DISEASES OF THE PARATHYROID

GLAND

By: HERMAN NDJAMENGROUP: 305

STRUCTURE OF GLAND

FUNCTION & REGULATION OF GLAND

DISEASE CLASSIFICATION

EXPLANATION

CONCLUSION

STRUCTURE

STRUCTURE CONTINUES This gland contains 3 groups of cells:

The chief cells which are the main cells with endocrine functioncontaining lots of secretary granules. The Oxyphil and transitional oxyphil cells are the larger cells that contain lots of mitochondria and glycogen lakes.

FUNCTION

• DIRECT REGULATION OF BLOOD CALCIUM ION LEVEL

• PARTICIPATES INDIRECTLY IN REGULATION OF PHOSPHATE

REGULATION

DISEASE CLASSIFICATION

HYPERPARATHYROIDISM

HYPOPARATHYROIDISM

PSEUDOHYPOPARATHYROIDISM

HYPERPARATHYROIDISM• It is classified into: - PRIMARY HYPERPARATHYROIDISM: an autonomous, spontaneous overproduction of PTH. Example: Tumor - SECONDARY HYPERPARATHYROIDISM: any condition that gives rise to chronic hypocalcemia, which in turn leads to compensatory overactivity of the parathyroid glands. Example Chronic Renal insufficiencyNB: Hypercalcemia occuring in these cases is unable to downregulate production of PTH.

RESULT• Two major sites of complication of primary

hyperparathyroidism are Kidneys and bones.

• The kidneys may have renal stones (nephrolithiasis) or diffuse deposition of calcium-phosphate complexes in the parenchyma (nephrocalcinosis).

• In skeleton a condition called “osteitis fibrosa cystica” could occur characterized by subperiosteal resorption of the distal phalanges, distal tappering of the clavicles, a “salt and pepper” appearance of the skull as well as bone cysts and brown tumors of the long bones.

Other clinical manifestations

• cardiac arrhythmias, tremors (Ca++ necessary for normal muscle contraction

• Anorexia, vomiting, constipation• Weakness• Polyuria, polydipsia, hypercalcuria• peptic ulcer disease, acute pancreatitis,

hypertension, gout and pseudo gout, and anaemia

HYPOPARATHYROIDISM• Deficient secretion of PTH CAUSES- Surgically induced hypoparathyroidism- Autoimmune hypoparathyroidism: associated with

autoimmune polyendocrine syndrome type 1.- Autosomal-dominant hypoparathyroidism is caused

by gain-of-function mutations in the calcium-sensing receptor (CASR) gene.

- Familial isolated hypoparathyroidism (FIH)- Congenital absence of parathyroid glands• Functional hypoparathyroidism: due to low level

of magnesium which is required for PTH release from the glands

Clinical manifestations

• The hallmark of hypocalcemia is tetany, which is characterized by neuromuscular irritability. Symptoms range from circumoral numbness or paresthesias (tingling) of the distal extremities and carpopedal spasm, to life-threatening laryngospasm and generalized seizures.

• Mental status changes include emotional instability, anxiety and depression, confusional states, hallucinations, and frank psychosis.

• Intracranial manifestations include calcifications of the basal ganglia, parkinsonian-like movement disorders, and increased intracranial pressure with resultant papilledema.

The major clinical manifestations of hypoparathyroidism are related to the severity and chronicity of the hypocalcemia.

• Ocular disease takes the form of calcification of the lens and cataract formation.

• Cardiovascular manifestations include a conduction defect that produces a characteristic prolongation of the QT interval in the electrocardiogram.

• Dental abnormalities occur when hypocalcemia is present during early development. These findings include: dental hypoplasia, failure of eruption, defective enamel and root formation, and abraded carious teeth.

PSEUDOHYPOPARATHYROIDISM

• Hypoparathyroidism occuring as a result of end-organ resistance to the actions of PTH.

• PTH like TSH, FSH & LH signal via G-protein–triggered second messengers, and the disorder results from genetic defects in this pathway.

• Thus level of PTH may be normal but all the symptoms of hypocalcemia are present.