Module 9 14 Aminoglycosides Tetracycline Nitrofurantoin Fosfomycin Flashcards
(323 cards)
1
Q
Question
A
Answer
2
Q
What is the primary spectrum of activity for aminoglycosides?
A
Aminoglycosides are narrow-spectrum antibiotics primarily used against aerobic gram-negative bacilli.
3
Q
What is the mechanism of action of aminoglycosides, and what does it result in?
A
Aminoglycosides disrupt protein synthesis, leading to rapid bacterial death.
4
Q
What are the potential toxic effects associated with aminoglycoside use?
A
Aminoglycosides have the potential to cause serious inner ear and kidney damage.
5
Q
Why are the indications for aminoglycosides limited?
A
The toxicities associated with aminoglycosides restrict their clinical use.
6
Q
Why are aminoglycosides not absorbed from the gastrointestinal (GI) tract?
A
Aminoglycosides carry multiple positive charges, preventing their absorption from the GI tract.
7
Q
How are aminoglycosides typically administered to treat systemic infections?
A
Aminoglycosides must be administered parenterally (via injection) to effectively treat systemic infections.
8
Q
How many aminoglycosides are approved for clinical use in the United States, and which ones are commonly employed?
A
In the United States, seven aminoglycosides are approved for clinical use, with gentamicin, tobramycin, and amikacin being the most commonly employed agents.
9
Q
What is the structural composition of aminoglycosides?
A
Aminoglycosides are composed of two or more amino sugars connected by a glycoside linkage.
10
Q
What is the electrochemical property of aminoglycosides at physiologic pH?
A
Aminoglycosides are highly polar polycations, carrying several positive charges.
11
Q
Why do aminoglycosides have limited ability to cross biological membranes?
A
Aminoglycosides cannot readily cross membranes due to their positive charge.
12
Q
How are aminoglycosides affected by their positive charge in terms of absorption?
A
Due to their positive charge, aminoglycosides are not absorbed from the gastrointestinal (GI) tract.
13
Q
Can aminoglycosides enter the cerebrospinal fluid (CSF)?
A
Aminoglycosides do not enter the cerebrospinal fluid (CSF).
14
Q
What is the fate of aminoglycosides in the body regarding excretion?
A
Aminoglycosides are rapidly excreted by the kidneys.
15
Q
What is the target of aminoglycosides in bacterial cells, and how do they disrupt protein synthesis?
A
Aminoglycosides target the 30S ribosomal subunit in bacterial cells. They disrupt protein synthesis by binding to this subunit.
16
Q
What are the three effects of aminoglycoside binding to the ribosomal subunit on protein synthesis?
A
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.
17
Q
Are aminoglycosides bactericidal or bacteriostatic antibiotics?
A
Aminoglycosides are bactericidal antibiotics, meaning they kill bacterial cells.
18
Q
How does the bactericidal activity of aminoglycosides relate to their concentration?
A
Bactericidal activity of aminoglycosides is concentration-dependent, meaning higher concentrations result in more rapid clearance of the infection.
19
Q
What is the postantibiotic effect, and how does it apply to aminoglycosides?
A
The postantibiotic effect is a phenomenon where bactericidal activity persists for several hours after serum levels of aminoglycosides drop below the minimal bactericidal concentration.
20
Q
What is the proposed mechanism of bacterial death by aminoglycosides, and how does it differ from other antibiotics?
A
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.
21
Q
What is the primary cause of bacterial resistance to aminoglycosides?
A
Bacterial resistance to aminoglycosides is mainly caused by the production of enzymes that can inactivate these antibiotics.
22
Q
How do gram-negative bacteria typically acquire the genetic information needed to produce aminoglycoside-inactivating enzymes?
A
Gram-negative bacteria often acquire the genetic information through the transfer of R factors.
23
Q
How many different aminoglycoside-inactivating enzymes have been identified, and what makes patterns of resistance complex?
A
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.
24
Q
Which aminoglycoside is least susceptible to inactivation by bacterial enzymes, and what is the result of this resistance pattern?
A
Amikacin is the least susceptible aminoglycoside to inactivation by bacterial enzymes. As a result, resistance to amikacin is uncommon.
25
What is the recommended approach to using amikacin to minimize the emergence of resistant bacteria?
To prevent the emergence of resistant bacteria, amikacin should be reserved for infections that do not respond to other aminoglycosides.
26
Which type of bacteria are primarily susceptible to the bactericidal effects of aminoglycosides?
Bactericidal effects of aminoglycosides are most effective against aerobic gram-negative bacilli.
27
Can you name some of the sensitive organisms to aminoglycosides?
Sensitive organisms include Escherichia coli, Klebsiella pneumoniae, Serratia marcescens, Proteus mirabilis, and Pseudomonas aeruginosa.
28
Are aminoglycosides generally effective against gram-positive bacteria?
Aminoglycosides are generally inactive against most gram-positive bacteria.
29
Why can't aminoglycosides kill anaerobic bacteria, and what is the oxygen-dependent process involved?
Aminoglycosides cannot kill anaerobic bacteria because they require oxygen-dependent transport across the bacterial cell membrane.
30
Why are anaerobic organisms resistant to aminoglycosides, and how does this relate to their oxygen requirements?
Anaerobic organisms, which live in the absence of oxygen, cannot take up aminoglycosides, making them resistant to these antibiotics.
31
Under what conditions are aminoglycosides inactive against facultative bacteria, and why?
Aminoglycosides are inactive against facultative bacteria when these organisms are living under anaerobic conditions because the antibiotics' transport process is oxygen-dependent.
32
What is the principal use of parenteral aminoglycosides in treating infections?
Parenteral aminoglycosides are primarily used to treat serious infections caused by aerobic gram-negative bacilli.
33
Which specific organisms are the primary targets of aminoglycosides in the treatment of infections?
The primary target organisms for aminoglycosides are Pseudomonas aeruginosa and the Enterobacteriaceae, which includes organisms like Escherichia coli, Klebsiella, Serratia species, and Proteus mirabilis.
34
In what circumstances is gentamicin, an aminoglycoside, used in combination with other antibiotics, and which gram-positive cocci are targeted?
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.
35
What are the three most commonly used aminoglycosides for parenteral therapy?
The most commonly used aminoglycosides for parenteral therapy are gentamicin, tobramycin, and amikacin.
36
What factors determine the choice of aminoglycoside among gentamicin, tobramycin, and amikacin for therapy?
The choice among these aminoglycosides depends mainly on patterns of resistance in a specific community or hospital.
37
In settings where resistance to aminoglycosides is uncommon, which aminoglycoside is often preferred, and why?
In settings with low resistance, either gentamicin or tobramycin is usually preferred. Gentamicin may be selected on the basis of being less expensive.
38
What is the aminoglycoside of choice when organisms are resistant to both gentamicin and tobramycin?
When organisms are resistant to both gentamicin and tobramycin, they are usually sensitive to amikacin.
39
In settings where resistance to gentamicin and tobramycin is common, which aminoglycoside may be preferred for initial therapy?
In settings with high resistance to gentamicin and tobramycin, amikacin may be preferred for initial therapy.
40
How are aminoglycosides used topically in the treatment of infections?
Aminoglycosides are used topically to treat infections.
41
Which aminoglycosides are used to treat eye infections?
Gentamicin and tobramycin are used to treat eye infections.
42
In addition to eye infections, which type of infections can neomycin be used to treat, and in which chapters are these uses discussed?
Neomycin can be used to treat infections of the ear and eye, as discussed in Chapters 87 and 89.
43
Which systemic aminoglycosides are commonly used for treatment, and what are their names?
Common systemic aminoglycosides include amikacin, gentamicin, and tobramycin.
44
How can the total daily dose of systemic aminoglycosides be administered?
The total daily dose may be given as one large dose each day or as two to three divided doses at equally spaced intervals.
45
Why should serum drug levels be measured when using systemic aminoglycosides?
Serum drug levels should be measured due to interpatient variability, and dosage should be adjusted based on these measurements.
46
What are the typical peak therapeutic levels for amikacin, gentamicin, and tobramycin when given in divided doses?
The peak therapeutic levels are typically 2-3 µg/mL for amikacin, gentamicin, and tobramycin when given in divided doses.
47
What are the recommended trough levels for amikacin, gentamicin, and tobramycin?
Recommended trough levels are less than 5-10 µg/mL for amikacin and less than 1-2 µg/mL for gentamicin and tobramycin.
48
Are the dosages different when gentamicin is used in combination with other antibiotics, and in which circumstances?
Yes, the dosages may differ when gentamicin is combined with vancomycin or a beta-lactam antibiotic to treat certain gram-positive infections.
49
Do peak values for gentamicin remain the same in all cases, and when may higher trough levels be acceptable?
Peak values for gentamicin may vary depending on the type of infection. Higher trough levels may be acceptable for severe infections.
50
What is the reason behind the limited oral effectiveness of aminoglycosides for systemic infections?
Aminoglycosides are polycations, which hinders their ability to cross membranes. Only about 1% of an oral dose is absorbed.
51
How are aminoglycosides administered for the treatment of systemic infections?
Aminoglycosides must be given parenterally, either intramuscularly (IM) or intravenously (IV), to effectively treat systemic infections.
52
Is there significant absorption of aminoglycosides when applied to intact skin?
No, absorption of aminoglycosides after application to intact skin is minimal.
53
In what situation might aminoglycosides be absorbed in amounts sufficient to produce systemic toxicity?
Aminoglycosides may be absorbed in amounts sufficient to produce systemic toxicity when used for wound irrigation.
54
What is the primary distribution site of aminoglycosides in the body?
Aminoglycosides are primarily distributed to extracellular fluid in the body.
55
Are aminoglycosides capable of entering the cerebrospinal fluid in sufficient quantities to treat meningitis in adults?
No, aminoglycosides are generally not capable of entering the cerebrospinal fluid in sufficient quantities to treat meningitis in adults.
56
Can aminoglycosides enter the cerebrospinal fluid in sufficient quantities to treat meningitis in adults?
No, aminoglycosides do not enter the cerebrospinal fluid in sufficient quantities to treat meningitis in adults.
57
Why do aminoglycosides achieve much higher levels in the kidneys compared to serum levels, and what can result from this?
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.
58
How can aminoglycosides cause ototoxicity, and where in the inner ear do they penetrate?
Aminoglycosides can penetrate the perilymph and endolymph of the inner ears, leading to ototoxicity.
59
Can aminoglycosides cross the placenta, and what potential risk does this pose?
Yes, aminoglycosides can cross the placenta, posing a potential risk of toxicity to the fetus.
60
Are aminoglycosides approved for use in treating bacterial infections in infants, and how is dosing determined for infants?
Aminoglycosides are approved for use in infants younger than 8 days. Dosing is based on the infant's weight and length of gestation.
61
Are aminoglycosides generally considered safe for treating bacterial infections in children and adolescents?
Yes, aminoglycosides are considered safe for use against bacterial infections in children and adolescents.
62
What is the potential concern when using aminoglycosides during pregnancy?
There is evidence that the use of aminoglycosides during pregnancy can harm the fetus.
63
Is gentamicin safe to use during lactation, and what is the available information regarding its use in breastfeeding women?
Gentamicin is likely safe to use during lactation, but there is limited information available regarding its use in breastfeeding women.
64
What caution should be exercised when using aminoglycosides in older adults, and why?
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.
65
How are aminoglycosides primarily eliminated from the body?
Aminoglycosides are primarily eliminated by the kidneys.
66
Are aminoglycosides subject to metabolism in the body?
No, aminoglycosides are not metabolized in the body.
67
What is the typical range of half-lives for aminoglycosides in patients with normal renal function?
In patients with normal renal function, the half-lives of aminoglycosides range from 2 to 3 hours.
68
How does renal impairment affect the elimination of aminoglycosides and their half-lives?
Renal impairment compromises the elimination of aminoglycosides, leading to significantly longer half-lives in affected patients.
69
Why is it necessary to adjust the dosage size or increase the dosing interval in patients with kidney disease when using aminoglycosides?
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.
70
Why do different patients receiving the same aminoglycoside dosage achieve widely different serum drug levels?
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.
71
What factors contribute to the interpatient variation in aminoglycoside serum levels?
Interpatient variation is influenced by factors such as age, percent body fat, and pathophysiological conditions like renal impairment, fever, edema, and dehydration.
72
Why is individualized dosing of aminoglycosides necessary for patients?
Individualized dosing of aminoglycosides is necessary to account for the significant variability in serum drug levels among patients.
73
Can you provide an example of the dramatic variation in aminoglycoside dosages observed in a clinical study?
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.
74
What are the primary sites of serious toxicity caused by aminoglycosides?
Aminoglycosides can produce significant toxicity, primarily affecting the inner ears and kidneys.
75
Why are the inner ears and kidneys vulnerable to aminoglycoside toxicity?
The inner ears and kidneys are particularly vulnerable to aminoglycoside toxicity because these drugs become highly concentrated within the cells of these structures.
76
How can aminoglycosides affect the inner ears, and what are the consequences?
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.
77
What is the primary factor contributing to the risk of aminoglycoside-induced ototoxicity?
The risk for ototoxicity is primarily related to elevated trough levels of aminoglycosides rather than excessive peak levels.
78
Why does prolonged exposure to aminoglycosides contribute to inner ear cellular injury?
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.
79
What are some risk factors that increase the likelihood of aminoglycoside-induced ototoxicity?
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.
80
What is the first sign of impending cochlear damage in patients on aminoglycoside therapy?
High-pitched tinnitus is often the initial sign of cochlear damage associated with aminoglycosides.
81
Is ototoxicity caused by aminoglycosides reversible?
Ototoxicity caused by aminoglycosides is largely irreversible.
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?
Aminoglycosides should be discontinued at the first signs of damage to prevent permanent injury.
83
How does hearing loss typically progress in patients with aminoglycoside-induced cochlear damage?
Initial high-frequency hearing loss is followed by low-frequency hearing loss with continued aminoglycoside use.
84
Why is audiometric testing essential for patients on aminoglycoside therapy?
Audiometric testing is necessary to detect the subtle initial decline in high-frequency hearing associated with aminoglycosides.
85
What is the first sign of impending vestibular damage in patients on aminoglycoside therapy?
A persistent headache, lasting for a day or two, is typically the initial sign of impending vestibular damage.
86
What are the subsequent symptoms of vestibular damage caused by aminoglycosides?
Nausea, unsteadiness, dizziness, and vertigo are common symptoms of vestibular damage due to aminoglycosides.
87
What should patients on aminoglycoside therapy be instructed to do regarding the signs and symptoms of cochlear and vestibular damage?
Patients should be educated about these signs and symptoms and instructed to report them promptly.
88
What is the consequence of aminoglycoside-induced ototoxicity?
Aminoglycosides can lead to irreversible ototoxicity, resulting in permanent damage to hearing and balance.
89
What are some neurotoxic symptoms associated with aminoglycoside use?
Neurotoxic symptoms may include numbness, tingling, muscle twitching, and seizures in individuals taking aminoglycosides.
90
When is the risk of neurotoxicity with aminoglycosides most significant?
The risk of neurotoxicity is highest in patients receiving high doses of aminoglycosides or using them for extended durations.
91
How does preexisting renal impairment affect the risk of aminoglycoside-induced neurotoxicity?
Patients with preexisting renal impairment are at an increased risk of experiencing neurotoxicity when using aminoglycosides.
92
What is nephrotoxicity associated with in the context of aminoglycoside use?
Nephrotoxicity refers to kidney damage associated with the use of aminoglycosides.
93
How does the risk of nephrotoxicity change in patients receiving high doses of aminoglycosides?
The risk of nephrotoxicity increases in patients receiving high doses of aminoglycosides.
94
What happens to the risk of nephrotoxicity with prolonged use of aminoglycosides?
Prolonged use of aminoglycosides is associated with an increased risk of nephrotoxicity.
95
Which patient population is at greater risk of aminoglycoside-induced nephrotoxicity?
Patients with preexisting renal impairment are at a greater risk of aminoglycoside-induced nephrotoxicity.
96
How do aminoglycosides affect cells in the proximal renal tubules of the kidneys?
Aminoglycosides can injure cells of the proximal renal tubules.
97
What factors are associated with aminoglycoside-induced nephrotoxicity?
Nephrotoxicity correlates with the total cumulative dose of aminoglycosides and high trough levels.
98
Do high peak levels of aminoglycosides significantly increase nephrotoxicity?
High peak levels of aminoglycosides do not significantly increase nephrotoxicity.
99
How does nephrotoxicity usually manifest when caused by aminoglycosides?
Nephrotoxicity caused by aminoglycosides usually presents as acute tubular necrosis.
100
What are some symptoms of aminoglycoside-induced nephrotoxicity?
Symptoms may include proteinuria, urine casts, production of dilute urine, and elevated levels of serum creatinine and BUN.
101
Why is monitoring of serum creatinine and BUN recommended for patients receiving aminoglycosides?
Monitoring helps assess kidney function and detect nephrotoxicity.
102
Who is at higher risk for aminoglycoside-induced nephrotoxicity?
Older adults, patients with preexisting kidney disease, and those taking other nephrotoxic drugs are at higher risk.
103
Is aminoglycoside-induced kidney damage usually reversible?
Yes, aminoglycoside-induced kidney damage is usually reversible because proximal tubule cells in the kidneys can regenerate.
104
What is the most significant consequence of renal damage due to aminoglycosides?
The accumulation of aminoglycosides in the body, which can lead to ototoxicity and further kidney damage.
105
What is the potential neuromuscular effect of aminoglycosides?
Aminoglycosides can inhibit neuromuscular transmission.
106
What can be the consequence of neuromuscular inhibition caused by aminoglycosides?
Neuromuscular blockade can result in flaccid paralysis.
107
Why is neuromuscular blockade due to aminoglycosides particularly concerning?
Neuromuscular blockade due to aminoglycosides can be life-threatening, especially if it affects the muscles responsible for respiration.
108
Where have most reported cases of neuromuscular blockade following aminoglycosides occurred?
Most cases have occurred after intraperitoneal or intrapleural instillation of aminoglycosides.
109
Why are penicillins and aminoglycosides frequently used in combination for bacterial infections?
They weaken the bacterial cell wall, allowing aminoglycosides better access to their site of action, further enhancing bacterial killing.
110
How do penicillins contribute to the effectiveness of this combination therapy?
Penicillins disrupt the bacterial cell wall.
111
What is the result of disrupting the bacterial cell wall in combination therapy with aminoglycosides?
Disruption of the cell wall facilitates the access of aminoglycosides to their site of action, further enhancing bacterial killing.
112
How can cephalosporins and vancomycin enhance bacterial killing in combination with aminoglycosides?
They weaken the bacterial cell wall, allowing aminoglycosides better access to their site of action.
113
What is the primary mechanism by which cephalosporins and vancomycin contribute to this combination therapy?
They weaken the bacterial cell wall, much like penicillins, to enhance bacterial kill.
114
What is the result of weakening the bacterial cell wall in this combination therapy?
It improves the effectiveness of aminoglycosides in killing bacteria.
115
What happens when aminoglycosides and loop diuretics are used together?
The risk of inner ear injury increases significantly.
116
Why is it important to avoid the concurrent use of aminoglycosides and loop diuretics?
To prevent ototoxicity and damage to the inner ears.
117
What are some examples of aminoglycosides that may pose a risk when combined with loop diuretics?
Gentamicin and tobramycin are common examples.
118
What happens when aminoglycosides are used concurrently with other nephrotoxic agents?
The risk of renal damage increases, and additive or potentiative nephrotoxicity may occur.
119
Can you name some nephrotoxic agents that may interact with aminoglycosides?
Examples include amphotericin B, cephalosporins, polymyxins, vancomycin, cyclosporine, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs).
120
What are the two common dosing schedules for systemic aminoglycosides?
They can be administered as a single large daily dose or as divided doses.
121
What was the traditional method of administering systemic aminoglycosides?
Traditionally, they were given in divided doses at equally spaced intervals around the clock (e.g., every 8 hours).
122
Why has once-daily dosing become the preferred schedule for aminoglycosides?
Once-daily dosing is considered both safe and effective and is more convenient and cost-effective.
123
Which patient groups may not be suitable for once-daily dosing of aminoglycosides?
Once-daily dosing is not appropriate for neonates, pregnant individuals, patients undergoing dialysis, and those with ascites.
124
Why is monitoring serum drug levels important for adjusting aminoglycoside dosage?
Monitoring ensures that peak levels are adequate for bacterial kill and that trough levels are low to minimize toxicity.
125
What determines the monitoring approach for aminoglycosides?
The dosing schedule (once-daily dosing or divided doses) determines the monitoring approach.
126
Is it necessary to measure peak levels when using once-daily dosing of aminoglycosides?
No, peak levels are not measured in once-daily dosing because high peak levels are guaranteed with this schedule.
127
When using divided doses for aminoglycosides, what levels need to be monitored?
With divided doses, both peak and trough levels should be monitored.
128
When should blood samples for peak levels of aminoglycosides be taken?
Peak levels should be measured 30 minutes after giving an IM injection or completing an IV infusion.
129
How is sampling for trough levels of aminoglycosides timed for patients receiving divided doses?
Trough samples should be taken just before the next dose for patients on divided doses.
130
When should a single sample for trough levels be drawn for patients receiving once-daily doses of aminoglycosides?
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.
131
What are the primary targets of gentamicin in the treatment of serious infections?
Gentamicin is primarily used to treat serious infections caused by aerobic gram-negative bacilli, including Pseudomonas aeruginosa and the Enterobacteriaceae.
132
Why is gentamicin often preferred for treating these infections in hospitals with low resistance?
Gentamicin is chosen in hospitals with low resistance due to its cost-effectiveness compared to tobramycin and amikacin.
133
What is the outcome when gentamicin and tobramycin are both ineffective due to resistance?
In cases of resistance to both gentamicin and tobramycin, amikacin is often an effective alternative.
134
Besides gram-negative bacilli, what other types of infections can gentamicin be used to treat?
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.
135
What is the therapeutic use of gentamicin?
Gentamicin is used to treat bacterial infections caused by aerobic gram-negative bacilli, including Pseudomonas aeruginosa and Enterobacteriaceae.
136
What is the usual adult dosage for tobramycin, and what are its common preparations?
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).
137
What is the therapeutic use and dosage of amikacin?
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.
138
For what purposes is neomycin used, and in what preparations?
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.
139
What is the therapeutic use and dosage of kanamycin, and are there any exceptions?
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.
140
What is the therapeutic use of streptomycin, and in what contexts is it employed?
Streptomycin is used in combination with other drugs to treat tuberculosis, as well as for tularemia and plague.
141
What is the therapeutic use and dosage of paromycin, and in what form is it available?
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.
142
What is the therapeutic use and dosage of plazomicin (Zemdri)?
Plazomicin is indicated for complicated urinary tract infections (UTIs) caused by Enterobacteriaceae, and the standard adult dosage is 15 mg/kg every 24 hours.
143
What are the potential toxicities associated with gentamicin?
Gentamicin can be toxic to the kidneys and inner ears.
144
Why should caution be exercised when combining gentamicin with other drugs?
Gentamicin should be combined cautiously with other nephrotoxic or ototoxic drugs to minimize the risk of these toxicities.
145
What should be avoided when administering gentamicin in a parenteral solution?
Gentamicin should not be mixed in the same parenteral solution with penicillins because it can be inactivated by direct chemical interaction.
146
How does tobramycin compare to gentamicin in terms of its uses and interactions?
Tobramycin is similar to gentamicin in its uses and interactions.
147
What is tobramycin's activity against Pseudomonas aeruginosa?
Tobramycin is more active than gentamicin against Pseudomonas aeruginosa.
148
For which patient population is tobramycin commonly used?
Tobramycin is often used for patients with cystic fibrosis.
149
What potential toxicities are associated with tobramycin?
Tobramycin, like other aminoglycosides, can cause inner ear and kidney damage.
150
How can the risk of tobramycin's toxicities be minimized?
It's advisable to avoid concurrent therapy with other ototoxic or nephrotoxic drugs when using tobramycin.
151
What adverse effect can tobramycin cause in some patients?
Tobramycin may lead to Clostridium difficile–associated diarrhea.
152
What are the two outstanding features of amikacin among aminoglycosides?
Amikacin is active against a broad spectrum of gram-negative bacilli and is less vulnerable to inactivation by bacterial enzymes.
153
How does amikacin's bacterial resistance incidence compare to that of gentamicin and tobramycin?
Amikacin has a lower incidence of bacterial resistance compared to gentamicin and tobramycin.
154
In what healthcare settings is amikacin typically the preferred agent for initial treatment of gram-negative infections?
Amikacin is the preferred agent in hospitals where resistance to gentamicin and tobramycin is common.
155
When should amikacin be reserved for treating infections in settings with infrequent resistance to other aminoglycosides?
Amikacin should be reserved for infections with proven aminoglycoside resistance to delay the emergence of amikacin-resistant organisms.
156
What caution should be exercised when using amikacin in combination with other drugs?
Caution should be exercised when using amikacin with other ototoxic or nephrotoxic drugs due to its potential kidney and inner ear toxicity.
157
What is the therapeutic goal of aminoglycoside treatment?
The therapeutic goal is to treat serious infections caused by gram-negative aerobic bacilli.
158
What baseline data should be collected before starting aminoglycoside therapy?
Blood and/or urine cultures should be obtained.
159
What aspects of aminoglycoside therapy should be monitored?
Aminoglycoside levels (peaks and troughs) and renal function should be monitored.
160
In which patient populations should aminoglycosides be used with caution?
Aminoglycosides should be used cautiously in patients with renal impairment, preexisting hearing impairment, and those receiving ototoxic and nephrotoxic drugs.
161
How should therapeutic effects of aminoglycoside treatment be evaluated?
Patients should be monitored for indications of antimicrobial effects, such as a reduction in fever, pain, or inflammation.
162
What precautions should be taken to minimize adverse effects of aminoglycosides?
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.
163
What is the potential outcome if interstitial fibrosis or renal tubular necrosis develops during aminoglycoside treatment?
Kidney damage may be permanent if interstitial fibrosis or renal tubular necrosis develops.
164
What is the primary mode of action of the drugs discussed in this chapter?
The primary mode of action of the drugs discussed in this chapter is inhibiting bacterial protein synthesis.
165
How do the drugs discussed in this chapter differ from aminoglycosides in terms of their bacteriostatic or bactericidal effects?
Unlike aminoglycosides, these drugs are largely bacteriostatic, meaning they suppress bacterial growth but do not produce outright bacterial kill.
166
When are the drugs discussed in this chapter typically used in clinical practice?
These drugs are considered second-line agents and are primarily used for infections that are resistant to first-line agents.
167
What are tetracyclines primarily used for in systemic therapy?
Tetracyclines are broad-spectrum antibiotics used for systemic therapy.
168
How many tetracyclines are available for systemic use in the United States, and what are their names?
There are seven tetracyclines available in the U.S.: tetracycline, demeclocycline, doxycycline, eravacycline, omadacycline, sarecycline, and minocycline.
169
What are the main similarities among the tetracyclines, and what distinguishes them from each other?
The tetracyclines share similarities in structure, antimicrobial actions, and adverse effects. Their main differences are in pharmacokinetics.
170
How are the tetracyclines discussed in this context?
Tetracyclines are discussed as a group due to their pronounced similarities, rather than focusing on a single prototype.
171
How do tetracyclines inhibit bacterial growth?
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.
172
What is the bacteriostatic nature of tetracyclines at clinically achieved concentrations?
Tetracyclines are bacteriostatic, meaning they suppress bacterial growth without causing bacterial death when present at clinically achieved concentrations.
173
What accounts for the selective toxicity of tetracyclines?
Tetracyclines' selective toxicity results from their limited ability to cross mammalian cell membranes, allowing them to affect bacterial cells but not mammalian cells.
174
How do tetracyclines enter bacterial cells, and why is this significant for their mechanism of action?
Tetracyclines enter bacterial cells through an energy-dependent transport system, essential for them to access the bacterial cell interior and influence protein synthesis.
175
Why do tetracyclines not harm mammalian cells despite their ability to inhibit protein synthesis?
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.
176
Are tetracyclines narrow- or broad-spectrum antibiotics?
Tetracyclines are broad-spectrum antibiotics.
177
Which types of bacteria are tetracyclines effective against?
Tetracyclines are effective against a wide range of bacteria, including both gram-positive and gram-negative species.
178
Can you name some sensitive organisms that respond well to tetracycline treatment?
Sensitive organisms to tetracyclines include Rickettsia, spirochetes, Brucella, Chlamydia, Mycoplasma, Helicobacter pylori, Borrelia burgdorferi, Bacillus anthracis, and Vibrio cholerae.
179
What has extensive use of tetracyclines led to?
Extensive use of tetracyclines has led to increased bacterial resistance.
180
Why are tetracyclines rarely the first choice of antibiotics today?
Tetracyclines are rarely the first choice of antibiotics due to resistance and the availability of more selective and less toxic alternatives.
181
In which disorders are tetracyclines still used as first-line treatments?
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.
182
How are tetracyclines used to treat severe acne vulgaris?
Tetracyclines are used both topically and orally for treating severe acne vulgaris.
183
What is the mechanism of action of tetracyclines in acne treatment?
Tetracyclines suppress the growth and metabolic activity of Propionibacterium acnes, an organism that secretes inflammatory chemicals.
184
What makes the use of oral tetracyclines for acne treatment advantageous?
Oral doses of tetracyclines for acne are relatively low, resulting in minimal adverse effects.
185
Where can further details about acne treatment be found?
Further details about acne treatment can be found in Chapter 88.
186
What is the role of Helicobacter pylori (H. pylori) in peptic ulcer disease?
H. pylori is a bacterium in the stomach and is a major contributing factor to peptic ulcer disease.
187
What is the recommended treatment for eradicating H. pylori in peptic ulcer disease?
Tetracyclines, in combination with metronidazole and bismuth subsalicylate, are a treatment of choice for eradicating H. pylori.
188
Where can you find more information about the involvement of H. pylori in ulcer formation?
The role of H. pylori in ulcer formation is discussed in Chapter 64.
189
How are doxycycline and minocycline used in the context of periodontal disease treatment?
Doxycycline and minocycline are employed for the treatment of periodontal disease.
190
What are the routes of administration for doxycycline in periodontal disease treatment?
Doxycycline is administered both orally and topically for periodontal disease.
191
How is minocycline applied in the management of periodontal disease?
Minocycline is exclusively applied topically for periodontal disease treatment.
192
How does oral doxycycline contribute to the treatment of periodontal disease?
Oral doxycycline aids in the treatment of periodontal disease by inhibiting collagenase, an enzyme responsible for breaking down gum tissue.
193
What is the typical dosage of oral doxycycline used for the treatment of periodontal disease?
The usual dosage of oral doxycycline for periodontal disease treatment is 20 mg taken twice daily.
194
Is the low dose of oral doxycycline used for periodontal disease treatment harmful to bacteria?
The low doses of oral doxycycline, commonly 20 mg twice daily, are not sufficient to harm bacteria.
195
How are topical minocycline and doxycycline used in the treatment of periodontitis?
Topical minocycline and doxycycline are employed as adjunct treatments alongside scaling and root planing in adults with periodontitis.
196
What is the primary objective of using topical antibiotics like minocycline and doxycycline in periodontal disease?
The main goal is to reduce pocket depth and bleeding associated with periodontal disease.
197
How do these topical antibiotics provide benefits in the treatment of periodontitis?
Benefits are achieved by inhibiting bacterial growth at the specific site of periodontal disease.
198
Where are these topical antibiotics applied within the oral cavity?
These antibiotics are applied directly to the affected area within the oral cavity.
199
What are the significant differences among individual tetracyclines in terms of pharmacokinetic properties?
Differences include half-life, route of elimination, and interactions with food.
200
Why are variations in the pharmacokinetics of tetracyclines important for medical practice?
Variations in the pharmacokinetics of tetracyclines are crucial for determining dosing and administration strategies for specific patients and treatment goals.
201
How can the choice of a particular tetracycline be influenced by its pharmacokinetic properties?
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.
202
What are the key pharmacokinetic properties that vary among different tetracyclines?
These properties include lipid solubility, oral dose absorption, the effect of food on absorption, route of elimination, and half-life.
203
Which tetracyclines are considered short-acting, and what are their characteristics in terms of lipid solubility, oral dose absorption, and elimination?
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.
204
What are the features of intermediate-acting tetracyclines, and which tetracyclines fall into this category?
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.
205
Which tetracyclines are classified as long-acting, and what sets them apart in terms of their pharmacokinetic properties?
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.
206
What should patients avoid taking with tetracyclines to prevent potential drug interactions?
Patients should avoid taking calcium supplements, milk products, iron supplements, magnesium-containing laxatives, and most antacids in combination with tetracyclines.
207
Do tetracyclines have good distribution in the body?
Yes, tetracyclines are widely distributed to various tissues and body fluids.
208
Are tetracyclines effective for treating meningeal infections?
No, their poor penetration into the cerebrospinal fluid limits their utility for this purpose.
209
Can tetracyclines cross the placenta and enter the fetal circulation?
Yes, tetracyclines can readily cross the placenta and enter the fetal circulation.
210
What are common gastrointestinal side effects associated with oral tetracycline therapy?
Common GI side effects include epigastric burning, cramps, nausea, vomiting, and diarrhea.
211
How can the GI irritation caused by tetracyclines be reduced?
Taking tetracyclines with meals can help reduce GI irritation, but it may decrease absorption.
212
What is the potential risk of taking tetracyclines at bedtime?
Taking tetracyclines at bedtime can occasionally lead to esophageal ulceration.
213
Why is it important to determine the cause of diarrhea in patients on tetracycline therapy?
Diarrhea may result from superinfection of the bowel, so determining the cause is essential.
214
How do tetracyclines affect tooth development?
Tetracyclines can bind to calcium in developing teeth, causing yellow or brown discoloration and potential enamel hypoplasia.
215
What factors influence the intensity of tooth discoloration caused by tetracyclines?
The intensity of tooth discoloration is related to the total cumulative dose, and staining is darker with prolonged and repeated treatment.
216
Can tetracycline use during pregnancy affect the baby's teeth?
Yes, when taken by a pregnant woman after the fourth month of gestation, tetracyclines can cause staining of the infant's deciduous teeth.
217
When does permanent tooth discoloration occur with tetracycline use, and who is at risk?
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.
218
Is there a tetracycline that may have a lower risk of tooth discoloration?
Yes, doxycycline may have a lower risk of tooth discoloration compared to other tetracyclines.
219
How does tetracycline use during pregnancy affect premature infants?
Tetracyclines taken by a pregnant woman can temporarily suppress the growth of long bones in premature infants, but this effect is reversible upon discontinuation.
220
What is superinfection?
Superinfection is the overgrowth of drug-resistant microbes that occurs when drug-sensitive organisms are suppressed.
221
How does the broad-spectrum nature of tetracyclines affect the risk of superinfection compared to narrower-spectrum antibiotics?
Tetracyclines, as broad-spectrum antibiotics, increase the risk of superinfection compared to antibiotics with a narrower spectrum.
222
What are the consequences of superinfection of the bowel, and which microbes can be involved?
Superinfection of the bowel can lead to severe diarrhea and life-threatening conditions. It may involve staphylococci or Clostridium difficile.
223
What is Clostridium difficile–associated diarrhea (CDAD), and what should patients do if they experience significant diarrhea?
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.
224
How should tetracyclines be managed if superinfection with staphylococci or C. difficile is diagnosed?
Tetracyclines should be discontinued immediately in cases of superinfection with staphylococci or C. difficile.
225
How is CDAD treated, and what are the components of its management?
CDAD is treated with oral vancomycin or metronidazole, along with vigorous fluid and electrolyte replacement.
226
What is superinfection with fungi, and what are common symptoms?
Superinfection with fungi, particularly Candida albicans, can occur in various body areas and result in symptoms such as itching and inflammatory lesions.
227
How can superinfection with Candida be managed when taking tetracyclines?
Superinfection with Candida can be managed by discontinuing tetracyclines or using antifungal therapy when discontinuation is not possible.
228
What is a potential hepatic (liver) side effect of tetracyclines?
Tetracyclines can lead to fatty infiltration of the liver, known as hepatotoxicity.
229
What are the clinical manifestations of hepatotoxicity caused by tetracyclines?
Hepatotoxicity may manifest with symptoms such as lethargy and jaundice.
230
In rare cases, how can hepatotoxicity from tetracyclines progress?
Rarely, hepatotoxicity may progress to massive liver failure.
231
Under what conditions is liver damage most likely to occur with tetracycline use?
Liver damage is most likely when tetracyclines are administered intravenously in high doses, exceeding 2 grams per day.
232
Who is at a particularly high risk of tetracycline-induced liver damage?
Pregnant and postpartum women with kidney disease are at an especially high risk for tetracycline-induced liver damage.
233
How can tetracyclines affect renal function in patients with preexisting kidney disease?
Tetracyclines can exacerbate renal impairment in patients with preexisting kidney disease.
234
Which tetracyclines are primarily eliminated by the kidneys?
Tetracycline and demeclocycline are mainly eliminated by the kidneys.
235
What should patients with renal impairment do regarding tetracycline and demeclocycline use?
Patients with renal impairment should avoid tetracycline and demeclocycline.
236
Which tetracyclines should be considered for patients with renal impairment who require treatment with a tetracycline?
For patients with renal impairment, doxycycline or minocycline should be chosen because these drugs are primarily eliminated by the liver.
237
How do tetracyclines affect the skin's response to ultraviolet (UV) light from the sun?
Tetracyclines can increase the skin's sensitivity to UV light, making it more prone to sunburn.
238
What precautions should patients taking tetracyclines follow regarding sun exposure?
Patients should avoid prolonged sun exposure, wear protective clothing like hats and long sleeves, and use sunscreen on exposed skin when outdoors.
239
What can tetracyclines form with certain metal ions, and which ions are involved?
Tetracyclines can form nonabsorbable chelates with metal ions, including calcium, iron, magnesium, aluminum, and zinc.
240
Which substances contain the metal ions that can interfere with tetracycline absorption?
Substances like milk products, calcium supplements, iron supplements, magnesium-containing laxatives, and most antacids contain these interfering metal ions.
241
How should tetracyclines be administered to minimize interference with absorption when taken with chelating agents?
Tetracyclines should be taken at least 1 hour before or 2 hours after ingesting chelating agents to reduce absorption interference.
242
How can tetracyclines affect digoxin levels in the body?
Tetracyclines can increase digoxin levels by enhancing its absorption in the gastrointestinal tract.
243
What impact can tetracyclines have on international normalized ratio (INR) levels?
Tetracyclines can alter INR levels by affecting the vitamin K-producing flora in the gut.
244
What is the recommended course of action for patients taking digoxin or warfarin when prescribed tetracyclines?
Patients on digoxin or warfarin should undergo careful drug level monitoring to ensure proper dosing and prevent potential adverse effects.
245
What is the dosing interval for short-acting tetracycline (Tetracycline), and what is the usual adult daily dose?
Tetracycline is taken every 6 hours, with a usual adult daily dose of 1000-2000 mg.
246
How often should intermediate-acting demeclocycline (Demeclocycline) be administered, and what is the adult dose?
Demeclocycline is taken every 12 hours with an adult dose of 600 mg.
247
What are the dosing intervals for long-acting doxycycline (Doxycycline), and what is the usual adult daily dose?
Doxycycline can be administered orally or intravenously every 24 hours with a usual adult daily dose of 100-200 mg.
248
What is the dosing interval for intravenous eravacycline (Xerava), and what is the adult dose?
Eravacycline is given intravenously every 12 hours with an adult dose of 1 mg/kg.
249
How often is minocycline (Minocin) administered, and what is the adult dose?
Minocycline can be taken orally or intravenously every 12 hours with an adult dose of 200 mg.
250
Describe the dosing interval and total daily dose for omadacycline (Nuzyra).
Omadacycline is administered orally and intravenously with a dosing interval of 24 hours and a daily dose of 300-450 mg for adults.
251
What is the dosing interval for sarecycline (Seysara), and what is the adult dose?
Sarecycline is taken orally every 24 hours, with adult doses ranging from 60-150 mg.
252
Why should tetracyclines not be used in children under 8 years?
Tetracyclines should not be used in children under 8 years because they may cause permanent discoloration of the teeth.
253
Why should tetracyclines be avoided during pregnancy?
Tetracyclines should be avoided during pregnancy because animal studies suggest potential fetal harm.
254
Why should breastfeeding women avoid tetracyclines?
Breastfeeding women should avoid tetracyclines to prevent permanent staining during tooth development.
255
What is a care concern for older adults taking tetracyclines, especially when they are on multiple medications?
Older adults taking tetracyclines, especially when on multiple medications, should be monitored for drug interactions, including interactions with drugs like digoxin.
256
Why should patients with kidney disease avoid tetracyclines like tetracycline and demeclocycline?
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.
257
What side effect of tetracyclines can be prevented by withholding these drugs from pregnant women and children under 8 years?
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.
258
What should patients do if they experience diarrhea while taking tetracyclines?
Patients should notify their prescribers if they experience diarrhea while taking tetracyclines, as it may indicate a potentially life-threatening superinfection of the bowel.
259
In what population is high-dose intravenous tetracycline therapy associated with the risk of severe liver damage?
High-dose intravenous tetracycline therapy is associated with the risk of severe liver damage, particularly in pregnant and postpartum women with kidney disease.
260
What is the therapeutic goal of tetracycline therapy?
Tetracyclines are used to treat tetracycline-sensitive infections, acne, and periodontal disease.
261
Is monitoring required for tetracycline therapy, and if so, what should be monitored?
There is no specific monitoring recommended for tetracycline therapy.
262
Who are the high-risk patients for whom tetracyclines are contraindicated?
Tetracyclines are contraindicated in pregnant women and in children younger than 8 years.
263
How can the therapeutic effects of tetracyclines be evaluated?
The therapeutic effects can be evaluated by monitoring for reductions in fever, pain, or inflammation.
264
How can gastrointestinal distress be minimized in patients taking tetracyclines?
Gastrointestinal distress can be reduced by taking tetracyclines with meals.
265
What advice should be given to patients regarding sunlight exposure during tetracycline therapy?
Patients should be advised to avoid prolonged exposure to sunlight.
266
What type of antibacterial drug is nitrofurantoin?
Nitrofurantoin is a broad-spectrum antibacterial drug.
267
What effects does nitrofurantoin produce at low concentrations, and what effects at high concentrations?
Nitrofurantoin produces bacteriostatic effects at low concentrations and bactericidal effects at high concentrations.
268
Where are therapeutic levels of nitrofurantoin primarily achieved?
Therapeutic levels of nitrofurantoin are primarily achieved in urine.
269
How does nitrofurantoin damage bacteria?
Nitrofurantoin damages bacteria by injuring their DNA.
270
What is required for nitrofurantoin to damage DNA in bacteria?
Enzymatic conversion of nitrofurantoin to a reactive form is required for it to damage DNA in bacteria.
271
Why is nitrofurantoin selectively toxic to bacteria?
Nitrofurantoin is selectively toxic to bacteria because bacteria possess relatively higher levels of the enzyme needed for drug activation compared to mammalian cells.
272
What types of bacteria are susceptible to nitrofurantoin?
Nitrofurantoin is effective against both gram-positive and gram-negative bacteria.
273
Can you name some of the susceptible organisms to nitrofurantoin?
Susceptible organisms include staphylococci, streptococci, Neisseria species, Bacteroides species, and most strains of E. coli.
274
Do the sensitive bacteria tend to develop resistance to nitrofurantoin?
Sensitive bacteria rarely acquire resistance to nitrofurantoin.
275
Which bacterial species are frequently resistant to nitrofurantoin?
Organisms commonly resistant to nitrofurantoin include Proteus, Pseudomonas, Enterobacter, and Klebsiella species.
276
What is the therapeutic indication for nitrofurantoin?
Nitrofurantoin is indicated for the treatment of acute infections of the lower urinary tract.
277
What type of organisms should be responsible for the lower urinary tract infections treated with nitrofurantoin?
The infections must be caused by susceptible organisms.
278
Besides treatment, for what other purpose can nitrofurantoin be used in urinary tract infections?
Nitrofurantoin can be used for prophylaxis to prevent recurrent lower urinary tract infections.
279
Is nitrofurantoin recommended for infections of the upper urinary tract?
No, it is not recommended for treating infections of the upper urinary tract.
280
What are the different formulations of nitrofurantoin used for UTI treatment?
Nitrofurantoin is available as microcrystals (Furadantin), macrocrystals (Macrodantin), and monohydrate/macrocrystals (Macrobid).
281
What is the usual dosage range for nitrofurantoin in the treatment of UTIs?
The usual doses for nitrofurantoin in the treatment of UTIs range from 50-100 mg, taken multiple times a day.
282
For what purpose can nitrofurantoin be used at bedtime?
Nitrofurantoin is used for UTI prophylaxis, and a typical dose of 50-100 mg is taken at bedtime.
283
What is the recommended dosage of methenamine hippurate (Hiprex, Urex) for UTI prophylaxis or suppression?
Methenamine hippurate is available in 1-g tablets and is taken twice a day for UTI prophylaxis or suppression.
284
What are the most frequent adverse reactions to nitrofurantoin?
The most common adverse reactions to nitrofurantoin are gastrointestinal disturbances, including anorexia, nausea, vomiting, and diarrhea.
285
How can GI side effects of nitrofurantoin be minimized?
GI side effects of nitrofurantoin can be minimized by administering the drug with milk or meals.
286
What other approaches can be taken to reduce GI distress associated with nitrofurantoin?
Reducing the dosage or using the macrocrystalline formulations of nitrofurantoin may also help in reducing GI distress.
287
What are the two types of pulmonary reactions that nitrofurantoin can induce?
Nitrofurantoin can induce acute and subacute pulmonary reactions.
288
What are the typical symptoms of acute pulmonary reactions to nitrofurantoin?
Acute pulmonary reactions to nitrofurantoin include dyspnea, chest pain, chills, fever, cough, and alveolar infiltrates.
289
How long does it usually take for the symptoms of acute pulmonary reactions to resolve after discontinuing nitrofurantoin?
The symptoms of acute pulmonary reactions usually resolve within 2 to 4 days after discontinuing nitrofurantoin.
290
What is the suspected cause of acute pulmonary reactions to nitrofurantoin?
Acute pulmonary reactions to nitrofurantoin are believed to be hypersensitivity reactions.
291
What should patients with a history of acute pulmonary reactions to nitrofurantoin do regarding the use of the drug?
Patients with a history of acute pulmonary reactions to nitrofurantoin should avoid using the drug again.
292
What are subacute reactions to nitrofurantoin, and when do they typically occur?
Subacute reactions to nitrofurantoin are rare and occur during prolonged treatment. They may include symptoms like dyspnea, cough, and malaise.
293
How long does it usually take for the symptoms of subacute reactions to regress after discontinuing nitrofurantoin?
In most cases, symptoms of subacute reactions regress over several weeks to months after discontinuing nitrofurantoin.
294
What potential complication may arise in some patients with subacute reactions to nitrofurantoin?
Some patients with subacute reactions to nitrofurantoin may experience permanent lung damage.
295
What are some hematologic reactions that nitrofurantoin can cause?
Nitrofurantoin can cause hematologic reactions such as agranulocytosis, leukopenia, thrombocytopenia, and megaloblastic anemia.
296
In which individuals can hemolytic anemia occur as a result of nitrofurantoin use?
Hemolytic anemia due to nitrofurantoin can occur in infants and in individuals with an inherited deficiency in glucose-6-phosphate dehydrogenase (G6PD).
297
Why is nitrofurantoin contraindicated for pregnant women near term?
Nitrofurantoin is contraindicated for pregnant women near term (close to delivery) due to the potential risk of hemolytic anemia in newborns.
298
Why should nitrofurantoin be avoided in infants younger than 1 month?
Nitrofurantoin should be avoided in infants younger than 1 month because of the risk of hemolytic anemia associated with its use.
299
What kind of nerve damage can result from nitrofurantoin use?
Nitrofurantoin use can lead to damage to sensory and motor nerves, potentially causing demyelination and nerve degeneration.
300
What are some early symptoms of nerve damage associated with nitrofurantoin?
Early symptoms of nerve damage include muscle weakness, tingling sensations, and numbness.
301
What should patients be instructed to do if they experience symptoms of nerve damage while taking nitrofurantoin?
Patients should be instructed to report symptoms of nerve damage immediately.
302
In which patients is neuropathy (nerve damage) most likely to occur with nitrofurantoin use?
Neuropathy is most likely to occur in patients with renal impairment and in those taking nitrofurantoin chronically.
303
What rare but serious adverse effect can nitrofurantoin cause in the liver?
Nitrofurantoin can rarely cause severe liver injury, presenting as hepatitis, cholestatic jaundice, and hepatic necrosis.
304
What are the potential consequences of severe liver injury caused by nitrofurantoin?
Severe liver injury from nitrofurantoin use can be life-threatening and has led to fatalities.
305
What should patients using nitrofurantoin do to monitor for signs of liver injury?
Patients using nitrofurantoin should undergo periodic tests of liver function to monitor for signs of liver injury.
306
What action should be taken if a patient develops liver injury while taking nitrofurantoin?
If a patient develops liver injury while taking nitrofurantoin, the drug should be discontinued immediately, and it should never be used again.
307
What does conflicting evidence regarding nitrofurantoin use during pregnancy suggest?
Conflicting evidence regarding nitrofurantoin use during pregnancy raises uncertainty about its safety in pregnant women.
308
What did a 2009 study reveal regarding nitrofurantoin and birth defects during pregnancy?
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.
309
What did a 2013 study from Norway discover about nitrofurantoin use during pregnancy?
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.
310
Why is nitrofurantoin contraindicated in pregnant patients at term?
Nitrofurantoin is contraindicated in pregnant patients at term (38–42 weeks of gestation) due to the potential risk of hemolytic anemia.
311
What is the suggested approach for nitrofurantoin use during pregnancy in light of the conflicting evidence?
Given the conflicting evidence, until more conclusive information is available, using alternative antibiotics during pregnancy may be considered a prudent approach.
312
What antibiotics are recommended to treat infants with urinary tract infections (UTIs)?
Ampicillin and gentamicin are recommended for the treatment of UTIs in infants.
313
Why is nitrofurantoin contraindicated in infants less than one month of age?
Nitrofurantoin is contraindicated in infants less than one month of age due to safety concerns.
314
What additional considerations are important in infants with UTIs?
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.
315
Which ages are methenamine hippurate and methenamine mandelate approved for in children?
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.
316
How should urinary tract infections (UTIs) in pregnant women be managed?
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.
317
What precautions should breastfeeding women take when using fluoroquinolones?
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.
318
In which patient group should nitrofurantoin be avoided, especially if they have decreased renal function?
Nitrofurantoin should be avoided in older adults with decreased renal function.
319
What is the approved use for fosfomycin (Monurol)?
Fosfomycin is approved for single-dose therapy in women with uncomplicated urinary tract infections (acute cystitis) caused by E. coli or E. faecalis.
320
How does fosfomycin work to kill bacteria?
Fosfomycin kills bacteria by disrupting the synthesis of peptidoglycan polymer strands, which form the bacterial cell wall.
321
What are the common adverse effects associated with fosfomycin?
Common adverse effects of fosfomycin include diarrhea, headache, vaginitis, nausea, abdominal pain, rhinitis, drowsiness, dizziness, and rash.
322
Is it necessary to take fosfomycin with food?
Fosfomycin dosing may be done with or without food.
323
When should improvement in cystitis symptoms be expected after taking fosfomycin?
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.
