Specially from what reason was the sending lung fiber caused? 's general knowledge

Specially from what reason was the sending lung fiber caused? 's general knowledge
Specially from what reason was the sending lung fiber caused?
The cause of disease of this disease has not been bright, the quality among the disseminated lung fiber is limited to the lung. Hamman and Rich reported several at first in 1935 and 1944 respectively, it was acute type, developed sharply, die from 6 weeks to half a year, so have another name called Hamman-Rich syndrome. This disease have illness coming on at 40-50 years old more, men exceed women slightly, spread all over disease in whole world, morbidity and case fatality rate are all raised in the past 10 years, the overwhelming majority is chronic type, the higher age of onset is, the longer the course of disease is. Acute type and rare. Most scholars think department's one's own immune disease, may relate to inherent cause in recent years.
IPF cause of disease is not clear, mechanism has not also totally expounded the onset, but already enough evidences have indicated to relate to the fact that immune inflammation has been damaged. The inflammatory response characteristic of immunity that different samples reveal is not the same, what the blood around reflected is that immunity is unusual more outstanding, and the bronchus alveolus irritates lotion to reveal inflammation reacts for the main fact, and the abnormal state of lung local organization is different to some extent. So it studies materials to need to consider this kind of difference to assess various.
Synthesize the research in recent years, have illness coming on about IPF mechanism and course summarize as follows:
A certain unknown antigen activates B cells, produce Ig and and form the immune complex, and then stimulate and activate alveolus macrophages. This immunoreaction is some in the lung, if alveolus wall B lymphocytes produced antibodies, then some compositions of the alveolus wall may be discerned as foreign matter wrongly. So someone thinks IPF can be regarded as one's own immune disease. But change and function of IPF patient T cells are indeterminate, only B cells are participated in not enough to prove it as one's own immune disease.
Activatory alveolus macrophages release many kinds of mediums, damage structure such as the ground substance, basilar membrane of lung cells, cells directly except protein hydrolase, collagenase, reactive oxygen supersession product and some cell factors, still there is medium including fiber that is formed and closely related with with the fiber that connects albumens (fibronectin, FN) , the original growth factor (alveolar macrophage derived growth factor, AMDGF) of macrophage of alveolus , the blood platelet derives growth factor (platelet derivedgrowth factor, PDGF) With one kind of growth factors(insulinlike growth factor, IGF) of insulin Wait, they can absorb into fibrous cells, and stimulate its hyperplasia, and lie between and lead the collagenic ground substance to shrink.
IL-8, TNF,etc. released in alveolus macrophages lie between, lead, lay neutral cells to hasten and melt, assemble and activate towards the alveolus, form and increase by neutral grains of cell rate (20%) It is alveolus inflammation of the characteristic, and neutral grains of cell inflammation react and release a series of medium again, cause or aggravate the lung to damage with the fiber.
Become hyperplasia of fibrous cell and produce important link and result that the glue was a disease. Normal people become fibrous cell grow have accurate adjustment, the intersection of prostaglandin and E2 for instance, become fibrous cell move, inhibit factor,etc. from belong to and shoulder and regulate the factor. In addition find a kind of C-sis gene which encodes PDGF in IPF, very similar to shifting virus cancer genetic V-sis. So emergence of IPF represent, succeed fibrous defeat of cell regulate, fail, or become fibrous cell " Tumour " Hyperplasia is a question very full of interest. Though someone finds the aggregate velocity or total amount that the quality is collagenic has not increased among IPF patient's lung, but type increase collagen, type rise rate when collagen is getting more collagenic for 2 type. Because type glue is to be high in every one for tension intensity, low to last sex, last one that arrange parallelly to cross by fibers belt, increasing shape and physiology sufficient to explain IPF to change of it, and no matter the collagenic total amount increases or not.
It is mainly alveolus inflammation that IPF early or acute issues of pathology change. It it is obvious on alveolus on wall and among lymphocyte, plasma cell, monocyte at quality, organize cell and a few grains of cells neutral acid not to be soaked. The alveolus needn't be involved, but there can be cells and the fibrin too to ooze out, include Model 2 alveolus cell and macrophage that is lossed. There can be albuminoid hyperplasia of network, but still little fibers in the interval of alveolus. As disease is developed, the inflammatory cell is oozed out and soaked and reduced gradually, become fibrous cell and collagenous thread hyperplasia, it increase alveolus wall thick,type alveolus cell reduce,Model 2 alveolus cell hyperplasia, there are out of shape and not destroying in structure on alveolus, and can involve alveolus managing and thin bronchus. Appear person who fill the air later stage the intersection of lung and fiber take, angry Out of shape, expand into a bag, the size is from 1cm to count cm, " honeycomb lung " called . The intersection of disease and alveolus - the intersection of capillary and membrane this can have unsymmetry or lean towards the disposition to increase thick, the lung capillary bed is reduced. But there is not vascular inflammation of artery or swollen pathological change of the granulation on IPF pathology; Have their, quality pulmonary tuberculosis when should consider desmosis or other.
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