- •13. Disturbances of the peripheral blood circulation
- •13.1. Name the main forms of the local disturbances of blood circulation:
- •13.2. What is arterial hyperemia?
- •13.3. What functional changes and clinical attributes characterize arterial hyperemia?
- •13.4. What factors can be a cause of arterial hyperemia? What mean the physiological and pathological arterial hyperemia?
- •13.5. Name the main mechanisms of the pathological arterial hyperemia development.
- •13.6. What is the essence of the neurotonic mechanism of development of the arterial hyperemia ?
- •13.7. Explain the neuroparalytic mechanism of development of the arterial hyperemia.
- •13.8. What humoral factors can be the cause of development of arterial hyperemia?
- •13.9. What is the role of endothelium of blood vessels in development of arterial hyperemia?
- •13.10. Name possible outcomes of arterial hyperemia.
- •13.11. What is venous hyperemia?
- •13.12. What factors can be the cause of venous hyperemia?
- •13.13. What attributes display venous hyperemia?
- •13.14. What local and common violations can be consequence of venous hyperemia?
- •13.15. What is ischemia?
- •13.16. What attributes are typical for ischemia?
- •13.17. Name the main types of ischemia depending on the reason and mechanisms of its occurrence.
- •13.18. How are defined the character of metabolic, functional and structural disturbances in a tissue in case of its ischemia?
- •13.19. What consecutive stages characterize the pathogenesis of alterations in ischemic tissues?
- •13.20. What is stasis?
- •13.21. Name the main variants of stasis and their reasons.
- •13.22. What is the thrombosis?
- •13.23. Name three major factors, promoting thrombosis formation (Virhov’s triad).
- •13.24. What phases is the process of blood clot forming consists of? What is their essence?
- •13.25. What negative consequences can thrombosis formation in pathology have?
- •13.26. What is embolism?
- •13.27. What kinds of embolism are assigned?
- •13.28. Name principal causes of embolism exogenous.
- •13.29. Name the principal causes of embolism of endogenous origins.
- •13.31. What is the essence of a phenomenon called "sludge"?
- •13.32. How the exchange of water between plasma of blood and an interstitial liquid is carried out?
- •13.33. How does hydrostatic and oncotic pressure of blood and an intercellular liquid changes influence on intensity of processes of a filtration-reabsorption of water in capillaries?
- •13.34. What is the insufficiency of lymphokinesia? Name its main forms.
13.17. Name the main types of ischemia depending on the reason and mechanisms of its occurrence.
The main types of ischemia are compressive, obturation and angiospastic.
The compressive ischemia arises as a result of squeezing of arteries by the outside ligature, cicatrix, a tumour, an alien body, etc.
The obturation ischemia is consequence of partial narrowing or full closing of arteries by atherosclerotic plaque, a blood clot or embolus.
The angiospastic ischemia arises owing to the spasm of arteries caused by emotional influence (fear, excitement, anger), physical factors (a cold, a trauma, mechanical irritation), chemical agents, biological irritants (toxins of bacteria), etc. The spasm can be initiated by nervous reflex mechanisms or direct action of different matters on smooth muscles of vessels (influence of vasopressin, angiotensin II, endothelin).
13.18. How are defined the character of metabolic, functional and structural disturbances in a tissue in case of its ischemia?
Character of such disturbances is defined by a degree of oxygen starvation. And the degree of the hypoxia, depends on speed of development, type of ischemia, its duration, localization, character of collateral blood circulations, the functional state of the organ or tissue.
Ischemia arises on the area of full of obturation or a compression of arteries, with other things being equal causes heavier changes, than at a spasm. The rapid ischemia, as well as long, proceeds more hard in comparison with witch has an insidious onset or short.
The ischemia of the vital important organs (brain, heart) has heavier consequences, than ischemia of kidneys, lungs, spleen, and ischemia of the last - heavier in comparison with the ischemia of skeletal muscles, bone or cartilaginous tissues. The brain and heart are characterized by a high level of a power exchange, but, despite of it, its collateral vessels functionally are not capable to compensate violation of blood circulation. On the contrary, skeletal muscles and especially connecting tissue, due to a low level of power exchange in them, are steadier in states of ischemia.
The difficulty of inflow of arterial blood at the raised functional activity of organ or a tissue is more dangerous, than in a condition of rest.
13.19. What consecutive stages characterize the pathogenesis of alterations in ischemic tissues?
The following stages of pathogenesis are assigned.
I. Violations of energy metabolism. They are shown by decrease in efficiency of pentose cycle and tissue breath, activation of glycolysis, and finally is reduction of the contents in cells of the macroergic compounds (phosphocreatine and ATP). Violation of formation of energy on a site of an ischemia is connected to insufficient delivery of oxygen and substrates necessary for oxidation, decrease in activity and synthesis of enzymes, an output of enzymes from the damaged cells, dissociation of oxidation and phosphorylation.
II. Violation of energy-dependent processes in the cells, caused by reduction of energy producing. Thus specific functions of cells (contractile, secretory, etc.), mechanisms of active transport of substances, in particular, work of ionic pumps are broken; biosynthesis of fibers of non-collagen type participating in the structural organization of cells and tissues goes down. Finally, develops damage of cells and necrobiotic changes which in the heaviest cases lead to formation of the necrosis of tissues - a heart attack.
III. Amplification of biosynthesis of components of a connecting tissue - collagen, glycosaminoglycans, glycoproteins, being a basis for the subsequent sclerosis of an ischemic site of a tissue or organ.