Benign Thyroid Disease: Sarah Rodriguez, MD Francis Quinn, MD
Benign Thyroid Disease: Sarah Rodriguez, MD Francis Quinn, MD
Benign Thyroid Disease: Sarah Rodriguez, MD Francis Quinn, MD
Diffuse and Nodular Goiter Toxic Multinodular Goiter Graves Disease Toxic Adenoma
Inflammatory Conditions
Anatomy
Anatomy
Histology
1. Iodide trapping 2. Oxidation of iodide and iodination of thyroglobulin 3. Coupling of iodotyrosine molecules within thyroglobulin (formation of T3 and T4) 4. Proteolysis of thyroglobulin 5. Deiodination of iodotyrosines 6. Intrathyroidal deiodination of T4 to T3
Fetal brain and skeletal maturation Increase in basal metabolic rate Inotropic and chronotropic effects on heart Increases sensitivity to catecholamines Stimulates gut motility Increase bone turnover Increase in serum glucose, decrease in serum cholesterol
Goitrogenesis
Iodine deficiency results in hypothyroidism Increasing TSH causes hypertrophy of thyroid (diffuse nontoxic goiter) Follicles may become autonomous; certain follicles will have greater intrinsic growth and functional capability (multinodular goiter) Follicles continue to grow and function despite decreasing TSH (toxic multinodular goiter) Sporadic vs. endemic goiter
Presentation
Usually picked up on routine physical exam or as incidental finding Patients may have clinical or subclinical thyrotoxicosis Patients may have compressive symptoms: tracheal, vascular, esophageal, recurrent laryngeal nerve
Flow-Volume Loop
Tracheal Compression
Suppressive Therapy Antithyroid Medications: Propylthiouracil and Methimazole I-131 Surgical Therapy
Graves Disease
Most common form of thyrotoxicosis Autoimmune etiology with familial predisposition Thyroid receptor stimulating antibody unique to Graves disease; other autoantibodies present (TgAb, TPOAb) Affects females five times more often than males
Thyrotoxicosis: palpitations, nervousness, easy fatigability, diarrhea, excessive sweating, intolerance to heat, weight loss Eye signs Diffuse goiter
Graves Ophthalmopathy
Class one: spasm of upper lids with thyrotoxicosis Class two: periorbital edema and chemosis Class three: proptosis Class four: extraocular muscle involvement Class five: corneal involvement Class six: loss of vision due to optic nerve involvement
Treatment
Antithyroid Drugs
Radioactive iodine
Surgery
Acute thyrotoxicosis: beta-blockers, barbiturates, cholestyramine Thyroid storm: manage aggressively with beta-blockers, calcium channel blockers, PTU, methimazole, sodium iodide, digitalis or diuretics for heart failure, fluid and electrolyte management
Toxic Adenoma
Autonomously functioning thyroid nodule hypersecreting T3 and T4 resulting in thyrotoxicosis (Plummers disease) Almost never malignant Manage with antithyroid drugs followed by either I-131 or surgery
Chronic Thyroiditis
Also known as Hashimotos disease Probably the most common cause of hypothyroidism in United States Autoantibodies include: thyroglobulin antibody, thyroid peroxidase antibody, TSH receptor blocking antibody
Painless goiter in a patient who is either euthyroid or mildly hypothyroid Low incidence of permanent hypothyroidism May have periods of thyrotoxicosis Treat with levothyroxine
Subacute Thyroiditis
Also known as De Quervain's thyroiditis Most common cause of thyroid pain and tenderness Acute inflammatory disease most likely due to viral infection Transient hyperthyroidism followed by transient hypothyroidism; permanent hypothyroidism or relapses are uncommon
Symptomatic: NSAIDS or a glucocorticoid Beta-blockers indicated if there are signs of thyrotoxicosis Levothyroxine may be given during hypothyroid phase
Riedels Thyroiditis
Rare disorder usually affecting middleaged women Likely autoimmune etiology Fibrous tissue replaces thyroid gland Patients present with a rapidly enlarging hard neck mass
Netter FH. Atlas of Human Anatomy 2nd ed. Novartis 1997. Plate 68 and 70. Braverman LE and Utiger RD. Werner and Ingbars The Thyroid A Fundamental and Clinical Text. 8th ed. Lippincott Williams and Wilkins 2000. Fig 76.1, Fig 76.2, Fig 29.16 Damjanov I and Linder J. Pathology A Color Atlas. Mosby 2000. Fig 10-12, Fig 10-13, Fig 10-14, Fig 10-16, Fig 10-17, Fig 10-19 Burkitt HG, Young B and Heath JW. Wheaters Functional Histology A Text and Color Atlas. Churchill Livingstone 1993. Fig 17.7 Greenspan FS and Gardner DG. Basic and Clinical Endocrinology 6th ed. Lange 2001. Fig 7-5, Fig 7-21