For a normal metabolism and energy in the body, he needs a constant supply of substrates from the outside, that is, with food, water and air. Their most important components are organic compounds, vitamins and mineral components - potassium, magnesium, sodium, copper, iron and many others. The last of these is part of red blood cells, the only oxygen-carrying cells in our blood, and therefore iron metabolism is so important for the body. And with its violations, one way or another, icteric syndrome develops, characterized in that the total bilirubin is elevated. Now we will understand all the important points.
Iron exchange
Man receives iron exclusively with food. Its highest concentration is observed in the liver of animals, some nuts (pistachios, peanuts, cedar, cashews), legumes (lentils, peas), cereals (buckwheat, wheat, oats, barley), spinach, and corn. At the same time, its necessary amount for the heme, which forms the basis of the red blood cell, is first replenished, and only then iron is deposited in its depot in our body, which is about 3-4 grams, it is ions bound mainly by plasma proteins and enzymes (ferritin, transferrin, xanthine oxidase, ferroflavoproteins, succinate and NADH dehydrogenase and others). But this is normal, now let's look at its losses and some pathological conditions.
The reasons for the loss of important minerals
One of the physiological processes in which iron loss occurs is menstruation and pregnancy in women. However, perhaps the most significant situations are blood loss, intoxication, anemia of various origins, severe diseases of internal organs, malignant neoplasms. If the loss was insignificant, then it manages to be replenished in a short time, and at the same time the patient does not have symptoms of his deficiency (sideropenic syndrome). However, there are those diseases in which the volume of iron is preserved, but its metabolism is severely impaired. Such cases include icteric syndrome of any genesis, since it reveals an increase in the main metabolite - bilirubin. To begin with, we will try to analyze its metabolism in the body and the causes of increased bilirubin in the blood: this is important for understanding the pathogenesis of these diseases.
Hemoglobin metabolism: first phase
Bilirubin is one of the most important pigments that make up bile and is excreted from the body precisely at its expense. It goes a long way through the vessels even in the form of hemoglobin, undergoes important transformations in hepatocytes and, finally, is secreted into the intestine for excretion into the environment with feces. So, this substance is formed during the breakdown of red blood cells and is immediately captured by carrier proteins for transport to the main laboratory - the liver. This fraction is called indirect or unbound, because the bilirubin in it is unchanged. This happens because in its free form it easily penetrates through the membranes of any cells and has a pronounced toxic effect primarily on neurons. Thus, its capture is a normal protective reaction.
Phases of neutralization and allocation of bilirubin
However, these proteins cannot accompany it to the intestines, because the body still needs them for many other functions, and therefore bilirubin must be subjected to such transformations so that it loses its property of passage into cells. To do this, in hepatocytes (structural cells of the liver parenchyma), it is conjugated, that is, binding by glucuronic acid, which, to put it simply, makes it heavier. Thus, under the action of the enzyme UDP-glucuronyl transferase, bilirubin-diglucuronide is formed. Further, from hepatocytes, it enters the bile and in its composition is excreted into the intestines during digestion. Now, going along with the food lump, first into the small and then into the large intestine, under the influence of the bacterial flora, it is again released and converted into urobilinogen, then into urobilin and sterkobilin, which are directly excreted in the feces. However, always an extremely small amount of bilirubin returns to the portal vein and is carried out to the kidneys, from where it is removed with urine.
Normal limits
Impaired metabolism of this important pigment can occur at three main stages: circulation in the blood during the breakdown of red blood cells, capture in the liver and excretion with bile. However, with all these options, it will be detected in the blood: the total bilirubin will be increased, mainly either due to its direct, or due to its indirect fraction. So, its normal plasma concentration is about 8.5-20.5 micromoles per liter. If this number increases to 85, then a state of mild hyperbilirubinemia occurs, from 86 to 169 - moderate and, finally, over 170 μmol / l - severe. This is the case if it is simply revealed that the total bilirubin is elevated. However, the norm also exists separately for fractions: direct - up to 5.1, unbound - up to 16.5 μmol / l.
Suprahepatic type of jaundice
So, in case of violation at the first stage, the total bilirubin in the blood is mainly due to the indirect fraction. This is explained by the etiology of the condition, namely, the increased decay of red blood cells in the vascular bed. This can occur with congenital forms of hemolytic anemia (defects at the genetic level of the red blood cells themselves, their enzymes, hemoglobin) or acquired (immunological diseases with attack of their own red blood cells, exposure to toxins and poisons, viruses, bacteria and other microorganisms). Thus, the pathogenesis is based on the increased formation of bilirubin, which is why liver cells simply do not have time to capture such a huge amount of it, and it accumulates in the skin and mucous membranes, and then in the internal organs, causing severe damage. So the suprahepatic form of jaundice is formed.
Hepatic type of jaundice
If the violation occurs in the second main stage, then the hepatocytes do not have time to capture and process even the normal amount of hemoglobin metabolite entering them, and as a result, the total bilirubin is increased due to both fractions. The reasons for this are severe destructive changes in the liver. These include hepatitis of various genesis (toxic, alcoholic, viral) and cirrhosis. Thus, the causes of increased bilirubin in the blood lie in the fact that hepatocytes cannot work adequately, either due to inflammation in them, or due to their insufficient number. The most common cause, of course, is A-type
viral hepatitis , B, C, delta, E or PP. This is how the hepatic (parenchymal) type of icteric syndrome develops, which is accompanied by vivid symptoms of mesenchymal inflammation and hepatociliary insufficiency.
Subhepatic type of jaundice
And, of course, a violation of bilirubin metabolism can occur at the third main stage, that is, with the excretion of bile. One way or another, with this option, its output is blocked along the pathways either from the liver, or already from vesicafellea. As a result of such changes, bile accumulates in the ducts and bladder, its pressure gradually increases, and as a result, it returns (this phenomenon is called regurgitation) to the intrahepatic ducts and further to the blood vessels, which is why total bilirubin is increased. In this case, of course, there are other changes in biochemical analyzes. So, cholemia occurs in the blood, that is,
bile acids and enzymes enter it, and cholestasis forms in the ducts themselves, that is, stagnation of the secret. Clinically, this will be expressed by jaundice of the sclera, mucous membranes and skin (yellowish with a green tint), and in the analyzes there will be not only general and direct bilirubin elevated, but also bile acids, cholesterol,
alkaline phosphatase level
, triglycerides, gamma-glutamyl transferase activity .
Development reasons
The etiology of obstructive or, as it is also called, subhepatic, jaundice, is quite extensive. The most common cause is stone blockage of the biliary tract during calculous cholecystitis or gallstone disease, as well as helminthic invasion, when a lump of worms is localized inside the ducts or pronounced cholangitis, when they are inflamed and the lumen is obstructed either due to swelling of the walls or due to infiltration of them. And, of course, this explains the fact that direct and total bilirubin is elevated. The causes of other pathologies, in any case, are caused by compression from the outside. Most often this is due to an increasing tumor process, usually affecting the head of the pancreas. But also such a situation can occur with biliary cirrhosis, when the ducts are compressed by the growing sections and cords of the connective tissue.
Physiological jaundice of newborns
However, not all jaundice are pathological conditions of the body. So, if total bilirubin is elevated in a child immediately at birth or several hours after it, and the skin and mucous membranes have a bright icteric hue, then do not immediately sound the alarm. Indeed, in newborns, this is a physiological state called transient, since it is transient. Of course, the question arises of his worried mother, who finds out that her child has increased bilirubin: "What to do?" The answer is simple: wait. In this case, only wait-and-see tactics are really shown, because over the course of several days (usually up to three to five), yellowness gradually disappears. And only if it is delayed, the baby's condition worsens, and the overall bilirubin remains elevated, the treatment is carried out urgently, namely, detoxification therapy and ultraviolet radiation are used. Now let's look at the pathogenesis of this condition.
Features of the blood circulation of newborns
The fact is that the blood circulation of the fetus in the womb is significantly different from what is observed in already born children. During pregnancy, the baby is immersed in a bubble with amniotic fluid, and therefore his lungs are not yet familiar with the air and are in a shriveled state, that is, inoperative. But a child really needs a constant supply of oxygen to his tissues for their formation, growth and differentiation. And therefore, his blood is so closely connected with the mother. In more detail, the baby’s erythrocytes simply take oxygen from a woman’s erythrocytes, and for this they need a more powerful exciting ability. Therefore, its hemoglobin is represented by the F-type, which means fetal. It easily receives oxygen and carries it to the cells of the fetus.
Summary
However, after birth, such his superpower is unnecessary, because from then on his lungs open, he breathes independently, and produces oxygen for himself. And if his hemoglobin remains the same, then he will not be able to give it to the cells. Therefore, after the first breath, an active change of this main erythrocyte protein from fetal to adult begins - type A. This determines the increased hemolysis of red blood cells and the urgent production of new, regular ones from the bone marrow. Thus, jaundice is observed in the first, suprahepatic type, which stops as soon as all the old red blood cells are destroyed, and new ones fill the bloodstream.
Therapy
The most important step in the treatment of elevated bilirubin is, of course, the treatment of the underlying disease that caused such metabolic disturbances, i.e. antibiotics for viral hepatitis, detoxification for poisoning with poisons, blood and red blood cell transfusion during hemolysis, or
liver transplantation for severe cirrhosis. However, physiotherapy, hepatoprotectors, a correct lifestyle without risk factors, and a special diet with
increased bilirubin should support this
. For this, firstly, it is necessary to give up smoking and alcohol, excess fat, cholesterol, spicy and fried foods. It is strictly forbidden to use pickles and pickled products. Salt and tea should be limited, and coffee should not be drunk at all. On the contrary, a diet with increased bilirubin includes frequent fractional nutrition with an increase in the number of lean porridges, compotes, and the replacement of white bread with gray. Indeed, thanks to the medications prescribed by the doctor, positive dynamics will begin and, ultimately, the disease will leave you.