5348741
Descripción
Fichas por lpgalbraith, actualizado hace más de 1 año
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Creado por lpgalbraith
hace más de 8 años
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| Pregunta | Respuesta |
| What are the stages of viral replication? | 1. Fusion 2. Uncoating 3. Nucleic acid replication 4. Protein synthesis 5. Assembly and release of new virus |
| Which viruses are RNA based? | Influenza A, B, C Measles, mumps Rabies Polio, rhinovirus HIV Rubella, hepatitis Rotavirus |
| Which viruses are DNA based? | HSV, varicella, adenovirus, papilloma virus, smallpox |
| Which drug targets the fusion of viruses? | Enfurvitide - used as salvage therapy in HIV |
| Mechanism of enfurvitide? | Binds to gp41 in HIV surface, inhibiting CD4/HIV interaction |
| Side effects of enfurvitide? | Injection site pain, depression, infections (especially bacterial pneumonia) |
| Which drug targets uncoating of viruses? | Amantadine (influenza) |
| Mechanism of amantadine | Inhibits viral ion channel (prone to mutations). Ion channel required to get H+ ions into bleb |
| Side effects of amantadine | CNS (dopaminergic effects) - nervousness, anxiety, insomnia |
| Drugs that target nucleic acid replication? | Zidovudine (HIV), nevirapine (HIV), acyclovir (herpes) |
| Mechanism of zidovudine? | Inhibits reverse transcriptase in HIV, incorporates into viral DNA (nucleoside reverse transcriptase (viral enzyme) inhibitor), slows replication |
| Mechanism of nevirapine? | Non-nucleoside inhibits reverse transcriptase by binding at a non active site in HIV |
| Side effects of zidovidine and nevirapine? | Anaemia, bone marrow suppression, liver toxicity |
| Mechanism of acyclovir? | Inhibits DNA polymerase in herpes, incorporates in viral DNA - leads to chain termination. Requires activation by viral enzymes (thymidine kinase) - increases specificity |
| Side effects of acyclovir | Nausea, vomiting, headache |
| Anti-virals that inhibit protein synthesis | Indinavir (HIV), |
| Mechanism of indinavir | Binds to active site of HIV protease (protease inhibitor). Prevents cleavage of new proteins required for formation and assembly of virus coat |
| Side effects of indinavir | Kidney stones, hyperlipidaemia, restriction on what food can be taken and requires precise dosing |
| What antivirals inhibits release of viruses? | Oseltavir (tamiflu) for influenza |
| Mechanism of oseltavir | Blocks viral release by inhibiting influenza neuraminidase activity |
| Side effects of oseltavir | Nausea, vomiting, diarrhoea, headache, possible neurological (self harm) |
| How does HIV resist RT nucleoside inhibitors? | Mutation of the drug binding site on RT enzyme |
| How does HIV resist RT non-nucleoside inhibitors? | Single point gene mutations |
| How does HIV resist protease inhibitors | Mutation in HIV target protein, multiple mutations required for high level resistance |
| What are the types of fungi? | True yeast - single celled eukaryotic organisms e.g. Cryptococcus Yeast-like fungi - non branching filaments e.g. Candida albicans Filamentous fungi - branching filaments e.g. aspergillus |
| What are the targets of antifungal drugs? | Cell wall synthesis, nucleic acid and mitotic spindle |
| What groups of antifungals are cell wall synthesis inhibitors? | Polyenes Imidazoles Triazole Terbinafine |
| Which group of antifungal is a nucleic acid synthesis inhibitor? | Flucytosine |
| Which group of antifungals is a mitotic spindle inhibitor? | Griseofulvin |
| What is the mechanism of polyenes? | Generates a pore in the cell wall by binding to ergosterol |
| Side effects of polyenes | Few, used topically, some GI upset internally, nephrotoxicity |
| Examples of polyenes | Amphotericin - IV used for systemic fungal infection (C. albicans) Nystatin - C. albicans infection of skin and mucous membranes, oesophageal and intestinal candidiasis |
| Mechanism of imidazoles | Lead to growth arrest by inhibiting lanosterol demethylase - fluidity of cell wall increases, cell permeability increases. (lanosterol demethylase required for conversion of lansosterol to ergosterol) |
| Types of imidazoles and uses | Clotrimazole - vaginal candidiasis, ringworm Miconazole - locally for oral infections, intestinal infections Ketoconazole - best oral absorption, fatal hepatotoxicity, systemic mycoses, vulval candiasis |
| What is the mechanism of triazoles? | Also inhibits lanosterol demethylase |
| What are the types of triazoles and what are their uses? | Fluconazole - CSF penetration, candida, cryptococcus Itraconazole - mucocutaneous candidiasis (used with caution in HF as contraindicated with Ca channel blockers) Voriconazole - wide spectrum, life threatening aspergillosis |
| What is the mechanism of terbinafine? | Inhibits squalene epoxidase (converts squalene to lansosterol). Toxic levels of squalene build up, active against dermatophyte (ringworm of nail) |
| What is terbinafine contraindicated against? | Sub-acute cutaneous lupus |
| What is the mechanism of griseofulvin? | Interferes with microtubules of mitotic spindle, inhibits division of fungal cells - active against dermatophytes |
| Drugs used in aspergillosis | Amphotericin*, voriconazole |
| Drugs used in candidiasis | Amphotericin*, nystatin, fluconazole, flucytosine + iv amphotericin |
| Drugs used in cryptococcus? | Amphotericin iv, fluconazole po, flucytosine |
| Drugs used in histoplasmosis | Itraconazole*, amphotericin iv if severe |
| Drugs used in skin and nail | *Itraconazole, griseofulvin |
| Drugs used in immunocompromised | Fluconazole, amphotericin iv |
| What is the mechanism of flucytosine? | Inhibit conversion of uracil to DNA, only used in combination with amphotericin or fluconazole |
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