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Infectious Diseases > HIV > Flashcards

HIV Flashcards

1
Q

what are the name of the type of drug that stops binding of the virus to target cell?

A

fusion inhibitors can stop the binding of the CD4-R/co-receptor (CCR5) to the HIV

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2
Q

protease inhibitors work how?

A

they stop the action of the viral protease from cleaving proteins into active forms

therefore it stops the virus from getting out of the cell and infecting other cells. it does not however, stop that cell from getting destroyed (c.f. Reverse transc inhibs)

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3
Q

what is the current theory about why patients with HIV get chronic immune activation?

A

in the initial infection with HIV, there is profound loss of the GALT/peyer’s patches (and this only partially returns even with full treatment)

because of this, there is quite significant loss of the barrier, and then a lot of chronic minor infection, particularly as the bugs are then moved up to the LNs

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4
Q

what is the better predictor of rate of decline of immune function in asymptomatic patient?

HIV RNA concentration or CD4 count?

A

RNA concentration is better

despite this, markers of immune activation are actually better.

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5
Q

how does the HIV molecule get into the cell?

A

it binds with the CD4-R. there is a coreceptor which it also needs to bind with

typically this is the CCR5

in patients with specific genetics that lead to loss of CCR5 (e.g. delta32 homozygotes with no CCR5 expression) have resistance to R5 isolates

if delta32 heterozygote, then delated progression to AIDS

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6
Q

what is the treatment regimen of choice for HIV patients?

A

The optimal antiretroviral (ARV) regimen for a treatment-naive patient consists of two NRTIs in combination with a third active ARV drug from one of three drug classes: an NNRTI, a PI boosted with ritonavir, or an INSTI.

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7
Q

what are some of the agents that you might know about?

let’s talk nucleoside RTIs

A

Kivexa is a combined tablet

  • abacavir and lamivudine
  • this agent should not be used in patients with high CVS risk
  • 5% of the population will have a hypersens to the abacavir. The way we check for this is the HLAB5701 (if pos, don’t use)

Truvada is a combined tablet

  • this is tenofovir plus emtricitabine
  • this is the drug of choice for Hep B co-infection (because these agents work against HBV)
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8
Q

what are the nNRTIs of choice?

A

Nevirapine

  • do not use if CD4 counts are above 250 in women, or 400 in men
  • this is because with high CD4 counts, it causes an increased risk of hep and rash.

Efavirenz

  • popular
  • potential teratogenicity
  • caution if preggo
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9
Q

PI first line agents?

A

lopinavir

atazanavir

Each of these should be boosted with ritonavir

  • ritonavir works by interacts with CYP-3A4 and leads to decreased hep clearance of other PIs.
  • overall it leads to IMPROVED PHARMACOKINETIC PROFILE
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10
Q

what are some mandatory pre-treatment tests in HIV?

A
  1. HLA B5701 (abacavir)
  2. Genotype resistance assay
  3. Hep B serology
  4. Pregnancy counselling
  5. CVD risk calculated
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11
Q

what is the characteristics of the abacavir hypersens reaction?

A

within the first 6 weeks (usually)

fever
rash
fatigue
malaise
sore throat/cough
myalgia

N/V/D

if this happens, stop immediately

do not rechallenge, for risk of anaphylactoid

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12
Q

what are some common toxicities seens with ART?

talk about NRTI

A

lipoatrophy (severe fat wasting) but better described as lipodystrophy because there is some central fat accumulation

MITOCHONDRIAL TOXICITY

peripheral neuropathy

renal disease - particularly tenofovir

zidovudine - N/V/headache/insomnia

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13
Q

what are some common toxicities seens with ART?

talk about nnRTI

A

rash and hepatitis

CNS toxicity - efavirenz causes this in almost all patients in the first few days of treatment, however it dissipates with time (this is usually nightmares and vivid dreams). Also dizziness (therefore give at night time)

SJ syndrome

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14
Q

what are some common toxicities seens with ART?

talk about PI

A

Metabolic complications such as hyperlipid and hyperglycaemia

CVS disease - this is ON TOP of the hyperlipid and hypergly (greater than expected for those RFs alone)

diarrhoea

jaundice is particularly common in ATA and IDV (?low yield?)

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15
Q

WHat does rifampicin do to some of the ART?

A

it decreases the level of PI

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16
Q

what does clarithromycin do to the ART?

A

it decreases the level of NNRTI

17
Q

how are statins affects by a type of ART?

A

PI increase the level of statins, particularly simvastatin

The best choice is pravastatin which is not affected by this

18
Q

which PI is affected by stomach acid?

A

atazanavir requires acidic environment to be well absorbed.

therefore, PPIs lead to poor absorption

19
Q

how are inhaled steroids affected by which ART?

A

ritonavir leads to increased levels of fluticasone and eventually, Cushings

20
Q

which ART is esp important in patients on methadone?

A

nevirapine leads to decreased levels of methadone

this can lead to clinically significant wirhdrawal

21
Q

which drug affects the COCP?

A

nevirapine leads to decreased level of the oestrogen component of COCP

22
Q

how does one manage the immune reconstitution inflammatory syndrome?

A

once drug toxicity and other differentials have been excluded, we continue ART

provide anti-inflamm
provide anti-microbial agents

you should aim to prevent it.

  • if CD4 <50 should have ophthalm review prior to ART (CMV)
  • CXR
  • MAC should be checked for - faeces and blood specimens
  • PCP prophylaxis
  • complete cryptococcal Ag
  • check for all the heps (serology and PCR)

consider MAC prophylaxis (?isoniazid)

23
Q

how do we provide ART in pregnancy?

A
  1. mother should start ART at least in second trimester with aim for undetectable viral load at time of delivery (this is the most important for reducing vertical transmission)
  2. baby gets ART for first 6 weeks of life
  3. if viral load undetect = can have SVD
    if any virus > must have C section
  4. no breast feeding

transmission can still occur, about 2%. but significantly better than baseline 30%!

24
Q

when do we need to start PEP?

how long do we continue it for?

what is the window period?

A

commence within 72 hours of exposure

ART should be continued for 4 weeks

the window period is extended to 6 months (there is a theory that the PEP could delay any possible seroconversion

25
Q

what are very strong reasons INDEPENDENT OF CD4 for initiation of ART

A

pregnancy

history of AIDS defining illness

HIV associated nephropathy

HIV/hep B coinfection

26
Q

how does the mitochondrial toxicity work?

A

it is particularly important in the nucleoside RTIs

this is because they are essentially DNA polymerase inhibitors. all of our cells are dependent on these. The major cellular DNA pol are not affected. However, the mitochondrial DNA pol are

this leads to adverse events such as:

lactic acidosis
peripheral neuropathy
CMP
pancreatitis
anaemia

the older agents were more problematic for this

d4T > ddI > AZT > ABC > 3TC

27
Q

which of the ART is most important to consider renal function?

A

Tenofovir is a NRTI

it can lead to renal impairment

the MoA is not clear yet

therefore measure urine protein:creat ratio

28
Q

what is the interplay between HIV and Hep C?

A

Hep C coinfection has little impact on the progression of HIV

HOWEVER,

HIV leads to higher HCV viral loads, more rapid progression and higher transmission

it is particularly difficult to assess the HCV when there is use of ART that can cause hepatotoxicity

29
Q

what sort of symptoms does one see with HIV dementia?

what sort of syndrome

A

global findings, such as memory impairment, irritability, behavioural change, poor concentration and possibly motor symptoms like loss of fine motor control

however, focal things like dysphasia are less common

Infectious Diseases (13 decks)

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