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Infectious Disease > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What is the mechanism of action for penicillins?

A
  • mimic PBP ligand and irreversibly inhibit transpeptidase

- activate murein hydrolases

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2
Q

Penicillins are limited to what bacteria cell populations?

A

those that are growing or proliferating

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3
Q

Penicillins are best for which classes of bacteria?

A

gram+, but anti-Staph, anti-pseudomonas, and extended spectrum penicillins are available

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4
Q

Penicillins are typically available in what preparations?

A
  • although it is acid liable, it is usually given orally

- also available in IV and depot preparations

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5
Q

Describe the distribution of penicillins.

A

it doesn’t reach the CNS, eyes, or prostate well

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6
Q

How are penicillins cleared and what is its half-life?

A
  • cleared via tubular secretion

- half-life of 30-60 minutes unless you add probenecid

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7
Q

What drug is often given alongside penicillins to extend their half life? How does this drug work?

A

probenecid inhibits tubular secretion of penicillins, extending their half life

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8
Q

Penicillin is a _____-dependent cell killer.

A

time dependent

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9
Q

What is ampicillin?

A

an extended spectrum penicillin

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10
Q

What is amoxicillin?

A

an extended spectrum penicillin

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11
Q

How do extended spectrum penicillins differ from penicillin G or V?

A
  • they have more gram- activity

- they are more susceptible to beta-lactamase

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12
Q

Name the two important extended spectrum penicillins.

A
  • ampicillin

- amoxicillin

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13
Q

List the four important anti-Staph penicillins.

A
  • methicillin
  • nafcillin
  • oxacillin
  • cloxacillin
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14
Q

How do anti-Staph penicillins differ from penicillin G or V?

A

they are beta-lactamase resistant

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15
Q

What is methicillin?

A

an anti-Staph penicillin (beta-lactamase resistant)

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16
Q

List the four important anti-pseudomonas penicillins.

A
  • ticarcillin
  • mezlocillin
  • piperacillin
  • carbenicillin indanyl
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17
Q

What is the problem with anti-pseudomonas penicillins? How is this overcome?

A

resistance is emerging so they must be used in combination with ahminoglycosides or fluroquinolones

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18
Q

How does MRSA achieve beta-lactam resistance?

A

it altered PBP structure, so penicillin could no longer bind

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19
Q

Describe the onset, cross-reactivity, and dose-dependence of the penicillin hypersensitivity reaction.

A
  • rapid onset
  • dose-independent response
  • complete cross-reactivity
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20
Q

List three ways bacteria achieve resistance to penicillins.

A
  • lack a cell wall or are dormant
  • produce a modified PBP that isn’t accessible to penicillin
  • produce beta-lactamases
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21
Q

What is the mechanism of action of cephalosporins?

A

they are beta-lactams

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22
Q

In what ways are cephalosporins better than penicillins?

A
  • greater gram- activity

- greater beta-lactamase resistance

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23
Q

What are the major side effects of cephalosporins?

A
  • renal toxicity (enhanced by ahminoglycosides)
  • inject site reaction
  • moderate cross-reactivity with PCN-sensitive patients
  • disulfiram effect with bleeding disorders (mostly cefotetan and cefoperazone)
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24
Q

Which cephalosporin has a disulfiram effect and causes bleeding disorders? How is this compensated for?

A
  • cefotetan

- co-administer Vit K

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25
Q

List the important first generation cephalosporins.

A
  • cephalothin
  • cephalexin
  • cefazolin
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26
Q

List the important second generation cephalosporins.

A
  • cefuroxime
  • cefotetan
  • cefactor
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27
Q

List the important third generation cephalosporins.

A
  • cefotaxime
  • ceftriaxone
  • ceftazidimine
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28
Q

What is cefepime?

A

the only fourth generation cephalosporin

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29
Q

What is the mechanism of action of aztreonam?

A

it is a beta-lactam and ICWS

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30
Q

List three advantages of aztreonam over penicillin.

A
  • beta-lactamase resistance
  • crosses the BBB
  • no cross-reactivity for PCN-sensitive patients
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31
Q

What is special about the distribution of aztreonam?

A

it crosses the BBB

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32
Q

Aztreonam is effective against which classes of bacteria?

A

only gram-, it has no gram+ or anaerobe activity

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33
Q

What is the mechanism of action of imipenem?

A

it is a beta-lactam

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34
Q

List three advantages of imipenem over penicillin.

A
  • it is broad spectrum
  • it crosses the BBB
  • it is beta-lactamase resistant
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35
Q

Why is imipenem co-adminsitered with cilastatin?

A

because cilastatin inhibits inactivation of impenem by renal dipeptidase

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36
Q

How is imipenem metabolized?

A

it is inactivated by renal dipeptidase

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37
Q

What is meropenem?

A

a carbapenem (beta-lactam) with renal dipeptidase resistance

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38
Q

What is the mechanism of action of clavulanic acid?

A

it is a beta-lactam

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39
Q

What is the mechanism of action of sulbactam?

A

it is a beta-lactam

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40
Q

What is the mechanism of action of tazobactam?

A

it is a beta-lactam

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41
Q

What is the mechanism of action of bacitracin?

A

it is a ICWS

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42
Q

What is the mechanism of action of vancomycin?

A

it is a ICWS that acts by inhibiting transglycosylation

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43
Q

Vancomycin is primarily used for which class of bacteria?

A

gram+

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44
Q

Vancomycin is a preferred treatment for which two difficult to treat infections?

A
  • MRSA

- C. diff

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45
Q

What are the major side effects of vancomycin?

A
  • it enhances the ototoxicity and renal toxicity of aminoglycosides
  • it triggers histamine release to cause “red man” syndrome
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46
Q

What is “red man” syndrome?

A

a major side effect of vancomycin caused by histamine release

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47
Q

What drug is preferred in the treatment of C. diff?

A

vancomycin

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48
Q

In what preparations is vancomycin available?

A
  • IV for systemic infection

- oral for C. diff infection

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49
Q

What is the mechanism of action of fosfomycin?

A

it inhibits the cytoplasmic step of cell wall precursor synthesis

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50
Q

What receptors mediate fosfomycin uptake?

A
  • glycerophosphate transporter

- G6P transporter

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51
Q

How is fosfomycin cleared from the system?

A

in the active form via the kidneys

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52
Q

What is one dose fosfomycin therapy administered for?

A

it’s active excretion from the kidneys makes it a good therapy for UTI

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53
Q

What is the mechanism of action of the polymixin drugs?

A

they are basic peptides that serve as detergents to disrupt cell membranes

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54
Q

What is colistin?

A

another name for polymixin E, a basic peptide that serves as a detergent to disrupt cell membranes

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55
Q

Which class of bacteria are polymixins effective against?

A

gram- bacteria except neisseria and proteus

56
Q

What are the limitations of polymixins?

A

they have systemic toxicity and are therefore restricted to topical applications or as salvage therapy for highly resistant bacteria

57
Q

Which three classes of antibiotics are inhibitors of protein synthesis?

A
  • tetracyclines
  • macrolides
  • aminoglycosides
58
Q

What is the mechanism of action for tetracyclines?

A

they reversibly bind and inhibit 30S ribosomal subunits as IPS

59
Q

What is the basis for the selectivity of tetracyclines?

A

bacterial uptake, not ribosomal affinity

60
Q

What are the five major side effects of tetracyclines?

A
  • GI irritation
  • photosensitization
  • liver impairment
  • superinfection
  • bone and teeth growth retardation or deformation
61
Q

Against which bacteria are tetracyclines effective.

A
  • broad spectrum

- particularly used against mycoplasma, chlamydia, rickettsia, and lyme disease

62
Q

Why does tetracycline cause bone deformities?

A

because it is a chelator of metal ions

63
Q

Describe the distribution of tetracyclines.

A
  • does not reach the CNS or synovial fluid

- does cross the placenta and enter breast milk

64
Q

List four important tetracyclines.

A
  • tetracycline
  • doxycycline
  • minocycline
  • tigecycline
65
Q

How do most bacteria achieve resistance to tetracyclines?

A

efflux pumps

66
Q

What is tigecycline?

A

a newer tetracycline that is resistant to most bacterial efflux pumps but has a black box warning for increased risk of death

67
Q

What is the mechanism of action of macrolides?

A

they are inhibitors of protein synthesis

68
Q

What is unique about macrolides compared to most other protein synthesis inhibitors?

A

they can be bacteriocidal at high dose

69
Q

How are macrolides administered?

A

orally with an enteric coating or as esters because they are acid liable

70
Q

What is special about azithromycin compared to other macrolides?

A

it has a 2-4 day half life

71
Q

What is the clinical utility of macrolides?

A

they are used for gram+ infections in PCN-sensitive patients

72
Q

What are side effects of macrolides?

A
  • GI distress
  • hepatotoxicity
  • DDIs with microsomal enzyme inhibition
73
Q

How do most bacteria achieve resistance to macrolides?

A

by methylation of rRNA

74
Q

Name the three important macrolides.

A
  • azithromycin
  • clarithromycin
  • erythromycin
75
Q

What is the mechanism of action of telithromycin?

A

it is a macrolide-like protein synthesis inhibitor

76
Q

What is telithromycin used to treat?

A

respiratory tract infections

77
Q

What are the two major side effects of telithromycin?

A
  • inhibits CYP3A4

- causes QT prolongation

78
Q

Which protein synthesis inhibitors can be bactericidal?

A
  • macrolides at high dose

- aminoglycosides

79
Q

What is the mechanism of action of aminoglycosides?

A
  • it targets 30s ribosomal subunits

- causes mRNA misreading, disrupts initiation, and breaks up polysomes

80
Q

What are strep monosomes?

A

a term used to describe the way streptomycin disrupts bacterial polysomes

81
Q

Which antibiotic was an example of concentration dependent cell killing?

A

aminoglycosides

82
Q

Describe the side effects of aminoglycosides.

A
  • time and dose dependent
  • nephrotoxicity likely reversible
  • ototoxicity may be reversible
  • causes a neuromuscular blockade at high dose
83
Q

What is gentamicin?

A

an aminoglycoside effective against pseudomonas

84
Q

List the three most important aminoglycosides.

A
  • gentamicine
  • streptomycin
  • neomycin
85
Q

What is the mechanism of action of chloramphenicol?

A

it is an inhibitor of protein synthesis

86
Q

How is chloramphenicol metabolized?

A

via glucuronidation

87
Q

What are the advantages of chloramphenicol?

A
  • excellent pharmacokinetics

- resistance is slow to development is minimal

88
Q

Under what circumstances do we use chloramphenicol?

A

only for typhoid and rocky mountain fever because of SEs

89
Q

Why is our use of chloramphenicol so limited?

A
  • despite good pharmacokinetics and limited resistance, it is high toxic
  • can cause aplastic anemia, grey baby syndrome, or fungal superinfection
90
Q

What are the side effects of chloramphenicol?

A
  • GI disturbance followed by fungal superinfection
  • aplastic anemia, which is often fatal
  • gray baby syndrome
91
Q

What is gray baby syndrome?

A

a side effect of chloramphenicol due to the poor glucuronidation abilities of babies

92
Q

What is the mechanism of action of clindamycin?

A

it is an IPS

93
Q

What is clindamycin used for?

A
  • mostly anaerobes
  • B. fragilis
  • MRSA
  • endocarditis prophylaxis
94
Q

What is the primary side effect of clindamycin?

A

it can cause of C. diff superinfection

95
Q

What are quinupristin and dalfopristin?

A

they are streptogrim protein synthesis inhibitors

96
Q

Why are streptogrims (quinupristin and dalfopristin) so clinically important?

A
  • they have no cross resistance with any other IPS

- they are approved for vancomycin and MD resistant E. faecium and MRSA

97
Q

What is the mechanism of action of oxazolidinones?

A

they inhibit 70s ribosomal formation

98
Q

What is the primary indication of oxazolidinones?

A

vancomycine resistant E. faecium

99
Q

What is the mechanism of action of sulfonamides?

A

they are PABA analogs that block folate synthesis via competitive inhibition of dihydrofolate synthesis

100
Q

What is silver sulfadiazine?

A

a sulfonamide used topically for burns

101
Q

What is sulfasalazine?

A

a sulfonamide used for ulcerative coilitis

102
Q

Sulfonamides are usually combined with what other therapy?

A

trimethoprim

103
Q

What are the adverse effects of sulfonamides?

A
  • Steven-Johnson syndrome reaction
  • hematuria
  • hematopoietic effects
104
Q

How do bacterial cells achieve resistance to sulfonamides?

A
  • overproduction of PABA
  • loss of permeability
  • modification of dihydropteroate synthesis
105
Q

What is co-trimoxazole?

A

trimethoprim-sulfamethoxazole combination therapy

106
Q

What two enzymes are used in the folate synthesis pathway?

A
  • dihydropteroate synthase

- dihydrofolate reductase

107
Q

What is the mechanism of action of trimethoprim?

A

it is a dihydrofolate reductase inhibitor

108
Q

How do we use trimethoprim clinically?

A
  • monotherapy for UTI

- with a sulfonamide (co-trimoxazole) otherwise

109
Q

What mediates the selectivity of trimethoprim?

A

high selectivity for bacteria dihydrofolate reductase

110
Q

What are the side effects of trimethoprim? How do we compensate for this?

A
  • anemia, leukopenia, etc.

- administer with folinic acid

111
Q

What is nalidixic acid?

A

the prototype quinolone

112
Q

What is the mechanism of action of quinolones?

A

they are DNA gyrase inhibitors and target topoisomerase II and IV

113
Q

Name the fluroquinolones.

A
  • ciproflaxacin
  • levofloxacin
  • ofloxacin
114
Q

What is the primary clinical use of fluroquinolones?

A

gram- bacteria, and particularly GI and GU infections

115
Q

How are fluroquinolones superior to nalidixic acid?

A

they are more slowly metabolized and excreted

116
Q

How do bacteria develop resistance against fluoroquinolones?

A

they modify their DNA gyrases

117
Q

What is the primary urinary tract antiseptic currently in use?

A

nitrofurantoin

118
Q

How can we increase the utility of nitrofurantoin against UTI?

A

keep urine pH below 5.5

119
Q

In what cases does nitrofurantoin cause side effects?

A

cleared so quickly, it has none unless the individual has a renal insufficiency

120
Q

List five first line anti-mycobacterial drugs.

A
  • isoniazid
  • ethambutol
  • rifampin
  • streptomycin (aminoglycoside)
  • pyrazinamide
121
Q

The primary drug used against leprosy is what?

A

dapsone

122
Q

What is the mechanism of action of isoniazid?

A

it blocks mycologic acid synthesis

123
Q

How is isoniazid used clinically?

A
  • alone for TB prophylaxis

- in combination for TB treatment

124
Q

Describe the adverse effects of isoniazid.

A

dose and time dependent nephropathy and hepatotoxicity

125
Q

How does resistance form against isoniazid?

A

bacteria delete KatG gene, which is needed for activation of isoniazid

126
Q

How is isoniazid metabolized?

A

via acetylation, and some polymorphisms make individuals fast acetylators requiring a higher dose

127
Q

What is the mechanism of action of ethambutol?

A

inhibit mycobacterial cell wall glycan synthesis

128
Q

What is the major side effect of ethambutol?

A

it has a dose-dependent optic neuritis that affects red-green differentiation and visual acuity

129
Q

What is the mechanism of action of rifampin?

A

it inhibits RNA synthesis

130
Q

How is rifampin used clinically?

A
  • in combination for active TB

- alone for TB prophylaxis if isoniazid isn’t an option

131
Q

What are the side effects of rifampin?

A
  • distinct orange color to body fluids
  • flu-like illness
  • inducer of microsomal enzymes (alters anticoagulants and oral contraceptive half life)
132
Q

What is pyrazinamide?

A

an anti-mycobacterial of unknown mechanism

133
Q

What are the disadvantages of using pyrazinamide?

A
  • requires bacterial activation
  • contraindicated by pregnancy
  • causes gout
134
Q

What is dapsone used to treat?

A
  • leprosy

- P. jiroveci pneumonia

135
Q

What two drugs are used form TB prophylaxis?

A

isoniazid and rifampin

Infectious Disease (9 decks)

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