Calcium & Phosphorus balance
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This document discusses the regulation of calcium and phosphorus balance in the body. It explains that calcium and phosphorus balance is principally maintained by parathyroid hormone (PTH), vitamin D (calcitriol), and fibroblast growth factor 23 (FGF23). PTH and calcitriol increase calcium levels while calcitonin, estrogen, and glucocorticoids decrease calcium. FGF23, PTH, and calcitonin lower phosphate levels, while vitamin D helps raise phosphate levels. The document then provides more details on how each of these regulators impacts calcium and phosphorus absorption, reabsorption, excretion, and bone resorption/formation to maintain appropriate levels in extracellular fluid and plasma.
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![Abstract – Regulation of absorption of calcium & phosphorus in GIT and regulation of
glomerular filtration through nephrons in kidney directly controls the calcium & phosphorus
balance in the body. The balance of calcium & phosphorus in extracellular fluid or plasma is
principally maintained by – Parathyroid hormone (PTH) vitamin D (calcitriol) & fibroblast
growth factor 23 (FGF23). Secondary regulators are – calcitonin, glucocorticoid & estrogen.
PTH & calcitriol increase plasma calcium level. Calcitonin, estrogen & glucocorticoid decrease
calcium concentration. FGF23, PTH & calcitonin lower phosphate level in plasma, but Vitamin d
helps rising phosphate level.
Keywords – Glomerular filtration, extracellular fluid, PTH, calcitriol, FGF23, calcitonin
Report –
Calcium balance –
Parathyroid hormone (PTH) - Secreted from parathyroid glands located in thyroid glands.
When plasma calcium level lowers, parathormone increases bone resorption & intestinal
absorption of calcium & phosphorus to increase their levels in plasma. So, lower
secretion of PTH causes Tetany disease. PTH also decreases excretion of calcium.
Vitamin D (calcitriol) - Calcitriol [1, 25 (OH)2 D3] & 1,25 (OH)2 D2 are active forms of
vitamin D. At high concentration, increases bone resorption through osteoclast, thus
increasing plasma calcium level. But at low concentration, induces bone calcification,
resulting in low plasma calcium level. Calcitriol Increases intestinal absorption of and
reduces glomerular filtration of calcium & phosphorus, rising their plasma level.
Calcitonin – Calcitonin inhibits osteoclastic bone resorption. In the kidney, calcitonin
reduces calcium reabsorption as well as reabsorption of other ions, including sodium,
potassium, and magnesium. Ability of calcitonin to block bone resorption and lower
serum calcium makes it a useful drug for the treatment of Paget’s disease, hypercalcemia,
and osteoporosis.
Glucocorticoid – Antagonizes vitamin D-stimulated intestinal calcium transport. Also
stimulates renal calcium excretion, and blocks bone formation.
Phosphorous balance –
Fibroblast Growth Factor 23 - FGF23 inhibits 1, 25(OH)2 D production and phosphate
reabsorption (via the sodium phosphate co-transporters NaPi 2a and 2c) in the kidney,
leading to hypophosphatemia. FGF23 binds to FGF receptors 1 and 3c in the presence of
the accessory receptor Klotho.
Parathyroid hormone & calcitonin lower phosphate level in plasma by increasing
excretion & reducing reabsorption respectively.
Vitamin D helps in rising of phosphate level by both increasing absorption from intestine
& decreasing excretion through kidney.](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
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1. Calcium homeostasis is regulated by parathyroid hormone (PTH), calcitonin, vitamin D, and the kidneys and bones. Abnormalities can cause hypo- or hypercalcemia.
2. Hypocalcemia presents with symptoms like numbness, cramps, and seizures. It is diagnosed through blood tests and may be treated with oral calcium or IV calcium gluconate.
3. Hypercalcemia has various causes like primary hyperparathyroidism and can be asymptomatic or cause polyuria, nausea, and kidney stones. Treatment involves rehydration, calcitonin, and bisphosphonates.
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- Histology of the gland.
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Calcium homeostasis is tightly regulated by several hormones and organs. Calcium levels are maintained within a narrow range through intestinal absorption, bone resorption and deposition, and renal excretion. Parathyroid hormone (PTH) increases calcium and phosphate levels by acting on bone, kidney, and intestine. Vitamin D facilitates intestinal calcium absorption and renal reabsorption. Calcitonin counters PTH by inhibiting bone resorption and reducing calcium and phosphate levels. Together these hormones work in a feedback loop to precisely control circulating calcium.
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Calcium homeostasis is tightly regulated by the interaction of the parathyroid hormone (PTH), calcitonin, vitamin D, bone, kidney, and intestine. PTH increases blood calcium levels by promoting bone resorption and calcium reabsorption in the kidney. Vitamin D assists by increasing intestinal calcium absorption. Hypocalcemia stimulates PTH release, while hypercalcemia inhibits PTH. Disorders occur if calcium levels become too high or low.
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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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1) Amino acids exist in an amino acid pool that increases after eating and decreases during fasting. Plasma amino acid levels range from 4-8 mg/dl.
2) Amino acids are used to synthesize proteins, peptides, and other biological molecules or undergo catabolism where the amino group is removed through transamination or deamination reactions.
3) Ammonia produced from amino acid catabolism is transported to the liver and converted to urea by the urea cycle. Elevated ammonia can be toxic and cause hyperammonemia.
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1. Calcium homeostasis is regulated by parathyroid hormone (PTH), calcitonin, vitamin D, and the kidneys and bones. Abnormalities can cause hypo- or hypercalcemia.
2. Hypocalcemia presents with symptoms like numbness, cramps, and seizures. It is diagnosed through blood tests and may be treated with oral calcium or IV calcium gluconate.
3. Hypercalcemia has various causes like primary hyperparathyroidism and can be asymptomatic or cause polyuria, nausea, and kidney stones. Treatment involves rehydration, calcitonin, and bisphosphonates.
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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.
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Calcitriol, the active form of vitamin D, is produced in the kidneys and increases calcium absorption in the intestines and bones. It binds to vitamin D binding proteins and is transported to tissues, where it binds to vitamin D receptors to increase intestinal calcium absorption, promote bone mineralization, and regulate calcium levels through effects on kidneys, muscles, and other tissues. Abnormalities associated with calcitriol include rickets and osteomalacia due to vitamin D deficiency, as well as hypervitaminosis D from extremely high vitamin D levels which can cause hypercalcemia and tissue calcification.
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This patient is most likely suffering from primary hyperparathyroidism. Two reasons support this diagnosis: 1) fluctuating calcium levels are typical of primary hyperparathyroidism and 2) a higher calcium level should be accompanied by a low PTH, but this patient has a high PTH with higher calcium levels. The commonest cause of primary hyperparathyroidism is a single adenoma of the parathyroid gland, present in around 85% of cases.
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- Histology of the gland.
- PTH biosynthesis.
- The calcium-sensing receptors (CaSR)
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This document summarizes key information about calcium homeostasis and metabolism. It discusses how calcium provides structural integrity to bones and is essential for many biochemical processes. It outlines recommended daily calcium intake and factors that influence calcium absorption and excretion. Key regulators of calcium levels like parathyroid hormone, calcitonin, and vitamin D are also described. The document discusses consequences of calcium deficiency and hypercalcemia, and treatments for correcting calcium levels.
Cal. po4 by dr tasnim
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.
Secondary hyperparathyroidism
The document discusses parathyroid glands and parathyroid hormone (PTH). It notes that parathyroid glands secrete PTH, which regulates calcium levels in the blood. PTH acts on bone, kidneys, and stimulates vitamin D production. Secondary hyperparathyroidism occurs in kidney disease and is caused by low calcium and vitamin D levels stimulating increased PTH secretion. Treatment focuses on controlling calcium, phosphate, PTH, and vitamin D levels through diet, binders, analogs, and calcimimetics. For refractory cases, parathyroidectomy may be required.
Parathyroid gland
The parathyroid glands secrete parathyroid hormone (PTH) which regulates blood calcium levels. PTH increases calcium resorption from bones and reabsorption from kidneys to raise calcium levels. It also increases vitamin D activation in kidneys to boost calcium absorption in the gut. PTH secretion is regulated by blood calcium and phosphate levels, increasing when calcium is low or phosphate is high to restore normal calcium concentrations.
parathormone.pptx
The parathyroid glands regulate calcium levels in the blood. They are located behind the thyroid gland and secrete parathyroid hormone (PTH). PTH increases calcium levels in the blood by releasing calcium from bones, reabsorbing calcium in the kidneys, and enhancing calcium absorption in the intestines. PTH also plays a key role in activating vitamin D, which further aids in intestinal calcium absorption. The level of calcium in the blood provides feedback to regulate PTH secretion, with lower calcium triggering more PTH release.
Calcium homeostasis
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.
PTH & Calcitonin for MBBS, BDS, Lab. Med..pptx
Parathyroid hormone (PTH) is one of three key hormones modulating calcium and phosphate homeostasis; the other two are calcitriol (1,25-dihydroxyvitamin D) and fibroblast growth factor 23 (FGF23).
Parathyroid, calcitonin
Parathyroid hormone (PTH) regulates calcium and phosphate levels by increasing their absorption in the intestines and bones and decreasing renal excretion. Excess PTH causes hypercalcemia by rapidly absorbing calcium from bones, while low PTH causes hypocalcemia. PTH is produced by the parathyroid glands and increases calcium levels while decreasing phosphate levels. Disorders of PTH include hypoparathyroidism, primary hyperparathyroidism, and secondary hyperparathyroidism.
Calcium 1
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 (
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Calcium metabolism and vitamin d deficiency
This document provides an overview of calcium metabolism and rickets. It discusses the roles of calcium, parathyroid hormone, vitamin D, and other factors in maintaining calcium homeostasis. Regarding rickets, it describes the causes as vitamin D deficiency, low calcium or phosphorus intake, or renal losses. Symptoms include bone deformities, growth retardation, and hypocalcemia. Treatment involves high-dose vitamin D and calcium supplementation. With nutritional deficiencies, prognosis is generally excellent with resolution of symptoms and bone healing with treatment.
Chronic Kidney Disease - MBD Part 2
The document discusses FGF-23 and Klotho, which are central regulators of phosphate homeostasis and calcitriol levels. FGF-23 is synthesized by bone cells and increases with declining renal function in CKD to regulate phosphate levels. It signals through Klotho and FGF receptors. Klotho exists in membrane and soluble forms and is necessary for FGF-23's phosphaturic effects. It has protective roles through antioxidant effects and inhibits TGF-β to prevent fibrosis. Higher FGF-23 levels in CKD are due to decreased clearance and a compensatory response to maintain phosphate levels.
Calcium
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/
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Here are the key steps in the procedure:
1. Protein is precipitated from 1 ml serum with 1 ml 10% TCA solution.
2. The mixture is centrifuged to separate precipitated protein.
3. Ammonium molybdate and ascorbic acid are added to the centrifugated serum to detect phosphates.
4. The volume is brought to 10 ml with water for measurement.
The procedure allows students to measure and compare phosphate levels in serum from a healthy woman and one with hyperparathyroidism, to observe the effects of the disorder on phosphate regulation.
Calcium Homeostasis.pptx
This document summarizes calcium homeostasis and the roles of parathyroid hormone (PTH) and vitamin D in regulating calcium levels. PTH and vitamin D work to maintain calcium levels in the blood by increasing calcium absorption in the intestines and kidneys. PTH acts directly on bones to increase calcium levels by promoting bone resorption, while vitamin D works indirectly by stimulating the kidneys to produce calcitriol, which then increases calcium absorption in the intestines. Together, PTH and vitamin D are the key hormones that regulate calcium homeostasis.
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Calcium & Phosphorus balance
- 1. CALCIUM & PHOSPHOROUS BALANCE NAME OF STUDENT – SHUVAM SAR ROLL NUMBER – 19320219008 CONTACT NUMBER - +918478098881 EMAIL ID – itzshuvam@gmail.com
- 2. Abstract – Regulation of absorption of calcium & phosphorus in GIT and regulation of glomerular filtration through nephrons in kidney directly controls the calcium & phosphorus balance in the body. The balance of calcium & phosphorus in extracellular fluid or plasma is principally maintained by – Parathyroid hormone (PTH) vitamin D (calcitriol) & fibroblast growth factor 23 (FGF23). Secondary regulators are – calcitonin, glucocorticoid & estrogen. PTH & calcitriol increase plasma calcium level. Calcitonin, estrogen & glucocorticoid decrease calcium concentration. FGF23, PTH & calcitonin lower phosphate level in plasma, but Vitamin d helps rising phosphate level. Keywords – Glomerular filtration, extracellular fluid, PTH, calcitriol, FGF23, calcitonin Report – Calcium balance – Parathyroid hormone (PTH) - Secreted from parathyroid glands located in thyroid glands. When plasma calcium level lowers, parathormone increases bone resorption & intestinal absorption of calcium & phosphorus to increase their levels in plasma. So, lower secretion of PTH causes Tetany disease. PTH also decreases excretion of calcium. Vitamin D (calcitriol) - Calcitriol [1, 25 (OH)2 D3] & 1,25 (OH)2 D2 are active forms of vitamin D. At high concentration, increases bone resorption through osteoclast, thus increasing plasma calcium level. But at low concentration, induces bone calcification, resulting in low plasma calcium level. Calcitriol Increases intestinal absorption of and reduces glomerular filtration of calcium & phosphorus, rising their plasma level. Calcitonin – Calcitonin inhibits osteoclastic bone resorption. In the kidney, calcitonin reduces calcium reabsorption as well as reabsorption of other ions, including sodium, potassium, and magnesium. Ability of calcitonin to block bone resorption and lower serum calcium makes it a useful drug for the treatment of Paget’s disease, hypercalcemia, and osteoporosis. Glucocorticoid – Antagonizes vitamin D-stimulated intestinal calcium transport. Also stimulates renal calcium excretion, and blocks bone formation. Phosphorous balance – Fibroblast Growth Factor 23 - FGF23 inhibits 1, 25(OH)2 D production and phosphate reabsorption (via the sodium phosphate co-transporters NaPi 2a and 2c) in the kidney, leading to hypophosphatemia. FGF23 binds to FGF receptors 1 and 3c in the presence of the accessory receptor Klotho. Parathyroid hormone & calcitonin lower phosphate level in plasma by increasing excretion & reducing reabsorption respectively. Vitamin D helps in rising of phosphate level by both increasing absorption from intestine & decreasing excretion through kidney.
- 3. Conclusion – calcium & phosphorous balance is very much vital in regulation of biochemical and other musculoskeletal activities throughout the body. Their regulation is studied very well to make the artificial agents to control the balance when disturbed.