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TREATMENT AND DRUGS MECHANISM OF ACTION SECONDARY SYPHILLIS M. ZHAFRAN DARWIS (C111 11 146) MAGHFIRAH MAHMUDDIN (C111 11 310) NURFADILLAH (c111 10 310)

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Page 1: Slide Sifilis

TREATMENT AND DRUGS MECHANISM OF ACTION

SECONDARY SYPHILLISM. ZHAFRAN DARWIS (C111 11 146)

MAGHFIRAH MAHMUDDIN (C111 11 310)NURFADILLAH (c111 10 310)

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What is SyphillisA disease caused by the

spirochete Treponema pallidum subspecies pallidum

that is usually sexually transmitted.

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Syphiliis StagesSyphilis passes through four distinct clinical phases:1. Primary stage, characterized by a chancre.2. Secondary stage, characterized typically by skin

eruption(s) with or without lymphadenopathy and organ disease.

3. A latent period of varied duration, characterized by the absence of signs or symptoms of disease, with only reactive serologic tests as evidence of infection.

4. Tertiary stage, with cutaneous, neurologic, or cardiovascular manifestations.

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Secondary syphillis Secondary syphilis is the stage when

generalized manifestations occur on the skin and mucous membranes. Serological tests are always positive in immunocompetent persons. Rashes in secondary syphilis have three common features:

1 they do not itch2 they are coppery red3 the lesions are symmetrically distributed

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Treatment of Syphillis

CDC recommendation

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Follow up syphillisFollow-up for clinical and serological

assessment should be done at 3, 6 and 12 months after the completion of treatment in early syphilis.

Non-treponemal antibody test titres correlate with disease activity and will usually become negative with time after successful treatment. In some patients

Treatment failure is suggested by a fourfold increase in titres

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titer for each person diagnosed with syphilis must be obtained on the day-of-treatment

In persons treated for secondary syphilis, the tests usually become nonreactive 12–24 months after treatment.

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The Jarisch–Herxheimer reaction The Jarisch–Herxheimer reaction is a self-limited

clinical syndrome consisting of Feverheadache flare of mucocutaneous lesionstender lymphadenopathy, pharyngitis, malaise,

myalgias, and leukocytosis.It occurs within 12 hours of initiating therapy and

resolves within 24–36 hours. The pathogenesis of the Jarisch–Herxheimer

reaction is unknown, but is thought to result from cytokine release mediated by the release of lipoproteins from dying T. pallidum organisms

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Penicilin Penicillins are members of the β-lactam

family.All penicillins have a nucleus composed of a thiazolidine ring and β-lactam ring, which

is required for antibiotic activity

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Penicilinpoorly absorbed and unstable at low PhPenicillins are widely distributed in body

fluids and tissuesNatural penicillins can interact with amines

(such as procaine and benzathine) to form salts with relatively low solubility; administered intramuscularly, penicillin is released more slowly, prolonging drug delivery

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bind to specific penicillin binding proteins (PNBs)

inhibit cell-wall peptidoglycan synthesis

inactivate an inhibitor of autolytic enzymes

present on bacterial cell walls.

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TetracyclineTetracycline is incompletely absorbed

primarily in the stomach and small intestineDoxycycline is excreted in the feces and no

adjustments for renal or hepatic failure are necessary

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Tetracycline

Tetracyclines inhibit bacterial protein synthesis by binding to the 30s ribosomal subunit and blocking

transfer RNA binding to the mRNA-ribosome complex

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