Tuesday, September 4, 2012

Hyperparathyroidism Definition, Etiology, Pathophysiology and Clinical Manifestations

Definition of Hyperparathyroidism

Hyperparathyroidism is excessive production of parathyroid hormone by the parathyroid glands, characterized by decalcification of bone and the formation of kidney stones, which contain calcium. Hyperparathyroidism is divided into two, namely primary and secondary hyperparathyroidism. Primary hyperparathyroidism occurs two or three times more often in women than men and in patients aged 60-70 years. While secondary hyperparathyroidism with manifestations similar to patients with chronic renal failure. Renal rickets, caused by retention of phosphorus will increase the stimulation of the parathyroid glands and increased secretion of parathyroid hormone. (Brunner & Suddath, 2001)

Hyperparathyroidism is a character of a disease caused by excess secretion of parathyroid hormone, amino acid polypeptide hormone. Secretion of parathyroid hormone is directly regulated by the concentration of calcium ion fluid. The major effect of parathyroid hormone is increased by increasing the concentration of liquid calcium and phosphate calcium release from bone matrix, increases the absorption of calcium by the kidneys, and the kidneys to increase production. Parathyroid hormone also causes phosphaturia, if dehydrated phosphate. Hyperparathyroidism is usually divided into primary, secondary and tertiary. (Lawrence Kim, MD, 2005, section 2).

Etiology of Hyperparathyroidism

According to Lawrence Kim, MD. 2005, the etiology of hyperparathyroidism are:
  1. Approximately 85% of cases of primary hyperparathyroidism caused by single adenoma.
  2. While the other 15% involves various glands (eg various adenoma or hyperplasia). Usually hereditary and frequency associated with other endocrine disorders.
  3. Few cases of primary hyperparathyroidism caused by parathyroid carcinoma. Etiology of adenoma and hyperplasia in most cases unknown. Family cases can occur either as part of various endocrine neoplasia syndrome, hyperparathyroidism tumor syndrome, or hyperparathyroidism derivatives. Familial hypercalcemia and hypocalcuric and neonatal severe hyperparathyroidism are also included into this category.
  4. Some surgeons and pathologist reported that enlargement of the gland adenoma types are generally multiple doubles. In about 15% of patients with hyper-function of all glands; chief cell parathyroid hyperplasia.
Pathophysiology of Hyperparathyroidism

Hyperparathyroidism can be primary (ie caused by hyperplasia or parathyroid neoplasm) or secondary, where cases are usually associated with chronic renal failure.

In 80% of cases of primary hyperparathyroidism caused by parathyroid adenomas are benign; 18% of cases caused by hyperplasia of the parathyroid glands: and 2% of cases are caused by parathyroid carcinoma (damjanov, 1996). Normally there are four parathyroid glands. Parathyroid adenoma or carcinoma is characterized by enlargement of the gland, with the other glands remained normal. In parathyroid hyperplasia, four enlarged glands. Because the diagnosis of adenoma or hyperplasia can not be enforced preoperative, so it is important for the surgeon to examine the four gland.

If one identified an enlarged adenomatous gland, the gland is usually removed and others left intact. If it is an enlarged lymph fourth surgeon will lift the third and leave one lymph gland that should be sufficient to maintain the homeostasis of calcium-phosphate.

Secondary parathyroid hyperplasia can be distinguished from primary hyperplasia, because the four symmetrically enlarged glands. Enlarged parathyroid glands and hiperfungsi are compensatory mechanisms that are triggered by the retention of the format and hypercalcemia associated with chronic kidney disease. Osteomalacia caused by hipovitaminosis D, as in rickets, can lead to the same effect.

Hyperparathyroidism is characterized by excess PTH in the circulation. PTH mainly working on bone and kidney. In bone, PTH increases calcium resorption from the renal tubules Limen. Thereby reducing the excretion of calcium in urine. PTH also increases the active form of vitamin D3 in the kidneys, which in turn facilitates the uptake of calcium from food in the intestines. Hypercalcemia and hypophosphatemia thus compensatory, is abnormlitas biochemical detected through blood analysis. Serum PTH concentrations also increased. (Rumahorbor, Hotma, 1999)

Excess production of parathyroid hormone is accompanied by kidney failure can cause a wide range of bone disease, which often occurs tulng is osteitis fibrosa cystica, a disease of increased bone resorption due to increased levels of parathyroid hormone. Other bone diseases are also common in these patients, but did not appear in person. (Lawrence Kim, MD, 2005, section 5)

Excess amounts of PTH secretion causes hypercalcemia can cause direct effects on receptors in bone, intestinal tract, and kidneys. Physiologically PTH secretion is inhibited by high serum calcium ions. The mechanism is not active in the state of adenomas, or gland hyperplasia, hypersecretion of PTH which coincides with hypercalcemia. Reabsorption of calcium from bone and increased absorption from the gut is a direct effect of the increase in PTH.

At the time of serum calcium levels approaching 12 mg / dL, renal tubular reabsorption of calcium causing excessive hypercalciuria circumstances. This can increase the incidence nefrolithiasis, which raises can decreased creatinine clearance and renal failure. Elevated levels of extracellular calcium can be deposited on soft tissue. The pain arises due to calcified nodules form on the skin, subcutaneous tissues, tendons (calcific tendonitis), and cartilage (chondrocalcinosis). Vitamin D plays an important role in calcium metabolism by PTH causes needed to work in the target organ.

Clinical Manifestations of Hyperparathyroidism

Patients may not be, or have signs and symptoms due to the disruption of multiple organ systems. Symptoms of apathy, fatigue complaints, muscle weakness, nausea, vomiting, constipation, hypertension, and cardiac arrhythmias may occur: all this is related to elevated levels of calcium in the blood. Psychological manifestations may range from irritability and emotional state of neurosis to psychosis caused by the direct effect of calcium on the brain and nervous system. Increased calcium levels will decrease the potential excitation of nerve and muscle tissue.

Stone formation in one or both kidneys associated with increased excretion of calcium and phosphorus is one of the complications of primary hyperparathyroidism. Kidney damage caused by precipitation of calcium phosphate in the pelvis, and renal parenchyma resulting in kidney stones (renal calculi), obstruction, pyelonephritis and renal failure.

Musculoskeletal symptoms accompanying hyperparathyroidism may occur due to demineralization of bone or bone tumors, which appears in the form of benign giant cells due to excessive osteoclast growth. Patients may experience skeletal pain and tenderness, especially in the back and joints; pain when supporting the body; pathologic fractures; deformity, and shortening of the body. Bone loss associated with hyperparathyroidism is a risk factor for fracture.

The incidence of peptic ulcer and prankreatitis increased in hyperparathyroidism and can cause symptoms gastroitestinal. (Brunner & Suddath, 2001)

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