1. Investigate & manage a chase of genital discharge 2. (a) PEP in HIV (b) Leprosy Vaccine 3. Mucocutaneous manifestations of HIV/AIDS 4. (a) Deformities in leprosy (b) Protease inhibitors 5. Classify trophic ulcers, its etiology and pathophysiology. How will you manage them & describe preventive measures? 6. (a) Newer drugs in leprosy (b) Bedside tests in STI 7. Diff relapse from reaction in leprosy. Mx of relapsed case of leprosy 8. Mx of HIV infection in women. Mx of ADRs to antiretroviral drugs 9. (a) Nail changes in leprosy (b) Inguinal bubo 10.Role of sex education with reference to STDs. How will you counsel a suspected case of HIV? In 10 marks format for 3rd yr post graduate theory examination

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These are 10 detailed postgraduate theory exam questions spanning STIs, HIV, leprosy, and trophic ulcers. Given the breadth and depth required for a 3rd-year PG exam format, let me search across all these topics simultaneously.

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I have sufficient foundational knowledge from the library and my training to now compile comprehensive, exam-format answers. Let me deliver all 10 answers in full PG theory format.Here are comprehensive answers for all 10 questions in 3rd Year PG Theory Examination format (10 marks each):

3rd Year Postgraduate Theory Examination

Dermatology, Venereology & Leprosy

Q1. Investigate & Manage a Case of Genital Discharge (10 Marks)

Introduction

Genital discharge is one of the most common presentations in STI clinics. It may arise from the urethra (urethral discharge in males) or vagina/cervix (vaginal discharge in females), and requires systematic syndromic or etiological management.

Causes

Males - Urethral Discharge:

Gonococcal urethritis: Neisseria gonorrhoeae
Non-gonococcal urethritis (NGU): Chlamydia trachomatis (most common), Ureaplasma urealyticum, Mycoplasma genitalium, Trichomonas vaginalis

Females - Vaginal/Cervical Discharge:

Physiological (commonest)
Bacterial vaginosis: Gardnerella vaginalis
Trichomoniasis: T. vaginalis
Candidiasis: Candida albicans
Cervicitis: N. gonorrhoeae, C. trachomatis

Clinical Features

Feature	Gonorrhea	Chlamydia	Trichomonas	BV
Discharge	Profuse, purulent, yellow-green	Scant, mucopurulent	Frothy, yellow-green	Grey, fishy odor
Dysuria	Yes	Mild	Yes	No
Onset	Acute (2-5 days)	Subacute (7-21 days)	Variable	Variable

Investigations

Bedside/Syndromic:

Whiff test (10% KOH) - positive fishy odor in BV
pH of discharge: >4.5 in BV/trichomonas, normal in candida
Wet mount microscopy: clue cells (BV), motile trichomonads, hyphae (candida)

Laboratory:

Gram stain of urethral smear: intracellular gram-negative diplococci (gonorrhea) - 95% sensitivity in males
Culture: Thayer-Martin medium (gonorrhea), specific for antibiotic sensitivity
NAAT (Nucleic Acid Amplification Test): gold standard for Chlamydia and N. gonorrhoeae; can be done on urine/swab
HIV, VDRL, Hepatitis B serology (always screen co-infections)
Tzanck smear if herpetic lesions present

Management

Syndromic Management (WHO/NACO approach): In resource-limited settings, all patients with urethral discharge are treated for both gonorrhea AND chlamydia simultaneously.

Gonorrhea: Ceftriaxone 500 mg IM single dose (first line; cefixime 400 mg oral if IM not available)
Chlamydia/NGU: Doxycycline 100 mg BD x 7 days OR Azithromycin 1 g single dose
Trichomonas: Metronidazole 2 g single dose (treat partner simultaneously)
BV: Metronidazole 400 mg BD x 7 days OR clindamycin 2% cream
Candidiasis: Fluconazole 150 mg single dose OR clotrimazole pessary

Etiological Management: When lab facilities are available, treat based on identification of organism.

General Measures:

Partner notification and treatment
Abstinence until treatment completed
Condom counseling
HIV testing, VDRL, Hepatitis B screening
Follow-up at 7 days
Report to health authorities (STI surveillance)

Q2 (a). PEP in HIV (5 Marks)

Definition

Post-Exposure Prophylaxis (PEP) is the use of antiretroviral drugs after a potential high-risk exposure to HIV to prevent seroconversion.

Indications

Occupational exposure: Needlestick injury, splash of blood/body fluids on mucous membranes/non-intact skin in healthcare workers
Non-occupational (nPEP): Unprotected sexual intercourse with HIV-positive person or unknown status, sexual assault, sharing of injecting equipment

When to Start

Must be started within 72 hours of exposure (ideally within 1-2 hours)
Every hour of delay reduces efficacy
Do NOT start if >72 hours have elapsed

Duration

28 days (4 weeks) of continuous therapy - non-negotiable

Recommended Regimen (WHO/NACO 2021)

Preferred: TDF (Tenofovir 300 mg) + 3TC/FTC (Lamivudine/Emtricitabine 300/200 mg) + DTG (Dolutegravir 50 mg) once daily x 28 days

Alternative: TDF + 3TC + LPV/r (Lopinavir/ritonavir)

Risk Assessment

Type of Exposure	Risk/10,000 exposures
Blood transfusion from HIV+	9,250
Receptive anal intercourse	138
Needlestick injury	23
Receptive vaginal intercourse	8
Insertive anal intercourse	11

Pre-initiation Workup

HIV rapid test (to confirm baseline HIV-negative status)
HBsAg, anti-HCV
Renal function (for TDF)
Pregnancy test in women

Follow-Up

HIV testing at baseline, 6 weeks, 3 months, 6 months
Counsel on window period, condom use during PEP

Efficacy

Reduces risk of seroconversion by approximately 80% after occupational needlestick. Efficacy declines sharply after 72 hours.

Q2 (b). Leprosy Vaccine (5 Marks)

Background

There is currently no licensed, dedicated leprosy-specific vaccine. However, several vaccines have been studied for immunoprophylaxis in leprosy.

1. BCG (Bacillus Calmette-Guerin) Vaccine

Most widely used
Provides variable but significant protection against leprosy: 20% (Malawi) to 80% (UK immigrants, Uganda)
Protection ranges from 20-80% in different geographic areas (geographic paradox - BCG efficacy varies by region)
Mechanism: cross-reactive immunity against M. leprae due to antigenic similarity
Repeated BCG doses may increase protection

2. BCG + Killed M. leprae (Combined Vaccine - India ICMR Trial)

Developed by Indian researchers (Talwar et al.)
Combined BCG + heat-killed M. leprae showed ~64% protection in South India trial
Not in routine use yet

3. Mycobacterium w (Mw) / ICRC Vaccine

Mw vaccine (Immunovaccine Technologies): Derived from Mycobacterium w (a non-pathogenic environmental mycobacterium)
Cross-reactive with M. leprae
Used as immunotherapeutic adjunct in multibacillary leprosy - reduces bacterial load, improves lepromin reactivity
Shown to reduce ENL reactions and prevent grade 2 disability in some trials

4. Mycobacterium vaccae

Also studied; limited evidence

5. Candidate vaccines under development

Recombinant BCG expressing M. leprae antigens (LID-1, NDO-LID)
DNA vaccines, subunit vaccines - still in research

Current Status

WHO recommends BCG vaccination for contacts of leprosy patients in high-endemic areas
Chemoprophylaxis with single-dose rifampicin (SDR) for contacts is now recommended alongside vaccination (WHO 2016 guidelines)

Q3. Mucocutaneous Manifestations of HIV/AIDS (10 Marks)

Introduction

Cutaneous manifestations occur in >90% of HIV-infected patients at some stage. They may be the first presenting feature and serve as markers of immune status. Can be classified by CD4 count level.

A. Viral Infections

1. Acute HIV Exanthem (Primary HIV Infection)

Occurs 2-6 weeks after inoculation in 50-70% of patients
Morbilliform/maculopapular rash - trunk, face, upper extremities
Resolves spontaneously in 1-2 weeks
Associated with fever, pharyngitis, lymphadenopathy (acute retroviral syndrome)

2. Herpes Simplex Virus (HSV)

Most common viral infection in HIV
Perianal, genital, orolabial herpes
Atypical, chronic, non-healing ulcers (>1 month = AIDS-defining)
More severe, less likely to spontaneously resolve
Treatment: Acyclovir 400 mg TDS; resistant cases - Foscarnet

3. Herpes Zoster (VZV)

20x more common in HIV
May involve multiple dermatomes (disseminated zoster)
Early or recurrent zoster in young adults - suspect HIV
Treatment: Acyclovir 800 mg 5x/day or Valacyclovir

4. Molluscum Contagiosum

Multiple, giant (>1 cm), atypical lesions on face (unusual site)
Inverse distribution (face, neck) suggests HIV
CD4 <200 cells/mm³

5. Warts (HPV)

Extensive, recalcitrant condylomata acuminata
Intraepithelial neoplasia risk increased (cervical, anal)

6. Oral Hairy Leukoplakia

EBV-induced
White, corrugated, non-removable plaques on lateral tongue
Pathognomonic of HIV (CD4 ~200-500)

B. Fungal Infections

1. Oral Candidiasis (Thrush)

Most common opportunistic infection in HIV
Pseudomembranous (white plaques), erythematous, angular cheilitis
Indicates CD4 usually <200
Treatment: Fluconazole

2. Cryptococcosis

Disseminated: Umbilicated papules resembling molluscum
Cryptococcus neoformans - primarily meningitis but skin involvement in 5-10%

3. Histoplasmosis, Penicilliosis (Talaromyces marneffei)

Endemic fungal infections with skin manifestations
Umbilicated necrotic papules in disseminated disease

C. Bacterial Infections

1. Bacillary Angiomatosis

Bartonella henselae/quintana
Vascular papules/nodules mimicking Kaposi's sarcoma
Treatment: Erythromycin 500 mg QID x 3 months

2. Impetigo, Folliculitis - more severe, widespread

3. Syphilis - atypical, aggressive; neurosyphilis risk higher

D. Seborrheic Dermatitis

Very common (up to 85% in AIDS)
Severe, recalcitrant, involves face, scalp, chest
Correlates with CD4 decline

E. Pruritic Papular Eruption (PPE)

Symmetric itchy papules, upper trunk and limbs
Eosinophilic folliculitis variant
Associated with low CD4 (<200)
Relatively specific for HIV in endemic areas

F. Drug Reactions

Severe drug hypersensitivity common with cotrimoxazole, nevirapine, abacavir
Stevens-Johnson Syndrome, DRESS syndrome

G. Malignancies

1. Kaposi's Sarcoma (KS)

Most common AIDS-defining malignancy
HHV-8 (KSHV) is the causative agent
Classic presentation: violaceous/purplish macules, plaques, nodules on skin + mucosa
Sites: lower limbs, oral mucosa, face; visceral involvement in AIDS-KS
CD4 usually <200
Treatment: ART (immune reconstitution causes regression), liposomal doxorubicin for advanced disease

2. Non-Hodgkin's Lymphoma - cutaneous involvement 3. Cervical/Anal Carcinoma (HPV-related)

H. Miscellaneous

Photosensitivity
Nail changes: onychomycosis, melanonychia
Psoriasis - severe, atypical, recalcitrant
Xeroderma, ichthyosis (late HIV)

Q4 (a). Deformities in Leprosy (5 Marks)

Introduction

Deformities in leprosy arise from nerve damage (leading to muscle paralysis and sensory loss), direct bacillary infiltration, and trophic changes. They are graded by the WHO disability grading system.

WHO Disability Grade

Grade 0: No anaesthesia, no visible deformity
Grade 1: Anaesthesia present but no visible deformity
Grade 2: Visible deformity/damage present

Mechanisms

Nerve damage - inflammation and destruction of peripheral nerves by M. leprae
Muscle paralysis - imbalance between intrinsic and extrinsic muscles
Anaesthesia - loss of protective sensation leading to trauma and trophic ulcers
Direct infiltration - of skin, subcutaneous tissue, bones
Reaction - Type 1 (reversal) and Type 2 (ENL) accelerate nerve damage

Nerves Commonly Affected and Resultant Deformities

Nerve	Site of Damage	Deformity
Ulnar nerve	Medial epicondyle	Clawing of ring & little finger, hypothenar wasting
Median nerve	Wrist (carpal tunnel)	Clawing of index & middle finger, thenar wasting, simian thumb
Combined ulnar + median	Both	"Main en griffe" - all 4 fingers clawed
Radial nerve	Spiral groove	Wrist drop
Common peroneal	Fibular neck	Foot drop
Posterior tibial	Behind medial malleolus	Clawing of toes, plantar anaesthesia
Facial nerve	Zygomatic arch	Lagophthalmos (inability to close eye)
Greater auricular	Neck	Thickened nerve

Specific Deformities

Hand:

Claw hand (Benediction hand) - ulnar nerve
Simian hand - median nerve involvement
Wrist drop - radial nerve

Face:

Lagophthalmos - leads to exposure keratitis, corneal ulceration, blindness
Saddle nose - collapse of nasal bridge due to septal perforation
Madarosis - loss of outer eyebrows (pathognomonic of lepromatous leprosy)
Leonine facies - thickened, ridged skin (LL)
Loss of anterior nasal spine

Foot:

Foot drop - peroneal nerve
Plantar ulcers (mal perforans) - anaesthesia + repeated trauma
Absorption/resorption of toes - concentric shortening

Eyes:

Lagophthalmos, corneal anaesthesia, iridocyclitis

Prevention of Deformities

Early diagnosis and MDT
Regular nerve function assessment (motor + sensory)
Corticosteroids for neuritis
Self-care education
Physiotherapy and splinting
Footwear modification
Reconstructive surgery (tendon transfer, etc.)

Q4 (b). Protease Inhibitors (5 Marks)

Mechanism of Action

HIV protease cleaves the Gag-Pol polyprotein precursor into structural proteins (p24, p17) and active enzymes. Protease Inhibitors (PIs) competitively inhibit this enzyme, resulting in production of immature, non-infectious viral particles.

Pharmacology - Key Features

Most PIs are substrates and inhibitors of CYP3A4
Ritonavir at low doses (100 mg) acts as a pharmacokinetic booster - inhibits CYP3A4 metabolism of other PIs, increasing their plasma levels ("boosted PI" concept)
Newer booster: Cobicistat (COBI)

Commonly Used PIs

Drug	Boosting	Dose	Key Feature
Lopinavir/r (LPV/r)	Self-boosted	400/100 mg BD	Long-term data; common in 2nd line
Atazanavir/r (ATV/r)	+Ritonavir	300/100 mg OD	Once daily; unconjugated hyperbilirubinemia
Darunavir/r (DRV/r)	+Ritonavir	600/100 mg BD or 800/100 OD	Active against resistant strains
Ritonavir	-	100 mg (booster)	Full dose not used now; CYP3A4 inhibitor
Saquinavir	+Ritonavir	1000/100 mg BD	First PI approved
Indinavir	+Ritonavir	800/100 mg BD	Nephrolithiasis; must hydrate well
Fosamprenavir	+Ritonavir	700/100 mg BD	Prodrug of amprenavir

Adverse Effects

Class effects:

Metabolic syndrome: Dyslipidemia (elevated TG, LDL), hyperglycemia, insulin resistance
Lipodystrophy: Peripheral fat atrophy (lipoatrophy) + central fat accumulation (lipohypertrophy) - "buffalo hump," "protease paunch"
Gastrointestinal: nausea, diarrhea (especially LPV/r)
Hepatotoxicity

Drug-specific:

Indinavir: Nephrolithiasis (drink 2L/day), indirect hyperbilirubinemia
Atazanavir: Unconjugated hyperbilirubinemia (benign, jaundice), PR interval prolongation
Darunavir: Sulfonamide allergy cross-reaction (sulfonamide moiety)

Drug Interactions

Ritonavir inhibits CYP3A4 - many interactions
Rifampicin (CYP3A4 inducer) - dramatically reduces PI levels; avoid; use rifabutin instead
Statins (lovastatin, simvastatin) - levels markedly increased; use pravastatin/rosuvastatin

Current Role

PIs (especially DRV/r) are used as:

Second-line ART (after NNRTI failure)
Third-line regimens
Special situations (pregnancy: LPV/r in some settings)

Q5. Classify Trophic Ulcers; Etiology, Pathophysiology, Management, and Preventive Measures (10 Marks)

Definition

A trophic ulcer is a chronic ulcer resulting from defective nutrition of the tissues, secondary to loss of sensation (neuropathy), vascular insufficiency, or both. Also called perforating ulcer or "mal perforans pedis."

Classification

I. By Etiology:

Neuropathic (neurogenic): Leprosy, diabetes mellitus, tabes dorsalis (syphilis), syringomyelia, hereditary sensory neuropathy
Vascular: Arterial (atherosclerosis, Buerger's disease), Venous (chronic venous insufficiency)
Mixed (neurovascular): Diabetic foot
Pressure ulcers: Bedsores in paralyzed/immobile patients

II. By Depth (Wagner's Classification for Diabetic Foot Ulcers):

Grade 0: Intact skin, at-risk foot
Grade 1: Superficial ulcer
Grade 2: Deep ulcer reaching tendon/capsule/bone
Grade 3: Deep ulcer with abscess/osteomyelitis/joint infection
Grade 4: Forefoot gangrene
Grade 5: Whole foot gangrene

Etiology

Leprosy - most important cause in India - posterior tibial nerve damage leads to plantar anaesthesia
Diabetes mellitus - peripheral sensory neuropathy + microangiopathy
Tabes dorsalis - posterior column disease
Syringomyelia - cervical cord; ulcers on hand
Peripheral vascular disease - Buerger's disease, atherosclerosis
Spinal cord injuries, paraplegia - pressure ulcers

Pathophysiology

Step 1 - Loss of protective sensation:

Neuropathy (e.g., leprosy) destroys small fiber sensory neurons
Patient cannot perceive pain, temperature, or pressure

Step 2 - Repetitive mechanical trauma:

Normal walking exerts high plantar pressures at metatarsal heads
Without pain sensation, patient continues walking despite injury
Repeated microtrauma leads to subepidermal hematoma, blister

Step 3 - Breakdown and ulceration:

Blister ruptures or bursts internally
Ulcer forms, typically over pressure points (metatarsal heads, heel, medial aspect of big toe)

Step 4 - Deepening and infection:

Absence of pain → patient ignores wound
Polymicrobial secondary infection
Destruction of deeper tissues: tendons, periosteum, bone
Osteomyelitis in late stages

Step 5 - Chronicity:

Impaired autonomic function → dry skin → fissuring
Impaired angiogenesis and tissue healing
Biofilm formation → chronic non-healing ulcer

Clinical Features

Painless ulcer (key feature - patient often unaware)
Location: plantar surface over metatarsal heads, heel
Surrounding callus/hyperkeratosis (in neuropathic type)
Well-defined punched-out edges with surrounding hyperkeratosis
Sloughy base
Absent protective sensation in surrounding area

Management

A. General Measures:

Address underlying cause (MDT for leprosy, glycemic control for diabetes)
Patient education on self-care
Regular foot inspection

B. Offloading - Most Important:

Remove pressure from ulcer site
Total Contact Cast (TCC) - gold standard
Removable cast walkers, padded shoes
Bed rest for severe ulcers

C. Wound Care:

Debridement of callus and necrotic tissue (dry debridement, sharp debridement)
Saline dressings - twice daily
Antiseptic soaks (potassium permanganate 1:10,000)
Advanced dressings: hydrocolloid, alginate for wound bed preparation
Maggot therapy for debriding necrotic tissue

D. Infection Management:

Superficial: topical antiseptics
Deep/cellulitis: systemic antibiotics (amoxicillin-clavulanate, or according to culture)
Osteomyelitis: prolonged IV antibiotics, surgical debridement

E. Surgical Management:

Excision of bony prominences (metatarsal head resection) to remove pressure point
Skin grafting for large clean ulcers
Amputation (last resort for grade 4-5)

F. Vascular Ulcers:

Revascularization (angioplasty, bypass grafting)

Prevention

Patient education - daily foot inspection using mirror for plantar surface
Proper footwear - insensitive feet shoe (Microcellular Rubber MCR footwear) - evenly distributes pressure; rigid-soled sandals
Regular callus paring - prevents areas of high pressure
Soaking feet - daily soaking and application of oil/moisturizer (prevents fissuring)
Early treatment of blisters, cuts - before they progress to ulcers
Avoidance of barefoot walking on rough surfaces
Regular physiotherapy - maintains range of motion
Leprosy control - early diagnosis and MDT reduces neuropathy
Glycemic control - in diabetics, HbA1c <7% significantly reduces risk
Regular foot examination by healthcare worker - at every follow-up visit

Q6 (a). Newer Drugs in Leprosy (5 Marks)

Background

Standard WHO-MDT (rifampicin, dapsone, clofazimine) has been the backbone of leprosy treatment for decades. However, newer agents have been studied for drug-resistant leprosy, single-lesion PB leprosy, and chemoprophylaxis.

1. Fluoroquinolones

Ofloxacin:

Highly bactericidal against M. leprae
MIC: lowest among fluoroquinolones for M. leprae
Used in ROM (Rifampicin + Ofloxacin + Minocycline) regimen for single-lesion PB leprosy
Dose: 400 mg/day
Also used in dapsone-resistant leprosy

Pefloxacin: Similar efficacy to ofloxacin Moxifloxacin: More potent; promising in multidrug-resistant leprosy (in research)

2. Minocycline

Tetracycline derivative with activity against M. leprae
Part of ROM regimen
Anti-inflammatory properties useful in reactions
Dose: 100 mg/day
Can cause reversible skin pigmentation (bluish-grey)

3. ROM Regimen (Single Dose)

For single-lesion PB leprosy (one patch):

Rifampicin 600 mg + Ofloxacin 400 mg + Minocycline 100 mg - all single dose
Non-inferior to 6 months of standard PB-MDT for 1 lesion
14-lesion criterion recently removed from PB leprosy classification (WHO 2018 revised)

4. Clarithromycin

Macrolide with bactericidal activity against M. leprae
Active against dapsone/rifampicin-resistant strains
Used in combination with other drugs

5. Thalidomide

Used for Type 2 lepra reaction (ENL)
Inhibits TNF-alpha production; down-regulates neutrophil function
Highly effective, but teratogenic (limb reduction defects - phocomelia) - absolutely contraindicated in women of childbearing age
Dose: 100-400 mg/day (taper)
Now replaced by clofazimine and steroids in most settings

6. Rifabutin

Rifamycin analogue
Active against rifampicin-resistant M. leprae
Fewer drug interactions than rifampicin
Used in combination regimens for resistant leprosy

7. Bedaquiline

Approved primarily for MDR-TB, but has in-vitro activity against M. leprae
Under investigation for MDR leprosy

Single-Dose Rifampicin (SDR) for Contacts

WHO 2016 guidelines recommend SDR prophylaxis for household contacts of newly diagnosed MB leprosy patients
Reduces risk of leprosy in contacts by ~57% over 2 years
Single dose: 600 mg rifampicin

Q6 (b). Bedside Tests in STI (5 Marks)

These are simple, rapid diagnostic tests performable in clinic without sophisticated laboratory equipment.

1. Dark Field Microscopy (DFM)

For: Treponema pallidum (primary and secondary syphilis)
Method: Serous exudate from chancre placed on slide; examined immediately under dark-field microscope
Result: Corkscrew motility of T. pallidum - spirochetes visible as bright coils on dark background
Sensitivity: ~80% for primary syphilis
Limitation: Cannot be used for oral/anal lesions (commensal treponemes)

2. Wet Mount Microscopy

For: Vaginal discharge
Saline wet mount: motile trichomonads (Trichomonas vaginalis), clue cells (Gardnerella/BV)
KOH preparation: hyphae/pseudohyphae/spores (Candida)
Sensitivity: 50-70% for trichomonas; improved with NAAT

3. Whiff Test (Amine Test)

For: Bacterial Vaginosis
Add 10% KOH to vaginal discharge on a glass slide
Positive: Fishy (amine) odor = BV
Simple, instant result

4. pH of Vaginal Discharge

Normal vaginal pH: 3.8-4.5 (acidic, lactobacillus-maintained)
pH >4.5: BV, Trichomonas, atrophic vaginitis
pH <4.5: Candida, normal
Use pH paper

5. Gram Stain

Urethral smear (males): Intracellular gram-negative diplococci (IGND) = gonorrhea (95% sensitive)
Vaginal smear: Less sensitive for gonorrhea in females
Clue cells: Epithelial cells studded with gram-variable coccobacilli (BV)
Hyphae/pseudohyphae: Candida

6. Tzanck Smear

For: Genital herpes (HSV), varicella
Scraping from base of fresh vesicle stained with Giemsa/Wright/Toluidine blue
Result: Multinucleated giant cells (syncytia) with intranuclear inclusions
Sensitivity: ~60%; cannot differentiate HSV-1 from HSV-2 or VZV

7. VDRL (Venereal Disease Research Laboratory) Test

Flocculation test for syphilis
Antigen: cardiolipin-lecithin-cholesterol
Rapid, cheap, bedside (though technically requires centrifuge)
Reactive in secondary syphilis (nearly 100%), less so in primary/tertiary
False positives: Malaria, autoimmune, pregnancy, TB

8. RPR (Rapid Plasma Reagin)

Similar principle to VDRL; can be done without centrifuge
Card test; truly bedside
Used for screening in resource-limited settings

9. POC NAAT

Emerging technology (GeneXpert, Xpert CT/NG)
Rapid, highly sensitive/specific; results in 90 minutes
Increasingly available in clinics

Q7. Differentiate Relapse from Reaction in Leprosy. Management of Relapsed Leprosy (10 Marks)

Definitions

Reaction: An immunological event (acute inflammation) occurring during the course of a chronic disease; not due to drug failure
Relapse: Re-appearance of active disease after completing a full course of adequate MDT, in a previously RFT (Released From Treatment) patient

Differentiation: Relapse vs. Reaction

Feature	Relapse	Type 1 Reaction (Reversal)	Type 2 Reaction (ENL)
Timing	Months to years after completing MDT	During treatment or after completion	During treatment or after completion
Onset	Insidious, gradual	Subacute (days to weeks)	Acute (hours to days)
Lesions	New skin lesions (may appear different)	Existing lesions become erythematous, edematous, tender	New crops of tender erythematous nodules
Nerves	May involve new nerves	New nerve involvement common	Tender but different mechanism
Systemic features	Absent	Absent	Fever, malaise, arthralgia, uveitis, orchitis, neuritis
Bacteriology (BI)	BI rises ≥2+ from nadir	BI may not change	BI may not change
Histopathology	Active inflammation, lymphocytes, macrophages with bacilli	Upgrading reaction - lymphocytes, no neutrophils, edema	Neutrophilic infiltrate, immune complex deposition
Lepromin test	Negative in MB	May become positive	Strongly positive
Response to steroids	No response	Dramatic response	Partial response
Treatment	Re-institute MDT	Prednisolone	Prednisolone; thalidomide

Key Distinguishing Points (Summary)

BI rising ≥2+ from nadir is the strongest indicator of relapse
In relapse: new lesions appear outside the area of previous lesions
In reaction: existing lesions become inflamed
Reaction: constitutional symptoms (ENL); Relapse: none
Slit skin smear (SSS) examination is essential to confirm relapse

Management of Relapsed Leprosy

Step 1 - Confirm Relapse

Clinical assessment + SSS + histopathology + BI
Exclude reaction (particularly important)
Drug susceptibility testing (DST) if available - look for rifampicin resistance (folP1, rpoB gene mutations)

Step 2 - Assess Type of Relapse

PB relapsed: Treat as MB-MDT (12 months)
MB relapsed: If susceptible strains, re-treat with standard WHO MB-MDT

Step 3 - Standard Re-treatment For suspected drug-sensitive relapse:

WHO MB-MDT x 24 months (extended course for relapse)
Rifampicin 600 mg once monthly (supervised)
Clofazimine 300 mg once monthly + 50 mg daily
Dapsone 100 mg daily

Step 4 - Drug-Resistant Relapse If dapsone resistance suspected (prior dapsone monotherapy, high BI, no response):

WHO Second-line regimen: Clofazimine + two of the following for 6 months, then one for 18 months:
- Clarithromycin 500 mg/day
- Minocycline 100 mg/day
- Ofloxacin 400 mg/day

If rifampicin resistance confirmed (QRDR mutations):

MDR-Leprosy regimen: Clarithromycin + Minocycline + Fluoroquinolone x 24 months
Bedaquiline being investigated

Step 5 - Ancillary Measures

Continue MDT for full prescribed course
Monitor for reactions during retreatment
Nerve function monitoring
Psychosocial support
Disability prevention

Q8. Management of HIV Infection in Women. Management of ADRs to Antiretroviral Drugs (10 Marks)

Part A: Management of HIV in Women

Specific Considerations in Women

Higher susceptibility to HIV than men per unprotected sexual act
Women-specific manifestations: recurrent vaginal candidiasis, cervical HPV/carcinoma, PID
Pregnant women: prevention of mother-to-child transmission (PMTCT)
Hormonal contraception interactions with ARVs

Diagnosis

HIV testing: Rapid test, ELISA, Western blot
Women should be offered HIV testing at first antenatal visit, family planning clinics
CD4 count, viral load, CBC, LFT, RFT, VDRL, HBsAg, anti-HCV, TB screening

When to Start ART

All women living with HIV should start ART regardless of CD4 count (Test and Treat)
Urgently in: pregnancy, CD4 <200, AIDS-defining illness

First-Line ART Regimen (Non-Pregnant Women) - WHO 2022/NACO

TDF + 3TC (or FTC) + DTG (Dolutegravir 50 mg) once daily

TDF: Tenofovir disoproxil fumarate 300 mg
3TC: Lamivudine 300 mg

Note on Dolutegravir: Previously avoided in first trimester due to neural tube defect concerns (Tsepamo study); updated data (2019 onwards) shows risk is very low (~0.1%); DTG is now recommended throughout pregnancy.

Alternative first-line: TDF + 3TC + EFV600 (Efavirenz 600 mg)

Special Situation: Pregnancy and PMTCT

Risk of MTCT without treatment: ~25-40% (breastfeeding increases risk) With ART: MTCT reduced to <1-2%

PMTCT components:

ART for mother: Start immediately, continue lifelong (Option B+)
For HIV-exposed infant: Nevirapine prophylaxis x 6 weeks (or 12 weeks if breastfeeding)
Infant HIV testing: DNA PCR at 6 weeks, 3 months
Infant feeding: Where safe water available - formula feeding; otherwise exclusive breastfeeding for 6 months with maternal ART
Delivery: Mode of delivery does not reduce MTCT if viral load is undetectable; cesarean section only for obstetric indications

Drugs Contraindicated/Avoided in Pregnancy:

Efavirenz: Avoid in 1st trimester (teratogenic in animal studies; current WHO allows after 8 weeks)
Stavudine (d4T): Avoid (lactic acidosis risk)
Didanosine (ddI) + Stavudine: Severe lactic acidosis in pregnancy

Women-Specific Complications and Management

Cervical cancer screening: Pap smear annually (HPV-related cancer risk 5x higher)
Recurrent VVC: Fluconazole 150 mg weekly prophylaxis
Menstrual irregularities: ARV interactions with hormonal contraception (especially EFV reduces OC levels - use barrier contraception additionally)
Osteoporosis risk: TDF reduces bone mineral density; calcium + Vitamin D supplementation

Part B: Management of ADRs to Antiretroviral Drugs

Overview

ADRs are common, affect adherence, and may be severe/life-threatening. Management depends on severity and the offending drug.

Key ARV ADRs and Management

1. NRTI-related ADRs

Drug	ADR	Management
Zidovudine (AZT)	Bone marrow suppression (anemia, neutropenia), macrocytosis, myopathy, lactic acidosis, lipodystrophy	If Hb <7.5 g/dL - switch to TDF or ABC; G-CSF for severe neutropenia
Stavudine (d4T)	Peripheral neuropathy, lactic acidosis, lipodystrophy (lipoatrophy), pancreatitis	Switch to TDF; avoid in new regimens
Tenofovir (TDF)	Nephrotoxicity (Fanconi syndrome, renal tubular acidosis), bone loss, weight gain (TAF form less toxic)	Monitor creatinine, urine protein; switch to TAF or ABC if renal impairment
Abacavir (ABC)	Hypersensitivity reaction (HSR) in HLA-B*5701 carriers - fever, rash, GI symptoms	Test HLA-B*5701 before prescribing; NEVER rechallenge
Lamivudine (3TC)	Well tolerated; minimal toxicity	-

2. NNRTI-related ADRs

Drug	ADR	Management
Nevirapine (NVP)	Severe rash (SJS, TEN), fulminant hepatotoxicity	Discontinue immediately; do NOT rechallenge; monitor LFTs in first 18 weeks; avoid if CD4 >250 (women) or >400 (men)
Efavirenz (EFV)	CNS effects (dizziness, nightmares, depression, vivid dreams), rash, hepatotoxicity	Take at bedtime; usually resolves in 2-4 weeks; if severe psychiatric effects - switch
Rilpivirine	Depression, insomnia, rash	-

3. PI-related ADRs

Metabolic: dyslipidemia, hyperglycemia, lipodystrophy - manage with dietary modification, statins (avoid simvastatin/lovastatin), metformin
GI: nausea, diarrhea (especially LPV/r) - anti-emetics, anti-diarrheals, loperamide
Nephrolithiasis (Indinavir): increased hydration 2L/day

4. Integrase Inhibitor ADRs

DTG: weight gain, insomnia, psychiatric effects, rarely rhabdomyolysis
Raltegravir: myopathy/rhabdomyolysis (rare)

General Approach to ARV ADRs

Step 1 - Assess severity (ACTG grading):

Grade 1-2 (mild-moderate): Symptomatic management, close monitoring
Grade 3-4 (severe, life-threatening): Discontinue offending drug, switch

Step 2 - Determine causative drug

Review all ARVs and concomitant medications
Timeline of drug initiation vs. ADR onset

Step 3 - Switch strategy

Substitute one drug while maintaining other two
Ensure new substitution maintains virological efficacy

Step 4 - Management of specific severe ADRs

Lactic acidosis: Stop all NRTIs; supportive care; IV bicarbonate; mortality high
Severe hepatotoxicity: Stop all ARVs if ALT >5x ULN with symptoms; restart cautiously
SJS/TEN: Stop offending drug (NVP, EFV); ICU care; skin barrier protection
ABC hypersensitivity: Stop ABC immediately; IV fluids; antihistamines; do NOT rechallenge

Q9 (a). Nail Changes in Leprosy (5 Marks)

Introduction

Nail changes in leprosy are not direct effects of M. leprae on nails, but rather result from nerve damage, vascular changes, and secondary infections.

Mechanisms

Autonomic neuropathy - impaired sweating and blood flow to nails
Sensory neuropathy - repeated trauma without protective pain
Direct infiltration in lepromatous leprosy
Secondary fungal/bacterial infections

Types of Nail Changes

1. Onychoschisis (nail splitting/lamination)

Most common nail change in leprosy
Transverse splitting of the nail plate

2. Onycholysis

Separation of nail plate from nail bed
Due to subungual infections or repeated minor trauma

3. Pterygium Unguis (nail pterygium)

Adherence of cuticle to nail plate
Forward extension of proximal nail fold over nail plate

4. Onychomycosis (fungal nail infection)

Very common in leprosy patients
Due to impaired local immunity and poor nail health
Discoloration, thickening, crumbling of nail

5. Leukonychia (white nails)

White discoloration

6. Nail atrophy and dystrophy

Thin, fragile, misshapen nails
In advanced neuropathy

7. Longitudinal ridging

Due to atrophy of nail matrix

8. Total nail loss

Anonychia - in advanced disease with bone resorption
Nail shedding due to infection, trauma, or direct infiltration

9. Brachyonychia (short nails)

Due to bone resorption of distal phalanx

10. Subungual hemorrhage

From minor unnoticed trauma (painless)

Clinical Significance

Nail changes indicate long-standing disease and nerve damage
Should prompt foot care, self-care education
Treat onychomycosis with oral antifungals (terbinafine 250 mg/day x 3 months for toenails)

Q9 (b). Inguinal Bubo (5 Marks)

Definition

An inguinal bubo is an enlarged, tender lymph node (or matted nodes) in the inguinal region due to infection or malignancy, most commonly STI-related.

Etiology - STI Causes

Disease	Organism	Type of Bubo
Lymphogranuloma Venereum (LGV)	Chlamydia trachomatis L1, L2, L3	Tender, matted, suppurative; groove sign
Chancroid	Haemophilus ducreyi	Tender, fluctuant, unilateral; may rupture
Primary Syphilis	Treponema pallidum	Non-tender, rubbery, bilateral ("sentinel nodes")
Donovanosis	Klebsiella granulomatis	Pseudobubo - subcutaneous nodule, not true LN
Genital Herpes	HSV-2	Tender, bilateral, non-fluctuant

Non-STI Causes of Inguinal Lymphadenopathy

Filariasis (Wuchereria bancrofti) - chronic, non-tender
Plague (Yersinia pestis) - painful, rapidly enlarging, can be inguinal
Tuberculosis - cold abscess
Lymphoma, metastatic carcinoma

Key Feature: Groove Sign of LGV

Inguinal ligament divides the enlarged nodes into groups above and below it
Creates a characteristic groove when the inguinal ligament is palpated
Pathognomonic of LGV

Clinical Approach to Inguinal Bubo

History: Painless or painful? Rapid or slow onset? Preceding genital ulcer? Travel? Sexual history?

Examination:

Size, consistency, tenderness, fluctuance, overlying skin changes
Look for primary lesion (chancre, ulcer) on genitals
Examine both inguinal regions and all lymph node groups

Investigations:

VDRL/RPR, TPHA (syphilis)
HSV PCR or culture
LGV: C. trachomatis NAAT (distinguish L1-L3 serovars)
Chancroid: H. ducreyi culture (difficult); clinical diagnosis usually
Biopsy if lymphoma/malignancy suspected
Aspirate: gram stain, culture, ZN stain, cytology

Management

STI	Treatment
LGV	Doxycycline 100 mg BD x 21 days
Chancroid	Azithromycin 1 g single dose OR Ceftriaxone 250 mg IM single dose
Primary Syphilis	Benzathine penicillin 2.4 MU IM single dose
Genital Herpes	Acyclovir 400 mg TDS x 7-10 days

Fluctuant bubo (LGV/Chancroid):

Needle aspiration (NOT incision - leads to chronic sinus)
Aspirate from adjacent normal skin

Q10. Role of Sex Education with Reference to STDs. Counseling of a Suspected Case of HIV (10 Marks)

Part A: Role of Sex Education in STDs

Definition

Sex education (sexuality education) refers to instruction on sexual health, human development, relationships, personal skills, sexual behavior, and sexual health - including STD prevention.

Importance

STDs/STIs are a major public health burden: 1 million STIs acquired per day globally (WHO)
Most STIs are preventable with correct information and behavior change
Young people are disproportionately affected
Stigma and lack of knowledge are major barriers to care

Components of Comprehensive Sex Education

Anatomy and physiology - reproductive system
Puberty, menstruation, reproductive health
Relationships and consent
STI/HIV - transmission, prevention, symptoms
Contraception - barrier methods (condom), hormonal methods
Correct and consistent condom use (male and female)
Partner communication and negotiation skills
Abstinence as a choice (but not the only message)
Healthcare seeking behavior - when and where to seek help
Reducing stigma around HIV and STIs

Role in STD Prevention

Primary Prevention (preventing infection):

Abstinence education
Delay of sexual debut
Reduction of number of partners
Correct and consistent condom use: reduces HIV transmission by 85%, gonorrhea/chlamydia by 50-80%
HPV vaccination awareness
PrEP awareness for high-risk individuals

Secondary Prevention (early detection):

Knowing symptoms of STIs (discharge, ulcer, rash)
Awareness of asymptomatic STIs (chlamydia)
Encouraging regular STI testing
Reducing fear and stigma of testing

Tertiary Prevention:

Adherence to treatment
Partner notification
Prevention of re-infection

Target Groups for Sex Education

School-going adolescents (age-appropriate)
Out-of-school youth
Sex workers, MSM, truckers, migrants (high-risk groups)
Married couples
Healthcare providers

National Programs

RKSK (Rashtriya Kishor Swasthya Karyakram) - adolescent health in India
ARSH clinics (Adolescent Reproductive and Sexual Health)
NACP (National AIDS Control Programme) - IEC (Information, Education, Communication)
School health programs

Part B: Counseling of a Suspected Case of HIV

Pre-Test Counseling (Before HIV Testing)

Purpose: Informed consent, risk assessment, emotional preparation for result

Steps:

1. Establish rapport and confidentiality

Reassure complete confidentiality (except mandatory partner notification)
Create non-judgmental atmosphere

2. Assess HIV risk

Sexual history (partners, condom use, high-risk behavior)
History of blood transfusion, surgery
IV drug use/needle sharing
History of STIs
Occupational exposure

3. Explain HIV - basics

What HIV is; difference from AIDS
Modes of transmission (sexual, blood-borne, mother-to-child)
Modes NOT transmitted (handshake, sharing food, mosquitoes)
Window period: 3-4 weeks to 3 months; modern 4th generation tests detect earlier

4. Explain the test

Confidential, voluntary
ELISA/rapid test; confirmatory by Western blot
False-positive/negative possibility (window period)

5. Discuss possible results

"What would it mean if the result is positive?"
Assess coping mechanisms, support system
Discuss impact on relationships, family

6. Obtain informed written consent for HIV testing

Post-Test Counseling

If Result is NEGATIVE:

Explain result is not conclusive if within window period - repeat test at 3 months
Reinforce risk reduction: condom use, single partner, avoid IV drug use
Offer PrEP if high-risk individual
Screen for other STIs

If Result is POSITIVE:

1. Breaking the news

Do so in private; allow patient to absorb; offer emotional support
Allow patient to express emotions (anger, denial, grief)

2. Clarify what HIV-positive means

HIV-positive ≠ AIDS; with ART, can live normal lifespan
ART works; explain viral load suppression, CD4 recovery
Reduce catastrophizing

3. Risk reduction counseling

Disclose to partner; partner testing
Condom use (even with HIV-positive partner to prevent superinfection and protect partner)
Avoid donating blood/organs/breast milk
Safe sex practices

4. Medical management

Referral to ART center
Explain ART: adherence is critical (>95%)
Regular follow-up: CD4, viral load monitoring
Prophylaxis for OIs (cotrimoxazole if CD4 <200)

5. Disclosure support

Discuss to whom to disclose (partner, family)
Legal protection against discrimination (in India - HIV/AIDS Act 2017)
Counseling for disclosure to partner

6. Psychosocial support

Support groups for PLHIV (People Living with HIV)
Mental health referral if needed
Address stigma and discrimination

7. Special groups

Pregnant women: PMTCT, ART immediately
Children: Pediatric ART, disclosure at age-appropriate time
Women: Reproductive counseling, contraception

References: Fitzpatrick's Dermatology; Harrison's Principles of Internal Medicine 22nd Ed; WHO Guidelines for the Treatment of STI (2016); NACO ART Guidelines (2021); WHO Guidelines for Leprosy Management (2018); Goldman-Cecil Medicine

---All 10 questions have been answered in full PG examination format. Here is a quick summary of what is covered:

Summary of Answers

Q	Topic	Key Points Covered
1	Genital Discharge - Investigation & Management	Causes (GC, chlamydia, BV, trichomonas, candida), clinical features table, bedside and lab investigations, syndromic + etiological management, partner notification
2a	PEP in HIV	Definition, indications, 72-hour window, TDF+3TC+DTG x28 days regimen, risk table, pre-initiation workup, follow-up
2b	Leprosy Vaccine	BCG (geographic paradox), Mw vaccine, ROM regimen, candidate vaccines, SDR chemoprophylaxis
3	Mucocutaneous Manifestations of HIV	Viral (acute exanthem, HSV, VZV, molluscum, OHL), fungal (candida, cryptococcus), bacterial (bacillary angiomatosis), seborrheic dermatitis, PPE, drug reactions, KS
4a	Deformities in Leprosy	Nerve-deformity table (ulnar, median, radial, peroneal, posterior tibial, facial), specific deformities by region, WHO grading, prevention
4b	Protease Inhibitors	Mechanism (HIV protease), boosting concept, drug table with doses, class ADRs (metabolic syndrome, lipodystrophy), drug-specific ADRs, drug interactions
5	Trophic Ulcers	Classification (neuropathic/vascular/mixed/pressure; Wagner's grade), etiology, 5-step pathophysiology, management (offloading, debridement, surgery), prevention (MCR footwear, daily foot inspection)
6a	Newer Drugs in Leprosy	Fluoroquinolones (ofloxacin, moxifloxacin), minocycline, ROM regimen, clarithromycin, thalidomide (ENL), rifabutin, SDR prophylaxis
6b	Bedside Tests in STI	DFM (syphilis), wet mount, whiff test, vaginal pH, gram stain, Tzanck smear, VDRL/RPR
7	Relapse vs Reaction + Management	Detailed comparison table (timing, onset, BI, histology, steroid response), confirmation of relapse, MDT re-treatment, MDR-leprosy regimen
8	HIV in Women + ARV ADRs	PMTCT (Option B+), DTG in pregnancy, women-specific issues (cervical cancer, VVC, contraception interactions), ADR management table (NRTI, NNRTI, PI), severity grading, switch strategies
9a	Nail Changes in Leprosy	10 nail changes (onychoschisis, onycholysis, pterygium, onychomycosis, brachyonychia, anonychia, etc.), mechanisms
9b	Inguinal Bubo	Etiology table (LGV, chancroid, syphilis, donovanosis, herpes), groove sign, clinical approach, management per STI, needle aspiration
10	Sex Education + HIV Counseling	Components of comprehensive sex education, primary/secondary/tertiary prevention, pre-test and post-test HIV counseling steps, disclosure, ART referral, PLHIV support

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Here are all 10 questions answered in full 3rd Year PG Theory Examination format:

3rd Year Postgraduate Theory Examination

Dermatology, Venereology & Leprosy

Q1. Investigate & Manage a Case of Genital Discharge (10 Marks)

Introduction

Causes

Males - Urethral Discharge:

Gonococcal urethritis: Neisseria gonorrhoeae
Non-gonococcal urethritis (NGU): Chlamydia trachomatis (most common), Ureaplasma urealyticum, Mycoplasma genitalium, Trichomonas vaginalis

Females - Vaginal/Cervical Discharge:

Physiological (commonest)
Bacterial vaginosis: Gardnerella vaginalis
Trichomoniasis: T. vaginalis
Candidiasis: Candida albicans
Cervicitis: N. gonorrhoeae, C. trachomatis

Clinical Features

Feature	Gonorrhea	Chlamydia	Trichomonas	BV
Discharge	Profuse, purulent, yellow-green	Scant, mucopurulent	Frothy, yellow-green	Grey, fishy odor
Dysuria	Yes	Mild	Yes	No
Onset	Acute (2-5 days)	Subacute (7-21 days)	Variable	Variable

Investigations

Bedside/Syndromic:

Whiff test (10% KOH) - positive fishy odor in BV
pH of discharge: >4.5 in BV/trichomonas, normal in candida
Wet mount microscopy: clue cells (BV), motile trichomonads, hyphae (candida)

Laboratory:

Gram stain of urethral smear: intracellular gram-negative diplococci (gonorrhea) - 95% sensitivity in males
Culture: Thayer-Martin medium (gonorrhea), specific for antibiotic sensitivity
NAAT (Nucleic Acid Amplification Test): gold standard for Chlamydia and N. gonorrhoeae; can be done on urine/swab
HIV, VDRL, Hepatitis B serology (always screen co-infections)
Tzanck smear if herpetic lesions present

Management

Syndromic Management (WHO/NACO approach): In resource-limited settings, all patients with urethral discharge are treated for both gonorrhea AND chlamydia simultaneously.

Gonorrhea: Ceftriaxone 500 mg IM single dose (first line; cefixime 400 mg oral if IM not available)
Chlamydia/NGU: Doxycycline 100 mg BD x 7 days OR Azithromycin 1 g single dose
Trichomonas: Metronidazole 2 g single dose (treat partner simultaneously)
BV: Metronidazole 400 mg BD x 7 days OR clindamycin 2% cream
Candidiasis: Fluconazole 150 mg single dose OR clotrimazole pessary

Etiological Management: When lab facilities are available, treat based on identification of organism.

General Measures:

Partner notification and treatment
Abstinence until treatment completed
Condom counseling
HIV testing, VDRL, Hepatitis B screening
Follow-up at 7 days
Report to health authorities (STI surveillance)

Q2 (a). PEP in HIV (5 Marks)

Definition

Post-Exposure Prophylaxis (PEP) is the use of antiretroviral drugs after a potential high-risk exposure to HIV to prevent seroconversion.

Indications

Occupational exposure: Needlestick injury, splash of blood/body fluids on mucous membranes/non-intact skin in healthcare workers
Non-occupational (nPEP): Unprotected sexual intercourse with HIV-positive person or unknown status, sexual assault, sharing of injecting equipment

When to Start

Must be started within 72 hours of exposure (ideally within 1-2 hours)
Every hour of delay reduces efficacy
Do NOT start if >72 hours have elapsed

Duration

28 days (4 weeks) of continuous therapy - non-negotiable

Recommended Regimen (WHO/NACO)

Preferred: TDF (Tenofovir 300 mg) + 3TC/FTC (Lamivudine/Emtricitabine 300/200 mg) + DTG (Dolutegravir 50 mg) once daily x 28 days

Alternative: TDF + 3TC + LPV/r (Lopinavir/ritonavir)

Risk of Transmission per 10,000 Exposures

Type of Exposure	Risk
Blood transfusion from HIV+	9,250
Receptive anal intercourse	138
Needlestick injury	23
Receptive vaginal intercourse	8
Insertive anal intercourse	11

Pre-initiation Workup

HIV rapid test (confirm baseline HIV-negative status)
HBsAg, anti-HCV
Renal function (for TDF)
Pregnancy test in women

Follow-Up

HIV testing at baseline, 6 weeks, 3 months, 6 months
Counsel on window period, condom use during PEP

Efficacy

Reduces risk of seroconversion by approximately 80% after occupational needlestick. Efficacy declines sharply after 72 hours.

Q2 (b). Leprosy Vaccine (5 Marks)

Background

There is currently no licensed, dedicated leprosy-specific vaccine. Several vaccines have been studied for immunoprophylaxis in leprosy.

1. BCG (Bacillus Calmette-Guerin) Vaccine

Most widely used
Provides variable but significant protection: 20% (Malawi) to 80% (Uganda, UK immigrants)
The "geographic paradox" - BCG efficacy varies markedly by region
Mechanism: cross-reactive immunity due to antigenic similarity between M. bovis and M. leprae
Repeated BCG doses may increase protection

2. BCG + Killed M. leprae (Combined Vaccine)

Developed by ICMR (Talwar et al.)
Combined BCG + heat-killed M. leprae showed ~64% protection in South India trials
Not in routine use yet

3. Mycobacterium w (Mw) / ICRC Vaccine

Derived from a non-pathogenic environmental mycobacterium with cross-reactivity to M. leprae
Used as an immunotherapeutic adjunct in multibacillary leprosy
Reduces bacterial load, improves lepromin reactivity
Shown to reduce ENL reactions and prevent Grade 2 disability in some trials

4. Candidate Vaccines Under Development

Recombinant BCG expressing M. leprae antigens (LID-1, NDO-LID)
DNA vaccines, subunit vaccines - still in research phase

Current Status

WHO recommends BCG vaccination for contacts of leprosy patients in high-endemic areas
Single-dose rifampicin (SDR) chemoprophylaxis for household contacts is now recommended alongside vaccination (WHO 2016 guidelines), reducing contact risk by ~57%

Q3. Mucocutaneous Manifestations of HIV/AIDS (10 Marks)

Introduction

Cutaneous manifestations occur in >90% of HIV-infected patients at some stage. They may be the first presenting feature and serve as markers of immune status (CD4 count).

A. Viral Infections

1. Acute HIV Exanthem (Primary HIV Infection)

Occurs 2-6 weeks after inoculation in 50-70% of patients
Morbilliform/maculopapular rash - trunk, face, upper extremities
Resolves spontaneously in 1-2 weeks
Associated with fever, pharyngitis, lymphadenopathy (acute retroviral syndrome)

2. Herpes Simplex Virus (HSV)

Most common viral infection in HIV
Perianal, genital, orolabial herpes
Atypical, chronic, non-healing ulcers (>1 month = AIDS-defining)
More severe, less likely to spontaneously resolve
Treatment: Acyclovir 400 mg TDS; resistant cases - Foscarnet

3. Herpes Zoster (VZV)

20x more common in HIV
May involve multiple dermatomes (disseminated zoster)
Early or recurrent zoster in a young adult - suspect HIV
Treatment: Acyclovir 800 mg 5x/day or Valacyclovir

4. Molluscum Contagiosum

Multiple, giant (>1 cm), atypical lesions on face (unusual site in immunocompetent)
Inverse distribution (face, neck) suggests HIV
Typically at CD4 <200 cells/mm³

5. Warts (HPV)

Extensive, recalcitrant condylomata acuminata
Increased risk of intraepithelial neoplasia (cervical, anal)

6. Oral Hairy Leukoplakia

EBV-induced
White, corrugated, non-removable plaques on lateral tongue
Virtually pathognomonic of HIV (CD4 ~200-500)

B. Fungal Infections

1. Oral Candidiasis (Thrush)

Most common opportunistic infection in HIV
Pseudomembranous (white plaques), erythematous, angular cheilitis forms
Indicates CD4 usually <200
Treatment: Fluconazole 150 mg

2. Cryptococcosis

Umbilicated papules resembling molluscum contagiosum in disseminated disease
Primarily meningitis but skin involvement in 5-10%

3. Histoplasmosis / Talaromycosis (Talaromyces marneffei)

Endemic fungal infections with umbilicated necrotic papules in disseminated disease

C. Bacterial Infections

1. Bacillary Angiomatosis

Bartonella henselae / quintana
Vascular papules/nodules closely mimicking Kaposi's sarcoma
Treatment: Erythromycin 500 mg QID x 3 months

2. Impetigo and Folliculitis - more severe, widespread, recurrent

3. Syphilis - atypical, aggressive presentation; higher risk of neurosyphilis

D. Seborrheic Dermatitis

Occurs in up to 85% of AIDS patients
Severe, recalcitrant; involves face, scalp, chest
Correlates with CD4 decline

E. Pruritic Papular Eruption (PPE)

Symmetric itchy papules, upper trunk and limbs
Eosinophilic folliculitis variant
Associated with low CD4 (<200); relatively specific for HIV in endemic areas

F. Drug Reactions

Severe drug hypersensitivity common with cotrimoxazole, nevirapine, abacavir
Stevens-Johnson Syndrome (SJS), TEN, DRESS syndrome

G. Malignancies

1. Kaposi's Sarcoma (KS)

Most common AIDS-defining malignancy
Caused by HHV-8 (KSHV)
Violaceous/purplish macules, plaques, nodules on skin + mucosa
Sites: lower limbs, oral mucosa, face; visceral involvement in AIDS-KS
CD4 usually <200
Treatment: ART (immune reconstitution causes regression); liposomal doxorubicin for advanced disease

2. Non-Hodgkin's Lymphoma - may have cutaneous involvement 3. Cervical/Anal Carcinoma - HPV-related; AIDS-defining

H. Miscellaneous

Photosensitivity
Nail changes: onychomycosis, melanonychia
Psoriasis - severe, atypical, recalcitrant
Xeroderma, ichthyosis (late HIV)

Q4 (a). Deformities in Leprosy (5 Marks)

Introduction

Deformities in leprosy arise from nerve damage (leading to muscle paralysis and sensory loss), direct bacillary infiltration, and trophic changes.

WHO Disability Grading

Grade 0: No anaesthesia, no visible deformity
Grade 1: Anaesthesia present, no visible deformity
Grade 2: Visible deformity/damage present

Mechanisms of Deformity

Peripheral nerve damage by M. leprae inflammation
Muscle imbalance - intrinsic vs. extrinsic muscle paralysis
Loss of protective sensation - repeated trauma, trophic ulcers
Direct bacillary infiltration of skin, subcutaneous tissue, bones
Lepra reactions (Type 1 and Type 2) accelerating nerve damage

Nerves Affected and Resultant Deformities

Nerve	Site of Entrapment	Deformity
Ulnar	Medial epicondyle	Claw hand (ring + little finger), hypothenar wasting
Median	Wrist (carpal tunnel)	Claw hand (index + middle), thenar wasting, simian thumb
Ulnar + Median (combined)	Both sites	"Main en griffe" - all 4 fingers clawed
Radial	Spiral groove	Wrist drop
Common peroneal	Fibular neck	Foot drop
Posterior tibial	Behind medial malleolus	Clawing of toes, plantar anaesthesia
Facial (zygomatic branch)	Zygomatic arch	Lagophthalmos

Specific Deformities by Region

Face:

Lagophthalmos - inability to close eye - leads to exposure keratitis, corneal ulceration, blindness
Saddle nose - collapse of nasal bridge due to septal perforation
Madarosis - loss of outer eyebrows (pathognomonic of lepromatous leprosy)
Leonine facies - thickened, ridged facial skin (LL)
Loss of anterior nasal spine

Hand:

Claw hand (Benediction hand) - ulnar nerve
Simian hand - median nerve
Wrist drop - radial nerve

Foot:

Foot drop - peroneal nerve
Plantar trophic ulcers (mal perforans)
Absorption/resorption of toes (concentric shortening)

Prevention of Deformities

Early diagnosis and MDT
Regular nerve function assessment (motor + sensory)
Corticosteroids for acute neuritis
Self-care education and physiotherapy
Footwear modification (MCR footwear)
Reconstructive surgery (tendon transfers) for established deformities

Q4 (b). Protease Inhibitors (5 Marks)

Mechanism of Action

Key Pharmacology

Most PIs are substrates and inhibitors of CYP3A4
Ritonavir at low doses (100 mg) acts as a pharmacokinetic booster - inhibits CYP3A4 metabolism of co-administered PIs, increasing their plasma levels ("boosted PI" concept)
Newer booster: Cobicistat (COBI)

Commonly Used PIs

Drug	Boosting	Dose	Key Feature
Lopinavir/r (LPV/r)	Self-boosted	400/100 mg BD	Long-term safety data; common 2nd-line
Atazanavir/r (ATV/r)	+ Ritonavir	300/100 mg OD	Once daily; benign hyperbilirubinemia
Darunavir/r (DRV/r)	+ Ritonavir	600/100 mg BD or 800/100 OD	Active against resistant strains; preferred
Ritonavir	-	100 mg (booster only)	Full dose no longer used; CYP3A4 inhibitor
Saquinavir	+ Ritonavir	1000/100 mg BD	First PI approved
Indinavir	+ Ritonavir	800/100 mg BD	Nephrolithiasis; requires high fluid intake

Adverse Effects

Class Effects (all PIs):

Metabolic syndrome: Dyslipidemia (elevated TG, LDL), hyperglycemia, insulin resistance
Lipodystrophy: Peripheral lipoatrophy + central lipohypertrophy ("buffalo hump," "protease paunch")
GI: nausea, diarrhea (especially LPV/r)
Hepatotoxicity

Drug-Specific:

Indinavir: Nephrolithiasis (drink 2L/day), indirect hyperbilirubinemia
Atazanavir: Unconjugated hyperbilirubinemia (benign), PR interval prolongation
Darunavir: Cross-reaction in sulfonamide allergy (sulfonamide moiety)

Drug Interactions

Rifampicin (strong CYP3A4 inducer) drastically reduces PI levels - avoid; use rifabutin instead
Statins (lovastatin, simvastatin) levels markedly increased - use pravastatin/rosuvastatin

Current Role

PIs (particularly DRV/r) are used as:

Second-line ART (after NNRTI-based regimen failure)
Third-line regimens
Special situations (e.g., pregnancy)

Q5. Classify Trophic Ulcers; Etiology, Pathophysiology, Management, and Preventive Measures (10 Marks)

Definition

Classification

I. By Etiology:

Neuropathic: Leprosy, diabetes mellitus, tabes dorsalis (syphilis), syringomyelia, hereditary sensory neuropathy
Vascular: Arterial (atherosclerosis, Buerger's disease), Venous (chronic venous insufficiency)
Mixed (neurovascular): Diabetic foot
Pressure ulcers: In paralyzed/immobile patients

II. By Depth - Wagner's Classification (Diabetic Foot):

Grade	Description
0	Intact skin, at-risk foot
1	Superficial ulcer
2	Deep ulcer reaching tendon/capsule/bone
3	Deep ulcer with abscess/osteomyelitis/joint infection
4	Forefoot gangrene
5	Whole foot gangrene

Etiology

Leprosy - most important cause in India; posterior tibial nerve damage leads to plantar anaesthesia
Diabetes mellitus - peripheral sensory neuropathy + microangiopathy
Tabes dorsalis - posterior column disease; Charcot joints
Syringomyelia - cervical cord lesion; ulcers on hands
Peripheral vascular disease - Buerger's disease, atherosclerosis obliterans
Spinal cord injuries, paraplegia - pressure sores

Pathophysiology

Step 1 - Loss of protective sensation: Neuropathy (e.g., leprosy, DM) destroys small-fiber sensory neurons. Patient cannot perceive pain, temperature, or pressure.

Step 2 - Repetitive mechanical trauma: Normal walking exerts high plantar pressures at metatarsal heads. Without pain sensation, patient continues activity despite injury. Repeated microtrauma leads to subepidermal hematoma and blister formation.

Step 3 - Breakdown and ulceration: Blister ruptures internally or externally. Ulcer forms over pressure points (metatarsal heads, heel, medial big toe).

Step 4 - Deepening and infection: Absence of pain means patient ignores the wound. Polymicrobial secondary infection. Progressive destruction of tendons, periosteum, bone - osteomyelitis in late stages.

Step 5 - Chronicity: Impaired autonomic function leads to dry skin and fissuring. Impaired angiogenesis and tissue healing. Biofilm formation leads to chronic non-healing state.

Clinical Features

Painless ulcer (key distinguishing feature)
Location: plantar surface over metatarsal heads, heel
Surrounding callus/hyperkeratosis (neuropathic type)
Well-defined, punched-out edges with surrounding hyperkeratosis
Sloughy base
Absent protective sensation in surrounding skin

Management

A. General Measures:

Address underlying cause (MDT for leprosy; glycemic control for diabetes)
Patient education

B. Offloading - Most Important Step:

Remove pressure from ulcer site
Total Contact Cast (TCC) - gold standard for offloading
Removable cast walkers, padded footwear
Bed rest for severe ulcers

C. Wound Care:

Debridement of callus and necrotic tissue (sharp/dry debridement)
Saline dressings twice daily
Antiseptic soaks (potassium permanganate 1:10,000)
Advanced dressings: hydrocolloid, alginate for wound bed preparation
Maggot therapy for debriding necrotic tissue

D. Infection Management:

Superficial: topical antiseptics
Deep infection/cellulitis: systemic antibiotics (amoxicillin-clavulanate, or culture-guided)
Osteomyelitis: prolonged IV antibiotics + surgical debridement

E. Surgical Management:

Excision of bony prominences (metatarsal head resection) to eliminate pressure points
Skin grafting for large, clean ulcers
Amputation as last resort (Grade 4-5)

F. Vascular Ulcers:

Revascularization (angioplasty, bypass grafting)

Prevention

Daily foot inspection using a mirror for plantar surface
Proper footwear - Microcellular Rubber (MCR) footwear distributes plantar pressure evenly
Regular callus paring to prevent high-pressure zones
Daily foot soaking and application of oil/moisturizer to prevent fissuring
Early treatment of blisters, cuts, and abrasions before progression
Avoidance of barefoot walking on rough surfaces
Regular physiotherapy - maintains range of motion
Early leprosy diagnosis and MDT to prevent neuropathy
Glycemic control in diabetics (HbA1c <7% significantly reduces risk)
Regular foot examination by a healthcare worker at every clinic visit

Q6 (a). Newer Drugs in Leprosy (5 Marks)

Background

Standard WHO-MDT (rifampicin, dapsone, clofazimine) has been the backbone of leprosy treatment since 1982. Newer agents are used for drug-resistant leprosy, single-lesion PB leprosy, and chemoprophylaxis.

1. Fluoroquinolones

Ofloxacin:

Highly bactericidal against M. leprae (lowest MIC among fluoroquinolones)
Part of the ROM regimen for single-lesion PB leprosy
Dose: 400 mg/day
Used in dapsone-resistant and rifampicin-resistant leprosy combinations

Moxifloxacin: More potent than ofloxacin; promising in MDR leprosy (under investigation)

2. Minocycline

Tetracycline derivative with bactericidal activity against M. leprae
Part of ROM regimen
Anti-inflammatory properties useful in reactions
Dose: 100 mg/day
Side effect: reversible bluish-grey skin pigmentation

3. ROM Regimen (Single-Dose)

For single-lesion PB leprosy (one patch):

Rifampicin 600 mg + Ofloxacin 400 mg + Minocycline 100 mg - all as single dose
Non-inferior to 6 months of standard PB-MDT for one lesion

4. Clarithromycin

Macrolide with bactericidal activity against M. leprae
Active against dapsone/rifampicin-resistant strains
Used in combination regimens

5. Thalidomide

Used for Type 2 lepra reaction (ENL)
Mechanism: inhibits TNF-alpha production; down-regulates neutrophil function
Highly effective for ENL
Absolutely contraindicated in women of childbearing age (causes phocomelia - limb reduction defects)
Dose: 100-400 mg/day (taper)
Now largely replaced by clofazimine + steroids in most settings

6. Rifabutin

Rifamycin analogue active against rifampicin-resistant M. leprae
Fewer drug interactions than rifampicin
Used in combination regimens for resistant leprosy

7. Single-Dose Rifampicin (SDR) for Contacts

WHO 2016 guidelines recommend SDR prophylaxis for household contacts of newly diagnosed MB leprosy patients
Single dose: 600 mg rifampicin
Reduces risk of leprosy in contacts by ~57% over 2 years

Q6 (b). Bedside Tests in STI (5 Marks)

Simple, rapid diagnostic tests performable in clinic without sophisticated laboratory equipment.

1. Dark Field Microscopy (DFM)

For: Treponema pallidum (primary and secondary syphilis)
Method: Serous exudate from chancre placed on slide; examined immediately under dark-field illumination
Result: Corkscrew motility of spirochetes - bright coils on dark background
Sensitivity: ~80% for primary syphilis
Limitation: Cannot be used for oral/anal lesions (commensal treponemes interfere)

2. Wet Mount Microscopy

Saline wet mount: motile trichomonads (T. vaginalis), clue cells (BV)
KOH preparation: hyphae/pseudohyphae/spores (Candida)
Sensitivity ~50-70% for trichomonas

3. Whiff Test (Amine Test)

For: Bacterial Vaginosis
Add 10% KOH to vaginal discharge on a glass slide
Positive: Fishy (amine) odor = BV
Instant result; no equipment needed

4. pH of Vaginal Discharge

Normal vaginal pH: 3.8-4.5 (acidic, maintained by lactobacilli)
pH >4.5: BV, Trichomonas, atrophic vaginitis
pH <4.5: Candida, normal discharge
Use narrow-range pH paper

5. Gram Stain

Urethral smear (males): Intracellular gram-negative diplococci (IGND) = gonorrhea (95% sensitive in males)
Vaginal smear: Less sensitive for gonorrhea in females
Clue cells: Epithelial cells studded with gram-variable coccobacilli = BV
Hyphae/pseudohyphae: Candida

6. Tzanck Smear

For: Genital herpes (HSV)
Scraping from base of fresh vesicle; stained with Giemsa/Wright/Toluidine blue
Result: Multinucleated giant cells (syncytia) with intranuclear inclusions
Sensitivity ~60%; cannot differentiate HSV-1 from HSV-2 or VZV

7. VDRL / RPR

VDRL: Flocculation test; antigen is cardiolipin-lecithin-cholesterol; requires centrifuge
RPR (Rapid Plasma Reagin): Card test; no centrifuge needed - truly bedside
Used for syphilis screening; false positives in malaria, autoimmune disease, pregnancy, TB

Q7. Differentiate Relapse from Reaction in Leprosy. Management of Relapsed Leprosy (10 Marks)

Definitions

Reaction: An acute immunological event occurring during the course of leprosy; not due to drug failure
Relapse: Re-appearance of active disease after completing a full, adequate course of MDT, in a previously Released From Treatment (RFT) patient

Differentiation: Relapse vs. Reaction

Feature	Relapse	Type 1 Reaction (Reversal)	Type 2 Reaction (ENL)
Timing	Months to years after completing MDT	During treatment or shortly after	During treatment or after completion
Onset	Insidious, gradual (weeks-months)	Subacute (days to weeks)	Acute (hours to days)
Lesions	New skin lesions outside previous distribution	Existing lesions become erythematous, edematous, tender	New crops of tender erythematous nodules
Nerve involvement	New nerves may be affected	New nerve involvement very common	Tender nerves, but different mechanism
Systemic features	Absent	Absent	Fever, malaise, arthralgia, uveitis, orchitis
Bacteriology (BI)	BI rises ≥2+ from nadir	BI unchanged or may improve	BI unchanged
Histopathology	Active inflammation; macrophages with bacilli	Lymphocytic infiltrate; upgrading; edema; no neutrophils	Neutrophilic infiltrate; immune complex deposition
Response to steroids	No response	Dramatic, rapid response	Partial response
Treatment	Re-institute MDT	Prednisolone	Prednisolone; thalidomide (ENL)

Key Points to Remember

BI rising by ≥2+ from nadir is the strongest indicator of relapse
In relapse: new lesions appear outside the area of previous lesions
In reaction: pre-existing lesions become inflamed
Reaction has constitutional symptoms in ENL; relapse does not
Slit-skin smear (SSS) examination is essential to confirm relapse

Management of Relapsed Leprosy

Step 1 - Confirm Relapse

Clinical + SSS + histopathology + BI assessment
Exclude reaction (critical distinction)
Drug susceptibility testing (DST) if available - check for rifampicin resistance (rpoB gene mutation) and dapsone resistance (folP1 mutation)

Step 2 - Assess Type of Relapse

PB relapsed case: re-treat as MB-MDT
MB relapsed case: re-treat with extended MB-MDT if drug-sensitive

Step 3 - Standard Re-treatment (Drug-Sensitive) WHO MB-MDT for 24 months (extended for relapse):

Rifampicin 600 mg once monthly (supervised)
Clofazimine 300 mg once monthly + 50 mg daily
Dapsone 100 mg daily

Step 4 - Drug-Resistant Relapse

If dapsone resistance: Substitute dapsone with clofazimine; continue rifampicin.

If rifampicin resistance confirmed (MDR Leprosy): Second-line regimen (WHO) - 6 months intensive + 18 months continuation:

Clarithromycin 500 mg/day
Minocycline 100 mg/day
Ofloxacin/Moxifloxacin 400 mg/day
Clofazimine 50 mg/day

Step 5 - Ancillary Measures

Continue full prescribed MDT course without interruption
Monitor for reactions during retreatment (immune reconstitution may trigger Type 1 reaction)
Nerve function monitoring (monthly)
Disability prevention: physiotherapy, footwear, self-care
Psychosocial support and anti-stigma counseling

Q8. Management of HIV Infection in Women. Management of ADRs to Antiretroviral Drugs (10 Marks)

Part A: Management of HIV in Women

Why Women Need Special Attention

Higher biological susceptibility to HIV per unprotected sexual act vs. men
Women-specific manifestations: recurrent vaginal candidiasis, cervical HPV/carcinoma, pelvic inflammatory disease
Pregnant women: prevention of mother-to-child transmission (PMTCT)
ARV interactions with hormonal contraception

Diagnosis and Initial Workup

HIV rapid test + confirmatory ELISA/Western blot
Testing offered at antenatal clinics, family planning clinics, ICTC
Baseline: CD4 count, viral load, CBC, LFT, RFT, VDRL, HBsAg, anti-HCV, TB screening

When to Start ART

All HIV-positive women start ART regardless of CD4 count (Test and Treat policy)
Urgently if: pregnancy, CD4 <200, AIDS-defining illness present

First-Line Regimen (Non-Pregnant Women) - WHO/NACO

TDF 300 mg + 3TC 300 mg + DTG 50 mg - once daily

Alternative: TDF + 3TC + EFV 600 mg OD

Special Situation: Pregnancy and PMTCT

Risk of MTCT without treatment: ~25-40% (breastfeeding adds risk) With ART: MTCT reduced to <1-2%

PMTCT Components (WHO Option B+ Strategy):

ART for all HIV-positive pregnant women: start immediately, continue lifelong
Neonatal prophylaxis: Nevirapine (NVP) syrup x 6 weeks (or 12 weeks if breastfeeding)
Infant HIV testing: DNA PCR at 6 weeks, then 3 months
Infant feeding: Exclusive breastfeeding for 6 months with maternal ART suppression (in resource-limited settings)
Delivery: Cesarean section only for obstetric indications if viral load undetectable

Drugs to Avoid in Pregnancy:

Efavirenz: Avoid in first trimester (teratogenic in animals; WHO now permits after 8 weeks)
Stavudine (d4T): Avoid - lactic acidosis risk
ddI + d4T combination: Severe lactic acidosis and fetal death

Note on Dolutegravir in Pregnancy: Earlier concerns about neural tube defects (Tsepamo study, Botswana) were updated. Risk is very low (~0.1%) - WHO now recommends DTG throughout pregnancy.

Women-Specific Monitoring

Cervical cancer screening: Pap smear annually (cervical carcinoma is AIDS-defining; HPV risk 5x higher)
Recurrent VVC: Fluconazole 150 mg weekly prophylaxis
Contraception: Efavirenz and PIs reduce OC plasma levels - advise barrier contraception additionally; DMPA injection is safe
Bone health: TDF reduces bone mineral density - calcium + Vitamin D supplementation

Part B: Management of ADRs to Antiretroviral Drugs

NRTI-Related ADRs

Drug	ADR	Management
Zidovudine (AZT)	Bone marrow suppression (anemia, neutropenia), macrocytosis, myopathy, lactic acidosis	If Hb <7.5 g/dL: switch to TDF or ABC; G-CSF for severe neutropenia
Stavudine (d4T)	Peripheral neuropathy, lactic acidosis, lipoatrophy, pancreatitis	Switch to TDF; avoid in all new regimens
Tenofovir (TDF)	Nephrotoxicity (Fanconi syndrome, RTA), bone loss	Monitor Cr, urine protein; switch to TAF or ABC if renal impairment
Abacavir (ABC)	Hypersensitivity reaction (HSR) in HLA-B*5701+ patients: fever, rash, GI distress	Screen HLA-B*5701 before prescribing; NEVER rechallenge after HSR
Lamivudine (3TC)	Minimal toxicity; very well tolerated	No specific management needed

NNRTI-Related ADRs

Drug	ADR	Management
Nevirapine (NVP)	Severe rash (SJS, TEN), fulminant hepatotoxicity	Discontinue immediately; do NOT rechallenge; avoid in CD4 >250 (women) or >400 (men)
Efavirenz (EFV)	CNS effects (dizziness, nightmares, vivid dreams, depression), rash	Take at bedtime; usually resolves in 2-4 weeks; switch if severe psychiatric effects

PI-Related ADRs

Dyslipidemia: dietary modification; statins (pravastatin or rosuvastatin - avoid simvastatin/lovastatin)
Hyperglycemia: metformin; insulin if needed
GI intolerance (LPV/r): loperamide, anti-emetics
Nephrolithiasis (Indinavir): increased hydration (2L/day)

General Approach to ARV ADRs

Step 1 - Assess severity (ACTG grading 1-4):

Grade 1-2 (mild-moderate): Symptomatic management + close monitoring
Grade 3-4 (severe-life-threatening): Stop offending drug; switch

Step 2 - Identify the causative drug (timeline of drug initiation vs. ADR onset)

Step 3 - Switch strategy: Substitute one drug while maintaining the other two to preserve virological efficacy

Management of Specific Severe ADRs:

Lactic acidosis (NRTIs): Stop all NRTIs; supportive care; IV bicarbonate; ICU care - high mortality
Severe hepatotoxicity: Stop all ARVs if ALT >5x ULN with symptoms; restart cautiously with different regimen
SJS/TEN (NVP, EFV): Stop offending drug immediately; ICU care; skin barrier nursing
Abacavir HSR: Stop immediately; IV fluids; antihistamines; never rechallenge (can be fatal)

Q9 (a). Nail Changes in Leprosy (5 Marks)

Introduction

Nail changes in leprosy are not a direct effect of M. leprae on nail tissue, but result from peripheral nerve damage, autonomic dysfunction, vascular changes, and secondary infections.

Mechanisms

Autonomic neuropathy - impaired sweating and blood flow to nail matrix and bed
Sensory neuropathy - repeated unnoticed trauma to nails
Direct infiltration of nail bed in lepromatous leprosy
Secondary fungal and bacterial superinfections

Types of Nail Changes

Nail Change	Description
Onychoschisis	Transverse splitting/lamination of nail plate - most common
Onycholysis	Separation of nail plate from nail bed
Pterygium unguis	Forward extension of cuticle/proximal nail fold over nail plate
Onychomycosis	Fungal nail infection - discoloration, thickening, crumbling (very common)
Leukonychia	White discoloration of nail
Nail atrophy/dystrophy	Thin, fragile, misshapen nails from matrix damage
Longitudinal ridging	Due to nail matrix atrophy
Brachyonychia	Short nails from resorption of distal phalanx
Subungual hemorrhage	From minor unnoticed trauma (painless)
Anonychia (total nail loss)	Advanced disease; shedding due to infection, trauma, bone resorption

Clinical Significance

Nail changes reflect long-standing disease and significant nerve damage
Should prompt foot/hand care education and self-care training
Treat onychomycosis actively: oral terbinafine 250 mg/day x 3 months for toenails
Protect nails from trauma with padded gloves/footwear

Q9 (b). Inguinal Bubo (5 Marks)

Definition

An inguinal bubo is an enlarged, tender lymph node (or matted nodes) in the inguinal region due to infection or malignancy, most commonly STI-related.

STI Causes

Disease	Organism	Type of Bubo
Lymphogranuloma Venereum (LGV)	C. trachomatis L1, L2, L3	Tender, matted, suppurative; groove sign
Chancroid	Haemophilus ducreyi	Tender, fluctuant, unilateral; may rupture spontaneously
Primary Syphilis	Treponema pallidum	Non-tender, rubbery, bilateral ("sentinel nodes")
Donovanosis	Klebsiella granulomatis	Pseudobubo - subcutaneous nodule, not true lymphadenopathy
Genital Herpes	HSV-2	Tender, bilateral, non-fluctuant

Non-STI Causes

Filariasis (Wuchereria bancrofti) - chronic, non-tender, rubbery
Plague (Yersinia pestis) - extremely painful, rapidly enlarging
Tuberculosis - cold abscess, non-tender
Lymphoma, metastatic carcinoma

Groove Sign of LGV (Classic Feature)

The inguinal ligament divides enlarged nodes into groups above and below it
Creates a characteristic groove on palpation - pathognomonic of LGV

Clinical Approach

History: Painful vs. painless? Preceding genital ulcer? Sexual history? Travel?

Examination:

Size, consistency, tenderness, fluctuance, overlying skin
Examine genitals for primary lesion (chancre, ulcer)
Examine both inguinal regions

Investigations:

VDRL/RPR + TPHA (syphilis)
C. trachomatis NAAT (LGV - L1-L3 serovars)
HSV PCR
Aspirate: gram stain, culture, cytology
Biopsy if lymphoma/malignancy suspected

Management

STI	Treatment
LGV	Doxycycline 100 mg BD x 21 days
Chancroid	Azithromycin 1 g single dose OR Ceftriaxone 250 mg IM single dose
Primary Syphilis	Benzathine penicillin 2.4 MU IM single dose
Genital Herpes	Acyclovir 400 mg TDS x 7-10 days

For fluctuant bubo (LGV/Chancroid):

Needle aspiration (NOT incision - leads to chronic sinus formation)
Aspirate through adjacent normal skin

Q10. Role of Sex Education with Reference to STDs. Counseling of a Suspected Case of HIV (10 Marks)

Part A: Role of Sex Education in STDs

Scale of the Problem

WHO estimates 1 million STIs are acquired every day globally
Most are preventable with correct information and behavioral change
Young people are disproportionately affected
Stigma and lack of knowledge are major barriers to care-seeking

Components of Comprehensive Sex Education

Anatomy and physiology of the reproductive system
Puberty, menstruation, and reproductive health
Relationships, consent, and personal boundaries
STI/HIV - transmission, prevention, symptoms, treatment
Contraception - barrier methods (male/female condom), hormonal methods
Correct and consistent condom use demonstration
Partner communication and refusal/negotiation skills
Abstinence as a valid choice (not the only message)
Healthcare-seeking behavior - when and where to seek help
Reducing stigma around HIV/STIs

Role in STD Prevention

Primary Prevention (preventing acquisition):

Delay of sexual debut
Reduction in number of sexual partners
Correct and consistent condom use: reduces HIV transmission by 85%, gonorrhea/chlamydia by 50-80%
HPV vaccination awareness
PrEP awareness for high-risk individuals

Secondary Prevention (early detection):

Recognizing symptoms of STIs (discharge, ulcer, rash)
Awareness of asymptomatic infections (especially chlamydia)
Encouraging regular STI testing
Reducing fear and stigma around testing

Tertiary Prevention:

Adherence to treatment
Partner notification and treatment
Prevention of re-infection and complications

Target Groups

School-going adolescents (age-appropriate curricula)
Out-of-school youth
High-risk groups: sex workers, MSM, truckers, migrants
Married couples
Healthcare providers

National Programs in India

RKSK (Rashtriya Kishor Swasthya Karyakram) - adolescent health
ARSH Clinics (Adolescent Reproductive and Sexual Health)
NACP (National AIDS Control Programme) - IEC (Information, Education, Communication) campaigns
School health programs under NHM

Part B: Counseling of a Suspected Case of HIV

Pre-Test Counseling

Purpose: Informed consent, risk assessment, emotional preparation for possible result

Steps:

1. Establish rapport and confidentiality

Reassure complete confidentiality
Create non-judgmental, supportive atmosphere

2. Assess HIV risk

Sexual history (partners, condom use, high-risk behavior)
Blood transfusion, surgery, invasive procedures
IV drug use/needle sharing
History of STIs
Occupational exposure

3. Explain HIV basics

What HIV is; difference between HIV and AIDS
Modes of transmission: sexual, blood-borne, mother-to-child
Modes NOT transmitted: handshake, sharing food, mosquitoes
Window period: 3-4 weeks to 3 months; modern 4th-generation tests detect earlier

4. Explain the test

Voluntary, confidential
ELISA/rapid test; confirmed by Western blot
Explain possibility of window-period false negative

5. Discuss possible results

Ask: "What would it mean to you if the result is positive?"
Assess coping mechanisms and support systems
Discuss potential impact on relationships

6. Obtain informed written consent for HIV testing

Post-Test Counseling

If Result is NEGATIVE:

Explain result is not conclusive if within the window period - repeat at 3 months
Reinforce risk reduction: condom use, single/fewer partners, avoid IV drug use
Offer PrEP counseling if high-risk
Screen for other STIs

If Result is POSITIVE:

1. Breaking the news

Private setting; allow patient to absorb the information
Allow time for emotional response (anger, denial, grief); do not rush

2. Clarify what HIV-positive means

HIV-positive does NOT mean AIDS
With ART, patients can live a normal, near-full lifespan
Viral load suppression protects the patient and prevents transmission (U=U: Undetectable = Untransmittable)

3. Risk reduction counseling

Disclose to partner; offer partner testing
Consistent condom use (even with another HIV-positive partner)
Avoid donating blood, organs, or breast milk
Safe injection practices if applicable

4. Medical management plan

Referral to ART center immediately
Explain ART: adherence >95% is critical for viral suppression
Regular follow-up: CD4 count, viral load every 6 months
OI prophylaxis: cotrimoxazole if CD4 <200

5. Disclosure support

Discuss to whom to disclose (partner, family)
Legal protection: India's HIV/AIDS (Prevention and Control) Act 2017 protects against discrimination
Counseling support for partner disclosure

6. Psychosocial support

Refer to PLHIV (People Living with HIV) support groups
Mental health referral if depression/anxiety present
Address workplace and social stigma

7. Special Populations:

Pregnant women: Start ART immediately (PMTCT); neonatal prophylaxis
Women of reproductive age: Reproductive and contraceptive counseling
Children: Pediatric ART; age-appropriate disclosure planning

References: Fitzpatrick's Dermatology (9th Ed.); Harrison's Principles of Internal Medicine (22nd Ed., 2025, McGraw-Hill); Goldman-Cecil Medicine; WHO Guidelines for the Treatment of STI (2016); NACO ART Guidelines (2021); WHO Global Leprosy Guidelines (2018)

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