Khan Antibiotic Review

Front 1

What works on the RIBOSOME in inhibiting bacterial protein synthesis?

Back 1

- tetracycline
- aminoglycosides.

Front 2

What is a METABOLIC and NUCLEIC ACID INHIBITOR?
- folate synthesis inhibitor
- DNA gyrase inhibitor
- RT inhibitor

Back 2

- sulfonamides
- fluoro
- AZT

Front 3

CELL MEMBRANE INHIBITOR?

Back 3

Antifungals - ketoconazole.

Front 4

Def. Active against a SINGLE species/ or a LIMITED group of pathogens

i.e.: gram (+) bacteria

Back 4

Narrow spectrum drugs.

Front 5

Agents active against wide spectrum of pathogens

Back 5

Broad spectrum

Front 6

What is a superinfection?

Broad effect causes more antibiotic on microorganism.

Back 6

- 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.

Front 7

Gram negative organism is resistant to:

Back 7

vanco......this is a characteristic of microbial resistance: growth not halted by max level of an antibiotic that is tolerated by the host.

Front 8

How do mutations occur?

substitution, deletion, or insertion.

Back 8

- during long exposure to antibiotic
- or subtherapeutic levels of drug.

Front 9

Microbial Resistance:

Back 9

Mutation
Transferable Resistance.

Front 10

Plasmid

Back 10

extrachromosomal DNA

Front 11

this results from bacterial conjugation and thre transfer of plasmids that confer drug resistance

Back 11

Transferable Resistance:

Bacterial conjugations: tranfer plasmids that have resistance to antibiotic :
(R FACTORS)

Front 12

TRANSFERABLE RESISTANCE:
- UPtake of naked DNA
- Transfer of bacterial DNA by bacteriophage (a virus that propagates on bacteria)

Back 12

- transformation
- transduction

Front 13

Mechanism of Resistance:

Back 13

1. Enzymatic inactivation of drugs
2. Decreased accumulation of the drug.
3. Alteration in target site components.

Front 14

1. Enzymatic inactivation of drugs:

Back 14

A. Beta-lactamase
B. Chloramphenical Acetyltransferase.
C. Aminoglycoside Modifying Enzyme:
- Phospho, acetyl, adenyltransferases

Front 15

Decreased accumulation of the drug:

Back 15

1. Increase efflux or decreased influx of antibiotics due to altered porins.

Front 16

Alteration in target site components:

Back 16

A. increased conc. of competing sub: PABA
b. Resistance target site components:
- reduced affinity for folate, DNA gyrase, PBP.

Front 17

What are fluproquinolones:

Back 17

- ORALLY ACTIVE
- bactericidal
- synthetic
- Broad Spectrum

Front 18

MOA of fluoroquinolones:

Back 18

- inhibit DNA gyrase and TOPO IV.

Front 19

Resistance of fluoro

Back 19

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.

Front 20

Where are fluoro quinolones absorbed?

Back 20

- Wide tissue distribution
- peak 1-3 hrs.
- Conc. in CSF, bone, prostatic fluid less than serum conc.

Front 21

How is MOXIFLOXACIN eliminated?

Back 21

- hepatically.

Front 22

Drug Interaction of fluoro?

Back 22

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.

Front 23

Drug interactions of ciprofloxacin?

Back 23

- increase theophylline and methyxanthine

Front 24

A.E. OF fluoroquinolones:

Back 24

- GI reactions
- Hematologic
- Photosenstivity
- CNS SIDE EFFECTS:
+ c/a with NSAIDs augment replacement of GABA --> Potentiate the CNS stimulant effect.
- HALLUCINATIONS, SEIZURES, DELIRIUM

Front 25

What is the pencillin wall composed of:

Back 25

- N-acetyl glucoamine
- N-acetylmuramic acid

It has a highly cross-linked lattice work structure:
gm(+) 50-100 thick
gm (-) 1-2 thick.

Front 26

MOA OF pencillins:

Back 26

1. inhibiting transpeptidase.
2. Binds to other PBPs and inhibit them.
3. Autolytic enzyme --> destruction of existing cell wall.

Front 27

Mechanism of resistance for pencillins?

Back 27

1. Production of beta-lactamases (deactivating enzymes: narrow vs. broad)
2. Modifications of target PBPs: changes in PBPs that alter the affinity for pencillin.

Front 28

Natural pencillins:

Back 28

Pencillin G (acid labile, poor oral absorption) I.M. depot--> respiratory prep.
- procaine and benzathine
- peak I.M. w/in 30 min.

Front 29

Advantages of pencillin G:

Back 29

1. released slow but persistent conc. of antibiotic

Front 30

Difference b/w Pencillin G and Pencillin V:

Back 30

Pencillin G: 60%
Pencillin V: 80%

Front 31

Pencillins in CSF:

Back 31

when normal does not enter CSF, when inflammed, pencillin enters into the CSF more readily.

Front 32

How are pencillins excreted?

Back 32

- Renally through TUBULAR SECRETION
- neonates and infants, renal disease increase the conc. due to decreased CL.

Front 33

A.E. OF Natural pencillins:

Back 33

- 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.

Front 34

Drug interactions of Pencillins:

Back 34

1. Probenecid: inhibit tubular secretion.
2. aminoglycosides:inactivation of aminoglycoside.
3. Tetracycline: static? vs. cidial
4. Methotrexate: decrease excretion of MTX......increased toxicity.

Front 35

Pencillin REsistance:

Back 35

MRSA due to decreased affinity for beta-lactam antibiotic.

Front 36

No sign clinical diff in:

Back 36

- oxacillin, clox, diclo..in oral bioavailability.

Front 37

Protein binding for pencillins is:

Back 37

- very high protein (>90%)

Front 38

Sign. portion of oxacillin metabolized by:

Back 38

liver, increases liver enzymes (hepatic damage)

Front 39

exretion of naficillin:
A.E. of nafcillin

Back 39

biliary secretion and hepatic inactivation.
A.E. of nafcillin:
1. Phlebitis
2. Na Overload
3. Reversible Neutropenia

Front 40

Aminopencillins has how many protein binding?

Back 40

20% protein binding.

Front 41

A.E. OF aminopencillins:

Back 41

Ampicillin + allopurinol = rash-toxic
- interfere O.C.
- SUPERINFECTION

Front 42

Antipseudomonal Pencillins:

Back 42

- hypernatremia
- bleeding via decreased platelet aggregration as a result of binding to platelet ADP.