HyperthyroidismHypothyroidism

Dr. Meg-angela Christi Amores

Thyroid Hormones

• Thyroxine (T4)• Triiodothyronine (T3)• Secreted by the THYROID G:AMD

• Regulated by the PITUITARY GLAND• TSH – secreted by the PITUITARY GLAND

Normal levels

• T4 = • T3 =• TSH

• T4 and T3 greater than normal: HYPERTHYROIDISM

• T4 and T3 lesser than normal: HYPOTHYROIDISM

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

Organification, Coupling, Storage, Release

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

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

Hypothyroidism

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

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

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)

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

Atrophic thyroiditis

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

Hypothyroidism• Clinical manifestations

Laboratory Evaluation

• TSH level• T4 level

• Circulating unbound T3 levels are normal in about 25% of patients

• elevated cholesterol and triglycerides, and anemia

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

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

Hyperthyroidism

• Causes:– Graves' disease– Toxic multinodular goiter– 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)

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

Graves Disease

• Clinical manifestations

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