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Anabolic Steroids Essay

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 categoriesprerenal, 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 r 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.

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StudyBoss » Steroids » Anabolic Steroids Essay

Anabolic Steroids Essay

Anabolic steroids are performance enhancing drugs. They are a synthetic form of the chemical testosterone that is normally found in the body. By taking anabolic steroids, a person’s testosterone level can be raised up to a hundred times more than the usual amount of 2. 5 to 10 mg. Per day. The increase in testosterone increases anabolic activity, which results in greater muscle bulk. It also increases protein synthesis and androgenic activity (enhanced secondary sexual characteristics) in males.

The users of steroids want to increase the anabolic effects and reduce the androgenic effects, but no steroid s known to have just anabolic effects. Use: Anabolic steroids can be taken in two ways, by injection or they can be taken orally. Both oral and injected steroids carry benefits and adverse effects. Orally taken steroids are well absorbed into the stomach and they are excreted fairly rapidly. The bad side of taking oral steroids is that they are more toxic than injected steroids. They are highly potent, which makes the risk of overdosing very high.

Steroids that are injected are less toxic to the liver and are less potent than oral steroids on an equal dosage basis. Injected teroids have a delayed take up, which makes them last longer. It also allows them to be detected in drug tests for a longer period of time. How they work in the body: When anabolic steroids are introduced into the body, under certain conditions they increase: protein synthesis, lean body mass, and the nitrogen balance in the body. A steroid receptor is formed which stimulates the synthesis of enzymes. With the stimulus of enzymes in the body, protein synthesis is also increased.

One enzyme system that is placed into the body by the receptor is the ribonucleic acid (RNA)-polymerose system. This system promotes cellular protein metabolism and synthesis which utilizes nitrogen. By utilizing the nitrogen, the anabolic action is increased, which leads to larger muscle size and strength. Anabolic steroids also increase nitrogen retention in the body. They move the nitrogen equilibrium to the positive side. This allows the body to utilize ingested protein better, but the balance does not last forever. The body’s homeostatic mechanisms regulate the balance and change it back to normal.

This is one set back to anabolic steroid use. In order to gain ean body mass a person may have to eat up to 10,000 calories / day and must continue a rigorous weight training program. If this is not followed, taking the steroids would be worthless. Adverse Effects: Despite the increase in muscle size and strength, anabolic steroids carry an even greater risk, the side effects. The side effects can be permanent or even deadly. Serious side effects are seen in the liver, the cardiovascular, central nervous and reproductive/endocrine systems. One major side effect that can be found in the liver is hepatotoxicity.

This is the poisoning of the liver. It shuts down the liver’s ability to process blood, which in turn shuts down the whole body. Prolonged use of anabolic steroids can cause cholestosis and jaundice (yellowish coloring of the eyes, skin and body fluids). Even though most adverse side effects in the liver are reversible upon discontinuation of steroids, fatalities can occur. The fatalities occur from hepatic cholestosis, liver tumors or peliosis hepatitis (blood filled cysts that can rupture and cause bleeding and liver failure). Very noticeable effects occur in the reproductive system.

In males the esticles shrink by about 20%. They become impotent. Their sperm count can decrease by 90%. Also gynecomastia can be seen in males. Gynecomastia is the enlargement of the breasts. One adverse effect that can be seen in both males and females using steroids is inappropriate hair growth. In females, anabolic steroids can cause irregularities in their menstrual cycles. It causes the female voice to deepen and clitoral hypertrophy. Clitoral hypertrophy is the enlargement of the clitoris. Many of these things are irreversible, but some can be changed with the discontinuation of steroid use.

In the cardiovascular system adverse effects can be very deadly. When taking steroids an increase in LDL (low density lipoprotein) cholesterol and a decrease in HDL (high density lipoprotein) cholesterol occurs in the bloodstream. This can carry a risk of coronary heart disease and myocardial infarctions. They can also cause retention of fluids. High blood pressure can cause an increased risk of congestive heart failure and strokes. The adverse effects in the musculoskeletal systems are not life threatening, but they are very noticeable.

Younger steroids users can have a remature closure of the epiphyses (growth plates) in the long bones. This irreversibly limits the full adult height potential. With the use of steroids, muscle/tendon strength changes. The muscles become stronger, but the tendons become stiffer and less able to withstand force. This causes an increase in muscle strains or ruptures. The central nervous system is also effected by the use of steroids. In the person taking steroids, aggressive behavior, self confidence and a sense of well being are seen. Also manic mood swings can occur.

These mood swings can ange from euphoria to sexual arousal to irritability and hostility. Cognitive impairment can also set in on the user. Cognitive impairment can involve distractibility, forgetfulness, and confusion. History: The use of steroids is nothing new to the world. Since the time of the Greek Olympics athletes have been using performance enhancing drugs in order to heighten their athletic performance. In 1886 the 1st person to die due to performance enhancing drugs was a French cyclist. He took a speed-ball, a mix of cocaine and heroin, which eventually killed him.

Physicians in the 20’s ran tests on athletes by inserting monkey testicles into male athletes to help boost their vitality. Adolf Hitler supposedly administered the hormone testosterone to himself and his troops in order to increase aggressiveness. In 1953 the first anabolic steroid was introduced. It had five times more strength building effects than natural hormones. In the 1960’s the IOC (International Olympic Committee) started to ban performance enhancing drugs due to their popular use. At the 1976 summer games in Montreal, the IOC initiated the first testing for teroids.

Today testing is done routinely on the collegiate and international level. The USOC (United States Olympic Committee) can suspend an athlete for up to two years if caught using steroids. Repeat offenders may be suspended from competing on the Olympic level for life. The NCAA does year round testing regardless if the athlete is in season or not. Selected teams are notified two days in advance of being tested, and 18 players are tested at that time. Positive testing results in a one year suspension of the student athlete.

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