Got milk?
happy thanksgiving!
Two red blood cells are talking to two platelets...
One red blood cell says "I heard you two finally tied the clot!"
The other says "Coagulations!"
One red blood cell says "I heard you two finally tied the clot!"
The other says "Coagulations!"
Thigh Roid Rage
Compliments to the Neph
100
A 63-year-old woman is evaluated after a recent diagnosis of multiple myeloma. The diagnosis was based on the presence of a large amount of monoclonal protein on serum electrophoresis and more than 10% bone marrow monoclonal plasma cells. She is asymptomatic. She takes no medications.
Physical examination findings, including vital signs, are normal. Serum calcium level is 11.2 mg/dL (2.8 mmol/L), and total protein is 9.2 g/dL (92 g/L).
Which of the following should be measured?
A) 24-Hour urine calcium
B) 25-Hydroxyvitamin D
C) Ionized calcium
D) Parathyroid hormone
C) Ionized calcium
- In clinical settings in which increased protein binding of calcium may occur, the serum total calcium level may be elevated without a rise in the actual serum ionized calcium concentration.
- Ionized calcium measurement is indicated in asymptomatic patients with multiple myeloma and elevated total serum calcium.
Her total calcium level is elevated, but she is without symptoms of hypercalcemia. Approximately 40% to 45% of the calcium in serum is bound to protein, principally albumin, although the physiologically active form of calcium is in an ionized (or free) state. In most patients with relatively normal serum albumin levels, the total calcium usually reflects an accurate ionized calcium fraction. However, in clinical settings in which increased protein binding of calcium may occur, the serum total calcium level may be elevated without a rise in the actual serum ionized calcium concentration. This may occur in patients with hyperalbuminuria (as may occur in those who are severely dehydrated) and in patients with a paraprotein capable of binding calcium (as occasionally occurs in some patients with multiple myeloma). This phenomenon is sometimes termed pseudohypercalcemia (or factitious hypercalcemia). If present, a normal ionized calcium level may indicate that the elevated total calcium level is the result of excessive protein binding and potentially eliminates the need for further evaluation for hypercalcemia. Ionized calcium measurement is indicated in asymptomatic patients with multiple myeloma and elevated total serum calcium.
A 24-hour urine calcium measurement (Option A) is indicated in the diagnosis of familial hypocalciuric hypercalcemia (FHH). FHH is an autosomal dominant condition and the most common type of familial hypercalcemia. In FHH, an inactivating mutation of the CaSR gene causes the parathyroid gland to perceive serum calcium concentrations as low, resulting in increased parathyroid hormone (PTH) secretion and a higher serum calcium level. Simultaneously, the mutated CaSR in the kidney increases kidney resorption of calcium, leading to paradoxical hypocalciuria in the setting of hypercalcemia. This patient with multiple myeloma and a large amount of serum monoclonal protein likely has pseudohypercalcemia, and measurement of the ionized calcium level is the most appropriate diagnostic test.
25-Hydroxyvitamin D (Option B) is the storage form of vitamin D in the body, and its measurement is the most appropriate test for assessing vitamin D stores but will not help evaluate patients with hypercalcemia. Measuring both 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D is useful in further assessing patients with non–PTH-mediated hypercalcemia to assess for excess vitamin D production.
PTH testing (Option D) is indicated in patients with hypercalcemia to differentiate between PTH-mediated and non–PTH-mediated hypercalcemia. Measurement of PTH and 1,25-dihydroxyvitamin D levels may be indicated as part of this patient's evaluation, but only after true hypercalcemia has been established by measuring the ionized calcium. However, the primary cause of hypercalcemia in patients with multiple myeloma is not primary hyperparathyroidism but rather tumor-induced, osteoclast-mediated bone resorption due to cytokines released by myeloma cells.
100
Who is Rebecca Raccoon?
Calvin Coolidge was gifted a live raccoon by Vinnie Joyce, a Mississippi resident, in 1926. The gift was intended to be used as Thanksgiving dinner. Coolidge, however, became attached to the raccoon, kept her as a pet and named her Rebecca.
100
A 50-year-old woman is evaluated in the ICU for painful changes in her fingers, as shown, following placement of a right radial artery catheter 5 days ago. She has been receiving heparin therapy since admission. Her platelet count was normal on admission but it is now 35,000/μL (35 × 109/L).
Which of the following is the most likely diagnosis?
A. Antiphospholipid antibody syndrome
B. Disseminated intravascular coagulation
C. Heparin-induced thrombocytopenia and thrombosis
D. Thrombotic thrombocytopenic purpura
C. Heparin-induced thrombocytopenia and thrombosis
The most likely diagnosis is heparin-induced thrombocytopenia and thrombosis (HITT). Up to 2% of patients treated with heparin develop heparin-induced thrombocytopenia, and approximately 30% of such patients develop HITT. In patients with HITT, venous thrombi occur two- to fourfold more often than do arterial thrombi, although in patients with underlying arterial disease this ratio is reversed. Thrombi have a propensity to form in areas of vascular damage, such as in vessels in which indwelling catheters have been placed, as in this patient.
In patients with suspected heparin-induced thrombocytopenia, use of the 4T score is recommended to guide clinical decisions and management.
Heparin should be discontinued in patients with suspected heparin-induced thrombocytopenia (HIT) and an intermediate or high 4T score, and HIT laboratory testing should be obtained; in most cases, a non-heparin anticoagulant should be initiated.
100
A 75-year-old woman is evaluated in follow-up for abnormal thyroid function test results. The test was obtained to evaluate unexplained weight gain over the previous 6 months. She reports no additional symptoms such as fatigue, cold intolerance, or constipation. She has no other medical concerns.
On physical examination, pulse rate is 82/min. BMI is 26. The thyroid is normal size and without nodules.
Laboratory studies show a thyroid-stimulating hormone level of 9 μU/mL (9 mU/L) and a free thyroxine level of 1.0 ng/dL (12.9 pmol/L).
Which of the following is the most appropriate management?
A) Initiate levothyroxine
B) Measure triiodothyronine level
C) Repeat thyroid function studies in 6 to 8 weeks
D) No additional management
C Repeat thyroid function studies in 6-8 weeks
- Subclinical hypothyroidism is typically asymptomatic and diagnosed by a serum thyroid-stimulating hormone level above the upper limit of the reference range and a normal free thyroxine level.
- No evidence supports that treatment of subclinical hypothyroidism improves quality of life, cognitive function, blood pressure, or weight.
The most appropriate management is to repeat the thyroid function studies in 6 to 8 weeks (Option C). This patient has subclinical hypothyroidism. Subclinical hypothyroidism is typically asymptomatic and diagnosed by a serum thyroid-stimulating hormone (TSH) level above the upper limit of the reference range and a normal free thyroxine (T4) level. It affects 5% to 10% of the general population. Transient elevation of serum TSH should be ruled out by repeating the measurement in 6 to 8 weeks. The rate of progression from subclinical to overt hypothyroidism is 2% to 4% per year, whereas normal thyroid function will spontaneously return in one third of patients. The normal range for TSH increases with age; a TSH level of up to 10 μU/mL (10 mU/L) is within the normal range for persons 80 years and older.
Initiating levothyroxine (Option A) for subclinical hypothyroidism with TSH less than 10 μU/mL (10 mU/L) should be considered in younger patients, those attempting to become pregnant, or if severe symptoms are present. This patient fulfills none of these criteria. Subclinical hypothyroidism with TSH greater than 10 μU/mL (10 mU/L) may be a risk factor for coronary artery disease and heart failure. There is no evidence that treating subclinical hypothyroidism improves quality of life, cognitive function, blood pressure, or weight; however, in patients with elevated LDL cholesterol, normalizing the TSH will lower LDL cholesterol. Overtreatment, however, is seen in more than one third of patients older than 65 years, which may increase risk for dysrhythmia and bone loss.
Measuring the triiodothyronine level (Option B) in the setting of hypothyroidism is not necessary or recommended; normal levels are maintained unless hypothyroidism is severe. TSH will become elevated in hypothyroidism first, followed by abnormalities in the T4 level.
This patient should have thyroid function tests repeated in 6 to 8 weeks to confirm the diagnosis of subclinical hypothyroidism and the need for ongoing monitoring. In this context, no additional management (Option D) is incorrect.
100
A 33-year-old man is evaluated for acute kidney injury 48 hours after being hospitalized for herpes simplex virus encephalitis. Diagnosis was confirmed with polymerase chain reaction testing of the cerebrospinal fluid. He is being treated with intravenous high-dose acyclovir. Empiric therapy with ceftriaxone plus vancomycin was initiated and then discontinued after the results of the cerebrospinal fluid analysis became available. Medical history is significant for chronic kidney disease due to hereditary nephritis and hypertension. Outpatient medications are lisinopril and hydrochlorothiazide, both held since admission.
On physical examination, vital signs are normal. The patient has some difficulty with attention and orientation to time but is otherwise neurologically intact. The remainder of the examination is normal.
Cr 2.3
Na 137
K 5.8
Cl 102
HCO3 27
UA: SG 1.01, pH 7.5, 1+ blood, 2+ protein, 1+ leukocytes, 3-5 erythrocytes/hpf, fine needle crystals
Kidney u/s shows 11 cm right kidney and 11.8 cm left kidney with normal cortical appearance and without hydronephrosis
Which of the following is the most likely cause of this patient's acute kidney injury?
A) Acute glomerulonephritis
B) Acute interstitial nephritis
C) Acute tubular necrosis
D) Intratubular obstruction
D: intratubular obstruction
- Intravenous acyclovir can cause acute kidney injury due to intratubular obstruction from acyclovir crystal precipitation.
- Correction of volume depletion is critical for the prevention and treatment of crystal-induced acute kidney injury
The most likely cause of this patient's acute kidney injury (AKI) is intratubular obstruction (Option D). Intratubular obstruction can cause AKI through precipitation of crystals within the tubular lumen. Urinary findings include hematuria, pyuria, and crystals. This patient received intravenous high-dose acyclovir, which can cause acute AKI due to intratubular obstruction from acyclovir crystal precipitation. Predisposing factors for crystal-induced AKI include chronic kidney disease and volume depletion. Aggressive volume expansion is recommended during high-dose acyclovir therapy for these patients. Correction of volume depletion is also critical for the treatment of crystal-induced AKI as well as discontinuation of the drug if possible.
Acute glomerulonephritis (Option A) is not a likely cause of this patient's AKI. This patient has hereditary nephritis, which can lead to chronic glomerular basement membrane changes but not acute glomerulonephritis. Furthermore, neither acute viral encephalitis nor acyclovir is associated with acute glomerulonephritis.
Acute interstitial nephritis (AIN) (Option B) is a common cause of AKI and is characterized by inflammation and edema of the interstitium. The classic clinical presentation of fever, rash, and peripheral eosinophilia occurs in only 10% to 30% of patients with AIN. Drug-induced AIN, especially due to antibiotics, is the most common cause of AIN and should be considered in any patient with AKI, a characteristic urinalysis, and history of any drug exposure. Drug-induced AIN typically takes 7 to 10 days to develop and is characterized by substantial pyuria and leukocyte casts, which is not seen in this patient's urinalysis results.
Acute tubular necrosis (Option C) is usually suggested by urine sediment that shows pigmented brown casts and debris, which are not seen in this patient's urinalysis results.
200
A 57-year-old man is evaluated during routine follow-up of hypoparathyroidism. He underwent resection of locally advanced squamous cell carcinoma of the tongue base with laryngectomy, thyroidectomy, tracheostomy, and percutaneous gastrostomy tube placement 2 years ago. He also received adjuvant radiation therapy. Hypoparathyroidism developed after treatment. He has no evidence of cancer recurrence and has maintained a normal weight and hydration. Medications are levothyroxine, calcium citrate, calcitriol, hydrochlorothiazide, and potassium chloride.
Serum calcium, magnesium, and urine calcium excretion are measured today.
Which of the following measurements should also be obtained for management of this patient's hypoparathyroidism?
A) 25-Hydroxyvitamin D
B) Ionized calcium
C) Parathyroid hormone
D) Serum phosphorus
D) Serum phosphorus
- Loss of parathyroid hormone–mediated renal excretion of phosphorus may result in hyperphosphatemia.
- Initial treatment of hyperphosphatemia is reduction of dietary phosphorus but occasionally requires the addition of oral phosphate binders if serum phosphorus exceeds the normal range.
Hypocalcemia is the most immediate manifestation and primary cause of symptoms attributable to hypoparathyroidism. Therefore, normalization of serum calcium is the primary goal and most frequently monitored endpoint of therapy. A reasonable goal for most patients is a serum calcium concentration at or just below the reference range without hypercalciuria. Monitoring of urine calcium excretion is mandatory because hypercalciuria often limits therapy. Correction of coexisting hypomagnesemia is also required. Thiazide diuretics are commonly used because they decrease urine calcium excretion. However, loss of parathyroid hormone (PTH)-mediated renal excretion of phosphorus may also result in hyperphosphatemia. In hypoparathyroidism management, serum phosphorus concentrations are ideally maintained in the normal range. Initial treatment of hyperphosphatemia is reduction of dietary phosphorus but occasionally requires addition of oral phosphate binders if serum phosphorus exceeds the normal range. Measurement of this patient's serum phosphorus level is an integral part of managing his hypoparathyroidism.
The most appropriate test to assess adequacy of vitamin D levels is measurement of serum 25-hydroxyvitamin D (Option A), which reflects dietary and skin-derived vitamin D. However, activation of vitamin D to 1,25-dihydroxyvitamin D requires both PTH and sufficient kidney function. Therefore, in the absence of PTH, as in this patient, measurement of 25-hydroxyvitamin D is of limited value. Vitamin D supplementation, 1000 to 4000 IU/d, and oral calcium carbonate or calcium citrate at doses of 1 to 3 g/d in divided doses may normalize or sufficiently treat mild or chronic hypocalcemia, as in this patient. If supplemental vitamin D and calcium cannot maintain a normal calcium level, then addition of calcitriol (1,25-dihydroxyvitamin D) will be necessary.
Measured calcium levels depend on the amount bound to albumin, which can be affected by nutrition and acid-base status. Hypoalbuminemia of any cause, such as cirrhosis or malignancy-related cachexia, will cause low total calcium levels. When albumin concentration is low, measurement of ionized calcium (Option B) or calculation of corrected total calcium is required to accurately assess calcium levels. In this well-nourished outpatient, the total serum calcium should reflect the expected ionized calcium concentration and measurement of ionized calcium is unnecessary.
During the assessment of new-onset hypocalcemia, measurement of PTH (Option C) establishes the mechanism of disease and guides treatment. However, if hypoparathyroidism is established and persists beyond 6 months, it is considered chronic hypoparathyroidism and management does not require continued monitoring of serum PTH levels.
200
which 2 NFL teams play every thanksgiving?
Detroit Lions
Dallas Cowboys (boo)
200
A 42-year-old woman is evaluated in the emergency department for 2-day history of headache, dizziness, and easy bruising. Her medical history is otherwise unremarkable, and she takes no medications.
On physical examination, temperature is 38.0 °C (100.4 °F), blood pressure is 150/98 mm Hg, pulse rate is 104/min, and respiration rate is 16/min. A neurologic examination is normal. She has no lymphadenopathy or organomegaly. Petechiae are noted on both legs.
Laboratory studies:
Haptoglobin - Undetectable
Hemoglobin - 8.2 g/dL (82 g/L)
Leukocyte count - 10,200/μL (10.2 × 109/L)
Platelet count - 8000/μL (8 × 109/L)
Reticulocyte count - 5% of erythrocytes
Creatinine - 1.1 mg/dL (97.2 μmol/L)
Peripheral blood smear is shown.
Which of the following is the most appropriate treatment?
A) Caplacizumab
B) Intravenous nitroprusside
C) Plasma exchange plus prednisone and rituximab
D) Platelet transfusion
E) Plasmapheresis with normal saline and 5% albumin replacement
C) Plasma exchange plus prednisone and rituximab
She has thrombotic thrombocytopenic purpura (TTP) based on the presence of thrombocytopenia and microangiopathic hemolytic anemia (MAHA), with supporting features of fever and headache. Acquired TTP is most often caused by production of an autoantibody that leads to a deficiency in the metalloprotease ADAMTS13, which is responsible for cleaving high-molecular-weight von Willebrand factor (vWF) multimers. An excess of high-molecular-weight vWF multimers causes platelet clumping in the microvasculature that leads to platelet consumption and MAHA. Plasma exchange with fresh frozen plasma is a crucial component of therapy that will remove the autoantibody and replace the deficient ADAMTS13. Prednisone is used to decrease continued autoantibody production. Rituximab further suppresses autoantibody production and the risk of recurrence.
Caplacizumab is a monoclonal antibody that binds to vWF and blocks the interaction of vWF to platelets (Option A). It is approved as an ancillary treatment for TTP in severe cases but would not be initiated before a trial of plasma exchange, glucocorticoids, and rituximab.
Although she has a low platelet count with evidence of petechiae, platelet transfusion should not be performed for a patient with TTP without life-threatening bleeding because it increases the risk of arterial thrombosis (Option D).
Performing plasmapheresis with non-plasma replacement, such as saline and albumin, will remove the autoantibody but does not correct the ADAMTS13 deficiency (Option E). Plasma exchange and immunosuppressive therapy are crucial to remove the autoantibody, replace the deficient ADAMTS13, and prevent the formation of new autoantibody.
200
A 32-year-old woman with an established diagnosis of primary hypothyroidism is evaluated during the fourth week of her first pregnancy. She is asymptomatic. Her only medications are levothyroxine, 125 µg/d, and prenatal vitamins with folic acid.
Physical examination findings are normal. Serum thyroid-stimulating hormone level is 4.2 µU/mL (4.2 mU/L), and free thyroxine level is 1.6 ng/dL (20.6 pmol/L).
Which of the following is the most appropriate management?
A) Increase the levothyroxine dosage by 10% now
B) Increase the levothyroxine dosage by 30% now
C) Increase the levothyroxine dosage by 50% in the second trimester
D) Continue current management
- B increase 30% now
- During pregnancy, the levothyroxine dosage is typically increased in the first trimester, with a possible total increase of 30% to 50%.
- During pregnancy, thyroid-stimulating hormone levels should be maintained in the lower half of the trimester-specific reference range, or less than 2.5 µU/mL (2.5 mU/L).
This patient's levothyroxine dosage should be increased by 30% now (Option B), and the thyroid function tests should be repeated in 2 to 4 weeks. Pregnancy is known to increase levothyroxine requirements in most patients receiving thyroid replacement therapy, and this expected increase should be anticipated by increasing her levothyroxine dosage. The levothyroxine dosage is typically increased in the first (and sometimes in the second) trimester of pregnancy, with a possible total increase of 30% to 50%. During pregnancy, thyroid-stimulating hormone (TSH) levels should be maintained in the lower half of the trimester-specific reference range, or less than 2.5 µU/mL (2.5 mU/L) if trimester-specific reference ranges are unavailable. In contrast, the upper range of normal for nonpregnant patients is approximately 4.5 to 5.0 µU/mL (4.5-5.0 mU/L).
Increasing the levothyroxine dosage by only 10% (Option A) will be insufficient; an increase in 30% to 50% is required to maintain the TSH level in the lower half of the trimester-specific reference range.
Increasing the thyroxine level by 50% in the second semester (Option C) will result in maternal hypothyroidism during the first trimester and places the fetus at substantial risk. The fetus is dependent on transplacental transfer of maternal thyroid hormones during the first 12 weeks of gestation. The presence of maternal subclinical or overt hypothyroidism may be associated with subsequent fetal neurocognitive impairment, increased risk for premature birth, low birth weight, increased miscarriage rate, and even an increased risk for fetal death. In pregnant patients with hypothyroidism, thyroid function testing should be frequent, preferably every 4 weeks, to protect the health of mother and fetus and to avoid pregnancy complications. When serum TSH values are inappropriately elevated, the dosage of levothyroxine is increased, and free thyroxine and TSH levels are monitored every 2 to 4 weeks.
Continuing the current levothyroxine dosage (Option D) is inappropriate in this patient because her TSH level is already too high at 4.2 µU/mL (4.2 mU/L) and requirements for thyroxine will continue to increase during the first and possibly the second trimester.
200
A 25-year-old man is evaluated in the emergency department for a 1-week history of fatigue, dyspnea, and hemoptysis. He has no other medical problems and takes no medications.
On physical examination, blood pressure is 155/95 mm Hg, and respiration rate is 25/min; other vital signs are normal. No rash is noted. The remainder of the examination is unremarkable.
Laboratory studies:
C3 - 95 mg/dL (950 mg/L)
C4 - 20 mg/dL (200 mg/L)
Creatinine - 2.3 mg/dL (203.3 µmol/L)
Antinuclear antibodies - Negative
Antimyeloperoxidase antibodies- Negative
Antiproteinase-3 antibodies- Negative
Urinalysis
3+ blood; 3+ protein; numerous erythrocytes and erythrocyte casts
Kidney biopsy shows necrotizing and crescentic glomerulonephritis with linear staining for IgG on immunofluorescence.
Which of the following is the most appropriate serologic test to perform next?
A) Anti–double-stranded DNA antibodies
B) Anti–glomerular basement membrane antibodies
C) Anti–phospholipase A2 receptor antibodies
D) Circulating IgA levels
B) Anti–glomerular basement membrane antibodies
This patient has rapidly progressive glomerulonephritis (RPGN), defined as an acute and steep rise in serum creatinine accompanied by hematuria and proteinuria. The differential diagnosis for RPGN is divided histologically into three patterns on immunofluorescence microscopy of the kidney biopsy: pauci-immune staining (ANCA-mediated glomerulonephritis), linear staining (anti-GBM glomerulonephritis), and granular staining (lupus nephritis). This patient has RPGN and a kidney biopsy showing linear staining, which is seen in anti-GBM antibody disease. Lung involvement (Goodpasture syndrome) occurs in >50% of patients with anti-GBM antibody disease; hemoptysis can be a presenting symptom, although shortness of breath or cough should also raise suspicion for a pulmonary-renal syndrome even in the absence of hemoptysis. Testing for anti-GBM antibodies is required as the next step in management to confirm diagnosis. For this patient, anti-GBM antibody titers would also be used to monitor treatment response. Up to one in three patients with anti-GBM antibody disease will have positive ANCA serologies, usually antimyeloperoxidase (MPO) antibodies, which can affect prognosis. Combined seropositivity is most commonly seen in patients with anti-GBM antibody disease who are older women. Therefore, it is appropriate to test for p-ANCA/anti-MPO and c-ANCA/antiproteinase 3 antibodies. Successful treatment, which typically includes glucocorticoids, plasmapheresis, and cyclophosphamide, will eradicate the patient's serum anti-GBM antibody titer.
Testing for anti–double-stranded DNA antibodies (Option A) is not required in this patient, as his antinuclear antibody test is negative and his kidney biopsy shows no granular staining suggestive of lupus nephritis.
Anti–phospholipase A2 receptor antibodies (Option C) can be checked in patients suspected of having primary membranous nephropathy, which typically presents with the nephrotic syndrome and preserved kidney function. The findings of erythrocytes and erythrocyte casts also argue against primary membranous nephropathy.
IgA nephropathy (IgAN) can present with any of the manifestations of the nephritic syndrome. Diagnosis can only be made when kidney biopsy shows dominant mesangial immune deposits of IgA with C3, and occasionally IgG or IgM. Circulating IgA levels (Option D) are not diagnostically useful, nor can they be reliably correlated with disease activity and should not be obtained. This patient's kidney biopsy shows linear staining, which is not consistent with IgAN.
300
A 22-year-old woman is evaluated in the office for a 6-month history of intermittent nausea, anorexia, and occasional constipation. She does not smoke cigarettes, drink alcohol, or use recreational drugs. She otherwise feels well and takes no medications. Family history is unremarkable.
Vital signs and physical examination are normal.
Hypercalcemia was noted on an initial metabolic profile.
Repeat laboratory studies:
Calcium - 11.1 mg/dL (2.8 mmol/L)
Creatinine - 1.0 mg/dL (88.4 μmol/L)
Phosphorus - 4.4 mg/dL (1.4 mmol/L)
Parathyroid hormone - <10 pg/mL (<10 ng/L)
25-Hydroxyvitamin D - 36 ng/mL (89.9 mmol/L)
1,25-Dihydroxyvitamin D - 97 pg/mL (233.0 pmol/L)
24-Hour urine calcium - 450 mg/24 h
Which of the following is the most appropriate additional test?
A) Chest radiography
B) Neck ultrasonography
C) Parathyroid hormone-related protein measurement
D) Urine calcium-creatinine ratio determination
A) Chest radiography
- Vitamin D-dependent hypercalcemia is associated with a suppressed parathyroid hormone level, hypercalcemia, a high or high-normal serum phosphorus level, and an elevated 1,25-dihydroxyvitamin D level.
- Unregulated conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D and resultant hypercalcemia may occur in granulomatous tissue associated with fungal infection, tuberculosis, sarcoidosis, and lymphoma.
This patient has mildly symptomatic hypercalcemia and a high-normal serum phosphorus level, suppressed parathyroid hormone (PTH), and an elevated 1,25-dihydroxyvitamin D level. Unregulated conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D may occur in granulomatous tissue associated with fungal infection, tuberculosis, sarcoidosis, and lymphoma, leading to increased intestinal absorption of calcium. Vitamin D-dependent hypercalcemia is associated with normal to elevated serum phosphorus levels because vitamin D enhances intestinal absorption of phosphorus, and suppressed PTH secretion reduces kidney phosphorus excretion. In the absence of an established cause of vitamin D-dependent hypercalcemia, such as documented ingestion, a chest radiograph to diagnose sarcoidosis, fungal infection, tuberculosis, or lymphoma is reasonable. In this young otherwise healthy patient, pulmonary sarcoidosis causing vitamin D-dependent hypercalcemia is probable.
Neck ultrasonography (Option B) may be reasonable to consider in a patient with PTH-dependent hypercalcemia to locate an adenoma before surgery. However, this patient's PTH is suppressed, making hyperparathyroidism unlikely.
Tumor-produced PTH-related protein (PTHrP) is the most common cause of hypercalcemia of malignancy. As in this patient, PTH would be suppressed but 1,25-dihydroxyvitamin D would not be elevated and serum phosphorus would be low. Most patients with humoral hypercalcemia of malignancy have advanced cancer associated with severe hypercalcemia; tumor-produced PTHrP is an unlikely mechanism of hypercalcemia in this otherwise well young patient. Therefore, PTHrP measurement is inappropriate for this patient (Option C).
Urine calcium-creatinine ratio determination (Option D) is useful to confirm the diagnosis of familial hypocalciuric hypercalcemia (FHH). Patients with this disorder are asymptomatic, have a history of hypercalcemia since childhood, and a family history of hypercalcemia. In this condition, the PTH level is elevated and the urine calcium excretion is low, resulting in paradoxical hypocalciuria in the setting of hypercalcemia. This patient's clinical and biochemical profiles are inconsistent with FHH, so measurement of the urine calcium-creatinine ratio is unnecessary.
300
How many turkeys per year are prepared for thanksgiving?
46 million
300
A 32-year-old man is evaluated for easy bruising. He has no other medical problems; takes no medications, recreational drugs, or supplements; and does not drink alcohol.
On physical examination, vital signs are normal. Two small ecchymoses are noted on the left thigh; he also has one small bruise on the right upper arm. No petechiae are visible. He has no lymphadenopathy or hepatosplenomegaly.
Laboratory studies:
Hemoglobin - 14.5 g/dL (145 g/L)
Leukocyte count - 5500/μL (5.5 × 109/L)
Mean corpuscular volume - 85 fL
Platelet count - 44,000/μL (44 × 109/L)
Reticulocyte count - 1.2% of erythrocytes
Creatinine - 0.7 mg/dL (61.9 μmol/L)
Urinalysis- Normal
Peripheral blood smear is unremarkable.
Which of the following are the most appropriate diagnostic tests?
A) Antinuclear antibodies and complement level
B) Antiplatelet antibodies and direct antiglobulin test
C) HIV and hepatitis C virus
D) Vitamin B12 and folate levels
C) HIV and hepatitis C virus
This patient has acute immune thrombocytopenic purpura (ITP). The initial evaluation for patients with ITP should include testing for HIV and hepatitis C virus because thrombocytopenia may be the initial presenting sign in these infections. Patients with HIV infection may have ITP independent of HIV viral load or CD4 cell count and may be otherwise asymptomatic. Although many patients with hepatitis C have symptoms, they are nonspecific and may not be directly related to the viral infection but rather to associated comorbid conditions. Testing for Helicobacter pylori may also be reasonable if the patient is from an endemic region.
Testing for systemic lupus erythematosus would be appropriate if the patient reported symptoms such as arthralgia, pleuritic chest pain, photosensitivity, or rash or had other cytopenias or evidence of kidney disease. Because none of these is present, antinuclear antibody and complement level testing is not necessary (Option A).
Although the pathogenesis of ITP is presumably related to autoantibody-mediated platelet destruction, the current methodology for antiplatelet antibody testing is not sensitive or specific enough to assist in the diagnosis. The patient also has no signs of concurrent hemolysis (normal hemoglobin level, reticulocyte count), so a direct antiglobulin test is not needed (Option B).
Vitamin B12 and folic acid are needed for normal hematopoiesis (Option D). However, isolated thrombocytopenia would be an unusual manifestation of these vitamin deficiencies. Although some patients with vitamin B12 deficiency are not anemic, they are apt to have macrocytosis, which is absent in this patient, as shown by the normal mean corpuscular volume. The patient has a normal leukocyte count, and no hypersegmented polymorphonuclear cells are noted on his peripheral blood smear, so a vitamin deficiency is unlikely to be the cause of his thrombocytopenia.
300
A 73-year-old woman is seen during a routine evaluation. She has been taking amiodarone for atrial fibrillation for 1 year with good control until a recurrence 1 week ago. Thyroid function tests were normal before starting amiodarone. She has no history of iodinated contrast use. She is otherwise well and takes no additional medications.
On physical examination, pulse rate is 110/min and irregular; remaining vital signs are normal. Other than an irregular tachycardia, the thyroid and remainder of the examination are normal.
Laboratory studies show a thyroid-stimulating hormone level of less than 0.01 μU/mL (0.01 mU/L) and free thyroxine level of 3.5 ng/dL (45.0 pmol/L).
ECG shows atrial fibrillation.
Which of the following is the most appropriate diagnostic test?
A) Serum thyroglobulin measurement
B) Thyroid peroxidase antibody titer
C) Thyroid scintigraphy with radioactive iodine uptake
D) Thyroid ultrasonography with Doppler studies
D: thyroid US with doppler
- Type 1 amiodarone-induced thyrotoxicosis (AIT) (hyperthyroidism) occurs in patients with Graves disease or thyroid nodules; type 2 AIT (destructive thyroiditis) occurs in patients without underlying thyroid disease.
- Thyroid ultrasonography with Doppler studies can help distinguish type 1 amiodarone-induced thyrotoxicosis (increased vascularity) from type 2 (decreased vascularity).
The most appropriate diagnostic test to perform next is thyroid ultrasonography with Doppler studies (Option D). This patient has developed thyrotoxicosis while taking amiodarone. Amiodarone has a high iodine content (37%) and prolonged half-life of approximately 60 days or longer. Thyrotoxicosis affects 5% of patients treated with amiodarone. Type 1 amiodarone-induced thyrotoxicosis (AIT) (hyperthyroidism) occurs in patients with Graves disease or thyroid nodules. This form of iodine-induced hyperthyroidism (Jod-Basedow phenomenon) is typically treated with methimazole. Type 2 AIT (destructive thyroiditis) is more common and occurs in patients without underlying thyroid disease. Type 2 AIT is usually self-limiting but sometimes requires treatment with glucocorticoids. Thyroid ultrasonography with Doppler studies, in addition to identifying thyroid nodules, allows assessment of the gland vascularity. Increased vascularity suggests type 1 AIT as the cause, whereas decreased vascularity suggests type 2 AIT. The decision to discontinue amiodarone depends on the patient's cardiac condition and type of thyrotoxicosis and should be done in consultation with a cardiologist.
Serum thyroglobulin measurement (Option A) is useful in distinguishing endogenous thyrotoxicosis from exogenous thyrotoxicosis, with the former leading to increased or normal levels and the latter leading to low levels. This test would be useful for patients who may be surreptitiously taking thyroid hormone. This patient has no history to suggest exogenous intake of thyroid hormone. Thyroid-stimulating immunoglobulins or thyroid-stimulating hormone receptor antibodies may be useful in identifying Graves disease as a potential cause of the thyrotoxicosis.
Thyroid peroxidase (TPO) antibodies are present in most patients with Hashimoto thyroiditis that is a cause of hypothyroidism; however, this patient has hyperthyroidism. Additionally, in evaluation of hypothyroidism, assessment of the TPO antibody titer (Option B) is unnecessary unless the diagnosis is unclear.
Typically, the evaluation of thyrotoxicosis is aided by thyroid scintigraphy with radioactive iodine uptake (Option C), which differentiates hyperthyroidism (Graves disease and toxic multinodular goiter) from destructive thyroiditis. The evaluation of AIT with thyroid scintigraphy is difficult and unreliable, however, because the high iodine load from amiodarone impairs thyroid uptake of iodine.
300
A 19-year-old woman is evaluated for a 2-week history of fatigue, poor appetite, arthralgia of the hands and knees, and a rash, all of which appeared 1 day after a trip to the beach. She has no other medical problems and takes no medications.
On physical examination, vital signs are normal. A malar rash characterized by pink-violet papules and plaques with sparing of the nasolabial folds is noted. The remainder of the examination, including joint examination, is normal.
Laboratory studies:
Albumin - 3.1 g/dL (31 g/L)
C3 - 50 mg/dL (500 mg/L)
C4 - 9 mg/dL (90 mg/L)
Creatinine - 1.1 mg/dL (97.2 µmol/L)
Antinuclear antibodies Titer, 1:160
Urinalysis
3+ blood; 3+ protein; many erythrocytes; occasional dysmorphic erythrocytes; rare erythrocyte casts
Kidney ultrasound shows kidneys of normal size and echogenicity.
Which of the following is the most appropriate diagnostic test to perform next?
A) Erythrocyte sedimentation rate
B) Extractable nuclear antigen panel
C) Kidney biopsy
D) Skin biopsy
C) Kidney biopsy
The 2019 European League Against Rheumatism/American College of Rheumatology classification criteria for systemic lupus erythematosus (SLE) include having antinuclear antibody (ANA) positivity at least once as obligatory entry criterion, followed by additive weighted criteria grouped into seven clinical and three immunologic domains. Patients with the entry criteria of a positive ANA, at least one clinical criterion, and having accumulated ≥10 points are classified as having SLE with a sensitivity of 96.1% and specificity of 93.4%. This patient has a positive ANA, acute cutaneous lupus erythematosus, and low serum complement levels (10 total points). The classic pattern of lupus nephritis is an immune complex–mediated glomerulonephritis with a varied pathology that includes six distinct classes of disease. The biopsy is crucial not only to establish the diagnosis but also to indicate which class of lupus nephritis she has, as the approach to treating lupus nephritis is guided by histologic class and the degree of kidney function impairment
This patient may test positive for one or more antibodies on the extractable nuclear antigen (ENA) (Option B) panel (e.g., anti-Smith, anti-U1-RNP, anti-Ro/SSA, anti-La/SSB), but this antibody panel test is not required to make a diagnosis of SLE. In addition, the results of an ENA panel are not expected to influence treatment plans compared with those of a kidney biopsy.
400
A 55-year-old woman is evaluated for hypercalcemia discovered during an emergency department visit 5 days ago. She had a 2-day history of vomiting and diarrhea that prompted her emergency department visit, where she was treated for volume depletion with intravenous 0.9% saline. She has since made a complete recovery and is asymptomatic.
Vital signs and physical examination are normal.
Emergency department laboratory studies:
Blood urea nitrogen - 35 mg/dL (12.5 mmol/L)
Calcium - 10.7 mg/dL (2.7 mmol/L)
Creatinine - 1.9 mg/dL (168.0 μmol/L)
Electrolytes
Sodium - 144 mEq/L (144 mmol/L)
Potassium - 4.5 mEq/L (4.5 mmol/L)
Chloride - 102 mEq/L (102 mmol/L)
Bicarbonate - 27 mEq/L (27 mmol/L)
Which of the following is the most appropriate test?
A) 25-Hydroxyvitamin D
B) Ionized calcium
C) Parathyroid hormone
D) Serum calcium
E) Serum phosphorus
D) Serum calcium
- Changes in blood protein, anion content, or blood pH can transiently change total calcium concentrations.
- Unless acute and severe, transient fluctuations in calcium binding or blood volume do not affect ionized calcium concentrations.
The most appropriate test to perform next is measurement of serum calcium (Option D). Total calcium is the sum of protein and anion-bound calcium as well as ionized calcium in serum. Changes in blood protein, anion content, or blood pH can transiently change total calcium concentrations. Volume loss results in an increase in the concentration of calcium in serum. Unless acute and severe, such fluctuations in binding or blood volume do not affect ionized calcium concentrations. The transient nature of these changes can be confirmed with a repeat measurement of total serum calcium after volume repletion and when issues related to calcium binding are resolved.
Vitamin D toxicity may present with hypercalcemia especially with concomitant calcium supplementation. The degree to which 25-hydroxyvitamin D levels are elevated varies widely in patients with hypervitaminosis D; therefore, levels are not diagnostic of toxicity independent of other indicators such as hypercalciuria or suppressed parathyroid hormone level (PTH). Therefore, measurement of 25-hydroxyvitamin D (Option A) is premature in this case.
Although ionized calcium (Option B) is the physiologically active form of calcium in blood, it should be a second-order test to evaluate abnormal calcium values in patients who are not critically ill. Methods of collection, transport, and analysis require resources that may not be readily available or are inefficient relative to other strategies for routine evaluation of hyper- or hypocalcemia.
PTH measurement (Option C) narrows the differential diagnosis of hypocalcemia and hypercalcemia and is indicated early in the evaluation of calcium disorders. However, in this patient with probable transient hypercalcemia, measurement of PTH is premature.
In the absence of metabolic bone disease, chronic kidney disease, or established calcium disorder, measurement of serum phosphorus (Option E) is unhelpful. Calcium disorders may affect phosphorus homeostasis given that they share multiple regulatory mechanisms. Serum phosphorus concentrations may be helpful in identifying the mechanism of hypercalcemia especially if data are ambiguous. However, a calcium disorder has yet to be verified.
400
When was the first thanksgiving celebrated?
1621
400
A 75-year-old man is hospitalized with sepsis secondary to community-acquired pneumonia. He has been otherwise well before hospital admission and was taking no medications.
On physical examination, temperature is 39.4 °C (102.9 °F), blood pressure is 90/52 mm Hg, pulse rate is 110/min, and respiration rate is 16/min. Oxygen saturation is 92% using a nonrebreathing mask. Cardiac examination reveals tachycardia. Bilateral basilar pulmonary crackles are noted.
Laboratory studies:
Activated partial thromboplastin time -55 s
D-dimer - 2.8 μg/mL (2.8 mg/L)
Hemoglobin - 9.1 g/dL (91 g/L)
Leukocyte count - 14,000/μL (14 × 109/L)
Platelet count - 55,000/μL (55 × 109/L)
Prothrombin time - 19 s
Fibrinogen - 105 mg/dL (1.05 g/L)
Peripheral blood smear is shown.
Cultures are collected. Fluid resuscitation is provided with 0.9% saline, and broad-spectrum antibiotics are initiated.
Which of the following is the most appropriate initial treatment for the coagulopathy?
A) Eculizumab
B) Prednisone
C) Therapeutic plasma exchange
D) No additional treatment
D) No additional treatment
He has disseminated intravascular coagulation (DIC), which has been triggered by sepsis. DIC is a systemic process with widespread and inappropriate activation of coagulation and concomitant fibrinolysis. In acute DIC, coagulation factors and platelets are rapidly consumed, leading to bleeding, organ dysfunction, and microangiopathic hemolytic anemia manifesting as schistocytes on the peripheral blood smear (see figure in Stem). Normal compensatory mechanisms are unable to keep up with the consumption of many blood components, resulting in depletion of platelets and coagulation proteins. Patients may have bleeding resulting from lack of available procoagulant factors in addition to large amounts of fibrin degradation products released from accompanying fibrinolysis, which interferes with normal platelet function and fibrin formation. Bleeding can often be seen at mucosal sites and areas of procedures (e.g., venous catheters). Organ dysfunction, including kidney and liver impairment, is also common. Laboratory findings in acute DIC include prolongation of the prothrombin and activated partial thromboplastin times, thrombocytopenia, low fibrinogen level, and markers of fibrinolysis such as an elevated D-dimer. Sepsis is the most common cause of acute DIC. Treatment focuses on addressing the underlying condition. Platelet transfusions, cryoprecipitate, and fresh frozen plasma are provided as needed for bleeding manifestations.
aHUS, ITP, AIHA, or TTP are not associated with coagulation abnormalities.
400
A 46-year-old man is evaluated for a thyroid nodule discovered 2 years ago. Thyroid ultrasonography performed at that time showed a 2-cm left upper pole isoechoic solid nodule without microcalcification or irregular margin. The sonographic pattern was characterized as low suspicion for malignancy. Fine-needle aspiration biopsy showed benign cytology.
On physical examination, vital signs are normal. A 2-cm left upper pole thyroid nodule is firm and mobile. No lymphadenopathy is evident.
Laboratory studies show a thyroid-stimulating hormone level of 2.0 μU/mL (2.0 mU/L).
Which of the following is the most appropriate next step in management?
A) Fine-needle aspiration biopsy
B) Levothyroxine initiation
C) Thyroid scintigraphy with radioactive iodine uptake
D) Thyroid ultrasonography
E) No further evaluation
D: Thyroid US
- Repeat ultrasonography should be performed in 6 to 12 months for all high-suspicion thyroid nodules, 12 to 24 months for intermediate- and low-suspicion nodules, and 24 months or longer for very low-suspicion nodules.
- Repeat fine-needle aspiration biopsy is indicated for all high-suspicion thyroid nodules, nodules with concerning new sonographic findings, and intermediate or low-suspicion nodules that increase significantly in size.
The most appropriate next step is thyroid ultrasonography (Option D). This patient has a persistent 2-cm thyroid nodule previously evaluated by thyroid ultrasonography and fine-needle aspiration biopsy (FNAB). Thyroid nodule evaluation begins with a thyroid-stimulating hormone (TSH) measurement; if it is normal or elevated, ultrasonography and FNAB are performed. Approximately 60% to 70% of biopsied nodules have benign cytology; 20% are indeterminate, and 5% to 10% have evidence of malignancy. Benign thyroid cytopathology results are associated with a 0% to 3% risk for malignancy. Repeat ultrasonography should be performed in 6 to 12 months for all high-suspicion nodules, 12 to 24 months for intermediate- and low-suspicion nodules, and 24 months or longer for very low-suspicion nodules.
FNAB (Option A) is inappropriate because the previous result of cytopathology was benign and the risk for malignancy remains low, without any clear change on examination. Repeat FNAB is indicated for all high-suspicion nodules, nodules with concerning new sonographic findings, and intermediate- or low-suspicion nodules that increase 20% in at least two dimensions or by 50% in nodule volume.
Based on past use to reduce TSH levels, levothyroxine initiation (Option B) may theoretically prevent thyroid nodule growth. However, studies have not shown the efficacy of this treatment, and the risk for thyrotoxicosis and adverse effects is increased.
Thyroid scintigraphy with radioactive iodine uptake (Option C) is useful in evaluating thyroid nodules associated with a suppressed TSH, indicating a possibly autonomously functioning and likely benign thyroid nodule. In this patient, the TSH is normal and thyroid scintigraphy with radioactive iodine uptake would not be warranted.
No further evaluation (Option E) of the thyroid nodule is inappropriate. Proceeding with a repeat ultrasonography in 6 to 24 months after the initial ultrasound is recommended by the American Thyroid Association to avoid the possibility of a false-negative test for malignancy with the first ultrasound and to detect interim changes in nodule morphology that may result in a change in treatment.
400
A 28-year-old man is evaluated for hematuria that he noted on awakening and a 3-day history of fever, runny nose, and cough. One year ago, he had an episode of gross hematuria after running a half marathon. Evaluation at that time resulted in a biopsy diagnosis of IgA nephropathy. He has no other medical problems and takes no medications.
On physical examination, temperature is 37.9 °C (100.2 °F), and blood pressure is 110/70 mm Hg; other vital signs are normal. The nasal mucosa is edematous, with serous discharge. Examination of the oropharynx reveals erythema without exudate. There is no lymphadenopathy. Lungs are clear to auscultation. The remainder of the examination is unremarkable.
Laboratory studies show a serum creatinine level of 0.9 mg/dL (79.6 µmol/L); urinalysis shows 3+ blood, trace protein, too numerous to count erythrocytes, and no casts. Streptococcal rapid antigen test is negative.
Which of the following is the most appropriate management?
A) Amoxicillin
B) CT of the abdomen and pelvis
C) Prednisone
D) Clinical observation
D) Clinical observation
This patient can be reassured that the gross hematuria is related to his underlying IgA nephropathy and will resolve spontaneously. Recurrent gross hematuria, in which the hematuria occurs in the setting of an upper respiratory infection (synpharyngitic hematuria) or after heavy exertion, is a common manifestation of IgA nephropathy in younger patients; it usually portends a benign clinical course with recurrent episodes of gross hematuria without progression to chronic kidney disease. Other predictors of a benign prognosis include a normal serum creatinine concentration and blood pressure as well as minimal proteinuria.
Glucocorticoid therapy, such as with prednisone (Option C), is unnecessary in a mild form of nonprogressive IgA nephropathy. The use of immunosuppression in progressive IgA nephropathy remains controversial: The STOP-IgAN study showed no benefit of glucocorticoid therapy in slowing the decline of kidney function, and the TESTING study was terminated early due to significantly increased risk for adverse events in patients treated with glucocorticoids. Therefore, glucocorticoid therapy is reserved for severe forms of IgA nephropathy deemed high risk for rapid progression to end-stage kidney disease.
500
A 52-year-old woman is evaluated for hypercalcemia that was incidentally discovered during a recent office visit. Serum calcium level was 10.7 mg/dL (2.7 mmol/L) three weeks ago. She is asymptomatic, has no other medical conditions, and takes no medications.
On physical examination, vital signs are normal; the examination is unremarkable.
Laboratory studies:
Calcium - 10.9 mg/dL (2.7 mmol/L)
Creatinine - 0.9 mg/dL (79.6 μmol/L)
Parathyroid hormone - 58 pg/mL (58 ng/L; N 10-65)
24-Hour urine calcium - 290 mg/24 h (N 100-300)
Which of the following is the most likely diagnosis?
A) Familial hypocalciuric hypercalcemia
B) Milk-alkali syndrome
C) Primary hyperparathyroidism
D) Surreptitious thiazide diuretic use
E) Vitamin D toxicity
C) Primary hyperparathyroidism
- Overt hypercalciuria or high-normal levels of urine calcium can help distinguish primary hyperparathyroidism from familial hypocalciuric hypercalcemia, which typically presents with low urinary calcium excretion.
- In patients with primary hyperparathyroidism, calcium levels are often only mildly elevated; parathyroid hormone levels may be frankly elevated or inappropriately normal.
This patient has a mildly elevated serum calcium level associated with an inappropriately normal parathyroid hormone (PTH) level. Primary hyperparathyroidism is usually caused by a parathyroid adenoma, and calcium levels are often only mildly elevated. PTH levels may be frankly elevated or inappropriately normal (typically the upper half of the reference range), as seen in this patient. Hypercalciuria may be present in up to 30% of patients. Overt hypercalciuria or high-normal levels of urine calcium, as seen in this patient, can help distinguish primary hyperparathyroidism from familial hypocalciuric hypercalcemia, which typically presents with low urinary calcium excretion.
Although familial hypocalciuric hypercalcemia (FHH) may also present with mild hypercalcemia and elevated or inappropriately normal PTH levels, an elevated or high-normal urinary calcium level (>200 mg/24 h), as seen in this patient, excludes the diagnosis of FHH (Option A). In FHH, a mutation of the CaSR gene causes the parathyroid glands to perceive serum calcium concentrations as low, resulting in elevated PTH and calcium levels. The CaSR gene also causes kidney resorption of calcium, leading to paradoxical hypocalciuria, usually less than 100 mg/24 h. This patient does not have hypocalciuria, which makes the diagnosis of primary hyperparathyroidism more likely.
Milk-alkali syndrome is caused by ingesting large amounts of calcium, such as with excessive antacid use, and results in kidney impairment and metabolic alkalosis (Option B). PTH levels are usually suppressed. This patient has an inappropriately normal PTH level and is unlikely to have milk-alkali syndrome.
Surreptitious thiazide diuretic use may cause mild hypercalcemia through reduction of urinary calcium excretion (Option D). This effect is more likely in the setting of previously unrecognized disease, and thiazide diuretics may “unmask” primary hyperparathyroidism. When thiazide diuretics are thought to be the cause of hypercalcemia, the medication should be stopped and calcium and PTH levels should be rechecked. This patient has a high-normal urinary calcium excretion, so surreptitious thiazide diuretic use is unlikely.
Vitamin D toxicity is unlikely in this patient (Option E). Vitamin D toxicity suppresses PTH and decreases urinary calcium excretion, neither of which is occurring in this patient.
500
how many feathers does a turkey have?
5000-6000
500
A 19-year-old woman is evaluated for easy bruising of 2 weeks' duration. She has no other symptoms, and medical history is unremarkable. She takes no medications.
On physical examination, vital signs are normal. Examination findings are limited to petechiae on the lower extremities and small, scattered ecchymoses.
Laboratory studies show a platelet count of 15,000/μL (15 × 109/L); the remainder of the complete blood count is normal.
The peripheral blood smear is shown.
Which of the following is the most appropriate management?
HIV and hepatitis C testing is pending.
A) Glucocorticoids
B) Plasma exchange
C) Platelet transfusion
D) Observation
A: Glucocorticoids
- Platelet transfusion is not generally indicated in patients with thrombocytopenia in the absence of trauma, surgery, or bleeding unless the platelet count decreases to less than 10,000 to 20,000/μL (10-20 × 109/L).
- Glucocorticoid treatment is indicated in patients with immune thrombocytopenic purpura and a platelet count less than 30,000/μL (30 × 109/L).
This patient should be treated with glucocorticoids (Option A). Clinical features and laboratory studies support the diagnosis of immune thrombocytopenic purpura (ITP). Petechiae and ecchymoses without lymphadenopathy or splenomegaly are supportive findings. Laboratory findings are limited to a low platelet count. On the peripheral blood smear, platelets appear as small purplish cells without a nucleus. As a rule of thumb, approximately seven platelets are normally seen per 100-power field. Giant platelets are typically associated with increased platelet production secondary to the stress of increased peripheral platelet destruction. In adults with newly diagnosed ITP and a platelet count less than 30,000/μL (30 × 109/L) who are asymptomatic or have minor mucocutaneous bleeding, treatment with glucocorticoids is recommended. Initial therapy includes a short course (<6 weeks) of prednisone or dexamethasone. The response to intravenous immune globulin is faster and may be indicated in patients with more severe thrombocytopenia and life-threatening bleeding.
Initial treatment of thrombotic thrombocytopenic purpura (TTP) involves therapeutic plasma exchange to remove the high-molecular-weight von Willebrand factor multimers and replace the deficient ADAMTS13 (Option B). Glucocorticoids are added to decrease autoantibody production. This patient lacks any evidence for microangiopathic hemolysis needed to establish the diagnosis of TTP such as schistocytes on the peripheral blood smear.
Platelet transfusion is not generally indicated in patients with thrombocytopenia in the absence of trauma, surgery, or bleeding unless the platelet count decreases to less than 10,000 to 20,000/μL (10-20 × 109/L); the lower platelet count is more applicable to patients with chronic thrombocytopenia who are otherwise stable. The transfusion threshold for patients with bleeding, trauma, or both is approximately 50,000/μL (50 × 109/L). This mildly symptomatic patient without overt bleeding does not require a platelet transfusion (Option C).
ITP may be asymptomatic and discovered in the evaluation of thrombocytopenia as an incidental finding on a routine complete blood count. Patients with such incidentally discovered ITP and platelet counts greater than 30,000/μL (30 × 109/L) may be observed without the need for drug therapy or platelet transfusions (Option D). This patient's symptoms indicate more severe thrombocytopenia requiring treatment with glucocorticoids; platelet transfusions are not indicated for patients with ITP who are not actively bleeding.
500
A 68-year-old woman is admitted to the ICU for urosepsis. She has a history of hypothyroidism, but levothyroxine is not found among her home medications supplied by her husband. Current therapy consists of Ringer lactate infusion, norepinephrine, vasopressin, and piperacillin-tazobactam.
On physical examination, temperature is 34.0 °C (93.2 °F), blood pressure is 90/40 mm Hg, pulse rate is 64/min, respiration rate is 8/min, and oxygen saturation is 90% with the patient breathing ambient air.
The patient has periorbital edema, loss of lateral third of eyebrows, 3+ lower extremity pitting edema, distant heart sounds, and absent deep tendon reflexes. She is lethargic with slow responses to questions.
Na 130
TSH 29
fT4 .1
Cortisol 21
Which of the following is the most appropriate treatment?
A) Active warming with heating pads
B) Administer hydrocortisone
C) Administer intravenous levothyroxine
D) Administer oral levothyroxine
C: IV Synthroid
- The most common clinical manifestations of myxedema coma include mental status changes and hypothermia with temperature less than 34.4 °C (94.0 °F).
- Initial treatment for myxedema coma is intravenous levothyroxine.
The most appropriate treatment is to administer intravenous levothyroxine (Option C). Myxedema coma is a rare life-threatening presentation of severe hypothyroidism with hemodynamic compromise. Mortality is high (up to 40%). Mental status changes ranging from lethargy to psychosis and coma, coupled with hypothermia (temperature <34.4 °C [94.0 °F]), are the most common clinical manifestations. Bradycardia, hypotension, or decreased respiration rate with resultant hypoxia and hypercapnia are also frequently present. Careful examination of the neck for thyroidectomy scar is critical. Free thyroxine (T4) is low in myxedema coma. Thyroid-stimulating hormone (TSH) is typically elevated, but without an overtly low free T4, myxedema coma is unlikely regardless of how high the TSH. Initial treatment for myxedema coma is intravenous levothyroxine with a loading dose of 200 to 400 μg, followed by an oral dose of 1.6 μg/kg/d. Lower levothyroxine doses are recommended in patients with advanced age and/or cardiac disease.
Aggressive supportive measures include fluids, vasopressors if necessary, ventilator support, and passive warming rather than active warming with heating pads (Option A) to avoid vasodilation, which can worsen hypotension. Passive warming includes the use of blankets. Heating pads are a form of active warming, as are forced warm air systems, and should not be used in this situation.
Stress-dose glucocorticoids are usually administered empirically before thyroid hormone is initiated to treat possible concomitant adrenal insufficiency. If a random cortisol level is above 18 μg/dL (497.0 nmol/L), hydrocortisone administration (Option B) can be avoided or discontinued. This patient's random cortisol is 21 μg/dL (580.0 nmol/L), so cortisol does not have to be administered.
Oral levothyroxine administration (Option D) is inappropriate because the severe hypothyroidism may cause bowel edema and slowed oral absorption of levothyroxine.
500
A 69-year-old man is evaluated 7 days after starting nafcillin to treat a culture-proven methicillin-sensitive Staphylococcal aureus sternal wound infection. The infection was diagnosed 10 days after coronary artery bypass surgery. History is significant for diabetes mellitus. Other medications are aspirin, metformin, metoprolol, atorvastatin, and acetaminophen as needed.
On physical examination, vital signs are normal. The sternal wound appears to be healing, with minimal tenderness and redness and decreased drainage. The remainder of the examination is unremarkable.
Laboratory studies:
C3 - 61 mg/dL (610 mg/L)
C4 - 13 mg/dL (130 mg/L)
Creatinine -2.0 mg/dL (176.8 µmol/L); before hospital admission: 0.9 mg/dL (79.6 µmol/L)
Urinalysis
3+ blood; 2+ protein; 30-40 erythrocytes/hpf; 2-5 leukocytes/hpf; dysmorphic erythrocytes; rare erythrocyte casts
Kidney biopsy shows a mild proliferative glomerulonephritis with infiltrating neutrophils, granular C3, and IgG and IgM staining on immunofluorescence; hump-shaped subepithelial electron-dense deposits are seen on electron microscopy.
Which of the following is the most appropriate treatment?
A) Add lisinopril
B) Add prednisone
C) Continue nafcillin
D) Initiate sodium restriction and furosemide
C) Continue nafcillin
Continuing nafcillin (Option C) is the most appropriate treatment for this patient with infection-related glomerulonephritis (IRGN). IRGN results from a recently resolved infection or an ongoing infection at the time of development of glomerulonephritis. Diabetes mellitus is the most common comorbidity, and older age (>65 years) is a key risk factor; both factors are present in this patient. Treatment of IRGN is typically supportive and aimed at the infectious etiology.
The prognosis for complete recovery from IRGN is excellent in children. However, in adults, the prognosis of the newly recognized forms of IRGN (e.g., due to Staphylococcus aureus and gram-negative organisms) is less favorable, with more patients developing severe kidney dysfunction, progressing to chronic kidney disease (CKD) and sometimes to end-stage kidney disease. Initiation of an ACE inhibitor such as lisinopril (Option A) at the time of acute kidney injury is not recommended. However, in this patient's long-term follow-up, lisinopril therapy is a reasonable option if he develops proteinuric CKD as a residual of IRGN.
Adding a trial of glucocorticoid therapy such as prednisone (Option B) to antibiotic therapy for IRGN is considered only in rare cases in which a severe proliferative glomerulonephritis on biopsy is accompanied by a rapid progression toward kidney failure. In this patient, the glomerular lesion is not described as severe, and his serum creatinine levels during his hospitalization do not indicate rapidly progressive glomerulonephritis defined by at least a 50% decline in glomerular filtration rate over a short time period.
The indication for diuretics and sodium restriction is the presence of hypertension and edema secondary to fluid retention. In these cases, sodium restriction and a loop diuretic (Option D) are recommended first-line therapies. Because this patient does not have evidence of hypertension or edema, these therapies are not indicated.