Hypothyroidism Diagnosis, Etiopathogenesis and Treatment

3,435 views 22 slides Apr 06, 2020
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About This Presentation

Hypothyroidism is a condition in which the thyroid gland doesn't produce enough thyroid hormone.
Hypothyroidism's deficiency of thyroid hormones can disrupt such things as heart rate, body temperature and all aspects of metabolism. Hypothyroidism is most prevalent in older women.
Major sympt...


Slide Content

HYPOTHYROIDISM Dr. Chavan P. R

DEFINITION A condition in which the thyroid gland doesn't produce enough thyroid hormone. Also called as underactive thyroid

PATHOPHYSIOLOGY The vast majority of hypothyroid patients have thyroid gland failure (primary hypothyroidism). The causes include chronic autoimmune thyroiditis (Hashimoto’s disease), iatrogenic hypothyroidism, iodine deficiency, enzyme defects, thyroid hypoplasia , and goitrogens . Pituitary failure (secondary hypothyroidism) is an uncommon cause resulting from pituitary tumors, surgical therapy, external pituitary radiation, postpartum pituitary necrosis, metastatic tumors, tuberculosis, histiocytosis , and autoimmune mechanisms.

CLINICAL PRESENTATION s

DIAGNOSIS A rise in the TSH level is the first evidence of primary hypothyroidism. Many patients have a free T4 level within the normal range (compensated hypothyroidism) and few, if any, symptoms of hypothyroidism. As the disease progresses, the free T4 concentration drops below the normal level. The T3 concentration is often maintained in the normal range despite a low T4.

Antithyroid peroxidase antibodies and antithyroglobulin antibodies are likely to be elevated. The RAIU is not a useful test in the evaluation of hypothyroidism because it can be low, normal, or even elevated. Pituitary failure (secondary hypothyroidism) should be suspected in a patient with decreased levels of T4 and inappropriately normal or low TSH levels.

DESIRED OUTCOMES To normalize thyroid hormone concentrations in tissue Provide symptomatic relief, Prevent neurologic deficits in newborns and children, and Reverse the biochemical abnormalities of hypothyroidism.

NONPHARMACOLOGIC TREATMENT

TREATMENT CHART

PHARMACOLOGIC TREATMENT Levothyroxine (L- thyroxine , T4) is the drug of choice for thyroid hormone replacement and suppressive therapy because it is chemically stable, relatively inexpensive, free of antigenicity , and has uniform Because T3 (and not T4) is the biologically active form, levothyroxine administration results in a pool of thyroid hormone that is readily and consistently converted to T3.

Young patients with long-standing disease and patients older than 45 years without known cardiac disease should be started on 50 mcg daily of levothyroxine and increased to 100 mcg daily after 1 month. The recommended initial daily dose for older patients or those with known cardiac disease is 25 mcg/day titrated upward in increments of 25 mcg at monthly intervals to prevent stress on the cardiovascular system

The average maintenance dose for most adults is about 125 mcg/day, but there is a wide range of replacement doses, necessitating individualized therapy and appropriate monitoring to determine an appropriate dose. Patients with subclinical hypothyroidism and marked elevations in TSH (greater than 10 milli -international units per liter [ mIU /L]) and high titers of TSAb or prior treatment with sodium iodide 131 may benefit from treatment with levothyroxine .

Levothyroxine is the drug of choice for pregnant women, and the objective of the treatment is to decrease TSH to 1 mIU /L and to maintain free T4 concentrations in the normal range. Cholestyramine , calcium carbonate, sucralfate , aluminum hydroxide, ferrous sulfate, soybean formula, and dietary fiber supplements may impair the absorption of levothyroxine from the GI tract. Drugs that increase nondeiodinative T4 clearance include rifampin , carbamazepine , and possibly phenytoin. Amiodarone may block the conversion of T4 to T3.

Thyroid , USP (or desiccated thyroid) is derived from hog, beef, or sheep thyroid gland. It may be antigenic in allergic or sensitive patients. Inexpensive generic brands may not be bioequivalent. Thyroglobulin is a purified hog-gland extract that is standardized biologically to give a T4:T3 ratio of 2.5:1. It has no clinical advantages and is not widely used.

Liothyronine (synthetic T3) has uniform potency but has a higher incidence of cardiac adverse effects, higher cost, and difficulty in monitoring with conventional laboratory tests. Liotrix (synthetic T4:T3 in a 4:1 ratio) is chemically stable, pure, and has a predictable potency but is expensive. It lacks therapeutic rationale because about 35% of T4 is converted to T3 peripherally.

Excessive doses of thyroid hormone may lead to heart failure, angina pectoris, and myocardial infarction. Allergic or idiosyncratic reactions can occur with the natural animal-derived products such as desiccated thyroid and thyroglobulin , but they are extremely rare with the synthetic products used today. Excess exogenous thyroid hormone may reduce bone density and increase the risk of fracture.

EVALUATION OF THERAPEUTIC OUTCOMES Serum TSH concentration is the most sensitive and specific monitoring parameter for adjustment of levothyroxine dose. Concentrations begin to fall within hours and are usually normalized within 2 to 6 weeks. TSH and T4 concentrations should both be checked every 6 weeks until a euthyroid state is achieved. An elevated TSH level indicates insufficient replacement. Serum T4 concentrations can be useful in detecting noncompliance, malabsorption , or changes in levothyroxine product bioequivalence. TSH may also be used to help identify noncompliance. In patients with hypothyroidism caused by hypothalamic or pituitary failure, alleviation of the clinical syndrome and restoration of serum T4 to the normal range are the only criteria available for estimating the appropriate replacement dose of levothyroxine .

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