Calcium- The miracle Mineral.
Calcium is an essential mineral to maintain good health. It is very important to build bone and teeth health.
Approximately 99% of the body’s calcium stored in the bones and teeth. It is also aids in neurotransmitter release and muscle contraction.
Everybody thinks and assumes the role that calcium plays in strengthening bones and teeth, but there is something people are not aware of and in calcium’s role.
For example: It is a mineral, most abundant in humans. Additional benefits like.
- Nerve transmission.
- Development of bones and teeth.
- Vascular function, nerve, and muscle activity signaling hormones.
- 99% stored in bones and teeth.
- The health of your heart.
- Blood coagulation.
And it is also essential this is almost indispensable when it comes to anything to do with our immune system.
Calcium is also believed to reduce the risk of high blood pressure, Dairy products, such as milk, and cheese, are a well-known source of calcium.
It is also very rich in milk, so we tend to drink milk with strong burns. Actually, there’s very little correlation between the amount of milk consumed in the rate of bone health or osteoporosis.
Osteoporosis is a disease
- Abnormal bone mineralization associated with aging.
- Bones become weak, brittle, and increased risk of fracture.
- Reabsorption exceeds deposition.
One of the reasons for this you use calcium without Vitamin D’ and magnesium.
Vitamin ‘D’ is required for calcium absorption. get little sunlight every day to aid calcium absorption.
It is an important nutrient to prevent osteoporosis in later life.
Avoid calcium robbers like caffeine and excess intake of salt in your food.
If you have too much calcium without magnesium you can actually be worse for your cardiovascular health.
Exceeding the recommended daily calcium intake for an extended period of time can result in hypocalcaemia and calcium metabolism disorder.
Women, especially, need to ensure the calcium intake in their foods to ensure a healthy life.
The research has shown that women who take 1200 milligrams have calcium per day have reduced symptoms of PMS by up to 50%.
Including headache, moodiness, food cravings, bloating, and, menstrual pain.
Pregnancy is a time when proper calcium intake is of particular importance.
The growing fetus depends on its mother to provide a daily supply and adequate nutrients including calcium for healthy growth and development.
Nursing mothers need to ensure the intake of calcium is adequate to ensure baby growth.
In a child’s deposition exceeds reabsorption leading to bone growth at the growth plats and adults this process is typically in equilibrium until we get into the later years of life.
Calcium has been proposed to reduce the risk of cardiovascular disease by several mechanisms such as decreasing absorption of fats and increasing their excretion as well as allowing total cholesterol levels in the blood.
How much calcium we need?
|Age 70 and younger – 1000 mg daily|
|Age 71 and older – 1200 mg daily|
|Age 50 and younger – 1000 mg daily|
|Age 51 and older – 1200 mg daily|
What is calcium deficiency?
A calcium deficiency disease also known as “hypocalcemia” is a condition where you are calcium levels are lower than average.
The normal range is a two-point one to two-point six millimoles per liter.
Levels less than two-point one millimoles per liter is defined as “hypocalcemia” and while low levels may not cause any symptoms at first.
As the condition develops signs may begin to show like numbness, tingling, weakness, or brittle fingernails, and more.
When you have low calcium intake you can also increase your risk of bone loss.
If your body doesn’t get enough calcium to keep its base functions running smoothly it will actually leach calcium from your bones to makeup for the short fall.
And if this goes for a too long your bone mineral density will deplete to the point of osteopenia or worsen osteoporosis.
Since calcium is so critical throughout the body low calcium symptoms can show up anywhere and they may manifest in many different ways.
But how does it come to this what causes hypocalcemia common causes of hypocalcemia can be low vitamin D levels because vitamin D increases your body’s ability to absorb calcium dietary,
Intolerance like a dairy allergy or gluten sensitivity or even genetic factors discovering your cause of calcium deficiency is crucial to reclaiming your overall health and your bone health now you know.
Know we are going to discuss the disorders of calcium and phosphorus.The learning objectives for this talk– we will review the hormonal regulation of calcium and phosphorous homeostasis, the etiology, clinical manifestations, and treatment of hypercalcemia, and hypocalcemia.
We will review also the etiology, clinical manifestations, and treatment of hyperphosphatemia and hypophosphatemia. Calcium and phosphorous regulation involve three tissues, namely the bone, kidney, and intestine.
It also involves three hormones– PTH, calcitonin, and activated vitamin D. About 98% of calcium is stored in the cells and bones.
The remainder circulates in the blood as ionized calcium in 50% bound to proteins such as albumin in 40% and bound to citrate, or phosphorous buffers, in 10%. Now, about 85% of phosphorus is stored in the bone, 14% is stored intracellularly, and only 1% is present extracellularly.
Inorganic phosphorous plays a critical role in skeletal development, cell membrane integrity, and function as phospholipids.
It’s also critical in intracellular signaling, platelet aggregation, and energy transfers in the cells. Here is the summary of the interactions between the three different organs and hormones involving the homeostasis of calcium and phosphorus.
The calcium concentration in plasma is tightly controlled as free calcium and bounded to proteins. A regular daily diet would contain around 400 milligrams of elemental calcium of which 30% to 35% is absorbed in the intestines Vitamin D increases the absorptions of both calcium and phosphorous in the intestine.
Vitamin D also favors the reabsorption of phosphorous in the proximal tubule. As a feedback mechanism, Vitamin D inhibits the production of the PTH hormone. Now, PTH is secreted by the chief cells in the parathyroid gland.
It stimulates the osteoclasts to increase the concentration of calcium in the blood. It also favors the tubular reabsorption of calcium and stimulates the production of 1,25 hydroxyvitamin D in the kidneys.
On the other hand, calcitonin, which is a hormone secreted by the parafollicular cells of the thyroid gland acts in the bone inhibiting bone reabsorption.
PTH is mainly secreted in response to hypocalcemia. In normal circumstances, after it releases, the serum calcium levels will increase while normal phosphorous levels are maintained. As we mentioned before, PTH acts directly in the bone, increasing the activity of osteoclasts.
It also increased the calcium levels, stimulating its absorption in the renal tubules. PTH indirectly acts, increasing the calcium reabsorption through stimulation on the synthesis of 1, 25 hydroxyvitamin D in kidneys.
Now, let’s review the role of vitamin D. Vitamin D or ergocalciferol, is derived from plants, while vitamin D3 or cholecalciferol is derived from animal sources such as fish oil.
But vitamin D2 and vitamin D3 are hydroxylated in the liver to 25 hydroxyvitamin D and then converted in the kidneys to 1, 25 hydroxyvitamin D3 by the one hydroxylase. Vitamin D increases the intestinal absorption of both calcium and phosphorus in the intestine and inhibits the synthesis of PTH.
Let’s review the topic about hypercalcemia. Hypercalcemia may cause different symptoms at the neurologic, gastrointestinal, renal, and cardiovascular systems.
In the neurologic system, hypercalcemia results in a decrease in mental activity, and patients might manifest lethargy and confusion.
As a gastrointestinal symptom, hypercalcemia results, in decreased bowel activity, and patients might manifest constipation anorexia, but commonly also produce nausea and vomiting.
Pancreatitis occurs because of the precipitation of calcium in the pancreas. However, severe pancreatitis is associated with hypocalcemia because of the binding of calcium to fat.
Also, diseases are caused by hypercalcemia for unclear reasons. In the renal system, hypercalcemia results in polyuria and polydipsia because of the induction of nephrogenic diabetes insipidus.
Calcium also precipitates in the kidney, resulting in both kidney stones and nephrolithiasis. In the cardiovascular system, hypercalcemia might play a role in hypertension.
30% to 50% of patients with hypercalcemia have hypertension. The EKG will show a short QT. Etiology– the most common causes of hypercalcemia are primary hyperparathyroidism.
The majority of patients with hyperparathyroidism do not have symptoms, and the diagnosis comes to light because of routine office-based testing.
The hypercalcemia of malignancy occurs due to a PTH-like protein and metastatic disease to the bone. Granulomatous diseases such as sarcoidosis, tuberculosis, berylliosis, histoplasmosis, and coccidioidomycosis are all associated with hypercalcemia.
These maybe increase vitamin D production. The causes of hypercalcemia include the use of thiazide diuretics, Paget’s disease of the bone, vitamin D intoxication, and prolonged immobilization.
Hyperthyroidism is also associated with hypercalcemia because of a partial effect of the thyroid hormone on osteoclast activity.
Treatment of hypercalcemia–
Severe, life-threatening hypercalcemia is treated first with aggressive fluid replacement using normal saline.
This is usually followed by the use of loop diuretics such as furosemide, which promotes calcium loss from the body. Bisphosphonates such as alendronate, zoledronate, and pamidronate all inhibit osteoclasts and stimulate osteoblasts.
However, the maximal effect of biphosphonates takes two to three days. Calcitonin can be used for a more rapid decrease in calcium levels.
Calcitonin works by inhibiting the activity of the osteoclasts. Primary hyperparathyroidism– primary hyperparathyroidism represents 90% of mild hypercalcemia.
It is most commonly due to one gland adenoma in 80% of the cases. But hyperplasia of all four glands can lead to primary hyperparathyroidism in 20% of the cases.
Parathyroid cancer is a rare cause of the disease and is present in only less than 1%. Primary hyperparathyroidism can occur as part of MEN or Multiple Endocrine Neoplasia syndrome.
There are two kinds of multiple endocrine neoplasia syndrome. In MEN type I, the patients suffer from hyperparathyroidism, pituitary tumors, and pancreatic tumors.
This is called the Ps. In MEN type II, the patients suffer from hyperparathyroidism, pheochromocytoma, and medullary carcinoma of the thyroid.
On half of the patients with hyperthyroidisms, no symptoms are found. But they might present with symptoms related to hypercalcemia.
Osteitis fibrosa cystica can be present and occurs because of the increased rate of osteoclastic bone resorption and results in bone pain, fractures, swelling, deformity in areas of demineralization as well as the production of bone cysts and brain tumors.
Diagnosis and treatment of hyperparathyroidism–
The diagnosis can be made by laboratory findings of serum calcium of 10.5 milligrams per deciliter with elevated PTH level.
Serum phosphorous is usually low, less than 2.5 milligrams per deciliter. The differential diagnosis includes all other causes of hypercalcemia.
Imaging studies are not used for the diagnosis of hyperparathyroidism. Surgical removal of the parathyroid glands is usually effective and should be performed if there are symptoms of hypercalcemia, bone diseases, or renal diseases, or if the patient is pregnant.
One of the common complications of surgery is the development of the hungry bone syndrome. Medical treatment is used in an asymptomatic or mild increase of calcium level, for example, if the calcium is less than 11.5 milligrams per deciliter.
Medical treatment is also used if there are contraindications for surgery. The medical management includes biphosphonates, reduction of calcium intake to less than 400 milligrams per deciliter, and oral hydration with 2 to 3 liters of fluid per day.
Cinacalcet has also a place in the treatment of hyperparathyroidism. Hypocalcemia– hypoglycemia results in increased neural hyperexcitability such as seizures, tetany, circumoral numbness, and tingling of the extremities.
Physical findings are the known Chvostek sign, which is a contraction of the facial muscles after percussion of the facial nerve, and the Trousseau sign, which is the spasm of outstretched hand after inflation of a blood pressure cuff higher than the systolic blood pressure for more than three minutes. Of note, arrhythmia may also develop as a result of a prolonged QT. Finally, cataracts may develop for unclear reasons.
Etiology and treatment of hypocalcemia.
Hypocalcemia is most commonly caused by hypoparathyroidism, acute pancreatitis, and renal failure. In renal failure, hypocalcemia develops as a decrease of their 1, 25 hydroxyvitamin D production.
Hypocalcemia is most commonly caused by hypoparathyroidism, acute pancreatitis, and renal failure. In renal failure, hypocalcemia develops as a decrease of their 1, 25 hydroxy vitamin D production.
Hyperphosphatemia might also cause hypocalcemia, vitamin D deficiency, and hypomagnesemia, which prevents the release of PTH by the parathyroid glands.
Some drugs like loop diuretics, phenytoin, alendronate, and foscarnet would also lower calcium levels in the blood.
Hyperphosphatemia will cause precipitation of calcium in tissues. Massive blood transfusions can cause hypocalcemia because of the binding of the calcium to the citrate that contains the transfused units of blood.
Finally, hypocalcemia occurs with a low albumin level. The treatment of hypocalcemia depends on the correction of the underlying etiology.
But in general, calcium should be replaced intravenously or orally, and vitamin D is often used if his replacement is necessary.
Hyperphosphatemia– in general, the acute development of hyperphosphatemia does not cause symptoms unless it is associated with hypocalcemia.
Persistent hyperphosphatemia occurs almost exclusively in renal failure. Acute hyperphosphatemia can result from increased intestinal absorption like vitamin D intoxication or after the use of high phosphorous-containing enemas.
A common etiology is the rapid release of cellular contents like happens in tumor lysing syndrome after chemotherapy or in fast cell turnover.
It also occurs in rhabdomyolysis, acute hemolysis, hyperthermia, or decreased renal excretion. Chronic kidney diseases cause hyperphosphatemia mainly due to the inability of the kidney to eliminate phosphorous.
Unfortunately, chronic hyperphosphatemia in advanced chronic kidney disease is associated with adverse sequelae including cardiovascular disease, soft tissue calcification, and multiple bone metabolism disturbances.
The treatment of hyperphosphatemia includes the use of phosphate-binding agents to prevent its absorption in the gut.
Hypophosphatemia is a common finding in hospitalized patients. It is present in 3% of all patients and near to the hospitals. It is more frequent in patients with a history of alcoholism and can present in up to 70% of patients in the intensive care units.
hypophosphatemia is usually asymptomatic. But in moderate or severe cases, it can be manifested as muscle weakness, cardiomyopathy in heart failure may cause hemolysis, platelet dysfunction, and neurologic disorders.
Hypophosphatemia is caused by decreased intestinal absorption secondary to the use of phosphorous binders, alcohol intake, or severe vitamin D deficiency.
Hypophosphatemia can also be secondary to urinary losses like renal tubular defects, glucosuria, and hyperparathyroidism.
Hypophosphatemia can be caused by cellular shifts like happens in diabetics ketoacidosis crisis, respiratory alkalosis, and angry bone syndrome.
Hypophosphatemia is usually treated with intravenous or oral replacement. In general, increasing his oral intake is the preferred treatment.
As a summary, calcium and phosphorous homeostasis is regulated by vitamin D, PTH, and calcitonin.
The most common cause of hypercalcemia is hyperparathyroidism. Cardinal symptoms of hypocalcemia are tetany.
Hyperphosphatemia is clinically most relevant when caused by tumor lysis syndrome or advanced chronic kidney disease. Hypophosphatemia is usually related to nutritional deficiencies and is extremely common in hospitalized patients.