Resistance to thyroid hormone (RTH) is an inherited condition characterized by reduced sensitivity of tissues to thyroid hormone (TH). Individuals with RTH have high levels of TH (T4 and T3) but normal or slightly elevated TSH levels. The condition is usually caused by mutations in the TH receptor beta gene. Affected individuals are often clinically euthyroid due to compensatory increased TH production. The diagnosis of RTH requires high T4, normal or high TSH, and confirmation of reduced tissue response to supra-physiologic TH doses. Most patients do not require treatment as the reduced sensitivity is adequately compensated by increased TH levels.
This document discusses thyroid function tests. It describes:
1) The thyroid gland produces the hormones thyroxine (T4) and triiodothyronine (T3) which are transported to tissues.
2) Thyroid function tests measure levels of TSH, free T3, total T3, free T4, and total T4 to determine if a patient is hypothyroid or hyperthyroid.
3) Interpretation of the test results can indicate primary hyperthyroidism, autoimmune Hashimoto's thyroiditis, or subclinical hypothyroidism with Hashimoto's thyroiditis.
The thyroid gland produces hormones that are essential for normal body metabolism. Blood testing is now commonly available to determine the adequacy of the levels of thyroid hormones. These blood tests can define whether the thyroid gland's hormone production is normal, overactive, or underactive.
Interpretation of laboratory thyroid function tests Hussam Elmouzi
This document discusses thyroid function tests and thyroid disease. It notes that 5% of the world population has thyroid disease. It describes the hypothalamic-pituitary-thyroid axis and how thyroid hormones affect many organs. It discusses the signs and symptoms of hypo- and hyperthyroidism as well as their laboratory findings. It also discusses subclinical thyroid disease, treatment of thyroid disorders, thyroid disease in pregnancy, and congenital hypothyroidism.
This document discusses thyroid function tests. It provides a classification of thyroid tests based on measuring hormone levels, thyroid function, metabolic effects, and detecting autoimmune diseases. Common tests described include TSH, free T4, T3, thyroid antibodies, radioactive iodine uptake, TRH stimulation, and thyroid scanning. Abnormalities in thyroid function testing can indicate hypothyroidism or hyperthyroidism. The document outlines causes and clinical features of each, and how to evaluate results based on hormone levels. Fine needle aspiration cytology of the thyroid is also summarized.
This document summarizes various endocrine tests used to assess different endocrine functions and disorders. It describes dynamic tests such as the insulin tolerance test used to evaluate the hypothalamic-pituitary-adrenal axis and growth hormone axis. It also summarizes tests used to evaluate disorders of the adrenal glands such as the ACTH stimulation test, dexamethasone suppression tests, and tests used to diagnose Cushing's syndrome and hyperaldosteronism. Precautions, interpretations and procedures are provided for many of the major endocrine dynamic tests.
Congenital hypothyroidism and Hashimoto's thyroiditis are the most common causes of hypothyroidism in children, with congenital hypothyroidism requiring lifelong thyroid hormone replacement treatment if detected by newborn screening which aims to identify affected infants before symptoms arise to prevent intellectual disability. Graves' disease is the most frequent cause of hyperthyroidism in children, presenting with symptoms like irritability, weight loss, and eye changes.
Thyroid function tests and their interpretationsBhargavi Patel
This document discusses various thyroid conditions and test results. It covers subclinical hypothyroidism, where TSH is elevated but symptoms are minimal. It is recommended to confirm elevated TSH over 3 months before treatment. Secondary hypothyroidism involves low TSH and thyroid hormones, often due to pituitary issues. Sick euthyroid syndrome describes abnormal thyroid tests during illness without underlying thyroid problems.
The document provides information about the thyroid gland and thyroid function tests. It discusses that the thyroid gland produces thyroid hormones that regulate metabolism and other bodily functions. It describes different thyroid disorders like hyperthyroidism and hypothyroidism. It then explains various thyroid function tests that evaluate thyroid hormone levels, the hypothalamic-pituitary-thyroid axis, and detect thyroid antibodies to help diagnose thyroid conditions.
This document discusses thyroid function tests. It describes:
1) The thyroid gland produces the hormones thyroxine (T4) and triiodothyronine (T3) which are transported to tissues.
2) Thyroid function tests measure levels of TSH, free T3, total T3, free T4, and total T4 to determine if a patient is hypothyroid or hyperthyroid.
3) Interpretation of the test results can indicate primary hyperthyroidism, autoimmune Hashimoto's thyroiditis, or subclinical hypothyroidism with Hashimoto's thyroiditis.
The thyroid gland produces hormones that are essential for normal body metabolism. Blood testing is now commonly available to determine the adequacy of the levels of thyroid hormones. These blood tests can define whether the thyroid gland's hormone production is normal, overactive, or underactive.
Interpretation of laboratory thyroid function tests Hussam Elmouzi
This document discusses thyroid function tests and thyroid disease. It notes that 5% of the world population has thyroid disease. It describes the hypothalamic-pituitary-thyroid axis and how thyroid hormones affect many organs. It discusses the signs and symptoms of hypo- and hyperthyroidism as well as their laboratory findings. It also discusses subclinical thyroid disease, treatment of thyroid disorders, thyroid disease in pregnancy, and congenital hypothyroidism.
This document discusses thyroid function tests. It provides a classification of thyroid tests based on measuring hormone levels, thyroid function, metabolic effects, and detecting autoimmune diseases. Common tests described include TSH, free T4, T3, thyroid antibodies, radioactive iodine uptake, TRH stimulation, and thyroid scanning. Abnormalities in thyroid function testing can indicate hypothyroidism or hyperthyroidism. The document outlines causes and clinical features of each, and how to evaluate results based on hormone levels. Fine needle aspiration cytology of the thyroid is also summarized.
This document summarizes various endocrine tests used to assess different endocrine functions and disorders. It describes dynamic tests such as the insulin tolerance test used to evaluate the hypothalamic-pituitary-adrenal axis and growth hormone axis. It also summarizes tests used to evaluate disorders of the adrenal glands such as the ACTH stimulation test, dexamethasone suppression tests, and tests used to diagnose Cushing's syndrome and hyperaldosteronism. Precautions, interpretations and procedures are provided for many of the major endocrine dynamic tests.
Congenital hypothyroidism and Hashimoto's thyroiditis are the most common causes of hypothyroidism in children, with congenital hypothyroidism requiring lifelong thyroid hormone replacement treatment if detected by newborn screening which aims to identify affected infants before symptoms arise to prevent intellectual disability. Graves' disease is the most frequent cause of hyperthyroidism in children, presenting with symptoms like irritability, weight loss, and eye changes.
Thyroid function tests and their interpretationsBhargavi Patel
This document discusses various thyroid conditions and test results. It covers subclinical hypothyroidism, where TSH is elevated but symptoms are minimal. It is recommended to confirm elevated TSH over 3 months before treatment. Secondary hypothyroidism involves low TSH and thyroid hormones, often due to pituitary issues. Sick euthyroid syndrome describes abnormal thyroid tests during illness without underlying thyroid problems.
The document provides information about the thyroid gland and thyroid function tests. It discusses that the thyroid gland produces thyroid hormones that regulate metabolism and other bodily functions. It describes different thyroid disorders like hyperthyroidism and hypothyroidism. It then explains various thyroid function tests that evaluate thyroid hormone levels, the hypothalamic-pituitary-thyroid axis, and detect thyroid antibodies to help diagnose thyroid conditions.
this is a series of notes on clinical pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
The document discusses thyroid disorders and summarizes key information about the thyroid gland, its hormones and functions. It describes hypothyroidism and hyperthyroidism, their causes, symptoms and treatment methods. Hypothyroidism is treated mainly with levothyroxine while hyperthyroidism can be treated with antithyroid drugs, beta blockers or radioactive iodine ablation.
The document summarizes thyroid gland structure and function. Some key points:
- The thyroid gland produces the hormones T3, T4, and reverse T3. It weighs about 30g in adults.
- Thyroglobulin, secreted into follicles, binds iodine to produce the hormones. The thyroid is the only tissue that can absorb iodine from the blood.
- Blood tests are essential to diagnose thyroid disorders, as symptoms are often subtle. Tests include measuring radioactive iodine uptake by the gland, serum thyroid hormone levels like T4 and T3, and stimulating the gland with TSH or TRH to assess function.
Thyroid Function Tests, NORMAL THYROID PHYSIOLOGY
, Anatomy of the Thyroid Gland, Hypothalamic-Pituitary-Thyroid AxisNegative Feedback Mechanism, Hypothalamic-Pituitary-Thyroid AxisPhysiology, PITUITARY-THYROTROPE CELL
, THYROID HORMONES
, FORMATION & SECRETION OF THYROID HORMONES , ION TRANSPORT BY THE THYROID FOLLICULAR CELL
, THYROGLOBULIN SYNTHESIS IN THE THYROID FOLLICULAR CELL
Thyroid function test ( TFT) in simple waybinaya tamang
This document provides information about thyroid function tests. It discusses the thyroid gland, thyroid hormones, and thyroid stimulating hormone. It covers the biological functions of thyroid hormones, their biochemistry and biosynthesis. It also describes hypothyroidism and hyperthyroidism, their causes, classifications, and clinical presentations. The role of thyroid stimulating hormone is explained. Additionally, the document outlines objectives of thyroid function tests and different classifications of tests based on their function.
The document discusses thyroid hormones and thyroid function tests. It states:
- The thyroid gland produces thyroxine (T4) and triiodothyronine (T3), which regulate metabolic rate. Iodine is essential for their synthesis.
- TSH secretion is regulated by a negative feedback loop involving the hypothalamus and pituitary gland. Thyroid hormones inhibit TSH release.
- Thyroid function tests measure thyroid hormones, binding proteins, antibodies, and other markers. Direct and indirect methods estimate free thyroid hormones.
- Abnormal test results can indicate primary or secondary hypothyroidism/hyperthyroidism, autoimmune disease, or other conditions. Serial testing
This document provides an overview of hypopituitarism, including its anatomy, etiology, clinical features, diagnosis, and treatment. Hypopituitarism is a clinical syndrome of deficiency in pituitary hormone production and secretion that can result from disorders of the pituitary gland, hypothalamus, or surrounding structures. Common causes include tumors, trauma, infections, infiltrative disorders, and genetic mutations. Clinical features vary depending on which hormones are deficient but may include fatigue, weight changes, dry skin, and visual disturbances. Diagnosis involves hormonal blood tests and dynamic testing. Treatment is lifelong hormone replacement therapy to mimic normal hormone levels.
This document discusses hypothyroidism, including three patient cases. It covers the epidemiology, causes, clinical presentation, diagnosis, and treatment of hypothyroidism. The key points are:
1) Hypothyroidism can be primary (thyroid gland failure) or secondary (insufficient TSH stimulation). The most common cause is autoimmune thyroid disease. Clinical symptoms vary but include fatigue, weight gain, and depression.
2) Diagnosis is made through lab tests - an elevated TSH with low free T4 indicates primary hypothyroidism. Subclinical hypothyroidism has an elevated TSH but normal free T4.
3) Treatment is lifelong levothyroxine
The document summarizes thyroid gland development, function, and congenital hypothyroidism. It discusses that the thyroid gland secretes thyroid hormones that regulate metabolism. Congenital hypothyroidism occurs when there is a deficiency of thyroid hormones at birth and can be caused by thyroid dysgenesis or defects in hormone synthesis. It is important to screen all newborns for congenital hypothyroidism through measuring TSH and T4 levels to detect cases early so treatment with thyroid hormone replacement can prevent intellectual and growth impairment.
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.
Second ppt on endocrine system, describing hypothalamus, pituitary and thyroid glands.
This describes the hormones from these glands and their mode of action etc
The thyroid hormones T4 and T3 are produced by the thyroid gland and regulate metabolism. TSH produced by the pituitary stimulates the thyroid gland. The thyroid secretes mostly T4 which is converted to the more active T3 in tissues. Thyroid hormones increase metabolism and are essential for growth and development. Abnormalities in thyroid hormone levels can cause hypothyroidism or hyperthyroidism with various symptoms. Diseases like Graves' disease and Hashimoto's thyroiditis can also affect thyroid function.
This document discusses an approach to a person with an abnormal thyroid stimulating hormone (TSH) level. It begins by introducing the thyroid gland and hormones T4 and T3, which are regulated by TSH. Several conditions can cause high or low TSH, including hypothyroidism, hyperthyroidism, thyroid hormone resistance, and TSH-secreting pituitary adenomas. Specific thyroid conditions discussed in detail include Hashimoto's thyroiditis, iodine deficiency, acute/subacute/silent/chronic thyroiditis, and subclinical hypothyroidism. Treatment depends on the underlying condition but may include levothyroxine, glucocorticoids, surgery, or radiation therapy.
This document discusses thyroid function tests (TFTs) which are important for evaluating thyroid function and detecting thyroid disorders. It provides details on:
1) The key hormones measured in TFTs including TSH, T3, T4, free T3, free T4, thyroglobulin, and thyroid antibodies.
2) The hypothalamic-pituitary-thyroid axis and how thyroid hormones are produced and transported.
3) The indications, limitations, and interpretation of TFT results for evaluating hyperthyroidism, hypothyroidism, and other thyroid conditions.
The thyroid gland secretes hormones that regulate metabolism. Disorders can cause hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid). Examination of the thyroid involves inspection for size/shape, palpation for consistency/nodules, and auscultation for bruits. Blood tests measure thyroid hormone levels while ultrasound images the gland. Mild cases may only require monitoring but severe or abnormal cases should be referred to an endocrinologist.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Thyroid function test , made by dr.boskey,suratBoskey Gandhi
This document discusses thyroid disease, including:
- Thyroid disorders affect over 4 crore people in India, with 90% undiagnosed.
- Thyroid function tests include TSH, FT3, FT4, T3, T4, thyroid antibodies, and urinary iodine.
- Hypothyroidism is more common than hyperthyroidism. Causes include iodine deficiency, Hashimoto's, and surgery. Signs include dry skin, weight gain, and fatigue.
- Hyperthyroidism causes include Graves' disease. Signs include warm moist skin, weight loss, and tachycardia.
- Subclinical
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
The thyroid gland produces hormones that regulate metabolism. Thyroid function tests measure levels of thyroid hormones like TSH, T3, and T4 to determine if the thyroid is functioning properly. Abnormal thyroid function can cause disorders like hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). Common thyroid disorders include hypothyroidism, hyperthyroidism, goiter, nodules, and cancer.
The thyroid gland produces the hormones thyroxine (T4) and triiodothyronine (T3) which regulate metabolism. Thyroid function tests measure these hormones and antibodies to evaluate thyroid status and identify disorders like hypothyroidism and hyperthyroidism. There are four main categories of tests: tests that measure thyroid hormones themselves; tests that evaluate the hypothalamic-pituitary-thyroid axis by measuring TSH; tests of intrinsic thyroid function like radioactive iodine uptake; and tests for antibodies against thyroid tissue. Together these provide a comprehensive picture of thyroid function and any abnormalities.
Thyroid function tests (TFTs) are a suite of blood tests designed to assess the health and performance of the thyroid gland, a crucial organ with a central role in regulating metabolism, energy production, and overall bodily function. Understanding these tests is vital for diagnosing and managing thyroid disorders effectively.
Thyroid-Stimulating Hormone (TSH):
TSH is a hormone produced by the pituitary gland that stimulates the thyroid to release thyroid hormones (T3 and T4).
Elevated TSH levels typically indicate an underactive thyroid (hypothyroidism), suggesting insufficient production of thyroid hormones.
Free T3 and Free T4:
Free T3 and Free T4 are the active forms of thyroid hormones produced by the thyroid gland.
Abnormal levels of these hormones can signify thyroid dysfunction. Low levels may suggest hypothyroidism, while high levels could indicate hyperthyroidism.
Thyroid Antibodies:
Thyroid antibodies, including thyroid peroxidase (TPO) and thyroglobulin antibodies, are markers of autoimmune thyroid diseases.
Elevated antibody levels may indicate conditions like Hashimoto's thyroiditis (where the immune system attacks the thyroid) or Graves' disease (causing overproduction of thyroid hormones).
Thyroid Ultrasound:
While not a blood test, thyroid ultrasound provides imaging of the thyroid gland's structure, helping to detect nodules, evaluate size, and identify potential abnormalities.
Ultrasound is particularly useful in assessing the thyroid's physical characteristics.
Interpreting TFT results involves understanding the dynamic relationship between TSH, Free T3, and Free T4. In cases of primary hypothyroidism, TSH is often elevated, indicating an underactive thyroid, with Free T3 and Free T4 possibly being low. Conversely, in hyperthyroidism, TSH is typically low, accompanied by elevated Free T3 and Free T4.
Regular monitoring of TFTs is essential for managing thyroid disorders. Medication adjustments, lifestyle changes, and ongoing collaboration with healthcare professionals are often necessary to optimize thyroid function. Periodic thyroid ultrasounds and antibody tests aid in tracking disease progression and treatment efficacy.
Individuals with thyroid conditions should work closely with their healthcare providers to develop personalized treatment plans. This collaborative approach ensures that interventions are tailored to specific needs, leading to effective management of thyroid disorders and overall well-being. Always consult with a healthcare professional for accurate interpretation of test results and personalized medical advice
Thyroid function tests (TFTs) are a suite of blood tests designed to assess the health and performance of the thyroid gland, a crucial organ with a central role in regulating metabolism, energy production, and overall bodily function. Understanding these tests is vital for diagnosing and managing thyroid disorders effectively.
Thyroid-Stimulating Hormone (TSH):
TSH is a hormone produced by th
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.
this is a series of notes on clinical pathology, useful for undergraduate and post graduate pathology students. Notes have been prepared from standard textbooks and are in a format easy to reproduce in exams.
The document discusses thyroid disorders and summarizes key information about the thyroid gland, its hormones and functions. It describes hypothyroidism and hyperthyroidism, their causes, symptoms and treatment methods. Hypothyroidism is treated mainly with levothyroxine while hyperthyroidism can be treated with antithyroid drugs, beta blockers or radioactive iodine ablation.
The document summarizes thyroid gland structure and function. Some key points:
- The thyroid gland produces the hormones T3, T4, and reverse T3. It weighs about 30g in adults.
- Thyroglobulin, secreted into follicles, binds iodine to produce the hormones. The thyroid is the only tissue that can absorb iodine from the blood.
- Blood tests are essential to diagnose thyroid disorders, as symptoms are often subtle. Tests include measuring radioactive iodine uptake by the gland, serum thyroid hormone levels like T4 and T3, and stimulating the gland with TSH or TRH to assess function.
Thyroid Function Tests, NORMAL THYROID PHYSIOLOGY
, Anatomy of the Thyroid Gland, Hypothalamic-Pituitary-Thyroid AxisNegative Feedback Mechanism, Hypothalamic-Pituitary-Thyroid AxisPhysiology, PITUITARY-THYROTROPE CELL
, THYROID HORMONES
, FORMATION & SECRETION OF THYROID HORMONES , ION TRANSPORT BY THE THYROID FOLLICULAR CELL
, THYROGLOBULIN SYNTHESIS IN THE THYROID FOLLICULAR CELL
Thyroid function test ( TFT) in simple waybinaya tamang
This document provides information about thyroid function tests. It discusses the thyroid gland, thyroid hormones, and thyroid stimulating hormone. It covers the biological functions of thyroid hormones, their biochemistry and biosynthesis. It also describes hypothyroidism and hyperthyroidism, their causes, classifications, and clinical presentations. The role of thyroid stimulating hormone is explained. Additionally, the document outlines objectives of thyroid function tests and different classifications of tests based on their function.
The document discusses thyroid hormones and thyroid function tests. It states:
- The thyroid gland produces thyroxine (T4) and triiodothyronine (T3), which regulate metabolic rate. Iodine is essential for their synthesis.
- TSH secretion is regulated by a negative feedback loop involving the hypothalamus and pituitary gland. Thyroid hormones inhibit TSH release.
- Thyroid function tests measure thyroid hormones, binding proteins, antibodies, and other markers. Direct and indirect methods estimate free thyroid hormones.
- Abnormal test results can indicate primary or secondary hypothyroidism/hyperthyroidism, autoimmune disease, or other conditions. Serial testing
This document provides an overview of hypopituitarism, including its anatomy, etiology, clinical features, diagnosis, and treatment. Hypopituitarism is a clinical syndrome of deficiency in pituitary hormone production and secretion that can result from disorders of the pituitary gland, hypothalamus, or surrounding structures. Common causes include tumors, trauma, infections, infiltrative disorders, and genetic mutations. Clinical features vary depending on which hormones are deficient but may include fatigue, weight changes, dry skin, and visual disturbances. Diagnosis involves hormonal blood tests and dynamic testing. Treatment is lifelong hormone replacement therapy to mimic normal hormone levels.
This document discusses hypothyroidism, including three patient cases. It covers the epidemiology, causes, clinical presentation, diagnosis, and treatment of hypothyroidism. The key points are:
1) Hypothyroidism can be primary (thyroid gland failure) or secondary (insufficient TSH stimulation). The most common cause is autoimmune thyroid disease. Clinical symptoms vary but include fatigue, weight gain, and depression.
2) Diagnosis is made through lab tests - an elevated TSH with low free T4 indicates primary hypothyroidism. Subclinical hypothyroidism has an elevated TSH but normal free T4.
3) Treatment is lifelong levothyroxine
The document summarizes thyroid gland development, function, and congenital hypothyroidism. It discusses that the thyroid gland secretes thyroid hormones that regulate metabolism. Congenital hypothyroidism occurs when there is a deficiency of thyroid hormones at birth and can be caused by thyroid dysgenesis or defects in hormone synthesis. It is important to screen all newborns for congenital hypothyroidism through measuring TSH and T4 levels to detect cases early so treatment with thyroid hormone replacement can prevent intellectual and growth impairment.
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.
Second ppt on endocrine system, describing hypothalamus, pituitary and thyroid glands.
This describes the hormones from these glands and their mode of action etc
The thyroid hormones T4 and T3 are produced by the thyroid gland and regulate metabolism. TSH produced by the pituitary stimulates the thyroid gland. The thyroid secretes mostly T4 which is converted to the more active T3 in tissues. Thyroid hormones increase metabolism and are essential for growth and development. Abnormalities in thyroid hormone levels can cause hypothyroidism or hyperthyroidism with various symptoms. Diseases like Graves' disease and Hashimoto's thyroiditis can also affect thyroid function.
This document discusses an approach to a person with an abnormal thyroid stimulating hormone (TSH) level. It begins by introducing the thyroid gland and hormones T4 and T3, which are regulated by TSH. Several conditions can cause high or low TSH, including hypothyroidism, hyperthyroidism, thyroid hormone resistance, and TSH-secreting pituitary adenomas. Specific thyroid conditions discussed in detail include Hashimoto's thyroiditis, iodine deficiency, acute/subacute/silent/chronic thyroiditis, and subclinical hypothyroidism. Treatment depends on the underlying condition but may include levothyroxine, glucocorticoids, surgery, or radiation therapy.
This document discusses thyroid function tests (TFTs) which are important for evaluating thyroid function and detecting thyroid disorders. It provides details on:
1) The key hormones measured in TFTs including TSH, T3, T4, free T3, free T4, thyroglobulin, and thyroid antibodies.
2) The hypothalamic-pituitary-thyroid axis and how thyroid hormones are produced and transported.
3) The indications, limitations, and interpretation of TFT results for evaluating hyperthyroidism, hypothyroidism, and other thyroid conditions.
The thyroid gland secretes hormones that regulate metabolism. Disorders can cause hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid). Examination of the thyroid involves inspection for size/shape, palpation for consistency/nodules, and auscultation for bruits. Blood tests measure thyroid hormone levels while ultrasound images the gland. Mild cases may only require monitoring but severe or abnormal cases should be referred to an endocrinologist.
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
Thyroid function test , made by dr.boskey,suratBoskey Gandhi
This document discusses thyroid disease, including:
- Thyroid disorders affect over 4 crore people in India, with 90% undiagnosed.
- Thyroid function tests include TSH, FT3, FT4, T3, T4, thyroid antibodies, and urinary iodine.
- Hypothyroidism is more common than hyperthyroidism. Causes include iodine deficiency, Hashimoto's, and surgery. Signs include dry skin, weight gain, and fatigue.
- Hyperthyroidism causes include Graves' disease. Signs include warm moist skin, weight loss, and tachycardia.
- Subclinical
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
The thyroid gland produces hormones that regulate metabolism. Thyroid function tests measure levels of thyroid hormones like TSH, T3, and T4 to determine if the thyroid is functioning properly. Abnormal thyroid function can cause disorders like hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). Common thyroid disorders include hypothyroidism, hyperthyroidism, goiter, nodules, and cancer.
The thyroid gland produces the hormones thyroxine (T4) and triiodothyronine (T3) which regulate metabolism. Thyroid function tests measure these hormones and antibodies to evaluate thyroid status and identify disorders like hypothyroidism and hyperthyroidism. There are four main categories of tests: tests that measure thyroid hormones themselves; tests that evaluate the hypothalamic-pituitary-thyroid axis by measuring TSH; tests of intrinsic thyroid function like radioactive iodine uptake; and tests for antibodies against thyroid tissue. Together these provide a comprehensive picture of thyroid function and any abnormalities.
Thyroid function tests (TFTs) are a suite of blood tests designed to assess the health and performance of the thyroid gland, a crucial organ with a central role in regulating metabolism, energy production, and overall bodily function. Understanding these tests is vital for diagnosing and managing thyroid disorders effectively.
Thyroid-Stimulating Hormone (TSH):
TSH is a hormone produced by the pituitary gland that stimulates the thyroid to release thyroid hormones (T3 and T4).
Elevated TSH levels typically indicate an underactive thyroid (hypothyroidism), suggesting insufficient production of thyroid hormones.
Free T3 and Free T4:
Free T3 and Free T4 are the active forms of thyroid hormones produced by the thyroid gland.
Abnormal levels of these hormones can signify thyroid dysfunction. Low levels may suggest hypothyroidism, while high levels could indicate hyperthyroidism.
Thyroid Antibodies:
Thyroid antibodies, including thyroid peroxidase (TPO) and thyroglobulin antibodies, are markers of autoimmune thyroid diseases.
Elevated antibody levels may indicate conditions like Hashimoto's thyroiditis (where the immune system attacks the thyroid) or Graves' disease (causing overproduction of thyroid hormones).
Thyroid Ultrasound:
While not a blood test, thyroid ultrasound provides imaging of the thyroid gland's structure, helping to detect nodules, evaluate size, and identify potential abnormalities.
Ultrasound is particularly useful in assessing the thyroid's physical characteristics.
Interpreting TFT results involves understanding the dynamic relationship between TSH, Free T3, and Free T4. In cases of primary hypothyroidism, TSH is often elevated, indicating an underactive thyroid, with Free T3 and Free T4 possibly being low. Conversely, in hyperthyroidism, TSH is typically low, accompanied by elevated Free T3 and Free T4.
Regular monitoring of TFTs is essential for managing thyroid disorders. Medication adjustments, lifestyle changes, and ongoing collaboration with healthcare professionals are often necessary to optimize thyroid function. Periodic thyroid ultrasounds and antibody tests aid in tracking disease progression and treatment efficacy.
Individuals with thyroid conditions should work closely with their healthcare providers to develop personalized treatment plans. This collaborative approach ensures that interventions are tailored to specific needs, leading to effective management of thyroid disorders and overall well-being. Always consult with a healthcare professional for accurate interpretation of test results and personalized medical advice
Thyroid function tests (TFTs) are a suite of blood tests designed to assess the health and performance of the thyroid gland, a crucial organ with a central role in regulating metabolism, energy production, and overall bodily function. Understanding these tests is vital for diagnosing and managing thyroid disorders effectively.
Thyroid-Stimulating Hormone (TSH):
TSH is a hormone produced by th
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.
This document discusses thyroid hormone and factors that affect thyroid function. It provides information on:
1. Thyroid disorders are common worldwide, especially hypothyroidism which contributes significantly to disease burden.
2. Many extra-thyroidal factors can influence thyroid function tests results, including age, gender, ethnicity, smoking, nutrition, medication and illness.
3. Interpreting thyroid function tests requires considering the pattern of TSH, free T4, antibodies and clinical factors. Subclinical hypothyroidism and hyperthyroidism are important to identify.
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.
1. The serum TSH test is the best initial test for evaluating thyroid function, with a high TSH indicating hypothyroidism and a low TSH indicating hyperthyroidism.
2. Additional tests like T4, T3, thyroid antibodies, and radioactive iodine uptake can help diagnose specific thyroid disorders like Hashimoto's thyroiditis or Graves' disease.
3. Examining TSH, T4, T3 levels together can differentiate between primary thyroid disorders and secondary disorders originating from the pituitary or hypothalamus.
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.
2012 Clinical Practice guidelines for hypothyroidism in adults: American Asso...Jibran Mohsin
This is presentation format of 2012 Clinical Practice guidelines for hypothyroidism in adults: American Association of Clinical Endocrinologists (AACE) / American Thyroid Association (ATA)
This document provides information about thyroid function tests. It discusses the thyroid gland and its role in producing thyroid hormones like T4 and T3. It describes the physiology of thyroid hormone production and regulation via the hypothalamic-pituitary-thyroid axis. The document outlines the common blood tests used to evaluate thyroid function, including TSH, T4, T3, and thyroid antibodies. It provides the normal ranges for these tests and discusses how they are used to diagnose hyperthyroidism and hypothyroidism. Non-blood tests like radioactive iodine uptake are also summarized.
The document discusses thyroid disease and its implications for dental care. It begins with background on the thyroid gland and thyroid diseases. It then reviews the literature on thyroid disease and dental care, finding few articles that specifically address the topic. The conclusions state that dental professionals should screen for undiagnosed thyroid disease and understand how thyroid conditions can impact dental treatment. Modifications to dental care may be needed for patients with thyroid disease.
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
The thyroid gland secretes the hormones T3 and T4, which are derived from tyrosine and necessary for proper functioning of cells and biological processes. Thyroid hormones increase the basal metabolic rate, promote growth and development, and stimulate RNA and protein synthesis. T4 and T3 are transported bound to thyroxine binding globulin in the blood, with the free forms being biologically active. Hypothalamic-pituitary-thyroid axis feedback controls TSH secretion and thyroid hormone levels. Laboratory tests can measure thyroid hormones, TSH, antibodies, and imaging can identify thyroid abnormalities.
This document discusses nonthyroidal illness syndrome (NTIS), also known as low T3 syndrome or euthyroid sick syndrome. NTIS is characterized by low serum T3, normal or low T4, and high rT3 levels. It reflects alterations in thyroid function tests in various clinical situations including starvation, sepsis, surgery, myocardial infarction, and other severe illnesses. NTIS is caused by changes at all levels of the hypothalamic-pituitary-thyroid axis, including decreased 5'-deiodinase activity leading to low T3, possible HP axis suppression, and altered peripheral thyroid hormone metabolism. Low T3 and T4 levels in NTIS have been associated with increased mortality risk.
1. The thyroid gland secretes two main hormones: thyroxine (T4) and triiodothyronine (T3) in a ratio of 15:1.
2. T4 and T3 are bound to serum proteins and transported through the bloodstream, with the free unbound levels regulating thyroid function.
3. Peripherally, T4 is converted to the more potent T3, which enters cells and binds nuclear receptors to increase protein synthesis and cellular metabolism.
case presentationof the endocrine 3.pptxssuserfd7cc21
1. The patient is a 48-year-old woman found to have subclinical hyperthyroidism on routine screening, with a TSH of 0.17 mU/L and no symptoms of hyperthyroidism.
2. Thyroid ultrasound showed multiple isoechoic and hyperechoic nodules bilaterally, with the largest measuring 1.5 cm and 2.0 cm.
3. Given her stable thyroid function, lack of symptoms, and normal bone density, the decision was made not to treat and monitor her thyroid levels every 6 months.
This document discusses thyroid hormones, their functions, synthesis, regulation, and mechanisms of action. It covers the receptors, transporters, and enzymes involved in thyroid hormone activity. It also describes the clinical features and management of hypothyroidism and hyperthyroidism, as well as laboratory tests for thyroid function. Various thyroid analogs and their selective actions on thyroid hormone receptors are also mentioned.
The document summarizes thyroid hormone synthesis and regulation. Iodine is incorporated into thyroglobulin to form the thyroid hormones thyroxine (T4) and triiodothyronine (T3). T4 is formed by coupling of two diiodotyrosine molecules, while T3 results from coupling a diiodotyrosine and a monoiodotyrosine. Only a small fraction of T4 and T3 circulate freely in the blood; the majority are bound to proteins. The free forms, free T4 and free T3, are biologically active. Thyroid stimulating hormone (TSH) regulates thyroid hormone production through negative feedback. Laboratory tests of TSH, total T4, total T3,
The document discusses thyroid gland disorders and hypothyroidism. It provides details on the causes, effects on organ systems, and types of hypothyroidism. The main causes of hypothyroidism are autoimmune thyroiditis, which results in the gradual destruction of the thyroid gland, and surgical or medical thyroid ablation for conditions like Graves' disease. Hypothyroidism can affect many organ systems by reducing the basal metabolic rate and impairing other metabolic processes. It discusses the different types of hypothyroidism, including congenital hypothyroidism and central hypothyroidism.
1) Congenital hypothyroidism is the most common preventable cause of mental retardation and can be diagnosed through newborn screening programs that measure TSH levels.
2) It is classified as permanent or transient, with permanent CH caused by thyroid dysgenesis, defects in hormone synthesis, TSH resistance, or central hypothyroidism.
3) Transient CH has various causes including antithyroid drugs, iodine excess or deficiency, prematurity, or blocking antibodies; it typically resolves on its own.
Hyperthyroidism is often caused by Graves' disease, which results from autoimmune production of thyroid stimulating hormone (TSH) receptor antibodies. This leads to excessive thyroid hormone production and symptoms of hyperthyroidism. Graves' disease is the most common cause of childhood hyperthyroidism. Treatment options include antithyroid medications, radioactive iodine therapy, or surgery, with the choice individualized for each patient.
The document discusses definitions of remission for rheumatoid arthritis (RA) and the goals of treating RA. It provides context on the history of RA treatment goals moving from symptom relief to preventing joint damage and achieving remission. The key points are:
1) Definitions of remission have evolved from the original ACR criteria to the 2011 ACR-EULAR definition, which includes boolean and index-based definitions for use in clinical trials.
2) Achieving early remission through aggressive treatment is associated with better long-term outcomes for RA patients.
3) The 2011 definition was developed for clinical trials but needs validation for use in practice to guide treatment and measure remission.
This document discusses the differential diagnosis and evaluation of various cardiac murmurs. It presents 6 clinical cases involving patients with different cardiac murmurs and conditions such as aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation, tricuspid regurgitation, and prosthetic valve dysfunction. For each case, it describes the history, physical exam findings, appropriate tests, diagnosis, complications, and management considerations for the underlying heart condition.
This document discusses congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency. It describes the key enzymes involved in cortisol and aldosterone synthesis, the genetics and clinical presentations of classic and nonclassic forms of the condition, diagnostic testing including elevated 17-hydroxyprogesterone levels, and treatment approaches using glucocorticoids like dexamethasone. The classic salt-losing form is most severe and presents in infancy while the nonclassic late-onset form involves androgen excess in adolescent/adult females and may be asymptomatic.
This document discusses the management of acute liver failure (ALF). It defines ALF and lists common causes such as drug-induced liver injury, viral hepatitis, and autoimmune liver disease. It provides details on diagnosis, evaluation of specific etiologies, and management strategies. Management involves intensive care support and treating any identified causes. Cerebral edema is a major complication, and grades of encephalopathy are described. Treatments aimed at reducing intracranial pressure such as mannitol, hyperventilation, and barbiturates are outlined. Liver transplantation is the definitive treatment for severe ALF from certain causes.
N-acetylcysteine (NAC) has various uses and potential side effects. It is used to treat acetaminophen overdose by replenishing glutathione stores in the liver. Optimal treatment is within 8 hours of ingestion. NAC may also be used as an expectorant for lung conditions like COPD. Potential side effects include nausea, rash, and bronchospasm. Precautions are needed with asthma, pregnancy, and some cancer treatments due to possible interference.
The document provides guidance on the initial assessment and management of patients presenting with acute stroke. It outlines goals of ensuring medical stability, diagnosing intracranial hemorrhage, and identifying conditions contributing to symptoms. A history and physical exam can help distinguish stroke from other disorders and detect potential causes. Immediate labs, imaging, and monitoring of vital signs are recommended. Guidelines for blood pressure and blood glucose management are provided based on the type of stroke and patient's condition.
Updates in managment of acute poisoned patientHaifa Alshwikh
This document summarizes recent guidelines from the American Academy of Clinical Toxicology and European Association of Poison Centres and Clinical Toxicologists on the management of acute poisoned patients. It finds that gastric lavage is not recommended as routine treatment and has not been shown to improve outcomes when administered over an hour after ingestion. Activated charcoal is established as the primary method of gastrointestinal decontamination. Whole bowel irrigation may be considered for ingestion of sustained-release preparations or foreign bodies when activated charcoal cannot be used.
Case presentation of primary hyperparathyroidismHaifa Alshwikh
This case presentation describes a 44-year-old woman who presented with left hip pain and was found to have hypercalcemia. The differential diagnosis for her hypercalcemia includes primary hyperparathyroidism, familial hypocalciuric hyperparathyroidism, and tertiary hyperparathyroidism. She underwent laboratory testing which showed elevated PTH, consistent with primary hyperparathyroidism. Localization testing with sestamibi scan and ultrasound were recommended to help guide minimally invasive parathyroidectomy.
Body packers, also known as internal carriers or mules, smuggle drugs internally by swallowing prepackaged drugs in plastic, latex, or condoms. Common drugs transported include cocaine, heroin, and ecstasy. Packets usually number between 50-100 and each contains 8-10 grams of drug. Diagnosis involves history, physical exam, and imaging like abdominal x-rays or CT scans to detect packets. Treatment depends on symptoms but typically involves monitoring and supportive care until packets pass naturally. Activated charcoal and bowel relaxants may speed passage. Intoxicated packers require specific treatment like naloxone for opioid overdose.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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3. RTSH is broadly defined as
high serum TSH (hyperthyrotropinemia) of normal
biological activity in the absence of goitre.
Affected individuals have normal or hypoplastic thyroid
glands, high serum TSH concentrations, and normal or low
serum T4 and T3 concentrations.
They are often identified at birth through neonatal
screening for congenital hypothyroidism ( with normally
located thyroid gland)
4. TSH is the predominant regulator of thyroid growth and T4
and T3 synthesis and secretion. These actions are mediated
through TSH-binding to the TSH receptor located on the
plasma membrane of thyroid follicular cells.
Activation of the TSH receptor results in activation of G
proteins and then of the adenylyl cyclase-cyclic AMP
pathway of signal transduction The result is stimulation of
thyroid follicular-cell growth and function
5.
6. two genetic causes of RTSH have been so far identified.
1-Inactivating mutations in the TSH receptor
The inheritance is recessive
2-Defect in the long arm of chromosome 15
The defect is inherited in an autosomal dominant
manner.
7. Fully compensated defect — The impaired response to
TSH is compensated by hypersecretion of TSH; this
overcomes the resistance, resulting in euthyroid
hyperthyrotropinemia.
Partially compensated defect — This occurs when
the high serum TSH cannot fully compensate for the
defect; affected individuals have mild hypothyroidism
("Subclinical hypothyroidism".)
Uncompensated defect — Complete lack of TSH
receptor function results in severe hypothyroidism.
This most often occurs when both alleles carry
mutant TSH receptors with complete lack of function
8. RTSH should be suspected in patients, particularly infants,
who have high serum TSH concentrations, normal or low
serum free T4 and T3 concentrations, and a normally located
thyroid gland.
The differential diagnosis includes all those conditions that
impair thyroid secretion. Because of the important role of
TSH in promoting thyroid growth, RTSH is unlikely if the
patient has a goiter or ectopically located thyroid tissue.
9. Individuals with fully compensated RTSH are euthyroid and
need no treatment. There is no evidence that in the absence
of other risk factors, persistent elevation of serum TSH
levels produces pituitary TSHomas or thyroid neoplasia.
Individuals with partially compensated or uncompensated
RTSH should be treated with L-T4, like any other
hypothyroid patient.
Because these individuals have normal responsiveness to
thyroid hormone, the goal is to normalize their serum TSH
concentration.
10. Resistance to TSH (RTSH) is broadly defined as high serum TSH
(hyperthyrotropinemia) of normal biological activity in the
absence of goiter.
Affected individuals have normal or hypoplastic thyroid glands,
high serum TSH concentrations, and normal or low serum T4
and T3 concentrations
RTSH should be suspected in patients, particularly infants, who
have high serum TSH concentrations, normal or low serum free
T4 and T3 concentrations, and a normally located thyroid
gland.
In patients with RTSH who are euthyroid (the impaired
response to TSH is fully compensated by hypersecretion of
TSH), we suggest NOT treating with thyroid hormone) (Fully
compensated defect)' , If the high serum TSH cannot fully
compensate for the defect (partially compensated or
uncompensated defects), the individual is hypothyroid and
should be treated with thyroid hormone, like any other
hypothyroid patient
11.
12. is an inherited syndrome characterized by reduced
responsiveness of target tissues to TH.
The disorder is characterized by high serum concentrations of
free T4 and usually free T3, accompanied by normal or slightly
high serum TSH concentrations.
The diagnosis of RTH is confirmed if supra-physiologic doses of T4
or T3 are required to reduce the TSH secretion.
13. RTH has been detected in 1 of 40,000 live births
and it occurs with equal frequency in both sexes.
it is inherited as an autosomal dominant trait.
14. Thyroid hormone receptor mutations:
There are two TRs, alpha and beta, which are encoded by
separate genes located on chromosomes 17 and 3,
respectively. The receptors have structural and sequence
similarities
In approximately 85 percent of cases, RTH is due to
mutations in the TR beta gene. One hundred and twenty-four
different mutations have been identified so far among 343
unrelated families. Most of the mutations are located in the
T3-binding domain of the TR
They interfere with the function of the normal TR (dominant
negative effect)
. No mutations in the TR alpha gene have been identified in
humans
.
15.
16. nonTR-RTH
In 15 percent of families, RTH is not caused by a TR beta
gene mutation; this is known as "nonTR-RTH". It is clinically
and biochemically indistinguishable from RTH with TR beta
gene mutations
17. In RTH, resistance of the pituitary thyrotrophs to TH raises
TSH secretion, which increases the synthesis and secretion
of T4 and T3 from the thyroid gland.
The elevated levels of these thyroid hormones fail to
downregulate the hypothalamic-pituitary-thyroid axis as
they would in an individual without RTH, As a result, these
patients have high levels of T4 and T3, and normal or high
levels of TSH..
18. Because of this apparent dissociation between serum TH and
TSH concentrations, the syndrome has been called
"inappropriate secretion of TSH". However, TSH secretion is
not really inappropriate because the response of the
thyrotrophs to TH is reduced; to the contrary, it is
compensatory and appropriate for the level of TH action
mediated through the defective TR beta
The TSH secreted by these patients is rich in sialic acid and
has increased bioactivity, as compared with normal TSH ,This
explains why patients with RTH have goiter and high serum
T4 and T3 concentrations even though their serum
immunoreactive TSH concentrations are normal or only
slightly high.
19. Because increased TH secretion compensates for TH
resistance, most patients with RTH are clinically euthyroid,
although the completeness of compensation varies in
different patients and in different tissues in the same
patient .
20. The hallmark of RTH is the paucity of symptoms and signs
of thyroid dysfunction despite the presence of high serum
T4 and T3 concentrations
Among all clinical findings, goiter is by far the most
common (65 to 95 percent), followed by hyperactivity (33
to 68 percent) and tachycardia (33 to 75 percent)
These abnormalities usually lead to evaluation of thyroid
function. The subsequent finding of high serum T4 and T3
concentrations often results in the erroneous diagnosis of
hyperthyroidism.
.
21. Patients with RTH may have some symptoms or signs of
hypothyroidism or hyperthyroidism, but these are variable
and, when present, often inconstant .
If hypothyroidism is present, clinical features may include
growth retardation, delayed bone maturation, learning
disabilities, mental retardation, sensorineural deafness, and
nystagmus.
Patients with symptoms of hyperthyroidism may have
tachycardia, hyperactivity, and increased basal metabolic
rate. Overt hypothyroidism is more common in these
patients because of erroneous diagnosis of hyperthyroidism,
they received ablative or antithyroid treatment to reduce
their TH level
23. a high serum free T4 concentration and non-suppressed TSH
are essential requirements for the diagnosis of RTH. Serum
levels of T3 and rT3 are usually also high.
The concentration of thyroglobulin (the protein within which
T3 and T4 are synthesized and stored) tends to be high,
reflecting the level of TSH-induced thyroid gland
hyperactivity.
The abnormalities should be confirmed by repeat
measurements several weeks later.
24. Determine if there are mutations in the TR beta gene by
direct sequencing. Several commercial laboratories offer
sequencing of the TR beta gene. This test provides a means
to confirm the diagnosis, to obtain prenatal diagnosis, and to
prevent inappropriate anti-thyroid treatment of patients with
high serum levels of free TH.
The response of TSH to TSH-releasing hormone is normal or
exaggerated, depending on the baseline TSH level. The
suppressive effect of administered TH on TSH, cholesterol
and creatine kinase is blunted. Similarly, the stimulatory
effect of TH on sex-hormone binding globulin and ferritin is
attenuated.
25.
26. All causes of high serum T4 and T3 concentrations in
association with normal to high serum TSH levels should be
considered in the differential diagnosis
1- T4-binding globulin excess TBG
2- transthyretin excess TTR
3- familial dysalbuminemic hyperthyroxinemia FDH
4-TSH-producing pituitary adenoma TSHoma
5-nonthyroidal illness NTI
27. The following steps are appropriate to establish the diagnosis
of RTH
To exclude abnormalities of TH binding in serum, including
familial dysalbuminemic hyperthyroxinemia, hereditary and
acquired thyroxine binding globulin excess, and transthyretin
excess, measure serum free T4 and T3 by equilibrium dialysis.
Normal values suggest a defect of TH binding in serum that
could be confirmed by measurement of the specific protein or
by genetic analysis.
To exclude a TSH-producing pituitary adenoma, measure the
alpha subunit of TSH , A high ratio of alpha subunit to whole
TSH is pathognomonic of TSH-secreting tumor. This disorder is
associated with a similar TH profile to RTH but most, if not
all, patients are hyperthyroid .
28.
29. There is no treatment that will correct the defect of TR
beta function in subjects with RTH.
Fortunately, in most patients, the hyposensitivity to TH
seems to be adequately compensated by the increase in
secretion of T4 and generation of T3. Thus, treatment is
usually not needed.
30. ablative treatment should be avoided. Large glands have
been successfully treated by the administration of a single
high dose of L-T3 given every other day.
Symptoms of thyrotoxicosis, more specifically tachycardia
and tremor, respond to the administration of the beta
adrenergic blocker, atenolol.
Attention deficit hyperactivity disorder should be treated as
indicated using drugs available for the treatment of this
disorder independently from RTH.
31. In some patients with RTH, several peripheral tissues may be
relatively more resistant than the thyrotrophs. Thus, the
compensation for the hormonal resistance in these tissues is
incomplete and judicious administration of a dose of T4
higher than that needed to restore TSH secretion to normal
may be indicated. The dose must be individually determined
by assessing tissue responses..
In children, this should be done by regular assessment of
growth, bone maturation, and mental development.
Levothyroxine should be given in incremental doses, and the
basal metabolic rate, nitrogen balance, and serum sex
hormone-binding globulin should be measured after
treatment for four to six weeks before the dose is changed;
bone age and growth should be followed on a longer-term
basis. Development of a catabolic state is an indication of
overtreatment.
32. Management of pregnancies in mothers with RTH who are
carrying unaffected fetuses may warrant judicious use of anti-
thyroid medication, depending on the wellbeing of the fetus .
In such mothers, free T4 should be maintained not higher than
20 percent above the upper limit of normal. This can be
achieved by judicious use of propylthiouracil, taking care to
avoid inducing hypothyroidism.
There is no basis for regular treatment of normal mothers
carrying affected fetuses unless the fetus is found to have a
large goiter or be in distress, in which case the only treatment
alternative is intraamniotic infusion of LT-4, although this has
not been reported. Further studies are needed before general
recommendations can be made.
33. Resistance to thyroid hormone (RTH) is an inherited syndrome
characterized by reduced responsiveness of target tissues to thyroid
hormone (TH).
the disorder is characterized by high serum concentrations of free T4
and usually also free T3, accompanied by normal or slightly high
serum TSH concentration.
The hallmark of RTH is the paucity of symptoms and signs of thyroid
dysfunction despite the presence of high serum T4 and T3
concentrations. Clinical features include goiter, hyperactivity, and
tachycardia.
The clinical disease is usually mild because the hyposensitivity to TH
is adequately compensated by the increase in secretion of T4 and
generation of T3.
In approximately 85 percent of cases, RTH is due to mutations in the
TH receptor beta gene. In approximately 15 percent of cases, RTH is
caused by yet undetermined genetic abnormalities.
Diagnosis of RTH depends on characteristic elevations in TH and
exclusion of other causes of hyperthyroxinemia, When RTH is
suspected, the diagnosis should be confirmed by direct sequencing of
the TR beta gene to identify mutation.