pth Flashcards
Parathyroid Glands
Chief cells – basic cell type, contain granules of PTH
Express calcium sensing receptor
Recall G-Protein Calcium Sensor for PTH release
Synthesize and secrete PTH in response to low calcium
Oxyphil cells – appear at puberty, present as single cells of small clusters
Have many mitochondria; secretory granules are absent
activity of the PT glands is controlled by the
evel of free (ionized) calcium in the bloodstream
Decreased levels of free calcium stimulate the synthesis and secretion of PTH
An increased level of free calcium, in turn, inhibits PTH secretion
Hypercalcemia
Serum PTH levels are inappropriately elevated for serum calcium levels
Clinically apparent hypercalcemia
Malignancies
Solid cancers secrete PTH related protein (PTHrp)
Solid tumors (lung, breast, head and neck and renal cancers) and hematologic malignancies mostly multiple myeloma
Primary hyperparathyroidism
Autonomous, spontaneous overproduction of PTH by PT tissue
Cyclin D1 and MEN1 mutations
5-10% are familial-associated with MEN 1 and MEN 2A syndromes
PT Hyperplasia
Sporadic/component of MEN syndrome
All 4 glands or asymmetric involvement with sparing of 1 or 2 glands
Parathyroid carcinomas
May involve 1 gland, gray-white irregular masses that exceed 10g, cytological similarity to adenomas
Invasion of surrounding tissues and metastasis are only reliable criteria for malignancy
Morphologic changes in other organs
Increased osteoclastic activity results in increased bone resorption
Increased osteoblastic activity results in formation of new bony trabeculae
Resultant bone comprises of widely spaced thin trabeculae and in severe cases, marrow with hemorrhage, cyst formation and fibrosis
Occasionally form masses composed of giant cells and hemorrhagic debris
Urinary tract – urinary tract stones, nephrocalcinosis (calcification of renal interstitium and tubules)
Secondary hyperparathyroidism
Due to conditions causing chronic DECREASED calcium which lead to compensatory PT hyperplasia
Chronic renal failure is most common cause – decreases phosphate excretion leading to elevated serum phosphate levels that directly depress serum calcium levels
Loss of renal substance reduces availability of alpha-1-hydroxylase
Tertiary hyperparathyroidism
When PT activity becomes autonomous and excessive with resultant hypercalcemia
Treatment – parathyroidectomy
Hypoparathyroidism
ongenital absence, surgery/radiation, autoimmune, familial
Clinical manifestations – related to severity and chronicity of hypocalcemia
Tetany, neuromuscular irritability
Anxiety and depression, confusional states, hallucinations, and frank psychosis
Calcifications of basal ganglia, Parkinsonian-like movement disorders, and increased intracranial pressure with resultant papilledema
Characteristic prolongation of QT interval in ECG
Pseudohypoparathyroidism
Hypoparathyroidism occurs because of end-organ resistance to actions of PTH
Serum PTH levels are normal or elevated
C cells of thyroid
Secrete the hormone calcitonin
Lowers serum calcium
Goitrogens
Chemical agents that inhibit function of thyroid gland
Suppress T3/T4 synthesis
Hyperthyroidism
Hypermetabolic state caused by elevated circulating levels of free T3 and T4
Primary
Diffuse hyperplasia (Graves disease) – 85% of cases
Toxic multinodular goiter, toxic adenoma, iodine-induced hyperthyroidism, neonatal thyrotoxicosis
Secondary – TSH-secreting pituitary adenoma
Thyroid storm
Abrupt onset of severe hyperthyroidism; results from an acute elevation in catecholamine levels,