Gastrointestinal

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 fibers 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 fibers 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 fibers 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 fibers 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 Reflexes
 GI reflexes can be considered;
 1. Local
 2. Regional
 3. Systemic
 Local reflexes are processed entirely within the enteric system and
control secretion, local motility, and mixing contractions.
 Regional reflexes go to the sympathetic ganglia, and are important
for reflexes at a distant, such as the gastro- colic reflex causing
evacuation of the colon, and messages from the intestine to the
stomach to inhibit emptying, the entero- gastric reflex, or the
colono- ilial reflex that inhibits emptying of the ilial contents into
the colon.
 Systemic reflexes are processed in the spinal cord or brainstem and
will control overall activity f the GI system, for example pain
reflexes 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 fluid and electrolytes

 Trophic (growth) effects

 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
emulsification 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 effects 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 Stimulus Stomach Pancreas Gall bladder
Motility and
Secretion
1. Secretin S cells lining Acid entering Inhibits Stimulates
the duodenum duodenum fluid secretion
(HCO3-)
2. CCK Cells lining the Fat and amino Inhibits Stimulates 1. Contraction
duodenum acids entering emptying enzyme 2. Relaxation
duodenum secretion sphincter
(Oddi)
3. Gastrin G cells of Stomach Stimulates
stomach distension
Antrum Parasymp
Duodenum Peptides
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 fluid into lower
esophagus
 Acid reflux 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 significant 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 fibers are predominantly cholinergic.
 The relaxation of the sphincter that occurs in response to primary peristalsis
in the esophagus is primarily mediated by vagal fibers 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 sufficiently 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 diffuse 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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 Clinical : DYSPHAGIA
 Def: Difficulty swallowing (affect esophagus), or
difficulties with the transition of ingested
substance from the mouth to stomach.