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مدمج
مدمج
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:
2. Longitudinal muscle.
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).
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)
• 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
[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.
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 drop in turn initiates a stretch reflex of the jaw muscles (the
masseter, medial pterygoid, and temporalis muscles) that leads
to rebound contraction.
[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.
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.
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.
[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.
• 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
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 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.
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:
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.
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:
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 :
[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).
[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:
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).
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.
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.
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
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.
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.
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.
[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 .
[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 .
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.
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.
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