Clinical Chemistry In Medicine Essay Research Paper

СОДЕРЖАНИЕ: Clinical Chemistry In Medicine Essay, Research Paper Of the diagnostic methods available to veterinarians, the clinical chemistry test has developed into a valuable aid for localizing pathologic

Clinical Chemistry In Medicine Essay, Research Paper

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


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

haptoglobulins, 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.


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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