DOH, DHA & MOH Internal Medicine Specialist Exam Questions

This patient meets GINA 2024 criteria for severe uncontrolled Type 2 high asthma: blood eosinophils ≥150 cells/μL (here 450), FeNO ≥25 ppb (here 55), and inadequate control despite optimised step 4 therapy. Dupilumab (anti-IL-4Rα, blocking both IL-4 and IL-13 signalling) is approved at GINA step 5 for this phenotype and does not require pre-treatment IgE or allergen sensitization data, making it the correct choice while those results are pending. Omalizumab targets free IgE and is indicated only when allergic sensitization and elevated total IgE are confirmed — not yet available here. Tiotropium (LAMA add-on) is a GINA step 4–5 option but is less effective than biologics for eosinophilic disease and would not adequately address this severity. Long-term oral corticosteroids carry significant systemic toxicity and are a last resort. Azithromycin has evidence in non-eosinophilic/neutrophilic severe asthma (AMAZES trial) and is less appropriate when Type 2 biomarkers are markedly elevated. Pearl: when IgE and sensitization data are unavailable, dupilumab is the biologic that can be initiated purely on eosinophil and FeNO criteria. Reference: GINA 2024, Step 5 add-on therapies; NICE NG245 (2024).

Why correct (D): This patient presents with recurrent acute anterior uveitis (AAU) associated with HLA-B27-positive axial spondyloarthropathy (ankylosing spondylitis, per the modified New York criteria supported by bilateral sacroiliitis on MRI and clinical features). The ocular findings — circumcorneal flush, fine non-granulomatous keratic precipitates, significant anterior chamber cells and flare, and posterior synechiae — are classic for HLA-B27-associated acute anterior uveitis. According to the American Uveitis Society consensus and the European League Against Rheumatism (EULAR) 2022 recommendations for spondyloarthropathy-associated uveitis, the first-line treatment for acute non-infectious anterior uveitis is intensive topical corticosteroids combined with a cycloplegic–mydriatic agent. Topical prednisolone acetate 1% is the gold-standard topical corticosteroid for anterior uveitis, applied hourly during waking hours initially and then tapered gradually based on clinical response (typically over 4–6 weeks to prevent rebound). Cyclopentolate 1% (an intermediate-acting cycloplegic) serves two critical purposes: it reduces pain from ciliary spasm and prevents further posterior synechiae formation by keeping the pupil mobile and dilated. The existing 2 mm posterior synechia at 6 o'clock underscores the urgency of cycloplegia. This combination is the established initial treatment for anterior uveitis in all major ophthalmological guidelines.

Why A is wrong: Oral methotrexate is a steroid-sparing immunosuppressive agent used for chronic or frequently recurrent uveitis that is refractory to topical therapy, or for sight-threatening intermediate/posterior/panuveitis. While this patient has had recurrent episodes, systemic immunosuppression is not the initial treatment for an acute flare of anterior uveitis. Starting methotrexate may be considered as a longer-term prophylactic strategy after the acute episode is controlled, particularly if recurrences become more frequent (generally >3 episodes per year), but it is not the immediate treatment for the acute inflammatory episode.

Why B is wrong: Oral prednisolone at 1 mg/kg/day is reserved for severe bilateral anterior uveitis unresponsive to topical therapy, or for intermediate, posterior, or panuveitis where topical therapy cannot reach the site of inflammation. In isolated unilateral acute anterior uveitis — even with moderate severity as in this case — topical therapy is the first-line approach. Systemic corticosteroids carry significant systemic side effects (hyperglycaemia, osteoporosis, adrenal suppression, weight gain) and are not warranted as initial therapy when topical treatment is expected to be effective.

Why C is wrong: Sub-Tenon (periocular) triamcinolone injection is a regional corticosteroid delivery method used primarily for intermediate uveitis, cystoid macular oedema secondary to uveitis, or anterior uveitis refractory to intensive topical therapy. It is not first-line for acute anterior uveitis. Furthermore, periocular depot steroids carry risks of elevated intraocular pressure and cataract formation that are avoidable when topical therapy suffices.

Why E is wrong: Topical ketorolac is a non-steroidal anti-inflammatory drug (NSAID) with insufficient anti-inflammatory potency to control true uveitis; it is used for post-operative inflammation or allergic conjunctivitis. Topical moxifloxacin is a fluoroquinolone antibiotic with no role in non-infectious uveitis. This combination entirely omits corticosteroid therapy and cycloplegia, both of which are essential. A registrar might be tempted by this option if misdiagnosing the presentation as infective keratitis or post-surgical inflammation, but the clinical picture is unambiguously non-infectious anterior uveitis.

Key learning point: HLA-B27-associated acute anterior uveitis is the most common form of anterior uveitis and is strongly linked to axial spondyloarthropathies. The cornerstone of initial treatment is intensive topical corticosteroid (prednisolone acetate 1% hourly) plus a cycloplegic agent (cyclopentolate 1%) to control inflammation, relieve pain, and prevent synechiae. Systemic or regional corticosteroids and immunosuppressive agents are reserved for refractory, chronic, or posterior segment disease.

Serum amylase, when elevated ≥3× the upper limit of normal in the appropriate clinical context (epigastric pain, vomiting, alcohol history), is a recognised diagnostic criterion for acute pancreatitis per BSG 2019 guidelines. However, the degree of elevation does not correlate with disease severity, and amylase does not feature in any validated prognostic scoring system — including Glasgow-Imrie, Ranson, or APACHE II. The correct answer is C. Option A is incorrect: amylase has no prognostic utility; CRP >150 mg/L at 48 hours is the preferred biochemical severity marker (BSG 2019). Option B is incorrect: serum lipase is more sensitive and more specific than amylase, particularly in alcohol-related pancreatitis and late presentations (longer half-life). Option D is incorrect: amylase specificity is ~90% but is elevated in salivary pathology, perforated viscus, mesenteric ischaemia, and DKA. Option E is incorrect: amylase clearly has diagnostic value. Clinical pearl: in late-presenting or alcohol-related pancreatitis, request lipase rather than amylase — amylase may have normalised by 48–72 hours even in severe disease.

Fibrates (e.g., fenofibrate) are the established first-line pharmacological treatment for type III hyperlipoproteinaemia (dysbetalipoproteinaemia). This rare disorder results from apoE2 homozygosity, impairing hepatic clearance of chylomicron and VLDL remnants (IDL), producing the characteristic elevation of both cholesterol and triglycerides with pathognomonic palmar xanthomata. Fibrates activate PPAR-α, upregulating lipoprotein lipase and reducing remnant accumulation — the core pathophysiological target. This is supported by the ESC/EAS Dyslipidaemia Guidelines (2019, reaffirmed in 2024 prevention context) and NICE CG181. Statins are effective adjuncts but address LDL-C via HMG-CoA reductase inhibition rather than remnant clearance, making them second-line. Omega-3 fatty acids lower triglycerides but are adjunctive. Secondary causes (hypothyroidism, diabetes, obesity) must always be excluded first, as treating them alone can resolve the phenotype. Ursodeoxycholic acid has no role in dyslipidaemia management.

Hydroxychloroquine blocks hERG potassium channels (Kv11.1), delaying cardiac repolarisation and prolonging the QT interval. When combined with other QT-prolonging agents — including macrolide antibiotics (azithromycin, erythromycin), antipsychotics (haloperidol, quetiapine, chlorpromazine), and class III antiarrhythmics (amiodarone, sotalol) — additive or synergistic QT prolongation markedly increases the risk of torsades de pointes (TdP), a potentially fatal polymorphic ventricular tachycardia. This is classified as a 'Known Risk' drug-drug interaction on the CredibleMeds/AZCERT QTDrugs database (2024), and was specifically highlighted in MHRA Drug Safety Updates during the COVID-19 pandemic. Option A is incorrect: beta-blockers and ACE inhibitors do not prolong QT and may actually be protective against arrhythmia. Option C is incorrect: furosemide does not cause QRS widening; its arrhythmic risk is indirect via hypokalaemia and hypomagnesaemia. Option D is incorrect: clinically significant CYP3A4-mediated statin–hydroxychloroquine interactions are not established in current pharmacokinetic guidance. Pearl: always cross-reference newly prescribed drugs against the CredibleMeds QTDrugs list for patients on hydroxychloroquine with a baseline QTc >450 ms.