CALCIUM AND IT S DEFICIENCY

CALCIUM A positive charge ion, abundant in skeletal system (99%) and the only one % seen in the plasma.

Normal total serum calcium level 8.6 to 10.2 mg/dL (2.2 to 2.6 mmol/L

ROLE of the CALCIUM Transmitting nerve impulses. Help regulate muscle contraction and relaxation including cardiac muscles. Instrumental in activating enzymes that stimulate many essential chemical reactions in the body Play a role in blood coagulation

Sources:
Milk Cheese Butter Ice cream REMEMBER!!!!
Calcium is absorbed from foods in the body presence of normal gastric acidity and Vit.D. Calcium is excreted primarily in the feces with the remainder excreted un the urine. The serum calcium level is controlled by Parathyroid Hormone and Calcitonin.

ABSTRACT
Hypercalcemia: a finding indicative of a prostatic adenocarcinoma
Abstract Calcemic alterations in prostate cancer are extremely rare. Hypercalcemia may be seen in cases of multiple osseous dissemination, and even in the absence of this in response to humoral mechanisms. The existence of hypercalcemia may indicate tumoural recurrence, and may at times be a datum prior to the diagnosis of the tumour. In cases of disseminated prostate adenocarcinoma hormones treatment may secure the normalization of blood calcium. We present a case of prostate carcinoma diagnosed in a 76-year-old patient, as a result of the presentation of a hypercalcemic metabolic syndrome, which was corrected after treatment by means of complete androgenic blocking.
http://www.researchgate.net/publication/20624118_Hypercalcemia_a_finding_indicative_of_a_prostatic_ade nocarcinoma

Postoperative parathyroid hormone testing decreases symptomatic hypocalcemia and associated emergency room visits after total thyroidectomy. Abstract
BACKGROUND: Symptomatic hypocalcemia, the most common complication of total thyroidectomy, can lead to postoperative emergency room visits for laboratory testing and intravenous calcium infusion. A method to identify patients reliably at risk for postoperative hypocalcemia could allow prophylactic treatment to avoid this. We hypothesized that quick parathyroid hormone testing within 4 hours of thyroidectomy and a protocol to treat parathyroid-hormone-deficient patients would reduce symptomatic hypocalcemia, eliminating the need for emergency room visits. METHODS: After January 1, 2006, 271 consecutive patients underwent total thyroidectomy with postoperative parathyroid hormone testing (group 1). Patients with parathyroid hormone levels <10 pg/mL were treated according to a newly instituted protocol with 0.25-ug calcitriol twice daily and 2-6 g of calcium carbonate daily for 1 week. Patients with parathyroid hormone levels 10 pg/mL were treated with calcium only. Group 2 consisted of 100 consecutive patients who underwent total thyroidectomy prior to 2006 without parathyroid hormone testing and were treated according to surgeon preference and serum calcium levels.

 RESULTS: Patients in the 2 groups were similar with regard to age, sex, and thyroiditis. However, patients in group 1, who had parathyroid hormone testing, had greater postoperative calcium levels (P < .005). Also, patients in group 2 had a higher incidence of malignancy (P = .04). Importantly, patients in group 1 had a lesser incidence of symptomatic hypocalcemia (7% vs 17%; P = .005). Furthermore, the number of patients who made visits to the emergency room was less in patients who had parathyroid hormone testing compared with those who did not (1.8% vs 8.0%; P = .008). CONCLUSION: Postoperative parathyroid hormone testing reliably identifies patients at risk for hypocalcemia after thyroid surgery. Moreover, parathyroid hormone testing and calcitriol administration to patients at risk decreases the incidence of hypocalcemia and associated emergency room visits after total thyroidectomy. Therefore, patients with postoperative serum parathyroid hormone levels <10 pg/mL after thyroid surgery should be treated with calcitriol and calcium to prevent symptomatic hypocalcemia. Copyright 2010 Mosby, Inc. All rights reserved. | PMID: 20723956

http://pubget.com/mesh_browser/Nutritional%20and%20Metabolic%20Dise ases/Metabolic%20Diseases/Calcium%20Metabolism%20Disorders/Hypoc alcemia/pg/1

Hypercalcemia and huge splenomegaly presenting in an elderly patient with B-cell nonHodgkin's lymphoma: a case report Abstract Introduction
Hypercalcemia is the major electrolyte abnormality in patients with malignant tumors. It can be due to localized osteolytic hypercalcemia or elaboration of humoral substances such as parathyroid hormone-related protein from tumoral cells. In hematological malignancies, a third mechanism of uncontrolled synthesis and secretion of 125(OH)2D3 from tumoral cells or neighboring macrophages may contribute to the problem. However, hypercalcemia is quite unusual in patients with B-cell non-Hodgkin's lymphoma.

Case presentation An 85-year-old Caucasian woman presented with low grade fever, anorexia, abdominal discomfort and fullness in her left abdomen for the last six months. She was mildly anemic and complained of fatigability. She had huge splenomegaly and was hypercalcemic. After correction of her hypercalcemia, she had a splenectomy. Microscopic evaluation revealed a malignant lymphoma. Her immunohistochemistry was positive for leukocyte common antigen, CD20 and parathyroid hormone-related peptide. Conclusion Immunopositivity for parathyroid hormone-related peptide clearly demonstrates that hypersecretion of a parathyroid hormone-like substance from the tumor had led to hypercalcemia in this case. High serum calcium is seen in only seven to eight percent of patients with B-cell non-Hodgkin's lymphoma, apparently due to different mechanisms. Evaluation of serum parathyroid hormonerelated protein and 1-25(OH)2D3 can be helpful in diagnosis and management. It should be noted that presentation with hypercalcemia has a serious impact on prognosis and survival. http://www.jmedicalcasereports.com/content/4/1/330/abstract

Hypocalcemia pathopysiology

 When extracellular fluid calcium concentration falls below normal, the parathyroid glands are directly stimulated by the low calcium levels to promote increased secretion of PTH. PTH regulates plasma calcium concentration through three main effects.
By stimulating bone resorption By stimulating activation of vitamin D, which then increases intestinal reabsorption of calcium. By directly increasing renal tubular calcium reabsorption.

Ca

Vit D3 Activation

PTH

Intestinal Ca Reabsorption

Renal Ca Reabsorption

Ca Release From Bones

 Hypocalcemia can also develop from an inadequate intake of vitamin D as a result of intentional changes of diet. Parathyroid disease decreases plasma calcium level a deficiency of parathyroid hormone results in a decreases in plasma calcium levels because of decreased bone resorption, decreased GI absorption, and increased urinary excretion of calcium.

 Hypocalcemia can develop in people with pancreatitis owing to release of lipase into soft tissue spaces, with subsequent binding of free fatty acids to calcium. Excess sodium, as seen in cushing disease, promotes the excreation of calcium. Over correction of acidosis may lead to hypocalcemia, because alkalosis causes decreased calcium ionization, leading to more calcium protein binding.

 Several medications have been linked with hypocalcemia: magnesium sulphate,colchicines,and neomycin Aspirin, anticonvulsant and estrogen Phosphate preparations Steroids Loop diuretics Antacids and laxatives

 Nursing Management in Hypocalcemia Clinical Management

Tetany Trousseau s sign Chvostek s sign Seizures Medical Management IV calcium administration Vitamin D therapy

 Nursing Management
Seizure precautions are initiated when hypocalcemia is severe. Airway is closely monitored because laryngeal stridor can occur. High risk for osteoporosis are instructed about the need for adequate dietary calcium intake. Value of regular weight-bearing exercise in decreasing bone loss should be emphasize. Strategies to reduce falls.

Hypercalcemia
Defined as a plasma Ca level greater than 5.5 mEq/L or 11mg/dl It is a common electrolyte disorder that can have serious physical complications ETIOLOGY AND RISK FACTORS: 1. Metastic malignancy 2. Hyperparathyriodism 3. Thiazide diuretic therapy

Pathophysiology
Increase serum Ca Increase resorption of Ca in the bones Destruction of bone tissues Ca is released in ECF

Increase Ca absorption in the intestine Release HCL, Gastrin and pancreatic enzyme

Excess Ca in the kidney

Cell membrane threshold becomes more positive Decrease neuromuscular excitability

Disturb cardiac muscle function and electrical conduction through the heart S/Sx: Increase in HR and Bp

Retention of Ca by the kidney

Slows bowel transit time

Causes osmotic diuresis

Constipation Polyuria S/Sx: Decrease motility Hypoactive bowel sound Abdominal Distention

Ca precipitates tend to form ureteral or kidney stones Urinary Blockage

Neurologic depression

Risk for thrombus formation

Bradycardia lethargy

S/Sx: increase urinary output Increase thirst

Impaired Glomerular Blood flow Renal Failure

Depressed sensorium Confusion Muscle weakness Decrease deep tendon reflex

Cardiac Arrest

S/Sx: polyuria,polydipsia,Nocturia

Dehydration Treatment: Diuretics Calcium chelators Fluid volume therapy

Coma

Death

S/Sx: Mild Hypercalcemia: slightly above 5.5mEq/L or 11mg/dl  Asymptomatic Moderate Hypercalcemia: Ca levels of 6.2 mEq/L or 13mg/dl  Anorexia  Nausea and vomiting  Polyuria  Muscle weakness  Fatigue  Lethargy  Dehydration  Constipation Chronic hypercalcemia: may develop similar symptoms to those of peptic ulcer.  Confusion  Impaired memory  Slurred speech

 Lethargy  Acute psychotic behavoir  Coma  The more severe symptoms tend to appear when the serum Ca level is approx. 16 mg/dl or above
Hypercalcemic crisis refers to an acute rise in the serum Ca level to 17mg/dl or higher.  S/Sx:  Severe thirst  Polyuria  Muscle weakness  Intractable nausea  Abdominal cramps  Obstipation or Diarrhea  Peptic ulcer symptoms  Bone pain

 Lethargy  Coma  This condition is very dangerous and may result in cardiac arrest.

Nursing Diagnosis Risk of constipation related to abdominal muscle weakness Excessive urination related to disturbed renal tubular function. Impaired physical mobility related to decreased tone in smooth and striated muscle.  Medical Management Goal:
Decrease the serum calcium level and reversing the process causing hypercalcemia. Treating the underlying cause of hypercalcemia.

Interventions:
Administer fluids to dilute serum calcium and promote its excretion by the kidneys. Restriction of dietary calcium intake.

Nursing Management
Interventions:

Encourage patient to ambulate as soon as possible. Adequate fiber should be provided in the diet to offset the tendency of constipation. Assess patient for signs and symptoms of digitalis toxicity. Cardiac rate and rhythm should be monitored for any abnormalities.

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Prepared by:
Bandiola, Rizaber Bataga, Mary Rose Bedua, Erika Buhat, April Ann Daarol, Lourilwin David, Jennifer Anne Dela Torre, Wilhelmina Joy BSN3-B