Clinical Chemistry Tests 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,
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,
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