Study your flashcards anywhere!
Download the official Cram app for free >
- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
- Read
Toggle OnToggle 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
42 Cards in this Set
- Front
- Back
What works on the RIBOSOME in inhibiting bacterial protein synthesis?
|
- tetracycline
- aminoglycosides. |
|
What is a METABOLIC and NUCLEIC ACID INHIBITOR?
- folate synthesis inhibitor - DNA gyrase inhibitor - RT inhibitor |
- sulfonamides
- fluoro - AZT |
|
CELL MEMBRANE INHIBITOR?
|
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:
|
Mutation
Transferable Resistance. |
|
Plasmid
|
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 : (R FACTORS) |
|
TRANSFERABLE RESISTANCE:
- 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:
|
- ORALLY ACTIVE
- 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. NO INACTIVATING ENZYME. |
|
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 - CNS SIDE EFFECTS: + c/a with NSAIDs augment replacement of GABA --> Potentiate the CNS stimulant effect. - HALLUCINATIONS, SEIZURES, DELIRIUM |
|
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, diclo..in 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. - SUPERINFECTION |
|
Antipseudomonal Pencillins:
|
- hypernatremia
- bleeding via decreased platelet aggregration as a result of binding to platelet ADP. |