Antibacterial Agents I Flashcards

1
Q

Selective toxicity definition

A

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

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2
Q

Typical gram-positive cocci

A

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

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3
Q

Typical gram-negative cocci

A

Neisseria (meningitidis, gonorrheae)

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4
Q

Typical gram-negative rods

A

E. Coli, Pseudomonas aeruginose

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5
Q

Typical anaerobic gram-positive rods

A

Clostridia (difficile, tetani, botulinum)

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6
Q

Typical anearobic gram-negative rods

A

Bacteriodes fragilis

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7
Q

Typical atypical bacteria

A

Chlamydia, Mycoplasma, Rickettsia

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8
Q

Examples of selective toxicity (5)

A
  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)
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9
Q

Narrrow spectrum antibiotic definition

A

treats gram-positive or gram-negative bacteria

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10
Q

Extended spectrum antibiotic definition

A

treats gram-positive and gram-negative bacteria

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11
Q

Broad spectrum antibiotic definition

A

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

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12
Q

Narrrow spectrum antibiotic examples (3)

A
  1. aminoglycosides 2. vancomyocin 3. penicillin
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13
Q

Extended spectrum antibiotic examples (3)

A
  1. cephalosporins 2. fluoroquinoloes (cip, levo) 3. carbapenems
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14
Q

Braod spectrum antibiotic examples (4)

A
  1. macrolides 2. sulfonamides 3. tetracyclines 4. fluoroquinoloes (moxi, gemi)
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15
Q

Natural (intrinsic) resistance definition and example

A

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

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16
Q

Escape resistance definition and example

A

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
Q

Acquired resistance definition and types

A

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

18
Q

Mutational (chromosomal) resistance process

A

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
Q

Plasmid-mediated resistance process

A

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

20
Q

Main mechanisms of resistance (5)

A
  1. altered targets/receptors 2. enzymatic destruction 3. alternative resistant metabolic pathway 4. decreased entry (natural) 5. increased efflux
21
Q

Steps to minimize resistance (3)

A
  1. only use antibiotics when needed 2. select antibiotic based on susceptibilty of pathogen 3. use adequate concentration and duration of antibiotic
22
Q

Action of Bactericidal agents

A

organisms are killed

23
Q

Action of Bacteriostatic agents

A

organisms are prevented from growing

24
Q

Bactericidal general mechanisms

A
  1. inhibition of cell wall synthesis 2. disruption of cell membrane function 3. interferes with DNA function/synthesis
25
Q

Bacteriostatic general mechanisms

A
  1. inhibtion of protein synthesis (except aminoglycosides) 2. inhibition of intermediary metabolic pathways
26
Q

Advantages of bactericidal agents (4)

A
  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
Q

Oral vs. IV route of administration of antibiotics

A

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

28
Q

Considerations regarding distribution when selecting antibiotics (3)

A
  1. CNS=will drug cross BBB if necc.? 2. Fetus=will drug cross placenta and harm fetus? 3. Selective distribution=will drug accumulate?
29
Q

Common beneficial antibiotic accumulations (4)

A
  1. clindamycin–>bone 2. marcolides –> pulmonary cells 3. tetracyclins –> gingival fluid & sebum) 4. nitrofurantoin –> urine
30
Q

Common toxic antibiotic accumulations (2)

A
  1. aminoglycoside–>inner ear & renal brush border 2. tetracyclines–>bind Ca++ in developing bone/teeth
31
Q

Elimination impact on antibiotic choice/dosing

A

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

32
Q

Consequence of inadequate duration or dose of antibiotic

A

can develop resistance and/or recurrence of infection

33
Q

Consequence of overextended duration of antibiotic

A

superinfection more likely

34
Q

Consequence of elevated dose of antibiotic

A

dose-related toxicities may occur

35
Q

Most important cell wall synthesis inhibitors (5)

A
  1. Penicillins (Acid-stable: Penicillin V & Extended Spectrum: Amoxicillin) 2. Cephalosporins (1st: Cephalexin 3rd: Cefdinir) 3. Vancomycin
36
Q

Most important protein synthesis inhibitors (6)

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