A 50-year-old obese woman has long-standing type 2 diabetes mellitus inadequately controlled on metformin and pioglitazone. Insulin glargine (15 units subcutaneously at bedtime) has recently been started because of a hemoglobin A1C level of 8.4. Over the weekend, she develops nausea, vomiting, and diarrhea after exposure to family members with a similar illness. Afraid of hypoglycemia, the patient omits the insulin for 3 nights. Over the next 24 hours, she develops lethargy and is brought to the emergency room. On examination, she is afebrile and unresponsive to verbal command. Blood pressure is 84/52. Skin turgor is poor and mucous membranes dry. Neurological examination is nonfocal; she does not have neck rigidity. Laboratory results are as follows:
Which of the following is the most likely cause of this patient’s coma?
This woman with poorly controlled diabetes has developed hyperglycemia and lethargy during an episode suggestive of viral gastroenteritis. Her presentation is most consistent with hyperosmolar nonketotic coma. This condition typically occurs in type 2 diabetics who become volume depleted and develop renal insufficiency. Glucose is no longer able to spill out into the urine, the blood glucose skyrockets, and severe hypertonicity leads to brain dysfunction and coma. Serum osmolarity is calculated by the formula:
This patient’s serum osmolality is as follows:
Thus, the serum osmolarity is greater than 350 mOsm/L. Although the serum sodium is usually the main determinant of osmolarity, extreme hyperglycemia contributes significantly to this patient’s hypertonicity. Osmotically active particles in the extracellular fluid space pull water out of the intracellular space. This causes cellular dehydration in the brain and consequently the patient’s CNS changes. Diabetic ketoacidosis would be associated with a much lower serum bicarbonate level and with an elevated anion gap. This patient’s anion gap is 9 mEq/L (126 − [95 + 22]), which is well within the normal range. This patient’s hyponatremia is minimal and is related to the osmotic effects of hyper-glycemia. Patients with SIADH have an inappropriate production of ADH, leading to water retention and consequent hypotonicity (not hypertonicity, as in this case). The diagnosis of SIADH or drug-induced hyponatremia cannot be made in the setting of severe hypovolemia. Although the oral hypoglycemic chlorpropamide can cause drug-induced hyponatremia, this patient was not taking a sulfonylurea. Although meningitis can be associated with hyponatremia, this patient’s hypertonicity and lack of meningeal signs point toward hyperosmolar nonketotic coma as the cause of her illness.
A 24-year-old white man presents with a persistent headache for the past few months. The headache has been gradually worsening and is unresponsive to over-thecounter medicines. He notices diminished peripheral vision while driving. He takes no medications. He denies illicit drug use but has smoked one pack of cigarettes per day since the age of 18. Past history is significant for passage of a kidney stone last year. At that time, he was told to increase his fluid intake. Family history is positive for diabetes in his mother. His brother (age 20) has had kidney stones from too much calcium and a “low-sugar problem.” His father died of some type of tumor at age 40. Physical examination reveals a deficit in temporal fields of vision and a few subcutaneous lipomas.
Laboratory results are as follows:
You suspect a pituitary tumor and order an MRI which reveals a 0.7-cm pituitary mass. Based on this patient’s presentation, which of the following is the most probable diagnosis?
This young man presents with two obvious serum abnormalities—hypercalcemia and hyperprolactinemia (most likely secondary to the pituitary tumor). This, along with his positive family history of a younger sibling with high calcium and low blood sugar and a father who died from an unknown tumor, indicates this family has one of the multiple endocrine neoplasia syndromes. MEN1 is associated with hyperparathyroidism, pituitary tumors (usually prolactinomas), and islet cell tumors (most commonly gastrinomas, occasionally insulinomas). This patient’s personal and family history, therefore, suggests MEN1. The MEN2 syndromes include medullary carcinoma of the thyroid and pheochromocytoma. MEN2A is associated with hyperparathyroidism; MEN2B with mucosal and GI tract neuromas. There is no pituitary abnormality with the MEN2 syndromes. It would not be prudent to treat the patient’s issues as two separate abnormalities (primary hyperparathyroidism and prolactinoma). Tension headache is untenable in the face of a pituitary tumor and visual field deficit.
A 50-year-old woman is 5 ft 7 in tall and weighs 185 lb. There is a family history of diabetes mellitus. Fasting blood glucose (FBG) is 160 mg/dL and 155 mg/dL on two occasions. HgA1c is 7.8%. You educate the patient on medical nutrition therapy. She returns for reevaluation in 8 weeks. She states she has followed diet and exercise recommendations, but her FBG remains between 130 and 140 and HgA1C is 7.3%. She is asymptomatic, and physical examination shows no abnormalities. Which of the following is the treatment of choice?
The classification of diabetes mellitus has changed to emphasize the process that leads to hyperglycemia. Type 2 DM is a group of heterogeneous disorders characterized by insulin resistance, impaired secretion of insulin, and increased glucose production. In this type 2 patient, the first intervention, medical nutrition therapy, failed to achieve the goal HgA1c of less than 7.0%. Medical nutrition therapy (MNT) is a term now used to describe the best possible coordination of calorie intake, weight loss, and exercise. It emphasizes modification of risk factors for hypertension and hyperlipidemia, not just weight loss and calorie restriction. Blood glucose control should be evaluated after 4 to 6 weeks and additional therapy should be added; therefore, continued observation is not the best option. Metformin is considered first-line therapy in that it promotes mild weight loss, has known efficacy and side-effect profile, and is available as a generic with very low cost. Thiazolidinediones (“glitazones”), sulfonylureas, and insulin are considered second-line or add-on therapy for most patients with type 2 DM.
A 24-year-old woman presents 6 months after the delivery of her first child, a healthy girl, for evaluation of fatigue. She suspects that the fatigue is related to getting up at night to breastfeed her baby, but she has also noticed cold intolerance and mild constipation. She recalls having a tremor and mild palpitations for a few weeks, beginning 3 months after delivery. On examination, her BP is 126/84 and her pulse rate is 56. The thyroid gland is 2 times normal in size and nontender. The rest of the physical examination is normal. Laboratory studies reveal a free T4 level of 0.7 ng/ml (normal 0.9-2.4) and an elevated TSH at 22 microU/mL (normal 0.4-4). What is the likely course of her illness?
This patient has postpartum thyroiditis. Like other forms of destructive thyroiditis (including subacute or de Quervain thyroiditis), this illness is triphasic. Initially there is hyperthyroidism due to inflammation and release of preformed thyroid hormone from the inflamed follicles; this phase usually lasts 2 to 4 weeks. In subacute thyroiditis, the initial phase is usually noticed because of pain and tenderness over the thyroid gland, but in postpartum thyroiditis the thyroid is usually painless, and the hyperthyroid phase may be overlooked. This phase is then followed by transient hypothyroidism, usually lasting 1 to 3 months. The third phase is resolution and euthyroidism. Whereas Hashimoto thyroiditis usually leads to permanent autoimmune hypothyroidism, most patients with destructive thyroiditis have a full recovery. Some will be symptomatic enough to require thyroid supplementation for 1 to 3 months until the process resolves. Although the initial hyperthyroid phase can suggest Graves disease, in thyroiditis the absence of infiltrative ophthalmopathy and a suppressed radioiodine uptake will make the distinction. Antithyroid drug treatment of thyroiditis is ineffective and puts the patient at unnecessary risk of toxicity such as agranulocytosis. Although hypothyroidism can cause amenorrhea and hence impair fertility, the hypothyroid phase of postpartum thyroiditis is transient. Low-level radiation exposure, but not thyroiditis, increases the risk of subsequent development of thyroid cancer. Interestingly, therapeutic RAI, such as is given for Graves disease, does not increase the long-term risk of cancer, probably because the thyroid cells are destroyed.
A 65-year-old white woman presents for an annual examination. She feels well except for occasional nocturnal leg cramp and mild abdominal bloating. She takes a multivitamin and a supplement containing 600 mg calcium carbonate and 200 international units of vitamin D twice daily. She takes no prescription medications. Physical examination is unremarkable for her age. In completing the appropriate screening tests, you order a dual x-ray absorptiometry (DXA) to evaluate whether the patient has osteoporosis. DXA results reveal a T-score of −3.0 at the total hip and −2.7 at the femoral neck (osteoporosis: less than −2.5). Since her Z-score is −2.0, you proceed with an evaluation of secondary osteoporosis. Laboratory evaluation reveals
What is the likely cause of her osteoporosis?
Screening for osteoporosis in women is recommended at age 65 for most women and at age 60 for those with risk factors, including hyperparathyroidism, corticosteroid use greater than 3 months, cigarette smoking, low body weight, or documented fragility fracture. Although most women with osteoporosis will have primary osteoporosis, her hypocalcemia and low vitamin D levels suggest that this woman’s osteoporosis is due to a secondary cause. The GI symptoms and the iron deficiency anemia suggest that her hypovitaminosis D is due to intestinal malabsorption. Celiac sprue is relatively common (as high as 1% of the Caucasian population) and often presents with mild symptoms. A tissue transglutaminase or antiendomysial antibody test will provide important diagnostic information. Hypoparathyroidism causes hypocalcemia but is not associated with vitamin D deficiency or osteoporosis. Estrogen deficiency is an important contributing factor to the skeletal loss of calcium that occurs in women at the time of menopause, but is associated with normal calcium and vitamin D levels and would not account for the iron deficiency. Hypercalciuria of any cause will lead to kidney stones but does not cause hypocalcemia or hypovitaminosis D. Although primary biliary cirrhosis may present with mild symptoms (usually pruritus) and vitamin D deficiency, the alkaline phosphatase is always elevated (often three to five times upper normal) in this disease. Again, recent studies show that sprue (gluten-sensitive enteropathy) is much commoner than PBC.
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