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Therapeutics > Antibiotic cases > Flashcards

Antibiotic cases Flashcards

1
Q

What is the origin of antibiotics and how are they defined in this context?

A

Antibiotics are derived from living organisms (e.g., penicillin) and in this context, they will be used to mean antibacterial drugs, including chemotherapeutic agents that were synthesized.

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2
Q

What is the emphasis of the lecture regarding antibiotics?

A

The emphasis is on drugs for community-acquired infections.

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3
Q

Are drugs for nosocomial infections included in the lecture?

A

Yes, drugs for nosocomial infections are included for completeness, denoted by an H in a red circle.

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4
Q

Which antibiotics exhibit concentration-dependent killing?

A

Antibiotics like aminoglycosides and quinolones exhibit concentration-dependent killing.

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5
Q

What determines the effectiveness of concentration-dependent antibiotics?

A

The effectiveness is directly related to the concentration achieved in the blood or at the site of infection.

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6
Q

What does the Area Under the Curve (AUC)/Minimum Inhibitory Concentration (MIC) ratio indicate?

A

The AUC/MIC ratio correlates with the efficacy of the antibiotic, with a higher ratio generally indicating better bacterial eradication.

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7
Q

What is the Minimal Inhibitory Concentration (MIC)?

A

MIC is the lowest concentration of the antibiotic that inhibits visible growth of the bacterium.

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8
Q

Why is it important to achieve concentrations well above the MIC for concentration-dependent antibiotics?

A

Achieving concentrations well above the MIC is crucial for effective treatment and bacterial killing.

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9
Q

What are the risks of underdosing concentration-dependent antibiotics?

A

Underdosing can lead to subtherapeutic levels, potentially resulting in treatment failure and the development of resistance.

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10
Q

Which antibiotics exhibit time-dependent killing?

A

Antibiotics like beta-lactams exhibit time-dependent killing.

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11
Q

What determines the effectiveness of time-dependent antibiotics?

A

The effectiveness is related to the duration of time that the drug concentration remains above the Minimum Inhibitory Concentration (MIC).

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12
Q

For beta-lactams, what percentage of the dosing interval should drug concentrations remain above the MIC to correlate with clinical cure?

A

Maintaining drug concentrations above the MIC for 40-60% of the dosing interval correlates with clinical cure.

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13
Q

In certain infections like meningitis, what is the optimal duration for drug levels to be above the MIC?

A

Optimal bacterial killing occurs when drug levels are above the MIC for 95-100% of the dosing interval in infections like meningitis.

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14
Q

Why is it important for patients to adhere to the prescribed dosing schedule for time-dependent antibiotics?

A

Adherence ensures that drug concentrations remain above the MIC, reducing the risk of subtherapeutic levels, treatment failure, and resistance.

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15
Q

What are the risks associated with skipping doses of time-dependent antibiotics?

A

Skipping doses can result in subtherapeutic levels, reducing the effectiveness of the antibiotic and increasing the risk of resistance.

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16
Q

B lactam antibiotics

A
  1. Penicillin
  2. Clavulanic (B lactamase inhibitor)
  3. Cephalosporin
  4. Carbapenem (H)
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17
Q

What is the primary target of beta-lactam antibiotics?

A

Beta-lactams target the synthesis of peptidoglycan, an essential component of the bacterial cell wall.

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18
Q

What role does peptidoglycan play in bacterial cells?

A

Peptidoglycan provides structural integrity and strength to the bacterial cell wall, helping to maintain its shape and prevent lysis.

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19
Q

How do beta-lactams exert their effect on bacteria?

A

Beta-lactams bind to and inhibit penicillin-binding proteins (PBPs), which are enzymes involved in the final stages of peptidoglycan synthesis.

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20
Q

What is the function of penicillin-binding proteins (PBPs)?

A

PBPs catalyze the cross-linking of peptidoglycan chains, a critical step in forming a strong, rigid cell wall.

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21
Q

What reaction is inhibited by beta-lactams, leading to a weakened cell wall?

A

Beta-lactams inhibit the transpeptidation reaction, which forms cross-links between peptidoglycan chains.

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22
Q

How does the inhibition of cell wall synthesis by beta-lactams lead to bacterial cell death?

A

The inhibition of cell wall synthesis activates autolytic enzymes within the bacterium, further degrading the cell wall and leading to bacterial cell lysis and death.

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23
Q

Are beta-lactams bactericidal or bacteriostatic?

A

Beta-lactams are typically bactericidal, meaning they kill bacteria rather than merely inhibiting their growth.

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24
Q

What determines the efficacy of beta-lactams?

A

The efficacy of beta-lactams depends on the duration of time that the drug concentration remains above the Minimum Inhibitory Concentration (MIC) during the dosing interval.

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25
Q

Do all beta-lactams have the same spectrum of activity?

A

No, different beta-lactams have varying spectra of activity, with some being effective against Gram-positive bacteria, others against Gram-negative bacteria, and some having broad-spectrum activity.

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26
Q

Where do beta-lactam antibiotics exert their action?

A

Beta-lactam antibiotics act on the bacterial cell wall.

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27
Q

What type of bactericidal action do beta-lactams have?

A

Beta-lactams have a time-dependent bactericidal action.

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28
Q

What is notable about the therapeutic index of beta-lactams?

A

Beta-lactams have a wide therapeutic index, but they can cause CNS toxicity at maximal doses

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29
Q

What is the main adverse effect of beta-lactam antibiotics?

A

The main adverse effect of beta-lactam antibiotics is hypersensitivity.

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30
Q

How are most beta-lactam antibiotics eliminated?

A

Most beta-lactam antibiotics are eliminated by renal tubular secretion.

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31
Q

What is the most common resistance mechanism against beta-lactam antibiotics?

A

The most common resistance mechanism is mediated by beta-lactamases.

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32
Q

Can beta-lactamase resistance be overcome by using higher doses of beta-lactams?

A

No, beta-lactamase resistance cannot be overcome by using higher doses.

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33
Q

What types of bacteria commonly produce beta-lactamases in the community?

A

In the community, most aerobic Gram negatives, anaerobes, and staphylococci produce beta-lactamases.

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34
Q

Where are extended spectrum beta-lactamases (ESBLs) typically found, and what is their impact?

A

ESBLs are typically found in aerobic Gram negatives in hospitals, leading to high-level resistance to all penicillins and cephalosporins.

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35
Q

What is the second resistance mechanism to beta-lactam antibiotics, and how can it be overcome?

A

The second resistance mechanism involves mutations in penicillin-binding proteins (e.g., S. pneumoniae), usually causing low-level resistance that can be overcome by using higher doses.

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36
Q

Against which types of bacteria is penicillin active?

A

Penicillin is active against Gram positives and spirochaetes.

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37
Q

For which infections is penicillin the drug of choice?

A

Penicillin is the drug of choice for:

  • Streptococci (with few S. pneumoniae being highly resistant)
  • Syphilis and other spirochaetes
  • Enterococci
  • Listeria
  • Actinomyces
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38
Q

Is penicillin susceptible to beta-lactamase?

A

Yes, penicillin is susceptible to beta-lactamase.

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39
Q

What are the different forms of penicillin administration and their uses?

A

Penicillin G: Intravenous injection (IVI)

Penicillin V: Oral (poorly absorbed, concentrations inadequate for S. pneumoniae)

Benzathine Penicillin: Long-acting injectable (intramuscular injection, IMI) that lasts for 21 days

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40
Q

What are the two types of aminopenicillins and their modes of administration?

A

Ampicillin: Intravenous (IV) only

Amoxicillin: Oral (well absorbed)

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41
Q

How do aminopenicillins compare with penicillin in terms of bacterial coverage?

A

Aminopenicillins cover the same bacteria as penicillin plus Haemophilus (except for the +15% that have beta-lactamase).

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42
Q

Why are aminopenicillins recommended for respiratory infections?

A

Aminopenicillins have excellent activity against S. pneumoniae, making them recommended for respiratory infections.

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43
Q

Which penicillins resist beta-lactamase from Staphylococci?

A

Cloxacillin and flucloxacillin

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44
Q

Which penicillin has better oral absorption?

A

Flucloxacillin is better absorbed orally than cloxacillin.

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45
Q

What type of bacteria are cloxacillin and flucloxacillin effective against?

A

Both are only effective against Gram-positive bacteria.

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46
Q

What are cloxacillin and flucloxacillin widely used for?

A

They are widely used for skin and soft tissue infections.

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47
Q

What are B-lactamase inhibitors?

A

B-lactamase inhibitors are compounds that bind irreversibly to B-lactamases, enzymes produced by bacteria that confer resistance to B-lactam antibiotics.

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47
Q

What are irreversible inhibitors of β-lactamases?

A

Substances that bind permanently to β-lactamases, preventing the enzyme from breaking down β-lactam antibiotics.

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48
Q

How do irreversible inhibitors of β-lactamases work?

A

They bind to the active site of β-lactamase, inhibiting its action and thus protecting the β-lactam antibiotic from degradation.

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49
Q

What is the benefit of combining β-lactam antibiotics with β-lactamase inhibitors?

A

This combination can reverse bacterial resistance, making the antibiotics effective against bacteria that produce β-lactamase enzymes

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49
Q

Can you name two examples of irreversible β-lactamase inhibitors?

A

Clavulanate and Tazobactam.

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50
Q

Give an example of a combination of a β-lactam antibiotic and a β-lactamase inhibitor

A

Amoxicillin-clavulanate.

Piperacillin-tazobactam (H)

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51
Q

What spectrum of activity does Amoxicillin-clavulanate have?

A

It has a broad spectrum of activity.

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52
Q

What types of infections can Amoxicillin-clavulanate treat?

A

It can treat community-acquired infections caused by Gram-positive, Gram-negative, and anaerobic bacteria.

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53
Q

Must know penicillin drugs

A

Penicillin (IV, oral and depot IM)

Cloxacillin/flucloxacillin

Amoxicillin

Amoxicillin-clavulanate

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54
Q
A
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55
Q
A
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55
Q

How were cephalosporins developed?

A

Cephalosporins were developed in successive waves or generations.

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56
Q

What is the spectrum of 1st generation cephalosporins?

A

The spectrum is largely limited to Streptococci and Staphylococci.

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57
Q

Can you name examples of 1st generation cephalosporins and their routes of administration?

A

Cefazolin (IV) and Cephalexin (PO).

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58
Q

What additional bacteria does the 2nd generation cephalosporin spectrum cover compared to the 1st generation?

A

It covers Haemophilus and community-acquired Gram negatives, in addition to Streptococci and Staphylococci.

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59
Q

Can you name examples of 2nd generation cephalosporins and their routes of administration?

A

Cefuroxime (PO & IV).

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60
Q

What additional bacteria and conditions does the 3rd generation cephalosporin spectrum cover compared to the 2nd generation?

A

It covers typhoid, spirochetes, and has good CSF penetration.

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61
Q

Can you name examples of 3rd generation cephalosporins?

A

Cefotaxime, ceftriaxone, and ceftazidime.

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62
Q

What is ceftazidime specifically effective against, and what is it poor for?

A

It is effective against Pseudomonas and poor for Streptococci, commonly used for hospital-acquired infections

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63
Q

What is the spectrum of 4th generation cephalosporins?

A

Similar to ceftazidime and cefotaxime.

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64
Q

Can you name an example of a 4th generation cephalosporin?

A

Cefepime.

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65
Q

What type of infections is cefepime commonly used for?

A

Hospital-acquired infections.

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66
Q

What is Cefazolin used for at induction?

A

It is used for surgical prophylaxis.

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67
Q

What type of serious infections is Cefazolin also used for?

A

Serious staphylococcal infections.

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68
Q

What are the routes of administration for Ceftriaxone?

A

Intravenous injection (IVI) and intramuscular injection (IMI).

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69
Q

How is Ceftriaxone primarily excreted from the body?

A

It is excreted mainly through the bile

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70
Q

What is the spectrum of Ceftriaxone?

A

It covers community-acquired Gram-positive (including most S. pneumoniae, but not ideal for S. aureus) and Gram-negative bacteria.

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71
Q

What is Ceftriaxone’s significance in the treatment of bacterial meningitis?

A

It has good CSF penetration and is the empiric drug of choice for bacterial meningitis.

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72
Q

For which serious infections is Ceftriaxone the drug of choice?

A

Typhoid and gonorrhea (IMI).

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73
Q

Why is Ceftriaxone considered a useful broad-spectrum agent?

A

It is effective for serious community-acquired infections.

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74
Q

What is the spectrum of activity for carbapenems?

A

Extremely broad spectrum covering most hospital-acquired Gram-positive, Gram-negative, and anaerobes.

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75
Q

What type of infections are carbapenems used for?

A

Only for nosocomial (hospital-acquired) infections.

76
Q

Are carbapenems effective against cloxacillin-resistant Staphylococci?

A

No, they are not active against cloxacillin-resistant Staphylococci.

77
Q

What is a significant drawback of using carbapenems?

A

They are very expensive

78
Q

With which class of antibiotics is the incidence of hypersensitivity reactions highest?

A

Penicillins, with an incidence of 1 to 6%.

79
Q

What is the most common hypersensitivity reaction to β-lactam antibiotics?

A

Maculopapular rash.

80
Q

When does a maculopapular rash typically appear after β-lactam administration?

A

After 72 hours.

81
Q

Which β-lactam antibiotic is usually associated with maculopapular rash?

A

Amoxicillin

82
Q

How soon can anaphylaxis occur after β-lactam administration?

A

Within 1 hour.

83
Q

What is the incidence rate of anaphylaxis due to β-lactam antibiotics?

A

Rare, 0.01 to 0.05%.

84
Q

Through which route is anaphylaxis most commonly triggered?

A

Mostly through parenteral (injection) administration.

85
Q

What immunoglobulin is associated with anaphylaxis?

A

IgE

86
Q

When can angioedema, urticaria, or bronchospasm occur after β-lactam administration?

A

Within 72 hours.

87
Q

What immunoglobulin is associated with angioedema, urticaria, or bronchospasm?

A

IgE.

88
Q

What is the incidence of cross reactions between cephalosporins and penicillins?

A

Less than 5%.

89
Q

What is the incidence of cross reactions between 3rd generation cephalosporins and penicillins?

A

Less than 1%.

90
Q

Is it safe to use cephalosporins in patients with a penicillin allergy?

A

It is OK to use if the hypersensitivity reaction was not IgE mediated.

91
Q

What should be done if the penicillin allergy was IgE-mediated?

A

Avoid the entire class of β-lactam antibiotics.

92
Q

What can be done in exceptional cases for patients with IgE-mediated reactions?

A

Desensitization may be considered.

93
Q

How common are cross reactions between carbapenems and other β-lactam antibiotics?

A

Cross reactions with carbapenems are rare.

94
Q

What type of infections are glycopeptides primarily used for?

A

Hospital-acquired infections.

95
Q

How do glycopeptides work?

A

They are active against cell walls

96
Q

What type of killing do glycopeptides exhibit?

A

Time-dependent killing.

97
Q

Are glycopeptides absorbed orally?

A

No, they are not absorbed orally.

98
Q

What is the spectrum of activity for glycopeptides?

A

They cover only Gram-positive bacteria.

99
Q

Which type of resistant bacteria are glycopeptides especially effective against?

A

Cloxacillin-resistant Staphylococci.

100
Q

Can you name an example of a glycopeptide?

A

Vancomycin.

101
Q

What is essential when administering Vancomycin?

A

A slow IV infusion to prevent red man syndrome.

102
Q

What are the potential toxicities of glycopeptides?

A

They are mildly nephrotoxic and ototoxic.

103
Q

When should the concentration of glycopeptides be measured?

A

In cases of renal failure and for selected organisms.

104
Q

What type of bacteria are aminoglycosides particularly potent against?

A

Aerobic Gram-negative bacilli.

105
Q

How do aminoglycosides work?

A

They are bactericidal inhibitors of protein synthesis.

106
Q

What type of killing do aminoglycosides exhibit?

A

Concentration-dependent killing.

107
Q

Do aminoglycosides require synergy with other antibiotics?

A

Synergy with β-lactams is seldom necessary.

108
Q

What is a characteristic of aminoglycosides in terms of tissue penetration?

A

They are polar compounds with poor tissue penetration.

109
Q

How are aminoglycosides typically administered?

A

They must be given parenterally.

110
Q

Where are aminoglycosides concentrated in the body?

A

They are concentrated in the urine.

111
Q

What is the recommended dosing schedule for aminoglycosides?

A

Single daily dosing is best, due to the post-antibiotic effect.

112
Q

When should aminoglycoside concentrations be measured?

A

If treatment is longer than 3 days or in cases of renal failure.

113
Q

Examples of aminoglycosides

A
  • Gentamicin
  • Amikacin
114
Q

What types of infections is Gentamicin used for?

A

Serious community infections, including pyelonephritis

115
Q

When is Gentamicin combined with β-lactams?

A

For polymicrobial infections or for synergy, such as in enterococci and streptococcal endocarditis.

116
Q

What type of infections is Amikacin used for?

A

Hospital-acquired infections.

117
Q

What is aminoglycoside toxicity related to?

A

Prolonged elevated trough concentrations.

118
Q

What are the two types of ototoxicity caused by aminoglycosides?

A

Cochlear ototoxicity (high tone deafness initially) and vestibular ototoxicity.

119
Q

Is aminoglycoside-induced ototoxicity reversible?

A

It is irreversible in many cases.

120
Q

What type of nephrotoxicity is caused by aminoglycosides?

A

Tubular toxin.

121
Q

Is aminoglycoside-induced nephrotoxicity reversible?

A

Yes, it is reversible.

122
Q

In which patient populations should aminoglycosides be avoided?

A

In the elderly and those with chronic kidney disease (CKD).

123
Q

What enzymes do quinolones target?

A

DNA gyrase and topoisomerase IV.

124
Q

What type of killing do quinolones exhibit?

A

Concentration-dependent killing.

125
Q

How well are older (first generation) quinolones absorbed?

A

They are poorly absorbed

126
Q

What is the spectrum of first generation quinolones?

A

Limited to Gram-negative aerobes.

127
Q

What is an example of a first generation quinolone?

A

Nalidixic acid.

128
Q

How readily does resistance arise with first generation quinolones?

A

Resistance arises readily.

129
Q

How well are second generation fluoroquinolones absorbed?

A

They are well absorbed

130
Q

What is the spectrum of second generation fluoroquinolones?

A

Includes Gram-negative aerobes (including Pseudomonas), but poor for Gram-positive bacteria.

131
Q

How well are third generation fluoroquinolones absorbed?

A

They are well absorbed.

132
Q

What is the spectrum of third generation fluoroquinolones?

A

Includes both Gram-positive bacteria (especially Streptococci) and Gram-negative bacteria (except Pseudomonas).

133
Q

What are the common toxicities associated with quinolones?

A

Rashes, CNS effects (headache, dizziness, excitation, seizures), and tendonitis.

134
Q

Why is the use of quinolones in children limited?

A

Due to animal toxicity, but they are OK for restricted indications.

135
Q

How does resistance to quinolones generally develop?

A

By mutations in the target genes.

136
Q

Due to recent toxicity concerns, for what type of infections are quinolones recommended?

A

Only for serious infections.

137
Q

What is the drug of choice for bacterial dysentery, pyelonephritis, and prostatitis?

A

Ciprofloxacin (a second generation fluoroquinolone).

138
Q

When can ciprofloxacin be used as an alternative to aminoglycosides?

A

For serious infections where aminoglycosides are typically used.

139
Q

What is a notable use of ciprofloxacin for systemic infections?

A

Typhoid, although resistance is increasing.

140
Q

What is moxifloxacin (a third generation fluoroquinolone) used for in the context of tuberculosis?

A

It is used for multi-drug resistant tuberculosis (MDR TB).

141
Q

When can moxifloxacin be used as an alternative for respiratory tract infections?

A

Only if there is a severe beta-lactam allergy, and it covers atypical pneumonia agents as well as conventional bacterial causes of community-acquired pneumonia.

142
Q

What is the mechanism of action of macrolides?

A

They inhibit protein synthesis by binding to the 50S ribosome subunit.

143
Q

Are macrolides bacteriostatic or bactericidal?

A

Bacteriostatic.

144
Q

What type of bacteria are macrolides primarily active against?

A

Gram-positive bacteria.

145
Q

What is a concern with the use of macrolides against S. pneumoniae?

A

There is increasing resistance to macrolides in S. pneumoniae.

146
Q

How is the bioavailability of erythromycin?

A

Erythromycin has fair bioavailability.

147
Q

Example of a macrolides

A

Erythromycin
clarithromycin
azithromycin

148
Q

How do newer macrolides like clarithromycin and azithromycin compare to erythromycin in terms of absorption and half-life?

A

Newer agents are better absorbed and have a longer half-life.

149
Q

What are common gastrointestinal toxicities associated with macrolides?

A

Nausea, vomiting, and diarrhea.

150
Q

Do macrolides inhibit CYP450 metabolism?

A

Yes, macrolides inhibit CYP450 metabolism, except azithromycin.

151
Q

For which type of infections can macrolides be used as an alternative to penicillin in allergic patients?

A

For mild streptococcal and staphylococcal infections.

152
Q

What atypical pneumonia agents are macrolides active against?

A

Legionella, Mycoplasma, and Chlamydophila.

153
Q

Which macrolides are drugs of choice for H. pylori infection?

A

Clarithromycin and azithromycin.

154
Q

Which macrolide is used as a single-dose treatment for Chlamydia urethritis and cervicitis?

A

Azithromycin.

155
Q

Are macrolides used in the treatment of pertussis?

A

Yes, macrolides are drugs of choice for pertussis.

156
Q

Can macrolides be used to treat chancroid?

A

Yes, macrolides are used in the treatment of chancroid.

157
Q

Which macrolides are used to treat M. avium complex infections in AIDS patients?

A

Clarithromycin and azithromycin.

158
Q

What is the mechanism of action of tetracyclines?

A

They inhibit protein synthesis by binding to the 30S ribosome subunit.

159
Q

Are tetracyclines bacteriostatic or bactericidal?

A

Bacteriostatic

160
Q

How can bacteria develop resistance to tetracyclines?

A

Through efflux pumps or enzymatic breakdown.

161
Q

How does the absorption of tetracyclines vary, and which tetracycline has excellent absorption?

A

Absorption varies among tetracyclines, and doxycycline has excellent absorption.

162
Q

What impairs the absorption of tetracyclines?

A

Divalent cations impair the absorption of tetracyclines.

163
Q

Do tetracyclines have good intracellular penetration?

A

Yes, tetracyclines have good intracellular penetration.

164
Q

What gastrointestinal toxicity is associated with tetracyclines?

A

Nausea and vomiting.

165
Q

What skin-related toxicity is associated with tetracyclines?

A

Photosensitivity.

166
Q

Why should tetracyclines be avoided in children under 8 years old and during pregnancy?

A

They can cause teeth discolouration.

167
Q

Which bacterial infection is treated with tetracyclines as the drug of choice?

A

Rickettsia

168
Q

Is tetracycline the drug of choice for brucellosis?

A

Yes, tetracycline is used for brucellosis

169
Q

For what dermatological condition are low doses of tetracycline used?

A

Acne

170
Q

Can tetracycline be used for prophylaxis of falciparum malaria?

A

Yes, it is used for prophylaxis of falciparum malaria.

171
Q

Which sexually transmitted infection (STI) can be treated with tetracyclines, although now often superseded by azithromycin?

A

Chlamydia, including urethritis and pelvic inflammatory disease (PID).

172
Q

Why is the usefulness of tetracyclines limited as a single agent for respiratory infections?

A

Because Streptococcus pneumoniae is often resistant.

173
Q

How does cotrimoxazole work?

A

It blocks successive steps in the bacterial folate pathway, preventing nucleic acid synthesis

173
Q

What are the two components of cotrimoxazole?

A

Sulfamethoxazole (a sulphonamide) and trimethoprim.

174
Q

How is cotrimoxazole absorbed?

A

It is well absorbed orally.

175
Q

What is the main side effect of cotrimoxazole?

A

Sulphonamide hypersensitivity, which can cause skin rashes.

176
Q

What severe skin reactions can cotrimoxazole cause?

A

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis.

177
Q

Why is cotrimoxazole of minimal value outside of HIV?

A

Due to its toxicity and high prevalence of resistance in community-acquired Gram negatives and Streptococcus pneumoniae.

178
Q

In HIV infection, what is cotrimoxazole the drug of choice for treating?

A
  • Pneumocystis jirovecii pneumonia
  • Toxoplasmosis
  • Cystoisospora belli diarrhoea
179
Q

What role does cotrimoxazole play in primary prophylaxis for HIV patients?

A

It prevents Pneumocystis jirovecii pneumonia, toxoplasmosis, and Cystoisospora belli diarrhoea, and reduces bacterial infections.

180
Q

Why do HIV+ patients have a much higher frequency of rash with cotrimoxazole?

A

Especially with higher doses, HIV+ patients are more prone to rashes.

181
Q

Is rechallenge or dose reduction often successful for cotrimoxazole-induced rashes in HIV+ patients?

A

Yes, rechallenge or dose reduction is often successful unless the reaction was severe

182
Q

How does metronidazole exert its toxic effect on bacteria?

A

It is toxic to DNA, forming a highly reactive nitro radical with anaerobic metabolism Fe: S proteins.

183
Q

How is metronidazole absorbed when taken orally?

A

It has good oral absorption

184
Q

Besides oral, in what other forms is metronidazole available?

A

It is also available as PR (rectal) and IVI (intravenous).

185
Q

How well is metronidazole tolerated in short courses?

A

It is well tolerated in short courses.

186
Q

What common side effect does metronidazole cause that affects taste?

A

It causes a metallic taste.

187
Q

What should be avoided when taking metronidazole due to a disulfiram-like effect?

A

Alcohol should be avoided.

188
Q

What are the potential long-term toxic effects of metronidazole?

A

Neurotoxicity and neutropenia.

189
Q

What types of anaerobic organisms is metronidazole effective against?

A

Cocci, Gram-negative bacilli, and Gram-positive spore-forming bacilli.

190
Q

Which protozoan infections, lacking mitochondria, can be treated with metronidazole?

A

Entamoeba histolytica, Trichomonas vaginalis, and Giardia lamblia.

Therapeutics (15 decks)

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