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53 Cards in this Set
- Front
- Back
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What are the names of the macrolides?
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erythromycin, clarithromycin, azithromycin
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Where are the macrolides distributed?
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widely, except for the CNS.
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How are the macrolides metabolized and excreted?
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primarily liver and bile
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What is azithromycine used for?
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S. pneum, Mcyoplasma, H. flu and Legionnaires
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What is doxycycline used for?
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GU chlamydia
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What is clairithromycin + amoxicillin or metronidazole used for?
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H. pylori causing ulcers
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How do macrolides cause GI distress?
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it is a motilin receptor agonist which causes GI secretions and contraction
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What is the primary reason for cessation of macrolides?
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GI distress
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What causes cholestatic jaundice?
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erythromycin estolate
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What does prolonged Qt interval lead to?
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polymorphic ventricular tachycardia
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What can occur if a calcium channel blocker and erythromycin are administered together?
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high risk of sudden cardiac death
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How does erythromycin cause polymorphic ventricular tachycardia?
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erythromycin inhibits K channel, leading to cardiac arrhythmia
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Describe what happens when erythromycin and verapamil are administered together.
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plasma erythromycin elevates via competition w/ Ca channel blockers for hepatic metabolism. increased cardiac concentrations of either drug due to competition at level of multi-drug efflex pump (P-glycoprotein)
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What are the key points to know about macrolides?
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orally active, not for CNS, useful for GU chlamydia, Leigonnaires, H pylori, streptococcus, MSSA and H. flu; causes GI distress and ventricular tachycardia
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What is the basic structure of aminoglycosides?
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highly polar, poor cellular penetration including the CNS
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What is the MOA for aminoglycosides?
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diffuses through the OM porins, active transport through the inner membrane. Acts at specific binding site on 30S; inhibition of protein synthesis as well as abberrant protein synthesis. insert these abberrant proteins into membranes, increasing membrane permeability and further increasing A.G entry into cell. cell death is secondary to disruption of cell envelope and other proteins
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How are aminoglycosides absorbed?
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parenteral only (IV or IM)
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What are the exceptions to the poor penetration rule for aminoglycosides?
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renal cortex and perilymph and endolymph of 8th nerve
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How is resistance conferred for aminoglycosides?
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bacterial drug metabolism-phosphorylation, adenylation, acetylation
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What type of dosing regimen should aminoglycosides be given?
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peak/trough
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How can penicillin interact with aminoglycosides?
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may decrease plasma half life of aminoglycoside and may also inactivate aminoglycoside via chemical interaction
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What are risk factors for oto and nephrotox associated with aminoglycosides?
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geriatric, dehydration, renal impairment, long term high dose therapy, other ototoxic or nephrotoxic drugs
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Why is aminoglycoside otoxtoxic?
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1/2 life in otic fluid is much greater than in blood. With a single daily dose, trough in plasma enhances back diffusion from otic fluids.
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What is ototoxicity caused by aminoglycosides exacerbated by?
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noise and loop diuretics (also ototoxic and may increase AG concentration in otic fluid)
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How are aminoglycosides nephrotoxic?
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they increase BUN and creatine, decrease urine specific gravity, proteinuria and cells or casts in urine.
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How can you minimize risk of nephrotoxicity with aminoglycosides?
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maintain hydration
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What drugs exacerbate nephrotoxicity of AG?
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indomethacin, vancomycin, some beta-lactams
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What patients are predisposed to neuromuscular blockade from AGs?
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anesthesia, myasthenia gravis, high dose direct application such as respiratory paralysis with topical application to chest
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What are other nervous system effects of AGs?
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h/a, peripheral neuropathies, tremor, depression, blurred vision w/ high doses
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What are key points to remember about aminoglycosides?
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peak-trough regimen, toxicities and adverse rxns (ototox, nephrotox), combination w/ penicillins and cephalosporins
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What is the mechanism of action for chloramphenicol?
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broad spectrum; bacteriostatic-binds to 50S ribosome and inhibits protein synthesis
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What type of organism is chloramphenicol good for?
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anaerobes
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What specific proteins does chloramphenicol inhibit?
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mitochondrial proteins
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How do organisms become resistant to chloramphenicol?
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inactivation of drug by bacterial acetylation; CA falis to bind 50S ribosome when acetylated. may also be decreased cellular permeability and mutations in 50S ribosomal binding site for CA
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What is unique about the distribution of chloramphenicol?
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it has uniquely high CSF/plasma distribution
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How is chloramphenicol metabolized/excreted?
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hepatic inactivation by glucuronidation
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How does gray baby syndrome happen?
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excessive plasma CA leads to undeveloped hepatic conjugation and inadequate renal elimination. presents with vomiting, decreased respiration, green color of loose stools, hypothermic, cyanotic and possible death
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What are therapeutic uses for chloramphenicol?
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H. flue meningitis (cidal in this case), alternative to penicillin for other causes of bacterial meningitis, anaerobes, Rickettsial disease
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What are the adverse effects of chloramphenicol?
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bone marrow toxicity, aplastic anemia/pancytopenia
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In chloramphenicol-induced anemia, what does the severity correlate with?
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the lag time between the end of therapy and toxicity; the longer it takes to develop, the more fatal.
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What are therapeutic uses of clindomycin?
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b. fragilis (except in CNS), necrotizing fascilitis
**anaerobic!** |
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How is clindamycin metabolized/eliminated?
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hepatic metabolism, renal excretion
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What are adverse effects of clindomycin?
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diarrhea, pseudomembranous colitis due to C. difficile (fever, abdominal pain, diarrhea, mucus and blood in stool, white/yellow plagues on mucosa of colon)
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What type of organism does metronidazole work on?
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anaerobes
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Where in metronidazole contraindicated?
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1st trimester pregnancy
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What are toxicities associated with metrinonidazole?
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ETOH intolerance, neuropathy, urethral burning, discolored urine
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What is the mechanism of action of metronidazole?
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pro drug metabolized to reactive products intra-cellularly in mammals and microbes. Products react with functional groups of DNA and protein.
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What is the distribution of metronidazole?
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CNS, absesses, vaginal secretions
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How is metronidazole excreted?
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determined by hepatic metabolism; adjust systemic dose for hepatic dysfunction
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What are therapeutic uses for metronidazole?
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antibacterial for anaerobes
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What are adverse effects of metronidazole?
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h/a, nausea, dry mouth/sharp unpleasant taste, neural (rare; peripheral (numb, tingle, parasthesia), CNS (vertigo, dizzy, ataxia, confusion)), GU (urethral burning/pressure in perineum/polyuria/incontinence, dark/reddish brown urine, blood dyscrasias, antabuse reaction
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Why is metronidazole contraindicated in 1st trimester?
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drug distribution, mechanism of action and mutagenic effects at high doses in experimental animals.
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How are oral contraceptives made less active with antibiotics?
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Liver conjugates steroids and changes them to become water soluble. bacteria will conjugate
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