Antimicrobials

Front 1

Penicillin

Back 1

Safe

Interferese with a site unique to the growth of mo's

Front 2

Chloramphenicol

Back 2

-less specific to mo's than penicillin, potentially more toxic

-used in developing countries

-In some peope damages bone marrow --> no white cells (no immunity) --> infection and death

No bone marrow --> no RBS (anemic) <--aplastic anemia

Front 3

H Pylori (peptic ulcers)

Back 3

Tetracycline, Metronidazole, Bismuth, Amoxiciliine, Clarithromycin <-- all used to treat H pylori

Front 4

Rational dosing

Back 4

-

Relationship of drug concentration totherapeutic (anti-microbial) effects

if increasing the dose will significantly increase the number of mo's killed --> go ahead

If not, probably not a good idea

Front 5

Classes of antimicrobial drugs

Back 5

penicillins

cephalosporins

tetracyclines

aminoglycosides

macrolides

fluoroquinolones

other

Front 6

Mycoplasma

Back 6

between bacteria and fungus but are not either

Front 7

Narrow spectrum antibiotics: example Isoniazid

Back 7

act on a single or a limited group of mo's

Front 8

Extended Spectrum antibiotics: example amoxicillin

Back 8

effective against gram + and few - bacteria

Front 9

Broad spectrum antibiotics: tetracyclin

Back 9

affect wide variety

dr will prolly prescribe 1st

Front 10

Aminoglycoside antibiotics

Back 10

-streptomycin a typical example

-widely prescribed

-maybe used to treat TB in combination with other drugs

-not metabolized much and is excreted by kidneys --> kidney toxicity

-ototoxicity- unique

Front 11

Aminoglycoside antibiotics: mechanism of action

Back 11

-Interfereswith the protein translation process

-These otherdrugs also interfere with protein translation (affect ribosome function atvarious levels)

-Erythromycin

-Tetracyclin

-Streptoycin

-Chloramphenicol

Front 12

Penicillin

Back 12

-Mechanismof action: doesn’t let bacteria to produce a cell wall

Front 13

Sulpha drugs

Back 13

can inhibit metabolism in bacteria –preventing bacteria from energyproduction àbacteria dies

Front 14

Fluoroquniolones

Rifampin

Back 14

inerefere with DNA synthesis

Front 15

Mechanism of Drug Resistance

Back 15

-genetic alterations in bacterial genome involved

-spontaneous mutation (insertion, deletion, subs of one or more nucleotide)

-DNA transfer or drug resistance between bacteria

-resistance properties often encoded by extrachomorosmal R factors (resistance plasmids)

-Plasmids enter cells by transduction (phage mediate, transformation or conjugation)

Front 16

Conjugation

Back 16

hfr cell passes resistant genes to normal bacteria

Front 17

Drug resistance table;

Back 17

Fluoroquinolones: alteration in the target enzyme, DNA gyrase --> resistance

B-lactams: alteration to porin channesl -->resistance. Also penicillinases destroy the antibiotic

tetracyclines: plasmid medieated protein that promotes efflux of the drug -->resistance

Front 18

Prophylactic antibiotics

Back 18

-to prevent streptococcal infections in patients with a history of rhhumatic heart disease

-prior to surgical procedure

-prior to dental work

-zidovoudine used for HIV+ mothers during birth

-pretreatment to prevent TB or menigititis

Front 19

Uses of antimicrobial drugs

Back 19

Sulfa drugs: UTI, Txoplasmosis

B-Lactams: pneumonia, gonorrhea, syphilis

Vancomycin: S. aureus, C. difficile, S. epidermidis

Tetracyclines: lyme disease, pneumonia, cholers, chlamydia

F-quinolones: UTI, GI infections, Anthrax

Rifampin: mycobacteria (TB, H. Influenza)