Disturbances in interstitial fluid amount
Interstitial fluid is located in the intercellular substance. The amount of interstitial fluid is controlled by neurohumoral system (aldosterone and pituitary antidiuretic hormone). It depends on the state of blood and lymph circulation as well as the level of vascular-tissue permeability.
Disturbances in interstitial fluid amount may be of the following types: increase (edema) and reduction (dehydration, exicosis).
Increase in interstitial fluid amount. Edema when transudate (which contains not more than 2% of protein) accumulates in the tissues or the cavities of the body. If transudate accumulates in subcutaneous fat it is called anasarca, in the heart cavity hydroperi-cardium, in the pleural cavity hydrothorax, in the abdominal cavity ascites, in the testis hydrocele. Edemas develop in the patients with cardiovascular, kidneys, liver, allergic diseases, infections, pathologic conditions of pregnancy (hestosis), in vein thrombosis, lymph congestion, disturbances of nervous trophism, etc. In these diseases, the following changes are observed: 1) those in hydrostatic blood pressure,
2) those in colloid osmotic pressure of blood plasma,
3) vascular wall permeability increases, 4) retention of water and electrolytes.
These factors accompany each other in the majority of cases, but as a rule one of them prevails, e.g. mechanical or congestive edema develops as a
result of increase in hydrostatic pressure in micro-vessels and in fluid filtration.
Oncotic edema results from reduction in colloid-osmotic pressure in the blood plasma. Membranogenic edema is associated with the increase in capillary permeability which results in plasma protein exit and its accumulation in the tissues. Electrolyte edema results from retention of water and electrolytes. Lymphogenic edema is caused by lymph congestion. According to the disease responsible for the edema and its cause, it can be:
1. Congestive (in thrombophlebitis, vein compression, lymphostasis). Most frequently edema is local. This is due to venous congestion resulting in increase in venous pressure, hypoxia, damage of endothelium and basement membranes of the capillaries, increase in vascular permeability, transudation of some amount of blood to the tissue.
2. Cardiac (in cardiac decompensation). This case edema is characterized by combination of pathogenesis of congestive edema as well as accompanying blood redistribution, increase in aldosterone secretion and reduction in its destruction by the liver. Aldosterone is known to retain Na and water resulting in edema.
3. Hepatic. The pathogenesis consists of oncotic factor and Na retention.
4. Degenerative. Protein deficiency. Hypo-proteinemia develops and oncotic blood pressure reduces.
5. Inflammatory edema develops in the focus of inflammation where vascular permeability increases.
The outcome of edema is favorable, the fluid resolves, but prolonged edema can result in degeneration, atrophy, sclerosis.
Reduction in interstitial fluid amount (exicosis) may occur in rapid loss of great amount of fluid (cholera, prolonged diarrhea).
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