This document discusses a case of hyperthyroidism in a 39-year-old female presenting with nervousness, anxiety, palpitations, diarrhea, and weight loss. On examination, she had a heart rate of 110 bpm, tremor, increased reflexes, and an enlarged thyroid. Laboratory tests found high free T3 and T4, low TSH, and positive thyroid stimulating immunoglobulins, consistent with a diagnosis of Graves' disease. Graves' disease is an autoimmune disorder causing hyperthyroidism through thyroid stimulating antibodies. If left untreated, hyperthyroidism can progress to a thyroid storm, a life-threatening condition of severe hypermetabolism.
The document provides an outline on the physiology and causes of hyperthyroidism, also known as thyrotoxicosis. It discusses the thyroid gland, thyroid hormone synthesis and regulation, clinical features of Graves' disease and toxic multinodular goiter, diagnosis of hyperthyroidism, and management approaches including antithyroid drugs, radioactive iodine therapy, surgery, and novel minimally invasive therapies. It also covers thyroid storm as a life-threatening emergency characterized by abrupt release of thyroid hormones.
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 storm is a life-threatening syndrome that results from an acute exacerbation of thyrotoxicosis. Prevention, prompt recognition, and appropriate intervention as discussed herein are key to the prevention of death and morbidity in affected patients. I hope you find it educating as well as enlightening.
This document discusses hyperthyroidism and thyrotoxicosis. It begins by defining the terms and describing the thyroid gland's normal function. It then discusses the various causes of hyperthyroidism including Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The document outlines the anatomy and physiology of the thyroid gland. It describes the clinical manifestations, diagnostic tests including thyroid function tests, ultrasound, and thyroid scintigraphy. It provides algorithms for diagnosis and outlines treatment options for hyperthyroidism including anti-thyroid medications, radioactive iodine treatment, and thyroidectomy.
A complete presentation on hypothroidism endocrine disorder based on latest editon of harrison and reference books. this presentation will help to learn about this second most common endocrine disorder.
This document provides information about acromegaly, a rare disorder caused by excess growth hormone in adults. It discusses the typical causes, signs and symptoms, and effects on organ systems. Pituitary adenomas that secrete growth hormone are responsible for over 95% of cases. Clinical features depend on when excess growth hormone begins, causing either gigantism in children or acromegaly in adults, characterized by enlarged extremities and soft tissues. Complications can include joint and cardiovascular problems, diabetes, and sleep apnea. Early diagnosis and treatment are important to prevent morbidity.
The document provides an outline on the physiology and causes of hyperthyroidism, also known as thyrotoxicosis. It discusses the thyroid gland, thyroid hormone synthesis and regulation, clinical features of Graves' disease and toxic multinodular goiter, diagnosis of hyperthyroidism, and management approaches including antithyroid drugs, radioactive iodine therapy, surgery, and novel minimally invasive therapies. It also covers thyroid storm as a life-threatening emergency characterized by abrupt release of thyroid hormones.
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 storm is a life-threatening syndrome that results from an acute exacerbation of thyrotoxicosis. Prevention, prompt recognition, and appropriate intervention as discussed herein are key to the prevention of death and morbidity in affected patients. I hope you find it educating as well as enlightening.
This document discusses hyperthyroidism and thyrotoxicosis. It begins by defining the terms and describing the thyroid gland's normal function. It then discusses the various causes of hyperthyroidism including Graves' disease, toxic multinodular goiter, subacute thyroiditis, and toxic adenoma. The document outlines the anatomy and physiology of the thyroid gland. It describes the clinical manifestations, diagnostic tests including thyroid function tests, ultrasound, and thyroid scintigraphy. It provides algorithms for diagnosis and outlines treatment options for hyperthyroidism including anti-thyroid medications, radioactive iodine treatment, and thyroidectomy.
A complete presentation on hypothroidism endocrine disorder based on latest editon of harrison and reference books. this presentation will help to learn about this second most common endocrine disorder.
This document provides information about acromegaly, a rare disorder caused by excess growth hormone in adults. It discusses the typical causes, signs and symptoms, and effects on organ systems. Pituitary adenomas that secrete growth hormone are responsible for over 95% of cases. Clinical features depend on when excess growth hormone begins, causing either gigantism in children or acromegaly in adults, characterized by enlarged extremities and soft tissues. Complications can include joint and cardiovascular problems, diabetes, and sleep apnea. Early diagnosis and treatment are important to prevent morbidity.
Hypothyroidism is caused by an underactive thyroid gland that produces insufficient thyroid hormones. The document summarizes the symptoms, complications, classifications, and treatments for hypothyroidism. It provides details on the thyroid gland, hormones, and regulating system. Treatment recommendations include dietary changes like increasing iodine, calcium and magnesium intake. Herbal supplements like bladderwrack, oats and makandi are also suggested to support thyroid function.
The document discusses hypothyroidism, including its causes, signs and symptoms, diagnosis, and treatment. Some key points:
- Primary hypothyroidism is caused by failure of the thyroid gland and accounts for 99% of cases. Secondary hypothyroidism is caused by pituitary failure.
- Hashimoto's thyroiditis is the most common cause of hypothyroidism in iodine-sufficient areas. It is an autoimmune disorder more common in women.
- Diagnosis is based on elevated TSH and low free T4 levels. Treatment involves daily levothyroxine replacement therapy with dosages adjusted based on follow up TSH levels.
This document discusses hypothyroidism, including its causes, signs and symptoms, diagnosis, and treatment. It notes that the most common causes are iodine deficiency, autoimmune disease like Hashimoto's thyroiditis, and treatment of hyperthyroidism. Hashimoto's thyroiditis causes lymphocytic infiltration and destruction of the thyroid gland. Symptoms include fatigue, dry skin, weight gain, and constipation. Treatment involves levothyroxine replacement to normalize TSH levels. Dosing may need adjustment during pregnancy to ensure normal thyroid function and prevent complications.
This document discusses hypertensive crises, including definitions, epidemiology, pathophysiology, assessment, diagnosis, and management. It defines hypertensive emergencies as elevated blood pressure with acute end-organ damage, while hypertensive urgencies involve impending end-organ damage. The typical patient presenting with crisis is middle-aged, noncompliant with medications, and may use substances. Treatment of emergencies requires immediate blood pressure reduction in the ICU to prevent further damage, while urgencies can be treated gradually as uncontrolled hypertension. Nitroprusside is very effective but has limitations like toxicity risks with prolonged use.
The document discusses a case of subclinical hypothyroidism in a 70-year-old woman named Ayesha who presented with fatigue, dry skin, and difficulty losing weight. Laboratory tests found her TSH level to be elevated at 8.1 mIU/L and her FT4 level to be low normal, confirming a diagnosis of subclinical hypothyroidism likely caused by Hashimoto's thyroiditis. The document then provides information on hypothyroidism, its causes, signs and symptoms, diagnosis, and treatment options including levothyroxine replacement therapy.
This document discusses hyperthyroidism and its treatment. It defines hyperthyroidism as increased secretion of thyroid hormones due to various stimuli. It then describes the clinical types of hyperthyroidism including diffuse toxic goitre (Graves' disease), toxic nodular goitre, and toxic nodule. The document outlines the symptoms, diagnosis, and principles of treatment for hyperthyroidism including anti-thyroid drugs, radioactive iodine therapy, and surgery. Treatment options depend on factors like the type and severity of hyperthyroidism, patient age and preferences.
Management of Thyroid Diseases & Emergenciesyuyuricci
Primary hypothyroidism is usually caused by autoimmune thyroiditis like Hashimoto's thyroiditis. It results from gradual destruction of the thyroid gland leading to decreased thyroid hormone production. Common symptoms include fatigue, cold intolerance, constipation, and weight gain. Secondary hypothyroidism is caused by pituitary or hypothalamic disease resulting in decreased TSH levels. Both can be confirmed through lab tests showing elevated TSH and low free T4 levels. Treatment involves thyroid hormone replacement therapy.
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.
This document discusses hyperthyroidism (excess thyroid hormone). There are two main types - those caused by excess hormone production and those caused by release of stored hormone. Primary causes include Graves' disease while secondary causes include Plummer's disease and toxic nodules. Signs and symptoms, investigations, and treatment options like antithyroid drugs, surgery, and radioiodine are described for different patient groups. Management involves controlling hyperthyroidism and returning the patient to a euthyroid state.
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.
The document discusses the thyroid gland and hypothyroidism. It provides details on the anatomy, histology, synthesis and secretion of thyroid hormones. It also describes the clinical features of hypothyroidism including constitutional symptoms like cold intolerance and fatigue. Laboratory tests for investigating thyroid function and disorders are outlined, including measurement of thyroid hormones and thyroid antibodies. Physical examination findings for the thyroid gland are also reviewed.
The document describes several cases of thyrotoxicosis and discusses potential causes. It outlines cases of three patients, two children and one infant, who presented with thyrotoxicosis. The potential causes discussed include Graves' disease, toxic multinodular goiter, toxic adenoma, neonatal Graves' disease, activated TSH receptor, excess TSH, thyroiditis, and thyrotoxicosis resulting from excess iodine or medications like amiodarone.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.
The document discusses various endocrine emergencies including diabetic ketoacidosis (DKA), hypoglycemia, and thyroid storm. It provides details on the causes, symptoms, diagnostic criteria and treatment approaches for each condition. DKA results from lack of insulin and needs urgent treatment including rehydration, insulin administration, and electrolyte correction. Hypoglycemia can be caused by too much insulin or too little food intake and requires glucose administration. Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires treatments to correct the hyperthyroidism and address any precipitating factors.
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.
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.
Cushing's syndrome is caused by chronic overexposure to cortisol and can be difficult to diagnose. It may be pituitary-dependent (Cushing's disease), adrenal-dependent (adenoma or carcinoma), or caused by an ectopic ACTH-secreting tumor. Diagnostic tests include urine and salivary cortisol levels, low and high dose dexamethasone suppression tests, and imaging of the pituitary and adrenal glands. Treatment depends on the cause but may involve surgery to remove tumors, adrenalectomy, or medication to suppress cortisol production while managing comorbidities. The prognosis has improved with effective treatments but risks remain high without treatment.
Thyrotoxicosis is a clinical syndrome caused by high levels of circulating thyroid hormones, with primary causes including Graves' disease and toxic nodular goiter, leading to symptoms of weight loss, fatigue, heat intolerance, and emotional changes. Diagnosis is based on examination findings of a goiter, tachycardia, and eye changes like exophthalmos, with treatment options including antithyroid drugs, radioactive iodine, or surgery to remove the overactive thyroid tissue.
This slide was prepared for teaching purpose to medical students. It contain information from different books and medical journals. please inform if any of the information given need to be changed.
Hyperthyroidism, Reference: Hyperthyroid, Harrison's Principles of Internal Medicine, Soheil Elahi, Islamic Azad University of Medicine- International Branch (IAUM-int)
The thyroid gland is located in the neck and produces hormones that regulate metabolism. It has two lobes connected by an isthmus. The gland contains follicles that produce thyroid hormones. Hashimoto's thyroiditis is the most common cause of hypothyroidism. It is an autoimmune disease where the immune system attacks the thyroid, destroying follicles and causing lymphocytic infiltration. This leads to decreased thyroid hormone production and symptoms like weight gain and fatigue. Treatment involves thyroid hormone replacement therapy.
Vasoactive drugs act on the heart and circulatory system by affecting adrenergic receptors. They can be classified as vasopressors, inotropes, or vasodilators. Common vasoactive drugs include adrenaline, noradrenaline, dopamine, dobutamine, milrinone, vasopressin, nitroglycerine, and nitroprusside. Each drug has distinct mechanisms of action and indications for use. Careful consideration of dosing and side effects is important when using these powerful cardiovascular medications.
Hypothyroidism is caused by an underactive thyroid gland that produces insufficient thyroid hormones. The document summarizes the symptoms, complications, classifications, and treatments for hypothyroidism. It provides details on the thyroid gland, hormones, and regulating system. Treatment recommendations include dietary changes like increasing iodine, calcium and magnesium intake. Herbal supplements like bladderwrack, oats and makandi are also suggested to support thyroid function.
The document discusses hypothyroidism, including its causes, signs and symptoms, diagnosis, and treatment. Some key points:
- Primary hypothyroidism is caused by failure of the thyroid gland and accounts for 99% of cases. Secondary hypothyroidism is caused by pituitary failure.
- Hashimoto's thyroiditis is the most common cause of hypothyroidism in iodine-sufficient areas. It is an autoimmune disorder more common in women.
- Diagnosis is based on elevated TSH and low free T4 levels. Treatment involves daily levothyroxine replacement therapy with dosages adjusted based on follow up TSH levels.
This document discusses hypothyroidism, including its causes, signs and symptoms, diagnosis, and treatment. It notes that the most common causes are iodine deficiency, autoimmune disease like Hashimoto's thyroiditis, and treatment of hyperthyroidism. Hashimoto's thyroiditis causes lymphocytic infiltration and destruction of the thyroid gland. Symptoms include fatigue, dry skin, weight gain, and constipation. Treatment involves levothyroxine replacement to normalize TSH levels. Dosing may need adjustment during pregnancy to ensure normal thyroid function and prevent complications.
This document discusses hypertensive crises, including definitions, epidemiology, pathophysiology, assessment, diagnosis, and management. It defines hypertensive emergencies as elevated blood pressure with acute end-organ damage, while hypertensive urgencies involve impending end-organ damage. The typical patient presenting with crisis is middle-aged, noncompliant with medications, and may use substances. Treatment of emergencies requires immediate blood pressure reduction in the ICU to prevent further damage, while urgencies can be treated gradually as uncontrolled hypertension. Nitroprusside is very effective but has limitations like toxicity risks with prolonged use.
The document discusses a case of subclinical hypothyroidism in a 70-year-old woman named Ayesha who presented with fatigue, dry skin, and difficulty losing weight. Laboratory tests found her TSH level to be elevated at 8.1 mIU/L and her FT4 level to be low normal, confirming a diagnosis of subclinical hypothyroidism likely caused by Hashimoto's thyroiditis. The document then provides information on hypothyroidism, its causes, signs and symptoms, diagnosis, and treatment options including levothyroxine replacement therapy.
This document discusses hyperthyroidism and its treatment. It defines hyperthyroidism as increased secretion of thyroid hormones due to various stimuli. It then describes the clinical types of hyperthyroidism including diffuse toxic goitre (Graves' disease), toxic nodular goitre, and toxic nodule. The document outlines the symptoms, diagnosis, and principles of treatment for hyperthyroidism including anti-thyroid drugs, radioactive iodine therapy, and surgery. Treatment options depend on factors like the type and severity of hyperthyroidism, patient age and preferences.
Management of Thyroid Diseases & Emergenciesyuyuricci
Primary hypothyroidism is usually caused by autoimmune thyroiditis like Hashimoto's thyroiditis. It results from gradual destruction of the thyroid gland leading to decreased thyroid hormone production. Common symptoms include fatigue, cold intolerance, constipation, and weight gain. Secondary hypothyroidism is caused by pituitary or hypothalamic disease resulting in decreased TSH levels. Both can be confirmed through lab tests showing elevated TSH and low free T4 levels. Treatment involves thyroid hormone replacement therapy.
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.
This document discusses hyperthyroidism (excess thyroid hormone). There are two main types - those caused by excess hormone production and those caused by release of stored hormone. Primary causes include Graves' disease while secondary causes include Plummer's disease and toxic nodules. Signs and symptoms, investigations, and treatment options like antithyroid drugs, surgery, and radioiodine are described for different patient groups. Management involves controlling hyperthyroidism and returning the patient to a euthyroid state.
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.
The document discusses the thyroid gland and hypothyroidism. It provides details on the anatomy, histology, synthesis and secretion of thyroid hormones. It also describes the clinical features of hypothyroidism including constitutional symptoms like cold intolerance and fatigue. Laboratory tests for investigating thyroid function and disorders are outlined, including measurement of thyroid hormones and thyroid antibodies. Physical examination findings for the thyroid gland are also reviewed.
The document describes several cases of thyrotoxicosis and discusses potential causes. It outlines cases of three patients, two children and one infant, who presented with thyrotoxicosis. The potential causes discussed include Graves' disease, toxic multinodular goiter, toxic adenoma, neonatal Graves' disease, activated TSH receptor, excess TSH, thyroiditis, and thyrotoxicosis resulting from excess iodine or medications like amiodarone.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires urgent treatment. It is diagnosed using criteria from Burch and Wartofsky that evaluate temperature dysregulation, neurological changes, gastrointestinal involvement, cardiovascular dysfunction, and precipitating events. Treatment involves high dose thioamides to block hormone synthesis, inorganic iodides to block hormone release, beta-blockers to inhibit peripheral T4 to T3 conversion, and correcting homeostatic decompensation and any precipitating illnesses.
The document discusses various endocrine emergencies including diabetic ketoacidosis (DKA), hypoglycemia, and thyroid storm. It provides details on the causes, symptoms, diagnostic criteria and treatment approaches for each condition. DKA results from lack of insulin and needs urgent treatment including rehydration, insulin administration, and electrolyte correction. Hypoglycemia can be caused by too much insulin or too little food intake and requires glucose administration. Thyroid storm is a life-threatening exacerbation of hyperthyroidism that requires treatments to correct the hyperthyroidism and address any precipitating factors.
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.
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.
Cushing's syndrome is caused by chronic overexposure to cortisol and can be difficult to diagnose. It may be pituitary-dependent (Cushing's disease), adrenal-dependent (adenoma or carcinoma), or caused by an ectopic ACTH-secreting tumor. Diagnostic tests include urine and salivary cortisol levels, low and high dose dexamethasone suppression tests, and imaging of the pituitary and adrenal glands. Treatment depends on the cause but may involve surgery to remove tumors, adrenalectomy, or medication to suppress cortisol production while managing comorbidities. The prognosis has improved with effective treatments but risks remain high without treatment.
Thyrotoxicosis is a clinical syndrome caused by high levels of circulating thyroid hormones, with primary causes including Graves' disease and toxic nodular goiter, leading to symptoms of weight loss, fatigue, heat intolerance, and emotional changes. Diagnosis is based on examination findings of a goiter, tachycardia, and eye changes like exophthalmos, with treatment options including antithyroid drugs, radioactive iodine, or surgery to remove the overactive thyroid tissue.
This slide was prepared for teaching purpose to medical students. It contain information from different books and medical journals. please inform if any of the information given need to be changed.
Hyperthyroidism, Reference: Hyperthyroid, Harrison's Principles of Internal Medicine, Soheil Elahi, Islamic Azad University of Medicine- International Branch (IAUM-int)
The thyroid gland is located in the neck and produces hormones that regulate metabolism. It has two lobes connected by an isthmus. The gland contains follicles that produce thyroid hormones. Hashimoto's thyroiditis is the most common cause of hypothyroidism. It is an autoimmune disease where the immune system attacks the thyroid, destroying follicles and causing lymphocytic infiltration. This leads to decreased thyroid hormone production and symptoms like weight gain and fatigue. Treatment involves thyroid hormone replacement therapy.
Vasoactive drugs act on the heart and circulatory system by affecting adrenergic receptors. They can be classified as vasopressors, inotropes, or vasodilators. Common vasoactive drugs include adrenaline, noradrenaline, dopamine, dobutamine, milrinone, vasopressin, nitroglycerine, and nitroprusside. Each drug has distinct mechanisms of action and indications for use. Careful consideration of dosing and side effects is important when using these powerful cardiovascular medications.
The document discusses the history and development of the internet over the past 50 years, from its origins as a US military program called ARPANET to the commercialization of the world wide web in the 1990s. It led to an explosion of new technologies and services over the following decades that have transformed how people live and work through greater connectivity and access to information.
Acute Decompensated Heart Failure : What is New ?drucsamal
1. The document discusses drug trials for acute decompensated heart failure and their results. Many trials tested drugs like nesiritide, milrinone, tezosentan, levosimendan, tolvaptan, and rolofylline but did not show clinical benefit.
2. It proposes classifying patients based on their clinical profile into those with volume overload, reduced cardiac output, or a combination, to help determine optimal treatment which may include diuretics, vasodilators, inotropes, or renal preservation agents.
3. The management of acute heart failure is divided into initial, in-hospital, and discharge phases, with goals like establishing diagnoses, treating precip
This document discusses types of shock, including hypovolemic, cardiogenic, obstructive, distributive, septic, anaphylactic, and neurogenic shock. It covers the pathophysiology, signs and symptoms, treatment principles of fluid resuscitation, and choices of intravenous fluids for each type of shock. The key aspects of fluid management in shock include initially restoring intravascular volume with crystalloids before considering colloids or blood transfusion to achieve hemodynamic goals.
The document discusses liver function tests and bilirubin metabolism. It describes that liver function tests are useful for diagnosing and monitoring liver diseases. A battery of tests are needed since the liver has diverse functions including excretion, metabolism, protein and plasma synthesis, and storage. Specific tests mentioned include liver enzymes, albumin, prothrombin time, tumor markers, bilirubin, and dye excretion tests. The types of jaundice - hemolytic, obstructive, and hepatic - are distinguished based on conjugated and unconjugated bilirubin levels as well as other factors. Various inborn errors affecting bilirubin metabolism are also outlined.
This document provides information on interscalene brachial plexus blocks, including indications, contraindications, anatomy, techniques, complications, and references. It describes Winnie's anterior approach using landmarks to identify the interscalene groove for injection, as well as a posterior approach. Areas of blockade, continuous techniques, and use of nerve stimulation are also summarized. Supraclavicular blockade as an alternative is outlined with similar details.
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
A 42-year-old male presented with abdominal pain for 20 days. Medical history revealed a past diagnosis of pancreatitis. Physical examination found a vague mass palpable in the epigastric and left hypochondrium region. Imaging studies including ultrasound and CT scan identified a cystic structure along the head and tail of the pancreas, with one cyst extending into the mediastinum. The patient underwent a laparotomy with roux-en-y cystojejunostomy to drain a pseudocyst measuring 15x12 cm communicating with a 10x8 cm cyst. Post-operative recovery was uneventful.
The document discusses enhanced recovery after surgery (ERAS) programs. It describes how ERAS utilizes a multimodal approach involving surgeons, nurses, dietitians and others to optimize patient care and recovery through measures like preoperative counseling and nutrition, minimal invasive surgery when possible, reduced use of tubes/drains, early mobilization and feeding, and well-managed postoperative pain control. The goal is to reduce length of stay without increasing complications through evidence-based practices compared to traditional postoperative care methods. Studies show ERAS programs can achieve these outcomes safely and cost-effectively across several surgery types.
A study compared outcomes for 32 patients undergoing fast-track colorectal surgery (Group A) to 32 patients receiving conventional care (Group B). Group A received no bowel preparation, no tubes, early feeding and early mobilization. Group A had significantly shorter hospital stays, time to first bowel movement, and time to liquid diet compared to Group B. There was no significant difference in postoperative pain between the groups.
This document defines various gallstone diseases and provides information on their risk factors, presentations, diagnoses, and treatments. It discusses the definitions of cholelithiasis, cholecystitis, choledocholithiasis, and other conditions. The risk factors include factors like female gender, obesity, and hemolytic states. Imaging studies like ultrasound and CT are used for diagnosis, and treatments involve analgesics, antibiotics, ERCP, and cholecystectomy.
This document provides information on the primary survey and resuscitation of trauma patients. It discusses the importance of the ABCDE approach to assess airway, breathing, circulation, disability, and exposure. Proper cervical spine control and airway management are emphasized as the first priorities in trauma resuscitation. Basic airway maneuvers like chin lift and jaw thrust are described, as well as advanced techniques like orotracheal intubation that provide a definitive airway. The document stresses the need for rapid evaluation and treatment of life-threatening injuries according to established trauma protocols.
2012 Clinical Practice guidelines for hypothyroidism in adults: American Asso...Jibran Mohsin
This is presentation format of 2012 Clinical Practice guidelines for hypothyroidism in adults: American Association of Clinical Endocrinologists (AACE) / American Thyroid Association (ATA)
The document discusses hepatic (liver) functions and manifestations of liver disease. It covers topics such as jaundice, hepatic encephalopathy, and different types of jaundice (prehepatic, hepatic, post-hepatic). Liver diseases discussed include toxic hepatitis, infectious hepatitis, parasitic hepatitis, and nutritional hepatitis. Clinical signs, nervous system signs, and laboratory tests for assessing liver function and disease are also summarized.
Damage control surgery (DCS) is an approach used for severely injured trauma patients that focuses on rapidly addressing life-threatening issues like hemorrhage rather than fully repairing anatomy. It aims to prevent the lethal triad of hypothermia, acidosis, and coagulopathy that can result from long operations and blood loss. Key aspects of DCS include temporary measures like packing bleeding liver injuries; stapling but not repairing some intestinal injuries; leaving unrepaired vascular injuries clamped; and rapidly closing the abdomen with clips rather than drains to allow reoperation once the patient is stabilized. The goal is definitive repair within 24 hours once the patient's physiology is corrected.
Thyroid disorders result from issues with thyroid hormone production or secretion, altering metabolism. Hyperthyroidism occurs when excessive thyroid hormones are produced, often due to Graves' disease, an autoimmune disorder. Hypothyroidism results from decreased thyroid hormone production, commonly caused by Hashimoto's thyroiditis or thyroid surgery/radiation treatment. Both conditions are managed through pharmacological interventions like antithyroid drugs or levothyroxine replacement therapy.
Hypothyroidism is a common endocrine disorder where the thyroid gland produces insufficient hormones. It affects 1.8% of the population and is more prevalent in females and the elderly. The most common cause is Hashimoto's thyroiditis which results in lymphocytic infiltration and thyroid damage. Symptoms of hypothyroidism are non-specific but include fatigue, weight gain, dry skin, and low heart rate. Treatment involves lifelong thyroid hormone replacement therapy with levothyroxine to normalize thyroid levels. Special care is needed in pregnancy, myxedema coma, and avoiding overtreatment.
The document summarizes key topics in endocrinology, including disorders of the thyroid, parathyroid, and adrenal glands. It discusses hypothyroidism and its causes, signs, symptoms, and treatment with levothyroxine replacement. It also covers thyrotoxicosis, hyperparathyroidism, Cushing's syndrome, and disorders of the adrenal cortex that can cause hormone deficiencies or excesses. The quiz at the end reviews topics like Cushing's syndrome and autoimmune destruction of pancreatic beta cells in type 1 diabetes.
Hyperthyroidism is a condition where the thyroid gland is overactive and produces too much thyroid hormone, leading to accelerated metabolism. It can be caused by Graves' disease in most cases. Symptoms include nervousness, rapid heartbeat, weight loss, and eye problems. Treatment involves anti-thyroid medications, radioactive iodine, surgery or beta blockers to reduce thyroid hormone levels and symptoms.
This document discusses various endocrine problems involving the pituitary gland and thyroid. It summarizes pituitary control of growth hormone and describes symptoms of growth hormone excess such as enlarged hands, feet, and tongue. It also discusses diagnostic studies and treatment for growth hormone excess. Transient diabetes insipidus and syndrome of inappropriate antidiuretic hormone are described as potential postoperative complications. Diabetes insipidus, its causes and goals of treatment are summarized. Hyperthyroidism, hypothyroidism, thyroid storm, thyroiditis, thyroid cancer, and thyroidectomy are briefly described. Cushing's syndrome, Addison's disease, hyperparathyroidism, and pheochromocytoma are also mentioned.
Thyroid disorders are common in endocrinology. The document discusses the anatomy and functions of the thyroid gland, as well as the regulation of hormone production and classification of thyroid disorders. It provides an overview of hyperthyroidism (thyrotoxicosis) and hypothyroidism, including their causes, signs, symptoms, and treatment approaches. Graves' disease is described as the most common cause of thyrotoxicosis. Treatment options for hyperthyroidism discussed include beta-blockers, antithyroid medications, radioactive iodine, and thyroidectomy.
- Shelley, a 14-year-old girl, presents with symptoms of hyperthyroidism including weight loss, tremors, and an enlarged thyroid gland. Laboratory tests confirm low TSH and high free T3 and T4 levels. She is diagnosed with Graves' disease based on her symptoms and positive thyroid receptor antibodies. Graves' disease is an autoimmune disorder causing hyperthyroidism due to stimulating antibodies to the TSH receptor. Treatment involves antithyroid drugs like carbimazole to control thyroid levels and beta blockers to control symptoms of thyrotoxicosis.
This document discusses endocrine disorders and their causes, symptoms, diagnosis and treatment. [1] Endocrine disorders can be caused by issues with the hypothalamus, pituitary gland, or hormone-producing glands and can result from congenital defects, infections, autoimmunity, tumors or unknown causes. [2] Too much or too little hormone production can occur due to failures in the feedback systems that control hormone levels or dysfunction of the endocrine glands themselves. [3] The document focuses on disorders of the thyroid gland (hypothyroidism, hyperthyroidism), adrenal gland (Addison's disease, Cushing's syndrome) and their clinical presentations and management.
This document discusses thyroid storm, a life-threatening condition caused by excess thyroid hormone levels. It begins by outlining the objectives of understanding the pathophysiology of hyperthyroidism, recognizing clinical presentations of thyroid storm, and providing optimal treatment guidelines. Key points include distinguishing primary from secondary hyperthyroidism, identifying potential triggers of thyroid storm like infection or trauma, and describing the classic presentation of fever, tachycardia, and altered mental status. Treatment involves supportive care as well as inhibiting thyroid hormone synthesis with drugs, blocking hormone release with iodine, treating symptoms like tachycardia, and using steroids or plasmapheresis in refractory cases. The goal is to reduce circulating thyroid hormone levels and control
The document provides information on the thyroid gland, including its anatomy, histology, physiology, pathology, and disorders. Some key points:
- The thyroid is one of the earliest endocrine organs to develop. It is located in the neck and weighs 15-25 grams.
- Graves' disease is the most common cause of hyperthyroidism. It is characterized by the triad of thyrotoxicosis, ophthalmopathy, and dermopathy due to autoantibodies that mimic TSH.
- Hypothyroidism is most commonly caused by Hashimoto's thyroiditis, an autoimmune disorder characterized by lymphocytic infiltration and antibody production. Clinical manifestations range from mild to
Hyperthyroidism, also known as overactive thyroid, results from excessive thyroid hormone production and secretion. Graves' disease, the most common cause, is an autoimmune disorder where antibodies stimulate the thyroid. It is characterized by diffuse thyroid enlargement, ophthalmopathy, and pretibial myxedema. Symptoms include palpitations, heat intolerance, weight loss and tremors. Diagnosis involves low TSH and high T4 levels and presence of thyroid autoantibodies. Treatment options include antithyroid medications, radioactive iodine ablation, or surgery. Thyroid storm is a medical emergency characterized by severe hyperthyroid symptoms that requires urgent beta-blockers, antithyroid drugs and supportive
Thyrotoxicosis- complete review of anatomy, physiology, types and clinical fe...Surjeet Acharya
this presentation covers extensive pictures for clear explanation. this includes the anatomy & physiology of thyroid gland, a case review, types, clinical features and treatment of thyrotoxicosis. and the most intersting part it, it also includes Recent Advances in field of thyrotoxicosis
This document discusses hyperthyroidism and its management. It begins with definitions of hyperthyroidism and thyrotoxicosis. It then discusses the prevalence, anatomy, physiology and causes of hyperthyroidism. The clinical manifestations involving multiple body systems are explained in detail. Diagnostic tests including blood tests, ultrasound and radioactive iodine uptake scans are outlined. Finally, the medical management including antithyroid drugs, radioactive iodine therapy and surgery are summarized.
Q: A 70 y.o. man is brought to ER by his nephew because he was found poorly responsive at home. The nephew had not checked on the patient for two weeks. The patient lives alone and has been noted by his nephew to be more confused and less active over the past few months.
The nephew was uncertain about the patient's past medical history. He recalls that the patient takes several pills per day for some 'heart issues,' blood pressure, and headaches.
He also recalls that the patient was seen in ER recently for muscle pains and was given opioid analgesics.
This document summarizes thyroid diseases and evaluation of thyroid nodules. It discusses the peripheral action of thyroid hormones, thyroiditis conditions including Hashimoto's, subacute, and Riedel's, hyperthyroidism including Graves' disease and toxic nodular goiter, evaluation of thyroid nodules including risk factors and initial workup, and treatment options for hyperthyroidism such as antithyroid medications, radioactive iodine, and surgery.
Most common thyroid disorders are hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid). Hyperthyroidism symptoms include nervousness, palpitations, sweating, and eye changes. Causes include Graves' disease and ingestion of excess thyroid hormone. Treatment involves anti-thyroid medications, radioactive iodine, or surgery. Hypothyroidism causes fatigue, weight gain, dry skin and is most often due to autoimmune disease or previous thyroid surgery/radiation. Levothyroxine replacement is the standard treatment monitored through thyroid hormone level testing.
This document provides an overview of hypothyroidism, including its definition, effects on different organ systems, types, causes, investigations, and treatment. Some key points are:
- Hypothyroidism is a deficiency in thyroid hormone secretion, occurring in 2-15% of the population more commonly in women. Risk increases with age.
- It affects the cardiovascular, respiratory, renal, central nervous, neuromuscular, gastrointestinal, and hematological systems, causing decreased metabolism.
- Types include primary, central, and congenital hypothyroidism. Causes include iodine deficiency, autoimmune disease, surgery, radiation, and certain drugs.
- Investigations include thyroid function tests and antibodies
Hyperthyoroidism and thyrotoxixosis grave's diseases.pptxPradeep Pande
This document provides tips and instructions for using a PowerPoint presentation on thyrotoxicosis and hyperthyroidism. It discusses:
1. How the presentation can be freely downloaded, edited, and modified.
2. How blank slides are included for active learning sessions, where students are asked questions before the next slide with information is shown.
3. Tips for using the presentation for self-study as well.
The presentation then provides information on hyperthyroidism vs thyrotoxicosis, thyroid hormone function, Graves' disease, etiology and pathogenesis, clinical presentation, diagnosis, and management.
Thyroid gland (anatomy and physiology) biochemical basisDeependra Shrestha
A 65-year-old female presented with fatigue, constipation, feeling cold, dry skin, and neck swelling. On examination, she had an enlarged, nontender thyroid, diminished reflexes, dry skin, and was taking fortified salt.
The most likely diagnosis is hypothyroidism. Laboratory tests would include measuring thyroid stimulating hormone (TSH) levels to confirm the diagnosis. Treatment would be thyroid hormone replacement therapy.
This case report describes a 5-year-old child presenting with bowed legs and frontal bossing. Laboratory tests found hypocalcemia, hypophosphatemia, elevated alkaline phosphatase, and hyperparathyroidism despite normal vitamin D levels before and elevated levels after supplementation. This constellation of findings led to a diagnosis of vitamin D resistant rickets, supported by the child's symptoms improving on high-dose calcitriol and calcium treatment. Vitamin D resistant rickets is a rare form of rickets caused by mutations impairing the vitamin D receptor.
1. Minimal change disease and focal segmental glomerulosclerosis are causes of nephrotic syndrome that involve damage to the glomerular filter, resulting in proteinuria.
2. Diabetic nephropathy is caused by chronic hyperglycemia damaging the kidneys through pathways like increased flux through the polyol pathway and production of advanced glycation end products.
3. Hypertensive nephropathy involves high blood pressure damaging the kidneys over time through arterial thickening, glomerular ischemia, and glomerular hypertension.
The document summarizes the structure and function of the renal (urinary) system. It describes the key components of the system including the kidneys, ureters, bladder, and urethra. It then discusses the functional units of the kidneys called nephrons and their role in filtering blood and regulating water and electrolyte balance through glomerular filtration, tubular reabsorption and secretion processes. Specifically, it explains how nephrons use active transport mechanisms like the sodium-potassium pump to reabsorb filtered materials and maintain blood pressure and pH levels.
The document discusses carbohydrates and their roles in glycoproteins, glycolipids, and proteoglycans. It explains that carbohydrates are covalently attached to proteins or lipids through glycosylation to form these glycoconjugates. Glycosaminoglycans are linear polysaccharides that help form the extracellular matrix. Common examples discussed include hyaluronic acid, chondroitin sulfate, dermatan sulfate, heparan sulfate, and keratan sulfate. Proteoglycans are core proteins with attached glycosaminoglycan chains that interact with extracellular proteins. Glycoproteins have oligosaccharide chains attached to asparagine or serine/threonine residues. Gly
This document summarizes carbohydrates and their classification. It defines glycosidic bonds as bonds that join carbohydrates. It describes oligosaccharides as short polymers of monosaccharides joined by glycosidic bonds, including common disaccharides formed from two monosaccharides like sucrose, lactose, and maltose. It also discusses polysaccharides including storage polysaccharides like starch and glycogen, structural homopolysaccharides like cellulose and chitin, and heteropolysaccharides like peptidoglycan and agar.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
2. Clinical Scenario
• A 39-year-old female presents to the clinic for a routine health maintenance
exam.
• She reports that she is feeling nervous and anxious all the time with frequent
palpitations.
• On further questioning she reports having diarrhea and has been losing weight.
• She has also noticed a change in hair and fingernail growth and frequently feels
warm while others are cold or comfortable.
• She denies any history of depression or anxiety disorder and is not taking any
medications.
• On examination, her heart rate is 110 beats per minute. She has a slight tremor
and has increased reflexes in all extremities.
• A nontender thyroid enlargement is appreciated in the thyroid region.
• Presence of Exophthalmos
7. On further investigation..
• Thyroid Stimulating Immunoglobulins (TSIs) test is positive
• TPO antibodies are negative
8. Discussion:
• The patients has symptoms of nervousness, weight loss,
gastrointestinal and skin alterations, heart palpitations, heat
intolerance, and physical signs of hyperreflexia and a goiter.
• Likely diagnosis:
• Hyperthyroidism, likely Graves disease.
• Supporting points from biochemistry
• T3- High
• T4- High
• TSH – Low
• TSIs- Positive
9. • Biochemical mechanism:
• The most frequent cause of hyperthyroidism, Graves disease, is an
autoimmune process in which thyroid hypersecretion is caused by
circulating immunoglobulins that bind to the TSH receptor on the
thyroid follicular cells and stimulate thyroid hormone production.
• The diagnosis is confirmed by increased thyroid stimulating IgG
antibodies and is frequently seen in other family members.
• Hyperthyroidism, thyroid excess causes a tachycardia, tremor,
nervousness, thin skin, weight loss through the hypermetabolic state,
and hyperreflexia.
• If unchecked, the high levels of thyroid hormone can sometimes even
cause adrenergic crisis (so called thyroid storm), which has a high
rate of mortality.
10. • Normally, the thyroid hormone (thyroxine) is under tight control. The
pituitary release of thyroid stimulating hormone is stimulated by
insufficient thyroxine, and suppressed by excess thyroxine.
• In Graves disease, the most common cause of hyperthyroidism, an
autoimmune immunoglobulin is produced that stimulates the TSH
receptor of the thyroid gland.
• This is confirmed by either assaying for the Thyroid Stimulating
Immunoglobulin, or a radionuclide scan revealing diffuse increased
uptake throughout the thyroid gland.
• Treatment acutely includes β-adrenergic antagonists and agents that
inhibit the catabolism of thyroid hormone such as propylthiouracil
(PTU).
14. Hyperthyroidism:
• Increase in activities of thyroid hormones.
• Decrease in TSH due to feedback mechanism.
• Causes:
• Graves’ disease
• Toxic adenoma/hot nodule
• Multinodular goiter
• Thyroiditis(Hasitoxicosis)
• Exogenous iodine ingestion
• Excessive T3 and T4 ingestion.
• Ectopic thyroid tissue
• HCG dependent
• TSH dependent: Pituitary tumor.
15. Clinical Features:
• Cardiovascular:
• High thyroid hormones have a direct stimulatory effect on cardiac
muscle.
• Increase heart rate and stroke volume even at rest.
• Peripheral vascular resistance is reduced.
• Increase in cardiac output.
• Arrhythmias.
• Gastrointestinal:
• Weight loss
• Increase bowel movement.
• Liver unction can be markedly deranged, with hypoalbuminaemia and
elevation of plasma aminotransferase and alkaline phosphatase
activities.
16. • Nervous system:
• Generalized hyperkinesia
• Fine tremor of outstretch finger
• Loss of sleep
• Musculoskeletal:
• Weakness particularly proximal muscles.
• Due to impaired phosphorylation of creatine.
• Periodic paralysis, associated with hypokalaemia during attacks of
weakness
17. • Respiratory:
• Due to generalized myopathy, respiratory muscle function may be
impaired and pulmonary compliance may also be reduced.
• Dyspnoea
• Breathlessness
• Skin and hair:
• Hair loss
• Brittle nails
• Warm and moist skin.
18. • Skeleton
• Significant loss of mineral from the skeleton, which results from increased
bone turnover
• Hypercalciuria and hyperphosphaturia are found
• urinary hydroxyproline excretion is increased, reflecting the increase in
collagen turnover.
• Kidney:
• Increase magnesium excretion
• Increase thirst and mild polyuria even in the absence of hypercalcemia of
hyperglycemia.
• Endocrine:
• Menstrual irregularity
• Reduced fertility.
• Decrease sex steroid due to decrease binding protein.
• Gynaecomastia.
19. Graves’ Disease:
• Basedow-Graves disease
• Most common cause of Hyperthyroidism.
• An autoimmune disease.
• Female/Male: 6:1
• Peak onset 3rd-4th decade, but can occur at any age
• It most commonly affects the thyroid, frequently causing it to enlarge to twice its
size or more (goitre)
• It can also affect the eyes, causing bulging eyes (exophthalmos).
• It affects other systems of the body, including the skin.
20. Mechanism:
• Thyroid Stimulating Immunoglobulins (TSIs) bind to the TSH receptor
and mimic the action of TSH.
• Activates adenylate cyclase and the formation of cAMP.
• Genetic factor: MHC class II antigen HLA-DR3 increases risk by 3 fold
25. Graves’ Ophthalmopathy:
• Pathogenesis
• Presumed autoimmune, likely due to shared antigens on thyroid and
retroorbital tissue (possibly the TSH receptor).
• Extraocular muscles enlarge with edema, glycosaminoglycan
deposition, mononuclear cell infiltrate, and fibrosis.
26.
27. Graves’ Dermopathy(Pretibial Myxedema)
• Patients with graves disease may develop indurated purple skin.
• It is due to glycosaminoglycan deposition
• Rare, generally accompanied by eye disease
• Usually asymptomatic
• Therapy typically topical glucocorticoids
29. Findings:
• TSH low (always measure this)
• Free T4, free T3 elevated (measure one or both if TSH is low)
• Radioiodine uptake increased (excludes subacute thyroiditis and
allows Rx with radioiodine)
• Thyroid stimulating antibodies present (could measure instead of
RAIU)
• Antithyroid (anti-TPO and Tg) antibodies often present (generally
don’t measure)
30.
31. Other biochemical changes:
• High calcium level:
• Increase bone turnover.
• Low magnesium level:
• Increase excretion.
• Low LDL cholesterol:
• Increase lipolysis.
• High liver enzymes:
• Increase plasma transaminase, alkaline phosphatase
33. • Surgery:
• Subtotal thyroidectomy is highly effective.
• Advantages:
• Rapid (but must pre-treat with antithyroid drugs or β-blockers), may
not cause hypothyroidism
• Disadvantages:
• Inpatient surgery, general anesthesia, complications
(hypoparathyroidism, recurrent laryngeal nerve palsy)
34. Toxic multinodular goitre:
• Thyroid has multiple nodules, some of which may be too small to
palpate.
• Some of the nodules function autonomously.
• “Toxic” multinodular goiter signifies that the level of autonomous
function is sufficient to cause hyperthyroidism
35. • Shows all features of hyperthyroidism as mention earlier
• Generally the cause is not known, although some nodules have
activating mutations of the TSH receptor.
• Treat with radioiodine or surgery, as spontaneous remissions do not
occur.
36.
37. Toxic adenoma:
• Less common cause of hyperthyroidism than Graves’ disease
• In most patients, the nodule produces too little thyroid hormone to
cause hyperthyroidism
• Generally must be >2.5 cm to cause clinical hyperthyroidism (“toxic
adenoma”)
• Constitutively activating mutations of the TSH receptor are causative
in many cases
38. • Lab findings are similar to Graves’ disease except TSI and anti-thyroid
Abs are negative.
• Spontaneous remissions are very rare.
• Thionamides will lower T4 and T3, but will not lead to cure.
• Therefore, preferred therapy is surgery or radioiodine.
39.
40. Exogeneous Iodine ingestion
• Jod-Basedow Effect:
• Opposite of the Wolff-Chaikoff effect
• Excessive iodine loads induce hyperthyroidism
• Observed in hyperthyroid disease processes
Graves’ disease
Toxic multinodular goiter
Toxic adenoma
• This effect may lead to symptomatic thyrotoxicosis in patients who
receive large iodine doses from
Dietary changes
Contrast administration
Iodine containing medication ( Amiodarone )
41. Iodine containing medication ( Amiodarone )
• Amiodarone has a structure similar to that of thyroid hormones and inhibits
the peripheral conversion of T 4 to T 3 catalyzed by iodothyronine
deiodinase D1.
• Resulting concentrations of T4 may be high and T 3 low, with an increase in
rT 3.
• Thyroid stimulating hormone may rise transiently during the first few weeks
of treatment, but by four months, most patients who are euthyroid will have
normal or sometimes suppressed concentrations of TSH.
• The drug inhibits both iodine uptake by the thyroid and entry of T4 into cells
and can also cause both iodine-induced hypothyroidism and
hyperthyroidism.
42. Ectopic thyroid tissue.
• Metastatic thyroid follicular carcinoma may rarely produce sufficient
thyroid hormone to result in hyperthyroidism.
• Other tumors, such as ovarian teratomas, may contain functional thyroid
tissue in sufficient quantity to produce symptoms and signs of
thyrotoxicosis (struma ovarii).
• Endogenous thyroid radioisotope uptake will be suppressed and
functioning tissue demonstrable in the tumor under these most
uncommon circumstances.
43. HCG dependent
• Human chorionic gonadotropin (hCG)–induced hyperthyroidism is observed in
gestational transient thyrotoxicosis.
• hCG possesses intrinsic human thyroid stimulating activity
• So causes hyperthyroidism
• Usually occurs during pregnancy.
• TSH receptor sensitivity to appropriate hCG concentrations during pregnancy,
and hCG-secreting tumors.
• Gestational transient thyrotoxicosis occurs in 2 to 3% of all pregnancies, and
results from activation of TSH receptors by hCG, which is greatly elevated
during pregnancy.
• Trophoblastic tumours such as choriocarcinoma, hydatidiform mole and
metastatic embryonal testicular carcinoma may secrete human chorionic
gonadotrophin (hCG).
• The degree of hyperthyroidism is typically mild, and treatment is not usually
required.
44. Hashitoxicosis
• During the clinical course of Hashimoto thyroiditis, if a period of
accelerated destruction of thyroid follicular cells occurs, subsequent
release of thyroid hormone can produce a transient interval of
hyperthyroidism, termed Hashitoxicosis.
• Hashitoxicosis should be differentiated from Graves’ disease because
the treatments for these two conditions are different.
• Hashitoxicosis is self-limited
• TSIs are usually positive in patients with Graves’ disease and negative
in Hashitoxicosis.
• In addition, the RAIU is elevated in Graves’ disease but is not elevated
in Hashitoxicosis.
45. Postpartum Thyroiditis
• Patients with postpartum thyroiditis can experience a period of
transient, usually self-limited, hyperthyroidism from accelerated
breakdown of thyroid tissue.
• Subacute or acute thyroiditis can produce a period of transient
hyperthyroidism.
46. Central hyperthyroidism
• It is caused by pituitary adenomas and is rare condition
• It secrete TSH hormone excessively which causes hyperthyroidism.
• This diagnosis is suggested by
• Clinical hyperthyroidism,
• Elevated FT4
• Normal to elevated TSH concentration,
• Evidence of a pituitary mass on computed tomography (CT) scan or magnetic
resonance imaging (MRI).
• Hyperthyroidism is also caused when there is pituitary resistance to
thyroid hormone in feedback mechanism
47. T3 Toxicosis
• T3 toxicosis is defined by the presence of clinical hyperthyroidism in a
patient with suppressed TSH, normal FT4, and elevated T3 (or FT3).
• When a very mild excess of thyroid hormone is causing increased
thyroidal and peripheral deiodination of T4 to T3.
• D1 conversion of T4 to T3 is enhanced in hyperthyroidism.
• Raise in T3 occurs in contrast to T4
• T3 toxicosis is also possible
• when hyperthyroidism occurs in the presence of mild iodine deficiency
• when iodine is sufficient to synthesize excessive amounts of T3 but not T4.
• TSHR enhances the production of T3 more than T4.
48. Thyroid Storm:
• Medical Emergency
• Occurs in ~ 1% of pregnant pts with hyperthyroidism
• Thyroid storm is a decompensated state of thyroid hormone–induced,
severe hypermetabolism involving multiple systems and is the most
extreme state of thyrotoxicosis.
• The clinical picture relates to severely exaggerated effects of THs due to
increased release (with or without increased synthesis) or increased
intake of TH.
• Thyroid storm, also referred to as thyrotoxic crisis, is an acute,
49. • Life-threatening, hypermetabolic state induced by excessive release
of thyroid hormones (THs) in individuals with thyrotoxicosis.
• The clinical presentation includes fever, tachycardia, hypertension,
and neurological and GI abnormalities.
• Hypertension may be followed by congestive heart failure that is
associated with hypotension and shock.