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+{"question": "A 21-year-old woman presents to her primary care physician due to a history of abdominal pain. She states that she has had recurrent bouts of mood swings, bloating, and abdominal pain that occur together approximately every 4 weeks. She states that when these symptoms occur, she gets into frequent arguments at work, is unable to concentrate, and sleeps longer than usual. Furthermore, she has episodes of extreme anxiety during these periods, leading her to take off time from work. She notes that these symptoms are causing distress in her interpersonal relationships as well. She has no past medical history and takes no medications. She experienced menarche at age 12 and has regular periods. Her temperature is 98.2\u00b0F (36.8\u00b0C), blood pressure is 100/70 mmHg, pulse is 75/min, and respirations are 12/min. Physical exam reveals a nontender abdomen. Pelvic exam reveals a closed cervix with no cervical motion or adnexal tenderness. Her cardiopulmonary and neurological exams are unremarkable. Which of the following is the most likely diagnosis?", "choicesA": "Premenstrual dysophoric disorder", "choicesB": "Premenstrual syndrome", "choicesC": "Major depressive disorder", "choicesD": "Generalized anxiety disorder", "answer_idx": "A", "answer": "Premenstrual dysophoric disorder", "explanation": "This patient with recurrent abdominal pain, bloating, and mood changes causing interpersonal difficulties related to the menstrual cycle likely has premenstrual dysphoric disorder. Premenstrual dysphoric disorder is a variant of premenstrual syndrome (PMS) characterized by prominent irritability and disruption of everyday life.\n\nPremenstrual dysphoric disorder is a variant of PMS characterized by recurrent physical and behavioral symptoms that manifest during the luteal phase of the menstrual cycle and resolve with menstruation. The diagnosis is made by criteria outlined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). To make a diagnosis of premenstrual dysphoric disorder, symptoms such as marked affective lability or marked irritability or anger must be present along with signs such as decreased concentration, hypersomnia or insomnia, and decreased interest in usual activities. These symptoms must cause significant distress or interfere with work, school, or relationships and must present 1 week before the onset of menses and resolve the week following menses. The initial management of premenstrual dysphoric disorder involves a pregnancy test to rule out pregnancy and a menstrual diary to prospectively confirm symptoms and their relationship to the menstrual cycle for 2 consecutive cycles. Following confirmation of a diagnosis of premenstrual dysphoric disorder, treatment involves lifestyle changes, antidepressant/anxiolytic medications, or hormonal therapies such as oral contraceptive pills (OCPs).\n\nBhatia et al. discuss premenstrual dysphoric disorder. They note that premenstrual dysphoric disorder affects 2-10% of women of reproductive age. They note that serotonin dysregulation may be relevant to the etiology and treatment of premenstrual dysphoric disorder.\n\nIncorrect Answers:\nAnswer A: Generalized anxiety disorder (GAD) is anxiety characterized by symptoms such as restlessness, fatigue, and irritability lasting > 6 months unrelated to any specific triggers. The topics of anxiety should be unrelated to one another. This patient's anxiety and symptoms are temporally related to her menstrual cycle, making premenstrual dysphoric disorder a more likely diagnosis.\n\nAnswer B: Major depressive disorder (MDD) is characterized by depressed mood and at least 5 of 9 \"SIG E CAPS\" symptoms for 2 weeks or longer. These symptoms include sleep disturbance, anhedonia, guilt, loss of energy, loss of concentration, appetite/weight changes, psychomotor retardation or agitation, and suicidal ideation. Though this patient exhibits some of these symptoms, premenstrual dysphoric disorder is a more likely diagnosis as she exhibits these symptoms temporally related to her menstrual cycle.\n\nAnswer C: Panic disorder is characterized by 4 or more panic attacks (sweating, palpitations, shaking, paresthesias) in a 4-week period or \u2265 1 panic attack followed by at least 1 month of fear of another panic attack. Though this patient experiences anxiety that leads her to avoid her work, she does not have any of the characteristic signs of a panic attack and therefore does not meet the criteria for diagnosis of panic disorder.\n\nAnswer E: PMS and premenstrual dysphoric disorder have overlap in their symptoms; however, premenstrual dysphoric disorder is characterized by symptoms that significantly affect daily functioning. This patient's symptoms have affected her work and relationships, making premenstrual dysphoric disorder a more likely diagnosis. Note that the workup and treatment is similar between these 2 conditions.\n\nBullet Summary:\nPremenstrual dysphoric disorder (PMDD) is a variant of premenstrual syndrome (PMS) characterized by more severe physical and mood symptoms that affect daily functioning.", "link": "https://step2.medbullets.com/testview?qid=216746"}
+{"question": "A 48-year-old woman, gravida 3 para 3, presents to the clinic with a 5-month history of intermittent loss of urine. Her urinary leaking occurs throughout the day and night, and she often has to get up to use the bathroom while asleep. Exercising does not affect the loss of urine. She states that she often cannot make it to the bathroom in time once she senses a need to void. Her last menstrual period was 2 weeks ago. Her urinalysis is unremarkable, and her postvoid residual volume is 40 mL. On pelvic examination, there is no dribbling of urine when the patient coughs. Physical exam is otherwise unremarkable. Which of the following is the most likely diagnosis?", "choicesA": "Overflow incontinence", "choicesB": "Urge incontinence", "choicesC": "Stress incontinence", "choicesD": "Mixed urinary incontinence", "answer_idx": "B", "answer": "Urge incontinence", "explanation": "This patient with a sudden need to void followed by loss of urine with urgency (unable to make it to the bathroom in time) most likely has urinary urge incontinence.\n\nUrge incontinence is a form of urinary incontinence characterized by a sudden urge to urinate, resulting in the involuntary leakage of urine. Normally, bladder contraction occurs due to the stimulation of muscarinic receptors in the detrusor muscle. Urinary urge incontinence is due to detrusor overactivity, leading to a sudden and frequently overwhelming need to void that occurs throughout the day and night. The most common cause is idiopathic, though it may be secondary to neurologic disorders (e.g., spinal cord injury or multiple sclerosis), bladder abnormalities, or chronic bladder inflammation. Workup is first centered on ruling out a urinary tract infection with a urinalysis. The diagnosis is made with urodynamic studies, and first-line treatment involves bladder training and pelvic floor exercises. Should first-line treatment of urge incontinence fail, antimuscarinic medications (such as oxybutynin) which reduce acetylcholine activity on muscarinic receptors can decrease detrusor contraction and thus the sense of urgency.\n\nNandy and Ranganathan review urge incontinence. They note that it presents with leakage of urine associated with a sudden urge to urinate. They recommend an appropriate history and workup to first rule out other causes.\n\nIncorrect Answers\nAnswer A: Genitourinary syndrome of menopause represents urinary symptoms (stress and/or urge incontinence) due to vaginal dryness and atrophy from menopause. This patient still has menstrual cycles and no symptoms of ovarian follicle depletion (narrowed introitus, vulvovaginal dryness and irritation, irregular vaginal bleeding), making this an unlikely diagnosis.\n\nAnswer B: Mixed urinary incontinence presents with features of both stress and urge incontinence. This patient lacks symptoms of stress incontinence given a lack of incontinence with increases in intrabdominal pressure (such as exercise, coughing, laughing, or sneezing).\n\nAnswer C: Overflow incontinence is caused by impaired detrusor muscle activity or bladder outlet obstruction. It presents with constant involuntary dribbling or urine and incomplete bladder emptying. Post-void residual volume is increased in patients with overflow incontinence.\n\nAnswer D: Stress incontinence is caused by urethral hypermobility and otherwise insufficient urethral support. It presents with urinary leakage with activities that increase intraabdominal pressure (such as coughing, sneezing, laughing, and exercising). This patient\u2019s symptoms are unrelated to exercise.\n\nBullet Summary:\nUrge incontinence presents with sudden urinary urgency with a normal post-void residual volume and absence of findings consistent with urinary tract infection.", "link": "https://step2.medbullets.com/testview?qid=216248"}
+{"question": "A 44-year-old man presents to the emergency department acutely confused. The patient\u2019s wife states she found him lethargic at home. He has been sick the past week with diarrhea and has been staying home from work. He is otherwise healthy and does not take any medications. His temperature is 97.5\u00b0F (36.4\u00b0C), blood pressure is 62/32 mmHg, pulse is 185/min, respirations are 25/min, and oxygen saturation is 98% on room air. The patient has profuse, bloody diarrhea while in the emergency department. The patient is given 3L of ringer lactate and subsequently appears less confused, with a blood pressure of 100/70 mmHg. He is able to drink oral fluids and protect his airway. An ECG is performed as seen in Figure A. He continues to have diarrhea while in the emergency department. Which of the following is contraindicated in the management of this patient?", "choicesA": "Loperamide", "choicesB": "Norepinephrine", "choicesC": "Ceftriaxone", "choicesD": "Normal saline", "answer_idx": "A", "answer": "Loperamide", "explanation": "This patient is presenting with infectious diarrhea (given his bloody diarrhea and hypotension) with unstable vitals that improve with fluids. In bloody diarrhea, loperamide is contraindicated and could worsen illness.\n\nBacterial diarrhea is commonly caused by organisms such as Campylobacter, Shigella, and Escherichia coli. It may present with bloody or purulent diarrhea and fever and may progress to sepsis or septic shock. Immediate management is centered on hydration. Unstable patients or those who cannot tolerate PO require IV fluids immediately. Otherwise, patients can rehydrate orally. Loperamide is an antimotility agent that decreases diarrheal output. It is contraindicated in bloody diarrhea as it can decrease the rate of fecal shedding and lead to bacteremia and a worsening clinical picture. Loperamide may be appropriate in controlling diarrhea in milder infectious forms of diarrhea, or in non-infectious conditions such as irritable bowel syndrome.\n\nBaker reviews loperamide. He discusses its indications, contraindications, and mechanism of action. They recommend that loperamide should not be given in invasive diarrhea.\n\nFigure/Illustration A demonstrates U waves on ECG (red arrows) that are significant for hypokalemia, which would be expected in a dehydrated patient with profuse diarrhea.\n\nIncorrect Answers:\nAnswer A: Ceftriaxone would be appropriate in this patient who has bacterial diarrhea and appears septic as his critically ill state warrants antibiotics. Note that this patient may receive broader antibiotics than ceftriaxone given how ill he appears. Antibiotics should not be routinely used for bacterial diarrhea in young, healthy patients with stable vitals.\n\nAnswer C: Magnesium could be appropriate in this patient even though his magnesium level is not stated as he is hypokalemic given his ECG is demonstrating U waves. The serum magnesium level does not adequately reflect intracellular magnesium levels. It requires replacement in many cases of hypokalemia.\n\nAnswer D: Norepinephrine could be appropriate in this patient if he remained persistently hypotensive despite fluid administration. Note that this patient could receive more fluids and is not frankly unstable. While norepinephrine may not be appropriate at this time, it is not contraindicated.\n\nAnswer E: Normal saline is generally avoided in diarrheal illness in patients who can tolerate PO as oral hydration is preferred to IV. However, IV fluids are not contraindicated and would be appropriate in this persistently hypotensive patient. Normal saline has a very high sodium and chloride load and can cause a hyperchloremic metabolic acidosis. For this reason, a lower-chloride solution may be preferred (e.g, Lactated Ringer).\n\nBullet Summary:\nLoperamide is contraindicated in bloody diarrhea.", "link": "https://step2.medbullets.com/testview?qid=216585"}
+{"question": "A 55-year-old man presents to the emergency department after fainting while moving furniture. He states that he has been working in a hot, humid attic all day and forgot his water bottle. He felt dizzy when standing up and then fainted and was unconscious for roughly 1 minute. He awoke at his neurologic baseline afterwards. The patient has a history of hypertension being managed by his primary care doctor. His temperature is 98.7\u00b0F (37.1\u00b0C), blood pressure is 149/82 mmHg, pulse is 86/min, respirations are 15/min, and oxygen saturation is 99% on room air. Physical exam reveals a diaphoretic man. He demonstrates an unremarkable cardiopulmonary exam. The patient walks with a steady gait and his neurologic exam is non-focal. An ECG is performed as seen in Figure A. The patient is given 2 liters of oral fluids and feels back to his baseline. Which of the following conditions is most likely to occur in this patient based on his current history and ECG?", "choicesA": "Atrial fibrillation", "choicesB": "Torsades des pointes", "choicesC": "Stroke", "choicesD": "Complete heart block", "answer_idx": "D", "answer": "Complete heart block", "explanation": "This patient is presenting with dizziness and syncope in the setting of likely dehydration (working in a hot/humid environment without water) and feels better after rehydration, suggesting a diagnosis of orthostatic hypotension. An ECG is performed and incidentally demonstrates a bifascicular block, which is at high risk of progressing to a complete heart block.\n\nBifascular block is a conduction abnormality in 2 of the 3 fascicles that conduct electricity from atria to ventricles. This leaves conduction to the ventricles via the single remaining fascicle. There are different possibilities that may present on ECG. One possibility is a right bundle branch block with a left anterior fascicular block; the other is a right bundle branch block with a left posterior fascicular block. Note that the pathophysiology of complete heart block is an inability to conduct electricity from the atria to the ventricles. If there is only 1 fascicle left to conduct electricity, the patient would be in complete heart block if this fascicle were to no longer work, which is a common outcome in patients with bifascicular block. Treatment of complete heart block involves the placement of a pacemaker.\n\nWiberg et al. discuss bifascicular block. They note the possible outcome of a complete heart block. It is recommended to look for this finding on ECG and appropriately workup patients to prevent progression of disease.\n\nFigure/Illustration A is an ECG demonstrating bifascicular block. Note the left axis deviation as suggested by the net upward deflection of the QRS in lead I and net downward deflection in lead II (blue arrows). Then, note the appearance of a right bundle branch block with the RSR pattern in aVR (black arrow) and upward R\u2019 in lead V1 (green arrow). This is a classic pattern for bifascicular block. Contrast this to the other pattern of bifascicular block which would present with a right bundle branch block and right axis deviation (upward QRS in lead II and downward in lead I), which was not seen in this case.\n\nIncorrect Answers:\nAnswer A: Atrial fibrillation may occur secondary to aging, hypertension, or ischemia and presents with an irregularly irregular rate and rhythm with an absence of P waves. It may cause complications such as stroke. Management typically involves rate control agents such as beta-blockers or calcium channel blockers.\n\nAnswer C: Myocardial infarction is a likely outcome in individuals with risk factors such as obesity, hypertension, smoking, and dyslipidemia, in particular, without proper preventive measures and medical therapy including statins, beta blockers, and ACE inhibitors. This patient may be at risk of a myocardial infarction with his hypertension, and his underlying bifascicular block could suggest undiagnosed cardiac ischemia; however, it is more likely this patient progresses to complete heart block in the setting of his bifascicular block.\n\nAnswer D: Stroke is a possible complication of atrial fibrillation. For this reason, most patients with atrial fibrillation are on blood thinners to prevent this complication. It occurs secondary to stasis of blood in the fibrillating left atrium. Patients are often risk stratified prior to starting blood thinners with tools such as CHADS2VASC and HASBLED. Isolated syncope is a rare manifestation of stroke.\n\nAnswer E: Torsades des pointes is a progression from QT prolongation which may occur secondary to genetic conditions, medications, and/or infection. It presents on ECG with QRS complexes that twist in amplitude around the electrical baseline. Treatment involves the administration of magnesium sulfate and, if needed, electrical cardioversion.\n\nBullet Summary:\nA bifascicular block can progress to complete heart block.", "link": "https://step2.medbullets.com/testview?qid=216637"}
+{"question": "A 55-year-old man with a history of polysubstance abuse is found down in his home acutely obtunded. Emergency medical services administered naloxone which immediately woke the patient up and improved his oxygen saturation from 40% to 90%. However, they noted subsequently that the patient demonstrated increased work of breathing and had crackles and wheezing on pulmonary exam. The patient arrives alert and oriented claiming he feels short of breath. He denies any chest pain or other symptoms aside from shortness of breath. He has a history of cocaine-induced cardiomyopathy and myocardial infarction from cocaine use 2 years ago. The patient has a 40 pack-year smoking history. His temperature is 96.0\u00b0F (35.6\u00b0C), blood pressure is 120/68 mmHg, pulse is 102/min, respirations are 26/min, and oxygen saturation is 88% on room air. Physical exam reveals increased work of breathing, pulmonary crackles, and wheezing. A chest radiograph is performed as seen in Figure A. Which of the following is the most likely etiology of this patient's current symptoms?", "choicesA": "Medication administration", "choicesB": "Community acquired pneumonia", "choicesC": "Atypical pneumonia", "choicesD": "Poor cardiac function", "answer_idx": "A", "answer": "Medication administration", "explanation": "This patient is presenting after administration of naloxone with respiratory distress, wheezing, crackles, and pulmonary edema on chest radiography, suggesting acute pulmonary edema. Given the presence of symptoms immediately following naloxone administration, the cause of the pulmonary edema is likely the naloxone (medication-induced) that was administered.\n\nOpioid use disorder is a common problem in the United States and can lead to overdose, which is life-threatening if not treated. Patients with symptoms of opioid intoxication including miosis, bradypnea, and altered mental status should be empirically given naloxone, as it may be life-saving and is relatively benign. Naloxone should only be given for patients with unstable vitals or who are failing to ventilate/oxygenate or protect their airway. Naloxone commonly precipitates withdrawal and may cause nausea, vomiting, diarrhea, and pain. It is possible for naloxone to cause pulmonary edema (via a poorly elucidated mechanism). Pulmonary edema presents with wheezing, tachypnea, and pulmonary crackles. The most important intervention when treating pulmonary edema is to address the underlying cause and start the patient on positive pressure ventilation. Diuretics may be administered if the patient is volume overloaded. An echogardiogram can rule out poor cardiac function as the underlying etiology as well.\n\nLassen et al. review naloxone use and pulmonary edema. They note that naloxone administration can cause non-cardiogenic pulmonary edema and that the mechanism is not well elucidated. They recommend that naloxone should only be used at the lowest dose possible to stabilize the patient.\n\nFigure A is a chest radiograph demonstrating \"fluffy\" interstitial infiltrates throughout both lung fields suggestive of pulmonary edema.\n\nIncorrect Answers:\nAnswer A: Atypical pneumonia may present with a dry cough, fever, hypoxia, and increased interstitial markings on chest radiograph. These patients are usually well appearing, and the opacities are not as \"fluffy\" as pulmonary edema. A common cause is Mycoplasma pneumoniae.\n\nAnswer B: Chronic obstructive pulmonary disease (COPD) presents with a flattened diaphragm and increased number of visible ribs on chest radiography as a result of air accumulation in the chest. Pneumonia may be present on chest radiograph and is a common cause of COPD flares. A COPD flare may present with wheezing, poor air movement, hypoxia, and hypercarbia.\n\nAnswer C: Community-acquired pneumonia presents with a fever, cough, hypoxia, and a lobar consolidation on chest radiograph. This infiltrate is usually confined to one lobe and is thus often called \"lobar pneumonia.\" Streptococcus pneumoniae is the most common cause.\n\nAnswer E: Poor cardiac function can cause pulmonary edema via increased hydrostatic pressure backing up into the lungs causing fluid leakage. Though the appearance of pulmonary edema would be the same, naloxone causes non-cardiogenic pulmonary edema. In this patient with a previous myocardial infarction, a low ejection fraction may plausibly be contributing to this patient's pulmonary edema; however, the association of symptoms with naloxone administration makes this a less likely etiology for this case.\n\nBullet Summary:\nNaloxone can cause non-cardiogenic pulmonary edema.", "link": "https://step2.medbullets.com/testview?qid=216360"}
+{"question": "A 42-year-old man presents to the urgent care clinic with low back pain. He was working on a home improvement project the day prior to presentation when the pain started. He describes the pain as \"achy and sore.\" It is not positional and does not radiate. He denies fevers, chills, paresthesias, and bowel or bladder incontinence. He has a history of a distal radius fracture 2 years ago from falling off a ladder. He drinks 3 alcoholic beverages weekly and denies illicit drug use. The patient\u2019s temperature is 98.4\u00b0F (36.9\u00b0C), blood pressure is 124/80 mmHg, pulse is 90/min, and respirations are 16/min. His body mass index (BMI) is 22.4 kg/m^2. There is tenderness to palpation of his paravertebral lumbar region bilaterally. Perineal and dermatomal sensation is symmetric and intact. Strength is 5/5 to knee flexion/extension and ankle dorsiflexion/plantarflexion. Patellar and Achilles reflexes are 2+ bilaterally. Raising either leg while the patient is in the supine position does not elicit any pain. Which of the following is the most likely diagnosis?", "choicesA": "Osteoarthritis", "choicesB": "Vertebral compression fracture", "choicesC": "Lumbar strain", "choicesD": "Disc herniation", "answer_idx": "C", "answer": "Lumbar strain", "explanation": "This patient presents with low back pain after activity with paravertebral tenderness and without red flag signs/symptoms, such as history of trauma or malignancy, intravenous drug use, saddle anesthesia (reduced perineal sensation), or neurological deficits. The most likely diagnosis is a lumbar strain.\n\nThe differential diagnosis of low back pain is broad and includes mechanical causes such as lumbar strain, osteoarthritis, spondylolisthesis, disc herniation, spinal stenosis, and fractures as well as non-mechanical etiologies such as osteomyelitis and malignancy. History and physical should focus on eliciting red flag symptoms, including traumatic etiology, constitutional symptoms (e.g., fever, weight loss), history of malignancy, intravenous drug use, steroid use, and neurological deficits (e.g., saddle anesthesia, incontinence). The presence of any red flags should prompt further evaluation with imaging. Lumbar strain typically presents with acute low back pain after a precipitating event (e.g., lifting weight) with no red flag signs/symptoms and responds well to conservative management including activity modification, ice, and non-steroidal anti-inflammatory drugs. Prevention measures include strengthening of core muscles and education on proper lifting techniques. Physical therapy is a core component of treating patients with muscle strains.\n\nKnezevic et al. review lower back pain. They note the many potential causes and symptoms that may present. They recommend a multimodal interdisciplinary approach to back pain given the many mechanisms, especially in complex cases.\n\nIncorrect Answers:\nAnswer A: Disc herniation presents with radicular symptoms due to compression of spinal nerve roots as they exit the spinal canal, manifesting as a burning or shooting pain that radiates down either leg. Dermatomal sensory changes or hyporeflexia may be present depending on the spinal level affected (e.g., reduced Achilles reflex with S1 radiculopathy). The straight leg raise reproduces pain radiating down the leg on the affected side.\n\nAnswer B: Lumbar stenosis characteristically causes low back pain or lower extremity paresthesias with walking or standing that resolves when leaning forward (\u201cshopping cart sign\u201d). This is referred to as neurogenic claudication. Involvement of spinal nerve roots can lead to sensory loss and weakness in the lower extremities.\n\nAnswer D: Osteoarthritis can cause low back pain and stiffness, but is an age-related degenerative disease that is less likely in this patient who presents acutely after activity. The patient also does not have the typical risk factors for osteoarthritis, which include advanced age, female sex, or obesity.\n\nAnswer E: Vertebral compression fracture occurs mainly in osteoporotic patients, whose reduced bone mineral density increases their risk for vertebral body collapse under stress. Vertebral compression fractures present with point tenderness at the midline over the site of fracture. Additionally, this patient has no risk factors for osteoporosis (e.g., advanced age, post-menopausal women, low BMI).\n\nBullet Summary:\nLumbar strain presents as low back pain without red flag signs or symptoms (e.g., constitutional symptoms, neurologic deficits) and is treated conservatively with activity modification, ice, and core strengthening.", "link": "https://step2.medbullets.com/testview?qid=216255"}
+{"question": "A 77-year-old man presents to the emergency department acutely obtunded. The patient lives alone and was found unresponsive by his son. Generally, the patient manages his own finances, medications, and works part-time. He has not been responding to phone calls for the past 3 days. The patient is unable to offer a history. He has a past medical history of hypothyroidism, depression, and diabetes. His temperature is 88.0\u00b0F (31.1\u00b0C), blood pressure is 92/62 mmHg, pulse is 35/min, respirations are 9/min, and oxygen saturation is 92% on room air. The patient is cold to the touch and moves all extremities to painful stimuli. His pupils are reactive and sluggish, and he does not follow commands. There are no signs of trauma or skin infections. The patient is started on IV fluids and hydrocortisone, is externally warmed, and is started on a norepinephrine drip. An ECG is performed as seen in Figure A. Which of the following is the most appropriate next step in management?", "choicesA": "Levothyroxine administration", "choicesB": "Free T4 level", "choicesC": "Thyroid stimulating hormone and free T4 level", "choicesD": "Triiodothyronine administration", "answer_idx": "A", "answer": "Levothyroxine administration", "explanation": "This elderly patient with a past medical history of hypothyroidism is presenting with altered mental status, hypotension, hypothermia, and bradycardia, which are concerning for myxedema coma. Empiric and immediate treatment with levothyroxine is the appropriate management of this condition prior to confirming the diagnosis with lab studies.\n\nMyxedema coma is a life-threatening complication of hypothyroidism. It presents with stupor/obtundation, bradycardia, hemodynamic instability, and hypothermia. With a high clinical suspicion, appropriate history, physical exam, and vitals, it is appropriate to first treat the patient with IV hydrocortisone (or another highly potent steroid) and levothyroxine prior to confirming the diagnosis given the high morbidity and mortality associated with this condition. Triiodothyronine is given in some circumstances as well (in more ill patients) but is less dire than first giving levothyroxine. Subsequently, the diagnosis can be confirmed with a serum thyroid stimulating hormone (TSH) and free T4 level. Patients are critically ill and typically require further care in an ICU.\n\nWall discusses the management of myxedema coma. He notes this is a potentially lethal condition. He recommends immediate administration of IV levothyroxine.\n\nFigure A is an ECG with sinus bradycardia.\n\nIncorrect Answers:\nAnswers 1, 3, & 4: Thyroid stimulating hormone and free T4 levels should certainly be obtained; however, the mortality for myxedema coma is so high that empiric treatment with levothyroxine should be started with clinical suspicion alone prior to confirming the diagnosis with laboratory studies, as a delay in therapy could increase morbidity and mortality. After administration of levothyroxine and initial supportive therapy, the diagnosis can be supported with laboratory studies.\n\nAnswer E: Triiodothyronine or T3 could be appropriate in patients with myxedema coma in severe scenarios where patients do not respond to levothyroxine. In some cases, it may also be given empirically but does not take priority over T4 administration.\n\nBullet Summary:\nIn myxedema coma, empiric treatment with levothyroxine is appropriate with a high clinical suspicion for the diagnosis prior to laboratory confirmation.", "link": "https://step2.medbullets.com/testview?qid=216587"}
+{"question": "A 52-year-old G3P3 woman presents to clinic with a 2-year history of urinary incontinence. She has had frequent, involuntary loss of urine over the last 2 years but presented today because of 10 days of dysuria. She has been treated for 2 urinary tract infections over the past 6 months. She does not endorse any loss of urine with coughing or laughter. She has no chronic medical illnesses and no surgical history. Her temperature is 99.5\u00b0F (37.5\u00b0C), blood pressure is 120/80 mmHg, pulse is 92/min, and respirations are 15/min. Her BMI is 30 kg/m^2. On pelvic examination, the vagina is dry and atrophic with a 2-cm tender, palpable anterior vaginal mass. The mass does not change with Valsava maneuver. Her postvoid residual volume is 60 mL. Which of the following is the most likely diagnosis?", "choicesA": "Urethral diverticulum", "choicesB": "Overflow incontinence", "choicesC": "Stress urinary incontinence", "choicesD": "Pelvic organ prolapse", "answer_idx": "A", "answer": "Urethral diverticulum", "explanation": "This patient is presenting with a history of dysuria, incontinence, and recurrent lower urinary tract infections in conjunction with a tender anterior vaginal wall mass. The most likely diagnosis is a urethral diverticulum.\n\nA urethral diverticulum is an abnormal, localized outpouching of the urethral mucosa often due to recurrent periurethral gland infection. The outpouching can often collect and store urine, resulting in slow postvoid dribbling and recurrent urinary tract infections. Urethral diverticula can often be associated with expressed purulent or bloody discharge on exam. Initial workup includes urinalysis and transvaginal ultrasound. Diagnosis can be confirmed with a pelvic MRI before referral for surgical excision.\n\nGreiman et al. review urethral diverticula and its treatment. They note that surgical repair is challenging. However, it is still recommended to perform surgery in appropriate candidates.\n\nIncorrect Answers:\nAnswer A: Overflow incontinence (caused by impaired detrusor activity or bladder outlet obstruction) can also present with involuntary loss of urine due to urinary retention. However, this patient\u2019s normal postvoid residual volume (< 150 mL) makes this an unlikely diagnosis. Patients will often present with a constant dribbling of urine and a sensation of incomplete voiding.\n\nAnswer B: Pelvic organ prolapse occurs due to weakened pelvic support and increased intraabdominal pressure and can be exacerbated by increasing parity. While it can also present with incontinence, physical exam often reveals a bulging mass that increases with Valsava maneuver - a finding that is absent in this patient.\n\nAnswer C: Stress urinary incontinence is caused by urethral hypermobility leading to urinary leakage from increased intraabdominal pressure. This patient\u2019s urinary loss is unrelated to coughing or laughing, and stress incontinence would not explain the anterior vaginal mass. On exam, urine may be released with coughing.\n\nAnswer E: Vesicovaginal fistula is an abnormal tract between the vagina and bladder that presents with constant leakage of urine due to the direct draining of urine from the bladder to the vagina. This patient\u2019s incontinence is intermittent and not constant, and a vesicovaginal fistula would not explain the anterior vaginal mass.\n\nBullet Summary:\nA urethral diverticulum presents with dysuria, intermittent urinary incontinence, and a tender anterior vaginal wall mass that may cause recurrent urinary tract infections.", "link": "https://step2.medbullets.com/testview?qid=216247"}
+{"question": "A 48-year-old man presents to the emergency room with a 2-hour history of severe abdominal pain, nausea, and vomiting. He states that he has not passed gas or had a bowel movement in 4 days and his pain has worsened and become constant over the past 2 hours. His only medical history includes an appendectomy that he underwent as a child, and he takes no daily medications. His temperature is 38.5\u00b0C (101.3\u00b0F), blood pressure is 92/60 mmHg, pulse is 138/min, and respirations are 25/min. His pulse oximetry is 99% on room air.There are no cardiopulmonary abnormalities on auscultation. His abdomen is distended and tender in all quadrants, with guarding and rebound present. He also has increased bowel sounds throughout. Laboratory results are as follows:\n\nHemoglobin: 11 g/dL\nLeukocyte count: 16,500/mm^3 with normal differential\nPlatelets: 250,000/mm^3\n\nSerum:\nCreatinine: 1.0 mg/dL\nGlucose: 95 mg/dL\nLipase: 45 U/L\nTotal bilirubin: 0.8 mg/dL\nAlkaline phosphatase: 74 U/L\nAspartate aminotransferase (AST, GOT): 32 U/L\nAlanine aminotransferase (ALT, GPT): 45 U/L\nLactate: 7.0 mmol/L\n\nWhich of the following is the most appropriate next step in management?", "choicesA": "Supportive care, NPO, and intravenous fluids", "choicesB": "Urgent surgical intervention", "choicesC": "Nasogastric tube placement", "choicesD": "CT angiography of the abdomen and pelvis", "answer_idx": "B", "answer": "Urgent surgical intervention", "explanation": "This patient with abdominal pain, vomiting, and obstipation is now hemodynamically unstable with fever, leukocytosis, rising lactate, and worsening pain. He most likely has a complicated small-bowel obstruction (SBO) and should undergo immediate surgical intervention.\n\nSBO occurs when the normal progression of intraluminal contents in the intestines is interrupted, with most cases stemming from mechanical blockages. A history of abdominal surgery is a risk factor for SBO due to the formation of adhesions. Patients with SBO can typically be managed conservatively including nasogastric tube suction (if discomfort and active vomiting), bowel rest, and intravenous fluid resuscitation. However, patients with findings of a complicated SBO (changes in abdominal pain, fever, leukocytosis, guarding, and hemodynamic instability) require emergent surgical intervention. Delay in abdominal exploration may lead to necrosis, perforation, infection and a significant risk of mortality.\n\nBower et al. review small bowel obstruction. They note the need for operative intervention only in those who fail conservative management. They recommend nonoperative management for most cases of small bowel obstruction.\n\nIncorrect Answers:\nAnswer A: Broad-spectrum antibiotics and serial abdominal radiographs alone would not be appropriate for this patient with a deteriorating clinical picture (hemodynamically unstable, worsening abdominal pain, fever, leukocytosis, high lactate). Antibiotics are not indicated in patients with uncomplicated SBO but may be useful in reducing infection risk in patients with complicated SBO. This patient should undergo emergent abdominal exploration in addition to receiving broad-spectrum antibiotics as it is possible he has already experienced bowel perforation.\n\nAnswer B: Computed tomography angiography (CTA) is useful in the diagnosis of acute mesenteric ischemia, which classically presents with abdominal pain out of proportion to exam (severe pain without much tenderness), vomiting, abdominal distention, and decreased bowel sounds. However, severe peritonitis and obstipation are more characteristic of SBO, and this patient is too hemodynamically unstable to undergo further imaging before proceeding to surgery.\n\nAnswers 3 & 4: Nasogastric tube placement with supportive care can be used to conservatively manage patients with uncomplicated SBO. This hemodynamically unstable patient has a fever, guarding, peritoneal signs, and newly worsened abdominal pain, indicative of a complicated SBO. He should be taken emergently to the operating room as the next step in management.\n\nBullet Summary:\nPatients with intestinal obstruction who have a surgical abdomen or hemodynamic instability should undergo immediate surgical intervention.", "link": "https://step2.medbullets.com/testview?qid=216246"}
+{"question": "A 26-year-old woman presents to the emergency department because she feels as though her heart is \"beating out of her chest.\" She states that she feels well apart from the discomfort of that sensation. Her temperature is 97.9\u00b0F (36.6\u00b0C), blood pressure is 124/84 mmHg, pulse is 180/min, respirations are 22/min, and oxygen saturation is 98% on room air. An ECG is obtained as seen in Figure A. After unsuccessful attempts at vagal maneuvers, the emergency physician administers an IV medication. The effect of the medication wears off in seconds. Which of the following is a potential side effect of this medication?", "choicesA": "Tachycardia", "choicesB": "Photosensitivity", "choicesC": "Flushing", "choicesD": "Seizure", "answer_idx": "C", "answer": "Flushing", "explanation": "This patient presents with a narrow complex tachycardia that is regular which is suggestive of supraventricular tachycardia (SVT) and was pharmacologically cardioverted with adenosine (as it has a very short half-life). Side effects of adenosine include flushing, hypotension, bronchospasm, and heart block.\n\nSVT presents with a narrow-complex, regular tachycardia. The diagnosis is made with these findings on ECG. Management in an unstable patient is centered on cardioversion. Otherwise, the first step in management is centered on vagal maneuvers. If these fail, adenosine is the first-line pharmacologic treatment. While a relatively safe drug, side effects of adenosine include hypotension, heart block, flushing, and bronchospasm. Patients may also report a \"sense of impending doom\" following administration, thought to be the result of the transient asystole adenosine produces. Persistent SVT refractory to adenosine may be further managed with calcium channel blockers, beta blockers, or cardioversion.\n\nColucci et al. review the diagnosis and management of common types of supraventricular tachycardias. The most common types of supraventricular tachycardia are caused by a reentry phenomenon producing accelerated heart rates. Symptoms may include palpitations, chest pain, lightheadedness or dizziness, and dyspnea. If Wolff-Parkinson-White syndrome is present, expedient referral to a cardiologist is warranted because ablation is a potentially curative option.\n\nFigure A is an ECG demonstrating SVT. Note the regular narrow complex tachycardia that is a defining feature of this condition.\n\nIncorrect Answers:\nAnswer A: A disulfiram-like reaction was once thought to be associated with medications such as metronidazole. Metronidazole is an antibiotic that covers anaerobes. When alcohol is consumed in a patient on disulfiram, headache, malaise, nausea, and vomiting may be experienced.\n\nAnswer C: Photosensitivity is associated with medications such as sulfonamides, amiodarone, and tetracycline. Patients should be advised to stay out of the sun on these medications.\n\nAnswer D: Seizures are not associated with adenosine. Isoniazid, bupropion, imipenem/cilastatin, tramadol, enflurane, and metoclopramide are all known to increase the risk of seizures. Seizures often present with tonic-clonic activity, tongue biting, urinary incontinence, and a postictal phase.\n\nAnswer E: Tachycardia can be associated with medications such as atropine which reduce vagal tone on the heart increasing the heart rate. Medications that block the AV node would be expected to cause bradycardia.\n\nBullet Summary:\nAdenosine is a first-line pharmacological agent in supraventricular tachycardia and can cause hypotension, heart block, flushing, and bronchospasm.", "link": "https://step2.medbullets.com/testview?qid=106849"}