- •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. Disturbances of the peripheral blood circulation
13.1. Name the main forms of the local disturbances of blood circulation:
Arterial hyperemia, venous hyperemia, ischemia, stasis, thrombosis and embolism.
13.2. What is arterial hyperemia?
Arterial hyperemia is an increasing of blood filling of some organ or a tissue due to superfluous receipt of blood on arterial vessels.
13.3. What functional changes and clinical attributes characterize arterial hyperemia?
During arterial hyperemia the expansion of small arteries, arterioles, veins and capillaries are observed; acceleration of the blood flow in them, the pulsation of fine arteries and capillaries, increase in number of vessels seen by an eye, increase in pressure in arterioles, capillaries and veins. As a result of the specified changes there is a diffuse redness, the local temperature raises, the volume of hyperemic site increases, turgor of tissue raises, increases the metabolism and functions of organ.
13.4. What factors can be a cause of arterial hyperemia? What mean the physiological and pathological arterial hyperemia?
The reason of arterial hyperemia can be influence of physical, chemical and biological factors of an environment; increase of loading on organ or the part of tissue; psychogenic influences.
Physiological arterial hyperemia arises as a result of influences of usual physiological matters (such like increasing the load on organ, psychogenic influences). Its main types are working and reactive hyperemia.
The working hyperemia is the increasing of blood flow in the body during amplification of its function (increasing of coronal blood flow in case of amplification of work of heart, hyperemia of salivary glands at reception of food, etc.).
Reactive hyperemia represents increase of blood flow after its short-term restriction. It develops usually in kidneys, brain, skin, intestines and muscles.
Pathological arterial hyperemia arises as a result of action of the unusual (pathological) factors or as a result of increase of sensitivity of vessels to usual influences. It accompanies with development of such pathological processes, as an inflammation, an allergy, burns, a fever. Its clinical examples can be an infectious or allergic spots, reddening of the skin at many infectious diseases (measles, a scarlet fever, a typhus), reddening of half of face at a neuralgia of a trigeminal nerve, etc.
13.5. Name the main mechanisms of the pathological arterial hyperemia development.
Two mechanisms are distinguished: neurogenic and myoparalytic - mechanism which is connected with activity of local chemical (metabolic) factors.
Depending on concrete mechanisms of development neurogenic arterial hyperemia can be of such types: neurotonic and neuroparalytic.
Myoparalytic (metabolic) arterial hyperemia caused by decreasing of contractile properties of smooth muscles of vessels as a result of influence of chemical agents.
13.6. What is the essence of the neurotonic mechanism of development of the arterial hyperemia ?
The neurotonic type of arterial hyperemia develops at increase of pulsation on vasodilating nerves (vasodilators), - such like parasympathetic nerves and sympathetic cholinergic nerves, which mediator is acetylcholine.
In experiment on animals this type of arterial hyperemia is reproduced by irritation of vasodilating nerves. So, irritation of chorda tympani (the branch of n. facialis) causes arterial hyperemia and amplification of submandibular salivary gland secretion (K. Bernara's experiment).
In clinic neurotonic hyperemia arises more often as a reflex at irritation of extra- and intra-receptors, and also at irritation of vasodilating nerves and their centers. In particular it can explain the reddening of the face and neck in case of progress of pathological processes in internal organs (ovaries, heart, and a liver).