HIV & opportunistic infections flashcards
28 high-yield MRCP Part 1 cards from the Intellect Medicos Infectious Diseases course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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HIV binds CD4 using envelope glycoprotein ______, and fusion with the host membrane is mediated by gp41.
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gp120
Why? Entry also needs a co-receptor, usually CCR5 or CXCR4. gp160 is the precursor cleaved into gp120 and gp41.
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HIV binds CD4 using envelope glycoprotein gp120, and fusion with the host membrane is mediated by ______.
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gp41
Why? Entry also needs a co-receptor, usually CCR5 or CXCR4. gp160 is the precursor cleaved into gp120 and gp41.
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What is the first-line HIV test, and what does it detect?
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A fourth-generation test: HIV-1/2 antibodies plus p24 antigen.
Why? p24 antigen appears before antibodies, so infection is detected earlier than with antibody-only tests.
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What is the window period of a fourth-generation laboratory HIV test?
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45 days.
Why? A negative result 45 days after exposure reliably excludes infection (BHIVA/BASHH/BIA 2020). Antibody-only point-of-care and self-tests have a longer window (90 days).
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What are the typical features of HIV seroconversion illness and when does it occur?
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A glandular-fever-like illness 2–6 weeks after infection: fever, sore throat, rash, lymphadenopathy, myalgia.
Why? It coincides with very high viral load; recognising it allows early diagnosis.
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What is the structure of a standard first-line antiretroviral regimen (BHIVA)?
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An integrase inhibitor-based regimen: two NRTIs plus dolutegravir or bictegravir (e.g. tenofovir/emtricitabine + dolutegravir), or the two-drug combination dolutegravir/lamivudine.
Why? The aim is an undetectable viral load; undetectable = untransmittable (U=U).
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What test must be done before starting abacavir, and why?
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HLA-B*57:01 testing — carriers are at high risk of a severe abacavir hypersensitivity reaction.
Why? The reaction can be fatal on rechallenge; HLA-B*57:01-positive patients must not receive abacavir.
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Which NRTI classically causes macrocytic anaemia and bone marrow suppression?
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Zidovudine (AZT).
Why? It also causes myopathy, lipodystrophy and insulin resistance. NRTIs as a class cause mitochondrial toxicity (e.g. peripheral neuropathy, lactic acidosis).
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Which organ toxicity is the main concern with tenofovir disoproxil?
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Renal toxicity — proximal tubulopathy (Fanconi-type) and falling eGFR; also reduced bone mineral density.
Why? Monitor renal function and urine protein. Tenofovir alafenamide has less renal and bone toxicity.
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How do NNRTIs such as efavirenz differ from NRTIs in mechanism?
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They bind reverse transcriptase directly at a non-active site and do not need intracellular phosphorylation.
Why? NRTIs are nucleoside analogues that must be phosphorylated and then terminate the DNA chain.
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Why is low-dose ritonavir added to other protease inhibitors?
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It is a potent CYP3A4 inhibitor ("booster"), raising levels of the partner drug.
Why? This allows once-daily dosing but causes many drug interactions (e.g. with statins, steroids, some anticoagulants).
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Which simple co-prescribed medicines reduce dolutegravir absorption?
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Antacids and supplements with polyvalent cations (calcium, iron, magnesium, aluminium).
Why? Integrase inhibitors chelate these cations; separate doses by several hours.
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Below what CD4 count is co-trimoxazole prophylaxis against Pneumocystis started?
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CD4 <200 cells/mm³.
Why? PCP risk rises steeply below this level. Prophylaxis can stop once CD4 is >200 for over 3 months on ART (or 100–200 with an undetectable viral load for 3–6 months).
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What CT finding and SPECT result suggest cerebral toxoplasmosis rather than primary CNS lymphoma in HIV?
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Multiple ring-enhancing lesions with SPECT negative (lymphoma: often single lesion, SPECT/thallium positive).
Why? Lymphoma is metabolically active, so takes up thallium; toxoplasma abscesses do not.
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What is the first-line treatment for cerebral toxoplasmosis?
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Pyrimethamine + sulfadiazine + folinic acid.
Why? Folinic acid protects the marrow from pyrimethamine's antifolate effect.
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Which CSF tests diagnose cryptococcal meningitis?
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Cryptococcal antigen (CrAg) and India ink stain (plus culture); opening pressure is usually very high.
Why? Cryptococcus neoformans is the commonest CNS fungal infection in HIV (CD4 <100).
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What is the induction treatment for cryptococcal meningitis?
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Liposomal amphotericin B + flucytosine, followed by fluconazole consolidation/maintenance.
Why? The combination clears CSF fastest; fluconazole prevents relapse.
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Which virus causes progressive multifocal leukoencephalopathy (PML)?
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JC virus (a polyomavirus).
Why? It destroys oligodendrocytes → non-enhancing white matter lesions. No specific antiviral; treatment is immune restoration with ART.
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What is the fundoscopic appearance of CMV retinitis?
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"Pizza pie" / "cheese and ketchup" retina — haemorrhages with white necrotic exudates along vessels.
Why? It occurs at CD4 <50 and causes painless progressive visual loss.
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What is the first-line treatment for CMV retinitis?
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Oral valganciclovir; immediately sight-threatening lesions also need intravitreal (± IV) ganciclovir. Foscarnet or cidofovir are alternatives.
Why? Valganciclovir is a prodrug of ganciclovir with good oral absorption.
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What is the classic histology of CMV colitis on biopsy?
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"Owl's eye" intranuclear inclusion bodies.
Why? CMV colitis (usually CD4 <50) presents with bloody diarrhoea, pain and risk of perforation; treat with IV ganciclovir.
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What is the first-line treatment of disseminated Mycobacterium avium complex (MAC) in HIV?
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Clarithromycin (or azithromycin) + ethambutol, adding rifabutin if severe.
Why? MAC occurs at CD4 <50 with fever, sweats, weight loss, anaemia and raised ALP; blood cultures are diagnostic.
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Which virus causes Kaposi's sarcoma?
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Human herpesvirus 8 (HHV-8).
Why? It causes purple vascular skin lesions with spindle cells, and can spread to lungs and GI tract.
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Which virus causes oral hairy leukoplakia, and how is it told apart from candida?
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EBV; the white lateral-tongue plaques cannot be scraped off (candida plaques can).
Why? It is a marker of immunosuppression in HIV and usually needs no specific treatment.
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A patient deteriorates with fever and enlarging lymph nodes 4 weeks after starting ART for HIV with TB. How should ART be managed?
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Continue ART and give supportive care (steroids may be used for severe IRIS).
Why? This is immune reconstitution inflammatory syndrome: recovering immunity attacks the existing infection.
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What mode of delivery does BHIVA recommend for a woman with HIV whose viral load is <50 copies/mL at 36 weeks?
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Planned vaginal delivery.
Why? With full suppression the transmission risk is very low and caesarean adds no benefit.
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What prophylaxis is given to a low-risk baby born to a mother with HIV and viral load <50 copies/mL?
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Zidovudine monotherapy for 2 weeks; the baby is tested with HIV PCR (nucleic acid testing).
Why? Antibody tests are useless in infants because maternal antibodies cross the placenta. High-risk babies get combination ART.
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Besides Pneumocystis, which CNS opportunistic infection does co-trimoxazole prophylaxis also prevent in toxoplasma-seropositive patients with low CD4 counts?
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Cerebral toxoplasmosis.
Why? Co-trimoxazole is active against Toxoplasma gondii, so one drug covers both infections until CD4 recovers on ART.
More Infectious Diseases topics
- Microbiology & antimicrobials
- Skin, soft tissue & Gram-positive infections
- Pneumonia & tuberculosis
- Meningitis & encephalitis
- Gastrointestinal infections
- Viral infections & hepatitis
- Zoonoses & rickettsial infections
- Malaria & tropical infections
- Worms & helminths
- Sexually transmitted infections
- Vaccines, PEP & asplenia