By: Abduljabbar Hamid Jabbar

University of Baghdad-College Of Medicine

M. B. Ch. B
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
The digestive system prepares food for use by cells through five basic activities:
1. Ingestion or the taking of food into the body.
2. Peristalsis or the physical movement or pushing of food along the digestive tract.
3. Digestion or the breakdown of food by both mechanical and chemical mechanisms.
4. Absorption or the passage of digested food from the digestive tract into the cardiovascular and lymphatic systems for
distribution to the body’s cells.
5. Defecation or the elimination from the body of those substances that are indigestible and cannot be absorbed.

The primary function of the alimentary tract is to break down food and to
provide the body with a continual supply of water, electrolytes and nutrients.
In order to achieve these functions, the gastrointestinal tract (GIT) must
perform the following processes:

ingestion, movement, digestion, absorption, secretion and defecation. The

adult GIT is a tube running through the body from mouth to anus.
Anatomical features: The organizations of the structures that
make up the wall of the gastrointestinal tract (GIT) from the
posterior pharynx to the anus generally are as follow from the
outer surface inward
1. Serosa which continues onto the mesentery, which contains the
nerves, lymphatics, and blood vessels supplying the tract.

2. Longitudinal muscle.

3. Myenteric (Auerbach’s) plexus which controls mainly the GIT

movement.

4. Circular muscle which causes a decrease in the diameter of the

lumen of the GI tract when it contracts.

5. Submucous (Meissner’s) plexus which is important in controlling

secretion and blood flow and also subserves many sensory
functions, receiving signals from chemoreceptors in the gut
epithelium and from stretch receptors in the gut wall.

6. Mucosa and submucosa which consists of epithelium and

subepithelial connective tissue and are specialized for secretion
and absorption.
The enteric nervous system (ENS): The GIT has an intrinsic nervous system of its own called the enteric nervous system
which controls most GI functions, especially GIT movements and secretion.

The enteric nervous system is composed of two layers of neurons and connecting fibers, the outer layer is called the
myenteric (Auerbach’s) plexus, the inner layer is called the submucous (Meissner’s) plexus. The degree of activity of this
enteric nervous system can strongly be altered by extrinsic (autonomic) nervous system, i.e. parasympathetic and
sympathetic nervous systems.

Both systems send signals to GIT from the brain and spinal cord to modulate the activity of the enteric nervous system.
The parasympathetic nerve fibers: Stimulation of the parasympathetic nerves fibers releases acetylcholine and causes in
general:
• An increase in the activity of most GIT functions.
• Relaxation of sphincters (except the lower esophageal sphincter, which they stimulate).

The parasympathetic supply to the gut is divided into:

I. Cranial division: Is mediated almost entirely through the vagus (X cranial nerve). Vagus nerves innervate esophagus,
stomach, pancreas, gallbladder and first half of the large intestine, and little innervations to the small intestine

II. Sacral divisions: The sacral divisions originate in S2, 3, 4 sacral segments of the spinal cord, and pass through the
pelvic nerves to the distal half of the large intestine. These fibers function especially in the defecation reflex. Because
the parasympathetic nervous system plays a dominant role in the digestive process, it is often referred to as the “rest
and digest”division.
Reflexes of GIT are either occur entirely within the
enteric nervous system (short reflex arc), or the reflex
arc is originated from the gut and to the CNS (spinal
cord or brain stem) and then back to the gut (long
reflex arc)

Signals transmitted through these reflexes can cause

reflex excitation or inhibition of intestinal movements
or secretion. In addition to its anatomic complexity,
the ENS utilizes many different neurotransmitters,
including acetylcholine, adenosine triphosphate (ATP),
nitric oxide, and numerous peptides.
• Hirschsprung’s disease is a congenital absence of the myenteric plexus, usually involving a portion of the
distal colon. The pathologic non-ganglionic section of large bowel lacks peristalsis and undergoes
continuous spasm, leading to a functional obstruction.

• The normally innervated proximal bowel dilates as a result of the obstruction and can lead to the most
feared complication of Hirschsprung’s disease, toxic megacolon.
Types of GIT smooth muscle contractions: The smooth muscle of GIT is almost exclusively unitary smooth muscle while
that of pharynx, upper one third of the esophagus, and external anal sphincter are striated muscles. Although the upper
esophageal sphincter surrounds the upper part of the esophagus consists of skeletal muscle, but is not under conscious or
voluntary control. There are two main types of smooth muscle contractions:

[A] Phasic (rhythmical) contractions that occur in the esophagus, stomach, and intestine. They include

1. Peristaltic
2. Migrating Motor Complex (MMC),
3. Segmentation and haustration contractions
4. Distention-induced contraction

[B] Tonic contractions

In peristalsis, contraction of a small section of proximal muscle is followed immediately by relaxation of the muscle just
distal to it. The resulting wavelike motion moves food along the GIT in a proximal to distal direction. Peristaltic wave could
be of two types:

[1] Primary peristaltic wave which is a continuation of the peristaltic wave that begins proximally and mediated by
vagovagal reflexes, long reflex arc.

[2] Secondary peristaltic wave which is generated by the enteric nervous system (short reflex pathway), initiated from the
distension of the viscus by the retained food if the primary peristaltic wave fails to move all the food that has entered the
viscus.
MMC is a distinct pattern of electromechanical activity observed in
gastrointestinal smooth muscle during the periods between meals,
and it is interrupted by feeding. It is thought to serve a
"housekeeping" role and sweep residual undigested material through
the digestive tube. The cycle recurs every 1.5 to 2 hours.

These motor complexes trigger peristaltic waves, which facilitate

transportation of indigestible substances such as bone, fiber, and
foreign bodies from the stomach, through the small intestine, past the
ileocecal sphincter, and into the colon. An intact enteric nervous
system is essential for propagation of migrating motor complexes
along the bowel.

The MMC is thought to be partially regulated by motilin (by a direct

action on smooth muscle and by activation of excitatory enteric
nerves and it is released during the interdigestive period). MMC is
initiated in the stomach as a response to vagal stimulation. Control of
the MMC is complex.

MMC with an antral origin can be induced in humans through

intravenous administration of motilin, erythromycin or ghrelin,
whereas administration of serotonin or somatostatin induces MMC
with duodenal origin.

The role of the vagus nerve in control of the MMC seems to be

restricted to the stomach, as vagotomy abolishes the motor activity in
the stomach, but leaves the periodic activity in the small bowel intact.
In segmentation contraction, nonadjacent segments of alimentary tract organs, especially small intestine, contract and
relax, moving food forward then backward, resulting in food mixing and slow food propulsion. Segmentation contraction is
the primary motility pattern of the digestive period in humans, and is defined as irregular and uncoordinated contraction of
the circular muscle layer. This pattern, which develops in response to intestinal wall distention, is determined by activation
of preprogrammed neural circuits within the myenteric plexus.

The combined contractions of the circular and longitudinal smooth muscle cause the unstimulated portion in large intestine
to bulge outward into baglike sacs called haustration. Therefore, the fecal material in the large intestine is squeezed,
moving back and forth along the colon in a manner similar to that for the segmentation contractions in the small intestine.
Distention-induced contraction of gastrointestinal smooth muscle develops as the result of long (vago-vagal) and local
(enteric nerves) reflexes. The importance of long versus local reflex pathways varies along the gut.

Secondary esophageal peristalsis, intestinal segmentation, and migrating motor complexes are unaffected by vagotomy,
whereas primary peristaltic wave and proximal stomach peristalsis is decreased but not abolished by vagotomy.
Electrical slow wave activity in the gastrointestinal tract appears to originate from specialized pacemaker cells (interstitial
cells of Cajal) located between the longitudinal and circular muscle layers and within the submucosal and myenteric
plexuses. These pacemaker cells input directly onto the smooth muscle and receive input from Autonomic nerves.
[B] Tonic contractions that occur in the lower esophageal sphincter, pyloric sphincter, ileocecal sphincter, and
internal anal sphincter. Tonic contraction is continuous, occasionally increases or decreases in intensity.
Different Types of Neurotransmitters Secreted by Enteric Neurons
1. Acetylcholine 7. Substance P
2. Norepinephrine 8. Vasoactive intestinal polypeptide
3. Adenosine triphosphate 9. Somatostatin
4. Serotonin 10. Leu-enkephalin
5. Dopamine Acetylcholine most often excites
11. Met-enkephalin gastrointestinal activity.
6. Cholecystokinin 12. Bombesin Norepinephrine and epinephrine almost
always inhibit gastrointestinal activity.
Thank You
17
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
Mastication (chewing): Is the process by which food taken into the
mouth is chewed by the teeth.

• The chewing reflex is controlled by nuclei in the medulla and

cerebral cortex. Most of the muscles of chewing are innervated
by the motor branch of the 5 th cranial nerve (trigeminal N).

• Voluntary contraction of the muscles of chewing is in response

to the presence of a bolus of food in the mouth compresses the
bolus against the linings of the mouth and push the food to
come in contact with the buccal receptors.

• The contact of food with buccal receptors causes reflex

inhibition of the muscles of mastication, which allows the lower
jaw to drop.

• The drop in turn initiates a stretch reflex of the jaw muscles (the
masseter, medial pterygoid, and temporalis muscles) that leads
to rebound contraction.

• This automatically raises the jaw to cause closure of the teeth,

but again, it also compresses the bolus against the linings of
the mouth and pushes the food to come in contact with the
buccal receptors, which inhibit the jaw muscles once again and
allowing the jaw to drop and rebound another time, and this is
repeated again and again.
Chewing is important because:

[1] Chewing breaks down the indigestible cellulose membranes around the nutrient portions of food before the food can be
utilized.

[2] Chewing increases the surface area of food so the rate of digestion of food by the digestive enzymes is increased.

[3] Chewing grinds the food to a very fine particulate consistency prevents excoriation of the GIT and increases the ease
with which food is swallowed and emptied from the stomach into the small intestine and thence into all succeeding
segments of the gut.

[4] Chewing mixes the food with salivary gland secretions which initiates the process of starch digestion (by salivary
amylase) and to much less extent of lipid digestion (by lingual lipase) and to lubricate and soften the bolus of food, making
it easier to swallow.

[5] Chewing brings food into contact with taste receptors and releases odors that stimulate the olfactory receptors. The
sensations generated by these receptors increase the pleasure of eating and initiate gastric secretions.
Salivary glands: The daily normal secretion of saliva is between 500—1500 ml. Saliva is secreted from the glands of
salivation, the parotids (25%), submandibular glands (70%), and sublingual glands (5%). In addition, there are many small
buccal glands. In comparison to plasma, saliva is:
• Hypotonic.
• Contains higher concentration of K ions and bicarbonate ions and lower concentrations of Na and Cl ions.
• Saliva has a pH 6.0 - 7.4.

HCO3 - Iodide , Ca+

The structure of each gland is similar to a bunch of grapes. The acinus is lined with acinar cells and secretes initial saliva
which is a plasma-like solution (isotonic) containing amylase and/or mucin. A branching duct system is lined with columnar
epithelial cell, which modify the initial saliva. Acinar cells secrete initial (primary) saliva which is a plasma-like solution
(isotonic) containing amylase and/or mucin and then modified by the ductal epithelial cells of the gland by:
Active absorption of Na+ (3Na+ -2K+ ATPase),
Passive reabsorption of Cl ions (due to electrical gradient) in exchange to HCO3 - ions which are secreted actively (Cl- -
HCO3 - secondary active counter-transport).
Saliva is an important route of iodide excretion; its concentration in saliva is 20–100 times that in plasma.
It is saturated with calcium ions; calcium salts are laid down as plaque on the teeth.
Saliva consists of two major types of protein secretions:

1. Serous secretion (watery saliva) containing ptyalin (α-amylase which is an enzyme for
digesting starches) and electrolytes.

2. Mucous secretion containing mucin (glycoprotein) for lubricating purposes.

The parotid glands secrete entirely the serous type.
The submandibular and sublingual glands secrete both the serous type and mucus.
The buccal glands secrete only mucus

Therefore, the composition of saliva varies with the salivary flow rate:

[1] At the lowest flow rates, saliva has the lowest osmolarity (about 100 mOsm/L) and lowest
Na+ , and Cl-concentrations, but has the highest K+ and HCO3 - ion concentration.

[2] At the highest flow rates, saliva is most like the initial secretion from the acinus and its
composition is closet to that of plasma.
Control of salivary secretion: Salivary glands are controlled by
salivatory nuclei which are located at the juncture of the medulla
and pons.

• Mainly through parasympathetic fibers through 7th cranial nerve

(Facial N) and 9th cranial nerve (Glossopharyngeal N) which leads
to abundant watery saliva rich in enzymes.

• And to less extent by sympathetic nervous signals originates from

the superior cervical ganglia and then travels along blood vessels
to the salivary glands which leads to scanty thick saliva rich in
mucus. This is why the mouth may feel sticky or dry under
conditions of stress.

Under basal conditions, saliva is almost entirely of the mucus type

and is secreted all the time except during sleep when the secretion
becomes very little. Unlike the autonomic nervous system
elsewhere in the body, sympathetic and parasympathetic responses
in the salivary glands are not antagonistic.
Salivatory nuclei are excited or inhibited by :

[A] Signals from the mouth: Taste (especially the sour taste is excitatory, bitter taste is inhibitory) and tactile stimuli
(especially smooth objects is excitatory) from the tongue and other areas of the mouth.

[B] Signals from higher centers of CNS: Salivation can also be stimulated or inhibited by impulses arriving in the salivatory
nuclei from higher centers of CNS. For instance, when a person smells or sees favorite foods, salivation is greater than
when disliked food is smelled or seen.

[C] Signals from GIT: Salivation also occurs in response to reflex originating in the stomach and upper intestine particularly
when very irritating foods are swallowed or when a person is nauseated. The swallowed saliva may help to remove the
irritating factor in the GIT by diluting or neutralizing the irritant substances.

Saliva production is decreased (via inhibition of the parasympathetic nervous system) by sleep, dehydration, fear, and
anticholinergic drugs (such as atropine).
Functions of saliva:
[A] Protection of the mouth by: by Cooling hot foods and By maintaining healthy oral tissues. The mouth is loaded with
pathogenic bacteria that can easily destroy tissues and can also cause dental caries. However, saliva helps prevent the
harmful effects of bacteria by:

• Continuous washing away the pathogenic bacteria as well as the food particles that provide the bacteria with metabolic
support.
• Saliva contains many factors that can kill bacteria such as thiocyanate ions, proteolytic enzymes, and antibodies (IgA).

[B] Digestion of starch by α-amylase (which is ultimately inactivated by the low pH of the stomach), and fat by lingual
lipase.

[C] Lubrication of food and making swallowing easier, and moisten the mouth, facilitating speech. It also neutralizes any
gastric acid that refluxes from stomach into the lower esophagus (heartburn)
Xerostomia is defined as dry mouth resulting from reduced or absent saliva flow. Xerostomia is not a disease,
but it may be a symptom of various medical conditions, a side effect of a radiation to the head and neck, or a
side effect of a wide variety of medications.

Xerostomia is a common complaint affecting approximately 20 percent of the elderly.

Thank You
12
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
Swallowing (deglutition): The voluntary initiation of swallowing takes place in higher brain centers and starts with oral
stage. From here on, the process of swallowing becomes entirely or almost entirely automatic and controlled by swallowing
(or deglutition) center which is located at the medulla and the pons.

• The afferent (sensory) fibers to this center are:

Trigeminal (5th cranial nerves),
Glossopharyngeal (9th cranial nerves),

• The efferent (motor) nerve fibers from the swallowing center are conducted through:
Trigeminal (5th cranial nerves),
Glossopharyngeal (9th cranial nerves),
Vagus (10th cranial nerves),
Hypoglossal (12th cranial nerves),
Few of the superior cervical nerves to the pharynx and upper esophagus

 Swallowing can be divided into the following stages:

Oral stage.
Pharyngeal stage.
Esophageal stage.
Relaxation of lower esophageal sphincter.
[A] Oral (voluntary) stage of swallowing: Food is voluntarily
squeezed posteriorly in the mouth to the oropharynx by
pressure of the tongue upward and backward against the hard
palate.
From here on, the process of swallowing becomes entirely or
almost entirely automatic and cannot be stopped.

[B] Pharyngeal (involuntary) stage: When the bolus of food is

pushed backward in the mouth,
It stimulates swallowing receptor areas around the opening of
the pharynx afferent impulses pass to Swallowing center to
initiate a series of automatic pharyngeal muscular contractions
and to inhibit the respiratory center of the medulla during
swallowing, halting respiration at any point in its cycle to allow
swallowing to proceed.

The sequence of events of the pharyngeal stage of the

swallowing is as follows:
1. The soft palate is pulled upward to close the posterior nares
preventing reflux of food into the nasal cavities.

2. The palatopharyngeal folds on either side of the pharynx are

pulled medial ward to approximate each other. In this way these
folds form sagital slit through which the food must pass into
the posterior pharynx. This slit performs a selective action,
allowing food that has been masticated properly to pass with
ease while impede the passage of large objects.
3. The vocal cords of the larynx are strongly
approximated, and the hyoid bone and larynx are pulled
upward and anteriorly by the neck muscles causing
epiglottis to swing backward over the superior opening of
the larynx. All these effects (especially the approximation
of vocal cords) prevent passage of food into the trachea.

4. The upward movement of the larynx also stretches the

opening of the esophagus. At the same time, the upper 3
to 4 cm of the esophagus, an area called the upper
esophageal sphincter (or pharyngeoesophageal sphincter
or the cricopharyngeal muscle), relaxes, thus allowing
food to move easily and freely from the posterior pharynx
into the upper esophagus.

This sphincter between swallows, remains tonically and

strongly contracted (by the continual firing of the vagal
fibers), thereby prevents air from going into the
esophagus during respiration.

5. At the same time that the larynx is raised and the upper
esophageal sphincter is relaxed, the superior constrictor
muscle of the pharynx contracts, giving rise to a rapid
peristaltic wave passing downward over the pharyngeal
muscles and into the esophagus, which also propels the
food into the esophagus.
Swallowing becomes a great concern for the elderly since strokes and Alzheimer's disease can interfere with the
autonomic nervous system.

there are multiple areas of the central nervous system which, if affected by a stroke, could disrupt the ability to swallow.
This is especially true for strokes of the medulla, as this is a relatively small area that contains multiple structures that are
critical in carrying out the swallowing reflex.

In fact, people with medullary strokes frequently require temporary or permanent feeding tube placement
[C] Esophageal stage of swallowing: The esophagus functions to conduct food from
the pharynx to the stomach. The movement of food down the esophagus is an active
process (primary esophageal peristalsis integrated at swallowing center) that does
not depend on gravity for its normal function. The upper esophageal sphincter and
lower esophageal sphincter are closed in normal resting state.

Closure of the upper esophageal sphincter prevents air from being drawn from the
mouth into the esophagus during inspiration. Closure of the lower esophageal
sphincter prevents gastric contents to move back from the stomach to the
esophagus.

Because most of the esophagus is contained within the thoracic cavity, the pressure
in the lumen of the resting esophagus is approximately equal to intra-thoracic
pressure (atmospheric or slightly below atmospheric) when the upper esophageal
sphincter and lower esophageal sphincter are closed (normal resting state). During
pulmonary inspiration, the intra-esophageal pressure will be sub-atmospheric.

The term secondary esophageal peristalsis describes esophageal peristalsis and

lower esophageal relaxation associated with distension or irritation of the smooth
muscle portion of the esophageal body.

The event is limited to the smooth muscle component of the esophagus and is the
result of activation of enteric nerves. Initiation of secondary peristalsis does not
involve extrinsic neural reflexes and, thus, is not accompanied by the oral-pharyngeal
phase of swallowing.
[D] Relaxation of lower esophageal sphincter: The lower
esophageal sphincter is not anatomically separate identifiable
muscles.

The fundus of the stomach and lower esophageal sphincter

extending about 2-5 cm above its junction with the stomach
both relax during a swallow while the bolus of food is still
higher in the esophagus. This phenomenon is called
receptive relaxation. Receptive relaxation is vagally mediated,
Nitric oxide is the neurotransmitter thought to mediate
receptive relaxation at the smooth muscle cell allowing food
to pass to the stomach.
Reflux of the acidic contents of the stomach up to
the esophagus damages the esophageal mucosa.
This is prevented by:

[1] The muscles of the lower esophageal sphincter

normally remains tonically contracted due to tonic
activity of the vagal fibers innervating the esophagus
(in contrast to the mid- and upper portions of the
esophagus which normally remain completely
relaxed).

Vagal efferent nerve fibers control contraction and

relaxation of the LES. Vagal excitatory fibers
synapse on post-ganglionic, enteric motor neurons
that release acetylcholine within the musculature of
the LES. Vagal inhibitory fibers synapse on enteric
inhibitory motor neurons that release nitric oxide
(NO).

These neurons may also utilize ATP and VIP as

inhibitory transmitters, but NO is the primary
inhibitory neurotransmitter. Sympathetic neurons
also provide excitatory input to the LES via
excitatory motor neurons.
[2] Another factor that prevents reflux is the oblique entrance of the esophagus to the stomach which acts like
a valve-like mechanism of that portion of the esophagus that lies immediately beneath the diaphragm.

Greatly increased intra-abdominal pressure caves the esophagus inward at this point at the same time that the
abdominal pressure also increases the intragastric pressure, preventing the high pressure in the stomach
from forcing stomach contents into the esophagus.
Esophageal reflux: Reflux of stomach acid to the esophagus causes esophageal pain (heartburn) and may
lead to esophagitis. An increase in the intraabdominal pressure (by the ingestion of a very large meal,
production of intestinal gas, pregnancy, an abdominal mass such as a tumor, bending at the waist, straining
against a closed glottis as in defecation) will facilitate gastro-esophageal reflux if the LES is not contracted or
there is distortion of the valve-like mechanism. Esophageal reflux may occur if:

[A] If the intragastric pressure raises high enough to force the lower esophageal sphincter open.
[B] If the lower esophageal sphincter is unable to maintain its normal tone.
[C] If the lower esophageal sphincter is forced through the diaphragm and into the thoracic cavity as in hiatal
hernia, in which the oblique entrance of the esophagus to the stomach is distorted, and consequently the
valve-like mechanism is impaired.
Belching (eructation): Following a heavy meal or the ingestion of large amounts of gas (e.g., from carbonated
beverages), the gas bubble that is usually in the fundus of the stomach is displaced to the cardia.

When lower esophageal sphincter relaxes during the swallowing process, gas enters the esophagus and is
regurgitated.
Dysphagia: Difficulty in swallowing. Persons with dysphagia usually report choking, coughing, or an abnormal sensation of
food sticking in the back of the throat or upper chest when they swallow. If swallowing is painful, it is referred to as
odynophagia. Dysphagia can result from altered nerve function or from disorders such as:

Narrowing of the esophagus.

Lesions of the central nervous system (CNS), such as a stroke, often involve the cranial nerves that control swallowing.

Strictures and cancer of the esophagus and strictures resulting from scarring can reduce the size of the esophageal
lumen and make swallowing difficult.
Achalasia: In which the lower esophageal sphincter fails to relax; food that has been swallowed has difficulty
passing into the stomach, and the esophagus above the lower esophageal sphincter becomes enlarged.

One or several meals may lodge in the esophagus and pass slowly into the stomach. There is danger of
aspiration of esophageal contents into the lungs when the person lies down.
Thank You
16
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
The stomach: The stomach can be divided into a. the fundus, b. the body, and c. the antrum.

Physiologically the fundus functions mainly as part of the body. The lining epithelium of the stomach mucosa is a simple
columnar epithelium composed entirely of mucous cells.

They produce a cloudy, protective two-layer coat of alkaline mucus in which the surface layer consists of viscous,
insoluble mucus that traps a layer of bicarbonate-rich fluid beneath it.

This otherwise smooth lining is dotted with millions of deep gastric pits, which lead into tubular gastric glands that produce
the stomach secretion called gastric juice.
1. Storage: Is mediated by the process of receptive relaxation
of the stomach until the food can be delivered to the small
intestine at the proper time. Normally, when food enters the
stomach a vago-vagal reflex greatly reduces the tone in the
muscular wall of the body of the stomach (active relaxation
of smooth muscles, vagally mediated, Nitric oxide is the
neurotransmitter thought to mediate receptive relaxation at
the smooth muscle cell) so that the wall can bulge
progressively outward accommodating greater and greater
quantities of food up to a limit of about 1 liter.

Stomach accommodation depends exclusively upon an

intact vago-vagal reflex. If vagal innervation is interrupted,
then intra-gastric pressure increases. This is a potential
cause of vomiting due to the inability of the proximal
stomach smooth muscle to undergo receptive relaxation.

2. Mixing and propelling of food: When the stomach is filled,

weak peristaltic and segmentation (mixing) contractions
move toward the antrum along the stomach wall, propelling
and mixing food with gastric juice until it forms a semifluid
mixture called chyme. This is due to distension of the
stomach which elicit vagovagal reflex
3. Emptying: Slow emptying of chyme from the stomach into the small intestine at a rate suitable for proper
digestion and absorption by the small intestine. The degree of constriction of the pyloric sphincter and the
intensity of antral peristaltic wave (mediated by myenteric reflexes) can be varied according to signals both,
from the stomach and from duodenum. The antral peristaltic waves provide a pumping action and are
frequently called the pyloric pump.

The stomach is a poor absorptive area of the gastrointestinal tract because it lacks the typical villus type of
absorptive membrane, and also because the junctions between the epithelial cells are tight junctions. Only a
few highly lipid-soluble substances, such as alcohol and some drugs like aspirin can be absorbed in small
quantities.
Regulation of gastric emptying (pyloric pump): Gastric emptying is a key control point in the gastrointestinal
tract to ensure the orderly delivery of nutrients in a form that can be digested and to give appropriate signals
of fullness (satiety).

Gastroparesis (“weak stomach”) is a common complication of poorly controlled diabetes mellitus and
significantly slows gastric emptying. The rate at which the stomach empties is regulated by signals both from
the stomach and duodenum. These signals will be discussed later in association with the factors that affect
gastric secretion. Gastric emptying takes about 3 hours and very closely regulated so that nutrient absorption
is maximized and H+ in the duodenum has time to be neutralized.
Gastric secretions aid in the breakdown of food into small
particles and continue the process of digestion which had begun
by the salivary enzymes. About 2 L / day of gastric secretions are
produced. The stomach mucosa contains two main types of
gastric glands

[A] Gastric glands which are located in the fundus and the body of
the stomach. They contain three types of secretory cells:

1. Mucus secreting cells which secretes mucus.

2. Parietal (oxyntic) cells which secrete intrinsic factor and HCl.

3. Peptic (chief) cells which secrete pepsinogen, the precursor for

the proteolytic enzyme pepsin.

4. Enteroendocrine cells (or enterochromaffin-like cells, ECL cell)

release a variety of chemical messengers directly into the
interstitial fluid of the mucosa of the stomach. Some of these are
histamine, serotonin, and somatostatin.
[B] Pyloric glands which are located in the antral and pyloric
regions of the stomach. They contain:
G cells and some mucous cells, G cells are responsible for the
release of the hormone gastrin.
D cells, which release somatostatin, a hormone that inhibits the
release of gastrin
Gastric intrinsic factor secretion: A substance called intrinsic factor is secreted by the oxyntic cells, and it is essential for
absorption of vitamin B12 in the ileum. If the acid producing cells of the stomach are destroyed as it occurs in chronic
gastritis, the person develops achlorhydria and pernicious anaemia because of failure of maturation of the RBC in the
absence of vitamins B12.

Although intrinsic factor is secreted by the oxyntic cells of the gastric mucosa, binding to cobalamin occurs in the
duodenum. The vitamin B12-intrinsic factor complex is propelled along the small intestine to the terminal ileum, where
specific transporters located on the enterocyte microvilli bind the vitamin B12-intrinsic factor complex. Binding requires
calcium and is optimal at pH 6.6. Absorption is an active transport process.
Gastric HCl secretion: HCl is secreted into the parietal cell canaliculi by the following steps :

[1] CO2 diffuses from blood to inside the parietal cells.

[2] Within the parietal cells, carbonic acid is formed from the reaction: CO2 + H2O H2CO3.
The formation of H2CO3 from CO2 is catalyzed by the enzyme carbonic anhydrase.

[3] HCO3 – diffuses back into the plasma in exchange for Cl- , thus providing Cl for the initial
step in the secretory process. As HCO3 – is added to the venous blood, the pH of the blood
drained from the stomach increases (alkaline tide). The active transport process is begun by
the transport of Cl ion into the canaliculi that open to the lumen of the stomach.

[4] The H+ that is supplied by the dissociation of carbonic acid into H+ and HCO3 - within the
parietal cells is exchanged for K+ by the H+ -K + -ATPase pump (proton pump).

[5] Chloride ions diffuse with the charged H+ .

[6] Water enters the canaliculi down the osmotic gradient created by the movement of HCl into
the canaliculi.
Most of the HCl that is secreted into the stomach is neutralized and reabsorbed within the small intestine.
However, if the gastric contents are lost before they enter the small intestine as in case of vomiting, sever
alkalosis may ensue. The pH of the parietal cell secretion can be as low as 0.8 (or almost 4 million times as
great as the H+ concentration of plasma).

Parietal cells bear receptors for three potent stimulators of acid secretion, reflecting a triad of neural,
paracrine and endocrine control:

Acetylcholine (muscarinic type receptor) Gastrin Histamine (H2 type receptor)

A variety of substances are capable of reducing gastric acid secretion including:

Prostaglandin E2 (PGE2),
Several peptides hormones, including Secretin, Gastric inhibitory polypeptide (GIP), Glucagon and,
Somatostatin.
GIP (also known as the glucose-dependent insulinotropic peptide) released from duodenal and jejunal
mucosa in response to the presence of chyme especially by hyperosmolarity of glucose in the duodenum and
inhibits gastric gastrin release and stimulate the release of insulin from pancreas, and inhibit the GI motility
and secretion of acid.

The amount of insulin secreted is greater when glucose is administered orally than intravenously. It is the
only gastrointestinal hormone released by all three major foodstuffs (fats, proteins, and carbohydrates).
PGE2, secretin and somatostatin may be physiologic regulators. Somatostatin inhibits secretion of gastrin
and histamine, and appears to have a direct inhibitory effect on the parietal cell.
The functions of HCl:

[1] It participates in the breakdown of protein: The high acidity of the chyme alters the protein molecules, thereby changing
protein structure so as to break up connective tissue and cells in the ingested food.

[2] It hinders the growth of pathogenic bacteria: HCl kills most of the bacteria that enter along with food. This process is
not 100% effective, and some bacteria survive to take up residence and multiply in the intestinal tract.

[3] It activates pepsinogens and provides an optimal pH for the action of pepsin: Several different types of pepsinogens are
secreted by the peptic cells of the gastric glands and all perform the same function. When the pepsinogens are secreted,
they have no digestive activity.

However, as soon as they come in contact with HCl and especially when they come in contact with previously formed
pepsin plus the HCl, they are immediately activated to form active pepsin which is an active proteolytic enzyme in a highly
acid medium.
Gastric mucus secretion: The surface of the stomach mucosa between glands has a continuous layer of mucous cells that
secrete large quantities of a viscid and alkaline mucus that coats the mucosa with a mucous gel layer (the gastric mucosal
barrier) often more than 1 mm thick, thus providing a major shell of protection for the stomach wall against acidity as well
as contributing to lubrication of food transport.

Even the slightest irritation of the mucosa directly stimulates the mucous cells to secrete copious quantities of this thick,
viscid mucus. This in turn forms a gastric barrier that prevents digestion of the gastric wall and also greatly reduces the
absorption of most substances by the gastric mucosa. If this barrier is damaged by toxic substances, such as occurs with
excessive use of aspirin, and other nonsteroidal anti-inflammatory drugs, or alcohol, the secreted acid does leak down an
electrochemical gradient into the mucosa, causing stomach mucosal damage
The luminal membranes of the gastric mucosal cells are impermeable to H+ so that HCI cannot penetrate into the cells.
The cells are joined by tight junctions that prevent HCI from penetrating between them.
A mucus coating over the gastric mucosa serves as a physical barrier to acid penetration.
The HCO3 - rich mucus also serves as a chemical barrier that neutralizes acid in the vicinity of the mucosa.
Even when luminal pH is 2, the mucus pH is 7.
Mild injury to the mucosal barrier results in increased
mucus secretion and surface desquamation followed
by regeneration. A more serious injury breaks
mucosal barrier and exposes the mucosal surface,
forming an ulcer, and produces bleeding. Breaks of
mucosal barrier and exposure of the mucosal surface
to damage occurs due to highly concentrated HCl,
10% ethanol, salicylic acid, or acetylsalicylic acid
(aspirin).

The damaged mucosa liberates histamine, which in

turn increases acid secretion and produces increased
capillary permeability and vasodilatation. The latter
two effects lead to edema. In addition, the exposure of
mucosal capillaries to the digestive process leads to
bleeding. Erosive gastritis can occur as a result of
chronic use of non-steroidal anti-inflammatory drugs
(NSAIDs).

The mechanism by which NSAIDS cause gastritis

involves the inhibition of prostaglandin synthesis in
the stomach. Prostaglandins normally maintain the
physicochemical barrier on the gastroduodenal
mucosal surface by stimulating the secretion of
mucus and bicarbonate. Loss of the protective mucus
and bicarbonate barrier renders the gastric mucosa
susceptible to damage by the acidic environment.
The H+ -K + -ATPase pump can be inhibited by the drug
omeprazole, which is now used for the treatment of
duodenal and gastric ulcers (peptic ulcers). Inhibition of
pump activity leads to a prolonged increase in gastric pH
and the removal of the inhibitory effect of low pH ( less
than 3) on gastrin release.

In addition, two other drugs can also be used for

treatment of peptic ulcer and these are cimetidin and
ranitidine (Histamine blockers) . They accomplish this by
two mechanisms:

(1) Histamine released by ECL cells in the stomach is

blocked from binding on parietal cell H2 receptors,
which stimulate acid secretion;

(2) therefore, other substances that promote acid

secretion (such as gastrin and acetylcholine) have a
reduced effect on parietal cells when the H2 receptors
are blocked.
Thank You
17
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
Gastric hormonal secretion: Gastrin, main gastrointestinal hormone,
is secreted by antral G cells and has the following effects:

It stimulates the parietal cells to secret HCl.

It stimulates the chief cells to secret pepsinogen.
It stimulates the enterochromaffin-like cells (ECL cell, or
enteroendorine cells) to release histamine.
It enhances muscle contractions of pyloric pump (minor effect)
and has a slight constrictor effect on the gastroesophageal
sphincter.

It stimulates contraction of intestinal muscle, relaxes ileocecal

valve, and stimulates mass movements. Other hormones such as
histamine, serotonin, and somatostatin release directly into the
interstitial fluid of the mucosa of the stomach and act as chemical
messengers.
Phases of gastric motility and secretion:
Cephalic phase (only nervous ) (30%)
Gastric phase ( nervous and hormonal )(60%)
Intestinal phase (only hormonal)(10%)
1. The cephalic phase: It occurs even before the food enters the stomach . It results from the sight, smell,
thought, tactile sensation in the mouth, taste of food, or emotional state.

Neurogenic signals causing the cephalic phase of secretion can originate in the cerebral cortex or in the
appetite centers of the amygdala or hypothalamus and transmitted through the vagi to the stomach (insulin
induced hypoglycemia also stimulates the vagus nerve).
Psychic states have marked effects on gastric secretion and motility. Anger and hostility were associated with
hypersecretion of the gastric mucosa and enhance gastric motility while fear and depression decrease gastric
secretion and inhibit gastric motility. Almost 30% of the gastric secretions released during a meal occur as a
result of cephalically induced vagal stimulation .

During this phase, the non-distended stomach secretes hormone Ghrelin from cells in the stomach. Ghrelin
the "hunger hormone” is a peptide hormone produced by cells in the gastrointestinal tract which functions as
a neuropeptide in the central nervous system. It acts on hypothalamic brain cells both to increase hunger, and
to increase gastric acid secretion and gastrointestinal motility to prepare the body for food intake. When the
stomach is empty, ghrelin is secreted. When the stomach is stretched, secretion stops.

Ghrelin is also a stimulator of the growth hormone secretagogue receptor in the anterior pituitary, a receptor
that mediates growth hormone release.
2. The gastric phase: 60% of gastric secretions are associated with this phase. It starts once the food enters the stomach
[A] The stomach excitatory signals:
• Distension of the antrum by food through myenteric reflexes, increase in the activity of the pyloric pump and at the
same time inhibits the pyloric sphincter.

• The presence of the protein (small peptides and amino acids or other substance like caffeine) in the diet (the presence of
protein digestion products in the diet is the most important determinant of acid secretion during the gastric phase) a
reflex stimulation of G cell of mucosa to release gastrin. Consequently increase in gastric secretion and motility of
pyloric pump. Therefore, carbohydrates empty fastest, followed by protein. Fats take longest to empty.

Less PH= more acid = More H+

 [B] The gastric inhibitory signals: The most potent inhibitor of HCl secretion and pyloric pump activity is the drop of pH
(increasing in gastric [H+ ]) of the gastric content below 2-3. This inhibition is mediated by two mechanisms:

1. A low pH directly inhibits G cells and gastrin secretion, consequently inhibits HCl secretion and pyloric pump activity.
Plasma gastrin levels are related inversely to acid secretory capacity because of a feedback mechanism by which antral
acidification inhibits gastrin release.

2. A low pH stimulates antral D cells to release somatostatin, which inhibit secretion of parietal cells, ECL cells, and G
cells, thus turning off the HCl-secreting cells and their most potent stimulatory pathway.

Less PH= more acid = More H+

Facts about Gastric emptying:
a. The rate of gastric emptying is fastest when the stomach contents are isotonic. If the
stomach contents are hypertonic or hypotonic, gastric emptying is slowed.

b. Fat inhibits gastric emptying (i.e., increases gastric emptying time) by stimulating the
release of CCK.

c. H + in the duodenum inhibits gastric emptying via direct neural reflexes. H+ receptors in
the duodenum relay information to the gastric smooth muscle via interneurons in the GI
plexuses.

d. The initial rate of the gastric emptying varies directly with the volume of the meal ingested.
 Another phase of acid secretion is known as the basal state which occurs in the times between meals (interdigestive
phase). The level of acid secretion during these times is regulated by body weight, individual, number of parietal cells, and
time of day.

Acid secretion is lowest in the morning before awakening and highest at night. The stomach secretes only few milliliters of
gastric juice per hour during the interdigestive period (between meals) when little or no digestion is occurring anywhere in
the gut which is almost entirely of non-oxyntic type i.e., it is composed mainly of mucus containing very little pepsin and
almost no acid.

However, strong emotional stimuli frequently increase the interdigestive secretion to 50 ml or more of highly peptic and
highly acidic gastric juice per hour in very much the same manner that the cephalic phase of the gastric secretion excites
secretion at the onset of a meal. This increase of secretion during the presence of emotional stimuli is believed to be one of
the factors in the development of peptic ulcers.
3. The intestinal phase: Intestinal receptors monitor the composition of chyme
and elicit feedback mechanisms that regulate gastric acid secretion and gastric
emptying. Absence of feedback leads to an increased presence of excitatory
mediators of gastric function. 10% of gastric secretion is associated with the
intestinal phase.

This is achieved through hormones and nervous reflexes. The rate at which the
stomach empties is regulated by signals from both the stomach and the
duodenum. However, the duodenum provides by far the more potent of the
signals, controlling the emptying of chyme into the duodenum at a rate no
greater than the rate at which the chime can be digested and absorbed in the
small intestine. These feedback inhibitory mechanisms work together to slow
the rate of emptying when

(1) too much chyme is already in the small intestine or

(2) the chyme is excessively acidic, contains too much unprocessed protein or
fat, is hypotonic or hypertonic, or is irritating.

[A] The intestinal excitatory signals:

1. Nervous Feedback: Slight stretching the wall of the upper portion of the
small intestine, particularly in the duodenum by food.

2. Hormonal Feedback: The presence of small amounts of food (especially

protein digestion products) stimulates small amount of intestinal gastrin to
be released from the duodenal mucosa. This can slightly increase the
activity of pyloric pump and gastric juice secretion (through the same
mechanism mentioned before).
[B] The intestinal inhibitory signals:
1. Nervous Feedback:
• Duodenal wall distension or irritation of duodenal mucosa provokes inhibitory reflex effect from the duodenum to the
stomach. When food enters the duodenum, multiple nervous reflexes are initiated from the duodenal wall receptors.
These reflexes are mediated through the enteric nervous system, or through long, and short nervous reflexes These
signals depress the gastric juice secretion and at the same time decrease pyloric pump activity and usually increase
pyloric tone to prevent the flow of chyme from exceeding the ability of the intestine to handle it.

Osmolarity of the chyme: Iso-osmotic gastric contents empty faster than hyper or hypo-osmotic contents due to feedback
inhibition produced by duodenal wall chemoreceptors (hyper more inhibitory than hypo).
pH of chyme: Small intestinal chyme of < 3.5-4 stimulates the duodenal wall chemoreceptos and will activate reflexes that
ultimately inhibits pyloric pump through.
Presence of fats and protein digestion products in the duodenum.

Speed of delivery of nutrients from

stomach to small intestine is as
follow: Carbohydrate > protein > fat
2. Hormonal Feedback: The chyme coming from the stomach is normally hypertonic, acidic, and contains high
concentrations of fat, protein, and carbohydrates. The intestinal inhibitory signals are:

Fats entering the duodenum stimulate inhibitory hormone CCK which inhibits the pyloric pump. CCK is
the most potent inhibitor of pyloric pump.

Acidic chyme in the duodenum stimulates inhibitory hormone secretin which inhibits the pyloric pump.
Fat, protein, and carbohydrates in the duodenum stimulate inhibitory hormones Gastric inhibitory
peptide (GIP) that has a general but weak effect of decreasing gastrointestinal motility. CCK and secretin
hormones are collectively called enterogastrones.
In summary: In humans, gastric acid secretion by the parietal cell occurs in response to:-
Excitatory neural (acetylcholine), hormonal (gastrin), and paracrine (histamine) stimuli.
Inhibitory feedback regulation of acid output also involves neural (enterogastric reflex), hormonal
(enterogastrone), and paracrine (somatostatin) influences.

Obviously, these feedback signals allow chyme to enter the duodenum only as rapidly as it can be processed
by small intestine.
Gastric digestion and absorption: Carbohydrate digestion in
the stomach depends on the action of salivary amylase, which
remains active until halted by the low pH in the stomach.

Protein digestion occurs in the stomach by about 10% and

mediated by HCl and later by gastric pepsin.

Fat digestion is minimal in the stomach due to restriction of

gastric lipase activity. Very little absorption of nutrients takes
place in the stomach.

The only substances absorbed to any appreciable extent are

highly lipid-soluble substances (e.g., the non-ionized
triglycerides of acetic, propionic, and butyric acids).

Aspirin at gastric pH is non-ionized and fat soluble, after

absorption, it ionizes intracellularly, damaging mucosal cells
and ultimately producing bleeding. Ethanol is rapidly absorbed
in proportion to its concentration. Water moves in both
directions across the mucosa. Water-soluble substances
including Na+ , K+ , glucose, and amino acids, are very poorly
absorbed.
Vomiting (emesis): It is a forceful expulsion of contents of the stomach and upper intestinal tract through the mouth.
Vomiting is a reflex coordinated by the region in the brain stem medulla known as the vomiting center.

From here, motor impulses that cause the actual vomiting are transmitted from the vomiting center through
parasympathetic vagal and sympathetic nerves to the lower tract and through motor spinal nerves to the diaphragm and
abdominal muscles. Stimuli that elicit vomiting include
1. Tactile (touch) stimulation of the back of the throat, which is one of the
most potent stimuli.
2. Irritation or distension of the stomach and duodenum.

3. Stimulation of higher cortical centers by memory, feel, anticipation,

sensory input (pain, smell, sight), elevated intracranial pressure (thus,
vomiting after a head injury is considered a bad sign; it suggests
swelling or bleeding within the cranial cavity).

4. Rotation or acceleration of the head producing dizziness, such as in

motion sickness.

5. Body chemistry disturbances and chemical agents, including drugs or

noxious substances that initiate vomiting (that is, emetics) either by
acting in the upper parts of the gastrointestinal tract or by stimulating a
specialized chemoreceptor trigger zone (CTZ, or postrema) next to the
vomiting center in the brain.

Activation of this zone triggers the vomiting reflex. For example,

chemotherapeutic agents used in treating cancer often cause vomiting by
acting on the chemoreceptor trigger zone.
The importance of vomiting is to remove the ingested toxic substances
before they can be absorbed. Moreover, the nausea that usually
accompanies vomiting may have the importance in conditioning the
individual to avoid the future ingestion of food containing the same toxic
substances. Vomiting begins with:

[1] Vomiting is usually preceded by increased salivation, sweating

increased heart rate, pallor, and feeling of nausea, all are characteristic of
a general discharge of the sympathetic nervous system in response to
stress. Vomiting is often proceeded by retching (is the reverse movement
(peristalsis) of the stomach and esophagus without vomiting).

[2] Deep inspiration, closure of the glottis, and elevation of the soft palate.

[3] The abdominal and thoracic muscles contract, raising the abdominal
pressure which is transmitted to the contents of the stomach. In addition,
the upper portion of small intestine contracts (retro peristalsis) and tends
to force some of the intestinal contents back into the stomach. Thus
some bile may be present in the vomitus.

[4] The lower esophageal sphincter relaxes, and the high abdominal
pressure forces the contents of the stomach into the esophagus.
Excessive vomiting can lead to large losses of fluid and salts which
normally would be absorbed in the small intestine. This can result in
severe dehydration, upset the salt balance of the body and produce
circulatory problems due to decrease in plasma volume. The loss of acid
results in a low of body acidity
The dumping syndrome: Is a condition that can develop after surgery to remove all or part of your stomach or after surgery
to bypass your stomach to help you lose weight. It occurs because food moves from stomach into small bowel too quickly.
Rapid emptying of the stomach can lead to low pH, elevated tonicity in the duodenum, incomplete digestion of food by the
pancreas, liver, and duodenal mucosa and in incompletely emulsified fats in the duodenum.

The increased rate of travel of food coupled with the reduced rate of digestion can ultimately result in incomplete digestion
and absorption, particularly of fat and protein. The unabsorbed food retains osmotically water, which in conjunction with
the increased rate of intestinal transport, can lead to diarrhea and steatorrhea (fat in the feces). The by-products of the
bacterial metabolism of undigested food in the terminal ileum and colon can cause intestinal cramping, gas, and bloating.
Weakness, dizziness, and sweating, are due in part to hypoglycemia, underly the presentation of dumping syndrome.
Another cause of the symptoms is rapid entry of a hypertonic meal into the intestine, which promotes the movement of an
abundance of water into the gut, producing significant hypovolemia and hypotension.
Thank You
21
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
By: Abduljabbar Hamid Jabbar
University of Baghdad-College Of Medicine
M. B. Ch. B
Small intestine: The small intestine is the major site of digestion and absorption of carbohydrates, proteins, and fats in the
GIT. The small intestine has three parts: the duodenum, the jejunum, and the ileum. Although the small intestine is
approximately 5 m long, it has an absorptive area of over 250 m2 .

Its large surface area is created by numerous folds of the intestinal mucosa (valvulae conniventes or plica circulares), by
densely packed finger-like projections of the mucosa called villi, which line the entire mucosal surface, and by microvilli,
which protrude from the surface of the intestinal epithelial cells (enterocytes). The microvilli give the intestinal mucosa its
characteristics brush border appearance
The life span of a typical epithelial cell varies from two to three days in the esophagus to six days in the large intestine. The
divisions of epithelial stem cells continuously renew the lining of the entire digestive tract. These divisions normally keep
pace with the rates of cell destruction and loss at epithelial surfaces.

This high rate of cell division explains why radiation and anticancer drugs that inhibit mitosis have drastic effects on the
digestive tract. Lost epithelial cells are no longer replaced. The cumulative damage to the epithelial lining quickly leads to
problems in absorbing nutrients. In addition, the exposure of the lamina propria to digestive enzymes can cause internal
bleeding and other serious problems.

Though peristalsis in the small intestine is normally very weak, intense irritation of the intestinal mucosa, as occur in some
sever case of infectious diarrhea, can cause both very powerful and rapid peristalsis called the peristaltic rush. This is
initiated mainly by vagovagal nervous reflexes to the brain stem and back again to the gut. The powerful peristaltic
contractions sweep the contents of the intestine into the colon and thereby relieving the small intestine of either irritative
chyme or excessive distension.
Function of the ileocecal valve: The principal function of the ileocecal valve is to prevent backflow of fecal content from the
colon into the small intestine. The wall of the ileum for several centimeters immediately preceding the ileocecal valve has a
thickened muscular coat called ileocecal sphincter which normally remains mildly constricted.
Following meal, gastroileal reflex intensifies peristalsis, and the hormone, gastrin, which is liberated from the stomach
mucosa in response to food in the stomach, has a relaxant effect on the ileocecal sphincter, both of them cause an increase
emptying.
On the other hand, when the cecum is distended, the degree of contraction of the ileocecal sphincter is intensified while
ileal peristalsis is inhibited, which greatly delays emptying of additional chyme from the ileum. Also, any irritant in the
cecum delays emptying. These reflexes from the cecum to the ileocecal sphincter and ileum are mediated both by way of
the enteric nervous system and through vagovagal reflexes.
Pancreatic secretions: Approximately 1200 to 1500 ml of clear pancreatic juice is produced daily (about pH 8). Pancreatic
juice is secreted mainly in response to the presence of chyme in the upper portions of the small intestine and the
characteristics of the pancreatic juice are determined to some extent by the types of food in the chyme.

Pancreatic juice contains enzymes for digesting all three major types of food proteins, carbohydrates, and fats. It also
contains large quantities of bicarbonate ions which play an important role in neutralizing the acid chyme emptied by the
stomach into the duodenum. Pancreatic juice is isotonic and with the same Na+ and K+ concentrations and much lower Cl
concentration than plasma. The digestive enzymes of the pancreas are:
The digestive enzymes for proteins (proteolytic
enzymes) which are trypsin, chymotrypsin,
carboxypolypeptidase, ribonuclease, and
deoxyribonuclease. By far the most abundant of
these is trypsin .

The digestive enzyme for carbohydrates is

pancreatic amylase which hydrolyzes starches,
glycogen and most other carbohydrates except
cellulose to form disaccharides and a few
trisaccharides.

The digestive enzyme for fat which is pancreatic

lipase that is capable of hydrolyzing neutral fat into
fatty acids and monoglycerides, cholesterol
esterase which cause hydrolysis of cholesterol
esters, and phospholipase which splits fatty acids
from phospholipids.
Pancreas protects itself from autodigestion by proteolytic enzymes by the following
ways:

[1] When synthesized in the pancreatic cells, the proteolytic enzymes are in the
inactive forms (inactive zymogens), trypsinogen, chymotrypsinogen, and
procarboxypolypeptidase, which are all enzymatically inactive.
[2] These become activated only by trypsin.

[3] Trypsin is activated only after it is secreted into the intestinal tract. Trypsinogen is
activated by an enzyme called enteropeptidase (enterokinase) which is secreted by the
intestinal mucosa when chyme comes in contact with the mucosa. Also, trypsinogen
can be autocatalytically activated by trypsin that is already been formed.
Chymotrypsinogen is activated by trypsin to form chymotrypsin, and
procarboxypolypeptidase is activated in a similar manner. It is important that the
proteolytic enzymes of the pancreatic juice not become activated until they have been
secreted into the intestine which otherwise would digest the pancreas itself.

[4] The same cells that secrete the proteolytic enzymes into the acini of the pancreas
secrete simultaneously another substance called trypsin inhibitor. This substance is
stored in the cytoplasm of the glandular cells surrounding the enzyme granules and it
prevents activation of trypsin both inside the secretory cells and in the acini and ducts
of the pancreas.

However, when the pancreas becomes severely damaged or when a duct becomes
blocked, large quantities of pancreatic secretion become pooled in the damaged areas
of the pancreas. Under these conditions, the effect of trypsin inhibitor is sometimes
overwhelmed, in which case the pancreatic secretions rapidly become activated and
digest the pancreas giving rise to the condition called acute pancreatitis.
The enzymes of the pancreatic juice are secreted entirely by the acini
of the pancreatic glands. On the other hand, two other important
components of the pancreatic juice, bicarbonate ions and water, are
secreted in large amounts mainly by the epithelial cells of the
ductules leading from the acini .

The alkaline ions or the pancreatic juice serves to neutralize acid

emptied into the duodenum from the stomach. The secretion of
bicarbonate ions by the pancreas is an active process. The
mechanism of bicarbonate secretion is similar to the process of HCI
secretion by the stomach, except that the events on the two sides of
the cells are reversed.

Because the amount of bicarbonate secreted by the pancreas is

reflexly regulated by the amount of acid entering the duodenum from
the stomach, the amount of bicarbonate secreted by the pancreas is
normally about equal to the amount of acid secreted by the stomach.
This also means that the bicarbonate released into the blood by the
stomach is normally equal to the amount of acid released into the
blood by the pancreas.

When the alkaline blood leaving the stomach mixes with the acidified
blood from the pancreas, the overall result is no change in the acidity
of the blood returning to the heart. However, a loss of large
quantities of bicarbonate ions from the intestinal tract during periods
of prolonged diarrhea leads to a net accumulation of acid in the
blood, just as, loss of acid from the stomach by vomiting leads to a
net alkalinization of the blood.
Regulation of pancreatic secretion: Pancreatic secretion is regulated by both nervous and hormonal mechanisms. However,
hormonal regulation is by far the more important. Like gastric secretion, pancreatic secretion is divided into the following
three phases:

[1] Cephalic phase: The thought, sight, smell, or taste of food produces the cephalic phase of pancreatic secretion via vagal
stimulation. It is scanty and rich in enzymes.

[2] Gastric phase: Pancreatic secretion is slightly enhanced during the gastric phase by:
[A] Distention of the antrum and the body of the stomach, which initiates a vagovagal reflex resulting in a low volume of
pancreatic secretion containing both bicarbonate ions and enzymes.

[B] Food breakdown digestion products (primarily amino acids and peptides) can stimulate pancreatic secretions because
of their ability to cause the G cells of the antrum to release gastrin. Gastrin produces a low-volume, high-enzyme
pancreatic secretion.
[3] Intestinal phase: The major stimulants
for pancreatic secretion are the hormone
CCK and secretin. They are released from
endocrine cells in the duodenum and
jejunum during the intestinal phase of
pancreatic secretion in response to the
entrance of chyme into the small intestine.

CCK, in addition to its effect on the

gallbladder, is a potent stimulant of
pancreatic enzyme secretion. Protein and
fat are the major stimuli for CCK secretion.
CCK induces secretion of enzyme-rich
pancreatic juice.

Secretin stimulates the HCO3 - secretion.

Low pH (< 4.5), caused by the presence of
gastric acid (HCl) in the intestine, is a
potent stimulus for the release of secretin.
Secretin causes secretion of HCO3 − -rich
pancreatic juice.
Secretin is very important for two reasons:
[A] Neutralization of the acidic chyme: Secretin is released from the mucosa of small intestine when the pH of
the duodenal contents falls below 4.5 and its release increases very greatly as the pH falls to 3.0.

This immediately causes large quantities of pancreatic juice containing abundant amounts of sodium
bicarbonate to be secreted. In this way, the acid contents emptied into the duodenum from the stomach
become neutralized, and peptic activity of the gastric juice is immediately blocked. Since the mucosa of the
small intestine cannot withstand the digestive action of acid gastric juice. This is a highly important and even
essential protective mechanism against the development of duodenal ulcers.

[B] Provides a proper alkaline medium for the action of pancreatic enzymes

Because CCK and secretin are potentiators of each other’s action, small concentrations of CCK and secretin
together can produce significant amounts of pancreatic bicarbonate ions and enzymes secretions, while
either one alone would have little or no effect.
Pancreatitis and Pancreatic Cancer: Pancreatitis is an inflammation of the pancreas that occurs quite
commonly. Pancreatitis involves the release of pancreatic enzymes within the pancreas itself, which digest
pancreatic tissue. It can result from alcoholism, the use of certain drugs, pancreatic duct blockage, cystic
fibrosis, viral infection, or pancreatic cancer. Symptoms can range from mild abdominal pain to systemic
shock and coma.

Cancer of the pancreas can obstruct the pancreatic and common hepatic ducts, resulting in jaundice.
Pancreatic cancer may not be detected until the tumor has become fairly large, and it can become so large as
to block off the pyloric region of the stomach.
Thank You
14