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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
When to stop prophylactic Tx if CD4 <200?
when CD4 >200 for > 3 months
26
MAC
mycobacterium avium complex
27
Sx of MAC
fever night sweats fatigue weight loss anorexia diarrhoea
28
Tx of MAC
macrolides + ethambutol
29
prophylactic Tx for MAC
azithromycin 1250mg WEEKLY
30
Mycobacterial TB Tx
pyrazinamide rifampicin ethambutol isoniazid
31
What has inc risk with mycobacterium TB?
risk of IRIS
32
malignancies at inc risk with HIV
- systemic NHL - primary cerebral - lymphoma - Kaposi's sarcoma - cervical cancer
33
enzymes in HIV virus not found in humans
reverse transcriptase integrase protease
34
4 types of HIV drugs
1. CCR5 inhibitors 2. nucleoside/nucleotide RT inhibitors &non-nucleoside RTIs 3. integrase inhibitors 4. protease inhibitors
35
goals of HIV Tx
- etended life expectancy and QOL - preserve and restore CD4 cell count - viral load undetectable within 4-6mths (<20 copies/ml) - prevent transmission
36
when to start Tx (4)
1. primary infection 2. chronic infection 3. presents ith AIDS or major infection 4. prevention of transmission
37
When to start Tx in primary infection?
only when patient ready, uness: - neurological involvelemt - any AIDS defining illness - CD4 persistently <350 cells/ul - diagnosis within 12 weeks of previous negative
38
When to start Tx if patient presents with AIDS/major infection?
start within 2 weeks of antimicrobials if - AIDS defining infection - serious bacterial infection with CD4 count <200 cells/ul
39
pros of early Tx
- inc immunological recovery - reduced transmission - reduced disease progression/morbidity - reassurance to pt
40
cons of early Tx
- not prepared for Tx, poor adherence leads to resistance - cost - LT s/e
41
factors to consider when starting Tx
- 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
IRIS
immune reconstitution inflammatory syndrome
43
What is IRIS?
- 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
patient factors to consider before starting Tx
- 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
2 types of ARV prophylaxis Tx?
1. PEP - post exposure prophylaxis 2. PrEP - preexposure prophylaxis
46
post exposure prophylaxis - PEP
28 days Tx started within 72hrs after exposure sexual, needle stick injury
47
pre-exposure prophylaxis - PrEP
taken daily or PRN by HIV -ve person to prevent transmission high risk, unprotected sex
48
What drugs are used as the backbone drugs?
NRTI - tenofovir and emtricitabine - abacavir and lamivudine
49
What are the NRTI backbone combined with?
protease inhibitors OR integrase inhibitors OR NNRTIs rarely CCR5 inhibitors
50
What are always used with protease inhibitors?
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
How to NRTIs work?
block addition of nucleosides to DNA chain during transcription terminate building of DNA chain
52
pros and cons of Truvada (tenofovir disoproxil fumarate & emtricitabine)
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
pros and cons of Descovy (tenofovir alafenamide & emtricitabine)
pros - equivalent to Truvada, benefit over Truvada if renal/bone disease cons - very expensive, NEW
54
pros and cons of Kivexa (abacavir & lamivudine)
pros - 2nd line, HLAB 5701 negative, no effect on BMD/renal fxn, only use if VL <100,000 cons - caution in CVD
55
cautions when using Truvada (tenofovir + emtricitabine)
CKD stage 3 low BMD - OP
56
cautions when using Kivexa (abacavir + lamividuine)
CVD
57
Tenofovir salts
TDF = tenofovir disoproxil fumarate (Truvada) TAF = temofovir alafenamide (Descovy)
58
difference between TDF and TAF
both prodrugs TDF activated in plasma TAF activated intracellulary - lower plasma concs - fewer s/e (BMD, renal fxn)
59
Abacavir problems
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
test before giving Abacavir
HLA-B 5701 gene
61
formulation of Abacavir that CAN be used if high VL
Triumeq (if co-formulated with this)
62
pros and cons of protease inhibitors
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
pros and cons of integrase inhibitors
pros - few s/e - few interactions (Ca, Mg supplements) - rapid dec in VL, response rapid cons - cost - low barrier to resistance
64
pros and cons of NNRTIs
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
resons for Tx failure
- resistance - poor adherence (s/e, forgetting, lifestyle) - drug interactions (Rx or OTC)
66
How often is VL measured when established on Tx?
about every 6 months
67
How often is VL measured when established on Tx?
about every 6 months
68
When to do resistance testing for HIV drugs?
* initiation * change * Tx failure
69
What % adherence is needed?
>95% (only missing 1 dose per month)
70
risks associated with poor adherence
- risk of Tx failure - disease progression - transmission of resistant virus - inc healthcare costs
71
What enzyme is used to convert HIV RNA to DNA?
reverse transcriptase
72
How does resistance occur?
- 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
What is WT HIV?
HIV without any genetic mutations that have resistance to Tx genetically superior
74
resistance and VL
low VL, resistance less likely high repliation - resistance more likely to produce mutations that are reisstance
75
drugs that only require 1/small number of mutations to become resistant
NNRTIs NRTIs integrase inhibitors
76
drugs that need multiple mutaitons for resistance to occur
protease inhibitors -> better for patient who has bad ahderence
77
2 reasons for taking HIV drugs with food
1. to reduce se eg. ritonavir, zidovudine 2. to inc absorption of lipid somuble drugs
78
types of drug-drug interactions
1. absorption 2. transporter proteins (intesitinal & hepatic) 3. metabolism 4. renal clearance
79
types of absorption interactions with HIV meds
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
How can trnasporter proteins cause drug interactions?
drugs can inhibit or induce transporter proteins intestinal, hepatic, BBB
81
How can metabolism cause drug interactions?
inhibition OR induction of CYP450 or UGT enzymes
82
drugs that effect CYP450
PI & NNRTIs they're substrates of CYP450, inducers and inhibitors
83
example of drugs that casue renal inufficiency
PIs and tenofovir

PHAM02 (32 decks)

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