The Liver And Biliary System

Published Date: 02 Nov 2017

Name: Rachael Houghton

Module Code: CPM1106M

Lecturer: Katie

List of Contents

Summary 2

Contents 4

Section 1. Normal structure and function of the liver and biliary system

1.1 The Anatomy of the liver. 4

1.2 The structure of the liver. 4

1.3 Organs associated with the liver. 4

1.4 Physiology of the liver. 4

1.5 Metabolic functions of the liver. 5

1.6 Other metabolic functions of the liver. 5

1.7 Physiologic anatomy of the biliary secretion. 5

1.8 Composition of bile. 5

1.9 Blood and the liver. 6

Section 2. Altered anatomy and physiology 7, 8

Section 3. Recent research into treatment 10

3.1 Current Research 10

3.2 Genes 10

Conclusion 11

Appendix 1: Figures 13

Fig 1 – Normal Liver – Liver with cirrhosis 13

Fig 2 – Cirrhosis histology 13

Fig 3 – Anatomy of the liver 13

References 14

Summary

This report attempts to discuss what happens when there is altered physiology, in this case cirrhosis and what happens during this change. The liver is the largest gland in the body and is one of the most critical organs as it has various functions one of the major functions is its digestive function. The liver is also responsible for the removal of toxins so that they can be removed from the body. The liver also has associated organs, one being the gall bladder, which is responsible for storing bile that the liver makes. Almost all of the blood circulating through the intestines to the heart goes through the liver. Therefore everything you eat that gets into the bloodstream passes through your liver, the liver then either stores the nutrients or break them down even more.

Section 1. Normal anatomy and physiology

1.1 The Anatomy of the Liver

The liver is the biggest gland/organ in the body and normally weighs about 2 per cent of the total body weight in the average human being (Guyton, 859). It is situated in the upper part of the abdominal cavity occupying the greater part of the hypochondriac region, part of the epigastric region and extending into the left hypochondriac region. It’s upper and anterior surfaces are smooth and curved to fit under surface of the diaphragm, its posterior surface is irregular in outline (Ross, 305)

1.2 The Structure of the Liver

The lobes of the liver are made up of small functional units called lobules, there are approximately 50,000 to 100,000 individual lobules in the human liver (Guyton, 859). Liver lobules are hexagonal in outline and are formed by cubical shaped cells called hepatocytes, which are arranged in pairs of columns and radiate from the central vein (Ross, 305).

1.3 Organs Associated with the Liver

Superiorly and interiorly – diaphragm and anterior abdominal wall

Inferiorly – stomach, bile ducts, duodenum, hepatic flexure of the colon, right kidney and adrenal gland.

Posteriorly – oesophagus, inferior vena cava, aorta, gall bladder, vertebral column, and diaphragm.

Laterally – lower ribs and diaphragm (Ross, 305).

Physiology of the Liver

The liver is responsible for three categories of functions: (1) Metabolic regulation, (2) haematological regulation, and (3) bile production. The liver has more than 200 functions. (Martini, 893) The liver has high blood flow and low vascular resistance, about 1050ml of blood flows from the portal vein into the liver sinusoids each minute (Guyton, 860).

1.5 Metabolic Functions of the Liver

Fat Metabolism – stored fat can be converted to a form in which it can be used by the tissues to provide energy (Ross, 305).

Carbohydrate Metabolism – The liver stabilises blood glucose levels, if blood glucose levels drop hepatocytes break down glycogen stores and discharges glucose into the bloodstream. They also amalgamate glucose from other carbohydrates or from vacant amino acids. This action is called gluconeogenesis. The following functions are also performed, storage of large amounts of glycogen and the conversion of galactose and fructose to glucose (Martini, 893).

Protein Metabolism – Deamination of amino acids and the process is (1) To remove nitrogenous portion from the amino acids not required for the formation of new protein, urea is formed in this mode, which is eliminated as urine, (2) to break down genetic material to form uric acid, which is also excreted in the urine (Valentina, 1998).

1.6 Other Metabolic Functions of the Liver

The liver is a repository site for vitamins, it stores iron as ferritin, the liver forms a grand proportion of the blood substances used in coagulation and the liver removes or excretes drugs, hormones and other substances (Guyton, 862)

1.7 Physiologic Anatomy of the Biliary Secretion

Bile is expelled in two stages by the liver, the initial portion is secreted by the principal functioning cells of the liver, the hepatocytes. This first stage contains copious amounts of bile acids, cholesterol, and other organic constituents. It is expelled into minute bile canaliculi that originate between the hepatic cells. In the second stage the bile flows in the canaliculi towards the interlobular septa where it then expels into the terminal bile ducts and then more into larger ducts, finally reaching the hepatic duct and common bile duct. The bile then either expels directly into the duodenum or it is deflected for minutes up to several hours through the cystic duct into the gall bladder (Guyton, 802).

1.8 Composition of Bile

About 500ml of bile are expelled by the liver daily. Bile consists of, water, mineral salts, mucus, bile pigments (mainly bilirubin), bile salts (which are derived from the primary bile acids, cholic acid and chenodeoxycholic acid), and cholesterol (Ross, 307)

1.9 The liver cells can regenerate, but if the organisational structure of the lobule, with its unique arrangements of blood vessels and bile ducts, is altered by necrosis and scar tissue, the regeneration areas may not be functional.

The hepatocytes (liver cells) are aligned in lobules, and from each central vein radiates plates of cells to which a lobule is found. which eventually drain blood back into the general circulation through the hepatic veins and inferior vena cava. Sinusoids (channels) are full of blood which comes from two places and these pass between the plates of the hepatocytes. Entering the sinusoids is blood from branches of the hepatic artery, carrying oxygen to the liver cells and venous blood from the portal vein, which delivers nutrients absorbed from the stomach and intestines (hepatic portal circulation), as well as from the pancreas and spleen. To aid the hepatocytes to do their job, the arterial and venous blood mix and flow slowly through the sinusoids. The sinusoids are lined with endothelial cells and kupffer’s cells, which remove the phagocytose any foreign material and bacteria from the digestive tract before the blood does into the general circulation.

As blood flows through the sinusoids, lots of substances are exchanged to facilitate liver functions. Absorbed nutrients are taken up by the hepatocytes to be stored (minerals, iron and copper, or vitamins A, B6, B12, D, and K and folic acid). Lots of blood components such as iron or amino acids are monitored, and those that have been reduced as the blood circulates through the body are replaced. Blood glucose levels are maintained, as glucose is essential for brain function.

In conjunction with the hormone insulin, the liver responds to high levels of blood glucose by glycogensis, converting glucose to glycogen, which is stored in the liver. Alternatively, the hepatocytes break down liver glycogen to glucose (glycogenolysis) when blood glucose levels decrease and glucagons secretion increases. Gluconeogenesis, the change of protein and fat into glucose, may take place when blood glucose levels decrease, under the influence of hormones such as cortisol or epinephrine.

Conversion of one amino acid into another takes place, as needed to maintain the amino acid pool in the blood. Synthesis and control of blood levels of other materials, such as plasma proteins, clotting factors, or lipoproteins, is accomplished. Synthesis of cholesterol occurs in the liver for use in the production of steroid hormones, such as cortisol or the sex hormones, and bile salts.

Hormones, such as aldosterone and estrogen, are inactivates and prepares for excretion. Ammonia, a nitrogen waste resulting from protein metabolism in the intestine or in the liver, is removed from the blood and converted to urea, enabling it to be excreted by the kidneys. Drugs and alcohol are detoxified before excretion. The detoxification process makes such substances less harmful and increases the solubility of many substances, facilitating their excretion.

Damaged or old erythocytes are removed from the blood to facilitate the recycling of iron and protein from haemoglobin. The liver serves as a blood reservoir because it is capable of releasing a large quantity of blood into the general circulation when blood volume is depleted.

The hepatocytes of the liver constantly produce bile, a mixture of water, bile salts, bile pigment (conjugated bilirubin), cholesterol, and electrolytes, including bicarbonate ions. Bile is vital for digestion and serves as a vehicle for the removal of bilirubin and excess cholesterol from the body. The bile salts, formed from cholesterol, are essential for the emulsification of fats and fat-soluble vitamins (A, D, E & K) before they can be absorbed from the intestine (Gould, 2006).

Section 2 – Altered anatomy and physiology

There are a number of different causes of Cirrhosis, some drugs, medicines and harmful chemicals, infections, chronic hepatitis B, C, or D – viral infections that attack the liver, Autoimmune hepatitis, which causes the body’s immune system to destroy liver cells, some inherited diseases that are passed from parent to child, Wilson’s disease and porphyria (Valentina, 1998).

The initial change in alcoholic liver disease is the accumulation of fat in liver cells, causing fatty liver. Other than the enlargement of the liver or hepatomegaly, this stage is asymptomatic and is reversible if alcohol intake is reduced, preferably ceased.

In the second stage, alcoholic hepatitis, inflammation and cell necrosis occur. Fibrous tissue forms, which is an irreversible change. Acute inflammation may develop when alcohol increases or binge drinking becomes more excessive or frequent. This second stage may also be asymptomatic or it may manifest with mild symptoms, such as anorexia, nausea, and liver tenderness.

The third stage, or end stage cirrhosis, is reached when fibrotic tissue replaces normal tissue, this alters significantly the basic liver structure to the extent that a very small amount of normal function remains. Signs of portal hypertension or impaired digestion and absorption are the usual early indicators (Gould, 2006).

Micronodular cirrhosis – where the liver is usually enlarged with small nodules of uniform size. This is associated with alcohol (yellow colour due to steatosis), haemochromatosis (dark reddish brown due to iron), drugs, chronic venous obstruction, chronic hepatitis, and chronic biliary disease (greenish colour). Macronodualr cirrhosis – where the liver is nearly always shrunken with large bulging nodules. This is the most common form seen in chronic viral hepatitis, chronic autoimmune hepatitis, Wilson’s disease and after fusion of micronodules in alcoholic liver disease and haemochromatosis.

Microscopically the nodules are made up of hyperplastic hepatocytes detached by fibrous tissue. The liver cells are enlarged and the vasculature distorted due to the fibrosis involving portal triads. Fistulous communications may be formed between portal veins & hepatic arterioles (Dassanayake, 2011).

Research

Section 3. Recent research into treatment

3.1 Current research areas and treatments:

Cirrhosis once established is irreversible however, there are many trials ongoing to reduce symptoms and lengthen life expectancy. It appears that this is slightly easier when the cause of the cirrhosis is known eg alcohol or viruses. With regards to alcohol cirrhosis the obvious tactic is to stop drinking however, to of got to the stage of cirrhosis through drinking they will often be alcohol dependent which makes this a hard task. The diet should also be looked at as this goes through the liver so a healthy diet is necessary. Often the patients with this disease will be on drugs to help with the symptoms eg oedema – diuretics this brings on its own issues as the drugs once again have to go through the liver. Antiviral drugs are often prescribed for viral hepatitis and for autoimmune hepatitis corticosteroids are used (NDDIC, 2012).

There is a current study being run to measure the effects of a high fibre diet, Fibre has been proven to increase the excretion of nitrogen products and consequently reduce its blood levels, and an adequate protein intake (1- 1.5 g per kg) has shown to decrease endogenous catabolism in cirrhotic patients (Torre Delgadillo, 2012).

3.2 Genes

Scientists have discovered a gene that interferes with the clearance of hepatitis C virus infection. Chronic infection with hepatitis C virus is a known cause of liver cirrhosis and liver cancer. Up to 80% of people who are acutely infected with hepatitis C do not clear the virus and develop chronic hepatitis C infection, and of these, approximately 5% go on to develop liver cancer. To find the new gene, the investigators used a technology involving RNA sequencing on human liver cells treated to mimic hepatitis C virus infection.

From this discovery, two medicines have been made and three new potential treatments to treat this virus have been made (Prokunina-Olsson, 2013).

Conclusion

The liver and biliary system are amazing organs and it seems to me that education is key into highlighting the dangers of abusing these organs. The liver and biliary system are responsible for so many important and necessary tasks and therefore should be respected and treated with care, whilst being fed what it requires and not what ‘we’ want. A healthy diet with exercise is all the liver and associated organs require, simple.

Appendix

Figure 1

liver in cirrhosis

(wikinut.com, 2009)

Figure 2

cirrhosis histology

(wikinut.com, 2009)

Figure 3

(scribd.com, 2008)