Cirrhosis, liver increase

Ultrasound examination is used routinely to evaluate cirrhosis a small, nodular liver with increased echogenicity is consistent with cirrhosis. Liver biopsy is the only way to diagnose cirrhosis definitively, but it is often deferred in lieu of a... 

Based on our studies, it is possible to recommend HBO in postoperative period for patients with Uver cirrhosis to increase the efficacy of the Uver detoxification function. Depending on the type of the morphological form of liver cirrhosis, this would help to optimise the process of surgical treatment of patients with fiver cirrhosis. 

Increased portal blood pressure Blood flow in the portal system is often obstructed in cirrhosis, resulting in an increased portal blood pressure. Further, colloidal osmotic pressure of the blood is decreased as a result of impaired synthesis of plasma proteins by the diseased liver. Increased portal blood pressure and low osmo-larity of the blood cause fluid to escape from the portal vascular system and collect in the abdomen. 

In delayed-phase imaging, the signal increase in the liver parenchyma does not necessarily increase the conspicuity or detection of lesions because residual hepatocytes of a tumor of hepatocytic origin, such as hepatocellular carcinoma (HCC) and focal nodular hyperplasia, may influence the contrast enhancement. Gd-BOPTA is effective for use with delayed-phase MRI to detect metastases [130]. In cirrhosis, liver functioning is impaired and the number of normal hepatocytes is reduced. The entry of Gd-BOPTA into cirrhotic hepatocytes decreases, but the accumulation in the liver increases due to reduced biliary excretion [131]. As a consequence, contrast enhancement is reduced and the window of acquisition is widened. The contrast enhancement of a cirrhotic liver is therefore different from that observed in normal liver parenchyma. 

Although inhibition of stem-cell proliferation is the most likely mechanism of hematological toxicity, increased platelet hepatic uptake has been suggested to account for thrombocytopenia (227). Raised serum thrombopoietin concentrations were found in patients with interferon alfa-induced thrombocytopenia (228). However, there is evidence that serum thrombopoietin concentrations in patients who have had thrombocytopenia during interferon alfa treatment for chronic viral hepatitis C either do not increase (in patients with compensated cirrhosis) or increase only moderately and less than expected (in non-cirrhotic patients) (229). The authors proposed that interferon alfa impairs liver production of thrombopoietin, raising the possibility of testing thrombopoietin administration in patients with severe thrombocytopenia before or during treatment with interferon alfa (230). 

Hepatic steatosis with Mallory inclusion bodies has been reported with nifedipine (28). In patients with liver cirrhosis, nifedipine increases portal pressure due to splanchnic vasodilatation (29) whether this increases the risk of variceal bleeding is unknown. 

Even in patients with histologically proven alcoholic hepatitis, serum alkaline phosphatase may remain within reference limits. Green et al. (G21) found normal serum alkaline phosphatase values in 20 out of 46 patients with alcoholic hepatitis, while only 4 patients showed values greater than 2.5 times the upper reference limit. Bradus et al. (B39) described 83 patients whose liver biopsies showed fatty change but no evidence of cirrhosis. Mild increases in serum alkaline phosphatase (up to 2.5 times the upper reference limit) were found in about 50%. 

Except for the less lipid-soluble aprobarbital and phenobarbital, nearly complete metabolism and/or conjugation of barbiturates in the liver precedes their renal excretion. The metabolic elimination of barbiturates is more rapid in young people than in the elderly and infants, and half-lives are increased during pregnancy partly because of the expanded volume of distribution. Chronic liver disease, especially cirrhosis, often increases the tj of the biotransformable barbiturates. Repeated administration, especially of phenobarbital, shortens the tj of barbiturates that are metabolized as a result of the induction of microsomal enzymes (see above). 

Established interactions. These increases in bioavailability might be expected to increase the extent of the sedation and amnesia due to these benzodiazepines, but in young healthy adults this is apparently of little importance. The clinical effects of the interaction with diazepam appear not to have been investigated. The effects of midazolam and triazolam may be more enhanced than those of other benzodiazepines, because these drugs are more dependent on CYP3A4 for their metabolism (see Mechanism, abovej.What is not clear is whether other factors such as old age or liver cirrhosis might increase the risk of adverse effects with concurrent use. 

In some studies of spray painters in the automobile and airplane industries and of house painters mortality from liver cirrhosis was increased. Another study investigating house painters, however, did not show an increase. ... 

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. 

There is very little evidence relating to the role of ROMs in cholestatic liver disease. Serum selenium and glutathione peroxidase activity are decreased in humans with intrahepatic cholestasis of pregnancy (Kauppila et al., 1987). Low levels of vitamin E have been reported in patients with primary biliary cirrhosis, and in children with Alagille s syndrome or biliary atresia (Knight et al., 1986 Jeffrey etal., 1987 Lemonnier etal., 1987 Babin etal., 1988 Kaplan et al., 1988 Sokol etal., 1989). Serum levels of Mn-SOD are increased in patients with all stages of primary biliary cirrhosis compared with patients with other forms of chronic liver disease, although whether this causes or results from the disease process is unclear (Ono etal., 1991). 

As stated at the beginning of this article, the liver is the most intensively studied animal tissue in biochemistry. In the context of the role of free radicals in human diseases, the liver is not obviously at centre stage, since heart disease and cancer are more important in the industrialized world than, for example, cirrhosis. Free-radical biochemistry of the liver will remain a fertile area of work, however, not least because so many original ideas and techniques are developed there and then applied to the study of other tissues. The increasing use of liver transplantation, following the acceptance of kidney and heart transplants as almost routine, will surely increase the interest in the study of ischaemia-reperfusion injury in... 

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

Sinusoidal damage from cirrhosis is the most common cause of portal hypertension. The sinusoids are porous vessels within the liver that surround radiating rows of hepatocytes, the basic functional cells of the liver (Fig. 19-2). Progressive destruction of hepatocytes and an increase in fibroblasts and connective tissue surrounding the hepatocytes culminate in cirrhosis. Fibrosis and regenerative nodules of scar tissue... 

Non-alcoholic fatty liver disease begins with asymptomatic fatty liver but may progress to cirrhosis. This is a disease of exclusion elimination of any possible viral, genetic, or environmental causes must be made prior to making this diagnosis. Non-alcoholic fatty liver disease is related to numerous metabolic abnormalities. Risk factors include diabetes mellitus, dyslipidemia, obesity, and other conditions associated with increased hepatic fat.26... 

The incidence of liver complications associated with PN ranges from approximately 7% to 84%, and end-stage liver disease develops in as many as 15% to 40% of adult patients on long-term PN.35 Patients often develop a mild increase in liver enzymes within 1 to 2 weeks of initiating PN, but this generally resolves when PN is discontinued. Severe liver complications include hepatic steatosis (fat deposition in liver), steatohepatitis (a severe form of liver disease characterized by hepatic inflammation that may progress rapidly to liver fibrosis and cirrhosis), cholestasis, and cholelithiasis.35... 

The problems of alcohol dependence and alcoholism are dealt with in Chapter 10. Suffice it to say here that problem drinkers risk numerous psychological problems, such as anxiety and depression, and may experience physical withdrawal symptoms. There are also numerous medical problems related to heavy, chronic alcohol consumption these include increased risk of coronary heart disease, liver cirrhosis, impotence and infertility, cancer and stroke (Chapter 10). It is estimated that alcohol plays a part in up to 33,000 deaths per year in the UK (DoH, 2001). Within the last year 1 in 4 adults will have experienced loss of memory following an alcoholic binge, injured themselves or... 

The potent antidiuretic hormone AVP orchestrates the regulation of free water absorption, body fluid osmolality, cell contraction, blood volume, and blood pressure through stimulation of three G-protein-coupled receptor subtypes Vi-vascular types a and b, V2-renal, and V3-pituitary. Increased AVP secretion is the trademark of several pathophysiological disorders, including heart failure, impaired renal function, liver cirrhosis, and SIADH. As a consequence, these patients experience excess water retention or inadequate free-water excretion, which results in the dilution of sodium concentrations, frequently manifesting as clinical hyponatremia (serum sodium concentration <135mmol/L). This electrolyte imbalance increases mortality rates by 60-fold. Selective antagonism of the AVP V2 receptor promotes water... 

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