1. Pathological anatomy: 1) definition, 2) objectives, 3) objects and methods of research, 4) place in medical science and healthcare practice, 5) levels of study of pathological processes.
1) Pathological anatomy is a fundamental medical and biological science that studies the structural basis of pathological processes and all human diseases.
Pathological anatomy studies and develops: 1) cell pathology 2) molecular basis, etiology, pathogenesis, morphology and morphogenesis of pathological processes and diseases 3) pathomorphosis of diseases 4) pathological embryogenesis 5) classification of diseases
2) ^ Tasks of pathological anatomy :
a) generalization of factual data obtained using various biomedical research methods
b) study of typical pathological processes
c) development of problems of etiology, pathogenesis, morphogenesis of human diseases
d) development of philosophical and methodological aspects of biology and medicine
e) formation of the theory of medicine in general and the doctrine of disease in particular
3) Objects and methods of research:
| ^ Object of study | Research method |
| living person | biopsy - intravital morphological examination ^ Types of biopsy: 1) puncture 2) excisional 3) incisional 4) aspiration a) diagnostic b) surgical cytobiopsy (rapid diagnostics) |
| dead man | autopsy - autopsy of a deceased person Purposes of autopsy:
|
| animals | experiment - actually refers to pathological physiology |
4) Pathological anatomy is the foundation of all clinical disciplines; it develops and studies not only the morphological basis of clinical diagnosis, but is also the theory of medicine as a whole.
5) Levels of study of pathological processes: a) organismal b) organ c) tissue d) cellular e) ultrastructural f) molecular
2. History of pathological anatomy: 1) works of Morgagni, 2) theory of Rokitansky, 3) theory of Schleiden and Schwann, 4) works of Virchow, 5) their significance for the development of pathological anatomy
Stages of development of pathological anatomy:
1. Macroscopic level (G. Morgagni, K. Rokitansky)
2. Microscopic level (R. Virchow)
3. Electron microscopic level
4. Molecular biological level
1) Before Morgagni, autopsies were carried out, but without analysis of the data obtained. Giovanni Batisto Morgagni:
a) began to conduct systematic autopsies with the formation of an idea of the essence of the pathological process
b) in 1861 he wrote the first book on pathological anatomy “On the location and causes of diseases identified anatomically”
c) gave the concepts of hepatization, cardiac rupture, etc.
2) Karl Rokitansky was the last representative of the theory of human humoral pathology.
Created one of the best in the 19th century. “Manual of pathological anatomy”, where he systematized all diseases on the basis of his huge personal experience(30,000 autopsies over 40 years of autopsy activity)
3) Schleiden, Schwann - theory of cellular structure (1839):
1. Cell - the minimum unit of living things
2. Animal and plant cells are fundamentally similar in structure
3. Cell reproduction is carried out by dividing the original cell
4. Cells within multicellular organisms are integrated
The significance of cell theory: it armed medicine with an understanding of the general laws of the structure of living things, and the study of cytological changes in a diseased organism made it possible to explain the pathogenesis of human diseases and led to the creation of pathomorphology of diseases.
4) 1855 - Virchow - the theory of cellular pathology - a turning point in pathological anatomy and medicine: the material substrate of the disease is cells.
5) The works of Morgagni, Rokitansky, Schleiden, Schwann, Virchow laid the foundation of modern pathology and determined the main directions of its modern development.
3. Schools of pathologists: 1) Belarusian, 2) Moscow, 3) St. Petersburg, 4) the main areas of activity of domestic schools of pathologists, 5) their role in the development of pathological anatomy.
1) The Department of Pathanatomy of the Moscow State Medical Institute was founded in 1921. Head until 1948 – prof. Titov Ivan Trofimovich - chairman of the republican scientific society, wrote a textbook on pathological anatomy in the Belarusian language.
Then the department was headed by Gulkevich Yuri Valentinovich. He was the head of the central pathological-anatomical laboratory. Autopsied the corpses of Hitler and Goebbels. He came to Minsk and began to actively develop perinatal pathology. The department defended many dissertations on the management of childbirth, cranial birth trauma, and studied listeriosis and cytoplasm. 1962 – a laboratory of teratology and medical genetics was opened, and active developmental studies began. The department created an entire institute of research institute of congenital and hereditary pathology (headed by Lazyuk Gennady Ilyich - student of Yu.V. Gulkevich). Currently there are three professors at the department:
1. Evgeniy Davydovich Cherstvoy – head of the department, honored worker of science. Multiple congenital malignancies, thyroid cancer in children
2. Kravtsova Garina Ivanovna – specialist in renal pathology, congenital kidney disease
3. Nedved Mikhail Konstantinovich – pathology of the central nervous system, congenital disorders of brain development
2) 1849 – the first department of pathological anatomy in Moscow. Head department - prof. Polunin is the founder of the clinical and anatomical direction of pathological anatomy. Nikiforov – a number of works, a textbook on pathological anatomy. Abrikosov – works in the field of pulmonary tuberculosis, pathology of the oral cavity, kidneys, a textbook that has gone through 9 reprints. Skvortsov – diseases of childhood. Davydovsky – general pathology, infectious pathology, gerontology. Strukov is the founder of the doctrine of collagenoses.
3) 1859 - the first department of pathological anatomy in St. Petersburg - head prof. Rudnev, also Shor, Anichkov, Glazunov, Sysoev and others.
4) Main directions - see questions 1-2
5) Role in the development of pathological anatomy: they were the founders of domestic pathological anatomy, determined the high level of its development at the present stage
4. Death: 1) definition, 2) classification of human death, 3) characteristics of clinical death, 4) characteristics of biological death, 5) signs of death and post-mortem changes.
1) Death is the irreversible cessation of human life.
2) Classification of human death:
a) depending on the reasons that caused it: 1) natural (physiological) 2) violent 3) death from illness (gradual or sudden)
b) depending on the development of reversible or irreversible changes in life activity: 1) clinical 2) biological
3) Clinical death - changes in the vital functions of the body that are reversible within a few minutes, accompanied by cessation of blood circulation and respiration.
State before clinical death - agony - uncoordinated activity of homeostatic systems in the terminal period (arrhythmias, sphincter paralysis, convulsions, pulmonary edema, etc.)
Clinical death is based on: hypoxia of the central nervous system due to cessation of blood circulation and respiration and disorders of their regulation.
4) Biological death - irreversible changes in the vital activity of the body, the beginning of autolytic processes.
It is characterized by non-simultaneous death of cells and tissues (the cells of the cerebral cortex die first, after 5-6 minutes; in other organs, cells die within several days, while their destruction can be immediately detected only with EM)
^ 5) Signs of death and post-mortem changes:
1. Cooling a corpse (algor mortis)- gradual decrease in body temperature.
Reason: cessation of heat production in the body.
Sometimes - in case of strychnine poisoning or death from tetanus - the temperature after death may rise.
2. ^ Rigor mortis (rigor mortis) - compaction of voluntary and involuntary muscles of the corpse.
Reason: disappearance of ATP in the muscles after death and accumulation of lactate in them.
3. ^ Corpse desiccation : localized or generalized (mummification).
Reason: evaporation of moisture from the surface of the body.
Morphology: clouding of the corneas, the appearance of dry brownish spots on the sclera, parchment spots on the skin, etc.
4. ^ Redistribution of blood in a corpse - overflow of blood in the veins, emptying of the arteries, post-mortem blood clotting in the veins and right parts of the heart.
Morphology of post-mortem clots: smooth, elastic, yellow or red, lying freely in the lumen of the vessel or heart.
Quick death - few post-mortem clots, death from asphyxia - absence of post-mortem clotting.
5. ^ Cadaveric spots- the appearance of cadaveric hypostases in the form of dark purple spots, most often in the underlying parts of the body that are not subject to compression. When pressed, the cadaveric spots disappear.
Reason: redistribution of blood in the corpse depending on its position.
6. ^ Corpse imbibition - late cadaveric spots of red-pink color that do not disappear with pressure.
Reason: impregnation of the area of cadaveric hypostases with plasma with hemoglobin from hemolyzed erythrocytes.
^ 7. Cadaveric decomposition with processes
A) autolysis - first of all occurs and is expressed in glandular organs with enzymes (liver, pancreas), in the stomach (gastromalacia), esophagus (esophagomalacia), during aspiration of gastric juice - in the lungs ("acid" softening of the lungs)
B) rotting of a corpse - the result of the proliferation of putrefactive bacteria in the intestines and their subsequent colonization of the tissues of the corpse; rotting tissue is dirty green and smells like rotten eggs
C) cadaveric emphysema - the formation of gases during the rotting of a corpse, swelling the intestines and penetrating into organs and tissues; in this case, the tissues acquire a foamy appearance, and crepitation is heard when palpated.
5. Dystrophies: 1) definition, 2) causes, 3) morphogenetic mechanisms of development, 4) morphological specificity of dystrophies, 5) classification of dystrophies.
1) Dystrophy– a complex pathological process, which is based on a violation of tissue (cellular) metabolism, leading to structural changes.
2) ^ The main cause of dystrophy - violation of the basic mechanisms of trophism, namely:
a) cellular (structural organization of the cell, cell autoregulation) and b) extracellular (transport: blood, lymph, MCR and integrative: neuroendocrine, neurohumoral) mechanisms.
3) ^ Morphogenesis of dystrophies:
A) infiltration– excessive penetration of metabolic products from the blood and lymph into cells or intercellular substances with their subsequent accumulation due to the insufficiency of enzymatic systems that metabolize these products [infiltration of the epithelium of the proximal tubules of the kidneys with protein in nephrotic syndrome]
b ) decomposition (phanerosis)– disintegration of cell ultrastructures and intercellular substance, leading to disruption of tissue (cellular) metabolism and accumulation of products of impaired metabolism in the tissue (cell) [fatty degeneration of cardiomyocytes during diphtheria intoxication]
V) perverted synthesis– synthesis in cells or tissues of substances not normally found in them [synthesis of alcoholic hyaline by hepatocytes]
G) transformation– the formation of products of one type of metabolism from common initial products that are used to build proteins, fats, carbohydrates [increased polymerization of glucose into glycogen]
4) A certain tissue is most often characterized by a certain mechanism of morphogenesis of dystrophy [renal tubules - infiltration, myocardium - decomposition] - orthology of dystrophies
5) ^ Classification of dystrophies.
I. Depending on the predominance of morphological changes in specialized elements of the parenchyma or stroma and vessels:
a) parenchymal dystrophies b) stromal-vascular (mesenchymal) dystrophies c) mixed dystrophies
II. According to the predominance of violations of one or another type of exchange:
a) protein b) fat c) carbohydrate d) mineral
III. Depending on the influence of genetic factors:
a) acquired b) hereditary
IV. According to the prevalence of the process:
a) general b) local
6. Parenchymatous protein dystrophies: 1) causes 2) morphology and outcomes of granular dystrophy 3) morphology and outcomes of hydropic dystrophy 4) morphology and outcomes of hyaline droplet dystrophy 5) morphology and outcomes of horny dystrophy.
1) Causes of parenchymal protein dystrophies: dysfunction of certain enzyme systems (see the example of certain types of parenchymal protein dystrophies)
Types of parenchymal protein dystrophies: 1. horny 2. granular 3. hyaline-droplet 4. hydropic
2) Morphology of granular dystrophy(dull, cloudy swelling): MaSk: organs are enlarged, dull, flabby on section; MiSk: cells are enlarged, swollen, with protein grains.
^ Development mechanism and reason: expansion of the ER cisterns and swelling of mitochondria as a result of hyperplasia in response to functional stress
Localization: 1) kidneys 2) liver 3) heart
Exodus: 1. elimination of the pathological factor cell restoration 2. transition to hyaline-droplet, hydropic or fatty degeneration.
3) ^ Morphology of hydropic (dropsy) dystrophy : cells are enlarged; the cytoplasm is filled with vacuoles with clear liquid; the nucleus is on the periphery, vesicular.
Localization: 1) skin cells 2) kidney tubules 3) hematocytes 4) NS ganglion cells
^ Development mechanism : increased permeability of cell membranes, activation of hydrolytic enzymes of lysosomes breaking of intramolecular bonds, attachment to water molecules hydration of cells.
Causes: kidneys - nephrotic syndrome; liver - toxic and viral hepatitis; epidermis - smallpox, swelling; ganglion cells are a manifestation of physiological activity.
^ Exodus: focal or total liquefaction necrosis of cells.
4) Morphology of hyaline droplet dystrophy: hyaline-like protein droplets in the cytoplasm with destruction of cellular organelles.
Localization: 1) liver 2) kidneys 3) myocardium (very rare)
^ Development mechanism and causes : kidneys - failure of the vacuolar-lysosomal apparatus of the epithelium of the proximal tubules of nephrocytes in nephrotic syndrome; liver - synthesis of hyaline-like Mallory bodies from alcoholic hyaline in alcoholic hepatitis.
^ Exodus: focal or total coagulative necrosis of cells.
5) Horny dystrophy (pathological keratinization):
a) hyperkeratosis - excessive formation of horny substance on the keratinizing epithelium
b) leukoplakia - pathological keratinization of mucous membranes; cancer pearls for squamous cell carcinoma
^ Reasons: violation of skin development; chronic inflammation; viral infections; avitaminosis
Exodus: elimination of the pathogen at the beginning of the process cell restoration; cell death
7. Parenchymal fatty degenerations: 1) causes 2) histochemical methods for identifying fats 3) macro- and microscopic characteristics of parenchymal myocardial degeneration 4) macro- and microscopic characteristics of fatty liver degeneration 5) outcomes of fatty degeneration
1) ^ Causes of parenchymal fatty degenerations:
A. tissue hypoxia in anemia, chronic lung diseases, chronic alcoholism
b. infections and intoxications with lipid metabolism disorders (diphtheria, sepsis, chloroform)
V. vitamin deficiencies, one-sided nutrition without protein with a deficiency of lipotropic factors.
2) ^ Histochemical methods for identifying fats : A. Sudan III, sharlah - red color; b. Sudan IV, osmic acid - black color c. Nile blue sulfate - dark blue fatty acids, red neutral fats.
3) ^ Morphology of parenchymal fatty degeneration of the myocardium:
MaSk: the heart is unchanged or enlarged, the chambers are stretched, flabby, clay-yellow on section; yellow-white striations on the side of the endocardium (“tiger heart”).
MiSk: dust-like obesity (tiny fat droplets in cardiomyocytes) fine-droplet obesity (replacement of the entire cytoplasm of cells with fat droplets, disappearance of cross-striations, breakdown of mitochondria). The focal process occurs along the venous end of the capillaries (“tiger heart”).
^ Development mechanism : myocardial energy deficiency (hypoxia, diphtheritic toxin) 1) increased supply of fatty acids into cells 2) impaired fat metabolism in the cell 3) breakdown of lipoproteins of intracellular structures.
4) ^ Morphology of parenchymal fatty liver degeneration:
MaSk: liver is enlarged, flabby, ocher-yellow, there is fat on the knife blade
MiSk: dust-like obesity small-droplet obesity large-droplet obesity (fat vacuole fills the entire cytoplasm and pushes the nucleus to the periphery).
^ Development mechanisms 1. excessive intake of fatty acids into the liver or an increase in their synthesis by hepatocytes (lipoproteinemia in diabetes, alcoholism, general obesity, hormonal disorders) 2. exposure to toxins that block the oxidation of fatty acids and the synthesis of lipoproteins in hepatocytes (ethanol, phosphorus, chloroform) 3. insufficient intake of lipotropic factors (vitaminosis)
5) Outcomes of parenchymal fatty degeneration: A. reversible while maintaining cellular structures b. cell death
8. Parenchymal carbohydrate dystrophies: 1) causes 2) histochemical methods for identifying carbohydrates 3) carbohydrate dystrophies associated with impaired glycogen metabolism 4) carbohydrate dystrophies associated with impaired glycoprotein metabolism 5) outcomes of carbohydrate dystrophy.
1) Carbohydrates: A. polysaccharides (glycogen) b. glycosaminoglycans (mucopolysaccharides) c. glycoproteins (mucus mucins, tissue mucoids).
^ Causes of parenchymal carbohydrate dystrophies : disturbance of glycogen metabolism (with diabetes), glycoproteins (with inflammation).
2) Histochemical methods for identifying carbohydrates:
a) all carbohydrates - CHIC reaction of Hotchkiss-McManus (red color)
b) glycogen - Besta carmine (red)
c) glycosamines, glycoproteins - methylene blue
3) ^ Carbohydrate dystrophies associated with impaired glycogen metabolism:
A) acquired- mainly in diabetes:
1. decrease in tissue glycogen reserves in the liver infiltration of the liver with fats inclusions of glycogen in the nuclei of hepatocytes ("holey", "empty" nuclei)
2. glucosuria glycogen infiltration of the epithelium of the narrow and distal segments glycogen synthesis in the tubular epithelium tall epithelium with light foamy cytoplasm
3. hyperglycemia diabetic microangiopathy (intercapillary diabetic glomerulosclerosis, etc.)
b) congenital- glycogenosis: deficiency of enzymes involved in the breakdown of stored glycogen.
4) ^ Carbohydrate dystrophies associated with impaired glycoprotein metabolism : accumulation of mucins and mucoids in cells and intercellular substance (mucosal dystrophy)
A) inflammation increased mucus production, changes in the physicochemical properties of mucus desquamation of secretory cells, obstruction of excretory ducts with cells and mucus a. cysts; b. obstruction of the bronchi atelectasis, foci of pneumonia c. accumulation of pseudomucins (mucus-like substances) colloid goiter
b) cystic fibrosis- hereditary systemic disease, secretion of thick viscous mucus by the epithelium of the glands retention cysts, sclerosis (cystic fibrosis) damage to all glands of the body
5) ^ Outcomes of carbohydrate dystrophies : A. at the initial stage - cell restoration when the pathogen is eliminated b. atrophy, mucosal sclerosis, cell death
9. Mesenchymal protein dystrophies: 1) definition and classification 2) etiology and morphogenesis of mucoid swelling 3) morphological picture and outcomes of mucoid swelling 4) etiology and morphogenesis of fibrinoid swelling 5) morphological characteristics and outcomes of fibrinoid swelling
1) ^ Mesenchymal protein dystrophies - disturbance of protein metabolism in the connective tissue of the stroma of organs and the walls of blood vessels.
Classification of mesenchymal protein dystrophies: 1. mucoid swelling 2. fibrinoid swelling (fibrinoid) 3. hyalinosis (three successive stages of connective tissue disorganization) 4. amyloidosis
At the core: plasmorrhagia, increased vascular permeability accumulation of blood plasma products in the main substance destruction of connective tissue elements.
2) Mucoid swelling- superficial and reversible disorganization of connective tissue.
Etiology of mucoid swelling: 1. hypoxia 2. streptococcal infection 3. immunopathological reactions.
Morphogenesis of mucoid swelling: accumulation of hydrophilic glycosaminoglycans (hyaluronic acid) in the connective tissue hydration and swelling of the main interstitial substance
^ Process localization : wall of arteries; heart valves; endo- and epicardium.
3) Morphological picture of mucoid swelling: MaSk organ or tissue is not changed, MiSk is a basophilic basic substance (the phenomenon of metachromasia due to the accumulation of chromotropic substances); collagen fibers swell and undergo fibrillar disintegration (painted yellow-orange with picrofuchsin).
Outcomes: 1. complete restoration of tissue 2. transition to fibrinoid swelling
4) Fibrinoid swelling- deep and irreversible destruction of connective tissue.
Etiology of fibrinoid swelling:
a) at the system (widespread) level:
1. infectious-allergic reactions (vascular fibrinoid in tuberculosis with hyperergic reactions)
2. allergic reactions (fibrinoid changes in blood vessels in rheumatic diseases)
3. autoimmune reactions (in the capillaries of the renal glomeruli during GN)
4. angioneurotic reactions (fibrinoid of arterioles in arterial hypertension)
b) at the local level - chronic inflammation in the appendix with appendicitis, in the bottom of a chronic gastric ulcer.
^ Morphogenesis of fibrinoid swelling : plasmorrhagia + destruction of the main substance and fibers of connective tissue formation of fibrinoid (fibrin + proteins + cellular nucleoproteins).
5) ^ Morphology of fibrinoid swelling : MaSk organs and tissues are not changed; MiSK homogeneous bundles of collagen fibers form insoluble compounds with fibrin, eosinophilic, yellow when stained with picrofuchsin, sharply CHIC-positive, argyrophilic.
Exodus: fibrinoid necrosis (complete destruction of connective tissue with a pronounced reaction of macrophages) replacement of the focus of destruction with connective tissue (hyalinosis; sclerosis).
10. Hyalinosis: 1) definition, mechanism of development and classification 2) pathological processes that result in the development of hyalinosis 3) pathomorphology of vascular hyalinosis 4) pathomorphology of connective tissue hyalinosis 5) outcome and functional significance of hyalinosis.
1) Hyalinosis- formation in the connective tissue of homogeneous translucent dense masses resembling hyaline cartilage - hyaline.
Hyaline consists of 1. fibrin and other blood plasma proteins 2. lipids 3. immunoglobulins. Strongly CHIC-positive, yellow-red when stained with picrofuchsin.
Development mechanism: destruction of fibrous structures, increased tissue-vascular permeability precipitation of plasma proteins on altered fibrous structures formation of hyaline.
Classification: 1. vascular hyalinosis a. systemic b. local 2. hyalinosis of the connective tissue itself a. systemic b. local
2) Pathological processes resulting in the development of hyalinosis:
A) vessels: 1. Hypertension, atherosclerosis (simple hyaline) 2. diabetic microangiopathy (diabetic arteriolohyalinosis - lipohyalin) 3. rheumatic diseases (complex hyaline) 4. local physiological phenomenon in the spleen of adults and the elderly (“glazed spleen”).
b) connective tissue itself: 1. rheumatic diseases 2. locally in the bottom of a chronic ulcer, appendix 3. in scars, fibrous adhesions of cavities, vascular wall with atherosclerosis.
3) Pathomorphology of vascular hyalinosis(mainly small arteries and arterioles are affected, it is systemic in nature, but most typical for the vessels of the kidneys, pancreas, brain, retina):
^ MiSk: hyaline in the subendothelial space; thinned media.
MaSk: glassy vessels in the form of dense tubes with a sharply narrowed lumen; atrophy, deformation, shrinkage of organs (for example, arteriolosclerotic nephrocirrhosis).
4) ^ Pathomorphology of hyalinosis of the connective tissue itself:
MiSk: swelling of connective tissue bundles; loss of fibrillarity, fusion into a homogeneous dense cartilage-like mass; cellular elements are compressed and undergo atrophy.
^ MaSk: the tissue is dense, whitish, translucent (for example, hyalinosis of the heart valves in rheumatism).
5) Outcomes of hyalinosis (usually unfavorable): 1. resorption (in keloids, in mammary glands in conditions of hyperfunction) 2. mucus formation 3. rupture of hyalinized vessels with high blood pressure, hemorrhage
Functional meaning: widespread hyalinosis of arterioles functional organ failure (CRF in arteriolosclerotic nephrocirrhosis); local hyalinosis of the heart valves heart disease.
11. Amyloidosis: 1) definition and methods of histochemical detection of amyloid 2) theories of the pathogenesis of amyloidosis 3) morpho- and pathogenesis of amyloidosis 4) classification of amyloidosis 5) perireticular and pericollagenous amyloidosis.
1) ^ Amyloidosis (amyloid dystrophy) - stromal vascular dysproteinosis, accompanied by deep violation protein metabolism, the appearance of abnormal fibrillar protein and the formation of a complex substance - amyloid - in the interstitial tissue and walls of blood vessels.
Amyloid detection methods(the reactions are based on the phenomenon of metachromasia):
1. coloring Congo red - red
2. staining with Lugol's solution with 10% sulfuric acid solution - blue
3. staining with methyl violet - red
4. dichroism and anisotropy in a polarizing microscope
2) Theories of the pathogenesis of amyloidosis:
a) immunological (amyloid as a result of the interaction of AG and AT)
b) theory of local cellular synthesis (amyloid is produced by cells of mesenchymal origin)
c) mutation theory (amyloid is produced by mutant cells)
3) ^ Amyloid consists of two components that have antigenic properties :
A) P-component(plasma) - plasma glycoproteins
b) F component(fibrillar) - heterogeneous, four types of F-component:
1. AA protein - not associated with Ig - from serum α-globulin SSA
2. AL protein - associated with Ig - from - and -light chains of Ig
3. FAP protein - formed from prealbumin
4. ASC1 protein - formed from prealbumin
Morphogenesis of amyloidosis:
1. Pre-amyloid stage - transformation of some cells (fibroblasts, plasma cells, reticular cells, cardiomyocytes, vascular SMCs) into amyloidoblasts
2. Synthesis of the fibrillar component
3. Interaction of fibrils to form the amyloid framework
4. Interaction of the framework with plasma components and chondroitin sulfate with the formation of amyloid
Pathogenesis of amyloidosis:
A) AA amyloidosis: activation of the monocytic phagocyte system release of IL-1 stimulation of SSA protein synthesis in the liver (its function is an immunomodulator) sharp increase SSA in the blood enhanced destruction of SAA by macrophages to AA assembly of amyloid fibrils from the AA protein on the surface of macrophages-amyloidoblasts under the influence of amyloid-stimulating factor synthesized by organs in the pre-amyloid stage.
b) AL-amyloidosis: disruption of the degradation of immunoglobulin light chains, the appearance of genetically altered light chains synthesis of amyloid fibrils from Ig L-chains by macrophages, plasma and other cells.
4) Classification of amyloidosis:
a) due to reason (origin):
1. idiopathic primary(AL amyloidosis)
2. hereditary(genetic, family): a. periodic illness (familial Mediterranean fever) b. Muckle-Wales syndrome (a and b - AA amyloidosis) c. familial amyloid polyneuropathy (FAP amyloidosis)
3. secondary acquired: A. reactive (AA amyloidosis in chronic infections, COPD, osteomyelitis, wound suppuration, rheumatoid arthritis) b. monoclonal protein (AL amyloidosis in paraproteinemic leukemia)
4. senile systemic amyloidosis(ASC1 amyloidosis) and local
b) according to the specificity of the fibril protein: 1. AL- (generalized damage to the heart, lungs, blood vessels) 2. AA- (generalized damage mainly to the kidneys) 3. FAP- (damage to peripheral nerves) 4. ASC1- (mainly damage to the heart and blood vessels)
c) by prevalence: 1. generalized: primary, secondary, systemic senile 2. local: forms of hereditary amyloidosis, senile local amyloidosis, “amyloid tumor”
d) according to clinical manifestations: 1. cardiopathic 2. epinephropathic 3. nephropathic 4. neuropathic 5. APUD amyloidosis 6. hepapathic
5) Amyloidosis is classified according to the location of the lesion:
1. perireticular (“parenchymatous”)- loss of amyloid along the reticular fibers of the membranes of blood vessels and glands, reticular stroma of the parenchyma (spleen, liver, kidneys, adrenal glands, intestines, intima of small and medium-sized vessels)
2. pericollagenous ("mesenchymal")- loss of amyloid along the collagen fibers of the adventitia of medium and large vessels, myocardium, striated muscles, SMC, nerves, skin.
12. Amyloidosis: 1) clinical and morphological forms of amyloidosis and organs affected by them 2) the most common causes of secondary amyloidosis 3) macro- and microscopic characteristics of spleen amyloidosis 4) macro- and microscopic characteristics of kidney amyloidosis 5) morphology of amyloidosis of the liver, intestines and brain.
1) CMF amyloidosis and organs predominantly affected by it: 1. cardiopathic (heart) 2. epinephropathic (adrenal glands) 3. nephropathic (kidneys) 4. neuropathic (nerves, brain) 5. APUD amyloidosis (APUD system) 6. hepapathic (liver)
2) The most common causes of secondary amyloidosis:
A. severe forms chronic infections (tuberculosis, syphilis)
b. COPD (bronchiectasis, abscesses)
V. osteomyelitis, wound suppuration
d. rheumatoid arthritis and other rheumatic diseases
d. multiple myeloma
^ 3) Pathomorphology of spleen amyloidosis:
A) "greasy" spleen: MiSk uniform deposition of amyloid in the pulp, MaSk spleen enlarged, dense, brown-red, smooth, greasy shine on the cut
b) "sago" spleen: MiSk deposition of amyloid in lymphoid follicles, which have the appearance of sago grains on a section, MaSk spleen is enlarged, dense
4) ^ Pathomorphology of renal amyloidosis : MiSk amyloid deposits in the vascular wall, capillary loops and vascular mesangium, in the basement membranes of the tubular epithelium and stroma, MaSk first dense large sebaceous (“big white kidney”), then amyloid-wrinkled kidney (see question 126 - amyloid nephrosis)
^ 5) Pathomorphology of amyloidosis:
A) liver: MiSk amyloid deposition between the stellate reticuloendotheliocytes of the sinusoids, along the reticular stroma of the lobules, in the walls of vessels, ducts, in the connective tissue of the portal tracts, MaSk liver is enlarged, dense, greasy on the section
b) intestines: amyloid deposits along the reticular stroma of the mucosa and in the walls of blood vessels; atrophy of the glandular apparatus of the intestinal mucosa
V) brain: amyloid in senile plaques of the cortex (markers of senile dementia, Alzheimer's disease), blood vessels and membranes of the brain.
13. Mesenchymal fatty degenerations: 1) definition and classification 2) definition, causes and mechanisms of development of obesity 3) morphology of obesity 4) lipomatosis 5) morphology of cholesterol metabolism disorders
1) ^ Mesenchymal fatty degenerations - stromal-vascular dystrophies, which occur when the metabolism of neutral fats and cholesterol is disrupted and are accompanied by either excessive accumulation of fat and cholesterol, or a decrease in its amount, or accumulation in an uncharacteristic location.
^ Classification of mesenchymal fatty degenerations:
1. disturbance of the metabolism of neutral fats: a. general: 1) obesity 2) exhaustion b. local
2. violation of the exchange of cholesterol and its esters.
2) Obesity (obesity)- an increase in the amount of neutral fats in fat depots, which are of a general nature.
Causes of obesity: 1. excess nutrition 2. physical inactivity 3. disturbance of neuroendocrine regulation of fat metabolism 4. hereditary factors.
Development mechanism: A. activation of lipoprotein lipase and inhibition of lipolytic lipases b. disruption of hormonal regulation in favor of antilipolytic hormones c. changes in the state of fat metabolism in the liver and intestines
^ Classification of general obesity:
1. by etiology: A. primary b. secondary (nutritional, cerebral in case of a brain tumor, endocrine in case of Itsenko-Cushing syndrome, hypothyroidism, hereditary)
2. by external manifestations: A. symmetrical (universal) type b. upper (in the area of the face, neck, shoulders, mammary glands) c. middle (in the subcutaneous tissue of the abdomen in the form of an apron) d. lower (in the area of the thighs and lower legs)
3. for excess body weight: I degree (up to 30%) II degree (up to 50%) III degree (up to 99%) IV degree (from 100% or more)
4. by number and size of adiposocytes: a) hypertrophic type (the number of adiposocytes is not changed, the cells are sharply enlarged, malignant course) b) hyperplastic type (the number of adiposocytes is increased, there are no metabolic changes in the cells, benign course)
^ 3) Morphology of obesity:
1. abundant deposition of fat in the subcutaneous tissue, omentum, mesentery, mediastinum, epicardium, as well as in uncharacteristic places: myocardial stroma, pancreas
2. adipose tissue grows under the epicardium and envelops the heart, sprouting muscle mass; the heart is significantly enlarged; cardiomyocyte atrophy; the border between the membranes of the heart is erased; in some cases, heart rupture is possible (the right parts are especially affected)
4) Lipomatosis- local increase in the amount of fatty tissue:
a) Dercum's disease (lipomatosis dolorosa) - painful nodular deposits of fat in the subcutaneous tissue of the trunk and limbs due to polyglandular endocrinopathy
b) vacant obesity - local increase in the amount of adipose tissue during organ atrophy (fat replacement of the thymus during its atrophy)
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Plan
Lecture 1. Pathological anatomy
1.1 Objectives of pathological anatomy
1.2 Objects of study and methods of pathological anatomy
1.3 Brief history of the development of pathological anatomy
1.4 Death and post-mortem changes, causes of death, thanatogenesis, clinical and biological death
1.5 Cadaveric changes, their differences from intravital pathological processes and significance for the diagnosis of the disease
Lecture 2. Necrosis
2.1 Definition, etiology and classification of necrosis
2.2 Pathomorphological characteristics of necrosis. Their importance for diagnosing diseases
Lecture 3. Pathological anatomy
Lecture 4. General doctrine of dystrophies
Lecture 5. Necrosis
5.1 Classification of necrosis
Lecture 6. Circulatory disorders
6.1 Hyperemia
6.2 Bleeding
6.3 Thrombosis
6.4 Embolism
6.5 Heart attack
Lecture 7. Inflammation
7.1 Macroscopic classification of foci of tuberculous inflammation
Lecture 8. Immunopathological processes
Lecture 9. Regeneration. Wound healing
Lecture 10. Processes of adaptation (adaptation) and compensation
Lecture 11. Sclerosis
Lecture 12. Tumors
12.1 Connective tissue tumors
12.2 Tumors bone tissue
12.3 Tumors of cartilage tissue
12.4 Tumors of vascular tissue
12.5 Muscle tumors
12.6 Tumors of hematopoietic tissue
Lecture 13. Blood diseases
13.1 Anemias and their classification
13.2 Hemoblastoses
13.3 Classification of tumors of hematopoietic and lymphatic tissue
13.4 Thrombocytopathies
Lecture 14. Diseases of the cardiovascular system
14.1 Endocarditis
14.2 Myocarditis
14.3 Heart defect
14.4 Cardiosclerosis
14.5 Atherosclerosis
14.6 Hypertension
14.7 Coronary heart disease
14.8 Cerebrovascular disorders
14.9 Vasculitis
Lecture 15. Respiratory diseases
15.1 Acute bronchitis
15.2 Acute inflammatory diseases lungs (pneumonia)
15.3 Acute destructive processes in the lungs
15.4 Chronic nonspecific lung diseases
Lecture 16. Diseases of the gastrointestinal tract
16.1 Diseases of the esophagus
16.2 Stomach diseases
16.3 Bowel diseases
Lecture 17. Diseases of the liver, gall bladder and pancreas
17.1 Liver diseases
17.2 Gallbladder diseases
17.3 Diseases of the pancreas
Lecture 18. Kidney diseases
18.1 Glomerulopathies
18.2 Tubulopathies
18.3 Interstitial nephritis
18.4 Kidney stones
18.5 Polycystic kidney disease
18.6 Nephrosclerosis
18.7 Kidney tumors
Lecture 19. Diseases of the genital organs and breast
19.1 Dyshormonal diseases
19.2 Inflammatory diseases of the genital organs and breast
19.3 Tumors of the genital organs and mammary glands
Lecture 20. Diseases of the endocrine glands
20.1 Pituitary disorders
20.2 Adrenal disorders
20.3 Thyroid gland
20.4 Pancreas
Lecture 21. Diseases of the central nervous system
21.1 Alzheimer's disease
21.2 Charcot's disease
21.3 Multiple sclerosis
21.4 Encephalitis
Lecture 22. Infectious diseases
22.1 Viral diseases
22.2 Diseases caused by bacteria
22.3 Fungal diseases
22.4 Diseases caused by protozoa
Lecture 1. Pathological anatomy
1.1 Tasks of pathological anatomy
Pathological anatomy - the science of the occurrence and development of morphological changes in a sick body. It originated in an era when the study of painfully altered organs was carried out with the naked eye, i.e., using the same method used by anatomy, which studies the structure of a healthy organism.
Pathological anatomy is one of the most important disciplines in the system veterinary education, in the scientific and practical activities of a doctor. She studies the structural, i.e., material basis of the disease. It is based on data from general biology, biochemistry, anatomy, histology, physiology and other sciences that study the general laws of life, metabolism, structure and functional functions of a healthy human and animal body in its interaction with the external environment.
Without knowing what morphological changes a disease causes in an animal’s body, it is impossible to have a correct understanding of its essence and mechanism of development, diagnosis and treatment.
The study of the structural basis of the disease is carried out in close connection with its clinical manifestations. Clinical and anatomical direction is a distinctive feature of Russian pathological anatomy.
The study of the structural basis of the disease is carried out at different levels:
· the organismal level allows us to identify the disease of the entire organism in its manifestations, in the interrelation of all its organs and systems. From this level begins the study of a sick animal in clinics, a corpse in a dissection room or a cattle burial ground;
· the system level studies any system of organs and tissues (digestive system, etc.);
· the organ level allows you to determine changes in organs and tissues visible with the naked eye or under a microscope;
· tissue and cellular levels - these are the levels of studying altered tissues, cells and intercellular substance using a microscope;
· the subcellular level makes it possible to observe using an electron microscope changes in the ultrastructure of cells and intercellular substance, which in most cases were the first morphological manifestations of the disease;
· the molecular level of studying the disease is possible using complex research methods involving electron microscopy, cytochemistry, autoradiography, immunohistochemistry.
Recognition of morphological changes in organ and tissue levels It is very difficult at the beginning of the disease, when these changes are minor. This is due to the fact that the disease began with changes in subcellular structures.
These levels of research make it possible to consider structural and functional disorders in their inextricable dialectical unity.
1.2 Objects of research and methods of pathological anatomy
Pathological anatomy deals with the study of structural disorders that arise at the very initial stages of the disease, during its development, up to the final and irreversible conditions or recovery. This is the morphogenesis of the disease.
Pathological anatomy studies deviations from the usual course of the disease, complications and outcomes of the disease, and necessarily reveals the causes, etiology, and pathogenesis.
Studying the etiology, pathogenesis, clinical picture, and morphology of the disease allows us to apply scientifically based measures for the treatment and prevention of the disease.
The results of observations in the clinic, studies of pathophysiology and pathological anatomy showed that a healthy animal body has the ability to maintain a constant composition internal environment, stable equilibrium in response to external factors - homeostasis.
In case of illness, homeostasis is disrupted, vital activity proceeds differently than in a healthy body, which is manifested by structural and functional disorders characteristic of each disease. Disease is the life of an organism in changed conditions of both the external and internal environment.
Pathological anatomy also studies changes in the body. Under the influence of drugs, they can be positive and negative, causing side effects. This is the pathology of therapy.
So, pathological anatomy covers a wide range of issues. She sets herself the task of giving a clear idea of the material essence of the disease.
Pathological anatomy strives to use new, more subtle structural levels and the most complete functional assessment of the altered structure at equal levels of its organization.
Pathological anatomy receives material about structural disorders in diseases with the help of autopsies, surgical operations, biopsies and experiments. In addition, in veterinary practice, for diagnostic or scientific purposes, forced slaughter of animals is carried out at different stages of the disease, which makes it possible to study the development of pathological processes and diseases on various stages. A great opportunity for pathological examination of numerous carcasses and organs is presented in meat processing plants during the slaughter of animals.
In clinical and pathomorphological practice, biopsies are of particular importance, i.e. intravital removal of pieces of tissue and organs, carried out for scientific and diagnostic purposes.
Particularly important for elucidating the pathogenesis and morphogenesis of diseases is their reproduction in experiment . Experimental The method makes it possible to create disease models for accurate and detailed study, as well as for testing the effectiveness of therapeutic and preventive drugs.
The possibilities of pathological anatomy have expanded significantly with the use of numerous histological, histochemical, autoradiographic, luminescent methods, etc.
Based on the objectives, pathological anatomy is placed in a special position: on the one hand, it is a theory of veterinary medicine, which, by revealing the material substrate of the disease, serves clinical practice; on the other hand, it is clinical morphology for establishing a diagnosis, serving the theory of veterinary medicine.
1.3 Brief history of the development of pathological anatomy
The development of pathological anatomy as a science is inextricably linked with the dissection of human and animal corpses. According to literary sources in the 2nd century AD. e. The Roman physician Galen dissected the corpses of animals, studying their anatomy, physiology, and described some pathological and anatomical changes. In the Middle Ages, due to religious beliefs, autopsies of human corpses were prohibited, which somewhat halted the development of pathological anatomy as a science.
In the 16th century in a number of countries in Western Europe, doctors were again given the right to perform autopsies on human corpses. This circumstance contributed to the further improvement of knowledge in the field of anatomy and the accumulation of pathological and anatomical materials for various diseases.
In the middle of the 18th century. The book of the Italian doctor Morgagni “On the localization and causes of diseases identified by the anatomist” was published, where the scattered pathological and anatomical data of his predecessors were systematized and his own experience was generalized. The book describes changes in organs in various diseases, which facilitated their diagnosis and contributed to the promotion of the role of pathological and anatomical research in establishing a diagnosis.
In the first half of the 19th century. in pathology, the humoral direction dominated, whose supporters saw the essence of the disease in changes in the blood and juices of the body. It was believed that what happens first qualitative violation blood and juices with subsequent rejection of “pathogenic matter” in the organs. This teaching was based on fantastic ideas.
The development of optical technology, normal anatomy and histology created the prerequisites for the emergence and development of cell theory (Virchow R., 1958). The pathological changes observed in a particular disease, according to Virchow, are a simple sum of the diseased state of the cells themselves. This is the metaphysical nature of R. Virchow’s teaching, since the idea of the integrity of the organism and its relationship with the environment was alien to him. However, Virchow's teaching served as an incentive for in-depth scientific study of diseases through pathological-anatomical, histological, clinical and experimental research.
In the second half of the 19th and early 20th centuries. In Germany, major pathologists Kip and Jost worked, authors of fundamental manuals on pathological anatomy. German pathologists conducted extensive research on equine infectious anemia, tuberculosis, foot and mouth disease, swine fever, etc.
The beginning of the development of domestic veterinary pathological anatomy dates back to the middle of the 19th century. The first veterinary pathologists were professors of the veterinary department of the St. Petersburg Medical-Surgical Academy I. I. Ravich and A. A. Raevsky.
Since the end of the 19th century, domestic pathological anatomy has received its further development within the walls of the Kazan Veterinary Institute, where since 1899 the department was headed by Professor K. G. Bol. He is the author of a large number of works on general and specific pathological anatomy.
The research conducted by domestic scientists is of great scientific and practical importance. A number of important studies have been carried out in the field of studying theoretical and practical issues pathologies of farm and commercial animals. These works made a valuable contribution to the development of veterinary science and animal husbandry.
1.4 Death and post-mortem changes,causes of death, thanatogenesis, clinical and biological death
Death is the irreversible cessation of the vital functions of the body. This is the inevitable end of life, which occurs as a result of illness or violence.
The process of dying is called agony. Depending on the cause, the agony can be very brief or last up to several hours.
Distinguish clinical and biological death. Conventionally, the moment of clinical death is considered cessation of cardiac activity . But after this, other organs and tissues with varying durations still retain vital activity: intestinal motility continues, gland secretion continues, and muscle excitability remains. After cessation of all vital functions biological death occurs in the body. Postmortem changes occur. Studying these changes is important for understanding the mechanism of death in various diseases.
For practical activities, the differences in morphological changes that occurred intravital and postmortem are of great importance. This helps to establish the correct diagnosis and is also important for forensic veterinary examination.
1.5 Cadaveric changes, their differences from intravital pathological processes and significance for the diagnosis of the disease
Cooling the corpse. Depending on the conditions, after various periods of time, the temperature of the corpse is equalized with the temperature of the external environment. At 18-20°C, the corpse cools by one degree every hour.
Rigor mortis. 2-4 hours (sometimes earlier) after clinical death, smooth and striated muscles contract somewhat and become dense. The process begins with the jaw muscles, then spreads to the neck, forelimbs, chest, belly and hind limbs. The greatest degree of rigor is observed after 24 hours and persists for 1-2 days. Then the rigor disappears in the same sequence as it appears. Rigor of the heart muscle occurs 1-2 hours after death.
The mechanism of rigor mortis has not yet been sufficiently studied. But the importance of two factors has been clearly established. During the post-mortem breakdown of glycogen, a large amount of lactic acid is formed, which changes the chemistry of muscle fiber and promotes rigor. The amount of adenosine triphosphoric acid decreases, and this causes the loss of elastic properties of the muscles.
· Cadaveric spots arise due to changes in the state of the blood and its redistribution after death. As a result of post-mortem contraction of the arteries, a significant amount of blood passes into the veins and accumulates in the cavities of the right ventricle and atria. Post-mortem blood clotting occurs, but sometimes it remains liquid (depending on the cause of death). In death from asphyxia, blood does not clot. There are two stages in the development of cadaveric spots.
The first stage is the formation of cadaveric hypostases, which occur 3-5 hours after death. The blood, due to gravity, moves to the underlying parts of the body and seeps through the vessels and capillaries. Spots form, visible in the subcutaneous tissue after removing the skin, and in the internal organs - upon opening.
The second stage is hypostatic imbibition (impregnation).
In this case, interstitial fluid and lymph penetrate into the vessels, thinning the blood and increasing hemolysis. The diluted blood again seeps out of the vessels, first onto the underside of the corpse, and then everywhere. The spots have indistinct outlines, and when cut, it is not blood that flows out, but sanguineous tissue fluid (different from hemorrhages).
Corpse decomposition and rotting. In dead organs and tissues, autolytic processes develop, called decomposition and caused by the action of the dead organism’s own enzymes. Tissue disintegration (or melting) occurs. These processes develop most early and intensively in organs rich in proteolytic enzymes (stomach, pancreas, liver).
Decomposition is then joined by rotting of the corpse, caused by the action of microorganisms that are constantly present in the body during life, especially in the intestines.
Rotting occurs first in the digestive organs, but then spreads to the entire body. During the putrefactive process, various gases are formed, mainly hydrogen sulfide, and a very unpleasant odor occurs. Hydrogen sulfide reacts with hemoglobin to form iron sulfide. A dirty greenish color appears in the cadaveric spots. The soft tissues swell, soften and turn into a gray-green mass, often riddled with gas bubbles (cadaveric emphysema).
Putrefactive processes develop faster with more high temperature and higher environmental humidity.
Lecture 2. Necrosis
2.1 Definition, etiology and classification of necrosis
Necrosis- necrosis of individual cells, tissue areas and organs. The essence of necrosis is the complete and irreversible cessation of vital activity, but not in the entire body, but only in some limited area (local death).
Depending on the cause and various conditions, necrosis can occur very quickly or over a period of very variable duration. With slow death, dystrophic changes occur, which increase and reach a state of irreversibility. This process is called necrobiosis.
Necrosis and necrobiosis are observed not only as a pathological phenomenon, but also occur as a constant process under physiological conditions. In the body, a certain number of cells constantly die and are replaced by others, this is especially clearly noticeable on the cells of the integumentary and glandular epithelium, as well as on the blood cells.
The causes of necrosis are very diverse: the action of chemical and physical factors, viruses and microbes; damage to the nervous system; disturbance of blood supply.
Necrosis that occurs directly at the site of application of harmful agents is called direct.
If they occur at a distance from the place of exposure to a harmful factor, they are called indirect. These include:
· angiogenic necrosis, which is formed as a result of cessation of blood flow. Under these conditions, oxygen starvation of the tissue develops, leading to cell death. The central nervous system is especially sensitive to hypoxia;
· neurogenic, caused by damage to the central and peripheral nervous system. When neurotrophic function is disturbed, dystrophic, necrobiotic and necrotic processes occur in tissues;
· allergic necrosis, which is observed in tissues and organs with altered sensitivity to a harmful agent that acts repeatedly. Skin necrosis in the chronic form of pig erysipelas, according to the mechanism of their formation, is also a manifestation of an allergic organism that is sensitized to the causative agent of this disease.
2. 2 Pathomorphological characteristics of necrosis. Their importance for diagnosing diseases
The sizes of dead areas vary: microscopic, macroscopically visible from barely visible to very large. Sometimes entire organs or individual parts die.
The appearance of necrosis varies depending on many conditions: the cause of necrosis, the mechanism of development, the state of blood circulation, the structure and reactivity of the tissue, etc.
The following types of necrosis are distinguished according to macroscopic signs.
A. Dry (coagulative) necrosis
Occurs when moisture is released into the environment. The reasons may be cessation of blood flow, the action of certain microbial toxins, etc. In this case, coagulation (clotting) of proteins in cells and interstitial matter occurs. Necrotic areas have a dense consistency, whitish-gray or grayish-yellow color. The cut surface is dry, the tissue pattern is erased.
An example of dry necrosis can be anemic infarctions - areas of organ necrosis that occur when the flow of blood is stopped. arterial blood; dead muscles - with paralytic hemoglobinemia of horses, white muscle disease and bedsores. The affected muscles are dull, swollen, and reddish-gray in color. Sometimes it resembles wax in appearance; This is where waxy, or Zenker's, necrosis occurs. Dry necrosis includes the so-called caseous (cheesy) necrosis, in which the dead tissue is a dry crumbling mass of yellowish-gray color.
B. Wet (colliquation) necrosis occurs in tissues rich in moisture (for example, the brain), and also provided that the area of necrosis does not dry out. Examples: necrosis in the substance of the brain, death of the fetus in the uterus. Sometimes foci of dry necrosis (secondary colliquation) may liquefy.
B. Gangrene is one of the necroses, but is characterized by the fact that it may not occur in the entire body, but only in areas in contact with the external environment, under conditions of exposure to air, thermal influences, moisture, infection, etc. (lungs, gastrointestinal tract, uterus, skin).
In dead areas, changes in hemoglobin occur under the influence of air. Iron sulfide is formed, and dead tissue becomes dark, gray-brown or even black.
Dry gangrene (mummification) is observed on the skin. Dead areas are dry and dense, brown or black in color. This process can occur due to frostbite, ergot poisoning, and certain infections (erysipelas, leptospirosis, pigs, etc.).
Wet gangrene (putrefactive or septic) is caused by the action of putrefactive microorganisms on dead tissue, resulting in liquefaction of dead materials. Affected areas are soft, decaying, dirty gray, dirty green or black in color, with a foul odor. Some putrefactive microbes produce a lot of gases that accumulate in the form of bubbles in dead tissue (gas, or noisy, gangrene).
Microscopic changes in the cell during necrosis
Changes in the nucleus have three types: - karyopyknosis - wrinkling; - karyorrhexis - decay or rupture; - karyolysis - dissolution.
With karyopyknosis, a decrease in nuclear volume occurs due to chromatin compaction; it wrinkles and therefore becomes more intensely colored.
Karyorrhexis is characterized by the accumulation of chromatin clumps of various sizes, which then separate and penetrate the damaged nuclear envelope. Remnants of chromatin remain scattered in the protoplasm.
During karyolysis, voids (vacuoles) are formed in the nucleus at the sites of chromatin dissolution. These voids merge into one large cavity, the chromatin disappears completely, the nucleus does not stain and dies.
Changes in the cytoplasm. At the beginning, coagulation (clotting) of proteins occurs due to the action of enzymes. The cytoplasm becomes more dense. This is referred to as plasmopyknosis, or hyalinization. Later, the cytoplasm breaks up into separate clumps and grains (plasmorhexis).
When there is a large amount of moisture in the tissues, liquefaction processes predominate. Vacuoles are formed and merge; the cells take the form of balloons filled with liquid, and the cytoplasm dissolves (plasmolysis).
Changes in the interstitial substance. Collagen, elastic and reticular fibers lose their outlines, become basophilically stained and fragmented, and later liquefy. Sometimes the dead interstitial substance becomes similar to fibrin fibers (fibrinoid transformation).
When the epithelium becomes necrotic, the soldering (cementing) substance liquefies. Epithelial cells are separated and torn away from the basement membrane: cell discomplexation and desquamation or desquamation.
Outcomes of necrosis. In areas of necrosis, tissue decay products (detritus) accumulate, which have an irritating effect on surrounding living tissues; inflammation develops in them.
A red stripe called a demarcation line forms at the boundary between living tissue and dead material.
During the process of inflammation, proteolytic enzymes act on dead materials, which are liquefied and absorbed by polynuclear cells and macrophages; thus, decomposition products are removed.
At the site of necrosis, granulation tissue forms, from which a scar is formed. The replacement of necrosis by connective tissue is called organization.
Calcium salts are easily deposited in dead material, which is called calcification or petrification.
If dead tissue is not liquefied and replaced, a connective tissue capsule forms around it - encapsulation occurs. When a capsule forms around the area of wet necrosis, a cyst is formed - a cavity with liquid contents.
If, during demarcation inflammation, increased emigration of leukocytes occurs, purulent softening occurs, leading to the delimitation of the necrotic focus from the surrounding tissues. This is called sequestration, and the isolated dead area is called sequestration. Granulation tissue develops around the sequester, from which a capsule is formed.
When there is necrosis in the outer parts of the body, they can be completely rejected from the body - mutilation.
The significance of necrosis is that the dead areas cease to function.
Necrosis in the heart and brain often leads to death. Absorption of tissue decay products causes poisoning of the body (autointoxication). At the same time there can be very severe violations vital activity of the body and even death.
Llecture3 . Pathological anatomy
Pathological anatomy studies the structural changes that occur in the patient's body. It is divided into theoretical and practical. Structure of pathological anatomy: general part, specific pathological anatomy and clinical morphology. The general part studies general pathological processes, patterns of their occurrence in organs and tissues in various diseases. Pathological processes include: necrosis, circulatory disorders, inflammation, compensatory inflammatory processes, tumors, dystrophies, cell pathology. Particular pathological anatomy studies the material substrate of the disease, that is, it is the subject of nosology. Nosology (the study of disease) provides knowledge of the etiology, pathogenesis, manifestation and nomenclature of diseases, their variability, as well as the construction of diagnosis, principles of treatment and prevention.
Tasks of pathological anatomy:
1) study of the etiology of the disease (causes and conditions of the disease);
2) study of the pathogenesis of the disease (mechanism of development);
3) study of the morphology of the disease, i.e. structural changes in the body and tissues;
4) study of the morphogenesis of the disease, i.e. diagnostic structural changes;
5) study of the pathomorphosis of the disease (persistent changes in cells and morphological diseases under the influence of drugs - medicinal metamorphosis, as well as under the influence of environmental conditions - natural metamorphosis);
6) the study of complications of diseases, the pathological processes of which are not obligatory manifestations of the disease, but arise and worsen it and often lead to death;
7) study of disease outcomes;
8) study of thanatogenesis (mechanism of death);
9) assessment of the functioning and condition of damaged organs.
Objectives of practical pathological anatomy:
1) control of the correctness and timeliness of the clinical diagnosis (autopsy). The percentage of discrepancy between clinical and pathological diagnoses ranges from 12-19%. Causes: rare diseases with a blurred clinical or laboratory picture; late presentation of the patient to medical institution. Timely diagnosis means that the diagnosis must be made within 3 days, if the patient’s condition is serious - in the first hours;
2) advanced training of the attending physician (the attending physician is always present at the autopsy). For each case of discrepancy in diagnosis, the clinic holds a clinical-anatomical conference, where a specific analysis of the disease takes place;
3) direct participation in making a lifetime clinical diagnosis (by biopsy and examination of surgical material).
Methods for studying pathological anatomy:
1) autopsy of the bodies of the dead;
2) biopsy (intravital histological examination carried out for the purpose of diagnosing and determining the prognosis of the disease).
The research material is called “biopsy”. Depending on the methods of obtaining it, biopsies are distinguished between closed and hidden.
Closed biopsies:
1) puncture (in the liver, kidneys, mammary glands, thyroid gland, lymph nodes etc.);
2) aspiration (by suction from bronchial tree);
3) trepanation (from dense bone tissue and cartilage);
4) diagnostic curettage of the uterine cavity, i.e. obtaining endometrial scrapings (used in obstetrics and gynecology);
5) gastrobiopsy (using a gastrofibroscope, the gastric mucosa is taken).
Hidden biopsies:
1) examination of surgical material (all material is taken);
2) experimental modeling of the disease.
The structure of the biopsy can be liquid, solid or soft. According to the timing, the biopsy is divided into planned (result on the 6th-7th day) and urgent (result within 20 minutes, i.e. at the time of surgery).
Methods for studying pathological material:
1) light microscopy using special dyes;
2) electron microscopy;
3) luminescence microscopy;
4) radiography.
Levels of research: organismal, organ, systemic, tissue, cellular, subjective and molecular.
Briefly about the history of pathological anatomy.
The works of the French morphologists M. Bichat, J. Corvisart and J. Cruvelier, who created the world's first color atlas on pathological anatomy, were of great importance for the development of pathological anatomy. R. Bayle was the first author of a complete textbook on private pathological anatomy, translated into Russian in 1826 by the doctor A.I. Kostomarov. K. Rokitansky was the first to systematize the pathological processes of body systems in various diseases, and also became the author of the first manual on pathological anatomy.
In Russia, autopsies began to be performed for the first time in 1706, when medical hospital schools were organized by order of Peter I. But the clergy prevented autopsies from being carried out. Only after the opening of the medical faculty at Moscow University in 1755, autopsies began to be performed regularly.
In 1849, the first department of pathological anatomy in Russia was opened. They succeeded each other as heads of the department: A. I. Polunin, I. F. Klein, M. N. Nikiforov, V. I. Kedrovsky, A. I. Abrikosov, A. I. Strukov, V. V. Serov.
Llecture4 . General doctrine of dystrophies
Dystrophy is a pathological process that is a consequence of metabolic disorders, which causes damage to cell structures and the appearance in the cells and tissues of the body of substances that are not normally detected.
Dystrophies are classified:
1) according to the scale of the process: local (localized) and general (generalized);
2) by reason of occurrence: acquired and congenital. Congenital dystrophies have a genetic cause of the disease.
Hereditary dystrophies develop as a result of a violation of the metabolism of proteins, carbohydrates, fats; in this case, the genetic deficiency of one or another enzyme that is involved in the metabolism of proteins, fats or carbohydrates is important. Subsequently, incompletely converted products of carbohydrate, protein, and fat metabolism occur in the tissues. This process can develop in various tissues of the body, but damage to the tissue of the central nervous system always occurs. Such diseases are called storage diseases. Children with these diseases die in the 1st year of life. The greater the deficiency of the necessary enzyme, the faster the disease develops and the sooner death occurs.
Dystrophies are divided into:
1) according to the type of metabolism that was disrupted: protein, carbohydrate, fat, mineral, water, etc.;
2) according to the point of application (according to the localization of the process): cellular (parenchymal), non-cellular (mesenchymal), which develop in connective tissue, as well as mixed (observed in both parenchyma and connective tissue).
There are four pathogenetic mechanisms.
1. Transformation- this is the ability of some substances to be transformed into others that have a similar structure and composition. For example, carbohydrates have this ability when they transform into fats.
2. Infiltration- this is the ability of cells or tissues to be filled with an excess amount of various substances. There are two types of infiltration. Infiltration of the first type is characterized by the fact that a cell that participates in normal life receives an excess amount of a substance. After some time, a limit comes when the cell cannot process and assimilate this excess. Infiltration of the second type is characterized by a decrease in the level of vital activity of the cell; as a result, it cannot cope even with the normal amount of substance entering it.
3. Decomposition- characterized by the collapse of intracellular and interstitial structures. The breakdown of protein-lipid complexes that make up the membranes of organelles occurs. In the membrane, proteins and lipids are bound and therefore not visible. But when membranes disintegrate, they form in cells and become visible under a microscope.
4. Perverted Synthesis- formation of abnormal foreign substances occurs in the cell, which are not formed during the normal functioning of the body. For example, with amyloid dystrophy, abnormal protein is synthesized in cells, from which amyloid is then formed. In patients with chronic alcoholism, the synthesis of foreign proteins begins to occur in liver cells (hepatocytes), from which the so-called alcoholic hyaline is subsequently formed.
Different types of dystrophies are characterized by their own dysfunction of tissue. In dystrophy, the disorder is twofold: quantitative, with a decrease in function, and qualitative, with a perversion of function, i.e., features appear that are unusual for a normal cell. An example of such a perverted function is the appearance of protein in the urine in kidney diseases, when there are degenerative changes in the kidney, or changes in liver tests that appear in liver diseases, and in heart diseases - changes in heart tones.
Parenchymal dystrophies are divided into protein, fat and carbohydrate.
Protein dystrophy is a dystrophy in which protein metabolism is disrupted. The process of degeneration develops inside the cell. Among the protein parenchymal dystrophies, granular, hyaline-droplet, and hydropic dystrophies are distinguished.
With granular dystrophy, during histological examination, protein grains can be seen in the cytoplasm of cells. Granular dystrophy affects parenchymal organs: kidneys, liver and heart. This dystrophy is called cloudy or dull swelling. This has a connection with macroscopic features. With this dystrophy, the organs become slightly swollen, and the surface on the cut looks dull, cloudy, as if “scalded by boiling water.”
Several reasons contribute to the development of granular dystrophy, which can be divided into 2 groups: infections and intoxications. A kidney affected by granular dystrophy increases in size, becomes flabby, and a positive Schorr test can be determined (when the poles of the kidney are brought together, the kidney tissue is torn). On a section, the tissue is dull, the boundaries of the medulla and cortex are blurred or may not be distinguishable at all. With this type of dystrophy, the epithelium of the convoluted tubules of the kidney is affected. In normal renal tubules, smooth lumens are observed, but in granular dystrophy, the apical section of the cytoplasm is destroyed, and the lumen becomes star-shaped. In the cytoplasm of the epithelium of the renal tubules there are numerous grains (pink).
Renal granular dystrophy ends in two ways. A favorable outcome is possible if the cause is eliminated; the tubular epithelium in this case returns to normal. An unfavorable outcome occurs with continued exposure to a pathological factor - the process becomes irreversible, dystrophy transforms into necrosis (often observed in cases of poisoning with kidney poisons).
The liver in granular dystrophy is also slightly enlarged. When cut, the fabric takes on the color of clay. The histological sign of granular liver dystrophy is the inconsistent presence of protein grains. It is necessary to pay attention to whether the beam structure is present or destroyed. With this dystrophy, proteins are divided into separately located groups or separately lying hepatocytes, which is called discomplexation of the hepatic beams.
Cardiac granular dystrophy: the heart is also slightly enlarged in appearance, the myocardium becomes flabby, and when cut it resembles boiled meat. Macroscopically, no protein grains are observed.
In histological examination, the criterion for this dystrophy is basophilia. Myocardial fibers perceive hematoxylin and eosin differently. Some areas of the fibers are intensely stained lilac by hematoxylin, while others are intensely stained blue by eosin.
Hyaline droplet dystrophy develops in the kidneys (the epithelium of the convoluted tubules is affected). Occurs in kidney diseases such as chronic glomerulonephritis, chronic pyelonephritis, and poisoning. Droplets of a hyaline-like substance form in the cytoplasm of the cells. This dystrophy is characterized by significant impairment of renal filtration.
Hydropic dystrophy can occur in liver cells with viral hepatitis. In this case, large light drops are formed in hepatocytes, often filling the cell.
Fatty degeneration. There are 2 types of fats. The amount of mobile (labile) fats changes throughout a person’s life; they are localized in fat depots. Stable (immobile) fats are included in the composition of cellular structures, membranes.
Fats perform a wide variety of functions - supporting, protective, etc.
Fats are determined using special dyes:
1) Sudan-III has the ability to color fat orange-red;
2) scarlet colors red;
3) Sudan-IV (osmic acid) turns fat black;
4) Nile blue has metachromasia: it colors neutral fats red, and all other fats under its influence become blue or light blue.
Immediately before dyeing, the starting material is processed using two methods: the first is alcohol wiring, the second is freezing. To determine fats, freezing tissue sections is used, since fats dissolve in alcohols.
Fat metabolism disorders represent three pathologies:
1) fatty degeneration itself (cellular, parenchymal);
2) general obesity or obesity;
3) obesity of the interstitial substance of the walls of blood vessels (aorta and its branches).
Fatty degeneration itself is the basis of atherosclerosis. The causes of fatty degeneration can be divided into two main groups: infections and intoxications. Nowadays, the main type of chronic intoxication is alcohol intoxication. Drug intoxications can often be observed, endocrine intoxications - developing with diabetes mellitus.
An example of an infection that provokes fatty degeneration is diphtheria, since diphtheria toxin can cause fatty degeneration of the myocardium. Fatty degeneration is observed in the same organs as protein degeneration - in the liver, kidneys and myocardium.
With fatty degeneration, the liver increases in size, it becomes dense, and when cut it is dull and bright yellow. This type of liver is figuratively called “goose liver”.
Microscopic manifestations: fat droplets of small, medium and large sizes appear in the cytoplasm of hepatocytes. As a rule, they are located in the center of the hepatic lobule, but they can occupy it all.
There are several stages in the process of obesity:
1) simple obesity, when the drop occupies the entire hepatocyte, but when the influence of the pathological factor ceases (when the patient stops drinking alcohol), after 2 weeks the liver returns to normal levels;
2) necrosis - infiltration of leukocytes occurs around the focus of necrosis as a response to damage; the process at this stage is reversible;
3) fibrosis - scarring; the process enters an irreversible cirrhotic stage.
The heart enlarges, the muscle becomes flabby, dull, and if you carefully examine the endocardium, under the endocardium of the papillary muscles you can observe a transverse striation, which is called the “tiger heart”.
Microscopic characteristics: fat is present in the cytoplasm of cardiomyocytes. The process is mosaic in nature - the pathological lesion spreads to cardiomyocytes located along small veins. The outcome can be favorable when a return to normal occurs (if the cause is eliminated), and if the cause continues to act, then cell death occurs and a scar forms in its place.
In the kidneys, fat is localized in the convoluted tubule epithelium. Such dystrophy occurs in chronic kidney diseases (nephritis, amyloidosis), poisoning, and general obesity.
In obesity, the metabolism of neutral labile fats, which are formed in excess in fat depots, is disrupted; body weight increases significantly as a result of the accumulation of fat in the subcutaneous fatty tissue, in the omentum, mesentery, in the perinephric, retroperitoneal tissue, and in the tissue covering the heart. With obesity, the heart becomes clogged with a thick fatty mass, and then fat penetrates into the thickness of the myocardium, which causes its fatty degeneration. Muscle fibers undergo pressure from the obese stroma and atrophy, which leads to the development of heart failure. Most often, the thickness of the right ventricle is affected, as a result of which developments develop in the systemic circulation. congestion. In addition, obesity of the heart can result in myocardial rupture. In literary sources, such a fatty heart is characterized as Pickwick syndrome.
In an obese liver, fat can form inside the cells. The liver takes on the appearance of a “goose liver”, as in dystrophy. It is possible to differentiate the formed fat in liver cells using color staining: Nile blue has the ability to color neutral fat in case of obesity red, and in case of developed dystrophy - blue.
Obesity of the interstitial substance of the walls of blood vessels (meaning cholesterol exchange): during infiltration from blood plasma into an already prepared vascular wall, cholesterol enters, which is then deposited on the vascular wall. Some of it is washed back, and some is processed by macrophages. Macrophages loaded with fat are called xanthoma cells. Over the fat deposits, connective tissue grows, which protrudes into the lumen of the vessel, thus forming an atherosclerotic plaque.
Causes of obesity:
1) genetically determined;
2) endocrine (diabetes, Itsenko-Cushing's disease);
3) physical inactivity;
4) overeating.
Carbohydrate dystrophy may be associated with impaired glycogen or glycoprotein metabolism. A violation of glycogen content manifests itself in a decrease or increase in its amount in tissues and its appearance in places where it is usually not detected. These disorders are expressed in diabetes mellitus, as well as in hereditary carbohydrate dystrophies - glycogenosis.
In diabetes mellitus, there is insufficient consumption of glucose by tissues, an increase in its amount in the blood (hyperglycemia) and excretion in the urine (glucosuria). Tissue glycogen reserves decrease sharply. In the liver, glycogen synthesis is disrupted, which leads to its infiltration with fats - fatty liver degeneration occurs. At the same time, glycogen inclusions appear in the nuclei of hepatocytes, they become light (“holey” and “empty” nuclei). With glucosuria, changes appear in the kidneys, manifested in glycogen infiltration of the tubular epithelium. The epithelium becomes tall, with light foamy cytoplasm; glycogen grains are also found in the lumen of the tubules. The kidney tubules become more permeable to plasma proteins and sugars. One of the manifestations of diabetic microangiopathy develops - intercapillary (diabetic) glomerulosclerosis. Glycogenosis is caused by the absence or deficiency of an enzyme that is involved in the breakdown of stored glycogen, and refers to hereditary enzymopathies (storage diseases).
In carbohydrate dystrophies associated with impaired glycoprotein metabolism, there is an accumulation of mucins and mucoids, also called mucous and mucus-like substances (mucosal dystrophy). The causes vary, but most often it is inflammation of the mucous membranes. Systemic dystrophy underlies hereditary systemic disease- cystic fibrosis. The endocrine apparatus of the pancreas, glands of the bronchial tree, digestive and urinary tracts, bile ducts, reproductive and mucous glands are affected. The outcome is different - in some cases, regeneration of the epithelium occurs and complete restoration of the mucous membrane, while in others it atrophies, becomes sclerotic, and the function of the organ is disrupted.
Stromal-vascular dystrophy is a metabolic disorder in connective tissue, mainly in its intercellular substance, accumulation of metabolic products. Depending on the type of impaired metabolism, mesenchymal dystrophies are divided into protein (dysproteinoses), fat (lipidoses) and carbohydrate. Dysproteinoses include mucoid swelling, fibrinous swelling, hyalinosis and amyloidosis. The first three are associated with impaired permeability of the vascular wall.
1. Mucoid swelling- this is a reversible process. Superficial, shallow changes in the structure of connective tissue occur. Due to the action of a pathological factor, decomposition processes occur in the main substance, i.e., the bonds of proteins and aminoglycans disintegrate. Aminoglycans are in a free state and are found in connective tissue. Due to them, the connective tissue is stained basophilic. The phenomenon of metachromasia occurs (the ability of tissue to change the color of the dye). Thus, toluidine blue is normally blue, but with mucoid swelling it is pink or lilac. Mucin (mucus) consists of proteins and therefore is colored in a unique way. Glycosoaminoglycans absorb fluid well that comes out of vascular bed, and the fibers swell but do not collapse. The macroscopic picture is not changed. Factors that cause mucoid swelling include: hypoxia (hypertension, atherosclerosis), immune disorders (rheumatic disease, endocrine disorders, infectious diseases).
2. Fibrinoid swelling is a deep and irreversible disorganization of connective tissue, which is based on the destruction of the main substance of the tissue and fibers, accompanied by a sharp increase in vascular permeability and the formation of fibrinoid. May be a consequence of mucoid swelling. The fibers are destroyed, the process is irreversible. The property of metachromasia disappears. The macroscopic picture is unchanged. Microscopically, collagen fibers are observed, impregnated with plasma proteins, stained yellow with pyrofuchsin.
The outcome of fibrinoid swelling can be necrosis, hyalinosis, sclerosis. Macrophages accumulate around the area of fibrinoid swelling, under the influence of which the cells are destroyed and necrosis occurs. Macrophages are capable of producing monokines, which promote the proliferation of fibroblasts. Thus, the necrosis zone is replaced by connective tissue - sclerosis occurs.
3. Hyaline dystrophy (hyalinosis). In the connective tissue, homogeneous transparent dense masses of hyaline (fibrillar protein) are formed, which are resistant to alkalis, acids, enzymes, are PAS-positive, readily accept acidic dyes (eosin, acid fuchsin), and are colored yellow or red by pyrofuchsin.
Hyalinosis is the outcome of various processes: inflammation, sclerosis, fibrinoid swelling, necrosis, plasma impregnation. A distinction is made between hyalinosis of blood vessels and the connective tissue itself. Each can be widespread (systemic) and local.
With vascular hyalinosis, predominantly small arteries and arterioles are affected. Microscopically, hyaline is found in the subendothelial space, destroying the elastic lamina, the vessel turns into a thickened glassy tube with a very narrowed or completely closed lumen.
Hyalinosis of small vessels is systemic in nature, but is significantly expressed in the kidneys, brain, retina, and pancreas. Characteristic of hypertension, diabetic microangiopathy and diseases with impaired immunity.
There are three types of vascular hyaline:
1) simple, resulting from the insudation of unchanged or slightly changed components of blood plasma (with hypertension, atherosclerosis);
2) lipohyalin, containing lipids and β-lipoproteins (for diabetes mellitus);
3) complex hyaline, built from immune complexes, collapsing structures of the vascular wall, fibrin (characteristic of diseases with immunopathological disorders - for example, rheumatic diseases).
Hyalinosis of the connective tissue itself develops as a result of fibrinoid swelling, which leads to the destruction of collagen and saturation of the tissue with plasma proteins and polysaccharides. The appearance of the organ changes, its atrophy occurs, deformation and wrinkling occur. The connective tissue becomes dense, whitish and translucent. Microscopically, the connective tissue loses its fibrillarity and merges into a homogeneous dense cartilage-like mass; cellular elements are compressed and undergo atrophy.
With local hyalinosis, the outcome is scars, fibrous adhesions of serous cavities, vascular sclerosis, etc. The outcome in most cases is unfavorable, but resorption of hyaline masses is also possible.
4. Amyloidosis- a type of protein dystrophy, which is a complication of various diseases (infectious, inflammatory or tumoral in nature). In this case, there is acquired (secondary) amyloidosis. When amyloidosis is a consequence of an unknown etiology, it is primary amyloidosis. The disease was described by K. Rakitansky and was called “greasy disease”, since the microscopic sign of amyloidosis is a greasy sheen of the organ. Amyloid is a complex substance - a glycoprotein, in which globular and fibrillar proteins have a close relationship with mucopolysaccharides. While proteins are characterized by approximately the same composition, polysaccharides always have a different composition. As a result, amyloid never has a constant chemical composition. The proportion of proteins makes up 96-98% of the total mass of amyloid. There are two fractions of carbohydrates - acidic and neutral polysaccharides. The physical properties of amyloid are represented by anisotropy (the ability to undergo birefringence, which manifests itself in polarized light); under a microscope, amyloid produces a yellow glow, which differs from collagen and elastin. Colorful reactions for the determination of amyloid: selective staining “Congo red” stains amyloid in a brick-red color, which is due to the presence of fibrils in the amyloid composition, which have the ability to bind and firmly hold the paint.
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The subject of pathological anatomy, its significance and place in medical science and healthcare practice. Study methods
Subject (content) of pathological anatomy. Pathological anatomy (pathology) studies the morphological manifestations of pathological processes in the human body at different levels (organ, tissue, cellular and subcellular).
Pathological anatomy consists of three main sections:
1. General pathological anatomy– the doctrine of typical pathological processes (metabolic disorders, blood and lymph circulation, inflammation, immunopathological processes, regeneration, atrophy, hypertrophy, tumor growth, necrosis, etc.).
2. Private(special) pathological anatomy studies morphological manifestations individual diseases(nosological forms), for example, tuberculosis, rheumatism, liver cirrhosis, etc.
3. Pathological practice– the doctrine of the organization of pathological services and the practical activities of a pathologist (pathologist). The pathologist carries out intravital and postmortem morphological diagnostics of pathological processes. Intravital morphological diagnostics are carried out on the material of biopsies and surgically removed organs or parts thereof. The term biopsy(from the Greek βίος - life; όψις - vision, glance, appearance; literal translation of the term - “looking at the living”) refers to the taking of tissue from a patient for diagnostic purposes. The resulting material (usually a piece of fabric) is called biopsy. The study of corpses of deceased people is called autopsy(from the Greek αύτός - myself; όψις - vision, glance, appearance; the literal translation of the term is “I look myself”). The results of the morphological study are formalized in the form of a pathological diagnosis (conclusion). Pathological diagnosis is most important in oncology.
Pathological human anatomy (medical pathological anatomy) makes extensive use of data obtained from experimental study pathological processes in laboratory animals.
Tasks of pathological anatomy . The main tasks of pathological anatomy are the following:
1. Identification etiology pathological processes, i.e. reasons ( causal genesis) and the conditions for their development.
2. Study pathogenesis– mechanism of development of pathological processes. In this case, the sequence of morphological changes is called morphogenesis. The term used to denote the mechanism of recovery (reconvalescence) sanogenesis, and the mechanism of dying (death) – thanatogenesis.
3. Characteristics morphological picture diseases (macro- and micromorphological signs).
4. Study complications And outcomes diseases.
5. Research pathomorphosis diseases, i.e. persistent and regular changes in the picture of the disease under the influence of living conditions or treatment.
6. Study iatrogeny– pathological processes that have developed as a result of diagnostic or therapeutic procedures.
7. Developing questions diagnosis theories.
METHODS OF PATHOLOGICAL ANATOMY
The concept of morphological methods. Feature morphological methods research in biology and medicine is the use of empirical information obtained directly when studying an object. In contrast, it is possible to study the properties of an object without directly perceiving it, but based on the nature of secondary changes in the environment caused by the very existence of the object (such research methods are widely used in pathological physiology and clinical medicine). In other words, the morphological method is based on direct perception of the subject being studied, first of all him visual characteristic(result observations).
Morphological methods, like any other scientific methods, are implemented in three stages:
1. Empirical stage– receiving primary information about an object from the senses. In pathological morphology, in addition to visual, tactile information is of great importance.
2. Theoretical stage– the stage of understanding the obtained empirical data and their systematization. This stage requires broad erudition of the researcher, since the effectiveness of perception of empirical information directly depends on the completeness of theoretical knowledge, which is expressed in the formula "We see what we know".
3. Practical implementation stage– use of research results in practical activities. The results of morphological research in medicine are basis of diagnosis, which determines the important practical significance of the method.
Descriptive method. Among morphological methods at the empirical stage, of particular importance is descriptive method (description method) – a method of recording perceived information using verbal symbols (means of language as a sign system). A correct description of pathological changes is a kind of information copy of the object of study. That is why it is necessary to strive to ensure that it is as complete and accurate as possible.
The method of describing macro-objects is used by almost all doctors of clinical specialties, which determines the need for students of all faculties to study this method. Most often, the method of describing macro-objects is used when a doctor detects changes in integumentary tissues (skin and visible mucous membranes) during an examination of a patient. Visible changes during surgery internal organs, especially those removed, the surgeon reflects in the operation protocol.
The main morphological methods include:
1. Macromorphological method– a method for studying biological structures without significantly enlarging the object. Examination using a magnifying glass with low magnification refers to the macromorphological method. The macromorphological method should not be called a macroscopic study, because the information received is not only visual.
2. Micromorphological (microscopic) method– a method of morphological research that uses instruments (microscopes) that significantly magnify the image of an object. Many variants of the microscopic method have been proposed, but the most widely used light microscopy (light-optical examination).
Macromorphological study
In pathological anatomy, the study and description of macroscopic objects is the first stage of morphological analysis of autopsy and surgical material, which is then supplemented by microscopic examination.
Macromorphological parameters. The description of pathological changes in organs is carried out using the following basic parameters:
1. Localization pathological process in an organ (when not the entire organ is affected, but part of it).
2. Magnitude an organ, its fragment or pathologically changed area (size parameter, volumetric characteristic).
3. Configuration(outline, shape) of a pathologically altered organ or part thereof.
4. Color characteristic tissue from the surface and in the cut.
5. Consistency pathologically altered tissue.
6. Degree of uniformity pathologically altered tissue by color And consistency.
If a parameter has not been changed, it is usually not reflected in the object description.
Micromorphological method
Tissue sections for conventional light-optical examination are prepared using special instruments ( microtomes) and stained using various methods. The optimal thickness of such sections is 5–7 µm. Histological specimen It is a stained tissue section enclosed between a slide and cover glass in transparent media (balsam, polystyrene, etc.).
There are overview and special (differential) painting methods. Special methods are used to identify certain tissue structures and certain substances (histochemical and immunohistochemical studies).
The most commonly used staining of tissue sections is hematoxylin and eosin. Hematoxylin– a natural dye, extract of the bark of a tropical logwood tree – stains cell nuclei (“nuclear dye”), deposits of calcium salts, colonies of gram-positive microorganisms and fibrous tissue in a state of mucoid edema blue. Hematoxylin is a basic (alkaline) dye, so the ability of tissue to accept it is called basophilia(from lat. basis– base). Eosin– synthetic pink paint, dawn color paint (named after ancient greek goddess morning dawn Eos). Eosin is an acidic dye, so the ability of tissue structures to perceive it is called acidophilia, or oxyphilia. Eosin stains the cytoplasm of most cells (“cytoplasmic dye”), fibrous structures and intercellular substance.
Methods for identifying fibrous structures of connective tissue, primarily collagen fibers, in tissue sections are widespread. In Russia, traditionally preference is given van Gieson method(van Gieson); in this case, cell nuclei, gram-positive microorganisms and calcium deposits are stained Weigert's iron hematoxylin black, collagen fibers and hyaline – red sour fuchsin, the remaining structures of the intercellular substance and the cytoplasm of cells are yellow picric acid. In Western countries, the so-called trichrome(three-color) methods staining of fibrous connective tissue using phosphotungstic and phosphomolybdic acids ( Mallory method, Masson's method and etc.). In this case, collagen fibers are painted blue, reticular (reticulin) fibers - blue, elastic fibers - red.
Destruction
Destruction – destruction of cells and tissues. This phenomenon is widespread and occurs both normally and in pathology. There are four forms of destruction of biological tissues: cell death, isolated destruction of intercellular substance, necrosis and decomposition of dead body tissue (see above).
Cell death– destruction of both individual cells and cells within dying tissue. There are two mechanisms of cell death:
1. active form of cell death ( apoptosis) – cell destruction with the participation of a special genetic dying program;
2. passive form of cell death ( "necrosis", oncosis) is a form of cell death in which the genetically determined mechanism of cell self-destruction does not activate.
Isolated destruction of the intercellular substance is designated by the terms degradation, depolymerization or lysis. Necrosis tissue destruction is called an independent form of biological destruction, i.e. cells and intercellular substance (and not just cells) in a living organism.
Cell death, degradation of intercellular structures and necrosis occur both in pathology and in conditions of normal life, for example, periodic necrosis of the uterine mucosa (endometrium) in women of reproductive age. Moreover, we can talk about cell death in the case of cell destruction in culture (in vitro), i.e. outside the body.
APOPTOSIS
Definition. Apoptosis– a form of cell death, realized with the participation of a special genetically determined mechanism of cell destruction. The apoptosis program can be activated by special receptors on the cell surface ( exogenous mechanism of apoptosis induction), under the influence of the p53 protein in case of irreversible DNA damage ( endogenous mechanism) and with insufficiency of apoptosis inhibitors in the intercellular substance ( "dying out by default").
NECROSIS
It should be noted that the term necrosis in modern pathology has two meanings - necrosis as an alternative form of cell death to apoptosis, and necrosis as tissue destruction in vivo. The scope of these concepts coincides only partially. In some cases, they characterize processes independent of each other.
Definition. Necrosis– death of tissue in a living organism. The distinctive signs of necrosis are the following:
1. Necrosis develops in living organism. Often necrosis of tissue of vital organs leads to the death of the body. In other cases, death occurs at the prenecrotic stage due to severe metabolic disorders of the damaged tissue.
2. Despite the fact that necrosis develops in tissue formed by both cells and intercellular substance, the key event of necrosis is cell death. Sometimes, under pathological conditions, tissue destruction begins with the degradation of the intercellular substance, and later cells are involved in the process. This happens during the development of the so-called fibrinoid changes in fibrous connective tissue and in the tissue of vascular walls. As long as the process is limited to lysis of intercellular structures, fibrinoid changes are called fibrinoid swelling; when cells die in the focus of fibrinoid swelling, the process is called necrosis ( fibrinoid necrosis).
Classification. The main principles of classification of forms of necrosis are pathogenetic (according to the mechanism of development of necrosis) and clinical and morphological. The content of these classifications partially coincides (for example, heart attack included in both classification principles). In addition, it should be remembered that the clinical and morphological classification is not logically correct, because its headings partially, and in some cases completely, overlap in the scope of concepts. Thus, dry gangrene can be attributed equally to coagulative necrosis, and intestinal infarction at the same time is gangrene. Essentially, the clinical and morphological typology of forms of necrosis includes all those used in practical medicine terms for necrosis.
A. Pathogenetic principle
I. straight necrosis:
1. traumatic necrosis.
2. toxic necrosis.
II. indirect necrosis:
1. heart attack(angiogenic or vascular necrosis).
2. trophoneurotic necrosis.
3. allergic necrosis.
Heart attack
Definition.Heart attack– necrosis that develops as a result of impaired blood circulation in the tissue.
Etymology of the term. From lat. infarctus– filled, stuffed, stuffed. This term began to be used to designate foci of necrosis that are whitish in color, different from the color of normal tissue (white infarcts in the myocardium, spleen, kidneys); at the same time, the organ looks as if it is filled, stuffed with whitish masses.
Classification. A heart attack is classified according to three basic principles - by the mechanism of development, by the color of the destroyed tissue and by the shape of the focus of necrosis on the section of the organ.
Gangrene
Definition. Gangrene– necrosis of tissues in contact with the external environment.
Etymology of the term. The term γάγγραινα (“gággraina”, transformed in Russian into the word gangrene) was introduced into the European medical tradition by Hippocrates and formed from the verb γραίνω - to gnaw, i.e. “Gangrene” literally translated from ancient Greek means “something gnawing [the body]”, “something devouring [flesh]”. With dry gangrene of the limb, the dying tissue turns black, and a bright red border forms at the border with living tissue. The presence of a halo of hyperemia around the blackened tissue creates the impression of “burning” and subsequent “charring” of the skin, which determined the old Russian name Antonov fire, which meant dry gangrene distal sections limbs.
Classification. There are two forms of gangrene:
1. dry gangrene (mummification).
2. wet gangrene.
Special types of wet gangrene are bedsore(decubitus) and noma.
Dry gangrene (mummification) – gangrene, in which detritus is a dense, dry mass.
Wet gangrene– gangrene, in which detritus is rich in moisture.
Bedsore (decubitus) – necrosis of integumentary tissues (skin or mucous membranes) in places of prolonged compression.
Noma– wet gangrene of the soft tissues of the face. Typical for children with severe measles.
Sequestration
Definition. Sequestration- a fragment of destroyed tissue, freely located among living tissues.
Etymology of the term. From lat. sequestrum- separating, tearing away.
Between the sequestrum and viable tissue there is a more or less pronounced space, usually slit-like. When the process worsens, this space is usually filled with purulent exudate. The sequestrum does not undergo autolysis (self-destruction) and organization (i.e., it is not replaced by fibrous connective tissue). Most often, sequesters form in bone tissue during osteomyelitis. Rejection of sequesters ( sequestration) occurs through forming channels in the surrounding tissues. Such channels ( fistulas, or fistulas) open on the surface of the skin or mucous membrane. The formation of fistulas is associated with the destruction of the tissues surrounding the sequestration by purulent exudate. Thanks to the purulent exudate, the sequester fragments; in this case, smaller fragments of detritus are formed, which are removed from the source of damage with pus flowing through the fistulas. Tissue restoration (reparation) occurs after complete removal of the sequestration.
It is necessary to distinguish from sequestration mutilation And necrectomy. Mutilation– spontaneous (spontaneous) rejection of a necrotic organ or part thereof. For example, mutilation of the hand with gangrene, mutilation of the appendix with gangrenous appendicitis. Necrectomy– surgical (operative) removal of necrotic tissue.
Structure of the sequestral “box”. The sequester is located in sequestral cavity. On the side of living tissue, the cavity is limited by a capsule of coarse fibrous (scar) tissue - sequestral capsule. Cavity and capsule are united by the concept sequestral "box".
MORPHOGENESIS OF NECROSIS
Tissue death under pathological conditions goes through several qualitatively different stages. Necrosis is preceded by changes in their vital activity in the form of metabolic disorders. In pathology, any metabolic disorders are designated by the term degeneration(dystrophy). The period of degenerative (dystrophic) changes in a cell preceding its death can be long or, conversely, short-term. It's called prenecrosis(pre-necrotic state). There are two phases of prenecrosis: phase reversible degenerative changes ( paranecrosis) and phase irreversible changes ( necrobiosis). The set of degenerative and necrotic processes in general pathology is called alteration (damage). Destruction of already dead tissues - necrolysis– can occur in three ways: by self-digestion ( autolysis), by phagocytosis of detritus by specialized cells ( heterolysis) and by rotting(destruction of detritus by microorganisms). Thus, we can distinguish pre-necrotic, necrotic and post-necrotic stages of tissue death:
I. prenecrosis (prenecrotic stage):
1. paranecrosis– reversible degenerative changes,
2. necrobiosis– irreversible changes.
II. necrosis (necrotic stage).
III. necrolysis (postnecrotic stage):
1. autolysis– destruction of dead tissue under the influence of the dead cells’ own hydrolytic enzymes,
2. heterolysis– phagocytosis of detritus by specialized cells,
3. rotting– destruction of detritus under the influence of microorganisms.
PROTEINOGENIC PIGMENTS
Proteinogenic pigments include melanin, the pigment of enterochromaffin cell granules, and adrenochrome, a product of the oxidation of adrenaline in the adrenal medulla. Melanin– brown-black pigment. Its synthesis occurs in melanocytes. First, promelanine (dioxyphenylalanine - DOPA) is formed from tyrosine under the influence of tyrosinase, which polymerizes into melanin. When the adrenal glands are damaged (tuberculosis, tumors), excess tyrosine, from which adrenaline is also formed, is converted into melanin. The skin takes on a bronze tint - bronze disease(Addison's disease). Focal accumulation of melanin in the skin is observed in pigment spots - pigmented nevi, freckles or in malignant tumors - melanomas. The absence of melanin in the skin, hair follicles or retina and iris of the eyes due to hereditary tyrosinase deficiency is called albinism (albus - white). The focal absence of melanin in the skin is called leukoderma (vitiligo) and can be observed in leprosy, diabetes, syphilis, etc.
LIPIDOGENIC PIGMENTS
Representatives of this group of pigments are lipofuscin and lipochromes. Lipofuscin Sudan III is colored yellow-orange. The pigment is detected in the cytoplasm of nerve cells, hepatocytes and cardiomyocytes in the form of golden grains. With atrophy and cachexia, organs acquire a brown color - brown atrophy of the liver and myocardium. Currently, lipofuscin is classified as a normal cell component. Its granules - cytosomes or keratinosomes - store oxygen. Under hypoxic conditions, lipofuscin provides oxidation processes. The pigment can accumulate in hepatocytes in hereditary hepatoses (Gilbert's syndrome, Rotor's syndrome, etc.) - primary lipofuscinosis. Secondary lipofuscinosis develops with hypoxia, in old age, with exhaustion as a result of certain diseases (tuberculosis, alimentary cachexia, etc.). Lipofuscin can accumulate in the cells of malignant tumors, because in them anaerobic glycolysis predominates over tissue respiration.
Liporomas contain carotenoids - precursors of vitamin A and color adipose tissue, blood serum, corpus luteum of the ovaries, and adrenal cortex yellow.
STONE FORMATION
The formation of stones is typical for hollow organs (gall, bladder) or ducts (urinary tract, bile ducts, pancreatic ducts and salivary glands). Less commonly, stones form in the lumen of the veins (phleboliths), bronchi, or in the large intestine (coprolites). Common factors for the formation of stones include metabolic disorders, primarily cholesterol, nucleoproteins, obesity, atherosclerosis, and gout. Local factors include secretion disorders, stagnation of secretions, and inflammatory processes in organs. The mechanism of stone formation consists of two processes: the formation of an organic matrix (mucus, desquamated cells of the mucous membranes) and crystallization of salts. Gallbladder stones, based on their chemical structure, can be divided into pigmented (they are often multiple, faceted and greenish in color), and calcareous (white). Kidney stones and Bladder More often they are urate (yellow), phosphate (white), oxalate (I often include blood pigments, because they have an uneven surface and injure the mucous membrane).
VENOUS FULL BLOOD
1. Increased blood supply to an organ or tissue due to a decrease (obstruction) of blood outflow, while the blood flow is not changed or reduced.
2. Stagnation of venous blood leads to dilation of veins and capillaries, slowing down blood flow in them and the development hypoxia.
3. Venous congestion can be general and local, acute and chronic
General acute venous congestion occurs in acute heart failure (acute myocardial infarction, acute myocarditis)
Due to hypoxia and an increase in hydrostatic pressure, the permeability of capillaries in the stroma of organs increases, plasma impregnation, edema, stasis in the capillaries, diapedetic hemorrhages in the parenchyma - dystrophic and necrobiotic changes develop.
General chronic venous congestion occurs with chronic heart failure (heart defects, chronic coronary disease hearts). A long-term state of tissue hypoxia leads not only to plasmorrhagia, edema, stasis and hemorrhage, dystrophy and necrosis, but also to atrophy and sclerosis. Stagnant compaction develops ( induration) organs and tissues. The skin, especially of the lower extremities, becomes cold, bluish (cyanosis), the veins are dilated and filled with blood, the dermis and subcutaneous tissue swollen, thickened. The liver is enlarged and dense, its capsule is stretched, the edges are rounded, on a section it is variegated gray-yellow with red speckles, reminiscent of nutmeg. Microscopically, only the central sections of the lobules are full-blooded, where hemorrhages are noted, the hepatocytes are compressed and atrophic, and on the periphery of the lobules hepatocytes are in a state of fatty degeneration. As a result of chronic venous stagnation, connective tissue grows in the liver - nutmeg fibrosis develops. With the progression of connective tissue proliferation, imperfect regeneration of hepatocytes appears with the formation of regenerated nodes, restructuring and deformation of organs - nutmeg (cardiac) cirrhosis develops. The lungs become large and dense, brown when cut. Microscopically, cells loaded with hemosiderin (sideroblasts, siderophages) and free-lying hemosiderin appear in the alveoli, bronchi, interalveolar septa, lymphatic vessels, nodes; the interalveolar septa are thickened due to fibrosis. The kidneys are enlarged, dense, bluish. The spleen is enlarged, dense, dark cherry-colored on section.
LOCAL VENOUS FULL BLOOD occurs when there is difficulty in the outflow of venous blood from a certain organ or part of the body due to the closure of the lumen of the vein (thrombus or embolus) or compression from the outside (tumor). In this case, the same changes occur in the organs as with general plethora.
15. Thrombosis. Mechanisms of thrombus formation. Structure and outcomes of blood clots. The importance of thrombosis for the body
Thrombosis– intravital blood coagulation with the formation of a clot – a thrombus – in the lumen of a vessel or the cavities of the heart.
Thrombosis is a pathological manifestation of hemostasis. Hemostasis is a protective mechanism and its activation occurs when a vessel is damaged or ruptured and prevents or stops bleeding. There are three parts of hemostasis: 1) platelet, 2) components of the vascular wall, 3) plasma coagulation factors. The platelet apparatus is the first to be included in the hemostasis process. Structural and functional changes in platelets occur when a vessel is damaged when the subendothelium comes into contact with them. Platelets do not adhere to intact endothelial cells. When they are damaged, platelet adhesion (spreading) occurs. The initial attachment and spreading of platelets on the subendothelium is regulated by the protein von Willebrand factor, synthesized by endothelial cells and megakaryocytes. As a result of a complex of biochemical reactions, the structure of the platelet membrane changes and a receptor complex is organized on their surface. Activated platelets secrete adhesive proteins (fibrinogen, fibronectin, thrombospondin) that bind to the cell membrane and endothelium. As a result, cell aggregates are formed. Plasma coagulation components carry out their action in the internal (blood) or external (tissue) systems. In the internal system, their source is platelets, in the external system - tissue factor. Both systems are closely related. Most of these components (factors) are aimed at the formation of active thromboplastin. Blood coagulation is an enzymatic autocatalytic process and, according to modern concepts, includes 4 stages:
I – prothrombokinase + activators → active thromboplastin;
II – prothrombin + Ca + active thromboplastin → thrombin;
III – fibrinogen + thrombin → fibrin monomer;
IV – fibrin monomer + fibrin stimulating factor → fibrin polymer.
B.A. Kudryashov proved that the liquid state of blood is ensured by the normal functioning of the coagulation and anticoagulation systems. The latter is represented by natural anticoagulants (antithrombin, heparin, fibrinolysin system) and reflex-humoral regulation of hemostasis. Thrombosis is a manifestation of impaired regulation of the unified system of hemostasis of the liquid state of blood in the vascular bed.
The formation of a blood clot can be considered as hemostasis, but causing harm to the body, with possible life-threatening consequences. The structural and functional basis of thrombosis includes the mechanisms of hemostasis:
1) reaction of the damaged vascular wall - expressed in vasoconstriction, reaction of the endothelium (produces antiplatelet and thrombogenic factors - an imbalance between them in favor of thrombogenic factors occurs when the endothelium is damaged, which leads to thrombosis) and subendothelium. The subendothelium contains a variety of protein compounds, in particular fibronectin, which forms bonds with fibrin and is involved in the attachment of blood clots to the vascular wall.
2) adhesion and aggregation of platelets in the area of damage. Adhesion occurs due to the receptor interaction of platelet receptors with components of the subendothelium. Platelet degranulation occurs with the release of fibrinogen, antiheparin, fibronectin, etc. It ends with platelet aggregation with the formation of a primary hemostatic plaque.
3) the coagulation process occurs in the form of a cascade of reactions involving the enzyme, cofactors and ends with the transformation of prothrombin into thrombin, which promotes the conversion of fibrinogen into fibrin. Next, the fibrin bundle captures leukocytes, erythrocytes, and precipitating blood plasma proteins. A secondary hemostatic plaque is formed.
Stages of thrombus morphogenesis:
1) agglutination of platelets with their previous loss from the blood flow, adhesion to the site of endothelial damage. Then they degranulate, releasing serotonin, a thromboplastic factor, which leads to the formation of active thromboplastin.
2) coagulation of fibrinogen with the formation of fibrin occurs upon activation of the blood coagulation system (coagulation cascade). The primary platelet plaque is stabilized.
3) agglutination of red blood cells.
4) precipitation of plasma proteins.
Causes of thrombosis:
violation of the integrity of the vascular wall
blood flow disturbance
imbalance between the coagulation and anticoagulation systems of the blood.
Morphology of the thrombus. A thrombus consists of blood cells, fibrin and the liquid part of the blood.
Depending on the structure and appearance There are white, red, mixed and hyaline thrombi. White thrombus consists mainly of platelets in the form of multi-storey beams, fibrin and leukocytes. It forms slowly, with fast blood flow, most often in the arteries, on the inner surface of the heart. Red blood clot formed by a fibrin network, in which a large number of red blood cells and small accumulations of platelets are detected. More often found in veins, it forms quickly, with slow blood flow. Mixed thrombus– consists of elements of both white and red thrombus, has a layered structure. Found in veins, arteries, aneurysms. Hyaline thrombi are formed in the vessels of the microvasculature; they are based on necrotic erythrocytes, platelets, and precipitating plasma proteins.
In relation to the lumen of the vessel, the thrombus can be parietal, i.e. leave part of the vessel free, or clogged. According to etiology, blood clots are divided into arrowroot (occur during exhaustion, when dehydration of the body develops and the blood becomes thicker, usually in structure they are mixed blood clots), tumor (when tumor cells grow into the lumen of the veins, their surface is covered with thrombotic masses of a mixed type), septic ( this is an infected, mixed thrombus) and in diseases of the hematopoietic system.
The size of the clot may vary. Its surface is usually dull, uneven, corrugated, blood clots break easily, and are always associated with vascular wall. Blood clots are not associated with the wall of the vessel, with a smooth shiny surface and elastic consistency.
Outcomes of thrombosis:
I. Favorable:
1) aseptic autolysis (dissolution)
2) calcification
3) organization - resorption with its replacement by connective tissue, which grows in from the intima; accompanied by canalization, vascularization and revascularization.
II. Unfavorable:
1) septic fusion of thrombus
2) detachment of a blood clot with the development of thromboembolism.
The significance of thrombosis is determined by the speed of its development, localization, prevalence, and possible outcome. More often, thrombosis is a dangerous phenomenon that can lead to the development of heart attacks and gangrene; thromboembolism, sepsis, etc.
Classification of granulomas.
According to etiology. I. Granulomas of established etiology: 1. infectious granulomas, 2. non-infectious granulomas (dust, drug-related, around foreign bodies). II. Granulomas of unknown etiology.
According to morphology. I. Mature macrophages. II. Epithelioid cell granulomas. The following division according to morphology is possible: 1) with the formation of granulomatous infiltrate (diffuse type), 2) with the formation of granulomas (tuberculoid type). Criteria for assessing granulomas include their specificity. Specific are called granulomas that are formed under the influence of specific pathogens and are characterized by relatively specific morphological manifestations. Depending on the characteristics of cell maturation, granulomas with slow metabolism are distinguished (for example, granulomas of foreign bodies, with long period life of monocytes) and granulomas with a high level of metabolism (in response to the penetration of bacteria into the body that live in macrophages for several days), they differentiate into epithelioid.
Outcomes of granulomas: 1. resorption, 2. necrosis, 3. suppuration, 4. scarring. In most cases, granulomatosis leaves behind a relatively long-term immunity, sometimes lifelong, to the same disease.
Tuberculosis granuloma . The causative agent is mycobacterium, Koch's bacillus. Granuloma – tubercle, macroscopically, a tubercle in the form of a gray nodule the size of a millet grain ( miliary tubercle). Microscopically, it consists of epithelioid cells, lymphocytes, and multinucleated Pirogov-Langhans cells. Typical cells may include plasma cells, macrophages, and a thin network of argyrophilic fibers. Subsequently (under unfavorable conditions), tissue permeability increases, and leukocytes and plasma proteins penetrate into the tubercle. This promotes the proliferation of mycobacteria and the release of toxins. A curdled necrosis appears in the center of the tubercles, and their color changes from gray to yellow, yellow-gray, resembling cottage cheese (curdled tubercle). If large areas of tissue with purulence are exposed to cheesy necrosis
Pathological anatomy obtains material for research during autopsies of corpses, surgical operations, biopsies and experiments.
When autopsies are performed on the corpses of the deceased, both advanced changes are found that led the patient to death, as well as initial changes, which are often discovered only during microscopic examination. This made it possible to study the stages of development of many diseases; at autopsy, the correctness of the clinical diagnosis is confirmed or a diagnostic error is revealed, the causes of death of the patient, and the features of the course of the disease are established.
Surgical material (removed organs and tissues) allows the pathologist to study the morphology of the disease at various stages of its development and explore various methods of morphological research.
Biopsy – intravital tissue collection for diagnostic purposes. Through a biopsy, the clinic receives objective data confirming the diagnosis, allowing us to judge the dynamics of the process, the nature of the course of the disease and prognosis, the feasibility of using and the effectiveness of a particular type of therapy, and the possible side effects of drugs.
The experiment is important for elucidating the pathogenesis and morphogenesis of diseases. Using models of human diseases, the effects of certain medications are studied and methods of surgical interventions are developed.
The study of the structural basis of the disease is carried out at different levels: organismal, systemic, organ, tissue, cellular, subcellular, molecular.
The organismal level allows us to see the disease of the entire organism in its diverse manifestations, in the interconnection of all organs and systems.
The system level is the level of study of any system of organs or tissues united by common functions.
The organ level makes it possible to detect changes in organs identified during macro-microscopic examination.
Tissue and cellular levels are the levels of studying altered tissues, cells and intercellular substances using light-optical research methods.
The subcellular level makes it possible to observe using an electron microscope changes in the ultrastructures of the cell and intercellular substance, which in most cases are the first morphological manifestations of the disease.
A molecular level study of the disease is possible using complex research methods involving electron microscopy, immunohistochemistry, cytochemistry, and autoradiography.
The problems that pathological anatomy solves place it in a special position among medical disciplines: on the one hand, it is a theory of medicine that considers the material substrate of the disease; on the other hand, it is clinical morphology for making a diagnosis, serving the practice of medicine. It should be emphasized that teaching pathological anatomy is based on the principles of unity and conjugation of structure and function, as well as its clinical and anatomical direction.
Brief historical data.
As an independent discipline, pathological anatomy developed very slowly in due to the fact that autopsy of the bodies of the dead was prohibited for a long time.
In 1761, the work of the Italian anatomist G. Morgagni (1682-1771) “On the location and causes of diseases identified by the anatomist” was published, based on the results of 700 autopsies, some of which were performed by the author personally. He tried to establish a connection between the described morphological changes and the clinical manifestations of diseases. Thanks to Morgagni’s work, the dogmatism of old schools was broken, new medicine appeared, and the place of pathological anatomy among clinical disciplines was determined.
The works of the French morphologists M. Bichat (1771-1802), J. Corvisart (1755-1821) and J. Cruvelier (1791-1874), who created the world's first color atlas on pathological anatomy, were of great importance for the development of pathological anatomy.
In the 19th century, pathological anatomy had already gained a strong position in medicine. Departments of pathological anatomy were opened in Berlin, Paris, Vienna, Moscow, and St. Petersburg. A representative of the Viennese school, K. Rokitansky (1804-1878), based on enormous personal experience (300,000 autopsies over 40 years of dissection work), created one of the best manuals on pathological anatomy at that time.
The creation in 1855 by the German scientist R. Virchow (1821-1902) of the theory of cellular pathology can be considered a turning point in the development of pathological anatomy and all medicine.
In the 20th century, pathological anatomy began to develop rapidly, involving biochemistry and biophysics, immunology and genetics, molecular biology, electronics and computer science in solving its problems.
In Russia, autopsies began to be performed for the first time in 1706, when, by decree of Peter 1, medical hospital schools were organized. However, the first organizers of the medical service in Russia, N. Bidloo, P. Foucher, P. Kondoidi, had to overcome the stubborn resistance of the clergy, who in every possible way prevented the autopsies. Only after the opening of the Faculty of Medicine at Moscow University in 1775, autopsies began to be carried out quite regularly.
The first pathologists were the heads of the clinics F.F. Keresturi and E.O. Mukhin. A.O. Over et al.
A special place in the Moscow school of pathologists was occupied by M.N. Nikiforov (1858-1915), who headed the department of pathological anatomy at Moscow University from 1897 to 1915. He created one of the best textbooks and trained a large number of students. The most talented student of M.N. Nikiforov was A. I. Abrikosov, who laid the scientific and organizational foundations of pathological anatomy. He authored outstanding research on the initial manifestations of pulmonary tuberculosis, myoblast tumors, oral pathology, kidney pathology, etc. He wrote a textbook for students, which went through 9 editions, A multi-volume manual on pathological anatomy for doctors has been created, and a large number of students have been trained.
Prominent representatives of the Moscow school of pathologists are M.A. Skvortsov (1876-3963), who created the pathological anatomy of childhood diseases, and I.V. Davydovsky (1887-1968), known for his work on general pathology, infectious pathology, gerontology and combat trauma, research on the philosophical foundations of biology and medicine.
The Department of Pathological Anatomy in St. Petersburg was created in 1895. On the initiative of N.I. Pirogov, the glory of Russian pathological anatomy was created here by M.M. Rudnev (1837-1878), G.V. Shore (1872-1948), N.N. Anichkov, M.F. Glazunov, F.F. Sysoev, V.G. Garshin, V.D. Zinzerling. They trained a large number of students, many of whom headed departments at Leningrad medical institutes: A.N. Chistovich, M.A. Zakharyevskaya, P.V. Sipovsky.
In the second half of the 19th and early 20th centuries, departments of pathological anatomy were opened in medical institutes of Kazan, Kharkov, Kyiv, Tomsk, Odessa, Saratov, Perm and other cities.
Pathologists deployed Scientific research in various areas of medicine, in particular infectious diseases. Subsequently, they developed issues of early diagnosis of tumors, paid a lot of attention to the study of cardiovascular and many other diseases, issues of geographic and regional pathology. Experimental pathology developed successfully.
A pathological anatomical service has been created in Ukraine. In large cities, central pathological laboratories have been created that organize the work of pathologists. All deaths in hospitals or clinics of medical institutes are subject to a pathological autopsy. It helps to establish the correctness of the clinical diagnosis, identify defects in the examination and treatment of the patient. To discuss medical errors identified during a pathological autopsy and develop measures to eliminate shortcomings in therapeutic work Clinical and anatomical conferences are organized.
The work of pathologists is regulated by regulations and orders of the Ministry of Health and is controlled by the chief pathologist.
Since 1935, the journal “Archive of Pathology” has been published. Its first editor was A.I. Abrikosov. Since 1976, the publication of the abstract journal “General Issues of Pathological Anatomy” began.
2. Objects of study and methods of pathological anatomy
3. Brief history of the development of pathological anatomy
4. Death and post-mortem changes, causes of death, thanatogenesis, clinical and biological death
5. Cadaveric changes, their differences from intravital pathological processes and significance for the diagnosis of the disease
1. Objectives of pathological anatomy
Pathological anatomy– the science of the occurrence and development of morphological changes in a sick body. It originated in an era when the study of painfully altered organs was carried out with the naked eye, i.e., using the same method used by anatomy, which studies the structure of a healthy organism.
Pathological anatomy is one of the most important disciplines in the system of veterinary education, in the scientific and practical activities of a doctor. She studies the structural, i.e., material basis of the disease. It is based on data from general biology, biochemistry, anatomy, histology, physiology and other sciences that study the general laws of life, metabolism, structure and functional functions of a healthy human and animal body in its interaction with the external environment.
Without knowing what morphological changes a disease causes in an animal’s body, it is impossible to have a correct understanding of its essence and mechanism of development, diagnosis and treatment.
The study of the structural basis of the disease is carried out in close connection with its clinical manifestations. Clinical and anatomical direction is a distinctive feature of Russian pathological anatomy.
The study of the structural basis of the disease is carried out at different levels:
· the organismal level allows us to identify the disease of the entire organism in its manifestations, in the interrelation of all its organs and systems. From this level begins the study of a sick animal in clinics, a corpse in a dissection room or a cattle burial ground;
· the system level studies any system of organs and tissues (digestive system, etc.);
· the organ level allows you to determine changes in organs and tissues visible with the naked eye or under a microscope;
· tissue and cellular levels - these are the levels of studying altered tissues, cells and intercellular substance using a microscope;
· the subcellular level makes it possible to observe using an electron microscope changes in the ultrastructure of cells and intercellular substance, which in most cases were the first morphological manifestations of the disease;
· the molecular level of studying the disease is possible using complex research methods involving electron microscopy, cytochemistry, autoradiography, and immunohistochemistry.
Recognition of morphological changes at the organ and tissue levels is very difficult at the beginning of the disease, when these changes are insignificant. This is due to the fact that the disease began with changes in subcellular structures.
These levels of research make it possible to consider structural and functional disorders in their inextricable dialectical unity.
2. Objects of study and methods of pathological anatomy
Pathological anatomy deals with the study of structural disorders that arise at the very initial stages of the disease, during its development, up to the final and irreversible conditions or recovery. This is the morphogenesis of the disease.
Pathological anatomy studies deviations from the usual course of the disease, complications and outcomes of the disease, and necessarily reveals the causes, etiology, and pathogenesis.
Studying the etiology, pathogenesis, clinical picture, and morphology of the disease allows us to apply scientifically based measures for the treatment and prevention of the disease.
The results of observations in the clinic, studies of pathophysiology and pathological anatomy have shown that a healthy animal body has the ability to maintain a constant composition of the internal environment, a stable balance in response to external factors - homeostasis.
In case of illness, homeostasis is disrupted, vital activity proceeds differently than in a healthy body, which is manifested by structural and functional disorders characteristic of each disease. Disease is the life of an organism in changed conditions of both the external and internal environment.
Pathological anatomy also studies changes in the body. Under the influence of drugs, they can be positive and negative, causing side effects. This is the pathology of therapy.
So, pathological anatomy covers a wide range of issues. She sets herself the task of giving a clear idea of the material essence of the disease.
Pathological anatomy strives to use new, more subtle structural levels and the most complete functional assessment of the altered structure at equal levels of its organization.
Pathological anatomy receives material about structural disorders in diseases with the help of autopsies, surgeries, biopsies and experiments. In addition, in veterinary practice, for diagnostic or scientific purposes, forced slaughter of animals is carried out at different stages of the disease, which makes it possible to study the development of pathological processes and diseases at various stages. A great opportunity for pathological examination of numerous carcasses and organs is presented in meat processing plants during the slaughter of animals.
In clinical and pathomorphological practice, biopsies are of particular importance, i.e. intravital removal of pieces of tissue and organs, carried out for scientific and diagnostic purposes.
Particularly important for elucidating the pathogenesis and morphogenesis of diseases is their reproduction in experiment . Experimental The method makes it possible to create disease models for accurate and detailed study, as well as for testing the effectiveness of therapeutic and preventive drugs.
The possibilities of pathological anatomy have expanded significantly with the use of numerous histological, histochemical, autoradiographic, luminescent methods, etc.
Based on the objectives, pathological anatomy is placed in a special position: on the one hand, it is a theory of veterinary medicine, which, by revealing the material substrate of the disease, serves clinical practice; on the other hand, it is clinical morphology for establishing a diagnosis, serving the theory of veterinary medicine.
