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PHAM02 > HIV > Flashcards

HIV Flashcards

1
Q

what type of virus is HIV?

A

single stranded RNA Lentivirus

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2
Q

variants of HIV

A

HIV-1 - more virulent, most common

HIV-2 - less common, W Africa

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3
Q

How is HIV transmitted?

A
  • sex without condom
  • from mother to baby during childbirth
  • sharing needles
  • contaminated blood transfusion/organ transplant
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4
Q

How to diagnosie HIV?

A
  1. POCT - point of care testing
  2. 4th generation assay
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5
Q

POCT - point of care test

A
  • HIV Ab test
  • finger prick test or mouth swab
  • results in 20-30mins
  • highly accurate >6 weeks after exposure
  • less sensitive (+ve results send for 4th gen test)
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6
Q

4th generation assay

A
  • HIV Ab and P24 Ag test
  • blood sample sent to lab
  • results can take 7 days
  • highly sensitive after 4 weeks
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7
Q

What is P24 antigen that 4th generation assay looks for?

A

protein produced 2-3 weeks after infection

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8
Q

Markers to monitor HIV

A
  1. CD4 count
  2. viral load
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9
Q

CD4 count

A

no of CD4+ T cells in 1ul of blood

represents how well the immune system is functioning

CD4% represents proportion of CD4+ cells in relation to other WBC

Tx aim = inc CD4 count/CD4%

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10
Q

CD4 levels in normal and HIV

A

normal CD4 = 500-1000
normal CD4% = > 14

HIV CD4 = less than that

CD4 <350 inc risk infection
CD4 <200 severe risk

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11
Q

What is viral load?

A
  • no. of copies of HIV RNA in 1ml of blood
  • represents the conc of virus in the blood, not the amount of virus in the patient’s body
  • Tx aim = dec VL to undetectable (<50-20)
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12
Q

Tx aims for CD4 and VL?

A

CD4 as high as possible

VL as low as possible

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13
Q

markers used to assess effectiveness of ARV Tx?

A

viral load

CD4 count

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14
Q

Reduced viral load leads to what CD4?

A

inc CD4 cell count or %

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15
Q

stages of HIV infection

A
  1. acute infection
  2. clinical latency
  3. declining CD4 count
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16
Q

acute infection stage (seroconversion illness)

A
  • 1-6 weeks
  • inc infectiousness, high viral load
  • unaware of HIV status
  • up to 50% asymptomatic
  • non-specific Sx, flu-like
  • diagnosis often missed
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17
Q

clinical latency stage

A
  • declining CD4 count
  • may last >8yrs
  • some decline rapidly (6-12mths)
  • non-progressors, never see decline in CD4 count
  • stable viral load
  • asymptomatic, few Sx, mild
  • may be unaware of infection
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18
Q

risks with declining CD4 count

A

inc risk of opportunistic infection and lymphomas

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19
Q

AIDS

A

advanced immuno deficiency syndrome

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20
Q

When is AIDS diagnosed?

A

low CD4 count and at least 1 AIDS defining illness

  • opportunistic infections
  • cancers
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21
Q

PCP

A

P jirovecci pneumonia

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22
Q

Sx of PCP

A
  • seen in new HIV diagnoses
  • non productive cough and exertional dyspnoea, thick mucous
  • weight loss
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23
Q

Tx for PCP

A

co-trimoxazole for 21 days

  • IV for severe
  • oral for mild/mod

(trimethoprim + sulfametoxazole)

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24
Q

prophylactic Tx for CD4 <200

A

co-trimoxazole 480mg OD PO

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25
Q

When to stop prophylactic Tx if CD4 <200?

A

when CD4 >200 for > 3 months

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26
Q

MAC

A

mycobacterium avium complex

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27
Q

Sx of MAC

A

fever
night sweats
fatigue
weight loss
anorexia
diarrhoea

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28
Q

Tx of MAC

A

macrolides + ethambutol

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29
Q

prophylactic Tx for MAC

A

azithromycin 1250mg WEEKLY

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30
Q

Mycobacterial TB Tx

A

pyrazinamide
rifampicin
ethambutol
isoniazid

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31
Q

What has inc risk with mycobacterium TB?

A

risk of IRIS

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32
Q

malignancies at inc risk with HIV

A
  • systemic NHL
  • primary cerebral - lymphoma
  • Kaposi’s sarcoma
  • cervical cancer
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33
Q

enzymes in HIV virus not found in humans

A

reverse transcriptase

integrase

protease

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34
Q

4 types of HIV drugs

A
  1. CCR5 inhibitors
  2. nucleoside/nucleotide RT inhibitors &non-nucleoside RTIs
  3. integrase inhibitors
  4. protease inhibitors
35
Q

goals of HIV Tx

A
  • etended life expectancy and QOL
  • preserve and restore CD4 cell count
  • viral load undetectable within 4-6mths (<20 copies/ml)
  • prevent transmission
36
Q

when to start Tx (4)

A
  1. primary infection
  2. chronic infection
  3. presents ith AIDS or major infection
  4. prevention of transmission
37
Q

When to start Tx in primary infection?

A

only when patient ready, uness:

  • neurological involvelemt
  • any AIDS defining illness
  • CD4 persistently <350 cells/ul
  • diagnosis within 12 weeks of previous negative
38
Q

When to start Tx if patient presents with AIDS/major infection?

A

start within 2 weeks of antimicrobials if

  • AIDS defining infection
  • serious bacterial infection with CD4 count <200 cells/ul
39
Q

pros of early Tx

A
  • inc immunological recovery
  • reduced transmission
  • reduced disease progression/morbidity
  • reassurance to pt
40
Q

cons of early Tx

A
  • not prepared for Tx, poor adherence leads to resistance
  • cost
  • LT s/e
41
Q

factors to consider when starting Tx

A
  • CD4 count
  • viral load
  • pt’s likely adherence
  • discordant couples where 1 has high VL
  • transmission risk
  • pregnancy
  • pt’s wishes
  • co-morbidities (AIDS, HepB/C, TB, neuro involvement, CVD risk, IRIS risk)
42
Q

IRIS

A

immune reconstitution inflammatory syndrome

43
Q

What is IRIS?

A
  • starting ART, immune system recovers
  • get infection, immune system can over react, high inflammatory response
  • can be fatal
  • treat the infection first, then start HIV meds, don’t start at same time as ART
44
Q

patient factors to consider before starting Tx

A
  • renal, liver fxn
  • CV risk
  • pregnancy
  • drug Hx, oral contraceptives
  • pill burden
  • psychiatric, mental health
  • concurrent infections (HepC, TB)
  • Tx experienced or naive
  • adherance
  • pt choice
  • allergies
  • viral load
45
Q

2 types of ARV prophylaxis Tx?

A
  1. PEP - post exposure prophylaxis
  2. PrEP - preexposure prophylaxis
46
Q

post exposure prophylaxis - PEP

A

28 days Tx started within 72hrs after exposure

sexual, needle stick injury

47
Q

pre-exposure prophylaxis - PrEP

A

taken daily or PRN by HIV -ve person to prevent transmission

high risk, unprotected sex

48
Q

What drugs are used as the backbone drugs?

A

NRTI

  • tenofovir and emtricitabine
  • abacavir and lamivudine
49
Q

What are the NRTI backbone combined with?

A

protease inhibitors
OR
integrase inhibitors
OR
NNRTIs

rarely CCR5 inhibitors

50
Q

What are always used with protease inhibitors?

A

always boosted with either cobicistat OR ritonavir

  • CYP inhibitors
  • inhibit metabolism of protease inhibitors by liver
  • lower doses, give less frequently, less s/e
51
Q

How to NRTIs work?

A

block addition of nucleosides to DNA chain during transcription

terminate building of DNA chain

52
Q

pros and cons of Truvada (tenofovir disoproxil fumarate & emtricitabine)

A

pro - 1st line, good at reducing VL

cons - tenofovir associated with kidney disease (caution CKD stage 3), LT effects on bone density

  • dec CrCl (<60) –> avoid
  • Hx bone density problems, OP –> AVOID
53
Q

pros and cons of Descovy (tenofovir alafenamide & emtricitabine)

A

pros - equivalent to Truvada, benefit over Truvada if renal/bone disease

cons - very expensive, NEW

54
Q

pros and cons of Kivexa (abacavir & lamivudine)

A

pros - 2nd line, HLAB 5701 negative, no effect on BMD/renal fxn, only use if VL <100,000

cons - caution in CVD

55
Q

cautions when using Truvada (tenofovir + emtricitabine)

A

CKD stage 3

low BMD - OP

56
Q

cautions when using Kivexa (abacavir + lamividuine)

A

CVD

57
Q

Tenofovir salts

A

TDF = tenofovir disoproxil fumarate (Truvada)

TAF = temofovir alafenamide (Descovy)

58
Q

difference between TDF and TAF

A

both prodrugs

TDF activated in plasma

TAF activated intracellulary
- lower plasma concs
- fewer s/e (BMD, renal fxn)

59
Q

Abacavir problems

A
  1. allergy, fatal allergic rxn
    - CANNOT GIVE if +ve for HLA-B 5701 gene
  2. significant CVD risk
    - cautioned
  3. high viral load, >100,000
    - not as effective
60
Q

test before giving Abacavir

A

HLA-B 5701 gene

61
Q

formulation of Abacavir that CAN be used if high VL

A

Triumeq (if co-formulated with this)

62
Q

pros and cons of protease inhibitors

A

pros
- high barrier to resistance (good if not adherent)
- effective

cons
- a lot of interactions (enzyme inhibitors, CYP)
- cost (expensive)
- a LOT OF S/E (redistribution of body lipids)

63
Q

pros and cons of integrase inhibitors

A

pros
- few s/e
- few interactions (Ca, Mg supplements)
- rapid dec in VL, response rapid

cons
- cost
- low barrier to resistance

64
Q

pros and cons of NNRTIs

A

pros
- were 1st line
- effective
- few s/e

cons
- psychiatric problems
- c/i if Hx mental health problems
- rilpivirine only if VL<100,000
- interactions
- low barrier to resistance

65
Q

resons for Tx failure

A
  • resistance
  • poor adherence (s/e, forgetting, lifestyle)
  • drug interactions (Rx or OTC)
66
Q

How often is VL measured when established on Tx?

A

about every 6 months

67
Q

How often is VL measured when established on Tx?

A

about every 6 months

68
Q

When to do resistance testing for HIV drugs?

A
  • initiation
  • change
  • Tx failure
69
Q

What % adherence is needed?

A

> 95%

(only missing 1 dose per month)

70
Q

risks associated with poor adherence

A
  • risk of Tx failure
  • disease progression
  • transmission of resistant virus
  • inc healthcare costs
71
Q

What enzyme is used to convert HIV RNA to DNA?

A

reverse transcriptase

72
Q

How does resistance occur?

A
  • reverse transcriptase is prone to errors
  • 1 in 10,000 bases of viral RNA
  • leads to mutationos
  • can lead to resistance, inc sensitivtity or have no effect on the drug
73
Q

What is WT HIV?

A

HIV without any genetic mutations that have resistance to Tx

genetically superior

74
Q

resistance and VL

A

low VL, resistance less likely

high repliation - resistance more likely to produce mutations that are reisstance

75
Q

drugs that only require 1/small number of mutations to become resistant

A

NNRTIs
NRTIs
integrase inhibitors

76
Q

drugs that need multiple mutaitons for resistance to occur

A

protease inhibitors

-> better for patient who has bad ahderence

77
Q

2 reasons for taking HIV drugs with food

A
  1. to reduce se eg. ritonavir, zidovudine
  2. to inc absorption of lipid somuble drugs
78
Q

types of drug-drug interactions

A
  1. absorption
  2. transporter proteins (intesitinal & hepatic)
  3. metabolism
  4. renal clearance
79
Q

types of absorption interactions with HIV meds

A
  1. chelation
    - binding prevents absorption
    - integrase inhibitors + ions (Ca, Fe supplements)
  2. changes to gastric pH
    - reducing absorption
    - atazanavir + rilpivirine c/i with PPIs
80
Q

How can trnasporter proteins cause drug interactions?

A

drugs can inhibit or induce transporter proteins

intestinal, hepatic, BBB

81
Q

How can metabolism cause drug interactions?

A

inhibition OR induction of CYP450 or UGT enzymes

82
Q

drugs that effect CYP450

A

PI & NNRTIs

they’re substrates of CYP450, inducers and inhibitors

83
Q

example of drugs that casue renal inufficiency

A

PIs and tenofovir

PHAM02 (32 decks)

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