(a) A sixty-year-old male develops central chest pain while walking uphill. The pain is squeezing in character, radiating to left…

(a) Evaluation and Treatment of Stable Angina Pectoris

The clinical presentation is indicative of stable angina pectoris, resulting from a transient myocardial oxygen supply-demand mismatch secondary to fixed atherosclerotic coronary artery narrowing. Disease severity is classified using the Canadian Cardiovascular Society (CCS) functional grading.

Evaluation begins with a baseline 12-lead resting ECG (often normal, or demonstrating resting ST-T wave changes) and serum cardiac troponins to rule out acute coronary syndrome. Baseline investigations include complete blood count, fasting lipid profile, renal function tests, and HbA1c. Non-invasive functional evaluation involves a Treadmill Exercise Stress Test (TMT) or stress echocardiography/SPECT myocardial perfusion imaging to assess inducible ischemia. Anatomical evaluation is performed using Coronary Computed Tomography Angiography (CCTA) or invasive Coronary Angiography (CAG) in patients with high-risk features or refractory symptoms.

Treatment comprises lifestyle modification, risk factor control, and stepwise pharmacotherapy. Acute symptom relief is achieved with sublingual Glyceryl Trinitrate (GTN 0.5 mg). First-line anti-anginal therapy includes beta-blockers (Metoprolol or Bisoprolol) titrated to a resting heart rate of 55–60 bpm, or calcium channel blockers (Amlodipine, Diltiazem). Long-acting nitrates, Nicorandil, or Trimetazidine are added as second-line agents. Disease-modifying secondary prevention includes antiplatelet therapy (Aspirin 75–150 mg daily), high-intensity statins (Atorvastatin 40–80 mg daily), and ACE inhibitors for concurrent hypertension or left ventricular dysfunction. Myocardial revascularization via Percutaneous Coronary Intervention (PCI) or Coronary Artery Bypass Grafting (CABG) is indicated for persistent symptoms despite optimal medical therapy or high-risk coronary anatomy (left main or multi-vessel disease).

(b)(i) Neonatal respiratory distress. Causes of respiratory distress in a newborn include Respiratory Distress Syndrome (surfactant deficiency), Transient Tachypnea of the Newborn (TTN), Meconium Aspiration Syndrome, congenital pneumonia, Congenital Diaphragmatic Hernia, cyanotic congenital heart disease (CHD), and neonatal sepsis.

To differentiate respiratory from cardiac causes, the Hyperoxia test is performed by administering 100% oxygen for 10 minutes; arterial PaO2 rises above 150 mmHg in primary respiratory disease, whereas it remains below 150 mmHg in cyanotic CHD due to fixed anatomical right-to-left shunts. A pre-ductal and post-ductal SpO2 gradient exceeding 10% indicates persistent pulmonary hypertension or ductal-dependent systemic circulation. Chest radiography reveals parenchymal infiltrates, reticulogranular patterns, or air-bronchograms in lung pathology, contrasted with cardiomegaly and altered pulmonary vascular markings (oligemia or plethora) in cardiac conditions. Bedside 2D-Echocardiography provides definitive differentiation.

(b)(ii) Complications of cyanotic CHD. These include secondary polycythaemia with hyperviscosity and relative iron deficiency, hypercyanotic (Tet) spells, clubbing and growth failure, cerebral thromboembolism and stroke, paradoxical embolism and brain abscess, infective endocarditis, congestive cardiac failure, arrhythmias, bleeding diathesis, and hyperuricaemia with gout.

(b)(iii) Management. Management of a 17-month-old child presenting with severe respiratory distress, fever, and cough (severe pneumonia) follows an emergency ABCDE approach. Maintain airway patency and administer humidified oxygen via nasal prongs or mask targeting SpO2 above 92%. Send a chest X-ray, blood count, blood culture and blood gas. Initiate empirical intravenous antibiotics: WHO/IMNCI recommends ampicillin with gentamicin, while IAP guidance commonly uses ceftriaxone (50–75 mg/kg/day); add staphylococcal cover (cloxacillin or vancomycin) if there is pneumatocele or empyema. Consider bronchiolitis, empyema and foreign-body aspiration. Administer restricted maintenance intravenous fluids (75–80% of normal requirement to avoid fluid overload and SIADH), provide antipyretics (Paracetamol 15 mg/kg), and monitor respiratory rate, sensorium, and hemodynamics. Indications for Pediatric Intensive Care Unit (PICU) transfer and mechanical ventilation include worsening hypoxemia (SpO2 < 90% despite high FiO2), severe subcostal indrawing, apnea, exhaustion, or altered sensorium.

(c)(i) Lichenoid. 'Lichenoid' literally means resembling lichen, that is, flat-topped shiny papules clinically. Histologically it denotes a pattern of interface dermatitis characterized by basal keratinocyte hydropic degeneration, necrotic keratinocytes (Civatte bodies), saw-toothed irregular epidermal hyperplasia, and a dense, continuous band-like lymphocytic infiltrate in the upper dermis hugging the dermo-epidermal junction.

(c)(ii) Prototype. The prototype of this reaction is lichen planus, a T-cell-mediated attack on basal keratinocytes; it is associated with hepatitis C, and lichenoid drug eruptions mimic it.

(c)(iii) Clinical features. Lichen planus clinically presents with the classic '6 Ps': Pruritic, Polygonal, Planar (flat-topped), Purple/Violaceous, Papules, and Plaques, characteristically distributed over the flexor aspects of the wrists and forearms, the shins and ankles, and the lumbar region, healing with marked post-inflammatory hyperpigmentation in Indian skin. Lesions exhibit fine, whitish reticular networks on their surface known as Wickham striae and demonstrate the Koebner isomorphic phenomenon along lines of trauma. Mucosal involvement typically presents as asymptomatic or painful lacy white streaks (striae) on the buccal mucosa. Genital lesions may be annular. Nail involvement is marked by longitudinal ridging, thinning, subungual hyperkeratosis, and dorsal pterygium formation, and scalp involvement (lichen planopilaris) causes scarring alopecia. Variants include hypertrophic, annular, actinic, bullous and LP pigmentosus. Most skin disease remits within 1–2 years, but oral erosive LP is chronic and carries a small risk of squamous cell carcinoma.