Parathyroid Gland (Gross Anatomy)

Small flattened, ovoid bodies that lie external to the thyroid capsule
It is four in number and are closely related to

posterior border of the thyroid gland. Measures 5mm in length, 4mm in width and 2mm in thickness, and weigh 25-50mg apiece. Origin: 3rd and 4th brachial pouches of early embryo.

Blood Supply
Superior Thyroid Artery
Inferior Thyroid Artery Thyroidea Ima

Venous Supply
Superior Thyroid Vein Middle Thyroid Vein Inferior Thyroid Vein

Nerve Supply
Vagus Nerve

(CN X) Sympathetic Nerve

Lymph Drainage
Deep cervical
Pre-tracheal

Parathyroid Gland
Enclosed with a thin capsule from which trabeculae

extends inward carrying blood vessels, nerves and lymphatic.

Endocrine gland that produces PTH that consist of 84

amino acid.
CALCIUM required for muscular contraction,

glandular secretion, blood coagulation.

Parathyroid Gland (Microscopically)

Chief cells - 6-8

microns, polygonal, central round nuclei, contain granules of parathyroid hormone (PTH) Basic cell type, other cell types are due to differences in physiologic activity 80% of chief cells have intracellular fat Chief cell is most sensitive to changes in ionized calcium

 Oxyphil cells - slightly

larger than chief cell (12 microns), acidophilic cytoplasm due to mitochondria; no secretory granules; first appear at puberty as single cells, then pairs, then nodules at age 40

Functions!
Parathyroid hormones (PTH) Stimulates osteoclastic activity in bones Mobilizes the bone calcium Increase the calcium level in the blood Stimulates the absorption of dietary calcium from the small intestine Stimulates the reabsorption of calcium in the proximal convoluted tubules of the kidney It also strongly diminishes the reabsorption of phosphate of the PCT of the kidney The secretion of PTH is controlled by the calcium levels in the blood

Primary Hyperparathyroidism
Autonomous, spontaneous overproduction of PTH by

parathyroid tissue, with no evidence of prior parathyroid stimulation by renal or intestinal disease Important cause of hypercalcemia (raised calcium levels).
Causes: There is over secretion of PTH due to adenoma, hyperplasia or, rarely, carcinoma of the parathyroid glands.

Symptoms:
Bone disease:Osteoporosis (from osteoclast prominence and

remodeling), with later deformities and fractures.Osteitis fibrosa cystica (aka brown tumors, Recklinghausens disease [not neurofibromatosis]): thin cortex, marrow with increased fibrous tissue, hemorrhage and cysts; often in jaw Stones: renal calcium stones in 20%; also nephrocalcinosis (calcification of renal interstitium and tubules); renal stones cause hypertension, are important cause of death; renal abnormalities may progress after treatment Groans from GI distress: nausea, peptic ulcers (associated with high serum gastrin that decreases after surgical excision), constipation, pancreatitis, gallstones Moans from CNS disturbance: depression, lethargy, seizures Also weakness, fatigue, calcifications of aortic and mitral valves; metastatic calcification in stomach, lungs, myocardium, blood vessels

Osteoporosis

Osteomalacia

Treatment: There are no medications or pills that work to cure or treat parathyroid problems or high calcium.
Surgical excision of enlarged gland plus one additional

gland for diagnostic purposes Use selective venous catheterization to localize abnormal gland preoperatively Also total parathyroidectomy with autotransplantation of parathyroid tissue into forearm muscle, but may get recurrence of hyperparathyroidism, and hyperplastic gland may infiltrate the skeletal muscle and look malignant

Secondary hyperparathyroidism
Hyperparathyroidism due primarily to non-PTH disease

Causes:

renal failure (phosphorus retention causes hypocalcemia), inadequate calcium intake, steatorrhea (failure to absorb Vitamin D), vitamin D deficiency or resistance. All cause hypocalcemia, which causes elevated PTH levels

Note: high serum phosphate levels DIRECTLY depress serum calcium levels
Bone changes usually less severe than primary

hyperparathyroidism Dialysis patients may have discrete, punched-out bone lesions with minimal resorption or osteoblast activity.

Gross: hyperplastic glands, may not be symmetrical

Hypoparathyroidism
decreased function of the parathyroid glands with

under production of parathyroid hormone. Causes: Low blood magnesium levels and Metabolic alkalosis Signs and Symptoms:
experience paresthesia, an unpleasant tingling sensation

around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet

 Treatment: PTH is commercially available for use in the treatment of osteoporosis. Its use for patients with hypoparathyroidism is not approved by the Food and Drug Administration.