Thyroiditis pdf

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In general, thyroiditis is defined as an inflammation of the thyroid gland. There are several kinds of thyroiditis, and they can be associated with either increased, decreased, or normal thyroid function. Furthermore, they can be classified as painful or painless, depending on the etiology. Typically, painful thyroiditis is caused by radiation, trauma, or infection, while painless thyroiditis is caused by autoimmune diseases or medications. This activity reviews the presentation of De Quervain thyroiditis and highlights the role of the interprofessional team in its treatment.

Objectives: Describe the presentation of De Quervain thyroiditis. Review the evaluation of a patient suspected of De Quervain thyroiditis. Summarize the treatment for De Quervain thyroiditis. Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by De Quervain thyroiditis.

Access free multiple choice questions on this topic. Differentiating between the different kinds is dependent on the clinical setting, medical and family history, how fast the symptoms progressed, and most importantly, the presence or absence of neck pain. Painless thyroiditis can be subdivided into Hashimoto thyroiditis, postpartum thyroiditis, subacute lymphocytic thyroiditis, drug-induced amiodarone, interferon-alpha, interleukin 2, lithium thyroiditis, and Riedel fibrosis thyroiditis.

This article will focus on subacute granulomatous thyroiditis, also known as subacute thyroiditis, painful thyroiditis, subacute nonsuppurative thyroiditis, giant cell thyroiditis, or de Quervain thyroiditis. It is an infrequent cause of hyperthyroidism. The common symptoms are neck pain or discomfort, tenderness to palpation, and a predictable course of hyperthyroidism followed by euthyroidism, hypothyroidism, and back to euthyroidism.

Viral infections are presumed as a cause of subacute thyroiditis. Many patients may have a history of viral upper respiratory infection 2 to 8 weeks before developing thyroiditis. Autoimmunity is not significant in subacute thyroiditis, unlike other thyroiditis, but it is commonly associated with human leukocyte antigen HLA - B Viral antigens or viral-host tissue damage particles bind to HLA - B 35; these complexes activate cytotoxic T cells, thus also damaging thyroid follicular cells.

The best available epidemiologic data on the incidence of subacute thyroiditis is from a study conducted by Fatourechi V et al. The overall age and sex-adjusted incidence of subacute thyroiditis during this period were 4. This disease affects women almost 4 to 5 times as often as men and typically occurs between 25 to 35 years.

With increasing age, the incidence of subacute thyroiditis decreases. The prevalence of subacute thyroiditis appears to be seasonal, as most cases occur in the summer and fall.

Thyroiditis causes damage to thyroid follicular cells, resulting in no new thyroid hormone production and excessive release of large amounts of triiodothyronine T3 and thyroxine T4. These excess hormones contribute to clinical and biochemical hyperthyroidism and inhibition of TSH negative feedback. With the release of the stored thyroid hormone and the absence of new thyroid hormone production, the phase of hyperthyroidism can last only for 2 to 8 weeks.

During this early inflammatory state, the thyroid gland is mildly enlarged and is tender to palpate. After the inflammation is subsided, new thyroid follicular cells are generated and resume thyroid hormone synthesis. This whole process may take 2 to 8 weeks, during which time the patient goes through a short phase of euthyroidism and hypothyroid before returning to normal thyroid function.

Hyperthyroidism in subacute thyroiditis is usually mild and transient, but it can rarely cause ventricular tachycardia and even thyroid storm. In subacute thyroiditis, the predominant inflammatory cells are lymphocytes with a unique type of follicular disruption with predominant histiocytes surrounding colloid masses, producing giant cells.

Interestingly, even though the entire thyroid gland is tender on gross examination, histologic examinations show patchy changes with varying stages of the disease. In the early phase, follicular cells are disrupted and are replaced with microabscesses and neutrophils. The classic granulomatous changes appear a little later in the disease with a large aggregation of lymphocytes, plasma cells, and large histiocytes in the damaged thyroid follicles.

Multinucleated giant cells surround the fragments of colloid, and sometimes colloid can also be seen in the giant cells. In the late stages, there are many lymphocytic infiltrates and fibrosis. Rarely different histologic stages can be found in the same gland suggesting the confluence nature of destruction.

Subacute thyroiditis has both granulomatous and non-granulomatous patchy lesions under electron microscope examination. The predominant finding seen in granulomatous lesions is loss of honeycomb cellular architecture of follicular cells with decreased or shortened size of follicular cell microvilli with predominant giant cells.

In the non-granulomatous lesions, the follicular basement membrane is disrupted and is replaced with T lymphocytes, monocytes, and histiocytes. It is essential to elicit from the patient the timing and duration of any symptoms, any sick contacts, any family or medical history pertinent to the patient's chief complaint, and any recent upper respiratory illness the patient has experienced. Family members may be a good source of information to help narrow down a differential if the patient's mental status is altered or confused for some other reason.

Pain is the most common complaint, and it can radiate to the jaw, upper chest, neck, and throat. It can be exacerbated by turning the head, coughing, and swallowing. Fever, malaise, body pains, fatigue, and anorexia are frequently associated with subacute thyroiditis. Patients can also have symptoms of hyperthyroidism like tachycardia, sweating, restlessness, and weight loss, but neck pain is the chief complaint.

A thorough physical exam should include a full HEENT head, eyes, ears, nose, and throat exam to rule out any other causes of neck pain. On examination, the thyroid gland is slightly enlarged and always tender to palpate.

In most cases, both the thyroid lobes are involved initially; rarely, it can be unilateral, start on one side, and migrate to the side, called "creeping thyroiditis. The diagnosis is based on history, clinical context, physical findings, and laboratory testing. Standard tests in the emergency department are thyroid studies including free thyroxine T4 , T3 and thyroid-stimulating hormone levels TSH , erythrocyte sedimentation rate ESR , and C-reactive protein along with other tests as needed based on patient presentation.

All patients have laboratory evidence of hyperthyroidism-mildly elevated serum free T4 and T3 and low TSH concentrations during the early stages of illness.

This hyperthyroidism is transient and lasts for 2 to 8 weeks, followed by a period of transient, asymptomatic, or sometimes subclinical hypothyroidism.

The interpretation of labs should be based on detailed history and examination findings. Patients with de Quervain thyroiditis will often have elevated ESR and CRP levels, along with elevated thyroglobulin concentrations, anemia, and mild leukocytosis. Liver function tests can be abnormal during the initial hyperthyroid phase and return to normal after 2 to 3 months.

Levels of antithyroid peroxidase and antithyroglobulin antibodies are generally undetectable or low normal. Because patients often present with a fever, a septic workup is usually done. EKG should be performed in the presence of tachycardia. It is differentiated from Graves' disease by the lack of a thyroid thrill or bruit, ophthalmopathy, pretibial myxedema, and thyroid-stimulating immunoglobulins, and by a low or absent rather than elevated RAIU. Treatment is similar to that of postpartum thyroiditis.

Amiodarone Cordarone , interferonalfa Infergen; Intron A, Roferon-A, Rebetron combination therapy , interleukin-2, and lithium may cause a destructive thyroiditis with hyperthyroidism or hypothyroidism, low RAIU, and variable presence of antithyroid peroxidase antibodies.

The thyroid abnormalities usually resolve with discontinuation of the drug responsible. Riedel's thyroiditis also known as fibrous thyroiditis is a rare condition characterized by an extensive fibrotic process of unknown etiology involving the thyroid and adjacent structures.

It may be associated with a diffuse fibrotic process affecting multiple tissues idiopathic multifocal fibrosclerosis 26 and may be unilateral or diffuse. Four times more women are affected than men, with the highest prevalence occurring in individuals between 30 and 60 years of age.

Patients present with a rock-hard, wood-like, fixed, painless goiter, often accompanied by symptoms of esophageal or tracheal compression. Approximately one third of patients have hypothyroidism because of extensive replacement of the gland by scar tissue. Antithyroid peroxidase antibodies are present in two thirds of patients, and RAIU typically is low. Open biopsy or resection is necessary for a definitive diagnosis because fine-needle aspiration may have a poor yield.

Surgery to relieve tracheal and esophageal compression is the mainstay of treatment. Steroids, methotrexate, and tamoxifen Nolvadex have been used as treatment, with some success. Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. While writing this article, Dr. He also holds the James R. Klinenberg Chair in Medicine at Cedars-Sinai. Address correspondence to Glenn D. Braunstein, M. Reprints are not available from the authors. Clinical features and outcome of subacute thyroiditis in an incidence cohort: Olmstead County, Minnesota, study.

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Painful Hashimoto's thyroiditis as an indication for thyroidectomy: clinical characteristics and outcome in seven patients. Subclinical thyroid dysfunction: a joint statement on management from the American Association of Clinical Endocrinologists, the American Thyroid Association, and the Endocrine Society.

Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. Subclinical hypothyroidism and pregnancy outcomes. Obstet Gynecol. Primary thyroid lymphoma is a heterogenous disease. Hashimoto's thyroiditis with papillary thyroid carcinoma PTC -like nuclear alterations express molecular markers of PTC.

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Endocr Rev. Volpe R. Is silent thyroiditis an autoimmune disease? Arch Intern Med. Woolf PD. Transient painless thyroiditis with hyperthyroidism: a variant of lymphocytic thyroiditis? The effects of amiodarone on the thyroid. Clinical review interferon-alpha-related thyroid disease: pathophysiological, epidemiological, and clinical aspects. Patients treated with interferon-alpha, interferon-beta, and interleukin-2 have a different thyroid autoantibody pattern than patients suffering from endogenous autoimmune thyroid disease.

Association between lithium use and thyrotoxicosis caused by silent thyroiditis. Clin Endocrinol. Lithium-associated thyroiditis. Clinical case seminar: Riedel's thyroiditis: report of a case complicated by spontaneous hypoparathyroidism, recurrent laryngeal nerve injury, and Horner's syndrome. Corticosteroid therapy in Riedel's thyroiditis. However, necrosis or calcification does not occur and would suggest a different diagnosis.

The organ system manifestations of Hashimoto thyroiditis are varied due to the nature of the disease. Initially, patients may have bouts of hyperthyroid symptoms, as the initial destruction of thyroid cells may lead to the increased release of thyroid hormone into the bloodstream.

Eventually, when enough destruction has been caused by the antibody response, patients exhibit symptoms of hypothyroidism. These symptoms are insidious and variable and may affect almost any organ system in the body. The classic skin characteristic associated with hypothyroidism is myxedema, which refers to the edema-like skin condition caused by increased glycosaminoglycan deposition.

This, however, is uncommon and only occurs in severe cases. Skin can be scaly and dry, especially on the extensor surfaces, palms, and soles.

Histologic examination reveals epidermal thinning. Increased dermal mucopolysaccharides cause water retention and, in turn, pale-colored skin. The rate of hair growth slows, and hair can be dry, coarse, dull, and brittle. Diffuse or partial alopecia is not uncommon. Bradycardia may result from a loss of chronotropic action of thyroid hormone directly on the sinoatrial cells. However, most patients have a few symptoms directly attributable to the cardiovascular system.

Fatigue, exertional dyspnea, and exercise intolerance are likely associated with a combination of limited pulmonary and cardiac reserve in addition to decreased muscle strength or increased muscle fatigue. Hypothyroid rats have been shown to have decreased endurance.

Biochemical changes in this population have shown decreased muscle oxidation of pyruvate and palmitate, increased utilization of glycogen stores, and diminished fatty acid mobilization.

Muscle weakness and myopathy are important features. The presentation may also be subclinical. Early symptoms may include constipation, fatigue, dry skin, and weight gain.

More advanced symptoms may include: cold intolerance, decreased sweating, nerve deafness, peripheral neuropathy, decreased energy, depression, dementia, memory loss, muscle cramps, joint pain, hair loss, apnea, menorrhagia, and pressure symptoms in the neck from goiter enlargement such as voice hoarseness. Furthermore, patients can have an accumulation of fluid in the pleural and pericardial cavities rarely. Myxoedema coma is the most severe clinical presentation and has to be managed as an endocrine emergency within patient care.

Hashimoto thyroiditis is an autoimmune disorder of inadequate thyroid hormone production. The biochemical picture indicates raised thyroid-stimulating hormone TSH in response to low free T4. Low total T4 or free T4 level in the presence of an elevated TSH level confirms the diagnosis of primary hypothyroidism.

Integrative and functional medicine practitioners may also asses free T3 and reverse T3 levels, however, Western medicine does not use this approach. There can be decreased glomerular filtration rate GFR , renal plasma flow, and renal free water clearance with resultant hyponatremia.

A thyroid ultrasound assesses thyroid size, echotexture, and whether thyroid nodules are present; however, it is usually not necessary for diagnosing the conditioning the majority. The mainstay of treatment for hypothyroidism is thyroid hormone replacement. The drug of choice is titrated levothyroxine sodium administered orally. It has a half-life of 7 days and can be given daily.

It should not be given with iron or calcium supplements, aluminum hydroxide, and proton pump inhibitors to avoid suboptimal absorption.

It is best taken early in the morning on an empty stomach for optimum absorption. The standard dose is 1. Patients less than 50 years old should be commenced on standard full dose; however, lower doses should be used in patients with cardiovascular diseases and the elderly. The theory behind the inflammation has to do with the leaky gut syndrome, where there is an insult to the gut mucosa, which allows penetrance of proteins that do not typically enter the bloodstream via transporters in the gut mucosa.

It is theorized that a response similar to molecular mimicry occurs, and antibodies are produced against the antigens. Unfortunately, the antigen may be very structurally similar to thyroid peroxidase, leading to antibody formation against this enzyme.

The concept of an autoimmune diet is based on healing the gut and decreasing the severity of the autoimmune response. More research is required on this topic before it becomes a part of the guidelines. Chronic autoimmune gastritis CAG is characterized by the partial or complete disappearance of parietal cells leading to impairment of hydrochloric acid and intrinsic factor production.

The patients go on to develop hypochlorhydria-dependent iron-deficient anemia, leading to pernicious anemia, and severe gastric atrophy. Thyrogastric syndrome was first described in the s when thyroid autoantibodies were found in a subset of patients with pernicious anemia and atrophic gastritis. The latest guidelines have incorporated the two aforementioned autoimmune disorders into a syndrome, now known as a polyglandular autoimmune syndrome PAS.

This is characterized by two or more endocrine and nonendocrine disorders. The thyroid gland develops from the primitive gut, and therefore the thyroid follicular cells share similar characteristics with parietal cells of the same endodermal origin. Iodine not only plays an essential role in the production of thyroid hormone, but it is also involved in the regulation of gastric mucosal cell proliferation and acts as an electron donor in the presence of gastric peroxidase and assists in the removal of free oxygen radicals.

It is important to note that due to the pharmaceutical formation of thyroxine available worldwide, there can be problems with absorption in patients with disorders of the gastric mucosa. Most levothyroxine is obtained by the salification with sodium hydroxide, making sodium levothyroxine.

Decreased gastric acid secretion can disrupt this percentage and may cause issues with decreased absorption of most pharmaceutical grade forms of levothyroxine, except for liquid-based or soft gel formations. Clinically, it is important to note the association between thyroid and gastric autoimmune diseases.

The presence of iron-deficiency anemia and thyroxine absorption issues should encourage further diagnostic workup. Hashimoto thyroiditis is a life long disorder with no cure; thus, it is best managed by an interprofessional team that includes an endocrinologist, primary care provider, and an internist.

The key is to follow up on the levels of thyroid hormone. Empirically prescribing one standard dose of levothyroxine may lead to hormone toxicity in some people. In addition, some patients may develop lymphoma, and thus a regular examination of the neck area is highly recommended.