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.
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 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 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
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
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The two most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
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.
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 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 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
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
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcemia is a condition where there are abnormally high levels of calcium in the blood. It affects around 0.5-1% of the general population. The two most common causes are primary hyperparathyroidism and hypercalcemia caused by malignancy, which together account for 90% of cases. Symptoms range from none to neurological effects like confusion, weakness, and coma. Treatment involves rehydration, calcitonin, bisphosphonates, and dialysis for severe cases. Ongoing treatment aims to prevent recurrence by addressing the underlying cause when possible.
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
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.
Calcium is an essential mineral that makes up 2% of body weight. Over 99% is stored in bones, with the rest in tissues and plasma. Calcium levels are tightly regulated by parathyroid hormone (PTH), calcitonin, and calcitriol (active vitamin D). PTH increases calcium levels by promoting bone resorption, while calcitonin and calcitriol decrease calcium levels by reducing resorption. Bisphosphonates are used to treat osteoporosis and Paget's disease by inhibiting bone resorption. They decrease osteoclast activity and survival. Calcium supplements are used to treat deficiencies and osteoporosis, while bisphosphonates and calcim
This document discusses calcium metabolism and provides details on calcium homeostasis, absorption, excretion, and the roles of parathyroid hormone and vitamin D. It also covers hypocalcemia and hypercalcemia, defining each condition and describing causes, clinical manifestations, diagnostic workup, and treatment approaches. Hypocalcemia can result from neonatal issues, vitamin D deficiency, hypoparathyroidism, or other causes. Hypercalcemia has causes including parathyroid hormone excess, malignancy, vitamin D excess, and genetic conditions.
This document discusses calcium homeostasis and hypercalcemia. It notes that approximately 1000-1200 mg of calcium is present in an adult, mostly in bone. It describes the distribution and protein binding of calcium in extracellular fluid and intracellular fluid. Factors that influence calcium absorption in the gut and renal handling of calcium are outlined. Mechanisms involved in response to changes in serum calcium levels, including the roles of TRPV5 calcium channels and calbindin D28k protein, are summarized. Causes, clinical features, pathophysiology, and treatment approaches for hypercalcemia and various hypercalcemic disorders like primary hyperparathyroidism and familial hypocalciuric hypercalcemia are described.
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 electrolyte abnormalities in children. It begins by reviewing body composition and water balance in the human body. It then covers the composition and regulation of sodium, potassium, and other electrolytes. Specific conditions that can cause electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia are defined and their causes and treatment approaches are outlined. The document emphasizes the importance of determining the underlying cause and correcting imbalances gradually to avoid complications.
This document discusses electrolyte abnormalities in children. It provides information on the composition of body fluids, water balance, and maintenance fluid and electrolyte requirements in children. It then focuses on abnormalities in sodium, potassium, and other electrolytes. For each abnormality, it describes the causes, clinical features, evaluation, and treatment approaches. It emphasizes the importance of determining the underlying cause and correcting abnormalities slowly and carefully to avoid complications.
This document provides an overview of acute renal failure in children. It defines acute renal failure, discusses causes (pre-renal, intrinsic renal, post-renal), pathogenesis, laboratory findings, biomarkers, management including fluid resuscitation, diuretics, electrolyte abnormalities, nutrition, and indications for dialysis. Management is aimed at treating the underlying cause and maintaining fluid, electrolyte and acid-base balance until renal function recovers.
This document summarizes alterations in calcium metabolism, including hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism, or increased intestinal calcium absorption. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood compartment, or by decreased calcium flow from intestines or bones into the blood, as seen in hypoparathyroidism. The document outlines the clinical presentations, diagnostic evaluations, and treatments for hypercalcemia and hypocalcemia.
This document summarizes alterations in calcium metabolism, including hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism, or increased intestinal calcium absorption. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood compartment, or by decreased calcium flow from intestines or bones into the blood, as seen in hypoparathyroidism. The document outlines the clinical presentations, diagnostic evaluations, and treatments for hypercalcemia and hypocalcemia.
Calcium and phosphorus are essential minerals found primarily in bones and teeth. Calcium makes up 1-2% of total body weight and is found mostly in bones, while phosphorus makes up 1% of body weight and is primarily intracellular. Dietary sources of calcium include dairy products, while phosphorus is obtained from foods like cereals, meat, and nuts. Absorption of both minerals can be affected by factors like vitamin D, pH, and other dietary constituents. Calcium and phosphorus are important for bone health, cell signaling, and other metabolic processes. Abnormal levels can cause issues like muscle problems or bone diseases. Their levels are tightly regulated and measured together to diagnose certain conditions.
Acute renal failure is a clinical syndrome where sudden deterioration of renal function results in the kidneys' inability to maintain fluid and electrolyte homeostasis. It has various etiologies like pre-renal, intrinsic renal, and post-renal factors. Management involves treating the underlying cause, fluid resuscitation, controlling electrolyte abnormalities, and starting dialysis for refractory volume overload, hyperkalemia, acidosis, or neurological symptoms. The healthcare team works to stabilize the patient and prevent long-term kidney damage.
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
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 alterations in calcium metabolism, specifically hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism or bone metastases from cancers like breast or lung cancer. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood into tissues, as seen in kidney failure, or by decreased intestinal calcium absorption, as seen in vitamin D deficiency. Symptoms, diagnosis, and treatment approaches are described for both hypercalcemia and hypocalcemia.
Approach to patient with hypo/hyper calcaemiaNassr ALBarhi
This document discusses calcium homeostasis and disorders of calcium metabolism. It begins by describing the functions of calcium in the body and where calcium is stored. It then discusses calcium regulation by parathyroid hormone, vitamin D, and calcitonin. Causes, signs and symptoms, and treatment approaches for hypercalcemia and hypocalcemia are reviewed. The key points are that calcium levels are tightly controlled by hormones to maintain levels between 2.25-2.62 mmol/L and that disorders can result from excess or deficiencies of these regulating hormones.
Calcium,magnesium,phosphate and chloride imbalances Jyothi Swaroop
Calcium,magnesium,phosphate and chloride imbalances
Their treatment,my main reference is Eric strong's lectures in youtube,and some of the websites.Hope everyone finding Serum electrolytes find atleast some use of it .
Thank you
Calcium,magnesium,phosphate and chloride imbalances jyothiswaroopb1
i could make best of me ,by collecting information from mainly Eric's strongs medical lectures in youtube and from many websites .
Hope you guys may find any important information.
Thank you
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
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.
Calcium is an essential mineral that makes up 2% of body weight. Over 99% is stored in bones, with the rest in tissues and plasma. Calcium levels are tightly regulated by parathyroid hormone (PTH), calcitonin, and calcitriol (active vitamin D). PTH increases calcium levels by promoting bone resorption, while calcitonin and calcitriol decrease calcium levels by reducing resorption. Bisphosphonates are used to treat osteoporosis and Paget's disease by inhibiting bone resorption. They decrease osteoclast activity and survival. Calcium supplements are used to treat deficiencies and osteoporosis, while bisphosphonates and calcim
This document discusses calcium metabolism and provides details on calcium homeostasis, absorption, excretion, and the roles of parathyroid hormone and vitamin D. It also covers hypocalcemia and hypercalcemia, defining each condition and describing causes, clinical manifestations, diagnostic workup, and treatment approaches. Hypocalcemia can result from neonatal issues, vitamin D deficiency, hypoparathyroidism, or other causes. Hypercalcemia has causes including parathyroid hormone excess, malignancy, vitamin D excess, and genetic conditions.
This document discusses calcium homeostasis and hypercalcemia. It notes that approximately 1000-1200 mg of calcium is present in an adult, mostly in bone. It describes the distribution and protein binding of calcium in extracellular fluid and intracellular fluid. Factors that influence calcium absorption in the gut and renal handling of calcium are outlined. Mechanisms involved in response to changes in serum calcium levels, including the roles of TRPV5 calcium channels and calbindin D28k protein, are summarized. Causes, clinical features, pathophysiology, and treatment approaches for hypercalcemia and various hypercalcemic disorders like primary hyperparathyroidism and familial hypocalciuric hypercalcemia are described.
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 electrolyte abnormalities in children. It begins by reviewing body composition and water balance in the human body. It then covers the composition and regulation of sodium, potassium, and other electrolytes. Specific conditions that can cause electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia are defined and their causes and treatment approaches are outlined. The document emphasizes the importance of determining the underlying cause and correcting imbalances gradually to avoid complications.
This document discusses electrolyte abnormalities in children. It provides information on the composition of body fluids, water balance, and maintenance fluid and electrolyte requirements in children. It then focuses on abnormalities in sodium, potassium, and other electrolytes. For each abnormality, it describes the causes, clinical features, evaluation, and treatment approaches. It emphasizes the importance of determining the underlying cause and correcting abnormalities slowly and carefully to avoid complications.
This document provides an overview of acute renal failure in children. It defines acute renal failure, discusses causes (pre-renal, intrinsic renal, post-renal), pathogenesis, laboratory findings, biomarkers, management including fluid resuscitation, diuretics, electrolyte abnormalities, nutrition, and indications for dialysis. Management is aimed at treating the underlying cause and maintaining fluid, electrolyte and acid-base balance until renal function recovers.
This document summarizes alterations in calcium metabolism, including hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism, or increased intestinal calcium absorption. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood compartment, or by decreased calcium flow from intestines or bones into the blood, as seen in hypoparathyroidism. The document outlines the clinical presentations, diagnostic evaluations, and treatments for hypercalcemia and hypocalcemia.
This document summarizes alterations in calcium metabolism, including hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism, or increased intestinal calcium absorption. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood compartment, or by decreased calcium flow from intestines or bones into the blood, as seen in hypoparathyroidism. The document outlines the clinical presentations, diagnostic evaluations, and treatments for hypercalcemia and hypocalcemia.
Calcium and phosphorus are essential minerals found primarily in bones and teeth. Calcium makes up 1-2% of total body weight and is found mostly in bones, while phosphorus makes up 1% of body weight and is primarily intracellular. Dietary sources of calcium include dairy products, while phosphorus is obtained from foods like cereals, meat, and nuts. Absorption of both minerals can be affected by factors like vitamin D, pH, and other dietary constituents. Calcium and phosphorus are important for bone health, cell signaling, and other metabolic processes. Abnormal levels can cause issues like muscle problems or bone diseases. Their levels are tightly regulated and measured together to diagnose certain conditions.
Acute renal failure is a clinical syndrome where sudden deterioration of renal function results in the kidneys' inability to maintain fluid and electrolyte homeostasis. It has various etiologies like pre-renal, intrinsic renal, and post-renal factors. Management involves treating the underlying cause, fluid resuscitation, controlling electrolyte abnormalities, and starting dialysis for refractory volume overload, hyperkalemia, acidosis, or neurological symptoms. The healthcare team works to stabilize the patient and prevent long-term kidney damage.
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
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 alterations in calcium metabolism, specifically hypercalcemia and hypocalcemia. Hypercalcemia is defined as elevated serum calcium levels and can be caused by increased bone resorption, as seen in primary hyperparathyroidism or bone metastases from cancers like breast or lung cancer. Hypocalcemia is defined as low serum calcium levels and can be caused by calcium exiting the blood into tissues, as seen in kidney failure, or by decreased intestinal calcium absorption, as seen in vitamin D deficiency. Symptoms, diagnosis, and treatment approaches are described for both hypercalcemia and hypocalcemia.
Approach to patient with hypo/hyper calcaemiaNassr ALBarhi
This document discusses calcium homeostasis and disorders of calcium metabolism. It begins by describing the functions of calcium in the body and where calcium is stored. It then discusses calcium regulation by parathyroid hormone, vitamin D, and calcitonin. Causes, signs and symptoms, and treatment approaches for hypercalcemia and hypocalcemia are reviewed. The key points are that calcium levels are tightly controlled by hormones to maintain levels between 2.25-2.62 mmol/L and that disorders can result from excess or deficiencies of these regulating hormones.
Calcium,magnesium,phosphate and chloride imbalances Jyothi Swaroop
Calcium,magnesium,phosphate and chloride imbalances
Their treatment,my main reference is Eric strong's lectures in youtube,and some of the websites.Hope everyone finding Serum electrolytes find atleast some use of it .
Thank you
Calcium,magnesium,phosphate and chloride imbalances jyothiswaroopb1
i could make best of me ,by collecting information from mainly Eric's strongs medical lectures in youtube and from many websites .
Hope you guys may find any important information.
Thank you
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1. HYPERCALCEMIA & HYPOCALCEMIA
MODERATOR
DR. RAKESH RANJAN
ASSISTANT PROFESSOR PEDIATRIC
DEPARTMENT
SHRI KRISHNA MEDICAL
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PRESENTER
DR. JAIKISHAN
AND
DR. AMANATULLAH
PG- DNB(1ST YEAR)
PEDIATRIC DEPARTMENT
SKMC, MUZZAFARPUR
2. CALCIUM HOMEOSTASIS
It involves interaction of GIT absorption , Bone resorption and Renal excretion .
PTH and Vit D are principle regulators of Calcium Homeostasis.
Normal Serum Calcium level is 9-11 mg /dL.
Calcitonin & PTH-related peptide are important primary regulator in fetus.
PTH is an 84 amino acid chain , but its biologic activity resides in the first 34 residues.
3. Most (99%) body calcium is stored in the bone and is in constant
equilibrium with serum calcium .
Approx 1-2% of body calcium exist in ECF for physiological function
like –
Blood Coagulation
Cellular Communication
Exocytosis and Endocytosis
Muscle contraction
Neuromuscular transmission
4. Most of the filtered Calcium is Reabsorbed in the
proximal convulted tubule (approx 70% ) ,
Ascending Loop of Henle (20%) & the Distal
convulted tubule and Collecting Duct (5-10%) .
5. Role of Calcium Sensing receptor
The body senses calcium levels using calcium sensing
receptors present in parathyroid gland and kidney.
The Calcium sensing receptor is GPCR
Plasma calcium exists in 3 different forms –
50 % as biologically active ionized form
45% bounded to plasma protein (mainly albumin)
5% complexed to phosphate
6.
7. Metabolic acidosis leads to increased ionized calcium
from reduced protein binding
Alkalosis has opposite effect .
Corrected Calcium can be calculated by
Corrected Ca = ( 4 – Plasma albumin in g/dL ) x 0.8
+ Measured Serum Calcium
[ for every 1g/dL drop in Serum Albumin below 4g/dL,
measured Sr. calcium decreased by 0.8 mg/dL ]
8.
9. HYPERCALCEMIA
Defined as Serum Calcium levels > 11mg/dL.
Hypercalcemia is often asymptomatic although it can cause
symptoms at levels 12mg/dL
10. Causes of Hypercalcemia
Hypercalcemia is uncommon in children as compared to Hypocalcemia .
➢ 1) Neonates
Neonatal primary hyperparathyroidism
Secondary hyperparathyroidism
Excessive supplementation of Calcium
William’s Syndrome
Familial Hypocalcemic Hypercalcemia
11. ➢ Older Children
Hyperparathyroidism – Parathyroid Adenoma
MEN-1
Malignancies - Non Hodgkin or Hodgkin Lymphoma
- Ewing’s Sarcoma
- Neuroblastoma
Granulomatous disease - Sarcoidosis
TB
Wegener disease .
Others - Vit D or Vit A intoxication
- Thiazide diuretic
- Milk-Alkali Syndrome
12. Symptoms and Signs of Hypercalcemia
Common Symptoms are –
Polyuria
Polydipsia
Poor weight gain
Failure to thrive
Easy Fatigability
Irritability
Confusion
Pain abdomen
Constipation
13. Severe Hypercalcemia inhibits neuromuscular and myocardial
depolarization causing arrhythmia and neuromuscular weakness.
Severe acute abdominal pain could be a clue to suspect
pancreatitis
Severe Calcium >14 mg/dL may result in encephalopathy .
Bone related symptoms are Bone pain and Fractures
CVS effect – Prolong PR interval
Short QT interval
Widened QRS complex
14.
15. Treatment of Hypercalcemia
Treatment is required for symptomatic hypercalcemia and
asymptomatic hypercalcemia with serum calcium > 15 mg/dL .
A) For increasing Calcium elimination
Twice maintenance fluid ( Isotonic Fluid )
Loop Diuretics – I.V Furosemide 1-2 mg/kg/day
in case of renal or cardiac disease only
Hemodialysis
16. b) Reducing Bone absorption – Bisphosphonates
Pamidronate (0.5-1 mg/kg)
as an infusion over 4-6 hrs
Calcitonin – 4 units /kg IM/S.C
q 12 hourly
c) Reducing calcium absorption – Steroids (1-2 mg/kg/day –
20-40 mg/day )
d) Surgical intervention may be needed in patients with
hyperparathyroidism, particularly with recurrent renal stones .
19. Causes of Hypocalcemia
1) Neonatal
a) Maternal disorder
Diabetes mellitus
Toximia of pregnancy
Vit D deficiency
Use of anti-convulsants
High intake of alkali or
magnesium sulfate
Hyperparathyroidism
21. (B) Acquired :
1) Autoimmune polygandular syndrome type 1 (AIRE Gene mutation)
2) Activating antibodies to the CaSR
3) Hypomagnesemia / Hypermagnesemia
3) VIT D Deficiency
4) Other Causes like –
1) Calcium deficiency due to Nutritional Deprivation , Hypercalcemia
2) Disorders of magnesium Homeostasis
3) Hyperphosphatemia – a) renal failure
b) phosphate administration
22. Clinical Manifestation
➢ The Symptoms of Hypocalcemia are related to disturbance in nerve and muscle conduction as
hypocalcemia causes neuromuscular excitability .
Muscular pain and Cramps ( early manifestations)
➢ Numbness, Stiffness and Tingling of hand and feet .
➢ Uncommon symptoms – Stridor secondary to laryngeal spasm and apnea in infants .
24. ECG reveals prolonged QTc interval ( > 0.4 s ) and
QoTc ( > 0.2 s )
25. Investigation
Basic investigation in hypocalcemia
1) Serum Calcium level is low and Phosphorus level is elevated
2) Serum Calcium , Phosphate , Alkaline phosphatase .
3) Serum Vit D , Parathyroid hormone , X ray Wrist or Knee
4) Serum albumin , Serum Creatinine , Serum Magnesium
5) Urine Calcium / Creatinine ratio .
26. Treatment
Depends on severity of symptoms and underlying etiology of hypocalcemia
- I/V Calcium required in case of Seizure , Laryngospasm , Tetany , Cardiovascular compromise
- 10 % Calcium Gluconate ( 1ml contains 9.3 mg of elemental calcium )
- I/V dose – 0.5-1 ml/kg (max 2 ml/kg )
Calcium Gluconate diluted with Ns or 5% dextrose ( 1:10 dilution ) over 20 min
- Not more than 5 mg of elemental calcium per minute
- Additionally 1,25 dihydroxycholecalciferol should be given
initial dose – 0.25 μg / 24 hr
maintenance dose – 0.01 – 0.10 μg / kg / 24 hr
maximum dose – 1 – 2 μg / 24 hr
27. - I/V calcium should be always infused under cardiac monitoring
- Once the acute symptoms are subsided discontinue I/V Supplementation
- For those children who don’t need urgent correction of serum calcium , oral calcium
supplementation can be administered upto 400 mg / kg /day .
- Magnesium deficiencies must be considered In patients with unexplained
hypocalcemia
- Concentration of serum Mg < 1.5 mg/dL are abnormal