Hyperthyoroidism and thyrotoxixosis grave's diseases.pptx

Lecture notes for medical students

1. Tips on using my ppt. You can freely download, edit, modify and put your name etc. Don’t be concerned about number of slides. Half the slides are blanks except for the title. First show the blank slides (eg. Aetiology ) > Ask students what they already know about ethology of today's topic. > Then show next slide which enumerates aetiologies. At the end rerun the show – show blank> ask questions > show next slide. This will be an ACTIVE LEARNING SESSION x three revisions. Good for self study also. See notes for bibliography.

2. Thyrotoxicosis and Hyperthyroidism

3. Hyperthyroidism

4. Hyperthyroidism It is a term reserved for disorder that result in overproduction of hormone by the thyroid gland. In short in hyperthyroidism the pathology is in the thyroid gland itself.

5. Thyrotoxicosis

6. Thyrotoxicosis Biochemical and physiological manifestation of Excessive thyroid hormone. Thyrotoxicosis need not be due to hyperthyroidism But hyperthyroidism mostly produce thyrotoxicosis .

7. Hyperthyroidism Vs thyrotoxicosis

8. Hyperthyroidism Vs thyrotoxicosis No Hyperthyroidism Toxicosis without hyperthyroidism 1, Grave’s disease Subacute thyroiditis 2, Toxic nodular goitre Ectopic functioning thyroid 3, Toxic adenoma Silent thyroiditis 4, Jod – Basedow’s disease Struma ovarii 5, Metastatic follicular carcinoma 6, Trophoblastic tumours 7, Postpartum thyroiditis 8, Thyrotoxicosis factitia

9. Thyroid Hormone Function

10. Thyroid Hormone Function Thyroid hormones affect almost every system in the body . T 3 increases oxygen consumption, basal metabolic rate, and heat production by stimulation of Na + /K + ATPase in various tissues

11. The  Jod - Basedow  effect (also  Jod - Basedow syndrome  and  Jod - Basedow  phenomenon) is hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as iodinated contrast for medical imaging.

12. Wolff - Chaikoff effect  is an autoregulatory phenomenon, whereby a large amount of ingested iodine acutely inhibits thyroid hormone synthesis within the follicular cells, irrespective of the serum level of thyroid-stimulating hormone 

13. Diffuse toxic goitre (Grave’s disease)

14. Diffuse toxic goitre (Grave’s disease) T his disorder is known as Graves' disease after Robert Graves, an Irish physician who described three patients in 1835. It is an autoimmune disease with a strong familial predisposition, female preponderance (5:1). Peak incidence between the ages of 40 to 60 years. Graves' disease is characterized by thyrotoxicosis, diffuse goiter, and extrathyroidal conditions including ophthalmopathy , dermopathy (pretibial myxedema), thyroid acropachy , gynecomastia , and other manifestations.

15. Etiology, Pathogenesis, and Pathology

16. Etiology, Pathogenesis, and Pathology The exact etiology of the initiation of the autoimmune process in Graves' disease is not known. Postpartum state, iodine excess, lithium therapy, and bacterial and viral infections have been suggested as possible triggers. Genetic factors also play a role-HLA-B8 and HLA-DR3 and HLADQA1*0501.

17. Etiology, Pathogenesis, and Pathology Some unknown factors S timulate B lymphocytes, which produce antibodies directed against the thyroid hormone receptor. TSIs or antibodies that stimulate the TSH-R, as well as TSH-binding inhibiting immunoglobulins or antibodies have been described. The thyroid-stimulating antibodies stimulate the thyrocytes to grow and synthesize excess thyroid hormone, which is a hallmark of Graves' disease. Graves' disease also is associated with other autoimmune conditions such as type I diabetes mellitus, Addison's disease, pernicious anemia, and myasthenia gravis.

18. Etiology, Pathogenesis, and Pathology Macroscopically, the thyroid gland in patients with Graves' disease is diffusely and smoothly enlarged, with a concomitant increase in vascularity. Microscopically, the gland is hyperplastic, and the epithelium is columnar with minimal colloid present. The nuclei exhibit mitosis, and papillary projections of hyperplastic epithelium are common.

19. Presentation

20. Presentation Variable. Increase in sympathetic nervous system symptoms. Younger patients >sympathetic activation, such as anxiety, hyperactivity, and tremor Older patients >more cardiovascular symptoms, including dyspnea and atrial fibrillation with unexplained weight loss

21. Clinical manifestation

22. Clinical manifestation D ivided into those related to hyperthyroidism and those specific to Graves' disease. Hyperthyroid symptoms - H eat intolerance - I ncreased sweating and thirst - W eight loss despite adequate caloric intake

23. Epidemiology

24. Epidemiology incidence of hyperthyroidism is estimated between 0.05% and 1.3 %  incidence increases with age.   Graves disease predominantly affects those aged 20-40 years A slight predominance of hyperthyroidism exists among females . White and Hispanic populations in the United States have a slightly higher prevalence 

25. Clinical manifestation

26. Clinical manifestation Symptoms of increased adrenergic stimulation - palpitations, nervousness, fatigue, emotional lability , hyperkinesis , heat intolerance and tremors. GI symptoms include increased frequency of bowel movements and diarrhea. Female patients often develop amenorrhea, decreased fertility, and an increased incidence of miscarriages. Children experience rapid growth with early bone maturation. Older patients may present with cardiovascular complications such as atrial fibrillation and congestive heart failure.

27. Other manifestation of Grave’s

28. Other manifestation of Grave’s Approximately 50% of patients with Graves' disease also develop clinically evident ophthalmopathy , and dermopathy occurs in 1 to 2% of patients. Eye signs - lid lag (von Graefe's sign), spasm of the upper eyelid revealing the sclera above the corneoscleral limbus ( Dalrymple's sign), and a prominent stare, due to catecholamine excess. True infiltrative eye disease results in periorbital edema, conjunctival swelling and congestion ( chemosis ), proptosis , limitation of upward and lateral gaze (from involvement of the inferior and medial rectus muscles, respectively), keratitis, and even blindness due to optic nerve involvement.

29. Von  Graefe's  sign is the lagging of the upper eyelid on downward rotation of the eye, 

30. Rare bony involvement leads to subperiosteal bone formation and swelling in the metacarpals (thyroid acropachy ). Onycholysis , or separation of fingernails from their beds, is a more commonly observed finding.

31. Clinical signs

32. Clinical signs W eight loss and facial flushing may be evident. The skin is warm and moist and African American patients often note darkening of their skin. Tachycardia or atrial fibrillation is present with cutaneous vasodilation leading to a widening of the pulse pressure and a rapid falloff in the transmitted pulse wave (collapsing pulse). A fine tremor, muscle wasting, and proximal muscle group weakness with hyperactive tendon reflexes often are present. The thyroid usually is diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe. O verlying bruit or thrill and loud venous hum in the supraclavicular space

33. Tests of Thyroid Function

34. Tests of Thyroid Function Serum Thyroid-Stimulating Hormone (Normal 0.5–5 U/mL): Serum TSH levels reflect the ability of the anterior pituitary to detect free T4 levels. Small changes in free T 4 lead to a large shift in TSH levels (Inverse relation). Total T 4 (Reference Range 55–150 nmol /L) and T 3 (Reference Range 1.5–3.5 nmol /L). Free T 4 (Reference Range 12–28 pmol /L) and Free T 3 (3–9 pmol /L). Thyroid Antibodies : Thyroid antibodies include anti- Tg , antimicrosomal , or anti-TPO and thyroid-stimulating immunoglobulin (TSI).

35. Diagnostic Tests

36. Diagnostic Tests S uppressed TSH with or without an elevated free T4 or T 3 level. If eye signs are present, other tests are generally not needed. I n the absence of eye findings, an 123 I uptake and scan should be performed. An elevated uptake, with a diffusely enlarged gland, confirms the diagnosis of Graves' disease It helps to differentiate it from other causes of hyperthyroidism. Anti- Tg and anti-TPO antibodies are elevated in up to 75% of patients. Elevated TSH-R or thyroid-stimulating antibodies ( TSAb ) are diagnostic of Graves' disease and are increased in about 90% of patients

37. Management

38. Management Guidelines for the management of hyperthyroidism and other causes of thyrotoxicosis  have been developed by the American Thyroid Association (ATA) and the American Association of Clinical Endocrinologists.   These guidelines include 100 evidence-based recommendations concerning the care of these patients.

39. Management Graves' disease may be treated by any of three treatment modalities— - A ntithyroid drugs - Thyroid ablation with radioactive 131 I - Thyroidectomy

40. Anti Thyroid Drugs

41. Anti Thyroid Drugs Antithyroid medications generally are administered in preparation for RAI ablation or surgery. The drugs commonly used are propylthiouracil (PTU, 100 to 300 mg three times daily) and methimazole (10 to 30 mg three times daily, then once daily). Both drugs reduce thyroid hormone production by inhibiting the organic binding of iodine and the coupling of iodotyrosines (mediated by TPO). PTU also inhibits the peripheral conversion of T4 to T 3 , making it useful for the treatment of thyroid storm. PTU has a lower risk of transplacental transfer.

42. Anti Thyroid Drugs Side effects of treatment include reversible granulocytopenia , skin rashes, fever, peripheral neuritis, polyarteritis , vasculitis , and, rarely, agranulocytosis and aplastic anemia. The catecholamine response of thyrotoxicosis can be alleviated by administering beta-blocking agents. Propranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily.

43. Radioactive Iodine Therapy ( 131 I)

44. Radioactive Iodine Therapy ( 131 I) RAI forms the mainstay of Graves' disease treatment in North America. The major advantages of this treatment are the avoidance of a surgical procedure and its concomitant risks. The 131 I dose is calculated after a preliminary scan, and usually consists of 8 to 12 mCi administered orally. After standard treatment with RAI, most patients become euthyroid within 2 months. However, only about 50% of patients treated with RAI are euthyroid 6 months after treatment, and the remaining are still hyperthyroid or already hypothyroid

45. Radioactive Iodine Therapy ( 131 I) RAI therapy is therefore most often used in older patients with small or moderate-sized goiters, those who have relapsed after medical or surgical therapy. Contraindication : Absolute : W omen who are pregnant or breastfeeding. Relative : Y oung patients (i.e., especially children and adolescents), those with thyroid nodules, and those with ophthalmopathy .

46. Surgical Treatment S urgery is recommended when RAI is contraindicated (a) Have confirmed cancer or suspicious thyroid nodules. (b) Young. (c) Pregnant or desire to conceive soon after treatment. (d) Severe reactions to antithyroid medications (e) Large goiters causing compressive symptoms. (f) R eluctant to undergo RAI therapy.

47. Surgical Treatment

48. Surgical Treatment What surgical Procedure ? 1) Near total thyroidectomy 2) Subtotal thyroidectomy 3) Total thyroidectomy 4) Hartley- Dunhill procedure - Solely based on discretion of surgeon and their experience.

49. Management of Ophthalmopathy  

50. Management of Ophthalmopathy  Tight-fitting sunglasses. Saline eye drops  Exposure keratitis   Saline gel or drops Taping eyelids closed with paper tape before sleep. Goggles at night to keep the eyes moist

51. Management of Ophthalmopathy   A medical emergency -Optic nerve compression with early loss of color vision and orbital pain>permanent vision loss. High-dose glucocorticoids Orbital decompression surgery Ocular radiation therapy.

52. Toxic MNG

53. Toxic MNG Toxic multinodular goiters usually occur in older individuals, who often have a prior history of a nontoxic multinodular goiter. Over several years, enough thyroid nodules become autonomous to cause hyperthyroidism. Hyperthyroidism also can be precipitated by iodide-containing drugs such as contrast media and the antiarrhythmic agent amiodarone ( J odbasedow hyperthyroidism). Symptoms and signs of hyperthyroidism are similar to Graves' disease, but extrathyroidal manifestations are absent.

54. Toxic MNG Blood tests are similar to Graves' disease with a suppressed TSH level and elevated free T4 or T 3 levels. USG shows nodules. RAI uptake also is increased, showing multiple nodules with increased uptake and suppression of the remaining gland. Treatment – After adequately controlling hyperthyroid state total thyroidectomy is treatment of choice.

55. Toxic Adenoma (Plummer's Disease)

56. Toxic Adenoma (Plummer's Disease) Hyperthyroidism from a single hyperfunctioning nodule typically occurs in younger patients who note recent growth of a long-standing nodule along with the symptoms of hyperthyroidism. Most hyperfunctioning or autonomous thyroid nodules have attained a size of at least 3 cm before hyperthyroidism occurs. Physical examination usually reveals a solitary thyroid nodule without palpable thyroid tissue on the contralateral side. RAI scanning shows a "hot" nodule with suppression the rest of the thyroid gland. These nodules are rarely malignant. Surgery (lobectomy and isthmusectomy ) is preferred to treat young patients and those with larger nodules.

57. Thyroid Storm

58. Thyroid Storm Thyroid storm is a condition of hyperthyroidism accompanied by fever, central nervous system agitation or depression, cardiovascular dysfunction that may be precipitated by infection, surgery, or trauma. Beta blockers are given to reduce peripheral T4 to T 3 conversion and decrease the hyperthyroid symptoms. Oxygen supplementation and hemodynamic support should be instituted. Non-aspirin compounds can be used to treat pyrexia and Lugol's iodine or sodium ipodate (intravenously) should be administered to decrease iodine uptake and thyroid hormone secretion. PTU therapy blocks the formation of new thyroid hormone and reduces peripheral conversion of T 4 to T 3 . Corticosteroids often are helpful to prevent adrenal exhaustion and block hepatic thyroid hormone conversion.

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