HIV Flashcards
(89 cards)
1
Q
what is HIV
A
chronic infection that results in the progressive destruction of CD4 and T lymphocytes
2
Q
what is AIDS
A
HIV positive and has a CD4 cell count below 200 or
CD4 cells account for fewer than 14% of all lymphocytes or
has been diagnosed with one or more of the aids defining illnesses
3
Q
what do CD4 cells do
A
direct and activate IR
4
Q
how is the virus transmitted
A
contact with body fluids
blood semen, breast milk, not urine or feces
5
Q
primary HIV symptoms
A
fever, sore throat weight loss, myalgia morbilliform rash lymphadenopathy, night sweats aseptic meningitis
6
Q
what is seroconversion, when does it happen
A
development of HIV antibody
convert within 6 months so may not test positve right away
7
Q
explain the stages of hiv infection
A
chronic asymptomatic - viral replication controlled by IR
chronic symptomatic infection - start getting infections to body would fight off
AIDS
advanced HIV infection - CD4 below 50
8
Q
methods of trasmission
A
sex
parenteral
perinatal or mother to child
9
Q
factors that increase the risk of transmission
A
increased viral load vaginal bleeding during intercourse being the reciever genital ulcers STIs lack of circumcision genetic
10
Q
what should someone with HIV who is breast feeding do
A
virus transmited in milk
resource rich countries with safe water exclusively formula
in resource poor may be appropriate to exclusively breastfeed
11
Q
all lwomen screened for HIV during pregnancy what do you do if positive
A
treat with antiretroviral during pregnancy, may delay until after 1st trimester
antiretroviral treatment during labour and delivery and to baby post delivery
IV zidovudine for mother during delivery
oral zidovudine for baby first 6 weeks
if viral load >1000 may require csection
12
Q
ways to decreased parenteral transmission
A
free needle exchange not sharing injection paraphernalia sterilize equipment safe disposal use of post exposure prophylaxis
13
Q
describe how the virus enters the cell and replicated
A
- binds to one of the receptors
- fuses with cell membrane
- uncoating of virus
- reverse transcription converts viral RNA to DNA
- viral integrasee splices viral DNA into cellular DNA
- cell uses the viral dna as template to reproduce the HIV genome
- cell uses HIV RNA as template to synthesize viral proteins
- protease enzyme cuts long protein chains into individual proteins
- new virus buds from cell and goes to infect other cells
14
Q
do antiretrovirals kill the virus
A
no prevents infectious virus from being made if taken daily and able to achieve and maintain therapeutic blood levels
15
Q
what are rthe 6 classes of antiretrovirals
A
NRTIs NNRTIs protease inhibitors integrase strand transfer inhibitors fusion inhibitors CCR5 receptor antagonist
16
Q
NRTIs
A
abacavir
emtricitabine
lamivudine
tenofovir
17
Q
NNRTIs
A
efavirenz
nevirapine
etravirine
rilpivirine
18
Q
integrase inhibitors
A
raltegravir
dolutegravir
19
Q
protease inhibitors
A
atazanavir
darunavir
lopinavir
ritonavir
20
Q
CC5 receptor inhibitor
A
maraviroc
21
Q
boosters
A
ritonavir
cobicistat
22
Q
how many ARV are needed to be used in combo
A
3, booster doesnt count
23
Q
goals of therapy
A
reduce the HIV associated morbidity and prolong the duration and quality of survival
restore and preserve immunologic function
maximally suppress plasma HIV viral load
prevent HIV transmission
24
Q
markers of disease progression
A
HIV RNA in the blood
CD4 T cell lymphocyte counts
25
do we delay ARV therapy
no
26
evaluation before initiation of HAART
physical
psychosocial
labs: CD4, viral load, hep A B C, toxoplasmosis, CBC, BUN< SCr, glucose, LFT, cholesterol, pap, STI
HIV drug resistance testing
27
whats the HLA B5701 test
for abacavir associated with hypersensitivity reaction which can be life threatening
identify patients at higher risk of hypersensitivity
28
what are the 3 types of regimens
2NRTIs and 1 NNRTI
2NRTIs and 1 PI
2 NRTIs and INSTI
29
what happens if patient gets low levels of the meds
virus mutates to become resistant and will always be present so can never use that med again
30
who shouldnt use atazanavir
people who requi >20mg omeprazole per day
31
who can use abacavir
people with HLA B5701 negative
32
advantages of INSTIs
NNRTI and PI options preserved for future use
| less negative effects on lipids
33
advantages of protease inhibitors
higher genetic barrier for resistance - multiple mutations to confer resistance
PI resistance uncommone with failure - give if think they wont remember to take their meds
34
disadvantages of protease inhibitors
GI adverse effects
greater potential for drug interaction, esp with ritonavir
metabolic complications - fat maldstribution, dyslipidemia
35
advantages of NNRTI
less fat maldistribution than PI based
long half life
PI and INSTI preserved for future use
36
NNRTI disadvantages
**low genetic barrier - single mutation can cause resistance
skin rash
hepatotoxicity
CNS effects
cyp DI
**transmitted resistance to NNRTIs more common than resistance to PI
37
AE of NRTIs
lactic acidosis and hepatic steatosis and lipodystrophy rare more common in the older ones
headache, GI intolerance
38
abacavir AE
hypersensitivity can be fatal
| have to get negative test
39
tenofovir AE
renal impairment
40
emtricitabine and lamivudine (interchangeable) AE
hyperpigmentation in patients with dark complexion
41
zidovudine AE
bone marrow suppression
42
AE for all the ARV
nausea
diarrhea
headache
43
raltegravir AE
insomnia
fatigue
CK elevation - rhabdo, myosistis
monitor
44
PI AE
hyperlipidemia
insulin resistance and diabetes
lipodystrophy
elevated LFT
45
AE of atazanavir
hyperbilirubinemia
all patients will get elevated bilirubin if they dont they arent taking their meds
if see yellowing of the skin levels too high
46
darunavir AE
rash
| food requirement
47
ritonavir AE
GI intolerance
elevated liver enzymes
only used for boosting other PIs at 100-200mg/day
48
AE if efavirenz
CNS - nightmares, depression, impaired concentration...
occurs within 6 weeks
usually get better over time
cna give at bedtime or on an empty stomach
teratogenic - dont start if planing on becoming pregnant
49
nevirapine AE
hepatotoxocity - increased risk in women
greatest risk during first 6 weeks
rash
50
nevirapine monitoring
transaminases at baseline, 2 weeks, 4 weeks, then monthly for 18 weeks
rash
51
when would you use 2nd gen NNRTI etravirine
treatment experiences patients with resistance to otther classes including NNRTIs
activity against K103N mutation
less cns effects
ae: rash, nausea
52
what does the use of CCR5 receptor antagonists require
tropism test
only effective if virus uses CCR5 exclusively to enter the cell
ae: cough, rash, URTI, fever
53
which is the only injectable antiviral
enfuvirtide - fusion inhibitor
54
when would you use a fusion inhibitor
treatement experienced patients with resistance to other classes
55
enfuvirtide AE
local injection site reaciton
| nodule, induration
56
triumeq advantages (dolutegravir, abacavir, lamivudine)
```
single tablet
less negative lipid effects
higher genetic resistance compared to other INSTI NNRTI
no pharmacoenhancer so less DI
no food requirement
```
57
triumeq disadvantages (dolutagravir, abacavir, lamivudine)
need b5701 test prior
| if taken on empty stomach have to space apart from polyvalent cation containing products
58
advantages of stribild and genvoya (elvitegravir, cobicistat, emtricitabine, tenofovir)
less negative lipid effects
59
disadvantages of stribild and genvoya
DI with cobistat
food requirement
lower genetic barrier to drug resistance than PI
60
difference between stribild and genvoya
pro drugs
disoproxil fumarate: cant start in crcl <70
alafenamide (genvoya): cant start in crcl <30
61
darunavir (2NRTIs + booster) advantages
no evidence of PI resistance mutations with virologic failure when used as inital PI
HIGHEST GENETIC BARRIER TO DRUG RESISTANCE
62
darunavir (2NRTIs and booster) disadvantages
```
rash
negative lipid effects
pill burden
food requirement
DI with booster
GI intolerance
```
63
advantages of 2 pill regimen (dolutegravir +tenofovir/emtricitabine)
```
higher genetic drug resistance
dont need HLA B5701 status
no booster
no food requirement
can crush
```
64
disadvantages of 2 pill regimen (dolutegravir +tenofovir/emtricitabane)
2 pill regimen
drug interactions with divalent cations
increase serum levels of metformin
65
what to do if there are interactions with cations
take 2 hr before or 6 hrs after
| or take with food
66
short term ADR toxicities
```
NV
diarrhea
headache
rash
CNS
```
67
long term ADR toxicities
```
bone marrow suppresion
mitochondrial toxicity
metabolic complications
nephrotoxicity
hepatotoxicity
```
68
NV management
take with food
take at bedtime
antiemetics: dimenhydrinate, ondansetron
antidiarrheals: loperamide
69
what to do if patient develops hyperglycemia AE
diet and exercise
switch off PI based regimen
oral hypoglycemis
monitor BG and A1C
70
rank the incidence of hyperlipidemia amoung the ARV
boosted PI > NNRTI > INSTI
71
what should you not use for hyperlipidemia that is caused by ARV
avoid lovastatin and simvastain
72
explain the desired DI of ritonavir and cobicistat
inhibitors of cyp 3A4 so boost the PI serum levels
| gives higher trough levels allowing less frequent dosing
73
what drug interactions result in subtherapeutic drug levels
antacids and atazanavir
boosted PI and statin
chelation with divalent cations and integrase inhibitors
74
what DI may result in elevated levels leading to toxic AE
etravirine and warfarin - etravirine inhibits warfarin metabolism
75
ritonavir and cobicistat interaction with steroids ***
fluticasone is extensively metabolized by cyp 3A4
increase in fluticasone plasma concentration and decrease plasma cortisol concentration
can result in corticosteroid excess (cushing syndrome, and adrenal insufficiency)
DO NOT WITHHOLD FOR TREATMENT OF ACUTE DISEASE
76
recommended steroid when on ritonavir or cobicistat
beclomethasone
77
ritonavir and cobicistat interaction with statins
statins metabolized by cyp 3a4
increase in plasma concentrations of atorvastatin and increase risk of rhabdomyolysis and myopathy
use lowest dose possible and monitor for signs and symptoms
78
when should you monitor HIV RNA and whats the goal
baseline then 2-8 weeks after treatment initiation or change in therapy
repeat every 3-4 months
goal to maintain viral load below limits of assay
79
other things to monitor while on HAART and how often
```
CD4 t cell count
CBC
electrolytes
liver function tests
kidney function
lipids
glucose tolerance
baseline and every 3-4 months
```
80
define virologic faulure
failure to achieve viral load <50 copies by 48 weeks or any return of the viral load to >50 copies
81
can you drink alcohol on HARRT
yes
82
preexposure prophylaxis
use antiretroviral med prior to exposure to HIV
tenofovir DF/emtricitabine oral daily
like birth control
83
post exposure prophylaxis
use combo of 3 antiretrovirals after potential exposure
initiation within 72 hrs
28 day treatment
like plan b
84
advantage and disavantage of raltegravir
adv: not metabolized through CYP
dis: BID, low genetic barrier
85
adv and dis of dolutegravir
adv: once daily, highest genetic barrier of that class
dis: UGT substrate
oral absorption decreased with polyvalent cations
86
adv and dis of elvitegravir
adv: once daily
dis: needs booster, low genetic barrier, only in STR
87
management of high cholesterol and triglycerides
atorv 10 for 4 months then add fibrate if needed
| monitor lipid at baseline, 3 months and then annually
88
causes of virlogic failure
incomplete adherance
inadequate antoretroviral potency
development of drug resistance
failure of drugs to reach target site
89
ways to enhance adherance
```
treat depression or substance abuse
social support
educate
involve patient in selction
simplify regimen
offer adherance aids
```
