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1
Q

15% of which conditions present with syncope?

A 
PE
Aortic dissection
ACS
Ectopic pregnancy
Ruptured AAA
Subarachnoid haemorrhage
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2
Q

What constitutes simple alcohol withdrawal?

A

Onset of symptoms 12 hours after last drink
Symptoms peak on day 2
Significant improvement by day 4/5

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3
Q

What are common symptoms of alcohol withdrawal?

A 
Anxious, restlessness, insomnia
Tremor
Sweating
Nausea + vomiting
Palpitations
Headache
Tachycardia
Ataxia
Nystagmus
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4
Q

When does alcohol hallucinosis occur? What does it involve?

A

12-24 hours after alcohol has stopped

Involves visual, auditory or tactile hallucinations

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5
Q

When do withdrawal seizures occur? What kind of seizures are they?

A

24-48 hours after alcohol has stopped

Generalised tonic-clonic seizures

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6
Q

When does delirium tremens occur?

A

48-72 hours after alcohol has stopped

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7
Q

How does delirium tremens present?

A 
Hallucinations
Delusions
Severe tremor
Confusion and disorientation
Autonomic hyperactivity - hyperreflexia, hypertension, fever
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8
Q

What is the clinical triad of Wernicke’s encephalopathy?

A

Ophthalmoplegia = paralysis of eye muscles
Gait ataxia
Confusion

(only 10% have all 3)

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9
Q

What causes Wernicke’s encephalopathy?

A

Thiamine deficiency

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10
Q

What is Korsakoff’s psychosis?

A

Persistent + dense cognitive impairment

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11
Q

What score assesses the severity of alcohol withdrawal?

A

CIWA score (Clinical Institutes Withdrawal Assessment) - it is measured based on common signs and symptoms e.g. hypertension, seizures, insomnia, hallucinations, nausea

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12
Q

What LFTs are raised in alcohol abuse?

A

GGT = best indicator

Triglycerides

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13
Q

What might be seen on FBC in alcohol abuse?

A

Macrocytic anaemia

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14
Q

What is the management for acute alcohol withdrawal?

A

Chlordiazepoxide (or diazepam) over 5-7 days with reducing dose
Pabrinex IV 250mg daily for 3-5 days (500mg daily for 3-5 days if WK syndrome)

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15
Q

What constitutes binge, hazardous and harmful drinking?

A

Binge = twice the recommended daily limit in one session (i.e. 6 units)

Hazardous = 14-35 units/week

Harmful = 35+ units/week

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16
Q

What is a complete heart block?

A

When atrial activity is not conducted to the ventricles

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17
Q

Where can a complete heart block occur in the heart?

A

Proximal block = AV node

Distal block = in or below bundle of His

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18
Q

What differences can be seen between proximal and distal AV blocks?

A

Proximal

  • Narrow QRS complexes
  • HR 45-60bpm

Distal

  • Wide QRS complexes
  • HR <45 bpm
  • Haemodynamically unstable
  • More likely to cause sudden death
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19
Q

What are the causes of complete heart block?

A 
Progression from 2nd degree heart block
IHD
SLE 
Congenital heart disease 
Digoxin toxicity
Aortic valve calcification
Hyperkalaemia
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20
Q

How does complete heart block present?

A

Proximal

  • Fatigue
  • Dizziness
  • Reduced exercise tolerance
  • Palpitations

Distal

  • Chest pain
  • Shortness of breath
  • Confusion
  • Syncope
  • Sudden death
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21
Q

What JVP sign is related to complete heart block?

A

JVP cannon A waves

They occur when there is simultaneous contraction of atria and ventricles (the atria are contracting against closed tricuspid valve)

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22
Q

What is seen on ECG in complete heart block?

A

Dissociation between P waves and QRS complexes

P waves remain regular

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23
Q

What drugs can be given to increase heart rate in complete heart block?

A

Atropine IV 0.5mg - repeat every 2-3 mins (max 3mg)

Adrenaline IV

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24
Q

What is diabetic ketoacidosis?

A

Hyperglycaemia
Acidosis
Ketonaemia

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25
Q

What is the pathophysiology behind DKA?

A

Insulin deficiency means that when there is an increase in plasma glucose the glucose cannot enter the cells
The body thinks it’s in starvation so lipolysis occurs which produces fatty acids that are oxidised in liver to ketones
High plasma glucose causes an osmotic diuresis with Na+ and water

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26
Q

What can cause DKA to occur?

A

Four I’s

Infection - UTI, RTI, skin
Infarction - MI, stroke, GI, PVD
Insufficient insulin
Intercurrent illness

Also:

  • Pregnancy
  • Cushing’s
  • Alcohol abuse
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27
Q

How does DKA present?

A

Dehydration

  • Polydipsia
  • Polyuria
  • Dry mouth
  • Decreased skin turgor
  • Hypotension

GI symptoms

  • Nausea + vomiting
  • Abdominal pain
  • Weight loss

Hyperventilation, then Kussmaul breathing
Ketotic breath
Confusion

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28
Q

What presents similarly to DKA in patients with T2DM?

A

Hyperosmolar hyperglycaemic state (HHS)

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29
Q

How can you differentiate DKA from HHS?

A

DKA

  • Rapid onset
  • Younger patients

HHS

  • Gradual onset
  • Older patients
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30
Q

What is the diagnostic criteria for DKA?

A

Hyperglycaemia:
Glucose > 11 or known T1DM

Ketonaemia or ketonuria:
Ketones > 3mmol/L or urinary 2++

Acidaemia:
Venous pH < 7.3 or bicarb <15

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31
Q

What changes might be seen on ECG in DKA?

A

Signs of hyperkalaemia:

  • Tall tented T waves
  • Increased PR interval
  • Broad QRS complexes
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32
Q

How do you manage DKA?

A
  • First 1L 0.9% sodium chloride over 1 hour, second bag over 2 hours, third bag over 2 hours and fourth bag over 4 hours (1, 2, 2, 4)
  • Fixed rate insulin 0.1units/kg/hour
  • Dextrose 10% 8 hourly if glucose falls below 14
  • Monitor potassium because at risk of hypokalaemia (insulin drives potassium into the cells)
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33
Q

When should you admit a DKA patient to ICU?

A

Very high ketones
Need for extra organ support
Renal failure
Heart failure - difficult to give lots of fluids to

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34
Q

What defines resolution of DKA?

A

Ketones < 0.3mmol/L

pH > 7.3

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35
Q

What should be included in your reassessment of DKA after initial treatment?

A

Hourly capillary blood glucose and ketones
Venous bicarb and K+ at 1hr, 2hrs and 2 hourly after
Continuous cardiac and sats monitoring

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36
Q

What treatment should be given depending on K+ levels in DKA patients?

A

< 3.5: send to HDU
3.5-4.5: 40mmol K+
4.5-5: 20mmol K+
>5.5: no replacement needed

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37
Q

What defines hyperosmotic hyperglycaemic state?

A

Very hyperglycaemic and profoundly dehydrated

  • Hypovolaemia
  • Hyperglycaemia > 30 mmol/L
  • Without significant hyperketonaemia
  • Without significant acidosis
  • Osmolality > 320mosmol/kg (glucose + urea + 2xNa)
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38
Q

How is HHS managed?

A
  • Mainstay = gradual fluid resuscitation (1L 0.9% saline over 30 min)
  • Consider IV insulin if remain hyperglycaemic (half as much as in DKA so 0.5units/kg/hr)
  • Prophylactic LMWH
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39
Q

What is primary brain injury?

A

Brain injury that occurs at the time of the head injury

Axonal shearing and disruption with associated area of haemorrhage

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40
Q

What is secondary brain injury?

A

Brain injury that occurs later due to various problems that commonly co-exist

  • Hypoxia
  • Hypovolaemia
  • Hyperglycaemia
  • Cerebral hypoperfusion
  • Raised ICP
  • Intracranial haematoma
  • Seizures
  • Infection
41
Q

What are signs of a basal skull fracture?

A 
Orbital bruising - panda eyes
Bruising over mastoid process - Battle sign (takes days to appear) 
Subconjunctival haemorrhage - red sclera
Bleeding from auditory meatuses
CSF otorrhoea/rhinorrhoea
42
Q

How do you calculate cerebral perfusion pressure?

A

CPP = MAP - ICP

43
Q

What occurs if there is an increased ICP?

A

Cushing’s response = reflex increased BP with bradycardia

Coning of the brain through the foramen magnum

44
Q

What causes ipsilateral pupillary dilatation in raised ICP?

A

Herniation of the temporal lobe through the tectorial hiatus compresses the oculomotor nerve resulting in ipsilateral pupillary dilatation

45
Q

What is the Monroe Kellie Doctrine?

A

It says that the brain has compensatory mechanisms (e.g. displacing venous blood and CSF) that maintain a normal ICP for a change in brain volume < 100-200ml

However, a limit is quickly reached where ICP increases and restricts CPP leading to cerebral ischaemia

46
Q

What factors are important in the history of a head injury?

A

Collateral history
Mechanism of injury
Time of injury
Any LOC
Amnesia
Subsequent symptoms e.g. headache, vomiting, weakness, vision changes, otorrhoea, rhinorrhoea
Drug history (esp. anticoagulants) incl. illicit drugs

47
Q

What examinations are important to do in a head injury?

A 
GCS
HR, BP, RR
Glucose
Smell alcohol on patient
Pupils - size, movements, reflexes
Cranial nerves
Limb neuro exam - tone, reflexes, power, sensation
PR exam for anal tone
48
Q

What cranial and intracranial injuries are possible in a head injury?

A

Cranial injuries:

  • Skull fracture
  • C-spine fracture

Intracranial injuries:

  • Diffuse axonal injury
  • Extradural bleed
  • Subdural bleed
  • Subarachnoid bleed
  • Intracerebral bleed
  • Cerebral contusion
49
Q

What are the indications for doing a CT head in a head injury?

A

Urgent CT head within 1 hour if:

  • GCS < 13 at initial assessment
  • GCS < 15 at 2h post injury
  • Suspected open/depressed fracture
  • Seizure
  • Focal neurological deficit
  • > 1 episode of vomiting
50
Q

What are the signs of cerebral oedema on a CT head?

A
  • Loss of sulcul patterns – brain pushed up against sides of skull
  • Loss of grey/white matter differentiation – all hazy grey
51
Q

What can be done to reduce the risk of secondary brain injury?

A

Avoid hypotension - maintain MAP above 90 with medications

Encourage venous drainage - Sit patients up by elevating head to 30-40 degrees

Avoid hypercapnia - hyperventilate if ventilated and keep PaCO2 between 4-4.5kPa

Avoid hypoxia - maintain PaO2>11 with oxygen

Restrict fluids to <1.5L/day

Osmotic agents e.g. mannitol

Seizure control - IV lorazepam/buccal midazolam

Reduce stress response from intubation - opiates

52
Q

Why is avoidance of hypercapnia important?

A

Reduced PaCO2 leads to cerebral vasoconstriction which reduces the effects of raised ICP

53
Q

What is the risk with mannitol (osmotic agents)?

A

They can lead to rebound increase in ICP if used over prolonged period of time

54
Q

What additional treatment should be given in skull fracture?

A

IV antibiotics - 1.5g cefurozime

55
Q

Describe the different elements of a seizure

A

Before:
- Prodrome (hours/days) - change in mood/behaviour

Seizure:

  • Partial seizure: aura = focal seizure (often from temporal lobe), deja vu, strange smells, flashing lights
  • Generalised seizure: loss of consciousness - tonic, clonic, absence, myoclonic, atonic

After:
- Post-ictal phase - headache, confusion, myalgia, temporary weakness, dysphasia, Todd’s palsy

56
Q

What is Todd’s palsy?

A

Focal deficit/hemiparesis lasting for up to 24 hours

Indicates a high chance of a structural lesion

57
Q

What is status epilepticus?

A

Continuous generalised seizure lasting longer than 5 mins

The distinguishing features diminish leading to coma with virtually no motor evidence of seizure (often just minimal ocular twitching)

58
Q

What are some complications of status epilepticus?

A

Hypoglycaemia
Pulmonary hypertension
Pulmonary oedema
Increased ICP

59
Q

What can precipitate status epilepticus?

A 
Cerebral infection
Trauma
CVD
Toxic substances
Childhood febrile seizures
Eclampsia in pregnancy
60
Q

What investigations should you do in seizures?

A

Anti-epileptic medication levels - check compliance if known epileptic
EEG
MRI - if focal onset or if seizures continue with medication
ECG - in all patients with altered consciousness
LP - if infection suspected
Pregnancy test + BP - if possible eclampsia
Glucose
Toxicology screen

61
Q

What is the management for seizures?

A

ABCDE assessment

Maintain airway (consider adjunct)
Recovery position
Oxygen 15L/min NRBM
IV lorazepam 4mg slow bolus - repeat after 10 mins if no response
Call senior
Consider IV phenytoin 15mg/kg
If still unresponsive call ICU and conduct rapid sequence induction

62
Q

What are the alternatives to IV lorazepam in management of seizure?

A
  • IV diazepam 10mg

If no IV access:

  • Buccal midazolam 10mg
  • Rectal diazepam
63
Q

What should be given in a pregnancy-related fit (eclampsia)?

A

IV magnesium sulphate

64
Q

What additional management is required if alcoholism suspected in seizure?

A

Pabrinex infusion - IV 250mg over 30 min

65
Q

What are the two sources of blood supply to the brain?

A

Internal carotid arteries = anterior circulation (anterior cerebral artery + middle cerebral artery)

Basilar artery = posterior circulation (posterior cerebral artery)

66
Q

What provides collateral circulation in the brain?

A

Anterior and posterior communicating arteries in the circle of Willis

They provide collateral circulation in cases of carotid artery stenosis

67
Q

How does an anterior circulation stroke present?

A
  • Unilateral weakness and/or sensory disturbance in limb
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial deficit)

If total anterior circulation stroke, all 3 present
If partial anterior circulation stroke, 2 of 3 present

68
Q

What does the posterior circulation of the brain supply?

A

Brainstem
Cerebellum
Occipital lobe

69
Q

How does a posterior circulation stroke present?

A

One of:

  1. Cerebellar or brainstem syndrome
  2. Loss of consciousness
  3. Isolated homonymous hemianopia
70
Q

What are the symptoms of cerebellar syndrome?

A

DANISH

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech
Hypotonia
71
Q

How does brainstem syndrome present?

A

Quadriplegia
‘Locked in syndrome’
Visual disturbance

72
Q

How does a lacunar stroke present?

A

One of:

  1. Unilateral weakness (and/or sensory deficit) to face and arm, arm and leg, or all three
  2. Pure sensory stroke
  3. Ataxic hemiparesis
73
Q

What is the first thing that should be done in suspected stroke?

A

CT head within 1 hour in order to rule out haemorrhage - don’t want to thrombolyse or anticoagulate if bleeding

74
Q

What score is calculated for strokes?

A

Rosier Score

Facial weakness +1
Arm weakness +1
Leg weakness +1
Speech disturbance +1
Visual disturbance +1
Loss of consciousness -1
Seizure episode -1

Stroke unlikely if score 0 or less

75
Q

What signs point more towards haemorrhagic stroke than ischaemic stroke?

A

Meningism
Severe headache
Coma

(however, these are unreliable signs)

76
Q

What areas of the brain do lacunar infarcts affect?

A

Basal ganglia
Internal capsule
Thalamus
Pons

77
Q

What score assesses severity of TIA?

A

ABCD2 Score

Age
Blood pressure
Clinical features of TIA
Duration
Diabetes
78
Q

What is the acute management of an ischaemic stroke?

A

Give alteplase within 4.5 hours once haemorrhage is excluded

If post-4.5 hours, give aspirin 300mg (continue for 2 weeks)

Thrombectomy (particularly with large artery occlusion in proximal anterior circulation)

79
Q

When should alteplase not be given?

A

Do not give after 4.5 hours since onset of stroke or if there is no clear onset time

Contraindications:

  • Previous haemorrhage
  • Aneurysm
  • Recent head injury
  • Known clotting disorder
  • Intracranial cancer
  • Acute pericarditis
  • Seizure at onset of stroke (suggests haemorrhage or tumour)
  • Recent lumbar puncture
  • Systolic BP > 185 mmHg
  • Very hypo/hyperglycaemic
80
Q

What is the difference between Broca’s and Wernicke’s aphasia?

A

Broca’s

  • Expressive aphasia
  • Motor issue
  • Understands what others say but unable to speak
  • Frontal lobe

Wernicke’s

  • Receptive aphasia
  • Sensory issue
  • Doesn’t understand what others say and speaks nonsense
  • Temporal lobe
81
Q

Describe the headache in a subarachnoid haemorrhage

A

Thunderclap headache
Worst ever headache
Like a blow to the back of the head

82
Q

What other symptoms accompany the headache in a subarachnoid haemorrhage?

A 
Neck pain
Vomiting
Photophobia
Syncope
Fits
Drowsiness
Confusion
Unilateral eye pain
83
Q

What usually causes a subarachnoid haemorrhage

A

Rupture of Berry aneurysm in circle of Willis (80%) - most are saccular (i.e. non-congenital) due to stressors such as smoking, hypertension, alcohol damaging the elastic lamina of the vessels

Arterio-venous malformations (15%)

84
Q

Name some genetic disorders that can predispose you to a subarachnoid haemorrhage

A

Marfan’s syndrome
Autosomal dominant polycystic disease
Ehlers-Danlos syndrome
Neurofibromatosis

85
Q

What can come on 6 hours after onset of SAH?

A

Neck stiffness
Kernig’s sign - positive when thigh is flexed at hip and knee is at 90 degrees, then subsequent extension of knee is very painful

86
Q

What investigations must be done in suspected SAH?

A

Urgent CT head - detects >95% of SAH within 24 hours - starfish shaped hyper-density

LP - if CT head negative but history is suggestive - yellow CSF due to bilirubin

Angiography - to identify aneurysms

87
Q

What score assesses the severity of SAH and what scores indicate suitability for surgery?

A

Hunt and Hess Scale

0 - Unruptured aneurysm
1 - asymptomatic, minimal headache, nuchal rigidity
2 - moderate to severe headache, no neurological deficit except for CN palsy
3 - drowsiness, confusion, mild focal deficit
4 - stuporous, hemiparesis
5 - coma, decerebrate posturing, moribound

Scores 1 and 2 can have surgery, others not suitable

88
Q

How do you manage a SAH?

A

Prevent vasospasm
- Calcium channel blockers - nimodipine

Prevent rebleeding

  • Clipping = craniotomy with clips around neck of aneurysm
  • Coiling = obliterate aneurysm by causing clot to form in it
89
Q

How would an aneurysm in the posterior communicating artery present?

A

Pupil dilatation due to CNIII palsy (compression)

90
Q

What is the most common cause of a CNIII palsy?

A

Diabetes

Down and out pupil

91
Q

Define vasovagal syncope

A

Sudden, transient loss of consciousness (less than 2 mins) with spontaneous prompt recovery

92
Q

What causes a vasovagal syncope?

A

Reflex bradycardia +/- peripheral vasodilation

Provoked by emotion, pain, standing for too long, over-warm environment

93
Q

Give examples of pre-syncopal symptoms

A 
Nausea
Pallor
Sweating
Narrowing of visual fields
Dizzy
Altered hearing
94
Q

What may occur during vasovagal syncope?

A 
Brief clonic jerking of limbs due to cerebral hypoperfusion
Urinary incontinence (uncommon)
95
Q

What is situation syncope?

A

Syncope with a clear precipitant e.g. cough, exercise, urination

96
Q

What causes Stokes-Adams attacks?

A

Transient arrhythmias (e.g. bradycardia due to complete heart block) lead to decreased cardiac output and LOC

97
Q

What investigations must be done in syncope?

A

ECG - exclude cardiac causes e.g. arrhythmias, heart block, long QT syndrome
Bloods - to exclude other causes

98
Q

What aspects in the history suggest epilepsy rather than syncope?

A 
Witness says they were stiff/floppy
Incontinence
Bitten sides of tongue 
Preceding aura 
Did it occur watching TV
Muscle ache 
Confused/sleepy

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