This document discusses thyrotoxicosis, which results from excess thyroid hormone production regardless of cause. It is one of the more common endocrine disorders seen by family physicians. The causes of thyrotoxicosis include Graves' disease, toxic multinodular goiter, solitary toxic nodule, and thyroiditis. Graves' disease is an autoimmune condition characterized by a diffuse goiter, ophthalmopathy, and dermopathy. Toxic multinodular goiter develops from autonomy in a pre-existing nodular goiter. A solitary toxic nodule refers to autonomy developing in an otherwise normal thyroid. Thyroiditis can cause a transient thyrotoxic phase followed by hypothyroidism. Treatment depends on
This document discusses thyrotoxicosis and hyperthyroidism. It begins by covering thyroid physiology including iodine metabolism and thyroid hormone synthesis. It then discusses the causes and clinical manifestations of Graves' disease (diffuse toxic goiter), toxic multinodular goiter, and toxic adenoma. Diagnostic tests and treatment options including antithyroid drugs, radioactive iodine therapy, and surgery are described for hyperthyroidism. Thyroid storm, a medical emergency, is also summarized.
This document provides an overview of thyrotoxicosis, including its epidemiology, pathophysiology, causes, clinical manifestations, diagnosis, and management. Some key points:
- Thyrotoxicosis is defined as thyroid hormone excess and can be caused by hyperthyroidism, thyroiditis, or excess hormone ingestion. The major causes of hyperthyroidism are Graves' disease, toxic multinodular goiter, and toxic adenomas.
- Clinical manifestations depend on severity and duration of thyrotoxicosis, and include symptoms like palpitations, sweating, weight loss as well as signs like goiter, tremor, eye changes. Diagnosis involves testing thyroid function through TSH,
The document describes several cases of thyrotoxicosis and discusses potential causes. It outlines cases of three patients, two children and one infant, who presented with thyrotoxicosis. The potential causes discussed include Graves' disease, toxic multinodular goiter, toxic adenoma, neonatal Graves' disease, activated TSH receptor, excess TSH, thyroiditis, and thyrotoxicosis resulting from excess iodine or medications like amiodarone.
Thyrotoxicosis and other thyroid diseases is a document discussing various thyroid conditions including hyperthyroidism, Graves' disease, toxic multinodular goiter, toxic adenoma, subacute thyroiditis, hypothyroidism, autoimmune thyroiditis, and other causes of hypothyroidism. It provides details on the epidemiology, etiology, clinical features, pathophysiology, diagnosis, differential diagnosis and management of these conditions.
This document discusses hyperthyroidism (excess thyroid hormone). There are two main types - those caused by excess hormone production and those caused by release of stored hormone. Primary causes include Graves' disease while secondary causes include Plummer's disease and toxic nodules. Signs and symptoms, investigations, and treatment options like antithyroid drugs, surgery, and radioiodine are described for different patient groups. Management involves controlling hyperthyroidism and returning the patient to a euthyroid state.
This document discusses a case of hyperthyroidism in a 39-year-old female presenting with nervousness, anxiety, palpitations, diarrhea, and weight loss. On examination, she had a heart rate of 110 bpm, tremor, increased reflexes, and an enlarged thyroid. Laboratory tests found high free T3 and T4, low TSH, and positive thyroid stimulating immunoglobulins, consistent with a diagnosis of Graves' disease. Graves' disease is an autoimmune disorder causing hyperthyroidism through thyroid stimulating antibodies. If left untreated, hyperthyroidism can progress to a thyroid storm, a life-threatening condition of severe hypermetabolism.
This document discusses the management of thyroid storm, a life-threatening condition characterized by a hypermetabolic state caused by underlying hyperthyroidism. Key points include:
- Thyroid storm is diagnosed clinically or using scoring tools like the Burch-Wartofsky Point Scale.
- Management aims to inhibit thyroid hormone synthesis/release and peripheral effects while reversing decompensation. This involves high-dose antithyroid drugs, beta blockers, corticosteroids, inorganic iodide, and treating any precipitating factors.
- Supportive treatments like IV fluids and nutrition are also important, along with considering urgent thyroidectomy or radioactive iodine in some cases. Patient education is crucial
The document discusses the thyroid gland and hypothyroidism. It notes that the thyroid gland regulates vital body functions through hormones like T3 and T4. Hypothyroidism is the most common endocrine disease and is often underdiagnosed. It presents with symptoms like fatigue, weight gain, and menstrual irregularities. Diagnosis involves low free T4 and high TSH levels. Treatment is typically lifelong levothyroxine supplementation to replace thyroid hormones. The goal is to alleviate symptoms and maintain normal TSH levels.
This document discusses thyrotoxicosis and hyperthyroidism. It begins by covering thyroid physiology including iodine metabolism and thyroid hormone synthesis. It then discusses the causes and clinical manifestations of Graves' disease (diffuse toxic goiter), toxic multinodular goiter, and toxic adenoma. Diagnostic tests and treatment options including antithyroid drugs, radioactive iodine therapy, and surgery are described for hyperthyroidism. Thyroid storm, a medical emergency, is also summarized.
This document provides an overview of thyrotoxicosis, including its epidemiology, pathophysiology, causes, clinical manifestations, diagnosis, and management. Some key points:
- Thyrotoxicosis is defined as thyroid hormone excess and can be caused by hyperthyroidism, thyroiditis, or excess hormone ingestion. The major causes of hyperthyroidism are Graves' disease, toxic multinodular goiter, and toxic adenomas.
- Clinical manifestations depend on severity and duration of thyrotoxicosis, and include symptoms like palpitations, sweating, weight loss as well as signs like goiter, tremor, eye changes. Diagnosis involves testing thyroid function through TSH,
The document describes several cases of thyrotoxicosis and discusses potential causes. It outlines cases of three patients, two children and one infant, who presented with thyrotoxicosis. The potential causes discussed include Graves' disease, toxic multinodular goiter, toxic adenoma, neonatal Graves' disease, activated TSH receptor, excess TSH, thyroiditis, and thyrotoxicosis resulting from excess iodine or medications like amiodarone.
Thyrotoxicosis and other thyroid diseases is a document discussing various thyroid conditions including hyperthyroidism, Graves' disease, toxic multinodular goiter, toxic adenoma, subacute thyroiditis, hypothyroidism, autoimmune thyroiditis, and other causes of hypothyroidism. It provides details on the epidemiology, etiology, clinical features, pathophysiology, diagnosis, differential diagnosis and management of these conditions.
This document discusses hyperthyroidism (excess thyroid hormone). There are two main types - those caused by excess hormone production and those caused by release of stored hormone. Primary causes include Graves' disease while secondary causes include Plummer's disease and toxic nodules. Signs and symptoms, investigations, and treatment options like antithyroid drugs, surgery, and radioiodine are described for different patient groups. Management involves controlling hyperthyroidism and returning the patient to a euthyroid state.
This document discusses a case of hyperthyroidism in a 39-year-old female presenting with nervousness, anxiety, palpitations, diarrhea, and weight loss. On examination, she had a heart rate of 110 bpm, tremor, increased reflexes, and an enlarged thyroid. Laboratory tests found high free T3 and T4, low TSH, and positive thyroid stimulating immunoglobulins, consistent with a diagnosis of Graves' disease. Graves' disease is an autoimmune disorder causing hyperthyroidism through thyroid stimulating antibodies. If left untreated, hyperthyroidism can progress to a thyroid storm, a life-threatening condition of severe hypermetabolism.
This document discusses the management of thyroid storm, a life-threatening condition characterized by a hypermetabolic state caused by underlying hyperthyroidism. Key points include:
- Thyroid storm is diagnosed clinically or using scoring tools like the Burch-Wartofsky Point Scale.
- Management aims to inhibit thyroid hormone synthesis/release and peripheral effects while reversing decompensation. This involves high-dose antithyroid drugs, beta blockers, corticosteroids, inorganic iodide, and treating any precipitating factors.
- Supportive treatments like IV fluids and nutrition are also important, along with considering urgent thyroidectomy or radioactive iodine in some cases. Patient education is crucial
The document discusses the thyroid gland and hypothyroidism. It notes that the thyroid gland regulates vital body functions through hormones like T3 and T4. Hypothyroidism is the most common endocrine disease and is often underdiagnosed. It presents with symptoms like fatigue, weight gain, and menstrual irregularities. Diagnosis involves low free T4 and high TSH levels. Treatment is typically lifelong levothyroxine supplementation to replace thyroid hormones. The goal is to alleviate symptoms and maintain normal TSH levels.
The document discusses the physiology of the thyroid gland and thyroid hormones such as T3 and T4. It describes how the pituitary-thyroid axis controls thyroid hormone production and discusses different types of thyroid enlargement including simple goiter, diffuse hyperplastic goiter, toxic nodular goiter, and Graves' disease. The principles and advantages/disadvantages of different treatment approaches for hyperthyroidism are provided, including anti-thyroid drugs, surgery, and radioiodine therapy. Potential postoperative complications of thyroid surgery are also listed.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.
The document provides an outline on the physiology and causes of hyperthyroidism, also known as thyrotoxicosis. It discusses the thyroid gland, thyroid hormone synthesis and regulation, clinical features of Graves' disease and toxic multinodular goiter, diagnosis of hyperthyroidism, and management approaches including antithyroid drugs, radioactive iodine therapy, surgery, and novel minimally invasive therapies. It also covers thyroid storm as a life-threatening emergency characterized by abrupt release of thyroid hormones.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can be fatal if not treated promptly and aggressively. It is usually precipitated by stress in individuals with poorly controlled hyperthyroidism. Signs and symptoms involve multiple organ systems and include fever, tachycardia, heart failure, gastrointestinal issues, and altered mental status. Treatment requires addressing the underlying hyperthyroidism with antithyroid drugs, iodine, beta-blockers, and glucocorticoids to suppress hormone production and effects. Managing precipitating factors, supportive care, and monitoring for complications are also important.
This document discusses the case of a 56-year-old woman who presented with fever, sore throat, and breathlessness and was diagnosed with thyroid storm. It provides details on her medical history, examination, labs, and treatment. The document also discusses two additional cases of thyroid storm and provides a summary of key points on diagnosing and treating thyroid storm.
Hypothyroidism can be primary, meaning it is caused by a problem in the thyroid gland itself, or secondary, caused by a lack of TSH from the pituitary gland. Primary causes include congenital defects, iodine deficiency, autoimmune disorders like Hashimoto's thyroiditis, and surgery or radiation treatment of the thyroid. Secondary hypothyroidism is caused by problems of the pituitary gland or peripheral resistance to thyroid hormone. Diagnosis is made through blood tests showing low T3 and T4 and high TSH for primary hypothyroidism. Treatment is lifelong thyroid hormone replacement, usually levothyroxine. Dosage depends on age, severity, and other factors.
Goiter is swelling of the thyroid gland that can be caused by iodine deficiency, autoimmune disorders, or abnormal thyroid function. Simple goiter involves an enlarged thyroid gland but is usually not cancerous, while toxic goiter causes hyperthyroidism. Diagnosis involves blood tests of thyroid hormones and ultrasound examination. Treatment depends on the underlying cause, and may include thyroid hormone replacement, radioactive iodine, or surgery. With proper treatment, the prognosis for goiter is generally good.
Hyperthyroidism is a condition where the thyroid gland produces too much thyroid hormone. Graves' disease is the most common cause of hyperthyroidism. It is an autoimmune disorder where the immune system produces antibodies that stimulate the thyroid gland to overproduce hormones. Symptoms include weight loss, rapid heartbeat, increased appetite, nervousness, tremors, and eye problems. Treatment options include anti-thyroid medications to slow hormone production, radioactive iodine therapy to destroy thyroid cells, and surgery to remove part or all of the thyroid gland. Lifestyle changes like a healthy diet and stress reduction can also help manage symptoms.
The document discusses the thyroid gland, its hormones, and abnormalities in thyroid function such as hypothyroidism and hyperthyroidism (goiter). It notes that the thyroid gland produces thyroxine (T4) and triiodothyronine (T3) which regulate metabolism. Goiter is classified as simple or toxic, and can be caused by iodine deficiency, genetic defects, or drugs/chemicals. Treatment options include surgery, radioactive iodine, levothyroxine medication, and dietary changes.
Graves' disease, also known as toxic diffuse goiter, is the most common cause of hyperthyroidism in the United States.
Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs.
A complete presentation on hypothroidism endocrine disorder based on latest editon of harrison and reference books. this presentation will help to learn about this second most common endocrine disorder.
This document discusses the thyroid gland and various thyroid conditions. It begins by explaining what the thyroid gland does, producing hormones that regulate metabolism. It then discusses different types of goiters (enlargement of the thyroid gland), including diffuse goiter, multi-nodular goiter, and solitary thyroid nodules. For each condition, it covers causes, symptoms, diagnostic evaluation, and treatment approaches. Key points are that toxic goiters are rarely malignant, solitary nodules need evaluation to exclude cancer, and surgery is rarely needed for autoimmune or inflammatory thyroid diseases.
Thyroiditis refers to an inflammation of the thyroid gland. The gland is located in the front of your neck and controls your metabolism by releasing a series of hormones.
The document provides information about thyroid gland disorders including hypothyroidism and hyperthyroidism. It discusses the anatomy and blood supply of the thyroid gland. It describes Hashimoto's thyroiditis as the most common cause of hypothyroidism due to an autoimmune reaction. Graves' disease is outlined as the most common cause of hyperthyroidism, also caused by an autoimmune process involving thyroid stimulating antibodies. The clinical features, investigations, and treatment approaches for hypothyroidism and hyperthyroidism are summarized.
Hypothyroidism is a common endocrine disorder characterized by reduced thyroid hormone production. It affects females more than males and rates increase with age. Primary hypothyroidism is caused by conditions like Hashimoto's thyroiditis or iatrogenic thyroid damage. Secondary hypothyroidism results from pituitary or hypothalamic dysfunction. Symptoms include fatigue, weight gain, dry skin and slowed thinking. Diagnosis is based on low free thyroxine and elevated TSH levels. Treatment involves thyroid hormone replacement therapy and monitoring to ensure proper thyroid function is maintained. Complications can occur if treatment is inadequate or excessive.
1. The document discusses various diseases of the thyroid gland including goiter, hypothyroidism, thyroiditis, and thyroid cancer. It describes the etiology, pathogenesis, clinical features, investigations, and management of these conditions.
2. Graves' disease is described as the most common cause of thyrotoxicosis, characterized by hyperthyroidism, goiter, eye signs, and thyrotoxicosis symptoms. It results from thyroid stimulating immunoglobulins that act on the TSH receptor.
3. Papillary carcinoma is the most common type of thyroid cancer, accounting for 60-80% of cases. It often affects women around age 40 and has a 40% rate of neck node metastasis.
Hyperthyroidism, also known as overactive thyroid, is a condition where the thyroid gland produces and secretes excessive amounts of thyroid hormones triiodothyronine (T3) and/or thyroxine (T4). Graves' disease, an autoimmune disorder, is the most common cause. Symptoms include weight loss, increased appetite, irritability, weakness, and heat intolerance. Signs include palpitations, tremor, and goiter. The excess thyroid hormone affects nearly every tissue in the body, increasing the body's metabolic rate. Tests can confirm the diagnosis by showing suppressed TSH and elevated free T4 levels, and imaging and antibody tests are also used.
Diffuse toxic goiter, also known as endemic goiter, is an autoimmune disease characterized by overproduction of thyroid hormones causing damage to organs like the nervous and cardiovascular systems. It is caused by iodine deficiency in the environment, especially in soil and water. People in iodine-deficient areas can develop an enlarged thyroid gland with a reduction in its function over time, along with symptoms like difficulty swallowing and changes to heart function. Treatment options include thyroid drugs, surgery to remove part of the thyroid gland, and preventing future cases by providing iodized salt and foods to populations.
The document discusses various thyroid cases commonly seen in clinical practice and provides guidance on thyroid examination and testing. It describes how to evaluate thyroid function test results using a "nine square" approach and discusses distinguishing postpartum thyroiditis from Graves' disease. It also addresses questions on thyroid testing in pregnancy, thyroid hormone replacement therapy and management of hypothyroidism and benign thyroid nodules.
This document discusses thyrotoxicosis, which is defined as thyroid hormone excess caused by hyperthyroidism or excessive thyroid function. It outlines the various causes of thyrotoxicosis including primary and secondary hyperthyroidism. Signs and symptoms as well as laboratory findings are described. Treatment options including antithyroid drugs, beta blockers, radioiodine, and surgery are discussed in detail. Thyrotoxic crisis, a life-threatening exacerbation of hyperthyroidism, is also covered.
1) The document discusses thyrotoxicosis and hypothyroidism, including the development, anatomy, histology, blood supply, physiology, and clinical features of the thyroid gland.
2) It describes the various causes, signs and symptoms, investigations, and treatment approaches for hyperthyroidism and hypothyroidism.
3) Key topics covered include Graves' disease, toxic multinodular goiter, toxic nodules, hypothyroidism, myxedema, and thyroid function tests.
Thyrotoxicosis is a clinical syndrome caused by high levels of circulating thyroid hormones, with primary causes including Graves' disease and toxic nodular goiter, leading to symptoms of weight loss, fatigue, heat intolerance, and emotional changes. Diagnosis is based on examination findings of a goiter, tachycardia, and eye changes like exophthalmos, with treatment options including antithyroid drugs, radioactive iodine, or surgery to remove the overactive thyroid tissue.
The document discusses the physiology of the thyroid gland and thyroid hormones such as T3 and T4. It describes how the pituitary-thyroid axis controls thyroid hormone production and discusses different types of thyroid enlargement including simple goiter, diffuse hyperplastic goiter, toxic nodular goiter, and Graves' disease. The principles and advantages/disadvantages of different treatment approaches for hyperthyroidism are provided, including anti-thyroid drugs, surgery, and radioiodine therapy. Potential postoperative complications of thyroid surgery are also listed.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.
The document provides an outline on the physiology and causes of hyperthyroidism, also known as thyrotoxicosis. It discusses the thyroid gland, thyroid hormone synthesis and regulation, clinical features of Graves' disease and toxic multinodular goiter, diagnosis of hyperthyroidism, and management approaches including antithyroid drugs, radioactive iodine therapy, surgery, and novel minimally invasive therapies. It also covers thyroid storm as a life-threatening emergency characterized by abrupt release of thyroid hormones.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can be fatal if not treated promptly and aggressively. It is usually precipitated by stress in individuals with poorly controlled hyperthyroidism. Signs and symptoms involve multiple organ systems and include fever, tachycardia, heart failure, gastrointestinal issues, and altered mental status. Treatment requires addressing the underlying hyperthyroidism with antithyroid drugs, iodine, beta-blockers, and glucocorticoids to suppress hormone production and effects. Managing precipitating factors, supportive care, and monitoring for complications are also important.
This document discusses the case of a 56-year-old woman who presented with fever, sore throat, and breathlessness and was diagnosed with thyroid storm. It provides details on her medical history, examination, labs, and treatment. The document also discusses two additional cases of thyroid storm and provides a summary of key points on diagnosing and treating thyroid storm.
Hypothyroidism can be primary, meaning it is caused by a problem in the thyroid gland itself, or secondary, caused by a lack of TSH from the pituitary gland. Primary causes include congenital defects, iodine deficiency, autoimmune disorders like Hashimoto's thyroiditis, and surgery or radiation treatment of the thyroid. Secondary hypothyroidism is caused by problems of the pituitary gland or peripheral resistance to thyroid hormone. Diagnosis is made through blood tests showing low T3 and T4 and high TSH for primary hypothyroidism. Treatment is lifelong thyroid hormone replacement, usually levothyroxine. Dosage depends on age, severity, and other factors.
Goiter is swelling of the thyroid gland that can be caused by iodine deficiency, autoimmune disorders, or abnormal thyroid function. Simple goiter involves an enlarged thyroid gland but is usually not cancerous, while toxic goiter causes hyperthyroidism. Diagnosis involves blood tests of thyroid hormones and ultrasound examination. Treatment depends on the underlying cause, and may include thyroid hormone replacement, radioactive iodine, or surgery. With proper treatment, the prognosis for goiter is generally good.
Hyperthyroidism is a condition where the thyroid gland produces too much thyroid hormone. Graves' disease is the most common cause of hyperthyroidism. It is an autoimmune disorder where the immune system produces antibodies that stimulate the thyroid gland to overproduce hormones. Symptoms include weight loss, rapid heartbeat, increased appetite, nervousness, tremors, and eye problems. Treatment options include anti-thyroid medications to slow hormone production, radioactive iodine therapy to destroy thyroid cells, and surgery to remove part or all of the thyroid gland. Lifestyle changes like a healthy diet and stress reduction can also help manage symptoms.
The document discusses the thyroid gland, its hormones, and abnormalities in thyroid function such as hypothyroidism and hyperthyroidism (goiter). It notes that the thyroid gland produces thyroxine (T4) and triiodothyronine (T3) which regulate metabolism. Goiter is classified as simple or toxic, and can be caused by iodine deficiency, genetic defects, or drugs/chemicals. Treatment options include surgery, radioactive iodine, levothyroxine medication, and dietary changes.
Graves' disease, also known as toxic diffuse goiter, is the most common cause of hyperthyroidism in the United States.
Hyperthyroidism is a disorder that occurs when the thyroid gland makes more thyroid hormone than the body needs.
A complete presentation on hypothroidism endocrine disorder based on latest editon of harrison and reference books. this presentation will help to learn about this second most common endocrine disorder.
This document discusses the thyroid gland and various thyroid conditions. It begins by explaining what the thyroid gland does, producing hormones that regulate metabolism. It then discusses different types of goiters (enlargement of the thyroid gland), including diffuse goiter, multi-nodular goiter, and solitary thyroid nodules. For each condition, it covers causes, symptoms, diagnostic evaluation, and treatment approaches. Key points are that toxic goiters are rarely malignant, solitary nodules need evaluation to exclude cancer, and surgery is rarely needed for autoimmune or inflammatory thyroid diseases.
Thyroiditis refers to an inflammation of the thyroid gland. The gland is located in the front of your neck and controls your metabolism by releasing a series of hormones.
The document provides information about thyroid gland disorders including hypothyroidism and hyperthyroidism. It discusses the anatomy and blood supply of the thyroid gland. It describes Hashimoto's thyroiditis as the most common cause of hypothyroidism due to an autoimmune reaction. Graves' disease is outlined as the most common cause of hyperthyroidism, also caused by an autoimmune process involving thyroid stimulating antibodies. The clinical features, investigations, and treatment approaches for hypothyroidism and hyperthyroidism are summarized.
Hypothyroidism is a common endocrine disorder characterized by reduced thyroid hormone production. It affects females more than males and rates increase with age. Primary hypothyroidism is caused by conditions like Hashimoto's thyroiditis or iatrogenic thyroid damage. Secondary hypothyroidism results from pituitary or hypothalamic dysfunction. Symptoms include fatigue, weight gain, dry skin and slowed thinking. Diagnosis is based on low free thyroxine and elevated TSH levels. Treatment involves thyroid hormone replacement therapy and monitoring to ensure proper thyroid function is maintained. Complications can occur if treatment is inadequate or excessive.
1. The document discusses various diseases of the thyroid gland including goiter, hypothyroidism, thyroiditis, and thyroid cancer. It describes the etiology, pathogenesis, clinical features, investigations, and management of these conditions.
2. Graves' disease is described as the most common cause of thyrotoxicosis, characterized by hyperthyroidism, goiter, eye signs, and thyrotoxicosis symptoms. It results from thyroid stimulating immunoglobulins that act on the TSH receptor.
3. Papillary carcinoma is the most common type of thyroid cancer, accounting for 60-80% of cases. It often affects women around age 40 and has a 40% rate of neck node metastasis.
Hyperthyroidism, also known as overactive thyroid, is a condition where the thyroid gland produces and secretes excessive amounts of thyroid hormones triiodothyronine (T3) and/or thyroxine (T4). Graves' disease, an autoimmune disorder, is the most common cause. Symptoms include weight loss, increased appetite, irritability, weakness, and heat intolerance. Signs include palpitations, tremor, and goiter. The excess thyroid hormone affects nearly every tissue in the body, increasing the body's metabolic rate. Tests can confirm the diagnosis by showing suppressed TSH and elevated free T4 levels, and imaging and antibody tests are also used.
Diffuse toxic goiter, also known as endemic goiter, is an autoimmune disease characterized by overproduction of thyroid hormones causing damage to organs like the nervous and cardiovascular systems. It is caused by iodine deficiency in the environment, especially in soil and water. People in iodine-deficient areas can develop an enlarged thyroid gland with a reduction in its function over time, along with symptoms like difficulty swallowing and changes to heart function. Treatment options include thyroid drugs, surgery to remove part of the thyroid gland, and preventing future cases by providing iodized salt and foods to populations.
The document discusses various thyroid cases commonly seen in clinical practice and provides guidance on thyroid examination and testing. It describes how to evaluate thyroid function test results using a "nine square" approach and discusses distinguishing postpartum thyroiditis from Graves' disease. It also addresses questions on thyroid testing in pregnancy, thyroid hormone replacement therapy and management of hypothyroidism and benign thyroid nodules.
This document discusses thyrotoxicosis, which is defined as thyroid hormone excess caused by hyperthyroidism or excessive thyroid function. It outlines the various causes of thyrotoxicosis including primary and secondary hyperthyroidism. Signs and symptoms as well as laboratory findings are described. Treatment options including antithyroid drugs, beta blockers, radioiodine, and surgery are discussed in detail. Thyrotoxic crisis, a life-threatening exacerbation of hyperthyroidism, is also covered.
1) The document discusses thyrotoxicosis and hypothyroidism, including the development, anatomy, histology, blood supply, physiology, and clinical features of the thyroid gland.
2) It describes the various causes, signs and symptoms, investigations, and treatment approaches for hyperthyroidism and hypothyroidism.
3) Key topics covered include Graves' disease, toxic multinodular goiter, toxic nodules, hypothyroidism, myxedema, and thyroid function tests.
Thyrotoxicosis is a clinical syndrome caused by high levels of circulating thyroid hormones, with primary causes including Graves' disease and toxic nodular goiter, leading to symptoms of weight loss, fatigue, heat intolerance, and emotional changes. Diagnosis is based on examination findings of a goiter, tachycardia, and eye changes like exophthalmos, with treatment options including antithyroid drugs, radioactive iodine, or surgery to remove the overactive thyroid tissue.
This document discusses the management of thyrotoxicosis, including investigations and treatment options. Key investigations include thyroid function tests, radioisotope scans, and antibody tests. Treatment options include anti-thyroid drugs, surgery, and radioactive iodine therapy. Anti-thyroid drugs are the first line treatment and help prepare patients for surgery or radioactive iodine therapy. Surgery involves removing parts of the thyroid gland and is indicated when drugs fail or for large goiters. Radioactive iodine therapy uses radiation to destroy the thyroid tissue and is preferred for older patients with no risk of genetic mutations. Long term management may require thyroid hormone replacement therapy.
Hyperthyroidism, or an overactive thyroid, is caused by excessive secretion of thyroid hormones from the thyroid gland. Common causes include Graves' disease, toxic nodular goiter, and thyroiditis. Symptoms include rapid heart rate, sweating, weight loss, and anxiety. Diagnosis involves blood tests to measure thyroid hormone levels. Treatment options are anti-thyroid medications, radioactive iodine therapy, or surgery to remove part of the thyroid gland.
Hyperthyroidism refers to excessive thyroid hormone production. Graves' disease is the most common cause. Symptoms include tremors, weight loss, palpitations, heat intolerance and eye changes. Diagnosis involves blood tests showing low TSH and high free T4 levels. Treatments include antithyroid drugs, radioactive iodine ablation, or surgery. Untreated hyperthyroidism can lead to thyroid storm, weight loss, osteoporosis, heart and eye complications. Follow-up care after treatment is needed to monitor for hypothyroidism or recurrence.
This document discusses the treatment of thyrotoxicosis. The main goals of treatment are to decrease hyperthyroid symptoms and establish a euthyroid state. The main treatment modalities are antithyroid drugs, radiotherapy, and surgery. Antithyroid drugs like methimazole and propylthiouracil work by inhibiting thyroid hormone production. Radioactive iodine treatment involves administering radioactive iodine which is taken up by the thyroid gland to destroy thyroid tissue. Surgery involves removing part or all of the thyroid gland. Selection of treatment depends on factors like severity of symptoms, comorbidities, risks of each treatment, and patient preferences. Long term follow up is needed to monitor thyroid hormone levels and watch
This document discusses thyrotoxicosis (hyperthyroidism) during pregnancy. It notes the physiological changes in thyroid function during pregnancy, including increases in thyroid binding globulin and decreases in plasma iodide levels. It describes the signs and symptoms of maternal hyperthyroidism as well as its most common cause, Graves' disease. Guidelines are provided for clinical management, including use of thionamide medications like propylthiouracil to control thyroid levels while monitoring the fetus. Treatment may also include beta blockers, iodine, or subtotal thyroidectomy in rare cases. Radioactive iodine therapy is contraindicated in pregnancy due to risks to the fetal thyroid.
Hyperthyroidism is a hypermetabolic state caused by increased thyroid secretion. There are several types, including Graves' disease (the most common cause), toxic nodular goitre, and toxic adenoma. Clinical features include symptoms like fatigue, heat intolerance, and weight loss, as well as signs like tachycardia, eye changes, and thyroid swelling. Diagnosis involves clinical evaluation, thyroid function tests, and scans. Treatment options are antithyroid drugs, surgery, and radioactive iodine.
The document summarizes thyroid disorders in pregnancy. Some key points:
- Thyroid disorders are among the most common endocrine conditions affecting 1-2% of pregnancies. Proper management is important for pregnancy outcomes.
- Hypothyroidism can cause complications for both mother and fetus like preeclampsia, preterm birth, and developmental delays. Treatment is levothyroxine.
- Hyperthyroidism in pregnancy is usually Graves' disease and may improve during pregnancy due to immunosuppressive effects but often worsens postpartum. Treatment focuses on maintaining normal thyroid levels.
- Postpartum thyroiditis is an autoimmune condition causing transient thyroid dysfunction after delivery
1) Thyroid eye disease (TED) is an autoimmune disorder associated with Graves' disease. It can affect the eye muscles, fatty tissue, and optic nerve.
2) Treatment depends on the severity and activity of TED. Mild and inactive cases may only require monitoring. Moderate to severe active TED is treated with intravenous steroids, radiation therapy, or surgery. Sight-threatening TED urgently requires treatments like steroids and orbital decompression.
3) Managing thyroid function and advising patients to stop smoking can help prevent progression of TED. Referral to a specialist TED clinic is recommended for persistent or worsening eye symptoms.
hyperthyroidism, thyrotoxicosis, grave disease, thyroid storm, pregnancy, high risk pregnancy, pregnancy complications, management of thyrotoxicosis and thyroid storm in pregnancy
This document summarizes the histological structure of the thyroid gland. It notes that the thyroid gland consists of two lobes and an isthmus, and its structural unit is the follicle. Each follicle contains a layer of epithelial cells surrounding a follicular cavity filled with colloid. The epithelial cells are cuboidal and can change shape depending on the gland's activity level. Additionally, parafollicular cells in the interfollicular spaces secrete thyrocalcitonin. The colloid within the follicular cavity is a gel-like secretion composed of nucleoproteins and enzymes used to synthesize thyroid hormones.
The document discusses thyroid gland disorders, including hyperthyroidism and hypothyroidism. It describes the anatomy and function of the thyroid gland, the hormones it produces, and how they are regulated. It then discusses the causes, symptoms, diagnosis and treatment of hyperthyroidism and hypothyroidism, focusing on Graves' disease and Hashimoto's thyroiditis. It also covers complications like myxedema coma and the effects of thyroid hormones on multiple body systems.
The thyroid gland is the body's largest single organ specialized for endocrine hormone production. Its function is to secrete an appropriate amount of the thyroid hormones, primarily (thyroxine, T4) , and a lesser quantity of triiodothyronine (T3) , which arises mainly from the subsequent extrathyroidal deiodination ofT4.
Diagnosis and treatment of hypothyroidism.pptxvivianOkoli1
Hypothyroidism is a common endocrine disorder where the thyroid gland does not produce enough hormones. It can be caused by iodine deficiency, autoimmune disease, or drugs/radiation affecting the thyroid. Symptoms are often subtle and vary in children, women, and elderly people. Laboratory tests show low thyroid hormones and high TSH. Treatment is with levothyroxine replacement to restore hormone levels, with dose adjustments over time based on symptoms and follow-up tests. In severe cases, myxoedema coma requires emergency treatment in hospital.
Khadeeja Nasser, a 35-year-old woman, presented with fatigue, weight gain, cold intolerance, dry skin, constipation, and irregular periods over the past six months. Examination found fatigue, puffy face, slow pulse, dry skin, and sluggish reflexes. Labs found elevated TSH and low T4, with positive thyroid peroxidase antibodies. This suggests Hashimoto's thyroiditis causing hypothyroidism. Hypothyroidism presents with the symptoms described and is diagnosed by elevated TSH and low T4. It is managed with levothyroxine replacement.
Hypothyroidism Diagnosis, Etiopathogenesis and TreatmentPranatiChavan
Hypothyroidism is a condition in which the thyroid gland doesn't produce enough thyroid hormone.
Hypothyroidism's deficiency of thyroid hormones can disrupt such things as heart rate, body temperature and all aspects of metabolism. Hypothyroidism is most prevalent in older women.
Major symptoms include fatigue, cold sensitivity, constipation, dry skin and unexplained weight gain.
Treatment consists of thyroid hormone replacement.
This document summarizes information about hypothyroidism and hyperthyroidism (thyrotoxicosis). It discusses the epidemiology, causes, clinical manifestations, investigations, treatment, and prevention of hypothyroidism. For hyperthyroidism/thyrotoxicosis, it covers the epidemiology, causes, clinical signs and symptoms, investigations, treatment options including anti-thyroid drugs, surgery and radioactive iodine, and considerations for treatment in pregnancy. It also provides details on myxedema coma, a rare but serious complication of severe untreated hypothyroidism.
- Shelley, a 14-year-old girl, presents with symptoms of hyperthyroidism including weight loss, tremors, and an enlarged thyroid gland. Laboratory tests confirm low TSH and high free T3 and T4 levels. She is diagnosed with Graves' disease based on her symptoms and positive thyroid receptor antibodies. Graves' disease is an autoimmune disorder causing hyperthyroidism due to stimulating antibodies to the TSH receptor. Treatment involves antithyroid drugs like carbimazole to control thyroid levels and beta blockers to control symptoms of thyrotoxicosis.
This document provides information about thyroid function tests. It begins with an introduction to the thyroid gland and its role in producing thyroid hormones that regulate metabolism. It then discusses disorders like hyperthyroidism and hypothyroidism. The bulk of the document describes various diagnostic tests used to evaluate thyroid function, including TSH, total and free T4 and T3, thyroid hormone uptake, and secretory capacity. Each test is explained in terms of its clinical significance and normal reference ranges. The document concludes with references.
Hashimoto's thyroiditis and subacute thyroiditis are the most common causes of primary hypothyroidism. Hashimoto's is an autoimmune disorder characterized by elevated TSH and the presence of anti-thyroid antibodies. Subacute thyroiditis causes a transient hypothyroid phase due to thyroid hormone release rather than increased synthesis, with low radioactive iodine uptake and no antibodies present. Graves' disease, the most common cause of hyperthyroidism, results from TSH receptor antibodies that mimic TSH and stimulate increased thyroid hormone production.
Introduction:
@ Thyroid releases T3 & T4
@ The ratio of T4 to T3 is 5:1, so most of the hormone released is
thyroxine
@ Most of the T3 in the blood is derived from thyroxine
@ T3 is three to four times more potent than T4
@ The affinity of the receptor site for T3 is about ten times higher than that for T4
The endocrine emergencies most commonly discussed by EMS provi.docxtodd701
The endocrine emergencies most commonly discussed by EMS providers typically deal with diabetes mel-litus, a condition associated with malfunction of the pancreas or its hormones and improper regulation of the blood glucose level. It is important to recognize that there are many other emergencies that may be related to
malfunctioning endocrine glands or hormones. These emergencies may produce acute life-threatening conditions that
exhibit a wide variety of clinical presentations based on the gland or hormones involved. Some patients may not readily
recognize, or may ignore, the slow and progressive clinical changes that are occurring and allow the disease to create an
acute life-threatening condition.
Since EMS providers may be called upon to manage the patient experiencing this acute and potentially life-threatening
condition, it is prudent for them to possess an awareness and understanding of other potential life-threatening endocrine
emergencies, such as those involving the thyroid gland and its related hormones.
By Joseph J. Mistovich, MEd, NREMT-P,
William S. Krost, BSAS, NREMT-P,
& Daniel D. Limmer, AS, EMT-P
Part 1: Hyperthyroidism and Thyroid Storm
This CE activity is approved
by EMS Magazine, an
organization accredited by
the Continuing Education
Coordinating Board
for Emergency Medical
Services (CECBEMS), for
1.5 CEUs.
OBJECTIVES
• Review anatomy of the
thyroid gland
• Discuss metabolic
disturbances
• Review emergency
management of
endocrine emergencies
Sponsored by
CONTINUING
EDUCATION FROM EMS
endocrine emergencies
This article is the first in a two-part series addressing endocrine emergencies involving thyroid hormone
disorders. The second part will follow in next month’s issue and cover conditions related to hypothyroid-
ism. The section below on anatomy and physiology of the thyroid gland pertains to both articles. It will be
important to review this section prior to reading the next article to completely understand the hypothyroid-
ism conditions covered in part two.
BEYOND THE BASICS:BEYOND THE BASICS:
Part 1: Hyperthyroidism and Thyroid Storm
This CE activity is approve
by EMS Magazine, an
organization accredited by
the Continuing Education
Coordinating Board
for Emergency Medical
Services (CECBEMS), for
1.5 CEUs.
OBJECTIVESJ
• Review anatomy of the
thyroid gland
• Discuss metabolic
disturbances
• Review emergencyThis article is the first in a two part series addressing endocrine emergencies involving thyroid hormoneThis article is the first in a two part series addressing endocrine emergencies involving thyroid hormone
ENDOCRINEENDOCRINE
EMERGENCIESEMERGENCIES
P
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D
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www.emsresponder.com ■ EMS ■ OCTOBER 2007 123
123-127 ce article.indd 123123-127 ce article.indd 123 9/18/2007 3:38:33 PM9/18/2007 3:38:33 PM
ANATOMY AND
PHYSIOLOGY OF THE
THYROID GLAND
The thyroid is a butterfly-shaped
endocrine gland l.
A 27-year-old female presents with palpitations. Exam finds an enlarged, tender thyroid. Labs show suppressed TSH, elevated T4 and low radioactive iodine uptake. The next appropriate test would be to check the ESR, as these findings are consistent with subacute thyroiditis, an inflammation of the thyroid gland often caused by a viral infection. The treatment is symptomatic with pain medication as the condition will typically resolve on its own over several months.
A 27-year-old female presents with palpitations. Exam finds an enlarged, tender thyroid. Labs show suppressed TSH, elevated T4 and low radioactive iodine uptake. The next appropriate test would be to check the ESR, as these findings are consistent with subacute thyroiditis, an inflammation of the thyroid gland often caused by a viral infection. The treatment is symptomatic with pain medication; the condition will typically resolve on its own over several months.
The document discusses various thyroid disorders including hyperthyroidism, hypothyroidism, thyroiditis, thyroid nodules, thyroid cancer, and parathyroid glands. It covers the causes, signs and symptoms, diagnostic tests, and treatment options for different thyroid conditions. Lab tests like TSH, T4, and radioactive iodine uptake can help evaluate thyroid function and differentiate disorders. Diseases discussed include Graves' disease, Hashimoto's thyroiditis, toxic nodular goiter, hypothyroidism, thyroiditis, and thyroid cancer.
DIFFICULTIES IN LAB. DIAGNOSIS OF THYROID DISEASEMoustafa Rezk
The document discusses common thyroid diseases and laboratory tests used in their diagnosis. It describes the main thyroid diseases as hypothyroidism, hyperthyroidism, goiters, thyroiditis, solitary thyroid nodules, and cancer. For each disease, it discusses causes, symptoms, and diagnostic tests. It emphasizes that no single test can diagnose thyroid disease and that a combination of tests is needed. It also notes that subtle thyroid abnormalities may be missed by standard lab ranges and that patient symptoms should be considered.
Thyroiditis is a general term that refers to “inflammation of the thyroid gland”. Thyroiditis includes a group of individual disorders causing thyroidal inflammation but presenting in different ways. For example, Hashimoto's thyroiditis is the most common cause of hypothyroidism in the United States.
1. The thyroid gland secretes thyroid hormones that regulate metabolism and growth. Thyroid hormones are synthesized within thyroid follicles by iodination of tyrosine residues on thyroglobulin.
2. Thyroid hormone synthesis and secretion is regulated by a negative feedback loop involving thyroid stimulating hormone (TSH) from the pituitary gland.
3. Disorders of the thyroid gland include hyperthyroidism (overproduction of hormones) and hypothyroidism (underproduction of hormones).
The thyroid gland produces thyroid hormones that regulate metabolism. It is located in the neck below the thyroid cartilage. The main thyroid hormones are T3 and T4, which are synthesized from iodine and tyrosine. Hormone production is regulated by TSH from the pituitary and TRH from the hypothalamus. Common thyroid disorders include hypothyroidism, in which hormone production is deficient, and hyperthyroidism, in which hormones are in excess. Blood tests can measure thyroid hormones and TSH/TRH to evaluate thyroid function and diagnose disorders.
Thyroid storm, or thyrotoxic crisis, is a life-threatening complication of hyperthyroidism characterized by multisystem involvement. It occurs when a precipitating event causes a sudden increase in thyroid hormone levels in a patient with hyperthyroidism. Common precipitants include discontinuing antithyroid medication or thyroid surgery. Thyroid storm requires prompt treatment with beta-blockers, antithyroid drugs, iodine, glucocorticoids, and supportive care to reduce mortality, which is estimated at 8-25% without treatment. Symptoms include fever, tachycardia, heart failure, neurological changes, and gastrointestinal issues. Diagnosis is clinical based on symptoms and elevated thyroid hormone levels
The thyroid gland secretes three hormones: T3, T4, and calcitonin. T3 and T4 regulate metabolism, while calcitonin regulates calcium levels. The thyroid is located in the neck below the Adam's apple. T3 and T4 are synthesized from tyrosine and stored bound to thyroglobulin. They are regulated by TSH from the pituitary and feedback to decrease TSH secretion. The main actions of thyroid hormones are to increase growth, metabolism, and heart rate. Hypothyroidism is treated with thyroxine replacement therapy.
Know the difference between Endodontics and Orthodontics.Gokuldas Hospital
Your smile is beautiful.
Let’s be honest. Maintaining that beautiful smile is not an easy task. It is more than brushing and flossing. Sometimes, you might encounter dental issues that need special dental care. These issues can range anywhere from misalignment of the jaw to pain in the root of teeth.
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Summer is a time for fun in the sun, but the heat and humidity can also wreak havoc on your skin. From itchy rashes to unwanted pigmentation, several skin conditions become more prevalent during these warmer months.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)MuskanShingari
Statistics- Statistics is the science of collecting, organizing, presenting, analyzing and interpreting numerical data to assist in making more effective decisions.
A statistics is a measure which is used to estimate the population parameter
Parameters-It is used to describe the properties of an entire population.
Examples-Measures of central tendency Dispersion, Variance, Standard Deviation (SD), Absolute Error, Mean Absolute Error (MAE), Eigen Value
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
1. Volume 32 Number 6, December 2005 407
Thyrotoxicosis:
Pathophysiology, assessment
and management
Marianne S Elston MBChB FRACP, Endocrinology Research Fellow, and John V Conaglen MD
FRACP, Consultant Endocrinologist
Thyrotoxicosis, which results from the
biochemical and physiologic effects
of excess thyroid hormone regardless
of cause, is one of the more common
endocrine disorders presenting to the
family physician. By definition,
hyperthyroidism is a term restricted
to situations in which the thyroid
gland is responsible for overproduc-
ing thyroid hormone. Arbitrarily the
causes of thyrotoxicosis can be dif-
ferentiated into those associated with
a high uptake on radioactive iodine
or technetium scanning (most com-
monly Graves disease) and those with
a low uptake (Table 1).
The normal adult thyroid is one
of the largest endocrine organs
weighing about 15–20 grams. It con-
sists of two lobes joined by an isth-
mus, with arterial blood supply from
both the superior and the inferior
thyroid arteries. The normally high
blood flow of 4–6mL/minute/g (com-
pared to the renal blood flow of 3mL/
min/g) may increase to over 1L/
minute in the diffuse toxic goitre of
John V Conaglen is Clinical Director of
Endocrinology at Waikato Hospital and As-
sociate Professor of Medicine in the Waikato
Clinical School, Faculty of Medical and Health
Sciences, University of Auckland. His research
interests include the role of growth factors
in cellular repair, the clinical impact of endo-
crine genetic disorders and the investigation
and management of sexual desire disorders.
Marianne Elston previously
workedasaseniorendocrinology
registrar at Waikato Hospital
and is currently working as a
Diabetes and Endocrinology Re-
search Fellow at Middlemore
Hospital, Auckland. Interests in-
clude familial endocrine disor-
ders and pituitary disease.
Graves disease, resulting in an audi-
ble bruit or palpable thrill. At a mi-
croscopic level the gland is composed
of follicles filled with thyroglobulin-
containing colloid in which thyroid
hormone is stored. In addition the
gland contains parafollicular (C cells)
cells, which secrete calcitonin. The
thyroid gland synthesises and secretes
thyroid hormones sufficient to meet
bodily needs. This involves active
uptake of iodide by the thyroid trans-
membrane sodium-iodide symporter,
subsequent oxidation of the iodide
by the enzyme thyroid peroxidase
(TPO) and incorporation into the thy-
roglobulin molecule in the form of
monoiodotyrosine (MIT) and
diiodotyrosine (DIT). These precur-
sors are joined or coupled to form
thyroxine (T4) and triiodothyronine
(T3) in the thyroglobulin molecule.
The thyroid stores large amounts of
thyroid hormones in the colloid, of
which only about 1% are secreted
daily. This excess storage protects
against hypothyroidism should thy-
roid hormone synthesis be temporar-
ily inhibited, for example by a di-
etary goitrogen. This excess storage
of thyroglobulin helps explain why
anti-thyroid medications may not
reduce the T4 levels for at least two
weeks. In addition, the thyrotoxico-
sis occurring after an inflammatory
thyroiditis in which the thyroid cells
are disrupted results from the release
of this preformed thyroid hormone
storage. All of the steps in thyroid
hormone synthesis and release are
stimulated by Thyroid Stimulating
Hormone (TSH), secreted from the
anterior pituitary. The thyroid gland
releases both T4 and T3, however in
the euthyroid state about 80% of the
T3 is produced peripherally from T4.
Being relatively lipid-soluble both
thyroid hormones circulate bound to
plasma proteins – Thyroxine-Bind-
ing Globulin (TBG) and transthyretin
and albumin and to a lesser extent as
the free hormone. Thyroid hormone
readily crosses the plasma membrane
and in the form of T3 binds to spe-
Continuing Medical Education
2. 408 Volume 32 Number 6, December 2005
cific intra-cellular thyroid hormone
receptors, which as a complex act as
transcription factors to up- or down-
regulate many specific genes. The
circulatory levels of T3 are control-
led by negative feedback loops in-
volving the thyroid, pituitary and
hypothalamus. Stability of thyroid
hormone levels are assisted by the
large intra-thyroidal hormone pool.
Although thyrotoxicosis is not
always obvious clinically, (commonly
presenting as tiredness), the bio-
chemical profile of an elevated Free
T3 (FT3), and/or Free T4 (FT4), with a
suppressed TSH make the diagnosis
relatively straightforward. In T3-toxi-
cosis the FT3 is elevated and TSH is
suppressed with a normal FT4.
Occasionally a family physician
receives laboratory results in which
the T3 and/or T4 levels are above the
upper limit of the reference range and
the TSH is not suppressed. The most
common cause of elevated free thy-
roid hormone levels with a measur-
able TSH is interference with the as-
say by heterophile antibodies in a
clinically euthyroid patient. Specific
tests for heterophile antibodies can
be requested from the laboratory.
Thyroid hormone resistance is an-
other cause of elevated thyroid hor-
mone levels with a normal or elevated
TSH. Recent intake of excess thyrox-
ine in a previously noncompliant
patient may also cause the same pat-
tern, as free thyroid hormone levels
will elevate before the TSH falls.
Secondary thyrotoxicosis (elevated
free thyroid hormone levels, with a
measurable levels of TSH in a clini-
cally thyrotoxic patient) due to a TSH-
secreting pituitary adenoma is rare,
(estimated incidence approximately
one per million per annum). Although
extremely rare, TSHomas are impor-
tant not to miss as treatment is prima-
rily directed towards the pituitary.
Given the complexity, patients
with elevated free thyroid hormone
levels and a nonsuppressed TSH
should be referred to an endocrin-
ologist for more detailed investiga-
tion to ensure correct diagnosis and
treatment.
Clinical features of thyrotoxicosis
Presenting symptoms resulting from
excess metabolic activity include
tiredness, heat intolerance, unex-
plained weight loss, excess sweating,
palpitations, tremor and irritability
(Table 2). Older patients with ‘apa-
thetic thyrotoxicosis’ may present
predominantly with weight loss, ano-
rexia, muscle weakness, depression
and lethargy. Occasional patients may
present with sudden onset profound
muscle weakness (which may
progress to a flaccid tetraparesis),
associated with severe hypokalaemia,
which resolves completely on resto-
ration of the serum potassium (thy-
rotoxic hypokalaemic periodic pa-
ralysis – THPP). THPP, which may be
precipitated by exercise or a large
carbohydrate meal, is more common
in males, especially Asian, Maori, and
Polynesian, and results from increased
intracellular uptake of potassium.
The severity of thyrotoxicosis can
vary from the patient who has very
few symptoms to those who present
with florid congestive cardiac heart
failure, life-threatening arrhythmias,
and even severe psychotic illness.
Thyroid storm, although extremely
rare, is usually of sudden onset and
may be precipitated by infection, sur-
gery or major illness. Fever is almost
always present, with profound tachy-
cardia and possibly arrhythmias.
Restlessness and delirium or even
frank psychosis may occur and
progress to coma. Nausea, vomiting
Table 1. Causes of thyrotoxicosis
Thyrotoxicosis with high radioiodine Thyrotoxicosis with low radioiodine
uptake uptake
Autoimmune – Graves disease Thyroiditis
– Subacute
Autonomous thyroid tissue – Postpartum
– Toxic multinodular goitre – Drug-induced
– Solitary toxic adenoma e.g. interferon, amiodarone
– Radiation
TSH-mediated
– TSHoma (rare) Autonomous thyroid tissue with iodine
load e.g. amiodarone/x-ray contrast
HCG-mediated
– Hyperemesis gravidarum Excessive exogenous thyroid hormone
– Hydatidiform mole/ intake
choriocarcinoma (rare)
– Testicular tumours (rare) Ectopic thyrotoxicosis
– Struma ovarii (ectopic thyroid
tissue)(rare)
– Metastatic follicular cancer with
with functioning metastases (rare)
Figure 1. Diffuse goitre Figure 2. Graves ophthalmopathy
Continuing Medical Education
3. Volume 32 Number 6, December 2005 409
and abdominal pain frequently oc-
curs early. Although this condition
is often exaggerated by the inexpe-
rienced clinician, unrecognised thy-
roid storm is usually fatal.
Graves disease
Graves disease is an autoimmune
condition with the thyrotoxicosis
caused by autoantibodies stimulating
the TSH receptor (TSHRAb or Thy-
roid Stimulating Immunoglobulins,
TSI). As in other autoimmune condi-
tions, Graves disease is more com-
mon in females (7–10:1) and a fam-
ily history of thyroid or other
autoimmune disease is often present.
The classical manifestations of Graves
disease include a diffuse toxic goitre
(Figure 1), congestive ophthalmopa-
thy (Figure 2) and dermopathy
(pretibial-myxoedema) (Figures 3
and 4). These three features of Graves
disease may occur simultaneously or
independently in a given individual.
In practice, patients commonly
present with thyrotoxicosis and a
diffuse goitre usually with a soft
bruit. Although congestive ophthal-
mopathy is often present, it is usu-
ally mild and may not be recognised.
Figures 3 and 4. Graves dermopathy
Dermopathy (pretibial myxoedema)
is relatively uncommon. It is impor-
tant to distinguish the congestive
ophthalmopathy of Graves disease
from the eye signs secondary to sym-
pathetic overactivity, which may oc-
cur in thyrotoxicosis from any cause.
Congestive ophthalmopathy is due to
swelling of the extraocular muscles
and orbital fat by accumulation of
excess water and glycosamino-
glycans secreted from fibroblasts.
This results in bulgy eyes (exophthal-
mos/proptosis) and conjunctival in-
jection, chemosis, periorbital oedema,
restriction in eye movements and, in
severe cases, visual loss. Thyrotoxi-
cosis from any cause may cause sym-
pathetic eye signs such as lid lag and
lid retraction and the stare (‘startled
rabbit’ look), which are not specific
to Graves disease.
Toxic multinodular goitre
Toxic multinodular goitre (MNG) is
due to the development of autonomy
in a (usually) long-standing pre-ex-
isting goitre. The thyroid feels nodu-
lar and there is no bruit. The thyro-
toxicosis may be precipitated by re-
cent iodine exposure, such as iodine
containing contrast from radiologi-
cal procedures, iodine from medica-
tions (e.g. amiodarone) or from health
shop preparations. Patients with toxic
multinodular goitre are often older
and more severely affected by the
hyperthyroidism. Radioactive iodine
is an effective treatment for toxic
MNG provided there hasn’t been re-
cent iodine exposure.
Solitary toxic nodule
Solitary toxic nodule refers to the
development of a (usually) solitary
nodule in a thyroid that is otherwise
normal. Most are due to a somatic
Table 2. Symptoms and signs of thyrotoxicosis
Symptoms Signs
Fatigue Finetremor
Heat intolerance Tachycardia
Weight loss (rarely weight gain) Sweating
Hyperphagia (rarely anorexia) Goitre
Palpitations Lid lag, retraction
Sweating Heart failure
Tremor Atrial fibrillation
Reduced exercise tolerance Ophthalmopathy
Increased frequency of defaecation Dermopathy
Loose bowel motions Proximal myopathy
Anxiety Gynaecomastia
Irritability Systolic hypertension
Poorsleep Hyperdynamic circulation
Irregular periods Hyperreflexia
Lighter periods Palmar erythema
Difficulty concentrating
Urinary frequency Other
Weakness Hypercalcaemia, raised alkaline
Shortness of breath phosphatase, deterioration in glycaemic
control
Continuing Medical Education
4. 410 Volume 32 Number 6, December 2005
mutation in the TSH Receptor gene
resulting in constitutive activation of
the receptor without TSH binding.
With increased growth and activity
of the nodule the remainder of the
gland becomes suppressed and even-
tually atrophic. It is more common
in young-middle-aged patients with
mild thyrotoxicosis and presents with
a single smooth palpable nodule (with
no bruit). T3-toxicosis is not uncom-
mon in this setting. Treatment is ei-
ther radioactive iodine (with a low
risk of subsequent hypothyroidism,
as the rest of the suppressed gland
usually recovers function) or surgi-
cal removal of the nodule.
Thyroiditis
Subacute viral thyroiditis is another
relatively common cause of thyro-
toxicosis. The patient presents
acutely with hyperthyroidism, with
or without neck pain, and general
features of malaise, fatigue and my-
algia. The thyroid gland may be im-
palpable or mildly enlarged, and may
or may not be tender. The erythro-
cyte sedimentation rate and other
inflammatory markers are usually
raised, associated with a mild nor-
mochromic anaemia. If the clinician
is uncertain of the diagnosis a Tech-
netium 99m thyroid scan will reveal
reduced uptake of the radioisotope
(in contrast to Graves disease in
which the uptake is increased). This
condition is self-limiting with an ini-
tial thyrotoxic phase due to release
of preformed thyroid hormone from
disrupted thyroid cells, followed by
a hypothyroid phase, which may per-
sist for several months before the re-
turn to euthyroidism. Treatment is
symptomatic with analgesia for any
thyroid discomfort (paracetamol be-
ing first-line, followed by NSAIDs.
Glucocorticoids such as prednisone
are only rarely required). It should
be noted that none of these treatments
alter the natural course of the dis-
ease. Beta-blockers can reduce the
symptoms of thyrotoxicosis such as
palpitations and can be weaned as the
thyrotoxicosis resolves. The hypothy-
roid phase typically doesn’t need
treatment but occasionally a short
course of thyroxine is required if the
patient is severely symptomatic. The
whole process may take six to nine
months. In about 5% of patients with
subacute thyroiditis the hypothy-
roidism may be permanent.
Investigations
The diagnosis usually just requires thy-
roid function tests – FT4, FT3, and TSH
followed by a subsequent good clini-
cal assessment. Measurement of thy-
roid antibodies may assist in determin-
ing the autoimmune nature of the con-
dition. Often the cause of thyrotoxi-
cosis is obvious from the history and
examination findings (e.g. a diffuse
goitre with bruit, with signs of con-
gestive ophthalmopathy is clearly
Graves disease and no further imaging
is required). When the diagnosis is not
obvious, e.g. the thyroid is not palpa-
ble, or when there is the suspicion of
silent thyroiditis, radionuclide (Tech-
netium 99m) imaging can be very
helpful. Patients with Graves disease
and a small thyroid gland will have
increased uptake of the isotope and in
those with thyroiditis, recent iodine
or thyroxine exposure, the uptake of
Tc99m will be reduced. In the major-
ity of thyrotoxic patients, ultrasound
is not useful as a first-line test (in con-
trast to euthyroid patients with a soli-
tary nodule).
Treatment
Treatment needs to be directed ac-
cording to the underlying cause. In
patients with the common causes of
primary hyperthyroidism (Graves,
toxic MNG and solitary toxic nod-
ule) there are generally three options
for management. The first is the tem-
porary use of oral medications in-
cluding Carbimazole (CBZ), or pro-
pylthiouracil (PTU). More permanent
Table 3. Comparison of radioactive iodine and surgery for thyrotoxicosis
Radioactive Iodine Surgery
Advantages Advantages
Noninvasive Rapid control of thyrotoxicosis
Well-tolerated even in the elderly Rapid relief from pressure symptoms
Lower risk of hypothyroidism especially No risk of recurrence (if total
if toxic nodular goitre thyroidectomy performed)
Can reduce size of goitre
No need for anaesthetic
Disadvantages Disadvantages
Doesn’t work immediately Invasive
Risk of late hypothyroidism - may be Risk of complications including
insidious so ongoing monitoring hypoparathyroidism, recurrent
required laryngeal nerve injury and other
surgical complications
Anaesthetic risk
Precautions required May not be suitable for patients with
significant underlying cardiac disease
Absolutely contraindicated in Scarring (keloid in some patients)
pregnancy
Risk of flare secondary to radiation Need for lifelong thyroxine
thyroiditis (uncommon) replacement therapy
May need a second or third dose Increased anaesthetic and surgical risk if
(especially if Maori) patientseverelythyrotoxicpreoperatively
Need for lifelong thyroxine Recurrent disease following incomplete
replacement therapy surgery
Continuing Medical Education
5. Volume 32 Number 6, December 2005 411
options include radioactive iodine
I131
, or surgery (Table 3). All these
options have their place in the man-
agement of primary hyperthyroidism
and, as with all good medical prac-
tice, treatment should be tailored to
the patient’s circumstances.
1. Anti-thyroid drugs are com-
monly used as first-line treatment
to achieve a euthyroid state and
allow time for the more defini-
tive options to be discussed and
considered by the patient. CBZ
can usually be safely taken once
per day, whereas PTU needs to
be taken 2–4x/d depending on
dose. PTU is preferred in preg-
nant women as increasing reports
suggest an association between
methimazole (which is the
metabolite of CBZ) and a rare
embryopathy. In non-pregnant
patients, CBZ is usually preferred
as it is effective when taken once
daily and, in New Zealand, PTU
currently requires an exceptional
circumstances form. Both drugs
can result in agranulocytosis and
the potential for death. Agranu-
locytosis is reported to occur in
<1% of patients, usually in the
first few weeks to months of treat-
ment. Because, severe neutro-
paenia can develop suddenly,
warning the patient of the risk is
more important than routine
monitoring of the neutrophil
count. It is critical that any pa-
tient commenced on anti-thyroid
medication should be fully edu-
cated about the risk of agranu-
locytosis. In addition, the patient
can be provided with a labora-
tory form for a full blood count
with the suggestion that should
they develop any sign of infec-
tion such as sore throat and fe-
ver, they must stop the medica-
tion, have a blood test and phone
their family doctor for the result
the same day. After confirming
the neutrophil count is normal
the anti-thyroid medication can
be recommenced. If the
neutrophils are low, the test must
be immediately confirmed, and
urgent referral is required as the
patient may require hospital ad-
mission for antibiotics and
granulocyte colony-stimulating
factor. Anti-thyroid medication
should never be used in such pa-
tients again. One clinical diffi-
culty is that some patients with
thyrotoxicosis have a low neu-
trophil count prior to the use of
anti-thyroid medications. In this
circumstance consultation with
colleagues in endocrinology
and/or haematology and close
monitoring is recommended.
Other side-effects from anti-thy-
roid medications include liver
dysfunction, arthralgia and rash.
Approximately 40% of patients
with Graves disease are reported
to remain in remission after
ceasing a 12–18 month period
of medical therapy. This figure
of 40% is clearly an overstate-
ment as many patients on anti-
thyroid drugs will be requiring
such high doses of CBZ or PTU
at 12 months that they certainly
require definitive therapy, and
many other patients just choose
to have either radioactive iodine
or surgery or they have reacted
adversely to the drugs.
2. Radioactive iodine I131
: This is an
effective treatment administered
as an outpatient drink which car-
ries a risk of permanent hypothy-
roidism, especially in Graves dis-
ease. Hypothyroidism is gener-
ally preferable to hyperthy-
roidism since thyroxine replace-
ment is usually simpler for the
patient and physician and re-
quires less monitoring than sup-
pression with CBZ, or PTU. I131
has been in use for more than 50
years, appears to be safe and is
the recommended option for the
majority of patients requiring
definitive treatment, especially
the elderly. It cannot be given to
pregnant women, especially af-
ter the first trimester when the
fetal thyroid can concentrate io-
dine. I131
can also worsen the con-
gestive ophthalmopathy in a
small number of patients al-
though this is usually only mild
and temporary. Precautions such
as avoiding close contact for sev-
eral days or two weeks off work
for those working in the food
industry are required following
therapeutic I131
administration.
One disadvantage of radioactive
iodine is that it may take weeks
to months to have an effect. In
addition, the development of
hypothyroidism may be insidi-
ous and occur years after therapy.
For this reason it is important to
continue monitoring thyroid
function tests in euthyroid pa-
tient following I131
treatment,
even if it was administered dec-
ades earlier. Rarely patients may
develop a radiation thyroiditis,
which results in a flare of the
thyrotoxicosis 10–14 days post-
treatment. Administration of ra-
dioactive iodine to children re-
mains controversial, especially
after the reports of thyroid can-
cer in young people after the
Chernobyl disaster.
3. Surgery: Prior to offering surgery
it is best to normalise the thyroid
function tests with anti-thyroid
drugs. Moderate to severe thyro-
toxicosis increases the anaesthetic
and surgical risk. Generally sur-
gery is considered for patients
with large goitres causing
compressive symptoms, amioda-
rone-induced thyrotoxicosis re-
fractory to treatment or in young
patients with a solitary toxic nod-
ule. However, some patients just
prefer surgery to the concept of
taking a drink of radioactive io-
dine. In addition, surgery has the
advantage of rapid control of the
thyrotoxicosis when compared to
I131
and many patients just want
to get on with their lives. With
the exception of the solitary toxic
nodule in an otherwise normal
gland, near total thyroidectomy
is the preferred operation because
of the risk of recurrence of thy-
rotoxicosis in both Graves disease
and toxic MNG. Surgery does
Continuing Medical Education
6. 412 Volume 32 Number 6, December 2005
carry a mortality risk (as does
every operation) as well as the
risk of permanent hypoparathy-
roidism and recurrent laryngeal
nerve injury. As the complication
rate is lower if thyroidectomy is
performed by an experienced thy-
roid surgeon, it is important that
the referring physician be aware
of their specific surgeon’s skills.
Subclinical hyperthyroidism
Low or undetectable TSH levels with
levels of FT4 and FT3 within the ref-
erence range are found in subclini-
cal hyperthyroidism. This state may
result from excessive exogenous thy-
roid hormone administration or due
to endogenous overproduction of
thyroid hormone, e.g. multinodular
goitre with some autonomy. Excess
exogenous thyroid hormone is com-
mon and may be intentional, as in
the treatment of metastatic or local-
ised thyroid cancer with high risk of
recurrence, or unintentional, as in
hypothyroid patients replaced with
thyroxine. It is important not to con-
fuse patients with hypopituitarism
who will have a similar biochemical
profile and low TSH levels as a re-
sult of pituitary gland hypofunction.
Overt thyro-
toxicosis is a risk
factor for oste-
oporosis and frac-
tures although this
is more controver-
sial in subclinical
disease.1
Patients
with subclinical
hyperthyroidism
receiving thyrox-
ine replacement
for benign thyroid
disease should have the dose re-
duced to ensure the TSH is in the
reference range. The treatment of
subclinical hyperthyroidism re-
mains controversial, although many
studies report increased rates of
atrial fibrillation and increased left
ventricular mass in these patients.1
A recent consensus panel supported
the treatment of patients with
undetectable TSH (<0.01mU/L) espe-
cially for patients older than 60
years, and those at increased risk of
heart disease, osteoporosis, or those
with symptoms suggestive of hyper-
thyroidism.2
Patients with endog-
enous subclinical hyperthyroidism
should be followed and referral to
an endocrinology service consid-
ered if the condition persists, par-
ticularly in those with atrial fibril-
lation or in whom thyrotoxicosis
would be poorly tolerated because
of comorbid disease.
Other causes of a low TSH and
normal free thyroid hormone levels
include central hypothyroidism (usu-
ally the free thyroid hormone levels
are at the lower end of the reference
range), recovery from hyperthy-
roidism and as a transient effect in
patients with nonthyroidal illness
(sick euthyroid syndrome).
Pregnancy
Pregnancy is a special situation and
pregnant women with thyrotoxico-
sis should be referred to an
endocrinology service. Normal preg-
nancy with thyroid enlargement and
hyperdynamic circulation can mimic
some features of hyperthyroidism. In
addition, TSH levels can be sup-
pressed in preg-
nancy especially
during the 8th–
14th weeks be-
cause of HCG
stimulation of the
TSH receptor. Hy-
peremesis gravi-
darum may be as-
sociated with
frankly elevated
thyroid hormones,
which then settle
around 14–16 weeks as the HCG lev-
els settle. Distinguishing this condi-
tion from Graves disease can be dif-
ficult with pre-existing thyroid dis-
ease, sleeping tachycardia, family his-
tory of autoimmune disease and posi-
tive TSH-receptor stimulating anti-
bodies being more indicative of
Graves disease. Thyrotoxicosis in
pregnancy is associated with an in-
creased rate of spontaneous miscar-
riage, stillbirth, preterm labour, low
birth weight, and preeclampsia.
Treatment with PTU, rather than CBZ,
is increasingly recommended be-
cause of rare reports of methimazole
embryopathy. While this has not been
reported with carbimazole as
carbimazole is metabolised to methi-
mazole it is probably reasonable to
opt for PTU. Both medications cross
the placenta and can cause fetal hy-
pothyroidism and goitre so the low-
est possible dose should be given and
the maternal free thyroid hormone
levels should be maintained at the
upper end of the reference range and
measured monthly over the gestation.
Obstetric involvement is indicated
given the complexity and the small
risk of fetal thyrotoxicosis. Women
with only very mild thyrotoxicosis
can be monitored carefully without
treatment. Graves disease improves
throughout pregnancy and often
women can have the anti-thyroid
medication stopped by the third tri-
Key Points
• Consider the underlying cause
of the thyrotoxicosis – making
a specific diagnosis will allow
the practitioner to proceed
directly to appropriate therapy.
Uncertainty about the diagno-
sis will require early referral to
endocrinology or further
investigation such as techne-
tium scanning.
• Early referral should be made
for patients with severe
thyrotoxicosis, those on
amiodarone and those with
reduced physiological reserve,
e.g. the elderly and patients
with cardiac disease.
• Anti-thyroid-induced agranu-
locytosis is rare, but can be
life-threatening. Any patient
started on anti-thyroid medica-
tion needs to be warned about
this risk and instructed what to
do in the event of illness.
Radioactive iodine is
absolutely contraindicated
during pregnancy, but
surgery occasionally is
required in special
situations with the safest
time being during the
second trimester
Continuing Medical Education
7. Volume 32 Number 6, December 2005 413
mester. Radioactive iodine is abso-
lutely contraindicated during preg-
nancy, but surgery occasionally is re-
quired in special situations with the
safest time being during the second
trimester. Post-partum flare of Graves
disease in the mother is common and
should be anticipated based on the
pre- or early-pregnancy thyroid sta-
tus of the mother. Women with a his-
tory of Graves disease who are now
euthyroid (e.g. post thyroid ablation
with radioactive iodine or surgery)
may still have TSH-R antibodies
which can cross the placenta and
cause hyper- or hypo-thyroidism in
the fetus so TSH-R
Abs should be meas-
ured at the end of the
second trimester and
obstetric involve-
ment is required to
monitor for evidence
of fetal thyrotoxico-
sis, although this is
rare. Overzealous
treatment with anti-
thyroid medications
in the third trimester
can result in a fetal goitre, which may
lead to difficulties with delivery as
the fetal neck may be unable to fully
flex or with airway compromise.
Elderly
Thyrotoxicosis in the elderly may
present more subtly so a high index
of suspicion is required. The older
patient often does not tolerate thy-
rotoxicosis well and has an increased
risk of atrial fibrillation, exacerba-
tion of preexisting ischaemic heart
disease and congestive cardiac fail-
ure. Any elderly patient with newly
diagnosed atrial fibrillation should
have their thyroid function measured,
as atrial fibrillation may be the only
manifestation of thyrotoxicosis.
Amiodarone-induced
thyrotoxicosis
Amiodarone is an iodine-rich medi-
cation (approximately 37% iodine by
weight) and, while most patients on
amiodarone remain euthyroid, it may
cause either hypo- or hyper-
thyroidism. Patients on amiodarone
should have regular monitoring of
their thyroid function every three
months. Amiodarone-induced thyro-
toxicosis (AIT) may
even occur months
after the amiodarone
isstoppedandcanbe
very resistant to
treatment. Urgent re-
ferral to an
endocrinology serv-
ice should occur as
the typical patient
has underlying car-
diac disease so the
thyrotoxicosis may
be poorly tolerated. As the amiodarone
takes months to clear (half-life is 50–
60 days) there is no need to stop it
immediately on diagnosis of
amiodarone-induced thyrotoxicosis,
and indeed it may provide some
cardioprotection from the thyrotoxi-
cosis initially. The decision to continue
or stop the amiodarone should be
Patient information
American Thyroid Association website: www.thyroid.org/patients/brochures.html
References
1. Biondi B, Palmieri EA, Klain M, Schlumberger M, Filetti S,
Lombardi G. Subclinical hyperthyroidism: clinical features and
treatment options. Eur J Endocrinol 2005; 152:1-9.
2. Surks MI, Ortiz E, Daniels GH, Sawin CT, Col NF, Cobin RH,
Franklyn JA, Burman KD, Denke MA, Cooper RS, Weissman NJ.
Subclinical thyroid disease. Scientific review and guidelines for
diagnosis and management. J Am Med Ass 2004; 291:228-238.
made by a cardiologist familiar with
the patient’s condition so that an al-
ternative therapy, e.g. beta-blockade,
can be considered. As amiodarone
blocks the uptake of iodide by the thy-
roid gland, the only effective thera-
pies for AIT include high dose antithy-
roid medications or surgery. Beta-
blockers or glucocorticoids may have
a role in treatment.
Iodine
Excess iodine from any source may
cause hyperthyroidism (iodine-in-
duced hyperthyroidism or the Jod-
Basedow effect). For this reason, for
patients with known nodular thyroid
disease, clinicians need to consider
whether it is necessary to administer
iodine-containing materials (e.g. ra-
diological contrast agents, or drugs
such as amiodarone) as the extra io-
dine load may result in subsequent
thyrotoxicosis.
Thyrotoxicosis factitia
This is thyrotoxicosis that occurs
from excessive exogenous intake of
thyroid hormone. Patients are usu-
ally aware that they are taking the
medication although may deny it. It
may also be taken inadvertently as
part of weight loss preparations.
Typically there are typical biochemi-
cal and clinical features of thyrotoxi-
cosis along with suppressed serum
thyroglobulin levels and reduced up-
take on technetium scanning.
Any elderly patient with
newly diagnosed atrial
fibrillation should have
their thyroid function
measured, as atrial
fibrillation may be the
only manifestation of
thyrotoxicosis
‘There are in fact two things, science and opinion; the former begets knowledge, the latter ignorance. ‘
Hippocrates, Law
Continuing Medical Education