Pharm Quiz 4 - Principles Of Antimicrobial Use

Front 1

Infection Pathogens

Back 1

Bacteria
Virus
Fungi
Parasites

Front 2

Pathogens Inhabit:

Back 2

Hospitals
Food Supply
Water
Animals
Humans

Front 3

Signs of Infection

Back 3

Fever
Increased WBCs

Front 4

Chain of Transportation

Back 4

Reservoir
Susceptible
Mode
Entry

Front 5

Examples of Reservoirs

Back 5

Human
Animal
Insect
Soil

Front 6

Examples of Susceptibles

Back 6

Malnourished
Unimmunized
Immunocompromised

Front 7

Examples of Modes

Back 7

Insect Bite
Nasal droplets
Semen

Front 8

Examples of Entry

Back 8

nasal/oral mucosa
abrasion puncture
sexual transmission

Front 9

Examples of drawbacks to overuse of antimicrobials

Back 9

Alters the body's natural
flora
Leads to resistant microbes

Front 10

Consequence of misuse?

Back 10

Obsolescense

Front 11

Cause of Superinfections

Back 11

Disruption of normal
nonpathogenic flora
Altered chemical environment
allows uncontrolled growth
of pathogenic bacteria or
fungus

Front 12

When are you at risk for a superinfection?

Back 12

Anytime you use an antibiotic (especially for long periods of time or for repeated therapy)

Front 13

Sites of Antibacterial Attack (5)

Back 13

1)Inhibition of synthesis of
the cell wall
2)Damage to cell membrane
3)Modification of DNA/RNA
synthesis
4)Modification of protein
synthesis (at Ribosome)
5)Modification of energy
metabolism on cell cytoplasm
(PABA-folic acid)

Front 14

Empiric Therapy

Back 14

When you don't know what the pathogen is and you have to start therapy by trial and error. Gradual and Slow.

Front 15

Direct Therapy

Back 15

When you know what the pathogen is and you can use specific antimicrobials to treat. Often, start with empirical while waiting to grow a culture that will identify the pathogen.

Front 16

Minimal Inhibitory Concentration (MIC)

Back 16

The lowest concentration of antimicrobial agent that presents visible growth after 18-24 hour incubation.

Front 17

Minimal Bacteriocidal Concentration (MBC)

Back 17

Kills 99.9% of cells. MIC dilution on agar until no growth.

Front 18

Bactericidal

Back 18

Kills Bacteria

Front 19

Bacteriostatic

Back 19

Stops growth of bacteria with help from host immune system.

Front 20

Concentration Dependent Effect

Back 20

Fluoroquinolones and Aminoglycosides kill bacteria at a faster rate at higher concentrations.

Front 21

Post-Antibiotic Effect

Back 21

When an antibiotic continues to inhibit growth for several hours after the concentrations fall below the MIC in the serum.

Front 22

Desired Peak Concentration of Drug at Site of Infection

Back 22

Greater than 4 x MIC

Front 23

Areas that are hard to reach with drugs

Back 23

Brain
Cerebrospinal Fluid
Eye
Prostate

Front 24

Toxicity in Antibiotics

Back 24

Most have favorable profiles.
Example: Aminoglycosides are nephrotoxic and ototoxic.

Front 25

Host Factors

Back 25

Allergy History
Age
Renal Function
Hepatic Function
Pregnancy
Genetics
Defenses

Front 26

Host Factors:
Allergy

Back 26

Penicillins and Sulfonamides especially.

Front 27

Host Factors:
Age

Back 27

Tetracyclines (Stain)
Sulfonamides (kernicterus)
Chloramphenicol (newborns)

Front 28

Host Factors:
Renal Function

Back 28

aminoglycosides: nephrotoxic
penicillin: ototoxic
quinolones: ototoxic

Front 29

Host Factors:
Hepatic Function

Back 29

Chloramphenicol
Erythromycin
Clarithromycin
Rifampin
Some Quinolones

Front 30

Host Factors:
Pregnancy Drugs to Avoid

Back 30

Metronidazole (X)
Rifampin (D)
Trimethoprim (D)
Quinolones (cartilage)
Tetracycline (bone and teeth)
Streptomycin (ototoxicity)
Sulfonamides (CNS toxicity)

Front 31

Host Factors:
Pregnancy Concerns

Back 31

Drugs can cross the placenta to some degree.
Also, drugs can be excreted in breast milk altering child's normal flora or sensitizing them for future allergies

Front 32

Host Factors:
Genetic and Metabolic Factors

Back 32

Hemolysis occurs in people who are glucose-6-phosphate-dehydrogenase-deficient when they take sulfonamides, chloramphenicol, and other certain drugs.

Front 33

Reasons for Multitherapy

Back 33

1)Lifethreatening Infection
2)Polymicrobial Infection
3)Empiric Therapy
4)To Achieve Synergy
5)Prevent emergence of
resistant bacteria
6)To permit a lower dose to
be used of one of the
antibiotics (b/c of S.E.s?)

Front 34

Interactions:
Indifferent Effects

Back 34

1+1=2

Front 35

Interactions:
Synergy

Back 35

1+1>2

Front 36

Interactions:
Antagonistic

Back 36

1+1<2

Front 37

3 Examples of synergistic combos

Back 37

1)Cell Wall Synthesis
Inhibitor + Aminoglycoside
2)Agents acting on
sequential steps in a
metabolic pathway.
3)Clavulanate + amoxicillin

Front 38

Antibiotic Decision Making... what should you do?

Back 38

Reassess regularly

Front 39

Antibiotic Prophylaxis

Back 39

To prevent infections when a patient may be especially vulnerable to infection.

Front 40

Intrinsic Bacterial Resistance

Back 40

A bacterium may be naturally resistant to some antibiotics because of a physical characteristic, like a thick cell wall.

Front 41

Acquired Bacterial Resistance

Back 41

Resistance gained by either mutation of an existing site, or acquisition of new genes.

Front 42

Ways that bacteria can acquire resistance

Back 42

Conjugation: exchange of
genetic materials (plasmids
with resistance genes.
Transposons: jumping genes)
Transformation: Bacteria
picks up DNA from environment
Trasduction: acquired through
a phage.

Front 43

4 Mechanisms of Resistance

Back 43

1)Development of altered
receptors or targets to
which the drug cannot bind
2)Altered rates of entry
and/or removal of the drug
from the bacterial cell can
cause a decrease in the
concentration of drug at
receptor sites.
3)Enhanced destruction or
inactivation of the drug.
4)Synthesis of resistant
metabolic pathways.