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Clinical Pharmacology II > Antiviral and Antiretroviral Therapies > Flashcards

Antiviral and Antiretroviral Therapies Flashcards

1
Q

Goal of antiviral and antiretroviral therapy ?

A
  • Theoretical
    1) Eliminate the virus
  • Reality
    1) Reduce viral load 2) Maintain viral load
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2
Q

Definition of Induction therapy ?

A
  • Reduce the viral load (Titer) to a level that is undetectable and/or has no S&S
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3
Q

Definition of maintenance therapy?

A
  • Maintain viral load at a undetectable / lowest possible state
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4
Q

Influenza A and B ?

A
  • Negative sense ssRNA viruses
  • Single agent therapy

or

  • No Treatment
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5
Q

Herpes virus (HSV1, HSV2 and CMV)?

A
  • dsDNA viruses
  • Single agent therapy

&

  • Short treatment duration
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6
Q

Hepatitis Virus (HBV & HCV) ?

A
  • Positive sense ssRNA viruses
  • Two agent therapy

&

  • Long treatment duration
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7
Q

Retrovirus (HIV)

A
  • Three + Agents therapy

&

  • Indefinite treatment
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8
Q

Antiretro virals simply inhibit the production of new viruses

T or F

A
  • True

- Have no effect on pre existing viruses

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9
Q

T or F

Immune system is critical for clearing mature viruses ?

A
  • True
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10
Q

Viral resistance to antiretro therapies generally occurs when ?

A
  • The virus mutates and still allows the target protein to continue to work even when the drug is present
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11
Q

T or F

The viral mutation prevents the drug from binding (Resistance) but such mutations result in less virulent viruses?

A
  • True
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12
Q

How many steps can antiviral therapy target in a virus?

A
  • 9 Steps in viral replication
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13
Q

What do M2 anti influenza agents target?

A
  • M2 inhibitors block viral unpacking
  • Blocks the M2 proton pump = No unpacking
  • A lot of resistance not recommended
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14
Q

Neuraminidase inhibitors block what ?

A
  • Block viral escape from the host cell
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15
Q

MOA of Oseltamivir (Tamiflu) ?

A
  • Neuraminidase inhibitor
  • Reversibly binds and inhibits the viral Neuraminidase to block viral detachment from host cell
  • Impairs cleavage of Neuraminic acid tether
  • Impairs the enzyme Sialidase
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16
Q

T or F

Oseltamivir (Tamiflu) is given as a prodrug, activated by hepatic esterases into active metabolite

A
  • True
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17
Q

What does Oseltamivir (Tamiflu) treat?

A
  • Influenza A and B
  • Very little resistance thus far
  • Some resistance for avian flu H7N9
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18
Q

Adverse effects of Oseltamivir (Tamiflu)?

A
  • Some neuropsychiatric events have been reported
  • Self-injury
  • Delirium
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19
Q

Anti-herpesvirus agents target what ?

A
  • limit the viral replication during the lytic active phase
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20
Q

What are the Major targets for herpesvirus inhibition are vDNA synthesis?

A

1) NucleoSIDE DNA polymerase inhibitors
2) NucleoTIDE DNA polymerase inhibitors
3) Pyrophosphate analog DNA polymerase inhibitors

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21
Q

T or F

A NucleoSIDE has a phosphate group attached ?

A
  • False

- Pentose
Base + Ribose or Deoxyribose

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22
Q

T or F

A NuleoTIDE has a phosphate group attached?

A
  • True

- Pentose
Base + Ribose or Deoxyribose + Phosphate group

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23
Q

T or F

All antiherpesviruse agents mimic some part of the dNTP structure to deceive the DNA polymerase?

A
  • True
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24
Q

Valacyclovir and Valganciclovir are nucleoside analogs, what do they require?

A
  • Requires conversion to dNTP analogs for activity
  • Depends on
    1) Viral thymidine kinase
    2) Viral UL97 kinase
    3) Host cell kinase
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25
Q

Cidofovir is a nucleotide analog (1 Phosphate), what does it require for activation?

A
  • Requires conversion to dNTP analog for activity
  • Depends on
    1) Host Kinase
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26
Q

Foscarnet is a pyrophosphate (Diphosphate) analog it requires viral and host kinase activation?

t or F

A
  • False
  • Mimics diphosphate product of DNA syn
  • Blocks DNA polymerase activity
  • Does not require viral or host cell kinase activation
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27
Q

Valacyclovir (Valtrex) (Improved nucleoside analog) MOA ?

A
  • Inhibition of viral DNA polymerase
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28
Q

T or F

Viral thymidine kinase able to phosphorylate any nucleoside (even though it’s not a “Thymidine)

A
  • True
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29
Q

Treatment of activity of Valcyclovir ?

A
  • Treats HSV 1 and HSV 2

- Some coverage for VZV

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30
Q

Valcyclovir is a pro drug, L-valyl ester of Aacyclovir, Converted to acyclovir via first pass metabolism

T or F

A
  • True

Better absorption

  • Less doses
  • Better efficacy
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31
Q

What is the most common resistance of Valcyclovir?

A

1) Viral Thymidine kinase mutations that prevent conversion to nucleotide analog (MOST COMMON)

or

2) Viral DNA Polymerase mutations that prevent drug from binding and DNA incorporation

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32
Q

T or F

Acyclovir can cause nephrotoxicity; Valacyclovir is much better tolerated

A
  • True
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33
Q

Valcyclovir is excreted via the kidneys, taking what increases the serum concentration?

A
  • Probenacid increases serum concentration
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34
Q

Valganciclovir (Improved nucleoside analog) mimics what?

A
  • Mimics pentose sugar
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35
Q

What does Valganciclovir treat?

A
  • > 100x more effective than Acyclovir against CMV
  • Approved for treatment of CMV in
    1) Immunocompromised patients
    2) HIV
    3) Organ transplant
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36
Q

T or F

Valganciclovir is given as a prodrug?

A
  • True

- Take with food
- Converted to Ganciclovir via first pass metabolism
Valganciclovir = L-valyl ester of ganciclovir

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37
Q

Resistance to Valganciclovir is caused by what ?

A
  • Mutations in viral UL97

- Prevents drug from being phosphorylated

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38
Q

Valganciclovir adverse effects ?

A
  • Myelosuppression
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39
Q

Valganciclovir is safe in pregnancy ?

T or F

A
  • False

- Teratogenic/mutagenic

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40
Q

T or F

Cidofovir is a Nucleotide analog?

A
  • True
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41
Q

MOA of Cidofovir ?

A
  • Inhibition of viral DNA polymerase
  • Converted to diphosphate by host cell kinases
  • “looks” like a triphosphate
  • Activity is independent of viral kinases
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42
Q

T or F

Cidofovir mimics a triphosphate?

A
  • True

- Only needs host kinase for activity

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43
Q

Cidofovir resistance occurs when?

A
  • Mutations in viral DNA polymerase that prevent it from binding drug
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44
Q

When is Cidofovir used?

A
  • > 100x more effective than acyclovir against CMV
  • Treatment of CMV in immunocompromised patients (HIV; organ transplant)
  • Used for acyclovir-resistant HSV infections (no cross-resistance)
    (val) acyclovir-resistant HSV infections
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45
Q

T or F

Cidofovir is used to treat acyclovir-resistant HSV infections
(val)acyclovir-resistant HSV infections

A
  • True

- No cross-resistance

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46
Q

T or F

Cidofovir has poor absoprtion and is given IV

A
  • True
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47
Q

Cidofovir is excreted via the Kidneys and is usually given with?

A
  • Probenecid
    Protects kidneys from damage
  • Saline
    To further dilute urine
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48
Q

Cidofovir is contraindicated with other nephrotoxic agents

T or F

A
  • True
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49
Q

Adverse Effects of Cidofovir?

A
  • Nephrotoxicity (proximal tubular nephropathy)
  • Fanconi syndrome
    Excess amounts of glucose, bicarbonate, phosphates (phosphorus salts), uric acid, potassium, and certain amino acids being excreted in the urine

-Acid-base imbalances common

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50
Q

T or F

Cidofovir is safe during pregnancy?

A
  • False

- Teratogen/mutagen, incorporated into human DNA should be avoided in pregnancy

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51
Q

Foscarnet (Pyrophosphate (Diphsophate) analog) MOA ?

A
  • Inhibition of viral DNA polymerase
  • Competitive inhibitor
  • Mimics Pyrophosphate (Diphosphate)
  • Competitively inhibits binding of new dNTP
52
Q

Foscarnet is used to treat?

A
  • CMV-induced retinitis in immunocompromised

patients (HIV; organ transplant; etc.)

53
Q

Foscarnet resistance occurs via mutations in viral DNA polymerase?

T or F

A
  • True

- Prevent it from binding drug

54
Q

T or F

Foscarnet cleared primarily by the kidneys, Dosage must be carefully calculated based on Cr clearance!

A
  • True
55
Q

Foscarnet and Cidofovir have the same adverse effects?

T or F

A
  • True
  • Nephrotoxicity (proximal tubular nephropathy)
  • Fanconi syndrome
    Excess amounts of glucose, bicarbonate, phosphates (phosphorus salts), uric acid, potassium, and certain amino acids being excreted in the urine

-Acid-base imbalances common

56
Q

Goal treatment of HepB?

A
  • Suppression of disease to slow progression of cirrhosis

- Reduce risk of liver cancer

57
Q

Goal treatment of HepC?

A
  • Eradication of virus
  • Absence of detectable virus 24 weeks after completion of therapy
  • Recommended for those at increased risk for progression to cirrhosis
58
Q

T or F

About 15-30% of patients clear HepC virus without treatment?

A
  • True
59
Q

PEGinterferon alfa (PEGylated interferon alpha) is used to treat?

A
  • HepB and HepC (IV; SQ)

- Coadministered with a broad-spectrum antiviral such as Ribavirin

60
Q

PEGinterferon alfa (PEGylated interferon alpha) MOA in treating HepB and HepC ?

A
  • Binds to interferon receptors on host cells to
  • “prime” them to resist infection
  • Inhibits viral
    1) Penetration
    2) Translation
    3) Transcription
    4) Protein processing
    5) Maturation
    6) Release
  • Increases expression of viral antigens
61
Q

PEGinterferon alfa (PEGylated interferon alpha) is contraindicated in pts with?

A

1) Hepatic decompensation
2) Autoimmune disease
3) Cardiac arrhythmia

62
Q

PEGinterferon alfa (PEGylated interferon alpha) adverse side effects?

A
  • Flu-like symptoms (30% of pts) resolve on their own
  • Neurologic symptoms
  • Autoantibodies
  • Arrhythmias
63
Q

T or F

Tenofovir Disoproxil Fumarate and Tenofovir Alafenamide are both prodrugs of Tenofovir

A
  • True
64
Q

Where is the prodrug Tenofovir Disoproxil Fumarate (TDF) converted to Tenofovir?

A
  • Plasma
65
Q

Where is the prodrug Tenofovir Alafenamide converted to Tenofovir?

A
  • Intracellularly
66
Q

3 Benefits of the prodrug Tenofovir Alafenamide (TA) converting to Tenofovir intracellularly?

A

1) Lower dosing
2) Improved antiviral activity
3) Better distribution into lymphoid tissues

67
Q

T or F

Tenofovir is an Adenine nucleotide analog ?

A
  • True
68
Q

Tenofovir MOA?

A
  • Developed as an Antiretroviral nucleotide
    1) Inhibits DNA polymerase
    2) Causes DNA chain termination
69
Q

Tenofovir clinical use?

A
  • HBV and HIV-1
  • Included in regimens for pts coinfected with both viruses HepB/HIV
  • Because its Anti-HIV activity
70
Q

Tenofovir is given PO and distribution is improved when given with fatty meals.

T or F

A
  • True
71
Q

Tenofovir as a AntiRetroViral for HIV MOA

A
  • Inhibits Reverse Transcriptase (rather than DNA polymerase)
  • Considered a Nucleotide RTI
72
Q

Tenofovir adverse effects ?

A
  • GI complaints
73
Q

Anti-HCV agents distribute broadly into three categories based on their target, what are the targets?

A

1) NS3 (Protease)
2) NS5A
3) NS5B (RNA polymerase)

74
Q

Ribavirin (guanosine nucleoside analog) has one exception when treating HepC, what is the exception?

A

Acts both nonspecifically on

1) mRNA
2) Viral RNA polymerase

75
Q

Ribavirin (guanosine nucleoside analog) MOA?

A
  • Broad-spectrum antiviral
  • Inhibits guanine capping of viral mRNA
  • Takes the place of 7-Methylguanosine Cap
  • Inhibits RNA-dependent RNA polymerase in RNA viruses
  • Preventing translation of viral mRNAs
76
Q

Clinical use of Ribavirin?

A
  • Only approved for HCV

But effective against - HCV

  • IVA (Influenza A)
  • IVB (Influenza B)
  • HIV
77
Q

Ribavirin contraindications include?

A
  • Hemolytic Anemia
  • Renal Disease
  • Extremely Teratogenic, Mutagenic & Embryotoxic
78
Q

Ribavirin is contraindicated in males and females trying to get pregnant

T or F

A
  • True
  • For six months prior to conception
  • Contraception during Tx and 6 months after
79
Q

Grazoprevir (NS3/4A inhibitor) MOA ?

A
  • Blocks NS3 viral protease activity that cleaves the polyprotein
  • Preventing the release of functional individual viral proteins
80
Q

Grazoprevir and Ribavirin are Co formulated

T or F

A
  • True
81
Q

T or F

Grazoprevir has a long half life?

A
  • True

- Extensively protein bound

82
Q

Grazoprevir prevents cleavage of HepC polyproteins?

T or F

A
  • True
83
Q

Why is Grazoprevir contraindicated in hepatic insufficiency?

A
  • Metabolized heavily by CYP3A4

- Contraindicated with many CYP3A4 inhibitors

84
Q

Ledipasavir (NS5A inhibitor) is often co formulated with ?

A
  • Grazoprevir
    NS5B (polymerase)/4A

or

  • Ribavirin
    NS5B inhibitors
85
Q

Ledipasavir has few drug drug interactions and well tolerated

T or F

A
  • True
86
Q

Ledipasavir (NS5A inhibitor) treats ?

A
  • HepC
87
Q

Sofosbuvir (NS5B/RNA-dependent RNA polymerase inhibitor) MOA?

A
  • Highly effective inhibitor of viral RNA polymerase
  • Yielding high cure rates
  • Prodrug nucleotide analog commonly coformulated with other anti-HCV agents
88
Q

Sofosbuvir (NS5B/RNA-dependent RNA polymerase inhibitor) requires what?

A
  • Requires prodrug conversion to nucleoside triphosphate (NTP) by HOST cellular kinases
  • Incorporated into elongating RNA strand and terminates chain
89
Q

T or F

Sofosbuvir (NS5B/RNA-dependent RNA polymerase inhibitor) is the newest most expensive drug

A
  • True
  • Very high cure rates up to 97%
  • Extremely expensive $84,000 (12-week course)
90
Q

Side effects of Sofosbuvir (NS5B/RNA-dependent RNA polymerase inhibitor) ?

A
  • HA

- Fatigue

91
Q

T or F

Sofosbuvir (NS5B/RNA-dependent RNA polymerase inhibitor) is a P Glycoprotein substrate ?

A
  • True

- Contraindicated with p Glycoprotein inducers

92
Q

What are the two receptors on the host cell membrane where Retroviruses attach?

A
  • CCR5 or CXCR4
93
Q

What are the three most targeted pathways for Antiretroviral drugs?

A

1) Nucleoside RT inhibitors (NRTI’s)
2) Necleotide RT inhibitors (Nucleotides)
3) Non-Nucleoside RT inhibitors (NNRTI’s)

94
Q

What do Proteases inhibitors (PI’s) Target on retroviruses?

A
  • Interfere with viral protein production
95
Q

What do Integrase inhibitors target on retroviruses?

A
  • Block vDNA into host genome

- Preventing trascription

96
Q

T or F

Antiretroviral (ART) therapy in indicated for ALL HIV infected pts?

A
  • True
  • Limits disease progression
  • Limits transmission
97
Q

T or F

Most current therapies for HIV consist of 3+ drugs from different families?

A
  • True
  • 2 NRTI’s +
  • 1 PI or
  • 1 NNRTI or
  • 1 INSTI
98
Q

T or F

25% of pt’s with HIV also have HepC ?

A
  • True
  • A lot of serous DD interactions with HepC meds
  • HepC compromises the liver & many ART drugs have hepatotoxicity
99
Q

Nucleoside RT inhibitors (NRTI’s) bind where?

A
  • RT enzyme active site
100
Q

Non-Nucleoside RT inhibitors (NNRTI’s) bind where ?

A
  • Adjacent to RT’s active site

- Alters is shape

101
Q

Non-Nucleoside RT inhibitors (NNRTI’s) interferes with the binding of nucleotides or NRTI’s on the RT enzyme?

T or F

A
  • False
  • Does not prevent from others binding
  • But does prevent OTHER NNRTI’s from binding (Competitive inhibition)
  • Only 1 NNRTI at a time
102
Q

Zidovudine AZT MOA ?

A
  • NRTI
  • Competitive inhibitor of RT
  • Dock into enzyme active site
  • Preventing vDNA synthesis
103
Q

Zidovudine is a Thymidine analog antimetabolite ?

T or F

A
  • True

- Prodrug requires host kinase for activation

104
Q

What are the common adverse effects for ALL NRTI’s ?

A

1) Hepatosteatitis (Fatty Liver)
2) Hepatotoxicicty
3) Lactic acidosis

105
Q

Where does AZT target?

A
  • T Cells
106
Q

What resistance can AZT have ?

A
  • Mutations of RT that prevent drug binding
107
Q

T or F

AZT Zidovudine is the First-line treatment in pregnant women due to excellent prevention of vertical transmission (mother to child)

A
  • True
108
Q

What medications can alter the metabolism of AZT Zidovudine causing an increase in the prodrug levels (CYP450) and impacting its clearance?

A
  • Probenecid
  • Valproic acid
  • Fluconazole
  • Atovaquone
109
Q

AZT Zidovudine toxicities include ?

A
  • Hematologic toxicity is increased upon coadministeration of other myelosuppressive agents
  • (val)ganciclovir
  • Ribavirin
  • Conventional cytotoxic chemotherapeutics
110
Q

Nevirapine (non-nucleoside reverse transcriptase inhibitor; NNRTI) MOA ?

A
  • Binds to RT and allosterically inhibits DNA synthesis
  • Binds to a hydrophobic pocket adjacent to the NTP-binding site in RT
  • Changes the shape of RT enough that it cannot synthesize DNA.
111
Q

Nevirapine (non-nucleoside reverse transcriptase inhibitor; NNRTI) is metabolized in the liver by CYP3A4, thus can act as an inducer or inhibitor depending on the drug

T or F

A
  • True
  • Often alters CYP3A4 function
  • Leading to DDI issues
112
Q

Nevirapine crosses the placenta and thus ?

A
  • Used to prevent vertical transmission during birth
113
Q

Nevirapine can cause Hepatotoxicity, severe hepatitis that can be life-threatening

(Sudden onset)

T or F

A
  • True
114
Q

Nevirapine can cause a macropapular rash

T or F

A
  • True

- Dose dependent

115
Q

Atazanavir (protease inhibitor) MOA?

A
  • Docks into the substrate-binding site (Basket) between the monomers of the retroviral protease
  • Competitively inhibits the cleavage of the polyprotein
  • Prevents production of mature viral particles
116
Q

Atazanavir (protease inhibitor) is associated with ?

A
  • Buffalo hump
  • Gynecomastia
  • Cushing appearance
  • Central obesity
117
Q

Atazanavir (protease inhibitor) can be coadministered with PPIs, H2-blockers, or other acid-reducing agents?

T or F

A
  • False
  • Requires low pH to function
  • Absorption impaired by divalent cations (antacids, Fe/Ca supplements)
118
Q

T or F

All PIs are extensively metabolized by CYP3A4 and many inhibit CYP3A4 and other CYP450s,

Sometimes exploited clinically to “boost” the levels of other antiretroviral agents

A
  • True
  • Glucouronidation by UGT1A1
  • Strong inhibitor of CYP3A4 and CYP2C9
119
Q

Atazanavir (protease inhibitor) mimics a polypeptide

T or F

A
  • True
120
Q

Atazanavir (protease inhibitor) can cause hyperbilirubinemia due to UGT1A1 inhibition

T or F

A
  • True
121
Q

Dolutegravir (integrase inhibitor) MOA ?

A
  • Bind to integrase enzyme
  • Prevents it from integrating the vDNA into the host genome
  • The third and final step of provirus integration
122
Q

Dolutegravir (integrase inhibitor) is imparied by divalent cations (antacids, Fe/Ca supplements, etc.)

T or F

A
  • True
123
Q

Dolutegravir (integrase inhibitor) toxicities include?

A
  • Hypersensitivity
  • Occasional liver dysfunction
  • Discontinue immediately and do not restart!
124
Q

Dolutegravir (integrase inhibitor) Integrase inhibitors are generally devoid of serious side effects and thus are extremely commonly included in modern antiretroviral cocktails

T or F

A
  • True
125
Q

Herpes medications

A

VVCF

1) Valacyclovir
2) Valganciclovir
3) Cidofovir
4) Foscarnet

126
Q

HepC Medications

A

RGLS (riggles!)

1) Ribavirin
2 Grazoprevir
3) Ledipasavir
4) Sofosbuvir)

127
Q

HIV medications

A

DANZ (dance!)

1) Dolutegravir
2) Atazanazvir
3) Nevirapine
4) Zidovudin

Clinical Pharmacology II (5 decks)

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