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Hyperthyroidism Hypothyroidism

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  1. HyperthyroidismHypothyroidism 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

  5. Organification, Coupling, Storage, Release

  6. 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

  7. 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

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

  9. Diagnosis and Treatment • Diagnosis • neonatal screening programs • based on measurement of TSH or T4 levels in heel-prick blood specimens • Treatment • T4 is instituted at a dose of 10–15 g/kg per day, and the dose is adjusted by close monitoring of TSH levels. T4 requirements are relatively great during the first year of life • Early treatment with T4 results in normal IQ levels

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

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

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

  13. Hypothyroidism • Clinical manifestations

  14. Laboratory Evaluation • TSH level • T4 level • Circulating unbound T3 levels are normal in about 25% of patients • elevated cholesterol and triglycerides, and anemia

  15. 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 (T4) daily • dose is adjusted on the basis of TSH levels • measured about 2 months after instituting treatment

  16. 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

  17. Hyperthyroidism • Causes: • Graves' disease • Toxic multinodulargoiter • Toxic adenoma • Functioning thyroid carcinoma metastases • Activating mutation of the TSH receptor • Activating mutation of Gsa (McCune-Albright syndrome) • Struma ovarii • Drugs: iodine excess (Jod-Basedow phenomenon)

  18. 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

  19. Graves Disease • Clinical manifestations

  20. Treatment • reducing thyroid hormone synthesis, using antithyroid drugs • reducing the amount of thyroid tissue with radioiodine (131I) 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