Pathological physiology Part 2 (topic #10-18) Content. № Name topic Page 1. Regional Blood Flow Disturbances. Arterial hyperemia 3 2. Venous Hyperemia 7 3. Ischemia 9 4. STASIS 11 5. Thrombosis 13 6. Mechanisms of hemostasis 16 7. Syndrome of disseminated intravascular coagulation (DIC-syndrome) 27 8. Embolism 30 9. INFLAMMATION 33 10. Pathogenesis of inflammation 35 11. Chronic inflammation 49 12. Local signs of inflammation 51 13. General manifestations of inflammation 52 14. Acute phase response 57 15. Fever 64 16. DIFFERENCES FROM FEVER HYPERTHERMIC STATES AND REACTIONS 73 17. NEOPLASIA 76 18. Antitumor resistance of the body 94 19 EXTREME CONDITION 96 20 Collapse 101 21 Shock 104 22. Coma 118 23. Allergy 128 24. Type I allergic reactions 133 25. Allergic reactions type II 134 26. Allergic reactions type III 136 27. Type IV allergic reactions 138 28 IMMUNOPATHOLOGY 142 29 IMMUNOPATHOLOGICAL STATES AND REACTIONS 155 30 IMMUNODEFICIENCIES 156 31 Pathological tolerance 167 32 The "graft versus host" reaction 168 Regional Blood Flow Disturbances Numerous disorders of the regional (peripheral, local) blood flow are subdivided into blood flow disturbances in the vessels of medium diameter and blood and lymph flow disturbances in the vessels of microcirculation. Blood flow disturbances in the vessels of medium diameter can be classified as: - pathological arterial hyperemia, - venous hyperemia, - ischemia, - stasis. Arterial hyperemia Arterial hyperemia is a typical form of violation of the local circulation, characterized by an increase in the blood supply of the organ or tissue due to increased blood flow through the arterial vessels (aorta, arterioles, arteries and arterial capillaries). Causes There is a physiological and pathological arterial hyperemia. Physiological arterial hyperemia Physiological arterial hyperemia is adequate to the effect and has an adaptive value. It can be functional and protective-adaptive. 1) Functional. It develops in organs and tissues due to an increase in the level of their functioning (for example, hyperemia in a contracting muscle or in a hard working organ). 2) Protective-adaptive. Develops in the implementation of protective reactions and processes (for example, in the focus of inflammation or around an alien transplant, a zone of necrosis or hemorrhage). In these cases, arterial hyperemia contributes to the delivery of oxygen, metabolic substrates, Ig, phagocytes, lymphocytes, other cells and agents necessary for local protective and regenerative reactions in tissues. Pathological arterial hyperemia Pathological arterial hyperemia is not adequate to the effect, is not associated with a change in the function of the organ or tissue, and plays a disadaptive, damaging role. Pathological hyperemia is accompanied by impaired blood supply, microhemocirculation, transcapillary exchange, sometimes - hemorrhages and bleeding. Examples. Pathological arterial hyperemia of the brain with hypertensive crisis. Pathological arterial hyperemia of various organs and tissues, developing according to the neuromyocarpathy mechanism [eg, in the organs of the abdominal cavity after ascites; In the skin and muscles of the limb after removing the long-lasting bundle; In the zone of chronic inflammation; In a place of long (several hours) exposure to heat - solar, when using a heating pad, mustard plasters; In the region with sympathetic denervation]. The causes of arterial hyperemia can have a different origin and nature. By the nature of the causative factor, arterial hyperemia is distinguished by mechanical, physical, chemical, biological and social genesis. 1. Mechanical (mechanical effect). 2. Physical (very high temperature, electric current, local reduction of atmospheric pressure, when setting the cans). 3. Chemical (organic and inorganic acids, alkalis, alcohols, aldehydes). 4. Biological (physiologically active substances formed in the body: adenosine, acetylcholine, prostacyclin, nitric oxide). 5. Social (emotional stress, stress). By origin, arterial hyperemia is distinguished, the causes of which are endogenous or exogenous factors. -Exogenous. Agents that cause arterial hyperemia affect the organ or tissue from the outside. These include infectious (microorganisms and / or their endo- and exotoxins) and non-infectious factors of various nature. - Endogenous. Factors leading to arterial hyperemia are formed in the body [for example, the deposition of salts and concrements in the tissues of the kidneys, liver, subcutaneous tissue; The formation of excess BAA, causing a decrease in the tone of the GMC arterioles (vasodilation), - adenosine, Pg, kinin; Accumulation of organic acids - lactic, pyruvic, ketoglutaric]. Conditions for the development of arterial hyperemia: 1. The site of the action of the stimulus (artery, surrounding its tissues, the corresponding neural formations); 2. The strength and duration of the action of the stimulus. If its action is adequate, then physiological arterial hyperemia arises. If the irritant is extreme - abnormal arterial hyperemia. 3. The state of individual reactivity of the body, sensitization of the body (the state of the autonomic nervous system). Types of pathological arterial hyperemia according to the mechanism development: 1. Neurotonic or reflex 2. Neuroparalytic 3. Inflammatory arterial hyperemia is due to humoral and reflex mechanisms/ 4. Vakat increase blood flow to the discharged space where the air pressure is reduced/ 5. Postanemic increased blood flow after ischemia/ 6. Postishemic increased blood flow after anemia 7. Collateral arterial hyperemia develops in sudden decrease in blood flow through the main vessel. Mechanisms of occurrence The pathogenesis of all types of pathological arterial hyperemia is the same and differs only in the starting moment. Expansion of the lumen of small arteries and arterioles is achieved due to the realization of neurogenic (neurotonic and neuroparalytic), humoral, neurohumoral and myoparalytic mechanisms or their combination. 1. Neurogenic mechanism. Distinguish between the neurotonic and neuroparalytic varieties of the neurogenic mechanism of arterial hyperemia development. - Neurotonic mechanism. It is in the predominance of the effects of parasympathetic nervous influences (in comparison with sympathetic) on the walls of arterial vessels. - Neuroparalytic mechanism. Characterized by a decrease or absence ("paralysis") of sympathetic nerve effects on the walls of arteries and arterioles. 1) Neuroparalytic arterial hyperemia. Etiology: occurs when the tone of the vasoconstrictor centers and nerves decreases. It is known that the sympathetic vasoconstrictor nerves are tonic (impulse in the state of rest 1-2 IU / sec, which determines the vasomotor component of the vascular tone). In humans and animals, tonic impulsation is inherent in sympathetic nerves, reaching the vessels of the skin of the upper limbs, ears, skeletal muscles, and the food canal. The cutting of these nerves causes a sharp increase in blood flow in each of these organs. This effect is based on the use of periarterial and ganglionic sympathectomy in the treatment of endarteritis, which is accompanied by prolonged vascular spasms. In man in the kidneys, brain, lungs, myocardium and some areas of the skin, the vasoconstrictor nerves under normal conditions do not carry tonic impulses and, thus, the transection of the sympathetic nerves of these organs is not accompanied by arterial hyperemia. Pathogenesis: one of the forms of neuroparalytic arterial hyperemia is hyperemia after previous ischemia, i.e. after the condition of local anemia. In conditions of ischemia, oxygenation of tissues and vessels due to paralysis of the neuromuscular apparatus of the vascular wall is impaired, they lose their tone. If the ischemia stops, the blood begins to flow into this area, but due to the reduced tone of the vasoconstrictors, the arteries sharply expand. Arterial hyperemia of the neuroparalytic type can also be obtained chemically by blocking the transfer of central nervous impulses to the sympathetic ganglia (with the help of ganglion blockers) or at the level of sympathetic nerve endings (with the help of sympatholytic or adrenolytic drugs). The neuroparalytic mechanism of arterial hyperemia partially underlies inflammatory hyperemia, ultraviolet erythema, and others. A classic example of the experimental reproduction of neuroparalytic hyperemia is Claude Bernard's experience, which has received an expansion of the vessels of the rabbit ear after extirpation of the cervical sympathetic nodes. Also, a frosty blush on the cheeks is a manifestation of physiological neuroparalytic arterial hyperemia. Her mechanism is this: with a decrease in skin temperature, her vessels initially undergo a neurogenic spasm. However, when the skin temperature falls below 15 ° C, due to cold paralysis of neuromuscular excitability and conduction, the dermal vessels begin to expand. 2) Neurotonic arterial hyperemia. Etiology and pathogenesis: neurotonic arterial hyperemia can occur both as a result of irritation of the parasympathetic part of the autonomic nervous system, as well as the redistribution of the sympathetic department. It also appears reflexively in connection with the irritation of the extro- and interoreceptors, the vasodilating nerves and centers under the influence of mental, mechanical, temperature factors, chemical and biological agents. This is the case, for example, with a neuroviral infection caused by herpes zoster, when arterial hyperemia arises in the