Git Physiology Compiled by Umah, Umah Victor

COMPILED AND EDITED BY UMAH, UMAH VICTOR
GASTROINTESTINAL PHYSIOLOGY
OUTLINE:
 Introduction
 Physiologic Anatomy
 Electrical activity of GIT smooth muscles
 Neural control of GIT
 Hormonal control of GIT
 Gastrointestinal motility
 Deglutition
 Gastroesophageal sphincter
 Disorder of the oesophagus
 Peristalsis
 Gastric motility
 Gastric emptying
 Intestinal motility
 Defecation
 Vomiting
 GIT Secretions
 Digestion and end products
 Absorption
 Problems of absorption
COMPILED AND EDITED

BY
UMAH, UMAH VICTOR
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The lions may grow weak and hungry,
But those who seek the lord lack no good thing.
Psalm 34: 10 (NIV)
INTRODUCTION
The gastrointestinal system starts from the mouth and ends in the anus, thus the
gastrointestinal system consists of the digestive tract and its associated glands. The digestive
tract is made up of mouth, pharynx, esophagus, stomach, small intestine and large intestine.
Accessory organs of the digestive system include: teeth, tongue, salivary glands, exocrine part
of pancreas, liver, gall bladder.
PHYSIOLOGIC ANATOMY:
Generally, a typical cross section of the intestinal wall includes the following layers from outer
surface inward;
1. Serosa
2. Longitudinal smooth muscle layer
3. Circular smooth muscle layer
4. Sub-mucosa
5. Mucosa
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In addition, sparse bundles of smooth muscles fibres, the mucosal muscle, lie in the
deeper layers of the mucosa, thus motor functions of the gut are performed by the different layers
of smooth muscles.
The oesophagus is a tubular structure and a derivative of the foregut made of non-keratinized
stratified squamous epithelium; skeletal muscle in muscularis externa(upper 1/3); smooth
muscle (lower 1/3). The oesophagus has upper and lower oesophageal sphincter that restrict
flow of food contents to optimize digestion and absorption.
The stomach is made up of the fundus, body, and pylorus. The fundus and the body is made
of ruggae, shallow pits and deep glands and the pylorus is made of deep pits and shallow
branched glands. The pylorus acts as a sphincter of the stomach and retards emptying of the
stomach. The stomach is made up of the mucous cells, chief cells, parietal cells and
enteroendocrine cells.
The small intestine is divided into duodenum, jejunum and ileum and made of columnar
absorptive cells. It is characterized by villi, plicae, and crypts. The duodenum is made of
Brunner glands which secrete an alkaline secretion, also contains globlet cells, paneth cells
and enteroendocrine cells.
The jejenum is made up of villi as well as developed plicae, crypts. It also contains the
same cell types as found in the duodenum epithelium.
The ileum contains aggregates of lymph nodules called peyer patches and contains M cells
found over lymphatics nodules and peyer patches.
Large intestine lacks villi, has crypts, and contains mainly mucous secreting and absorptive
cells. The ileocecal valve retains colonic contents (including large number of bacteria) in the
large intestine, and the inner and outer anal sphincter).
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ELECTRICAL ACTIVITY OF GASTROINTESTINAL SMOOTH MUSCLE

The smooth muscle of the gastrointestinal tract is excited by almost continual slow, intrinsic
electrical activity along the membranes of muscle fibres.
This activity has two basic types of electrical waves:
1. Slow waves
2. Spikes
Slow waves: Most gastrointestinal contractions occur rhythmically, and this rhythm is
determined mainly by the frequency of slow waves of the smooth muscle membrane which are
not action potentials. Their intensity usually varies between 5 and 15 millivolts and their
frequency ranges in different parts of the human gastrointestinal tract from 3 to 12 per minute.
It is about 3 in the body of the stomach, as much as 12 in the duodenum and 8 or 9 in terminal
ileum. They are slow, undulating changes in the resting membrane potential.
SPIKE POTENTIALS: The spike potentials are the action potentials. They occur
automatically when the resting membrane potential of the gastrointestinal smooth muscles
becomes more positive than about -40millivolts (the normal resting membrane potential in the
smooth muscle fibres of the gut is between -50 and 60 millivolts.
 The higher the slow wave potential rises, the greater the frequency of the spike potentials,
usually ranging between1 and 10 spikes per second.
Difference between spike potentials and action potentials:

1. The spike potentials last longer in gastrointestinal muscle than the action potential in large nerve
fibers.
2. Action potential of the gastrointestinal smooth muscle are caused by calcium-sodium channels
where large numbers of calcium ions enter along with smaller number of sodium. These
channels are much slower to open and close than the rapid sodium channels of large nerve
fibres, thus, the slowness of opening and closing of the calcium- sodium channels account for the
long duration of action potential in GIT smooth muscle. Whereas, in nerve fibres, the action
potentials are caused by rapid entry of sodium ions through sodium channels to the interior of
the fibers.
NEURAL CONTROL OF GIT

GIT has 2 main types of nerve supply
1. Intrinsic nerve supply

2. Extrinsic nerve supply
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INTRINSIC NERVE supply include: Myenteric plexus and submucosal plexus.
EXTRINSIC NERVE supply include: parasympathetic and sympathetic nerve fibers.
Myenteric plexus(Auebach’s plexus):is an outer plexus lying between the longitudinal

and circular muscle layers. It controls mainly the gastrointestinal movement .Submucosal
plexus or Meissner’s plexus: is an inner plexus that lies in the submucosa. It controls mainly
GIT secretion and local blood flow.
Differences between the myenteric and submucosal plexuses:

1. The myenteric plexus consists mostly of a linear chain of interconnecting neurons that extends
the entire length of the gastrointestinal tract.
2. It lies between the longitudinal and circular layers of intestinal smooth muscle.
When it is stimulated, its effects are:
a) Increased tonic contraction or tone of the gut wall.

b) Increased intensity of the rhythmical contraction.
c) Slightly increased rate of the rhythm of contraction.
d) Increased velocity of conduction of excitatory waves along the gut wall.
This causes more rapid movement of the gut peristaltic waves.The myenteric plexus is
not entirely excitatory as some of its neurons are inhibitory; their fibres endings secrete an
inhibitory transmitter, vasoactive intestinal polypeptide or other inhibitory peptide which helps to
inhibit some intestinal sphincter muscles that impede movement of food along the segments of
the GIT such as the pyloric sphincter which control emptying of the stomach into the duodenum
and the sphincter of the ileocaecal valve which control emptying from small intestine to the
caecum. Whereas the sub mucosal plexus is found in submucosal layer of GIT. It controls
intestinal secretion, local absorption and local contraction of submucosal muscle.
NEUROTRANSMITTERS SECRETED BY INTRINSIC (ENTERIC)

NEURONS
1. Acetylcholine
2. Adenosine triphosphate
3. Dopamine
4. Serotonine
5. Norepinephrine
6. Cholecystokinin
7. Substance P
8. Vasoactive intestinal polypeptide
9. Somatostatin
10. Leu-enkenphalin
11. Met-enkephalin
12. Bombesin
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Acetylcholine excites GIT activity. Norepinephrine and epinephrine almost inhibit GIT
activity. The extrinsic sympathetic and parasympathetic fibres connect to both myenteric and
submucosal plexuses. Although the enteric nervous system can function independently of these
extrinsic nerves, stimulation by the parasympathetic and sympathetic systems can greatly
enhance or inhibit GIT functions. Sensory nerve ending that originates in the GIT epithelium or
gut wall send afferent fibres to both plexuses of the enteric system as well as:
a. To the prevertebral ganglia of the sympathetic nervous system
b. Spinal cord
c. In the vagus nerves all the way to the brain stem.
The sensory can elicit local reflexes within the gut wall itself and still other reflexes that are
relayed to the gut from either the prevertebral ganglia or the basal region of the brain.
AUTONOMIC CONTROL OF THE GIT:

This is done by the extrinsic nerve supply which includes:
1. The parasympathetic supply to the gut: include the cranial and sacral division. The
cranial. Parasympathetic nerve fibers are almost entirely in the vagus nerves which
supply the oesophagus, stomach, pancreas and the first half of the large intestines. The
sacral parasympathetic originates in the second, third and fourth sacral segment of the
spinal cord and pass through the pelvic nerves to the distal half of the large intestine and
to the anus.
The preganglionic and postganglionic parasympathetic nerve fibres to the mouth and
salivary glands pass through facial (vii) and glossopharyngeal (ix) nerves. The
preganglionic parasympathetic nerves fibres to oesophagus, stomach, small intestine and
upper part of large intestine pass through vagus(x). The preganglionic nerve fibres to
lower part of large intestine arise from 2nd,3rd,4th sacral segments of the spinal cord
and pass through pelvic nerve. All preganglionic parasympathetic nerve fibres synapse
with postganglionic nerve cells in the myenteric and submucosal plexus. Parasympathetic
supply is by fibres of vagus(x) nerves. Neurotransmitter by parasympathetic nerves is
acetylcholine. The functions of parasympathetic system are:
i. Increases the motility of GIT but relaxes sphincters.

ii. It increases the secretory activities of glands of GIT.
2. Sympathetic nerve fibres to GIT: preganglionic originate in the spinal cord between
T5 to L2. The postganglionic fibres is distributed in the GIT.
Function of sympathetic: inhibition of GIT movement and secretion.Neurotransmitter
by sympathetic nerve fibres is norepinephrine.
HORMONAL CONTROL OF THE GIT

These are polypeptides that are produced by nerve and glands and act on the same area of
their secretion(paracrine) or immediate neighbourhood.
Function of GIT hormones: Regulation of the secretion and motility of GIT structure
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These hormones are divided into 2 groups based on their structure and functional similarities.
a) Gastrin family
b) Secretin family
Gastrin family include: Gastrin and CCK (Cholecystokinin)
Secretin family include: secretin, glucagon, vasoactive inhibitory polypeptide, gastric
inhibitory polypeptide.
Others do not belong to these groups include: somatostatin, motilin, glicetin, peptide YY,
Neuropepide Y, Substance P.
GASTRIN FAMILY:
1. Gastrin: It is produced by the G cells of the antrum of the gastric mucosa, duodenum .The
precursor, preprogastrin is divided into 3 fragments containing 34, 17, 14 aminoacids residues
and thus called G34, G17 and G14 forms respectively. G17 is the principal form for gastric acid
secretion. Gastrin acts via the receptor CCK-b.
G17 and G14 have half-life of 2-3 mins in circulation while G34 has half- life of 15 mins.
Gastrin are inactivated in the small intestine and kidneys.
Stimulants for Gastrin secretion include:
a) Presence of food in the stomach especially peptides and amino acids e.g. phenylalanine and
tryptophan.
b) Stimulation of local nervous plexus in stomach and small intestine.
c) Vago-vagal reflex (increase vagal discharge): Neurotransmitter is gastrin releasing
polypeptide(GRP) and not acetylcholine hence it is not blocked by atropine.
d) A rise in blood borne factors e.g. Ca2+, adrenaline.
Actions of Gastrin:
1. Gastrin stimulates pepsin secretion and gastric acid (HCl) secretion. This is a negative
feedback control as gastrin stimulates acid secretion and a high acidity inhibits gastrin secretion.
2. Stimulates growth of mucosa of stomach and small intestine.
3) Stimulates gastric motility and emptying
4) Contracts the musculature that closes lower oesophageal sphincter.
5) Stimulates insulin secretion after a protein meal
2. Cholecystokinin (CCK): Produced by I cells in the mucosa of duodenum, jejenum mainly, and
small quantity in the ileum.
CCK is produced from a large precursor, Prepro-CCK which is made of 3 fragments: CCK
58,CCK-38, CCK-33. CCK-33 is the most abundant. CCK acts via the receptor, CCK-A.
Stimulants of CCK secretion include:
1. Presence of proteins in food being digested
2. Fats
3. Acid
Actions of CCK:
a) Stimulates contraction of the gall bladder
b) Stimulates the secretion of enzyme rich pancreatic juice
c) Inhibits gastric motility and emptying
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d) Exerts a trophic effect on pancreas

e) Increases the secretion of enterokinase
f) Augments the action of secretin in producing alkaline pancreatic juice.
g) May enhance motility of small intestine and colon.
h) Along with secretin, augments contraction of pyloric sphincter.
i) Also stimulate glucagon secretion.
j) CCK secretion occurs during meals and is sustained by a positive feedback control (unlike
gastrin).
CCK secretion is triggered by presence of products of protein and fat digestion in the
duodenum and jejenum. It stimulates the pancreas to secrete powerful enzymes which digest
proteins and fats and result in more protein and fat that stimulates more CCK secretion.
SECRETIN FAMILY
1. Secretin: produced by S cells of mucosa of the upper small intestine. Its structure is similar to
CCK,VIP and GIP. It has half- life of 5 mins.
Stimulants for secretion of secretin include: acid in the small intestine aminoacids and fatty
acids in the upper intestine.
Actions of Secretin
1. It enhances the action of CCK in stimulating pancreatic enzyme secretion.
2. Stimulates watery alkaline pancreatic secretion rich in bicarbonates.
3. It stimulates biliary bicarbonate secretion.
4. It causes pyloric sphincter contraction.
5. It inhibits gastric acid secretion.
Control of secretion of Secretin:
Secretin causes alkaline pancreatic juice to flood the duodenum thereby neutralizing the acid
from the stomach and thus inhibiting further secretion of the hormone.
2. Gastric inhibitory peptide (GIP): peptide contains 42 amino acids, produced by K cells from
the mucosa of duodenum and jejunum in response to presence of fat and glucose in these areas.
Actions of GIP:
1. Inhibition of gastric secretion and motility when released in large amount.
2. Stimulation of insulin release.
3. Vasoactive Intestinal Polypeptide(VIP): It contains 28 amino acids and produced by GIT

nerve, thus it is not a hormone itself. VIP is however seen in blood. It has a half -life of 2 mins.
Stimulant for VIP secretion is presence of acid chyme in the intestine.
Actions of VIP
1) It stimulates intestinal secretion of electrolyte and water.
2) It causes relaxation of intestinal smooth muscle including sphincters
3) It dilates the peripheral blood vessels.
4) It inhibits gastric acid secretion.
5) It potentiates the action of acetylcholine on salivary glands.
4. Glucagon: It is secreted by the alpha cells of the islet of langerhans in pancreas. It is also
secreted by A cell in the stomach and duodenum.
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Stimulants for Glucagon:

1. Hypoglycaemia
2. Food rich in fat and protein.
Actions of glucagon:
It increases blood sugar level by promoting glycogenolysis (in liver), gluconeogenesis and
lipolysis.
OTHERS INCLUDE:
1. Somatostatin: Somatostatin, the growth-hormone-inhibiting hormone originally isolated from
the hypothalamus, is secreted as a paracrine by D cells in the pancreatic islets and by similar D
cells in the gastrointestinal mucosa. It exists in tissues in two forms, somatostatin 14 and
somatostatin 28 and both are secreted. Its secretion is stimulated by acid in the lumen.
Actions of Somatostatin:
a. Somatostatin inhibits the secretion of gastrin, VIP, GIP, secretin, and motilin.
b. It inhibits gastric secretion and motility.
c. It also inhibits pancreatic exocrine secretion.
d. It inhibits gallbladder contraction and the absorption of glucose, amino acids, and
triglycerides.
e. It inhibits secretion of GH and TSH.
2. MOTILIN: Motilin is a polypeptide containing 22 amino acid residues that is secreted by

enterochromaffin cells and Mo cells in the stomach, small intestine, and colon. It acts on G
protein coupled receptors on enteric neurons in the duodenum and colon and produces
contraction of smooth muscle in the stomach and intestines in the period between meals.
3. Substance P is found in endocrine and nerve cells in the gastrointestinal tract and may enter the
circulation. It increases the motility of the small intestine.
GASTROINTESTINAL MOTILITY
This involves movement of food from the mouth down to the anus and the activities that occur at
different parts of the gastrointestinal tract.
Types of motility:
1. Mixing
2. Propulsive
Mixing: keeps the gastrointestinal contents thoroughly mixed at all times.
Propulsive: cause food to move forward along the tract at an appropriate rate to accommodate
digestion and absorption.
GIT motility includes:

1. Mastication(Chewing):
Chewing is the process in which large food is broken down to smaller substances to help
digestion and absorption. Chewing is reflex process, it can be voluntary. The teeth are involved
in chewing. The anterior teeth (incisors) provide a strong cutting action and the posterior teeth
(molars) a grinding action.
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Reasons for mastication:

a. It reduces large molecules into smaller molecules to make swallowing easy
b. It makes available the nutrient portion of most vegetable and fruits because it breaks down the
cellular cell wall in leaves.
c. It also makes the food to be smooth as saliva is mixed with food so that excoriation of GIT wall
is prevented when swallowed.
d. Chewing helps to break down food into smaller particles so that the taste of the food is
appreciated. This is achieved by liquefaction of food so that taste buds that can pick the taste.
Initiation of chewing reflex begins with:

Opening of the mouth  Stretching of muscles of the mouth  rebound contraction 
compresses the food unto the upper palate  inhibition of mouth muscle  closing of the
mouth.
The muscles involved in mastication are the masseter, temporalis, medial pterygoids and
buccinators. These supplied muscles are by mandibular part of trigeminal nerve(cranial
nerve V). Chewing breaks food particles into smaller bits thus increasing the surface area so that
the digestive enzymes can act on them. Chewing is a mixing process. This automatically raises
the jaw to cause closure of the teeth, but it also compresses the bolus again against the linings of
the mouth, which inhibits the jaw muscles once again, allowing the jaw to drop and rebound
another time; this is repeated again and again.
2. Deglutition(swallowing):
This is a process whereby a properly masticated food is propelled from the mouth through
the oesophagus to the stomach. This is reflex response that is triggered by afferent impulses in
the trigeminal, glossophargeal and vagus nerves.
There are two (2) phases of swallowing:
a. Voluntary phase
b. Involuntary phase
Voluntary phase:
This initiates the swallowing process. It occurs in the mouth and involves collecting the food
contents on the tongue, and propelling them backward into the pharynx. In this phase, you can
decide to stop.
Involuntary phase:
Once started cannot be stopped and Involuntary phase has 2 divisions:
i. Pharyngeal phase: This receives the voluntary phase. This constitutes passage of food through
the pharynx into the oesophagus by involuntary contraction of the pharyngeal muscles. Pharynx
receptors called swallowing receptors , are sensitive to presence of food because of stretching of
pharyngeal muscles. Thus stimulating the pharyngeal receptors, impulses are then sent through
the afferent nerves (5th & 9th CN) to a swallowing centre located in the brainstem. After
integration in the swallowing centre, impulses are sent via efferent pathways via the 5th, 9th ,
10th & 12th CNS.
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RESPONSES INCLUDE
 There is flipping upward of the soft palate such that it covers the posterior nares.
 There is tight approximation of palatopharyngeal folds leaving only a sagittal slot (small
opening) that selectively allows properly masticated foods to pass through easily.
 There is also tight approximation of the vocal cords to prevent foods from entering into the
trachea.
 There is enlargement of the opening of the oesophagus so as to make it easier for the swallowed
food to pass into the oesophagus.
 There is forceful, muscular contraction of the pharynx to generate a contractile force that pushes
the swallowed food into the oesophagus.
 This contractile force initiates perilstalsis- forceful contraction of the pharynx.
ii. Oesophageal phase:

This transports food from the pharynx to the stomach. The oesophagus normally exhibits two
types of peristaltic movements: primary peristalsis and secondary peristalsis. Primary
peristalsis is simply continuation of the peristaltic wave that begins in the pharynx and spreads
into the oesophagus during the pharyngeal stage of swallowing. This wave passes all the way
from the pharynx to the stomach in about 8 to 10 seconds. If the primary peristaltic wave fails to
move into the stomach all the food that has entered the oesophagus, secondary peristaltic waves
result from distention of the oesophagus itself by the retained food. These waves continue until
all the food has emptied into the stomach. The secondary peristalsis occurs when the primary
peristalsis is not strong enough to push the food through the lower oesophageal sphincter.
Control of oesophageal Peristalsis;

The control of oesophageal is both intrinsic and extrinsic. In the smooth muscle areas of the
oesophagus, peristalsis occurs after bilateral vagotomy, or in an isolated excised oesophagus in
an organ bath. It is therefore believed that peristalsis can be mediated by intrinsic nerve plexuses.
Vagal control of oesophageal (and pharygneal) peristalsis is presumed to be coordinated by
the swallowing centres in the medulla which sends a series of sequential impulses to
progressively distal segments of the oesophagus, causing the affected segments to contract. Thus,
if the oesophagus is cut across, the peristaltic wave begins below the cut as it dies out above the
cut.
DEGLUTITION REFLEX
This occurs during the involuntary stage of swallowing ie the pharyngeal and oesophageal
stages. As a reflex, it goes through a reflex arc.
Receptor: When food enters the oropharyngeal region, the receptors here are stimulated.
Afferent pathway: Afferent impulses from the oropharyngeal receptors pass to the deglutition
center.
Deglutition center: is at medulla oblongata of the brain.
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Efferent pathway: Impulses from deglutition center travel through the glossopharyngeal and
vagus nerve to reach the soft palate, pharynx and oesophagus. The glossopharyngeal nerve is
concerned with pharyngeal stage of swallowing. The vagus nerve is concerned with oesophageal
stage.
Response: The reflex causes upward movement of soft palate, to close nasophaynx and upward
movement of larynx, to close the respiratory passage so the food bolus enter the oesophagus.
Thus, peristalsis occurs in the esophagus, pushing the food bolus into the stomach.
Gastroesopharygeal Sphincter:
The musculature of the gastroesophageal junction (lower oesophageal sphincter; LES) is
tonically active but relaxes on swallowing. The tonic activity of the LES between meals prevents
reflux of gastric contents into the oesophagus. The LES is made up of three components.
i. The oesophageal smooth muscle which is more prominent at the junction with the stomach
(intrinsic sphincter).
ii. Fibres of the crural portion of the diaphragm, a skeletal muscle which surround the oesophagus
at this point (extrinsic sphincter)
iii. Phrenoesophageal ligament.
The oblique fibres of the stomach wall create a flap valve that helps close off the
oesophagogastric junction and prevent regurgitation when intragastric pressure rises. The tone of
the LES is under neural control. Release of acetylcholine from vagal endings causes the intrinsic
sphincter to contract and release of NO (Nitric Oxide) and VIP from interneurons innervated by
other vagal fibres causes it to relax.
Contraction of the crural portion of the diaphragm, which is innervated by the phrenic nerves,
is coordinated with respiration and contractions of chest and abdominal muscles. Thus, the
intrinsic and extrinsic sphincters operate together to permit orderly flow of food into the stomach
and to prevent reflux of gastric contents into the oesophagus.
VOMITTING (EMESIS)
This is reversed swallowing. It is also a reflex process.
Causes of vomiting
a) It is usually due to irritation, over distension or over excitability of upper GIT (mouth to
stomach).
b) Infection of the meninges, peritoneum, genitourinary tract and childhood infections
c) Pregnancy
d) Raised intracranial pressure
d) Migraine.
e) Uraemia
f) Drugs e.g apomorphine, morphine, digoxin
g) Psychogenic factors
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VOMITING REFLEX
This may or may not be preceded by nausea and salivation. Vomiting receptors are stimulated;
impulses are generated and pass through the afferent pathways (sympathetic and
parasympathetic) to the vomitting centre (medulla) near the nucleus tractus solitarius.
Appropriate messages are sent via the efferent pathways (5th, 7th, 9th, 10th, & 12th CNs) +
spinal nerves.
Efferent responses are as follows:
 Take in deep breath

 There is glottis closure
 There is superior and anterior opening of the larynx & closure of d posterior nares
 Contraction of diaphragm so as to increase intra-gastric pressure
 Relaxation of the LES sphincters and upper oesophageal sphincters.
 Psychological factors goes straight to vomiting centre
Some drugs trigger vomiting by stimulating chemoreceptor trigger zone (CTZ) located on the
floor of the 4th ventricle.
Vomiting as a rapid linear or circular motion sickness--->stimulate receptors in the ear called
labyrinthine receptors--->vestibular nuclei stimulation cerebellum CTZ.
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DISORDERS OF SWALLOWING AND OESOPHAGUS:

1. Difficulty in swallowing(dysphagia):
Causes
a) Oesophagal strictures due to reflux of gastric acid causing oesophagitis (inflammation of
oesophagus) or swallowed corrosives;
b) Damage to the 5th, 9th, 10th, CNs will lead to paralysis of the swallowing mechanism.
c) Diseases such as polio and encephalitis can prevent normal swallowing by damaging the
swallowing centre in the brainstem
d) Paralysis of swallowing muscles such as in muscle dystrophy or failure of neuromuscular
transmission such as in myasthenia gravis.
e) Carcinoma of oesophagus
2. Achalasia(Failure to relax):
This is a condition in which food accumulates in the oesophagus, thus it become massively
dilated. It is due to increased resting lower oesophageal sphincter tone and incomplete relaxation
on swallowing. The myenteric plexus of the oesophagus is deficient at the lower oesophageal
sphincter and the release of nitric-oxide (NO) and vasoactive inhibitory peptide is defective.
Treatment of Achalasia:
This can be treated by pneumatic dilation of sphincter or incision of the oesophageal muscle
(myotomy). Inhibition of acetylcholine release by injection of botulinum toxin into LES is also
effective and produces relief that last for months.
3. Gastroesophageal reflux disease:

This is most frequent digestive disorder. It causes heartburn and oesophagitis and can lead to
ulceration and stricture of the oesophagus due to scarring. In severe cases, the intrinsic sphincter,
the extrinsic, and sometimes both are weak.
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Treatment for Gastroesophageal reflex disease:

a) Inhibition of acid secretion with hydrogen receptors blockers or proton pump inhibitors.
b) Fundoplication: surgical treatment in which a portion of the fundus of the stomach is wrapped
around lower oesophagus so that the LES is inside a short tunnel of stomach. It is not a lasting
solution.
PROPULSIVE MOVEMENT
The basic propulsive movement of the gastrointestinal tract is peristalsis.
PERISTALSIS:
This is slow rhythmic movement which involves a wave of contraction, followed by the
wave of relaxation of muscle fibres of the gastrointestinal tract thus food is moved down along
the tract. It is an inherent property of many syncytial smooth muscle tubes. Stimulation at any
point in the gut can cause a contractile ring to appear in the circular muscle, and this ring then
spreads along the gut tube. Peristalsis also occurs in the bile ducts, glandular ducts, ureters,
and many other smooth muscle tubes of the body.
The usual stimulus for intestinal peristalsis is distension of the gut. That is, if a large
amount of food collects at any point in the gut, the stretching of the gut wall stimulates the
enteric nervous system to contract the gut wall 2 to 3 centimetres behind this point, and a
contractile wave appears that initiates a peristaltic movement. Other stimuli that can initiate
peristalsis include chemical or physical irritation of the epithelial lining in the gut. Also,
strong parasympathetic nervous signals to the gut will elicit strong peristalsis.
The motor functions of the stomach are:

1. Storage of large quantities of food until the food can be processed in the stomach (receptive
relaxation)
2. Mixing of this food with gastric secretions until it forms a semifluid mixture called chyme.
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3. Slow emptying of the chyme from the stomach into the small intestine at a rate suitable for
proper digestion and absorption by the small intestine.
1. RECEPTIVE RELAXATION
When food enters the stomach, the fundus and upper portion of the body relax and
accommodate the food with little if any increase in pressure (receptive relaxation) Receptive
relaxation is in part, vagally mediated and triggered by movement of the pharynx and
oesophagus.
Intrinsic reflexes also lead to relaxation as the stomach wall is stretched. Peristalsis then
begins in the lower portion of the body, mixing and grinding the food and permitting small,
semiliquid portions of it to pass through the pylorus and enter the duodenum. Peristaltic waves
controlled by the gastric BER (Basic Electrical Rhythm) begin soon thereafter and sweep toward
the pylorus.
The contraction of the distal stomach caused by each wave is sometimes called antral
systole and can last up to 10s. Waves occur 3–4 times per minute.
HUNGER CONTRACTIONS
Besides the peristaltic contractions that occur when food is present in the stomach,
another intense contractions called hunger contractions often occur when food the stomach has
been empty for several hours or more. They are rhythmic peristaltic contractions in the body of
the stomach. They are most intense in young healthy people who have high degree of
gastrointestinal tonus. They are greatly increased when the person is having lower than normal
levels of blood sugar.
When hunger contractions occur in the stomach, the person sometimes experiences mid
pain in the stomach called hunger pangs. Hunger pangs usually do not begin until 12 to 24 hours
after the last ingestion of food. In starvation, they reach the greatest intensity in 3 to 4 days and
gradually weaken in succeeding days.
2. MIXING AND PROPULSION OF FOOD IN THE STOMACH-BASIC ELECTRICAL

RHYTHM OF THE STOMACH WALL
The digestive juices of the stomach are secreted by gastric glands, which are present in
almost the entire wall of the body of the stomach except along a narrow strip on the lesser
curvature of the stomach.
These secretions come immediately into contact with that portion of the stored food lying
against the mucosal surface of the stomach.
As long as food is in the stomach, weak peristaltic constrictor waves, called mixing
waves, begin in the mid to upper portions of the stomach wall and move toward the antrum about
once every 15 to 20 seconds. These waves are initiated by the gut wall basic electrical rhythm,
consisting of electrical "slow waves" that occur spontaneously in the stomach wall. As the
constrictor waves progress from the body of the stomach into the antrum, they become more
intense and providing powerful peristaltic action potential-driven constrictor rings that force the
antral contents under higher and higher pressure toward the pylorus.
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3. Gastric emptying:
This refers to periodic expulsion of the liquefied food into the duodenum. Food remains
in the stomach for about 3 hours. Digestion takes place during this period. Gastric emptying is
coordinated action of GIT hormones and nervous system. Peristaltic waves in the body and
pyloric part of the stomach and simultaneous relaxation of pyloric sphincter are necessary for
normal gastric emptying.
Factors that influence gastric emptying
a. Volume of gastric content: Gastric emptying is directly proportional to the volume. If the
content of the stomach is large, large amount is emptied into the intestine. This is mainly due to
stretching of the stomach wall which elicits local myenteric reflexes in the wall that greatly
increases the activity of the pyloric pump and at the same time inhibits the pylorus.
b. Consistency of gastric content: Gastric emptying depends upon the consistency of the contents.
Liquids leave the stomach rapidly and solid move out of stomach after being converted into fluid
or semi fluid. Undigested solid particles are not easily emptied.
c. Chemical composition of the food: Carbohydrates leave the stomach more rapidly than the fat.
Fatty food remains in the stomach for a longer period. Protein rich foods also slow down gastric
emptying. The mechanisms are both humeral and neural.
d. PH of gastric content: Gastric chyme with low pH leaves the stomach slowly.
e. Osmolarity of gastric content: Hyperosmolarity and increased acidity inhibit gastric emptying.
Hyperosmolality of the duodenal contents is sensed by “duodenal osmoreceptors” that initiate a
decrease in gastric emptying, which is probably neural in origin. Gastric content which is
isotonic to blood leaves the stomach rapidly than hypertonic or hypotonic content.
f. Excitement hastens gastric emptying.
g. Fear slows gastric emptying.
Regulation of gastric emptying:
Gastric factors:
i. Stretching
ii. Gastrin
Gastrin has mild to moderate stimulatory effects on motor functions in the body of the
stomach and enhances the activity of the pyloric pump. Thus, gastrin promotes stomach
emptying.
Emptying of stomach stops mainly due to the inhibition of gastric motility. This
inhibition is caused by both neural and hormonal factors (duodenal factors).
Neural factors: This is due to enterogastric reflex controlled by nervous system.
Humoral factors: Humoral factors are due to VIP, GIP, Secretin, CCK, Somatostatin and
peptide YY.
ENTEROGASTRIC REFLEX
When acid chyme enters the duodenum, the mucosa releases some hormones which enter
the stomach through blood and inhibit the motility of stomach. When food enters the duodenum,
multiple nervous reflexes are initiated from the duodenal wall. They pass back to the stomach to
slow or even stop stomach emptying if the volume of chyme in the duodenum becomes too
much.
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These reflexes are mediated by three routes:

1. Directly from the duodenum to the stomach through the enteric nervous system in the gut wall.
2. Through extrinsic nerves that go to the prevertebral sympathetic ganglia and then back
through inhibitory sympathetic nerve fibers to the stomach, and
3. Probably to a slight extent through the vagus nerves all the way to the brain stem, where they
inhibit the normal excitatory signals transmitted to the stomach through the vagi.
All these parallel reflexes have two effects on stomach emptying:
First, they strongly inhibit the "pyloric pump" propulsive contractions, and second, they increase
the tone of the pyloric sphincter.
The types of factors that are continually monitored in the duodenum and that can initiate
enterogastric inhibitory reflexes include the following:
 The degree of distension of the duodenum.
 The presence of any degree of irritation of the duodenal mucosa.
 The degree of acidity of the duodenal chyme.
 The degree of osmolality of the chyme.
 The presence of certain breakdown products in the chyme, especially breakdown products of
proteins and, perhaps to a lesser extent, of fats.
The enterogastric inhibitory reflexes are especially sensitive to the presence of irritants
and acids in the duodenal chyme, and they often become strongly activated within as little as 30
seconds. For instance, whenever the pH of the chyme in the duodenum falls below about 3.5 to
4, the reflexes frequently block further release of acidic stomach contents into the duodenum
until the duodenal chyme can be neutralized by pancreatic and other secretions.
Breakdown products of protein digestion also elicit inhibitory enterogastric reflexes; by
slowing the rate of stomach emptying, sufficient time is ensured for adequate protein digestion in
the duodenum and small intestine.
Finally, either hypotonic or hypertonic fluids (especially hypertonic) elicit the inhibitory
reflexes. Thus, too rapid flow of non-isotonic fluids into the small intestine is prevented, thereby
also preventing rapid changes in electrolyte concentrations in the whole-body extracellular fluid
during absorption of the intestinal contents.
INTESTINAL MOTILITY
DR. C UGURU
There are three types of smooth muscle contractions:
A) Peristaltic waves/ propulsion
B) Segmentation contractions/ mixing
C) Tonic contractions
These contractions are initiated by focal increases in calcium influx with waves of
increased calcium concentration spreading from each focus.
A. Peristalsis:
Peristalsis Propels the intestinal contents (chyme) toward the large intestines. longitudinal
layer executes this task. Movement controlled by auerbach plexus. (Location: between the
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circular and longitudinal muscle of the GIT ) Electrical rhythm is faster in the intestinal (12 per
minute unlike 3 per minute for the stomach).
Recall: BER (basic electrical rhythm) by interstitial cells of Cajal.
B. Segmentation contractions:
This moves the chyme to and fro and increases its exposure to the mucosal surface. It is
done by the circular layer, and assumes a sausage like appearance. It mixes chyme with
enzymes and involves retrograde movement unlike peristalsis
C. Tonic contractions
Theseare relatively prolonged contractions that in effect isolate one segment of the
intestine from another.
These last two types of contractions slow transit in the small intestine to the point that the transit
time is actually longer in the fed than in the fasted state. This permits longer contact of the
chyme with the enterocytes and facilitates absorption.
CONTROL OF PERISTALSIS
Peristaltic activity of the small intestine is greatly increased after a meal. This is caused partly by
the beginning entry of chyme into the duodenum causing stretch of the duodenal wall. Also,
peristaltic activity is increased by the so-called gastroenteric reflex that is initiated by
distension of the stomach and conducted principally through the myenteric plexus.
Hormonal Control
They include gastrin, CCK, insulin, motilin, and serotonin, all of which enhance intestinal
motility and are secreted during various phases of food processing. Conversely, secretin and
glucagon inhibit small intestinal motility.
The function of the peristaltic waves in the small intestine is not only to cause
progression of chyme toward the ileocecal valve but also to spread out the chyme along the
intestinal mucosa.
As the chyme enters the intestines from the stomach and elicits peristalsis, this
immediately spreads the chyme along the intestine; and this process intensifies as additional
chyme enters the duodenum. On reaching the ileocecal valve, the chyme is sometimes blocked
for several hours until the person eats another meal; at that time, a gastroileal reflex intensifies
peristalsis in the ileum and forces the remaining chyme through the ileocecal valve into the
cecum of the large intestine.
PERISTALTIC RUSH
Irritation of the intestinal mucosa, as occurs in some severe cases of infectious diarrhoea
causes both powerful and rapid peristalsis, called the peristaltic rush.This is initiated partly by
nervous reflexes involving the autonomic nervous system and brainstem and partly by intrinsic
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enhancement of the myenteric plexus reflexes within the gut wall itself. The powerful peristaltic
contractions travel long distances in the small intestine within minutes, sweeping the contents of
the intestine into the colon and thereby relieving the small intestine of irritative chyme and
excessive distension.
MOVEMENT OF VILLI
This consists of alternate shortening and elongation of villi by contraction and relaxation
of muscles. It is initiated by local nervous reflexes and villikinin and helps to empty lymph from
central lacteal and increase surface area for absorption.
MOTILITY OF THE COLON

The colon serves as a reservoir for the residues of meals that cannot be digested or
absorbed. Motility in this segment is slowed to allow the colon to absorb water, sodium, and
other minerals. By removing about 90% of the fluid, it converts the 1000–2000ml of isotonic
chyme that enters it each day from the ileum to about 200–250 mL of semisolid faeces. The
ileocecal valve and sphincter restricts reflux of colonic content and commensal bacteria, into the
relatively sterile ileum. The portion of the ileum containing the ileocecal valve projects slightly
into the cecum and ncrease in colonic pressure squeezes it shut, while increase in ileal pressure
open it. It is normally closed.
Each time a peristaltic wave reaches it, it opens briefly, permitting some of the ileal
chyme to squirt into the cecum. When food leaves the stomach, the sphincter relaxes and the
passage of chyme through the ileocecal valve increases (gastroileal reflex). This is presumably a
vago-vagal reflex. The movements of the colon include :
• Segmentation contractions
• Peristaltic waves like those occurring in the small intestine.
• Mass action contraction.
Segmentation contractions mix the contents of the colon and, by exposing more of the
contents to the mucosa, facilitate absorption. Haustrations are formed along the length of the
colon as segmentation contractions take place.
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Peristaltic waves propel the contents toward the rectum, although weak antiperistalsis is
sometimes seen. The movements of the colon are coordinated by the BER of the colon. The
frequency of this wave, unlike the wave in the small intestine, increases along the colon, from
about 2/min at the ileocecal valve to 6/min at the sigmoid.
A third type of contraction that occurs only in the colon is the mass action contraction,
occurring about 10 times per day, in which there is simultaneous contraction of the smooth
muscle over large confluent areas. These contractions move material from one portion of the
colon to another. They also move material into the rectum, and rectal distention initiates the
defecation reflex.
DISORDER OF COLON MOTILITY

A. Constipation
This refers to a pathological decrease in bowel movements. It is due to alterations in the
balance between secretion and absorption in the colon which could contribute to symptom onset.
Patients with persistent constipation, and particularly those with a recent change in bowel habits,
should be examined carefully to rule out underlying organic disease.
However, many normal humans defecate only once every 2–3 days, even though others
defecate once a day and some as often as three times a day.
Symptoms caused by constipation are slight anorexia and mild abdominal discomfort and
distension.
Treatment of constipation:
Most cases of constipation are relieved by a change in the diet to include more fibre, or
the use of laxatives that retain fluid in the colon, thereby increasing the bulk of the stool and
promoting reflexes that lead to evacuation.
B. Hirschsprung disease or aganglionic megacolon

This is characterized by abdominal distension, anorexia, and lassitude. The disease is typically
diagnosed in infancy, and affects as many as 1 in 5000 live births. It is due to a congenital
absence of the ganglion cells in both the myenteric and submucous plexuses of a segment of
the distal colon, as a result of failure of the normal cranial-to-caudal migration of neural crest
cells during development.
The absence of peristalsis in patients with this disorder causes faeces to pass the
aganglionic region with difficulty, and children with the disease may defecate as infrequently as
once every 3 weeks.
Management of Hirshsprung disease:

The symptoms of Hirschsprung disease can be relieved completely if the aganglionic
portion of the colon is resected and the portion of the colon above it anastomosed to the rectum.
DEFAECATION:
This is a process by which unwanted faecal matters are sent out of GIT through the anus.
Distension of the rectum with faeces initiates reflex contractions of its musculature and the desire
to defecate.
Control: In humans, the sympathetic nerve supply to the internal (involuntary) anal sphincter is
excitatory, whereas the parasympathetic supply is inhibitory. This sphincter relaxes when the
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rectum is distended. The nerve supply to the external anal sphincter, a skeletal muscle, comes
from the pudendal nerve.
The urge to defecate first occurs when rectal pressure increases to about 18 mm Hg.
When this pressure reaches 55 mm Hg, the external as well as the internal sphincter relaxes and
there is reflex expulsion of the contents of the rectum. This is why reflex evacuation of the
rectum can occur even in the setting of spinal injury. Before the pressure that relaxes the external
anal sphincter is reached, voluntary defecation can be initiated by straining.
Normally, the angle between the anus and the rectum is approximately 90º, and this plus
contraction of the puborectalis muscle inhibits defecation. With straining, the abdominal muscles
contract, the pelvic floor is lowered 1–3 cm, and the puborectalis muscle relaxes. The anorectal
angle is reduced to 15º or less. This is combined with relaxation of the external anal sphincter
and defecation occurs.
GIT SECRETION
There are various secretions in the GIT which include:
Bile is not a digestive juice, although it helps to make fat accessible to enzymes.
SALIVA
This is the fluid that is found in the mouth. It is produced and secreted by glands in the
mouth that opens via ducts into the oral cavity. The salivary glands are compound tubular
glands with secretory cells that are arranged in groups called acini around a central duct. There
are 2 types of secretory cells
a) Serous
b) mucous
c) mixed
The serous secretory cells have zymogen granules. The mucous secretory cells have
translucent granules and secrete mucin which makes saliva slippery. The serous cells secrete
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Ptyalin (salivary α- amylase) that digest carbohydrates in the mouth. Saliva is produced by
three pairs of salivary glands :
- parotid,
-submandibular, and
-sublingual glands
1. Parotid gland: produces 25% of saliva. It is the largest of the salivary glands and secretes
serous saliva. Secretions are emptied into the oral cavity by Stensen’s duct into the mouth
opposite the upper and molar tooth on either side.
2. Submandibular or Submaxillary glands: Produce 70% of saliva. Secretes mixed saliva.
Each gland empties its saliva into oral cavity by whartons duct.
3. Sublingual gland: Produces 5% of saliva. It is smallest of the 3 pairs of major salivary glands.
Secretes mucous saliva. It opens into the oral cavity by several fine ducts, the Rivinus(5-15
small ducts)
NEURAL CONTROL OF SALIVARY GLANDS:

-Sympathetic and
-Parasympathetic nerves.
All salivary glands receive sympathetic. Parotid gland is supplied by glossopharyngeal
nerve. Submandibular and sublingual glands supplied by facial nerve.
SALIVA SECRETION:
Approximately 1-1.5 litres per day of saliva is secreted. Salivary gland is a secretory
acinus which produces the primary secretion conducted through short intercalated ducts till it
gets to the main collecting ducts. Primary secretion in the acini is like an ultra-filtrate of
plasma.
Saliva is viscous, colourless, cloudy and slimy liquid. It has a pH about 7.0 and specific
gravity 1.002-1.012. It is hypotonic.
The secretion is modified during its passage through the intralobular ducts.
The ductal modification is under the influence of aldosterone as Na+ is actively reabsorbed with
Cl-. K+ and HCO3- are actively reabsorbed into the saliva. Thus, the composition of saliva is
variable.
Composition of Saliva
-Organic
-Inorganic
1. Organic components include:
a. Enzymes:
 -amylase (ptyalin) produced by the serous cell, optimal pH is 6.7.
 Lingual lipase: produced by glands known as ebner’s gland located on the dorsal surface of the
tongue. It is also active in the stomach until it is inhibited by gastric juice, digests about 30% of
fats.
Other enzymes like acid phosphatase, peroxidase and kallikrein.
b. Mucin: is a glycoprotein. It lubricates food and protects the oral mucosa. It causes food and
faecal matter to bind together, hence makes swallowing and defaecation easy. It is viscus for
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easy passage of food. It is strongly resistant to digestion by enzymes. It is amphoteric (acid or

base) hence acts as a buffer.
c. Immunoglobulins mainly IgA with smaller amount of IgG & IgM, hence saliva plays a role in
immunity.
d. Lysozyme: When this enzyme combines with thiocyanate, it is very effective at destroying
bacteria.
e. Lactoferrin: binds to iron and also effective at attacking bacteria. It is bacteriostatic.
f. Proline-rich proteins: These protect tooth enamel and also bind toxic substances.
g. Others are urea, blood group antigens, kallikrein
2. Inorganic constituents include:

a. Water: constitute about 99% of saliva
b. Ions: both cations and anions. Cation- mainly K+ and Na+. Anion- mainly Cl- and HCO32-.
Others are PO4- and Ca2+
The relative concentration of these ions will depend on the modification of saliva by the ducts.
Saliva ions in the gland are equivalent to ions in the plasma unless it is modified by the duct
depending on body’s need.
Functions of Saliva:
1. It facilitates swallowing.
2. keeps the mouth moist
3. Serves as a solvent for the molecules that stimulate the taste buds.
4. Aids speech by facilitating movements of the lips and tongue
5. keeps the mouth and teeth clean as the saliva also has some antibacterial action, and patients with
deficient salivation (xerostomia)have a higher than normal incidence of dental caries.
6. The buffers in saliva help maintain the oral pH at about 7.0.
Regulation of Salivary Secretion:

Secretion of saliva is mainly under neural control via parasympathetic and sympathetic
mechanisms. It is a reflex process, makes use of receptors that are located in the mouth. Once the
receptors are stimulated, impulses generated are sent via afferent pathway (CNs 7, 9) to the
salivary nuclei in the brainstem. The impulses will then be decoded and appropriate message
will be sent via efferent pathway (CNs 7, 9) to salivary glands. Quantity of saliva released
depends on the activity.
 It is increased during mastication of food and anxiety.
 It decreases during sleep. Food in the mouth, sour taste and smooth objects increase salivation.
 Rough object decrease salivation by direct inhibition of salivary gland.
 Smell, thought, sight and taste of flavoury food stimulate salivation.
 Disliked food will reduce salivation.
 Smell of faeces can increase salivation
Disorders of Salivary Secretion:

1. Hyposalivation(decreased saliva secretion): could be due to fear, fever, dehydration, hypoplasia
of salivary gland(congenital absence), Bell’s palsy(paralysis of facial nerve VII).
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2. Hypersalivation(increased salivation):could occur in pregnancy, tooth decay, neoplasm of

mouth and tongue(due to irritation of nerve endings in the mouth)
3. Gastritis, esophagitis, neurological disorders e.g. Parkinsonism, cerebral palsy and mental
retardation.
GASTRIC SECRETION
This is secretions by the gastric glands.
There are 2 types of gland in the stomach
1. Oxyntic or gastric glands
2. Pyloric glands
1. The oxyntic glands are located on the inside surfaces of the
body and fundus of the stomach. It contributes about 80% of
gastric secretion.
There are 3 types of cells in the oxyntic glands
a. Mucus neck cell: secrete mainly mucus
b. Peptic or Chief cells: secrete mainly pepsinogen
c. Parietal or Oxyntic cells: secrete HCL and intrinsic factor
Intrinsic factor is important for the later absorption of vitamin B12 or cobalamin and is
reabsorbed in the distal ileum.
2. The Pyloric glands are found in the antral and pyloric regions of the stomach or the distal 20% of
the stomach.
They contribute about 20% to gastric secretion. Pyloric glands secrete mainly mucus, in
addition to pepsinogen and hormone gastrin. About 2-3 litres of gastric secretions is produced
per day. The pH is 1 to 3.5.
COMPOSITION OF GASTRIC SECRETION
a. Organic composition
b. Inorganic composition
Organic composition:
i. Pepsin: this begins the digestion of protein in the stomach.
ii. Gelatinase: an enzyme that hydrolyses gelatin.
iii. Gastric α-amylase
iv. Gastric lipase
These last 2 play insignificant role
v. Intrinsic factor: plays a significant role in the formation of blood,
vi. Mucus: Secretion is stimulated by prostaglandins
Inorganic composition:
i. Water
ii. Cations: Na+ , K+ , mg2+ , H2+
iii. Anions: Cl- ,HPO4, so42+
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FUNCTIONS OF GASTRIC SECRETION

1. Pepsin: is an active proteolytic enzyme, has an optimal PH of 1.8 to 3.5. At Ph >5.0, it
becomes inactive. It begins the process of protein digestion, digests about 10-20% of the total
proteins ingested. Also digests collagen.
2. Gelatinase: digests gelatin in meat
3. Gastric lipase: is mainly a tributyrase, digest a kind of butter fat called Tributylin.
4. Gastric α-amylase: plays an insignificant role.
5. Intrinsic factor: helps in the absorption of vitamin B12 which helps with maturation of red
blood cells. Intrinsic factor coats VitaminB12 preventing it from absorption until it reaches the
appropriate place of absorption. Lack of it causes pernicious anaemia.
6. Mucus: forms a flexible gel that coats the mucosal surface of the stomach, thus preventing the
digestion of mucosa by acid. This coating forms a part of mucosal defense against gastric acid.
Other mucosal defense against gastric acid mechanism includes the following:
i. The surface membranes of mucosal cells are impermeable to acid

ii. The tight junction are also impermeable to hydrogen ion.
Control/Regulation of acid secretion

This can be Neural or Hormonal. Neural control is mainly through the vagus nerve
(parasympathetic) and the Hormonalcontrol is through gastrin.
Regulation is divided into 3 phases:
a. Cephalic
b. Gastric
c. Intestinal phases
Cephalic: the sight, smell, thought, or taste of food will increase acid secretion. This phase
contributes about 20% to gastric secretions. Emotional factors also affect gastric secretion e.g.
anger increases secretion but fear and depression reduce secretion.
Gastric: presence of food in the stomach contributes >70% of gastric secretions.
Intestinal: mainly inhibitory thru enterogastric reflex. Inhibition can also be through the
hormones: secretin, cholecytokinin, somatostatin.
MECHANISM OF ACID SECRETION
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The main driving force for hydrochloric acid secretion by the parietal cells is a hydrogen-
potassium pump (H+-K+ ATPase).The chemical mechanism of hydrochloric acid formation
consists of the following steps:
1. Water inside the parietal cell becomes dissociated into H+ and OH- in the cell cytoplasm. The
H+ is then actively secreted into the canaliculus in exchange for K+, an active exchange process
that is catalyzed by H+ - K+ ATPase. Potassium ions transported into the cell by the Na+-K+
ATPase pump on the basolateral (extracellular) side of the membrane tend to leak into the lumen
but are recycled back into the cell by the H+-K+ ATPase.
2. The pumping of H+ out of the cell by the H+-K+ ATPase permits OH- to accumulate and form
bicarbonate from CO2, either formed during metabolism in the cell or entering the cell from the
blood. This reaction is catalysed by carbonic anhydrase. The bicarbonate is then transported
across the basolateral membrane into the extracellular fluid in exchange for chloride ions,
which enter the cell and are secreted through chloride channels into the canaliculus, giving a
strong solution of hydrochloric acid in the canaliculus. The hydrochloric acid is then secreted
outward through the open end of the canaliculus into the lumen of the gland.
3. Water passes into the canaliculus by osmosis because of extra ions secreted into the canaliculus.
Thus, the final secretion from the canaliculus contains water, hydrochloric acid at a
concentration of about 150 to 160 mEq/L, potassium chloride at a concentration of 15 mEq/L,
and a small amount of sodium chloride.
FUNCTIONS OF GASTRIC SECTRETION
1. Kills many ingested bacteria
2. Helps protein digestion (pepsinogenpepsin)
3. Provides optimal pH for pepsin activity
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4. Increases the flow of bile and pancreatic juice.
EFFECT OF HYPERSECRETION OF ACID

Peptic Ulcer Disease (PUD):
Peptic ulcer is an ulcer in the wall of stomach or duodenum caused by digestive action of the
HCl. It is irritation or degradation or digestion of the gastric and duodenal mucosa as a result of
the breakdown of the mucosal barrier that normally protects this irritation or digestion. It is
characterized by recurrent epigastric pains, relieved by food, antacids or vomiting with periods
of spontaneous remission. Peptic ulcer is more common in persons of blood group O. Peptic
ulcer disease tends to run in families.
Causes:
There are 2 main groups of causes:
*disruption of mucosal barrier
*prolonged secretion of acid
Disruption of mucosal barrier could be either through infections with helicobacter pylori or
ethanol, NSAIDs, bile salts prolonged secretion of acid is seen in some patients with Zollinger-
ellison syndrome usually characterized by tumours of gastrin producing cells (gastrinomas).
Treatment:
Try and evaluate the cause Gastric and duodenal ulcers can be given a chance to heal by
inhibition of acid secretion with drugs such as omeprazole and related drugs that inhibit
H+ - ATPase (“proton pump inhibitors”). If present, Helico pylori can be eradicated with
antibiotics, and NSAID-induced ulcers can be treated by stopping the NSAID. Gastrinomas can
sometimes be removed by surgery.
PANCREATIC SECRETION
The pancreas is an organ with dual functions namely: exocrine and endocrine functions.
The endocrine function involves the production of the hormones which pass into the
bloodstream. These hormones secreted by endocrine part of pancreas are: insulin, glucagon,
somatostatin and pancreatic polypeptide from islet of langerhans. The exocrine part of the
pancreas secretes pancreatic juice.
As an exocrine gland, the digestive secretion is poured into the duodenum.
The pancreas is made of three types of cells.
1. Acinar cells
2. Islet cells of langerhans
3. Duct cells
Islet cells are concerned with endocrine function and consist of 3 types of cells:
1) A or  cells secrete glucagon.
2) B or  cells secrete insulin.
3) D or  cells secrete somatostatin.
Pancreatic Juice:
The pancreatic digestive enzymes are secreted by pancreatic acini, and large volumes of
sodium bicarbonate solution are secreted by the small ductules and larger ducts leading from
the acini. The combined product of enzymes and sodium bicarbonate then flows through a long
pancreatic duct that normally joins the hepatic duct immediately before it empties into the
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duodenum through the ampulla of Vater, surrounded by the sphincter of Oddi. Pancreatic juice
is secreted most abundantly 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.
Between 0.5 to 1.5 L/day (up to 2L during maximal secretion) of pancreatic juice is produced.
The pH is between 8.0 – 9.0
Composition:
*Organic
*Inorganic
Organic compositions are mostly enzymes.
a. Trypsinogen which is converted to trypsin by the action of an enzyme called Enterokinase.
This enzyme is increased by CCK.
b. Trypsin inhibitor: produced by the cell that produces trpsinogen. It inhibits any trypsin that is
formed along the duct. It is a protective mechanism. It prevents digestion of pancreas by formed
trypsin in the duct.
c. Chymotrypsinogen: activated to chymotrypsin by trypsin
d. Procarboxypolypeptidase: also converted to active form carboxypolypeptidase by trypsin.
e. Ribonuclease: plays a role in the digestion RNA.
f. Deoxyribonuclease: plays a role in the digestion of DNA.
g. Proelastase: converted to active form, elastase by trypsin. It helps in the digestion of elastin.
h. Prophospholipase A2 : converted to phospholipase A2 (PLA2). Then this PLA2 will convert
lecithin to lysolecithin and a free fatty acid is generated. Lysolecithin is powerful in damaging
cell membranes and is a major factor in what happens in pancreatitis that is due to blockage
pancreatic duct.
i. Procolipase: activated by trypsin to give colipase which facilitates the exposure of active site of
pancreatic lipase.
j. Pancreatic α-amylase: is a powerful enzyme of all carbohydrate digestion except cellulose.
k. Pancreatic lipase: a lipid digesting enzyme.
l. Cholesteryl ester hydrolase: hydrolyses cholesterol esters.
m. Trypsin and chymotrypsin split whole and partially digested proteins into peptides of various
sizes but do not cause release of individual amino acids.
n. carboxypolypeptidase splits some peptides into individual amino acids, thus completing
digestion of some proteins all the way to the amino acid state.
Inoganic Compositions:
a. Cations: Na, Mg, Ca, K
b. Anions: HCO3 ,Cl, SO4. H2PO4
c. Water
The bicarbonate ions play an important role in neutralizing the acidity of the chyme
emptied from the stomach into the duodenum.
When the pancreas becomes severely damaged or when a duct becomes blocked, large
quantities of pancreatic secretion sometimes become pooled in the damaged areas of the
pancreas. Under these conditions, the effect of trypsin inhibitor is often overwhelmed, in which
case the pancreatic secretions rapidly become activated and can literally digest the entire
pancreas within a few hours, giving rise to the condition called acute pancreatitis. This is
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sometimes lethal because of accompanying circulatory shock; even if not lethal, it usually leads
to a subsequent lifetime of pancreatic insufficiency.
Secretion of Bicarbonate Ions
Although the enzymes of the pancreatic juice are secreted entirely by the acini of the
pancreatic glands, the other two important components of pancreatic juice, bicarbonate ions and
water, are secreted mainly by the epithelial cells of the ductless and ducts that lead from the
acini. When the pancreas is stimulated to secrete copious quantities of pancreatic juice, the
bicarbonate ion concentration can rise to as high as 145 mEq/L, a value about five times that of
bicarbonate ions in the plasma. This provides a large quantity of alkali in the pancreatic juice that
serves to neutralize the hydrochloric acid emptied into the duodenum from the stomach. This
provides a large quantity of alkali in the pancreatic juice that serves to neutralize the
hydrochloric acid emptied into the duodenum from the stomach. The basic steps in the cellular
mechanism for secreting sodium bicarbonate solution into the pancreatic ductless and ducts are
as follows:
1. Carbon dioxide diffuses to the interior of the cell from the blood and, under the influence of
carbonic anhydrase, combines with water to form carbonic acid (H2CO3). The carbonic acid in
turn dissociates into bicarbonate ions and hydrogen ions (and H+). Then the bicarbonate ions are
actively transported in association with sodium ions (Na+) through the luminal border of the cell
into the lumen of the duct.
2. The hydrogen ions formed by dissociation of carbonic acid inside the cell are exchanged for
sodium ions through the blood border of the cell by a secondary active transport process.
This supplies the sodium ions (Na+) that are transported through the luminal border into the
pancreatic duct lumen to provide electrical neutrality for the secreted bicarbonate ions. The
overall movement of sodium and bicarbonate ions from the blood into the duct lumen creates an
osmotic pressure gradient that causes osmosis of water also into the pancreatic duct, thus
forming an almost completely isosmotic bicarbonate solution.
Regulation of Pancreatic Secretion:

Three basic stimuli are important in causing pancreatic secretion:
1) Acetylcholine, which is released from the parasympathetic vagus nerve endings and from
other cholinergic nerves in the enteric nervous system
2) Cholecystokinin, which is secreted by the duodenal and upper jejunal mucosa when food
enters the small intestine
3) Secretin, which is also secreted by the duodenal and jejunal mucosa when highly acidic food
enters the small intestine.
Acetylcholine and cholecystokinin stimulate the acinar cells of the pancreas, causing
production of large quantities of pancreatic digestive enzymes but relatively small quantities of
water and electrolytes to go with the enzymes. CCK acts on the acinar cells to cause the release
of zymogen granules and production of pancreatic juice rich in enzymes but low in volume. Its
effect is mediated by phospholipase C.
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Like CCK, acetylcholine acts on acinar cells via phospholipase C to cause discharge of
zymogen granules, and stimulation of the vagi causes secretion of a small amount of pancreatic
juice rich in enzymes. There is evidence for vagally mediated conditioned reflex secretion of
pancreatic juice in response to the sight or smell of food.
Secretin, in contrast to the first two basic stimuli, acts on the pancreatic ducts to cause
copious secretion of a very alkaline pancreatic juice that is rich in HCO3 and poor in enzymes.
The effect on duct cells is due to an increase in intracellular cAMP. Secretin also
stimulates bile secretion. Although HCO3 is secreted in the small ducts, it is reabsorbed in the
large ducts in exchange for Cl- The magnitude of the exchange is inversely proportionate to the
rate of flow.
Multiplicative Effects of Different Stimuli:
When all the different stimuli of pancreatic secretion occur at once, the total secretion is
far greater than the sum of the secretions caused by each one separately.Therefore, the various
stimuli are said to "multiply," or "potentiate," one another. Thus, pancreatic secretion normally
results from the combined effects of the multiple basic stimuli, not from one alone.
Phases of Pancreatic Secretion
These occur in three phases:
 The cephalic phase,
 The gastric phase, and
 The intestinal phase.
Cephalic phase:
Here, the same nervous signals from the brain that cause secretion in the stomach also cause
acetylcholine release by the vagal nerve endings in the pancreas. This causes moderate amounts
of enzymes to be secreted into the pancreatic acini, accounting for about 20% of the total
secretion of pancreatic enzymes after a meal. But little of the secretion flows immediately
through the pancreatic ducts into the intestine because only small amounts of water and
electrolytes are secreted along with the enzymes.
Gastric phase:
During the gastric phase, the nervous stimulation of enzyme secretion continues, accounting for
another 5 to 10% of pancreatic enzymes secreted after a meal. But, again, only small amounts
reach the duodenum because of continued lack of significant fluid secretion
Intestinal Phase:
After chyme leaves the stomach and enters the small intestine, pancreatic secretion becomes
copious, mainly in response to the hormone secretin. This accounts for >70% of pancreatic
secretion.
Effect Of Secretin On Stomach Chyme:
Secretin is a polypeptide, containing 27 amino acids (molecular weight about 3400), present in
an inactive form, prosecretin, in so-called S cells in the mucosa of the duodenum and jejunum.
When acid chyme with pH less than 4.5 to 5.0 enters the duodenum from the stomach, it causes
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duodenal mucosal release and activation of secretin, which is then absorbed into the blood. The
one truly potent constituent of chyme that causes this secretin release is the hydrochloric acid
from the stomach. Secretin in turn causes the pancreas to secrete large quantities of fluid
containing a high concentration of bicarbonate ion (up to 145 mEq/L) but a low concentration of
chloride ion. The secretin mechanism is especially important for two reasons:
First, secretin begins to be released from the mucosa of the small intestine when the pH
of the duodenal contents falls below 4.5 to 5.0, and its release increases greatly as the pH falls to
3.0. This immediately causes copious secretion of pancreatic juice containing abundant amounts
of sodium bicarbonate. In this way, the acid contents emptied into the duodenum from the
stomach become neutralized, so further peptic digestive activity by the gastric juices in the
duodenum is immediately blocked. Because the mucosa of the small intestine cannot withstand
the digestive action of acid gastric juice, this is an essential protective mechanism to prevent
development of duodenal ulcers.
BILIARY SECRETION
Organic Constituents of Bile
A. Bile Salts and Micelles: Primary bile acids are cholic acid and chenodeoxycholic acid because
they are formed de novo by the liver from cholesterol. The lipid-soluble bile acids are then
conjugated primarily with either glycine or taurine forming either glycocholic acid or
taurocholic acid. The conjugated forms are water-soluble but contain a lipid-soluble segment. In
the alkaline pH of bile, the bile acids are converted to Na+ and K+ referred to as bile salts. Bile
salts are actively secreted by the liver.mSecondary bile acids are formed by deconjugation and
dehydroxylation of the primary bile salts by bacteria in the colon forming deoxycholic acid (from
cholic acid) and lithocholic acid (from chenodeoxycholic acid).nLithocholic acid is hepatotoxic,
not soluble and is excreted in faeces. Deoxycholic acid is reabsorbed and re-excreted by the liver
as bile salt.
Micelle Formation:
When bile salts become concentrated, they form micelles. They are water-soluble spheres
with a lipid-soluble interior. As such, they provide a vehicle to transport lipid-soluble materials
in the aqueous medium of the bile fluid and the small intestine.
Micelle Function:
Micelles are vital in the digestion, transport and absorption of lipid –soluble substances
from the duodenum to the distal ileum. In the distal ileum, the bile salts be actively reabsorbed
and recycled (Enterohepatic circulation).Lack of active reabsorbing mechanism (or a distal
ileum) causes loss in the stool and a general deficiency in bile salts, as the liver has a limited
capacity to manufacture them. This deficiency can lead to fat malabsorption and cholesterol gall
stones.
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B. Bile Pigments:
1. Bilirubin: A major bile pigment, bilirubin is a lipid soluble metabolite of hemoglobin.
Transported to the liver attached to protein, it is then conjugated and excreted as water-soluble
glucoronides. These give a golden yellow colour to bile.
2. Stercobilin: Produced from metabolism of bilirubin by intestinal bacteria. It gives a brown
colour to the stool.
Haemoglobin Biliverdin Bilirubin Urobilinogen Stercobilinogen (oxidized to
stercobilin in the colon)
C. Cholesterol: Present in small amount. It is insoluble in water and must be solubilized by bile salt
micelles before it can be secreted in the bile.
FUNCTIONS OF BILE
a. Emulsification of fats
b. Transport of endproducts of fat digestion
c. Activation of pancreatic lipase
d. Neutralization of acid
e. Excretion of various substances eg cholesterol, bile pigments, drugs, toxins
ENTEROHEPATIC CIRCULATION OF BILE

Greater than 90% of bile salts are reabsorbed in the terminal ileum. Greater than 5%
enter the colon where they form deoxycholic acid and lithocholic acid. The reabsorbed salts then
enter the blood where they move into the liver and then re-secreted into the bile. The enteric pool
of bile is about 3.5g and this amount circulate twice per meal in about 6 to 8 times per day.
Normal bile synthesis is about 0.3g per day. In bile deficiency, >50% of fat is lost, causing
Steatorrhea (presence of fat in faeces).
Control of bile secretion

 Mainly Neural and Hormonal
 Neural is mainly via vagal stimulation ↑vagal stimulation↑parasympathetic↑bile secretion
 Hormonal:
 secretin increases ductal secretion
 liver blood flow also increases secretion
 choleretics like secretin,bile salts and bile acids
 increase the flow of bile
 cholagogues like CCK increase gall bladder
 contraction
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PROBLEMS OF BILE SECRETION AND STORAGE OF BILE

A. Jaundice (icterus):
This refers to yellowing of skin, scleras and mucous membranes due to accumulation of free or
conjugated bilirubin in the blood. It is usually detectable when the total plasma bilirubin is
greater than 2 mg/dl (34 μmol/L). Hyperbilirubinemia may be due to :
1) excess production of bilirubin (haemolytic anaemia, etc.
2) decreased uptake of bilirubin into hepatic cells.
3) disturbed intracellular protein binding or conjugation .
4) disturbed secretion of conjugated bilirubin into the bile
Canaliculi
When it is due to one of the first three processes, the free bilirubin rises (unconjugated).
When it is due to disturbed secretion of conjugated bilirubin or bile duct obstruction, bilirubin
glucuronide regurgitates into the blood, and it is predominantly the conjugated bilirubin in the
plasma that is elevated.
Types of Jaundice:
1) Haemolytic jaundice seen in ABO incompatibility, erythroblastosis foetalis, SCA.
2) Hepatocellular jaundice: seen in those with impaired hepatic uptake of bilirubin or those with
impaired conjugation of bilirubin
3) Obstructive jaundice includes intrahepatic and extrahepatic obstruction.
B. Cholelithiasis: This is the presence of gallstones. It is a common condition.

Its incidence increases with age. The stones are of two types:
calcium bilirubinate stones and cholesterol stones.
Three factors appear to be involved in the formation of cholesterol stones:
1. Bile stasis: stones form in the bile that is
sequestrated in the gallbladder rather than the bile that is flowing in the bile ducts.
2. Inflammation of gall bladder
C. Supersaturation of the bile with cholesterol:

Cholesterol is very insoluble in bile, and it is maintained in solution in micelles only at
certain concentrations of bile salts and lecithin. The bile is supersaturated and contains small
crystals of cholesterol in addition to micelles. Gallstones that obstruct bile outflow from the liver
can result in obstructive jaundice. If the flow of bile out of the liver is completely blocked,
substances normally excreted in the bile, such as cholesterol, accumulate in the bloodstream.The
interruption of the enterohepatic circulation of bile also induces the liver to synthesize bile at a
greater rate.
The Treatment Of Gallstones:
• Depends on their nature, and the severity of any symptoms.
• Many, particularly if small and retained in the gallbladder, may be asymptomatic.
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• Larger stones that cause obstruction may need to be removed surgically.

• Oral dissolution agents may dissolve small stones composed of cholesterol, but the effect is slow
and stones often return once therapy is stopped.
• A definitive cure for patients who suffer from recurrent attacks of symptomatic cholelithiasis is
to have the gallbladder removed.
INTESTINAL SECRETIONS
There are 2 major glands in the intestine that contribute to the intestinal secretions:
1) Brunner’s gland
2) Crypts of lieberkuhn
1. Brunner’s glands:
Found mainly in the duodenum btw the pylorus and the duodenal papilla (ampulla of vater).It
secretes an alkaline fluid composed of mucin. Its main function is to protect the duodenal
mucosal wall from digestion by acidic gastric juice.
Regulation of the secretion is mainly neural which is mainly sympathetic. Sympathetic
stimulation inhibits secretion.
2. Crypts of Lieberkuhn:
Found on the entire surfaces of the small intestine btw villi. They are lined by low columnar
epithelium with 3 cell types:
*goblet cells that secrete mucus
*argentaffin cells that secrete secretin and
serotonin
*acidophillic paneth cells which secrete enzymes that are capable of digesting proteins, CHO,
fats. Such enzymes include dipeptidase, tripeptidase, isomaltase, intestinal lipase etc.
Epithelial cells at the bottom of the crypts are mitotically active producing cells that migrate
upwards to replace worm out cells at the tips of the villi every 5 to 7 days.
REGULATION OF INTESTINAL SECRETION

Mainly neural and hormonal. Neural mainly through local reflexes like myenteric
reflexes that are stimulated by touch. The greater the chyme reaching the small intestine, the
greater the stimulation of crypts of lieberkuhn. Hormonal is mainly by secretin and CCK.
LARGE INTESTINE SECRETION

Large intestine has no villi on the mucosa. Crypts of lieberkuhn is present but no brunner
gland. No enzyme secreting cells. They consist mainly of mucus secreting cells- goblet cells.
Secretion is stimulated by neural mechanism through parasympathetic and local reflexes
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END PRODUCT OF DIGESTION AND ABSORBTION

Carbohydrate:
In the mouth: Salivary -amylase begins the digestion of carbohydrates and its activity
continues in the stomach until acid penetrates the bolus.In the small intestine: Pancreatic -
amylase, a required enzyme for carbohydrate digestion continues the process. Hydrolysis of
starch by -amylase goes on in solution in the lumen of the small intestine mostly in the
duodenum.
Farther splitting of these trisaccharides, disaccharides and oligosaccharides occurs on the
brush border. The enzymes --glucoamylase, isomaltase, and maltase are all bound to the brush
border (apical membrane of enterocytes). Brush border enzymes have their highest activity in the
upper jejunum.These brush border enzymes are required for digestion mainly because
disaccharides e.g. sucrose, lactose are not absorbed from the gut.
The -glcoamylase (-dextrinase) cleaves terminal -1,4,bonds producing free glucose.

Lactase hydrolyses lactose into glucose and galactose. Lactase deficiency( lactose intolerance)
leads to osmotic diarrhoea. Sucrase splits sucrose and fructose. Maltase breaks down the maltose
and maltotriose to form 2 and 3 glucose units, respectively. The monosaccharide end products-
glucose, galactose and fructose are readily absorbed from the small intestine, also mainly in the
jejenum.
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Protein:
In the stomach pepsin begins the digestion of protein in the acid medium of the stomach.
In the small intestine: Digestion continues with the pancreatic proteases (trypsin, chymotrypsin,
elastase, and carboxypeptidases (A and B),which are essential enzymes. All these pancreatic
enzymes are secreted as inactive proenzymes(zymogenes). Protein digestion is completed by the
small intestinal brush border enzymes, dipeptidases, and an aminopeptidase. The main end
products are amino acids (40%) and dipeptides and tripeptides (60%).
Triglycerides:
In the stomach: Fatty materials broken down to decrease particle size and increase
surface area.In the small intestine. Bile micelles emulsify the fat, and pancreatic lipases digest it.
Micelle and pancreatic lipase are required for triglyceride digestion. The major end products is 2-
monoglycerides and fatty acids.
DIAGRAM SHOWING PROTIEN DIGESTION
ABSORPTION
Carbohydrate:
At the luminal membrane: Glucose and galactose are actively absorbed thru’ secondary
active transport via the same carrier. The transporter is a carrier which is Sodium Dependent
Glucose Transporter 1 (SGLT-1). Fructose is absorbed independently. It makes use of GLUT-
5 to move into the cells. In the enterocyte, much of fructose is converted to glucose which is then
transported to ECF by GLUT-2. At the basal membrane: Glucose is absorbed passively via
facilitated diffusion, although some simple diffusion may also contribute.
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NOTE: SGLT-2 is responsible for glucose transport out of the renal tubules.
DIAGRAM FOR ABSORPTION FOR CARBOHYDRATE ABSORPTION
Protein:
At the luminal membrane: Secondary active transport linked to sodium and receptor-
mediated endocytosis occurs. At the basal membrane: Simple diffusion of amino acids and some
protein-mediated transport also occurs. At least seven different transport systems transport amino
acids into enterocytes. Five of these 7 are sodium dependent and co-transport amino acids and
Na+. Two of these 5 also require Cl-, that is 2 require NaCl. The di- and tripeptides are
transported into enterocytes by a system known as PepT1 (or peptide transporter 1) that requires
H- instead of Na+. There is very little absorption of larger peptides.
In the enterocytes, amino acids released from the peptides by intracellular hydrolysis plus
the amino acids absorbed from the intestinal lumen and brush border are transported out of the
enterocytes along their basolateral borders by at least five transport systems. From there, they
enter the hepatic portal blood. Absorption of amino acids is rapid in the duodenum and
jejunum. There is little absorption in the ileum in health, because the majority of the free amino
acids have already been assimilated at that point.
In humans, a congenital defect in the mechanism that transports neutral amino acids in
the intestine and renal tubules causes Hartnup disease. A congenital defect in the transport of
basic amino acids causes Cystinuria. However, most patients do not experience nutritional
deficiencies of these amino acids because peptide transport compensates.
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LIPIDS
Absorption depends on the size of FFA molecule. Those with carbon chain <10 are
absorbed directly into the capillaries as FFA. Those > 10 are absorbed by the same system that is
used to absorbed 2-monoglycerides, cholesterol, lysolecithin etc. These molecules diffuse into
the enterocytes where they are re-esterified and then coated with cholesterol, phospholipids and
proteins to form chylomicrons. Chylomicrons leave the enterocytes thru’ exocytosis and then
diffuse into central lacteal embedded inside the villiMove on via the lymphatics to thoracic
ductgeneral circulation.
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Micelles diffuse to the border of the intestine. The diffusion through the unstirred layer is
the rate-limiting step of fat absorption. The digested lipids then diffuse across the brush border in
the lipid matrix. In the mucosal cell, triglyceride is re-synthesized and forms lipid droplets
(chylomicrons). These leave the intestine via the lymphatic circulation (lacteals).They then enter
the blood stream via the thoracic duct. The more water- soluble short-chain fatty acids can be
absorbed by diffusion directly into the blood stream. The bile salts are actively reabsorbed in the
distal ileum.
Water:
About 9 litres of water is presented to GIT per day, 2 litres by ingestion and 7 litres by
secretion. Water can either move from blood to enterocyte to lumen of GIT or from lumen to
enterocyte to blood depending on concentration or osmolarity of the content of the GIT. End
products of digestion will usually increase the concentration of GIT lumen, hence it pulls water
to the lumen. Net movement of water is towards the blood. About 98% of water is reabsorbed
leaving about 200ml in faeces.
Sodium:
About 25 to 38 grams of Na+ are presented to the GIT per day, of which 5-8 grams are
ingested and 20-30 grams are secreted. All the mucosal cells of small and large intestines are
permeable to Na+ ion. Sodium diffuses into the enterocyte from where it is actively pumped out
by Na-k ATPase. Some sodium is absorbed with glucose and amino acid. This is the basis of
ORT. About 25-35g of sodium is absorbed per day.
Chloride:
Usually Cl- enters the enterocyte from the interstitial fluid by Na, K, 2Cl ATPase
transporters that are located in the basolateral membrane. The Cl is then secreted into the lumen
by mechanism that depends on cAMP.
ABSORPTION OF VITAMINS AND ESSENTIAL MINERALS

Vitamins:
 Fat soluble - A, D, E, K
 Water soluble – B6, B12 , C, Folic acid etc.
Fat soluble vitamins are absorbed with fats  enterocytes  leave as chylomicrons via
exocytosis central lacteal
Water soluble vitamins: The absorption of folic acid and B12 are sodium dependent,
follows the absorption of sodium. Others like thiamine, riboflavin, niacin, pyridoxine, and biotin
are NOT sodium dependent.
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IRON
About 3-6% of ingested iron is absorbed. Iron is more readily absorbed in ferrous state
(Fe ) but most of the dietary iron is in the ferric state (Fe3+). Ferric iron is reduced by HCL and
2+
ascorbic acid. Most iron is absorbed in the small intestine. Haem iron (part of Hb) from meat,
liver and other iron containing fluids are absorbed directly from where the Fe2+ is then released
intracellular. Non-haem iron makes use of a more complex mechanism.
Inside the mucosal cell, the haem is split open to release Fe2+. A large part of the ferrous
iron is retained in the mucosal cells bound to a protein known as apoferritin to form ferritin.
Some of the Fe2+ is transported out of the mucosal cell to the plasma where it is oxidized and
bound to a ß-globulin called transferrin. This transports it to phagocytes presence in the liver,
spleen and bone marrow for storage as ferritin. If apoferritin is exhausted, the iron is stored as
haemosiderin. Haemosiderin accumulates in tissues in prolonged iron overload to form
Haemosiderosis which cause tissue damage called Haemochromatosis.
PROBLEMS OF DIGESTION AND ABSORPTION

A. Malabsorption:
This refers to abnormal absorption of nutrients resulting from abnormalities in the normal of
digestion and absorption. It is usually due to inadequate absorption but sometimes due to
excessive absorption.
Causes:
i. Inadequate digestion: usually due to inadequacy of enzymes, unsuitable pH for enzyme activity
and/or deficiency of bile salts.
ii. Inadequate absorption: due to insufficient available absorptive surface, absorptive surface
defective in function and/or use of drugs that increases intestinal motility.
iii. Excessive absorption which may be due to genetic factors, use of drugs that will decrease
intestinal motility or voluntary inhibition of defaecation reflexes
SYMPTOMS OF MALABSORPTION
Malabsorption can give rise to the following:
1. Diseased conditions eg pernicious anaemia
2. Change in bowel habit eg diarrhoea cases, steatorrhea and constipation.
B. Diarrhea:
This is passage of very liquid stool that is associated with increased frequency and urgency.
Diarrhea leads to loss of electrolytes like Na, K, Cl and water which leads to dehydration,
hypovolaemia, cardiovascular collapse and shock then death if not treated.
Causes:
 Infections
 Toxins
 Drugs
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The above can cause any of the following:

a. Decreased solute and water absorption from the GIT
b. Increase electrolyte secretion into the G.I lumen
c. Presence of osmotically active solute in the G.I lumen
d. Increased intestinal motility
CLASSIFICATION OF DIARHEA
1. Secretory diarrhoea: This refers to the passage of copious and watery stool caused by
abnormalities in the absorption and secretion of electrolytes
2. Osmotic diarrhoea: This is caused by accumulation of poorly absorbed solutes in the G.I
lumen e.g. in cases of:
(i) disacharidase deficiency as seen in lactase deficiency in lactose intolerance
(ii) steatorrhea
3. Diarrhoea due to abnormal intestinal motility. E.g.
(i) Decrease peristalsis
(ii) Increased small intestinal motility  reduced contact time btw
digested products and absorptive surface
(iii) Increased colonic emptying.
TREATMENT:
This is usually according to the cause. If infection use antibiotics Fluid and electrolyte
replacement using ORS. Use of drugs which affect intestinal motility which will depend on what
is causing the diarrhoea.
C. CONSTIPATION:
This refers to the passage of hard stool caused by infrequent bowel movement and excessive
contact btw faecal matter and absorptive surfaces of the colon.
Causes:
(i) Intake of low fibre diet
(ii) Drugs especially anticholinergic drugs which are drug that inhibit ACH release
(iii) Voluntary inhibition of defaecation reflex.
SYPTOMS OF CONSTIPATION
 Anorexia
 Abdominal discomfort
 Abdominal distension
 Headache
Treatment:
 Intake of high fibre diet
 Evacuation of rectum with laxatives, suppositories
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 Use of saline solution like solution of magnesium salts which are poorly absorb and pool
water to themselves
D. STEATORRHEA
This refers to the passage of fatty, bulky, clay-coloured and foul smelling stools bcos of
impaired digestion and absorption of fats,
Causes:
Mostly due to lipase deficiency
Decreased bicarbonate in the G.I lumen  loss of buffering effect  acidic Ph  enzyme
dysfunction and precipitation of bile salt
Defective reabsorption of bile salt in the terminal ileum hence loss of bile salt
Treatment:
(i) Use of pancreatic enzyme preparation
(ii) Use of drugs that can increase bicarbonate secretions
E. LACTOSE INTOLERANCE
Intestinal lactase activity is high at birth, then declines to low levels during childhood and
adulthood. The low lactase levels are associated with intolerance to milk (lactose
intolerance). When such individuals ingest dairy products, they are unable to digest lactose
sufficiently, and so symptoms such as bloating, pain, gas, and diarrhoea are produced by the
unabsorbed osmoles that are subsequently digested by colonic bacteria.
TREATMENT:
 The simplest treatment for lactose intolerance is to avoid dairy products in the diet.
 Symptoms can be ameliorated by administration of commercial lactase preparations, but
this is expensive.
 Yogurt is better tolerated than milk in intolerant individuals because it contains its own
bacterial lactase.
THANK YOU FOR LISTENING.
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COMPILED AND EDITED BY UMAH, UMAH VICTOR

 Electrical activity of GIT smooth muscles

 Neural control of GIT

 Hormonal control of GIT

COMPILED AND EDITED

ELECTRICAL ACTIVITY OF GASTROINTESTINAL SMOOTH MUSCLE

This activity has two basic types of electrical waves:

Difference between spike potentials and action potentials:

NEURAL CONTROL OF GIT

1. Intrinsic nerve supply

INTRINSIC NERVE supply include: Myenteric plexus and submucosal plexus.

EXTRINSIC NERVE supply include: parasympathetic and sympathetic nerve fibers.

Myenteric plexus(Auebach’s plexus):is an outer plexus lying between the longitudinal

Differences between the myenteric and submucosal plexuses:

When it is stimulated, its effects are:

a) Increased tonic contraction or tone of the gut wall.

NEUROTRANSMITTERS SECRETED BY INTRINSIC (ENTERIC)

AUTONOMIC CONTROL OF THE GIT:

i. Increases the motility of GIT but relaxes sphincters.

HORMONAL CONTROL OF THE GIT

d) Exerts a trophic effect on pancreas

3. Vasoactive Intestinal Polypeptide(VIP): It contains 28 amino acids and produced by GIT

Stimulants for Glucagon:

2. MOTILIN: Motilin is a polypeptide containing 22 amino acid residues that is secreted by

GIT motility includes:

Reasons for mastication:

Initiation of chewing reflex begins with:

ii. Oesophageal phase:

Control of oesophageal Peristalsis;

 Take in deep breath

DISORDERS OF SWALLOWING AND OESOPHAGUS:

3. Gastroesophageal reflux disease:

Treatment for Gastroesophageal reflex disease:

The motor functions of the stomach are:

2. MIXING AND PROPULSION OF FOOD IN THE STOMACH-BASIC ELECTRICAL

These reflexes are mediated by three routes:

MOTILITY OF THE COLON

DISORDER OF COLON MOTILITY

B. Hirschsprung disease or aganglionic megacolon

Management of Hirshsprung disease:

NEURAL CONTROL OF SALIVARY GLANDS:

easy passage of food. It is strongly resistant to digestion by enzymes. It is amphoteric (acid or

2. Inorganic constituents include:

Regulation of Salivary Secretion:

Disorders of Salivary Secretion:

2. Hypersalivation(increased salivation):could occur in pregnancy, tooth decay, neoplasm of

FUNCTIONS OF GASTRIC SECRETION

i. The surface membranes of mucosal cells are impermeable to acid

Control/Regulation of acid secretion

Gastric: presence of food in the stomach contributes >70% of gastric secretions.

MECHANISM OF ACID SECRETION

4. Increases the flow of bile and pancreatic juice.

EFFECT OF HYPERSECRETION OF ACID

Regulation of Pancreatic Secretion:

ENTEROHEPATIC CIRCULATION OF BILE

Control of bile secretion

PROBLEMS OF BILE SECRETION AND STORAGE OF BILE