Gastrointest

inal
Physiology I
Part 1
Dr Lwiindi
(Medical
Physiologist)
 Functions
 4 major activities of GI tract
1. Motility
 Propel ingested food from mouth toward rectum
2. Secretion
 Aid in digestion and absorption
3. Digestion
 Food broken down into absorbable molecules
4. Absorption
 Nutrients, electrolytes, and water are absorbed
 Structure of GI Tract
 Arranged linearly in following
sequence
 Mouth, esophagus, stomach, small
intestine, large intestine, and anus

 Other structures of GI tract

 Salivary glands, pancreas, liver, and
gallbladder
 Structure of GI Tract
 Layers of GI Wall
1. Mucosa
 Innermost layer (faces lumen)
 It consists of an epithelium, the lamina propria,
and the muscularis mucosae
 Layer of epithelial cells specialized for absorption and
secretion
2. Submucosa
 Consists of collagen, elastin, glands, and blood
vessels
3. Circular and Longitudinal Smooth Muscle
 Provides motility for GI tract
4. Serosa
 Faces the blood
Layers of GI Wall
 Innervation of GI Tract
 Autonomic Nervous System has an
extrinsic and an intrinsic component
 Extrinsic
 Sympathetic and Parasympathetic
innervation of GI tract
 Intrinsic
 Called Enteric Nervous System
 Contained within wall of GI tract

 Communicates with Extrinsic component

 Intrinsic Innervation
 Can direct all functions of GI in absence
of extrinsic innervation
 Controls contractile, secretory, and
endocrine functions of GI tract
 Receives input from
1. Parasympathetic and sympathetic nervous
systems
2. Mechanoreceptors and chemoreceptors in
mucosa
 Sends information directly to smooth
muscle, secretory, and endocrine cells
 EXTRINSIC NERVES
 I. PARASYMPATHETIC FIBERS
 are supplied by the vagus nerve and pelvic nerves
which are of sacral origin. Parasympathetic fbers
are cholinergic and innervate both plexuses of the
enteric NS. Increased parasympathetic activity
increases smooth muscle activity. Motility and
secretion is increased, there is a reduction in
constriction of sphincters. An increase in
parasympathetic activity promotes digestive and
absorptive processes.
 The proximal half of the nervous system is
innervated from the cranial parasympathetic
nerve fbers via the vagal nerve. The distal half is
innervated via Sacral Parasympathetic nerves,
which gives supply to the sigmoid colon, rectum
and anus, and are important in controlling
defecation
 SYMPATHETIC INNERVATION
 The fbers originate in the sympathetic ganglia of T-5

to L-2 and terminate on the enteric nervous plexus,

but also a few nerves terminate in the mucosa it self

 SYMPATHETIC FIBERS innervation of the GI is

noradrenergic postganglionic. Increased sympathetic
discharge inhibit acetylcholine secretion from
cholinergic neurons.
 Some sympathetic fbers innervate smooth muscle

cells directly and some innervate splanchnic blood

vessels and act to cause vasocostriction, leading to
decreased motility and secretions, increase in
constriction of sphincters.
Gastrointestinal Refexes
 GI refexes can be considered;
 1. Local
 2. Regional
 3. Systemic
 Local refexes are processed entirely within the enteric
system and control secretion, local motility, and mixing
contractions.
 Regional refexes go to the sympathetic ganglia, and are
important for refexes at a distant, such as the gastro- colic
refex causing evacuation of the colon, and messages from
the intestine to the stomach to inhibit emptying, the entero-
gastric refex, or the colono- ilial refex that inhibits
emptying of the ilial contents into the colon.
 Systemic refexes are processed in the spinal cord or
brainstem and will control overall activity f the GI system, for
example pain refexes that will inhibit the entire GI system.
 GIT REGULATION
 Includes hormones, neurocrines, and
paracrines
 Regulate functions of GI tract
 Contraction and relaxation of smooth muscle
wall and sphincters
 Secretion of enzymes for digestion

 Secretion of fuid and electrolytes

 Trophic (growth) efects

 Some regulate secretion of other GI peptides

 GI Peptides
 Hormones
 Peptides released from endocrine cells of GI tract
 Secreted into portal circulation and enter systemic
circulation
 Target cells may be in GI tract or may be located
elsewhere in body
 Gastrin, Cholecystokinin, Secretin, and Gastric Inhibitory
Peptide
 Paracrines
 Secreted by endocrine cells of GI tract
 Act locally within same tissue that secretes them
 Somatostatin (inhibitory actions)
 Neurocrines
 Released by neurons of GI tract following an AP
 ACh, norepinephrine, Vasoactive Intestinal Peptide (VIP),
Gastrin-Releasing Peptide (GRP), Neuropeptide Y, and
Substance P
 GI Hormones
 Gastrin
 Secreted by G cells in stomach in response
to eating
 Stimuli include proteins, distention of stomach,
and vagal stimulation
 Gastrin-releasing peptide (GRP) is released from
vagal nerve endings onto G cells
 Secretion is inhibited by low pH in stomach
 Promotes H+ secretion by gastric parietal
cells
 Stimulates growth of gastric mucosa
 GI Hormones
 Cholecystokinin
 Secreted by I cells of small intestine in response to fatty
acids and small peptides
5 Actions:
1. Contraction of gallbladder
 Eject bile from gallbladder into small intestine necessary
for emulsifcation lipids
2. Secretion of pancreatic enzymes
 Digest lipids, carbohydrates, and proteins
3. Secretion of bicarbonate (HCO3-) from
pancreas
4. Growth of exocrine pancreas and gallbladder
5. Inhibition of gastric emptying
 Ensures adequate time for digestive and absorptive
 GI Hormones
 Secretin
 Secreted by S cells of duodenum in response
to H+ and fatty acids
 Promotes secretion of pancreatic HCO3-
 Neutralizing H+ allows for pancreatic enzymes to
digest fats
 Inhibits efects of gastrin on parietal cells (H+
secretion and growth)
 Gastric Inhibitory Peptide (GIP)
 Secreted by small intestine in response to all 3
types of nutrients
 Stimulates insulin secretion by pancreas
 Inhibits gastric H+ secretion
 GI Paracrines
 Somatostatin
 Secreted by endocrine cells in response
to decreased luminal pH
 Inhibits secretion of other GI hormones
 Inhibits gastric H+ secretion

 Histamine
 Secreted in H+-secreting region of
stomach
 Stimulates H+ secretion by gastric
parietal cells (along with gastrin and ACh)
 GI Neurocrines
 Synthesized in cell bodies of GI
neurons
 AP causes release of neurocrine
which interacts with receptors on
postsynaptic cell

 ACh (released from cholinergic neurons)

 Norepinephrine (released from

adrenergic neurons)
Hormone Source Stmulus Stomach Pancreas Gall bladder
Motlity and
Secreton
1. Secretn S cells lining Acid entering Inhibits Stmulates
the duodenum duodenum fluid secreton
(HCO3-)
2. CCK Cells lining the Fat and amino Inhibits Stmulates 1. Contracton
duodenum acids entering emptying enzyme 2. Relaxaton
duodenum secreton sphincter
(Oddi)

3. Gastrin G cells of Stomach Stmulates

stomach distension
Antrum Parasymp
Duodenum Peptdes
Stomach acid
inhibits

4. GIP Duodenum Fat, CH0, Inhibits

amino acids

CCK = Cholecystokonin, GIP = Gastric inhibitory peptide (glucose insulintropic peptide)

Note: In a non-acid producing stomach (e.g, chronic gastritis), the reduced negative feedback
increases circulating gastrin.
All four hormones stimulate insulin release.
 Esophagus
 Muscular tube that conveys food
from pharynx to stomach
 Inner circular muscle
 Outer longitudinal muscle

 Food passes through quickly

because of peristalsis
Esophagus
 Esophagus
 Pyrosis (heartburn)—common esophageal
discomfort
 Result of regurgitation of food and gastric fuid
into lower esophagus
 Acid refux can cause esophagitis
 Control of LES tone.
 The resting pressure in the LES is about 20 mm Hg. The tonic
contraction of the circular musculature of the sphincter is
regulated by nerves, both intrinsic and extrinsic, and by hormones
and neuromodulators.
 A signifcant fraction of this basal tone in this sphincter is
mediated by vagal cholinergic nerves. Stimulation of sympathetic
nerves to the sphincter also causes the LES to contract
 Relaxation of the LES.
 The intrinsic and extrinsic innervation of the LES is both
excitatory and inhibitory
 Vagal excitatory fbers are predominantly cholinergic.
 The relaxation of the sphincter that occurs in response to
primary peristalsis in the esophagus is primarily mediated by
vagal fbers that inhibit the circular muscle of the LES. Although
the inhibitory neurotransmitter is not known with certainty, it is
thought that VIP and NO mediate this relaxation of the LES.
 In some individuals, the sphincter fails to relax suficiently during
swallowing to allow food to enter the stomach.
 This condition is known as achalasia.
 Therapy for achalasia involves either mechanically dilating or
surgically weakening the LES or administering drugs that inhibit its
tone. In individuals with difuse esophageal spasm, prolonged and
painful contraction of the lower part of the esophagus occurs after
swallowing, instead of the normal esophageal peristaltic wave. In
individuals with incompetence of the LES, gastric juice can move
back up into the lower esophagus and erode the esophageal
mucosa.
 Mechanical Digestion
 Mastication – reducing the food
particle size through chewing, and
mixes food with saliva
 Deglutition – swallowing
1. Oral Stage (moth to oropharynx)
2. Pharyngeal Stage (oropharynx to
esophagus)
3. Esophageal Stage (esophagus to
stomach)
DIGESTION: MECHANICAL
 Deglutition: process of swallowing; complex
process requiring coordinated, rapid movements
(Figure 26-2)
 Oral stage (mouth to oropharynx): voluntarily controlled;
formation of a food bolus in the middle of the tongue;
tongue presses bolus against the palate and food is then
moved into the oropharynx
 Pharyngeal stage (oropharynx to esophagus): involuntary
movement; to propel bolus from the pharynx to the
esophagus, the mouth (tongue), nasopharynx (soft palate),
and larynx (epiglottis) must be blocked; a combination of
contractions and gravity move bolus into esophagus
 Esophageal stage (esophagus to stomach): involuntary
movement; contractions and gravity move bolus through
esophagus and into stomach

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