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Spring 2018 Pharm Exam 4 > #6: Antiviral Drugs > Flashcards

#6: Antiviral Drugs Flashcards

1
Q

What 2 drugs are acyclic guanosine derivatives and metabolically activated by 3 phosphorylations

A

Acyclovir and Ganciclovir

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2
Q

Acyclovir MOA
- what is the 1st phosphorylation done by
(leads to drug becoming active)

A

Acyclovir MOA

  • 1st phosphorylation done by VIRAL thymidine kinase (TK)
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3
Q

Acyclovir ADME

  1. what is unique about its admin (2 ways to give it)
  2. what tissue does it diffuse into
  3. how is it cleared
A

Acyclovir ADME

  1. admin = given PO or IV (unique)
  2. diffuse into CSF
  3. Renally cleared
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4
Q

Acyclovir AEs

  1. 2 major AEs when given IV
  2. how to prevent them (2 ways)
A

Acyclovir AEs

  1. 2 major AEs when given IV
    - Renal toxicity (nephropathy, nephritis)
    - Neurotoxicity (tremors, delirium, seizures)
  2. how to prevent them (2 ways)
    - hydration
    - slow infusion
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5
Q

Acyclovir AEs/interactions

  1. what other types of drugs incr renal toxicity
  2. how do Probenecid and cimeditine alter acyclovir’s metab
A

Acyclovir AEs/interactions

  1. nephrotoxic drugs incr renal toxicity
  2. how do Probenecid and cimeditine alter acyclovir’s renal elimination
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6
Q
  1. genital herpes
  2. long term genital herpes, cutaneous zoster, varicella - decr sxmptomatic outbreaks/transmission
  3. recurrent orolabial herpes if take during prodrome

uses for which form of Acyclovir

A

PO Acyclovir Uses:

  1. genital herpes
  2. long term genital herpes, cutaneous zoster, varicella - decr sxmptomatic outbreaks/transmission
  3. recurrent orolabial herpes if take during prodrome
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7
Q

IV Acyclovir is 1st line Tx for what 3 things

A

IV Acyclovir is 1st line Tx

  1. HSV Encephalitis
  2. Neonatal HSV
  3. severe HSV or VZV infxns
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8
Q

Topical Acyclovir

  1. less eff than PO for what type of HSV
  2. ineff vs what type of HSV infxn
A

Topical Acyclovir

  1. less eff than PO for primary HSV
  2. ineff vs recurrent HSV infxn
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9
Q

Acyclovir Mechanism of Resistance

  1. alteration/mutation in what 2 things –> resis
  2. what is the Tx for Acyclovir Resis
A

Acyclovir Mechanism of Resistance

  1. alteration/mutation –> resis
    - TK (thymidine kinase)
    - DNA Polymerase
  2. Tx for Acyclovir Resis = Foscarnet
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10
Q

What are the 2 Anti-CMV agents

- what type of pts are CMV infxns common in (gen and 2 spp ex)

A

Anti-CMV agents

  1. Ganciclovir
  2. Foscarnet

CMV infxns common in immunosuppressed

  • HIV pts
  • after organ transplant
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11
Q

Ganciclovir

  1. MOA: what is the 1st phosphorylation catalyzed by
  2. what is the major AE (occurs at high doses)
  3. how is it used for Tx/ppx
A

Ganciclovir

  1. MOA: 1st phosphorylation catalyzed by CMV kinase
  2. major AE = Myelosuppresion (high doses)
  3. Tx/ppx of CMV after transplant
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12
Q

What drug is a Pyrophosphate analog

A

Foscarnet

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13
Q

Foscarnet

  1. MOA: what 3 things does it inhibit
  2. how does it differ from Ganciclovir (and Acyclovir)
  3. what is the only way it can be admin and where is most of its serum conc
A

Foscarnet

  1. MOA: inhibits VIRAL DNA polymerase, RNA polymerase and RT
  2. does NOT need to be activate
    - differs from Ganciclovir (and Acyclovir)
  3. IV ONLY
    - most serum conc = CSF
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14
Q

Foscarnet AEs

  1. What organ toxicity does it have
  2. Electrolytes:
    - incr the levels of what
    - decr levels of what 3 things
  3. what is resis d/t (mutations in what 2 things)

Others: chrom damage, arrhythmias, seizures

A

Foscarnet AEs

  1. Renal toxicity
  2. Electrolytes:
    - HYPERphosatemia
    - HYPO: K, Ca, Mg
  3. Resis d/t mutations in DNA polymerase or RT
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15
Q

Foscarnet uses

  1. strains resistant to
  2. what d/o in AIDS pts
  3. synergistic when combined w/acyclovir to Tx
A

Foscarnet uses

  1. strains resistant to acyclovir
  2. CMV retinitis AIDS pts
  3. synergistic when combined w/acyclovir to Tx CMV retinitis
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16
Q

Influenza Drugs

  1. name of drug and name of class
  2. what type of influenza is the only type to cause mass infxns
  3. if given quickly after Sx onset (48hrs) what is the benefit(2)
  4. who should be given these drugs (gen + 3 spp)
A

Influenza Drugs

  1. Amantidine + Neurominidase Inhibitors
  2. influenza A = only type to cause mass infxns
  3. given quickly after Sx onset (48hrs) –> decr dz severity/duraiton
  4. For pts w/high risk of complications
    - extremes of age
    - immunocompromised
    - comorbidities
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17
Q

Amantidine

  1. what does it inhibit
  2. what types of drugs are they
  3. why is this drug NOT used
A

Amantidine

  1. inhibits uncoating of viral RNA
  2. NMDA Antagonists
  3. NOT used b/c resistance common
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18
Q

Neurominidase inhibitors

  • what 2 drugs in this class
  • which given orally, which given by inhalation
A

Neurominidase inhibitors

  1. Oseltamivir/Tamiflu (PO)
  2. Zanamivir/Relenza (inhaled)
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19
Q

Neurominidase inhibitors: “mivirs”

  1. what are they analogs of
  2. what is the MOA (what do they inhibit the rel of)
A

Neurominidase inhibitors: “mivirs”

  1. sialic acid analogs
  2. MOA: inhibit the rel of influenza progeny
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20
Q

Neurominidase inhibitors: “mivirs” Uses

  1. what 2 types of influenza are they active vs
  2. which can be used for strains that are resistant in the other
A

Neurominidase inhibitors: “mivirs” Uses

  1. active vs Type A and B influenza
  2. Zanamivir used for Oseltamivir resistant strains
21
Q

Antiretroviral Agents

- 3 major classes

A

Antiretroviral Agents: classes

  1. RT inhibitors
  2. Protease Inhibitors
  3. Fusion, entry and integration inhibitors
22
Q

Antiretroviral Agents: General Info

  1. what is combo therapy (HAART) std of care
  2. Retroviral replication is error prone –> incr of what 2 things
A

Antiretroviral Agents: General Info

  1. combo therapy (HAART) std of care b/c need to target diff life cycles of virus
  2. Retroviral replication is error prone –> incr mutations –> incr resistance
23
Q

RTIs: General Info MOA

  1. how do they stop viral elongation by competitive inhib of RT
  2. how are they activated to triphosphate
A

RTIs: General Info MOA

  1. competitive inhib of RT –> incorp into viral DNA –> stop viral elongation
  2. activated to triphosphate by cellular phosphorylation
24
Q

RTIs: General Info AEs

  1. what is the main AE d/t interactions in cell
  2. what AE is life threatening
A

RTIs: General Info AEs

  1. main AE = mitochondrial toxicity
    - d/t interactions in cell

2.life threatening lactic acidosis w/ hepatic steatosis

25
Q

What NRTI (Nucleoside RTI) is a guanosine analog

A

Abacavir = guanosine analog

26
Q

Abacavir AEs

  1. Why is there cautioned used in CVD pts
  2. What pts is it CI in d/t HSN rxn that can be fatal

Other AE = skin rash

A

Abacavir AEs

  1. cautioned used in CVD pts –> MI
  2. CI in pts w/ HLA-b5701 polymorphism
    - HSN rxn that can be fatal

Other AE = skin rash

27
Q

What NRTI is a cytosine analog

A

Lamuvidine = cytosine analog

28
Q

What NRTI is a fluorinated analog of Lamivudine

- has long t 1/2 –> once daily dosing

A

Emtricitabine = fluorinated analog of Lamivudine

- has long t 1/2 –> once daily dosing

29
Q

What NRTI is used for HBV Tx

A

Lamuvidine used for HBV Tx

30
Q

What is the drug prototype for NtRTIs (Nucleotide RTI)

A

Nucleotide RT Inhibitor = Tenofovir

31
Q

Tenofovir: Nucleotide RT Inhibitor

  1. what is it an analog of
  2. competitively inhibits HIV RT –> causes what to occur
  3. how does this drugs activation differ from others

1st line therapy in combo w/Emtricitabine

A

Tenofovir: Nucleotide RT Inhibitor

  1. adenosine analog
  2. competitively inhibits HIV RT –> chain termination after incorp into DNA
  3. only needs 2 P’s for activation (nucleotide so already has 1)
32
Q

2 major AEs a/w Tenofovir

- which form has less toxicity

A

Tenofovir AEs

  1. Renal toxicity
  2. Ostepenia/bone loss
  • less toxicity w/AF
33
Q

3 examples of Renal toxicity that occur w/ Tenofovir

A

Tenofovir Renal Toxicity

  1. Tubular Necrosis
  2. Renal failure
  3. Fanconi’s Syndrome
34
Q

What is the drug prototype for the Non-Nucleoside RT Inhibitor (NNRTI)

A

Non-Nucleoside RT Inhibitor (NNRTI)

- Efavirenz

35
Q

What drug binds directly to HIV-1 RT and inhbits RNA and DNA dep DNA Polymerase

A

Efavirenz

- binds directly to HIV-1 RT and inhbits RNA and DNA dep DNA Polymerase

36
Q

How does the binding site of NNRTIs differ from NRTIs

A

NNRTIs bind to allosteric sites

NRTIs bind to active site (competitively inhibit)

37
Q

Efavirenz

  1. does it need phosphorylation to be activated
  2. major AE a/w start of tx that later resolves
  3. what severe HSN rxn can it cause that limits the drugs use
  4. Drug interactions are d/t what

Note: resis occurs rapidly (only need 1 mutation in RT)

A

Efavirent
1. does NOT need phosphorylation to be activated

  1. major AE a/w start of tx that later resolves
    - Nightmares/Psychiatric Disturbances
  2. severe HSN rxn –> SJS
    - limits the drugs use
  3. Drug interactions d/t P450/CYP34A

Note: resis occurs rapidly (only need 1 mutation in RT)

38
Q

3 Examples of Protease Inhibitors

- what types of drugs are they (what do they resemble)

A

Protease Inhibitors = “navir”

  1. Ritonavir
  2. Darunavir
  3. Atazanavir
  • peptidomimetics (resemble peptide bonds)
39
Q

Protease Inhibitors (all)

  1. MOA: what do the inhibit
  2. do they need activation
  3. why are they used in combo
  4. what inhibition –> drug interactions
  5. Class toxicities
    - incr levels of what 2 things, other toxicity
A

Protease Inhibitors (all)

  1. MOA: what do the inhibit proteolytic cleavage
  2. DONT need activation
  3. used in combo b/c resis common
  4. CYP34A inhibition –> drug interactions
  5. Class toxicities
    - incr levels TGs and LDL
    - lipodystrophy
40
Q

Which protease inhibitor is a booster

- it inhibits CYP34A and is used with other PIs to incr their serum levels –> less freq dosing, more tolerable

A

Ritonavir = booster

  • it inhibits CYP34A and is used with other PIs to incr their serum levels –> less freq dosing, more tolerable
41
Q

Ritonavair

- major AE

A

Ritonavair

  • major AE = elevated serum aminotranferase
42
Q

What two combos of PIs are the ToC for naive pts

A

ToC for naive pts

  1. Ritonavir/Darunavir
  2. Ritonavair/Atazanavir
43
Q

Fusion entry and integration Inhibitors

  • 3 drugs in this class
  • which inhibits fusion, entry, integration
A

Fusion entry and integration Inhibitors

  1. Enfuvirtide = inhibits fusion
  2. Maraviroc = inhibits entry
  3. Dolutegravir = inhibits integration
44
Q

Enfuvrtide: Fusion inhibitor

  • what does it bind to that prevents fusion

(not for HIV-2)

A

Enfuvrtide: Fusion inhibitor

  • binds to gp41 subunit of viral envelope glycoprotein –> prevents fusion
45
Q

Maraviroc: entry inhibitor

  • what does it bind selectively to

(for HIV-1 resistant strains)

A

Maraviroc: entry inhibitor

  • binds selectively to CCR5
46
Q

Maraviroc: entry inhibitor

  • binds selectively to CCR5 –> how does this prevent entry
A

Maraviroc: entry inhibitor

binds selectively to CCR5
- CCR5 = corec needed for HIV to enter CD4 cells –> binding prevents entry

47
Q

Dolutegravir: integration inhibitor

  • what enzyme does it bind to that –> inhibits viral DNA strand from integrating into host genome

(eff in HIV resis to other INSTIs)

A

Dolutegravir: integration inhibitor

  • binds to integrase –> inhibits viral DNA strand from integrating into host genome
48
Q

PEP vs PrEP meds

A

PEP
- raltegravir or dolutegravir + Tenofovir DF/emtricitabine

PrEP
- same as above but only last 2 drugs

Spring 2018 Pharm Exam 4 (7 decks)

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