Thyroid storm and myxedema coma are life-threatening thyroid emergencies. Thyroid storm is an exacerbation of hyperthyroidism caused by precipitating factors and is treated with anti-thyroid drugs, beta-blockers, steroids, and iodine to control symptoms rapidly within 1-2 days. Myxedema coma develops in severe, prolonged hypothyroidism and is treated with thyroid hormone replacement along with treating any precipitating causes while providing ventilatory support. Both have high mortality rates even with treatment.
1) Myxedema coma is a life-threatening emergency that occurs in severe hypothyroidism and is characterized by hypothermia, hypoventilation, and unconsciousness.
2) Thyroid storm is a severe exacerbation of thyrotoxicosis that can cause multi-organ failure if not treated promptly. It is usually precipitated by infection or other stressors.
3) Treatment for both conditions involves stabilizing vital functions, administering thyroid hormones, and treating any underlying causes. Myxedema coma has high mortality even with treatment while thyroid storm mortality can be reduced to 10-20% with early diagnosis and comprehensive management.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.
This document discusses the case of a 56-year-old woman who presented with fever, sore throat, and breathlessness and was diagnosed with thyroid storm. It provides details on her medical history, examination, labs, and treatment. The document also discusses two additional cases of thyroid storm and provides a summary of key points on diagnosing and treating thyroid storm.
This document discusses hypothyroidism and myxedema coma. It begins with an introduction defining hypothyroidism and its causes. Myxedema coma is described as a metabolic crisis characterized by uncorrected hypothyroidism and precipitating stressors causing mental status changes, hypothermia, and other symptoms. Diagnosis involves clinical evaluation and lab tests. Treatment involves supportive care and thyroid hormone replacement, with myxedema coma being a medical emergency. Special populations like pregnant and elderly patients require careful management.
This document discusses the management of thyroid storm, a life-threatening condition characterized by a hypermetabolic state caused by underlying hyperthyroidism. Key points include:
- Thyroid storm is diagnosed clinically or using scoring tools like the Burch-Wartofsky Point Scale.
- Management aims to inhibit thyroid hormone synthesis/release and peripheral effects while reversing decompensation. This involves high-dose antithyroid drugs, beta blockers, corticosteroids, inorganic iodide, and treating any precipitating factors.
- Supportive treatments like IV fluids and nutrition are also important, along with considering urgent thyroidectomy or radioactive iodine in some cases. Patient education is crucial
This document summarizes the case of a patient presenting with symptoms of myxedema crisis including loss of consciousness for 5 days. On examination, the patient was found to have hypothyroid features including an unrousable mental state, dry skin, bradycardia, and hypothermia. Laboratory tests confirmed very high TSH levels and low FT3 and FT4, consistent with severe untreated hypothyroidism. The patient was treated with intravenous thyroxine, hydrocortisone, saline and antibiotics. Myxedema crisis carries high mortality if not treated but can be managed with thyroid hormone replacement and treating any underlying infections or precipitating causes.
1) Thyroid storm, or a thyrotoxic crisis, is a life-threatening exacerbation of hyperthyroidism caused by an abrupt release of thyroid hormones into circulation.
2) It presents with fever, tachycardia, arrhythmias, heart failure, tremors, and gastrointestinal issues like nausea and vomiting.
3) Treatment involves controlling adrenergic symptoms with beta blockers, treating the underlying thyroid abnormality with antithyroid drugs like PTU, and providing supportive care like fluids and electrolyte replacement.
The document discusses thyroid storm, an acute, life-threatening exacerbation of hyperthyroidism. It describes the anatomy and functions of the thyroid gland. Thyroid storm is a medical emergency caused by excessive thyroid hormones and can be precipitated by events like surgery or infection. Symptoms include high fever, rapid heart rate, nausea, and confusion. Treatment aims to reduce thyroid hormone levels through medications, control symptoms, and maintain homeostasis.
1) Myxedema coma is a life-threatening emergency that occurs in severe hypothyroidism and is characterized by hypothermia, hypoventilation, and unconsciousness.
2) Thyroid storm is a severe exacerbation of thyrotoxicosis that can cause multi-organ failure if not treated promptly. It is usually precipitated by infection or other stressors.
3) Treatment for both conditions involves stabilizing vital functions, administering thyroid hormones, and treating any underlying causes. Myxedema coma has high mortality even with treatment while thyroid storm mortality can be reduced to 10-20% with early diagnosis and comprehensive management.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.
This document discusses the case of a 56-year-old woman who presented with fever, sore throat, and breathlessness and was diagnosed with thyroid storm. It provides details on her medical history, examination, labs, and treatment. The document also discusses two additional cases of thyroid storm and provides a summary of key points on diagnosing and treating thyroid storm.
This document discusses hypothyroidism and myxedema coma. It begins with an introduction defining hypothyroidism and its causes. Myxedema coma is described as a metabolic crisis characterized by uncorrected hypothyroidism and precipitating stressors causing mental status changes, hypothermia, and other symptoms. Diagnosis involves clinical evaluation and lab tests. Treatment involves supportive care and thyroid hormone replacement, with myxedema coma being a medical emergency. Special populations like pregnant and elderly patients require careful management.
This document discusses the management of thyroid storm, a life-threatening condition characterized by a hypermetabolic state caused by underlying hyperthyroidism. Key points include:
- Thyroid storm is diagnosed clinically or using scoring tools like the Burch-Wartofsky Point Scale.
- Management aims to inhibit thyroid hormone synthesis/release and peripheral effects while reversing decompensation. This involves high-dose antithyroid drugs, beta blockers, corticosteroids, inorganic iodide, and treating any precipitating factors.
- Supportive treatments like IV fluids and nutrition are also important, along with considering urgent thyroidectomy or radioactive iodine in some cases. Patient education is crucial
This document summarizes the case of a patient presenting with symptoms of myxedema crisis including loss of consciousness for 5 days. On examination, the patient was found to have hypothyroid features including an unrousable mental state, dry skin, bradycardia, and hypothermia. Laboratory tests confirmed very high TSH levels and low FT3 and FT4, consistent with severe untreated hypothyroidism. The patient was treated with intravenous thyroxine, hydrocortisone, saline and antibiotics. Myxedema crisis carries high mortality if not treated but can be managed with thyroid hormone replacement and treating any underlying infections or precipitating causes.
1) Thyroid storm, or a thyrotoxic crisis, is a life-threatening exacerbation of hyperthyroidism caused by an abrupt release of thyroid hormones into circulation.
2) It presents with fever, tachycardia, arrhythmias, heart failure, tremors, and gastrointestinal issues like nausea and vomiting.
3) Treatment involves controlling adrenergic symptoms with beta blockers, treating the underlying thyroid abnormality with antithyroid drugs like PTU, and providing supportive care like fluids and electrolyte replacement.
The document discusses thyroid storm, an acute, life-threatening exacerbation of hyperthyroidism. It describes the anatomy and functions of the thyroid gland. Thyroid storm is a medical emergency caused by excessive thyroid hormones and can be precipitated by events like surgery or infection. Symptoms include high fever, rapid heart rate, nausea, and confusion. Treatment aims to reduce thyroid hormone levels through medications, control symptoms, and maintain homeostasis.
Hyperthyroidism and thyrotoxicosis occur when the thyroid gland overproduces thyroid hormones. Thyroid storm is a life-threatening exacerbation of thyrotoxicosis caused by factors like infection, surgery, or medication changes. It involves fever, sweating, tachycardia, anxiety, and heart failure. Treatment focuses on cooling the patient, blocking further hormone production with antithyroid drugs and iodine, and supporting heart and brain function with beta-blockers and glucocorticoids. Thyroidectomy may be required for severe cases not responding to medical management.
This document summarizes thyroid storm, an extreme manifestation of hyperthyroidism. It describes the etiology as usually involving a precipitating factor in addition to hyperthyroidism. Signs and symptoms are severe and can involve multiple organ systems. Management requires promptly blocking thyroid hormone synthesis and secretion, blocking peripheral thyroid hormone action, and providing supportive care measures to stabilize the patient's homeostasis and address underlying causes.
Myxoedema coma is a life-threatening manifestation of severe, untreated hypothyroidism. It occurs when the body's compensatory mechanisms for coping with low thyroid hormone levels are overwhelmed, such as by infection, drugs, or other illness. Left untreated, it can affect multiple organ systems as the adaptations that help maintain homeostasis start to fail. Symptoms include deterioration of mental status, reduced brain function, hypothermia, slowed metabolism and reflexes, bradycardia, edema, and respiratory issues. Prompt diagnosis and treatment are needed to avoid permanent brain damage or death.
This document discusses myxedema coma, a life-threatening complication of severe hypothyroidism. It can be precipitated by a stressful event in someone who is already hypothyroid. Primary symptoms include altered mental status, low body temperature, low blood pressure, slow heart rate, and hypoventilation. Treatment involves supportive care in the intensive care unit, treating hypothermia, hyponatremia, and providing thyroid hormone replacement through intravenous levothyroxine and possibly liothyronine, as well as hydrocortisone therapy.
Myxoedema coma Pharmacotherapeutic viewPranatiChavan
Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration. The term myxedema is often used interchangeably with hypothyroidism and myxedema coma. Myxedema also refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid. Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can be fatal if not treated promptly and aggressively. It is usually precipitated by stress in individuals with poorly controlled hyperthyroidism. Signs and symptoms involve multiple organ systems and include fever, tachycardia, heart failure, gastrointestinal issues, and altered mental status. Treatment requires addressing the underlying hyperthyroidism with antithyroid drugs, iodine, beta-blockers, and glucocorticoids to suppress hormone production and effects. Managing precipitating factors, supportive care, and monitoring for complications are also important.
This document provides guidelines from the American Thyroid Association and American Association of Clinical Endocrinologists for the management of hyperthyroidism and thyrotoxicosis. It includes over 30 recommendations regarding the evaluation, treatment, and management of Graves' disease, toxic multinodular goiter, toxic adenoma, and thyroid storm using radioactive iodine therapy, antithyroid medications, or thyroidectomy. Recommendations cover pre-treatment procedures, dosing, monitoring, and follow-up care for patients undergoing treatment for hyperthyroidism.
This document discusses how various drugs can interfere with thyroid function. It begins by defining primary and central hypothyroidism. It then explains how drugs can disrupt thyroid hormone synthesis, alter thyroid autoimmunity, and affect follicular cell activity. Specific drugs like amiodarone, lithium, and cytokines are highlighted. The document also discusses how drugs can interfere with T4 metabolism and conversion to T3. It provides examples of medications that can alter thyroid function tests or T4 binding. Finally, it emphasizes the importance of recognizing drug interactions to correctly interpret thyroid tests and treat patients.
This document discusses drug-induced hematological disorders, focusing on drug-induced aplastic anemia, hemolytic anemia, and megaloblastic anemia. It defines each condition, describes their mechanisms, symptoms, risk factors, prevention, and treatment approaches. Drug-induced aplastic anemia is the most serious as it damages stem cells and reduces blood cell counts, potentially causing infections and bleeding. Treatment involves discontinuing the causative drug, immunosuppression, supportive care like transfusions, and sometimes stem cell transplantation. Drug-induced hemolytic anemia and megaloblastic anemia are also explained in terms of their causes, presentations, and management through removal of the offending drug and supplementation.
This document discusses principles of drug therapy and pharmacology in heart disease. It covers topics such as variability in drug effects due to pharmacokinetic, pharmacodynamic, and pharmacogenomic factors. It discusses optimizing drug dosages starting at low levels and monitoring for adverse effects. Special considerations for drug therapy in the elderly population and issues with polypharmacy are also covered. The risks of non-adherence to drug regimens in elderly patients are described.
Hyperthyroidism is caused by excess thyroid hormone production. Treatment aims to normalize thyroid hormone levels, minimize symptoms, and provide individualized therapy based on disease severity and patient factors. Treatment options include antithyroid medications, radioactive iodine, surgery, and beta blockers. Antithyroid drugs work by inhibiting thyroid hormone synthesis and are given for 12-24 months to induce remission. Radioactive iodine is the treatment of choice for Graves' disease and destroys overactive thyroid cells with radiation. Surgery may be considered for large goiters or lack of drug treatment response. Therapy for thyroid storm involves rapidly suppressing hormone levels along with antiadrenergic and corticosteroid treatment.
This document discusses different types of hypothyroidism including cretinism, adult hypothyroidism, and myxoedema. Cretinism is fetal or infantile hypothyroidism which can be endemic or sporadic and causes symptoms like a hoarse cry and umbilical hernia. Adult hypothyroidism causes symptoms like bradycardia, cold extremities, dry skin/hair, puffy eyes, hoarse voice, slowed movements, and delayed ankle jerks. Myxoedema is a severe form of hypothyroidism that requires treatment with oral thyroxine, triiodothyronine, or intravenous thyroxine along with corticosteroids and antibiotics.
This document summarizes key endocrine emergencies including thyroid storm, adrenal crisis, and hypoglycemia. Thyroid storm is a life-threatening complication of hyperthyroidism caused by Graves' disease or toxic multinodular goiter in 1-2% of cases, with a mortality rate of 20% without treatment. Adrenal crisis can occur due to primary or secondary adrenal insufficiency and presents with low blood pressure. Hypoglycemia is most commonly caused by insulin therapy in diabetic patients but can occur in non-diabetics, defined as a blood glucose below 50-60 mg/dL.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can develop in patients with undiagnosed or untreated hyperthyroidism when stressed. It is characterized by worsening signs and symptoms of thyrotoxicosis including cardiac dysfunction, hyperglycemia, altered mental status, and seizures. Diagnosis is based on clinical features and scoring systems, with a Burch-Wartofsky score of over 45 suggestive of thyroid storm. Treatment involves supportive care, administration of beta blockers, antithyroid medications, iodine, and glucocorticoids to reduce thyroid hormone levels and symptoms.
hypertension is a condition arrising due to increased symphathetic tone so drugs therapies are administered for minimising disease sevearity and further complications. Drug therapy includes drugs like alpha blockers, beta blockers, ACE INHIBITORS, ARBs, vasodilators,direct renin inhibitors, reserpine,prostaglandin analogs, calcium channel blockers for minimising excessive pressure and increased contractility of the heart.
The document discusses hypertension, noting that its prevalence is increasing worldwide and discusses its classification, treatment options including various classes of antihypertensive drugs and their mechanisms of action, experimental models used to study hypertension, and approaches to it in Ayurveda.
This document discusses drugs used to treat hypertension. It classifies antihypertensive drugs into diuretics, sympathoplegics, direct vasodilators, and agents that block the renin-angiotensin-aldosterone system. Specific drugs discussed include furosemide, hydrochlorothiazide, amlodipine, captopril, and losartan. Their mechanisms of action, uses, and potential adverse effects are explained. The document emphasizes that blood pressure can be controlled through multiple pathways and drug classes.
A 27-year-old female presents with palpitations. Exam finds an enlarged, tender thyroid. Labs show suppressed TSH, elevated T4 and low radioactive iodine uptake. The next appropriate test would be to check the ESR, as these findings are consistent with subacute thyroiditis, an inflammation of the thyroid gland often caused by a viral infection. The treatment is symptomatic with pain medication as the condition will typically resolve on its own over several months.
1. Rate control has equivalent efficacy to rhythm control for managing atrial fibrillation and has less drug-related side effects.
2. Drugs like digoxin, beta blockers, and calcium channel blockers can be used for rate control, while antiarrhythmics like amiodarone, dofetilide and sotalol are used for rhythm control.
3. Electrical cardioversion can be used to restore sinus rhythm but has a risk of recurrence, so anticoagulation is recommended afterwards to prevent stroke from clots that may form during the arrhythmia.
Hyperthyroidism and thyrotoxicosis occur when the thyroid gland overproduces thyroid hormones. Thyroid storm is a life-threatening exacerbation of thyrotoxicosis caused by factors like infection, surgery, or medication changes. It involves fever, sweating, tachycardia, anxiety, and heart failure. Treatment focuses on cooling the patient, blocking further hormone production with antithyroid drugs and iodine, and supporting heart and brain function with beta-blockers and glucocorticoids. Thyroidectomy may be required for severe cases not responding to medical management.
This document summarizes thyroid storm, an extreme manifestation of hyperthyroidism. It describes the etiology as usually involving a precipitating factor in addition to hyperthyroidism. Signs and symptoms are severe and can involve multiple organ systems. Management requires promptly blocking thyroid hormone synthesis and secretion, blocking peripheral thyroid hormone action, and providing supportive care measures to stabilize the patient's homeostasis and address underlying causes.
Myxoedema coma is a life-threatening manifestation of severe, untreated hypothyroidism. It occurs when the body's compensatory mechanisms for coping with low thyroid hormone levels are overwhelmed, such as by infection, drugs, or other illness. Left untreated, it can affect multiple organ systems as the adaptations that help maintain homeostasis start to fail. Symptoms include deterioration of mental status, reduced brain function, hypothermia, slowed metabolism and reflexes, bradycardia, edema, and respiratory issues. Prompt diagnosis and treatment are needed to avoid permanent brain damage or death.
This document discusses myxedema coma, a life-threatening complication of severe hypothyroidism. It can be precipitated by a stressful event in someone who is already hypothyroid. Primary symptoms include altered mental status, low body temperature, low blood pressure, slow heart rate, and hypoventilation. Treatment involves supportive care in the intensive care unit, treating hypothermia, hyponatremia, and providing thyroid hormone replacement through intravenous levothyroxine and possibly liothyronine, as well as hydrocortisone therapy.
Myxoedema coma Pharmacotherapeutic viewPranatiChavan
Myxedema coma is an extreme complication of hypothyroidism in which patients exhibit multiple organ abnormalities and progressive mental deterioration. The term myxedema is often used interchangeably with hypothyroidism and myxedema coma. Myxedema also refers to the swelling of the skin and soft tissue that occurs in patients who are hypothyroid. Myxedema coma occurs when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can be fatal if not treated promptly and aggressively. It is usually precipitated by stress in individuals with poorly controlled hyperthyroidism. Signs and symptoms involve multiple organ systems and include fever, tachycardia, heart failure, gastrointestinal issues, and altered mental status. Treatment requires addressing the underlying hyperthyroidism with antithyroid drugs, iodine, beta-blockers, and glucocorticoids to suppress hormone production and effects. Managing precipitating factors, supportive care, and monitoring for complications are also important.
This document provides guidelines from the American Thyroid Association and American Association of Clinical Endocrinologists for the management of hyperthyroidism and thyrotoxicosis. It includes over 30 recommendations regarding the evaluation, treatment, and management of Graves' disease, toxic multinodular goiter, toxic adenoma, and thyroid storm using radioactive iodine therapy, antithyroid medications, or thyroidectomy. Recommendations cover pre-treatment procedures, dosing, monitoring, and follow-up care for patients undergoing treatment for hyperthyroidism.
This document discusses how various drugs can interfere with thyroid function. It begins by defining primary and central hypothyroidism. It then explains how drugs can disrupt thyroid hormone synthesis, alter thyroid autoimmunity, and affect follicular cell activity. Specific drugs like amiodarone, lithium, and cytokines are highlighted. The document also discusses how drugs can interfere with T4 metabolism and conversion to T3. It provides examples of medications that can alter thyroid function tests or T4 binding. Finally, it emphasizes the importance of recognizing drug interactions to correctly interpret thyroid tests and treat patients.
This document discusses drug-induced hematological disorders, focusing on drug-induced aplastic anemia, hemolytic anemia, and megaloblastic anemia. It defines each condition, describes their mechanisms, symptoms, risk factors, prevention, and treatment approaches. Drug-induced aplastic anemia is the most serious as it damages stem cells and reduces blood cell counts, potentially causing infections and bleeding. Treatment involves discontinuing the causative drug, immunosuppression, supportive care like transfusions, and sometimes stem cell transplantation. Drug-induced hemolytic anemia and megaloblastic anemia are also explained in terms of their causes, presentations, and management through removal of the offending drug and supplementation.
This document discusses principles of drug therapy and pharmacology in heart disease. It covers topics such as variability in drug effects due to pharmacokinetic, pharmacodynamic, and pharmacogenomic factors. It discusses optimizing drug dosages starting at low levels and monitoring for adverse effects. Special considerations for drug therapy in the elderly population and issues with polypharmacy are also covered. The risks of non-adherence to drug regimens in elderly patients are described.
Hyperthyroidism is caused by excess thyroid hormone production. Treatment aims to normalize thyroid hormone levels, minimize symptoms, and provide individualized therapy based on disease severity and patient factors. Treatment options include antithyroid medications, radioactive iodine, surgery, and beta blockers. Antithyroid drugs work by inhibiting thyroid hormone synthesis and are given for 12-24 months to induce remission. Radioactive iodine is the treatment of choice for Graves' disease and destroys overactive thyroid cells with radiation. Surgery may be considered for large goiters or lack of drug treatment response. Therapy for thyroid storm involves rapidly suppressing hormone levels along with antiadrenergic and corticosteroid treatment.
This document discusses different types of hypothyroidism including cretinism, adult hypothyroidism, and myxoedema. Cretinism is fetal or infantile hypothyroidism which can be endemic or sporadic and causes symptoms like a hoarse cry and umbilical hernia. Adult hypothyroidism causes symptoms like bradycardia, cold extremities, dry skin/hair, puffy eyes, hoarse voice, slowed movements, and delayed ankle jerks. Myxoedema is a severe form of hypothyroidism that requires treatment with oral thyroxine, triiodothyronine, or intravenous thyroxine along with corticosteroids and antibiotics.
This document summarizes key endocrine emergencies including thyroid storm, adrenal crisis, and hypoglycemia. Thyroid storm is a life-threatening complication of hyperthyroidism caused by Graves' disease or toxic multinodular goiter in 1-2% of cases, with a mortality rate of 20% without treatment. Adrenal crisis can occur due to primary or secondary adrenal insufficiency and presents with low blood pressure. Hypoglycemia is most commonly caused by insulin therapy in diabetic patients but can occur in non-diabetics, defined as a blood glucose below 50-60 mg/dL.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can develop in patients with undiagnosed or untreated hyperthyroidism when stressed. It is characterized by worsening signs and symptoms of thyrotoxicosis including cardiac dysfunction, hyperglycemia, altered mental status, and seizures. Diagnosis is based on clinical features and scoring systems, with a Burch-Wartofsky score of over 45 suggestive of thyroid storm. Treatment involves supportive care, administration of beta blockers, antithyroid medications, iodine, and glucocorticoids to reduce thyroid hormone levels and symptoms.
hypertension is a condition arrising due to increased symphathetic tone so drugs therapies are administered for minimising disease sevearity and further complications. Drug therapy includes drugs like alpha blockers, beta blockers, ACE INHIBITORS, ARBs, vasodilators,direct renin inhibitors, reserpine,prostaglandin analogs, calcium channel blockers for minimising excessive pressure and increased contractility of the heart.
The document discusses hypertension, noting that its prevalence is increasing worldwide and discusses its classification, treatment options including various classes of antihypertensive drugs and their mechanisms of action, experimental models used to study hypertension, and approaches to it in Ayurveda.
This document discusses drugs used to treat hypertension. It classifies antihypertensive drugs into diuretics, sympathoplegics, direct vasodilators, and agents that block the renin-angiotensin-aldosterone system. Specific drugs discussed include furosemide, hydrochlorothiazide, amlodipine, captopril, and losartan. Their mechanisms of action, uses, and potential adverse effects are explained. The document emphasizes that blood pressure can be controlled through multiple pathways and drug classes.
A 27-year-old female presents with palpitations. Exam finds an enlarged, tender thyroid. Labs show suppressed TSH, elevated T4 and low radioactive iodine uptake. The next appropriate test would be to check the ESR, as these findings are consistent with subacute thyroiditis, an inflammation of the thyroid gland often caused by a viral infection. The treatment is symptomatic with pain medication as the condition will typically resolve on its own over several months.
1. Rate control has equivalent efficacy to rhythm control for managing atrial fibrillation and has less drug-related side effects.
2. Drugs like digoxin, beta blockers, and calcium channel blockers can be used for rate control, while antiarrhythmics like amiodarone, dofetilide and sotalol are used for rhythm control.
3. Electrical cardioversion can be used to restore sinus rhythm but has a risk of recurrence, so anticoagulation is recommended afterwards to prevent stroke from clots that may form during the arrhythmia.
This document outlines the work done by the Alexandria University Hospitals Healthcare Quality Directorate Center for Evidence-Based Clinical Practice Guidelines to adapt clinical practice guidelines in Egypt. It discusses how the center has adapted over a dozen guidelines on various pediatric topics through master's theses. It also describes workshops held to train on adapting guidelines using the ADAPTE process and resources. The center has produced several adapted clinical practice guidelines on treating conditions like asthma in children.
this presentation was present by my friend during emergency posting seminar with Dr.Mohd. Kamal Mohd. Arshad. I upload this ppt here for all of us and my own reference too.
الفوائد العظيمة وراء الكشف المبكر لسرطان الثدي
جراحة بسيطة
يمكن الاستغناء عن العلاج الكيمائي في المراحل المبكرة
يمكن ايضا الاستغناء عن العلاج الاشعاعي في المراحل المبكرة
العودة الي الحياة الطبيعية بسرعة
فائدة للفرد والاسرة والمجتمع والدخل القومي
معهد حنوب مصر للاورام
The document discusses the anatomy and infections of the hand spaces. It describes the various spaces in the hand including the finger pulp space, web spaces, mid palmar space, thenar space, and forearm space of Parona. Common infections of these spaces include nail fold infections, pulp space infections (felons), and web space infections. The document outlines the clinical features, treatment, and complications of infections in each of these hand spaces.
This document provides information about chest pain, including its definition, common causes, symptoms, and guidelines for patient care. Chest pain can be caused by issues with the heart, lungs, esophagus, or other organs in the chest cavity. The physical examination and diagnostic tests are aimed at evaluating the chest, heart, and lungs to determine the underlying cause and appropriate treatment for the patient's chest pain.
Outcomes of primary unilateral cheiloplastyin same-day surgical settingsMansoor Khan
This study evaluated outcomes of primary unilateral cleft lip repair performed as single-day surgery in Pakistan. Of 23 patients, most clefts were mild (44.9%) or severe (40.2%). Fisher's technique was most commonly used. Postoperative outcomes were good in 89.8% of cases. Nasal symmetry outcomes improved over the study period. Single-day surgery reduced hospital costs by 19% without increasing complication rates compared to overnight admission. The study demonstrated primary unilateral cleft lip repair can be performed safely and cost-effectively as single-day surgery.
This document discusses wound classification and management. It defines acute and chronic wounds and describes simple, complex, and problem wounds. For problem wounds, it identifies key causative factors like infection, ischemia, and age. It recommends thorough debridement and discusses various adjunct treatments like negative pressure wound therapy, hyperbaric oxygen therapy, and different types of dressings. It provides guidance on managing specific wound types like pressure sores, diabetic wounds, and venous stasis ulcers.
1. Diabetic ketoacidosis is caused by insulin deficiency and presents with hyperglycemia and metabolic acidosis. Symptoms include confusion, abdominal pain, and fruity breath odor. Treatment involves fluid resuscitation, insulin therapy, and bicarbonate for severe acidosis.
2. Hyperosmolar hyperglycemic state is characterized by extreme hyperglycemia without significant ketoacidosis. It presents with dehydration, confusion, and hypernatremia. Management consists of aggressive fluid replacement and insulin therapy to lower blood glucose levels.
3. Hypoglycemia can cause neurological symptoms like confusion and seizures. Treatment involves oral glucose for conscious patients or IV dextrose for
A 58-year-old man presented with intermittent chest pain for 2 weeks. His initial ECG showed ST elevation but serial troponins were negative. This could represent either benign early repolarization or a subtle anterior STEMI. A repeat ECG 12 hours later helped determine the diagnosis. While early repolarization commonly shows widespread, concave ST elevation in leads V2-V5 and is rare in those over 50, STEMI can still present with negative troponins initially. A study evaluated a mathematical formula to distinguish between the two using measurements of ST elevation, QTc interval, and R wave progression, finding it 86% sensitive and 91% specific. A separate trial found that 1 in 6 patients admitted for syncope
This document provides information on evaluating and diagnosing chest pain. It begins by defining chest pain and noting that it is a common reason patients present for medical care. It then discusses the causes of chest pain and provides details on distinguishing ischemic from non-ischemic chest pain. Key factors for ischemic cardiac pain are discussed such as onset during exertion and relief with rest. The document provides guidance on evaluating a patient's chest pain by taking a thorough history addressing 10 specific points. Differential diagnoses for chest pain are also reviewed.
Sugical anatomy of hand and its infectionssanyal1981
1. The document discusses the anatomy and clinical infections of the hand. It describes the parts of the hand and their blood supply, nerves and fascial spaces.
2. Common infections like paronychia, felon, herpes simplex virus infection and flexor tenosynovitis are explained in terms of their causes, presentations, and treatments.
3. Surgical management of hand infections is outlined, emphasizing the importance of adequate drainage while avoiding injury to critical structures like nerves and tendons. Post-operative splinting and irrigation are also discussed.
The document discusses various hand infections including paronychia, felon, pyogenic flexor tenosynovitis, and deep space infections. Paronychia typically involves the nail fold and is usually caused by Staphylococcus aureus, while a felon is a deep pulp space abscess of the finger that requires surgical drainage. Pyogenic flexor tenosynovitis is a surgical emergency that infects the closed flexor tendon sheath and can lead to tendon necrosis if not promptly drained.
This document discusses the management of solitary thyroid nodules. It defines thyroid nodules and states that 12-28% of nodules are malignant. A thorough clinical evaluation and tests like FNAC, thyroid function tests, thyroid scintiscan, and ultrasound can help determine if a nodule is benign or malignant. For nodules found to be malignant through these tests, total thyroidectomy is recommended. For nodules deemed benign, conservative treatment like TSH suppression is usually sufficient. Hemithyroidectomy may be considered for indeterminate or suspicious nodules.
Ueda2016 thyroid nodule in practice - khaled el hadidyueda2015
The document discusses thyroid nodules and guidelines for their evaluation and management. It provides definitions of thyroid nodules and discusses their prevalence in the population. Risk factors for malignancy are outlined. The American Thyroid Association guidelines from 2009 and 2015 are summarized, including recommendations on ultrasound characteristics warranting biopsy and nodule size thresholds for biopsy consideration. Systems for stratifying nodules based on ultrasound features, such as the TI-RADS system, are also covered briefly.
This document discusses the anatomy and clinical evaluation of median nerve injuries as well as various management strategies. It describes the anatomy of the median nerve and its branches that innervate different muscle groups in the arm and hand. Clinical presentations of high and low median nerve palsies are outlined. Surgical techniques for restoring function are proposed, including nerve transfers to regain opposition, sensation, flexion and pronation. Tendon transfers are also mentioned to help with opposition and finger flexion.
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterized by hyperglycemia, dehydration, and metabolic acidosis. It is diagnosed based on blood sugar over 14 mmol/L, presence of ketones, pH below 7.3, and bicarbonate below 18 mmol/L. Management involves rapid intravenous fluid resuscitation, gradual rehydration and electrolyte replacement, and insulin therapy to reverse hyperglycemia and ketosis while closely monitoring for complications. The goals are to correct estimated fluid deficits over 24 hours and lower blood glucose by 3-4 mmol/L per hour.
This document summarizes information about hyperthyroidism and hypothyroidism, including their common causes, symptoms, signs, investigations, and treatment approaches. The most common causes are Graves' disease, multinodular goiter, and solitary thyroid adenomas. Common symptoms include weight loss, heat intolerance, palpitations, and tremors. Diagnostic testing involves measuring T3, T4, and TSH levels. Treatment depends on the underlying cause, and may include antithyroid drugs, radioactive iodine, surgery, or beta-blockers to control symptoms.
Graves' disease is the most common cause of thyrotoxicosis, accounting for 60-80% of cases. It is an autoimmune disorder causing hyperthyroidism due to thyroid stimulating immunoglobulins that activate the TSH receptor. Symptoms include anxiety, heat intolerance, palpitations, weight loss and goiter. Treatment involves antithyroid medications, radioactive iodine therapy or surgery to control the hyperthyroidism. Radioactive iodine is often the preferred treatment option. Graves' disease can also cause eye changes and pretibial myxedema. Managing the condition during pregnancy requires careful titration of antithyroid medications.
Thyroid storm and myxedema coma are life-threatening emergencies caused by excess or deficiency of thyroid hormones respectively. Thyroid storm results from excessive thyroid hormones and causes hypermetabolism affecting multiple systems. Myxedema coma occurs in severe long-standing hypothyroidism when precipitated by an event and causes physiological decompensation. Both require rapid diagnosis and aggressive treatment in an ICU setting to prevent high mortality rates. Treatment involves supportive care, thyroid hormone replacement, glucocorticoids, and correcting underlying conditions.
Graves' disease is an autoimmune disorder causing hyperthyroidism in 60-80% of cases. Genetic and environmental factors contribute to susceptibility. Smoking increases the risk of ophthalmopathy. Hyperthyroidism is caused by thyroid stimulating immunoglobulins that activate the TSH receptor and cause overproduction of thyroid hormones. Treatment involves antithyroid drugs, radioiodine ablation, or surgery. Ophthalmopathy may cause eye swelling, bulging, and vision issues. Thyroiditis refers to inflammation of the thyroid and can be acute, subacute, or chronic depending on duration and symptoms. Subacute thyroiditis causes thyroid pain and temporary changes in thyroid function. Pregnancy causes changes in
This document discusses drugs used to treat hyperthyroidism. It describes the mechanisms and effects of common drug classes including thioamides like methimazole and propylthiouracil which inhibit thyroid hormone synthesis; iodides which block hormone production and conversion; radioactive iodine which destroys thyroid tissue; and beta blockers which relieve symptoms. Adverse effects, clinical uses, and special considerations for conditions like Graves' disease and pregnancy are covered.
This document discusses thyrotoxicosis, which is defined as thyroid hormone excess caused by hyperthyroidism or excessive thyroid function. It outlines the various causes of thyrotoxicosis including primary and secondary hyperthyroidism. Signs and symptoms as well as laboratory findings are described. Treatment options including antithyroid drugs, beta blockers, radioiodine, and surgery are discussed in detail. Thyrotoxic crisis, a life-threatening exacerbation of hyperthyroidism, is also covered.
Hyperthyroidism and hypothyroidism are disorders caused by excess or deficiency of thyroid hormones. Hyperthyroidism causes symptoms of hypermetabolism like weight loss, heat intolerance, palpitations and anxiety. Hypothyroidism causes symptoms of slowed metabolism like fatigue, cold intolerance, dry skin and constipation. Both disorders affect multiple body systems and can be treated with medications, radioactive iodine or surgery to restore normal thyroid function.
This document discusses endocrine diseases and their implications for anesthesia. It covers both hyperthyroidism and hypothyroidism in detail. For hyperthyroidism, it describes the signs and symptoms, causes, effects on the cardiovascular system, and treatment approaches including antithyroid medications, beta blockers, iodine, and surgery. It provides guidance on preoperative preparation and intraoperative management. For hypothyroidism, it discusses signs and symptoms, effects on the cardiovascular system, diagnosis, and treatment with levothyroxine. It notes risks for anesthesia and importance of rendering patients euthyroid prior to elective surgery.
Thyroid storm, or thyrotoxic crisis, is a life-threatening complication of hyperthyroidism characterized by multisystem involvement. It occurs when a precipitating event causes a sudden increase in thyroid hormone levels in a patient with hyperthyroidism. Common precipitants include discontinuing antithyroid medication or thyroid surgery. Thyroid storm requires prompt treatment with beta-blockers, antithyroid drugs, iodine, glucocorticoids, and supportive care to reduce mortality, which is estimated at 8-25% without treatment. Symptoms include fever, tachycardia, heart failure, neurological changes, and gastrointestinal issues. Diagnosis is clinical based on symptoms and elevated thyroid hormone levels
This document summarizes information about hypothyroidism and hyperthyroidism (thyrotoxicosis). It discusses the epidemiology, causes, clinical manifestations, investigations, treatment, and prevention of hypothyroidism. For hyperthyroidism/thyrotoxicosis, it covers the epidemiology, causes, clinical signs and symptoms, investigations, treatment options including anti-thyroid drugs, surgery and radioactive iodine, and considerations for treatment in pregnancy. It also provides details on myxedema coma, a rare but serious complication of severe untreated hypothyroidism.
This document discusses the diagnosis and management of two endocrine emergencies: myxedema coma and thyroid storm. It describes the key features of each condition, including precipitating factors, clinical presentation, diagnostic criteria, and treatment approach. For myxedema coma, treatment involves intravenous thyroid hormone replacement after excluding adrenal insufficiency, glucocorticoid therapy, rewarming, and treating any precipitating infections. For thyroid storm, treatment involves intensive care monitoring, fluid management, beta-blockade, antithyroid medications, iodine, glucocorticoids, and addressing any precipitating factors. Careful monitoring is needed for both conditions given their high mortality risks if not properly treated.
A 58-year-old woman presents with symptoms of hyperthyroidism including anxiety, tremors, sweating, palpitations and insomnia. On exam she has a modest, non-tender goiter. Thyroid function tests show a suppressed TSH and elevated free T4, consistent with primary hyperthyroidism. A thyroid uptake scan shows diffuse homogeneous uptake, consistent with Graves' disease. She is started on methimizole to treat her hyperthyroidism due to Graves' disease.
This document discusses the endocrine system and various endocrine disorders. It outlines the major glands of the endocrine system including the hypothalamus, pituitary, thyroid, parathyroids, adrenals, pancreas, ovaries/testes, kidneys, thymus and pineal gland. It then provides details on various disorders that can affect these glands such as disorders of the pituitary including tumors and growth hormone deficiency. It also discusses thyroid disorders including hypothyroidism, hyperthyroidism and Graves disease. Disorders of the parathyroids including hyperparathyroidism are outlined as well as hypoparathyroidism.
The document discusses the endocrine system and various endocrine disorders. It describes the major endocrine glands including the hypothalamus, pituitary gland, thyroid gland, parathyroid gland, adrenal glands, pancreas, ovaries, testes, thymus, pineal gland, kidneys, and prostaglandins. It then examines disorders of the pituitary gland including pituitary tumors and diabetes insipidus. Finally, it discusses thyroid disorders like hypothyroidism, hyperthyroidism, Graves' disease, and thyroid storm.
The thyroid gland is located in the lower neck and produces thyroid hormones that regulate metabolism. Hyperthyroidism occurs when the thyroid gland is overactive and produces excessive thyroid hormones. Graves' disease is the most common cause of hyperthyroidism and results in symptoms like nervousness, rapid heartbeat, weight loss, and bulging eyes. Treatment options for hyperthyroidism include radioactive iodine therapy which destroys the thyroid gland, anti-thyroid medications that reduce hormone production, or surgery to remove part of the thyroid gland.
Hyperthyroidism about goiter medical Ppt.pptxabbashshah09
Hyperthyroidism is caused by excessive thyroid function and can be due to Graves' disease in 60-80% of cases. Graves' disease is an autoimmune disorder where antibodies stimulate the thyroid. Common symptoms include weight loss, tremors, rapid heart rate, and goiter. Treatment options include antithyroid medications, radioactive iodine therapy, or surgery to reduce thyroid tissue. Antithyroid drugs work to block thyroid hormone production and are generally the first treatment approach. Radioactive iodine or surgery may be used if antithyroid medications do not control the hyperthyroidism or if the patient prefers a more permanent treatment option.
Thyroid Hormone Disorders lecture :-
-Thyroid gland & Thyroid hormones.
-How does Thyroid hormone is formed ?
-Regulation of secretion.
-Hypothyroidism.
-Treatment of hypothyroidism .
-Administration of Levothyroxin.
-Levothyroxin interactions.
-Levothyroxin cautions.
-Hyperthyroidism .
-Symptoms & treatment of Hyperthyroidism.
-Removal of part or all of the thyroid.
-Blockade of hormone release .
-Inhibition of thyroid hormone synthesis.
-Mechanism of action of antithyroid.
-Administration of antithyroid drugs.
-Antithyroid drugs interactions.
-Antithyroid drugs cautions.
-General notes.
-Practical notes on levothyroxin.
-Practical notes on antithroid drugs.
-Rapid review.
-Test yourself.
The pituitary gland is a small structure located at the base of the brain that secretes hormones controlling other endocrine glands. Hypopituitarism occurs when the pituitary gland fails to secrete sufficient hormones, causing weight loss, hair loss, and hypometabolism if hormones are not replaced. Pituitary tumors can cause gigantism, acromegaly, or Cushing's syndrome depending on location and are assessed using imaging and hormone level tests. Surgical removal of the pituitary treats tumors but requires lifelong hormone replacement.
This document discusses thyroid storm, which is a life-threatening exacerbation of hyperthyroidism. It can have a mortality rate of 20-30%. Causes include infections, discontinuing thyroid medications, and other systemic stresses. Patients experience high metabolism, tachycardia, hypertension, and other symptoms. Treatment involves medications to stop thyroid hormone synthesis and block peripheral effects, supportive care, treating any precipitating causes, and monitoring for complications. Early diagnosis and treatment are important to reduce the high mortality risk associated with thyroid storm.
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Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
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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).
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
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One health condition that is becoming more common day by day is diabetes.
According to research conducted by the National Family Health Survey of India, diabetic cases show a projection which might increase to 10.4% by 2030.
4. ACCELERATED HYPERTHYROIDISM OR THYROID STORM IS AN EXTREME ACCENTUATION OF THYROTOXICOSIS Thyroid stom It is an uncommon but serious complication, usually occurring in association with Graves' disease but sometimes with toxic multinodular goiter crisis frequently followed thyroidectomy in hyperthyroid patients The mortality rate due to cardiac failure, arrhythmia, or hyperthermia is as high as 30%, even with treatment.
5. General: Infection. Non-thyroidal trauma or surgery. Psychosis. Parturition. Myocardial infarction or other acute medical problems. Thyroid specific: Radioiodine. High doses of iodine-containing compounds (for example, radiographic contrast media). Discontinuation of antithyroid drug treatment. Thyroid injury (palpation, infarction of an adenoma). New institution of amiodarone therapy. Precipitating factors in thyroid storm
6. DELIRIUM, SEVERE TACHYCARDIA, VOMITING, DIARRHEA, DEHYDRATION IN MANY CASES, VERY HIGH FEVER. Clinical features Thyrotoxic crisis is usually of abrupt onset and occurs in patients in whom preexisting thyrotoxicosis has been treated incompletely or has not been treated at all.
7. RELATED TO CYTOKINE RELEASE AND ACUTE IMMUNOLOGIC DISTURBANCE CAUSED BY THE PRECIPITATING CONDITION. THE SERUM THYROID HORMONE LEVELS IN CRISIS ARE NOT APPRECIABLY GREATER THAN THOSE IN SEVERE UNCOMPLICATED THYROTOXICOSIS, BUT THE PATIENT CAN NO LONGER ADAPT TO THE METABOLIC STRESS. The mechanism by which such factors worsen thyrotoxicosis
8. NOTE THAT FINDINGS ARE NOT DIFFERENT THAN THAT OF HYPERTHYROIDISM, BUT THE DIFFERENCE IS IN THE SETTING; KEY IS FEVER (TYPICALLY > 40 C / 104 F) YOU CAN BE ADMITTED WITH HYPERTHYROIDISM THAT IS SEVERE YET IS NOT THYROID STORM (HYPERTHYROID TACHYARRHYTHMIAS ARE SERIOUS BUT NOT “STORM”) THYROID HORMONE LEVELS ARE NOT MUCH DIFFERENT IN STORMING THAN IN OTHER CASES SO LIKELY OTHER PREDISPOSING FACTORS (STRESS, METABOLIC FACTORS) Hyperthyroid vs Thyroid Storm
9. MAJOR PART IS SUPPORTIVE CARE WITH HYDRATION, COOLING BLANKETS, AND ANTIPYRETICS (ACETAMINOPHEN ) management Avoid aspirin (case reports that it releases thyroid hormone from its binding globulin, worsens case) Intensive therapy with anti-thyroid drugs, beta-blockers, steroids, iodine solutions
10. PROPYLTHIOURACIL , WHICH INHIBITS THYROID HORMONE SYNTHESIS AND CONVERSION OF THYROXINE TO TRI IODOTHYRONINE IS GIVEN BY MOUTH, NASOGASTRIC TUBE, OR RECTALLY AT A RATE OF 300 TO 400 MG EVERY 4–6 HOURS. Anti-thyroid drugs: Carbimazole is less useful since it does not inhibit conversion of thyroxine to tri-iodothyronine. One hour after starting propylthiouracil, iodide ( for example, eight drops of Lugol’s iodine every six hours ) is given to inhibit thyroid hormone release. Alternatively, if available, the radiographic contrast media, sodium ipodate or iopanoic acid, can be given orally, with a loading dose of 2 g followed by 1 g daily. These agents also inhibit conversion of thyroxine to tri-iodothyronine
11. Theoretically, propylthiouracil should be administered before iodine to inhibit the synthesis of additional thyroid hormone from the administered iodide. Nonetheless, because iodide is the only agent that will block release of preformed thyroid hormones from the thyroid gland and it blocks its own organification through the Wolff-Chaikoff effect, its administration should not be delayed or omitted in the severely toxic patient if propylthiouracil (or methimazole) is not immediately available.
12. Beta-blockade High doses of b-blocker should be given, and propranolol at a dose of 80–120 mg every six hours is recommended. High output thyrotoxic cardiac failure will respond to control of the heart rate and therefore b-blockade should be used (with caution), while in general the response to digoxin and diuretics is poor. In the absence of cardiac insufficiency or asthma, a β-adrenergic blocking agent should be given to ameliorate the hyperadrenergic state.
13. If β-adrenergic blocking agents are contraindicated, a calcium channel blocker (diltiazem) may be used to slow the heart rate a very short-acting β-adrenergic blocker such as labetalol or esmolol may be safer than propranolol in this situation High-output congestive heart failure can develop in patients with severe thyrotoxicosis, and a β-adrenergic antagonist may further reduce cardiac output.
14. Steroids Large doses of dexamethasone (8 mg orally once daily) should be given to support the response to stress, inhibit both the release of hormone from the gland and the peripheral generation of T 3 from T 4 , synergizing with iodide and propylthiouracil, respectively, in these actions. The combined use of propylthiouracil, iodide, and dexamethasone can restore the concentration of T 3 to normal within 24 to 48 hours
15. Cholestyramine, 4 g every 6–8 hours, binds thyroid hormone in the gut and thus interrupts the modest enterohepatic circulation of thyroid hormone; its use will lead to a more rapid lowering of circulating thyroid hormones Cholestyramine
16. Supportive measures correction of dehydration and hypernatremia, if present, and administration of glucose Hyperpyrexia should be treated vigorously In mild cases, acetaminophen may suffice, but a cold blanket or ice packs may be required. Salicylates should be avoided because they compete with T 3 and T 4 for binding to TBG and transthyretin (TTR) and therefore increase the free hormone levels. In addition, high doses of salicylates increase the metabolic rate.
17. If heart failure or pulmonary congestion is present, appropriate diuretics are indicated. In patients with atrial fibrillation, the rapid ventricular response requires appropriate blockade of atrioventricular node conduction.
18. When treatment is successful, improvement is usually manifested within 1 or 2 days and recovery occurs within a week. At this time, iodide and dexamethasone can be withdrawn and plans for long-term management are made. Follow up After implementation of this four-pronged approach to management of thyrotoxic storm, dramatic clinical improvement is usually seen within 12 to 24 hours in most patients who survive.
19. Myxedema coma Myxedema coma is a severe, life-threatening sequela of profound hypothyroidism. Myxedema coma is the ultimate stage of severe longstanding hypothyroidism Severe hypothyroidism with metabolic shutdown (cardiac, hepatic, other organs) This state, which almost invariably affects older patients, occurs most commonly during the winter months and is associated with a high mortality rate. Very high mortality 1:3 Typical patient: elderly female with longstanding hypothyroidism.
22. Clinical features The three main features are: Altered mental state ranging from poor cognitive function through psychosis to coma; Hypothermia (as low as 23˚C) or absence of fever in spite of severe infection (prognosis worsens as the core Temperature fall); The presence of a precipitating event. Hallmark signs of hypothyroidism will be present— dry, coarse, scaly skin; sparse or coarse hair; nonpitting edema of the periorbital regions, hands, and feet; macroglossia; hoarseness; and delayed deep tendon reflexes.
23. cns manifestations : The patient may have a history of using a CNS depressant, narcotic, or sedative. About 25% of patients with myxedema coma have focal or generalized seizures. Severe sensorial depression, ……coma. CARDIAC MANIFESTATION : Although frank heart failure is rare, cardiomegaly, bradycardia, and decreased cardiac contractility are common features of cardiovascular involvement in myxedema coma. Cardiac enlargement (" myxedema heart" ) is often due to pericardial effusion.
24. GI tract manifestation : astrointestinal tract involvement in myxedema coma may result in decreased intestinal motility, paralytic ileus, or megacolon, causing patients to present with abdominal pain, constipation, and nausea Oral medications may be ineffective because of these problems. Renal manifestation : Hyponatremia and decreased glomerular filtration rate occur, the kidneys lose their ability to excrete a water load because of decreased delivery of water to the distal nephron, as well as increased production of antidiuretic hormone.
25. Biochemical abnormalities hyponatraemia, normal or increased urine sodium excretion raised creatine phosphokinase and lactate dehydrogenase, hypoglycaemia normocytic or macrocytic anaemia Thyroid stimulating hormone values may only bemodestly raised (and will be normal or low in secondary hypothyroidism) but free thyroxine levels are usually very low.
26. Three major etiologies: Undiagnosed hypothyroidism (autoimmune thyroiditis, radiation hypothyroidism, etc) More commonly discontinuation of therapy or running out of medication (for months) Iatrogenic: stopping patients for I-131 cancer Rx
27. MANAGEMENT The importance of the difficulty in diagnosing myxedema coma is that a delay in therapy worsens the prognosis Consequently, the diagnosis should be made on clinical grounds, and, after sending serum for thyroid function tests, therapy should be initiated without awaiting the results of confirmatory tests because mortality may be 20% or higher. Even with prompt recognition and treatment, mortality is 20%–30%.
28. The three principles of management are 1. Rapid institution of thyroid hormone replacement, 2. Treatment of the precipitating cause, and 3. provision of ventilatory and other support. ‘‘ High dose’’ regimens may be given as follows: if intravenous thyroxine is available, this can be given as a bolus of 300–500 mg, followed by 50–100 mg daily. Oral thyroxine in similar doses can be given (usually by nasogastric tube), but absorption may be impaired. thyroid hormone replacement
29. There is a theoretical concern that conversion of thyroxine to triiodothyronine will be impaired due to the effects of any illness on deiodinase activity, and therefore the use of triiodothyronine instead of thyroxine has been advocated, but this also has the potential to cause adverse cardiac effects when given too rapidly. The usual intravenous dose of triiodothyronine is 10–20 mg initially, followed by 10 mg every four hours for 24 hours, then 10 mg every six hours. Oral treatment with similar doses is also possible. A further variation is to give 200 mg thyroxine with 10 mg triiodothyronine initially, and then tri-iodothyronine 10 mg every 12 hours and thyroxine 100 mg every 24 hours, until the patient resumes normal thyroxine orally.
30. The authors recommend ECG monitoring and careful titration of thyroid replacement therapy against any definite ischaemic ECG abnormalities. steroid Hydrocortisone (5 to 10 mg/hr) should also be given because of the possibility of relative adrenocortical insufficiency as the metabolic rate increases. ANTIBIOTICS Treatment of the underlying precipitant is usually straightforward. Broad spectrum antibiotics should be considered if there is no obvious cause, as the signs of an infection may be obscure, yet this is the underlying cause in up to a third of cases.
31. OTHER S A critical element in therapy is support of respiratory function by means of assisted ventilation and controlled oxygen administration All patients should be admitted to intensive care or the HDU: most patients require ventilatory support for 1–2 days. Hypothermia should be treated with space blankets, since active external rewarming leads to circulatory collapse due to peripheral vesodilatation. Cautious volume expansion using intravenous saline usually suffices, but hypertonic saline may need to be considered if the serum sodium is very low (,120 mmol/l)
32. Intravenous glucose may be required for hypoglycaemia. General measures applicable to the comatose patient should be undertaken, such as frequent turning, prevention of aspiration, and attention to fecal impaction and urinary retention. Finally, the physician should assess the patient for the presence of coexisting disease, such as infection and cardiac or cerebrovascular disease. In particular, the myxedematous patient may be afebrile despite a significant infection. As soon as the patient is able to take medication by mouth, treatment with oral levothyroxine should be instituted
34. Pituitary apoplexy is caused by haemorrhagic infarction of a pituitary tumour or less commonly the normal pituitary gland Acute pituitary apoplexy This may cause volume expansion with local mass effect. Apoplexy is an endocrine emergency that may result in severe hypoglycemia, hypotension, central nervous system (CNS) hemorrhage, and death. Prompt recognition is needed to prevent cardiovascular collapse secondary to pituitary-adrenal hypofunction. There is an equal sex incidence.
35. Pituitary apoplexy may occur spontaneously in a preexisting adenoma; post-partum (Sheehan's syndrome); or in association with diabetes, hypertension, sickle cell anemia, or acute shock The hyperplastic enlargement of the pituitary during pregnancy increases the risk for hemorrhage andinfarction.
36.
37. Clinical features These resemble those of subarachnoid haemorrhage , severe headache, nausea (80%), vomiting (60%), photophobia(50%), and loss of consciousness (10%). Neuro-ophthalmic signs include ocular paresis in up to 70% of cases with IIIrd (67%), IVth (4%), and Vth (29%) nerve palsies, Visual field defects, and even blindness. Pre-existing endocrine dysfunction is present in 20%–30%. patient may have circulatory collapse.
38. Management If pituitary apoplexy is suspected (or confirmed by urgent magnetic resonance imaging or computed tomography), hydrocortisone 100 mg intramuscularly six hourly, or 4 mg/ hour intravenously should beadministered without delay and continued until the crisis is over. Those with significant or progressive visual loss or loss of consciousness require urgent surgical decompression. Visual recovery after surgery is inversely correlated with the length of time after the acute event. Therefore, severe ophthalmoplegia or visual deficits are indications for early surgery.
39. Early neurosurgical intervention is associated with improved neuro-ophthalmic outcome with reported improvements in visual acuity and fields of 86% and 76% respectively.
41. 1. Following Stress (trauma, surgery, infection, or prolonged fasting) in patient with latent insufficiency. 2. Following sudden withdrawal of adrenocortical hormone in a patient with chronic insufficiency 3. Following bilateral adrenalectomy or a functioning adrenal tumor that had suppressed the other adrenal 4. Following sudden destruction of the pituitary gland (pituitary necrosis) or when thyroid hormone is given to a pt with hypoadrenalism 5. Following injury to both adrenals by trauma, hemorrhage, anticoagulant therapy, thrombosis, infection, or metastatic carcinoma. Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. N Engl J Med 2003;348:727-734 Causes
42. Dehydration, hypotension, or shock out of proportion to severity of current illness Nausea and vomiting with a history of weight lost and anorexia Abdominal pain, so-called acute abdomen Unexplained hypoglycemia Unexplained fever CLINICAL AND LABORATORY FEATURES OF AN ADRENAL CRISIS Hyponatremia, hyperkalemia, azotemia, hypercalcemia, or eosinophilia Hyperpigmentation or vitiligo Other autoimmune endocrine deficiencies, such as hypothyroidism or gonadal failure
43.
44. TREATMENT OF ACUTE ADRENAL INSUFFICIENCY (ADRENAL CRISIS) EMERGENCY MEASURE 1. Establish intravenous access with a large-gauge needle. 2. Draw blood for stat serum electrolytes and glucose and routine measurement of plasma cortisol and ACTH. Do not wait for laboratory results. 3. Infuse 2 to 3 L of 154 mmol/L NaCl (0.9% saline) solution or 50 g/L (5%) dextrose in 154 mmol/L NaCl (0.9% saline) solution as quickly as possible. Monitor for signs of fluid overload by measuring central or peripheral venous pressure and listening for pulmonary rales. Reduce infusion rate if indicated. 4. Inject intravenous hydrocortisone (100 mg immediately and every 6 hr) 5. Use supportive measures as needed.
45. SUBACUTE MEASURES AFTER STABILIZATION OF THE PATIEN 1. Continue intravenous 154 mmol/L NaCl (0.9% saline) solution at a slower rate for next 24 to 48 hr. 2. Search for and treat possible infectious precipitating causes of the adrenal crisis. 3. Perform a short ACTH stimulation test to confirm the diagnosis of adrenal insufficiency, if patient does not have known adrenal insufficiency. 4. Determine the type of adrenal insufficiency and its cause if not already known. 5. Taper glucocorticoids to maintenance dosage over 1 to 3 days, if precipitating or complicating illness permits. 6. Begin mineralocorticoid replacement with fludrocortisone (0.1 mg by mouth daily) when saline infusion is stopped.