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A 33-year-old woman presents to her primary care physician with fever, malaise, and rash 3 weeks after returning from a weekend camping trip. She states the rash is painless but feels hot to the touch and has been gradually expanding since it first appeared on her stomach 2 weeks prior to the onset of her current symptoms. On examination, there is circumferential periumbilical erythema measuring approximately 5 cm in diameter with central clearing that is consistent with erythema migrans. Which of the following is the most appropriate therapeutic intervention at this time?
The most appropriate therapeutic intervention at this time is administration of oral doxycycline. Erythema migrans is a classic skin finding in early Lyme disease, a tick-borne illness caused by three Borrelia spirochete species, with B. burgdorferi the main causative pathogen in the United States. Lyme disease manifests clinically in three stages: early localized disease characterized by erythema migrans possibly with associated constitutional symptoms within 1 month of tick exposure, early disseminated disease characterized by multiple skin lesions and possible neurologic or cardiac findings, and late disease characterized by mono- or polyarthritis with potential neurologic manifestations such as encephalopathy or polyneuropathy. The standard treatment for early localized Lyme disease includes oral doxycycline 100 mg bid for 10–14 days, or amoxicillin 500 mg tid or cefuroxime axetil 500 mg bid each for 2–3 weeks. The facial palsy of early disseminated disease can be treated with doxycycline for 14–28 days. Doxycycline is also not contraindicated for early treatment of Lyme disease in pregnant women.
Administration of IV ceftriaxone (A) at a standard dose of 2 grams daily is used interchangeably with cefotaxime or penicillin G to treat acute cardiac and CNS manifestations in early disseminated Lyme disease, particularly when oral doxycycline cannot be tolerated. Other indications include neurological symptoms with associated abnormal cerebrospinal fluid (CSF) findings or parenchymal involvement such as encephalitis and cardiac symptoms, second- or third-degree atrioventricular (AV) block, or first-degree AV block with PR interval of 300 milliseconds or greater. IV antibiotics may also be used to treat some cases of late-stage arthritis. Administration of IV penicillin G (B) at a standard dose of 18–24 million units daily is used interchangeably with ceftriaxone or cefotaxime for the treatment of cardiac and neurologic manifestations of early disseminated disease and some cases of late-stage arthritis as noted above. However, these antibiotics are not recommended for early localized disease as seen in this patient. Administration of oral azithromycin (C) or other macrolides such as clarithromycin and erythromycin is not considered first-line therapy for the treatment of Lyme disease agents because of lower efficacy than preferred agents and spirochete strain-specific resistance. Azithromycin 500 mg PO daily for 10 days can be used in patients with combined intolerance to tetracyclines and beta-lactams.
A 45-year-old woman presents with a rash. The rash is located on her face; it is hyperpigmented, scaly, and erythematous. She noticed the rash two months ago and it has progressed in size. She also complains of recent joint pain involving her knees, hips, and wrists. Her past medical history is notable for chronic obstructive pulmonary disease, hypertension, hyperlipidemia, and diabetes. Her medications include tiotropium, albuterol as needed, hydralazine, and atorvastatin. She has a 30 pack-year smoking history and currently smokes a pack per day. She does not drink alcohol and denies drug use. On examination, an erythematous, scaly rash on the brim of her nose and over her maxilla is appreciated. Her wrists, knees, and hip joints are swollen and tender. Anti-histone antibodies are positive. Anti-double-stranded DNA antibodies are negative. Which of the following is the most likely diagnosis?
This patient has drug-induced lupus caused by chronic treatment of her hypertension with hydralazine. Hydralazine, procainamide, and certain tumor necrosis factor-alpha-inhibitors may cause a lupus-like syndrome that presents as a rash on sun-exposed areas such as the face, scalp, ears, and chest, that is erythematous and scaly, photosensitivity, serositis, fever, oral ulcers, and arthritis. Unlike systemic lupus erythematosus, the central nervous system and the kidneys are rarely involved in drug-induced lupus. The majority of patients with drug-induced lupus are positive for anti-histone antibodies, and anti-double-stranded DNA antibodies are absent except in cases induced by anti-TNF agents. Management includes discontinuation of the offending medication.
The rash of discoid lupus (A) presents as erythematous, scaly, hypo- or hyperpigmented lesions on sun-exposed regions of the body. Drug-induced lupus however rarely presents as a discoid lupus rash. Rheumatoid arthritis (C) often presents with symmetrical arthritis commonly involving the wrist joints. Anti-rheumatoid factor and anti-cyclic citrullinated antibodies are often positive. The rash described in this patient is not typical of rheumatoid arthritis. Systemic lupus erythematosus (D) is an autoimmune disorder that may affect any organ of the body and commonly affects the central nervous system, the kidneys, and the vascular system. Anti-double-stranded DNA antibodies and hypocomplementemia are usually present in idiopathic systemic lupus erythematosus and are usually absent (except in cases brought on by anti-TNF agents) in drug-induced lupus. Idiopathic systemic lupus erythematosus usually presents gradually while the signs and symptoms of drug-induced lupus come on more abruptly as seen in this patient.
A 67-year-old man is recovering in the hospital after undergoing left knee surgery five days ago. His laboratory investigations on admission showed a platelet count of 300,000/mcL, hemoglobin of 14.0 g/dL and the white blood cell count of 6,000/mcL. On admission, he was started on subcutaneous heparin injections to prevent deep venous thrombosis. One day ago, he was found to have swelling in his left upper extremity. A Doppler ultrasound examination revealed thrombosis of the left axillary vein extending into the subclavian vein. He was switched to enoxaparin at the therapeutic dose. Today, his laboratory investigations show a platelet count of 120,000/mcL, hemoglobin level of 12.5 g/dL, and white blood cell count of 7,000/mcL. The peripheral blood smear shows reduced platelets and the red blood cell morphology appears unremarkable with no schistocytes. Which of the following is the most appropriate next step in management?
Argatroban is used to treat heparin-induced thrombocytopenia, the most likely diagnosis in this patient. Heparin-induced thrombocytopenia results from antibodies directed against heparin-platelet factor 4 (PF4) complexes. It is a prothrombotic state due to the activation of platelets and monocytes, most commonly associated with unfractionated heparin. Thrombocytopenia typically develops 5 -10 days after starting heparin or even sooner if there is history of prior exposure to heparin, with the platelet count drop of 50% or more from the baseline. Thrombosis is seen in both arterial and venous systems and can happen in unusual locations like visceral vessels or cerebral sinuses. The 4T scoring system is used to determine pretest probability for the diagnosis of heparin-induced thrombocytopenia. Diagnostic tests include enzyme-linked immunoassay (ELISA) and the more specific serotonin release assay. The treatment includes discontinuing all forms of heparin and anticoagulation with non-heparin anticoagulants such as argatroban, bivalirudin and danaparoid. Other options include fondaparinux and there is an emerging role of direct oral anticoagulants like dabigatran or rivaroxaban in the treatment for heparin- induced thrombocytopenia.
High dose dexamethasone (A) is used to treat immune thrombocytopenia, which is caused by antiplatelet antibodies. Patients usually present with symptoms of bleeding. Plasma exchange (C) is indicated if thrombotic thrombocytopenic purpura is suspected. It is caused by deficiency of von Willebrand factor-cleaving protease ADAMTS13. Patients are usually sick and present with fever, neurologic and renal dysfunction, microangiopathic hemolytic anemia and thrombocytopenia. Schistocytes are present upon review of peripheral blood smear. Warfarin (B) is not used in the initial management of heparin-induced thrombocytopenia as it can cause skin necrosis and venous limb gangrene due to rapid depletion of protein C leading to hypercoagulable state. It is started once the platelet count has normalized on treatment with another non-heparin anticoagulant.
A 30-year-old woman presents to her primary care physician to review the results of her recent hepatitis B testing that was drawn as part of an executive health screening. She is asymptomatic and has no known medical conditions. Her serum serologies reveal a negative hepatitis B surface antigen, positive total hepatitis B core antibody, negative IgM antibody to hepatitis B core antigen, and positive hepatitis B surface antibody. Which of the following is the most likely clinical situation for this patient?
Diagnostic testing showing a negative hepatitis B surface antigen, positive total hepatitis B core antibody, negative IgM antibody to hepatitis B core antigen, and positive hepatitis B surface antibody is most consistent with immunity to hepatitis B due to prior resolved infection. Elevated levels of hepatitis B surface antigen can be detected during acute or chronic hepatitis B infection and indicate infectivity. Total hepatitis B core antibody is an IgG antibody that appears upon symptom onset in acute hepatitis B and remains for life, hence indicating ongoing or prior infection. Presence of IgM antibody to hepatitis B core antigen signals acute infection with hepatitis B. The presence of hepatitis B surface antibody would indicate recovery and immunity to hepatitis B.
Serologies in patients with acute hepatitis B infection (A) would reveal a positive hepatitis B surface antigen, positive total hepatitis B core antibody, positive IgM antibody to hepatitis B core antigen, and negative hepatitis B surface antibody. A patient with chronic hepatitis B infection (B) would present with a positive hepatitis B surface antigen, positive total hepatitis B core antibody, negative IgM antibody to hepatitis B core antigen, and negative hepatitis B surface antibody. A negative hepatitis B surface antigen, negative total hepatitis B core antibody, negative IgM antibody to hepatitis B core antigen, and positive hepatitis B surface antibody would be suggestive of a patient with immunity to hepatitis B due to prior immunization (C).
A 67-year-old woman with a history of hypertension, coronary artery disease, and prior myocardial infarction presents to her cardiologist for follow-up evaluation six months after undergoing placement of an implantable cardioverter-defibrillator for sustained monomorphic ventricular tachycardia. She was prescribed amiodarone and sotalol shortly after device implantation due to repetitive shocks delivered by the implantable cardioverter-defibrillator. She is pleased with the results, stating that she cannot recall any painful shocks since. On presentation today, she is concerned due to recent weight gain, constipation, and fatigue over the past two months. She denies chest pain, dyspnea, low mood, anhedonia, and suicidal ideation. Her current medications include lisinopril, amiodarone, sotalol, and a melatonin supplement. She does not smoke tobacco, drink alcohol, or use illicit drugs. Her temperature is 98.5°F, HR is 57/min, and BP is 131/73 mm Hg. The lungs are clear to auscultation bilaterally. Physical examination is otherwise unremarkable. Which of the following is the most appropriate next step in this patient’s management?
This patient’s presentation (i.e., fatigue, constipation, weight gain, and bradycardia) in the setting of amiodarone therapy is suggestive of amiodarone-induced hypothyroidism. Therefore, test thyroid function is the best next step in management. Amiodarone is associated with thyroid dysfunction due to its high iodine content and direct toxic effect on thyroid follicular cells. Both hypo- and hyperthyroidism may occur with amiodarone use, although hypothyroidism is more common. Amiodarone reduces triiodothyronine (T3) production, resulting in elevated levels of reverse T3. It also inhibits T3 receptor binding to nuclear receptors and decreases expression of several thyroid hormone-related genes. Adjunctive pharmacologic therapy with amiodarone, a class III antidysrhythmic drug, is often used in patients with implantable cardioverter-defibrillators for the prevention of ventricular dysrhythmias. Shocks delivered by implantable cardioverter-defibrillators can be painful and significantly impact patient quality of life. Amiodarone can be used to reduce the risk of shocks delivered by the device. Patients with implantable cardioverter-defibrillators on chronic amiodarone therapy should be monitored with thyroid function testing every three months.
Discontinue amiodarone (A) is unnecessary in this patient, as hypothyroidism secondary to amiodarone therapy can be treated with levothyroxine. Prescribe sertraline (C), a selective serotonin reuptake inhibitor, is inappropriate for this patient. Her symptoms are due to an underlying medical condition, and she does not meet the diagnostic criteria for major depression. Prescribe methimazole (B), an antithyroid drug, would worsen this patient’s condition. Methimazole is the primary pharmacologic agent used for the treatment of hyperthyroidism.
A 58-year-old man presents to the emergency department for a 2-day history of severe headache. He also reports nausea without vomiting, subjective fever, and inability to tolerate bright lights. His symptoms have been interfering with his work as a computer technician. He reports no vision changes, chest pain, palpitations, shortness of breath, diarrhea, or recent trauma, travel, or sick contacts. His past medical history includes hypertension and hyperlipidemia. His only medications are amlodipine 10 mg and atorvastatin 40 mg daily. On physical examination, his temperature is 38.4°C (101.1°F), blood pressure is 131/72 mm Hg, pulse is 108 bpm, and he is saturating 97% on room air. His physical exam, including a detailed neurologic exam, is unremarkable, except that when his neck is flexed, his hips and knees flex as well. A basic metabolic panel, complete blood count, and urinalysis are unremarkable. A lumbar puncture is performed at the bedside, and analysis of the cerebrospinal fluid reveals an elevated leukocyte count with neutrophilic predominance, decreased glucose, and increased protein. Samples for Gram stain and culture of the cerebrospinal fluid are sent to the laboratory. What is the most appropriate antibiotic regimen for this patient?
This patient has bacterial meningitis, given his symptoms of headache, fever, and neck stiffness in the setting of cerebrospinal fluid findings of increased leukocyte count, low glucose level, and increased protein level. He does not have known immunocompromising conditions and should be treated empirically with intravenous ampicillin, ceftriaxone, and vancomycin. The most common causes of bacterial meningitis are Streptococcus pneumoniae and Neisseria meningitidis, so empiric treatment should cover for these two organisms. Empiric coverage should include antibiotics able to penetrate the blood-brain barrier, such as third-generation cephalosporins combined with vancomycin to cover for penicillin-resistant organisms. Patients over 50 years of age are at risk for infection with Listeria monocytogenes, so ampicillin should also be added to the empiric regimen in this patient. Treatment can be adjusted once culture results and antibiotic sensitivities are known.
Ceftazidime and vancomycin (B), ceftriaxone and nafcillin (C), and meropenem (D) are incorrect. This patient is over the age of 50 and would need coverage for Listeria. Nafcillin would not cover for penicillin-resistant organisms. In the setting of bacterial meningitis, meropenem can be used in combination with another antibiotic with coverage for penicillin-resistant organisms in patients with immunocompromising conditions when extended gram-negative coverage is necessary.
A 58-year-old man presents to the emergency department for respiratory symptoms. In the past week, he developed rhinorrhea, cough, dyspnea, and subjective fever. Medical history includes hypertension for which he takes hydrochlorothiazide and lisinopril. Review of systems is also positive for two months of fatigue and a nonhealing ulcer in his left nostril and negative for sputum, hemoptysis, chest pain, hematuria, and gastrointestinal complaints. Temperature is 100.8°F, blood pressure is 125/88 mm Hg, pulse is 72 bpm, and respiratory rate is 18/min. On physical examination, there is a 5 mm ulcer on the nasal aspect of the right nostril. Lung auscultation reveals clear lung fields. Serum creatinine level is 1.8 mg/dL. Hilar adenopathy and a pulmonary nodule are seen on chest X-ray. PR3-antineutrophil cytoplasmic autoantibody is positive, and a biopsy of the lung nodule reveals necrotizing granulomatous inflammation and vasculitis. Which of the following is the most likely diagnosis?
Granulomatosis with polyangiitis is more common in older adults and presents with nonspecific symptoms such as fatigue, fever, rhinosinusitis, cough, and dyspnea. Nasal manifestations include crusting, sinusitis, persistent rhinorrhea, purulent or bloody discharge, ulcers, and polychondritis. Renal manifestations are common and include asymptomatic hematuria, a rise in creatinine, proteinuria, and rapidly progressive glomerulonephritis. Other symptoms may include arthralgias, urinary abnormalities, purpura, and neurologic dysfunction. Any organ system may be affected, but renal and respiratory system involvement is most common. Symptoms may begin acutely or insidiously, and prodromal symptoms may precede specific organ involvement by weeks or months. In patients with lung involvement, chest X-ray findings may include nodules, patchy or diffuse opacities, fleeting pulmonary infiltrates, and hilar adenopathy. By definition, patients must have the presence of granulomas in any organ on biopsy and respiratory tract involvement for diagnosis. A positive PR3-antineutrophil cytoplasmic autoantibody (PR3-ANCA) implies the diagnosis, but a definitive diagnosis is made with a biopsy of the affected organ. Biopsy findings include necrotizing inflammation and small-vessel vasculitis in the respiratory tract and necrotizing glomerulonephritis in the kidneys.
Patients with microscopic polyangiitis (C) present with similar clinical manifestations but no granulomatous inflammation on biopsy. Myeloperoxidase (MPO)-ANCA is commonly associated with microscopic polyangiitis. Additionally, ear, nose, and throat manifestations are more common in patients with granulomatosis with polyangiitis. Eosinophilic granulomatosis with polyangiitis (A) most commonly presents as nonspecific constitutional symptoms in a patient with existing asthma or lung disease. This patient did not have lung disease prior to this acute presentation. Polyarteritis nodosa (D) is an ANCA-negative vasculitis that presents with constitutional systemic symptoms and skin lesions, hypertension, renal insufficiency, neurologic dysfunction, and abdominal pain.
A 68-year-old man presents to his primary care physician for preoperative evaluation prior to an elective laminectomy for severe spinal stenosis. He reports no acute symptoms but notes that, over the past year, he has been increasingly fatigued with diminished exercise capacity. Past medical history is notable for type 2 diabetes, hypertension, hyperlipidemia, and chronic kidney disease. His medications are insulin glargine and hydrochlorothiazide. He has no history of known cardiac disease or myocardial infarction. He is able to feed and dress himself and walk short distances inside his home, but he is unable to walk up a flight of stairs due to dyspnea on exertion. Review of systems is negative for chest pain or palpitations. ECG is unremarkable. He has an elevated calculated major adverse cardiac event score. Which of the following is the most appropriate next step in evaluation?
Pharmacologic stress testing is the most appropriate next step in evaluation. This patient is planning to undergo an elective laminectomy, which is a nonemergent, intermediate-risk surgery. Intermediate-risk surgeries, including orthopedic, head and neck, intraperitoneal, and prostate surgeries, carry a 1–5% risk of nonfatal myocardial infarction and cardiac death. Calculation of the patient’s perioperative major adverse cardiovascular event risk using the National Surgical Quality Improvement Program risk calculator or the revised cardiac risk index is recommended. Patients with a risk of a major adverse cardiovascular event of < 1% can proceed to surgery without preoperative cardiovascular stress testing. However, those with an elevated risk of a major adverse cardiovascular event should undergo assessment of their functional capacity to perform daily activities, which is quantified in metabolic equivalents (METs). Patients capable of at least four METs (such as climbing up a flight of stairs) can proceed to surgery without further cardiovascular stress testing. However, those who are not capable of performing at least four METs or who have unknown functional capacity should undergo pharmacologic stress testing if it will affect medical decision-making or perioperative care. A positive stress test finding in this patient would likely alter management since treatment and optimization of coronary artery disease could potentially be performed prior to elective surgery.
A pharmacologic stress test, rather than cardiac catheterization (A), is the most appropriate next step. Cardiac catheterization may be warranted in certain patients with positive pharmacologic stress test findings. A Holter monitor (B) is a device that records the heart’s rhythm for 24–48 hours. It is not indicated in this patient at this time, as he does not complain of palpitations or syncope and does not have evidence of a dysrhythmia on exam and has a normal ECG. No additional testing should be considered (C) is not correct, given this patient’s elevated major adverse cardiovascular event risk, poor functional capacity, and potential that stress testing could change management.
A 75-year-old man presents to his primary care physician for his physical exam. He feels well today. Past medical history is notable for hypertension treated with lisinopril 20 mg daily, coronary artery disease treated with aspirin 81 mg daily, and bipolar I disorder, which has been well controlled on olanzapine 20 mg daily without recurrence for the past five years. He also takes a daily 2,000 IU vitamin D supplement. He has a history of a mechanical fall three weeks ago after tripping on the bathroom rug as well as a mechanical fall after slipping on ice 10 months ago. He did not experience head injury or complications from either fall and has not had other falls or fractures in the past. Family history is notable for his father, who died at age 60 from three-vessel coronary artery disease. He does not smoke or use recreational drugs, and he drinks one beer weekly. Review of systems is negative for headache, lightheadedness, dizziness, chest pain, depression, anhedonia, manic episodes, or bleeding. On vital signs, he has a temperature of 98.5°F, supine and standing pulse of 76 bpm, supine blood pressure of 140/86 mm Hg, standing blood pressure of 136/82 mm Hg, respiratory rate of 16 breaths per minute, and oxygen saturation of 100%. Physical examination is normal. Complete blood count, comprehensive metabolic panel, and serum vitamin D level are within normal limits. Which of the following is the best next step for this patient to prevent future falls?
The best next step for this patient to prevent future falls is to reduce the dose of olanzapine. Falls are common in older patients, affecting 30–40% of community-dwelling adults older than the age of 65. Older patients should be screened for falls or risk of falling at least annually. Patients with an acute fall, two or more falls in the past year, or balance or gait difficulties should undergo a focused history including a fall history as well as physical exam. A multifactorial fall risk assessment should be performed, including evaluation of balance, gait, mobility, hearing, vision, cognitive or neurologic abnormalities, strength, and feet. Measurement of pulse and blood pressure and evaluation for postural hypotension are also recommended. Medications should also be reviewed to identify those that may increase risk of falls and to consider reducing or stopping the offending medication. Certain psychotropic medications are associated with an increased risk of falls. Neuroleptics, including atypical antipsychotics such as olanzapine and risperidone, increase fall risk secondary to sedation, sensory and motor instability, and postural hypotension. Other psychotropic medications such as sedatives, benzodiazepines, and antidepressants may also increase fall risk. This patient has been stable on maximum-dose olanzapine for years without bipolar disorder recurrence, so decreasing the olanzapine dose should be considered at this time.
It would not be recommended to reduce the dose of lisinopril (B), as this patient has a history of hypertension with an elevated blood pressure and no evidence of orthostatic hypotension. It would not be advised to increase the dose of vitamin D (A). Although guidelines on vitamin D supplementation for fall prevention may vary, older adults at risk for falls may consider 600–1,000 IU of vitamin D supplementation. This patient is already on a higher dose of vitamin D supplementation with a normal serum vitamin D level. Stop the aspirin (D) is incorrect, as this patient has a history of coronary artery disease and has no evidence of bleeding. He should be continued on low-dose aspirin therapy for cardiovascular risk reduction.
A 45-year-old man presents with galactorrhea that began 1 week ago. He has a medical history of hyperlipidemia and diabetes mellitus managed with atorvastatin and metformin. He has a 20 pack-year smoking history and smokes one pack of cigarettes daily. He reports no illicit drug use. On examination, discharge is expressed on compression of the nipples bilaterally. Morning testosterone level on two separate occasions is 150 ng/dL and 160 ng/dL. Follicle-stimulating hormone level is 0.9 mIU/mL, and luteinizing hormone level is 2.6 mIU/L. Prolactin level is 186 ng/mL. MRI shows pituitary adenoma measuring 0.5 cm. Which of the following is indicated for management?
This patient has hyperprolactinemia. Hyperprolactinemia is secondary to excessive secretion of prolactin hormone from the anterior pituitary gland, commonly due to an adenoma or the decreased clearance of prolactin, which is usually secondary to renal or hepatic failure. Excessive secretion of prolactin hormone may result from decreased dopaminergic inhibition of prolactin secretion such as the use of antipsychotic medications and damage of dopaminergic neurons in the hypothalamus. Other causes of excessive secretion include hypothalamic tumors and infiltrative disease of the hypothalamus, such as that in the setting of sarcoidosis, among others. Hyperprolactinemia may result in hypogonadism manifesting in infertility, oligomenorrhea, and amenorrhea in premenopausal women. Premenopausal women may also experience decreased bone mineral density and galactorrhea. Hyperprolactinemia is generally symptomatic in postmenopausal women in the setting of macroadenomas that impinge on the optic chiasm, causing visual disturbances. The condition in men may cause hypogonadism manifesting as erectile dysfunction, infertility, gynecomastia, or galactorrhea. Hypogonadism in men is confirmed on the finding of a low morning testosterone level on two separate occasions. Primary hypogonadism manifests as elevated gonadotropin levels, and secondary hypogonadism, such as that due to a prolactinoma, is associated with low gonadotropins. Hyperprolactinemia is further diagnosed by serum prolactin level. Prolactinomas are treated when they are greater than 10 mm, enlarging, cause infertility, gynecomastia, testosterone deficiency, oligomenorrhea, or acne, and in the presence of hirsutism. Dopamine agonists such as bromocriptine and cabergoline are first-line treatments for both micro- and macroadenomas. Disease refractory to medical therapy requires surgical resection of adenoma, commonly by transsphenoidal route.
Glucocorticoid administration (B) may inhibit gonadotropin-releasing hormone levels, causing further hypogonadism. Spironolactone (C), an androgen antagonist, is indicated for the management of hyperandrogenism in patients who have polycystic ovarian syndrome for whom oral contraceptive pills are contraindicated, or it may be used as an adjunct to oral contraceptive pills for treatment. Surgical resection of pituitary mass (D) may be indicated if medical therapy is unsuccessful. Testosterone replacement therapy (E) is not indicated, as hyperprolactinemia is the underlying pathology.
A 47-year-old woman presents to the emergency department with fever, cough, and shortness of breath. She describes a persistent cough of yellow sputum, subjective fever, and dyspnea that has progressively worsened over the past 5 days. She has no recent sick contacts and no recent travel. Her past medical history is significant for hypertension and hyperlipidemia. Her medications include amlodipine and pravastatin. She is allergic to morphine and vancomycin. On physical exam, temperature is 38.1°C (100.6°F), heart rate is 81 bpm, blood pressure is 108/72 mm Hg, and respiratory rate is 31/min with an oxygen saturation of 91% while breathing ambient air. A chest radiograph reveals an area of focal opacification in the lower lobe of the left lung. She is started on empiric antibiotic treatment with ceftriaxone and azithromycin. She shows no improvement after 3 days of treatment. Sputum cultures are obtained and grow gram-positive cocci in clusters that are resistant to oxacillin. What is the most appropriate antibiotic regimen for this patient?
This patient has methicillin-resistant Staphylococcus aureus (MRSA) pneumonia, indicated by the presence of gram-positive cocci in clusters that are resistant to oxacillin. Common intravenous antibiotics used to treat MRSA infections include linezolid and vancomycin. This patient has an allergy to vancomycin. which makes linezolid the best choice. Linezolid is a bacteriostatic agent that acts by inhibiting bacterial protein synthesis. It binds to the 23S ribosomal RNA of the 50S subunit, which prevents formation of a functioning 70S initiation complex, thereby inhibiting the bacterial translation process.
Cefepime (A) is a fourth-generation cephalosporin with broad-spectrum activity against gram-positive and gram-negative bacteria, including Pseudomonas, but it is not effective for treating MRSA. Levofloxacin (C) is a fluoroquinolone with broad-spectrum activity against gram-positive, gram-negative, and atypical respiratory pathogens, but it is not effective for treating MRSA. Daptomycin (B) has broad-spectrum activity against many multidrug-resistant gram-positive bacteria, including MRSA, but it is inactivated by pulmonary surfactant and doesn’t achieve adequate levels in the respiratory tract.
A 67-year-old woman presents with left knee pain. She complains of daily pain with walking and climbing stairs and says that the pain has progressed to the point that it now limits her activities of daily living. She reports no trauma. She has a history of hyperlipidemia, hypertension, and diabetes mellitus. Her medications include atorvastatin, lisinopril, amlodipine, and metformin. Body mass index is 36 kg/m2. Physical examination is notable for tenderness along the left medial knee. Mild swelling of the left knee is appreciated without warmth. There is crepitus with passive movement of the joint. Active and passive range of motion are limited. A number of the distal interphalangeal joints of the hands bilaterally are enlarged, but no other joint abnormalities are noted. Which of the following X-ray findings is most consistent with her underlying condition?
This patient most likely has osteoarthritis of the knee. Osteoarthritis of the knee presents more commonly in patients who are obese, those who have had a knee injury or previous knee surgery, and those who bend and lift on a repetitive basis. It may present as sharp and predictable pain associated with forceful movements that progresses to daily aching pain with limitation of function. Physical examination is notable for joint line tenderness, limitation of active and passive range of motion, joint swelling, and in the case of severe disease, joint deformity or instability. Plain radiograph is notable for osteophytes, joint space narrowing, subchondral sclerosis, and cysts. Although unnecessary for evaluation, magnetic resonance imaging may reveal disease earlier than plain radiographs. Ultrasonography is useful for evaluation of synovial inflammation and effusion. Management of risk factors, including weight loss in patients who are obese and regular exercise, are indicated for patients who have osteoarthritis of the knee. Oral and topical nonsteroidal anti-inflammatory drugs and topical capsaicin are indicated for mild pain relief.
Bone erosions (A) and osteopenia (D) are noted on radiograph in patients who have rheumatoid arthritis. Bone erosions with new bone formation (B) is characteristic of psoriatic arthritis.
An 81-year-old woman presents to the hospital with chest pain. She reports intermittent chest pain for 1 week, exacerbated by activity and alleviated by rest. Today her symptoms worsened and the pain now persists even at rest. She experienced moderate persistent squeezing pain for more than 30 minutes with radiation to the jaw, prompting her to call the ambulance. Her past medical history is significant for hypertension, type 2 diabetes mellitus, dyslipidemia, and coronary artery disease. Prior to arrival, paramedics administered 325 mg of aspirin. Vital signs are notable for a temperature of 98.9°F, HR of 50 beats/min, RR of 24 breaths/min, BP of 88/54 mm Hg, and pulse oximetry of 92% on room air. The patient is ill appearing, diaphoretic, and in mild respiratory distress. She also is noted to have JVD, rales throughout both lungs, and peripheral edema. Her ECG shows ST segment depressions in the inferior leads but no ST segment elevations. Her cardiac troponin level is 1.9 ng/mL. Which of the following is the best next step in management of this patient?
This patient is having a non-ST segment elevation myocardial infarction (NSTEMI), as indicated by her elevated troponin, symptoms, and history. She has multiple high-risk features that would prompt consideration for immediate percutaneous coronary intervention. Squeezing chest pain exacerbated by activity and radiating to the jaw are classic symptoms that should raise suspicion for acute coronary syndrome. Hypertension, type 2 diabetes mellitus, dyslipidemia, and coronary artery disease are risk factors for acute coronary syndrome. Patients with NSTEMI should receive aspirin, nitroglycerin, beta-blockers, statin therapy, and anticoagulation. However, nitroglycerin is contraindicated in this patient because of hypotension, and beta-blockers are contraindicated because of bradycardia. This patient has evidence of hemodynamic instability and congestive heart failure, as indicated by hypotension, JVD, rales, and peripheral edema. Patients with these findings are at very high risk for short-term adverse cardiovascular events and should proceed to immediate angiography and revascularization. Resuscitative efforts should be performed while getting her to the catheterization lab.
Administration of alteplase (A) is incorrect. There is no evidence of a benefit of fibrinolytics in NSTEMI. Administration of heparin (B) is incorrect. Although anticoagulation is part of a management plan in patients with NSTEMI, the best step in management for this patient is immediate percutaneous coronary intervention. Administration of nitroglycerin (C) is incorrect. Patients with acute coronary syndrome may require nitroglycerin, but hypotension is a contraindication in this patient.
An 85-year-old woman with advanced breast cancer and congestive heart failure is admitted to home hospice after an extended hospitalization for multiple spinal compression fractures and a congestive heart failure exacerbation. She has undergone exhaustive treatment of her breast cancer including bilateral mastectomies, chemotherapy, radiation therapy, and biologic therapies without success. Her oncologist, cardiologist, and palliative care physician agree that further curative therapy would not be beneficial and are in agreement that she will likely not survive more than several days due to her grave condition. She and her family agree to pursue home hospice care. At home, she is experiencing bothersome dyspnea with a sensation of air hunger and breathlessness. Review of systems is negative for significant pain or anxiety. Oxygen saturation is within normal limits. Which of the following therapies is recommended for management of this patient’s dyspnea?
Sublingual morphine is recommended for this patient. Patients with advanced illness at the end of life may commonly experience dyspnea, especially in the setting of advanced cancer, chronic obstructive pulmonary disease, heart disease, AIDS, and kidney disease. Dyspnea refers to difficulty breathing or shortness of breath and may be described as breathlessness, air hunger, increased work of breathing, or a sensation of suffocation. Evaluation and management of underlying reversible causes of dyspnea are recommended when possible. At the end of life and in patients with irreversible underlying causes of dyspnea, general supportive measures may be beneficial. Techniques to promote relaxation and the use of a fan to blow cool air on the face may be helpful. Short-acting oral or sublingual opiates are the cornerstone of therapy for treating dyspnea at the end of life. They also can be helpful for treating concurrent pain. Depending on the patient’s clinical situation, it may be beneficial to offer opiates regularly or on a set schedule, since some patients may not be able to ask for them. Long-acting opiates should be avoided to minimize the risk of excess sedation.
There is not sufficient evidence to support the use of nebulized morphine (A) for the management of dyspnea at the end of life. Some have used sublingual atropine (B) to manage end-of-life airway secretions, but there is insufficient evidence to support its use for managing secretions. Sublingual atropine is not recommended for the management of dyspnea at the end of life. Sublingual lorazepam (C) may be considered as an adjunctive therapy for patients with dyspnea who also have concomitant anxiety at the end of life.
An 18-year-old man presents to his physician for a routine examination. He has no acute complaints and reports feeling otherwise well. He has a medical history of asthma, for which he takes an albuterol inhaler. His body mass index is 30 kg/m2. Physical examination is unremarkable. His serum studies are notable for a hemoglobin A1C of 6.7% which is persistently elevated on repeat testing. Which of the following laboratory findings supports type 1 diabetes mellitus over type 2 diabetes mellitus?
Diabetes mellitus (DM) is a medical condition caused by abnormal carbohydrate metabolism leading to hyperglycemia. Diabetes is associated with decreased or absent insulin secretion and peripheral resistance to insulin. DM can be divided into type 1 and type 2. Type 1 DM is a common and chronic disease of childhood that persists into adulthood. It is characterized by destruction of the pancreatic beta cells that produce insulin. Type 2 DM is typically seen in adult patients who are overweight and obese and is characterized by peripheral insulin resistance, where the cells do not adequately respond to the serum glucose-lowering effects of insulin. DM itself is diagnosed by one of the following measures, confirmed by repeat testing: 1) having a plasma glucose ≥ 126 mg/dL, 2) plasma glucose of ≥ 200 mg/dL at 2 hours after receiving a 1.75 g/kg oral glucose tolerance test, or 3) having a hemoglobin A1C ≥ 6.5%. Diagnosis can also be established in a patient with symptoms of hyperglycemia (e.g., polyuria) and a random venous plasma glucose ≥ 200 mg/dL. With regards to laboratory studies, the presence of pancreatic autoantibodies against glutamine acid decarboxylase 65 (GAD65) is supportive of type 1 DM.
Elevated fasting insulin (B) is supportive of type 2 DM. There is increased peripheral resistance to insulin in type 2 DM, thus, the increased serum glucose will encourage increased insulin secretion by the pancreas. Elevated C-peptide (A) is supportive of type 2 DM. C-peptide is a product of cleaving proinsulin to insulin within the pancreatic beta cells. Therefore, an elevated C-peptide is expected in states of increased insulin secretion. Fasting plasma glucose of 130 mg/dL (C) is a laboratory abnormality that is supportive of DM but does not differentiate between type 1 and type 2.
A 57-year-old man is hospitalized for management of worsening pneumonia. He was diagnosed with pneumonia 3 days ago by his primary care physician and started on outpatient azithromycin therapy. However, his cough progressively worsened on therapy. This morning, he became lightheaded with altered mental status and was brought into the emergency room 2 hours ago by his wife. A diagnosis of a left lower lobe pneumonia was confirmed on chest radiography. On admission, he had a temperature of 102.8°F, pulse of 110 bpm, blood pressure of 78/50 mm Hg, respiratory rate of 22 breaths per minute, and oxygen saturation of 96%. Intravenous fluid resuscitation with three 1-liter boluses of normal saline was administered, and central venous and arterial lines were placed. Blood cultures were drawn, and empiric intravenous vancomycin and piperacillin-tazobactam therapy was initiated. Because he remained hypotensive after fluid resuscitation, he was started on a norepinephrine infusion. After titration of the norepinephrine infusion for over an hour, his pulse is now 99 bpm with a blood pressure of 84/52 mm Hg. Complete blood count reveals a white blood cell count of 18,400/mcL with a neutrophil count of 13,000/mcL. Serum lactate level is 2.6 mmol/L. Which of the following is the best next step in management for this patient?
Administer intravenous hydrocortisone is the best next step for this patient. Sepsis is defined as a dysregulated host response to infection that results in life-threatening organ dysfunction. Septic shock may be diagnosed in a septic patient who, despite adequate fluid resuscitation, necessitates vasopressors in order to maintain a mean arterial pressure of at least 65 mm Hg and has a serum lactate level higher than 2 mmol/L. Norepinephrine is generally the initial first-line intravenous vasopressor for management for hypotension in patients with septic shock. Glucocorticoids are not routinely recommended for initial therapy in patients with sepsis, as absolute adrenal insufficiency is uncommon among patients who are critically ill. However, intravenous hydrocortisone may be considered in patients with septic shock who are refractory to fluid resuscitation and vasopressors. Refractory shock may be defined as a systolic blood pressure < 90 mm Hg for longer than 1 hour after adequate fluid resuscitation and administration of vasopressors.
It would not be recommended to initiate low-dose dopamine infusion (B). Low-dose dopamine causes selective vasodilation by acting at dopamine-1 receptors in the renal, coronary, mesenteric, and cerebral beds. It is not generally a recommended treatment for patients with septic shock. Measure a plasma cortisol level (C) and perform an adrenocorticotropic hormone stimulation test (D) are incorrect. Studies have found that plasma cortisol measurements and adrenocorticotropic hormone stimulation tests are not reliable in patients who are critically ill. Also, these tests are not beneficial in determining which patients with septic shock ultimately benefit from the use of glucocorticoids.
A 48-year-old woman presents to the emergency department for evaluation of new-onset blurred vision and headache. Her medical history is notable for a history of diffuse cutaneous systemic sclerosis. Blood pressure on arrival is 179/109 mm Hg. She has no prior history of hypertension. Physical examination reveals digital pitted scars, palmar erythema, telangiectasias on the chest and face, and calcinosis of the extensor surfaces of the forearms and several digits. Funduscopic examination reveals retinal exudates and papilledema. Serum creatinine is 2.2 mg/dL on presentation, despite a history of normal kidney function. Urine sediment reveals mild proteinuria and no casts or cells. Which of the following is the best therapeutic intervention at this time?
Captopril and nitroprusside is the best therapeutic intervention at this time. This patient’s presentation is concerning for a rare but serious complication of systemic sclerosis known as scleroderma renal crisis. This occurs in a minority of patients with diffuse cutaneous systemic sclerosis. It is characterized by new-onset kidney disease, sudden-onset hypertension, and a normal urine sediment. The development of hypertension is associated with increased plasma renin activity. This patient’s creatinine is elevated above baseline, suggesting new-onset kidney disease. She has an acutely elevated blood pressure greater than 150/85 mm Hg, with associated retinal changes of exudates and papilledema as well as headache. In scleroderma renal crisis, the urine sediment is generally notable only for mild proteinuria. Treatment centers around the use of captopril to return the patient’s blood pressure to baseline within 3 days. A rapid reduction in blood pressure is generally permitted, given the acute nature of the patient’s hypertension. Captopril has been studied most for use in scleroderma renal crisis, although all angiotensin-converting enzyme inhibitors may be appropriate. Moreover, captopril has a short duration of action and onset that allows easy dose titration and increases. Nitroprusside is initially added for acute blood pressure management in patients with central nervous system effects such as retinal changes, papilledema, or encephalopathy.
While captopril is the agent of choice in scleroderma renal crisis, this patient should also initially receive intravenous nitroprusside, given the evidence of retinal exudates and papilledema. This is preferred to captopril alone (A). Epoprostenol (C) is a prostacyclin that has been used anecdotally for the treatment of scleroderma renal crisis. Its effectiveness has not been validated in clinical trials. Losartan (D) and other angiotensin II receptor blockers have not yet been studied in the treatment of scleroderma renal crisis.
A 67-year-old man is being evaluated in the ED for chest pain. The pain began 2 hours ago while at rest, is located substernally, and radiates down his left arm. He feels nauseated and vomited once. His history is notable for hyperlipidemia, hypertension, and diabetes mellitus. His medications include atorvastatin, lisinopril, and insulin. He has a 40 pack-year smoking history and smokes two packs of cigarettes daily. He does not use illicit drugs. Troponin I is 2.54 ng/mL, and his ECG reveals a regular rate and rhythm at 40 bpm and ST segment elevations in leads II, III, and aVF. What is the most common dysrhythmia that is seen in this condition?
This patient is having an acute myocardial infarction, diagnosed based on the typical findings of coronary occlusion: chest pain accompanied by elevation of the cardiac enzyme troponin I and ST segment elevations in leads II, III, and aVF on ECG, which is characteristic of an inferior myocardial infarction. Inferior myocardial infarctions are secondary to rupture or erosion of an atherosclerotic plaque in the right coronary artery, an artery that serves the sinoatrial nodal artery in 60% of patients. Sinus bradycardia, as seen in this patient, is the most common conduction abnormality in the setting of an acute inferior myocardial infarction. First-degree atrioventricular block also can occur secondary to occlusion of the right coronary artery or the left circumflex artery, and Mobitz type I second-degree atrioventricular block may present in patients with inferior myocardial infarction. Anterior myocardial infarctions, diagnosed on electrocardiogram by ST segment elevations in leads V3 and V4, are less commonly associated with conduction abnormalities than are inferior myocardial infarctions. However, when present, they may be associated with more severe findings. First-degree, Mobitz type I and II second-degree, and third-degree atrioventricular block may present as a complication of an anterior myocardial infarction.
Atrial fibrillation (A) is not commonly associated with myocardial infarction. First-degree atrioventricular block (B) may present in patients with inferior myocardial infarctions but less often than sinus bradycardia. Second-degree atrioventricular block (C), Mobitz type I, may occur secondary to an inferior myocardial infarction but less frequently than sinus bradycardia. Mobitz type II is more common in anterior myocardial infarctions.
A 57-year-old woman with moderately severe chronic obstructive pulmonary disease, hypertension, and diabetes presents to clinic with postprandial epigastric abdominal pain for one month. She has not had weight loss, difficulty swallowing, or melena. She has been hospitalized several times in the last year for exacerbations of chronic obstructive pulmonary disease, including a hospitalization three weeks ago during which she was treated with steroids and azithromycin. Medications include inhaled albuterol, prednisone, budesonide-salmeterol, and subcutaneous insulin. She is allergic to penicillin, to which she reports anaphylaxis as a child. Complete blood count, kidney function, and electrolytes are normal. Fecal antigen testing for Helicobacter pylori is positive. Which of the following is the most appropriate management strategy at this time?
This patient, with abdominal pain and positive non-invasive testing for Helicobacter pylori (H. pylori), without other “red flags” to indicate a serious cause of abdominal pain, should be treated with an effective regimen based on her patient profile. In this case, the most effective therapy listed is bismuth-based quadruple therapy which includes bismuth subsalicylate, tetracycline, metronidazole, and a proton pump inhibitor for 14 days. H. pylori is a gram-negative, seagull-shaped bacterium that is spread through the fecal-oral route and has a relatively high prevalence worldwide. The bacteria colonizes and infects the gastric antrum, where it is able to survive the harsh pH of the gastric mucosa by producing urease, an enzyme that allows it to produce ammonia and raise the local pH. H. pylori produces inflammatory and carcinogenic factors, and is implicated in the development of gastric mucosal associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma; importantly, in some situations, eradication of H. pylori can lead to resolution of the neoplasm. H. pylori is also one of the main causes (along with nonsteroidal anti-inflammatory drugs) of peptic ulcer disease, and is also implicated in iron deficiency anemia, immune thrombocytopenia purpura, and functional dyspepsia. In patients under 60 years of age with dyspepsia and no alarm features, it is reasonable to perform non-invasive testing for H. pylori; it is diagnosed by non-invasive testing with the urea breath test, fecal antigen testing, or serology. Urea breath testing and fecal antigen testing have diminished accuracy in the setting of proton pump inhibitor (PPI) use but are useful to prove active infection, while serology is unaffected by PPI use but does not distinguish active from past infection. Endoscopy with gastric biopsies can also diagnose active infection, as the bacteria can be seen histopathologically but is not superior to noninvasive testing if there is not another indication for endoscopy. Any patient who tests positive should be offered therapy due to the long-term risks of malignancy and peptic ulcer disease. There are multiple therapeutic options for H. pylori, all of which are multi-drug regimens due to high levels of drug resistance. Traditional first-line therapy has been amoxicillin, clarithromycin, and PPIs; however, patients who have been recently treated with macrolides or who have penicillin allergy may be treated with an alternative regimen. Of the available options, a bismuth-based quadruple therapy is the best first-line option and has a cure rate of over 90%. A longer treatment duration of 14 days has a higher cure rate than shorter treatment duration. After treatment, patients should have test of cure to verify eradication.
Levofloxacin, clarithromycin, metronidazole, and a proton pump inhibitor for 14 days (B) is not a recommended treatment regimen for H. pylori. The most common levofloxacin-based regimen is levofloxacin, amoxicillin, and a PPI. Levofloxacin and clarithromycin are both potentially QT-prolonging agents and have not been studied in combination in the treatment of H. pylori. Penicillin desensitization followed by treatment with amoxicillin, clarithromycin, and a proton pump inhibitor for 14 days (C) is incorrect because there are alternative, effective treatment regimens for H. pylori that do not require penicillin desensitization. In addition, even if the patient were to undergo penicillin desensitization, this is not an appropriate first-line treatment in this patient due to recent macrolide exposure. Previous macrolide exposure is used as a proxy for drug resistance testing, which is not routinely performed in H. pylori due to difficulty culturing the bacteria. This is an important element of the history because clarithromycin resistance reduces the likelihood of effective therapy by 50%. Amoxicillin, clarithromycin, and a PPI is otherwise a reasonable first-line treatment for H. pylori in patients who do not have penicillin allergy or recent macrolide exposure. Upper endoscopy with biopsies of the gastric body, incisura, and antrum (D) is an acceptable diagnostic approach to demonstrate active H. pylori infection. Since this patient already has positive non-invasive testing for the bacterium and has no other indication for endoscopy such as dysphagia, melena, or iron deficiency anemia, the answer is incorrect as there is no need for further invasive diagnostic testing at this time.
An 18-year-old woman is brought into the emergency department by a friend complaining of lethargy, abdominal pain, nausea, and vomiting. She has no known past medical history and takes no medications. She does not smoke, drink alcohol, or use recreational drugs. Family history is notable for her mother, who has type 1 diabetes. On vital signs, she has a temperature of 98.8°F, pulse of 109 bpm, blood pressure of 110/70 mm Hg, respiratory rate of 18/min, and oxygen saturation of 98%. Physical exam is significant for decreased skin turgor and a fruity breath odor. She is alert and oriented to person, place, and time without focal neurologic deficits. Comprehensive metabolic panel is significant for a serum potassium level of 3.0 mEq/L, serum bicarbonate level of 14 mEq/L, and serum glucose level of 424 mg/dL. Serum anion gap is 21 mEq/L. Urine and serum ketones are both positive. Intravenous fluids are initiated with 0.9% normal saline. Which of the following is the most appropriate next step?
Administration of intravenous potassium chloride is the most appropriate next step. Diabetic ketoacidosis is an acute complication of diabetes marked by hyperglycemia, ketoacidosis, and an anion gap metabolic acidosis. Diabetic ketoacidosis develops in patients with type 1 diabetes in the setting of acute infection or illness, inadequate insulin therapy, or use of certain medications. Patients can also present with diabetic ketoacidosis as the initial manifestation of new-onset type 1 diabetes, as in this patient. Patients with type 2 diabetes present less frequently with diabetic ketoacidosis, typically in settings of serious illness or stressors. Diabetic ketoacidosis has a rapid onset, usually over 24 hours. Symptoms include polydipsia, polyuria, lethargy, nausea, vomiting, and abdominal pain. Physical exam findings can involve decreased skin turgor, low jugular venous pressure, or other manifestations of volume depletion. Deep respirations and a fruity breath odor can also be present. Hyperglycemia is present, with serum glucose levels usually between 250–800 mg/dL. Serum and urine ketones are typically present, and decreased serum bicarbonate and an anion-gap metabolic acidosis are characteristic. Patients with diabetic ketoacidosis often have potassium deficits due to increased urinary potassium losses. This patient has a low serum potassium concentration. Even in the setting of potassium deficits, patients can often present with normal, or less commonly, elevated serum potassium concentration due to potassium shifts from intracellular to extracellular fluid. The initial step in management of diabetic ketoacidosis involves correcting fluid and electrolyte abnormalities. Intravenous isotonic saline is administered to replenish extracellular fluid volume and free water deficits. Repletion of potassium deficit is also recommended unless the serum potassium is > 5.3 mEq/L. Patients with serum potassium levels < 3.3 mEq/L should be given intravenous potassium chloride to raise the serum potassium concentration to > 3.3 mEq/L prior to administering insulin therapy.
Low-dose intravenous insulin (B), subcutaneous long-acting insulin (C), and subcutaneous rapid-acting insulin (D) are incorrect. Insulin therapy is advised only after serum potassium has been repleted to > 3.3 mEq/L. Insulin causes potassium to enter cells, thereby decreasing the serum potassium concentration and potentially leading to life-threatening dysrhythmias in patients who are already hypokalemic. After potassium replacement, low-dose intravenous insulin (typically with regular insulin) is the recommended regimen in patients with moderate to severe diabetic ketoacidosis. For patients with mild diabetic ketoacidosis, subcutaneous insulin regimens can be considered.
A 34-year-old man presents to the emergency department after being found profoundly disoriented by his friends. He has a past medical history of untreated AIDS and hypertension. His only medication is amlodipine. He has no known drug allergies. He smokes cigarettes but does not drink alcohol or use illicit drugs. On physical exam, he is febrile with a temperature of 38.2°C (100.8°F), pulse rate is 94 bpm, respiratory rate is 18/min, and blood pressure is 152/94 mm Hg. He is awake but drowsy and oriented to person but not to place or time. His neurologic examination is unremarkable. A lumbar puncture is performed and laboratory testing detects cryptococcal antigen in the CSF. What is the most appropriate treatment?
This patient has cryptococcal meningitis, which is especially common in patients with untreated AIDS who have a CD4 count < 100 cells/mcL. The treatment for cryptococcal meningitis involved three phases: induction, consolidative, and maintenance therapy. The combination of liposomal amphotericin B and flucytosine is recommended for initial induction therapy for a 2-week period typically. Amphotericin B works by binding ergosterol and forming holes in the fungal membrane to allow the leakage of electrolytes. It is highly toxic and can cause fever, chills, hypotension, dysrhythmias, anemia, nephrotoxicity, and phlebitis at the injection site. It is combined with flucytosine, a nucleic acid synthesis inhibitor, to treat cryptococcal meningitis. Flucytosine can also have adverse effects, such as bone marrow suppression, hepatic toxicity, and gastrointestinal symptoms. Patients being treated with these two drugs should have their blood counts, electrolyte levels, and renal function monitored closely during treatment. IV hydration before and after administration helps to decrease the nephrotoxicity of amphotericin B. Additionally, liposomal amphotericin B is less toxic, especially to the kidneys, and should be used when available.
Dexamethasone (A) is a glucocorticoid that can be used to decrease inflammation in some forms of meningitis, but it is associated with no reduction in mortality and increased adverse events in HIV-associated cryptococcal meningitis. Fluconazole and amphotericin B (B) therapy has been shown to be less effective in treating patients with cryptococcal meningitis when compared to treatment with amphotericin B and flucytosine. Micafungin (D) is an echinocandin that is used to treat Aspergillus and Candida. It has no role in treatment of cryptococcal meningitis.
A 78-year-old man with a 15-year history of osteoarthritis is evaluated for 4 days of severe pain and swelling of the left knee. His past medical history is significant for hypertension, type 2 diabetes mellitus, and chronic kidney disease. His medications include glyburide, lisinopril, and low-dose aspirin. On physical examination, vital signs are normal. He is unable to bear weight on the left leg secondary to pain. The left knee is swollen, erythematous, and warm to touch. There are no tophi present. Range of motion of the joint is limited secondary to pain. Arthrocentesis of the left knee is performed. Synovial fluid analysis reveals a leukocyte count of 24,000 cells/mm3. Microscopy under polarized light reveals negatively birefringent needle-shaped crystals. Which of the following is the most appropriate treatment for this patient?
This patient is having an acute episode of gout. The presence of negatively birefringent needle-shaped crystals in the synovial fluid is diagnostic of gout. Acute episodes of gout should be treated with glucocorticoids, NSAIDs, or colchicine. Oral glucocorticoids are considered first-line therapy for treating acute gout flares. They inhibit inflammatory pathways and decrease the innate immune response. Caution should be used in patients with heart failure, poorly controlled hypertension, or brittle diabetes. Unlike NSAIDs and colchicine, glucocorticoids can be used in patients like this one with renal insufficiency. Glucocorticoids may also be combined with NSAIDs or colchicine in the treatment of acute gout.
Acetaminophen (A) is not indicated for the treatment of gout. It is an antipyretic and analgesic without anti-inflammatory properties. Allopurinol (B) is used for prophylaxis in gout, but it is not useful in acute flares. Allopurinol should not be started in an acute gout flare because fluctuations in uric acid levels frequently trigger acute exacerbations. Indomethacin (C) is an NSAID and should not be used in patients with chronic kidney disease.
A 68-year-old man with a history of osteoarthritis of the hip and hypertension presents to his primary care physician for a preoperative evaluation prior to a left hip replacement. He recently had a mechanical mitral valve placed 6 months ago, for which he is maintained on warfarin and low-dose aspirin. He has no history of atrial fibrillation, left ventricular dysfunction, hypercoagulability, or prior thromboembolic event. Which of the following is the most appropriate plan regarding anticoagulation prior to his procedure?
The most appropriate plan is to hold warfarin 3 days prior to the procedure, continue aspirin, and bridge with heparin until the day of surgery. This patient is at risk of thromboembolism, one of the most common complications of mechanical prosthetic valves. Patients with mitral valve prostheses are twice as likely to experience systemic embolization as those with prosthetic aortic valves. Generally speaking, elective noncardiac surgeries should be postponed until at least 3 months after valve surgery. These first several months after a mitral valve replacement present the highest risk of thromboembolism. This patient undergoing hip replacement surgery is also at a high risk of bleeding. Because he has no known risk factors for thrombotic events aside from the presence of a mechanical mitral valve replacement, vitamin K antagonist therapy (such as warfarin) should be stopped for the minimum amount of time possible while initiating bridging anticoagulation. Preferred options for anticoagulant bridging include intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin. Vitamin K antagonists are held 2–4 days prior to the procedure to obtain a goal international normalized ratio (INR) less than 1.5 on the morning of the procedure. Aspirin should be continued, bridging anticoagulation started, and vitamin K antagonists restarted 12–24 hours after the procedure, assuming adequate hemostasis.
Warfarin should be held 2–4 days prior to the surgery to allow for the INR to become subtherapeutic and avoid significant bleeding risk. To hold warfarin and aspirin the morning of the procedure (D) would not allow adequate time for the INR to decrease. Moreover, because this patient underwent mechanical mitral valve replacement, he is at increased risk for a thrombotic event and should receive bridging anticoagulation preoperatively. To hold warfarin and aspirin 3 days prior to the procedure (C) is thus not correct, as he needs bridging anticoagulation. To hold warfarin 3 days prior to the procedure, hold aspirin, and bridge with heparin until the day of surgery (B) is incorrect because aspirin should be continued for patients with mechanical valve prostheses.
A 56-year-old woman presents to her primary care physician for fatigue. She reports no chest pain, shortness of breath, and unexplained weight gain or swelling. She has a medical history of ulcerative colitis, for which she takes oral mesalamine. Physical examination is unremarkable. Her laboratory studies are shown below:
Sodium: 142 mEq/L
Chloride: 100 mEq/L
Potassium: 3.7 mEq/L
Bicarbonate: 24 mEq/L
Urea nitrogen: 12 mg/dL
Glucose: 105 mg/dL
Creatinine: 0.71 mg/dL
Alkaline phosphatase: 400 U/L
Aspartate aminotransferase: 105 U/L
Alanine aminotransferase: 110 U/L
Which of the following is most likely to confirm the diagnosis?
Primary sclerosing cholangitis is a progressive disorder that affects the intra- or extrahepatic biliary tree, leading to inflammation, fibrosis, and stricture formation. The cause of primary sclerosing cholangitis is unknown and is most commonly associated with ulcerative colitis. Patients can be asymptomatic or may develop symptoms of fatigue and pruritus due to biliary obstruction. If the obstruction is significant, patients may have jaundice, hepatosplenomegaly, and excoriations from pruritus on physical examination. However, approximately 50% of cases have a normal physical examination when the diagnosis is made. Serum studies typically demonstrate a cholestatic pattern on liver function tests, where the alkaline phosphatase level is predominantly elevated with mild elevation of serum aminotransferases. Patients with inflammatory bowel disease with a cholestatic pattern on serum labs raise suspicion for primary sclerosing cholangitis and merit imaging of the biliary tree. Magnetic resonance cholangiopancreatography is a noninvasive method of establishing the diagnosis and is seen as strictures visualized in the biliary tree, leading to a beaded appearance along the bile duct.
Complete blood count (A) can evaluate for anemia in patients with fatigue. However, it would not address the elevated alkaline phosphatase level and would not establish a diagnosis. Esophagogastroduodenoscopy (B) visualizes the upper gastrointestinal tract to evaluate for malignancy, ulcers, and a source of bleeding, which could result in anemia and subsequent fatigue. It would not explain the cholestatic pattern on the liver function test. Serum antimitochondrial antibodies (D) are present in primary biliary cholangitis and are usually absent in primary sclerosing cholangitis.
A 36-year-old woman is brought into the emergency department by her husband for evaluation of altered mental status, fever, and sweats. Her husband recounts that the patient developed nausea, vomiting, and diarrhea 3 days ago and was diagnosed with acute viral gastroenteritis at a local urgent care clinic. Their 3-year-old daughter had recently contracted norovirus in a confirmed outbreak at her preschool. This morning, when the patient awoke, she had a fever of 105°F, and her husband noticed she was acutely confused and not responding appropriately to questioning. Past medical history is notable for hyperthyroidism of unclear etiology, for which she is prescribed methimazole, although her husband reports that she skipped multiple doses in the past week. On vital signs, she has a temperature of 105°F, pulse of 130 bpm, blood pressure of 112/66 mm Hg, respiratory rate of 18 breaths per minute, and oxygen saturation of 99%. Physical exam shows bilateral lid lag, an enlarged thyroid gland, and moist skin. Complete blood count, comprehensive metabolic panel, and thyroid function tests are drawn. An ECG reveals sinus tachycardia without other abnormalities. The patient is admitted to the intensive care unit, and propranolol and hydrocortisone are administered. Which of the following therapies is also recommended?
It is recommended to administer propylthiouracil now followed by iodine solution in 1 hour. Thyroid storm is a severe, life-threatening thyrotoxicosis. It can occur in patients who have untreated hyperthyroidism secondary to Graves disease or other conditions such as a toxic multinodular goiter. Additional predisposing factors are commonly present, such as surgery, acute illness, an acute iodine load, or cessation of or irregular use of antithyroid medications. Clinical presentation involves high fevers to 104–106°F, tachycardia or atrial fibrillation, hypotension, altered mental status, anxiety, sweats, and high-output cardiac failure. Patients can also have associated nausea, vomiting, abdominal pain, and diarrhea. The diagnosis of thyroid storm is established on the basis of clinical presentation, and there are clinical scoring systems that can aid in diagnosis, such as the Burch-Wartofsky Point Scale. Biochemical evidence of hyperthyroidism, namely an increased free T3 or free T4 level in the setting of a suppressed TSH, can confirm the diagnosis. However, treatment of thyroid storm should be promptly initiated in patients with clinical thyroid storm features before laboratory results return to avoid delays in therapy. Admission to the intensive care unit is recommended. The beta-blocker propranolol is typically administered to control heart rate and other manifestations due to increased adrenergic tone. Glucocorticoids, such as hydrocortisone, are also administered to lower conversion of T4 to T3, support vasomotor stability, and also potentially decrease the autoimmune process in patients with associated Graves disease. Additionally, administration of the thioamide propylthiouracil is recommended to block further thyroid hormone synthesis. Iodine solution should also be given 1 hour after the initial dose of thioamide in patients with thyroid storm to inhibit the release of T3 and T4 from the thyroid gland. Bile acid sequestrants, such as cholestyramine, can also be considered as a treatment adjunct, especially in those who cannot take thionamides.
Methimazole now followed by iodine solution in 1 hour (C) is not the preferred treatment. Although methimazole is less hepatotoxic and has a longer duration of action, propylthiouracil administered every 4 hours is recommended for acute management of life-threatening thyroid storm for patients in the intensive care unit. Propylthiouracil results in a 45% decrease in T3 levels within 24 hours versus a 10–15% decrease in T3 levels with methimazole. Iodine solution now followed by methimazole in 1 hour (A) and iodine solution now followed by propylthiouracil in 1 hour (B) are incorrect. Iodine solution should not be administered until at least 1 hour after propylthiouracil initiation. If the patient develops thyroid storm secondary to a toxic multinodular goiter or a toxic adenoma, iodine can potentially be used as a substrate for new thyroid hormone synthesis. Therefore, propylthiouracil should be administered before giving iodine therapy to block thyroid hormone synthesis.