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Pharm Final > Antibacterial Basics > Flashcards

Antibacterial Basics Flashcards

1
Q

Antibiotics (ABs) are substances produced to kill microorganisms or to protect from toxins produced by microorganisms, what are the 3 ways ABs are produced?

A

by microorganism
precursor by microorganism - semi synthetic
synthetic

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2
Q

in 1936 what noted to kill streptococci?

A

sulfanilamide

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3
Q

what was discovered in 1928 and began mass production of it in 1941

A

penicillin

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4
Q

most of the over 100 AB drugs in clinical use are what?

A

semi synthetic

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5
Q

What are the properties of a ideal AB

A

stability, Solubility, diffusibility (crosses the BBB), slow excretion (protein binding, drug combos), and large therapeutic index= SELECTIVE

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6
Q

PEN G (Benzyl penicillin) vs PEN V (phenoxy-benzyl penicillin), which one is stable in acids thus can be take orally

A

PEN V is stable in ACIDS

PEN G is NOT stable in acids

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7
Q

Therapeutic index = TD50 / ED50
what is TD 50?
what is ED50?
do you want a large or small Therapeutic index?

A

TD50= toxic dose
ED50= effective dose
want a HIGH therapeutic index bc that means drug is safer and more SELECTIVE

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8
Q

the microbe response to a AB can be resistance or secondary products of bacterial destruction, what 3 things are taken into consideration when resistance by a microbe is occurring?

A

resistance tells you to consider:

  1. choice of drug
  2. the dosage of the drug
  3. drug combos
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9
Q

what 5 ABs are considered Bacteriostatic?

A 
sulfonamides
trimethoprim
tetracyclines
erythromycin
Vancomycin*
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10
Q

what 5 ABs are considered Bactericidal?

A 
Vancomycin *
quinolones
penicillins
cephalosporins
aminoglycosides
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11
Q

what is the 1 AB that was considered bactericidal but due to INC resistance has led to it becoming more of a bacteriostatic drug

A

Vancomycin

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12
Q

what do bacteriostatic drugs do

A

bacteriostatic drugs stop the growth of that microbe. so on a graph static drugs will just halt the growth thus not allowing microbe to inc in number

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13
Q

what do bactericidal drugs do

A

bacteriocidal kills the microbe! so on a graph cidal drugs will bring the amount of microbe to 0

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14
Q

what is prophylaxis?

how much AB drug use is for prophylaxis?

A

prophylaxis temporarily decs the most likely pathogens below a critical level required to cause infection.
Prophylaxis accounts for .25-.5 of AB drug use

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15
Q

what is empiric therapy?

A

initiation of treatment (tx) before etiology of infection is known with agents known to be effective against the most likely pathogen acquired (suspected from source of infection)

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16
Q

what are the differences between gram + and gram - bacteria

A

gram + : many lactamases, thick cell wall of peptidoglycans, membrane has PBPs, 1 cell membrane

gram - : few lactamases, thin cell wall of 1-2 layers of peptidoglycan, 2 cell membranes, 1 on outside then cell wall layer then 2 cell membrane

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17
Q

What is MIC

A

MIC - minimum inhibitory concentration - the lowest concentration of drug which completely inhibits growth at 24 hrs

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18
Q

what is MBC

A

MBC- minimum bactericidal concentration

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19
Q

what does Vancomycin work against?

A

GRAM + bacteria!

Too big to work against gram -

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20
Q

what is the note about choosing a AB

A

once sensitivity profile is known, choose the effective drug with the narrowest spectrum to avoid emergence of resistance microbes

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21
Q

what variables are used to determine AB sensitivity? aka susceptibility guided therapy.

A

MIC
MBC
disk diffusion assays and etest

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22
Q

what is the Gold Standard for determining MIC

A

Broth dilution assay

23
Q

the location of infection is important for choosing AB and agents in the CNS are hard to treat, what kind of AB will treat a CNS infection

A

ABs that are lipophilic that can cross the BBB will treat a CNS infection

24
Q

what are the variables of pharmacokinetics that need to be taken into consideration about ABs?

A

ADME+T

absorption, distribution/ excretion, metabolism + toxicity (nephro, ototoxicity, hypersensitivity)

25
Q

Metabolism is important in Prodrugs why?

A

Prodrugs require activation and are based on cytochrome p450 activation or inactivation

26
Q

What host factors must be considered when prescribing a AB?

what is the importance of age?

A

age (young people metabolize, clear drugs faster than older)
allergies, food/ hydration (Ca can limit absorption of ciprofloxacin)
hepatic function (will pro drug be activated?)
pharmacogenetics (fast vs slow metabolism)
pregancy
immune status

27
Q

Describe the 3 AB cocktail situations

a) empiric therapy
b) mixed infections
c) synergism

A

a) empiric therapy- for serious infections of unknown etiology
b) mixed infections: intra abdominal- potentially several microbes, use 2 narrow spectrum ABs
c) synergism: more than additive effects of using 2+ ABs, different MoA leading to one drug making the other more effective

28
Q

An example of synergism is use of B lactam and aminoglyoside combo, what are the functions of each and how is this synergism?

A

B lactam: cell wall synthesis inhibitors
Aminoglycosides: inhibitors of protein synthesis
use of B lactam compromises cell walls allowing Aminoglycosides to accumulate inside the cell thus killing it

29
Q

An example of synergism is the use of trimethoprim and sulfamethoxazole, what is the combo used for?

A

tx of gram - urinary tract infections

30
Q

what is antagonism? what example was provided?

A

antagonism- less than additive effects.
use of bacteriostatic drug with B lactam, bacteriostatic drug inhibits cell growth thus requiring no new cell wall synthesis making B lactam useless

31
Q

what 4 ABs of inhibitors of Nucleic acid synthesis?

2 classes describe the two classes and the drugs in each class

A

Inhibits folic acid synthesis= sulfonamides, trimethoprim and antifolates

RNA synthesis inhibitor= Rifampin

32
Q

Rifampin does what

A

inhibits RNA synthesis

33
Q

sulfonamides, trimethoprim and antifolates do what

A

inhibits folic acid synthesis

34
Q

What 4 Abs are DNA damaging agents?

A

quinolones
Nitrofurantoin
Metronidazole
Methenamine

35
Q

what do quinolones do?

A

DNA gyrase A, Topoisomerase 4 inhibitors

36
Q

what do Nitrofurantoins do?

A

free radical generator

37
Q

What do Metronidazoles do?

A

anaerobic enzymatic reduction then metabolite DNA binding

38
Q

What do Methenamines do?

A

breaks down to form formaldehyde which alkylates DNA and protein

39
Q

what 3 ABs are inhibitors of cell wall synthesis

A

B Lactams
Vancomycin
Bacitracin

40
Q 
What do B lactams do? 
What drugs are under the class of B lactams?
A 
B lactams inhibit the transpeptidation cross linking of peptidoglycan
B lactams include: 
penicillin
cephalosporins, monobactams (aztreonam)
carbadpenems (imipenem)
41
Q

what does Vancomycin do?

what bacteria does Vancomycin work against?

A

Vancomycin binds to D-ala-D-Ala preventing polymerization of cell wall components
Vancomycin= Gram +!!

42
Q

what does Bacitracin do?

A

binds to and prevents functioning of lipid carrier of peptidoglycan

43
Q

Penicillin is what type of drug and MoA?

A

penicillin is a beta lactam that inhibits cell wall synthesis by inhibition of transpeptidation cross linking of peptidoglycan

44
Q

What 2 Abs are responsible for damage of cell membrane?

A

polymyxins

daptomycin

45
Q

polymyxins do what to damage cell membrane

A

polymyxins are cationic detergents that disrupts the cell membrane

46
Q

daptomycin does what?

A

daptomycin is a lipopeptide that disrupts membrane function

47
Q

cephalosporins are what type of drug and what is its MoA

A

Cephalosporins are a beta lactam that inhibits cell wall synthesis by inhibition of transpeptidation cross linking of peptidoglycan

48
Q

What are the 7 (1 combo) Abs that are inhibitors of protein synthesis by ribosomal protein binding to 30s or 50s

A 
aminoglycosides- bactericidal
tetracyclines= bacteriostatic
tigecycline
macrolides 
clindamycin
linezolid
Quinupristin/ dalfopristin= bactericidal
49
Q

monobactams are what type of drug and what is its MoA

A

monobactams are a beta lactam that inhibits cell wall synthesis by inhibition of transpeptidation cross linking of peptidoglycan

50
Q

what are the 3 Abs under the class called macrocodes? and what are their MoA

A

Macrolides= erythromycin, clarithromycin, azithromycin

Macrocodes are inhibitors of protein synthesis

51
Q

carbapenems are what type of drug and what are their MoA

A

carbapenems are a beta lactam that inhibits cell wall synthesis by inhibition of transpeptidation cross linking of peptidoglycan

52
Q

what is a inhibitor of dihydrofolate reductase (DHFR) that is a structural analog of pteridine?
is it bacteriostatic or tidal?

A

trimethoprim
Trimethoprim is bacteriostatic!!
can be tidal if with a sulfonamide

53
Q

what is trimethoprims selectivity

A

very selective needs much higher concentration to inhibit human DHFR

Pharm Final (13 decks)

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