This is a disorder characterized by weight gain, cold intolerance, coarse skin, a dull facial expression, prolongation of the relaxation phase of deep tendon reflexes, weakness, fatigue, diastolic hypertension, bradycardia, constipation, menorrhagia and mental impairment secondary to a deficiency of thyroid hormone. Primary hypothyroidism is more commonly seen and is the result of a hypofunctioning thyroid gland, which is in contrast to secondary hypothyroidism (rare) which occurs when the hypothalamic-pituitary axis fails resulting in a deficiency of thyroid stimulating hormone (TSH) secretion from the pituitary. Secondary hypothyroidism may be the result of pituitary failure causing decreased TSH production/secretion, or it may result from failure of the hypothalamus to secrete thyrotropin releasing hormone (TRH). A deficit of TRH results in decreased stimulation of the pituitary to secrete TSH. Secondary hypothyroidism should be suspected when symptoms include amenorrhea rather than menorrhagia, and when hypotension and hypoglycemia are present secondary to adrenal and growth hormone deficiencies, respectively.

The diagnosis of hypothyroidism is confirmed by characteristic abnormalities on thyroid function tests. Primary hypothyroidism is diagnosed when the TSH is elevated in the presence of low T4 level. Secondary hypothyroidism is characterized by decreased levels of TSH and T4. Subclinical hypothyroidism should be diagnosed when there is a persistent minimal elevation of the TSH in the presence of a normal T4 level. Primary hypothyroidism is often associated with hypercholesterolemia whereas the serum cholesterol is usually low in secondary hypothyroidism. The hyperlipidemia associated with hypothyroidism corrects with adequate thyroid hormone replacement therapy. Therefore, therapy for hyperlipidemia should not be instituted until the patient has been euthyroid for an adequate time and only if repeat lipid testing shows a persistent elevation. Other associated lab abnormalities include elevations of AST and CPK which are released from muscle, anemia and hyponatremia which is secondary to an increased ADH release and a decreased GFR.

Treatment of hypothyroidism entails daily replacement therapy with oral exogenous thyroid hormone. Treatment should be titrated to normalize the TSH; however, it is important to remember that it takse six weeks for the TSH to change in response to a dosage adjustment. In patients with known or suspected coronary artery disease, thyroid replacement should be initiated at a lower starting dose (12. 5-50 micrograms/day) and the patients should be cautioned about the symptoms of coronary ischemia and where to present if these symptoms manifest. Dosage adjustments in patients with ischemic heart disease should be made in minor increments and occur no more than once every six weeks. Patients with subclinical hypothyroidism may be considered as candidates for thyroid replacement therapy when they meet any of the following criteria: (1) the serum TSH level is greater than 14 mU/L, (2) the serum TSH is 10 mU/L or more in the presence of a positive antimicrosomal antibody test, (3) the antimicrosomal antibody titer is greater than 1:1,600, regardless of the TSH level, or (4) there is the presence of a goiter or symptoms attributable to hypothyroidism.

Myxedema coma is diagnosed in patients with a history or signs of hypothyroidism, hypothermia, mental confusion and bradycardia. This represents a severe and prolonged deficiency of thyroid hormone and is a life threatening emergency. This must be differentiated from Addisonian crisis, and patients should receive treatment for Addisonian crisis before therapy for myxedema is begun if the two disorders coexist. Treatment of myxedema coma entails thyroxine 500 mcg intravenously initially and then 100 mcg per day intravenously. Patients should be monitored for hyponatremia and hypoglycemia and bacterial infections should be aggressively sought after. External warming should be avoided as it may potentiate cardiovascular collapse.