BSPh 103 Topic 8 Major Intracellular & Extracellular Electrolytes PDF

Major Intracellular and Extracellular Electrolytes Georchelle Faith Darcey, RPh BSPh 103: Inorganic Pharmaceutical Chemistry (Topic 8)  Major Intra- and Extracellular Electrolytes The body’s fluids are solutions of inorganic and organic solutes. The...

Major Intracellular and Extracellular Electrolytes Georchelle Faith Darcey, RPh BSPh 103: Inorganic Pharmaceutical Chemistry (Topic 8)  Major Intra- and Extracellular Electrolytes The body’s fluids are solutions of inorganic and organic solutes. The concentration balances of the various components are maintained in order for the cells and tissues to have a constant environment. Ions present in ICF: 1. Potassium – major cation 2. Phosphate – major anion 3. Magnesium – second major cation 4. Sulfate - second major anion Ions present in ECF: 1. Sodium – major cation 2. Chloride – major anion 3. Calcium – second major cation 4. Bicarbonate – second major anion PHOSPHATE (–– PO4-2) 1. Hexoses are metabolized as phosphate esters. 2. The phosphoric acid anhydride linkage is the body’s means of storing potential chemical energy as ATP. 3. The monohydrogen phosphate / dihydrogen phosphate is an important buffer system. 4. Phosphorus is essential for proper calcium metabolism. Phosphorus is essential for normal bone and tooth development since it is a component of hydroxyapatite, the main calcium salt found in bones and teeth. Serum phosphate levels usually correlate with serum calcium values. ATP molecule Osteogenesis Hyperphosphatemia may be found in: a. Hypervitaminosis D (w/c increases intestinal phosphate absorption along with calcium) b. Renal failure due to inability to excrete phosphate into the urine c. Parathyroidism (the lack of parathyroid hormone permits renal tubular reabsorption of phosphate w/c results in decreased urinary phosphate and a rise in serum phosphate – leading to the formation of phosphatic urinary calculi (a form of kidney stone) Hypophosphatemia may be seen in: a. Vitamin D deficiency (Rickets) – caused by decreased intestinal calcium absorption b. Lack of phosphate reabsorption by the kidney tubule from other causes (infection, cancers) c. Hyperparathyroidism d. Long-term aluminum hydroxide gel antacid therapy (it forms insoluble aluminum phosphate salts from dietary phosphate therapy, thus preventing the absorption of dietary phosphate from the intestinal tract) BICARBONATE (–– HCO-3) A lack of bicarbonate causes metabolic acidosis and an excess causes metabolic alkalosis. SODIUM (–– Na+1) This ion is responsible for maintaining normal hydration and osmotic pressure. Conditions causing hyponatremia (low serum sodium level): a. Extreme urine loss (such as seen in diabetes insipidus) b. Metabolic acidosis in which sodium is excreted c. Addison’s disease (with decreased excretion of ADH, aldosterone) d. Diarrhea and vomiting e. Kidney damage Conditions causing hypernatremia: a. Hyperadrenalism (Cushing’s syndrome) with increased aldosterone production b. Severe dehydration c. Certain type of brain injury d. Excess treatment with sodium salts – resulting to edema POTASSIUM (–– K+1) It is the major intracellular cation, present in a concentration approximately 23 times higher than the concentration of potassium in the extracellular fluid compartments. During transmission of a nerve impulse, potassium leaves the cell and sodium enters the cell. Potassium salts have been used for their diuretic action. Hypopotassemia (hypokalemia) can occur from: a. Vomiting b. Diarrhea c. Burns d. Hemorrhages e. Diabetic coma f. IV infusion of solutions lacking in potassium g. Overuse of thiazide diuretics h. Alkalosis Hyperpotassemia (hyperkalemia) can occur from: – is less common and usually occurs during certain types of kidney damage. If the kidney is functioning properly, the body can eliminate excess potassium readily. CALCIUM (–– Ca+2) 99% of body calcium is found in the bones; the remaining calcium is largely found in the ECF compartments Its absorption across the intestinal membranes is controlled by the parathyroid hormone and a metabolite of vitamin D. The other hormone involved in calcium control is calcitonin, or thyrocalcitonin. The intestinal absorption and serum level of calcium are heavily influenced by phosphate. Increased serum phosphorus levels will lower serum calcium levels. The administration of phosphorus salts has been used in the treatment of hypercalcemia. Calcium is essential for blood clotting. Citrate is added to whole blood to complex the blood calcium and thereby prevent clot formation in the collected blood. Hypocalcemia can be caused by: 1. Hypoparathyroidism 2. Vitamin D deficiency 3. Osteoblastic metastasis (spreading bone cancer) 4. Steatorrhea (fatty stool) 5. Cushing’s syndrome (hyperactive adrenal cortex) 6. Acute pancreatitis 7. Acute hyperphosphatemia Bone diseases: 1. Osteoporosis – a serious condition of bone degeneration commonly associated with aging; there is a reduced volume of bone tissue per unit volume of anatomical bone. Probable causes include: Decreased calcium absorption due to diet or some problem associated with intestinal calcium absorption Vitamin D deficiency Increased sensitivity to parathyroid hormone, particularly in postmenopausal women Bone dissolution 1. Paget’s disease – is due to faulty calcium metabolism characterized by an initial phase of decalcification and softening of the bone followed by calcium deposition with resultant thickening and deformity. Hypercalcemia is found in: 1. Hyperparathyroidism 2. Hypervitaminosis D 3. Some bone neoplastic diseases Symptoms of hypercalcemia: Fatigue Muscle weakness Constipation Anorexia (loss of appetite) Cardiac irregularities MAGNESIUM (–– Mg+2) It is the second most abundant cation in the intracellular fluid compartment and the fourth most abundant cation in the body. It is an essential component of many of the enzymes involving phosphate metabolism which also require adenosine triphosphate (ATP). Indispensable for protein synthesis and for the smooth functioning of the neuromuscular system. Magnesium salts when injected IM or IV have a powerful general anesthetic action. Soluble magnesium salts, usually magnesium sulfate, have been used as CNS depressants in obstetrics, convulsant states, and for the symptoms of tetanus.  Electrolytes Used for Replacement Therapy The main purpose of electrolyte replacement therapy is to overcome the electrolyte imbalance & to restore the composition of body fluid & body volume. This electrolyte imbalance seen in different abnormal conditions like diarrhea, vomiting, dehydration, prolonged treatment without adding any source of nutrients. There are few electrolytes present in the body which are responsible for different actions in the body like sodium, potassium, phosphate, bicarbonates, sulphate, calcium, chloride, & magnesium.  1. Sodium replacement Sodium chloride, USP XVIII – its uses range from replacement therapy and manufacture of isotonic solutions to a flavor enhancer. In order to be isotonic, a salt solution should be 0.9% w/v. Ordinary table salt does not meet USP standards. Isotonic solutions are used as wet dressings, for irrigating body cavities or tissues, and as injections when fluid and electrolytes have been depleted in isotonic proportions. Hypotonic solutions are administered for maintenance therapy when patients are unable to take fluid and nutrients orally for one to three days. Hypertonic injections are used when there is loss of sodium in an excess of water. 2. Potassium replacement Potassium chloride - drug of choice for oral replacement of potassium, preferably s a solution. It is irritating to the GIT and solutions must be well diluted. 3. Calcium replacement Calcium gluconate - used as electrolyte replenisher. Added to that patient diet which have the hypoglycemic condition. It is also used to treat conditions caused by low calcium levels such as: Bone loss (osteoporosis) Weak bones (osteomalacia/rickets) Decreased activity of the parathyroid gland (hypoparathyroidism) A certain muscle disease (latent tetany) Thank you for listening!