Pharm Final - Selection And Clinical Use Of Antimicrobials

Front 1

there is increasing evidence that antimicrobials are ___ and _____ used

Back 1

over, improperly

Front 2

T/F choosing an antimic. is just matching a drug to a bug

Back 2

F

Front 3

4 steps of the systematic approach for AM selection

Back 3

1. Confirm presence of infxn
2. ID the pathogen
3. select presumptive (empiric) therapy
4. monitor therapeutic response

Front 4

_____ are substances that cause fever

Back 4

pyrogens

Front 5

T/F you must have an infxn to have a fever

Back 5

F

Front 6

what is a drug induced fever

Back 6

persistent fever in absence of infxn which coincides w/ drug use and disappears when drug is D/Ced

Front 7

What is the normal range for body temp in C

Back 7

36-37.8

Front 8

3 ways to confirm presence of infxn

Back 8

fever
drug induced fever
WBC count

Front 9

normal WBC count range

Back 9

4-10K/mm

Front 10

bact. infxns are associated w/ increased ___ counts

Back 10

granulocyte

Front 11

what type of WBC is especially elevated in bact. infxn

Back 11

neutrophils

Front 12

what form of neutrophil becomes more common in bact. infxn? What is this called?

Back 12

immature forms
shift to the left

Front 13

factors that predispose to infxn

Back 13

-alterations in normal flora of host
-disruption of natural barriers
-Age
-immunosuppression from malnutrition, DZ, hormones, drugs

Front 14

what should you get before any AM therapy and should you do it sooner or later?

Back 14

a culture!
soon! delay can cause false negative esp. if drugs are given (will mask infxn)

Front 15

what is MIC?

Back 15

minimum inhibitory conc. - the smallest conc. that will inhibit growth

Front 16

what is MBC?

Back 16

min. bactericidal conc. - the smallest conc. that will kill the org.

Front 17

T/F it is more important to consider national and regional susceptibility data than local

Back 17

F!

Front 18

T/F every AM kills the bug that it treats

Back 18

F

Front 19

what bacteriostatic AM is hard to get in the US b/c of it's toxic side effects?

Back 19

chloramphenicol

Front 20

what do bacteriostatic AMs do?

Back 20

inhibit protein synth. which prevents orgs. from growing

Front 21

what is conc. dependent killing and give 2 examples of AMs with it

Back 21

rate and extent of killing increases with increasing drug conc.
-ex. aminoglycosides and quinolones (floxacins)

Front 22

what is time dependent killing and give an example

Back 22

bactericidal activity continues as long as serum conc. are greater than MBC
-ex. beta-lactams

Front 23

do you get better killing with a time dependent killing AM if you increase AM conc. above MBC?

Back 23

NOPE

Front 24

combination therapy ____ the spectrum of coverage and is esp. useful in what two types of infxns?

Back 24

broadens,
mixed and nosocomial infxns

Front 25

what are the disadvantages of combo therapy?

Back 25

-additive toxicity --> nephrotoxicity
-possible antagonism among agents
ex. aminoglycosides are inactivated by penicillin

Front 26

what is the post-antibiotic effect (PAE) and what is it's mechanism?

Back 26

persistent suppression of growth after drug is gone
-mechanism unknown (may be lag phase of bact. growth)

Front 27

what is the clinical relevance of post-antibiotic effect?

Back 27

-once daily dosing
-enhanced bactericidal activity
-less toxicity*
-lower monitoring costs

Front 28

what is post-antibiotic leukocyte enhancement (PALE)?

Back 28

increased susceptibility of bact. to the phagocytic and bactericidal action of neutrophils

Front 29

synergism can result in a __ fold or greater reduction in MIC/MBC of each drug when used in combo vs. alone

Back 29

4

Front 30

what are 3 mechanisms of synergism?

Back 30

-blockade of sequential steps in a metabolic sequence ex. TMP/sulfa
-inhibition of enzymatic inactivation ex. penicillins and cephalosporings (unisyn)
-enhancement of AM agent uptake
ex. penicillin and aminoglycosides (break down cell wall and then kill)

Front 31

what are the mechanisms of antagonism

Back 31

-inhibition of 'cidal' activity by 'static' agents
-induction of enzymatic inactivation
ex. imipenem, cefoxitin, ampicillin
-direct drug interaction

Front 32

What 2 AMs require serum conc. monitoring?

Back 32

Aminoglycosides and Vanco

Front 33

AMs are _____ in preventing infxns

Back 33

effective

Front 34

AM prophylaxis may be divided into ____ and ____

Back 34

surgical and non-surg

Front 35

surgical wound infxns increase the average hospital stay by __ days and inc. the bill by $_____

Back 35

7.3,
$3152

Front 36

surgical procedures that require AM prophylaxis include:

Back 36

-contaminated and clean-contaminated operations
-ops in which postop infxn would be catastrophic i.e. open heart surg
-clean procedures that involve prosthetics
-any procedure in immunocompromised pt

Front 37

for surg. prophylaxis the AM must achieve conc. greater than ____ and must be present by _____

Back 37

MIC
Time of incision

Front 38

T/F the surgical prophylaxis AM should have as broad of coverage as possible

Back 38

F, should be active against common surgical wound pathogens

Front 39

the _____ course of the ______ effective and _____ toxic AM should be used for surg. proph.

Back 39

shortest possible;
most;
least;

Front 40

What are some common errors in AM prophylaxis?

Back 40

-selection of wrong AM
-admin. the 1st dose too late
-failure to repeat doses during long procedures
-excessive duration of proph.
-inappropriate use of broad spectrum AM

Front 41

when do you administer nonsurgical prophylaxis

Back 41

-indicated for those at high risk for temp. exposure to pathogens or b/c of underlying DZ

Front 42

what is nonsurgical prophylaxis?

Back 42

-prevention of colonization/asymptomatic infxn
-administration of drugs following colonization/inoculation BUT before development of DZ