Open in TheBrain

Calcium

Calcium is an essential mineral in the body that plays a crucial role in several vital functions, including:

  1. Bone Health: Calcium is a primary building block of bone tissue. About 99% of the body's calcium is stored in bones and teeth, helping them stay strong and dense.
  2. Muscle Function: It helps muscles contract and relax. Calcium ions are involved in muscle contraction, and a deficiency can lead to muscle cramps or spasms.
  3. Nerve Transmission: Calcium helps transmit nerve signals. It plays a key role in the release of neurotransmitters, which are chemicals that carry signals between nerve cells.
  4. Blood Clotting: Calcium is necessary for blood coagulation. It works with other proteins to help blood clot when needed, such as after an injury.
  5. Hormonal Secretion: It is involved in the release of hormones and enzymes that regulate many body processes.

Dietary Sources:

Calcium is found in many foods, including:

Recommended Daily Intake:

The recommended daily calcium intake varies by age and gender:

Deficiency:

A calcium deficiency can lead to weakened bones (osteoporosis), muscle cramps, numbness, and fatigue. Long-term deficiency can significantly affect bone health and increase fracture risk.

Supplements:

If you're not getting enough calcium from food, supplements are an option. However, it’s important to balance calcium with magnesium and vitamin D, as they help with calcium absorption.

Hypercalcaemia

From Wikipedia, the free encyclopedia

**Hypercalcaemia** (British English) or **hypercalcemia** (American English) is an elevated calcium (Ca2+) level in the blood.[1] (Normal range: 9–10.5 mg/dL or 2.2–2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a workup should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

Contents

[hide]

Signs and symptoms[edit]

The neuromuscular symptoms of hypercalcemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarization.[2] There is a general mnemonic for remembering the effects of hypercalcaemia: "Stones, Bones, Groans, Thrones and Psychiatric Overtones"

  • Stones (renal or biliary)
  • Bones (bone pain)
  • Groans (abdominal pain, nausea and vomiting)
  • Thrones (polyuria)
  • Psychiatric overtones (Depression 30–40%, anxiety, cognitive dysfunction, insomnia, coma)

Other symptoms can include fatigue, anorexia, and pancreatitis.[citation ^needed]

Abnormal heart rhythms can result, and ECG findings of a short QT interval[3] and a widened T wave suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.[4] Hypercalcaemia has also been known to cause an ECG finding mimicking hypothermia, known as an Osborn wave.[5]

Hypercalcaemia can increase gastrin production, leading to increased acidity so peptic ulcers may also occur.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result. Hypercalcaemia causes the opposite[clarify] – the high levels of calcium ions decrease neuronal excitability, which leads to hypotonicity of smooth and striated muscle. This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups. In the gut this causes constipation. The sluggish nerves also explain drowsiness, confusion, hallucinations, stupor and / or coma.

Causes[edit]

Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.[6][7]

Abnormal parathyroid gland function[edit]

Malignancy[edit]

[](http://en.wikipedia.org/wiki/File:Small_cell_carcinoma_of_the_ovary_hypercalcemic_type-high_mag.jpg)

[](http://en.wikipedia.org/wiki/File:Small_cell_carcinoma_of_the_ovary_hypercalcemic_type-high_mag.jpg "Enlarge")

Micrograph of ovarian small cell carcinoma of the hypercalcemic type. H&E stain.

Vitamin-D metabolic disorders[edit]

Disorders related to high bone-turnover rates[edit]

Renal failure[edit]

Treatments[edit]

The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause.

Initial therapy: fluids and diuretics[edit]

  • hydration, increasing salt intake, and forced diuresis.
    • hydration is needed because many patients are dehydrated due to vomiting or renal defects in concentrating urine.
    • increased salt intake also can increase body fluid volume as well as increasing urine sodium excretion, which further increases urinary calcium excretion (In other words, calcium and sodium (salt) are handled in a similar way by the kidney. Anything that causes increased sodium (salt) excretion by the kidney will, en passant, cause increased calcium excretion by the kidney)
    • after rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload andpulmonary oedema. In addition, loop diuretics tend to depress renal calcium reabsorption thereby helping to lower blood calcium levels
    • can usually decrease serum calcium by 1–3 mg/dL within 24 h
    • caution must be taken to prevent potassium or magnesium depletion

Additional therapy: bisphosphonates and calcitonin[edit]

  • bisphosphonates are pyrophosphateanalogues with high affinity for bone, especially areas of high bone-turnover.
    • they are taken up by osteoclasts and inhibit osteoclastic bone resorption
    • current available drugs include (in order of potency): (1st gen) etidronate, (2nd gen) tiludronate, IV pamidronate, alendronate (3rd gen) zoledronate and risedronate
    • all patients with cancer-associated hypercalcaemia should receive treatment with bisphosphonates since the 'first line' therapy (above) cannot be continued indefinitely nor is it without risk. Further, even if the 'first line' therapy has been effective, it is a virtual certainty that the hypercalcaemia will recur in the patient with hypercalcaemia of malignancy. Use of bisphosphonates in such circumstances, then, becomes both therapeutic and preventative
    • patients in renal failure and hypercalcaemia should have a risk-benefit analysis before being given bisphosphonates, since they are relatively contraindicated in renal failure.
  • Calcitoninblocks bone resorption and also increases urinary calcium excretion by inhibiting renal calcium reabsorption
    • Usually used in life-threatening hypercalcaemia along with rehydration, diuresis, and bisphosphonates
    • Helps prevent recurrence of hypercalcaemia
    • Dose is 4 Units per kg via subcutaneous or intramuscular route every 12 hours, usually not continued indefinitely

Other therapies[edit]

Hypercalcaemic crisis [edit]

A hypercalcaemic crisis is an emergency situation with a severe hypercalcaemia, generally above approximately 14 mg/dL (or 3.5 mmol/l).[14]

The main symptoms of a hypercalcaemic crisis are oliguria or anuria, as well as somnolence or coma.[15] After recognition, primary hyperparathyroidism should be proved or excluded.[15]

In extreme cases of primary hyperparathyroidism, removal of the parathyroid gland after surgical neck exploration is the only way to avoid death.[15] The diagnostic program should be performed within hours, in parallel with measures to lower serum calcium.[15] Treatment of choice for acutely lowering calcium is extensive hydration and calcitonin, as well as bisphosphonates (which have effect on calcium levels after one or two days).[16]

See also[edit]

References[edit]

  1. Jump up "hypercalcemia" at Dorland's Medical Dictionary
  2. Jump up Armstrong, C.M., Cota, Gabriel.; Cota (1999). "Calcium block of Na+ channels and its effect on closing rate". Proceedings of the National Academy of Sciences of the United States of America 96 (7): 4154–4157.Bibcode:1999PNAS...96.4154A. doi:10.1073/pnas.96.7.4154. PMC 22436.
  3. Jump up http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/hypercalcemia/
  4. Jump up Wesson, L.; Suresh, V.; Parry, R. (2009). "Severe hypercalcaemia mimicking acute myocardial infarction". Clinical medicine (London, England) 9 (2): 186–187. doi:10.7861/clinmedicine.9-2-186. PMID 19435131. edit
  5. Jump up Serafi S, Vliek C, Taremi M (2011) "Osborn waves in a hypothermic patient" The Journal of Community Hospital Internal Medicine Perspectives http://www.jchimp.net/index.php/jchimp/article/view/10742/html
  6. Jump up Table 20-4 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.
  7. Jump up Tierney, Lawrence M.; McPhee, Stephen J.; Papadakis, Maxine A. (2006). Current Medical Diagnosis and Treatment 2007 (Current Medical Diagnosis and Treatment). McGraw-Hill Professional. p. 901. ISBN 0-07-147247-9.
  8. Jump up Online 'Mendelian Inheritance in Man' (OMIM) 146200
  9. Jump up Online 'Mendelian Inheritance in Man' (OMIM) 145980
  10. Jump up Online 'Mendelian Inheritance in Man' (OMIM) 145981
  11. Jump up Online 'Mendelian Inheritance in Man' (OMIM) 600740
  12. Jump up Non-Small Cell Lung Cancer at medscape. Author: Winston W Tan.Chief Editor: Jules E Harris. Updated: Mar 30, 2011
  13. Jump up Online 'Mendelian Inheritance in Man' (OMIM) 143880
  14. Jump up Hypercalcemia in Emergency Medicine at Medscape. Author: Robin R Hemphill. Chief Editor: Erik D Schraga. Retrieved April 2011
  15. ^ Jump up to:^a b c d Ziegler R (February 2001). "Hypercalcemic crisis". J. Am. Soc. Nephrol. 12 Suppl 17: S3–9. PMID 11251025.
  16. Jump up Page 394 in: Roenn, Jamie H. Von; Ann Berger; Shuster, John W. (2007). Principles and practice of palliative care and supportive oncology. Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-9595-8.
  17. Jump up Dauber, Andrew; Nguyen Thutrang T; Sochett Etienne; Cole David E C; Horst Ronald; Abrams Steven A; Carpenter Thomas O; Hirschhorn Joel N (Nov 2011). "Genetic Defect in CYP24A1, the Vitamin D 24-Hydroxylase Gene, in a Patient with Severe Infantile Hypercalcemia". The Journal of Clinical Endocrinology and Metabolism (in ENG) 97 (2): E268–74. doi:10.1210/jc.2011-1972. PMC 3275367. PMID 22112808.

[show]

Inborn error of metal metabolism (E83, 275)



[show]

Paraneoplastic syndromes



Categories: