Parathyroid Gland

Question 1

Familial Hypocalciuric Hypercalcemia (FHH)

Answer 1

Asymptomatic, modest, lifelong hypercalcemia
Hypocalciuria 
PTH not suppressed
Autosomal dominant
Surgery not indicated

Question 2

Mutation in FFH1

Answer 2

CaSR mutation

Codominant –> neonatal severe hyperparathyroidism

Question 3

What does the skeleton look like in primary hyperparathyroidism?

Answer 3

1. Not known if similar to osteoporosis
2. Baseline BMD is more decreased at cortical sites with relative sparing of trabecular bone; subset with spinal osteopenia
3. Fractures may be increased
4. Newer techniques suggest trabecular bone may not be normal

Question 4

What are some causes of PTH-independent Hypercalcemia?

Answer 4

Malignancy
Calcitriol-mediated (granulomatous, inflammatory)
Hyperparathyroidism
Milk-alkali syndrome or calcium alkali syndrome
Immobilization
Rare causes

Question 5

What are some things that may causes Calcitriol (1,25[OH]2D) - mediated Hypercalcemia

Answer 5

Sarcoid
Lymphoma
TB

Question 6

What is the first test that you get for a work up of Hypercalcemia?

Answer 6

PTH

Question 7

What are some treatments for Hypercalcemia?

Answer 7

IV fluids - normal saline
Loop diuretics - furosemide, augments Ca2+ excretion
Calcitonin - rapid reduction in Ca2+
Bisphosphonates - potently inhibit osteoclastic bone resorption

Question 8

What drug is an agonist for the calcium sensing receptor that may be used in primary hyperparathyroidism when surgery is not an option?

Answer 8

Cinacalet –> fools the PT into thinking calcium is higher so PTH decreases

Question 9

What are some signs and symptoms of Hypocalcemia?

Answer 9

Neuromuscular irritability (parathesias, muscle cramps, tetany) 
Lowered seizure threshold
Mental status changes
Cardiac - prolonged QT, arrhythmias, CHF
Basal ganglia calcification
Cataracts
Positive Chvostek's and Trousseau's sign

Question 10

Treatment for hypocalcemia

Answer 10

Acute – IV calcium gluconate

Chronic - d/t hypoparathyroidism is treated with calcium supplements and either vitamin D2 or D3 or calcitriol

Question 11

What makes FGF23? What does it do?

Answer 11

Made by bone cells (osteocytes)
Increases urinary phosphate excretion
Decreases renal production of 1,25(OH)2D

Question 12

What does excess FGF23 cause?

Answer 12

Hypophosphatemia and impaired one mineralization (genetic form of rickets, tumor induced osteomalacia)

Question 13

What does decreased FGF23 cause?

Answer 13

Hyperphosphatemia and tumoral calcinosis

Question 14

What are some causes of hypophosphatemia?

Answer 14

Reduced renal tubular phosphate reabsorption (PTH/PTHrP-dependent and PTH/PTHrP-independent)

Impaired intestinal phosphate absorption

Shifts of extracellular phosphate into cells (IV glucose, insulin therapy for prolonged hyperglycemia or diabetic ketoacidosis, catecholamines, acute respiratory alkalosis, rapid cellular proliferation)

Accelerated net bone formation

Question 15

What are some causes of hyperphosphatemia?

Answer 15

Impaired renal phosphate excretion (renal insufficiency, hypoparathyroidism, pseudohypoparathyroidism, tumoral calcinosis)

Vitamin D intoxication

Sarcoidosis, granulomatous diseases

Massive extracellular fluid phosphate loads (rapid admin or exogenous phosphate, extensive cellular injury or necrosis)

Transcellular phosphate shifts (metabolic acidosis, respiratory acidosis)