Anatomy of Human Body, Liver - Essay Example

ANATOMY In human anatomy Liver, although an accessory organ, is the largest organ in our body. It constitutes about 50 of the entire weight of thebody. The weight of liver in an adult is approximately 1500 gms. Thousands of functional units called 'liver lobules' are there in liver. These liver lobules number about 50,000 to 100,000 in human liver. They are of several millimeters in length and 0.8 to 2.0 mm in diameter. The lobule is found in a central vein, which empties into hepatic vein and then into the vena cava. The lobule itself is composed of many hepatic cellular plates. These plates radiate from the central vein. Each of these plates is of thickness of two cells. Between the adjacent cells lie small bile canaliculi that empty into bile ducts in the fibrous septa separating the adjacent liver lobules. Blood from the venous outflow of the gastro intestinal tract reaches small portal venules in the septa by way of portal vein. Flat branching hepatic sinusoids, which lie between hepatic plates receive the blood from the portal venules. Afterwards the blood goes to central vein. Thus hepatic cells are continuously exposed to portal venous blood. In the interlobular septa, hepatic arterioles supply arterial blood to the septal tissues between the adjacent lobules. Many of these arterioles empty directly into the hepatic sinusoids in such a way that one third of the distance is away from the interlobular septa. The venous sinusoids are lined by two other types of cells namely, typical endothelial cells and larger Kupfer cells. The latter is also known as reticuloendothelial cells. The Kupfer cells are capable of phagocytosis, the process by which bacteria and other foreign matter in hepatic sinus blood are engulfed. The large pores in the lining of the endothelial cells facilitate free flow of the substances in plasma. Some pores are big enough to the tune of 1 micrometer in diameter. Millions of narrow tissue spaces called 'Spaces of Disse' lie between endothelial cells and hepatic cells. In the interlobular septa, these Spaces of Disse are connected with lymphatic vessels. Overflowing fluid in these spaces are thus removed by lymphatics. The large pores are helpful in diffusing even the large portions of plasma protein freely into this space. The functions of liver are versatile. Liver maintains filtration and storage of blood. Carbohydrates, protein, fats, hormones and foreign chemicals that are found in medications are metabolized at liver only. Liver stores vitamins and iron, which are necessary for the growth. The very important function of liver is formation of bile. It is through this bile secretion that many waste materials are excreted from liver. During medication, we consume many drugs such as sulfonamides, penicillin, ampicillin, and erythromycin. The active chemical medium present in liver detoxifies or excretes those drugs into bile. Accumulation of some steroid hormones like estrogen, coristol, aldosterone secreted by endocrine glands causes over activity of hormonal systems. Theses hormones are either chemically changed into other substances or excreted by the liver. Unwanted Calcium is excreted from the body only with help of the secretion from liver; from bile secretion the calcium reaches the gut and is lost finally in faeces. (Arthur C.Guyton and John E. Hall, 2000) One of the important excretory jobs carried out by the liver is removal of bilirubin. Bilirubin is formed continuously in the usual breakdown of the red blood cells. After circulating in the blood stream for about 120 days, in a normal healthy adult, the red blood cells wear out. These worn out red blood cells, haemoglobin, are converted into bilirubin, a yellow pigment. This bilirubin passes through the blood stream to liver, which is the only organ in our body capable of removing it. Metabolism of bilirubin takes places in three phases--- prehepatic, intrahepatic and post hepatic. In prehepatic phase about 80% of haemogulobin halves are metabolized to form bilirubin. Nearly 4mg/kg of bilirubin is produced in a day. This bilirubin reaches liver for conjugation and excretion. In the intrahepatic phase, the unconjugated bilirubin, which is soluble in fats, is conjugated in hepatocyte with a sugar through an enzyme called 'glicuronosyltransferase' and becomes soluble in aqueous bile. Posthepatic phase of bilirubin metabolism occurs outside the liver, when the bile-soluble bilirubin enters the gallbladder, duodenum and intestine. From the intestine the bilirubin is excreted in stool and urobilinogens are excreted through urine. (Sean P Roche, Rebecca Kobos, 2004) Abnormal accumulation1 of this yellow pigment, bilirubin in extracellular fluids is the cause of jaundice. Normal plasma concentration of bilirubin is about 0.5mg/dl of plasma. Mostly bilirubin in unconjugated or free form is found in the normal concentration. In some abnormal situations this rises to 40mg/dl during when the form of bilirubin is effectively conjugated. The skin of a jaundice patient becomes yellow when the concentration rises thrice its normal level ie, 1.5mg/dl. The causes for such accumulation of bilirubin vary. Jaundice is consequently of four types. They are: hemolytic jaundice, obstructive jaundice, liver jaundice and constitutional jaundice. In hemolytic jaundice the excretory function of the liver is normal. But when the destruction rate of red blood cells are far more higher, the hepatic cells in the liver become simply unable to excrete the bilirubin in the same speed. This leads to the raise of plasma concentration of bilirubin much above normal. This type of jaundice often affects people with sickle-cell anemia or any other inherited RBC disorders. Infants are prone to be easily attacked by this type. In many cases infants are jaundiced from birth with unconjugated hyperbilirubinemia in addition to the development of cholestasis. Sometimes it dates back to its foetal life. (Prof AJW Miller, 2001) Erystoblastosis fetalis, a disorder in which the antibodies from the mother's blood stream pass to the infant's blood stream destroys the RBCs of the infant especially when the baby has a different blood group than that of the mother. Such blood group incompatibility2 can be prevented with an injection of Rh immune globulin to the mother within 72 hours of delivery. This jaundice is a dangerous one as the brain parts of the infant is affected. Unattended infants are liable to be subjected to kernicterus, which can cause deafness, delayed development or a form of cerebral palsy3. In hemolytic jaundice, very similar to the fast formation of bilirubin, urobilinogen is also speedily formed. In a normal healthy body about of bilirubin is converted by bacterial action into urobilinogen. This urobilinogen is highly soluble and hence some of it is reabsorbed into blood by the intestinal mucosa. The absorbed urobilinogen again enters the liver and gets excreted by the liver through the gut. However kidneys excrete some percentage of this into urine. The glaring difference in the color of urine of this type of jaundice patients is due to the presence of this urobilinogen. Urobilinogen in urine exposed to air gets oxidized to form urobilin and the same in faeces on exposure becomes stercobilin. Obstructive jaundice is usually caused by obstruction of bile ducts or by damage to hepatic cells. Damage of hepatic cells happens to occur in hepatitis. Obstruction of bile ducts occurs when gallstone or cancer blocks the ducts. The speed of bilirubin formation is normal in this case but the bilirubin formed is unable to reach intestine through liver because of this blockade. However the free or unconjugated bilirubin enters the liver cells and gets conjugated there. Due to the rupture of congested bile canaliculi this conjugated bilirubin is then returned to the blood stream emptying the bile into the lymph. Thus in this type of jaundice most of the bilirubin in plasma is of conjugated type. While diagnosing jaundice the difference between hemolytic jaundice and obstructive jaundice can easily be detected by Van den Bagh test. In hemolytic jaundice all the bilirubin are in free form whereas the obstructive jaundice shows only conjugated bilirubin in the tests. When there is a total blockade of bile passage, no bilirubin enters intestine for getting converted into urobilinogen. This eliminates the possibility of re-absorption of urobilinogen into blood resulting in a negetive urobilinogen indication in the urine test. The stool also is clay colored for the lack of stercobilin and the bile pigments. By this test a major difference can also be detected. Kidneys excrete small quantities of conjugated bilirubin but not the albumin-bound free bilirubin. Simply by shaking the urine in test tube to form foam the presence of conjugated bilirubin can be ascertained, if the foam turns intense yellow. Constitutional jaundice is caused by an impairment in the transfer of bilirubin from blood to the liver cells whereas the liver jaundice is caused by the impairment of the excretion of bilirubin from liver cells to the bile ducts due to damage of hepatic cells as in hepatitis. Hepatitis is cellular inflammation of liver. Infectious agents, chemical compounds, metabolic disturbances or any other autoimmune phenomena may be the cause behind hepatitis. Glutamic oxaloacetic transaminase (GOAT) and glutamic pyruvic transaminase(GPT) are the two enzymes in the cytoplasm of hepatocytes. The function of these enzymes is facilitating transamination of amino acids. In hepatitis these enzymes are released from damaged cells to the serum thus raising the normal transaminase concentration of up to 40 Karmen units. In addition to liver, the GOAT is present in heart, kidney and skeletal muscle also. But GPT is specific for liver tissue alone. Hence a rise in the level of SGPT indicates liver cell necrosis. Although the inflamed liver is capable of maintaining its coagulation function, an accumulation of bilirubin occurs in the liver parenchyma due to the defective mechanism of excretion. Consequently the bilirubin regurgitates into the plasma elevating the total serum bilirubin above the normal level with half of it in coagulated form. (J.Rosewell Gallagher, Felix P. Herald and Dale C Garell, 1976) Before starting the treatment for jaundice, the cause-source of it is ascertained in a systematic way by going through all the three phases - prehepatic, intrahepatic and posthepatic. Prehepatic causes are normally the excessive hemolysis or re-absorption of large haematoma. Hemolytic anemia may also be the reason for jaundice. Intrahepatic causes are of two types: they are unconjugated hyperbilirubinemia and conjugated hyper bilirubinemia. Gilbert syndrome is a common hereditary factor, in which the activity of 'glucuroronosyltransferase' is slightly decreased. Conjugated hyperbilirubinemia is mainly due to intrahepatic cholestasis and obstruction of bile ducts. Posthepatic causes are chiefly the intrinsic or extrinsic obstruction of the duct system. Gallstones are the main entity causing obstruction. A common duct, which drains both biliary and pancreatic system is blocked by gallstones in pancreatitis. Impacted gallstones are removed endoscopically.( Sean P Roche, Rebecca Kobos, 2004) Some rare phenomenons of obstructive jaundice are ganglioneuroblastoma and metastatic tumor of pancreas from breast cancer. Obstructive jaundice being the rare symptom in the neuroblastic tumor, five courses of chemotherapy proves a better solution in reducing the size of the tumor and complete resection thereafter. (Ito, Aya; Uno, Takeji; Gunji, Yuji; Yamauchi, Tadahiko ; Egami, Satoshi ; Kawarasaki, Hideo; Momoi, Mariko Y ,2005).Immunohistochemical staining using antibodies unique to the mammary gland is an effective method of diagnosis of secondary tumor of pancreas.( Naomi Kitamura, Satoshi Murata, Hajime Abe, Kazuyoshi Hanasawa, Shizuki Tsukashita and Tohru Tani , 2003) For the treatment of obstructive jaundice caused by metastases from non biliary and non pancreatic cancers (PTBD) Percutanous Transhepatic Biliary Drainage is useful, since obstructive jaundice is most often attributable to metastases to the lymph nodes.( M Iwasaki, J Furuse, M Yoshino, M Konishi, N Kawano, T Kinoshita and M Ryu , 1996) Apart from jaundice hepatitis is a direct attack on liver. Presence of hepatitis B surface antigen (HBsAg) in the blood confirms the viral attack of hepatitis B. To nullify the infection our immune system produce antibodies to trounce the antigens or foreign proteins, which make up the virus. The antigens are namely, the surface antigen, core antigen and "e"antigen. Some special cells are let free by the immune system to kill the liver cells that are infected by the virus. Presence of alanine aminotransferase (ALT) indicates that large numbers of infected liver cells are damaged by the immune system.(Christine M.Kukka,@ www.hbvadvocate.org) Liver transplantation is a widely accepted course of treatment in cases of patients of end-stage liver diseases. However liver transplant brings along with it many post-operative complications. Infection of liver with hepatitis B and hepatitis C viruses are found common on those recipients. Cholestatic liver diseases, hepato cellular carcinoma, biliary complications, hyperlipidemia and obesity are susceptible to sprout out of liver transplantation. Reference List - Arthur C.Guyton and John E. Hall, 2000: "Text Book of Medical Phisiology" 10th edition, Saunders, Pensylvania, pp797-801 Christine M.Kukka, HBV Project manager, http;//www.hbvadvocate.org/hepatitis/hepB/Acute_HBV_FS.html Ito, Aya MD; Uno, Takeji MD, PhD; Gunji, Yuji MD, PhD; Yamauchi, Tadahiko MD; Egami, Satoshi MD ; Kawarasaki, Hideo MD, PhD; Momoi, Mariko Y MD, PhD "Obstructive Jaundice as a Presentation of Ganglioneuroblastoma." Journal of Pediatric Hematology/Oncology. 27(2):112-114, February 2005 M Iwasaki, J Furuse, M Yoshino, M Konishi, N Kawano, T Kinoshita and M Ryu Japanese Journal of Clinical Oncology, Vol 26, Issue 6 465-468, 1996 Naomi Kitamura, Satoshi Murata, Hajime Abe, Kazuyoshi Hanasawa, Shizuki Tsukashita and Tohru Tani Obstructive Jaundice in a Metastatic Tumor of the Pancreas from Breast Cancer Japanese Journal of Clinical Oncology 33 no2:93-97 2003 Prof AJW Miller: "Infant Surgical Jaundice",The Medicine Journal Vol 43No.3, Apr,2001 J.Rosewell Gallagher, Felix P. Herald and Dale C Garell, 1976: "Medical Care of the Adolescent", Appleton-Century Crofts,NewYork, p466 Sean P Roche, Rebecca Kobos,: "Jaundice in the Adult Patient",Journal of American Academy of Family Physicians, Vol. 69/No2 , Jan,15,2004 Read More