Pathologic anatomy violations pigmentary exchange

Metabolic disorders pigments coming in excessive quantities into the body from outside, referred to as exogenous, and pigment formed in the body, is the endogenous pigmentations.
Exogenous pigmentation observed in professional diseases, such as pneumoconiosis (see), rarely with medication (preparations of silver, gold, bismuth and others).
Endogenous pigmentation is conventionally divided into autogenous and actually endogenous. The first associated with the production of pigments in neuroectodermal pigment cells localized in the skin of the nipple, anal, scrotum, in the mucous membrane of the large intestine, in the choroid, the iris, in the soft brain membranes and produce melanin (see). In fact endogenous pigments are formed as of tissue proteins (proteinogenic) with the participation of lipids (lipopigments), and directly from hemoglobin and products of its metabolism (hemoglobinuria).
Proteinogenic pigments and lipopigments together in a large group Angelo-globalagenda. These include carotenoids, lipochrome, lutein, lipofuscin, zeroed and agronomicheskaya pigment. Carotenoids - unsaturated carbon compounds, deprived of nitrogen, contain carotene and xenophile have photosensitizing properties, are capable of fluorescence, optical active. Carotene - orange-yellow pigment, the predecessor of vitamin a, is contained in vascular endothelium, yellow body of the ovaries, the adrenal gland, bone marrow, liver, heart, placenta, nervous tissue; serves as a source of formation of visual purple (the lack of it in the body leads to a chicken blindness). Carotenoids soluble in lipids cells and connecting with cholesterol can give lipochrome. Common lipochromes observed in diabetes mellitus. This lipogram is deposited in the endothelium of the capillaries of the brain and liver. The deposition of pigment in the skin turn yellow palms, soles, nose, nasolabial fold, face and ears. In severe cases, the palm take ohrany color (xanthosis diabetica). Limited lipochromes is manifested in the development of the so-called xanthelasma (see).
Very similar chemically to the lipofuscin (see) ceroid - shiny granules brownish-yellow, adapalene, acid, insoluble in fat. Color zeroed caused by oxidation products a highly saturated fatty acids. In the body it is deposited in the form of generalized and focal zerodata. In the pathogenesis of generalized zerodata plays the role of the human intake of fats and fat-soluble vitamins for chronic failure of the pancreas and the liver (experimentally diffuse zerodot can be induced in rats liver cirrhosis). The pigment is deposited in the smooth muscles of the gastrointestinal tract, the vascular membrane of the uterus. Muscle fibers thus shortened, swell, their nuclei arise dystrophic changes, until marialisa. Less zeroed is deposited in the cytoplasm phagocytes, coppersky liver cells, reticular cells of the lymph nodes. With limited forms zeroed determined oleogranulomas, atherosclerotic plaques in the brain when contusions near deposits of hemosiderin. The appearance in the organism agronomicheskaja pigment is accompanied by Ahronot (see).
To hemoglobinopathy pigments belong hemosiderin, hematoidin, enomelanin, bilirubin, hematoporphyrin. They are formed by extra - and intravascular destruction of red blood cells. Hemosiderin - grained, yellow-brown pigment containing iron, not soluble in water, alcohol, ether, alkalis, soluble in acids. Occurs when an intracellular enzyme systems in the outer area of the bleeding in the form of tracks are already in a day, and to 7-10 th day it is determined in large numbers. The pigment is localized in macrophages (brown induration lung macrophages containing hemosiderin, are called "cells cardiac defect"). Deposits can be focal and diffuse. In the latter case is common gemosideros with rusty colouring of the spleen, liver and skin. Occurs it with a massive intravascular destruction of red blood cells as a symptom of various diseases.
Hematoidin - crystalline pigment that does not contain iron, insoluble in water, alcohol, ether, soluble in chloroform, sulphur carbon; is formed without participation of the cells, when the hemorrhage is localized in the depth of focus, outside the cells, appearing to 6-7-th day, and there for two months.
In malaria circulating in the blood, the parasite occurs in the red blood cells and leads to the formation within them look like melanin pigment, called by analogy with enomelanin. In the period of the liberation of parasites of erythrocytes last destroyed and pigments in the form of black and brown beans that contain iron, into the blood, and from there to the reticulo-endothelial system. The spleen and liver while significantly increasing purchasing slate-grey. When comatose malaria smoky color takes on even the brain. Deposits enomelanin may be subject to reverse the development of education hemosiderin and bilirubin. Bilirubin is produced in cells of the reticuloendothelial system and in the blood is bound to serum albumin. It is assumed that in the destruction of the red blood cells formed verchromen that, losing iron, enters biliverdin, and the last - in bilirubin. Yellowish staining of tissue may be associated with impaired excretion of bilirubin and excessive his education (see Jaundice).
Hematoporphyrin - grained pigment, fluorescence close to bilirubin, contains iron, not defined histochemically. In the norm there are in a small amount in the blood and urine, playing the role of antagonist of melanin. The excess of hematoporphyrin in the blood with lead poisoning, sulfonamides, barbiturates, during avitaminosis (pellagra), liver failure due to violations of enzyme synthesis in the body, in congenital hereditary metabolic hemoglobin - the so-called congenital porphyria. It is noted diffuse the deposition of hematoporphyrin in the gastrointestinal tract (accompanied by diarrhoea), skin, bones, nervous system. The deposition of pigment in the skin accompanied by a sharp increase in the sensitivity to ultraviolet rays, until burns.