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[MT 6314] Pharmacology & Toxicology > [3S] Sulfonamides, Trimethoprim & Quinolones > Flashcards

[3S] Sulfonamides, Trimethoprim & Quinolones Flashcards

1
Q

Antifolate Drugs

A

● Sulfonamides
● Trimethoprim
● Trimethoprim-Sulfamethoxazole mixtures

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2
Q

MOA

  1. Inhibit dihydropteroate synthase and folate production.
  2. Bacteriostatic when given alone.
  3. Usually given in combination with trimethoprim or
    pyrimethamine.
A

Antifolate drugs

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3
Q

One of the earliest and most successful antibiotics ever developed

A

Sulfa drugs

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4
Q

SULFONAMIDES

Introduced in 1935 by _______ ______ and marketed as ___________.

A

Gerhard Domagk, Prontosil

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5
Q

ANTIFOLATE DRUGS PKINETICS

● Similar to p-aminobenzoic acid (PABA)
● Weakly acid compounds

A

Sulfonamides

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6
Q

ANTIFOLATE DRUGS PKINETICS

Modest tissue absorption

A

Sulfonamides

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7
Q

ANTIFOLATE DRUGS PKINETICS

Sulfonamides metabolism & excretion

A

M = Liver
E = Urine

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8
Q

ANTIFOLATE DRUGS PKINETICS

Triple Sulfa
1) Short-acting
2) Intermediate-acting
3) Long-acting

A

1) Sulfisozaxole
2) Sulfamethosaxole
3) Sulfadoxine

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9
Q

ANTIFOLATE DRUGS

Sulfonamides ROA

A

Oral absorbable, Oral non-absorbable, Topical

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10
Q

MOA

● Competitive inhibitor of Dihydropteroate synthase and folate production
● Usually given in combination with Trimetophrim or Pyrimethamine

A

Antimetabolites

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11
Q

ANTIFOLATE DRUGS MOA

• Bacteriostatic (when given alone)
• Competitive inhibitor of dihydropteroate synthase
• Antimetabolate of PABA
• Act as substrates
• Selective toxicity

A

Sulfonamides

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12
Q

ANTIFOLATE DRUGS RESISTANCE MECHANISM

  1. Plasmid-mediated
  2. Decreased accumulation of the drug
  3. Increase production of PABA by bacteria
  4. Decrease in the sensitivity of dihydropteroate synthase
A

Sulfonamides

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13
Q

RESISTANCE MECHANISM

• Some bacteria depends on exogenous sources of folate
• Mutations in the following:
o Overproduction of PABA
o Production of a folic acid synthesizing enzyme that has low affinity for sulfonamides
o Impaired permeability to the sulfonamides
• Antibiotic efflux

A

Antimetabolites

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14
Q

Provides synergistic activity because of
sequential inhibition of folate synthesis

Resistance occurs but development is slow.

A

Sulfonamides and Trimethoprim

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15
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

• Gram (+)
• Gram (-)
o Klebsiella pneumoniae o Salmonella
o Shigella
o Enterobacter sp.
o Nocardia sp.
o Chalmydia trachomatis

A

Sulfonamides

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16
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

• Poor against: anaerobes
• Not active against:
o Ricketssiae
o P. aeruginosa

A

Sulfonamides

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17
Q

SULFONAMIDES CLINICAL APPLICATIONS

Simple UTI

A

Oral Triple sulfa & Sulfisoxazole

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18
Q

SULFONAMIDES: NON-ABSORBABLE CLINICAL APPLICATIONS

Ocular infection

A

Topical Sulfacetamide

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19
Q

SULFONAMIDES: NON-ABSORBABLE CLINICAL APPLICATIONS

Burn infections

A

Topical Mafenide & Silver sulfadiazine

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20
Q

SULFONAMIDES: NON-ABSORBABLE CLINICAL APPLICATIONS

● Ulcerative colitis (oral)
● Rheumatoid arthritis (oral)
● Enteritis
● Other Inflammatory Bowel Diseases (IBDs)

A

Sulfasalazine

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21
Q

SULFONAMIDES: NON-ABSORBABLE CLINICAL APPLICATIONS

Effective in the treatment of bacterial conjunctivitis; considered to be second-line

A

Sodium Sulfacetamide

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22
Q

ANTIFOLATE DRUGS TOXICITIES

Common toxicity of sulfonamides

A

Hypersensitivity

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23
Q

ANTIFOLATE DRUGS TOXICITIES

• Hypersensitivity
o Skin rash & fever (common)
o Exfoliative dermatitis (rare)
o Polyarteritis nodosa (rare)
o Stevens-Johnson syndrome (rare)
o Cross-allergenicity

A

Sulfonamides

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24
Q

ANTIFOLATE DRUGS TOXICITIES

Gastrointestinal
o Nausea, vomiting, & diarrhea
o Mild hepatic dysfunction
o Hepatitis (rare)

A

Sulfonamides

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25
Q

ANTIFOLATE DRUGS TOXICITIES

Nephrotoxicity
o Crystalluria and hematuria

A

Sulfonamides

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26
Q

ANTIFOLATE DRUGS TOXICITIES

Kernicterus (3rd trimester of pregnancy)

A

Sulfonamides

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27
Q

ANTIFOLATE DRUGS TOXICITIES

Hematotoxicity (Hematopoietic Disturbances)
○ Rare
○ Granulocytopenia
○ Thrombocytopenia
○ Aplastic anemia
○ Leukemoid reactions
○ May provoke acute hemolysis in G6PD patients

A

Sulfonamides

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28
Q

ANTIFOLATE DRUGS PKINETICS

● Structurally similar to folic acid
● Weak base

A

Trimethoprim

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29
Q

ANTIFOLATE DRUGS PKINETICS

● Trapped in acidic environments
● High conc: prostatic and vaginal fluids

A

Trimethoprim

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30
Q

ANTIFOLATE DRUGS PKINETICS

Trimethoprim excretion

A

Urine

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31
Q

ANTIFOLATE DRUGS

Trimethoprim ROA

A

PO, IV

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32
Q

ANTIFOLATE DRUGS MOA

• Bactericidal (with sulfamethoxazole)
• Selective inhibitor of bacterial dihydrofolate reductase

A

Trimethoprim

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33
Q

ANTIFOLATE DRUGS RESISTANCE MECHANISM

  1. Production of dihydrofolate reductase that has reduced affinity for the drug
  2. Reduced cell permeability
  3. Overproduction of dihydrofolate reductase
  4. Production of an altered reductase with reduced drug binding
A

Trimethoprim

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34
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

Acute UTIs

A

Oral Trimethoprim

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35
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

o P. jirovecii
o UTIs
o Prostatitis
o Shigella
o Salmonella
o Nontuberculous mycobacteria

A

Oral Trimethoprim-Sulfamethoxazole (TMP-SMZ)

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36
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

Effective against most Staphylococcus aureus strains (MRSA) and respiratory tract pathogens such as Haemophilus sp., Moraxella catarrhalis, and K pneumoniae (but not Mycoplasma pneumoniae)

A

Trimethoprim

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37
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

Commonly used for the treatment of uncomplicated skin and soft tissue infections

A

Trimethoprim

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38
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

  • Moderately severe to severe pneumocystis pneumonia
  • G(-) bacteremia
  • MDR: Enterobacter & Serratia, Shigellosis, or Typhoid
  • Preferred alternate therapy for serious Listeria infections
A

IV Trimethoprim-Sulfamethoxazole

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39
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS - TRIMETHOPRIM

Used in the treatment of toxoplasmosis

A

Oral Pyrimethamine with Sulfonamide

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40
Q

TRIMETHOPRIM CLINICAL APPLICATIONS

○ Aka folinic acid
○ 10 mg orally each day should be administered
to minimize bone marrow suppression seen with pyrimethamine

A

Leucovorin

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41
Q

ANTIFOLATE DRUGS TOXICITIES

Megaloblastic anemia, Leukopenia, & Granulocytopenia

A

Trimethoprim

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42
Q

ANTIFOLATE DRUGS TOXICITIES

• HIV patients
o Fever
o Rashes
o Leukopenia
o Diarrhea
• Mild elevation of blood creatinine

A

Trimethoprim

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43
Q

ANTIFOLATE DRUGS ROA

TMP-SMX ROA

A

PO, IV

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44
Q

ANTIFOLATE DRUGS MOA

● Bactericidal
● Sequential blockade of folate synthesis

A

TMP-SMX

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45
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

• Urinary tract
• Respiratory
• Ear

A

TMP-SMX

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46
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

Sinus infections caused by
o H. influenzae
o M. catarrhalis

A

TMP-SMX

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47
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

DOC
o Pneumocystis pneumonia o Toxoplasma
o Nocardiosis

A

TMP-SMX

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48
Q

ANTIFOLATE DRUGS CLINICAL APPLICATIONS

Treatment of infections
o MR staphylococci
o L. monocytogenes

A

TMP-SMX

49
Q

ANTIFOLATE DRUGS TOXICITIES

● Nausea
● Vomiting
● Drug fever
● Vasculitis
● Renal damage
● CNS disturbances

A

TMP-SMX

50
Q

ANTIFOLATE DRUGS TOXICITIES

HIV: Fever Rashes Leukopenia Diarrhea

A

Trimethoprim & TMP-SMX

51
Q

SULFONAMIDES: NON-ABSORBABLE CLINICAL APPLICATIONS

Can cause metabolic acidosis

A

Mafenide Acetate & Silver Sulfadiazine

52
Q

SULFONAMIDES: ORAL ABSORBABLE AGENTS CLINICAL APPLICATIONS

● P. jirovecii pneumonia
● Toxoplasmosis
● Nocardiosis

A

Sulfamethoxazole

53
Q

SULFONAMIDES: ORAL ABSORBABLE AGENTS CLINICAL APPLICATIONS

First line for Acute Toxoplasmosis

A

Sulfadiazine + Pyrimethamine

54
Q

SULFONAMIDES: ORAL ABSORBABLE AGENTS CLINICAL APPLICATIONS

● Marketed in some countries
● Second-line antimalarial agent

A

Sulfadoxine + Pyrimethamine

55
Q

DNA GYRASE INHIBITORS PKINETICS

Originally developed because of their gram-negative aerobic coverage (with gram+ coverage as well)

A

Fluoroquinolones

56
Q

DNA GYRASE INHIBITORS PKINETICS

Impaired absorption when combined with antacids, divalent, and trivalent cations

A

Fluoroquinolones

57
Q

DNA GYRASE INHIBITORS PKINETICS

Fluoroquinolones excretion

A

Both = Dela & Gemi
Renal (tubular/glomerular)
Liver = Moxi

58
Q

DNA GYRASE INHIBITORS PKINETICS

Long half-lives permit once-a-day dosing

A

○ Levofloxacin
○ Gemifloxacin
○ Moxifloxacin

59
Q

DNA GYRASE INHIBITORS MOA

• Interfere with bacterial DNA synthesis
o Topoisomerase II (relaxation)
o Topoisomerase IV (separation)
• Bactericidal
• Exhibit post-antibiotic effects

A

Fluoroquinolones

60
Q

DNA GYRASE INHIBITORS MOA

Prevents the relaxation of positively charged supercoiled DNA that is required for normal transcription and replication

A

Topoisomerase II (DNA gyrase)

61
Q

DNA GYRASE INHIBITORS MOA

Interferes with separation of replicated
chromosomal DNA into the respective
daughter cells during cell division

A

Topoisomerase IV

62
Q

DNA GYRASE INHIBITORS MOA

Primary target for gram negative

A

DNA Gyrase

63
Q

DNA GYRASE INHIBITORS MOA

Primary target for gram positive

A

Topoisomerase IV

64
Q

Fluoroquinolone Resistance Mechanism

A
  1. Mutation / Change permeability
  2. Efflux pumps
  3. Changes in porin
  4. Changes in sensitivity (point mutations)
65
Q

DNA GYRASE INHIBITORS RESISTANCE MECHANISM

Resistant organism appears in about every 107-109

A

o Staphylococci
o P. aeruginosa
o S. marcesens

66
Q

DNA GYRASE INHIBITORS RESISTANCE MECHANISM

Emerged rapidly for 2nd generation:
o C. jejuni and gonococci
o Gram (+) cocci (MRSA)
o Pseudomonas and Serratia

A

Fluoroquinolones

67
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Urogenital and gastrointestinal tract infection
• Atypical and intracellular pathogens

A

Fluoroquinolones

68
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gr (+) bacteria
• Gram (-) organisms
o Gonococci
o E. coli
o K. pneumoniae
o C. jejuni
o Enterobacter
o P. aeruginosa o Salmonella
o Shigella

A

Fluoroquinolones

69
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Bacterial diarrhea
• Meningococcal carriers
• Prophylaxis of bacterial infections w/ neutropenia

A

Fluoroquinolones

70
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

Effectiveness is variable due to resistance
o Respiratory tract
o Skin and soft tissue infection

A

Fluoroquinolones

71
Q

DNA GYRASE INHIBITORS TOXICITIES

Fluoroquinolones most common toxicity

A

Gastrointestinal distress

72
Q

DNA GYRASE INHIBITORS TOXICITIES

• Occasionally: headache, dizziness, insomnia, skin rash or abnormal LFTs
• Tendinitis and tendon rupture
• Superinfection caused by C. albicans and streptococci

A

Fluoroquinolones

73
Q

DNA GYRASE INHIBITORS TOXICITIES

Photosensitivity

A

Lomefloxacin, Pefloxacin, Sparfloxacin

74
Q

DNA GYRASE INHIBITORS TOXICITIES

• Temporary to Permanent Peripheral Neuropathy
• Increase levels of theophylline and other methylxanthines

A

Fluoroquinolones

75
Q

DNA GYRASE INHIBITORS TOXICITIES

• May damage growing cartilage and cause arthropathy
• Avoid in pregnancy

A

Fluoroquinolones

76
Q

DNA GYRASE INHIBITORS PKINETICS

Derived from nalidixic acid (earliest)

A

1st Gen - Norfloxacin

77
Q

DNA GYRASE INHIBITORS PKINETICS

• Common pathogens that cause UTI
• Does not achieve adequate plasma levels for use in systemic infections
• Oral bioavailability: 80%

A

1st Gen - Norfloxacin

78
Q

DNA GYRASE INHIBITORS PKINETICS

Norfloxacin excretion

A

Renal

79
Q

DNA GYRASE INHIBITORS PKINETICS

Fluoroquinolones ROA

A

PO

80
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

Least active of the fluoroquinolones against both gram negative and gram positive organisms

A

1st Gen - Norfloxacin

81
Q

DNA GYRASE INHIBITORS PKINETICS

• Synthetic fluorinated derivatives
• Oral bioavailability: 70%

A

2nd Gen - Ciprofloxacin

82
Q

DNA GYRASE INHIBITORS PKINETICS

Ciproflaxin excretion

A

Renal

83
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gram (-): greater activity
o P. aeruginosa
• Gram (+) cocci
• Gonococcus
• Mycobacteria
• MSSA
• Atypical organisms (M. pneumoniae)
• N. gonorrhea (single oral doses)
o Alternative to 3rd generation cephalosporin
• Anthrax

A

2nd Gen - Ciprofloxacin

84
Q

DNA GYRASE INHIBITORS PKINETICS

Oral bioavailability: 95%

A

2nd Gen - Ofloxacin

85
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gram (-): greater activity
• Gram (+) cocci
• Gonococcus
• Mycobacteria
• MSSA
• Atypical organisms (M. pneumoniae)
• Will eradicate accompanying organisms like Chlamydia (7 day course)
o Urethritis

A

2nd Gen - Ofloxacin

86
Q

DNA GYRASE INHIBITORS PKINETICS

• Synthetic fluorinated derivatives
• Oral bioavailability: 95%

A

3rd Gen - Levofloxacin

87
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Slightly less active against gram (-)
• Greater activity against gram (+) cocci
• Streptococci
• S. pneumoniae
• Staphylococci
• MRSA
• MSSA
• Some strains of enterococci

A

3rd Gen - Levofloxacin & Gatifloxacin

88
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Community-acquired pneumonia
• Atypical pneumonia (M. pneumoniae)
• Anthrax prophylaxis

A

3rd Gen - Levofloxacin

89
Q

DNA GYRASE INHIBITORS TOXICITIES

QT Prolongation

A

3rd Gen - Levofloxacin & Gatifloxacin
4th Gen - Moxifloxacin & Gemifloxacin

90
Q

DNA GYRASE INHIBITORS PKINETICS

Levofloxacin excretion

A

Renal

91
Q

DNA GYRASE INHIBITORS PKINETICS

Gatifloxacin excretion

A

Renal

92
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

Gram (+)
o S pneumoniae
o Some staphylococci

A

3rd Gen - Gatifloxacin

93
Q

DNA GYRASE INHIBITORS TOXICITIES

• QT prolongation
• Hypoglycemia when given with oral
hypoglycemic agents

A

3rd Gen - Gatifloxacin

94
Q

DNA GYRASE INHIBITORS PKINETICS

Sparfloxacin excretion & elimination

A

• Excretion: renal
• Eliminated partly by hepatic metabolism and biliary excretion

95
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Enhanced activity against anaerobes
• Gram (+) organisms
• Penicillin-resistant pneumococci

A

3rd Gen - Sparfloxacin

96
Q

DNA GYRASE INHIBITORS TOXICITIES

• Risk for cardiac arrhythmia
• Photosensitivity

A

Sparfloxacin

97
Q

DNA GYRASE INHIBITORS PKINETICS

• Broadest spectrum
• Oral bioavailability: >85%

A

4th Gen - Moxifloxacin

98
Q

DNA GYRASE INHIBITORS PKINETICS

Moxifloxacin elimination

A

Eliminated partly by hepatic metabolism and biliary excretion

99
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

Enhanced activity against anaerobes

A

4th Gen

100
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gram (+)
o S pneumoniae
o Some staphylococci
• Gram (-) organisms

A

4th Gen - Moxifloxacin & Trovafloxacin

101
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Anaerobic bacteria
• Lacks appreciable activity against:
o P. aeruginosa

A

4th Gen - Moxifloxacin

102
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Used in meningococcal carrier state
• Tuberculosis
• Neutropenia prophylaxis

A

4th Gen - Moxiflaxocin

103
Q

DNA GYRASE INHIBITORS PKINETICS

Broadest spectrum

A

4th Gen

104
Q

DNA GYRASE INHIBITORS PKINETICS

Trovafloxacin elimination

A

Eliminated partly by hepatic metabolism and biliary excretion

105
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Prophylactic management: neutropenic patients

A

4th Gen - Trovafloxacin

106
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gram (+)
• Gram (-) organisms
• Anaerobic bacteria
• Used in meningococcal carrier state
• Tuberculosis

A

4th Gen - Trovafloxacin & Moxifloxacin

107
Q

DNA GYRASE INHIBITORS TOXICITIES

Hepatotoxic potential

A

4th Gen - Trovafloxacin

108
Q

DNA GYRASE INHIBITORS PKINETICS

• Broadest spectrum
• Oral bioavailability: 70%

A

4th Gen - Gemifloxacin

109
Q

DNA GYRASE INHIBITORS PKINETICS

Gemifloxacin excretiom

A

Renal & Nonrenal

110
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gram (+)
o S. pneumoniae
o Some staphylococci
• + Azithromycin o Lower RTIs

A

4th Gen - Gemifloxacin

111
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

Gram (+)
o S. pneumoniae
o Some staphylococci
o Pneumococci
o Beta-hemolytic streptococci
o MSSA
o MRSA

A

4th Gen - Delafloxacin

112
Q

DNA GYRASE INHIBITORS CLINICAL APPLICATIONS

• Gram (-): similar to ciprofloxacin
o P. aeruginosa
• In vitro activity against anaerobes but not proven

A

4th Gen - Delafloxacin

113
Q

DNA GYRASE INHIBITORS ANTIBACTERIAL ACTIVITY

T/F: Most exist in zwitterionic forms in vivo except delafloxacin. Anionic at neutral pH & no charge at acidic pH.

A

T

114
Q

DNA GYRASE INHIBITORS

Modest activity against anaerobic bacteria

A

4th Gen - Moxiflaxocin

115
Q

DNA GYRASE INHIBITORS

Most active agent of this group against gram-negative organisms particularly P aeruginosa

A

2nd Gen - Ciprofloxacin

116
Q

DNA GYRASE INHIBITORS

● L-isomer of ofloxacin
● Has greater activity than ciprofloxacin against
gram-positive organisms especially Streptococcus pneumoniae

A

3rd Gen - Levofloxacin

117
Q

DNA GYRASE INHIBITORS

Minimum inhibitory concentrations fourfold to eightfold higher than those of ciprofloxacin

A

1st Gen - Norfloxacin

118
Q

DNA GYRASE INHIBITORS

Has threefold to fivefold more potent in vitro activity against most gram-positive organisms including pneumococci, beta-hemolytic streptococci, MSSA, and MRSA

A

4th Gen - Delafloxacin

119
Q

Occasionally used as part of a treatment regimen for tuberculosis and nontuberculous mycobacterial infection (same goes for ciprofloxacin and moxifloxacin)

A

Levofloxacin

[MT 6314] Pharmacology & Toxicology (20 decks)

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