Ribosomal Agents

Front 1

Spectinomycin- Class, MOA, Resistance

Back 1

Class: related to aminoglycosides
MOA: bacterioSTATIC, binds to 30S subunits and inhibits initiation complex
Res: binding site alteration or drug inactivating enzymes

Front 2

Spectinomycin- Use, PK

Back 2

- gonorrhea, though not DOC
PK: poorly absorbed by GI

Front 3

Aminoglycosides- MOA, Use,

Back 3

MOA: bind to 30S subunit and inhibit initiation complex, cause misreading of genetic code on mRNA template, are bacteriCIDAL, transported across the membrane by O2 DEPENDENT process, very highly polar, acidic environment limits absorption

Front 4

Aminoglycosides- Use, PK

Back 4

Use: aerobic gram negatives, often used w/ beta lactam antibiotics, good for pseudomonas
PK excreted UNCHANGED in urine, 1x/day dosing b/c ototox related to trough levels

Front 5

Aminoglycosides- AE, Resistance

Back 5

AE: nephrotoxic (acute tubular necrosis), neurotoxic (neuromuscular blockade), OTOTOXIC
Res: group transferases-- transfer of groups, such as acetylation to the drug itself

Front 6

Aminoglycoside drugs

Back 6

- streptomycin, gentamycin, tobramycin, neomycin, and amikacin

Front 7

- Streptomycin, Gentamycin, Tobramycin, Neomycin, and AMikacin- Class

Back 7

Aminoglycosides

Front 8

Streptomycin- Special use
Amikacin- special use

Back 8

Streptomycin: TB
Amikacin: resistant to inactivating enzymes, used when widespread ressistance to gentamycin/tobramycin in the hospital.

Front 9

Would aminoglycosides be able to be transported across the cell wall of an anaerobic bacteria? Does low extracellular pH help in transport of aminoglycosides?

Back 9

1. NO
2. NO
- anaerobic and acidic conditions inhibit aminoglycoside transport

Front 10

What is one very unique mechanism of resistance for aminoglycosides?
Which aminoglycoside is resistnat to many inactivating enzymes?

Back 10

- plasmid mediated production of group transferases which inactivate the drug
- Amikacin

Front 11

Aminoglycosides- PK, AE

Back 11

PK: not absorbed by GI tract, usually require IV or IM
AE: ototox, nephrotox, NM blockade, and skin rxns

Front 12

Aminoglycoside- Use, what drugs are often used synergistically?

Back 12

Use- aerobic gram (-) organisms, strict anaerobes are resistant
- often used w/ beta lactam drugs synergistically

Front 13

Tetracyclines- MOA

Back 13

- inhibit binding of aminoacyl t RNA to the mRNA ribosomal complex
- bind to 30S subunit, are bacterioSTATIC

Front 14

Tetracyclines- MOR

Back 14

- efflux of drugs by plasmid coded efflux protein pump= TEST Q
- altered drug permeability/enzymatic inactivation of the drug

Front 15

Tetracyclines- PK, AE, Use, CI

Back 15

PK: oral, does not absorb well into the CNS
AE: hepatotoxicitiy, teeth discoloration
CI: preggers, young children
Use: BROAD spectrum- both gram - and gram +
- also works of rricketsiae, chlamydiae, and mycoplasma infections, borrelia bergdorfiri (lyme dz)

Front 16

Chloramphenicol- MOA

Back 16

- bind ot 50 S subunit and inhibit the peptidyl transferase- in transpeptidation
- bacterioSTATIC

Front 17

Chloramphenicol- MOR

Back 17

- production of plasmid coded drug inactivating enzyme-- chloramphenicol acetyltransferase

Front 18

Chloramphenicol- PK(absorption)

Back 18

- GI tract absorption, well distributed in body including the CSF
- hepatic inactivation

Front 19

Chloramphenicol- AE

Back 19

- Grey baby syndrome
- dose dependent bone marrow suppression- inhibition of mitochondrial ribosomes
- dose independent aplastic anemia

Front 20

Chloramphenicol- Use

Back 20

- BROAD spectrum, typhoid fever, (big 3) meningitis, children and pregnant women w/ rocky mt spotted fever

Front 21

Macrolides- MOA, Drugs

Back 21

- erythromycin, clarithromycin, azithromycin, and telithromycin
- MOA: bind to 50S, prevent the ribosome form translocating down the mRNA

Front 22

Macrolides(thromycins)- MOR

Back 22

- methylation of receptor on the 50 S ribosome results in decreased affinity for the drug
- production of drug inactivating enzymes
- reduced permeability of the drug

Front 23

Macrolides- Absorption/Distribution, Use

Back 23

- GI tract absorption, wide distribution, concentration INSIDE cells
Use: broad spectrum, respiratory infections (even severe atypicals- legionairres, mycoplasma, corny dip, bordatella pertussis)

Front 24

Lincosamides- Drugs, MOA

Back 24

- LIncosamide, Clindomycin
- MOA: bind to 50S subunit, prevents ribosome from translocating down the mRNA

Front 25

Lincosamide- MOR

Back 25

- methylaiton of ribosomal receptor site
- production of drug inactivating enzymes
- reduced permeability to the drug

Front 26

Lincosamides- Absorption/PK, Use

Back 26

- concentrated INSIDE cells
- excreted in urine and BILE
Use: ANaerobic infection above diaphragm, aerobic gram + cocci infections

Front 27

Streptogramins- MOA

Back 27

- bind to different sites on 50 S ribosomal subunit and work to prevent ribosom from translocating down the mRNA
- bacteriaCIDAL

Front 28

Streptogramins- MOR

Back 28

- methylation of quiniupristin binding site
- production of drug inactivating enzyme
- active transport efflux

Front 29

Streptogramins- Use

Back 29

- penicillin resistant pneumococci- PRSP
- methicillin resistant stap aureus- MRSA
- vanc resistant staph aurus
- vanc resistant enterococci

Front 30

Linezolid- MOA

Back 30

- bacteriaCIDAL- binds to a unique site on 50S subunit and inhibits formation of 70S ribosome
- inhibits initiation complex
- inhibits translocation of peptidyl tRNA

Front 31

LInezolid- MOR

Back 31

- mutation of binding site rRNA
- no cross resistance w/ other drugs

Front 32

LInezolids- USe

Back 32

- PRSP
- MRSA
- VRSA
- VRE

Front 33

Macrolides, LIncosamides, and streptogramins share what type of resistance mechanism?

Back 33

- constitutive methylase production which confers resistance b/c they share the same ribosomal binding site-- called MLS type B resistance