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Module 2 > Antiretroviral therapy > Flashcards

Antiretroviral therapy Flashcards

1
Q

How many patients undergo rapid HIV progression?

A

<5%

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2
Q

What iss the percetnage of patinets who are long-term non-progressors?

A

5%

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3
Q

What is the typical HIV progression?

A

7-10 years

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4
Q

What is seen with primary HIV disease in terms of viral count and CD4?

A

during primary, there is very high viraemia with rapid decrease in CD4, then with seroconversion, CD4 count rises

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5
Q

What did the SMART study look at?

A

continuous ART vs drug conservation strategy

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6
Q

What is the drug conservation strategy with ART?

A

defer use of ART til CD4 <250 then episodic ART based on CD4 count to increase counts to >350

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7
Q

What were the results of the SMART study?

A

opportunistic disease and all-cause death were both considerably lower in the virologic suppression cohort– first evidence that HIV doesn’t just affect immune system but also results in inflammatory disease eg MIs; strokes which can be reduced with ART

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8
Q

What was the START study looking at?

A

immediate vs deferred ART for asymptomatic, ART-naive patients

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9
Q

What was the result of the START study?

A

60% reduction in serious events or death with immediate ART vs deferred—everyone with HIV gets ART

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10
Q

What are the 2 types of entry inhibitor?

A

CCR5 inhibitor- maraviroc and fusion gp41- T20

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11
Q

What is the problem with CCR5 inhibitors?

A

have to ensure that the patietns has an R5 tropic virus

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12
Q

How can you determine if a patients virus is R5 or X4 tropic?

A

viral culture to look at characteristcs- phenotypic test ; genotypic test- sequence the envelope of the virus

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13
Q

How does T20 work?

A

big peptide which stops the receptor changing shape therefore prevents entry

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14
Q

What is the problem with T20?

A

has to be injected as it is a large peptide but is exogenous so there are injection site reactions

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15
Q

What are the 3 types of reverse transcriptase inhibitor?

A

NRTI (nucleoside RTI); NTRTI (nucleotide RTI) and NNRTI (non-nucleoside)

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16
Q

How do the NNRTIs work?

A

enzmye inhibitors- bind to RT

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17
Q

How do the NRTIs and NTRTIs work?

A

chain terminators

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18
Q

Why are integrase inhibitors now first line?

A

massively reduced SE profile

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19
Q

What is the MOA of AZT?

A

acts as an analogue for thymidine in growing pro-viral DNA chain

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20
Q

How many HIV viral particles are produced each day?

A

10^11

21
Q

How does HIV resistance develop?

A

error prone reproduction, drug resistant mutatns have no advantage (are less fit) but drug pressure selects out and creates mutants

22
Q

How long does AZT work for?

A

6 months (resistance)

23
Q

Which drugs were the first developed using rationale drug design

A

protease inhibitors (after protease enzyme structure established)

24
Q

What is the best HAART combination?

A

2 nucleoside RTIs and another drug- usually integrase

25
Q

Which NRTIs are recommended first line?

A

tenofovir; emtricitabine

26
Q

What was the prupose of the ESPIRIT study?

A

look at whether you can boost a patietns immune system to fight HIV by giving IL-2

27
Q

What were the results of the ESPIRIT study?

A

got massive CD4 response to IL-2 but there was not difference in OI or death between arms

28
Q

What is the minimum adherence required to prevetn resistance?

A

a dose every 6 months

29
Q

What were the main side effects with the historical NRTIs?

A

mitochondrial toxicity; lipoatrophy; individual drug toxicities

30
Q

What is the mechanism behind the SE of historical NRTIs?

A

some cross-reactivity between RT and DNA polymerase, lots of DNA polymerase in mitochondria–drugs tend to hit a specific organs mitochondria

31
Q

What is a problem with abacavir?

A

4% of caucasians have a genetic hypersensitivity to abacavir; increased risk of MI

32
Q

How can the hypersensitivity to abacavir be avoided?

A

screen patietns for HLA-B27 01 before using; only give to patients with a low risk of MI- QRISK score

33
Q

What organs does tenofovir affect?

A

renal and bone

34
Q

What is the difference bewteen the 2 forms of tenofovir (DF and AF)?

A

different prodrugs- AF gives v. high concentrations in lymphocytes vs kidneys and bones so has less SE than DF version

35
Q

What are the general SE of NNRTIs?

A

rash; hepatotoxicity; CNS effects

36
Q

What are the specific SEs of nevirapine?

A

allergic rash and hepatitis/ SJS

37
Q

What are the specific SE of efavirenz?

A

insomnia; vivd dreams; pychosis; rash

38
Q

What are hte main SE with protease drugs?

A

metabolic syndrome- hyperlipidaemia; hyperglycaemia; body fat accumulation

39
Q

What is a specific SE of indinavir?

A

renal stones

40
Q

What is a specific SE of atazanavir?

A

scleral icterus

41
Q

When would the TAF version of tenofovir be used instead of TDF?

A

if decreased GFR and abnormal BMD or young patient (bones still growing)

42
Q

What metabolises the protease inhibitors?

A

CYP 3A4

43
Q

Why are CYP 3A4 inhibitors given with protease inhibitors?

A

as without there are a lot of peaks and troughs in drug levels so reduces doses needed

44
Q

What is a major problem with protease inhibitors?

A

lots of drug interactions

45
Q

When is T20 used?

A

in patietns resistance to all other classes

46
Q

What adverse effect is more common in integrase inhibitors?

A

insomnia- CNS toxicity?

47
Q

What comorbdities are more common in HIV persons?

A

hypertension; angina; MI ; liver disease; renal failure and cancer

48
Q

What are the future challenges with HIV treatment?

A

less drug-drug interactions; less imapct on comorbidities and easier adherence

Module 2 (38 decks)

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