For normal metabolism and energy in the body, he needs constant supply of substrates from the outside, that is, with food, water and air. Their most important constituents are organic compounds, vitamins and mineral components - potassium, magnesium, sodium, copper, iron and many others. The last of these is included in the red blood cells, the only cells-carriers of oxygen in our blood, and therefore the exchange of iron is so important for the body. And with its violations one way or another develops icteric syndrome, characterized by the fact that bilirubin is common. Now let's look at all the important points.
Exchange of iron
Causes of 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 genesis, severe diseases of internal organs, malignant neoplasms. If the loss was insignificant, then it can replenish in a short time, and the patient does not have symptoms of its deficiency (sideropenic syndrome). However, there are also those diseases in which the volume of iron remains, but its exchange is sharply disrupted. To such cases the icteric syndrome of any genesis concerns, as at it the increase in the basic metabolite - bilirubin is revealed. To begin with, we will try to disassemble 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 exchange: first phase
The phases of neutralization and excretion of bilirubin
However, these proteins can not accompany it to the intestine, because they are still needed by the body for many other functions, and therefore bilirubin should be subjected to such transformations that it lost its property of passage into the cells. To do this, in hepatocytes (structural cells of the liver parenchyma), its conjugation occurs, that is, binding by glucuronic acid, which, to put it simply, makes it heavier. So, under the action of the enzyme UDF-glucuronyltransferase, bilirubin-diglucuronide is formed. Further from hepatocytes, it enters bile and in its composition is released into the intestines during digestion. Now, passing the path together with the food lump first into the thin and then into the large intestine, under the influence of the bacterial flora it is again released and transformed into urobilinogen, then into urobilin and sterocilin, which are directly excreted with feces. However, always an extremely small amount of bilirubin returns to the portal vein and is carried to the kidneys, where it is removed from the urine.
Limits of the norm
Disturbance of the metabolism of this important pigment can occur at three main stages: circulation in the blood during the decay of erythrocytes, capture in the liver and excretion with bile. However, for all these variants, it will be detected in the blood: bilirubin will be generally elevated, mainly by either a direct or indirect fraction. So, its normal concentration in the plasma is about 8.5-20 micromolar per liter. If this number increases to 85, then there is a state of mild hyperbilirubinemia, from 86 to 169 - the average and, finally, more than 170 μmol / l - severe. This is the case, if it is simply revealed that the total bilirubin is elevated. However, the norm exists separately for fractions: direct - up to 5.1, unbound - up to 16.5 micromol / l.
Superhepatic type of jaundice
So, if there is a violation at the first stage, bilirubin is generally increased in the blood mainly due to the indirect fraction. This is explained by the etiology of the condition, namely, the increased disintegration 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 the attack of their own red blood cells, the effects of toxins and poisons, viruses, bacteria and other microorganisms). Thus, the basis of pathogenesis is the increased formation of bilirubin, which is why the 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 their severe damage. This is how the superhepatic form of jaundice is formed.
Liver type of jaundice
Subhepatic type of jaundice
Causes of development
The etiology of the obturation or, as it is called, subhepatic, jaundice, is quite extensive. The most common cause is a blockage of the biliary tract by calculus in calculous cholecystitis or cholelithiasis, as well as helminthic invasion, when a lump of worms is localized within ducts or expressed cholangitis, when they are inflamed and the lumen is obturating either due to swelling of the walls or due to infiltration from them. And, of course, this explains the fact that direct and total bilirubin is elevated. The causes of other pathologies in any case are determined by compression from the outside. Most often this is observed because of the growing tumor process, which usually affects the head of the pancreas. But such a situation can also occur with biliary cirrhosis, when the ducts are squeezed by growing areas and connective tissue strands.
Physiological jaundice of newborns
Features of the blood circulation of newborns
The fact is that the blood circulation of the fetus in the womb is significantly different from that observed in already-born children. During pregnancy, the baby is immersed in a bladder with an amniotic fluid, and therefore his lungs are not yet familiar with the air and are in a shrunken state, that is, non-working. But in fact the child is vital to the constant supply of oxygen to his tissues for their formation, growth and differentiation. So his blood is so closely communicated with the mother. To put it in more detail, the baby's erythrocytes simply take oxygen from the erythrocytes of a woman, and for that they need a stronger ability that captures it. Therefore, its hemoglobin is represented by F-type, which means fetal. He easily receives oxygen and carries it to the cells of the fetus.
However, after birth, such a super-force is unnecessary, because from this time his lungs open, he breathes himself, and he himself extracts oxygen. And if his hemoglobin remains the same, he will not be able to give it to the cells. Therefore, after the first sigh, the active replacement of this main protein of erythrocytes from fetal to adult type A begins. This causes increased hemolysis of red blood cells and the urgent development of new, regular, from the bone marrow. Thus, jaundice is observed in the first, superhepatic type, which stops as soon as all old red blood cells are destroyed, and new ones fill the bloodstream.