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AMC MCQ Teaching: All 4 Questions

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Q1 - 6-year-old girl who doesn't talk at school, communicates fine at home

Why this is the right answer - step by step reasoning

• She does talk at home (communication with family is good)
• She does study well (so cognition is intact)
• She won't talk in certain situations (school/social settings)
• No separation anxiety mentioned
• No developmental or autism-spectrum features

How to eliminate the distractors

AMC key teaching points on Selective Mutism

• Onset typically ages 4-8 years; often preschool shy, but becomes apparent when the child must speak aloud at school
• The child is not globally mute - they speak fluently at home and in familiar settings
• Strongly related to social anxiety disorder - the same neural substrate, but situation-specific
• Children may use gestures, nods, or whispering as alternatives at school
• Do not diagnose in the first month of school (adjustment period)
• Exclude: communication disorders (e.g. stuttering, dysphasia), autism, intellectual disability, language barrier
• Treatment: behavioural therapy (stimulus fading, shaping), CBT; SSRIs (e.g. fluoxetine) are used pharmacologically
• Kaplan & Sadock's Synopsis of Psychiatry, p.646-648

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Q2 - Man back from Bali, monogamous, fever, cervical lymphadenopathy (tender, mild), hepatosplenomegaly

Why EBV is correct

1. Fever
2. Lymphadenopathy (typically cervical, tender)
3. Hepatosplenomegaly (splenomegaly in ~50%, hepatomegaly common)

How to eliminate distractors

AMC key teaching points on EBV / Infectious Mononucleosis

• Caused by Epstein-Barr virus (HHV-4), transmitted via saliva ("kissing disease")
• Incubation 4-6 weeks
• Investigations: FBC - atypical lymphocytes (Downey cells); monospot test (heterophile antibodies); EBV IgM for definitive diagnosis
• AVOID ampicillin/amoxicillin - causes a florid non-allergic morbilliform rash in ~80% of EBV patients
• Treatment is supportive; no specific antiviral
• Avoid contact sports for 21 days minimum due to risk of splenic rupture
• Steroids only for: severe tonsillar obstruction, massive splenomegaly, myocarditis, haemolytic anaemia, HLH
• Red Book 2021 (Committee on Infectious Diseases), p.547-553

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Q3 - Patient with diplococci on gram stain - most appropriate treatment?

The framework

Why not Flucloxacillin?

• Neisseria infections
• Pneumococcal infections (amoxicillin is preferred here)

AMC key points

• N. gonorrhoeae: Gram-negative intracellular diplococci (kidney-bean shaped, found inside neutrophils). Treatment: ceftriaxone 500mg IM single dose (now the standard due to quinolone resistance)
• N. meningitidis: Gram-negative diplococci; treatment: ceftriaxone IV for meningococcal meningitis/septicaemia
• S. pneumoniae: Gram-positive diplococci (lancet-shaped, in pairs). Sensitive to penicillin/amoxicillin; for meningitis, use ceftriaxone + consider vancomycin pending sensitivities
• The question stem says "diplococci positive infection" - this likely means Gram-positive diplococci (pneumococci), making amoxicillin the best answer over flucloxacillin
• Harrison's Principles of Internal Medicine 22E, p.910+

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Q4 - RA patient on tocilizumab + others, presents with GI perforation - which drug is most responsible?

Mechanism - why tocilizumab causes GI perforation

• Mucosal repair is impaired
• Diverticulitis can progress to perforation without the usual inflammatory warning signs (pain may be blunted due to suppression of IL-6-mediated inflammation)
• The incidence of lower GI perforation (particularly diverticular) is significantly elevated compared to other biologics

"Gastrointestinal perforation has been reported in patients receiving tocilizumab for rheumatoid arthritis." - Katzung's Basic & Clinical Pharmacology, 16th Ed., p.1383

Why not the other options?

AMC key teaching point

• Rheumatology, 2-Volume Set (Elsevier 2022)
• Katzung's Basic & Clinical Pharmacology 16th Ed.

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Quick Summary Table

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AMC MCQ Teaching - All 4 Questions

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Q1 - 6yo girl, doesn't talk (at school), studies well, talks fine with family

The Logic - Eliminate First, Confirm Last

• Hallmark is excessive fear/distress when separated from attachment figures
• Child cries, refuses school, has physical symptoms (nausea, headache) anticipating separation
• The stem says no separation is mentioned - if it were separation anxiety, the examiner would tell you the child cries when mum leaves
• This child is simply not talking - no distress about being away from family is described

• Requires an identifiable psychosocial stressor (death in family, divorce, moving house, new school)
• The stem explicitly says "no stress" - this is a direct elimination clue
• Symptoms must develop within 3 months of the stressor and resolve within 6 months of its removal

• DSM-5 requires deficits in TWO core domains:
  1. Social communication and social interaction - must be pervasive (everywhere, not just school)
  2. Restricted, repetitive patterns of behaviour
• This girl communicates normally at home - ASD does not switch on and off depending on location
• Good academic performance also argues against ASD
• The AMC will never give you ASD without mentioning repetitive behaviours, restricted interests, or developmental concerns

1. Consistent failure to speak in specific social situations where speaking is expected (school)
2. Ability to speak in other situations (home, family)
3. Interferes with educational achievement or social communication
4. Duration at least 1 month (not limited to the first month of school)
5. Not better explained by a communication disorder, ASD, or language barrier

Key AMC Points to Remember

• Age of onset: typically 4-8 years - becomes obvious when the child must speak aloud in class
• It is classified under anxiety disorders in DSM-5, not communication disorders
• Closely related to social anxiety disorder - same pathophysiology, different expression
• The child is not defiant - they genuinely cannot speak due to anxiety in that context
• Some children whisper, gesture, or use eye contact as substitutes
• Risk factors: family history of anxiety, immigrant families (language barrier can overlap), overprotective parenting
• Treatment: behavioural therapy (stimulus fading, shaping), CBT, SSRIs (fluoxetine is first-line pharmacotherapy)
• Do NOT diagnose in the first month of starting a new school

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Q2 - Man from Bali, monogamous, fever + cervical LAD (tender, mild) + hepatosplenomegaly

The Diagnostic Triad for EBV

Fever + Lymphadenopathy + Hepatosplenomegaly = Infectious Mononucleosis until proven otherwise

Eliminate the Distractors

• Requires high-risk sexual behaviour: multiple partners, unprotected sex with unknown status partners, MSM, IV drug use
• The stem explicitly states he only had sex with his regular partner - this is a deliberate clue to exclude HIV
• ARS presents with: flu-like illness, diffuse truncal rash, oral ulcers, myalgia, generalised LAD
• Hepatosplenomegaly is not a dominant feature of ARS

• Bali IS an endemic area, so travel history fits - this is a deliberate distractor
• But Zika's classic triad is: rash + conjunctivitis (red eyes) + arthralgia/joint pain
• Zika does NOT typically cause significant lymphadenopathy or hepatosplenomegaly
• The stem has none of Zika's key features (no rash, no red eyes, no joint pain)
• The AMC is testing whether you know what Zika looks like, not just where it comes from

AMC Key Points on EBV

• Causes a florid, non-allergic morbilliform rash in ~80% of patients
• This is a type of immune complex reaction, not true penicillin allergy

• Supportive - rest, analgesia, hydration
• No antiviral (acyclovir has no clinical benefit in immunocompetent patients)
• Avoid contact sports for at least 21 days - risk of splenic rupture
• Steroids only if: airway obstruction from massive tonsils, haemolytic anaemia, myocarditis, HLH

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Q3 - Patient with diplococci infection - most appropriate treatment?

The Master Rule

Why Flucloxacillin is WRONG

• MSSA (Staphylococcus aureus - Gram-positive cocci in clusters)
• Skin and soft tissue infections, septic arthritis, osteomyelitis caused by Staph

• Gram-negative organisms (no coverage of Neisseria)
• Streptococcus pneumoniae (amoxicillin is used instead)
• Any diplococci arrangement

The AMC Logic

Extra AMC Facts on Gonorrhoea Treatment

• Current Australian standard: ceftriaxone 500mg IM single dose (500mg not 250mg - updated due to resistance)
• Add azithromycin 1g oral if chlamydia co-infection not excluded
• Resistance has made ciprofloxacin and penicillin no longer appropriate empirically in Australia

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Q4 - RA patient on tocilizumab + other drugs, develops GI perforation

Your notes say "steroids are more specific for perforation" - let me clarify this precisely

The Key Distinction the AMC Tests

• NSAIDs and steroids cause ulcers - which can secondarily perforate
• Tocilizumab causes direct lower GI perforation (especially diverticular) - this is in the black-box warning
• The mechanism is unique: IL-6 blockade impairs gut wall integrity AND simultaneously suppresses the inflammatory signals that would otherwise warn you (pain, fever) that something is going wrong
• This means perforation can be clinically silent until it is severe in patients on tocilizumab

Why Tocilizumab is the Best Answer

1. It is a labelled/black-box adverse effect specific to this drug class
2. The mechanism (IL-6 inhibition) directly damages intestinal mucosa
3. Studies comparing RA biologics show tocilizumab has the highest rate of GI perforation compared to TNF inhibitors, abatacept, and others
4. Steroids and NSAIDs cause ulcers primarily - perforation is a downstream consequence, not the primary association

"Gastrointestinal perforation has been reported in patients receiving tocilizumab for rheumatoid arthritis." - Katzung's Basic & Clinical Pharmacology, 16th Ed.

AMC Exam Tip

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Final Summary - All 4 Answers

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AMC MCQ Teaching - 5 Questions

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Q1 - Chronic alcohol abuse + long-standing epigastric pain - best investigation to establish diagnosis

Why CT is the answer - the full reasoning

The STEP approach to diagnosing chronic pancreatitis

Why CT specifically?

• Sensitivity 75-90% for chronic pancreatitis
• Specificity 85%
• MRCP is equivalent and an acceptable alternative

Why not other options?

AMC Key Points

• In a chronic alcohol user with long-standing epigastric pain, the first investigation is CT
• Alcohol is the most common cause of chronic pancreatitis (70-80%)
• Serum enzymes are unreliable in chronic pancreatitis - do not use them to exclude the diagnosis
• Pancreatic calcification on CT = chronic pancreatitis until proven otherwise
• The pain is typically epigastric, radiating to the back, worse after food or alcohol
• Complications to look for: exocrine insufficiency (steatorrhoea), endocrine insufficiency (diabetes mellitus type 3c)
• Washington Manual of Medical Therapeutics; Harrison's Principles of Internal Medicine 22E

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Q2 - Diabetic foot ulcer treated with IV flucloxacillin → profound hypotension

Why adrenaline is the immediate first intervention

Why Adrenaline First - The Mechanism

The AMC Sequence for Anaphylaxis Management

1. STOP the offending agent (stop the flucloxacillin infusion immediately)
2. Call for help / activate emergency response
3. Adrenaline IM 0.5mg (1:1000) into the outer thigh - FIRST drug, no delay
4. Lay patient flat, legs elevated (unless airway concerns)
5. Oxygen high-flow
6. IV access + IV fluid bolus (500ml-1L normal saline)
7. Antihistamine (promethazine) - second-line, does NOT replace adrenaline
8. Corticosteroids (hydrocortisone 200mg IV) - second-line, takes hours to work, prevents biphasic reaction

Common AMC Traps on Anaphylaxis

Adrenaline Dose - AMC Must Know

• Adults: 0.5mg IM (0.5mL of 1:1000 solution) into the outer mid-thigh
• Children: 0.01mg/kg IM (max 0.5mg)
• Thigh > deltoid - faster, more consistent peak blood levels
• Repeat every 5-10 minutes if no response

"Epinephrine is the treatment of choice for anaphylaxis. The α1-receptor activation reduces mucosal edema and treats hypotension, β1-receptor stimulation increases heart rate and myocardial contractility, and β2-receptor stimulation provides bronchodilation and limits further mediator release." - Tintinalli's Emergency Medicine

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Q3 - Elderly patient on antihypertensives with symptomatic orthostatic hypotension

The Principle - Address the Cause First

The AMC First-Line Management Sequence

Which antihypertensives most commonly cause orthostatic hypotension?

• Alpha-1 blockers (prazosin, doxazosin) - highest risk
• Diuretics (frusemide, thiazides) - volume depletion
• Nitrates - venous pooling
• Tricyclic antidepressants - if co-prescribed
• ACE inhibitors / ARBs - less so but contribute

Why CCB (the given wrong answer) is incorrect

• Calcium channel blockers (amlodipine, nifedipine) are antihypertensives - they would further lower blood pressure
• Amlodipine causes peripheral vasodilation and can itself worsen postural hypotension
• You never add another antihypertensive to treat hypotension caused by antihypertensives

AMC Key Rule

If the patient is symptomatic (dizzy, falls, near-syncope) from orthostatic hypotension on antihypertensives - the first and most appropriate step is to stop or reduce the medication.

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Q4 - New-onset bilateral ankle oedema - which antihypertensive is the most likely cause?

The Mechanism

• Blocking L-type voltage-gated calcium channels in arteriolar smooth muscle
• Causing selective arteriolar vasodilation (reduces afterload)
• This lowers blood pressure effectively

• Increased hydrostatic pressure in the capillary bed
• Fluid shifts into the interstitial space
• Dependent (gravity-dependent) oedema - bilateral ankle swelling

Why this is specific to dihydropyridine CCBs

AMC Key Points

• Bilateral ankle oedema + antihypertensive = amlodipine (or other dihydropyridine CCB) - this is a very high-yield AMC association
• It is NOT heart failure - there is no raised JVP, no orthopnoea, no pulmonary oedema
• Management: reduce dose, switch to ACE inhibitor/ARB, or add a low-dose ACE inhibitor (some evidence it counteracts the oedema)
• Other dihydropyridines: nifedipine, felodipine - same effect
• Non-dihydropyridines (verapamil, diltiazem) cause less peripheral oedema

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Q5 - Post-abdominal trauma, epigastric pain, visible bruising, hypotension - next investigation

The Critical Rule - Haemodynamic Status Determines Your Investigation

Why NOT CT in an unstable patient?

• Transporting the patient out of the resuscitation bay
• Waiting 10-30 minutes for the scan
• IV contrast administration
• A cooperative, reasonably stable patient

"The decision to proceed to CT with a hemodynamically unstable patient must be made cautiously. A repeat FAST and x-rays must be obtained to identify evolving injuries." - Sabiston Textbook of Surgery

What FAST tells you

1. Pericardium - cardiac tamponade
2. Right upper quadrant (Morrison's pouch) - liver/kidney
3. Left upper quadrant (splenorenal fossa) - spleen/kidney
4. Pelvis (pouch of Douglas) - pelvic free fluid

The Retroperitoneal vs Intraperitoneal Distinction

• Grey Turner's sign - flank ecchymosis (bruising) - retroperitoneal bleeding
• Cullen's sign - periumbilical ecchymosis - retroperitoneal/peritoneal bleeding
• Flank/back pain, haematuria (renal injury)
• Upper abdominal pain (pancreatic injury)

The Management Algorithm in Hypotensive Trauma

Hypotensive abdominal trauma
         ↓
    FAST scan (bedside)
         ↓
Free fluid present?
    YES → Activate MTP, go to theatre (haemoperitoneum)
    NO → Repeat FAST, consider retroperitoneal source
         → Stabilise → CT when stable

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Summary Table - All 5 Questions

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AMC MCQ Teaching - 9 Questions

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Q1 - Driver with open chest wound + flail chest, gasping for breath - most immediate management

1. Open pneumothorax (sucking chest wound)
2. Flail chest

The Problem with an Open Chest Wound

• Collapse of the lung on the affected side
• Mediastinal shift with each breath (pendulum breathing)
• Hypoxia + hypercapnia = gasping for breath

Why the 3-Sided Occlusive Dressing is the IMMEDIATE answer

• 3 sides taped shut = prevents air entering the pleural space on inspiration
• 1 side open (untaped, usually the bottom) = allows accumulated air to escape on expiration
• This prevents conversion to a tension pneumothorax (which would occur if all 4 sides were sealed)

"Temporary management of this injury includes covering the wound with an occlusive dressing that is taped on three sides. This acts as a flutter valve, permitting effective ventilation on inspiration while allowing accumulated air to escape from the pleural space on the untaped side, so that a tension pneumothorax is prevented." - Schwartz's Principles of Surgery, 11th Ed.

Why the Other Options Are Wrong as the IMMEDIATE step

What About the Flail Chest?

• Adequate analgesia (reduces splinting, encourages deep breathing)
• Oxygen
• Intubation + mechanical ventilation if respiratory failure develops
• Pulmonary contusions worsen over the first 12 hours - monitor closely

AMC Scene Sequence

Open chest wound + gasping
         ↓
IMMEDIATE: 3-sided occlusive dressing (stops air entering)
         ↓
Secure airway (intubation if needed)
         ↓
Chest tube insertion (remote from the wound - definitive)
         ↓
Closure of chest wall defect (surgical - definitive)

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Q2 - H. pylori infection - most appropriate first-line pharmacological eradication therapy

The Global Standard

• PPI (omeprazole 20mg or equivalent) twice daily
• Clarithromycin 500mg twice daily
• Amoxicillin 1g twice daily

The Australian Context - Critical AMC Point

• PPI (standard dose) twice daily
• Bismuth subcitrate 120mg four times daily
• Tetracycline 500mg four times daily
• Metronidazole 400mg three to four times daily

The AMC Rule

• Never use PPI + Amoxicillin + Metronidazole as triple therapy in Australia (high metronidazole resistance makes this unreliable)
• Preferred: PPI + Clarithromycin + Amoxicillin (clarithromycin triple) OR Bismuth quadruple depending on local resistance patterns
• Duration: 14 days is superior to 7 or 10 days
• Confirm eradication with urea breath test at least 4 weeks after completing therapy (not stool antigen or repeat endoscopy as first choice)
• Harrison's Principles of Internal Medicine 22E; Yamada's Gastroenterology 7E

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Q3 - Perimenopausal woman, previous hysterectomy, seeks HRT for vasomotor symptoms

The Fundamental Rule of HRT

Why This Matters

• Oestrogen alone reduces vasomotor symptoms (hot flushes, night sweats) effectively
• Oestrogen + progestogen (combined/sequential) is ONLY for women with a uterus
• Combined HRT carries higher risk of breast cancer than oestrogen-only
• The Women's Health Initiative (WHI) data showed oestrogen-only HRT had a lower breast cancer risk than combined HRT

AMC Exam Rules on HRT

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Q4 - Breastfed infant, persistent jaundice for 3 months, elevated liver enzymes, NORMAL GGT

The GGT Rule in Infant Jaundice

The Correct Answer: Ask About Family History of Liver Disease

• 3 months old (beyond the breastfeeding jaundice window)
• Persistent jaundice
• Elevated liver enzymes
• Normal GGT

• Progressive Familial Intrahepatic Cholestasis (PFIC) - types 1 and 2 have LOW/normal GGT despite cholestasis
• Alagille syndrome - usually elevated GGT
• Alpha-1 antitrypsin deficiency - can have normal GGT early
• Citrin deficiency

Why the Other Options Are Wrong

AMC Key Teaching Points

• Any jaundice beyond 14 days in a formula-fed infant, or 21 days in a breastfed infant, requires investigation - measure conjugated vs unconjugated bilirubin first
• Conjugated (direct) bilirubin >20% of total = always pathological, always investigate
• Normal GGT in a jaundiced infant with elevated transaminases = ask about family history of liver disease (inherited metabolic condition)
• First investigation after recognising conjugated hyperbilirubinaemia: split bilirubin, LFTs, GGT, USS abdomen
• PFIC types 1 and 2 have LOW GGT despite cholestasis - this is a classic AMC distinction

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Q5 - Post-forceps delivery, urinary leakage only on coughing

The Diagnostic Rule

The Pathophysiology

• Levator ani muscle (pelvic floor)
• Pudendal nerve (innervates external urethral sphincter)
• Urethral support ligaments

Why NOT Vesicovaginal Fistula (VVF)

• VVF = continuous, uncontrollable leakage of urine through the vagina, at rest and with activity, day and night
• There is no voluntary control - the patient is constantly wet
• VVF follows obstructed labour, pelvic surgery, or radiation
• This patient only leaks on coughing - there IS voluntary control between episodes = not a fistula

Initial Management of SUI (AMC order)

1. Exclude UTI (MSU - midstream urine) - UTI can mimic or worsen any incontinence
2. Pelvic floor exercises (Kegel) - first-line non-surgical
3. Bladder retraining
4. Physiotherapy referral
5. If conservative measures fail: surgical (mid-urethral sling - TVT/TOT)

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Q6 - Elderly woman with cystocele + urinary incontinence on coughing - investigation before surgery

Why UDS Before Surgery is Mandatory

1. Urge incontinence / Overactive bladder (OAB) - caused by detrusor overactivity, NOT by pelvic floor weakness. Surgery will NOT fix this and may worsen it.
2. Mixed incontinence - component of both stress and urge. Surgery addresses only the stress component.
3. Voiding dysfunction - poor detrusor contractility. Surgery (especially sling) may cause urinary retention post-operatively.

What UDS measures

The AMC Rule

If a woman with cystocele/pelvic organ prolapse is going to surgery, she MUST have urodynamic studies first to:

• Confirm the incontinence type
• Exclude detrusor overactivity (which needs anticholinergics/mirabegron, not surgery)
• Detect occult stress incontinence that may unmask after prolapse repair

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Q7 - Acute bacterial infection of the lower eyelid - management

The AMC Distinction

Management of Acute Bacterial Eyelid Infection (Hordeolum/Stye)

1. Warm compresses 4x daily (10-15 minutes each) - promotes spontaneous drainage
2. Gentle lid massage after warming
3. Most resolve spontaneously within 1-2 weeks

• Warm compresses + lid scrubs (diluted baby shampoo) = cornerstone, long-term
• Artificial tears for dry eye
• Topical antibiotics for moderate-severe flares
• Oral doxycycline (low-dose, 50mg/day for 6-12 weeks) for rosacea-associated blepharitis or meibomian gland dysfunction

AMC Key Distinction

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Q8 - Recurrent SCC left cheek, deeply invading underlying muscle

Why Combined Modality Treatment

• Recurrent (has already been excised once)
• High-risk (deeply invading muscle = T4 disease)

Risk Stratification of SCC

Indications for Adding RT

• Deep/muscle invasion
• Perineural invasion
• Positive or close surgical margins
• Regional lymph node involvement
• Immunosuppression

AMC Rule for SCC Management

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Q9 - Recurrent pulmonary infections + chronic constipation + iron deficiency anaemia

Why CF fits all three features

Why NOT Coeliac Disease

Other CF Features to Know (AMC)

• Neonatal: meconium ileus (10-15%), prolonged jaundice
• Paediatric/adult: failure to thrive, clubbing, barrel chest, nasal polyps
• Endocrine: CF-related diabetes mellitus (CFRD) - type 3c
• Reproductive: male infertility (bilateral absence of vas deferens)
• Diagnosis: Sweat chloride test >60 mmol/L (gold standard) + CFTR gene testing
• Treatment: Airway clearance, CFTR modulators (ivacaftor, elexacaftor/tezacaftor/ivacaftor = Trikafta), pancreatic enzyme replacement, fat-soluble vitamin supplementation

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Final Summary - All 9 Questions