Hypothyroidism
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Hashimoto's Thyroiditis
AMERICAN THYROID ASSOCIATION® www.thyroid.org Hashimoto’s Thyroiditis (Lymphocytic Thyroiditis) WHAT IS THE THYROID GLAND? HOW IS THE DIAGNOSIS OF HASHIMOTO’S The thyroid gland is a butterfly-shaped endocrine gland THYROIDITIS MADE? that is normally located in the lower front of the neck. The diagnosis of Hashimoto’s thyroiditis may be made The thyroid’s job is to make thyroid hormones, which are when patients present with symptoms of hypothyroidism, secreted into the blood and then carried to every tissue often accompanied by a goiter (an enlarged thyroid in the body. Thyroid hormones help the body use energy, gland) on physical examination, and laboratory testing of stay warm and keep the brain, heart, muscles, and other hypothyroidism, which is an elevated thyroid stimulating organs working as they should. hormone (TSH) with or without a low thyroid hormone (Free WHAT IS HASHIMOTO’S THYROIDITIS? thyroxine [Free T4]) levels. TPO antibody, when measured, is usually elevated. The term “Thyroiditis” refers to “inflammation of the thyroid gland”. There are many possible causes of thyroiditis (see Occasionally, the disease may be diagnosed early, Thyroiditis brochure). Hashimoto’s thyroiditis, also known especially in people with a strong family history of thyroid as chronic lymphocytic thyroiditis, is the most common disease. TPO antibody may be positive, but thyroid cause of hypothyroidism in the United States. It is an hormone levels may be normal or there may only be autoimmune disorder involving chronic inflammation of isolated mild elevation of serum TSH is seen. Symptoms of the thyroid. This condition tends to run in families. Over hypothyroidism may be absent. -
Thyroid Hormones in Fetal Growth and Prepartum Maturation
A J FORHEAD and A L FOWDEN Thyroid hormones and fetal 221:3 R87–R103 Review development Thyroid hormones in fetal growth and prepartum maturation A J Forhead1,2 and A L Fowden1 Correspondence should be addressed 1Department of Physiology, Development and Neuroscience, University of Cambridge, Physiology Building, to A L Fowden Downing Street, Cambridge CB2 3EG, UK Email 2Department of Biological and Medical Sciences, Oxford Brookes University, Oxford OX3 0BP, UK [email protected] Abstract The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are essential for normal Key Words growth and development of the fetus. Their bioavailability in utero depends on " thyroid hormones development of the fetal hypothalamic–pituitary–thyroid gland axis and the abundance " intrauterine growth of thyroid hormone transporters and deiodinases that influence tissue levels of bioactive " maturation hormone. Fetal T4 and T3 concentrations are also affected by gestational age, nutritional and " neonatal adaptation endocrine conditions in utero, and placental permeability to maternal thyroid hormones, which varies among species with placental morphology. Thyroid hormones are required for the general accretion of fetal mass and to trigger discrete developmental events in the fetal brain and somatic tissues from early in gestation. They also promote terminal differentiation of fetal tissues closer to term and are important in mediating the prepartum maturational effects of the glucocorticoids that ensure neonatal viability. Thyroid hormones act directly through anabolic effects on fetal metabolism and the stimulation of fetal oxygen Journal of Endocrinology consumption. They also act indirectly by controlling the bioavailability and effectiveness of other hormones and growth factors that influence fetal development such as the catecholamines and insulin-like growth factors (IGFs). -
Beyond the Fixed Setpoint of the Hypothalamus–Pituitary–Thyroid Axis
E Fliers and others Hypothalamus–pituitary– 171:5 R197–R208 Review thyroid axis MECHANISMS IN ENDOCRINOLOGY Beyond the fixed setpoint of the hypothalamus–pituitary–thyroid axis Eric Fliers1, Andries Kalsbeek1,2 and Anita Boelen1 Correspondence should be addressed 1Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, 1105 AZ to E Fliers Amsterdam, The Netherlands and 2Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Email Amsterdam, The Netherlands e.fl[email protected] Abstract The hypothalamus–pituitary–thyroid (HPT) axis represents a classical example of an endocrine feedback loop. This review discusses dynamic changes in HPT axis setpoint regulation, identifying their molecular and cellular determinants, and speculates about their functional role. Hypothalamic thyrotropin-releasing hormone neurons were identified as key components of thyroid hormone (TH) setpoint regulation already in the 1980s, and this was followed by the demonstration of a pivotal role for the thyroid hormone receptor beta in negative feedback of TH on the hypothalamic and pituitary level. Gradually, the concept emerged of the HPT axis setpoint as a fixed entity, aiming at a particular TH serum concentration. However, TH serum concentrations appear to be variable and highly responsive to physiological and pathophysiological environmental factors, including the availability or absence of food, inflammation and clock time. During food deprivation and inflammation, TH serum concentrations decrease without a concomitant rise in serum TSH, reflecting a deviation from negative feedback regulation in the HPT axis. Surprisingly, TH action in peripheral organs in these conditions cannot be simply predicted by decreased serum TH concentrations. Instead, diverse environmental stimuli have differential effects on local TH metabolism, e.g. -
Study Guide Medical Terminology by Thea Liza Batan About the Author
Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails proficiencyincommunicatingwithhealthcareprofessionalssuchasphysicians,nurses, or dentists. -
Endocrinology Review – Adrenal and Thyroid Disorders
FOCUS: ENDOCRINOLOGY Endocrinology Review – Adrenal and Thyroid Disorders LINDA S. GORMAN, JANELLE M. CHIASERA LEARNING OBJECTIVES This article represents the first of three articles focusing 1. Define endocrinology and list the major endocrine on the endocrine system. The first article will provide glands of the body. you with fundamental theory regarding the endocrine system that will serve as a basis for understanding the 2. Explain how feedback (positive and negative) Downloaded from promotes maintenance of normal levels of next two articles focusing on two specific endocrine hormones. glands, the thyroid and adrenal glands. 3. Differentiate between steroid and peptide hormones with regard to their mechanism of Endocrinology is the branch of medical science that action. deals with the endocrine system, a system that consists 4. Provide examples of peptide and steroid hormones. of several glands located in different parts of the body http://hwmaint.clsjournal.ascls.org/ 5. Explain how endocrine disorders are categorized. that secrete hormones directly into the bloodstream. Although every organ system in the body may respond ABBREVIATIONS: ACTH - adrenocorticotropic hor- to hormones, endocrinology focuses specifically on mone; ADH - antidiuretic hormone; CRH – cortico- endocrine glands whose primary function is hormone tropin releasing hormone; DHEA – dehydroepian- secretion. Major endocrine glands include the pituitary drosterone; FSH - follicle stimulating hormone; GHRH (anterior and posterior), hypothalamus, thyroid, - growth hormone -
Thyroiditis: an Integrated Approach LORI B
Thyroiditis: An Integrated Approach LORI B. SWEENEY, MD, Virginia Commonwealth University Health System, Richmond, Virginia CHRISTOPHER STEWART, MD, Bayne-Jones Army Community Hospital, Fort Polk, Louisiana DAVID Y. GAITONDE, MD, Dwight D. Eisenhower Army Medical Center, Fort Gordon, Georgia Thyroiditis is a general term that encompasses several clinical disorders characterized by inflammation of the thyroid gland. The most common is Hashimoto thyroiditis; patients typically present with a nontender goiter, hypothyroid- ism, and an elevated thyroid peroxidase antibody level. Treatment with levothyroxine ameliorates the hypothyroid- ism and may reduce goiter size. Postpartum thyroiditis is transient or persistent thyroid dysfunction that occurs within one year of childbirth, miscarriage, or medical abortion. Release of preformed thyroid hormone into the bloodstream may result in hyperthyroidism. This may be followed by transient or permanent hypothyroidism as a result of depletion of thyroid hormone stores and destruction of thyroid hormone–producing cells. Patients should be monitored for changes in thyroid function. Beta blockers can treat symptoms in the initial hyperthyroid phase; in the subsequent hypothyroid phase, levothyroxine should be considered in women with a serum thyroid-stimulating hormone level greater than 10 mIU per L, or in women with a thyroid-stimulating hormone level of 4 to 10 mIU per L who are symptomatic or desire fertility. Subacute thyroiditis is a transient thyrotoxic state characterized by anterior neck pain, suppressed thyroid-stimulating hormone, and low radioactive iodine uptake on thyroid scanning. Many cases of subacute thyroiditis follow an upper respiratory viral illness, which is thought to trigger an inflammatory destruction of thyroid follicles. In most cases, the thyroid gland spontaneously resumes normal thyroid hormone production after several months. -
Treating Thyroid Disease: a Natural Approach to Healing Hashimoto's
Treating Thyroid Disease: A Natural Approach to Healing Hashimoto’s Melissa Lea-Foster Rietz, FNP-BC, BC-ADM, RYT-200 Presbyterian Medical Services Farmington, NM [email protected] Professional Disclosures I have no personal or professional affiliation with any of the resources listed in this presentation, and will receive no monetary gain or professional advancement from this lecture. Talk Objectives • Define hypothyroidism and Hashimoto’s. • Discuss various tests used to identify thyroid disease and when to treat based on patient symptoms • Discuss potential causes and identify environmental factors that contribute to disease • Describe how the gut (food sensitivities) and the adrenals (chronic stress) are connected to Hashimoto’s and how we as practitioners can work to educate patients on prevention before the need for treatment • How the use of adaptogens can enhance the treatment of Hashimoto’s and identify herbs that are showing promise in the research. • How to use food, exercise, and relaxation to improve patient outcomes. Named for Hakuro Hashimoto, a physician working in Europe in the early 1900’s. Hashimoto’s was the first autoimmune disease to be recognized in the scientific literature. It is estimated that one in five people suffer from an autoimmune disease and the numbers continue to rise. Women are more likely than men to develop an autoimmune disease, and it is believed that 75% of individuals with an autoimmune disease are female. Thyroid autoimmune disease is the most common form, and affects 7-8% of the population in the United States. Case Study Ms. R is a 30-year-old female, mother of three, who states that after the birth of her last child two years ago she has felt the following: • Loss of energy • Difficulty losing weight despite habitual eating pattern • Hair loss • Irregular menses • Joints that ache throughout the day • A general sense of sadness • Cold Intolerance • Joint and Muscle Pain • Constipation • Irregular menstruation • Slowed Heart Rate What tests would you run on Ms. -
Hashimoto Thyroiditis
Hashimoto thyroiditis Description Hashimoto thyroiditis is a condition that affects the function of the thyroid, which is a butterfly-shaped gland in the lower neck. The thyroid makes hormones that help regulate a wide variety of critical body functions. For example, thyroid hormones influence growth and development, body temperature, heart rate, menstrual cycles, and weight. Hashimoto thyroiditis is a form of chronic inflammation that can damage the thyroid, reducing its ability to produce hormones. One of the first signs of Hashimoto thyroiditis is an enlargement of the thyroid called a goiter. Depending on its size, the enlarged thyroid can cause the neck to look swollen and may interfere with breathing and swallowing. As damage to the thyroid continues, the gland can shrink over a period of years and the goiter may eventually disappear. Other signs and symptoms resulting from an underactive thyroid can include excessive tiredness (fatigue), weight gain or difficulty losing weight, hair that is thin and dry, a slow heart rate, joint or muscle pain, and constipation. People with this condition may also have a pale, puffy face and feel cold even when others around them are warm. Affected women can have heavy or irregular menstrual periods and difficulty conceiving a child ( impaired fertility). Difficulty concentrating and depression can also be signs of a shortage of thyroid hormones. Hashimoto thyroiditis usually appears in mid-adulthood, although it can occur earlier or later in life. Its signs and symptoms tend to develop gradually over months or years. Frequency Hashimoto thyroiditis affects 1 to 2 percent of people in the United States. -
Thyroid and Polycystic Ovary Syndrome
S Gabersˇcˇek and others Thyroid and PCOS 172:1 R9–R21 Review MECHANISMS IN ENDOCRINOLOGY Thyroid and polycystic ovary syndrome Simona Gabersˇcˇek1,2, Katja Zaletel1, Verena Schwetz3, Thomas Pieber3, Barbara Obermayer-Pietsch3 and Elisabeth Lerchbaum3 Correspondence should be addressed to 1Department of Nuclear Medicine, University Medical Centre Ljubljana, Zalosˇka 7, 1525 Ljubljana, Slovenia, B Obermayer-Pietsch 2Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1104 Ljubljana, Slovenia and 3Division of Endocrinology Email and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, barbara.obermayer@ 8036 Graz, Austria medunigraz.at Abstract Thyroid disorders, especially Hashimoto’s thyroiditis (HT), and polycystic ovary syndrome (PCOS) are closely associated, based on a number of studies showing a significantly higher prevalence of HT in women with PCOS than in controls. However, the mechanisms of this association are not as clear. Certainly, genetic susceptibility contributes an important part to the development of HT and PCOS. However, a common genetic background has not yet been established. Polymorphisms of the PCOS-related gene for fibrillin 3 (FBN3) could be involved in the pathogenesis of HT and PCOS. Fibrillins influence the activity of transforming growth factor beta (TGFb). Multifunctional TGFb is also a key regulator of immune tolerance by stimulating regulatory T cells (Tregs), which are known to inhibit excessive immune response. With lower TGFb and Treg levels, the autoimmune processes, well known in HT and assumed in PCOS, might develop. In fact, lower levels of TGFb1 were found in HT as well as in PCOS women carrying allele 8 of D19S884 in the FBN3 gene. -
Vitamin D Status and Its Relationship with Thyroid Function Parameters in Patients with Hypothyroidism
Medical Laboratory Journal, Sep-Oct, 2019; Vol 13: No 5 Original Article Vitamin D Status and its Relationship with Thyroid Function Parameters in Patients with Hypothyroidism Mojtaba Zare Ebrahimabad (MSc) ABSTRACT Department of Biochemistry and Background and Objectives: Vitamin D is an essential secosteroid that plays a Biophysics, Metabolic Disorders Research Center, Faculty of Medicine, crucial role in the homeostasis of a few mineral elements, particularly calcium. Since vitamin Golestan University of Medical D deficiency and thyroid diseases are two important global health problems, we aimed to Sciences, Gorgan, Iran investigate a possible relationship of vitamin D and calcium levels with hypothyroidism in an Hanieh Teymoori (MSc) Department of Biochemistry and Iranian population. Biophysics, Metabolic Disorders Methods: This case-control study was conducted on 175 subjects with Research Center, Faculty of Medicine, hypothyroidism (75 males and 100 females) and 175 euthyroid controls (85 males and 90 Golestan University of Medical Sciences, Gorgan, Iran females) who were referred to a laboratory in Gorgan, Iran. Serum levels of 25- Hamid Reza Joshaghani (PhD) hydroxyvitamin D, calcium, thyroid-stimulating hormone (TSH), free triiodothyronine (free Professor of Clinical Biochemistry, T3) and thyroxine (total T4) were measured in all participants. Laboratory Sciences Research Center (LSRC), Golestan University of Results: Vitamin D and calcium were significantly lower in patients with Medical Sciences, Gorgan, Iran hypothyroidism (P<0.0001). Free T3 and calcium levels differed significantly among Corresponding author: Hamid Reza hypothyroid patients based on their vitamin D status (P<0.0001), but vitamin D levels were Joshaghani Tel: +98-1732436108 within sufficient range in all groups. -
Graves' Disease Following the Occurrence of Hypothyroidism
Henry Ford Hospital Medical Journal Volume 28 Number 2 Richmond W. Smith Jr. Testimonial Article 14 Issue 6-1980 Graves' Disease Following the Occurrence of Hypothyroidism A. R. Guansing D. D. Klink N. Engbring Y. Leung J. Chakravarty See next page for additional authors Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Guansing, A. R.; Klink, D. D.; Engbring, N.; Leung, Y.; Chakravarty, J.; and Wilson, S. (1980) "Graves' Disease Following the Occurrence of Hypothyroidism," Henry Ford Hospital Medical Journal : Vol. 28 : No. 2 . Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol28/iss2/14 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Graves' Disease Following the Occurrence of Hypothyroidism Authors A. R. Guansing, D. D. Klink, N. Engbring, Y. Leung, J. Chakravarty, and S. Wilson This article is available in Henry Ford Hospital Medical Journal: https://scholarlycommons.henryford.com/ hfhmedjournal/vol28/iss2/14 Henry Ford Hosp Med j Vol 28, No 2 and 3, 1980 Graves' Disease Following the Occurrence of Hypothyroidism A. R. Guansing, MD,* D. D. Klink, MD,* N. Engbring, MD,** Y. Leung, MD,*** J. chakravarty, MD,*** and S. Wilson, MD** Three patients with hypothyroidism of 15-48 months' dura negative antithyroglobulin and antimicrosomal antibody tion developed Graves' disease while on thyroid hormone titers. Two had demonstrable long-acting thyroid stimulator replacement therapy. -
The Relationship Between Vitamin D Deficiency and Thyroid Function in the First Trimester of Pregnancy
Original Article The relationship between Vitamin D deficiency and thyroid function in the first trimester of pregnancy Farahnaz Rostami 1, Lida Moghaddam-Benaem2, Navid Ghasemi 3, Sedighe Hantoushzadeh 4* 1Department of Midwifery & Reproductive Health, Faculty of Medical Sciences, Tarbiat Modares University, Al-e-Ahmad Highway, Tehran, Iran. 2 Department of Reproductive Health & Midwifery, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. 3 Department of medicine, faculty of Medical Sciences Tehran, Islamic Azad University, Tehran, Iran.4 Maternal, fetal & Neonatal Research Center, Tehran University of Medical Sciences, Tehran, Iran. Abstract Aims and Objective: There are few studies about the relationship between vitamin D deficiency and thyroid hormone levels in pregnancy. This study aimed to assess the relation serum vitamin D levels with thyroid hormones in the first trimester of pregnancy in Iran. Methods: In this case-control research 430 pregnant women (215 mothers with vitamin D deficiency, and 215 without this deficiency) attending prenatal clinics in Tehran, Iran were studied. 25 hydroxy vitamin D levels and thyroid function tests [free tetraiodothyronine (FT4), thyroid stimulating hormone (TSH), and free triiodothyronine (FT3)] were measured in all mothers. Data were analyzed using SPSS version 22 software. Kolmogorov-Smirnov test was used for normality testing of continuous variables; Student T-Test, and Mann-Whitney U test were used to compare the continuous parametric and nonparametric variables respectively in the 2 study groups; Linear regression model was used to assess the effect of potentially effective variables besides vitamin D on thyroid function tests. Results: In Mann-Whitney U test performed, T4 levels (mean± SD) were significantly higher in vitamin D deficiency group compared with the control group (20.8 ±32.5 vs.14.4 ± 24.1 ng/dl, P-value: 0.04), but there were no significant differences between the 2 study groups regarding TSH, and free T3 levels.