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Flashcards in ANTIRETROVIRAL DRUGS Deck (50):
1

HIV TRANSMISSION

DIAGNOSIS

Contact with body fluids (blood, semen, vaginal secretions, breast milk etc)

• From mother to child transplacentally or perinatally in 30-50% cases

• Transmission by saliva or droplets produced by coughing or sneezing is extremely unlikely

HIV DIAGNOSIS: 

• Antibody or antigen testing (usually within few weeks of infections)
• ELISA / Western Blot

New rapid tests (< 30 min) on blood & saliva available (usually confirmed by standard blood tests)

 

2

HIV TREATMENT

WHEN TO START? 

WHAT CONDITIONS STRONGLY RECOMMEND STARTING?

Therapy is usually initiated when CD4+ cells ≤500 cellsmm3

 

Regardless of CD4 count, initiation of therapy is strongly recommended for individuals with the following conditions:

• 1) Pregnancy

• 2) History of an AIDS-defining illness
• 3) HIV-associated nephropathy (HIVAN)
• 4) HIV/hepatitis B virus (HBV) co-infection

3

HIV PRIMARY TREATMENT GOALS: 

 

Primary treatment goals:

• reduce HIV-related morbidity and prolong survival,

• improve quality of life,
• restore and preserve immunologic function,
• maximally and durably suppress viral load, and

• prevent vertical HIV transmission

4

CURRENT HIV TREATMENTS 

(DRUG CLASSES and examples) 

 

1) Nucleoside/-tide Reverse Transcriptase Inhibitors (NRTIs)

  • Abacavir, Didanosine, Emtricitabine, Lamivudine, Stavudine,Tenofovir, Zidovudine

2) Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)

  • Delavirdine, Efavirenz, Etravirine, Nevirapine

3) Protease Inhibitors

  • Atazanavir, Darunavir, Indinavir, Lopinavir, Nelfinavir, Ritonavir, Tipranavir

4) Entry Inhibitors

  • Enfuvirtide, Maraviroc

5) Integrase Inhibitor

Raltegravir

5

COMBINATOIN THERAPY/HAART

Current studies suggest a prevalence of HIV drug resistance of 6%–16% in antiretroviral treatment-naïve patients.

HAART (Highly Active Antiretroviral Therapy) / combination therapy was initiated in 1996

6

NUCLEOSIDE/TIDE REVERSE TRANSCRIPTASE INHIBITORS (NRTI'S) 

MOA

MOA

• Analogs of native ribosides (lack 3’OH)

• Phosphorylated by cellular enzymes and incorporated into viral DNA by reverse transcriptase

Lack of 3’OH terminates DNA elongation
--> ie. they are competitive inhibitors of reverse

transcriptase***
• Most have activity against BOTH HIV-2 as well as HIV-1

7

NUCLEOSIDE/TIDE REVERSE TRANSCRIPTASE INHIBITORS (NRTI'S) 

RESISTANCE

PK

AE

RESISTANCE:

• Emerges rapidly if used alone
• Most common mutation at viral codon 184: lamivudine

(restores sensitivity to zidovudine & tenofovir)
• Cross-resistance between agents of same analog class

can occur

PK: dosage adjustements required with RENAL INSUFFICIENCY

AE: 

• If more than one NRTI given toxicities may overlap

• AE mainly due to inhibition of ****mitochondrial DNA polymerase: peripheral neuropathy, myopathy, lipoatrophy (localized loss of fat tissue) & lactic acidosis******

• Pancreatitis, myelosuppression & cardiomyopathy can also occur

Liver toxicity is rare but fatal (lactic acidosis, hepatomegaly with steatosis).

• Zidovudine & stavudine may be particularly associated with dyslipidemia & insulin resistance

8

NRTI'S

DRUG INTERACTIONS

T, increases D (Titties increase Dick), when coadministered 

---> therefore must decrease D dose (don't let as many dicks in the bar) 

• Didanosine & tenofovir

  • Tenofovir increases plasma didanosine levels ~60%.
  • Doses of didanosine have to be reduced.

NRTIs are not generally metabolized by cytochrome enzymes

9

ZIDOVUDINE

NRTI

ZIDOVUDINE --> causes BONE MARROW SUPPRESSION --> causes bone marrow to "ZZZZZZZ"

-is a nucleoSIDE analog

PK: oral, penetrates the BBB well

--> dosage adjustement required in patients with CIRRHOSIS

AE: 

  • ***BONE MARROW SUPPRESSION*** (neutropenia, anemia)
  • GI INTOLERANCE, headaches, insomnia

CONTRAINDICATIONS: 

• Toxicity potentiated by coadmin. of probenecid, acetaminophen, lorazepam, indomethacin & cimetidine.

• Stavudine & ribavirin activated by same pathways (might reduce active levels of zidovudine)

10

STAVUDINE

 

NRTI

STAVUDINE --> STAB U DINING --> stabs both the Boy (beta) and Girl (gamma) DNA (dinner) polymerases 

Strong inhibitor of beta and gamma DNA polymerases (high affinity for mitochondrial DNA polymerase, which can lead to toxicity) --> can cause PERIPHERAL NEUROPATHY (b/c just got stabbed, as well as MUSCLE BREAKDOWN --> therefore LACTIC ACIDOSIS 

Nucleoside Analog = Thymidine

Pharmacokinetics

• Oral
• Dosage adjustment required in renal insufficiency

AE: PERIPHERAL NEUROAPTHY, LACTIC ACIDOSIS

--> HYPERLIPIDEMIA, NEUROMUSCULAR WEAKNESS

11

DIDANOSINE 

NRTI

DIDANOSINE = DI DAN SIGN --> smart drug because take in FASTING state (acid labile) and combined with an ANTACID --> but DAN PAN DAN --> look out for PANCREATITIS --> don't give it to somebody who already has pancreas problems!!!!!! 

NucleoSIDE Analog --> Adenosine

Pharmacokinetics

• Absorption best if taken in fasting state (ACID LABILE) or

combined with antacid

• Penetrates into CSF
• Dosage adjustment required in renal insufficiency

Adverse Effects

High affinity for mitochondrial DNA polymerase

Pancreatitis*** (esp. alcoholics and patients with hypertriglyceridemia)

• Peripheral neuropathy, diarrhea, hepatic dysfunction

• CNS effects

NOTE IF PATIENT ALREADY HAS PANCREAS PROBLEMS, THIS DRUG IS CONTRAINDICATED!!! 

12

TENOFOVIR

NRTI

TENOFOVIR --> is 10/10 --> IS THE PREFERRED NRTI IN CURRENT REGIMENS!! 

--> Remember TEN TITTIES --> raises DICKS (didanosine) 

**One of preferred NRTIs in currently recommended regimens**

Nucleotide Analog --> Adenosine

Fixed-Dose Combinations Available

• Tenofovir + emtricitabine
• Tenofovir + emtricitabine + efavirenz

Pharmacokinetics

• Should be taken with food to increase bioavailability***

• Long t1/2 (can dose once daily)

Adverse Effects

• GI (nausea, diarrhea, vomiting, flatulence)

13

TENOFOVIR 

CONTRAINDICATIONS

NRTI

REMEMBER: TENOFOVIR (Ten TITTIES) raises DICKS, but it DECREASES AT AZZZZ

• Serum creatinine monitored with renal insufficiency

Only NRTI with sig. drug interactions

  • 1) increases DIDANOSINE concentrations and dosage reductions are usually required****
  • 2) Decreases concentrations of atazanavir.
    • Atazanavir can be ‘boosted’ with ritonavir

14

LAMIVUDINE

LAMIVUDINE --> LAME DINING --> does NOT have many AE, does not affect mitochondrial DNA synthesis, or bone marrow precursor cells 

 

****DOES NOT affect mitochondrial DNA synthesis or bone marrow precursor cells****

Nucleoside Analog --> Cytosine

Resistance

• High level resistance occurs with single amino acid substitutions

Pharmacokinetics

• Dosage adjustment required with renal insufficiency

Adverse effects (very few!!!) 

• Few significant (headache, dry mouth)

15

EMTRICITABINE

NRTI

EMTRICITABINE --> Where's Seattle from? "Emmm.. Tricity? obivously.. EM-TRICITY --> SEATTLE --> HYPERPIGMENTATION  of PALMS + SOLES b/c WALKING (soles) to their local starbucks and holding onto the coffee (palms) --> is one of the preferred NRTIs in currently recommended regimens 

Structural relative of lamivudine

One of preferred NRTIs in currently recommended regimens

Nucleoside Analog --> Cytosine

Pharmacokinetics

Once-a-day administration

AE: ***HYPERPIGMENTATION OF PALMS + SOLES*** (occurs most frequently in dark-skinned people) 

16

ABACAVIR

 

NRTI

ABACAVIR --> think of ABACADABRA!!! --> POOF all of a sudden get a quick hypersensitivity reaciton --> sensitized inidivuals should never be rechallenged 

--> is a GUANISINE ANOLOG (guanisine for GENIE) 

Nucleotide Analog --> Guanosine

Resistance

• HIV resistance requires several mutations and tends to develop slowly.

Adverse Effects

• GI, headache, dizziness

• 5% - ***‘hypersensitivity’ reaction**** (one or more of rash, GI, malaise, respiratory distress).

Sensitized individuals should NEVER be rechallenged (can be genetically screened)

17

NNRTIs

MOA

NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS

MOA (only works on HIV-1, NOT on HIV-2) 

Highly selective, noncompetitive inhibitors of HIV-1 RT

• Bind at a distinct site away from active site (NNRTI pocket)

• All NNRTI’s bind within the same pocket

• All result in inhibition of RNA- and DNA-dependent DNA polymerase

DO NOT REQUIRE PHOSPHORYLATION BY CELLULAR ENZYMES

• Lack in vitro activity against HIV-2

18

NNRTIs

Advantages + Disadvantages

AEs

Advantages

• Lack of effect on host blood-forming elements

• Lack of cross resistance with NRTIs (binding sites are distinct)

Disadvantages

Cross-resistance with NNRTIs (ie with itself) 

• Drug interactions

High incidence of hypersensitivity reactions (eg, rash)

AE: 

• 1) *****Skin rash (including Stevens-Johnson syndrome)*****

• GI intolerance

All are CYP3A4 substrates and can act as inducers, inhibitors or both of CYPs

19

NEVIRAPINE

PK + AE 

NEVER A PINE --> is an NNRTI --> can never cut down a pine right away --> need 14 day titration period to get sapp out, at half dose? --> if not syrup can be sour and can cuase potential severe HEPATOTOXICITY + RASH (from pine needles) 

Pharmacokinetics

• Excreted mainly in urine as metabolites (CYP 3A4 & CYP 2B6)

Adverse Effects

Potential severe hepatotoxicity (don’t use in women with CD4+ counts >250 cells/mm3 & men >400 cells/mm3)

Rash (16%), dermatologic effects (Stevens-Johnson syndrome & toxic epidermal necrolysis)

14 day titration period at 1⁄2 dose is mandatory to reduce risk of serious epidermal reactions

20

NEVIRAPINE 

 

CONTRAINDICATIONS 

 

RESISTANCE 

NEVER-A-PINE --> contraindicated in most popular places = CYP3A4 --> it INDUCES A RIOT b/c people want those trees to still stand --> INDUCES THE METABOLISM OF PROTEASE INHIBS 

Contraindications

Inducer of CYP 3A4

• Increases metabolism of PI’s (no dosage adjustment necessary), oral contraceptives, ketoconazole, methadone, metronidazole, quinidine, theophylline & warfarin

Resistance

• Target site of nevirapine is HIV-1 specific & not essential to enzyme (reverse transcriptase), thus mutations and resistance can develop rapidly

21

DELAVIRDINE

 

CLINICAL APPLICATIONS

 

PHARMACOKINETICS

 

AEs

DEL-A-VIRDINE --> DELL --> think of DELL COMPUTERS --> not used as much anymore because they have short half lives --> RASH = #1 ADVERSE EFFECT, IF ASK RASH IT WILL BE ABOUT DELL COMPUTERS --> because people putting them togetehr exposed to so many chemicals --> is also TERATOGENIC (contraindicated in pregnancy) 

Clinical Applications

Not as widely used as other NNRTIs due to short t1/2

 

Pharmacokinetics

• Well absorbed orally (especially at pH <2; antacids, H2

blockers etc may decrease absorption)

• Excreted mainly in urine as metabolites (CYP 3A4 & 2D6)

• Non-linear PK (t1/2 increases with increasing doses)

Adverse Effects

Rash (18-36%), ****Stevens-Johnson syndrome & toxic epidermal necrolysis

• Fever, headache & depression also common

Teratogenic

 

22

DELAVIRDINE

DELL COMPUTERS --> won't let you do ANYTHING --> is an INHIBITOR 

Contraindications

Inhibitor of and substrate of CYP3A4
• CYP 3A4 inducers (eg, rifampin, phenytoin) may decrease

delavirdine concentrations

• Pregnancy (Cat C)

Resistance

• Target site of delavirdine is HIV-1 specific & not essential to enzyme (reverse transcriptase) therefore resistance develops rapidly

23

ETRAVIRINE

clinical applications

PK

ETRAVIRINE --> see the E think EXPERIENCED PATIENTS

Clinical Applications

Approved for use in treatment-experienced patients

• May be effective against HIV strains resistant to first-generation NNRTIs

Pharmacokinetics

Metabolized by CYP 3A4, 2C9 and 2C19
• Metabolites have ~10% HIV activity of parent compound

24

ETRAVIRINE

 

ADVERSE EFFECTS

 

CONTRAINDICATIONS 

ETRAVIRINE --> think EXPERIENCED PATIENTS and also think ENZYME ELEVATION --> TRANSAMINASE ELEVATIONS!!!

Adverse Effects

Rash (normally resolves within 1-2 weeks), nausea, diarrhea

Transaminase elevations (esp. in patients co-infected with hepatitis)

Contraindications

CYP 3A4 inducer
CYP 2C9 and 2C19 inhibitor
• Some interactions are difficult to predict

25

EFAVIRENZ (not ETRAVINE)

CLINICAL APPLICATIONS

PHARMACOKINETICS

• ********Preferred NNRTI on DHHS guidelines*********** EFAVIRENZ DOES ERRRYTHINGGGGG B/C DRUG GOES ALL THE WAY TO THE END OF THE ALPHABET (Z)
• Results in increased CD4+ counts & decreased viral load

 

Pharmacokinetics

• Oral
• t1/2 >40h (once-a-day dosing)*****
• Extensively metabolized to inactive products

26

ETRAVIRENZ

AE

Contraindications

EFAVIRENZ --> it ZZZZZZZ'S --> dizziness, vivid DREAMZZZZZZ

DON'T GIVE TO PZYCHHOOOOOSSSS

Adverse Effects

• 1) Mostly CNS (50%) (dizziness, headache, vivid dreams, loss of concentration) – resolve after few weeks.

• 2) Rash (25%)

• 3) Increased triglycerides, HDL and total cholesterol (lipid levels must be monitored at beginning of and during therapy)

Contraindications

Potent inducer of CYP P450 enzymes.

Pregnancy (D) (can be used after 1st trimester if considered best choice)

27

PROTEASE INHIBITORS

MOA: 

Reversible inhibitors of HIV aspartyl protease (enzyme responsible for cleavage of viral polyprotein into RT, protease & integrase)

• Protease inhibition prevents virus maturation & results in production of non-infectious virions

DO NOT REQUIRE INTRACELLULAR ACTIVATION

• Active against both HIV-1 and HIV-2

28

PROTEASE INHIBITORS

PK

Pharmacokinetics

• Poor oral bioavailability

• High-fat meals can increase (nelfinavir) or decrease (indinavir) bioavailability

Substrates for CYP 3A4

Substrates for P-glycoprotein pump

• Bound to plasma proteins (a1-acid glycoprotein which can increase in response to trauma & surgery)

29

PROTEASE INHIBITORS

AE

PROTEASE INHIBS ---> MAKE YOU A PORKER!!!! ---> FUCKS WITH LIPID METABOLISM --> FAT REDISTRIBUTION + ACCUMULATION 

Adverse Effects

Parathesias, nausea, vomiting, diarrhea
Disturbances in lipid metabolism (diabetes, hypertriglyceridemia, hypercholesterolemia)

• Chronic admin -->  *****fat redistribution & accumulation***** resulting in central obesity, dorsocervical fat enlargement, peripheral & facial wasting, breast enlargement and a cushingoid appearance

Atazanavir has less side effects than other PI’s

A image thumb
30

PROTEASE INHIBITORS

DRUG INTERACTIONS 

• Potent inhibitors and substrates of CYP isoforms

eg, rhabdomyolysis (simvastatin or lovastatin),

excessive sedation (midazolam or triazolam),

respiratory depression (fentanyl)

• Warfarin, sildenafil & phenytoin require dosage adjustments

Rifampin & St.Johns Wort are contraindicated

RESISTANCE

• Accumulation of stepwise mutations of protease gene. Can lead to high levels of resistance.

31

RITONAVIR

 

PROTEASE INHIBITOR

RITONAVIR --> RIT --> RAMPS UP IE ENHANCER/BOOSTER OF OTHER PI'S d/t INHIBITION OF CYP3A4

CLINICAL APPLICATION: 

-- enhancer/booster of other PIs

-potent INHIBITOR of CYP3A4 

CONTRINDICATIONS:

-numerous d/t inhibition of CYP 

32

ATAZANAVIR

ATAZANAVIR --> ATAZMANIAN DEVIL --> can't give with PPI's b/c it inhibits them (give 12 hours apart from PPIs) --> thrives in the acidic environment (that tazmanian devil) --> go home and watch 1 CARTOON A DAY --> IS THE PREFERRED CARTOON TO WATCH, is the ONCE-DAILY PREFERED PI

--> is structurally unrealted to  the others because is just a cartoon (not a human) 

Clinical Application: 

- is a once-daily preferred PIs (as is Ritonavir) 

 

PK:

-structurally UNRELATED to other PIs

--> is well absorbed with food, highly protein bound 

CONTRAINDICATIONS:

-metabolized by and inhibits CYP3A4

-contraindicated with a proton pump inhibitor 

-administration must be >12 HOURS APART FROM H2 BLOCKERS + ANTACIDS 

-less incidence of side-effects than other PIs 

33

DARUNAVIR

PROTEASE INHIBITOR

DA-RUN-AVIR --> think about running, in order to run well, need to absorb what you're taking quickly, so is BEST ABSORBED WITH FOOD 

-inhibits HIV protease resistant to other PIs

-well absorbed with FOOD

-is metabolized by CYP3A4, but also INHIBITS it as well

34

INDINAVIR

PROTEASE INHIBITOR

INDIAN-AVIR --> must be given with RITONAVIR b/c INDIANS AREN'T THAT STRONG 

--> eat way too much INDIAN FOOD --> GET RENAL STONES!!! 

-is given with RITONAVIR

-least protein bound (60%) 

--> absorption DECREASED when taken with meals

-dosage should be REDUCED with hepatic insufficiency

AEs:

-is well tolerated but can also get 

-NEPHROLITHIASIS + HYPERBILIRUBINEMIA (adequate hydration important) 

35

LOPINAVIR

PROTEASE INHIBITOR

LOPINAVIR --> LOW-PIN-AVIR --> can cause INSULIN RESISTANCE

--> is an INducer --> contains alcohol which makes you do things, therefore don't give with disulfiram or metro) 

--> warts are the size of PINS --> CYP INDUCER FOR ST. JOHNS WARTS 

-one of the PREFERRED Protease Inhibitors

-is given with RITONAVIR

-has poor intrinsic stability

CONTRAINDICATIONS: 

--> is an ENZYME INDUCER, therefore St. Johns Wort should be avoided 

-oral solution contains EtOH (avoid disulfiram or metronidazole) 

36

NELFINAVIR

PROTEASE INHIBITOR

NELFINAVIR --> NEW ELF --> is the best elf that santa has --> it is already working at maximum efficiency so cannot be boostd by RTV 

-CANNOT be boosted by Ritonavir

-metabolized by SEVERAL CYPs 

--> major metabolite (CYP2C19) has antiviral actiivity equal to parent compound

CONTRAINDICATIONS: NUMEROUS (d/t inhibition of CYP)

AE:

-diarrhea (controlled by loperamide), nausea, flatulence 

37

TIPRANAVIR

PROTEASE INHIBITOR (don't confuse with DARUNAVIR which is well-absorbed w food)

TIPRANOVIR --> if run on TIPTOES --> will make your head go crazy --> INTRACRANIAL HEMORRHAGE --> can also cause FATAL HEPATITIS --> can feel the TIP of your liver while you're RUNNING (can feel the stich with your right hand) 

-inhibits HIV protease resistant to other PIs

-twice-daily should be given with RITONAVIR

-is well absorbed with food

-is an INDUCER of CYP P450

AES:

1) SEVERE + FATAL HEPATITIS

2) FATAL + NONFATAL INTRACRANIAL HEMORRHAGES

38

ENTRY/FUSION INHIBITORS

FUSION INHIBITOR

1) ENFUVIRTIDE

 

ENTRY INHIBITOR

1) MARAVIROC 

39

ENFUVIRTIDE

 

FUSION INHIBITOR

ENFUVIRTIDE --> like the thing tries to enter but it hits the cell and hits the tide and bounces back, ie it is a FUSION INHIBITOR --> is structurally --> when do u see the tide? when you're 41 years old, able to afford a YACHT ---> acts like a gp41

• First approved drug that inhibits viral fusion
Approved for use in treatment-experienced adults with evidence of HIV replication

No activity against HIV-2

-most common adverse effect = PAIN AT INJECTION SITE!!! --> ENFU as in EFF YOU!!!!

MOA

Structurally similar to gp41 (HIV protein mediates membrane fusion)

• Binds to gp41 subunit of the viral envelope glycoprotein, preventing ability of virion to fuse cell membrane

PK: parenteral administration only 

AE: 

Injection-related (3% discontinue)

• Hypersensitivity reactions & eosinophilia rarely

No drug interactions with other antiretrovirals have been noted

40

MARAVIROC

ENTRY INHIBITOR

MARAVIROC ---> think MARRY --> ENTRY INTO MAIRRAGE/NEW PART IN YOUR LIFE --> CCR5 is the song that you play at your mairrage --> binds on surface of T cells/monocytes, inhibiting interaction with gp120.

MOA

Binds specifically and selectively to CCR5 (one of two coreceptors necessary for entrance of HIV into CD4+ cells)

• Result in blocking HIV entry (only CCR5-tropic virus can be treated with maraviroc)

 

Pharmacokinetics

• Metabolized by CYP 3A4 (reduce dose when given with PIs)

AE's:

--> well tolerated, risk of hepatotoxicity 

41

RALTEGRAVIR

INTEGRASE STRAND TRANSFER INHIBITOR (INSTI)

RALTEGRAVIR ---> R GRAVE --> when you're dying you start decomposing, start INTEGRATING into the soil --> this INHIBITS the INTEGRASE enzyme --> Leads to specific inhibition of the final step in integration of viral DNA into host cell DNA --> ie you're put in grave and eveyrthign is allowed to occur but the final step of decomposition is inhibited 

--> metabolized by UGT1A1-mediated glucuronidation  ie think GUT (ugt mixed around) 

--> note also that PPI's INCREASE the concentration for when you're decomposing 

Clinical Applications

• In combination with other antiretrovirals, raltegravir is approved for treatment-experienced and treatment- naive patients with evidence of viral replication

MOA

Binds integrase (enzyme essential to the replication of both HIV-1 and HIV-2)

• Leads to specific inhibition of the final step in integration of viral DNA into host cell DNA

Pharmacokinetics

• Metabolism via UGT1A1-mediated glucuronidation

AE: 

Well tolerated (nausea, headache, diarrhea)
• Can cause increases in creatine phosphokinase

Drug Interactions

• Rifampin, tipranavir & efavirenz may decrease [raltegravir]

• PPI’s may increase [raltegraivr]

42

TREATMENT FOR NAIVE PATIENTS

Goals:

• Maximally & durably suppress viral load replication

• Restore & preserve immunologic function
• Reduce HIV-related morbidity & mortality
• INCREASE QUALITY OF LIFE

 

43

WHICH REGIMINS TO START FOR NAIVE PATIENT?

Start with one of the following regimens:
(1) NNRTI & 2 x NRTI


(2) PI (preferably boosted with ritonavir) & 2 x NRTI

 

(3) INSTI & 2 x NRTI

44

FACTORS TO CONSIDER WHEN SELECTING AN INTIAL REGIMEN IN A NAIVE PATIENT 

Factors to consider when selecting an initial regimen:

• Comorbid conditions
• Potential adverse drug effects
• Potential drug interactions
• Pregnancy or pregnancy potential
• Results of genotypic drug resistance testing

• Patient adherence potential
• Convenience

45

SELECTION IS BASED ON: 

 

Selection is based on:

• Avoiding the use of 2 agents of the same nucleotide analog

• Avoiding overlapping toxicities and genotypic and phenotypic characteristics of the virus

• Patient factors such as disease symptoms and concurrent illnesses

• Impact of drug interactions; and

• Ease of adherence to a frequently complex administration regimen

46

CURRENT RECOMMENDATIONS FOR TREATMENT OF NAIVE PATIENTS: 

 

A image thumb
47

CURRENT REGIMEN FOR PREGNANT PATIENTS: 

 

 

1) RITONAVIR-BOOSTED LOPINAVIR (twice daily)

AND

2) ZIDOVUDINE/LAMIVUDINE

 

48

CURRENT RECOMMENDATIONS FOR INFANT BORN TO HIV INFECTED MOTHER

 

1) ZIDOVUDINE (start immediately after birth and administer for 6 weeks) 

49

HIV PROPHYLAXIS following a NEEDLE STICK 

Upon exposure to HIV, healthcare personnel should immediately receive a postexposure prophylaxis regimen containing at least 3 antiretroviral drugs

Preferred regimen:

1) Raltegravir + (Integrase inhibitor) 

2) tenofovir + (NRTI) 

3) emtricitabine (NRTI)

Regimen is given for 28 days and can be stopped if source is shown to be HIV-negative.

50

HIV PROPHYLACTIC VACCINES 

recommended?

contraindicated? 

• 1) Streptococcus pneumoniae

• 2) Hepatitis A
• 3) Hepatitis B and
• 4) Influenza

are generally recommended for all HIV-infected patients

CONTRAINDICATED: 

Live vaccines eg,

• MMR
• Varicella and

• Zoster

Other vaccines may be administered without regard to the patient’s CD4+