A 64-year-old Caucasian female presents to the clinic with vague symptoms of non- specific abdominal pain, myalgias, constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had about of kidney stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy or other interventions. She was told by the urologist to follow up with her primary care provider after the kidney stones has resolved.

A 64-year-old Caucasian female presents to the clinic with vague symptoms of non- specific abdominal pain, myalgias, constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had about of kidney stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy or other interventions. She was told by the urologist to follow up with her primary care provider after the kidney stones has resolved.

 

The APRN examining the patient orders a Chem 7 which revealed a serum Ca++ of 13.1 mg/dl. The APN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist who does a complete work up and concurs with the APRN’s diagnosis.

Question:

What is the role of parathyroid hormone in the development of primary hyperparathyroidism? 

      
Correct Answer:  

 

Primary hyperparathyroidism is the unregulated overproduction of parathyroid hormone (PTH) resulting in abnormal calcium balance. PTH secretion is increased and is not under the usual feedback control mechanisms. The Ca++ level in the blood increase because of increased resorption and GI absorption of calcium but fails to inhibit PTH secretion at normal levels of calcium because the feedback threshold for calcium is set at a higher level in the abnormal parathyroid tissues. Hypercalcemia and hypophosphatemia are the clinical hallmarks of hyperparathyroidism.

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