153. Parathyroid gland

Question 1

Parathyroid gland

Answer 1

development: pharyngeal arches
chief cells: regulated by free Ca in blood –> secrete PTH –> increase ca in blood by:
- increased Ca reabsorption by kidneys
- increased Ca absorption by GI (Vit. D)
- increased phosphate excretion by kidneys
- increased osteoblast activity
oxyphil cells: no function

Question 2

Primary Hyperparathyroidism

Answer 2

cause: spontaneous idiopathic
types: adenoma > primary hyperplasia > carcinoma
pathogenesis:
-cyclin D overexpression, MEN-1 mutations
morphology:
-parathyroid adenoma (single gland enlargement,
encapsulated, chief cell endocrine atypia)
-primary parathyroid hyperplasia (multiglandular
enlargement, diffuse or multinodular pattern)
- parathyroid carcinoma (same features as adenoma,
diagnosed by tissue invasion and metastasis)
clinical features: hypercalcemia
- bone: osteitis fibrosa cystica, brown tumors
- renal: nephrolithiasis, nephrocalcinosis
- GI: constipation, peptic ulcer, gall stones, pancreatitis
- neuromuscular: muscular weakening, hypotonia
- CNS: depression, lethargy, seizures

Question 3

Secondary Hyperparathyroidism

Answer 3

definition: chronic depression of calcium due to renal failure –> overactivity of parathyroid gland –> hyperparathyroidism
pathogenesis: chronic hypocalcemia –> stimulate parathyroid gland –> hyperplasia
- renal failure –> decreased phosphate excretion –>
binds to Ca –> decreased free Ca
- decreased alpha-1 hydroxylase –> decreased active
form of Vit D –> decreased intestinal absorption of
Ca
morphology:
- like primary parathyroid hyperplasia, increased chief
cells or water clear cells
clinical features:
- Ca blood levels remain normal due to compensatory
mechanisms by PTH
- Calciphylaxis: ischemic damage to blood vessels
caused by metastatic calcification secondary to
hyperphosphatemia

Question 4

Tertiary hyperparathyroidism

Answer 4

hypercalcemia due to autonomous activity of the gland

Question 5

Hypoparathyroidism

Answer 5

causes:
- surgical removal
- congenital absence (Di George syndrome,
chromosome 22 deletion)
- autoimmune hypoparathyroidism (AIRE)
clinical features (secondary to hypocalcemia)
-increased neuromuscular irritability (spasm, tetany)
- cardiac arrhythmias
- increased intracranial pressure
- chronic hypoparathyroidism –> cataract, basal ganglia
calcification, dental abnormalities