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SURGICAL WEBSITES BREAST DISEASE LIVER ABSCESS Anatomy of liver
SURGICAL WEBSITES KIDNEY SURGERY POSTGRADUATE SURGERY LINKS
BREAST DISEASE Breast cancer Breast lump Breast awareness Breast calcifications Breast cysts Breast pain Duct ectasia Fat necrosis Fibroadenoma Hyperplasia Intraductal papilloma Phyllodes tumour Sclerosing adenosis
LIVER ABSCESS Anatomy of liver Physiology of liver Method of examination of liver Haematology of liver disease. Amoebic liver abscess .Pyogenic liver abscess. Percutaneous needle aspiration of liver abscess. Case study. Result Result continued Discussion
CHOLECYSTECTOMY Introduction Historical Review Anatomy of Gallbladder Physiology of Gallbladder Physiologic effects of pneumoperitoneum Pathology of Gallbladder Investigations Pre- operative preparation of laparoscopic cholecystectomy Contraindications Treatment modalities for gallstones. Anaesthesia
INGUINAL HERNIA HOW SURGICAL OPERATION IS DONE THYROID EXAMINATION MANAGEMENT OF SEVERELY INJURED PATIENT SEPSIS AND MULTIPLE ORGAN FAILURE CHEST TRAUMA BRONCHOGENIC CARCINOMA TETANUS AND ANAEROBIC INFECTIONS
PHYSIOLOGY OF LIVER
PHYSIOLOGY OF LIVER
Although the liver has been examined by the anatomist for many centuries, a knowledge of its function is relatively modern. Claude Bernard was the first to demonstrate its importance in carbohydrate metabolism and was responsible for identification and naming of glycogen. In 1922, Mann and his colleagues, by perfecting a technique of experimental total hepatectomy in dogs, were able to give the first full account of liver function.
Within few hours of total hepatectomy the sugar concentration falls rapidly, and a hypoglycaemia develops, there is increasing weakness followed convulsions coma and death. When the state first develops, it can be rapidly reversed by administering glucose. A few hours later a somewhat similar state occurs but accompanied by vomiting, ataxia and apparent loss of sight and hearing. This final state is uninfluenced by giving glucose, and so is not hypoglycaemic in origin. The storage of glycogen in muscle only a little even when the animal is dying of hypoglycaemia, and it is concluded that liver is responsible solely for replenishing the liver sugar.
The importance of the liver in the formation of urea was suspected before experimental hepatectomy was became practicable. The liver was known to have a higher urea content than other tissues and it was also known that the fluid perfused through the liver acquire a higher urea content in transit. If the liver is removed from the animal, the blood urea concentration falls to almost zero after about 24 hours, but remains stable if the kidneys have also been removed. Blood urea rises progressively in animals with an intact liver with bilateral nephrectomy, and it follows that the urea formation is dependent on liver.
Hepatectomised dogs become increasingly jaundiced throughout the period of their survival. The plasma bilirubin begins to rise early and yellow colour of plasma is visible to naked eye with in about three hours. The sclera are jaundiced in dogs which survive about 16 hours and at the post mortem the fat through out the body is found to be stained. The formation of bilirubin is not prevented by removing all the abdominal viscera including the liver and spleen and extra bilirubin is still formed after the injection of haemoglobin. It can be concluded that the liver is not only the organ formation of bilirubin but it is the principal organ of the bilirubin excretion.
The functions include formation of bile, carbohydrate storage, ketone body formation, and other functions in control of carbohydrate metabolism: reduction and conjugation of adrenal and gonadal steroid hormones; detoxifictions of many drugs and toxins; manufacture of plasma proteins; inactivation of polypeptide hormones; urea formation and many important functions in the metabolism of fat.
The liver occupies a key position in the carbohydrate metabolism. It stores carbohydrates as glycogen, a condensation product of many molecules of glycogen. Glycogen can be formed from monosaccharides in the portal venous blood (glycogenesis), from the glycerol of fat, and from deaminated amino acids (neoglycogenesis). The stored glycogen is converted into glucose (glycogenolysis) as required to maintain blood glucose concentration at constant level.
The formation of glycogen and its release as glycogen is under the influence of hormones. Insulin favours the laying down of glycogen and retards the liberation of glucose, while the hormones of the anterior pituitary, the adrenal cortex and the thyroid favours the break down of glycogen and the liberation of glucose. Glucagon and adrenaline also liberate glucose from the glycogen.
The liver glycogen is the only readily available reserve of the glucose for maintaining the concentration of the blood sugar; muscle glycogen is not available for this purpose, as shown by experiments in totally hepatectomised animals where hypoglycaemic death occurred before very much glycogen had disappeared from muscles.
The average adult liver contains about 100 grams of glycogen. The store is exhausted by about 24 hours of starvation after which the whole body requirement for glucose must be met by the formation of glucose from body fat and protein. This process at its normal speed results in the liberation of small amounts of ketone bodies, and the ketosis of starvation represents the normal process carried to excess. In children the reserve of the liver glycogen is similar and the metabolic rate higher, and the ketosis of starvation begins correspondingly earlier.
Glycogen in addition to its fundamental role in carbohydrate metabolism, protects the liver from damage by many poisons, of which chloroform is the classical example.
The liver is also the site of metabolism to glucose of other monosaccharides, such as fructose, and of lactic pyruvic and ketoglutaric acids produced by the utilisation of glucose in muscle and other tissues 12.
AMINO ACID METABOLISM: FORMATION OF UREA.
The liver is concerned in breakdown of food and body protein and particularly in the deamination of the amino acids. The amino acids set free by digestion of protein are absorbed by the small intestine, pass into portal blood to the liver and some pass through the liver into the systemic blood. The average concentration of the amino acids in the blood is 3-4 mg/dl, but this may rise to 10 mg/dl after a meal rich in protein. The absorbed amino acids together with those released by the breakdown of body protein from the amino acid pool which is available for the re-synthesis into protein or for combustion as a source of energy. The amino acid pool is in a continual state of flux, with amino acids being added, transformed or removed all the time.
Many of the 20 amino acids can be synthesised in the body by transformation from other amino acids, or by the amination of the carbohydrates but there is a group of 8 amino which cannot be synthesised and are termed essential since they must be supplied in diet.
Oxidative deamination occurs principally in the liver. The reaction involves the transformation of the amino acid (e.g. alanine) to the corresponding keto-acid (pyruvic acid) and the liberation of ammonia. The keto- acid can be used for synthesising other compounds or burned as a source of energy. Most of the ammonia released in the process of deamination is converted to urea and excreted in the urine, and the reminder is used in the synthesis of other amino acids (reamination). Oxidative deamination occurs in the tissues other than the liver, but urea formation is probably a hepatic function only. The formation of urea CO(NH2)2 requires the union of carbon dioxide and ammonia with the elimination of water:
CO2 + 2NH3 ---> CO(NH2)2 + H2O
Deamination of amino acids may also be coupled with the simultaneous amination of a ketoacid, the enzymes facilitating these reactions being termed transaminases. The result is the transference of the NH2 group from one amino acid and its use to synthesise another as in the formation of glutamic acid from alinine facilitated by alanine amino transferase (ALT).
The amino transferases are intracellular enzymes but small quantities are normally present in the circulation. When significant cellular damage occurs in an organ, their serum concentration rises an example of which is increase in ALT following damage to liver.
PROTEIN METABOLISM: The liver manufacture albumin and the proteins concerned with blood clotting (fibrinogen, prothrombin, and factors V, VII, IX, and X). Furthermore the hepatic Kupffer cells able to synthesise a and b-globulin, and remove g-globulin, and to remove g-globulin from portal blood.
The evidence that the liver is the major source of plasma albumin is both experimental and clinical. In dogs after total hepatectomy, there is slow but progressive fall in the concentration of the plasma albumin, suggesting albumin is being slowly utilised without replacement. In man, the ability to make albumin is reduced in liver failure and hepatic cirrhosis, and the plasma concentration of albumin is often much less than the normal value of 40-50g/l.
The characteristic change in the chronic liver disease is a fall in the serum albumin accompanied by a rise in serum g-globulin. It is therefore necessary to measure fractions as total value may be within the normal range. It should be noted that the serum albumin and g-globulin concentrations measure different hepatic functions: the albumin is formed in the liver whereas g–globulin is formed in extrahepatic reticuloendothelial system and removed from the circulation by hepatic Kupffer cells.
BLOOD COAGULATION: As indicated above the liver is the site of synthesis of the coagulation factors V, VII, IX, and X as well as fibrinogen and prothrombin is dependent on the presence of vitamin K from intestine. Synthesis of many of the coagulation factors may thus be impaired either by extensive parenchymatous disease or damage or by failure to absorb vitamin K from gut and may cause the development of significant bleeding tendency. Lack of labile factor V occurs with severe liver disease and never with vitamin K deficiency.
The problem is most often associated with resection for injury when the bleeding tendency is caused by large quantities of stored blood which is deficient in factor. The liver is the only site for synthesis of fibrinogen but impaired formation is rare even in severe hepatic failure. The only common cause of fibrinogen lack is increased fibrinolysis which may occur in all forms of liver disease and especially in patients with cirrhosis.
Tests for defect in blood coagulation include the one stage prothrombin time and this should be measured in all patients with hepatobiliary disease. A prolonged prothrombin time may indicate deficient prothrombin synthesis, especially in the presence of obstructive jaundice. Operation and such procedures as splenic venography or liver biopsy should be postponed until the patient has responded to treatment with vitamin K given parentally. Failure to respond promptly to vitamin K may be an index of synthesis, however, reflecting severe hepatocellular dysfunction.
The liver plays an important role in the metabolism of fat and is concerned not only with the digestion and absorption of fat by virtue of secreting bile salts into the duodenum but also in the removal of fat from the blood stream after absorption has taken place.
The bile salts assist in the intestinal absorption of dietary fat by breaking up fat globules into a fine emulsion thus allowing greater contact with lipases for hydrolysis and also a reduction in particle size; they also form water soluble complexes (micelles) with lipids which promotes their absorption. The products of hydrolysis (free fatty acids, monoglycerides and to a lesser extent diglycerides and triglycerides) and probably absorbed as a mixture by the mucosal cells of the intestine. Long chain fatty acids are converted into triglycerides, enter the lymphatic and pass by way of thoracic duct to the systemic vein together with the particulate fat. Short chain fatty acids are water soluble and enter the portal blood and pass to the liver some is metabolised and some continues to be deposited in the body fat depots.
Fatty infiltration impairs the live function and interferes with the detoxication of barbiturates and makes dangerous the administration of fat-soluble anaesthetics such as ether chloroform, methoxyflurane, enflurane or halothane.
The liver protects the body against many endogenous and exogenous toxic substances. The substances are dealt with by conjugation, by destructive oxidation or by a combination of these processes. The method of dealing with toxin appears to be fortuitous, depending on the resemblance of the toxin to the physiological compounds.
Conjugation may be with amino-acids glucuronic acids sulphates or ascetic acid. Oxidative destruction is the method of dealing with many compounds foreign to the body. The alkaloid, strychnine and nicotine and the short lasting barbiturates are destroyed in this way. Liver disease or damage may make a patient unduly susceptible to the agents normally conjugated or destroyed in the liver and this often influences the drug dosage in these conditions.
The hepatic Kupffer cells which are found lining the sinusoids are an important part of the reticulo-endothelial (mononuclear phagocytic) system, the remainder being located in the bone marrow, lymph nodes and spleen. These hepatic cells are able to ingest colloidal particles, their main function is ingestion of bacteria and bacterial products such as endotoxin the removal of g-globulin, the destruction of erythrocytes and the extraction of injected colloids from the circulation.
By the ingestion of bacteria the phagocytic cells are concerned in the defence of the body against infection they greatly increase in number resulting in enlargement of the organs rich in globulins.
Washington, DC Registry
Last modified: Monday, 29-Nov-2004 06:52:26 EST