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Flashcards in Antimicrobials Deck (194):
1

MOA for Penicillin G (IV and IM), V (oral)

  • Bind penicillin-binding proteins (transpeptidases).
  • Block transpeptidase cross-linking of peptidoglycan.
    • Activate autolytic enzymes 

2

  • Bind penicillin-binding proteins (transpeptidases).
  • Block transpeptidase cross-linking of peptidoglycan.
  • Activate autolytic enzymes 

MOA for Penicillin G (IV and IM), V (oral)

3

Clinical Use: Pen G and V

  • Mostly used for gram+ orgs (S. pneumoniae, S. pyogenes, Actinomyces). Also used for N. meningitidis and T. pallidum.
  • Bactericidal for gram + cocci and rods, gram- cocci, and spirochetes.
  • Penicillinase sensitive 

4

  • Mostly used for gram+ orgs (S. pneumoniae, S. pyogenes, Actinomyces). Also used for N. meningitidis and T. pallidum.
  • Bactericidal for gram + cocci and rods, gram- cocci, and spirochetes.
  • Penicillinase sensitive 

Clinical Use: Pen G and V

5

Toxicity for Penicillin G, V

Hypersensitivity reactions, hemolytic anemia

6

Hypersensitivity reactions, hemolytic anemia

Toxicity for Penicillin G, V

7

Resistance to Pen G and V

Penicillinase in bacteria cleaves β-lactam ring 

8

Penicillinase in bacteria cleaves β-lactam ring 

Resistance to Pen G and V

9

MOA for Ampicillin, amoxicillin (aminopenicillins; penicillinase-sensitive penicillins)

  • Same as penicillin but wider spectrum
  • penicillinase sensitive.
  • combine with clavulanic acid to protect against β-lactamase. 

10

  • Same as penicillin but wider spectrum
  • penicillinase sensitive.
  • combine with clavulanic acid to protect against β-lactamase. 

MOA for Ampicillin, amoxicillin (aminopenicillins; penicillinase-sensitive penicillins)

11

which has greater oral bioavailability- amoxicillin or ampicillin?

AmOxicillin has greater Oral bioavailability

12

Clinical Use for aminopenicillins

  • Extended-spectrum penicillin—Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci 
  • ampicillin/amox HELPSS kill enterococci

13

  • Extended-spectrum penicillin—Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci 
  • ampicillin/amox HELPSS kill enterococci

Clinical Use for aminopenicillins

14

Toxicity of aminopenicillins

Hypersensitivity reactions; rash; pseudomembranous colitis 

15

Hypersensitivity reactions; rash; pseudomembranous colitis 

Toxicity of aminopenicillins

16

mechanisms of resistance for aminopenicillins

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring 

17

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring 

mechanisms of resistance for aminopenicillins

18

penicillinase resistant penicillins

oxacillin, nafcillin, dicloxacillin

19

oxacillin, nafcillin, dicloxacillin

penicillinase resistant penicillins

20

MOA of oxacillin, nafcillin, dicloxacillin

  • Same as penicillin but NARROW spectrum
  • penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring. 

21

  • Same as penicillin but NARROW spectrum
  • penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring. 

MOA of oxacillin, nafcillin, dicloxacillin

22

Clinical use of oxacillin, nafcillin, dicloxacillin

S. aureus (except MRSA; resistant bc of altered penicillin-binding protein target site). 

23

  • S. aureus (except MRSA; resistant bc of altered penicillin-binding protein target site). 
  • Use "naf" for staph

Clinical use of oxacillin, nafcillin, dicloxacillin

24

toxicity of oxacillin, nafcillin, dicloxacillin

Hypersensitivity reactions, interstitial nephritis. 

25

Hypersensitivity reactions, interstitial nephritis. 

toxicity of oxacillin, nafcillin, dicloxacillin

26

antipseudomonals

Tircarcillin, piperacillin

27

Tircarcillin, piperacillin

antipseudomonals

28

MOA for ticarcillin, piperacillin

Same as penicillin but extended spectrum 

29

Same as penicillin but extended spectrum 

MOA for ticarcillin, piperacillin

30

Clinical Use for ticarcillin, piperacillin

  • Pseudomonas spp. and gram- rods
  • susceptible to penicillinase
  • use with β-lactamase inhibitors. 

31

  • Pseudomonas spp. and gram- rods
  • susceptible to penicillinase
  • use with β-lactamase inhibitors. 

Clinical Use for ticarcillin, piperacillin

32

Toxicity for antipseudomonals

Hypersensitivity reactions 

33

Hypersensitivity reactions 

Toxicity for antipseudomonals

34

beta lactamase inhibitors

  • Clavulanic Acid, Sulbactam, Tazobactam.
  • Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase). 
  • "CAST"

35

  • Clavulanic Acid, Sulbactam, Tazobactam.
  • Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase). 
  • "CAST"

beta lactamase inhibitors

36

MOA for cephalosporins (generations 1-5)

  • β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal 

37

  • β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal 

MOA for cephalosporins (generations 1-5)

38

organisms typically not covered by cephalosporins and the exception

 

  • LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci.
  • Exception: ceftaroline covers MRSA. 

39

  • LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci.
  • Exception: ceftaroline covers MRSA. 

organisms typically not covered by cephalosporins and the exception

 

40

1st generation cephalosporins

cefazolin, cephalexin 

41

cefazolin, cephalexin 

1st generation cephalosporins

42

Use for 1st generation cephalosporins

  • gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae.
  • Cefazolin used prior to surgery to prevent S. aureus wound infections. 

43

  • gram + cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae.
  • Cefazolin used prior to surgery to prevent S. aureus wound infections. 

Use for 1st generation cephalosporins

44

2nd generation cephalosporins

cefoxitin, cefaclor, cefuroxime 

45

cefoxitin, cefaclor, cefuroxime 

2nd generation cephalosporins

46

Use of 2nd generation cephalosporins

  • gram + cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens 
  • HEN PEcKS

47

  • gram + cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens 
  • HEN PEcKS

Use of 2nd generation cephalosporins

48

3rd generation cephalosporins

ceftriaxone, cefotaxime, ceftazidime 

49

ceftriaxone, cefotaxime, ceftazidime 

3rd generation cephalosporins

50

Use of 3rd generation cephalosporins

  • serious gram-negative infections resistant to other β-lactams
  • Ceftriaxone—meningitis and gonorrhea.
  • Ceftazidime—Pseudomonas  

51

  • serious gram-negative infections resistant to other β-lactams
  • Ceftriaxone—meningitis and gonorrhea.
  • Ceftazidime—Pseudomonas  

Use of 3rd generation cephalosporins

52

4th generation cephalosporin

cefepime 

53

cefepime 

4th generation cephalosporin

54

Use of cefepime

 increase activity against Pseudomonas and gram-positive organisms. 

55

 increase activity against Pseudomonas and gram-positive organisms. 

Use of 4th generation cephalosporins

56

5th generation cephalosporin

ceftaroline 

57

ceftaroline 

5th generation cephalosporin

58

Use of cefaroline

broad gram-positive and gram-negative organism coverage, including MRSA; does not cover Pseudomonas. 

59

broad gram-positive and gram-negative organism coverage, including MRSA; does not cover Pseudomonas. 

Use of cefaroline

60

toxicity of cephalosporins

  • Hypersensitivity reactions, vitamin K deficiency.
  • Low cross-reactivity with penicillins. 
  • increased nephrotoxicity of aminoglycosides 

61

  • Hypersensitivity reactions, vitamin K deficiency.
  • Low cross-reactivity with penicillins. 
  • increased nephrotoxicity of aminoglycosides 

toxicity of cephalosporins

62

MOA of Aztreonam

  • A monobactam
  • resistant to β-lactamases.
  • Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3.
  • Synergistic with aminoglycosides.
  • No cross-allergenicity with penicillins 

63

  • A monobactam
  • resistant to β-lactamases.
  • Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3.
  • Synergistic with aminoglycosides.
  • No cross-allergenicity with penicillins 

MOA of Aztreonam

64

Use of Aztreonam

  • Gram-negative rods only—no activity against gram + or anaerobes.
  • For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides 

65

  • Gram-negative rods only—no activity against gram + or anaerobes.
  • For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides 

Use of Aztreonam

66

toxicity for aztreonam

  • Usually nontoxic; occasional GI upset. 

67

  • Usually nontoxic; occasional GI upset. 

toxicity for aztreonam

68

carbapenem drug group

Imipenem, meropenem, ertapenem, doripenem 

69

Imipenem, meropenem, ertapenem, doripenem 

carbapenem drug group

70

MOA of Imipenem

  • broad-spectrum, β-lactamase– resistant carbapenem.
  • Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules. 
  • Newer carbapenems include ertapenem (limited Pseudomonas coverage) and doripenem 

71

  • broad-spectrum, β-lactamase– resistant carbapenem.
  • Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules. 
  • Newer carbapenems include ertapenem (limited Pseudomonas coverage) and doripenem 

MOA of Imipenem

72

Use of Imipenem

  • Gram + cocci, gram-negative rods, and anaerobes.
  • Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.

73

  • Gram + cocci, gram-negative rods, and anaerobes.
  • Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.

Use of Imipenem

74

unique to meropenem

decreased risk of seizures and is stable to dehydropeptidase I 

75

decreased risk of seizures and is stable to dehydropeptidase I 

unique to meropenem

76

Toxicity of carbapenems

  • GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels. 

77

  • GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels. 

Toxicity of carbapenems

78

MOA of Vancomycin

  • Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.
  • Bactericidal. 

79

  • Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.
  • Bactericidal. 

MOA of Vancomycin

80

Use of Vancomycin

  • Gram + only—serious, multidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis). 

81

  • Gram + only—serious, multidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis). 

Use of Vancomycin

82

Toxicity of vancomycin

  • Well tolerated in general—but NOT trouble free --> Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing—red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate). 

83

  • Well tolerated in general—but NOT trouble free --> Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing—red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate). 

Toxicity of vancomycin

84

mechanism of resistance to vancomycin

  • Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac. “Pay back 2 D-alas (dollars) for vandalizing (vancomycin).” 

85

  • Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac. “Pay back 2 D-alas (dollars) for vandalizing (vancomycin).” 

mechanism of resistance to vancomycin

86

drugs that inhibit 30S ribosome

  • A = Aminoglycosides [bactericidal]
  • T = Tetracyclines [bacteriostatic] 

87

  • A = Aminoglycosides [bactericidal]
  • T = Tetracyclines [bacteriostatic] 

drugs that inhibit bacterial 30S ribosome

88

drugs that inhibit bacterial 50S subunit

C = Chloramphenicol, Clindamycin [bacteriostatic]

E = Erythromycin (macrolides) [bacteriostatic]

L = Linezolid [variable] 

89

C = Chloramphenicol, Clindamycin [bacteriostatic]

E = Erythromycin (macrolides) [bacteriostatic]

L = Linezolid [variable] 

drugs that inhibit bacterial 50S subunit

90

aminoglycosides 

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin 

“Mean” (aminoglycoside) GNATS caNNOT kill anaerobes 

 

 

91

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin 

“Mean” (aminoglycoside) GNATS caNNOT kill anaerobes 

 

 

aminoglycosides 

92

MOA of aminoglycosides

  • Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Also block translocation.
  • Require O2 for uptake; therefore ineffective against anaerobes. 

93

  • Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Also block translocation.
  • Require O2 for uptake; therefore ineffective against anaerobes. 

MOA of aminoglycosides

94

Use of aminoglycosides

  • Severe gram-negative rod infections. Synergistic with β-lactam antibiotics.

  • Neomycin for bowel surgery. 

95

  • Severe gram-negative rod infections. Synergistic with β-lactam antibiotics.

  • Neomycin for bowel surgery. 

Use of aminoglycosides

96

toxicity of aminoglycosides

  • Nephrotoxicity (especially when used with cephalosporins) 
  • Neuromuscular blockade 
  • Ototoxicity (especially when used with loop diuretics)
  • Teratogen 

97

  • Nephrotoxicity (especially when used with cephalosporins) 
  • Neuromuscular blockade 
  • Ototoxicity (especially when used with loop diuretics)
  • Teratogen 

toxicity of aminoglycosides

98

mechanism of resistance for aminoglycosides

  • Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation 

99

  • Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation 

mechanism of resistance for aminoglycosides

100

tetracyclines

Tetracycline, doxycycline, minocycline. 

101

Tetracycline, doxycycline, minocycline. 

tetracyclines

102

MOA of tetracyclines

  • Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
  • Doxycycline is fecally eliminated and can be used in patients with renal failure.
  • Do not take with milk (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit its absorption in the gut 

103

  • Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.
  • Doxycycline is fecally eliminated and can be used in patients with renal failure.
  • Do not take with milk (Ca2+), antacids (Ca2+ or Mg2+), or iron-containing preparations because divalent cations inhibit its absorption in the gut 

MOA of tetracyclines

104

Use of tetracyclines

  • Borrelia burgdorferi, M. pneumoniae.
  • Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia.
  • Also used to treat acne. 

105

  • Borrelia burgdorferi, M. pneumoniae.
  • Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia.
  • Also used to treat acne. 

Use of tetracyclines

106

toxicity of tetracycline

  • GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity.
  • Contraindicated in pregnancy 

107

  • GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity.
  • Contraindicated in pregnancy 

toxicity of tetracycline

108

mechanism of resistance of tetracycline

 decreased uptake or  increased efflux out of bacterial cells by plasmid-encoded transport pumps. 

109

 decreased uptake or  increased efflux out of bacterial cells by plasmid-encoded transport pumps. 

mechanism of resistance of tetracycline

110

macrolides

Azithromycin, clarithromycin, erythromycin. 

111

Azithromycin, clarithromycin, erythromycin. 

macrolides

112

MOA of macrolides

  • Inhibit protein synthesis by blocking translocation (“macroslides”); bind to the 23S rRNA of the 50S ribosomal subunit.
  • Bacteriostatic 

113

  • Inhibit protein synthesis by blocking translocation (“macroslides”); bind to the 23S rRNA of the 50S ribosomal subunit.
  • Bacteriostatic 

MOA of macrolides

114

Use of macrolides

  • Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STDs (for Chlamydia), and gram- positive cocci (streptococcal infections in patients allergic to penicillin). 

115

  • Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STDs (for Chlamydia), and gram- positive cocci (streptococcal infections in patients allergic to penicillin). 

Use of macrolides

116

toxicity of macrolides

  • MACRO: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia.
  • Increases serum concentration of theophyllines, oral anticoagulants. 

117

  • MACRO: Gastrointestinal Motility issues, Arrhythmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia.
  • Increases serum concentration of theophyllines, oral anticoagulants. 

toxicity of macrolides

118

mechanism of resistance to macrolides

Methylation of 23S rRNA-binding site prevents binding of drug. 

119

Methylation of 23S rRNA-binding site prevents binding of drug. 

mechanism of resistance to macrolides

120

MOA of chloramphenicol

  • Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic 

121

  • Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic 

MOA of chloramphenicol

122

Use of chloramphenicol

  • Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and Rocky Mountain spotted fever (Rickettsia rickettsii).

  • Limited use owing to toxicities 

123

  • Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and Rocky Mountain spotted fever (Rickettsia rickettsii).

  • Limited use owing to toxicities 

Use of chloramphenicol

124

toxicity of chloramphenicol

  • Anemia (dose dependent)
  • aplastic anemia (dose independent)
  • gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase). 

125

  • Anemia (dose dependent)
  • aplastic anemia (dose independent)
  • gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase). 

toxicity of chloramphenicol

126

mechanism of resistance to chloramphenicol

  • Plasmid-encoded acetyltransferase inactivates the drug 

127

  • Plasmid-encoded acetyltransferase inactivates the drug 

mechanism of resistance to chloramphenicol

128

MOA of clindamycin

  • Blocks peptide transfer (translocation) at 50S ribosomal subunit.
  • Bacteriostatic. 

129

  • Blocks peptide transfer (translocation) at 50S ribosomal subunit.
  • Bacteriostatic. 

MOA of clindamycin

130

Use of Clindamycin

  • Anaerobic infections (e.g., Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections.
  • Also effective against invasive Group A streptococcal (GAS) infection. 
  • Treats anaerobes above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)

131

  • Anaerobic infections (e.g., Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections.
  • Also effective against invasive Group A streptococcal (GAS) infection. 
  • Treats anaerobes above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)

Use of Clindamycin

132

toxicity of clindamycin

  • Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea. 

133

  • Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea. 

toxicity of clindamycin

134

sulfonamides

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine 

135

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine 

sulfonamides

136

MOA of sulfonamides

  • Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase.
  • Bacteriostatic. 

137

  • Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase.
  • Bacteriostatic. 

MOA of sulfonamides

138

use of sulfonamides

  • Gram-positive, gram-negative, Nocardia, Chlamydia.
  • Triple sulfas or SMX for simple UTI 

139

  • Gram-positive, gram-negative, Nocardia, Chlamydia.
  • Triple sulfas or SMX for simple UTI 

use of sulfonamides

140

toxicity for sulfonamides

  • Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g., warfarin). 

141

  • Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g., warfarin). 

toxicity for sulfonamides

142

mechanism of resistance for sulfonamides

  • Altered enzyme (bacterial dihydropteroate synthase),  decreased uptake, or increased PABA synthesis 

143

  • Altered enzyme (bacterial dihydropteroate synthase),  decreased uptake, or increased PABA synthesis 

mechanism of resistance for sulfonamides

144

MOA for trimethoprim

  • Inhibits bacterial dihydrofolate reductase.
  • Bacteriostatic 

145

  • Inhibits bacterial dihydrofolate reductase.
  • Bacteriostatic 

MOA for trimethoprim

146

Use of trimethoprim

  • Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP- SMX]), causing sequential block of folate synthesis.
  • Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis. 

147

  • Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP- SMX]), causing sequential block of folate synthesis.
  • Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis. 

Use of trimethoprim

148

toxicity of trimethoprim

  • Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid). 
  • TMP: Treats Marrow Poorly. 

149

  • Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid). 
  • TMP: Treats Marrow Poorly. 

toxicity of trimethoprim

150

Fluoroquinolones

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gemifloxacin, enoxacin (fluoroquinolones), nalidixic acid (a quinolone) 

151

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gemifloxacin, enoxacin (fluoroquinolones), nalidixic acid (a quinolone) 

Fluoroquinolones

152

MOA of fluoroquinolones

  • Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
  • Bactericidal.
  • Must not be taken with antacids. 

153

  • Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
  • Bactericidal.
  • Must not be taken with antacids. 

MOA of fluoroquinolones

154

Use of fluoroquinolones

  • Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram-positive organisms. 

155

  • Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram-positive organisms. 

Use of fluoroquinolones

156

fluoroquinolone toxicity

  • GI upset, superinfections, skin rashes, headache, dizziness.
  • Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias.
  • Contraindicated in pregnant women, nursing mothers, and children under 18 years old due to possible damage to cartilage.
  • Some may cause prolonged QT interval.
  • May cause tendon rupture in people > 60 years old and in patients taking prednisone
  • Fluoroquinolones hurt attachments to your bones 

157

  • GI upset, superinfections, skin rashes, headache, dizziness.
  • Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias.
  • Contraindicated in pregnant women, nursing mothers, and children under 18 years old due to possible damage to cartilage.
  • Some may cause prolonged QT interval.
  • May cause tendon rupture in people > 60 years old and in patients taking prednisone
  • Fluoroquinolones hurt attachments to your bones 

fluoroquinolone toxicity

158

Mechanism of resistance to fluoroquinolones

Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps. 

159

Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps. 

Mechanism of resistance to fluoroquinolones

160

MOA of metronidazole

  • Forms free radical toxic metabolites in the bacterial cell that damage DNA.
  • Bactericidal, antiprotozoal 

161

  • Forms free radical toxic metabolites in the bacterial cell that damage DNA.
  • Bactericidal, antiprotozoal 

MOA of metronidazole

162

Use of metronidazole

  • Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile).
  • Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori. 

163

  • Treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile).
  • Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori. 

Use of metronidazole

164

Toxicity of metronidazole

  • Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol; headache, metallic taste. 

165

  • Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol; headache, metallic taste. 

Toxicity of metronidazole

166

MOA for isoniazid (INH)

  • decreased synthesis of mycolic acids. Bacterial catalase- peroxidase (encoded by KatG) needed to convert INH to active metabolite 

167

  • decreased synthesis of mycolic acids. Bacterial catalase- peroxidase (encoded by KatG) needed to convert INH to active metabolite 

MOA for isoniazid (INH)

168

Use of Isoniazid

  • Mycobacterium tuberculosis.
  • The only agent used as solo prophylaxis against TB.
  • Different INH half-lives in fast vs. slow acetylators  

169

  • Mycobacterium tuberculosis.
  • The only agent used as solo prophylaxis against TB. 

Use of Isoniazid

170

Toxicity for isoniazid

  • Neurotoxicity, hepatotoxicity. Pyridoxine (vitamin B6) can prevent neurotoxicity, lupus 
  • INH Injures Neurons and Hepatocytes 

171

  • Neurotoxicity, hepatotoxicity. Pyridoxine (vitamin B6) can prevent neurotoxicity, lupus 
  • INH Injures Neurons and Hepatocytes 

Toxicity for isoniazid

172

Rifamycins

Rifampin, rifabutin 

173

Rifampin, rifabutin 

Rifamycins

174

MOA of rifamycins

Inhibits DNA-dependent RNA polymerase 

175

Inhibits DNA-dependent RNA polymerase 

MOA of rifamycins

176

Use of rifamycins

  • Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy.
  • Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B 

177

  • Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy.
  • Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B 

Use of rifamycins

178

toxicity of rifamycins

  • Minor hepatotoxicity and drug interactions (increased P-450) 
  • orange body fluids (nonhazardous side effect).
  • Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation 

179

  • Minor hepatotoxicity and drug interactions (increased P-450) 
  • orange body fluids (nonhazardous side effect).
  • Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation 

toxicity of rifamycins

180

4 R's of Rifampin

  • RNA polymerase inhibitor

  • Ramps up microsomal cytochrome P-450 Red/orange body fluids

  • Rapid resistance if used alone

  • Rifampin ramps up cytochrome P-450, but rifabutin does not 

181

  • RNA polymerase inhibitor

  • Ramps up microsomal cytochrome P-450 Red/orange body fluids

  • Rapid resistance if used alone

  • Rifampin ramps up cytochrome P-450, but rifabutin does not 

4 R's of Rifampin

182

MOA of pyrazinamide

  • Mechanism uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid.
  • Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found. 

183

  • Mechanism uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid.
  • Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found. 

MOA of pyrazinamide

184

Use of pyrazinamide

Mycobacterium tuberculosis. 

185

Mycobacterium tuberculosis. 

Use of pyrazinamide

186

toxicity of pyrazinamide

Hyperuricemia, hepatotoxicity. 

187

Hyperuricemia, hepatotoxicity. 

toxicity of pyrazinamide

188

MOA of ethambutol

  • decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase 

189

  • decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase 

MOA of ethambutol

190

Use of ethambutol

Mycobacterium tuberculosis.

191

Mycobacterium tuberculosis.

Use of ethambutol

192

Toxicity of ethambutol

Optic neuropathy (red-green color blindness). 

193

Optic neuropathy (red-green color blindness). 

Toxicity of ethambutol

194