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24 Cards in this Set
- Front
- Back
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Member Drugs in the Macrolide class (3)
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1. ERYTHROMYCIN
2. CLARITHROMYCIN 3. AZITHROMYCIN |
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Spectum of action of Macrolides |
BROAD SPECTRUM
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Mechanism of action of Macrolides (2)
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- INHIBIT PROTEIN SYNTHESIS, and
- INHIBITION OF SYNTHESIS 50S ribosomal sub-unit |
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Mechanisms ofresistance of Macrolides (3)
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- IMPAIRED INFLUX OR INCREASEDEFFLUX
- RIBOSOME PROTECTIVE –MODIFICATION OF BINDING SITE or METHYLASES (Constitutive or Inducible) - INCREASED METABOLISM(ESTERASES) |
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Three important things to remember |
- Cross-Resistanceoccurs across all macrolides,
- Constitutive methylase confers resistance to structurallydifferent but mechanistically similar compounds e.g. CLINDAMYCIN andSTREPTOGRAMIN-B. [This resistance is referred to as Macrolide-Lincosamide-Streptogramin(MLS-type B) resistance] - Non-Macrolides do not induce methylase production |
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Absorption of Macrolides
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- Erythromycinbase – destroyed by gastric acid. Enteric coated tablets.
- Foodinterferes with absorption - Steratesand esters are acid resistant |
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Distribution of Macrolides
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- Goodbut not in the CNS
- Crossesthe Blood Placenta Barrier - Takenup by polymorphonuclear leukocytes |
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Metabolismof Macrolides
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Byliver enzymes
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Excretionof Macrolides
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- Bilemajorly
- Half-lifeincreased in anuric patients BUT dose adjustment not necessary |
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Clinical Uses of Erythromycin (10)
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- Chlamydiasp (trachomatis, pneumoniae)
- Mycoplasmapneumoniae - Legionellapneumophilia - Listeriamonocytogens - Helicobacterpylori (gastro-duodenal ulcers) - Bordetellapertussis (Whooping cough) - Rickettsiaeinfections - Bartonellasp - Campylobactersp. (C.jejuni – secretory or bloody diarrhoea) - Treponemapallidum (Syphillis) |
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Adverse Reactions of Macrolides (4)
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- GIT– Anorexia, nauseas, vomiting, and diarrhoea
- AcuteChoestatic Jaundice - Metabolistesinhibit Cytochrome P450 enzymes - Increasesbioavailability of digoxin |
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CLARITHROMYCIN
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Drug derived from erythromycin |
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Why is CLARITHROMYCIN is better than Erythromycin? (4) |
- More acid stable
- More active against H.influenzae,Mycobactera Avium Complex, and Toxoplasma gondi - Longer half-life (6 hours) - Distribution good – even CNS |
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Metabolism and dosage (in renal failure) of CLARITHROMYCIN |
- Liver; metabolite has antibacterial activity
- Dosage adjustment recommended in renal failure of CrCl <30mL/min |
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AZITHROMYCIN
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Also derived from erythromycin |
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Spectrum of action for Azithromycin |
- Activity against Staph and Strep << than clarithromycin anderythromycin; but more active against H. influenza.
- Highly active againstchlamydia |
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Distribution of Azithromycin |
- Penetrates tissues and phagocytes VERY WELL, but not CNS!
- Concentrationin tissues 10-100x plasma concentrations. Tissue t ½ 2-4 days - Eliminationt ½ is ~3 days; permits once daily dosing, and for a few days |
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Absorption of Azithromycin |
- Absorption is rapid, and is well tolerated orally.
- Administer 1hourbefore or 2 hours after meals |
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Something special of Azithromycin |
Does not inhibit CYP450
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What the hell is KETOLIDES– TELITHROMYCIN?
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- Semisynthetic macrolide
- Cladinose substituted by a 3-keto group |
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Clinical USE of Ketolides - Telithomycin |
Community Acquired Pneumonia
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Excretion of Ketolides - Telithomycin
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- biliary and urinary
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Mechanism of action of Ketolides - Telithomycin |
CYP3A4 reversibly |
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Adverse effects of Ketolides - Telithomycin |
Hepatitis and liver failure
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