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Clinical 2.0 > HIV > Flashcards

HIV Flashcards

1
Q

what is HIV

A

chronic infection that results in the progressive destruction of CD4 and T lymphocytes

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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

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3
Q

what do CD4 cells do

A

direct and activate IR

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4
Q

how is the virus transmitted

A

contact with body fluids

blood semen, breast milk, not urine or feces

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5
Q

primary HIV symptoms

A 
fever, sore throat
weight loss, myalgia
morbilliform rash
lymphadenopathy, night sweats 
aseptic meningitis
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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

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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

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8
Q

methods of trasmission

A

sex
parenteral
perinatal or mother to child

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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
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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

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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

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12
Q

ways to decreased parenteral transmission

A 
free needle exchange 
not sharing injection paraphernalia 
sterilize equipment 
safe disposal 
use of post exposure prophylaxis
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13
Q

describe how the virus enters the cell and replicated

A
  1. binds to one of the receptors
  2. fuses with cell membrane
  3. uncoating of virus
  4. reverse transcription converts viral RNA to DNA
  5. viral integrasee splices viral DNA into cellular DNA
  6. cell uses the viral dna as template to reproduce the HIV genome
  7. cell uses HIV RNA as template to synthesize viral proteins
  8. protease enzyme cuts long protein chains into individual proteins
  9. new virus buds from cell and goes to infect other cells
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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

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15
Q

what are rthe 6 classes of antiretrovirals

A 
NRTIs
NNRTIs
protease inhibitors
integrase strand transfer inhibitors
fusion inhibitors
CCR5 receptor antagonist
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16
Q

NRTIs

A

abacavir
emtricitabine
lamivudine
tenofovir

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17
Q

NNRTIs

A

efavirenz
nevirapine
etravirine
rilpivirine

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18
Q

integrase inhibitors

A

raltegravir

dolutegravir

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19
Q

protease inhibitors

A

atazanavir
darunavir
lopinavir
ritonavir

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20
Q

CC5 receptor inhibitor

A

maraviroc

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21
Q

boosters

A

ritonavir

cobicistat

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22
Q

how many ARV are needed to be used in combo

A

3, booster doesnt count

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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

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24
Q

markers of disease progression

A

HIV RNA in the blood

CD4 T cell lymphocyte counts

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25
Q

do we delay ARV therapy

A

no

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26
Q

evaluation before initiation of HAART

A

physical
psychosocial
labs: CD4, viral load, hep A B C, toxoplasmosis, CBC, BUN< SCr, glucose, LFT, cholesterol, pap, STI
HIV drug resistance testing

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27
Q

whats the HLA B5701 test

A

for abacavir associated with hypersensitivity reaction which can be life threatening
identify patients at higher risk of hypersensitivity

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28
Q

what are the 3 types of regimens

A

2NRTIs and 1 NNRTI
2NRTIs and 1 PI
2 NRTIs and INSTI

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29
Q

what happens if patient gets low levels of the meds

A

virus mutates to become resistant and will always be present so can never use that med again

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30
Q

who shouldnt use atazanavir

A

people who requi >20mg omeprazole per day

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31
Q

who can use abacavir

A

people with HLA B5701 negative

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32
Q

advantages of INSTIs

A

NNRTI and PI options preserved for future use

less negative effects on lipids

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33
Q

advantages of protease inhibitors

A

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

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34
Q

disadvantages of protease inhibitors

A

GI adverse effects
greater potential for drug interaction, esp with ritonavir
metabolic complications - fat maldstribution, dyslipidemia

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35
Q

advantages of NNRTI

A

less fat maldistribution than PI based
long half life
PI and INSTI preserved for future use

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36
Q

NNRTI disadvantages

A

**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
Q

AE of NRTIs

A

lactic acidosis and hepatic steatosis and lipodystrophy rare more common in the older ones
headache, GI intolerance

38
Q

abacavir AE

A

hypersensitivity can be fatal

have to get negative test

39
Q

tenofovir AE

A

renal impairment

40
Q

emtricitabine and lamivudine (interchangeable) AE

A

hyperpigmentation in patients with dark complexion

41
Q

zidovudine AE

A

bone marrow suppression

42
Q

AE for all the ARV

A

nausea
diarrhea
headache

43
Q

raltegravir AE

A

insomnia
fatigue
CK elevation - rhabdo, myosistis
monitor

44
Q

PI AE

A

hyperlipidemia
insulin resistance and diabetes
lipodystrophy
elevated LFT

45
Q

AE of atazanavir

A

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
Q

darunavir AE

A

rash

food requirement

47
Q

ritonavir AE

A

GI intolerance
elevated liver enzymes
only used for boosting other PIs at 100-200mg/day

48
Q

AE if efavirenz

A

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
Q

nevirapine AE

A

hepatotoxocity - increased risk in women
greatest risk during first 6 weeks
rash

50
Q

nevirapine monitoring

A

transaminases at baseline, 2 weeks, 4 weeks, then monthly for 18 weeks
rash

51
Q

when would you use 2nd gen NNRTI etravirine

A

treatment experiences patients with resistance to otther classes including NNRTIs
activity against K103N mutation
less cns effects
ae: rash, nausea

52
Q

what does the use of CCR5 receptor antagonists require

A

tropism test
only effective if virus uses CCR5 exclusively to enter the cell
ae: cough, rash, URTI, fever

53
Q

which is the only injectable antiviral

A

enfuvirtide - fusion inhibitor

54
Q

when would you use a fusion inhibitor

A

treatement experienced patients with resistance to other classes

55
Q

enfuvirtide AE

A

local injection site reaciton

nodule, induration

56
Q

triumeq advantages (dolutegravir, abacavir, lamivudine)

A 
single tablet 
less negative lipid effects 
higher genetic resistance compared to other INSTI NNRTI
no pharmacoenhancer so less DI 
no food requirement
57
Q

triumeq disadvantages (dolutagravir, abacavir, lamivudine)

A

need b5701 test prior

if taken on empty stomach have to space apart from polyvalent cation containing products

58
Q

advantages of stribild and genvoya (elvitegravir, cobicistat, emtricitabine, tenofovir)

A

less negative lipid effects

59
Q

disadvantages of stribild and genvoya

A

DI with cobistat
food requirement
lower genetic barrier to drug resistance than PI

60
Q

difference between stribild and genvoya

A

pro drugs
disoproxil fumarate: cant start in crcl <70
alafenamide (genvoya): cant start in crcl <30

61
Q

darunavir (2NRTIs + booster) advantages

A

no evidence of PI resistance mutations with virologic failure when used as inital PI
HIGHEST GENETIC BARRIER TO DRUG RESISTANCE

62
Q

darunavir (2NRTIs and booster) disadvantages

A 
rash
negative lipid effects
pill burden 
food requirement 
DI with booster
GI intolerance
63
Q

advantages of 2 pill regimen (dolutegravir +tenofovir/emtricitabine)

A 
higher genetic drug resistance 
dont need HLA B5701 status 
no booster
no food requirement 
can crush
64
Q

disadvantages of 2 pill regimen (dolutegravir +tenofovir/emtricitabane)

A

2 pill regimen
drug interactions with divalent cations
increase serum levels of metformin

65
Q

what to do if there are interactions with cations

A

take 2 hr before or 6 hrs after

or take with food

66
Q

short term ADR toxicities

A 
NV 
diarrhea
headache
rash
CNS
67
Q

long term ADR toxicities

A 
bone marrow suppresion 
mitochondrial toxicity 
metabolic complications
nephrotoxicity 
hepatotoxicity
68
Q

NV management

A

take with food
take at bedtime
antiemetics: dimenhydrinate, ondansetron
antidiarrheals: loperamide

69
Q

what to do if patient develops hyperglycemia AE

A

diet and exercise
switch off PI based regimen
oral hypoglycemis
monitor BG and A1C

70
Q

rank the incidence of hyperlipidemia amoung the ARV

A

boosted PI > NNRTI > INSTI

71
Q

what should you not use for hyperlipidemia that is caused by ARV

A

avoid lovastatin and simvastain

72
Q

explain the desired DI of ritonavir and cobicistat

A

inhibitors of cyp 3A4 so boost the PI serum levels

gives higher trough levels allowing less frequent dosing

73
Q

what drug interactions result in subtherapeutic drug levels

A

antacids and atazanavir
boosted PI and statin
chelation with divalent cations and integrase inhibitors

74
Q

what DI may result in elevated levels leading to toxic AE

A

etravirine and warfarin - etravirine inhibits warfarin metabolism

75
Q

ritonavir and cobicistat interaction with steroids ***

A

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
Q

recommended steroid when on ritonavir or cobicistat

A

beclomethasone

77
Q

ritonavir and cobicistat interaction with statins

A

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
Q

when should you monitor HIV RNA and whats the goal

A

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
Q

other things to monitor while on HAART and how often

A 
CD4 t cell count 
CBC
electrolytes
liver function tests 
kidney function 
lipids
glucose tolerance 
baseline and every 3-4 months
80
Q

define virologic faulure

A

failure to achieve viral load <50 copies by 48 weeks or any return of the viral load to >50 copies

81
Q

can you drink alcohol on HARRT

A

yes

82
Q

preexposure prophylaxis

A

use antiretroviral med prior to exposure to HIV
tenofovir DF/emtricitabine oral daily
like birth control

83
Q

post exposure prophylaxis

A

use combo of 3 antiretrovirals after potential exposure
initiation within 72 hrs
28 day treatment
like plan b

84
Q

advantage and disavantage of raltegravir

A

adv: not metabolized through CYP
dis: BID, low genetic barrier

85
Q

adv and dis of dolutegravir

A

adv: once daily, highest genetic barrier of that class
dis: UGT substrate
oral absorption decreased with polyvalent cations

86
Q

adv and dis of elvitegravir

A

adv: once daily
dis: needs booster, low genetic barrier, only in STR

87
Q

management of high cholesterol and triglycerides

A

atorv 10 for 4 months then add fibrate if needed

monitor lipid at baseline, 3 months and then annually

88
Q

causes of virlogic failure

A

incomplete adherance
inadequate antoretroviral potency
development of drug resistance
failure of drugs to reach target site

89
Q

ways to enhance adherance

A 
treat depression or substance abuse
social support
educate
involve patient in selction 
simplify regimen 
offer adherance aids

Clinical 2.0 (24 decks)

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