Hyperthyroidism propranolol

Propranolol Inhibition of adrenoreceptors inhibit T4 to T3 conversion (only propranolol) Hyperthyroidism, especially thyroid storm adjunct to control tachycardia, hypertension, and atrial fibrillation Onset within hours duration of 4-6 h (oral propranolol) Toxicity Asthma, AV blockade, hypotension, bradycardia... 

Non-selective P-adrenergic receptor antagonists (e.g. propranolol) can suppress tachycardia and tremor in patients with hyperthyroidism or tremor caused by... 

The patient with hyperthyroidism is likely to have cardiac symptoms such as tachycardia or palpitations. Propranolol, a adrenergic blocking drug (see Chap. 21), may be prescribed by tlie primary health care provider as adjunctive treatment for several weeks until tlie therapeutic effects of tlie antithyroid drug are obtained. 

The answer is d. (Hardman, p 1401.) In patients who are suspected of having hyperthyroidism, propranolol can be administered to provide temporary relief of the peripheral manifestations of the disease while the patient is further evaluated. Propranolol suppresses adrenergic symptoms such as tremors and tachycardia it has no effect on the release of thyroid hormones from the gland. 

Patients with hyperthyroidism tend to have enhanced metabolism leading to weight loss, tremor and palpitations. Propranolol may be indicated to reduce the sympathetic symptoms, such as tremor and palpitations. 

As the symptoms of hyperthyroidism mimic in many aspects those of sympathic stimulation propranolol, and probably also other non-selective beta blockers (see Chapter 20), give rapid relieve in thyrotoxicosis while having no effect on the underlying disease. 

Hyperthyroidism Propranolol blocks the peripheral conversion of thyroxine to triiodothyronine. It controls palpitation, nervousness, tremor sweating etc. 

Excessive catecholamine action is an important aspect of the pathophysiology of hyperthyroidism, especially in relation to the heart (see Chapter 38). The 13 antagonists are beneficial in this condition. The effects presumably relate to blockade of adrenoceptors and perhaps in part to the inhibition of peripheral conversion of thyroxine to triiodothyronine. The latter action may vary from one 13 antagonist to another. Propranolol has been used extensively in patients with thyroid storm (severe hyperthyroidism) it is used cautiously in patients with this condition to control supraventricular tachycardias that often precipitate heart failure. 

Propranolol Block 3i and 32 receptors Lower HR and BP reduce renin Hypertension angina pectoris arrhythmias migraine hyperthyroidism Oral, parenteral Toxicity Bradycardia worsened asthma fatigue vivid dreams cold hands... 

Beta blockers without intrinsic sympathomimetic activity (eg, metoprolol, propranolol, atenolol) are effective therapeutic adjuncts in the management of thyrotoxicosis since many of these symptoms mimic those associated with sympathetic stimulation. Propranolol has been the 3 blocker most widely studied and used in the therapy of thyrotoxicosis. Beta blockers cause clinical improvement of hyperthyroid symptoms but do not typically alter thyroid hormone levels. Propranolol at doses greater than 160 mg/d may also reduce T3 levels approximately 20% by inhibiting the peripheral conversion of T4 to T3. 

Propranolol inhibits the conversion of thyroxine (T4) to tri-iodothyronine (T3) by peripheral tissues (180), resulting in increased formation of inactive reverse T3. There have been several reports of hyperthyroxinemia in clinically euthyroid patients taking propranolol for non-thyroid reasons in high dosages (320-480 mg/day) (181,182). The incidence was considered to be higher than could be accounted for by the development of spontaneous hyperthyroidism, but the mechanism is unknown. 

Harrower AD, Fyffe JA, Horn DB, Strong JA. Thyroxine and triiodothyronine levels in hyperthyroid patients during treatment with propranolol. Clin Endocrinol (Oxf) 1977 7(l) 41-4. 

During the acute phase of a viral infection of the thyroid gland, there is destruction of thyroid parenchyma with transient release of stored thyroid hormones. A similar state may occur in patients with Hashimoto s thyroiditis. These episodes of transient thyrotoxicosis have been termed "spontaneously resolving hyperthyroidism." Supportive therapy is usually all that is necessary, such as propranolol for tachycardia and aspirin or nonsteroidal anti-inflammatory drugs to control local pain and fever. Corticosteroids may be necessary in severe cases to control the inflammation. 

Propranolol 3-Blockers are effective in blunting the widespread sympathetic stimulation that occurs in hyperthyroidism (see p. 75). 

Endocrine uses Hyperthyroidism P-blockade reduces unpleasant symptoms of sympathetic overactivity there may also be an effect on metabolism of thyroxine (peripheral deiodination from T to Tj. A nonselective agent (propranolol) is preferred to counteract both the cardiac (Pj and p ) effects, and tremor (p ). 

A decrease in concentration of proteins and an increase in concentration of free fatty acids in plasma are observed in hyperthyroidism. For propranolol and warfarin, an increase of up to 20-30 % in the unbound plasma fractions has been reported. ... 

The effect of beta-adrenoceptor antagonists on thyroid hormone metabolism is unlikely to play a significant role in their use in hyperthyroidism. Since D-propranolol has similar effects on thyroxine metabolism to those seen with the racemic mixture, membrane-stabilizing activity may be involved (176). 

Talley JD, Wathen MS, Hurst JW. Hyperthyroid-induced atrial flutter-fibrillation with profound sinoatrial nodal pauses due to small doses of digoxin, verapamil, and propranolol. Clin Cardiol 1989 12(l) 45-7. 

Clinica use Primarily as an antihypertensive agent. Also used for controlling ventricular rate in AF, post-Mi,CHF, angina, and hyperthyroidism. Additionally, propranolol maybe used for migraine headaches, essential tremors, and anxiety. The nonselectlve faeta-blockers are useful in the treatment of hepatic portal hypertension in patients with liver cirrhosis. Topical agents are used to lower intraocular pressures in patients with glaucoma. 

Case Conclusion HP began methimazole therapy for her Graves hyperthyroidism. She also began propranolol to help control her tachycardia and tremor. During this time HP should avoid excessive exercise or other sympathomimetic drugs until her symptoms of tachycardia have subsided. HP will return to the clinic for follow-up in 4 weeks. At that time, methimazole dose, tolerability, compliance, and thyroid function tests will be reassessed. 

Hyperthyroidism P-Antagonists Reduce peripheral sympathetic hyperresponsiveness Propranolol... 

C. Pantos, I. Mourouzis, S. Tzeis, V. Malliopoulou, D. D. Cokkinos, Asimakopoulos, H.C. Carageorgiou, D.D. Varonos, D.V. Cokkinos, Propranolol diminishes cardiac hypertrophy but does not abolish acceleration of the ischemic contracture in hyperthyroid hearts, J Cardiovasc Pharmacol 36, 384-389 (2000). 

Hypokalemic periodic paralysis is a rare complication of hyperthyroidism commonly observed in Asian and Hispanic populations. It presents as recurrent proximal muscle flaccidity ranging from mild weakness to total paralysis. The paralysis may be asymmetric and usually involves muscle groups that are strenuously exercised before the attack. Cognition and sensory perception are spared, whereas deep tendon reflexes are commonly markedly diminished. Hypokalemia results from a shift of potassium from extracellular to intracellular sites. High carbohydrate loads and exercise provoke the attacks. Treatment includes correcting the hyperthyroid state, potassium administration, spironolactone to conserve potassium, and propranolol to minimize intracellular shifts. ... 

The 24-hour RAIU wiU be suppressed to less than 2% during the thyrotoxic phase of painless thyroiditis. Antithyroglobuhn and antimicrosomal antibody levels are elevated in more than 50% of patients. Painless thyroiditis frequently occurs during the immediate postpartum period, and individual patients may experience recurrence of the disease with subsequent pregnancies. Patients with mild hyperthyroidism and painless thyroiditis should be reassured that they have a self-hmited disease. Adrenergic symptoms may be ameliorated with propranolol. Antithyroid drugs are not indicated because they do not decrease the release of preformed thyroid hormone. 

Because many of the manifestations of hyperthyroidism are mediated by /S-adrenergic receptors, /3-blockers (especially propranolol) have been used widely to ameliorate thyrotoxic symptoms such as palpitations, anxiety, tremor, and heat intolerance. Although /S-blockers are quite effective for symptom control, they have no effect on the urinary excretion of calcium, phosphorus, hydroxypro-line, creatinine, or various amino acids, suggesting a lack of effect on peripheral thyrotoxicosis and protein metabolism. Furthermore, /3-blockers do not reduce TSAb nor prevent thyroid storm. EYopra-nolol and nadolol partially block the conversion of T4 to T3, but this contribution to the overall therapeutic effect is small in magnitude. Inhibition of conversion of T4 to T3 is mediated by rf-propranolol, which is devoid of /3-blocking activity, and /-propranolol, which is responsible for the antiadrenergic effects and has little effect on the conversion. 

Answer E. Increased sympathetic activity is a major problem in hyperthyroidism and is best managed by use of beta blockers, which can offset cardiac stimulatory effects. Propranolol has an ancillary action in thyrotoxicosis in that it prevents conversion of T4 to T3 via its inhibition of 5 deiodinase. Amiodarone causes difficult-to-predict adverse effects on thyroid function and would not be appropriate in a patient with hyperthyroidism. Bretylium is an IV agent reserved for ventricular arrhythmias. Digoxin is not ideal because of its complex actions on the heart, which include both inhibition and stimulation. 

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