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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°F (36.8°C), 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?
|
{
"A": "Premenstrual dysophoric disorder",
"B": "Premenstrual syndrome",
"C": "Major depressive disorder",
"D": "Generalized anxiety disorder",
"E": ""
}
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A
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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.
Premenstrual 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).
Bhatia 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.
Incorrect Answers:
Answer 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.
Answer 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.
Answer C: Panic disorder is characterized by 4 or more panic attacks (sweating, palpitations, shaking, paresthesias) in a 4-week period or ≥ 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.
Answer 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.
Bullet Summary:
Premenstrual dysphoric disorder (PMDD) is a variant of premenstrual syndrome (PMS) characterized by more severe physical and mood symptoms that affect daily functioning.
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A 62-year-old woman is brought to a physician by her husband for fluctuating changes in behavior and hallucinations over the past 2 years. On occasion, she becomes difficult to understand and her speech becomes disorganized. She also frequently sees "small people" and animals on the dining room table, which is disturbing to her. Her medical problems include hypertension and chronic obstructive pulmonary disease for which she takes amlodipine, albuterol, ipratropium, and a fluticasone inhaler. She was formerly an executive at a software company but had to retire due to frequent memory lapses. Her temperature is 98.6°F (37°C), blood pressure is 120/80 mmHg, pulse is 80/min, and respirations are 12/min. Physical exam is notable for slowed movements and difficulty with balance at rest, which were not present at her wellness visit 1 year ago. Which of the following pathological findings (Figures A-E) would most likely be seen if a brain biopsy were performed?
|
{
"A": "Figure D",
"B": "Figure E",
"C": "Figure B",
"D": "Figure C",
"E": ""
}
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D
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This patient with fluctuating changes in behavior and cognition, visual hallucinations, memory loss, and extrapyramidal symptoms (bradykinesia, postural instability) most likely has Lewy body dementia. Lewy body dementia is characterized histologically by Lewy bodies, which are intracytoplasmic eosinophilic inclusions of alpha-synuclein (shown in Figure C).
Alpha-synuclein is normally abundantly present in its unfolded form in neurons. Abnormal folding of alpha-synuclein leads to aggregation into insoluble fibrils. These intracytoplasmic aggregates (Lewy bodies) are seen in Parkinson disease, Lewy body dementia, and multiple system atrophy, which are collectively referred to as alpha-synucleinopathies. Lewy body dementia is the second most common degenerative dementia and presents with fluctuating cognition, visual hallucinations, parkinsonism (bradykinesia, postural instability, rigidity, and a resting tremor), rapid eye movement (REM) sleep disorder, autonomic dysfunction, and sensitivity to antipsychotics. Lewy body dementia can be distinguished from Parkinson disease with dementia by the timing of symptoms. In Lewy body dementia, cognitive symptoms begin at the same time as or 1 year prior to the onset of movement symptoms whereas in Parkinson disease the cognitive symptoms classically occur over 1 year after motor symptoms. There is no cure for Lewy body dementia, and treatment is aimed at alleviating symptoms.
Arnaoutoglou et al. reviewed the epidemiology, pathology, treatment, and future directions for research of Lewy body dementia. The authors found potential genetic bases for Lewy body dementia, including mutations in the GBA gene. They recommended that further research be conducted on the therapeutic implications of these genetic findings.
Figure/Illustration A shows a hematoxylin and eosin (H&E) stained brain biopsy of a patient with Creutzfeldt-Jakob disease. Characteristic spongiform changes in neurons (yellow boxes) and agglomerated prions (orange arrows) are seen in this slide.
Figure/Illustration B shows an H&E stained brain biopsy of a patient with a small lacunar infarct on low magnification. A central area of tissue loss (yellow outline) and surrounding residual gliosis (orange arrows) are seen in this slide.
Figure/Illustration C shows a brain biopsy of a patient with Lewy body dementia stained with mouse anti-alpha-synuclein antibody and counterstained with hematoxylin. Lewy bodies (intracytoplasmic eosinophilic inclusions of alpha-synuclein) are indicated by orange arrows. Note that Lewy bodies are always found intracellularly (neurons highlighted by blue boxes).
Figure/Illustration D shows an H&E stained brain biopsy of a patient with Alzheimer disease. Extracellular neurofibrillary tangles found in Alzheimer disease are indicated by black arrows.
Figure/Illustration E shows an H&E stained brain biopsy of a patient with frontotemporal dementia. A characteristic Pick cell (red box), or ballooned neuron, with dissolved chromatin (yellow arrow), is seen in this slide.
Incorrect Answers:
Answer A: Figure A shows an H&E stained brain biopsy of a patient with Creutzfeldt-Jakob disease. Creutzfeldt-Jakob disease is a rapidly progressive dementia that manifests with poor concentration, declining executive function, startle myoclonus, 14-3-3 protein on lumbar puncture, and synchronous sharp wave complexes on electroencephalogram (EEG). Clinical decline occurs over the course of weeks and months, culminating in death within a year. Creutzfeldt-Jakob disease shows spongiform vacuolation due to the accumulation of abnormal prion protein (PrPsc).
Answer B: Figure B shows an H&E stained brain biopsy of a patient with a small lacunar infarct. Lacunar infarcts may be asymptomatic or cause focal neurologic deficits such as motor hemiparesis, pure sensory stroke, ataxic hemiparesis, or dysarthria-clumsy hand syndrome depending on the territory involved. Lacunar strokes will show diffuse eosinophilia of the affected area, followed by liquefactive necrosis with neutrophilic infiltration, followed by macrophages with surrounding reactive gliosis, finally leading to an area of tissue loss with residual gliosis.
Answer D: Figure D shows an H&E stained brain biopsy of a patient with Alzheimer disease. Alzheimer disease presents with a gradual cognitive decline with difficulty completing activities of daily living. Memory is the most prominently affected domain. Visual hallucinations, fluctuating levels of cognition, and extrapyramidal symptoms are not common in Alzheimer disease. Amyloid plaques and neurofibrillary tangles may be seen on brain biopsy.
Answer E: Figure E shows an H&E stained brain biopsy of a patient with frontotemporal dementia (Pick disease). The behavioral variant of frontotemporal dementia is associated with early-onset personality and behavioral changes, and it may be associated with extrapyramidal symptoms. Unlike Lewy body dementia, memory is usually not affected in frontotemporal dementia until late in the disease course. frontotemporal dementia is characterized by Pick cells (ballooned neurons with dissolved chromatin) and Pick bodies, round intracellular aggregates of hyperphosphorylated tau protein.
Bullet Summary:
Lewy body dementia presents with alterations in consciousness, disorganized speech, visual hallucinations, extrapyramidal symptoms, early compromise of executive functions, and eosinophilic intracytoplasmic inclusions of alpha-synuclein (Lewy bodies) on biopsy.
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303
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A 55-year-old woman is brought to the emergency department by her husband with a 1 hour history of an unremitting headache. The headache started suddenly while she was eating dinner and she says it feels like the “worst headache of my life.” An emergent CT scan of the head without contrast confirms the diagnosis, and a CT angiogram identifies the source of bleeding. The patient undergoes surgical management of her condition. On hospital day 3, she is found to be disoriented to person, place, and time. She also develops nausea and vomiting. Her medical problems consist of heart failure for which she takes furosemide, spironolactone, and metoprolol, which were continued at admission. Her temperature is 99.6°F (37.6°C), blood pressure is 100/60 mmHg, pulse is 112/min, and respirations are 16/min. Physical examination shows poor skin turgor. Capillary refill time is 4 seconds. Serum laboratory results are shown below: Na+: 120 mEq/L Cl-: 92 mEq/L K+: 3.9 mEq/L HCO3-: 26 mEq/L BUN: 32 mg/dL Creatinine: 1.0 mg/dL Serum osmolality is 265 mEq/L and urine osmolality is 340 mEq/L. Urine sodium is 44 mEq/L. Which of the following is the most likely diagnosis?
|
{
"A": "Addison disease",
"B": "Cerebral salt wasting",
"C": "Diuretic overuse",
"D": "Syndrome of inappropriate anti-diuretic hormone",
"E": ""
}
|
B
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This patient presents with a subarachnoid hemorrhage (“worst headache of my life”) which is treated and then subsequently develops nausea, vomiting, and altered mental status with reduced serum sodium concentration, indicative of symptomatic hyponatremia. In the setting of serum hypo-osmolality, urine hyper-osmolality, urine sodium concentration > 20 mEq/L, and hypovolemia (low blood pressure, decreased skin turgor, and prolonged capillary refill), this is indicative of cerebral salt wasting.
The mechanism of cerebral salt wasting is unclear, although some hypotheses point to increased release of brain natriuretic peptide after injury leading to suppression of renal sodium reabsorption, or sympathetic nervous system injury resulting in an impaired renin response. Patients classically present several days after cerebral injury or neurosurgery with hypovolemic hyponatremia and hypochloremia. Water retention results in serum hypo-osmolality, hyponatremia, and hypochloremia with urine hyper-osmolality and increased urine sodium excretion. In patients with prolonged cerebral salt wasting, hypokalemia can also occur (potassium may be normal in acute states). Treatment in mild or moderate cases consists of normal saline infusion to correct both volume status and hyponatremia. Treatment in severe cases consists of hypertonic saline. During correction, serum sodium must be monitored closely to prevent central pontine myelinolysis.
Cui et al. describe the differences between syndrome of inappropriate anti-diuretic hormone (SIADH) and cerebral salt wasting. They discuss how volume status serves as the key differentiator between these conditions. They recommend paying closer attention to total body electrolyte balance in understanding these conditions.
Incorrect Answers:
Answer A: Addison disease, also known as primary adrenal insufficiency, results in salt wasting due to decreased mineralocorticoid activity. Because of reduced aldosterone release, patients also have hyperkalemia and metabolic acidosis. In contrast, this patient’s potassium and bicarbonate levels are normal. Treatment is with steroids.
Answer C: Diuretic overuse is occasionally observed in patients using loop diuretics. Overuse of loop diuretics can cause hyponatremia, hypokalemia, and hypochloremia. Metabolic alkalosis is commonly seen due to volume contraction. Cerebral salt wasting is more likely in this patient presenting after a recent cerebral injury. Treatment is the cessation of the causative medication.
Answer D: Primary polydipsia can cause symptomatic hyponatremia. The urine would be maximally diluted (urine osmolality < 100 mEq/L) due to an appropriate physiological response to hyponatremia and excess free water intake. Treatment is cessation of excessive water consumption.
Answer E: Syndrome of inappropriate anti-diuretic hormone (SIADH) presents with identical findings as cerebral salt wasting with the exception of euvolemia as opposed to hypovolemia. An assessment of volume status is essential to differentiate. This patient has clear signs of hypovolemia. Treatment of SIADH is fluid restriction followed by ADH inhibitors, if needed.
Bullet Summary:
Cerebral salt wasting presents with hyponatremia, hypochloremia, and hypovolemia in the setting of recent cerebral injury or neurosurgery.
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A 1-year-old girl is brought to a neurologist due to increasing seizure frequency over the past 2 months. She recently underwent a neurology evaluation which revealed hypsarrhythmia on electroencephalography (EEG) with a mix of slow waves, multifocal spikes, and asynchrony. Her parents have noticed the patient occasionally stiffens and spreads her arms at home. She was born at 38-weeks gestational age without complications. She has no other medical problems. Her medications consist of lamotrigine and valproic acid. Her temperature is 98.3°F (36.8°C), blood pressure is 90/75 mmHg, pulse is 94/min, and respirations are 22/min. Physical exam reveals innumerable hypopigmented macules on the skin and an irregularly shaped, thickened, and elevated plaque on the lower back. Which of the following is most strongly associated with this patient's condition?
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{
"A": "Cardiac rhabdomyoma",
"B": "Glaucoma",
"C": "Optic glioma",
"D": "Polyostotic fibrous dysplasia",
"E": ""
}
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A
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This patient with a seizure disorder, ash-leaf spots (innumerable hypopigmented macules), Shagreen patch (elevated irregular plaque on the lower back), and West syndrome (hypsarrhythmia on EEG and movements consistent with infantile spasms) likely has tuberous sclerosis. Tuberous sclerosis is associated with cardiac rhabdomyomas.
Tuberous sclerosis is a neurocutaneous disorder that is inherited in an autosomal dominant fashion. Mutations in TSC1 and TSC2 lead to unregulated cell growth, leading to the formation of hamartomas in various locations. Manifestations of tuberous sclerosis include seizures (secondary to subependymal nodules and cortical dysplasia), mental retardation, renal angiomyolipomas, facial angiofibromas, mitral regurgitation, and hypomelanotic macules (ash-leaf spots). Cardiac rhabdomyoma is strongly associated with tuberous sclerosis and can lead to arrhythmias. West syndrome, which is characterized by infantile spasms, intellectual disability, and hypsarrhythmia (a chaotic mixture of high-amplitude slow waves, multifocal spikes, and intrahemispheric-interhemispheric asynchrony) on EEG, is also associated with tuberous sclerosis. Diagnosis of tuberous sclerosis is made with genetic testing. Advanced imaging (CT or MRI) may reveal cortical tubers and lesions in the third and fourth ventricles. Abdominal imaging may reveal renal angiomyolipomas. The management of seizures in tuberous sclerosis includes anti-seizure medications, though surgery may also be pursued in select cases.
Hinton et al. studied the cardiac manifestations of tuberous sclerosis. They found that cardiac rhabdomyomas can lead to arrhythmia later in life. They recommended that infantile spasms in tuberous sclerosis be treated with vigabatrin but other seizure types should be treated similar to other epileptic disorders.
Incorrect Answers:
Answer B: Glaucoma may occur in patients with Sturge-Weber syndrome, which is characterized by "tram-track" calcifications in the brain, port-wine stains of the face, mental retardation, and epilepsy. Diagnosis is with MRI of the brain with contrast to demonstrate leptomeningeal vascular malformations that are characteristic of the disease.
Answer C: Optic glioma is associated with neurofibromatosis type 1 (NF1), which presents with hyperpigmented macules (cafe-au-lait spots), axillary freckling, and cutaneous neurofibromas. Neurofibromas in NF1 may also grow on peripheral nerves, leading to malignant peripheral nerve sheath tumors. Lisch nodules, or benign growths of the iris, may also be seen in NF1. Diagnosis of NF1 is clinical, but can be aided by genetic testing.
Answer D: Polyostotic fibrous dysplasia is associated with McCune-Albright syndrome. Polyostotic fibrous dysplasia causes fibrous tissue in bones, leading to growth abnormalities and pathologic fractures. McCune-Albright syndrome is also associated with cafe-au-lait macules, which have irregular borders, and endocrine abnormalities such as precocious puberty and hyperthyroidism. Diagnosis is supported with endocrine tests as well as genetic testing.
Answer E: Renal cell carcinoma is associated with Von-Hippel-Lindau syndrome (VHL), which presents with tumors arising in multiple organs. Patients with VHL present with hemangioblastomas in the brain, spinal cord, cerebellum, and retina, and pheochromocytoma. Pheochromocytomas release catecholamines, leading to episodic hypertension, diaphoresis, and palpitations. Diagnosis of VHL is with genetic testing.
Bullet Summary:
Tuberous sclerosis has numerous manifestations including seizures, angiofibromas, mitral regurgitation, renal angiomyolipoma, ash-leaf spots, mental retardation, and cardiac rhabdomyoma.
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A 72-year-old man with a history of type 2 diabetes mellitus, hypertension, and hyperlipidemia presents to his primary care provider for concerns about his cognitive decline. His wife has noticed that he has a worsening ability to organize, plan, and exhibit impulse control over the last month. The patient states that he is able to complete his activities of daily living without assistance, but has some weakness of his left upper and lower extremities that began 3 months prior. He needs reminders from his wife about daily tasks to complete. He enjoys spending time with his spouse, playing cards with his friends, and taking daily walks around his neighborhood. His temperature is 98.2°F (36.8°C), blood pressure is 149/87 mmHg, pulse is 87/min, and respirations are 12/min. Physical exam reveals an elderly man who is oriented to person, place, and time. He has 4/5 left-sided weakness of the upper and lower extremities and associated pronator drift of the left upper extremity. A mini-mental status exam reveals he is able to remember 2 out of 3 words after 4 minutes. He is able to appropriately draw a clock. A magnetic resonance imaging study of the brain is shown in Figure A. Which of the following is the most likely diagnosis?
|
{
"A": "Normal aging",
"B": "Vascular dementia",
"C": "Pseudodementia",
"D": "Mild cognitive impairment",
"E": ""
}
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B
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This patient with cardiovascular risk factors (hypertension, type 2 diabetes mellitus, hyperlipidemia) who presents with sudden cognitive decline of executive function and neurologic symptoms consistent with vasculopathy and possible prior stroke given his neurologic exam likely has vascular dementia, which can be corroborated with magnetic resonance imaging revealing white matter focal involvement consistent with vascular infarcts.
Vascular dementia is a form of dementia that results from compromise of blood supply to the brain, such as minor strokes or microinfarcts to the white matter. These insults lead to worsening cognitive abilities and presents classically as a stepwise decline (sudden/sharp declines in cognitive function that occur at distinct periods of time, not gradually) in cognitive function (thinking, planning, self-control, flexibility in thought). This is often associated with neurologic deficits as byproducts of these strokes. Unlike other forms of dementia, this presentation is step-wise. Treatment involves optimizing medical management to treat underlying medical comorbidities (managing cardiovascular risk factors such as hypertension, type 2 diabetes mellitus, hyperlipidemia), physical therapy/rehab for stroke symptoms, and caregiver support at home. Magnetic resonance imaging reveals focal white matter changes consistent with small vascular infarcts.
Khan et al. review the diagnosis and management of vascular dementia while including commentary on recent updates in the literature. They found that risk factors for vascular diseases such as stroke, high blood pressure, high cholesterol, and smoking also raise the risk of vascular dementia. They thus recommend medical management of underlying medical comorbidities such as hypertension, diabetes mellitus, or hyperlipidemia as treatments for vascular dementia.
Figure/Illustration A shows magnetic resonance imaging with white matter small vessel ischemic changes (red arrows) characteristic of vascular dementia within a background of diffuse generalized atrophy.
Incorrect Answers:
Answer A: Alzheimer disease is a form of dementia that presents with progressive forgetfulness as the first and most jarring clinical symptom, followed by worsening visual/spatial recognition, and then worsening behavioral function. It is most common in patients over the age of 75. It is not associated with focal deficits or weakness on neurological exam.
Answer B: Mild cognitive impairment is a stage between the expected cognitive decline of normal aging and forms of dementia. Patients and family members may notice problems with memory, thinking, or judgment, but they are not significant enough to cause interference with activities of daily living.
Answer C: Normal aging does not involve a noticeable decline in cognition and does not involve neurologic deficits. Declines are present, but are infrequent and do not impede activities of daily living.
Answer D: Pseudodementia is the result of untreated depression, which can present as forgetfulness in the elderly. This etiology can be distinguished by screening for signs or symptoms of depression, which might include sleep disturbance, anhedonia, lack of energy, increased or decreased appetite, fatigue, and/or loss of concentration. These symptoms are absent in this case.
Bullet Summary:
Vascular dementia presents with a step-wise decline in executive cognitive function and neurologic deficits in a patient with cardiovascular risk factors and is associate with MRI findings including white matter changes consistent with vascular infarcts.
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A 55-year-old woman presents to a primary care physician with persistent nausea and abdominal discomfort. She has experienced these symptoms daily for the past 3 months. She feels bloated and has episodic loose and watery stools. She has a history of hypertension and hyperlipidemia for which she takes amlodipine and atorvastatin. She immigrated from Vietnam 6 months ago. Her temperature is 98.6°F (37.0°C), blood pressure is 110/60 mmHg, pulse is 70/min, and respirations are 18/min. Physical exam reveals a thin-appearing woman in no acute distress. Her mucous membranes are moist. Cardiac and lung examinations are unremarkable. Laboratory results are as follows: Leukocyte count: 13,000/mm^3 Segmented neutrophils: 54% Bands: 2% Eosinophils: 6% Basophils: 0.4% Lymphocytes: 30% Monocytes: 5% A vitamin D level is 26 ng/mL (reference: >= 30 ng/mL). Which of the following is the most appropriate test in making the diagnosis?
|
{
"A": "Lower endoscopy",
"B": "Bowel wall biopsy",
"C": "CT scan of the abdomen",
"D": "Stool ova and parasite assay",
"E": ""
}
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D
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This patient who presents with persistent abdominal discomfort, nausea, bloating, diarrhea, eosinophilia, and signs of malabsorption (thin-appearing, vitamin D deficiency) in the setting of immigration from a resource-limited country most likely has a gastrointestinal parasite infection (Ascaris lumbricoides). The most appropriate next step in management is to obtain a stool ova and parasite assay.
Ascaris lumbricoides is a roundworm that is transmitted via the fecal-oral route (egg ingestion). While most patients are asymptomatic, there can be pulmonary and intestinal manifestations in the early and late phases, respectively. Pulmonary signs include dry cough, dyspnea, fever, and wheezing. Intestinal signs include abdominal discomfort, diarrhea, nausea, vomiting, malabsorption, and/or anorexia. The diagnosis should be suspected in patients with vague abdominal symptoms with travel history to an endemic area. The diagnosis is secured with stool microscopy for eggs or worms. Complications of this condition include intestinal obstruction or hepatobiliary/pancreatic involvement, presenting as biliary colic, obstructive jaundice, and/or ascending cholangitis. Treatment in patients with uncomplicated infection is with anti-helminth therapy (albendazole or mebendazole).
Parija et al. review the epidemiology of helminth infections globally. The authors note that many cases are caused by Ascaris species. They recommend prompt identification of these infections as they can cause lack of school attendance, anemia, and cognitive deficits if left untreated.
Incorrect Answers:
Answer A: Bowel wall biopsy is used in the diagnostic work-up of suspected Whipple disease, which presents with chronic diarrhea, malabsorption, weight loss, and joint symptoms (arthralgias). This disease is progressive over years and would be less likely in this patient with disease onset of 3 months.
Answer B: CT scan of the abdomen is used in the diagnostic work-up of small bowel obstruction, which presents as crampy abdominal pain, constipation, obstipation, and/or vomiting. Bowel obstruction is an acute process that would be unlikely in this patient with chronic symptoms. Although bowel obstruction is a complication of Ascaris infection, this patient has no signs of obstruction. Diarrhea may occur secondary to infection of the colon as well including colitis or diverticulitis; however, these conditions typically cause pain and low grade fever.
Answer C: Lower endoscopy (colonoscopy) is used in the diagnosis of inflammatory bowel disease, consisting of Crohn disease and ulcerative colitis. Ulcerative colitis presents with bloody diarrhea, abdominal pain, weight loss, and fatigue. Eosinophilia would be unexpected, and this patient does not have bloody diarrhea.
Answer E: Stool toxin assay is used to diagnose Clostridioides difficile infection. This presents after recent antibiotic use with watery diarrhea, dehydration, fever, and nausea. It presents acutely and generally without eosinophilia.
Bullet Summary:
Parasitic gastrointestinal infections present with chronic diarrhea, abdominal discomfort, malabsorption, and eosinophilia, and are diagnosed using stool ova and parasite assays.
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A 53-year-old African-American woman presents to her primary care doctor with increasing difficulty climbing the stairs. She noticed the weakness approximately 3 months ago. It has gotten progressively worse since that time. She has also noticed increasing difficulty combing her hair, standing from a seated position, and experiences muscle aches. Her medical history is significant for hypertension treated with lifestyle modification and gastroesophageal reflux disease (GERD). Her temperature is 98.6°F (37.0°C), blood pressure is 130/65 mmHg, pulse is 80/min, and respirations are 16/min. She has 3/5 strength to shoulder abduction and hip flexion bilaterally. Her strength is 5/5 to wrist extension and ankle plantar flexion. No skin rashes are noted. Which of the following is the most accurate test to confirm this patient’s diagnosis?
|
{
"A": "Serum creatine kinase",
"B": "Muscle biopsy",
"C": "Electromyography",
"D": "Serum aldolase",
"E": ""
}
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B
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This patient with insidious, subacute, progressive, symmetric proximal muscle weakness (difficulty climbing the stairs, combing her hair, standing from a seated position) without associated skin lesions most likely has polymyositis. The most accurate diagnostic test for polymyositis is muscle biopsy.
Polymyositis is caused by an autoimmune reaction that leads to cell-mediated cytotoxicity against unidentified skeletal muscle antigens, primarily affecting the endomysium. It is more often found in women, patients between 30-60 years of age, and African-Americans. Clinical features of polymyositis include symmetric proximal muscle weakness that may be accompanied by myalgia, dysphagia (due to pharyngeal muscle weakness), restrictive lung disease (due to respiratory muscle weakness), cardiac involvement (myocarditis, heart failure), interstitial lung disease, and increased risk of malignancy. There are no accepted diagnostic criteria for polymyositis; however, diagnosis is usually secured with a combination of clinical features and other tests. Routine initial studies can include a complete blood count, complete metabolic panel, C-reactive protein, erythrocyte sedimentation rate, lactate dehydrogenase, aldolase, creatine kinase, autoantibodies (anti-nuclear antibody, anti-Jo-1), and electromyography (EMG). Muscle biopsy of an affected muscle is the gold standard for diagnosis and will typically show muscle fiber damage, CD8+ T cells in the endomysium, and overexpression of MHC-I on the sarcolemma. First-line treatment of polymyositis includes glucocorticoids and a steroid-sparing agent (methotrexate, azathioprine). Subsequent treatments can include intravenous immunoglobulins, rituximab, or plasmapheresis.
Amato et al. review the evaluation and treatment of inflammatory myopathies such as polymyositis, dermatomyositis, and inclusion body myositis. They found that polymyositis typically presents in adult life with symmetric proximal leg greater than arm weakness. They recommend that a muscle biopsy be done on any patient considered to have polymyositis, preferably prior to starting immunosuppressive treatment.
Incorrect Answers:
Answer A: Electromyography (EMG) can help distinguish myopathic weakness (e.g., polymyositis) from neuropathic causes of weakness (e.g., amyotrophic lateral sclerosis, myasthenia gravis). Characteristic EMG findings include fibrillations, early recruitment of motor unit potentials, and abnormal low-amplitude motor unit potentials. EMG is not a confirmatory test and is less sensitive than muscle biopsy for diagnosing myositis.
Answer B: MRI can be used to demonstrate areas of edema, atrophy, fatty replacement, and calcification in patients with suspected polymyositis. MRI can assess large regions of muscle, thus avoiding sampling error with muscle biopsy. The findings in MRI are nonspecific and require correlation with muscle biopsy for definitive diagnosis. MRI can also be used to help select the site of muscle biopsy.
Answer D: Serum aldolase can occasionally be used in the diagnostic investigation of suspected polymyositis if creatine kinase is normal. Aldolase elevation is nonspecific and may be seen in fasciitis, drug-induced myositis, and connective tissue disease-associated interstitial lung disease.
Answer E: Serum creatine kinase (CK) is the most sensitive muscle enzyme exam and should be part of the initial diagnostic investigation of any patient with suspected polymyositis. CK elevation is nonspecific and may be seen in myriad conditions such as inflammatory insult, metabolic injury, drug-induced injury, and infection.
Bullet Summary:
Muscle biopsy is the gold standard for the diagnosis of polymyositis.
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A 34-year-old man presents to the emergency room with pain behind his eyes. He had a similar episode about 1 month ago which resolved after a few hours. The pain feels like a stabbing sensation behind his right eye. He denies any symptoms on the left side. The last time he had an episode like this, his eye was tearing. His temperature is 98.2°F (36.8°C), blood pressure is 120/90 mmHg, pulse is 110/min, and respirations are 12/min. Physical exam reveals a 2 mm pupil on the right and a 5 mm pupil on the left. Extraocular movements are intact bilaterally. The remainder of the neurologic exam is unremarkable. Which of the following is the most appropriate prophylactic treatment?
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{
"A": "Sumatriptan",
"B": "Verapamil",
"C": "Ibuprofen",
"D": "Propranolol",
"E": ""
}
|
B
|
This patient with a history of retro-orbital pain, unilateral miosis (2 mm pupil on the right), and history of lacrimation during a similar episode is likely experiencing cluster headaches. Verapamil may be used as prophylaxis in the treatment of cluster headaches.
Cluster headaches occur more commonly in men and present with severe, unilateral, retro-orbital pain. Typical episodes last 15 minutes to 3 hours. Attacks may be associated with the circadian rhythm, as patients may notice that they get headaches at night. Because of the extreme pain, cluster headaches are sometimes colloquially referred to as "suicide" headaches. These headaches may present with autonomic symptoms, such as lacrimation and rhinorrhea. Horner syndrome may also occur, defined by a unilateral triad of ptosis, miosis, and anhidrosis. Acute management of cluster headaches includes administration of 100% oxygen. Other options include triptans. The first-line medication for prophylaxis of cluster headaches is verapamil. Studies have shown that lithium, topiramate, and ergotamine may also be effective as prophylaxis for cluster headaches; however, these therapies are less established than verapamil.
Blau and Engel review the use of medications for cluster headaches. They note that most of patients with episodic cluster headaches had complete suppression of attacks with the use of verapamil. It is recommended to give verapamil in this patient population.
Incorrect Answers:
Answer A: Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) that is used in the treatment of migraine and tension headaches. Migraine headaches present with unilateral, pulsating pain with photophobia and phonophobia, whereas tension headaches present with constant bilateral pain. Ibuprofen should not be used as prophylaxis for any type of headache as it has side effects including kidney dysfunction, ulcers, and even premature aging.
Answer B: Oxygen is first-line treatment for acute cluster headaches; however, it does not have any role in the prophylaxis of cluster headaches.
Answer C: Propranolol is a beta-blocker that is a prophylactic medication for migraine headaches. Migraines are more common in women and typically present as a unilateral headache with photophobia or phonophobia. They may also be associated with an aura, which presents as a visual, auditory, olfactory, or motor disturbance.
Answer D: Sumatriptan is a triptan that is used as an abortive treatment for migraine headaches and cluster headaches. It should not be used as prophylaxis for headaches.
Bullet Summary:
Verapamil may be used as prophylaxis for cluster headaches.
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https://step2.medbullets.com/testview?qid=217746
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