1- Antifungals and Antivirals
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44 terms
Terms | Definitions |
|---|---|
| oSignificant difference in membrane is ergosterol in membrane instead of cholesterol [Major target] oSo drugs inhibit synthesis or inhibit it from working oBeta-glucans link together to make cell wall, so recently new drugs target the synthesis of this wall oazoles inhibit step of ergosterol synthesis |  How Antifungal Drugs work |
| Amphotericin B Flucytosine Caspofugin Itraconazole | What are the 4 Systemic Antifungals Drugs |
| Nystatin Terbinafine Miconazole | What are the 3 superficial antifungal drugs |
| Not much resistance to this drug and no superinfections | Amphotericin B- resistance |
| •binds ergosterol (complex 1-1, forming a pore through the membrane) ocholesterol has sigmoidal shape so can't bind to it •disrupt fungal cell membrane function | Amphotericin B-Mechanism |
| •used for most systemic fungal infections •broad spectrum: treat leishmaniasis •not absorbed orally; must be IV | Amphotericin B- therapuetic uses |
| •nephrotoxicity (lipid formulations of drug less nephrotoxic) •transient fever and chills following intravenous administration | Amphotericin B- Adverse Effects |
| •inhibits synthesis of cell wall polysaccharides (beta-glucans) | Echinocandins (caspofungin)- mechanism |
| •alternate therapy for the treatment of serious systemic fungal infections •poor oral absorption; give IV | Echinocandins (caspofungin)- therapeutic uses |
| prodrug form •selectively activated by fungal-specific enzyme (cytosine deaminase) oamine group is removed and converted into 5-fluorouracil (anticancer drug) •inhibits DNA synthesis oinhibits thymidylate synthetase enzyme (makes thymine nucleotides) | flucytosine- mechanism |
| •used in combo with Amphotericin B or itraconazole (syntergistic); allows for drug to inside membrane | flucytosine- therapeutics |
| •enterocolitis ocan act on proliferating cells in GI tract •bone marrow suppression oin GI tract, the bacteria there have thymidylate synthetase to suppress bone marrow or if pt has underlying bone marrow problem already obad for pt on chemotherapy | flucytosine- adverse effects |
| •inhibits cytochrome P-450 mediated synthesis of ergosterol by fungi | itraconazole- mechanism |
| •broad spectrum antifungal agent | itraconazole- therapeutics |
| •can increase the plasma levels of other drugs (phenytoin, cyclosporine) odue to P-450 inhibition by inhibiting the drug's metabolism by the liver | itraconazole- drug interactions |
| mechanism: same as amphotericin B/ binds ergosterol only useful for treatment of candidiasis not absorbed in GI tract, can take orally | nystatin: mechaism, therapeutic use, how taken |
| mechanism same as itraconazole (inhibits biosynthesis of ergosterol) useful for treatment of candidiasis and tinea pedia (athlete's foot) primarily used as a cream | micronazole: mechanism, theraputic use, how taken |
| •inhibits ergosterol biosyntehsis by a different mechanism than Miconazole | terbinafine: mechanism |
| •taken orally for treatment of severe or extensive superficial infections oconcentrates in keratin (keratinophilic) oespecially in toe and fingernails •can also be used topicaly | terbinafine: therapeutic uses |
| ohemagglutinin and neuraminidase on cell surface, allows virus to bind to membrane that it is going to affect odrug that targets late step of process is oseltamivir (prevent release of virus from infected cell) | Antiinfluenza agents - how work |
| •neuraminidase inhibitor (reduces viral spread in respiratory tract) •active against influenza A and B virus | oseltamivir: mechanism |
| •treatment and prophylaxis of influenza | oseltamivir: clinical use |
| oDNA viral infection; envelope virus that binds to surface and releases DNA which then transcripts and replicates and assembles into new viral particles Most drugs selectively against replication phase (target DNA polymerase and a viral thymidine kinase) | herpes virus drugs: how work |
| acyclovir, foscarnet | 2 Types of herpes virus drugs |
| looks like deoxyguanosine; missing part of surgar PRODRUG •blocks viral DNA synthesis oselectively phosphorylated by viral thymidine kinase inhibits viral DNA polymerase causes chain termination when incorporated into viral DNA | acyclovir: mechaism |
| •herpetic infections (herpes simplex, varicella zoster) onot very active against cytomegalovirus (CMV) •ganciclovir: nucleoside analogue; more active against CMV (can cause bone marrow suppression) •drug-resistant strains emerging in AIDS patients | acyclovir: clinical use |
| •renal toxicity when solubility levels exceeded: drug precipitates •does not appear to be carcinogenic or mutagenic or teratogenic | acyclovir: adverse effects |
| •pyrophosphate-like compound (diphosphate, byproduct of DNA replication) •selectively inhibits viral DNA polymerases and HIV reverse transcriptase by interacting with pyrophostphate binding site •does not require activation to inhibit polymerase, acts directly (unlike acyclovir) | foscarnet: mechanism |
| •herpetic infections (CMV, varicella zoster, HSV) •HIV infections | foscarnet: clinical use |
| •Nephrotoxicity •Hypocalcemia | foscarnet: adverse effects |
| -binds to cell surface oReverse transcription is blocked by NRTIs and NNRTIs oIntegration is blocked by integrase inhibitors oBudding and maturation is blocked by protease inhibitors | HIV life cycle |
| reverse transcriptase inhibitors and protease inhibitors | Anti HIV drug mechanisms |
| -NRTI (thymidine analogs, cytidine analogs, purine analogs] -NNRTI (looks nothing like nucleosides) | types of Anti HIV reverse transcriptase inhibitors |
| Zidovudine/AZT | Example of a NRTI drug (nucleoside reverse transcriptase inhibitor) |
| Dideoxynucleoside analogue Pyrimidine nucleoside analogue similar to thymidine Prodrug: triphosphate form of drug inhibits viral polymerase Incorporation into viral nucleic acid causes chain termination | Zitdovudine/AZT: mechanism |
| Bone marrow suppression Mitochondrial syndrome (lactic acidosis) •Probably due to inhibition of mitochondrial DNA polymerase | Zitdovudine/AZT: adverse effects |
| Nevirapine | Example of a NNRTI (non-nucleoside reverse transcriptase inhibitor) |
| Does not require activation and binds to different (non-essential) site than AZT away from enzyme catalytic site Synergistic in combo with nucleoside HIV inhibitors (AZT) Active against HIV1 (what see in clinics) but not HIV 2 | Nevirapine: mechanism |
| don't overlap with nucleoside HIV inhibitors (NRTI drugs) | Nevirapine: toxicity and resistance patterns |
| Hypersensitivity reaction: SJS Liver toxicity | Nevirapine: adverse effects |
| Can increase the hepatic metabolism of other drugs | Nevirapine: drug interaction |
| Ritonavir | Example of a Protease inhibitor |
| opeptidomimetic drug that inhibits HIV encoded aspartate protease | Ritonavir: mechanism |
| oLipdystrophy (buffalo hump) oDrug interactions: can inhibit the metabolism of other drugs | Ritonavir: adverse effects |
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