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Immunity, Infection and Disease > Antivirals > Flashcards

Antivirals Flashcards

1
Q

Mechanism of action for the acyclovir family of drugs and the disease they are used to treat

A

Treat Herpes Virus. They are guanosine analogs. Acyclovir and penciclovir are active, valacyclovir and famciclovir are prodrugs

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2
Q

How might a virus become resistant to the acyclovir family of drugs?

A

Alterations in its thymidine kinase (viral thymidine kinase catalyzes first phosphorylation of the acyclovirs), or change in its DNA pol

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3
Q

Most important severe AE of acyclovir

A

nephrotoxicity (esp at high IV doses), cna also cause neurotoxicity

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4
Q

If your patient has herpetic encephalitis, which drug from the acyclovir family should you use and why?

A

Acyclovir, it is only drug available IV (and this method of admin helps drug cross BBB)

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5
Q

What type of drug is ganciclovir, is it active or prodrug, and what disease is it used for?

A

Guanosine analog, it is active (valganciclovir is its prodrug), used to treat CMV

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6
Q

What viral enzymes interact with the acyclovir and ganciclovir families respectively?

A

Acyclovir interacts with viral thymidine kinase, ganciclovir interacts with viral phosphotransferase

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7
Q

Which drug can be used orally to treat CMV

A

Valganciclovir (ganciclovir has a bioavailability which is too low, requires IV admin for active infection)

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8
Q

AEs for ganciclovir family of drugs

A

Myelosuppression, fever, rash, increased LFTs, carcinogenic, embryotoxic

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9
Q

How does cidofovir work and what diseases does it treat?

A

Cytosine nucleotide analog, used for CMV and HSV infections

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10
Q

Difference between a nucleotide and nucleoside and the pharmacologic implication

A

Nucleoside still needs to be phosphorylated to be used in DNA replication. Nucleotide analogs can be used in infections with mutated thymidine kinase, whereas nucleoside analogs wont work here

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11
Q

Disadvantages of cidofovir

A

IV only, nephrotoxic, also neutropenia and metabolic acidosis (rare)

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12
Q

Cidofovir has significant AEs (eg nephrotoxicity). Why would we use cidofovir?

A

CMV pts who do not tolerate ganciclovir or HSV pts who have resistance to the acyclovir family

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13
Q

How does Foscarnet work and what diseases is it used to treat?

A

Inorganic pyrophosphate (complexes with viral DNA pol), used for CMV and HSV infections

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14
Q

Will foscarnet show cross-resistance with other CMV/HSV drugs (eg acyclovir family, ganciclovir)?

A

No, has unique mechanism of action from them

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15
Q

Disadvantages of foscarnet

A

IV only, nephrotoxicity, anemia

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16
Q

NRTIs

A

Nucleoside Reverse Transcriptase Inhibitors. Structural analogs to nucleoside bases, used in retroviruses (eg HIV)

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17
Q

AEs of NRTIs

A

Lactic acidemia, hepatomegaly with steatosis, also Zidovudine - myelosuppression, Abacavir - hypersensitivity, Savudine and didanosine - peripheral neuropathy

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18
Q

Why do NRTIs have few drug interactions?

A

Because they are primarily metabolized by kidney (dont interact with CYP system)

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19
Q

Only Nucleotide Reverse Transcriptase Inhibitor

A

Tenofovir (is an adenosine base analog, most properties similar to NRTIs)

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20
Q

NNRTIs

A

Non-Nucleoside Reverse Transcriptase Inhibitors, non-competitive binding to RT, bind adjacent to catalytic site of enzyme

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21
Q

Causes of NNRTI resistance

A

Mutation in viral DNA pol

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22
Q

AEs of NNRTIs

A

Hypersensitivity reactions, Rash (Stevens-Johnson), Efavirenz - CNS symptoms, dose in evening

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23
Q

What metabolizes NNRTIs and what is the clinical impact of this?

A

CYP3A4 (Liver), causes drug-drug interactions

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24
Q

What type of drug is efavirenz?

A

NNRTI (non-nucleoside reverse transcriptase inhibitor)

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25
Q

What do protease inhibitors prevent?

A

Bind to protease to prevent production of mature of the virus (by preventing cleavage of Gag-Pol polyprotein)

26
Q

AEs of protease inhibitors

A

Metabolic syndrome - Lipodystrophy, hyperlipidemia, hypertriglyceridemia, hyperglycermia, also indinavir - nephrolithiasis, nelfinavir - diarrhea, atazenavir - increase bilirubin and prolonged QT, tipranavir - intracranial hemorrhage

27
Q

Metabolizism of protease inhibitors and the impact of this

A

CYP3A4 (Liver), drug-drug interactions

28
Q

Protease Inhibitor Boosting

A

Giving two protease inhibitors concomitantly to utilize the CYP3A4 inhibition to your advantage (increase drug levels)

29
Q

What PI is the most potent CYP inhibitor, and what use does that presdispose it for?

A

Ritonavir, it is frequently used for boosting

30
Q

List protease inhibitors

A

Ritonavir, lopinavir, atazanavir sulfate, duranivir

31
Q

What do integrase inhibitors do?

A

Inhibits insertion of HIV DNA into human DNA

32
Q

List integrase inhibitors

A

Raltegravir (Isentress)

33
Q

Fusion inhibitors

A

Binds gp41 on viral envelope to prevent fusion of virus with cell membrane

34
Q

Class of HIV drugs that are not first line therapy

A

Fusion inhibitors, entry inhibitors

35
Q

List fusion inhibitors

A

Enfuvirtide (T-20)

36
Q

Which HIV med is not an oral med and by what method is it adminstered?

A

Enfuvirtide (a fusion inhibitor), it is given subcutaneous

37
Q

Are integrase inhibitors and fusion inhibitors metabolized by CYP450?

A

No

38
Q

Entry inhibitors

A

Coreceptor antagonists preventing HIV entry into cells

39
Q

List entry inhibitors

A

Maraviroc (Selzentry)

40
Q

What types of HIV does maraviroc (an entry inhibitor) work against?

A

CCR5 trophic HIV-1 only (virus must use CCR5 as coreceptor for entry)

41
Q

Why is compliance a huge issue with NNRTI therapy?

A

Because if the pt doesnt take meds, a single mutation in thymidine kinase can confer resistance of the virus to the whole class of drugs

42
Q

What classes of HIV drugs most commonly show drug interactions?

A

NNRTIs and PIs

43
Q

3 options for HAART regimens

A

1) NNRTI + 2 NRTIs, 2) PI (boosted) + 2 NRTIs, 3) Integrase inhibitor + 2 NRTIs

44
Q

Two types of Hep B drugs and list drugs in each

A

Suppress viral replication - Lamivudine, Tenofovir (also adefovir, entecavir, telbivudine), and Modulate immune system - Interferons

45
Q

Hepatitis B is a DNA virus. Why do we use RT inhibitors against it?

A

It replicates via an RNA intermediate which requires reverse transcriptase

46
Q

Disadvantages of nucleoside/nucleotide analog therapy in Hep B?

A

Drug resistance develops, relapse once therapy discontinued

47
Q

Which two nucleoside/nucleotide analogs are preferable in treatment of Hep B and why?

A

Entecavir and tenofovir, because they lead to lower rates of resistance

48
Q

Effects of interferons in treating Hep B

A

Enzyme induction, suppress cell proliferation, inhibit viral replication

49
Q

What is done to increase the half life of injected interferons?

A

Conjugating it to poly ethelene glycol (Pegylating it)

50
Q

AEs of interferons

A

Flu-like symptoms, myelosuppression, neuropsychiatric effects

51
Q

Ribavirin

A

Guanosine analog, inhibits viral RNA pol, used for influenza, HCV, RSV

52
Q

AEs of ribavirin

A

Hemolytic anemia (another note, ribavirin used with interferon for Hep C)

53
Q

List agents for treating Hepatitis C

A

Interferon with either ribavirin or telaprevir/boceprevir

54
Q

How do telaprevir and boceprevir work and what are they used to treat?

A

Protease inhibitors, block cleavage of HCV polyprotein, used for Hep C

55
Q

AEs of PIs used in Hep C (Telaprevir and Boceprevir)

A

Anemia, rash

56
Q

Anti-influenza agents and what each targets

A

Amantadine/Rimantadine (target M2, which is uncoating protein), and Zanamivir/Oseltamivir (target Neuraminidase which is used for virion release)

57
Q

What are the classes of interferons given as antivirals and what is each class given for?

A

Alpha-2b - HBV and HCV, Alpha-2a - chronic HCV, Alphacon-2 - chronic HCV

58
Q

Hep B treatment options

A

Interferon monotherapy (16-48 weeks), or Nucleoside RT inhibitor monotherapy (minimum one year)

59
Q

Hep C treatment options

A

Pegylated interferon + Ribavirin or Pegylated interferon + ribavirin + telaprevir or boceprevir

60
Q

Which of the drugs targeting influenza M2 is more efficacious?

A

Rimantadine is much more than Amantadine

61
Q

Why are amantadine and rimantadine not recommended as monotherapy in influenza infection anymore?

A

Because significant resistance now exists in the population

Immunity, Infection and Disease (86 decks)

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