Finding Dependable Contractors
As most of you already know LiverFoundation-NE.org has been renovating it’s office for around 7 or 8 months. The entire renovation was supposed to only take 3 months to finish, but we’ve had numerous issues with a few different contractors. We can’t even begin to explain how difficult it has been to find reliable, local contractors who will tell you how it is instead of just saying what you want to hear. We initially chose contractors that offered the best prices, but we quickly found out that they purposely bid low just to win the contract and then they would just keep adding fees. We had trouble finding roofing contractors, concrete contractors, and HVAC contractors until we found Proven Contractor. Proven Contractor has been a total life saver, and we will never hire a contractor that’s not on ProvenContractor.com ever again. Proven Contractor reviews and verifies that contractors are licensed and insured (more difficult than it sounds) and all of the contractors we’ve hired from them have been reliable and affordable and most importantly honest. Check out ProvenContractor.com for more information or to find a local contractor in your area.
The Liver Explained
medicinenet Liver cancer (hepatocellular carcinoma) is a cancer arising from the liver. It is also known as primary liver cancer or hepatoma. The liver is made up of different cell types (for example, bile ducts, blood vessels, and fat-storing cells). However, liver cells (hepatocytes) make up 80% of the liver tissue. Thus, the majority of primary liver cancers (over 90%-95%) arises from liver cells and is called hepatocellular cancer or carcinoma. When patients or physicians speak of liver cancer, however, they are often referring to cancer that has spread to the liver, having originated in other organs (such as the colon, stomach, pancreas, breast, and lung). More specifically, this type of liver cancer is called metastatic liver disease (cancer) or secondary liver cancer. This is a much more common problem around the world than primary liver cancer and frequently leads to confusion, because the term liver cancer actually can refer to either metastatic liver cancer or hepatocellular cancer. The subject of this article is hepatocellular carcinoma, which I will refer to as liver cancer. What is the scope of the liver cancer problem? Liver cancer is the third most common cancer in the world.
A deadly cancer, liver cancer will kill almost all patients who have it within a year. In 2000, it was estimated that there were about 564,000 new cases of liver cancer worldwide, and a similar number of patients died as a result of this disease. About three-quarters of the cases of liver cancer are found in Southeast Asia (China, Hong Kong, Taiwan, Korea, and Japan). Liver cancer is also very common in sub-Saharan Africa (Mozambique and South Africa). The frequency of liver cancer in Southeast Asia and sub-Saharan Africa is greater than 100 cases per 100,000 population. In contrast, the frequency of liver cancer in North America and Western Europe is much lower, less than five per 100,000 population. However, the frequency of liver cancer among native Alaskans is comparable to that seen in Southeast Asia. This reflects the prevalence of hepatitis B infection, which is the most common cause of this cancer worldwide. Recent data show, however, that the frequency of liver cancer in the U.S. overall is rising. This increase is due primarily to rising obesity and diabetes rates, and to chronic hepatitis C, another infection of the liver that causes liver cancer.In the U.S., the highest frequency of liver cancer occurs in immigrants from Asian countries, where liver cancer is common.
The frequency of liver cancer among Caucasians is the lowest, whereas among African-Americans and Hispanics, it is intermediate. The frequency of liver cancer is high among Asians because liver cancer is closely linked to chronic hepatitis B infection. This is especially so in individuals who have been infected with chronic hepatitis B for most of their lives (it is usually a childhood disease in Asia). If you take a world map depicting the frequency of chronic hepatitis B infection, you can easily superimpose that map on a map showing the frequency of liver cancer. On the other hand, in Japan, North America and Europe, hepatitis C infection is a much more common cause; alcohol abuse is also an important contributing factor. All of these diseases cause continual damage to the liver, which can result in severe scarring (cirrhosis) that then can lead to cancer. In areas where liver cancer is more common and associated with hepatitis B, the cancer usually develops in people in their 30s and 40s, as opposed to other areas of the world, where they are in their 60s and 70s. This is because it generally takes about 30 years of chronic damage to the liver before the cancer grows large enough to become obvious. Men are much more likely than women to have liver cancer, especially if they have hepatitis and cirrhosis. Regardless of the cause, patients with a history of alcohol abuse as well are much sicker when they initially develop the cancer. In North America, up to one-quarter of people with liver cancer have no obvious risk factors; they are generally healthier and do much better with treatment. What are liver cancer causes and risk factors? Hepatitis B can be caught from contaminated blood products or used needles or sexual contact but is frequent among Asian children from contamination at birth or even biting among children at play. The role of hepatitis B virus (HBV) infection in causing liver cancer is well established.
Several lines of evidence point to this strong association. As noted earlier, the frequency of liver cancer relates to (correlates with) the frequency of chronic hepatitis B virus infection. In addition, the patients with hepatitis B virus who are at greatest risk for liver cancer are men with hepatitis B virus cirrhosis (scarring of the liver) and a family history of liver cancer. Perhaps the most convincing evidence, however, comes from a prospective (looking forward in time) study done in the 1970s in Taiwan involving male government employees over the age of 40. In this study, the investigators found that the risk of developing liver cancer was 200 times higher among employees who had chronic hepatitis B virus as compared to employees without chronic hepatitis B virus infection. Studies in animals also have provided evidence that hepatitis B virus can cause liver cancer. For example, we have learned that liver cancer develops in other mammals that are naturally infected with viruses related to the hepatitis B virus. Finally, by infecting transgenic mice with certain parts of the hepatitis B virus, scientists caused liver cancer to develop in mice that do not usually develop liver cancer. (Transgenic mice are mice that have been injected with new or foreign genetic material.) How does chronic hepatitis B virus cause liver cancer? In patients with both chronic hepatitis B virus and liver cancer, the genetic material of hepatitis B virus is frequently found to be part of the genetic material of the cancer cells. It is thought, therefore, that specific regions of the hepatitis B virus genome (genetic code) enter the genetic material of the liver cells.
This hepatitis B virus genetic material may then disrupt the normal genetic material in the liver cells, thereby causing the liver cells to become cancerous. The vast majority of liver cancer that is associated with chronic hepatitis B virus occurs in individuals who have been infected most of their lives. In areas where hepatitis B virus is not always present (endemic) in the community (for example, the U.S.), liver cancer is relatively uncommon. The reason for this is that most of the people with chronic hepatitis B virus in these areas acquired the infection as adults, and very few develop an ongoing (chronic active) infection, which happens as often as 15% of the time in Asia. Hepatitis C virus (HCV) infection is more difficult to get than hepatitis B. It usually requires direct contact with infected blood, either from contaminated blood products or needles. HCV is also associated with the development of liver cancer. In fact, in Japan, hepatitis C virus is present in up to 75% of cases of liver cancer. As with hepatitis B virus, the majority of hepatitis C virus patients with liver cancer have associated cirrhosis (liver scarring). In several retrospective-prospective studies (looking backward and forward in time) of the natural history of hepatitis C, the average time to develop liver cancer after exposure to hepatitis C virus was about 28 years. The liver cancer occurred about eight to 10 years after the development of cirrhosis in these patients with hepatitis C.
Several prospective European studies report that the annual incidence (occurrence over time) of liver cancer in cirrhotic hepatitis C virus patients ranges from 1.4%-2.5% per year. In hepatitis C virus patients, the risk factors for developing liver cancer include the presence of cirrhosis, older age, male gender, elevated baseline alpha-fetoprotein level (a blood tumor marker), alcohol use, and co-infection with hepatitis B virus. Some earlier studies suggested that hepatitis C virus genotype 1b (a common genotype in the U.S.) may be a risk factor, but more recent studies do not support this finding. The way in which hepatitis C virus causes liver cancer is not well understood. Unlike hepatitis B virus, the genetic material of hepatitis C virus is not inserted directly into the genetic material of the liver cells. It is known, however, that cirrhosis from any cause is a risk factor for the development of liver cancer. Therefore, it has been argued that hepatitis C virus, which causes cirrhosis of the liver, is an indirect cause of liver cancer. On the other hand, there are some chronic hepatitis C virus-infected individuals who have liver cancer without cirrhosis. So, it has been suggested that the core (central) protein of hepatitis C virus is the culprit in the development of liver cancer. The core protein itself (a part of the hepatitis C virus) is thought to impede the natural process of cell death or interfere with the function of a normal tumor suppressor (inhibitor) gene (the p53 gene). The result of these actions is that the liver cells go on living and reproducing without the normal restraints, which is what happens in cancer. Cirrhosis caused by chronic alcohol consumption is the most common association of liver cancer in the developed world. In fact, at autopsy, as many as half of alcoholics previously unsuspected to have cancer will have early evidence of cancer hidden within the liver. Many of these people are also infected with chronic hepatitis C virus.
The usual setting is an individual with alcoholic cirrhosis who has stopped drinking for 10 years and then develops liver cancer. It is somewhat unusual for an actively drinking alcoholic to develop liver cancer. What happens is that when the drinking is stopped, the liver cells try to heal by regenerating (reproducing). It is during this active regeneration that a cancer-producing genetic change (mutation) can occur, which explains the occurrence of liver cancer after the drinking has been stopped. More importantly, if an alcoholic does not stop drinking, he or she is unlikely to live long enough to develop the cancer. Alcoholics who are actively drinking are more likely to die from non-cancer related complications of alcoholic liver disease (for example, liver failure). Indeed, patients with alcoholic cirrhosis who die of liver cancer are about 10 years older than patients who die of non-cancer causes. Finally, as noted above, alcohol adds to the risk of developing liver cancer in patients with chronic hepatitis C virus or hepatitis B virus infections. Aflatoxin B1 is the most potent liver cancer-forming chemical known. It is a product of a mold called Aspergillus flavus, which is found in food that has been stored in a hot and humid environment. This mold is found in such foods as peanuts, rice, soybeans, corn, and wheat. Aflatoxin B1 has been implicated in the development of liver cancer in Southern China and sub-Saharan Africa. It is thought to cause cancer by producing changes (mutations) in the p53 gene. These mutations work by interfering with the gene’s important tumor suppressing (inhibiting) functions. There are no medications that cause liver cancer, but female hormones (estrogens) and protein-building (anabolic) steroids are associated with the development of hepatic adenomas.
These are benign liver tumors that may have the potential to become malignant (cancerous). Thus, in some individuals, hepatic adenoma can evolve into cancer. Certain chemicals are associated with other types of cancers found in the liver. For example, thorotrast, a previously used contrast agent for diagnostic imaging studies, caused a cancer of the blood vessels in the liver called hepatic angiosarcoma. Also, vinyl chloride, a compound used in the plastics industry, can cause hepatic angiosarcomas that appear many years after the exposure. Liver cancer will develop in up to 30% of patients with hereditary hemochromatosis (a disorder in which there is too much iron stored in the body, including in the liver). Patients at the greatest risk are those who develop cirrhosis with their hemochromatosis. Unfortunately, once cirrhosis is established, effective removal of excess iron (the treatment for hemochromatosis) will not reduce the risk of developing liver cancer. Over the past decade, the incidence of liver cancer in the United States has risen significantly, paralleling the rise in obesity revitol hair removal cream. Although it is hard to separate the effects of diabetes from obesity on the liver, both conditions can cause chronic damage and accumulation of fat within the liver.. This is a disease called NASH (non-alcoholic steatohepatitis), which is present in up to 5% of North Americans. Fatty liver disease like this causes damage to the individual liver cells and may lead to cirrhosis in some people, thereby increasing the risk of liver cancer. Not only is the chance of developing the cancer enhanced, but patients with diabetes who undergo surgical removal of liver cancer have a higher chance of the cancer returning than do those without diabetes.
Individuals with most types of cirrhosis of the liver are at an increased risk of developing liver cancer. In addition to the conditions described above (hepatitis B, hepatitis C, alcohol, and hemochromatosis), alpha 1 anti-trypsin deficiency, a hereditary condition that can cause emphysema and cirrhosis, may lead to liver cancer. Liver cancer is also strongly associated with hereditary tyrosinemia, a childhood biochemical abnormality that results in early cirrhosis. Certain causes of cirrhosis are less frequently associated with liver cancer than are other causes. For example, liver cancer is rarely seen with the cirrhosis in Wilson’s disease (abnormal copper metabolism) or primary sclerosing cholangitis (chronic scarring and narrowing of the bile ducts). It used to be thought that liver cancer is rarely found in primary biliary cirrhosis (PBC) as well. Recent studies, however, show that the frequency of liver cancer in PBC is comparable to that in other forms of cirrhosis. The initial symptoms (the clinical presentations) of liver cancer are variable. It is becoming much more common for patients to be identified by screening people at high risk for the cancer and finding the cancer before there are any symptoms at all. In countries where liver cancer is very common, the cancer generally is discovered at a very advanced stage of disease for several reasons. For one thing, areas where there is a high frequency of liver cancer are generally developing countries where access to health care is limited. For another, screening examinations for patients at risk for developing liver cancer are not available in these areas. In addition, patients from these regions may actually have more aggressive liver cancer disease. In other words, the tumor usually reaches an advanced stage and causes symptoms more rapidly. In contrast, patients in areas of low liver cancer frequency tend to have liver cancer tumors that progress more slowly and, therefore, remain without symptoms longer.
There Kent Wedding Photographer are no specific symptoms of liver cancer, and in fact, the earliest signs are usually subtle and can be mistaken for simple worsening of cirrhosis and liver function. Abdominal pain is uncommon with liver cancer and usually signifies a very large tumor or widespread involvement of the liver. Additionally, unexplained weight loss or unexplained fevers are warning signs of liver cancer in patients with cirrhosis. These symptoms are less common in individuals with liver cancer in the U.S. because these patients are usually diagnosed at an earlier stage. However, whenever the overall health of a patient with cirrhosis deteriorates, every effort should be made to look for liver cancer. A common initial presentation of liver cancer in a patient with compensated cirrhosis (meaning that there are no complications of liver disease) is the sudden onset of a complication. For example, the sudden appearance of ascites (abdominal fluid and swelling), jaundice (yellow color of the skin), or muscle wasting without causative (precipitating) factors (for example, alcohol consumption) suggests the possibility of liver cancer. What’s more, the cancer can invade and block the portal vein (a large vein that brings blood to the liver from the intestine and spleen). When this happens, the blood will travel paths of less resistance, such as through esophageal veins. This causes increased pressure in these veins, which results in dilated (widened) veins called esophageal varices.
The patient then is at risk for hemorrhage from the rupture of the varices into the gastrointestinal tract. Rarely, the cancer itself can rupture and bleed into the abdominal cavity, resulting in bloody ascites. On physical examination, an enlarged, sometimes tender, liver is the most common finding. Liver cancers are very vascular (containing many blood vessels) tumors. Thus, increased amounts of blood feed into the hepatic artery (artery to the liver) and cause turbulent blood flow in the artery. The turbulence results in a distinct sound in the liver (hepatic bruit) that can be heard with a stethoscope in about one-quarter to one-half of patients with liver cancer. Any sign of advanced liver disease (for example, ascites, jaundice, or muscle wasting) means a poor prognosis. Rarely, a patient with liver cancer can become suddenly jaundiced when the tumor erodes into the bile duct. The jaundice occurs in this situation because both sloughing of the tumor into the duct and bleeding that clots in the duct can block the duct. In advanced liver cancer, the tumor can spread locally to neighboring tissues or, through the blood vessels, elsewhere in the body (distant metastasis). Locally, liver cancer can invade the veins that drain the liver (hepatic veins). The tumor can then block these veins, which results in congestion of the liver. The congestion occurs because the blocked veins cannot drain the blood out of the liver. (Normally, the blood in the hepatic veins leaving the liver flows through the inferior vena cava, which is the largest vein that drains into the heart.) In African patients, the tumor frequently blocks the inferior vena cava.
Blockage of either the hepatic veins or the inferior vena cava results in a very swollen liver and massive formation of ascites. In some patients, as previously mentioned, the tumor can invade the portal vein and lead to the rupture of esophageal varices. Regarding distant metastases, liver cancer frequently spreads to the lungs, presumably by way of the bloodstream. Usually, patients do not have symptoms from the lung metastases, which are diagnosed by radiologic (X-ray) studies. Rarely, in very advanced cases, liver cancer can spread to the bone or brain. These are an infrequent problem in many patients who do not live long enough to develop these complications.The liver is a vital organ present in vertebrates and some other animals. It has a wide range of functions, including detoxification, protein synthesis, and production of biochemicals necessary for digestion. The liver is necessary for survival; there is currently no way to compensate for the absence of liver function. This organ plays a major role in metabolism and has a number of functions in the body, including glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone production, and detoxification. It lies below the diaphragm in the thoracic region of the abdomen. It produces bile, an alkaline compound which aids in digestion, via the emulsification of lipids. The liver’s highly specialized tissues regulate a wide variety of high-volume biochemical reactions, including the synthesis and breakdown of small and complex molecules, many of which are necessary for normal vital functions. Medical terms related to the liver often start in hepato- or hepatic from the Greek word for liver, h?par The liver is a reddish brown organ with four lobes of unequal size and shape.
A human liver normally weighs between 1.4–1.6 kg (3.1–3.5 lb), and is a soft, pinkish-brown, triangular organ. It is both the largest internal organ (the skin being the largest organ overall) and the largest gland in the human body. It is located in the right upper quadrant of the abdominal cavity, resting just below the diaphragm. The liver lies to the right of the stomach and overlies the gallbladder. It is connected to two large blood vessels, one called the hepatic artery and one called the portal vein. The hepatic artery carries blood from the aorta whereas the portal vein carries blood containing digested nutrients from the small intestine and the descending colon. These blood vessels subdivide into capillaries which then lead to a lobule. Each lobule is made up of millions of hepatic cells which are the basic metabolic cells. The liver receives a dual blood supply from the hepatic portal vein and hepatic arteries. Supplying approximately 75% of the liver’s blood supply, the hepatic portal vein carries venous blood drained from the spleen, gastrointestinal tract, and its associated organs. The hepatic arteries supply arterial blood to the liver, accounting for the remainder of its blood flow. Oxygen is provided from both sources; approximately half of the liver’s oxygen demand is met by the hepatic portal vein, and half is met by the hepatic arteries. Blood flows through the sinusoids and empties into the central vein of each lobule. The central veins coalesce into hepatic veins, which leave the liver and empty into the inferior vena cava. The term biliary tree is derived from the arboreal branches of the bile ducts.
The bile produced in the liver is collected in bile canaliculi, which merge to form bile ducts. Within the liver, these ducts are called intrahepatic (within the liver) bile ducts, and once they exit the liver they are considered extrahepatic (outside the liver). The intrahepatic ducts eventually drain into the right and left hepatic ducts, which merge to form the common hepatic duct. The cystic duct from the gallbladder joins with the common hepatic duct to form the common bile duct. Bile can either drain directly into the duodenum via the common bile duct or be temporarily stored in the gallbladder via the cystic duct. The common bile duct and the pancreatic duct enter the second part of the duodenum together at the ampulla of Vater. Apart from a patch where it connects to the diaphragm (the so-called “bare area”), the liver is covered entirely by visceral peritoneum, a thin, double-layered membrane that reduces friction against other organs. The peritoneum folds back on itself to form the falciform ligament and the right and left triangular ligaments. These “lits” are in no way related to the true anatomic ligaments in joints, and have essentially no functional importance, but they are easily recognizable surface landmarks. An exception to this is the falciform ligament, which attaches the liver to the posterior portion of the anterior body wall. Traditional gross anatomy divided the liver into four lobes based on surface features. The falciform ligament is visible on the front (anterior side) of the liver. This divides the liver into a left anatomical lobe, and a right anatomical lobe. If the liver is flipped over, to look at it from behind (the visceral surface), there are two additional lobes between the right and left. These are the caudate lobe (the more superior), and below Car Share this the quadrate lobe.
From behind, the lobes are divided up by the ligamentum venosum and ligamentum teres (anything left of these is the left lobe), the transverse fissure (or porta hepatis) divides the caudate from the quadrate lobe, and the right sagittal fossa, which the inferior vena cava runs over, separates these two lobes from the right lobe. Each of the lobes is made up of lobules; a vein goes from the centre of each best acne treatment lobule which then joins to the hepatic vein to carry blood out from the liver. On the surface of the lobules there are ducts, veins and arteries that carry fluids to and from them. Correspondence between anatomic lobes and Couinaud segments The central area where the common bile duct, hepatic portal vein, and hepatic artery proper enter is the hilum or “porta hepatis”. The duct, vein, and artery divide into left and right branches, and the portions of the liver supplied by these branches constitute the functional left and right lobes. The functional lobes are separated by an imaginary plane joining the gallbladder fossa to the inferior vena cava. The plane separates the liver into the true right and left lobes. The middle hepatic vein also demarcates the true right and left lobes. The right lobe is further divided into an anterior and posterior segment by the right hepatic vein. The left lobe is divided into the medial and lateral segments by the left hepatic vein. The fissure for the ligamentum teres also separates the medial and lateral segments.
The medial segment is also called the quadrate lobe. In the widely used Couinaud (or “French”) system, the functional lobes are further divided into a total of eight subsegments based on a transverse plane through the bifurcation of the main portal vein. The caudate lobe is a separate structure which receives blood flow from both the right- and left-sided vascular branches. The liver is found in all vertebrates, and is typically the largest visceral organ. Its form varies considerably in different species, and is largely determined by the shape and arrangement of the surrounding organs. Nonetheless, in most species it is divided into right and left lobes; exceptions to this general rule include snakes, where the shape of the body necessitates a simple cigar-like form. The internal structure of the liver is broadly similar in all vertebrates. An organ sometimes referred to as a liver is found associated with the digestive tract of the primitive chordate Amphioxus. However, this is an enzyme secreting gland, not a metabolic organ, and it is unclear how truly homologous it is to the vertebrate liver.The various functions of the liver are carried out by the liver cells or hepatocytes. Currently, there is no artificial organ or device capable of emulating all the functions of the liver. Some functions can be emulated by liver dialysis, an experimental treatment for liver failure. Further information: Proteins produced and secreted by the liver A large part of amino acid synthesis The liver performs several roles in carbohydrate metabolism: Gluconeogenesis (the synthesis of glucose from certain amino acids, lactate or glycerol).
Note that humans and some other mammals cannot synthesize glucose from glycerol. Glycogenolysis (the breakdown of glycogen into glucose) Glycogenesis (the formation of glycogen from glucose)(muscle tissues can also do this) The liver is responsible for the mainstay of protein metabolism, synthesis as well as degradation The liver also performs several roles in lipid metabolism: Cholesterol synthesis Lipogenesis, the production of triglycerides (fats). The liver produces coagulation factors I (fibrinogen), II (prothrombin), V, VII, IX, X and XI, as well as protein C, protein S and antithrombin. In the first trimester fetus, the liver is the main site of red blood cell production. By the 32nd week of gestation, the bone how to get your ex boyfriend back marrow has almost completely taken over that task. The liver produces and excretes bile (a yellowish liquid) required for emulsifying fats. Some of the bile drains directly into the duodenum, and some is stored in the gallbladder. The used car prices liver also produces insulin-like growth factor 1 (IGF-1), a polypeptide protein hormone that plays an important role in childhood growth and continues to have anabolic effects in adults. The liver is a major site of thrombopoietin production. Thrombopoietin is a glycoprotein hormone that regulates the free iphone production of platelets by the bone marrow. The breakdown of insulin and other hormones The liver breaks down hemoglobin, creating metabolites that are added to bile as pigment (bilirubin and biliverdin). The liver breaks down or press release distribution modifies toxic substances (e.g., methylation) and most medicinal products in a process called drug metabolism. This sometimes results in toxication, when the metabolite is more toxic than its precursor. Preferably, the toxins are conjugated to Best Man Speeches avail excretion in bile or urine. The liver converts ammonia to urea. The liver stores a multitude of substances, including glucose (in healthy living the form of glycogen), vitamin A (1–2 years’ supply), vitamin D (1–4 months’ supply), vitamin B12 (1-3 years’ supply), iron, and copper. The liver is responsible for immunological effects- the good health reticuloendothelial system of the liver contains many immunologically active cells, acting as a ‘sieve’ for antigens carried to it via the portal system. The liver produces albumin, the major osmolar wrinkle cream component of blood serum. The liver synthesizes angiotensinogen, a hormone that is responsible for raising the blood pressure when activated by renin, an enzyme that is released wholesale silver jewellery when the kidney senses low blood pressure. The liver supports almost every organ in the body and is vital for survival. Because of its strategic location and multidimensional pyxism functions, the liver is also prone to many diseases. The most common include: Infections such as hepatitis A, B, C, E, alcohol damage, fatty liver, cirrhosis, cancer, drug damage (especially diy repair acetaminophen, cancer drugs) Many diseases of the liver are accompanied by jaundice caused by increased levels of bilirubin in the system.
The bilirubin results from the breakup of the solar power systems haemoglobin of dead red blood cells; normally, the liver removes bilirubin from the blood and excretes it through bile. There are also many pediatric liver diseases including USPS change of address biliary atresia, alpha-1 antitrypsin deficiency, alagille syndrome, progressive familial intrahepatic cholestasis, and Langerhans cell histiocytosis, to name but a few. Diseases that interfere with liver function will lead to derangement of these baby gift baskets processes. However, the liver has a great capacity to regenerate and has a large reserve capacity. In most cases, the liver only produces symptoms after extensive reverse phone lookup damage. Liver diseases may be diagnosed by liver function tests, for example, by production of acute phase proteins.The classic signs of liver damage include the following: Pale stools occur when stercobilin, a brown pigment, is absent from the stool. Stercobilin is derived from bilirubin metabolites best acne treatment produced in the liver. Dark urine occurs when bilirubin mixes with urine Bilirubin when it deposits in skin, causes an intense itch. Itching is the most common complaint Houston Personal Injury Lawyer by people who have liver failure. Often this itch cannot be relieved by drugs. Swelling of the abdomen, ankles and feet occurs because the liver fails to make Diamond Engagement Rings albumin. Excessive fatigue occurs from a generalized loss of nutrients, minerals and vitamins. Bruising and easy bleeding are other features of liver disease. The liver makes substances which help prevent bleeding. When liver damage occurs, these substances are no longer present and severe bleeding can occur. The diagnosis of liver function is made by blood tests. Liver function tests can readily pinpoint the extent of liver damage. If infection is suspected, then other serological tests are done. Sometimes one may require an ultrasound or a cars forum CT scan to image the liver. Physical exam of the liver is not accurate in determining the extent of liver damage.
Physical exam can only reveal presence of tenderness or size of liver but in all cases some type of radiological study is required to look at the liver. The ideal way to look at damage to the liver is with a biopsy. A biopsy is not required in all cases but may be necessary when the cause is unknown. The procedure is video interviewing done at the bedside and only requires local anesthetic. A small thin needle is inserted into the skin just below the rib cage and a biopsy is obtained. The tissue is sent to the laboratory where it is analyzed under a microscope. Sometimes the radiologist may perform a liver biopsy under ultrasound cash advance guidance if only a small area is involved. The liver is the only internal human organ capable of natural regeneration of lost tissue; as little as 25% of a liver can green marketing regenerate into a whole liver. This is predominantly due to the hepatocytes re-entering the cell cycle. That is, the hepatocytes go from the quiescent G0 phase to the G1 phase and undergo mitosis. This process is activated by the p75 receptors. There is also some evidence of bipotential stem cells, called ovalocytes or hepatic oval cells, which are thought to reside in the canals of Hering. These cells can differentiate into table tennis either hepatocytes or cholangiocytes, the latter being the cells that line the bile ducts. The capability for the liver to regenerate itself has been known since at least the times of the ancient Greeks, whose mythology includes a story about Prometheus being chained to a rock in the Caucasus seo company mountain and his liver being partially eaten during the day by an eagle only to “regenerate” in the night. The story, however, embellishes the speed with which this occurs. Human liver transplants were first performed by Thomas Starzl in the United States and Roy Calne in Cambridge, England in 1963 and 1965, respectively.
After resection of left lobe liver tumor Liver transplantation is the only option for those with irreversible liver failure. Most transplants are done for chronic liver diseases leading to cirrhosis, such as chronic hepatitis C, alcoholism, autoimmune hepatitis, and many tourbillon watches others. Less commonly, liver transplantation is done for fulminant hepatic failure, in which liver failure occurs over days to weeks. Liver allografts for transplant usually come from non-living donors who have died from fatal brain injury. Living donor liver transplantation is a technique in which a portion of a living person’s liver is removed and used to replace the entire liver of the recipient. This was first performed in 1989 for pediatric liver transplantation. Only 20% of an adult’s liver (Couinaud segments 2 and 3) is needed to serve as a liver allograft for an infant or small child. More recently, adult-to-adult liver transplantation has been done using the donor’s right hepatic lobe which amounts to 60% of the fat burning furnace review liver. Due to the ability of the liver to regenerate, both the donor and recipient end up with normal liver function if all goes well. This procedure is more controversial as it Group Halloween Costumes entails performing a much larger operation on the donor, and indeed there have been at least 2 donor deaths out of the first several hundred cases. A recent publication has addressed the outdoor table tennis table problem of donor mortality, and at least 14 cases have been found. The risk of postoperative complications (and death) is far greater in right-sided operations than that in left-sided operations. With the recent advances of non-invasive imaging, living liver donors usually have to undergo tinnitus treatment imaging examinations for liver anatomy to decide if the anatomy is feasible for donation. The evaluation is usually performed by multi-detector row computed tomography (MDCT) and magnetic resonance imaging (MRI). MDCT is good in vascular anatomy and volumetry. MRI is used for biliary tree anatomy. Donors with very unusual vascular anatomy, which makes them unsuitable for donation, could be screened out to avoid unnecessary operations. MDCT image. Arterial anatomy contraindicated for liver donation. MDCT fish oil image.
Portal venous anatomy contraindicated for liver donation. MDCT image. 3D image created by MDCT can clearly visualize the liver, measure the liver volume, and plan the dissection plane to corporate entertainment facilitate the liver transplantation procedure. Phase contrast CT image. Contrast is perfusing the right liver but not the left due to a left portal vein thrombus. In the growing fetus, a major bedroom furniture source of blood to the liver is the umbilical vein which supplies nutrients to the growing fetus. The umbilical vein enters the abdomen at the umbilicus, and passes upward CD replication along the free margin of the falciform ligament of the liver to the inferior surface of the liver. There it joins with the left branch of the portal vein. The ductus venosus Portable Staging carries blood from the left portal vein to the left hepatic vein and then to the inferior vena cava, allowing placental blood to bypass the liver. In the fetus, the liver develops nature sounds throughout normal gestation, and does not perform the normal filtration of the infant liver. The liver does not perform digestive processes because the fetus does not consume meals directly, but receives nourishment from the mother via the placenta. The fetal liver releases some blood stem cells that migrate to the fetal thymus, so 18th birthday ideas initially the lymphocytes, called T-cells, are created from fetal liver stem cells. Once the fetus is delivered, the formation of blood stem cells in infants shifts to the red bone marrow. After birth, the umbilical vein and ductus venosus are completely obliterated in two to five days; the former becomes the ligamentum teres and the latter becomes the ligamentum venosum. In the disease state of cirrhosis and portal hypertension, the umbilical vein can open up again. The liver has always been an important symbol in occult physiology. As the largest organ, the CD replication one containing the most blood, it was regarded as the darkest, least penetrable part of man’s innards.
Thus it was considered to contain the secret of fate and was used for fortune-telling. In Plato, and in later physiology, the liver represented the darkest passions, particularly the bloody, smoky ones of wrath, jealousy, and greed which drive men to action. Thus the liver meant the impulsive attachment to life itself. In Greek mythology, Prometheus was punished by the gods for revealing fire to humans, by being chained to a rock where a vulture (or an eagle) would peck out his liver, which would regenerate overnight. (The liver is the only human internal Portable Staging organ that actually can regenerate itself to a significant extent.) Many ancient peoples of the Near East and Mediterranean areas practised a type of divination called nature sounds haruspicy, whereby they tried to obtain information from examining the livers of sheep and other animals. The Talmud (tractate Berakhot 61b) refers to the liver as the Hair Transplant seat of anger, with the gallbladder counteracting this. The Persian, Urdu, and Hindi languages refer to the liver in figurative speech to indicate courage and strong feelings, or “their best”; e.g., “This Mecca has thrown to you the pieces of its liver!”. The term jan e jigar, literally “the strength (power) of my liver”, is a term of endearment in Urdu. In Persian slang, jigar is used as an adjective for any object which is desirable, especially women. In the Zulu language, the word for liver (isibindi) is the same as the word for courage. The louis vuitton handbags legend of Liver-Eating Johnson says that he would cut out and eat the liver of each man killed after dinner. In the motion picture The Message, Hind bint Utbah is implied or portrayed eating the liver of Hamza ibn ‘Abd al-Muttalib during the Battle of Uhud. Although there are narrations that suggest that Hind did “taste”, rather than eat, the liver of Hamza, the authenticity of these narrations have to be questioned. Bile or gall is a bitter-tasting, dark green to yellowish brown fluid, produced by the liver of most vertebrates, that aids the process of digestion of lipids in the small intestine. In many species, bile is stored in the gallbladder and upon eating is discharged into the duodenum. In the medical theories prevalent in the West from Classical Antiquity up to the Middle Ages, the body’s health depended on the equilibrium between four “humors” or vital fluids: blood, phlegm, “yellow bile” (or ichor) and “black bile”.
Excesses of the last two humors were supposed to produce aggression and depression, respectively; and the Greek names for them gave rise to the English words “cholera” and “melancholia”. Those same theories explain the derivation of the English word “bilious” from “bile”, and the meaning of “gall” in English as “exasperation” or “impudence”. Bile is produced by hepatocytes in the liver, draining through the many bile ducts that penetrate the liver. During this process, the epithelial cells add a watery solution that is rich in bicarbonates that dilutes and increases alkalinity of the solution. Bile then flows into the common hepatic duct, which joins with the cystic duct from the gallbladder to form the common bile duct. The common bile duct in turn joins with the pancreatic duct to empty into the duodenum. If the sphincter of Oddi is closed, bile is prevented from draining into the intestine and instead flows into the gallbladder, where it is stored and concentrated to up to five times its original potency between meals. This concentration occurs through the absorption of water and small electrolytes, while retaining all the original organic molecules. Cholesterol is also released with the bile, dissolved in the acids and fats found in the concentrated solution. When food is released by the stomach into the duodenum in the form of chyme, the duodenum releases cholecystokinin, which causes the gallbladder to release the concentrated bile to complete digestion. The human liver can produce close to one litre of bile per day (depending on body size). About 95% of the salts secreted in bile are reabsorbed in the terminal ileum and re-used. Blood from the ileum flows directly to the hepatic portal vein and returns to the liver where the hepatocytes reabsorb the salts and return them to the bile ducts to be re-used, sometimes two to three times with each meal. Action of bile salts in digestion Bile acts to some extent as a surfactant, helping to emulsify the fats in the food. Bile salt anions have a hydrophilic side and a hydrophobic side, and therefore tend to aggregate around droplets of fat (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic towards the outside.
The hydrophilic sides are positively charged due to the lecithin and other phospholipids that compose bile, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles. Ordinarily, the micelles in the duodenum have a diameter of around 14-33 ?m. The dispersion of food fat into micelles thus provide a largely increased surface area for the action of the enzyme pancreatic lipase, which actually digests the triglycerides, and is able to reach the fatty core through gaps between the bile salts. A triglyceride is broken down into two fatty acids and a monoglyceride, which are absorbed by the villi on the intestine walls. After being transferred across the intestinal membrane, fatty acids are reformed into triglicerides, then absorbed into the lymphatic system through lacteals. Without bile salts, most of the lipids in the food would be passed out in feces, undigested. Since bile increases the absorption of fats, it is an important part of the absorption of the fat-soluble substances, such as the vitamins D, E, K and A. Besides its digestive function, bile serves also as the route of excretion for bilirubin, a byproduct of red blood cells recycled by the liver. Bilirubin derives from hemoglobin by glucuronidation. The alkaline bile also has the function of neutralizing any excess stomach acid before it enters the ileum, the final section of the small intestine. Bile salts also act as bactericides, destroying many of the microbes that may be present in the food. Bile from slaughtered animals can be mixed with soap. This mixture, called bile soap, can be applied to textiles a few hours save marriage before washing and is a traditional and rather effective method for removing various kinds of tough stains. Bile also helps to neutralise the chyme from the stomach with sodium bicarbonate. The cholesterol contained in bile will occasionally accrete into lumps in the gallbladder, forming gallstones.
On an empty stomach – after repeated vomiting, for example – a person’s vomit may be green or dark yellow, and very bitter. The bitter and greenish component is bile. (The color of bile is often likened to “fresh-cut grass”, but in a vomit it may be mixed with other components in the stomach to look greenish yellow or dark yellow.) In the absence of bile, fats become indigestible and are instead excreted in feces, a condition called steatorrhea. Feces lack their characteristic brown colour and instead are white or grey, and greasy. Steatorrhea can lead to deficiencies in essential fatty acids and fat-soluble vitamins. In addition, past the small intestine (which is normally responsible for absorbing fat from food) the gastrointestinal tract and gut flora are not adapted to processing fats, leading to problems in the large intestine. Liver function tests (LFTs or LFs), which include liver enzymes, are groups of clinical biochemistry laboratory blood assays designed to give information about the state of a patient’s liver. Most liver diseases cause only mild symptoms initially, but it is vital that these diseases be detected early. Hepatic (liver) involvement in some diseases can be of crucial importance. This testing is performed by a medical technologist on a patient’s serum or plasma sample obtained by phlebotomy. Some tests are associated with functionality (eg. albumin); some with cellular integrity (eg. transaminase) and some with conditions linked to the biliary tract (gamma-glutamyl transferase and alkaline phosphatase). Several biochemical tests are useful in the evaluation and management of patients with hepatic dysfunction. These tests can be used to (1) detect the presence of liver disease, (2) distinguish among different types of liver disorders, (3) gauge the extent of known liver damage, and (4) follow the response to treatment.
This section is missing citations or needs footnotes. Please help add inline citations to guard against copyright violations and factual inaccuracies. (November 2008) Measurement Significance Reference range (Normal Values) Albumin (Alb) Albumin is a protein made specifically by the liver, and can be measured cheaply and easily. It is the main constituent of total protein; the remaining fraction is called globulin (including the immunoglobulins). Albumin levels are decreased in chronic liver disease, such as cirrhosis. It is also decreased in nephrotic syndrome, where it is lost through the urine. Poor nutrition or states of protein catabolism may also lead to hypoalbuminaemia. The half-life of albumin is approximately 20 days. Albumin is not considered to be an especially useful marker of liver synthetic function; coagulation factors (see below) are much more sensitive. 3.9 to 5.0 g/dL Alanine transaminase (ALT) Alanine transaminase (ALT), also called Serum Glutamic Pyruvate Transaminase (SGPT) or Alanine aminotransferase (ALAT) is an enzyme present in hepatocytes (liver cells). When a cell is damaged, it leaks this enzyme into the blood, where it is measured. ALT rises dramatically in acute liver damage, such as viral hepatitis or paracetamol (acetaminophen) overdose. Elevations are often measured in multiples of the upper limit of normal (ULN). 9 to 60 IU/L Aspartate transaminase (AST) Aspartate transaminase (AST) also called Serum Glutamic Oxaloacetic Transaminase (SGOT) or aspartate aminotransferase (ASAT) is similar to ALT in that it is another enzyme associated with liver parenchymal cells. It is raised in acute liver damage, but is also present in red blood cells, and cardiac and skeletal muscle and is therefore not specific to the liver. The ratio of AST to ALT is sometimes useful in differentiating between causes of liver damage.Elevated AST levels are not specific for liver damage, and AST has also been used as a cardiac marker. 10 to 40 IU/L Alkaline phosphatase (ALP) Alkaline phosphatase (ALP) is an enzyme in the cells lining the biliary ducts of the liver. ALP levels in plasma will rise with large bile duct obstruction, intrahepatic cholestasis or infiltrative diseases of the liver.
ALP is also present in bone and placental tissue, so it is higher in growing children (as their bones are being remodelled) and elderly patients with Paget’s disease. 30 to 120 IU/L Total bilirubin (TBIL) Bilirubin is a breakdown product of heme (a part of haemoglobin in red blood cells). The liver is responsible for clearing the blood of bilirubin. It does this by the following mechanism: bilirubin is taken up into hepatocytes, conjugated (modified to make it water-soluble), and secreted into the bile, which is excreted into the intestine. Increased total bilirubin causes jaundice, and can signal a number of problems: 1. Prehepatic: Increased bilirubin production. This can be due to a number of causes, including hemolytic anemias and internal hemorrhage. 2. Hepatic: Problems with the liver, which are reflected as deficiencies in bilirubin metabolism (e.g. reduced hepatocyte uptake, impaired conjugation of bilirubin, and reduced hepatocyte secretion of bilirubin). Some examples would be cirrhosis and viral hepatitis. 3. Posthepatic: Obstruction of the bile ducts, reflected as deficiencies in bilirubin excretion. (Obstruction can be located either within the liver or in the bile duct. Direct bilirubin (Conjugated Bilirubin) The diagnosis is narrowed down further by looking at the levels of direct bilirubin. If direct (i.e. conjugated) bilirubin is normal, then the problem is an excess of unconjugated bilirubin, and the location of the problem is upstream of bilirubin excretion. Hemolysis, viral hepatitis, or cirrhosis can be suspected. If direct bilirubin is elevated, then the liver is conjugating bilirubin normally, but is not able to excrete it. Bile duct obstruction by gallstones or cancer should be suspected. Gamma glutamyl transpeptidase (GGT) Although reasonably specific to the liver and a more sensitive marker for cholestatic damage than ALP, Gamma glutamyl transpeptidase (GGT) may be elevated with even minor, sub-clinical levels of liver dysfunction. It can also be helpful in identifying the cause of an isolated elevation in ALP. GGT is raised in alcohol toxicity chronic).