(a) (i) Discuss in short about the different modalities used in the diagnosis of Extra-Pulmonary Tuberculosis. (10 marks) (ii)…

(a)(i) Diagnostic modalities for extra-pulmonary tuberculosis

Extra-pulmonary TB (EPTB) is paucibacillary and its specimens are hard to obtain, so diagnosis combines several tests.

• Specimen collection: fluid (pleural, ascitic, CSF, synovial, pericardial), FNAC or excision biopsy of lymph nodes, tissue biopsy, urine, pus.
• Molecular tests (preferred under NTEP): CBNAAT/GeneXpert MTB/RIF (Ultra) or Truenat on the specimen give rapid detection and rifampicin resistance. Line probe assay on positive cultures detects isoniazid and fluoroquinolone resistance.
• Microscopy and culture: Ziehl-Neelsen or fluorescent smear has low sensitivity. Liquid culture (MGIT) is the reference standard and also allows drug-susceptibility testing, but takes weeks.
• Cytology and histopathology: epithelioid-cell granulomas with caseous necrosis and Langhans giant cells support the diagnosis.
• Biochemical markers: raised adenosine deaminase (ADA) in pleural, peritoneal or pericardial fluid and in CSF; lymphocytic exudate with high protein and low glucose.
• Imaging: chest X-ray for co-existing lung disease; ultrasound for abdominal TB and effusions; CT for nodes, abdomen and genitourinary tract; MRI for spinal TB (Pott's) and CNS TB (tuberculomas, basal exudates).
• Immunological tests: IGRA and tuberculin skin test show infection only, not active disease, and are of limited value in adults.

(a)(ii) Clinical features of malabsorption syndrome

• Intestinal: chronic diarrhoea, steatorrhoea (bulky, pale, greasy, foul-smelling stools that float), abdominal distension, bloating and flatulence.
• General: weight loss, fatigue and, in children, failure to thrive and short stature.
• Protein loss: hypoalbuminaemic oedema and muscle wasting.
• Iron, folate and B12 deficiency: anaemia, glossitis and angular cheilitis.
• Fat-soluble vitamins: night blindness (A), osteomalacia or rickets and tetany (D and calcium), bruising and bleeding (K).
• Other deficiencies: peripheral neuropathy (B12), dermatitis (zinc, niacin), and infertility.

Clues to the cause include dermatitis herpetiformis and anti-tTG antibodies in coeliac disease, travel or residence in the tropics with folate deficiency in tropical sprue, and arthralgia with PAS-positive macrophages in Whipple's disease.

(b)(i) Ten steps of the Baby-friendly Hospital Initiative (revised 2018)

Critical management procedures:

1. (a) Comply fully with the International Code of Marketing of Breast-milk Substitutes and the relevant World Health Assembly resolutions. (b) Have a written infant-feeding policy that is routinely communicated to staff and parents. (c) Establish ongoing monitoring and data-management systems.
2. Ensure that staff have sufficient knowledge, competence and skills to support breastfeeding.

Key clinical practices:

3. Discuss the importance and management of breastfeeding with pregnant women and their families.
4. Facilitate immediate and uninterrupted skin-to-skin contact and support mothers to initiate breastfeeding as soon as possible after birth.
5. Support mothers to initiate and maintain breastfeeding and to manage common difficulties.
6. Do not give breastfed newborns any food or fluids other than breast milk, unless medically indicated.
7. Enable mothers and their infants to remain together and to practise rooming-in 24 hours a day.
8. Support mothers to recognise and respond to their infants' cues for feeding (responsive feeding).
9. Counsel mothers on the use and risks of feeding bottles, teats and pacifiers.
10. Coordinate discharge so that parents and their infants have timely access to ongoing support and care.

In India, the MAA (Mothers' Absolute Affection) programme promotes these practices.

(b)(ii) Advantages of breastfeeding

• For the infant: ideal, easily digested nutrition; protective factors (secretory IgA, lactoferrin, lysozyme, bifidus factor, cells) that reduce diarrhoea, pneumonia and otitis media; less necrotising enterocolitis in preterm babies; lower risk of later obesity and diabetes; and better cognitive development.
• For the mother: faster uterine involution and less postpartum bleeding, lactational amenorrhoea (LAM, a temporary contraceptive), weight loss, and lower risk of breast and ovarian cancer and type 2 diabetes.
• For the family and society: it is cheap, clean, always available at the right temperature, and builds mother–infant bonding.

(c) Depigmented chalky-white macules on the face and around body orifices

(i) Diagnosis: vitiligo (acquired, autoimmune loss of melanocytes), here of the non-segmental, acrofacial or generalised type.

(ii) Associated findings:

• Skin: Koebner phenomenon, leukotrichia (white hair), trichrome and confetti-like lesions in active disease, and accentuation under Wood's lamp; the lesions are non-scaly with normal texture and sensation.
• Autoimmune associations: thyroid disease (Hashimoto's, Graves'), type 1 diabetes, pernicious anaemia, Addison's disease, alopecia areata and halo naevi.
• Eye and ear: pigmentary changes in the retina and uvea, and sometimes hearing changes (as in Vogt-Koyanagi-Harada syndrome).

(iii) Classification (Vitiligo Global Issues Consensus Conference, 2012):

• Non-segmental vitiligo: acrofacial, mucosal (more than one site), generalised (vulgaris), universal (more than 80% of body surface), mixed, and rare variants.
• Segmental vitiligo: uni-, bi- or plurisegmental.
• Undetermined/unclassified: focal and isolated mucosal lesions.

(iv) Clinical course:

• Non-segmental vitiligo has an unpredictable, chronic course with periods of activity (new lesions, enlarging lesions, Koebner phenomenon, confetti lesions) and stability; it rarely repigments spontaneously.
• Segmental vitiligo starts early, spreads rapidly within its segment for 1–2 years and then stabilises; leukotrichia is common and it responds poorly to medical treatment but well to grafting.
• Repigmentation usually starts as perifollicular dots or from the margins.
• Prognosis is better with recent onset, lesions on the face and trunk, and perifollicular repigmentation. It is worse with acral and lip-tip lesions, mucosal involvement, leukotrichia and long-standing disease.
• Psychosocial impact (stigma, depression) is significant, particularly in India.