Chapter 21: Parathyroid

Question 1

What are the cell types in the parathyroid, and what do they do?

Answer 1

Chief cells: Clear with glycogen, make PTH. Contain chromogranin A, synaptophysin, cytokeratins.

Oxyphil cells: Deep eosinophilic cytoplasm with mitochondria, nonsecretory and nongranular.

Question 2

What does PTH do?

Answer 2

Stimulate increased plasma Ca/Mg.
Kidney: Ca2+ reabsorption increase and PO4 decrease
Bone: Ca2+ and PO4 release
Intestine: Vitamin D mediated, increase Ca2+ and PO4 absorption.

Question 3

What are symptoms of hypoparathyroidism?

Answer 3

Hypocalcemia - tingling, cramps, tetanus, stridor, convulsions, depression, paranoia/psychosis.
Hyperphosphatemia.

Causes:
Iatrogenic
DiGeorge syndrome - agenesis of PT gland
Familial isolated
Familial polyglandular syndrome

Question 4

What is pseudo-hypoparathyroidism?

Answer 4

Reduced responsiveness of target tissues to PTH. Hypocalcemia with high PTH levels.

Albright syndrome!
GNAS1 gene - defective reabsorption at kidney renal tubular cells.

Question 5

Patient presents with osteodystrophy and bone abnormalities, short stature, obesity, mental retardation, subcutaneous cacification.

Answer 5

Albright syndrome.

Question 6

Patient presents with fatigue, weight loss, polyuria and polydipsia. Also has gastric ulcers, tarry stools, nausea/vomiting, anorexia.

Chondrocalcinosis and nephrocalcinosis are seen,
Nephrolithiasis with renal colic is seen.

Osteitis fibrosis cystica is seen.

Blood serum shows high PTH, high calcium, and low phosphate

Answer 6

Primary hyperparathyroidism (PTH production despite hypercalcemia).

PT adenoma most common - chief cell neoplasm. MEN1/2A.

Question 7

Patient presents with high PTH and a history of chronic renal failure and bone disease.

Answer 7

Secondary hyperparathyroidism.

Also occurs during Fanconi syndrome, renal tubular acidosis, vitamin D deficiency, intestinal malabsorption.