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Renal 16 Antibiotics

Bridges: Antibiotics - Protein synthesis inhibitors

Inhibit bacterial cell wall synthesis Beta-lactams Vancomycin Bacitracin
Anti-metabolic activity Sulfonamides Trimethoprim
Inhibition of bacterial protein synthesis. Aminoglycosides Tetracyclins Chloramphenicol Macrolides
Inhibit bacterial nucleic acid syntheses Fluoroquinolones
Which drug classes target the bacterial ribosome? Aminoglycosides Tetracyclins Macrolides Chloramphenicol
This class is of protein synthesis inhibitors are bacteriocidal Aminoglycosides
Classes that work on the 50s unit Macrolides Streptogramins Chloramphenicol Lincosamides Oxazolidinones
Classes that work on the 30s unit Aminoglycosides Tetracyclins
Animoglycoside that is topically OTC Neomycin
Aminoglycosides are frequently used in Serious infxn from aerobic G-
Use is limited due to Toxicity
Used in combination with... Beta-lactams Vancomycin
Why does it work best in aerobics G-? Uptake of the drug requires O2 dependent transport system
Frequently used for infxns due to... PEPS Pseudomonas (DoC) Enterobacter Proteus Serratia
Can also be used to treat Invasive enterococcal infxn Serious staph. infxn Y. pestis and Francisella tularenis
Clinical applications of aminoglycosides -Serious infxns- Septicemia Nosocomial RTI Complicated UTI Osteomyelitis
When are aminoglycosides discontinued? Once the organism is identified and susceptibility is known
Aminoglycoside MoA Irreversibly binds to 30s ribosome 1. interferes with initiation complex formation 2. Causes misreading of mRNA 3. Restricts polysome formation
What contributes to the bacteriocidal nature? Concentration-dependent killing Long PAE
AG uptake into G- Diffuse across the outer membrane via porin channels Cross the inner membrance via O2 dependent active transport Inner membrane potential drives transport
What can block the transport of AG? Anaerobic environment Low extracellular pH
Aminoglycoside resistance Inactivation of drug by microbial enzymes (aminoglycoside modifying enzymes)
Aminoglycoside kinetics Very polar compounds Don't cross the membrane well
Aminoglycoside pharmacokinetics Concentrated in the proximal tubular cells Largely eliminated by GF
What must you do in renal compromised pts? Adjust the dose/dosing frequency Blood levels are very important Must adjust dose relative to creatintine clearance
Advantages of consolidated therapy Comparable efficacy Decreased nephrotoxicity Long PAE
Toxicity is dependent on Concentration and time above threshold
Consolidation therapy is not recommended for what situations? Pregnant pts Osteomyelitis Infective endocarditis Pts recieving concurrent ototoxins Pts undergoing solid organ transplantation
Aminoglycosides therapeutic index Narrow
Primary toxicities of aminoglycosides Nephrotoxicity Ototoxicity Neuromuscular blockade
Which of these are reversible/irreversible? -Reversible- Nephrotoxicity Neuromuscular blockade -Irreversible- Ototoxicity
Makes nephrotoxicity and ototoxicity more likely Therapy > 5 days In elderly pts In pts with renal dysfunction Tox incidence related to drug concentration
Nephrotoxicity Reversible Involves an acute tubular necrosis
The most important result of nephrotoxicity Decreased AG excretion -Increased AG plasma levels -Predisposes to ototoxicity
AGs accumulate and are retained in.. Proximal tubular cells
Results of AG accumulation Impairs renal concentrating ability Mild proteinuria Appearance of hyalin and granular casts GFR decreases
2 drugs that are nephrotoxic Amphotericin B Cyclosporine
Why is ototoxicity is difficult to determine? May occur after drug is stopped
Where do AGs accumulate in the ear? Perilymph and endolymph in the inner ear
Ototoxicity manifestations Tinnitus High freq. hearing loss Vestibular damage
What is special about ototoxicity? Irreversible Damage accumulates with repeat courses
This class of drugs may enhance ototoxicity. Loop diuretics
Absolute contraindication for AG use Pts with Myasthenia gravis
What may be seen with neuromuscular blockade? Acute respiratory paralysis May enhance effects skeletal muscle relaxants
Mechanism of NM blockade May inhibit prejunctional relase of acetylcholine Reduce postsynaptic sensitivity
Streptomycin use Limited by resistance and advent of newer AGs
Streptomycin used alone to treat... Tularemia and plague (DoC)
Streptomycin used in combination to treat Tuberculosis Brucellosis (DoC with doxy) Endocarditis (w/ cillin)
Gentamycin One of the most frequently used Generally chosen first
Gentamycin used in combination for... (used with cillin) Pseudomonas (DoC) Enterococcal (DoC)
Amakacin primarily used for Pseudomonas Other serious infxns caused by *organisms resistant to other AGs*
Amikacin has The broadest spectrum Resistance to inactivating enzymes
What makes amikacin more effective than other AGs? There is only one site susceptible to enzyme anabolism
Neomycin is... Not used systemically Used topically The most toxic AG
Only time Neomycin is used orally/systemically To sterilize the gut When organisms are resistant to other agents
Tetracycline (class) spectrum G+, G-, aerobic, anaerobic Intracellular bacteria -Chlamydia, Rickettsia, Mycoplasm p.)
Doxycycline and minocycline 2 of the most widely prescribed drugs
Doxycycline One of the most active and clinically used Preferred in pts with poor renal fxn
Minocycline Meningococcal carrier state Crosses the blood-brain-barrier
Tetracyclines are Docs or alternatives for Mycoplasma p Chlamydia Rickettsiae Lyme Dz Plague, tularemia, brucellosis, malaria prophylaxis
Tetracycline (group) MoA Reversibly binds to 30s Prevents tRNA binding to acceptor site Prevents addition of amino acids to growing peptide
How does it get into the cell? Passive diffusion (porin Om in G-) Active transport (plasma membrane)
Why are tetracyclins and penicillina antagonistic? Tetra's stop bacterial growth Penicillions need bacterial growth
Primary mechanism of resistance to tetras Efflux pumps *Ribosome protection* -Proteins interfere with binding and dislodge drug form ribosome
This provides a cross-resistance among tetracyclines except for Tigrecyclin
Tetracycline pharmacokinetics GI absorption is variable For stable chelates with cations
DD interactions Milk Antacids Pepto-Bismol
Tetracycline that gets into the CSF Minocycline
Chelates with Ca effecting Bones and teeth
Don't give to which patient population? Pregnant women
Tetracycline elimination Eliminated by the kidneys
Which 3 tetras are less dependent on the kidneys for excretion? Doxy, mino, and Tige Excreted by the bile
Tigecycline spectrum of action Very broad spectrum antibiotic Effective in resistant organisms (MRSA, Staph epi, PRSP, VRE)
What makes tigecycline so useful? Not susceptible to efflux pumps and ribosome protection
Tigecyclin route of administration and excretion IV Poor oral absorption Biliary excretion
Tigecycline uses Complicated skin and skin structure infxn Intraabdominal infxn Community-acquired pneumonia
Tetracycline adverse effects GI Boney structures and teeth Liver tox Local Tissus Tox Photosensitivity Vestibular reactions
Tetracycline AE: GI Oral dosing can cause GI distress NVD
Tetracycline AE: Bone Bind Ca, esp. in newly formed bone of young kids Kids may develop permanent brown discoloration
What increases the risk of permanent brown discoloration? Use in the last half of pregnancy and up to 8 y/o Crosses the placenta and accumulates in fetus
Tetracycline AE: Liver Tox Rare but fatal Occurs more commonly with tetra and mino
Tetracycline AE: Local tissue tox Directly irritating to tissues IV: thromboplebitis IM: painful
Tetracycline AE: Photosensitivity Fair skin pts ate major risk
Tetracycline AE: Vestibular Rxn May be produced by Mino Ataxia Dizziness NV
Tetracycline AE: Superinfections Pseudomembranous colitis
Precautions with Tetracyclines Don't give to: Pregnant pts kids <8 Discard unused drugs as it may cause Fanconi syndrome
Drug classes that act on the 50s Chloramphenicol Macrolides Lincosamides Streptogramins Oxazolidinones
Chloramphenicol Rarely used Serious toxicity limits use Reserved for life-threatening infxn due to resistance or allergies to safer drugs
Chloramphenicol occasionally used for Rickettsial infxn Menengitis Anaerobic infxn
Chloramphenicol spectrum and MoA Broad spectrum -Aerobic, anaerobic, G+, G- Reversibly binds to inhibit peptidyl transferase (Peptide bond formation)
Chloramphenicol Toxicity Hematological Toxicity Bone marrow suppression -anemia, leukocytopenia, thrombocytopenia Dose dependent and reversible
Chloramphenicol: Idiosyncratic response Serious and fatal Aplastic anemia-> fatal pancytopenia Rare; does NOT containdicate
Chloramphenicol: Idiosyncratic drug reaction Abnormal Rare and unpredictable Occurs sporadically Not related to dose
Chloramphenicol: Adverse Effects Gray syndrome/gray baby syndrome -Gray color, shock, hypothermia, vomiting, flaccidity Can be fatal in 2 days
Gray baby syndrome: Mechanism Lack of glucuronyl transferare activity
Macrolides Good substitute for penicillins G+ activity
Clarithromycin and Azrithromycin: Spectrum G+ and some G- Camylobacter jejuni H. pylori Shingella spp E. Coli Meisseria gonorrhoeae
Macrolides are DoC for Kids and pregnant women Pts allergic to penicillin Preferred for community-acquired RTIs
Restrictions for macrolide use in CAP Uncomplicated pneumonia not requiring hospitalization No sig. comorbidities No ABx use in past 3 mo. No sig. macrolide-resistant strains locally
Macrolides also DoC for... Mycoplasma p Chlamydia Bordetella Campylobacter Mycobacterium avian complex (MAC)
Macrolides: Mechanism of Action Bacteriostatic Inhibits peptide chain elongation (translocation or peptidyl tRNA from A to P site is inhibited
Macrolides: Resistance Efflux pumps Ribosome modification -Alters macrolide binding site on the bacterial ribosome
Macrolides: Pharmacokinetics New macrolides are more acid-stable Clarithro: less freq dosing Azithro has 1/2 life ~70hrs
Macrolides: Drug interactions **Inhibit CYP3A4** P450 inhibition
Macrolides: Toxicity (Primarily seen with Erythromycin) GI -Anorexia, NVD -Epigastric distress Cholestatic hepatitis -Fever, jaundice, impaired liver fxn
Lincosamides Clindamycin: Spectrum and Clinical use Anaerobic, strept, staph infxns DoC for C. perfringens Aerobic G- bacilli are intrinsically resistant
Lincosamides Clindamycin: Mechanism of Action Binds close to erythromycin and chloramphenicol binding sites Inhibits peptide bond formation
Lincosamides Clindamycin: Resistance Alterations of ribosomal binding site -Cross resistance with erythro Metabolism of drug G- intrinsic resistance
Lincosamides Clindamycin: Pharmacokinetics Does not cross BBB Penetrates into bone (high levels) Actively transported into PMN leukocytes and macrophages (high levels)
Lincosamides Clindamycin: Adverse effects Severe diarrhea -May cause antibiotic associated diarrhea
Lincosamides Clindamycin and pseudomembranous colitis Clindamycin classically assoc. with this disorder
Streptogramins Quinupristin + Dalfopristin: Spectrum G+ bacteria -Staph resistant to: Methacillin, quinolones, vanc -Strept. pneumonia resistant to Pens Vanc-resistant E. farcium
Streptogramins Quinupristin + Dalfopristin: Principle Clinical Use Drug resistant G+ cocci infxn -Skin and soft tissue Serious or life-threatening VRE Complicated skin infxn -MSSA and S. pyrogenes
Streptogramins Quinupristin + Dalfopristin: Mechanism of Action Q: binds same site as macrolides D: directly interferes with polypeptide chain formation Binds near Q, enhances binding of Q Bactericidal
Streptogramins Quinupristin + Dalfopristin: Resistance D: enzymatic inactivation, efflux pumps Q: binding site mods by methylase, enzymatic inactivation
Streptogramins Quinupristin + Dalfopristin: Drug Interactions **POTENT CYP3A4 inhibitor**
Streptogramins Quinupristin + Dalfopristin: Adverse Effects Pain and phlebitis at infusion site Severe arthalgias and myalgias
Oxazolidinones Linezolid: Spectrum Similar to quinupristin+dalfopristin (G+) plus e. faecalis Should be reserved for MDR G+
Oxazolidinones Linezolid: Clinical Use Hospital and community AP -Strep pneumoniae Tx of skin and soft tissue -Complicated/uncomplicated -MRSA & MSSA VR enterococcus
Oxazolidinones Linezolid: Mechanism of Action Block formation of initiation complex Mostly bacteriostatic -Cidal to strep.
Oxazolidinones Linezolid: Resistance and Pharmacokinetics R: mutation or rRNA binding site P: MAO inhibitor Weak, reversible Tyramine rich foods can cause sudden and severe high BP
Oxazolidinones Linezolid: Adverse Effects Myelosuppression -Thrombocytopenia (most common effect) Anemia, Leukopenia
Created by: bcriss