Practical class 3 Metabolic disease. Morphology of pathologic accumulation of endogenous and exogenous pigments. Morphology of mineral metabolism disease icon

Practical class 3 Metabolic disease. Morphology of pathologic accumulation of endogenous and exogenous pigments. Morphology of mineral metabolism disease




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Practical class 3

Metabolic disease. Morphology of pathologic accumulation of endogenous and exogenous pigments. Morphology of mineral metabolism disease


Importance of the topic: metabolic disease rather often occurs in practice of clinicians and should be considered as a manifestation of general pathologic processes. Often it occurs at endocrine diseases, as well as at pathology of gastrointestinal tract and hepatobiliary system and it reveals through structural morphologic changes. Knowledge of issues of this topic enlarges the minds of would-be clinicians concerning the kind of changes that underlie various pathologic processes at one or another disease.

Purpose: to study causes, development mechanism, morphologic manifestations and consequences of accumulation of endogenous and exogenous pigments, as well as mineral metabolism disease.

Specific goals: 1 To learn varieties of metabolic diseases and their development mechanisms.

2 To study causes, development mechanism, pathogenesis and morphogenesis, morphologic presentations and consequences of accumulation of endogenous and exogenous pigments, as well as mineral metabolism disease.

3 To learn to differentiate various kinds of pigment metabolic diseases and mineral metabolism diseases according to morphologic signs.

4 To evaluate functional importance and consequences of accumulation of endogenous and exogenous pigments, as well as mineral metabolism diseases, to know how to diagnose their morphologic manifestations in cells and tissues.



^ Basic matters for self-training


Iron metabolic disease and metabolic disorder of hematogenous pigments. Metabolism and pathogenic action of iron, formation of anabolic and catabolic ferritin. Classification of hematogenous pigments. Toxic forms of ferritin: causes and consequences of their formation.

Hemosiderosis (topical and extensive): causes, pathogenesis, morphologic characteristics and consequences. Acquired and congenital hemochromatosis: morphologic characteristics and consequences.

Hematoidin, hematin, porphyrin: features and area of formation, morphologic characteristics and consequences of their accumulation.

Bilirubin metabolic disease: causes, pathogenesis and anatomical pathology of hemolytic jaundice, hepatic jaundice, obstructive jaundice. Pathogenic effect of increased bilirubin, complications and causes of death at jaundice.

Melanin formation disorder. Causes, pathogenesis, morphologic characteristics of hypopigmentation (leukoderma, vitiligo, albinism) and hyperpigmentation (common melanoderma, local melanosis, pigmented nevus).

Nucleoprotein metabolic disease. Podagra and gouty arthritis: classification, aetiology, pathogenesis, stage of disease and morphologic characteristics of joints’ changes, clinical presentations, complications and consequences. Podagric nephropathy. Clinicopathologic characteristics.

Copper metabolic disease. Hepatolenticular degeneration (Wilson's disease).

Potassium metabolic disease. Periodic paralysis.

Calcium metabolic disease. Acute hypocalcemia and hypercalcemia: definition, pathogenesis, consequences and their role in thanatogenesis. Calcinosis (calcification): definition, classification, morphogenesis of metastatic calcification, dystrophic calcification and metabolic calcinosis; consequences, the role of calcification of organs in thanatogenesis.

Stone formation: localization, causes, pathogenesis, types of stones, consequences and complications of stone formation.

І Auxiliary materials for self-training to practical lesson

Pathologic accumulation of endogenous pigments rather often is represented in metabolic disease of complex proteins – chromoproteins, nucleoproteins, glucoproteins and lipoproteins. Chromoproteins, or colored proteins, are endogenous pigments, to which hematogenous, proteinogenous and lipidogenous pigments are referred. Metabolic disease of complex proteins is observed in parenchyma, as well as in stroma of tissues and organs.


^ Iron metabolic disease and metabolic disorder of hematogenous pigments

Ferritin, hemosiderin, bilirubin are referred to hematogenous pigments. There are pigments which may be accumulated in organism at physiological conditions and at some diseases; hematoidin, hematin, porphyrin are pigments which are formed only at pathologic processes. They are generated from hemoglobin at destruction (hemolysis) of erythrocytes.


Ferritin is generated from hemoglobin at intensive intravascular hemolysis of erythrocytes – catabolic form. Anabolic form is generated from iron absorbed in bowels . At conditions of hypoxia ferritin is restored into an active form (SH-ferritin) which is an adrenalin antagonist, that’s why it acts vasoparesically, i.e. as vasodilator. An active ferritin is accumulated at incompatible blood transfusion and collapse of vessels is observed, then a syncope takes place.


Hemosiderin is generated from hemoglobin only in macrophages (intracellularily). It appears outside the cell only after cell destruction. It looks like small brown seeds; tissue acquires brown coloration at evident hemosiderosis. One can distinguish common and topical hemosiderosis. Common hemosiderosis is developed at intensive intravascular hemolysis of erythrocytes (incompatible blood transfusion, hemolytic poisoning). Unconjugated hemoglobin is captured by macrophages of unitary mononuclear phagocyte system of liver, spleen, lymph nodes, bone marrow, thymus gland in which hemoglobin turns into hemosiderin. Listed organs acquire brown coloring.

Topical hemosiderosis arises at areas of extravasation. Erythrocytes are absorbed outside the vessels by macrophages, in which hemoglobin turns into hemosiderin. An example of topical hemosiderosis is pulmonary hemosiderosis which is developed at venous plethora of lungs accompanied by diapedetic extravasations.

Hemochromatosis is a peculiar disease closely related to common hemosiderosis. There could be primary and secondary one. Primary (hereditary) hemochromatosis is referred to storage diseases, caused by a hereditary defect of small intestine ferments. A secondary one is conditioned by acquired enzymatic deficiency of systems providing food iron metabolism.


Bilirubin is a bile pigment generated at destruction of hemoglobin and detachment of haem in reticulum- endothelial (mononuclear) system. Increased bilirubin (bilirubinhemia) is evidence of jaundice. One can distinguish hemolytic jaundice, hepatocellular jaundice and obstructive (mechanical) jaundice. Hemolytic jaundice arises at infectious diseases, intoxications, isoimmune and autoimmune conflicts, massive hemorrhage, as well as erythrocytopathy and hemoglobinopathy.

Hepatocellular jaundice arises at liver diseases of various aetiology, in case defective hepatocytes are not able to capture bilirubin, its conjugation to glucuronic acid and excretion are disturbed. Obstructive (mechanical) jaundice arises at retention of bile outflow from liver.


Hematoidin is a pigment which doesn’t contain iron. It is accumulated in central areas of hemorrhage in the distance of living tissues.


Hematin – is an oxidized form of haem. The following pigments are referred to: malarial pigment which is generated from hemoglobin under influence of malarial plasmodia, muriatic hematin which is generated at hemoglobin interaction with intestinal juice ferments and hydrochloric acid (it colours erosions and bottom of bleeding ulcer into black and brown), as well as formalin pigment which occurs in histologic specimen fixed by acid formalin.


Hematoporphyrin is a pigment which is melanin antagonist. Its small quantity is contained in blood, urine and stool, it heightens light sensibility of skin. Excess accumulation of this pigment is called porphyria. It could be caused by congenital defect of porphyrin metabolism or acquired one: lead or barbiturate poisoning, avitaminosis PP, etc. Such patients are UV hypersensitive which causes burns, ulcers, skin atrophy and depigmentation. Bones and teeth are coloured into brown.



^ Metabolic disorder of proteinogenous pigments. Melanin chromogenesis disorder.

Melanin, as well as adrenochrome and pigment of enterochromaffin cell granules are referred to proteinogenous (tyrosinogenous) pigments which are tyrosine and tryptophan metabolic derivatives.

Melanin is a brown-black pigment which determines color of skin, hair and eyes. Melanin chromogenesis disorder could appear in increase or decrease of this pigment in skin. There could be local or extensive process. There could be congenital or acquired pathology. Extensive hypopigmentation or hypomelanosis (albinism) appears as a result of hereditary deficiency of tyrosinase. Local hypomelanosis (vitiligo, leukoderma) appears as a result of disorder of neuroendocrine control of melanogenesis at leprosy, diabetes mellitus, hyperparathyroidism, Hashimoto's thyroiditis, syphilitic skin affection. Extensive acquired hypermelanosis declares itself in excessive accumulation of melanin in skin (melanoderma) and is observed at emaciation, Addison's disease, endocrine disorders, pellagra, scurvy. Extensive congenital hypermelanosis declares itself in spotted skin pigmentation, hyperkeratosis and edema – pigmentary xeroderma. Local congenital hypermelanosis is represented by birthmarks or nevus, acquired one is observed at pregnancy, pituitary adenoma, lentigo, melanosis coli at constipation.


Adrenochrome is an adrenalin oxidation product. It occurs in the form of granules in cells of medullary substance of adrenal glands.


^ Pigment of enterochromaffin cell granules occurs in cells of diffuse endocrine system: enterochromaffin cells of stomach, bowels, B and C cells of thyroid gland, cells of juxtaglomerular apparatus of kidney, cells of Langans’s islands of pancreas. It is considered to be a serotonin analog. Carcinoids or tumors made of above mentioned cells possess a significant serotonin activity. In such cases patients get carcinoid syndrome.


^ Metabolic disorder of lipidogenous pigments

Lipofuscin and lipochromes are referred to lipidogenous pigments.


Lipofuscin is a pigment of goldish colour. Its perinuclear location is an evidence of active metabolic processes. Its accumulation (lipofuscinosis) at the periphery of a cell is an evidence of activity decrease of respiratory ferments in a cell. Lipofuscinosis is occurred at aging, cachexy. The organs are colored into brown – brown atrophy of myocardium, liver.


Lipochrome colours lipocytes, adrenal gland cortex, blood serum, yellow body of ovary into yellow. At pathologic conditions the quantity of lipochromes is increased in fatty tissue at diabetes mellitus, lipidic-vitaminous metabolic disorder, drastic emaciation.


^ Metabolic disorder of nucleoproteids

It could be often observed at excessive formation of uric acid and its salts which determines development of podagra, urolithiasis, uric acid infarct. At most cases pathology is determined by congenital purine metabolic disorder. Over-use of animal proteins, kidney diseases are of a significant importance for disease pathogenesis. Uric acid sodium deposits in joints (synovial membrane, articular cartilages of hands and feet), synovial membranes of tendon with necrosis areas developed, granulomatosis giant-cell reaction, painful arthroliths, deformation of joints are typical for podagra and gouty arthritis. Podagric nephropathy – uric acid salt deposits in ducts and gathering tubes with obstruction of their lumens and inflammatory, sclerotic and atrophic changes – arises as complication.


^ Copper metabolic disorder

It could be most often observed at hereditary hepatolenticular degeneration or Wilson's disease. Copper accumulation is observed in liver, brain, kidneys, pancreas,


Potassium metabolic disorder cornea – typical green-brown Kaiser- Fleischer ring at the periphery of cornea. Dystrophic and sclerotic changes are the result of copper accumulation in organs.

It could declare itself in increase of potassium in blood and tissues which is observed at Addison’s disease as result of affection of adrenal glands. Decrease of potassium causes periodic paralysis – fit of weakness and motor paralysis development.


^ Calcium metabolic disorder

It could declare itself in increase or decrease of calcium concentration in blood (hypocalcemia and hypercalcemia). Calcium metabolic disorder results in development of calcifications (calcinosis) – calcium salts deposits in intercellular substance or cells, that’s why calcifications are divided into intercellular and extracellular ones. According to development mechanism there are metastatic, dystrophic, metabolic calcifications. Calcifications also could be systemic or local.

^ Metastatic calcifications are more often systemic and appear at hypercalcemia caused by the following:

  • disorder of endocrine control of calcium metabolism (hyperproduction of parathyroid hormone, calcitonin deficiency), excessive vitamin D content;

  • intensive calcium excretion from bones (multiple fractures, myelomatosis, tumor deposits of bones, osteomalacia, hyperparathyroidic osteodystrophy);

  • disorder of calcium excretion from organism (colonic involvement, chronic dysentery, mercuric chloride poisoning, kidney diseases: polycystic renal disease, chronic nephritis).

Most often there are calcium salts deposits in lungs, mucous coat of stomach, kidneys, miocard, walls of arteries.


^ Dystrophic calcifications or petrifications are of local character and result in calcium salts deposits formation in necrosis areas or areas of severe dystrophic changes of tissues (tuberculosis, gumma, infarction, atherosclerosis of vessel wall, mitral valve at endocarditis, dead parasites).

Change of physicochemical composition of tissues and local increase in phosphatase activity determine their development, there is no hypercalcemia observed at the same time.


^ Metabolic calcinosis appears at instability of buffer systems of organism (calcium gout, interstitial calcinosis). Consequences of calcifications are unfavorable in most cases.


Stone formation is appearance of solid concrements in caval organs or excretory ducts of glands. Stones appear in biliary and urinary tracts, excretory ducts of pancreas and salivary glands, bronchi and bronchiectasis, as well as in vessels and bowels. Stone formation is caused by acquired or hereditary metabolic diseases (metabolic disorders of carbohydrates, fats, nucleoproteins, minerals). Among local factors there are secretion disorder, secretion congestion, inflammation. Depending on localization and form of organ in which stones appear there are solitary, multiple, round, oval stones, stones with processes, cylindrical, smooth and shaggy stones. Cholelithic disease and urolithiasis, pressure bedsore, perforation of organs, fistulas, inflammation of walls of caval organs, jaundice, hydronephrosis are the consequences of stone formation.


^ II Algorithm of practical part of the lesson

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