Increased pleural capillary permeability
Introduction
Introduction In view of the fact that the two main components of pathogenic microorganisms, namely white blood cells and antibodies, are transported by blood, the three changes in hemodynamic changes, increased vascular permeability and leukocyte exudation are evident in acute inflammation. As a result, protein-rich exudates, fibrin, and leukocytes accumulate in the extravascular space at the site of injury. This is the main feature of acute inflammatory histopathology.
Cause
Cause
Causes of increased pleural capillary permeability
Maintenance of microcirculatory vascular permeability depends primarily on the integrity of endothelial cells. During inflammation, the following mechanisms can cause an increase in vascular permeability.
1. Endothelial cell contraction After the binding of histamine, bradykinin and other inflammatory mediators to endothelial cell receptors, endothelial cell contraction can be rapidly induced, resulting in the formation of a gap of about 0.5 to 1.0 m wide between endothelial cells. Since these inflammatory mediators have a short half-life of only 15 to 30 minutes, this response is called an immediate transient response. This reaction only involves venules of 20 to 60 m caliber, while the arterioles and capillaries are not involved. Antihistamines can inhibit this reaction.
2. Direct endothelial injury: severe stimuli such as severe burns and pyogenic infections can directly cause endothelial cell damage, causing necrosis and shedding. Increased vascular permeability occurs rapidly and persists for several hours to several days at high levels until a thrombus forms in the damaged vessel. This process is called an immediate-sustained response. Microcirculatory vessels at the level of arterioles, capillaries, and venules can be affected.
Light and moderate thermal damage, X-ray and UV damage, and direct damage to endothelial cells caused by certain bacterial toxins occur later, often after 2 to 12 hours, but can last for hours to days, called late Delayed prolonged response. This reaction only involves the capillaries and venules.
3. Leukocyte-mediated endothelial damage: In the early stages of inflammation, leukocytes adhere to the wall and adhere to endothelial cells, causing activation of leukocytes, releasing active oxygen metabolites and proteolytic enzymes. The latter can cause damage or shedding of endothelial cells and increase vascular permeability.
4. The high permeability of the new capillary wall The new capillary bud formed during the repair process, the endothelial cell junction development is immature, which can explain the liquid extravasation and edema in the re-inflammation.
Examine
an examination
Related inspection
Dynamic electrocardiogram (Holter monitoring) ECG
1 pleural effusion routine, biochemical, culture can determine the nature of the effusion, and found tuberculosis or other pathogenic bacteria.
2 tuberculin test and tuberculosis antibody positive for the diagnosis of tuberculous pleurisy.
3 blood routine examination white blood cell count can be normal or increased, ESR often accelerates.
Diagnosis
Differential diagnosis
Differential diagnosis of increased pleural capillary permeability:
Excessive exudate can affect organ function and oppress adjacent organs. For example, accumulation of exudate in the lung can affect ventilation function. Pericardial and pleural effusion can compress heart, lung, severe laryngeal edema can cause asphyxia, etc. Wait. If the cellulosic exudate is not completely absorbed, it will be mechanized. For example, in the lung, the lung meat may be caused to change in the serosal cavity, which may cause serosal adhesion or even serosal cavity atresia.
1 pleural effusion routine, biochemical, culture can determine the nature of the effusion, and found tuberculosis or other pathogenic bacteria.
2 tuberculin test and tuberculosis antibody positive for the diagnosis of tuberculous pleurisy.
3 blood routine examination white blood cell count can be normal or increased, ESR often accelerates.
