A 33-year-old woman with a history of poorly controlled Graves disease is interested in radioactive iodine (RAI) therapy to permanently treat her hyperthyroidism. She is currently trying to get pregnant.
Which of the following should the physician warn the patient about as a possible side effect of RAI treatment?
Worsening of Graves ophthalmopathy. There are several ways to treat Graves disease. One option is antithyroid drugs such propylthiouracil (PTU and methimazole (MMI). If patients are interested in permanent treatment of their hyperthyroidism, then surgery (thyroidectomy) and RAI should be considered. With RAI treatment, iodine concentrates in the follicular cells of the thyroid and ablates them completely within 2 to 4 months. Although RAI therapy will treat the hyperthyroidism through destruction of thyroid tissue, it will not decrease circulating levels of TSH receptor antibodies, and thus it will not treat Graves ophthalmopathy. Through an unclear mechanism, it can actually worsen Graves ophthalmopathy. In order to prevent this, some practitioners give glucocorticoids prior to RAI treatment.
(A) Agranulocytosis is a side effect of antithyroid drugs (PTU and MMI). (B) Recurrent laryngeal nerve injury can occur in surgical thyroidectomy. (D) First-trimester teratogenicity can occur with MMI treatment. Therefore, a pregnant female interested in antithyroid medication should be offered PTU instead of MMI.
A 29-year-old woman presents with rapid hair growth over her torso and face for the last 2 months. During this time she has not menstruated; however, she reports always being “regular” in the past. Her boyfriend reports that she is looking more “masculine” than she did before and has developed acne and a lower voice. Her past medical history is insignificant. On physical examination, a significant amount of coarse terminal hair is present on her jawline, chest, and lower abdomen. In addition, bitemporal hair thinning is noted. The patient refused genitourinary examination. Gynecologic ultrasound reveals normal and functionally intact ovaries.
Which of the following is the next best step in management?
Testosterone and DHEAS levels. The patient in this question likely has an androgen-secreting neoplasm of either the ovary or the adrenal gland. She reports rapid onset of hyperandrogenism and virilization (acne, voice lowering, androgenic alopecia, and masculine features). Anytime a virilizing neoplasm is suspected, the first step is always to order serum testosterone and DHEAS levels. This will determine the likely site of the neoplasm: Increased testosterone levels with normal DHEAS levels make an androgen-secreting ovarian tumor likely, whereas increased DHEAS levels with normal or slightly increased testosterone levels make an androgen-secreting adrenal tumor likely. Of note, DHEAS (the sulfated form of DHEA) is exclusive to the adrenal glands; DHEA, on the other hand, is secreted from the ovaries and the adrenal glands. (A) 17-hydroxyprogesterone levels is the screening test in diagnosing congenital adrenal hyperplasia (CAH) and is elevated in the 21-hydroxylase and 11-β hydroxylase deficiency forms of CAH. The classical form of this disease is usually diagnosed early in life and rapidly developing virilization is rare in this condition. (C) LH and FSH levels would be the answer if polycystic ovarian syndrome (PCOS) were suspected. PCOS, however, is very unlikely to have rapidly developing virilization. In PCOS, we typically see an increased ratio of LH to FSH. However, our patient is likely to have undetectable LH and FSH levels due to suppression by increased androgen levels. The lack of polycystic ovaries on ultrasound makes the diagnosis of PCOS unlikely with this patient. (D) Abdominal CT scan and other imaging studies are usually performed after serologic testing.
A 54-year-old woman presents with nausea and generalized muscle weakness. She was recently diagnosed with small cell lung cancer. She presents with a temperature of 36.8°C, blood pressure of 134/86 mmHg, heart rate of 96 beats per minute, respiratory rate of 16 breaths per minute, and oxygen saturation of 96% on room air. Physical examination is unremarkable and laboratory results reveal the following:
Which of the following do you expect to be present in this patient?
No jugular venous distention. The patient in this question has hyponatremia secondary to SIADH likely from small cell lung cancer. The key to answering this question is to recognize that SIADH causes euvolemic hyponatremia in which there is no volume expansion in the body, as opposed to hypovolemic hyponatremia (adrenal insufficiency, diuretic use) or hypervolemic hyponatremia (cirrhosis, congestive heart failure, nephrotic syndrome). Thus, physical examination will not demonstrate jugular venous distention. (A, B) Peripheral edema and paroxysmal nocturnal dyspnea are signs of hypervolemia. (C) Delayed capillary refill time is seen in hypovolemia.
A 54-year-old obese woman with a history of type 2 diabetes mellitus presents to the physician for her annual visit. She currently takes metformin and a multivitamin. She reports being compliant with her medication; however, she has noticed that her blood sugar levels have consistently been in the high 200s to 300s for the last month. Laboratory results reveal a fasting blood glucose of 172 mg/dL and an HbA1c of 8.3%. The physician informs her that a second agent will need to be prescribed for her diabetes. The patient requests an antidiabetic medication that will help her lose weight as well as control her blood sugars.
Which of the following medications should be added to the patient’s current regimen?
Exenatide. The preferred initial medication in patients with type 2 diabetes is metformin. Contraindications to metformin include renal insufficiency. Of note, metformin can cause adverse effects such as gastrointestinal irritation (diarrhea, cramps, increased flatulence) and lactic acidosis. However, most people with type 2 diabetes eventually require more than one medication for maintaining optimal glycemic control. If metformin is not sufficient in controlling a patient’s blood sugars, then the second medication depends on several factors, one of which is patient preference. The patient here desires to lose weight as well as control her blood sugars, so a GLP-1 receptor agonist such as exenatide is used. (A) Although sulfonylureas (glipizide) are usually the second drug added to metformin in patients with suboptimal blood sugar levels, side effects include weight gain and hypoglycemia. (C) Insulin would definitely assist in improving glycemic control but is associated with weight gain and hypoglycemia. Insulin is usually added to metformin if HbA1c >8.5%. (D) A thiazolidinedione such as pioglitazone can be used in patients with renal insufficiency; however, it is associated with weight gain, CHF, and edema.
A 44-year-old woman with a history of type 2 diabetes presents with nausea, confusion, and lethargy. She has a temperature of 36.8°C, blood pressure of 134/86 mmHg, heart rate of 88 beats per minute, respiratory rate of 24 breaths per minute, and oxygen saturation of 94% on room air. Laboratory results reveal the following:
Which of the following is a possible cause of this acid–base abnormality?
Diarrhea. The patient in this question is presenting with a nonanion gap metabolic acidosis. Given that the pH is less than 7.4, it is an acidosis. To determine if it is a metabolic acidosis versus respiratory acidosis, one must then look at the PaCO2 and bicarbonate. If bicarbonate and PaCO2 are both low, it signifies that it is a metabolic acidosis since a decreased bicarbonate will signal the lungs to hyperventilate in order to decrease the PaCO2 to compensate for the decreased bicarbonate. Finally, the presence of an anion gap or nonanion gap must be determined. Anion gap (AG) represents the concentration of unmeasured serum anions and is calculated by subtracting the bicarbonate (HCO3) and the chloride (Cl) from the sodium [AG = Na – (HCO3 + Cl)]. Normal anion gap value is between 6 and 12 mEq/L. This patient has an anion gap of 10, making this a nonanion gap metabolic acidosis. The most common cause of nonanion gap metabolic acidosis is diarrhea, which involves a GI loss of bicarbonate. (B) Diabetic ketoacidosis causes an anion gap metabolic acidosis. (C) Acute respiratory acidosis, on the other hand, occurs when inadequate ventilation occurs (so CO2 is retained (increased), which lowers the pH). This will then cause a rise in bicarbonate to compensate for the acidic pH. Myasthenia gravis and other neuromuscular diseases (muscular dystrophy, Guillain– Barré syndrome) are causes of respiratory acidosis. (D) High altitude causes a respiratory alkalosis since low atmospheric pressure of oxygen stimulates increased ventilation. (E) Vomiting causes a metabolic alkalosis.
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