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Pa Tho Physiology of Liver Cirrhosis_Mercy

Pa Tho Physiology of Liver Cirrhosis_Mercy

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Published by: mersenie_Theovercomer on Dec 18, 2009
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Pathophysiology of Liver Cirrhosis
Cirrhotic ascites forms as the result of a particular sequence of events (Fig. 1
). The currentaccepted theory of ascites formation is the peripheral arterial vasodilation hypothesis. This doesnot directly refute older hypotheses, but rather incorporates them into one uniform theory thatmatches actual hemodynamic data most closely.
Development of portal hypertension is the first abnormality to occur in cirrhotic patients whodevelop ascites. Cirrhosis itself increases the resistance to blood flow within the liver, therebycausing the development of portal hypertension and shunting of blood to the systemiccirculation. Portal pressures higher than 12 mm Hg are generally required for the accumulationof fluid in cirrhosis. This concept is important, because reducing portal pressure to lower than 12mm Hg is the goal of many modern therapeutic maneuvers.As portal hypertension develops, a local release of vasodilators occurs. These vasodilators affectthe splanchnic arteries and thereby decrease the effective arterial blood flow and arterial pressures. The precise agent(s) responsible for vasodilation is a subject of wide debate; however,most the recent literature has focused on the role of nitric oxide. Observations that implicatenitric oxide as the likely mediator of vasodilation in cirrhosis include the following:
1.Increased activity of nitric oxide synthase detected in the arteries of cirrhoticrats2.High serum nitrite and nitrate levels (an index of nitric oxide synthesis)measured in cirrhotic patients
3.Inhibition of nitric oxide, leading to increased arterial pressure and systemicvascular resistance in animals
Progressive vasodilation leads to the activation of vasoconstrictor and antinatriureticmechanisms, both in an attempt to restore normal perfusion pressures. Mechanisms involvedinclude the renin-angiotensin system, sympathetic nervous system, and antidiuretic hormone(vasopressin). The ultimate effect is sodium and water retention. In the late stages of cirrhosis,free water accumulation is more pronounced than the sodium retention and leads to a dilutionalhyponatremia. This explains why cirrhotic patients with ascites demonstrate urinary sodiumretention, increased total body sodium, and dilutional hyponatremia, a challenging concept tomany physicians.
Liver Cirrhosis
Cirrhosis is a chronic medical condition of liver abandoning the usual biochemical functioning of liver in the body. Cirrhosis is resulted from the surrogation of the liver tissues by regenerativenodules and fibrotic scar nodules that lead to the progressive loss of biochemical function of theliver. The common causes of Cirrhosis are hepatitis C, chronic hepatitis B; Wilson's disease,autoimmune hepatitis, hereditary hemochromatosis, alcoholism etc. and this become a crucialhealth problem of the mankind.The nodule formation and fibrosis lead to the alteration of the ordinary liver structure whichobstructs the blood flow throughout the liver is the condition of Cirrhosis. Cirrhosis also leads toan incapability of performing liver biochemical functions. The pathophysiology of cirrhosis, thenormal and anatomy of the liver provide the better understanding of the hazards of Cirrhosis. Theliver is an important organ in the animal body where also where metabolism of toxins and drugsincluding alcohol are carried out.The biochemical functions of liver includes the synthesis of blood clotting factors, secretion andsynthesis of albumin, the chief blood protein, secretion of bile and modification of itscomponents. In addition, cholesterol metabolism and the conversion of fats and proteins intoglucose like primary biochemical functions are also performed by the liver. Thus liver plays animportant role in the functioning of the human body and deterioration in its functioning like bycirrhosis is of major biomedical concern and diagnosing the disease and immediate treatment isthe best solution.Liver biopsy through a transjugular, percutaneous, fine-needle or laparoscopic approach is the best way to diagnose cirrhosis. On the basis of the results obtained from the histological studiescirrhosis can be divided into macronodular, micronodular, or mixed, but it is unfocused to theetiology and these may loss with the progress of the disease and serological sign are greatlyspecific. If the laboratory, clinical, and radiological records suggests cirrhosis them there is norequirement of going for liver biopsy.The only treatment of liver cirrhosis is the elimination of the causes and preventingcomplications of the disease. There is no such treatment to get the liver cirrhosis reversed back tothe original healthy liver. Abstaining from alcoholism, timely treatment of hepatitis associatedcirrhosis and other cirrhosis causing diseases are the ways for eliminating cirrhosis. If the causeis Wilson's disease then chelation therapy for removing the copper that build up in the body bythis disease is effective.Medications including antibiotics are the best ways of preventing the complications of cirrhosisdue to different causes. If the complications outbreaks the limit of control then liver transplantation is preferable. With advancement in the biomedical sciences the chances of 
survival on liver transplantation or the success of it inflating and thus giving new hope of curingto the cirrhosis sufferers.
 The liver plays a vital role in synthesis of proteins (e.g.albumin,clotting factorsand complement), detoxification and storage (e.g.vitamin A). In addition, it participates in the metabolism of lipidsandcarbohydrates. Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are still fullyreversible. The pathological hallmark of cirrhosis is the development of scar tissue thatreplaces normalparenchyma, blocking the portal flow of blood through the organand disturbing normal function. Recent research shows the pivotal role of stellatecell, a cell type that normally storesvitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to activation of the stellate cell, whichbecomes contractile (calledmyofibroblast) and obstructs blood flow in thecirculation. In addition, it secretes TGF-β
, which leads to a fibrotic response andproliferation of connective tissue. Furthermore, it disturbs the balance betweenmatrix metalloproteinasesand the naturally occurring inhibitors (TIMP 1 and 2),leading tomatrixbreakdown and replacement by connective tissue-secreted matrix.
 The fibrous tissue bands (septa) separate hepatocyte nodules, which eventuallyreplace the entire liver architecture, leading to decreased blood flow throughout. Thespleenbecomes congested, which leads tohypersplenismand increased sequestration of platelets. Portal hypertension is responsible for most severecomplications of cirrhosis.

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