Clinical Chemistry In Medicine

.. toglobulins, which bind hemoglobin. Iron transport is related to beta-globulins. The glycoprotein that binds the iron is transferrin (Lehninger, 1993). Gamma-globulins (immunoglobulins) are associated with antibody formation.

There are five different classes of immunoglobulins. IgG is the major circulating antibody. It gives immune protection within the body and is small enough to cross the placenta, giving newborns temporary protection against infection. IgM also gives protection within the body but is too large to cross the placenta. IgA is normally found in mucous membranes, saliva, and milk.

It provides external protection. IgD is thought to function during the development and maturation of the immune response. IgE makes of the smallest fraction of the immunoglobulins. It is responsible for allergic and hypersensitivity reactions. Altered levels of alpha- and beta- globulins are rare, but immunoglobulin levels change in various conditions.

Serum immunoglobulin levels can increase with viral or bacterial infection, parasitism, lymphosarcoma, and liver disease. Levels are decreased in immunodeficiency. Albumin is a serum protein that affects osmotic pressure, binds many drugs, and transports fatty acids. Albumin is produced in the liver and is the most prevalent serum protein, making up 40 to 60 percent of the total protein. Serum albumin levels are decreased (hypoalbuminemia) by starvation, parasitism, chronic liver disease, and acute glomerulonephritis (Sodikoff, 1995). Albumin is a weak acid and hypoalbuminemia will tend to cause nonrespiratory alkalosis (de Morais, 1995).

Serum albumin levels are often elevated in shock or severe dehydration. Creatine Kinase (CK) is an enzyme that is most abundant in skeletal muscle, heart muscle, and nervous tissue. CK splits creatine phosphate in the presence of adenosine diphosphate (ADP) to yield creatine and adenosine triphosphate (ATP). During periods of active muscular contraction and glycolysis, this reaction proceeds predominantly in the direction of ATP synthesis. During recovery from exertion, CK is used to resynthesize creatine phosphate from creatine at the expense of ATP.

After a heart attack, CK is the first enzyme to appear in the blood (Lehninger, 1993). CK values become elevated from muscle damage (from trauma), infarction, muscular dystrophies, or inflammation. Elevated CK values can also be seen following intramuscular injections of irritating substances. Muscle diseases may be associated with direct damage to muscle fibers or neurogenic diseases that result in secondary damage to muscle fibers. Greatly increased CK values are usually associated with heart muscle disease because of the large number of mitochondria in heart muscle cells (Bistner, 1995).

When active muscle tissue cannot be supplied with sufficient oxygen, it becomes anaerobic and produces pyruvate from glucose by glycolysis. Lactate dehydrogenase (LDH) catalyzes the regeneration of NAD+ from NADH so glycolysis can continue. The lactate produced is released into the blood. Heart tissue is aerobic and uses lactate as a fuel, converting it to pyruvate via LDH and using the pyruvate to fuel the citric acid cycle to obtain energy (Lehninger, 1993). Because of the ubiquitous origins of LDH, the total serum level is not reliable for diagnosis; but in normal serum, there are five isoenzymes of LDH which give more specific information.

These isoenzymes can help differentiate between increases in LDH due to liver, muscle, kidney, or heart damage or hemolysis (Bistner, 1995). Calcium is involved in many processes of the body, including neuromuscular excitability, muscle contraction, enzyme activity, hormone release, and blood coagulation. Calcium is also an important ion in that it affects the permeability of the nerve cell membrane to sodium. Without sufficient calcium, muscle spasms can occur due to erratic, spontaneous nervous impulses. The majority of the calcium in the body is found in bone as phosphate and carbonate.

In blood, calcium is available in two forms. The nondiffusible form is bound to protein (mainly albumin) and makes up about 45 percent of the measurable calcium. This bound form is inactive. The ionized forms of calcium are biologically active. If the circulating level falls, the bones are used as a source of calcium. Primary control of blood calcium is dependent on parathyroid hormone, calcitonin, and the presence of vitamin D.

Parathyroid hormone maintains blood calcium level by increasing its absorption in the intestines from food and reducing its excretion by the kidneys. Parathyroid hormone also stimulates the release of calcium into the blood stream from the bones. Hyperparathyroidism, caused by tumors of the parathyroid, causes the bones to lose too much calcium and become soft and fragile. Calcitonin produces a hypocalcemic effect by inhibiting the effect of parathyroid hormone and preventing calcium from leaving bones. Vitamin D stimulates calcium and phosphate absorption in the small intestine and increases calcium and phosphate utilization from bone. Hypercalcemia may be caused by abnormal calcium/phosphorus ratio, hyperparathyroidism, hypervitaminosis D, and hyperproteinemia.

Hypocalcemia may be caused by hypoproteinemia, renal failure, or pancreatitis (Bistner, 1995). Because approximately 98 percent of the total body potassium is found at the intracellular level, potassium is the major intracellular cation. This cation is filtered by the glomeruli in the kidneys and nearly completely reabsorbed by the proximal tubules. It is then excreted by the distal tubules. There is no renal threshold for potassium and it continues to be excreted in the urine even in low potassium states.

Therefore, the body has no mechanism to prevent excessive loss of potassium (Schmidt-Nielsen, 1995). Potassium plays a critical role in maintaining the normal cellular and muscular function. Any imbalance of the body’s potassium level, increased or decreased, may result in neuromuscular dysfunction, especially in the heart muscle. Serious, and sometimes fatal, arrythmias may develop. A low serum potassium level, hypokalemia, occurs with major fluid loss in gastrointestinal disorders (i.e., vomiting, diarrhea), renal disease, diuretic therapy, diabetes mellitus, or mineralocorticoid dysfunction (i.e., Cushing’s disease).

An increased serum potassium level, hyperkalemia, occurs most often in urinary obstruction, anuria, or acute renal disease (Bistner, 1995). Sodium and its related anions (i.e., chloride and bicarbonate) are primarily responsible for the osmotic attraction and retention of water in the extracellular fluid compartments. The endothelial membrane is freely permeable to these small electrolytes. Sodium is the most abundant extracellular cation, however, very little is present intracellularly. The main functions of sodium in the body include maintenance of membrane potentials and initiation of action potentials in excitable membranes.

The sodium concentration also largely determines the extracellular osmolarity and volume. The differential concentration of sodium is the principal force for the movement of water across cellular membranes. In addition, sodium is involved in the absorption of glucose and some amino acids from the gastrointestinal tract (Lehninger, 1993). Sodium is ingested with food and water, and is lost from the body in urine, feces, and sweat. Most sodium secreted into the GI tract is reabsorbed.

The excretion of sodium is regulated by the renin-angiotensin-aldosterone system (Schmidt-Nielsen, 1995). Decreased serum sodium levels, hyponatremia, can be seen in adrenal insufficiency, inadequate sodium intake, renal insufficiency, vomiting or diarrhea, and uncontrolled diabetes mellitus. Hypernatremia may occur in dehydration, water deficit, hyperadrenocorticism, and central nervous system trauma or disease (Bistner, 1995). Chloride is the major extracellular anion. Chloride and bicarbonate ions are important in the maintenance of acid-base balance.

When chloride in the form of hydrochloric acid or ammonium chloride is lost, alkalosis follows; when chloride is retained or ingested, acidosis follows. Elevated serum chloride levels, hyperchloremia, can be seen in renal disease, dehydration, overtreatment with saline solution, and carbon dioxide deficit (as occurs from hyperventilation). Decreased serum chloride levels, hypochloremia, can be seen in diarrhea and vomiting, renal disease, overtreatment with certain diuretics, diabetic acidosis, hypoventilation (as occurs in pneumonia or emphysema), and adrenal insufficiency (de Morais, 1995). As seen above, one to two milliliters of blood can give a clinician a great insight to the way an animals’ systems are functioning. With many more tests available and being developed every day, diagnosis becomes less invasive to the patient.

The more information that is made available to the doctor allows a faster diagnosis and recovery for the patient. Bibliography Bibliography Barrie, Joan and Timothy D. G. Watson. Hyperlipidemia. Current Veterinary Therapy XII.

Ed. John Bonagura. Philadelphia: W. B. Saunders, 1995. Bistner, Stephen l.

Kirk and Bistners Handbook of Veterinary Procedures and Emergency Treatment. Philadelphia: W. B. Saunders, 1995. de Morais, HSA and William W.

Muir. Strong Ions and Acid-Base Disorders. Current Veterinary Therapy XII. Ed. John Bonagura.

Philadelphia: W. B. Saunders, 1995. Fraser, Clarence M., ed. The Merck Veterinary Manual, Seventh Edition. Rahway, N.

J.: Merck & Co., 1991. Garrett, Reginald H. and Charles Grisham. Biochemistry. Fort Worth: Saunders College Publishing, 1995.

Lehninger, Albert, David Nelson and Michael Cox. Principles of Biochemistry. New York: Worth Publishers, 1993. Schmidt-Nielsen, Knut. Animal Physiology: Adaptation and environment. New York: Cambridge University Press, 1995.

Sodikoff, Charles. Labratory Profiles of Small Animal Diseases. Santa Barbara: American Veterinary Publications, 1995. Science.