ABIM - Hypoparathyroidism & Calcium Imbalances

Here are key facts for ABIM Certification Exam from the Parathyroid Hormone & Calcium Homeostasis tutorial, as well as points of interest at the end of this document that are not directly addressed in this tutorial but should help you prepare for the boards. See the tutorial notes for further details and relevant links.

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1. Parathyroid hormone increases ECF calcium levels. 2. Regulated by calcium and vitamin D. 3. Typical reference blood calcium range is 2.2-2.6 mmol/L (8.6-10.3 mg/dL). 4. In response to reduced extracellular calcium concentration, the parathyroid glands secrete parathyroid hormone (PTH). 5. Both calcium and phosphate are stored within the hydroxyapatite crystals of bone, and calcium can be retained or excreted in renal and digestive systems, depending on the body's needs. 1. Prolonged exposure to parathyroid hormone promotes resorption of old bone, and, therefore, the release of calcium and phosphate into extracellular fluid. 2. Parathyroid hormone increases calcium reabsorption in the distal convoluted tubule of the nephrons. 3. It also stimulates activation of Vitamin D (activated form = 1,25(OH)2-VD). 4. The total effect of parathyroid hormone is to elevate extracellular calcium levels. 5. If Vitamin D levels are high, parathyroid hormone secretion is inhibited. 1. Most often the result of surgical removal or damage to the parathyroid glands. 2. Other causes include autoimmune destruction (i.e., Autoimmune polyglandular syndrome type 1), congenital lack of functioning parathyroid glands, and very low magnesium levels. 3. Low parathyroid hormone leads to low levels of calcium and high levels of phosphate. 4. Two key signs of tetany in hypoparathyroidism: Chvostek sign and Trousseau's sign. 5. Treatments include activated Vitamin D and calcium supplements, possibly magnesium supplements.

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1. Prolonged exposure to parathyroid hormone promotes resorption of old bone, releasing calcium and phosphate into extracellular fluid. 2. Episodic, transient binding of parathyroid hormone causes an increase in new bone synthesis. 3. Parathyroid hormone increases calcium reabsorption in the distal convoluted tubule of the nephrons. 4. It also stimulates activation of Vitamin D (activated form = 1,25(OH)2-VD). 5. Vitamin D acts on the nephron to increase reabsorption of calcium and phosphate. 6. In the small intestine, Vitamin D increases calcium and phosphate reabsorption. 7. In the bones, Vitamin D works with parathyroid hormone to facilitate skeletal remodeling. 1. Muscle weakness 2. Paresthesia (tingling or burning, especially in the feet, hands, and around the mouth) 3. Cramping 4. Tetany 5. Laryngospasms, bronchospasms, and stridor 1. Psychiatric effects: Irritability and confusion. 2. Cardiovascular effects: Include prolonged QT interval or heart failure. 3. Ocular: Cataracts 1. Typical reference blood calcium range is 2.2-2.6 mmol/L (8.6-10.3 mg/dL). 2. Chvostek sign: tapping the facial nerve (in the parotid gland/masseter muscle area) produces facial muscle spasms. 3. Trousseau's sign: carpopedal spasm seen after a few minutes of wearing an inflated blood pressure cuff (20 mmHg above systolic pressure). In the spasm, the patient will have flexed wrist, thumb, and metacarpophalangeal but hyperextended fingers. 1. Activated Vitamin D and calcium supplements, possibly magnesium supplements. 2. Dietary recommendations: high in calcium (green leafy vegetables, legumes, fortified cereals) and low in phosphorous (less meat, soft drinks, and dairy products). 1. Pseudohypoparathyroidism: Patients present with signs and symptoms associated with hypoparathyroidism but normal or elevated levels of parathyroid hormone – these patients have hormone resistance in the target organs. 1. Disorders that cause excessive bone resorption: Cancers, Paget disease, hyperthyroidism, Familial hypocalciuric hypercalcemia, Vitamin D toxicity. 2. Disorders that cause excessive gastrointestinal calcium absorption: Sarcoidosis, other granulomatous diseases. 3. Drugs that increase extracellular calcium, including lithium and thiazide diuretics. 1. Vitamin D deficiency or resistance (including antiseizure drugs that alter vitamin D metabolism) 2. Pancreatitis 3. Magnesium imbalances

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Below is information not explicitly contained within the tutorial but important for ABIM. 1. Most common cause of hypercalcemia in outpatients 2. Clinical presentation spectrum: asymptomatic to classical "stones, bones, abdominal groans, and psychic moans" 3. Laboratory profile: elevated calcium with inappropriately normal or elevated PTH 4. Surgical indications: symptomatic disease, age <50, significantly elevated calcium, reduced bone density, kidney stones 1. Secondary: compensatory PTH elevation due to another cause (e.g., chronic kidney disease, vitamin D deficiency) 2. Tertiary: autonomous parathyroid function after long-standing secondary hyperparathyroidism 3. Management approaches: vitamin D, phosphate binders, calcimimetics 4. Indications for parathyroidectomy in refractory cases 1. Hypercalcemic crisis: aggressive IV hydration, calcitonin, bisphosphonates, consideration of hemodialysis 2. Acute symptomatic hypocalcemia: IV calcium gluconate, correction of underlying causes 3. Recognition and management of calcium disorders in critically ill patients 4. Medication-induced calcium abnormalities: recognition and management 1. Parameters for chronic hypoparathyroidism therapy 2. Management of complications: hypercalciuria, nephrocalcinosis, kidney stones 3. Monitoring bone density in conditions affecting calcium metabolism 4. Emerging therapies: recombinant PTH, calcimimetics, newer vitamin D analogs