PowerPoint Presentation Lecture 7 Harper CollegePowerPoint演示文稿讲座7 哈珀学院.pptVIP

Lecture 7Chapter 25 Antibacterials: Penicillins Cephalosporins Antibacterials Antibacterials/antimicrobial drugs - Substances that inhibit the growth of or kill bacteria or other microorganisms (microscopic organisms = bacteria, viruses, fungi, protozoa) Bacteriostatic = Inhibits growth of bacteria Bactericidal = Kills bacteria Peaks Troughs = Serum antibacterial levels for drugs w/ a narrow therapeutic index - Too high = drug toxicity (Peak - 1 hr. after drug infused) - Too low = therapeutic range (Trough - before dose) Antibacterials Mechanism of Action: 1. Inhibition of cell wall synthesis - Bactericidal 2. Alteration in membrane permeability - ‘Cidal’ or ‘Static’ 3. Inhibition protein synthesis - ‘Cidal’ or ‘Static’ 4. Inhibition of bacterial RNA DNA - Inhibits synthesis of RNA DNA 5. Interferes with metabolism in the cell - ‘Static’ Antibacterials Drugs - 1. Penetrate bacterial cell wall in sufficient concentrations 2. Affinity to the binding sites on the bacterial cell: - Time drug remains at binding sites = effect - Time controlled by pharmacokinetics Antibacterials Pharmacodynamics - - Concentration at site or exposure time for drug plays an important role in bacteria eradication - Duration of time for use of antibacterial varies according to type of pathogen, site of infection condition of host - With some severe infections - continuous infusion more effective than intermittent - Body defense drugs work together to stop infectious process - Effect = drug host’s defense mechanisms Effects of concentrated drug dosing Antibacterials Bacterial Resistance - result naturally or may be acquired * Natural (inherent) = w/o previous exposure to antibiotic ie. pseudomonas resistant to Penicillin G * Acquired = prior exposure to antibacterial ie. staph aureus was sensitive to PCN G, now it’s not Nosocomial infections - infections acquired while clients are in the hosp. Many are mutant strains resistant to