Module 9 14 Aminoglycosides Tetracycline Nitrofurantoin Fosfomycin

Question 1

Question

Answer 1

Answer

Question 2

What is the primary spectrum of activity for aminoglycosides?

Answer 2

Aminoglycosides are narrow-spectrum antibiotics primarily used against aerobic gram-negative bacilli.

Question 3

What is the mechanism of action of aminoglycosides, and what does it result in?

Answer 3

Aminoglycosides disrupt protein synthesis, leading to rapid bacterial death.

Question 4

What are the potential toxic effects associated with aminoglycoside use?

Answer 4

Aminoglycosides have the potential to cause serious inner ear and kidney damage.

Question 5

Why are the indications for aminoglycosides limited?

Answer 5

The toxicities associated with aminoglycosides restrict their clinical use.

Question 6

Why are aminoglycosides not absorbed from the gastrointestinal (GI) tract?

Answer 6

Aminoglycosides carry multiple positive charges, preventing their absorption from the GI tract.

Question 7

How are aminoglycosides typically administered to treat systemic infections?

Answer 7

Aminoglycosides must be administered parenterally (via injection) to effectively treat systemic infections.

Question 8

How many aminoglycosides are approved for clinical use in the United States, and which ones are commonly employed?

Answer 8

In the United States, seven aminoglycosides are approved for clinical use, with gentamicin, tobramycin, and amikacin being the most commonly employed agents.

Question 9

What is the structural composition of aminoglycosides?

Answer 9

Aminoglycosides are composed of two or more amino sugars connected by a glycoside linkage.

Question 10

What is the electrochemical property of aminoglycosides at physiologic pH?

Answer 10

Aminoglycosides are highly polar polycations, carrying several positive charges.

Question 11

Why do aminoglycosides have limited ability to cross biological membranes?

Answer 11

Aminoglycosides cannot readily cross membranes due to their positive charge.

Question 12

How are aminoglycosides affected by their positive charge in terms of absorption?

Answer 12

Due to their positive charge, aminoglycosides are not absorbed from the gastrointestinal (GI) tract.

Question 13

Can aminoglycosides enter the cerebrospinal fluid (CSF)?

Answer 13

Aminoglycosides do not enter the cerebrospinal fluid (CSF).

Question 14

What is the fate of aminoglycosides in the body regarding excretion?

Answer 14

Aminoglycosides are rapidly excreted by the kidneys.

Question 15

What is the target of aminoglycosides in bacterial cells, and how do they disrupt protein synthesis?

Answer 15

Aminoglycosides target the 30S ribosomal subunit in bacterial cells. They disrupt protein synthesis by binding to this subunit.

Question 16

What are the three effects of aminoglycoside binding to the ribosomal subunit on protein synthesis?

Answer 16

Aminoglycoside binding results in (1) inhibition of protein synthesis, (2) premature termination of protein synthesis, and (3) production of abnormal proteins due to misreading of the genetic code.

Question 17

Are aminoglycosides bactericidal or bacteriostatic antibiotics?

Answer 17

Aminoglycosides are bactericidal antibiotics, meaning they kill bacterial cells.

Question 18

How does the bactericidal activity of aminoglycosides relate to their concentration?

Answer 18

Bactericidal activity of aminoglycosides is concentration-dependent, meaning higher concentrations result in more rapid clearance of the infection.

Question 19

What is the postantibiotic effect, and how does it apply to aminoglycosides?

Answer 19

The postantibiotic effect is a phenomenon where bactericidal activity persists for several hours after serum levels of aminoglycosides drop below the minimal bactericidal concentration.

Question 20

What is the proposed mechanism of bacterial death by aminoglycosides, and how does it differ from other antibiotics?

Answer 20

Bacterial death by aminoglycosides involves the production of abnormal proteins, which are inserted into the bacterial cell membrane, causing it to leak. This is distinct from other antibiotics like tetracyclines and chloramphenicol, where complete blockade of protein synthesis is usually bacteriostatic, not bactericidal.

Question 21

What is the primary cause of bacterial resistance to aminoglycosides?

Answer 21

Bacterial resistance to aminoglycosides is mainly caused by the production of enzymes that can inactivate these antibiotics.

Question 22

How do gram-negative bacteria typically acquire the genetic information needed to produce aminoglycoside-inactivating enzymes?

Answer 22

Gram-negative bacteria often acquire the genetic information through the transfer of R factors.

Question 23

How many different aminoglycoside-inactivating enzymes have been identified, and what makes patterns of resistance complex?

Answer 23

Over 20 different aminoglycoside-inactivating enzymes have been identified. Patterns of resistance are complex because each aminoglycoside can be modified by more than one of these enzymes, and each enzyme can act on more than one aminoglycoside.

Question 24

Which aminoglycoside is least susceptible to inactivation by bacterial enzymes, and what is the result of this resistance pattern?

Answer 24

Amikacin is the least susceptible aminoglycoside to inactivation by bacterial enzymes. As a result, resistance to amikacin is uncommon.

Question 25

What is the recommended approach to using amikacin to minimize the emergence of resistant bacteria?

Answer 25

To prevent the emergence of resistant bacteria, amikacin should be reserved for infections that do not respond to other aminoglycosides.

Question 26

Which type of bacteria are primarily susceptible to the bactericidal effects of aminoglycosides?

Answer 26

Bactericidal effects of aminoglycosides are most effective against aerobic gram-negative bacilli.

Question 27

Can you name some of the sensitive organisms to aminoglycosides?

Answer 27

Sensitive organisms include Escherichia coli, Klebsiella pneumoniae, Serratia marcescens, Proteus mirabilis, and Pseudomonas aeruginosa.

Question 28

Are aminoglycosides generally effective against gram-positive bacteria?

Answer 28

Aminoglycosides are generally inactive against most gram-positive bacteria.

Question 29

Why can’t aminoglycosides kill anaerobic bacteria, and what is the oxygen-dependent process involved?

Answer 29

Aminoglycosides cannot kill anaerobic bacteria because they require oxygen-dependent transport across the bacterial cell membrane.

Question 30

Why are anaerobic organisms resistant to aminoglycosides, and how does this relate to their oxygen requirements?

Answer 30

Anaerobic organisms, which live in the absence of oxygen, cannot take up aminoglycosides, making them resistant to these antibiotics.

Question 31

Under what conditions are aminoglycosides inactive against facultative bacteria, and why?

Answer 31

Aminoglycosides are inactive against facultative bacteria when these organisms are living under anaerobic conditions because the antibiotics’ transport process is oxygen-dependent.

Question 32

What is the principal use of parenteral aminoglycosides in treating infections?

Answer 32

Parenteral aminoglycosides are primarily used to treat serious infections caused by aerobic gram-negative bacilli.

Question 33

Which specific organisms are the primary targets of aminoglycosides in the treatment of infections?

Answer 33

The primary target organisms for aminoglycosides are Pseudomonas aeruginosa and the Enterobacteriaceae, which includes organisms like Escherichia coli, Klebsiella, Serratia species, and Proteus mirabilis.

Question 34

In what circumstances is gentamicin, an aminoglycoside, used in combination with other antibiotics, and which gram-positive cocci are targeted?

Answer 34

Gentamicin is used in combination with either vancomycin or a beta-lactam antibiotic to treat serious infections caused by certain gram-positive cocci, specifically Enterococcus species, some streptococci, and Staphylococcus aureus.

Question 35

What are the three most commonly used aminoglycosides for parenteral therapy?

Answer 35

The most commonly used aminoglycosides for parenteral therapy are gentamicin, tobramycin, and amikacin.

Question 36

What factors determine the choice of aminoglycoside among gentamicin, tobramycin, and amikacin for therapy?

Answer 36

The choice among these aminoglycosides depends mainly on patterns of resistance in a specific community or hospital.

Question 37

In settings where resistance to aminoglycosides is uncommon, which aminoglycoside is often preferred, and why?

Answer 37

In settings with low resistance, either gentamicin or tobramycin is usually preferred. Gentamicin may be selected on the basis of being less expensive.

Question 38

What is the aminoglycoside of choice when organisms are resistant to both gentamicin and tobramycin?

Answer 38

When organisms are resistant to both gentamicin and tobramycin, they are usually sensitive to amikacin.

Question 39

In settings where resistance to gentamicin and tobramycin is common, which aminoglycoside may be preferred for initial therapy?

Answer 39

In settings with high resistance to gentamicin and tobramycin, amikacin may be preferred for initial therapy.

Question 40

How are aminoglycosides used topically in the treatment of infections?

Answer 40

Aminoglycosides are used topically to treat infections.

Question 41

Which aminoglycosides are used to treat eye infections?

Answer 41

Gentamicin and tobramycin are used to treat eye infections.

Question 42

In addition to eye infections, which type of infections can neomycin be used to treat, and in which chapters are these uses discussed?

Answer 42

Neomycin can be used to treat infections of the ear and eye, as discussed in Chapters 87 and 89.

Question 43

Which systemic aminoglycosides are commonly used for treatment, and what are their names?

Answer 43

Common systemic aminoglycosides include amikacin, gentamicin, and tobramycin.

Question 44

How can the total daily dose of systemic aminoglycosides be administered?

Answer 44

The total daily dose may be given as one large dose each day or as two to three divided doses at equally spaced intervals.

Question 45

Why should serum drug levels be measured when using systemic aminoglycosides?

Answer 45

Serum drug levels should be measured due to interpatient variability, and dosage should be adjusted based on these measurements.

Question 46

What are the typical peak therapeutic levels for amikacin, gentamicin, and tobramycin when given in divided doses?

Answer 46

The peak therapeutic levels are typically 2-3 µg/mL for amikacin, gentamicin, and tobramycin when given in divided doses.

Question 47

What are the recommended trough levels for amikacin, gentamicin, and tobramycin?

Answer 47

Recommended trough levels are less than 5-10 µg/mL for amikacin and less than 1-2 µg/mL for gentamicin and tobramycin.

Question 48

Are the dosages different when gentamicin is used in combination with other antibiotics, and in which circumstances?

Answer 48

Yes, the dosages may differ when gentamicin is combined with vancomycin or a beta-lactam antibiotic to treat certain gram-positive infections.

Question 49

Do peak values for gentamicin remain the same in all cases, and when may higher trough levels be acceptable?

Answer 49

Peak values for gentamicin may vary depending on the type of infection. Higher trough levels may be acceptable for severe infections.

Question 50

What is the reason behind the limited oral effectiveness of aminoglycosides for systemic infections?

Answer 50

Aminoglycosides are polycations, which hinders their ability to cross membranes. Only about 1% of an oral dose is absorbed.

Question 51

How are aminoglycosides administered for the treatment of systemic infections?

Answer 51

Aminoglycosides must be given parenterally, either intramuscularly (IM) or intravenously (IV), to effectively treat systemic infections.

Question 52

Is there significant absorption of aminoglycosides when applied to intact skin?

Answer 52

No, absorption of aminoglycosides after application to intact skin is minimal.

Question 53

In what situation might aminoglycosides be absorbed in amounts sufficient to produce systemic toxicity?

Answer 53

Aminoglycosides may be absorbed in amounts sufficient to produce systemic toxicity when used for wound irrigation.

Question 54

What is the primary distribution site of aminoglycosides in the body?

Answer 54

Aminoglycosides are primarily distributed to extracellular fluid in the body.

Question 55

Are aminoglycosides capable of entering the cerebrospinal fluid in sufficient quantities to treat meningitis in adults?

Answer 55

No, aminoglycosides are generally not capable of entering the cerebrospinal fluid in sufficient quantities to treat meningitis in adults.

Question 56

Can aminoglycosides enter the cerebrospinal fluid in sufficient quantities to treat meningitis in adults?

Answer 56

No, aminoglycosides do not enter the cerebrospinal fluid in sufficient quantities to treat meningitis in adults.

Question 57

Why do aminoglycosides achieve much higher levels in the kidneys compared to serum levels, and what can result from this?

Answer 57

Aminoglycosides bind tightly to renal tissue, leading to levels in the kidneys that can be up to 50 times higher than in the serum. This can result in nephrotoxicity.

Question 58

How can aminoglycosides cause ototoxicity, and where in the inner ear do they penetrate?

Answer 58

Aminoglycosides can penetrate the perilymph and endolymph of the inner ears, leading to ototoxicity.

Question 59

Can aminoglycosides cross the placenta, and what potential risk does this pose?

Answer 59

Yes, aminoglycosides can cross the placenta, posing a potential risk of toxicity to the fetus.

Question 60

Are aminoglycosides approved for use in treating bacterial infections in infants, and how is dosing determined for infants?

Answer 60

Aminoglycosides are approved for use in infants younger than 8 days. Dosing is based on the infant’s weight and length of gestation.

Question 61

Are aminoglycosides generally considered safe for treating bacterial infections in children and adolescents?

Answer 61

Yes, aminoglycosides are considered safe for use against bacterial infections in children and adolescents.

Question 62

What is the potential concern when using aminoglycosides during pregnancy?

Answer 62

There is evidence that the use of aminoglycosides during pregnancy can harm the fetus.

Question 63

Is gentamicin safe to use during lactation, and what is the available information regarding its use in breastfeeding women?

Answer 63

Gentamicin is likely safe to use during lactation, but there is limited information available regarding its use in breastfeeding women.

Question 64

What caution should be exercised when using aminoglycosides in older adults, and why?

Answer 64

Caution should be exercised in older adults due to the potential for decreased renal function, which can affect drug clearance and increase the risk of toxicity.

Question 65

How are aminoglycosides primarily eliminated from the body?

Answer 65

Aminoglycosides are primarily eliminated by the kidneys.

Question 66

Are aminoglycosides subject to metabolism in the body?

Answer 66

No, aminoglycosides are not metabolized in the body.

Question 67

What is the typical range of half-lives for aminoglycosides in patients with normal renal function?

Answer 67

In patients with normal renal function, the half-lives of aminoglycosides range from 2 to 3 hours.

Question 68

How does renal impairment affect the elimination of aminoglycosides and their half-lives?

Answer 68

Renal impairment compromises the elimination of aminoglycosides, leading to significantly longer half-lives in affected patients.

Question 69

Why is it necessary to adjust the dosage size or increase the dosing interval in patients with kidney disease when using aminoglycosides?

Answer 69

To prevent serious toxicity, it is necessary to adjust the dosage size or increase the dosing interval in patients with kidney disease when using aminoglycosides.

Question 70

Why do different patients receiving the same aminoglycoside dosage achieve widely different serum drug levels?

Answer 70

Interpatient variation in serum levels is influenced by factors such as age, percent body fat, and pathophysiological conditions, leading to significant differences in drug levels.

Question 71

What factors contribute to the interpatient variation in aminoglycoside serum levels?

Answer 71

Interpatient variation is influenced by factors such as age, percent body fat, and pathophysiological conditions like renal impairment, fever, edema, and dehydration.

Question 72

Why is individualized dosing of aminoglycosides necessary for patients?

Answer 72

Individualized dosing of aminoglycosides is necessary to account for the significant variability in serum drug levels among patients.

Question 73

Can you provide an example of the dramatic variation in aminoglycoside dosages observed in a clinical study?

Answer 73

In one clinical study, doses to achieve equivalent serum drug levels ranged from as little as 0.5 mg/kg in one patient to as high as 25.8 mg/kg in another, representing a difference of more than 50-fold.

Question 74

What are the primary sites of serious toxicity caused by aminoglycosides?

Answer 74

Aminoglycosides can produce significant toxicity, primarily affecting the inner ears and kidneys.

Question 75

Why are the inner ears and kidneys vulnerable to aminoglycoside toxicity?

Answer 75

The inner ears and kidneys are particularly vulnerable to aminoglycoside toxicity because these drugs become highly concentrated within the cells of these structures.

Question 76

How can aminoglycosides affect the inner ears, and what are the consequences?

Answer 76

Aminoglycosides can accumulate within the inner ears, causing damage to sensory hair cells. This can lead to both hearing impairment, due to cochlear damage, and disruption of balance, resulting from damage to the vestibular apparatus.

Question 77

What is the primary factor contributing to the risk of aminoglycoside-induced ototoxicity?

Answer 77

The risk for ototoxicity is primarily related to elevated trough levels of aminoglycosides rather than excessive peak levels.

Question 78

Why does prolonged exposure to aminoglycosides contribute to inner ear cellular injury?

Answer 78

Prolonged exposure occurs when trough levels of aminoglycosides remain persistently elevated, preventing the drug from diffusing out of inner ear cells. This extended exposure leads to cellular injury in the inner ear.

Question 79

What are some risk factors that increase the likelihood of aminoglycoside-induced ototoxicity?

Answer 79

Risk factors for ototoxicity include renal impairment (causing drug accumulation), concurrent use of loop diuretics, and administering aminoglycosides in excessive doses or for more than 10 days.

Question 80

What is the first sign of impending cochlear damage in patients on aminoglycoside therapy?

Answer 80

High-pitched tinnitus is often the initial sign of cochlear damage associated with aminoglycosides.

Question 81

Is ototoxicity caused by aminoglycosides reversible?

Answer 81

Ototoxicity caused by aminoglycosides is largely irreversible.

Question 82

What action should be taken to prevent permanent injury if signs of cochlear damage, such as tinnitus or persistent headache, appear during aminoglycoside therapy?

Answer 82

Aminoglycosides should be discontinued at the first signs of damage to prevent permanent injury.

Question 83

How does hearing loss typically progress in patients with aminoglycoside-induced cochlear damage?

Answer 83

Initial high-frequency hearing loss is followed by low-frequency hearing loss with continued aminoglycoside use.

Question 84

Why is audiometric testing essential for patients on aminoglycoside therapy?

Answer 84

Audiometric testing is necessary to detect the subtle initial decline in high-frequency hearing associated with aminoglycosides.

Question 85

What is the first sign of impending vestibular damage in patients on aminoglycoside therapy?

Answer 85

A persistent headache, lasting for a day or two, is typically the initial sign of impending vestibular damage.

Question 86

What are the subsequent symptoms of vestibular damage caused by aminoglycosides?

Answer 86

Nausea, unsteadiness, dizziness, and vertigo are common symptoms of vestibular damage due to aminoglycosides.

Question 87

What should patients on aminoglycoside therapy be instructed to do regarding the signs and symptoms of cochlear and vestibular damage?

Answer 87

Patients should be educated about these signs and symptoms and instructed to report them promptly.

Question 88

What is the consequence of aminoglycoside-induced ototoxicity?

Answer 88

Aminoglycosides can lead to irreversible ototoxicity, resulting in permanent damage to hearing and balance.

Question 89

What are some neurotoxic symptoms associated with aminoglycoside use?

Answer 89

Neurotoxic symptoms may include numbness, tingling, muscle twitching, and seizures in individuals taking aminoglycosides.

Question 90

When is the risk of neurotoxicity with aminoglycosides most significant?

Answer 90

The risk of neurotoxicity is highest in patients receiving high doses of aminoglycosides or using them for extended durations.

Question 91

How does preexisting renal impairment affect the risk of aminoglycoside-induced neurotoxicity?

Answer 91

Patients with preexisting renal impairment are at an increased risk of experiencing neurotoxicity when using aminoglycosides.

Question 92

What is nephrotoxicity associated with in the context of aminoglycoside use?

Answer 92

Nephrotoxicity refers to kidney damage associated with the use of aminoglycosides.

Question 93

How does the risk of nephrotoxicity change in patients receiving high doses of aminoglycosides?

Answer 93

The risk of nephrotoxicity increases in patients receiving high doses of aminoglycosides.

Question 94

What happens to the risk of nephrotoxicity with prolonged use of aminoglycosides?

Answer 94

Prolonged use of aminoglycosides is associated with an increased risk of nephrotoxicity.

Question 95

Which patient population is at greater risk of aminoglycoside-induced nephrotoxicity?

Answer 95

Patients with preexisting renal impairment are at a greater risk of aminoglycoside-induced nephrotoxicity.

Question 96

How do aminoglycosides affect cells in the proximal renal tubules of the kidneys?

Answer 96

Aminoglycosides can injure cells of the proximal renal tubules.

Question 97

What factors are associated with aminoglycoside-induced nephrotoxicity?

Answer 97

Nephrotoxicity correlates with the total cumulative dose of aminoglycosides and high trough levels.

Question 98

Do high peak levels of aminoglycosides significantly increase nephrotoxicity?

Answer 98

High peak levels of aminoglycosides do not significantly increase nephrotoxicity.

Question 99

How does nephrotoxicity usually manifest when caused by aminoglycosides?

Answer 99

Nephrotoxicity caused by aminoglycosides usually presents as acute tubular necrosis.

Question 100

What are some symptoms of aminoglycoside-induced nephrotoxicity?

Answer 100

Symptoms may include proteinuria, urine casts, production of dilute urine, and elevated levels of serum creatinine and BUN.

Question 101

Why is monitoring of serum creatinine and BUN recommended for patients receiving aminoglycosides?

Answer 101

Monitoring helps assess kidney function and detect nephrotoxicity.

Question 102

Who is at higher risk for aminoglycoside-induced nephrotoxicity?

Answer 102

Older adults, patients with preexisting kidney disease, and those taking other nephrotoxic drugs are at higher risk.

Question 103

Is aminoglycoside-induced kidney damage usually reversible?

Answer 103

Yes, aminoglycoside-induced kidney damage is usually reversible because proximal tubule cells in the kidneys can regenerate.

Question 104

What is the most significant consequence of renal damage due to aminoglycosides?

Answer 104

The accumulation of aminoglycosides in the body, which can lead to ototoxicity and further kidney damage.

Question 105

What is the potential neuromuscular effect of aminoglycosides?

Answer 105

Aminoglycosides can inhibit neuromuscular transmission.

Question 106

What can be the consequence of neuromuscular inhibition caused by aminoglycosides?

Answer 106

Neuromuscular blockade can result in flaccid paralysis.

Question 107

Why is neuromuscular blockade due to aminoglycosides particularly concerning?

Answer 107

Neuromuscular blockade due to aminoglycosides can be life-threatening, especially if it affects the muscles responsible for respiration.

Question 108

Where have most reported cases of neuromuscular blockade following aminoglycosides occurred?

Answer 108

Most cases have occurred after intraperitoneal or intrapleural instillation of aminoglycosides.

Question 109

Why are penicillins and aminoglycosides frequently used in combination for bacterial infections?

Answer 109

They weaken the bacterial cell wall, allowing aminoglycosides better access to their site of action, further enhancing bacterial killing.

Question 110

How do penicillins contribute to the effectiveness of this combination therapy?

Answer 110

Penicillins disrupt the bacterial cell wall.

Question 111

What is the result of disrupting the bacterial cell wall in combination therapy with aminoglycosides?

Answer 111

Disruption of the cell wall facilitates the access of aminoglycosides to their site of action, further enhancing bacterial killing.

Question 112

How can cephalosporins and vancomycin enhance bacterial killing in combination with aminoglycosides?

Answer 112

They weaken the bacterial cell wall, allowing aminoglycosides better access to their site of action.

Question 113

What is the primary mechanism by which cephalosporins and vancomycin contribute to this combination therapy?

Answer 113

They weaken the bacterial cell wall, much like penicillins, to enhance bacterial kill.

Question 114

What is the result of weakening the bacterial cell wall in this combination therapy?

Answer 114

It improves the effectiveness of aminoglycosides in killing bacteria.

Question 115

What happens when aminoglycosides and loop diuretics are used together?

Answer 115

The risk of inner ear injury increases significantly.

Question 116

Why is it important to avoid the concurrent use of aminoglycosides and loop diuretics?

Answer 116

To prevent ototoxicity and damage to the inner ears.

Question 117

What are some examples of aminoglycosides that may pose a risk when combined with loop diuretics?

Answer 117

Gentamicin and tobramycin are common examples.

Question 118

What happens when aminoglycosides are used concurrently with other nephrotoxic agents?

Answer 118

The risk of renal damage increases, and additive or potentiative nephrotoxicity may occur.

Question 119

Can you name some nephrotoxic agents that may interact with aminoglycosides?

Answer 119

Examples include amphotericin B, cephalosporins, polymyxins, vancomycin, cyclosporine, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs).

Question 120

What are the two common dosing schedules for systemic aminoglycosides?

Answer 120

They can be administered as a single large daily dose or as divided doses.

Question 121

What was the traditional method of administering systemic aminoglycosides?

Answer 121

Traditionally, they were given in divided doses at equally spaced intervals around the clock (e.g., every 8 hours).

Question 122

Why has once-daily dosing become the preferred schedule for aminoglycosides?

Answer 122

Once-daily dosing is considered both safe and effective and is more convenient and cost-effective.

Question 123

Which patient groups may not be suitable for once-daily dosing of aminoglycosides?

Answer 123

Once-daily dosing is not appropriate for neonates, pregnant individuals, patients undergoing dialysis, and those with ascites.

Question 124

Why is monitoring serum drug levels important for adjusting aminoglycoside dosage?

Answer 124

Monitoring ensures that peak levels are adequate for bacterial kill and that trough levels are low to minimize toxicity.

Question 125

What determines the monitoring approach for aminoglycosides?

Answer 125

The dosing schedule (once-daily dosing or divided doses) determines the monitoring approach.

Question 126

Is it necessary to measure peak levels when using once-daily dosing of aminoglycosides?

Answer 126

No, peak levels are not measured in once-daily dosing because high peak levels are guaranteed with this schedule.

Question 127

When using divided doses for aminoglycosides, what levels need to be monitored?

Answer 127

With divided doses, both peak and trough levels should be monitored.

Question 128

When should blood samples for peak levels of aminoglycosides be taken?

Answer 128

Peak levels should be measured 30 minutes after giving an IM injection or completing an IV infusion.

Question 129

How is sampling for trough levels of aminoglycosides timed for patients receiving divided doses?

Answer 129

Trough samples should be taken just before the next dose for patients on divided doses.

Question 130

When should a single sample for trough levels be drawn for patients receiving once-daily doses of aminoglycosides?

Answer 130

For once-daily dosing, a single sample can be drawn 1 hour before the next dose, aiming for a very low value, preferably close to zero.

Question 131

What are the primary targets of gentamicin in the treatment of serious infections?

Answer 131

Gentamicin is primarily used to treat serious infections caused by aerobic gram-negative bacilli, including Pseudomonas aeruginosa and the Enterobacteriaceae.

Question 132

Why is gentamicin often preferred for treating these infections in hospitals with low resistance?

Answer 132

Gentamicin is chosen in hospitals with low resistance due to its cost-effectiveness compared to tobramycin and amikacin.

Question 133

What is the outcome when gentamicin and tobramycin are both ineffective due to resistance?

Answer 133

In cases of resistance to both gentamicin and tobramycin, amikacin is often an effective alternative.

Question 134

Besides gram-negative bacilli, what other types of infections can gentamicin be used to treat?

Answer 134

Gentamicin can be combined with other antibiotics to treat infections caused by certain gram-positive cocci, such as Enterococcus species, some streptococci, and Staphylococcus aureus.

Question 135

What is the therapeutic use of gentamicin?

Answer 135

Gentamicin is used to treat bacterial infections caused by aerobic gram-negative bacilli, including Pseudomonas aeruginosa and Enterobacteriaceae.

Question 136

What is the usual adult dosage for tobramycin, and what are its common preparations?

Answer 136

Tobramycin is employed at a usual adult dosage of 1–1.7 mg/kg every 8 hours. It is available in injection form (IV/IM) and nebulizer solution (300 mg/5 mL).

Question 137

What is the therapeutic use and dosage of amikacin?

Answer 137

Amikacin is used for bacterial infections caused by gram-negative bacilli. The usual adult dosage is 15 mg/kg per day, divided every 8–12 hours.

Question 138

For what purposes is neomycin used, and in what preparations?

Answer 138

Neomycin is used topically for various purposes, including the treatment of topical infections, prevention in minor cuts, and ocular bacterial infections. It is available as a topical cream and ointment.

Question 139

What is the therapeutic use and dosage of kanamycin, and are there any exceptions?

Answer 139

Kanamycin is used for bacterial infections caused by gram-negative bacilli, with the exception of Serratia and Pseudomonas. The usual adult dosage is 7.5 mg/kg every 12 hours.

Question 140

What is the therapeutic use of streptomycin, and in what contexts is it employed?

Answer 140

Streptomycin is used in combination with other drugs to treat tuberculosis, as well as for tularemia and plague.

Question 141

What is the therapeutic use and dosage of paromycin, and in what form is it available?

Answer 141

Paromycin is used for the treatment of intestinal amebiasis and is available in 250-mg capsules. The usual adult dosage is 25–35 mg/kg per day, divided every 8 hours.

Question 142

What is the therapeutic use and dosage of plazomicin (Zemdri)?

Answer 142

Plazomicin is indicated for complicated urinary tract infections (UTIs) caused by Enterobacteriaceae, and the standard adult dosage is 15 mg/kg every 24 hours.

Question 143

What are the potential toxicities associated with gentamicin?

Answer 143

Gentamicin can be toxic to the kidneys and inner ears.

Question 144

Why should caution be exercised when combining gentamicin with other drugs?

Answer 144

Gentamicin should be combined cautiously with other nephrotoxic or ototoxic drugs to minimize the risk of these toxicities.

Question 145

What should be avoided when administering gentamicin in a parenteral solution?

Answer 145

Gentamicin should not be mixed in the same parenteral solution with penicillins because it can be inactivated by direct chemical interaction.

Question 146

How does tobramycin compare to gentamicin in terms of its uses and interactions?

Answer 146

Tobramycin is similar to gentamicin in its uses and interactions.

Question 147

What is tobramycin’s activity against Pseudomonas aeruginosa?

Answer 147

Tobramycin is more active than gentamicin against Pseudomonas aeruginosa.

Question 148

For which patient population is tobramycin commonly used?

Answer 148

Tobramycin is often used for patients with cystic fibrosis.

Question 149

What potential toxicities are associated with tobramycin?

Answer 149

Tobramycin, like other aminoglycosides, can cause inner ear and kidney damage.

Question 150

How can the risk of tobramycin’s toxicities be minimized?

Answer 150

It’s advisable to avoid concurrent therapy with other ototoxic or nephrotoxic drugs when using tobramycin.

Question 151

What adverse effect can tobramycin cause in some patients?

Answer 151

Tobramycin may lead to Clostridium difficile–associated diarrhea.

Question 152

What are the two outstanding features of amikacin among aminoglycosides?

Answer 152

Amikacin is active against a broad spectrum of gram-negative bacilli and is less vulnerable to inactivation by bacterial enzymes.

Question 153

How does amikacin’s bacterial resistance incidence compare to that of gentamicin and tobramycin?

Answer 153

Amikacin has a lower incidence of bacterial resistance compared to gentamicin and tobramycin.

Question 154

In what healthcare settings is amikacin typically the preferred agent for initial treatment of gram-negative infections?

Answer 154

Amikacin is the preferred agent in hospitals where resistance to gentamicin and tobramycin is common.

Question 155

When should amikacin be reserved for treating infections in settings with infrequent resistance to other aminoglycosides?

Answer 155

Amikacin should be reserved for infections with proven aminoglycoside resistance to delay the emergence of amikacin-resistant organisms.

Question 156

What caution should be exercised when using amikacin in combination with other drugs?

Answer 156

Caution should be exercised when using amikacin with other ototoxic or nephrotoxic drugs due to its potential kidney and inner ear toxicity.

Question 157

What is the therapeutic goal of aminoglycoside treatment?

Answer 157

The therapeutic goal is to treat serious infections caused by gram-negative aerobic bacilli.

Question 158

What baseline data should be collected before starting aminoglycoside therapy?

Answer 158

Blood and/or urine cultures should be obtained.

Question 159

What aspects of aminoglycoside therapy should be monitored?

Answer 159

Aminoglycoside levels (peaks and troughs) and renal function should be monitored.

Question 160

In which patient populations should aminoglycosides be used with caution?

Answer 160

Aminoglycosides should be used cautiously in patients with renal impairment, preexisting hearing impairment, and those receiving ototoxic and nephrotoxic drugs.

Question 161

How should therapeutic effects of aminoglycoside treatment be evaluated?

Answer 161

Patients should be monitored for indications of antimicrobial effects, such as a reduction in fever, pain, or inflammation.

Question 162

What precautions should be taken to minimize adverse effects of aminoglycosides?

Answer 162

Caution should be exercised when aminoglycosides are used in combination with other nephrotoxic or ototoxic drugs, and patients should be instructed to report symptoms of ototoxicity.

Question 163

What is the potential outcome if interstitial fibrosis or renal tubular necrosis develops during aminoglycoside treatment?

Answer 163

Kidney damage may be permanent if interstitial fibrosis or renal tubular necrosis develops.

Question 164

What is the primary mode of action of the drugs discussed in this chapter?

Answer 164

The primary mode of action of the drugs discussed in this chapter is inhibiting bacterial protein synthesis.

Question 165

How do the drugs discussed in this chapter differ from aminoglycosides in terms of their bacteriostatic or bactericidal effects?

Answer 165

Unlike aminoglycosides, these drugs are largely bacteriostatic, meaning they suppress bacterial growth but do not produce outright bacterial kill.

Question 166

When are the drugs discussed in this chapter typically used in clinical practice?

Answer 166

These drugs are considered second-line agents and are primarily used for infections that are resistant to first-line agents.

Question 167

What are tetracyclines primarily used for in systemic therapy?

Answer 167

Tetracyclines are broad-spectrum antibiotics used for systemic therapy.

Question 168

How many tetracyclines are available for systemic use in the United States, and what are their names?

Answer 168

There are seven tetracyclines available in the U.S.: tetracycline, demeclocycline, doxycycline, eravacycline, omadacycline, sarecycline, and minocycline.

Question 169

What are the main similarities among the tetracyclines, and what distinguishes them from each other?

Answer 169

The tetracyclines share similarities in structure, antimicrobial actions, and adverse effects. Their main differences are in pharmacokinetics.

Question 170

How are the tetracyclines discussed in this context?

Answer 170

Tetracyclines are discussed as a group due to their pronounced similarities, rather than focusing on a single prototype.

Question 171

How do tetracyclines inhibit bacterial growth?

Answer 171

Tetracyclines inhibit bacterial growth by binding to the 30S ribosomal subunit, preventing transfer RNA from binding to the messenger RNA-ribosome complex, and blocking amino acid addition to the growing peptide chain.

Question 172

What is the bacteriostatic nature of tetracyclines at clinically achieved concentrations?

Answer 172

Tetracyclines are bacteriostatic, meaning they suppress bacterial growth without causing bacterial death when present at clinically achieved concentrations.

Question 173

What accounts for the selective toxicity of tetracyclines?

Answer 173

Tetracyclines’ selective toxicity results from their limited ability to cross mammalian cell membranes, allowing them to affect bacterial cells but not mammalian cells.

Question 174

How do tetracyclines enter bacterial cells, and why is this significant for their mechanism of action?

Answer 174

Tetracyclines enter bacterial cells through an energy-dependent transport system, essential for them to access the bacterial cell interior and influence protein synthesis.

Question 175

Why do tetracyclines not harm mammalian cells despite their ability to inhibit protein synthesis?

Answer 175

Although tetracyclines have the potential to inhibit protein synthesis in mammalian cells, they do not cause harm because their levels within host cells remain too low due to the absence of an active transport system in mammalian cells.

Question 176

Are tetracyclines narrow- or broad-spectrum antibiotics?

Answer 176

Tetracyclines are broad-spectrum antibiotics.

Question 177

Which types of bacteria are tetracyclines effective against?

Answer 177

Tetracyclines are effective against a wide range of bacteria, including both gram-positive and gram-negative species.

Question 178

Can you name some sensitive organisms that respond well to tetracycline treatment?

Answer 178

Sensitive organisms to tetracyclines include Rickettsia, spirochetes, Brucella, Chlamydia, Mycoplasma, Helicobacter pylori, Borrelia burgdorferi, Bacillus anthracis, and Vibrio cholerae.

Question 179

What has extensive use of tetracyclines led to?

Answer 179

Extensive use of tetracyclines has led to increased bacterial resistance.

Question 180

Why are tetracyclines rarely the first choice of antibiotics today?

Answer 180

Tetracyclines are rarely the first choice of antibiotics due to resistance and the availability of more selective and less toxic alternatives.

Question 181

In which disorders are tetracyclines still used as first-line treatments?

Answer 181

Tetracyclines are used as first-line treatments for disorders including rickettsial diseases, Chlamydia trachomatis infections, brucellosis, cholera, Mycoplasma pneumoniae pneumonia, Lyme disease, anthrax, and H. pylori gastric infections.

Question 182

How are tetracyclines used to treat severe acne vulgaris?

Answer 182

Tetracyclines are used both topically and orally for treating severe acne vulgaris.

Question 183

What is the mechanism of action of tetracyclines in acne treatment?

Answer 183

Tetracyclines suppress the growth and metabolic activity of Propionibacterium acnes, an organism that secretes inflammatory chemicals.

Question 184

What makes the use of oral tetracyclines for acne treatment advantageous?

Answer 184

Oral doses of tetracyclines for acne are relatively low, resulting in minimal adverse effects.

Question 185

Where can further details about acne treatment be found?

Answer 185

Further details about acne treatment can be found in Chapter 88.

Question 186

What is the role of Helicobacter pylori (H. pylori) in peptic ulcer disease?

Answer 186

H. pylori is a bacterium in the stomach and is a major contributing factor to peptic ulcer disease.

Question 187

What is the recommended treatment for eradicating H. pylori in peptic ulcer disease?

Answer 187

Tetracyclines, in combination with metronidazole and bismuth subsalicylate, are a treatment of choice for eradicating H. pylori.

Question 188

Where can you find more information about the involvement of H. pylori in ulcer formation?

Answer 188

The role of H. pylori in ulcer formation is discussed in Chapter 64.

Question 189

How are doxycycline and minocycline used in the context of periodontal disease treatment?

Answer 189

Doxycycline and minocycline are employed for the treatment of periodontal disease.

Question 190

What are the routes of administration for doxycycline in periodontal disease treatment?

Answer 190

Doxycycline is administered both orally and topically for periodontal disease.

Question 191

How is minocycline applied in the management of periodontal disease?

Answer 191

Minocycline is exclusively applied topically for periodontal disease treatment.

Question 192

How does oral doxycycline contribute to the treatment of periodontal disease?

Answer 192

Oral doxycycline aids in the treatment of periodontal disease by inhibiting collagenase, an enzyme responsible for breaking down gum tissue.

Question 193

What is the typical dosage of oral doxycycline used for the treatment of periodontal disease?

Answer 193

The usual dosage of oral doxycycline for periodontal disease treatment is 20 mg taken twice daily.

Question 194

Is the low dose of oral doxycycline used for periodontal disease treatment harmful to bacteria?

Answer 194

The low doses of oral doxycycline, commonly 20 mg twice daily, are not sufficient to harm bacteria.

Question 195

How are topical minocycline and doxycycline used in the treatment of periodontitis?

Answer 195

Topical minocycline and doxycycline are employed as adjunct treatments alongside scaling and root planing in adults with periodontitis.

Question 196

What is the primary objective of using topical antibiotics like minocycline and doxycycline in periodontal disease?

Answer 196

The main goal is to reduce pocket depth and bleeding associated with periodontal disease.

Question 197

How do these topical antibiotics provide benefits in the treatment of periodontitis?

Answer 197

Benefits are achieved by inhibiting bacterial growth at the specific site of periodontal disease.

Question 198

Where are these topical antibiotics applied within the oral cavity?

Answer 198

These antibiotics are applied directly to the affected area within the oral cavity.

Question 199

What are the significant differences among individual tetracyclines in terms of pharmacokinetic properties?

Answer 199

Differences include half-life, route of elimination, and interactions with food.

Question 200

Why are variations in the pharmacokinetics of tetracyclines important for medical practice?

Answer 200

Variations in the pharmacokinetics of tetracyclines are crucial for determining dosing and administration strategies for specific patients and treatment goals.

Question 201

How can the choice of a particular tetracycline be influenced by its pharmacokinetic properties?

Answer 201

The choice of tetracycline can be based on the patient’s specific needs, such as the desired duration of action or potential interactions with food.

Question 202

What are the key pharmacokinetic properties that vary among different tetracyclines?

Answer 202

These properties include lipid solubility, oral dose absorption, the effect of food on absorption, route of elimination, and half-life.

Question 203

Which tetracyclines are considered short-acting, and what are their characteristics in terms of lipid solubility, oral dose absorption, and elimination?

Answer 203

Short-acting tetracyclines include tetracycline and demeclocycline. They have low to moderate lipid solubility, 60-80% oral dose absorption, and are largely affected by food. They are eliminated primarily through urine with half-lives of 8-12 hours.

Question 204

What are the features of intermediate-acting tetracyclines, and which tetracyclines fall into this category?

Answer 204

Intermediate-acting tetracyclines include doxycycline, eravacycline, and minocycline. They have high lipid solubility (except eravacycline), 90-100% oral dose absorption, varying effects of food on absorption, and are eliminated via urine and/or the gastrointestinal route (feces) with half-lives ranging from 16 to 20-22 hours.

Question 205

Which tetracyclines are classified as long-acting, and what sets them apart in terms of their pharmacokinetic properties?

Answer 205

Long-acting tetracyclines include omadacycline and sarecycline. They have high lipid solubility, varying rates of oral dose absorption, significantly affected by food, and are eliminated through renal and GI routes with half-lives of 16 to 21 hours.

Question 206

What should patients avoid taking with tetracyclines to prevent potential drug interactions?

Answer 206

Patients should avoid taking calcium supplements, milk products, iron supplements, magnesium-containing laxatives, and most antacids in combination with tetracyclines.

Question 207

Do tetracyclines have good distribution in the body?

Answer 207

Yes, tetracyclines are widely distributed to various tissues and body fluids.

Question 208

Are tetracyclines effective for treating meningeal infections?

Answer 208

No, their poor penetration into the cerebrospinal fluid limits their utility for this purpose.

Question 209

Can tetracyclines cross the placenta and enter the fetal circulation?

Answer 209

Yes, tetracyclines can readily cross the placenta and enter the fetal circulation.

Question 210

What are common gastrointestinal side effects associated with oral tetracycline therapy?

Answer 210

Common GI side effects include epigastric burning, cramps, nausea, vomiting, and diarrhea.

Question 211

How can the GI irritation caused by tetracyclines be reduced?

Answer 211

Taking tetracyclines with meals can help reduce GI irritation, but it may decrease absorption.

Question 212

What is the potential risk of taking tetracyclines at bedtime?

Answer 212

Taking tetracyclines at bedtime can occasionally lead to esophageal ulceration.

Question 213

Why is it important to determine the cause of diarrhea in patients on tetracycline therapy?

Answer 213

Diarrhea may result from superinfection of the bowel, so determining the cause is essential.

Question 214

How do tetracyclines affect tooth development?

Answer 214

Tetracyclines can bind to calcium in developing teeth, causing yellow or brown discoloration and potential enamel hypoplasia.

Question 215

What factors influence the intensity of tooth discoloration caused by tetracyclines?

Answer 215

The intensity of tooth discoloration is related to the total cumulative dose, and staining is darker with prolonged and repeated treatment.

Question 216

Can tetracycline use during pregnancy affect the baby’s teeth?

Answer 216

Yes, when taken by a pregnant woman after the fourth month of gestation, tetracyclines can cause staining of the infant’s deciduous teeth.

Question 217

When does permanent tooth discoloration occur with tetracycline use, and who is at risk?

Answer 217

Discoloration of permanent teeth occurs when tetracyclines are taken by children aged 4 months to 8 years while tooth enamel is forming. Children younger than 8 years should avoid tetracyclines to prevent permanent tooth discoloration.

Question 218

Is there a tetracycline that may have a lower risk of tooth discoloration?

Answer 218

Yes, doxycycline may have a lower risk of tooth discoloration compared to other tetracyclines.

Question 219

How does tetracycline use during pregnancy affect premature infants?

Answer 219

Tetracyclines taken by a pregnant woman can temporarily suppress the growth of long bones in premature infants, but this effect is reversible upon discontinuation.

Question 220

What is superinfection?

Answer 220

Superinfection is the overgrowth of drug-resistant microbes that occurs when drug-sensitive organisms are suppressed.

Question 221

How does the broad-spectrum nature of tetracyclines affect the risk of superinfection compared to narrower-spectrum antibiotics?

Answer 221

Tetracyclines, as broad-spectrum antibiotics, increase the risk of superinfection compared to antibiotics with a narrower spectrum.

Question 222

What are the consequences of superinfection of the bowel, and which microbes can be involved?

Answer 222

Superinfection of the bowel can lead to severe diarrhea and life-threatening conditions. It may involve staphylococci or Clostridium difficile.

Question 223

What is Clostridium difficile–associated diarrhea (CDAD), and what should patients do if they experience significant diarrhea?

Answer 223

CDAD, also known as antibiotic-associated pseudomembranous colitis, is a condition that can result from bacterial superinfection. Patients should inform their prescriber if they experience significant diarrhea.

Question 224

How should tetracyclines be managed if superinfection with staphylococci or C. difficile is diagnosed?

Answer 224

Tetracyclines should be discontinued immediately in cases of superinfection with staphylococci or C. difficile.

Question 225

How is CDAD treated, and what are the components of its management?

Answer 225

CDAD is treated with oral vancomycin or metronidazole, along with vigorous fluid and electrolyte replacement.

Question 226

What is superinfection with fungi, and what are common symptoms?

Answer 226

Superinfection with fungi, particularly Candida albicans, can occur in various body areas and result in symptoms such as itching and inflammatory lesions.

Question 227

How can superinfection with Candida be managed when taking tetracyclines?

Answer 227

Superinfection with Candida can be managed by discontinuing tetracyclines or using antifungal therapy when discontinuation is not possible.

Question 228

What is a potential hepatic (liver) side effect of tetracyclines?

Answer 228

Tetracyclines can lead to fatty infiltration of the liver, known as hepatotoxicity.

Question 229

What are the clinical manifestations of hepatotoxicity caused by tetracyclines?

Answer 229

Hepatotoxicity may manifest with symptoms such as lethargy and jaundice.

Question 230

In rare cases, how can hepatotoxicity from tetracyclines progress?

Answer 230

Rarely, hepatotoxicity may progress to massive liver failure.

Question 231

Under what conditions is liver damage most likely to occur with tetracycline use?

Answer 231

Liver damage is most likely when tetracyclines are administered intravenously in high doses, exceeding 2 grams per day.

Question 232

Who is at a particularly high risk of tetracycline-induced liver damage?

Answer 232

Pregnant and postpartum women with kidney disease are at an especially high risk for tetracycline-induced liver damage.

Question 233

How can tetracyclines affect renal function in patients with preexisting kidney disease?

Answer 233

Tetracyclines can exacerbate renal impairment in patients with preexisting kidney disease.

Question 234

Which tetracyclines are primarily eliminated by the kidneys?

Answer 234

Tetracycline and demeclocycline are mainly eliminated by the kidneys.

Question 235

What should patients with renal impairment do regarding tetracycline and demeclocycline use?

Answer 235

Patients with renal impairment should avoid tetracycline and demeclocycline.

Question 236

Which tetracyclines should be considered for patients with renal impairment who require treatment with a tetracycline?

Answer 236

For patients with renal impairment, doxycycline or minocycline should be chosen because these drugs are primarily eliminated by the liver.

Question 237

How do tetracyclines affect the skin’s response to ultraviolet (UV) light from the sun?

Answer 237

Tetracyclines can increase the skin’s sensitivity to UV light, making it more prone to sunburn.

Question 238

What precautions should patients taking tetracyclines follow regarding sun exposure?

Answer 238

Patients should avoid prolonged sun exposure, wear protective clothing like hats and long sleeves, and use sunscreen on exposed skin when outdoors.

Question 239

What can tetracyclines form with certain metal ions, and which ions are involved?

Answer 239

Tetracyclines can form nonabsorbable chelates with metal ions, including calcium, iron, magnesium, aluminum, and zinc.

Question 240

Which substances contain the metal ions that can interfere with tetracycline absorption?

Answer 240

Substances like milk products, calcium supplements, iron supplements, magnesium-containing laxatives, and most antacids contain these interfering metal ions.

Question 241

How should tetracyclines be administered to minimize interference with absorption when taken with chelating agents?

Answer 241

Tetracyclines should be taken at least 1 hour before or 2 hours after ingesting chelating agents to reduce absorption interference.

Question 242

How can tetracyclines affect digoxin levels in the body?

Answer 242

Tetracyclines can increase digoxin levels by enhancing its absorption in the gastrointestinal tract.

Question 243

What impact can tetracyclines have on international normalized ratio (INR) levels?

Answer 243

Tetracyclines can alter INR levels by affecting the vitamin K-producing flora in the gut.

Question 244

What is the recommended course of action for patients taking digoxin or warfarin when prescribed tetracyclines?

Answer 244

Patients on digoxin or warfarin should undergo careful drug level monitoring to ensure proper dosing and prevent potential adverse effects.

Question 245

What is the dosing interval for short-acting tetracycline (Tetracycline), and what is the usual adult daily dose?

Answer 245

Tetracycline is taken every 6 hours, with a usual adult daily dose of 1000-2000 mg.

Question 246

How often should intermediate-acting demeclocycline (Demeclocycline) be administered, and what is the adult dose?

Answer 246

Demeclocycline is taken every 12 hours with an adult dose of 600 mg.

Question 247

What are the dosing intervals for long-acting doxycycline (Doxycycline), and what is the usual adult daily dose?

Answer 247

Doxycycline can be administered orally or intravenously every 24 hours with a usual adult daily dose of 100-200 mg.

Question 248

What is the dosing interval for intravenous eravacycline (Xerava), and what is the adult dose?

Answer 248

Eravacycline is given intravenously every 12 hours with an adult dose of 1 mg/kg.

Question 249

How often is minocycline (Minocin) administered, and what is the adult dose?

Answer 249

Minocycline can be taken orally or intravenously every 12 hours with an adult dose of 200 mg.

Question 250

Describe the dosing interval and total daily dose for omadacycline (Nuzyra).

Answer 250

Omadacycline is administered orally and intravenously with a dosing interval of 24 hours and a daily dose of 300-450 mg for adults.

Question 251

What is the dosing interval for sarecycline (Seysara), and what is the adult dose?

Answer 251

Sarecycline is taken orally every 24 hours, with adult doses ranging from 60-150 mg.

Question 252

Why should tetracyclines not be used in children under 8 years?

Answer 252

Tetracyclines should not be used in children under 8 years because they may cause permanent discoloration of the teeth.

Question 253

Why should tetracyclines be avoided during pregnancy?

Answer 253

Tetracyclines should be avoided during pregnancy because animal studies suggest potential fetal harm.

Question 254

Why should breastfeeding women avoid tetracyclines?

Answer 254

Breastfeeding women should avoid tetracyclines to prevent permanent staining during tooth development.

Question 255

What is a care concern for older adults taking tetracyclines, especially when they are on multiple medications?

Answer 255

Older adults taking tetracyclines, especially when on multiple medications, should be monitored for drug interactions, including interactions with drugs like digoxin.

Question 256

Why should patients with kidney disease avoid tetracyclines like tetracycline and demeclocycline?

Answer 256

Patients with kidney disease should avoid these tetracyclines because they can accumulate to toxic levels in the body due to primarily being eliminated through the urine.

Question 257

What side effect of tetracyclines can be prevented by withholding these drugs from pregnant women and children under 8 years?

Answer 257

Tooth discoloration is a side effect of tetracyclines that can be prevented by not using these drugs in pregnant women and children under 8 years.

Question 258

What should patients do if they experience diarrhea while taking tetracyclines?

Answer 258

Patients should notify their prescribers if they experience diarrhea while taking tetracyclines, as it may indicate a potentially life-threatening superinfection of the bowel.

Question 259

In what population is high-dose intravenous tetracycline therapy associated with the risk of severe liver damage?

Answer 259

High-dose intravenous tetracycline therapy is associated with the risk of severe liver damage, particularly in pregnant and postpartum women with kidney disease.

Question 260

What is the therapeutic goal of tetracycline therapy?

Answer 260

Tetracyclines are used to treat tetracycline-sensitive infections, acne, and periodontal disease.

Question 261

Is monitoring required for tetracycline therapy, and if so, what should be monitored?

Answer 261

There is no specific monitoring recommended for tetracycline therapy.

Question 262

Who are the high-risk patients for whom tetracyclines are contraindicated?

Answer 262

Tetracyclines are contraindicated in pregnant women and in children younger than 8 years.

Question 263

How can the therapeutic effects of tetracyclines be evaluated?

Answer 263

The therapeutic effects can be evaluated by monitoring for reductions in fever, pain, or inflammation.

Question 264

How can gastrointestinal distress be minimized in patients taking tetracyclines?

Answer 264

Gastrointestinal distress can be reduced by taking tetracyclines with meals.

Question 265

What advice should be given to patients regarding sunlight exposure during tetracycline therapy?

Answer 265

Patients should be advised to avoid prolonged exposure to sunlight.

Question 266

What type of antibacterial drug is nitrofurantoin?

Answer 266

Nitrofurantoin is a broad-spectrum antibacterial drug.

Question 267

What effects does nitrofurantoin produce at low concentrations, and what effects at high concentrations?

Answer 267

Nitrofurantoin produces bacteriostatic effects at low concentrations and bactericidal effects at high concentrations.

Question 268

Where are therapeutic levels of nitrofurantoin primarily achieved?

Answer 268

Therapeutic levels of nitrofurantoin are primarily achieved in urine.

Question 269

How does nitrofurantoin damage bacteria?

Answer 269

Nitrofurantoin damages bacteria by injuring their DNA.

Question 270

What is required for nitrofurantoin to damage DNA in bacteria?

Answer 270

Enzymatic conversion of nitrofurantoin to a reactive form is required for it to damage DNA in bacteria.

Question 271

Why is nitrofurantoin selectively toxic to bacteria?

Answer 271

Nitrofurantoin is selectively toxic to bacteria because bacteria possess relatively higher levels of the enzyme needed for drug activation compared to mammalian cells.

Question 272

What types of bacteria are susceptible to nitrofurantoin?

Answer 272

Nitrofurantoin is effective against both gram-positive and gram-negative bacteria.

Question 273

Can you name some of the susceptible organisms to nitrofurantoin?

Answer 273

Susceptible organisms include staphylococci, streptococci, Neisseria species, Bacteroides species, and most strains of E. coli.

Question 274

Do the sensitive bacteria tend to develop resistance to nitrofurantoin?

Answer 274

Sensitive bacteria rarely acquire resistance to nitrofurantoin.

Question 275

Which bacterial species are frequently resistant to nitrofurantoin?

Answer 275

Organisms commonly resistant to nitrofurantoin include Proteus, Pseudomonas, Enterobacter, and Klebsiella species.

Question 276

What is the therapeutic indication for nitrofurantoin?

Answer 276

Nitrofurantoin is indicated for the treatment of acute infections of the lower urinary tract.

Question 277

What type of organisms should be responsible for the lower urinary tract infections treated with nitrofurantoin?

Answer 277

The infections must be caused by susceptible organisms.

Question 278

Besides treatment, for what other purpose can nitrofurantoin be used in urinary tract infections?

Answer 278

Nitrofurantoin can be used for prophylaxis to prevent recurrent lower urinary tract infections.

Question 279

Is nitrofurantoin recommended for infections of the upper urinary tract?

Answer 279

No, it is not recommended for treating infections of the upper urinary tract.

Question 280

What are the different formulations of nitrofurantoin used for UTI treatment?

Answer 280

Nitrofurantoin is available as microcrystals (Furadantin), macrocrystals (Macrodantin), and monohydrate/macrocrystals (Macrobid).

Question 281

What is the usual dosage range for nitrofurantoin in the treatment of UTIs?

Answer 281

The usual doses for nitrofurantoin in the treatment of UTIs range from 50-100 mg, taken multiple times a day.

Question 282

For what purpose can nitrofurantoin be used at bedtime?

Answer 282

Nitrofurantoin is used for UTI prophylaxis, and a typical dose of 50-100 mg is taken at bedtime.

Question 283

What is the recommended dosage of methenamine hippurate (Hiprex, Urex) for UTI prophylaxis or suppression?

Answer 283

Methenamine hippurate is available in 1-g tablets and is taken twice a day for UTI prophylaxis or suppression.

Question 284

What are the most frequent adverse reactions to nitrofurantoin?

Answer 284

The most common adverse reactions to nitrofurantoin are gastrointestinal disturbances, including anorexia, nausea, vomiting, and diarrhea.

Question 285

How can GI side effects of nitrofurantoin be minimized?

Answer 285

GI side effects of nitrofurantoin can be minimized by administering the drug with milk or meals.

Question 286

What other approaches can be taken to reduce GI distress associated with nitrofurantoin?

Answer 286

Reducing the dosage or using the macrocrystalline formulations of nitrofurantoin may also help in reducing GI distress.

Question 287

What are the two types of pulmonary reactions that nitrofurantoin can induce?

Answer 287

Nitrofurantoin can induce acute and subacute pulmonary reactions.

Question 288

What are the typical symptoms of acute pulmonary reactions to nitrofurantoin?

Answer 288

Acute pulmonary reactions to nitrofurantoin include dyspnea, chest pain, chills, fever, cough, and alveolar infiltrates.

Question 289

How long does it usually take for the symptoms of acute pulmonary reactions to resolve after discontinuing nitrofurantoin?

Answer 289

The symptoms of acute pulmonary reactions usually resolve within 2 to 4 days after discontinuing nitrofurantoin.

Question 290

What is the suspected cause of acute pulmonary reactions to nitrofurantoin?

Answer 290

Acute pulmonary reactions to nitrofurantoin are believed to be hypersensitivity reactions.

Question 291

What should patients with a history of acute pulmonary reactions to nitrofurantoin do regarding the use of the drug?

Answer 291

Patients with a history of acute pulmonary reactions to nitrofurantoin should avoid using the drug again.

Question 292

What are subacute reactions to nitrofurantoin, and when do they typically occur?

Answer 292

Subacute reactions to nitrofurantoin are rare and occur during prolonged treatment. They may include symptoms like dyspnea, cough, and malaise.

Question 293

How long does it usually take for the symptoms of subacute reactions to regress after discontinuing nitrofurantoin?

Answer 293

In most cases, symptoms of subacute reactions regress over several weeks to months after discontinuing nitrofurantoin.

Question 294

What potential complication may arise in some patients with subacute reactions to nitrofurantoin?

Answer 294

Some patients with subacute reactions to nitrofurantoin may experience permanent lung damage.

Question 295

What are some hematologic reactions that nitrofurantoin can cause?

Answer 295

Nitrofurantoin can cause hematologic reactions such as agranulocytosis, leukopenia, thrombocytopenia, and megaloblastic anemia.

Question 296

In which individuals can hemolytic anemia occur as a result of nitrofurantoin use?

Answer 296

Hemolytic anemia due to nitrofurantoin can occur in infants and in individuals with an inherited deficiency in glucose-6-phosphate dehydrogenase (G6PD).

Question 297

Why is nitrofurantoin contraindicated for pregnant women near term?

Answer 297

Nitrofurantoin is contraindicated for pregnant women near term (close to delivery) due to the potential risk of hemolytic anemia in newborns.

Question 298

Why should nitrofurantoin be avoided in infants younger than 1 month?

Answer 298

Nitrofurantoin should be avoided in infants younger than 1 month because of the risk of hemolytic anemia associated with its use.

Question 299

What kind of nerve damage can result from nitrofurantoin use?

Answer 299

Nitrofurantoin use can lead to damage to sensory and motor nerves, potentially causing demyelination and nerve degeneration.

Question 300

What are some early symptoms of nerve damage associated with nitrofurantoin?

Answer 300

Early symptoms of nerve damage include muscle weakness, tingling sensations, and numbness.

Question 301

What should patients be instructed to do if they experience symptoms of nerve damage while taking nitrofurantoin?

Answer 301

Patients should be instructed to report symptoms of nerve damage immediately.

Question 302

In which patients is neuropathy (nerve damage) most likely to occur with nitrofurantoin use?

Answer 302

Neuropathy is most likely to occur in patients with renal impairment and in those taking nitrofurantoin chronically.

Question 303

What rare but serious adverse effect can nitrofurantoin cause in the liver?

Answer 303

Nitrofurantoin can rarely cause severe liver injury, presenting as hepatitis, cholestatic jaundice, and hepatic necrosis.

Question 304

What are the potential consequences of severe liver injury caused by nitrofurantoin?

Answer 304

Severe liver injury from nitrofurantoin use can be life-threatening and has led to fatalities.

Question 305

What should patients using nitrofurantoin do to monitor for signs of liver injury?

Answer 305

Patients using nitrofurantoin should undergo periodic tests of liver function to monitor for signs of liver injury.

Question 306

What action should be taken if a patient develops liver injury while taking nitrofurantoin?

Answer 306

If a patient develops liver injury while taking nitrofurantoin, the drug should be discontinued immediately, and it should never be used again.

Question 307

What does conflicting evidence regarding nitrofurantoin use during pregnancy suggest?

Answer 307

Conflicting evidence regarding nitrofurantoin use during pregnancy raises uncertainty about its safety in pregnant women.

Question 308

What did a 2009 study reveal regarding nitrofurantoin and birth defects during pregnancy?

Answer 308

A 2009 study found an association between nitrofurantoin use during pregnancy and specific birth defects, including anophthalmia, hypoplastic left heart syndrome, atrial septal defects, and cleft lip with cleft palate.

Question 309

What did a 2013 study from Norway discover about nitrofurantoin use during pregnancy?

Answer 309

A 2013 study from Norway did not find an increased incidence of the previously mentioned birth defects in babies delivered by mothers who had taken nitrofurantoin. However, it revealed an increased incidence of neonatal jaundice in neonates exposed to nitrofurantoin in the last 30 days of gestation.

Question 310

Why is nitrofurantoin contraindicated in pregnant patients at term?

Answer 310

Nitrofurantoin is contraindicated in pregnant patients at term (38–42 weeks of gestation) due to the potential risk of hemolytic anemia.

Question 311

What is the suggested approach for nitrofurantoin use during pregnancy in light of the conflicting evidence?

Answer 311

Given the conflicting evidence, until more conclusive information is available, using alternative antibiotics during pregnancy may be considered a prudent approach.

Question 312

What antibiotics are recommended to treat infants with urinary tract infections (UTIs)?

Answer 312

Ampicillin and gentamicin are recommended for the treatment of UTIs in infants.

Question 313

Why is nitrofurantoin contraindicated in infants less than one month of age?

Answer 313

Nitrofurantoin is contraindicated in infants less than one month of age due to safety concerns.

Question 314

What additional considerations are important in infants with UTIs?

Answer 314

UTIs in infants can often coincide with other infections or urinary tract abnormalities, necessitating immediate source investigation. Trimethoprim/sulfamethoxazole should be avoided in the early stages of infancy.

Question 315

Which ages are methenamine hippurate and methenamine mandelate approved for in children?

Answer 315

Methenamine hippurate is approved for use in children between 6 and 12 years of age, while methenamine mandelate can be used in children less than 6 years of age.

Question 316

How should urinary tract infections (UTIs) in pregnant women be managed?

Answer 316

UTIs in pregnant women should be treated as complicated infections. Nitrofurantoin is contraindicated in the third trimester of pregnancy, and fluoroquinolones should be avoided during pregnancy.

Question 317

What precautions should breastfeeding women take when using fluoroquinolones?

Answer 317

Fluoroquinolones have been detected in breast milk at low doses. Short-term use during breastfeeding is acceptable. For maximum safety, breastfeeding should be avoided between 4 and 6 hours after a dose.

Question 318

In which patient group should nitrofurantoin be avoided, especially if they have decreased renal function?

Answer 318

Nitrofurantoin should be avoided in older adults with decreased renal function.

Question 319

What is the approved use for fosfomycin (Monurol)?

Answer 319

Fosfomycin is approved for single-dose therapy in women with uncomplicated urinary tract infections (acute cystitis) caused by E. coli or E. faecalis.

Question 320

How does fosfomycin work to kill bacteria?

Answer 320

Fosfomycin kills bacteria by disrupting the synthesis of peptidoglycan polymer strands, which form the bacterial cell wall.

Question 321

What are the common adverse effects associated with fosfomycin?

Answer 321

Common adverse effects of fosfomycin include diarrhea, headache, vaginitis, nausea, abdominal pain, rhinitis, drowsiness, dizziness, and rash.

Question 322

Is it necessary to take fosfomycin with food?

Answer 322

Fosfomycin dosing may be done with or without food.

Question 323

When should improvement in cystitis symptoms be expected after taking fosfomycin?

Answer 323

Improvement in cystitis symptoms is typically expected within 2 to 3 days after taking fosfomycin. If symptoms do not improve, additional doses are not recommended.