Clinical Chemistry Tests In Medicine Essay Example For Students

Clinical Chemistry Tests In Medicine Essay Of the diagnostic methods available to veterinarians, the clinicalchemistry test has developed into a valuable aid for localizing pathologicconditions. This test is actually a collection of specially selected individualtests. With just a small amount of whole blood or serum, many body systems canbe analyzed. Some of the more common screenings give information about thefunction of the kidneys, liver, and pancreas and about muscle and bone disease. There are many blood chemistry tests available to doctors. This paper coversthe some of the more common tests. Blood urea nitrogen (BUN) is an end-product of protein metabolism. Likemost of the other molecules in the body, amino acids are constantly renewed. Inthe course of this turnover, they may undergo deamination, the removal of theamino group. Deamination, which takes place principally in the liver, resultsin the formation of ammonia. In the liver, the ammonia is quickly converted tourea, which is relatively nontoxic, and is then released into the bloodstream. In the blood, it is readily removed through the kidneys and excreted in theurine. Any disease or condition that reduces glomerular filtration or increasesprotein catabolism results in elevated BUN levels. Creatinine is another indicator of kidney function. Creatinine is awaste product derived from creatine. It is freely filtered by the glomerulusand blood levels are useful for estimating glomerular filtration rate. Muscletissue contains phosphocreatinine which is converted to creatinine by anonenzymatic process. This spontaneous degradation occurs at a ratherconsistent rate (Merck, 1991). Causes of increases of both BUN and creatinine can be divided into threemajor categories: prerenal, renal, and postrenal. Prerenal causes includeheart disease, hypoadrenocorticism and shock. Postrenal causes include urethralobstruction or lacerations of the ureter, bladder, or urethra. True renaldisease from glomerular, tubular, or interstitial dysfunction raises BUN andcreatinine levels when over 70% of the nephrons become nonfunctional (Sodikoff,1995). Glucose is a primary energy source for living organisms. The glucoselevel in blood is normally controlled to within narrow limits.Inadequate orexcessive amounts of glucose or the inability to metabolize glucose can affectnearly every system in the body. Low blood glucose levels (hypoglycemia) may becaused by pancreatic tumors (over-production of insulin), starvation,hypoadrenocorticism, hypopituitarism, and severe exertion. Elevated bloodglucose levels (hyperglycemia) can occur in diabetes mellitus, hyperthyroidism,hyperadrenocorticism, hyperpituitarism, anoxia (because of the instability ofliver glycogen in oxygen deficiency), certain physiologic conditions (exposureto cold, digestion) and pancreatic necrosis (because the pancreas producesinsulin which controls blood glucose levels). Diabetes mellitus is caused by a deficiency in the secretion or action ofinsulin. During periods of low blood glucose, glucagon stimulates the breakdownof liver glycogen and inhibits glucose breakdown by glycolysis in the liver andstimulates glucose synthesis by gluconeogenesis. This increases blood glucose. When glucose enters the bloodstream from the intestine after a carbohydrate-richmeal, the resulting increase in blood glucose causes increased insulin secretionand decreased glucagon secretion. Insulin stimulates glucose uptake by muscletissue where glucose is converted to glucose-6-phosphate. Insulin alsoactivates glycogen synthase so that much of the glucose-6-phosphate is convertedto glycogen. It also stimulates the storage of excess fuels as fat (Lehninger,1993). With insufficient insulin, glucose is not used by the tissues andaccumulates in the blood. The accumulated glucose then spills into the urine. Additional amounts of water are retained in urine because of the accumulation ofglucose and polyuria (excessive urination) results. In order to preventdehydration, more water than normal is consumed (polydipsia). In the absence ofinsulin, fatty acids released form adipose tissue are converted to ketone bodies(acetoacetic acid, B-hydroxybutyric acid, and acetone). Although ketone bodiescan be used a energy sources, insulin deficiency impairs the ability of tissuesto 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 areexcreted by the kidneys, drawing water with them into the urine. Ketones arealso negatively charged and draw positively charged ions (sodium, potassium,calcium) with them into urine. Some other results of diabetes mellitus arecataracts (because of abnormal glucose metabolism in the lens which results inthe accumulation of water), abnormal neutrophil function (resulting in gr eatersusceptibility to infection), and an enlarged liver (due to fat accumulation)(Fraser, 1991). Bilirubin is a bile pigment derived from the breakdown of heme by thereticuloendothelial system. The reticuloendothelial system filters out anddestroys spent red blood cells yielding a free iron molecule and ultimately,bilirubin. Bilirubin binds to serum albumin, which restricts it from urinaryexcretion, and is transported to the liver. In the liver, bilirubin is changedinto bilirubin diglucuronide, which is sufficiently water soluble to be secretedwith other components of bile into the small intestine. Impaired liver functionor blocked bile secretion causes bilirubin to leak into the blood, resulting ina yellowing of the skin and eyeballs (jaundice). Determination of bilirubinconcentration in the blood is useful in diagnosing liver disease (Lehninger,1993). Increased bilirubin can also be caused by hemolysis, bile ductobstruction, fever, and starvation (Bistner, 1995). Two important serum lipids are cholesterol and triglycerides. Cholesterol is a precursor to bile salts and steroid hormones. The principlebile salts, taurocholic acid and glycocholic acid, are important in thedigestion of food and the solubilization of ingested fats. The desmolasereaction converts cholesterol, in mitochondria, to pregnenolone which istransported to the endoplasmic reticulum and converted to progesterone. This isthe precursor to all other steroid hormones (Garrett, 1995). Triglycerides are the main form in which lipids are stored and are thepredominant type of dietary lipid. They are stored in specialized cells calledadipocytes (fat cells) under the skin, in the abdominal cavity, and in themammary glands. As stored fuels, triglycerides have an advantage overpolysaccharides because they are unhydrated and lack the extra water weight ofpolysaccharides. Also, because the carbon atoms are more reduced than those ofsugars, oxidation of triglycerides yields more than twice as much energy, gramfor gram, as that of carbohydrates (Lehninger, 1993). Camera Obscura Experience EssayCalcium is involved in many processes of the body, includingneuromuscular excitability, muscle contraction, enzyme activity, hormonerelease, and blood coagulation. Calcium is also an important ion in that itaffects the permeability of the nerve cell membrane to sodium. Withoutsufficient calcium, muscle spasms can occur due to erratic, spontaneous nervousimpulses. The majority of the calcium in the body is found in bone as phosphateand carbonate. In blood, calcium is available in two forms. The nondiffusibleform is bound to protein (mainly albumin) and makes up about 45 percent of themeasurable calcium. This bound form is inactive. The ionized forms of calciumare biologically active.If the circulating level falls, the bones are used asa source of calcium. Primary control of blood calcium is dependent on parathyroid hormone,calcitonin, and the presence of vitamin D. Parathyroid hormone maintains bloodcalcium level by increasing its absorption in the intestines from food andreducing its excretion by the kidneys. Parathyroid hormone also stimulates therelease of calcium into the blood stream from the bones. Hyperparathyroidism,caused by tumors of the parathyroid, causes the bones to lose too much calciumand become soft and fragile. Calcitonin produces a hypocalcemic effect byinhibiting the effect of parathyroid hormone and preventing calcium from leavingbones. Vitamin D stimulates calcium and phosphate absorption in the smallintestine and increases calcium and phosphate utilization from bone. Hypercalcemia may be caused by abnormal calcium/phosphorus ratio,hyperparathyroidism, hypervitaminosis D, and hyperproteinemia. Hypocalcemia maybe caused by hypoproteinemia, renal failure, or pancreatitis (Bistner, 1995). Because approximately 98 percent of the total body potassium is found atthe intracellular level, potassium is the major intracellular cation. Thiscation is filtered by the glomeruli in the kidneys and nearly completelyreabsorbed 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 theurine even in low potassium states. Therefore, the body has no mechanism toprevent excessive loss of potassium (Schmidt-Nielsen, 1995). Potassium plays a critical role in maintaining the normal cellular andmuscular function. Any imbalance of the bodys potassium level, increased ordecreased, may result in neuromuscular dysfunction, especially in the heartmuscle. Serious, and sometimes fatal, arrythmias may develop. A low serumpotassium level, hypokalemia, occurs with major fluid loss in gastrointestinaldisorders (i.e., vomiting, diarrhea), renal disease, diuretic therapy, diabetesmellitus, or mineralocorticoid dysfunction (i.e., Cushings disease). Anincreased serum potassium level, hyperkalemia, occurs most often in urinaryobstruction, anuria, or acute renal disease (Bistner, 1995). Sodium and its related anions (i.e., chloride and bicarbonate) areprimarily responsible for the osmotic attraction and retention of water in theextracellular fluid compartments. The endothelial membrane is freely permeableto these small electrolytes. Sodium is the most abundant extracellular cation,however, very little is present intracellularly. The main functions of sodiumin the body include maintenance of membrane potentials and initiation of actionpotentials in excitable membranes. The sodium concentration also largelydetermines the extracellular osmolarity and volume. The differentialconcentration of sodium is the principal force for the movement of water acrosscellular membranes. In addition, sodium is involved in the absorption ofglucose 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. Theexcretion of sodium is regulated by the renin-angiotensin-aldosterone system(Schmidt-Nielsen, 1995). Decreased serum sodium levels, hyponatremia, can be seen in adrenalinsufficiency, inadequate sodium intake, renal insufficiency, vomiting ordiarrhea, and uncontrolled diabetes mellitus. Hypernatremia may occur indehydration, water deficit, hyperadrenocorticism, and central nervous systemtrauma or disease (Bistner, 1995). Chloride is the major extracellular anion. Chloride and bicarbonateions are important in the maintenance of acid-base balance. When chloride inthe form of hydrochloric acid or ammonium chloride is lost, alkalosis follows;when chloride is retained or ingested, acidosis follows. Elevated serumchloride levels, hyperchloremia, can be seen in renal disease, dehydration,overtreatment with saline solution, and carbon dioxide deficit (as occurs fromhyperventilation). Decreased serum chloride levels, hypochloremia, can be seenin diarrhea and vomiting, renal disease, overtreatment with certain diuretics,diabetic acidosis, hypoventilation (as occurs in pneumonia or emphysema), andadrenal insufficiency (de Morais, 1995). As seen above, one to two milliliters of blood can give a clinician agreat insight to the way an animals systems are functioning. With many moretests available and being developed every day, diagnosis becomes less invasiveto the patient. The more information that is made available to the doctorallows a faster diagnosis and recovery for the patient. BibliographyBarrie, Joan and Timothy D. G. Watson. Hyperlipidemia. Current VeterinaryTherapy XII. Ed. John Bonagura. Philadelphia: W. B. Saunders, 1995. Bistner, Stephen l. Kirk and Bistners Handbook of VeterinaryProcedures and Emergency Treatment. Philadelphia: W. B. Saunders, 1995. de Morais, HSA and William W. Muir. Strong Ions and Acid-BaseDisorders. Current Veterinary Therapy XII. Ed. JohnBonagura. Philadelphia: W. B. Saunders, 1995. Fraser, Clarence M., ed. The Merck Veterinary Manual, SeventhEdition. Rahway, N. J.: Merck ; Co., 1991. Garrett, Reginald H. and Charles Grisham. Biochemistry. FortWorth: Saunders College Publishing, 1995. Lehninger, Albert, David Nelson and Michael Cox. Principles ofBiochemistry. New York: Worth Publishers, 1993. Schmidt-Nielsen, Knut. Animal Physiology: Adaptation andenvironment. New York: Cambridge University Press, 1995. Sodikoff, Charles. Labratory Profiles of Small Animal Diseases. Santa Barbara: American Veterinary Publications, 1995. Category: Science