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Pharm Block 12 > Antivirals > Flashcards

Antivirals Flashcards

1
Q

“Avir”

A

AIDS

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2
Q

“Ovir”

A

Herpes

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3
Q

“Ivir”

A

Influenza

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4
Q

Why a kind of virus is herpes

A

DNA

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5
Q

What kind of drugs treat DNA viruses?

A

“Ovir”

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6
Q

What kind of virus is influenza

A

RNA

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7
Q

What kind of drug treats an RNA virus

A

“Ivir”

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8
Q

What kind of virus if HIV

A

Retrovirus

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9
Q

What kind of drugs treat retroviruses

A

“Avir”

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10
Q

Clinical presentation of HIV

A

High viral load and persistent decrease in CD4 lymphocytes

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11
Q

Drugs used for HIV

A
  • reverse transcriptase inhibitors: NRTIs, NtRTIs, NNRTIs
  • protease inhibitors
  • fusion inhibitors
  • integrate inhibitors
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12
Q

What are the main enzymes involved in the HIV virus

A

Reverse transcriptase
Protease
Integrase

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13
Q

What kind of HIV drugs stop entry into the cell?

A

Fusion inhibitors

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14
Q

What do reverse transcriptase inhibitors do

A

Stop DNA

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15
Q

What do proteases do in HIV

A

Matures virus to infect other cells

-use protease inhibitors

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16
Q

What do protease inhibitors do in HIV treatment

A

Prevents virus from maturing and infecting other cells

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17
Q

What does integrase do in HIV

A

Integrates genetic material into host DNA

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18
Q

What do integrase inhibitors do in treating HIV

A

Prevent the virus from integrating genetic material into host DNA

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19
Q

Nucleoside

A

DNA + sugar

-not active, no phosphates

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20
Q

Nucleotides

A

DNA base + sugar +3 phosphates

-active

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21
Q

How can a nucleoside become active

A

Get 3 phosphates attached to it and become a nucleotide

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22
Q

What are the nucleoside reverse transcriptase inhibitors (NRTIs) used for HIV

A

Zidovudine
Lamivudine
Emtrictabine

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23
Q

MOA of NRTIs

A
  • host enzyme activates the drug by adding on 3 phosphates to the drug (host kinases)
  • 5’-triphosphate-DRUG terminates DNA elongation, competes with natural deoxynucleotides for reverse transcriptase
  • competitive inhibitor, looks like DNA but just inhibits it
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24
Q

How do NRTIs differ from thymidine

A

They lack the 3’ hydroxyl

  • cant elongate with this
  • chain termination of DNA
  • looks like nucleotide in body, but stops chain because no 3’ hydroxyl
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25
Q

Adverse effects of NRTIs

A

Bone marrow suppression: AZT (zidovudine)

  • could make you sicker because more immunosuppression
  • lower risk today because of combination therapy allowing a lower dose of this drug
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26
Q

What are considered the least toxic NRTIs

A

Lamivudine and emtricitabine

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27
Q

How do you use NRTIs

A

Always in combination, use two at a time

  • cant do laivruline and emtrictabine together because Rhett both look like cystine and will compete with each other
  • have to use one of those with zidovudine
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28
Q

What is the nucleotide reverse transcriptase inhibitors used for HIV (NtRTI)

A

Tenofovir (TDF)

-there’s an O in there but it does not treat herpes!

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29
Q

MOA of NtRTIs (tenofovir (TDF))

A

Has a single phosphate on its sugar residue and must be further phosphorylated to the active form tenofovir triphosphate

Drug with a single phosphate that needs two more

Prodrugs

30
Q

How is tenofovir Rxed

A

With emtricitabine

31
Q

What are the non-nucleoside reverse transcriptase inhibitors (NNRTIs)

A

Efavirenz

32
Q

MOA of NNRTIs (efavirenz)

A

Bind to reverse transcriptase at a site below the catalytic site (allosteric inhibition)

Does NOT require phosphorylation to become active

33
Q

Which HIV drugs need phosphorylated?

A

NRTIs

NtRTIs

34
Q

Which HIV drugs do not need phosphorylated

A

NNRTIs

35
Q

Adverse effects of NNRTIs (efavirenz)

A

CNS effects (vivid dreams)

36
Q

What is the protease inhibitor used to treat HIV

A

Ritonavir

37
Q

MOA of ritonavir

A

Protease cleansed viral precursor proteins; critical for producing mature infectious visions, inhibits this

38
Q

Adverse effects of protease inhibitors (ritonavir)

A

Central adiposity and insulin resistance

-hyperglycemia

39
Q

Is ritonavir a P450 inhibitor or inducer

A

Inhibitor

40
Q

Why is ritonavir (a P450 inhibitor) frequently given together with other PIs?

A

Because it boosts other PIs

  • give other PI at low dose because plasma levels will be increased due to ritonavir
  • used with lopinavir usually
41
Q

Fusion inhibitors in HIV treatment (enfuvirtide)

A
  • enfuvirtide

- blocks gp41 protein on T cell surface to prevent viral entry

42
Q

What are the fusion inhibitors to treat HIV

A

Enfuvirtide

Maraviroc

43
Q

Maraviroc, fusion inhibitor in HIV treatment

A

Blocks CCR5 protein on macrophage (or T cell) surface to prevent viral entry

44
Q

Integrase inhibitor in treating HIV

A

Raltegravir
-inhibits the HIV enzyme integrase; this enzyme integrates the viral genetic material into human chromosomes

“Avir”=HIV
“Teg”=integrase

45
Q

What is the best way to treat HIV

A 
Combination therapy 
-2 NRTIS with one of the following:
—1-2 PIs
—and NNRTI
—raltegravir
46
Q

How is post exposure prophylaxis treated in HIV

A

The same way as it regularly is

47
Q

Evaluating therapeutic outcomes of HIV

A

Check CD4

Decreased CD4=risk of opportunistic infections

48
Q

What is PrEP in HIV

A

Pre-exposure prophylaxis
-used for people who do not have HIV but are high risk or exposure through sex or IV dirt use

-combination of tenofovir and emtricitabine

49
Q

HSV-1

A

Cold sores

50
Q

HSV-2

A

Genital herpes

51
Q

Herpes zoster

A

Shingles

52
Q

What is herpes zoster (shingles) caused by

A

Herpesvirus varicella-zoster, same virus that causes chickenpox

  • reactivation of citrus causes shingles
  • pain in one dermatome
53
Q

What are the anti herpes drugs we talk about

A

Acyclovir
Cidofovir
Ganciclovir
Foscarnet

54
Q

MOA of acyclovir

A

Prodrug

  • nucleoside that needs 3 phosphates
  • herpes donates a phosphate to it and then human enzymes donate two phosphates to it
  • competitive inhibitor of DNA polymerase
55
Q

Adverse effects of acyclovir

A

Well tolerated, fe side effects

56
Q

What enzyme puts a phosphate onto the acyclovir drug

A

Thymidine kinase

-this from the viral genome phosphorylated acyclovir over a hundred times faster than host cell enzyme

57
Q

Resistance of acyclovir

A

Downregulate the enzyme TK

58
Q

Why cant you use acyclovir on TK- strains of herpes

A

Because it needs TK to add a phosphate to it to activate it. If there isn’t any TK, it wont activate

59
Q

Which herpes medication can be used in TK- strains and works by getting phosphorylated by host kinases

A

Cidofovir

60
Q

Ganciclovir and herpes

A

Used like acyclovir but used for CMV retinitis; bone marrow suppression is major toxicity

61
Q

What herpes medication can be used to CMV retinitis?

A

Ganciclovir

62
Q

What is the side effect of ganciclovir

A

Bone marrow suppression

-“gangs” up on bone marrow

63
Q

MOA of foscarnet

A
  • Herpes
  • not prodrug
  • selectively inhibits the pyrophosphate binding site on virus-specific DNA polymerases and reverse transcriptase
  • works on TK- strains
64
Q

What are the two herpes drugs that can work on TK- strains of herpes

A

Foscarnet and cidofovir

65
Q

Spectrum of foscarnet

A

CMV retinitis

66
Q

What drugs can treat CMV retinitis

A

Ganciclovir and foscarnet

67
Q

Adverse effects of foscarnet

A

Nephrotoxicity

68
Q

What two viruses cause influenza in humans

A

Influenza A and B

-hemagglutinin and neuraminidase on surface

69
Q

Main types of influenza in the past 3 decades

A

H3N2 and H1N1

70
Q

Drugs to treat influenza

A

Oseltamivir

71
Q

MOA of oseltamivir

A

-block neuraminidases thereby inhibiting the budding and release of virus from the cells

72
Q

Antiviral spectrum of oseltamivir

A

Influenza A and B prophyalxis and treatment

Pharm Block 12 (7 decks)

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