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Hyperthyroidism

Hyperthyroidism

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Hyperthyroidism

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  1. Hyperthyrodism

  2. Outlines Definition of hyperthyroidism and its Causes Clinical features Diagnosis and treatment 2 1 3

  3. 1 Definition of hyperthyroidism and its Causes

  4. Thyroid gland The thyroid gland is a butterfly-shaped organ located anteriorly in the neck. The thyroid's hormones regulate vital body functions, including: Breathing Heart rate Central and peripheral nervous systems Body weight Muscle strength Menstrual cycles› Body temperature Cholesterol levels

  5. Hyperthyroidism

  6. Thyroid hormons Thyroxine Less active form. Created in grater amount than T3. Half life ( 6 to 8 days). Highly active form. Half life ( 1 to 2 days) Triiodothyronine T3 T4

  7. Gravies disease Plummer disease (multinodular toxic goiter) 15% of all cases. Toxic thyroid adenoma (single nodule) 2% of all cases. (diffuse toxic goiter) is the most common cause 80% of all cases. Causes of hyperthyroidism

  8. Hashimoto thyroiditisand subacute (granulomatous) thyroiditis(both can cause transient hyperthyroidism). Other causes Postpartum thyroiditis (transient hyperthyroidism) Iodine-induced hyperthyroidism Excessive doses of levothyroxine (e.g., iatrogenic by health care provider or surreptitious self-administration) Causes of hyperthyroidism

  9. 2 Clinical features

  10. Symptoms Nervousness, insomnia, irritability Excessive sweating, heat intolerance, Palpitations (due to tachyarrhythmias) Hand tremor, hyperactivity, tremulousness, Muscle weakness Weight loss despite increased appetite, Diarrhea

  11. Signs Graves disease: a diffusely enlarged (symmetric), nontender thyroid gland; a bruit may be present. Plummer disease and Hashimoto thyroiditis (if multinodularity is present): thyroid gland is bumpy, irregular, and asymmetric. Subacute thyroiditis: an exquisitely tender, diffusely enlarged gland (with a viral illness). Toxic adenoma: single nodule with an otherwise atrophic gland. Thyroid gland

  12. Signs Eyes: Proptosis, due to edema of the extraocular muscles and retro orbital tissue, is a hallmark of Graves disease (but not always present). Irritation and excessive tearing are common due to corneal exposure. Lid retraction may be the only sign in milder disease Lid lag may be present. Extrathyroidal

  13. Eyes signs

  14. Signs Skin changes: warm and moist, pretibial myxedema (edema over tibial surface due to dermal accumulation of mucopolysaccharides) Cardiovascular effects: arrhythmias (sinus tachycardia, atrial fibrillation, and premature ventricular contractions), elevated BP Neurologic: brisk deep tendon reflexes, tremor. Extrathyroidal

  15. Pretibial Myxedema

  16. 3 Diagnosis and treatment

  17. Serum TSH level (low)—initial test of choice: If TSH is normal or high, hyperthyroidism is unlikely. Next order thyroid hormone levels: T4 level should be elevated. Testing the T3 level is usually unnecessary but may be helpful if TSH level is low and free T4 is not elevated, because excess T3 alone can cause hyperthyroidism. Diagnosis

  18. Diagnosis 4. Other tests (less commonly used but often tested). a. Radioactive T3 uptake. b. Free thyroxine index (FTI).

  19. Treatment types Radioiodine 131 (131I). Pharmacologic Surgical subtotal thyroidectomy.

  20. Thionamides— Methimazole and propylthiouracil (PTU) inhibit thyroid hormone synthesis, and PTU also inhibits conversion of T4 to T3 . Treatment with thionamides results in long-term remission in a minority of patients; a major serious side effect is agranulocytosis. Other side effects shared by both methimazole and PTU include skin rash, arthralgias, and hepatotoxicity. β-Blockers—for acute management of some symptoms such as palpitations, tremors, anxiety, tachycardia, sweating, and muscle weakness. Sodium ipodate or iopanoic acid—lowers serum T3 and T4 levels and causes rapid improvement of hyperthyroidism; appropriate for acute management of severe hyperthyroidism that is not responding to conventional therapy. Pharmacologic

  21. Causes destruction of thyroid follicular cells. Most common therapy in the United States for Graves hyperthyroidism. Main complication is hypothyroidism and occurs in majority of patients. If the first dose does not control the hyperthyroidism within 6 to 12 months, then administer another dose. Contraindicated during pregnancy and breastfeeding due to risk of cretinism (stunted physical and mental growth from severe hypothyroidism). Radioiodine 131

  22. Very effective, but only 1% of patients with hyperthyroidism are treated with surgery due to the following side effects: permanent hypothyroidism (30%), recurrence of hyperthyroidism (10%), recurrent laryngeal nerve palsy (1%), and permanent hypoparathyroidism (1%). Often reserved for patients with very large goiters (more common in toxic multinodular goiter), those who are allergic to antithyroid drugs, or patients who prefer surgery over medication. Watch for clinical manifestations of hypocalcemia after surgery that may not return to normal due to parathyroid inflammation or accidental removal. Surgical

  23. For immediate control of adrenergic symptoms of hyperthyroidism (of any cause): β-blocker (propranolol). For nonpregnant patients with Graves disease. Start methimazole (in addition to the β-blocker). Taper β-blocker after 4 to 8 weeks (once methimazole starts to take effect). Continue methimazole for 1 to 2 years. Measure thyroid-stimulating IgG antibody at 12 months. If it is absent, then discontinue therapy. If relapse occurs, then resume methimazole for about 1 more year or consider radioiodine therapy. Treatment

  24. 3. For pregnant patients with Graves disease. PTU is preferred. 4. Radioactive iodine ablation therapy. Leads to hypothyroidism over time in many patients. Consider therapy with 131I for the following patients: Elderly patients with Graves disease. Patients with a solitary toxic nodule. Patients with Graves disease in whom therapy with antithyroid drugs fails (e.g., due to relapse, agranulocytosis). Treatment

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