Parathyroid and Bone Pathophysiology

Question 1

Etiology (Primary and Secondary) and Pathogenesis (Primary and Secondary) of Hyperparathyroidism

Answer 1

Etiology
Primary: Hyperplasia, adenoma
Secondary Chronic Renal Failure, Chronic malabsorption of calcium
Pathogenesis
Primary: Hypercalcemia + Hypercalciuria. Chronic resorption of bone
Secondary (Renal disease) Early: Decreased Calcium + Vitamin D -> Increased PTH. Later: Parathyroid becomes more resistant to feedback regulation -> hyperplasia. Calcification of soft tissue + vessels

Question 2

What is the function of Vitamin D in regards to calcium and phosphate in blood and how do we obtain Vitamin D?

Answer 2

Increased Vitamin D (+ PTH) -> Increased calcium and phosphate absorption in intestines
Increased Vitamin D (+ PTH) -> Increased resorption + Decreased formation of bone
Sources Food (fish, liver, milk) and UV light

Question 3

What is the function of calcitonin in regards to calcium and where is it produced?

Answer 3

Calcium binding in bone cells, Decreased osteoclast activity, Decreased reabsorption Calcium and phosphate kidneys. Secreted by C cells in thyroid.

Question 4

What is the overall function of PTH in regards to calcium and phophate?

Answer 4

Keeps calcium from falling below normal level + Prevents phosphate from rising above normal

Question 5

How does PTH work in intestines, kidneys and bones?

Answer 5

Intestines Activation of Vitamin D -> Increased absorption of calcium and phosphate
** Kidneys** Conservation of calcium + Excretion of phosphate
Skeletal First: Calcium is released from bone fluid. Later: Bone is resorbed

Question 6

Etiology, clinical manifestations and treatment of hypoparathyroidism

Answer 6

Etiology Congenital absence, surgery, autoimmune destruction
Manifestations Decreased calcium in plasma -> Muscle cramps, convulsions, cardiac abnormalities, anxiety, personality changes
Treatment Replacement of calcium and vitamin D