DOH, DHA & MOH Internal Medicine Specialist Exam Questions

Heroin-associated nephropathy (HAN) classically presents as FSGS — the correct answer — characterised by progressive proteinuria (often nephrotic-range), gradual decline in GFR, and an absence of haematuria unless a superimposed nephritic process exists. Light microscopy shows focal and segmental sclerosis with hyalinosis; electron microscopy demonstrates diffuse podocyte foot-process effacement. FSGS is also associated with HIV, sickle cell disease, obesity, and reflux nephropathy (KDIGO Glomerular Diseases Guidelines 2021). AA amyloidosis (B) can complicate chronic heroin use due to recurrent skin infections and abscess formation causing sustained acute-phase response, but typically presents with nephrotic-range proteinuria and enlarged echogenic kidneys — a plausible but less common cause. Mesangiocapillary GN (C) and IgA nephropathy (D) typically feature haematuria. Chronic pyelonephritis (E) causes tubular defects and scarring rather than significant proteinuria. Clinical pearl: always check HIV status in IVDU with FSGS, as HIV-associated nephropathy (HIVAN) is a distinct collapsing variant requiring antiretroviral therapy as primary treatment.

This presentation is classic for intrahepatic cholestasis of pregnancy (ICP): pruritus predominating on palms and soles, no primary rash, elevated serum bile acids (≥10 µmol/L diagnostic; ≥40 µmol/L high-risk threshold), and mildly elevated transaminases. Per RCOG Green-top Guideline No. 43 (2022), bile acids ≥40 µmol/L are associated with significantly increased risk of stillbirth, spontaneous preterm birth, and meconium-stained liquor. Management includes ursodeoxycholic acid for symptom relief, serial bile acid and LFT monitoring, and planned delivery at 37–38 weeks for bile acids >40 µmol/L. The other options describe conditions without hepatic involvement or elevated bile acids: PUPPP (urticarial plaques on abdomen, benign), atopic eruption (eczematous, no LFT changes), and polymorphic eruption (self-limiting, no fetal risk). Pearl: serum bile acids, not bilirubin or ALT, are the key diagnostic and prognostic marker in ICP.

Weight gain (E) is the most common clinically significant adverse effect of sulfonylureas, including gliclazide. Sulfonylureas stimulate pancreatic beta-cell insulin secretion independently of ambient blood glucose, producing a sustained anabolic state that promotes glucose uptake and adipogenesis. This is a well-recognised management consideration when choosing therapy in overweight or obese patients with type 2 diabetes (ADA Standards of Care 2024, Section 9; NICE NG28). Hypoglycaemia is the other major adverse effect. Peripheral neuropathy (A) is a complication of diabetes itself, not gliclazide. Cholestasis (B), photosensitivity (C), and SIADH (D) are rare, idiosyncratic class effects of sulfonylureas — recognised but uncommon compared to weight gain, which affects a substantial proportion of users. Clinical pearl: When initiating sulfonylureas in patients who are already overweight, consider the weight trajectory and discuss the risk explicitly, as per ADA 2024 shared decision-making recommendations.

Per IMWG diagnostic criteria (reaffirmed in NCCN Multiple Myeloma v2.2025), multiple myeloma is confirmed by clonal bone marrow plasma cells ≥10% (or biopsy-proven plasmacytoma) together with one or more CRAB criteria or a myeloma-defining event (e.g. >60% clonal plasma cells, serum FLC ratio ≥100). This patient fulfils all four CRAB features: hyperCalcaemia (Ca 11.9 mg/dL), Renal insufficiency (creatinine 2.1 mg/dL), Anaemia (Hb 8.8 g/dL), and Bone lesions (lytic lesions on CT). The clonal plasma cell threshold ≥10% is therefore the confirmatory bone marrow finding. Option B describes features of Hodgkin lymphoma (Reed-Sternberg cells). Option C describes AML with maturation. Option D describes myelodysplastic syndrome with ring sideroblasts (MDS-RS). Pearl: clonality must be demonstrated (κ/λ light-chain restriction by immunohistochemistry or flow cytometry); hypercellular marrow alone is insufficient.

Felty syndrome is defined by the triad of seropositive rheumatoid arthritis, splenomegaly, and neutropaenia (ANC <2.0 × 10⁹/L, often <0.5 × 10⁹/L in severe cases). It occurs in fewer than 1% of RA patients, typically after ≥10 years of active, seropositive disease, and confers markedly increased susceptibility to bacterial infections — the clinical scenario here. Management per EULAR 2022 RA recommendations includes optimisation of DMARDs (methotrexate first-line), G-CSF for severe or symptomatic neutropaenia, and splenectomy reserved for refractory cases. Adult-onset Still's disease presents with quotidian fever, rash, and arthritis in a younger patient without established RA. Caplan syndrome describes pulmonary nodules in RA patients with pneumoconiosis. Large granular lymphocyte (LGL) syndrome can mimic Felty syndrome with neutropaenia and splenomegaly but is driven by a clonal LGL expansion — an important differential to exclude. Primary Sjögren's overlap does not cause this specific triad. Clinical pearl: Felty syndrome shares the HLA-DR4 haplotype with seropositive RA and can occur even when joint disease is quiescent.