Morphology of cells and tissues reversible and irreversible injury. Intracellular and extracellular accumulation (uptake) of proteins, hydrocarbons and lipids.
(Parenchimatous and mesenchimal dystrophies)
Cells and tissue reversible changes occurs in the result of tissue or cell metabolism disturbance and are accompanied with these substances (proteins, fats, hydrocarbons) which exists as norm intracellular or tissue uptakes and appearance of those pathological which do not exist in the norm. These changes are named metabolic products pathologic uptakes or dystrophies (from Lat. dys – disturbance, trophe – nutrition). Intracellular uptake of substances causes parenhymatous degenerations development. Parenhymatous degenerations occurs mostly in highly specialized cells of parenhymatous organs (kidneys, liver, heart, cerebrum, etc.). Acquired or congenital fermentopathies underlie parenhymatous degenerations development. These fermentopathies make a big group of storage diseases or thesaurismoses. Latter contain a big group of storage diseases or thesaurismoses.
Causes of metabolism products abnormal uptake
1 Cell pathology. Cells are not able to utilize substances as energy or plastic material or release them. This is caused mostly by cells structure injury with various factors, sometimes by congenital or acquired ferments pathology, which participate in metabolism (fermentopathies).
2 Function disturbance of transport systems, providing both substances supply to tissues and cells and metabolism products excretion. It is often observed under cardiovascular collapse and pulmonary insufficiency.
3 Endocrine and nervous regulation of trophism disorders.
Mechanisms of metabolism products abnormal uptake Infiltration is excessive penetration of metabolism products from blood into cells and intercellular substance with their subsequent uptake due to ferment system, providing their metabolism, insufficiency. Substances metabolism products abnormal uptake by way of infiltration is observed in liver, kidneys, aorta wall.
Decomposition (phanerosis) occurs under cell and intercellular substance ultrastructures destruction due to intoxication, hypoxia or other reasons. Ultrastructures membranes are made of proteins, fats and hydrocarbons, so under their destruction these substances are accumulated and stored in cells.
Distored synthesis is synthesis of those substances in cells and tissues which are not observed in them as a norm. As an example, it’s glycogen synthesis in nephron tubules epithelium under diabetes mellitus, alcohol hyaline synthesis in hepatocytes.
Transformation is the creation of one kind of metabolism products from intermediate disintegration products, which should be utilized for proteins, fats and hydrocarbons synthesis. For example, it’s fats and hydrocarbons components transformation into proteins under starvation, fats and hydrocarbons components transformation
into glycogen under diabetes mellitus.
Metabolism products abnormal uptake classification
Classification by the kind of metabolism disturbance prevail:
a) protein, b) fat, c) hydrocarbon, d) mineral
By pathologic process localization:
a) parenchymatous (modifications in the organs parenchymatous cells - cardiomyocytes, hepatocytes, ganglionic cells of cerebrum, etc.);
b) stromal-vascular (modifications in organs stroma);
c) mixed (changes in parenchyma and stroma).
Depending on genetic factors influence:
a) congenital, b) acquired.
By process spread:
a) general, b) local.
Morphology of proteins abnormal uptake (proteinosis)
Occurs under proteins metabolism disturbance. Tissues proteins form cells as plastic materials (capsule, nucleus, cytoplasm, intracellular organelles) as well as intercellular stroma – collagen, elastic, reticulin fibers, basic intercellular substance, vessels, nerves. By proteins metabolism disturbance development location proteinosises are divided into parenchymatous, stromal-vascular and mixed. .
Under parenchymatous proteinosis physical-chemical features of intracellular proteins are violated. At the beginning grain effect occurs in cytoplasm at the cost of protein inclusions, which is manifestation of cell ultrastructures overstrain (hyper function). This process is reversible. Quite often proteins disbolism is combined with Na-K-pump operation faults, which is accompanied with natrium ions uptake and cells hydration. In case intoxication, hypoxia, inflammation or other reasons of proteinosis increase this cause cells destructive changes intensification. The following kinds of parenchymatous proteinaceous degenerations (proteinosis) are recognized: hyaline-drop, hydropic (vacuolar), keratinization.
At hyaline-drop proteinosis proteins compacts and become similar to hyaline cartilage. Big hyalinoid drops of protein occur in cells cytoplasm. Sometimes coagulation necrosis develops and cells die, organ function decreases, but macroscopic changes are not found. This kind dystrophy is often observed in hepatocytes under alcoholic hepatitis (Mellori bodies), in renal tubules epithelium under nephrotic syndrome, etc.
Cytoplasmic organelle damage leads to a variety of injury patterns, most of which are best seen by electron microscopy. Acute injuries tend to damage an entire cell, so specific organelle damage is beside the point. However, in some cases the damage can be cumulative over many years. Here are Mallory bodies (the red globular material) composed of cytoskeletal filaments in liver cells chronically damaged from alcoholism. These are a type of "intermediate" filament between the size of actin (thin) and myosin (thick).
Intracellular accumulations of a variety of materials can occur in response to cellular injury. Here is fatty metamorphosis (fatty change) of the liver in which deranged lipoprotein transport from injury (most often alcoholism) leads to accumulation of lipid in the cytoplasm of hepatocytes.
Hydropic or dropsy proteinosis is characterized by intracellular fluid increase, in which cytoplasm proteins are dissolved due to hydrolytic pigments action. Vacuoles full of cytoplasm fluid occur in cells. Further on cells cytoplasm transforms into blisters full with fluid, intracellular organelles destroy, cell dies off and coliquation necrosis develops. Organs also didn’t change macroscopically. Hydropic proteinosis often develops in liver under viral hepatitis, in kidneys under glomerulonephritis, etc.
Sometimes cellular injury can lead to accumulation of a specific product. Here, the red globules seen in this PAS stained section of liver are accumulations of alpha-1-antitrypsin in a patient with a congenital defect involving cellular metabolism and release of this substance.
Many inherited disorders of metabolism involving enzymes in degradation pathways can lead to accumulation of storage products in cells, as seen here with Gaucher disease involving spleen. The large pale cells contain an accumulated storage product from lack of the glucocerebrosidase enzyme.
The yellow-brown granular pigment seen in the hepatocytes here is lipochrome (lipofuscin) which accumulates over time in cells (particularly liver and heart) as a result of "wear and tear" with aging. It is of no major consequence, but illustrates the end result of the process of autophagocytosis in which intracellular debris is sequestered and turned into these residual bodies of lipochrome within the cell cytoplasm.
Keratinization proteinosis is characterized with excessive keratin generation on the surface of plane keratinized epithelium – hyperkeratosis, ichthyosis. The causes of keratinization development is chronic inflammation, avitaminosis, skin development abnormalities. Leukoplakia which is mucous tunics epithelium pathologic keratinization, also belongs to this process and can become a source of malignant growth.
Extracellular uptakes occur in the result of metabolism disturbance in organs stroma or in vessels walls, so they are named stromal-vascular or mesenchymal proteinosis. Important attention is paid to proteinosis developing in the result of proteins metabolism in conjunctive tissue and are found in stroma and vessels walls. Primary pathologic changes are developed on histion level, consisting of microcirculation channel: basic substance, fibers (collagen, reticulum, elastic), cells (fibroblasts, fibrocytes, lymphocytes, labrocytes, histiocytes), nerves. Basic substance is connecting, cementing, fiber and cells are situated in it. By chemical composition it is polymer of composite protein-hydrocarbon molecules – mucopolysaccharides (glycosamineglycanes). The following relates to stromal-vascular proteinosis: mucoid swelling, fibrinoid swelling (fibrinoid), hyalinosis, which are considered to be consequent stages of conjunctive tissue destruction.
Mucoid swelling – is primary disorganization of conjunctive tissue. Causes: hypoxia, allergy, endocrine pathologies. It often occurs under rheumatic and infection diseases, atherosclerosis, it is found in artery walls, cardiac valves, endocardium, heart. Basic substance depolymerization underlies its development. As a consequence it becomes hydrophilic, attracts liquid, vessel wall penetrability increases. Basic substance hydration, collagen fibers swelling occurs. With vascular-tissue penetrability growth conjunctive tissue saturates with blood plasm proteins, in first turn with albumines and globulins. Macroscopically organ or tissue mostly doesn’t change. Microscopically phenomenon of metachromasia is observed: glycosamineglycanes are painted with toluidine blue in red color. Described changes in conjunctive tissue provided that the reason was eliminated are reversible and tissue structure is rehabilitated.
This Congo red stain reveals orange-red deposits of amyloid, which is an abnormal accumulation of breakdown products of proteinaceous material that can collect within cells and tissues.
Fibrinoid swelling is following stage of conjunctive tissue disorganization. Under substantial growth of vascular-tissue penetrability fibrinogen sweats in stroma from vessels clearance, which rather quickly precipitates in strings of fibrin, collagen fibers are destroyed (broken, fragment), conjunctive tissue basic substance chemical composition is changed. Under fibrinoid swelling deep and irreversible disorganization of conjunctive tissue is observed, which is accompanied with basic substance and fibers destruction against the background of considerable increase of balls vascular permeability. Macroscopically organ doesn’t change, microscopically collagen fibers become homogenous, eosinophilic, becomes yelow when painted with picrofuchsin, pyroninophil and argyrophil. Consequence Fibrinoid necrosis is developed in the final of the process. Significance – organ function disturbance under heart disease formation, joints immobility, luminal narrowing and vessel wall elasticity decrease, organ function termination under renal insufficiency at malignant hypertension, when fibrinoid changes as well as arterioles and cappilars necrosis develops.
Hyalinosis is the final stage of tissue disorganization and is characterized with uptake of collagen destruction products, plasm proteins, polysaccharides, which merge into homogenous mass which consolidates as time passes, becomes semi-transparent similar to hyaline cartilage, so it is called hyaline. This is complex fibrillar protein. Hyalinosis occurs as a consequence of fibrinoid swelling, plasmorrhagia, sclerosis, necrosis. It develops as the result of peculiar completion of sclerosis in scarring, cardiac valves under rheumatism (local conjunctive tissue hyalinosis). Macroscopically fibrous conjunctive tissue becomes dense, cartilaginous, whitish, semi-transparent. Microscopically collagen fibers loss fibrillarity and merge into homogenous dense cartilaginous mass, cells squeeze and atrophy.
Heart in such cases is enlarged, ventricular cavities are dilated, mitral valve flappers are dense, whitish color, conjoint in between each other, considerably deformed. This kind of hyalinosis is peculiarly expressed in rough vicious cicatrix after burns (keloid). Consequences are unfavorable because of considerable deterioration of organ or injured tissue function.
Systemic hyalinosis develops in vessels walls under hypertension disease, diabetes mellitus (vascular hyalinosis) and is mostly expressed in kidneys, cerebrum, eye retina, pancreas. Considering occurrence pathogenesis three kinds of vascular hyaline are recognized: simple is observed under hypertension disease, atherosclerosis; lipohyaline is developed under diabetes mellitus; complex hyaline occurs in the result of immunopathologic disturbances and vessel wall fibrinoid disorganization at collagenosis.
Morphology of lipids pathological uptake (lipidosis)
Occurs as the result of fats metabolism disturbance.
Lipidosis are divided into parenchymatous and stromal-vascular (mesenchymal) fatty (adipose) degenerations. To reveal fats frozen sections are colored with sudan ²²² or ²V.
Parenchymatous lipidosis are manifested with neutral lipids (triglycerides) drops uptake in cells cytoplasm and are the results of cytoplasm fats metabolism disturbance. Mostly they are found in myocardium, lever, kidneys.
Myocardium lipidosis is characterized with lipoproteids drops uptake in cardiac hystiocytes. As a rule it is observed under intoxications (diphtherial, alcohol, with phosphoric compounds, arsenic, diseases of liver, kidneys, thyrotoxicosis, etc.), long time general hypoxia (anemia, chronic pulmonary and cardiovascular insufficiency), Under oxygen deficiency process of oxidative phosphorylation and ATP synthesis in cardiomyocytes decreases, fatty acids beta-oxidation violates. So fats coming into cell are not completely utilized as plastic and power material and they accumulate in cytoplasm. Besides that under hypoxia membrane lipoprotein complexes destruction is observed (decomposition or phanerosis). Macroscopically heart at this process enlarges in size, its chambers stretch, myocardium becomes flaccis, of clay-yellow color, retraction ability of cardial muscle decreases. From myocardium side especially on papillary muscles surface, trabeculas, it is observed yellow-grey striation– “ tiger heart”, which is caused by dystrophy. Microscopically fat uptakes in muscular cells groups, situated downstream cappilars venous elbow and small veins where hypoxia factor is mostly expressed.
Liver lipidosis is characterized with fat content increase in hepatocytes. Quite often it is the result of imbalance between increased fats supply under hyper lipidemia (alcoholism, diabetes mellitus, general obesity), their decreased assimilation (fatty acids oxidation in mitochondrions under hypoxia or toxic influences) and lipids excretion decrease by liver cells under apoprotein production decrease which transports fats in the form of lipoproteins. This is observed in case protein insufficiency in food or under gastrointestinal disturbances, poisoning with ethanol, phosphor, etc., congenital defects of ferments metabolizing fats. Microscopically first occurs saw type, then small drop and large drop degeneration. Three stages of liver lipidosis are distinguished:
1- fat uptake in hepatocytes, 2- fat uptake with mesenchymal reaction development, 3- fat uptake with liver fibrosis and cirrhosis development. Fat fills all cytoplasm and gradually pushes nucleus aside to periphery and modified hepatocytes becomes similar to adipocytes. Fatty degeneration prevalence in peripheral portions of liver part confirms infiltration mechanism of its development, which is observed under hyperlipidemia. Fatty degeneration development prevalence in central portions of liver part is connected with decompensation mechanism and is observed under hypoxia or intoxication. Macroscopically liver is enlarged, loose (of pastry consistency), yellow or clay color.
Kidneys lipidosis is often observed under nephrotic syndrome, chronic renal insufficiency when hyperlipidemia and lipiduria occur. Fat excess is excreted from organism with kidneys and constipates them. Microscopically fat occurs in proximal, distal or convoluted renal tubules epithelium in cells basal portions. Nephrocytes lipidosis often joins hyaline-drop degeneration and hydropic proteinosis. Macroscopically kidney is enlarged, flaccid, cortical layer is dilated with signs of swelling, of grey color with yellow specks.
Congenital lipid metabolism disturbances are manifested with systemic lipidosis and pertain to fermentopathies (diseases of storage or uptake). The following diseases are marked out: cerebrosine lipidosis (Gaucher's disease), sphingomyelin lipidosis (Niemann-Pick disease), generalized gangliosidosis (Tay-Sachs disease), generalized gangliosidosis (Norman-Landig disease), which are accompanied with liver, spleen, marrow, nervous system and other organs and tissues damage.
Stromal-vascular lipidosis include neutral fat metabolism disturbance in adipose tissue and adipose depot as well as cholesterol and its ethers in arteries walls under atherosclerosis.
General disturbance of neutral fats metabolism is manifested with neutral fat stocks increase or decrease in hypodermic fat tissue, mesentery, pericardium, marrow, etc. General uptake of neutral fat in fat depots is called obesity. The following is recognized: primary or idiopathic obesity the cause of which is unknown and secondary obesity which occurs under endocrine, cerebral and hereditary diseases. By external signs obesity kinds are as follows: upper, mid, lower and universal symmetric. By morphologic signs hyper plastic type is marked out characterized with fat cells (adipocytes) quantity increase in organism as well as hypertrophic (malignant) type the basis of which is adipose cells size increase several times and triglycerides content increase in cytoplasm several times.
Under general obesity the important clinical attention is paid to heart injury. In this case adipose tissue grows under pericardium, surrounding organ like case. Lipocytes uptake in myocardium stroma between cardiac hystiocytes, squeezing the latter ones which causes their atrophy. Right portion of the heart is the most injured one. Sometimes the whole thickness of right ventricle myocardium is changed with adipose tissue, that can cause cardiac rupture or accelerate decompensation process.
Neutral fat local uptake is observed under Madelung's syndrome, Dercum's disease and Weber-Krischen’s desease, as well as vacant obesity when organ atrophied portion is substituted. The essence of Dercum's disease is in painful lipomas occurrence in subcutaneous adipose tissue of extremities and trunk. Weber-Krischen’s disease is characterized with recurrent nonpurulent cellulites with productive granulomatous inflammation development around sphacelous adipose tissue.
General decrease of adipose tissue occurs under emaciation (cachexia). Tissue becomes loose, flabby, is saturated with liquid, sliming.
Cholesterol and its ethers’ metabolism imbalance is a basis of atherosclerosis development. Uptake of cholesterol fractions, lipoproteins of various density, proteins in arteries’ walls causes formation of fat detritus (atheroma) and conjunctive tissue enlargement (sclerosis). Hereditary cholesterol metabolism disturbance is observed under family hypercholesterolemic xanthomatosis, manifested with xanthalasms formation (cholesterol deposition in skin, big vessels’ walls, heart valves and other organs).
Carbohydrates pathologic uptake (glycogenosis) morphology
The most valuable in carbohydrates metabolism disturbance is glycogen, glycosamineglycanes and glycoproteins. The most important in this pathology is glycogen metabolism disturbance occurring under diabetes mellitus. In case insulin deficiency in blood the tissues utilize sugar insufficiently causing sugar level increase in blood (hyperglycemia), and glycogen quantity in tissues decreases. Kidneys remove sugar excess with urine (glucosuria). In the result of glucose polymerization under its resorption from plasma ultrafiltrate glycogen is accumulated in tubules epithelium, mesangium and membranes of glomerule vessels. The most of it is in epithelial cells and in Henle’s loop lumens (narrow segment). Epithelium in these sections of nephron becomes high, with light and foamy cytoplasm. Changes in kidneys under diabetes mellitus are finalized with sclerosis development called diabetic glomerulosclerosis.
Hereditary (glycogenosis) occurs under deficiency of ferment which splits glycogen and the latter accumulates in cells. These includes hepatorenal glygenosis, Pompe disease, MacArdles and Gerce’s under which glycogen structure is not damaged, as well as Forbes-Cori (type 3 glycogenosis) and Anderson’s disease (type 4 glycogenosis) under which this structure is changed.
Under glycoproteins metabolism disturbance (mucins and mucoids which are the base of mucus) mucus degeneration develops. The typical manifestation of it is mucoviscidosis which is systemic disease, charactristic of which is high viscosity of mucus, causing development of retention cysts and sclerosis in pancreas, bronchi, digestive and other glands. Besides that this degeneration is often observed under catarrhal inflammation of nose mucous tunic (rhinitis), mucous tunic of larynx (laryngitis), bronchi (bronchitis), stomach (gastritis), etc. Macroscopically excess of mucus is seen on mucous tunic, and this mucous trickles down from the surface. Microscopically wine glass like cells appear in mucous tunic and release mucus. Also desquamation or cells necrosis is observed, glands’ excretory ducts are clogged with mucus which is accompanied with cysts formation.
Glycoproteins and glycosamineglycanes uptake in organs’ stroma is accompanied with collagen fiber as well as cartilage and adipose tissue substitute with mucus-like mass. Damaged tissues cells have star-like shape. This process is called tissue sliming and it is observed under cachexias and myxedema. Carbohydrates uptake consequence can be reversible and under process progress they become semi-transparent, looks like mucus, colliquative necrosis develops.
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.
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.
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.
A Prussian blue reaction is seen in this iron stain of the liver to demonstrate large amounts of hemosiderin that are present within the cytoplasm of the hepatocytes and Kupffer cells. Ordinarily, only a small amount of hemosiderin would be present in the fixed macrophage-like cells in liver, the Kupffer cells, as part of iron recycling.
The brown coarsely granular material in macrophages in this alveolus is hemosiderin that has accumulated as a result of the breakdown of RBC's and release of the iron in heme. The macrophages clear up this debris, which is eventually recycled.
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.
These renal tubules contain large amounts of hemosiderin, as demonstrated by the Prussian blue iron stain. This patient had chronic hematuria.
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.
The yellow-green globular material seen in small bile ductules in the liver here is bilirubin pigment. This is hepatic cholestasis.
The black streaks seen between lobules of lung beneath the pleural surface are due to accumulation of anthracotic pigment. This anthracosis of the lung is not harmful and comes from the carbonaceous material breathed in from dirty air typical of industrialized regions of the planet. Persons who smoke would have even more of this pigment.
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.
Here is anthracotic pigment in macrophages in a hilar lymph node. Anthracosis is nothing more than accumulation of carbon pigment from breathing dirty air. Smokers have the most pronounced anthracosis. The anthracotic pigment looks bad, but it causes no major organ dysfunction.
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.
This is dystrophic calcification in the wall of the stomach. At the far left is an artery with calcification in its wall. There are also irregular bluish-purple deposits of calcium in the submucosa. Calcium is more likely to be deposited in tissues that are damaged.
Here is so-called "metastatic calcification" in the lung of a patient with a very high serum calcium level (hypercalcemia).
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.
Cells and tissues damage and death. Necrosis and apoptosis. Pathologic anatomy of organ deficiency. Fundamentals of thanatology.
Death, definition, signs of death
Critical alteration of specialized cells. Definition, etiology and consequences.
Molecular mechanisms of cells critical alteration. Concepts of endogenous metabolic catastrophe: cells biological combustion insufficiency, cell acidotic alteration, plasma membrane transportaion mechanisms injury, activation of cytoplasm lipid peroxidation and cell membranes, injury with free radicals and nitrogen oxide excess, catastrophic increase of free calcium in cell, cell injury with transmitters excess, abnormal proteins accumulation in cell. Critical injury of cell with external factors: external physics-chemical factors, pathogenic infects (ultramicrobs, Rickettsias, bacteria, fungi).
Kinds of specialized cells death in organism.
Cell necrosis: definition, terms and phases of development, morphologic characteristic of coagulation necrosis and cells necrosis, their consequences.
Pathogenic inductive apoptosis: definition, molecular mechanisms, term of development, microscopic manifestation, consequences.
Immune destruction of cells. Immune destruction of cells in organism conditions and designation. Phagocytosis: definition, main cells-phagocytes, phagocytosis mechanisms and microscopic manifestation. Immune cells killing: definition, cytotoxical cells, mechanisms and microscopic manifestations, consequences. Cells destruction with activated complement: definition, mechanisms and microscopic manifestations.
Pathological anatomy of organ insufficiency.
Autoimmune (lymphocytic) destruction of all specialized structures of organ: definition, stages of development, clinical-morphological characteristics, consequences.
Postishemic-markfusional organs injury: definitions, morphogenesis peculiarities, clinical-morphologic characteristics, consequences.
Necrosis of organ or its portion. Morphologic types of tissues necrosis (colliquative, coagulative): definition, causes, pathological anatomy. Organ necrosis: definition, causes, development stages (ore-necrotic, necrosis and tissues destruction). Post necrotic transformation of organ’s sphacelus (necrosis demarcation and encapsulation, regeneration, infection and inflammation, formation of ulcer, cyst, sequester, sclerosis/gliosis foci, calcinosis foci).
Clinical-morphological classification of organ necrosis basic kinds.
Infarction: definition, morphogenesis, pathological anatomy of main types, consequences. Gangrene: definition, morphogenesis, pathological anatomy of dry, wet and anaerobic, consequences. Morphologic characteristics of infarction, gangrene. Decubitus: definition, trophoneurotic necrosis morphogenesis, consequences. Noma: definition, morphogenesis, pathological anatomy, consequences. Morphogenesis, pathological anatomy of liver toxic necrosis and enzymatic pancreatonecrosis. Sequester: definition, morphogenesis, pathological anatomy, consequences.
Fundamentals of thanatology.
Human being birth and death. Organism death from biological, social and medical positions: idea of natural, violent death and death from diseases (untimely and sudden). Intrauterine death definition.
Thanatogenesis. Cause, molecular-metabolic and structural mechanisms of vital parts activity cessation under natural course of disease. Immidiate consequences of heart, lungs, cerebrum, kidneys and liver work cessation.
Clinical-pathological characteristics of the main periods of thanatogenesis. Modern acknowledged periods of thanatogenesis: critical period, apparent death, post reanimation period, natural death. Consequences of vital parts activity cessation.
Critical and agonal periods of disease: definition, clinical-pathological features, consequences.
Clinical death: definition, features and terms of development, idea of cardiopulmonary reanimation and its consequences.
Post reanimation period: definition, molecular and clinical-pathological anatomy features of vital parts injury and their functions recovery.
Natural death: definition, immediate (main) causes and development terms under natural clinical course and under sudden death of a person. Precursory and delayed signs of natural death and resuscitated patient. Morphological characteristic of cadaveric changes. Basic reasons and morphological signs of intrauterine fetal death and neonate death.
Critical alteration of specialized cells is manifested with their death being the final result of their damage. The most often cell’s death is caused by acute hypoxia or ischemia; physical factors (mechanical trauma, burns, frostbites, radiation, electric shock); chemical substances and medicines; infections, intoxications, immune reactions and other conditions.
Mechanisms of cells damage
Mechanisms of cells damage are extremely various. Under ischemia damage develops in the result of oxygen scarcity in tissues and its free radicals creation causing lipids peroxidation and cellular breakdown. Critical damage can develop under calcium homeostasis disturbance. Under cytolemma hyperpermeability free calcium ions concentration grows causing activation of numerous ferments’ damaging cell: phospholipase, protease, ATPase, endonuclease. ATP content decrease causes cytolemmas damage and induces cell death.
Types of specialized cells death.
Three basic types of specialized cells death in organism are recognized: ischemic or hypoxic, toxic and damage with oxygen free radicals. Hypoxic and ischemic damage occurs in the result of arterial flow cessation. Herewith oxidative phosphorilation is ceased and ATP formation is terminated, anaerobic glycolysis enhances, lactic acid, inorganic phosphate accumulates, intracellular pH decreases, chromatin consenses, cell becomes dropsical, membrane structures destruct. Cell damage by free radicals is caused by membranes lipids peroxidation, autocatalytic reactions development, oxic proteopepsis, DNA damage. Toxic damage occurs under chemical substances action on cell membrane or intracellular organelles.
Two types of local death exists: necrosis and apoptosis. Necrosis (from Greek nekros – dead) which is local death, death is characterized with cells death in living body. Specific cells, a group of cells, the portion of the organ, organ in full can be subject to death.
Cell necrosis is cell death under the influence of extreme negative exogenic and endogenic factors and it is manifested with considerable cells edema or cellular breakdown, cytoplasmic proteins denaturation and coagulation, cell organelles breakdown. Three stages are differentiated in necrosis development: pre-necrotic, necrotic and post necrotic. Pre-necrotic stage is characterized with severe degenerative changed which are ended with necrosis. At necrosis stage the following is broken-down and decomposed (kariorrhexis, kariolysis), cellular cytoplasm (plasmorrhexis, plasmolysis) and intercellular substance – fibrinoid necrosis.
In the post necrotic stage necrosis products are subject to autolysis, meaning dilation or dispersion or organization. Macroscopically necrosis region differs from surrounding living tissues. Its of dirty black color in skin and bowels and whitish yellow in the other organs (myocardium, liver, kidneys, spleen).
By etio-pathogenetic principle the following direct necrosis is differentiated: traumatic, toxic and the following indirect ones: trophoneurotic, allergic, vascular.
Microscopic signs of necrosis:
Cell nucleus change: karyopyknosis, karyorrhexis, kariolysis.
Cell cytoplasm chang: plasma coagulation, plasmorrhesis, plasmolysis.
Intracellular substance change: mucoid swelling, fibrinoid swelling, fibers disintegration.
Necrosis classification by etiology: trophoneurotic, toxic, traumatic, vascular, allergic.
Trophoneurotic necrosis occurs under central nervous system and peripheral nerves injury. Traumatic necrosis occurs in the result of physical, electrical, chemical, thermal trauma direct action. Toxic necrosis occurs in the result of toxins, mostly of bacterial origin influence on tissues. Allergic necrosis develops on condition of tissues hypersensitivity (sensibilization). Vascular (ischemic) necrosis occurs in the result of tissues blood supply significant decrease or termination.
Clinicopathologic classification of the main types of organs’ and tissues’ necrosis
The following types of necrosis are differentiated: coagulation, colliquative, infarction, gangrene, decubitus, sequester.
Coagulation (dry) necrosis is characterized with sphacelus portion deaquation and induration. It includes cheesy (caseation) necrosis under tuberculosis, lues, lymphogranulomatosis as well as cereous myonecrosis under abdominal and flea-borne typhus, cholera, fibrinoid necrosis under allergic and lymphocytic diseases, malignant hypertension as well as adiponecrosis which is distributed into ferment, which occurs under pancreatitis and non-ferment caused by trauma.
Colliquative (wet) necrosis is characterized with necrotic tissue rarefication and fusion in the result of hydrolytic processes activation. It is developed in tissues rich with moisture, for example in cerebrum.
Infarction is necrosis caused by blood supply deficiency. Occurs in the result of thrombosis, embolism, long term arteriostenosis and long term, functional overexertion of organ in hypoxia conditions. By its shape infarction could be wedge-like (spleen, lung, kidneys) and irregular shape (heart, cerebrum). By its appearance it is distributed into white (ischemic), which the most often is found in cerebrum, spleen; red (hemorrhagic) which occurs in lungs, bowel, amphiblestrodes; white with hemorrhagic crown – in heart, kidneys. Infarction form and appearance depends on the features of organ’s vascular system, types of vessels branching, anastomosis development, structural-functional features of the organ (for detail see the theme of circulatory disturbances).
Gangrene is death of tissues contacting with air (bowel, extremities). Under the influence of air ferric sulphide is formed from hemoglobin, and this ferric sulphide colors necrotic portion in black. Dry and wet gangrenes are differentiated. Dry occurs mostly in the result of insufficient arterial blood supply. Necrotic portion dries up, densifies, mummifies. Wet gangrene occurs in the cases when lymph and black blood outflow is disrupted or when necrosis portion is subject to putrefactive mycronychia action. Necrotic portion is hydropic, diluted, of dirty black color with very unpleasant smell. Anaerobic gangrene development is based also on blood outflow disrupted. It is caused by a group of anaerobic activators. During that gases squeeze microvasculature structures.
Decubitus is a kind of gangrene. It is caused by blood supply and nervous trophism disturbance of subiculum in the place of squeezing (sacral bone, bladebones, calx) under seriously ill patient long term decubitus, for example, cerebrovascular accident.
Sequestrum is sphacelus which is not subject for autolysis for a long time. As a rule sequestra are observed in bones under osteomyelitis.
Demarcation line of red color with a tinge of yellow occurs surrounding necrotic portion. This is reactive inflammation characterized with vascular distention in living tissue, edema, leukocytic infiltration, macrophages incipiency. Lytic ferments of heterophilic leukocytes expedite dead zymolyte maceration and resolution similar to the one observed under wet necrosis, for example in cerebrum with cisterns formation and cyst buildup or rejection (autoamputation) of external necrotic body parts. In favorable cases mesenhymal origin cells proliferation starts around necrotic portion, spacelous aggregate either grow with conjunctive tissue (organization) or encrust with it (encapsulation) or are subject to calcification (petrification). Sometimes necrotic portion purulence is observed with abscess formation.
Apoptosis is genetically programmed death of unnecessary or defective cells in living body and the following causes these cells destruction in the process of embryogenesis and physiologic involution: cutaneous epithelium, white and red corpuscles extinction. Herewith chromatin condensation and fragmentation in cells is observed. In case apoptosis decrease neoplastic process is developed and in case apoptosis increase – atrophy. Apoptosis differs from necrosis in:
- inflammation absence,
- only several cells or their groups are involved in the process,
- cell membrane is saved,
- cellular breakdown is done not by activated hydrolytic ferments, but in participation of special calcium-magnesium dependent endonucleases which cut nucleus into numerous fragments,
- formed cells fragments (apoptosis corpuscles) phagocytized by parenchymatous or stromal cells which are situated nearby.
Apoptosis morphogenesis develops in several stages:
- chromatin condensation and margination, nucleus becomes fragmented,
- intracellular organelles condensation and cells shrinkage,
- apoptosis corpuscles formation,
- apoptosis corpuscles phagocytosis with parenchymatous cells or macrophages .
Under histological investigation apoptosis cells are round or oval particles with intensively colored cytoplasm and dark fragments of nucleus chromatin.
Fundamentals of thanatology
Thanatology is doctrine of organism dying starting from initial signs up to full corruption of the body. In the course of dying organism stays in terminal (critical) condition and is capable for reversible development occur prior to death coming. Herewith progressive functions decrement of various organism’s systems is observed, first of all respiratory depression as well as blood flow organs depression occurs, organism’s homeostatic systems incoordination has place: pulmonary edema, arrhythmia, paroxysm, respiration disturbance, constrictors paralyses, etc. Hypoxia and blood circulation disturbance cause pathologic changes in organs and tissues, which are called moribund state. Blood circulation directed to support functions of cerebrum causes microcirculation disturbance on periphery resulting in parenhymal organs structure and functions failure. Energy metabolism switches to anaerobic glycolysis causing lactic acid accumulation, acidosis, hypoxia intensifies. Biologically active substances come into blood causing microcirculation channel paresis and paralysis, increase of vascular permeability, blood clotting, stasis occurrence, clots formation. Terminal condition development and signs depend on pathological process caused death agony. In case dying is going on, terminal condition can be divided into several stages: pre-agony, terminal pause, agony, apparent death, natural death. During pre-agony stage arterial tension gradually decreases, inhibition of sensorium and electric activity of cerebrum. Tachycardia passes into bradycardia, trunkal reflex disturbance occur. In terminal phase temporary breath holding is observed, and periodic asystolia changes bradycardia. Agony is characterized with sudden activation of bulbar centers on the background of cerebral cortex full shutdown. Such disintegration of vegetal centers is accompanied with temporary and short time arterial tension increase, sinus automatism initiation and respiratory movements intensification. Apparent death is characterized with the deepest inhibition of central nervous system which expands also on spinal bulb with blood circulation termination and apnea.
Death, types, signs, postmortem changes
Depending on the causes the following types of death are recognized: natural (physiologic) death from age and organism depreciation, violent death from trauma or other negative influence on organism which ends with death and from diseases. Depending on reversible or irreversible changes in organism apparent death and natural death are specified. Apparent death is characterized with apnea, blood circulation termination and lasts for 5-6 minutes until cerebral cells death. Apparent death is reversible process of dying. Reversibility depends on the stage of hypoxic changes in cerebrum. Natural death is manifested with irreversible changes development and autolytic processes beginning in all the organs. It has characteristic signs and postmortem changes in tissues: dead body cooling, postmortem rigidity, mummification, blood relocation, postmortem lividity, cadaveric disintegration. In case death process in fast, it is observed liquid blood in the heart and vessels caused by fibrinolysis, postmortem face lividity, ecchymosis in conjunctiva, intensive and wide spread cadaveric lividity, urine, fecal matter discharge as well as red mucus presence in respiratory passages, considerable venous plethora of internal organs, hemicardia engorgement, punctuate hemorrhage on heart, lungs surface.
In case agony comes prior to death dense blood clots are observed in the heart and vessels – red in case of short term agony and yellowish-white or white under long term agony. Following basic vital functions of organism termination, early and late signs of natural death gradually develop in organism. Early signs are as follows: cadaveric lividity (occur in 30 –60 minutes post mortem), cadaveric rigidity (occurs in 2-4 hours), cooling (every hour of death gives 1 degree dead body temperature decrease, desiccation of specific parts of skin and mucous coats (the most clearly it can be seen on opened eye sclera – Lyarshe spots) and autolysis. Late signs of natural death occur on 2-3 day port mortem. They are ruining (putrefaction, dead body damage by plants, animals) and preserving (grave wax, mummification, turfy tannage, etc.). Putrefaction occurs with microorganisms participation and is characterized with dead body organic substances destruction. This is accompanied with gases formation, tissues mollities and dilution. First signs of putrefaction occur in large bowel in 24-36 hours, abdominal wall derma turns green because of sulfgemoglobin accumulation.
Autopsy procedure and methods in medical and preventive treatment facilities
Dead body stays in the ward for two hours after the fact of natural death is established by in-patient hospital’s physician. Surname, name, father’s name, date and time of death, department are to be written on the hip with brilliant green. Usually rubber-coated label on which above mentioned passport data is written is fixed to the arm. The latter method is better to use in those medical and preventive treatment facilities in which sporadic death cases occur.
Under body lift and its further examination it’s necessary to keep all moral-ethical and professional requirements. Ethical requirements include medical secrecy keeping regarding everything revealed at autopsy (thanatopsy). It’s also should be taken in mind that dead body serving for science has relatives and family. For example, Professor V.Gruberg required from students and those working in autopsy room to take off hats, as "hats wearing does not correspond the credit of the room". It’s advised to warn junior health professionals of the fact that cadaveric hypostasis can disfeature the face in case body stays dorsum upwards. It should be kept in mind that after natural death fact is etsbalished it’s necessary to close eyes, fasten up lower jaw, to cover the body with clean linen, etc. Simultaneously with diseased body completely filled-in medical records should be submitted to mortuary.
Prior to deceased body autopsy anatomist studies all the data regarding patient’s life, disease and death which can be found in medical card of hospital patient, asks attending doctor missed facts relating to course of disease and dying. Sometimes it’s useful to clarify some data from relatives, especially in case patient’s short term stay in the hospital. The following should be carefully investigated: laboratory, tolls and other methods of investigations, methods of treatment, medicines potions taken by patient, diagnosis written on title page of medical records as well as all working diagnosis written in log books. All this circumstances study pursues one more important aim – to exclude or to find out medicolegal aspect.
It’s desirable that anatomist examining all necessary data independently formulated diagnosis which can differ of attending doctor diagnosis. Doing this, as P.Kalitiyevskyi mentions, anatomist in a certain manner puts her/himself in the position of attending doctor, which is really important for mutual understanding between anatomist and clinician.
There is certain algorithm in autopsy fulfillment:
1 To carry out autopsy in day light as artificial lighting changes color transfer.
2 To put on gown and rubberized apron and oversleeves. It’s advisable to use anatomical gloves. This will ensure contagious diseases prevention, as well as cadaveric alkaloid penetration through possible defects of skin.
3 External examination of diseased body. The following should be established: sex, body-type, nutrition, state of integumentum, existence of death signs, eruptions, hematomas, wounds, ulcerations, edema, etc. It’s desirable that attending doctor could confirm passport data of diseased.
4 Main incision. It’s necessary to watch to prevent it coming through after surgical sections, cicatrix and other defects.
5 Detailed examination of cavities establishing the position and interlocation of organs, presence of joints, exudates, transudate, foreign objects, etc.
6 Organs’ withdrawal from the cavities and their investigations (size, weight, color, consistency, shape, etc.) with simultaneous necropsy taking and, depending on tasks set for anatomist, material for bacteriologic, serologic, biochemical and virology investigations. Sometimes X-ray examination of bones is done.
7 Short summary incorporating paragnosis, the cause of death, possible