PHYSIO EXAM 3 STUDY GUIDE
PHYSIO EXAM 3 STUDY GUIDE PGY 451LEC
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This page Study Guide was uploaded by Ndidiamaka Okorozo on Friday November 6, 2015. The Study Guide belongs to PGY 451LEC at University at Buffalo taught by Baizer, J S in Fall 2015. Since its upload, it has received 181 views. For similar materials see Human Physiology I in Physiology at University at Buffalo.
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Date Created: 11/06/15
PHYSIO EXAM 3 STUDY GUIDE INTRO TO DIGESTIVE SYSTEM The GI tract is a hollow tube that brings the outside world inside Inside the lumen of the esophagus is considered external outside world because it connects with the outside Helps maintain homeostasis Its primary function is to digest food and absorb nutrients electrolytes and water into the body s internal environment Functions Motility Secretion Digestion Absorption Excretion and Protection Epithelium is a single layer of cells that protects the inside from the outside world It is involved in regulation of materials across compartments Layers of the stomach a Longitudinal muscle increases volume b Circular muscle causes propulsion and mixing c Oblique causes stomach to twist because of contractions These three layers makes up muscularis externae and engage in motility lnvagination called gastric glands increase surface area in the stomach Intestinal surface have invaginations called crypts This is found in Small intestine SI and large intestine However Sl also has villi that enable further increased absorption GI Physiology Regulation a Endocrine hormone is released and it circulates in blood before reaching target cells b Neurocrine a neuron innervates the target cell using neurotransmitter c Paracrine cell releases hormone to neighboring cells Enteric Nervous System intrinsic network of the gut Can function independently of the ANS However it is modulated by the parasympathetic Ach and sympathetic NE nervous systems Parasympathetic is controlled by medulla oblongata and uses the vagus nerve ENS network is imbedded in submucosal plexus and myenteric plexus lts receptors are mechanoreceptors and chemical receptors The ENS and two branches of ANS are all interconnected GI MOTILITY Two functions a Movement of food from the mouth to the anus b Mechanically mixing food to break it into smaller particles and to mix with digestive juices Muscle types Striated Skeletal muscles of moth pharynx upper esophagus and external anal sphincter These are innervated by the somatic motor neurons Smooth muscles rest of the GIT GI Tract and are innervated by autonomic motor neurons They are involuntary and contract spontaneously Smooth muscles are driven by pace makers electrically connected by gap junctions and different regions exhibit different types of contractions Tonic contractions can contract and remain like that for long periods of time Enables them to be used in sphincters Phasic contraction changes contracts and relaxes They also exhibit slow wave potential RMP is not xed but continuously wavering Because of the gap junctions information is passed easily and the cells contract or relax at the same time Not all slow waves reach threshold GI Motility processes include ingestion mastication deglutition swallowing food peristalsis rhythmic wavelike contractions that move food forward and segmentation mixing contractions in different segments and defecation Interstitial Cells of Cajal Pacemaker cells where slow waves are initiated Have gap junctions These slow waves affect the opening of Ca2 channels and therefore can lead to contraction when threshold is reached Amplitude and frequency are modulated by extrinsic and intrinsic nerves and hormones Ach and substance P excite while VIP amp NO nitric oxide will inhibit Slow waves are 35 per min in stomach 1220 per min in small intestine and 68 per min in colon The force and duration of muscle contraction are directly related to the amplitude and frequency of the action potentials Contraction of GI smooth muscle Threshold is reached l Ca2 enters associates with CAM l activates MLCK which uses ATP to activate inactive myosin l myosin and actin contract This complex stay intact as long as myosin stays phosphorylated and when it stops being phosphorylated myosin and actin relax Exhibits the tonic contraction characteristic Motor patterns of Small Intestine SI a Peristalsis wavelike movement from side to side which produces pressure that pushes the food forward b Segmentation mixing the food in different segments but there is not net movement c Migrating Motor Complex MMC involved in the house keeping function Strongest set of contractions that are forcing out and cleaning the SI region These activities occur between meals to keep the SI clean Chewing Involuntary re ex in the mouth from food and voluntary consciously chewing your food Mechanoreceptors sense the presence of food in the mouth and sends info to the brain stem Mixing food with saliva to lubricate and facilitate swallowing Reduces size of food particles to facilitate swallowing Mixes ingested carbohydrate39s with salivary amylase to begin carbohydrate digestion Swallowing Both voluntary and involuntary Re ex portion controlled by the swallowing center in the medulla evoked by the presence of food in the mouth Vagus and glossopharyngeal nerves provide both afferent and efferent pathways between sensory neurons swallowing center and the striated muscle of the pharynx and upper esophagus Three phases 1 Oral creates bolus of food using muscles of mouth and tongue by mixing it with saliva the pushes it to be swallowed 2 Pharyngeal phase complex re ex makes sure that gottis is closed so food doesn t end up in trachea And it opens upper esophageal sphincter while propelling food forward 3 esophageal phase food moves down via peristalsis Oropharyngeal stage is the last voluntary act in processing food until the anal end of the GIT In the upper esophageal tract the pharynx and upper esophageal sphincter UES are made of striated muscles and are controlled by the somatic system while the esophagus and lower esophageal sphincter LES are smooth muscles controlled by the autonomous system Process of motility The UES opens the bolus enters into the esophagus and UES closes Peristaltic contractions move the bolus down the esophagus and the LES is opened by peptidergic bers in the vagus nerve that release VIP as their neurotransmitter Then as food enters the stomach and the upper potion relaxes because of receptive relaxation This allows it to increase in volume without increasing pressure GI Transit Time 50 of stomach contents emptied 25 to 3 hours Total emptying of the stomach 4 to 5 hours 50 emptying of the small intestine 25 to 3 hours Transit through the colon 30 to 40 hours Note that the small intestine can no handle a large amount of liquid and that transit time can increase across different individuals Regulation of Motility 1 GI hormones a Cholecystokinin CCK secreted by I cells in the duodenum Has receptors in smooth muscles all over the gut It is the strongest inhibitor of gastric emptying and it stimulates intestinal and colonic motility b Motilin secreted by M cells in the crypts of the SI small intestine It increases MMC which does the house keeping function so motilin is secreted between meals 2 Neural activity Enteric nervous system a Myenteric plexus between circular and longitudinal muscles Uses Ach Substance P VIP and nitic oxide They are modi ed by the ANS b Extrinsic nerves parasympathetic and sympathetic nervous systems Seven sphincters of the GIT UES LES Pyloric sphincter lleocecal sphincter Internal anal sphincter External anal sphincter Sphincter of Oddi controls ow of pancreatic and liver products into the duodenum Only the UES and he external anal sphincter are striated muscles and voluntary the rest are smooth Processing of an lngested Meal 1 Cephalic Phase Visual and olfactory stimuli creates anticipation for a meal which activates the GIT to receive a meal Auditory conditioned re ex has been linked to involvement in GIT anticipation as in the case of Pavlov and his dog where the dog was conditioned to relate a particular sound with food There is also increased parasympathetic out ow 2 Oral Phase Similar responses 5 the cephalic phase Main difference here is the actual physical presence of the food in the mouth which is FP P FP NI sensed mechanoreceptors and chemoreceptors gustatorysweet biter salty umami and sour nociceptors damaging stimuli It also involves chewing Secretions of the GIT Salivary glands pancreas liver glands of the gut wall and from intestinal mucosa The secretions contain water electrolytes proteins and signaling molecules hormones Daily secretions of GI Juices Secretion Daily Volume ml pH Saliva 1000 6070 Gastric 1500 1035 Pancreatic 1000 8083 Bile 1000 78 Small lntestine 1800 7580 Brunner s gland 200 8089 Large lntestine 200 7580 Total 6700 All uid 5 reabsorbed to maintain homeostasis Tubuloalveolar Gland typical in salivary gland and exocrine pancreas Lined with epithelial cells and found in ducts Has serous cells which produce salt and water uid and mucus cells which produce mucus There are three major salivary glands 1 parotid has serous cells 2 submandibular has mixed cells 3 sublingual has mucus cells with many small buccal glands Control of Salivary Secretion controlled by the parasympathetic and sympathetic branches of the ANS but parasympathetic is dominant via vagal nerve Anxiety affects secretion Regulation of Salivary Secretion Stimuli like food nausea conditioning and smell increases parasympathetic out ow while dehydration fear and sleep decrease out ow o Parasympathetic Stimuli D release of Ach which bind to muscarinic receptors D increase in Ca2 and P3 in acinar or ductal cell D release of saliva Sympathetic Stimuli l release of norepinephrine binds to B receptors in cell l saliva release Salivary Gland Secretions Has a high ow rate 1mLming of food and hypotonic environment Electrolytes like Na K HC03 Ca2 Mg2 and Cl Mucin a complex mixture of glycoproteins is also released Amylase and lipase are released for digestion of carbs and fats Degree of digestion here Is dependent on how long the food is chewed Lysozyme is an antibacterial that s present for protection lmmunoglobulins generate immune response if needed and lactoferrin binds upon iron n to prevent bacterial growth Therefore immunoglobulin lactoferrin and lysozyme provide protection 0 Composition changes as ow rate increases Secretion vs Absorption Main difference is that in absorption molecules is moved from outside to inside the body and it is vice versa in secretion ln secretion however hormonal and paracrine secretions resemble absorption Characteristics of Epithelial Transport Symmetrical cell equal transport of molecules from all sides no net movement The K conduction polarizes the membrane and Na produces can move in and out of cell depending on its electrochemical gradient with the use of ATP Tight junction allows the passage of molecules lon Transport by Salivary Gland Acinar cells end of duct cells Secretes k Cl and HCO3 The primary active transporter generates energy used for secondary active transporters Because it s releasing more negative than positive sodium travels passive through paracellular pathway to balance the charge Duct cells slow owing reabsorbs Na and Cl leaving HC03 behind so the environment becomes hypotonic Water ows in the direction with high concentration of electrolytes GASTRIC PHASE Stomach Orad region the most proximal region to the esophagus lt s thin walled and exhibits receptive relaxation to prevent change in pressure with increased volume of food Relaxes when food is present Fundus contained in the orad region the topmost part of the stomach Rugae folded area in stomach that stretches to provide more surface area for digestion Body the middle part of stomach Antrum the most distal part of the stomach Has the thickest wall Connects to the SI Caudad region thick walled and has strong contractions that mixes the chyme food in stomach Moves the food through the pyloric sphincter The pyloric sphincter controls the passage of chyme from the stomach into the SI Region Secretion Motility LES and cardia Mucus Prevention of re ux HCO3 Entry of food Regulation of belching Fundus and body H Reservoir Intrinsic factor Tonic force during Mucus emptying HCO3 Pepgnogens Lipase Antrum and pylorus Mucus Mixing HCO3 Grinding Sieving Regulation fog gastric emptying Mucus neutralizes food to keep the pH at 78 Intrinsic factor coming from the acid producing cells It is ESSENTIAL to only the stomach Oxyntic ganduar mucus in fundus and body Pepsinogens inactive pepsin that are activated in the presence of acids Gastric Mucosa The gastric glands secrete the mucus that protects the stomach cells from the acid Note that cells in the stomach is same as every other GIT part but the production of mucus protects them from being damaged by the low pH Surface epithelial cells makes mucus and HCO3 The chief cells produce pepgnogen Neural Regulation in Gastric Phase Cephalic phase initiates 30 of acid secretion in the stomach Acid unfolds pepsinogen and it becomes active produces pepsin l starts breaking peptide bonds in proteins including pepsinogen l more pepsinogens made active more pepsin Positive Feedback Once pepsin reaches SI it s inactivated because it only works in pH less than 35 Both vasovagal re ex and endocrine release of gastrin stimulate acid and pepsinogen secretion during gastric phase Parietal Cell sole producer of acid H It is lled with mitochondria which implies high aerobic metabolism so it s able to actively pump HCl out Parietal cell is regulated by neural hormonal and paracrine pathways Have tight junctions Ach from Enteric nervous system which was innervated by ANS release Ach on parietal cell and it produces and release HCl Ach is also released on ECL cell electrochlorophary which makes histamine Histamine further increase the secretion of acid by parietal cells Another neuron innervates GRP that activates G cell s production of Gastrin Gastrin endocrine factor travels through a hormonal pathway and increases the production of acid by parietal cell So parietal cell is regulated by a Neural neuron releasing Ach b Hormonal Gastrin released by G cell c Paracrine Histamine Feedback Regulation of Gastric Acid Acid in the antrum most distal part of stomach stimulates the release of somatostatin by D cells which binds to G cells and inhibits its production of Gastrin Somatostatin is the strongest inhibitor of gastrin production Also remember that gastrin causes the production of acid Therefore somatostatin indirectly inhibits acid secretion Parasympathetic Stimulation of Gastric Secretions via Enteric Neurons Parasympathetic vagal efferent out ow excites enteric nervous system which also releases Ach on a Chief cell produces pepsinogen b Parietal cell produces HCl c ECL cell produces histamine in lamina propria in mucosa The ENS activates GRP which causes stimulates G cell to secrete gastrin into the blood HCl and pepsinogen are released in the lumen of the stomach Mechanism of HCl production in parietal cell Water diffuse into the cell is broken down into H and OH H is actively pumped out to the lumen while K is being pumped into the cell K leaks back out into the lumen which hyperpolarizes the cell As a result Cl is forced out into the lumen to balance the charge Cl binds with H in the lumen and produces HCl acid C02 diffuses into the cell and is catalyzed by Carbonic Anhydrase CA with OH from H20 to produce HCO3 The HCO3 is pumped to the interstitial space The amount of the H pumped into the lumen is equivalent to the amount of HCO3 pumped out into the interstitial space If more HC03 is pumped out than H it causes nausea which leads to less K being pumped in and less H being pumped out Hypokalemia results Direct and indirect actions of three acid secretagogues Direct Pathway in direct pathway the Ach Gastrin and Histamine directly stimulate the secretion of H by the parietal cell Indirect Pathway here the Ach and gastrin activate ECL cells which produces histamine that will stimulate the production of acid by parietal cells Signal Transduction in Parietal Cells a Vagus l Ach M3 muscurinic receptor l increases Ca2 and P3 l H secretion b G cells l Gastrin l CCKB receptor l increases Ca2 and P3 l H secretion c ECL cells l Histamine l H2 receptor l increases cAMP l H secretion d Somastatin l inhibits cAMP e Prostaglandins l inhibits cAMP All these work via GProteins Atropine blocks binding of Ach to M3 receptors Cimetidine blocks binding of histamine to H2 receptors Omeprazole blocks the ATP pump that pumps out H very effective Secretion of mucus by gastric mucosa Mucus gel undegraded glycoprotein polymer and has high viscosity more sticky In the presence of pepsin becomes degraded and with low viscosity less sticky Mucus Layer as Diffusion Barrier Mucus layer protects layer from acid It produces aqueous solution as much as acid is produced to neutralize H to prevent damage of stomach cells When it s not produced l damages cell l produces histamine l more H release damages cells more Positive feedback Trituration of solid l its breakdown The jetlike repulsion through the ori ce of antral contraction triturates the solid particles Force for the repulsion is increased pressure in the antrum as the antral contraction approaches closed pylorus Gastric Emptying Liquids empty faster than solids isotonic content are faster than hypo or hypertonic content The rate is also slowed by fat content and presence of H in the duodenum Contribution of phases in turning on the GIT Cephalic 30 Gastric 60 Intestinal 10 INTESTINAL PHASE Primary functions of the SI digestion and absorption Increase in pancreatic secretion l gall bladder GB contraction l Sphincter of Oddi relaxes and opens l regulate gastric emptying by inhibiting acid and gastrin secretion Enterogastric re ex releases enterogastrones that inhibit production of H and pepsinogen GIP is signal for the release of insulin by endocrine system CCK down regulates acid secretion Secretin causes inhibition too but it s minor A lot of absorption occur in the small intestine Volumes secreted and absorbed in GIT are equivalent Exocrine Pancreas Duct cells secrete aqueous NaHC03 and acinar cells secrete digestive enzymes Regulation of pancreatic secretion a Presence of fatty acids l I cells produce CCK l increase in Ca2 and P3 acinar cells l release of enzymes inactive b Acid in lumen l S cells produce Secretin l cAMP ductal cells l aqueous secretion basic Activation of gastrointestinal proteases SI Trypsinogen l trypsin Activated by enterokinase brush border enzyme Trypsinogen l trypsin Proelastase l elastase Chymotrysinogen l chymotrypsin Trypsin activates all the other enzympes Digestion hydrolysis breaks the bonds between monomers of glucose by creating water molecules Absorption 2 paths transcellular crosses 2 barriers and ows across cells Paracellular goes around the cells Absorption along GIT Stomach absorbs alcohol and drugs SI duodenum shortest common area for ulser jejunum does most of the absorption ileum absorbs whatever that s left electrolytes and water reabsorbed Acids and gases from mechanisms of bacteria If you resection the distal parts of SI ability to absorb 812 and bile salts is lost Carbs have a lower transit time in SI than proteins and proteins pass faster than fats Microbiota is made up of different types of bacteria everybody has a different constitution Colon is the hidden organ Intestinal Feedback to Stomach Chyme entering duodenum generates feedback signals that control the rate of gastric emptying Neural vagal afferents respond to nutrients H hyperosmotic content Hormonal CCK inhibits gastric emptying among other actions The volume of chyme in duodenum decreases as it moves down the intestine reducing the strength of the feedback inhibition Carbohydrates Monosaccharides monomers Glucose fructose galactose Disaccharides Maltose 2 glucose sucrose glucose and fructose lactose glucose and galactose Enzymes are maltase sucrose and lactase respectively Oligosaccharides short polymers Polysaccharides long polymers Amylose straightchain glucose polymer d14 linear linkage broken by amylase l maltotriose 3 glucose and maltose 2 glucose Amylopectin massive branched glucose polymer Starch plant d16 branch points Glycogen animal starch many more d16 branch points broken by amylase l maltotriose maltose and dlimit dextrins Amylase can t break it down further Different enzymes break the 14 and 16 bonds lsomaltase breaks down dlimit dextrins maltotriose and maltose l glucose Cellulose has 314 which is broken by cellulase and unable to be broken by amylase so we don t consume it because we don t produce cellulase Brush Border Enzymes on enterocytes on the SI Have maltase sucrose and lactase on its surface Disorders of Carb Digestion and Absorption if not fully broken down it won t be absorbed and remains in lumen with water increases osmotic pressure l osmotic diarrhea Carb Absorption Glucose and galactose are transported along with Na passively with GLUT1 channel Fructose are transported with GLUT5 All are facilitated They all exit into the blood via GLUT 2 Protein Digestion and Absorption proteins are broken into oligopeptides or amino acids before absorption by SI done by hydrolysis before absorption Digestion 4 phases Four phases of enzymatic action a Pepsin in gastric lumen stomach b Pancreatic proteases c Brush border peptidases d Cytosolic peptidase of enterocytes rest are SI Amino acidAA Absorption by enterocyte Na drives AA into the cell Gastric and pancreatic peptidases break proteins down to oligopeptides and AAs which are transported into the cell via H coupled channels Di and tripeptidases them down and they are pushed into the interstitial space There are at least seven different transporters because there are different AAs Tri and Dipeptide absorption is dependent on sodium and proton gradients because pumping Na into cells creates a gradient for H which drags tripeptides in too Absorption of Whole Protein neonatal period is important because apical pinocytosis cell drinking occurs where there is a passive immunity from mother to child It closes after 6 months and corticosteroids promote early closure Immune system is developed in the child with the lumen content absorbed from the mother 70 of our immune system is in the lumen of our gut M cell and Peyer s patches collection of cells receiving proteins from lumen of gut Follicles of lymphoid tissues that are in the lamina propria of the SI They make sure proteins are not contaminated Lipid Absorption Dietary lipids include triglycerides cholesterol and phospholipids Hydrophobic prefers aqueous solution Salivary and gastric lipase begins digestion 10 but bulk of the work is done in the small intestine by pancreatic lipase Most import role of stomach in the digestion of lipid is to control release of chyme into duodenum Triglycerides are digested to monoglyceride and free fatty acids not bound to glycerol Trypsin activates enzymes Colipase coming from the pancreas is released as procolipase Trypsin converts the procolipase to colipase in duodenum Colipase changes the structure of lipase to more hydrophobic and active Bile makes hydrophobic lipid more digestive It s a watery mixture of organic and inorganic compounds Bilirubin breaks down heme portion of red blood cells RBC gives feces and urine their color Phosphatidylcholine lecithin allows for transmission between aqueous environments Conjugated bile acids I bile salts Amphipathic and is an emulsifying agent a Bile salts coat lipids to emulsify them break the down Polar hydroxyl part faces the water while the nonpolar methyl part bind to the lipid b Lipids are broken down by lipase into micelles small disks with bile salts phospholipids fatty acids cholesterol and mono and diglycerides Lipase l micelles l diffuse into enterocytes after brush border enzymes have turned them to triglycerides amp cholesterol l inside the cell reassembled into chylomicron triglyceride cholesterol and proteins l packaged into vesicle and instead of being transported into the blood like proteins and carbs it is transported to lacteals to enter the lymphatic system Bile Salt Recycling or Enterohepatic Circulation Cholesterol in liver is converted to bile salts l translocated into bile duct I if the sphincter of oddi is closed l goes to gall bladder CCK signals for presence of lipid l gall bladder contracts l sphincter of oddi opens up delivered in to the duodenum and mixes with lipid Only lipid component are taken up by enterocytes so bile salts are bile acids by now so they are converted back to bile salts by conjugating them with amino acids glycine and taurine and then returned to liver via portal circulation Bile is always being produced Synthesis of Bile Acids and Conversion to Bile Salts Cholesterol is converted to primary bile salts by liver and primary bile salts is converted to secondary bile salts by intestinal bacteria Disorder of Lipid Digestion amp Absorption pancreatic insufficiency to release pancreatic lipase inadequate bicarbonate and bacterial overgrowth Overgrowth will deconjugate bile salts and make them insoluble LIVER A quotchemical factoryquot an excretory system an exocrine gland and an endocrine gland The liver plays a key role in handling foodstuffs assimilated by the small intestine Receives portal blood from the stomach small intestine large intestine pancreas and spleen a Largest internal organ and can regenerate itself Heptoportal Circulation Left side pumps blood into systemic circulation Celiac artery Superior mesenteric artery and inferior mesenteric artery supply the GIT The blood that absorbs nutrients from food goes straight to the liver via the portal vein b Hepatic artery supplies the blood with oxygenated blood Bile secreted by liver is secreted into the common bile duct for storage in GB Then it is secreted into the lumen via the common bile duct If sphincter of oddi doesn t close between meals there could be re ux c Hepatocytes of liver are organized in lobules hexagonal units Lobules have veins that drain to hepatic portal vein which drains into the inferior vena cava Hepatocyte membrane faces the bile canaliculi which is where bile is secreted and drain into bile duct Cycle Cholesterol parents converted to bile salts converted l primary bile acid by liver converted secondary bile acids by intestinal bacteria back to circulation l conjugation with amino acids glycine and taurine l bile salts and transported back to liver through enterohepatic circulation Bile goes through this process at least 2 times Gall Bladder has epithelium that reabsorbs Na amp C Into the blood Cl is done actively and through transcellular pathway while Na travels passively and through paracellular pathway Water follows into the blood concentrating bile in the gall bladder Neurohumoral control of gall bladder CCK causes GB to contract VIP and NO inhibit the sphincter of oddi and it relaxes and opens CCK send stimulus that activates the dorsal vagal complex COLONIC PHASE Large Intestine area of bacterial actions Teniae coli creates haustrum where the muscles are arranged Rectal valves function to control ow of chime through colon Internal anal sphincter is smooth muscle and controlled by ANS Sympathetic branch keep it contracted while parasympathetic branch relaxes it Sodium transport by colonocyte of Large Intestine function is to give water and electrolyte back to the body of the intestine The Na channel is not excitable Release of Na into blood causes CI to travel paracellularly to counteract the positive charge Short chain fatty acid SCFA uptake is produced from intestinal fatty acid uptake It s secondary active transport as transport of SFCA is coupled with sodium Mechanism of chloride secretion in the small and large intestine Cystic brosis transconductance regulator CFTR is responsible for secreting C NaCl is secreted within the crypts Active transcellular chloride secretion and passive Na paracellular secretion Water follows and electrolytes and water enter the lumen Fluid Balance in the GI System water is taken back towards blood There has to be balance in absorption and secretion of uid If not balanced it leads to diarrhea Diarrhea a Osmotic caused by unabsorbed component which causes water to be retained in gut b Secretory Most common and deadly over activation of secretion in crypt Example is cholera c Motilityrelated irritating the gut to decrease transit time and prevent absorption d In ammatory gut is sensitized by microorganism Cholera cholera toxin activates cholera secretion Toxins turn on crypt cells and in the presence of cAMP Cl will be released Na and H20 travel too to balance the uid in the system Enterotoxin cholera toxin secreted when when you have cholera Secretion into lumen from the body Absorption into body from the lumen Cholera toxin causes more secretion than absorption Oral Rehydration Therapy Very useful in children because they are very susceptible to cholera Cholera toxin doesn t kill by itself but it causes excessive loss of body uids even in the cardiovascular system Intake of sugar salt and water restores balance and supplies the body with uid It stimulates the uptake of salt and water in the brush border AcidBase balance within the GIT and blood When acidic chyme moves into the duodenum the base neutralizes it Pancreas needs to keep up with bicarbonate secretion to maintain neutral pH Vomiting or diarrhea disrupts acidbase balance Gastric Acid Barrier if the mucus coating is breached acid passes through and causes acid to digest the epithelial layer and mucosal layer cells The acid in submucosa stimulates histamine release that stimulates parietal cell to release more acid into the lumen of the stomach Postive feedback Gastric Ulcer To stop the process Antacids don t work well it acts as buffer for HCL To prevent release of HCl use PPI to block the parietal cell from releasing H Ach and gastrin inhibitors too will prevent stimulation of parietal cells Helicobacter pylori creates an environment that allows the mucosa or lining to live in the presence of the ulcer It neutralizes the H around it Sulforaphane natural inhibitor of helicobacter
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