THYROID

1. THYROID Presented by : Hind Al_Osaimi Supervised by: Dr_ Suliman Justania

2. ANATOMY The thyroid gland consist of two lobes joint by an isthmus ,with occasionally an embryological extension of the isthmus superiorly called the pyramidal lobe. The normal gland weighs 20-25 g. The functioning unit is the lobule supplied by a single arteriole and consisting of 24-40 follicle which are lined by cuboidal epithelium. The resting follicle contain colloid in which thyroglobulin is stored.

3. B. Blood Supply: 1-Superior thyroid arteries ____arise from external carotid artery. 2-Inferior thyroid arteries ____ branch of thyrocervical trunk.( which arise from 1st part of subclavian A.) 3-Thyroidea ima _____arise from aorta or brachiocephalic A.

4. - venous drainage : 1-superior thyroid vein __Internal jugular v. 2- Middle thyroid vein __ Internal jugular v. 3-Inferior thyroid vein__ Brachiocephalic v.

5. C.Lymphatic drainage : -The lymph from thyroid gland drain mainly laterally into the deep cervical lymph nodes. -Some lymphatic vessels pass to pre-laryngeal , pretracheal and paratracheal lymph node.

6. D .laryngeal nerves: 1-Recurrent laryngeal __variable position about 70% run in the tracheoesophageal groove , 60% posterior to inferior thyroid artery . 2- Superior laryngeal nerve __run near the superior thyroid arteries.

7. PATHOPHYSIOLOGY • The thyroid gland operates as part of a feedback mechanism involving the hypothalamus and the pituitary gland. • The hypothalamus sends a signal to the anterior pituitary gland through a hormone called TRH (thyrotropin releasing hormone) which exerts a +ve feedback on it, causing release of TSH (thyroid stimulating hormone) which stimulate the thyroid gland to take up iodine to form its own hormones, T4 and T3, which are stored by binding to thyroglobuline in follicles.

8. T3& T4 enter the bloodstream __bound mainly to thyroid binding globulin & to lesser extend to thyroid binding albumin . A small proportion remain free in circulation. • AT tissue level ,deiodinase enzyme convert T4 to T3 which is physiologcally active hormone.

9. The peripheral levels of circulating free T4 constitute a feedback mechanism on the pituitary TSH secreting capacity __ the low circulating level induce increased TSH secretion (as in Hashimoto’s disease) and vise versa (as in oral thyroxine therapy).

10. Common Disorders of the Thyroid

11. Thyroid disorders fall into three broad categories a – Hypofunction b – Hyperfunction c – Enlargements (1)Diffuse __ termed goiter regardless of functional status. (2)Nodule.

12. Management • History: -sings &symptom of hypo or hyperthyroidism -pressure symptom as dysphagia ,dysphonia ,dyspnea &choking sensation -Change in voice -presence of mass__ duration ,progression& pain. -H/O exposure to radiation , diet , drugs -Family hx.

13. Physical Examination: -Inspection -palpation -percussion -Auscultation

14. Hypothyroidism

15. classification • Autoimmune thyroiditis (chronic lymphocytic thyroiditis) - goitrous :Hashimoto’s thyroditis - non-goitrous : primary myxoedema • Iatrogenic : - post thyroidectomy. - after radioiodine therapy. -drug induced (antithyroid drugs)

16. Dyshormonogenrsis. • Goitrogens. • Secondary to pituitary or hypothalamic disease.

17. Clinical picture • Symptoms: -tiredness. -mental lethargy. -Headaches & dementia. -cold intolerance. -weight gain . -constipation. -Menstrual disturbance.

18. Signs: -Bradycardia. -Cold extremities. -periorbital puffiness. -Hoarse voice , slow speech -enlarged toung. -Hair become dry & brittle. -Skin become dry, thickened &puffy. -Bradykinesia (slow movement ). -Delay relaxation of ankle jerk reflex.

19. Diagnosis: 1-Low T4 & T3level with high TSH . 2- High serum titers of antithyroid antibodies are characteristic of autoimmune disaese. Treatment: L-thyroxine _____0.1-0.2 mg orally once daily.

20. Thyroid Enlargement

21. classification • Simple goiter (euthyroid) 1-Diffuse hyperplastic: -physiological -Pubertal -pregnancy 2-Multinodular goiter • Toxic 1-Diffuse __ graves’ disease 2-Multinodular 3-Toxic adenoma

22. Neoplastic 1-Bengin 2-Malignant • Inflammatory 1-Autoimmune : -Chronic lymphocytic thyroditis -Hashimoto’s disease 2-Granulomatous -De quervain’s thyroditis 3-Fibrosing -Riedel’s thyroiditis 4-Infective -Acute (bacterial , viral thyroiditis ‘subacute thyroiditis’) -Chronic ( tuberculous , syphilitic ) • Other: __ amyloid.

23. Simple goiter • Aetiology: -Simple goiter may develop as a result of stimulation of thyroid gland by TSH ,either as a result of inappropriate secretion from a microadenoma in the anterior pituitary gland or in response to a chronically low level of circulating thyroid hormones .

24. -The most important factor in endemic goiter is dietary iodine deficiency. -Defective hormone synthesis probably accounts for many sporadic goiter.

25. Stages in goiter formation • 1-persistant growth stimulation cause diffuse hyperplasia ,all lobules are composed of active follicles and iodine uptake is uniform .This is a diffuse hyperplastic goiter . • 2-later on a mixed pattern develops with areas of active lobules and areas of inactive lobule as a result of fluctuating stimulation.

26. 3-Active lobules become more vascular & hyperplastic untill haemorrhage occure, causing central necrosis & leaving only a surrounding rind of active follices. • 4-Necrotic lobules __ form nodules filled with either iodine-free colloid or a mass of new but inactive follicles. • 5-Continual repetition of this process result in a nodular goiter.

27. Diffuse hyperplastic goiter • The goiter usually occur at puberty when metabolic demand are high , it appears in childhood in endemic area . • IF TSH stimulation stops the goiter may regress but tend to be recur later at times of stress such as pregnancy. • The goiter is soft diffuse & may become large enough to cause discomfort .

28. A colloid goiter is a late stage of diffuse hyperplasis when TSH stimulation has fallen off & many follicle are in active and full of colloid. • Treatment: • -thyroxine 0.15-.2 mg daily should be given to suppress TSH . • -Thyroidectomy may be required for pressure symptom or cosmotic.

29. Nodular goiter (nontoxic) • Nodules are usually multiple forming a multinodular goiter. • Nodules may be may be colloid or cellular • Cystic degeneration & haemorrhage are common . • All type of simple goiter are common in F more than M, and the presence of estrogen receptor in normal thyroid tissue and in nodular goiter is relevant.

30. , • The pt is euthyroid ,presented with smooth firm ,painless goiter . • Hardness and irregularity occur due to calcification __ may stimulate carcinoma. • Painful nodule & rapid enlargement of a nodule raise suspicion of carcinoma but is usually due to haemorrhage into a simple nodule.

31. Complications: • Tracheal obstruction__due to compression in a lateral or anteroposterior plane by retrosternal extention of the goiter .acute respiratory obstruction may follow Hge into a nodule impacted in thoracic inlet. • Secondary thyrotoxicosis. • Carcinoma_ which is usually of follicular pattern.It is un common.

32. Investigation: • Test of thyroid function to exclude mild hyperthyroidism. • Fine-needle aspiration . • Ultrasound may confirm multiple nodule. • Plain x-ray of chest & thoracic inlet__ may show calcification or tracheal deviation.

33. Treatment: -most of the pt are asymptomatic & do not require operation . -Retrosternal extention with tracheal compression is an indication for operation. -Operation may be indicated on cosmetic ground. -The surgical operation either : (a) subtotal thyroidectomy. (b) Total thyroidectomy with immediate & lifelong replacement of thyroxin __ for gland above 100 g in weight.

34. Solitary thyroid nodule • 50% of STN are truly solitary, the reminder are a part of nodular goitre and constitute a dominant nodule . • The majority of STN are benign ,about 5% are malignant. • Causes: -Multinodular goitre -Haemorrhage or necrosis into a hyperplastic nodule -Thyroid cyst -Benign follicular adenoma (including toxic adenoma) -Carcinoma ( papillary or follicular ) -Enlargement of the one lobe by a thyroiditis

35. Investigation : • Thyroid function test to exclude solitary toxic nodule. • Autoantibody titer __determine if the swelling is a manifestation of chronic lymphocytic thyroditis. • FNA to exclude malignancy. • Ultrasound__ diff. b/w solid & cystic ,determine whether the STN is a dominant nodule within MNG. • Thyroid isotope scan __give idea of the function of the nodule( hot or cold) .

36. If the isotope scan show a hot nodule & TSH is suppressed __ so it is a asolitary toxic nodule. • If the isotope scan show a cold nodule __ there is increase risk of malignancy.

37. Treatment: • Benign thyroid nodule does not required treatment unless symptomatic or cosmetic. • FNA should be repeated after 1 year __if remaine benign then further treatment. • Pt with suspicious nodule on FNA should under go thyroid lobectomy . • If the nodule is solitary , solid ,hot & cytology benign __it is a follicular adenoma __ for total lobectomy with excision of isthmus.

38. If the nodule is cold &the cytology show benign or atypical __ it is probably follicular adenoma - - - Total lobectomy with isthmus is necessary. • If the paraffin histopathology show carcinoma a second operation to complete a near total thyroidectomy is indicated. • if cytology show undoubted malignancy near total thyroidectomy is advisable at least to parathyroid gland & minimal protecting thyroid gland about 1 g.

39. Hyperthyroidism Hyperthyroidism is clinical state in which there is excess circulating thyroid hormones leading to an alteration in the basal metabolic rate.

40. Causes • Diffuse toxic goiter (Graves disease) • Toxic multi-nodular goiter • Toxic adenoma. • De quervains thyroiditis. • Thyroid cancer.

41. Clinical feature • Symptoms include: -tiredness -nervousness &irritability -tremor -insomnia -sweating -heat intolerance -weight loss -excessive appetite -palpitation -diarrhea

42. Signs of thyrotoxicosis: -Thyroid goiter -Tachycardia -Hot , moist palms -Agitation -Eye sign__ exophthalmos Lid lag & lid retraction supraorbital &infraorbital swelling ophthalmoplegia ( double vision) chemosis

43. Graves’ Disease( Diffuse toxic goiter) • Autoimmune thyrotoxicosis (primary thyro-toxicosis)_ caused by an antibody raised against the TSH receptor (TRAB). • A diffuse vascular goiter appearing at the same time as the hyperthyroidism. • Usually in young women. • Frequently associated with eye signs. • The hypertrophy & hyperplasia are due to abnormal thyroid stimulating antibodies. • Total thyroidectomy will cure grave’s disease with postoperative hypothyroidism

44. Toxic multinodular goiter • Simple nodular goiter is present for a long time before the hyperthyroidism. • Usually in middle age or elderly. • Pressure sing in the neck may be present. • Not frequently associated with eye manifestation. • The gland is irregularly enlarged, and its cut surface reveals many nodule which are solid (cellular) or cystic (colloid-filled). • Cardiac arrhythmia & insidious cardiac failure are common • In many cases the nodules are inactive & it is the internodular thyroid tissue that is overactive.

45. Toxic nodule • This is a solitary overactive nodule which may be a part of a generalized nodularity or a true toxic adenoma. • Because TSH secretion is suppressed by the high level of circulating thyroid hormones , the normal thyroid tissue surrounding the nodule is itself suppressed & inactived. • Cut surface shows a single lesion with a thin capsule , the nodule may show cystic change .fibrosis and calcification. • Technetium scan will show a solitary hot nodule.

46. De quervain’s thyroiditis • It is a true subacute inflammation of the thyroid gland. • IT is often associated with mild hyperthyroidism . • IT may be caused by viral infection. • Main complaint is a sudden appearance of a painful swelling in the neck • The pt may complain of malaise ,sore throat& fever. • IT is a self-limiting , it disappears in 1-3 month.

47. Diagnosis • Most of the cases are readily diagnosed clinically. • Low TSH level & high T3 &T4.

48. Treatment • Nonspecific measures ___ rest & sedation. • Antithyroid drug :e.g: propylthiouracil & carbimazole. • Radioiodine__ destroy thyroid cell& reduce the mass of functioning thyroid tissue to below a critical level.

49. Surgery: 1-In diffuse toxic goiter & toxic nodular goiter with overactive inter nodular tissue surgery cure by reducing the mass of overactive tissue (i.e reduce a thyroid tissue below a critical mass) 2- In toxic nodular goiter & toxic nodule surgery cure by removing all of the overactive thyroid tissue.__ this allow the supressed normal tissue to function again.

50. Choice of therapeutic agent • 1- Diffuse toxic goiter : - over 45 __ radioiodine . -under 45_surgey for large goiter & antithyroid drugs for small goiter. • 2- Toxic nodular goiter: -surgery ( because it doesn’t response as well to radioiodine or antithyroid drugs as dose a diffuse toxic goiter)