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. -
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. -
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. -
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. -
Thyroid Disease
Thyroid Disease Thyroid disease occurs when the thyroid (a small, butterfly-shaped gland in the front of your neck) does not produce the right amount of thyroid hormone. These hormones control how your body uses energy. If you are feeling fatigued, notice skin or hair changes, or have hoarseness or pain, your doctor may conduct a physical exam and order blood tests. If these tests indicate a problem, your doctor may order thyroid scan and uptake, thyroid biopsy, or imaging tests to help diagnose and evaluate a thyroid condition. Treatment will depend on the specific nature of your thyroid condition and its underlying cause. What is thyroid disease? The thyroid is a small, butterfly-shaped gland in the front of your neck that wraps around your windpipe (trachea). The two halves of the thyroid gland are connected in the middle by a thin layer of tissue known as the isthmus. The thyroid gland uses iodine (mostly absorbed from food) to produce hormones that control how your body uses energy. Nearly every organ in the body is affected by the function of the thyroid gland. The pituitary gland and hypothalamus, an area at the base of the brain, control the rate at which the thyroid produces and releases these hormones. The main function of the thyroid gland is to release a hormone called thyroxine or T4, which is converted into a hormone called T3. Both of these hormones circulate in the bloodstream and help regulate your metabolism. The amount of T4 produced by the thyroid gland is determined by a hormone produced by the pituitary gland called TSH or thyroid-stimulating hormone. -
Hypothyroidism and Resistance to Thyroid Hormone Panel
Hypothyroidism and Resistance to Thyroid Hormone Panel Test code: EN0701 Is a 22 gene panel that includes assessment of non-coding variants. Is ideal for patients with a clinical suspicion of congenital hypothyroidism or thyroid hormone resistance. About Hypothyroidism and Resistance to Thyroid Hormone Primary congenital hypothyroidism is a permanent thyroid hormone deficiency that is present from birth. About 1 in 5,000 babies is born with congenital hypothyroidism, in which the thyroid fails to grow normally and cannot produce enough hormone. There is no identifiable cause for most cases of congenital hypothyroidism but in 15-20% are caused by an inherited defect in genes that play a role in the proper growth, function and development of the thyroid gland. Primary congenital hypothyroidism may be due to a thyroid dysgenesis where the thyroid gland fails to develop normally or it may occur as a result of an inborn error of thyroid hormone biosynthesis (also known as dyshormonogenesis) or as a result of thyroid- stimulating hormone (TSH) receptor mutations. In iodine sufficient countries, 85% of permanent congenital hypothyroidism is due to thyroid dysgenesis. The remaining 10-15% of cases can be attributed to dyshormonogenesis or to defects in peripheral thyroid hormone transport, metabolism or action. Primary congenital hypothyroidism may also be idiopathic. The prevalence is estimated at 1:2,000-1:4,000. For reasons that remain unclear, congenital hypothyroidism affects more than twice as many females as males. Thyroid dyshormonogenesis results from mutations in one of the several genes involved in the production of thyroid hormones. These genes include DUOX2, SLC5A5, TG, and TPO. -
Primary Hyperparathyroidism
Primary Hyperparathyroidism The parathyroid glands are 4 glands that reside within the thyroid glands: there are two parathyroid glands attached to each thyroid gland. The thyroid/parathyroid glands lie on either side of the trachea (wind pipe) about midway down the neck. The job of the parathyroid glands is to regulate calcium in the body. They secrete a hormone called parathyroid hormone (PTH), and this hormone draws calcium out of the bone where it is stored, as well as acting on the kidney and intestine to increase blood calcium. This is a normal process in response to fluctuations in blood calcium levels. The calcium in the blood is regulated by PTH (increases blood calcium) and calcitonin (a hormone secreted by the thyroid gland to decrease calcium) in order to keep it within a normal range. When the calcium gets too high or too low, symptoms arise. The most common symptoms of high calcium are increased thirst and urination. Other signs include: lethargy, weakness, diarrhea, inappetance, weight loss, tremors or stiffness. In about 50% of dogs with high calcium, urinary stones +/- urinary tract infection is present. Tumors (enlargement) of the parathyroid gland are typically not malignant, but they do over-secrete PTH. In 90% of cases only one of the four glands is enlarged. By one gland enlarging and over-secreting PTH, the three other glands typically shrink and temporarily stop functioning. Parathyroid tumors are suspected based on consistent blood work that shows elevated or normal PTH in the face of elevated calcium (the normal feedback mechanism would mean that when calcium is high, PTH is not needed and therefore is low). -
Hypothyroidism and Pregnancy: What Should I Know?
Fact Sheet From ReproductiveFacts.org The Patient Education Website of the American Society for Reproductive Medicine Hypothyroidism and pregnancy: what should I know? What is hypothyroidism? to protect you against bacterial and viral infections. Sometimes, Hypothyroidism (underactive thyroid) is when the thyroid gland however, the immune system can make antibodies against produces less thyroid hormone than it should. The thyroid gland is your own body—such as against your thyroid. T4 is a hormone found in the lower part of the throat and partially wraps around the produced directly by the thyroid gland. It is typically low in patients upper windpipe (trachea). with hypothyroidism. An autoantibody is an antibody that attacks the cells and tissues of the organism that made it. Thyroid What does the thyroid gland do? autoantibodies are seen in patients with Hashimoto’s (autoimmune) The thyroid gland produces two hormones: triiodothyronine (T3) thyroiditis. and thyroxine (T4). These hormones play an important role in metabolism. Metabolism is the body’s ability to transform food How does hypothyroidism affect my fertility and into energy. The thyroid gland is controlled (regulated) by thyroid- my baby if I become pregnant? stimulating hormone (TSH). TSH is produced by the pituitary gland, Hypothyroidism can prevent the release of the egg from the ovary which is located in the brain. (ovulation). Typically, for women who have periods (menstruate) each month, an egg is released from the ovary each month. What are the symptoms of hypothyroidism? But women who have hypothyroidism may release an egg less When the thyroid gland produces less thyroid hormone than it frequently or not at all.