• Primary hyperparathyroidism with hypercalcemic crisis.
  
  

2. What things exclude benign familial hypercalcemia? 

• The patient had symptoms, an increased urinary calcium excretion, and a high PTH.
  
  

3. What would you anticipate as possibilities at cervical exploration? 

• Solitary parathyroid adenoma or parathyroid carcinoma. 
• In most cases of primary hyperparathyroidism, a mass would not be palpable. 
• However, the adenoma is felt in about fifty percent of patients with calcium values greater than 14.0 mg/dl.
  
  

4. What do you think caused the initial excessive urinary output? 

• Hypercalcemia-induced failure of renal tubular concentrating ability.
  
  

5. What were helpful and harmful occurrences associated with the patient’s hypomagnesemia?

• Initially, the hypomagnesemia caused by diuresis helped by reducing the secretion of parathyroid hormone and by making bone inert to the effects of parathyroid hormone. 
• Harm was near when the patient required treatment with magnesium sulfate to avert primary hypomagnesemic tetany unrelated to the normal calcium value.
  
  

6. Outline the principles involved in the treatment of the patient’s hypercalcemia with each of the following:

• NaCl. Volume repletion increased glomerular filtration followed by solium induced renal calcium clearance at the loop.
• Furosemide. Inhibits Na reabsorption in the ascending loop of Henle. The increased Na in the distal tubule causes direct inhibition of calcium absorption. Thiazide diuretics are not used here because they cause increased distal renal tubular calcium reabsorption.
• Calcitonin. Immediately decreases PTH-mediated bone resorption and also increases renal calcium clearance.
• Pamidronate. Causes greater decreased PTH-mediated bone resorption than calcitonin with onset about 24-48 hours after use.
  
  

7. Assuming the patient became hypocalcemic shortly postoperatively, to what would you attribute the hypocalcemia? What clues would you have about the cause?

• Pamidronate might continue to suppress bone resorption, causing low calcium and low phosphate.
• Because of the previous hypercalcemia, the remaining parathyroid glands remain suppressed, causing low calcium and high phosphate (transient hypoparathyroidism). 
• Patients with severe osteitis fibrosa cystica may make new bone quickly. 
• This "bone hunger" is detected by low calcium and low phosphate concentrations. 
• Parathyroprivic hypoparathyroidism, detected by low calcium and high phosphate, may occur if the surgeon has removed all the parathyroid tissue.