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I3 Exam 3 > Antivirals (O'Brien) > Flashcards

Antivirals (O'Brien) Flashcards

1
Q

Anti-herpes/CMV drugs (non-HIV)

A

acyclovir, ganciclovir, foscarnet

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2
Q

Anti-influenza drugs (non-HIV)

A

amantidine, oseltamivir, zanamivir

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3
Q

Acyclovir mechanism

A

Viral thymidine kinase phos. acyclovir –> monophosphate –> more phos. happens with our thymidine kinase –> blocks DNA synthesis via competitive inhibition of viral DNA synthesis

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4
Q

How much phosphorylations does acyclovir undergo

A

3 (first one is viral thymidine kinase)

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5
Q

How is acyclovir administered

A

topically and IV

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6
Q

Is acyclovir a first line agent?

A

indeed!

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7
Q

What toxicity should you worry about for acyclovir?

A

renal, interactions

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8
Q

acyclovir resistance mechanisms

A

alteration in viral thymidine kinase

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9
Q

What drug can you give if pt. is resistant to acyclovir?

A

foscarnet

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10
Q

Anti-CMV agents

A

ganciclovir, foscarnet

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11
Q

ganciclovir mechanism

A

acyclic guanosine analog; first phos catalyzed by CMV kinase

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12
Q

Can ganciclovir be given orally?

A

no!

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13
Q

Ganciclovir active against

A

CMV (100x>acyclovir)

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14
Q

This is used as treatment/prophylaxis for CMV post-transplantation

A

ganciclovir

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15
Q

Ganciclovir toxicity

A

myelosuppression

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16
Q

Foscarnet mechanism of actions

A

inhibits viral DNA and RNA polymerase, HIV RT

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17
Q

Does foscarnet require phos?

A

No!

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18
Q

How is foscarnet administered

A

IV only

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19
Q

Foscarnet used in strains resistant to…

A

acyclovir

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20
Q

Foscarnet toxicities

A

renal; hyperphosphatemia, hypokalemia/calcemia/magnesemia

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21
Q

T:F - Anti-influenza agents must be given quickly after onset of symptoms

A

true

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22
Q

Oseltamivir (tamiflu, oral) and zanamivir (inhaled) are ______ inhibitors

A

neuraminidase inhibitors (analogs of sialic acid

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23
Q

Oseltamivir (tamiflu, oral) and zanamivir (inhaled) have activity against influenza…

A

A and B

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24
Q

Zanamivir is useful against ______-resistance strains

A

oseltamivir

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25
Q

Reverse Transcriptase Inhibitors (RTIs)

A

RTIs
Nucleoside: abacavir, emtricitibine/lamivudine
Non-nucleoside: efavirenz
Nucleotide: tenofovir

HIV protease inhibitors: atazanavir, darunavir, ritonavir

Fusion, entry, integration inhibitors: enfuvirtide, maraviroc, dolutegravir

26
Q

What was wrong with AZT?

A

retroviral replication is error prone and increase mutation frequency and increase resistance

27
Q

What is the standard of care of HIV?

A

combo therapy

28
Q

How are drugs selected for HIV?

A

based on pt strain resistance (genotype strain for mutations in RT and protease genes for mutations that can lead to resistance

29
Q

NRTIs=nucleoside reverse transcriptase inhibitors act by…

A

competitive inhib of RT and incorporation into viral DNA

30
Q

How are NRTIs activated?

A

cellular phosphorylation to triphosphate

31
Q

How does NRTI resistance occur?

A

mutations in viral RT

32
Q

NRTI toxicity

A

lactic acidosis w/ hepatic steatosis (life-threatening) –> due to NRTI-mediated inhib of mitochon fn (causes build-up of triglycerides = hepatic steatosis) –> due to lack of specificity

33
Q

Abacavir is a ____

A

reverse transcriptase inhib

34
Q

Abacavir toxicity (2)

A

myocardial infarction (caution exercised in CV disease; potentially increases platelet aggregation)

hypersensitivity rxn (can be fatal and with HLAB5701 should never take abacavir)

35
Q

Lamivudine and emtricitabine are ______ analogs and are used in ____ treatment

A
  • cytosine analog

- used in HBV treatment

36
Q

Emtricitabine is a fluorinated analog and is favored because____

A

longer half life and once daily dosing

37
Q

Truvada is a combo of

A

emtricitabine and tenofovir

38
Q

What does tenofovir do?

A

nucleotide analog of adenosine

39
Q

Does tenofovir require phosphorylation?

A

No! nucleoTIDE

40
Q

Tenofovir mech of action

A

competitively inhib HIV RT - chain termination after incorporation into DNA

41
Q

Tenofovir is coadministered w….

A

emtricitabine as a first-line RIT backbone therapy

42
Q

Tenofovir toxicity

A

renal accumulation: tubular necrosis, renal failure, Fanconi’s Syndrome

43
Q

Efavirenz is a ____

A

non-nucleoside RTI

44
Q

Efavirenz binds___and inhibits____

A

directly to HIV-1 RT and inhibits RNA and DNA-dependent DNA polym activity

45
Q

What kind of inhibitor is efavirenz?

A

allosteric (NRTIs are competitive)

46
Q

What limits the use of efavirenz?

A

extensive metabolism/induction via CYP3A4

47
Q

Efavirenz toxicity

A

nightmares/psychiatric disturbances (at start then resolve)

48
Q

HIV protease inhibitors are pepitdomimetics which means they…

A

mimic peptides and inhibit proteolytic cleavage

49
Q

HIV protease inhibitors toxicity

A

redistribution and accumulation of body fat (lipodystrophy)

increased triglycerides/LDL

50
Q

Ritonavir inhibitor of CYP3A4; used with other PIs to increase their serum levels, which means…

A

less frequent dosing, more tolerability (“boosting”)

51
Q

Ritonavir toxicity

A

increase triglycerides/LDL; elevated serum aminotransferase levels

52
Q

Name the three HIV protease inhibitors

A

ritonavir; atazanavir; darunavir

53
Q

Maraviroc is a…

A

entry inhibitor/CCR5 receptor antagonist

54
Q

Maraviroc binds…

A

selectively to CCR5

55
Q

Maraviroc used in…

A

HIV-1 strains resistant to other drugs

56
Q

Enfuvirtide is a…

A

fusion inhibitor

57
Q

Enfuvirtide binds to…

58
Q

Enfuvirtide is given by…

A

subq injection (peptide)

59
Q

What is the treatment for experienced HIV pt w/ ongoing HIV replication?

A

enfuvirtide

60
Q

Dolutegravir is a….

A

integrase strand transfer inhibitor (INSTIs)

61
Q

Dolutegravir inhibits…

A

viral DNA strand integration in host genome

62
Q

Dolutegravir appears effective in HIV that is…

A

resistant to other INSTIs

I3 Exam 3 (9 decks)

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