Case-based MCQ

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👍B Nocturnal enuresis, or nighttime urinary incontinence at age ≥5, is a common childhood condition, particularly in boys.  In an otherwise asymptomatic child, enuresis is typically genetic (most have ≥1 parents affected during childhood) and developmental, with self-resolution expected as bladder control matures.  However, an underlying medical condition should be suspected when other signs or symptoms are present, as in this case. In addition to wetting the bed, this child is irritable and inattentive with tonsillar hypertrophy.  These findings are concerning for obstructive sleep apnea (OSA) as the underlying cause of his enuresis.  Enuresis may reflect apnea effects on arousal response (eg, effects on bladder pressure, urinary hormone secretion) or difficulties awakening in response to a full bladder.  Instead of daytime somnolence seen in adults with OSA, behavioral concerns (eg, inattention, impulsivity) and mood changes (eg, emotional lability) are common manifestations of sleep disturbance in children.  OSA is also associated with increased blood pressure (as seen here); chronic symptoms can result in poor growth (decreased nocturnal growth hormone secretion) and cardiovascular complications (eg, cor pulmonale). Evaluation of OSA is with nocturnal polysomnography (ie, sleep study), which detects and quantifies respiratory pauses and desaturations during sleep.  Treatment of OSA (eg, adenotonsillectomy, positive airway pressure) can lead to resolution of associated enuresis. A trial of methylphenidate may be indicated for attention deficit hyperactivity disorder (ADHD), which can also present with irritability and inattention and has association with enuresis.  However, ADHD would not explain this child’s tonsillar hypertrophy. Urodynamic testing can be considered in a patient with findings concerning for bladder dysfunction, such as daytime incontinence, weak stream, dribbling, straining, or urgency, none of which is present in this patient. Imipramine is a tricyclic antidepressant that can be considered for nocturnal enuresis that is not due to an underlying medical problem and is refractory to first-line management (eg, desmopressin, bed-wetting alarm).  Evaluation and management of coexisting conditions, such as OSA, should be prioritized before initiating pharmacotherapy for enuresis. Reassurance and follow-up are appropriate for normal bed-wetting behaviors in an otherwise asymptomatic child age <5.  This patient with behavioral concerns, enlarged tonsils, and hypertension requires further workup for his enuresis. Nocturnal enuresis secondary to obstructive sleep apnea should be considered in a child who has bed-wetting in addition to inattention, behavioral concerns, hypertension, and/or tonsillar hypertrophy.  Evaluation is with nocturnal polysomnography.

A 7-year-old boy comes to the office with his parents due to bed-wetting.  He achieved daytime dryness at age 4 but has never stayed dry overnight for more than 3 consecutive nights.  His urinary stream is strong, and there is no dribbling, straining, or urgency.  The child is irritable and inattentive, often interrupting his teacher and disrupting his classmates at school.  His mother and father both achieved nighttime dryness at age 5.  Height and weight are tracking along the 75th and 25th percentiles, respectively.  Blood pressure is at the 90th percentile.  On examination, the tympanic membranes are clear, and the tonsils are symmetrically enlarged.  Cardiopulmonary, abdominal, and genital examinations are normal.  Urinalysis and serum creatinine are normal.  Which of the following is the best next step in management of this patient? A. Initiate a trial of methylphenidate B. Obtain nocturnal polysomnography C. Obtain urodynamic study D. Prescribe imipramine E. Reassure and follow up in 6 months

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🧩 Medical Mnemonics 👀 Low RAIU in Thyrotoxicosis?

When the thyroid isn’t making hormone — just leaking it, receiving it, or faking it — radioactive iodine uptake (RAIU) drops.

Remember " 🎭  FACTITIOUS 🎭 " ▫Factitious thyrotoxicosis (e.g., levothyroxine abuse)  ▪Amiodarone-induced thyrotoxicosis (Type 2) ▫Congenital thyroiditis ▪Thyroiditis (subacute, silent, postpartum)  ▫ Iodine excess (Jod-Basedow) ▪Tumor (Struma ovarii) hormone, thyroid stays quiet  ▫Infiltrative disease ▪Overdose of iodine contrast  ▫Unusual causes: Interferon-induced or mixed mechanisms  ▪Suppressed TSH (central~Pituitary dysfunction) #endocrinology 〰〰〰〰〰〰〰〰〰〰〰 ©Medical Mnemonics

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B👍 This patient with an acute ischemic stroke has polycythemia, defined as a hematocrit level >49% in men or >48% in women.  Hematocrit is the main determinant of blood viscosity; therefore, significant elevations in hematocrit can result in cerebral microcirculation sludging and potentially life-threatening ischemic events. Polycythemia is generally classified as follows: Primary polycythemia is largely caused by malignant transformation of erythrocyte progenitor cells, which results in unregulated erythrocyte production (eg, polycythemia vera).  Erythropoietin (EPO), the hormone that stimulates red blood cell production, will be low or absent because elevated red blood cell mass exerts a negative feedback effect on EPO-producing cells in the renal cortex. Secondary polycythemia is typically due to elevated circulating EPO levels.  Most cases are caused by conditions associated with chronic hypoxia (eg, cardiopulmonary disease, obstructive sleep apnea), which stimulates EPO secretion, or by EPO-producing tumors (eg, renal cell carcinoma). This patient’s elevated EPO level indicates secondary polycythemia.  Given the patient’s normal BMI, pulse oximetry, and chest x-ray, chronic hypoxia is unlikely.  Therefore, exploration for an EPO-secreting tumor should be undertaken.  Because the kidney is the primary site of EPO production, renal cell carcinoma, a primary malignant neoplasm of the kidney, is most likely (and may explain her several weeks of generalized weakness); abdominal CT scan is the first test of choice for diagnosis.  CT would also evaluate for hepatocellular carcinoma, which sometimes causes EPO production (although it does not always lead to polycythemia, possibly due to inhibited erythropoiesis). Primary polycythemia, which is associated with low (not high) EPO levels, requires bone marrow aspiration/biopsy with JAK2 mutation testing (to evaluate for polycythemia vera).  Secondary polycythemia does not usually require bone marrow evaluation. Factor V Leiden is an autosomal dominant disease associated with venous thromboembolism (VTE), myocardial infarction, and stroke; it is generally suspected when a patient has a family history of VTE or develops VTE at a young age (<50).  Lupus anticoagulant is an antiphospholipid antibody associated with autoimmune diseases and certain drugs/infections; it can cause VTE, thrombocytopenia, stroke, and fetal loss.  Neither factor V Leiden nor lupus anticoagulant is associated with polycythemia. Polycythemia with high circulating erythropoietin (EPO) levels (secondary polycythemia) is usually due to tumors that produce EPO (eg, renal cell carcinoma) or chronic hypoxia (eg, cardiopulmonary disease, obstructive sleep apnea).  Individuals with secondary polycythemia and no evidence of hypoxia should undergo abdominal CT scan to evaluate for renal cell carcinoma.

A 54-year-old woman is admitted to the hospital with a day of right-sided weakness.  The stroke team was activated, but no intervention was performed due to long length of time since symptom onset.  The patient also notes 6 weeks of headaches and generalized weakness.  She has not had recent fever, shortness of breath, cough, chest pain, palpitations, or syncope.  She has no chronic medical conditions and does not take medications.  The patient smoked a pack of cigarettes daily for 20 years but quit 15 years ago.  She does not use alcohol or illicit drugs.  Temperature is 37.1 C, blood pressure is 160/96 mm Hg, and pulse is 80/min and regular.  Oxygen saturation is 99% on room air.  BMI is 25 kg/m2.  Cardiopulmonary examination shows no abnormalities.  Abdomen is soft and tender; there is no hepatosplenomegaly.  Extremities have no cyanosis, clubbing, or edema.  A right facial droop is present.  Motor strength is 2/5 in right upper extremity, 3/5 in right lower extremity, and 5/5 in left upper and left lower extremities.  Sensation is intact diffusely.  Laboratory results are as follows: Hemoglobin 20.2 g/dL Hematocrit 61% Leukocytes 7,200/mm3 Platelets 180,000/mm3 Creatinine 106 umol/L LDL cholesterol 3.11 mmol/L Erythropoietin level 22.9 mU/mL (normal: 4.1-19.5) MRI of the brain reveals an acute infarction involving the left internal capsule.  Chest x-ray is normal.  ECG shows normal sinus rhythm.  Echocardiogram shows no abnormalities.  Which of the following is most likely to establish a diagnosis in this patient? A. Bone marrow aspiration B. CT scan of the abdomen C. Factor V Leiden mutation testing D. Lupus anticoagulant E. Serologic test for syphilis