19. Local hemosiderosis: causes, mechanisms of development. Macro- and microscopic changes in organs, detection methods. Examples of pathological processes.

Local hemosiderosis is a condition that develops with extravascular destruction of red blood cells (extravascular hemolysis) in hemorrhage foci.

Micro-: erythrocytes outside the vessels lose hemoglobin and turn into pale round corpuscles, free hemoglobin and fragments of erythrocytes go to build pigment. Leukocytes, histiocytes, reticular cells, endothelium, and epithelium become sideroblasts and siderophages.

Macro-: Siderophages can persist for a long time at the site of a former hemorrhage, they are often transferred by lymph current to nearby lymph nodes, where they linger, and the nodes become rusty.

Hemosiderin is formed in all hemorrhages, both small and large. In small hemorrhages, which are more often diapedetic, only hemosiderin is detected. Hemosiderin is formed along the periphery of large hemorrhages in living tissue, and hematoidin crystals appear in the center of the hemorrhage, where autolysis occurs without oxygen access and cell involvement.

Depending on the conditions of development, local hemosiderosis can occur within not only a tissue site (hematoma), but also an entire organ. This is the hemosiderosis of the lungs observed in rheumatic mitral heart disease, cardiosclerosis. Chronic venous congestion in the lungs leads to multiple diapedetic hemorrhages, which is why a large number of hemosiderin-loaded cells appear in the interalveolar septa, alveoli, lymphatic vessels and nodes of the lungs.

20. Pathology of hematins: types, structural features, examples of diseases. Macro- and microscopic changes in organs with the accumulation of malarial pigment.

Hematins are an oxidized form of heme, they are formed during the hydrolysis of oxyhemoglobin, they look like dark brown or black diamond-shaped crystals or grains. Hematins detected in tissues are hemomelanin (malarial pigment), hematin hydrochloric acid (gemin) and formalin pigment.

1.Hemomelanin (malaria pigment) is formed from the prosthetic part of hemoglobin under the influence of malaria plasmodium parasitizing in erythrocytes. When red blood cells are destroyed, the malarial pigment enters the bloodstream. It is phagocytized by macrophages of the spleen, liver, bone marrow, lymph nodes, and brain. Hemomelanosis develops, the organs acquire a slate-gray color. In them, along with the malarial pigment, hemosiderin deposition is observed.

2. Hydrochloric acid hematin (gemin) is found in erosions and ulcers of the stomach, where it is formed as a result of the action of enzymes of gastric juice and hydrochloric acid on hemoglobin. The area of the defect of the gastric mucosa acquires a brownish-black color.

3. Formalin pigment in the form of dark brown needles or granules is found in tissues when they are fixed in acidic formalin.

21. Jaundice: definition, classification, normal bilirubin metabolism. Prehepatic jaundice: causes, macro-, microscopic changes in organs, clinical signs, complications, outcomes.

A violation of bilirubin metabolism is associated with a disorder of its formation and excretion. This leads to an increased content of bilirubin in blood plasma and yellow staining of the skin, sclera, mucous membranes and serous membranes and internal organs, jaundice develops. The mechanism of jaundice development is different, which makes it possible to distinguish three types of jaundice: suprahepatic (hemolytic), hepatic (parenchymal) and subhepatic (mechanical).

Suprahepatic (hemolytic) jaundice is an increased formation of bilirubin due to increased breakdown of red blood cells. Under these conditions, the liver forms a larger amount of pigment than normal, but due to insufficient bilirubin uptake by hepatocytes, its level in the blood remains elevated.

Causes: Hemolytic jaundice is observed in infections (sepsis, malaria, recurrent typhus) and intoxication (hemolytic poisons), in isoimmune (hemolytic disease of newborns, drinking incompatible blood) and autoimmune (hemoblastosis, systemic connective tissue diseases) conflicts. Hemolytic jaundice may be caused by a defect in red blood cells. These are hereditary fermentopathin (microspherocytosis, ovalocytosis), hemoglobinopathies or hemoglobinoses (thalassemia or hemoglobinosis F; sickle cell anemia or hemoglobinosis S), paroxysmal nocturnal hemoglobinuria, the so-called shunt jaundice with vitamin 12 deficiency, some hypoplastic anemia.

Micro-: It can also develop in massive hemorrhages, hemorrhagic infarctions due to excessive bilirubin intake into the blood from the red blood cell breakdown site, where the bile pigment is detected in the form of crystals.

Macro-: The formation of bilirubin in hematomas is associated with a change in their color, jaundice staining of the skin, sclera, mucous membranes with a lemon-yellow tinge, there is often pallor of the skin and enlargement of the spleen (due to anemia).