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Pharm 323 - Royce > Antivirals - HIV > Flashcards

Antivirals - HIV Flashcards

1
Q

HIV attacks which human cells?

A

CD4, macrophages, microglial

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2
Q

goal of antiviral HIV therapy

A

reduce viral load

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3
Q

which 2 classes of HIV antivirals BLOCK VIRAL ENTRY INTO CELLS

A
  1. CCR5 antagonists

2. fusion inhibitors

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4
Q

which 3 classes of HIV antivirals INHIBIT ENZYMES REQUIRED FOR HIV REPLICATION

A
  1. reverse transcriptase inhibitors
  2. integrase inhibitors
  3. protease inhibitors
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5
Q

what are the 2 subclasses of reverse transcriptase inhibitors?

A

nucleoside + non-nucleoside

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6
Q

what is the receptor on CD4 cells that HIV virus likes to bind with for entry into cell?

A

CCR5

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7
Q

mechanism of action for CCR5 antagonists?

A

blocks CCR5 receptor from binding with gp 120 on HIV virion

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8
Q

which receptor on the CD4 cell is present much more often at the START of infection?

A

CCR5

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9
Q

main thing to know / test for before administering CCR5 antagonists for HIV treatment?

A

test client to determine if their HIV strain is CCR5 tropic

using this receptor ro gain entry into CD4 cell

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10
Q

what is the prototype for CCR5 antagonists?

A

maraviroc (SelzENTRY)

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11
Q

AE/risk of maraviroc

A

hepatotoxicity risk

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12
Q

mechanism of action for fusion inhibitors

A

blocks fusion of HIV cells with CD4 cell (drug binds to gp41 on HIV cell to prevent fusion)

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13
Q

prototype of fusion inhibitor

A

enFUvirtide (FUZEon)

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14
Q

when are fusion inhibitors used?

A

when there is resistance to other HIV antivirals

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15
Q

2 downsides to fusion inhibitors (r/t patient access)

A
  1. costly!!
  2. Subcut injections BID
    =not an easy drug
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16
Q

most common AE of enFUvirtide (FUZEon) + how to avoid

A

injection site rxns (98%)
erythema, tenderness, pain, ecchymosis

prevention: rotate sites + avoid deep injections

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17
Q

mechanism of action for: nucleotide/nucleoside reverse transcriptase inhibitors (NRTI) aka NUKES

A

subs a dummy base pair –> inhibits creation of viral DNA

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18
Q

what class of drug is used mostly for initial regimen?

A

nukes (NRTIs)

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19
Q

what are the 2 prototype for NRTI/nukes

A
  1. zidovudine (AZT)

2. abacavir (Ziagen, ABC)

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20
Q

side effects of AZT (long term use)

A

anemia + neutropenia (affects bone marrow) = low H+H/low WBCs

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21
Q

re: pharmacogenomics, what do we need to look for with abacavir? if they have this, what are they at risk for if they take the drug?

A

test for genetic variant HLA-B*5701 –> @ risk for severe hypersensitivity rxn (anaphylaxis)

22
Q

what is the mechanism of action for non-nukes/non-nucleotide reverse transcriptase inhibitors (NNRTIs)

A

a cog in a wheel - binds to center of enzyme and causes direct inhibition –> STOPS it!

23
Q

AE of non-nukes

A

rash
hypersensitivity rxns
–> SJS (STOP if they have a severe rxn!!!)
a lot of drug-drug interactions

24
Q

what is the prototype for non-nukes

A

efaVIRenz (Sustiva)

reVERse Nukes = VIR enZ

25
Q

3 main points to know for effects of non-nukes

A

NO TO THE 3 B’s!!!!!! (BBB, babies, BC)

  1. crosses BBB (can be good OR bad thing)
  2. teratogenic
  3. can interfere with oral contraceptives - need new method
26
Q

adverse effects of protease inhibitors (5)

A
  1. dyslipidemia
  2. hyperglycemia/DM (secondary)
  3. lipodystrophy (central obesity)
  4. increased liver enzymes
  5. decreased cardiac conduction
27
Q

how can you recognize integrase inhibitors by their name?

A

“___tegr___”

28
Q

are INTEGRASE inhibitors tolerated well? Y or N?

A

YES! well tolerated and rarely cause hypersensitivity reactions

29
Q

what is the mechanism of action for integrase inhibitors?

A

prevents HIV genetic material from being INTEGRATED into DNA of CD4 cell

30
Q

name one side effect of integrase inhibitors (patient teaching/prepare them)

A

weight gain

31
Q

which type of HIV antiviral has recently risen to the top of the list for tx b/c they’re tolerated so well?

A

integrase inhibitors

32
Q

what type of HIV antiviral is the most effective antiviral available and can reduce viral load to undetectable levels?

A

protease inhibitors

33
Q

what is the mechanism of action of protease inhibitors?

A

prevents cutting of the HIV polyprotein, so it can’t be made into smaller virions

34
Q

re: the adverse effects of protease inhibitors, what kind of condition can this cause in the body? and could lead to what type of problems?

A

metabolic syndrome –> cardiovascular problems

35
Q

what is lipodystrophy r/t protease inhibitors?

A

redistribution of fat (back, trunk, face)

36
Q

re: increased liver enzymes as an AE of protease inhibitors, what is your concern for the patient?

A

if they’re co-infected with hep B or C

37
Q

re: decreased cardiac conduction as an AE of protease inhibitors, what other class of drug would you be concerned about the patient might be taking?

A

beta blockers

38
Q

pharmacokinetic enhancers are also known as what?

A

boosters!!

39
Q

ritonavir (Norvir) and Cobicistat (Tybost) are known as what? and act in what kind of fashion re: pharmacokinetics?

A

boosters ; synergistic = one drug increases the level of the other drug

40
Q

what is the point of a booster?

A

to be able to use lower levels of HIV drugs and have better effects :)

41
Q

mechanism of action for cobicistat (tybost)

A

blocks CYP450 3A4 enzyme

42
Q

mneumonic for NNRTIs (non-nukes) to recognize them by their name

A

___vir___ = “THROW A WRENCH IN THE MIDDLE”

43
Q

mneumonic for protease inhibitors

A

____navir = “NAVIR/NEVER tease a PRO”

44
Q

mneumonic for CCR5 and fusion inhibitors

A

“Preventing the ROC and the TIDE from coming to together”

MaraviROC + EnfuvirTIDE

45
Q

when does tx happen during L+D of positive pregnant person?

A

before delivery, during delivery, tx baby after delivery

46
Q

if a pregnant person had a viral load >1000 copies, what would you expect re: delivery?

A

C/S @ 38 weeks

47
Q

what is the pre-exposure prophylaxis drug for HIV?

A

Trevada

48
Q

when is post-exposure prophylaxis tx most effective?

A

1-2 hours after exposure –> up to 72 hours

49
Q

what is the best test to predict clinical outcomes and response to meds (HIV)

A

HIV viral load

50
Q

you should see a dramatic change in HIV viral load within _______ (time frame) of starting medication

A

6 weeks

Pharm 323 - Royce (28 decks)

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