Jaundice

What is Jaundice?

By jaundice we mean the yellowish and uniform color that the skin, the sclerae and other tissues take on in response to a pathological increase in blood bilirubin values, with consequent accumulation of the substance locally.

Similar symptoms, but less evident and mostly localized to the frenulum of the tongue and to the ocular sclerae, are also found in the presence of sub-jaundice (considered the "antechamber of actual jaundice").

In most cases, jaundice results from liver or gallbladder disease.

Causes of Yellow Skin

For further information: Yellow Skin

Apart from jaundice, the skin can take on a yellowish color in various conditions, such as carotenosis or the skin accumulation of urochrome or colors absorbed through the skin; in these cases - called pseudohythera - the chromatic alterations are distinguished from those typical of jaundice for the less uniformity and for the sparing of the ocular sclerae and mucous membranes.

Jaundice occurs when the circulating bilirubin in the blood (bilirubinemia) exceeds 2-2.5 mg per 100 ml, while sub-jaundice occurs when these values border the abnormality (1.5-2 mg / dl) without reaching this threshold; this allows to direct the patient towards an early diagnosis and thus undertake an adequate therapy to prevent its evolution.

Types of Jaundice

The classification of jaundice can be made on the basis of several elements. In relation to the serum concentration of bilirubin, for example, jaundice can be mild, medium or severe, while depending on the skin nuances we speak of flavin, rubinic, verdinic and melanic jaundice.

Causes

What is Bilirubin?

To understand the pathogenesis of jaundice it is necessary to know the metabolism of bilirubin, amply illustrated in the following article. Briefly, let us recall how this pigment deriving from the catabolism of aged red blood cells, is made water-soluble by the liver, which transforms it into direct bilirubin to facilitate its "urinary elimination. Once the jaundice has been recognized, it is therefore necessary to establish whether it is due to the excess of direct bilirubin (conjugated with glucuronic acid) or indirect (not yet processed by the liver); the orientation towards one or the other diagnosis, confirmed only by blood tests, can be based in the first instance on the physical examination of the urine: if these appear dark it means that the conjugated bilirubin is regularly eliminated, while the absence of the typical straw-yellow reflexes induces to think that something in the liver is not working properly. Similarly, it is good to remember that the typical staining of the stool is due to the chemical conversion of bilirubin into urobilin and stercobilin by intestinal bacteria and enteric enzymes.

Types of Jaundice

Obstructive jaundice

The premises of the previous chapter are particularly useful in "examining" obstructive jaundice, a condition in which the urine accentuates its color, while the faeces appear clear.

From what has been said, it is evident that in such situations the liver is able to perform its function (only the conjugated bilirubin is eliminated by the kidney), but that the outflow of bile towards the intestine is prevented.

This impediment can be caused by:

from "obstruction of the bile ducts (for example due to the presence of stones or sclerosing cholangitis)
or from liver diseases of various origins (hepatitis, liver cirrhosis) which hinder the excretion of bile from the liver (we can therefore have intra or extrahepatic obstructions).

Since the bile cannot leave the liver, we will have dark urine and light stools.

Obstructive jaundice, which is characterized by an increase in bilirubin levels direct in the blood, it allows us to make a further reference to human physiology; in fact, we remember how bile is essential for the digestion of fats, which is why in the presence of obstructive jaundice the stools, in addition to appearing clear, are rich in fats (steatorrhea). The symptomatological picture is completed by bradycardia and itching, due to the presence of bile salts in the circulation.

Hepatocellular jaundice

Hepatocellular jaundice is linked to the reduced function of liver cells; as such, it is characterized by an increase in bilirubin levels live in the bloodstream and can be caused by:

inability to pick up indirect bilirubin due to anatomical or functional deficit of two proteins, ligandins Y and Z, which retain it in the hepatocyte freeing it from albumin (to which it is associated in the bloodstream); this is the case of Gilbert's syndrome.
Inability to conjugate indirect bilirubin: for example in "neonatal jaundice (physiological condition especially typical of premature babies) or as a side effect of some drugs.
Congenital defect of the enzyme glucuronyltransferase (implicated in the salification of indirect bilirubin with glucuronic acid): Crigler-Najjar syndrome.

Hemolytic jaundice

In the hemolytic jaundice and in the overproduction of bilirubin, urine and faeces retain their color, which is often accentuated.

This condition is linked to the massive destruction of red blood cells (as in the presence of haemolytic anemia, a condition that can be caused by:

bacterial infections,
autoimmune or genetic diseases such as favism;
hyperfunctionality of the spleen)
an "ineffective erythropoiesis (pernicious anemia, thalassemias, leukemias, etc.)
an "increased production of bilirubin (in the liver or bone marrow).

In similar conditions, the liver increases the metabolism of unconjugated bilirubin (with hyperpigmentation of urine and faeces) but this is not enough to prevent its increase in circulation; therefore there is a jaundice with indirect hyperbilirubinemia.