Clinical Chemistry In Medicine Essay Example For Students

Clinical Chemistry 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 bodysystems can be analyzed. Some of the more common screenings giveinformation about the function of the kidneys, liver, and pancreas andabout muscle and bone disease. There are many blood chemistry testsavailable to doctors. This paper covers the some of the more commontests. Blood urea nitrogen (BUN) is an end-product of protein metabolism. Likemost of the other molecules in the body, amino acids are constantlyrenewed. In the course of this turnover, they may undergo deamination,the removal of the amino group. Deamination, which takes placeprincipally 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 readilyremoved through the kidneys and excreted in the urine. Any disease orcondition that reduces glomerular filtration or increases proteincatabolism results in elevated BUN levels. Creatinine is another indicator of kidney function. Creatinine is a wasteproduct derived from creatine. It is freely filtered by the glomerulus andblood 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 includeurethral obstruction or lacerations of the ureter, bladder, or urethra. Truerenal disease from glomerular, tubular, or interstitial dysfunction raisesBUN and creatin ine levels when over 70% of the nephrons becomenonfunctional (Sodikoff, 1995). Glucose is a primary energy source for living organisms. The glucoselevel in blood is normally controlled to within narrow limits. Inadequateor excessive amounts of glucose or the inability to metabolize glucosecan affect nearly every system in the body. Low blood glucose levels(hypoglycemia) may be caused by pancreatic tumors (over-production ofinsulin), starvation, hypoadrenocorticism, hypopituitarism, and severeexertion. Elevated blood glucose levels (hyperglycemia) can occur indiabetes mellitus, hyperthyroidism, hyperadrenocorticism,hyperpituitarism, anoxia (because of the instability of liver glycogen inoxygen deficiency), certain physiologic conditions (exposure to cold,digestion) and pancreatic necrosis (because the pancreas produces insulinwhich controls blood glucose levels). Diabetes mellitus is caused by a deficiency in the secretion or action of insulin. During periods of low blood glucose, gl ucagonstimulates the breakdown of liver glycogen and inhibits glucosebreakdown by glycolysis in the liver and stimulates glucose synthesis bygluconeogenesis. This increases blood glucose. When glucose enters thebloodstream from the intestine after a carbohydrate-rich meal, theresulting increase in blood glucose causes increased insulin secretion anddecreased glucagon secretion. Insulin stimulates glucose uptake bymuscle tissue where glucose is converted to glucose-6-phosphate. Insulinalso activates glycogen synthase so that much of theglucose-6-phosphate is converted to glycogen. It also stimulates thestorage 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 theurine. Additional amounts of water are retained in urine because of theaccumulation of glucose and polyuria (excessive urination) results. Inorder to prevent dehydration, more water than normal is consum ed(polydipsia). In the absence of insulin, fatty acids released form adiposetissue are converted to ketone bodies (acetoacetic acid, B-hydroxybutyricacid, and acetone). Although ketone bodies can be used a energysources, insulin deficiency impairs the ability of tissues to use ketonebodies, which accumulate in the blood. Because they are acids, ketonesmay exhaust the ability of the body to maintain normal pH. Ketones areexcreted by the kidneys, drawing water with them into the urine. Ketonesare also negatively charged and draw positively charged ions (sodium,potassium, calcium) with them into urine. Some other results of diabetesmellitus are cataracts (because of abnormal glucose metabolism in thelens which results in the accumulation of water), abnormal neutrophilfunction (resulting in greater susceptibility to infection), and an enlargedliver (due to fat accumulation) (Fraser, 1991). Bilirubin is a bile pigment derived from the breakdown of heme by thereticuloendothelial system. T he reticuloendothelial system filters out anddestroys spent red blood cells yielding a free iron molecule andultimately, bilirubin. Bilirubin binds to serum albumin, which restricts itfrom urinary excretion, and is transported to the liver. In the liver,bilirubin is changed into bilirubin diglucuronide, which is sufficientlywater soluble to be secreted with other components of bile into the smallintestine. Impaired liver function or blocked bile secretion causesbilirubin to leak into the blood, resulting in a yellowing of the skin andeyeballs (jaundice). Determination of bilirubin concentration in the bloodis useful in diagnosing liver disease (Lehninger, 1993). Increasedbilirubin can also be caused by hemolysis, bile duct obstruction, fever,and starvation (Bistner, 1995). Two important serum lipids are cholesterol and triglycerides. Cholesterolis a precursor to bile salts and steroid hormones. The principle bile salts,taurocholic acid and glycocholic acid, are important in the dige stion offood and the solubilization of ingested fats. The desmolase reactionconverts cholesterol, in mitochondria, to pregnenolone which istransported 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 thepredominant type of dietary lipid. They are stored in specialized cellscalled adipocytes (fat cells) under the skin, in the abdominal cavity, andin the mammary glands. As stored fuels, triglycerides have an advantageover polysaccharides because they are unhydrated and lack the extrawater weight of polysaccharides. Also, because the carbon atoms aremore reduced than those of sugars, oxidation of triglycerides yields morethan twice as much energy, gram for gram, as that of carbohydrates(Lehninger, 1993). Hyperlipidemia refers to an abnormally high concentration of triglycerideand/or cholesterol in the blood. Primary hyperlipidemia is an inheriteddisorder of lipid metabolism. Secondary hyperlipidemias are usuallyassociated with pancreatitis, diabetes mellitus, hypothyroidism, proteinlosing glomerulonephropathies, glucocorticosteroid administration, a nd avariety of liver abnormalities. Hypolipidemia is almost always a result ofmalnutrition (Barrie, 1995). Alkaline phosphatase is present in high concentration in bone and liver. Their Eyes Were Watching God Essay ThesisThe ionized forms of calcium are biologically active. If the circulatinglevel 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 hormonemaintains blood calcium level by increasing its absorption in theintestines from food and reducing its excretion by the kidneys. Parathyroid hormone also stimulates the release of calcium into theblood stream from the bones. Hyperparathyroidism, caused by tumors ofthe parathyroid, causes the bones to lose too much calcium and becomesoft and fragile. Calcitonin produces a hypocalcemic effect by inhibitingthe effect of parathyroid hormone and preventing calcium from leavingbones. Vitamin D stimulates calcium and phosphate absorption in thesmall intestine and increases calcium and phosphate utilization frombone. Hypercalcemia may be caused by abnormal calcium/phosphorusratio, hyperparathyroidism, hypervitaminosis D, and hyperproteinemia. Hypocalcemia may be caused by hypoproteinemia, renal failure, orpancreatitis (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 distaltubules. There is no renal threshold for potassium and it continues to beexcreted in the urine even in low potassium states. Therefore, the bodyhas no mechanism to prevent 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 or decreased, may result in neuromuscular dysfunction,especially in the heart muscle. Serious, and sometimes fatal, arrythmiasmay develop. A low serum potassium level, hypokalemia, occurs withmajor fluid loss in gastrointestinal disorders (i.e., vomit ing, diarrhea),renal disease, diuretic therapy, diabetes mellitus, or mineralocorticoiddysfunction (i.e., Cushings disease). An increased serum potassiumlevel, hyperkalemia, occurs most often in urinary obstruction, anuria, oracute renal disease (Bistner, 1995). Sodium and its related anions (i.e., chloride and bicarbonate) areprimarily responsible for the osmotic attraction and retention of water inthe extracellular fluid compartments. The endothelial membrane is freelypermeable to these small electrolytes. Sodium is the most abundantextracellular cation, however, very little is present intracellularly. Themain functions of sodium in the body include maintenance of membranepotentials and initiation of action potentials in excitable membranes. Thesodium concentration also largely determines the extracellular osmolarityand volume. The differential concentration of sodium is the principalforce for the movement of water across cellular membranes. In addition,sodium is involved in the a bsorption of glucose and some amino acidsfrom the gastrointestinal tract (Lehninger, 1993). Sodium is ingestedwith 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 ofsodium 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 nervoussystem trauma or disease (Bistner, 1995). Chloride is the major extracellular anion. Chloride and bicarbonate ionsare important in the maintenance of acid-base balance. When chloride inthe form of hydrochloric acid or ammonium chloride is lost, alkalosisfollows; when chloride is retained or ingested, acidosis follows. Elevatedserum chloride levels, hyperchloremia, can be seen in renal disease,dehydration, overtreatment with saline solution, and carbon dioxidedeficit (as occurs from hyperventilation). Decreased serum chloridelevels, hypochloremia, can be seen in diarrhea and vomiting, renaldisease, overtreatment with certain diuretics, diabetic acidosis,hypoventilation (as occurs in pneumonia or emphysema), and adrenalinsufficiency (de Morais, 1995). As seen above, one to two milliliters of blood can give a clinician a greatinsight to the way an animals systems are functioning. With many moretests available and being developed every day, diagnosis becomes lessinvasive to the patient. The more information that is made available tothe doctor allows a faster diagnosis and recovery for the patient. BibliographyBibliography 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 Bistners 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. Science