. standing, being scared (blood, needles), straining (micturition, defacation)

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3
Q

What may cause orthostatic hypotension

A

Reduced intravascular volume (e.g. dehydration)
Normal autonomic response (transient tachycardia and peripheral vasoconstriction) or standing is blunted e.g. druggs or autonomic nueropathy

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4
Q

What are the reflex causes of blackouts

A

Vasovagal syncope

Carotid sinus hypersensitivity
Situational syncope e.g. micturition

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5
Q

What are the cardiac causes of blackout

A

Arrhythmias

Structural cardiac pathology causing outflow obstruction e.g. aortic stenosis, hypertrophic obstructive cardiomyopathy

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6
Q

What are the orthostatic causes of blackout

A

Drugs (anti-hypertensives, anti-sympathetics)

Dehydration
Autonomic instability
Baroreceptor dysfunction

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7
Q

What are the cerebrovascular causes of blackout

A

Vertebrobasilar insufficiency
Subclavian steal
Aortic dissection

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8
Q

What are the non-syncopal causes of blackout

A 
Intoxication
Head trauma
Metabolic (hypoglycaemia)
Psychogenic (non-epileptic_ seizures
Narcolepsy
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9
Q

What is the main cause of loss of consciousness in a patient aged 25

A

Vasovagal syncope

Warning or presyncopal sensation (stomach, going pale, clammy)

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10
Q

What is the main cause of loss of consciousness in a patient aged 55

A

Vasovagal syncope and cardiac arrhythmias (usually secondary to IHD)
No warning, while playing sport or without trigger

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11
Q

What is the main cause of loss of consciousness in a patient aged 85

A

Orthostatic hypotension secondary to medications (diuretics, ACEi, beta blockers, CCBs)
Causes morbidity from broken bones, loss of consciousness and independence and mortality

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12
Q

What questions do you ask about before the loss of consciousness

A

Was there any warning
Were there any precipitating factors
Was there any recent head trauma

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13
Q

What does warning before the blackout tell you

A

no warning -> more likely cardiac cause e.g. arrhythmia, AS or cerebrovascular disease e.g. subclavian steal syndrome (although may be preceded by palpitations)
Most other blackout causes will have warning e.g. aura before epileptic seizure, dizziness before vasovagal

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14
Q

What does precipitating factors tell you about the loss of consciousness

A

Postural - orthostatic hypotension
Head turning - carotid sinus hypersensitivity
Sitting or lying down - arrhythmia
Exercise - primary cardiac pathology e.g. AS, cardiomyopathy
Vigorous arm activity - subclavian steal

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15
Q

What questions do you ask about during the loss of consciousness

A

How long were they unconscious for

Did they bite their tongue or move their limbs, or where they incontinent of urine or faeces

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16
Q

What does tongue biting or spasms during blackouts tell you

A

tongue-biting - epileptic seizure

twitching an incontinence - vasovagal or other

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17
Q

What questions do you ask about after the loss of consciousness

A

Did they recover spontaneously
How long did it take to recover if not
Were they confused

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18
Q

Summarise the before, during and after features of epilepsy

A

May have stereotyped aura before (partial) or none (general)
Can last minutes, same episodes every time, tongue biting
Slow recovery, confused for 5-30 minutes

19
Q

Summarise the before, during and after features of Vasovagal attack

A

Vagal symptoms (sweating, pallor, nausea) may have precipitant
Last seconds, may twitch or be incontinent
Rapid recovery on sitting or lying

20
Q

Summarise the before, during and after features of cardiac arrhythmias

A

No warning
Last seconds, may twitch or be incontinent
Rapid spontaneous recover

21
Q

What is important to ask about in the past medical history for blackouts

A 
Has it happened before
Diabets
Cardiac illness 
Peripheral vascular disease 
epilepsy 
Anaemia 
Psychiatric illness
22
Q

What is important to ask about in the drug history for blackouts

A

insulin
Antihypertensives
Vasodilators
Antiarrhythmics
Antidepressants (SE of Tricyclic antidepressants)
Warfarin or anticoagulants (subdural haemorrhage>)

23
Q

What is important to ask about in the social history for blackouts

A

Alcohol

Recreational drugs e.g. cocaine, amphetamines

24
Q

What is important to ask about in the family history for blackouts

A

Sudden death in anyone <65 years of age

25
Q

What signs do you look for on examination for blackout patients

A

Tongue bitting
Dehydration (tachycardia, dry tongue, hypotension)
head trauma
Heart rate and murmurs (slow, irregular pulse, AS murmur)
Carotid bruits (carotid artery stenosis)
Blood pressure (orthostatic)
Focal neurological signs (peripheral neuropathy or parkinsonism due to autonomic dysfunction)

26
Q

What is orthostatic hypotension defined as

A

drop of 20 mmHg in systolic blood pressure or 10 mmHg diastolic on standing

27
Q

What are the first line investigations for blackout

A

Bloods (capillary blood glucose, FBC, U&Es)

ECG

28
Q

What are the investigations specific to suspicion of structural cardiac abnormality e.g. valve lesion

A

Echo

29
Q

What are the investigations specific to suspicion of carotid sinus sensitivity

A

Carotid sinus massage

30
Q

What are the investigations specific to suspicion of epilepsy

A

Brain scan (CT or MRI) to look for intracranial abnormality that can precipitate a seizure e.g. tumour + EEG

31
Q

What is a Stokes Adams attack and what is the treatment

A

Sudden transient loss of consciousness induced by a slow or absent pulse -> loss of CO
Either due to third degree HB or sinoatrial disease
Lasts seconds, more than 15 -> twitching due to cerebral anoxia
After attack - patient is flushed
Treatment - pacemaker

32
Q

What is epilepsy and what are seizures

A

Epilepsy is the tendency to have recurrent unprovoked seizures
Seizure - transient excessive electrical activity with motor, sensory or cognitive manifestations

33
Q

What are the types of generalised seizure

A

Tonic clonic/grand mal: rigid -> convulse with rhythmic muscular contractions
Absence: loses consciousness -> vacant and unresponsive
Atonic: loss of tone
Tonic: rigid
Clonic: convulsion
Myoclonic: extremely brief muscle contraction(jerk)

34
Q

What can partial seizures be split into

A

Simple - consciousness unimpaired

Complex - impaired

35
Q

What is the tilt table test

A

Helps to determine whether there is a vasovagal cause
Patient placed on tilt table supine, and rotated upright. Test is positive if:
there is loss of consciousness, fall in HR or BP or symptoms develop

36
Q

What are the main side effects of anticonvulsants in general

A

Teratogenic
valproate - weight gain, hair loss/curling, nausea, rash, tremor
Lamotrigine - Steven Johnson syndrome, headache, dizziness
Carbamazepine - rash, nausea, ataxia, diploplia, agranulocytosis, hypontraemia
Phenytoin - acne, rash, ataxia, sedation, ophthalmoparesis

37
Q

What are the interactions of anticonvulsants

A

Carbamazepine and phenytoin interfere with Contraceptive pill -> double dose
Same interfere with warfarin

38
Q

How do you test for carotid sinus hypersensitivity

A

Carotid sinus massage -> ECG and BP monitored for bradycardia/hypotension.

39
Q

What is HOCM

A

Genetic mutation (inherited via dominant or sporadic)
Non-physiological left ventricular hypertrophy
Asymmetrical septal hypertrophy leads to left ventricular outflow obstruction
Exacerbated by systolic anterior movement of the mitral valve
Exacerbated by exercise

40
Q

What is Long QT syndrome

A

Genetic mutation of cardiac channels (Na, K)
Prolonged repolarisation and a long QT interval on ECG, particularly on exertion
Associated with ventricular tachy

41
Q

What is Brugada syndrome

A

Mutation of cardiac sodium channel gene
Autosomal dominant
RBBB + saddle shaped ST elevation V1-V3

42
Q

What is arrhythmogenic right ventricular dysplasia

A

Myocardium is partially replaces by fatty tissue

ECG - T wave inversion V1-3, RBBB and epsilon wave

43
Q

What is the treatment for rare cardiac causes of loss of consciousness

A

Implantable cardioverter defibrillator device

Beta blockers adjunct

Y3 Oxford Cases (29 decks)

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