MEDICINE 1

Question 1

1. Hypertension: classification and management

Answer 1

• stage 1: 140/90 clinic, 135/85 ABPM
• stage 2: 160/100 clinic, 150/95 ABPM
• stage 3: 180/110+
• <55yr, male/non-fertile female: ACE/ARB
• <55yr, fertile female: beta-blocker
• > 55yr, black of any age: CCB
• diabetic of any age: ACE/ARB

Question 2

2. Angina pectoris

Answer 2

• presentation: chest pain on exertion; heavy, gripping, tight etc
• investigations: ECG, FBC, U&Es, LFTs, TFTs, lipid profile, HBA1c
• management: GTN (x2 for immediate relief), BB/CCB prophylactic, Mx of cardio Rx by 4 A’s (atorvastatin, aspirin, ACE inhibitor, atenolol)

Question 3

3. Acute Coronary Syndrome: classification, investigation, management

Answer 3

• classification: 1 (spontaneous), 2 (2ndry to ischaemia), 3 (sudden cardiac death/SCD), 4a (PCI), 4b (stent thrombosis), 5 (CABG)
• Ix: ECG, U&Es, LFTs, troponins
• immediate Mx [MONA]: morphine, o2 (if sats <96/92), nitrates (GTN/isosorbide), aspirin
• Mx [STEMI]: is PCI available within 120 min?
  – yes: prasugrel, UFH, gp IIa/IIIb inhibitor, radial access for PCI
  – no: thrombolysis, ticagrelor
• Mx [NSTEMI]: fondaparinux and 6 month mortality tool (e.g. GRACE)
  – mortality low (<3%): ticagrelor
  – mortality high (>3%): prasugrel or ticagrelor and PCI
• Mx [Recovery]: DABS [dual antiplatelets, ACE inhibitor, beta-blocker, statin]
  – ACS [no PCI]: aspirin (lifelong), ticagrelor (12 months)
  – ACS [PCI]: aspirin (lifelong), ticagrelor OR prasugrel (12 months)
  – ACS [aspirin C/I]: clopidogrel (lifelong)
  – PAD clopidogrel (lifelong), aspirin (lifelong) only if clopidogrel C/I

Question 4

3a. Primary C/I to cardiac drugs: ACE inhibitors, beta-blockers, aspirin and clopidogrel, statins

Answer 4

• ACEi/ARBs: pregnancy/breastfeeding, bilateral renal stenosis, angioedema
• beta-blockers: hypotension, bradycardia, asthma/COPD
• aspirin/clopidogrel: aspirin 1st line EXCEPT with evidence of PAD/stroke, then clopidogrel 1st line

Question 5

3b. Complications after ACS: timescale (inc. pathology), Dressler’s syndrome

Answer 5

• 0-24hr: arrhythmia (esp. VF)
• 0-48hr: pericarditis
  – 20min-3days: cells shrink (pyknosis) and neutrophils arrive
  – 3-7days: macrophages replace neutrophils
• 3-14days: ventricular septal defect
• 5-14days: cardiac tamponade
• 1-2wk: ventricle free wall rupture
• 2-6wk: Dressler’s
  – 2-6wk: fibroblasts lay down collagen, weakening the heart
• Dressler’s: believed to arise as the result of neo-antigens. Sx include malaise, dyspnoea, chest pain (better on sitting forward), PR depression and ST elevation. Mx: aspirin and steroids

Question 6

4. Congestive heart failure: pathology, classification, investigations, management

Answer 6

• pathology: sustained increase in mechanical work causes myocyte hypertrophy. this leads to vulnerability to ischaemic disease.
• classification: by Killip
  – I: no evidence of CHF
  – II: rales in <1/2 lung fields, S3 heart sound, systolic BP >90
  – III: frank pulmonary oedema (>1/2 lung fields), systolic BP >90
  – IV: cardiogenic shock, tissue hypoperfusion, hypotension (SBP <90)
• Ix: BNP/NT-pro BNP measured first to guide echo urgency. Echo is diagnostic.
  – others: FBC, U&Es, LFTs, TFTs
  – CXR: ABCDE [Alveolar bat wings, kerley B lines, Cardiomegaly, Dilated upper vessels, Effusion (pleural)
• Mx:
  – immediate [OMFG]: O2, morphine, furosemide, GTN, consider mechanical assist devices
  – maintenance: AB + S + D

Question 7

5. Pulmonary embolism: Virchow’s triad, scoring systems,, investigation, management

Answer 7

• Virchow’s triad: hypercoagulability (cancer, thrombophilia, inflammation etc.), vessel wall injury (surgery, irritation etc.), stasis (immobility, varicose veins etc.)
• Ix: depends on whether risk for PE is low or high.
  – [low]: PERC (PE rule-out criteria) requires all to be absent: age >50, HR>100bpm, O2<94%, previous DVT/PE, recent surgery/trauma, haemoptysis, unilateral leg swelling, oestrogen use (HRT/contraception)
  – [high]: Well’s score; a score of >4 indicates PE.
  — 3 points: clinical signs of DVT
  — 1.5 points: tachycardia, recent surgery/immobility, history of PE/DVT
  — 1 point: haemoptysis, malignancy
  – high likelihood of PE: CTPA (C/I renal disease, contrast allergy: V/Q)
  – low likelihood: DVT US scan
• Mx: DOAC (apixaban, rivaroxaban) continued for 3 months (unless PE is unprovoked, then 6 months)
  – renal impairment: LMWH, then UFH/warfarin
  – APLS: LMWH, then warfarin
  – circulatory failure: thrombolysis

Question 8

6. Orthostatic hypotension and falls: presentation, causes, investigation, management

Answer 8

• presentation: common in the elderly, dizziness, syncope, falls, fractures. definition: a fall of 20SBP or 10DBP from sitting to standing within 3 mins
• causes: drugs [vasodilators, diuretics, negative inotropes, antidepressants, opiates]; chronic HTN; dehydration; sepsis; autonomic dysfunction [e.g. Parkinson’s]; adrenal insufficiency
• investigations: FBC, neurological history [?Parkinson’s, ?peripheral neuropathy –> CT head], echo, ECG, urinary history [urine dip, bladder scan, PR exam]
• Mx: lifestyle [rise slowly from sitting, hydration, polypharmacy, soft flooring etc.]; consider compression stockings or abdominal binders; drugs [fludrocortisone, anticholinergics]

Question 9

7. Asthma: pathology, presentation, investigations, management

Answer 9

• pathology: reversible airway obstruction, type I hypersensitivity assc. with IgE and mast cells
• presentation: wheezing, dyspnoea, chest tightness, cough worse diurnally. triggers include infection, smoke, cold air, stress, exercise
• Ix: primarily a clinical diagnosis; Ix can include bronchial provocation [histamine, methacholine], exercise tests, exhaled NO2, ?skin prick test
• Mx: SABA + low-dose inhaled steroids [ICS] (beclomethasone)
  – +LTRA (e.g. montelukast)
  – +LABA (stop LTRA in children, continue in adults)
  – switch LABA/ICS to a MART
  – consider increasing ICS dose or adding theophylline
  – specialist: consider monoclonal antibodies, such as omalizumab

Question 10

7a. Status asthmaticus: presentation classification [severe, lifethreatening], management

Answer 10

• severe asthma: unable to complete a sentence, RR>25, HR>100, PEFR <50%
• life-threatening: [remember 33 92 CHEST] <33% PEFR, <92% FiO2, Cyanosis, Hypotension, Exhaustion, Silent chest, Tachycardia (severe)
• Mx [O SHIT MAN]: O2, salbutamol, hydrocortisone/ prednisolone (strong steroid), ipratropium (a SAMA), ?theophylline, magnesium sulphate, aminophylline (with senior medical staff input), nebuliser.
• discharge: patient stable without nebulizer or O2 for 12-24hr, inhaler technique, PEFR >75%

Question 11

8. COPD: classification, symptoms, investigations, diagnostic guideline, management

Answer 11

• classification: emphysema (irreversible enlargement of terminal bronchioles; ‘pink puffers’) and chronic bronchitis (cough >3months in at least 2 consecutive years; ‘blue bloaters’)
• symptoms: progressive dyspnoea, cough, wheeze, weight loss, barrel chest, accessory muscle use, poor chest expansion
• Ix: spirometry (raised TC, RV, ERV; decreased IRV; conserved TV –> FEV1/FVC <70%); CXR (flat diaphragm); blood gas; a1-antitrypsin levels (non-smokers, young patients)
• diagnostic guideline [GOLD]: I (>80%, dyspnoea on hill); II: (50-79%, walks slow on level); III (30-49%, dyspnoea on level); IV (<30%, has to stop after 100m exertion)
• Mx: SABA + LABA + LAMA [+ ICS if steroid responsive features present]
  – azithromycin, carbocysteine, roflumilast, LTOT

Question 12

9. Cystic Fibrosis: genetics, presentation, diagnosis

Answer 12

• 1 in 2,500 live births, autosomal recessive to chromosome 7 (CFTR chloride channel, F508)
• mucus obstruction leads to infections, chronic bronchitis, bronchiectasis, abscesses, malabsorption of fat (causing steatorrhoea), cor pulmonale, sinonasal polyps, liver disease
• diagnosis: heel prick test (raised trypsinogen), sweat electrolyte concentration, CFTR gene sequencing
• Mx: antimicrobials, pancreatic enzyme replacement (Creon), lung transplant, airway clearance, drugs (e.g. Ivacaftor, Lumacaftor, Trikefta, Symkevi)

Question 13

10. Bronchiectasis: definition, causes, morphology, treatment

Answer 13

• definition: permanent dilation of the airways, leading to obstruction and chronic infection
• causes: congenital (CF, Kartanager’s, Young’s); infection (pneumonia, measles, TB)
• bronchial obstruction (tumour, foreign bodies)
• morphology: HRCT shows signet rings, tramlines, and tram-tracks
• treatment: physical training, airway clearance, bronchodilators, antibiotics, transplantation.

Question 14

11. Obstructive sleep apnoea: epidemiology, clinical features, management

Answer 14

• epidemiology: affects older, overweight men > women
• clinical features: disruption of REM sleep, personality change, cognitive impairment, loud snoring, pulse oximetry will show sawtooth pattern. Diagnosis with sleep studies showing 10-15 apnoeas in any hour of sleep
• Mx: polyp removal, CPAP, modafinal (short term, CNS stimulant), mandibular advancement (younger patients)

Question 15

12a. Causes of lung fibrosis: upper vs. lower zones

Answer 15

• more common types of fibrosis affect the lower zones. these include IPF, connective tissue disorders (but NOT ankylosing spondylosis), drugs (amiodarone, bleomycin, methotrexate)
• upper zone causes [CHARTS]: Coal worker pneumoconiosis, Hypersensitivity, Ankylosing spondylitis, Radiation, TB, Silicosis/Sarcoidosis

Question 16

12b. Idiopathic pulmonary fibrosis: presentation, diagnosis, management

Answer 16

• presentation: dyspnoea, tachypnoea, end-inspiratory crackles, cyanosis, clubbing. M 2> F
• diagnosis: exclude reversible causes. spirometry shows restrictive defect. HRCT gold standard, showing honeycombs
• Mx: antifibrotics (pirfenidone), tyrosine kinase inhibitor (Nintedanib), oxygen, lung transplant [steroids are NOT effective]

Question 17

13a. Arrhythmia: BLS management guidelines

Answer 17

• ABCDE, ECG, BP, IV access, identify reversible causes (4T’s and P’s)
• adverse effects (shock, syncope, myocardial ischaemia, heart failure): DC shock synchronised, amiodarone
• narrow QRS (<0.12s)
  – regular: vagal manoeuvres, adenosine 6+12+12mg
  – irregular: probable AF; give BB/CCB
• broad QRS
  – irregular: amiodarone
  – regular: probable VT, give amiodarone

Question 18

13b. AV Heart Block: types, management

Answer 18

• first degree: constant prolonged PR interval (>0.22s, 5 boxes)
• second degree, Mobitz I/Wenckebach; ‘longer, longer, longer, dropped; that is a Wenckebach’
• second degree, Mobitz II: every nth beat is missed
• third degree: complete heart block, no co-ordination between P wave and QRS complex
• Mx: atropine, adrenaline, dopamine, temporary transvenous pacing

Question 19

13c. AF: presentation, causes, classification, management short term and long term

Answer 19

• presentation: dyspnoea, light-headedness, increased risk of stroke
• causes [THE ATRIAL FIBS]: thyroid, hypothermia, embolism (e.g. PE), alcohol, trauma, resp (pneumonia, lung malignancy), ischaemic, atrial enlargement, lone (idiopathic), fever, (ischaemia), bad valves (mitral stenosis), stimulants (caffiene, cocaine, theophylline) / surgery (CABG)
• classification: paroxysmal (<48h), persistent (>7 days), long-standing (>1 year), permanent (accepted)
• short-term Mx: rate > rhythm control, unless [reversible cause, new <48h, causes CHF]
  – rate control: beta-blockade [1st line], diltiazem [CCB, 2nd line], digoxin [sedentary]. do not combine BB + CCB [risk of bradycardia]
  – rhythm control: pharmacologic [flecanide, amiodarone], electrical cardioversion
• long-term Mx: balance CHA2DS2VASc and ORBIT [previously HAS-BLED]. use warfarin [requires INR monitoring] or DOAC [e.g. apixaban]

Question 20

13d. SVTs: differential, ECG findings, management

Answer 20

• four main differentials: SVT, AF, Atrial Flutter, AVRT (WPW syndrome)
  – SVT: regular fast QRS complexes, P waves slurred upward
  – AF: irregularly irregular, no discernible P waves
  – AFlutter: saw tooth ECG
  – AVRT (WPW): delta waves (up-slurring of P wave), ST depression
• Mx: cardiovert with haemodynamic compromise, otherwise vagal maneouvres (Valsalva –> carotid body), then adenosine (C/I verapamil)

Question 21

13e. VTs and channelopathies: differential, genetics, ECG findings, management

Answer 21

• VT, VF, Brugada syndrome, long QT syndrome
• Brugada: autosomal dominant to cardiac sodium channels (SCN5A)
• Long QT:
  – Romano-Ward: autosomal dominant, associated with weakness, bone abnormality, autism
  – Jervell & Lange-Nielsen: autosomal recessive, associated with bilateral SN deafness
• ECG findings:
  – VT: monomorphic peaks (including Torsades de Pointes)
  – VF: pulseless, ‘squiggly line’
  – Brugada: pseudo-RBBB with ST elevation in V1-3
  – long QT: prolonged QTc, may result in TdP
• Mx: emergency DC cardioversion + amiodarone (then adrenaline if required)

Question 22

13f. Reversible causes of cardiac arrest

Answer 22

4Hs and 4Ts.
- Hypoxia: respiratory conditions (e.g. asthma)
- Hypovolaemia: haemorrhage, laceration or trauma
- Hyper / hypo metabolic: DKA, toxins
- Hypothermia: exposure to cold
- Thrombosis: coronary or PE
- Tamponade: post-MI, dissection, trauma
- Toxins
- Tension pneumothorax

Question 23

13g. BLS algorithm for management of cardiac arrest

Answer 23

• assess ABC: airway patent, breathing? circulation?
• call resus team (e.g., DRS ABCDE)
• commence CPR. 30:2 compression to rescue breaths
• attach defibrillator or monitor and assess cardiac rhythm
  – shockable [VF or pulseless VT]: give a shock then recommence CPR for 2 min
  – non-shockable [PEA/asystole]: recommence CPR for 2 min
• return of spontaneous circulation (ROSC): ABCDE, O2, ECG, temp control, assess for reversible cause

Question 24

14. Aortic aneurysm: definition and types, presentation, management, screeing

Answer 24

• dilation of the aorta 2x normal size of all three layers (adventitia, media, intima)
• 60% occur in the AAA between L2-4
• 40% occur in the thoracic aorta
• presentation: pulsatile, expansile mass, severe left flank/abdominal pain. 75% asymptomatic
• Mx: EVAR (endoscopic vascular aneurysm repair), laparoscopic surgery 2nd line
• screening: men 65-74 (women much lower risk)
  – <3cm: aneurysm not present
  – 3-4.4cm: small aneurysm. annual screening
  – 4.5-5.4cm: medium aneurysm. 3-monthly checkup
  – >5.5cm: large aneurysm. 2wk referral to surgery

Question 25

15. Aortic dissection: definition, types, presentation, investigations, management

Answer 25

• definition: splitting of tunica media, forming a false lumen and blood fills between the tunica intima and media
• types: Stanford A (ascending aorta), B (descending aorta). A is more common than B and is much more deadly.
• presentation: sharp, ripping chest pain (may mimic MI), BP differs in each arm. may cause hypotension and shock.
• Ix: CXR, transoesophageal echo, MRI, CT angio
• Mx:
  – type A: surgical graft, usually emergency presentation
  – type B: beta-blockers, nitroprusside, endovascular intervention

Question 26

16. Peripheral arterial disease: presentation, investigations and types, management

Answer 26

• presentation [ARTS]: absent pulses and hair, red and round sores, toes and feet pale, sharp leg pain on exertion. others include haemosiderin deposits, lipodermatosclerosis, gangrene
• Ix: ABPI (ankle-brachial pressure index)
  – >0.9: normal
  – 0.4-0.85: intermittent claudiation
  – <0.4: critical limb ischaemia
• Mx: smoking cessation, management of lipids, chiropody (DM), clopidogrel (>aspirin), consider PDE3 inhibition and surgery in severe cases

Question 27

17. Peripheral venous disease (including DVT): presentation, management

Answer 27

• presentation [VEINY]: voluptuous pulses and varicose veins, (o)edema, irregular shapes, no pain on exercise, yellow and brown ankles
• DVT presentation: pain, swelling, redness, engorged superficial veins, Homan’s sign (pain on dorsiflexion).
• Mx:
  – varicose veins: compression stockings (NB: also used for DVT prevention), endothermal ablation (radiofrequency or laser ablation; if C/I foam guided sclerotherapy)
  – DVT: warfarin for 4wk to 3mnth, cover initially with LMWH until INR in target range (2.5-3.5)

Question 28

18. Valvular disease: types and auscultation findings, management

Answer 28

• aortic stenosis: most common, caused by age, bicuspid valve, or rheumatic fever. opening click, s2 (soft S2), S4. Mx: valve replacement
• aortic regurgitation: collapsing pulse, wide pulse pressure, displaced apex. early diastolic murmur.
  – superior to inferior signs: Murmurs Don’t Cease Quickly, They Die Hard: Muller’s (uvular pulsation), De-Musset (head bobbing), Corrigan’s (distension of arterial pulse), Quincke’s (nail bed pulsations on compression), Traube’s (pistol shots over femoral artery), Duroziez’s (bruits over femoral artery), Hill’s (popliteal pressure exceeds brachial by 60mmHg)
• mitral stenosis: rare, caused by rheumatic fever. loud S1, opening snap, rumbling diastolic. malar flush. Mx: warfarin (assc. AF) and surgery/balloon valvuloplasty
• mitral regurgitation: pansystolic, s1, sp2, S3. Mx: mitroclip (infancy), or ACE inhibitor/diuretic

Question 29

19a. Embryology of the cardiovascular system: how the heart forms, foetal circulation

Answer 29

• forms from mesoderm. initially formed of 5 parts: truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, sinus venosus. endocardial cushion gives rise to septa + mitral + tricuspid valves.
• oxygenated blood from the umbilical veins to foetal IVC meeting the hepatic vein, which meet the right atrium.
• shunts to left atrium via foramen ovale and ductus arteriosus (maintained by prostaglandin E2)
• deoxygenated blood returns to the placenta via the umbilical arteries.

Question 30

19b. Atrial congenital defects: findings and management

Answer 30

• ASD: left to right shunt, acyanotic. fixed splitting of S2, ejection systolic murmur. Closure via surgery or endoscopy to prevent haemodynamic abnormalities
• PFO: left to right shunt. aspirin and warfarin, or surgery-based closure of PFO
• tricuspid atresia: requires right to left shunt via ASD and PFO. High mortality.

Question 31

19c. Tetralogy of Fallot: features, clinical features, management.

Answer 31

• 4 cardinal features: VSD, pulmonary stenosis, overriding aorta, RVH
• clinical: right to left shunt, cyanosis, ejection systolic murmur. CXR shows a boot shaped heart. Tet’s spells are paroxysms of hypoxia; older children may squat to increase blood flow to the heart.
• Mx: shunting, intracardiac repair (both surgical).

Question 32

19d. Transposition of the great arteries (TOGA): features, management.

Answer 32

• aorta and pulmonary arteries are swapped and therefore incompatible with life unless VSD present
• RVH and left ventricular atrophy; CXR shows ‘egg on side’ or ‘egg on strings’ appearance
• Mx: atrial switch operation, balloon atrial septostomy early in life

Question 33

19e. Marfan syndrome: genetics, clinical features, management

Answer 33

• genetics: autosomal dominant to fibrillin 1 (FBN1) on chromosome 15. FBN1 normally sequesters TGF-beta so tissue growth is excessive
• clinical features [CLAVATE]: chest (pectus excavatum, carinatum), lungs (bullae, ptx), arachnodactyly, valve prolapse (mitral), aorta (regurgitation), tall and thin, eyes (ectopia lentis)
• Mx: beta-blocker (atenolol), ARB (losartan)

Question 34

20a. Pneumonia: classification, clinical features, investigation, management

Answer 34

• CAP unless within hospital for 48hr prior (HAP)
• clinical features: high fever, dyspnoea, rigor, cough (productive or dry), pleuritic pain, friction rub
• Ix: CURB-65 (CRB-65 in GP): confusion, urea >7mmol/l, RR >30, BP <90/60, age 65. identify organism (with sputum culture, gram stain, or PCR). CXR shows consolidation.
• Mx: O2, fluids, abx
  – CURB-65 of 0-1: amoxicillin (doxycycline) or macrolide (atypical)
  – 1-2: amoxicillin (doxycycline) +/- macrolide (atypical)
  – 3-4: co-amoxiclav (levofloxacin) + macrolide
  – mycoplasma: macrolide (doxycycline)
  – legionella: macrolide (quinolone)

Question 35

20b. Pneumonia: microbiology

Answer 35

• strep pneumoniae: rapid onset, herpes labialis
• haemophilus: exacerbation of COPD
• moraxella: elderly
• staph aureus: IVDUs, following viral infection
• klebsiella: red-current sputum, alcoholics and malnourished
• pseudomonas: CF, immunocompromised
• legionella: contaminated water/AC units. confusion, renal and GI features
• mycoplasma: closed communities (prisons)
• pneumocystis jiroveci: HIV
• chlamydia pneumoniae, coxiella burnetti
• chlamydia psittaci: exposed to avian proteins
• influenza A, B, C: may be superimposed by staph aureus
• SARS-CoV (2): COVID

Question 36

21. TB: pathology, epidemiology, presentation, investigation, treatment (including drug s/e)

Answer 36

• pathology: TB enters macrophages, activated by IFN-y and forms granulomas. the initial bacilli consolidation is the Ghon focus.
• epidemiology: most common in poverty, crowding, racial / ethnic minorities (India, China, southern Africa, Eastern Europe). strongly associated with HIV (get HIV test)
• presentation: weight loss, night sweats, anorexia, haemoptysis, low-grade fever
• Ix: CXR, sputum culture (microscopy, ZN stain, culture, PCR)
• Mx: RIPE (2 months), RI (4 months)
  – rifampicin: induces liver enzymes, raises bilirubin, pink secretions (‘R’ = red), decreases COCP efficacy
  – isoniazid: B6 deficiency (co-prescribe pyridoxine)
  – pyrazinamide: hepatic toxicity, gout
  – ethambutol: red-green colour blindness
  – streptomycin is occasionally used; may cause damage to the vestibular nerve

Question 37

22. ENT Infections (pertussis, rhinitis and sinusitis, coryza, diphtheria): clinical features and management.

Answer 37

• pertussis: paroxysms of whooping cough. incubation ~1wk. nasal congestion, cough, low grade fever. vaccine is available. treat with abx (macrolides) and isolation.
• rhinitis is typically atopic. history may reveal triggers, confirmed with skin prick. remove triggers and consider drugs such as H1-antihistamines (loratidine, cetirizine), alpha-adrenergics, sodium cromoglicate, steroids, leukotriene antagonists
• sinusitis: pain, swelling and tenderness of cheeks, blocked nose, toothache, headache. Mx: decongestants, abx, steroids
• coryza: runny nose, cough, fever, sore nose and throat. self-limiting.
• diphtheria: pseudomembrane and lymphadenopathy. vaccine available. treat with penicillin or erythromycin.

Question 38

23. Sarcoidosis: pathology, clinical features, investigations, treatment

Answer 38

• pathology: systemic granulomatous disease, type IV hypersensitivity (T lymphocytes against an unknown antigen)
• clinical features [SARCOID]: skin (erythema nodosum), arthritis, respiratory (bilateral hilar lymphadenopathy, raised ACE), cardiac (arrhythmia), ocular (uveitis), intracranial (haemorrhage), deranged metabolites (raised Ca2+)
• Ix: serum ACE, Ca2+, HRCT, biopsy
• Mx: steroids, methotrexate, HCQ, azathioprine etc.

Question 39

24. Inflammation of the cardiac system (myocarditis, pericarditis, endocarditis): causes, clinical features, management.

Answer 39

• myocarditis: coxsackie, echovirus, other viruses, Chagas disease. Aschoff bodies on biopsy
  – fatigue, dyspnoea, palpitation, praecordial discomfort, fever
  – bed rest and antibiotics. avoid steroids and NSAIDs
• pericarditis: idiopathic, coxsackie, Dressler’s, uraemia, autoimmune, radiation
  – fever, chest pain worse on heavy breathing and leaning forward, decreased heart sounds etc.
  – ST elevation and PR depression, heart ‘dances’ on echo
  – colchicine + aspirin, pericardiocentesis if severe
• endocarditis is typically infective, rheumatic, or due to lupus (Libman-Sacks)
  – fever, malaise, weight loss, fatigue, dyspnoea, splinter haemorrhage, Roth spots, Janeway lesions, Osler nodes
  – Duke’s criteria: 2M+1m, 3m, or 5m
  — M: [EC] Endocardial involvement (echo, new murmur), Cultures (2+)
  – m: [FEVER] Fever, Evidence of immunologic phenomena (Roth, Osler, glomerulonephritis), Vascular phenomena (emboli, infarct, Janeway, haemorrhage), Early culture result (1+), Risk (PWIDs, CHF)

Question 40

25a. Dilated cardiomyopathy: causes, clinical features, management

Answer 40

• causes [CATCH DEAD]: cocaine, alcohol, thiamine deficiency, Chagas, haemochromatosis, doxorubicin, endocrine, AF, Duchenne dystrophy
• clinical features: dyspnoea, easy fatiguability, systolic dysfunction
• Mx: mechanical support, pharmacologic therapy (as heart failure), transplant

Question 41

25b. Arrhythmogenic right ventricular cardiomyopathy (ARVC) pathology, clinical features, Naxos syndrome, management

Answer 41

• pathology: autosomal dominant, variable penetrance. causes right ventricular failure and VF/VT. associated with malfunction to gene that transcribes dermatomes in cardiac cells.
• clinical features: usually asymptomatic, may present with VT/VF, syncope, or SCD. ECG shows inverted T waves, epsilon wave, and RBBB in V1-4.
• Naxos syndrome: ARVC + hyperkeratosis on palmar + plantar skin
• Mx: beta-blockers, amiodarone. step up to ICD/transplant for more severe disease

Question 42

25c. Hypertrophic cardiomyopathy: pathology, clinical features, ECG findings, management.

Answer 42

• pathology: autosomal dominant affecting sarcomere proteins (e.g. B-MHC, TnT, a-tropomyosin, MYBP-C). associated with Friedreich ataxia
• clinical features: dyspnoea, S4, ejection systolic murmur, pansystolic murmur, SCD in young athletes
• ECG findings: left axis deviation, convex ST segment in V5/6
• Mx: beta-blockers +/- verapamil. consider amiodarone in lower risk and ICD in higher risk.

Question 43

25d. Restrictive cardiomyopathy: pathology, clinical features, management

Answer 43

• pathology: decreased ventricular compliance (diastolic dysfunction). causes: idiopathic, radiation, amyloidosis, sarcoidosis, tumours.
• clinical features: dyspnoea, fatigue, Friedreich sign (raised JVP with diastole), Kussmaul sign (JVP elevation with inspiration)
  – rarer: hepatomegaly, ascites, oedema, S3/4
• Mx: transplantation

Question 44

25e. Takotsubo cardiomyopathy

Answer 44

• ‘broken heart syndrome’, brought on by extremely stressful events and can mimic MI with ST elevation in V1-4. diagnostic coronary angiography demonstrates unobstructed coronary arteries
• most common in middle-aged to elderly women
• recovery of function is common within 4-6 weeks, although may reoccur

Question 45

26. Pneumothorax: risk factors, presentation (including tension ptx), investigation, management.

Answer 45

• risk factors: tall thin men, asthma, COPD, TB, cancer
• presentation: dyspnoea, hypoxia, tachycardia, sharp chest pain, hyperresonant percussion, quiet breath note
  – tension ptx: raised JVP, hypotension, tracheal deviation to opposite side
• investigation: CXR, unless tension pneumothorax present (decompress immediately to convert to simple pneumothorax).
• Mx:
  – decompress tension: thoracocentesis on 2nd intercostal space, midclavicular line
  – chest drain (thoracostomy) in 5th intercostal space, anterior axillary line

Question 46

27. Pleural effusion: clinical features, types, management.

Answer 46

• clinical features: dyspnoea, pleuritic chest pain (worse on inspiration), assymetrical chest expansion, decreased tactile fremitus, diminished breath sounds
• types:
  – transudate (<30g/l protein, <2/3 ULN HDL): systemic, e.g. cardiac failure (straw-coloured fluid)
  – exudate (>30g/l protein, >2/3 ULN HDL): local, e.g. cancer, TB, pneumonia
• Mx: pleural tap, tubular drain. consider diuretics for heart failure

Question 47

28. Paediatric respiratory infections (croup, epiglottitis, bronchiolitis): onset, pathogen, fever, symptoms, management.

Answer 47

• croup: gradual onset, parainfluenza virus, low grade fever. barking cough, hoarseness, improves in cool air (e.g. outside at night).
  – nebulised adrenaline, single dose dexamethasone (0.15mg/kg), O2 and IV fluids
• epiglottitis: rapid onset, haemophilus influenzae B, high grade fever. stridor, tripod position, drooling and odynophagia.
  – intubation (trained staff only), O2, IV antibiotics
• bronchiolitis: gradual onset, RSV, low grade fever. rales, expiratory wheeze, tachypnoea and hypoxaemia.
  – supportive Mx, no vaccine but monoclonal antibodies available.

Question 48

29a. Lung cancer: types and their location and paraneoplastic syndromes, risk factors

Answer 48

• small cell: central, develops from neuroendocrine cells. may cause Cushing’s (ACTH), SIADH (ADH), Lambert-Eaton (neoantigens), and/or myasthenia gravis
• squamous: central, apex. strongly associated with smoking. may cause hypercalcaemia (PTHrP).
• adenocarcinoma: peripheral (Pancoast tumour). may cause HPOA (clubbing), hoarseness (recurrent laryngeal nerve), Horner’s (sympathetic chain). most common in non-smokers.
• risk factors: cigarettes, second-hand smoke, industrial hazards, air pollution

Question 49

29b. Lung cancer: presentation, investigations, management

Answer 49

• clinical features: cough, chest pain, haemoptysis, cachexia, tiredness, hoarseness, wheeze, recurrent infection, fever, paraneoplastic syndromes etc.
• investigations: CXR, CT (stages disease by TNM), PET-CT (lymph nodes, metastases), biopsy
• Mx: MDT. options include radical surgery (I to IIIA), chemo/radiotherapy, adjuvant chemo, palliation

Question 50

30a. Tonsillitis: presentation, differential, management.

Answer 50

• presentation: reddening, oedema, tonsillar enlargement, pseudomembrane, exudate
• DDx: Centor or Fever PAIN used to differentiate between bacterial and viral. 3-4 Centor criteria indicate use of penicillin.
  – Centor: fever, tonsil exudate, lymphadenopathy, no cough/coryza
  – FeverPAIN: fever, purulence, attended <72hr, inflamed tonsils, no cough/coryza
• Mx: if bacterial (3-4 Centor) give phenoxymethylpenicillin (allergy: clarithromycin) for 7-10 days

Question 51

30b. Tonsillectomy: indications, complications

Answer 51

• indications:
  – suspected malignancy
  – febrile convulsions, repeated
  – sleep apnoea
  – recurrent (7x1y, 5x2y, 3x3y)
  – quinsy with a Hx of recurrent tonsillitis
• complications:
  – primary (<24hr): haemorrhage (inadequate haemostasis)
  – secondary (24hr-10dy): haemorrhage (infection), pain

Question 52

30c. Infectious mononucleosis: pathogen, presentation, investigation, management.

Answer 52

• pathogen: EBV
• presentation: triad of fever, pharyngitis, and lymphadenopathy (with atypical lymphocytes)
  – jaundice, hepatitis, rash, leucocytosis, splenomegaly, palatal petichae
• investigation: Paul-Bunnel (sheep RBCs), Monospot (horse RBCs) 1st line. 2nd line antibodies
• Mx: non-specific. bed rest, analgesia, avoidance of sport (splenomegaly).

Question 53

30d. Herpes simplex: presentation, lifecycle, complications, management

Answer 53

• vesicles filled with clear, serous fluid which rupture to yield painful, red-rimmed, shallow ulcers
• lymphadenopathy, fever, anorexia, irritability
• transmission via saliva. after primary infection, travels to ganglia (1 to CN V, 2 to sacral) and stored as latency-associated transcripts (LATs) where they may reactivate at any time
• complications:
  – herpetic whitlow: affects the finger
  – encephalitis: fever, headache, seizure, focal neurological signs, impaired consciousness
  – primary gingivostomatitis
• management: acyclovir, famciclovir, valcyclovir, mouthrinse anaesthetic

Question 54

31. Otitis media (AOM): pathology, presentation, otoscopy findings, management, complications.

Answer 54

• pathology: viral URTIs thought to disturb nasopharyngeal microbiome, allowing bacteria to settle and infect
• presentation: pain (otalgia), ear tugging, fever, hearing loss, coryza
• otoscope: bulging erythematous membrane, otorrhoea, decreased mobility on pneumatic otoscopy
• management: conservative (NSAIDs) <72hr unless meets criteria for immediate abx 5-7 day course (amoxicillin 1st line, C/I erythromycin or clarithromycin)
  – systemically unwell but does not require admission
  – immunocompromised or significant organ disease
  – <2yr with bilateral otitis media
  – otitis media with perforation/discharge
• complications: perforation (leading to CSOM), hearing loss, labyrinthitis, mastoiditis, meningitis, brain abscess, facial nerve paralysi

Question 55

32. Otitis externa: pathology, presentation, otoscopy findings, management, malignant otitis externa

Answer 55

• pathology: natural barriers to infection overcome (i.e. by chlorine in swimming pools) and infection occurs with staph aureus or pseudomonas
• presentation: discharge, itch, swelling, lymphadenopathy
• otoscopy: swollen auditory canal, debris, tympanic membrane normal tympanic membrane
• Mx: topical antibiotics or combined antibiotic (dexamethasone, framycetin sulphate, gramicidin, hydrocortisone, gentamicin)
• malignant OE: occurs in HIV/DM with pseudomonas, deep-seated otalgia, temporal headache, otorrhoea

Question 56

33. Hearing loss: types, causes, clinical examination findings.

Answer 56

• conductive and sensorineural
• conductive: otitis (OME, AOM, otitis externa), obstruction (cholesteatoma, wax), perforation, otosclerosis
• sensorineural: neurological (prebycusis, acoustic neuroma, Meniere’s disease), noise-induced, ototoxicity (aminoglycosides, loop diuretics)
• Weber and Rinne clinical examination findings:
  – normal: W central, R AC>BC
  – left SN loss: W R (louder), AC>BC
  – left C loss: W L (louder), BC>AC L, AC>BC R

Question 57

34. Secretory otitis media with effusion (OME, ‘glue ear’): pathology, risk factors, presentation, otoscopy findings, management

Answer 57

• pathology: non-infectious (unlike AOM), vacuum from poor ventilation leads to effusion
• Rx: male, siblings with OME, winter/spring season, bottle feeding, day care, parental smoking
• presentation: hearing loss, speech delay, balance or behavioural problems
• otoscopy: dull tympanic membrane, loss of light reflex, air bubbles in middle ear
• Mx: grommet insertion (ventilates middle ear) for 6 months-2 years, also consider antibiotic-glucocorticoid drops

Question 58

35. Cholesteatoma: pathology, risk factor, clinical features, otoscopy findings, management

Answer 58

• pathology: associated with chronic otitis media, non-neoplastic keratinising squamous epithelium
• risk factors: chronic otitis media, cleft palate (100-fold)
• clinical features: foul-smelling non-resolving discharge, hearing loss, vertigo, facial nerve paralysis, cerebellopontine angle syndrome
• otoscopy: defect in tympanic membrane, ‘attic crust’
• Mx: ENT referral for mastoid surgery

Question 59

36. Otosclerosis: pathology, clinical features, management.

Answer 59

• pathology: abnormal bone deposition in the middle ear near the oval window and stapes bone. autosomal dominant with variable penetrance
• clinical features: usually begins 20-40yr, conductive deafness, tinnitus, normal tympanic membrane (10% have a ‘flamingo tinge’)
• Mx: hearing aid, stapedectomy

Question 60

37. Vertigo: types (pathology, episode length, clinical features, diagnosis/management)

Answer 60

• BPPV: due to otoconia (stones formed of calcium carbonate) dislodging into the semicircular canals
  – seconds
  – precipitated by movements (e.g. rolling over)
  – Dix-Hallpike is diagnostic, Epley treats vertigo
• Meniere’s: caused by buildup of endolymphatic fluid
  – minutes-hours
  – aural fullness, vertigo, N&V, tinnitus (aural fullness = high yield)
  – low salt and caffiene, cinnarizine, labyrinthectomy
• vestibular neuronitis: due to recent viral infection affecting vestibular part of CN VIII
  – hours-days
  – vertigo, tinnitus, Neuritis = No hearing loss
  – antihistamines, motion sickness medications, antibiotics
• labyrinthitis: due to a viral infection, affecting both parts o CN VIII
  – weeks
  – hearing loss, tinnitus, vertigo
  – Mx as for vestibular neuronitis

Question 61

38. Branchial pouches (embryology): muscles, skeletal / cartilage, nerves, arteries arose

Answer 61

• 1st [‘M’]:
  – muscles: Mastication, Mylohyoid, (anterior belly digastric, tensor tympani and veli palatini)
  – cartilage: Maxilla, Mandible, Malleus, Meckel, (incus)
  – nerves: trigeMinal (V2, 3)
  – artery: Maxillary
• 2nd [‘S’]:
  – muscles: facial expreSSion, Stapedius, Stylohyoid, (posterior belly digastric)
  – cartilage: Stapes, Styloid process of temporal bone, leSSer horn of hyoid, (Reichart)
  – nerves: facial (‘Smiling’)
  – arteries: Stapedial, (hyoid)
• 3rd [‘pharyngeal’]:
  – muscle: stylopharyngeus
  – parathyroid glands
  – nerve: glossopharyngeal
  – arteries: internal and common carotid
• 4th (upper vagus)
  – muscle: cricothyroid
  – cartilage: thyroid cartilage, epiglottic
  – nerve: vagus (superior)
  – arteries: R (subclavian), L (aortic arch)
• 5th (little significance)
• 6th (lower vagus)
  – muscles: all intrinsic larynx muscles (except cricothyroid (4th)
  – cartilages: cricoid, arytenoid, corniculate
  – nerve: vagus (recurrent)
  – arteries: R (R pulmonary), L (L pulmonary, ductus arteriosis)

Question 62

39. Epistaxis: pathology, emergency management, definitive management

Answer 62

• pathology: Little’s (aka Kiesselbach’s) area is a frequent site of nasal haemorrhage where 5 arteries (anterior ethmoid, posterior ethmoid, sphenopalatine, superior labial [septal], greater palatine) anastomose
• emergency Mx: external digital compression of the anterior lower nose (also ice pack) and lean forward for 10 mins. avoid swallowing blood (causes nausea)
• definitive management: if haemodynamic instability, ABCDE + fluid resus
  – bleeding stops with compression: naseptic cream (reduces recurrence)
  – bleeding point can be seen: cautery (silver nitrate)
  – bleeding point cannot be seen: nasal packing or sphenopalatine artery ligation

Question 63

40a. Aphthous ulcers (‘canker sores’): risk factors and associations, types of ulcer, management

Answer 63

• Rx: idiopathic, female, non-smokers, young adults (20-40) family history
• associations: Coeliac’s, IBD, Behcet disease, deficient in iron, folic acid, B12
• types:
  – minor aphthous: <10mm diameter, grey/white centre, thin erythematous halo, heal within 14 days
  – major aphthous: >10mm, persist for weeks and months
• Mx: non-specific; may involve reducing oral trauma, acidic food/drinks. corticosteroids may be considered

Question 64

40b. Behcet disease: diagnostic criteria, epidemiology, management

Answer 64

• diagnosis: recurrent oral ulcers (3/year or more), plus two of
  – genital ulcers
  – eye: anterior uveitis
  – skin: erythema nodosum, pseudofolliculitis, papulopustular lesions
  – positive skin pathergy test
• epidemiology: east Mediterranean, men, young adults (20-40), FHx, HLA-B51 allele
• Mx: non-specific; immunosuppression, colchicine (joint pain), thalidomide (not in pregnant women)

Question 65

41. Oesophageal lacerations: clinical features, management

Answer 65

• Mallory-Weiss tears typically cross the GOJ and occur secondary to increased intra-abdominal pressure (coughing, retching, vomiting). usually stops spontaneously, but may require endoscopy clipping or oversewing
• Boerhaave syndrome: rupture of distal oesophagus, causing deep pain and haematesis (may mimic MI). high yield = subcutaneous emphysema. requires surgical intervention

Question 66

42. Eosinophilic oesophagitis: clinical features, endoscopy findings, management.

Answer 66

• clinical features: food impaction, dysphagia, Hx of allergy or atopy. typical patient is 35, male, white
• endoscope: oesophagus appears ‘trachealised’.
• Mx: take endoscope forceps biopsy and eosinophil count taken. treatment is with diet restriction and topical/systemic steroids

Question 67

43. GORD: presentation, investigation, complications, management

Answer 67

• presentation: heartburn (chest pain exacerbated by changes in position), dysphagia, waterbrash (hypersalivation), weight loss, hoarseness, cough, regurgitation
• Ix: patients <45 with no red flag symptoms do not require Ix. otherwise Ix is with endoscopy or pH monitoring (yields DeMeester score) or manometry
• complications: ulceration, haematesis, melena, strictures, aspiration pneumonia, Barrett’s oesophagus
• Mx:
  – lifestyle: reduce alcohol, caffeine, smoking
  – pharmacologic: PPIs (e.g. omeprazole), H2 antagonist (e.g. ranitidine)
  – surgical: endoluminal gastroplication, Nissen fundoplication

Question 68

44. Oesophageal varices: pathology, causes, clinical features, management.

Answer 68

• pathology: venous blood from the GI tract passes through the liver via the portal vein prior to returning to systemic circulation (‘first pass’). diseases that impede this flow cause portal hypertension and cause shunting (e.g., to oesophageal veins).
• causes: cirrhosis (typically ALD), schistosomiasis, autoimmune disease, sepsis
• clinical features: those of ALD, including spider naevi, palmar erythema, leukonychia, encephalopathy, ascites, jaundice etc. may be picked up on endoscopy or with haematemesis.
• Mx: ABCDE, resus, haemastasis, treat underlying cause
  – beta-blockers, ligation can be used prophylactically

Question 69

45. Oesophageal cancer: types and risk factors, location, presentation, management

Answer 69

• adenocarcinoma: Barrett’s oesophagus, smoking, radiation (risk reduced by fruit, veg)
  – distal 1/3 oesophagus due to metaplasia
• SCC: alcohol, smoking, poverty, caustic injury, Plummer-Vinson
  – upper 2/3 oesophagus
• presentation: pain (food impaction), weight loss, haematemesis, chest pain, vomiting, subconscious adaptation to a liquid diet
• Mx: surgery (tumour has not invaded oesophageal wall), neo-adjuvant and adjuvant therapy, palliation

Question 70

46. Plummer-Vinson syndrome: clinical features, investigations, management

Answer 70

• clinical features [5]: iron deficiency anaemia (microcytic), dysphagia, glossitis, cheilosis, oesophageal webs
• Ix: bloods (iron deficiency anaemia), endoscopy (webs)
• Mx: correct iron deficiency anaemia and dilate webs (bougies).

Question 71

47. Achalasia: presentation, Chagas disease, investigation, management.

Answer 71

• presentation: progressive dysphagia, nocturnal regurgitation, aperistalsis (due to degenerative changes to inhibitory neurones in the lower oesophagus), cough, aspiration pneumonia
• Chagas: associated with travel to S America and infection of T cruzi, (incubation 2 weeks). cardiac signs include cardiomyopathy [dilated: ‘CATCH DEAD’]
• Ix: CXR, barium swallow (‘bird’s beak’), endoscopy, CT (excludes cancer), manometry
• Mx: Heller’s cardiomyotomy

Question 72

48. Gastritis and Helicobacter pylori: causes of gastritis, pathology, microbiology of H pylori, clinical features (ulceration), investigation, management

Answer 72

• causes [ABCD]: autoimmune, bugs (H pylori), chemical (NSAIDs, reflux), distress (stress ulcers)
  – autoimmune: 10% of cases, loss of parietal cells and intrinsic factor and anaemia (vitamin B12 deficiency). antibodies against parietal cells present
  – bugs: H pylori. 90% of cases. gram-negative aerophillic helical bacteria. features include flagella (motility), urease (ammonia, combats stomach acid), adhesins, toxins
  – chemical: NSAIDs (prevents COX and prostaglandin-mediated repair of stomach cells), bile reflux
  – distress: Curling ulcers (proximal duodenum, burns/trauma), Cushing ulcers (intracranial pressure stimulates CN X to secrete stomach acid)
  – others: eosinophilic, lymphocytic (Coeliac’s), granulomatous
• features (PUD): epigastric pain (gastric - more painful after eating; duodenal - less painful after eating), iron deficiency anaemia, haemorrhage, N&V, bloating, belching, weight loss
• Ix: test for H pylori (rapid urease test, faecal antigen test, bacterial culture, PCR)
• Mx: triple therapy [TACO]: Triple of Amoxicillin, Clarithromycin, and Omeprazole

Question 73

49. Gastric cancer: types and their pathologies, clinical features, and management.

Answer 73

• adenocarcinoma (90%). may be intestinal or diffuse morphology. usually occurs in the pylorus, antrum or lesser curve.
  – H pylori, Barrett’s, smoking, nitrites, smoked food, salt
  – Virchow’s node (supraclavicular node)
• lymphoma (aka MALToma). B-cell tumours
  – associated with H pylori and autoimmune gastritis
• carcinoid tumours: arises from G cells causing secretion of serotonin, histamine, bradykinin etc.
  – carcinoid syndrome (flushing, sweating, bronchospasm, colic, diarrhoea)
• clinical features: weight loss, anorexia, early satiety, anaemia, haemorrhage, palpable mass; carcinoid syndrome in carcinoid tumours
• Mx: endoscopic removal, chemo, palliation
  – carcinoid tumours: somatostatin analogue (e.g. octreotide, lanreotide)

Question 74

50. Upper GI bleed: causes, scoring systems, risk factors, presentation, management.

Answer 74

• causes [PIVOT]: peptic ulcers, inflammation (stomach, duodenum), varices, oesophagitis, tears (Mallory-Weiss, Boerhaave)
• scoring: Blatchford score determines need for endoscopy; Rockall score bases risk on findings [ABCDE]: age, BP fall (shock?), co-morbidities, diagnosis (e.g., Mallory-Weiss), evidence of blood
• risk factors: age, co-morbidity, signs of shock, signs of liver disease
• presentation: haematemesis, malaena, shock (bleed is massive)
• Mx: history, ABCDE, group and save, bloods. high yield = urea helps distinguish upper GI from lower GI bleed (digested blood), IV access, monitor BP/pulse for shock and arrange endoscopy
• varices: adrenaline (thermal coagulation or clipping), haemostatic powder (more severe), give PPI

Question 75

51. Coeliac’s disease: pathology, presentation, investigation, management, complications.

Answer 75

• pathology: auto-antibodies against gliadin (IgA) and tissue transglutaminase (TTG), triggered in the presence of gluten. causes villous atrophy
• presentation: chronic diarrhoea, gallstones, bloating, fatigue, anaemia (vitamin malabsorption). F 2x M. dermatitis herpitiformis is an eruption associated with Coeliac’s
• Ix: blood IgA antibodies against TTG. patients should eat gluten in at least one meal every day prior for 6 weeks (gluten challenge test)
  – +ve: diagnosis is made
  – -ve: IgA or IgG EMA (endomysial) tests
  – consider biopsy of the second part of the duodenum
  – in all cases of suspected IBS, test for Coeliac’s
• Mx: only current option is a gluten-free diet
• complications: osteoporosis, malignancy (typically lymphoma), splenic atrophy (pneumococcal vaccination)

Question 76

52. IBS: pathology, clinical features, classification, investigations, management

Answer 76

• pathology: interplay between psychological stress, diet, disturbance of gut microbiome (e.g. gastroenteritis), and abnormal motility
• clinical features: 20-40 yr, female, abdominal pain, bloating, change in bowel habit [ABC]
• Ix: Rome III, Manning criteria. test all patients for Coeliac’s. faecal calprotectin (can distinguish between IBS and IBD)
• IBS-C (constipation):
  – dietary changes: increase fruit and veg, avoid seeds, mushroom, garlic, onion etc.
  – antispasmodics: mebeverine etc., fibre supplements (e.g. ispagula husk), osmotic laxitaves, serotonin-4 antagonists
• IBS-D (diarrhoea)
  – dietary changes: avoid fruit and veg, skin, and bran. consider FODMAP diet
  – antispasmodics as for IBS-C (mebeverine, fibre supplements etc.). loperamide, codiene, TCAs/SSRIs

Question 77

53. IBD: pathology and risk factors, presentation, differences, investigations, treatment, complications.

Answer 77

• pathology: alterations in host interactions with intestinal bacteria, epithelial dysfunction, altered mucosal immune responses and gut microbiome
• risk factors: family history, genetics (160+ genes), T-cells (TH1, TH17, IL-13)
• Crohn’s disease: occurs anywhere in GI tract but most commonly at terminal ilieum, ileocaecal valve and caecum.
  – morphology: skip lesions, strictures, aphthous ulcers, cobblestoning, crypt abscesses, Paneth cell metaplasia, non-caseating granulomas
  – smoking worsens disease
  – Mx: 6-8wk high dose tapering steroids. maintenance immunosuppression with azathioprine, mercaptopurine, methotrexate, infliximab, increased dietary nutrients, supplementation
• UC: always involves the rectum and spreads proximally to the colon (pancolitis)
  – pseudopolyps, atrophy, toxic megacolon, tenesemus, mucus/pus diarrhoea, associated with PSC
  – smoking appears to be protective
  – Ix: Truelove/Witt criteria
  – Mx: as for Crohn’s, but 5-ASA may be used as maintenance therapy
• Ix: colonoscopy and histology, barium enema, MRI, bloods (CRP, albumin, AXR, LFTs, faecal calprotectin which can distinguish IBS and IBD)

Question 78

54. Bowel obstruction: causes and their pathologies, presentation, investigations, management.

Answer 78

• pathology [HAVIC]:
  – hernia: weakness or defect in the abdominal wall which permits protrusion of bowel
  – adhesion: most common cause. fibrous bridges between structures
  – volvulus: twisting of loop of bowel around its mesenteric point of attachment
  – intussusception: segment of intestine constricted by peristalsis, telescopes into immediate distal segment and pulls mesentery along
  – colorectal cancer
• presentation: N&V, cramping abdominal pain, obstipation, distension, fever, tachycardia
• Ix: AXR shows a ‘caterpillar’ like appearance
• Mx: ABCDE, resus, CT, gastrographic studies. drip and suck (resus and removal of food). treat obstruction with surgery

Question 79

55. Hernias: types and their anatomy, cause, risk, age, and gender.

Answer 79

• direct inguinal: protrudes through Hesselbach triangle, medial to inferior epigastric artery. caused by weakness in the transversalis fascia. low risk of strangulation, adults, male
• indirect inguinal: protrudes through inguinal ring, lateral to inferior epigastric artery. caused by failure of closure of the processus vaginalis. low risk of strangulation, more common in infants and males
• femoral: below the inguinal ligament and lateral to the pubic tubercle. high risk of strangulation. more common in adults and females

Question 80

56. Ischaemic bowel disease: pathology, causes, presentation, investigations, management.

Answer 80

• pathology: blockage of coeliac, superior or inferior mesenteric arteries. hypoxic injury occurs and reperfusion causes damage. most vulnerable are the splenic flexure and sigmoid colon/rectum.
• causes: severe atherosclerosis, aortic aneurysm, hypercoagulable state, COCP use, AF emboli, illicit drugs (e.g. cocaine)
• presentation: usually elderly patient. severe left lower abdominal pain, cramping, desire to defecate, blood PR
• Ix: CT angiogram and laparotomy. FBC shows raised WCC and metabolic acidosis (high yield)
• Mx: surgical. resection (portion of bowel is not viable), emblectomy (portion of bowel is viable).

Question 81

57. Gastroenteritis: microbiology (stereotypical history, incubation period, need for abx), investigation, aspects of management.

Answer 81

• microbiology based on incubation periods [1st line abx; 2nd line abx]:
  – child, ~3-5 days: watery diarrhoea, rotavirus
  – any age, ~3 days, projectile vomiting and watery diarrhoea (semi-closed environments): norovirus
  – 1-6h: staph aureus (severe vomiting), b. cereus (reheated rice)
  – 12-48h: e coli o157 (traveller’s diarrhoea); salmonella [amox/ceftriaxone; trimethoprim]
  – 48-72h: campylobacter jejuni (flu-like prodrome, bloody diarrhoea, tenesmus, may mimic appendicitis, can cause GBS [azithromycin; cipro, vanco]); shigella (~3d bloody diarrhoea [azithromycin, ceftriaxone; cefixime, cipro])
  – >7 days: giardiasis, ETEC (prolonged, non-bloody diarrhoea); amoebiasis (bloody diarrhoea)
  – C. diff: new onset neutrophilia after abx treatment of other infection [metro; vanco]
  – cholera: rice-water diarrhoea, severe dehydration [azithromycin; doxy, cipro]
  – C. perfringins: inadequate storage or reheating of meat
• Ix: history, exam (if appropriate), admit systemically unwell patients (dehydration, shock, sepsis), stool culture and sensitivity if bacterial cause suspected
• Mx (home): rehydration (water, ORS)
• Mx (social): do not attend work/school until 48hr after last episode of D/V
• notify local health protection team

Question 82

58. Intestinal polyps (benign): types (and associated syndromes), clinical features

Answer 82

• hyperplastic polyps: patients 60-70yrs, no malignant potential. most common in left colon and typically multiple.
• inflammatory: IBD, presents with rectal bleeding, mucus discharge. caused by impaired relaxation of the anorectal sphincter causing abrasion and ulceration
• hamartomas:
  – juvenile polyposis: SMAD4 gene, macrocephaly, hypotonia
  – Peutz-Jeghers syndrome: hyperpigmented macules (dark blue ‘freckles’) on lips, nostrils, hands, feet, genitalia, perianal. Mx by endoscopic polypectomy, screening (CEA: colon cancer, CA19-9: pancreatic cancer, CA-125: ovarian)

Question 83

59a. Colorectal cancer (genetic syndromes): FAP (Gardner’s) and HNPCC (Lynch’s).

Answer 83

• FAP: autosomal dominant, hundreds of polyps form. caused by mutation to tumour suppressor APC. 100 polyps required to diagnose. Gardner’s includes extra-colonic polyps (osteoma of skull and mandible, epidermoid cysts, thyroid carcinoma, retinal pigmentation. prophylactic total colectomy with ileo-anal pouch formation
• HNPCC: small number of polyps. autosomal dominant against DNA replication mismatch repair, causing microsatellite instability. also confers high risk for endometrial cancer.

Question 84

59b. Colorectal cancer: screening

Answer 84

• FIT (faecal immunochemical test) is a type of FOB (faecal occult blood test) that screens specifically for human Hb
• Scotland: ages 50-74, England: ages 60-74.
• abnormal result prompts colonoscopy. 50% will be normal, 40% will have polyps (removed due to their premalignant potential), and 10% will have colorectal cancer.

Question 85

59c. Colorectal cancer: epidemiology, locations of malignancy, risk factors, how patients may present, referral critera

Answer 85

• epidemiology: third most diagnosed in UK (after lung and breast cancer), 150,000 new cases and 50,000 deaths per annum
• locations: 40% rectal, 30% sigmoid colon, 15% ascending colon and caecum, 10% transverse colon, 5% descending colon. small intestine accounts for <1% (duodenum/jejunum)
• risk factors: low fibre, high carbohydrate and red meat intake, smoking, obesity. theorised that low fibre reduces stool bulk and alters the microbiome
• presentation: bowel screening, urgent referral, or emergency (e.g. obstruction)
• referral criteria (2-wk pathway):
  – >40 weight loss + abdo pain
  – >50 rectal bleed
  – >60 iron deficiency anaemia
  – >60 change in bowel habit
• consider for 2-wk referral:
  – rectal/abdo mass
  – unexplained anal mass or ulceration
  – <50 with rectal bleeding + 1 of (abdo pain, change in bowel habit, weight loss, iron deficiency anaemia)

Question 86

59d. Colorectal cancer: investigations and management

Answer 86

• diagnosis: sigmoidoscopy or colonoscopy (dependent on location), MRI (below peritoneal reflection)
• staging: CT chest, abdomen and pelvis
• Mx: resection (curative) with anastamosis
  – caecum to proximal transverse colon: R hemicolectomy + ileo-colic anastomosis
  – distal transverse to descending colon: L hemicolectomy + colo-colon anastomosis
  – sigmoid colon: high anterior resection + colo-rectal anastamosis
  – upper rectum: anterior (TME) + colo-rectal anastomosis
  – lower rectum: anterior (low TME) + colorectal anastomosis with defunctioning stoma
  – anal verge: abdominoperineal excision of rectum, no anastomosis

Question 87

60. Acute appendicitis: pathology, clinical features and signs, diagnosis, management.

Answer 87

• pathology: increases in intraluminal pressure compromise venous outflow. causes include faecoliths, gallstones, tumours, or mass of worms. stasis of venous flow triggers ischaemia and inflammation. contact with the omentum may cause peritonitis.
• clinical features: abdominal pain, N&V, anorexia, low-grade fever, tachycardia, leucocytosis
• clinical signs: McBurney point, guarding, Rosving’s (palpation of LLQ causes pain in RLQ), Psoas, Obturator, Aaron’s (pointing sign)
• Dx: history and exam + leucocytosis generally adequate for diagnosis. other tests: urinalysis (pregnancy, renal colic, UTI). USS may be useful in women, CT (not generally used in UK)
• Mx: laparoscopic appendicectomy. prognosis by Alvarado score (MATRELS)
  – Migration of pain (1)
  – Anorexia (1)
  – Nausea (1)
  – Tenderness RLQ (2)
  – Rebound (1)
  – Elevated temp (1)
  – Leucocytosis (2)
  – Shift of WBC [leucocytosis] {1}

Question 88

60. Ascites: definition, pathology, diagnosis, management.

Answer 88

• definition: accumulation of fluid within the peritoneal cavity
• pathology: portal hypertension causes increased hydrostatic pressure, leading to transudation of fluid
• Dx: ascitic tap with SAAG (serum ascites albumin gradient)
  – high SAAG [>1.1]: cirrhosis, CHF, Budd-Chiari, constrictive pericarditis, hepatic
  – low SAAG [<1.1]: mesothelial cancer, TB, pancreatitis, nephrotic syndrome
• Mx: salt and fluid restriction, spironolactone +/- furosemide +/- therapeutic paracentesis

Question 89

61. Haemorrhoids: pathology, risk factors, terminology, presentation, differentials, staging, management.

Answer 89

• pathology: enlarged, congested, symptomatic vascular cushions (sinusoids rather than veins, meaning not varices). found mainly at 3’, 7’, and 11’oclock. portal hypertension forms shunts. exposed vasculature so subject to trauma, inflammation, thrombosis, ulceration
• terminology: internal/endoderm (above anorectal line), external/ectoderm (below anorectal line)
• risk factors: straining (e.g. at defecation), constipation, venous stasis of pregnancy
• presentation: discomfort, fullness in rectum, pruritis, pain
• DDx:
  – fissure (lacks mass; treated with laxatives and topical GTN)
  – abscess (fever, surrounding cellulitis)
  – polyps (lacks pain)
• staging: I (no prolapse, prominent vessels), II (prolapse on bearing down, spontaneous reduction), III (prolapse on bearing down, manually reduced), IV (prolapse, not able to be reduced).
• Mx:
  – I, II: high fibre, fruit and veg diet; sitz bath and steroid cream or pramoxine
  – III, IV: sclerotherapy, rubber band ligation, infrared coagulation, haemorrhoidectomy

Question 90

62a. Acute/fulminant liver failure: causes, clinical features, investigation, management.

Answer 90

• causes [ABCDEF]: A (acetominophen, hep A, autoimmune), B (hep B), C (hep C), D (drugs, hep D), E (hep E), F (fatty changes to liver)
• clinical features: high yield = encephalopathy (raised ammonia, causes asterixis, personality change) and coagulopathy (easy bruising). also N&V, jaundice, icterus, high oestrogen (spider naevi, gynaecomastia, palmar erythema)
• Ix: thorough Hx, LFTs, PT (best screen for liver function), USS, virology
• Mx: rest, fluids, nutrition, N-acetylcysteine in paracetamol overdose

Question 91

62b. Alcoholic liver disease (ALD): risk factors, pathology, clinical features, management, prognosis

Answer 91

• risk factors: women (more susceptible to damage), African American ethnicity, co-morbidities (iron, HBC, HCV)
• pathology: acetaldehyde (product of alcohol breakdown by ADH) induces lipid production and disrupts cytoskeleton and membrane function, decreasing methionine and glutathione levels, sensitising the liver to oxidative injury
  – 2-3 days: hepatic steatosis (lipid buildup)
  – 4-6 weeks: alcoholic hepatitis, necrosis, Mallory-Denk bodies, neutrophils
  – months-yrs: fibrosis (chicken-wire fence pattern)
  – yrs: cirrhosis
• clinical features: raised bilirubin, ALP. malaise, anorexia, weight loss, abdominal discomfort, hepatomegaly. chronically: dementia, Wernicke-Korsakoff, anaemia, MSK, endocrine, reproductive disease, spider naevi, encephalopathy, raised PT, low albumin, caput medusae, hypersplenism, thrombocytopaenia
• Mx:
  – short term: prednisolone, PTX.
  – long term: alcohol cessation, transplant
• prognosis: 90% 5-yr survival in abstinence. risks include hepatic coma, GI haemorrhage, infection, hepatorenal syndrome, HCC (1-6% yr)

Question 92

63a. Primary biliary cholangitis (PBC): pathology, investigations, presentation, management.

Answer 92

• pathology: non-suppurative inflammatory destruction of small-medium sized intrahepatic bile ducts
• investigations: anti-mitochondrial antibodies present, plus raised ALP and IgM
• presentation: fatigue, pruritis, xanthelasma. extrahepatic signs include hyperpigmentation, steatorrhoea, osteomalacia, RA, Raynaud’s, Coeliac’s
• Mx: ursodeoxycholic acid (pruritis), liver transplant

Question 93

63b. Primary sclerosing cholangitis (PSC): pathology, investigations, presentation, management.

Answer 93

• pathology: inflammation and obliterative fibrosis of intrahepatic and extrahepatic bile ducts
• investigations: pANCA in 94%, MCRP gold standard investigations, raised ALP, associated with UC
• presentation: fatigue, pruritis, jaundice, steatorrhoea, risk of cholelithiasis and cholangiocarcinoma, chronic pancreatitis and cholecystitis
• Mx: symptomatic: cholestyramine, ERCP with dilatation. definitive: transplantation

Question 94

63c. Bilirubin disorders: pathology of the four bilirubin disorders (Gilbert’s, Crigler-Nijjar, Dubin, and Rotor syndromes)

Answer 94

• Gilbert’s: increased unconjugated bilirubin due to immature UGT (UDP-glucuronosyltransferase). Stresses and exercise results in jaundice
• Crigler-Nijjar: UGT not present
• Dubin: bilirubin cannot be excreted from the liver, resulting in dark liver
• Rotor: milder form of Dubin syndrome

Question 95

63d. NAFLD/NASH: pathology, presentation, management

Answer 95

• pathology: insulin resistance (metabolic syndrome) and oxidative injury (liver cell necrosis and inflammation). associated with hypertension, dyslipidaemia, central obesity, microalbuminuria
• presentation: metabolic syndrome including cardiovascular disease
• Mx: reversing steatosis, preventing cirrhosis by managing underlying factors (e.g. obesity, insulin resistance)

Question 96

63e. Haemochromatosis: pathology, presentation, investigation, management

Answer 96

• pathology: excessive iron absorption, autosomal recessive. affects men > women as menstruation counteracts accumulation. occurs with genetic defect to hepcidin, which removes iron
• clinical signs: hepatomegaly, abdominal pain, hyperpigmentation, arthritis, cardiomyopathy and arrhythmia
• Mx: weekly phlebotomy (venesection)

Question 97

63d. Wilson disease: pathology, clinical features, investigations, management

Answer 97

• pathology: autosomal recessive (chr13), causing impaired copper excretion into bile. copper accumulation promotes formation of free radicals causing oxidative damage
• clinical features: steatosis, asterixis, chorea, psychiatric disturbance, Kayser-Fleisher rings
• Ix: decreased ceruloplasmin, increased urinary excretion of copper
• Mx: D-penicillinamine or zinc-based therapy. transplant is definitive

Question 98

63e. a1-antitrypsin deficiency: pathology, clinical features, investigation, management

Answer 98

• pathology: autosomal recessive deficiency of a1-AT, which normally inhibits elastin (a neutrophil protease released at the site of inflammation)
• clinical features: pulmonary (emphysema, bronchitis or bronchiectasis), hepatic (cirrhosis)
• Ix: pulmonary or hepatic symptom Ix (e.g. CXR or liver biopsy). periodic acid-Schiff positive stain
• Mx: smoking cessation, IV a1-AT, COPD medication, lactulose for hepatic encephalopathy

Question 99

64a. HAV (hepatitis A virus): epidemiology, virology, disease.

Answer 99

• epidemiology: endemic in developing countries, especially those with poor sanitation and hygiene. spread via faecal-oral route (sporadic infection with shellfish).
• virology: positive-strand RNA picornavirus. vaccine is available.
• disease: causes Acute infection (fatigue, anorexia, jaundice). cannot cause chronic hepatitis.

Question 100

64b. HBV (hepatitis B virus): epidemiology, virology, presentation, serology, management, progression

Answer 100

• epidemiology: transmitted via the 3 B’s (blood, birthing, ‘bonking’).
• virology: DNA hepadnavirus. includes surface Ag/Ab (HbSAg), core Ag/Ab (HbCAg), and E Ag/Ab (HbEAg).
• presentation: asymptomatic (65%), constitutional (25%), chronic infection (10%)
• serology [HbSAg / HbSAb / HbCAb]
  – no infection: -/-/-
  – vaccinated: -/+/-
  – previous infection: -/+/+
  – acute infection: +/-/IgM
  – chronic infection: +/-/IgG
  – unclear: -/-/+
• Mx: acute (monitor for encephalopathy and resolution, inform public health and vaccinate contacts). chronic: prevent progression to cirrhosis or cancer (peginterferon first line, other antivirals if not tolerated)
• progression: chronic hepatitis, HCC, polyarteritis nodosa

Question 101

64c. HCV (hepatitis C virus): epidemiology, virology, presentation, management.

Answer 101

• epidemiology: IV drug abuse (54%), multiple sex partners (36%), surgery (16%), needle stick injury, childbirth, medical or dental employment
• virology: single-stranded RNA virus of Flaviviridae family
• presentation: milder than HBV acutely, but almost always leads to Chronic hepatitis (80-90%)
• Mx: HAART (as used for HIV), transplant

Question 102

64d. HDV and HEV (hepatitis D/E virus).

Answer 102

• HDV: delta virus, requires HBV for propagation. typically restricted to PWIDs. vaccination for HBV also protects against HDV.
• HEV: transmitted via faecal-oral route and, like HAV, causes only acute hepatitis. no vaccine. high mortality in pregnant women. zoonotic with animal reservoirs (cats, dogs, monkeys, pigs)

Question 103

65a. Benign liver tumours: types, risk of dysplasia and neoplasia, other features

Answer 103

• HNF1-a inactivated HC adenomas: 90% somatic, more common in women, almost 0% risk of neoplasia
• B-catenin activated HC adenomas: equal risk to both men and women, high risk of dysplasia so should be resected
• inflammatory HC adenomas: associated with NAFLD/NASH. medium risk of dysplasia so should be resected. overproduction of CRP and amyloid.

Question 104

65b. HCC (hepatocellular carcinoma): risk factors, clinical features, screening, management, metastasis

Answer 104

• risk factors: HBV, HCV, aflatoxin (Aspergillus), alcohol injury, metabolic disease (haemochromatosis, Wilson’s, a1-AT deficiency)
• clinical features: malaise, upper abdominal pain, fatigue, weight loss, hepatomegaly, liver bruit (rare)
• screening: in those with known cirrhosis, screen for varices and AFP levels (>100ng/ml suggestive). USS, CT/ MRI with vascular or contrast allows staging
• Mx: transplantation, resection, ablation
• metastasis: most commonly to colon, lung, breast, and pancreas.

Question 105

65c. CCA (cholangiocarcinoma): risk factors, pathology, presentation.

Answer 105

• risk factors: PSC, HBV, HCV, NAFLD, liver flukes
• pathology: chronic inflammatory disease of large bile ducts cause neoplasia
• presentation: obstruction of biliary flow, symptomatic liver mass

Question 106

66. Biliary disease: differential diagnosis

Answer 106

• [RUQ pain / fever / jaundice]
  – biliary colic: +/-/-. Five F’s: Female, Fat, Fertile, Fair, Forty. Mx: analgesia, dietary change, laparoscopic cholecystectomy, ERCP/MRCP
  – cholecystitis: +/+/-. Murphy’s sign is positive. Mx: IV abx, nil by mouth, USS to confirm Dx. ERCP may be used to remove.
  – cholangitis: +/+/+
  – carcinoma: -/-/+

Question 107

67. Acute pancreatitis: pathology, clinical features, investigations, management, prognosis

Answer 107

• pathology: I GET SMASHED: idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpions, hypercalcaemia, ERCP, drugs (e.g. azathioprine). acute pancreatitis results from inappropriate release and activation of pancreatic enzymes, which destroy pancreatic tissue
• clinical features: abdominal pain (constant, intense, radiates to back and left shoulder). anorexia, N&V, erythema abgine, Cullen’s sign, Grey Turner’s sign
• Ix: USS, CT, raised amylase (first 24h), raised lipase (72-96h)
• Mx: rest the pancreas by nil by mouth. IV fluids and analgesia. correct electrolytes
• prognosis: Glasgow score [PANCREAS]:
  – PaO2 <8kPa
  – Age >55
  – Neuts >15x10(9)/l
  – Ca2+ <2mmol/l
  – Renal (urea >16mmol/l)
  – Enzymes (AST/ALT >200, LDH >600)
  – Albumin <32g/l
  – Sugar >10mmol/l

Question 108

68. Pancreatic carcinoma: pathology, epidemiology, clinical features, management

Answer 108

• pathology: genes: KRAS (PI3K/AKT pathways), CDKN2A, SMAD4, TP53. marker: CA19-9
• epidemiology: risk factors include age (60-80), black or Jewish ethnicity, smoking, fat-rich diet, charred meats
• clinical features: asymptomatic, then pain, obstructive jaundice, weight loss, anorexia, malaise, weakness, steatorrhoea, dark urine, back pain, Trosseau sign (migratory thrombophlebitis)
• Mx: inoperable (>80%): ERCP/PTC and stents. operable: Whipple’s, pancreatectomy