Respiratory_Bridges_Intro To Antimicrobials

Front 1

Do bacteriostatic or bactericidal drugs work better in a healthy person with a normal immune system?

Back 1

Both of these drugs work just as well in a normal immune system

Front 2

MOA: Bacteriostatic Agents

Back 2

Inhibit growth and reproduction of bacteria without killing them

Front 3

Which drugs work with the immune system to rid bacteria from the body?

Back 3

Bacteriostatic drugs

Front 4

Tetracyclines and Macrolides are what?

Back 4

Bacteriostatic drugs

**Protein Synthesis Inhibitors**

Front 5

These drugs are critical when the immune system is depressed

Back 5

Bactericidal

Front 6

In general, cell wall agents are what type of drugs?

Back 6

Bactericidal

Front 7

Penecillin is a bactercidal drug with a time-dependent effect. What does that mean?

Back 7

Once you reach the Minimum Inhibitory Concentration of penecillin it begins and continues killing as long as you are still at MIC.

Upping dosage will not increase penicillin's affect once @ MIC

Front 8

Some bacteria have concentration dependent effects. What does this mean?

Back 8

Must reach a certain concentration of drug in body before it begins to kill bacteria

Front 9

What type of agent is required for:

-Endocarditis or other endovascular infxn

-Meningitis

-Infxn in neutropenic cancer patients

Back 9

Bactericidal

Front 10

T/F

All drugs can be harmful at high concentrations

Back 10

TRUE

Front 11

Table for Antimicrobial TI's

Back 11

Therapeutic Index

Front 12

What does selective toxicity mean?

Back 12

Drug affects only one type of cell (bacteria, etc.) and spares host cells

Front 13

In order to obtain selective toxicity, what is targeted?

Back 13

Microorganism

-Cell wall

-protein synthesis

-nucleic acid synthesis

**no effect on host cells**

Front 14

What is the therapeutic index?

Back 14

Relates the dose of desired effects to dose of undesired effects

Front 15

High therapeutic index

Back 15

less likely to be toxic to patients

Front 16

Low therapeutic index

Back 16

More likely to be toxic to patient

**May require patient monitoring for toxicity**

Front 17

What are some potential side effects of antimicrobial drugs?

Back 17

Allergic Reaction

Toxicity--> renal damage

Supression of Normal Flora

Front 18

Suppression of normal flora in the gut can cause what?

Back 18

C. diff -->pseudomembranous colitis

Front 19

What are the 5 principle targets of antibiotics?

Back 19

1. Inhibition of cell wall synthesis

2. Disruption of cell membrane function

3. Inhibition of protein synthesis

4. Inhibition of nucleic acid synthesis

5. Action as antimetabolites

Front 20

MOA: Agents that inhibit synthesis of bacterial cell walls

Back 20

Inhibit different stages of cell wall sytnthesis

Beta-lactams --> penicillins and cephalosporins

Front 21

What cells have peptidoglycan?

Back 21

Only bacteria have peptidoglycan

It makes up cell walls and is targeted by agents that inhibit cell wall synthesis

Front 22

MOA: Agents that act directly on the cell membrane

Back 22

Increase permeability leading to leakage of intracellular components

Front 23

Examples of Agents that act directly on the cell membrane

Back 23

polymyxin and daptomycin

Front 24

Agents that reversibly inhibit bacterial protein synthesis are bacteriostatic/bactericidal

Back 24

Bacteriostatic

Front 25

Aminoglycosides reversibly/irreversibly inhibit bacterial protein synthesis and are considered bacteriostatic/bactericidal

Back 25

Irreversibly inhibit

Bactericidal

Front 26

MOA: Agents that affect bacterial nucleic acid metabolism

Back 26

**affect bacterial DNA replication**
- inhibit DNA gyrase (eg, fluoroquinolones)

**inhibit RNA polymerase** (eg, rifampin)

Front 27

MOA: Inhibition of synthesis of essential metabolites

Back 27

antimetabolites that block essential
enzymes of FOLATE metabolism

(eg,trimethoprim and the sulfonamides)

Front 28

What are the essential metabolites of FOLATE metabolism?

Back 28

p-Aminobenzoic acid

Didhydrofolic acid

Tetrahydrofolic acid

Front 29

Big summary slide of ABX actions

Back 29

Front 30

Explain Intrinsic Drug Resistance

Back 30

-Bacteria resistant naturally, without prior exposure to antibiotics

-There is no drug target or drug cannot access target

Front 31

Explain Acquired Drug Resistance

Back 31

Bacteria change or acquire new DNA resulting in resistance

(genetic change)---> Plasmid

Front 32

Why would a drug not reach its target?

Back 32

decreased uptake or increased efflux

Front 33

Why would a drug not be active?

Back 33

increased rate of inactivation

limited formation of active drug

Front 34

How is a drug target altered?

Back 34

-target deleted

-target modified

- acquisition of a resistant form of native, susceptible target

Front 35

What are these examples of?

Altered Porins can prevent certain drugs from entering

Increased efflux --> efflux pumps increase capacity to eliminate drug

Back 35

Drug does not reach target

Front 36

Mutation and ABX selection of a resistant mutant are the molecular basis of resistance to:

Back 36

*streptomycin*
- ribosomal mutation

*quinolones*
- gyrase or topoisomerase gene mutation

*linezolid*
-ribosomal RNA mutation

Front 37

This mechanism underlies all resistance to M. tuberculosis

Back 37

Mutation and selective pressure

Front 38

DNA of one bacteria introduced into another ...PHAGE MEDIATED ... same species

Important in the transfer of resistance among
strains of S. aureus

Back 38

Transduction

Front 39

DNA uptake from lysed bacteria (related species)

Molecular basis of penicillin-resistance in pneumococci and Neisseria

Back 39

Transformation

Front 40

What is the major mechanism of resistance transfer?

Back 40

Conjugation

Front 41

Gene transfer through direct cell-to-cell contact

- R determinant DNA plasmids encode drug resistance

- Occurs between same strain, different strains,different species

- Can transfer multiple drug resistance (MDR)

Back 41

Conjugation

Front 42

Transposons - ‘jumping genes’ -sticky ends

Can move from plasmid to plasmid or plasmid to chromosome

These occur in:

Back 42

Conjugation

Front 43

What are the 3 general uses of antibiotics?

Back 43

empirical therapy

definitive therapy

prophylactic therapy

Front 44

What are some situations where empiric therapy is highly justified?

Back 44

-Neutropenic, febrile cancer patients

-Community acquired pneumonia

Front 45

Name the antimicrobial therapy:

-organism not yet identified

- broad spectrum agent used

Back 45

empirical therapy

Front 46

Name the antimicrobial therapy:

-organism and susceptibilities known

-narrow spectrum agent used

Back 46

definitive therapy

Front 47

Name the antimicrobial therapy:

-prevent initial or recurrent infection

-spectrum of agent depends on situation

Back 47

prophylactic therapy

Front 48

this is the appearence of a new infection during therapy of a primary infection

Back 48

Superinfection

Front 49

What are some Disadvantages of
Antimicrobial Combinations?

Back 49

- Increased risk of toxicity

- Increased cost
*Selection of multi-drug resistant microorganisms*

- Eradication of normal host flora