Liver Function Tests Literature Review and Practice

Liver Function Tests Literature check and PracticeIntroductionThe coloured is the largest internal organ in the body. In adult the coloured-colored weighs approximately 1-2.5 kilograms. It is wedge-shaped, soft and reddish-brown in colour. It is situated underneath the diaphragm. The colored-colored is change integrity into right and left everywhere hand lobes by the middle hepatic venous melodic line vessel. The right lobe is bigger and consists of caudate and quadrate lobes. The breed is supplied to the liver constitute 25% of the resting cardiac output and through deuce major blood vessels hepatic artery and portal vein. Blood leaves the liver via the hepatic vein, which drains directly into the inferior vena cava. Bile is wreaked in the liver and it is collected in the saddle sore capillaries which drain into the right and left hepatic ducts.The liver is organised in lobules within which blood f miserables byg bingle hepatic booths via sinusoids from branches of the portal vein (bringing absorbed materials from gastroin straininal tract) to the central vein of each lobule. Hepatic artery blood (providing oxygen needed for many of the metabolic fermentes carried out by the liver) also enters the sinusoids. The central veins coalesce to carcass the hepatic veins which drain into the inferior vena cava. Each liver cell is also apposed to several bile goataliculi. The canaliculi coalesce to form the right and left hepatic ducts, which join outside the liver to form the common hepatic duct. The cystic duct drains the fussbladder. The hepatic duct unites with the cystic duct to form the common bile duct. The common bile duct enters the duodenum at the papilla. Ganong, (1995)Hepatocytes or pargonnchymal (liver cells) which further classified on the basis of their site in the lobule compensate about 60% kupffer cells lining the hepatic sinusoids comprise 30% of the liver cells and the remaining 10% of cells consist of vascular and supporting tissue and bile ducts.The significant important of the liver came from the skill of this organ to perform a wide variety of intents which contri entirelye in the body homeostasis, in contingent regulation of blood sugar. When in that respect is an excess sugar, the pancreatic cells secret the endocrine gland insulin that converts excess sugar into glycogen (storage form of glucose). Glycogen provide rapid accessible source of energy for the body when blood glucose decrease. Also gluconeogenesis (formation of tender glucose) from amino acids such(prenominal) as alanine and ascorbic acid take place in liver. The coagulation factors which atomic number 18 required for blood clotting, white and various lipoproteins which argon required for transport of lipid in blood stream argon synthesized in the liver. The only exception of protein synthesis is the synthesis of immunoglobulin. Cholesterol which serves as precursor of steroid hormones is close toly synthesized in by the liv er. Also liver has the ability to excrete and detoxify e.g. ammonia formed from the sectionalization of amino acids or microbial action in the gastrointestinal tract born-again to urea. Steroid hormones which ar inactivated by conjugation with glucuronate and sulphate excreted into urine as water soluble forms.A wide range of medications (drugs) inactivated by endoplasmic reticulum enzymes and some atomic number 18 excreted in the bile. Kupffer cells in the hepatic sinusoid distill toxins absorbed from the gastrointestinal tract. Other important excretory function is the voiding of bile acid formed from cholesterol in the liver to gall bladder where it stored until required for lipid digestion in the small intestine. The ability of liver to carry out its excretory function of the metabolism end products depends on, thinking(a) functioning hepatocytes, adequate blood flow through the liver and plain biliary duct. The other important function of liver is Storage of vitamins such as vitamin A, D and vitamin B12.In addition, metabolism and excretion of bilirubin is one of the major functions of the liver. hematoidin is an ecteric waste product pigment formed from the breakdown of hemoglobin (Hb) in the red blood cells in the lymph reticular placement at the end of their life span which is approximately 120 days. usually an adult produces about 450 umol/L daily. Gaw et al, (1999). Hb contains four haem group, an exhort atom and prophyrin ring draw togethered to each haem group. When Hb molecules metabolize, the smoothing iron atoms ar extinguishd and reused again in the mathematical processing of a hot Hb molecule. The prophyrin ring breaks to form a open tetrapyrole derivative biliverdin fibril which is further reduced to form un joinedd bilirubin (lipid soluble).Whitby, (1988).The lipid-soluble bilirubin can violate cell membrane include mental capacity barrier and cause brain cell damage. Therefore it has to be transported by a special newsboy called ovalbumin in the plasma in order to be converted to water-soluble so that can be excreted into bile. The binding of albumin urbane by being non enter cells readily and also non filtered through glumerulus unless there is glomerular proteinuria. When the albumin-bilirubin complex reach the liver, it dissociates by the receptors on the plasma at the same eon. Inside hepatocytes, bilirubin molecules join to comparatively non-specific anion binding proteins called ligandin (Y protein), is soluble transport protein in the smooth endoplasmic reticulum. Calbreath, (1992). The glucuronic acid molecules attach to unconjugated bilirubin molecules to form bilirubin glucuronides in a reaction intermediate by uridine diphosphate (UDP). hematoidin glucuronides complex is water-soluble conjugated bilirubin which so excreted into small intestine. The conjugation process depends on the active secretion of bile acids and therefore serum bile acids tightfistedness atomic number 18 more minute index of hepatic transport function than the natural bilirubin. Small touchstone undergoes reabsorption in the small intestine and the rest is degraded by bacterial action mainly in the colon where it is de-conjugated to form urobilinogen. Portions of urobilinogen re-enter the hepatic circulation and excreted by the liver into bile. Small fraction filtered by kidney into urine, but the majority is excreted in faeces providing its orange-yellow characteristic.If the bilirary tract becomes blocked, serum bilirubin slow-wittedness will rise as uncojugated bilirubin not excreted and the unhurried becomes strain. Jaundice is a yellow discoloration of the skin or the sclera of the eye. The yellowish coloration is caused by an excess amount of bilirubin in the plasma which is not detectable until the concentration is greater than 40 umol/L. gaw, et al (1999). The prescript concentration is up to 20 umol/L. causes of tartness classified into ternary categories incl uding haemolytic (prehepatic) jaundice characterized by an change magnitude breakdown of haemoglobin, hepatic jaundice referable to failure of the conjugation mechanism and post hepatic or obstructive jaundice because of obstruction of biliary system. Most neonate babies are characterized with physiological or neonatal jaundice due(p) to natural process of breaking down RBCs. As their livers are immature, they can not process bilirubin as quickly as when they are old. This increase in bilirubin concentration and has no significance to do with liver. Marshal, (2000).In clinical practice usually all the tests related to liver diseases are called liver function tests (LFT). Biochemical tests include measurement of bilirubin, the aminotransferases (ALT and AST), albumin total protein and alkalescent pkosphatase in serum specimen. albumin and total protein reflect the synthetical liver function. ALT and AST used to measure the severity of liver cells damage although they are not sp ecific index of acute damage to hepatocytes, but they are sensitve indicators to cytoplasmic and mitochondrial membrane. Gaw, et al (1999). Increased conjugation bilirubin concentration and increased ALP activity at curved surface indicate cholestasis, a law of closure in the bile flow. Prolonged cholestasis can pass in severe jaundice with real high bilirubin concentration result in deposition of bile salts, characterized by itching, bleeding due to vitamin K malabsorption, cholesterol retention and dark urine with pale stool. The prothrombin time (PT) which is used to asses the synthetic function of liver is prolonged due to cholestasis. quantity of glutamyl transferase can give an indication of hepatocellular enzyme induction due to drugs or alcohol.Materials and modePlease refer to medical biochemistry practical book (BMS2).Result numerationDetermination of ALPThe equation seeed from the graph is used to calculate the amount of phenylic acid liberated by the action of A LP. The equation isY = 0.1753The enzyme activity is metrical in international unit per 1 minute (IU/1) therefore to obtain the activity, the result has to be converted first to umol/1 and then divided by the incubation time (15 minutes) as follow(Value of phenol concentration in mmol/1 X 1000) / 15 = IU/LPatient 1Result 0.207 / 0.1753 = 1.18083 x 1000 = 1180.8 umol/LTo get the enzyme activity in 1 minute= 1180.8 / 15 = 78.7 IU/LALP enzyme activity of unhurried 1= 78.7 IU/LPatient 2Result 0.215 / 0.1753 = 1.2264 x 1000 = 1226.4 umol/LTo get the enzyme activity in 1 minute= 1226.4 / 15 = 81.7 IU/LALP enzyme activity of unhurried 2 = 81.7 IU/LDetermination of bilirubinThe concentration of bilirubin is calculated by using the following equationAbsorbance of the test x STD concentrationAbsorbance of STDResultPatient 1 = (0.413/0.431) x 350 = 335.3 umol/LPatient 2 = (0.037/0.431) x 350 = 30 umol/LThe results of Aspartate transaminase (AST), albumin and total protein were provided by th e tutor.ConclusionThe biochemical finding displays that patient 1 whitethorn re plait haemolytic disease where as the other patient (patient 2) suffer from acute hepatitis.DiscussionLiver function test are done to asses the integrity of the liver to carry out its approach pattern synthetic and metabolic functions. This is achieved through series of numerical tests that reflect the healthiness of the liver when comparing the result obtained with normal reference ranges. The measurements of enzyme activities are very usable in following the progress of the liver disease once the diagnosing has been made.From the result it is obvious that patient 1 has got normal TP, ALB, AST and ALP results, which means that there is liver damage. Total protein is combined of immunoglobulin proteins and other proteins. A persons total protein take gives information about the liver damage, kidney damage and nutritional health. Albumin is small protein made in the liver. If a person suffers from li ver damage, the albumin concentration will drop because the liver can not hold in the normal yield of albumin. Aspartate transminase (AST) is the enzyme appoint in the liver, heart and muscle. Levels of this enzyme are usually assessed in conjugation with reading for other liver enzyme to determine or monitor the liver involvement.On other hand the bilirubin is very high above the normal range (hyperbilirubiaemia) and normally the bilirubin which is perplex in plasma is unconjugated bilirubin. Since the unconjugated bilirubin is high it indicates that is excessive red blood cells (RBCs) destruction (haemolysis) which make outs in haemolytic anaemia. Normally the red blood cells choice is 120 days, but in haemolytic anaemia is less. Because of that the RBCs are sunk in large quantities in the RE system (particularly the spleen). When the RBCs are destroyed, the haemoglobin is released and bilirubin is produced. It is mainly produced from the haem moiety of the haemoglobin (it i s also produced from myoglobin, cytochroms and peroxidase, which are widely distributed in the body). The liver can not conjugate and remove this large amount of unconjugated bilirubin and since it is protein bound the renal glomeruli can not filter it. That leads to overflow of unconjugated bilirubin in blood circulation. These mean that this patient may subscribe haemolytic jaundice (prehepatic jaundice), because the protein synthesis is normal and ALP, AST are normal which means that there is no liver involvement.Haemolytic jaundice also occurs in haemolytic Disease of Newborn, transfusion of incompatible blood, catching spherocytosis and autoimmune red cell destruction. Marshall,(2000).The results of patient 2 show normal total protein, albumin and ALP. There is a slight increase in bilirubin level (hyperbilirubinaemia) and AST is above the very high. AST is an intracellular enzyme and is mostly found in the cytoplasmic and mitochondrial membrane of hepatocytes. So it is a sen sitive marker for the severity of damage hepatocytes. ALP concentration usually rises in cholestasis (this is by extra-hepatic obstruction of the bile duct) but in this patient was normal, which means that the kupffer cells and sinusoidal surface is not yet damaged. Total protein and albumin were also normal and that indicates that the metabolism and synthesis in the liver is not yet affected. Bilirubin was slightly high which support that there is liver disease and due to this, there is defect of bile salt and bile pigment excretion. In addition to that, conjugation and detoxification functions are come up defected because of hepatic cells damaged. These happen due to a condition called Hepatitis (liver inflammation).Hepatitis is the common cause of acute liver injury. keen hepatitis usually occurs due to viral infection particularly with hepatitis viruses A, B, C, D and E, but also Epstein-bar virus and cytomegalovirus or toxin (e.g. alcohol and paracetamol). Marshall, (2000) I n the primeval stages of hepatitis, increased plasma ALT and AST activities may be the only irregular chemical finding.There will be also an increased level of urobilinogen and bilirubin in urine (the urine will be darkened). The stool may be very pale due to damage biliary excretion of bilirubin and urobilinogen then disappears more or less completely from the urine. Marshall, (2000)The above results reveal that liver is functioning well but partly defected because of the early stage of the disease. This patient may have acute liver disease (Acute hepatitis). To confirm these results hepatitis virus profiles should be done. oppugnJaundice in the newborn is common. Why?Jaundice in the newborn is called Neonatal Jaundice. It is common because before birth, an infant get rid of bilirubin through the mothers blood and liver system. After birth, the babys liver has to take over processing on its own. The activity of the hepatic conjugation enzyme is usually low at birth but increases rapidly thereafter. Almost all newborns have higher than normal level of bilirubin because the immaturity of their livers. In most cases, the babys system continues to develop and can soon process bilirubin. However, some infants may need medical treatment to prevent serious complications which can occur due to the accumulation of bilirubin. There are at least ii significant processes that predispose normal infants to jaundiceThe rate of bilirubin production is higher in infants than adults because their red blood cells have half-life and turn over more rapidly.Infants have a relatively limited ability to conjugate bilirubin and conjugation in the liver is necessary for efficacious elimination.Write short notes on Gilberts disease.Gilberts disease is a harmless transmitted condition in which the unconjugated bilirubin level in the blood is increased. Bilirubin is an end product of haemoglobin breakdown and it is conjugated in the liver with glucuronate. This process is catalysed by specific enzyme called uidine diophosphate glucuronyl transferase which is found in endoplasmic reticulum, which helps the body to conjugate bilirubin and get rid of it. Thus Gilberts syndrome is a genetic unhinge which means that there is slight deficiency of this enzyme.Patient with Gilberts disease can have intermittent bilirubin level but the values are often increased when blood is drown after a point in time of fasting or during a time of concurrent viral malady or when the person is stressed, either physically or mentally. People with Gilberts syndrome are not ill but they may complain of vague ab discomfort and general fatigue for which no cause found. The condition is not usually apparent until adolescence or early adult life. It is sometimes observed incidentally, in the course of investigations done for related reasons. All liver function tests (LFTs) are normal, except for serum bilirubin which is raised. X-ray and liver biopsy show that there is no liver diseas e. Gilberts syndrome should not be regarded as a disease and people with the syndrome are not ill.