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Lecture notes, cheat sheets
pathological physiology. Cheat sheet: briefly, the most important
Directory / Lecture notes, cheat sheets Table of contents
1. General etiology and pathogenesis. The value of the reactivity of the organism in pathology Etiology - the doctrine of the causes and conditions for the occurrence and development of diseases and pathological processes. Etiological factor (EF) - the main, leading, causing factor, without which there would be no disease (for example, Koch's bacillus in tuberculosis). The etiological factor can be simple (mechanical effect) or complex (damaging factors of a nuclear explosion), acting for a long time, throughout the entire disease (microbes, viruses, toxins), or only triggering a pathological process (thermal factor during a burn). The organism has a fundamental property - reactivity, which is understood as the ability of the organism to react in a certain way to the influence of environmental factors. Reactivity is an integral characteristic of the whole organism, which determines the possibility and nature of the development of the disease and undergoes changes in the course of the disease. We can talk about local (local) reactivity and general reactivity, which determines the integral response of the organism to the impact. It is necessary to distinguish between the normal reactivity of the body (when the reaction is adequate to the stimulus) and pathologically altered reactivity (for example, the formation of increased sensitivity to an allergen during sensitization). One of the most important properties of the body is resistance, i.e., the ability to withstand the effects of pathogenic factors. There are non-specific and specific resistance (immunity). Nonspecific resistance is provided by barrier systems, protective proteins, phagocytic cells, integral vascular tissue reactions (inflammation), and systemic neurohumoral mechanisms. Fever is a systemic nonspecific defense reaction. Immunity as a way of specific protection of the body's internal environment from substances and agents bearing signs of alien genetic information is realized through humoral mechanisms (production of protective antibodies) and with the participation of specialized cells (T-lymphocytes). The third element of causal interaction is environmental conditions (external and internal), which can significantly modify the process of interaction of the etiological factor with the body. This includes the influence of climatic and geographical factors (for example, "diseases in hot countries"), the nature of nutrition, seasonality, social factors, stressful situations, temperature, humidity, background radiation, etc. The basis of any disease is damage to any structures of a living organism, leading to a violation of its normal functioning. Various exogenous and endogenous factors can act as damaging (altering) agents. Pathogenesis of the disease - a dialectically contradictory process that includes two opposite tendencies: on the one hand, these are the mechanisms of damage, damage, deviation from the norm, and on the other hand, the mechanisms of protection, adaptation, compensation and reparation. 2. The role of hereditary factors in human pathology. Chromosomal and molecular diseases All human inherited traits are recorded using the genetic code in the macromolecular structure of DNA. The DNA double helix, interacting with alkaline proteins (pistons), forms a complex supramolecular structure - the chromosome. Each chromosome contains one continuous DNA molecule, has a certain gene composition and can only transmit hereditary information inherent in it. The human chromosome set (karyotype) includes 22 pairs of autosomes and 2 sex - XX or XY - chromosomes. Mutations in germ cells phenotypically manifest themselves as a hereditary predisposition or hereditary disease. Hereditary predisposition is a genetically determined increased susceptibility to a disease, which is realized in certain environmental conditions. Molecular diseases - an extensive group of diseases, the nature of which is associated with damage to individual genes. More than 2500 molecular diseases are now known. The cause of this pathology is gene (point) mutations, i.e. changes in the nucleotide sequence in the DNA molecule. An important stage in the implementation of the genetic program is the posttranscriptional modification of mRNA. A poly-A segment consisting of 50–200 idenyl nucleotides is attached to one end of the mRNA. The other end of the mRNA is subjected to capping, i.e., it is connected to a chemical group containing methylguanosine. Violation of these processes leads to a reduction in the lifetime of mRNA, its rapid destruction by nucleases and, consequently, the impossibility of translation of genetic information. The mRNA released from the nucleus combines with cytoplasmic proteins to form nucleoprotein particles - informosomes. Informosome pathology disrupts the regulated entry of mRNA into the protein-synthesizing system. Thus, the basis of molecular diseases is a violation of the synthesis of various body proteins. To diagnose the most common enzymopathies, simple express methods are used - the so-called screening tests (screening - "sifting"). Screening for enzymopathies is based on determining the activity of an abnormal enzyme, studying the amount of end products of the reaction and precursors, as well as identifying unusual metabolic products in biological fluids. In chromosomal diseases and syndromes, light microscopy reveals changes in the chromosome set either in the form of aneuploidy, i.e. changes in the number of autosomes (Down's disease, Edwards and Patau syndromes) or sex chromosomes (Klinefelter, Shereshevsky-Turner syndromes, trisomy-X), or in the form of changes in the structure of chromosomes (deletions, duplications, inversions, translocations). For the diagnosis of chromosomal diseases, a study of the human chromosome set (karyotype) is carried out, and X- and Y-sex chromatin are also determined, which makes it possible to detect a change in the number of sex chromosomes in the karyotype. 3. Mechanisms of carcinogenesis Tumor - this is an excessive, uncoordinated by the body, potentially unlimited proliferation of tissue, consisting of qualitatively altered cells, which are characterized by uncontrolled proliferation, impaired differentiation, morphological, biochemical and functional atypism. The tumor process is an unbalanced tissue growth, excessive cell reproduction that does not meet the needs of the tissue and the body as a whole. In pathology, there are other processes accompanied by tissue growth, but they differ significantly from true tumor growth. So, one of the tissue manifestations of the inflammatory response is cell proliferation. The growth of the tumor is carried out due to the multiplication of cells of the same type, which are descendants of one cell that has undergone transformation. Classification of tumors There are benign and malignant tumors. Benign tumors grow slowly over years, while malignant tumors grow rapidly and can evolve noticeably over several months or even weeks. Benign tumors, increasing in size, move away (push apart) the surrounding tissues, are mobile on palpation and have a flat surface. Malignant tumors are usually dense, with a bumpy surface, adjacent tissues germinate, and are inactive. Malignant neoplasms, in addition to pronounced changes in neighboring tissues, cause depletion of the body, are capable of spreading, forming metastases, relapses, and without treatment are fatal. The modern international classification of tumors is histogenetic. In accordance with this classification, the following types of tumors are distinguished: 1) epithelial tumors without specific localization; 2) tumors of exo- and endocrine glands; 3) mesenchymal tumors; 4) tumors of melanin-forming tissue; 5) tumors of the nervous tissue and membranes of the brain; 6) tumors of the blood system; 7) teratoma. In clinical practice, the classification of tumors according to TNM is accepted: T (from Latin "tumor") - characterizes the spread of the primary tumor; N (from Latin "nodulus") - reflects the state of regional lymph nodes; M (from Latin "metastasis") - indicates the presence or absence of metastases. The numbers added to each of the symbols (1, 2, 3, 4) indicate: for T - local spread of the primary tumor, for N - the degree of regional lymph node metastases, for M - the absence of distant metastases (0) or their presence (1 ). 4. Biological features of tumors The set of features that distinguish the tumor tissue and its constituent cells from normal precursors is referred to as "atypism". Tissue atypia. Tumors can arise in any tissue, from all types of its constituent cells capable of active division, and therefore can be localized in any part of the body. The form of tumors is various. Cellular atypia. The unusualness of cancer cells can be considered in terms of the features of their structure (morphological atypism), metabolic processes (metabolic atypism) and the peculiarity of behavior (functional atypism). Morphological atypism. Morphological atypism primarily consists in a variety of shapes, size and unusual structure of tumor cells. Typical for cancer cells is the depletion of cytoplasmic membranes with receptors that perceive regulatory neurohumoral signals ("receptor simplification"). Pronounced morphological changes were also found in the cellular organelles of tumor cells. The nuclei have an irregular shape, there is an unequal degree of their staining. In cancer cells, the number of mitochondria noticeably decreases, their structure changes. metabolic atypia. In a tumor cell, molecular forms of enzymes (isoenzymes) unusual for a normal cell appear. Carbohydrate metabolism. Tumor cells take up glucose from the incoming blood, even at low concentrations when normal cells are unable to take it up. Protein exchange. Cancer cells are characterized by an anabolic orientation of metabolism. Tumor cells intensively extract amino acids from the flowing blood, becoming a kind of "nitrogen trap". At the same time, amino acid synthesis is 50 times more intense in tumor cells than in normal cells. Fat exchange. Tumor cells intensively absorb free fatty acids, various lipoproteins, cholesterol ("fat trap") from the blood, which they use as substrates for building lipids that are part of cytoplasmic membranes. Exchange of nucleic acids. In tumor cells, the activity of DNA and RNA polymerases is increased, there is an intensive synthesis of nucleic acids - replication and transcription are activated. The synthesis of both chromosomal and mitochondrial DNA is stimulated. The activity of nucleases is low in cancer cells. Functional atypism. 1. The most important and fundamental feature of cancer cells is their immortality (immortalization). 2. An unlimited ability to reproduce is combined in tumor cells (primarily malignant tumors) with a violation of their maturation (differentiation). 3. Transformed cells, as a rule, lose the ability to perform the function inherent in the original tissue. The degree of dysfunction depends on the level of dedifferentiation: usually, some tumor cells can retain their tissue-specific function. 4. In tumor cells, the need for growth factors decreases. 5. Stages of the tumor process. Factors contributing to carcinogenesis The first stage of transformation (induction) - the process of transformation of a normal cell into a tumor (cancerous). Transformation is the result of the interaction of a normal cell with a transforming agent (carcinogen). The second stage of the tumor process is the activation (promotion) stage, the essence of which is the reproduction of the transformed cell, the formation of a clone of cancer cells and a tumor. A growing tumor is not a frozen, stationary formation with unchanged properties. The evolution of tumor properties is called "tumor progression". Progression This is the third stage of tumor growth. Finally, the fourth stage is the outcome of the tumor process. Allocate the following factors contributing to carcinogenesis. 1. Hereditary predisposition. The presence of family forms of cancer, when cancer of the same localization is detected among members of the same family in several generations. Thus, the presence of breast cancer in a mother increases the risk of detecting cancer of this localization in a proband by 5 times, and the presence of a mother and sister by 10-15 times. 2. Immunosuppression. Protection of the body from a growing tumor is provided by the mechanisms of cellular and, to a lesser extent, humoral immunity. The immune system recognizes cancer cells, causes their destruction or inhibits reproduction by inhibiting the promotion phase. Any immunosuppression promotes tumor growth. Immunodeficiency states of various origins (especially with a defect in the T-system) predispose to the occurrence of tumors. Thus, the development of breast cancer is most often observed against the background of a decrease in both cellular and humoral links of immune defense. 3. A certain endocrine background. Hormones that stimulate cell growth play an important role in the process of carcinogenesis. These are somatoliberin and growth hormone, prolactoliberin and prolactin, thyroliberin and TSH, melanoliberin and melanotropic hormone, gonadoliberins, estrogens. An excess of these hormones (as well as an imbalance between them) creates conditions conducive to the development of tumors. An example is breast cancer that occurs against the background of an excess of estrogen, thyroid cancer with an excess of TSH, etc. 4. Chronic inflammatory and sluggish proliferative processes. With these pathological conditions, a favorable background is created for the action of carcinogenic factors. 5. Old age. Tumors are diseases mainly of the elderly. If we take into account that the development of a tumor is a multistage process of the emergence, accumulation and implementation of genetic changes and the selection of altered cells, it becomes clear that the probability of "accumulating" the required number of mutations increases with age. 6. Etiology of tumors The precursor of a cancer cell in the body is always a normal cell of some tissue. Factors (agents) that can cause the transformation (transformation) of a normal cell into a tumor cell are called carcinogens. Carcinogens are the etiological factors of the tumor process. Depending on the nature of carcinogens are divided into physical, chemical and biological. Physical carcinogens include various types of ionizing radiation (X-rays, g-rays, elementary particles - protons, neutrons, a-, b-particles), as well as ultraviolet radiation. Most often, under the influence of radiation, leukemias, tumors of the lungs, skin and bones, as well as endocrine-dependent tumors (mammary gland, reproductive system, thyroid gland) occur. The introduction of radioactive isotopes into the body can cause the development of tumors in various organs, primarily in those where radioactive substances accumulate. Chemical carcinogens are an extensive group of compounds of organic and inorganic nature, different in structure. They are widely distributed in the environment. It is believed that 80-90% of all human malignant tumors can be caused by chemicals. It is accepted to distinguish the following groups of chemical carcinogens. 1. Polycyclic aromatic hydrocarbons (PAHs) are heterocyclic compounds containing active sites capable of interacting with a DNA molecule. 2. Aromatic amines and amino-azo compounds. Classical representatives of this group are benzidine dyes, as well as aniline and its derivatives. 3. Nitro compounds (NS) are used in the national economy as food preservatives, in the synthesis of dyes, drugs, polymeric materials, pesticides, etc. 4. Nitrosamines are included in the group of "single dose" carcinogens, since they are supposed to be able to cause tumor transformation of the cell even with a single exposure. 5. Metals and metalloids. Some minerals have a carcinogenic effect - nickel, chromium, arsenic, cobalt, lead, etc. In the experiment, they cause tumors at the injection site. Some substances used as medicines have carcinogenic properties. These are phenacetin, phenobarbital, diethylstilbestrol, estrone, cyclophosphamide, imuran, isopicotinic acid hydrazide, etc. 6. Chemical carcinogens of biological origin. This group includes aflatoxins - "single dose" carcinogens. 7. Endogenous blastomogenic substances. This group includes carcinogens that are formed in the body itself as a result of a violation of normal metabolism. Thus, in violation of the metabolism of hormones (estrogens, thyroxine), substances are formed that have a carcinogenic effect. The blastomogenic properties of some steroids - metabolites of cholesterol and bile acids have been proven. 7. Mechanisms of carcinogenesis The main provisions of the theory of oncogenes were formulated in the early 70s. XNUMXth century R. Huebner and G. To-daro, who suggested that the genetic apparatus of every normal cell contains genes that, if not activated or disrupted in time, a normal cell can turn into a cancer cell. These genes are called proto-oncogenes. Proto-oncogenes are common (normal) cellular genes that control cell growth, reproduction, and differentiation. Some proto-oncogenes work only at the early stages of ontogeny, others also function in differentiated cells, but the work of these genes is under strict control. As a result of mutation of the proto-oncogenes themselves or a persistent change in their activity after the mutation of regulatory genes, the proto-oncogene is converted into a cellular oncogene. Therefore, the appearance of an oncogene is associated with inadequate (quantitative, qualitative, or temporal) expression (or activation) of the proto-oncogene. As is known, the total number of genes in the human genome is about 100. Among them, there are about 000 true proto-oncogenes, i.e., cellular genes, the disruption of the normal function of which can lead to their transformation into oncogenes and tumor transformation of the cell. Proto-oncogenes are tissue specific. To date, more than 100 proto-oncogenes have been identified, grouped into seven main types. The following reasons for the transformation of a proto-oncogene into an oncogene are possible: point mutation, translocation or intrachromosomal rearrangement, amplification, activation of enhancer genes and (or) inhibition of silencers, transduction of proto-oncogenes by viruses, activation of a cellular oncogene promoter by an integrated virus genome. The transformation of a protooncogene into an oncogene leads to the synthesis of an oncoprotein - a quantitatively or qualitatively altered product of the protooncogene. An oncoprotein appears in the cell either in an increased amount or acquires a changed structure and properties, which provides this protein with increased activity and disrupts its response to regulatory influences. By localization in the cell, nuclear, cytoplasmic and membrane oncoproteins are distinguished. Under the influence of oncoproteins, the regulation of cell growth, proliferation and differentiation is disturbed, conditions are created for accelerated DNA replication and continuous cell division. These are tumor suppressor genes or anti-oncogenes that are functional antagonists of oncogenes. More than 10 anti-oncogenes have been identified so far. The anti-oncogenic function is also performed by polyamines synthesized by cells of different tissues - spermine and spermidine. These substances are involved in the regulation of cell proliferation and differentiation, their level increases with tissue growth and regeneration. At the same time, polyamines stabilize chromatin and nuclear proteins by forming complexes with negatively charged groups of proteins and DNA. A decrease in the level of polyamines leads to the induction of apoptosis. 8. The effect of the tumor on the body A growing malignant tumor affects both the tissues immediately surrounding it and the entire body of the patient. The most important manifestations of the systemic action of the tumor are as follows. 1. Cancer cachexia - General depletion of the body. Cancer cachexia is the result of many factors. Tumor cells successfully compete with normal cells for a number of vitamins and microelements. 2. Immunosuppression. The growth of a malignant tumor is accompanied by the development of secondary immunodeficiency, which is associated, on the one hand, with excessive production of glucocorticoids, and, on the other hand, with the production of special factors by the tumor that inhibit the host's immune response and promote the reproduction of transformed cells. 3. Anemia. As the tumor process develops, patients develop progressive anemia. Anemia in cancer has a complex genesis. First, the tumor secretes substances that reduce the iron content in the blood, inhibit erythropoiesis in the bone marrow and reduce the lifespan of red blood cells. Secondly, anemia may be the result of occult bleeding due to tumor invasion of the vessel wall. Thirdly, the deficiency of vitamin B12 (folic acid) that occurs in the body of the tumor carrier can affect. Finally, tumor metastases to the bone marrow are possible. 4. Thrombosis and hemorrhagic complications. Typical for malignant tumor processes is the development of changes in the system of regulation of the aggregate state of the blood with the development of DIC. 5. Universal membrane-damaging action. It develops as a result of activation of lipid peroxidation processes. The tumor is a trap for vitamin E, one of the most powerful natural antioxidants. In the cells of the tumor-bearing organism, the activity of antioxidant defense enzymes - catalase, SOD and glutathione reductase - decreases. 6. Production of ectopic hormones. Due to the derepression of certain loci of the genome, the tumor cell can produce hormones that are unusual for this tissue. 7. Intoxication. Since the proliferation of endothelial cells and the associated neoplasm of vessels, as a rule, lag behind the growth of the tumor itself, areas of necrotic decay are almost always found in its center. The decay products of the tumor can enter the bloodstream and cause general intoxication. 8. Edema. The following factors are involved in the genesis of tumor edema: hypoproteinemia, increased vascular permeability, compression of the veins and lymphatic vessels by the tumor with impaired outflow, development of secondary aldosteronism, increased production of ADH. 9. Metastasis. As a result of metastasis, a variety of secondary symptoms may develop. Serious dysfunction of distant organs may occur. 9. Pathology of water-electrolyte metabolism Water and electrolyte disturbances accompany and aggravate the course of many diseases. All the variety of these disorders can be divided into the following main forms: hypo- and hyperelectrolytemia, hypohydration (dehydration, exsicosis) and hyperhydration. Edema - this is an excessive accumulation of fluid in the intercellular space due to a violation of the exchange of water between the blood and the interstitium at the level of the capillary. Edema can be local, i.e. localized in a limited area of the body, and generalized, it can be hidden and obvious. Depending on the etiological factors, it is customary to distinguish the following edema: inflammatory, toxic, allergic, cardiac, cirrhotic, renal (nephritic and nephrotic), hungry (cachectic), lymphatic, neurogenic, endocrine. The development of edema is the result of a number of, as a rule, interconnected pathogenetic mechanisms, the main of which are the following. 1. An increase in hydrostatic (venous) pressure inside the vessels. The latter can be associated both with an increase in resistance to venous outflow in case of circulatory failure, compression, blockage, narrowing of the veins, and with the expansion of arterioles and precapillary sphincters, leading to an increase in blood flow and a sharp increase in intracapillary pressure. 2. Decreased oncotic pressure of blood plasma in vessels due to hypoalbuminemia. Wherein the ability of plasma proteins to retain fluid inside the vessels decreases. 3. An increase in the permeability of the vascular wall under the influence of a number of biologically active substances (histamine, serotonin, kinins, prostaglandins), toxic substances (venom of snakes, insects, bacterial toxins, biologically active substances), severe hypoxia. The reasons for the increase in the permeability of the vascular wall can also be overstretching of capillaries (for example, with arterial hyperemia), damage to endothelial cells (with acidosis), and a violation of the structure of the basement membrane. 4. Increasing the hydrophilicity of tissues due to hyperosmia and hyperoncia of tissues. Hyperosmia and hyperonkia of tissues can occur due to the accumulation of electrolytes, proteins, osmotically active metabolic products in them, as a result of tissue alteration, a decrease in the active transport of ions through cell membranes during tissue hypoxia, impaired leaching of electrolytes and metabolites from tissues in violation of microcirculation. Hyperosmia and hyperon-kia increase the flow of fluid from the capillaries into the tissues. 5. Violation of the outflow of lymph as a result of damage, compression or obstruction of the lymphatic vessels. In this case, there is an accumulation in the interstitial space of excessively filtered and not subjected to reabsorption into the vascular bed of the fluid. 6. Violation of the neurohormonal regulation of water and electrolyte metabolism. 10. Violation of the acid-base state One of the necessary conditions for the existence of an organism is to maintain a constant acid-base ratio (CBS). Violation of the CBS inevitably entails the development of pathological changes in the body, up to its death. A shift in pH - a value that characterizes the state of CBS - even by 0,1 already causes pronounced disorders in the cardiovascular and respiratory systems, and a shift in blood plasma pH above 7,8 or below 6,8 is incompatible with life. CBS disorders can be of exogenous and endogenous origin. In the direction of the shift in the acid-base balance, two forms of acid-base imbalance are distinguished - acidosis and alkalosis. Non-gas acidosis is characterized by a decrease in blood pH and buffer bases in blood plasma. The latter is associated with the neutralizing effect of bicarbonates on non-volatile acids. An increase in the concentration of hydrogen ions stimulates ventilation of the lungs, which leads to a compensatory decrease in CO2 tension. Compensation also includes intracellular buffer mechanisms. Hydrogen ions pass, in particular, into erythrocytes, from which sodium and calcium ions enter the plasma instead. The final compensation is carried out by the kidneys, which begin to intensively remove excess hydrogen ions in the urine. Gas acidosis, or respiratory, develops with an increase in the concentration of CO2 in the blood. This may be due either to inhalation of air with a high content of CO2, or a violation of the release of carbon dioxide by the lungs due to impaired airway patency, extensive damage to the lung parenchyma, suppression of the activity of the respiratory center, or as a result of circulatory failure, when, due to a sharp decrease in blood flow, the removal of CO2 from the lungs slows down. blood. Non-gas alkalosis is characterized by an increase in the concentration of buffer bases in plasma, an increase in the pH value. Respiratory compensation leads to a decrease in pulmonary ventilation and an increase in CO2 tension. However, such compensation cannot be long-term, since the accumulated carbon dioxide stimulates respiration. In non-gas alkalosis, the maximum pCO2 value is usually 60 mm Hg. Art. The compensation process involves intracellular buffer systems that donate hydrogen ions to the plasma, binding sodium cations. Gas alkalosis is caused by increased removal of carbon dioxide from the blood through the lungs during hyperventilation. This is observed during shortness of breath resulting from brain damage, with hyperthermia, severe fever, severe anemia. The development of gaseous alkalosis is possible when breathing rarefied air at high altitude, with hyperventilation during artificial respiration. The main disturbance in gaseous alkalosis is a decrease in CO2 tension in the blood. The initial compensatory reaction to respiratory alkalosis consists in the release of hydrogen ions from the cells into the extracellular fluid, in an increase in the production of lactic acid. 11. Kinetoses. Pathogenic effect of electric current Mechanical factors include the pathogenic effect of accelerations. Uniform rectilinear and rotational movement is not accompanied by disease-causing phenomena, but a change in the speed of movement (acceleration) can dramatically change the state of the body. The symptom complex of kinetosis consists of four types of reactions that manifest differently in different people, such as: 1) motor reactions, changes in the tone of the striated muscles; 2) autonomic disorders, manifested by blanching, cold sweat, lack of appetite, nausea, vomiting, bradycardia; 3) sensory reactions, characterized by dizziness, impaired spatial orientation; 4) mental disorders. These changes are mainly reflex in nature and are due to the effect on various receptors: 1) vestibular analyzer; 2) proprioceptors of muscles, tendons; 3) visual receptors; 4) receptors of the mucous and serous membranes of the abdominal organs. Among the physical factors that the body is most often exposed to, electric current can be distinguished. The defeats arising from influence of an electric current belong to a special kind of injuries. Unlike all other lesions inflicted on the body by mechanical, chemical and other physical agents, electricity affects a person not only by contact, but also indirectly. Moreover, electricity can strike a person from a distance. The biological effect of electric current is determined by its physical parameters, as well as the state of the body. It is believed that the pathogenic effect depends mainly on the strength of the current. The pathogenic effect of electric current is the stronger, the higher its voltage. Alternating current below 40 V is considered harmless, current up to 100 V is conditionally pathogenic, over 200 V is absolutely pathogenic. The most dangerous is alternating current with a frequency of 40-60 Hz, with an increase in frequency, its damaging effect decreases. The pathogenic effect of electric current depends on the direction of passage ("loop" current). Especially dangerous is the passage of current through the region of the heart and the brain. The danger increases with the increase in the time the current passes through the body. The damage that occurs in the body under the action of electric current is made up of local changes (electrical signs, burns, electrolysis) and general manifestations of the body's reaction to injury (such as loss of consciousness, respiratory arrest, ventricular fibrillation, changes in blood pressure, myocardial ischemia, contraction of skeletal muscles, etc.). 12. Stages of traumatic shock Traumatic shock - an acute neurogenic phasic pathological process that develops under the action of an extreme traumatic agent and is characterized by the development of peripheral circulatory insufficiency, hormonal imbalance, a complex of functional and metabolic disorders. In the dynamics of traumatic shock, erectile and torpid stages are distinguished. In the case of an unfavorable course of shock, the terminal stage occurs. erectile stage shock is short, lasts a few minutes. Outwardly, it is manifested by speech and motor anxiety, euphoria, pallor of the skin, frequent and deep breathing, tachycardia, and some increase in blood pressure. At this stage, there is a generalized excitation of the central nervous system, excessive and inadequate mobilization of all adaptive reactions aimed at eliminating the disorders that have arisen. There is a spasm of arterioles in the vessels of the skin, muscles, intestines, liver, kidneys, i.e., organs that are less important for the survival of the body during the action of the shock factor. Simultaneously with peripheral vasoconstriction, a pronounced centralization of blood circulation occurs, provided by dilatation of the vessels of the heart, brain, and pituitary gland. The erectile phase of shock quickly turns into a torpid one. The transformation of the erectile stage into the torpid stage is based on a complex of mechanisms: a progressive disorder of hemodynamics, circulatory hypoxia leading to severe metabolic disorders, macroergic deficiency, the formation of inhibitory mediators in the CNS structures, in particular GABA, type E prostaglandins, increased production of endogenous opioid neuropeptides. Torpid phase traumatic shock is the most typical and prolonged, it can last from several hours to 2 days. It is characterized by lethargy of the victim, adynamia, hyporeflexia, dyspnea, oliguria. During this phase, inhibition of the activity of the central nervous system is observed. In the development of the torpid stage of traumatic shock, in accordance with the state of hemodynamics, two phases can be distinguished - compensation and decompensation. The compensation phase is characterized by the stabilization of blood pressure, normal or even somewhat reduced central venous pressure, tachycardia, the absence of hypoxic changes in the myocardium (according to ECG data), the absence of signs of cerebral hypoxia, pallor of the mucous membranes, and cold, wet skin. The decompensation phase is characterized by a progressive decrease in the IOC, a further decrease in blood pressure, the development of DIC, the refractoriness of microvessels to endogenous and exogenous pressor amines, anuria, and decompensated metabolic acidosis. The stage of decompensation is a prologue to the terminal phase of shock, which is characterized by the development of irreversible changes in the body, gross violations of metabolic processes, and massive cell death. 13. Pathogenesis of traumatic shock characteristic feature traumatic shock is the development of pathological deposition of blood. Concerning the mechanisms of pathological blood deposition, it should be noted that they are formed already in the erectile phase of shock, reaching a maximum in the torpid and terminal stages of shock. The leading factors of pathological blood deposition are vasospasm, circulatory hypoxia, the formation of metabolic acidosis, subsequent degranulation of mast cells, activation of the kallikrein-kinin system, the formation of vasodilatory biologically active compounds, microcirculation disorders in organs and tissues, characterized initially by prolonged vasospasm. Pathological deposition of blood leads to the exclusion of a significant part of the blood from the active circulation, exacerbates the discrepancy between the volume of circulating blood and the capacity of the vascular bed, becoming the most important pathogenetic link in circulatory disorders in shock. An important role in the pathogenesis of traumatic shock is played by plasma loss, which is caused by an increase in vascular permeability due to the action of acid metabolites and vasoactive peptides, as well as an increase in intracapillary pressure due to blood stasis. Plasma loss leads not only to a further deficit in the volume of circulating blood, but also causes changes in the rheological properties of the blood. At the same time, the phenomena of aggregation of blood cells, hypercoagulation with the subsequent formation of DIC syndrome develop, capillary microthrombi are formed, completely interrupting the blood flow. Under conditions of progressive circulatory hypoxia, there is a deficiency in the energy supply of cells, suppression of all energy-dependent processes, pronounced metabolic acidosis, and an increase in the permeability of biological membranes. There is not enough energy to ensure the functions of cells and, above all, such energy-intensive processes as the operation of membrane pumps. Sodium and water rush into the cell, and potassium is released from it. The development of cell edema and intracellular acidosis leads to damage to lysosomal membranes, the release of lysosomal enzymes with their lytic effect on various intracellular structures. In addition, during shock, numerous biologically active substances, which enter the internal environment of the body in excess, exhibit a toxic effect. Thus, as shock progresses, another leading pathogenetic factor, endotoxemia, comes into play. The latter is also enhanced by the intake of toxic products from the intestine, since hypoxia reduces the barrier function of the intestinal wall. Of particular importance in the development of endotoxemia is a violation of the antitoxic function of the liver. Endotoxemia, along with severe cellular hypoxia caused by a microcirculation crisis, restructuring of tissue metabolism to an anaerobic pathway, and impaired ATP resynthesis, plays an important role in the development of irreversible shock phenomena. 14. Arterial hyperemia Arterial hyperemia called the state of increased blood filling of the organ and tissue, resulting from increased blood flow to them through dilated arteries. General arterial plethora develops with a significant increase in the volume of circulating blood (for example, with erythrocytosis). With physiological arterial hyperemia, the blood flow increases adequately to the increased needs of an organ or tissue in oxygen and energy substrates. Pathological arterial hyperemia occurs regardless of the metabolic needs of the organ. The myoparalytic mechanism is associated with a decrease in myogenic vascular tone under the influence of metabolites (lactate, purines, pyruvic acid, etc.), mediators, an extracellular increase in the concentration of potassium, hydrogen and other ions, and a decrease in oxygen content. The essence of the neurogenic mechanism is to change the neurogenic constrictor and dilator effects on the vessels, leading to a decrease in the neurogenic component of vascular tone. This mechanism underlies the development of neurotonic, neuroparalytic hyperemia, as well as inflammatory arterial plethora in the implementation of the axon reflex. Neurotonic arterial hyperemia occurs when the tone of parasympathetic or sympathetic cholinergic vasodilating nerves increases or when their centers are irritated by a tumor, scar. Post-ischemic arterial hyperemia is an increase in blood flow in an organ or tissue after a temporary cessation of blood circulation. Vacate (Latin vacutio - "empty") hyperemia is observed with a decrease in barometric pressure over any part of the body. Inflammatory arterial hyperemia occurs under the action of vasoactive substances (inflammatory mediators), causing a sharp decrease in basal vascular tone, as well as due to the implementation of neurotonic, neuroparalytic mechanisms and axon reflex in the alteration zone. Collateral arterial hyperemia is adaptive in nature and develops as a result of reflex expansion of the vessels of the collateral bed with difficulty in blood flow through the main artery. Hyperemia due to arteriovenous fistula can develop when arterial and venous vessels are damaged as a result of the formation of an anastomosis between an artery and a vein. For arterial hyperemia, the following changes in microcirculation are characteristic: 1) expansion of arterial vessels; 2) increase in linear and volumetric blood flow velocity in microvessels; 3) increase in intravascular hydrostatic pressure, increase in the number of functioning capillaries; 4) increased lymph formation and acceleration of lymph circulation; 5) a decrease in the arteriovenous difference in oxygen. 15. Venous congestion Venous congestion - this is a state of increased blood filling of an organ or tissue, due to the obstructed outflow of blood through the veins. Venous plethora can be local and widespread. Local venous plethora occurs when the outflow of blood through large venous trunks is difficult. A condition conducive to venous congestion is a long-term non-physiological position of one or another part of the body, unfavorable for local outflow of blood. In this case, hypostasis is formed - gravitational venous hyperemia. The most common causes of widespread venous plethora are: 1) insufficiency of heart function in rheumatic and congenital malformations of its valves, myocarditis, myocardial infarction; 2) decompensation of a hypertrophied heart; 3) a decrease in the suction action of the chest with exudative pleurisy, hemothorax, etc. According to the rate of development and duration of existence, this pathology can be acute and chronic. Prolonged venous hyperemia is possible only with insufficiency of collateral venous circulation. Microcirculatory disorders in venous hyperemia are characterized by: 1) expansion of capillaries and venules; 2) slowing down of blood flow through the vessels of the microvasculature up to stasis; 3) loss of blood flow division into axial and plasma; 4) increased intravascular pressure; 5) pendulum or jerky movement of blood in venules; 6) a decrease in the intensity of blood flow in the area of hyperemia; 7) violation of lymphatic circulation; 8) an increase in the arteriovenous difference in oxygen. External signs of venous hyperemia include: 1) increase, compaction of an organ or tissue; 2) development of edema; 3) the appearance of cyanosis, i.e. cyanotic color. In acute venous plethora, there may be an exit of erythrocytes from small vessels into the surrounding tissues. With the accumulation of a significant amount of them in the mucous membranes and serous membranes, small, pinpoint hemorrhages are formed in the skin. Due to increased transudation, edematous fluid accumulates in the tissues. Under conditions of hypoxia, granular and fatty degeneration, mucoid swelling of the interstitial substance develops in the cells of parenchymal organs. In chronic venous plethora, dystrophic processes develop in the tissues, atrophy of parenchymal elements with simultaneous replacement growth of stromal cells and accumulation of collagen fibers in it. 16. Edema Edema - a typical pathological process, which consists in excessive accumulation of extracellular tissue fluid in the interstitial space. According to the etiology, pathogenesis, prevalence, edema is divided into: 1) systemic (general); 2) local (local). Systemic edema occurs as a result of a violation of the leading mechanisms of regulation of water-salt metabolism, which is possible with diseases of the heart, kidneys, liver, and gastrointestinal tract. In accordance with the characteristics of the etiological factor and development mechanisms, edema can be: 1) inflammatory nature, caused by exudation; 2) non-inflammatory in nature, associated with an increase in the process of extravasation and (or) impaired lymphatic drainage. Depending on the leading factor that determines the development of edema, there are: 1) congestive (mechanical) edema caused by impaired blood and lymph flow and increased hydrostatic pressure in microvessels; 2) oncotic, resulting from a decrease in the colloid osmotic pressure of blood plasma; 3) membranogenic, appearing with an increase in the permeability of the capillary wall; 4) edema associated with active retention in the tissues of electrolytes, mainly sodium, and water; 5) lymphogenous, arising from the stagnation of lymph. Depending on the leading cause of development, local edema can be divided into: 1) inflammatory; 2) hemodynamic; 3) lymphodynamic. The pathogenesis of any local edema is based on Starling imbalance, which is reduced to an increase in intravascular hydrostatic pressure, a decrease in the oncotic gradient, an increase in the permeability of the vascular walls, or a combination of these mechanisms. The following factors contribute to the development of general edema. 1. Hyperfunction of the renin-angiotensin-aldosterone system and a general excess of sodium in the body. 2. Insufficiency of the formation of atrial natriuretic factor (PNUF). 3. Reducing the oncotic pressure of the blood plasma due to the loss of oncotic active proteins (loss of proteins in nephrotic syndrome, burn plasmorrhea, prolonged vomiting, etc.). 4. An increase in hydrostatic pressure in the exchange vessels of the microvasculature. 5. Increasing the permeability of the vascular walls. 6. Increasing the hydrophilicity of tissues. 17. Thrombosis Thrombosis - intravital local parietal formation in the vessels or heart of a dense conglomerate of blood cells and stabilized fibrin, i.e. a thrombus. Thrombosis is a physiological protective process aimed at preventing bleeding in case of tissue injury, strengthening the walls of aneurysms, accelerating contraction and healing of wounds. However, if thrombosis is excessive, insufficient, or has lost its necessarily local limited character, severe pathology may develop. Thrombosis as a natural way to stop bleeding reflects the nature of the interaction between the mechanisms of the hemostasis system and fibrinolysis. It is customary to distinguish three main links of hemostasis: 1) vascular link (hemostatic mechanisms of the vascular wall, aimed at spasm of the damaged vessel and triggering thrombus formation and blood coagulation); 2) cellular (platelet-leukocyte) link, which ensures the formation of a white blood clot; 3) fibrin link (a coagulation system that provides the formation of fibrin, resulting in the formation of red and mixed blood clots). A white thrombus is formed in 2-5 minutes. The formation of a fibrin-rich red thrombus requires 4-9 minutes. The process of thrombus formation begins with the gradual formation of a white blood clot. White blood clots stop capillary bleeding. A red thrombus is formed under conditions of predominance of coagulation over agglutination, with rapid blood clotting and slow blood flow. It is able to stop bleeding from arterial and venous vessels. A red thrombus consists of a head, which is an analogue of a white thrombus, a layered body in which platelet and fibrin deposits alternate, and a fibrin tail that traps erythrocytes. Mixed thrombi are called layered thrombi with several agglutinating white heads. The activation of thrombus formation in various pathological processes is based on the Virchow triad: damage to the endothelium of the vascular wall, slowing of blood flow, and activation of coagulation hemostasis. This cascade of reactions can be induced by gram-negative bacteria endotoxins, exotoxins, hypoxia, excessive accumulation of hydrogen ions, biogenic amines, kinins, leukotrienes, proetaglandins, free radicals, and many cytokines produced in excess by neutrophils, monocytes, and lymphocytes. The consequences of thrombosis can be varied. Thrombosis is a protective mechanism aimed at stopping bleeding when a vessel is damaged or ruptured. The nature of circulatory disorders and the degree of organ dysfunction in thrombosis can be different and depend on the localization of the thrombus, the rate of its formation, and the possibilities of collateral circulation in this place. 18. Embolism embolism called blockage of a blood or lymphatic vessel by particles brought with the blood or lymph flow and not usually found in the blood and lymph flow. Orthograde embolism occurs most often and is characterized by the movement of the embolus in the direction of blood flow. With retrograde embolism, the embolus moves against the blood flow under the influence of its own gravity. Paradoxical embolism has an orthograde direction, but occurs due to defects in the interatrial or interventricular septum. Air embolism occurs due to the ingress of air from the environment into the vascular system. Gas embolism is associated with the release of bubbles of dissolved gases (nitrogen and helium) in the blood during a rapid transition from high atmospheric pressure to normal or from normal to low. Microbial embolism occurs with septicopyemia, when a large number of microorganisms are in the bloodstream. Parasitic embolism occurs in helminthiases. Fat embolism occurs when the vessels are blocked by endogenous lipoprotein particles, chylomicron aggregation products or exogenous fat emulsions and liposomes. Tissue embolism is divided into: 1) amniotic; 2) tumor; 3) adipocyte. Amniotic fluid embolism leads to blockage of the pulmonary vessels by conglomerates of cells suspended in the amniotic fluid and thromboembolism, formed under the action of the procoagulants contained in it. Tumor embolism is a complex process of hematogenous and lymphogenous metastasis of malignant neoplasms. Tissue and, in particular, adipocyte embolism can be the result of trauma, when particles of crushed tissues enter the lumen of damaged vessels. A type of endogenous embolism - thromboembolism - occurs due to blockage of blood vessels by detached blood clots or their particles. One of the most severe forms of thromboembolism is pulmonary embolism (PE). The nature of clinical manifestations and the severity of the consequences of PE may depend on the caliber of the occluded vessel, the rate of development of the process, and the reserves of the fibrinolysis system. According to the nature of the course of PE, there are forms: 1) lightning fast; 2) acute; 3) subacute; 4) recurrent. According to the degree of damage to the pulmonary vascular bed, the following forms are distinguished: 1) massive; 2) submassive; 3) a form with damage to the small branches of the pulmonary artery. 19. Ischemia ischemia (from the Greek isho - "delay") is called anemia of tissues caused by insufficient or complete cessation of arterial blood flow. According to the causes and mechanisms of development, several types of ischemia are distinguished: 1) angiospastic, resulting from spasm of the arteries, caused either by an increase in the tone of vasoconstrictors, or by the effect of vasoconstrictor substances on the walls of blood vessels; 2) compression, caused by compression of the arteries by a scar, a tumor, a tourniquet applied, shedding blood; 3) obstructive, developing with partial or complete closure of the lumen of the artery by a thrombus, embolus, atherosclerotic plaque, etc.; 4) redistributive, which takes place during interregional, interorgan redistribution of blood; 5) obstructive, resulting from the mechanical destruction of blood vessels in trauma; 6) ischemia due to a significant increase in blood viscosity in small vessels in combination with vasoconstriction. The ischemic area is characterized by pallor, a decrease in volume and turgor due to impaired blood supply. There is a decrease in the temperature of the ischemic area due to a violation of the influx of warm arterial blood and a decrease in the intensity of metabolic processes. The magnitude of the pulsation of the arteries decreases as a result of a decrease in their systolic filling. Ischemia is characterized by the following disorders of microcirculatory blood flow: 1) narrowing of arterial vessels; 2) slowing down blood flow through microvessels; 3) a decrease in the number of functioning capillaries; 4) decrease in intravascular hydrostatic pressure; 5) a decrease in the formation of tissue fluid; 6) a decrease in oxygen tension in the ischemic tissue. Due to impaired delivery of oxygen and metabolic substrates, metabolic, structural and functional disorders develop in the ischemic tissue, the severity of which depends on the following factors: 1) on the rate of development and duration of ischemia; 2) from tissue sensitivity to hypoxia; 3) on the degree of development of collateral blood flow; 4) from the previous functional state of the organ or tissue. Ischemic areas experience a state of oxygen starvation, the intensity of metabolic processes decreases, dystrophy of parenchymal cells develops up to their death, glycogen disappears. With prolonged transcendental ischemia, tissue necrosis may occur. 20. Heart attack. Stasis Myocardial (from Latin infarctus - “stuffed, stuffed”) is a focus of necrosis resulting from the cessation of blood flow to organs with functional end vessels, i.e., either without or having an extremely insufficient number of anastomoses. These organs include the brain, lungs, spleen, kidneys, liver, small intestine, where the vessels have anastomoses only in the area of the microcirculatory bed and therefore, with a delay in blood flow along the main trunk, the collaterals are insufficient to stop ischemia in the basin of the damaged vessel. There are the following types of heart attacks, depending on various signs and mechanisms of development: 1) white and red; 2) aseptic and infected; 3) coagulation and colliquation; 4) pyramidal-conical and irregular shape. White (ischemic) infarctions occur in organs with absolutely or relatively insufficient collaterals and are characterized by the absence of secondary filling of the blood vessels of the necrotic area with blood. Red (hemorrhagic) infarctions occur with secondary blood flow into the vessels of the necrosis zone from collaterals or through portal systems and pronounced blood diapedesis (lungs, intestines, gonads, retina, etc.). Heart attacks of internals are more often aseptic. An infected infarction develops in the case of primary bacterial contamination of the site. In all organs, a heart attack develops as a coagulative necrosis with an outcome in a connective tissue scar. Only cerebral infarctions proceed according to the type of collimation necrosis with an insignificant participation of neutrophilic leukocytes, activation of microglial elements and outcome in the form of a cyst. Stasis (from the Greek. stasis - "stop") is a reversible stop of blood flow in the vessels of the microvasculature. Stasis can be caused by a decrease in the pressure difference along the microvessel or an increase in resistance in its lumen. true stasis is associated with a significant primary increase in resistance to blood flow in the vessels, which occurs due to a violation of the rheological properties of the blood. Ischemic and venous stasis are based on dyscirculatory disorders: a sharp slowdown or complete cessation of arterial blood inflow or a violation of venous blood outflow. With stasis, blood flow stops completely, erythrocytes stick together and form aggregates in the form of so-called coin columns up to the homogenization of blood cells. short-term stasis reversible, with the rapid elimination of the causes of stasis, the movement of blood is restored. Prolonged stasis leads to the disintegration of platelets, followed by the loss of fibrin and the formation of a thrombus, which is accompanied by the development of progressive circulatory hypoxia and tissue necrosis. 21. Bleeding Bleeding, hemorrhage (from the Greek. haema - "blood", rhagos - "break") - this is the exit of blood from the heart or blood vessels. It is called external if blood flows into the external environment, and internal when blood accumulates in tissues or natural cavities of the body: in the pleural - hemothorax, in the pericardium - hemopericardium, in the abdominal cavity - hemoperitoneum, joints - hemarthrosis. According to the nature of the bleeding vessel, bleeding is divided into: 1) arterial; 2) venous; 3) capillary; 4) mixed. According to the mechanism of violation of the integrity of the vascular wall, the following types of bleeding are distinguished: 1) per rhexin (from lat. geho - “I tear”) - bleeding as a result of rupture of the walls of blood vessels or the heart, which occurs with mechanical trauma, necrosis of the walls of blood vessels or the heart, rupture of the wall of a congenital or acquired aneurysm, with primary pathological processes in the vessel wall (with syphilis, atherosclerosis, etc.); 2) per diabrosin (from the Greek diabrosin - "corrosion") - bleeding due to corrosiveness of the walls of blood vessels, i.e. enzymatic digestion of the components of the vessel wall in hemorrhagic pancreatitis, peptic ulcer of the stomach or duodenum, purulent fusion of tissue, etc.; 3) per diapedesin (Greek dia - "through", pedeo - "jump") - the exit of erythrocytes through the walls of blood vessels that do not have visible damage; it occurs in the area of the microvasculature due to an increase in the permeability of arterioles, venules and capillaries in infectious, vascular diseases, with lesions of the hematopoietic apparatus. In appearance, there are several types of hemorrhages: 1) petechial (small, punctate), arising from diapedesis from small-caliber vessels. They often occur in the skin, mucous membranes and serous membranes during infections, blood diseases, hypoxia, etc. Larger hemorrhages are called ecchymosis. Multiple petechiae and ecchymosis are characterized as purpura; 2) bruises ("bruises"). These are lamellar hemorrhages in loose subcutaneous tissue, which occur during injuries due to rupture of small vessels and diapedesis; 3) hemorrhagic infiltration (suffusion). This is a surface that is extensive in length, characterized by the accumulation of blood in the interstitial crevices, "impregnation" of the tissue with blood; 4) hematoma. It is characterized by local tissue destruction and the formation of a cavity containing blood and (or) clots. Typical formation of hematomas in the brain with atherosclerosis, rheumatism, hypertension. The mechanism of hematoma formation can be complex. 22. Disseminated intravascular coagulation (DIC) DIC syndrome - a nonspecific pathological process characterized by widespread blood clotting and aggregation of blood cells in the microcirculation, leading to blockade of microcirculation, hypoxia, acidosis, organ dystrophy, and the development of multiple organ failure. DIC complicates a wide variety of forms of pathology: myocardial infarction, cardiogenic shock, various types of malignant neoplasms, extensive surgical interventions, severe hypoxia, obstetric pathology, incompatible blood transfusion, systemic lupus erythematosus, immunocomplex diseases, liver cirrhosis. Disseminated intravascular coagulation - a dynamic pathological process characterized by a succession of generalized hypercoagulability with intravascular coagulation, platelet aggregation, blockade of microcirculation and hypocoagulation with hypofibrinogenemia and consumption thrombocytopenia. Concerning the pathogenesis of disseminated intravascular blood coagulation, it should be noted the general patterns of its development, including the following initiating mechanisms. 1. Primary lesion of the vascular wall, desquamation of the endothelium, exposure of subendothelial proteins 2. The primary predominant effect of the pathogenic factor on platelets. 3. Combined simultaneous effect of bacterial, toxic, immunoallergic factors on the platelet-vascular and coagulation links of the hemostasis system. 4. Development of alternative mechanisms of hemocoagulation due to the activation of monocyte-macrophage and erythrocyte links of the hemostasis system. Pathogenic factors of various nature cause activation of the procoagulant blood system due to massive generalized damage to the vascular wall, an increase in its adhesive properties, activation of the platelet link of the hemostasis system, and in some cases, monocyte-macrophage and erythrocyte alternative ways of hemocoagulation. In the development of DIC, the following phases should be distinguished: 1) hypercoagulation and aggregation of blood cells - I phase; 2) the transition of hypercoagulation to hypocoagulation - phase II; 3) the stage of deep hypocoagulation up to complete blood incoagulability, phase III; 4) the recovery stage with a favorable course of the disease or the formation of multiple organ failure - phase IV. DIC can be acute, subacute, chronic, and recurrent. The acute form occurs with septic infections, extensive surgical interventions, blood loss, burns, transfusion of incompatible blood, etc. The subacute course of DIC occurs with renal failure, malignant neoplasms, and leukemia. Recurrent and chronic forms can occur in cancer, systemic inflammatory, autoimmune diseases. 23. Vascular reactions and emigration of leukocytes in the focus of acute inflammation Inflammation - a typical pathological process that occurs in response to the action of various altering factors and is manifested by the development of a complex of vascular tissue changes. The main signs of inflammation are pain, swelling, redness, fever, and impaired function. Vasospasm - a short-term reaction associated with direct irritation, an altering factor of vasoconstrictors and vascular smooth muscles. Arterial hyperemia is characterized by a moderate expansion of arterioles, capillaries, an increase in blood flow velocity, the phenomenon of capillary neoformation, an increase in volumetric blood flow velocity, an increase in intracapillary pressure, and some increased filtration of the liquid part of the blood. Venous hyperemia is characterized by further vasodilation, slowing of blood flow, the phenomenon of marginal standing of leukocytes and their emigration, the development of exudation, and a violation of the rheological properties of blood. The most important sign of venous hyperemia is the emigration of leukocytes, i.e., the release of white blood cells outside the vascular bed into the area of inflammation. The sequence of leukocyte release is called Mechnikov's law, according to which, a few hours after the action of the altering factor, neutrophils intensively emigrate, and then monocytes and lymphocytes. An important role in the mechanisms of adhesion and emigration of leukocytes is played by the elimination of the negative charge of the endothelial cell and leukocyte due to the accumulation of hydrogen and potassium ions, as well as cationic proteins, in the focus of inflammation. Complement, fibronectin, immunoglobulins, histamine, leukotrienes are the most significant factors initiating adhesion of leukocytes to the vessel wall. In most cases of acute inflammation, the dominant position in emigration during the first 6-24 hours is occupied by neutrophils, after 24-48 hours - by monocytes, and somewhat later - by lymphocytes. Neutrophils are active phagocytes, producers of endopyrogens, a source of vasoactive compounds - leukotrienes, leukokinins, prostaglandins, free radicals, non-enzymatic cationic proteins with pronounced bactericidal activity, lysozyme, lactoferrin, as well as a complex of lysosomal hydrolases that cause destructive processes in the alteration zone. Exudation - the release of the liquid part of the blood - is one of the signs of venous hyperemia and at the same time determines the nature of tissue changes in the area of inflammation. Exudation is usually biphasic and includes an immediate and a delayed phase. The immediate phase is completed on average within 15-30 minutes. The delayed phase develops gradually, reaches a maximum after 4-6 hours, lasts up to 100 hours, is associated with damage to the vascular wall by leukocyte factors - lysosomal enzymes, active oxygen metabolites. 24. Changes in metabolism in the focus of inflammation. Mechanisms of proliferation in inflammation The development of alteration, vascular changes in the area of inflammation is naturally combined with typical metabolic disorders. Moreover, at the stage of arterial hyperemia, there is a sharp increase in the intensity of metabolism due to increased oxygenation, trophism of the inflamed tissue due to an increase in blood flow in the microcirculation system. However, the successive change of arterial venous hyperemia in the area of inflammation leads to the development of prestasis, stasis, a sharp decrease in oxygen tension, which leads to the suppression of redox reactions, the accumulation of intermediate products of glycolysis, lipolysis, proteolysis, in particular lactic, pyruvic, fatty acids, amino acids, etc. Excessive accumulation of acid metabolites underlies the development in the alteration zone at the beginning of compensated and then decompensated metabolic acidosis. In the phase of venous hyperemia, due to the development of local metabolic acidosis, a complex of typical disorders occurs: swelling of mitochondria, uncoupling of the processes of oxidative phosphorylation and respiration, a decrease in the level of macroergic compounds in cells, suppression of various energy-dependent reactions, in particular transmembrane ion transport, protein synthesis, etc. Under conditions of acidosis, a pronounced destabilization of biological membranes occurs, in particular, cytoplasmic and lysosomal ones. Secretion of proteinases, cathepsins, myeloperoxidase, cationic proteins, acid hydrolases, elastase in the alteration zone by neutrophils and monocytes affects the intercellular matrix of the inflammatory focus, leading to its degradation. Products of stimulated neutrophils cause degranulation of mast cells, activate the complement system, kallikrein-quinine system, blood coagulation and fibrinolysis system. Proliferation is the final phase of the development of inflammation, providing reparative proliferation of tissues at the site of the focus of alteration. Reproduction of cellular elements begins along the periphery of the focus of inflammation, while in the center of it, the phenomena of alteration and exudation can still persist. Recovery and replacement of damaged tissues begins with the release of fibrinogen molecules from the vessels and the formation of fibrin, which forms a kind of network, a framework for subsequent cell reproduction. Division, growth and movement of fibroblasts is possible only after their binding to fibrin or collagen fibers. Along with fibroblasts, other tissue and hematogenous cells also multiply. Endothelial cells proliferate from tissue cells and form new capillaries. Fibroblasts together with newly formed vessels form granulation tissue. This is, in essence, a young connective tissue, rich in cells and thin-walled capillaries, the loops of which protrude above the surface of the tissue in the form of granules. The granulation tissue gradually turns into a fibrous tissue called a scar. 25. Fever Fever - a typical pathological process that occurs when pyrogens act on the heat-regulating center, characterized by an active temporary restructuring of thermoregulation and aimed at increasing the temperature of the internal environment of the body, regardless of the ambient temperature. The development of fever is due to the shift of the set point of temperature homeostasis to a higher level under the influence of pyrogenic substances. Exogenous pyrogens of infectious origin are high-molecular lipopolysaccharide complexes of endotoxins, which are a component of the membranes of gram-negative microbes and are released when many bacterial cells are damaged. The main carrier of pyrogenic activity is the lipoid A contained in them. Highly active exopyrogens practically do not have toxic, antigenic properties and species pyrogenic specificity. With repeated exposure to them, tolerance is formed to them. The toxic effect of lipopolysaccharide pyrogens in the body is manifested under the influence of doses hundreds of thousands of times higher than the minimum pyrogenic dose. Exogenous infectious pyrogens also include thermolabile protein substances isolated from exotoxins of hemolytic streptococcus, diphtheria bacilli, pathogens of dysentery, tuberculosis and paratyphoid. The effect of infectious pyrogens is mediated through endogenous pyrogens formed in the body, which are adequate irritants of the hypothalamic center of thermoregulation. Endogenous pyrogens represent a heterogeneous group of biologically active substances, united by the concept of "cytokines". The heat- and cold-sensitive neurons that form the measurement department ("thermostat") perceive direct and reflex temperature influences through the corresponding receptors. Serotonin and norepinephrine serve as mediators of heat impulses, and acetylcholine serves as cold impulses. These thermoneurons transmit impulses about the nature of the temperature effect to the interneurons of the comparison apparatus ("setting point"), which have spontaneous impulse activity, which perceive information and form the "setting point" of temperature homeostasis. The role of the mediator in the neurons of the "setting point" is performed by acetylcholine. The mismatch signal generated by the intercalary neurons is transmitted to the autonomic sympathetic, parasympathetic and somatic neurons that make up the effector section of the thermoregulation center. The mediators of efferent impulses are norepinephrine and acetylcholine, which regulate the mechanisms of heat transfer, heat production and temperature maintenance in full accordance with the "set point" of temperature homeostasis. The comparison signal arising in interneurons is necessary for feedback and stabilization of the function of thermosensitive neurons, ensuring the constancy of the normal temperature level and returning to it after its decrease or increase. 26. Stages of fever First stage of fever characterized by limited heat transfer and subsequent increase in heat production. The mechanisms of changes in thermoregulation during this period can be represented as follows. When exposed to endopyrogens, about 20 different "fever mediators" are formed in the anterior hypothalamus. Among them, prostaglandins E (PGE), which are produced under the influence of IL-1, IL-6 and TNF, are of the greatest importance in increasing the "setting point" of temperature homeostasis. PGEs activate adenylate cyclase and inhibit phosphodiesterase, which leads to the accumulation of c3,5-AMP in the neurons of the heat-regulating center. Under conditions of accumulation of c3,5-AMP, Na ions and a decrease in the concentration of calcium ions, the sensitivity of neurons to cold increases and the sensitivity to thermal direct and reflex influences decreases, the activity of the intercalary neurons of the comparison apparatus and the "set point" of temperature homeostasis increase. This leads to an increase in the production of catecholamines, spasm of peripheral vessels, to a decrease in blood supply to the skin and heat transfer through convection, irradiation and sweating. Thus, the increase in body temperature occurs primarily due to the limitation of heat loss and accumulation of heat in the body. Due to further activation of cold thermoneurons of the anterior hypothalamus and adrenergic neurons of the posterior hypothalamus, the activating effects of the reticular formation of the brain stem on the neurons of the red nuclei of the midbrain and the nucleus of the cranial nerves, on the spinal a-, b- and g-motor neurons increase. Second stage of fever is that with increased heat production in the body, heat transfer gradually begins to increase, and these processes are balanced. An increase in the temperature of the internal environment of the body causes some activation of the heat receptors of the heart, kidneys, veins of the abdominal organs, heat-sensitive neurons of the spinal cord and anterior hypothalamus. In parallel, there is a limitation of the impulse activity of cold thermoneurons of the heat-regulating center, a decrease in the activity of adrenergic neurons of the posterior hypothalamus and sympathetic influences, some activation of parasympathetic neurons and cholinergic influences. All this leads to the expansion of peripheral vessels, an increase in the flow of warm blood to the internal organs and skin, an increase in its temperature, sweating and heat transfer. An increase in heat transfer against the background of a limited increase in heat production prevents a further increase in body temperature and contributes to its establishment at a higher level. Third stage of fever characterized by a significant predominance of heat transfer over heat production and the return of body temperature to its original level. The latter is due to a decrease in the concentration of pyrogens in the body, a gradual restoration of the sensitivity of neurons of the hypothalamic center to cold and thermal direct and reflex effects. In full accordance with the normalization of the sensitivity of the interneurons of the comparison apparatus, the "setting point" of temperature homeostasis returns to its original value. 27. Allergens that induce the development of allergic reactions of the humoral type Allergy (from the Greek alios - "other", different, ergon - "action") is a typical immunopathological process that occurs against the background of exposure to an allergen antigen on an organism with a qualitatively altered immunological reactivity and is accompanied by the development of hyperergic reactions and tissue damage. There are allergic reactions of immediate and delayed type (humoral and cellular reactions, respectively). Allergic antibodies are responsible for the development of allergic reactions of the humoral type. For the manifestation of the clinical picture of an allergic reaction, at least two contacts of the body with the antigen-allergen are necessary. The first dose of exposure to the allergen (small) is called sensitizing. The second dose of exposure is large (permissive), accompanied by the development of clinical manifestations of an allergic reaction. Allergic reactions of the immediate type can occur within a few seconds or minutes, or 5-6 hours after repeated contact of the sensitized organism with the allergen. In some cases, long-term persistence of the allergen in the body is possible, and in this regard, it is practically impossible to draw a clear line between the impact of the first sensitizing and repeated resolving doses of the allergen. Allergen antigens are divided into bacterial and non-bacterial antigens. Non-bacterial allergens include: 1) industrial; 2) household; 3) medicinal; 4) food; 5) vegetable; 6) animal origin. Complete antigens are isolated that can stimulate the production of antibodies and interact with them, as well as incomplete antigens, or haptens, consisting only of determinant groups and not inducing the production of antibodies, but interacting with ready-made antibodies. There is a category of heterogeneous antigens that resemble the structure of determinant groups. Allergens can be strong or weak. Strong allergens stimulate the production of a large number of immune or allergic antibodies. Soluble antigens, usually of a protein nature, act as strong allergens. An antigen of a protein nature is the stronger, the higher its molecular weight and the more rigid the structure of the molecule. Weak are corpuscular, insoluble antigens, bacterial cells, antigens of damaged cells of one's own body. There are also thymus-dependent allergens and thymus-independent allergens. Thymus-dependent are antigens that induce an immune response only with the mandatory participation of three cells: a macrophage, a T-lymphocyte and a B-lymphocyte. Thymus-independent antigens can induce an immune response without the involvement of helper T-lymphocytes. 28. General patterns of development of the immunological phase of allergic reactions of immediate type The immunological stage begins with the exposure to a sensitizing dose of the allergen and the latent period of sensitization, and also includes the interaction of the resolving dose of the allergen with allergic antibodies. The essence of the latent period of sensitization lies primarily in the macrophage reaction, which begins with the recognition and absorption of the allergen by the macrophage (A-cell). In the process of phagocytosis, most of the allergen is destroyed under the influence of hydrolytic enzymes; the non-hydrolyzed part of the allergen (determinant groups) is exposed to the outer membrane of the A-cell in combination with the Ia-proteins and m-RNA of the macrophage. The resulting complex is called superantigen and is immunogenic and allergenic. In the latent period of sensitization, after the macrophage reaction, the process of specific and nonspecific cooperation of three types of immunocompetent cells occurs: A-cells, T-lymphocyte-helpers and antigen-reactive clones of B-lymphocytes. First, the allergen and Ia-proteins of the macrophage are recognized by specific receptors of T-lymphocyte-helper cells, then the macrophage secretes interleukin-1, which stimulates the proliferation of T-helper cells, which, in turn, secrete an immunogenesis inducer that stimulates the proliferation of antigen-sensitive clones of B-lymphocytes, their differentiation and transformation into plasma cells - producers of specific allergic antibodies. The process of antibody formation is influenced by another type of immunocytes - T-suppressors, the action of which is opposite to the action of T-helpers: they inhibit the proliferation of B-lymphocytes and their transformation into plasma cells. Normally, the ratio of T-helpers to T-suppressors is 1,4: 2,4. Allergic antibodies are divided into: 1) antibodies-aggressors; 2) witness antibodies; 3) blocking antibodies. Each type of allergic reactions (anaphylactic, cytolytic, immunocomplex pathology) is characterized by certain aggressor antibodies that differ in immunological, biochemical and physical properties. When a permissive dose of an antigen penetrates, the active centers of antibodies interact with the determinant groups of antigens at the cellular level or in the systemic circulation. The pathochemical stage consists in the formation and release into the environment in a highly active form of allergy mediators, which occurs during the interaction of the antigen with allergic antibodies at the cellular level or the fixation of immune complexes on target cells. The pathophysiological stage is characterized by the development of the biological effects of immediate-type allergy mediators and the clinical manifestations of allergic reactions. 29. Anaphylactic (atonic) reactions There are generalized (anaphylactic shock) and local anaphylactic reactions (atopic bronchial asthma, allergic rhinitis and conjunctivitis, urticaria, angioedema). Allergens that most often induce the development of anaphylactic shock: 1) allergens of antitoxic serums, allogeneic preparations of g-globulins and blood plasma proteins; 2) allergens of protein and polypeptide hormones; 3) medicines; 4) radiopaque substances; 5) insect allergens. Local anaphylactic reactions occur when an allergen enters the body in a natural way and develop in the places of the entrance gate and the fixation of allergens. Antibodies-aggressors in anaphylaxis are homocytotropic antibodies (reagins or atopenes) related to immunoglobulins of classes E and G4, capable of fixing on various cells. With anaphylaxis, two waves of release of allergy mediators are distinguished: The first wave occurs approximately 15 minutes later, when mediators are released from cells with high affinity receptors; The second wave - after 5-6 hours, the sources of mediators in this case are cells - carriers of low-affinity receptors. Mediators of anaphylaxis and sources of their formation: 1) mast cells and basophils synthesize and secrete histamine, serotonin, eosinophilic and neutrophilic, chemotactic factors, heparin, arylsulfatase A, galactosidase, chymotrypsin, superoxide dismutase, leukotrienes, prostaglandins; 2) eosinophils are a source of arylsulfatase B, phospholipase D, histaminase, cationic proteins; 3) leukotrienes, histaminase, arylsulfatases, prostaglandins are released from neutrophils; 4) from platelets - serotonin; 5) basophils, lymphocytes, neutrophils, platelets and endothelial cells are sources of formation of platelet activating factor in case of activation of phospholipase A2. Anaphylactic shock is characterized by the rapid development of general manifestations of pathology: a sharp drop in blood pressure up to a collaptoid state, disorders of the central nervous system, disorders of the blood coagulation system, spasm of the smooth muscles of the respiratory tract, gastrointestinal tract, increased vascular permeability, skin itching. A lethal outcome can occur within half an hour with symptoms of asphyxia, severe damage to the kidneys, liver, gastrointestinal tract, heart and other organs. Local anaphylactic reactions are characterized by an increase in the permeability of the vascular wall and the development of edema, the appearance of skin itching, nausea, abdominal pain due to spasm of smooth muscle organs, sometimes vomiting, and chills. 30. Cytotoxic reactions. Immunocomplex pathology. Principles and methods of hyposensitization Varieties: blood transfusion shock, maternal and fetal Rh incompatibility, autoimmune anemia, thrombocytopenia and other autoimmune diseases, a component of transplant rejection. The antigen in these reactions is a structural component of the membrane of the cells of one's own organism or an antigen of an exogenous nature, firmly fixed on the cells and changing the structure of the membrane. Cytolysis of the target cell under the influence of a resolving dose of the antigen-allergen is provided in three ways: 1) due to complement activation; 2) due to the activation of cell phagocytosis; 3) through the activation of antibody-dependent cellular cytotoxicity. The main mediators of complement-mediated cytotoxicity are activated complement fragments. Distinguish between a generalized form of immunocomplex pathology (serum sickness) and local reactions such as the Arthus phenomenon. Antitoxic sera, allogeneic d-globulins, food products, bacterial and viral allergens take part in the formation of immune complexes as antigens. The composition of immune complexes in immunocomplex pathology includes precipitating and complement-fixing antibodies (IgG1-3 and IgM). Soluble complexes of medium size usually have a damaging effect. Specific hyposensitization can be carried out by: 1) elimination of contact with a certain antigen-allergen; 2) the introduction of small doses of antigen according to various schemes; 3) fractional administration of therapeutic antitoxic sera according to Bezredko. Nonspecific hyposensitization is a decrease in sensitivity to various allergen antigens. For the purpose of non-specific hyposensitization, methods are used that prevent the development of allergic reactions in different phases. Suppression of the pathochemical and pathophysiological phases of allergic reactions is achieved using a complex of pharmacological preparations with different directions of action: 1) drugs that either increase the content of cAMP in cells, or reduce the level of cGMP (anticholinergics), or change their ratio (levamisole, etc.); 2) antihistamines; 3) serotonin antagonists; 4) inhibitors of the lipoxygenase pathway of arachidonic acid metabolism, which suppress the formation of leukotrienes; 5) antiprotease drugs; 6) antioxidants (α-tocopherol, etc.); 7) inhibitors of the kallikrein-kinin system; 8) anti-inflammatory drugs. 31. Delayed-type hypersensitivity reactions. Principles of hyposensitization Delayed type hypersensitivity (HRT) is one of the pathologies of cellular immunity carried out by immunocompetent T-lymphocytes against antigens of cell membranes. For the development of DTH reactions, prior sensitization is necessary, which occurs upon initial contact with the antigen. HRT develops in animals and humans 6-72 hours after penetration into the tissues of a permissive (repeated) dose of the allergen antigen. Antigens-allergens that induce the development of the HRT reaction: 1) infectious; 2) cells of own tissues with altered antigenic structure (autoantigens); 3) specific tumor antigens; 4) protein histocompatibility antigens; 5) complex compounds formed during the interaction of certain chemicals (arsenic, cobalt) with tissue proteins. In allergic reactions of the cellular type, as a rule, methods of non-specific hyposensitization are used, aimed at suppressing the afferent link, the central phase and the efferent link of delayed-type hypersensitivity. The afferent link is provided by tissue macrophages - A-cells. Synthetic compounds suppress the afferent phase - cyclophosphamide, nitrogen mustard, gold preparations. To suppress the central phase of cell-type reactions, various immunosuppressants are used - corticosteroids, antimetabolites, in particular analogues of purines and pyrimidines (mercaptopurine, azathioprine), folic acid antagonists (ametopterin), cytotoxic substances. To suppress the efferent link of cell-type hypersensitivity reactions, including the damaging effect on target cells of T-killers, as well as delayed-type allergy mediators - lymphokines - anti-inflammatory drugs are used - salicylates, antibiotics with a cytostatic effect - actinomycin C and rubomycin, hormones and biologically active substances , in particular corticosteroids, prostaglandins, progesterone, antisera. It should be noted that most of the immunosuppressive drugs used do not cause a selective inhibitory effect only on the afferent, central, or efferent phases of cell-type allergic reactions. It should be noted that in the vast majority of cases, allergic reactions have a complex pathogenesis, including, along with the dominant mechanisms of delayed (cellular) hypersensitivity reactions, auxiliary mechanisms of humoral type allergies. In this regard, to suppress the pathochemical and pathophysiological phases of allergic reactions, it is advisable to combine the principles of desensitization used in humoral and cellular types of allergies. 32. General mechanisms for the development of a delayed-type hypersensitivity reaction The allergen antigen, when it enters the body, is phagocytosed by a macrophage (A-cell), in the phagolysosome of which, under the influence of hydrolytic enzymes, a part of the allergen antigen is destroyed (about 80%). The unfragmented part of the antigen-allergen in complex with Ia-protein molecules is expressed on the A-cell membrane as a superantigen and presented to antigen-recognizing T-lymphocytes. Following the macrophage reaction, there is a process of cooperation between the A-cell and T-helper, the first stage of which is the recognition of a foreign antigen on the surface of the A-cell by antigen-specific receptors on the membrane of T-helper cells, as well as recognition of macrophage Ia proteins by specific T-helper receptors. Further, A-cells produce interleukin-1 (IL-1), which stimulates the proliferation of T-helpers (T-amplifiers). The latter secrete interleukin-2 (IL-2), which activates and maintains blast transformation, proliferation and differentiation of antigen-stimulated T-producers of lymphokines and T-killers in regional lymph nodes. When T-producers-lymphokines interact with the antigen, more than 60 soluble mediators of DTH-lymphokines are secreted, which act on various cells in the focus of allergic inflammation. Along with lymphokines, other biologically active substances play a role in the development of allergic inflammation in HRT: leukotrienes, prostaglandins, lysosomal enzymes, and chalones. If T-producers of lymphokines realize their effect remotely, then sensitized T-killers have a direct cytotoxic effect on target cells, which is carried out in three stages. Stage I - target cell recognition. The T-killer is attached to the target cell through cellular receptors for a specific antigen and histocompatibility antigens (H-2D and H-2K proteins - products of the MHC D and K loci genes). In this case, there is a close membrane contact between the T-killer and the target cell, which leads to the activation of the metabolic system of the T-killer, which subsequently lyses the target cell. II stage - a lethal blow. T-killer has a direct toxic effect on the target cell. Stage III - osmotic lysis of the target cell. This stage begins with a series of successive changes in the membrane permeability of the target cell and ends with a rupture of the cell membrane. Primary damage to the membrane leads to a rapid entry of sodium and water ions into the cell. Phases of delayed-type allergic reactions: 1) immunological - includes the period of sensitization after the first dose of the allergen antigen, the proliferation of the corresponding clones of T-lymphocyte-effectors, recognition and interaction with the target cell membrane; 2) pathochemical - the phase of the release of HRT mediators; 3) pathophysiological - manifestation of the biological effects of DTH mediators and cytotoxic T-lymphocytes. 33. Separate forms of HRT contact dermatitis. Allergy of this type often occurs in low molecular weight substances of organic and inorganic origin. Contact dermatitis can also be caused by substances of plant origin - cotton seeds, citrus fruits. Allergens, penetrating the skin, form stable covalent bonds with the SH and MH2 groups of skin proteins. These conjugates have sensitizing properties. infectious allergy. HRT develops in chronic bacterial infections caused by fungi and viruses, as well as in diseases caused by protozoa (toxoplasmosis), with helminthic invasions. Sensitization to microbial antigens usually develops with inflammation. transplant rejection. During transplantation, the recipient's body recognizes foreign transplantation antigens (histocompatibility antigens) and carries out immune responses leading to transplant rejection. Mechanisms of graft rejection 1. Cellular factors. Sensitized by donor antigens, lymphocytes of the recipient migrate into the graft after graft vascularization, exerting a cytotoxic effect. As a result of exposure to T-killers and under the influence of lymphokines, the permeability of target cell membranes is disrupted, which leads to the release of lysosomal enzymes and cell damage. 2. Humoral factors. With allotransplantation of the skin, bone marrow, and kidney, hemagglutinins, hemolysins, leukotokeins, and antibodies to leukocytes and platelets are often formed. Autoimmune diseases Autoimmune diseases are divided into two groups. The first group is represented by collagenoses - systemic diseases of the connective tissue, in which auto-antibodies are found in the blood serum without strict organ specificity. The second group includes diseases in which organ-specific antibodies are detected in the blood (Hashimoto's thyroiditis, pernicious anemia, Addison's disease, autoimmune hemolytic anemia, etc.). Several possible mechanisms have been identified in the development of autoimmune diseases. 1. Formation of autoantibodies against natural (primary) antigens - antigens of immunologically barrier tissues. 2. Formation of autoantibodies against acquired (secondary) antigens. 3. Formation of autoantibodies against cross-reacting or heterogeneous antigens. 4. Autoimmune lesions may occur as a result of a breakdown in immunological tolerance to one's own unaltered tissues. 34. Primary CIDs Primary CIDs - this is a genetically determined feature of the body to implement one or another link of the immune response. They are caused by a genetic block at various levels of transformation of stem cells into T- and B-lymphocytes or at subsequent stages of their differentiation. The manifestation of IDS depends on the level of the defect. IDS with a predominant violation of the cellular link of immunity. DiGeorge Syndrome - occurs with hypo-and aplasia of the thymus gland. The synthesis of humoral antibodies is not impaired, but there is a defect in the differentiation of stem cells into T cells. Frequent infections of the respiratory and urinary tract, persistent digestive disorders are characteristic. Lymphocytic dysgenesis (Nezelof's syndrome) is a quantitative and qualitative insufficiency of the T-system as a result of atrophy of the thymus and lymph nodes. It is characterized by purulent-inflammatory foci in the internal organs and in the skin. Children often die in the first months of life from sepsis. IDS with predominant damage to the B-system Bruton's disease - occurs when there is a defect in the maturation of B-cell precursors into B-lymphocytes. Only boys get sick. The content of d-globulins in the blood serum is less than 1%. Resistance to opportunistic bacteria and fungi is sharply reduced. Selective manifestations of immunodeficiency. Perhaps the development of IDS with a selective violation of the synthesis of IgG, IgA or IgM. Their formation can be based on both blockade of the development of individual subpopulations of B-lymphocytes and an increase in the activity of suppressor T-lymphocytes. Combined IDS are characterized by a violation of stem cell differentiation, a block in the maturation of T- and B-lymphocytes, and their deficiency. Reticular dysgenesis syndrome is characterized by a decrease in the number of stem cells in the bone marrow. Intrauterine fetal death is characteristic, or children die shortly after birth. The Swiss type of immunodeficiency is characterized by damage to the Ti B systems and, consequently, the absence of cellular and humoral reactions of immunological protection. Louis-Bar syndrome is caused by a maturation defect, a decrease in the function of T-lymphocytes, a decrease in their number in the blood (especially T-helpers), a deficiency of immunoglobulins (especially IgA, IgE, less often IgG). Wiskott-Aldrich Syndrome characterized by a deficiency of peripheral T-lymphocytes, a violation of their structure and physico-chemical properties of membranes, a decrease in cellular immunity in the absence of changes in the morphological structure of the thymus. Principles of treatment of primary IDS. Treatment depends on the type of primary immunological deficiency and includes targeted replacement therapy (transplantation of immunocompetent tissues, transplantation of embryonic thymus, bone marrow). 35. Secondary CIDs Secondary IDS develop under the influence of various exogenous influences on a normally functioning immune system. The list of major diseases accompanied by secondary immunodeficiency, proposed by WHO experts: 1) infectious diseases: a) protozoal and helminthic diseases; b) bacterial infections; c) viral infections; d) fungal infections; 2) malnutrition - malnutrition, cachexia, intestinal absorption disorders, etc.; 3) exogenous and endogenous intoxications - with renal and hepatic insufficiency, with herbicide poisoning; 4) tumors of lymphoreticular tissue (lympholeukemia, thymoma, lymphogranulomatosis), malignant neoplasms of any localization; 5) metabolic diseases (diabetes mellitus, etc.); 6) loss of protein in intestinal diseases, nephrotic syndrome, burn disease, etc.; 7) the effect of various types of radiation, especially ionizing radiation; 8) strong, prolonged stress effects; 9) the effect of drugs (immunosuppressants, corticosteroids, antibiotics, sulfonamides, salicylates, etc.); 10) blockade by immune complexes and antibodies of lymphocytes in some allergic and autoimmune diseases. Secondary CIDs can be divided into 2 main forms: 1) systemic, developing as a result of systemic damage to immunogenesis (with radiation, toxic, infectious, stress lesions); 2) local, characterized by regional damage to immunocompetent cells (local disorders of the immune apparatus of the mucosa, skin and other tissues, developed as a result of local inflammatory, atrophic and hypoxic disorders). Principles of treatment of secondary IDS. 1. Replacement therapy - the use of various immune preparations (g-globulin preparations, antitoxic, anti-influenza, anti-staphylococcal sera, etc.). 2. Correction of the effector link. It includes the impact on the immune system by pharmacological drugs that correct its work (decaris, diucefon, imuran, cyclophosphamide, etc.), hormones and mediators of the immune system (thymus drugs - thymosin, thymalin, T-activin, leukocyte interferons). 3. Removal of inhibitory factors that bind antibodies and block the effect of immunocorrection (hemosorption, plasmapheresis, hemodialysis, lymphopheresis, etc.). 36. AIDS Etiology of AIDS. The causative agent of AIDS is a retrovirus and is referred to as HIV (human immunodeficiency virus) or LAV (lymphoadenopathic virus). The virus enters the body with blood, with cells during transplantation of organs and tissues, blood transfusion, with sperm and saliva through damaged mucous membranes or skin. Anti-HIV antibodies appear 6-8 weeks after infection. AIDS pathogenesis. The AIDS pathogen invades cells that have the T4 receptor, to which the viral envelope glycoproteins have a high affinity (T-helpers, macrophages, neuroglial cells, neurons). Then there is a release from the viral envelope, and the viral RNA leaves the core structure. Under the influence of reverse transcriptase, viral RNA becomes a template for the synthesis of double-stranded DNA, which enters the nucleus. Next, the virus-specific DNA is integrated into the chromosomes of the host cell and the virus passes into the next cell generations with each cell division. The massive death of T-helpers also occurs in connection with the interaction of the viral protein on the surface of infected cells. One infected cell can attach up to 500 uninfected cells, which is why lymphopenia develops. The number of B-lymphocytes, as a rule, remains within the normal range, and their functional activity often decreases. The number of macrophages usually does not change, however, there is a violation of chemotaxis and intracellular digestion of foreign agents. Cells also die due to the activity of the immune system itself (the production of neutralizing antibodies to HIV proteins, the production of autoantibodies to T-helpers). All this disables the immune defense in general and deprives the body of the ability to resist any infections. Clinical variants of AIDS. 1. Pulmonary type. It is characterized by the development of pneumonia caused by concomitant infection, often pneumocystis. 2. With predominant damage to the central nervous system by the type of encephalitis or meningitis. 3. Gastrointestinal type. It is characterized by signs of damage to the gastrointestinal tract, primarily diarrhea (in 90-95% of patients). 4. Feverish type. It is characterized by the occurrence of prolonged fever, not associated with other diseases, accompanied by a significant decrease in body weight, weakness. In all forms of AIDS, there is an increased tendency to form tumors. AIDS treatment. There is no effective treatment for AIDS. Therapeutic measures for AIDS: 1) blockade of HIV reproduction (suppression of the replication of its nucleic acid by inhibiting revertase; suppression of the processes of translation and "assembly" of the virus); 2) suppression and prevention of infections and tumor growth; 3) restoration of the body's immune competence (introduction of thymus preparations, bone marrow tissue, interleukin-2). 37. Physiology of phagocytosis Phagocytosis - this is a kind of cellular immunity, characterized by the recognition, absorption and digestion of various foreign corpuscular objects by phagocytes. Classification of phagocytes. I. By morphological and functional features: 1) microphages - neutrophils, eosinophils, basophils; 2) macrophages - blood and bone marrow monocytes, tissue macrophages II. According to the ability to actively move: 1) fixed - Kupffer cells of the liver, histocytes of the connective tissue, macrophages of the bone marrow, lymph nodes, synovial membranes, CNS, etc.; 2) mobile - macrophages of serous cavities, inflammatory exudates, alveolar macrophages, monocytes. Stages of phagocytosis: I - the approach of the phagocyte to the object of phagocytosis; II - attraction; III - absorption of the object by the phagocyte; IV - killing of viable objects; V - digestion of non-viable objects. The stage of approaching the phagocyte to the object of phagocytosis is carried out due to a random collision of the phagocyte with a foreign object in the bloodstream or the directed active movement of the phagocyte towards the object of phagocytosis, which is called positive chemotaxis. The attraction stage includes opsonization, recognition and attachment of the phagocyte to the object of phagocytosis. Opsonization - the process of adsorption on the surface of a foreign object of opsonins - substances that are molecular mediators in the interaction of phagocytes with a phagocytosed object. Opsonins facilitate recognition and increase the intensity of phagocytosis. The uptake stage is an active, energy-dependent process consisting in successive coverage of the particle by pseudopodia from all sides and its immersion into the cytoplasm of the phagocyte together with the surrounding area of the plasma membrane. The result of the absorption stage is the formation of a phagosome containing a foreign particle. The killing stage is provided by the presence of bactericidal factors in the phagocyte, which are released into the phagosome or into the environment surrounding the phagocyte, which can provide a distant bactericidal effect. The stage of digestion is possible only if the phagocytosed object has lost its viability. Digestion is due to the release of the contents of the lysosomes of the phagocyte into the phagosome. Lysosomes contain about 60 different enzymes - hydrolases (proteases, lipases, phospholipases, elastases, collagenases, DNases, RNases, amylases, glucosidases, etc.). As a result of the fusion of lysosomes and phagosomes, a phagolysosome is formed, in which the final degradation of the components of a foreign object occurs. 38. Changes in the total amount of blood The total amount of blood in the human body is normally 6-8% of body weight. The percentage of red blood cells in relation to the total volume of plasma is called the hematocrit index. Hypervolemia is an increase in the total amount of blood. There are three types of hypervolemia. 1. Simple hypervolemia - a proportional increase in cellular elements and plasma, observed as a temporary phenomenon after the transfusion of a large amount of blood, as well as during intense physical work, when deposited blood and tissue fluid enter the vascular bed. 2. Oligocythemic hypervolemia - an increase in the total amount of blood due to its liquid part. This condition occurs with certain kidney diseases (insufficient filtration), during the subsidence of edema (inflow of interstitial fluid into the vessels), after the introduction of saline and blood-substituting fluids. 3. Polycythemic hypervolemia - an increase in blood volume due to red blood cells. An increase in the number of red blood cells may be compensatory. Hyperproduction of red blood cells may be the result of a malignant disease of the hematopoietic system (erythremia). Hypovolemia, or oligemia, is a decrease in the total amount of blood. Hypovolemia occurs in three variants. 1. Simple hypovolemia - a proportional decrease in plasma and cellular elements - occurs as a short-term phenomenon immediately after acute blood loss or in a state of shock, when a significant amount of blood is not involved in the circulation. The hematocrit does not change. 2. Oligocythemic hypovolemia - a decrease in blood volume due to a drop in the content of red blood cells. Such a condition is observed, for example, after acute blood loss, when the reduced blood volume is replenished by the entry of tissue fluid into the vascular bed. The hematocrit falls. 3. Polycythemic hypovolemia - a decrease in blood volume due to the loss of the liquid part. At the same time, the number of erythrocytes remains normal, however, in a unit of blood volume, there are more of them due to its thickening (relative erythrocytosis). Blood loss. The causes of acute blood loss can be: wounding of blood vessels during external injuries (external bleeding), or bleeding from internal organs (internal bleeding), for example, gastrointestinal bleeding, pulmonary, uterine, etc. The main link in the pathogenesis of disorders of body functions during blood loss are: a decrease in the volume of circulating blood and the onset of hypoxemia, followed by hypoxia of organs and tissues. Hypoxemia causes the development of both compensatory-adaptive reactions and pathological changes. 39. Change in the quantitative and qualitative composition of erythrocytes An increase in the number of red blood cells (erythrocytosis) is a symptom of various diseases or pathological conditions. There are absolute and relative erythrocytosis. Absolute erythrocytosis characterized by an increase in the number of red blood cells due to the activation of erythropoiesis. The most common cause of erythrocytosis is enhanced compensatory regeneration of the bone marrow in various hypoxic conditions (hydroxic erythrocytosis). Relative erythrocytosis occurs when the body is dehydrated. With the loss of fluid, the plasma volume decreases, the blood thickens, which leads to the relative predominance of red blood cells. Erythremia (Wakez's disease). Erythremia, unlike erythrocytosis, is a nosological form of a disease of the hematopoietic system. The disease is caused by total bone marrow hyperplasia, which is most intense in the erythroid lineage. The main signs of erythremia are an increased number of erythrocytes (up to 8 million or more per 1 mm3 of blood), high hemoglobin numbers (18-22 g), an increase in circulating blood volume due to the volumetric mass of erythrocytes (hematocrit may exceed 70%). Anemia, or anemia, is a decrease in the content of red blood cells and hemoglobin per unit volume of blood. Anemia occurs due to various diseases, intoxications, lack of factors involved in hematopoiesis, bone marrow hypoplasia, erythrocyte hemolysis, etc. With anemia, the respiratory function of the blood is disturbed - the delivery of oxygen to the tissues. The body's need for oxygen is compensated to some extent by the mobilization of protective and adaptive reactions. Changes in the qualitative composition of blood erythrocytes in anemia Anisochromia - the presence of red blood cells with different degrees of color due to the unequal content of hemoglobin in them. The content of hemoglobin in each individual erythrocyte can be judged by a color indicator, which is normally conventionally taken as a unit. hypochromia - depletion of erythrocytes in hemoglobin. They are weakly stained, sometimes they become like a ring (anulocytes). The predominance of hypochromic erythrocytes in the blood causes a decrease in the color index to a value less than one; such anemia is called hypochromic. Hyperchromia - more intense staining of erythrocytes with the absence of a central zone of enlightenment. Anemia with the presence of hyperchromic erythrocytes in the blood and a color index exceeding one is called hyperchromic. Poikilocytosis - the appearance in the blood of erythrocytes of various shapes. They can take the form of a sickle, pear, kettlebell, mulberry, etc. Anisocytosis - the presence of red blood cells of different sizes (microcytes, macrocytes, megalocytes). 40. Change in the quantitative and qualitative composition of leukocytes The function of leukocytes becomes insufficient when their number decreases or when immature and degenerative forms of leukocytes enter the bloodstream. The insufficiency of the protective function of leukocytes is expressed in a sharp decrease in the body's resistance to infections. In the blood of healthy adults at rest on an empty stomach, the number of leukocytes averages from 5000 to 8000 per 1 mm3 of blood. Leukopenia. It is characterized by a drop in the content of leukocytes below 4000 in 1 mm3 of blood. Leukopenia is observed with a uniform decrease in the number of all white blood cells and leukopenia with a predominant decrease in the number of certain types of leukocytes (neutropenia, eosinopenia, lymphocytopenia, etc.). Redistributive leukopenia is observed, for example, in hemotransfusion or anaphylactic shock as a result of the accumulation of leukocytes in the dilated capillaries of the lungs, liver, and intestines. Distributive leukopenia is temporary and is usually replaced by leukocytosis. Leukocytes can be destroyed under the influence of allergic and antileukocyte antibodies. Allergic leukopenia sometimes occurs in individuals who are hypersensitive to such allergen drugs. Leukopenia due to violation or inhibition of leukopoiesis. Violation of leukopoiesis can manifest itself as a delay in the maturation and release of leukocytes into the blood, which is observed, for example, in systemic lesions of the hematopoietic organs (acute leukemia) occurring with leukopenia. Deep inhibition of leukopoiesis is caused by the following reasons: chronic poisoning with chemicals at work (benzene, tetraethyl lead); exposure to x-rays or ionizing radiation, to which lymphoid tissue is especially sensitive; lymphopenia is found already in the initial stage of radiation sickness; autoallergic reactions developing in hematopoietic organs; metastasis of tumor cells to the bone marrow; poisoning with overwintered cereals that are affected by a fungus. Leukocytosis. Physiological leukocytosis. Physiological leukocytosis includes: 1) leukocytosis of newborns (the number of leukocytes during the first 2 days of life is 15-000 per 20 mm000 of blood); 2) digestive leukocytosis, which develops 2-3 hours after a meal; 3) myogenic leukocytosis associated with physical work. Pathological leukocytosis occurs in many infectious diseases, intoxications, inflammatory processes, endocrine disorders, disorders of the nervous regulation of hematopoiesis. The number of leukocytes can increase from 10 to 000 in 40 mm000 of blood. 41. Pathophysiology of the cardiovascular system Cardiac circulatory failure develops as a result of a weakening of the contractile function of the myocardium. Its reasons are: 1) overwork of the myocardium caused by the working overload of the heart; 2) direct myocardial damage; 3) disorders of the coronary circulation; 4) disorders of the function of the pericardium. Mechanisms of development in heart failure. With any form of heart damage from the moment of its occurrence, compensatory reactions develop in the body, aimed at preventing the development of general circulatory failure. Along with the general "extracardiac" mechanisms of compensation in case of heart failure, compensatory reactions are included that take place in the heart itself. At the first stages of damage to the heart, the work performed by it increases, and the strengthening of the work of the heart (its hyperfunction) gradually leads to hypertrophy of the heart muscle. Myocardial hypertrophy is characterized by an increase in the mass of the heart muscle, mainly due to the volume of muscle elements. There are physiological (or working) and pathological hypertrophy. Heart failure from overload develops with heart defects, hypertension of the small and large circulation. More rarely, overload can be caused by diseases of the blood system (anemia) or endocrine glands (hyperthyroidism). Heart failure during overload in all cases develops after a more or less long period of compensatory hyperfunction and myocardial hypertrophy. At the same time, energy generation in the myocardium is sharply increased: the tension caused by the myocardium is increased, the work of the heart is enhanced, but the efficiency is significantly reduced. Heart defects are characterized by a violation of intracardiac hemodynamics, which causes an overload of one or another chamber of the heart. Heart failure due to myocardial damage can be caused by infections, intoxications, hypovitaminosis, coronary insufficiency, autoallergic processes. Myocardial damage is characterized by a sharp decrease in its contractile function. Disturbances in energy metabolism in the myocardium may be the result of insufficient oxidation, the development of hypoxia, a decrease in the activity of enzymes involved in the oxidation of substrates, and uncoupling of oxidation and phosphorylation. The lack of substrates for oxidation most often occurs due to a decrease in the blood supply to the heart and a change in the composition of the blood flowing to the heart. Sclerosis of the coronary vessels is the most common cause of reduced blood supply to the heart muscle. Relative cardiac ischemia may result from hypertrophy, in which an increase in muscle fiber volume is not accompanied by a corresponding increase in the number of blood capillaries. 42. Disorders of the coronary circulation The amount of coronary blood flow depends on the tone of the coronary vessels. Irritation of the vagus nerve usually causes a decrease in coronary blood flow, which, apparently, depends on a slowing of the heart rate (bradycardia) and a decrease in mean pressure in the aorta, as well as a decrease in the heart's need for oxygen. Excitation of the sympathetic nerves leads to an increase in coronary blood flow, which is obviously due to an increase in blood pressure and an increase in oxygen consumption, which occurs under the influence of norepinephrine released in the heart and adrenaline brought in by the blood. Acute coronary insufficiency It is characterized by a mismatch between the need of the heart for oxygen and its delivery with blood. Most often, insufficiency occurs with atherosclerosis of the arteries, spasm of the coronary (mostly sclerotic) arteries, blockage of the coronary arteries by a thrombus, rarely an embolism. The result of acute coronary insufficiency is myocardial ischemia, causing a violation of oxidative processes in the myocardium and excessive accumulation of underoxidized metabolic products in it. Myocardial infarction - focal ischemia and necrosis of the heart muscle that occurs after a prolonged spasm or blockage of the coronary artery (or its branches). The coronary arteries are terminal, therefore, after the closure of one of the large branches of the coronary vessels, the blood flow in the myocardium supplied by it decreases tenfold and recovers much more slowly than in any other tissue in a similar situation. The contractility of the affected area of the myocardium drops sharply and then completely stops. Cardiogenic shock is a syndrome of acute cardiovascular insufficiency that develops as a complication of myocardial infarction. Clinically, it manifests itself as a sudden sharp weakness, blanching of the skin with a cyanotic tint, cold sticky sweat, a drop in blood pressure, a small frequent pulse, lethargy of the patient, and sometimes a short-term impairment of consciousness. In the pathogenesis of hemodynamic disorders in cardiogenic shock, three links are essential: 1) decrease in stroke and minute volume of the heart (cardiac index below 2,5 l/min/m2); 2) a significant increase in peripheral arterial resistance (more than 180 dynes/sec); 3) violation of microcirculation. In severe shock, a vicious circle occurs: metabolic disorders in tissues cause the appearance of a number of vasoactive substances that contribute to the development of vascular disorders and erythrocyte aggregation, which, in turn, support and deepen existing disorders of tissue metabolism. As tissue acidosis increases, deep violations of enzyme systems occur, which leads to the death of cellular elements and the development of small necrosis in the myocardium, liver, and kidneys. 43. Pathophysiology of digestion Indigestion - a condition of the gastrointestinal tract, when it does not ensure the absorption of food entering the body. Digestive insufficiency, in addition to disorders of the digestive tract, is characterized by a negative nitrogen balance, hypoproteinemia, exhaustion of the body, and changes in reactivity. Examples of insufficiency of digestion in adulthood are achilia and a decrease in the secretion of pancreatic juice. In old age, insufficiency of digestion develops as a result of a decrease in the secretory function of the digestive glands and absorption processes. The main causes of indigestion are: 1) malnutrition; 2) causative agents of a number of infections; 3) getting into the digestive tract of poisons (salts of heavy metals, poisons of plant origin, etc.); 4) tumors; 5) postoperative conditions; 6) abuse of alcohol and nicotine; 7) mental trauma, negative emotions; 8) congenital anomalies of the gastrointestinal tract. Decrease in appetite - anorexia - observed as a result of inhibition of the secretion of the digestive glands in many diseases of the gastrointestinal tract, with infectious diseases, negative emotions. Pathological increase in appetite - hyperrexia (bulimia) - usually combined with increased food intake - polyphagia. Bulimia can develop with thyrotoxicosis (due to an increase in the specific dynamic action of the protein, as well as an increase in basal metabolism and oxidative processes) and some other diseases of the endocrine system. Sometimes a pathological increase in appetite is observed with lesions of the central nervous system, after resection of the cardial part of the stomach, etc. Insufficient grinding of food in the oral cavity is often associated with disturbances in the functioning of the chewing apparatus. This apparatus includes teeth, chewing muscles, muscles of the tongue and bones of the skull, to which the chewing muscles are attached. The most common causes of decreased chewing ability are dental lesions - caries, periodontal disease. With the defeat of the teeth chewing pressure is significantly reduced. Chewing is disturbed by inflammation of the masticatory muscles, violations of its innervation (bulbar paralysis), injuries of the jaw bones. Inflammatory processes in the oral cavity make chewing difficult, making it painful. With poor chewing of food, the reflex separation of gastric and pancreatic juices decreases. Poorly crushed food injures the mucous membrane of the oral cavity and stomach, which, near the anastomosis, contracts spastically and forms a muscle roller that prevents the passage of food along a new path. Violation of the movement of food through the esophagus can also lead to a violation of the digestion of food in general. 44. Indigestion in the stomach Indigestion in the stomach manifested by changes in its evacuation function, digesting, secretory, etc.; this leads to disruption of the normal functioning of the whole organism. Types of gastric secretion. 1. Normal type of gastric secretion: the amount of secreted gastric juice and its acidity (free and total) naturally increase in accordance with the two applied stimuli. 2. The excitable type of gastric secretion is characterized by its increase in response to both mechanical and chemical stimuli. The acidity of the juice is usually increased. 3. The asthenic type of gastric secretion is characterized by an increase in the excitability of the gastric glands to mechanical irritation and a decrease in its excitability to chemical. This type of secretion is noted with increased irritability and rapid exhaustion of the gastric glands. In the first hour of observation (mechanical irritation) secretion exceeds normal, in the second hour (chemical irritation) it is reduced. Accordingly, the acidity of gastric juice also changes. The total amount of it in the asthenic type of secretion is below normal. 4. The inert type of gastric secretion is characterized by a decrease in the excitability of the secretory cells of the stomach to the action of a mechanical stimulus with normal or increased excitability to chemical irritation. The total amount of gastric juice is usually higher than normal. 5. For the inhibitory type of gastric secretion, a decrease in the excitability of the gastric glands to mechanical and chemical irritation is characteristic. The total amount of gastric juice is very small, its acidity is low, free acid is often absent. Changes in the amount of gastric juice and its acidity. Quantitative changes in the secretory function of the stomach (hypo- or hypersecretion) are often combined with its qualitative changes: an increase in acidity or a decrease in it up to the complete absence of free hydrochloric acid in gastric juice. The combination of the absence of free hydrochloric acid and pepsin in gastric juice is called achilia. In pathology, there may be a dissociation between the amount of juice separated, its acidity and digestive power. Hyposecretion can be combined with high, and hypersecretion - with low digestive power of the juice. Violation of the absorption function of the stomach. Normally, this function is small, but with damage to the stomach, it can be significantly enhanced. Absorptive function of the stomach can be enhanced by inflammatory processes in it (gastritis). In this case, the gastric mucosa becomes permeable to toxins and some digestion products. Violation of the excretory function of the stomach. The excretory function of the stomach can be judged by the rate of appearance of a neutral dye solution administered intravenously in the gastric juice (normally after 12-15 minutes). 45. Digestive disorders in the intestines Violation of bile secretion. Insufficient flow of bile into the intestine is called hypocholia, a complete cessation of its flow is called acholia. These phenomena are possible with blockage or compression of the common bile duct, with a violation of the bile-forming function of the liver. With acholia, the digestion and absorption of fat suffers especially sharply, since the lipase of the pancreatic juice in the absence of bile is inactive, and the fats are not emulsified and their contact with the lipolytic enzyme is difficult. With a lack of bile, the absorption of fatty acids, cholesterol, and fat-soluble vitamins suffers. Violation of the external secretion of the pancreas. Violations of the external secretion of the pancreas can be due to a number of reasons: 1) duodenitis - inflammatory processes of the duodenum, accompanied by a decrease in the formation of secretin; 2) neurogenic inhibition of pancreatic function (vagal dystrophy, atropine poisoning); 3) blockage or compression of the gland duct; 4) destruction of the gland by a tumor; 5) allergic restructuring of the body; 6) development of inflammatory processes in the pancreas (acute and chronic pancreatitis). With disorders of the pancreas function, the formation of enzymes in it decreases, and therefore duodenal digestion is disturbed. The digestion of fat suffers especially sharply, since pancreatic juice contains the most active lipolytic enzyme. The appearance of a large number of muscle fibers in the feces after eating meat food indicates insufficient protein digestion. Indigestion in the small intestine. Violations of the secretory function of the intestine may depend on a decrease in the amount of separated juice, a decrease in the content of enzymes in it, and a violation of parietal digestion. With a weakening of intestinal digestion, the digestion of fats and proteins changes little, since the secretion of lipase and amylase of pancreatic juice increases compensatory. Slow absorption may be due to: 1) insufficient splitting of food masses in the stomach and duodenum; 2) violations of parietal digestion; 3) congestive hyperemia of the intestinal wall (paresis of vessels, shock); 4) ischemia of the intestinal wall; 5) inflammation of the small intestine (enteritis), when its mucous membrane becomes edematous, swollen; 6) resection of most of the small intestine; 7) intestinal obstruction in the upper segments of the intestine. Due to prolonged malabsorption, depletion of the body develops, hypovitaminosis occurs (rickets in children) and other manifestations of indigestion. Pathological enhancement of absorption is associated with an increase in the permeability of the intestinal wall. 46. Violation of the motor function of the intestine Violation of the motor function of the intestine is manifested in the acceleration or deceleration of peristalsis and the alternation of these processes, as well as in violation of pendulum movements. Acceleration of peristalsis. As a result of the acceleration of peristalsis, the food slurry moves through the intestines faster and diarrhea develops. The most common causes of diarrhea are inflammatory changes in the gastrointestinal tract. At the same time, the excitability of the receptors of the intestinal wall increases, which causes the acceleration of peristalsis under the action of various, including adequate, stimuli. Diarrhea occurs when unusual irritants act on the intestinal wall: undigested food (for example, with achilia), fermentation and decay products, toxic substances. The acceleration of peristalsis in this case has a protective value. Deceleration of peristalsis. At the same time, the movement of food gruel through the intestines is inhibited and constipation develops. Constipation can be spastic and atonic. Spastic constipation occurs under the influence of toxic factors (lead poisoning), psychogenic influences, as well as viscero-visceral reflexes from various parts of the abdominal cavity. All these factors lead to spastic contraction of individual sections of the intestine and the accumulation of feces in it. Atonic constipation is caused by those factors that cause a decrease in the tone of the intestinal wall and a weakening of peristalsis. Intestinal obstruction occurs when there is an obstruction in the intestines for the passage of food masses. Distinguish mechanical obstruction due to mechanical closure of the intestinal lumen, and dynamic obstruction caused by paralysis or spasm of the intestinal muscles. The pathogenesis of intestinal obstruction is complex. Intoxication of the body due to the absorption of toxic intestinal contents, pathological reflex effects with an altered intestinal wall, dehydration of the body and a drop in the level of blood chlorides are important, since they pass into the abdominal cavity together with water. Violation of defecation can occur in the following cases: 1) with strong mental shocks (fear, fright): the influence of the cerebral cortex on the spinal center of defecation may fall out, while defecation becomes involuntary (reflex); 2) in case of damage nn. pelvici: defecation is disturbed due to dysfunction of the muscles involved in this act; 3) with inflammatory processes in the rectum: the sensitivity of its receptors increases and there are frequent false urges to defecate (tenesmus); 4) with injuries of the lumbosacral spinal cord due to the defecation center being turned off, fecal incontinence occurs. 47. Pathophysiology of the liver The liver is the largest glandular organ, the removal or sharp damage of which leads to the death of a person. The main functions of the liver: 1) synthesis and secretion of bile; 2) participation in the metabolism of carbohydrates, fats and proteins; 3) the formation of fibrinogen; 4) the formation of prothrombin; 5) formation of heparin; 6) participation in the regulation of the total blood volume; 7) barrier function; 8) hematopoiesis in the fetus; 9) deposition of iron and copper ions; 10) the formation of vitamin A from carotene. Insufficiency of liver functions in the body is manifested in metabolic disorders, bile formation disorders, lowering of the barrier function of the liver, changes in the composition and properties of the blood, changes in the function of the nervous system, and impaired water metabolism. Among the large number of etiological factors that lead to insufficiency of liver function, the most important role is played by factors that cause an inflammatory process in the liver - hepatitis. Often, liver failure occurs on the basis of a long-term violation of the diet (eating fatty foods, alcoholic beverages, lack of protein in food). The final stage in the development of chronic hepatitis is usually cirrhosis of the liver. Liver function disorders may be of a secondary nature, for example, in violation of the general circulatory system. imagination, violation of bile secretion, general amyloidosis. Lack of liver function is also characterized by a violation of its barrier function. Violation of bile formation and bile secretion. With cirrhosis, hepatitis, starvation, insufficient intake of methionine and cysteine in the body, the formation of paired bile acids is weakened, and then the amount of free bile acids in the bile increases. The process of formation of bile pigments mainly occurs in the cells of the reticuloendothelial system from the hemoglobin of destroyed erythrocytes. The so-called indirect bilirubin released from these cells is transported with the blood stream to the liver cells, where it conjugates with two molecules of glucuronic acid, and turns into direct bilirubin and is excreted with bile into the intestinal lumen. The weakening or complete cessation of the flow of bile into the duodenum significantly changes the content of urobilin and stercobilin in the urine and feces, which can serve as an important indicator for characterizing the state of the liver. Under the action of certain substances (egg yolk, fats, peptone, magnesium sulphate), bile secretion is accelerated. Most of these substances have an effect on the formation of bile, but mainly they act on the pressure in the bile ducts or on the relaxation of the sphincter of Oddi. 48. Violation of diuresis Causes of kidney dysfunction: 1) disorders of the nervous and endocrine regulation of kidney function; 2) impaired blood supply to the kidneys (atherosclerosis, shock conditions); 3) infectious diseases of the kidneys (pyelonephritis, focal nephritis); 4) autoallergic kidney damage (diffuse glomerulonephritis); 5) violation of the outflow of urine (formation of stones, compression of the ureters, etc.); 6) kidney damage in severe infectious diseases and intoxications (sepsis, cholera, poisoning with salts of heavy metals); 7) congenital anomaly of the kidneys (hypoplasia, polycystic); 8) a hereditary defect in the enzymatic systems of the tubules (Fanconi's syndrome, etc.). For a day in adults, the amount of urine excreted (daily diuresis) is about 1,5 liters (from 1 to 2 liters). A decrease in the daily amount of urine is called oliguria, and a complete cessation of urination is called anuria. Increased urine production is called polyuria. Excitation of cortical cells usually leads to polyuria, and their inhibition - to oliguria. Cases of complete cessation of urination in people who have undergone extreme mental trauma are described. With various lesions of the hypothalamus and pituitary gland (hemorrhage, tumors, trauma to the skull), diuresis may increase or decrease. Suppression of secretion of antidiuretic hormone (ADH) leads to severe polyuria. Polyuria occurs because ADH deficiency disrupts the reabsorption of water in the distal tubules and collecting ducts (facultative reabsorption). Painful anuria may occur. In various reflexogenic zones (skin, intestines, ureters, bladder), reflex inhibition of urination is possible. The mechanism of occurrence of reflex pain anuria is complex, nervous and humoral factors are involved. With pain irritation, the sympathetic nervous system is excited, hormones - adrenaline and ADH are released into the blood. Under the influence of an excess of adrenaline, the tone of the renal arterioles increases, which leads to a drop in glomerular filtration. Excess ADH promotes more intense reabsorption in the tubules. Ultimately, diuresis decreases up to anuria. In addition to adrenaline and ADH, other hormones also influence diuresis. An increase in diuresis in hyperfunction of the thyroid gland is due to the fact that the hormone thyroxine enhances filtration in the renal glomeruli. Hydrocortisone, a glucocorticoid hormone of the adrenal glands, has the same effect. With an excess of aldosterone (the mineralocorticoid hormone of the adrenal glands), polyuria is noted. Its occurrence is apparently associated with the inhibition of ADH secretion, as well as the intensive release of potassium, along with which water is lost. 49. Violation of filtration, reabsorption and secretion Ultrafiltration of plasma with the formation of primary urine is carried out in the glomeruli of the kidneys. The filtering membrane of the glomerulus consists of three layers: the capillary endothelium, the basement membrane, and the epithelial cells of the inner part of the capsule, which are called podocytes. Podocytes have processes that tightly rest against the basement membrane. The filtering membrane of the glomerulus is capable of passing almost all substances with a molecular weight below 70 present in the blood plasma, as well as a small part of albumins. Filtration in the glomeruli occurs under the influence of filtration pressure (PD). PD \u75d 25 - (10 + 40) \uXNUMXd XNUMX mm Hg. Art., where 75 mm Hg. Art. - hydrostatic pressure in the capillaries of the glomeruli; 25 mmHg Art. - oncotic pressure of plasma proteins; 10 mmHg Art. - intrarenal pressure. Filtration pressure can vary within 25-50 mm Hg. Art. Approximately 20% of the blood plasma flowing through the glomerular capillaries undergoes filtration. To determine the filtration capacity of the kidneys, the definition of the purification index is used. The indicator of purification, or clearance (from the English to clear - "clear"), is the volume of blood plasma, which is completely released by the kidneys from a given substance in 1 minute. Reduced filtration. The decrease in the amount of primary urine produced depends on a number of extrarenal and renal factors: 1) drop in blood pressure; 2) narrowing of the renal artery and arterioles; 3) increased oncotic blood pressure; 4) violation of the outflow of urine; 5) decrease in the number of functioning glomeruli; 6) damage to the filter membrane. Reducing the filtration area. In an adult, the number of glomeruli in both kidneys exceeds 2 million. The reduction in the number of functioning glomeruli leads to significant restrictions on the filtration area and a decrease in the formation of primary urine, which is the most common cause of uremia. The filtration surface in the glomerulus may be reduced due to damage to the filtration membrane, which can be caused by: 1) thickening of the membrane due to the proliferation of cells of the endothelial and epithelial layers, for example, in inflammatory processes; 2) thickening of the basement membrane due to the deposition of anti-renal antibodies on it; 3) germination of the filtering membrane by connective tissue (sclerosis of the glomerulus). An increase in glomerular filtration is observed in the following cases: 1) increase the tone of the efferent arteriole; 2) decrease in the tone of the afferent arteriole; 3) decrease in oncotic blood pressure. 50. Violation of tubular reabsorption The most common mechanisms of impaired tubular reabsorption include: 1) overstrain of reabsorption processes and depletion of enzyme systems due to an excess of reabsorbed substances in the primary urine; 2) a decrease in the activity of enzymes of the tubular apparatus; 3) damage to the tubules in case of circulatory disorders or kidney disease. reabsorption of glucose. Glucose penetrates into the epithelium of the proximal tubules, undergoing the process of phosphorylation under the influence of the enzyme hexokinase. With hyperglycemia of various origins (pancreatic diabetes, alimentary hyperglycemia), a lot of glucose is filtered through the glomeruli and enzymatic systems are not able to ensure its complete reabsorption. Glucose appears in the urine, glucosuria occurs. protein reabsorption. Primary urine contains up to 30 mg of albumin, and in just a day 30-50 g of protein is filtered through the glomeruli. There is practically no protein in the final urine. The appearance of protein in the urine is called proteinuria. More often found albuminuria - excretion of albumin in the urine. amino acid reabsorption. In adults, about 1,1 g of free amino acids are excreted in the urine. Increased excretion of amino acids compared to the norm is called aminoaciduria. Aminoaciduria occurs with a hereditary defect in the enzymes that ensure the absorption of amino acids in the renal tubules, and with kidney diseases accompanied by damage to the tubular apparatus. Reabsorption of sodium and chloride. About 10-15 g of sodium chloride is excreted in the urine per day. The rest is absorbed back into the blood. The process of absorption of chlorides in the proximal tubules is determined by the active transfer of sodium. A decrease in sodium reabsorption leads to depletion of alkaline reserves in the blood and disruption of the water balance. Reabsorption of water and the concentration ability of the kidneys. About 120 ml of water (1-119%) is sucked back out of 96 ml of filtrate in 99 minute. Of this amount, approximately 85% of water is absorbed in the proximal tubules and the loop of Henle (mandatory reabsorption), 15% in the distal tubules and collecting ducts (facultative reabsorption). Facultative reabsorption of water is suppressed with a lack of ADH (antidiuretic hormone), since without it the cells of the tubules become impermeable to water. Excess secretion of ADH is accompanied by oliguria due to intense absorption of water. In a healthy person, the specific gravity of urine with a normal diet is not lower than 1,016-1,020 and varies depending on the intake of food and water within 1,002-1,035. The inability of the kidneys to concentrate urine is called hypostenuria. The specific gravity of urine with hypostenuria does not exceed 1,012-1,014 and fluctuates slightly during the day. Hypostenuria with relatively sufficient glomerular function leads to the development of an early stage of chronic nephritis, pyelonephritis. 51. Violation of tubular secretion. kidney disease In diseases of the kidneys, secretion processes in the tubules are disrupted and all substances secreted by secretion accumulate in the blood. Violation of the secretion of uric acid occurs as a hereditary defect. The accumulation of uric acid and uric acid salts in the blood leads to the development of the so-called renal gout. Increased secretion of potassium is noted with an excess of the hormone aldosterone and with the use of diuretics, inhibitors of the carbonic anhydrase enzyme contained in the epithelium of the tubules. Loss of potassium (potassium diabetes) leads to hypokalemia and severe dysfunction. An excess of parathyroid hormone contributes to intensive secretion and loss of phosphates (phosphate diabetes), changes occur in the skeletal system, and the acid-base balance in the body is disturbed. A formidable sign is isostenuria, when the specific gravity of urine approaches the specific gravity of the glomerular filtrate (1,010) and remains fixed at a low figure in different daily portions of urine (monotonic diuresis). Isosthenuria indicates a violation of the tubular reabsorption of water and salts, the loss of the ability of the kidneys to concentrate and dilute urine. As a result of destruction or atrophy of the tubular epithelium, the tubules turn into simple tubes that carry the glomerular filtrate to the renal pelvis. The combination of isosthenuria with oliguria is an indicator of severe renal insufficiency. Kidney stone disease is one of the types of disorders in the excretion of salts by the kidneys. The cause of this disease is not well understood. A number of factors contribute to stone formation in the kidneys: a violation of mineral metabolism, infection of the urinary tract, stagnation of urine, kidney injury, lack of vitamins A and D in food, a hereditary metabolic defect (oxalosis). Stones are composed of phosphates (calcium salts of phosphoric acid), oxalates (calcium salts of oxalic acid), urates (salts of uric acid) and may have a mixed composition. There are cystine stones with a hereditary disease (cystinuria), sulfanilamide stones with an increased concentration of sulfanilamide drugs in the urine, xanthine stones. Stone growth occurs by deposition of alternating concentric layers of mucopolysaccharides and crystalloids on it. Kidney stones and sediments in the urine have a variety of shapes and vary in size. They are found in the form of small grains of sand or large formations that fill the cavity of the pelvis. 52. Insufficiency of kidney function Insufficiency of kidney function is called the inability to purify the blood of metabolic products and maintain the constancy of the composition of the blood plasma. Acute insufficiency can occur with kidney injury, shock conditions, blockage of the urinary tract with a stone, massive hemolysis of red blood cells, etc. Chronic insufficiency is characteristic of the final stage of development of a number of progressive chronic kidney diseases with the transition to a wrinkled kidney. Azotemia. A significant limitation of the filtration surface in kidney diseases is accompanied by the accumulation in the blood of the end products of protein metabolism (urea, uric acid, creatinine, ammonia, indican). The content of residual nitrogen in the blood increases to 290-400 mg, primarily due to an increase in urea. The concentration of urea in the blood rises above the upper limit of the norm, and its concentration in the urine falls. The content of creatinine in the blood reaches 30-35 mg. Violation of the electrolyte composition of plasma and acid-base balance. In acute renal failure due to impaired filtration, the potassium content in the blood increases from 4-5 to 7,5 meq / l. Hyperkalemia can contribute to sudden cardiac arrest due to impaired excitability and conduction. For chronic renal failure, hypokalemia is most characteristic due to impaired potassium reabsorption. Loss of sodium and other alkaline cations (potassium, calcium) leads to acidosis. The state of acidosis in renal failure is due not only to the loss of alkaline cations and bicarbonates, but also to the retention of acid radicals in the blood due to a drop in the filtration capacity of the kidneys. Hypertension and anemia of the kidneys. Patients with chronic kidney failure develop persistent hypertension (200/120 mm Hg and above), severe anemia with a drop in the number of erythrocytes to 2 per 000 mm000 and below, toxic leukocytosis with a shift to the left is noted. Uremia is self-poisoning of the body resulting from kidney failure. Due to the retention of nitrogen metabolic products in the blood, their exit from tissues and cells is difficult, damage occurs at the cellular level due to metabolic disorders. Uremia is characterized by pronounced disorders of the functions of the central nervous system: severe headache, apathy and drowsiness, attacks of excitement and convulsions, shortness of breath. A state of loss of consciousness (uremic coma) may occur. With uremia, the blood supply to the brain is sharply disrupted due to vasospasm. Hypoxia and intoxication of the respiratory center cause periodic respiration of the Cheyne-Stokes type. An artificial kidney (hemodialysis) is used to free patients from toxic metabolic products and normalize homeostasis. Repeated use of hemodialysis in acute forms of renal failure allows you to gain time during which renal function can recover. 53. Disorders of external respiration External (or pulmonary) respiration consists of: 1) air exchange between the external environment and the alveoli of the lungs (pulmonary ventilation); 2) exchange of gases (CO2 and Cy) between alveolar air and blood flowing through the pulmonary capillaries. The main function of external respiration is to ensure the arterialization of blood in the lungs at the proper level, that is, to maintain a strictly defined gas composition of the blood flowing from the lungs by saturating it with oxygen and removing excess carbon dioxide from it. The insufficiency of pulmonary respiration is understood as the inability of the respiratory apparatus to provide the blood with oxygen at the proper level and the removal of carbon dioxide from it. Hyperventilation of the lungs means an increase in ventilation more than is required to maintain the necessary tension of oxygen and carbon dioxide in the arterial blood. Hyperventilation leads to an increase in O2 tension and a fall in CO2 tension in the alveolar air. Correspondingly, the CO2 tension in the arterial blood decreases (hypocapnia), and gaseous alkalosis occurs. Hypoventilation of the lungs. Depends, as a rule, on the defeat of the respiratory apparatus - diseases of the lungs, respiratory muscles, circulatory disorders and innervation of the respiratory apparatus, oppression of the respiratory center by drugs. Hypoventilation leads to hypoxia (decreased arterial pO2) and hypercapnia (increased arterial pCO2). Uneven ventilation. It is observed under physiological conditions even in healthy young people and, to a greater extent, in the elderly, as a result of the fact that not all lung alveoli function simultaneously, and therefore different parts of the lungs are also ventilated unevenly. This unevenness is especially pronounced in certain diseases of the respiratory apparatus. Uneven ventilation can occur with loss of elasticity of the lungs (for example, with emphysema), difficulty in bronchial patency (for example, with bronchial asthma), accumulation of exudate or other fluid in the alveoli, with pulmonary fibrosis. Uneven ventilation, like hypoventilation, leads to hypoxemia, but is not always accompanied by hypercapnia. The vital capacity of the lungs (normally it ranges from 3,5 to 5 liters) mainly characterizes the amplitude within which respiratory excursions are possible. Its decrease indicates that some reasons prevent free chest excursions. A decrease in VC is observed with pneumothorax, exudative pleurisy, bronchospasm, stenosis of the upper respiratory tract, movement disorders of the diaphragm and other respiratory muscles. Residual volume is the volume of the lungs occupied by alveolar air and dead space air. Its value under normal conditions is such that a sufficiently rapid gas exchange is ensured. 54. Upper respiratory disorders Turning off nasal breathing, in addition to disrupting a number of important functions of the body (stagnation of blood in the vessels of the head, sleep disturbance, memory loss, performance, etc.), leads to a decrease in the depth of respiratory movements, minute breathing volume and lung capacity. Sneeze - irritation of the receptors of the nasal mucosa - causes a sneezing reflex, which under normal conditions is a protective reaction of the body and helps to cleanse the respiratory tract. In case of inflammation (for example, allergic rhinitis) or irritation of the nasal mucosa BAS (biologically active substances), prolonged sneezing leads to an increase in intrathoracic pressure, respiratory rhythm disturbance, and circulatory disorders. Dysfunction of the larynx and trachea. The narrowing of the lumen of the larynx and trachea is observed with the deposition of exudate (diphtheria), edema, tumors of the larynx, spasm of the glottis, inspiration of foreign bodies (coins, peas, toys, etc.). Partial tracheal stenosis is usually not accompanied by gas exchange disorders due to compensatory increased breathing. Pronounced stenosis leads to hypoventilation and gas exchange disorders. Asphyxia is a condition characterized by insufficient supply of oxygen to the tissues and the accumulation of carbon dioxide in them. Most often, it occurs when strangulation, drowning, swelling of the larynx and lungs, aspiration of foreign bodies, etc. The following periods of asphyxia are distinguished. I period - deep and somewhat rapid breathing with an extended breath - inspiratory dyspnea. During this period, there is an accumulation of carbon dioxide in the blood and its depletion of oxygen, which leads to the excitation of the respiratory and vasomotor centers - heart contractions become more frequent and blood pressure rises. At the end of this period, breathing slows down and expiratory dyspnea occurs. II period - an even greater slowdown in breathing and its short-term stop, a decrease in blood pressure, a slowdown in cardiac activity. III period - the extinction of reflexes due to the depletion of the nerve centers, the pupils greatly dilate, the muscles relax, blood pressure drops sharply, heart contractions become rare and strong, after several terminal respiratory movements, breathing stops. Cough - a reflex act that contributes to the cleaning of the respiratory tract from both foreign bodies that have entered from the outside, and from endogenously formed products. Bronchospasm and dysfunction of the bronchioles are characteristic of bronchial asthma. As a result of the narrowing of the lumen of the bronchi (bronchospasm, hypersecretion of the mucous glands, swelling of the mucous membrane), resistance to the movement of the air stream increases. At the same time, the act of exhalation becomes especially difficult and lengthens, and expiratory dyspnea occurs. Alveolar dysfunction. These disorders occur in inflammatory processes (pneumonia), edema, emphysema, lung tumors, etc. The leading link in the pathogenesis of respiratory disorders in these cases is a decrease in the respiratory surface of the lungs and a violation of oxygen diffusion. 55. Violations of the function of the pleura Pleural dysfunction occur most often in inflammatory processes (pleurisy), pleural tumors, air entering the pleural cavity (pneumothorax), accumulation of exudate, edematous fluid (hydrothorax) or blood (hemothorax) in it. With all these pathological processes (with the exception of dry, i.e., without the formation of serous exudate, pleurisy), the pressure in the chest cavity rises, the lung is compressed, atelectasis occurs, leading to a decrease in the respiratory surface of the lungs. Pleurisy (inflammation of the pleura) is accompanied by the accumulation of exudate in the pleural cavity, which makes it difficult to expand the lung during inspiration. Usually, the affected side participates little in respiratory movements, and for the reason that irritation of the endings of sensory nerves in the pleural sheets leads to reflex inhibition of respiratory movements on the diseased side. Clearly expressed disorders of gas exchange occur only in cases of large (up to 1,5-2 liters) accumulation of fluid in the pleural cavity. Pneumothorax. In this condition, air enters the pleural cavity through a damaged chest wall or from the lungs in violation of the integrity of the bronchi. There are open pneumothorax (the pleural cavity communicates with the environment), closed (without communication of the pleural cavity with the environment, for example, therapeutic pneumothorax in pulmonary tuberculosis) and valve, or valve, that occurs when the integrity of the bronchi is violated. Collapse and atelectasis of the lung. The collapse of the lung, which occurs when the contents of the pleural cavity (air, exudate, blood) are pressed against it, is called lung collapse. The collapse of the lung in violation of bronchial patency is called atelectasis. Changes in the structure of the chest, leading to respiratory failure, occur when the vertebrae and ribs are immobile, premature ossification of the costal cartilages, ankyloses joints and anomalies in the shape of the chest. Respiratory muscle dysfunction may occur as a result of damage to the muscles themselves (myositis, muscle atrophy, etc.), disruption of their innervation (with diphtheria, poliomyelitis, tetanus, botulism, etc.) and mechanical obstacles to their movement. The most pronounced respiratory disorders occur with damage to the diaphragm - most often with damage to the nerves innervating it or their centers in the cervical part of the spinal cord, less often - from changes in the places of attachment of the muscle fibers of the diaphragm itself. 56. Disorders of internal breathing Impaired transport of oxygen from lungs to tissues occurs as a result of either a decrease in the amount of hemoglobin in the blood (anemia, blood loss, etc.), or a shift in the hemoglobin dissociation curve in various pathological conditions, a decrease in the partial pressure of oxygen in the alveoli. Violation of the transport of carbon dioxide from tissues to the lungs. Most carbon dioxide is transported in the blood in the form of plasma bicarbonates and red blood cells. The value of carbon dioxide physically dissolved in plasma for its general transport is small. In addition, carbon dioxide also enters into a chemical bond with hemoglobin, forming carbaminohemoglobin (or carbohemoglobin). At the same time, reduced hemoglobin binds more carbon dioxide than oxyhemoglobin. Oxygenation of hemoglobin in the pulmonary capillaries promotes the breakdown of carbohemoglobin and the removal of carbon dioxide from the blood. Violation of the transport of carbon dioxide from tissues to the lungs most often occurs with anemia for the following reasons: 1) the loss of hemoglobin disrupts not only the supply of oxygen to tissues, but also the removal of carbon dioxide from there, as well as the release of this gas in the lungs; 2) the loss of bicarbonates contained in erythrocytes reduces the capacity of the blood in relation to carbon dioxide, which makes it difficult to release it in the tissues. Violation of tissue respiration. Tissue respiration is the process of oxygen uptake by tissues. Both the respiratory apparatus, the circulatory apparatus, and the blood system are involved in providing tissues with oxygen. It is conditionally possible to distinguish between exogenous and endogenous causes of impaired tissue respiration. Exogenous causes are factors that, acting on the body from the outside, affect the oxidative processes in tissues. This group of factors should include phosphorus, arsenic, cyanide compounds, drugs. Endogenous causes are all those factors that, arising in the body itself, disrupt the oxidative processes in tissues. Violations of tissue respiration occur in disorders of the function of some endocrine glands. Oxygen starvation of tissues (hypoxia) - a condition that occurs in the human or animal body as a result of a violation of both the delivery of oxygen to tissues and its use in them. Insufficient delivery of oxygen to tissues may be due to diseases of the respiratory, circulatory, blood systems or a decrease in the partial pressure of oxygen in the inhaled air. Acute hypoxia occurs extremely quickly and can be caused by the inhalation of physiologically inert gases such as nitrogen, methane and helium. Chronic hypoxia occurs with blood diseases, heart and respiratory failure, after a long stay high in the mountains or under the influence of repeated exposure to conditions of insufficient oxygen supply. Authors: Barsukov V.I., Selezneva T.D.
▪ Constitutional (state) law of the Russian Federation. Crib ▪ Foreign economic activity. Crib
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