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Pharmacology > Antivirals > Flashcards

Antivirals Flashcards

1
Q

Patients being treated for HIV should be on at least ______ drugs.

A

3

typically 2 NRTIs and a 3rd drug

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2
Q

What is the MOA of NRTIs (Nuceloside Reverse Transcriptase Inhibitors)?

A

Eliminates action of reverse transcriptase which inhibits the virus from transcribing RNA to DNA

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3
Q

What type of toxicity can NRTIs cause?

A

Mitochondrial

Off target inhibition of mitochondrial DNA polymerase

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4
Q

S/s of NRTIs mitochondrial toxcity:

A 
Peripheral neuropathy 
Lipodystrophy (lipoatrophy)
Lactic acidosis
Hepatic steatosis 
Pancreatitis
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5
Q

How are NRTIs eliminated?

A

Renally

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6
Q

Which NRTI should be used if a patient has renal dysfunction?

A

Abacavir

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7
Q

The NRTIs, Lamivudine and emtricitabine are very commonly used and have _____ toxicity risk.

A

Minimal

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8
Q

The NRTI, tenofovir, carries which type of toxicity risk?

A

Nephrotoxicity

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9
Q

The NRTI, abacavir, has which AE?

A

HSR (pts with HLA B-5701 allele are at greater risk)

Increased risk of MI

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10
Q

Zidovudine (AZT), one of the first NRTIs is still used in patients who have multiple _____ _____ and may cause ______.

A

drug resistance

anemia, neutropenia (d/t BM suppression)

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11
Q

What is the largest concern with patients on NNRTIs (Non-nucleotide Reverse Transcriptase Inhibitors)?

A

DI

CYP450 substrates and induce CYP3A4

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12
Q

SE of NNRTIs include:

A

rash, increased transaminases

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13
Q

What is concern is associated with the long half lives of NNRTIs like Efavirenz?

A

Patients will typically be on two NRTIs and an NNRTI, if regimen is stopped, the NRTIs will exit the body faster than the NNRTI which could have a half life up to 3 weeks. Having only the NNRTI in the body can lead to drug resistance by the virus

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14
Q

AE of the NNRTI Efavirenz include:

A

Teratogenic in 1st trimester
CNS SE
False positive cannabinoid and benzo tests

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15
Q

AE of NNRTI Nevirapine:

A

Hepatotoxicity secondary to HSR

Stevens-Johnson syndrome

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16
Q

AE of the NNRTI Etravirine:

A

2nd gen

Induces CYP3A4, inhibits 2C9(incr warfarin levels) and 2C19 (prevents activation of plavix)

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17
Q

What is the pharmokinetic enhancement of drug levels called?

A

Boosting

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18
Q

Protease inhibitors: lopinavir, saquinavir, darunavir, and tipranavir are always _______
Nelfinavir is _____ ______.

A

boosted

never boosted

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19
Q

How does the PI Ritonavir work to boost other PI’s?

A

Ritonavir is a potent inhibitor of CYP3A4, PI’s are substrates of CYP3A4. By inhibiting CYP3A4 this increases the bioavailability of PIs, decreases elimination of PIs, and results in increased efficacy, and/or a longer dosing interval
(Rotanavir has effect on HIV replication, was used at higher doses to treat HIV in the ‘90’s)

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20
Q

Common DI associated with Ritonavir:

A 
CYP3A4 substrates (increase levels of those drugs also)
Inhibits CYP2D6
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21
Q

Protease Inhibitors DI’s are related to:

A

Substrates of CYP3A4

Inhibitors of CYP3A4

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22
Q

SE of PI use:

A

Dyslipidemia
Increased glucose
GI intolerance

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23
Q

Which drugs are CI for patients using PI’s?

A 
Midazolam, triazolam
Rifampin (potent inducer of 3A4=cancel out effect of ritonavir)
Simvastatin, lovastatin 
Fluticasone
St. John's Wort
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24
Q

The PI Atazanavir should not be used with:

A

acid suppressing agents. Atazanavir needs acidic environment to be absorbed

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25
Which drugs required dose adjustments in patients using PI's?
``` Rifabutin Clarithromycin Atorvastatin Oral contraceptives Voriconazole, ketoconazole Sildenafil, vardenafil, tadalafil Anticonvulsants ```
26
Which PK enhancer/booster works by inhibiting CYP3A4 but has no effect of HIV replication?
Cobicistat
27
While ritonavir has mainly lipid and GI concerns what potential AE dose cobicistat have?
Renal AEs
28
How do the Integrase Inhibitors Raltegravir and Elvitegravir differ?
Raltegravir is metabolized by the glucoronidation pathway so is not renally eliminated and not metabolized by CYP3A4. Elvitegravir is metabolized by 3A4 and usually boosted by Cobicistat
29
Which type of HIV meds are given to patients who do not have other options?
Fusion inhibitors | CCR5 Inhibitors
30
How does the fusion inhibitor Enfuviritide work, how is it administered, AE, metabolism?
Binds to the gp41 rc to prevent fusion Injection AE: injection site reactions Metabolized via non-CYP450 pathways
31
What is the MOA and what is different about the CCR5 Inhibitor, Maraviroc?
MOA: CCR5 antagonist at the rc on the surface of CD4 cells inhibiting fusion It is the only drug that has a target of the human cell vs. viral target
32
Which drugs inhibit mature HIV cells?
Protease Inhibitors
33
Which drugs inhibit integration in human DNA?
Integrase inhibitors
34
Which drugs prevent formation of HIV DNA?
NRTIs, NNRTIs
35
Which drugs inhibit fusion of the virus to the host cell?
Fusion inhibitors and CCR5 antagonists
36
Herpes viruses are what kinds of viruses?
DNA
37
Why is valacyclovir given and what is it converted into?
Valacyclovir is a prodrug for acyclovir. It is given because it is more lipophillic, has better bioavailability, and is better absorbed orally.
38
Why is famciclovir given and what is it converted into?
Famciclovir is a prodrug for penciclovir. It is more lipophillic and better absorbed orally. Penciclovir is only available topically.
39
What is the MOA of acyclovir and penciclovir?
These drugs are selectively activated by HSV and VZV enzymes, thymidine kinase. The drugs are triphosphorylated by the virus, these triphosphorylated metabolites selectively inhibit DNA synthesis halting the viral replication
40
Why is HSV easier to treat?
The thymidine kinase produced by HSV when exposed to acyclovir or penciclovir is more efficient
41
How does docosonol work?
(Abreva) Prevents fusion of HSV to plasma membranes
42
When do all drugs for the treatment of HSV and VZV work best?
Before manifestation of lesions occur. Once lesions occur, drugs do not heal what has already manifested but prevent further lesions
43
What drugs are used topically for herpes labialis?
Penciclovir/docosonal
44
What drug is used in the treatment of HSV encephalitis and herpes zoster in immunocompromised patients?
IV acyclovir
45
AE of docosonal include:
Burning/stinging sensation
46
AE of systemic HSV, VSV agents:
GI disturbances HA Rash (acyclovir/valcyclovir) Fatigue (Famciclovir)
47
What DI can occur with acyclovir and penciclovir?
Probenecid blocks renal secretion of these drugs
48
What can cause drug resistance in acyclovir/pencyclovir?
Thymidine kinase deficiency (virus no longer producing this) Thymidine kinase mutants (virus producing faulty form) =drug can no longer be activated More common in immunocompromised patients Suspect resistance if patients show poor clinical response to drugs
49
Treatment of CMV includes what antibiotics?
Ganciclovir Valganciclovir Cidofivir Foscarnet
50
Cidovir and Foscarnet can also be used to treat what?
Acyclovir-resistant HSV
51
What is the prodrug for ganciclovir?
Valganciclovir
52
MOA of ganciclovir:
Once triphosphorylated to its active form, it inhibits viral DNA synthesis by inhibiting viral DNA polymerase
53
AE of ganciclovir:
**Anemia, neutropenia, thrombocytopenia | GI disturbances
54
Ganciclovir does have HSV activity but has cross-resistance with _______.
acyclovir
55
MOA of Cidofivir:
Inhibits viral DNA synthesis by inhibiting DNA polymerase
56
MOA of Foscarnet:
Inhibits DNA polymerase and reverse transcriptase
57
Why are Cidofivir and Foscarnet active against acyclovir resistant HSV?
Their activation is not dependent on thymidine kinase
58
One common adverse effect for both Cidofivir and Foscarnet is:
Nephrotoxicity
59
Fever, N/V/D, anemia can also be associated with which drug used in the treatment of CMV and acyclovir-resistant HSV?
Foscarnet
60
What DI is present with Cidofivir?
Probenecid blocks renal secretion
61
Indications for use of Ribavirin: (3)
1. Symptomatic relief in young children with influenze A and B 2. RSV pneumonia (inhalation) 3. Chronic Hep C inf (most common)
62
MOA of Ribavirin:
Inhibits viral-specific RNA synthesis | Inhibits formation of viral proteins/enzymes necessary for replication
63
AE of Ribavirin:
- Serious: cardiac arrest, apnea, bacterial pneumonia, pulmonary deterioration - **Anemia, neutropenia, thrombocytopenia (may require Epo) - Rash, conjunctivitis
64
What should female patients be counseled about regarding ribavirin?
Category X: teratogenic | Use 2 forms of birth control during and for 6mos after discontinuation of treatment
65
In what patients is inhaled ribavirin contraindicated?
Vented patients
66
How is PO ribavirin eliminated?
Renally
67
Adamantanes: Amantadine and Rimantidine were at one time used for the prophylaxis and treatment of influenza ____. Why are they not used often?
A | CDC advises against use d/t resistance
68
What is the MOA of Adamantanes?
Interference with viral attachment and uncoating
69
What other disease can Amantadine be effective against and why?
Parkinson's Causes the release of dopamine (AE: ataxia, nightmares, insomnia)
70
Neuraminidase Inhibitors, the most commonly used antivirals to treat influenza, include:
Oseltamivir (Tamiflu) | Zanamivir (Relenza)
71
Oseltamivir(Tamiflu) and Zanamivir (Relenza) are effective against:
Influenza A and B, pandemic H1N1, H5N1 (avian influenza) Treatment and prophylaxis
72
MOA of neuraminidase inhibitors:
Inhibits neuraminidase, preventing budding from the host cell (halting reproduction) Prevents spread of infection
73
When should neuraminidase inhibitors be given?
First 48hrs of s/s to limit number of days with s/s
74
Oseltamivir (Tamiflu): route of administration, AE, type of drug
PO prodrug AE: N/V, serious skin and hypersensitivity reactions, neuropsychiatric side effects
75
Zanamavir (Relenza): Route of administration, AE
Oral inhalation | AE: Cough, bronchospasm in patients with asthma and COPD
76
When is Peramivir (IV) given?
To patients in the ICU who cannot take oral or inhaled agents

Pharmacology (48 decks)

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