{"id":8871,"date":"2025-07-17T20:01:19","date_gmt":"2025-07-18T00:01:19","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathology\/?post_type=chapter&#038;p=8871"},"modified":"2025-08-23T23:53:49","modified_gmt":"2025-08-24T03:53:49","slug":"test-dylan","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/test-dylan\/","title":{"raw":"Graves' Disease","rendered":"Graves&#8217; Disease"},"content":{"raw":"<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Learning Objectives<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nBy the end of this section, you will be able to:\r\n<ul>\r\n \t<li>Describe normal thyroid function and anatomy, highlighting key hormones and processes.<\/li>\r\n \t<li>Outline the autoimmune mechanism behind Graves disease incidence.<\/li>\r\n \t<li>Describe symptoms, treatment, and diagnosis of Graves disease.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<h2>Introduction<\/h2>\r\n<div>Graves' disease is an autoimmune disorder that causes hyperthyroidism, the result of excess release of thyroid hormones. It is estimated to effect approximately 1 in 100 Canadians.<\/div>\r\n<h2>Normal Thyroid Function and Anatomy<\/h2>\r\n<div>In healthy individuals, the hypothalamus detects low levels of thyroid hormones in the blood and releases [pb_glossary id=\"8929\"]thyrotropin releasing hormone[\/pb_glossary] (TRH). TRH is released from the hypothalamus into the hypophyseal portal system, a network of capillaries linking the hypothalamus to the anterior pituitary gland. When exposed to TRH, the anterior pituitary gland produces and releases [pb_glossary id=\"8930\"]thyroid stimulating hormone[\/pb_glossary] (TSH), which stimulates the thyroid gland located in the neck. The thyroid gland is made up of numerous follicles, which are small spheres lined with follicular cells. Follicular cells convert the protein thyroglobulin into two important iodine-containing hormones. These include [pb_glossary id=\"8931\"]triiodothyronine[\/pb_glossary] (T3) and [pb_glossary id=\"8932\"]thyroxine[\/pb_glossary]\u00a0(T4). Once released from the thyroid gland, T3 and T4 enter the blood and bind to circulating plasma proteins, and the hormones are picked up by nearly every cell in the body. Once in the cells, most T4 is converted into T3, which is the more active hormone. T3 has many effects, including speeding up basal metabolic rate, increasing cardiac output, stimulating bone resorption, and activating the sympathetic nervous system.<\/div>\r\n<div>\r\n\r\n[caption id=\"attachment_8743\" align=\"aligncenter\" width=\"705\"]<img class=\"size-full wp-image-8743\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles-.png\" alt=\"Thyroid follicle section under light microscope\" width=\"705\" height=\"636\" \/> Thyroid follicle section under light microscope \u00a9 Panzer is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\" rel=\"license\">CC BY-SA (Attribution ShareAlike)<\/a>\u00a0license[\/caption]\r\n\r\n<\/div>\r\n\r\n[caption id=\"attachment_8744\" align=\"aligncenter\" width=\"1080\"]<img class=\"size-full wp-image-8744\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal-.png\" alt=\"The hypophyseal portal vein connects the hypothalamus to the anterior pituitary\" width=\"1080\" height=\"915\" \/> The hypophyseal portal vein connects the hypothalamus to the anterior pituitary\u00a0\u00a9 OpenStax College is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a>\u00a0license[\/caption]\r\n<h2>Autoimmune Mechanism<\/h2>\r\n<div>While the trigger of the autoimmune attack leading to Graves' disease remains unclear, pathogenesis of this disease is influenced by a combination of genetic and environmental factors. For example, middle aged women, smokers, and people who experience high levels of stress are at increased risk for developing Graves. In what is deemed as a [pb_glossary id=\"8933\"]type II hypersensitivity reaction [\/pb_glossary], [pb_glossary id=\"8475\"]B cells[\/pb_glossary]\u00a0begin to produce [pb_glossary id=\"8516\"] antibodies[\/pb_glossary] against thyroid proteins. The most common of such antibodies is thyroid stimulatory [pb_glossary id=\"8934\"]immunoglobulin[\/pb_glossary], which binds to TSH receptors on thyroid cells and stimulates increased release of T3 and T4. Thyroid protein antibodies can also have direct effects on certain tissues. They may cause thyroid [pb_glossary id=\"271\"]hypertrophy[\/pb_glossary], which is characterized by growth of thyroid tissue, and hyperplasia, which results in an increased number of follicular cells. Hypertrophy and [pb_glossary id=\"8935\"]hyperplasia [\/pb_glossary] together cause thyroid enlargement, resulting in a goiter. In response to thyroid stimulatory antibodies, follicular cells begin to express molecules on their surface that attract nearby T cells that may infiltrate the thyroid gland. [pb_glossary id=\"8936\"]Fibroblasts[\/pb_glossary]\u00a0in tissue surrounding the eyes and skin may also be stimulated by thyroid stimulating antibodies. As thyroid stimulating antibodies accumulate, fibroblasts divide and make extracellular matrix proteins called glycosaminoglycans.<\/div>\r\n<div>\r\n\r\n[caption id=\"attachment_8745\" align=\"aligncenter\" width=\"1126\"]<img class=\"size-full wp-image-8745\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism-.png\" alt=\"Graves disease autoimmune mechanism, including important players leading to hyperthyroidism\" width=\"1126\" height=\"636\" \/> Graves disease autoimmune mechanism, including important players leading to hyperthyroidism \u00a9 He et al. is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a> license[\/caption]\r\n\r\n<\/div>\r\n<h2>Symptoms<\/h2>\r\nThe main symptoms of Graves' disease include hyperthyroidism, ophthalmopathy, and dermopathy.\r\n\r\nUntreated hyperthyroidism can lead to significant weight loss despite increased appetite due to increased basal metabolic rate, which coincides with overall heat intolerance. Hyperthyroidism also causes an increase in sympathetic nervous system activity, which may cause rapid heart rate, sweating, hyperactivity, anxiety, and insomnia. As described above, hyperthyroidism may also lead to a goiter, characterized by hyperplasia and hypertrophy of the thyroid tissue.\r\n<div>\r\n\r\n[caption id=\"attachment_8746\" align=\"aligncenter\" width=\"1100\"]<img class=\"size-full wp-image-8746\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter-.png\" alt=\"Thyroid enlargement, a symptom of hyperthyroidism can result in a structure called a Goiter\" width=\"1100\" height=\"710\" \/> Thyroid enlargement, a symptom of hyperthyroidism can result in a structure called a Goiter. Licensed under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\" rel=\"license\">CC BY-SA (Attribution ShareAlike)<\/a> license[\/caption]\r\n\r\n<\/div>\r\nIn Graves ophthalmopathy, a buildup of glycosaminoglycans causes inflammation and swelling in and around the eye's follicular cells. This process can lead to exophthalmos, which is an outward bulging of the eyeball. Furthermore, this weakens the muscles that control upper eyelid movement and may damage the cornea as the individual has a difficult time blinking efficiently. Together, Graves ophthalmopathy symptoms lead to an increased risk of corneal ulcers.\r\n<div>\r\n\r\n[caption id=\"attachment_8747\" align=\"aligncenter\" width=\"613\"]<img class=\"size-full wp-image-8747\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes-.png\" alt=\"Graves' disease induced ophthalmopathy\" width=\"613\" height=\"368\" \/> Graves' disease induced ophthalmopathy \u00a9 Sim Peini is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a> license[\/caption]\r\n\r\n<\/div>\r\nGraves dermopathy is characterized by localized thickening and swelling of the skin due to glycosaminoglycan build-up. This is a rare skin condition marked by non-pitting edema, particularly over the shins.\r\n<div>\r\n\r\n[caption id=\"attachment_8748\" align=\"aligncenter\" width=\"514\"]<img class=\"size-full wp-image-8748\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg-.png\" alt=\"Graves induced dermopathy, most commonly resulting in non pitting edema on the shins\" width=\"514\" height=\"389\" \/> Graves induced dermopathy, most commonly resulting in non pitting edema on the shins \u00a9 Gardner et al. is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by-nd\/4.0\/\" rel=\"license\">CC BY-ND (Attribution NoDerivatives)<\/a> license[\/caption]\r\n\r\n<\/div>\r\nPeople with Graves' disease can experience an acute flair in their disease called a \u2018thyroid storm\u2019. A [pb_glossary id=\"8937\"]thyroid storm [\/pb_glossary]\u00a0is a life-threatening increase in hyperthyroidism where the body goes into a state of sever hypermetabolism. A flare such as this can develop when a patient stops their treatment, develops infection, or has surgery. During a thyroid storm, all normal symptoms of hyperthyroidism become exaggerated. For example, heat intolerance can develop into high fever and a rapid heart rate can develop into cardiac arrythmia.\r\n<h2>Diagnosis and Treatment<\/h2>\r\nDiagnosis of hyperthyroidism is done through blood tests, where levels of TSH, T3, and T4 are measured. To confirm if hyperthyroidism is caused by Graves' disease, a blood test measuring thyroid stimulating antibodies would be performed. To further support diagnosis, radioiodine scans and measurements of iodine uptake would subsequently be tested. Radioiodine scans work by injecting small amounts of radioactive iodine, which can be traced endogenously through advanced cameras. Imaging allows medical professionals to monitor iodine absorption and function of the thyroid.\r\n\r\nThe main treatment approach for Graves' disease includes medication. Beta blockers treat the immediate symptoms of hyperthyroidism. Beta blockers do not act by directly reducing thyroid hormone production; instead, they block beta-adrenergic receptors. These receptors are the site of induction of sympathetic nervous system activity. Therefor the use of beta-blockers causes a reduction in the sympathetic nervous system hormones epinephrine and norepinephrine. Specific beta blockers may also help reduce or block the conversion of T4 into the more potent thyroid hormone T3. Anti-thyroid drugs however may directly block thyroid hormone production and release. In severe cases, the thyroid may need to be destroyed or removed. Radio-iodine therapy partially destroys thyroid function but requires subsequent hormone replacement therapy. If the goiter becomes so large that it presses against surrounding tissue, thyroid tissue can be removed through surgery. Graves ophthalmopathy is treated separately, using steroids, radiation therapy, and surgery. Graves dermopathy is generally treated through overall stabilization of the disease, however topical immunosuppressant may be used to specifically reduce the autoimmune response in affected areas.\r\n<h1>Review Questions<\/h1>\r\n[h5p id=\"424\"]","rendered":"<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Learning Objectives<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>By the end of this section, you will be able to:<\/p>\n<ul>\n<li>Describe normal thyroid function and anatomy, highlighting key hormones and processes.<\/li>\n<li>Outline the autoimmune mechanism behind Graves disease incidence.<\/li>\n<li>Describe symptoms, treatment, and diagnosis of Graves disease.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<h2>Introduction<\/h2>\n<div>Graves&#8217; disease is an autoimmune disorder that causes hyperthyroidism, the result of excess release of thyroid hormones. It is estimated to effect approximately 1 in 100 Canadians.<\/div>\n<h2>Normal Thyroid Function and Anatomy<\/h2>\n<div>In healthy individuals, the hypothalamus detects low levels of thyroid hormones in the blood and releases <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8929\">thyrotropin releasing hormone<\/a> (TRH). TRH is released from the hypothalamus into the hypophyseal portal system, a network of capillaries linking the hypothalamus to the anterior pituitary gland. When exposed to TRH, the anterior pituitary gland produces and releases <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8930\">thyroid stimulating hormone<\/a> (TSH), which stimulates the thyroid gland located in the neck. The thyroid gland is made up of numerous follicles, which are small spheres lined with follicular cells. Follicular cells convert the protein thyroglobulin into two important iodine-containing hormones. These include <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8931\">triiodothyronine<\/a> (T3) and <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8932\">thyroxine<\/a>\u00a0(T4). Once released from the thyroid gland, T3 and T4 enter the blood and bind to circulating plasma proteins, and the hormones are picked up by nearly every cell in the body. Once in the cells, most T4 is converted into T3, which is the more active hormone. T3 has many effects, including speeding up basal metabolic rate, increasing cardiac output, stimulating bone resorption, and activating the sympathetic nervous system.<\/div>\n<div>\n<figure id=\"attachment_8743\" aria-describedby=\"caption-attachment-8743\" style=\"width: 705px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-8743\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles-.png\" alt=\"Thyroid follicle section under light microscope\" width=\"705\" height=\"636\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles-.png 705w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles--300x271.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles--65x59.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles--225x203.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/follicles--350x316.png 350w\" sizes=\"auto, (max-width: 705px) 100vw, 705px\" \/><figcaption id=\"caption-attachment-8743\" class=\"wp-caption-text\">Thyroid follicle section under light microscope \u00a9 Panzer is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\" rel=\"license\">CC BY-SA (Attribution ShareAlike)<\/a>\u00a0license<\/figcaption><\/figure>\n<\/div>\n<figure id=\"attachment_8744\" aria-describedby=\"caption-attachment-8744\" style=\"width: 1080px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-8744\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal-.png\" alt=\"The hypophyseal portal vein connects the hypothalamus to the anterior pituitary\" width=\"1080\" height=\"915\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal-.png 1080w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal--300x254.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal--1024x868.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal--768x651.png 768w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal--65x55.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal--225x191.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/hypophyseal--350x297.png 350w\" sizes=\"auto, (max-width: 1080px) 100vw, 1080px\" \/><figcaption id=\"caption-attachment-8744\" class=\"wp-caption-text\">The hypophyseal portal vein connects the hypothalamus to the anterior pituitary\u00a0\u00a9 OpenStax College is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a>\u00a0license<\/figcaption><\/figure>\n<h2>Autoimmune Mechanism<\/h2>\n<div>While the trigger of the autoimmune attack leading to Graves&#8217; disease remains unclear, pathogenesis of this disease is influenced by a combination of genetic and environmental factors. For example, middle aged women, smokers, and people who experience high levels of stress are at increased risk for developing Graves. In what is deemed as a <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8933\">type II hypersensitivity reaction <\/a>, <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8475\">B cells<\/a>\u00a0begin to produce <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8516\"> antibodies<\/a> against thyroid proteins. The most common of such antibodies is thyroid stimulatory <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8934\">immunoglobulin<\/a>, which binds to TSH receptors on thyroid cells and stimulates increased release of T3 and T4. Thyroid protein antibodies can also have direct effects on certain tissues. They may cause thyroid <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_271\">hypertrophy<\/a>, which is characterized by growth of thyroid tissue, and hyperplasia, which results in an increased number of follicular cells. Hypertrophy and <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8935\">hyperplasia <\/a> together cause thyroid enlargement, resulting in a goiter. In response to thyroid stimulatory antibodies, follicular cells begin to express molecules on their surface that attract nearby T cells that may infiltrate the thyroid gland. <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8936\">Fibroblasts<\/a>\u00a0in tissue surrounding the eyes and skin may also be stimulated by thyroid stimulating antibodies. As thyroid stimulating antibodies accumulate, fibroblasts divide and make extracellular matrix proteins called glycosaminoglycans.<\/div>\n<div>\n<figure id=\"attachment_8745\" aria-describedby=\"caption-attachment-8745\" style=\"width: 1126px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-8745\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism-.png\" alt=\"Graves disease autoimmune mechanism, including important players leading to hyperthyroidism\" width=\"1126\" height=\"636\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism-.png 1126w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism--300x169.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism--1024x578.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism--768x434.png 768w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism--65x37.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism--225x127.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-mechanism--350x198.png 350w\" sizes=\"auto, (max-width: 1126px) 100vw, 1126px\" \/><figcaption id=\"caption-attachment-8745\" class=\"wp-caption-text\">Graves disease autoimmune mechanism, including important players leading to hyperthyroidism \u00a9 He et al. is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a> license<\/figcaption><\/figure>\n<\/div>\n<h2>Symptoms<\/h2>\n<p>The main symptoms of Graves&#8217; disease include hyperthyroidism, ophthalmopathy, and dermopathy.<\/p>\n<p>Untreated hyperthyroidism can lead to significant weight loss despite increased appetite due to increased basal metabolic rate, which coincides with overall heat intolerance. Hyperthyroidism also causes an increase in sympathetic nervous system activity, which may cause rapid heart rate, sweating, hyperactivity, anxiety, and insomnia. As described above, hyperthyroidism may also lead to a goiter, characterized by hyperplasia and hypertrophy of the thyroid tissue.<\/p>\n<div>\n<figure id=\"attachment_8746\" aria-describedby=\"caption-attachment-8746\" style=\"width: 1100px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-8746\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter-.png\" alt=\"Thyroid enlargement, a symptom of hyperthyroidism can result in a structure called a Goiter\" width=\"1100\" height=\"710\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter-.png 1100w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter--300x194.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter--1024x661.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter--768x496.png 768w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter--65x42.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter--225x145.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/goiter--350x226.png 350w\" sizes=\"auto, (max-width: 1100px) 100vw, 1100px\" \/><figcaption id=\"caption-attachment-8746\" class=\"wp-caption-text\">Thyroid enlargement, a symptom of hyperthyroidism can result in a structure called a Goiter. Licensed under a <a href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\" rel=\"license\">CC BY-SA (Attribution ShareAlike)<\/a> license<\/figcaption><\/figure>\n<\/div>\n<p>In Graves ophthalmopathy, a buildup of glycosaminoglycans causes inflammation and swelling in and around the eye&#8217;s follicular cells. This process can lead to exophthalmos, which is an outward bulging of the eyeball. Furthermore, this weakens the muscles that control upper eyelid movement and may damage the cornea as the individual has a difficult time blinking efficiently. Together, Graves ophthalmopathy symptoms lead to an increased risk of corneal ulcers.<\/p>\n<div>\n<figure id=\"attachment_8747\" aria-describedby=\"caption-attachment-8747\" style=\"width: 613px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-8747\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes-.png\" alt=\"Graves' disease induced ophthalmopathy\" width=\"613\" height=\"368\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes-.png 613w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes--300x180.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes--65x39.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes--225x135.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/eyes--350x210.png 350w\" sizes=\"auto, (max-width: 613px) 100vw, 613px\" \/><figcaption id=\"caption-attachment-8747\" class=\"wp-caption-text\">Graves&#8217; disease induced ophthalmopathy \u00a9 Sim Peini is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a> license<\/figcaption><\/figure>\n<\/div>\n<p>Graves dermopathy is characterized by localized thickening and swelling of the skin due to glycosaminoglycan build-up. This is a rare skin condition marked by non-pitting edema, particularly over the shins.<\/p>\n<div>\n<figure id=\"attachment_8748\" aria-describedby=\"caption-attachment-8748\" style=\"width: 514px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"size-full wp-image-8748\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg-.png\" alt=\"Graves induced dermopathy, most commonly resulting in non pitting edema on the shins\" width=\"514\" height=\"389\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg-.png 514w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg--300x227.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg--65x49.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg--225x170.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/06\/graves-leg--350x265.png 350w\" sizes=\"auto, (max-width: 514px) 100vw, 514px\" \/><figcaption id=\"caption-attachment-8748\" class=\"wp-caption-text\">Graves induced dermopathy, most commonly resulting in non pitting edema on the shins \u00a9 Gardner et al. is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by-nd\/4.0\/\" rel=\"license\">CC BY-ND (Attribution NoDerivatives)<\/a> license<\/figcaption><\/figure>\n<\/div>\n<p>People with Graves&#8217; disease can experience an acute flair in their disease called a \u2018thyroid storm\u2019. A <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8871_8937\">thyroid storm <\/a>\u00a0is a life-threatening increase in hyperthyroidism where the body goes into a state of sever hypermetabolism. A flare such as this can develop when a patient stops their treatment, develops infection, or has surgery. During a thyroid storm, all normal symptoms of hyperthyroidism become exaggerated. For example, heat intolerance can develop into high fever and a rapid heart rate can develop into cardiac arrythmia.<\/p>\n<h2>Diagnosis and Treatment<\/h2>\n<p>Diagnosis of hyperthyroidism is done through blood tests, where levels of TSH, T3, and T4 are measured. To confirm if hyperthyroidism is caused by Graves&#8217; disease, a blood test measuring thyroid stimulating antibodies would be performed. To further support diagnosis, radioiodine scans and measurements of iodine uptake would subsequently be tested. Radioiodine scans work by injecting small amounts of radioactive iodine, which can be traced endogenously through advanced cameras. Imaging allows medical professionals to monitor iodine absorption and function of the thyroid.<\/p>\n<p>The main treatment approach for Graves&#8217; disease includes medication. Beta blockers treat the immediate symptoms of hyperthyroidism. Beta blockers do not act by directly reducing thyroid hormone production; instead, they block beta-adrenergic receptors. These receptors are the site of induction of sympathetic nervous system activity. Therefor the use of beta-blockers causes a reduction in the sympathetic nervous system hormones epinephrine and norepinephrine. Specific beta blockers may also help reduce or block the conversion of T4 into the more potent thyroid hormone T3. Anti-thyroid drugs however may directly block thyroid hormone production and release. In severe cases, the thyroid may need to be destroyed or removed. Radio-iodine therapy partially destroys thyroid function but requires subsequent hormone replacement therapy. If the goiter becomes so large that it presses against surrounding tissue, thyroid tissue can be removed through surgery. Graves ophthalmopathy is treated separately, using steroids, radiation therapy, and surgery. Graves dermopathy is generally treated through overall stabilization of the disease, however topical immunosuppressant may be used to specifically reduce the autoimmune response in affected areas.<\/p>\n<h1>Review Questions<\/h1>\n<div id=\"h5p-424\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-424\" class=\"h5p-iframe\" data-content-id=\"424\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"Graves&#039;\"><\/iframe><\/div>\n<\/div>\n<div class=\"media-attributions clear\" prefix:cc=\"http:\/\/creativecommons.org\/ns#\" prefix:dc=\"http:\/\/purl.org\/dc\/terms\/\"><h2>Media Attributions<\/h2><ul><li about=\"https:\/\/commons.wikimedia.org\/wiki\/File:Thyroid_follicle.jpg \"><a rel=\"cc:attributionURL\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:Thyroid_follicle.jpg \" property=\"dc:title\">Thyroid follicle section under light microscope<\/a>  &copy;  Panzer    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\">CC BY-SA (Attribution ShareAlike)<\/a> license<\/li><li about=\"https:\/\/commons.wikimedia.org\/wiki\/File:1808_The_Anterior_Pituitary_Complex.jpg\"><a rel=\"cc:attributionURL\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:1808_The_Anterior_Pituitary_Complex.jpg\" property=\"dc:title\">The hypophyseal portal vein connects the hypothalamus to the anterior pituitary<\/a>  &copy;  OpenStax College    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY (Attribution)<\/a> license<\/li><li about=\"https:\/\/www.frontiersin.org\/journals\/pharmacology\/articles\/10.3389\/fphar.2022.862831\/full\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.frontiersin.org\/journals\/pharmacology\/articles\/10.3389\/fphar.2022.862831\/full\" property=\"dc:title\">Graves disease autoimmune mechanism, including important players leading to hyperthyroidism<\/a>  &copy;  He et al.    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY (Attribution)<\/a> license<\/li><li about=\"https:\/\/commons.wikimedia.org\/wiki\/File:A_woman_suffering_from_Goiter.png\"><a rel=\"cc:attributionURL\" href=\"https:\/\/commons.wikimedia.org\/wiki\/File:A_woman_suffering_from_Goiter.png\" property=\"dc:title\">Thyroid enlargement, a symptom of hyperthyroidism can result in a structure called a Goiter<\/a>  <a rel=\"dc:creator\" href=\"https:\/\/www.myupchar.com\/en\" property=\"cc:attributionName\"><\/a>    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-sa\/4.0\/\">CC BY-SA (Attribution ShareAlike)<\/a> license<\/li><li about=\"https:\/\/universe.roboflow.com\/sim-peini-zfk8r\/eye-diseases-classification\"><a rel=\"cc:attributionURL\" href=\"https:\/\/universe.roboflow.com\/sim-peini-zfk8r\/eye-diseases-classification\" property=\"dc:title\">Graves&#8217; disease induced ophthalmopathy<\/a>  &copy;  Sim Peini    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY (Attribution)<\/a> license<\/li><li about=\"https:\/\/dermnetnz.org\/topics\/pretibial-myxoedema \"><a rel=\"cc:attributionURL\" href=\"https:\/\/dermnetnz.org\/topics\/pretibial-myxoedema \" property=\"dc:title\">Graves induced dermopathy, most commonly resulting in non pitting edema on the shins<\/a>  &copy;  Gardner et al.    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nd\/4.0\/\">CC BY-ND (Attribution NoDerivatives)<\/a> license<\/li><\/ul><\/div><div class=\"glossary\"><span class=\"screen-reader-text\" id=\"definition\">definition<\/span><template id=\"term_8871_8929\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8929\"><div tabindex=\"-1\"><p>hormone produced in the hypothalamus that stimulates the release of thyroid-stimulating hormone in the anterior pituitary gland <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8930\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8930\"><div tabindex=\"-1\"><p>hormone produced by the anterior pituitary gland that stimulates the thyroid gland to produce thyroid hormones<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8931\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8931\"><div tabindex=\"-1\"><p>thyroid hormone that has many regulating effects in the body such as metabolism, growth, body temperature, and heart rate. <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8932\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8932\"><div tabindex=\"-1\"><p>primary hormone produced by the thyroid gland. Is the pro hormone form of the more active form thyroid hormone triiodothyronine. <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8933\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8933\"><div tabindex=\"-1\"><p>type of hypersensitivity reaction in which antibodies bind to antigens on the surface of cells or extracellular materials, triggering an immune response that damages or destroys those cells or tissues<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8475\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8475\"><div tabindex=\"-1\"><p>lymphocytes that mature in the bone marrow and differentiate into antibody-secreting plasma cells<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8516\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8516\"><div tabindex=\"-1\"><p>protein that is produced by plasma cells after stimulation by an antigen; also known as an immunoglobulin<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8934\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8934\"><div tabindex=\"-1\"><p>Proteins produced by the immune system which recognize and neutralize antigens. Also known as antibodies<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_271\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_271\"><div tabindex=\"-1\"><p>tissue is enlarged due to each individual cell becoming larger, often with an increase of cytoplasmic contents such as contractile proteins as in the case with muscle tissue<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8935\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8935\"><div tabindex=\"-1\"><p>An enlargement of a tissue or organ caused by an abnormal increase in the number of cells in a tissue or organ<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8936\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8936\"><div tabindex=\"-1\"><p>Cell type found in connective tissue, responsible for producing and maintaining the extracellular matrix<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8871_8937\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8871_8937\"><div tabindex=\"-1\"><p>occurs when the thyroid gland releases excessive amounts of thyroid hormones into the bloodstream. Can lead to dramatic increase in hyperthyroidism and its symptoms. <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><\/div>","protected":false},"author":2432,"menu_order":11,"template":"","meta":{"pb_show_title":"on","pb_short_title":"Graves' Disease","pb_subtitle":"Graves' Disease","pb_authors":["dylanmann","morganalford"],"pb_section_license":""},"chapter-type":[],"contributor":[538,535],"license":[58],"class_list":["post-8871","chapter","type-chapter","status-publish","hentry","contributor-dylanmann","contributor-morganalford","license-all-rights-reserved"],"part":8316,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8871","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/users\/2432"}],"version-history":[{"count":8,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8871\/revisions"}],"predecessor-version":[{"id":9523,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8871\/revisions\/9523"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/parts\/8316"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8871\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/media?parent=8871"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapter-type?post=8871"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/contributor?post=8871"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/license?post=8871"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}