A 28-year-old woman presenting with diarrhea, sweating, palpitations, and anxiety is found to have a diminished TSH (0.1 μU/mL) and an elevated free T4 (32 μg/dL).
What is the next best step in management?
Radioactive iodine uptake (RAIU) scan. The patient is presenting clinically with hyperthyroidism and laboratory values (decreased TSH and elevated free T4) confirm a diagnosis of primary hyperthyroidism. However, there are several etiologies of primary hyperthyroidism, including Graves disease (the most common), toxic multinodular goiter, functioning adenoma, and other rare causes (thyroiditis, struma ovarii, thyrotoxicosis factitia). The next best step to distinguish these causes from each other is an RAIU scan. If the RAIU scan reveals diffuse iodine uptake, then it is Graves (if it is homogeneously diffuse) or toxic multinodular goiter (if it is heterogeneously diffuse). If the RAIU scan reveals focal iodine update, it is likely a functioning adenoma. (B) If the RAIU scan reveals no iodine uptake, then serum thyroglobulin should be ordered as an increased level indicates thyroiditis, struma ovarii, or iodine load and a decreased level indicates thyrotoxicosis factitia. (C) Thyroid antibodies are a good test to order, but this is not the next best step in working up primary hyperthyroidism. Antithyroid peroxidase (anti-TPO) antibodies are seen in Hashimoto disease, and TSH receptor antibodies are seen in Graves disease. (D) FNA biopsy is typically performed in the workup of a thyroid nodule, particularly after TSH returns normal or RAIU confirms a cold nonfunctional nodule, in order to rule in/out malignancy.
A 58-year-old man with a 50-pack-year smoking history presents with forgetfulness. He constantly forgets to lock the door when he leaves for work and locked his keys in his car two times last week. He 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 is the best subsequent step in managing this condition?
Fluid restriction. This patient is presenting with hyponatremia and the etiology must be determined before management proceeds. Given the low serum osmolality, high urine osmolality, and high urine sodium, this patient likely has SIADH in the context of normal creatinine, potassium, and thyroid laboratory values. Other causes of decreased serum osmolality include primary polydipsia and malnutrition, but these would cause low urine osmolality (in contrast with our patient). Given the patient’s smoking history, he likely has lung cancer (small cell lung cancer) which is a common malignancy causing SIADH.
This question goes beyond diagnosing SIADH though; it asks for the appropriate management. In SIADH, treatment depends on severity of symptoms. In an asymptomatic or mildly symptomatic (forgetfulness, gait changes) patient, the treatment is fluid restriction to less than 800 mL/d. A loop diuretic can be administered as well if the urine osmolality is greater than 2× the serum osmolality. (C) Hypertonic saline is given as the first treatment in SIADH if the patient presents with moderate (confusion, lethargy) or severe (seizures, comatose) state. Our patient is clearly demonstrating mild symptoms so fluid restriction is the next best step in management. (A) Normal saline would worsen the hyponatremia here since it ultimately leads to sodium chloride excretion; however, in SIADH, the amplified ADH response would further concentrate the urine and dilute the blood and theoretically worsen the hyponatremia. In addition, administering a fluid with lower osmolality than the urine will cause net reabsorption of water. (D) Dexamethasone is a steroid and can be used in many inflammatory conditions, but is not useful in treating hyponatremia caused by SIADH.
A 34-year-old woman with an insignificant past medical history presents with unrelenting headaches for the past 2 weeks. She has a temperature of 36.8°C, blood pressure of 168/102 mmHg, heart rate of 96 beats per minute, respiratory rate of 16 breaths per minute, and oxygen saturation of 98% on room air. One year prior to this episode, her recorded blood pressure was 134/86 mmHg. Physical examination was unremarkable except for a faint bruit on the left side just inferior to the costal margin. Laboratory studies reveal a serum sodium of 148 mEq/L and a serum potassium of 2.8 mEq/L. Magnetic resonance angiography (MRA) shows a “string of beads” appearance of the left renal artery.
Which of the following laboratory values do you expect with this condition?
Increased plasma renin and decreased plasma aldosterone to plasma renin ratio. The patient in this question has fibromuscular dysplasia, a condition that commonly affects young women of childbearing age. The patient is presenting with new-onset hypertension along with laboratory values that reflect hyperaldosteronism (hypernatremia and hypokalemia). In this situation, the physical examination finding of a faint bruit inferior to the left costal margin and the “string of beads” MRA finding supports an etiology of secondary hyperaldosteronism, specifically fibromuscular dysplasia. Other causes of secondary hyperaldosteronism include renal artery stenosis, chronic renal failure, CHF, cirrhosis, and even nephrotic syndrome. All these conditions have an important characteristic in common: Kidney perception of low intravascular volume which upregulates the renin–angiotensin system. (C, D) Decreased plasma renin would be seen in primary hyperaldosteronism (caused by adrenal hyperplasia or an aldosterone-secreting adrenal adenoma) because in these disorders the kidneys perceive high intravascular volume which downregulates the renin–angiotensin system. (A) The overactive renin– angiotensin system seen in secondary hyperaldosteronism contributes to high plasma renin level and accordingly, a decreased (or sometimes normal) plasma aldosterone to plasma renin ratio.
A 29-year-old woman presents with heat intolerance, weight loss, and diarrhea. Her past medical history is significant for type 2 diabetes. She has a temperature of 36.8°C, blood pressure of 136/64 mmHg, heart rate of 102 beats per minute, respiratory rate of 20 breaths per minute, and oxygen saturation of 98% on room air. Physical examination is significant for a palpable 3-cm spherical and well-demarcated nodule on the right lobe of her thyroid gland. Her skin is moist. Laboratory studies reveal the following:
The patient is opposed to surgery and very hesitant to receive medical treatment for the condition. If she opts for no treatment, what is she at risk for developing?
Atrial fibrillation. The patient in this question has a toxic thyroid adenoma, a common cause of hyperthyroidism that results in focal hyperplasia of thyroid follicular cells that function independently of regulation by TSH. Although relatively common, it is less common than Graves disease. This question requires the student to not only know the diagnosis, but to also understand the side effects if left untreated. If no treatment is given, patients with hyperthyroidism can develop life-threatening cardiac arrhythmias secondary to the direct action of free thyroid hormone causing an elevated circulatory demand. This increased metabolic state can cause tachycardia, systolic hypertension, and certain tachyarrhythmias like atrial fibrillation. (A) Thyroid malignancy resulting from toxic adenoma of the thyroid gland is exceedingly rare. However, it is important to note that “cold” or nonfunctioning nodules are more concerning for cancer. (B) Infiltrative ophthalmopathy occurs in Graves disease and results from glycosaminoglycans building up in the retro-orbital and extraocular muscles. Graves disease is associated with diffuse enlargement (goiter) of the thyroid gland and pretibial myxedema. (D) Bone growth is the opposite of what one would expect in untreated hyperthyroidism. Rather, rapid bone loss can occur because thyroid hormone acts directly on bone cells, causing osteoclastic bone resorption (and hypercalcemia from the increased calcium release from the bones).
A 53-year-old man with a history of type 2 diabetes presents with swollen legs for the last month. The patient is asymptomatic otherwise. His current medications include a multivitamin and metformin. HbA1c was 7.9% at his annual visit in the previous year. He has a temperature of 36.8°C, blood pressure of 142/78 mmHg, heart rate of 68 beats per minute, respiratory rate of 16 breaths per minute, and oxygen saturation of 98% on room air. Physical examination reveals 2+ bilateral pitting edema up to his midtibia region. Laboratory results reveal the following:
Which of the following should be administered to reduce the progression of this patient’s underlying renal condition?
Lisinopril. The patient in this question has diabetic nephropathy and macroproteinuria (urine protein excretion greater than 300 mg/d). Diabetic nephropathy first manifests itself through an increased GFR and then microalbuminuria before progressing to macroproteinuria. Strict blood pressure control is the only effective treatment for reducing the progression of diabetic nephropathy. In diabetic patients, the blood pressure goal must be below 130/80 mmHg and ACE inhibitors (Lisinopril) are the antihypertensive drug of choice to prevent or slow the progression of nephropathy. ACE inhibitors are beneficial for diabetic patients because they slow the decline in GFR by reducing the hyperfiltration occurring at the level of the nephron. Potassium levels must be monitored very carefully in patients taking an ACE inhibitor due to the risk for hyperkalemia. (A) This patient is demonstrating azotemia with a BUN of 41 mg/dL and optimizing blood glucose control with an additional antidiabetic agent (although important with the patient’s recent HbA1c level) is not superior to strict blood pressure control in reducing progression of his diabetic nephropathy. (C, D) Lipid control and aspirin are beneficial for reducing the likelihood of coronary heart disease, but has not been shown to be effective in improving diabetic nephropathy.