Parathyroid hormone is the main hormone that maintains a balance of calcium and phosphate in our bodies.  When released, parathyroid hormone increases the release of calcium from the bone, reabsorption from the kidney, and secondarily stimulates absorption of calcium from the intestines.  It also stimulates secretion of phosphate in the kidney.  Hyperparathyroidism is the abnormal secretion of parathyroid hormone.

Clinical findings:

The classic medical school clinical findings are "Stones, Bones, abdominal moans, and psychiatric overtones," referring to renal calculi, bone pain, peptic ulcers, pancreatitis, and CNS symptoms (confusion lethargy, weakness).  Depending on the etiology, the serum calcium may be elevated and phosphate may be decreased.

Etiology:

Primary Hyperparathyroidism

Excessive parathyroid hormone due to a parathyroid gland abnormality

80% parathyroid adenoma

12% parathyroid hyperplasia (rarely from Multiple endocrine neoplasia)

1-3% parathyroid carcinoma

Secondary Hyperparathyroidism

Excessive parathyroid hormone due to an abnormality elsewhere in the body.

Most often this is from chronic renal failure where elevated phosphate and +/- decreased calcium lead to chronic stimulation of the parathyroid gland. 

Tertiary Hyperparathyroidism

Excessive parathyroid hormone due to autonomous secretion of parathyroid hormone.

Often this is from prolonged secondary hyperparathyroidism from renal failure.  Then, when the patient receives a renal transplant, cause of the secondary hyperparathyroidism is taken away, but the parathyroid glands continue to over secrete parathyroid hormone.

Radiology of Hyperparathyroidism

Osteopenia and bone demineralization are present in all forms of hyperparathyroidism

Subperiosteal resorption is virtually pathognomonic for hyperparathyroidism and is typically seen at the radial aspect of the middle phalanx of the index and middle fingers

Figure 1: Subperiosteal resorption as well as acroosteolysis, the next sign of hyperparathyroidism

Figure 2: Subperiosteal resorption in a child

Figure 3: Compare the finger on a patient with hyperparathyroidism, to his normal appearing finger after treatment

Phalangeal tuff resorption/acroosteolysis

Figure 4: Acroosteolysis (also subperiosteal resorption)

Acroosteolysis differential diagnosis Mnemonic from The Primer:  

(Presented because I can never remember it)

PINCH FO

Psoriasis

Injury (thermal/frostbite)

Neuropathy (congenital insensitivity to pain, diabetes, leprosy, myelomeningocele)

Collagen vascular disease (Scleroderma, Raynaud's)

Hyperparathyroidism

Familial (Hadju-Cheney)

Other (Polyvinyl chloride exposure, snake/scorpion venom)

Subchondral resorption

Sacroiliac joints

Distal clavicle

Pubic symphysis

Salt and pepper skull

Figure 5: Salt and pepper skull

Figure 6: Normal skull in the same patient following treatment of hyperparathyroidism

Brown Tumor

Brown tumors are more common in patients with primary hyperparathyroidism, however, due to the increased prevalence of secondary hyperparathyroidism, there are more brown tumors from secondary hyperparathyroidism than form primary hyperparathyroidism.  It is difficult to differentiate a Brown Tumor from a giant cell tumor or fibrous dysplasia; however, other signs of hyperparathyroidism should be present.

Figure 7:  Brown tumor in the phalanx (also subperiosteal resorption, tuft resorption, and osteopenia)

Figure 8: Brown tumor in the inferior obturator ramus

Soft tissue calcification 

Primary > Secondary

Chondrocalcinosis

Secondary > Primary

Knee

Triangular fibrocartilage

Symphysis Pubis