Principles of Antimicrobial Chemo Flashcards Preview

Mini II > Principles of Antimicrobial Chemo > Flashcards

Flashcards in Principles of Antimicrobial Chemo Deck (46):
1

what 3 classes of antibiotics cause superinfection?

1) broad spectrum penicillins (ampicillin)
2) Cephalosporins- 3rd/4th gen
3) Clindamycin

2

selective toxicity

antibiotics can kill microbes while having no effect or minimal effect on host cell

3

Cell wall synthesis inhibitors
(4 b-lactams, 2 other)

B-lactams:
1) penicillins
2) cephalosporins
3) carbapenems
4)monobactams

Others:
1) vancomycin
2) fosfomycin

4

protein synthesis inhibitors

1) aminoglycosides
2) macrolides and ketolide
3) clindamycin
4) tetracyclines and glycylcyclines
5) streptogramins
6) other (chlroamphenicol, Linezolid)

5

inhibitors of nucleic acid synthesis or function

1) sulfonamides
2) trimethoprim
3) fluroquinolones
4) nitroimidazoles (metronidazole)

6

antimycobacterial drugs

Rifamycins (rifampin)
(aminoglycosides)
(fluoroquinolones)
Others (isoniazid, prazinamide, ethambutol)

7

Bactericidal drugs

kill sensitive organisms at serum levels achievable in patient so number of viable organisms falls rapidly after exposure to drug

8

what is the first line treatment for seriously ill or immunocompromised patients?

bactericidal drugs

9

bacteriostatic drugs

arrests growth and replication of bacteria at serum levels achievable in patient thus limited spread of infection.

10

6 main bacteriostatic drugs

1) Sulfonamides
2) Macrolides
3) Clindamycin
4) Tetracyclines
5) chloramphenicol
6) Linezolid

11

MIC (Minimum inhibitory concentration)

lowest concentraiton of antibiotic that inhibits growth of tested bacteria

12

MBC (Minimum bactericidal concentration)

lowest concentration of antibiotic that kills tested bacteria

13

concentration dependent killing

(+ examples)

increase of bacterial killing as blood concentration of bactericidal antibiotics increases

ex: aminoglycosides, fluoroquinolones

14

time-dependent killing

(+ examples)

some bactericidal antibiotics do not significantly increase rate of killing as concentration increases

rate of killing is proportional to time the blood concentration remains above the minimum bactericidal concentration.

ex: penicillins, cephalosporins, vanco

15

postantibiotic effect

(+ examples)

some antibiotics show persistent suppression of microbial growth after drug plasma levels have fallen below minimum inhibitory concentration.

could be due persistence of drug at binding site and need to synthetize new enzymes before growth can resume

(ex: aminoglycosides and fluroquinolones)

16

b-lactam (site & MOA)

cell-wall
inhibition of transpeptidases

17

vancomycin (site & MOA)

cell wall
inhibition of transglycosylase

18

fofomycin (site & MOA)

inhibition of enolpyruvate transferase

19

aminoglycosides (site & MOA)

30S

blockade of initiation complex, misreading code of mRNA template, and blockade of translocation reaction

20

macrolides (site & MOA)

50S

blockade of translocation reaction

21

Chloramphenicol (site & MOA)

50S

blockade of transpeptidation reaction

22

Tetracyclines (site & MOA)

30S

blockade of aminoacyl-tRNA binding

23

Quinupristin (site & MOA)

50S

blockade of translocation reaction

24

Dalfopristin (site & MOA)

50S

blockade of translocation reaction

25

Linezolid (site & MOA)

50S

blockade of initiation complex

26

Sulfonamide (site & MOA)

cytoplasm

inhibition of dihydropteroate syntehtase

27

Trimethoprim (site & MOA)

cytoplasm

inhibition of dihydrofolate reductase

28

Quinolones (site & MOA)

cytoplasm

inhibition of topoisomerases

29

Metronidazole (site & MOA)

DNA

DNA damage

30

drug resistance can result from what 2 changes in microbial DNA?

1) spontaneous mutation

2) DNA transfer of drug resistance (Plasmid)

31

What 4 mechanisms are responsible for antimicrobial drug resistance?

1) production of microbial enzymes that inactivate drug (ex: beta-lactamase)
2) development of microbial targets with decreased drug affinity (i.e. decreased topoisomerase affinity, 50S, 30S)
3) decreased drug concentration inside bacteria due to decreased permeability of cell membrane or multidrug efflux pump
4)increased production of essentail metabolite (i.e. PABA)

32

empiric therapy

antimicrobial treatment without laboratory identification of specific pathogen.
used when:
1) history and site of infection
2) severity of disease requires immediate treatment

33

specific therapy

specific antimicrobial treatment done after identifying causative pathogen by cultures nad susceptibiliyt testing of sample from infection site

34

prophylactic therapy

to prevent rather than treat infection. Indiscriminate use of prophylactic therapy can result in bacterial resistance and super infections

35

impaired immune systems can affect antimicrobail drug therapy. what clinical situations would this include?

1) advanced age
2)DM
3) alcoholism
4) malnutrition
5) HIV
6) immunosuppressive therapy
7) cancer chemo

36

T or F-- bactericidal antibiotics are preferred inpatients with impaired immunity

T

37

when must surgical drainage occur before proper action of antibiotics can be achieved?

abscesses

38

why are some antibiotics contraindicated in very young or very old?

becauser renal and hepatic functions are poorly developed in newborns and diminished in elderly

39

do most antimicrobials cross placenta?

yes

40

what antibiotics should be avoided during pregnancy? (5 major classes)

1) tetracyclines/glycylcylines
2) aminoglycosides
3) some macrolides
4) fluoroquinolones
5) sulfonamides

41

direct cytotoxicity

when some antibiotics cause dose-related cytotoxicity to some organs or tissues

42

allergic reactions and antimicrobials

when some antibiotics or their metabolites have intrinsic ability to induce hypersensitiviy.

most allergenic antibiotics = beta-lactams, sulfonamides, and tetracyclines

43

drug interactions

mainly due to induction (i.e. by rifampin) or inhibitions (i.e. erythromycin) or metabolism of concamitant drug

44

superinfection

broad specturm antibiotics can lead to alteration of normal microflora of respiratory, intestinal, and GU tracts leading to opportunistic infections

45

what are 4 reasons why antibiotic combinations are used?

1) treat empirically severe infections (i.e. endocarditis)
2) delay drug resistance (i.e. TB)
3) treat mixed infection (i.e. periotneal infection)
4) achieve a synergistic effect (i.e. P. aeruginosa)

46

What are the 3 main mechanims of antibiotic synergism?

1) sequential blockade ( combine duse of drugs may cause inhibition of two steps in a bacterial metabolic pathway-- ie.e trimethoprim-sulfametoxazole combo)
2) blockade of drug inactiving enzymes (i.e. clavulanic acid inhibits penicillinases)
3) enhanced bacterial drug uptake (i.e. b-lactam drugs increase bacterial permeability to aminoglycosides)