Armour Thyroid, Thyrar
Classifications: hormone; thyroid agent;
Therapeutic: thyroid hormone replacement

Prototype: Levothyroxine sodium
Pregnancy Category: A


15 mg (1/4 grain), 30 mg (? grain), 60 mg (1 grain), 90 mg (1? grain), 120 mg (2 grain), 180 mg (3 grain), 240 mg (4 grain), 300 mg (5 grain) tablets


Preparation of desiccated animal thyroid gland containing active thyroid hormones, l-thyroxine (T4) and l-triiodothyronine (T3). Action mechanism unknown; T4 is largely converted to T3, which exerts the principal effects. Influences growth and maturation of various tissues (including skeletal and CNS) at critical periods. Promotes a generalized increase in metabolic rate of body tissues.

Therapeutic Effect

Effectiveness indicated by diuresis, accompanied by loss of weight and puffiness, followed by sense of well-being, increased pulse rate, increased pulse pressure, increased appetite, increased psychomotor activity, loss of constipation, normalization of skin texture and hair, and increased T3 and T4 serum levels.


Replacement or substitution therapy in primary hypothyroidism (cretinism, myxedema, simple goiter, deficiency states in pregnancy and older adults) and secondary hypothyroidism caused by surgery, excess radiation, or antithyroid drug therapy. May be given as adjunct to antithyroid agents when it is desirable to limit release of thyrotropic hormones and to prevent goitrogenesis and hypothyroidism.


Thyrotoxicosis; acute MI not associated with hypothyroidism, cardiovascular disease; morphologic hypogonadism; nephrosis; uncorrected hypoadrenalism.

Cautious Use

Angina pectoris, hypertension, older adults who may have occult cardiac disease; renal insufficiency; concomitant administration of catecholamines; diabetes mellitus; hyperthyroidism (history of); malabsorption states; pregnancy (category A).

Route & Dosage

Mild to Moderate Hypothyroidism
Adult: PO 60 mg/d, may increase q30d to 60–180 mg/d

Severe Hypothyroidism
Adult: PO 15 mg/d, increased q2wk to 60 mg/d, then may increase q30d if needed
Child: PO 15 mg/d, may increase by 15 mg q2wk if needed


  • Give as a single dose, preferably on an empty stomach.
  • Initiate dosage generally at low level and systematically increase in small increments to desired maintenance dose.
  • Store in dark bottle to minimize spontaneous deiodination. Keep desiccated thyroid dry.

Adverse Effects (≥1%)

Endocrine: Hyperthyroidism, thyroid storm [high temperature (as high as 41° C [106° F])], tachycardia, vomiting, shock, coma. Special Senses: Staring expression in eyes. CV: CHF, angina, cardiac arrhythmias, palpitation, tachycardia. Body as a Whole: Weight loss, tremors, headache, nervousness, fever, insomnia, warm and moist skin, heat intolerance, leg cramps, menstrual irregularities, shock, changes in appetite. GI: Diarrhea or abdominal cramps. Metabolic: Hyperglycemia (usually offset by increased tissue oxidation of sugar).

Diagnostic Test Interference

Thyroid increases basal metabolic rate; may increase blood glucose levels, creatine phosphokinase, AST, LDH, PBI. It may decrease serum uric acid, cholesterol, thyroid-stimulating hormone (TSH), iodine 131 uptake. Many medications may produce false results in thyroid function tests.


Drug: oral anticoagulants potentiate hypoprothrombinemia; may increase requirements for insulin, sulfonylureas; epinephrine may precipitate coronary insufficiency; cholestyramine may decrease thyroid absorption.


Absorption: Variably absorbed from GI tract. Peak: 1–3 wk. Distribution: Does not readily cross placenta; minimal amounts in breast milk. Metabolism: Deiodination in thyroid gland. Elimination: In urine and feces. Half-Life: T3, 1–2 d; T4, 6–7 d.

Nursing Implications

Assessment & Drug Effects

  • Observe patient carefully during initial treatment for untoward reactions such as angina, palpitations, cardiac pain.
  • Be alert for symptoms of overdosage (see ADVERSE EFFECTS) that may occur 1–3 wk after therapy is started. If they develop, interrupt treatment for several days and restart with reduced dosage.
  • Monitor response until regimen is stabilized to prevent iatrogenic hyperthyroidism. In drug-induced hyperthyroidism, there may also be increased bone loss. Such a patient is vulnerable to pathologic fractures.
  • Monitor vital signs: Pulse rate is an important clue to drug effectiveness. Assess pulse before each dose during period of dosage adjustment. Consult physician if rate is 100 or more or if there has been a marked change in rate or rhythm.
  • Lab tests: Monitor thyroid function q3mo during dose adjustment period. Monitor prothrombin time closely if patient is receiving concurrent anticoagulant therapy. A decrease in requirement usually develops within 1–4 wk after starting treatment with thyroid.
  • Be aware that toxic effects of thyroid develop slowly and disappear gradually. T4 effects require up to 3–6 wk to dissipate; T3 effects last 6–14 d after drug withdrawal.

Patient & Family Education

  • Adhere to established dosage regimen; do not change dose intervals without approval of the physician.
  • Be aware that replacement therapy for hypothyroidism is life-long; continued follow-up care is important.
  • Do not change brands of thyroid unless physician approves. Hormone content varies among brands.
  • Monitor pulse rate and report increases greater than parameter set by physician.
  • Report onset of chest pain or other signs of aggravated CV disease (dyspnea, tachycardia) to physician promptly.
  • Report evidence of any unexplained bleeding to physician when taking concomitant anticoagulant.
  • Use serial height and weight measurement to monitor growth in juvenile undergoing treatment.

Common adverse effects in italic, life-threatening effects underlined; generic names in bold; classifications in SMALL CAPS; Canadian drug name; Prototype drug

© 2006-2022 Last Updated On: 11/16/2022 (0)
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