Antibacterial Agents I Flashcards Preview

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Flashcards in Antibacterial Agents I Deck (36):
1

Selective toxicity definition

ability of an antimicrobial agent to target only pathogens and not normal body cells

2

Typical gram-positive cocci

Streptococci (pneumonia, pyogenes), Staphyloccoci (aureaus: MRSA), Enterococci (faecium)

3

Typical gram-negative cocci

Neisseria (meningitidis, gonorrheae)

4

Typical gram-negative rods

E. Coli, Pseudomonas aeruginose

5

Typical anaerobic gram-positive rods

Clostridia (difficile, tetani, botulinum)

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Typical anearobic gram-negative rods

Bacteriodes fragilis

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Typical atypical bacteria

Chlamydia, Mycoplasma, Rickettsia

8

Examples of selective toxicity (5)

1. folate metabolism: intracell (bacteria) vs. absorb (mammal) 2. protein synthesis: different ribosomes 3. DNA synthesis: gyrase (bacteria) vs. topoisomerase (mammal) 4. cell wall: no peptidoglycan in eukaryotes 5. ergosterol (fungal membrane) vs. cholesterol (mammal)

9

Narrrow spectrum antibiotic definition

treats gram-positive or gram-negative bacteria

10

Extended spectrum antibiotic definition

treats gram-positive and gram-negative bacteria

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Broad spectrum antibiotic definition

treats gram-positive and gram-negative bacteria and atypical organisms

12

Narrrow spectrum antibiotic examples (3)

1. aminoglycosides 2. vancomyocin 3. penicillin

13

Extended spectrum antibiotic examples (3)

1. cephalosporins 2. fluoroquinoloes (cip, levo) 3. carbapenems

14

Braod spectrum antibiotic examples (4)

1. macrolides 2. sulfonamides 3. tetracyclines 4. fluoroquinoloes (moxi, gemi)

15

Natural (intrinsic) resistance definition and example

microbe lacks target for drug action; e.g. fungal cell walls do not contain peptidoglycan

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Escape resistance definition and example

microbe sensitive but "escapes" consequences due to mitigating factors; e.g. availabilty of purines, tymidine, serine, and methionine w/in purulent infections generates sulfonamide resistance

17

Acquired resistance definition and types

Selective pressure produces successive generations w/traits that resist action of durgs; mutational (chromosomal) or plasmid-mediated resistance

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Mutational (chromosomal) resistance process

Each suceeding generation of bacteria becomes slightly more resistant if some survive treatment; proper dosing and duration of antibiotic prevents survival of resistant strains

19

Plasmid-mediated resistance process

Extrachromosomal ring of DNA that confers antibiotic resistance is taken up via conjugation, transduction, and transformation; clincially important source of multiple drug resistance

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Main mechanisms of resistance (5)

1. altered targets/receptors 2. enzymatic destruction 3. alternative resistant metabolic pathway 4. decreased entry (natural) 5. increased efflux

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Steps to minimize resistance (3)

1. only use antibiotics when needed 2. select antibiotic based on susceptibilty of pathogen 3. use adequate concentration and duration of antibiotic

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Action of Bactericidal agents

organisms are killed

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Action of Bacteriostatic agents

organisms are prevented from growing

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Bactericidal general mechanisms

1. inhibition of cell wall synthesis 2. disruption of cell membrane function 3. interferes with DNA function/synthesis

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Bacteriostatic general mechanisms

1. inhibtion of protein synthesis (except aminoglycosides) 2. inhibition of intermediary metabolic pathways

26

Advantages of bactericidal agents (4)

1. preferred in sever infections 2. act more quickly, act irreversably 3. compensate for pts w/impaired host defense 4. treat infections unable to be accessed by host immune system

27

Oral vs. IV route of administration of antibiotics

Oral=cheaper, easily accepted but possible GI upset vs. IV=most rapid, predictable plasma levels but greater expense, requires strict aseptic conditions

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Considerations regarding distribution when selecting antibiotics (3)

1. CNS=will drug cross BBB if necc.? 2. Fetus=will drug cross placenta and harm fetus? 3. Selective distribution=will drug accumulate?

29

Common beneficial antibiotic accumulations (4)

1. clindamycin-->bone 2. marcolides --> pulmonary cells 3. tetracyclins --> gingival fluid & sebum) 4. nitrofurantoin --> urine

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Common toxic antibiotic accumulations (2)

1. aminoglycoside-->inner ear & renal brush border 2. tetracyclines-->bind Ca++ in developing bone/teeth

31

Elimination impact on antibiotic choice/dosing

renal exretion may require renal dosing; hepatic metabolism --> drug-drug interaction; hepatotoxicity

32

Consequence of inadequate duration or dose of antibiotic

can develop resistance and/or recurrence of infection

33

Consequence of overextended duration of antibiotic

superinfection more likely

34

Consequence of elevated dose of antibiotic

dose-related toxicities may occur

35

Most important cell wall synthesis inhibitors (5)

1. Penicillins (Acid-stable: Penicillin V & Extended Spectrum: Amoxicillin) 2. Cephalosporins (1st: Cephalexin 3rd: Cefdinir) 3. Vancomycin

36

Most important protein synthesis inhibitors (6)

1. Macrolides (Azithromycin) 2. Tetracyclines (Doxycycline, Minocycline) 3. Lincosamides (Clindamycin) 4. Chloramphenicol 5. Aminoglycosides (Streptomycin)