Thyroid hormone drugs are natural or synthetic preparations containing tetraiodothyronine T 4levothyroxine sodium or triiodothyronine T 3liothyronine sodium or both. T 4 and T 3 are liothyronine and vitamin c in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. T 4 contains four iodine atoms and is formed by the coupling of two molecules of diiodotyrosine DIT.
T 3 contains three atoms of iodine and is formed by the coupling of one molecule of DIT with one molecule of monoiodotyrosine MIT. Both hormones are stored in the thyroid colloid as thyroglobulin. Thyroid hormone preparations belong to two categories: Natural preparations include desiccated thyroid and thyroglobulin.
Desiccated thyroid is derived from domesticated animals that are used for food by man either beef or hog thyroidand thyroglobulin is derived from thyroid glands of the hog. Iodine content is only an indirect indicator of true hormonal biologic activity. Cytomel liothyronine sodium Tablets contain liothyronine L-triiodothyronine or LT 3a synthetic form of a natural thyroid hormone, and is available as the sodium salt.
The structural and empirical formulas and molecular weight of liothyronine sodium are given below. Twenty-five mcg of liothyronine is equivalent to approximately 1 grain of desiccated thyroid or thyroglobulin and 0. Each round, white to off-white Cytomel liothyronine sodium tablet liothyronine and vitamin c liothyronine sodium equivalent to liothyronine as follows: Inactive ingredients consist of calcium sulfate, liothyronine and vitamin c, gelatin, corn starch, stearic acid, sucrose and talc.
The mechanisms by which thyroid hormones exert their physiologic action are not well understood. These hormones enhance oxygen consumption by most tissues of the body, increase the basal metabolic rate and the metabolism of carbohydrates, lipids and proteins.
Thus, they exert a profound influence on every liothyronine and vitamin c system in the body and are of particular importance in the development of the central nervous system.
Liothyronine and vitamin c liothyronine sodium T 3 is not firmly bound to serum protein, liothyronine and vitamin c, it is readily available to body tissues. The onset of activity of liothyronine sodium is rapid, occurring within a few hours. Maximum pharmacologic response occurs within 2 or 3 days, providing early clinical response.
T 3 is almost totally absorbed, 95 percent in 4 hours. The hormones contained in the natural preparations are absorbed in a manner similar to the synthetic liothyronine and vitamin c. Liothyronine sodium has a rapid cutoff of activity which permits quick dosage adjustment and facilitates control of the effects of overdosage, should they occur.
The higher affinity of levothyroxine T 4 for both thyroid-binding globulin and thyroid-binding prealbumin as compared to triiodothyronine T 3 partially explains the higher serum levels and longer liothyronine and vitamin c of the former hormone. Both protein-bound hormones exist in reverse equilibrium with minute amounts of free hormone, the latter accounting for the metabolic activity. As replacement or supplemental therapy in patients with hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis.
This category includes cretinism, myxedema and ordinary hypothyroidism in patients of any age pediatric patients, adults, liothyronine and vitamin c, the elderlyor state including pregnancy ; primary hypothyroidism resulting from functional deficiency, primary atrophy, partial or total absence of thyroid gland, liothyronine and vitamin c, or the effects of surgery, radiation, or drugs, with or without the presence of goiter; and secondary pituitary or tertiary hypothalamic hypothyroidism see Warnings.
As diagnostic agents in suppression tests to differentiate suspected mild hyperthyroidism or thyroid gland autonomy. Cytomel liothyronine sodium Tablets can be used in patients allergic to desiccated thyroid or thyroid extract derived from pork or beef. Thyroid hormone preparations are generally contraindicated in patients with diagnosed but as yet uncorrected adrenal cortical insufficiency, untreated thyrotoxicosis and apparent hypersensitivity to any of their active or extraneous constituents.
There is no well-documented evidence from the literature, however, of true allergic or idiosyncratic reactions to muscle milk and weight loss hormone. Drugs with thyroid hormone activity, alone or together with other therapeutic agents, have been used for the treatment of obesity, liothyronine and vitamin c. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction.
Larger doses may produce serious or even life-threatening manifestations of toxicity, liothyronine and vitamin c, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects.
The use liothyronine and vitamin c thyroid hormones in the therapy ic and augmentin obesity, alone or combined with other drugs, is unjustified and has been shown to be ineffective. Neither is their use justified for the treatment of male or female infertility unless this condition is accompanied by hypothyroidism.
Thyroid hormones should be used with great caution in a number of circumstances where the integrity of the cardiovascular system, liothyronine and vitamin c the coronary arteries, liothyronine and vitamin c, is suspected. These include patients with angina pectoris or the elderly, in whom there is a greater likelihood of occult cardiac disease.
In these patients, liothyronine sodium therapy should be initiated with low doses, with due consideration for its relatively rapid onset liothyronine and vitamin c action. Starting dosage of Cytomel liothyronine sodium Tablets is 5 mcg daily, and should be increased by no more than 5 mcg increments at 2-week intervals. When, in such patients, a euthyroid state can only be reached at the expense of an aggravation of the cardiovascular disease, thyroid hormone dosage should be reduced, liothyronine and vitamin c.
Morphologic hypogonadism and nephrosis should be ruled out before the drug is administered. If hypopituitarism is present, the adrenal deficiency must be corrected prior to starting the drug.
Myxedematous patients are very sensitive to thyroid; dosage should be started at a very low level and increased gradually. Severe and prolonged hypothyroidism can lead to a decreased level of adrenocortical activity commensurate with the lowered metabolic state. When thyroid-replacement therapy is administered, the metabolism increases at a greater rate than adrenocortical activity.
This can precipitate adrenocortical insufficiency. Therefore, in severe and prolonged hypothyroidism, supplemental adrenocortical steroids may be necessary. In rare instances the administration of thyroid hormone may precipitate a hyperthyroid state or may aggravate existing hyperthyroidism. Thyroid hormone therapy in patients with concomitant diabetes mellitus or insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms.
Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required.
Hypothyroidism decreases and hyperthyroidism increases the sensitivity to oral anticoagulants, liothyronine and vitamin c. Prothrombin time should be closely monitored in thyroid-treated patients on oral anticoagulants and dosage of the latter agents adjusted on the basis of frequent prothrombin time determinations. In infants, excessive doses of thyroid hormone preparations may produce craniosynostosis. Patients on thyroid hormone preparations and parents of pediatric patients on thyroid therapy should be informed that:.
Replacement therapy is to be taken essentially for life, with the exception of cases of liothyronine and vitamin c hypothyroidism, liothyronine and vitamin c, usually associated with thyroiditis, and in those patients receiving a therapeutic trial of the liothyronine and vitamin c. They should immediately report during the course of therapy any signs or symptoms of thyroid hormone toxicity, e.
In case of concomitant diabetes mellitus, the daily dosage of antidiabetic medication may need readjustment as thyroid hormone replacement is achieved.
If thyroid medication is stopped, a downward readjustment of the dosage of insulin or oral hypoglycemic agent may be necessary to avoid hypoglycemia. At all times, liothyronine and vitamin c, close monitoring of urinary glucose levels is mandatory in such patients. In case of concomitant oral anticoagulant therapy, the prothrombin time should be measured frequently to determine if the dosage of oral anticoagulants is to be readjusted, liothyronine and vitamin c.
Partial loss of hair may be experienced by pediatric patients in the first few months of thyroid therapy, but this is usually a transient phenomenon and later recovery is usually the rule.
Treatment of patients with thyroid hormones requires the periodic assessment of thyroid status by means of appropriate laboratory tests besides the full clinical evaluation. The TSH suppression test can be used to test the effectiveness of any thyroid preparation, bearing in mind the relative insensitivity of the infant pituitary to the negative feedback effect of thyroid hormones.
Serum T 4 levels can be used to test the effectiveness of all thyroid medications except products containing liothyronine sodium. When the total serum T 4 is low but TSH is normal, a test specific to assess unbound free T 4 levels is warranted.
Specific measurements of T 4 and T 3 by competitive protein binding or radioimmunoassay are not influenced by blood levels of organic or inorganic iodine and have essentially replaced older tests of thyroid hormone measurements, i. Thyroid hormones appear to increase catabolism of vitamin K-dependent clotting factors. If oral anticoagulants are also being given, compensatory increases in clotting factor synthesis are impaired.
Patients stabilized on oral anticoagulants who are found to require thyroid replacement therapy should be watched very closely when thyroid is started. If a patient is truly hypothyroid, it is likely that a reduction in anticoagulant dosage will be required. No special precautions appear to be necessary when oral anticoagulant therapy is begun in a patient already stabilized on maintenance thyroid replacement therapy.
Initiating thyroid replacement therapy may cause increases in insulin or oral hypoglycemic requirements. The effects seen are poorly understood and depend upon a variety of factors such as dose and type of thyroid preparations and endocrine status of the patient. Patients receiving insulin or oral hypoglycemics should be closely watched during initiation of thyroid replacement therapy. Cholestyramine binds both T 4 and T 3 in the intestine, thus impairing absorption of these thyroid hormones.
In vitro studies indicate that the binding is not easily removed. Liothyronine and vitamin c, 4 to 5 hours should elapse between administration of cholestyramine and thyroid hormones. Estrogens tend to increase serum thyroxine-binding globulin TBg. In a patient with a nonfunctioning thyroid gland who is receiving thyroid replacement therapy, free levothyroxine may be decreased when estrogens are started thus increasing thyroid requirements. Therefore, patients without liothyronine and vitamin c functioning thyroid gland who are on thyroid replacement therapy may need to increase their thyroid dose if estrogens or estrogen-containing oral contraceptives are given.
Use of thyroid products with imipramine and other tricyclic antidepressants may increase receptor sensitivity and enhance antidepressant activity; transient cardiac arrhythmias have been observed, liothyronine and vitamin c. Thyroid hormone activity may also be enhanced. Thyroid preparations may potentiate the toxic effects of digitalis.
Thyroid hormonal replacement increases metabolic rate, which requires an increase in digitalis dosage. When administered to patients on a thyroid preparation, this parenteral anesthetic may cause hypertension and tachycardia. Use with caution and be prepared to treat hypertension, if necessary. Thyroxine increases the adrenergic effect of catecholamines such as epinephrine and norepinephrine.
Therefore, injection of these agents into patients receiving thyroid preparations increases the risk of precipitating coronary insufficiency, especially in patients with coronary artery disease. Careful observation is required. The following drugs or moieties are known to interfere with laboratory tests performed in patients on thyroid hormone therapy: Changes in TBg concentration should be taken into consideration in the interpretation of Liothyronine and vitamin c 4 and T 3 values.
In such cases, the unbound free hormone shouldbemeasured. Pregnancy, estrogens liothyronine and vitamin c estrogen-containing oral contraceptives increase TBg concentrations. TBg may also be increased during infectious hepatitis.
Decreases in TBg concentrations are observed in nephrosis, acromegaly and after androgen or corticosteroid therapy. Familial hyper- or hypo-thyroxine-binding-globulinemias have been described. The incidence of TBg deficiency approximates 1 in Perioral dermititis and milk allergy binding of thyroxine by thyroxine-binding prealbumin TBPA is inhibited by salicylates.