Cology, Antimicrobial Tx 1

Front 1

microbial susceptibility:

wide variety of organism

Back 1

broatd spectrum

Front 2

microbial susceptibitlity:

active against selective organist

Back 2

narrow spectrum

Front 3

sensitivity testing done by:

Back 3

disk diffusion

microdilution

e-test

Front 4

the oldest sensitivity

Back 4

disk diffusion

Front 5

dose for effective tx determined by

Back 5

MIC: minimum inhibitory concentration

Front 6

when to determine mic

Back 6

when there's no replication

Front 7

whcih is more effective:

MIC

or

MBC

Back 7

MBC: minimal bacterial concentration

Front 8

what can stain ur teeth as a child

Back 8

tetracylcine

binds to Ca and is put into the enamel

(also binds to bones)

Front 9

when shouldn't you give tetracycline

Back 9

< 14 yrs old

Front 10

what will cause gray baby syndrome

Back 10

chloramphenicol

Front 11

why will chloramphenicol cause gray baby syndrome

Back 11

babies unable to glucoronidate

they become lethargic and die

Front 12

chloramphenicol is a -- spectrum

Back 12

broad

Front 13

w/ a wound what's the best way to give an abx

Back 13

clean the wound so the enzymes won't inactivate the abx

Front 14

pcn can cause

Back 14

seizures

Front 15

time dependent: ability to kill dependent on -- ----

Back 15

blood concentration

Front 16

conc dependent: independent of ----

even if drug falls below window still able to kill; so ok to give ------

Back 16

time

QD

inside bacteria; so still killing

Front 17

combto used for tx of :

--- ---- infections

---microbial infections

--- antimicrobial activity

tx of --- strains

permit --- doses of antimicrobial agents

possibly reduce emergence of ---- ------

Back 17

life threatening

polymicrobial

enchanced

resistanct strains

lower doses

resistant strains

Front 18

how are pcn and aminoglycosides synergistic

Back 18

pcn's act on the cell wall

amino's act on protein synthesis

pcn's will weaken the cell wall, which will let amino's get in easier.

Front 19

develop of resistance:

----

--- to destory active drug

change in -- to drug

change in -- pathway

Back 19

selection

enzymes (pcnase, carbapenemases, cephalopsorinases)

permeability (b lactams get thru thru porins, so change this to prevent from get in)

efflux (tetracyclines, chloramphenicol, macrolides)

Front 20

development of reisistance:

change in --- of site of active drug

develop altered --- pathways

develop altered enzyme w/ less ------

Back 20

affinity (loss/alteration of binding proteins. . . protein synthesis inhibitors)

metabolic (sulfonamides/PABA)

affinity: protein synthesis inhibitor

Front 21

origin of resistance:

microoraginsh is in -- stage. . . surveis thousands of years. . .spores

specific --- structure lost after several -----

Back 21

dormant

target

replications (ex. cell wall)

Front 22

genetic changes that contribute to resistance include

Back 22

mutational resistance

conjugation

transduction

transformation

Front 23

t/f

mutation resistance is easy when there's only a few bac

Back 23

f

easier when there's millions

Front 24

conjugation:

-- resistance

common among gram -- bacteria

Back 24

plamid

negative

(vancomycin)

Front 25

transduction:

bacterial dna transferred thru -----

Back 25

phages

important in s. aureus

(resistant bac inject dna into sensitive and then it becomes resistant)

Front 26

when free dna absorbed from environment

Back 26

transformation

. . . cell scavengers eat up resistant stuff and become resistant

Front 27

when to use prophylatic abx

Back 27

heart valves

sx

Front 28

problems w/ prophylatic abx

Back 28

resistance

Front 29

misuse of antimicrobial agents:

tx of --- infections

--- of undetermined origins

improper ----

omission of --- drainage

lacke of adequate --- info

prolong tx after ---

Back 29

nonbacterial

fever

dosage (use whole dose)

surgical drainage

bacteriological

cure