Systemic disorders in liver disease

Diseases of the liver often manifest common symptoms and disorders.

Circulation disorders

Arterial hypotension in the progression of liver failure may contribute to impaired renal function. The pathogenesis of hyperdynamic circulation (an increase in the minute volume of the heart and heart rate) and arterial hypotension, which develop with the progression of liver failure or cirrhosis, is not fully understood. However, these disorders can be caused by peripheral arterial vasodilation. Specific circulatory disorders in the liver (for example, Badd-Chiari syndrome).

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10],

Endocrine disorders

Glucose intolerance, hyperinsulinism, insulin resistance and hyperglucagonemia are often observed in patients with cirrhosis; an increase in insulin levels reflects a decrease in the rates of its disintegration in the liver rather than an increase in secretion, whereas the reverse is more characteristic of hyperglucagonemia. Changes in the parameters of thyroid function more likely reflect the violation of the exchange of thyroid hormones in the liver and the disruption of the binding of hormones to blood plasma proteins than the violation of the thyroid gland itself.

Chronic liver diseases usually cause irregularities in the menstrual cycle and fertility. In men with cirrhosis of the liver, especially those with alcoholism, hypogonadism (including testicular atrophy, erectile dysfunction, decreased spermatogenesis) and feminization (gynecomastia, effeminate) are often observed. The biochemical mechanisms of these changes are not fully understood. The gonadotropin reserve of the hypothalamic-pituitary system is often reduced. The level of testosterone circulating in the blood is reduced mainly due to a decrease in synthesis, but also due to increased peripheral conversion to estrogens. The level of estrogens, in addition to estradiol, is usually elevated, but the relationship between estrogen and feminization is quite complex. These disorders are more pronounced in alcoholic liver disease than with cirrhosis of another etiology. It is assumed that the cause of these changes is directly alcohol, and not liver disease. It is proved that alcohol itself is toxic against testicles.

[11], [12], [13], [14], [15], [16], [17]

Hematologic disorders

Anemia is typical for patients with liver disease. This is promoted by bleeding, a deficiency of folic acid, hemolysis, suppression of hematopoiesis by alcohol and a direct effect of chronic liver disease. Leukopenia and thrombocytopenia are often combined with splenomegaly in the progression of portal hypertension.

Characteristic violations of coagulation, the mechanism of their occurrence is complicated. Hepatocellular dysfunction and reduced absorption of vitamin K disrupt the synthesis of clotting factors in the liver. Depending on the changes in the parameters of PV or MHO and the severity of hepatocellular dysfunction, there may be a different response to parenteral administration of phytonadione (vitamin K 5-10 mg once daily for 2-3 days.Trombocytopenia, disseminated intravascular coagulation and fibrinogen level also affect hemostasis in most patients.

Renal and electrolyte disorders

Often there are kidney and electrolyte disorders, especially in patients with ascites.

Hypokalemia can be the result of a loss of potassium in the urine due to an increase in aldosterone in the blood, kidney failure of ammonium ions in exchange for potassium, secondary renal tubular acidosis, or diuretic therapy. Treatment includes prescribing potassium chloride and potassium-sparing diuretics.

Hyponatremia is common even with Na retention; as a rule, hyponatremia is observed with progressive hepatocellular disorders and is difficult to correct. To a greater extent this is due to the relative excess of water than to the general losses of sodium; the value of potassium also has a value. Fluid restriction and potassium intake may be effective; The use of diuretics that increase the clearance of free water is controversial. Intravenous administration of saline solutions is indicated only if there is severe hyponatremia, causing paroxysms, or if there is a suspicion of complete depletion of sodium; this should be avoided in patients with cirrhosis of the liver with fluid retention, as this worsens the course of ascites and only temporarily increases the level of sodium in the serum.

Progressing liver failure can change the acid-base balance, usually leading to metabolic alkalosis. The concentration of urea blood, as a rule, is low due to impaired synthesis by the liver; Gastrointestinal bleeding is associated more with increased enteral load than with impaired renal function. In the latter case, the normal concentration of creatinine confirms the normal renal function.

Renal failure in liver diseases can reflect rare disorders that directly affect both the kidneys and the liver (eg, carbon tetrachloride poisoning); circulatory disorders with decreased renal perfusion with visible acute tubular necrosis or without; or functional renal failure, often called hepatorenal syndrome. Hepatorenal syndrome is manifested by progressive oliguria and azotemia in the absence of structural damage to the kidney; this is usually found in patients with fulminant hepatitis or progressive liver cirrhosis with ascites. In the mechanism of pathogenesis, the expressed vasodilation of the arterial vessels of the internal organs is probably involved, which leads to a decrease in the effective arterial blood flow. There is a decrease in the neurogenic or humoral regulation of the renocortical blood flow, leading to a decrease in glomerular filtration. Low sodium concentration in urine and unchanged urinary sediment usually distinguish it from tubular necrosis, but this condition is difficult to distinguish from prerenal azotemia; in doubtful cases, a kidney response to a water load can be assessed. It is established that renal failure as a result of hepatorenal syndrome usually progresses rapidly, leading to a lethal outcome (type 1 hepatorenal syndrome), but some cases are more favorable, with a stable course of renal failure (type 2). Liver transplantation is the only method of treatment for patients with hepatorenal syndrome type 1; trans hepatic intrahepatic portosystemic shunting (TIPS) and the use of vasoconstrictors show encouraging results, but require more observations.

Asymptomatic flow with altered laboratory results

Since aminotransferases and alkaline phosphatase are included in the routine laboratory test report, changes are often observed in patients without signs or symptoms of liver disease. In such cases, the doctor should receive information about possible toxic effects on the liver, including alcohol use; prescription and over-the-counter medicines, herbal products and home remedies; on the exposure of an industrial or other chemical substance. Moderate elevations in ALT or ACT levels (<2 times ULN) require only a re-examination; they occur in about 1/3 of the cases. If the changes are observed in other laboratory tests and they are significant or persist after a second study, further examination is necessary.

With an increase in the level of aminotransferases, fatty hepatosis must be excluded, the suspicion of which often occurs in a clinical trial. If fatty hepatosis is excluded, screening for hepatitis B and C should be performed. Patients over 40 years of age should be examined for hemochromatosis; patients younger than 30 years old - on Wilson's disease. Most patients, especially young or middle-aged women, should be examined for autoimmune diseases. Certain groups of patients (at risk) should be screened for malaria and schistosomiasis. If the results are negative in such cases, a study is shown to identify a-antitrypsin deficiency. If the cause is not established, a liver biopsy is recommended.

In asymptomatic isolated elevations of alkaline phosphatase levels, it is necessary to confirm the hepatic origin of this phenomenon (this is confirmed by elevated levels of 5'-nucleotidase or gamma-glutamyltranspeptidase). If the presence of hepatic pathology is confirmed, an instrumental examination of the liver is indicated, usually using ultrasonography or magnetic resonance cholangiopancreatography. If no structural disorders are detected, one can think of intrahepatic cholestasis and presume toxic effects of drugs or hepatotrones. Need to clarify the infiltrative changes and metastases in the liver (eg, colon cancer).

Women need the definition of antimitochondrial antibodies. Persistent unexplained increases in indices or suspicion of intrahepatic cholestasis are an indication for liver biopsy.

[18], [19], [20], [21], [22], [23]