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Query: UMLS:C1389183 (autodigestion)
 317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal Ileus is Gut Shock caused by Bowel Hypoxia. The morbidity and mortality of Intestinal Ileus has puzzled more than two generations of investigators because they have overlooked the fact that the gas which collects in obstructed small intestine is mostly (90+%) Nitrogen. For some strange reason a gut full of nitrogen has not been looked on as comparable to a lung full of nitrogen, even though the lung and gut have a common embryological origin. My proposal is that intestinal epithelium lining a nitrogen filled lumen becomes as oxygen starved as alveolar lining in a similar circumstance. Bowel hypoxia may be brought about either by failure of the intestine to "breathe out", having breathed in due to mechanical block, or gut paralysis, from any cause, of which one may be failure of blood borne oxygen transport to the bowel, Individually, or together, these may reduce or stop the flow of air and/or aerated intestinal contents along the lumen. Local (bowel) or general underperfusion +/- hypovolaemia +/- anaemia may be a particular cause of paresis or paralysis (aperistalsis) of intestinal muscle. The non-contracting gut then fails to transport the luminal current of fluid and air (oxygen), and adds lumenal to blood-borne oxygen deficiency. The intestinal mucosa utilises oxygen from the current of air churned along the bowel by normal peristalsis to mix with and dissolve in the luminal contents. Should this current be obstructed or the propulsive churning activity cease, oxygen will be "used up", the residual gas become almost entirely nitrogen, and the mucosa must necessarily become oxygen starved and suffocated. Hypoxic mucosa lives in a dangerous environment, at risk of autodigestion by self-produced proteolytic or other enzymes secreted into the lumen by exocrine glands, and it may rapidly become necrotic and gangrenous. Different presentations of Ileus are different degrees of the same Gut Shock due to different levels and durations of tissue hypoxia brought about by different mechanisms with that final common path, complicated by different degrees of autodigestive mucosal destruction, bowel wall oedema, and fluid exudation into the lumen comparable to that through BURNED skin. This idea is new only in so far as it has been put together in this way. Parts have been anticipated by other writers. No new ways of managing ileus are proposed, but it is suggested that existing empirical methods be rationalised and applied more widely and logically.
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PMID:The physiology of intestinal oxygenation and the pathophysiology of intestinal ileus. 355 73

Physiologists have long pondered the riddle of why the stomach is itself not digested by the very juice it secretes. One explanation is that a mucus-bicarbonate barrier, coating the stomach lumen as well as superficial portions of gastric glands, prevents autodigestion. However, this leaves unanswered the question of what protects cells deeper in the glands, which seem to lack a mucus barrier. These are the parietal and chief cells, which secrete acid and pepsin. Using perfused single gastric glands from rabbit, we recently found that intracellular pH is uniquely resistant to extreme degrees of luminal acidification, suggesting that the apical (luminal) barrier might also exclude ammonia and carbon dioxide, to which cell membranes are generally highly permeable. We now show that this is indeed the case. There are three reports of membranes with very low permeabilities to NH3 (refs 5-7), and none of membranes impermeable to CO2.
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PMID:Unusual permeability properties of gastric gland cells. 812 67

Pancreatitis presents clinically as acute and chronic form. A common characteristic of these two forms is enzymatic autodigestion of pancreas in the course of the disease. It results from premature activation of pancreatic digestive enzymes and disturbance of subtle balance between proteolytic enzymes and their inhibitors. The way to understand the character of mechanisms leading to development of pancreatitis has been simplified by discovery of genetic factors, which are able to initiate pathological changes at tissue level. Mutations in the PRSS1 gene (first of all R122H and N29I mutations), which encodes for cationic trypsin, cause trypsin to be protected from autodegradation. These mutations also cause precursor of trypsin - trypsinogen, to be activated easier. On the other hand mutations in the SPINK1 gene have been identified. SPINK1 gene encodes for the most important protease inhibitor of the pancreatic fluid. The most frequent mutation, namely N34S, decrease SPINK1 protein in its activity. The link between the genotype and phenotype is not clear in every case. It is probable that pancreatitis will be recognized as poligenic with many genes engaged in the disease development. Pancreatic cancer is a frequent consequence of pancreatitis. It is a very invasive cancer with high mortality. In the course of pancreatic inflammation intensive cell proliferation takes place for regeneration of pancreas damage. It is the chance for amplification of pathological changes in DNA, which have arisen as a ROS's (Reactive Oxygen Species) and RNOS's (Reactive Nitrogen Oxide Species) action effect. ROS and RNOS are generated in the course of pancreas inflammation.
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PMID:[Hereditary aspects of pancreatitis]. 1313 Jan 70