8/20/15 The All-of-Endocrinology-in-ONE-hour AM Report!

Clinical Pearls:

  • Over 90% of hypercalcemia is caused by primary hyperparathyroidism or malignancy.
  • Malignancy etiologies could be due to bone metastasis and/or PTHrP
  • Granulomatous diseases can cause hypercalcemia by expressing 1a-hydroxylase, which induces production of active Vitamin D.
  • Severe hypercalcemia (over 13mg/dL) is usually associated with malignancy and is most commonly seen in the inpatient setting
  • Mild to moderate hypercalcemia (11-13mg/dL) is usually seen in patients with primary hyperparathyroidism. It is most commonly seen in the outpatient setting.
  • Metastatic tumors to the hypothalamus/pituitary space are usually caused by lung or breast cancer
  • Management of hypercalcemia
    • IV Fluids to improve GFR immediately for calcium excretion.
    • Calcitonin intermediate onset of 4-6 hours. Be aware of tachyphylaxis
    • IV bisphosphonates, onset 24-48 hours (pamidronate, zolendronate)
  • A normal to high level of PTH in a patient with hyperparathyroidism almost always suggests primary hyperparathyroidism as the etiology.
  • V1 receptors are present in the blood vessels whereas V2 receptors are present in the collecting tubule. Activation of V2 receptors causes aquaporin channels within the membrane to allow reabsorption of water.
  • The hypernatremia from Diabetes insipidus may be masked until the patient is unable to satisfy their thirst or if they are unable to access water (for example, outpatients with DI usually don’t have hypernatremia because they can obtain free water from the most powerful sensing mechanism – thirst)
  • The etiologies for hypernatremia include poor water intake (inability to access water) versus diabetes insipidus.
  • Central DI will respond appropriately to ddAVP whereas nephrogenic DI will have a suboptimal response
  • Nephrogenic DI can be caused by electrolyte abnormalities (hypercalcemia, hypokalemia), medications (lithium, demeclocycline, etc), and genetic factors
  • Prolactin levels will INCREASE with pituitary stalk compression due to the lack of inhibition from hypothalamic dopamine, while all other anterior pituitary hormones (FSH, LH, ACTH, TSH, GNRH) would decrease.

A Very Special Thank you to Dr. Crapo for joining us!!! Also a special thank you to Dr. Kevin Ku for bringing in yummy bagels!

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