Hyperthyroidism Etiology Levin Avi

Clinical Exam. of Thyroid  Have patient seated on a stool / chair  Inspect neck before & after swallowing  Examine with neck in relaxed position  Palpate from behind the patient  Use the tips of fingers for palpation  Palpate firmly down to trachea

Where to look for Thyroid ?

Clinical Anatomy of Thyroid

What is Hyperthyroidism Hyperthyroidism refers to over activity of the thyroid gland leading to excessive synthesis of thyroid hormones thyroxine (T4), triiodothyronine (T3), and acceleratedthyroxine triiodothyronine metabolism in the peripheral tissues.

Etiology 1 Grave’s disease Autoimmune disease caused by antibodies to TSH receptors Can be familial and associated with other autoimmune diseases The most important autoantibodys are: Thyroid Stimulating Immunoglobulin (TSI) or TSA TSI acts as proxy to TSH and stimulates T 4 and T 3 Anti thyro globulin (anti-TG) Anti Microsomal and other Anti thyro peroxidase (anti-TPO) antibodies

Graves Disease I 123 or TC 99m Normal v/s Graves

Etiology 2 Toxic multi-nodular goiter 5% of all cases 10 times more common in iodine deficient area Typically occurs in older than 40 with long standing goiter

Etiology 3 Toxic adenoma More common in young patients Autonomically functioning nodule Plummer's disease is named after the American physician Henry Stanley Plummer but refers to a single toxic nodule (adenoma) which may present with the background of a suppressed multinodular goitre

Etiology 4 Thyroiditis Subacute Known as silent thyroiditis or painless thyroiditis. Abrupt onset due to leakage of hormones Follows viral infection Resolves within eight months Can re-occur Lymphatic and postpartum-De Quervain's thyroiditis Transient inflammation-Viral causes include Coxsackie virus, mumps and adenoviruses Postpartum can occur in 5-10% cases in the first 3-6 months Transient hypothyroidism occurs before resolution

Hashimoto's thyroiditis Autoimmune disease believed to be the most common cause of primary hypothyroidism in North America- An average of 1 to 1.5 in a 1000 people Various autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors. may be associated with the HLA-DR5 gene and with CTLA-4 gene since the CTLA-4 antigen acts as an inhibitor to T-Cell activation.

Hashimoto ’ s Thyroiditis Identical male twins with Hashimoto's thyroiditis were photographed at age 12. At age 8, they had the same height and appearance. During the intervening 4 years, small goiters developed and the growth of the twin on the right almost stopped. Biopsy indicated Hashimoto's thyroiditis in each twin's thyroid.

Etiology 5 Treatment Induced Hyperthyroidism Iodine Induced Excess iodine indirect Exposure to radiographic contrast media Medication Excess iodine increases synthesis and release of thyroid hormone in iodine deficient and older patients with pre-existing goiters

Etiology Amiodarone Induced Thyroiditis Up to 12% of patients, especially in iodine deficient cases Most common cause of iodine excess in US. Two types: *Type I - due to excess iodine Amiodarone contains 37% iodine. *Type II –– occurs in normal thyroid

Etiology Thyroid Hormone Induced Hyperthyroidism in accidental or intentional ingestion to lose weight- oral consumption of excess thyroid hormone tablets as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone "hamburger hyperthyroidism" Tumors -Metastatic thyroid cancer -Ovarian tumor that produces thyriod hormone (struma ovarii) -Trophoblastic tumor -TSH secreting tumor

Postpartum thyroiditis It affects about 5% of all women within a year after giving birth may involve hyperthyroidism, hypothyroidism or the two sequentially-The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism believed to result from the modifications to the immune system necessary in pregnancy. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism

Clinical Presentations

MNG and Graves Huge Toxic MNGDiffuse Graves Thyroid

Grade IV Toxic MNG Huge Toxic MNG

Exophthalmos Thyroid Ophthalmopathy

Ophthalmopathy in Graves Periorbital edema and chemosis

Ophthalmopathy in Graves Occular muscle palsy

Thyroid Dermopathy Pink and skin coloured papules, plaques on the shin

Graves with Acropathy Graves GoiterAcropathy

subperiosteal new bone formation Clubbing and Osteoarthropathy Thyroid Acropathy

Onycholysis-nail detachment