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Phase 3B Infectious Diseases > HIV > Flashcards

Flashcards in HIV Deck (18)
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1
Q

HIV epidemiology:
a) Virus subtypes
b) At-risk groups

A

a) HIV-1:
- most common worldwide and in Europe
- subtypes M (main), O (outlier), and N (non-M or O)

HIV-2
- more common in West Africa.
- subtypes A and B

b) - Endemic areas
- IVDU
- MSM
- Prostitutes
- Infants of HIV+ mothers (vertical transmission)
- Co-existing Hepatitis / other STI

2
Q

HIV structure:
a) 2 main receptors
b) Attaches to what receptor? (found on what cells?)
c) 9 genes encoded by HIV
d) 3 enzymes targeted by ARVT (function of each)

A

a) GP-120 (attaches to CD4 receptor, found on CD4 cells and also macrophages and others) and GP-41

b) CD4 receptor:
- Helper T-lymphocytes, monocytes, macrophages and neural cells

c) Gag, Pol, Env, Tat, Rev, Nef, Vif, Vpr and Vpu

d) - Reverse transcriptase: converts HIV viral RNA into DNA before its incorporation into the cell genome
- Integrase: integrates the viral DNA with host DNA
- Protease: produces mature infectious viral particles by cleaving large structural proteins and enzymes

3
Q

CD4 count.
a) Normal range
b) Annual decline without ARVT
c) AIDS diagnosed when CD4 is below…?

A

a) 500-1500

b) 50/year

c) < 200

4
Q

AIDS-defining illnesses: pathogenesis
a) Viral
b) Fungal
c) Bacterial
d) Parasitic
e) Neoplasm
f) Other

A

a) - CMV disease (other than liver, spleen or nodes), eg. CMV retinitis (with loss of vision)
- Progressive multifocal leukoencephalopathy (JC virus)
- Herpes simplex: chronic ulcer(s) (>1 month’s duration)

(Note: OHL and shingles are more common in HIV, bua are not AIDS-defining illnesses)

b) - Pneumocystis jirovecii pneumonia (PCP)
- Candidiasis of trachea, bronchi, lungs, or oesophagus
- Coccidioidomycosis (disseminated or extrapulmonary)
- Cryptococcosis (extrapulmonary)

c) - Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary)
- Mycobacterium avium complex (MAC) or M. kansasii (disseminated or extrapulmonary)
- Mycobacterium, other species or unidentified species, (disseminated or extrapulmonary)
- Pneumonia, recurrent.
- Salmonella septicaemia, recurrent.

d) - Toxoplasmosis of brain
- Histoplasmosis, disseminated or extrapulmonary.
- Cryptosporidiosis, chronic intestinal (>1 month’s duration)
- Isosporiasis, chronic intestinal (>1 month’s duration)

e) - Kaposi’s sarcoma.
- Lymphoma: CNS, Burkitt’s or immunoblastic.
- Cervical carcinoma, invasive.

f) - Encephalopathy, HIV-related.
- Wasting syndrome due to HIV.

5
Q

AIDS-defining illnesses: body region.
a) Brain/CNS
b) Eyes
c) GI
d) Pulmonary
e) Skin
f) Disseminated infection
g) Other

A

a) - Neurotoxoplasmosis
- HIV-related encephalopathy
- CNS lymphoma
- PML.

b) - CMV retinitis
(note: ocular toxoplasmosis is common in HIV but not an AIDS-defining illness)

c) HSV oral ulcers (> 1 month)
- Candida oesophagitis
- Cryptosporidiosis, isosporiasis (> 1 month)

d) - PCP
- Candidiasis of bronchi, trachea or lungs
- Pulmonary TB

e) - Kaposi Sarcoma.

f) - Mycobacteria
- Coccidioidomycosis
- Cryptococcosis
- Histoplasmosis
- Salmonella sepsis (recurrent)

g) - Invasive cervical cancer.
- Burkitt’s or immunoblastic lymphoma.

6
Q

Pneumocystis jirovecci (PCP).
a) Risk factors
b) Clinical features
c) CXR appearance
d) Management of suspected infection
e) Cautions and side effects of treatment

A

a) - HIV infection (50% have AIDS)
- Other immunosuppression: chemotherapy, taking immunosuppressive medication, transplant patients, haematological malignancy

b) - Cough (usually dry), SOB, fever, etc.
- Signs of HIV/AIDS (thrush, OHL, wasting, etc.)
- O/E: often normal, may be scattered creps/wheeze

c) - Abnormal, but non-specific findings (usually bilateral)
- Examples: perihilar fluffy shadows, pneumatoceles, interstitial reticular shadowing

d) - HIV testing: antibodies for ELISA
- Imaging: plain XR +/- HRCT
- Sputum sample; if negative but PCP is still suspected - do a bronchoscopy with bronchoalveolar lavage or transbronchial biopsy
- Co-trimoxazole (oral if mild-moderate; IV if severe)
- Adjuvant steroids (in moderate-severe disease)

e) Co-trimoxazole.
- Cautions: severe hepatic/ renal dysfunction, porphyria, pregnancy, breastfeeding
- Side effects: nausea, vomiting, skin rash, neutropenia, thrombocytopenia, hepatitis, cholestatic jaundice

7
Q

HIV risk factors
- Mnemonic: SHARP

A
  • Sexual partner - “Have you ever had a Sexual partner who is known to be HIV positive?”
  • Homosexual - “Have you ever had sex with a bisexual man/engaged in male homosexual activity?”
  • Abroad - “Have you ever had sex with someone abroad, or who was born in a different country?”
  • Recreational drugs - “Have you ever injected drugs?” “Are you aware of any of your previous partners having ever injected drugs?”
  • Prostitution - “Have you ever paid someone for sex, or been paid for sex?”
8
Q

Diagnosing HIV.
a) Who is screened? (screening test used)
b) Diagnostic tests (chronology of appearance in serum)
c) Other tests
d) What should be done before and after testing?
e) Test in infants born to HIV+ mothers

A

a) Pregnant women, sexual health clinics:
- Rapid POC blood test - HIV antibodies for ELISA

b) - HIV RNA and p24 antigen appear first - do PCR
- HIV antibody appears later (negative in seroconversion)
- Combination test: HIV antibody AND p24 antigen
(most accurate - takes ~ 4 weeks to get the result)

c) - FBC: anaemia, thrombocytopenia, lymphocytopenia, with reduced CD4 cell count
- ESR raised
- STI screen (chlam/gono, etc.)
- Other infection screen - Hep B/C, syphilis, TB
- Baseline CXR
- Cervical smear

d) Counselling

e) HIV DNA PCR and virus culture
(antibody test unreliable due to maternal antibodies)

9
Q

Stages of HIV infection.
a) Seroconversion illness
b) Following seroconversion - ?
c) Once CD4 counts begin falling - ?
d) Final stage

A

a) - 1 - 6 weeks post-infection (~ 50% present here)
- Glandular fever-type illness: fever, pharyngitis, lymphadenopathy, malaise, myalgia, headaches, diarrhoea, neuralgia or neuropathy, maculopapular rash
- Viral load high
- Antibody negative; p24 antigen/HIV RNA positive

b) Asymptomatic phase: from ~ 12 weeks post-infection
- May have persistent generalised lymphadenopathy
- Viral load low (but gradually increasing)
- HIV antibody positive; antigen/RNA positive

c) Symptomatic phase (prodrome to AIDS):
- Constitutional symptoms (eg. fever, weight loss, night sweats, chronic diarrhoea)
- Opportunistic infections* (eg. shingles, recurrent oral or vaginal candidiasis, oral hairy leukoplakia)

*excluding those that are AIDS-defining

d) AIDS:
- Presence of AIDS-defining illness in context of HIV
- CD4 count usually < 200

10
Q

AIDS - definition

A

One or more of:
- Presence of AIDS-defining illness in context of HIV
- CD4 count < 200

11
Q

Management of HIV: non-drug

A
  • Emotional support, counselling, education
  • Annual health screen
  • 6-monthly sexual health screen
  • Contraception and fertility advice (+ antenatal care in pregnancy)
  • Confidentiality
  • Sexual partner notification
  • Immunisations: Hep A/B, annual influenza, pneumococcal (NOT BCG)
12
Q

HIV management: HAART
a) How is response to treatment monitored?
b) Why are 3 different drugs usually used?
c) 3 main enzymes acted on
d) 4 main classes
e) Usual regimen
f) In patients with HIV-2

A

a) - Clinical assessment
- Bloods: HIV RNA (viral load) and CD4 count

b) Prevent drug resistance

c) Reverse transcriptase, integrase, protease

d) - Nucleoside reverse transcriptase inhibitors (NRTI)
- non-nucleoside RTI (NNRTI)
- protease inhibitors (PI)
- integrase inhibitors (II)

e) 3 drugs: 2 NRTIs plus… 1 NNRTI or 1 PI or 1 II
(eg. tenofovir, emtricibatine + raltegravir)

f) - Refer to centre specialising in HIV-2 treatment
- Don’t use non-nucleoside RTIs (HIV-2 resistant to them)
- Otherwise, therapies are the same

13
Q

Example HAART drugs.
a) Nucleoside reverse transcriptase inhibitors (NRTI); one also used to treat Hep B
b) Non-nucleoside reverse transcriptase inhibitors (NNRTI)
c) Protease inhibitors
d) Integrase inhibitors
e) Pill that combines 3 drugs

A

a) Tenofovir (used also to treat Hep B), emtricitabine, zidovudine (AZT)
- Note: often given as one Truvada® tablet (245 mg tenofovir and 200 mg emtricitabine)

b) Efavirenz

c) Darunavir

d) raltegravir (inTEGgrase - ralTEGravir)

e) Atripla® (efavirenz/emtricitabine/tenofovir disoproxil)

14
Q

HIV in pregnancy.
a) Management
b) Breastfeeding

A

a) - Specialist antenatal care
- HAART to reduce vertical transmission (however, risk of foetal toxicity and preterm birth)

b) If HIV+, avoid breastfeeding (not the case in deprived areas with poor access to infant nutrition)

15
Q

Treatment of co-existing disease.
a) TB (prevention/treatment)
b) PCP/toxoplasmosis
c) CMV retinitis
d) HSV
e) Salmonella (prevention/treatment of septicaemia)

A

a) Isoniazid prevention, or RIPE if active

b) Co-trimoxazole

c) Ganciclovir

d) Aciclovir

e) Ciprofloxacin

16
Q

Post-exposure prophylaxis.
a) For what exposures?
b) Define an ‘exposure’
c) Window of opportunity (and efficacy)
d) Duration of treatment
e) Drugs used
f) Follow-up

A

a) - Occupational exposure to Hep B, Hep C and HIV (eg. needlestick injury)
- Non-occupational exposure to Hep B, Hep C and HIV (eg. sexual - only penetrative or ejaculative; i.e. not fellatio without ejaculation or cunnilingus)

b) Exposure: contact with potentially infected sample via percutaneous injury, mucocutaneous contact (including the eye) or through a break in the skin (eg. bad eczema)

c) HIV - ideally within 1 hour; or at least 72 hours (to prevent viral replication)
- Around 80% effective if initiated early

d) 28 days

e) Normal 3-drug regimen (2x NRTI + 1 other)

f) - HIV antibody testing using ELISA 12 weeks post-completion of PEP (or if not taking PEP, 6 weeks post-exposure)

17
Q

HIV transmission risk.
a) Occupational: percutaneous vs mucocutaneous
b) Non-occupational: highest to lowest risk

A

a) - Percutaneous: 3 in 1000
- Mucocutaneous: < 1 in 1000
(note: through cracked skin, risk is even lower)

b) - Blood transfusion (highest)
- Receptive anal intercourse.
- Receptive vaginal intercourse.
- Insertive anal/vaginal intercourse
- Receptive oral sex

18
Q

HAART: side effects of treatment

A
  • GI upset and headaches
  • Liver damage (especially NRTIs)
  • Blood disorders: anaemia, neutropenia, thrombocytopenia)
  • Rashes/Stevens-Johnson syndrome (especially NNRTIs)
  • Metabolic: raised cholesterol, fat redistribution, lipodystrophy, insulin resistance
  • P450 effects - drug interactions