Clinical Biomechanics of Podium Bones
During phase flexia PDM. podium bone makes the movement of outdoor rotation. At the same time, the rear parts of large horns are diverted down the book, Kepened and Knab. Thus, the lift bone is revealed. The body descends, slightly turning the stop.
During phase extension PDM. subject bone makes the movement of internal rotation. At the same time, the rear parts of large horns converge up, for the stop and knutrice. Podium bone is thus closed. The body of the bone rises, slightly turning the kleon.
1. Novoseltsev S.V. Introduction to osteopathy. Crane diagnostics and correction techniques. St. Petersburg, LLC "Publishing Foliant", 2007. - 344 C.: IL.
2. Caporossi R., Peyralade F. Traite Pratique D`osteopatique Cranienne. S.i.O. Paris, ED. D`Verlaque, 1992.
3. Liem T. CraniosaCral Osteopathy. Principles and Practice. ELSEVIER, 2004. - 706 p.
4. Magoun H.I. Osteopathy In The Cranial Field, 3 Rd ED., 1976. - PP.5, 165.
5. Retzlaff E.W., Mitchell F.L., Jr. The Cranium and Its Sutures, Berlin, Springer Verlag, 1987.
6. SUTHERLAND W.G. Contributions of the Thougoht. - IDAHO: SUTHERLAND CRANIAL TEACHING FOUNDATION, 1967. - P. 90-92.
Introduction
Anatomy and clinical biomechanics of the bones of the skull. General
Palpator landmarks skull
Anatomy and clinical biomechanics of the occipital bone
Anatomy and clinical biomechanics of wedge-shaped bone
Anatomy and clinical biomechanics of temporal bone
Anatomy and clinical biomechanics of parietal bones
Anatomy and clinical biomechanics of the frontal bone
Anatomy and clinical biomechanics of lattice bone
Anatomy and clinical biomechanics of the upper jaw
Anatomy and clinical biomechanics of zicky bone
Anatomy and clinical teachnik biomechanics
Anatomy and clinical biomechanics sky bones
Anatomy and clinical biomechanics of the lower jaw
Anatomy and clinical biomechanics of sub-speaking bones
Pathological anatomy gets material on structural disorders
Diseases with the help of opening corpses, surgical operation, biopsy
and experiment.
When opening the corpses (autopsy-from Greek. AutoPsia - Vision
own eyes) dead from various diseases confirmed
clinical diagnosis vulnence or diagnostic error is detected,
The cause of the death of the patient, the features of the course of the disease,
is the effectiveness of the use of therapeutic drugs, tools,
Working statistics for mortality and mortality, etc. At the opening of
go as far as far as the changes that led the patient to death,
so the initial changes that detect more often with micro
Skopic study. That is how all stages were studied.
The development of tuberculosis, currently well-known doctors. By-
Once studied early manifestations of such a disease like cancer,
Revealed changes preceding its development, i.e. the precancer
processes.
Organs and tissues taken on autopsy are studied using not only ma-
Croskopic, but also microscopic research methods. At the same time
reproduced mainly by a light-optical study, since
Changes (autolysis) limit the use of thinner methods of morpho
logical analysis.
Operational material allows the pathologist to study
morphology of the disease at various stages of its development and use when
This is a variety of morphological research methods.
Biopsy (from Greek. BIOS - Life and Opsis - Vision) - Lifting Taking
Fabrics and microscopic examination with a diagnostic purpose. Already bo
Leu 100 years ago, as soon as the light microscope appeared, pathologists
Began to study the biopsy material - biopsy. Thus
way they supported a clinical diagnosis of morphological research
. Over time, the use of tissue biopsy available for research
Doves expanded. Currently, it is impossible to present therapeutic institutions
The railway in which they would not be resorted to biopsies to clarify the diagnosis.
In modern medical institutions, biopsy is produced to each third
Mu patient.
Until recently, biopsy was used mainly to diagnose
Packs of tumors and urgent solving further medicinal tactics, result
Tatti research biopsy was interested in most often surgeons and dermatology
gov. Over the past 30 years, the picture has changed dramatically. Medical equipment
Created special needles with which you can carry out the so-called
puncture biopsies of different organs (liver, kidneys, lungs, heart, bone
Brain, synovial shells, lymph nodes, spleen, head
Brain), as well as devices for the production of endobiopsy (bronchi, stomach, ki-
Schaine, etc.).
Currently, not only biopsy is improved, but also expands
The task, which with its help solves the clinic. By biopsy,
Rarely repeated, the clinic receives objective data confirming
diagnosis to judge the process dynamics, the nature of the flow of disease
nor and forecast, the feasibility of using and the effectiveness of this or
A different type of therapy, about the possible side effect of drugs. So
zoom, the pathologist becomes a full participant in the diagnosis,
Rapeutic or surgical tactics and disease forecasting.
Biopsy make it possible to explore the most initial and subtle changes
cells and tissues using an electron microscope, biochemical, histo-
Chemical, histoimmunochemical and enzymological methods. It's known
cheat that with the help of modern methods of morphological research
You can identify those initial changes in diseases, clinical manifestations
which are still missing due to the consistency of compensatory
processes. In such cases, only the pathologist has
opportunities early diagnosis. The same modern methods of cyto- and
Stochemistry, immunohistochemistry, radioautography, especially in combination with
throne microscopy, allow you to give a functional assessment of the changed
in case of disease structures, to obtain a submission not only about the essence and PATO
The genesis of the developing process, but also on the degree of compensation for disturbed
functions. Thus, biopsytat is currently becoming one of
new research objects in solving both practical and theoretical
There are problems of pathological anatomy.
Experiment is very important to clarify pathogenesis and morphogenesis
Diseases. The experimental method found particularly widespread use.
in pathological physiology, to a lesser extent - in the pathological anatom
Mia. However, the latter uses an experiment in order to trace
All phases of the development of the disease.
In the experiment it is difficult to create an adequate model of human disease, so
as his diseases are closely related not only with the effects of the pathogenic factor,
But also by the special working conditions and life. Some diseases such as rheum
TIM, meet only in humans, and still attempts to reproduce them
Animals did not give the desired results. However, the model of many
human pains are created and created, they help deeper to understand the PATO
Genesis and morphogenesis of diseases. On the models of human diseases, they study
These or other drugs are developing methods
Operational interventions before they find clinical use.
Thus, modern pathological anatomy is experiencing a period
Modernization, it became clinical pathology.
Tasks that are currently pathological anatomy
They have it among medical disciplines in a special position: on the one hand -
This is the theory of medicine, which, revealing the material substrate
The clinical practice serves directly clinical practice; On the other - it is
Clinical morphology to establish a diagnosis that serves
Waria medicine.
The main method of pathological anatomy is the opening of a deceased person - autopsy. The goal of autopsy is to establish a diagnosis of illness, identify complications that led the patient to death, the features of pathogenesis, pathomorphosis and etiology of the disease. On the basis of autopsy material, new nosological forms of disease are described and studying.
The autopsy conducts a pathologist in the presence of attending doctors, guided by the provisions of the relevant orders of the Ministry of Health of the Republic of Belarus. During autopsy, the doctor of the pathologist makes a fence of pieces of various organs for histological examination, and, if necessary, for bacteriological and bacterioscopic studies. At the end of the opening, the pathologist discharges a medical certificate of death and draws up an autopsy protocol.
Of the slices of organs recorded in a 10% neutral formal solution, the laboratory technicians of the pathoanatomic separation prepare histological preparations. After the microscopic study of such drugs, the patrol monastery makes the final pathologist diagnosis and compares clinical and pathologist diagnoses. The most interesting cases and cases of discrepancies of diagnoses are dealt with clinical and anatomical conferences. With the order of clinical and anatomical conferences, students get acquainted during the passage of classes on the biopsy-section cycle at the senior courses.
The main method of pathological anatomy should also include the biopsy research method. Biopsy - From the Greek Words of Bios -zhizn and Opsis -Curty perception. Under the biopsy, they understand the histological examination of pieces of tissues taken from a living person to diagnostic purposes.
Distinguish diagnostic biopsies. taken specifically to establish a diagnosis and operationalWhen the histological examination is sent to the organs and tissues removed during operation. Quite often in therapeutic institutions use the method express biopsyWhen histological research is carried out directly during operational intervention to solve the issue of the volume of operational intervention. Currently widespread method punction biopsies (aspiration biopsy). Such biopsy is carried out with the help of appropriate needles and syringes by puncture of internal organs and suction in a syringe of material from the organ (kidney, liver, thyroid gland, blood-forming organs, etc.).
Modern methods of pathological anatomy. Among them are the main importance of immunohistochemistry and hybridization in place. These methods gave the main impetus to the development of modern pathological anatomy, they combine elements of classical and molecular pathology.
Immunohistochemical Methods (IGH). They are based on the specific interaction of tissue and cellular antigens of a person with specially obtained antibodies that carry a variety of labels. Today it is not much difficult to get antibodies to almost any antigen. IHG methods can be studied the most different molecules, the receptor apparatus of cells, hormones, enzymes, immunoglobulins, etc. studying concrete molecules, IGH allows you to obtain information about the functional state of the cell, its interaction with the microenvironment, to determine the cell phenotype, to establish the cell affiliation to a certain tissue, What is crucial in the diagnosis of tumors, the evaluation of cell differentiation, histogenesis. Phenotyping of cells can be carried out using light and electron microscopy.
To visualize the results of the reaction, the antigen antibody uses labels. For light microscopy, enzymes and fluorochromas are used for electronically dense markers. IGH also serves to assess the expression of cellular genes on appropriate protein products in tissues and cells encoded by data genes.
Hybridization on site (GIS) - This is a method for direct detection of nucleic acids directly in cells or histological preparations. The advantage of this method is the possibility of not only the identification of nucleic acids, but also correlation with morphological data. The accumulation of information about the molecular structure of viruses using this method made it possible to identify the alien genetic material in histological preparations, and also to understand what many years were called morphologists with viral inclusions. GIS, as a highly sensitive method, is necessary for the diagnosis of hidden or latent infections, such as cytomegalovirus, herpetic infections, hepatitis viruses. The use of GIS can contribute to the diagnosis of viral infection in the seronegative patients with AIDS, viral hepatitis; With it, it is possible to study the role of viruses in carcinogenesis (thus the connection of the Epstein-Barr virus with NazoFaring Karcinoma and Lymphoma of Berkitta, etc.).
Electronic microscopy.. To diagnose pathological processes on the material taken during the patient's life, the necessary cases use electron microscopy (transmission - in a passing light beam like light-optical microscopy and scanning - removing surface relief). The transmission EM is used more often to study the material in ultra-thin cloth sections, to study the parts of the cell structure, detecting viruses, microbes, immune complexes, etc. The main stages of the material processing are as follows: a small piece of fresh fabric (diameter 1.0-1.5 mm) It is immediately fixed in glutaraldegitis, less often - another lock, and then - in the four-rock osmium. After the wiring, the material is poured into special resins (epoxy), the ultra-thin sections are prepared with ultramicrothomes, painted (contrast), are placed on special grids and explore.
EM is a laborious and expensive method, it should be applied only in cases where other methods have exhausted themselves. Most often, such a need arises in monomorphology and virology. For the diagnosis of certain types of histiocytosis, for example, histiocytosis, tumors from the process of epidermal macrophages, the marker of which are Birbek granules. Another example, a rhabomiosarcoma, its marker is z-discs in tumor cells.
2. Objects of research and methods of pathological anatomy
3. Brief history of the development of the Patanatomy
4. Death and post-mortem changes, causes of death, tanatogenesis, death clinical and biological
5. Conductive changes, their differences from the lifetime pathological processes and the importance for diagnosing the disease
1. Tasks of pathological anatomy
Pathological anatomy- Science on the emergence and development of morphological changes in the sore organism. It originated in the era, when the study of painfully altered organs was carried out by the naked eye, i.e., the same method, which is used by anatomy that studies the structure of a healthy body.
Pathological anatomy is one of the most important disciplines in the system of veterinary education, in the scientific and practical activity of the doctor. It studies structural, i.e., the material foundations of the disease. It relies on the data of general biology, biochemistry, anatomy, histology, physiology and other sciences, which are studying the general patterns of life, metabolism, structure and functional shipments of a healthy human body and animals in the interaction of it with the external environment.
Without knowledge of what morphological changes in the animal body causes a disease, it is impossible to correctly understand its essence and the mechanism of development, diagnosis and treatment.
The study of the structural foundations of the disease is carried out in close connection with its clinical manifestations. The clinical and anatomical direction is a distinctive feature of the domestic patanatomy.
The study of the structural foundations of the disease is carried out at different levels:
· The organism level allows you to identify the disease of the holistic organism in its manifestations, in the relationship of all its organs and systems. From this level begins the study of the patient of the animal in clinics, the corpse - in the sectional hall or crookogenesis;
· The system level studies any system of organs and tissues (digestive system, etc.);
· The organ level allows to determine changes in organs and tissues visible to a simple eye or under a microscope;
· Tissue and cellular levels are levels of study of altered tissues, cells and an intercellular substance using a microscope;
· Sub-cell level allows you to observe with an electron microscope change in the ultrastructure of cells and the intercellular substance, which in most cases were the first morphological manifestations of the disease;
· The molecular level of the study of the disease is possible using integrated research methods with the involvement of electron microscopy, cytochimia, radioautographics, immunohistochemistry.
Recognition of morphological changes on the organ and fabric 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 a change in subcellular structures.
These levels of research make it possible to consider structural and functional disorders in their inseparable dialectical unity.
2. Objects of research and methods of pathological anatomy
Pathological anatomy is engaged in the study of structural disorders arising at the most initial stages of the disease, in the course of its development, up to finite and irreversible states or recovery. This is morphogenesis of the disease.
Pathological anatomy studies deviations from the usual flow of illness, complications and outcomes of the disease, necessarily reveals the causes, etiology, pathogenesis.
The study of etiology, pathogenesis, clinics, morphology of the disease allows us to apply scientifically based treatment and prevention of disease.
The results of observations in the clinic, research of pathophysiology and pathological anatomy have shown that the healthy body of the animal has the ability to maintain the constancy of the internal environment, a steady equilibrium in response to external factors - homeostasis.
During the disease, homeostasis is broken, life activity occurs otherwise than in a healthy body, which is manifested by the structural and functional disorders characteristic of each disease. The disease is the life of the body in the changed conditions of both the outer and the inner medium.
Pathological anatomy also examines 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 large range of issues. It puts the task to give a clear idea of \u200b\u200bthe material essence of the disease.
Pathological anatomy seeks to use new, thinner structural levels and the most complete functional assessment of the changed structure at equal levels of its organization.
Pathological anatomy receives material on structural disorders in diseases with opening of corpses, surgical operations, biopsy and experiments. In addition, in veterinary practice with a diagnostic or scientific goal, a forced kill of animals is carried out in different terms of the disease, which makes it possible to study the development of pathological processes and illness at various stages. The great possibility of a pathologist examination of numerous carcasses and organs is represented on meat processing plants when riding animals.
In clinical and pathological practice, biopsy, i.e., have a certain meaning, that is, the lifetime taking pieces of tissues and organs carried out with a scientific and diagnostic target.
Especially important to clarify pathogenesis and morphogenesis of diseases is to reproduce them in the experiment . Experimental The method makes it possible to create a disease model for accurate and detailed examination, as well as to test the effectiveness of therapeutic and preventive drugs.
The possibilities of pathological anatomy have significantly expanded with the use of numerous histological, histochemical, autoradographic, luminescent methods, etc.
Based on the tasks, the pathological anatomy is put in a special position: on the one hand, this is the theory of veterinary medicine, which, disclosing the material substrate of the disease, serves clinical practice; On the other hand, it is a clinical morphology to establish a diagnosis that serves the theory of veterinary medicine.
1. Pathological anatomy: 1) Definition, 2) Tasks, 3) Objects and methods of research, 4) Place in medical science and health practice, 5) Levels of study of pathological processes.
1) Pathological anatomy - Fundamental medical and biological science that studies the structural foundations of pathological processes and all human diseases.
Pathological anatomy he studies and develops: 1) Cell pathology 2) Molecular bases, etiology, pathogenesis, morphology and morphogenesis of pathological processes and diseases 3) Patomorphosis of diseases 4) Pathological embryogenesis 5) Classification of diseases
2) ^ Tasks of pathological anatomy :
a) summarizing the actual data obtained using various medical and biological 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) the formation of the theory of medicine in general and the teachings of the disease in particular
3) Objects and research methods:
| ^ Object of study | Research method |
| live man | biopsy - Lifting Morphological Study ^ Types of biopsy: 1) puncture 2) Excisional 3) incision 4) aspiration a) diagnostic b) operating cytobiopsy (express diagnostics) |
| dead man | autopsy - opening a deceased person Objectives of autopsy:
|
| animals | experiment - actually refers to pathological physiology |
4) Pathological anatomy is the foundations of all clinical disciplines, it develops and examines not only the morphological basis of the clinical diagnosis, but also is the theory of medicine as a whole.
5) Levels of study of pathological processes: a) organized b) organized in) tissue d) cellular d) ultrastructural E) molecular
2. History of pathological anatomy: 1) Morgali works, 2) Rokitansky theory, 3) The theory of Shleiden and Schwann, 4) works of Virhov, 5) their importance for the development of pathological anatomy
Patanatomy development stages:
1. Macroscopic level (J. Morganya, K. Rokitansky)
2. Microscopic level (R. Virhov)
3. Electron microscopic level
4. Molecular biological level
1) To the morgot of autopsy was carried out, but without analyzing the data obtained. Giovanni Batisto Morgania:
a) began to conduct systematic autopsies with the formation of the idea of \u200b\u200bthe 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) hepatitization gave the concepts, the gap of the heart, etc.
2) Karl Rokitansky was the last representative of the theory of humoral human pathology.
Created one of the best in the XIX century. "Pathological Anatomy Guide", where I systematized all diseases based on your huge personal experience (30000 openings for 40 years of transactors)
3) Shleden, Svann - the theory of cellular structure (1839):
1. Cell - minimum alive unit
2. Cells of animals and plants are fundamentally similar to the structure
3. The reproduction of cells is carried out by dividing the original cell
4. Cells in the composition of multicellular organisms integrated
The value of the cell theory: armed with medicine with the understanding of the general patterns of the structure of the living, and the study of cytological changes in the patient organism made it possible to explain the pathogenesis of human diseases, led to the creation of pattomorphology of disease.
4) 1855 - Virchov - the theory of cell pathology - a turning point in pathological anatomy and medicine: a material substrate disease - cells.
5) The works of Morgali, Rokitansky, Shleiden, Svanna, Virchova laid the foundation of modern pathologistics, determined the main directions of its modern development.
3. Schools of pathologists: 1) Belorusskaya, 2) Moskovskaya, 3) Petersburg, 4) the main activities of domestic schools of pathologists, 5) their role in the development of pathological anatomy.
1) The Department of Patanatomy MGMI emerged in 1921. Head of up to 1948- prof. Titov Ivan Trofimovich - Chairman of the Republican Scientific Society, wrote a tutorial on Patanatomy in Belarusian.
Then the department headed Gulkevich Yuri Valentinovich. He was the head of the central path-anatomical laboratory. Okrew the corpses of Hitler, Gebels. I arrived in Minsk, I began to actively develop perinatal pathology. The department is protected by many of the dissertations for childbirth, cerpentine injury, lesteriosis, cytoplasm, are studied. 1962 - the laboratory of teratology and medical genetics was opened, an active study of development began. The department created a whole institution of regenerate and hereditary pathology (head of Lazyuk Gennady Ilyich - President Gulkevich Yu.V.). Currently, three professors at the department:
1. Related Evgeny Davydovich - Head of the Department, Honored Science Worker. Multiple PRD, thyroid cancer in children
2. Kravtsova Garina Ivanovna - Specialist in renal pathology, Arch Republic
3. Near Mikhail Konstantinovich - Pathology of CNS, congenital violations of brain development
2) 1849 - The First Patanatomy Department in Moscow. Head Department - prof. Polunin - the nambler of the clinical and anatomical direction of the Patanatomy. Nikiforov - a number of works, a padanatomy textbook. Apricot - work in the field of pulmonary tuberculosis, the pathology of the oral cavity, kidneys, a textbook, withstood 9 reprints. Skvortsov - Diseases of Children's Age. Davydovsky - general pathology, infectious pathology, gerontology. Stops - the founder of the teachings on collagenisas.
3) 1859 - the first Department of Patanatomy in St. Petersburg - the head of prof. Rudnev, also Shor, Anichkov, Glazunov, Sysoev, etc.
4) main directions - see questions 1-2
5) the role in the development of the Patanatomy: appeared by the Radonarchists of the Russian Patanatomy, led to a 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 posthumous changes.
1) Death is an 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 the disease (gradual or sustainable)
b) depending on the development of reversible or irreversible changes in life: 1) clinical 2) biological
3) Clinical death is reversible within a few minutes of changes in the life of the body, accompanied by stopping blood circulation and respiration.
Condition before clinical death - agony - non-coordinated activity of homeostatic systems in the terminal period (arrhythmia, paralysis of sphincter, convulsions, pulmonary edema, etc.)
At the heart of clinical death: Hypoxia CNS due to cessation of blood circulation and respiration and disorders of their regulation.
4) Biological death - irreversible changes in the life of the body, the beginning of the autolytic processes.
It is characterized by an unlimited death of cells and tissues (first, after 5-6 minutes, the cells of the cortex of the brain are dying, in other cells, the cells are dying during several days, while their destruction can be immediately detected only with EM)
^ 5) Signs of death and posthumous changes:
1. Cooling corpse (Algor Mortis) - gradual decrease in the temperature of the corpse.
Reason: cessation of heat generation.
Sometimes - with strikhnin poisoning, death from the tetanus - the temperature after death can increase.
2. ^ Pocketer (Rigor Mortis) - Sealing arbitrary and involuntary muscles of the corpse.
Reason: disappearance in the muscles after the death of ATP and the accumulation of lactate in them.
3. ^ Dry drying : Localized or generalized (mummification).
Cause: evaporation of moisture from the body surface.
Morphology: clouding of cornea, appearance on the sclera of dry drowned spots, parchment spots on the skin, etc.
4. ^ Redistribution of blood in the corpse - Overflow of blood blood, the insertion of the arteries, the posthumous coagulation of blood in the veins and the right hearts.
Morphology of posthumous clots: smooth, elastic, yellow or red, lie freely in the lumen of the vessel or heart.
Fast death - few posthumous clots, death from asphyxia is the absence of posthumous coagulation.
5. ^ Capor spots - The occurrence of body hypostasis in the form of dark purple spots is most often in the underlying parts of the body that are not subjected. When pressing, the pipe stains disappear.
Reason: Redistribution of blood in the corpse depending on its position.
6. ^ Corpse immibilation - Late coupling spots of red-pink coloring, not disappearing when pressed.
Reason: impregnation of the area of \u200b\u200bbody hypostasis plasma with hemoglobin from hemolyzed erythrocytes.
^ 7. Corpent decomposition with processes
A) autolysis - earlier arises and expressed in ferrous organs with enzymes (liver, pancreas), in the stomach (gastromayag), the esophagus (esophagomying), with the aspiration of the gastric juice - in the lungs ("sour" softening of the lungs)
B) the rotation of the corpse is the result of the reproduction of rotten bacteria in the intestine and the subsequent settlement of the tissues of the corpse; Gliding fabrics dirty green, make the smell of rotten eggs
C) body emphysema - the formation of gases in the rotation of the corpse, swelling the intestines and penetrating the organs and tissues; At the same time, the fabrics acquire a foamy look, when ticking, the attitudes are heard.
5. Dystrophy: 1) Definition, 2) Causes, 3) Morphogenetic mechanisms of development, 4) Morphological specificity of dystrophy, 5) Classification of dystrophy.
1) Dystrophy- A complex pathological process, which is based on a disturbance of tissue (cellular) metabolism leading to structural changes.
2) ^ The main cause of dystrophy - violation of the main mechanisms of trophic, namely:
a) cellular (block cell organization, cell retardation) and b) extracellular (transport: blood, lymph, ICR and integrative: neuroendocrine, neurogumoral) mechanisms.
3) ^ Distrophy morphogenesis:
but) infiltration - Excessive penetration of blood exchange products and lymphs in cells or intercellular goods, followed by their accumulation due to insufficiency of enzymatic systems, metabolizing these products [Infiltration of the epithelium protein of the proximal kidney tubules with nephrotic syndrome]
b. ) Decomposition (Plyeroz) - disintegration of cell ultrastructures and an intercellular substance, leading to a violation of tissue (cellular) metabolism and accumulation of products of impaired exchange in tissue (cell) [Cardiomyocyte fatty dystrophy, diphtheriaxication]
in) perverted synthesis- Synthesis in the cells or tissues of substances that are not found in them [Synthesis of alcoholic hyaline hepatocytes]
d) transformation - the formation of products of one type of exchange from general source products that go to the construction of proteins, fats, carbohydrates [reinforced polymerization of glucose in glycogen]
4) For a certain tissue, a certain mechanism of morphogenesis of dystrophy is characterized most often [Renal Channels - Infiltration, Myocardium - Decomposition] - distrophy orthology
5) ^ Distrophy classification.
I. Depending on the prevalence of morphological changes in specialized elements of parenchyma or stroma and vessels:
a) parenchymal dystrophy b) stromal-vascular (mesenchymal) dystrophy c) mixed dystrophy
II. According to the prevail of violations of a particular 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. Parenchimato protein dystrophy: 1) Causes 2) Morphology and outcomes of grainy dystrophy 3) Morphology and outcomes of hydropic dystrophy 4) Morphology and outcomes of hyalin-drip dystrophy 5) morphology and outcomes of horny dystrophy.
1) Causes of parenchymal protein dystrophy: violation of the function of certain enzyme systems (see examples of certain types of parenchymal protein dystrophy)
Types of parenchymal protein dystrophy: 1. Horny 2. Grainy 3. Hylin-drip 4. Hydropic
2) Morphology of grainy dystrophy (dim, muddy swelling): mask: organs are increased, dull, flabby on the section; Misk: Cells are enlarged, swollen, with protein grains.
^ Development mechanism and reason: expansion of EPS tanks and swelling mitochondria as a result of hyperplasia in response to functional voltage
Localization: 1) kidneys 2) liver 3) heart
Exodus: 1. Elimination of the pathological factor Cell recovery 2. Transition to hyalin-drip, hydropic or fatty dystrophy.
3) ^ Morphology of hydropic (water) dystrophy : Cells are enlarged; cytoplasm is filled with vacuoles with transparent liquid; The core on the periphery, bubble-shaped.
Localization: 1) skin cells 2) kidney channels 3) hematocytes 4) ganglion ns cells
^ Development mechanism : Increase the permeability of cell membranes, activation of hydrolytic enzymes with lysosomes Gap in intramolecular bonds, attaching to water molecules cell hydration.
The reasons: kidneys - nephrotic syndrome; liver - toxic and viral hepatitis; Epidermis - OSP, swelling; Ganglion cells - manifestation of physiological activities.
^ Exodus: focal or total combination cells of cells.
4) Morphology of hyalino-drop dystrophy: Hyali-like protein drops in cytoplasm with destruction of cellular organelles.
Localization: 1) liver 2) kidneys 3) myocardium (very rarely)
^ Development mechanism and reasons : kidneys - insufficiency of the vacuolar-lysomal apparatus of the epithelium of the proximal tubules of nephrocytes with nephrotic syndrome; The liver is the synthesis of Hyalino-like Taurus Mallory from alcoholic hyaline with alcoholic hepatitis.
^ Exodus: Focal or total coagulation cells of cells.
5) Horny dystrophy (pathological oroging):
a) hyperkeratosis - excessive formation of a horny matter at the burdensome epithelium
b) leukoplakia - pathological energization of mucous membranes; Cancer pearls with flat drainage cancer
^ Reasons: violation of skin development; chronic inflammation; viral infections; Avitaminosis
Exodus: Elimination of the pathogen at the beginning of the process recovery of cells; Cell death
7. Parenchimato fatty dystrophy: 1) Causes 2) Histochemical methods for detecting fat 3) Macro- and microscopic characteristics of parenchymal dystrophy of myocardium 4) Macro- and microscopic characteristics of liver dystrophy 5) Exodes of fatty dystrophy
1) ^ Causes of parenchymal fatty dystrophy:
but. Fabric hypoxia for anemia, chronic diseases of the lungs, chronic alcoholism
b. infections and intoxication with violation of lipid metabolism (diphtheria, sepsis, chloroform)
in. avitaminosis, one-sided nutrition without a protein with a deficit of lipotropic factors.
2) ^ Histochemical methods for detecting fat : but. Sudan III, Charles - color in red; b. Sudan IV, Osmisian Acid - Color in black in. Nile blue sulfate - dark blue fatty acids, red neutral fats.
3) ^ Morphology of parenchymal health dystrophy of myocardium:
Mask: The heart is not changed or increased, the chambers are stretched, a flabby, on the cut clay and yellow; Yellow-white is allocated from endocardium ("Tiger heart").
Misk: Dusty obesity (the smallest fat droplets in cardiomyocytes) fine-flowered obesity (substitution of the fat drops of the entire cytoplasm of cells, the disappearance of transverse allocations, the decay of mitochondria). The focal process - along the venous end of the capillaries ("Tiger Heart").
^ Development mechanism : Energy Self Deficiency (hypoxia, diphtheric toxin) 1) Increase the intake of fatty acids in cells 2) Violation of the exchanging of fats in the cell 3) the decay of lipoproteins of intracellular structures.
4) ^ Morphology of the parenchymal fatty liver dystrophy:
Mask.: liver is increased, flaky, hidden yellow, on the blade knife fat
Misk: Pull-like obesity fine-closed obesity Large-cap obesity (fatty vacuol fills the entire cytoplasm and moves the kernel to the periphery).
^ Development mechanisms : 1. Excessive receipt of the LCD into the liver or an increase in their synthesis of hepatocytes (lipoprotehemia for diabetes, alcoholism, general obesity, hormonal disorders) 2. The impact of toxins blocking oxidation of fatty acids and synthesis of leipoproteins in hepatocytes (ethanol, phosphorus, chloroform) 3. Insufficient Admission of lipotropic factors (avitaminosis)
5) Exodes of parenchymal fatty dystrophy: but. Removing while maintaining cell structures b. Cell death
8. Parenchimato carbohydrate dystrophy: 1) Causes 2) Histochemical methods for detecting carbohydrates 3) Carbohydrate dystrophy associated with a violation of glycogen exchange 4) Carbohydrate dystrophy associated with violation of glycoprotein exchange 5) Exodes of carbohydrate dystrophy.
1) Carbohydrates: but. polysaccharides (glycogen) b. Glicosaminoglycans (mucopolysaccharides) in. Glycoproteins (mucines of mucus, fabric mucoids).
^ Causes of parenchymal carbohydrate dystrophy : Violation of the metabolism of glycogen (at SD), glycoproteins (with inflammation).
2) Histochemical methods of detecting carbohydrates:
a) All carbohydrates - Chic-reaction of the Khiksa-Mac-Manusa (Red Color)
b) Glycogen - Carmin Besz (red)
c) glycosamines, glycoproteins - methylene blue
3) ^ Carbohydrate dystrophy associated with a violation of glycogen exchange:
but) acquired - Mainly at SD:
1. Reducing the tissue glybogen reserves in the liver intiltribration of liver fats inclusion of glycogen in hepatocyte kernels ("hole", "empty" kernels)
2. Glucosuria glycogenic infiltration of the epithelium of narrow and distal segments Synthesis of glycogen in the tubular epithelium High epithelium with light foamy cytoplasm
3. Hyperglycemia Diabetic microangiopathy (intercapillary diabetic glomerosclerosis, etc.)
b) congenital - Glycogenesis: Insufficiency of enzymes involved in the splitting of deposited glycogen.
4) ^ Carbohydrate dystrophy associated with violation of glycoprotein metabolism : accumulation of mucins and mucoids in cells and intercellular substance (mucous dystrophy)
but) inflammation Increase mucus formation, change in the physicochemical properties of mucus Desqumation of secretory cells, the obturation of output ducts by cells and mucus a. cysts; b. Obbitation of bronchi atelectase, foci of pneumonia in. The accumulation of pseudoomycins (mucus-like substances) colloidate goiter
b) mukobovysidosis - hereditary systemic disease, highlighting the epithelium of glands with a thick viscous poorly outlined mucus Retention cysts, sclerosis (cystic fibrosis) Defeat of all organism glasses
5) ^ Exodes of carbohydrate dystrophy : but. At the initial stage - the recovery of cells in the elimination of the pathogen b. Atrophy, sclerosis of mucous, cell death
9. Mesenchimal protein dystrophy: 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) ^ Mesenchimal protein dystrophy - violation of the exchange of proteins in the connective tissue of the etch of organs and the walls of the vessels.
Classification of mesenchymal protein dystrophy: 1. Mulcoid swelling 2. Fibrinoid swelling (fibrinoid) 3. Hylinosis (three consecutive stages of disorganization of connective tissue) 4. amyloidosis
Based on: Plasmoria, an increase in vascular permeability accumulation of blood plasma products in the main substance destruction of connective tissue elements.
2) Mucoid swelling - Surface and reversible disorganization of connective tissue.
Etiology of Mucoid swelling: 1. Hypoxia 2. Streptococcal infection 3. Immunopathological reactions.
Morphogenesis of mukoidal swelling: accumulation in the connective tissue of hydrophilic glycosaminoglycans (hyaluronic acid) hydration and swelling of the main intermediate substance
^ Localization of the process : wall arteries; heart valves; Endo- and epicard.
3) Morphological picture of mukoid swelling: Mask organ or fabric has not been changed, a basophilic basophilic substance (a metacromasque phenomenon due to the accumulation of chromotropic substances); Collagen fibers swell, subjected to fibrillary collapsion (painted with picrofoxin in yellow-orange).
Exodes: 1. Full fabric restoration 2. Transition to fibrinoid swelling
4) Fibrinoid swelling - Deep and irreversible destruction of connective tissue.
Etiology of fibrinoid swelling:
a) on a systematic (common) level:
1. Infectious-allergic reactions (fibrinoid of vessels with tuberculosis with hypergic reactions)
2. Allergic reactions (fibrinoid changes of vessels with rheumatic diseases)
3. Autoimmune reactions (in kidney clusters at GG)
4. angioedema reactions (fibrinoide arterioles in arterial hypertension)
b) at the local level - chronic inflammation in a heart-shaped process during appendicitis, in the bottom of the chronic ulcer of the stomach.
^ Morphogenesis of fibrinoid swelling : Plasmoria + destruction of the main substance and fibers of the connective tissue Fibrinoid formation (fibrin + proteins + cellular nucleoproteides).
5) ^ Morphology of fibrinoid swelling : Mask organs and fabrics are not changed; Misk homogeneous bunches of collagen fibers form insoluble compounds with fibrin, eosinophilic, yellow when painting with picropuxin, sharply chic-positive, argirofils.
Exodus: fibrino-shaped necrosis (complete destruction of connective tissue with a pronounced macrophage reaction) Replace the focus of destruction by connecting tissue (hyaline; sclerosis).
10. Hyalos: 1) Definition, Development Mechanism and Classification 2) Pathological processes, in the outcome of which the hyaline is developing 3) Pathomorphology of vessel hyalinosis 4) Patomorphology of connecting tissue hyalinosis 5) Exodus and functional meaning of hyalinose.
1) Hylia - Education in the connective tissue of homogeneous translucent dense masses, reminiscent of hyaline cartilage - hyaline.
Hyaline It consists of 1. fibrin and other blood plasma proteins 2. lipids 3. Immunoglobulins. Sharply chic-positive, yellow-red when painting with picropuxin.
Development mechanism: Destruction of fibrous structures, an increase in tissue-vascular permeability Precipient plasma proteins on altered fibrous structures Education of hyaline.
Classification: 1. Hyalosa vessels a. System b. Local 2. Hyalos of connective tissue itself a. System b. local
2) Pathological processes, in the outcome of which the hyaliosis develops:
but) vessels: 1. AG, atherosclerosis (simple hyaline) 2. Diabetic microangiopathy (diabetic arterialosis - lipogalin) 3. Rheumatic diseases (sophisticated hyaline) 4. Local-physiological phenomenon in the spleen of adults and the elderly ("glaze spleen").
b) actually connective tissue: 1. Rheumatic diseases 2. locally in the bottom of chronic ulcers, appendix 3. in scars, fibrous spikes of cavities, vascular wall during atherosclerosis.
3) Patomorphology of hyalinose vessels (Mostly small arteries and arterioles are affected, is systemic in nature, but most characteristic of the kidney vessels, pancreas, brain, retinal eyes):
^ Misk: hyaline in subendothelial space; Endaged media.
Mask.: vitreous vessels in the form of dense tubes with sharply narrowed lumen; Atrophy, deformation, arranging organs (for example, arteriolosclerotic nephrocyrousz).
4) ^ Patomorphology of hyalinosis actually connective tissue:
Misk: swelling of connecting bunches; loss of fibrillarity, fusion into a homogeneous dense cartilage mass; Cell elements are squeezed, atrophy are subjected.
^ Mask.: The fabric is dense, whitish, translucent (for example, hyaline heart valves during rheumatism).
5) Exodes of hyalinosis (more often unfavorable): 1. Razing (in keloids, in lactic glands in the condition of hyperfunction) 2. Ending 3. The gap of the hyalinized vessels with elevated blood pressure, hemorrhage
Functional value: Common hyaline arterioles functional insufficiency of organs (CPR in arteriolosclerotic nephrocyrosis); Local hyaline heart valves heart disease.
11. AMILOIDOS: 1) Definition and methods of histochemical detection of amyloid 2) The theory of the pathogenesis of amyloidosis 3) morpho and pathogenesis of amyloidosis 4) classification of amyloidosis 5) perieticular and periclagen amyloidosis.
1) ^ Amyloidosis (amyloid dystrophy) - Stromally-vascular dispennosis, accompanied by a deep disruption of protein metabolism, the appearance of anomalous fibrillar protein and the formation of a complex substance in the intermediate tissue and the walls of vessels - amyloid.
Methods for identifying amyloida (The basis of reactions is the phenomenon of metacromasia):
1. Coloring Congo Red - in red
2. The painting solution of a lugol with a 10% solution of sulfuric acid - in blue
3. Coloring methyl purple - in red
4. Dichroism and anisotropy in the polarization microscope
2) The theories of the pathogenesis of amyloidosis:
a) immunological (amyloid as a result of the interaction of AG and AT)
b) the theory of local cell synthesis (amyloid produced by cells of mesenchymal origin)
c) mutational theory (amyloid produced by mutant cells)
3) ^ Amilide consists of two components with antigenic properties :
but) P-component (plasma) - plasma glycoproteins
b) F-component (fibrilla) - heterogen, four varieties of the F-component:
1. Aa-protein - non-dissociated with IG - from serum -globulin SSA
2. Al-protein - associated with Ig - from and -light chains Ig
3. FAP protein - formed from the prehalation
4. ASC1 protein - is formed from the prehalation
Amiloidosis morphogenesis:
1. Pre-formidoid stage - converting part of cells (fibroblasts, plasma cells, reticular cells, cardiomyocytes, MMC vessels) in amyloidoblasts
2. Synthesis of the fibrillar component
3. Interaction of fibrils with the formation of the carcass of amyloid
4. The interaction of the frame with plasma components and chondroitin sulfate with the formation of amyloid
Pathogenesis of amyloidosis:
but) Aa-amyloidosis: Activation of the monocytic phagocyte system Isolation of IL-1 Stimulation of SSA protein synthesis in the liver (according to the function is an immunomodulator) a sharp increase in SSA in the blood reinforced destruction of SAA macrophages to AA Assembly on the surface of macrophage-amyloidoblasts AMA protein fibrils Amyloidthimulating factor synthesized by the bodies in the pre-formidoid stage.
b) BUTL.-Alamidosis: Violation of the degradation of light chains of immunoglobulins, the appearance of genetically modified light chains synthesis of amyloid fibrils from L-circuits Ig macrophages, plasma and other cells.
4) Classification of amyloidosis:
a) due to (origin):
1. idiopathic primary(Al-amyloidosis)
2. hereditary (genetic, family): a. Periodic disease (family Mediterranean fever) b. Macla Wales syndrome (A and B - AA-amyloidosis) in. Family amyloid polyneuropathy (FAP-amyloidosis)
3. secondary acquired: but. Jet (aa-amyloidosis in chronic infections, HNZL, osteomyelitis, wound suppurations, rheumatoid arthritis) b. Monoclon-protein (Al-amyloidosis in paraproteinemic leukemia)
4. senile Systemic amyloidosis (ASC1-amyloidosis) and local
b) on the specifics of protein fibrils: 1. Al- (generalized lesion of the heart, lungs, vessels) 2. AA- (generalized damage predominantly kidney) 3. FAP- (damage to peripheral nerves) 4. ASC1- (mainly damage to the heart and vessels)
c) in prevalence: 1. Generalized: primary, secondary, systemic senile 2. Local: forms of hereditary amyloidosis, senile local amyloidosis, "amyloid tumor"
d) on clinical manifestations: 1. Cardiopathic 2. Epinephropathic 3. Nephropathic 4. Neuropathic 5. Apud-amyloidosis 6. Hepatopathic
5) the lesion localization is distinguished by amyloidosis:
1. perieticular ("parenchymal") - Amyloida drops along the reticular fibers of the membranes of vessels and glands, reticular stroma parenchyma (spleen, liver, kidneys, adrenal glands, intestines, intima of small and medium vessels)
2. periclagen ("mesenchymal") - Amoloid falling in the course of collagen fibers Adventization of medium and large vessels, myocardium, cross-striped muscles, MMC, nerves, skin.
12. Amilidosis: 1) Clinical-morphological forms of amyloidosis and organs affecting them 2) The most frequent causes of secondary amyloidosis 3) Macro- and microscopic characteristic of amyloidosis spleen 4) Macro- and microscopic characteristics of amyloidosis kidneys 5) liver amyloidosis morphology, intestine and brain.
1) CMF amyloidosis and organs predominantly affecting them: 1. Cardiopathic (heart) 2. Epinephropathic (adrenal glands) 3. Nephropatic (kidney) 4. Neuropathic (nerves, brain) 5. Apud-amyloidosis (Apud system) 6. Hepatopathic (liver)
2) the most frequent causes of secondary amyloidosis:
but. Heavy forms of chronic infections (tuberculosis, syphilis)
b. HNZL (bronchiectase, abscesses)
in. osteomyelitis, wound suppuration
g. Rheumatic Arthritis and other rheumatic diseases
d. myeloma disease
^ 3) Patomorphology of amyloidosis spleen:
but) "Song" spleen: Misk Uniform Amoloid's Deposition in the Pulp, Mask Spleca is increased, dense, brown-red, smooth, greasy shine on the cut
b) "Sagovaya" spleen: Misk Deposition of amyloid in lymphoid follicles, having a sectional view of sage grains, Mask spleen is increased, dense
4) ^ Patomorphology of amyloidosis kidneys : Misk deposition of amyloid in the wall of vessels, capillary hinges and mesangia vessels, in the basal membranes of the epithelium of the tubules and stroma, the mask at the beginning is dense large ("big white kidney"), then amyloid worn kidney (see question 126 - amyloid nephrisosis)
^ 5) Amoidosis Patomorphology:
but) liver: Misk Deposition of Amiloid Between Star Sinusoid ReticuloDoteliocytes, along the Reticular Stroma, in the walls of vessels, ducts, in the connective tissue of portal paths, mask The liver is increased, dense, silent
b) intestine: sediments of amyloid in the course of the reticular stroma of the mucous and in the walls of the vessels; Atrophy of the ferrous apparatus of the intestinal mucosa
in) brain: amyloid in sedenive plaques of the crust (markers of senile dementia, alzheimer's diseases), vessels and brain shells.
13. Mesenchimal fatty dystrophy: 1) Definition and classification 2) Definition, causes and mechanisms for the development of obesity 3) Morphology of obesity 4) Lipomatosis 5) Morphology of cholesterol exchange disorders
1) ^ Mesenchimal fatty dystrophy - Stromally-vascular dystrophy arising from violation of the exchange of neutral fats and cholesterol and accompanied by either excessive accumulation of fat and xs, or in a decrease in its number, or in accumulation in an uncharacteristic place for it.
^ Classification of mesenchymal fatty dystrophy:
1. Violation of the exchange of neutral fats: a. General: 1) Obesity 2) Exhaustion b. Local
2. Violation of the exchange of hs and its esters.
2) Obesity (obesity) - an increase in the number of neutral fats in fatty depots that are common.
Causes of obesity: 1. Excessive nutrition 2. Hydgodina 3. Disrupting the neuro-endocrine regulation of fat metabolism 4. Hereditary factors.
Development mechanism: but. Activation of lipoproteinlipase and inhibition of lipolytic lipase b. Violation of hormonal regulation in favor of anti-polytic hormones in. Changing the state of fat metabolism in the liver and intestines
^ Common obesity classification:
1. by etiology: but. primary b. Secondary (alimentary, cerebral with a brain tumor, endocrine with Izeno-Cushing syndrome, hypothyroidism, hereditary)
2. on external manifestations: but. Symmetric (universal) type b. Upper (in the field of face, neck, shoulders, mammary glands) in. Middle (in the subcutaneous tissue of the belly in the form of apron) of the lower (in the field of hips and lower legs)
3. to exceed body weight: I degree (up to 30%) II degree (up to 50%) III degree (up to 99%) IV degree (from 100% or more)
4. in terms of the number and size of adiposocytes: a) hypertrophic type (the number of adiposocytes has not been changed, the cells are sharply increased, malignant flow) b) hyperplastic type (the number of adiposocytes is increased, metabolic changes in cells are absent, benign for)
^ 3) Morphology of obesity:
1. Abundant deposition of fats in subcutaneous tissue, gland, ear, mesenter, mediastinum, epicardium, as well as in uncharacteristic places: stoma myocardium, pancreas
2. Fatty tissue grows under epicardium and envelops the heart, sprinkle muscle mass; Heart increased significantly; Atrophy of cardiomyocytes; The border between the shells of the heart is erased, in some cases a heart break is possible (the right departments are especially affected)
4) Lipomatosis - Local increase in the number of fatty fiber:
a) Derkuma disease (Lipomatosis Dolorosa) - painful noded fat deposits in subcutaneous fiber of the body and limbs due to polyglandular endocrinopathy
b) vacanistic obesity - local increase in the number of adipose tissue in atrophy of the organ (fat replacement of thymus during its atrophy)
Time: 3 hours.
Motivational characteristics of the topic: The knowledge of the theme is necessary for the assimilation of other general and private courses of pathological anatomy, as well as for clinical and anatomical analysis when studying clinical disciplines and in the practical work of the doctor.
Total purpose of learning: to explore the content, objectives, the subject, the main methods and levels of study of pathological anatomy, familiarize themselves with the main historical stages of the development of discipline. Specific objectives:
1. To be able to define the object of pathological anatomy;
2. To be able to explain the tasks of pathological anatomy;
3. To be able to explain the main methods and levels of research in pathological anatomy;
4. Be able to assess the value of the pathological anatomy at the present stage.
The necessary initial level of knowledge: the student must recall the levels of research in morphology, the stages of the manufacture of microcreparations, histological color.
Questions for self-preparation (source level of knowledge):
2. Tasks of discipline;
3. Macroscopic, microscopic, ultrastructural levels of research;
4. The value of pathological anatomy in science and practice; Terminology
Outopcia (Autopsia - vision with their own eyes) - opening the corpse.
Biopsy (BIOS - Life and Opsis - Vision) - Lifting tissue with a diagnostic purpose.
Morphogenesis is the morphological basis of development mechanisms (pathogenesis).
Patomorphosis - variability of disease.
Santogenesis - recovery mechanisms.
Tanatogenesis - death mechanisms.
Ethiology - causes.
Hatrogen (Iatros is a doctor) - diseases arising from the activities of the doctor.
Pathological anatomy is an integral part of the pathology (from Greek. Pathos - a disease), which is an extensive area of \u200b\u200bbiology and medicine that studies various aspects of the disease. Pathological anatomy studies structural (material) bases of the disease. These knowledge serve as the basis for the theory of medicine and clinical practice. Theoretical, scientific importance of pathological anatomy is most fully revealed in the study of the general patterns of the development of cell pathology, pathological processes and diseases, i.e. General human pathology. The clinical, applied, the value of the pathological anatomy is to study the structural foundations of the entire diversity of human diseases, the specifics of each disease or the clinical anatomy of a patient person. This section deals with a course of private pathological anatomy.
The study of general and private pathological anatomy is inextricably linked, since the utility processes in various combinations of their combinations are the content of both syndromes and human diseases. The study of the structural foundations of syndromes and diseases is carried out in close connection with their clinical manifestations. The clinical and anatomical direction is a distinctive feature of the domestic pathological anatomy.
In case of illness, which should be considered as a violation of the normal life functions of the organism, as one of the forms of life, structural and functional changes are inextricably linked. Functional changes not caused by the appropriate structural changes does not exist.
Therefore, the study of pathological anatomy is based on the principle of unity and conjugation of the structure and function.
When studying pathological processes and diseases, pathological anatomy is interested in the causes of their occurrence (etiology), developmental mechanisms (pathogenesis), the morphological foundations of these mechanisms (morphogenesis), various outcomes of the disease, i.e. Recovery and its mechanisms (sovenesis), disabled, complications, as well as death and death mechanisms (tanatogenesis). The task of pathological anatomy is also the development of a diagnosis of a diagnosis.
In recent years, pathological anatomy has paid special attention to the variability of diseases (pathomorphosis) and diseases arising
in connection with the activities of the doctor (ITRAGEN). Patomorphosis is a wide concept reflecting, on the one hand, changes in the structure of morbidity and mortality associated with changes in human living conditions, i.e. Changes in general panorama of diseases, on the other - persistent changes in the clinical and morphological manifestations of a certain disease, nosology (nosomorphosis), usually arising in connection with the use of drugs (therapeutic pathomorphosis).
Objects, methods and levels of research in pathological anatomy. Material for research in pathological anatomy is obtained by opening corpses, surgical operations, biopsies and experiment.
At the opening of the dead corpses, they find both far changes that led to death and initial changes that detect more often during microscopic examination. This allows you to study the stages of the development of many diseases. Organs and tissues taken on autopsies are studied using macroscopic and microscopic methods. At the same time, they are predominantly a light-optical study. At the opening, the correctness of the clinical diagnosis is confirmed or the diagnostic error is detected, the causes of the patient's death, the features of the disease, the effectiveness of the use of therapeutic drugs, diagnostic manipulations is revealed, the statistics of mortality and mortality are being developed, etc.
Operational material (remote organs and tissues) allows the pathologist to study the morphology of the disease at various stages of its development and use the various methods of morphological research.
Biopsy is a lifetime taking of fabric with a diagnostic purpose. The material obtained by biopsy is called biopsy.
The experiment is very important to clarify pathogenesis and morphogenesis of diseases. Although in the experiment it is difficult to create an adequate model of a person's disease, the models of many human diseases are created and created, they help to deeper the pathogenesis and morphogenesis of diseases. On the models of human diseases, the action of certain drugs is being studied, the methods of operational interventions are developing before they find clinical use.
The study of the structural bases of the disease is carried out on the organismant, systemic, organ, fabric, cellular, sub cell and molecular levels.
The organism level allows you to see the disease of the holistic organism in its diverse manifestations, in the relationship of all organs and systems.
The system level is the level of studying any system of organs or tissues, combined with the generality of functions (for example, a system of connective tissue, blood system, digestive system, etc.).
The organ level allows you to detect the changes of the organs, which in some cases are well visible to the naked eye, in other cases it is necessary to resort to microscopic examination.
Tissue and cellular levels are levels of study of altered tissues, cells and an intercellular substance using light-optical methods.
The sub-cell level allows you to observe with an electron microscope change of ultrastructures of cells and an intercellular substance, which in most cases are the first morphological manifestations of the disease.
The molecular level of study of the disease is possible when using comprehensive research methods with the involvement of electron microscopy, immunohistochemistry, cytochimia, radioautography.
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