Clinical Chemistry In Medicine Essay
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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 different surface charge distribution than
...
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.
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