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Renal 16 Antibiotics

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Created by: bcriss

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Question	Answer
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