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Research paper topic: Clinical Chemistry In Medicine - 1442 words
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Clinical Chemistry In Medicine Of the diagnostic methods available to veterinarians, the clinical chemistry test has developed into a valuable aid for localizing pathologic conditions. This test is actually a collection of specially selected individual tests. With just a small amount of whole blood or serum, many body systems can be analyzed. Some of the more common screenings give information about the function of the kidneys, liver, and pancreas and about muscle and bone disease. There are many blood chemistry tests available to doctors.
This paper covers the some of the more common tests. Blood urea nitrogen (BUN) is an end-product of protein metabolism. Like most of the other molecules in the body, amino acids are constantly renewed. In the course of this turnover, they may undergo deamination, the removal of the amino group. Deamination, which takes place principally in the liver, results in the formation of ammonia. In the liver, the ammonia is quickly converted to urea, which is relatively nontoxic, and is then released into the bloodstream.
In the blood, it is readily removed through the kidneys and excreted in the urine. Any disease or condition that reduces glomerular filtration or increases protein catabolism results in elevated BUN levels. Creatinine is another indicator of kidney function. Creatinine is a waste product derived from creatine. It is freely filtered by the glomerulus and blood levels are useful for estimating glomerular filtration rate. Muscle tissue contains phosphocreatinine which is converted to creatinine by a nonenzymatic process. This spontaneous degradation occurs at a rather consistent rate (Merck, 1991).
Causes of increases of both BUN and creatinine can be divided into three major categories: prerenal, renal, and postrenal. Prerenal causes include heart disease, hypoadrenocorticism and shock. Postrenal causes include urethral obstruction or lacerations of the ureter, bladder, or urethra. True renal disease from glomerular, tubular, or interstitial dysfunction raises BUN and creatinine levels when over 70% of the nephrons become nonfunctional (Sodikoff, 1995). Glucose is a primary energy source for living organisms.
The glucose level in blood is normally controlled to within narrow limits. Inadequate or excessive amounts of glucose or the inability to metabolize glucose can affect nearly every system in the body. Low blood glucose levels (hypoglycemia) may be caused by pancreatic tumors (over-production of insulin), starvation, hypoadrenocorticism, hypopituitarism, and severe exertion. Elevated blood glucose levels (hyperglycemia) can occur in diabetes mellitus, hyperthyroidism, hyperadrenocorticism, hyperpituitarism, anoxia (because of the instability of liver glycogen in oxygen deficiency), certain physiologic conditions (exposure to cold, digestion) and pancreatic necrosis (because the pancreas produces insulin which controls blood glucose levels). Diabetes mellitus is caused by a deficiency in the secretion or action of insulin.
During periods of low blood glucose, glucagon stimulates the breakdown of liver glycogen and inhibits glucose breakdown by glycolysis in the liver and stimulates glucose synthesis by gluconeogenesis. This increases blood glucose. When glucose enters the bloodstream from the intestine after a carbohydrate-rich meal, the resulting increase in blood glucose causes increased insulin secretion and decreased glucagon secretion. Insulin stimulates glucose uptake by muscle tissue where glucose is converted to glucose-6-phosphate. Insulin also activates glycogen synthase so that much of the glucose-6-phosphate is converted to glycogen. It also stimulates the storage of excess fuels as fat (Lehninger, 1993). With insufficient insulin, glucose is not used by the tissues and accumulates in the blood.
The accumulated glucose then spills into the urine. Additional amounts of water are retained in urine because of the accumulation of glucose and polyuria (excessive urination) results. In order to prevent dehydration, more water than normal is consumed (polydipsia). In the absence of insulin, fatty acids released form adipose tissue are converted to ketone bodies (acetoacetic acid, B-hydroxybutyric acid, and acetone). Although ketone bodies can be used a energy sources, insulin deficiency impairs the ability of tissues to use ketone bodies, which accumulate in the blood.
Because they are acids, ketones may exhaust the ability of the body to maintain normal pH. Ketones are excreted by the kidneys, drawing water with them into the urine. Ketones are also negatively charged and draw positively charged ions (sodium, potassium, calcium) with them into urine. Some other results of diabetes mellitus are cataracts (because of abnormal glucose metabolism in the lens which results in the accumulation of water), abnormal neutrophil function (resulting in greater susceptibility to infection), and an enlarged liver (due to fat accumulation) (Fraser, 1991). Bilirubin is a bile pigment derived from the breakdown of heme by the reticuloendothelial system. The reticuloendothelial system filters out and destroys spent red blood cells yielding a free iron molecule and ultimately, bilirubin.
Bilirubin binds to serum albumin, which restricts it from urinary excretion, and is transported to the liver. In the liver, bilirubin is changed into bilirubin diglucuronide, which is sufficiently water soluble to be secreted with other components of bile into the small intestine. Impaired liver function or blocked bile secretion causes bilirubin to leak into the blood, resulting in a yellowing of the skin and eyeballs (jaundice). Determination of bilirubin concentration in the blood is useful in diagnosing liver disease (Lehninger, 1993). Increased bilirubin can also be caused by hemolysis, bile duct obstruction, fever, and starvation (Bistner, 1995). Two important serum lipids are cholesterol and triglycerides. Cholesterol is a precursor to bile salts and steroid hormones.
The principle bile salts, taurocholic acid and glycocholic acid, are important in the digestion of food and the solubilization of ingested fats. The desmolase reaction converts cholesterol, in mitochondria, to pregnenolone which is transported to the endoplasmic reticulum and converted to progesterone. This is the precursor to all other steroid hormones (Garrett, 1995). Triglycerides are the main form in which lipids are stored and are the predominant type of dietary lipid. They are stored in specialized cells called adipocytes (fat cells) under the skin, in the abdominal cavity, and in the mammary glands.
As stored fuels, triglycerides have an advantage over polysaccharides because they are unhydrated and lack the extra water weight of polysaccharides. Also, because the carbon atoms are more reduced than those of sugars, oxidation of triglycerides yields more than twice as much energy, gram for gram, as that of carbohydrates (Lehninger, 1993). Hyperlipidemia refers to an abnormally high concentration of triglyceride and/or cholesterol in the blood. Primary hyperlipidemia is an inherited disorder of lipid metabolism. Secondary hyperlipidemias are usually associated with pancreatitis, diabetes mellitus, hypothyroidism, protein losing glomerulonephropathies, glucocorticosteroid administration, and a variety of liver abnormalities. Hypolipidemia is almost always a result of malnutrition (Barrie, 1995). Alkaline phosphatase is present in high concentration in bone and liver. Bone remodeling (disease or repair) results in moderate elevations of serum alkaline phosphatase levels, and cholestasis (stagnation of bile flow) and bile duct obstruction result in dramatically increased serum alkaline phosphatase levels.
The obstruction is usually intrahepatic, associated with swelling of hepatocytes and bile stasis. Elevated serum alkaline phosphatase and bilirubin levels suggest bile duct obstruction. Elevated serum alkaline phosphatase and normal bilirubin levels suggest hepatic congestion or swelling. Elevations also occur in rapidly growing young animals and in conditions causing bone formation (Bistner, 1995). Aspartate aminotransferase (AST) is an enzyme normally found in the mitochondria of liver, heart, and skeletal muscle cells. In the event of heart or liver damage, AST leaks into the blood stream and concentrations become elevated (Bistner, 1995).
AST, along with alkaline phosphatase, are used to differentiate between liver and muscle damage in birds. Alanine aminotransferase (ALT) is considered a liver-specific enzyme, although small amounts are present in the heart. ALT is generally located in the cytosol. Liver disease results in the releasing of the enzyme into the serum. Measurements of this enzyme are used in the diagnosis of certain types of liver diseases such as viral hepatitis and hepatic necrosis, and heart diseases. The ALT level remains elevated for more than a week after hepatic injury (Sodikoff, 1995). Fibrinogen, albumin, and globulins constitute the major proteins of the blood plasma.
Fibrinogen, which makes up about 0.3 percent of the total protein volume, is a soluble protein involved in the clotting process. The formation of blood clots is the result of a series of zymogen activations. Factors released by injured tissues or abnormal surfaces caused by injury initiate the clotting process. To create the clot, thrombin removes negatively charged peptides from fibrinogen, converting it to fibrin. The fibrin monomer has a different surface charge distribution than fibrinogen. These monomers readily aggregates into ordered fibrous arrays.
Platelets and plasma globulins release a fibrin-stabilizing factor which creates cross-links in the fibrin net to stabilize the clot. The clot binds the wound until new tissue can be built (Garrett, 1995). The alpha-, beta-, and gamma-globulins compose the globulins. Alpha-globulins transport lipids, hormones, and vitamins. Also included is a glycoprotein, ceruloplasmin, which carries copper and hap ...
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