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Phase 1 - 2025 > Ch 7 - Antibiotics > Flashcards

Ch 7 - Antibiotics Flashcards

1
Q

What does PK stand for in pharmacology?

A

Pharmacokinetics

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2
Q

What does PD stand for in pharmacology?

A

Pharmacodynamics

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3
Q

Why is it important to consider PK and PD MIC when designing a dose regimen?

A

To ensure effective drug dosing and therapeutic outcomes

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4
Q

What are the important PK parameters for time and concentration dependent drugs?

A

Maximum drug concentration and elimination half-life

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5
Q

For time-dependent drugs, what is a critical PK parameter?

A

Elimination half-life

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6
Q

What is the aim for T>MIC in time-dependent PD index?

A

50-75%

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7
Q

What is the exception for T>MIC in carbapenems?

A

25%

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8
Q

What is the Cmax/MIC ratio for concentration-dependent PD index?

A

Cmax/MIC ≥ 10

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9
Q

What is the AUC/MIC range for concentration-dependent PD index?

A

125 to 250

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10
Q

What does MBC stand for?

A

Minimum Bactericidal Concentration

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11
Q

What does MPC stand for?

A

Minimum Concentration needed to block growth of less susceptible bacteria

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12
Q

What type of drugs target the bacterial cell wall?

A

Beta-Lactam

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13
Q

What are the two main types of beta-lactam antibiotics?

A

Penicillins and Cephalosporins

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14
Q

What is the origin of natural penicillin?

A

Mold Penicillium

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15
Q

What is the significance of the beta-lactam ring in beta-lactam antibiotics?

A

It is the active site for inhibiting bacterial cell wall synthesis

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16
Q

What is the effect of the six-member ring in cephalosporins compared to the five-member ring in penicillins?

A

More stable and less susceptible to degradation and resistance

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17
Q

What is the mechanism of action for beta-lactams?

A

Interference with bacterial cell wall synthesis

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18
Q

What are the key components of the bacterial cell wall that beta-lactams target?

A

Peptidoglycan strands

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19
Q

What leads to bacterial cell lysis when affected by beta-lactams?

A

Loss of cell wall rigidity and osmotic pressure

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20
Q

What is the relationship between beta-lactams and ribosomal inhibitors?

A

They have well-documented antagonistic effects

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21
Q

What is the activity spectrum of natural penicillin G?

A

Effective against gram-positive cocci and some gram-negative anaerobes

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22
Q

What type of penicillins are resistant to beta-lactamase?

A

Beta-lactamase-resistant penicillins such as dicloxacillin, cloxacillin, methicillin, and oxacillin

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23
Q

What are aminopenicillins?

A

Amoxicillin and ampicillin

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24
Q

What is the significance of beta-lactamase inhibitors?

A

They improve the efficacy of beta-lactams against resistant organisms

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25
Q

What is the role of carbapenems?

A

Broad-spectrum antibiotics with resistance to beta-lactamase

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26
Q

What is the MOA of carbapenems?

A

Bind to PBPs and are effective against a wide range of bacteria

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27
Q

What is the significance of the mecA gene in MRSA?

A

It alters the penicillin-binding protein, leading to resistance

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28
Q

What are ESBLs?

A

Extended-Spectrum Beta-Lactamases that confer resistance to certain cephalosporins

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29
Q

What is a common challenge in detecting ESBLs?

A

They may be missed in routine susceptibility testing

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30
Q

What is the role of pharmacokinetics in beta-lactam treatment?

A

Determines absorption, distribution, metabolism, and excretion of the drugs

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31
Q

Fill in the blank: Many beta-lactams are _______ bound to plasma proteins.

A

highly

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32
Q

What is the significance of protein binding in beta-lactams?

A

Prolongs their half-life and duration in circulation

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33
Q

What is the elimination route for most beta-lactams?

A

Primarily via the kidneys

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34
Q

What is the Cmax and half-life of amoxicillin at the label dose?

A

Low Cmax and short half-life increase likelihood of therapeutic failure even with susceptible isolates

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35
Q

How do procaine and benzathine penicillin G esters differ in terms of absorption duration?

A

Procaine lasts 24 hours, benzathine up to 120 hours

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36
Q

What is the MIC90 for amoxicillin-clavulanic acid against S. pseudintermedius?

A

<0.5 μg/mL

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37
Q

What is the MIC90 for E. coli?

A

8 μg/mL

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38
Q

What is the protein binding characteristic of imipenem in dogs?

A

Minimally protein bound

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39
Q

What is the clearance rate of imipenem in dogs?

A

0.26 L/hr/kg

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40
Q

What is the preferred administration route for meropenem for faster onset?

A

Intravenous administration

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41
Q

What is the half-life of cefalexin at a 20 mg/kg dose?

A

5 hours

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42
Q

What is the Cmax of cefazolin after a 22 mg/kg IV dose?

A

178 μg/mL

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43
Q

What is the Cmax of cefuroxime after subcutaneous administration in Beagles?

A

29 μg/mL

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44
Q

What is the oral bioavailability of cefpodoxime?

A

63%

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45
Q

What is the protein binding percentage of cefovecin?

A

96%-98% at low concentrations

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46
Q

What is the dosing interval for cefpodoxime to stay above MIC90 for E. coli?

A

12-24 hours

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47
Q

What is the risk associated with combining beta-lactams and bacteriostatic drugs?

A

Beta-lactams may become bacteriostatic rather than bactericidal

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48
Q

Which beta-lactam may not exhibit antagonism with certain Enterobacteriaceae?

A

Chloramphenicol

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49
Q

What is a common side effect of beta-lactam antibiotics?

A

Diarrhea

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50
Q

What may reduce gastrointestinal upset when using amoxicillin-clavulanic acid?

A

Higher amoxicillin to clavulanic acid ratio

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51
Q

What serious condition may arise from overuse of cefovecin?

A

Emergence of methicillin-resistant Staphylococcus aureus (MRSA)

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52
Q

What is the main mechanism of action of vancomycin?

A

Binding to D-Ala-D-Alanine precursor in bacterial cell walls

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53
Q

What type of bacteria is vancomycin primarily used to treat?

A

Methicillin-resistant Staphylococcus and other Gram-positive bacteria

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54
Q

What is a potential toxicity associated with vancomycin?

A

Nephrotoxicity

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55
Q

How does teicoplanin differ from vancomycin?

A

More lipid-soluble structure

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56
Q

What is the spectrum of activity for teicoplanin?

A

Effective against Gram-positive bacteria

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57
Q

What type of bond characterizes fosfomycin?

A

Carbon–phosphorus bond

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58
Q

What is the mechanism of action of the drug similar to vancomycin?

A

It interferes with bacterial cell wall synthesis by binding to the D-Ala-D-Alanine precursor.

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59
Q

What spectrum of bacteria is the drug effective against?

A

Effective against Gram-positive bacteria, including Staphylococcus, Streptococcus, and some anaerobes.

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60
Q

What has largely replaced the clinical role of the drug similar to vancomycin?

A

Vancomycin and daptomycin due to similar efficacy and better options available.

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61
Q

What is fosfomycin?

A

A phosphonic acid with a carbon–phosphorus bond, produced by Streptomyces fradiae.

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62
Q

What is the mechanism of action of fosfomycin?

A

Inhibits phosphoenolpyruvate transferase, which catalyzes the first step in bacterial cell wall peptidoglycan synthesis.

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63
Q

What type of infections is fosfomycin particularly effective for?

A

Uncomplicated urinary tract infections (UTIs), including those caused by multidrug-resistant E. coli.

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64
Q

What is the oral bioavailability of fosfomycin?

A

30%, with a dose-dependent increase in plasma concentration.

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65
Q

What can decrease the bioavailability of fosfomycin?

A

Food.

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66
Q

What is the half-life of fosfomycin?

A

Short half-life (~1.3 hours).

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67
Q

What are common adverse effects of fosfomycin?

A

Mild gastrointestinal upset, such as diarrhea.

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68
Q

What type of drugs are aminoglycosides?

A

A class of antibiotics that target ribosomes and are bactericidal.

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69
Q

Name some aminoglycosides.

A
  • Amikacin
  • Gentamicin
  • Neomycin
  • Tobramycin
  • Streptomycin
  • Netilmicin
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70
Q

What is the structure of aminoglycosides composed of?

A

Amino sugars linked to an aminocyclitol core.

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71
Q

How do aminoglycosides enter gram-negative bacteria?

A

Through porins in the lipopolysaccharide layer.

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72
Q

What ribosomal subunit do aminoglycosides bind to?

A

30S ribosomal subunit.

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73
Q

What type of killing mechanism do aminoglycosides exhibit?

A

Concentration-dependent killing.

74
Q

What is the recommended dosing strategy for aminoglycosides?

A

Once daily at high dosages.

75
Q

What type of bacteria are aminoglycosides primarily effective against?

A

Aerobic gram-negative bacteria and some aerobic gram-positive organisms.

76
Q

What is the synergy effect of aminoglycosides?

A

Enhances effectiveness when combined with penicillins or vancomycin.

77
Q

What are the common resistance mechanisms to aminoglycosides?

A
  • Enzymatic destruction
  • Decreased cell entry
  • Altered ribosomal structure
78
Q

What is the most common resistance mechanism to aminoglycosides?

A

Enzymatic destruction.

79
Q

What is the main adverse effect associated with aminoglycosides?

A

Nephrotoxicity.

80
Q

What are the risk factors associated with nephrotoxicity from aminoglycosides?

A
  • Hypocalcemia
  • Hypomagnesemia
  • Dehydration
  • Renal diseases
81
Q

What can cause ototoxicity when using aminoglycosides?

A

Active uptake of the drug into cochlear hair cells.

82
Q

What is a significant pharmacokinetic characteristic of aminoglycosides?

A

They are poorly absorbed from the GI tract.

83
Q

What is the elimination route for aminoglycosides?

A

Excretion is proportional to GFR.

84
Q

What can enhance the effectiveness of aminoglycosides in patients with renal disease?

A

Monitoring serum creatinine levels to adjust dosing intervals.

85
Q

What type of toxicity is associated with aminoglycosides?

A

Auditory & vestibular toxicity

Aminoglycosides can lead to hearing loss and balance issues due to damage in cochlear hair cells.

86
Q

What is the mechanism of auditory toxicity caused by aminoglycosides?

A

Active uptake into cochlear hair cells results in cell damage

This mechanism contributes to hearing loss and balance issues.

87
Q

What trough levels of aminoglycosides should be avoided to minimize ototoxicity?

A

Above 2-5 µg/mL

Higher trough levels are associated with increased risk of ototoxicity.

88
Q

Why should drugs not be used in patients with a perforated eardrum?

A

Increased risk of ototoxicity

Perforated eardrums can enhance the risk of drug-induced hearing loss.

89
Q

What neuromuscular effects can aminoglycosides have?

A

Impair calcium release, leading to muscle weakness and respiratory paralysis

Risk increases with intravenous administration, hypocalcemia, or combination with other neuromuscular affecting drugs.

90
Q

What can be used to reverse neuromuscular blockade caused by aminoglycosides?

A

Cholinesterase inhibitors and calcium

These treatments help restore neuromuscular function.

91
Q

What changes can prolonged therapy or high doses of aminoglycosides cause?

A

Progressive kidney damage

Kidney damage can be monitored through changes in urine osmolality, creatinine levels, and renal enzyme markers.

92
Q

Which drugs increase the risk of ototoxicity and nephrotoxicity when combined with aminoglycosides?

A

Other aminoglycosides, NSAIDs, loop diuretics, ACE inhibitors, amphotericin B

These combinations can elevate toxicity risks.

93
Q

What are the primary targets of fluoroquinolones in bacterial cells?

A

DNA gyrase and topoisomerase IV

These topoisomerases are essential for DNA replication and separation.

94
Q

What is the mechanism of action of fluoroquinolones?

A

Cause irreversible breaks in bacterial DNA

This action leads to inhibition of DNA replication.

95
Q

What is the significance of the Cmax/MIC ratio for fluoroquinolones?

A

It should exceed 10 for optimal efficacy

This ratio indicates effective bacterial killing.

96
Q

What are the four generations of fluoroquinolones based on spectrum and potency?

A

1st: Narrow spectrum, 2nd: Broader spectrum, 3rd: Enhanced potency, 4th: Broadest spectrum

Each generation has different effectiveness against gram-negative and gram-positive bacteria.

97
Q

Which gram-negative bacteria are commonly targeted by fluoroquinolones?

A

E. coli, Klebsiella, Pasteurella, Pseudomonas spp.

These bacteria are susceptible to fluoroquinolone antibiotics.

98
Q

What is the major mode of resistance to fluoroquinolones?

A

Mutation in target topoisomerase enzymes

Resistance can also involve reduced drug uptake and increased efflux pump activity.

99
Q

What pharmacokinetic properties do fluoroquinolones exhibit?

A

Excellent tissue distribution due to lipid solubility

They can accumulate in phagocytic white blood cells and cross the blood-brain barrier.

100
Q

What is the role of pradofloxacin among fluoroquinolones?

A

Targets P. aeruginosa and many anaerobes

It features a cyclopropyl ring that enhances bacterial killing.

101
Q

What is a key drug interaction concern with fluoroquinolones?

A

They can inhibit hepatic enzymes, prolonging elimination of other drugs

Notable interactions include theophylline, cyclosporine, and warfarin.

102
Q

What is the effective concentration of fluoroquinolones for pathogens with low MICs?

A

4.7 μg/mL

This concentration suggests their use is most effective for specific pathogens.

103
Q

What do fluoroquinolones inhibit that can prolong the elimination of other drugs?

A

Certain hepatic enzymes

This can lead to various drug interactions.

104
Q

Which drug’s metabolism can be impaired by fluoroquinolones like ciprofloxacin?

A

Theophylline

This can lead to toxicity in both dogs and humans.

105
Q

What effect do fluoroquinolones have when combined with cyclosporine?

A

Increase cyclosporine concentrations

This may necessitate monitoring.

106
Q

What are the potential effects of combining fluoroquinolones with warfarin?

A

Prolonged anticoagulant effects

This can increase the risk of bleeding.

107
Q

Fill in the blank: Fluoroquinolones may enhance the hypoglycemic effects of _______.

A

Oral Hypoglycemics and Insulin

108
Q

What type of activity do fluoroquinolones have when given with aminoglycosides?

A

Synergistic activity

Effective against gram-negative organisms.

109
Q

What CNS effects may occur when fluoroquinolones are combined with drugs that inhibit GABA receptors?

A

Increased risk of seizures and other CNS disorders

110
Q

What can enrofloxacin cause in terms of glucose readings?

A

False glucosuria

This can complicate diabetes management.

111
Q

What gastrointestinal issues are associated with fluoroquinolone use?

A

Vomiting, nausea, and diarrhea

Particularly with oral administration.

112
Q

What cardiovascular toxicity is linked to levofloxacin?

A

Hypotension and decreased left ventricular function

113
Q

What type of damage can fluoroquinolones like enrofloxacin cause in growing animals?

A

Cartilage and connective tissue damage

Especially in dogs.

114
Q

What is the risk associated with magnesium in relation to fluoroquinolones?

A

Magnesium antagonism leading to cartilage damage

115
Q

What can fluoroquinolones inhibit that contributes to seizures?

A

The release of GABA

116
Q

What retinal issue can occur in cats treated with fluoroquinolones?

A

Dose-dependent retinal degeneration

Clinical signs may include mydriasis and acute blindness.

117
Q

Which fluoroquinolone is least likely to cause retinal degeneration in cats?

A

Marbofloxacin

118
Q

What is a potential consequence of impaired bone healing associated with fluoroquinolones?

A

Impaired fracture healing

119
Q

What can fluoroquinolones induce in certain bacteria, potentially worsening conditions?

A

Bacteriophage lysis

Examples include S. canis and E. coli.

120
Q

What are fluoroquinolones derived from?

A

Nalidixic acid

121
Q

What is the primary therapeutic use of fluoroquinolones?

A

Effective against a wide range of organisms in life-threatening infections

122
Q

What is a concern regarding the use of fluoroquinolones?

A

Development of antimicrobial resistance

123
Q

What must be monitored to prevent resistance development with fluoroquinolones?

A

Minimum Bactericidal Concentration (MBC) and mutant prevention concentrations (MPC)

124
Q

What is the mechanism of action of rifampin?

A

Inhibits the B unit of DNA-dependent RNA polymerase in bacteria

125
Q

Which organisms is rifampin mainly effective against?

A

Gram-positive organisms

Includes Staphylococcus and Mycobacterium.

126
Q

What is a significant adverse effect associated with rifampin?

A

GI disturbances and liver function abnormalities

127
Q

What drug interactions are important to consider with rifampin?

A

Induces microsomal enzymes including CYP450 enzymes

128
Q

What is the mechanism of action of metronidazole?

A

Inhibits microbial RNA/DNA synthesis via nitrous reduction in anaerobic environments

129
Q

What types of bacteria is metronidazole effective against?

A

Anaerobic bacteria

Includes B. fragilis and Clostridium spp.

130
Q

What are common adverse effects of metronidazole?

A

Gastrointestinal upset and CNS toxicity

131
Q

What is the mechanism of action of sulfonamides?

A

Inhibit bacterial folic acid synthesis by competing with PABA

132
Q

What is the spectrum of activity for sulfonamides?

A

Broad spectrum but effectiveness varies due to resistance

133
Q

What is a common adverse effect of sulfonamides?

A

Keratoconjunctivitis sicca

134
Q

What is the mechanism of action for tetracyclines?

A

Bacteriostatic, concentration dependent

135
Q

Fill in the blank: Tetracyclines are obtained from _______.

A

Streptomyces

136
Q

What type of activity do tetracyclines exhibit?

A

Bacteriostatic, concentration dependent

Tetracyclines inhibit bacterial growth without killing bacteria directly.

137
Q

Name three naturally occurring tetracyclines.

A
  • Chlortetracycline
  • Oxytetracycline
  • Demethylchlortetracycline

These are the foundational tetracyclines from which semisynthetic derivatives are derived.

138
Q

List the classification of tetracyclines by half-life.

A
  • Short-acting: tetracycline, oxytetracycline, chlortetracycline
  • Intermediate-acting: demethylchlortetracycline, methacycline
  • Long-acting: doxycycline, minocycline

This classification affects the dosing and administration of these drugs.

139
Q

What is the mechanism of action for tetracyclines?

A

Bind to the 30S ribosomal subunit, preventing the binding of amino-acyl tRNA

This inhibition impairs protein synthesis in bacteria.

140
Q

What is the spectrum of activity for tetracyclines?

A

Broad-spectrum: effective against gram-positive and gram-negative bacteria, anaerobes, rickettsial organisms, mycoplasma, Chlamydia, Hemobartonella, and spirochetes

However, they are not effective against P. aeruginosa unless specified.

141
Q

True or False: Tetracyclines can be used in immunocompromised patients.

A

False

Tetracyclines are bacteriostatic and may not be effective in patients with weakened immune systems.

142
Q

What are the main adverse effects of tetracyclines?

A
  • Gastrointestinal upset
  • Hepatotoxicity
  • Renal toxicity
  • Esophageal erosions
  • Discoloration of teeth
  • Enamel hypoplasia
  • Hypersensitivity reactions
  • Fanconi-like syndrome

These effects vary by individual and specific tetracycline used.

143
Q

What is the pharmacokinetic profile of doxycycline?

A

100% bioavailable, penetrates tissues well, including CNS

Doxycycline’s bioavailability makes it a preferred choice in many cases.

144
Q

How do tetracyclines interact with cations?

A

Chelation with cations reduces absorption

Tetracyclines should not be given with antacids, sucralfate, or calcium supplements.

145
Q

What is the mechanism of action for chloramphenicol and florfenicol?

A

Both bind to the 50S ribosomal subunit, inhibiting peptidyl transferase

This action impairs protein synthesis in bacteria.

146
Q

What are the primary uses for florfenicol?

A

Approved for bovine respiratory disease and has fewer toxicity concerns compared to chloramphenicol

It is commonly used in small animals, especially cats.

147
Q

What is a notable adverse effect of chloramphenicol?

A

Bone marrow suppression

This can be reversible or irreversible and is more common in cats.

148
Q

What is the main advantage of florfenicol over chloramphenicol?

A

Fewer adverse effects and less risk of irreversible bone marrow suppression

This makes florfenicol a safer alternative in many cases.

149
Q

What types of bacteria are lincosamides effective against?

A
  • Aerobic gram-positive cocci
  • Nocardia
  • Anaerobes
  • Cell wall-deficient organisms like Mycoplasma

Clindamycin is more effective than lincomycin, especially against anaerobes.

150
Q

What is a potential side effect of clindamycin?

A

Pseudomembranous colitis

This condition is caused by an overgrowth of C. difficile due to disruption of normal intestinal microbiota.

151
Q

How do macrolides inhibit bacterial growth?

A

By binding to the bacterial 50S ribosomal subunit, inhibiting protein synthesis

This can be bacteriostatic or bactericidal depending on the concentration.

152
Q

What are some examples of macrolides?

A
  • Erythromycin
  • Azithromycin
  • Tylosin
  • Tilmicosin

These drugs vary in their specific applications and safety in different animal species.

153
Q

What are the adverse effects associated with erythromycin?

A
  • Gastrointestinal upset
  • Cholestatic hepatitis

Gastrointestinal upset can occur in up to 50% of animals treated.

154
Q

What is the role of azithromycin in terms of pharmacokinetics?

A

Has a large volume of distribution and is well distributed in tissues

Its half-life ranges from 1.5 hours in dogs to 35 hours in humans.

155
Q

What is a significant drug interaction concern with macrolides?

A

Macrolides can inhibit cytochrome P450 enzymes, increasing drug concentrations

This can lead to toxicity with other medications.

156
Q

What effect do anti-acids have on azithromycin absorption?

A

Anti-acids extend the absorption of azithromycin

This may influence the effectiveness of the drug.

157
Q

How do macrolides affect cytochrome P450 enzymes?

A

Macrolides can inhibit cytochrome P450 enzymes, increasing drug concentrations

This can lead to potential drug interactions.

158
Q

Which macrolides are most likely to interact with CYP 3A4?

A

Azithromycin and clarithromycin

They affect drugs like theophylline, digoxin, and warfarin.

159
Q

What type of effects can occur when azithromycin is combined with other antibiotics?

A

Synergistic effects

Examples include cefamandole or sulfadiazine/trimethoprim.

160
Q

What is azithromycin used for in cystic fibrosis treatment?

A

Azithromycin impairs P. aeruginosa adhesion in the respiratory tract

This helps in managing lung infections.

161
Q

What is Tylosin classified as?

A

Technically classified as a macrolide

It is structurally different from erythromycin.

162
Q

What is the mechanism of action for Tylosin?

A

Targets the 50S ribosomal subunit

Similar to erythromycin.

163
Q

What is the stability characteristic of Tylosin?

A

Stable in gastric environment

No need for enteric coating for oral administration.

164
Q

What type of infections is Tylosin used to treat in small animals?

A

Gastrointestinal infections and bacterial pyodermas

Example includes chronic inflammatory bowel disease.

165
Q

What is the first ketolide approved for human use?

A

Telithromycin

It is developed for treating respiratory tract infections.

166
Q

What is the mechanism of action for ketolides?

A

Bind to 50S ribosomal subunit

Similar to macrolides and azalides.

167
Q

What is the primary use of linezolid?

A

Effective against gram-positive bacteria

Examples include MRSA and vancomycin-resistant enterococci.

168
Q

What is the mechanism of action for oxazolidinones?

A

Binds to the 50S ribosomal subunit, inhibits protein synthesis at the P site

This action leads to its antibacterial effects.

169
Q

What are the adverse effects associated with linezolid?

A

Myelosuppression, peripheral neuropathies, and hyperlactatemia

These effects are more common in humans.

170
Q

What is the mechanism of action for daptomycin?

A

Binds to bacterial cell membranes, causing cell death

This mechanism is specific to gram-positive organisms.

171
Q

What is the main adverse effect of daptomycin in dogs?

A

Can cause skeletal muscle damage and peripheral neuropathies

Adverse effects are dose-dependent.

172
Q

What class does fusidic acid belong to?

A

Steroid like antimicrobial

It has a unique mechanism of action.

173
Q

What is the spectrum of activity for fusidic acid?

A

Primarily gram-positive bacteria

Especially effective against staphylococci.

174
Q

What is the mechanism of action for bacitracin?

A

Inhibits peptidoglycan synthesis

This action targets gram-positive organisms.

175
Q

What are polymyxins primarily effective against?

A

Primarily gram-negative organisms

Example includes P. aeruginosa.

176
Q

What is the limitation of using novobiocin systemically?

A

Systemic toxicity, such as bone marrow suppression

It is used topically only.

177
Q

What is the mechanism of action for mupirocin?

A

Inhibits incorporation of isoleucine into proteins

It binds to isoleucyl transfer-RNA synthetase.

178
Q

What is the spectrum of activity for silver sulfadiazine?

A

Effective against P. aeruginosa and broad-spectrum against gram-positive and other gram-negative organisms

Primarily used for burn wounds.

179
Q

What are nitrofurans used for?

A

Effective against gram-positive and gram-negative organisms, and some protozoa

Examples include nitrofurantoin and furazolidone.

180
Q

What is the mechanism of action for methenamine?

A

Bactericidal in acidic conditions; bacteriostatic in more alkaline environments

This dual action makes it versatile.

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