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Terms in this set (151)

A. Trimethoprim-sulfamethoxazole

Rationale:
The patient's initial severe purulent SSTI was managed by daptomycin and I&D. Culture results from the initial I&D of the infected site returned positive for methicillin-resistant Staphylococcus aureus (the pathogen is resistant to the beta-lactam antibiotic cefazolin) with susceptibilities that can be used to guide therapeutic decision making. Trimethoprim-sulfamethoxazole would be the most appropriate choice for this patient because of his substantial clinical improvement since admission, the susceptibility of the isolated pathogen to the drug, and the need for oral therapy due to his history of injection drug use.

Although daptomycin was an appropriate choice for empiric treatment of this patient's severe purulent SSTI now known to be caused by methicillin-resistant Staphylococcus aureus (the pathogen is resistant to the beta-lactam antibiotic cefazolin), daptomycin is available only for parenteral administration. Although the patient appears to have responded to initial daptomycin therapy, it is not the best choice for him to use at home because of his history of injection drug use. An oral antibiotic, such as trimethoprim-sulfamethoxazole, is preferred.

Rifampin is available for oral administration, but it should not be used alone for the treatment of SSTIs caused by Staphylococcus aureus (S. aureus), regardless of the susceptibility test results. Rifampin use in patients with SSTIs should be reserved for cases involving S. aureus and prosthetic materials, such as joints, and the drug should be used only in combination with another active agent.

Linezolid is available for oral administration, and it is an appropriate choice for the treatment of a severe, purulent SSTI caused by methicillin-resistant Staphylococcus aureus (the pathogen is resistant to the beta-lactam antibiotic cefazolin). However, use of linezolid is contraindicated in this patient because of his use of sertraline for depression. The use of selective serotonin reuptake inhibitors, like sertraline, in combination with linezolid has been shown to increase the risk for serotonin syndrome, so it should be avoided if possible.
A. Amoxicillin-clavulanate 750 mg (amoxicillin component) orally every 12 hr x 10 days

Rationale:
Oral amoxicillin-clavulanate is the most appropriate therapy for this patient's acute otitis media (AOM). She received amoxicillin for AOM within the past 30 days, so it would not be prudent for her to receive this drug alone again. The dosage of amoxicillin-clavulanate is important because this 18-kg patient should receive 80-90 mg/kg/day of the amoxicillin component. A dosage of 750 mg (amoxicillin component) every 12 hours provides approximately 83 mg/kg/day. Finally, because she is only 1 year of age, the duration of therapy should be 10 days.

Oral amoxicillin-clavulanate is the most appropriate therapy for this patient's acute otitis media (AOM). The use of amoxicillin alone is not appropriate because this patient received the drug within the past 30 days, so the likelihood of an isolate growing that is resistant to amoxicillin is high.

Oral amoxicillin-clavulanate is the most appropriate therapy for this patient's acute otitis media (AOM). Oral cefdinir is indicated for initial immediate or delayed therapy for AOM, but it is reserved for patients with non-type 1 penicillin allergies. Because this patient has already received amoxicillin safely, there is no concern about an allergy.

Oral amoxicillin-clavulanate is the most appropriate therapy for this patient's acute otitis media (AOM). Intramuscular ceftriaxone is indicated for initial immediate or delayed therapy for AOM, but it is reserved for patients with non-type 1 penicillin allergies. Because this patient has already received amoxicillin safely, there is no concern about an allergy.
B. A 62-year-old woman who presents with a 2-week history of facial pressure, anosmia, and nasal congestion

Rationale:
Although this patient is immunocompromised by his HIV infection, immune compromise does not contribute to a diagnosis of ABRS. His symptoms of nasal congestion, facial pain, and cough reflect classic rhinosinusitis, none represent severe symptoms and have been present for only 5 days. Therefore, the likelihood of ABRS is not high in this patient.

According to the 2012 IDSA clinical practice guideline, diagnosis with bacterial rhinosinusitis requires meeting one of the following criteria: persistent symptoms of rhinosinusitis for >10 days without improvement OR onset of severe symptoms including fever >102°F, purulent nasal discharge, or facial pain lasting 3-4 days beyond the beginning of illness OR worsening of symptoms following initial onset and improvement after 5-6 days that include fever, headache, or increase in nasal discharge. This patient has been experiencing rhinosinusitis symptoms of facial pressure, anosmia, and nasal congestion for 14 days. Therefore, the likelihood of ABRS is high in this patient.

This patient's symptoms (cough and fever) have been present for only 2 days. Both of these symptoms represent minor symptoms for the diagnosis of sinusitis, have lasted only 2 days and could be caused by a number of other infectious diseases. Therefore, the likelihood of ABRS is not high in this patient.

Bronchopulmonary diseases (e.g., COPD) and recent hospitalization may predispose to a wide variety of infections, but these factors do not contribute to a diagnosis of ABRS. Although this patient has some major symptoms of ABRS, such as headache and purulent nasal discharge, she has been experiencing these symptoms for only the past 24 hours. Therefore, the likelihood of ABRS is not high in this patient.
D. Obtain a throat swab for a rapid antigen detection test (RADT) for GAS

Rationale:
Although a culture may be useful in the diagnosis of infectious diseases, the initial approach for diagnosing GAS pharyngitis involves a RADT. If there is high clinical suspicion for GAS pharyngitis, but the RADT is negative, obtaining a throat culture would be an appropriate next step due to the lower sensitivity of the RADT.

Although LL has classic GAS pharyngitis symptoms (rapid-onset sore throat and fever), clinical symptoms alone cannot be used to make the diagnosis of GAS (or other bacterial) pharyngitis. Clinical symptoms that are suggestive of a viral etiology for the pharyngitis in the absence of any symptoms suggestive of GAS disease may not require any testing at all.

There is no urine antigen test approved for diagnosing GAS pharyngitis, although urinary antigen testing for Streptococcus pneumoniae (which can cause a variety of other upper and lower respiratory tract infections) is available.

Any patient who presents with symptoms suggesting acute pharyngitis that are not consistent with a viral origin should be tested for GAS using a RADT. This patient's age of 12 years, rapid-onset sore throat, and fever are consistent with GAS pharyngitis, but a diagnosis cannot be made on based clinical symptoms alone and requires the use of a RADT. This testing is more than 95% sensitive for GAS, and results take 24-48 hours less time than a throat culture. Therefore, obtaining a throat swab for a RADT for GAS is the best choice to confirm a diagnosis of GAS pharyngitis in LL.
D. Ceftriaxone + doxycycline

Rationale:
Use of a fluoroquinolone in conjunction with amiodarone is contraindicated because of the potential for prolongation of the QTc interval. Therefore, cefuroxime plus levofloxacin is not appropriate for this patient who takes amiodarone for atrial fibrillation.

Use of a fluoroquinolone in conjunction with amiodarone is contraindicated because of the potential for prolongation of the QTc interval. Therefore, moxifloxacin is not appropriate for this patient who takes amiodarone for atrial fibrillation.

Use of a macrolide antibiotic in conjunction with amiodarone is contraindicated because of the potential for prolongation of the QTc interval. Therefore, this patient should not receive azithromycin because he takes amiodarone for atrial fibrillation. Additionally, this patient does not present with any specific risk factors for methicillin-resistant Staphylococcus aureus (MRSA), so the use of linezolid for its anti-MRSA activity is not warranted.

The combination of an antipneumococcal beta-lactam antibiotic plus a macrolide antibiotic or a respiratory fluoroquinolone alone is appropriate for treating CAP in patients hospitalized in a non-intensive care unit. Empiric coverage for Streptococcus pneumoniae, Haemophilus influenzae, and atypical pathogens is needed in patients with suspected CAP. This patient has a history of atrial fibrillation for which he takes amiodarone and presents with a rapid, racing heart, so drugs that can prolong the QTc interval (e.g., fluoroquinolones, macrolide antibiotics) should be avoided. Therefore, the use of theanti-pneumococcal beta-lactam antibiotic ceftriaxone plus the tetracycline doxycycline is appropriate to provide the necessary antimicrobial coverage without prolonging the QTc interval in this patient.
A 72-year-old man presents to the emergency department complaining of abdominal pain, cramping, and profuse, watery diarrhea that slowly worsened over the past week. He completed a course of ciprofloxacin for a urinary tract infection (UTI) 3 weeks ago. The patient is admitted to the hospital, and a stool sample is sent to the lab. Results of a stool Clostridioides difficile (C. difficile) toxin assay and glutamate dehydrogenase (GDH) test are positive. He is given fluids and started on oral vancomycin. The patient is discharged after 4 days and completes a 10-day course of vancomycin therapy with full resolution of his initial gastrointestinal signs and symptoms. Two weeks after completing vancomycin therapy he again experiences a sudden onset of profuse, watery diarrhea. On return to the clinic, his stool C. difficile toxin assay again is positive. Other reported lab test results include a white blood cell (WBC) count of 14.1 x 103/mm3 and serum creatinine (SCr) of 1.2 mg/dL. Which of the following is the most appropriate management for this patient's ongoing diarrhea based on the 2017 clinical practice guidelines for C. difficile infection (CDI) from the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA)?

A. Fidaxomicin 200 mg orally twice daily x 10 days
B. Vancomycin 125 mg orally four times daily x 10 days
C. Metronidazole 500 mg orally three times daily and probiotics each day for 14 days
D. Vancomycin 500 mg orally four times daily and probiotics each day for 14 days
A. Fidaxomicin 200 mg orally twice daily x 10 days

Rationale:
The patient is experiencing his first recurrence of C. difficile infection (CDI) following his initial infection 3 weeks ago. According to the 2017 IDSA/SHEA clinical practice guidelines for CDI, in cases where vancomycin was used to treat the initial episode, a course of oral fidaxomicin for 10 days should be used to treat a first recurrence.

This patient is experiencing his first recurrence of C. difficile infection (CDI), so his treatment should not be the same as it was for the initial episode (oral vancomycin for 10 days), according to the 2017 IDSA/SHEA clinical practice guidelines for CDI. This is a change from previous CDI guidelines, which recommended use of the same regimen as was used initially for treatment of the first recurrence. If vancomycin was chosen for this patient, the only viable approach would be a prolonged tapered and pulsed oral regimen lasting 6 to 14 weeks.

The role of probiotics in treating C. difficile infection is not clearly established, and the IDSA/SHEA guidelines definitively state that there is no clear evidence to support the use of probiotics. In some instances, bloodstream infection has been reported after use of probiotics.

The role of probiotics in treating C. difficile infection is not clearly established, and the IDSA/SHEA guidelines definitively state that there is no clear evidence to support the use of probiotics. In some instances, bloodstream infection has been reported after use of probiotics.
B. Vancomycin 500 mg orally every 6 hr, metronidazole 500 mg IV every 8 hr, and rectal vancomycin 500 mg every 12 hr

Rationale:
This patient has a C. difficile infection (CDI) based on his symptoms (profuse diarrhea that has stopped, elevated WBC count, colonic inflammation, and ileus) as well as PCR testing that reveals C. difficile. This patient's episode would be classified as initial, fulminant based on the diagnosis of CDI and presence of ileus. Recommendations for treating initial episode, fulminant CDI include vancomycin 500 mg orally every 6 hours (vancomycin 125 mg orally every 6 hours is inappropriate because the dosage is too low). Metronidazole 500 mg IV every 8 hours and rectal vancomycin 500 mg every 12 hours should also be used because ileus is present and there is concern that vancomycin administered orally may not reach the site of infection in adequate concentrations..

This patient has a C. difficile infection (CDI) based on his symptoms (profuse diarrhea that has stopped, elevated WBC count, colonic inflammation, and ileus) as well as PCR testing that reveals C. difficle. This patient's episode would be classified as initial, fulminant based on the diagnosis of CDI and presence of ileus.
Recommendations for treating initial episode, fulminant CDI include vancomycin 500 mg orally every 6 hours. Metronidazole 500 mg IV every 8 hours and rectal vancomycin 500 mg every 12 hours should also be used because ileus is present and there is concern that vancomycin administered orally may not reach the site of infection in adequate concentrations.

This patient has a C. difficile infection (CDI) based on his symptoms (profuse diarrhea that has stopped, elevated WBC count, colonic inflammation, and ileus) as well as PCR testing that reveals C. difficile. This patient's episode would be classified as initial, fulminant based on the diagnosis of CDI and presence of ileus. Recommendations for treating initial episode, fulminant CDI include vancomycin 500 mg orally every 6 hours (vancomycin 125 mg orally every 6 hours is inappropriate because the dosage is too low). Metronidazole 500 mg IV every 8 hours and rectal vancomycin 500 mg every 12 hours should also be used because ileus is present and there is concern that vancomycin administered orally may not reach the site of infection in adequate concentrations.

This patient has a C. difficile infection (CDI) based on his symptoms (profuse diarrhea that has stopped, elevated WBC count, colonic inflammation, and ileus) as well as PCR testing that reveals C. difficile. This patient's episode would be classified as initial, fulminant based on the diagnosis of CDI and presence of ileus. Recommendations for treating initial episode, fulminant CDI include vancomycin 500 mg orally every 6 hours. Metronidazole 500 mg IV every 8 hours and rectal vancomycin 500 mg every 12 hours should also be used because ileus is present and there is concern that vancomycin administered orally may not reach the site of infection in adequate concentrations. Intravenous immunoglobulin is not recommended for management of CDI.
B. Double the dose every 2 weeks but only if symptoms of volume overload are absent

Rationale:
ß-blockers should be titrated very carefully in patients with heart failure with reduced ejection fraction. The fastest documented titration schedule (i.e., shortest interval between dosage adjustments) in clinical trials was every 2 weeks under very careful supervision. Guidelines do not suggest a more aggressive titration schedule than what was used in clinical trials. Therefore, doubling the b-blocker dose every day regardless of symptoms is inappropriate.

ß-blockers should be titrated very carefully in patients with heart failure with reduced ejection fraction, taking into consideration symptoms of volume overload. The fastest documented titration schedule (i.e., shortest interval between dosage adjustments) in clinical trials was every 2 weeks under very careful supervision. Guidelines do not suggest a more aggressive titration schedule than what was used in clinical trials. Doubling the dose every 2 weeks only if symptoms of volume overload are absent is appropriate.

ß-blockers should be titrated very carefully in patients with heart failure with reduced ejection fraction. The fastest documented titration schedule (i.e., shortest interval between dosage adjustments) in clinical trials was every 2 weeks under very careful supervision. Guidelines do not suggest a more aggressive titration schedule than what was used in clinical trials. Therefore, doubling the b-blocker dose every day is inappropriate even if symptoms of overload are absent.

ß-blockers should be titrated very carefully in patients with heart failure with reduced ejection fraction, taking into consideration symptoms of volume overload. The fastest documented titration schedule (i.e., shortest interval between dosage adjustments) in clinical trials was every 2 weeks under very careful supervision. Guidelines do not suggest a more aggressive titration schedule than what was used in clinical trials. There are no guideline recommendations for b-blocker dose titration based on heart rate > 70 beats per minute.
D. There are currently no medications shown to reduce mortality

Rationale:
There are currently no clinical trial data that have shown a survival benefit in patients with heart failure with preserved ejection fraction. The I-PRESERVE trial compared irbesartan versus placebo in patients with heart failure with preserved ejection fraction. Irbesartan did not reduce mortality compared with placebo. Similarly, candesartan did not reduce mortality compared with placebo in the CHARM-Preserved trial.β-blocker therapy has not shown a reduction in cardiovascular mortality in patients with heart failure with preserved ejection fraction

There are currently no clinical trial data that have shown a survival benefit in patients with heart failure with preserved ejection fraction. β-blocker therapy has not shown a reduction in cardiovascular mortality in patients with heart failure with preserved ejection fraction. The I-PRESERVE trial compared irbesartan versus placebo in patients with heart failure with preserved ejection fraction. Irbesartan did not reduce mortality compared with placebo. Similarly, candesartan did not reduce mortality compared with placebo in the CHARM-Preserved trial.

There are currently no clinical trial data that have shown a survival benefit in patients with heart failure with preserved ejection fraction. The I-PRESERVE trial compared irbesartan versus placebo in patients with heart failure with preserved ejection fraction. Irbesartan did not reduce mortality compared with placebo. Similarly, candesartan did not reduce mortality compared with placebo in the CHARM-Preserved trial. β-blocker therapy has not shown a reduction in cardiovascular mortality in patients with heart failure with preserved ejection fraction

There are currently no clinical trial data that have shown a survival benefit in patients with heart failure with preserved ejection fraction. The I-PRESERVE trial compared irbesartan versus placebo in patients with heart failure with preserved ejection fraction. Irbesartan did not reduce mortality compared with placebo. Similarly, candesartan did not reduce mortality compared with placebo in the CHARM-Preserved trial. β-blocker therapy has not shown a reduction in cardiovascular mortality in patients with heart failure with preserved ejection fraction
B. A 60-year-old male with heart failure with reduced ejection fraction (left ventricular ejection fraction 30%) receiving metoprolol succinate 200 mg daily, enalapril 10 mg twice daily, and spironolactone 25 mg daily, with a blood pressure of 110/70 mm Hg and heart rate of 85 beats per minute.

Rationale:
According to the 2017 ACC/AHA/HFSA guidelines, ivabradine can be beneficial for reducing heart failure hospitalization for patients with symptomatic (New York Heart Association class II-III) stable chronic heart failure with reduced ejection fraction (left ventricular ejection fraction ≤ 35%) who are receiving goal-directed evaluation and management, including a b-blocker at the maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 beats per minute or greater at rest. This patient is not yet receiving the target b-blocker dosage (200 mg daily for metoprolol succinate). A higher dosage of the b-blocker should be tried before considering ivabradine in this patient.

According to the 2017 ACC/AHA/HFSA guidelines, ivabradine can be beneficial for reducing heart failure hospitalization for patients with symptomatic (New York Heart Association class II-III) stable chronic heart failure with reduced ejection fraction (left ventricular ejection fraction ≤ 35%) who are receiving goal-directed evaluation and management, including a b-blocker at the maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 beats per minute or greater at rest. This 60-year-old male with heart failure with reduced ejection fraction (30%) receiving metoprolol succinate 200 mg daily (the target dosage), enalapril 10 mg twice daily, and spironolactone 25 mg daily, with a blood pressure of 110/70 mm Hg and HR 85 bpm is a candidate for ivabradine therapy.

According to the 2017 ACC/AHA/HFSA guidelines, ivabradine can be beneficial for reducing heart failure hospitalization for patients with symptomatic (New York Heart Association class II-III) stable chronic heart failure with reduced ejection fraction (left ventricular ejection fraction ≤ 35%) who are receiving goal-directed evaluation and management, including a b-blocker at the maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 beats per minute or greater at rest. Ivabradine is not appropriate for this patient because his heart rate (65 beats per minute) is less than 70 beats per minute.

According to the 2017 ACC/AHA/HFSA guidelines, ivabradine can be beneficial for reducing heart failure hospitalization for patients with symptomatic (New York Heart Association class II-III) stable chronic heart failure with reduced ejection fraction (left ventricular ejection fraction ≤ 35%) who are receiving goal-directed evaluation and management, including a b-blocker at the maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 beats per minute or greater at rest. Ivabradine is not appropriate for this patient because he has permanent atrial fibrillation and is not in sinus rhythm. In a clinical trial known as SHIFT of patients with heart failure with reduced ejection fraction, ivabradine was associated with a higher incidence of atrial fibrillation than placebo.
B. Insulin glargine 10 units subcutaneously every evening

Rationale:
Insulin should be initiated if symptoms of hyperglycemia are present (e.g., polyuria, polydipsia), which is the case for this patient. Adding the sodium glucose cotransporter-2 inhibitor canagliflozin probably would not be sufficient for this patient to reach her goal A1c of <7.0%.

Results of a meta-analysis suggest that each new class of noninsulin agent added to initial therapy generally lowers A1c by approximately 0.7-1.0%. Adding an additional oral medication probably would not be sufficient for this patient to reach her A1c goal of <7.0%. The addition of the basal insulin glargine is the best choice for this patient because it has the greatest potential to lower her A1c to goal. In addition, insulin should be initiated if symptoms of hyperglycemia are present (e.g., polyuria, polydipsia), which is the case for this patient.

Insulin should be initiated if symptoms of hyperglycemia are present (e.g., polyuria, polydipsia), which is the case in this patient. Adding the dipeptidyl peptidase 4 inhibitor (DPP-4i) sitagliptin probably would not be sufficient for this patient to reach her goal A1c of <7.0%. It also would be inappropriate for her to receive both a DPP-4i and the glucagon-like peptide 1 receptor agonist liraglutide.

Insulin should be initiated if symptoms of hyperglycemia are present (e.g., polyuria, polydipsia), which is the case in this patient. Adding the thiazolidinedione pioglitazone probably would not be sufficient for this patient to reach her goal A1c of <7.0%.
D. Empagliflozin 10 mg orally once daily

Rationale:
An agent with proven cardiovascular disease benefit (e.g., empagliflozin) is recommended as add-on therapy with metformin in patients with type 2 diabetes mellitus and established cardiovascular disease if the A1c is above target. Sitagliptin has not been shown to provide cardiovascular disease benefit in patients with type 2 diabetes mellitus and established cardiovascular disease. Therefore, it is not the best choice for CJ.

An agent with proven cardiovascular disease benefit (e.g., empagliflozin) is recommended as add-on therapy with metformin in patients with type 2 diabetes mellitus and established cardiovascular disease if the A1c is above target. Rosiglitazone has not been shown to provide cardiovascular disease benefit in patients with type 2 diabetes mellitus and established cardiovascular disease. Therefore, it is not the best choice for CJ.

An agent with proven cardiovascular disease benefit (e.g., empagliflozin) is recommended as add-on therapy with metformin in patients with type 2 diabetes mellitus and established cardiovascular disease if the A1c is above target. Glipizide has not been shown to provide cardiovascular disease benefit in patients with type 2 diabetes mellitus and established cardiovascular disease. Therefore, it is not the best choice for CJ.

An agent with proven cardiovascular disease benefit is recommended as add-on therapy with metformin in patients with type 2 diabetes mellitus and established cardiovascular disease if the A1c is above target. Adding empagliflozin is appropriate for reduction of cardiovascular mortality in adults like CJ with type 2 diabetes mellitus, atherosclerotic cardiovascular disease, and an elevated A1c (CJ's A1c of 8.8% is above his goal of <7.0%).
D. History of medical conditions

Rationale:
The 2015 ADA/EASD recommendations call for a less stringent A1c goal in patients with a history of severe hypoglycemia, long duration of diabetes, limited life expectancy, advanced complications, extensive comorbid conditions, or difficulty attaining goals despite maximal combination therapy and counseling. In this case, a less strict A1c goal is appropriate due to the patient's history of established cardiovascular disease. She is not on any medications with a high risk for hypoglycemia, and no recent hypoglycemic events are reported.

The 2015 ADA/EASD recommendations call for a less stringent A1c goal in patients with a history of severe hypoglycemia, long duration of diabetes, limited life expectancy, advanced complications, extensive comorbid conditions, or difficulty attaining goals despite maximal combination therapy and counseling. In this case, a less strict A1c goal is appropriate due to the patient's history of established cardiovascular disease. The patient was diagnosed with diabetes only 4 years ago.

The 2015 ADA/EASD recommendations call for a less stringent A1c goal in patients with a history of severe hypoglycemia, long duration of diabetes, limited life expectancy, advanced complications, extensive comorbid conditions, or difficulty attaining goals despite maximal combination therapy and counseling. In this case, a less strict A1c goal is appropriate due to the patient's history of established cardiovascular disease. The American Diabetes Association does not support a less strict A1c goal solely based on a specific age.

The 2015 ADA/EASD recommendations call for a less stringent A1c goal in patients with a history of severe hypoglycemia, long duration of diabetes, limited life expectancy, advanced complications, extensive comorbid conditions, or difficulty attaining goals despite maximal combination therapy and counseling. In this case, a less strict A1c goal is appropriate due to the patient's history of established cardiovascular disease.
B. Insulin aspart before breakfast

Rationale:
The patient's reported fasting blood glucose (FBG) values over the last month (95-115 mg/dL) are well controlled based on the goal range of 80-130 mg/dL. Insulin glargine is a long-acting insulin that would decrease FBG, so this would not be the best medication to adjust.

The patient's reported fasting blood glucose (FBG) values over the last month (95-115 mg/dL) are well controlled based on the goal range of 80-130 mg/dL. Her 2-hour post-dinner plasma glucose readings (165-178 mg/dL) are also well controlled based on the goal range of <180 mg/dL. However, her reported pre-lunch plasma glucose readings (165-178 mg/dL) exceed 130 mg/dL, the upper limit of the recommended range. Insulin aspart is a rapid-acting analog. If given before breakfast, it primarily affects pre-lunch plasma glucose or 2-hour post-breakfast plasma glucose. Therefore, insulin aspart before breakfast should be addressed when modifying her diabetes drug regimen.

The patient's 2-hour post-dinner plasma glucose readings (165-178 mg/dL) are well controlled based on the goal range of <180 mg/dL. However, her reported pre-lunch plasma glucose readings (165-178 mg/dL) exceed 130 mg/dL, the upper limit of the recommended range. Insulin aspart is a rapid-acting analog. If given before lunch, it primarily affects pre-dinner plasma glucose or 2-hour post-lunch plasma glucose. If given before breakfast, it primarily affects pre-lunch plasma glucose or 2-hour post-breakfast plasma glucose. Based on the provided information, insulin aspart before breakfast should be addressed when modifying her diabetes drug regimen.

The patient's 2-hour post-dinner plasma glucose readings (165-178 mg/dL) are well controlled based on the goal range of <180 mg/dL. However, her reported pre-lunch plasma glucose readings (165-178 mg/dL) exceed 130 mg/dL, the upper limit of the recommended range. Insulin aspart is a rapid-acting analog. If given before dinner, it primarily affects bedtime plasma glucose or 2-hour post-dinner plasma glucose. If given before breakfast, it primarily affects pre-lunch plasma glucose or 2-hour post-breakfast plasma glucose. Based on the provided information, insulin aspart before breakfast should be addressed when modifying her diabetes drug regimen.
B. 8 units as IV bolus followed by 8 units/hr IV continuous insulin infusion

Rationale:
For diabetic ketoacidosis, regular insulin should be administered intravenously as 0.1 units/kg as IV bolus followed by 0.1 units/kg/hr IV continuous insulin infusion or as 0.14 units/kg/hr as IV continuous infusion without IV bolus per the American Diabetes Association. The patient weighs 176 pounds or 80 kg. Therefore, the appropriate regimen would be 8 units as IV bolus followed by 8 units/hr IV continuous insulin infusion or 11 units/hr as IV continuous insulin infusion without IV bolus.

For diabetic ketoacidosis, regular insulin should be administered intravenously as 0.1 units/kg as IV bolus followed by 0.1 units/kg/hr IV continuous insulin infusion or as 0.14 units/kg/hr as IV continuous infusion without IV bolus per the American Diabetes Association. The patient weighs 176 pounds or 80 kg. Therefore, the appropriate regimen would be 8 units as IV bolus followed by 8 units/hr IV continuous insulin infusion or 11 units/hr as IV continuous insulin infusion without IV bolus.

For diabetic ketoacidosis, regular insulin should be administered intravenously as 0.1 units/kg as IV bolus followed by 0.1 units/kg/hr IV continuous insulin infusion or as 0.14 units/kg/hr as IV continuous infusion without IV bolus per the American Diabetes Association. The patient weighs 176 pounds or 80 kg. Therefore, the appropriate regimen would be 8 units as IV bolus followed by 8 units/hr IV continuous insulin infusion or 11 units/hr as IV continuous insulin infusion without IV bolus.

For diabetic ketoacidosis, regular insulin should be administered intravenously as 0.1 units/kg as IV bolus followed by 0.1 units/kg/hr IV continuous insulin infusion or as 0.14 units/kg/hr as IV continuous infusion without IV bolus per the American Diabetes Association. The patient weighs 176 pounds or 80 kg. Therefore, the appropriate regimen would be 8 units as IV bolus followed by 8 units/hr IV continuous insulin infusion or 11 units/hr as IV continuous insulin infusion without IV bolus.
C. Increased risk of gastrointestinal bleeding

Rationale:
This answer is incorrect. This response makes the assumption that the drug interaction between amiodarone and warfarin would result in a decrease in the warfarin concentration, which would reduce the effectiveness of warfarin. As described in answer choice C below, the opposite is true - the concentration of warfarin would be increased, not decreased, when used in combination with amiodarone. As a side note, this drug interaction could potentially result in an increased risk of hemorrhagic stroke associated with an elevated warfarin concentration and INR, but not an ischemic stroke.

This response makes the assumption that this potential drug interaction would result in an increase in the amiodarone concentration, thereby increasing the risk for proarrhythmia. Warfarin is a substrate for shared CYP P450 isoenzymes with amiodarone, but it is not an inhibitor and does not adversely affect amiodarone exposure.

Amiodarone is a substrate for and potent inhibitor of several cytochrome (CYP) P450 isoenzymes, including CYP 2C9, 2D6, and 3A4. Warfarin is metabolized by CYP 1A2 (R-warfarin) and CYP 2C9 (S-warfarin). When these two medications are used in combination, amiodarone inhibits the metabolism of warfarin, resulting in an increased warfarin concentration, which would increase the prothrombin time/INR and thereby increase the risk for bleeding.

This response makes the assumption that this potential drug interaction would result in a decrease in the amiodarone concentration, thereby decreasing the efficacy of amiodarone and resulting in a break through or worsening of atrial fibrillation (i.e., rapid ventricular response). Warfarin is a substrate for shared CYP P450 isoenyzmes with amiodarone, but warfarin is not an inducer of these isoenzymes and does not adversely affect amiodarone exposure.
D. A 56 year-old female with a history of transient ischemic attack with atrial fibrillation that was discovered incidentally on routine ECG testing

Rationale:
Treatment guidelines recommend stroke risk stratification for each patient with atrial fibrillation. The recommended risk stratification tools is the CHADS2-VASc score, which assigns a risk score for a concomitant diagnosis of Congestive heart failure (1 point), Hypertension (1 point), Age greater than 75 years (2 points), Diabetes mellitus (1 point), Stroke, transient ischemic attack, or thromboembolism (2 points), Vascular disease (1 point), Age 65—74 years (1 point), and Sex category (i.e., female gender, 1 point). As the CHADS2-VASc score increases, the risk for stroke increases. Using this risk stratification tool, this patient's CHADS2 score is 2 (1 point for age 64—74 years and 1 point for hypertension), which is lower than that of the patient in answer choice D.

This patient's CHA2DS2-VASc score is 1 (1 point for female gender), which is lower than that of the patient in answer choice D.

This patient's CHA2DS2-VASc score is 1 (1 point for hypertension), which is lower than that of the patient in answer choice D.

As described in answer choice A above, this patient's CHA2DS2-VASc score is 3 (1 point for female gender and 2 points for prior transient ischemic attack), which is the highest score of all of the patients described in this question, thus placing this patient at the greatest risk for future stroke associated with atrial fibrillation.
A. Metoprolol

Rationale:
The beta-adrenergic receptor antagonists (beta-blockers), including metoprolol, are the most effective for rate control in patients with atrial fibrillation. Furthermore, this patient has a past medical history of coronary artery disease with recent myocardial infarction and heart failure, which are compelling indications for long-term use of a beta-blocker.

Non-dihydropyridine calcium channel antagonists (calcium channel blockers), such as diltiazem, may considered as a second-line treatment alternative to beta-blockers for rate control in atrial fibrillation for those patients who have not achieved adequate rate control with a beta-blocker or in those patients with compelling indications. In addition, the use of a non-dihydropyridine calcium channel blocker in a patient with a history of heart failure (as in this case) is generally not recommended due to potential worsening of the heart failure.

Digoxin can be used for rate control in atrial fibrillation, but due to the narrow therapeutic index of the drug, the significant toxicity profile, and other viable treatment options, digoxin is generally resigned to a last-line treatment alternative in atrial fibrillation.

Amiodarone is generally used for rhythm control in patients with atrial fibrillation, although it does possess beta-adrenergic receptor blockade and provides additional benefit for rate control. However, due to the significant toxicity and need for extensive monitoring associated with amiodarone, it is generally considered only as a last-line treatment option for rate control in those patients with atrial fibrillation in which other treatment options have failed.
A. Begin warfarin 5 mg daily

Rationale:
A determination of a patient's risk for stroke due to atrial fibrillation must first be completed to determine the appropriate stroke prevention treatment strategy. The recommended risk stratification tools is the CHA2DS2-VASc score, which assigns a risk score for a concomitant diagnosis of Congestive heart failure (1 point), Hypertension (1 point), Age greater than 75 years (2 points), Diabetes mellitus (1 point), Stroke, transient ischemic attack, or thromboembolism (2 points), Vascular disease (1 point), Age 65—74 years (1 point), and Sex category (i.e., female gender, 1 point). As the CHA2DS2-VASc score increases, the risk for stroke increases. Using this risk stratification tool, this patient's CHA2DS2-VASc score is 5 (1 for hypertension, 1 point for diabetes mellitus, 1 point for vascular disease, 1 point for age 65—74, and 1 point for female gender). The recommendation for stroke prevention is based upon the CHA2DS2-VASc risk score. Patients with a CHA2DS2-VASc risk score of 0 may receive no therapy; patients with a CHA2DS2-VASc risk score of 1 may receive either oral anticoagulation, aspirin, or no therapy; and patients with a CHA2DS2-VASc risk score of two or more should receive anticoagulation. This patient's CHA2DS2-VASc risk score is 5, placing her at increased risk for stroke, warranting the need for anticoagulation. Treatment guidelines recommend oral anticoagulation with warfarin, dabigatran, rivaroxaban, or apixaban for patients at high risk for stroke. Dabigatran and rivaroxaban should not be used in patients with a creatinine clearance less than 15 mL/min and/or receiving hemodialysis, which is applicable to this patient with a history of chronic renal insufficiency requiring hemodialysis. Therefore, warfarin would be the recommended anticoagulant in this patient, with a goal INR 2—3 and a target INR of 2.5.

As described above, this patient is at high risk for stroke associated with atrial fibrillation and should receive anticoagulation. Dabigatran is contraindicated in patients with a creatinine clearance less than 15 mL/min or those that require hemodialysis, which is applicable to this patient with a history of chronic renal insufficiency requiring hemodialysis. Therefore, dabigatran should not be used.

As described above, this patient is at high risk for stroke associated with atrial fibrillation and should receive anticoagulation. Rivaroxaban should not be used in patients with a creatinine clearance < 15 mL/min, which is applicable to this patient with a history of chronic renal insufficiency requiring dialysis.

Aspirin therapy alone for the prevention of stroke in patients with atrial fibrillation is limited only to those patients who are assessed to be at low risk for stroke (CHA2DS2-VASc score 0 or 1). As described above, this patient is at high risk for stroke and anticoagulation is recommended.
D. Delay cardioversion, and begin anticoagulation with dose-adjusted warfarin for three weeks prior to and four weeks after cardioversion

Rationale:
Cardioversion is associated with an increased risk for stroke in patients with atrial fibrillation. This risk greatly increases as the duration of atrial fibrillation increases. Therefore, prior to cardioversion, all patients with atrial fibrillation should be evaluated for the need for anticoagulation. The exact duration of atrial fibrillation in this patient is not known; the patient reports that he has experienced intermittent symptoms (palpitations, shortness of breath) for the past three weeks. It would be prudent to assume that the duration of atrial fibrillation in this patient is at least 3 weeks, which necessitates the use of anticoagulation prior to cardioversion, followed by at least 4 weeks of anticoagulation thereafter, provided the patient is stable. Based on the provided subjective complaints and vital signs, this patient is stable and cardioversion could be delayed.

As described above, the exact duration of atrial fibrillation in this patient is not known. The patient reports intermittent symptoms (palpitations, shortness of breath) for the past three weeks; it would be prudent to assume that the duration of atrial fibrillation in this patient is at least 3 weeks, which necessitates the use of anticoagulation prior to cardioversion. The duration of anticoagulation prior to cardioversion is dictated based on the patient's status. At this point, this patient is hemodynamically stable: the patient is not hypotensive (is hypertensive in fact), has a normal heart rate, and from the details of the case, does not appear to have an altered mental status or ischemic changes on the electrocardiogram (ECG). Because the patient is hemodynamically stable, emergent cardioversion is not needed. Because of this assessment combined with the risk of stroke associated with cardioversion, it would be prudent to delay cardioversion until the patient receives cardioversion for at least three weeks prior to cardioversion. If this delay is not desired, a transesophageal echocardiogram could be performed to evaluate for thrombus and to serve as a guide for the risk of stroke and to determine an optimal duration of anticoagulation.

As described above, the patient is hemodynamically stable and emergent cardioversion is not needed. Because of this assessment combined with the risk of stroke associated with cardioversion, it would be prudent to delay cardioversion until the patient receives cardioversion for at least three weeks prior to cardioversion. If this delay is not desired, a transesophageal echocardiogram could be performed to evaluate for thrombus and to serve as a guide for the risk of stroke and to determine an optimal duration of anticoagulation.

In a patient with a duration of atrial fibrillation greater than 48 hours or unknown, the preferred recommendation is to administer anticoagulation for at least 3 weeks prior to and for at least 4 weeks following cardioversion. This treatment strategy would reduce the risk of stroke associated with cardioversion, although the success of cardioversion does decrease as the duration of atrial fibrillation increases. Treatment options for anticoagulation prior to cardioversion include warfarin (INR 2—3), low molecular-weight heparin or unfractionated heparin at treatment doses, dabigatran, rivaroxaban, or apixaban. It is important to note that this recommendation only applies to patients in which a delay in cardioversion would be acceptable. In those patients in need of emergent cardioversion (e.g., hemodynamically unstable), anticoagulation should not delay cardioversion. Finally, as noted above, a transesophageal echocardiogram may be performed prior to cardioversion to evaluate for thrombus and to guide the duration of anticoagulation therapy.
D. Amiodarone

Rationale:
Amiodarone and sotalol are the preferred antiarrhythmic drugs for secondary prevention of ventricular arrhythmias. Currently, dofetilide is only indicated for the treatment of atrial arrhythmias, specifically atrial fibrillation and atrial flutter. Dofetilide is primarily excreted renally as the unchanged drug, which requires dose adjustment in patients with reduced creatinine clearance due to the risk for accumulation and subsequent toxicity, including proarrhythmias. Dofetilide is contraindicated in patients with a creatinine clearance less than 20 mL/min. Due to the potential for increased toxicity associated with decreased renal function in this patient and other suitable treatment alternatives that are preferred for prevention of ventricular arrhythmias, dofetilide is not the preferred treatment option for this patient.

Amiodarone and sotalol are the preferred antiarrhythmic drugs for secondary prevention of ventricular arrhythmias. Currently, dronedarone is only indicated in select patients for the treatment of atrial fibrillation. Due to a risk for increased mortality, dronedarone is contraindicated in patients with New York Heart Association (NYHA) functional Class IV heart failure or in patients with NYHA Class II-III heart failure with recent decompensation. Due to the potential for increased mortality associated with a concomitant diagnosis of heart failure in this patient and other suitable treatment alternatives, dronedarone is not the preferred treatment option in this patient.

Sotalol is one of the preferred antiarrhythmic drugs for secondary prevention of ventricular arrhythmias. Sotalol is primarily excreted renally as the unchanged drug, which requires dose adjustment in patients with reduced creatinine clearance due to the risk for drug accumulation and subsequent toxicity. Sotalol is a Class III antiarrhythmic drug, but also exhibits significant beta-adrenergic receptor blockade, which may be of particular concern related to the potential for heart failure exacerbation in this patient, particularly in the setting of drug accumulation. Due to this potential for increased toxicity associated with decreased renal function in this patient, and the presence of a suitable treatment alternative, sotalol would not be the preferred treatment option in this patient.

Amiodarone is one of the preferred antiarrhythmic drugs for secondary prevention of ventricular arrhythmias. Amiodarone is considered a safe treatment option for patients with heart failure, prior myocardial infarction, and in renal insufficiency. Amiodarone is metabolized by and is an inhibitor of several cytochrome (CYP) P450 isoenzymes, which dictates the need for monitoring for potential drug-drug interactions, particularly when used in combination with other cardiovascular medications. Amiodarone does have a significant adverse reaction profile, which requires appropriate monitoring with long-term therapy.
C. 115 g

Rationale:
In critically ill patients without renal disease, the recommended daily amount of protein is 1.2 g/kg - 2.0 g/kg, or about 95 g - 155 g for this 77-kg man. This patient is not obese, so his actual weight may be used for the protein calculation. Providing 70 g/day in the parenteral solution will provide 0.9 g/kg/d which is not within the recommended daily amount of protein range.

In critically ill patients without renal disease, the recommended daily amount of protein is 1.2 g/kg - 2.0 g/kg, or about 95 g - 155 g for this 77-kg man. This patient is not obese, so his actual weight may be used for the protein calculation. Providing 85g/day in the parenteral solution will provide 1.1 g/kg/d which is not within the recommended daily amount of protein range.

In critically ill patients without renal disease, the recommended daily amount of protein is 1.2 g/kg - 2.0 g/kg, or about 95 g - 155 g for this 77-kg man. This patient is not obese, so his actual weight may be used for the protein calculation. Providing 115 g/day in the parenteral solution will provide 1.5 g/kg/d which is within the recommended daily amount of protein range.

In critically ill patients without renal disease, the recommended daily amount of protein is 1.2 g/kg - 2.0 g/kg, or about 95 g - 155 g for this 77-kg man. This patient is not obese, so his actual weight may be used for the protein calculation. Providing 170 g/day in the parenteral solution will provide 2.2 g/kg/d which is within the recommended daily amount of protein range.
B. 1523

Rationale:
The calorie content of 1800 mL is calculated based on the percentage of amino acids (5.5%), dextrose (9%), and fat (3.2%) in the solution and the calorie content per g of each component (4 kcal/g amino acids, 3.4 kcal/g dextrose, and 10 kcal/g fat). The total calories amounts to 1523 based on the following calculations: Amino acids 5.5 g/100 mL x 1800 mL = 99 g 99 g x 4 kcal/g = 396 kcal; Dextrose 9 g/100 mL x 1800 mL = 162 g 162 g x 3.4 kcal/g = 551 kcal; Fat 3.2 g/100 mL x 1800 mL = 57.6 g 57.6 g x 10 kcal/g = 576 kcal; Total kcal: 396 + 551 + 576 = 1523 kcal.

The calorie content of 1800 mL is calculated based on the percentage of amino acids (5.5%), dextrose (9%), and fat (3.2%) in the solution and the calorie content per g of each component (4 kcal/g amino acids, 3.4 kcal/g dextrose, and 10 kcal/g fat). The total calories amounts to 1523 based on the following calculations: Amino acids 5.5 g/100 mL x 1800 mL = 99 g 99 g x 4 kcal/g = 396 kcal; Dextrose 9 g/100 mL x 1800 mL = 162 g 162 g x 3.4 kcal/g = 551 kcal; Fat 3.2 g/100 mL x 1800 mL = 57.6 g 57.6 g x 10 kcal/g = 576 kcal; Total kcal: 396 + 551 + 576 = 1523 kcal.

The calorie content of 1800 mL is calculated based on the percentage of amino acids (5.5%), dextrose (9%), and fat (3.2%) in the solution and the calorie content per g of each component (4 kcal/g amino acids, 3.4 kcal/g dextrose, and 10 kcal/g fat). The total calories amounts to 1523 based on the following calculations: Amino acids 5.5 g/100 mL x 1800 mL = 99 g 99 g x 4 kcal/g = 396 kcal; Dextrose 9 g/100 mL x 1800 mL = 162 g 162 g x 3.4 kcal/g = 551 kcal; Fat 3.2 g/100 mL x 1800 mL = 57.6 g 57.6 g x 10 kcal/g = 576 kcal; Total kcal: 396 + 551 + 576 = 1523 kcal.

The calorie content of 1800 mL is calculated based on the percentage of amino acids (5.5%), dextrose (9%), and fat (3.2%) in the solution and the calorie content per g of each component (4 kcal/g amino acids, 3.4 kcal/g dextrose, and 10 kcal/g fat). The total calories amounts to 1523 based on the following calculations: Amino acids 5.5 g/100 mL x 1800 mL = 99 g 99 g x 4 kcal/g = 396 kcal; Dextrose 9 g/100 mL x 1800 mL = 162 g 162 g x 3.4 kcal/g = 551 kcal; Fat 3.2 g/100 mL x 1800 mL = 57.6 g 57.6 g x 10 kcal/g = 576 kcal; Total kcal: 396 + 551 + 576 = 1523 kcal.
A. Intrinsic

Rationale:
This patient recently received a contrast dye for an imaging procedure, and contrast dye is a known toxin that causes direct damage to the renal tubules. Nonsteroidal anti-inflammatory drugs, such as meloxicam, and angiotensin converting-enzyme inhibitors, such as lisinopril, are also known nephrotoxins. Therefore, this patient probably has acute tubular necrosis. Additionally, the FENa > 2%, normal urine sodium, and presence of granular casts, WBC, and RBC are indicative of intrinsic AKI.

This patient has no evidence of dehydration, such as a blood urea nitrogen (BUN):SCr ratio > 20:1, reduced urine sodium, and reduced FENa. She recently received a contrast dye for an imaging procedure, and contrast dye is a known toxin that causes direct damage to the renal tubules. Nonsteroidal anti-inflammatory drugs, such as meloxicam, and angiotensin converting-enzyme inhibitors, such as lisinopril, are also known nephrotoxins. Therefore, this patient probably has acute tubular necrosis. Additionally, the FENa > 2%, normal urine sodium, and presence of granular casts, WBC, and RBC are indicative of intrinsic AKI.

This patient has no evidence of obstruction or anatomical concerns that would result in postrenal AKI. She recently received a contrast dye for an imaging procedure, and contrast dye is a known toxin that causes direct damage to the renal tubules. Nonsteroidal anti-inflammatory drugs, such as meloxicam, and angiotensin converting-enzyme inhibitors, such as lisinopril, are also known nephrotoxins. Therefore, this patient probably has acute tubular necrosis. Additionally, the FENa > 2%, normal urine sodium, and presence of granular casts, WBC, and RBC are indicative of intrinsic AKI.

This patient is not receiving any medications that would affect the serum creatinine value without altering her creatinine clearance and falsely indicating the presence of AKI. She recently received a contrast dye for an imaging procedure, and contrast dye is a known toxin that causes direct damage to the renal tubules. Nonsteroidal anti-inflammatory drugs, such as meloxicam, and angiotensin converting-enzyme inhibitors, such as lisinopril, are also known nephrotoxins. Therefore, this patient probably has acute tubular necrosis. Additionally, the FENa > 2%, normal urine sodium, and presence of granular casts, WBC, and RBC are indicative of intrinsic AKI.
C. SC darbepoetin alfa and oral ferrous sulfate

Rationale:
Anemia of chronic kidney disease is primarily due to a deficiency in erythropoietin production. This patient will require an erythropoiesis-stimulating agent (ESA) based on the severity of his symptoms and his low hemoglobin level. Based on this patient's low ferritin and transferrin saturation, he also has iron deficiency that is contributing to his anemia and will require treatment. Iron supplementation as monotherapy generally is not adequate to treat the anemia in patients with iron deficiency anemia and CKD.

This patient will require an erythropoiesis-stimulating agent (ESA) based on the severity of his symptoms and his low hemoglobin level. However, based on this patient's low ferritin and transferrin saturation, he also has iron deficiency that is contributing to his anemia and will require treatment. Therefore, ESA therapy alone is not adequate for this patient.

Anemia of chronic kidney disease is primarily due to a deficiency in erythropoietin production. This patient will require an erythropoiesis-stimulating agent (ESA) based on the severity of his symptoms and his low hemoglobin level. Based on this patient's low ferritin and transferrin saturation, he also has iron deficiency that is contributing to his anemia and will require treatment. Therefore, SC darbepoetin alfa and oral ferrous sulfate are appropriate for this patient.

Anemia of chronic kidney disease is primarily due to a deficiency in erythropoietin production. This patient will require an erythropoiesis-stimulating agent (ESA) based on the severity of his symptoms and his low hemoglobin level. Based on this patient's low ferritin and transferrin saturation, he also has iron deficiency that is contributing to his anemia and will require treatment. Iron dextran is available only for administration by the IV route, and this patient is not receiving dialysis. Therefore, he probably does not have IV access for administration of iron dextran. Furthermore, this patient has a history of anaphylaxis to multiple medications, so iron dextran is not preferred for supplementation because it is associated with a very high risk of anaphylaxis (more than other iron products).
D. Ferric citrate

Rationale:
The first line therapy for CKD-MBD is treatment of hyperphosphatemia using phosphate binders. This patient's corrected calcium is 10.3 mg/dL, which is at the high end of the normal range. The KDIGO guidelines recommend to minimize calcium-based phosphate binders in Stage 3-5 CKD to avoid hypercalcemia. Therefore, a non-calcium-based phosphate binder is appropriate to treat this patient's hyperphosphatemia. Non-calcium-based phosphate binders for non-dialysis patients include sevelamer, lanthanum carbonate, ferric citrate, and aluminum hydroxide. Because this patient has not yet tried (and failed) a safer non-calcium-based phosphate binder, the risks of using aluminum (especially neurotoxicity) outweigh the benefits. Ferric citrate is a better choice for this patient.

Vitamin D therapy would not be appropriate in this patient because his serum calcium and phosphorus are elevated. Active forms of vitamin D and vitamin D analogs are used when the PTH remains elevated despite use of phosphate binders and adequate nutritional vitamin D, and this patient has a nutritional vitamin D deficiency that needs to be addressed first. Therefore, active vitamin D (calcitriol) is not indicated in this patient.

The first-line therapy for CKD-MBD is treatment of hyperphosphatemia using phosphate binders. Calcimimetic agents are appropriate if the PTH remains elevated once the phosphorus is in the normal range. However, because the PTH and phosphorous both are elevated in this patient, a phosphate binder, such as ferric citrate, would be more appropriate than the calcimimetic agent etelcalcetide at this time.

The first line therapy for CKD-MBD is treatment of hyperphosphatemia using a phosphate binder. This patient's corrected calcium is 10.3 mg/dL, which is at the high end of the normal range. The KDIGO guidelines recommend to minimize calcium-based phosphate binders in Stage 3-5 CKD to avoid hypercalcemia. Therefore, a non-calcium-based phosphate binder is appropriate to treat this patient's hyperphosphatemia. Non-calcium-based phosphate binders for non-dialysis patients include sevelamer, lanthanum carbonate, ferric citrate, and aluminum hydroxide. Because this patient has not yet tried (and failed) a safer non-calcium-based phosphate binder, the risks of using aluminum (especially neurotoxicity) outweigh the benefits. Therefore, ferric citrate is the best choice for this patient.
B. Add metolazone 5 mg orally daily

Rationale:
Dialysis can be used for volume control but it is reserved for use after multiple diuretic strategies, including a loop diuretic plus a thiazide diuretic, have failed. This patient is experiencing fluid retention and decreased urine output despite taking a very high dose of a loop diuretic (bumetanide), which probably reflects diuretic resistance. Because she is clinically stable, adding the thiazide-like diuretic metolazone is a good choice to overcome the sodium reabsorption in the distal tubule associated with bumetanide and improve the response to the loop diuretic.

This patient is experiencing fluid retention and decreased urine output despite taking a very high dose of a loop diuretic (bumetanide), which probably reflects diuretic resistance. Because she is clinically stable, adding the thiazide-like diuretic metolazone is a good choice to overcome the sodium reabsorption in the distal tubule associated with bumetanide and improve the response to the loop diuretic.

Fluid restriction generally is not recommended to maintain sodium and water homeostasis in patients with CKD because dehydration increases the risk of acute kidney injury (due to intravascular volume depletion). More judicious diuretic use is preferred.

This patient is experiencing fluid retention and decreased urine output despite taking a very high dose of a loop diuretic (bumetanide), which probably reflects diuretic resistance. Increasing the loop diuretic dosage will not overcome this problem. Because she is clinically stable, adding the thiazide-like diuretic metolazone is a good choice to overcome the sodium reabsorption in the distal tubule associated with bumetanide and improve the response to the loop diuretic.
C. Biopsy of the prostate gland

Rationale:
RJ has asymptomatic bacteriuria. The only compelling reasons to treat a patient who has no symptoms, a negative urinalysis, and microbes isolated in the urine are if a patient is pregnant, or if there are plans to manipulate the genitourinary tract (e.g., biopsy the prostate gland). Treatment is recommended in pregnancy due to concern about the development of complications for the mother and fetus. Genitourinary tract instrumentation poses a risk for introducing organisms into the bloodstream during a procedure. Antimicrobial therapy is not warranted solely for removal of the urinary catheter.

RJ has asymptomatic bacteriuria. The only compelling reasons to treat a patient who has no symptoms, a negative urinalysis, and microbes isolated in the urine are if a patient is pregnant, or if there are plans to manipulate the genitourinary tract (e.g., biopsy the prostate gland). Treatment is recommended in pregnancy due to concern about the development of complications for the mother and fetus. Genitourinary tract instrumentation poses a risk for introducing organisms into the bloodstream during a procedure. Antimicrobial therapy is not warranted solely for insertion of a central line.

Biopsy of the prostate gland is a guideline-supported indication for antimicrobial therapy in patients with asymptomatic bacteriuria.

RJ has asymptomatic bacteriuria. The only compelling reasons to treat a patient who has no symptoms, a negative urinalysis, and microbes isolated in the urine are if a patient is pregnant, or if there are plans to manipulate the genitourinary tract (e.g., biopsy the prostate gland). Treatment is recommended in pregnancy due to concern about the development of complications for the mother and fetus. Genitourinary tract instrumentation poses a risk for introducing organisms into the bloodstream during a procedure. Antimicrobial therapy is not warranted solely for loss of medical supervision after hospital discharge.
A. Cefadroxil

Rationale:
This patient has a UTI that would be classified as complicated based on her comorbidities, including diabetes mellitus. The infection has most likely recurred due to levofloxacin failure (i.e., resistance). Cefadroxil may have a small effect on her INR, but not to the same extent as trimethoprim/sulfamethoxazole. Additionally, the patient's prior culture data suggest that the narrowest spectrum agent that is not a quinolone should be sufficient to treat the current infection. Therefore, cefadroxil is the best choice.

Nitrofurantoin is not a good choice because of the patient's compromised renal function (elevated serum creatinine of 2.3 mg/dL) since this drug depends on glomerular filtration to deliver therapeutic concentrations to the bladder.

Ciprofloxacin is not the best choice because it would not be prudent to use the drug after the use of levofloxacin. There is no information about whether the patient took the levofloxacin as prescribed but the drug appears to have failed, suggesting the development of resistance.

Trimethoprim/sulfamethoxazole is an appropriate empiric therapy, however, in this case it should be avoided because the patient's INR is stable on warfarin therapy and there is likely to be a significant drug interaction between this antibiotic and warfarin, particularly since a longer course of therapy is required for this patient's complicated UTI than for an uncomplicated UTI. Additionally, the patient's prior culture data suggest that the narrowest spectrum agent that is not a quinolone should be sufficient to treat the current infection. Therefore, trimethoprim/sulfamethoxazole is not the best choice.
B. Vancomycin 30 mg/kg IV daily in 2 equally divided doses

Rationale:
The majority of cases of infective endocarditis in injectable drug users are caused by coagulase-negative Staphylococcus species (CNS) or Staphylococcus aureus (S. aureus). Oxacillin is recommended for infective endocarditis caused by all Staphylococcus species but it would not provide coverage if beta-lactam antibiotic resistance is present, which is very common among CNS. Anti-staphylococcal beta-lactam antibiotics also do not provide coverage for methicillin-resistant S. aureus. Therefore, oxacillin is not a good choice for this patient.

Vancomycin is the most appropriate empiric therapy for pathogens commonly associated with infective endocarditis until susceptibilities are known at which time therapy should be reevaluated. Vancomycin is the best choice for this patient.

The majority of cases of infectious endocarditis in injectable drug users are caused by coagulase-negative Staphylococcus species (CNS) or Staphylococcus aureus (S. aureus). The addition of gentamicin to a beta-lactam antibiotic or vancomycin in patients with native valve endocarditis is no longer recommended in guidelines from the American Heart Association. Additionally, the combination of gentamicin and oxacillin would not provide coverage if beta-lactam antibiotic resistance is present, which is very common among CNS. Anti-staphylococcal beta-lactam antibiotics also do not provide coverage for methicillin-resistant S. aureus.

Ampicillin + gentamicin is recommended therapy for infective endocarditis caused by susceptible Enterococcus species but it would not provide coverage for penicillin-resistant pathogens, which are common. Therefore, this combination is not a good choice for this patient.
A. Ceftriaxone and vancomycin

Rationale:
Vancomycin plus a third-generation cephalosporin (cefotaxime or ceftriaxone) is recommended as a first-line therapy in the treatment of suspected bacterial meningitis. In this case, the reported penicillin allergy requires additional consideration. A delayed rash from childhood is not characteristic of a severe, type-I allergic reaction (e.g. angioedema or anaphylaxis) and does not preclude the use of a cephalosporin. Acute bacterial meningitis warrants prompt administration of antimicrobials and delays for penicillin skin testing and/or graded-dose challenges are not always feasible and would be impractical in this scenario when immediate treatment is warranted.

No data are available to support the use of ciprofloxacin for treatment of bacterial meningitis, and its use is not guideline-supported.

Chloramphenicol is a second-line agent for treatment of infection caused by both Neisseria meningitidis and Haemophilus Influenzae that can be combined with vancomycin to provide adequate coverage in adult patients with presumptive pathogen identification by pathogen Gram stain. In this case, first-line therapies are available to treat the patient empirically.

Trimethoprim/sulfamethoxazole is a second-line recommendation for patients with bacterial meningitis requiring coverage for Listeria monocytogenes (patients >50 years of age), but it does not have reliable activity against Neisseria meningitidis or Haemophilus Influenzae, which are common pathogens. WW is only 37 years old.
A. 1st CVP 8-12 mm Hg; 2nd MAP 65-90 mm Hg; 3rd ScvO2 >70%.

Rationale:
The hemodynamic goals and sequence used as early goal-directed therapy in the landmark study by Rivers et al were 1st CVP 8-12 mm Hg; 2nd MAP 65-90 mm Hg; and 3rd ScvO2 >70%. In-hospital mortality was significantly lower and organ dysfunction was less severe with this early goal-directed therapy compared with standard therapy.

The hemodynamic goals and sequence used as early goal-directed therapy in the landmark study by Rivers et al were 1st CVP 8-12 mm Hg; 2nd MAP 65-90 mm Hg; and 3rd ScvO2 >70%. In-hospital mortality was significantly lower and organ dysfunction was less severe with this early goal-directed therapy compared with standard therapy. The goals in answer #2 are correct, but the sequence is incorrect.

The hemodynamic goals and sequence used as early goal-directed therapy in the landmark study by Rivers et al were 1st CVP 8-12 mm Hg; 2nd MAP 65-90 mm Hg; and 3rd ScvO2 >70%. In-hospital mortality was significantly lower and organ dysfunction was less severe with this early goal-directed therapy compared with standard therapy. The goals in answer #3 are correct, but the sequence is incorrect.

The hemodynamic goals and sequence used as early goal-directed therapy in the landmark study by Rivers et al were 1st CVP 8-12 mm Hg; 2nd MAP 65-90 mm Hg; and 3rd ScvO2 >70%. In-hospital mortality was significantly lower and organ dysfunction was less severe with this early goal-directed therapy compared with standard therapy. The goals in answer #4 are correct, but the sequence is incorrect.
C. Suggest managing the BPH with an alpha-antagonist alone initially

Rationale:
Starting tadalafil alone is not appropriate because the PDE-5 inhibitor has been shown to provide benefit in patients with BPH only when used with an alpha antagonist. Because BPH can lead to ED, treating the BPH using an alpha-antagonist alone is a logical first step after which the need for ED should be reassessed. If the ED persists, adding tadalafil to the alpha-antagonist would be appropriate.

Improvement in International Prostate Symptom Score, which reflects a variety of lower urinary tract symptoms associated with BPH, has been reported from tadalafil therapy. However, tadalafil has been shown to provide benefit in patients with BPH only when used with an alpha antagonist. Because BPH can lead to ED, treating the BPH using an alpha-antagonist alone is a logical first step after which the need for ED should be reassessed. If the ED persists, adding tadalafil to the alpha-antagonist would be appropriate.

The PDE-5 inhibitor tadalafil has been shown to provide benefit in patients with BPH only when used with an alpha antagonist, and the combination did not affect the flow rate or the post void residual volume. Because BPH can lead to ED, treating the BPH using an alpha-antagonist alone is a logical first step after which the need for ED should be reassessed. If the ED persists, adding tadalafil to the alpha-antagonist would be appropriate.

The PDE-5 inhibitor tadalafil has been shown to provide benefit in patients with BPH only when used with an alpha antagonist, and the combination did not affect the flow rate or the post void residual volume. Because BPH can lead to ED, treating the BPH using an alpha-antagonist alone is a logical first step after which the need for ED should be reassessed. If the ED persists, adding tadalafil to the alpha-antagonist would be appropriate.
D. Defer ED treatment until after further CV treatment

Rationale:
The use of PDE-5 inhibitors, such as tadalafil, is not appropriate until GM's elevated blood pressure is treated and controlled so that he can undergo an exercise tolerance test demonstrating that use of these drugs and sexual activity are safe. His risk for cardiovascular events is elevated because he has type 2 diabetes, hyperlipidemia, and obesity as well as hypertension.

The use of PDE-5 inhibitors, such as vardenafil, is not appropriate until GM's elevated blood pressure is treated and controlled so that he can undergo an exercise tolerance test demonstrating that use of these drugs and sexual activity are safe. His risk for cardiovascular events is elevated because he has type 2 diabetes, hyperlipidemia, and obesity as well as hypertension.

Treatment for ED should be deferred until after GM's elevated blood pressure is treated and controlled, which is needed before he can undergo an exercise tolerance test to ensure that use of PDE-5 inhibitors and sexual activity are safe. His risk for cardiovascular events is elevated because he has type 2 diabetes, hyperlipidemia, and obesity as well as hypertension.

Treatment for ED should be deferred until after GM's elevated blood pressure is treated and controlled, which is needed before he can undergo an exercise tolerance test to ensure that use of PDE-5 inhibitors and sexual activity are safe. His risk for cardiovascular events is elevated because he has type 2 diabetes, hyperlipidemia, and obesity as well as hypertension.
C. Mammography annually beginning now without routine breast self-exams or clinical breast exams

Rationale:
The American Cancer Society (ACS) recommends annual mammograms for screening beginning at age 45 if a woman is at average risk for breast cancer and asymptomatic. The ACS does not recommend clinical breast examination for screening in women at average risk for breast cancer at any age. The ACS makes no recommendation about routine performance of or instruction of women about breast self-examination for cancer screening. Therefore, annual mammography beginning now without breast self-exams or clinical breast exams is appropriate for MG.

The American Cancer Society (ACS) recommends annual mammograms for screening beginning at age 45 if a woman is at average risk for breast cancer and asymptomatic. The ACS does not recommend clinical breast examination for screening in women at average risk for breast cancer at any age. The ACS makes no recommendation about routine performance of or instruction of women about breast self-examination for cancer screening. Therefore, annual mammography beginning now without breast self-exams or clinical breast exams is appropriate for MG.

The American Cancer Society (ACS) recommends annual mammograms for screening beginning at age 45 if a woman is at average risk for breast cancer and asymptomatic. The ACS does not recommend clinical breast examination for screening in women at average risk for breast cancer at any age. The ACS makes no recommendation about routine performance of or instruction of women about breast self-examination for cancer screening. Therefore, annual mammography beginning now without breast self-exams or clinical breast exams is appropriate for MG.

The American Cancer Society (ACS) recommends annual mammograms for screening beginning at age 45 if a woman is at average risk for breast cancer and asymptomatic. The ACS does not recommend clinical breast examination for screening in women at average risk for breast cancer at any age. The ACS makes no recommendation about routine performance of or instruction of women about breast self-examination for cancer screening. Therefore, annual mammography beginning now without breast self-exams or clinical breast exams is appropriate for MG.
B. Diet (plus dietary supplements if needed) consisting of 1200 mg/day of calcium and 800-1000 IU/day of vitamin D and bone mineral density testing since she is >65 years of age

Rationale:
The NOF recommends an intake of adequate amounts of calcium (1000 mg per day for men 50-70; 1200 mg per day for women 51 and older and men 71 and older) and vitamin D intake (800-1000 IU/day of cholecalciferol) primarily from the diet, with supplements if necessary. Bone mineral density testing is indicated in all women >65 years of age and men >70 years of age, regardless of clinical risk factors.

The NOF recommends an intake of adequate amounts of calcium (1000 mg per day for men 50-70; 1200 mg per day for women 51 and older and men 71 and older) and vitamin D intake (800-1000 IU/day of cholecalciferol) primarily from the diet, with supplements if necessary. Bone mineral density testing is indicated in all women >65 years of age and men >70 years of age, regardless of clinical risk factors.

The NOF recommends an intake of adequate amounts of calcium (1000 mg per day for men 50-70; 1200 mg per day for women 51 and older and men 71 and older) and vitamin D intake (800-1000 IU/day of cholecalciferol) primarily from the diet, with supplements if necessary. Bone mineral density testing is indicated in all women >65 years of age and men >70 years of age, regardless of clinical risk factors.

The NOF recommends an intake of adequate amounts of calcium (1000 mg per day for men 50-70; 1200 mg per day for women 51 and older and men 71 and older) and vitamin D intake (800-1000 IU/day of cholecalciferol) primarily from the diet, with supplements if necessary. Bone mineral density testing is indicated in all women >65 years of age and men >70 years of age, regardless of clinical risk factors.
A. Osteopenia of the hip and spine; pharmacologic treatment should be initiated

Rationale:
According in the World Health Organization, a T-score between -1.0 and -2.5 is classified as osteopenia and a T-score of -2.5 or lower is osteoporosis. Pharmacologic treatment should be initiated in postmenopausal women and men ≥ 50 years with osteopenia and a 10-year probability of a hip fracture ≥ 3% based on the U.S. adapted FRAX.® Pharmacotherapy should be initiated for this postmenopausal woman who has osteopenia of both the hip and spine and a high 10-year probability of hip fracture.

According in the World Health Organization, a T-score between -1.0 and -2.5 is classified as osteopenia and a T-score of -2.5 or lower is osteoporosis. Pharmacologic treatment should be initiated in postmenopausal women and men ≥ 50 years with osteopenia and a 10-year probability of a hip fracture ≥ 3% based on the U.S. adapted FRAX.® Pharmacotherapy should be initiated for this postmenopausal woman who has osteopenia of both the hip and spine and a high 10-year probability of hip fracture.

According in the World Health Organization, a T-score between -1.0 and -2.5 is classified as osteopenia and a T-score of -2.5 or lower is osteoporosis. Pharmacologic treatment should be initiated in postmenopausal women and men ≥ 50 years with osteopenia and a 10-year probability of a hip fracture ≥ 3% based on the U.S. adapted FRAX.® Pharmacotherapy should be initiated for this postmenopausal woman who has osteopenia of both the hip and spine and a high 10-year probability of hip fracture.

According in the World Health Organization, a T-score between -1.0 and -2.5 is classified as osteopenia and a T-score of -2.5 or lower is osteoporosis. Pharmacologic treatment should be initiated in postmenopausal women and men ≥ 50 years with osteopenia and a 10-year probability of a hip fracture ≥ 3% based on the U.S. adapted FRAX.® Pharmacotherapy should be initiated for this postmenopausal woman who has osteopenia of both the hip and spine and a high 10-year probability of hip fracture.
B. Ibandronate

Rationale:
Evidence is available demonstrating a reduction in hip and other nonvertebral fractures in women with postmenopausal osteoporosis from the use of alendronate, risedronate, and zoledronic acid, but not ibandronate. A reduction in vertebral fractures has been demonstrated from use of all four bisphosphonates in this patient population. FG has osteoporosis based on her femoral neck T-score of -2.6 but her bone mineral density is normal at the spine based on a T-score of -0.8. Therefore FG is at higher risk for a nonvertebral fracture than a vertebral fracture and alendronate, risedronate, and zoledronic acid would all be acceptable first-line options.

Evidence is available demonstrating a reduction in hip and other nonvertebral fractures in women with postmenopausal osteoporosis from the use of alendronate, risedronate, and zoledronic acid, but not ibandronate. A reduction in vertebral fractures has been demonstrated from use of all four bisphosphonates in this patient population. FG has osteoporosis based on her femoral neck T-score of -2.6 but her bone mineral density is normal at the spine based on a T-score of -0.8. Therefore FG is at higher risk for a nonvertebral fracture than a vertebral fracture and ibandronate would not be the best bisphosphonate option.

Evidence is available demonstrating a reduction in hip and other nonvertebral fractures in women with postmenopausal osteoporosis from the use of alendronate, risedronate, and zoledronic acid, but not ibandronate. A reduction in vertebral fractures has been demonstrated from use of all four bisphosphonates in this patient population. FG has osteoporosis based on her femoral neck T-score of -2.6 but her bone mineral density is normal at the spine based on a T-score of -0.8. Therefore FG is at higher risk for a nonvertebral fracture than a vertebral fracture and alendronate, risedronate, and zoledronic acid would all be acceptable first-line options.

Evidence is available demonstrating a reduction in hip and other nonvertebral fractures in women with postmenopausal osteoporosis from the use of alendronate, risedronate, and zoledronic acid, but not ibandronate. A reduction in vertebral fractures has been demonstrated from use of all four bisphosphonates in this patient population. FG has osteoporosis based on her femoral neck T-score of -2.6 but her bone mineral density is normal at the spine based on a T-score of -0.8. Therefore FG is at higher risk for a nonvertebral fracture than a vertebral fracture and alendronate, risedronate, and zoledronic acid would all be acceptable first-line options.
A. Depot medroxyprogesterone acetate

Rationale:
Depot medroxyprogesterone acetate (DMPA) has been associated with a loss in bone mineral density, although it has not been linked to an increase in the rate of fractures. Because this patient has several risk factors for osteoporotic fracture (small stature, high caffeine consumption, and vitamin D insufficiency), DMPA should be promptly excluded as a hormonal option for this patient.

Depot medroxyprogesterone acetate (DMPA) has been associated with a loss in bone mineral density, although it has not been linked to an increase in the rate of fractures. Because this patient has several risk factors for osteoporotic fracture (small stature, high caffeine consumption, and vitamin D insufficiency), DMPA should be promptly excluded as a hormonal option for this patient. The contraceptive transdermal patch is less of a concern for this patient.

Depot medroxyprogesterone acetate (DMPA) has been associated with a loss in bone mineral density, although it has not been linked to an increase in the rate of fractures. Because this patient has several risk factors for osteoporotic fracture (small stature, high caffeine consumption, and vitamin D insufficiency), DMPA should be promptly excluded as a hormonal option for this patient. The combined oral contraceptive is less of a concern for this patient.

Depot medroxyprogesterone acetate (DMPA) has been associated with a loss in bone mineral density, although it has not been linked to an increase in the rate of fractures. Because this patient has several risk factors for osteoporotic fracture (small stature, high caffeine consumption, and vitamin D insufficiency), DMPA should be promptly excluded as a hormonal option for this patient. The levonorgestrel-releasing intrauterine device is less of a concern for this patient.
B. Discontinue atorvastatin

Rationale:
An increased risk of teratogenic effects has not been observed following maternal use of acetaminophen during pregnancy. The use of acetaminophen in recommended doses is not associated with an increased risk of miscarriage or still birth.

HMG-CoA reductase inhibitors (statins) are contraindicated in pregnancy due to evidence of fetal abnormalities. If treatment of dyslipidemias is needed in pregnant women or in women of reproductive age, other agents are preferred. The discontinuation of lipid lowering medications temporarily during planned conception and pregnancy is not expected to have significant impact on long-term outcomes of primary hypercholesterolemia treatment. It would be prudent to discontinue atorvastatin today given JH's plan to conceive soon and reassess need for future treatment of her hyperlipidemia at future visits.

Intranasal corticosteroids are recommended for the treatment of rhinitis during pregnancy with the utilization of the lowest effective dose. If JH's allergic rhinitis is controlled, a dose reduction to one spray per nostril daily could be recommended.

Human data supports adverse effects to the fetus have been observed with systemic corticosteroids. However, no associations have been found with the very limited data evaluating topical corticosteroids in pregnancy. When topical corticosteroids are needed during pregnancy, low to mid potency preparations are recommended for the shortest time possible. JH is using a very low potency topical steroid and therefore the atorvastatin is more prudent to discontinue today. If JH becomes pregnant, her eczema and hydrocortisone therapy should be reassessed.
D. Zolmitriptan intranasal for acute treatment; melatonin for prophylaxis

Rationale:
This patient probably is suffering from cluster headaches based on his clinical presentation. Prophylactic therapy is indicated upon diagnosis of cluster headaches, and verapamil is considered an appropriate prophylactic choice. Although the triptans are first-line options for the management of cluster headaches, the oral formulations are not considered preferred therapy due to their delayed onset of action. An intranasal triptan, such as zolmitriptan, is preferred.

This patient probably is suffering from cluster headaches based on his clinical presentation. Prophylactic therapy is indicated upon diagnosis of cluster headaches, and lithium (titrated to a concentration of 0.4-0.8 mEq/L) is considered an appropriate prophylactic choice. Ibuprofen could be tried for the treatment of cluster headaches, but it probably would not provide adequate pain relief because of the severity of the headaches. Additionally, enteral medications do not provide a sufficiently rapid onset of action, so they are not considered first-line therapies.

This patient probably is suffering from cluster headaches based on his clinical presentation. Acetaminophen could be tried for the treatment of cluster headaches, but it probably would not provide adequate pain relief because of the severity of the headaches. Additionally, enteral medications do not provide a sufficiently rapid onset of action, so they are not considered first-line therapies. Amitriptyline is considered a first-line prophylactic option for tension-type headaches, but currently available evidence is not sufficient to support its use for cluster headache prophylaxis.

This patient probably is suffering from cluster headaches based on his clinical presentation. Because of the severity of this headache disorder, treating the acute pain with a non-enteral formulation is recommended to hasten the onset of action. Zolmitriptan intranasal is considered an appropriate first-line choice for cluster headaches. Prophylactic therapy is indicated upon diagnosis of cluster headaches, and melatonin is considered an appropriate prophylactic agent.
D. Naproxen for acute treatment; mirtazapine for prophylaxis

Rationale:
This patient probably is suffering from tension-type headaches based on her clinical presentation. Amitriptyline is an appropriate prophylactic agent for tension-type headaches. However, triptans, such as sumatriptan, are not effective for the management of tension-type headaches.

This patient probably is suffering from tension-type headaches based on her clinical presentation. Continuing to recommend acetaminophen for acute headache treatment is not the best recommendation for this patient who has tried the drug without much success. Verapamil is indicated for cluster headache prophylaxis, but it does not currently have a role in tension-type headache prophylaxis.

This patient probably is suffering from tension-type headaches based on her clinical presentation. Metoprolol is an appropriate prophylactic agent for migraine headaches, and it may be an appropriate choice for tension-type headache prophylaxis. However, triptans, such as rizatriptan, are not effective for the acute management of tension-type headaches.

This patient probably is suffering from tension-type headaches based on her clinical presentation. Acetaminophen has not worked well for acute treatment to date, so a nonsteroidal anti-inflammatory drug, like naproxen, would be an appropriate first-line treatment alternative at this time. Prophylactic therapy may be indicated based on the frequency of her headaches, and mirtazapine is considered an appropriate prophylactic choice.
C. 6 hours

Rationale:
For patients who receive a 5-HT3 antagonist and droperidol as a part of triple therapy for PONV prophylaxis and subsequently experience PONV, the 5-HT3 antagonist and droperidol can be repeated for nausea and vomiting more than 6 hours after the surgery. However, if nausea and vomiting occurs 6 hours or less after the surgery, an antiemetic from a different class should be used instead.

For patients who receive a 5-HT3 antagonist and droperidol as a part of triple therapy for PONV prophylaxis and subsequently experience PONV, the 5-HT3 antagonist and droperidol can be repeated for nausea and vomiting more than 6 hours after the surgery. However, if nausea and vomiting occurs 6 hours or less after the surgery, an antiemetic from a different class should be used instead.

For patients who receive a 5-HT3 antagonist and droperidol as a part of triple therapy for PONV prophylaxis and subsequently experience PONV, the 5-HT3 antagonist and droperidol can be repeated for nausea and vomiting more than 6 hours after the surgery. However, if nausea and vomiting occurs 6 hours or less after the surgery, an antiemetic from a different class should be used instead.

For patients who receive a 5-HT3 antagonist and droperidol as a part of triple therapy for PONV prophylaxis and subsequently experience PONV, the 5-HT3 antagonist and droperidol can be repeated for nausea and vomiting more than 6 hours after the surgery. However, if nausea and vomiting occurs 6 hours or less after the surgery, an antiemetic from a different class should be used instead.