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Hyperthyroidism

  1. 1. Hyperthyroidism DR.HARDIK SHAH ST.STEPHEN’S HOSPITAL DELHI
  2. 2. • Hyperthyroidism results from excessive secretion of thyroid hormone. • Graves disease is the most common cause of hyperthyroidism.
  3. 3. CAUSES OF HYPERTHYROIDISM • CIRCULATING THYROID STIMULATORS:  Graves disease  Neonatal Graves disease  Thyrotropin-secreting tumor (Pituitary adenoma)  Choriocarcinoma • THYROIDAL AUTONOMY: • Toxic multinodular goiter • Toxic solitary adenoma • Congenital hyperthyroidism • Iodine-induced hyperthyroidism (Jod-Basedow)
  4. 4. • DESTRUCTION OF THYROID FOLLICLES (THYROIDITIS)  Subacute thyroiditis  Painless or postpartum thyroiditis  Amiodarone-induced thyroiditis  Acute (infectious) thyroiditis • EXOGENOUS THYROID HORMONE  Iatrogenic Excess ingestion of thyroid hormone  Factitious Excess ingestion of thyroid hormone  Hamburger thyrotoxicosis • ECTOPIC THYROID TISSUE  Struma ovarii - Ovarian teratoma containing thyroid tissue  Metastatic follicular thyroid cancer  Pituitary resistance to thyroid hormone
  5. 5. Graves Disease • It is an autoimmune disorder; production of thyroid-stimulating immunoglobulin (TSI) results in diffuse toxic goiter. • Graves disease occurs in approximately 0.02% of children (1 : 5,000). • It has a peak incidence in the 11- to 15-yr old; there is a 5 : 1 female to male ratio. • Most children with Graves disease have a positive family history of some form of autoimmune thyroid disease.
  6. 6. Etiology and Pathology: • Enlargement of the thymus, splenomegaly, lymphadenopathy, infiltration of the thyroid gland and retro-orbital tissues with lymphocytes and plasma cells, and peripheral lymphocytosis are well-established findings in Graves disease. • In the thyroid gland, T helper cells (CD4+) predominate in dense lymphoid aggregates; in areas of lower cell density, cytotoxic T cells (CD8+) predominate. • The percentage of activated B lymphocytes infiltrating the thyroid is higher than in peripheral blood. • A postulated failureof T suppressor cells allows expression of T helper cells, sensitized to the TSH antigen, which interact with B cells. • These cells differentiate into plasma cells, which produce thyrotropin receptor–stimulating antibody (TRSAb). • TRSAb binds to the receptor for TSH and stimulates cyclic adenosine monophosphate, resulting in thyroid hyperplasia and unregulated overproduction of thyroid hormone. • In addition to TRSAb, thyrotropin receptor-blocking antibody (TRBAb) may also be produced, and the clinical course of the disease usually correlates with the ratio between the two antibodies.
  7. 7. • In whites, Graves disease is associated with HLA-B8 and HLA-DR3. • Graves disease is also associated with other HLA-D3–related disorders such as Addison disease, type 1 diabetes mellitus, myasthenia gravis, and celiac disease. • In family clusters, the conditions associated most commonly with Graves disease are autoimmune lymphocytic thyroiditis and hypothyroidism.
  8. 8. CLINICAL MANIFESTATIONS: • The earliest signs in children may be emotional disturbances accompanied by motor hyperactivity. • The children become irritable and excitable, and they cry easily because of emotional lability. • They are restless sleepers and tend to kick their covers off. • Their schoolwork suffers as a result of a short attention span and poor sleep. • Tremor of the fingers can be noticed if the arm is extended. • There may be a voracious appetite combined with loss of or no increase in weight. • Recent height measurements might show an acceleration in growth velocity.
  9. 9. Symptoms: • Hyperactivity, irritability, altered mood, insomnia, anxiety • Heat intolerance, increased sweating • Palpitations • Fatigue, weakness • Dyspnea • Weight loss with increased appetite (weight gain in 10% of patients) • Pruritus • Increased stool frequency • Thirst and polyuria • Oligomenorrhea or amenorrhea
  10. 10. Signs: • Sinus tachycardia, atrial fibrillation (rare in children), supraventricular • tachycardia • Fine tremor, hyperkinesis, hyperreflexia • Warm, moist skin • Palmar erythema, onycholysis • Hair loss • Osteoporosis • Muscle weakness and wasting • High-output heart failure • Chorea • Periodic (hypokalemic) paralysis (primarily in Asian men) • Psychosis (rare
  11. 11. MANIFESTATIONS OF GRAVES DISEASE • Diffuse goiter • Ophthalmopathy  Upper eyelid retraction (the most common sign of Graves ophthalmopathy)  Infrequent or incomplete blinking (Stellwag sign)  Lid lag upon infraduction (Von Graefesign) or globe lag on supraduction (Kocher sign)  Widened palpebral fissure during fixation (Dalrymple sign)  Incapacity to close eyelids completely (lagophthalmos)  Prominent stare (Binswanger sign)  Inability to keep the eyeballs converged (Mobius sign)  Limited extraocular gaze (especially upward)  Blurred vision due to inadequate convergence and accommodation  Swollen orbital contents and puffy lids  Chemosis  Globe pain  Exophthalmos  Enlarged lacrimal glands (visible on inspection and palpable)  Dysfunctional lacrimal glands with decreased quantity and abnormal composition of tears  Corneal injection, ulceration, punctate epithelial erosions, or superior limbic keratoconjunctivi (rare)  Decreased visual acuity due to papilledema, retinal edema, retinal hemorrhages, or optic nerv damage (rare) • Localized dermopathy (rare in children) • Lymphoid hyperplasia • Thyroid acropachy (rare in children)
  12. 12. • Many scoring systems have been used to gauge the extent and activity of the orbital changes in Graves' disease. • The "NO SPECS" scheme is an acronym derived from the following eye changes: 0 = No signs or symptoms 1 = Only signs (lid retraction or lag), no symptoms 2 = Soft tissue involvement (periorbital edema) 3 = Proptosis (>22 mm) 4 = Extraocular muscle involvement (diplopia) 5 = Corneal involvement 6 = Sight loss
  13. 13. • Thyroid crisis, or thyroid storm, is a form of hyperthyroidism manifested by an acute onset, hyperthermia, severe tachycardia, heart failure, and restlessness. • There may be rapid progression to delirium, coma, and death. Precipitating events include trauma infection, radioactive iodine treatment, or surgery. • Apathetic, or masked, hyperthyroidism is another variety of hyperthyroidism characterized by extreme listlessness, apathy, and cachexia. • A combination of both forms can occur. • These symptom complexes are rare in children.
  14. 14. LABORATORY FINDINGS • Serum levels of thyroxine (T4), triiodothyronine (T3), free T4, and free T3 are elevated. • In some patients, levels of T3 may be more elevated than those of T4. • Levels of TSH are suppressed to below the lower range of normal. • Antithyroid antibodies, including thyroid peroxidase antibodies, are often present. • Most patients with newly diagnosed Graves disease have measurable TRSAb; • Measurement of TSI or TBII is useful in confirming the diagnosis of Graves disease. • Radioiodine is rapidly anddiffusely concentrated in the thyroid, but this study is rarely necessary. • Children who experience an acceleration of growth might also have advanced skeletal maturation. • Bone density may be reduced at diagnosis but returns to normal with treatment.
  15. 15. TREATMENT: 1. Antithyroid drugs 2. Radioactive iodine (131I) 3. Surgery
  16. 16. 1. Antithyroid drugs 1. Propylthiouracil (PTU) and 2. Methimazole (Tapazole). • Both compounds inhibit incorporation of trapped inorganic iodide into organic compounds, and they might also suppress TRSAb levels by directly affecting intrathyroidal autoimmunity. • Methimazole is at least 10 times more potent than PTU, longer serum half-life (6-8 hr vs 0.5 hr); PTU generally is administered 3 times daily, but methimazole can be given once daily. • Unlike methimazole, PTU is heavily protein bound and has a lesser ability to cross the placenta and to pass into breast milk; theoretically, PTU is the preferred drug during pregnancy and for nursing mothers. • Due to reports of severe liver disease in patients treated with PTU, with some patients requiring liver transplant or potentially suffering a fatal outcome, the consensus is to use only methimazole to treat children with Graves disease.
  17. 17. • The initial dosage of methimazole is 0.25-1.0 mg/kg/24 hr given once or twice daily. • Smaller initial dosages should be used in early childhood. • Rising serum levels of TSH to greater than normal indicates overtreatment and leads to increased size of the goiter. • Clinical response becomes apparent in 3-6 wk, and adequate control is evident in 3-4 mo. • The dose is decreased to the minimal level required to maintain a euthyroid state.
  18. 18. • Transient granulocytopenia (<2,000/mm3) is common; it is asymptomatic . • Transient urticarial rashes are common. • They may be managed by a short period off therapy, and then restarting the antithyroid drug. • The most severe reactions are hypersensitive and include agranulocytosis (0.1-0.5%), hepatitis (0.2-1%), a lupus-like polyarthritis syndrome, glomerulonephritis, and an ANCA- positive vasculitis involving the skin and other organs.
  19. 19. • Radioiodine treatment or surgery is indicated: - when adequate cooperation for medical management is not possible, - when adequate trial of medical management has failed to result in permanent remission, or - when severe side effects preclude further use of antithyroid drugs.
  20. 20. 2. Radioiodine • It is an effective, relatively safe first or alternative therapy for Graves disease in children >10 yr of age. • Pretreatment with antithyroid drugs is unnecessary; if a patient is taking them, they should be stopped a week before radioiodine administration. • Many pediatric endocrinologists prefer to select a dose of radioiodine to ensure complete ablation of thyroid tissue. • A dose of 300 μCi/g of thyroid tissue, or a total dose of approximately 15 mCi, will achieve this goal. • Essentially all patients treated at this dose will become hypothyroid; the time course to hypothyroidism averages 11 wk, with a range of 9-28 wk. • Because the full effects of treatment may not be complete for 1-6 mo, adjunctive therapy with a β-adrenergic antagonist and lower doses ofantithyroid drugs are recommended.
  21. 21. 3. Surgery • Subtotal thyroidectomy, a safe procedure when performed by an experienced team, is done only after the patient has been brought to a euthyroid state. • This may be accomplished with methimazole over 2-3 mo. • After a euthyroid state has been attained, a saturated solution of potassium iodide, 5 drops/24 hr, are added to the regimen for 2 wk before surgery to decrease the vascularity of the gland. • Complications of surgical treatment are rare and include hypoparathyroidism (transient or permanent) and paralysis of the vocal cords. • The incidence of residual or recurrent hyperthyroidism or hypothyroidism depends on the extent of the surgery. • Most recommend near-total thyroidectomy. • The incidence of recurrence is low, and most patients becomehypothyroid.
  22. 22. • A β-adrenergic blocking agent such as propranolol (0.5- 2.0 mg/kg/24 hr orally, divided 3 times daily) or atenolol (1-2 mg/ kg orally given once daily) is a useful supplement to antithyroid drugs in the management of severely toxic patients.

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