2. HYPERTHYROIDISM - Increased serum levels of thyroid hormones, - Surgical correction is frequently appropriate

3. NORMAL THYROID FUNCTION The follicular cells- T3, T4 T3, T4 bind with thyroglobulin, stored on the gland until released onto the bloodstream Release is under the control of TSH and TRH A feed-back mechanism regulating T3, T4 release is related to the level of circulating T3, T4.

5. HORMONAL ACTION The thyroid hormones: - increase the metabolic rate, - increase the O2 consumption, - increase glycogenolysis, - enhance the actions of catecholamines The result is: Increase in the PR, CO. Nervousness, irritability, muscular tremor, muscle wasting These effects can be blocked by the use of beta-blockers

6. HORMONAL ACTION The parafollicular or C-cells- produce thyrocalcitonin Thyrocalcitonin action: - to lower serum calcium and phosphate concentration, - reduces bone resorption - in the kidney accelerates calcium and phosphate excretion:

7. THYROID GLAND CLINICAL EXAMINATION Hyperthyroidism Symptoms: dyspnea on effort, palpitation, tiredness, preferance for cold, sweating, nervousness, weight loss, good appetite Signs: palpable thyroid, exophtalmos, lid lag, hyperkinesis, finger tremor, hot and moist hands, rapid PR

8. INVESTIGATIONS TSH- raised in primary hypothyroidism and after treatment of thyrotoxicosis by surgery or radioiodine, - reduced in hyperthyroidism Free T3, T4- radioimmunoassays, Radioiodine uptake, Thyroid isotope scanning Ultrasonography, CT, MRI Fine needle aspiration cytology Thyroid autoantibodies (ab.to thyroglobulin)

9. Thyroid scintigram Autonomous adenoma in the right lobe of the struma. The test substance accumulates almost exclusively in the range of the autonomous adenoma. The other areas of the struma show a considerable reduced accumulation of activity.

10. GOITER ENLARGEMENT OF THE THYROID GLAND Simple goiter - diffuse hyperplastic goitre, - nodular goitre Toxic goiter - diffuse (Grave’s disease), - toxic multinodular goitre, - toxic solitary nodule Neoplastic goiter - benign, - malignant Thyroiditis - subacute (de Quervain’s), - autoimmune(Hashimoto’s), - invasive fibrous thyroiditis (Riedel’s) - acute suppurative

11. HYPERTHYROIDISM Common causes: - diffuse toxic goitre (Graves’s disease), - toxic multinodular goitre (Plummer’s disease), - toxic solitary nodule, - exogenous thyroid hormone excess, - thyroiditis

12. HYPERTHYROIDISM Rare causes: - metastatic thyroid carcinoma, - pituitary tumour secreting TSH

13. GRAVE’S DISEASE The most common cause of hyperthyroidism It is an immunological disorders Thyroid stimulating antibodies (IgG type) bind to the TSH receptor of the thyroid cells- excess of the thyroid hormones The thyroid gland hypertrophies Diffuse enlargement

14. GRAVE’S DISEASE Clinical Diagnosis Symptoms and signs of thyrotoxicosis result from excess thyroid hormones: Cardio vascular Neurological Metabolic Exophtalmos Diffuse enlargement of the thyroid

15. GRAVE’S DISEASE Ophthalmopathy- two major components: -Non-infiltrating ophthalmopathy-sympathetic activity: - upper lid retraction, - a stare, - infrequent blinking -Infiltrative ophthalmopathy- edema of the orbital contents, lids, periorbital tissue, cellular infiltration within the orbit

17. HYPERTHYROIDISM PREOPERATIVE PREPARATION Surgery must be done in the euthyroid state ATD for a period then discontinue Betablockers to control cardiac symptoms Lugol’s solution, 10 days, will diminish the peroperative hemorrhagic risk

19. GRAVES’ DISEASE TREATMENT To restore the euthyroid state: Antithyroid drugs + beta-blockers Radioactive iodine - distroys overactive tissue Surgery - bilateral subtotal/total thyroidectomy

20. Grave’s disease Multiple nodules and hypervascularity

21. Grave’s disease Pressure symptoms

22. Recurrent Grave’s disease after subtotal thyroidectomy, nodule at the piramidal lobe

23. Right thyroid nodules after subtotal thyroidectomy

24. Nodules with cystic degeneration after subtotal thyroidectomy

25. Left upper nodule with cystic degeneration

26. MULTINODULAR GOITRE MANAGEMENT Hyperthyroid- iodine scan Large- ATD & surgery Small- iodine therapy Euthyroid No dominant nodule-observe Dominant nodule-FNAC Benign, no sy-observe Malignant- surgery Suspicious- surgery Inadequate- repeat FNAC Retrosternal- surgery Cosmetic- surgery

27. SOLITARY THYROID NODULE MANAGEMENT Hyperthyroid- FNAC & isotope scan Greater than 3 cm.- surgery Less than 3 cm.- iodine therapy Euthyroid- FNAC Benign-no pressure sy.-observe, repeat FNAC in 6 months Benign- with pressure sy.- surgery Thyoiditis- T4 treatment Suspicious- surgery Malignant- surgery Inadequate FNAC- repeat Cystic benign- observe, review in 6 weeks Cystic malignant- surgery

28. TOXIC SOLITARY NODULE TREATMENT This condition is caused by a single autonomous thyroid nodule Best option- surgery- unilateral thyroid lobectomy

30. Toxic compressive goiter

31. POSTOPERATIVE COMPLICATIONS 1. Postoperative bleeding 2.Postoperative thyrotoxic crisis 3.Postoperative voice changes 4. Hypoparathyroidism 5. Hypothyroidism

32. POSTOPERATIVE BLEEDING Postoperative bleeding there is always a risk of postop.bleeding, it is rare but sometimes dramatic The bleeding may occur in one of two sites, - deep to the myofascial layer in relation to thyroid vessels-evacuation must be done quickly - deep to the skin flaps, from veins Compressive hematoma- respiratory embarrasment- evacuation is mandatory

33. POSTOPERATIVE THYROTOXIC CRISIS Serious complication-where there has not been adequate preop.preparation It occurs within the first 24 hours of thyroidectomy Symptoms: confusion, hyperactive, fever, profuse sweating, rapid PR. Treatment: beta-blockers, iv steroids, iodine

34. POSTOPERATIVE VOICE CHANGES Rare due to any damage to recurrent laryngeal nerves- this occurs in less than 1% Probably minor changes in the muscles around the cricoid and thyroid cartilages are the most important, inevitable with the mobilization of the gland Trauma to external laryngeal nerve- cricothyroid muscle- voice change- difficulty in achieving vocal cord tension Trauma t the internal laryngeal nerve can occur where there is difficulty in mobilizing the superior pole

35. POSTOPERATIVE HYPOPARATHYROIDISM Hypocalcemia- usually a consequance of a metabolic changes- re-entry of calcium into bone demineralized by hyperthyroidism (“hungry bones”) Parathyroids are small and are not always easy to identify The incidence of hypoparathroidism after surgery shoud be less than 1%

36. POSTOPERATIVE HYPOTHYROIDISM All forms of treatment for thyrotoxicosis will produce a population of patients prone to develop hypothyroidism Greatest risk after radioiodine therapy