NR 566 Advanced Pharmacology Care of the Family Midterm SATISFIED Study Guide
REAL
NR566 Advanced Pharmacology
NR566 Week One PI Support: Chapter
... [Show More] 70-76
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Chapter 70
Table 70.1: Classifications of Antimicrobial Drugs by Susceptible Organisms:
➢ Narrow vs. Broad spectrum?
o The Difference in antibiotic coverage
▪ broad: covers more and possibly gram – and gram +
▪ narrow: covers just a few microorganisms
o Which one is often used as initial treatment when treatment is used before test results?
▪ broad – covers more bacteria and use your knowledge of which bacterium will be likely at that site (UTI- e. coli use narrow spectrum because you know)
o Which one is more likely to facilitate emergence of drug-resistant organisms and superinfections?
▪ broad – affecting more bacteria
▪ secondary infection when treating something else
▪ more common in inappropriate dose/high dose
➢ Give examples of superinfections?
o Ex of superinfection: vaginal candida
➢ What antibiotics cover gram + cocci and gram – bacilli?
o Ex: narrow spectrum pcn G and V, 3rd gen cephalosporin, broad spectrum pcn (ampicillin), tetracyclines, trimethoprim, sulfonamides, fluoroquinolones (cirpo), vanco, erythromycin, clindamycin, Carbapenems (imipenem)
➢ What antibiotics cover Mycobacterium tuberculosis?
o Isoniazid, Rifampin, Ethambutol, Pyrazinamide Antimicrobials MOA
➢ Aminoglycosides (Gentamicin) vs. Tetracyclines MOA?
o Gentamicin causes lethal inhibition of protein synthesis
▪ breaks into the cells
o Tetracycline causes slowing (nonlethal) of protein synthesis
➢ Bactericidal drugs vs. bacteriostatic drug?
o bactericidal: more lethal at clinically achievable concentrations
o bacteriostatic: slows bacterial growth without killing
➢ Is Gentamicin bactericidal or bacteriostatic?
o bactericidal
➢ Is Tetracycline bactericidal or bacteriostatic?
o bacteriostatic
➢ What happens when a bacteriostatic and bactericidal agent are used at the same time?
o antagonism will occur - decreased effects of bactericidal agent because they cannot kill bacteria unless they are actively growing (bacteriostatic agent suppresses growth)
Table 70.3: Drugs for Highly Resistant Bacteria
➢ Microbes have 4 basic mechanisms for resisting drugs:
o reduction of drug concentration at its site of action
o alteration of drug target molecules
o antagonist production
o drug activation
➢ What antibiotic has resistance to C. diff?
o metronidazole
➢ What antibiotic choices are there to treat C. diff?
o vanco. rifaximin
o vanco ORAL (needs to go to site where growth is – gut) Mechanisms by which resistance is acquired
➢ 1. Spontaneous mutation
➢ 2. conjugation (acquisition of DNA R-factors from one bacterium to next- often gram- bacteria and normal flora)
➢ Can antibiotics promote overgrowth of normal flora?
o yes- if they are resistant
➢ Normal flora can transfer resistance to pathogens
o Guess # patients who end up with health-care associated infections
▪ 1/20-5%
▪ This is problematic if antibiotics are overused when not needed, risk is it may not work when needed (ie. for HAI)
Common Infections and Treatment (Table 70.4-70.5)
➢ What are the 4 main kind of bacteria found in community acquired pneumonia (CAP):
o streptococcus pneumonae
o mycoplasma pneumonae
o H influenzae
o staphylococcus aureus
➢ Main bacteria found in CAP? streptococcus pneumonae (adults)
➢ 2 most common bacteria found in UTI? e. coli and Enterobacteriaceae
➢ What abx is 1st choice for uncomplicated gram + UTI? amoxicillin
➢ What alt abx is used in UTI cipro resistant caused by pseudomonas aeruginosa gram-? levofloxacin, piperacillin-tazobactam (Zosyn), ceftazidime, cefepime, meropenem, gentamicin, tobramycin, aztreonam
➢ What abxs is used to treat meningitis? Cefotaxime, ceftriaxone, cephalosporin
➢ What abx if used to treat upper resp infection (URI) or bronchitis (bacterial, most are viral)? Bactrim
➢ Alternative abx for H. pylori (1st treatment ineffective or allergy)? tetracycline + metronidazole + subsalicylate + Protonix
Empiric Antibiotic Therapy and Tests
➢ First rule: Match the drug with the bug
➢ Determine drug susceptibility if resistance is common (checking for C. diff; strep sensitivity never done why tho?)
➢ What is the quickest, simplest way to ID microorganisms? gram stain to visualize under microscope
➢ What test can detect very low titers of bacteria/viruses? PCR
o PCR can detect bacterial pathogens of C. diff, S. aureus, mycobacterium tuberculosis, Neisseria gonorrhoeae, chlamydia trachomatis, and H. pylori
➢ What viral pathogens can be detected by PCR? HIV and influenza virus Host Factors Affect Rx
➢ Host defenses (immune system and phagocytic cells)
➢ Site of infection (need adequate MIC- the amt of abx at the site of infection in a concentration > than that to be effective)
o how much drug levels at a site to be effective? 4-8x MIC
➢ Why is minimum inhibitory concentration (MIC) important with abx?
➢ What are some foreign (medical) materials in body that phagocytes attempt to destroy? cardiac pacemakers, shuts, heart valves, prostatic joints
➢ Previous allergic reactions to Rx and generic factors (avoid giving abx that break RBCs in patients with G6PD deficiency and do not give isoniazid to slow metabolizers (Asians?) as toxic accumulation may occur)
➢ Reason: abx pass thru milk – sulfonamide can cause kernicterus (neuro damage)
➢ What: heightened drug sensitivity, greater levels = toxic levels
Chapter 71: Drugs that Weaken the Bacterial Cell Wall I
Beta-Lactams: Penicillin
➢ Widely prescribed d/t safety and efficacy as NO direct effects on cells of the host (host cells do not have walls, but bacterial cells do have cell walls)
➢ PCNs weaken cells walls, which allows water to enter and eventually bursts cell
➢ So are they bactericidal or bacteriostatic?
➢ Inhibit transpeptidases and activated autolysins by binding to those enzymes (PCP) Mechanisms of Bacterial Resistance to PCN
➢ Inability of PCN to reach their targets (PBP)
o Gram- bacteria walls have 3 layers (outer membrane difficult to penetrate to get to thin wall)
o Gram+ bacteria walls that have 2 layers (no outer membrane, but thicker wall) of envelope around their cells
o Which one is more difficult to penetrate and why?
➢ Inactivation of PCN by bacterial enzymes
o Some bacteria produce b-lactamases; Production of PBPs have low affinity for PCN (MRSA)
▪ What are beta-lactamases/how do they inactivate PCN?
Penicillin
➢ Absorption: PCN salts dissociate to release PCN G, with K and Na PCN G absorbs faster than procaine and benzathine salts
➢ Distribution: well to most tissues and body fluids, may penetrate meninges if inflammation present
➢ Metabolism: minimal
➢ Elimination: excreted through kidneys mostly by active tubular secretion as unchanged drug
➢ May need to monitor kidney function or reduce dosage if renal impairment present as it can increase half-life and lead to neurotoxicity (seizures, confusion, hallucinations)
➢ 1% of patients with PCN allergies have cross sensitivity to cephalosporins (avoid if PCN allergy severe)
➢ An allergy to PCN can decrease overtime so important to know what prior reaction was (if mild ORAL cephalosporin can be given)
➢ What are safe alt for PCN allergy?
➢ What happens if inadvertent arterial injection?
➢ What happens if accidental injection into peripheral nerve?
➢ How is PCN given in “desensitization procedure” if necessary to PCN allergic patient if alt treatments to PCN are ineffective (i.e.. enterococcal endocarditis) [Show Less]