Hyperthyroidism PDF

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 13: Altered Hormonal and Metabolic Regulation Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathoph...

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 13: Altered Hormonal and Metabolic Regulation Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lecture Series Copyright © 2017 Wolters Kluwer Health | Lippincott Williams &Wilkins  Hyperthyroidism Pathophysiology Clinical manifestations Diagnostic criteria Treatment  Thyroid Hormone Function Major metabolic hormone and affects virtually every cell in body Increases metabolic rate for energy production Heat production Thyroid hormone release: (calorigenic effect → body temp regulation) Increased glucose absorption Glucose production Release of lipids from adipose tissue Promoting tissue growth and development Metabolism of proteins from muscle tissue Increased cholesterol breakdown in the liver Mental development and sexual Increased production of metabolic by-products Maintenance of blood pressure: Increased oxygen consumption ↑ heart rate and cardiac output Increased body heat production Increased cardiac output Increased gastric motility Increased muscle tone and reactivity Increased activation of cognitive processes  Thyroid Hormone Function Thyroid hormone is actually two related compounds T4 (thyroxine); has 2 tyrosine molecules + 4 bound iodine atoms T3 (triiodothyronine); has 2 tyrosine molecules + 3 bound iodine atoms T3 >>> T4 (10 times more active) T4 converted to T3 at target cells ↑TRH  Thyroid Hormone Function Negative feedback regulation of TH release Changing TH levels provide negative feedback inhibition on release of TSH and TRH Hypothalamic thyrotropin-releasing hormone (TRH) can overcome negative feedback during pregnancy or exposure to cold Cold is one of the strongest stimuli for increased thyroid hormone production McCance KL, Huether S. Pathophysiology. 7th ed. N.S.W, Mosby; 2015  Hyperthyroidism Pathophysiology Thyrotoxicosis: hypermetabolic state caused by elevated circulating levels of free T3 and T4 Hyperthyroidism is the most common form of thyrotoxicosis As a result: the two terms are often used interchangeably 5 Condition of excess thyroid hormone due to Primary hyperthyroidism: Excess stimulation of thyroid gland (1) Disease of the thyroid gland (2, 3) Iodine-induced hyperthyroidism (4) External sources with large amount of iodine: medications, food supplements Secondary hyperthyroidism: Excess production of TSH by pituitary adenoma (5) McCance KL, Huether S. Pathophysiology. 7th ed. N.S.W, Mosby; 2015  Hyperthyroidism Pathophysiology Strayer D, Rubin E. Rubin's Pathology: Clinicopathologic Foundations of Medicine. 7th ed. UK, Wolters Kluwer/Lippincott Williams & Wilkins; 2014 Graves disease is most common form of hyperthyroidism: excessive stimulation 50-80% of cases More common in women (7-10x) Autoimmune disease: IgG binds to TSH receptors Cause unknown Genetic (family, gender) Environmental (smoking, stress) Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby;2011  Hyperthyroidism Pathophysiology Thyrotoxic crisis (thyroid storm) Acute worsening of thyrotoxic state High fever, extreme cardiovascular effects, extreme CNS effects (delirium) High mortality rate: death can occur within 48 hours Spontaneous cause Patients with hyperthyroidism Stress from other causes: Infection, trauma, burns, injury, thyroid surgery, emotional distress Rapid diagnosis and treatment required  Hyperthyroidism Clinical Manifestations Goiter: enlargement of thyroid gland – follicular epithelial cell hyperplasia Excess metabolic rate: heat intolerance, weight loss Increased tissue sensitivity to sympathetic stimulation of ANS: agitation, palpitations, tachycardia, sweating, oily skin Increased neuromuscular effects: weakness, tremors Increased cardiorespiratory functions: increased ventilation, cardiac output Increased gastrointestinal functions: diarrhea Exophthalmos (a protrusion of the eyeballs in Graves Disease) Pretibial myxedema (subcutaneous swelling in Graves Disease) Treatment does not reverse these McCance KL, Huether S. Pathophysiology. 7th ed. N.S.W, Mosby; 2015  Hyperthyroidism Diagnostic Criteria History and physical examination Patient family history of autoimmune disease: Graves Thyroid disease Emigration from iodine deficient location Laboratory tests Primary hyperthyroidism (problem with thyroid gland) decreased TSH due to high thyroid hormone level (feedback loop) increased T3 and T4 levels Secondary (pituitary tumor secretes TSH): normal to increased level of TSH Serum free thyroxine level (not bound to globulins) and Increased uptake of radioactive iodine by the thyroid gland confirms diagnosis Ability of gland to remove and concentrate iodine Imaging studies (differentiate cyst from solid lesions) Needle biopsy to differentiate benign from malignant disease  Hyperthyroidism Treatment Main goal: to reduce thyroid hormone level (production or secretion) to block action of hormone Destruction of all or part of gland with radioactive iodine Surgical removal of all or part of gland Lifelong thyroid hormone replacement therapy Pharmacologic treatment to block thyroid hormone production Main complications for all treatment approach: hypothyroidism