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Chlamydia trachomatis
- ADO
- A- azithromycin (single oral dose)
- D- Doxycycline (bis 7D oral)
- O- ofloxacin
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Adverse rxn of drugs for chlamydia trachomatis
- mostly GI
- mild to moderate
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Gonococcal
- ceftriaxone - single IM + single oral of azithromycin
- cefixime - single oral
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PID (in-patient)
- cefoxitin/ cefotetan (IV) + doxycyline (oral)
- clindamycin + amyloglycoside
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PID (out-patient)
ceftriaxone (IM) + doxycycline +/- metronidazole for 14D
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Bacterial vagionosis
- infected by anaerobes
- metroniazole (oral 7D/ intravaginal gel)
- clidamycin (oral/ intravaginal)
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Trichomoniasis
- infected by protozoa
- metronidazole/ tinidazole (single dose)
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Vulvovaginal candidiasis
- infected by fungi
- ropical azole antifungal agents
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Syphilis
- penicillin G (all stages)
- benzathine penicillin G (single IM as slow release for early latent stage)
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Genital warts
- podofilax (gel on visible lesion)
- imiquimod, 5-flurouracil, trichoroacetic acid
- intralesional alpha interferon (inject into warts; for recurrences)
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mechanism of imiquimod, 5-flurouracil, trichloroacetic acid
denatures proteins and warts
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mechanism of intralesional alpha interferon
cytokines
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Genital Herpes
- acyclovir (prototype)
- valacyclovir, famciclovir (prodrugs/ ACV derivatives)
- foscarnet, cidofovir (reserved for severe/ complications)
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mechanism of acyclovir
- ACV -> ACV triphosphate (active form)
- first phosphorylation -> viral thymidine kinase; second and third phosphorylation -> host's cellular kinases
- competitive inhibition of viral DNA polymerase by ACV triphosphate -> chain termination -> incorporation into viral DNA
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pharmacology of acyclovir
- an acyclic guanosine derivative with clinical activity against herpes infections
- first clinical -> oral, severe -> IV
- oral less effective for recurrences
- long term prophylaxis -> lower recurrences
- low bioavailability (15%)
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mechanism and pharmacology of valacyclovir
- an ester of ACV being converted to ACV by hepatic and intestinal enzymes
- only first clinical & recurrent
- bioavailability: 15-55%
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mechanism and pharmacology of famciclovir
- converted to penciclovir with similar action as ACV in viral shedding, lesion healing and resolution of symptoms
- only first clinical and recurrent
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HIV
HAART highly active antiretroviral therapy
- NRTI/ NtRTI (nucleoside/nucleotide reverse transcriptase inhibitor)
- NNRTI (non-nucleoside reverse transcriptase inhibitor)
- PIs (protease inhibitor)
- Entry inhibitor
- INSTI (intergrase inhibitor)
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Primary Goals of HAART
- prolong duration & quality of survival + reduce HIV-associated morbidity
- restore/preserve immunity
- maximally & durably suppress viral load
- prevent transmission
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example of NRTI/ NtRTI
- Zidovudine (NRTI)
- Tenofofir (NtRTI)
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mechanism of NRTI/ NtRTI
- active form: triphosphate form
- competitively inhibit HIV reverse transcriptase + viral DNA chain termination
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common toxicities of NRTI/ NtRTI
- lactic acidosis
- hepatic steatosis
- lipodystrophy
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example of NNRTI
- nevirapine
- efavirenz
- delavirdine
- etravirine
- rilpivirine
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mechanism of NNRTI
directly inhibit HIV-1 reverse transcriptase in a reversible and non-competitive manner
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common toxicities of NNRTI
- rash
- CNA
- interaction (met. by P450)
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toxicities of nevirapine
- hepatotoxicity
- rash e.g. Steven- Johnson Syndrome
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toxicities of efavirenz
- neuropsychiatric (vivid dreams)
- tetragenic (not prescribed in preg)
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use of NRTI
- slow disease progression
- prolong survival
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use of NNRTI
- suppress viral replication
- prevent perinatal HIV transmission
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examples of PIs
- saquinavir
- ritonavir
- lopinavir
- atazanavir
- darunavir
- fosamprenavir
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mechanism of PI
specifically inhibit HIV-1 protease
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toxicities of PI
- hyperlipidemia
- insulin resistance and diabetes
- lipodystrophy
- increase liver function test
- increase risk of bleeding in hemophiliacs
- interaction (P450)
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examples of entry inhibitors
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mechanism of enfuvirtide
inhibit fusion of viral gp41 with host cell
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mechanism of maraviroc
antagonise CCR5 chemokine co-receptor on CD4 T cells
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use of entry inhibitors
treatment of multi-drug resistance (MDR) CCR5- trophic HIV-1
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mechanism of INSTI
inhibit HIV-1 intergrase -> prevent propagation of viral infection
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indication of INSTI
treatment of HIV-1 infection in treatment-experienced adult patients who have evidence of viral replication and HIV-1 strains resistant to multiple antiretroviral agents
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