Thyroid-benign-2003-0514 - Benign Thyroid Disease Benign...

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Unformatted text preview: Benign Thyroid Disease Benign Thyroid Disease Sarah Rodriguez, MD Francis Quinn, MD Benign Thyroid Disease Benign Thyroid Disease Benign Nontoxic Conditions Benign Toxic Conditions Diffuse and Nodular Goiter Toxic Multinodular Goiter Graves’ Disease Toxic Adenoma Inflammatory Conditions Chronic (Hashimoto’s) Thyroiditis Subacute (De Quervain’s) Thyroiditis Riedel’s Thyroiditis Anatomy Anatomy Anatomy Anatomy Histology Histology Thyroid Hormone Synthesis Thyroid Hormone Synthesis 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 Hypothalamic Pituitary Axis Hypothalamic Pituitary Axis Effects of Thyroid Hormone Effects of Thyroid Hormone 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 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 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 Flow­Volume Loop Flow­Volume Loop Tracheal Compression Tracheal Compression Gross and Microscopic Pathology Gross and Microscopic Pathology Multinodular Goiter Treatment of Diffuse or Treatment of Diffuse or Multinodular Goiter Suppressive Therapy Antithyroid Medications: Propylthiouracil and Methimazole I­131 Surgical Therapy Graves’ Disease 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 Presentation of Graves’ Disease Presentation of Graves’ Disease Thyrotoxicosis: palpitations, nervousness, easy fatigability, diarrhea, excessive sweating, intolerance to heat, weight loss Eye signs Diffuse goiter Graves’ Ophthalmopathy 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 Graves’ Gross and Microscopic Graves’ Gross and Microscopic Pathology Treatment Treatment Antithyroid Drugs Radioactive iodine May require prolonged therapy May worsen ophthalmopathy unless followed by steroids Surgery Make patient euthyroid prior to surgery Potassium iodide two weeks prior to surgery can decrease the vascularity of the gland Thyrotoxicosis and Thyroid Storm Thyrotoxicosis and Thyroid Storm Acute thyrotoxicosis: beta­blockers, barbiturates, cholestyramine Thyroid storm: manage aggressively with beta­blockers, calcium channel blockers, PTU, methimazole, sodium iodide, digitalis or diuretics for heart failure, fluid and electrolyte management Toxic Adenoma Toxic Adenoma Autonomously functioning thyroid nodule hypersecreting T3 and T4 resulting in thyrotoxicosis (Plummer’s disease) Almost never malignant Manage with antithyroid drugs followed by either I­131 or surgery Chronic Thyroiditis Chronic Thyroiditis Also known as Hashimoto’s disease Probably the most common cause of hypothyroidism in United States Autoantibodies include: thyroglobulin antibody, thyroid peroxidase antibody, TSH receptor blocking antibody Gross and Microscopic Pathology Gross and Microscopic Pathology of Chronic Thyroiditis Presentation and Course Presentation and Course 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 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 Treatment of Subacute Thyroiditis Treatment of Subacute Thyroiditis Symptomatic: NSAIDS or a glucocorticoid Beta­blockers indicated if there are signs of thyrotoxicosis Levothyroxine may be given during hypothyroid phase Histopathology of Subacute Histopathology of Subacute Thyroiditis Riedel’s Thyroiditis Riedel’s Thyroiditis Rare disorder usually affecting middle­ aged women Likely autoimmune etiology Fibrous tissue replaces thyroid gland Patients present with a rapidly enlarging hard neck mass Histopathology of Riedel’s Histopathology of Riedel’s Thyroiditis Sources (photographs and figures) Sources (photographs and figures) Netter FH. Atlas of Human Anatomy 2nd ed. Novartis 1997. Plate 68 and 70. Braverman LE and Utiger RD. Werner and Ingbar’s 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 10­12, Fig 10­13, Fig 10­14, Fig 10­16, Fig 10­17, Fig 10­19 Burkitt HG, Young B and Heath JW. Wheater’s 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 7­5, Fig 7­21 ...
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