Mixed dystrophies ( parenchymal-mesenchymal dystrophies , parenchymal-stromal dystrophies ) are dysmetabolic processes that develop in both the parenchyma and the stroma of organs .
Classification
Mixed dystrophies are classified as follows:
I. Disorders of the metabolism of complex proteins
- Endogenous pigmentation - metabolic disorders of chromoproteins
- Uric acid diathesis - disorders of the metabolism of nucleoproteins
- Disorders of lipoprotein metabolism (primarily cholesterol- containing lipoproteins).
Ii. Mineral metabolism disorders ( mineral dystrophies )
- Metabolism disorders of mineral macronutrients ( potassium , sodium , calcium , magnesium , phosphorus , chlorine , sulfur )
- Microelementoses - metabolic disorders of trace elements ( iron , copper , manganese , selenium , silicon, and others).
Previously, the term “proteids” (lipoproteins, nucleoproteins, chromoproteins, etc.) was used to designate complex proteins . In 1985 , the International Union of Theoretical and Applied Chemistry recommended naming complex proteins using the suffix "-in" (lipoproteins, nucleoproteins, chromoproteins, etc.), and fixing the notion " proteids " with protein-like substances.
Among the mineral macroelementoses, calcium metabolism disorders are of primary importance for human pathological anatomy, and among the microelementosis, metabolic iron and copper metabolism . Mineral dystrophy also includes the formation of stones ( stones ).
Endogenous pigmentation
Endogenous pigmentation is a metabolic disorder of chromoproteins ( endogenous pigments ) and their metabolites. Endogenous pigments are called dyed proteins or metabolic products of amino acids, which are formed in the body. In contrast, exogenous pigments denote colored substances that enter the human body from the external environment.
Classification of endogenous pigmentation
The main forms of metabolic disorders of chromoproteins are the following pathological processes:
- Hemosiderosis
- Icteric syndrome
- Porphyrias
- Melanin metabolism disorders
- Lipofuscinosis.
Hemosiderosis
Hemosiderosis - an increase in the content of ferritin and hemosiderin in the tissues. Deposition in organs (liver, pancreas, myocardium) of these pigments results in progressive destruction of parenchymal cells, substitution of fibrous connective tissue ( cirrhosis of the liver , pancreas fibrosis, cardio ) and development of a functional organ failure (chronic hepatic and cardiac insufficiency , diabetes ) .
Classification of hemosiderosis forms
There are general and local hemosiderosis. A special form of general hemosiderosis is hemochromatosis .
I. General hemosiderosis
- Caused by hemolysis
- Hemochromatosis (primary hemochromatosis and acquired forms)
Ii. Local hemosiderosis
- In areas of hemorrhage and in the tissue of regional lymph nodes
- Pulmonary hemosiderosis (hereditary forms and brown induration)
General hemosiderosis
General hemosiderosis (widespread hemosiderosis) - hemosiderosis due to intravascular or pronounced extravascular hemolysis.
Intravascular hemolysis develops with:
- intoxication (snake venom, benzene derivatives),
- infections (malaria, septicemia),
- immunopathological (for example, autoimmune) processes.
Pronounced extravascular hemolysis occurs with multiple extensive hemorrhages. Mostly catabolic ferritin and hemosiderin are deposited in organs and tissues rich in macrophages that come in contact with blood (in the liver, spleen, lymph nodes, bone marrow), so they turn bright brown and brown in color (their fabric becomes “rusty”). A microscopic examination of macrophages ( sideroblasts ) and in the extracellular substance reveals numerous brown granules, which are stained in the Perls reaction .
Hemochromatosis
Hemochromatosis is a common hemosiderosis, in which anabolic ferritin and hemosiderin formed from it accumulate in tissues due to enhanced absorption of nutritional iron in the small intestine. There are hereditary ( primary ) and acquired ( secondary ) hemochromatosis. Primary hemochromatosis is an independent disease and is formed in childhood. Secondary hemochromatosis occurs, as a rule, in adults, complicating any other diseases, surgical interventions and drug therapy.
I. Hereditary hemochromatosis ( primary hemochromatosis , " bronze diabetes ").
Ii. Acquired hemochromatosis ( secondary hemochromatosis )
- Alcohol hemochromatosis
- Postgastroectomy hemochromatosis
- Medicinal hemochromatosis .
Primary hemochromatosis. A feature of hereditary hemochromatosis is an increase in the content in the tissues of not only ferritin and hemosiderin, but also melanin (in the skin) and lipofuscin (in the internal organs). The disease manifests itself in three major syndromes: (1) bronze dermatosis (darkening of the skin due to increased melanin production), (2) secondary diabetes mellitus , developing as a result of pancreatic lesions, and (3) liver pigmented cirrhosis . The first two syndromes caused another name for the disease - bronze diabetes . In addition, in some cases, there is (4) severe heart damage ( pigmented cardiomyopathy ).
Secondary hemochromatosis is most common in chronic alcoholism (alcoholic hemochromatosis), after surgical removal of the stomach (postgastroectomy hemochromatosis), and with the abuse of iron preparations (drug hemochromatosis).
Local Hemosiderosis
Local hemosiderosis develops in areas of hemorrhage (“old” hemorrhages), in lymph nodes, regional to the site of hemorrhage, and also in the lungs ( pulmonary hemosiderosis ).
There are two options for hemosiderosis of the lungs - hereditary and acquired.
I. Hereditary pulmonary hemosiderosis
- Goodpasture syndrome
- Selena-Gellerstedt disease .
Ii. Acquired pulmonary hemosiderosis ( brown induction of the lungs ) in chronic heart failure.
Hereditary pulmonary hemosiderosis is characteristic of two rare diseases: Goodpasture pneumorenal syndrome , in which, in addition to the lungs, kidney damage is observed, and Selena-Gellerstadt disease . In these diseases, repeated hemorrhages in the lung tissue develop, resulting in hemosiderosis. Acquired lung hemosiderosis is formed in patients with chronic heart failure syndrome and is called brown lung induration .
Jaundice syndrome (icterus)
Yellow syndrome ( icterus ) - accumulation of bilirubin in the tissues.
Jaundice classification
There are three pathogenetic types of icteric syndrome:
I. Hemolytic jaundice .
Ii. Parenchymal jaundice
- Hereditary parenchymal jaundice
- Acquired parenchymal jaundice .
Iii. Mechanical jaundice
- Obstructive jaundice
- Compression jaundice .
Hemolytic jaundice
Hemolytic jaundice develops as a result of intravascular or pronounced extravascular hemolysis. More often it accompanies hemolytic anemia .
Parenchymal jaundice
Parenchymal jaundice - jaundice due to impaired bilirubin metabolism in hepatocytes (the main parenchymal cells of the liver). Parenchymal jaundice may be hereditary ( hereditary hepatic hyperbilirubinemia ) and acquired (hepatitis, hepatosis, liver cirrhosis, liver tumors and other acquired liver diseases).
I. Hereditary parenchymal jaundice
- Gilbert's syndrome — Lilestrand — Meulengracht
- Kriegler-Nayyar syndrome
- Dabin-Johnson syndrome (" black liver disease ")
- Rotor Syndrome .
Ii. Acquired parenchymal jaundice .
Hereditary parenchymal jaundice occurs in the following diseases: (1) Gilbert's syndrome — Liléstrand-Meilengracht (this disrupts the first stage of the exchange of bilirubin in hepatocytes - the absorption of unconjugated bilirubin from the blood from sinusoidal cells in the form of the card, I am not using the card ) , I am using the options I’m using the card, I’m not using this option to make use of the following options: bilirubin in hepatocytes — conjugation of bilirubin with two glucuronic acid molecules and the formation of bilirubin-diglucuronide), (3) Dabin – Johnson syndrome and (4) Rotor syndrome (the third stage of bilirubin metabolism in hepatocytes is disturbed - excretion of conjugated bilirubin to bile). Dabin-Johnson syndrome differs from Rotor syndrome in the presence of dark lipofuscin in the liver, which gives the body an almost black color (" black liver disease "). All of the above syndromes, with the exception of the severe form of Crigler-Nayar syndrome, proceed easily, and there are often no signs of liver failure. The severe form of Crigler-Nayar syndrome is fatal in the first weeks or months of life.
Mechanical jaundice
Mechanical jaundice is a form of jaundice that develops when the outflow (passage) of bile is difficult. Obstructive jaundice is divided into obstructive and compression variants.
1. Obstructive jaundice - obstructive jaundice that develops when there is an obstruction in the flow of bile inside the duct (stone, exophytic tumor, cicatricial stenosis, cytomegalovirus cholangiohepatitis, cystic fibrosis).
2. Compressed jaundice - mechanical jaundice due to compression (compression) of the bile ducts from the outside (tumor, ligature, regenerating nodes in liver cirrhosis, etc.).
With prolonged obstructive jaundice in the liver, (1) cholestasis develops (bile capillaries and ducts overflow with bile and expand) and (2) biliary necrosis (tissue necrosis , infiltrated bile, when the wall of the bile ducts ruptures). Increasing the pressure of bile in the ducts leads to the secretion of its components into the blood through the sinusoidal pole of the hepatocyte, cholemia occurs. Biliary necrosis in the liver is replaced by coarse-fibrous connective tissue, as a result of which cirrhosis of the liver, which is called secondary biliary cirrhosis, can develop. Cholemia causes (1) general intoxication, (2) pruritus and (3) hemorrhagic syndrome. The most aggressive components of bile are bile acids (their presence in the blood is denoted by the term holleemia ). Bile acids due to the detergent effect cause the destruction of tissue elements, in particular, the structures of the vascular wall, which underlies the hemorrhagic manifestations of obstructive jaundice.
Porphyrias
Porphyrins are pathological processes by which porphyrins accumulate in tissues.
Porphyry Classification
There are hereditary and acquired forms of porphyria.
I. Hereditary porphyria ( primary porphyria )
- Erythropoietic Porphyrias
- Hepatic porphyrias
- Neurological porphyria .
Ii. Acquired porphyrias ( secondary porphyrias )
- Porphyria with Pellagra
- Medicinal porphyria
- Lead porphyria .
Hereditary Porphyrias
Among the hereditary porphyrias, there are (1) erythropoietic, (2) hepatic and (3) neurological forms.
1. Among the erythropoietic porphyrias, Gunter’s erythropoietic uroporphyria is the most severe. Often it leads to disability and death in early childhood. Before the advent of antibiotics, death occurred mainly from sepsis. Currently, patients often live to mature age (25-30 years), but the face and neck and they are disfigured by scars. The disease is manifested by (1) hemolytic anemia, (2) severe photodermatitis, (3) brown staining of hard tissues of the teeth, and (4) red urine. Hemolytic anemia is caused by excessive destruction of red blood cells in the spleen (“intracellular hemolysis”). Photodermatitis develops due to increased sensitivity of the skin to the sun's rays under the influence of porphyrins (porphyrins are photosensitizers). In various areas of the skin appear blisters, after opening which remain poorly healing ulcers, often infected. The benign forms of erythropoietic porphyria include Magnus erythropoietic protoporphyria and erythropoietic coproporphyria .
2. The hepatic form of hereditary porphyria is the so-called late skin porphyria ( uroproporphyria ) - the most common hereditary porphyria in Russia. The manifestation of the disease usually occurs over the age of 40 years (hence the “late” in the name of the form). Alcohol abuse, the action of hepatotropic poisons, contact with gasoline, liver tumors, and severe hepatitis are provoked by the manifestations of the disease. Treatment of the disease is effective only in case of complete abandonment of alcoholic beverages. The main changes in cutaneous late porphyria are (1) photodermatitis and (2) liver damage. Photodermatitis is accompanied by redness, swelling of the skin, the formation of blisters, with a long course leads to atrophy and dry skin. In some cases, the affected areas of the skin are thickened due to fibrosis ( scleroderma-like form ), in others, they are hyperpigmented due to the accumulation of melanin ( melanodermic form ). The liver often increases, its function is impaired. The most effective treatment for the disease is the antimalarial drug delagil ( chloroquine ): it binds porphyrins in hepatocytes and removes them with urine. An electron microscopic study has established that delagil causes the destruction of part of the mitochondria of hepatocytes, in endomembranes of which the synthesis of porphyrins takes place. The destruction of mitochondria facilitates the release of delagil-porphyrin complexes from hepatocytes into the blood and bile. However, large doses of delagil can lead to the destruction of hepatocytes and the development of liver failure.
3. From neurological forms of hereditary porphyria, (1) acute intermittent porphyria, (2) hereditary Berger – Goldberg coproporphyria, (3) coproprotoporphyria (variegated porphyria) and (4) Chester porphyria (described in residents of the English city Chester) are distinguished. Acute intermittent porphyria is characterized by damage to the nervous system, primarily the peripheral (neuritis, plexitis, ganglionitis), as well as the pink color of urine during the period of exacerbation of the disease. A characteristic symptom of the disease is abdominal pain (in the epigastrium or in the right iliac region, in the right hypochondrium), in the lumbar region, in the extremities. Patients are often operated on with suspected acute appendicitis or cholecystitis , but the source of the pain syndrome is not detected and the operation does not alleviate the patient’s condition. A fatal complication is respiratory muscle paralysis.
Acquired Porphyrias
Acquired porphyrias complicate the course of (1) lead intoxication, (2) pellagra (PP hypovitaminosis), and (3) are a side effect of the use of certain drugs.
Melanin metabolism disorders
Disorders of the metabolism of melanin are manifested by hypomelanosis (a decrease in its content) and hypermelanosis (increased production of pigment).
I. Hypomelanosis
- Albinism (full, incomplete, partial)
- Vitiligo ( dog )
- Leucoderma ( leucoderma ).
Ii. Hypermelanosis
- Common Hereditary Hypermelanosis
- Common Acquired Hypermelanosis
- Local congenital hypermelanosis
- Local acquired hypermelanosis.
Hypomelanosis
Three forms of hypomelanosis are distinguished: albinism , vitiligo (pece), and leucoderma (leucoderma).
1. Albinism (from an armor. Albus - white) - the hereditary hypomelanosis which is shown right after the birth. Различают три варианта альбинизма: полный (отсутствие меланина во всех тканях организма), неполный (снижение содержания меланина в коже по сравнению с расовой нормой) и частичный ( очаговый ). Неполный альбинизм ( альбиноидизм ) особенно характерен для северных европеоидов (жители российского Севера и Скандинавии). Частичный альбинизм представляет собой наследственную форму местного гипомеланоза (например, «седая прядь» волос).
2. Витили́го ( песь ) — наследственный очаговый гипомеланоз, проявляющийся не сразу после рождения, а через несколько месяцев, лет и даже десятилетий. О наследственной природе процесса свидетельствует его семейный характер.
3. Лейкоде́рма ( лейкодерми́я ) — приобретённый очаговый гипомеланоз. Различают два основных типа лейкодермии: (1) инфекционный и (2) эндокринный. Инфекционная лейкодермия встречается при таких заболеваниях, как сифилис (например, « ожерелье Венеры ») или проказа (лепра). Эндокринная лейкодермия характерна для гипотиреоза, сахарного диабета и болезни Реклингаузена (гиперпаратиреоза).
Распространённый гипермеланоз
Различают (1) наследственные и (2) приобретённые формы распространённого гипермеланоза. Примером наследственного распространённого гипермеланоза является усиление пигментации кожи при пигментной ксеродерме . Приобретённый распространённый гипермеланоз наблюдается при тяжёлой форме хронической надпочечниковой недостаточности ( болезни Аддисона ).
Пигме́нтная ксероде́рма (от лат. xeroderma — сухая кожа) — наследственное заболевание , в основе которого лежит недостаточность ферментов репарации ДНК . Энзимы репарации ДНК прежде всего необходимы клеткам эпидермиса , на которые в течение всей жизни воздействуют ультрафиолетовые лучи солнечного спектра (основной естественный мутаген для человека ), поэтому именно в этих клетках отмечается их высокая активность. При пигментной ксеродерме основные изменения развиваются в коже: на открытых участках кожного покрова формируется фотодерматит . Одним из проявлений фотодерматита является реактивный гипермеланоз. С течением времени мутации в клетках кожи приводят к развитию злокачественной опухоли (карциномы, меланомы или саркомы), от которой больные погибают обычно на втором десятилетии жизни. Более лёгкая форма заболевания носит название пигментный ксеродермо́ид Ю́нга ; злокачественные опухоли при этом развиваются примерно на 10—15 лет позже. Больным пигментной ксеродермой необходимо с детства избегать солнечного и артифициального (искусственного) ультрафиолета.
Болезнь Аддисона (тяжёлая форма хронической недостаточности коры надпочечников ) характеризуется увеличением продукции аденогипофизом меланотропного гормона ( меланотропинов ). Меланотропины способствуют увеличению числа меланоцитов в коже, поэтому при этом заболевании отмечается распространённый гипермеланоз кожи ( меланодермия ). Болезнь Аддисона развивается вследствие разрушения ткани обоих надпочечников при аутоиммунном и туберкулёзном адреналите, а также при двусторонних метастазах злокачественной опухоли в надпочечники.
Местный гипермеланоз
Hereditary and acquired forms of local hypermelanosis are distinguished. Hereditary local hypermelanosis occurs in some oncogenetic syndromes (for example, Peitz-Yegers disease and the Karni complex) and is characterized by the appearance of congenital melanocytic nevi. Acquired local hypermelanosis is (1) tumor (acquired melanocytic nevi, malignant melanoma) and (2) reactive. Reactive local hypermelanosis occurs in many diseases and pathological processes: skin hypermelanosis in chronic dermatitis, colon hypermelanosis in prolonged constipation, etc.
Black acanthosis. Of particular importance among the forms of acquired local melanosis is black acanthosis ( acanthosis nigricans , pigment-papillary dystrophy of the skin ). At the same time, on the skin, especially in the area of natural folds, outgrowths appear (papillae), at least 0.5 cm high. The skin is pigmented. When micromorphological study in the epidermis revealed reactive changes, especially acanthosis (thickening of the spinous layer due to the active proliferation of epidermocytes). Black acanthosis is usually a nonspecific paraneoplastic process , that is, it accompanies the development of malignant neoplasms and, if it is found in an adult, it is necessary to exclude a tumor process (in children, similar changes may be a developmental defect of the skin). Black acanthosis has to be differentiated with black pseudo- acanthosis found in obese people. The main difference between black pseudo-acactosis is the height of papillary growths of the skin less than 0.5 cm.
Lipofuscinosis
Lipofuscinosis - accumulation in the parenchymal cells of lipofuscin pigment . Lipofuscinosis is traditionally considered in domestic pathological anatomy among mixed dystrophies, however, in essence, this process is a typical parenchymal dystrophy , since changes are detected exclusively in the parenchymal elements of the organ .
There are hereditary ( primary ) and acquired ( secondary ) variants of lipofuscinosis.
Primary lipofuscinosis occurs:
- with hereditary hepatic hyperbilirubinemia ( Gilbert , Crigler-Nayar, Dabin-Johnson, Rotor syndromes)
- with hereditary brain lesions (Hegberg-Santavuori, Bilshovsky-Yanovsky , Kufs , Spielmeyer-Vogt syndromes ).
At the same time, lipofuscin accumulates in hepatocytes and neurons, respectively. Dabin-Johnson syndrome is accompanied by the appearance of dark brown lipofuscin, due to which the liver becomes almost black (“ black liver disease ”). Primary neuronal lipofuscinosis is manifested by the syndrome of amaurotic idiocy ( amaurosis - complete blindness, idiocy - a severe form of oligophrenia ).
Of the secondary lipofuscinosis are more common:
- cardiomyocyte lipofuscinosis in alcoholism ,
- brown atrophy of myocardium and liver with cachexia ,
- iatrogenic lipofuscinosis with prolonged use of NSAIDs ,
- lipofuscinosis with hypovitaminosis E.
Urine acid diathesis
Urinary diathesis - the accumulation in the body of uric acid (urate) and its salts. The main forms of uric acid diathesis are (1) gout , (2) urolithiasis caused by urates, and (3) uric acid infarction .
Gout is subdivided into hereditary ( primary ) and secondary (for example, in chronic leukemia, chronic renal failure). The disease is characterized by (1) kidney damage (" gouty kidneys "), (2) joints (especially the first metatarsophalangeal joint) and (3) focal urate deposition in soft tissues ( gouty bumps - tophi urici ).
Uricine infarction - the deposition of urates in the kidneys of newborns who have lived for at least 2 days (the result of birth stress ). At the same time in the kidney tissue found orange stripes converging in the papillae of the pyramids. Uricine infarction, despite the name, does not lead to necrosis of the renal tissue and refers to the transient states of the neonatal period .
Calcium metabolism disorders
Two forms of calcium metabolism are distinguished: (1) a decrease in its content in tissues, primarily in bone ( osteoporosis ), and (2) excessive calcium accumulation outside the bones ( calcification , calcification , calcareous dystrophy ). In autopsy practice, calcification is of primary importance.
Classification of Calcification Forms
There are three options for calcification:
I. Metastatic calcification ( calcareous metastases ).
Ii. Dystrophic calcification ( petrification )
- Necrocalcinosis
- Thrombocalcinosis
- Fibrocalcinosis
- Chondrocalcinosis
- Calcification of dead parasites
- Lithopedion .
Iii. Metabolic calcification ( interstitial calcification ).
- Systemic metabolic calcification
- Lime gout .
Metastatic calcification ( calcareous metastases ) is a common calcification associated with hypercalcemia (for example, with hyperparathyroidism, multiple bone destruction, hypervitaminosis D, severe lesions of the kidneys and colon). Favorite localization of calcareous metastases are (1) lungs, (2) gastric mucosa, (3) myocardium, (4) artery walls and (5) kidneys, tissues of which are more alkaline and are able to accumulate calcium.
Dystrophic calcification ( petrification ) - local calcinosis that develops in areas of pathological tissue changes (necrobiosis and necrosis, scars), as well as in blood clots. Accordingly, they speak about three main variants of petrification: necro , fibro , and thrombocalcinosis . Less common is the pathological calcification of cartilage tissue, primarily hyaline cartilage ( chondrocalcinosis ), petrification of dead parasites (for example, trichinella) and the dead fetus during ectopic pregnancy (such a fetus is called lithopedion ). Dystrophic calcification due to tissue alkalosis and alkaline phosphatase activity. Calcification foci for this type of calcification are called petrification .
Metabolic calcification - calcification, developing without concomitant hypercalcemia and local tissue changes. Distinguish between systemic and focal forms of metabolic calcification. The systemic form may resemble metastatic calcification, but more often affects tendons, fasciae, aponeuroses, skeletal muscles, blood vessels, nerve trunks, skin, and subcutaneous tissue. The focal form ( lime gout ) is characterized by the deposition of lime in the form of plates in the skin of the fingers, less often of the feet.
Morphological picture
In a macromorphological study, the site of calcification is distinguished by a solid consistency (rocky density) and usually has a whitish-gray color. In tissue sections, calcium deposits intensively perceive alkaline dyes and are stained in blue with ordinary hematoxylin and in black with Weigert's iron hematoxylin (van Gieson color). If necessary, carry out histochemical verification of the process; using the Kossa silver impregnation method.
Stones (concretions)
In pathological anatomy, the formation of stones or concrements (from the Latin concrementum - intergrowth ) is traditionally referred to as mineral dystrophy.
Stones - solid, intensely mineralized bodies, formed in the hollow structures of the body (abdominal organs, ducts of the glands, bronchi, vessels). Stone formation causes the development of:
- obturation syndrome. (for example, mechanical jaundice or hydronephrotic transformation),
- inflammatory process
- bedsore organ wall with its subsequent ulceration or perforation.
In the pathogenesis of stone formation, local factors are of primary importance, first of all:
- lithogenic composition of secretion (for example, a decrease in the concentration of phospholipids and an increase in the content of cholesterol in the bile),
- its stagnation and thickening as well
- chronic inflammatory process.
The direct mechanism of stone formation consists of two events, each of which may be primary:
- formation of an organic matrix,
- crystallization of salts.
Stones formed in the human body are classified as follows:
I. Localization
- Gallstones - gallbladder , bile ducts
- Urinary stones - calyx and pelvis kidney, bladder
- Salivary stones - salivary gland ducts
- Pancreatic stones - pancreatic ducts
- Bronchial stones - bronchial lumen
- Stones in the crypts of the tonsils
- Phleboliths - lumen of veins
- Coproliths - intestinal stones.
Ii. Chemical composition
- Gallstones:
- cholesterol,
- pigment (brown or green),
- calcareous,
- combined.
- Urinary stones:
- urats (yellow)
- phosphates (white)
- oxalates,
- cystine
- xanthine
- combined.
Iii. View of the cut
- Radar structure stones ( crystal stones )
- Stones with a layered structure ( colloidal stones )
- Stones with a layered-radar structure ( colloidal crystalloid stones ).
Iv. Stone shape
- Round and oval stones
- Process stones
- Cylindrical stones
- Faceted stones - with flat edges, closely adjacent to each other.
V. Number of stones
- Solitary (single)
- Multiple.
Vi. The size of the stones
- Macrolites (large stones)
- Microliths (small but not microscopic).
VII. Surface character
- Stones with a smooth surface - usually do not injure the surrounding tissue
- Stones with a rough surface (for example, oxalate stones in the form of mulberry berries) - traumatize the surrounding tissue.
The main diseases, the development of the clinical picture of which is closely related to the formation of stones, are:
- cholelithiasis ( cholelithiasis ),
- urolithiasis ( urolithiasis ),
- nephrolithiasis ( kidney disease ),
- sialolithiasis ( calculous sialadenitis ).
See also
- Pathological anatomy
- Alterative processes
- Destructive processes
- Natural apoptosis
- Parenchymal dystrophy
- Parenchymal dysproteinosis
- Mesenchymal dystrophy
- Mesenchymal dysproteinosis
- Endogenous pigments
- Circulatory disorders
- Inflammatory response
- Immunopathological processes
- Adjustment and compensation processes
- Tumor growth
- Etiology of malignant tumors
Literature
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- Davydovskiy I.V. General pathological anatomy. 2nd ed. - M., 1969.
- Kaliteevsky PF Macroscopic differential diagnosis of pathological processes.— M., 1987.
- Microscopic technique: a guide for doctors and technicians / ed. D.S. Sarkisova and Yu. L. Perova. - M., 1996.
- General human pathology: a Guide for doctors / Ed. A.I. Strukova, V.V. Serov, D.S. Sarkisova: In 2 t. — T. 1.— M., 1990.
- Pathological anatomy of diseases of the fetus and child / Ed. T. E. Ivanovskaya, B. S. Gusman: In 2 t. M., 1981.
- V. V. Serov, V.S. S. Spiders. Ultrastructural Pathology. M., 1975.
- Strukov A. I., Serov V.V. Pathological Anatomy. M., 1995.