Peptic cell

Figure 3-14. Mean SEM number of labeled parietal cells found among 5,000 cells examined in mouse gastric mucosa after the last injection of tritiated thymidine. The difference between control mice injected with saline and those injected with gastrin solution is significant, except for the day immediately following cessation of thymidine injection. (From Willems G, Lehy T. Radioautographic and quantitative studies on parietal and peptic cell kinetics In the mouse. Gastroenterology 69 416-426, 1975.)...

When Boris Babkin himself reviewed the subject in 1950, he concluded that there was no proof that the sympathetic nervous system has any direct effect upon parietal or peptic cells any inhibition is probably the result of vasoconstriction." On the other hand, Babkin thought that sympathetic stimulation causes some as yet unidentified cells to secrete mucus. That opinion was based on work his student Stewart Baxter had done in 1934. In acute experiments in dogs and cats, Baxter has found that prolonged stimulation of newly severed splanchnic nerves resulted in secretion of a small amount of alkaline mucus having only low peptic power. Secretion was not abolished by atropine, and the pyloric glands seemed to be the chief source of the secretion. Baxter found paralytic secretion of mucus in two eso-phagostomized cats with gastric fistulas whose splanchnic nerves he had severed earlier." " ... 

Willems G, Lehy T. Radioautographic and quantitative studies on parietal and peptic cell kinetics in the mouse. Gastroenterology 69 416-426, 1975. 

These latter synthesize ptyalin, an endoamylase which is also an a-amy-lase. When we come to the gastric mucosa, besides mucous cells we find present parietal cells specialized for the secretion of hydrochloric acid by a mechanism of active transport, and peptic cells which can synthesize pepsinogen, from which an endopeptidase, pepsin, is formed. 

Protein digestion starts in the stomach where the acid secreted by the oxyntic cells both assists the denaturation of the proteins and activates the pepsinogen secreted by the peptic cells by removing about 20% of the molecule. Activation is autocatalytic exposure to the very low pH of the stomach contents also provides optimum conditions for the activity of the enzyme. Pepsin is not very specific but is most active with respect to bonds in which an aromatic amino acid... 

The cells of the gastric fundic epithelium that appear clinically relevant are the surface epithelial cells, the neck cells, the parietal and chief cells, and the endocrine cells, mainly the ECL and D cells. In the antrum, there are the surface cells, the neck and gland cells, the D and G cells, and a chief cell that secretes a different isoform of pepsinogen. The neck region of the glands contains the progenitor cells for the surface, parietal, and peptic cells. 

Amylase enters the blood largely via the lymphatics. An increase in hydrostatic pressure in the pancreatic ducts leads to a fairly prompt rise in the amylase concentration of the blood. Neither an increase in volume flow of pancreatic juice nor stimulation of pancreatic enzyme production will cause an increase in senm enzyme concentration. Elevation of intraductal pressure is the important determinant. Stimulation of flow in the face of obstruction can, however, augment the entry of amylase into the blood, as can disruption of acinar cells and ducts. A functional pancreas must be present for the serum amylase to rise. Serum amylase determination is indicated in acute pancreatitis in patients with acute abdominal pain where the clinical findings are not typical of other diseases such as appendicitis, cholecystitis, peptic ulcer, vascular disease or intestinal obstruction. In acute pancreatitis, the serum amylase starts to rise within a few hours simultaneously with the onset of symptoms and remains elevated for 2 to 3 days after which it returns to normal. The peak level is reached within 24 hours. Absence of increase in serum amylase in first 24 hours after the onset of symptoms is evidence against a diagnosis of acute pancreatitis (76). 

Prostaglandins, one of the most important epithelial growth factors, inhibit gastric acid secretion and have numerous mucosal protective effects, the most important of which include the stimulation of both mucus and phospholipid production, promotion of bicarbonate secretion, and increased mucosal cell turnover. Damage to the mucosal defense system is the primary method by which HP or NSAIDs cause peptic ulcers. 

There are certain histologic subtypes of diffuse, aggressive NHL that respond less well to treatment with conventional regimens such as CHOP. Burkitt s lymphoma, lymphoblastic lymphoma, mantel cell lymphoma, and primary CNS lymphoma are examples of disease that benefit from more intensive therapy. Regimens such as hyper-CVAD, which alternate cycles of hyperfractionated cyclophosphamide, doxorubicin, vincristine, and dexamethasone with high-dose cytarabine and methotrexate, often are substituted for CHOP. Intrathecal therapy with methotrexate is indicated with documented CNS infiltration of tumor or involvement of the sinuses. The recent appreciation of the etiology of Helicobacter pylori in the etiology of peptic ulcer disease and the association between colonization and mucosal-associated lymphoma (MALT) has spurred... 

The anti-ulcer agents omeprazole, lanzoprazole, and pantoprazole have been introduced during the past decade for the treatment of peptic ulcers. Gastric acid secretion is efficiently reduced by prazole inhibition of H+K+-ATPase in the parietal cells of the gastrointestinal mucosa [75]. The prazoles themselves are not active inhibitors of the enzyme, but are transformed to cyclic sulfenamides in the intracellular acidic compartment of parietal cells [76]. The active inhibitors are permanent cations at pH < 4, with limited possibilities of leaving the parietal cells, and thus are retained and activated at the site of action. In the neutral body compartments the prazoles are stable, and only trace amounts are converted to the active drugs. (For a review on omeprazole, see Ref. [77].)... 

Alterations in mucosal defense induced by HP or NSAIDs are the most important cofactors in peptic ulcer formation. Mucosal defense and repair mechanisms include mucus and bicarbonate secretion, intrinsic epithelial cell defense, and mucosal blood flow. Maintenance of mucosal integrity and repair is mediated by endogenous prostaglandin production. 

Prostaglandins inhibit the secretion of protons by the parietal cells in the stomach, which is normally increased in response to food and the hormone gastrin. Consequently, inhibition of prostaglandin synthesis by aspirin or other similar drugs results in increased secretion of protons by the stomach, which can result in considerable gastric discomfort and can, if chronic, lead to the development of a peptic ulcer. Consequently, there is some conflict between the use of such inhibitors to relieve chronic pain (see below), in diseases such as arthritis, and the risk of development of ulcers. 

Decubitus ulcer (e.g. bed sores, pressure sores) Diabetic ulcers Varicose ulcers Rodent ulcers Peptic ulcers Ulcer due to continuous pressure exerted on a particular area of skin often associated with bed-ridden patients Ulcers (e.g. diabetic leg ) caused by complications of diabetes Due to defective circulation, sometimes associated with varicose veins An ulcerous cancer (basal cell carcinoma), usually affecting the face Ulcer of the digestive tract, caused by digestion of the mucosa by acid and pepsin may occur in e.g. the duodenum (duodenal ulcer), or the stomach (gastric ulcer)... 

Physiologically, body stores are maintained by extracting approximately 10% of the iron provided in a balanced diet and this corresponds to 1.5 mg each day for males and slightly more for females to compensate for pregnancy and menses. The trace element is derived from food by peptic digestion and after reduction the ferrous form crosses the enterocyte to be released at the serosal pole via the ferroportin-hepcidin mechanism to be transported, by plasma transferrin, to developing red cells in the marrow for haemoglobin synthesis. At the end of their life span effete erythrocytes are removed by the reticuloendothelial system in the spleen, bone marrow and the liver. 

Large doses of glucocorticoids have been associated with the development of peptic ulcer, possibly by suppressing the local immune response against Helicobacter pylori. They also promote fat redistribution in the body, with increase of visceral, facial, nuchal, and supraclavicular fat, and they appear to antagonize the effect of vitamin D on calcium absorption. The glucocorticoids also have important effects on the hematopoietic system. In addition to their effects on leukocytes, they increase the number of platelets and red blood cells. 

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