As you study the patient with liver.

That is, everything you wanted to know about the liver from your doctor and have not had the courage to ask.

personal notes and reflections from experience dr. Claudio Italian, hepatologist

With this page, apologizing for Mr. hepatologists and gentlemen, we turn to the large audience of friends surfers, especially those who abuse alcohol, or eat badly, we continue to ask about scientific studies on how the patient's liver disease. In this first part we will discuss, in general, and briefly, investigation serum chemistry and how it approaches the patient's liver disease. Main topics, gradually leads to links which are listed below in the text. Deacon once that all comments are wrong, but rooted in the general public, that if I have a "bitter mouth" or lay "odor from the mouth" are sick and it takes me a liver detoxification with glutathione! How many patients come to my attention by glutathione vials made with care, vitamins and drugs for detoxifying the liver! The liver, once you are ill, have trouble, so we need to carefully read what's on this page and implement the hygiene standards of living and diet (see What foods to eat a proper diet? The concept of style life and the new food pyramid eggs, milk, yogurt and cheese: The nutritional value of cereals, these noble strangers to be invited to the table! fruits and vegetables: when, how and why, from patient to patient. fatty liver, which by ?).

.. One of the most serious problems to face, in fact, is the study of patients with liver failure and try to understand what treatments implemented by the signs. Basically, if I have a patient with cirrhosis, belly swollen with massive ascites, I do, how to treat ascites? And if, instead, I am a patient in front of his eyes yellow with jaundice, what? And if instead, another is to me and speaks of esophageal varices? As you can see the problems are many and the treatment is arduous. But we do not get discouraged and try to explain what we do, always taking into account that will be your doctor to have you treated us and not to cure you from this website because the information contained herein is simply reading!

So, in summary say that the liver has a "profile" in the sense that, like a beautiful woman, has a silhouette, a normal line and its physiological, that can be affected.

The profile control liver takes place after the control of:

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... The transaminases are enzymes located inside the liver cell and are precisely the AST in the cytosol and mitochondria in the cytoplasm while the ALT. So more damage while a damage free AST ALT less free. The monitoring of transaminases is essential for control of liver profile (AST, ALT, see approach to the patient), if these enzymes are elevated, such as x 2 or 3, then we think of chronic hepatitis, liver from alcohol (but we make differential diagnosis with the cytolysis of muscle cells, for example in myalgia rheumatica or in athletes after exercise, or to myocardial infarction), but if transaminases are definitely increased ox 15 x 10, then think of acute viral hepatitis (Hepatitis A Hepatitis B Hepatitis C Hepatitis acute hepatitis from drug poisoning or poison mushrooms etc..)

Serum bilirubin: is divided into direct or conjugated with glucuronic acid, ie a product produced by the liver that combines, that the bride and bilirubin bound to life with this carrier, and indirect, ie as a product of catabolism of red blood cells, which is not yet passed through the liver and has not yet been taken up by liver cells, hepatocytes. E 'increased especially in its share is often the first sign of liver distress, and rscontra in patients with jaundice, that is, with yellow eyes and skin, but may have an innocent meaning in prolonged fasting (cf. M. Gilbert) is the breakdown product of hemoglobin, because the liver is an organ emocateretico, ie a kind of scavenger body, which is responsible to clean the body of waste products represented by the aged red blood cells, which are replaced every three months from new. For precise information on bilirubin, I refer you to the page whose link is above, say here that bilirubin travels in the blood bound to albumin, as we travel in cars is a fat soluble substance and why it is not filtered by the kidneys but passes directly in bile and is excreted into the digestive tract through the bile ducts. Stones in the bile, therefore, its excretion is prevented, because the calculations may be impacted in the papilla of Vater and the toilet may be needed for the bile tract endoscopy (ERCP, or endoscopic retrograde pancretografia operational) to remove obstruction represented by the calculations and allow the excretion of bile and bilirubin, to resolve the condition of the patient's jaundice. In these cases, typically, the patient when the patient epigastric abdominal colic and right upper quadrant (see abdominal pain) and bilirubin, which is hovering around 60-10 mg%, the share of direct or conjugated bilirubin .

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.. The conjugated bilirubin, which was mentioned above, under normal conditions, once released from the liver, passes into the biliary tract, reaches the terminal ileum, where the bacteria separate from the carriers and pass faeces to color brown, which is good and right, while in acute hepatitis, in which the liver is unable to work because it is destroyed, and I am like clay, and you say acholic. Other times I have just black, as if the patient had consumed squid ink, and there is talk of melena (see upper intestinal bleeding), usually for gastric and duodenal ulcers or cancer of the upper tract. When bilirubin is indirect, however, think of hemolytic anemia or ineffective eritroiesi, that the body produces blood cells, but these are inadequate and are destroyed in steps through emocateretici organs, mainly liver and spleen and free bilirubin. Under the conditions of cirrhosis, biliary cirrhosis, sclerosing cholangitis, there will be significant increase in conjugated bilirubin or direct and this is due to the syndrome with ecstatic that the stasis of bile in the urinary tract.
Alkaline phosphatase, an enzyme localized in cell membranes canalicolari which different forms (isoenzymes). His determination is an expression of cholestasis, ie if there is obstruction in the bile is an increase of its production and the same happens in cholangitis, that is borne infectious processes of the biliary tract. If its development is driven by biliary stasis, then the other is the enzyme that increases 5-nucleotidase, otherwise you can think of other conditions such as increased absorption of bone, such as Paget's disease.

gammaGT, gamma-glutamyl transpeptidase: its increase occurs in conditions of cholestasis but also in pancreatic pain, in myocardial infarction in diabetes mellitus. It is also an excellent marker of alcoholism in the sense that the more you drink, the greater its value.

Group impairment: this involves checking and electrolytes, especially sodium and potassium in order to calibrate the diuretic treatment in patients with ascites (ascites and therapy). The patient with decompensated cirrhosis, in fact, have reduced renal excretion of sodium ions, which reduces up to 10 mEq / day, which added to other losses of the body brings it to 30-35 mEq / day. If the diet you make 130 or 260 mEq / day is easy to see that you go into positive sodium balance, resulting in water retention. Reduced renal sodium excretion is justified by the fact that several physio-pathological conditions influencing it, including the action of aldosterone on the distal renal tubule, resulting in reabsorption of sodium action that is reduced in cirrhosis, because the effective volume arterial blood with activation of the renin-angiotensin-aldosterone and consequent hyperaldosteronism. Furthermore, aldosterone in normal subjects and also degrades in the liver and cirrhosis in its catabolic elimination is reduced. The treatment of ascites therapy uses loop diuretics (furosemide) working on the elimination of sodium, plus the action of spironolattore and canrenoato. Determination of sodium, therefore, and potassium, as well as controlling blood urea nitrogen and creatinine mine, is the basis for monitoring of patients with cirrhosis.

Albumin, we have already spoken of this protein in the importance of this protein is very important for the homeostasis of the organism, protein, 69,000 daltons, produced by liver and vehicles, which owes its name to egg albumen, which is rich. The normal range of albumin concentration in the human body ranges from 3.5 to 5.0 g / dL, and constitutes approximately 60% of all plasma proteins, representing about 50% of the whole protein pool, which is essential to adjust and maintain plasma oncotic pressure or osmotic pressure necessary for proper distribution of body fluid compartments intervascolari. Put simply, the albumin is like a "magnet" intervascolare water, which draws the liquid into the bloodstream to the kidney and allows a more effective diuretic. For more insight we refer to the link specified on this website (albumin). Here, we will say, however, that albumin is used for monitoring of liver profile, ie for conditions of an insufficient liver, similar to the dose of pseudo-cholinesterase and attitude control of coagulation.

Weight of the patient with cirrhosis is the fundamental weight control of patients with liver failure in order to know if there was fluid retention. An increase of weight is always determined by sodium retention and accumulation of ascites.

Coagulation structure: mainly relies control of prothrombin. The liver produces many coagulation factors: fibrinogen, prothrombin, V, VI, VII, IX and X, which have short half-life. Except V, other factors are vitamin K dependent. The prothrombin time is useful in determining the severity and prognosis and the prognosis of liver disease. The use of oral vitamin K is often in itself sufficient to control the trim dell'epatopaziente coagulation.


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