Digestive System GIT Part 2 PDF

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Summary

This presentation covers the digestive system, focusing on the liver, bile, and pancreas. It details functions, structures, and related processes. The material is suitable for secondary-level biology.

Full Transcript

DIGESTIVE SYSTEM GIT- part 2 LIVER The liver is the largest gland and solid organ in the body, weighting app. 1.8 kg in men and 1.3 kg in women. It holds app. 13% of total blood supply at any given time and has over 500 functions. About 60% of the liv...

DIGESTIVE SYSTEM GIT- part 2 LIVER The liver is the largest gland and solid organ in the body, weighting app. 1.8 kg in men and 1.3 kg in women. It holds app. 13% of total blood supply at any given time and has over 500 functions. About 60% of the liver is made up of liver cells called hepatocytes- a hepatocyte has an average lifespan of 150 days. Liver can regenerate- regeneration can be observed after surgical removal or destruction of a part of a liver. LIVER STRUCTURE LIVER-FUNCTIONS LIVER FAILURE CLINICAL SIGNS OF LIVER FAILURE BILARY AND PANCREATIC DUCTS BILE Bile is a physiological aqueous solution produced and secreted by the liver. Hepatocytes produce bile by secreting conjugated bilirubin, bile salts, cholesterol, phospholipids, proteins, ions and water into their canaliculi (canals between adjacent hepatocytes that join to form bile ducts). Bile travels through a series of ducts joining in the common hepatic duct and flows through this duct into the gallbladder, where it is concentrated and stored. Cholesterol catabolism by hepatocytes results in the synthesis of the 2 major primary bile acids- they are conjugated by the liver with aminoacid taurine or glycine and are known as bile salts. BILE COMPOSITION BILE SECRETION The small ducts connect with interlobular bile ducts, accompanied by branches of the portal vein and hepatic artery, forming portal triads. Bile is subsequently modified by ductular epithelial cells as it passes through the biliary tree-these cells- cholangiocytes- dilute and alkalinize the bile through hormone-regulated absorptive and secretory processes. The cholangiocytes have receptors that modulate the bicarbonate-rich ductular bile flow, which hormones regulate: for secretin, somatostatin, cystic fibrosis transmembrane conductance regulator (CFTR), and chloride-bicarbonate exchanger. Secretin enhances bile flow, hhile bombesin, vasoactive intestinal polypeptide (VIP), acetylcholine, somatostatin, gastrin, insulin, and endothelin inhibit the flow. CONTROL OF BILE SECRETION 1/ secretin stimulates watery alkaline bile secretion from the bile ducts 2/ food in duodenum causes release of CCK ( cholecystokinin)- contraction of gallbladder and flow the bile to the duodenum 3/secretin effectively expands the volume of bile entering the duodenum- by stimulating biliary and pancreatic ductular cells to secrete bicarbonate and water in response to the presence of acid in the duodenum 4/ in the small intestine, bile acids facilitate lipid digestion and absorption; app. 5% of these bile acids are eventually excreted- most bile acids are efficiently reabsorbed from the ileum, secreted into the portal venous system, and returned to the liver through enterohepatic recirculation. GALLSTONES PANCREAS PANCREAS The pancreas has both exocrine and endocrine functions. Acinar cells comprise 75-90% of the gland, and release digestive enzymes into ducts which empty into the duodenum. Pancreatic duct cells secrete fluid and bicarbonate ions, which neutralize the acidity of gastric contents that enter the duodenum. Endocrine cells of pancreas are assembled in islets that are scattered throughout the gland. The pancreas is innervated by sympathetic and parasympathetic nerves. The parasympathetic efferent fibers originate from the dorsal motor nucleus of the vagus (DMV) nerve (located in the brain stem) and activate post-ganglionic neurons. Neurotransmitters such as acetylcholine and peptide hormones modulate pancreatic secretion via changes in parasympathetic activity. PANCREATIC JUICE Pancreatic juice is a transparent isotonic fluid (1-1.5 l/day) The exocrine pancreas secretes throughout 24 hours Rate of secretion: without stimulation-0.2-0.3 ml/min. after stimulation-3 ml/min. pH=8-9- slightly alkaline PANCREATIC JUICE CONTENTS PANCREATIC SECRETION PANCREATIC SECRETION App. 20-25% of the total pancreatic exocrine secretion occurs during the cephalic phase. This phase is initiated by sensory inputs such as sight, smell and tast of food, and long chain fatty acids (but not triglycerides or medium chain fatty acids) with receptors in the oral cavity. The cephalic phase is under the control of the vagus nerve. Sensory inputs arising from anticipation of food are integrated in the dorsal vagal complex (located in the brainstem) and transmitted to the exocrine pancreas via the vagus nerve. PANCREATIC PHASE The gastric phase accounts for app. 10% of pancreatic secretion. It is initiated by entry of food into the stomach where pepsin and gastric lipases catabolize proteins and fats into peptides and triglycerides and fatty acids, respectively, while salivary amylase contributes to the continued digestion of carbohydrates. Peptic digests of proteins are effective in stimulating the intestinal phase. When gastric chyme enters the duodenum, it stimulates the intestinal phase of pancreatic secretion. PANCREATIC SECRETION In the intestinal phase, pancreatic response is regulated primarily by the hormones secretin and CCK, and by neural influences including the enteropancreatic reflex which is mediated by the enteric nervous system and amplifies the pancreatic secretory response. Entry of low pH gastric chyme into the intestine stimulates release of secretin from S cells into the blood. The main action of secretin is to stimulate bicarbonate release from pancreatic duct cells, but it also has a direct effect on acinar cells and potentiates enzyme secretion. CCK stimulates enzyme secretion by both neural and hormonal pathways and is a key physiologic regulator of intestinal phase pancreatic digestive enzyme secretion. PANCREATIC SECRETION CCK stimulates pancreatic secretion by two possible mechanisms: 1/ CCK binds CCK-1 receptors on pancreatic acinar cells and stimulates release of enzymes. 2/ CCK binds CCK-1 receptors on capsaicin-sensitive C-type vagal afferent fibers. Stimulation of vagal afferent nerves generates a signal that is sent to the medial nucleus tractus solitarius (NTS) located in the brain stem and eventually transmitted via cholinergic postganglionic vagal efferent fibers to the pancreas and other target organs. Acetylcholine released from the efferent nerve endings, binds M3 muscarinic receptors on the pancreatic acinar cells and causes release of pancreatic enzymes. ACUTE PANCREATIC DISEASE

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