Hypoparathyroidism Definition, Etiology, Clinical Manifestations and Pathophysiology

Definition of Hypoparathyroidism

Hypoparathyroidism is a combination of symptoms of parathyroid hormone production is inadequate. This situation rarely found and are generally often caused by damage to or removal of the parathyroid glands during parathyroid or thyroid surgery, and rarer still is the absence of the parathyroid glands (in congenital). Sometimes a specific cause is not known.

Etiology of Hypoparathyroidism

Rare primary hypoparathyroidism, and if there is usually found in children under the age of 16 years. There are three categories of hypoparathyroidism:

1. Deficiency of parathyroid hormone secretion, there are two main causes:
   • Post surgical removal of the gland partiroid and total thyroidectomy.
   • Idiopathic, the disease is rare and can be congenital or acquired.
2. Hipomagnesemia
3. Secretion of parathyroid hormone is not activated.
4. Resistance to parathyroid hormone (pseudohypoparathyroidism).

Clinical Manifestations of Hypoparathyroidism

Hypocalcaemia causes irritability neuromuskeler system and helped cause the main symptoms of hypoparathyroidism in the form of tetanus.

Tetanus is a comprehensive muscle hipertonia with tremors and spasmodic or uncoordinated contractions that occur with or without an attempt to commit voluntary movement. In a state of latent tetanus symptoms are tingling and cramps in the extremities with complaints of feeling stiffness in both hands and feet. In a real situation tetanus, signs include bronchospasm, laryngeal spasm, carpopedal spasm (flexion of the elbow and wrist joints and extension sensi carpophalangeal), dysphagia, photophobia, cardiac arrhythmias and seizures. Other symptoms include anxiety, irritability, depression and even delirium. Changes in the ECG and hypotension may occur. (Brunner & Suddath, 2001)

Pathophysiology of Hypoparathyroidism

In hypoparathyroidism are disorders of the metabolism of calcium and phosphate, which decreased serum calcium (up to 5 mgr%) and elevated serum phosphate (up 9.5 to 12.5 mgr%).
In the post-surgery due to inadequate production of parathyroid hormone due to removal of the parathyroid glands during surgery. The first operation was to deal with the situation by lifting hyperparathyroidism the parathyroid glands. The aim is to overcome the excessive secretion of parathyroid hormone, but usually too much tissue is removed.

Second operation associated with the operation of total thyroidectomy. This is because the location of the thyroid and parathyroid gland anatomy nearby (get blood from a vein of the same) so that the parathyroid glands can be affected by incision or lifted. It is very rare and is usually less than 1% in thyroid surgery. In many patients an inadequate production of parathyroid hormone secretion transient postoperative thyroid or parathyroid glands, so the diagnosis can not be made immediately after the operation.

In Pseudohypoparathyroidism symptoms and signs of hypoparathyroidism but normal levels of PTH in the blood or increased. Since the network does not respond to the hormone, the disease is a disease of the receptor. There are two forms:

• in the form of more frequent, occurring congenital reduction in Gs activity by 50%, and PTH normally can not increase the concentration of cyclic AMP,
• the form of the rarer, but the normal cyclic AMP response fosfaturik disturbed hormone effects.

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Pathophysiology of Acute Gastritis and Chronic Gastritis

Pathophysiology of Acute Gastritis

Acute gastritis can be caused by stress, chemical substances such as drugs and alcohol, spicy foods, hot and sour. In experiencing the stress will occur sympathetic nerve stimulation NV (vagus nerve), which will increase the production of hydrochloric acid (HCl) in the stomach. The presence of HCl that is in the stomach will cause nausea, vomiting and anorexia.

Chemicals or stimulating foods will cause columnar epithelial cells, whose function is to produce mucus, reducing production. While it is the function of mucus to protect gastric mucosa that did not participate undigested. The response of the gastric mucosa due to decreased vasodilation, mucous secretion varies among gastric mucosal cells. There gastric mucosal lining cells produce HCl (especially the fundus) and blood vessels. Vasodilatation gastric mucosa will cause increased production of HCl. Anorexia can also cause pain. The pain inflicted by HCl contact with the gastric mucosa. Response due to decreased gastric mucosal mucus secretion may be eksfeliasi (exfoliation). Gastric mucosal cell exfoliation will lead to erosion of the mucosal cells. Mucosal cell loss due to erosion lead to bleeding. Bleeding happens to people with life-threatening, but it can also stop yourself because the process of regeneration, so that erosion disappear within 24-48 hours after hemorrhage.

Pathophysiology of Chronic Gastritis

Helicobacter pylori is a gram-negative bacteria. These organisms invade the gastric surface cells, aggravate the onset of cell desquamation and chronic inflammatory responses appeared on gastric ie: destruction of the gland and metaplasia. Metaplasia is one of the body's defense mechanism against irritation, namely by replacing the gastric mucosal cells, such as cells desquamosa stronger. Because cell desquamation stronger then the elasticity is also reduced. At the time of digesting food, the stomach peristaltic movement but as a replacement cells will give rise to inelastic stiffness, which in turn cause pain. Metaplasia also cause loss of mucous cells in the lining of the stomach, so it will cause damage to the mucosal lining of the blood vessels. Damage to blood vessels will cause bleeding (Price, Sylvia and Wilson, Lorraine, 1999: 162).

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