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Stomach and Duodenum Anatomy, Histology and Physiology I

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STOMACH AND DUODENUM ANATOMY, HISTOLOGY AND PHYSIOLOGY I. Anatomy and histology II. Functions of the stomach III. Review of gastric secretion IV. Tests of gastric acid secretion (gastric analysis) V. Abnormalities of gastric acid secretion VI. Gastric mucosal defense factors VII. Antibacterial function VIII. Pepsinogen secretion IX. Vitamin B12 physiology X. Ghrelin physiology XI. Gastric Motility I. Anatomy and Histology Stomach: The four anatomical regions of the stomach are the cardia, fundus, body and antrum. The mucosa of each of these regions contains gastric pits into which several types of mucosal glands empty. Cardiac glands are lined by mucous cells, which secrete mucus and small amounts of pepsinogen. Oxyntic glands are found in the fundus and body of the stomach. These glands contain a variety of cell types including mucous cells, parietal cells, chief cells, endocrine cells and enterochromaffin-like (ECL) cells. The gastric antrum contains pyloric glands composed of mucous and endocrine cells, especially G cells which produce gastrin and D cells which produce somatostatin. Table 1 lists the major cell types in the stomach, their respective products, and their functions. Table 1: Review of the Cell Types in the Stomach Cell Type Product Function Hydrochloric acid Kill enteric pathogens; Parietal cell facilitate activity of pepsin Intrinsic factor Cobalamin absorption Chief cell Pepsinogen I Digest protein Mucous cells Pepsinogen I and II Digest protein Stimulate ECL cell G Gastrin Stimulate parietal cell D Somatostatin Endogenous "brake" ECL Histamine Stimulate parietal cell Pylorus: tubular structure separating the stomach from the duodenum and containing the circular muscle-pyloric sphincter. Duodenum: The duodenal mucosa is characterized by the presence of Brunner’s glands, an important source of bicarbonate. These glands are located primarily in the submucosa. Vascular Supply: The stomach and duodenum are furnished with blood from branches of the celiac artery trunk. This trunk can give rise to the common hepatic, left gastric, splenic artery, and the gastroduodenal artery. This generous blood supply explains why vascular insufficiency syndromes of the stomach are rare. Venous drainage follows the arterial system and empties into the portal vein, splenic or superior mesenteric veins. Lymphatic drainage is primarily into the celiac nodes. Innervation: Sympathetic innervation is from fibers derived from the thoracic area T6 to T8. Parasympathetic innervation is primarily via branches of the vagus nerve, which play important roles in gastric acid secretion, gastrin release and gastric motility. Vagal afferent fibers are important in several gastric reflexes. The stomach is also innervated by the intrinsic enteric nervous system, with cell bodies found in Meissner’s and Auerbach’s plexus. II. Functions of the Stomach The anatomy and histology of the stomach combine to partially digest food prior to passage into the small intestine. The digestive process requires the integration of two functions: motility and secretion. Gastric motility can be divided into 3 categories that are region specific: receptive relaxation of the fundus, peristalsis of the body and antrum and antro-pyloric peristalsis. These 3 functions store the food, triturate (grind) it and empty the resulting chime into the small intestine in a coordinated manner. The interstitial cells of Cajal(ICC) are the gastric pacemakers and responsible for the generation of slow waves of the stomach. The pacemaker potentials originate from a site from an area in the greater curve in an area between the fundus and body. The stomach secretes numerous compounds that are responsible for digestion and regulation. The proximal stomach where oxyntic(parietal) cells are located secretes gastric acid whereas the pyloric gland area in the antrum acts as an endocrine organ releasing gastrin (to stimulate acid secretion) and somatostatin (a feedback inhibitor) to reduce acid secretion.. Additional functions of the stomach include facilitation of cobalamin (vitamin B12) absorption via intrinsic factor secretion, initiation of protein digestion (via pepsinogen secretion and pH-dependent peptic activity) and an antimicrobial function protecting against ingested pathogens (via the acidity of gastric juice). Ghrelin produced by endocrine cells of the gastric fundus and other hormones and neurotransmitters are involved in the regulation of hunger and satiety. III. Review of Gastric Secretion Gastric acid secretion is the result of paracrine, neural, intracellular and hormonal regulatory pathways. Gastric juice is a combination of parietal (hydrochloric acid) and non-parietal secretions. Parietal cells secrete pure hydrochloric acid at a concentration of 150-160 mmol/L. The volume secreted by parietal cells is determined by the number of actively-secreting cells and also varies according to food intake (low with fasting; high after meals). Non-parietal secretions + - + include water, electrolytes such as Na and HCO3 (but not H ), and mucus. The overall volume of gastric juice produced during any given period is determined by the relative proportions of parietal and non-parietal secretions and is roughly 2.5 L/day. The acidity (hydrogen ion concentration) of gastric juice depends on the relative proportions of parietal and non-parietal secretions. The basolateral membrane of the parietal cell has receptors for three stimulatory ligands: a histamine (H2) receptor (for histamine released by ECL cells), a muscarinic (M3) cholinergic receptor (for acetylcholine released from postganglionic neurons), and a cholecystokinin B (CCK-B) receptor for gastrin (released from pyloric and duodenal G cells) (Figure 1). Thus the parietal cell responds to paracrine, neurocrine and endocrine stimuli. The parietal cell also appears to have basolateral receptors for inhibitors of its function: somatostatin and prostaglandins (Figure 1). Figure 1: Model of gastric acid secretion by the parietal cell: Histamine is the most important stimulant of acid secretion. Released from ECL cells in the lamina propria, histamine interacts in a paracrine manner with local parietal cell histamine H2 receptors to increase acid secretion (Figure 1). There is also recent evidence that histamine may also act through H3 receptors on D cells to suppress the release of somatostatin thereby further augmenting acid secretion. Acetylcholine is released from postganglionic nerve endings as the final result of vagal nerve stimulation to interact with muscarinic M3 receptors located on a variety of cells in the stomach. This neurocrine/cholinergic action directly stimulates parietal cells and also stimulates the local release of histamine from ECL cells. Vagal activity also stimulates G cells to release gastrin, and suppresses the release of inhibitory somatostatin from D cells. Gastrin is a true hormone released into the bloodstream from G cells in the gastric antrum. Stimulation above basal levels results from the presence of food (particularly amino acids) in the gastric lumen as well as from vagal activity. There is still some controversy regarding how gastrin stimulates acid secretion in humans. Although gastrin binds directly to CCK-B (gastrin) receptors on the parietal cell basolateral surface, this action is likely to predominantly affect parietal cell proliferation and to be less important in mediating acid secretion than is its action on similar receptors located on ECL cells resulting in histamine release. Thus, gastrin's secretory effects on parietal cell acid production are probably mediated primarily through histamine release from ECL cells. Somatostatin, an inhibitor of parietal cell function, plays an important role in modulating gastrin release. The proximity of D and G cells in the gastric antrum suggests that somatostatin serves a paracrine function as an endogenous "brake" on gastrin release. Hydrogen ions in the gastric lumen "turn on" D cells to assist in the feedback inhibition of gastrin release by acid. Animal studies have also shown that acetylcholine, released via vagal stimulation, "turns off" D cells, thereby enhancing gastrin release providing an additional indirect means by which acetylcholine promotes acid secretion. Cholinergic release of gastrin does not appear to occur in humans. Cholecystokinin (CCK) is released into the blood from duodenal and jejunal I cells in response to diet-derived amino acids and fatty acids. CCK acts on both CCK-1 and -2 receptors, but the former effect is more prominent at physiological concentrations, with the net effect on the stomach to inhibit acid secretion, mediated through stimulation of somatostatin released from D cells. Prostaglandins are secreted by virtually every epithelial and non-epithelial cell in the stomach. The major prostaglandins produced by the human stomach are PGE2, PGF2α and PGI2 (prostacyclin). A receptor for PGE2 linked to an inhibitory G protein has been demonstrated on the parietal cell. Parietal cell PGE2 receptors have effects opposite to those of H2-receptors, i.e., they reduce adenylate cyclase activity, lower intracellular cyclic AMP (c-AMP) levels and protein kinase A activity thereby inhibiting acid production. Prostaglandin E analogs, such as misoprostol, reduce acid secretion. Parietal cell stimulation and inhibition. Following binding of a ligand to its receptor on the parietal cell, a second intracellular messenger is produced. For acetylcholine, this messenger is calcium, which is probably produced by hydrolysis of inositol
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