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
This document discusses calcium homeostasis and hypercalcemia. It notes that calcium is critical for many physiological functions and is mainly stored in bones. Hypercalcemia can be caused by primary hyperparathyroidism, vitamin D excess, certain malignancies, and other conditions. The diagnostic approach involves distinguishing between hyperparathyroidism and hypercalcemia of malignancy based on lab tests. Treatment focuses on rehydration, increasing calciuresis, and decreasing bone resorption or intestinal calcium absorption using medications like calcitonin, bisphosphonates, glucocorticoids, or dialysis depending on the severity of hypercalcemia.
This document discusses hypokalemia, defined as a serum potassium level below 3.6 mEq/L. It notes that potassium is critical for nerve impulse transmission and muscle function. The major causes of hypokalemia include decreased intake, intracellular shifts, non-renal losses like vomiting/diarrhea, and renal losses due to drugs like diuretics. Clinical features range from muscle weakness to cardiac arrhythmias. Diagnosis involves evaluating electrolytes, ECG changes, urine studies, and considering underlying causes. Treatment focuses on replacing potassium losses and correcting the underlying etiology.
This document discusses hypercalcemia and hypocalcemia. It defines hypercalcemia as a serum calcium level above 10.1 mg/dL and lists various causes including excessive PTH production, hypercalcemia of malignancy from PTHrP or bone metastases, excessive vitamin D production, and increased bone resorption. Symptoms can include neuropsychiatric issues, GI symptoms, ECG changes, and kidney stone formation. Evaluation involves correcting for albumin and measuring PTH to determine the cause. Treatment depends on the underlying condition but may include IV fluids, bisphosphonates, glucocorticoids, or gallium nitrate. Hypocalcemia is then discussed, outlining causes such as hy
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.
This document defines hypercalcemia and discusses its causes, evaluation, clinical presentation, and management. The main causes are parathyroid hormone dependent (primary hyperparathyroidism, tertiary hyperparathyroidism) and independent (malignancy, vitamin D related, endocrinopathies). Evaluation involves history, exam, and labs. Acute management is rehydration and medications to increase calcium excretion. Long term management depends on the underlying cause and may involve surgery, bisphosphonates, glucocorticoids, or ketoconazole.
Hypocalcemia has various presentations and can lead to significant morbidity if left untreated. The most common cause is hypoalbuminemia from conditions like cirrhosis or malnutrition that lower serum calcium levels. Other potential causes include vitamin D deficiency, parathyroid issues, medications, and critical illnesses like sepsis. Treatment involves identifying and addressing the underlying cause, as well as replacing calcium, often intravenously, to resolve symptoms and normalize calcium levels. Calcium levels must be closely monitored during treatment until stabilized.
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.
Hypercalcemia was causing the patient's acute renal failure. Treatment for hypercalcemia included intravenous fluids, furosemide, steroids, bisphosphonates, and dialysis which lowered the calcium levels and improved renal function. The underlying cause of hypercalcemia could not be determined after extensive testing, but was likely a malignancy given the persistent pancytopenia. Hypercalcemia can directly damage the kidneys by decreasing medullary osmolality and inducing nephrogenic diabetes insipidus, nephrolithiasis, and renal tubular acidosis. It also causes vasoconstriction and activation of the calcium-sensing receptor which stimulates renin release and worsens volume
This document discusses calcium homeostasis and hypercalcemia. It notes that calcium is critical for many physiological functions and is mainly stored in bones. Hypercalcemia can be caused by primary hyperparathyroidism, vitamin D excess, certain malignancies, and other conditions. The diagnostic approach involves distinguishing between hyperparathyroidism and hypercalcemia of malignancy based on lab tests. Treatment focuses on rehydration, increasing calciuresis, and decreasing bone resorption or intestinal calcium absorption using medications like calcitonin, bisphosphonates, glucocorticoids, or dialysis depending on the severity of hypercalcemia.
This document discusses hypokalemia, defined as a serum potassium level below 3.6 mEq/L. It notes that potassium is critical for nerve impulse transmission and muscle function. The major causes of hypokalemia include decreased intake, intracellular shifts, non-renal losses like vomiting/diarrhea, and renal losses due to drugs like diuretics. Clinical features range from muscle weakness to cardiac arrhythmias. Diagnosis involves evaluating electrolytes, ECG changes, urine studies, and considering underlying causes. Treatment focuses on replacing potassium losses and correcting the underlying etiology.
This document discusses hypercalcemia and hypocalcemia. It defines hypercalcemia as a serum calcium level above 10.1 mg/dL and lists various causes including excessive PTH production, hypercalcemia of malignancy from PTHrP or bone metastases, excessive vitamin D production, and increased bone resorption. Symptoms can include neuropsychiatric issues, GI symptoms, ECG changes, and kidney stone formation. Evaluation involves correcting for albumin and measuring PTH to determine the cause. Treatment depends on the underlying condition but may include IV fluids, bisphosphonates, glucocorticoids, or gallium nitrate. Hypocalcemia is then discussed, outlining causes such as hy
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.
This document defines hypercalcemia and discusses its causes, evaluation, clinical presentation, and management. The main causes are parathyroid hormone dependent (primary hyperparathyroidism, tertiary hyperparathyroidism) and independent (malignancy, vitamin D related, endocrinopathies). Evaluation involves history, exam, and labs. Acute management is rehydration and medications to increase calcium excretion. Long term management depends on the underlying cause and may involve surgery, bisphosphonates, glucocorticoids, or ketoconazole.
Hypocalcemia has various presentations and can lead to significant morbidity if left untreated. The most common cause is hypoalbuminemia from conditions like cirrhosis or malnutrition that lower serum calcium levels. Other potential causes include vitamin D deficiency, parathyroid issues, medications, and critical illnesses like sepsis. Treatment involves identifying and addressing the underlying cause, as well as replacing calcium, often intravenously, to resolve symptoms and normalize calcium levels. Calcium levels must be closely monitored during treatment until stabilized.
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.
Hypercalcemia was causing the patient's acute renal failure. Treatment for hypercalcemia included intravenous fluids, furosemide, steroids, bisphosphonates, and dialysis which lowered the calcium levels and improved renal function. The underlying cause of hypercalcemia could not be determined after extensive testing, but was likely a malignancy given the persistent pancytopenia. Hypercalcemia can directly damage the kidneys by decreasing medullary osmolality and inducing nephrogenic diabetes insipidus, nephrolithiasis, and renal tubular acidosis. It also causes vasoconstriction and activation of the calcium-sensing receptor which stimulates renin release and worsens volume
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 hypokalemia (low potassium levels). It notes that serum potassium levels do not accurately reflect total body potassium levels, as most potassium is intracellular. Transcellular shifts and actual losses/gains can affect serum levels. Tight regulation of potassium is critical for cardiac and neuromuscular function. Causes of hypokalemia include redistribution, GI loss, renal loss, and low intake. Clinical manifestations include muscle weakness and cardiac arrhythmias. Treatment depends on the underlying cause and includes oral and intravenous potassium supplementation, with close monitoring needed in some cases.
The document discusses potassium metabolism and disorders of potassium levels. It covers:
1) Normal potassium metabolism and regulation by the kidneys, factors that influence renal secretion/excretion.
2) Causes and pathophysiology of hypokalemia and hyperkalemia, including excessive renal/gastrointestinal loss or intake, shifts between intracellular/extracellular fluid.
3) Effects of abnormal potassium levels on neuromuscular and cardiac function, including changes in membrane potential and electrical activity.
This document discusses hypocalcemia, which occurs when calcium levels in the blood are too low. It defines normal calcium levels and describes the causes of hypocalcemia, including kidney disease, hypoparathyroidism, vitamin D deficiency, certain drugs, and other conditions. Symptoms can include tingling, muscle cramps, seizures, and cardiac issues. Diagnosis involves testing serum calcium, phosphate, albumin, magnesium, parathyroid hormone, and vitamin D levels. Treatment depends on severity but may include oral calcium supplements or intravenous calcium for more severe cases.
Hypernatremia is defined as a plasma sodium concentration >145 mEq/L. It is usually caused by a water deficit rather than sodium gain. Common causes include impaired thirst, diarrhea, insensible losses from fever/ventilation, and renal losses from osmotic diuresis or diabetes insipidus. Symptoms range from none in chronic cases to neurologic issues like altered mental status. Treatment involves gradually correcting the sodium level by about 10-12 mEq/L/day using oral or IV water while monitoring for complications like cerebral edema. Replacing volume deficits and identifying underlying causes are also important.
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.
This document discusses sodium metabolism and disorders of sodium concentration. It provides details on:
- Water distribution in the body and fluid compartments
- Causes and types of hyponatremia, including hypovolemic, hypervolemic, and euvolemic hyponatremia
- Evaluation and management of hyponatremia, including treatment based on severity and rate of sodium correction
- Causes and clinical features of hypernatremia
The document is a comprehensive review of sodium disorders and approaches to diagnosis and treatment of hypo- and hypernatremia.
This document discusses hypocalcemia, defined as a serum calcium level below 8.5 mg/dl. It may be caused by low or high parathyroid hormone levels. Causes of low PTH include parathyroid gland agenesis, destruction, or dysfunction. Causes of high PTH include vitamin D deficiency, kidney disease impairing vitamin D activation, or drugs. Symptoms include increased neuromuscular excitability. Investigations include calcium, albumin, phosphorus, magnesium and PTH levels. Treatment involves vitamin D, calcium supplements, and magnesium as needed.
This document provides an overview of hypopituitarism, including its anatomy, etiology, clinical features, diagnosis, and treatment. Hypopituitarism is a clinical syndrome of deficiency in pituitary hormone production and secretion that can result from disorders of the pituitary gland, hypothalamus, or surrounding structures. Common causes include tumors, trauma, infections, infiltrative disorders, and genetic mutations. Clinical features vary depending on which hormones are deficient but may include fatigue, weight changes, dry skin, and visual disturbances. Diagnosis involves hormonal blood tests and dynamic testing. Treatment is lifelong hormone replacement therapy to mimic normal hormone levels.
This document discusses magnesium disorders and hypomagnesemia. It begins by providing background on magnesium, including where it is stored in the body and its many functions. It then discusses the causes, clinical manifestations, diagnosis, and treatment of hypomagnesemia. Hypomagnesemia can be caused by renal magnesium wasting due to drugs, diseases, or genetic disorders, or by extrarenal losses from poor nutrition, malabsorption, diarrhea, or sweat losses. Symptoms affect the cardiovascular, neuromuscular, skeletal, and central nervous systems. Treatment involves identifying and addressing the underlying cause, as well as oral or parenteral magnesium supplementation.
Calcium homeostasis and hypercalcemia/hypocalcemia are summarized. Calcium plays important roles and is tightly regulated. Hypercalcemia can be caused by primary hyperparathyroidism, malignancy, vitamin D excess, or renal failure. Symptoms involve bones, kidneys, GI tract, and neuromuscular systems. Treatment focuses on increasing calcium excretion and decreasing absorption or treating the underlying cause. Hypocalcemia has causes like hypoparathyroidism or vitamin D deficiency. Symptoms include weakness, tingling, and muscle spasms. Treatment provides calcium supplementation and addresses the underlying condition.
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its serum level is tightly regulated between 3.5-5 mEq/L. Mechanisms involve sodium-potassium pumps and renal excretion. Causes of hyperkalemia include reduced renal excretion, intracellular shifts, and inadequate aldosterone levels. Symptoms range from none to muscle weakness to arrhythmias. Treatment focuses on antagonizing cardiac effects, driving potassium intracellularly, and removing excess potassium.
The document discusses parathyroid glands and parathyroid hormone (PTH). It notes that parathyroid glands secrete PTH, which regulates calcium levels in the blood. PTH acts on bone, kidneys, and stimulates vitamin D production. Secondary hyperparathyroidism occurs in kidney disease and is caused by low calcium and vitamin D levels stimulating increased PTH secretion. Treatment focuses on controlling calcium, phosphate, PTH, and vitamin D levels through diet, binders, analogs, and calcimimetics. For refractory cases, parathyroidectomy may be required.
Hypoparathyroidism is a condition characterized by decreased function of the parathyroid glands and low levels of parathyroid hormone, resulting in low calcium and high phosphorus levels in the blood. Symptoms range from tingling in the extremities to seizures and altered mental state. The condition is diagnosed based on low calcium and parathyroid hormone levels in the blood. Treatment involves calcium and vitamin D supplements to manage calcium levels, with some patients also requiring parathyroid gland transplants.
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 summarizes definitions and guidelines for the diagnosis and management of sepsis. It defines sepsis as a clinical syndrome resulting from infection along with systemic inflammatory response syndrome (SIRS). The onset of sepsis focuses on dysregulation of inflammation and can lead to multiple organ dysfunction syndrome (MODS) and high mortality. Diagnostic criteria for sepsis require confirmed or suspected infection along with general, inflammatory, hemodynamic, or organ dysfunction variables. Management of severe sepsis and septic shock prioritizes early supportive care to correct hypoxemia and hypotension, rapid fluid resuscitation, vasopressors if hypotension persists, and control of the septic focus. Early goal-directed resuscitation aims to optimize perfusion parameters like mean
Renal regulation of potassium balance is critical for maintaining normal potassium levels. The kidneys excrete most of the daily potassium intake and reabsorb potassium in the proximal tubule. In the distal tubule and collecting duct, aldosterone stimulates potassium secretion. Hyperkalemia occurs when potassium levels shift from cells to extracellular fluid or potassium excretion is decreased. Hypokalemia is usually caused by increased potassium excretion due to mineralocorticoid excess or drugs like diuretics. Both conditions can cause cardiac arrhythmias.
Hypercalcemia and hypocalcemia are disorders of calcium homeostasis. Hypercalcemia is defined as a serum calcium level >10.2 mg/dL and can be caused by primary hyperparathyroidism, malignancy, vitamin D excess, or renal failure. Symptoms include nausea, constipation, weakness and arrhythmias. Treatment focuses on rehydration, bisphosphonates, calcitonin and addressing the underlying cause. Hypocalcemia is a serum calcium <8.5 mg/dL and can result from hypoalbuminemia, hypoparathyroidism, vitamin D deficiency or sepsis. Symptoms include tingling, muscle spasms and seizures. Acute treatment involves calcium supplementation while long
This document discusses hypercalcemia and hypocalcemia. It covers the roles and homeostasis of calcium, along with the causes, clinical features, and management of hypercalcemia and hypocalcemia.
For hypercalcemia, the main causes discussed are primary hyperparathyroidism, malignancy, vitamin D excess, and renal failure. Symptoms involve the bones, muscles, kidneys, gastrointestinal and cardiovascular systems. Diagnostic tests include serum electrolytes, PTH, and imaging. Treatment focuses on increasing urinary excretion, inhibiting bone resorption, and decreasing intestinal absorption.
For hypocalcemia, chronic and acute causes are outlined. Symptoms include weakness, tingling, spasms and seizures
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 hypokalemia (low potassium levels). It notes that serum potassium levels do not accurately reflect total body potassium levels, as most potassium is intracellular. Transcellular shifts and actual losses/gains can affect serum levels. Tight regulation of potassium is critical for cardiac and neuromuscular function. Causes of hypokalemia include redistribution, GI loss, renal loss, and low intake. Clinical manifestations include muscle weakness and cardiac arrhythmias. Treatment depends on the underlying cause and includes oral and intravenous potassium supplementation, with close monitoring needed in some cases.
The document discusses potassium metabolism and disorders of potassium levels. It covers:
1) Normal potassium metabolism and regulation by the kidneys, factors that influence renal secretion/excretion.
2) Causes and pathophysiology of hypokalemia and hyperkalemia, including excessive renal/gastrointestinal loss or intake, shifts between intracellular/extracellular fluid.
3) Effects of abnormal potassium levels on neuromuscular and cardiac function, including changes in membrane potential and electrical activity.
This document discusses hypocalcemia, which occurs when calcium levels in the blood are too low. It defines normal calcium levels and describes the causes of hypocalcemia, including kidney disease, hypoparathyroidism, vitamin D deficiency, certain drugs, and other conditions. Symptoms can include tingling, muscle cramps, seizures, and cardiac issues. Diagnosis involves testing serum calcium, phosphate, albumin, magnesium, parathyroid hormone, and vitamin D levels. Treatment depends on severity but may include oral calcium supplements or intravenous calcium for more severe cases.
Hypernatremia is defined as a plasma sodium concentration >145 mEq/L. It is usually caused by a water deficit rather than sodium gain. Common causes include impaired thirst, diarrhea, insensible losses from fever/ventilation, and renal losses from osmotic diuresis or diabetes insipidus. Symptoms range from none in chronic cases to neurologic issues like altered mental status. Treatment involves gradually correcting the sodium level by about 10-12 mEq/L/day using oral or IV water while monitoring for complications like cerebral edema. Replacing volume deficits and identifying underlying causes are also important.
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.
This document discusses sodium metabolism and disorders of sodium concentration. It provides details on:
- Water distribution in the body and fluid compartments
- Causes and types of hyponatremia, including hypovolemic, hypervolemic, and euvolemic hyponatremia
- Evaluation and management of hyponatremia, including treatment based on severity and rate of sodium correction
- Causes and clinical features of hypernatremia
The document is a comprehensive review of sodium disorders and approaches to diagnosis and treatment of hypo- and hypernatremia.
This document discusses hypocalcemia, defined as a serum calcium level below 8.5 mg/dl. It may be caused by low or high parathyroid hormone levels. Causes of low PTH include parathyroid gland agenesis, destruction, or dysfunction. Causes of high PTH include vitamin D deficiency, kidney disease impairing vitamin D activation, or drugs. Symptoms include increased neuromuscular excitability. Investigations include calcium, albumin, phosphorus, magnesium and PTH levels. Treatment involves vitamin D, calcium supplements, and magnesium as needed.
This document provides an overview of hypopituitarism, including its anatomy, etiology, clinical features, diagnosis, and treatment. Hypopituitarism is a clinical syndrome of deficiency in pituitary hormone production and secretion that can result from disorders of the pituitary gland, hypothalamus, or surrounding structures. Common causes include tumors, trauma, infections, infiltrative disorders, and genetic mutations. Clinical features vary depending on which hormones are deficient but may include fatigue, weight changes, dry skin, and visual disturbances. Diagnosis involves hormonal blood tests and dynamic testing. Treatment is lifelong hormone replacement therapy to mimic normal hormone levels.
This document discusses magnesium disorders and hypomagnesemia. It begins by providing background on magnesium, including where it is stored in the body and its many functions. It then discusses the causes, clinical manifestations, diagnosis, and treatment of hypomagnesemia. Hypomagnesemia can be caused by renal magnesium wasting due to drugs, diseases, or genetic disorders, or by extrarenal losses from poor nutrition, malabsorption, diarrhea, or sweat losses. Symptoms affect the cardiovascular, neuromuscular, skeletal, and central nervous systems. Treatment involves identifying and addressing the underlying cause, as well as oral or parenteral magnesium supplementation.
Calcium homeostasis and hypercalcemia/hypocalcemia are summarized. Calcium plays important roles and is tightly regulated. Hypercalcemia can be caused by primary hyperparathyroidism, malignancy, vitamin D excess, or renal failure. Symptoms involve bones, kidneys, GI tract, and neuromuscular systems. Treatment focuses on increasing calcium excretion and decreasing absorption or treating the underlying cause. Hypocalcemia has causes like hypoparathyroidism or vitamin D deficiency. Symptoms include weakness, tingling, and muscle spasms. Treatment provides calcium supplementation and addresses the underlying condition.
This document discusses potassium homeostasis and hyperkalemia. It notes that potassium is mainly intracellular and its serum level is tightly regulated between 3.5-5 mEq/L. Mechanisms involve sodium-potassium pumps and renal excretion. Causes of hyperkalemia include reduced renal excretion, intracellular shifts, and inadequate aldosterone levels. Symptoms range from none to muscle weakness to arrhythmias. Treatment focuses on antagonizing cardiac effects, driving potassium intracellularly, and removing excess potassium.
The document discusses parathyroid glands and parathyroid hormone (PTH). It notes that parathyroid glands secrete PTH, which regulates calcium levels in the blood. PTH acts on bone, kidneys, and stimulates vitamin D production. Secondary hyperparathyroidism occurs in kidney disease and is caused by low calcium and vitamin D levels stimulating increased PTH secretion. Treatment focuses on controlling calcium, phosphate, PTH, and vitamin D levels through diet, binders, analogs, and calcimimetics. For refractory cases, parathyroidectomy may be required.
Hypoparathyroidism is a condition characterized by decreased function of the parathyroid glands and low levels of parathyroid hormone, resulting in low calcium and high phosphorus levels in the blood. Symptoms range from tingling in the extremities to seizures and altered mental state. The condition is diagnosed based on low calcium and parathyroid hormone levels in the blood. Treatment involves calcium and vitamin D supplements to manage calcium levels, with some patients also requiring parathyroid gland transplants.
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 summarizes definitions and guidelines for the diagnosis and management of sepsis. It defines sepsis as a clinical syndrome resulting from infection along with systemic inflammatory response syndrome (SIRS). The onset of sepsis focuses on dysregulation of inflammation and can lead to multiple organ dysfunction syndrome (MODS) and high mortality. Diagnostic criteria for sepsis require confirmed or suspected infection along with general, inflammatory, hemodynamic, or organ dysfunction variables. Management of severe sepsis and septic shock prioritizes early supportive care to correct hypoxemia and hypotension, rapid fluid resuscitation, vasopressors if hypotension persists, and control of the septic focus. Early goal-directed resuscitation aims to optimize perfusion parameters like mean
Renal regulation of potassium balance is critical for maintaining normal potassium levels. The kidneys excrete most of the daily potassium intake and reabsorb potassium in the proximal tubule. In the distal tubule and collecting duct, aldosterone stimulates potassium secretion. Hyperkalemia occurs when potassium levels shift from cells to extracellular fluid or potassium excretion is decreased. Hypokalemia is usually caused by increased potassium excretion due to mineralocorticoid excess or drugs like diuretics. Both conditions can cause cardiac arrhythmias.
Hypercalcemia and hypocalcemia are disorders of calcium homeostasis. Hypercalcemia is defined as a serum calcium level >10.2 mg/dL and can be caused by primary hyperparathyroidism, malignancy, vitamin D excess, or renal failure. Symptoms include nausea, constipation, weakness and arrhythmias. Treatment focuses on rehydration, bisphosphonates, calcitonin and addressing the underlying cause. Hypocalcemia is a serum calcium <8.5 mg/dL and can result from hypoalbuminemia, hypoparathyroidism, vitamin D deficiency or sepsis. Symptoms include tingling, muscle spasms and seizures. Acute treatment involves calcium supplementation while long
This document discusses hypercalcemia and hypocalcemia. It covers the roles and homeostasis of calcium, along with the causes, clinical features, and management of hypercalcemia and hypocalcemia.
For hypercalcemia, the main causes discussed are primary hyperparathyroidism, malignancy, vitamin D excess, and renal failure. Symptoms involve the bones, muscles, kidneys, gastrointestinal and cardiovascular systems. Diagnostic tests include serum electrolytes, PTH, and imaging. Treatment focuses on increasing urinary excretion, inhibiting bone resorption, and decreasing intestinal absorption.
For hypocalcemia, chronic and acute causes are outlined. Symptoms include weakness, tingling, spasms and seizures
Calcium homeostasis and hypercalcemia/hypocalcemia are summarized. Calcium plays important roles and is tightly regulated. Hypercalcemia can be caused by primary hyperparathyroidism, malignancy, vitamin D excess, or renal failure. Symptoms involve bones, kidneys, GI tract, and neuromuscular systems. Treatment focuses on increasing calcium excretion and inhibiting bone resorption. Hypocalcemia has causes like hypoparathyroidism, vitamin D deficiency, and alkalosis. Symptoms are weakness, tingling, and muscle spasms. Treatment provides calcium supplementation and addresses the underlying cause.
Control of calcium homeostasis involves parathyroid hormone, vitamin D, PTHrP, and calcitonin. Vitamin D is produced in skin and converted to its active form in liver and kidneys to regulate calcium absorption and bone mineralization. Disorders like rickets and osteomalacia can result from vitamin D deficiency. Primary hyperparathyroidism is a common cause of hypercalcemia where an overactive parathyroid gland increases bone resorption and renal calcium reabsorption. Hypocalcemia can occur in chronic kidney disease or hypoparathyroidism and cause neuromuscular symptoms. Multiple endocrine neoplasia type 1 involves tumors of the parathyroid glands, pancreas
This document discusses oncological emergencies, including tumor lysis syndrome, malignant hypercalcemia, superior vena cava syndrome, and others. It provides details on the definitions, causes, clinical presentations, diagnostic criteria, and treatment approaches for these time-sensitive cancer complications. Tumor lysis syndrome can result from cell lysis releasing uric acid and electrolytes, and requires aggressive hydration, allopurinol or rasburicase, and renal replacement therapy if severe. Malignant hypercalcemia is most common in breast and lung cancers and multiple myeloma, presenting with nausea, fatigue, and neurological symptoms, treated initially with hydration and bisphosphonates. Superior vena cava syndrome ob
This document discusses hypercalcemia in malignancy. It begins with an introduction defining hypercalcemia and its prevalence in certain cancers. It then covers normal calcium metabolism regulation involving bone, plasma, vitamin D, and the RANK/RANKL pathway. Etiologies of hypercalcemia in malignancy include PTHrP-mediated humoral hypercalcemia, local osteolytic hypercalcemia, 1,25-dihydroxyvitamin D mediated, and hyperparathyroidism. Clinical presentation involves neurologic, gastrointestinal, cardiovascular, and renal symptoms. Diagnostic evaluation includes calcium levels and approaches based on etiology. Management involves increasing urinary calcium excretion, inhibiting bone resorption with bisphosphonates or den
The document discusses calcium homeostasis and disorders of calcium and phosphate metabolism. It provides details on:
1. The functions of parathyroid hormone (PTH) and how it regulates calcium levels.
2. Causes of hypocalcemia including hypoparathyroidism and vitamin D deficiency.
3. Causes of hypercalcemia including primary hyperparathyroidism and malignant diseases.
4. How laboratory tests can help diagnose disorders like hypocalcemia and hyperparathyroidism.
This document reviews literature on hypercalciuria, which is defined as excessive calcium in the urine. It discusses the various causes of hypercalciuria including absorptive, renal leak, and resorptive types. Dietary factors like calcium, protein, sodium, alcohol and caffeine intake can also impact hypercalciuria. Treatment involves confirming the diagnosis, ruling out other conditions, trialing dietary modifications, and potentially using medications like thiazide diuretics, phosphates, or bisphosphonates. Care must be taken with treatment to monitor urine and blood levels and address other risk factors for kidney stones.
A 20-month-old girl presented with vomiting and dehydration due to hypercalcemia from Williams syndrome. She had experienced 4 episodes of hypercalcemia in the past 2 months. Treatment involved IV hydration, lasix, and steroids to lower her calcium levels. Steroids were able to maintain her calcium below 3 mmol/L. The main treatments for hypercalcemia include IV hydration to increase urinary calcium excretion, loop diuretics like furosemide to further promote calciuresis, and bisphosphonates to inhibit bone resorption for more severe cases. The choice of treatment depends on the severity and underlying cause of the hypercalcemia.
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.
Tumor lysis syndrome occurs when cancer cells release their contents into the bloodstream, causing electrolyte imbalances like hyperkalemia, hyperuricemia, and hyperphosphatemia that can damage organs. It is diagnosed when a patient develops acute kidney injury, arrhythmias, or seizures from their electrolyte changes. Treatment involves rapid hydration, uric acid-lowering drugs like allopurinol or rasburicase, and dialysis for severe electrolyte abnormalities or kidney injury. With advances in prevention and management, the prognosis for tumor lysis syndrome has improved in recent years.
This document discusses disorders of the parathyroid glands. It covers the anatomy and function of the parathyroid glands, parathyroid hormone, and disorders involving abnormal parathyroid function such as hyperparathyroidism and hypoparathyroidism. Hyperparathyroidism can be primary, secondary, or tertiary and involves excessive PTH production leading to hypercalcemia. Hypoparathyroidism is a deficiency of PTH causing hypocalcemia. Surgical removal of the parathyroid glands can cause hypoparathyroidism as a complication.
Tumor lysis syndrome is a potentially life-threatening condition caused by the rapid breakdown of tumor cells during cancer treatment, releasing electrolytes into the bloodstream. It can cause severe electrolyte abnormalities like hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. These abnormalities are due to the release of intracellular contents from dying tumor cells and can lead to acute kidney injury. Tumor lysis syndrome is most common in patients with high-grade lymphomas and leukemias undergoing aggressive chemotherapy and requires careful monitoring and prevention with hydration and medications to reduce complications.
Tumor lysis syndrome is a potentially life-threatening condition caused by the rapid breakdown of tumor cells during cancer treatment, releasing electrolytes into the bloodstream. It can cause severe electrolyte abnormalities like hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. These abnormalities are due to the release of intracellular contents from dying tumor cells and can lead to acute kidney injury. Tumor lysis syndrome is most common in patients with high-grade lymphomas and leukemias undergoing aggressive chemotherapy and requires careful monitoring and prevention with hydration and medications to avoid complications.
Tumor lysis syndrome is caused by massive tumor cell lysis and release of electrolytes into circulation, potentially causing kidney damage. Risk factors include large tumor burden, rapid proliferation, sensitivity to treatment, preexisting kidney conditions, and inadequate hydration or electrolyte control. Prevention focuses on aggressive hydration, uric acid reduction via allopurinol or rasburicase, electrolyte management, and sometimes dialysis for severe cases.
This document discusses calcium imbalances, including hypercalcemia and hypocalcemia. It begins with introducing calcium, its functions, and homeostasis. Hypercalcemia is defined as a calcium level above 10.5 mg/dL and can be caused by primary hyperparathyroidism, malignancy, or excessive vitamin D and calcium supplementation. Clinical features of hypercalcemia include neurological, cardiovascular, and renal symptoms. Treatment involves rehydration, bisphosphonates, calcitonin, surgery for severe cases. Hypocalcemia is a calcium level below 8.5 mg/dL and can result from vitamin D deficiency, kidney disease, or certain drugs. Symptoms include numbness and tetany. Treatment focuses on calcium and
This document discusses oncologic emergencies in pediatrics. It begins with an introduction and overview of common pediatric malignancies. It then categorizes oncologic emergencies and discusses several examples in more depth, including metabolic emergencies like tumor lysis syndrome, hematologic emergencies such as hyperleukocytosis and bleeding disorders, and cardiothoracic emergencies like superior vena cava syndrome. For each emergency, it covers pathophysiology, risk factors, diagnostic criteria, evaluation and management strategies. The document provides a comprehensive review of potential life-threatening complications that may arise from pediatric cancers or their treatment and strategies for rapid recognition and management.
Tumor lysis syndrome (TLS) describes metabolic derangements that occur from rapid tumor breakdown associated with cytotoxic therapy. It is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. TLS requires immediate intervention as it can overwhelm homeostatic mechanisms. It occurs primarily in hematologic malignancies with high proliferation rates that are sensitive to therapy. Prevention through hydration, hypouricemic agents, and monitoring of at risk patients is important to manage TLS.
INTRODUCTION
SOURCES OF CALCIUM
RDA OF CALCIUM
FUNCTIONS OF CALCIUM
CALCIUM BALANCE
ABSORPTION OF CALCIUM
EXCHANGE OF CALCIUM BETWEEN BONE AND ECF
EXCRETION OF CALCIUM
REGULATION OF PLASMA CALCIUM LEVEL
APPLIED ASPECTS
Retinoblastoma is a rare cancer that affects the retina. It is caused by mutations in the RB1 gene. There are two main types - hereditary retinoblastoma, which requires only one mutation, and sporadic retinoblastoma, which requires two mutations. Symptoms include leukocoria. Diagnosis involves ophthalmoscopy, imaging like ultrasound and MRI, and sometimes biopsy. Treatment depends on factors like tumor size and location, and may include focal therapies like cryotherapy, chemotherapy, external beam radiation, plaque brachytherapy, or enucleation of the eye. Prognosis depends on extent of disease and risk of metastasis.
1) Megavoltage electron beams represent an important treatment modality for superficial tumors up to 5 cm deep, sparing deeper tissues. They are commonly used to treat skin lesions and boost areas previously treated with photon irradiation.
2) Electron beams have high surface dose that decreases with depth, reaching half the maximum dose around the practical range. Bremsstrahlung production increases with energy. Beam energy is selected based on the required depth of treatment.
3) Tissue heterogeneities like air cavities or bone can shift dose distributions. Bolus and beam obliquity are used to compensate. Treatment planning considers target coverage and critical structure sparing.
1) Megavoltage photon therapy uses high energy photon beams, typically above 1 MV, generated via linear accelerators or cobalt-60 sources.
2) The three main interactions between photons and tissue are the photoelectric effect, Compton scattering, and pair production. Compton scattering is the most common interaction for megavoltage beams between 6-20 MV.
3) Key characteristics of megavoltage photon beams include percentage depth dose curves, beam profiles, isodose charts, and considerations for tissue heterogeneities. Wedge filters can also be used to modify beam profiles for uniform target coverage.
This document discusses the clinical response of normal tissues to radiation. It begins by explaining the inherent radiosensitivity of different tissues based on Casarett's and Michalowski's classifications. It then discusses the kinetics of normal tissue radiation injury, including acute, subacute, late responses. It explains how tissue organization into functional subunits and volume effects impact the response. The document outlines factors like regeneration and retreatment tolerance. It briefly introduces quantitative guidelines from projects like QUANTEC and LENT/SOMA for evaluating normal tissue effects from radiation therapy.
1) The document provides an overview of the anatomy, blood supply, lymphatic drainage, clinical features, radiological anatomy, pathology, and staging of carcinoma of the cervix.
2) It describes the external and internal female genital organs and their blood supply, lymphatic drainage, and innervation.
3) The clinical features of various gynecologic malignancies including cervical, endometrial, ovarian, fallopian tube, vaginal, urethral, and vulvar cancers are outlined. CT and MRI images of female pelvic organs are also shown.
This document provides information on carcinoma of the esophagus, including:
- Esophageal cancer is the 8th most common cancer worldwide, with high incidence rates in parts of Africa and Asia. Squamous cell carcinoma and adenocarcinoma account for most cases.
- The esophagus has three layers - mucosa, submucosa, and muscularis propria. It lacks a serosa, allowing early extraesophageal spread.
- Staging uses AJCC TNM and other systems to assess tumor size, lymph node involvement, and metastasis.
- Risk factors include smoking, alcohol, hot foods/liquids, micronutrient deficiencies, GERD, and Barrett's
Hyperthermia involves raising tumor temperature to 39.5-43°C as an additive cancer treatment to chemotherapy and radiation therapy. It can be combined with radiotherapy as thermoradiotherapy or with both radiotherapy and chemotherapy as thermochemoradiotherapy. Hyperthermia directly kills cells through protein denaturation and indirectly through vascular and oxygenation changes in the tumor microenvironment. Response depends on factors like temperature, duration, and combination with other treatments. Delivery methods include electromagnetic waves, ultrasound, or thermal conduction to heat tissues selectively.
- Cell survival curves relate the radiation dose to the proportion of cells that survive. They are generated through in vitro experiments where cells are exposed to radiation doses and then assessed for their ability to proliferate into colonies.
- The linear-quadratic model describes cell survival as having both a linear component related to single radiation hits and a quadratic component related to multiple radiation hits. It is used to design fractionated radiotherapy regimens and understand acute vs late tissue responses.
- Key factors in the model include the alpha coefficient representing intrinsic radiosensitivity, the beta coefficient representing repair capacity, and the alpha/beta ratio which indicates the dose where linear and quadratic death are equal.
This document provides information on Non-Hodgkin's lymphoma (NHL), including its subtypes, risk factors, presentation, classification, staging, diagnostic workup, prognostic factors, and treatment approaches. It discusses the most common subtypes of NHL - diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) - in more detail. For DLBCL, it outlines treatment protocols based on stage, prognostic factors, and management of relapsed/refractory disease. For FL, it discusses grading, clinical features, treatment based on stage including immunochemotherapy regimens and radiation therapy options. It also summarizes marginal zone lymphomas regarding clinical features, treatment including antibiotics for gastric M
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
2. Introduction
Calcium is one of the most abundant minerals in the human body and it has many important
biologicalfunctions.
Functionsof calcium :
1. Musclecontraction
2. Neuromuscular / nerve conduction
3. Intracellular signalling
4. Bone formation
5. Coagulation
6. Enzyme regulation
7. Maintenance of plasma membrane stability
3. NORMAL DISTRIBUTION:
• A 70 kg person has approximately 1.2kg of calcium in the body, 99%
is stored as hydroxyapatite in bones.
• <1% (5-6 g) of this calcium is in the intracellular and extracellular
compartments.
• Only 1.3 g is located extracellularly.
• Total normal calcium concentration in the plasma is 8.9-10.1 mg/dL.
• 50% of plasma calcium is ionized ,the active form of calcium which is
clinically significant
• 40% is bound to proteins (90% to albumin), 10% circulates bound to
anions (eg, phosphate, carbonate, citrate, lactate, sulfate).
4. Calculation of calcium levels:
• Step1:Ensurethatthealterationinserumcalciumlevelsisnotduetoabnormal
albuminconcentration(sinceionizedformistheactiveformofcalcium)
• Directmeasurementof ionisedcalciumiseasilyinfluencedbycollection
methodsandotherartefacts,hencewe prefertomeasurecorrectedcalcium
fromtotalcalciumandalbumin.
Corrected calcium:
• For every 1-g/dL drop in serum albumin below 4 g/dL, measured serum calcium
decreasesby0.8 mg/dL.
• Correctedcalcium=MeasuredCa+[0.8x(4–measuredalbumin)]
(Calciuminmg/dl;albumining/dl)
5. Calcium Homeostasis
• Extracellular calcium concentration - (8.9-10.1 mg/dl)
• Feedback mechanisms that involve parathyroid hormone ,calcitonin and the active Vitamin
D metabolite (1,25 dihydroxyvitaminD)
6.
7. I. HYPERCALCEMIA
• Causes :
1. Too much calcium enters the ECF.
2. There is insufficient calcium excretion from the kidney.
* ~ 90% are caused by malignancy or hyperparathyroidism.
MILD MODERATE CRISIS
TOTAL CALCIUM 10.5-11.9 mg/dl 12-13.9 mg/dl 14-16 mg/dl
IONISED CALCIUM 5.6-8 mg/dl 8-10 mg/dl 10-12 mg/dl
8.
9. Causes of hypercalcemia:
I.Parathyroid-related
• Primary hyperparathyroidism –Adenoma , Multiple
endocrine neoplasia , Carcinoma
• Lithium therapy
• Familial hypocalciuric hypercalcemia
II.Malignancy-related
• Solid tumour with metastases (breast)
• Solid tumour with humoral mediation of hypercalcemia
(lung , kidney)
• Hematologic malignancies (multiple myeloma,
lymphoma, leukaemia)
III. Vitamin D-related
• Vitamin D Intoxication
• Increased 1,25(OH)2D; sarcoidosis and other
granulomatous diseasesimpaired metabolism due to 24-
hydroxylase deficiency
IV.Associated with high bone turnover
• Hyperthyroidism
• Immobilization
• Thiazides
• Vitamin A intoxication
• Fat necrosis
V.Associated with renal failure
• Severe secondary hyperparathyroidism
• Aluminium intoxication
• Milk-alkali syndrome
10. Clinical manifestations
• Mild hypercalcemia – asymptomatic.
- Recognized on routine calcium measurements.
- Vague neuropsychiatric symptoms – concentration deficit, personality changes,
or depression.
- Others : Peptic ulcer, nephrolithiasis, fracture risk.
• Severe hypercalcemia – Acutely Lethargy, stupor, or coma, GI symptoms
(nausea, anorexia, constipation, or pancreatitis).
(decreases renal concentrating ability polyuria and polydipsia).
• Longstanding hyperparathyroidism bone pain/ pathologic fractures.
---------------------------------------------------------------------------------------------------------
• Hypercalcemia - significant ECG changes bradycardia, AV block, short QT
interval
• Changes in serum calcium - monitored by following the QT interval.
11. Renal “stones”
Nephrolithiasis
Nephrogenic diabetes insipidus
Dehydration
Nephrocalcinosis
Skeleton “bones”
Bone pain
Arthritis
Osteoporosis
Osteitis fibrosa cystica in hyperparathyroidism
(subperiosteal resorption, bone cysts)
Gastrointestinal “abdominal
moans”
Nausea, vomiting, Anorexia,
weight loss ,Constipation
Abdominal pain , Pancreatitis
Peptic ulcer diseaseNeuromuscular “psychic groans”
Impaired concentration and memory Confusion,
stupor, coma
Lethargy and fatigue
Muscle weakness
Corneal calcification (band
keratopathy)
Cardiovascular
Hypertension
Shortened QT interval on E C G Cardiac arrhythmias
Vascular calcification
12.
13. MALIGNANCY-RELATED HYPERCALCEMIA
• Hypercalcemia is the most common paraneoplastic syndrome, occurring in
10% to 30% of patients with advanced cancer
• Main mechanisms in cancer hypercalcemia
1. Bone mets-Local invasion and destruction of bone by tumor cells.(breast
cancer ,multiple myeloma)
2. Humoral hypercalcemia of malignancy is by PTHrP(PTH related peptide)
by a variety of carcinomas like squamous cell ca lung ,renal tumours
,breast
3. In some lymphomas- increased blood level of 1,25(OH)2D by the
abnormal lymphocytes.
4. Prostaglandins and interleukin 1 produced by various tumours enhances
bone resorption
5. Ectopic parathyroid hormone –very rare
Squamous cell tumors are most frequently associated with hypercalcemia, particularly tumors of the
lung, kidney, head and neck, and urogenital tract.
14. Investigations:
• Serum calcium(ionised ,total) , phosphorus(2.5 to 4.5mg/dl) and albumin
• Serum ALP
• Blood urea nitrogen and serum creatinine
• ECG
• PTH (10-65 pg/ml)
• PTHrP assay
• Bone scans
• Bone marrow biopsy
Treatment : (malignancy hypercalcemia)
• First to control of tumor; reduction of tumor mass usually corrects hypercalcemia.
• If a patient has severe hypercalcemia yet has a good chance for effective tumor therapy, treatment of the
hypercalcemia should be vigorous while awaiting the results of definitive therapy.
• If hypercalcemia occurs in the late stages of a tumor that is resistant to antitumor therapy, the treatment of
the hypercalcemia should be judicious as high calcium levels can have a mild sedating effect.
15. Management of Hypercalcemia
a.)Hydration and saline diuresis
Volume Restoration expansion and saline diuresis are most useful and
effective measures to correct hypercalcemia
0.9 % NaCl is infused to correct dehydration for volume expansion and
diuresis.(almost @ 200 to 300ml/hr and then tapered as required)hence
always use cautiously in HEART FAILURE AND ELDERLY patients to avoid
pulmonary oedema
Furosemide – Additive effect with 0.9 NS as it leads to forced Diuresis.
Precautions – fluid intake, output, blood levels of ca,k,mg every 8-12 hours
16. b.) BISPHOSPHONATES
MOA- Analogues of pyrophosphate with high affinity for increased bone turnover sites and inhibits osteoclysis
ZOLEDRONATE(4/8MG in 100 ml NS over 15 mins) is the most effective
PAMIDRONATE(60-90 mg in 500ML NS over 2-4 hours)
Doses may be repeated every 7 to 30 days
S.E –Osteonecrosis of jaw ,subtrochanteric #
c.) CALCITONIN
MOA-Inhibits bone resorption and increases urinary excretion
useful in acute crisis
DOSAGE-4IU/KG s.c 12hourly
Indications –diuresis , other drugs are contraindicated (RF , CHF)
S.E - tachyphylaxis
d.) DENOSUMAB
MOA-antibody that blocks RANK ligandand so reduces
osteoclast number and function
DOSAGE-120mg/s.c monthly
e.) HAEMODIALYSIS- Reserved for treatment of
patients with severe hypercalcemia and in CRF
17. • GLUCOCORTICOIDS
MOA- Causes decreased absorption and increases urinary excretion ,
decrease 1,25 OH dihydroxy vitamin production
Are effective in sarcoidosis,malignancy,vit d toxicity but not in primary
hyperparathyroidism
• SPECIFIC TREATMENT
Discontinue drugs responsible
Surgical treatment in primary
hyperparathyroidism
Specific treatment in cases of malignancy
and granulomatous conditions
18.
19. II. HYPOCALCEMIA
A decrease in serum calcium
less than 8.5mg/dl or ionized
calcium less than 3-4.4mg/dl
is termed as Hypocalcemia.
20. Mechanisms of hypocalcemia in malignancy
1. Paraneoplastic syndrome leading to hypocalcemia –very rare
2. Osteoblastic bone mets
3. CA prostate , breast on hormonal agents because of rapid bone healing.
4. Calcitonin –by medullary carcinoma of thyroid
5. Magnesium deficiency( both PTH secretion and its action)
• Prolonged nasogastric drainage
• On TPN without any magnesium supplementation
• Cisplatin therapy induced renal tubular dysfunction –urinary loss
• Chronic alcoholism
• Chronic diarrhoea
• EGFR blocking antibodies: cetuximab and panitumumab
6. Therapy for hypercalcemia
21. TUMOUR LYSIS SYNDROME
• Tumor cell death with the release of intracellular
contents can lead to a constellation of metabolic
abnormalities is tumor lysis syndrome (TLS).
• it can occur spontaneously in rapidly proliferating
tumors, it occurs most frequently following
administration of cytotoxic chemotherapy to patients
with hematologic malignancies, with a large percentage
of proliferating, drug-sensitive cells . Ex: acute leukemias
,large bulky high-grade non-Hodgkin lymphomas [NHL],
especially Burkitt lymphoma
• TLS occurs a few hours to a few days after the initiation
of therapy.
• Cell death leads to the release of potassium, phosphate,
uric acid, and other purine metabolites overwhelming
the kidney’s capacity for clearance with resultant
hyperkalemia, hyperphosphatemia and secondary
hypocalcemia, and hyperuricemia
• Unchecked, TLS can progress to acute renal failure and
metabolic acidosis . Established TLS is associated with a
high morbidity and mortality.
Cairo Bishop classification system
22. • The best management for TLS is prevention.The preventive regimen
consists of ,
1. IV hydration- goal is urine output of 80 to100ml/hr/m2. Recommended fluids
are 5% dextrose/0.45% NS. In hyponatremic patients 0.9% NS .Furosemide can
be added .
2. Urinary alkalinisation- pH as high as 7 (uric acid crystals form only in acidic
environment)
3. Hypouricemic drugs
• Allopurinol-100mg/m2 every 8 hours
• Rasburicase-0.15 to 0.2mg/kg once daily for 5 days
• Febuxostat- safe in liver and renal disease
23. Clinical Manifestations
• Usually asymptomatic if mild /chronic
• Moderate to severe parasthesia(fingers,toes,circumoral
region).Clinically Chovstek’s sign , trousseau’s sign are seen
• Severe seizures,carpopedal spasm,laryngospasm,prolongation of
QT interval
Carpopedal spasm Chovstek’s sign:
24. DIAGNOSTIC APPROACH
In addition to measuring serum calcium, it is useful to determine albumin, phosphorus, and magnesium levels.
• A suppressed (or “inappropriately low”) PTH level in the setting of hypocalcemia establishes absent or reduced PTH
secretion (hypoparathyroidism) as the cause of the hypocalcemia. Further history will often elicit the underlying
cause (i.e., parathyroid agenesis vs. destruction).
• By contrast, an elevated PTH level (secondary hyperparathyroidism) should direct attention to the vitamin D axis as
the cause of the hypocalcemia.
• Nutritional vitamin D deficiency is best assessed by obtaining serum 25-hydroxyvitamin D levels(20-100 ng/ml),
which reflect vitamin D stores. In the setting of renal insufficiency or suspected vitamin D resistance, serum
1,25(OH)2D levels are informative.
25. Management of Hypocalcemia
The approach to treatment depends on the severity of the hypocalcemia, the rapidity with
which it develops, and the accompanying complications (e.g., seizures, laryngospasm).
• Severe Acute, symptomatic hypocalcemia (S.ca<6mg/dl)-
a.) calcium gluconate 1gm diluted in 50 mL of 5% dextrose or 0.9% sodium chloride, given
intravenously over 10 to 20mins.
b.) followed by slow infusion of 11gm calcium gluconate in D5% /NS @50 ml/hr
c.)Magnesium sulphate 1gm IV every 8 hrs to 12 hrs if levels unknown or <1.5mg/dl
d.)Serum ca2+ levels every 2 hours
AVOID RINGER LACTATE WHEN INFUSING CALCIUM PREPARATIONS
26. • Moderate hypocalcemia: (6-8 mg/dl)
a.) calcium either oral or IV (1000mg of elemental iron daily)
b.) magnesium 1gm IV once/twice daily
c.) patients recovering from hypercalcemia are in risk
• Chronic hypocalcemia due to hypoparathyroidism is treated with calcium
supplements (1000–1500 mg/d elemental calcium in divided doses) and either
vitamin D2 or D3 (25,000–100,000 U daily) or calcitriol [1,25(OH)2D, 0.25–2
μg/day].
• Vitamin D deficiency, however, is best treated using vitamin D supplementation,
with the dose depending on the severity of the deficit and the underlying cause.
27.
28.
29. Management of Hypercalcemia
• Hydration and saline diuresis
• Bisphosphonates
• Calcitonin
• Denosumab
• Glucocorticoids
• Haemodialysis
Management of Hypocalcemia
• Calcium gluconate
• Magnesium sulphate
• Vit D supplementation
1.especially with certain types of tumor such as lung carcinoma), often severe and difficult to manage, and, on rare occasions, difficult to distinguish from primary hyperparathyroidism. Although malignancy is often clinically obvious or readily detectable by medical history, hypercalcemia can occasionally be due to an occult tumor
Trousseau’s sign- inflation of a blood pressure cuff over 20mm of the pt’s systolic for 3 mins