Assistant Surgeon / Casualty Medical Officer — 2023 — Provisional Answer Key — Kerala PSC PYQ Practice with Answers

Correct answer (Option D):\nPericarditis is clinically recognized as the most common cardiac manifestation found in patients suffering from Systemic Lupus Erythematosus (SLE). It can present acutely with characteristic chest pain or run an asymptomatic course accompanied by minor pericardial effusions.\n\nWhy others are wrong:\nOption A (Libman-Sacks endocarditis) is a classic, highly specific stereotypic non-bacterial verrucous endocarditis associated with SLE, but it occurs less frequently than pericarditis. Options B and C are rarer complications or chronic sequelae rather than the most common presentation.\n\nRemember:\nWhen evaluating cardiac issues in multi-system autoimmune diseases like SLE, look out for pericardial rubs or distinctive ECG changes associated with fluid collection around the pericardial sac.

Correct answer (Option C):\nChronic myeloid leukaemia (CML) is uniquely driven by the hallmark BCR-ABL1 fusion gene resulting from the reciprocal translocation t(9;22), widely known as the Philadelphia chromosome. It is not fundamentally associated with Janus kinase 2 (JAK2) mutations.\n\nWhy others are wrong:\nOptions A, B, and D describe classic BCR-ABL1 negative myeloproliferative neoplasms (Polycythemia vera, Primary Myelofibrosis, and Essential Thrombocythemia). These conditions heavily exhibit somatic JAK2 V617F mutations in a significant percentage of presenting clinical cases.\n\nRemember:\nJAK2 mutations alter tyrosine kinase signaling within the hematopoietic cell lines, accelerating standard cell line propagation without dependency on normal erythropoietin regulators.

Correct answer (Option A):\nIn Von Willebrand disease (vWD), the Prothrombin Time (PT) remains entirely normal. PT evaluates the extrinsic and common pathways of the coagulation cascade, which are completely unaffected by the deficiency or dysfunction of Von Willebrand Factor.\n\nWhy others are wrong:\nOption B and D are true because vWF stabilizes coagulation Factor VIII; hence, its deficiency leads to secondary systemic depletion of Factor VIII, extending the Activated Partial Thromboplastin Time (APTT). Option C is true because vWF is vital for functional platelet-to-endothelium adhesion, and its absence directly prolongs cellular Bleeding Time.\n\nRemember:\nvWD stands out as the most common inherited structural bleeding disorder, displaying diverse patterns of clinical severity across its qualitative and quantitative classification types.

Correct answer (Option D):\nConn's syndrome (primary hyperaldosteronism) is caused by autonomous aldosterone overproduction from the adrenal cortex. Excess aldosterone triggers substantial sodium retention and excessive renal potassium excretion, culminating directly in systematic arterial hypertension alongside hypokalemia.\n\nWhy others are wrong:\nOption A causes hyperdynamic circulatory symptoms but not direct hypokalemic pathology. Option B (Addison's disease) features aldosterone deficiency, bringing about hypotension and hyperkalemia. Option C typically displays fluid retention with variable or normal potassium presentation.\n\nRemember:\nAlways investigate for primary hyperaldosteronism whenever an operational clinical workup encounters unexplained hypokalemia paired with stubborn, drug-resistant hypertension.

Correct answer (Option A):\nA loud first heart sound (S1) in rheumatic mitral stenosis indicates that the valve leaflets remain pliable and flexible. The heightened intensity is produced when the wide-open pliable leaflets slam shut abruptly with great force under elevated intra-atrial pressures during ventricular systole.\n\nWhy others are wrong:\nOption B (calcified valve) results in a soft or completely muffled S1 because rigid, calcified leaflets lose their mobility. Options C and D generally act to diminish the operational intensity of S1 due to irregular ventricular filling patterns or structural valvular coaptation defects.\n\nRemember:\nThe preservation of a loud S1 and a clear opening snap are pivotal acoustic markers that support the clinical choice of executing a percutaneous balloon mitral valvuloplasty.