Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

42 Cards in this Set

  • Front
  • Back
What works on the RIBOSOME in inhibiting bacterial protein synthesis?
- tetracycline
- aminoglycosides.
- folate synthesis inhibitor
- DNA gyrase inhibitor
- RT inhibitor
- sulfonamides
- fluoro
Antifungals - ketoconazole.
Def. Active against a SINGLE species/ or a LIMITED group of pathogens

i.e.: gram (+) bacteria
Narrow spectrum drugs.
Agents active against wide spectrum of pathogens
Broad spectrum
What is a superinfection?

Broad effect causes more antibiotic on microorganism.
- alt. of microbial pop. of the intestinal
- upper repiratory tract
- genitourinary tract

This occurs due to the removal of normal flora that can anti-bacterial effects itself.
Gram negative organism is resistant to:
vanco......this is a characteristic of microbial resistance: growth not halted by max level of an antibiotic that is tolerated by the host.
How do mutations occur?

substitution, deletion, or insertion.
- during long exposure to antibiotic
- or subtherapeutic levels of drug.
Microbial Resistance:
Transferable Resistance.
extrachromosomal DNA
this results from bacterial conjugation and thre transfer of plasmids that confer drug resistance
Transferable Resistance:

Bacterial conjugations: tranfer plasmids that have resistance to antibiotic :
- UPtake of naked DNA
- Transfer of bacterial DNA by bacteriophage (a virus that propagates on bacteria)
- transformation
- transduction
Mechanism of Resistance:
1. Enzymatic inactivation of drugs
2. Decreased accumulation of the drug.
3. Alteration in target site components.
1. Enzymatic inactivation of drugs:
A. Beta-lactamase
B. Chloramphenical Acetyltransferase.
C. Aminoglycoside Modifying Enzyme:
- Phospho, acetyl, adenyltransferases
Decreased accumulation of the drug:
1. Increase efflux or decreased influx of antibiotics due to altered porins.
Alteration in target site components:
A. increased conc. of competing sub: PABA
b. Resistance target site components:
- reduced affinity for folate, DNA gyrase, PBP.
What are fluproquinolones:
- bactericidal
- synthetic
- Broad Spectrum
MOA of fluoroquinolones:
- inhibit DNA gyrase and TOPO IV.
Resistance of fluoro
1. drug permeation (active transport of drug out of the bacteria.
2. Mutation: mutation of chromosomal gene encoding DNA gyrase or TOPO IV.

Where are fluoro quinolones absorbed?
- Wide tissue distribution
- peak 1-3 hrs.
- Conc. in CSF, bone, prostatic fluid less than serum conc.
How is MOXIFLOXACIN eliminated?
- hepatically.
Drug Interaction of fluoro?
1. Chelations by cations (Ca, Al, Mg, Fe)
= antacids, sucralfate, hematinic: should not be administered for at least 2 hours before and after.
----> decrease absorb.fluoro.
2. Enchance oral anticoag.
3. increase QT interaval -- arrythmia.
Drug interactions of ciprofloxacin?
- increase theophylline and methyxanthine
A.E. OF fluoroquinolones:
- GI reactions
- Hematologic
- Photosenstivity
+ c/a with NSAIDs augment replacement of GABA --> Potentiate the CNS stimulant effect.
What is the pencillin wall composed of:
- N-acetyl glucoamine
- N-acetylmuramic acid

It has a highly cross-linked lattice work structure:
gm(+) 50-100 thick
gm (-) 1-2 thick.
MOA OF pencillins:
1. inhibiting transpeptidase.
2. Binds to other PBPs and inhibit them.
3. Autolytic enzyme --> destruction of existing cell wall.
Mechanism of resistance for pencillins?
1. Production of beta-lactamases (deactivating enzymes: narrow vs. broad)
2. Modifications of target PBPs: changes in PBPs that alter the affinity for pencillin.
Natural pencillins:
Pencillin G (acid labile, poor oral absorption) I.M. depot--> respiratory prep.
- procaine and benzathine
- peak I.M. w/in 30 min.
Advantages of pencillin G:
1. released slow but persistent conc. of antibiotic
Difference b/w Pencillin G and Pencillin V:
Pencillin G: 60%
Pencillin V: 80%
Pencillins in CSF:
when normal does not enter CSF, when inflammed, pencillin enters into the CSF more readily.
How are pencillins excreted?
- Renally through TUBULAR SECRETION
- neonates and infants, renal disease increase the conc. due to decreased CL.
A.E. OF Natural pencillins:
- hypersensitivity/allergic reactions
- I.M.: pain and sterile inflammatory response
- I.V.: thrombophlebitis.
- Jarisch-Herxheimer Reaction: release of spirochetal antigen
- Hyperkalemia
- decreased platelet aggregration and bone marrow depression.
Drug interactions of Pencillins:
1. Probenecid: inhibit tubular secretion.
2. aminoglycosides:inactivation of aminoglycoside.
3. Tetracycline: static? vs. cidial
4. Methotrexate: decrease excretion of MTX......increased toxicity.
Pencillin REsistance:
MRSA due to decreased affinity for beta-lactam antibiotic.
No sign clinical diff in:
- oxacillin, clox, oral bioavailability.
Protein binding for pencillins is:
- very high protein (>90%)
Sign. portion of oxacillin metabolized by:
liver, increases liver enzymes (hepatic damage)
exretion of naficillin:
A.E. of nafcillin
biliary secretion and hepatic inactivation.
A.E. of nafcillin:
1. Phlebitis
2. Na Overload
3. Reversible Neutropenia
Aminopencillins has how many protein binding?
20% protein binding.
A.E. OF aminopencillins:
Ampicillin + allopurinol = rash-toxic
- interfere O.C.
Antipseudomonal Pencillins:
- hypernatremia
- bleeding via decreased platelet aggregration as a result of binding to platelet ADP.