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IOS 10 Exam 2

Aminoglycosides & Vancomycin

Aminoglycoside resistance Plasmid- via modifying enzymes (acetyl, phosp, adenyltrasferace
Aminoglycoside ADME Poor abs, poor CNS& pulminory, 2% metabolized, glomular and renal secretion
Aminoglycoside SE risks Nephrotoxcity (dose, duration, female, liver dx) ototoxcity
Vancomycin ADME Poor, (treatment of C.diff), Poor CNS, 50% protein bound, Vd-0.7L/Kg, 5% metabolism, glomerular filtration CL=0.7*CrCl
Vancomycin SE risks Nephrotoxcity (other nephrotoxicns, age, renal dys, elevated troughs)
Vancomycin resistance Alterations in D-alanyl-D-lactate to inhibit binding
Aminoglycoside monitoring parameters Cmax, Cmin, CrCL, ototoxcity
Vancomicym monitoring parameters Cmin, and in patients with comorbidities, CrCl, Camx
What are peak and trough levels for Tobra, Genta, neli Peak severe 8-10mg/L, moderate 6-8mg/L, low 1-6mg/L Trough <2mg/L
What are peak and trough levels for amikacin Peak severe 25-30mg/L other 20-25mg/L Trough <10mg/L
Efficacy considerations of aminoglycosides Concentration dependant drug, post-receptor effect, adaptive resistance= Get Cmax:MIC 10-12 ratio
Post antibiotic effect is Suppression of growth after concnetraton falls below MIC due to inhibition of doubling of organism. Initial dose very important
Adaptive resistance Organisms that initially survive adapt and can see MIC change after second dose= Huuge Cmax
Aminoglycoside toxcity is related to Duration of therapy. Glomerular is saturated thus maxing dose does not hurt kidneys not inner ear.
Aminoglycoside high dose advantages High Cmax bug, decrease adaptive resistance, decrease toxcity,decrease drug monitoring, decrease cost, convience
Diadvantage of Aminoglycoside 1 day dosing Little clinical experience or comfort, Lack of data in certain patient populations (higher risk sepsis, febrile neutropenia) monitoring and ranges not well established
Initial dosing of aminoglycosides is 6-7mg/kg QD. We may need to increase or decrease the length of the interval
Problems to consider in 1 daily dosing of aminoglucosides Renal insufficiency, neutropenic infections, endocarditis, critically ill, burn pt., pregnancy, neonates, cystic fibrosis
Hartford nomogram dosing Administer 7mg/kg to every patient and infuse over 1 hr. Based on CrCl patients are then dosed and interval is adjusted as well.
Hartford monitoring Obtain midpoint between 6 and 14 hours after startign infusion and plot on nomogram.
Limitations od Hartford Assumes that 7mg/kg will reach a Cmax:MIC ratio of 10 for P. auriginosa, and Vd =0.31 what if altered, ClCr
Method of monitoring Aminoglycoside-Peak Measures efficacy but not toxcity (Cmin)
Methods of monitoring aminoglycosides Peak and Trough Consider peak and trough w/in 3 first doses(PK alterations) but trough can become undetectable-no calculations
Methods of monitoring aminoglycosides peak and midpoint Avoids unreadable trough and allows calculations
Methods of monitoring aminoglycosides Trough only Only assures toxicity but lacks efficacy monitoring
Vancomycin peak and trough concentrations are Peak-25-40mg/L and trough 5-15mg/L if sever trough15-20mg/L and if patient is failing 20-25mg/L
Vancomycin risk of neprotoxicity Combo therapy, age, renal dys, prolonged therapy with trough >15mg/L
Vancomycin risk of ototoxcity Reported at peak>80mg/L
vancomycin monitoring positions Standard of practive, potential ADE if outside TI, monitoring unwarranted, monitoring only for high risk patients
Moniring parameters for vancomycin are Cmin is major parameter, it is a time dependant drug. CL from patient specific concentrations
MOA of Sulfonamides Bacteriostatic analogue of PABA, bnds dihydropeteroate which catalyzes first step of dihydrofolic acid synthesis (decrease purine, thymidine-DNA)
MOA of trimethoprim Bacteriostatic, Structural analoge of dihydrofloic acid, binds enzyme dihydrofolate reductase and inhibits the concersion of dihydrofolate to tetrahydrofolic acid (decrease DNA)
MOA of rifampin Bactericidal binds B-subunit of bacterial RNA polymerase and inhibits the initiation of transcription
MOA of nitrofurantion Low concentrations bacteriostatic, high it is a bacteriocidal. Initially it is reduced to reactive metabolite which ROS react with nucleophilic sites.
MOA of Chlorampenicol Bacteriostatic, binds the 50 S ribosomal subunit. Bacteriocidal against S. pneumoniae, H.infl, N. meningitis
Resistance of Sulfonamides Intrinsic resistance- auxotrophic (E. faecailis uses exogenous folic acid) Aquired resistance -Single chromonomal mutation or plasmid mediated resistance
Resistance of Trimethoprim Aquired resistance via chromosoaml or plasmid mediated, decrease enzyme affinity, over production of enzyme, decreased porin permibility
Resistance of Rifampin Aquired mutation-single monotherapy leads to mutations to the RNA polymerase B-subunit. Always use as COMBO DRUG
Resistance of Nitrofurantion Aquired mutation to reduce ROS activityless active metabolite
Sulfonamide Gram + aerobe activity Actinomycetes, Listeria, nocardia, mycobacterium, Staph aures, Streptococci
Sulfonamides Gram - activity Burkholderia, enterobacteriaw,hameophilus, neisseria, Pseudomonas, stenotrophomas
Created by: liza001