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ANTIVIRAL
| Question | Answer |
|---|---|
| Fusion inhibitors | Block ATTACHMENT: Maraviroc Block PENETRATION: Enfuvirtide |
| Integrase inhibitors | Raltegravir |
| Protease inhibitors | (-navir): Lopinavir, Atazanavir, Darunavir, Fosamprenavir, Saquinavir, Ritonavir, lndinavir |
| Reverse transcriptase inhibitors | 1. NRTI´s 2. NNRTI´s |
| NRTI´s (Nucleoside Reverse Transcriptase Inhibitors) | Tenofovir (TDF) Emtricitabine (FTC) Abacavir (ABC) Lamivudine (3TC) Zidovudine (ZDV,formerly AZT) Didanosine (ddl) Stavudine (d4T) |
| NNRTI´s (Non-Nucleoside Reverse Transcriptase Inhibitors) | END E= Efavirenz N= Nevirapine D= Delavirdine |
| Prevent maturation of new viruses | Protease inhibitors |
| Protease inhibitor that can "boost" other drug concentrations by inhibiting cytochrome P-450. | Ritonavir |
| Protease inhibitors; TOXICITY | 1. Hyperglycemia 2. GI intolerance (nausea, diarrhea) 3. Lipodystrophy. 4. Nephropathy 5. Hematuria (indinavir). |
| NRTI that´s a nucleotide analog and does NOT have to be ACTIVATED | Tenofovir |
| NRTI used for general prophylaxis and during pregnancy to reduce risk of fetal transmission. | Zidovudine (ZDV) |
| NRTI´s (Nucleoside Reverse Transcriptase Inhibitors); TOXICITY | 1. Bone marrow suppression 2. Peripheral neuropathy 3. Lactic acidosis (nucleosides) 4. Rash (non-nucleosides) 5. Anemia (ZDV). 6. Pancreatitis (Didanosine) |
| Bone marrow suppression caused by NRTI´s can be reversed with | Granulocyte colony stimulating factor (G-CSF) and erythropoietin |
| Reversibly inhibiting HIV integrase. | Raltegravir (Integrase inhibitors) |
| Raltegravir (Integrase inhibitors); TOXICITY | Hypercholesterolemia |
| Binds gp41, inhibiting viral entry | Enfurvitide |
| Skin reaction at injection site | Enfurvitide |
| Binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120 | Maraviroc |
| Inhibit influenza neuraminidase, decreasing the release of progeny virus. | Zanamivir, Oseltamivir |
| Zanamivir, Oseltamivir; CLINICAL USE | BOTH Inlfuenza A and B |
| Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase | Ribavirin |
| RSV, Chronic Hepatitis C | Ribavirin |
| Ribavirin; CLINICAL USE | RSV, Chronic Hepatitis C |
| Ribavirin; TOXICITY | 1. Hemolytic anemia 2. Severe Teratogen |
| Acyclovir (Nucleoside analog); MOA | Inhibits viral DNA polymerase by chain termination. |
| Acyclovir; CLINICAL USE | 1. HSV and VZV 2. HSV encephalitis; Prophylaxis in immunocompromised patients. |
| Prodrug of acyclovir, has better oral bioavailability. | Valacyclovir |
| Herpes zoster | Famciclovir |
| Acyclovir; TOXICITY | Obstructive crystalline nephropathy and acute renal failure if NOT adequately HYDRATED!!! |
| Acyclovir; MECHANISM OF RESISTANCE | Mutated viral thymidine kinase |
| CMV | Ganciclovir, Foscarnet |
| Ganciclovir; TOXICITY | MORE toxic to host enzymes than Acyclovir 1. Leukopenia 2. Neutropenia 3. Thrombocytopenia 4. Renal toxicity |
| MORE toxic to host enzymes than Acyclovir | Ganciclovir |
| Foscarnet; MOA | Pyrophosphate analog |
| Inhibit viral Nucleic Acid synthesis | 1. Guanine nucleotide synthesis: -Ribavirin (RSV, HCV) 2. Viral DNA Polymerase inhibitors: -Foscarnet (CMV) -Cidofovir (HSV Acyclovir resistant) 3. Guanosine analogs: -Acyclovir (HSV, VZV) -Ganciclovir (CMV) |
| Foscarnet; CLINICAL USE | 1. CMV retinitis in immunocompromised patients when ganciclovir fails 2. Acyclovir-resistant HSV. |
| Foscarnet; MECHANISM OF RESISTANCE | Mutated DNA polymerase |
| What decreases Cidofovir toxicity | Coadminister with Probenecid and IV saline |
| Glycoproteins synthesized by virus-infected cells | Interferons |
| Interferons; MOA | block replication of both RNA and DNA viruses. |
| IFN-Alpha | 1. Chronic Hepatitis B and C 2. Kaposi sarcoma 3. Hairy cell leukemia 4. Condyloma acuminatum 5. Renal cell carcinoma 6. Malignant melanoma |
| IFN-Beta | Multiple sclerosis |
| IFN-Gamma | Chronic granulomatous disease |