Liver diseases often cause systemic symptoms and changes.
See also liver structure and function and assessment of patients with liver disease.) Liver diseases often cause systemic symptoms and changes. Changes in the circulation Hypotension with advanced liver disease may contribute to renal dysfunction. The pathogenesis of hyperdynamic circulation (increased cardiac ejection volume and increased heart rate), and hypotension, resulting in advanced liver dysfunction or cirrhosis, is only partially known. Peripheral arterial vasodilation probably contributes to the development of both constellations. Factors that contribute to cirrhosis, an altered sympathetic tone, production of nitric oxide and other endogenous vasodilators and an increased activity of humoral factors (eg. As glucagon) may be. With respect to specific changes in the hepatic circulation (eg. B. Budd-Chiari syndrome), vascular diseases of the liver. Endocrine disorders glucose intolerance, hyperinsulinemia, insulin resistance and hyperglucagonemia are often found in patients with liver cirrhosis. The elevated insulin levels are more an expression of a reduced degradation in the liver as an increased secretion, whereas the opposite is true for the Hyperglukonämie. Pathological thyroid function values ??have rather to a change in the hepatic metabolism of thyroid hormones and changes in thyroid hormone binding proteins in the plasma, as in primary thyroid dysfunction. Sexual disorders are common. Chronic liver diseases lead to impairment of menstruation and fertility. Men with cirrhosis, v. a. Alcoholics often show a hypogonadism (incl. Testicular atrophy, erectile dysfunction, decreased spermatogenesis) and feminization (gynecomastia, female habitus). The biochemical causes are poorly understood. The Gonadotropinreserven the hypothalamic pituitary axis are often exhausted. The circulating testosterone levels are low, this is due v. a. in the synthesis and reduced less in the increased peripheral conversion to estrogen. Estrogen levels are in contrast to those of the estradiols increased, but the dependence between estrogens and feminization is complex. These changes are evident on at alcoholic liver disease than in cirrhosis of other etiology and suggest that the alcohol and not the liver disease is the cause in question. In fact, there is evidence of the toxic effects of alcohol on the testes. Hematologic changes Anemia is a common side effect of liver diseases. Causative factors may be blood loss, lack of Fol (folic acid), hemolysis, alcohol-toxic bone marrow damage and a direct effect of chronic liver diseases. Leukopenia and thrombocytopenia are usually associated with splenomegaly in advanced portal hypertension. Coagulation changes are frequent and complex. Both the liver dysfunction as well as the insufficient intake of vitamin K lead to decreased synthesis of coagulation factors. A pathological prothrombin time, depending on the severity of liver dysfunction may respond to parenteral administration of phytonadione (vitamin K1) from 5 to 10 mg once daily for two to three days. Thrombocytopenia, disseminated intravascular coagulation and Fibrinogenveränderungen also contributes in many patients for blood clotting disorder. Kidney and electrolyte changes kidney and electrolyte changes are frequent, v. a. in patients with ascites. Hypokalemia is the result of excessive potassium loss due to the increased circulating aldosterone, renal retention of ammonium ions in exchange for potassium, renal tubular acidosis, or a secondary diuretic therapy. The treatment consists of the administration of oral potassium chloride and discontinuation of potassium-sparing diuretics. A hyponatremia is often, although the kidney intense sodium retinieren (ascites: Pathophysiology). It occurs usually in advanced liver disease and can be corrected only with difficulty. More often, a relative water retention is responsible, as a reduction of sodium. A Potassium reduction can also help. Therapeutically restricting the water supply and the replacement of potassium may be helpful. Diuretics, which increase water excretion may be given in severe or refractory cases. Administration of intravenous saline solution is indicated only in cases of severe hyponatremia that trigger convulsions, or any suspicion of a general sodium depletion of the organism; their administration should be avoided in patients with cirrhosis and water retention because it leads to a Verschlechtung of ascites and can increase the sodium levels only temporarily. Advanced liver disease can disrupt the acid-base balance and usually cause metabolic alkalosis. The blood urea concentration is often reduced in the liver due to decreased synthesis. Gastrointestinal bleeding lead to an increase due to an increased attack in the intestine and less due to a deterioration in renal function. If gastrointestinal bleeding let the blood urea concentration increase, normal creatinine indicate a normal renal function. In renal failure in liver diseases the following should be considered rare diseases that directly affect both the kidney and the liver (z. B. poisoning with carbon tetrachloride) circulatory failure with reduced renal perfusion, with or without acute tubular necrosis Functional renal failure, often called hepatorenal syndrome called hepatorenal syndrome This syndrome is defined as a progressive oliguria, azotemia in the absence of organic damage to the kidneys. It usually occurs in patients with fulminant hepatitis or advanced cirrhosis with ascites. Its unknown pathogenesis is likely due in part to an extreme vasodilation in the arterial circulation of the Splanchnikusgefäße, resulting in decreased central arterial volume. Neural and humoral reduction of renokortikalen blood flow are the result, leading to a decreased glomerular filtration rate. A pre-renal azotemia is often difficult to distinguish. A low concentration of sodium in the urine and a corresponding benign sediment distinguishes it from the tubular necrosis. In unclear cases, the response to a volume load should be investigated. Once established, the course of renal failure in untreated hepatorenal syndrome is usually rapidly progressive and fatal (hepatorenal syndrome type 1), there are also less severe clinical cases with stable renal function at a low level (hepatorenal syndrome type 2). Combination therapy with vasoconstrictors (typically midodrine, octreotide or terlipressin) and volume expander (typically albumin) can be effective. Liver transplantation is another accepted treatment hepatorenal syndrome type 1. A transjugular intrahepatic portosystemic shunt (TIPS) is promising, but further studies are needed.