AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
1. Host factors af- - Allergy
fecting antibiot- - Immune status (use bacteriacidal drugs in immunocompromised)
ic use - Infection site complications (BBB, foreign bodies, perfusion)
- Age
- Pregnancy & lactation
- genetics
- drug enzymes & DDI
2. Misuses of An- 1) Tx for viral infections
tibiotics 2) Tx for FUO (except in immunocompromised pts)
3) No bacterial information
4) Inappropriate dose or patient
5) Absence of other interventions i.e. drainage, removal of foreign bodies, etc.
3. Examples of in- 1) Common cold - abx are ineffective
appopriate Abx 2) Bronchitis - abx are ineffective except in some cases
prescription 3) Sore throat - abx only in confirmed Strep
4) Sinusitis - abx should be withheld for 10D in the absence of facial pain
4. Abx selective tox- Abx unique MOA that makes them selectively toxic to bacteria
icity & mecha- - ability to disrupt bacterial cell wall or inhibit cell wall synthesis
nism of antibiotic - lethal or nonlethal inhibition of bacterial protein synthesis
action - inhibition of bacterial nucleic acid synthesis
- antimetabolites
5. DNA or RNA syn- fluoroquinolones, rifampin
thesis inhibitors
6. T/F: any antibi- True
otic may pro-
mote resistance,
but *broad spec-
trum* agents are
, AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
the most likely to
cause it
7. Mechanisms of 1) production of drug-metabolizing enzymes
antibiotic resis- 2) decreased drug uptake
tance 3) change in drug receptor w/ decreased binding of abx
4) synthesis of compounds that antagonize the antibiotic
8. Ways organisms 1) *spontaneous mutation* - occurs only to one drug
become resistant 2) *conjugation*
to antibiotics - mostly in GN bacteria, occur b/w normal flora & pathogens
-*R-factor* w/c is extra-chromosomal DNA encoding for resistance that is passed
from one bacteria to the next
- responsible for multiple-drug resistant bugs
9. CDC's campaign *Infection Prevention*
to prevent an- - vaccinate
timicrobial resis- - remove catheters
tance
*Diagnose & Tx infections effectively*
- target the pathogen
- contact the experts
*Use ABX wisely*
- practice antimicrobial control
- use local data
- tx infection, NOT contamination or colonization
- know when to say "NO" to Vanco
- stop ABX when infection has cleared or unlikely a bacterial infection
*Prevent transmission*
- isolate the pathogen
- break the chain of contagion
, AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
10. Who should re- 1) Select *surgical patients* - cardiac, peripheral vascular, orthopedics, GI, GYN
ceive ABX pro- (hysterectomy)
phylaxis? 2) *severely neutropenic*
3) pt at risk for *bacterial endocarditis*
4) pts w/ *recurrent UTIs, severe rheumatic endocarditis*
11. Indications for 1) *initial therapy for severe infection* - until organism is ID'd
ABX combina- 2) *mixed infections* - common in GI, pelvic, brain abscesses
tions 3) *prevent emergence of resistance* - TB, HIV, certain parasites
4) *to decrease toxicity*
5) *to promote synergistic effect* - PCN + gentamicin, TMP-SMZ*
12. ABX combination 1) increased risk of *adverse effects* like allergy or toxicity
disadvantages 2) risk of *suprainfection* (ex. C. diff & yeast infection*
3) risk for *drug resistance*
4) increase *cost*
13. Cell wall synthe- PCN, cephalosporins, carbapenems, aztreonam, vancomycin, fosfomycin, te-
sis inhibitors icoplanin
14. Penicillins - *inhibit transpeptidases necessary for cell wall synthesis* & activate autolysis w/c
cleave bonds in the cell wall.
- *target the PCN binding proteins (PBP) - PBP1 & PBP3 (crucial targets)
- *resistance* is d/t inability of drug to reach PBPs or enzymatic inactivation of the
drug
- PCN resistant drugs produce beta-lactamase which cuts into the beta-lactam
ring of the drug which inactivates the ABX so the ABX is no longer become
anti-infective.
, AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
•Allergic reactions (1-5%); Anaphylaxis (.004-.015%)
•Cross reaction - 3-7% PCN to Ceph
•Prolonged high dose = granulocytopenia, interstitial nephritis
15. Bacterial cell wall Gram positive vs Gram negative
Gram negative has an outer membrane and gram positive does not w/c prevents
PCN from reaching PBPs (target molecules)
16. PCN: *PCN G, PCN V K*
*Narrow-spec- useful for Strep, Neisseria, many anaerobes, & spirochetes
trum PCNase
sensitive*
17. PCN: *Nafcillin, Oxacillin*, Cloxacillin, Dicloxacillin
*Narrow-spec- - useful for Staph aureus
trum PCNase
resistant*
18. PCN: *Ampicillin, Amoxicillin*, Bicampicillin
*Broad-spec- - useful for H. flu, E. coli, P. mirabilis, N. gonorrheae, enterococci
trum*
susceptible to beta-lactamase
19. PCN: *Extend- - *Piperacillin*, Carbenicillin, Ticarcillin, Mezlocillin
ed-spectrum* useful for H. flu, E. coli, P. mirabilis, N. gonorrheae, enterococci
*PLUS*
*pseudomonas*, enterobacter, proteus, *B. fragilis*, & Klebsi
Study online at https://quizlet.com/_js58wa
1. Host factors af- - Allergy
fecting antibiot- - Immune status (use bacteriacidal drugs in immunocompromised)
ic use - Infection site complications (BBB, foreign bodies, perfusion)
- Age
- Pregnancy & lactation
- genetics
- drug enzymes & DDI
2. Misuses of An- 1) Tx for viral infections
tibiotics 2) Tx for FUO (except in immunocompromised pts)
3) No bacterial information
4) Inappropriate dose or patient
5) Absence of other interventions i.e. drainage, removal of foreign bodies, etc.
3. Examples of in- 1) Common cold - abx are ineffective
appopriate Abx 2) Bronchitis - abx are ineffective except in some cases
prescription 3) Sore throat - abx only in confirmed Strep
4) Sinusitis - abx should be withheld for 10D in the absence of facial pain
4. Abx selective tox- Abx unique MOA that makes them selectively toxic to bacteria
icity & mecha- - ability to disrupt bacterial cell wall or inhibit cell wall synthesis
nism of antibiotic - lethal or nonlethal inhibition of bacterial protein synthesis
action - inhibition of bacterial nucleic acid synthesis
- antimetabolites
5. DNA or RNA syn- fluoroquinolones, rifampin
thesis inhibitors
6. T/F: any antibi- True
otic may pro-
mote resistance,
but *broad spec-
trum* agents are
, AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
the most likely to
cause it
7. Mechanisms of 1) production of drug-metabolizing enzymes
antibiotic resis- 2) decreased drug uptake
tance 3) change in drug receptor w/ decreased binding of abx
4) synthesis of compounds that antagonize the antibiotic
8. Ways organisms 1) *spontaneous mutation* - occurs only to one drug
become resistant 2) *conjugation*
to antibiotics - mostly in GN bacteria, occur b/w normal flora & pathogens
-*R-factor* w/c is extra-chromosomal DNA encoding for resistance that is passed
from one bacteria to the next
- responsible for multiple-drug resistant bugs
9. CDC's campaign *Infection Prevention*
to prevent an- - vaccinate
timicrobial resis- - remove catheters
tance
*Diagnose & Tx infections effectively*
- target the pathogen
- contact the experts
*Use ABX wisely*
- practice antimicrobial control
- use local data
- tx infection, NOT contamination or colonization
- know when to say "NO" to Vanco
- stop ABX when infection has cleared or unlikely a bacterial infection
*Prevent transmission*
- isolate the pathogen
- break the chain of contagion
, AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
10. Who should re- 1) Select *surgical patients* - cardiac, peripheral vascular, orthopedics, GI, GYN
ceive ABX pro- (hysterectomy)
phylaxis? 2) *severely neutropenic*
3) pt at risk for *bacterial endocarditis*
4) pts w/ *recurrent UTIs, severe rheumatic endocarditis*
11. Indications for 1) *initial therapy for severe infection* - until organism is ID'd
ABX combina- 2) *mixed infections* - common in GI, pelvic, brain abscesses
tions 3) *prevent emergence of resistance* - TB, HIV, certain parasites
4) *to decrease toxicity*
5) *to promote synergistic effect* - PCN + gentamicin, TMP-SMZ*
12. ABX combination 1) increased risk of *adverse effects* like allergy or toxicity
disadvantages 2) risk of *suprainfection* (ex. C. diff & yeast infection*
3) risk for *drug resistance*
4) increase *cost*
13. Cell wall synthe- PCN, cephalosporins, carbapenems, aztreonam, vancomycin, fosfomycin, te-
sis inhibitors icoplanin
14. Penicillins - *inhibit transpeptidases necessary for cell wall synthesis* & activate autolysis w/c
cleave bonds in the cell wall.
- *target the PCN binding proteins (PBP) - PBP1 & PBP3 (crucial targets)
- *resistance* is d/t inability of drug to reach PBPs or enzymatic inactivation of the
drug
- PCN resistant drugs produce beta-lactamase which cuts into the beta-lactam
ring of the drug which inactivates the ABX so the ABX is no longer become
anti-infective.
, AGACNP Barkley ABX
Study online at https://quizlet.com/_js58wa
•Allergic reactions (1-5%); Anaphylaxis (.004-.015%)
•Cross reaction - 3-7% PCN to Ceph
•Prolonged high dose = granulocytopenia, interstitial nephritis
15. Bacterial cell wall Gram positive vs Gram negative
Gram negative has an outer membrane and gram positive does not w/c prevents
PCN from reaching PBPs (target molecules)
16. PCN: *PCN G, PCN V K*
*Narrow-spec- useful for Strep, Neisseria, many anaerobes, & spirochetes
trum PCNase
sensitive*
17. PCN: *Nafcillin, Oxacillin*, Cloxacillin, Dicloxacillin
*Narrow-spec- - useful for Staph aureus
trum PCNase
resistant*
18. PCN: *Ampicillin, Amoxicillin*, Bicampicillin
*Broad-spec- - useful for H. flu, E. coli, P. mirabilis, N. gonorrheae, enterococci
trum*
susceptible to beta-lactamase
19. PCN: *Extend- - *Piperacillin*, Carbenicillin, Ticarcillin, Mezlocillin
ed-spectrum* useful for H. flu, E. coli, P. mirabilis, N. gonorrheae, enterococci
*PLUS*
*pseudomonas*, enterobacter, proteus, *B. fragilis*, & Klebsi
