Clinical Pharm Antiviral & Antifungal

Front 1

1. Identify drugs that inhibit viral uncoating by blocking the influx of protons through proton channels in the viral envelop and prevent pH-dependent dissociation of the viral matrix protein from the viral RNA genome of the influenza virus.

Back 1

Amantadine and rimantadine

Front 2

2. Identify drugs, which are nucleoside analogues that inhibit HSV and VZV genome replication by inhibiting DNA polymerases and, as they become incorporated into the growing DNA chain, terminate elongation.

Back 2

a. Acyclovir or Valacyclovir
a. Penciclovir or Famciclovir

Front 3

3. Identify drugs, which are nucleoside analogues that inhibit HIV replication by inhibiting DNA polymerase (reverse transcriptase) and, as they become incorporated into the DNA chain, terminate elongation.

Back 3

a. Abacavir
b. Didanosine
c. Entricitabine
d. Stavudine
e. Tenofovir
f. Zalcitabine
g. Zidovudine

Front 4

4. Protease inhibitors (amprenavir, atazanavir, indinavir, lopinavir, nelfinavir, ritonavir, and saquinavir) block the cleavage of viral proteins during assembly and maturation and are used in the treatment of which type of viral infection?

Back 4

Retroviruses, particularly HIV

Front 5

5. Identify the drug that appears to inhibit viral RNA polymerase and in combination with interferon is used in the treatment of chronic HCV infection.

Back 5

Ribavirin

Front 6

1. What are the pharmaco-dynamic and pharmacokinetic characteristics of azole antifungal agents (ketoconazole, itraconazole, voriconazole, and fluconazole)?

Back 6

The azole antifungal agents, which inhibit 14-sterol demethylase, promote structural and functional damage and cell death. Unfortunately, the azoles are not entirely selective for the 14-sterol demethylase enzyme. They also inhibit hepatic cytochrome P450 enzymes and are responsible for many drug-drug interactions. However, the extent of this inhibition is variable.

The access of antifungal agents to the site of infection depends on such factors as (1) their route of administration, (2) protein binding, (3) the concentration of the free drug in plasma and extracellular fluid, and (4) passive diffusion into foci of infection.

Front 7

2. What toxic reactions are associated with amphotericin B

Back 7

(1) an immediate systemic reaction or “cytokine storm” (release of TNF- and IL-1), characterized by fever, chills, and hypotension;
(2) renal toxicity, characterized by afferent arteriole constriction leading to renal ischemia;
(3) hematologic toxicity, characterized by anemia secondary to decreased production of erythropoietin.

Front 8

3. Because of severe systemic toxicity, the use of nystatin is strictly limited to the treatment of ______________.

Back 8

Superficial infections (oral & vaginal)

Front 9

4. What is the mechanism of action flucytosine?

Back 9

Inside the fungal cell, flucytosine is converted to 5-fluorouracil (5-FU) by the enzyme cytosine deaminase. 5-FU inhibits thymidylate syntase, an enzyme that mediates nucleotide synthesis, and prevents DNA and RNA synthesis.

Front 10

5. What is the mechanism of action of griseofulvin?

Back 10

Griseofulvin inhibits the assembly of microtubules and the activity of accessory proteins essential for the formation of the mitotic spindle and is preferentially toxic to cells in the M-phase of the cell cycle.