47
GI Physiology – I Dr Bhawana Neupane Pant Lecturer, Department of Physiology

GIT Physiology I

Embed Size (px)

Citation preview

Page 1: GIT Physiology I

GI Physiology – I

Dr Bhawana Neupane PantLecturer, Department of Physiology

Page 2: GIT Physiology I

Gastrointestinal System: Processes

• Motility• Digestion• Secretion• Absorption

Page 3: GIT Physiology I
Page 4: GIT Physiology I

Structure of the GI TractInnervation of the GI Tract

GI Peptides

Structure 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

Page 5: GIT Physiology I

1) Serosa - Continuous with the mesenteries

2) Muscularis- Longitudinal muscle- Circular muscle

3) Submucosa

4) Mucosa- Muscularis mucosae- Lamina propria- Epithelial cells

Layers of the GI tract

Structure of GI Tract

Page 6: GIT Physiology I

General Anatomy of Gut Wall

(Contains connective tissue, immune cells, capillaries, nerve endings)

(Might have role in villus movement)

Page 7: GIT Physiology I

1) Serosa

2) Muscularis:- Longitudinal muscle

- Circular Muscle

3) Submucosa:

4) Mucosa

Submucosal plexus (= Meissner’s plexus

Myenteric plexus (= Auerbach’s plexus)

2. Innervation of the GI Tract

Page 8: GIT Physiology I

a) The Enteric/ Intrinsic Nervous System

Primarily controls motility (length, intensity, frequency, velocity of peristaltic waves)Decreases tension of sphincters

Controls secretion, absorption, submucosal motility and blood flow

Page 9: GIT Physiology I

The Enteric Nervous System

Local Reflexes = “Short Reflexes.”

Can be influenced by CNS = “Long Reflexes.”

Page 10: GIT Physiology I

Parasympathetic and Sympathetic Innervation

Page 11: GIT Physiology I

Afferent Efferentsensory neurons from enteric NS (local afferents)

afferent sympathetic nerve fibers afferent parasympathetic nerve fibers2

1

en

te

ri

c

ne

rv

ou

s

sy

st

em

CN

S

mechanoreceptors chemoreceptors thermoreceptors

nociceptors

1

2

Integration of neuronal control of GI function

Page 12: GIT Physiology I

Effector system of GI innervation:

(modified from B&L)

Interaction of ANS and ENS

Page 13: GIT Physiology I

• 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

Page 14: GIT Physiology I

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.

Page 15: GIT Physiology I

Diabetic Stomach

• Gastroparesis is a disorder affecting people with both type 1 and 2 diabetes in 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.

Page 16: GIT Physiology I

Cholinergic (Acetylcholine) - excitatory

Adrenergic (Norepinephrine) - inhibitory

Non-adrenergic, non-cholinergic neurotransmitter (NANC)

• Vasoactive Intestinal Peptide (VIP)

• Gastrin Releasing Peptide (GRP) or Bombesin

• Enkephalins (opiates)

• Neuropeptide Y

• Substance 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.

Page 17: GIT Physiology I

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

Page 18: GIT Physiology I

In children with Hirschsprung’s 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)

Page 19: GIT Physiology I

Gastrointestinal Peptides:

Page 20: GIT Physiology I

Gastrointestinal Hormones:

Page 21: GIT Physiology I

Gastrin:

• Secreted by G cells in the antrum of stomach

• Principal physiologic actions: – Gastric acid secretion– Pepsin secretion– Trophic action (growth of the mucosa of the stomach, small and large

intestine)

Page 22: GIT Physiology I

What happens in Zollinger-Ellison Syndrome?

What happens when gastric antrum is resected?

H+ secretion is increased

Hypertrophy of gastric mucosa

Duodenal ulcer

Steatorrhea

H+ secretion is decreased

Gastric mucosa atrophies

Page 23: GIT Physiology I

Gastrin Stimulation

Inhibition 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 tryptophan Secretin

Page 24: GIT Physiology I

Cholecystokinin- secreted by I cells in the mucosa of the duodenum, the jejunum

• Primary functions:- Stimulation of pancreatic enzyme secretion

- The contraction of the gall bladder and relaxation of sphincter of

Oddi

- Growth of the exocrine pancreas and gallbladder

• Secondary functions:- Augments the action of secretin in producing secretion of an

alkaline pancreatic juice

- Increases the synthesis of enterokinase

- May enhance the motility of the small intestine and colon

Page 25: GIT Physiology I

CCK Functions

Page 26: GIT Physiology I

CCK Stimulation

Stimulation by:- Digestion products of fat and protein (most potent long fatty acid chains)

- Meals stimulate CCK secretions of gut and CNS simultaneously

Page 27: GIT Physiology I

Secretin

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.

Page 28: GIT Physiology I

Secretin Stimulation

- contact with acidic chyme- also stimulated by fatty acids

Page 29: GIT Physiology I

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

Page 30: GIT Physiology I

GIP Functions

Major function:- Release of insulin

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

??

Page 31: GIT Physiology I

GIP Stimulation

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

Page 32: GIT Physiology I

C. Candidate Hormones

• produced 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

Page 33: GIT Physiology I

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 Polypeptide• Secreted by the pancreas• Stimulated by ingestion of carbohydrates, proteins, or lipids• Inhibits pancreatic secretion of HCO3

- and enzymes • Physiologic role uncertain

I: Motilin• primarily in duodenum by M cells• physiologic stimuli not known• initiates the MMC migrating motor complex (see motility lecture)

Candidate Hormones

Page 34: GIT Physiology I

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.

1. Somatostatin

2. Histamine

Page 35: GIT Physiology I

Somatostatin• Secreted by D-cells in gastric mucosa• Delta cells in the pyloric antrum, the duodenum and the pancreatic

islets• Both paracrine and endocrine

• Suppresses gastric secretions• Inhibits motility and tone of stomach and small intestines and gall

bladder• Inhibits formation of liver bile• Inhibits the release of ALL known GI hormones• Inhibits saliva, gastric, pancreatic, small intestinal and liver

secretions• Inhibits splanchnic blood flow• Inhibits intestinal absorption

• In brain it inhibits GH release• In pancreas, inhibitor of insulin and glucagon

Octreotide : analogue of somatostatin

Page 36: GIT Physiology I

Action Gastrin CCK Secretin GIP

Acid secretion

Pancreatic HCO3- secretion

Pancreatic enzyme secretion

Bile HCO3-

Gallbladder contraction

Gastric emptying

Gastric Mucosal growth

Pancreatic growth

Insulin Secretion

S = stimulates; I = inhibits

Actions of GI hormones

ISS

S

S

S

SS S

I

S

S

I

Page 37: GIT Physiology I

GI Motility

Page 38: GIT Physiology I

Skeletal muscle:• Upper esophagus• External anal sphincter

Smooth muscle: (of the visceral or unitary type): • Rest of GI tract

GI Muscles

Page 39: GIT Physiology I

In comparison to skeletal muscle:

Energy: Low (up to 300x less)

Force: High

Shortening: High

Time: Long (tonic)

Speed: Slow

Page 40: GIT Physiology I
Page 41: GIT Physiology I

Basic Electrical Activity

SLOW 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

Page 42: GIT Physiology I

• Frequency of electric activity determines the frequency of contractions

• Basic Electrical Rhythm in different parts• Stomach ~ 3/min• Duodenum ~ 11-12/min• Distal Ileum ~ 6-7/min

Page 43: GIT Physiology I

Objectives of Today’s 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

Page 44: GIT Physiology I

MotilityMouth and Esophagus: Chewing, Swallowing,

Peristalsis

Stomach: Filling, Churning, Peristalsis, Emptying

Small Intestine: Segmental Contractions, Peristalsis

Large Intestine: Haustral Shuttling, Mass Movements, Defecation.

Sphincters: Regulation of Movement

Page 45: GIT Physiology I
Page 46: GIT Physiology I

Tonic Contractions

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

Page 47: GIT Physiology I

Phasic Contractions

Peristalsis Segmentation