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Varices (variceal bleeding) One consequence of chronic liver disease can be portal hypertension. This is an increase in the blood pressure in the portal vein, which carries the blood from the bowel and spleen to the liver. The pressure in the portal vein may rise because there is a blockage, such as a blood clot, or because the resistance in the liver is increased because of scarring (fibrosis) or cirrhosis. As a result, the pressure in the portal vein rises. This is known as portal hypertension.  As the blood tries to find another way back to the heart, new blood vessels open up. Among these vessels are those that run along the wall under the lining of the upper part of the stomach and the lower end of the oesophagus (gullet). These veins protrude into the gullet and the stomach and can bleed. The dilated veins in the gullet are known as varices. Bleeding may be a gentle ooze in which case anaemia is the commonest symptom. Sometimes there can be a major bleed; a person may have a haemorrhage and either vomits blood or passes blood through their bowels. This blood may appear to be black, since it is often changed as it passes through the body.  Oesophageal varices represent a significant complication of cirrhosis and some other types of liver damage.   Ascites In people with a liver disorder, ascitic fluid leaks from the surface of the liver and intestine and accumulates within the abdomen. A combination of factors is responsible. They include the following:  *Portal hypertension *Fluid retention by the kidneys  Alterations in various hormones and chemicals that regulate body  fluids. Also, albumin usually leaks from blood vessels into the  abdomen. Normally, albumin, the main protein in blood, helps keep  fluid from leaking out of blood vessels. When albumin leaks out of blood vessels, fluid also leaks out.    Hepatic Encephalopathy Hepatic encephalopathy is a brain disorder and refers to the changes in the brain that occur in patients with advanced, acute or chronic liver disease and is one of the major complications of cirrhosis. Hepatic encephalopathy may occur suddenly in people with acute liver failure however, the condition is more often seen in people with chronic liver disease.  An important job of the liver is to change harmful substances that are either made by the body or taken into the body (such as medicines) and make  them harmless. However, when the liver is damaged and unable to  function fully, these “toxins” may build up in the bloodstream.  HE occurs when the liver cannot remove chemicals, such as ammonia (see Useful from the blood. These chemicals then enter the brain, and can affect both the mental and physical condition of patients Often certain factors can be responsible for triggering an episode of HE in liver patients. The following factors may trigger an episode of HE:  • Dehydration (loss of water from the body) • Low oxygen levels in the body • Eating too much protein • Constipation • Medications that affect the nervous system, such as tranquiliser or sleep medications • Infections • Intestine, stomach, or oesophagus bleeding • Kidney problems • Surgery  Patients with acute liver disease, who have an episode of HE, generally find once the trigger is removed and their liver condition is treated, the HE disappears. However, some patients with chronic liver disease find they will have recurring episodes of HE. Episodes of HE usually result in hospitalisation, as without treatment, patients remain at high risk for recurrence. Other complications of untreated HE can be brain swelling, permanent nervous system damage, increased risk of heart failure, kidney failure, respiratory failure and sepsis (blood poisoning) and in severe cases coma.  HE symptoms can present at a range of stages from mild to overt (severe). Mild Symptoms of HE can be observed in nearly 70% of patients with cirrhosis. Overt HE occurs in about 30-45% of patients with cirrhosis. HE symptoms can vary from person to person; they can develop rapidly or slowly over time. Patients with HE can have both physical symptoms and reduced mental function.  Type 2 Diabetes For me this is a thorny subject as I’ve come across quite a number of diabetic nurses  who for some reason seem to once again adopt an American approach by putting all  Type 2 Diabetes suffers in the same little box, and labelling everyone with the  same condition, “It’s because your pancreas isn’t producing enough insulin”. This then  puts the blame on the poor pancreas, when in truth it’s having to work flat out.   I have carried out a lot of my own research into Type 2 Diabetes, and while I tend to avoid a lot of the American websites, I must confess that a huge amount of research has been done in to Type 2 Diabetes by our cousins across the pond. It makes sense to me, that when the liver becomes damaged through scaring, or alcohol-related liver disease.  Strange things will start to happen.  This is my own understanding as to what is going on:  The Liver is one of the most complicated organs in the body, and possibly the least understood. It plays a huge role in handling sugars and starches, making sure our bodies have enough fuel to function. When there’s a lot of sugar in the system, it stores some of the excess in a storage form of carbohydrate called glycogen. When blood sugar levels get low, as in times of hunger or at night, it converts some of the glycogen to glucose and makes it available for the body to use.  Easy to say, but how does the liver know what to do and when to do it? Scientists have found a “molecular switch” called CRTC2 that controls this process. When the CRTC2 switch is on, the liver pours sugar into the system. When there’s enough sugar circulating, CRTC2 should be turned off. The turn-off signal is thought to be insulin. This may be an oversimplification, though.  In a post transplant patient – here the medications used to prevent rejection can alter the way hepatocytes handle sugars and drive overproduction and release of glucose into the blood. Also patients with diabetic risks before transplant are more likely to experience it after transplant.  The CRTC2 gene is interesting the protein does indeed act as a switch to produce more sugar in fasting situations and is down regulated when abundant sugar is present. Levels change in type 2 diabetes and this makes the hyperglycemia worse. What’s most interesting is that the signals that act through this molecule are linked to a protein called calcineurin which is activated and causes the liver to make more sugar.  The calcineurin levels increase in insulin-resistant states. CRCT2 is found in many cells including immune cells, heart and placenta and some studies suggest in liver cells too. Also down regulated in some cancers  However Calcineurin is also in immune cells and is linked to growth and functional responses. So some anti rejection medications used after transplant, target calcineurin to dampen down anti-graft immune responses. Tacrolimus and cyclosporin are calcineurin inhibitors.  Thus you can see how there might be a connection between anti rejection medication and function of CRCT2. As you say however its quite a new area of research and it takes a while for new advances to make it into clinic.  Cancer of the Liver (Tumours) The human body is composed of billions of cells that are continually ageing, dying and being replaced. Cell death, replacement, growth and development are normally tightly controlled. If this control breaks down, cells begin to grow and divide abnormally, clustering together to form a lump known as a tumour. These tumours are either benign or malignant. Cancer is the name given to a malignant tumour. There are two broad categories of liver cancer: secondary and primary.  1.	Secondary liver cancer is a cancer that first develops elsewhere in the body and  then spreads    	(metastasises) to the liver. It is sometimes called metastatic cancer.  2.	Primary liver cancers are cancers that start in the liver. The two main types are: Hepatoma, also called  hepatocellular carcinoma (HCC) and Biliary tree cancer, which includes cholangiocarcinoma (bile duct  cancer) and gallbladder cancer.  Using heat to destroy cancer cells (Ablation)
The Allen Enterprise Project
          Alcohol-related Liver Disease

Medical Consequences

Ablation uses heat to destroy cancer cells. There are three types of ablation that produce heat in different ways. These are: Microwave Radiofrequency Laser ablation. Each type destroys cancer cells by heating them to a high temperature. They may be used if you have previously had surgery or if you’re not fit enough to have surgery. You will be given a sedative drug to make you feel drowsy and a local anaesthetic to numb the skin of your abdomen. Sometimes ablation is performed using a general anaesthetic. The doctor puts a fine needle through the skin over your liver and into the centre of each tumour. They use an ultrasound or CTscan to guide them. The microwave, radio-frequency or laser then produces heat which passes through the needle and into the tumour. This treatment takes about 30–60 minutes and can be used to treat tumours up to 5cm (2in) in size. You can usually go home a few hours after you’ve had your treatment. The side effects of ablation are usually mild and may last up to a week. They include pain in the liver area, which you can control by taking regular painkillers. Other side effects are a fever (high temperature) and feeling tired and generally unwell. These side effects are due to the body getting rid of the cells that have been destroyed. Try to drink plenty of fluids and get enough rest. Your doctor or nurse may ask you to contact the hospital if your temperature doesn’t settle within a few days or if it goes higher than 38˚C (100.4°F). This is to make sure you don’t have an infection. Your specialist can give you more information about the possible benefits and risks of these procedures.
TIPSS (Transjugular Intrahepatic PortoSystemic Shunt)
I’ve been trolling the internet to find a suitable presentation of this procedure, but sadly there appears to be nothing available from a British perspective as to how this procedure is carried out over here. I have therefore used an American video as I suspect that the procedure to be pretty much the same. This video maybe a little heavy for some people, But this procedure does look to be a little tricky. The best way of describing what TIPSS is, is to explain what the letters stand for:  
T is for TRANSJUGULAR. This means that the radiologist will put a fine, hollow needle into the jugular vein in your neck while you are asleep. Through this needle he, or she, will pass a fine, thin wire in a straight line until it reaches the veins from your liver. This is much easier than you would imagine. Over this wire the radiologist will pass a fine plastic tube called a catheter, about the size of a very long piece of spaghetti. I is for INTRAHEPATIC. The catheter that the radiologist has inserted will be passed down one of your liver veins into the liver itself. The radiologist will then take the wire out and insert a long curved needle.   PS is for PORTO-SYSTEMIC. The long needle will be pushed from your liver vein, (or SYSTEMIC vein) into your PORTAL vein, which lies close to it. It is this portal vein which has become partially blocked up by your liver disease. Because of the blockage, there is high blood pressure in this part of your circulation, and this procedure is designed to relieve this.   S  is for SHUNT. Once the needle has been passed between your liver vein and the portal vein, a wire will be passed through the needle and the needle withdrawn. Over the wire the radiologist will pass a metal spring called a stent. This stent will expand to create a channel between the two veins. Blood will then flow from the high-pressure portal vein into the low-pressure liver (or systemic) vein. The high pressure in the portal vein which is causing your problem, will consequently be reduced, back towards normal.