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A+E Flashcards

1
Q

RFs for AKI?

A 
Age >65
Diabetes
HTN
Dehydration
Nephrotoxic medications 
CKD
Heart failure
Rhabdomyolysis
Renal tract obstruction 
Myeloma
Liver disease
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2
Q

Pre-renal causes of AKI?

A
  1. Hypovolaemia (dehydration, bleeding)
  2. Septic shock
  3. Cardiogenic shock
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3
Q

Renal causes of AKI?

A
  1. Acute tubular necrosis
  2. Glomerulonephritis
  3. Vasculitis
  4. Interstitial nephritis
  5. Tubular toxicity ie CT contrast
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4
Q

What are the post-renal causes of AKI?

A
  1. Urinary tract obstruction
  2. Intraluminal ie stone
  3. Extraluminal ie cancer compression on ureter
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5
Q

What are the diagnostic criteria for AKI?

A
  1. Increase in serum creatinine over 0.3umol/L within 48 hrs
  2. Or inc. in serum creatinine 1.5x baseline
  3. Or urine volume less than 0.5mL/kg/hr for >6 hrs
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6
Q

What are the creatinine levels for Stage 1 AKI?

A

1.5-1.9x baseline

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7
Q

What are the creatinine levels for Stage 2 AKI?

A

2-2.9x baseline

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8
Q

What are the creatinine levels for Stage 3 AKI?

A

3x baseline

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9
Q

Management aims for AKI?

A
  1. Treat underlying cause

2. Prevent further damage by optimising renal blood flow with fluid challenge

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10
Q

What forms the AKI bundle?

A
  1. Restore perfusion
  2. Stop nephrotoxins
  3. Exclude obstruction
  4. Treat complications
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11
Q

How is perfusion restored in AKI?

A
  1. Fluid challenge

2. Consider vasoconstrictors or inotropes

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12
Q

How do you exclude obstruction in AKI?

A
  1. Measure urine output
  2. CT (stones)
  3. Renal USS (hydronephrosis)
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13
Q

What are some nephrotoxic drugs?

A

ACEis/ARBs, NSAIDs
Aminoglycosides (ie gentamicin)
Contrast media
Furosemide and some other diuretics

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14
Q

How does septic shock cause pre-renal AKI?

A

Sepsis causes leaky vessels; fluid moves from the vessels into the interstitium

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15
Q

What is the main medical cause of acute interstitial nephritis causing AKI?

A

NSAIDs

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16
Q

What is a side effect of gentamicin? Which drug interacts synergistically?

A

Ototoxic

Furosemide

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17
Q

Which metabolic abnormalities occur from an AKI and why?

A
  1. Hyperkalaemia
  2. Metabolic acidosis
    The transporters work less effectively causing a build up of H+ and K+ and a loss of Na
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18
Q

How is hyperkalaemia treated?

A

1) Calcium gluconate
2) 10 units Actrapid + 10% glucose
3) Calcium resonium

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19
Q

3 complications of AKI?

A
  1. Uraemia
  2. Metabolic acidosis
  3. Fluid overload
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20
Q

Headache. What would first and worst/ thunderclap headache suggest?

A

Subarachnoid haemorrhage

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21
Q

Headache. What would unilateral headache and eye pain suggest?

A

Cluster headache

Acute glaucoma

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22
Q

Headache. What would unilateral headache and ipsilateral symptoms suggest?

A

Migraine
Tumour
Vascular

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23
Q

Headache. What would cough-initiated/ worse in morning/ when bending over headache suggest?

A

Raised ICP/ venous thrombosis

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24
Q

Headache. What would a persisting headache with scalp tenderness in >50s suggest?

A

Giant cell arteritis

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25
Q

Headache. What would headache with fever/ neck stiffness suggest?

A

Meningitis

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26
Q

Headache. Aside from associated symptoms, what other questions should you ask a patient presenting with a headache?

A
  1. Any recent travel? (?malaria)
  2. Pregnant? (?pre-eclampsia; esp if proteinuria and HTN)
    Also check for any change in pattern of ‘usual’ headaches, and any change in consciousness.
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27
Q

Headache. Differential diagnoses for someone presenting with headaches?

A
  1. Tension, cluster, migraine
  2. Post-traumatic
  3. Drugs (nitrates, CCBs)
  4. Carbon monoxide poisoning/ anoxia
  5. Subarachnoid haemorrhage, Stroke, Subdural haematoma
  6. Tumour, Cerebral abscess
  7. Malignant hypertension
  8. Idiopathic intracranial hypertension
  9. Any CNS infection
  10. Encephalitis, meningitis, TB meningitis
  11. GCS, Acute glaucoma, Certebral artery dissection, Cervical spondylosis, Sinusitis, Paget’s disease, Altitude sickness
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28
Q

Breathlessness. What might be the cause of breathlessness if the patient is wheezing?

A
  1. Asthma
  2. COPD
  3. Heart failure
  4. Anaphylaxis
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29
Q

Breathlessness. What might be the cause of breathlessness if the patient has stridor?

A
  1. Foreign body/ tumour
  2. Acute epiglottis (younger patients)
  3. Anaphylaxis
  4. Trauma, e.g. laryngeal fracture
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30
Q

Breathlessness. What might be the cause of breathlessness if the patient has crepitations?

A
  1. Heart failure
  2. Pneumonia
  3. Bronchiectasis
  4. Fibrosis
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31
Q

Breathlessness. What might be the cause of breathlessness if the patient has a clear chest?

A
  1. Pulmonary embolism
  2. Hyperventilation
  3. Metabolic acidosis (e.g. DKA)
  4. Anaemia
  5. Drugs, e.g. salicylates
  6. Shock
  7. Pneumocystis jirovecii pneumonia
  8. CNS causes
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32
Q

Breathlessness. What might be the cause of breathlessness if there is ‘stony dullness’ to percussion of the chest?

A

Pleural effusion

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33
Q

Breathlessness. What key investigations should be carried out?

A
  1. Baseline observations (O2, sats, temp, peak flow)
  2. ABG if SpO2 <94% or concern about acidosis/ drugs/ sepsis
  3. ECG (signs of PE, LVH, MI?)
  4. CXR
  5. Baseline bloods: glucose, FBC, U&E, consider drug screen
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34
Q

Chest pain. Give 6 life-threatening causes

A 
Acute MI
Angina/ACS
Aortic dissection
Tension/open pneumothorax
Pulmonary embolism
Oesophageal rupture
Sickle-cell crisis
Cardiac tamponade/pericardial effusion
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35
Q

Chest pain. What are the 3 key investigations you would carry out?

A
  1. CXR
  2. ECG
  3. Bloods: FBC, U+E, troponin. Consider D-dimer
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36
Q

Coma. What is a coma?

A

Unrousable unresponsiveness

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37
Q

Give 7 metabolic causes of coma

A
  1. Drugs, poisoning (carbon monoxide, alcohol, tricyclics)
  2. Hypo/hyperglycaemia (HONK, ketoacidotic)
  3. Hypoxia, CO2 narcosis (COPD)
  4. Septicaemia
  5. Hypothermia
  6. Myxoedema, Addisonian crisis
  7. Hepatic/uraemic encephalopathy
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38
Q

Give 5 neurological causes of coma

A
  1. Trauma
  2. Infection: meningitis, encephalitis (herpes simplex - give IV aciclovir if slight suspicion), malaria, typhoid, etc.
  3. Tumour (primary or secondary)
  4. Vascular: stroke, subdural/subarachnoid, hypertensive encephalopathy
  5. Epilepsy: non-convulsive status or post-octal state
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39
Q

Coma. What is the immediate management?

A

Airway: protect C-spine; check patent; intubate if GCS <8
Breathing: give 4L high-flow O2
Circulation: IV access
Disability/glucose: give 50ml 20% glucose IV stat if hypo possible
Exposure

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40
Q

Coma. At what GCS would you consider intubation?

A

If GCS <8

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41
Q

What is the GCS composed of?

A

EMV (eyes, motor, verbal) 456

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42
Q

What drug would be administered in suspected Wernicke’s encephalopathy?

A

Pabrinex IV

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43
Q

What drug would be given for opiate intoxication?

A

Naloxone IV/ IM/ via ETT

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44
Q

What drug would be given for benzodiazepine intoxication?

A

Flumazenil IV (only if airway compromised)

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45
Q

What is Pabrinex?

A

Pabrinex is an injection that contains vitamins B and C (thiamine, riboflavin, pyridoxine, nicotinamide and ascorbic acid).

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46
Q

What is the alternative name for Vitamin B1?

A

Thiamine

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47
Q

What is the alternative name for Vitamin B9?

A

Folate

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48
Q

Coma. What are the key investigations to be carried out?

A
  1. Bloods: ABG, FBC, U&E, ESR/CRP, ethanol, toxic screen, drug levels
  2. Cultures: blood, urine, consider malaria
  3. Imaging: CXR, CT head
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49
Q

What alternative to GCS may be used to assess the critically ill?

A

AVPU (alert; responds to verbal stimuli; responds to pain; unresponsive)

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50
Q

GCS: what does extensor response to pain indicate?

A

Midbrain damage below the level of the red nucleus

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51
Q

Coma. Which brain pathway is affected?

A

ARAS (ascending reticular activating sytem)

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52
Q

What causes Cheyne-Stokes breathing?

A

Brainstem lesions/compression

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53
Q

Define: apneustic

A

Breath-holding

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54
Q

What may cause ataxic/apneustic breathing?

A

Brainstem damage (bad prognosis)

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55
Q

Shock. How is MAP (mean arterial pressure) calculated from the systolic and diastolic blood pressure?

A

1/3 (Systolic BP - Diastolic BP) + Diastolic BP

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56
Q

Shock. How is cardiac output calculated from stroke volume?

A

CO = SV x HR

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57
Q

Shock. How is MAP calculated from CO?

A

MAP = CO x SVR (systemic vascular resistance)

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58
Q

Shock. What is shock? What SBP/MAP values might be seen?

A

Circulatory failure resulting in inadequate organ perfusion
SBP <90mmHg
MAP <65mmHg

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59
Q

Shock. What signs of tissue hypoperfusion might be seen in shock?

A 
Mottled skin/ pallor, cool peripheries, slow CRT
Oliguria (Urine output <0.5ml/kg/hr)
Serum lactate >2mmol/L
Low GCS/agitation
Tachycardia
Tachypnoea
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60
Q

Shock. What are the two broad causes of inadequate cardiac output?

A
  1. Hypovolaemia

2. Pump failure

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61
Q

Shock. Give 2 broad causes of hypovolaemia, and an example of each.

A
  1. Bleeding (trauma, ruptured aortic aneurysm, GI bleed)

2. Fluid loss (vomiting, burns, ‘third space’ losses, e.g. pancreatitis, heat exhaustion)

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62
Q

Shock. Give 3 causes of bleeding that may result in hypovolaemia

A
  1. Trauma
  2. Ruptured aortic aneurysm
  3. GI bleed
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63
Q

Shock. Give 2 causes of fluid loss that may result in hypovolaemia

A
  1. Vomiting
  2. Burns
  3. ‘Third space’ losses - e.g. pancreatitis, heat exhaustion
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64
Q

Shock. What are the four main causes of shock due to peripheral circulatory failure (loss of SVR)?

A
  1. Sepsis
  2. Anaphylaxis
  3. Neurogenic (e.g. spinal cord injury, epidural, spinal anaesthesia)
  4. Endocrine failure (Addison’s disease, hypothyroidism)
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65
Q

What is SIRS?

A

Systemic inflammatory response syndrome

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66
Q

What are the criteria for SIRS?

A

2 or more of the following:

  1. Temp >38 or <36
  2. Tachycardia >90bpm
  3. Resp rate >20
  4. WBC v high or v low
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67
Q

What is sepsis?

A

SIRS in the presence of infection

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68
Q

What is severe sepsis?

A

Sepsis with evidence of organ hypoperfusion (eg hyperaemia, oliguria, lactic acidosis, altered cerebral function)

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69
Q

What is septic shock?

A

Sepsis with hypotension despite adequate fluid resus (or requirement of vasopressors/inotropes to maintain BP)

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70
Q

What type of hypersensitivity reaction is anaphylactic shock?

A

Type-I IgE-mediated

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71
Q

Give 3 signs of anaphylaxis

A
  1. Itching, sweating, D+V, erythema, urticaria, oedema
  2. Wheeze, laryngeal obstruction, cyanosis
  3. Tachycardia, hypotension
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72
Q

Give 4 differentials for anaphylaxis

A

Exacerbation of asthma/COPD

Carcinoid
Phaeochromocytoma
Systemic mastocytosis
Hereditary angioedema

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73
Q

Why would you measure serum tryptase in a patient?

A

To check whether they have had an anaphylactic reaction

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74
Q

Anaphylaxis. Which cells release tryptase?

A

Mast cells

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75
Q

Anaphylaxis. What is the immediate management for anaphylaxis?

A

ABCDE

  1. Secure airway - give 100% O2; intubate if necessary
  2. Remove cause; raise feet to restore circulation
  3. Adrenaline IM 0.5mg of 1 in 1000; repeat every 5min if needed
  4. IV access
  5. Chlorphenamine (Piriton) 10mg IV and Hydrocortisone 200mg IV
  6. IVI 0.9%NaCl as needed
  7. Admission to ICU if still hypotensive
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76
Q

Anaphylaxis. How would a patient be further managed once admitted to ICU?

A
  1. IVI adrenaline may be needed +/- aminophylline
  2. Nebulised salbutamol
  3. Admit to ward, monitor ECG
  4. Measure mast cell tryptase 1-6h after suspected anaphylaxis
  5. Continue chlorphenamine if still itching
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77
Q

Anaphylaxis. What dose of adrenaline would be given IM?

What are the risks of giving adrenaline IV?

A

0.3-0.5mg of 1 in 1000 adrenaline
Indicated in extremes of each system, e.g. stridor/wheeze, hypoTN, drowsy

Risks of IV: palpitations, SoB, N+V, MI, arrhythmia

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78
Q

STEMI. What would the initial investigations be?

A
  1. History and examination
  2. ECG
  3. Bloods: FBC, U&E, troponin, glucose, cholesterol
  4. CXR
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79
Q

STEMI. Initial management?

A

Offer pain relief asap (GTN or morphine)

ECG and IV access (take bloods, inc Trop I/T)
Aspirin 300mg
Morphine 5-10mg IV + antiemetic (e.g. metoclopramide)
Primary PCI (STEMI on ECG and PCI <120 mins)
OR
Fibrinolysis if not

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80
Q

Shock. What is cariogenic shock?

A

When the decline in CO is due to a decrease in contractility or dysrhythmias

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81
Q

Shock. What signs might suggest anaphylactic shock?

A

Lip/tongue swelling (angioedema)
Inspiratory stridor
Urticaria
Hx of atopy

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82
Q

Shock. What is the shock index?

A

HR/SBP

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83
Q

Shock. What shock index value indicates shock?

A

Shock index >0.8

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84
Q

Shock. What might an elevated eosinophil count suggest?

A
  1. Anaphylaxis

2. Adrenal insufficiency

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85
Q

Shock. What are band cells, and what do they suggest?

A

Immature neutrophils

Fairly specific for sepsis

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86
Q

Shock. What might elevated BUN (blood urea nitrogen) and Creatinine levels indicate?

A

Pre-renal AKI secondary to hypovolaemia

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87
Q

Shock. If an MI is suspected, what investigation should be carried out?

A

Troponin levels

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88
Q

Shock. If congestive heart failure is suspected, what 2 investigations should be carried out?

A
  1. CXR

2. BNP levels

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89
Q

Shock. What are the 2 types of hypovolaemic shock?

A
  1. Haemorrhagic

2. Non-haemorrhagic

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90
Q

Shock. What are the main causes of non-haemorrhagic hypovolaemic shock?

A
  1. GI: D&V
  2. Renal: excessive diuresis (DKA) or diabetes insipidus
  3. Excessive sweating
  4. Third-spacing
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91
Q

Shock. What is third spacing?

A

Anything that causes intravascular fluid to shift into the interstitial/intracellular space

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92
Q

Shock. Give 3 examples of ‘third space’ losses that could cause hypovolaemic shock

A
  1. Burns
  2. Intestinal obstruction
  3. Acute pancreatitis
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93
Q

Shock. What would you want to rule out in an elderly patient presenting with back/flank pain, syncope and hypotension?

A

Ruptured AAA

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94
Q

Shock. What type of blood can be given if the patient’s blood type is unknown?

A

O negative

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95
Q

Shock. What is an anaphylactoid reaction?

A

When a trigger (e.g. opioids) induce release of mediators in a non-IgE-dependent fashion

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96
Q

Anaphylaxis. How does adrenaline work to manage anaphylaxis?

A
  1. Vasoconstriction
  2. Increases CO
  3. Relaxes smooth muscle of the airway
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97
Q

Anaphylaxis. What is the issue with giving adrenaline to someone on a beta blocker?

A

Beta blockers can blunt the effect of adrenaline

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98
Q

Anaphylaxis. What can be given to potentiate the effects of adrenaline in someone who is on a beta blocker?

A

Glucagon

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99
Q

What can cause a delayed deterioration in anaphylaxis?

A

Digestion of food

Delayed histamine response

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100
Q

Anaphylaxis. What is the ‘biphasic reaction’?

A

When a less severe episode of anaphylaxis recurs within 72 hours of the initial reaction

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101
Q

Anaphylaxis. What can be given to reduce the risk of a biphasic reaction?

A

Glucocorticoids such as methylprednisolone (delayed onset of action)

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102
Q

Anaphylaxis. What is Kounis syndrome?

A

MI following anaphylaxis
Occurs in people with pre-existing CHD as they have lost of mast cells in coronary circulation which can trigger plaque rupture when anaphylaxis occurs

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103
Q

Neurogenic Shock. What is the sympathetic innervation of the heart?

A

T1 to T5

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104
Q

Neurogenic Shock. How might injury to T1-T5 affect the blood pressure? Why?

A

Hypotension
T1-T5 responsible for sympathetic innervation to the heart; injury results in unopposed parasympathetic stimulation -> vasodilation and bradycardia

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105
Q

Neurogenic Shock. How is it treated?

A
  1. IV Crystalloid fluids

2. Vasopressors (noradrenaline, phenylephrine, dopamine)

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106
Q

What is spinal shock?

A

Temporary state of flaccid paralysis and loss of sensation below the level of spinal cord injury

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107
Q

Shock. Which hormones are depleted in adrenal insufficiency?

A
  1. Cortisol

2. Aldosterone

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108
Q

What type of hormone is cortisol?

A

Glucocorticoid

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109
Q

What type of hormone is aldosterone?

A

Mineralocorticoid

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110
Q

Shock. What typically causes adrenal insufficiency?

A
  1. Sudden cessation of chronic exogenous glucocorticoids (e.g. in someone with asthma or COPD)
  2. Failure to increase the dose during stress (e.g. infection, surgery)
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111
Q

Shock. How is shock due to adrenal insufficiency treated?

A
  1. IV Hydrocortisone (to replace cortisol)

2. IV Fludrocortisone (to replace aldosterone)

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112
Q

Shock. What causes toxic shock syndrome?

A

Bacterial endotoxins that act as superantigens - generate hyperactive immune response

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113
Q

AKI. Pre-renal AKI is characterised by an ___ ratio of BUN:Creatinine and a ___ fractional excretion of sodium

A
  1. Elevated BUN:Creat ratio (>20)

2. Low fractional excretion of sodium (<1%)

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114
Q

Shock. What type of shock is associated with loss of sympathetic nervous system stimulation throughout the body?

A

Neurogenic shock

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115
Q

Shock. In a patient with bradycardia, hypotension, poikilothermia and priapism, what type of shock would be suspected?

A

Neurogenic shock

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116
Q

Shock. What is poikilothermia?

A

Inability to control body temperature; seen in neurogenic shock

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117
Q

Shock. What is Beck triad?

A
  1. Distended neck veins
  2. Muffled heart sounds
  3. Hypotension

its presence is characteristic of cardiac tamponade

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118
Q

Shock. Why is the patient warm and flushed without perspiration in neurogenic shock?

A

Systemic vasodilation -> warm and flushed

Without perspiration -> sweat glands are sympathetically controlled

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119
Q

Shock. What happens to the systemic vascular resistance in neurogenic shock?

A

Decreases (due to lack of sympathetic signalling -> widespread vasodilation)

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120
Q

Anaphylaxis. What type of reaction is associated with contact dermatitis or a delayed hypersensitivity reaction?

A

Type IV hypersensitivity

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121
Q

Shock. 26F comes to A&E w/ altered mental status, high fever and diffuse rash on lower limbs.
She is lethargic but arousable. T 39°C, HR 110bpm, Resp 33/min, BP 90/50mmHg. She is given 2 IV fluid boluses - no change in BP.
Started on treatment. Blood culture shows ++ G-ve diplococci.
Which of the following molecules is primarily involved in this patient’s condition?
a) IFN-beta
b) IL-10
c) IL-2
d) IL-3
e) TNF-alpha

A

e) TNF-alpha

Major mediator of septic shock

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122
Q

Shock. Which molecule is the major mediator of septic shock?

A

TNF-alpha

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123
Q

Shock. What type of cell releases TNF-alpha?

A

Macrophages

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124
Q

Shock. Which of the following parameters when re-evaluated serially over time is best for guiding fluid resuscitation efforts in sepsis?

  1. Anion gap
  2. Central venous oxygen saturation
  3. Central venous pressure
  4. CXR
  5. Venous lactate
A

Venous lactate

125
Q

Shock. How does increasing the systemic vascular resistance (SVR) affect cardiac output?

A

Increasing SVR leads to increased afterload; this leads to decrease in CO.

126
Q

Anaphylaxis. How does adrenaline affect:

  1. α1 receptors
  2. β1 receptors
  3. β2 receptors
A
  1. Activates; increases peripheral vascular resistance
  2. Activates; increases HR and contractility
  3. Activates; causes bronchodilation
127
Q

Shock. Chest pain, respiratory distress, hypotension, jugular venous distention, crackles in both lower lung fields heard on auscultation, and ECG findings (ST-elevation on anterior leads) are suggestive for what type of shock?

A

Cardiogenic

128
Q

List some things to check in an A-E assessment

A

A - secure airway (guedel, ETT/LMA)
B - RR, SpO2. Give O2, salbutamol/ ipratropium news
C - BP, HR, CRT, UO. Fluid resus, vasopressors, catheterisation
D - GCS, AVPU, BM. CT, IV dex
E - Rash, burns, bleeding, etc

129
Q

What is the Canadian C Spine Score?

A

Score used to determine need for CT scanning post neck injury
Use if patient is alert (GCS 15) and stable following trauma

130
Q

Outline the components of the Canadian C Spine Score

A
  1. If HIGH RF: CT/imaging

2. If LOW RF: assess ROM (if can’t rotate neck actively (45 degrees L and R -> imaging)

131
Q

What are the high RFs from the Canadian C Spine Score?

A
  1. Age 65+ yrs
  2. Dangerous mechanism
  3. Paraesthesia in the extremities
132
Q

What are the low RFs from the Canadian C Spine Score?

A
  1. Simple rear-end RTA
  2. Sitting position in ED
  3. Ambulatory at any time
  4. Delayed (not immediate) presentation
  5. Absence of midline C spine tenderness
133
Q

What counts as a ‘dangerous mechanism’ in the Canadian C Spine Score?

A
  1. Fall >2ft/5 stairs
  2. Axial load to head (e.g. diving)
  3. High speed, rollover or ejection RTA
  4. Bicycle collision with object (post, car)
  5. Motorised recreational vehicles (quad bike)
134
Q

Difference between burn and scald?

A 
Burn = injury by thermal, chemical, electrical or radiation energy
Scald = contact with hot liquid or steam
135
Q

What age categories are high risk groups with burns?

A

Kids <5

Adults >75

136
Q

What initial assessment should be done in a burns patient?

A

ABCDE, prevent hypothermia, assess need for fluid resus

Check nostrils for inhalational injury (smoke)

137
Q

Outline the rule of nines for burns

A 
Determines % body burnt (2nd/3rd degree only)
Arm = 9%
Head = 9%
Torso front = 18%
Torso back = 18%
Leg = 18%
Groin = 1%
138
Q

What charts should be used to assess paediatric burns?

A

Lund and Browder (accounts for age and growth; head and leg are different - in <1yr old, head = 18% and leg = 14%. For each extra year -1% head and +0.5% leg)

139
Q

What are Lund and Browder charts used for?

A

Assessing paediatric burns

140
Q

What are the 5 different depths of burns?

A
  1. Superficial (1st degree only involves epidermis)
  2. Partial (2nd degree, involves superficial dermis)
  3. Partial (2nd degree, involves deep dermis)
  4. Full thickness (3rd degree, involves epidermis and dermis)
  5. Full thickness and involves deeper tissue e.g. muscle and bone

NB burns are dynamic; should reassess in 24-72h

141
Q

Give 5 features of an epidermal (first degree) burn

A
  1. Painful
  2. Red
  3. Glistening
  4. NO blisters
  5. Brisk CRT
142
Q

Give 4 features of a superficial dermal (second degree) burn

A
  1. Pale pink/mottled
  2. Swelling
  3. SMALL blisters +/- weeping
  4. Brisk CRT
143
Q

Give 6 features of a deep dermal (second degree) burn

A
  1. Cherry red, blotchy
  2. Blistering
  3. Dry
  4. No blanching
  5. No CRT
  6. Reduced sensation
144
Q

Give 5 features of a full thickness (third degree) burn

A
  1. White/black and dry
  2. NO blisters
  3. No cap refill, No sensation
145
Q

What is a hallmark feature of second degree burns?

A

Blisters

146
Q

What is a severe complication that can occur if a burn goes all the way around an arm or leg? Why does this happen?

A

Compartment syndrome

Occurs due to swelling; restricts blood flow

147
Q

For each burn depth, how does it heal?

A
  1. Superficial: 1 wk, no scar
  2. Superficial dermal: 3 wks, minimal scarring
  3. Deep dermal: 3-8 wks healing with scarring +/- surgical Rx
  4. 3rd degree: Surgical repair/graft
  5. 4th degree: Reconstruction/ amputation
148
Q

What Ix are needed for burns victims?

A
  1. Bloods (FBC, crossmatch, HbCO, serum glucose, U&E, ABG)
  2. CXR
  3. ECG (check for dysrhythmias)
  4. Circulation monitoring (BP can be difficult so unreliable)
  5. Catheter for UO monitoring
149
Q

Treatment of minor burns after first aid measures?

A

Dressing and analgesia

  • leave blisters <1cm intact, aspirate larger blisters
  • non-adhesive gauze dressing and re-examine 48hrs
  • if infection: daily wound inspection and dressing change and 1/52 fluclox
  • analgesia, check tetanus status
150
Q

What % body surface area is represented by the palm?

A

0.75%

151
Q

What signs would indicate airway burns?

A 
Hoarseness
Stridor
Dysphagia
Facial/mouth burns
Singeing of nasal hair
Soot in nostrils/palate
152
Q

How would you manage the airway and C-spine in a patient with severe burns?

A
  1. Treat airway obstruction
  2. Continue O2
  3. Apply hard cervical collar (if ?spinal injury)
  4. Call for anaesthetist if risk of airway obstruction (GA and ETT may be needed)
153
Q

How would you check and manage breathing in a severe burns patient?

A
  1. ABG (don’t use PaO2 if CO poisoning)
  2. 100% O2
  3. Continue O2 therapy until COHb levels normal
  4. Make sure the burns are not restricting chest movement
154
Q

How do burns cause fluid loss?

A

Heat increases capillary permeability, leading to oedema and visible fluid loss exudates and blisters

155
Q

How would you manage circulation in a major burns patient?

A

2 x large peripheral cannulae
Fluid replacement if >15% surface area in adults (>10% in kids)
Warm fluids to prevent hypothermia

156
Q

Burns. What is Parkland formula?

A

How much fluid to give in major burns

Hartmanns = 4ml x kg x %total body area affected

157
Q

What is flail chest?

A

Fracture of 3+ ribs in 2 places allows part of chest wall to move paradoxically to rest of chest wall

158
Q

Which drugs should manage a small and medium PE?

A

Small: LMWH

Big: Alteplase

159
Q

How should broad complex tachycardia be managed immediately?

A

HELP
ABCDE
Repeat ECG
(wide and fast = bad)

160
Q

8 key endocrine emergencies?

A
  1. Hyponatraemia
  2. Addisonian crisis
  3. Phaeochromocytoma
  4. Pituitary apoplexy
  5. Thyroid storm
  6. Myxoedema coma
  7. Hypercalcaemia
  8. DKA
161
Q

What is the biochemical definition for hyponatraemia?

A

Sodium <135 mmol/L

162
Q

What are the 3 main categories of causes of hyponatraemia?

A
  1. Hypervolaemic
  2. Euvolaemic
  3. Hypovolaemic
163
Q

Give 5 causes of HYPERvolaemic hyponatraemia

A
  1. CHF
  2. Renal failure
  3. Nephrotic syndrome
  4. Cirrhosis/liver failure
  5. Hyperglycaemia
164
Q

Give 6 causes of EUvolaemic hyponatraemia

A 
Diuretics
SIADH
Primary polydipsia
Low Na intake
Advanced renal failure
Hormonal insufficiency (Addison's, Hypothyroidism, Pregnancy)
165
Q

List some causes of HYPOvolaemic hyponatraemia

A

Renal: Diuretics, Addison’s, Nephropathy
GI: D+V
Other: Burns, Rhabdomyolysis, Pancreatitis, Peritonitis

166
Q

What are the clinical features of hyponatraemia?

A

Confusion
Lethargy
Seizures
Coma

167
Q

How is acute hyponatraemia treated?

A

3% saline

- 150ml bolus over 20 mins

168
Q

What is the general rule for treating endocrine emergencies?

A

Treat on clinical suspicion and don’t wait for test results

169
Q

What are the symptoms of acute adrenal failure (Addisonian crisis)?

A 
Pain (lower back, abdo, legs)
Severe D+V
Low BP
LoC
Hyperkalaemia
Hyponatraemia (confusion, lethargy, coma)
170
Q

Give 2 key causes of an Addisonian crisis

A

Can be 1st presentation

  1. Sepsis can cause acute exacerbation of chronic insufficiency
  2. Steroid withdrawal
171
Q

How is Addisonian crisis managed?

A

Hydrocortisone 100mg IV or IM
0.9% NaCl IVI over 30-60 mins

Hydrocortisone 6 hrly until patient stable
Oral replacement after 24 hrs and reduced to maintenance over 3/4 days

172
Q

What is extreme hypertension and tachycardia unless proven otherwise?

A

Phaeochromocytoma

173
Q

3 complications of burns?

A
  1. Fluid loss
  2. Infection
  3. Scarring
174
Q

What does flail chest indicate?

A 
Pulmonary contusion (bruising of the lung)
May puncture lung and cause pneumothorax
175
Q

Management of flail chest?

A 
PPV (positive pressure ventilation)
Pain control (intercostal blocks)
Pulmonary hygiene (clear mucus and fluid from lungs)
176
Q

Reversible causes of cardiac arrest?

A 
Hypoxia
Hypovolaemia
Hypo/hyperkalaemia
Hypothermia
H+ ions - acidosis

Thrombosis (coronary or pulmonary)
Tamponade (cardiac)
Toxins
Tension pneumothorax

177
Q

What are the 5 sites of major haemorrhage? Brief Rx for each

A

“Blood on the floor and four more”
1. External sources

  1. Chest (chest drain for haemothorax)
  2. Pelvic # (pelvic binder)
  3. Abdo/retroperitoneal (laparotomy)
  4. Thigh/long bones, e.g. #femur (splint)
178
Q

What is the “lethal triad”?

A

Hypothermia
Acidosis (due to tissue hypoperfusion)
Coagulopathy

179
Q

Management of major haemorrhage?

A

Stop the bleeding: splint, pressure, haemostat agents (tranexamic acid IV), REBOA (resuscitative balloon occlusion of aorta - for chest/abdo/pelvis)

Replace the fluids - fluids + blood + blood products (FFP, cryoprecipitate)

180
Q

What blood products are given according to the major haemorrhage protocol?

A

1 unit RBCs
1 unit FFP
1 unit platelets

1:1:1 ratio in trauma
then call haematologist

181
Q

What is a sensible target UO when fluid resus-ing?

A

0.5ml/kg/hr

182
Q

What is the overarching principle of wound management?

A

Take a dirty ragged wound and make it a nice clean wound that can be simply reconstructed

183
Q

Key points in wound/laceration management?

A

Irrigation (0.9% saline)
Infiltrate with lidocaine
Remove debris, FBs, necrotic tissue
Deep sutures: absorbable (Vicryl) to bring skin edges together
Superficial sutures: interrupted nylon sutures
Remove sutures (face 5 days, upper body 7-10 days, lower limb 14 days)

184
Q

Alternatives to sutures in treating a wound/laceration?

A

Steri-strips

Glue

185
Q

What is the max dose of lidocaine used in treating a laceration? How does adrenaline affect this?

A

3mg/kg

7mg/kg if given with adrenaline

186
Q

Components of the ATLS primary survey?

A

C: Catastrophic haemorrhage! (identify and control)

A: airway, 100% O2, immobilise C spine

B: breathing +/- ventilation

C: circulation + haemorrhage control - apply direct pressure to visible haemorrhage, 2x large bore cannula, ?pelvic binder

D: disability, check GCS/AVPU, pupils, gross neurology for spinal cord injury, BM

E: exposure, ensure body temp maintained, rewarm as needed. Undress to check all over

187
Q

What are the 5 components of ‘damage control resus’ in trauma?

A
  1. Early haemostasis with tourniquet/direct pressure/surgery/splints etc
  2. Awareness and Rx of lethal triad
  3. Reduce excessive crystalloid/colloid use
  4. Early use of blood products in 1:1:1 ratio
  5. Hypotensive resus/”permissive hypotension”
188
Q

What drug can be given in major haemorrhage to help limit bleeding? Dose?

A

Tranexamic acid IV - 1g given over 10mins, then 1g over 4hrs
ONLY if given within 3hrs of initial injury
Antifibrinolytic properties

189
Q

What are the components of the secondary survey?

A 
Thorough head-to-toe exam after A-E and pt is responding to initial resus
Survey:
Head/skull
Maxillofacial
C spine
Chest, Abdo, Pelvis
Perineum
Orifices (PR/PV)
Neuro
MSK
Diagnostic tests
190
Q

What is a tension pneumothorax?

A

Air between visceral and parietal pleura

Penetrating injury creates one-way valve, forcing air from lung or through chest wall into thoracic cavity

Affected lung collapses and mediastinum displaced

191
Q

Management of pneumothorax?

A

Immediate decompression of affected side - large bore cannula in 2nd intercostal space midclavicular line

Definitive Rx: chest drain

192
Q

Difference between primary and secondary traumatic brain injury?

A

Primary: occurs at time of impact

Secondary: occurs mins-days later from neurophysiological consequences + anatomic damage, e.g. ^ICP, cerebral oedema, expanding haematomas, seizures, infection

193
Q

What are the main cranial and intracranial injuries?

A

Cranial = skull#, C spine#

Intracranial = diffuse axonal injury, ExD/SubD/SubA bleed, intracerebral bleed, cerebral contusion

194
Q

How do you assess a head injury patient coming into A+E?

A

A-E
Focus on GCS trends, pupil sizes and C-spine protection
Unequal pupils not good if unconscious
Look for localising neurology
Check for priapism and anal tone (spinal cord injury)
Low BP + low HR = ?sympathetic disruption in C spine

195
Q

Outline medical management of head injury?

A

Avoid hypotension, hypoxia, hypercapnia

Opiates - reduces stress of intubation, helps prevent surge in ICP

Mannitol - can reduce ICP in acute situ, but avoid if systemically hypotensive

Aggressively Rx any seizures (IV Loraz/ Buccal Midaz) - stress from seizures ^ICP

Raise head to 30 degrees helps jugular venous return

Avoid hyperglycaemia (damages brain tissue

Refer to neurosurgery if necessary

196
Q

Biochemical test to carry out in 1st few mins after arrival in A+E of unconscious patient?

A

BM

?DKA or hypo

197
Q

Pt found unconscious in stairwell.
A = patent
B = RR 12, SpO2 100% on O2
C = HR 92, BP 120/90
D = slight response to pain, pupils equal + reacting
What further examination points are relevant?

A

GCS
Exposure - needlesticks/injuries
Examine head for injury
Neuro exam

198
Q

Pt found unconscious in stairwell.
A = patent
B = RR 12, SpO2 100% on O2
C = HR 92, BP 120/90
D = slight response to pain, pupils equal + reacting
What other basic observation is important and why?

A

Temp:

  • ?Hypothermia (found outside)
  • ?pyrexia (sepsis - LoC from reduced organ perfusion)
199
Q

Why DON’T you use GCS in stroke?

A

May not be able to speak/slurred, arm weakness, etc

200
Q

Methods for applying painful stimuli to assess GCS?

A

Trapezius squeeze
Supraorbital notch pressure
Nail bed pressure
Jaw thrust

201
Q 
Pt found unconscious in stairwell. 
A = patent
B = RR 12, SpO2 100% on O2
C = HR 92, BP 120/90
D = slight response to pain, pupils equal + reacting
5 most important investigations?
A 
BM
CT head
ABG/VBG
ECG
Urine toxicology
FBC, U+E, CRP
?LP
202
Q

Pt found unconscious in stairwell. RR = 8, resps shallow. Pinpoint pupils (miosis). Diagnosis? + Ddx for pinpoint pupils + coma

A

Heroin overdose

Pontine lesions (infarct/haemorrhage)
Metabolic encephalopathy
Sedatives (opioids, clonidine, barbiturates, chloral hydrate, GHB)
Antipsychotics (chlorpromazine, atypicals)
Cholinergic agents (nicotine, mushrooms)
Valproate

203
Q

5 key components of neuro exam in coma patient?

A

GCS (EVM 456)
Pattern of breathing
Pupils (size + reactivity)
Eye movements and oculovestibular responses
Motor responses (tone, reflexes, posturing)

204
Q

Management of heroin overdose?

A

ABCDE
Naloxone 400mg bolus, + 800mg if no response in 1 min
(IV in hospital; IM if community)

Naloxone has short half-life, so must monitor patient incase resp deterioration after the initial improvement

205
Q

Examination findings that might alert you to the possibility of a heroin overdose?

A

Shallow slow resps
Pinpoint pupils
Myoclonic jerks
Track marks

206
Q

What GCS needs intubation/ventilation?

A

<8 - can’t protect own airway

less than 8, intubate

207
Q

A+E pt with base of skull# and large subdural haematoma. How do you prepare the pt for transfer to another hospital?

A 
O2, fluids
Defib paddles
Emergency drugs (2.5x normal required)
Anaesthetist + ODP
Paperwork, handover
208
Q

Signs of base of skull fracture?

A

Periorbital bruising (racoon/panda eyes)
Mastoid bruising
CSF rhinorrhea/otorrhoea
Haemotympanum (blood adjacent to tympanic membrane)

209
Q

What prophylaxis do you need to give base of skull fracture patient?

A

Pneumococcal and meningococcal vaccines

210
Q

Why is it important to continue monitoring a patient who has been treated with naloxone?

A

It only has a short half-life, so wears off quickly and the patient may develop later respiratory depression

211
Q

How does the ABCDE approach for assessing the patient change in major trauma?

A

CABCDE
Catastrophic haemorrhage
+ immobilise C-spine

212
Q

What is the pathological process behind tension pneumothorax?

A

Air between visceral and parietal pleura

Penetrating injury creates one-way valve, forcing air from lung or through chest wall into thoracic cavity

Affected lung collapses and mediastinum displaced

213
Q 
Major trauma Pt in RTC, suddenly deteriorates, says he can't breathe.
Pulse 130
Sats 89%
BP 93/59
What has happened?
A

Massive haemothorax/tension pneumothorax

214
Q

Management of tension pneumothorax?

A

Immediate decompression with large bore cannula in 2nd intercostal space mid-clavicular line

215
Q

Management of massive haemothorax?

A

Large bore chest drain

IV fluid/blood replacement

216
Q

What is Becks triad of cardiac tamponade?

A

Rising JVP
Falling BP
Muffled HS
(+/- pulsus paradoxus)

217
Q

How would you diagnose cardiac tamponade in acute setting?

A

US - black stripe around heart indicates fluid

218
Q

What is the management of cardiac tamponade?

A

Emergency pericardiocentesis

Thoracotomy + pericardotomy

219
Q

What is cardiac tamponade?

A

Fluid in the pericardium builds up, resulting in compression of the heart

220
Q

6 life-threatening chest injuries?

A 
AATOM FC
Aorta/airway obstruction
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Flail chest
Cardiac tamponade
221
Q

What is a FAST scan?

A

Focussed Assessment with Sonography for Trauma

Rapid bedside ultrasound scan used to screen for pericardial effusion/ haemoperitoneum after trauma

222
Q

What is a WBCT?

A

Whole body CT scan

Non-contrast + contrast-enhanced CT of head, neck, chest, abdo, pelvis

223
Q

What are the indications for a WBCT?

A

Suspected injury in 2+ body regions
Early disease detection, e.g. cancer (if one tumour find, scan for others to stage)
Abnormal physiology (eg tachycardia) with unknown cause
Significant mechanism (fall from height, high speed RTA) with reduced GCS
Death at the scene

224
Q

What are the indications for an eFAST scan?

A

Blunt trauma
Penetrating trauma
Unexplained HYPOtension
Trauma in pregnancy

225
Q

What is the difference between a FAST and eFAST scan?

A

eFAST = extended FAST scan

Extra 2 views assessing thorax to look for pneumothorax

226
Q

What are the 4 questions the eFAST scan answers?

A 
Is there free fluid in the:
1) Pericardial cavity?
2) Peritoneal cavity?
3) Chest cavity?
or
4) Is there a pneumothorax?
227
Q

Give 2 causes of tachycardia in a trauma patient?

A

Pain

Haemorrhage (initial catecholamine surge causes tachycardia)

228
Q

What is the SBP if a patient’s radial pulse is palpable?

A

> 80mmHg

229
Q

How can you prevent/treat hypothermia in a trauma patient?

A 
Resus with blood products
Warmed fluids
Bair Hugger/ warm blankets
Minimise exposure
^ambient temp
Continuous temp monitoring
230
Q

What are the 3 components of damage control resuscitation (DCR)?

A

1) Permissive hypotension
2) Early haemostatic resus
3) Damage control surgery

231
Q

What is the aim of permissive hypotension?

A

Avoid excessive fluid leading to:

1) haemodilution
2) fluid overload
3) clot disruption

232
Q

What is the SBP aim in permissive hypotension?

A

SBP 80-100

233
Q

Why is it not advisable to initiate fluid resus with 1-2L crystalloid in a major haemorrhage patient?

A

Dilutional coagulopathy
Impaired O2 delivery due to dilution anaemia
Hypothermia
Worsening metabolic acidosis
Clot dislodgement and haemorrhage from ^BP

These feed into the lethal triad (acidosis, coagulopathy, hypothermia)

234
Q

Benefits of splinting suspected #femur?

How can you make the procedure more comfortable for the Pt?

What would you check before and after splinting?

A

Pain relief

Nerve block

Pulses and neurology

235
Q

Name of the rash typically associated with allergy? Describe it

A

Urticaria

Wheals - raised pink circular with white centre

236
Q

Which systems can be affected in an allergic reaction, and what corresponding features should you look for O/E?

A 
Airway: stridor, swollen lips + tongue
Lungs: Wheeze, ^RR, cyanosis, low sats
Skin: rash
Circulatory: low BP, pale, clammy
Brain: reduced consciousness
237
Q

What is the mechanism of anaphylactic reactions?

A

IgE, IgG, complement -> mast cell degranulation -> histamine release -> vasodilation and contraction of bronchial muscles

238
Q

Anaphylaxis. What is the follow-up/discharge plan after anaphylaxis admission?

A 
Epipen (adrenaline)
3-5 days prednisolone
PO antihistamine
Salbutamol inhaler
R/V with allergist
239
Q

Anaphylaxis. What is the risk if someone else picked up an epipen and accidental needlestick?

A

Finger ischaemia (vasoconstrictor)

240
Q

32F, 3 day Hx L-sided CP. Worse on inspiration + cough. Sharp at times, feels SoB, occasional dry cough. Only DHx is marvelon (COCP). Smokes 20/day. Drinks 20-30 units/week.
4 differentials?

A

PE
MSK pain (chostochondritis?)
LRTI
Pneumothorax

241
Q

O/E what would be suggestive of MSK chest pain?

A

Tenderness on palpation

Tender shoulder movements

242
Q

32F, 3 day Hx L-sided CP. Worse on inspiration + cough. Sharp at times, feels SoB, occasional dry cough. Only DHx is marvelon (COCP). Smokes 20/day. Drinks 20-30 units/week.
4 useful tests?

A 
CTPA
D dimer
ABG
ECG, CXR
FBC, U+E, LFT, clotting
243
Q

What is a D-dimer?

A

Fibrin degradation product

244
Q

List 5 clinical findings suggestive of DVT

A 
Distension of superficial veins
Unilateral swelling (>3cm)
Pain
Warmth
Erythema
245
Q

Scoring system for PE, + what factors are taken into account?

A

Wells (also PERC - good initial screen)

Clinical signs/Sx of DVT
HR >100bpm
Immobilisation (3 days)/ surgery in last 4 weeks
Previous PE/DVT
Haemoptysis
Malignancy
246
Q

Pt started on warfarin. What range should INR be?

A

2-3

247
Q

How long should a Pt with Pulmonary Embolism be on warfarin for?

A

3-6 months

If recurrent, lifelong

248
Q

Management of large Pulmonary Embolism?

A 
O2 if hypoxic 
Morphine w/ antiemetic
LMWH/fondaparinux
Fluid bolus if low BP
Consistent low BP -> noradrenaline/dobutamine
IV thrombolysis (alteplase)
Long term anticoagulation
249
Q

Paracetamol overdose. Sx of paracetamol overdose?

A

Vomiting
RUQ pain
Jaundice, encephalopathy, AKI (later)

NB may be no symptoms

250
Q

Paracetamol overdose. How long does it take for paracetamol toxicity to occur?

A

Hepatic enzymes ^ around 24hrs
Then jaundice, hepatomegaly at around 48hrs

NB blood tests done 4h after paracetamol ingestion to predict likelihood of toxicity. If high risk, need Rx

251
Q

Paracetamol overdose. Why do you do bloods at 4hrs in paracetamol overdose if toxicity takes 24hrs?
Why not sooner?

A

Paracetamol levels, to predict future toxicity

Time for digestion/absorption from GI tract

And Rx is same efficacy up to 8hrs after overdose

252
Q

Paracetamol overdose. Liver is main site of paracetamol toxicity. What other organs are commonly affected in serious toxicity?

A

Brain

Kidney (AKI)

253
Q

Paracetamol overdose. Which patients are re at risk of toxicity?

A

Factors that induce hepatic enzymes (therefore ^NAPQI)

  • alcoholics
  • drugs e.g. carbamazepine, rifampicin

Low glutathione reserves

  • malnutrition/anorexia/cachexia
  • HIV infection
  • CF
254
Q

Paracetamol overdose. In paracetamol overdose, in what circumstances should you start the NAC ASAP, prior to seeing 4hr paracetamol levels?

A
  1. Staggered overdose (>1hr)
  2. If >8hrs after overdose (NAC efficacy drops after 8hrs - up to this point, efficacy is same so no benefit to rapid Rx
  3. Unresponsive patient (can not find out when overdose taken)
255
Q

Paracetamol overdose. Give 4 instances in which you could stop Parvolex (NAC)

A

1) If paracetamol level <10mg >4hrs after last tablet
2) Normal ALT
3) INR <1.3
4) No Sx liver toxicity

256
Q

Paracetamol overdose. See Pt 11hrs after paracetamol overdose, what bloods should you take?

A 
U+E
LFT
Paracetamol level
Clotting/INR
Glucose
257
Q

Paracetamol overdose. See Pt 11 hrs after paracetamol overdose. Should you give charcoal?

A

No

Should be given within 1 hr.

258
Q

Paracetamol overdose. See Pt 11hrs after paracetamol overdose. When should you start NAC?

A

Immediately as it is >8hrs since ingestion

-after 8hrs NAC becomes less effective

259
Q

Paracetamol overdose. Pt receiving NAC for PCM overdose, flushed and vomited. Obs normal. What should you do?

A

Rash is common S/E
Continue. Chlorphenamine + Antiemetics. Observe.
Can reduce to 1/2 rate.
Don’t stop unless anaphylaxis w/shock (BP here is normal)

260
Q

Management of broad complex tachycardia?

A 
O2
Sedate and DC shock
Correct electrolytes
Amiodarone
If known SVT/BBB, adenosine
Torsades: give Mg2+
261
Q

Management of narrow-complex/supraventricular tachycardia?

A

O2 (if sats <90)
Unstable: Sedate + DCCV
Correct electrolytes
Amiodarone

Stable + regular: Vagal manoevres
Adenosine
(Verapamil)

262
Q

Management of bradycardia?

A 
O2 if hypoxic
Correct electrolytes
Unstable: atropine
Transcutaneous pacing
Isoprenaline
Adrenaline
263
Q

Management of acute asthma?

A 
O2
Salbutamol neb
Ipratropium neb
Hydrocortisone IV/ prednisolone PO
MgSO4 IV

ICU: aminophylline, ventilation, IV salb

264
Q

Investigations in acute asthma?

A

PEF
ECG for arrhythmias
ABG

265
Q

Management of acute COPD exacerbation?

A 
Salbutamol neb
Ipratropium neb
Controlled O2
IV hydrocortisone + PO prednisolone
Amoxi/clarith/doxy if infection
Physio to aid sputum clearance

IV aminophylline

CPAP

Resp stimulant doxapram

Intubate/ ventilate

266
Q

Management of large PE?

A 
O2 if hypoxic
Morphine (w/ antiemetic)
Fondaparinux/ LMWH
Fluids/ vasopressors if hypovolaemic
Consider alteplase
Long term anticoagulation
267
Q

Pt with acute upper GI bleed who is shocked. What drug can you add to management if suspected cause is oesophageal varices? (i.e. in known liver disease)

A

Terlipressin

268
Q

Management of raised ICP?

A

Correct hypotension
Elevate bed head
If intubated, hyperventilate to achieve low CO2 (leads to cerebral vasoconstriction)

Mannitol

If oedematous tumour - dexamethasone

269
Q

In a fitting patient, what is another possible cause other than epilepsy in a female pt?

A

Eclampsia

270
Q

IV lorazepam given to fitting Pt. What SE are you most worried about?
What dose of lorazepam is given?

A

Respiratory arrest

4mg in adults (carefully as some people are more susceptible than others)

271
Q

What is the risk of phenytoin infusion in fitting Pt and when would you not give it?

A

Bradycardia

Bradycardia or heart block

272
Q

What are the causes/ Ddx of status epilepticus?

A 
1st presentation epilepsy/poor compliance with meds
Hypoxia/hypercapnia
Eclampsia (3rd tri)
Excess/withdrawal drugs/alcohol
Metabolic (glucose, uraemia, ^Ca2+, hypoNa)
Vascular (strokes/haemorrhage/trauma)
CNS infection/ lesion
Psychogenic
273
Q

Medical complications of status epilepticus?

A

Neuro: Brain damage, Intracranial HTN

Resp: Hypoxia, Resp acidosis, Aspiration

Cardio: HTN->HypoTN, tachycardia, dysrhythmias

Metabolic: lactic acidosis, hyperpyrexia, hyperglycaemia->hypoglycaemia

Other: rhabdomyolysis, blood leukocytosis

274
Q

What drug would be given in status epilepticus patient?

What drug would be given if haven’t obtained IV access?

A

IV lorazepam (0.1mg/kg) - 4mg usually given for adults

Rectal diazepam

275
Q

Why is lorazepam used in preference to diazepam?

A

Diazepam = less predictable outcome (lipid-soluble)

Lorazepam more CNS-targeted, so less distributed throughout body

276
Q

What is Keppra?

A

Levetiracetam
Used to treat epilepsy
Alternative to phenytoin

277
Q

How does phenytoin work?

A

Sodium channel blocker

278
Q

What key things should you check before giving someone phenytoin?

A

Check not already taking phenytoin

Check not pregnant (teratogenic, esp in 1st tri)

Check HR and BP (pro-arrhythmic - ensure cardiac monitoring in place)

!!allergies!!

279
Q

What could you give a patient who is fitting if they are already on phenytoin?

A

A phenobarbital can be given

280
Q

In a patient with status epilepticus who required RSI, which anaesthetic agent is best and why?

A

Thiopenthal

Has anti-seizure activity

281
Q

ECG criteria for thrombolysis in MI?

A

1) ST elevation >1mm in 2+ consecutive limb (I and aVL or II, III or aVF) leads
or
>2mm in 2+ consecutive chest leads (V1-V4 or V5-V6)

2) Post. elevation MI (ST dep, tall R waves V1-V3)
3) New LBBB

282
Q

Head injury. Primary traumatic brain injury occurs at time of impact. What neurophysiological/ anatomical consequences cause secondary injury mins-days later?

A 
^ICP
Cerebral oedema
Expanding haematomas
Seizures
Infection
283
Q

ABCDE. What aspects should be paid particular attention to in Pt w/ head injury?

A

GCS
Pupils (?PEARL)
C-spine protection
Neuro examination

284
Q

Trauma patient: low BP + inappropriately low pulse rate indicates injury to what aspect and what level of spinal cord?

A

Sympathetic

Cervical

285
Q

Pt w/ head injury and reduced GCS. What imaging should be arranged within 1st hour of injury?

A

CT head

286
Q

Following head injury, what aspects of Pt’s presentation might warrant urgent CT head?

A 
Reduced GCS
Open/ depressed/ basal skull fracture
Focal CNS deficit
Fit (post-injury)
>1 comit

LOC + coagulopathy

287
Q

When would you add C-spine CT to head CT in head injury Pt?

A 
Intubated (?could exacerbate C-spine injury)
GCS <13
Dangerous mechanism of injury
Focal CNS deficit
Upper/lower limb paraesthesia
288
Q

Elderly Pt w/ unwitnessed fall + poor Hx.

Takes warfarin. GCS 15. No focal neuro deficits. What Ix needed?

A

CT head within 1 hour

289
Q

Risk of OCH is higher for patents on warfarin or clopidogrel?

A

Clopidogrel

290
Q

3 aspects of medical management of head injury?

A

Avoid hypoTN (SBP >90)
Don’t overload (cerebral oedema)
Don’t use glucose (damages brain tissue)

Avoid hypoxia/hypercapnia > hypervent

Opiates

Mannitol

IV loraz/buccal midaz for seizure

Raise head

Avoid ^glycaemia and pyrexia

291
Q

ECG changes in PE?

A

Sinus tachycardia = most common

Also new AF
Any sign of R-sided heart strain (RBBB, R-axis deviation)
S1Q3T3
Non-specific ST changes
T wave inversion in chest leads
292
Q

What is thrombophilia?

A

Hereditary/acquired predisposition to clotting

293
Q

What is the most common heritable thrombophilia in Caucasians?

What is the mode of inheritance?

What is the gene mutation?

A

Factor V Leiden

Autosomal Dominant

V:G1691A mutation (gene for clotting factor V)

294
Q

What are the 4 key investigations required in ?pulmonary embolism?

A

ABG (?resp alkalosis, T2 RF)
ECG
CXR (exclude other causes/ wedge-shaped area of infarcted lung in PE)
D-dimer

295
Q

What are the components of ATMIST?

A 
Age
Time of incident/injury
Mechanism of injury
Injuries
Signs
Treatment

Used in handover of trauma patient

296
Q

How do you move a patient with C-spine injury?

A

Log roll

297
Q

Which is preferable for assessing injuries, FAST or WBCT?

A

WBCT - more accurate info and can be treated faster

298
Q

What is the name for the femoral shaft splint used in A+E?

A

Thomas splint

299
Q

RTA patient complains of pain in abdominal LUQ. No guarding/rebound tenderness. Bowel sounds present. What organ could be damaged?

A

Spleen

300
Q

Paracetamol overdose. What is the toxic product of paracetamol metabolism?

What usually renders it harmless?

A

NAPQI

Glutathione

301
Q

Paracetamol overdose. How does Parvolex (NAC) treat an overdose?

A

Analogue of glutathione

Binds to NAPQI

302
Q

Paracetamol overdose. What can be given if acetylcysteine (Parvolex/NAC) is not available, or the patient refuses IV treatment?

A

Methionine PO

303
Q

Paracetamol overdose. What is the criteria for liver transplant after paracetamol overdose?

A

Modified Kings Score

304
Q

Paracetamol overdose. How would you manage a patient who becomes flushed + starts vomiting after NAC administration?

A

1) Stop Rx
2) Treat symptomatically (entiemetic, fluid, antihistamine)
3) Re-start NAC at slower (1/2) rate

305
Q

Paracetamol overdose. How is NAC given? How fast is each bag administered?

A

IV
1st bag - 1hr
2nd bag - 4hrs
3rd bag - 16hrs

306
Q

What is the mnemonic for remembering the Mental State Examination?

A 
ABCDE SHIT
Appearance
Behaviour
Cognition
Delusions
Emotion + Mood

Speech
Hallucinations
Insight
Thoughts

Or ASEPTIC (appearance/behaviour, speech, emotion and mood, perceptions, thoughts, insight, cognition)

307
Q

Paracetamol overdose. What is the key test for liver toxicity?

A

INR or Prothrombin Time

308
Q

What is the difference between a single time point paracetamol overdose and a staggered overdose?

A

Single time point = >4g taken at single defined time point

Staggered = ingestion of 2+ supratherapeutic doses over >8hrs, resulting in cumulative dose of >4g/day

OD is considered staggered if all tablets not taken within 1 hour

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