(a) (i) Enumerate the topical antifungal drugs along with their indication and side effects. 5 marks (ii) Name antihelminitic…

(a)(i) Topical antifungals

The topical antifungals, with indications and side effects, are enumerated below:

Imidazoles — clotrimazole, miconazole, ketoconazole, econazole: indicated in dermatophytosis (tinea corporis, cruris, pedis), cutaneous candidiasis and tinea versicolor; side effects are local burning, itching, erythema and rarely contact dermatitis.

Allylamines — terbinafine, naftifine: indicated in dermatophytosis and tinea versicolor; side effects include local irritation, burning and rarely taste disturbance.

Polyenes — nystatin, amphotericin B: nystatin is indicated in oral and cutaneous candidiasis; amphotericin B topically for candidiasis and keratomycosis. Side effects are local irritation; systemic absorption is negligible from intact skin.

Ciclopirox olamine: indicated in tinea versicolor, dermatophytosis and cutaneous candidiasis; side effects are local irritation and burning.

Others — Whitfield's ointment (benzoic acid plus salicylic acid) for dermatophytosis, selenium sulfide and sodium thiosulfate for tinea versicolor, and griseofulvin (oral, not topical) is excluded. Rarely, systemic absorption from large eroded areas may cause systemic toxicity.

(a)(ii) Antihelminthics in neurocysticercosis

Albendazole (15 mg/kg/day in two divided doses for 28 days) and praziquantel (50 mg/kg/day in three divided doses for 15 days) are the first-line drugs; combination therapy is used in some cases. Corticosteroids are co-administered to control the inflammatory reaction to dying cysts. Side effects: headache, seizures, raised intracranial pressure, nausea, alopecia, hepatotoxicity (albendazole), and dizziness, drowsiness, abdominal pain and raised transaminases (praziquantel).

(b)(i) Cells of the lymphoreticular system

The cells are: lymphocytes (T cells, B cells, natural killer cells), plasma cells, macrophages, dendritic cells (including Langerhans cells and follicular dendritic cells), reticular cells and sinusoidal lining cells of lymphoid organs.

B-cell maturation, schematically:

Bone marrow: stem cell → pro-B cell (Ig gene rearrangement begins) → pre-B cell (cytoplasmic μ chain) → immature B cell (surface IgM) → exit to periphery.

Peripheral lymphoid organ: naive B cell → follicular mantle zone → antigen encounter in germinal centre → somatic hypermutation and class switching → memory B cell or plasma cell (antibody secretion).

(b)(ii) Pathogenesis of enteric fever

Schematic flowchart:

Ingestion of contaminated food/water → bacilli survive gastric acid → invade M cells of Peyer's patches → multiply in lamina propria and mesenteric lymph nodes → primary bacteraemia (asymptomatic) → seeding of gallbladder, liver, spleen, bone marrow → multiplication in gallbladder → secondary bacteraemia → systemic illness with fever, rose spots, splenomegaly, relative bradycardia → ileal Peyer's patch ulceration (third week) with risk of perforation and haemorrhage.

Two important categories of drug resistance in Salmonella typhi: chromosomal resistance — mutations in gyrA and parC (fluoroquinolone resistance) and decreased outer membrane permeability; and plasmid-mediated resistance — extended-spectrum β-lactamases, AmpC β-lactamases and NDM-1 carbapenemase, besides the classic multidrug resistance to chloramphenicol, ampicillin and cotrimoxazole.

(c) Risk factors for lung carcinoma

Smoking is the dominant risk factor, accounting for about 90% of cases, with risk proportional to pack-years; passive smoking adds risk. Radon exposure, asbestos, arsenic, chromium, nickel, silica and polycyclic aromatic hydrocarbons are occupational carcinogens. Air pollution, including biomass fuel and chulha smoke in Indian households, is an important India-specific factor. Genetic susceptibility, EGFR and ALK alterations in never-smokers, and chronic scarring (tuberculosis, interstitial fibrosis) contribute.

Morphological features of three major histological types:

Squamous cell carcinoma: typically central, arising from main or lobar bronchi; shows keratin pearls, intercellular bridges, squamous differentiation, cavitation and local invasion; strong association with smoking.

Adenocarcinoma: typically peripheral; shows glandular or lepidic patterns, mucin production, and is the commonest type in non-smokers and women; EGFR mutations are frequent in Asian populations.

Small cell carcinoma: central, arising from neuroendocrine cells; shows small cells with scant cytoplasm, hyperchromatic nuclei, nuclear moulding, crush artefact and high mitotic rate; strongly associated with smoking and paraneoplastic syndromes.

(d) Classification of CIN/SIL

Cervical intraepithelial neoplasia is classified as CIN 1 (dysplasia confined to the lower one-third of epithelium; Bethesda: low-grade squamous intraepithelial lesion, LSIL), CIN 2 (lower two-thirds; HSIL) and CIN 3 (full thickness, including carcinoma in situ; HSIL). The Bethesda system groups CIN 1 as LSIL and CIN 2 with CIN 3 as HSIL, reflecting the biological behaviour and management.

Role of HPV in pathogenesis: high-risk HPV types 16 and 18 cause about 70% of cervical cancers. Viral E6 oncoprotein binds and degrades p53, and E7 inactivates pRb, releasing E2F and driving uncontrolled proliferation. Integration of viral DNA into the host genome, with loss of E2 repression, leads to persistent E6/E7 expression, genomic instability, accumulation of mutations and progression from LSIL to HSIL to invasive carcinoma. Co-factors include early age at first intercourse, multiple partners, multiparity, smoking, immunosuppression and long-term oral contraceptive use.

(e) Classification of poisons by chief symptoms

Corrosives — strong acids and alkalis: cause burning pain in mouth, throat and stomach, with haematemesis and stricture formation.

Irritants — metallic salts, phosphorus, arsenic: cause vomiting, diarrhoea, abdominal pain and dehydration.

Neurotics — CNS depressants (barbiturates, alcohol, opioids) cause coma and respiratory depression; CNS stimulants (strychnine, organophosphates) cause convulsions and fasciculations.

Asphyxiants — carbon monoxide, cyanide, hydrogen sulphide: cause cyanosis, hypoxia and respiratory failure.

Cardiac poisons — aconite, digitalis, oleander: cause arrhythmias, bradycardia and cardiac arrest.

Miscellaneous — drugs, food poisons, snake and scorpion venom, and pesticides.

Legal duties of a medical practitioner in suspected poisoning, under Indian law: inform the police immediately (Section 39 CrPC, now Section 40 BNSS), preserve the stomach wash, vomitus, urine and blood for chemical analysis, maintain detailed and legible records of history, treatment and findings, record a dying declaration if the patient's condition is critical, and attend court as a witness when summoned. The doctor must not refuse treatment, must report suspected homicide or suicide, and must be aware of Section 304B IPC (dowry death) and Section 302 IPC where poisoning is suspected to be homicidal.