1. Hyperthyroidism Hypothyroidism Dr. Meg-angela Christi Amores

2. Thyroid Hormones Thyroxine (T4) Triiodothyronine (T3) Secreted by the THYROID G:AMD Regulated by the PITUITARY GLAND TSH – secreted by the PITUITARY GLAND

3. Normal levels T4 = T3 = TSH T4 and T3 greater than normal: HYPERTHYROIDISM T4 and T3 lesser than normal: HYPOTHYROIDISM

4. Thyroid Hormone Synthesis Iodide uptake is a critical first step in thyroid hormone synthesis In areas of relative iodine deficiency, there is an increased prevalence of goiter iodine deficiency remains the most common cause of preventable mental deficiency

6. Organification, Coupling, Storage, Release

7. Hypothyroidism Iodine deficiency remains the most common cause of hypothyroidism worldwide In areas of iodine sufficiency, autoimmune disease (Hashimoto's thyroiditis) and iatrogenic causes (treatment of hyperthyroidism) are most common

8. Congenital Hypothyroidism occurs in about 1 in 4000 newborns due to thyroid gland dysgenesis in 80–85% due to inborn errors of thyroid hormone synthesis in 10–15% TSH-R antibody-mediated in 5% of affected newborns

9. Hypothyroidism Clinical manifestations prolonged jaundice feeding problems Hypotonia enlarged tongue delayed bone maturation umbilical hernia

10. Diagnosis and Treatment Diagnosis – neonatal screening programs – based on measurement of TSH or T 4 levels in heel- prick blood specimens Treatment – T 4 is instituted at a dose of 10–15 g/kg per day, and the dose is adjusted by close monitoring of TSH levels. T 4 requirements are relatively great during the first year of life – Early treatment with T 4 results in normal IQ levels

11. Autoimmune Hypothyroidism may be associated with a goiter (Hashimoto's, or goitrous thyroiditis) or, at the later stages of the disease, minimal residual thyroid tissue (atrophic thyroiditis)

12. Hashimoto’s Thyroiditis marked lymphocytic infiltration of the thyroid with germinal center formation atrophy of the thyroid follicles accompanied by oxyphil metaplasia, absence of colloid, and mild to moderate fibrosis

13. Atrophic thyroiditis fibrosis is much more extensive, lymphocyte infiltration is less pronounced, and thyroid follicles are almost completely absent

14. Hypothyroidism Clinical manifestations

16. Laboratory Evaluation TSH level T 4 level Circulating unbound T 3 levels are normal in about 25% of patients elevated cholesterol and triglycerides, and anemia

17. Treatment daily replacement dose of levothyroxine is usually 1.6 ug/kg body weight (typically 100– 150 ug) Adult patients under 60 without evidence of heart disease may be started on 50–100 g levothyroxine (T 4 ) daily dose is adjusted on the basis of TSH levels measured about 2 months after instituting treatment

18. Treatment Patients may not experience full relief from symptoms until 3–6 months after normal TSH levels are restored Once full replacement is achieved and TSH levels are stable, follow-up measurement of TSH is recommended at annual intervals

19. Hyperthyroidism Causes: – Graves' disease – Toxic multinodular goiter – Toxic adenoma – Functioning thyroid carcinoma metastases – Activating mutation of the TSH receptor – Activating mutation of G sa (McCune-Albright syndrome) – Struma ovarii – Drugs: iodine excess (Jod-Basedow phenomenon)

20. Graves disease combination of environmental and genetic factors stress is an important environmental factor, presumably operating through neuroendocrine effects Due to TSI synthesized in the thyroid gland as well as in bone marrow and lymph nodes

21. Graves Disease Clinical manifestations

23. Treatment reducing thyroid hormone synthesis, using antithyroid drugs reducing the amount of thyroid tissue with radioiodine ( 131 I) treatment or by thyroidectomy Propranolol (20–40 mg every 6 h) or longer- acting beta blockers such as atenolol, may be helpful to control adrenergic symptoms Radioiodine causes progressive destruction of thyroid cells