Antibacterial Agents I

Question 1

Selective toxicity definition

Answer 1

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

Question 2

Typical gram-positive cocci

Answer 2

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

Question 3

Typical gram-negative cocci

Answer 3

Neisseria (meningitidis, gonorrheae)

Question 4

Typical gram-negative rods

Answer 4

E. Coli, Pseudomonas aeruginose

Question 5

Typical anaerobic gram-positive rods

Answer 5

Clostridia (difficile, tetani, botulinum)

Question 6

Typical anearobic gram-negative rods

Answer 6

Bacteriodes fragilis

Question 7

Typical atypical bacteria

Answer 7

Chlamydia, Mycoplasma, Rickettsia

Question 8

Examples of selective toxicity (5)

Answer 8

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)

Question 9

Narrrow spectrum antibiotic definition

Answer 9

treats gram-positive or gram-negative bacteria

Question 10

Extended spectrum antibiotic definition

Answer 10

treats gram-positive and gram-negative bacteria

Question 11

Broad spectrum antibiotic definition

Answer 11

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

Question 12

Narrrow spectrum antibiotic examples (3)

Answer 12

1. aminoglycosides 2. vancomyocin 3. penicillin

Question 13

Extended spectrum antibiotic examples (3)

Answer 13

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

Question 14

Braod spectrum antibiotic examples (4)

Answer 14

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

Question 15

Natural (intrinsic) resistance definition and example

Answer 15

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

Question 16

Escape resistance definition and example

Answer 16

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

Question 17

Acquired resistance definition and types

Answer 17

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

Question 18

Mutational (chromosomal) resistance process

Answer 18

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

Question 19

Plasmid-mediated resistance process

Answer 19

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

Question 20

Main mechanisms of resistance (5)

Answer 20

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

Question 21

Steps to minimize resistance (3)

Answer 21

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

Question 22

Action of Bactericidal agents

Answer 22

organisms are killed

Question 23

Action of Bacteriostatic agents

Answer 23

organisms are prevented from growing

Question 24

Bactericidal general mechanisms

Answer 24

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

Question 25

Bacteriostatic general mechanisms

Answer 25

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

Question 26

Advantages of bactericidal agents (4)

Answer 26

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

Question 27

Oral vs. IV route of administration of antibiotics

Answer 27

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

Question 28

Considerations regarding distribution when selecting antibiotics (3)

Answer 28

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

Question 29

Common beneficial antibiotic accumulations (4)

Answer 29

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

Question 30

Common toxic antibiotic accumulations (2)

Answer 30

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

Question 31

Elimination impact on antibiotic choice/dosing

Answer 31

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

Question 32

Consequence of inadequate duration or dose of antibiotic

Answer 32

can develop resistance and/or recurrence of infection

Question 33

Consequence of overextended duration of antibiotic

Answer 33

superinfection more likely

Question 34

Consequence of elevated dose of antibiotic

Answer 34

dose-related toxicities may occur

Question 35

Most important cell wall synthesis inhibitors (5)

Answer 35

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

Question 36

Most important protein synthesis inhibitors (6)

Answer 36

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