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Ok Pharmacology... Let's Do This... Be Gentle > Antimicrobial Pharmacology > Flashcards

Antimicrobial Pharmacology Flashcards

1
Q

what does the mechanism of antimicrobial drug action identify

A

the drug target

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2
Q

knowledge of the drug target gives you info about what 3 things

A
  1. selective toxicity
  2. drug resistance
  3. bactericidal vs bacteroistatic
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3
Q

what are the gram positive cocci

A

strep pneumo

strep pyogenes

staph aureus (MSSA and MRSA)

enterococcus faecium

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4
Q

what are the gram negative cocci

A

n. gonorrhea
n. meningitidis
m. catarrhalis

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5
Q

what are the gram positive rods

A

bacillus anthracis

listeria monocytogenes

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6
Q

what are the gram negative rods

A

h. flu
e. coli

pseudomonas

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7
Q

what are the anaerobic gram positive rods

A

c. diff

tetani

botulinum

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8
Q

what are the anaerobic gram negative rods

A

bacteroides fragilis

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9
Q

what are the atypical bacteria

A

chlamydia

mycoplasma

rickettsia

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10
Q

what abx target cell wall synthesis

A

vancomycin

bacitracin

penicillins

cephalosporins

monobactams

carbapenems

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11
Q

which stage of cell wall synthesis does vancomycin target

A

2

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12
Q

which abx target cell membranes

A

daptomycin

polymixin B

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13
Q

which abx target nucleic acids

A

fluoroquinolones

rifampin

nitrofurantoin

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14
Q

which abx target protein synthesis

A

aminoglycosides

tetracyclines

clindamycin

macrolides

chloramphenicol

streptogramins

muciporin

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15
Q

which abx target intermediary metabolism (folate metabolism)

A

sulfonamides

trimethoprim

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16
Q

what is selective toxicity

A

a feature of abx therapy that ensures abx selectively exert effects on microbe and not the host

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17
Q

name 4 methods of selective toxicity

A
  1. inhibition of metabolic pathway → folate metabolism
  2. differences in enzyme structure → ribosomes and DNA gyrase
  3. macromolecular structure → cell wall synthesis
  4. macromolecular structure → fungal cell membrane
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18
Q

what is the difference in folate metabolism between bacteria and humans

A

bacteria must synthesize folate

humans can take it up from the environment

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19
Q

what are the 2 bacterial ribosomes

A

30s

50s

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20
Q

what are the human ribosomes

A

40s

60s

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21
Q

humans use __ for nucleic acid synthesis

bacteria use __ for nucleic acid synthesis

A

humans: topoisomerase
bacteria: DNA gyrase

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22
Q

what do bacterial cell walls contain that eukaryotes do not contain

A

peptidoglycan

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23
Q

what is the difference between fungal cell membranes and human cell membranes

A

humans: cholesterol
fungal: ergosterol

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24
Q

what are the 4 mechanisms of abx resistance

A
  1. antibiotic target site alteration
  2. antibiotic inactivating or modifying enzyme
  3. reduced permeability → natural resistanve
  4. increased efflux → restricts abx access
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25
Q

what are the 4 methods of abx target site alteration

A

penicillin binding proteins

DNA gyrase

peptidoglycan side chain

50s ribosome methylation

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26
Q

what are the penicillin binding protein bacteria

A

MRSA

strep pneumo

enterococci

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27
Q

what bacteria use DNA gyrase for abx resistance

A

s. aureus

pseudomonas

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28
Q

what bacteria use peptidoglycan side chains for abx resistance

A

enterococci (VRE)

staphylococci (VRSA)

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29
Q

which bacteria use 50s ribosome methylation for resistance

A

strep

staph

enterococci

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30
Q

which bacteria use beta lactamase for abx modification or inactivation

A

s. aureus
p. aeruginosa

bacteroides

enterococci

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31
Q

which bacteria use acetyl-phospho-adenylyl transferases for resistance

A

enterococci

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32
Q

which bacteria use decreased entry (natural resistance)

A

pseudomonas

e.coli

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33
Q

which bacteria use increased efflux for abx resistance

A

streptococci

staphylococci

enterococci

pseudomonas

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34
Q

which type of abx resistance is this: microbes lack a susceptible target for drug action

A

natural (intrinsic) resistance

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35
Q

list 3 examples of natural (intrinsic) resistance

A
  1. fungal cell walls do not have peptidoglycans
  2. mycoplasma do not have cell walls at all
  3. pseudomonas - drugs can not penetrate outer membrane
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36
Q

what type of resistance is this: microbes are sensitive and abx reaches target, but something prevents the drug form working

A

escape resistance

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37
Q

which type of resistance is important for surgical drainage

A

escape → abx tolerance

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38
Q

what is acquired abx resistance

A

selective pressure of abx administration produces successive generations of organisms with biochemical traits that minimize drug action

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39
Q

what prevents acquired abx resistance

A

proper dosing and duration of abx therapy

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40
Q

which mode of acquired resistance is an important source of multiple drug resistance

A

plasmid mediated resistance

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41
Q

bacteria develop resistance to beta lactam abx by what mechanism

A

target site alteration

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42
Q

bacteria develop resistance to fluoroquinolones by what mechanism

A

abx target site alteration

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43
Q

bacteria develop resistance to vancomycin by what mechanism

A

target site alteration

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44
Q

bacteria develop resistance to erythromycin and clindamycin by what mechanism

A

target site alteration

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45
Q

what are the 5 drugs to which bacteria develop resistance using target site alteration

A
  1. beta lactams
  2. fluoroquinolones
  3. vancomycin
  4. erythromycin
  5. clindamycin
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46
Q

bacteria develop resistance to aminoglycosides and beta lactams via what mechanism

A

antibiotic modification or inactivation

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47
Q

bacteria develop resistance to beta lactams, fluoroquinolones, and aminoglycosides via what mechanism

A

decreased entry → natural resistance

48
Q

bacteria develop resistance to tetracyclines, macrolides, and fluoroquinolones using what mechanism

A

increased efflux

49
Q

MRSA, strep pneumo, and enterococci have developed resistance to what abx via target site alteration

A

beta lactams

50
Q

s. aureus and pseudomonas species have developed resistance to what abx via target site alteration

A

fluoroquinolones

51
Q

enterococci (VRE), and staphylococci (VRE) have developed resistance to what drug via target site alteration

A

vancomycin

52
Q

streptococci, staphylococci, and enterococci have developed resistance to what 2 drugs via target site alteration

A

erythromycin

clindamycin

53
Q

s.aureus, p.aeruginosa, bacteroides, and enterococci have developed resistance to what drug via abx modification or inactivation

A

beta lactams

54
Q

enterococci have developed resistance to what drug via abx modification or inactivation

A

aminoglycosides

55
Q

pseudomonas have developed resistance to what drug via decreased entry (natural resistance)

A

beta lactams

56
Q

pseudomonas species have developed resistance to what drug via decreased entry (natural resistance)

A

fluoroquinolones

57
Q

e.coli and pseudomonas have developed resistance to what drug via decreased entry (natural resistance)

A

aminoglycosides

58
Q

streptococci, staphylococci, and enterococci have developed resistance to what 2 drugs via increased efflux

A

tetracyclines

macrolides

59
Q

pseudomonas species have developed resistance to what drug via increased efflux

A

fluoroquinolones

60
Q

what are 3 methods to minimize abx resistance

A
  1. only use abx when need is established
  2. select abx on basis of susceptibility tests
  3. use adequate concentration and duration
61
Q

what is bactericidal action

A

organisms are killed

62
Q

what is bacteriostatic action

A

organisms are prevented from growing

63
Q

what determines whether an abx is -cidal or -static (3)

A
  1. mechanism of action → target
  2. concentration achieved in vivo
  3. specific microorganism
64
Q

what are the 3 bactericidal mechanisms

A
  1. inhibition of cell wall synthesis
  2. disruption of cell membrane fxn
  3. interference w. DNA fxn or synthesis
65
Q

what are the 2 bacteriostatic mechanisms

A
  1. inhibition of protein synthesis
  2. inhibition of intermediary metabolic pathways
66
Q

are aminoglycocides -static or -cidal

A

-cidal

67
Q

are -cidal or -static abx preferred in severe infxns

A

-cidal

68
Q

which abx class acts quickly and irreversibly with sustained effect

A

-cidal

69
Q

which class of bacteria is preferred in CNS and endocarditis infxns (immune sanctuaries)

A

-cidal

70
Q

what are the 4 categories of bacteria

A
  1. cocci
  2. rods
  3. anaerobes
  4. atypical
71
Q

in the op setting, when C&S is infrequently available, what 4 factors should you consider in selecting abx

A
  1. symptoms
  2. anatomic site
  3. local patterns of infxn
  4. patient demographics
72
Q

what are the 3 classes of abx spectrum

A
  1. narrow
  2. extended
  3. broad
73
Q

narrow spectrum abx cover

A

either gram (+)

OR

gram (-)

74
Q

extended abx cover

A

gram (+)

AND

gram (-)

75
Q

broad spectrum abx cover

A

gram (+)

AND

gram (-)

AND

atypical

76
Q

which spectrum of abx have the least disturbance of host flora → less diarrhea

A

narrow

77
Q

which spectrum of abx are most effective on susceptible organism

A

narrow

78
Q

which spectrum of abx are more likely to cause superinfections

A

broad

79
Q

which spectrum of abx sacrifices efficacy for greater scope and is used for initial tx

A

broad

80
Q

which spectrum of abx should be used for severe infxns of unknown etiology

A

empiric

81
Q

what are mixed infxns

A

oral or intraabdominal

82
Q

what is an ex of a synergistic abx effect

A

penicillin plus an aminoglycocide against enterococci

83
Q

what are 3 advantages of oral routes of administration

A
  1. ease of administration
  2. patient acceptance
  3. lower cost
84
Q

what are 3 cons of oral routes of administration

A
  1. GI upset
  2. lack of absorption for some drugs
  3. unsuitable for npo
85
Q

taking a drug on an empty stomach is recommended when

A

the abx is unstable dt increased gastric acidity when food is in the stomach

86
Q

taking a drug with food is recommended when

A

the drug is acid stable but may be irritating to stomach

87
Q

taking a drug on an empty stomach protects

A

the drug

88
Q

taking a drug with food protects

A

the stomach

89
Q

when are IV drugs indicated

A
  1. when rapid and predictable plasma levels are needed
  2. pt w. life threatening infxns
90
Q

what are cons of IV administration (3)

A
  1. greater training needed
  2. greater expense
  3. requires strict aseptic conditions
91
Q

abx vary greatly in ability to cross

A

bbb

92
Q

which class of drugs is excellent at crossing bbb

A

ceftriaxone → 3rd gen cephalosporins

93
Q

what is accumulation

A

a characteristic of certain drugs that can result in beneficial and harmful effects

94
Q

which drug has a beneficial accumulation effect in bone

A

clindamycin

95
Q

which drug has a beneficial accumulation effect in pulmonary cells

A

macrolides

96
Q

which drug has a beneficial accumulation effect in gingival crevicular fluid and sebum (peridontitis and acne)

A

tetracyclines

97
Q

which drug has a beneficial accumulation effect into urine (UTIs)

A

nitrofurantoin

98
Q

which drug can cause ototoxicity and nephrotoxicity via accumulation

A

aminoglycocides

99
Q

which drug can cause abnormal bone growth and tooth discoloration via accumulation

A

tetracyclines

100
Q

renal status is monitored via

A

SCr

CrCl

101
Q

how do you monitor hepatotoxicity with abx

A

you can’t! → must avoid hepatotoxic drugs if liver dysfxn

102
Q

what does DCRIMES mean

A

hepatotoxic abx

103
Q

what does DCRIMES stand for

A

Doxycycline

Clindamycin

Rifampin

Isoniazid

Metronidazole

Erythromycin-like (Macrolides)

Sulfonamides

104
Q

what class of drugs can cause urea crystalluria

A

sulfonamides

105
Q

what are 2 consequences if abx therapy is too short

A
  1. resistance develops
  2. recurrence possible
106
Q

what are 2 consequences if abx duration is too long

A
  1. superinfxn more likely via alteration of normal flora
  2. dose-related toxicities more likely
107
Q

what 2 abx can be dosed less frequently dt high initial cp levels (concentration dependent killing)

A

aminoglycosides

fluoroquinolones

108
Q

what 3 abx kill best when cp is above MIC for longer durations (time dependent killing)

A
  1. beta-lactams
  2. vancomycin
  3. macrolides
109
Q

what is direct toxicity

A

when abx effect on microbes affects host cellular processes → lack of selective toxicity

110
Q

what 5 systems does direct toxicity usually involve

A
  1. GI tract
  2. liver
  3. kidney
  4. nervous system
  5. blood and blood forming systems
111
Q

what are 3 examples of indirect toxicity

A
  1. allergic rxns and hypersensitivity
  2. salt effects → dt salt administered w. abx not abx itself
  3. drug-drug interactions → ex alteration of CYP450 metabolizing enzyme
112
Q

disturbances of host microflora (superinfection) usually occurs with what spectrum of abx

A

broad

113
Q

what is an example of superinfection related to disturbance of host microflora

A

pseudomembranous colitis dt c.diff overgrowth

114
Q

what 3 host factors can increase risk for toxicity

A
  1. age → very old and very young
  2. pregnancy/nursing → consider harm to fetus
  3. drug hypersensitivity → pt allergies
115
Q

what is post antibiotic effect

A

the persistent suppression of bacterial growth that may occur after limited exposure to some abx

116
Q

what side effects should you know w. abx

A
  1. most common
  2. most severe

Ok Pharmacology... Let's Do This... Be Gentle (6 decks)

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