Cirrhosis Of The Liver
Cirrhosis of the liver is cirrhosis that affects the liver tissue as a final result of various chronic diseases. The consequences of cirrhosis of the liver on the health of individuals depend critically on the degree of functionality that the liver can retain despite the histological alteration.
The primary abnormality of cirrhosis of the liver is the presence of fibrosis, which is the deposition of collagen fibers in the liver, but so that it can make the pathological diagnosis of cirrhosis, the accumulation of fibers hasdelimiting nodes, ie is to isolate areas of liver tissue, altering the architecture of the organ and preventinghepatocytes relationship between the fine blood vessels and through which they exert their synthesis andpurification function and through which feed.
Schematically, fibrosis form something like a three dimensional network within the liver, in which the cords of the net would fibrosis and areas therebetween remaining nodules cells that regenerate therein. This alteration is called a node of regeneration and is the feature that allows the diagnosis of cirrhosis. There are other liver disorders that are accompanied by fibrosis, cirrhosis not considered to meet the condition of being regenerative nodules.
The main causes of cirrhosis of the liver in developed countries
- Excessive consumption of alcohol (hepatic cirrhosis of Laennec, alcoholic, alcohol or alcoholic cirrhosis)
- Chronic hepatitis C virus (HCV cirrhosis)
- Other viruses, such as chronic hepatitis B virus and hepatitis virus infection mixed chronic hepatitis B andhepatitis D.
- Chronic cholestatic diseases (affecting production or output of bile from the liver), such as primary biliary cirrhosisor primary sclerosing cholangitis.
- Congenital metabolic liver diseases such as primary hemochromatosis (hepatic iron overload-quite frequently), Wilson‘s disease (hepatic copper overload-very rarely) and alpha-1 antitrypsin (also quite rare); or acquiredmetabolic diseases such as nonalcoholic steatohepatitis associated with diabetes or dyslipidemia.
- Other: autoimmune hepatitis. Liver toxicity hepatotoxic drugs or other chemicals. There are other much rarercauses and some specific early childhood that cause cirrhosis of the liver in children or adolescents.
All abovementioned diseases usually require years of evolution to eventually produce cirrhosis. Moreover, in manycases, excessive alcohol consumption or chronic hepatitis C virus never fail to produce cirrhosis and the patient dies by an independent cause of liver disease.
Similar to what happens in other tissues, liver inflammation is the basic process by which the liver responds to damage, whatever it. Through this process, the liver tissue is able to recognize the damage and repair it if possible. If repair is not possible, then destroy the damaged tissue. Normally, this type of response restores theoriginal structure and function and maintains tissue homeostasis, but sometimes the injury is too severe or persistent, and the inflammatory process itself compromises the structural integrity through processes such asfibrosis, with posterior sclerosis, as the abnormal tissue damaged structures are replaced.
The different etiological agents of cirrhosis of the liver diseases mentioned in the previous section can causetissue damage, inflammation and hepatocyte necrosis, but the type of cell repair predominates (regeneration orfibrosis) determine that the liver tissue recovers, or fibrosis progresses and this abnormal tissue regenerationleading to cirrhosis.
The predominance of one type or another of response depends on the characteristics and persistence of offending agent, and the characteristics of the individual
Micrograph showing cirrhosis. Trichrome stain.For the diagnosis of cirrhosis of the liver is usually sufficient with noninvasive procedures such as the combination of imaging techniques such as ultrasound, and laboratory findings. Liver biopsy is also used, however, today this procedure is used only in selected cases and nothing else.
Stages of cirrhosis cirrhosis of the liver
In the course of the disease, we can distinguish two phases: compensated and decompensated cirrhosis. This differentiation takes into account whether or not patients developed complications of the disease.
While compensated, patients may not have any symptoms, and this phase can live years. At this stage there are a significant number of patients who have not yet been diagnosed. Also, patients with compensated cirrhosis of the liver are similar to that of the general population survival. This is because under normal conditions the body does not need all the “potential” that the liver has. You can have 100% of the affected liver and not have any symptoms, detecting if anything increased transaminases in blood tests.
Defining complications decompensated cirrhosis of the liver are:
- Ascites: accumulation of intra-abdominal free fluid with transudate characteristics I transudado This also can be infected (spontaneous bacterial peritonitis), usually due to bacterial translocation (step into the bloodstream of bacteria that comprise the intestinal flora).
- Hepatorenal syndrome: prerenal functional and reversible without any structure impaired renal kidney failure.Occurs due to intense renal vasoconstriction leading to kidney failure established within days or weeks, very aggressively and has a fatal short-term prognosis in most cases weeks (hepatorenal syndrome type I) or more insidiously, with a slightly better prognosis and a median survival of about six months (hepatorenal syndrome typeII).
- Hepatic encephalopathy: impairment of neurological function, usually episodic and reversible, related to the passage from the portal circulation substances cleared by the liver into the general circulation.
- Gastrointestinal bleeding from esophageal varices.
- Jaundice: yellowish tint of the skin and mucous membranes as a result of accumulation of bilirubin.
Decompensated cirrhosis, however, usually predicts a significant decrease in survival, and poor short-term prognosis.
In developing these complications involved basically two pathogenic factors:
- Portal hypertension (increased normal stress of the portal vein)
- The hepatocellular insufficiency
In addition to the complications described, may appear many others, among which the increased risk with patientswith cirrhosis of the liver develop hepatocellular carcinoma.