Clinical Chemistry In Medicine Term paper

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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...

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 Bistner’s 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. You should cite this paper as follows:

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