HYPERPARATHYROIDISM
PRIMARY
BROWN TUMOUR
SALT AND PEPPER APPEARANCE OF SKULL
COD FISH SPINE
,
normal calicum metabolism
,
secondary hyperparathyroidism
,
albert hereditary osteodystrophy
,
pseudopseudohypoparathyroidism
,
hypocalcemia
HIGH YIELD
This patient presented with seizure, circumoral paresthesias, hyperreflexia, and carpopedal spasm after a recent total thyroidectomy. These symptoms are consistent with hypoparathyroidism caused by parathyroid gland damage or removal during thyroid surgery. Laboratory tests would likely show low ionized calcium levels as the cause of her symptoms. IV calcium replacement is the appropriate treatment.
This document provides information on parathyroid glands and parathyroid hormone (PTH). It discusses the anatomy and blood supply of the parathyroid glands. It describes PTH, its functions, and how it regulates calcium levels. It outlines primary hyperparathyroidism, including causes, clinical features, investigations, and treatment via parathyroidectomy. It also briefly discusses secondary and tertiary hyperparathyroidism, acute hyperparathyroidism, MEN syndrome, apudomas, and hypoparathyroidism.
The document discusses disorders of the parathyroid glands and tetany. It notes that the parathyroid glands regulate calcium and phosphate levels and vitamin D metabolism. Disorders can cause hypercalcemia or hypocalcemia. Hypercalcemia symptoms include polyuria and renal problems. Hypocalcemia can cause tetany with muscle spasms. Primary causes, clinical features, investigations, and management are described for various parathyroid disorders including primary hyperparathyroidism and hypoparathyroidism. Tetany is defined as muscle spasms caused by parathyroid dysfunction and low calcium levels.
This document provides an evidence-based presentation on parathyroid disorders. It begins with an introduction and objectives to define hyper and hypo parathyroidism, describe epidemiology and causes, identify diagnostics, state management protocols, and mention nursing interventions. It then covers the anatomy and function of parathyroid glands, disorders of parathyroid hormone, epidemiology of hyperparathyroidism, causes, pathophysiology, clinical manifestations, diagnostic evaluation including imaging and guidelines, management including surgical and medical protocols, complications, and prognosis. The presentation aims to educate on parathyroid disorders and their nursing management.
This document discusses a case of hypoparathyroidism in a 33-year-old female patient who presented with a grand mal seizure. The case involves radiological findings of brain calcification secondary to hypoparathyroidism. Hypoparathyroidism results from parathyroid hormone deficiency, which can be caused by thyroid surgery, irradiation, or autoimmune destruction of the parathyroid glands. In the absence of PTH, calcium and phosphorus levels in the blood are disrupted, which can lead to neurological symptoms and brain calcification over time.
The document discusses diseases of the parathyroid glands, including hyperparathyroidism and hypoparathyroidism. It covers the physiology and functions of the parathyroid glands and parathyroid hormone. It describes the etiology, pathogenesis, and classification of primary, secondary, and tertiary hyperparathyroidism. The clinical features of hyperparathyroidism are also outlined.
This document provides an overview of parathyroid glands and parathyroid disorders. It discusses the anatomy and embryology of the parathyroid glands. It describes parathyroid hormone (PTH) and its role in regulating calcium levels. The document summarizes primary, secondary, and tertiary hyperparathyroidism, including their causes, clinical manifestations, diagnostic imaging, and treatment options. It also discusses hypercalcemic crisis, persistent/recurrent hyperparathyroidism, surgical approaches, complications, and hypocalcemia.
This patient presented with seizure, circumoral paresthesias, hyperreflexia, and carpopedal spasm after a recent total thyroidectomy. These symptoms are consistent with hypoparathyroidism caused by parathyroid gland damage or removal during thyroid surgery. Laboratory tests would likely show low ionized calcium levels as the cause of her symptoms. IV calcium replacement is the appropriate treatment.
This document provides information on parathyroid glands and parathyroid hormone (PTH). It discusses the anatomy and blood supply of the parathyroid glands. It describes PTH, its functions, and how it regulates calcium levels. It outlines primary hyperparathyroidism, including causes, clinical features, investigations, and treatment via parathyroidectomy. It also briefly discusses secondary and tertiary hyperparathyroidism, acute hyperparathyroidism, MEN syndrome, apudomas, and hypoparathyroidism.
The document discusses disorders of the parathyroid glands and tetany. It notes that the parathyroid glands regulate calcium and phosphate levels and vitamin D metabolism. Disorders can cause hypercalcemia or hypocalcemia. Hypercalcemia symptoms include polyuria and renal problems. Hypocalcemia can cause tetany with muscle spasms. Primary causes, clinical features, investigations, and management are described for various parathyroid disorders including primary hyperparathyroidism and hypoparathyroidism. Tetany is defined as muscle spasms caused by parathyroid dysfunction and low calcium levels.
This document provides an evidence-based presentation on parathyroid disorders. It begins with an introduction and objectives to define hyper and hypo parathyroidism, describe epidemiology and causes, identify diagnostics, state management protocols, and mention nursing interventions. It then covers the anatomy and function of parathyroid glands, disorders of parathyroid hormone, epidemiology of hyperparathyroidism, causes, pathophysiology, clinical manifestations, diagnostic evaluation including imaging and guidelines, management including surgical and medical protocols, complications, and prognosis. The presentation aims to educate on parathyroid disorders and their nursing management.
This document discusses a case of hypoparathyroidism in a 33-year-old female patient who presented with a grand mal seizure. The case involves radiological findings of brain calcification secondary to hypoparathyroidism. Hypoparathyroidism results from parathyroid hormone deficiency, which can be caused by thyroid surgery, irradiation, or autoimmune destruction of the parathyroid glands. In the absence of PTH, calcium and phosphorus levels in the blood are disrupted, which can lead to neurological symptoms and brain calcification over time.
The document discusses diseases of the parathyroid glands, including hyperparathyroidism and hypoparathyroidism. It covers the physiology and functions of the parathyroid glands and parathyroid hormone. It describes the etiology, pathogenesis, and classification of primary, secondary, and tertiary hyperparathyroidism. The clinical features of hyperparathyroidism are also outlined.
This document provides an overview of parathyroid glands and parathyroid disorders. It discusses the anatomy and embryology of the parathyroid glands. It describes parathyroid hormone (PTH) and its role in regulating calcium levels. The document summarizes primary, secondary, and tertiary hyperparathyroidism, including their causes, clinical manifestations, diagnostic imaging, and treatment options. It also discusses hypercalcemic crisis, persistent/recurrent hyperparathyroidism, surgical approaches, complications, and hypocalcemia.
This document provides information on disorders of the parathyroid glands. It discusses the anatomy and function of the parathyroid glands, including their role in calcium regulation and production of parathyroid hormone (PTH). It describes primary hyperparathyroidism, which results from excessive PTH production, and its clinical features. The document also covers hypoparathyroidism, which is a deficiency of PTH, and its signs, symptoms and treatment with calcium and vitamin D supplementation. In summary, the document outlines key endocrine disorders of the parathyroid glands, their effects on calcium levels, and management approaches for hyperparathyroidism and hypoparathyroidism.
This document discusses disorders of the parathyroid gland that result in hypercalcemia and hypocalcemia. It covers the physiology of calcium and phosphate homeostasis, the roles of parathyroid hormone (PTH) and vitamin D, and differentials for hyper- and hypocalcemia. Causes of hypoparathyroidism include DiGeorge syndrome and autoimmune polyglandular syndrome type 1. Pseudohypoparathyroidism is described as a genetic defect causing tissues to fail responding to PTH. Primary hyperparathyroidism is most often due to adenomas or hyperplasia while secondary and tertiary hyperparathyroidism occur in kidney disease.
Surgical diseases of the thyroid gland and parathyroid glandMD Specialclass
- The document discusses surgical diseases of the parathyroid glands, including primary hyperparathyroidism which is caused by inappropriately increased amounts of parathyroid hormone relative to calcium levels. The three histologic patterns are single adenoma, hyperplasia, and parathyroid carcinoma.
- Secondary hyperparathyroidism is caused by malfunction of another organ like the kidneys in chronic renal failure patients. Tertiary hyperparathyroidism is persistent hyperparathyroidism after the underlying disorder is resolved, such as after a successful kidney transplant.
- Surgery is the treatment for primary hyperparathyroidism and tertiary hyperparathyroidism, while treatment for secondary hyper
This document provides information on disorders of the parathyroid gland. It discusses the anatomy and histology of the parathyroid glands. It describes how parathyroid hormone is synthesized and its role in calcium regulation. It covers different types of hyperparathyroidism including primary, secondary, and tertiary. Primary hyperparathyroidism can be caused by adenomas, hyperplasia, or carcinoma. It discusses clinical manifestations, diagnosis, and differential diagnosis of primary hyperparathyroidism. It also covers hypercalcemia associated with other conditions like malignancy, immobilization, and familial hypocalciuric hypercalcemia.
The document discusses diseases of the parathyroid gland. It describes the structure and regulation of parathyroid hormone (PTH) secretion, including how calcium levels control PTH levels. It also discusses hyperparathyroidism, the most common form being primary hyperparathyroidism caused by a single adenoma or hyperplasia of the parathyroid glands leading to elevated PTH levels and hypercalcemia. Signs and symptoms include fatigue, weakness, kidney stones, and bone disease. The genetics and clinical manifestations of primary hyperparathyroidism are also summarized.
The parathyroid glands are small endocrine glands located near the thyroid gland that regulate calcium homeostasis. They secrete parathyroid hormone (PTH) which increases blood calcium levels. There are usually four parathyroid glands receiving blood supply from the inferior thyroid arteries. Primary hyperparathyroidism is most commonly caused by a single adenoma. Investigations for hypercalcemia include PTH and calcium levels. Treatment involves surgical removal of the affected gland(s), with preoperative localization using ultrasound or sestamibi scans to allow for minimally invasive surgery.
The parathyroid glands are small endocrine glands located on the thyroid gland that secrete parathyroid hormone (PTH) to regulate calcium levels. Primary hyperparathyroidism is usually caused by a solitary parathyroid adenoma. Pre-operative localization with sestamibi scanning is accurate for adenomas. Surgical treatment involves either unilateral or bilateral neck exploration to remove the abnormal gland(s), with minimally invasive radioguided parathyroidectomy being an option for localized disease.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
This document discusses disorders of the parathyroid gland including hypoparathyroidism and hyperparathyroidism. It describes various causes of hypoparathyroidism including genetic disorders, autoimmune disorders, surgical complications, and functional immaturity in infants. Symptoms include low calcium levels, muscle cramps, and seizures. Treatment involves calcium and vitamin D supplementation. Causes of hyperparathyroidism are also outlined such as tumors and genetic disorders. Symptoms include high calcium levels and bone abnormalities. Treatment is surgical removal of the overactive parathyroid gland.
This document summarizes parathyroid gland anatomy and physiology and various types of hyperparathyroidism. It discusses the role of parathyroid hormone in calcium homeostasis, causes of primary, secondary, and tertiary hyperparathyroidism, associated symptoms and complications, diagnostic testing, treatment options including medication and surgery, and other related conditions like familial benign hypercalcemia and hypercalcemia of malignancy.
This presentation is about Parathyroid Disorders which are hypo and hyperparathyroidism and their relationship to teeth and oral cavity including oral and dental manifestation of these disorders , and correct management patients seeking dental care with these disorders.
A 24-year-old female presented with abnormal body movements and was found to have hypocalcemia. Laboratory workup showed low serum calcium, high phosphorus, and normal parathyroid hormone. She was diagnosed with hypoparathyroidism and treated with calcium supplementation, resulting in symptom improvement. The cause was determined to be idiopathic hypoparathyroidism.
The document discusses parathyroid disorders including:
- The parathyroid glands' location and functions in regulating calcium levels by secreting parathyroid hormone.
- Primary hyperparathyroidism which is caused by adenomas, hyperplasia or carcinoma of the parathyroid glands and results in hypercalcemia.
- Hypoparathyroidism which is a deficiency of PTH that can be congenital or acquired after surgery and results in hypocalcemia.
- The diagnosis and treatment of both conditions including surgery, medication, and managing calcium levels.
<PARATHYROID HORMONES (The Calcium Regulating Gland)> first recognized in 1850 by Richard Owen.
<INTRODUCTION>Parathyroid glands are small glands of the endocrine system which are located in the neck behind the thyroid.><Called parathyroid due to proximity to the thyroid gland.><Yellowish brown, small ovoid bodies about 6 mm long, 3mm wide and 2mm thick.><Human being have 4 tiny parathyroid glands.><Each weighting around 30-50mg, but may weight as much as 70 mg, and in diameter is 3-4 or till 8 millimeters>
<Each parathyroid gland is made up of chief cells and oxyphil cells.><Chief cells more numerous, smaller, with a slightly eosinophilic cytoplasm.><secrete Parathyroid hormone (PTH). Also known as parathormone or parathyrin.>
<PARATHORMONE>Protein in nature (84 amino acids)><Molecular weight= 9,500.>< Half- life = 10 minutes><Normal plasma level of PTH = 1.5 to 5.5 ng/dL>
<SYNTHESIS OF AND SECRETION OF PARATHORMONE>PTH is encoded by a gene in chromosome 11><After translation, it become pre-pro-parathyroid hormone (pre-pro-PTH) contains 115 amino acids><In endoplasmic reticulum 29 amino acids removed, so it called pro-parathyroid hormone (pro-PTH) contains 89 amino acids><In the Golgi, removed more amino acids by peptidase to become mature hormone (PTH).><It is stored in secretory vesicles within the cells, and released when required>
<METABOLISM OF PTH>Half-life= 4 minute><60- 70 % of PTH is degraded by kupffer cells of liver, by means of proteolysis><Degradation of about 20-30% PTH occurs in kidneys and to a lesser extent in other organs>
<Half life – 4 min. How does PTH produce its effect on biological system?>
<REGULATION OF PARATHORMONE SECRETION>Regulators of secretion of PTH include calcium, vit D and phosphorus.>
<MECHANISM OF SECRETION OF PARATHORMONE> <CALCIUM-SENSING RECEPTORS (CaSR)><CaSR is a plasma membrane or a cell surface receptor, structured as G protein-coupled that is expressed in the parathyroid hormone-producing chief cells of the parathyroid gland and the cells lining the kidney tubule. (Hendy & et al., 2000)><PTH RECEPTORS>PTHR1 is physiologically more important than others two.><PTHR = 60-80 kDa membrane glycoprotein.>
<ACTION OF PTH>Important role in maintaining blood calcium level.>< Also controls blood phosphate level>
<DISORDERS OF PARATHORMONE.><increased pth secretion leads to an increase in serum levels by increasing bone resorption and enhancing renal calcium reabsorption. >
<3 TYPES>Primary hyperparathyroidism, Secondary hyperparathyroidism, Tertiary hyperparathyroidism.><The most common cause of hypercalcaemia is primary hyperparathyroidism>
The document outlines a seminar on disorders of the parathyroid glands presented by Ms. Gautami S. Tirpude. It discusses the general and specific objectives of gaining knowledge about parathyroid gland disorders and their application in nursing practice. The seminar covers topics like hyperparathyroidism and hypoparathyroidism including their definition, etiology, pathophysiology, clinical manifestations, diagnostic studies, and medical and surgical management. It also discusses the nursing role in managing related complications through various nursing interventions.
This document discusses diseases of the parathyroid gland, including its structure and functions in regulating blood calcium levels. The diseases are classified into hyperparathyroidism, hypothyroidism, and pseudohypoparathyroidism. Primary hyperparathyroidism is caused by autonomous overproduction of PTH, often due to a tumor. It can result in kidney stones, bone abnormalities, and other clinical issues. Hypothyroidism is a deficiency of PTH secretion and causes low calcium levels and tetany. Pseudohypoparathyroidism occurs when there is end-organ resistance to PTH despite normal levels.
This document discusses vitamin D and hyperparathyroidism. It notes that vitamin D is a fat-soluble vitamin that is converted to its active form in the kidney and regulates calcium levels. Hyperparathyroidism occurs when the parathyroid glands overproduce parathyroid hormone (PTH), which regulates calcium levels. There are three types: primary (excess PTH from parathyroid glands), secondary (increased PTH to compensate for hypocalcemia), and tertiary (PTH secretion becomes unregulated even after correcting the underlying cause). The document outlines the causes, clinical features, investigations, and treatments for each type of hyperparathyroidism.
The document discusses the parathyroid glands, which regulate calcium and phosphate levels and produce parathyroid hormone (PTH). It describes hyperparathyroidism and hypoparathyroidism, conditions caused by excessive or deficient PTH respectively, and their symptoms, causes, assessments, and treatment including diet modifications and medications. Surgical removal of the parathyroid glands may be required to treat hyperparathyroidism.
The parathyroid glands secrete parathyroid hormone (PTH) which regulates calcium levels. PTH increases bone resorption and calcium absorption from the gut while decreasing calcium excretion by the kidneys. Hyperparathyroidism is an increased secretion of PTH and can be primary, secondary, or tertiary. Primary hyperparathyroidism is usually caused by a single adenoma and presents with increased serum calcium levels and bone, kidney, or gastrointestinal problems. Imaging tests can locate enlarged parathyroid glands and surgery is the treatment of choice for removing adenomas or hyperplastic glands.
Case presentation of primary hyperparathyroidismHaifa Alshwikh
This case presentation describes a 44-year-old woman who presented with left hip pain and was found to have hypercalcemia. The differential diagnosis for her hypercalcemia includes primary hyperparathyroidism, familial hypocalciuric hyperparathyroidism, and tertiary hyperparathyroidism. She underwent laboratory testing which showed elevated PTH, consistent with primary hyperparathyroidism. Localization testing with sestamibi scan and ultrasound were recommended to help guide minimally invasive parathyroidectomy.
The document discusses disorders of the parathyroid glands. It describes how parathyroid hormone (PTH) regulates calcium and phosphate levels in the blood by stimulating bone resorption and calcium reabsorption in the kidneys. PTH also stimulates vitamin D production, which increases calcium absorption in the intestines. Disorders discussed include hyperparathyroidism, hypoparathyroidism, and hypercalcemia of malignancy. Treatment involves managing calcium levels, identifying and removing tumors, and replacing hormones.
Calcium and phosphorus metabolism are regulated by hormones like calcitriol, parathyroid hormone, and calcitonin to maintain normal levels in the body. Calcium is important for bone health, muscle function, and other cellular processes. The majority of calcium is stored in bones. Phosphorus also has important roles in energy storage and cellular processes. Both are absorbed in the small intestine and levels are regulated by hormones and excretion through the kidneys. Abnormal levels can cause diseases like rickets, osteomalacia, and osteoporosis. Dental issues may also arise from metabolic bone diseases like brown tumors and osteitis deformans.
This document provides information on disorders of the parathyroid glands. It discusses the anatomy and function of the parathyroid glands, including their role in calcium regulation and production of parathyroid hormone (PTH). It describes primary hyperparathyroidism, which results from excessive PTH production, and its clinical features. The document also covers hypoparathyroidism, which is a deficiency of PTH, and its signs, symptoms and treatment with calcium and vitamin D supplementation. In summary, the document outlines key endocrine disorders of the parathyroid glands, their effects on calcium levels, and management approaches for hyperparathyroidism and hypoparathyroidism.
This document discusses disorders of the parathyroid gland that result in hypercalcemia and hypocalcemia. It covers the physiology of calcium and phosphate homeostasis, the roles of parathyroid hormone (PTH) and vitamin D, and differentials for hyper- and hypocalcemia. Causes of hypoparathyroidism include DiGeorge syndrome and autoimmune polyglandular syndrome type 1. Pseudohypoparathyroidism is described as a genetic defect causing tissues to fail responding to PTH. Primary hyperparathyroidism is most often due to adenomas or hyperplasia while secondary and tertiary hyperparathyroidism occur in kidney disease.
Surgical diseases of the thyroid gland and parathyroid glandMD Specialclass
- The document discusses surgical diseases of the parathyroid glands, including primary hyperparathyroidism which is caused by inappropriately increased amounts of parathyroid hormone relative to calcium levels. The three histologic patterns are single adenoma, hyperplasia, and parathyroid carcinoma.
- Secondary hyperparathyroidism is caused by malfunction of another organ like the kidneys in chronic renal failure patients. Tertiary hyperparathyroidism is persistent hyperparathyroidism after the underlying disorder is resolved, such as after a successful kidney transplant.
- Surgery is the treatment for primary hyperparathyroidism and tertiary hyperparathyroidism, while treatment for secondary hyper
This document provides information on disorders of the parathyroid gland. It discusses the anatomy and histology of the parathyroid glands. It describes how parathyroid hormone is synthesized and its role in calcium regulation. It covers different types of hyperparathyroidism including primary, secondary, and tertiary. Primary hyperparathyroidism can be caused by adenomas, hyperplasia, or carcinoma. It discusses clinical manifestations, diagnosis, and differential diagnosis of primary hyperparathyroidism. It also covers hypercalcemia associated with other conditions like malignancy, immobilization, and familial hypocalciuric hypercalcemia.
The document discusses diseases of the parathyroid gland. It describes the structure and regulation of parathyroid hormone (PTH) secretion, including how calcium levels control PTH levels. It also discusses hyperparathyroidism, the most common form being primary hyperparathyroidism caused by a single adenoma or hyperplasia of the parathyroid glands leading to elevated PTH levels and hypercalcemia. Signs and symptoms include fatigue, weakness, kidney stones, and bone disease. The genetics and clinical manifestations of primary hyperparathyroidism are also summarized.
The parathyroid glands are small endocrine glands located near the thyroid gland that regulate calcium homeostasis. They secrete parathyroid hormone (PTH) which increases blood calcium levels. There are usually four parathyroid glands receiving blood supply from the inferior thyroid arteries. Primary hyperparathyroidism is most commonly caused by a single adenoma. Investigations for hypercalcemia include PTH and calcium levels. Treatment involves surgical removal of the affected gland(s), with preoperative localization using ultrasound or sestamibi scans to allow for minimally invasive surgery.
The parathyroid glands are small endocrine glands located on the thyroid gland that secrete parathyroid hormone (PTH) to regulate calcium levels. Primary hyperparathyroidism is usually caused by a solitary parathyroid adenoma. Pre-operative localization with sestamibi scanning is accurate for adenomas. Surgical treatment involves either unilateral or bilateral neck exploration to remove the abnormal gland(s), with minimally invasive radioguided parathyroidectomy being an option for localized disease.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
This document discusses disorders of the parathyroid gland including hypoparathyroidism and hyperparathyroidism. It describes various causes of hypoparathyroidism including genetic disorders, autoimmune disorders, surgical complications, and functional immaturity in infants. Symptoms include low calcium levels, muscle cramps, and seizures. Treatment involves calcium and vitamin D supplementation. Causes of hyperparathyroidism are also outlined such as tumors and genetic disorders. Symptoms include high calcium levels and bone abnormalities. Treatment is surgical removal of the overactive parathyroid gland.
This document summarizes parathyroid gland anatomy and physiology and various types of hyperparathyroidism. It discusses the role of parathyroid hormone in calcium homeostasis, causes of primary, secondary, and tertiary hyperparathyroidism, associated symptoms and complications, diagnostic testing, treatment options including medication and surgery, and other related conditions like familial benign hypercalcemia and hypercalcemia of malignancy.
This presentation is about Parathyroid Disorders which are hypo and hyperparathyroidism and their relationship to teeth and oral cavity including oral and dental manifestation of these disorders , and correct management patients seeking dental care with these disorders.
A 24-year-old female presented with abnormal body movements and was found to have hypocalcemia. Laboratory workup showed low serum calcium, high phosphorus, and normal parathyroid hormone. She was diagnosed with hypoparathyroidism and treated with calcium supplementation, resulting in symptom improvement. The cause was determined to be idiopathic hypoparathyroidism.
The document discusses parathyroid disorders including:
- The parathyroid glands' location and functions in regulating calcium levels by secreting parathyroid hormone.
- Primary hyperparathyroidism which is caused by adenomas, hyperplasia or carcinoma of the parathyroid glands and results in hypercalcemia.
- Hypoparathyroidism which is a deficiency of PTH that can be congenital or acquired after surgery and results in hypocalcemia.
- The diagnosis and treatment of both conditions including surgery, medication, and managing calcium levels.
<PARATHYROID HORMONES (The Calcium Regulating Gland)> first recognized in 1850 by Richard Owen.
<INTRODUCTION>Parathyroid glands are small glands of the endocrine system which are located in the neck behind the thyroid.><Called parathyroid due to proximity to the thyroid gland.><Yellowish brown, small ovoid bodies about 6 mm long, 3mm wide and 2mm thick.><Human being have 4 tiny parathyroid glands.><Each weighting around 30-50mg, but may weight as much as 70 mg, and in diameter is 3-4 or till 8 millimeters>
<Each parathyroid gland is made up of chief cells and oxyphil cells.><Chief cells more numerous, smaller, with a slightly eosinophilic cytoplasm.><secrete Parathyroid hormone (PTH). Also known as parathormone or parathyrin.>
<PARATHORMONE>Protein in nature (84 amino acids)><Molecular weight= 9,500.>< Half- life = 10 minutes><Normal plasma level of PTH = 1.5 to 5.5 ng/dL>
<SYNTHESIS OF AND SECRETION OF PARATHORMONE>PTH is encoded by a gene in chromosome 11><After translation, it become pre-pro-parathyroid hormone (pre-pro-PTH) contains 115 amino acids><In endoplasmic reticulum 29 amino acids removed, so it called pro-parathyroid hormone (pro-PTH) contains 89 amino acids><In the Golgi, removed more amino acids by peptidase to become mature hormone (PTH).><It is stored in secretory vesicles within the cells, and released when required>
<METABOLISM OF PTH>Half-life= 4 minute><60- 70 % of PTH is degraded by kupffer cells of liver, by means of proteolysis><Degradation of about 20-30% PTH occurs in kidneys and to a lesser extent in other organs>
<Half life – 4 min. How does PTH produce its effect on biological system?>
<REGULATION OF PARATHORMONE SECRETION>Regulators of secretion of PTH include calcium, vit D and phosphorus.>
<MECHANISM OF SECRETION OF PARATHORMONE> <CALCIUM-SENSING RECEPTORS (CaSR)><CaSR is a plasma membrane or a cell surface receptor, structured as G protein-coupled that is expressed in the parathyroid hormone-producing chief cells of the parathyroid gland and the cells lining the kidney tubule. (Hendy & et al., 2000)><PTH RECEPTORS>PTHR1 is physiologically more important than others two.><PTHR = 60-80 kDa membrane glycoprotein.>
<ACTION OF PTH>Important role in maintaining blood calcium level.>< Also controls blood phosphate level>
<DISORDERS OF PARATHORMONE.><increased pth secretion leads to an increase in serum levels by increasing bone resorption and enhancing renal calcium reabsorption. >
<3 TYPES>Primary hyperparathyroidism, Secondary hyperparathyroidism, Tertiary hyperparathyroidism.><The most common cause of hypercalcaemia is primary hyperparathyroidism>
The document outlines a seminar on disorders of the parathyroid glands presented by Ms. Gautami S. Tirpude. It discusses the general and specific objectives of gaining knowledge about parathyroid gland disorders and their application in nursing practice. The seminar covers topics like hyperparathyroidism and hypoparathyroidism including their definition, etiology, pathophysiology, clinical manifestations, diagnostic studies, and medical and surgical management. It also discusses the nursing role in managing related complications through various nursing interventions.
This document discusses diseases of the parathyroid gland, including its structure and functions in regulating blood calcium levels. The diseases are classified into hyperparathyroidism, hypothyroidism, and pseudohypoparathyroidism. Primary hyperparathyroidism is caused by autonomous overproduction of PTH, often due to a tumor. It can result in kidney stones, bone abnormalities, and other clinical issues. Hypothyroidism is a deficiency of PTH secretion and causes low calcium levels and tetany. Pseudohypoparathyroidism occurs when there is end-organ resistance to PTH despite normal levels.
This document discusses vitamin D and hyperparathyroidism. It notes that vitamin D is a fat-soluble vitamin that is converted to its active form in the kidney and regulates calcium levels. Hyperparathyroidism occurs when the parathyroid glands overproduce parathyroid hormone (PTH), which regulates calcium levels. There are three types: primary (excess PTH from parathyroid glands), secondary (increased PTH to compensate for hypocalcemia), and tertiary (PTH secretion becomes unregulated even after correcting the underlying cause). The document outlines the causes, clinical features, investigations, and treatments for each type of hyperparathyroidism.
The document discusses the parathyroid glands, which regulate calcium and phosphate levels and produce parathyroid hormone (PTH). It describes hyperparathyroidism and hypoparathyroidism, conditions caused by excessive or deficient PTH respectively, and their symptoms, causes, assessments, and treatment including diet modifications and medications. Surgical removal of the parathyroid glands may be required to treat hyperparathyroidism.
The parathyroid glands secrete parathyroid hormone (PTH) which regulates calcium levels. PTH increases bone resorption and calcium absorption from the gut while decreasing calcium excretion by the kidneys. Hyperparathyroidism is an increased secretion of PTH and can be primary, secondary, or tertiary. Primary hyperparathyroidism is usually caused by a single adenoma and presents with increased serum calcium levels and bone, kidney, or gastrointestinal problems. Imaging tests can locate enlarged parathyroid glands and surgery is the treatment of choice for removing adenomas or hyperplastic glands.
Case presentation of primary hyperparathyroidismHaifa Alshwikh
This case presentation describes a 44-year-old woman who presented with left hip pain and was found to have hypercalcemia. The differential diagnosis for her hypercalcemia includes primary hyperparathyroidism, familial hypocalciuric hyperparathyroidism, and tertiary hyperparathyroidism. She underwent laboratory testing which showed elevated PTH, consistent with primary hyperparathyroidism. Localization testing with sestamibi scan and ultrasound were recommended to help guide minimally invasive parathyroidectomy.
The document discusses disorders of the parathyroid glands. It describes how parathyroid hormone (PTH) regulates calcium and phosphate levels in the blood by stimulating bone resorption and calcium reabsorption in the kidneys. PTH also stimulates vitamin D production, which increases calcium absorption in the intestines. Disorders discussed include hyperparathyroidism, hypoparathyroidism, and hypercalcemia of malignancy. Treatment involves managing calcium levels, identifying and removing tumors, and replacing hormones.
Calcium and phosphorus metabolism are regulated by hormones like calcitriol, parathyroid hormone, and calcitonin to maintain normal levels in the body. Calcium is important for bone health, muscle function, and other cellular processes. The majority of calcium is stored in bones. Phosphorus also has important roles in energy storage and cellular processes. Both are absorbed in the small intestine and levels are regulated by hormones and excretion through the kidneys. Abnormal levels can cause diseases like rickets, osteomalacia, and osteoporosis. Dental issues may also arise from metabolic bone diseases like brown tumors and osteitis deformans.
This document summarizes calcium homeostasis and disorders of calcium metabolism. It discusses that calcium is critical for numerous biological functions and exists in serum in ionized, protein-bound, and complexed forms. Hypocalcemia can result from hypoalbuminemia, hypoparathyroidism, pseudohypoparathyroidism, or hypomagnesemia. Symptoms include tetany, seizures, and Trousseau's sign. Treatment involves calcium and vitamin D supplementation. Hypercalcemia can be caused by primary hyperparathyroidism or malignancy. Symptoms include polyuria, nausea, and kidney stones. Evaluation involves measuring PTH and localizing an abnormal parathyroid gland with sestamibi
1. Parathyroid hormone (PTH) plays a key role in regulating calcium and phosphate levels. It stimulates bone resorption and calcium reabsorption in the kidney to increase calcium levels.
2. PTH also stimulates vitamin D production, which then increases calcium absorption in the intestines.
3. Hypercalcemia can be caused by primary hyperparathyroidism or certain cancers that produce PTH-related protein. Hypocalcemia is commonly caused by hypoparathyroidism after thyroid surgery.
Hypercalcemia is commonly caused by primary hyperparathyroidism or malignancy. It can be life-threatening in severe cases. Diagnosis involves measuring serum calcium, PTH, and assessing for underlying causes. Treatment depends on the underlying condition but may involve surgery for hyperparathyroidism or addressing the malignancy. Complications can impact the kidneys, GI tract, cardiovascular system, muscles and bones.
Tubular disorders of kidney REVISION NOTESTONY SCARIA
This document discusses various tubular disorders of the kidney. It begins by describing autosomal dominant polycystic kidney disease (ADPKD), noting its genetic causes and characteristic late age of onset and progression. Symptoms of ADPKD include flank pain, hypertension, hematuria and urinary infections appearing in the third or fourth decade. It then discusses autosomal recessive polycystic kidney disease (ARPKD), medullary sponge kidney disease, nephronophthisis, multicystic renal dysplasia and other tubular disorders. It provides details on acute kidney injury including causes, pathogenesis, clinical features and management. It also discusses specific conditions like cystinuria, cystinosis and hyper
1. Disorders of the parathyroid glands involve abnormalities in the regulation of calcium and phosphate levels by parathyroid hormone (PTH). Hyperparathyroidism and hypoparathyroidism can both lead to changes in calcium levels.
2. Hyperparathyroidism is most commonly caused by a single parathyroid adenoma and results in elevated PTH and calcium levels. It can cause symptoms of bone loss, kidney stones, and abdominal pain. Hypoparathyroidism results from low PTH levels and causes low calcium levels and symptoms of muscle spasms.
3. Diagnosis involves measuring calcium and PTH levels, and imaging tests may be used to locate parathy
The document discusses disorders of calcium metabolism. It presents two clinical scenarios: a 59-year-old woman with hypercalcemia found on labs during a routine visit, and a 9-year-old boy admitted to the emergency department with acute pancreatitis and hypocalcemia after falling off his bike. It then outlines topics like the different forms of calcium, calcium homeostasis, regulation of calcium metabolism by parathyroid hormone, vitamin D, and calcitonin, and disorders like hypercalcemia, hypocalcemia, hyperparathyroidism, and hypoparathyroidism.
This document discusses calcium homeostasis and hypercalcemia. It notes that approximately 99% of calcium in the body is stored in bones and teeth, with the remaining 1% distributed in the extracellular fluid, intracellular fluid, and soft tissues. Hypercalcemia is defined as a serum calcium level above 10.5 mg/dL. Causes include primary hyperparathyroidism in about 50% of cases of hypercalcemia, as well as malignancy, vitamin D toxicity, hyperthyroidism, and certain genetic conditions. Symptoms range from being mild or absent with mild increases in calcium to severe symptoms like confusion and coma with rapid or large rises in calcium levels.
This document discusses disorders of the parathyroid glands. It covers the role of parathyroid hormone (PTH) in regulating calcium and phosphate levels through effects on bone, kidney and intestines. It describes hypercalcemia and hypocalcemia, their causes, signs/symptoms, and management. Hyperparathyroidism, hypoparathyroidism, and pseudohypoparathyroidism are discussed in detail including their genetics, clinical features, investigations and treatment.
The document discusses calcium homeostasis and hypercalcemia. It provides details on:
- Calcium distribution in the body, with 99% located in bones and teeth.
- Intestinal and renal handling of calcium and the roles of TRPV5 channel and calbindin D28k protein.
- Causes of hypercalcemia including primary hyperparathyroidism, malignancy, and vitamin D excess.
- Presentation of hypercalcemia ranging from asymptomatic to severe symptoms like confusion.
- Workup and treatment of hypercalcemia depending on its underlying cause and severity.
Calcium & phosphorus metabolism and its applied aspectsdrshyam222
This document summarizes calcium and phosphorus metabolism. Calcium is essential for bone structure, nerve function, muscle contraction and more. The body tightly regulates calcium levels through hormones like PTH and calcitriol. Disorders occur when levels are too high or low, impacting bones, kidneys and other organs. Phosphorus also has key roles and is regulated similarly, with deficiencies or excesses also causing health issues. A variety of diseases like rickets, osteomalacia and osteoporosis result from imbalances in calcium and phosphorus metabolism.
This document discusses hypercalcemia and hypocalcemia, including their causes, symptoms, and management. Hypercalcemia can be caused by hyperparathyroidism, certain malignancies, vitamin D toxicity, and other conditions. Symptoms range from none in mild cases to fatigue, nausea, and cognitive issues in severe cases. Treatment focuses on rehydration, bisphosphonates, calcitonin, surgery, and addressing the underlying cause. Hypocalcemia is usually asymptomatic but can cause tingling and seizures in severe cases. It is often caused by hypoparathyroidism, vitamin D deficiency, or tumor lysis syndrome. Treatment involves calcium and vitamin D supplementation to address the deficiency. Laboratory tests are important to
- Disorders of the parathyroid glands can lead to abnormalities in calcium homeostasis. The main hormones involved are parathyroid hormone (PTH) and calcitonin, which work in opposition to maintain normal calcium levels.
- Primary hyperparathyroidism is caused by excessive PTH from overactive parathyroid glands. This disrupts the normal feedback inhibition and leads to hypercalcemia. It is usually treated with surgical removal of the affected gland(s).
- Medical treatments for hypercalcemia aim to increase calcium excretion and inhibit bone resorption through hydration, diuretics, calcitonin, bisphosphosphonates, and glucocorticoids in some cases
Hypercalcemia is a common condition seen in up to 4% of hospitalized patients. The most common causes are primary hyperparathyroidism and malignancy-associated hypercalcemia. Hypercalcemia occurs when calcium influx into the extracellular fluid exceeds renal excretory capacity. It is defined as a total serum calcium level greater than 10.2 mg/dL. Treatment involves stabilizing the patient with intravenous fluids, promoting calcium excretion with diuretics, and administering bisphosphonates to reduce bone resorption in malignancy-associated cases. Surgical removal of parathyroid adenomas is required for symptomatic primary hyperparathyroidism.
This document discusses hypercalcemia, which is defined as a serum calcium level above 10.5 mg/dl. It outlines the causes of hypercalcemia including primary hyperparathyroidism, certain cancers, and excessive vitamin D or calcium supplementation. Signs and symptoms are noted such as abdominal pain, nausea, weakness and cardiac issues. Diagnostic testing including PTH, calcium, and phosphate levels as well as imaging are covered. Treatment focuses on rehydration, bisphosphonates, glucocorticoids, calcitonin, surgery if needed, and addressing the underlying cause. Complications of untreated hypercalcemia include osteoporosis, kidney stones, and kidney failure.
Calcium metabolism can be disrupted, resulting in hypercalcemia or hypocalcemia. Hypercalcemia is caused by increased bone resorption, GI absorption, or decreased renal excretion and may be due to primary hyperparathyroidism, certain cancers, or excessive vitamin D intake. Hypocalcemia occurs when ionized calcium levels decrease below normal due to hypoparathyroidism, vitamin D deficiency, or other conditions. Symptoms of hypercalcemia include fatigue, nausea, and renal problems while hypocalcemia causes muscle spasms, tingling, and seizures. Treatment depends on the underlying cause and severity but aims to restore normal calcium levels through rehydration, diuretics, bisphosphonates
Tumor lysis syndrome and hypercalcemia of malignancyGaurav Kumar
This document discusses hypercalcemia and tumor lysis syndrome. It defines hypercalcemia as calcium levels above normal physiological range. The main causes of hypercalcemia include parathyroid disorders, malignancy, vitamin D abnormalities, and renal failure. Symptoms range from mild to severe depending on calcium level. Tumor lysis syndrome occurs when large numbers of cancer cells break down rapidly, releasing electrolytes. This can cause hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, potentially leading to renal failure. The document outlines evaluation, treatment and prevention of both conditions.
The document provides a history and overview of parathyroid glands and diseases of the parathyroid glands. It discusses that in 1849, Sir Richard Owen first accurately described normal parathyroid glands. In 1879, tetany was described in a patient after thyroidectomy and parathyroid glands were first microscopically identified. Primary diseases discussed include primary hyperparathyroidism, caused by increased PTH secretion independent of calcium levels, and hypoparathyroidism, caused by PTH deficiency resulting in hypocalcemia. Surgical treatment of diseases like parathyroid adenomas and management of complications are summarized.
Mucormycosis is a rare but aggressive fungal infection caused by fungi of the class Zygomycetes, including Rhizopus, Mucor, and Absidia. It mainly affects immunocompromised patients or those with uncontrolled diabetes. The fungi thrive in high glucose, acidic conditions. Common forms include rhinocerebral affecting the sinuses and orbit, pulmonary, gastrointestinal, cutaneous from skin injuries, and disseminated infection of multiple organs. Diagnosis involves tissue biopsy and culture. Treatment requires intravenous amphotericin B antifungal therapy and surgical debridement of infected tissues.
- The document discusses histograms generated by cell counters that graphically represent cell population data. It focuses on histograms for red blood cells (RBCs), white blood cells (WBCs), and platelets.
- Key parameters for each type of histogram are defined, such as how cells are counted and measured, normal ranges, and flags that indicate potential issues. Common causes for shifts or abnormalities in the histograms are also outlined.
- The information provides guidance on interpreting cell counter histograms and histograms to help evaluate a patient's blood cell counts and detect possible blood disorders or interferences.
Magnesium is an important intracellular cation that plays a key role in many cellular processes. Hypomagnesemia can result from reduced intake, malabsorption, renal losses due to drugs or conditions like Gitelman syndrome, while hypermagnesemia commonly occurs in renal failure or with magnesium-containing drugs. Both conditions can impact neuromuscular and cardiac function. Treatment of hypomagnesemia involves oral or IV magnesium supplementation while hypermagnesemia may require calcium, diuretics, or dialysis. Magnesium levels also influence PTH secretion and activity.
Special senses physiology revison topics TONY SCARIA
Rods and cones are the photoreceptive cells in the retina. Rods are more abundant than cones and are responsible for vision in low light levels. Cones are involved in color vision and are concentrated in the fovea. The retina contains approximately 120 million rods and 6 million cones. Signals from the photoreceptors are transmitted through the optic nerve, composed of approximately 1 million fibers, to the optic chiasm and lateral geniculate nucleus before reaching the visual cortex. Lesions of the optic chiasm can cause bitemporal hemianopia while lesions of the visual cortex can cause macular sparing.
CSF PHYSIOLOGY ANALYSIS NORMAL AND DISEASE TONY SCARIA
Cerebrospinal fluid is produced by the choroid plexus in the ventricles and circulates through the subarachnoid space around the brain and spinal cord. It is absorbed by arachnoid villi into venous blood. CSF turnover is approximately 3.7 times per day and pressure is normally maintained between 60-180 mmH2O by a balance of production and absorption. Elevated intracranial pressure can cause headache, impaired consciousness, papilledema and herniation syndromes. Treatment involves managing fluid balance, hyperventilation, osmotherapy and surgery in severe cases. Lumbar puncture analysis examines CSF opening pressure, composition and cytology to diagnose central nervous system infections
The plantar reflex is an important superficial reflex that involves polysynaptic pathways. A normal plantar reflex results in flexion of the toes when the sole is scratched, while an extensor plantar response (Babinski's sign) involves dorsiflexion of the great toe and fanning of the other toes and suggests corticospinal tract dysfunction. There are several methods to elicit the plantar reflex and variations in responses provide information about neurological conditions.
This document discusses parvovirus B19, which is a single-stranded DNA virus that causes fifth disease or slapped cheek appearance. It has the smallest viral genome and can cause aplastic crisis in children with chronic hemolytic anemia or arthralgia and arthritis in adults. Transplacental transmission occurs in 30% of cases and can result in nonimmune fetal hydrops.
Deep neck space infection ENT REVISION NOTES TONY SCARIA
This document summarizes different types of deep neck space infections including peritonsillar abscess, parapharyngeal abscess, retropharyngeal abscess, and Ludwig's angina. It describes the etiology, clinical features, examination findings, complications, and treatment for each type of infection. Key information provided includes the most common causative bacteria for each infection, symptoms like pain, swelling and difficulty swallowing, examination findings of swollen areas, and treatments involving antibiotics, incision and drainage, or tracheostomy if the airway is compromised.
Antirheumatic drugs & anti gout drugs PHARMACOLOGY REVISION NOTES TONY SCARIA
This document summarizes various drugs used to treat rheumatoid arthritis and gout. It describes disease-modifying antirheumatic drugs (DMARDs) like methotrexate, hydroxychloroquine, leflunomide, d-penicillamine, gold salts, and biological response modifiers that target TNF-α, IL-1, IL-6, and T cells. It also discusses corticosteroids, NSAIDs, and drugs for acute and chronic gout including colchicine, allopurinol, febuxostat, probenecid, and drugs that increase uric acid metabolism like rasburicase and pegloticase.
This document discusses various types of eye trauma including open globe injuries, closed globe injuries, and injuries to specific structures within the eye. It provides details on blunt and penetrating trauma, complications like sympathetic ophthalmia, investigations like water's view, and foreign bodies involving metals like iron and copper. Trauma can cause injuries to the cornea, iris, lens, retina, and other structures and may lead to complications such as cataracts, glaucoma, or phthisis bulbi if not properly treated.
This document discusses the anatomy and surgical procedures related to the orbit. It describes the bones that form the medial, lateral, roof and floor of the orbit. It also discusses the openings of the orbit like the superior and inferior orbital fissures. Common causes of proptosis in children and adults are listed. Surgical procedures like enucleation, evisceration and exenteration are described along with their indications. The document provides a comprehensive overview of the orbit anatomy and orbital surgeries.
Vision 2020 is a global initiative to eliminate preventable blindness by 2020. It targets diseases like cataract, refractive errors, childhood blindness, trachoma, and onchocerciasis globally. In India, it also focuses on glaucoma, corneal opacity, and diabetic retinopathy. The program implements a 4-tier system of primary vision centers, secondary service centers, tertiary training centers, and centers of excellence. Onchocerciasis is not included for India since it is not prevalent, and epidemic conjunctivitis is excluded globally and nationally. Cataract is the major cause of blindness in India. School screening programs help identify and refer children who cannot read certain lines to community health centers
The document summarizes information about the structure and function of the lens and different types of cataracts. It notes that the lens has a refractive index of 1.386 and refractive power of 14-16 D. It is avascular and composed of tightly packed lens fibers without organelles. Transport of water and glycerol is mediated by aquaporins like AQP0. Increased amounts of insoluble proteins and HMW3&4 contribute to cataract formation. Different types of cataracts discussed include congenital, developmental, cortical, nuclear, posterior subcapsular, and Christmas tree cataract. Pioneers in cataract surgery mentioned are Sir Harold Ridley and Charles Kelman.
Uvea consists of the iris, ciliary body, and choroid. Uveitis refers to inflammation of the uveal tract. It can be classified anatomically as anterior, intermediate, or posterior depending on the location of inflammation. Clinically it is classified as acute or chronic based on duration of symptoms. Infectious causes include bacteria, viruses, fungi and parasites. Anterior uveitis presents with eye pain, photophobia, and hypopyon may be seen on examination. Posterior uveitis can lead to complications like exudative retinal detachment. Treatment involves topical steroids and immunosuppressants depending on severity and cause of uveitis.
This document discusses several childhood tumors. It begins by focusing on retinoblastoma, noting that it is the most common ocular tumor in children under 5 years old. It then discusses various characteristics, presentations, histological findings, treatments and prognosis. The document then discusses neuroblastoma, noting it is a common abdominal tumor in infants. It provides details on characteristics, sites of occurrence, metastasis patterns, treatments and prognosis. Finally, it briefly discusses acute lymphoblastic leukemia, noting it is the most common childhood leukemia. It compares subtypes and provides information on characteristics, treatments and prognosis factors.
This document discusses various topics in genetics and genomics including:
- Genome and genomics, which refers to the study of the entire genetic content of an individual.
- Karyotyping techniques used to analyze chromosomes such as G-banding and C-banding.
- Types of genetic variation like single nucleotide polymorphisms and copy number variations.
- Non-coding RNAs including microRNAs and long non-coding RNAs that regulate gene expression.
- Different patterns of inheritance for genetic disorders like autosomal dominant, autosomal recessive, and X-linked inheritance.
- Examples of genetic disorders and their inheritance patterns including Marfan syndrome, Ehlers-Danlos syndrome, and Fabry disease
The document discusses various topics related to pathology including causes of cell injury, hypoxia, cellular adaptive responses, mechanisms of cell injury, features of reversible and irreversible injury, necrosis, apoptosis, calcification, pigmentation, and cellular aging. The key points are:
1. Hypoxia is the most common cause of cell injury, usually due to ischemia. Neurons are the most susceptible tissue to hypoxic damage.
2. Cellular adaptive responses to injury include atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia.
3. Apoptosis is an active and programmed form of cell death, while necrosis is unprogrammed cell death due to severe injury
Morphology of bacteria revision notes microbiologyTONY SCARIA
This document appears to be notes from a lecture or textbook on microbiology. It covers several topics related to bacterial structure and function, including:
- The types of microorganisms (bacteria, archaea, fungi, etc.)
- Bacterial cell structure, including the cell membrane, cell wall, flagella, and pili.
- Mechanisms of gene transfer between bacteria, such as transformation, transduction, conjugation, and transposition. Plasmids and bacteriophages are discussed in the context of horizontal gene transfer.
- Production of exotoxins and endotoxins by bacteria and their differences.
- Mechanisms of antibiotic resistance in bacteria, including
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
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.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
DECLARATION OF HELSINKI - History and principlesanaghabharat01
This SlideShare presentation provides a comprehensive overview of the Declaration of Helsinki, a foundational document outlining ethical guidelines for conducting medical research involving human subjects.
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
3. • Normal calcium level in the body
• Normal serum Ca = 9 – 11 mg%,
• Ionized Ca = 50%,
• Ca bound to protein = 40%,
• Ca bound to anions - 10%
TONY SCARIA 2010 KMC
5. ALP is raised in conditions a/w increased
osteoblastic activity
Raised ALP (d/t osteoblastic activity) ALP is normal in
• Paget disease,
• Bone metastases,
• Rickets, osteomalacia*,
• osteoporosis and
• multiple myeloma
TONY SCARIA 2010 KMC
6. Action of PTH
• ↑osteoclast activity releasing Ca2+ & phosphate from bones
• ↑Ca2+ & ↓phosphate reabsorption in the kidney;
• ↑Active 1,25 dihydroxy-vitamin D3 production
TONY SCARIA 2010 KMC
7. Primary hyperparathyroidism Secondary hyperparathyroidism Tertiary hyperparathyroidism
• Autonomous secretion of PTH,
usually by a single parathyroid
adenoma
• physiological increase in PTH
secretion to compensate for
prolonged hypocalcaemia (such
as in vitamin D deficiency)
continuous stimulation of the
parathyroids over a prolonged
period of time
adenoma formation and
autonomous PTH secretion
TONY SCARIA 2010 KMC
10. Primary hyperparathyroidism
• ↑Ca, ↓PO4, ↑PTH
• The most common cause of primary hyperparathyroidism is
parathyroid solitary adenoma.
• A single solitary abnormal gland is the cause of approximately 80% of patients
• Adenomas are most often located in the inferior parathyroid gland.
• Chief cells are predominant in both hyperplasia and adenoma.
• The abnormality of the gland is usually a benign neoplasm or adenoma and
rarely a parathyroid carcinoma.
TONY SCARIA 2010 KMC
11. Types of primary hyperparathyroidism
Sporadic Familial
Most common type Less common
• Cyclin D1 gene inversions leading to
overexpression of cyclin D1
• MEN1 mutations
• Multiple Endocrine Neoplasia, type 1 (MEN1 gene
on chromosome 11
• Multiple Endocrine Neoplasia, type 2(RET gene on
chromosome 10
• familial hypocalciuric hypercalcemia autosomal
dominant disorder caused by loss-of-function
mutations in the parathyroid calcium-sensing
receptor gene (CASR), which results in decreased
sensitivity to extracellular calcium
TONY SCARIA 2010 KMC
12. CF
• bones, stones and abdominal groans
• PTH-induced hypercalcemia favors formation of urinary tract stones
(nephrolithiasis) as well as calcifcation of the renal interstitium
and tubules (nephrocalcinosis)
TONY SCARIA 2010 KMC
13. Brown tumour in primary
hyperparathyroidism
• Osteitis fibrosa cystica
• Bone loss predisposes to microfractures and secondary
hemorrhages that elicit an influx of macrophages and an
ingrowth of reparative fibrous tissue, creating a mass
of reactive tissue, known as a brown tumor
TONY SCARIA 2010 KMC
18. Radiological features of primary
hyperparathyroidism
• Irregular diffuse rarefaction of bone
• Salt & pepper appearance of skull
• Subperiosteal resorption of phalanges
• Multiple cyst in pelvis & other bones
• Brown tumour
TONY SCARIA 2010 KMC
19. Salt & pepper appearance of skull
TONY SCARIA 2010 KMC
24. Cod fish spine
Intervertebral disk becomes
ballooned as they indent soft
vertebral bodies forming the
'Cod Fish spine
TONY SCARIA 2010 KMC
25. To localise adenoma
• 99_Tc sestamibi scan.
• After one hour of injection, uptake is done by both thyroid and parathyroid
gland.
• After 3 hrs uptake evidence is there only in parathyroid. So by computer
subtraction adenoma is located.
TONY SCARIA 2010 KMC
26. Indications for surgical removal of adenoma
• individuals aged less than 50 years,
• with clear-cut symptoms or documented complications (such as
peptic ulceration, renal stones, renal impairment or osteoporosis),
• (in asymptomatic patients) signifcant hypercalcaemia (corrected
serum calcium > 2.85 mmol/L (> 11.4 mg/dL))
TONY SCARIA 2010 KMC
30. CKD
Decrease in GFR
Increased phosphate
load in blood
Defective conversion of 25hydroxyvitamin D
to its active metabolite,1,25-
dihydroxyvitamin D,
• due in part to renal tubular cell damage
• elevated FGF23 levels
hypocalcaemia
increased PTH production by the parathyroid glands
Elevated FGF23
The FGF23 promotes
phosphate excretion,
thereby compensating in
part for the reduced
glomerular fltration of
phosphate.
TONY SCARIA 2010 KMC
32. • Rugger Jersey spine is
seen in CRF
• d/t 2*
hyperparathyroidism
TONY SCARIA 2010 KMC
33. Secondary hyperparathyroidism
• In CRF
• Ca2+↓
• PTH↑
• ↑PO4
• In malnutrition, ricket osteomalacia
• Ca↓
• PTH ↑
• ↓ PO4
TONY SCARIA 2010 KMC
34. TERTIARY HYPERPARATHYROIDISM
• Occurs after prolonged secondary hyperparathyroidism, causing
glands to act autonomously having undergone hyperplastic or
adenomatous change.
• This causes Ca2+ from secretion of PTH unlimited by feedback
control. Seen in chronic renal failure.
TONY SCARIA 2010 KMC
36. Malignant hyperparathyroidism
• Hypercalcemia in malignancy occur due to increase level of PTHrp. In
this PTH level are not raised
• Parathyroid-related protein (PTHrp)
• squamous cell lung cancers,
• breast
• renal cell carcinomas
TONY SCARIA 2010 KMC
40. Nephrogenic DI in hypercalcemia
• Polyuria results from effect of hypercalcemia on renal tubules
reducing their concentrating ability, a form of nephrogenic diabetes
insipidus
TONY SCARIA 2010 KMC
46. CF
• Mild
• Asymptomatic
• vague neuropsychiatric symptoms
• Trouble concentrating, personality changes, or depression
• peptic ulcer disease
• Nephrolithiasis
• nausea, anorexia, constipation, or pancreatitis
• NEPHROGENIC DI
• POLYURIA POLYDYPSIA
• electrocardiographic changes
• bradycardia, AV block, and short QT intervalTONY SCARIA 2010 KMC
47. Mx of A/C hypercalcemia
Mild hypercalcemia • Adequate hydration
Severe hypercalcemia (13-15mg/dl) • IV 0.9% saline 2–4 L/day
• use of loop diuretics to enhance sodium and
calcium excretion
• Zoledronic acid 4 mg IV or pamidronate 60–90 mg
IV
• IM/SC calcitonin 100 U 3 times daily for frst 24–48
hours in life-threatening hypercalcaemia
TONY SCARIA 2010 KMC
48. Management of c/c hypercalcemia
• Bisphosphonates
• Glucocorticoids :
• Effective in particular situations such as Vitamin D intoxication, Sarcoidosis,
Malignancy
• Calcitonin
• Phosphate*:
• 5. *Dialysis* - Quick and effective and is likely to be needed in
• severe cases with renal failure
• 6. *Plicamycin*
• 7. *Gallium Nitrate*
TONY SCARIA 2010 KMC
49. Cinacalcet
• Cinacalcet
• calcimimetic which enhances
the sensitivity of the calcium-
sensing receptor, so reducing
PTH levels, and is licensed for
tertiary hyperparathyroidism
and as a treatment for patients
with primary
hyperparathyroidism who are
unwilling to have surgery or are
medically unft
TONY SCARIA 2010 KMC
50. Familial hypocalciuric hypercalcemia
• AD
• Loss of function mutation of CaSR gene resulting in decreased
sensitivity to extracellular calcium increased PTH secretion
increased renal absorption of ca2+
TONY SCARIA 2010 KMC
53. Primary (due to gland
failure)
Secondary Pseudohypoparathyroidism Pseudopseudohypoparathyr
oidism
• Infantile
hypoparathyroidism: It is
associated with thymic
aplasia (Di George
syndrome)
• Idiopathic (Autoimmune)
(associated with other
autoimmune disorders),
• Post operative : surgery
(thyroidectomy).
• Post radio iodine therapy
• Hypomagnesemia – (Mg
is required for PTH
secretion)
It is a group of disorders
characterized by
hypocalcemia due to renal
resistance to PTH.
PTH levels are high.
Various phenotypic
abnormalities may be
associated—classically,
short stature, round face,
obesity, short fourth
metacarpals,ectopic bone
formation, and mental
retardation. *Cataract*.
Treatment is same as for
primary
Patients without
hypocalcemia but sharing
the phenotypic
abnormalities (as of
pseudohypoparathyroidism).
These patient have normal
serum calcium and high
serum PTH. In
pseudohypoparathyroidism,
defect lies at PTH receptor
level. While in pseudo
pseudohypoparathyroidism
defect lies at gene
transcription level beyond
the PTH receptors.
TONY SCARIA 2010 KMC
62. • females affected by either PHP-Ia or PPHP will have offspring with
PHP-Ia, if these children inherit the allele carrying the GNAS
mutation; in contrast, if the mutant allele is inherited from a male
affected by either disorder, the offspring will exhibit PPHP
TONY SCARIA 2010 KMC
63. PHP Ia PPHPP PHP Ib PHP II
• hypocalcemia due to
renal resistance to PTH.
• PTH levels are high.
• normal serum calcium
and high serum PTH
hypocalcemia and
hyperphosphatemia
Elevated serum PTH
• Epigenetic mutation in
Gsα allele from mother
• Epigenetic mutation in
Gsα allele from father
• there is reduced
synthesis of cAMP in
response to PTH so
there is no appropriate
increase in the urinary
cAMP occurs
• there is increased
synthesis of cAMP in
response to PTH so
there is increase in the
urinary cAMP occurs
Decreased cAMP release Normal cAMP in urine
• Albert hereditary
osteodystrophy
• Albert hereditary
osteodystrophy
TONY SCARIA 2010 KMC
64. • Pseudopseudohypoparathyroidism (PPHP)
• Patients without hypocalcemia but sharing the phenotypic abnormalities (as
of pseudo hypoparathyroidism)
• Serum PTH is normal
• Serum Ca2+ PO4 is normal
TONY SCARIA 2010 KMC
68. Chvostek’s sign
Chvostek’s sign (twitching of the circumoral
muscles in response to gentle tapping of the facial nerve just
anterior
to the ear)
TONY SCARIA 2010 KMC
69. Carpal spasm may be induced by inflation of a blood
pressure cuff to 20 mmHg above the patient’s systolic blood
pressure for 3 min (Trousseau’s sign)
TONY SCARIA 2010 KMC
71. Tetany
• Increase excitability of peripheral nerve due either to a low serum
calcium or low serum magnesium or alkalosis
Low serum Ca2+ Low serum Mg2+ Alkalosis
• Malabsorption
• Osteomalacia
• Hypoparathyroidism
• Acute pancreatitis
• Repeated vomiting
• Hyperventilation
• Primary
hyperaldosteronism
TONY SCARIA 2010 KMC
72. • In CRF, Hypocalcemia is a feature but tetany does not occurs due to
acidosis which prevents tetany
TONY SCARIA 2010 KMC
73. • In children
• Carpopedal spasm
• Stridor
• Convulsions.
• In adults
• Tingling sensation in the hands,
feet and around the mouth.
• Carpopedal spasm (Main
d’accoucheur position)
TONY SCARIA 2010 KMC
74. • Latent tetany signs are
• 1. Trousseau’s sign
• 2. Chvostek sign
TONY SCARIA 2010 KMC
75. • Treatment of tetany
• Injection calcium gluconate I/V
• In case of persistent vomiting – I/V saline
• In hyperventilation – Re breath from same bag
TONY SCARIA 2010 KMC
77. • Normal serum magnesium = 1.5 to 2.3 mg
TONY SCARIA 2010 KMC
78. • Magnesium is required for PTH secretion and for PTH action
TONY SCARIA 2010 KMC
79. • Serum Ca and Serum Mg level always go parallel in the body.
• The notable exceptions
• CRF (Hypocalcemia and Hypermagnesemia),
• Gitelman syndome (Normocalcemia and hypomagnesemia)
TONY SCARIA 2010 KMC
80. • Causes of hypomagnesemia
• 1. Reduce intake especially common in alcoholic patient and on TPN
• 2. GI losses - chronic diarrhea
• 3. Kidney loss – diuretics, Gitelman syndrome.
• 4. Acute pancreatitis
• 5. Drugs - Foscarnet (It is an anti herpes group of drug used generall in zoster
ophthalmitis).
TONY SCARIA 2010 KMC
85. CF
• Occur due to vasodilatation and neuromuscular blockage.
• There is paradoxical Bradycardia, Hypotension, Altered sensorium,
respiratory depression
TONY SCARIA 2010 KMC