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GI System GI Physiology Functions: - Ingestion - Mastication - Deglutition - Digestion (chemical and mechanical) - Absorption - Elimination Histology of Wall of GI Tract Five Layers (from outside to in) 1- Serrosa Layer – protects from outside structures. protects tube from ‘nasty’ stuff around it 2-Muscularis Layer – divided into two distinct layers 2A- Longitudinally Oriented Muscle Fiber (parallel to the length of the tract) - shorten the tract when it contracts 3A- Circular Muscle Fibers - segment the tract 4- Submucosa Layer- involved with absorption and secretion and is well supplied with blood vessels 5- Mucosal Layer - secretion of mucus along ENTIRE tract - lubricate Organs and structure in GI tract are divided into: 1- Tract Organs – mouth, stomach, small intestine, large intestine, sigmoid canal, anus 2- Structures vs. Accessory Organs – liver, gallbladder, pancreas, salivary glands The sections of tract are isolated from eachother by IMPORTANT sphincters Sphincters – two way flow Upper Esophageal Sphincter – near the proximal area of the esophagus Lower Esophageal Sphincter - cardiac or lower esophageal sphincter Pyloric Sphincter – between distal end of stomach and duodenum Ilioseco Valve - between the end of the small intestine and the beginning of the large intestin - strongest valve – resists a lot of pressure developed in the colon GI Muscle (Will come back to this later) - smooth muscle: large amount of this in the GI tract - Hypopolarized (closer to threshold) by: - stretch of the muscle - takes place everytime you put something into the tract - anytime you distend the tract, the muscle tends to become active - leads it toward depolarize - the parasympathetic division – increases GI activity (opposite of cardiac) - certain hormones – gastrin being one of them - Hyperpolarized (further from threshold) by: - Norepinephrine or Epinephrine - stimulation by nerves within the GI tract Enteric Nervous System - specialized group of neurons within the wall of the GI tract from the esophagus all the way to the anus Two Layers of Neurons: 1- Myenteric Plexus (Auerback’s Plexus) - located between the longitudinal and circular muscle fibers in the wall of the GI tract - becomes active GI tract movement - innervates those muscles 2- Submucosal Layer (Meissner’s Plexus) - submucosal plexus of nerve fibers located in the submucosal layer of the GI tract - initiating secretory activity and sensory functions in the tract along with some sensory functions ANS Parasympathetic Division - **Except for a few fibers to the mouth and the larynx, cranial parasympathetic fibers are from the Vagus nerve (CNX)** - these fibers provide innervation to the esophagus, stomach, pancreas, first half of the large intestine, and a very small segment of the small intestine Sacral Parasympathetic Nerves - are from S2, S3, S4 to the gut - supply the distal half of the large intestine Including: - sigmoid colon - rectal regions - anal regions -Parasympathetic Innervation INCREASE GI activity The whole parasympathetic division is formed from cranial nerves AND sacrospinal nerves Sympathetic Division (Thoracolumbar Division) - formed by thoracic and lumbar nerves T8-L2 Sympathetic Innveration Associated with the Tract Formed from: Spinal Nerves from T8-L2 - where sympathetic nerves originate that associate with the tract These fibers go to ALL parts of the tract These sympathetic nerve endings secrete norepinephrine, which generally decrease GI activity GI Reflexes Three Categories 1- Reflexes that occur entirely within the enteric nervous system - local reflexes These Reflexes include: - control GI secretions - control peristalsis - control mixing contraction - control inhibitory effects 2- Reflexes that involve sympathetic ganglia - go from gut to sympathetic ganglia, and then back A - Gastrocolic Reflex - starts in stomach and goes to sympathetic ganglia then back to the colon - results in evacuating the colon B - Enterogastric Reflex - from small intestine to the stomach - causing a decrease in gastric activity - occurs because there is stuff in the small intestine being digested C - Colonoileal Reflex - from the colon to the ileum - preventing ileal emptying because the colon is full 3- Reflexes from the GI tract to the CNS (spinal cord or brain) - from spinal cord or brain and back to the gut Include: A - Pain Reflexes - decrease GI activity B - Defication Reflex - produces powerful colonic, rectal, and abdominal contractions Functions of GI movement: -mixing movements- a result of alternation movement between muscular layers -Propulsive movement- aka parastalsis, distention is the stimulation for peristalsis. Peristalsis is due to a contraction 2-3 cm above the distention coupled with a relaxation 2-3 cm below the distention. **Atropine paralized cholinergic nerve endings blocking peristalsis.** Peristalsis usually dies out as it moves in an aurad direction because the mienteric plexus polarized in an anal direction, refered to as the “law of the gut” resulting in food always going in an anal direction. Ingestion - put something in your mouth causing distention pushing on wall of the mouth stimulation the salivary secretion and chew it. GI ALWAYS starts at the lips Mastication: -important because it begins mechanical digestion. It is especially important in breaking down cellulose which covers most of the fruits and vegetables that we eat. Deglutition Includes: - Voluntary Phase - moves food to back of the mouth - Involuntary Phase 1- soft palate elevates to cover posterior nares (openings between nose and nasopharynx) and preventing reflux into the nose 2- elevation of the vocal cords and hyoid bone causing the epiglottis to close off the airway 3- relaxation of the upper 3-4cm of the esophagus where the upper esophageal sphincter is located 4- contraction of the superior constrictor muscle pushing the food into the esophagus Sensory Portions of the Trigeminal and Glossopharygeal - associated with the involuntary phase - transmit impulses to the medulla, once here, region of medulla (swallowing center) takes over and orchestrates an orderly sequence of neuronal and mechanical activity and inhibits respiratory center Gastroesophageal Sphincter (Cardiac Sphincter or Lower Esophageal Sphincter) Primary Function: -peristalsis - to prevent the reflux of stomach contents with their proteolytic enzymes into the stomach -this sphincter is 2-3 centimeters above the junction of the esophagus and stomach Stomach **Responsible for:** - storage of food - mixing of food (esp with digestive enzymes, esp pepsin) - SLOW expelling food into the small intestine Divided into: - Fundis (Upper part) - associated with mixing of food - Antrum - distal end of the stomach just proximal to the pyloric sphincter When stomach is finished with whatever you eat chyme (milky white substance that is left) - white – bleached by HCl Emptying of the Stomach contents into the Duodenum - prevented by the pyloric sphincter - facilitated when the pyloric sphincter is inhibited and there are strong antral contractions Regulation of Gastric Emptying -When the stomach becomes distended there is a major stimulus for regulating the strength in antral contractions -Secretion of gastrin from the antral mucosa increase antral contractions Several Duodenal Factors that Prevent Gastric Emptying Include: 1- Degree of duodenal extension 2- pH of the duodenal chime - pH is too low gastric emptying slows 3- Presence of high concentrations of protein and fat in the chime of the duodenum decrease gastric emptying Hormonal Factors Hormones are released when there are FATS in the duodenal chime that inhibit gastric emptying - enter bloodstream and travel through stomach ALL hormones travel through the vascular system Travel together as Enterogastrones - groups of hormones that DECREASE gastric activity due to fat in the duodenum Include: 1- Cholecystokinin (CCK) - released by the jejunum in response to fatty chyme - causes a decrease in gastric activity because it INHIBITS the action of gastrin Gastrin – increases GI activity 2- Secretin - released by the duodenal mucosa - decreases gastric motility 3- Gastric Inhibiting Peptide (GIP) - inhibits gastric activity and motility -Peristalsis in the stomach is so slow that it averages 1cm/min, taking about 3-5 hours for the pass from the pylorus to the iliosecal valve. Where at the end we get to the iliosecal valve, whose primary function is to prevent back flow from the secum to the ilium (without question it is the strongest valve in the GI system) -Movements in the colon are also very sluggish and because of this there is plenty of time for reabsorption of water and electrolytes and only about 80-150 ml of the original chyme are finally left Secretions of the GI Tract Allow for two major Function: - secretion of chemical enzymes for chemical digestion to break down complex foods - Lubricate the tract (mucous) ALL areas of the tract (top to bottom) contain VARYING amounts of mucus secreting goblet cells (allowing for better protection with higher amounts of goblet cells) - all areas are lubricated by mucus and protect the GI tract Stimulation of glands that secrete these substances is by: - mechanical pressure - distension of the tract (push on walls of tract ?????) - parasympathetic nerve stimulation - hormone secretion (esp CCK and secretin) Saliva -lubricating the wall of the tract -buffering effect (hightly resistant to digestive enzymes) -binding of food together Glands: Parotid, Submandibular, Sublingual, buccal Saliva Contains: - salivary amylase(ptylin) - initiates carbohydrate digestion - mucus -electrolytes, esp potassium and bicarbonate ions - lysozyme and thiocyanate – both of which are antibacterial agents - kill bacteria before they can cause any harm -contain antibodies that also help to kill bacteria before becoming harmful - people without salivary secretion are prone to cavities and ulcerated and infected oral tissue Nervous Regulation of Salivary Secretion - via CNVII (Facial) and CNIX (Glossopharyngeal) both very active in triggering saliva secretion. - Under amylase secretions, starch starts it’s digestion in the mouth Esophageal Secretion - lining of the esophagus secretes ONLY mucus (no chemical enzymes) so, - NO digestive enzymes in esophageal secretion but what started in the mouth continues down the esophagus Stomach Wall The gastric mucousa is most complecated vs other mucosa in the tract. In addition to the thick mucous that is S&S by the goblet cells, the stomach wall, in addition to a very high secretion of mucus secreting cells, contains: - Oxyntic glands Contain: S&S - mucus secreting cells - chief cells (peptic cells) – release pepsinogen into the stomach - oxyntic cells (parietal cells) – release HCl into the stomach and intrinsic factor (nothing to do with digestion) [involved with vitamin B12 absorption] - Pyloric Glands - responsible for releasing gastrin Pepsinogen is inactivated when released - then activated by HCl to pepsin, which begins protein digestion in the stomach Whatever was happening under the influence of salivary amylase STOPS, because ONLY pepsin can work in a pH environment between 1.8 and 3.5 (in stomach b/c of HCl), the only one to work at such a low pH. Pepsin BEGINS protein digestion (not finishes) Regulation of Gastric Secretion By: - Vagal innervation which stim the enteric system - Gastrin – released due to gastric distension (stimulates secretion into the stomach) Pancreas - endocrine AND exocrine Pancreatic Juice: Exocrine – synthesis and secretion in the INACTIVE FORM of: - amylase (carbohydrate digesting enzyme) - proteases (protein digesting enzyme) - lipase (fat digesting enzyme) Amylase, when released in pancreatic juice, breaks down carboyhydrates to the disaccharide level Lipase, when released in pancreatic juice, digest (hydrolyzes) fats into glycerol and free fatty acids Protease Three proteases in pancreatic juice – that reach the duodenum via the pancreatic duct 1- trypsinogen: activated when it reaches the small intestine. It is activated by enterokinase which is waiting in the duodenum and turned into trypsin. Trypsin then activates the other two. 2- chymotrypsinogen 3- procarboxypeptidase These are ALL INACTIVE – NOT released in their active form Not activated UNTIL they get into the small intestine - When they get there, trypsinogen is ACTIVATED into trypsin by an enzyme – enterokinase – secreted in duodenal secretions Trypsin then activates chymotrypsinogenchymotrypsin Procarboxypeptidase carboxypeptidase These are POWERFUL protein digesting enzymes To prevent their activation, pancreatic juice also contains trypsin inhibiting factor - this is how the pancreas protects itself If trypsinogen is activated (in pancreas) before it gets to the dudodenum, trypsin will activate the other two pancreas will digest itself within 4-5 hours Breakdown by Enzymes Trypsin, or all three of these enzymes break down proteins ALL THE WAY to the amino acid level Trypsin and Chymotripsin break proteins dipeptides Carboxypeptidase breaks dipeptides amino acids This completes the protein digestion Pancreatic Juice - contains bicarbonate ions, in addition to the enzymes -Pancreatic amylase digest CHO to the disaccharide level (not complete, still need to break down to monosaccharide) -pancreatic lypase digests fat all the way down to the components free fatty acids and glycerol Regulation of pancreatic Juice release -regulated to neural and hormonal mechanisms -Neural are much more significant. The presents of chyme in the duodenum will trigger duodenal secretion of secretin and CCK in varying amounts Two Main Hormones : (remember these are both enterogastrins) 1- Secretin -does not stimulate the cells in the pancreas that secrete digestive enzymes - released by the duodenal mucosa when the chyme entering the small intestine has a low pH (VERY acidic) - triggers the pancreas to release pancreatic juice with a HIGH concentration of bicarbonate ions in it (bicarbonate neutralizes acid) - neutralize chyme and digest what’s in the duodenum (unless it is neutralized the enzymes, accept peptin, can’t work since they don’t do well in acidic environments) 2- CCK - released by the duodenum - triggers the pancreas to released pancreatic juice that has a LOW concentration of bicarbonate ion - happens when the chime is NOT very acidic Low pH Secretin Normal pH CCK -Gastrin release in the stomach, which increases motility, also affects the pancreas in the same way that CCK does Liver REVIEW Billiary Tree!!! Bile - is continuously produced by ALL hepatic cells (about 700-1200 ml / day) but maximum capacity for the gallbladder is about 65 ml. The bile that makes it here is concentrated because water is reabsorbed out of the bile leaving behind the main constituents of bile (bile salts, small amount of cholesterol, lecithin and bilirubine) - passes from the liver and drains through hepatic ducts backs up in the Cystic Duct (gall bladder) and meets up with the Hepatic Duct and make the Common Bile Duct enters the duodenum There is a Pancreatic Duct coming in at the sphincter between the common bile duct and duodenum In order for the bile to enter the duodenum and empty, the Sphincter of Oddi, which is located where the CBD and the duodenum are, must be relaxed (inhibited), and gallbladder must contract to force the bile out at the same time that the sphincter of Oddi is inhibited – this is caused by the release of CCK (Cholecystokinin) CCK – released when there are fats in the small intestine -stimulates the gall bladder to contract, causing bile to enter CBD - released when fat in the duodenum - prevents gastrin from acting in the stomach (get a decrease in gastric activity) Bile - a biological detergent effect on fat - emulsifies the fat into smaller pieces - More surface area Better digestion - allows the water soluble digestive enzymes to mix with the fat so you can digest it -bile salts also help in the absorption of fatty acids because bile salts form small complexes with the lipids called MYCELLES. These cells are highly soluble and absorbed through the mucosa. with out bile salts, as much as 30-40 percent of lipids are lost and excreted in the feces. -When fat is not absorbed adequately, there is a deficiency in the fat soluble vitamins (A,D,E,K). A,D,E are usually stored by the body. Vit K not stored by the body and without adequate vitamine K absorption the liver can’t synthesise many of the important clotting factors, (esp prothrombin, and factors 7,9, and 10) Gallstones caused by: - cholesterol can percipitate out causeing gall stones in the gallbladder. - too much reabsorption of water from bile could also cause this to happen. - And too much absorption of lecethin and bile salts Small Intestine - lots of mucus secreted in the small intestine - NO digestive enzymes in intestinal secretions Enzymes that digest disaccharides into monosaccharides are IN the cell that line the small intestine - are NOT secreted in the small intestine Disaccharides Types: - sucrose - maltose - lactose - digested into their monosaccharides AFTER they are absorbed into the cell that line the small intestine Sucrose - digested by sucrase - into fructose and glucose (monosaccharides) Maltose - digested by maltase - into two glucose molecules Lactose - digested by lactase – into glucose and galactose Large Intestine - primarily dealing with ONLY mucus to lubricate and to compact fecal material together Absorption: Villi and Microvilli (in small intestine) - increase surface area for absorption by 20 fold. SA of small intestin is approximated to be 20 sq meters (about the size of a tennis court) There are central lacteals in each villi - assist in absorption of fats (lymph) delivered to liver via the hepatic portal system for processing - and to direct absorbed nutrients to the liver - reabsorption can be active or passive and in the cells are many mitochondria for ATP synth to drive the active reabsorption. - along with nutrients, electrolytes are reabsorbed (sodium, potassium) - and the disaccharides (cleaved to monosaccharides once they are absorbed), amino acids, free fatty acids and glycerol are reabsorbed - of the 1500 ml of what’s left of the chyme, 90% of it is reabsorbed and that reabsorption occurs in the proximal half of the large intestine. The distal half is mainly for the storage of fecal matter before it is eliminated.