Emergency care Flashcards

1
Q

What acid-base imbalance does aspirin overdose initially cause and then turn to?

A

Starts as respiratory alkalosis (initial respiratory centre stimulation)
Turns to metabolic acidosis (compensation for high resp rate)

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2
Q

Into which categories can shock be classified?

A

Class 1 - Compensated
Class 2 - Tachycardia
Class 3 - Hypotension
Class 4 - Loss of consciousness

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3
Q

How can cardiogenic, septic and hypovolaemic shock be distinguished clinically?

A

Cardiogenic: only one with raised JVP
Septic: warm peripheries (others will be cold)

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4
Q

What is the management for cardiogenic vs septic vs hypovolaemic shock?

A

Cardiogenic: dobutamine, dopamine
Septic: noradrenaline
Hypovolaemic: blood

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5
Q

Define sepsis vs septic shock

A

Sepsis: life-threatening organ dysfunction caused by dysregulated host response to an infection

Septic shock: sepsis + lactate >2 despite fluid resus OR
patient needs vasopressors to maintain MAP > 65mmHg

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6
Q

Recall the management of sepsis

A

Cannulate (+ bloods)
Catheterise

3 out: 
- lactate (VBG) 
- UO (catheterise)
- Blood cultures 
3 in: 
- 15L/min oxygen (even if sats okay) 
- ABx (as per local guidelines) 
- Fluids 

Investigate for the source of infection

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7
Q

Recall some key elements to ask in the history in suspected spesis

A
AMPLE
Allergies
Medications 
Past medical history 
Last meal 
Events surrounding
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8
Q

Recall the immediate management of anaphylaxis

A

Secure airway –> remove cause –> raise legs
Then (alphabetical order, (doses on different card)):
- Adrenaline
(insert IV line for following drugs)
- Chlorphenamine IV
- Hydrocortisone IV

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9
Q

Recall the dosing for adrenaline in anaphylaxis in each different age group, and the max dose you can give

A

> 12y: 500mcg doses, up to 0.5mg
6-12y: 300mcg doses, up to 0.3mg
6m-6y: 150mcg doses, up to 0.3mg
0-6m: same as above

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10
Q

Recall the dosing for chlorphenamine in each different age group given in anaphylaxis

A

> 12y: 10mg
6-12y: 5mg
6m-6y: 2.5mg
0-6m: 250mcg/kg

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11
Q

Recall the dosing for hydrocortisone in each different age group given in anaphylaxis

A

> 12y: 200mg
6-12y: 100mg
6m-6y: 50mg
0-6m: 25mg

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12
Q

Describe the changes to the A to E approach in trauma

A

Before A to E:
- If massive haemorrhage, tamponade the massive bleeding prior to A to E

A
- Never do head tilt (just jaw thrust) because you always assume C spine injury until proven otherwise

B same as usual

C

  • If significant haemorrhage, replace with 1-1-1 plasma, platelets and packed rbcs when you get to circulation
  • If history of haemorrhage or ongoing bleeding (less massive) then give type O blood
  • FAST scan
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13
Q

At what GCS do you intubate?

A

<8

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14
Q

What is the Canadian C-Spine rule used for?

A

Criteria that, if any are met, mean you need to immobilise the spine

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15
Q

What are the NEXUS criteria used for?

A

If any of these criteria are met you cannot clear the C spine clinically

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16
Q

What is the gold-standard form of imaging for investigating a possible cervical spine fracture?

A

CT neck (or MRI in children <16y)

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17
Q

What is a FAST scan?

A

A point of care ultrasound scan used to identify intraperitoneal free fluid (assumed to be haemoperitoneum in the context of trauma)

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18
Q

Systematically recall some causes of coma

A

Metabolic: COMA CAUSES

Cold (hypothermia)
Oxygen (hypoxia)
Medication OD (eg TCAs)
Addisonian…

Crisis
Alcohol 
Underactive thyroid (myxoedema) 
Sepsis 
Encephalopathy (uraemic or hepatic) 
Sugars high/ low

Vascular: THEISM

Trauma 
Haemorrhage 
Epilepsy 
Infection 
Stroke 
Malignancy
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19
Q

Recall the elements of the Glasgow Coma Scale in people >5 years old

A
Eyes: 
1: no response 
2: open to pain 
3: open to voice
4: open spontaneously 
C = closed by swelling or bandage 
Voice: 
1: no response 
2: sounds 
3: words 
4: confused 
5: orientated 
T = intubated 

Motor:

1: no response
2: abnormal extension (decerebrate)
3: abnormal flexion (decorticate)
4: withdraw from pain
5: localise pain
6: obey commands

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20
Q

What is Cheyne-Stokes hyperventilation?

A

Type of central sleep apnoea where there are periods of apnoea followed by fast ventilation
If seen when patients are awake it indicates a poor prognosis

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21
Q

What is apneustic breathing?

A

Regular deep inspirations with an inspiratory pause followed by inadequate expiration
Caused by injury to the pons

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22
Q

What is ataxic breathing?

A

Completely irregular pattern of breathing that eventually becomes agonal breathing

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23
Q

If pupils are mid-position (3-5mm) and non-reactive (may be irregular or not), what does this indicate?

A

Midbrain lesion

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24
Q

If pupils are unilaterally fixed and dilated what does this indicate?

A

3rd nerve compression

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25
Q

If pupils are small but reactive what does this indicate?

A

Pontine lesion or drugs

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26
Q

How can you test the vestibulo-ocular reflex?

A

Doll’s head manoevre:
Head is moved laterally quickly
Normal if eyes keep looking at same point in space
Abnormal if eyes turn in opposite direction of rotation

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27
Q

In the most simplistic terms, how do you decide between a PCI or a CABG to manage ACS?

A

PCI for 1 or 2 vessel disease, not including LAD

CABG for >2 vessel disease, or including LAD

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28
Q

Recall the reversible causes of MI

A
5 Hs and 4 Ts
Hypoxia 
Hypovolaemia 
Hypothermia 
Hypokalaemia/ hyperkalaemia 
Hypoglycaemia 

Toxins
Tamponade
Thrombosis
Tension pneumothorax

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29
Q

Recall the possible complications of an MI

A
DARTH VADER 
Death 
Arrhythmia 
Rupture (left ventricular free wall, interventricular septum) 
Thrombosis 
Haemorrhage 
Valvular heart disease 
Aneurysm 
Dressler's syndrome 
Embolism 
Re-infarct
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30
Q

In what time period might LVFW rupture occur post-MI?

A

5 days to 2 weeks

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31
Q

What are the differentials for cardiac rupture 3-5days post MI?

A

1) Acute mitral regurgitation due to papillary muscle rupture
2) Ventricular septal rupture

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32
Q

What are the signs and symptoms of papillary muscle rupture?

A

Acute mitral regurgitation
Pulmomary oedema
Hypotension
New pansystolic murmur (harsh thrill)

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33
Q

What are the signs and symptoms of ventricular septal rupture post MI?

A

Chest pain
Biventricular failure
Shock
New PSM

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34
Q

What are the signs and symptoms of LVFW rupture post-MI?

A

Heart failure

Tamponade

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35
Q

What are the signs of cardiac tamponade?

A

Raised JVP
Muffled heart sounds
Hypotension
Pulsus paradoxus

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36
Q

How should heart block be managed following an anterior vs inferior MI?

A

If they had an anterior MI then got heart block:
- Temporary transcutaneous pacing –> permanent pacemaker

If they had an inferior MI then got heart block:
- Medical management with atropine

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37
Q

What is the most common cause of death post-MI?

A

Ventricular fibrilation

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38
Q

Describe the broad principles of immediate management of MI (this is your big ‘ol card when you turn over warning)

A

Offer 300mg aspirin loading dose asap

For symptom mx: 10mg IV morphine and 10mg IV metoclopramide (O2 if SpO2 <94%)

Immediately assess suitability for reperfusion therapy
- Can offer reperfusion therapy within 12 hours of symptom onset (or slightly otherwise in some circumstances)
- If it’s >12 hours since symptom onset –> medical mx only
Reperfusion options:
1. PCI - if you can offer within 120 mins (need to add aspirin + one other antiplatelet for this, choice depends on a number of factors)
2. Fibrinolysis - if you can’t offer PCI within 120 mins (1st line is enoxaparin - can also use unfractionated heparin/ fondaparinux)
3. If GRACE score low –> just fondaparinux

Medical mx:
- Aspirin and ticagrelor (180mg PO) unless high bleeding risk

Source: https://www.nice.org.uk/guidance/ng185/resources/visual-summary-stemi-pdf-8900623405

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39
Q

When would beta blockers be contra-indicated in immediate management of an MI?

A

Bradycardia
Hypotension
Heart failure/ block
COPD/asthma

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40
Q

Recall the long-term management of MI

A
ACE inhibitor (although consider spironolactine in HF) 
Beta blocker (OR verapamil/ dilitiazem) 
Cardiac rehab (diet and exercise) 
DAPT (aspirin + ticagrelor) 
Statin
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41
Q

Systematically recall some causes of acute onset pulmonary oedema

A

Cardiovascular (LVF –> elevated PAWP)
ARDS (normal PAWP)
Fluid overload
Neurogenic (head injury)

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42
Q

Recall the management of acute pulmonary oedema

A

(1) Sit them up - high flow O2 if sats low
(2) IV diamorphine (3mg) + IV metoclopramide (10mg)
(3) IV furosemide
(4) GTN spray x 2 SL (can use IV if SBP >100)
(5) Continue furosemide and nitrate infusions until stable

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43
Q

How can RA/RV/PAWP be measured?

A

Swan-Gantz catheter

Inserted through a central vein

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44
Q

What is the management of VF?

A

Non-synchronised DC shock (no R waves to trigger defib)

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45
Q

What is the management of VT?

A

Synchronised DC shock (synchronise to R waves)
Medical:
- Amiodarone, lidocaine, procainamide
- VERAPAMIL is a contraindication

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46
Q

How is Torsades de Pointes managed?

A

Depends on aetiology
Congenital: high dose beta blockers
Drug-induced: MgSO4

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47
Q

How is stable, regular, broad complex tachycardia managed?

A

IV amiodarone

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48
Q

How is narrow-complex tachycardia managed?

A

Vagal manoevres –> IV adenosine

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49
Q

How is bradycardia managed?

A

Give O2 if hypoxic
ECG, IV access, BP
Identify reversible causes (eg electrolyte imbalances)
If adverse signs (shock/ syncope, HF, myocardial ischaemia): IV ATROPINE 500mcg
If no adverse signs: assess risk of asystole (recent asystole? mobitz II? complete heart block?)
If risk –> atropine
If no risk –> continue observation

If atropine does not –> satisfactory response you can repeat it every 3-5 mins (3mg/6 doses max)

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50
Q

When would you admit someone for an acute exacerbation of asthma?

A
If no response to treatment in A&E or
CHEST: 
Cyanosis 
Hypotension 
Exhaustion (PEFR <33%) 
Silent chest 
Tachyarrhythmia
Near fatal (pCO2 raised)  
(Asthma management cards in respiratory deck)
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51
Q

How should tension pneumothorax be managed?

A

NB. these are NEW ATLS GUIDELINES 2018 - it USED to be 2nd ICL at MCL but NOW IS:

Safety triangle - aim for 4th/5th ICS MAL 
Boundaries: 
- lateral edge of pec major 
- 5th ICS
- Base of axilla 
- Lateral edge of lat dorsi 

Insert 14-16g needle - plunger removed - partially filled with saline (facilitates a one way valve)

https://www.fortunejournals.com/articles/changing-trends-in-the-decompression-of-tension-pneumothorax.pdf

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52
Q

What score is used to determine if someone is likely to have a PE, and how many points do you need to justify a CTPA?

A

Well’s score
>4 points
(if <5 points –> D dimer)

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53
Q

What are some possible signs of PE on ECG, and which is the most common?

A

Most common: sinus tachycardia

Also: RBBB, RAD, S1Q3T3

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54
Q

How will a CXR appear in PE?

A

Normal

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55
Q

How should pulmonary embolism be managed if a patient is haemodynamically stable?

A

For all PEs: O2 if hypoxic, morphine/ anti-emetic for pain/ distress, IV fluids if low BP, get IV access

1st line: DOAC
3 months if provoked
Minimum 6 months if unprovoked

2nd line: IVC filter

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56
Q

Recall some provoking factors for PE

A
Immobility 
Trauma 
Surgery 
COCP/ HRT
Pregnancy/ puerperium
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57
Q

How should pulmonary embolism be managed if a patient is haemodynamically unstable?

A

For all PEs: O2 if hypoxic, morphine/ anti-emetic for pain/ distress, IV fluids if low BP, get IV access

If no contra-indication to thrombolysis:
Unfractionated heparin + alteplase –> DOAC

If contra-indication to thrombolysis:
Unfractionated heparin WITHOUT alteplase –> DOAC
Consider embolectomy

If contraindication to thrombolysis AND anticoagulation:
Noradrenaline OR dobutamine
Consider embolectomy

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58
Q

What are some absolute contraindications to thrombolysis?

A
Brain things: 
Previous intracerebral haemorrhage 
Ischaemic stroke 
Cerebral malignancy
Major trauma/surgery to head

Bleeding things:

  • GI bleeding
  • Bleeding disorder
  • Aortic dissection
  • Non-compressible punctures (eg LP/ liver biopsy)
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59
Q

What are the markers of mild, moderate and severe ARDS?

A

Based on PaO2/FiO2 ratio
Mild: 200-300mmHg
Moderate: 101-200mmHg
Severe <101mmHg

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60
Q

What are some signs and symptoms of ARDS?

A

BL CXR opacities

Respiratory failure not explained by HF or fluid overload

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61
Q

What are the appropriate investigations for ARDS?

A
Sepsis 6 
Bloods: BC, FBC, U&E, LFT, glucose, clotting, FDPs, D-Dimer, G&S
MSU 
ECG 
CXR
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62
Q

How should ARDS be managed?

A

All patients:

  • Central venous access –> inotropes
  • Peripheral venous access –> broad spec abx, diuretics
  • O2

Non-shocked: sit upright

Shocked: colloid infusion

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63
Q

Recall some causes of UGI bleed, and which of these is most common

A

PUD (most common)
Mallory-Weiss tear
Erosions, oesophagitis, varices, malignancy

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64
Q

What anatomical landmark separates UGI from LGI bleeds?

A

Ligament of Treitz (suspends duodenal-jejunal flexure)

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65
Q

Recall the headings under which UG bleeds should be managed (other cards will go into each one)

A

(1) Resuscitation
(2) Risk assess
(3) Endoscopy
(4) Manage
(5) Prophylaxis

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66
Q

How should patients be resuscitated following an UGI bleed?

A

Packed RBCs
Platelets (if active bleeding or count <50)
FFP (if active bleeding and APTT is normal)
PCC if active bleeding on warfarin (prothrombin complex concentrate)

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67
Q

How can you perform a risk assesment for an UGI bleed?

A

Pre-endoscopy: Blatchford score

Post-endoscopy (to guide prognosis): Rockall score

68
Q

When should endoscopy be performed following an UGI bleed?

A

Immediately if after severe acute resuscitation

Otherwise within 24 hours

69
Q

How should variceal bleeds be managed?

A

For all:
IV Terlipressin
IV antibiotics as per local guidelines

For gastric varices:
1st line = endoscopic injection of butyl cyanoacrylate
2nd line = TIPS (transjugular intrahepatic portosystemic shunt)

For oesophageal varices:
1st line: endoscopic band ligation
2nd line: Sengstaken-Blakemore tube and TIPS (definitive)

70
Q

How should non-variceal bleeds be managed?

A

Endoscopic options:

  • Mechanical clips
  • Thermal coagulation
  • Fibrin/ thrombin

PPI after endoscopy

71
Q

How can variceal bleeding with portal HTN be prevented?

A

PO propranolol

72
Q

Recall some gram pos cocci and bacilli that may cause meningitis

A

Cocci:
Staph aureus (coag pos)
Staph epidermidis (coag neg)
Strep (pneumoniae, viridians etc)

Bacilli: 
ABCDL
- Actinomyces 
- Bacillus 
- Clostridium 
- Diptheriae 
- Listeria
73
Q

In what type of meningitis would the opening pressure of an LP be normal rather than raised?

A

Viral

74
Q

What would the expected glucose be on LP in viral vs bacterial vs TB meningitis?

A

Viral: normal
Bacterial: low
TB: low

75
Q

In which types of meningitis might the WCC be normal on LP?

A

Viral

TB

76
Q

What are the 2 most common causes of acute meningitis in adults?

A

Strep pneumoniae

Neisseria meningitidis

77
Q

How should contacts be treated of someone with acute meningitis?

A

PO ciprofloxacin

78
Q

Which bacterium is an important cause of both meningitis and encephalitis?

A

L monocytogenes

79
Q

Which demographic groups are most likely to be affected by listeria meningitis?

A

Neonates and the elderly

80
Q

Recall 3 causes of chronic meningitis

A

TB
Cryptococcus
Syphillis
(chronic only really affects the immunosuppressed)

81
Q

If the MRI report read, “leptomeningeal enhancement, basal cistern enhancement, dilation of ventricles”, what would be the likely diagnosis?

A

TB meningitis

82
Q

What is the most common cause of aseptic/viral meningitis?

A

Enterovirus (coxsackie A and B, echovirus)

83
Q

What is the most common cause of encephalitis in the UK vs worldwide?

A

UK: HSV-2
Worldwide: WNV

84
Q

How should encephalitis be treated?

A
IV acyclovir (10mg/kg, TDS) is first line 
If CMV/EBV --> ganciclovir
85
Q

What are the signs and symptoms of cerebral abscesses?

A

Raised ICP + fever

86
Q

Which types of cerebral abscess are most likely to be peripheral vs deep?

A

Peripheral: bacterial abscesses
Deep: toxoplasma asbscesses

87
Q

How long does a seizure need to last to count as status epilepticus?

A

> 5 mins

>30 mins is OLD definition

88
Q

Recall the stepwise management of status epilepticus

A

(1) Open and secure airway
(2) Oxygen and suction as required

(3) IV access and take blood:
- FBC, U&E, LFT
- Glucose
- Ca2+
- Toxicology screen if indicated
- Anticonvulsant levels

(4) IV bolus
- Lorazepam 4mg IV
- Give 2nd dose of lorazepam if no response after 10 minutes

(4.5)
If alcoholism/ malnourishment suspected –> thiamine
If glucose is low –> 50% glucose IV
If hypotensive –> correct with fluids

(5) (If seizures continuing)
- Phenytoin (monitor ECG and BP)

(6) If continuing seizures after 60 mins –> general anaesthesia

89
Q

What should be done in addition to an A to E assesment when assessing a head injury?

A
  • Assess events (retrogate and anterograde amnesia)
  • CNS examination
  • Early involvement of anaesthetics and ITU
90
Q

What are the 5 criteria for immediate CT head?

A
  • GCS <13 or <15 2 hours post-injury
  • Suspected skull fracture
  • Post-traumatic seizure
  • Focal neurological deficit
  • > 1 vomit
91
Q

Recall 4 signs of skull fracture

A

Haemotypanum
‘Panda eyes’
CSF rhinorrhoea/ otorrrhoea
Battle sign (mastoid ecchymosis)

92
Q

Recall 4 criteria for soon (within 8 hours) CT head following trauma

A

ABCD

  • Age >65
  • Bleeding/ clotting disorders (including current anticoagulation)
  • (Re)Collection of events before missing (retrograde amnesia)
  • Dangerous mechanism of action (eg involving a motor vehicle, or fall from >1m/ 5 stairs)
93
Q

Recall 4 criteria for an immediate CT spine

A
  • GCS <13 on initial assesment
  • Patient intubated
  • Ruling out needed (eg for surgery)
  • Clinical suspicion and age >65/ focal neurology/ high-impact injury/ limb paraesthesia
94
Q

What would the expected pupil size and light response be in 3rd nerve compression secondary to tentorial herniation?

A

Unilateral dilated pupil

Light response sluggish or fixed

95
Q

What would the expected pupil size and light response be in BL 3rd nerve palsy/ poor CNS perfusion?

A

BL dilated pupils with sluggish/fixed light response

96
Q

What would the expected pupil size and light response be in optic nerve injury?

A

Unilaterally dilated/ equal and cross-reactive light response

97
Q

What is a normal ICP?

A

<15mmHg

98
Q

If a headache is described as ‘worse when leaning forward’ what is this typical of?

A

Raised ICP

99
Q

What is Cheyne-Stokes respiration and what is it a sign of?

A

Sign of raised ICP

Periods of gradual hypopnoea and hyperpnoea interspersed by periods of apnoea

100
Q

What can be done in ventilated patients to help bring ICP down?

A

Hyperventilate –> cerebral vasoconstriction –> reduced ICP

101
Q

What are the 3 subtypes of cauda equina syndrome, and what are their symptoms?

A

CES-S: CES-suspected = BL sciatica, perianal sensory issues + sphincter issues

CES-I: CES-incomplete = voluntary control of micturition, objective signs/evidence of CES

CES-R: CES-retention/complete = complete urinary retention, overflow incontinence

102
Q

At what spinal level does the cauda equina begin?

A

L2

103
Q

Recall 2 ‘white flags’ for cauda equina

A

White flags = too late
Urinary retention
Urinary/faecal incontinence

104
Q

Recall 3 red flags for cauda equina

A

Red flag = ACT NOW, before it is too late
BL sciatica
Saddle anaesthesia
Lower limb weakness

105
Q

Recall and justify some useful investigations in suspected cauda equina syndrome

A

Lower limb neuro exam (will be abnormal in CE compression)
Saddle anaesthesia (will be reduced sensation in CE compression)
DRE (reduced anal tone in CE compression)
Bladder scan (will show urinary retention in CES as lose sensation of fullness)
MRI as 2nd line to visualise cause

106
Q

Recall 2 options for cauda equina management

A

If metasatic disease –> PO dexamethosone whilst awaiting MRI resluts
If within 48 hours of bladder dysfunction –> decompressive laminectomy

107
Q

Which 3 types of cancer are most likely to cause spinal cord compression?

A

Lung, breast and prostate

108
Q

What 2 things typically make back pain worse in spinal cord compression?

A

Lying down

Coughing

109
Q

What is the difference in symptoms between a spinal cord compression above vs below L1?

A

Above L1: UMN signs and sensory level

Below L1: LMN signs and peripheral numbness

110
Q

How should suspected spinal cord compression be investigated

A

Whole spine MRI within 24 hours

111
Q

How should spinal cord compression be managed?

A

Dexamethosone +/- radiotherapy (if frail, or multiple lesions) or surgery (if not frail, and there are fewer lesions)

112
Q

What investigations are important in DKA?

A

To establish DKA: BM, ketones, pH
Any needed to find cause (eg infection/ surgery/ chemo depending on BG)
Assess the damage (CRP, ECG, CXR, BC)

113
Q

At what level of ketones would you consider transfer to ITU/HDU?

A

> 6

114
Q

Recall 4 possible complications of DKA

A

VTE
Aspiration pneumonia
Cerebral oedema
Electrolyte imbalances (low K+/Mg2+/PO4,3-)

115
Q

How much KCL should you add per litre of saline in hypokalaemia (during DKA)?

A

40mmol

If K+ <3.5, contact HDU/ITU for higher doses

116
Q

In hypoglycaemia, when would you give IM/IV treatment rather than PO treatment?

A

BM <4 and unconscious/ no swallow

117
Q

Recall how to manage hypoglycaemia based on the BM

A

BM >4: long acting CHO (eg bread)
BM <4: if able to swallow - glucotabs
if unable to swallow - IM glucagon or IV glucose 20%

118
Q

How should myxoedema coma be managed?

A
IV T3 (5-20mcg/12 hours) 
IV hydrocortisone (100mg/8 hours)
119
Q

How should thyroid storm be immediately managed?

A

1st - propranolol (or digoxin if beta blockers CI)
2nd - carbimazole
3rd - hydrocortisone or dexamethosone
4th - treat cause

120
Q

What is the ongoing management for thyroid storm?

A
  • 4 hours after first dose of carbimazole –> Lugol’s iodine for 10 days
  • after 5 days of carbimazole treatment, reduce carbimazole from 20mg to 15mg, TDS, PO
  • After 10 days, stop propranolol and iodine; adjust carbimazole
121
Q

What is the mechanism of action of carbimazole?

A

Inhibits TPO

122
Q

What are the 2 main symptoms of an Addisonian crisis?

A

Hypoglycaemia

Shock

123
Q

Recall the management of Addisonian crisis

A

IM hydrocortisone 100mg STAT then ongoing

IV fluid bolus +/- glucose then ongoing fluid mx

124
Q

What is the most useful investigation for phaeochromocytoma?

A

Urinary catecholamines

125
Q

What is the management of phaeochromocytoma?

A

1st - short acting alpha blockade –> long-acting alpha blockade
2nd –> beta blockade
3rd (delayed a few weeks) –> surgery

126
Q

What 3 investigations should be ordered in ALL suspected poisonings?

A

Glucose
Paracetamol
Salicylate

127
Q

Recall 5 drugs in which haemodialysis may be indicated in OD?

A
BLAST 
Barbiturates 
Lithium 
Alcohol 
Salicylates 
Theophylline
128
Q

Recall the reversing agent for BDZs

A

Flumenazil

129
Q

Recall the reversing agent for opiates

A

Naloxone

130
Q

Recall the reversing agent for paracetamol

A

N-acetylcysteine

131
Q

Recall the reversing agent for aspirin

A

sodium bicarbonate

132
Q

Recall the reversing agent for TCAs

A

sodium bicarbonate

133
Q

Recall the reversing agent for beta blockers

A

Atropine

134
Q

Recall the reversing agent for ethylene glycol (anti-freeze)

A

Fomepizole

135
Q

What is the most common side effect of NAC?

A

Rash (non-IgE mediated allergic reaction)

136
Q

Recall the management of paracetamol OD

A

If <2 hours: activated charchoal followed by paracetamol levels >4 hours after ingestion –> NAC if indicated

If 2-8 hours: do a paracetamol level >4 hours post-ingestion –> NAC if indicated

If >8 hours, and ingested amount >75mg/kg –> NAC then paracetamol level

If ingestion time unknown or staggered OD (taken over 1 or more hours) –> NAC

137
Q

When do AST and ALT peak post paracetamol OD ingestion?

A

72 hours

138
Q

What LFT result will likely be normal in paracetamol OD?

A

ALP

139
Q

When is transplantation indicated in paracetamol OD?

A

If PT>180s on day 4

140
Q

Recall 3 specific symptoms of salicylate OD

A

Tinnitus
Hyperventilation
Vertigo

141
Q

Within what time window can you give activated charcoal for salicylate overdose?

A

<1 hour

142
Q

How do you choose between sodium bicarbonate and haemodialysis in salicylate OD?

A

Severe metabolic acidosis –> IV NaHCO3

Organ dysfunction/seizures –> haemodialysis

143
Q

What % of TBSA burned is an indication for fluid resuscitation?

A

10% (children)

15% (adults)

144
Q

What is the gold-standard assesment tool for calculating TBSA affected in burns?

A

Lund and Browder chart

145
Q

What 2 prognostic parameters are affected by burn depth?

A

Healing time

Scarring

146
Q

How should burns be temporarily cooled?

A

Saline/paraffin gauze and clingfilm

147
Q

What is the definitive management for partial thickness burns?

A

Silver sulfadiazine cream +/- cerium nitrate

148
Q

What is the Parkland formula?

A

4 x weight(kg) x %burn = mL Hartmann’s in first 24 hours (give 50% in first 8 hours)

149
Q

What is escharotomy?

A

Removal of tough, leathery eschar following burn rehydration - if it is left it can –> impaired circulation and compartment syndrome

150
Q

Roughly recall Wallace’s rule of 9s

A

18% of TBSA = back, chest, each leg
9& TBSA = head, each arm
1% = perineum

151
Q

Describe the appearance of each different thickness of burn

A

Superficial epidermal = red and painful
Superficial dermal = pale pink, painful, blistered
Deep dermal = white with patches of non-blanching erythema, reduced sensation
Full thickness = white/brown/black in colour, no blisters or pain

152
Q

What temperature counts as ‘hypothermia’?

A

Rectal temp <35C

153
Q

How can you tell if hypothermia is mild or severe?

A
Mild = shivering 
Severe = no shivering
154
Q

What ecg finding is pathognemonic of hypothermia?

A

J waves (Osborne waves)

155
Q

How quickly should you rewarm someone who is hypothermic?

A

0.5C/hour

156
Q

What must be remembered about CPR attempts in hypothermia?

A

Must be continued until core temp >33C as rarely successful when temp <30C

157
Q

What are the 3 most common symptoms of carbon monoxide poisoning?

A

Headache
Nausea and vomiting
Vertigo

158
Q

What investigations should be done in suspected CO poisoning?

A

Pulse oximetry will be falsely high –> do VBG/ABG

Need to check carboxyhaemaglobin levels

159
Q

How high will carboxyhaemoglobin levels be in CO poisoning?

A

10-30%

160
Q

How should CO poisoning be managed?

A

100% high-flow oxygen through nrb mask

161
Q

What are the signs and symptoms of hypoactive vs hyperactive delirium?

A

Hypoactive: lethargy, bradykinesia, excessive somnolence, inattention

Hyperactive: agitation, hallucinations/ delusions, wandering, aggression

162
Q

How should delirium be investigated?

A

Confusion assesment method/ AMTS
Bedside: exam, obs, urine dip, cap blood glucose
Bloods: baseline (FBC, U&Es), LFTs, B12, folate, TFTs, glucose, clotting, bone profile, blood culture
Imaging: CXR, CT head

163
Q

How should delirium be managed?

A
  1. Treat cause, modify RFs, well-lit room with familiar people
  2. PO haloperidol
164
Q

Recall 3 drug classes that can precipitate delirium

A

BDzs
Anti-cholinergics
Opioids

165
Q

How should tetanus-prone injuries be managed?

A

If they’ve had full course of tetanus vaccines with the last dose <10y –> nothing

If they’ve had the full course of tetanus vaccines with the last dose >10y –> reinforcing vaccine, and if a very high risk wound –> tetanus IV Ig

If they have an incomplete or unknown vaccine history –> reinforcing dose of vaccine + tetanus immunoglobin