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CMD Block 2 > Sweatman Antimicrobial Reading > Flashcards

Sweatman Antimicrobial Reading Flashcards

1
Q

What does mutations in penicillin binding proteins have in common with methylation of ribosomal subunits?

A

they are alterations that microbes have developed to subvert the target of antibiotics = 2 ways microbes have developed resistance

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2
Q

How have microbes decreased the entry of a drug or forced the efflux of a drug?

A

altered their porin structure (to resist cell wall synthesis inhibitors) and they have developed efflux pumps to remove the drug (tetracylines)

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3
Q

Microbes have become resistant to sulfa drugs by…

A

aquiring alternative metabolic pathways to bypass the pathway sulfa drugs block (they block folate synthesis)

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4
Q

What are 2 ways that microbes can keep drugs inactive?

A
  1. cause a failure for the prodrug to convert to it’s active form (isoniazid)
  2. inactivate a drug (penicillin by B-lactamase)
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5
Q

WHat are the 3 major factors to consider when selecting an anti-infective?

A
  1. microorganism factors
  2. host factors
  3. drug factors
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6
Q

Factors to consider when selecting anti-microbial: Microorganism factors (2)

A
  1. ID organism

2. susceptibility of organism

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7
Q

Factors to consider when selecting anti-microbial: Host factors (8)

A
  1. Drug allergies
  2. pharmacokinetic variables
  3. effect of food on drug
  4. effect of other drugs
  5. renal/hepatic function
  6. pregnancy/lactation
  7. signs and symptoms
  8. Fever, malaise, leukocytosis, pus
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8
Q

Factors to consider when selecting anti-microbial: Drug factors (6)

A
  1. economics
  2. tissue penetration
  3. drug toxicity
  4. preventing resistance
  5. bad drug combos
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9
Q

What are the 4 major mechanisms of action for antimicrobials?

A
  1. inhibition of cell wall synthesis (i.e. must have proliferating pop of microbes)
  2. inhibition of protein synthesis
  3. inhibition of folic acid biosynthetic pathways
  4. inhibition of DNA/RNA synthesis
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10
Q

T or F: Sometimes, you need to combine drugs that work by different mechanisms of action to achieve synergistic killing effects

A

true

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11
Q

What are the 5 classes that interfere with cell wall synthesis?

A 
penicilins
chephlasporins
carbapenems
monobactams
vancomyosins
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12
Q

Describe penicillin’s mechanism of action.

A

they bind to transpeptidase to inhibits the crosslinking of NAM and NAG

(they also activate the autolysins, carboxypeptidases, and endopeptidases that hydrolyze and destroy components of the cell wall)

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13
Q

What are penicillin binding proteins?

A

bacterial proteins that penicillin binds

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14
Q

T or F: for penicillins to function, they must penetrate the cell wall.

A

true

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15
Q

What are the 4 ways bacteria may become resistant to penicillins?

A
  1. modification of their PBPs
  2. active pumping of drugs back out of cells
  3. developing B-lactamases to cleave of the B-lactam ring structure (this occurs w/in the periplasmic space)
  4. altered porins (gram - bac only) that prevent the drugs from reaching the PBPs
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16
Q

What is the MIC?

A

minimum inhibitory concentration = lowest conc of an antimicrobial that will inhibit the visible growth of a microog after overnight incubation

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17
Q

T or F: the lower the MIC, the better the antimicrobial agent.

A

true: a lower conc is needed to stop the growth the microbe

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18
Q

What is the MBC?

A

minimum bactericidal concentration = lowest conc of antibiotic required to kill a particular bacterium

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19
Q

What is the difference between MIC and MBC?

A

MIC is the lowest conc of drug needed to stop the bac from reproducing and MBC is the lowest conc of antibiotic needed to kill the microbe

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20
Q

Describe the quantitative method of susceptibility testing.

A

a single colony of bacteria added into liquid cultures in varying antibiotic conc. The lowest conc in which there is no visible growth = MIC.

The remaining liquid cultures are plated onto agar that contains no antibiotic. The lowest dose/conc of the liquid antibiotic dilution in which bacteria does not grow on the petri dish = MBC.

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21
Q

Describe the qualitative method of susceptibility testing.

A

Disks with “impregnated” drugs are placed onto a petri dish that has been swabbed with bacteria. After incubation, the size of zones of inhibition around the disks indicate the bacterial susceptibility of the drug

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22
Q

What drugs target cell wall synthesis?

A

B-lactams (penicillin, cepthalasporins, carbapenems, monobactams) and Vancomyosin

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23
Q

What drugs inhibit folic acid synthesis?

A

trimethoprim

sulfonamides

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24
Q

What 2 enzymes are targeted to inhibit DNA/RNA synthesis?

A

DNA gyrase

DNA-directed RNA polymerase

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25
Q

What drug targets DNA gyrase?

A

quinolones

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26
Q

What drug targets DNA-directed RNA polymerase?

A

rifampin

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27
Q

What drugs inhibit protein syntheis by binding the 50S ribosomal subunit?

A 
chloramphenicol
macrolides
lincosamides
ketolides
Retapamulin 
linezolid
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28
Q

What drugs target the 30S ribosomal subunit?

A

tetracylines

aminoglycosides

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29
Q

Should penicillin be combined with tetracycline?

A

No. Tetracycline is bacteriostatic so it woud antagonize the penicillin

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30
Q

Why are oral contraceptives less effective when taken with an antibiotic?

A

Gut flora becomes disrupted and the enterohepatic recirculation of estrogenic components becomes impaired–> decreasing t1/2 of the OC –> less duration of action –> betta wrap that junk!

**Under normal circumstances, gut flora cleave estrogen-glucuronide conjugates to allow the estrogenic component to be absorbed. This cleavage decreases with decreasing gut flora function during antibiotic therapy

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31
Q

What are the 4 subclasses of penicillins?

A
  1. natural penicillins
  2. aminopenicillins
  3. penicillinase-resistant penicillins
  4. antipseudomonal penicillins
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32
Q

Why would you want to co-administer penicillin with an irreversible B-lactamase inhibitor?

A

broadens the antimicrobial spectrum to include coverage of B-lactasmase producing organisms

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33
Q

What types of penicillin is used to treat gram positive microorganisms?

A

natural penicillins and penicillinase-resistant penicillins

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34
Q

What cell wall synthesis inhibitors are used to fight infections with gram - bacteria?

A

Aminopenicillins
Antipseudomonal
Cycloserine
Polymixin B

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35
Q

What are examples of natural penicillins?

A

penicillin G and penicillin V

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36
Q

Why must penicillin ___ must be administered by IV. Why?

A

G: it is readily destroyed in acidic environments (i.e. digestive tract)

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37
Q

IM injections of penicillin G are used to prevent ____ and treat ____

A

rheumatic fever

syphilis

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38
Q

How is penicillin V be administered?

A

orally but on an empty stomach (1 hr before meals or 2-3 hrs after meals for maximal efficacy)

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39
Q

What are examples of aminopenicillins?

A

ampicillin and amoxicillin

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40
Q

How is ampicillin administered?

A

enterally or parenterally; if oral, must be on an empty stomach

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41
Q

Which aminopenicillin can be taken with or without food?

A

amoxicililin

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42
Q

What are examples of penicillinase-resistant penicillins?

A

dicloxacillin
methicillin
oxacillin
nafcillin

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43
Q

What is the MOA for penicillinase-resistant penicillins?

A

they contain side groups that protect the drugs from being inactivated by B-lactamases

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44
Q

How is methicillin usually administered?

A

parenterally

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45
Q

How is dicloxacillin usually administered?

A

orally

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46
Q

How is oxacillin usually administered?

A

parenterally

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47
Q

How is nafcillin usually administered?

A

parenterally

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48
Q

Where do B-lactamases reside?

A

periplasmic space

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49
Q

What are the 2 effects penicllin binding PBPs has?

A
  1. blocks transpeptidase of peptidoglycan to prevent cell wall syntheis
  2. activates autolytic enzymes in the cell wall that cause lesions –> bacterial cell death
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50
Q

What are examples of antipseudomonal penicillins?

A

carbenicillin
ticarcillin
mezlocillin
piperacillin

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51
Q

How are antipseudomonal penicillins usually administered?

A

parenterally

carbenicillin the the only one to be administered orally (but therapeutic levels are only found in the uninary tract = treatment only for UTIs and prostate infections

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52
Q

What penicillin is restricted to treating UTIs an prostate infections?

A

carbenicillin

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53
Q

T or F: Irreversible B-lactamases can be administered as a stand alone antimicrobial therapy.

A

False: they are have no anti-microbial activity by themselves. They need to be co-administered with penicillins to expand coverage against B-lactamase resistant microorgs

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54
Q

Cephlophlasporins structurally resemble ____ because they possess _____

A

penicillins bc they have a B-lactam chemical backbone

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55
Q

How are cephalopsorins different than penicillins?

A

cephalosporins are relatively stable to pH changes and may be taken with or without food

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56
Q

What drugs are irreversible inhibitors of B-lactamases?

A

clavulanic acid
sulbactam
tazobactam

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57
Q

Why can penicillin-allergic patients also be hypersensitive to cephalosporins?

A

bc of their structural similarities

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58
Q

T or F: As a rule, it is wise to refrain from prescribing ______ to patients with a well documented history of anaphylactic reactions to penicillins.

A

cephalosporins

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59
Q

Other than allergic reactions, what are some adverse effects of cephalosporins? (7)

A
  1. GI irritation
  2. local irritation at the site of injection
  3. renal toxicity (bc excreted by kidneys) = trouble for pt. with kidney disease
  4. disulfriam-like reactions
  5. hypoprothrombinemia
  6. seizures in pt with impaired kidney function (bc drug accumulates)
  7. 2ndary infections (disrupt normal flora)
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60
Q

What are examples of carbapenems?

A

imipenem/cilastatin
doripenem
ertapenem
meropenem

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61
Q

T or F: Carbapenems are bacteriostatic and inhibit cell wall synthesis.

A

False: they are bactericidal

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62
Q

How are carbapenems different then penicillin and cephalosporins?

A

they have a different stereochemical structure in their B-lactam ring that renders them resistant to B-lactamases

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63
Q

What drugs interfere with cell wall synthesis by blocking polymerization and crosslinking by binding to D-ala D-ala portion of the cell walls?

A

telavancin

vancomycin

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64
Q

What are the MOA for telavancin?

A
  1. blocking polymerization and cross-linking by binding D-ala pair
  2. disruption of the cell membrane potential and changes in cell permeability bc of the presence of a lipophillic side chain moiety
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65
Q

WHat is the MOA for cycloserine?

A

inhibits cell wall synthesis in gram-NEG microbes but is usually reserved for treating TB infections resistant to first line anti-tubercular drugs

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66
Q

What is the MOA for polymyxin B? What kind of microbes does it target?

A

It is a cationic detergent that disrupts the lipoproteins in bacterial cell walls –> inc membrane permeability

bactericidal to nearly all gram-neg bacilli with the exception of Proteus

67
Q

What are examples of aminoglycosides?

A 
amikacin
gentamicin
kanamycin
netilmicin
streptomycin
tobramycin
neomycin
68
Q

What is the MOA for aminoglycosides?

A

Bind to bacterial 30s and interferes with protein synthesis in at least 3 ways:

  1. formation of the initiation complex
  2. misread mRNA and miscode aa in the growing peptides
  3. cause ribosomes to separate from mRNA–> monosome = inefficient protein synthesis
69
Q

How are aminoglycosides typically administered? Why?

A

parenterally because they are too water soluble to be given orally

70
Q

Where do aminoglycosides accumulate?

A

inner ear and renal cortex

*accounts for nephrotoxic and ototoxic side effects

71
Q

What is the postantibiotic effect?

A

microbes continue to die even as plasma levels of the drug decline

72
Q

T or F: aminoglycosides exhibit the post-antibiotic effect.

73
Q

What type of microbes are aminoglycosides used to treat?

A

ONLY gram-negative

74
Q

What general type of bacteria have developed a resistance to aminoglycosides?

A

anaerobes (they have altered receptor proteins on their ribosomes that prevent the drug from binding

or any bacteria that have enzymatically or postranslationally altered the drug (via phosphorylation, acetylation, etc.) which interferes with the drug’s ability to efficiently bind the ribosomal subunits

75
Q

What are examples of tetracycline?

A

(all ending with -cycline)

76
Q

What is the MOA of tetracycline?

A

inhibit protein synthesis by reversibly bindind the 30S subunit to prevent the binding of new/incoming aa = interferes with peptide growth

*blocks the A site

77
Q

What are glycyclines?

A

antibiotics derived from tetracycline that are designed to overcome resistance medated by efflux pumps and ribosomal protection

78
Q

What tetracycline derivative most closely structurally resembles minocycline?

A

tigecycline

79
Q

T or F: tetracyclines are bactericidal only to gram negatives microbes.

A

False: they are BACTERIOSTATIC to both gram neg and gram pos

80
Q

How does tetracycline enter a gram neg cell? gram positive?

A

neg: passive diffusion
pos: active transport

81
Q

What limits gastric absorption of tetracycline?

A

chelation due to divalent cations (iron, Al, Mg, CALCIUM CONTAINING ANTACIDS and MILK or bile acid resins

82
Q

What tetracycline is the safest option for patients in renal dysfunction? Why?

A

doxycycline bc it is metabolized hepatically and excreted in the feces

83
Q

What mech of resistance do gram positives use against tetracycline?

A

efflux pump

84
Q

What mech of resistance do gram negatives use against tetracycline?

A

changes to outer membrane that prevent tetracylines from entering.

85
Q

T or F: Minocycline is not affected by tetracycline resistance mechanisms?

A

False: tigecycline is not affected by resistance to prevent tetracyclines from entering but microbes have developed resistance to minocycline

86
Q

Chloraphenicol is (bacteriostatic or bactericidal).

A

bacteriostatic

87
Q

Describe the MOA of chloramphenicol.

A

binds to the 50S ribosomal subunit and interferes with the enzyme peptidyl transferase to block the linkage of incoming aa

88
Q

What type of phase II reaction metabolizes chloramphenicol?

A

glucuronidation

89
Q

What can happen to infants and adults with hepatic disease that also are taking chloramphenicol?

A

the drug accumulates and is inefficiently glucuronidated resulting i n “gray baby/adult’ syndrome (fail to eat, thrive, pallor, cyanotic, abd distension, and may die of respiratory or vasomotor collapse)

90
Q

What type of drug is clindamycin?

A

lincosamides

91
Q

What is the MOA of clindamycin?

A

binds 50S subunit and prevents TRANSLOCATION of aa from A site to P site

92
Q

What are examples of macrolides?

A 
drugs that have erythromycin base:
erythromycin estolate
erythromycin sterate
erythromycin ethylsuccinate
clarithromycin 
azithromycin
93
Q

Describe the MOA for macrolides.

A

bind to the 50S subunit to prevent translocation of the amino acids from the A site to the P site

94
Q

What drugs prevent the translocation of amino acids from the P to A site? What is a possible consequence of this?

A

clindamycin
chloramphenicol
macrolides

they may interfere with one another and cross-resistance may develop between them

95
Q

Macrolides are (bacteriostatic or bactericidal)

A

both, it depends on drug conc

96
Q

Microbes become resistant to macrolides in the following circumstances (3):

A
  1. when their permeability for macrolides is altered
  2. when the microbes methylate the 50S subunit
  3. When the bacteria develop mechanisms to enzymatically destroy the drugs
97
Q

What are some adverse effects associated with erythromycin? (4)

A
  1. GI distress
  2. cholestatic hepatitis (elevated liver enzymes, malaise, nausea, vomiting, abd cramps, jaundice, and fever)
  3. inhibit CYP34A –> toxicity
  4. fatal arrhythmia (from prolong the QT interval)
98
Q

T or F: clarithromycin is associted with more GI distress than erythromycin.

A

False: less

99
Q

How is azithromycin different than erythromycin and clarithromycin?

A
  • does not prolong QT interval

- does not inhibit hepatic microsomal P450s

100
Q

What is an example of ketolides?

A

telithromycin

101
Q

What is the MOA of telithromycin?

A

inhibits 50S by binding at TWO locations

102
Q

Why is it difficult for bacteria to develop resistance to telithromycin?

A

must have mutations in 2 diff domains of 50S and this drug is a poor substrate for eflux pumps

103
Q

What is the MOA for retapamulin? How is it administered?

A
  • binds 50S to prevent formation of active 50S subunit
  • inhibits peptidyl trasferase
  • blocks P site interactions

-topical ointment

104
Q

What is the MOA of mupirocin?

A

inhibits tRNA that transports isoleucine

105
Q

T or F: Mupirocin can partake cross-resistance to other antimicrobials.

A

False: to does not (bc it is a unique MOA)

106
Q

What is cross resistance in antimicrobials?

A

resistance to a particular antibiotic that often results in resistance to other antibiotics

107
Q

What is the MOA of linezolid?

A

binds to a unique RNA site on the 50S to prevent formation of the 70S complex.

108
Q

What type of drug is a combination of quinupristin and dalfopristin?

A

streptogramins

109
Q

What is the MOA of the quinupristin/dalfopristin?

A

quinupristin irreversible blocks ribosomes to inhibit the late phase of protein synthesis.
Dalfopristin inhibits early phases of protein synthesis.

110
Q

What is the quinupristin/dalfopristin combination used to treat?

A

to treat life-threatening infections caused by vancomycin-resistant enterococci and complicated skin infections caused by MRSA

111
Q

Folic acid is a ____ vitamin

112
Q

T or F: bacteria can use folic acid obtained from the environment.

A

false: they cannot use it

113
Q

What drugs target dihydropteroate synthetase?

A

sulfonamides

114
Q

What drugs target dihydrofolate reductase?

A

trimethoprim

115
Q

What are examples of sulfonamides?

A 
sulfadiazine
silver sulfadiazine 
sulfamethoxazole
sulfacetaminde
sulfasalazine
116
Q

Describe the MOA for sulfonamides

A

compete with para-aminobenzoic acid (PABA) for binding to dihydropteroate synthetase (1st step in pathway) –> if it binds the pathway is blocked

117
Q

Sulfonamides are highly bound to ______

A

plasma proteins

118
Q

What are complications that can arises from concurrent administration of sulfonamides and warfarin, NSAIDs, and sulfonylurases

A

if they outcompete these drugs for binding to plasma proteins, the conc of these drugs will drastically rise and potentially become toxic

119
Q

Why are sulfonamides contraindicated for pregnant women in later term and infants less that 2 mo old?

A

they displace bilirubin from protein binding sites in neonates and hyperbilirubinemia in neonates may cause kernicterus (CNS disorder)

120
Q

What are the 4 ways bacteria develop resistance to sulfonamides?

A
  1. reduce uptake of drug
  2. develop alt pathways to make folic acid
  3. produce excess PABA to outcompete sulfonamides
  4. mutated dihydropteroate synthetase (rate limiting enzyme)
121
Q

How are sulfonamides metabolized?

A

hepatically by acetylation, oxidation, and/or glucuronidation

122
Q

Who are at an increased risk of hypersensitivity reactions to sulfonamides?

A

slow acetylators

123
Q

____(type of metabolic reaction) ___ of sulfonamides likely is responsible for many of the adverse affects associated with sulfonamides.

124
Q

How are sulfonamide metabolites excreted?

125
Q

Trimethoprim inhibits ____

A

dihydrofolate reductase (last set of folic acid synthesis)

126
Q

Bacteria may become resistant to trimethoprim by…

A
  1. reduced uptake of drug
  2. mutations in dihydrofolate reductase
  3. overproduction of dihydrofolate reductase
127
Q

What are some examples of fluoroquinolones?

A

all ending in “-floxacin”

128
Q

What is the MOA of fluoroquinolones?

A

inhibit DNA gyrase or topoisomerase IV

129
Q

What is the function of DNA gyrase?

A

relaxes supercoiled DNA and is essential in replication, Tx, and DNA repair

130
Q

What is the role of topoisomerase IV?

A

seperating DNA into daughter cells during replication

131
Q

What must bacteria become resistant to evade the effects of fluoroquinolone or gemifloxacin?

A

must acquire mutations in both DNA gyrase and topoisomerase IV

132
Q

What can impair the absorption of fluoroquinolones?

A

food or cations (Ca, Fe, Al, Mg, Zn) or sucralfate

133
Q

T or F: Fluoroquinolones penetrates and distributes mainly to the CNS.

A

false: they do not penetrate CNS and they distribute to nearly all other body compartments

134
Q

What type of drug is Daptomycin?

A

lipopeptide

135
Q

What is the MOA of daptomycin?

A

binds bacterial membranes and cuases rapid depolarization of the cell –> stops DNA, RNA, and protein synthesis => cell death

136
Q

T or F: cross resistance between daptomycin and rifaximin has developed.

A

false: daptomycin has not developed cross resistance with any other antibiotics

137
Q

T or F: Datomycin metabolites are excreted in the urine.

A

False: Daptomycin (UNCHANGED) is excreted in urine

138
Q

What antibiotic is selcetively absorbed by anaerobic bac and sensitive protozoa?

A

metronidazole

139
Q

Describe the MOA for metronidazole in anaerobes.

A

taken up and non-enzymatically reduced by reacting with reduced ferredoxin –> produces metabolites that are toxic –> DNA and nucleic acid synthesis is inhibited and existing DNA is degraded or strand breaks are introduced –> CELL DEATH

140
Q

What is the MOA for nitazonxanide?

A

inferfeeres with pyruvate/ferredoxin oxidoreductase enzyme dept e- transfer (necessary for anaerobic bacteria metabolism)

141
Q

WHat is the MOA for tinidazole?

A

causes DNA damage–> inhibiting DNA synthesis

142
Q

What antibiotics can be mutagenic and possibly carcinogenic?

A

metronidazole
nitazoxanide
tinidazole

143
Q

When are metronidazole and tinidazole contraindicated?

A

first timester of pregnancy

144
Q

T or F: Metronidazole penetrate the CNS and therefore can be used to treat meningitis and brain abscesses caused by aerobic bacteria.

A

False: All is true except it must be caused by an anaerobic bactera

145
Q

What is the MOA of rifaximin?

A

inhibits bacterial RNA synthesis by binding bacterial DNA dept RNA polymerase

146
Q

How is rifaximin excreted?

A

It is NOT abs in GI tract and therefore it is excreted in feces

147
Q

What are the difference between rifaximin and rifampin?

A
  • rifaximin does not interfere with CYP450s while rifampin does
  • rifaximin is excreted in feces
148
Q

What are mycobacteria?

A

gram positive rod-like bacteria that are aerobic and can form filamentous branching structures

149
Q

Why are mycobacterial infections (like TB and leprosy) hard to treat? (5)

A
  1. mycobac grows slowly
  2. they can lie dormant
  3. they have thick cell walls that are relatively impermeable
  4. they can reside n host cells
  5. become resistant quickly
150
Q

What is the MOA for isoniazid?

A

inhibits synthesis of mycolic acids (essental component of mycobacterial cell wall)

151
Q

T or F: Isoniazid diffuses throughout total body water, even the CNS.

152
Q

Metabolism of isoniazid occurs by _____

A

acetylation

153
Q

What consequences do “fast acetylators” have on the use of isoniazid as a treatment?

A

isoniazid may not reach therapeutic levels because they have a short plasma half life

154
Q

Will fast or slow acetylators be at a greater risk for drug-related toxicity with izoniazid?

155
Q

What is the MOA of rifampin?

A

binds upstream of RNA pol binding site to physically prevent the Tx of a gene (inhibits RNA pol)

156
Q

Rifampin is a potent inducer of _____

A

CYP450s –> DRUG-DRUG INXS are a major concern.

157
Q

What is the MOA of pyrazinamide?

A

unclear but thought that it lowers the pH in the tubercle cavity and inhibits growth of mycobacterium

158
Q

What is the MOA of ethambutol?

A

inhibits RNA synthesis and decreases replication of the tubercle bacilli

159
Q

What is the MOA of clofazimine?

A

binds to mycobacterial DNA to inhibit RNA pol actions. Tx is very slow and requires pt to be treated for a min of 2 yrs and possible for life

160
Q

What antibiotics are used to treat mycobacterial infections?

A 
isoniazid
rifampin
pyrazinamide 
ethambutol
clofazimine
161
Q

T/F: Aminopenicillin is unaffected by B-lactamase.

162
Q

What type of bacteria can become resistant by altering their porin structure?

163
Q

Where in the bacterial cell do B lactams work?

A

periplasmic space

164
Q

What cell wall inhibitors (other than penicillin) are used to treat gram - infections?

A
  • polymyxin B (proteus resistant)

- (cycloserines, but these are usually reserved for TB)

CMD Block 2 (38 decks)

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