Page 713 - Basic _ Clinical Pharmacology ( PDFDrive )

CHAPTER 38 Thyroid & Antithyroid Drugs 699

D. Adjuncts to Antithyroid Therapy or esmolol, 50–100 mg/kg per min, is helpful to control the severe
During the acute phase of thyrotoxicosis, β-adrenoceptor–blocking cardiovascular manifestations. If β blockers are contraindicated by
agents without intrinsic sympathomimetic activity are appropriate the presence of severe heart failure or asthma, hypertension and
in symptomatic patients aged 60 years or more, in those with heart tachycardia may be controlled with diltiazem, 90–120 mg orally
rates greater than 90 beats/min, and in those with cardiovascular three or four times daily or 5–10 mg/h by intravenous infusion
disease. Propranolol, 20–40 mg orally every 6 hours, or metopro- (asthmatic patients only). Release of thyroid hormones from the
lol, 25–50 mg orally every 6–8 hours, will control tachycardia, gland is retarded by the administration of saturated solution of
hypertension, and atrial fibrillation. Beta-adrenoceptor–blocking potassium iodide, 5 drops orally every 6 hours starting 1 hour
agents are gradually withdrawn as serum thyroxine levels return after giving thioamides. Hormone synthesis is blocked by the
to normal. Diltiazem, 90–120 mg three or four times daily, can administration of propylthiouracil, 500–1000 mg as a loading
be used to control tachycardia in patients in whom β blockers are dose, followed by 250 mg orally every 4 hours. If the patient is
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contraindicated, eg, those with asthma. Dihydropyridine calcium unable to take propylthiouracil by mouth, a rectal formulation
channel blockers may not be as effective as diltiazem or vera- can be prepared and administered in a dosage of 400 mg every
pamil. Adequate nutrition and vitamin supplements are essential. 6 hours as a retention enema. Methimazole may also be pre-
Barbiturates accelerate T breakdown (by hepatic enzyme induc- pared for rectal administration in a dose of 60–80 mg daily.
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tion) and may be helpful both as sedatives and to lower T levels. Hydrocortisone, 50 mg intravenously every 6 hours, will pro-
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Bile acid sequestrants (eg, cholestyramine) can also rapidly lower tect the patient against shock and will block the conversion of
T levels by increasing the fecal excretion of T . T to T , rapidly reducing the level of thyroactive material in
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the blood.
Supportive therapy is essential to control fever, heart failure,
TOXIC UNINODULAR GOITER & TOXIC and any underlying disease process that may have precipitated the
MULTINODULAR GOITER acute storm. In rare situations, where the above methods are not
adequate to control the problem, oral bile acid sequestrants (eg,
These forms of hyperthyroidism occur often in older women cholestyramine), plasmapheresis, or peritoneal dialysis has been
with nodular goiters. Free thyroxine is moderately elevated or used to lower the levels of circulating thyroxine.
occasionally normal, but FT or T is strikingly elevated. Single
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toxic adenomas can be managed with either surgical excision of Ophthalmopathy
the adenoma or with radioiodine therapy. Toxic multinodular
goiter is usually associated with a large goiter and is best treated Although severe ophthalmopathy is rare, it is difficult to treat. A
by preparation with methimazole (preferable) or propylthiouracil 15–20% risk of aggravating severe eye disease may occur follow-
followed by subtotal thyroidectomy. ing RAI, especially in those who smoke. Management requires
effective treatment of the thyroid disease, usually by total surgical
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excision or I ablation of the gland plus oral prednisone therapy
SUBACUTE THYROIDITIS (see below). In addition, local therapy may be necessary, eg,
elevation of the head to diminish periorbital edema and artificial
During the acute phase of a viral infection of the thyroid tears to relieve corneal drying due to exophthalmos. Smoking
gland, there is destruction of thyroid parenchyma with transient cessation should be advised to prevent progression of the ophthal-
release of stored thyroid hormones. A similar state may occur in mopathy. For the severe, acute inflammatory reaction, prednisone,
patients with Hashimoto’s thyroiditis. These episodes of transient 60–100 mg orally daily for about a week and then 60–100 mg
thyrotoxicosis have been termed spontaneously resolving hyperthy- every other day, tapering the dose over 6–12 weeks, may be effec-
roidism. Supportive therapy is usually all that is necessary, such tive. If steroid therapy fails or is contraindicated, irradiation
as β-adrenoceptor–blocking agents without intrinsic sympatho- of the posterior orbit, using well-collimated high-energy X-ray
mimetic activity (eg, propranolol) for tachycardia and aspirin or therapy, will frequently result in marked improvement of the
nonsteroidal anti-inflammatory drugs to control local pain and acute process. Threatened loss of vision is an indication for sur-
fever. Corticosteroids may be necessary in severe cases to control gical decompression of the orbit. Eyelid or eye muscle surgery
the inflammation. may be necessary to correct residual problems after the acute
process has subsided.
SPECIAL PROBLEMS
Dermopathy
Thyroid Storm Dermopathy or pretibial myxedema will often respond to topical

Thyroid storm, or thyrotoxic crisis, is sudden acute exacerba- corticosteroids applied to the involved area and covered with an
tion of all of the symptoms of thyrotoxicosis, presenting as a occlusive dressing.
life-threatening syndrome. Vigorous management is mandatory.
Propranolol, 60–80 mg orally every 4 hours, or intravenous pro- * To prepare a water suspension propylthiouracil enema, grind eight
pranolol, 1–2 mg slowly every 5–10 minutes to a total of 10 mg, 50-mg tablets and suspend the powder in 90 mL of sterile water.