Calcium metabolism involves the distribution, daily requirements, dietary sources, functions, absorption, and factors regulating plasma calcium levels. Calcium is primarily stored in bones and teeth, with 99% located in the skeleton. Dietary sources of calcium include milk, dairy products, leafy greens, and fish. Calcium is important for bone formation, muscle contraction, blood coagulation, and enzyme activation. Absorption occurs primarily in the small intestine and is influenced by vitamin D, PTH, pH, and dietary factors like oxalates. Plasma calcium levels are tightly regulated by vitamin D, PTH, and calcitonin. Disorders of calcium metabolism include hypercalcemia, hypocalcemia, rickets, and oste
1. Calcium homeostasis is regulated by parathyroid hormone (PTH), calcitonin, and vitamin D. PTH increases calcium absorption in the gut and kidneys while decreasing urinary calcium excretion. Calcitonin decreases calcium levels by inhibiting bone resorption. Vitamin D facilitates intestinal calcium absorption.
2. The normal plasma ionized calcium level is 2.12-2.65 mmol/L. Calcitonin and the kidneys play major roles in calcium homeostasis. Absorption of calcium from the gut is regulated by PTH and vitamin D.
3. A patient lacking PTH after parathyroid damage would have low calcium and phosphate levels, increased muscle excitability (
Calcium homeostasis involves tightly regulating plasma calcium levels through a complex interplay of hormones like parathyroid hormone (PTH), calcitriol, and calcitonin. PTH acts to raise calcium levels by stimulating bone resorption and renal reabsorption of calcium. Calcitriol promotes intestinal calcium absorption. Calcitonin lowers calcium levels by inhibiting bone resorption. The body maintains 99% of its calcium stores in bones. Imbalances can result in hypercalcemia from overactive PTH or hypocalcemia from vitamin D deficiency.
Calcium homeostasis is tightly regulated to keep plasma calcium levels within a narrow range. Three hormones - parathyroid hormone (PTH), calcitriol, and calcitonin - work together to regulate calcium levels by moving calcium between bones and extracellular fluid. The kidneys also play an important role by reabsorbing around 80% of filtered calcium in the proximal tubule and regulating further calcium reabsorption in other parts of the nephron in response to these hormones and other factors like calcium levels and pH. Disruptions to this regulatory system can lead to hypocalcemia or hypercalcemia.
Calcium homeostasis is tightly regulated by parathyroid hormone, calcitonin, and vitamin D. These hormones act on the intestines, bones, and kidneys to maintain calcium levels. When calcium levels decrease, parathyroid hormone signals the intestines to absorb more calcium from food and the bones to release calcium into the bloodstream. Calcitonin acts in opposition to parathyroid hormone by inhibiting bone calcium release. Vitamin D assists in intestinal calcium absorption. Disorders occur when these regulatory mechanisms are disrupted, leading to either hypercalcemia or hypocalcemia.
The document summarizes key aspects of the citric acid cycle (TCA cycle):
1) The TCA cycle involves the oxidation of acetyl-CoA to CO2 and generates most of the cell's ATP through oxidative phosphorylation.
2) Reactions of the TCA cycle involve the condensation of acetyl-CoA with oxaloacetate to form citrate, followed by several oxidation, isomerization and decarboxylation reactions that generate NADH and FADH2.
3) The TCA cycle is regulated by enzymes like citrate synthase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase which respond to cellular energy levels like ATP/ADP
Calcium homeostasis refers to the body's ability to maintain calcium levels in the blood within a normal range of 9-11 mg/100 ml. Approximately 99% of the body's 1 kg calcium stores are found in bones, while 1% circulates in blood and tissues. Calcium levels are regulated by parathyroid hormone (PTH), calcitonin, vitamin D, and through absorption in the intestines and reabsorption/excretion in the kidneys. PTH increases calcium levels by promoting bone resorption and kidney reabsorption, while calcitonin decreases them by inhibiting bone resorption and increasing kidney excretion. Vitamin D facilitates intestinal calcium absorption. Abnormally low calcium can cause tetany
Ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) are water-soluble molecules produced by the liver from fatty acids during periods of low food intake (fasting or starvation), prolonged intense exercise, and uncontrolled diabetes. The liver exports ketone bodies to be used as an energy source by the brain, heart, and skeletal muscles in place of glucose. Ketone body production is regulated by controlling fatty acid release from adipose tissue, fatty acid oxidation in the liver, and partitioning of acetyl-CoA between ketogenesis and the citric acid cycle. Excessive ketone body accumulation can overwhelm acid-base buffering mechanisms and lead to ketoacidosis, as
1. Calcium homeostasis is regulated by parathyroid hormone (PTH), calcitonin, and vitamin D. PTH increases calcium absorption in the gut and kidneys while decreasing urinary calcium excretion. Calcitonin decreases calcium levels by inhibiting bone resorption. Vitamin D facilitates intestinal calcium absorption.
2. The normal plasma ionized calcium level is 2.12-2.65 mmol/L. Calcitonin and the kidneys play major roles in calcium homeostasis. Absorption of calcium from the gut is regulated by PTH and vitamin D.
3. A patient lacking PTH after parathyroid damage would have low calcium and phosphate levels, increased muscle excitability (
Calcium homeostasis involves tightly regulating plasma calcium levels through a complex interplay of hormones like parathyroid hormone (PTH), calcitriol, and calcitonin. PTH acts to raise calcium levels by stimulating bone resorption and renal reabsorption of calcium. Calcitriol promotes intestinal calcium absorption. Calcitonin lowers calcium levels by inhibiting bone resorption. The body maintains 99% of its calcium stores in bones. Imbalances can result in hypercalcemia from overactive PTH or hypocalcemia from vitamin D deficiency.
Calcium homeostasis is tightly regulated to keep plasma calcium levels within a narrow range. Three hormones - parathyroid hormone (PTH), calcitriol, and calcitonin - work together to regulate calcium levels by moving calcium between bones and extracellular fluid. The kidneys also play an important role by reabsorbing around 80% of filtered calcium in the proximal tubule and regulating further calcium reabsorption in other parts of the nephron in response to these hormones and other factors like calcium levels and pH. Disruptions to this regulatory system can lead to hypocalcemia or hypercalcemia.
Calcium homeostasis is tightly regulated by parathyroid hormone, calcitonin, and vitamin D. These hormones act on the intestines, bones, and kidneys to maintain calcium levels. When calcium levels decrease, parathyroid hormone signals the intestines to absorb more calcium from food and the bones to release calcium into the bloodstream. Calcitonin acts in opposition to parathyroid hormone by inhibiting bone calcium release. Vitamin D assists in intestinal calcium absorption. Disorders occur when these regulatory mechanisms are disrupted, leading to either hypercalcemia or hypocalcemia.
The document summarizes key aspects of the citric acid cycle (TCA cycle):
1) The TCA cycle involves the oxidation of acetyl-CoA to CO2 and generates most of the cell's ATP through oxidative phosphorylation.
2) Reactions of the TCA cycle involve the condensation of acetyl-CoA with oxaloacetate to form citrate, followed by several oxidation, isomerization and decarboxylation reactions that generate NADH and FADH2.
3) The TCA cycle is regulated by enzymes like citrate synthase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase which respond to cellular energy levels like ATP/ADP
Calcium homeostasis refers to the body's ability to maintain calcium levels in the blood within a normal range of 9-11 mg/100 ml. Approximately 99% of the body's 1 kg calcium stores are found in bones, while 1% circulates in blood and tissues. Calcium levels are regulated by parathyroid hormone (PTH), calcitonin, vitamin D, and through absorption in the intestines and reabsorption/excretion in the kidneys. PTH increases calcium levels by promoting bone resorption and kidney reabsorption, while calcitonin decreases them by inhibiting bone resorption and increasing kidney excretion. Vitamin D facilitates intestinal calcium absorption. Abnormally low calcium can cause tetany
Ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) are water-soluble molecules produced by the liver from fatty acids during periods of low food intake (fasting or starvation), prolonged intense exercise, and uncontrolled diabetes. The liver exports ketone bodies to be used as an energy source by the brain, heart, and skeletal muscles in place of glucose. Ketone body production is regulated by controlling fatty acid release from adipose tissue, fatty acid oxidation in the liver, and partitioning of acetyl-CoA between ketogenesis and the citric acid cycle. Excessive ketone body accumulation can overwhelm acid-base buffering mechanisms and lead to ketoacidosis, as
This document discusses ketone body metabolism. Ketone bodies (acetoacetate, 3-hydroxybutyrate, acetone) are produced in the liver through fatty acid catabolism when glucose levels are low, such as during starvation or uncontrolled diabetes. They provide energy for other tissues when carbohydrates are limited. Excess ketone body production can lead to ketosis or ketoacidosis if ketones accumulate and cause a metabolic acidosis. The key steps in ketone body synthesis and utilization are described along with the regulation of ketogenesis and conditions that can cause diabetic or starvation ketoacidosis.
This document provides an overview of calcium metabolism. It discusses the regulatory mechanisms that control calcium levels in the blood and bones. The key hormones involved - parathyroid hormone (PTH), calcitonin, and vitamin D - and how they work to increase or decrease blood calcium levels by affecting absorption in the gut and resorption/deposition in bones. It also covers calcium storage in bones, excretion by the kidneys, interactions with other minerals, and disorders that can arise from issues with calcium regulation.
Calcium is essential for bone mineralization and plays an important role in many physiological processes; it is tightly regulated by parathyroid hormone and vitamin D. Hypocalcemia can result from hypoalbuminemia, chronic kidney disease, hypoparathyroidism, or hypomagnesemia, while hypercalcemia is usually caused by primary hyperparathyroidism or certain cancers. Both total and ionized calcium levels should be measured and interpreted carefully due to various pre-analytical factors that can affect results.
This document summarizes calcium, phosphate, and magnesium metabolism. It discusses that these minerals have important intracellular and extracellular functions regulated by hormones like PTH and vitamin D. The majority of calcium is stored in bone, while phosphate and magnesium also have roles in cell structures and energy processes. Tight homeostasis maintains mineral levels in the blood and body through balances of absorption, excretion, and bone remodeling. Disorders can develop if these processes are disrupted.
This document summarizes ketone body metabolism. It describes that ketone bodies (acetone, acetoacetate, and beta-hydroxybutyrate) are produced in the liver from fatty acids during periods of low carbohydrate availability like starvation and untreated diabetes. The liver converts fatty acids into ketone bodies which can be used as fuel by other tissues. High glucagon and low insulin levels promote ketone body formation and their levels in the blood (ketonemia) and urine (ketonuria) increase if their production exceeds utilization, causing the metabolic condition of ketosis.
Calcium homeostasis involves absorption of calcium from the intestine, regulation by parathyroid hormone (PTH), vitamin D, and calcitonin, and storage in bone. PTH increases calcium levels by stimulating bone resorption and renal reabsorption and vitamin D absorption. Vitamin D increases intestinal calcium absorption. Calcitonin decreases calcium by inhibiting bone resorption. Hypocalcemia causes neurological symptoms and hypercalcemia causes gastrointestinal and renal issues. Conditions are diagnosed by calcium levels and other tests and treated by calcium supplementation or intravenous calcium for hypocalcemia and hydration and medications for hypercalcemia.
This document summarizes bone physiology and calcium metabolism. It describes the organic and inorganic constituents of bone, including collagen, calcium hydroxyapatite, and other minerals. It outlines the cells involved in bone remodeling including osteoprogenitor cells, osteoblasts, osteocytes, and osteoclasts. It also discusses the roles of vitamin D, parathyroid hormone, and calcitonin in regulating calcium levels in the body and maintaining bone health. Key bone diseases like osteoporosis, Paget's disease, and renal osteodystrophy are also summarized.
They are water soluble substances.
2. They are synthesized at a relatively low rate in well nourished individuals.
3. Plasma level of ketone bodies < 1mg/dl.
4. Urinary level of ketone bodies <3 mg/24 hour urine.
This document summarizes ketone bodies and their synthesis during periods of starvation or uncontrolled diabetes. It notes that ketone bodies are normally a negligible source of energy but their levels can increase up to 500mg/dl during prolonged fasting as fatty acids are broken down and converted to ketone bodies in the liver. The key ketone bodies, acetoacetate and 3-hydroxybutyrate, can then be used as an energy source by tissues like cardiac muscle when glucose levels are low. The document also explains that ketone body synthesis is regulated by the lipolysis of fatty acids from adipose tissue and their conversion to acetyl-CoA in the liver mitochondria.
Phosphate homeostasis & its related disordersenamifat
This document discusses phosphate homeostasis and related disorders. It covers the functions, regulation, and normal ranges of phosphate in the body. Phosphate is essential for many processes like bone mineralization and energy metabolism. The kidneys play a major role in regulating phosphate levels through reabsorption and excretion. Parathyroid hormone (PTH) and vitamin D help regulate phosphate absorption in the intestines and its levels in blood and bones. Abnormalities can cause either high or low phosphate levels. Causes and effects of hyperphosphatemia and hypophosphatemia are explained.
Calcium metabolism involves three tissues (bone, intestine, kidney), three hormones (PTH, calcitonin, vitamin D), and three cell types that maintain normal calcium levels. Calcium is important for bone health, muscle function, and other processes. The daily requirement is 400-500mg for adults. PTH and calcitonin work to maintain calcium within normal ranges in plasma. Hypocalcemia can cause tetany and hypercalcemia can damage organs if severe. Tests are used to diagnose and treat imbalances.
it is about how ammonia is detoxified to urea and its biomedical significance. This PPT can be used by students of MBBS, MD, BDS and general Biochemistry students
Ketone bodies are produced when fatty acids are broken down in the liver. They serve as an alternative energy source for tissues when glucose is limited, such as during fasting or diabetes. Ketone bodies are synthesized in the liver through a series of reactions starting with acetyl CoA. Their production is regulated by substrate availability, fatty acid oxidation, ATP levels, and the enzyme HMG CoA synthase. Tissues such as the brain can use ketone bodies for energy through another series of reactions. Excessive ketone body production causes ketosis, characterized by ketonemia, ketonuria, and metabolic acidosis. Ketosis is managed by restoring carbohydrate metabolism and correcting electrolyte and acid-base imbalances.
The document discusses metabolic acidosis and ketosis. It defines metabolic acidosis as a condition where the blood pH is low due to buildup of acid in the body. Common causes include diarrhea, kidney failure, and loss of bicarbonate ions. Symptoms include nausea, vomiting, shortness of breath, and increased heart rate. Treatment involves administering bicarbonate ions intravenously to raise the pH level. Ketosis occurs when the liver produces ketone bodies during fasting to be used as fuel. It helps conserve protein and is a more efficient fuel than glucose. However, excessive ketone buildup can lead to ketoacidosis.
Calcium 101 The Fundamentals of CalciumDesiree Lotz
This document provides an overview of calcium and how the supplement Instant CalMag-C can help maintain calcium levels. It discusses that calcium is essential for the nervous, muscular and skeletal systems and is regulated by the parathyroid gland. For calcium to be active, it must work with magnesium in a 2:1 ratio and be in the form of calcium gluconate. Instant CalMag-C contains this precise calcium to magnesium ratio plus vitamin C to aid absorption. Maintaining balanced calcium and magnesium levels through supplements like Instant CalMag-C can support overall health.
This document discusses calcium, iron, copper, zinc, and selenium metabolism. It describes how calcium levels are regulated by the bone, kidney, and intestine, as well as hormones like calcitriol, PTH, and calcitonin. Iron transport involves uptake in the intestine and binding to transferrin in the bloodstream. Copper is an essential cofactor for many enzymes. Zinc and selenium deficiencies can cause growth problems and cardiac issues.
This document discusses ketone bodies, their metabolism, and conditions of excess ketone body production. Ketone bodies are produced in the liver from acetyl-CoA when fatty acid breakdown exceeds the ability of the citric acid cycle to process acetyl-CoA. They can be used as an energy source by other tissues. Excess ketone body production occurs in starvation and uncontrolled diabetes, leading to ketosis or ketoacidosis as ketone levels rise and pH decreases due to ketone acid buildup.
This document discusses calcium homeostasis and its regulation in the human body. It covers the following key points:
- Calcium is essential for structural integrity of bones and normal function of biochemical processes. Its levels are tightly regulated by parathyroid hormone (PTH), vitamin D, and calcitonin.
- 99% of calcium in the body is stored in bones, with the remaining 1% divided between intracellular and extracellular fluids. PTH acts to mobilize calcium from bones and enhance renal reabsorption when calcium levels drop.
- Vitamin D aids calcium absorption from the gut and reabsorption from kidneys. The active form is produced by PTH and kidney enzymes. Together with PTH, vitamin
This document discusses ketosis, including the three main types of ketone bodies, acetone, acetoacetic acid, and beta-hydroxybutyric acid. It describes how ketosis occurs when the rate of ketone body synthesis exceeds the rate of their utilization, as seen in starvation and diabetes mellitus. Factors that can aggravate ketosis are also summarized, such as decreased carbohydrate availability and increased free fatty acid levels. The clinical effects of ketosis include ketoacidosis, dehydration, and potentially death if left untreated. Treatment involves administering insulin, glucose, and bicarbonate to correct acidosis.
This document provides an overview of calcium homeostasis and the regulation of blood calcium levels. It discusses the distribution, storage, and biochemical functions of calcium in the body. The key hormones and mechanisms involved in maintaining calcium levels are parathyroid hormone (PTH), calcitriol (the active form of vitamin D), and calcitonin. PTH acts to increase blood calcium levels by promoting bone resorption and renal reabsorption of calcium. Calcitriol increases intestinal calcium absorption. Calcitonin acts to decrease blood calcium levels. Together these hormones tightly control calcium concentrations to ensure levels remain within their normal range.
Calcium is essential for bone development, muscle contraction, blood clotting and nerve transmission. 99% of calcium is stored in bones while the remaining 1% circulates in blood. Dietary sources like milk aid absorption while factors like phytates inhibit it. Calcium levels are tightly regulated by parathyroid hormone, calcitriol, and calcitonin. Hypocalcemia and hypercalcemia and disorders like rickets impact bone mineralization. Oral manifestations include dry mouth and enamel defects while radiographs show hypoplasia and resorption.
This document discusses ketone body metabolism. Ketone bodies (acetoacetate, 3-hydroxybutyrate, acetone) are produced in the liver through fatty acid catabolism when glucose levels are low, such as during starvation or uncontrolled diabetes. They provide energy for other tissues when carbohydrates are limited. Excess ketone body production can lead to ketosis or ketoacidosis if ketones accumulate and cause a metabolic acidosis. The key steps in ketone body synthesis and utilization are described along with the regulation of ketogenesis and conditions that can cause diabetic or starvation ketoacidosis.
This document provides an overview of calcium metabolism. It discusses the regulatory mechanisms that control calcium levels in the blood and bones. The key hormones involved - parathyroid hormone (PTH), calcitonin, and vitamin D - and how they work to increase or decrease blood calcium levels by affecting absorption in the gut and resorption/deposition in bones. It also covers calcium storage in bones, excretion by the kidneys, interactions with other minerals, and disorders that can arise from issues with calcium regulation.
Calcium is essential for bone mineralization and plays an important role in many physiological processes; it is tightly regulated by parathyroid hormone and vitamin D. Hypocalcemia can result from hypoalbuminemia, chronic kidney disease, hypoparathyroidism, or hypomagnesemia, while hypercalcemia is usually caused by primary hyperparathyroidism or certain cancers. Both total and ionized calcium levels should be measured and interpreted carefully due to various pre-analytical factors that can affect results.
This document summarizes calcium, phosphate, and magnesium metabolism. It discusses that these minerals have important intracellular and extracellular functions regulated by hormones like PTH and vitamin D. The majority of calcium is stored in bone, while phosphate and magnesium also have roles in cell structures and energy processes. Tight homeostasis maintains mineral levels in the blood and body through balances of absorption, excretion, and bone remodeling. Disorders can develop if these processes are disrupted.
This document summarizes ketone body metabolism. It describes that ketone bodies (acetone, acetoacetate, and beta-hydroxybutyrate) are produced in the liver from fatty acids during periods of low carbohydrate availability like starvation and untreated diabetes. The liver converts fatty acids into ketone bodies which can be used as fuel by other tissues. High glucagon and low insulin levels promote ketone body formation and their levels in the blood (ketonemia) and urine (ketonuria) increase if their production exceeds utilization, causing the metabolic condition of ketosis.
Calcium homeostasis involves absorption of calcium from the intestine, regulation by parathyroid hormone (PTH), vitamin D, and calcitonin, and storage in bone. PTH increases calcium levels by stimulating bone resorption and renal reabsorption and vitamin D absorption. Vitamin D increases intestinal calcium absorption. Calcitonin decreases calcium by inhibiting bone resorption. Hypocalcemia causes neurological symptoms and hypercalcemia causes gastrointestinal and renal issues. Conditions are diagnosed by calcium levels and other tests and treated by calcium supplementation or intravenous calcium for hypocalcemia and hydration and medications for hypercalcemia.
This document summarizes bone physiology and calcium metabolism. It describes the organic and inorganic constituents of bone, including collagen, calcium hydroxyapatite, and other minerals. It outlines the cells involved in bone remodeling including osteoprogenitor cells, osteoblasts, osteocytes, and osteoclasts. It also discusses the roles of vitamin D, parathyroid hormone, and calcitonin in regulating calcium levels in the body and maintaining bone health. Key bone diseases like osteoporosis, Paget's disease, and renal osteodystrophy are also summarized.
They are water soluble substances.
2. They are synthesized at a relatively low rate in well nourished individuals.
3. Plasma level of ketone bodies < 1mg/dl.
4. Urinary level of ketone bodies <3 mg/24 hour urine.
This document summarizes ketone bodies and their synthesis during periods of starvation or uncontrolled diabetes. It notes that ketone bodies are normally a negligible source of energy but their levels can increase up to 500mg/dl during prolonged fasting as fatty acids are broken down and converted to ketone bodies in the liver. The key ketone bodies, acetoacetate and 3-hydroxybutyrate, can then be used as an energy source by tissues like cardiac muscle when glucose levels are low. The document also explains that ketone body synthesis is regulated by the lipolysis of fatty acids from adipose tissue and their conversion to acetyl-CoA in the liver mitochondria.
Phosphate homeostasis & its related disordersenamifat
This document discusses phosphate homeostasis and related disorders. It covers the functions, regulation, and normal ranges of phosphate in the body. Phosphate is essential for many processes like bone mineralization and energy metabolism. The kidneys play a major role in regulating phosphate levels through reabsorption and excretion. Parathyroid hormone (PTH) and vitamin D help regulate phosphate absorption in the intestines and its levels in blood and bones. Abnormalities can cause either high or low phosphate levels. Causes and effects of hyperphosphatemia and hypophosphatemia are explained.
Calcium metabolism involves three tissues (bone, intestine, kidney), three hormones (PTH, calcitonin, vitamin D), and three cell types that maintain normal calcium levels. Calcium is important for bone health, muscle function, and other processes. The daily requirement is 400-500mg for adults. PTH and calcitonin work to maintain calcium within normal ranges in plasma. Hypocalcemia can cause tetany and hypercalcemia can damage organs if severe. Tests are used to diagnose and treat imbalances.
it is about how ammonia is detoxified to urea and its biomedical significance. This PPT can be used by students of MBBS, MD, BDS and general Biochemistry students
Ketone bodies are produced when fatty acids are broken down in the liver. They serve as an alternative energy source for tissues when glucose is limited, such as during fasting or diabetes. Ketone bodies are synthesized in the liver through a series of reactions starting with acetyl CoA. Their production is regulated by substrate availability, fatty acid oxidation, ATP levels, and the enzyme HMG CoA synthase. Tissues such as the brain can use ketone bodies for energy through another series of reactions. Excessive ketone body production causes ketosis, characterized by ketonemia, ketonuria, and metabolic acidosis. Ketosis is managed by restoring carbohydrate metabolism and correcting electrolyte and acid-base imbalances.
The document discusses metabolic acidosis and ketosis. It defines metabolic acidosis as a condition where the blood pH is low due to buildup of acid in the body. Common causes include diarrhea, kidney failure, and loss of bicarbonate ions. Symptoms include nausea, vomiting, shortness of breath, and increased heart rate. Treatment involves administering bicarbonate ions intravenously to raise the pH level. Ketosis occurs when the liver produces ketone bodies during fasting to be used as fuel. It helps conserve protein and is a more efficient fuel than glucose. However, excessive ketone buildup can lead to ketoacidosis.
Calcium 101 The Fundamentals of CalciumDesiree Lotz
This document provides an overview of calcium and how the supplement Instant CalMag-C can help maintain calcium levels. It discusses that calcium is essential for the nervous, muscular and skeletal systems and is regulated by the parathyroid gland. For calcium to be active, it must work with magnesium in a 2:1 ratio and be in the form of calcium gluconate. Instant CalMag-C contains this precise calcium to magnesium ratio plus vitamin C to aid absorption. Maintaining balanced calcium and magnesium levels through supplements like Instant CalMag-C can support overall health.
This document discusses calcium, iron, copper, zinc, and selenium metabolism. It describes how calcium levels are regulated by the bone, kidney, and intestine, as well as hormones like calcitriol, PTH, and calcitonin. Iron transport involves uptake in the intestine and binding to transferrin in the bloodstream. Copper is an essential cofactor for many enzymes. Zinc and selenium deficiencies can cause growth problems and cardiac issues.
This document discusses ketone bodies, their metabolism, and conditions of excess ketone body production. Ketone bodies are produced in the liver from acetyl-CoA when fatty acid breakdown exceeds the ability of the citric acid cycle to process acetyl-CoA. They can be used as an energy source by other tissues. Excess ketone body production occurs in starvation and uncontrolled diabetes, leading to ketosis or ketoacidosis as ketone levels rise and pH decreases due to ketone acid buildup.
This document discusses calcium homeostasis and its regulation in the human body. It covers the following key points:
- Calcium is essential for structural integrity of bones and normal function of biochemical processes. Its levels are tightly regulated by parathyroid hormone (PTH), vitamin D, and calcitonin.
- 99% of calcium in the body is stored in bones, with the remaining 1% divided between intracellular and extracellular fluids. PTH acts to mobilize calcium from bones and enhance renal reabsorption when calcium levels drop.
- Vitamin D aids calcium absorption from the gut and reabsorption from kidneys. The active form is produced by PTH and kidney enzymes. Together with PTH, vitamin
This document discusses ketosis, including the three main types of ketone bodies, acetone, acetoacetic acid, and beta-hydroxybutyric acid. It describes how ketosis occurs when the rate of ketone body synthesis exceeds the rate of their utilization, as seen in starvation and diabetes mellitus. Factors that can aggravate ketosis are also summarized, such as decreased carbohydrate availability and increased free fatty acid levels. The clinical effects of ketosis include ketoacidosis, dehydration, and potentially death if left untreated. Treatment involves administering insulin, glucose, and bicarbonate to correct acidosis.
This document provides an overview of calcium homeostasis and the regulation of blood calcium levels. It discusses the distribution, storage, and biochemical functions of calcium in the body. The key hormones and mechanisms involved in maintaining calcium levels are parathyroid hormone (PTH), calcitriol (the active form of vitamin D), and calcitonin. PTH acts to increase blood calcium levels by promoting bone resorption and renal reabsorption of calcium. Calcitriol increases intestinal calcium absorption. Calcitonin acts to decrease blood calcium levels. Together these hormones tightly control calcium concentrations to ensure levels remain within their normal range.
Calcium is essential for bone development, muscle contraction, blood clotting and nerve transmission. 99% of calcium is stored in bones while the remaining 1% circulates in blood. Dietary sources like milk aid absorption while factors like phytates inhibit it. Calcium levels are tightly regulated by parathyroid hormone, calcitriol, and calcitonin. Hypocalcemia and hypercalcemia and disorders like rickets impact bone mineralization. Oral manifestations include dry mouth and enamel defects while radiographs show hypoplasia and resorption.
Introduction
History
Distribution in body
Daily requirement
Sources
Absorption – active , passive
Factors promoting absorption
Factors inhibiting absorption
Excretion
Effect of Excess/ Low Calcium Level
Functions
Homeostasis of plasma calcium-calcium balance
Parathormone
Vit D3
Calcitonin
Role in orthodontic tooth movement
INTRODUCTION
Calcium is among the seven principal elements (macroelements).
Of which calcium is the most abundant.
Calcium is an important component of a healthy diet and a mineral necessary for life.
It has role in Orthodontic tooth movement
HISTORY
Latin calx or calcis meaning “live”.
Known as early as first century when ancient Romans prepared lime as calcium oxide.
Isolated in 1808 by Englishman Sir Humphrey Davy through the electrolysis of a mixture of lime (CaO) and mercuric oxide (HgO).
In 1883 Sydney Ringer demonstrated the biological significance of calcium .
DISTRIBUUTION OF Ca ++ IN BODY
DAILY REQUIREMENT
SOURCES
BEST SOURCES – MILK
MILK PRODUCTS
GOOD SOURCES – BEANS
LEAFY VEGETABLES
CEREALS
FISH
CABBAGE
EGG YOLK
ABSORPTION OF CALCIUM
Calcium absorption occurs across the intestinal wall in the blood by 2 major mechanics:
Active transport (transcellularly)
Passive transport ( paracellularly)
Active transport of calcium is dependent on the action of calcitriol and the intestinal vitamin D receptor (VDR).
Absorption of calcium at low and moderate intake levels.
Mostly in duodenum.
Passive diffusion or paracellular uptake involves the movement of calcium between mucosal cells and is dependent on luminal: serosal electrochemical gradients.
Occurs more readily during higher calcium intakes.
Occurs throughout the length of the intestine.
Mean Calcium Absorption (“fractional calcium absorption,” which is the percentage of a given dose of calcium that is absorbed) in men and non-pregnant women—across a wide age range— has been demonstrated to be approximately 25% of calcium intake (Hunt and Johnson, 2007).
FACTORS PROMOTING Ca ABSORPTION
FACTORS INHIBITATING Ca ABSORPTION
EXCRETION
Excess Calcium Level
It can cause constipation.
Increase the risk of kidney stones.
Increased risks of prostate cancer and heart disease.
Orthodontic consideration- It inhibit tooth movement.
Low Calcium Level
Bone breakdown occurs as the body uses its stored calcium to maintain normal biological functions.
Hypocalcemia.
Osteoporosis.
It can also cause rickets.
FUNCTIONS
BONE
Mineralisation of Bones and teeth.
Bone is a mineralized connective tissue.
It contains organic (collagen – protein) and inorganic (mineral) component, HYDROXY APATITE, Ca10(Po4)6 (OH)2.
MUSCLE CONTRACTION
controlled by tropomyosin binding to actin filaments and three types of troponin (troponin I, C, and T).
Troponin C is a calcium-binding protein.
In the normal state, the Ca2+ concentration in the cytoplasm is maintained at low levels. As Ca2+ will not bind to troponin C in this state, the myosin bin
Calcium homeostasis & its related disordersenamifat
Calcium homeostasis is tightly regulated by three hormones - calcitriol, parathyroid hormone, and calcitonin. Calcium is important for bone formation, blood clotting, hormone release, and muscle contraction. Hypocalcemia can cause tetany and muscle spasms while hypercalcemia increases risk of kidney stones and cardiac arrhythmias. The kidneys play a key role in calcium balance by reabsorbing over 95% of the filtered calcium and regulating excretion.
Calcium plays an important role in many biochemical functions such as bone and teeth development, membrane integrity, muscle contraction, blood coagulation, and hormone release. Calcium is regulated by hormones like parathyroid hormone, calcitonin, and vitamin D to maintain homeostasis. When calcium levels decrease in the blood, these hormones work to increase absorption from the intestines and resorption from bones to restore normal levels. The kidneys and bones also help regulate calcium balance in the body.
The document discusses mineral metabolism, with a focus on calcium and phosphorus. It covers the following key points:
- Calcium and phosphorus are important minerals that make up bones and teeth and are involved in many vital functions.
- Their metabolism involves absorption in the small intestine, regulation by calcitriol, parathyroid hormone, and calcitonin, and excretion primarily through feces and urine.
- Disorders of calcium and phosphorus metabolism can result from deficiencies or excesses and cause issues like hypocalcemia, hypercalcemia, rickets, and osteoporosis. Maintaining proper levels of these minerals is important for overall health.
Calcium homeostasis refers to the body's ability to maintain calcium levels in the blood within a normal range of 9-11 mg/100 ml. Calcium is important for many functions including nerve and muscle function, blood clotting, and bone formation. The body tightly regulates calcium levels through a balance of absorption from the gut, resorption from bones, and excretion by the kidneys. This involves the hormones parathyroid hormone (PTH), calcitonin, and vitamin D. PTH increases calcium levels while calcitonin decreases them. Vitamin D promotes calcium absorption. Imbalances can lead to hypercalcemia or hypocalcemia and related conditions like tetany.
Hypercalcemia and hypocalcemia can both occur due to disruptions in calcium homeostasis, which is tightly regulated by parathyroid hormone (PTH), vitamin D, and calcitonin. Hypocalcemia causes increased neuromuscular excitability and can lead to tetany, seizures, or cardiac issues if severe. Hypercalcemia suppresses the nervous system and can cause gastrointestinal symptoms, renal problems, or cardiac changes. Anesthetic implications include treating underlying calcium abnormalities, fluid management, drug interactions, and positioning patients carefully due to potential muscle weakness or brittleness.
This document discusses calcium and phosphate metabolism and related disorders. It covers the distribution, functions, absorption and excretion of calcium and phosphate. It describes the roles of parathyroid hormone, vitamin D, and calcitonin in regulating calcium and phosphate levels. Disorders resulting from calcium and phosphate imbalance like hypercalcemia, hypocalcemia, rickets, and osteomalacia/osteoporosis are explained. Factors affecting calcium and phosphate levels and their clinical importance are also summarized.
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Calcium is essential for many physiological processes. It is absorbed in the small intestine through both passive diffusion and active transport aided by vitamin D. Hormonal regulation of calcium levels involves parathyroid hormone, calcitonin, and vitamin D acting on the intestine, kidneys, and bone. Parathyroid hormone increases calcium levels by facilitating bone resorption and renal reabsorption. Calcitonin decreases calcium levels by inhibiting bone resorption and increasing urinary excretion. Vitamin D enhances intestinal calcium absorption. Together these hormones tightly control calcium concentration in the blood and body.
Minerals are inorganic compounds that are required for the body as one of the nutrients.
The inorganic elements (minerals) constitute only small potion of body weight.
Human body needs number of minerals for its functioning.
The document summarizes key information about calcium and phosphorus metabolism. It discusses their daily requirements, distribution in the body, dietary sources, functions, factors controlling absorption such as vitamin D, parathyroid hormone, and calcitonin. It also outlines hormonal control of calcium and phosphorus metabolism and clinical importance of hypo- and hypercalcemia and hyperphosphatemia. The objectives are to understand the role of calcium and phosphorus in the body and factors influencing their metabolism.
This document discusses calcium metabolism and homeostasis. It notes that calcium levels are tightly regulated by the intestine, kidneys, bones, and hormones. The parathyroid hormone (PTH) increases calcium absorption from the intestine and bones while decreasing urinary calcium excretion. Vitamin D increases intestinal calcium absorption. Calcitonin decreases bone resorption. Together, these organs and hormones work to maintain calcium levels within a narrow range. Imbalances can lead to hypo- or hypercalcemia with various neurological, cardiac, and musculoskeletal symptoms.
This document provides an overview of calcium-phosphate metabolism. It discusses the roles of calcium and phosphorus in the body, how they are regulated, and factors that influence their absorption and excretion. Key points covered include the functions of calcium in bones, teeth, and other tissues; hormones that regulate calcium levels such as PTH, vitamin D, and calcitonin; calcium absorption in the gut and reabsorption in kidneys; and disorders that can arise from abnormalities in calcium regulation. The document also reviews phosphorus metabolism, distribution, requirements, and excretion.
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Calcium is essential for many physiological processes in the body. It makes up 1-1.5% of total body weight, with 99% located in bones and teeth. Dietary sources include dairy products, eggs, fish, and leafy greens. The recommended daily intake is 500 mg for adults and 1200 mg for children. Calcium is absorbed in the duodenum and jejunum through an active transport process requiring energy and carrier proteins. Homeostasis is maintained by calcitriol, parathyroid hormone, and calcitonin which regulate absorption from the intestine and resorption from bones. Imbalances can cause hypercalcemia with symptoms like confusion and arrhythmias, or hypocalcemia/
This document summarizes key information about calcium balance and drugs that affect it. It discusses the physiological roles of calcium, how plasma calcium levels are regulated by parathyroid hormone (PTH), calcitonin, and calcitriol. It describes calcium absorption and excretion, preparations of calcium supplements, and uses of calcium supplements and drugs like PTH, calcitonin, and calcitriol to treat conditions like tetany, osteoporosis, and hypercalcemia. The actions, pharmacokinetics, and clinical uses of PTH, calcitonin, and calcitriol are also summarized.
Calcium homeostasis is tightly regulated by the interaction of the parathyroid gland, kidneys, bone, intestine, and hormones. Parathyroid hormone (PTH) increases blood calcium levels by promoting bone resorption and renal calcium reabsorption. Vitamin D assists PTH by increasing intestinal calcium absorption. Disorders occur when calcium levels decrease or increase outside the normal range, which can cause symptoms like numbness, seizures, or kidney stones. Maintaining balanced calcium levels requires the coordinated functions of multiple organ systems and hormones.
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This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
3. INTRODUCTION
Hundreds of reactions simultaneously take place in a living cell, in a well-organised and
integrated maanner.
The entire spectrum of chemical reactions, occuring in the living system, are collectively
reffered to as metabolism.
The term metabolite, is applied to a substrate or an intermediate or a product in the
metabolic reactions.
Metabolism is broadly divided into two categories.
1) Catabolism and
2) Anabolism.
4. INTRODUCTION
1) Catabolism: The degradative processses
concerned with the breakdown of complex
molecules to simpler ones, with a concomitant
release of energy.
2) Anabolism: the biosynthetic reactions
involving the formation of complex molecules from
simple precursors.
5. CALCIUM
Calcium is the most abundant among the minerals in the
body.
Calcium regulation can be explain using RULE OF 3
1) Three tissues: BONE, INTESTINE,KIDNEY
2) Three hormones: PTH, CALCITONIN AND VITAMIN D3
3) Three cell types: OSTEOBLASTS, OSTEOCYTES AND
OSTEOCLAST
7. DAILY REQUIREMENTS
ADULT MEN AND WOMEN- 800 mg/ day
WOMEN DURING PREGNANCY,
LACTATION AND - 1.5 g/ day
POST MENOPAUSE
CHILDREN (1-18yrs) - 0.8-1.2 g/day
INFANTS(< 1 YEAR) - 300-500 mg/day
8. DIETARY SOURCE
BEST SOURCES - MILK AND MILK PRODUCTS
GOOD SOURCES- BEANS, LEAFY VEGETABLES, FISH,
CABBAGE, EGG YOLK.
9. FUNCTIONS
1) DEVELOPMENT OF BONES AND TEETH
a) Calcium along with phosphate, is requried for the formation( of
hydroxyapatite) and physical strength of skeletal tissue.
b) Osteoblast are responsible for bone formation while osteoclasts result in
demineralaization.
10. FUNCTIONS
2) MUSCLE
A) Calcium mediates EXCITATION AND CONTRACTION of muscle fiber.
b) Calcium activates ATPase: increases action of actin and myosin and facilates
excitation-contraction coupling.
c) Calcium decreases neuromuscular irritability.
d) calcium deficiency causes tetany.
11. FUNCTIONS
3) BLOOD COAGULATION
a) Calcium is known as foctor IV in blood coagulation cascade.
4) NERVE TRANSMISSION
a) ca2+ is necessory for the transmission of nerve impulse.
5) MEMBRANE INTERGRITY AND PERMEABILITY
a) Ca2+ influences the membrane structure and transport of water and several ions across it.
6) ACTIVATION OF ENZYMES
a) Ca2+ is needed for the direct activation of enzymes such as lipase( pancreatic), ATP ase and succinate
dehydrogenase.
12. FUNCTIONS
7) CALCIUM AS INTRACELLULAR MESSENGER
a) Certain hormones exert their action through the mediation ofCa2+( Instead
of cAMP).
b) Calcium is regarded as a second messenger for such hormonal action e.g.
epinephrine in liver glycogenolysis.
C) Calcium serves as a third messenger for some hormones e.g antidiuretic
hormone acts through cAMP, and then ca2+
13. FUNCTIONS
8) MYOCARDIUM:
A) Ca++ PROLONGS SYSTOLE.
B) In hypercalcemia, Caediac arrest is seen in systole.
C) This fact should be kept in mind when calcium is administrated intravenously.
D) It should be given very slowly.
9) RELEASE OF HORMONES
A) The release of certain hormones( insulin, PTH, calcitonin) from the endocrine
glands is facilitated by ca2+
14. ABSORPTION
The absorption of calcium mostly occurs in the
duodenum by an energy dependent active process.
It is influenced by several factors
1) Factors promoting Ca absorption
2) Factors inhibiting Ca absorption
15. ABSORPTION
FACTORS PROMOTING Ca absorption
1) Vitamin D ( through the active form calcitriol) induces
the synthesis of calcium binding protien in the intestine
epithelial cells and promotes Ca absorption.
2) parathyroid hormone enhances Ca absorption through
the increased synthesis of calcitriol.
3) Acidity( low PH) is more favourable for Ca absorption.
16. ABSORPTION
FACTORS PROMOTING Ca absorption
4) Lactose promotes calcium uptake by intestinal cells.
5) The amino acids lysin and arginine facilates Ca
absorption.
17. ABSORPTION
FACTORS INHIBITING Ca absorption
1) Phytates and oxalates form insoluble salts and interfere
with Ca absorption.
2) High content of dietary phosphate results in the
formation of insoluble calcium phosphate and prevent Ca
uptake. The dietary ration of Ca and P between 1:2 and
2:1 is ideal for optimum Ca absorption by intestinal cells
18. ABSORPTION
FACTORS INHIBITING Ca absorption
4) Alkaline condition (high PH) is unfavourable for Ca
abosrption.
5) Higher content of dietary fiber interferes with Ca
absorption.
19. PLASMA CALCIUM
Normal concentration of plasma or serum Ca is
9-11 mg/dl.
At least 1mg/dl serum Ca is found in association
with citrate and or phosphate
The other half of serum Ca ( 4-5 mg/dl ) is bound
to protiens, mostly albumin and, to a lesser
extend, globulin.
20. FACTORS REGULATING PLASMA CALCIUM LEVEL
The major factors that regulate the plasma calcium within a narrow range
Vitamin D
Calcitriol
Parathyroid hormone and
Calcitonin .
23. FACTORS REGULATING PLASMA CALCIUM LEVEL
Calcitriol
1) Active form of vitamin D is a hormone, namely calcitriol or 1,25- dihydroxy-cholecalciferol.
2) Its main action is to increase the blood calcium level by increasing the calcium absorption
from the small intestine.
3) Furthermore, Calcitriol stimulates calcium uptake by osteoblasts of bone and promotes
calcifications or mineralization( deposition of calcium and phosphate) and remodelling.
24. FACTORS REGULATING PLASMA CALCIUM LEVEL
PARATHYROID HORMONE
1) It is a protein hormone secreted by parathyroid gland.
2) Molecular weight is 95,000 is a single chain polypeptide,
containing 84 amino acids
2) Its main function is to increase the blood calcium level.
25. FACTORS REGULATING PLASMA CALCIUM LEVEL
MECHANISM OF ACTION OF PTH
1) PTH binds to a membrane receptor protein on the target cell and activates
adenylate cyclase to liberate c AMP.
2) This, in turn, increases intracellular calcium that promotes the phosphorylation
of proteins which, finally brings about the biological actions.
3) PTH has three independent tissues
Bone
Kidneys and
Intestine
4) The PRIME FUNCTION OF PTH IS TO ELEVATE SERUM CALIUM
LEVEL.
27. FACTORS REGULATING PLASMA CALCIUM LEVEL
MECHANISM OF ACTION OF PTH
ACTION ON BONE:
1) PTH causes decalcification or DEMINERALIZATION OF BONE , a process
carried out by OSTEOCLAST.
2) This is brought out by PTH stimulated increased activity of the enzymes
pyrophosphatase and collagenase.
3) These enzyme result in bone resorption. Demineralization ultimately leads to an
increase in the blood Ca level.
4) The action of PTH on bone is quantitatively very significant to maintain Ca
homeostasis.
28. FACTORS REGULATING PLASMA CALCIUM LEVEL
MECHANISM OF ACTION OF PTH
ACTION ON KIDNEY:
1) PTH increases the Ca reabsorption by kidney tubules.
2) This is the most rapid action of PTH to elevate blood Ca levels.
3) PTH promotes the production of calcitriol in the kidney by stimulating 1
hydroxylation of 25 hydroxycholecalciferol.
29. FACTORS REGULATING PLASMA CALCIUM LEVEL
MECHANISM OF ACTION OF PTH
ACTION ON INTESTINE:
1) The action on PTH on intestine is indirect.
2) It increases the intestinal absorption of Ca
by promoting the synthesis of CALCITRIOL.
30. FACTORS REGULATING PLASMA CALCIUM LEVEL
MECHANISM OF ACTION OF PTH
CALCITONIN
1) It is a peptide containing 32 aminoacids.
2) It is secreated by parafollicular cells of thyroid gland.
3) Calcitonin promotes calcification by increasing the activity of osteoblasts.
4) Further, calcitonin decreases bone resorption and increases the excretion of Ca into
urine.
5) CT, therefore, has a DECREASING INFLUENCE ON BLOOD CALCIUM.
31. EXCRETION OF CALCIUM
1) Calcium is excreted partly through the kidneys and mostly
through the intestine.
2) The renal threshold for serum Ca is 10mg/dl.
STOOLS
Unabsorbed
calcium in the
diet
60-70%
URINE
50-
200mg/day
SWEAT
15mg/dy
32. CALCIUM IN THE TEETH
The teeth calcium is not subjected to regulation as observed for
bone calcium.
Thus the adult teeth, once formed, do not undergo decalcification
to meet the body needs of calcium.
However, proper calcium of teeth is important in the growing
children.
33. SYMPTOMS OF CALCIUM IMBALANCE
HYPERCALCEMIA
Hyperparathyroidism
Metastatic disease of bone
Vitamin A/D excess
Milk-alkali syndrome
Sarcoidosis
Immobilization (in setting of posttrauma
or osteoporosis)
Hyperthyroidism
HYPOCALCEMIA
Renal Failure
Hypoparathyroidism
Vitamin D deficiency
Tetany
35. HYPERCALCEMIA
The serum Ca level (normal 9-11 mg/dl) is elevated in hypercalcemia.
Hypercalcemia is associated with HYPERPARATHYROIDISM caused by increased activity of
parathroid glands.
The symptoms of hypercalcemia include lethary, muscle weakness, loss of appetite, constipation,
nausea, increased myocardial contractility and susceptibility to fractures.
36. HYPERPARATHYROIDISM
Hyperparathyroidism is characterized by hypersecretion of PTH. HPT occurs in three categories:
Etiology
1) Primary
Usually caused by a tumor (adenoma in 85% of all cases) or hyperplasia of the gland that produces an
increase in PTH secretion resulting in hypercalcemia and hypophosphatemia.
2) Secondary
When the parathyroid glands are stimulated to produce increased amounts of hormones to correct
abnormally low serum calcium levels in different physiologic or pathologic conditions like renal failure,
intestinal malabsorption syndrome, decrease of Vitamin D production, thus resulting in parathyroid
hyperplasia.
3) Tertiary
When long-standing secondary hyperplasia becomes autonomous in spite of correction of the underlying
stimulant (renal transplant).
37. ORAL MANIFESTATIONS OF HYPERPARATHYROIDISM
Dental abnormalities
Obliteration of pulp chamber by pulp stone
Alteration in dental eruption
Loosening and drifting of teeth
Malocclusions
Spacing of teeth
Partial loss of lamina dura
Periodontal ligament widening
Teeth become sensitive to percussion and mastication.
Floating teeth.
38. ORAL MANIFESTATIONS OF HYPERPARATHYROIDISM
Brown tumor
Generalized bone rarification of jaw
Soft tissue calcification
Hypercalcemia may results in sialolithiasis
Mandibular tori
Complaint of vague jaw bone pain.
39. ORAL MANIFESTATIONS OF HYPERPARATHYROIDISM
PALATAL ENLARGMENT IS CHARACTERISTIC OF RENAL OSTEODYSTROPHY ASSOCIATED
WITH SECONDARY HYPERPARATHYROIDISM
40. ORAL MANIFESTATIONS OF HYPERPARATHYROIDISM
THE PERIAPICAL RADIOGRAPH
REVEALS THE ‘GROUND GLASS’
APPEARANCE OF THE TRABECULAAE
AND LOSS OF LAMINA DURA IN A
PATIENT WITH SECONDARY
HYPERPARATHYROIDISM.
THE OCCLUSAL RADIOGRAPH OF THE
EDENTULOUS MAXILLARY ANTERIOR REGION
SHOWS A MULTILOCULAR RADIOLUCENCY
CHARACTERISTIC OF BROWN TUMOUR OF
PRIMARY HYPERPARATHROIDISM.
41. HYPOCALCEMIA
A DECREASE IN TOTAL PLASMA CALCIUM CONCENTRATION
BELOW 8.8mg/dl IN THE OF NORMAL PROTIEN CONCENTRATION.
42. HYPOPARATHYROIDISM
Hypoparathyroidism is a metabolic disorder characterized by low serum calcium and high serum
phosphorus concentrations due to a deficiency or absence of PTH secretion.
SIGNS AND SYMPTOMS
1) Hypoparathyroidism can cause hypocalcemia with consequent circumoral numbness, paresthesias of
distal extremities (finger and toes), muscle pain, abdominal pain or muscle cramping which can progress to
spasm or tetany. Laryngospasm or bronchospasm and seizures may also occur.
43. HYPOPARATHYROIDISM
Increased neuromuscular irritability (due to hypocalcemia) may be demonstrated by eliciting a Chvostek or
Trousseau sign. In positive Chvostek’s sign tapping, the facial nerve at its point of origin (anterior to ear
tragus) will cause spasm of facial musculature particularly of the lip and the alae of the nose. In Tousseau’s
sign Carpal, spasm occurs after inflation of the blood pressure cuff.
44. ORAL MANIFESTATIONS
1) The two most frequent dental abnormalities are enamel hypoplasia (enamel is thin), delayed eruption, and
there may be multiple unerupted teeth.
2) Teeth appear dull white in color with hypoplastic pitting. Crowns are small (microdontia) and the roots are
often short with blunt ends. In some teeth, roots are malformed, resulting from nontreated hypocalcemia
during the developmental phase of the dentition. A delay or cessation of dental growth and development, a
full complement of teeth is not always developed, premolars being the teeth most usually missing
(hypodontia). The teeth may show ankylosis, the jaws are generally short and wide with high arch palate.
Severe dental caries is usually noted in the deciduous and permanent teeth, the teeth are lost early due to
caries.
3) There may be chronic candidiasis of the oral mucosa and nail, paresthesia of the tongue or lips, and facial
twitching can occur.
45. CAUSES OF HYPOCALCEMIA
VITAMIN D DEFICIENCY
It is an important cause of hypocalcemia.
Vitamin D deficiency may result from inadequate dietary intake or decreased absorption due to
hepatobiliary disease or intestinalmalabsorption.
It can also occur because of alterations in vitamin D metabolism as occurs with certain drugs (phenytoin,
phenobarbital, and rifampin) or lack of skin exposure to sunlight.
46. RICKETS
RICKETS
1) Rickets in children is characterised by bone deformities due to incomplete
mineralization, resulting in soft and pliable bones and delay in teeth formation
49. HYPOPHOSPHATEMIC RICKETS
HYPOPHOSPHATEMIC rickets mainly results from defective renal
tubular reabsorption of phosphate. Supplementation of vitaminD long
with phosphate is found to be useful.
50. VITAMIN D RESISTANCE RICKETS
VITAMIN D RESISTANT RICKETS
1) Vitamin D-resistant rickets (VDRR), also known as hereditary or familial hypophosphatemia, is
characterized by a metabolic disturbance which causes defective calcification of mineralized structures.
2) VDRR is well established genetically as an X-linked dominant metabolic disorder, that may be
characterized by persistent hypophosphatemia and hyperphosphaturea associated with decreased renal
tubular reabsorption of inorganic phosphates.
51. VITAMIN D RESISTANCE RICKETS
RADIOGRAPHIC FEATURES
Dental radiographs reveal hypocalcification of teeth and the presence of large pulp chambers and alveolar
bone loss.
52. DENTAL FINDINGS
Dental findings that are often characteristic include dentin defects, unusually
large pulp chambers and enlarged pulp horns, in some cases the enamel is
hypoplastic.
These dental problems are more commonly associated with the primary than the
permanent dentition.
The most common intraoral radiologic findings include large pulp chambers,
short roots, poorly defined lamina dura and hypoplastic alveolar ridge.
53. RENAL RICKETS
In kidney diseases, even if vitamin D is available, Calcitriol is not synthesized.
Theses cases will respond to administration of calcitriol.
54. OSTEOMALACIA
The term is derived from greek ‘OSTEON’ = BONE AND ‘MALAKIA’= SOFTNESS.
The bones are softened due to insufficient mineralization and increases osteoporosis.
Patient are more prone to get fractures.
The abnormalities in BIOCHEMICAL PARAMETERS are slightly LOWER SERUM CALCIUM AND A
LOW SERUM PHOSPHATE.
Serum ALKALINE PHOSPHATASE, bone isoenzyme, is markedly increased.
55. OSTEOMALACIA
In osteomalacia (adult rickets) demineralization of bones occurs (bones become softer), increasing their
susceptibility to fractures.
Common cause is vitamin D deficiency.
56. OSTEOMALACIA
CLINICAL FEATURES
Pain and Chronic fatigue, starting insidiously.
Proximal muscles weakness.
Waddling gait.
Deformed pelvis and exaggerated lordosis.
Bowing of Lower limbs
57. OSTEOPOROSIS
Osteoporosis is characterized by demineralization of bone
resulting in progressive loss of bone mass.
OCCURRENCE
The elderly people(over 60 yr.) of both sexes are at risk for
osteoporosis.
It is more predominantly occurs in the postmenopausal women.
Osteoporosis results in frequent bone fractures which are a
major cause of disability among elderly.
58. OSTEOPOROSIS
ETIOLOGY
Etiology of osteoporosis is largely unknown, but it is believed
that several causitive factors may contribute to it.
The ability of calcitriol from vitamin D is decresaed with age,
particulary in he postmenopausal women.
Deficiency of sex hormones (in women) has been implicated in
the development of osteoporosis.
59. OSTEOPOROSIS
TREATMENT
Estrogen administration along with calcium supplementation(in combination with
vitamin D) TO POSTMENOPAUSAL WOMEN REDUCES THE RISK OF
FRACTURES .
Higher dietary intake of Ca (about) 1.5g/dy) is recommended for elderly people.
60. COMPARISON OF CALCIUM, PHOSPHORUS AND ALKALINE
PHOSPHATASE VALUES IN THE MORE COMMON DISORDERS OF BONE
AND CALCIUM METABOLISM
SERUM CALCIUM SERUM PHOSPHORUS SERUM ALKALINE
PHOSPHATASE
1) NORMAL 8.8B to 10.5 mg
ca/dl blood
2 to 5 mg p/dl
blood
1 to 4 units /dl
bood in adult
2)RICKETS Usually normal except in
tetany
Decreased Increased 20 to 40
x normal
3) OSTEOMALACIA Decreased Little if any change
4) PAGETS DISEASES Usually normal Usually normal elevated
5) HYPER
PARATHYROIDISM
Marked increase usually
decreased
Increaed 2 to 50
x normal
6) OSTEOGENESIS
IMPERFECTA
usually normal usually normal usually normal –at
times increased
7) SOLITARY BONE CYST Normal Normal Normal
8) TETANY 7mg ca /dl blood or
less
Normal or elevated Normal