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Pharm - Exam 2 - Antiviral Agents
Terms in this set (25)
Drugs used for viral infections:
STRATEGY: Inhibit/Block _________-___________ replication steps.
- So, they ________________ (they don't "kill") viruses.
•Many of these drugs are nucleic acid analogs.
•Cause some toxicity to host, since viruses are genetic "parasites" that hijack host machinery to replicate.
•Major problem to effective Tx: Viral mutations that result in ________________ viral variants.
A. RNA virsuses
a. Enter cell --> _____________ --> exit cell --> ______ cell on release
B. DNA viruses
a. Enter cell --> exit cell --> ________ from cell membrane
Drugs used for Influenza (RNA) Viruses
Influenza A and B
Two drug categories:
2) neuraminidase (N) inhibitors
1) _______________________ and rimantadine
-MOA: Block the virus from ________________
•most influenza strains are now resistant
2) _________________ (Tamiflu)
MOA: Prevent _______________ and
release of new virus
1) Amantadine, uncoating
2) Oseltamivir, budding
To be effective, the drugs used for Influenza (RNA) Viruses need to be taken within ____ to ______ h (and no later than ________hrs) after symptom onset.
**Otherwise, the infection has established itself in the body, and the benefits of the drug (which shortens the time of illness and reduces symptom severity) will be much less.
To be effective, they need to be taken within 30 to 36 h (and no later than 48h) after symptom onset.
_____________ is a leading cause of hospitalization and morbidity and mortality in infants and young children
-______________ (inhaled); generally well tolerated; given as aerosol for 3d -1wk. Pregnancy category X!!
-_________________ (Synagis) - a monoclonal antibody (MoAb) used in preemies & in young children with chronic lung disease. Given IM; no side effects except for rare hypersensitivity reactions.
RSV (Respiratory Syncytial Virus)
**study tip: my pal from MoAb has chronic lung disease; his older brother always Rib's him about it
Drugs to treat HIV infections: ART (Antiretroviral Therapy) Options
•Nucleoside reverse transcriptase inhibitors (NRTI)
•Protease inhibitors (PI)
Non-nucleoside reverse transcriptase inhibitor
Integrase strand transfer inhibitor
-They are _____________; activated within cell --> inhibit reverse transcriptase (RT) --> so cause _____________ chain termination.
•Special side effects:
-All NRTIs can cause a rare but potentially fatal syndrome: lactic ______________ with hepatic ____________ (fatty liver).
•Only used as _________________ Tx with other drug classes
What is the main A/E to the following NRTIs:
1) bone marrow depression
2) hyperpigmentation of palms and soles
Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
•Also inhibit RT activity- individual agents differ in structure and in MOA
•Active only against __________; directly bind to & inhibit RT
-Well tolerated; resistance develops quickly
•________________ use + other antiretroviral drugs.
•All are metabolized by the _______________________ system.
**Tx compliance is critical to prevent NNRTI resistance
liver cytochrome P450
Protease Inhibitors (PI)
HIV codes for a protease required for cutting its polypeptide precursors that generate its structural proteins and enzymes, including RT, integrase, and the protease itself.
-MOA: Protease inhibitors bind to the protease's _________ site and prevent it from cleaving the protein precursors- thus blocking viral ________________.
Protease Inhibitors (PI)
______________ used in Combination Therapy: a protease inhibitor + two nucleoside analogues.
•______________ (Prezista): newer PI used for treatment of naïve patients (except for those with sulfonamide allergies)
Integrase Inhibitors (INSTI)
MOA: They inhibit the ability of the HIV _______________________ to insert HIV __________ into host DNA, thus stopping HIV replication
-->abacavir, lamivudine, dolutegravir - one tablet
Side /Adverse effects: well tolerated, other than some GI effects
integrase enzyme, DNA
Fusion Inhibitors (FI)
enfuvirtide: (Fuzeon), a synthetic peptide
MOA: prevents the HIV ________________ from fusing with the CD4 HIV receptor on cell membranes, thus stopping viral ____________ and _______________
Triple therapy with a _____________________ + two _________________ analogs is more effective (i.e., "drug cocktails")
ART (antiretroviral therapy)
-2 NRTI + 1 NNRTI
-2 NRTI + 2 protease inhibitors
-2 NRTI + Integrase Inhibitor or Fusion Inhibitor
protease inhibitor, nucleoside
•When patients follow the prescribed ART regimens, HIV can be combatted successfully and turns into a __________________ with most sufferers, although the drugs we've covered have many unpleasant side effects.
•However, 1.2 million Americans have HIV, and out of those, about 10,000 have MDR HIV, which means _________________ to all medications used to treat HIV.
-NOTE WELL :
•although viral load decreases to nearly undetectable levels with some treatments in many patients, retroviruses are ____________________________ by antiviral treatments
MDR HIV = resistance to all meds used to treat HIV
never completely eliminated
Some Antiviral Drugs for Agents of Chronic hepatitis:
(a _______________ virus): No known cure- so vaccinate!!
NOT considered a retrovirus, but has a _______________ transcriptase.
Others we don't cover here
(a ___________ virus)
Ribavirin + interferon alfa
Others we don't cover here
**Hep C (i.e. HCV) is the leading cause of ______________________ & death (greater than HIV deaths)
RNA, liver transplants
**Study Tip: Heppy BDay, here's a gift of Hep CRayons
Drugs for chronic HBV Infection
•The standard therapy consists of two different types of drugs, nucleotide or nucleoside analogues.
•They stop HBV reproduction by acting as false substrates for the reverse transcriptase (RT) in the replication cycle of the virus; so, they terminate the elongation of viral genome DNA prematurely.
•Newer drugs like _______________ (nucleoSide analogue) and ____________(nucleoTide analogue) have reduced the risk of drug resistance.
•Patients compliant with NRTI therapy (which is well-tolerated) can expect sustained _______________ viral suppression with reliably achievable, undetectable HBV DNA levels.
**study tip: T's go together for tenofovir and nucleotide
Interferon (IFN) alfa-2b [Intron A]
•_____________ cells make IFN as part of the antiviral ______________ response. It increases patient immune response to viruses.
•IFN also inhibits viral replication cycles by multiple inhibitory effects. After binding to receptors on host cell membranes, IFN blocks:
-viral entry into cells and other steps in the viral replication cycle
•Parenteral administration for HBV infection:
-Adverse effects include _____________ symptoms, diarrhea, abdominal pain, bone marrow suppression, and cardiotoxicity; neuropsychiatric symptoms- notably __________________.
Drugs for chronic Hepatitis C (HCV) Infection
**used in combinations; expensive; many adverse effects and multiple drug interactions
•ribavirin + __________________
-ribavirin (remember, it is also used to treat RSV (respiratory syncytial virus)
•_____________ (Incivek) - A Protease Inhibitor
•____________ (Sovald) - A nucleoside analog viral DNA polymerase inhibitor
**study tip: P for telaPrevir matches Protease Inhibitor; S with SofoSbuvir matches nucleoSide analog viral DNA polymerase inhibitor
Drugs for DNA Virus Infection (i.e. Herpes, varicella-zoster, CMV)
Drugs used are _____________________________________
Nucleic Acid Inhibitors
-must first be activated by the viral thymidine kinase enzyme
-can be administered orally, IV, and topically
-oral Acyclovir ___________ during pregnancy
•MOA: Inhibits ____________________ by stopping viral DNA strand growth after it is incorporated
•ONLY Effective against ____________viruses like VZV (chicken pox) and herpes simplex [HSV-1 (oral herpes) and HSV-2 (genital herpes)] - CMV strains are generally resistant
•Adverse effects: __________- nausea, diarrhea; headache, vertigo
•Low oral bioavailability; topical not significantly absorbed into system
•Short T1/2 ~ 2.5 h (so must be given orally 5x/day); inexpensive
________________ (Valtrex, a prodrug of acyclovir with higher bioavailability); used for genital herpes to reduce transmission risk between _________________ heterosexual partners
•Deoxyguanosine; needs intracellular activation by viral enzyme.
•Administration: Oral, IV, ocular implants, ocular gels
•MOA: blocks viral ____________ strand growth.
-->Reproductive system toxin; can cause infertility; __________________ and ________________________.
•Indication: Used almost exclusively to prevent & Tx existing ____________ infection in immunocompromised, immunosuppressed, and __________ patients.
•Adverse effects: ______________ toxic than Acyclovir; causes bone marrow suppression (granulocytopenia, thrombocytopenia)
______________________ (Abreva) - OTC
-A fat-derived molecule used for Herpes labialis (HSV-1) - caused cold sores and fever blisters.
•Moderate relief; _______________________ reported.
-inhibits fusion between the cell plasma membrane and the HSV viral envelope --> ________________ entry so virus can't replicate; ________________ inactivate the virus!
-Viral replication NOT affected- so does NOT ______________ resistance.
No side effects
Review Slide 31 on Antiviral PP
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