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DR11.1-2 | HIV Dermatology — Graded Quiz
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A 32-year-old HIV-positive man presents with hyperpigmented, indurated plaques over his cheeks, ears and forearms with sensory loss. CD4 count is 420 cells/μL. Slit-skin smear reveals acid-fast bacilli. Which aspect of his management is MOST directly relevant to HIV co-management?
Correct. Rifampicin strongly induces CYP3A4, reducing PI and NNRTI plasma concentrations — a critical interaction in HIV-leprosy co-infection requiring ART regimen review.
Rifampicin in leprosy MDT is a potent CYP3A4 inducer and significantly reduces plasma levels of protease inhibitors and NNRTIs. This drug interaction must be anticipated and ART adjusted. Leprosy is not an AIDS-defining illness.
The key co-management challenge in HIV-leprosy is the rifampicin–ART drug interaction (CYP3A4 induction), not the diagnostic timing or HLA screening.
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A patient with HIV (CD4 55 cells/μL) presents with painful vesiculobullous eruption following a dermatomal distribution on the trunk, crossing the midline slightly with bilateral involvement. The MOST likely diagnosis and its implication is:
Correct. Bilateral/disseminated VZV reactivation at CD4 55 indicates advanced HIV and risk of visceral zoster. IV acyclovir is indicated; start/optimise ART.
Disseminated herpes zoster (>2 non-contiguous dermatomes or crossing midline with bilateral vesicles) is an AIDS-defining condition and indicates CD4 <100. It carries risk of visceral dissemination (pneumonitis, hepatitis, encephalitis). Requires IV acyclovir and urgent ART initiation/optimisation.
The bilateral involvement crossing the midline distinguishes disseminated from localised zoster; at CD4 55 and with bilateral distribution, disseminated zoster is the diagnosis with implications for visceral involvement.
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A woman with HIV on efavirenz presents with a non-tender, skin-coloured to slightly erythematous lipodystrophy — truncal obesity, buffalo hump, and peripheral lipoatrophy of the face and limbs. Which statement BEST describes this manifestation?
Correct. Thymidine-analogue NRTIs (stavudine, zidovudine) cause peripheral lipoatrophy via mitochondrial DNA polymerase-gamma inhibition. Switching to non-thymidine NRTIs (tenofovir, abacavir) partially reverses lipoatrophy.
ART-associated lipodystrophy includes peripheral lipoatrophy (mainly thymidine-analogue NRTIs: stavudine > zidovudine, via mitochondrial toxicity) and central lipohypertrophy (PI-related and NNRTI-related metabolic effects). Lactic acidosis from NRTI mitochondrial toxicity is a related metabolic complication.
Lipodystrophy in HIV is primarily ART-related — not solely HIV viral effect. Thymidine analogue NRTIs are the primary lipoatrophy culprits.
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A 40-year-old woman with HIV (CD4 65 cells/μL) has new onset of firm papules with central umbilication on her face. Some lesions have coalesced into large plaques. KOH mount of expressed material reveals encapsulated yeast. Diagnosis and appropriate treatment is:
Correct. Molluscum-like umbilicated papules with encapsulated yeast on KOH = disseminated cryptococcosis. LP essential. Amphotericin B + flucytosine induction is the current standard.
Disseminated Cryptococcus neoformans can manifest as molluscum-like umbilicated papules in advanced HIV (CD4 <100). The encapsulated yeast on KOH/India ink distinguishes it from molluscum. Cryptococcal meningitis must be excluded (LP). Treatment: amphotericin B + flucytosine induction, fluconazole consolidation and maintenance.
The encapsulated yeast on KOH distinguishes cryptococcosis from molluscum (which would show molluscum bodies, not yeast). This diagnosis requires antifungal treatment, not just ART.
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A patient on nevirapine-based ART develops fever (39.2°C), widespread morbilliform rash, facial oedema, lymphadenopathy, and ALT 3× ULN on day 21. Blood count shows eosinophilia. The MOST likely diagnosis and FIRST action is:
Correct. DRESS: delayed onset, rash + systemic features (fever, lymphadenopathy, eosinophilia, hepatitis) = stop nevirapine immediately. Systemic corticosteroids indicated for DRESS.
DRESS is characterised by delayed onset (typically 2–8 weeks), morbilliform rash with facial oedema, fever, lymphadenopathy, eosinophilia, and internal organ involvement (hepatitis, nephritis). Nevirapine is a major culprit. Immediate drug withdrawal is mandatory; systemic corticosteroids are used for DRESS (unlike SJS/TEN where they are controversial). DRESS has 10% mortality.
Eosinophilia, hepatitis, lymphadenopathy, and facial oedema with rash constitute DRESS, not SJS/TEN (which requires mucosal involvement and skin blistering) and not IRIS (which occurs in the context of immune reconstitution).
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A 29-year-old man with advanced HIV and low CD4 is started on ART. Three weeks later, facial molluscum contagiosum lesions worsen dramatically and multiply. CD4 has risen from 30 to 140 cells/μL, viral load is suppressed. On re-examination, no new infections are identified. The MOST appropriate management is:
Correct. Molluscum IRIS: paradoxical worsening with CD4 rise + VL suppression after ART. Continue ART — this is an expected, self-limiting immune reconstitution phenomenon.
Molluscum contagiosum IRIS is a classic example of unmasking or paradoxical IRIS. The key diagnostic features are: lesion worsening after ART initiation, simultaneous CD4 rise and VL suppression, and no evidence of new infection. Management: continue ART; the lesions typically regress as CD4 stabilises. Topical treatment may be added but is not the primary intervention.
Stopping or switching ART because of IRIS is incorrect and counterproductive. The clinical picture (VL suppressed, CD4 rising) confirms ART is working. IRIS requires ART continuation.
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A medical student reads that nevirapine causes SJS/TEN and that the BSA cut-off for TEN is >30%. Which of the following best integrates the SJS/TEN spectrum with nevirapine's clinical significance?
Correct. Nevirapine can cause the full SJS-TEN spectrum. BSA cut-offs: SJS <10%, overlap 10–30%, TEN >30%. Early drug withdrawal saves lives.
The SJS-TEN spectrum is defined by BSA epidermal detachment: SJS <10%, overlap 10–30%, TEN >30%. Nevirapine (NNRTI) is the ART drug most implicated in the full spectrum including TEN. Early drug withdrawal is the single most important determinant of survival in severe cases. Tenofovir has minimal dermatological toxicity.
Nevirapine is the ART drug with the highest SJS/TEN risk and can produce any point on the spectrum. The BSA thresholds are: SJS <10%, overlap 10–30%, TEN >30%.
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A patient with HIV on ART regimen containing indinavir (a protease inhibitor) complains of dry, cracked heels, brittle nails and generalised xerosis. There are no mucosal lesions or systemic symptoms. The MOST likely ART-related cutaneous side effect accounting for these features is:
Correct. Indinavir's retinoid-like effects — xerosis, paronychia, cracked heels, brittle nails — are a recognised class effect of this protease inhibitor.
Indinavir (and some other protease inhibitors) causes a retinoid-like syndrome: xerosis, cheilitis, paronychia, alopecia, and ingrown toenails — due to retinoid-receptor-like activity. This is distinct from DRESS, SJS/TEN, or morbilliform rash and is managed with emollients and, where needed, dose adjustment.
SJS/TEN and DRESS both involve systemic features and/or blistering, neither of which is present here. The retinoid-like mucocutaneous syndrome is a specific indinavir/PI class effect.
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In a patient with HIV and CD4 count 160 cells/μL presenting with a new white plaque on the buccal mucosa that can be SCRAPED OFF, leaving a raw erythematous base, the MOST appropriate initial treatment is:
Correct. Removable white plaques = oral candidiasis (thrush). First-line: topical nystatin or oral fluconazole for moderate disease. Address ART to restore immune control.
Oral candidiasis (thrush) presents as removable white plaques revealing erythematous raw base. Oral hairy leukoplakia (EBV) is non-removable. Oral candidiasis is treated with topical nystatin suspension or oral fluconazole (for moderate-severe or oropharyngeal disease). ART will help long-term immune recovery but immediate antifungal treatment is required.
The removable nature distinguishes this from OHL (which is not removable and is caused by EBV). Oral candidiasis requires antifungal therapy, not antivirals or steroids.
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A PLHIV (CD4 320 cells/μL) is found to have extensive genital warts (condylomata acuminata) and perianal lesions. She is not on ART. Regarding management and risk, which statement is MOST accurate?
Correct. HIV impairs HPV immune control, increasing oncogenic risk. ART reduces but does not abolish the elevated cancer risk. Ongoing cancer screening is essential.
HIV-related immunosuppression impairs local mucosal immunity against HPV, leading to greater viral persistence, higher lesion burden, higher recurrence rate after treatment, and significantly elevated risk of anogenital squamous cell carcinoma. ART (by restoring immunity) reduces but does not eliminate the excess risk — cervical and anal cancer screening must continue even in virologically suppressed PLHIV.
HPV-related lesions in HIV are not self-limiting and require treatment; ART does not fully restore oncogenic risk to HIV-negative levels.
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