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GI Physiology – I Dr Bhawana Neupane Pant Lecturer, Department of Physiology

GIT Physiology I

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GI Physiology I Dr Bhawana Neupane PantLecturer, Department of Physiology

GI Physiology: Motility1

Gastrointestinal System: ProcessesMotilityDigestionSecretionAbsorption



Structure of the GI TractInnervation of the GI TractGI PeptidesStructure of the GI Tract a) Layers of the GI tract b) GI muscles

Innervation of the GI Tract a) Intrinsic/Enteric nervous system b) Extrinsic/Autonomic and central NS

Hormonal Control of GI functions

Costanzo 327-335

GI Physiology: GI structure4

Serosa - Continuous with the mesenteries

2) Muscularis- Longitudinal muscle- Circular muscle

3) Submucosa

4) MucosaMuscularis mucosaeLamina propriaEpithelial cellsLayers of the GI tractStructure of GI Tract

GI Physiology: GI structure5


General Anatomy of Gut Wall(Contains connective tissue, immune cells, capillaries, nerve endings)(Might have role in villus movement)


1) Serosa

2) Muscularis:- Longitudinal muscle

- Circular Muscle3) Submucosa:

4) MucosaSubmucosal plexus (= Meissners plexus Myenteric plexus (= Auerbachs plexus)

2. Innervation of the GI Tract

GI Physiology: GI structure7


a) The Enteric/ Intrinsic Nervous SystemPrimarily controls motility (length, intensity, frequency, velocity of peristaltic waves)Decreases tension of sphinctersControls secretion, absorption, submucosal motility and blood flow

GI Physiology: GI Innervation, GI peptides

Enteric Nervous System23

The Enteric Nervous SystemLocal Reflexes = Short Reflexes.Can be influenced by CNS = Long Reflexes.

GI Physiology: GI structure9

Parasympathetic and Sympathetic Innervation

Integration of neuronal control of GI function

Interaction of ANS and ENS

The enteric nervous system coordinates digestion, secretion, and motility to optimize nutrient absorption.

Its activity is modified by information from the CNS and from local chemical and mechanical sensors.

Enteric Nervous System


What Is "Diabetic Stomach"?My niece takes an oral medicine for diabetes. At least once a week, she throws up at night. The doctor calls it "diabetic stomach." I have never heard of this, and I have had diabetes for 36 years. What could be the cause of her stomach problems, and what foods may be causing flare-ups?Hint:Type II diabetic patients have autonomic neuropathy and motor neuropathy.

Diabetic StomachGastroparesis is a disorder affecting people with both type 1 and2 diabetesin which gastric emptying is delayed.

Symptoms: Nausea Vomiting of undigested food Early feeling of fullness when eating Weight loss Abdominal bloating

Avoid high-fat and high-fiber foods.

Cholinergic (Acetylcholine) - excitatoryAdrenergic (Norepinephrine) - inhibitoryNon-adrenergic, non-cholinergic neurotransmitter (NANC)Vasoactive Intestinal Peptide (VIP)Gastrin Releasing Peptide (GRP) or BombesinEnkephalins (opiates)Neuropeptide YSubstance P

Neurotransmitters and Neuromodulators in the Enteric Nervous System:Note: There are list of putative transmitters is long; often, their physiologic significance is uncertain; but their potential pharmacological value is high.

GI Physiology: GI Innervation, GI peptides

Enteric Nervous System24

Is a disorder caused by the absence of enteric neurons.

In the majority of affected people, the disorder affects the short segment of the distal colon.

In rarer cases it affects the whole colon or even the whole GI system.

Hirschsprung disease or congenital megacolon

GI Physiology: GI structure17

In children with Hirschsprungs disease, nerves fail to form in all or part of the large intestine (colon). Waste from digestion cannot pass through the part of the colon lacking nerve tissue. The normal colon swells with blocked stool.

Clinical Presentation: Failure to pass meconium, abdominal distension, vomiting, enterocolitis

Treatment: Surgical removal of part (Pull through procedure)

Gastrointestinal Peptides:

Gastrointestinal Hormones:

Gastrin:Secreted by G cells in the antrum of stomach

Principal physiologic actions: Gastric acid secretionPepsin secretionTrophic action (growth of the mucosa of the stomach, small and large intestine)

GI Physiology: GI Innervation, GI peptides

Hormonal Control35

What happens in Zollinger-Ellison Syndrome?

What happens when gastric antrum is resected?H+ secretion is increasedHypertrophy of gastric mucosaDuodenal ulcerSteatorrheaH+ secretion is decreased Gastric mucosa atrophies

GI Physiology: Motility22

Gastrin StimulationInhibition by:- Somatostatin (H+ stimulates, N. vagus inhibits D-cells)- Low pH (partly at pH 3.5, completely at pH 2)- Secretin

Stimulation by:- N. Vagus- Distention of the stomach- Protein digestion products- Calcium, alcohol, coffee - CNS (anticipation of meal, olfactory stimuli)AA: phenylalanine and tryptophanSecretin

GI Physiology: GI Innervation, GI peptides


Cholecystokinin secreted by I cells in the mucosa of the duodenum, the jejunumPrimary functions:Stimulation of pancreatic enzyme secretionThe contraction of the gall bladder and relaxation of sphincter of OddiGrowth of the exocrine pancreas and gallbladderSecondary functions:Augments the action of secretin in producing secretion of an alkaline pancreatic juiceIncreases the synthesis of enterokinase May enhance the motility of the small intestine and colon

GI Physiology: GI Innervation, GI peptides.CCK41

CCK Functions

GI Physiology: GI Innervation, GI peptides


CCK StimulationStimulation by:- Digestion products of fat and protein (most potent long fatty acid chains)- Meals stimulate CCK secretions of gut and CNS simultaneously

GI Physiology: GI Innervation, GI peptides



Secreted by S cells in upper small-intestinal mucosa.

Stimulates water and alkali secretions from pancreas and biliary tract

Inhibits gastrin release, suppresses gastric acids

It also augments the action of CCK in producing pancreatic secretion of digestive enzyme

The secretion of secretin is increased by the products of protein digestion and by acid bathing the mucosa of the upper small intestine.

GI Physiology: GI Innervation, GI peptides


Secretin Stimulation- contact with acidic chymealso stimulated by fatty acids

IV: GIPold name: Gastric Inhibitory Peptidenew name: Glucose-dependent Insulinotropic Peptide- Secreted by K-cells in duodenum and jejunum

GI Physiology: GI Innervation, GI peptides


GIP Functions

Major function:Release of insulin

Action as enterogastrone controversial:- Inhibits gastrin release and acid secretion- Inhibits gastric and intestinal motility??

GI Physiology: GI Innervation, GI peptides


GIP Stimulation

Stimulated by- Glucose in upper small intestine- Long-chain fatty acids- Certain AA (different than those for gastrin and CCK) Inhibited byHigh levels of insulin or glucagon (unclear if physiologic?)

C. Candidate Hormonesproduced by pancreatic islet cells and endocrine cells

released most potently by protein digestion products

also released by vagal stimulation and Ach

I: MotilinII: Pancreatic PolypeptideIII: Enteroglucagon

GI Physiology: GI Innervation, GI peptides

Candidate Hormones50

II: Enteroglucagon secreted by intestinal mucosal cells of colon and terminal ilium stimulated by intraluminal glucose and fat same effects as glucagon but less potent (glycogenolysis and gluconeogenesis, lipolysis) might inhibit gastrin release and gastric acid secretion (not established)III: Pancreatic PolypeptideSecreted by the pancreasStimulated by ingestion of carbohydrates, proteins, or lipidsInhibits pancreatic secretion of HCO3- and enzymes Physiologic role uncertainI: Motilinprimarily in duodenum by M cellsphysiologic stimuli not knowninitiates the MMC migrating motor complex (see motility lecture)Candidate Hormones

GI Physiology: GI Innervation, GI peptides

Candidate Hormones51

D. Paracrines

Secreted into the interstitial fluid and diffuse to adjacent cells

The site of secretion must be only a short distance from the site of action.



GI Physiology: GI Innervation, GI peptides


SomatostatinSecreted by D-cells in gastric mucosaDelta cellsin thepyloric antrum, theduodenumand thepancreatic isletsBoth paracrine and endocrine

Suppresses gastric secretionsInhibits motility and tone of stomach and small intestines and gall bladderInhibits formation of liver bileInhibits the release of ALL known GI hormonesInhibits saliva, gastric, pancreatic, small intestinal and liver secretionsInhibits splanchnic blood flowInhibits intestinal absorption

In brain it inhibits GH releaseIn pancreas, inhibitor of insulin and glucagonOctreotide : analogue of somatostatin

GI Physiology: GI Innervation, GI peptides


Action Gastrin CCK Secretin GIP

Acid secretionPancreatic HCO3- secretionPancreatic enzyme secretionBile HCO3-Gallbladder contractionGastric emptyingGastric Mucosal growthPancreatic growthInsulin Secretion

S = stimulates; I = inhibits

Actions of GI hormones ISSSSSSSSISSI

GI Physiology: Motility36

GI Motility

Skeletal muscle:Upper esophagusExternal anal sphincter

Smooth muscle: (of the visceral or unitary type): Rest of GI tractGI Muscles

GI Physiology: GI structure38

In comparison to skeletal muscle: Energy: Low (up to 300x less)Force: HighShortening: HighTime: Long (tonic) Speed: Slow

GI Physiology: Motility40

Basic Electrical ActivitySLOW WAVES:Due to rhythmic changes in membrane potential initiated by Interstitial cells of Cajal (pacemaker cells)Not responsible for contractions but determine the frequency of contractions

SPIKE POTENTIALS: Develop on top of slow waves when they reach threshold potential (~ -40mV) The higher amplitude the more spike potentials the stronger gut motility

Membrane potential

GI Physiology: Motility41

Frequency of electric activity determines the frequency of contractions Basic Electrical Rhythm in different partsStomach ~ 3/minDuodenum ~ 11-12/minDistal Ileum ~ 6-7/min

GI Physiology: Motility42

Objectives of Todays Class:Structure of GI Wall

Enteric Nervous System and Its Interaction with ANS and CNS

Understanding GI Hormones

Electric Basis of Motility in GI Slow Waves

MotilityMouth and Esophagus: Chewing, Swallowing, PeristalsisStomach: Filling, Churning, Peristalsis, Emptying

Small Intestine: Segmental Contractions, Peristalsis

Large Intestine: Haustral Shuttling, Mass Movements, Defecation.

Sphincters: Regulation of Movement



Tonic Contractions

Latch Mechanism and slow myosin ATPase allow SM to maintain contraction with little energy and excitatory signal from nerves or hormones

Phasic Contractions


GI Physiology: Motility47