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16 Cards in this Set
- Front
- Back
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Selective Toxicity |
Ability of an antibiotic to harm microbial pathogens without harming host cells. Three mechanisms to achieve selective toxicity: disruption of bacterial cell wall (causes lysis), inhibition of a unique enzyme (typically used to synthesize folic acid), disruption of bacterial protein synthesis (targets bacterial ribosomes). |
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Narrow Spectrum Antibiotics |
Active against only a few species Generally preferred because they kill only the causative agent |
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Broad Spectrum Antibiotics |
Active against a wide variety of species More likely to cause bacterial resistance More likely to kill off normal flora leading to superinfections Used when the group of bacteria causing the infection is unknown or when multiple groups are suspected |
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Mechanisms of Resistance Development |
Reduction of drug concentration at site of action Alteration of drug target molecules Antagonist production Drug inactivation (by producing drug-metabolizing enzymes) |
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Spontaneous Mutations |
Method of how bacteria can acquire resistance Produce random changes in bacterial DNA that gradually increase resistance; confer resistance to only one drug |
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Conjugation and R Factors |
Method of how bacteria can acquire resistance Extrachromosomal DNA (an R factor) is transferred between bacteria; is not species specific Can confer resistance to multiple drugs |
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Indications for Prophylactic Antibiotic Treatment |
Surgery Bacterial endocarditis (can occur with people with heart disease and prosthetic heart valves) Neutropenia |
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Consequences and Examples of Misuse of Antibiotics |
About 50% of antibiotic prescriptions are used inappropriately Attempted treatment of viral infection: patient unlikely to benefit; may develop severe adverse/allergic reactions Treatment of fever of unknown cause: can delay correct diagnosis of infection/cause Improper dosage: too low (patient is exposed to adverse effects without beneficial treatment), too high (can cause superinfection and adverse effects) Treatment without adequate knowledge of bacteria Omission of surgical drainage: antibiotics often don’t help |
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Gram-Positive Bacteria |
Two layers to cell wall Cell wall is easily penetrated |
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Gram-Negative Bacteria |
Three layers to cell wall Thin cell wall with additional membrane that is hard to penetrate |
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Mechanism of Action of Penicillins |
Bactericidal Disrupt cell wall synthesis Weakening the cell wall causes bacteria to take up excess water and burst Core structure of penicillins is called the beta-lactam ring |
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Inactivation of Penicillins |
Bacteria can produce penicillinases (beta-lactamases) that can inactivate the beta-lactam ring of beta-lactam antibiotics |
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Allergic Reactions to Penicillin |
Allergy test for penicillin should be performed before administration If patient has history of mild reaction, cephalosporins can be considered If history of anaphylaxis, avoid penicillins and cephalosporins |
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Hypersensitivity Reactions to Penicillin |
Immediate: onset is 2-30 minutes; anaphylaxis (laryngeal edema, bronchoconstriction, hypotension) Accelerated: onset is 1-72 hours Delayed: onset is days or weeks |
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Characteristics of Vancomycin (Vancocin) |
Given IV Action: inhibits cell wall synthesis; doesn’t contain beta-lactam ring Uses: severe infections only that have resistance to many other drugs (MRSA, staph., C. Diff) Many adverse effects: ototoxicity, nephrotoxicity, red man syndrome, thrombophlebitis, thrombocytopenia, allergy |
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Serum Lab Values that Test Vancomycin Levels |
Peak: 25-40 mcg/mL; drawn 30 min after giving dose Trough: 5-10 mcg/mL; drawn 30 min before giving dose Creatine and BUN levels for kidney function |
