Question

1. Discuss why viral infections are uniquely hard to treat (compared to bacterial or fungal infections, for examples). Discuss the (limited) role of medication in the prevention and treatment of viral infections. 2. Identify the drug that is the agent of choice for most systemic mycoses; describe its main mechanism of antifungal action; and state whether it is best used for minor or more serious fungal infections and why. 3. Discuss why acyclovir is the drug of choice for most herpes simplex and varicella-zoster virus infections and explain the drug's main actions, uses, and other key clinical pharmacologic properties. 4. Discuss the education for patients regarding the transmission/prevention of Herpes Simplex. 5. Discuss some of the main impediments to proper, optimal therapy of HIVIAIDS, including not only pharmacologic considerations but also economic and compliance factors.

Answer 1

#. Viral infections are particularly difficult to treat because the pathogen is within the human host's cells and b/c the genetic info of the virus is directing the human cell to make viruses rather than to synthesize normal cell materials.

ANTIVIRAL Drugs :-

ACTION: Inhibit viral replication, Inhibit viral attachment, Prevent genetic copying of virus, Prevent viral protein production. Key characteristics: Able to enter the cells infected with virus. Interfere with viral nucleic acid synthesis and/or regulation. Some interfere with ability of virus to bind to cells. Some stimulate the body's immune system to kill the virus (ex: Interferon's)

#. 3 basic strategies for antiviral pharmacotherapy

1. Prevent viral infection through administration of vaccines

2. Treat active infections w/ drugs such as Zovirax that interrupt an aspect of the virus replication cycle.

3. For prophylaxis use drugs that boost pt immune response (immunostimulants)

#. Amphotericin B is active against a broad spectrum of pathogenic fungi and is a drug of choice for most systemic mycoses. Because of its potential for harm, amphotericin B should be employed only against infections that are progressive and potentially fatal.

Mechanism of action :-

It binds to ergosterol and disrupt the fungal cell membrane causing leakage of cells . Decrease viability of fungal cells.

#. Acyclovir is the drug of choice for most herpes simplex and varicella virus infections because of its mechanism of action

Mechanism of action:

Acyclovir

1. Monophosphorylated by viral thymidine kinase(TK), then further bioactivated by host-cell kinases to the triphosphate

2. Acyclovir-triphosphate is both a substrate for and inhibitor of viral DNA polymerase

Mechanism of action 2:

Acyclovir

1. When incorporated into the DNA molecule, acts as a chain terminator because it lacks the equivelent of ribosyl 3 hydroxyl group

2. Resistance possibly due to the changes in DNA polymerase to decreased activity of TK

3. >50% of HSV strains resistant to acyclovir completely lack thymidine kinase(TK-strains)

#. Prevention of herpes simplex :-

Avoidance of contact with a known infected lesion during the blistering phase can prevent the primary lesion .

Patients should also be taught to avoid sharing contaminated items such as toothbrushes, lipsticks, and drinking glasses. This disease can recur spontaneously. Avoidance of stressors, such as sunburn, injury, and fatigue, may delay a recurrence. The use of sunscreens, especially on the lips, may be helpful.