The Brain and Spine Institute is made up of experts in the field of neuroscience in order to bring patients the best healthcare in East Tennessee for a full range of neurological diseases and disorders.
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The Brain and Spine Institute is made up of experts in the field of neuroscience in order to bring patients the best healthcare in East Tennessee for a full range of neurological diseases and disorders.
We provide a comprehensive continuum of cancer services, including prevention, outreach, diagnostic, treatment and support services delivered by our highly skilled staff with compassion and care.
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The Heart Lung Vascular Institute brings together expertise in clinical care, teaching and research. Patients receive exceptional healthcare combined with patient-centered care.

Hypoparathyroidism is is an endocrine disorder in which the parathyroid glands in the neck do not produce enough parathyroid hormone (PTH).
See also: Hyperparathyroidism
The parathyroid glands help control calcium use and removal by the body. They do this by producing parathyroid hormone, or PTH. PTH helps control calcium, phosphorus, and vitamin D levels within the blood and bone.
Hypoparathyroidism occurs when the glands produce too little PTH. Blood calcium levels fall, and phosphorus levels rise.
The most common cause of hypoparathyroidism is injury to the parathyroid glands during head and neck surgery. Rarely, hypoparathyroidism is a side effect of radioactive iodine treatment for hyperthyroidism.
Hypoparathyroidism may also be caused by
DiGeorge syndrome is a childhood disease in which hypoparathyroidism occurs because all the parathyroid glands are missing at birth. Familial hypoparathyroidism occurs with other endocrine diseases, such as adrenal insufficiency, in a syndrome called type I polyglandular autoimmune syndrome (PGA I).
The risk factors for hypoparathyroidism include recent thyroid or neck surgery, a family history of parathyroid disorder, or certain autoimmune diseases such as Addison's disease.
Additional symptoms may include:
Blood tests will be done to check calcium, phosphorus, magnesium, and PTH levels. An ECG may show abnormal heart rhythms.
A urine test may be done to determine how much calcium is being removed from the body.
The goal of treatment is to restore the calcium and mineral balance in the body.
Treatment involves calcium carbonate and vitamin D supplements, which usually must be taken for life. Blood levels are measured regularly to make sure that the dose is correct. A high-calcium, low-phosphorous diet is recommended.
Persons who have life-threatening attacks of low calcium levels or prolonged muscle contractions are given calcium through a vein (IV). Precautions are taken to prevent seizures or larynx spasms. The heart is monitored for abnormal rhythms until the person is stable. When the life-threatening attack has been controlled, treatment continues with medicine taken by mouth.
The outcome is likely to be good if the diagnosis is made early. However, changes in the teeth, the development of cataracts, and brain calcifications are irreversible.
Hypoparathyroidism in children may lead to stunted growth, malformed teeth, and slow mental development.
Overtreatment with vitamin D and calcium can cause hypercalcemia (high blood calcium) and may sometimes interfere with kidney function.
Hypoparathyroidism increases your risk of pernicious anemia, Addison's disease, cataracts, and Parkinson's disease.
Call your health care provider if you develop any symptoms of hypoparathyroidism.
Seizures or breathing problems are an emergency. Call 911 or your local emergency number immediately.
Wysolmerski JJ. Insogna KL. The Parathyroid Glands, Hypercalcemia, and Hypocalcemia. In: Kronenberg HM, Schlomo M, Polansky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. St. Louis, Mo: WB Saunders; 2008: chap. 266.
Bringhurst FR, Demay MB, Kronenberg HM. Disorders of Mineral Metabolism. In: Kronenberg HM, Schlomo M, Polansky KS, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. St. Louis, Mo: WB Saunders; 2008: chap. 27.
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