Question 1

A 17-year-old boy is evaluated for abnormal urinalysis findings. He came to the clinic 2 weeks ago with low back pain, and a urinalysis at that time showed 2+ protein. He currently feels fine and has no urinary complaints. The patient has not exercised vigorously or taken any medications. He has no other medical problems and received all appropriate childhood vaccinations. He does not use tobacco or illicit drugs. The patient is not sexually active. His father had early coronary disease and a stroke. His blood pressure is 112/70 mm Hg and pulse is 77/min. BMI is 24 kg/m². Physical examination shows no abnormalities. Laboratory results from this visit are as follows: Urine sediment microscopy is unremarkable for casts. A 24-hour urine collection shows 600 mg of protein (normal <150 mg). Ultrasound of the kidneys shows no abnormalities. Split urine collection shows 40 mg of protein overnight (8 hours) and 500 mg of protein during the day (16 hours). Which of the following is the best next step in management of this patient?

Accepted Answer

Explanation: Long-term studies have shown that orthostatic proteinuria in adolescents is a benign condition that usually resolves spontaneously and does not have a significant effect on renal function. As a result, patients do not require further diagnostic workup or treatment (Choice D). Although very subtle glomerular abnormalities may be seen, orthostatic proteinuria has an excellent prognosis and does not predict development of significant glomerular pathology in the future. The patient should be reassured about the benign nature of orthostatic proteinuria and the tendency to resolve with age. He should be monitored periodically and have orthostatic proteinuria reconfirmed if he has persistent proteinuria. (Choice A) Angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers) are preferred for treating proteinuria due to glomerular damage (eg, diabetic nephropathy, glomerulonephritis, nephrotic syndrome). These medications reduce proteinuria and slow the progression of chronic kidney disease. However, orthostatic proteinuria has an excellent prognosis and does not require specific treatment. (Choice C) Oral prednisone is typically given empirically to children or adolescents with nephrotic syndrome due to minimal change disease. This patient's 24-hour protein <3-3.5 g makes this unlikely. (Choice E) First-degree relatives of children with nephrotic syndrome who do not respond to prednisone should undergo urine protein testing to diagnose rare genetic mutations that affect podocyte function. Educational objective: Orthostatic proteinuria is a benign finding and requires no invasive diagnostic workup (eg, kidney biopsy) or treatment (eg, angiotensin-converting enzyme inhibitors or oral steroids). References: Mechanisms of orthostatic proteinuria: lessons from a transplant donor. (http://www.ncbi.nlm.nih.gov/pubmed/8400067) Fixed and reproducible orthostatic proteinuria: results of a 20-year follow-up study. (http://www.ncbi.nlm.nih.gov/pubmed/7125410)

Question 2

A 76-year-old man comes to the office for a follow-up visit after a recent admission for acute decompensated heart failure. He reports persistent shortness of breath on mild exertion but has no other symptoms. Medical history includes hypertension, type 2 diabetes mellitus, coronary artery disease, coronary artery bypass grafting 5 years ago, heart failure with reduced ejection fraction (ejection fraction 20%), benign prostate hyperplasia, and osteoarthritis. The patient has been hospitalized 4 times over the last year for acute decompensated heart failure. He had an implantable cardioverter-defibrillator placed 2 years ago. His medications include low-dose aspirin, metoprolol, lisinopril, simvastatin, insulin glargine, spironolactone, empagliflozin, and furosemide. Temperature is 36.7 C, blood pressure is 106/72 mm Hg, pulse is 72/min, and respirations are 16/min. Jugular venous pressure is estimated at 12 cm H₂O. Lung examination shows bibasilar crackles. Cardiovascular examination shows regular heart sounds and an audible S3 over the cardiac apex. There is bilateral lower extremity edema. Laboratory evaluation shows a serum sodium concentration of 121 mEq/L and serum creatinine of 1.0 mg/dL. His serum sodium concentration 6 weeks ago was 124 mEq/L and serum creatinine was 0.9 mg/dL. In addition to adjusting the loop diuretic regimen, which of the following is the most appropriate next step in management of this patient's hyponatremia?

Accepted Answer

Explanation: Hyponatremia in patients with decompensated heart failure (DHF) usually parallels the severity of heart failure and is an independent predictor of adverse clinical outcomes. Low cardiac output and decreased perfusion pressure at the baroreceptors and renal afferent arterioles leads to neurohumoral activation with the release of renin and norepinephrine, and secretion of antidiuretic hormone (ADH). ADH (vasopressin) binds to V2 receptors in the renal collecting ducts and promotes water reabsorption; renin (via angiotensin II) and norepinephrine increase proximal sodium and water reabsorption and limit water delivery to the distal tubules. These actions promote free water retention and lead to dilutional hyponatremia. Angiotensin II and low cardiac output also stimulate thirst, leading to increased water intake and worsening hyponatremia. Water intake restriction is the mainstay of initial therapy for hyponatremia in patients with DHF. Correction of hyponatremia does not improve the clinical outcomes associated with heart failure and is indicated only in patients with symptoms (eg, confusion, seizures) or severe asymptomatic hyponatremia (serum sodium <120 mEq/L). Vasopressin-2 receptor antagonists (eg, tolvaptan) may be considered in patients with chronic heart failure and serum sodium <120 mEq/L. (Choice A) Desmopressin is a vasopressin analog with a potent antidiuretic effect that is used in the treatment of diabetes insipidus. It promotes free water retention and will worsen hyponatremia. (Choice B) Hypertonic saline is generally used as emergency therapy in patients with severe symptoms due to hyponatremia (eg, seizures, coma) or in those with acute hyponatremia with mild symptoms (due to risk of cerebral edema and herniation). It is not indicated in stable patients with chronic hyponatremia and mild or no symptoms. (Choice C) Angiotensin receptor blockers (eg, losartan) do not have a direct action in correcting hyponatremia, and adding an angiotensin receptor blocker to an ACE inhibitor is generally contraindicated due to increased risk of adverse effects (eg, hyperkalemia, acute kidney injury). Angiotensin receptor-neprilysin inhibitors (eg, sacubitril-valsartan) may worsen hyponatremia (due to neprilysin inhibition-induced natriuresis) and are relatively contraindicated in heart failure complicated by significant hyponatremia. (Choice D) Oral salt tablets (in addition to fluid restriction) can be used in patients with hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion. They should not be used in edematous patients with volume overload (ie, decompensated heart failure). Educational objective: Water intake restriction is the mainstay of initial therapy for correcting hyponatremia in patients with decompensated heart failure. Vasopressin-2 receptor antagonists (eg, tolvaptan) may be considered in patients with chronic heart failure and serum sodium <120 mEq/L. References: Hyponatremia in congestive heart failure. (http://www.ncbi.nlm.nih.gov/pubmed/15847851) Vasopressin receptor antagonists and their role in clinical medicine. (http://www.ncbi.nlm.nih.gov/pubmed/22470853)

Question 3

A 12-year-old boy is brought to the emergency department due to brown urine for the past 2 days.  In addition, the patient has had decreased urine output and a mild headache.  He has no chronic medical conditions but was treated with oral amoxicillin 18 days ago for pharyngitis.  The patient's family history is unremarkable.  Temperature is 36.8 C (98.2 F), blood pressure is 150/92 mm Hg, pulse is 89/min, and respirations are 15/min.  Physical examination shows a tired-appearing boy with edema in the scrotum and bilateral lower extremities.  Laboratory results are as follows:  Complement component C3 levels are low.  Which of the following is the best next step in management of this patient?

Accepted Answer

Explanation: 11ec2b69_c09c_93f6_8f63_956c4ab636e3_MD0005_00 This patient has hypertension, hematuria, and low complement component C3 several weeks after group A Streptococcus infection (eg, pharyngitis), findings consistent with acute poststreptococcal glomerulonephritis (APSGN). APSGN, a nephritic syndrome, results from immune complex deposition between the glomerular basement membrane (GBM) and the mesangium, as well as from glomerular damage due to complement (C3) activation and inflammation. Although many cases are characterized by asymptomatic microscopic hematuria that resolves within weeks, fulminant nephritic syndrome can occur, as in this patient. Damage to the glomerulus results in gross hematuria (tea- or cola-colored) usually with red blood cell casts, as well as increased urinary loss of protein, causing decreased intravascular oncotic pressure and third spacing. Acute kidney injury with decreased glomerular filtration (eg, ↑ serum creatinine) and impaired sodium excretion is also characteristic. The aggregate consequence of both sodium and water retention is volume overload with hypertension and edema. Management of APSGN is supportive, and first-line treatment for hypertension and edema is loop diuretics (eg, furosemide). Fluid restriction may be indicated, and caution should be used with intravenous fluids because they may worsen edema and hypertension. Most patients do not require adjunctive therapy with antihypertensives, but calcium channel blockers (eg, nifedipine) should be considered for hypertensive encephalopathy or hypertension refractory to diuresis. (Choice A) Cyclophosphamide is an immunosuppressant used in several nephritic syndromes (eg, anti-GBM disease, pauci-immune vasculitis). However, in APSGN, the deposition of antigen-antibody complexes spontaneously resolves, so immunosuppressive therapy is not needed. (Choice B) Dialysis is rarely required for patients with APSGN. Indications include medically refractory hyperkalemia, marked uremia, or pulmonary edema, none of which are present in this patient. (Choice D) ACE inhibitors (eg, lisinopril) are generally avoided for hypertension in the setting of acute kidney injury because of the risk of exacerbating hyperkalemia. Moreover, this patient's hypertension should be treated with diuresis first. Educational objective: Acute poststreptococcal glomerulonephritis, a complication of group A Streptococcus infection (eg, pharyngitis), typically presents with hematuria, edema, and hypertension. Management is supportive and includes loop diuretics (eg, furosemide) for symptoms of volume overload (eg, hypertension, edema). References: Acute poststreptococcal glomerulonephritis: the most common acute glomerulonephritis. (http://www.ncbi.nlm.nih.gov/pubmed/25554106)

Question 4

A 40-year-old man is evaluated for perioral paresthesias and cramping of both hands.  The patient has a history of alcoholic cirrhosis and was admitted 24 hours ago due to recurrent episodes of hematemesis.  Evaluation revealed acute variceal bleeding for which the patient received endoscopic therapy.  He also received 6 units of packed red blood cells and 4 units of fresh frozen plasma since admission.  The patient reports feelings of anxiety and worsening tingling and numbness around the mouth for the past 2 hours.  He has also had severe muscle spasms of the hands and legs.  Temperature is 37.1 C (98.8 F), blood pressure is 116/68 mm Hg, and pulse is 92/min.  Jugular venous pressure is normal.  The lungs are clear to auscultation and heart sounds are normal.  Abdominal examination reveals moderate ascites with no tenderness.  He has generalized mild muscle weakness and periodic spontaneous twitching in the major muscle groups.  Laboratory studies at the time of admission are as follows:  Hemoglobin level after the transfusions is 8.9 g/dL.  Further diagnostic testing is pending.  Intravenous administration of which of the following is most likely to improve this patient's current symptoms?

Accepted Answer

Explanation: 11ec2b69_c095_8f05_8f63_099389f0d28d_MD0005_00 This patient with liver disease who received several units of packed red blood cells over a short period developed perioral paresthesias and muscle cramping and twitching, raising suspicion for symptomatic hypocalcemia. Packed red blood cells are preserved and anticoagulated using sodium citrate and citric acid. These agents are rapidly cleared by the liver, kidney, and skeletal muscles and usually generate no adverse effects. However, patients who receive massive transfusions (usually >10 units) or those with certain underlying conditions (eg, hepatic disease, renal failure, hypothermia, shock) can fail to clear citrate quickly enough to prevent physiologic effects. As citrate binds ionized calcium, these patients are at risk for symptomatic hypocalcemia due to ionized (free) calcium deficiency. Diagnosis requires an ionized calcium level as serum calcium may be normal. Treatment with calcium gluconate or calcium chloride is usually curative, but several dosages may be required. (Choice B) Dextrose and thiamine are used as part of the treatment for Wernicke encephalopathy in patients with alcoholism or severe malnutrition. Wernicke encephalopathy is marked by oculomotor dysfunction, ataxia, and encephalopathy, not paresthesias and muscle cramping. (Choice C) Lorazepam can be used to treat seizures, which can occasionally present with muscle cramps and paresthesias. However, most patients will have additional neurologic findings such as episodic confusion, sleepiness, or clumsiness. As this patient with liver disease developed symptoms shortly after several blood transfusions, ionized calcium deficiency is more likely than seizures. (Choice D) High levels of citrate often result in metabolic alkalosis (from bicarbonate production with citrate metabolism), which can lead to hypokalemia due to the exchange of extracellular potassium for intracellular hydrogen. Although hypokalemia can cause muscle weakness and rhabdomyolysis, paresthesias and muscle spasms are less common. (Choice E) Sodium bicarbonate is typically used to treat severe metabolic acidosis as commonly seen in renal failure. Citrate causes a metabolic alkalosis; a sodium bicarbonate infusion would worsen the alkalosis. Educational objective: Packed red blood cells are preserved and anticoagulated using sodium citrate. Patients who receive massive transfusions or those with certain underlying conditions (eg, liver or renal failure, hypothermia, shock) can fail to adequately clear citrate. As citrate binds ionized calcium, these patients are at risk for symptomatic hypocalcemia due to ionized calcium deficiency. An ionized calcium level is required for diagnosis, as serum calcium is often normal.

Question 5

A 15-year-old boy with chronic kidney disease is being evaluated for kidney transplantation.  He has had chronic glomerulonephritis for the last 3 years.  His current estimated glomerular filtration rate is 12 mL/min.  He also has hypertension and mild intermittent asthma.  His sister, who is 22 years old, is willing to donate her kidney.  She has no medical problems.  The initial testing shows an ABO antigen match and one human leukocyte antigen mismatch.  The sister should be appropriately counseled about which of the following long-term risks of kidney donation?

Accepted Answer

Explanation: The complications of donor nephrectomy can be divided into immediate and long-term risks. In the immediate period, risks are primarily those typical of surgical procedures, such as deep venous thrombosis and hospital-acquired infections. The overall surgical mortality rate is very low at 3.1/10,000 donors. The long-term risks of donor nephrectomy are also quite low. Although there is an immediate decrease in net glomerular filtration rate following donor nephrectomy, compensatory hypertrophy in the remaining kidney largely replaces the lost renal function. As a result, there is no increased risk of end-stage renal disease in kidney donors (Choice C). Overall mortality in kidney donors is also similar to that of the general population (Choice A). Kidney donation is, however, associated with an increased risk of gestational complications in female donors of childbearing age. These complications include fetal loss, preeclampsia, gestational diabetes, and gestational hypertension. They have been seen at higher rates in women after donor nephrectomy compared to the same women with pregnancies that occurred prior to nephrectomy (although the overall rates are not significantly higher than in the general population). It is generally recommended that women complete their planned childbearing prior to kidney donation. However, this is not an absolute contraindication to donation, and it is possible for women who have not completed childbearing to proceed with the procedure if they are appropriately informed of the risks. (Choice B) Kidney donors do not have an increased risk of depression and actually appear to have a somewhat lower risk than the general population. Possible factors include increased sense of well-being associated with organ donation and extensive pre-donation psychological screening. (Choice E) There is no increased risk of renal cell carcinoma or other malignancy among patients who have had a donor nephrectomy. Educational objective: The immediate and long-term complications of donor nephrectomy are low. Patients have an increased risk of gestational complications after donor nephrectomy compared to pregnancies before the procedure. However, the rate is similar to that of the general population. The risk of end-stage renal disease and overall mortality following kidney donation are the same as in the general population. References: Long-term consequences of kidney donation. (http://www.ncbi.nlm.nih.gov/pubmed/19179315) Pregnancy and birth after kidney donation: the Norwegian experience. (http://www.ncbi.nlm.nih.gov/pubmed/18853953) Pregnancy outcomes after kidney donation. (http://www.ncbi.nlm.nih.gov/pubmed/19353771)

Question 6

A 40-year-old man comes to the nephrology clinic for follow-up due to poststreptococcal glomerulonephritis.  He initially had gross hematuria and edema associated with hypertension and required treatment with a diuretic.  Two weeks prior to the onset of symptoms, the patient had acute pharyngitis that resolved without treatment.  At the time of diagnosis, the serum C3 level was decreased, and the antistreptolysin O titer was elevated.  Which of the following factors most likely indicates a poor long-term prognosis for this patient's condition?

Accepted Answer

Explanation: 11ec2b69_c09c_1ec4_8f63_833f6745f343_MD0005_00 Poststreptococcal glomerulonephritis (PSGN) is a nonsuppurative complication of a pharyngeal or skin infection (eg, impetigo). Infection with nephritogenic strains of group A Streptococcus (GAS) (eg, S pyogenes) results in the formation of antigen-antibody complexes, which are deposited on the glomerular basement membrane. Subsequent activation of complement and inflammation results in the development of nephritic syndrome 2-4 weeks after initial infection. Common clinical features include gross hematuria, hypertension, and edema (periorbital or generalized). Urine studies show red blood cells and casts and mild proteinuria, whereas serum studies commonly demonstrate elevated creatinine, antistreptococcal antibodies (eg, antistreptolysin O), and low C3 (due to consumption). PSGN is most common in children age 5-12 and has an excellent prognosis in this group, with most patients achieving complete normalization of renal function. However, up to 40% of adults diagnosed with PSGN develop chronic kidney disease, persistent hypertension, or recurrent proteinuria, with 10% progressing to end-stage renal disease. Preexisting kidney disease, metabolic syndrome, and diabetes are also poor prognostic indicators. (Choices B, D and E) Gross hematuria and hypertension are common features of PSGN. Antistreptococcal antibodies are typically elevated in patients with recent GAS infection and can be used to help confirm the diagnosis. However, antistreptolysin O antibodies may be falsely low in patients who received antibiotic therapy or in those with a GAS skin infection. None of these findings significantly affects the prognosis, whereas the difference in prognosis between adults and children has been noted in multiple studies. (Choice C) Corticosteroid treatment is recommended for minimal change disease, which also is far more common in children and has a worse prognosis in adults; however, this condition causes nephrotic syndrome (eg, heavy proteinuria, edema, hyperlipidemia). Corticosteroids are not indicated in PSGN. Educational objective: Poststreptococcal glomerulonephritis, a complication of group A Streptococcus species, presents with nephritic syndrome (eg, renal failure, hypertension, hematuria, red blood cell casts) 2-4 weeks after infection. It is most common in children and has an excellent prognosis in this age group; however, adults and those with a history of chronic kidney disease, metabolic syndrome, or diabetes have a worse prognosis and may develop end-stage renal disease. References: Bacterial infection-related glomerulonephritis in adults. (http://www.ncbi.nlm.nih.gov/pubmed/23302723) Post-streptococcal glomerulonephritis. (http://www.ncbi.nlm.nih.gov/pubmed/26866231)

Question 7

A 17-year-old boy is evaluated for abnormal urinalysis findings. He came to the clinic 2 weeks ago with low back pain, and a urinalysis at that time showed 2+ protein. He currently feels fine and has no urinary complaints. The patient has not exercised vigorously or taken any medications. He has no other medical problems and received all appropriate childhood vaccinations. He does not use tobacco or illicit drugs. The patient is not sexually active. His father had early coronary disease and a stroke. His blood pressure is 112/70 mm Hg and pulse is 77/min. BMI is 24 kg/m². Physical examination shows no abnormalities. Laboratory results from this visit are as follows: Urine sediment microscopy is unremarkable for casts. A 24-hour urine collection shows 600 mg of protein (normal <150 mg). Which of the following is the best next step in management of this patient?

Accepted Answer

Explanation: This patient's isolated proteinuria on urinalysis is consistent with orthostatic proteinuria, a higher than normal protein excretion during the day (when upright) but normal protein excretion at night (when supine). Orthostatic proteinuria is the most common cause of proteinuria in adolescents (60%-75% prevalence) and rarely occurs after age 30. Possible mechanisms of proteinuria include an exaggerated normal response to upright posture, increased glomerular capillary pressure due to an exaggerated angiotensin II response with standing, subtle glomerular abnormality (eg, focal mesangial hypercellularity and/or basement membrane thickening), or left renal vein entrapment. Diagnosis can be confirmed by comparing the urine protein-to-creatine ratio in urine samples collected in both the supine and standing positions. Another confirmatory test is to compare protein excretion in a split 24-hour urine collection divided between the daytime (after morning void until bedtime) and nighttime periods. Orthostatic proteinuria is confirmed in patients with a significant elevation in daytime protein excretion but a normal nighttime rate. Clinical features suggesting an alternate diagnosis include history of nephrotoxic agents, acute glomerulonephritis (eg, hypertension, hematuria, acute kidney injury), or nephrotic syndrome (eg, proteinuria >3-3.5 g/24 hr, hypoalbuminemia, edema). (Choice A) Positive antinuclear antibody screen and low serum complements (C3 and C4) suggest lupus nephritis in patients with acute glomerulonephritis. However, this patient has no findings of lupus (eg, malar rash, arthritis) or acute glomerulonephritis. (Choice B) CT scan of the abdomen with intravenous contrast can evaluate for malignancy in patients with renal masses or hematuria. However, it is not as useful for evaluating proteinuria. (Choice D) Ultrasound-guided kidney biopsy may be required if this patient has persistent proteinuria or other renal abnormalities (eg, hematuria, hypertension, peripheral edema). (Choice E) Urine protein electrophoresis can detect monoclonal light chains or immunoglobulins in conditions such as multiple myeloma, which is more common in older adults and is rare in young adults. Educational objective: Orthostatic proteinuria is the most common cause of proteinuria in adolescents. The degree of proteinuria is mild and other significant renal abnormalities (eg, hematuria, acute kidney injury, hypertension) are absent. Orthostatic proteinuria can be diagnosed by split (day and night) 24-hour urine collection showing elevated daytime but normal nighttime protein excretion rates. References: Mechanisms of orthostatic proteinuria: lessons from a transplant donor. (http://www.ncbi.nlm.nih.gov/pubmed/8400067) Orthostatic proteinuria and the spectrum of diurnal variability of urinary protein excretion in healthy children. (http://www.ncbi.nlm.nih.gov/pubmed/20165888)

Question 8

An elderly male is brought to the emergency department by the police when he was found wandering on the street in the night.  He is confused, disoriented, and intermittently complaining of generalized abdominal pain and thirst.  Any further history is unobtainable.  His blood pressure is 110/80 mmHg, pulse is 98/min, temperature is 36.7C (98 F) and respirations are 22/min.  There is no abdominal rigidity or rebound tenderness.  Laboratory examination shows that his urine is positive for ketones.  His plasma glucose level is 167 mg/dL.  Other laboratory results are pending.
What is the best next step in the management of this patient?

Accepted Answer

Explanation: Most patients with alcoholic ketoacidosis respond to an administration of dextrose normal saline. Insulin is generally not required. Dextrose leads to an increase in insulin secretion, which leads to the metabolism of ketone bodies to bicarbonate. Almost all alcoholics are likely to be thiamine-deficient unless proven otherwise. (Choice B) There is no need to give insulin in patients with alcoholic ketoacidosis. (Choice C)This patient does not have a surgical abdomen; therefore, NPO, ultrasound, and surgical consultation are not required. (Choice D)Discharging the patient after the initial treatment is not an appropriate choice. These patients are likely to develop alcohol withdrawal, electrolyte imbalance and aspiration pneumonia. Furthermore, the administration of glucose can increase the utilization of thiamine, thus aggravating thiamine deficiency and leading to Wernicke' s encephalopathy. (Choice E)IV hydrocortisone is not indicated in the management of alcoholic ketoacidosis. Educational Objective: Most patients with alcoholic ketoacidosis will respond to an administration of intravenous dextrose containing normal saline and thiamine. Insulin is generally not required. All patients need to be hospitalized for treatment.

Question 9

A 42-year-old woman comes to the office for evaluation of elevated blood pressure.  She says, "I checked my blood pressure on a machine at the pharmacy, and it was 160/90 mm Hg.  The pharmacist said I should see a doctor."  The patient has no history of hypertension and has had no chest pain, headache, or focal weakness or numbness.  She notes occasional episodes of pain in her flanks, which she ascribes to muscle tension.  The patient has had several urinary tract infections over the course of her life but has no chronic medical problems and takes no medication regularly.  She does not use tobacco, alcohol, or illicit drugs.  The patient is married and has a son.  Her mother has hypertension, her father died at an early age in a motor vehicle collision, and her uncle has renal failure and receives dialysis.  Blood pressure is 156/94 mm Hg on the right arm and 152/96 mm Hg on the left arm.  Pulse is 80/min and respirations are 16/min.  Jugular venous pressure is within normal limits.  Breath sounds are normal bilaterally with no crackles.  Point of maximal impulse is displaced to the left and down.  Heart sounds are normal with no murmur or gallops.  The abdomen is soft with bilateral flank fullness.  Bowel sounds are active.  Laboratory results are as follows.  Urinalysis shows dysmorphic erythrocytes and mild proteinuria.  ECG shows left ventricular hypertrophy with nonspecific ST-T wave changes. 
Which of the following is the best next step in management of this patient?

Accepted Answer

Explanation: This patient has evidence of left ventricular hypertrophy on examination (eg, displaced point of maximal impulse) and on ECG, suggesting long-standing hypertension. Given the presence of bilateral flank pain/fullness and a family history of end-stage renal disease, the hypertension is likely due to underlying autosomal dominant polycystic kidney disease (ADPKD). ADPKD is an inherited disorder with a prevalence of approximately 1 in 500. Hypertension is a common early manifestation. Patients also frequently develop hematuria, proteinuria, and flank pain. Most patients with ADPKD have progressive renal insufficiency as they age; approximately 50% require renal replacement therapy by age 60. Patients with suspected ADPKD should be screened with renal ultrasound. The presence of enlarged kidneys with multiple bilateral cysts is usually diagnostic. multiple bilateral cysts (Choice A) Pheochromocytoma can also cause secondary hypertension and is usually diagnosed with urine and plasma metanephrine testing. Patients with pheochromocytoma typically have paroxysmal hypertension, diaphoresis, headaches, and sinus tachycardia. This patient with flank pain and fullness is more likely to have ADPKD. (Choice B) Patients with essential hypertension are often treated with lifestyle modifications. This patient with evidence of long-standing hypertension at a relatively young age and flank fullness should undergo further evaluation with renal ultrasonography. (Choice C) Primary hyperaldosteronism can also cause secondary hypertension and is typically diagnosed when plasma renin levels are very low (often undetectable) and aldosterone levels are inappropriately high. Primary hyperaldosteronism is often associated with hypokalemia. (Choice E) Home blood pressure monitoring is often used when a true diagnosis of hypertension is unclear (eg, white coat hypertension). This patient with signs of long-standing hypertension (likely left ventricular hypertrophy), bilateral flank pain/fullness, and urinalysis abnormalities should undergo renal ultrasound to examine for ADPKD. Educational objective: Autosomal dominant polycystic kidney disease is an inherited disorder characterized by multiple bilateral renal cysts. Patients are often asymptomatic, but many develop hypertension, hematuria, proteinuria, renal insufficiency, and/or flank pain. Diagnosis is usually made by renal ultrasound.

Question 10

A 56-year-old man comes to the clinic for follow-up. The patient has a history of end-stage renal disease due to hypertensive nephropathy and underwent renal transplantation 2 weeks ago. The surgery had no complications and he had good initial graft function. The patient has no other medical conditions. His immunosuppression medications include prednisone, tacrolimus, and mycophenolate sodium. The patient does not use tobacco, alcohol, or illicit drugs. Vital signs are normal. BMI is 31.8 kg/m². Physical examination shows a healing lower abdominal surgical scar with no erythema or drainage. Fasting serum chemistry reveals the following: Which of the following is this patient at greatest risk of developing within the next several months?

Accepted Answer

Explanation: The risk of new-onset diabetes mellitus (DM) is increased following renal transplant and highest within the first few months. The cause of the increased risk is likely multifactorial and related to the following: Immunosuppression medication adverse effects: Following renal transplant, patients are typically maintained on a multidrug regimen that can consist of glucocorticoids (eg, prednisone), calcineurin inhibitors (eg, tacrolimus, cyclosporine), and antimetabolic agents (eg, mycophenolate). Glucocorticoids cause weight gain and decreased insulin sensitivity, and calcineurin inhibitors cause reversible toxicity to pancreatic islet cells, leading to impaired insulin secretion. Improved renal function: The healthy, transplanted kidney causes increased insulin excretion and is capable of increased gluconeogenesis. Many cases of new-onset DM following renal transplant likely represent patients with preexisting susceptibility to type 2 DM. Risk factors include increased age (eg, >45), BMI >30 kg/m², and family history of DM. The development of new-onset DM following renal transplant has been shown to both increase patient mortality and shorten graft survival time. (Choice B) There are increased rates of subclinical hypothyroidism following renal transplant, likely related to adverse effects of glucocorticoids. However, the rates of hyperthyroidism are not significantly increased. (Choice C) The incidence of nephrolithiasis in renal transplant recipients is not increased and may be decreased compared to the general population; the reasons are unclear. (Choice D) The risk of osteoporosis is increased following renal transplant, likely due to adverse effects of both glucocorticoids and calcineurin inhibitors on bone metabolism. However, over the next several months the development of osteoporosis is less likely than DM in this overweight male patient. (Choice E) The lifetime risk of renal cell carcinoma (RCC) of the native kidneys is significantly increased in renal transplant recipients. This is likely due to immunosuppression and may also be related to structural changes that occur in the native kidneys during the period of advanced renal disease that precedes renal transplant. However, cancer is slow growing and the risk of developing RCC within the first few months following transplant is low. Educational objective: The risk of new-onset diabetes mellitus is increased following renal transplant, predominantly in the first few months. The cause of this increased risk is likely multifactorial, related to adverse effects of immunosuppression medications (eg, glucocorticoids, calcineurin inhibitors) as well as increased insulin excretion and gluconeogenesis by the healthy, transplanted kidney. References: New-onset diabetes mellitus in transplant patients: pathogenesis, complications, and management. (http://www.ncbi.nlm.nih.gov/pubmed/15168375)

Question 11

A 29-year-old woman, gravida 1 para 0, at 18 weeks gestation comes to the emergency department due to severe right flank pain. The pain is sharp and paroxysmal and radiates to her labia. When the pain occurs, she has associated nausea and vomiting. The patient has no fever, hematuria, dysuria, or increased urinary frequency. She has no chronic medical conditions and has had no surgeries. Her pregnancy had been uncomplicated and initial prenatal laboratory testing was normal. The patient takes a daily prenatal vitamin and does not use tobacco, alcohol, or illicit drugs. Temperature is 36.7 C (98 F), blood pressure is 110/60 mm Hg, and pulse is 100/min. BMI is 32 kg/m². The abdomen is tender to palpation along the right side, but there is no rebound or guarding. Pelvic examination reveals an 18-week-sized uterus. Laboratory results are as follows: Which of the following is the most appropriate next step in management of this patient?

Accepted Answer

Explanation: 11ec2b69_c09e_1a9a_8f63_b30ccd5ac5a2_MD0005_00 This patient's paroxysmal, severe flank pain that radiates to the labia is likely due to nephrolithiasis. Other clinical features of nephrolithiasis include nausea, vomiting, dysuria, hematuria, and pyuria. During pregnancy, nephrolithiasis is most common in the second and third trimesters. An increase in urinary calcium excretion, urinary stasis, and decreased bladder capacity predispose pregnant patients to the development of nephrolithiasis. Additional risk factors include obesity, hyperparathyroidism, diabetes mellitus, irritable bowel syndrome, and a history of nephrolithiasis outside of pregnancy. To avoid fetal radiation exposure, diagnosis of nephrolithiasis during pregnancy is via renal and pelvic ultrasound (US) (Choice B). Ultrasonography usually does not visualize a stone; however, US findings of hydronephrosis and hydroureter are consistent with ureteral obstruction due to nephrolithiasis. Most stones pass spontaneously; therefore, management of nephrolithiasis in pregnancy is generally supportive with pain control as needed. Nephrolithiasis that is complicated by persistent obstruction, intractable pain, or urinary tract infection may require surgical management. (Choice A) MRI urography is a second-line imaging modality for the diagnosis of nephrolithiasis during pregnancy and is indicated if US is nondiagnostic. (Choice C) A noncontrast helical CT scan is the most sensitive test for diagnosing nephrolithiasis and is the first-line modality in nonpregnant patients. However, CT scans are associated with fetal radiation exposure and are relatively contraindicated during pregnancy. CT scan may be considered during the second and third trimesters if US and/or MRI is not diagnostic or available. (Choice D) A quantitative β-hCG is indicated in the evaluation of an early pregnancy of unknown location. At this patient's gestational age, a β-hCG level provides no information; the pregnancy is better evaluated via US. Educational objective: Nephrolithiasis during pregnancy is most commonly seen during the second and third trimesters and can present with flank pain that radiates to the labia. During pregnancy, first-line imaging is with a renal and pelvic ultrasound as it minimizes fetal radiation exposure. References: Radiology of renal stone disease. (http://www.ncbi.nlm.nih.gov/pubmed/27816704)

Question 12

A 42-year-old woman comes to the office for evaluation of elevated blood pressure.  She says, "I checked my blood pressure on a machine at the pharmacy, and it was 160/90 mm Hg.  The pharmacist said I should see a doctor."  The patient has no history of hypertension and has had no chest pain, headache, or focal weakness or numbness.  She notes occasional episodes of pain in her flanks, which she ascribes to muscle tension.  The patient has had several urinary tract infections over the course of her life but has no chronic medical problems and takes no medication regularly.  She does not use tobacco, alcohol, or illicit drugs.  The patient is married and has a son.  Her mother has hypertension, her father died at an early age in a motor vehicle collision, and her uncle has renal failure and receives dialysis.  Blood pressure is 156/94 mm Hg on the right arm and 152/96 mm Hg on the left arm.  Pulse is 80/min and respirations are 16/min.  Jugular venous pressure is within normal limits.  Breath sounds are normal bilaterally with no crackles.  Point of maximal impulse is displaced to the left and down.  Heart sounds are normal with no murmur or gallops.  The abdomen is soft with bilateral flank fullness.  Bowel sounds are active.  Laboratory results are as follows.  Urinalysis shows dysmorphic erythrocytes and mild proteinuria.  ECG shows left ventricular hypertrophy with nonspecific ST-T wave changes. Imaging reveals enlarged kidneys with multiple bilateral cysts.  Which of the following is the best management for this patient?

Accepted Answer

Explanation: 11ec2b69_c09b_5b71_8f63_1ff6d7bee327_MD0005_00 Autosomal dominant polycystic kidney disease (ADPKD) usually causes slowly progressive renal insufficiency. Although no specific therapies are available to halt the illness, rigorous control of blood pressure with ACE inhibitors has been shown to reduce the rate of renal decline. Aggressive control of lipid levels using statins is also recommended to limit risk of cardiovascular disease. (Choice A) Patients with ADPKD do not appear to be at increased risk of renal carcinoma. Bilateral nephrectomy is not required. Focus should be placed on reducing the risk of renal failure and cardiovascular disease. (Choice B) Most patients with ADPKD are diagnosed when renal ultrasound shows enlarged kidneys with multiple bilateral cysts. Genetic testing is usually reserved for those with suspected ADPKD who do not have a clear diagnosis by ultrasound. (Choice C) Renal ultrasound is not typically used for monitoring progression of ADPKD as sensitivity is too low to determine rate of cyst growth. (Choice E) Patients with ADPKD are at increased risk of berry aneurysms, but a screening MRI of the brain is typically reserved for the minority with high-risk features (eg, family history of intracranial bleed, previous intracranial bleed). Although patients with ADPKD often have liver and pancreas cysts, a screening MRI of the abdomen is not necessary. Educational objective: ACE inhibitors are considered the drug of choice to control hypertension and prevent progression of chronic kidney disease in patients with autosomal dominant polycystic kidney disease.

Question 13

A 22-year-old man comes to the office to discuss laboratory test results.  He is a competitive cross-country skier and is required to have periodic blood testing to comply with international rules.  The patient feels well except for occasional heartburn for which he takes antacids.  He trains strenuously on a regular basis and is on a very high protein diet.  The patient's medical history is unremarkable except for a concussion at age 17; at that time, his serum calcium was noted to be borderline high, but the patient did not follow up with his physician after discharge from the hospital.  His father was also found to have hypercalcemia at a young age but has not required any specific treatment and is otherwise healthy.  The patient takes no prescription medications and does not use tobacco, alcohol, or illicit drugs.  Laboratory results are as follows:  Which of the following clinical findings is most likely present in this patient?

Accepted Answer

Explanation: This patient has mild (eg, <12 mg/dL), asymptomatic hypercalcemia. In light of his chronic course, normal renal function, and family history of benign hypercalcemia, this is most likely due to familial hypocalciuric hypercalcemia (FHH), an autosomal dominant disorder due to inactivating mutations of the calcium-sensing receptor. Normally, high-normal calcium levels suppress parathyroid hormone (PTH) secretion, but in FHH, higher calcium concentrations are required to suppress PTH release. Concurrently, the defective calcium-sensing receptor causes increased reabsorption of calcium in renal tubules. higher calcium concentrations The first step in evaluation of hypercalcemia is to measure PTH; patients with FHH typically have high-normal PTH levels. FHH can then be differentiated from primary hyperparathyroidism by measurement of urinary calcium excretion, which will be elevated in hyperparathyroidism and low in FHH. Patients with FHH have no clinical findings and no treatment is necessary. (Choices A and B) Chvostek sign (contraction of the facial muscles when the facial nerve is tapped) and hyperreflexia are features of hypocalcemia, not hypercalcemia. (Choices D and E) Patients (and family members) with multiple endocrine neoplasia (MEN) types 1 and 2A may present with hypercalcemia due to primary hyperparathyroidism. However, they are less likely than patients with FHH to follow a benign course and usually have additional features. MEN 1 also causes pituitary tumors (eg, visual field defects) and enteropancreatic neuroendocrine tumors, whereas MEN 2A also causes medullary thyroid cancer (palpable neck mass) and pheochromocytoma. FHH does not affect the pituitary gland or cause palpable parathyroid findings. Educational objective: Familial hypocalciuric hypercalcemia is an autosomal dominant disorder due to inactivating mutations of the calcium-sensing receptor. Patients with familial hypocalciuric hypercalcemia have mild hypercalcemia without any clinical findings and do not require any treatment. References: Familial hypocalciuric hypercalcaemia: a review. (http://www.ncbi.nlm.nih.gov/pubmed/21986511)

Question 14

A 64-year-old man comes to the emergency department due to 2 days of nausea, vomiting, and abdominal distension.  The patient has no abdominal pain.  He has hypertension, hypercholesterolemia, coronary artery disease, and congestive heart failure.  The patient also has chronic back pain due to a compression fracture 6 months ago.  Medications include aspirin, oxycodone, furosemide, losartan, vitamin D, calcium gluconate, and simvastatin.  Temperature is 36.7 C (98 F), blood pressure is 130/70 mm Hg, and pulse is 92/min.  The abdomen is distended but soft and nontender.  There is no rebound tenderness or rigidity.  Bowel sounds are decreased.  There is 1+ peripheral edema.  Laboratory results are as follows:  An electrocardiogram (ECG) shows normal sinus rhythm.  Abdominal x-rays show diffuse bowel distension with a gas pattern in the colon and rectum.  Which of the following is the most appropriate next step in management of this patient?

Accepted Answer

Explanation: Nausea and vomiting with a soft, distended abdomen, decreased bowel sounds, and gaseous distension of small and large bowels shown on x-ray suggest ileus. Presence of gas in the colon and rectum and absence of air fluid levels is evidence against small bowel obstruction. In the absence of obvious obstruction and no history of surgery, metabolic causes of ileus are most likely. small bowel obstruction This patient has hypokalemia, which can cause paralytic ileus. Loop diuretics can produce hypokalemia and hyponatremia. Persistent vomiting may also cause hypokalemia but is usually accompanied by other metabolic abnormalities (eg, hypochloremia, metabolic alkalosis). As this patient has normal chloride and bicarbonate levels, he most likely has loop diuretic-induced hypokalemia. Oral potassium replacement is recommended in patients able to tolerate oral intake. Parenteral potassium replacement is necessary in those unable to tolerate oral intake, such as in this patient with dysfunctional bowel and also in patients with cardiac or neurologic complications of hypokalemia. (Choice A) Gastrointestinal infections can be occasionally complicated by ileus. There is usually preceding diarrhea and leukocytosis. (Choice C) Opioids most commonly cause constipation; they can also occasionally cause/worsen ileus. Methylnaltrexone selectively blocks mu opioid receptors on the gut mucosa without reversing the analgesic effect of opioids. It is used to reverse opioid-induced constipation. This patient does not have constipation as there is gas (not stool) in the colon and rectum. Furthermore, in the presence of hypokalemia, intravenous potassium should be administered first. (Choice D) Spironolactone is used to counter chronic diuretic-induced hypokalemia. It will not increase potassium levels in acute hypokalemia. (Choice E) An abdominal CT is indicated when there is diagnostic uncertainty or when bowel obstruction is suspected. Educational objective: Diuretic-induced hypokalemia is a common complication of antihypertensive/congestive heart failure therapy, especially with loop diuretics. Dysfunctional bowel, as in paralytic ileus, and cardiac and neurologic complications are indications for prompt parenteral potassium replacement. References: A physiologic-based approach to the treatment of a patient with hypokalemia. (http://www.ncbi.nlm.nih.gov/pubmed/22901631)

Question 15

A 42-year-old woman comes to the office for evaluation of elevated blood pressure.  She says, "I checked my blood pressure on a machine at the pharmacy, and it was 160/90 mm Hg.  The pharmacist said I should see a doctor."  The patient has no history of hypertension and has had no chest pain, headache, or focal weakness or numbness.  She notes occasional episodes of pain in her flanks, which she ascribes to muscle tension.  The patient has had several urinary tract infections over the course of her life but has no chronic medical problems and takes no medication regularly.  She does not use tobacco, alcohol, or illicit drugs.  The patient is married and has a son.  Her mother has hypertension, her father died at an early age in a motor vehicle collision, and her uncle has renal failure and receives dialysis.  Blood pressure is 156/94 mm Hg on the right arm and 152/96 mm Hg on the left arm.  Pulse is 80/min and respirations are 16/min.  Jugular venous pressure is within normal limits.  Breath sounds are normal bilaterally with no crackles.  Point of maximal impulse is displaced to the left and down.  Heart sounds are normal with no murmur or gallops.  The abdomen is soft with bilateral flank fullness.  Bowel sounds are active.  Laboratory results are as follows.  Urinalysis shows dysmorphic erythrocytes and mild proteinuria.  ECG shows left ventricular hypertrophy with nonspecific ST-T wave changes. After learning about the disease, the patient becomes worried that her 19-year-old son may also have the same condition.  Which of the following is the most appropriate response to the patient?

Accepted Answer

Explanation: Patients age ≥18 with a family history of autosomal dominant polycystic kidney disease (ADPKD) should be screened for the disorder using renal ultrasound. Early recognition of ADPKD aids in family planning and the management of potential disease complications (eg, hypertension, renal insufficiency). Counseling is performed as a diagnosis of ADPKD often can result in psychological consequences, have an impact on career decisions, and potentially affect ability to obtain life insurance. (Choice A) Because ADPKD is autosomal dominant, offspring of a single affected parent have a 50% chance of getting the disorder. If both parents are affected, the child has a 75% chance of getting the disease. (Choice B) Renal insufficiency is usually a late manifestation of ADPKD. A diagnosis prior to the development of renal insufficiency allows for the initiation of targeted interventions (eg, blood pressure control) that may reduce risk of renal decline. (Choice C) Although blood pressure should be monitored, the development of hypertension is not diagnostic of ADPKD. Renal ultrasonography is the best screening test. (Choice E) Genetic testing is more expensive than ultrasound and is typically reserved for patients who have equivocal ultrasound results. Educational objective: Patients age >18 with a family history of autosomal dominant polycystic kidney disease should be screened for the disorder using renal ultrasound. Counseling should be done prior to screening as positive testing can have psychological, insurability, and employment ramifications.

Question 16

A 74-year-old woman comes to the emergency department because of an episode of syncope.  She has generalized weakness, fever, nausea, dysuria, and urinary frequency.  She has a 3-day history of decreased oral intake.  She lives alone at home.  She does not use tobacco, alcohol, or drugs.  Her medications include aspirin, lisinopril, and ibuprofen.  Her blood pressure is 102/45 mm Hg and pulse is 48/min.  Examination shows dry mucus membranes.  The abdomen is mildly tender, soft, and non-distended.  Cardiac and lung exam show no abnormalities.  The lab studies show:  An ECG shows a rate of 48/min, a regular rhythm, wide QRS complexes, and absent P waves.  Which of the following is the most appropriate next step in management?

Accepted Answer

Explanation: This patient's symptoms of fever, dysuria, and increased urinary frequency as well as a positive leukocyte esterase and nitrites on urinalysis confirm the diagnosis of a urinary tract infection. This patient has had reduced oral intake, which has led to decreased circulating volume and subsequent acute renal failure. The labs show an anion gap acidosis that is secondary to renal failure. However, the most abnormal laboratory value present is the elevated serum potassium. Some of the most common manifestations of hyperkalemia, including weakness and abnormalities in cardiac conduction on ECG, are exhibited in this case. Several factors, including acute renal failure, NSAID use, and lisinopril use have likely contributed to this patient's elevated potassium level. On ECG, hyperkalemia initially manifests as peaked T waves and subsequently as prolongation of the PR interval and QRS complex, disappearance of the P waves, and eventually a sine wave. Various arrhythmias, including sinus bradycardia (as seen in this patient), are also seen with hyperkalemia. 11ec2b69_c095_19d3_8f63_c362a47b8ad9_MD0005_00 In this case, the most appropriate next step in management is intravenous calcium gluconate. Calcium rapidly stabilizes the cardiac membrane potential in patients who have severe ECG manifestations of hyperkalemia (e.g. prolonged PR interval, prolonged QRS interval, or disappearance of P waves). However, the effect of calcium gluconate is short lived, so other treatments are subsequently necessary to lower the serum potassium level. (Choice A) Amiodarone is an antiarrhythmic medication but is not used in the treatment of hyperkalemia-associated arrhythmia. (Choice C) Dobutamine can reduce serum potassium but is not generally used for treatment of hyperkalemia. (Choice D) There is good evidence that sodium bicarbonate is ineffective in treating hyperkalemia even in patients with renal failure and acidosis. A combination of glucose and insulin is more effective to drive potassium intracellularly. (Choice E) Placement of a transvenous pacemaker is impractical when compared to more rapid and less invasive alternatives such as calcium gluconate. Educational objective: Calcium gluconate or calcium chloride is the first line treatment for hyperkalemia if severe ECG manifestations (i.e. ECG changes more severe than peaked T waves) are present. Beta-agonists or a combination of glucose and insulin are then typically given to reduce serum potassium by driving potassium intracellularly. References: Therapeutic approach to hyperkalemia. (http://www.ncbi.nlm.nih.gov/pubmed/12401936) Combined effect of bicarbonate and insulin with glucose in acute therapy of hyperkalemia in end-stage renal disease patients. (http://www.ncbi.nlm.nih.gov/pubmed/8852501)

Question 17

A 26-year-old woman comes to the office due to excessive fatigue and decreased exercise capacity for the past several weeks. She delivered a healthy boy 5 months ago with no complications and has been attributing her symptoms to "baby blues." The patient enjoys spending time with her son and is excited to return to work. She has had no change in appetite but has been gaining weight. The patient has had no insomnia, excessive urination, feelings of worthlessness, or suicidal ideations. She takes no medications and does not use alcohol, tobacco, or illicit drugs. Temperature is 36.5 C (97.7 F), blood pressure is 136/92 mm Hg, and pulse is 64/min. Weight is 70 kg (154 lb) and BMI is 27 kg/m². Physical examination shows moist mucous membranes and no scleral icterus, lymphadenopathy, or jugular venous distension. The lungs are clear on auscultation and heart sounds are normal. The abdomen is soft and nontender. There is mild, nonpitting edema of the hands and feet. Laboratory results are as follows: Which of the following is the definitive treatment for this patient's hyponatremia?

Accepted Answer

Explanation: 11ec2b69_c096_c789_8f63_315fd588f095_MD0005_00 This patient has euvolemic hypo-osmolar hyponatremia. In addition, she has fatigue, weight gain, and a significant elevation in TSH consistent with primary hypothyroidism. In light of her recent pregnancy, this is most likely due to postpartum thyroiditis, an autoimmune disorder that is considered a variant of chronic lymphocytic (Hashimoto) thyroiditis. Moderate to severe hypothyroidism (with significant elevations in TSH) can be associated with mild hyponatremia, possibly due to decreased clearance of free water and increased release of antidiuretic hormone. Classic postpartum thyroiditis is characterized by a brief thyrotoxic phase, followed by a self-limited hypothyroid phase and eventual return to a euthyroid state. Mild hypothyroidism due to postpartum thyroiditis does not require treatment and typically resolves within a few months. However, moderate to severe hypothyroidism, as in this symptomatic patient, should be treated with levothyroxine, which will likely correct the hyponatremia. (Choice A) Restricting free water would improve this patient's hyponatremia but would not be the definitive therapy as it would not correct the underlying hypothyroidism. (Choice B) Glucocorticoids are recommended in the initial management of adrenal insufficiency. Primary adrenal insufficiency can cause hyponatremia, but this patient has no other signs of primary adrenal insufficiency (eg, hyperpigmentation, weight loss, hypotension, hyperkalemia), and her elevated TSH is consistent with hypothyroidism. (Choice C) Isotonic saline is used for treating hypovolemic hyponatremia (eg, gastrointestinal losses). Infusion of isotonic saline in euvolemic hypo-osmolar hyponatremia with an inappropriately elevated antidiuretic hormone level can worsen the hyponatremia. (Choice E) Vasopressin receptor antagonists (eg, tolvaptan) may be considered for treating severe hypervolemic or euvolemic hyponatremia that is symptomatic and resistant to fluid restriction. They are not needed for mild hyponatremia. Educational objective: Moderate to severe hypothyroidism can be associated with mild euvolemic hyponatremia. Treatment of the underlying hypothyroidism with levothyroxine can correct the hyponatremia. References: Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. (http://www.ncbi.nlm.nih.gov/pubmed/24074529) Management of endocrine disease: hypothyroidism-associated hyponatremia: mechanisms, implications and treatment. (http://www.ncbi.nlm.nih.gov/pubmed/27484454)

Question 18

A 66-year-old man comes to the clinic for a routine physical examination.  He has chronic kidney disease, diabetes mellitus, hypercholesterolemia, and hypertension.  His medications include aspirin, atorvastatin, hydrochlorothiazide, and metformin.  The patient has smoked 2 packs of cigarettes daily for the past 22 years.  His temperature is 37.2 C (99 F), blood pressure is 140/90 mm Hg, pulse is 80/min, and respirations are 12/min.  Physical examination shows a palpable abdominal mass, and auscultation shows a bruit below his umbilicus.  A CT angiogram with intravenous iodinated contrast is performed.  His creatinine level on the day of the scan was 1.8 mg/dL and 2 days later was 2.6 mg/dL.  Which of the following would most likely have prevented this complication in the patient?

Accepted Answer

Explanation: 11ec2b69_c09a_49fc_8f63_0fa0dd62e27b_MD0005_00 This patient with chronic kidney disease developed acute kidney injury (AKI) after exposure to iodinated contrast. Contrast-induced nephropathy (CIN) refers to AKI seen within 2-3 days of contrast exposure and lasts about 5-7 days. Impaired renal function (estimated glomerular filtration rate <40 mL/min/1.73 m² or serum creatinine >1.5 mg/dL) and volume depletion are important risk factors. Contrast-induced renal vasoconstriction is the proposed mechanism of injury. Intravenous volume expansion with isotonic solution (sodium chloride or sodium bicarbonate) is the only intervention that has been shown consistently to reduce the risk of contrast-induced acute kidney injury. The efficacy of oral hydration or oral sodium bicarbonate is unclear. This is likely due to these measures not rapidly expanding intravascular volume to effectively counter renal vasoconstriction (Choices C and E). N-acetylcysteine has also been used to prevent CIN but has not been shown to be superior to intravenous saline or sodium bicarbonate. (Choice A) Hemodialysis does not counter effects of contrast media on the kidney once exposure has occurred. Therefore, it does not reduce the risk of contrast nephropathy and is not recommended. (Choice B) Adjusting the diuretic dose to increase urine flow does not prevent contrast nephropathy. Diuretics may cause volume depletion that can increase the risk of contrast nephropathy. As a result, diuretics are usually held around the time of the contrast study, particularly in patients at high risk of AKI. Metformin should also be held to avoid risk of metformin-associated lactic acidosis Educational objective: Contrast-induced renal vasoconstriction is thought to cause contrast-induced nephropathy (CIN). Patients at high risk of CIN should receive intravenous sodium chloride or sodium bicarbonate infusion before and after contrast exposure to prevent renal hypoperfusion. References: Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (part 2). (http://www.ncbi.nlm.nih.gov/pubmed/23394215)

Question 19

An elderly male is brought to the emergency department by the police when he was found wandering on the street in the night.  He is confused, disoriented, and intermittently complaining of generalized abdominal pain and thirst.  Any further history is unobtainable.  His blood pressure is 110/80 mmHg, pulse is 98/min, temperature is 36.7C (98 F) and respirations are 22/min.  There is no abdominal rigidity or rebound tenderness.  Laboratory examination shows that his urine is positive for ketones.  His plasma glucose level is 167 mg/dL.  Other laboratory results are pending.
What is the most likely cause of this patient's condition?

Accepted Answer

Explanation: The patient most likely has alcoholic ketoacidosis, as suggested by his impaired mental function with ketonuria and mildly elevated plasma glucose levels. Plasma glucose levels can be low, high, or normal. High plasma glucose levels are speculated to be due to impaired insulin secretion combined with increased insulin resistance. Biochemically, the patients with alcoholic ketoacidosis will have increased anion and osmolal gap. (Choice A) The patient is unlikely to have acute appendicitis, as he does not have tenderness in his right lower quadrant; however, appendicitis can be associated with starvation ketoacidosis. (Choice B)Similarly, the patient does not have cholecystitis because his pain is not localized to the right upper quadrant. (Choice D)Henoch-Schonlein purpura is mainly seen in the pediatric age group. It is characterized by abdominal pain, skin rashes and joint inflammation. Mental status change is not a feature of Henoch-Schonlein purpura. (Choice E)The patient is unlikely to have diabetic ketoacidosis in the presence of mild hyperglycemia. Blood glucose levels are generally higher than 250 mg/dL in patients with diabetic ketoacidosis. Educational Objective: Alcoholic ketoacidosis is characterized by anion gap acidosis, increased osmolal gap, ketonemia or ketonuria and variable blood glucose levels. Blood glucose levels are generally higher than 250 mg/dL in patients with diabetic ketoacidosis.

Question 20

A 66-year-old hospitalized man is evaluated after an episode of generalized tonic-clonic seizure.  The patient has no previous history of seizure.  He underwent right hemicolectomy for cecal adenocarcinoma the previous day.  Postoperatively, the patient had hypotensive episodes, which responded to fluid resuscitation.  He has been receiving intravenous infusion of 5% dextrose with 0.45% saline.  He is also receiving morphine via a patient-controlled device.  On physical examination, he is postictal.  Temperature is 36.7 C (98 F), blood pressure is 112/60 mm Hg, pulse is 68/min, and respirations are 12/min.  Pulse oximetry shows 96% on room air.  Laboratory results are as follows:  Which of the following is the most appropriate next step in management of this patient?

Accepted Answer

Explanation: 11ec2b69_c096_2b47_8f63_53ae6c536d87_MD0005_00 This patient has developed severe hyponatremia, most likely due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Postoperative SIADH is common due to prominent nonosmotic stimuli for ADH secretion (eg, pain, nausea, physical and emotional stress). The resulting hyponatremia can be worsened by postoperative administration of intravenous fluids (eg, 5% dextrose with 0.45% saline), which, in the setting of SIADH, can lead to further water retention. nonosmotic stimuli The symptoms of SIADH depend on the degree of hyponatremia and the rate at which it occurred. Patients with serum sodium of 130-135 mEq/L are usually asymptomatic, and those with slowly developing hyponatremia with serum sodium of 120-130 mEq/L may be asymptomatic or display only mild symptoms (eg, lethargy, forgetfulness). However, rapid decreases (within <48 hours) in serum sodium concentration can lead to large fluid shifts and severe symptoms (eg, profound confusion, seizures, coma). The tonic-clonic seizure in this patient with severe hyponatremia (eg, serum sodium <120 mEq/L) suggests the development of cerebral edema and an associated risk of brainstem herniation. Such patients require an urgent increase in their serum sodium concentration, which is best accomplished with the administration of hypertonic (3%) saline. (Choice A) Fluid restriction is appropriate management in asymptomatic patients with SIADH or those with only mild symptoms. However, this patient with severe symptoms (eg, seizure) is at risk for rapid neurologic deterioration and death, and should be treated with hypertonic saline to correct the hyponatremia. (Choices C and E) Both lactated Ringer solution and normal saline are forms of isotonic fluid. Infusion of isotonic fluid is appropriate for patients who are hypovolemic with hyponatremia; however, it can result in net free water retention and worsening hyponatremia in those with SIADH (who are characteristically euvolemic). (Choice D) Naloxone is an opiate receptor antagonist used to reverse the effects of opiate overdose (eg, morphine). Patients with opiate (or opioid) overdose typically present with somnolence and depressed respiratory rate, but seizures are not typical. Educational objective: Patients with the syndrome of inappropriate antidiuretic hormone secretion who are asymptomatic or have mild symptoms usually respond to fluid restriction. Patients with severe symptoms are at high risk of rapid neurologic deterioration and death and require treatment with hypertonic (3%) saline. References: The treatment of hyponatremia. (http://www.ncbi.nlm.nih.gov/pubmed/19523575) Diagnosing and treating the syndrome of inappropriate antidiuretic hormone secretion. (http://www.ncbi.nlm.nih.gov/pubmed/26584969)

Exam 1: Advanced Clinical Medicine