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Interview Prep > Clinical Interview COPY > Flashcards

Clinical Interview COPY Flashcards

1
Q

Hyperkalaemia?

A

K+ > 5.2
Mild 5.3 - 6.0
Moderate 6.0 - 7.0
Severe > 7.0

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2
Q

ECG changes in hyperkalaemia?

A
  • peaked t-wave
  • flat p-waves
  • PR prolongated
  • Wide QRS
  • Pulled up from the t-wave *
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3
Q

ECG changes in hypokalaemia?

A

t-wave inversion
ST depression
prominent U-waves
pushed down on T-segment

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4
Q

Clinical manifestation of hyperkalaemia? Pathophysiology?

A

Bradycardia, conduction blocks & cardiac arrest.
Suppressed SA node.
Reduced conduction at AVN / His-purkinje

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5
Q

Causes of hyperkalaemia? (6-themes)

A
  • increased intake (oral/IV)
  • increased production [tissue injury -> rhabdo, tumour lysis, burns, ischaemia, comparment syndrome]
  • decreased excretion [renal failure, hypoaldosteronism, obstructive uropathy]
  • transcellular shift [metabolic/resp acidosis, hyperglycaemia]
  • Pseudohyperkalaemia [lab error, haemolysed sample, thrombocytosis]
  • Drugs [aldost inhib; inhibition]
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6
Q

Drug causes of hyperkalaemia?

A
  • ACEi / ARB
  • Heparin, spironoloactone, BBs
  • Digoxin
  • Suxamethonium, phenylephrine
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7
Q

Management of hyperkalaemia?

A
  1. Cardiac stabilisation - calcium chloride/gluconate
  2. ECF -> ICF shift - insulin/dex, salbutamol, bicarb
  3. Removal of K+ - fruse (from urine), resonium (from gut), dialysis (from blood)
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8
Q

Dose of calcium chloride/gluconate?

A

10mls of 10%

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9
Q

Dose of insulin-dex for HyperK+?

A

10 units insulin 50g dextrose, IV over 20-30mins

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10
Q

Hypokalaemiea?

A

Mild 3.0-3.5
Mod 2.5-3.0
Severe <2.5

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11
Q

Causes of hypokalaemiea?

A
  1. decreased intake
  2. Mg depletion -> renal potassium loss
  3. Mineralocorticoid excess [cushing’s, addison’s, HTN, renin, barters]
  4. Increased loss [drugs, burns, GI, renal, endocrine, dialysis]
  5. Transcellular shift [insulin-dex, beta-agonists, alkalosis]
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12
Q

Mx of hypokalaemia?

A
  • non-acute = 10-20mmol/hr
  • acute (life threatening arrhythmia) = 20mmol in 10mins
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13
Q

Status epilepticus?

A
  1. continuous seizure > 5 minutes
  2. recurrent seizures without neurological recovery
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14
Q

Causes of status epilepticus?

A

epilepsy
infective
hypoxic
vascular
metabolic
physical (hyperthermia)
drug induced / withdrawal

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15
Q

Ix in status epilepticus?

A
  • bedside [BM, VBG/lactate]
  • laboratory [UEs, toxins, TFTs, LP]
  • imaging [CT / MRI brain]
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16
Q

Mx of status epileptics?

A

1st. Bolus benzodiazepines (IV, IM, buccal, PR)
2nd. Typically requires I+V
- phenytoin, valproic acid, levetiracetam
3rd. Refractory status
- propofol, midazolam, barbituates
4th. thiopentone, volatile, ketamine, lignocaine
Monitor EEG
Generally require HDU/ICU + neurology consult

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17
Q

Principles of mx of status?

A

Resuscitation, maintain CPP
Terminate seizure
Decrease cerebral metabolic rate
Diagnose + treat cause
Treat copmlications

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18
Q

Complications of status epilepticus?

A
  • aspiration
  • neurogenic pulm oedema
  • rhabdomyolysis
  • hyperthermia
  • trauma (HI, post shoulder dislocation)
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19
Q

DKA?

A

Life threatening complication of DM - insulin deficiency

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20
Q

Diagnostic criteria for DKA?

A
  1. pH < 7.3
  2. Ketosis (ketonaemia/ketonuria)
  3. HCO3 < 15
  4. Hyperglycaemia - may be mild/euglycaemic
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21
Q

Pathogenesis of DKA?

A
  • increased glucagon, cortisol, catecholamines, GH
  • decreased insulin
    —> hyperglycamiea -> hyperosmolality -> electrolye lost -> ketone production from metabolism of triglycerides -> acidosis
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22
Q

Goals of mx DKA?

A
  • establish precipitant + treat
  • assess degree of metabolic derangement
  • fluid resuscitation
  • insulin provision
  • electrolyt replacement
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23
Q

Mx of DKA?

A

-insulin infusion 0.1u/kg/hr
- balanced salt solution fluid resuscitation
- when glucose<15 -> dextrose 5% 100mls/hr
- monitor ketones
- monitor pH
– LOCAL GUIDELINES

Find cause + treat - e.g. infection [cultures, CXR, CT-A/P, bloods etc]

Continue background insulin

Early escalation to medical team/DM, ITU

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24
Q

Classification of tachycardia?

A
  1. regular vs irregular
  2. narrow vs wide complex
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25
Q

Types of regular narrow complex tachycardia?

A
  • sinus tachy
  • atrial tachy
  • atrial flutter
  • SVT
  • AVNRT
  • Narrow complex VT
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26
Q

Types of irregular narrow complex tachycardia?

A
  • AF
  • Atrial flutter w/ variable blcok
  • Multifocal atrial tachy
  • Digoxin toxicity
  • Tachycardia w/ premarture
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27
Q

Types of regular wide complex tachycardia?

A
  • Monomorphic VT
  • Ventricular flutter
  • Hyperkalaemia
  • Ischaemia
  • Regular tachycardia w/ BBB
  • Sodium channel blocker toxicity (e.g. TCA, cocaine)
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28
Q

Types of irregular wide complex tachycardia?

A
  • TdP
  • Irregular VT
  • VF
  • Irreg tachy w/ BBB
  • AF w/ pre-excitation syndrome
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29
Q

Causes of tachycardia?

A
  • Cardiac dysrhytmia
  • Non-cardiac
    – Electrolyte imbalance (hypoK/Mg)
    – Fever/sepsis
    – HyperThy
    – Ischaemia
    – Pain
    – Poisoning
    – PE
    – Resp diseases (CAP, PTx)
    – Shock
    – Trauma
    – Withdrawal
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30
Q

Management of narrow complex tachycardia?

A
  1. vagal manoeuvre
  2. adenosine 6mg-12mg-18mg IV
  3. cardioversion
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31
Q

Life-threatening features in tachycardia? (clinically unstable)

A
  • Shock
  • Syncope
  • MI
  • Severe heart failure
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32
Q

If life-threatening features in tachycardia what is management?

A
  • Synchronised DC shock up to x3 attempts
    – Under sedation
  • If unsuccessful - amiodarone 300mg IV over 10-20mins
  • Rpt DCCV
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33
Q

Mx of VT?

A
  1. amiodarone 300mg IV over 10-60mins
  2. DC cardioversion
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34
Q

What is Torsades de pointes?

A
  • polymorphic VT due to prolonged QTc interval
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35
Q

Mx of unstable TdP?

A

Synchronised DC cardioversion

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36
Q

Mx of stable TdP?

A

IV Mg
Stop causative drugs
Treat other QT prolonging factors - e.g. hypokalaemia

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37
Q

Approach to arrhythmias?

A
  • fast or slow
  • ventricular / SVT
  • compromised?
  • does it need management
  • underlying cause? trigger?
  • will it recur?
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38
Q

Narrow regular bradycardias?

A
  • sinus
  • junctional
  • complete AV block
  • Atrial flutter with block
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39
Q

Narrow irregular bradycardias?

A
  • sinus arrhythmia
  • AF with SVR
  • Second degree AV block
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40
Q

Wide complex regular bradycardias?

A
  • idioventricular rhythm
  • complete AV bock
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41
Q

Wide complex irreg bradycardias?

A
  • irreg brady w/ BBB
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42
Q

Mx of bradycardia with adverse features?

A
  • Atropine 500mcg IV
    – repeat up to max of 3mg
  • Alternate drugs (isoprenaline, adrenaline)
  • Transcutaenous pacing
  • Transvenous pacing - expert help
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43
Q

Life threatening signs of bradycardia?

A
  • shock
  • syncope
  • MI
  • HF
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44
Q

Reversible causes of arrest?

A

Hypoxia, hypovolaemia (think bleeding in post-op/trauma), hyperkalaemia, hypothermia
Tamponade, tension, thrombus (PE/MI), toxin

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45
Q

Shockable vs non-shockable rhythms?

A

Shockable = VF, pulseless VT
Non-shockable = asystole, PEA

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46
Q

Principles of arrest care?

A
  • Get help! 2222
  • High quality chest compression w/ minimal interruptions
  • Early defib
  • Basic airway –> ?intubation + ventilation
  • Adrenaline
  • POCUS for diagnosis
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47
Q

How to deliver a shock?

A
  • Chest compressions ongoing
  • Pause for 5s for rhythm recognition
  • If shockable, continue compressions, charge, then all hands off + O2 mask removed from patient to deliver shock
  • Immediately resume CPR - only stop if clinical + physiological signs of ROSC
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48
Q

Shockable algorithm?

A
  • VF / pVT
  • 2min cycles of chest compressions
  • Up to 3 shocks
  • Then adrenaline 1mg IV/IO every 3-5mins
  • Amiodarone 300mg IV/IO after shocks
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49
Q

Signs of peri-arrest in arrhythmia?

A
  • Shock (SBP<90) + increased sympathetic activity
  • Syncope
  • HF (pulm oedema (L), raised JVP (R))
  • MI
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50
Q

Indications for cardiac pacing?

A

Unstable, symptomatic bradycardia refractory to drug therapy

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51
Q

Causes of pancreatitis?

A

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpions
Hypercalcamiea
ERCP
Drugs [NSAID, thiazides, azathioprine]

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52
Q

Glasgow-Imrie score?

A

PaO2 < 8
Age > 55
Neutrophils > 15
Calcium < 2
Renal function [Ur>16]
Enzymes [LDH>600 / AST > 2000]
Albumin < 32
Sugar [BM > 10]

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53
Q

Presentation of pancreatitis?

A

Severe abdominal pain, radiating to back.
N&V
Anorexia

Often presence of risk factors [gallstones, EtOH, recent ERCP, hypertriglyceridemia]

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54
Q

Signs of pancreatitis?

A

Tender epigastrium +/- guarding
Cullen’s / Grey-Turner’s

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55
Q

Mx of pancreatitis?

A
  • Supportive [fluid resuscitation, analgesia, anti-emetic. Nutrition]
  • Risk stratification [Glasgow-Imrie score OA + 48hrs]
    –> Escalation to ITU if severe
  • Surgical - ERCP/lap chole
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56
Q

Complications of pancreatitis?

A

Local [pseudocyst, pancreatic necrosis]
Systemic [SIRS, ARDS, AKI, multi-organ failure, death]

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57
Q

DDx RUQ pain?

A
  • GI [PUD, cholecystitis, appendicitis, hepatitis]
  • Urinary [pyelonephritis]
  • Resp [pneumonia]
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58
Q

DDx epigastric pain?

A
  • GI [PUD, cholecystitis, oesophagitis/perf]
  • Cardiac [MI]
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59
Q

DDx LUQ pain?

A
  • GI [PUD, perforation, splenic rupture]
  • Urinary [Pyelonephritis]
  • Resp [pneumonia]
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60
Q

DDx RLQ pain?

A
  • GI [appendicitis, crohn’s, perforation]
  • Gynae [ovarian torsion/abscess; ectopic]
  • Urinary [calculus, pyelo]
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61
Q

DDx LLQ pain?

A
  • GI [diverticulitis, hernia, perforation, UC]
  • Gynae [ovarian, ectopic
  • Urinary [calculus, pyelo]
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62
Q

What is compartment syndrome?

A
  • Limb threatening condition caused by raised pressure within a fascial compartment
  • Causes compression of blood vessels, muscles and nerves within the compartment
    –> irreversible muscle & nerve damage
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63
Q

Presentation of compartment syndrome?
Caused by?

A
  • pain out of proportion
  • 6Ps
  • Caused by:
    – Trauma [fracture, crush injury, burns]
    – External compression [casts, dressings]
    – Bleeding disorder
    – Reperfusion injury [tourniquests; thrombectomy]
    – Extravasation
    – Arterial injury
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64
Q

Signs of compartment syndrome?

A
  • pain with passive stretch
  • paraesthesia
  • tense compartment (woody)
  • paralysis
  • pulseless
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65
Q

Common locations of CS?

A
  • forearm (esp volar)
  • lower leg (esp anterior) - tibial shaft
  • thigh
  • upper arm
  • hand
  • foot
  • back
  • abdomen
  • buttocks
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66
Q

Ix in compartment syndrome?

A
  • XR (?fracture)
  • Bloods (FBC, UE, CK, G&S)
  • Compartment pressure measurement
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67
Q

Mx of compartment syndrome?

A
  • IV access [fluid, analgesia, anti-emetic]
  • Relieve pressure
  • Reduce + splint any fractures
  • Urgent referral to ortho/plastics
    –> fasciotomy
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68
Q

Complications of compartment syndrome?

A
  • Local [gangrene, loss of limb, muscle contracture]
  • Systemic [rhabdomyolysis, renal failure]
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69
Q

Abdominal compartment syndrome?

A
  • intra-abdominal hypertension with new organ failure
    –> compression, thrombosis. Renal failure. Decreased tidal volumes. Decreased CO
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70
Q

Management of abdominal compartment syndrome?

A
  • Monitor IAP
  • Improve compliance - sedation, analgesia, neuromuscular block
  • NG tube, rectal decompression, enemas
  • Correct positive fluid balance
  • Organ support

+/- surgery - decompression with delayed closure

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71
Q

What is anaphylaxis?

A

Severe, life-threatening, systemic hypersensitivity reaction

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72
Q

Characteristics of anaphylaxis?

A

Rapidly developing airway, breathing and circulation problems associated with skin + mucosal changes

  • Pharyngeal/laryngeal oedema
  • Bronchospasm / tachypnoea
  • Hypotension / tachycardia
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73
Q

Causes of anaphylaxis?

A
  • Allergens (insect stings, nuts, eggs, dairy, fruit)
  • Medications (abx, NSAIDs, contrast)
  • Unidentified
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74
Q

DDx of anaphylaxis? (conditions which mimic anaphylaxis)

A
  • Urticaria
  • Angioedema
  • Dystonic reactions
  • Carcionoid
  • Red-man syndrome (Vanc)
  • Acute resp distress
  • Shock
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75
Q

Pathophysiology of anaphylaxis?

A
  • IgE mediated hypersensitivity
  • Profound histamine and serotonin release from basophils / mast cell degranulation
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76
Q

Symptoms of anaphylaxis?

A
  • angioedema
  • stridor
  • resp distress
  • bronchospasm
  • hypotension / collapse
  • abdo cramps
  • diarrhoea
  • flushing
  • urticaria
  • coagulopathy
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77
Q

Ix in anaphylaxis?

A
  • Clinical diagnosis, but investigations can help in longterm managment
    – tryptase, RAST, CAP, skin testing
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78
Q

Mx of anaphyalxis?

A
  • Stop trigger. Get help.
  • Supine. 100% O2
  • Adrenaline 0.5mg IM (rpt every 5 mins)
  • IV access + fluid boluses
  • Hydrocortisone IV
  • If persistent hypotension after x2 adrenaline -> infusino
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79
Q

Mx of anaphylactic cardiac arrest?

A
  • Extended CPR
  • Raise legs
  • 2L IV fluids stat
  • Increasing adrenaline
  • H1/H2 antagonist
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80
Q

Mx of persistent bronchospasm / angioedema in anaphylaxis?

A
  • Bronchospasm [as per asthma emergency]
  • Angioedmea [nebulised adrenaline; ETT; cricothyrdoiotomy/tracheostomy]
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81
Q

What are biphasic reactions?

A
  • Recurrence of anaphylaxis symptoms soon after the initial episode
  • may occur >24 hrs after initial episode, usually less severe
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82
Q

Risk factors for biphasic anaphylaxis reactions?

A
  • delayed adrenaline
  • slow response to adrenaline
  • repeated doses of adrenaline
83
Q

Does of adrenaline in anaphylaxis in kids?

A
  • IM adrenaline 1:1000 (1mg/mL) 0.01mg/kg
  • Repeat every 3-5mins
84
Q

What is sepsis?

A
  • Life threatening organ dysfunction due to dysregulated host response to infection
    – qSOFA (sequential organ failure assessment) ‘HAT’
    — Hypotension
    — Altered mental status
    — Tachypnoea
85
Q

Septic shock?

A
  • Sepsis +
    – Persistent hypotension - requiring vasopressors
    – Lactate >=2
86
Q

Criteria for SIRS?

A
  • Systemic inflam response syndrome
  • > =2 of the following
    T >38 or <36
    HR>90
    RR>20 / PaCO2 < 32mmHg
    WCC>12

Sepsis = SIRS + confirmed infection

87
Q

Mx of sepsis?

A
  • Resuscitation
  • Sepsis 6 (Lactate, BCs, UO; abx, IVI, O2)
  • Source control
  • IVI. +/- vasopressors
88
Q

Causes of APH? Features?

A
  • Abruption - bleeding, painless
  • Praevia - small bleeds, painless
  • Uterine rupture - painful, fetal distress, no UO
89
Q

Causes of PPH?

A
  • Uterine atony - assos w/ multiples, prolonged labour, polyhydramnios
  • Retained PoC / placenta
  • Genital tract trauma
  • Uterine inversion
  • Ac-/In-/Per- Creta
90
Q

Causes of haemorrhage in pregnancy? (Ts)

A
  • Tone
  • Trauma
  • Tissue
  • Thrombin
91
Q

Management of haemorrhage in pregnancy?

A
  • MDT [obstetrics, haematology, radiology, GenSurg, blood bank; neonatologist; ODPs/orderlies]
  • Left lateral tilt
  • CTG
  • O2
  • IV fluids +/- O- blood (6 Units)
  • Warming
  • Correct coagulopathy (TXA, RBCs, FFP, Cryo, Platelets)
  • Uterotonics [bimanual copmression; syntocinon; ergometrine; carboprost]
  • Surgery [embolistaion; clamp iliacs; caesarian hysterectomy]
92
Q

Mx of Obstetric arrest?

A
  • Left lateral position / manual displacement of uterus (relieves aortocaval compression)
  • O2, IV access, fluids etc
  • Algorithm is the same as non-pregnant women (DCCV & drug doses the same)
  • If no response at 4 minutes -> peri-mortem CS
93
Q

DDx of maternal collapse?

A
  • Anaphylaxis
  • PE
  • Amniotic fluid embolus [collapse during labour]
  • APH (abruption, praevia, rupture, ectopic)
  • Eclampsia
  • Intracranial haemorrhage
94
Q

ROTEM?

A

Rotational thromboelastography
- gives information about bloods ability to clot

(rather than individual components values)

95
Q

What types of analgesia are there?

A

Huge variety. Different classes, different routes. depending on patient situation - acute / chronic; duration required

  • Simple (paracetamol. COX-inhibitors: aspirin, diclofenac, ibuprofen, parecoxib)
  • Weak opiate (codeine, dihydro-, tramadol)
  • Strong opiate (morphine, fentanyl)
  • Neuropathic (amitriptyline,
  • Sedative (ketamine)
  • Inhaled (NO2, penthrox)
  • Regional (local anaesthetics; regional)
  • Spinal (opiates/ anaesthetics)

– Given by doctors/nurses (PO, IV, SC)
– Patient administered (PCA, PCEA)

96
Q

What is adrenal crisis?

A
  • Acute deterioration with hypotension, resolving with IV steroid
  • Chronic adrenal insufficiency + trigger
    OR
  • Acute adrenal sufficiency
97
Q

Causes of chronic adrenal insufficiency?

A
  • Chronic steroid therapy
  • Chronic adrenal grand dysfunction (Addison’s, malignancy, infection)
  • Chronic anterior pituitary dysfunction (granulomatous disease [TB/sarcoid], neoplasm, iatrogenic)
98
Q

Acute stressors precipitating adrenal crisis?

A
  • Infection [especially gastro]
  • Trauma/surgery
  • Reduced steroid dose [non-adherent, tapering]
  • Stress
  • Pregnancy
  • Drugs
99
Q

Causes of acute hypothalamic-pituitary-adrenal axis? (Rare)

A

Pituitary failure
- Pituitary apoplexy [post-partum / adenoma]
- Complication of neurosurgery

Adrenal gland failure
- Waterhouse-Friedrichsen [adrenal infarction due to DIC]
- Checkpoint-inhibitor immunotherapy

100
Q

Signs & symptoms of adrenal crisis?

A
  • Hypotension, vasodilatory shock
  • Fever
  • Nausea/vomiting
  • Abdo pain + tenderness
    – Can mimic abdominal sepsis/pancreatitis
  • Delirium
  • Features of trigger [trauma/surgery/infection]
101
Q

Signs in chronic adrenal insufficiency?

A
  • Hyperpigmentation
  • Vitiligo
  • Chronic fatigue
  • Anorexia
  • Vomiting
  • Weight loss
102
Q

Mineralocorticoid deficiency leads to..?

A

Occurs in primary adrenal insufficiency (Addisons)
- Hyperkalaemia
- Non-anion gap metabolic acidosis

103
Q

Glucocorticoid deficiency leads to..?

A
  • Hyponatraemia
  • Hypoglycaemia
104
Q

Renin-angiotensin-aldosterone axis?

A
  • Renin released due to high K+
  • Catalyzes production of angiotensin
  • Angiotensin stimulates adrenals to secrete aldosterone
  • Aldosterone signals kidney to excrete potassium
105
Q

Diagnosing adrenal insufficiency?

A
  • Random cortisol
  • ACTH stimulation test (synacthen)
106
Q

Mx of adrenal crisis?

A
  • Treat trigger
  • IV Hydrocortisone 100mg stat
    – 50mg IV Hydrocortisone QDS
  • Resuscitation with fluid +/- vasopressors
107
Q

Prevention of adrenal crisis?

A
  • Maintenance steroids (hydrocortisone, fludrocortisone)
  • Sick day rules (double dose)
  • Severe stress (major surgery, severe infection) - 50mg IV Hydrocortisone QDS
108
Q

Pathophysiology of adrenal crisis?

A
  • Cortisol and aldosterone deficiency
    – Aldosterone deficiency -> Na wasting; retentino of K+ & H+ -> Hypotension, hyperkalaemia, metabolic acidosis (non-anion-gap)
    – Cortisol deficiency -> increased inflam cytokines, vasodilation, hypoglycaemia, decreased fatty acids
109
Q

What does adrenal gland produce?

A
  • Zona Glomerulosa -> mineralocorticoids -> aldosterone
  • Zona Fasciculata -> glucocorticoids -> cortisol
  • Zona Reticularis -> sex steroids -> testosterone
  • Adrenal medulla -> catecholamines -> adrenaline
110
Q

Effects of cortisol?

A

– Released in response to ACTH
- Suppress inflammation (cytokines)
- Vasoconstriction (w/ catecholamines)
- Catabolism (gluconeogenesis, production of free fatty acids & amino acids)

111
Q

Mx of STEMI?

A
  • Monitored resus bed
  • IV access, bloods, ECG
  • O2 >93%
  • Analgesia (IV morphine titrated to effect) + antiemetic
  • GTN, anti-platelet (aspirin 300mg + ticagrelor 180mg)
  • Reperfusion strategy: PCI vs thrombolysis
  • PPCI within 2 hours of medical contact
  • Secondary prevention
112
Q

When to use fibrinolysis in STEMI?

A
  • <12 hours of symptoms
  • PCI not possible in 2 hours
113
Q

Mx of NSTEMI?

A
  • Monitored resus bed
  • IV access, bloods, ECG
  • O2 > 93% (or if pt shocked)
  • Analgesia titrated to effect; + antiemetic
  • GTN, DAPT (aspirin 300, ticagrelor 180); anticoagulation (fonda)
114
Q

Mx of acute asthma?

A
  • O2 > 92%
  • Beta-agonist - salbutamol neb/MDI/IV
  • Anticholinergic - ipratropium neb
  • Corticosteroids - HC / pred
  • Aminophyline

+/- adrenaline, Mg

115
Q

Markers of severe asthma?

A
  • Accessory muscle use
  • HR > 110
  • RR 25-30
  • PEFR < 50%
  • SpO2 < 92%
116
Q

Markers of imminent resp arrest in acute asthma?

A
  • Altered mental status
  • Paradoxical respiration
  • Bradycardia
  • Silent chest
  • High pCO2 on ABG
117
Q

Causes of pulmonary oedema?

A
  • Cardiogenic
    – acute heart failure, MI,
  • Non-cardiogenic
    – ARDS, reperfusion, neurogenic, transfusion reaction (TRALI), allergic alveolitis, HAPE, contusion
118
Q

Problems with ventilation in acute asthma?

A
  • Breath stacking (dynamic hyperinflation)
    – Barotrauma -> PTx
    – Increased intrathoracic pressure -> obstructive shock -> arrest
119
Q

Emergency mx of acute cardiogenic pulmonary oedema?

A
  • A - positioning
  • B - High flow O2, consider early CPAP
  • C - nitrates, furosmide
  • D - morphine
  • E - positionging
120
Q

Presentation of acute pulmonary oedema?

A
  • Breathless, sweaty, agitated

+/- precipitating event (cardiac ischaemia, MVR, arrhythmia, sepsis)

121
Q

Define anaphylaxis?

A

Life threatening generalised hypersensitivity reaction

122
Q

Characteristics of anaphylaxis?

A

Life threatening, rapidly developing A/B/C problems.
Usually associated with mucosal/skin change

123
Q

Mx of anaphylaxis?

A
  • STOP trigger
  • Call for help
  • O2 15L NRB
  • Adrenaline 0.5mg IM, repeat at 2 mins, onto infusion if no improvement
  • Fluids
  • Consider steroid / antihistamine
124
Q

Classification of hyponatraemia?
Brief explaination?

A
  • Hypovolaemic (Na loss > water loss)
  • Normovolaemic
  • Hypervolaemic (increased TBW relative to Na -> oedematous)
  • Pseudohyponatraemia [hyperglycaemia; hyperlipidaemia; hyperproteinaemia]
125
Q

Causes of hypovolaemic hyponatraemia?

A
  • Renal (urine Na > 20)
    – Addisions; CKD; RTA; diuretics; cerebral salt wasting
  • Extra-renal (urine Na < 20)
    – 3rd space losses [burns; pancreatitis; SBO; cirrhosis]; sweating/D&V with continued water intake
126
Q

Causes of euvolaemic hyponatraemia?

A
  • SIADH (Urine Osm > Serum Osm)
  • Exercise
  • Iatrogenic
  • Amphetamines
  • Tea & toast diet
  • polydipsia (water/beer)
127
Q

Causes of hypervolaemic hyponatraemia?

A
  • Renal failure
  • Heart failure
  • Cirrhosis
  • Nephrotic syndrome
  • Hepato-renal syndrome
128
Q

Causes of SIADH?

A

Malignancy [SCLC]
ADH secretion
Drugs [SSRI, carbamaz, amitrip]
CNS disease [meningitis, SAH]
Hormone deficiency [Thyroid/ Addisions]
Other
Pulmonary

129
Q

Mx of Hyponatraemia?

A

ASYMPTOMATIC
- SLOW correction
- Water restriction
- Demeclocycline

SYMPTOMATIC
- Hypertonic saline

130
Q

Complications of hyponatraemia?

A
  • Cerebral oedema
  • ECG changes
  • Pontine myelinolysis in overcorrection
131
Q

What is necrotising fasciitis?

A
  • Severe rapidly progressing bacterial soft tissue infection of subcut tissues + fascia
132
Q

Causative organisms of Nec Fasc?

A
  • Strep (grp A)
  • Staph aureus
  • Clost. pefringes
  • Vibrio vulficians
133
Q

Risk factors for Nec Fasc?

A
  • DM
  • EtOH
  • PVD
  • Renal failure
  • Malignancy
  • Skin trauma including surgery
134
Q

Symptoms/signs of Nec Fasc?

A
  • Rapid spreading cellulitis
  • Sepsis + haemodynamic instability
  • Pain out of proportion
  • Erythema -> tense swelling -> dark blisters -> gangrene
  • Crepitus
    – Rapid spread
135
Q

Investigations in Nec Fasc?

A
  • Do not delay surgical intervention!
  • Bloods [cultures; full panel; CRP; CK]
  • Imaging [XR/CT/MRI will reveal subcut gas]
136
Q

Management of Nec Fasc?

A
  • Supportive resuscitation
  • Extensive surgical debridement
  • Broad spec abx as per local guidelines
  • Often require ITU post-op +/- hyperbaric O2
137
Q

What is in a massive transfusion pack?

A
  • Packed RBCs
  • Platelets
  • Fresh frozen plasma

Ratio of 2:1:1

138
Q

5 commonest causes of critical bleeding?

A
  • Trauma
  • GI haemorrhage
  • Ruptured AAA
  • Obstetric haemorrhage
  • Surgical
139
Q

What is trauma’s lethal triad?

A

In the context of bleeding
- Hypothermia
- Coagulopathy
- Acidosis

140
Q

How does Tranexamic Acid work?

A
  • Antifibrinolytic; competitively inhibits plasminogen -> plasmin
141
Q

What are recommendations for TXA in trauma?

A

CRASH2 trial showed improved survival in trauma patients given TXA
1g loading dose, 1g infusion

142
Q

What is damage control surgery in trauma?

A

Damage control surgery = abandonment of definitive surgery, rapid haemostasis, packing and closure -> transfer to ICU for warming, correction of coagulopathy and inotropes -> definitive treatment undertaken later

  • Used when ongoing bleeding after 10 U RBC; pH<7.2 / T<35
143
Q

MDT involved in Obstetric haemorrhage?

A
  • Anaesthetics + ODP
  • Obstetrics
  • Haematology / blood bank
  • Radiology
  • GenSurg/Urology
  • Neonatologists
  • Orderlies
144
Q

Causes of major haemorrhage in trauma?

A
  • Blunt vs penetrating trauma
  • Chest
  • Abdomen
  • Pelvis
  • Long bones
  • Retroperitoneum
145
Q

Define critical bleeding?

A

Major haemorrhage that is life threatening and likely to require massive transfusion.

OR smaller volume of bleeding into critical area/organ - intra-cranial, spinal or occular

146
Q

Goals of management of major trauma?

A
  • Find the bleeding + stop the bleeding
  • Rapidly restore blood volume
  • Maintain blood composition (and so function)
  • Avoid hypothermia
147
Q

What is Rhesus disease?

A
  • Rh(-) mother exposed to Rh(+) blood will produce Anti-D antibody which can cross placenta and cause abortion of a Rh(+) foetus
  • can occur with: incompatible blood or foetal-maternal haemorrhage
148
Q

What are transfusion reactions?

A

Adverse event associated with transfusion of blood products. Can be classified as: acute (<24hrs) or delayed (>24hrs); and as immunological or non-immunological

149
Q

Acute, immunological transfusion reactions?

A
  • ABO incompatibility
  • Haemolytic
  • Febrile
  • Urticaria
  • Anaphylaxis
  • TRALI
150
Q

Pathophysiology of Transfusion Related Acute Lung Injury?

A

TRALI -> activated pulmonary neutrophils leads to non-cardiogenic pulmonary oedema; fever & shock

151
Q

Symptoms of ABO incompatibility?

A
  • chest pain, jaundice, shock, DIC
  • rapid intravascular haemolysis
152
Q

Acute, non-immunological transfusion reactions?

A
  • TACO
  • Sepsis
153
Q

Pathophysiology of TACO?

A
  • Increased intravascular volume -> pulmonary oedema
154
Q

Define massive transfusion?

A
  • > half of circulating volume in 4 hours
  • Whole circulating volume in 24 hours

(Circulating vol is approx 70mls/kg)

155
Q

Complications of massive transfusions?

A
  • Air embolism
  • Hypothermia
  • Hypocalcaemia
  • Citrate toxicity
  • Lactic acidosis
156
Q

How is blood stored?

A
  • Fridge approx 4’C
  • Solution: saline, adenine, glucose, mannitol
  • Citrate
    – Binds Ca++ preventing clotting
157
Q

Treatment for tension pneumothorax?

A

Life threatening emergency.
- O2 (15L NRB)
- Urgent needle decompression -> cannula, 2nd intercostal space in mid-clavicular line
- Progress to chest drain

158
Q

What is a pneumothorax?

A

Air in the pleural cavity

159
Q

Types & causes of pneumothorax?

A
  • Spontaneous
    – Primary (thin, smoker)
    – Secondary to Resp disease (COPD, bullae)
  • Traumatic
    – Blunt
    – Penetrating
  • Iatrogenic
    – Ventilation - barotrauma
    – CPR
    – CVC
160
Q

Treatments for recurrent pneumothoraces?

A
  • Pleurodesis
  • Surgery (thoracostomy, pleurectomy)
161
Q

Contraindication to pleurodesis? Why?

A
  • Cystic Fibrosis
  • May require lung transplant in future, pleurodesis makes this complicated/impossible
162
Q

What is asthma?

A

Chronic, reversible airway inflammation / obstruction due to bronchoconstriction.
Sensitivity to variety of stimuli.

Extrinsic - allergic
Intrinsic - non-allergic

163
Q

Pathophysiology behind acute asthma attack?

A
  • Early = bronchospasm
  • Later = airway oedema and mucus
164
Q

Indications for intubation in acute asthma?

A
  • Hypoxia (PaO2 < 8)
  • Hypercapnia (PaCO2 > 6)
  • Drowsiness/tiring
165
Q

When to refer acute asthma to ITU?

A
  • Early!
  • Acute severe / life-threatening, failing to respond to therapy
    – i.e [reduced PEFR; persistent/worsening hypoxia; hypercapnia; acidosis; exhaustion; drowsiness]
  • Have a high index of suspicion if prev ITU admissions
166
Q

Management of acute asthma?

A
  • A-E
  • Risk stratify mild / mod / severe / life-threatening
  • Neb salbutamol
  • PO/IV steroid
  • Neb ipratropium
  • IV salbutamol
  • IV Mg
  • Regular ABG monitoring + early escalation to critical care
167
Q

Management of chronic asthma?

A

1) B agonist
2) + ICS
3) + LABA
4) + LTRA
5) Daily steroid

168
Q

What is shock?

A
  • Life threatening state of cellular + tissue hypoxia most commonly occurring due to circulatory failure
  • If untreated -> organ dysfunction + death
169
Q

Types of shock?

A

CHODE
- Cardiogenic
- Hypovolaemic
- Obstructive
- Distributive (due to vasodilation eg sepsis)
- Endocrine

170
Q

Causes of acute renal failure?

A
  • Pre-renal: hypovolaemia; sepsis; low CO
  • Renal: ATN; hypoxia/hypoperfusion; toxin/drugs; abdominal compartment syndrome; hepatorenal syndrome
  • Post-renal: obstructive uropathy
171
Q

Signs of shock?

A
  • Drowsiness
  • Reduced cap refil
  • Oliguria
  • Hyperlactaemia
172
Q

Causes of cardiogenic shock?

A
  • Impaired contractility (MI, cardiomyopathy)
  • Dysrhythmia
  • Valvular dysfunction
  • Left ventricular outflow obstruction
173
Q

Causes of obstructive shock?

A
  • Intravascular: PE, other emboli (Eg air)
  • Extravascular: tamponade, tension PTx, hyperinflation (severe asthma), abdominal compartment syndrome,
174
Q

Causes of hypovolaemic shock?

A
  • Haemorrhage.
    — Traumatic
    — Non-traumatic (GI bleed, obstetric, epistaxis, coagulopathy)
  • Fluid loss
    — DKA
    — Burns
    — 3rd space (pancreatitis, burns, anaphylaxis)
    — Iatrogenic
175
Q

Causes of distributive shock?

A
  • Neurogenic
  • Liver failure
  • Adrenal insufficiency
  • Anaphylaxis
  • Sepsis
  • Drugs
176
Q

Endocrine causes of shock?

A
  • Adrenal insufficiency
  • ## Hypothyroid
177
Q

Uterotonic management options?

A
  • Bimanual compression
  • Syntocinon
  • Ergometrine
  • Carboprost
178
Q

Causes of venous thromboembolism?

A

Virchow’s triad
- Circulatory stasis
- Vessel wall injury
- Hypercoagulable state

179
Q

Risk factors for VTE?

A

Primary
- coagulant deficiency
- Factor V Leiden

Secondary
- immobility, surgery, malignancy, smoking, pregnancy, COCP

180
Q

ECG findings in right ventricular strain?

A
  • T-wave inversion in II, III, aVF, V1-V4
181
Q

Treatment options for PE?

A
  • LMWH
  • Thrombolysis if clinically massive PE + haemodynamic compromise
  • IVC filter if anti-coag contraindiciated
182
Q

Causes of cirrhosis?

A
  • Alcohol
  • NAFLD
  • Congenital: haemochromatosis, wilson’s
  • Autoimmune: PBC/PSC, hepatitis
183
Q

Causes of ascites?

A
  • Portal HTN
  • CCF
  • Intra-abdominal malignancy
184
Q

Causes of abdominal distension?

A
  • Fat
  • Fluid
  • Faeces
  • Flatus
  • Foetus
185
Q

Complications of cirrhosis?

A
  • Portal HTN
  • Varices
  • Coagulopathy
  • Encephalopathy
  • Hepatorenal syndrome
  • HCC
186
Q

ECG changes in Tricyclic Antidepressant overdose?

A
  • QRS prolongation
  • Right axis deviation of terminal QRS

– often also tachycardia, RBBB

187
Q

Presentation of TCA overdose?

A
  • CNS: agitation, seizures, coma
  • CVS: tachycardia, broad complex tacyhydysrhhythmia
  • Anticholinergic:
188
Q

Treatment of TCA overdose?

A
  • Intubation + ventilation - hyperventilation for pH > 7.5
  • IV Sodium Bicarbonate
  • IV fluids
  • ITU
189
Q

Patholophysiology of TCA overdose?

A
  • Blocks fast Na+ channels (most common in right heart)
  • Anti-cholinergic
190
Q

Antibiotic use in neutropenic sepsis?

A
  • Broad spectrum (Gent / Pip/Taz)
  • If abdominal source + metronidazole
  • If MSRA+ -> + vancomycin
  • If failure to improve -> + anti-fungal
  • Remove indwelling lines
  • Reverse barrier nurse in side room
191
Q

Causes of hypercalcaemia?

A
  • Hyperparathyroid
  • Malignancy (lysis of bone or PTHrP)
  • Drugs (thiazide)
  • Hyperthyroidism
  • Addison’s
  • Sarcoid
192
Q

Symptoms of hypercalcaemia?

A
  • Bone pain
  • Depression
  • Abdominal pain
  • Renal stones
193
Q

Symptoms/signs of hypocalcaemia?

A
  • Tingling
  • Cramps
  • Chvostek (tap -> mouth twitch)
  • Trousseau’s (carpopedal spasm with BP cuff)
  • Hyperreflexia
  • Seizure
194
Q

Calcium regulation?

A
  • PTH
  • Calcitonin
  • VItamin D
195
Q

what is myeloma?

A
  • Haematological cancer
  • Proliferation of plasma cells
  • Treatable but not curable
196
Q

Complications of sickle cell disease?

A
  • Vaso-occlusive crisis
  • Aplastic crisis
  • Sequestration crisis
  • Haemolytic crisis
197
Q

Pathophysiology of vaso-occlusive crisis in sickle cell disease?

A
  • Sickle-shaped RBCs obstruct capillaries and restrict blood flow –> ischaemia, pain, necrosis, organ damage
198
Q

Management of vaso-occlusive crisis?

A
  • Supportive
  • Analgesia
  • RBC transfusion
199
Q

Causes of haemolysis?

A
  • Acquired [autoimmune; prosthetic valves; malaria; drugs]
  • Congenital [hereditary spherocytosis; G6PD deficiency; sickle cell; thalassaemia]
200
Q

What is sickle cell disease?

A
  • Congenital
  • HbS haemoglobinopathy causing rigid, distorted & dysfunctional erythrocytes
201
Q

Precipitants to sickle cell crisis?

A
  • Infection
  • Dehydration
  • Hypoxia
  • Drugs
202
Q

What triggers aplastic crisis in sickle cell?

A
  • Parvovirus
203
Q
A

Interview Prep (5 decks)

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