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IOS 10 Exam 2
Aminoglycosides & Vancomycin
| Question | Answer |
|---|---|
| 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
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