The document discusses hormone stimulation tests and their purposes. Stimulation tests measure the response of endocrine glands to injected hormones like ACTH or insulin. They are used to diagnose conditions like growth hormone deficiency, pituitary tumors, and adrenal insufficiency. The document provides examples of specific stimulation tests for growth hormone, thyroid function, and cortisol. It explains the procedures, normal and abnormal results, and purposes of these important clinical endocrinology tests.
Gonadotrophins are hormones that include LH and FSH, which are produced by the pituitary gland. LH and FSH levels are controlled by GnRH from the hypothalamus. FSH stimulates growth of ovarian follicles and testosterone production, while LH stimulates estrogen and progesterone production. Abnormalities in FSH and LH secretion can indicate hypothalamic, pituitary, or gonadal issues and impact fertility.
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.
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.
Hyperthyroidism, also known as thyrotoxicosis, results from elevated thyroid hormones in the blood and causes hypermetabolism. Graves' disease is the most common cause, an autoimmune disorder where thyroid receptor antibodies stimulate excess thyroid hormone production. Women are more frequently affected than men. Laboratory tests show suppressed TSH and increased thyroid hormone levels. Graves' disease in pregnancy can cause fetal and neonatal hyperthyroidism or hypothyroidism if not properly managed.
Hyperlipidemia involves abnormally elevated levels of lipids and lipoproteins in the blood. Lipids include cholesterol, triglycerides, and phospholipids, which are transported around the body within lipoproteins like chylomicrons, VLDL, LDL, IDL, and HDL. High cholesterol and triglycerides are major risk factors for cardiovascular disease, and very high triglycerides can cause pancreatitis. Hyperlipidemias can be primary or secondary, and are classified based on which lipids are predominantly elevated, such as cholesterol, triglycerides, or both. Primary causes include genetic defects or polygenic influences, while secondary causes include hypothyroidism, pregnancy, liver disease
Neonatal hypocalcemia can present with jitteriness, seizures, and other neurological symptoms. It is commonly seen in preterm infants, infants of diabetic mothers, and those with perinatal asphyxia or maternal conditions affecting calcium homeostasis. Diagnosis is made via serum calcium and magnesium levels. Treatment involves calcium gluconate administered intravenously or orally as well as magnesium supplementation if hypomagnesemia is also present. Close monitoring is needed given risks of complications. Late onset hypocalcemia may require increased oral calcium intake and reduced phosphate intake.
This document provides an overview of the pharmacological management of congestive heart failure. It discusses the pathophysiology of heart failure and compensatory mechanisms. It describes the renin-angiotensin-aldosterone system and its role in heart failure. The document outlines the classification, causes, signs and symptoms, and diagnostic criteria of heart failure. It discusses the goals and types of drugs used to treat heart failure, including vasodilators, diuretics, beta blockers, and angiotensin-modulating agents like ACE inhibitors. The document provides details on commonly used ACE inhibitors and their mechanisms and effects in treating heart failure.
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.
Gonadotrophins are hormones that include LH and FSH, which are produced by the pituitary gland. LH and FSH levels are controlled by GnRH from the hypothalamus. FSH stimulates growth of ovarian follicles and testosterone production, while LH stimulates estrogen and progesterone production. Abnormalities in FSH and LH secretion can indicate hypothalamic, pituitary, or gonadal issues and impact fertility.
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.
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.
Hyperthyroidism, also known as thyrotoxicosis, results from elevated thyroid hormones in the blood and causes hypermetabolism. Graves' disease is the most common cause, an autoimmune disorder where thyroid receptor antibodies stimulate excess thyroid hormone production. Women are more frequently affected than men. Laboratory tests show suppressed TSH and increased thyroid hormone levels. Graves' disease in pregnancy can cause fetal and neonatal hyperthyroidism or hypothyroidism if not properly managed.
Hyperlipidemia involves abnormally elevated levels of lipids and lipoproteins in the blood. Lipids include cholesterol, triglycerides, and phospholipids, which are transported around the body within lipoproteins like chylomicrons, VLDL, LDL, IDL, and HDL. High cholesterol and triglycerides are major risk factors for cardiovascular disease, and very high triglycerides can cause pancreatitis. Hyperlipidemias can be primary or secondary, and are classified based on which lipids are predominantly elevated, such as cholesterol, triglycerides, or both. Primary causes include genetic defects or polygenic influences, while secondary causes include hypothyroidism, pregnancy, liver disease
Neonatal hypocalcemia can present with jitteriness, seizures, and other neurological symptoms. It is commonly seen in preterm infants, infants of diabetic mothers, and those with perinatal asphyxia or maternal conditions affecting calcium homeostasis. Diagnosis is made via serum calcium and magnesium levels. Treatment involves calcium gluconate administered intravenously or orally as well as magnesium supplementation if hypomagnesemia is also present. Close monitoring is needed given risks of complications. Late onset hypocalcemia may require increased oral calcium intake and reduced phosphate intake.
This document provides an overview of the pharmacological management of congestive heart failure. It discusses the pathophysiology of heart failure and compensatory mechanisms. It describes the renin-angiotensin-aldosterone system and its role in heart failure. The document outlines the classification, causes, signs and symptoms, and diagnostic criteria of heart failure. It discusses the goals and types of drugs used to treat heart failure, including vasodilators, diuretics, beta blockers, and angiotensin-modulating agents like ACE inhibitors. The document provides details on commonly used ACE inhibitors and their mechanisms and effects in treating heart failure.
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.
This document discusses thalassemia syndrome and provides information on its epidemiology, molecular structure of hemoglobin, inheritance, types, pathogenesis, clinical features, complications, investigations, classifications, treatment including blood transfusion, iron chelation, splenectomy and prevention through counseling and screening. It addresses the basics of thalassemia, its management, and importance of genetic counseling to prevent affected births.
Hypertension, or high blood pressure, is a major global health issue. It is defined as a systolic blood pressure over 140 mmHg or a diastolic over 90 mmHg. Risk factors include age, family history, stress, obesity, alcohol, sodium intake and lack of exercise. Complications can include heart disease, stroke, kidney disease and eye damage if left untreated. Treatment involves lifestyle changes like diet, exercise and weight loss as well as medications that lower blood pressure such as diuretics, ACE inhibitors, calcium channel blockers and beta blockers. Nurses play an important role in educating patients about hypertension management.
This document discusses hereditary hemochromatosis (HH), an inherited disorder characterized by excessive absorption of dietary iron, which can lead to iron overload. The key points are:
- HH is caused by mutations in the HFE gene, most commonly the C282Y mutation, and results in excessive iron absorption from the diet.
- Left untreated, iron accumulates in organs like the liver, heart and pancreas over many years and can cause organ damage and increased risk of conditions like cirrhosis, diabetes and liver cancer.
- Diagnosis involves blood tests showing elevated ferritin and transferrin saturation; genetic testing can confirm mutations and help screen at-risk family members; liver biopsy may also
Copy Of Investigation Of Endocrine Diseaseguest633bcb
Endocrinology involves understanding hormone levels and stimulating or suppressing hormones that are too high or too low. The pituitary gland regulates other endocrine glands and has anterior and posterior divisions. Diagnosis of endocrine diseases involves hormone stimulation tests, hormone level measurements, and imaging tests. The thyroid, parathyroid, adrenal and other glands are involved in various metabolic processes and their functions and diseases are described.
This document discusses gonadal hormone disorders and abnormalities in both males and females. It covers topics like hypothalamic-pituitary-gonadal axis function in males, male reproductive abnormalities classified into 5 types, defects in androgen action, and female reproductive abnormalities including polycystic ovary syndrome, amenorrhea, precocious puberty, hirsutism, and virilization. Causes, features, and diagnostic evaluation of each condition are described in detail. Congenital adrenal hyperplasia is also explained as a common cause of female pseudohermaphroditism.
This document provides an overview of hemoglobin disorders including:
1) Thalassemias are genetic disorders caused by reduced production of the alpha or beta globin chains. Alpha thalassemia causes mild to severe anemia while beta thalassemia major requires lifelong blood transfusions.
2) Sickle cell anemia is caused by a mutation in the beta globin gene, resulting in rigid, misshapen red blood cells and blockage of blood flow. It causes episodes of pain, anemia, and increased susceptibility to infection.
3) Hemoglobin C disease and Hemoglobin SC disease are hemoglobin variants that cause relatively mild chronic anemia without painful crises.
4
Prolactin is a unique hormone that has more than 300 functions across multiple body systems. It is produced primarily in the pituitary gland but also in other tissues. Prolactin levels have a circadian rhythm and are regulated by the hypothalamus. Abnormal prolactin levels can be caused by prolactinomas, drugs, or physiological states. Prolactinomas are benign pituitary tumors but macroadenomas larger than 1 cm require treatment. High or low prolactin impacts fertility in both males and females. Treatment involves lowering prolactin levels through dopamine agonists like bromocriptine or newer drugs.
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 discusses various diagnostic procedures and dynamic tests used in chemical pathology, focusing on tests for disorders of growth hormone, cortisol, and aldosterone metabolism. It provides details on insulin hypoglycemic tests, glucose stimulation tests, clonidine stimulation tests, and exercise stimulation tests. These tests measure hormonal responses to stimuli like insulin-induced hypoglycemia, glucagon administration, clonidine administration, or exercise to evaluate the functioning of the hypothalamic-pituitary-end organ axes. The document outlines the procedures, normal responses, and interpretations for each type of dynamic test.
Disorders of pituitary gland (( THE MASTER )) BY M.SASIcardilogy
The pituitary gland acts as the control center of the endocrine system. Disorders of the pituitary gland can cause either pituitary hyperfunction (hyperpituitarism) or hypopituitarism. Pituitary hyperfunction is usually caused by a pituitary adenoma and can result in excess secretion of hormones like prolactin, growth hormone, ACTH, or TSH. Prolactinomas, which cause excess prolactin secretion, are the most common type of pituitary adenoma. Symptoms of a prolactinoma include menstrual irregularities in women, infertility, and galactorrhea. Diagnosis involves measuring prolactin levels and treating the underlying cause.
This document provides information on liver function tests. It begins with an overview of liver anatomy and functions including synthesis, metabolism, and excretion. It then discusses specific tests that evaluate these hepatic functions and their clinical implications. Details are provided on liver zonation and regeneration. Key proteins and enzymes synthesized by the liver are outlined. Metabolic functions like ammonia, carbohydrate, and xenobiotic metabolism are reviewed. Inherited disorders of bilirubin metabolism that can cause jaundice are also summarized.
This document discusses non-transfusion dependent thalassemia (NTDT), including HbE/β thalassemia. It classifies HbE/β thalassemia into severe, moderate, and mild based on hemoglobin levels and clinical symptoms. It also discusses transfusion therapy for NTDT, indicating when regular transfusions should start based on hemoglobin drop, organ enlargement, and other factors. The document further discusses chelation therapy for managing iron overload in NTDT, covering various chelating agents like deferoxamine, deferiprone, and deferasirox.
Dyslipidemia, specially high LDL cholesterol is the key risk factor for cardiovascular diseases. The presentation discusses metabolism and structure of lipoproteins, their screening and interpretation, risk assessment methods, targets for various lipoproteins and its step by step treatment.
This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
This document discusses lipids and hyperlipidemia. It begins by explaining how chylomicrons, LDL, and HDL transport lipids between the intestines and cells. High levels of oxidized LDL can lead to atherosclerosis. Hyperlipidemia is characterized by abnormally high levels of fats and lipids in the blood. It causes atherosclerosis and conditions like heart disease. Various drugs are used to treat hyperlipidemia including statins, fibrates, niacin, bile acid sequestrants, and omega-3 fatty acids. The document explains the mechanisms of these drug classes.
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.
Thyroid Stimulating Hormone (TSH) is a glycoprotein produced by the anterior pituitary gland that regulates the thyroid gland and increases production of thyroxine and triiodothyronine. TSH binds to receptors on thyroid cells and activates cyclic AMP, which causes phosphorylation within the cell and increases both immediate and prolonged thyroid hormone secretion and growth. TSH production is regulated by thyrotropin-releasing hormone from the hypothalamus in a feedback loop, where high thyroid hormone levels decrease TSH secretion.
This document provides an overview of diabetes mellitus, including its classification, pathophysiology, clinical features, investigations, diagnostic criteria, and management. It discusses the different types of diabetes, risk factors, characteristics, and laboratory findings. Type 1 diabetes results from beta cell destruction leading to insulin deficiency, while type 2 involves insulin resistance with relative insulin deficiency. Gestational diabetes occurs during pregnancy.
This document discusses hypothyroidism and is presented by Maghan Das. It will state the functions of thyroid hormone, discuss the pathologic mechanisms of hypothyroidism including cretinism, myxedema, and Hashimoto's disease. Hypothyroidism can be congenital or acquired. Congenital hypothyroidism is caused by lack of TSH or abnormal thyroid hormone biosynthesis and can cause cretinism if untreated. Acquired hypothyroidism causes myxedema in adults and slows metabolism. Hashimoto's thyroiditis is an autoimmune cause of hypothyroidism that can destroy the thyroid gland.
Hereditary hemochromatosis, also known as Celtic Curse or Bronze Diabetes, is an autosomal recessive genetic disorder characterized by abnormal iron accumulation in organs. It is most commonly caused by mutations in the HFE gene and results in increased intestinal iron absorption. Symptoms include liver disease, arthritis, diabetes, skin pigmentation changes and heart/endocrine issues. Diagnosis involves blood tests showing elevated iron levels. Treatment is regular phlebotomy to reduce iron stores to normal levels and prevent organ damage. Screening of at-risk family members allows early detection before complications arise.
The document discusses panhypopituitarism, which refers to a deficiency of multiple pituitary hormones. It can be caused by pituitary tumors, head trauma, aneurysms, surgery, radiation, infections, infiltrative diseases, and autoimmune conditions. Symptoms include dry skin, weight gain, cognitive issues, headaches, and vision problems. Laboratory tests can help diagnose deficiencies in cortisol, thyroid hormones, sex hormones, and growth hormone. Treatment involves lifelong hormone replacement therapy for deficiencies.
This document discusses thalassemia syndrome and provides information on its epidemiology, molecular structure of hemoglobin, inheritance, types, pathogenesis, clinical features, complications, investigations, classifications, treatment including blood transfusion, iron chelation, splenectomy and prevention through counseling and screening. It addresses the basics of thalassemia, its management, and importance of genetic counseling to prevent affected births.
Hypertension, or high blood pressure, is a major global health issue. It is defined as a systolic blood pressure over 140 mmHg or a diastolic over 90 mmHg. Risk factors include age, family history, stress, obesity, alcohol, sodium intake and lack of exercise. Complications can include heart disease, stroke, kidney disease and eye damage if left untreated. Treatment involves lifestyle changes like diet, exercise and weight loss as well as medications that lower blood pressure such as diuretics, ACE inhibitors, calcium channel blockers and beta blockers. Nurses play an important role in educating patients about hypertension management.
This document discusses hereditary hemochromatosis (HH), an inherited disorder characterized by excessive absorption of dietary iron, which can lead to iron overload. The key points are:
- HH is caused by mutations in the HFE gene, most commonly the C282Y mutation, and results in excessive iron absorption from the diet.
- Left untreated, iron accumulates in organs like the liver, heart and pancreas over many years and can cause organ damage and increased risk of conditions like cirrhosis, diabetes and liver cancer.
- Diagnosis involves blood tests showing elevated ferritin and transferrin saturation; genetic testing can confirm mutations and help screen at-risk family members; liver biopsy may also
Copy Of Investigation Of Endocrine Diseaseguest633bcb
Endocrinology involves understanding hormone levels and stimulating or suppressing hormones that are too high or too low. The pituitary gland regulates other endocrine glands and has anterior and posterior divisions. Diagnosis of endocrine diseases involves hormone stimulation tests, hormone level measurements, and imaging tests. The thyroid, parathyroid, adrenal and other glands are involved in various metabolic processes and their functions and diseases are described.
This document discusses gonadal hormone disorders and abnormalities in both males and females. It covers topics like hypothalamic-pituitary-gonadal axis function in males, male reproductive abnormalities classified into 5 types, defects in androgen action, and female reproductive abnormalities including polycystic ovary syndrome, amenorrhea, precocious puberty, hirsutism, and virilization. Causes, features, and diagnostic evaluation of each condition are described in detail. Congenital adrenal hyperplasia is also explained as a common cause of female pseudohermaphroditism.
This document provides an overview of hemoglobin disorders including:
1) Thalassemias are genetic disorders caused by reduced production of the alpha or beta globin chains. Alpha thalassemia causes mild to severe anemia while beta thalassemia major requires lifelong blood transfusions.
2) Sickle cell anemia is caused by a mutation in the beta globin gene, resulting in rigid, misshapen red blood cells and blockage of blood flow. It causes episodes of pain, anemia, and increased susceptibility to infection.
3) Hemoglobin C disease and Hemoglobin SC disease are hemoglobin variants that cause relatively mild chronic anemia without painful crises.
4
Prolactin is a unique hormone that has more than 300 functions across multiple body systems. It is produced primarily in the pituitary gland but also in other tissues. Prolactin levels have a circadian rhythm and are regulated by the hypothalamus. Abnormal prolactin levels can be caused by prolactinomas, drugs, or physiological states. Prolactinomas are benign pituitary tumors but macroadenomas larger than 1 cm require treatment. High or low prolactin impacts fertility in both males and females. Treatment involves lowering prolactin levels through dopamine agonists like bromocriptine or newer drugs.
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 discusses various diagnostic procedures and dynamic tests used in chemical pathology, focusing on tests for disorders of growth hormone, cortisol, and aldosterone metabolism. It provides details on insulin hypoglycemic tests, glucose stimulation tests, clonidine stimulation tests, and exercise stimulation tests. These tests measure hormonal responses to stimuli like insulin-induced hypoglycemia, glucagon administration, clonidine administration, or exercise to evaluate the functioning of the hypothalamic-pituitary-end organ axes. The document outlines the procedures, normal responses, and interpretations for each type of dynamic test.
Disorders of pituitary gland (( THE MASTER )) BY M.SASIcardilogy
The pituitary gland acts as the control center of the endocrine system. Disorders of the pituitary gland can cause either pituitary hyperfunction (hyperpituitarism) or hypopituitarism. Pituitary hyperfunction is usually caused by a pituitary adenoma and can result in excess secretion of hormones like prolactin, growth hormone, ACTH, or TSH. Prolactinomas, which cause excess prolactin secretion, are the most common type of pituitary adenoma. Symptoms of a prolactinoma include menstrual irregularities in women, infertility, and galactorrhea. Diagnosis involves measuring prolactin levels and treating the underlying cause.
This document provides information on liver function tests. It begins with an overview of liver anatomy and functions including synthesis, metabolism, and excretion. It then discusses specific tests that evaluate these hepatic functions and their clinical implications. Details are provided on liver zonation and regeneration. Key proteins and enzymes synthesized by the liver are outlined. Metabolic functions like ammonia, carbohydrate, and xenobiotic metabolism are reviewed. Inherited disorders of bilirubin metabolism that can cause jaundice are also summarized.
This document discusses non-transfusion dependent thalassemia (NTDT), including HbE/β thalassemia. It classifies HbE/β thalassemia into severe, moderate, and mild based on hemoglobin levels and clinical symptoms. It also discusses transfusion therapy for NTDT, indicating when regular transfusions should start based on hemoglobin drop, organ enlargement, and other factors. The document further discusses chelation therapy for managing iron overload in NTDT, covering various chelating agents like deferoxamine, deferiprone, and deferasirox.
Dyslipidemia, specially high LDL cholesterol is the key risk factor for cardiovascular diseases. The presentation discusses metabolism and structure of lipoproteins, their screening and interpretation, risk assessment methods, targets for various lipoproteins and its step by step treatment.
This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
This document discusses lipids and hyperlipidemia. It begins by explaining how chylomicrons, LDL, and HDL transport lipids between the intestines and cells. High levels of oxidized LDL can lead to atherosclerosis. Hyperlipidemia is characterized by abnormally high levels of fats and lipids in the blood. It causes atherosclerosis and conditions like heart disease. Various drugs are used to treat hyperlipidemia including statins, fibrates, niacin, bile acid sequestrants, and omega-3 fatty acids. The document explains the mechanisms of these drug classes.
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.
Thyroid Stimulating Hormone (TSH) is a glycoprotein produced by the anterior pituitary gland that regulates the thyroid gland and increases production of thyroxine and triiodothyronine. TSH binds to receptors on thyroid cells and activates cyclic AMP, which causes phosphorylation within the cell and increases both immediate and prolonged thyroid hormone secretion and growth. TSH production is regulated by thyrotropin-releasing hormone from the hypothalamus in a feedback loop, where high thyroid hormone levels decrease TSH secretion.
This document provides an overview of diabetes mellitus, including its classification, pathophysiology, clinical features, investigations, diagnostic criteria, and management. It discusses the different types of diabetes, risk factors, characteristics, and laboratory findings. Type 1 diabetes results from beta cell destruction leading to insulin deficiency, while type 2 involves insulin resistance with relative insulin deficiency. Gestational diabetes occurs during pregnancy.
This document discusses hypothyroidism and is presented by Maghan Das. It will state the functions of thyroid hormone, discuss the pathologic mechanisms of hypothyroidism including cretinism, myxedema, and Hashimoto's disease. Hypothyroidism can be congenital or acquired. Congenital hypothyroidism is caused by lack of TSH or abnormal thyroid hormone biosynthesis and can cause cretinism if untreated. Acquired hypothyroidism causes myxedema in adults and slows metabolism. Hashimoto's thyroiditis is an autoimmune cause of hypothyroidism that can destroy the thyroid gland.
Hereditary hemochromatosis, also known as Celtic Curse or Bronze Diabetes, is an autosomal recessive genetic disorder characterized by abnormal iron accumulation in organs. It is most commonly caused by mutations in the HFE gene and results in increased intestinal iron absorption. Symptoms include liver disease, arthritis, diabetes, skin pigmentation changes and heart/endocrine issues. Diagnosis involves blood tests showing elevated iron levels. Treatment is regular phlebotomy to reduce iron stores to normal levels and prevent organ damage. Screening of at-risk family members allows early detection before complications arise.
The document discusses panhypopituitarism, which refers to a deficiency of multiple pituitary hormones. It can be caused by pituitary tumors, head trauma, aneurysms, surgery, radiation, infections, infiltrative diseases, and autoimmune conditions. Symptoms include dry skin, weight gain, cognitive issues, headaches, and vision problems. Laboratory tests can help diagnose deficiencies in cortisol, thyroid hormones, sex hormones, and growth hormone. Treatment involves lifelong hormone replacement therapy for deficiencies.
Hyperprolactinemia Quiz - Case PresentationUsama Ragab
Hyperprolactinemia Quiz - Hyperprolactinemia Workshop
In light of 3rd Annual Endo-ISMA Conference 2021
By Dr. Usama Ragab Youssif
Importance of History Taking and Hypothyroidism as a cause of hyperprolactinemia
The document discusses the hypothalamus-pituitary axis. It describes how the hypothalamus secretes releasing hormones that stimulate the anterior pituitary to release hormones like growth hormone, prolactin, and thyroid-stimulating hormone. The pituitary hormones then target various endocrine glands like the thyroid to regulate processes like metabolism and development. Disruptions to the hypothalamus-pituitary communication can lead to hormonal deficiencies. The feedback loops between the hypothalamus, pituitary and target glands allow for coordinated control of the endocrine system.
This case describes a 15-year-old boy who presents with short stature and social/behavioral issues. The main potential causes of his short stature are growth hormone (GH) deficiency, constitutional delay of growth, or familial short stature. Key tests to diagnose GH deficiency include low levels of insulin-like growth factor 1 (IGF-1) and GH stimulation tests such as the insulin tolerance test or GHRH+arginine stimulation test. Further investigations to confirm the diagnosis would include assessing his family history, measuring sex hormone levels, and checking for signs of other hormonal deficiencies or genetic disorders like Laron syndrome.
Male hypogonadism is caused by androgen deficiency which can negatively impact organ functions and quality of life. The goal of testosterone replacement therapy is to restore hormone levels to the normal range and alleviate symptoms. Common treatment options include injections, patches, gels, and implants which can restore sexual function, muscle strength, and bone density. Therapy requires monitoring for side effects like prostate issues or blood clots. Gonadotropins may also be used to stimulate testosterone production and spermatogenesis in hypogonadotropic hypogonadism.
This document provides guidance on evaluating male breast enlargement (gynecomastia). Key recommendations include examining the breasts to distinguish true gynecomastia from pseudogynecomastia caused by obesity, asking about medications associated with gynecomastia, and ordering tests if initial examination is insufficient. Causes of gynecomastia include physiological factors, drugs, decreased androgen production or effect, and increased estrogen production. A thorough history and physical exam can help identify contributing factors. The evaluation should include differentiating gynecomastia from pseudogynecomastia, checking for bilateral involvement, and inquiring about medical history, medications, weight changes and symptoms to identify
1) Endocrine diseases are often difficult to diagnose due to low hormone levels that require specialized assays for detection. Hormone levels also vary based on timing of tests and dynamic testing is often needed.
2) Common causes of pituitary diseases include tumors, trauma, infections, and genetic disorders which can cause either hormone excess or deficiency.
3) Pituitary tumors are usually benign adenomas that can be classified based on size and hormone production. Larger tumors may cause local pressure effects while smaller tumors often only cause hormone imbalance.
James is a 5-year old boy who is smaller than his classmates and has experienced a marked drop in growth rate over the past year. His bone age is that of a 3-year old. Biochemical tests appropriate to investigate this boy would include tests of anterior pituitary hormones like growth hormone, TSH, and ACTH, as deficiencies in these hormones could cause stunted growth. The anterior pituitary is controlled by hormones from the hypothalamus and secretes hormones including growth hormone, TSH, ACTH, prolactin, FSH, and LH that regulate growth, metabolism, and reproduction.
The anterior pituitary gland secretes several important hormones. Growth hormone promotes growth and development. Prolactin stimulates lactation. Gonadotropins such as LH and FSH regulate the reproductive system. ACTH regulates cortisol production and TSH controls thyroid function. These hormones are regulated by hypothalamic factors and provide feedback control of their target organs. Disorders can arise from excess or deficiency of anterior pituitary hormones, leading to important diseases like acromegaly, Cushing's syndrome, and hypothyroidism.
This document provides information about disorders of the anterior pituitary gland, focusing on pituitary adenomas. It begins with basic principles of endocrinology, describing the hypothalamic-pituitary feedback systems. It then discusses the pituitary gland and various types of pituitary adenomas, their effects and investigations. Specific adenomas covered in detail include Acromegaly (growth hormone excess), Hyperprolactinaemia, Cushing's Syndrome, and Hypopituitarism. For each condition, the document outlines causes, clinical features, investigations and management.
The hypothalamus and pituitary gland work together to regulate many endocrine systems. The hypothalamus controls the pituitary gland through neural and hormonal signals. The pituitary gland has an anterior and posterior lobe and is very small, sitting at the base of the brain. The hypothalamus releases hormones that stimulate or inhibit different hormone releases from the anterior pituitary gland to regulate other endocrine glands.
This document discusses acromegaly, a condition caused by excessive growth hormone production leading to disproportionate skeletal and soft tissue growth. It begins by describing the causes and effects of excess growth hormone, then discusses clinical features of acromegaly including organ enlargement and metabolic complications. The document outlines diagnostic tests for acromegaly focusing on growth hormone and IGF-1 levels. Treatment aims to control growth hormone levels and includes surgery, radiation therapy, somatostatin analogues, dopamine agonists, and growth hormone antagonists.
Hypothyroidism and thyroid screening can be caused by primary or secondary issues. Neonatal screening uses dried blood samples to test TSH levels to detect congenital hypothyroidism. TSH is the most sensitive indicator for primary hypothyroidism. Precocious and delayed puberty can have various causes like tumors, infections, or genetic defects. Puberty is evaluated based on physical signs, lab tests, and sexual maturity ratings which characterize development. Treatment depends on the underlying cause and aims to initiate normal development.
The document discusses several hormones produced by the pituitary gland and their effects. It begins by describing growth hormone (GH) and its role in promoting insulin-like growth factors (IGFs) which cause cell growth. GH increases growth during childhood and maintains muscle and bone mass in adults. Thyroid stimulating hormone regulates thyroid hormones, while follicle stimulating hormone and luteinizing hormone control reproduction. Prolactin induces milk production. The hypothalamus regulates pituitary hormone secretion through releasing and inhibiting hormones. Conditions caused by pituitary hormone imbalances like gigantism, dwarfism, and acromegaly are also summarized.
This note will be helpful for Pharmacy Students searching for analogues and inhibitors of various hormones in human body.
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Sarah is a 38-year-old woman who presented with amenorrhea, headaches, and joint pains. She reported changes in her facial features and enlargement of her hands, feet, and fingers. Examination found coarse facial features, prominent jaw, and enlarged hands and feet. Tests found elevated growth hormone and fasting blood glucose, decreased FSH, and elevated prolactin. An MRI revealed a pituitary adenoma. She was diagnosed with acromegaly due to the pituitary adenoma causing elevated growth hormone secretion after her growth plates had fused.
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Provocative test by sidra bibi d/o farzand ali taxila cantt
1.
2. For some of the hormones, a substance is given that would
normally affect hormone production and then the level of the
hormone is measured. For example, if insulin is injected, the levels
of ACTH, GH and prolactin should increase. Sometimes, rather
than measuring GH levels directly, another hormone, insulin like
growth factor I (IGF-1) is often measured. GH is produced in
bursts and its levels quickly fall, but IGF-1 levels reflect the
overall daily production of GH.
A stimulation/provocation test is a test that is performed to reveal
a clinical condition; suspected but not fully manifested clinically.
Any procedure in
which
a
suspected
pathophysiological abnormality is deliberately induced by
manipulating conditions known to provoke the abnormality.
The test can be either stimulation for hypoactive medical problem,
or suppression for hyperactive function.
4. Indications
Confirming suspected diagnosis.
Monitoring the course of disease.
Following the effect of therapy.
Establishing the significance of borderline low values by
stimulation tests.
Document the presence of hyperfunction by suppression
tests.
Distinguish primary from secondary causes of endocrine
dysfunction.
5. Clinical applications
Almost every system disorder in clinical evaluation of disease
could use a stimulation test.
It can be the only test available in certain situations like in “drug
induced diseases” by challenging the patient with the suspected
drug.
Stimulation testing is commonly used in endocrinology based on
the feedback system.
There are several different types of stimulation testing that can be
ordered to help the doctor diagnose child’s medical condition.
All stimulation testing can take several hours to complete. The
test should take from 1 to 3 hours, including registration, the test,
and a snack afterward.
Most stimulation tests are “fasting,” meaning that child should
not eat or drink before the test. Follow specific instructions given
about eating and drinking before the test.
6. The child will need to have an intravenous (IV) line placed to
start the testing. Blood samples will be removed from the IV
line at different times throughout the test.
Stimulation testing measures the response of certain glands
within the endocrine system to different types of
hormones. Some of the stimulation tests that might be ordered
include:
Growth Hormone Stimulation — used to find out if child’s
pituitary gland is producing enough growth hormone
Lupron Stimulation — used to diagnose precocious (too
early) or delayed (too late) puberty in boys and girls
Glucose Tolerance — used to rule out diabetes, hypoglycemia
and insulin resistance
ACTH Stimulation — used to find out if your child’s adrenal
glands are producing enough cortisol and to rule out congenital
adrenal hyperplasia
7.
8. PURPOSE
Growth hormone tests are ordered for the following reasons:
to identify growth deficiencies, including delayed puberty and
small stature in adolescents that result from pituitary or thyroid
malfunction
to aid in the diagnosis of hyperpituitarism that is evident in
gigantism or acromegaly
to screen for inadequate or reduced pituitary gland function
to assist in the diagnosis of pituitary tumors or tumors related
to the hypothalamus, an area of the brain
to evaluate hGH therapy
9. GROWTH HORMONE
Quantitative GH
Fasting level
Provocative test for suspected deficiency
Hypoglycemia causes GH levels to rise
Give
insulin, L-dopa or arginine
take samples at 0, 15, 39, 45, 60, 90, and 120 minutes
Small rise partial deficiency
No rise inability to secrete GH
Suppression test
Hyperglycemia suppresses GH but not in autonomous or
elevated GH
Give glucose
10. NORMAL RESULTS
Results are reported in nanograms per milliliter (ng/ml). Normal
results may vary from laboratory to laboratory depending upon the
method used for measurement, but results are usually within the
following ranges.
SOMATOTROPIN (hGH):
men: 5 ng/ml
women: less than 10 ng/ml
children: 0–10 ng/ml
newborn: 10–40 ng/ml
SOMATOMEDIN C:
adult: 42–110 ng/ml
child: 0–8 years; girls 7–110 ng/ml; boys 4–87 ng/ml
9–10 years: girls 39–186 ng/ml; boys 26–98 ng/ml
11–13 years: girls 66–215 ng/ml; boys 44–207 ng/ml
14–16 years: girls 96–256 ng/ml; boys 48–255 ng/ml
11. ABNORMAL RESULTS
Somatotropin hormone: Excess hGH is responsible for the
syndromes of gigantism and acromegaly. Excess secretion is
stimulated by anorexia nervosa, stress, hypoglycemia, and
exercise. Decreased levels are seen in hGH deficiency, dwarfism,
hyperglycemia, failure to thrive, and delayed sexual maturity.
Somatomedin C: Increased levels contribute to the syndromes of
gigantism
and
acromegaly.
Stress,
major
surgery,
hypoglycemia, starvation, and exercise stimulate hGH secretion,
which in turn stimulates somatomedin C.
Growth hormone stimulation: Decreased levels are seen in
pituitary deficiency and hGH deficiency. Diseases of the pituitary
can result in failure of the pituitary to secrete hGH and/or all the
pituitary hormones. As a result, the hGH stimulation test will fail
to stimulate hGH secretion.
12. Pitfalls
False negative or positive results if the test is not
conducted properly.
Failure to provide safety measures during a challenge
test may harm the patients.
Inadequate preparation following the exact procedure
for the test can provide misleading results.
Lab errors may confuse the results (wrong sample
labeling, wrong time, poor calibration).
13.
14. Thyroid hormone production is under the control of pituitary
TSH and in turn hypothalamic TRH. Plasma TSH levels
normally increase rapidly (2 to 5 minutes) after an IV bolus of
TRH, with a subsequent more gradual increase in T3 secretion
from the thyroid. The TRH test thus allows the integrity of the
thyroid axis to be tested.
Abnormalities of the prolactin response to TRH may occur in
pituitary tumors (especially GH or prolactin producing) or in
pituitary stalk pathology. Responses are not diagnostically
pathognomonic, but indicate axis disruption or dysregulation.
In GH excess states (gigantism/acromegaly), TRH may cause
an elevation of GH, but not in normal subjects.
15. Indications secretion and thyroid
1.To assess the response of pituitary TSH
hormone production to stimulation. The main indication is in
suspected secondary (pituitary) or tertiary (hypothalamic)
hypothyroidism. Less frequently may be of assistance in mild
primary hypothyroidism.
2.To assess the response of prolactin to stimulation
3.Less commonly used in investigation of gigantism/acromegaly.
Often performed as part of a combined pituitary function test
(triple test).
Dose:
200 micrograms/m2 BSA by slow intravenous injection over 1 min.
Sample:
0 min, 15min, 30min, 45min, 60min, 90min and 120min
Analysis:
TSH, Free T3, Free T4, Prolactin
16. Interpretation
A normal response is a rapid rise in TSH, peaking between 10-
30 mU/l at 20-30 minutes, then gradually declining to reach
baseline after 2 to 3 hrs. T3 values show a rise, but do not peak
until 3-4 hrs (30-70% rise from baseline).
Prolactin levels are age dependent. Above 1 year age, mean
basal levels are approximately 240 mU/l, rising to
approximately 725 mU/l with TRH stimulation (i.e. a 2-3 fold
rise).
In hyperthyroidism (Grave's disease), T3 and T4 are elevated
and TSH levels are suppressed and unresponsive to TRH
stimulation.
In primary hypothyroidism basal T3 and T4 are low, with
elevated basal TSH and an exaggerated TSH response (usually
to a peak > 30 mU/l at 30-40 min).
17. Conti……
In secondary (pituitary) hypothyroidism T3 and T4 levels are
likely to be low and there is a poor TSH response and poor T3
response.
In tertiary (hypothalamic) hypothyroidism, an exaggerated and
prolonged TSH peak may be seen, and a T3 response occurs.
While prolactin responses are variable, an exaggerated
prolactin response suggests hypothalamic disease or stalk
disruption, owing to loss of inhibitory effects of dopamine.
A poor prolactin response suggests pituitary disease.
In normal subjects TRH induces no rise in GH levels, but it
may do so in pituitary gigantism / acromegaly.
18. Adverse effects
Nausea, flushing, dizziness, urinary urgency, unusual taste
in mouth, occasionally headaches.
Increases in BP and pulse rate frequently observed
Caution in heart failure, myocardial ischemia and asthma.
Caution in severe hypopituitarism - risk of hypoglycemia
Certain drugs may diminish response.
21. Rationale
ACTH is the primary regulator of glucocorticoid production,
and also plays some role in adrenal androgen production.
Synacthen is a synthetic form of ACTH, is used to assess the
stimulated cortisol response of the adrenal cortex and is
valuable in diagnosing suspected primary adrenal
insufficiency.
The test is also useful in suspected secondary or tertiary
adrenal insufficiency since chronic CRH/ACTH deficiency or
dysregulation results in temporary quiescence of the adrenal
cortex and inability to respond acutely.
22. Conti…..
Furthermore, the test is not reliable in assessing secondary or
tertiary insufficiency within 2 weeks of surgery to the
hypothalamic-pituitary region or a major alteration in any
glucocorticoid therapy.
In congenital adrenal hyperplasia, Synacthen test is useful in
diagnosing milder or rare enzyme blocks by examining ratios
of various adrenal steroids to their precursor compounds. The
commonest ratio examined is that of 17-hydroxyprogesterone /
cortisol in suspected non-classical or simple virilizing CAH or
the heterozygote state.
23. Standard doze of synacthen
Over 1 yr: Single IM or IV injection of 250 micrograms.
Under 1 yr: Single IM or IV dose of 125 micrograms.
Alternatively a dose of 250 micrograms/m2 BSA may be
used.
24. Blood sampling
Samples are collected at 0 min, 30 min and 60 min.
Cortisol, 17-OHProgesterone, ACTH and Androgens
(DHEAS, Androstendione & Testosterone).
25. Interpretation
Serum cortisol rise of > 280 nmol/l with maximal level >
600 nmol/l.
Normal ratio of 17-OHP to cortisol at 30 mins < 0.023.
Ratios up to 0.08 suggest heterozygosity for 21-
hydroxylase deficiency.
ratios > 0.1 suggest CAH (21-hydroxylase deficiency).
28. GnRH (gonadotropin releasing hormone) is a decapeptide
secreted by the hypothalamus which stimulates the
production and secretion of LH and FSH by the anterior
pituitary.
The GnRH stimulation test evaluates the ability of
gonadotropes to secrete LH and FSH after exposure to the
natural hypothalamic releasing hormone, GnRH, or an
analog.
The GnRH test is extensively evaluated for the discrimination
of disorders of precocious or delayed puberty and
amenorrhea.
The GnRH test is useful to monitor adequate treatment of
gonadotropin-dependent precocious puberty.
29. Methods
This test may be done with either recombinant GnRH or a GnRH
agonist, such as leuprolide.
Several different methods have been used:
Administer 100 micrograms of GnRH (or GnRH analogue)
IV x 1 at time 0. Measure serum LH at time -15 minutes, 0,
+15, +30, +45, and +60 minutes after GnRH administration.
Administer 25 micrograms/M2 of GnRH IV at 8am after an
overnight fast. Measure serum LH and FSH at time 0, 15 min,
30 min, 60 min, and 90 min after GnRH injection.
Administer leuprolide 20 mcg/kg x 1, measure LH and FSH
at baseline and after 30 and 60 minutes.
30. Assay requirements
In general, assays for LH and sex hormones (estradiol and
testosterone) must be sensitive enough to detect pre-pubertal
levels. Prepubertal LH is less than 0.1 IU/L and pre-pubertal
E2 is <1 pg/L (undetectable with most available assays).
Immunochemiluminometric assays are much more sensitive
than radioimmunoassay for gonadotropin levels in the prepubertal, thus these should be used, especially when measuring
basal gonadotropin levels.
31. Interpretation
In general, in gonadotropin dependent precocious puberty
(GDPP), basal LH is elevated (pubertal range) and increases
further with GnRH stimulation (peak LH >5-8 IU/L suggests
GDPP), and in gonadotropin independent precocious puberty
(GIPP), basal LH is low (in the pre-pubertal range) and does
not increase with GnRH stimulation. In addition, stimulated
LH/FSH ratio may be help distinguish GDPP (higher LH:FSH)
from nonprogressive PP, which does not require treatment with
exogenous GnRH. Otherwise, the FSH values (basal or
stimulated) are generally not useful.
With either GnRH or GnRHa tests, the ratio of peak to basal
LH is also used to define precocious puberty. In general, a
ratio of LH (peak): LH (basal) <3.0 is considered normal and a
ratio of LH (peak): LH (basal) >3.0 is consistent with
precocious puberty.
32. Side effects
The patient may react to the side effect of GnRH, transient
thirst may occur. Abdominal or stomach discomfort, flushing
(lasting only a short time), headaches, lightheadedness, nausea
may also occur but less common.
Hypersensitivity reactions to GnRH, such as itching, redness or
swelling of skin at place of injection, skin rash, breathing
difficulty etc may occur but they are rare.
Rarely, GnRH injection has been associated with pituitary
apoplexy.