DOCSLIB.ORG

Myxedema Coma in the Elderly

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Myxedema Coma in the Elderly J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from Myxedema Coma In The Elderly (vnthia G. Olsen, M[) Background: Myxedema coma in the elderly, although uncommon, is frequently overlooked and has a high mortality rate. Signs and symptoms are many and are often insidious. Nearly every organ system is involved. Prompt recognition and treatment are mandatory for a successful outcome. Methods: A case study is presented. Using the key words "myxedema" with the word "aged," MEDLINE files were searched from 1989 to present. Articles dating before 1989 were accessed from the reference lists of the more recent articles. Results and Conclusions: This review describes the signs and symptoms of myxedema coma in the elderly. Epidemiology and histopathology of the disorder are discussed. Prompt recognition and emergency medical treatment are essential for a successful outcome. Prevention requires screening of elderly patients at risk for hypothyroidism and assuring thyroid hormone replacement therapy. (J Am Board Fam Pract 1995; 8:376-83.) Myxedema coma, the extreme expression of sodium depletion. A history of thyroidectomy for hypothyroidism, is a medical emergency re­ goiter in the remote past was discovered, and the quiring a high degree of clinical suspicion. The patient had not received thyroid hormone re­ term myxedema was proposed by Ord in 1878 placement therapy. A family history was notable to describe the peculiar nonpitting swelling in that her son had a thyroid goiter. of skin in the hypothyroid adult and has been During the physical examination the woman used interchangeably with hypothyroidism in was obtunded and unable to communicate with the medical literature. 1 Although the actual inci­ the examiner. She weighed 72.7 kg, her tempera­ dence is unknown, myxedema coma is uncom­ ture was 36.3° C, her pulse was ret,Tular at 80 beats mon; only 200 cases were reported between 1953 per minute, respirations were 24/min, and her and 1986.2 The mortality rate in these patients is blood pressure was 178/94 mmHg. On appear­ 50 percent or greater even with immediate thy­ ance her face was swollen, especially about the roid hormone replacement therapy and support­ eyes. Her mucous membranes were dry and the ive measures. Early recognition and intervention tongue was thickened. Neck masses were not can be lifesaving. found. Her skin was cool and doughy in consis­ tency, and there was marked pitting edema of the http://www.jabfm.org/ Illustrative Case lower extremities up to the knees. Lung examina­ A 90-year-old woman who had been residing in a tion demonstrated bilateral pulmonary edema nursing home for several years was brought in for with pleural effusions. The heart had a regular cOllSultation. The nursing staff and family re­ rate and rhythm with a grade IIM systolic ejec­ ported gradually increasing lethargy, depression, tion murmur. Neurologically the patient was and diminished mental alertness. semicomatose. Deep tendon reflexes were dimin­ on 24 September 2021 by guest. Protected copyright. She had a history of cerebrovascular accidents, ished with a slowed response. Rectal examination which precipitated her nursing home admission. found a fecal impaction. The medical chart reflected persistent chronic La bora tory studies discl osed the following hyponatremia unresponsive to fluid restriction. values: sodium 127 mEq/L, potassium 3.9 mEqlL, The patient had increasing pulmonary and pe­ chloride 93 mEqlL, and carbon dioxide 25 mEqlL. ripheral edema as a result of congestive heart fail­ Blood urea nitrogen (BUN) and serum creati­ ure. '[reatment with diuretics had worsened her nine were 17 mg/dL and 0.6 mg/dL, respectively. Serum osmolality was 250 mOsm/kg. Her fast­ ing blood glucose was 128 mg/dL. The serum Submittl'd, ITviSl'd, ~ May 1')');. total protein was 5.8 g/dL, and serum albumin From thl' Department of Family rvkdicillc, V\rright State Uni­ was 3.l g/dL. A complete blood count showed a versity School of Medicine, Dayton, Ohio. Address rl'print re­ mild microcytic, normochromic anemia. A urin­ quests to Cynthia G Olsen, MD, Department of Family Ml'di­ cinc, School of ,Vlcdicine, \Vright St'ltc University, (,27 Edwin alysis was positive for pyuria and bacteriuria. C. .'vloses Boulcvard, Dayton, 011 .:tHOll. Thyroid function studies showed a depressed 37(' JABFP Sept.-Oct.1995 Vol. R No.5 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from thyroxine level of3.0 ,...g/dL and an elevated thy­ Table 1. Precipitating Causes of Myxedema Coma. roid stimulating hormone (TSH) of 53 ,...U/mL. Cause Type An adrenocorticotropic hormone (ACTH) level was normal at 34 pg/mL. A blood gas determina­ Infections Pneumonia tion on 2 L of nasal cannula oxygen revealed aci­ Urinary tract infection dosis with a pH of 7.24, p02 of 118 mmHg, Influenza pC02 of 145 mmHg, and a bicarbonate of 50.4 Drugs mEq/L. A chest radiograph showed marked car­ Sedating Narcotics diomegaly with bilateral pleural effusions. A Phenothiazines two-dimension echo cardiogram showed mild Tranquilizers and barbiturates aortic stenosis and a dilated left ventricle with Other central nervous preserved function. system depressants The patient was hospitalized for myxedema General anesthesia coma caused by untreated hypothyroidism with Cardiac drugs f3- Blockers concurrent metabolic derangement, possible Amiodarone heart failure, and urinary tract infection. She re­ Stressors Surgery ceived intravenous hydrocortisone 75 mg every 6 hours. An initial bolus of 400 mg of synthetic Hospitalization thyroxine was followed by 200 mg on day 2 and Burns 100 mg daily thereafter. She received treatment Trauma of her heart failure with diuretics, supplemental Exposure to cold oxygen and potassium, and digoxin. On day 5 she was switched to oral medications of pred­ to the water-binding capacity of the acid gly­ nisone 10 mg, levothyroxine 125 mg, digoxin 25 cosaminoglycans within the papillary and reticu­ mg, and indapamide 2.5 mg. A follow-up chest lar layers.7 Other changes of the skin that contrib­ radiograph showed resolution of the pulmonary ute to edema in myxedema are increased capillary congestion. permeability, lymphatic obstruction, and perivas­ The patient returned to the nursing home on culitis. Acid glycosaminoglycans are also found in supplemental oxygen. During the next few the tissues of the tongue, myocardium, striated months the patient had an improved level of muscle, and intestines.8 Thyroid hormone re­ alertness and was able to recognize family mem­ placement treatment reduces hyaluronic acid http://www.jabfm.org/ bers. Her cardiac failure improved, and her meta­ concentrations in the skin, whereas the three bolic problems stabilized. other glycosaminoglycans remain unchanged.9 Muscle biopsy in severe myxedema reveals type II Epidemiology muscle fiber loss and atrophy, an increased num­ Myxedema coma occurs almost exclusively during ber of mitochondria, and an accumulation of gly­ or after the 6th decade with 80 percent of the cogen and lipids on the membranes. This effect is on 24 September 2021 by guest. Protected copyright. cases occurring in women.3,4 More than 90 percent also somewhat reversible with treatment. 10 of cases have been reported to have occurred dur­ ing winter months and are frequently associated Clinical Presentations with intercurrent illness or stressors (Table 1). Because the patient is in a coma, the initial diag­ Pneumonia or other infections and sedating drugs nosis is suggested by a history of clinical signs and are common precipitants.4-6 About 50 percent of symptoms of hypothyroidism and a history of myxedema coma patients have lapsed into coma thyroid surgery, high-dose external radiation of after admission to the hospital, probably as the re­ the neck, or discontinuation of thyroid hormone sult of stress caused by diagnostic and therapeutic replacement therapy (Table 2). interventions encountered during hospitalization. In addition to knowing the symptoms preced­ ing the onset of coma, physical findings will also Histopathology aid the physician in making the diagnosis. The The clinical manifestations of myxedema are in- patient typically has periorbital swelling, ptosis, duration and thickening of the skin, attributable and a thickened tongue. Nonpitting edema of the Myxedema Coma 377 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from Table 2. (;linical Signs and Symptoms of Myxedema atony. This serious condition can lead to visceral (;oma. perforation. The resulting colonic ileus can he in­ distinguishahle from mechanical ohstrllction. H (\rea Si~n or Sy1l1pt' 1111 Barium enem,) shows localized transverse thick­ Constitlltion,d, g·eneral Lethargy ening of the colonic haustration. l ) Myxedema \Veight gain or loss megacolon appearing as pseudomembranolls \\'eakness Sleep disturhance colitis and intestinal ischemia is rare. II) Ilypotonia of the esophagus, stomach, duodenum, gallblad­ I lead and neck llearing imp,]innent Obstructive sleep apnea der, and small intestine can also occur. M,]Croglossia The lowered metabolic state in myxedema Periorbital swellin~ coma patients results in bradycardia, slowed res­ Lid ptosis piratory rate, hypothermia, and hypotension. 17 I)erm,](ologic I Llir 10" Coarse, dry skin Shivering is diminished or absent. Hypothermia, I'retihiallllyxedellla common in the aging population, can also he Edema found with hypoglycemia and occasionally septi­ ( ;,]strointestinal Fecal impaction cemia. IH A core temperature of less than 35 .5°C Megacolon occurs in about HO percent of comatose patients. llrologic Bladder atony In fact, a normal temperature in a myxedema Urinary rdention coma patient should be considered relative hyper­ Musculo'ikelctal Muscle hypertrophy thermia. Underlying infection in these patients is Neurologic and psychiatrie Psychosis common and might be the precipitating factor Restlessness Delirium leading to coma. Reduced immune defenses often Dementia obscure the signs of infection. PsychoJl]otor retardation In the severe, chronic hypothyroid patient, the heart can be dilated and the myocardium atonic.
Load more

Recommended publications
  • 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.
    [Show full text]
  • The Subacute Thyroiditis, Since Its First Description by De Quervain (1904), Has Been Reported Under Many Synonyms
    Endocrinol. Japon. 1964, 11 (2), 119～138 STUDIES ON SUBACUTE THYROIDITIS SHOZO SAITO Department of Radiology, School of Medicine, Gunma University, Maebashi The subacute thyroiditis, since its first description by de Quervain (1904), has been reported under many synonyms. Terms given with reference to the histo- logic features of this disease include "pseudotuberculous thyroiditis", "granulo- matous thyroiditis", "gaint-cell thyroiditis", "de Quervain's thyroiditis", "struma granulomatosa" or "struma fibrosa, giant cell variant". The clinical findings have given rise to such names as" acute and subacute nonsuppurative thyroiditis", "acute noninfectious thyroiditis"and"subacute thyroiditis" . In recent writings, the disease is most commonly referred to as subacute thyroiditis. Later, de Quervain and Giordanengo (1936) collected reports of 54 cases of the disease, appearing in the literature since de Quervain's original description, and clearly distinguished it from other forms of thyroiditis. Several years ago, the disease had been considered relatively rare, but with recent advance in endocrinology, more attentions have been drawn by it, and more reports published on it. For the past six years, the author has treated 51 cases of subacute thyroiditis, and obtained findings of interest, which are outlined in this paper. METHODS OF EXAMINATION The disease was confirmed by Silverman's needle biopsy (Crile and Rumsey, 1950; Crile and Hazard, 1951) of the thyroid in 36 of them, and the others were diagnosed by typical clinical symptoms, characteristic results of thyroidal function test and accelerated red cell sedimentation rate and its clinical course. Thyroid function test Basal metabolic rate (BMR) was examined by Knipping's method (normal range•}15%), and serum protein-bound iodine (PBI) by modification of Barker's method (Barker and Humphrey, 1950).
    [Show full text]
  • 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.
    [Show full text]
  • Disease/Medical Condition
    Disease/Medical Condition HYPOTHYROIDISM Date of Publication: January 27, 2017 (also known as “underactive thyroid disease”; includes congenital hypothyroidism [also known as “neonatal hypothyroidism”] and Hashimoto’s thyroiditis [also known as “autoimmune thyroiditis”]; may manifest as “cretinism” [if onsets during fetal or early life; also known as “congenital myxedema”] or “myxedema” [if onset occurs in older children and adults]) Is the initiation of non-invasive dental hygiene procedures* contra-indicated? No. ◼ Is medical consult advised? – Yes, if previously undiagnosed hypothyroidism or enlarged (or shrunken) thyroid gland is suspected1, in which case the patient/client should see his/her primary care physician. Detection early in childhood can prevent permanent intellectual impairment. – Yes, if previously diagnosed hypothyroidism is suspected to be undermedicated (with manifest signs/symptoms of hypothyroidism) or overmedicated (with manifest signs/symptoms of hyperthyroidism2), in which case the patient/client should see his/her primary care physician or endocrinologist. Major stress or illness sometimes necessitates an increase in prescribed thyroid hormone. Is the initiation of invasive dental hygiene procedures contra-indicated?** Possibly, depending on the certainty of diagnosis and level of control. ◼ Is medical consult advised? – See above. ◼ Is medical clearance required? – Yes, if undiagnosed or severe hypothyroidism is suspected. ◼ Is antibiotic prophylaxis required? – No. ◼ Is postponing treatment advised? – Yes, if undiagnosed hypothyroidism is suspected (necessitating medical assessment/management) or severe hypothyroidism is suspected (necessitating urgent medical assessment/management in order to avoid risk of myxedema coma). In general, the patient/client with mild symptoms of untreated hypothyroidism is not in danger when receiving dental hygiene therapy, and the well managed (euthyroid) patient/client requires no special regard.
    [Show full text]
  • 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.
    [Show full text]
  • Myopathy in Acute Hypothyroidism
    Postgrad Med J: first published as 10.1136/pgmj.63.742.661 on 1 August 1987. Downloaded from Postgraduate Medical Journal (1987) 63, 661-663 Clinical Reports Myopathy in acute hypothyroidism A.W.C. Kung, J.T.C. Ma, Y.L. Yu, C.C.L. Wang, E.K.W. Woo, K.S.L. Lam, C.Y. Huang and R.T.T. Yeung Department ofMedicine, University ofHong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong. Summary: Hypothyroid myopathy has so far been reported in long standing cases ofhypothyroidism. We describe two adult patients with myopathy associated with acute transient hypothyroidism. Both presented with severe muscle aches and cramps, stiffness and spasms. Muscle enzymes were markedly elevated and electromyography in one patient showed myopathic features. Histological changes were absent in muscle biopsy, probably because of the short duration of metabolic disturbance. The myopathy subsided promptly when the hypothyroid state was reversed. Introduction Hypothyroid myopathy has been described in patients however no muscle weakness or symptoms of hypo- with long-standing hypothyroidism.' 3 We report two thyroidism. She had no preceding viral infection. Chinese patients with muscle involvement in acute Examination revealed that the goitre had decreased in copyright. transient hypothyroidism, who improved after rever- size and she was clinically euthyroid. Motor and sal of the hypothyroid state, sensory functions were completely normal. Investigation showed a T4 of 44nmol/l, triiodo- thyronine (T3) 1.2 nmol/I (normal 0.77-2.97 nmol/1), Case reports and TSH 5.1 AIU/ml (normal up to 7). The serum creatine kinase level was 11,940ILmol/min.l (normal Case I 5-165) and the lactic dehydrogenase was 397;Lmol/ min.l (normal 130-275), and glutamic-oxalacetic A 42 year old woman presented at another hospital transaminase was 120limol/min.l (normal 28-32).
    [Show full text]
  • 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.
    [Show full text]
  • Screening for Thyroid Dysfunction: U.S. Preventive Services Task Force Recommendation Statement Michael L
    Annals of Internal Medicine CLINICAL GUIDELINE Screening for Thyroid Dysfunction: U.S. Preventive Services Task Force Recommendation Statement Michael L. LeFevre, MD, MSPH, on behalf of the U.S. Preventive Services Task Force* Description: Update of the 2004 U.S. Preventive Services Task Recommendation: The USPSTF concludes that the current ev- Force (USPSTF) recommendation on screening for thyroid idence is insufficient to assess the balance of benefits and harms disease. of screening for thyroid dysfunction in nonpregnant, asymptom- atic adults. (I statement) Methods: The USPSTF reviewed the evidence on the benefits and harms of screening for subclinical and “overt” thyroid dysfunction without clinically obvious symptoms, as well as the Ann Intern Med. 2015;162:641-650. doi:10.7326/M15-0483 www.annals.org effects of treatment on intermediate and final health outcomes. For author affiliation, see end of text. * For a list of USPSTF members, see the Appendix (available at www.annals Population: This recommendation applies to nonpregnant, .org). asymptomatic adults. This article was published online first at www.annals.org on 24 March 2015. he U.S. Preventive Services Task Force (USPSTF) clinicians. Thyroid dysfunction represents a continuum Tmakes recommendations about the effectiveness of from asymptomatic biochemical changes to clinically specific preventive care services for patients without re- symptomatic disease. In rare cases, it can produce life- lated signs or symptoms. threatening complications, such as myxedema coma or It bases its recommendations on the evidence of thyroid storm (1, 2). both the benefits and harms of the service and an as- Subclinical hypothyroidism is defined as an asymp- sessment of the balance.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Care Step Pathway – Thyroiditis (Inflammation of the Thyroid Gland)
    Care Step Pathway – Thyroiditis (inflammation of the thyroid gland) Assessment Look: Listen: Recognize: - Appear unwell? - Appetite/weight changes? - Other immune-related toxicity? - Changes in weight since last visit? - Hot or cold intolerance? - Prior thyroid dysfunction? o Appear heavier? Thinner? - Change in energy, mood, or behavior? - Prior history of radiation therapy? - Changes in hair texture/thickness? - Palpitations? - Signs of thyroid storm (fever, tachycardia, sweating, dehydration, cardiac - Appear hot/cold? - Increased fatigue? decompensation, delirium/psychosis, liver failure, abdominal pain, - Look fatigued? - Bowel-related changes? nausea/vomiting, diarrhea) - Sweating? Constipation/diarrhea - Hyperactive or lethargic? o - Signs of airway compression - Difficulty breathing? - Shortness of breath/edema? - Clinical presentation: Occasionally thyroiditis with transient hyperthyroidism - Swollen neck? - Skin-related changes? (low TSH and high free T4) may be followed by more longstanding - Voice change (e.g., deeper voice) o Dry/oily hypothyroidism (high TSH and low free T4) - Differential diagnosis-- Primary hypothyroidism: High TSH with low free T4; secondary (central) hypothyroidism due to hypophysitis: both TSH and free T4 are low (see HCP Assessment below for more detail about testing) Grading Toxicity HYPOTHYROIDISM Definition: A disorder characterized by decreased production of thyroid hormones from the thyroid gland Asymptomatic, subclinical Asymptomatic, subclinical Symptomatic, primary Severely symptomatic, Life-threatening,
    [Show full text]
  • 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.
    [Show full text]