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CALCIUM (serum)
Increased in:
-Hyperparathyroidism, primary (due to hyperplasia or adenoma of parathyroids) or secondary
-Hyperparathyroidism due to parathormone-secreting cancer -Hematologicmalignancies (e.g., myeloma, lymphoma, leukemia)
-Excess vitamin D intake
-Bone tumor (Metastatic carcinoma (10% of patients))
-Acute osteoporosis (e.g., immobilization of young patients or in Paget's disease)
-Milk-alkali (Burnett's) syndrome
-Idiopathic hypercalcemia of infants
-Infantile hypophosphatasia
-Hyperthyroidism (some patients)
-Cushing's syndrome (some patients)
-Addison's disease (some patients)
-Myxedema (some patients)
-Hyperproteinemia (Sarcoidosis, -Multiple myeloma (some patients))
-Thiazide drugs
-Artifactual (e.g., venous stasis during blood collection, use of corkstoppered test tubes)
Decreased in:
-Hypoparathyroidism (Surgical; Idiopathic; Pseudohypoparathyroidism)
-Malabsorption of calcium and vitamin D (Obstructive jaundice)
-Hypoalbuminemia (Cachexia, Nephrotic syndrome, Sprue, Celiac disease,Cystic fibrosis of pancreas)
-Chronic renal disease with uremia and phosphate retention
-Acute pancreatitis with extensive fat necrosis
-Insufficient calcium, phosphorus, and vitamin D ingestion (Bone disease (osteomalacia, rickets); Starvation; Late pregnancy).
Total serum protein should always be known for proper interpretation of serum calcium levels.
CHLORIDE (serum)
Elevated in:
-Dehydration, excessive infusion of normal saline
-Hyperparathyroidism, renal tubular disease, metabolic acidosis, prolonged diarrhea
-Drugs (ammonium chloride administration, acetazolamide, boric acid, triamterene)
Decreased in:
CHF, SIADH, Addison's disease, vomiting, gastric suction, salt-losing nephritis, continuous infusion of D5W, thiazide diuretic administration, diaphoresis, diarrhea, burns.
COPPER (serum)
Increased in:
-Anemias (Pernicious anemia, Megaloblastic anemia of pregnancy, Iron deficiency anemia, Aplastic anemia, Leukemia, acute and chronic,Infection, acute and chronic, Malignant lymphoma, Hemochromatosis)
-Collagen diseases (including SLE, rheumatoid arthritis, acute rheumatic fever, glomerulonephritis)
-Frequently associated with increased C-reactive protein
Decreased in:
-Nephrosis (ceruloplasmin lost in urine)
-Wilson's disease
-Acute leukemia in remission
-Some iron deficiency anemias of childhood (that require copper as well as iron therapy)
FERRITIN (serum)
Elevated in:
Hyperthyroidism, inflammatory states, liver disease (ferritin elevated from necrotic hepatocytes), neoplasms (neuroblastomas, Iymphomas,leukemia, breast carcinoma), iron replacement therapy, hemochromatosis
Decreased in:
Iron deficiency anemia.
Increased in:
-Renal failure
-Diabetic coma before treatment
-Addison's disease and after adrenalectomy
-Controlled diabetes mellitus in older patients
-Administration of antacids containing magnesium
Decreased in:
-GI disease showing malabsorption and abnormal loss of GI fluids (e.g.,nontropical sprue, small bowel resection, biliary and intestinal fistulas, abdominal irradiation, prolonged aspiration of intestinal
contents, celiac disease and other causes of steatorrhea)
-Acute alcoholism and alcoholic cirrhosis
-Insulin treatment oof diabetic coma
-Lytic tumors of bone
-Diuretic drug therapy (e.g., ethacrynic acid, furosemide)
-Some cases of renal disease (e.g., glomerulonephritis, pyeloneI phritis, renal tubular acidosis)
-Acute pancreatitis
-Excessive lactation
-Idiopathic disorders
Magnesium deficiency may cause apparently unexplained hypocalcemia and hypokalemia; the patients may have neurologic and GI symptoms.
Increased in:
-Hypoparathyroidism (Idiopathic, Surgical, Pseudohypoparathyroidism)
-Excess vitamin D intake
-Secondary hyperparathyroidism (renal rickets)
-Bone disease (Healing fractures, Multiple myeloma (some patients),Paget's disease (some patients), Osteolytic metastatic tumor in bone(some patients))
-Addison's disease
-Myelogenous leukemia
-Acute yellow atrophy
-High intestinal obstruction
-Sarcoidosis (some patients)
-Milk-alkali (Burnett's) syndrome (some patients)
-Artifactual increase by hemolysis of blood
Decreased in
-Diabetes mellitus*
-Nutritional recovery syndrome* (rapid refeeding after prolonged starvation)
-Alkalosis, respiratory (e.g., gram-negative bacteremia) or metabolic
-Acute gout
-Salicylate poisoning
-Administration of glucose intravenously (e.g., recovery after severe burns, hyperalimentation)
-Administration of anabolic steroids, androgens, epinephrine, glucagon, insulin
-Acidosis (especially ketoacidosis)
-Renal tubular defects (e.g., Fanconi syndrome)
-Administration of diuretics
-Prolonged hypothermia (e.g., open heart surgery)
-Vitamin D deficiency and/or resistance, osteomalacia
-Malnutrition, vomiting, diarrhea
-Administration of phosphate-binding antacids*
-Primary hypophosphatemia
*Indicates conditions associated with severe hypophosphatemia.Mechanismsof hypophosphatemia are intracellular shift of phosphate,increased loss (via kidney or intestine), or decreased intestinal absorption; usually associated with prior phosphorus depletion. Often, more than one mechanism is operative.
Increased in:
-Renal failure: (Acute with oliguria or anuria; Chronic end-stage with oliguria (glomerular filtration rate <3-5 ml/minute); Chronic nonoliguric associated with dehydration, obstruction, trauma, or excess
-Decreased mineralocorticoid activity: (Addison's disease; Hypofunction of renin-angiotensin-aldosterone system; Pseudohypoaldosteronism;
Aldosterone antagonist (e.g., spironolactone)
-Increased supply of potassium: (Red blood cell hemolysis (transfusion reaction, hemolytic anemia); Excess dietary intake or rapid potassium infusion; Striated muscle (statusepilepticus, periodic paralysis);
Potassium-retaining drugs (e.g., triamterene); Fluid-electrolyte imbalance (e.g., dehydration, acidosis))
-Laboratory artifacts (e.g., hemolysis during venipuncture, conditions associated with thrombocytosis, incomplete separation of serum and clot)
Decreased in:
-Renal and adrenal conditions with metabolic alkalosis:(Administration of diuretics, Primary aidosteronism,Pseudoaldosteronism,Saltlosing nephropathy, Cushing's syndrome)
-Renal conditions associated with metabolic acidosis: (Renal tubularacidosis, Diuretic phase of acute tubular necrosis, Chronic pyelonephritis, Diuresis following relief of urinary tract obstruction)
-Gastrointestinal conditions: (Vomiting, gastric auctioning; Villous adenoma; Cancer of colon; Chronic laxative abuse; Zollinger-Ellison syndrome; Chronic diarrhea; Ureterosigmoidostomy).
SODIUM (serum)
Increased in:
Excess loss of water...
-Conditions that cause loss via gastrointestinal tract (e.g., in vomiting), lung (hyperpnea), or skin (e.g., in excessive sweating)
-Conditions that cause diuresis (Diabetes insipidus, Nephrogenicdiabetes insipidus, Diabetes mellitus, Diuretic drugs, Diuretic phase of acute tubular necrosis, Diuresis following relief of urinary tract
obstruction, Hypercalcemic nephropathy, Hypokalemic nephropathy),Excess administration of sodium (iatrogenic), e.g., incorrect replacement following fluid loss. ""Essential"" hypernatremia due to hypothalamic lesions,
Decreased in: (serum osmolality is decreased):
-Dilutional: (e.g., congestive heart failure, nephrosis, cirrhosis with ascites)
-Sodium depletion: (Loss of body fluids (e.g., vomiting, diarrhea, excessive sweating) with incorrect or no therapeutic replacement, diuretic drugs (e.g., thiazides); Adrenocortical insufficiency; Saltlosing
nephropathy; Inappropriate secretion of antidiuretic hormone)
-Spurious (serum osmolality is normal or increased): (Hyperlipidemia;Hyperglycemia (serum sodium decreases 3 mEq/L for every increase of serum glucose of 100 mg/100 ml).

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