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TnJ > ANTIBIOTICS > Flashcards

ANTIBIOTICS Flashcards

1
Q

goal for concentration dependent drug dosing

A

Cmax/MIC > or = 10-12

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2
Q

goal for time dependent drug dosing

A

time should be > MIC for 50-75% of dosing intervalEXCEPTION: Carbapenem may be 25-50% of dose interval because of rapid tidal activity

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3
Q

list rx based on bacterioSTATIC property

A

MOST protein synthesis/ribosome inhibitors–tetracyclines –phenicols–macrolides–lincosamidesSingle therapy folic acid inhibitors–sulfonamides–trimethoprim**accumulation in WBC/phagocytic cells may make them CIDAL

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4
Q

list rx based on bacterioCIDAL property

A

Cell wall inhibitors–B lactams (Penicillins, Cephalosporins, Carbapenems)–Glycopedtides (Vancomycin)DNA/RNA inhibitors–Fluorinated quinolones–Rifampin–MetronidazolePOTENTIATED folic acid sun inhibitors–TMSSOME protein synthesis inhibitors–Aminoglycosides–Macrolides–Lincosamides**accumulation in WBC/phagocytic cells may make them CIDAL

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5
Q

list concentration dependent drugs

A

–Fluorinated Quinolones–Aminoglycosides–Azithromycin (type of Macrolide)–Metronidazole

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6
Q

list of time dependent drugs

A

beta lactams (Penicillin, Cephalosporins, Carbapenems)glycopeptides (vancomycin)tetracyclinesmacrolides (EXCEPT azithromycin which is concentration dep)lincosamides

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7
Q

with the exception of concentration dependent drugs, which drugs have enhanced efficacy at higher doses

A

tetracyclinesmacrolideslincosamides

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8
Q

steps to avoid antimicrobial resistance

A

3 D’s1. de-escalate–don’t use Ab if you don’t have to2. design–make proper dosing regimes3. decontaminate–proper environmental safety and avoid exposure risks

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9
Q

general ways microbial resistance occurs within the bacT

A

inherent vs acquiredchromosomal mutations or transfer of genetic material outside of the chromosome( plasmid, bacteriophage-mediated)mechanisms:1. transposons– resistant genes that move back and forth btwn chromosome and plasmid2. conjugation–sexual transmission btwn bacT3. transduction–specific receptor transfers information via bacteriophage4. transformation–(human) naked DNA from previously lysed cell enters another bacT

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10
Q

Drugs that accumulate in phagocytic WBC

A

MacrolidesLincosamidesFluoroquinolonesRifampinSelective sulfonamidesdrug accumulation in WBC does not always = enhanced efficacy bc sometimes the drug is not released

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11
Q

drugs that do NOT accumulate in WBC

A

Beta lactamsAminoglycosidesMetronidazole

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12
Q

T/Flipid soluble drugs are more likely (than water soluble drugs) to move beyond extracellular fluid

A

TRUEand lipid soluble drugs should be used for infections that are more difficult to treat (ex. IC bacteria or tissues with barriers difficult to penetrate)

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13
Q

3 antimicrobial classes with good tissue penetration based on lipophilicity

A

FluoroquinolonesMacrolidesTMS combos

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14
Q

T/Fmost endotoxic release occurs with B lactams

A

TRUE least with amino glycosides (pg. 175)

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15
Q

B lactamMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Cell wall inhibitor of PBP–transpeptidase–>perm–>lysisTIMECIDALMostly gm +Some gm - Some anaerobes(incr spectrum with incr generations of penicillins)(spectrum favors gm- with incr generation of ceph)

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16
Q

Types of B lactams

A

PenicillinsCephalosporinsCarbapenems

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17
Q

Mx of resistance for B lactams

A
  1. Beta lactamase production by bacT 2. Alteration in mecA gene (change in PBP)3. Efflux pumps4. Loss/Change in porins
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18
Q

Glycopeptide/VancomycinMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Cell wall synthesis inhibitor and prevents elongation of cell wallTIMECIDALMostly gm + (Mainly used VRSA, VISA in humans)NO gm - Some anaerobes

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19
Q

AminoglycosidesMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Inhibit binding of 30s ribosome to complete unit (70s)Concentration dependentCIDAL Mostly gm - NO anaerobes (O2 required!)some main gm + (staph not strep)do not get absorbed or penetrate well

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20
Q

Mx of resistance for aminoglycosides

A

Plasmid mediated 1. enzymatic destruction2. decreased cell entry3. altered ribosome structure

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21
Q

Side effects of aminoglycosides

A

Nephrotoxicity (tubular)OtotoxicityNM blockage

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22
Q

Types of anti-pseudomonal penicillins

A

TicarcillinPiperacillin(parenteral only)

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23
Q

B lactamase inhibitors added to penicillins

A

sulbactamclavulonic acid

24
Q

characteristics of 2 newer 3rd generation cephalosporins

A

Convenia–Cefovecinhighly protein bound–>long half lifecats 166 hr dogs 133 hr; 3 week SQ shotSimplecef–Cefpoximelong half life for once daily dosing

25
Q

1, 2, 3 generation cephalosporins

A

incr generation incr gm- and anaerobe spectrum but at the cost of gm + spectrum decreasing1. cefazolin, cephalexin, cefadroxil2. Cefoxitin3. Ceftiofur, Cefpodoxime, Cefovecin, Ceftazidime

26
Q

tetracyclinesMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Inhibit binding of 16s part of 30s ribosome (prevents translation) also inhibits MMPTIMEStatic (but efficacy incr with incr dose) gm +, gm - Some anaerobes, IC bacT (tick borne diseases, Lepto)

27
Q

side effects of tetracyclines

A

Gastrointestinalesophageal stricture/esophagitis in catscollapse if rapid IVnephrotoxicity (high dose)enamel hypoplasia, bone growth problemsAVOID IN PREGNANT ANIMALS

28
Q

Types of tetracyclines

A

tetracylineoxytetracyclinedoxycyclineminocycline

29
Q

Advantages of doxy and minocyclin

A

TETRACYLINE GROUP–inhibitors of protein sunmost lipophilic of group and biliary excretionbetter penetrating hard to reach areas

30
Q

Mx of resistance for tetracyclines

A

Plasmid Mediated/Induced;-interfer w influx and efflux-enzymatic destruction-change binding to ribosome

31
Q

Spectrum of activity gentamicin vs amikacin aminoglycosides

A

gentamicin STAPH sppamikacin PSEUDOMONAS

32
Q

PhenicolsMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Inhibit Protein Synthesis – Binds 50s (peptidyl transferase)TIMESTATICGm +, -, anaerobes NOT pseudomonas

33
Q

Which phenicol drug is more resistant to bacterial destruction

A

Florfenicol is more resistant than chloramphenicol

34
Q

Side effects of phenicol drugs

A

Anemia (Non-Regen in animals and Aplastic in People) prolong barbituates (potent cyp inhib)affect active immunization procedures

35
Q

Mx of resistance for phenicol drugs

A

Plasmid Mediated–inactivation by transacetylase action on drug **florfenicol is more resistant to destruction by bacT

36
Q

MacrolidesMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Inhibit Protein Synthesis – Binds 50s at 2 sites (peptidyl transferase and translocation)TIME (Concen del at high doses)STATIC (cidal at high doses)very lipid soluble; can accumulate in WBC (azithromycin)Gm + Azithromycin/Clarithromycin may have incr spectrum for gm - bacT

37
Q

additional activity of erythromycin macrolide

A

GI prokineticMimics motilin and stimulates gastric, pyloric, and duodenal contractions

38
Q

list macrolides

A
  1. erythromycin, tylosin, tilmicosyn2. azithromycin, clarithromycin
39
Q

LincosamidesMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Inhibit Protein Synthesis – Binds 50s (translocation)TIME STATIC (*cidal at high doses)can accumulate in WBC Gm + , anaerobes

40
Q

list types of lincosamides

A

clindamycin, lincomycin

41
Q

Main side effect of clindamycin

A

clostridial overgrowth and diarrhea

42
Q

mx of resistance for lincosamides

A

Plasmid MediatedMutation in 50s ribosome that prevents drug binding

43
Q

mx of resistance for macrolides

A

Plasmid Mediated–increased efflux from cells–mutation in 50 S ribosome that prevents drug binding

44
Q

RifampinMOA, Time vs Conc, Static vs Cidal, Spectrum

A

inhibits RNA SYNTHESIS (DNAdep RNA pol inhibitor)CIDAL but used in COMBO THERAPY ONLY because incr risk resistanceonly gm +can cause incr ALP and red/orange urine

45
Q

mx of resistance for rifampin

A

Single mutation in bindingoccurs quicklyonly use in combo therapy

46
Q

NitroimidazolesMOA, Time vs Conc, Static vs Cidal, Spectrum

A

METRONIDAZOLEinhibits BOTH RNA and DNA synthesisCIDALCONCENTRATION DEPANAEROBES ONLY

47
Q

side effects metronidazole

A

GI upsetdose related neurotoxicity (cerebellum most sensitive)Teratogenic–DO NOT GIVE DURING PREGNANCY

48
Q

T/F metronidazole is “re-generated” on death of the microbe increasing and facilitating its efficacy

A

TRUEmetronidazole is “re-generated” on death of the microbe increasing and facilitating its efficacy

49
Q

FluoroquinolonesMOA, Time vs Conc, Static vs Cidal, Spectrum

A

Inhibit DNA synthesis (DNA gyrase/topoisomerase II AND topoisomerase IV inhibition)CIDALConcentration dependentGM +, GM -lipid soluble, into WBC!

50
Q

side effects fluoroquinolones

A

GI signsanaphylactoid reactionsseizuresDose dep retinal degeneration in cats ( less risk w marbofloxacin)cartilage damage in young animalsinduction of bacteriophage supergenes

51
Q

Mx of resistance for fluoroquinolones

A

CHROMOSOMALLY mediated;-Dec cell wall permeability (decr expression of porins)-Efflux pump activation-Mutation of topoisomerasesGM + bacT resist topoisomerase IVGM - bacT resist topoisomerase II/DNA gyrase

52
Q

Sulfonamides ALONEMOA, Time vs Conc, Static vs Cidal, Spectrum

A

inhibit folic acid pathway (folic acid synthetase)Static TimeGM + , Gm -, anaerobes(should be given potentiated)

53
Q

POTENTIATED SulfonamideMOA, Time vs Conc, Static vs Cidal, Spectrum

A

inhibit folic acid pathway (folic acid synthetase AND reductase)CIDAL TimeGM + , Gm -, anaerobes(should be given potentiated–TMS)

54
Q

Why are sulfonamides/TMS specific for bacterial folic acid pathways

A

mammal cells are not dependent on making own folic acid and they can get it from their dietbacT depend in FA synthesis for purine and nucleic acid synthesis

55
Q

side effects of sulfonamides/TMS

A

KCSHypersensitivity (polyarthritis, fever, thrombocytopenia, hepatitis)Doberman’s predisposed to reactions (AVOID)thyroid suppression w chronic use?

56
Q

mx of resistance for sulfonamides/TMS

A

Plasmid and chromosomal mediated–Decr drug penetration–decr affinity for substrate

TnJ (128 decks)

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