The document summarizes key aspects of gastrointestinal physiology, including: 1. The gastrointestinal tract has four layers - mucosa, submucosa, muscularis, and serosa. The mucosa secretes digestive juices and absorbs nutrients. 2. The gastrointestinal tract is innervated by the parasympathetic and sympathetic nervous systems. Parasympathetic stimulation increases secretion and motility while sympathetic stimulation decreases these functions. 3. Digestion begins in the mouth where chewing and saliva containing amylase begin breaking down food. Swallowing propels food through the esophagus to the stomach via peristalsis.

1. 1
PHYSIOLOGY OF THE GASTROINTESTINAL TRACT
By Elvis Ng’ala
Functions of the GIT
1. Motility: mixing and propulsion
2. Secretion: enzymes
3. Digestion: breaking down complex molecules into smaller ones
4. Absorption
5. Excretion
Structure of the GIT Wall and its Functions
The wall of the GIT has four layers;
 Mucosa: secretes digestive juices and certain hormones. Absorption occurs here and small
blood vessels run through here.
 Submucosa: consists of dense connective tissue and houses the Meissner nerve plexus, also
known as the submucosal nerve plexus.
 Muscularis layer: contains the smooth muscles of contraction. The inner circular muscles
and the outer longitudinal muscles. It houses the Auerbach nerve plexus, also known as the
myenteric nerve plexus.
 Serosa; covers the entire GIT except at the oesophagus and the rectal canal
Nerve Supply
The GIT is supplied by parasympathetic (cholinergic) nerve supply and sympathetic nerve supply.
Parasympathetic supply is by the vagus nerve (CN X) and the pelvic nerve, sympathetic supply is
by celiac and mesenteric ganglia in the abdomen (T5 to L2). These nerves reach the GIT via
splanchnic nerves. The GIT also has an intrinsic nervous system called the enteric nervous system,
in the form of the submucosal and myenteric plexuses.
The parasympathetic nervous system does not initiate intrinsic nervous activity but it regulates it.
The vagus nerve supplies

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 Oesophagus
 Stomach
 Small Intestine
 Upper part of the large intestine
The pelvic nerve supplies
 Lower part of the large intestine
 Rectum and anal canal
Parasympathetic Stimulation
a) Increase in secretion of digestive juice
b) Increased motility
c) Relaxation of sphincters
d) Dilation of blood vessels
Sympathetic Stimulation
a) Decrease in secretion of digestive juice
b) Decreased motility
c) Constriction of sphincters
d) Vasoconstriction
Enteric Nervous System
It has 3 types of neurons:
I. Motor neurons: motility and contraction of smooth muscle
II. Secretory neurons: innervate endocrine and exocrine glands
III. Sensory neurons: innervate the mucosa and respond to stretch and changes in pH
The myenteric (Auerbach) plexus is responsible for motor activity of the GIT.
The submucosal (Meissner) plexus regulates the secretory functions of the GIT.
Blood Supply

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Branches of the abdominal aorta supply the GIT and the hepatic portal vein drains it.
Regulation Of GI Function
The GIT is under nervous and hormonal regulation
1) Nervous Regulation
Is faster than hormonal regulation and contains three kinds of reflexes; local axon reflexes,
ganglionic reflexes and central nervous reflexes.
a) Local Axon Reflex; short reflexes that occur entirely within the enteric nervous system
e.g. secretion of gastrin, peristalsis
b) Ganglionic Reflexes: the interpreting centre is in the ganglion. For example:
i) Enterogastric Reflex
Consists of a local reflex and a reflex integrated within the medulla oblongata. It
inhibits gastric secretion and motility. It occurs due to the distension of intestinal mucosa
and is mediated by the myenteric (Auerbach) plexus and the vagus nerve.
Mechanism of Reflex
Presence of chyme in the duodenum causes a generation of nerve impulses which are
transmitted to the stomach by the myenteric plexus. Upon reaching the stomach these
impulses inhibit gastric emptying. Impulses from the duodenum pass through the extrinsic
sympathetic fibres to the stomach and inhibit emptying. Some impulses from the duodenum
travel through the afferent vagal fibres to the brain-stem. Normally the brain-stem neurons
send excitatory impulses to the stomach through efferent vagal fibres and stimulate gastric
emptying, however, impulses from the duodenum inhibit these neurons thereby inhibiting
gastric emptying.
ii) Gastrocolic Reflex
Controls the motility of the GIT. Involves an increase in motility of the colon in response
to stretch in the stomach and the by-products in the small intestine. It is responsible for the
urge to defecate following a meal and helps make room for food in the stomach.
iii) Gastroileal Reflex

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Works in tandem with the gastrocolic reflex to stimulate the urge to defecate. The urge is
stimulated by the opening of the ileocecal valve and the movement of the digested contents
from the ileum to the colon for compaction.
c) Central Nervous Reflex: these are long reflexes whose integrating centre is in the CNS
e.g. vagovagal reflex.
2) Hormonal Regulation
Gastrin Family: gastrin, cholecystokinin (CCK)
Secretin Family: secretin, GIP, VIP, glucagon
Digestion In The Mouth
The first step in the digestive process is mastication, or chewing, the motility of the mouth that
involves the slicing, tearing, grinding, and mixing of ingested food by the teeth. The teeth, cheeks,
tongue and palette are involved. The initiation of chewing is voluntary but the continuation is not.
Functions of Chewing
(a) To grind and break food into smaller pieces to facilitate swallowing and to increase the food
surface area on which salivary enzymes will act.
(b) Helps in swallowing mix food with saliva thereby forming a bolus
(c) To stimulate the taste buds and savour ingested food
(d) Reduce mechanical damage to the GIT
The third function also reflexly increases salivary, gastric, pancreatic, and bile secretion to prepare
for the arrival of food.
Muscles Of Mastication And Their Action
Muscles Action
 Temporalis
 Masseter
 Medial pterygoid
Close the jaw
 Lateral pterygoid Open the jaw
 Masseter Protraction and medial and lateral excursion

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 Medial pterygoid
 Lateral pterygoid
of the jaw
 Temporalis Retraction of the jaw
The Chewing Reflex
The chewing, or mastication, reflex, which is integrated in the medulla oblongata, controls the basic
movements involved in chewing. The presence of food in the mouth (hard palette) stimulates
sensory receptors, which activate a reflex that causes the muscles of mastication to relax. The
muscles are stretched as the mandible is lowered, and stretch of the muscles activates a reflex that
causes contraction of the muscles of mastication. Once the mouth is closed, the food again
stimulates the muscles of mastication to relax, and the cycle is repeated. Descending pathways from
the cerebrum strongly influence the activity of the mastication reflex so that chewing can be
initiated or stopped consciously. The rate and intensity of chewing movements can also be
influenced by the cerebrum.
Salivary Glands
There are three main salivary glands; parotid (largest), submandibular and the sublingual (smallest)
glands. Other salivary glands include lingual glands, palatine glands, buccal glands and labial
glands.
All the glands are compound alveolar glands (branching glands with clusters of alveoli resembling
grapes). They produce thin serous secretions (parotid), mixed secretions (submandibular; more
serous than mucinous) and mucus secretions (sublingual). The serous part of saliva contains
salivary amylase that breaks down starch to maltose and isomaltose. Saliva also prevents bacterial
infection because it contains lysozymes and IgA. The mucinous part of saliva contains mucin, a
proteoglycan that gives a lubricating quality to the secretions of the salivary glands.
Innervation Of Salivary Glands
Parasympathetic
Favours serous secretion and occurs via the cranial nerves. Substance P and acetylcholine are
released. Parotid gland is innervated by the glossopharyngeal nerve (CN IX), sublingual gland and
the submandibular glands are innervated by the facial nerve.
Sympathetic

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Favours viscous (mucoid) secretion and occurs via preganglionic nerves in the thoracic segment of
the spinal cord. Nor-epinephrine is released. Indirect sympathetic stimulation occurs via the blood
vessels supplying the glands.
Composition and Formation of Saliva
 Saliva has a volume of 1.5 L/day and a pH of 7.0 on average.
 During active saliva secretion, it tends to be alkaline (8.0) due to addition of HCO3
-.
 It is hyposmotic/hypertonic
 99.5% water and 0.5% solids.
 Classification of solids: organic and inorganic.
 Organic solids: mucin, α-salivary amylase, IgA, lysozymes, lactoferin (bacteriostatic),
proline-rich proteins (protect the tooth enamel), glucagon, somatostatin, renin.
 Inorganic solids: K+
, Na+
, Cl-
, HCO3
-
 Cells that produce saliva are called acinar cells and are of two types: serous and mucinous.
 Saliva production is by a primary active secretory process in acinar cells.
 Initially saliva is isotonic and as it moves to the top of the cell, K+
and HCO3
-
are added and
Na+
and Cl-
are reabsorbed.
 The walls of the duct are impermeable to water so it doesn’t get reabsorbed.
 Aldosterone influences the quality of saliva by increasing K+
secretion and Na+
absorption.
Functions Of Saliva
1. Digestion: α-amylase starts the process of carbohydrate digestion into trisaccharides and
disaccharides and α-limit dextrine. Lingual lipase initiates lipid breakdown from Ebner’s
glands.
2. Keeps buccal cavity moist that helps with articulation of speech.
3. Lubrication of food so it can easily be swallowed (mucin component).
4. Solvent where food particles can dissolve and aids with taste sensation.
5. Lysozymes and IgA provide an anti-bacterial effect.

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6. Buffers such as HCO3
-
and mucin maintain a neutral pH
Importance of Maintaining pH
a) Enzyme activity.
b) Enamel protection or else the calcium in the enamel dissolves.
c) Helps in reducing occurrence of heartburn.
7. Helps with heat loss in dogs
8. Serve as a signal to the peripheral thirst receptors during dehydration due to the reduced
salivary production.
9. Excretory route for some heavy metals such as mercury, iodine and fluorine.
Deglutition
This is the transfer of food from the buccal cavity to the stomach. It is studied by contrast X-ray and
occurs in three stages:
A) Buccal Phase
The tongue is voluntarily elevated against the palette by the mylohyoid muscle that presses
the bolus and sends it to the back of the pharynx. The mouth should be closed.
B) Pharyngeal Phase
Is mediated by a swallowing reflex that occurs as follows: the bolus on its way to the
pharynx stimulates receptors in the tonsilar pillar (swallowing receptor area), signals are
picked up by efferent fibres of CN V and CN IX and are relayed to the swallowing centre in
the medulla oblongata. Impulses are then discharged to CN IX, X and XII leading to two
effects:
a) Protective effect: protects food from going into the trachea by elevation of the soft palette
(closing the nasal cavity), elevation of the larynx against the epiglottis (closing the superior
laryngeal opening, preventing food from entering the trachea), approximation of the vocal
cords (closing the glottis), temporary apnoea, continued contraction of the mylohyoid
muscles (preventing regurgitation). If the mouth is kept open during swallowing the food
won’t touch the receptors.
b) Pharyngeal peristalsis: the superior pharyngeal muscles contract and initiate a rapid
peristaltic movement passing the bolus down to the medial and inferior pharyngeal muscles.

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While they contract, the pharyngeal-oesophageal sphincter is relaxing and the bolus enters
the oesophagus. The process takes 1-2 seconds.
C) Oesophageal Phase
Mucus from the epithelial lining lubricates the oesophagus for swallowing and protects the
lower oesophageal wall from regurgitated gastric juice. There are two types of oesophageal
peristalsis:
a) Primary peristalsis
This is a continuation of pharyngeal peristalsis induced by impulses discharged by by
efferent vagal nerve fibres.
b) Secondary peristalsis
Occurs in the primary primary peristaltic phase to propel the bolus down and originates in
the oesophagus itself. Distension in the oesophagus sends signals to the vagus nerve. This is
an example of a vagovagal reflex. It occurs at a speed of 3 cm/s and in a standing position
this increases to 4 cm/s due to the effect of gravity.
Differences Between Upper 1/3 And Lower 1/3 Of The Oesophagus
Upper 1/3 Lower 1/3
Musculature Skeletal Smooth
Nerve Supply Vagal nerve Vagal nerve and enteric nervous
system
Bilateral Vagotomy Complete paralysis Secondary peristalsis persists
Oesophageal Sphincters
Upper Oesophageal Sphincter
 3 cm of oesophagus at the pharyngeal-oesophageal junction.
 Resting tension is always high and the sphincter is always tight.
 Prevents air from entering the stomach during breathing.
 Relaxes to allow the bolus to enter the oesophagus.
Lower Oesophageal Sphincter
 4 cm above the gastro-oesophageal junction.

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 Functional sphincter also known as the cardiac sphincter.
 Always contracted when food is not passing through to prevent gastric reflux (tonically
contracted).
 Relaxes to allow food to pass through under the influence of vasointestinal peptide (VIP) or
nitric oxide.
 Incompetence occurs when tone reduces and this causes gastro-oesophageal reflux.
 Large doses of gastrin increase the tone.
Swallowing Disorders
(1) Dysphagia (difficulty swallowing)
Occurs as a result of lesions on CN IX and X as in diphtheria or as a result of damage to the
swallowing centre in poliomyelitis. Myasthenia gravis also causes dysphagia due to
malfunctioning of swallowing muscles. Oesophageal strictures as in cancer or complication
of oesophageal ulceration.
(2) Achalasia (increased tension in the lower oesophageal sphincter)
Food transfer from oesophagus to stomach is delayed or blocked leading to accumulation of
food in the oesophagus. Megaoesophagus due to reduced VIP producing neurons.
Stomach
Has 3 functional parts; the fundus, body and antrum. The entrance to the stomach is guarded by the
cardiac sphincter and the exit by the pyloric sphincter.
Gastric Mucosa
Simple tubular glands that open into the mucosa. The mucosa has folds called rugae and the glands
in the cardia region and pyloric region contain mucus-secreting cells. The glands in the fundus and
body contain the following:
a) Peptic cells (chief cells): proteolytic enzymes e.g. pepsinogen.
b) Oxyntic cells (parietal cells): secrete HCl and intrinsic factor. Intrinsic factor helps in the
absorption of B12 at the ileum.
c) Mucus cells: mucus.
The pyloric antrum contains all the above cells with one addition of G cells that produce gastrin.

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Nerve Supply
Sympathetic
Celiac ganglion via the greater splanchnic nerve. Sympathetic stimulation will cause relaxation of
the proximal part of the stomach, constriction of the pyloric sphincter, no gastric motility thereby
delaying gastric emptying, decrease in secretion of gastric juice and vasoconstriction of gastric
vessels.
Parasympathetic
The vagal nerve supplies it. Parasympathetic stimulation will cause contraction of the proximal part
of the stomach, relaxation of the pyloric sphincter, increases gastric motility thereby increasing
gastric emptying, increase in secretion of gastric juice and vasodilation of gastric vessels.
Mechanism of Gastric Secretion
I. Cephalic Phase
Occurs before food enters the mouth and is mediated by the vagal nerve. Conditioned and
unconditioned reflexes controlled by the vagal nerve and can be abolished by bilateral
vagotomy and administration of atropine. The vagal nerve terminates at the nerve plexuses
in the GIT wall. It stimulates the oxyntic cells to produce HCl and the G cells to produce
gastrin and the peptic cells to produce pepsinogen. 20% of the gastric juice volume is
produced in this phase.
II. Gastric Phase
Occurs when the food enters the stomach. This is the main mechanism of gastric secretion
and continues for 3 hours or more. 70% of the gastric juice volume is produced in this
phase. Two mechanisms constitute this phase
a) Nervous: local enteric reflex which is a series of short reflexes that occur due to
distension of the stomach (stretch). Chemical substances activate receptors in the
submucosal plexus leading to secretion. The vasovagal reflex is a long reflex occurs due to
distension and chemical irritation of the mucosa. Both afferent and efferent fibres are in the
stomach. Chemicals such as alcohol and caffeine directly stimulate the vasovagal reflex.
b) Hormonal: gastrin from the G cells enters the blood, vagal nerve terminals produce GRP
that stimulate gastrin release.
III. Intestinal Phase

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When gastric contents enter the duodenum, chyme stimulates gastrin production by
stimulation of G cells. This gastrin release is stimulated by products of protein digestion.
Pathway Inhibiting Gastric Secretion
Inhibitory factors are stronger than the excitatory factors.
1. Distension of the duodenum
2. Excess acid and fat
3. Irritant substances
Occurs by two mechanisms:
i. Secretion of inhibitory hormones
Excess fats, proteins and carbohydrates stimulate the release of inhibitory hormones such as
cholecystokinin, secretin, GIP, somatostatin and VIP
ii. Enterogastric reflexes
Occurs when there is distension in the duodenum and is mediated by local enteric,
ganglionic and vasovagal reflexes.
Factors Affecting Gastric Secretion
A) Stimulatory Factors
Food ingestion (conditioned and unconditioned reflexes)
Food enters the stomach (gastrin secretion)
Alcohol and caffeine
Emotions such as anxiety
Hypoglycaemia impulse from feeding centre
IV injections of certain amino acids like glycine and alanine
B) Inhibitory Factors
When the acidity of the stomach goes below 2, inhibitory hormones are released.
Distension of the duodenum
Gastric Juice

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2.5 L of gastric juice is secreted on average per day. It is highly acidic with a pH of 1 to 2. It is rich
in HCl, water, inorganic ions (Na+
, Mg2+
, H+
, K+
, PO4
3-
, Cl-
and SO4
2-
), enzymes (pepsinogen,
gastric lipase), gelatinine, intrinsic factor and mucus. Mucus can be soluble or insoluble.
Soluble Mucus
 Secreted by neck cells of gastric glands in the body and fundus.
 Is the main secretion of the cardiac, antrum and pyloric regions.
 Its function is to prevent auto-digestion.
Insoluble Mucus
 A thick alkaline secretion from surface of epithelium of the gastric mucosa and is rich in
HCO3
-
.
 It forms a flexible layer about 1.5 mm that lines the entire gastric mucosa
 It protects the gastric wall and lubricates the food for transport.
Mechanism of Protection of the Gastric Mucosa
Two assaults affect the gastric mucosa; acidity of the stomach (HCl) and pepsin.
i. Nature of the mucosa cell membrane which has tight junctions between the cells that
prevents diffusion of HCl.
ii. Gel layer provided by the insoluble mucus
iii. HCO3
-
and mucus layer forms an unstirred layer of pH 7 that provides a barrier.
Pepsinogen Secretion
There are two types of pepsinogen. Type I and Type II present in zymogen granules and are
secreted by exocytosis. The release of pepsinogen is stimulated by secretagogues e.g. gastrin,
histamine and acetylcholine. Pepsinogens are inactive forms and are activated to pepsin by HCl and
pepsins (auto-activation).
Pepsins are proteolytic enzymes, they begin the digestion of proteins. Endopeptidases break down
protein molecules to peptones, proteases and polypeptides. The optimum pH for pepsin activity is
1.6-3.2.
Mechanism of HCl Formation

13. 13
HCl is formed in the canaliculi of parietal cells. In the canaliculi, the H+
and Cl+
combine and HCl
is released into the gastric lumen. The sodium potassium ATPase pump keeps the level of
potassium high in the cell for exchange at the H+
,K+
-ATPase pump.
Apical Surface
CO2 + H2O------> H2CO3
Under action of carbonic anhydrase H2CO3 dissociates to HCO3
-
and H+
. A proton pump H+
,K+
-
ATPase pumps out H+
and pumps in K+
into the cell.
Basolateral Surface
The HCO3
-
,Cl-
anti-port moves Cl-
into the cell and HCO3
-
out of the cell. The Na+
, K+
-ATPase
pumps Na+
out of the cell and K+
out of the cell
Postprandial Alkaline Tide
When the gastric acid secretion increases after a meal, excess HCO3
-
is added to the blood by
parietal cells thereby raising the pH of systemic blood and the urine becomes alkaline.
Control of HCl Secretion
Inhibitory Factors
 Certain GI hormones e.g. CCK, secretin, VIP, GIP
CO2+H2O--->H2CO3
H2CO3--->HCO3
-
+ H+
Gastric Lumen
Interstitial Fluid
Parietal Cell
Parietal Cell

14. 14
 Enterogastric reflex
 Prostaglandins e.g. PGE inhibits HCl secretion by decreasing intracellular cAMP levels
Stimulatory Factors
 Secretagogues
i) Acetylcholine: acts through M1 muscarinic receptors and increases intracellular Ca++
levels.
ii) Histamine: released from enterochromaffin-like cells (like mast cells) in the gastric
mucosa. It acts through H2 receptors and increases intracellular cAMP levels. These
receptors can be blocked by H2 blockers only e.g. cimetidine. Histamine on its own can’t
produce a significant amount of HCl. It is an additive to the other two.
Iii) Gastrin: acts through gastrin receptors in parietal cells by increasing intracellular free
calcium levels.
Functions Of HCl
1) Activates pepsinogens to pepsin and provides an optimum pH for its activity.
2) Kills most ingested bacteria leading to sterilisation of the stomach. In gastroenteritis, there is
a reduced amount of gastric acid.
3) Stimulates bile flow and pancreatic secretion. CCK and secretin do this while inhibiting
gastric acid secretion.
4) Causes curdling of milk which helps in digestion by keeping it longer in the stomach. In
young animals this is done by renin.
5) Helps in absorption of iron by converting ferric iron to ferrous iron (Fe3+
to Fe2+
).
6) Helps in absorption of calcium by preventing the precipitation of calcium salts.
7) Regulates gastric emptying through the enterogastric reflex.
Functions Of The Stomach
(1) Storage of food
(2) Mixing if food with gastric juice

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(3) Empty chyme at a slow and steady rate optimal for duodenal digestion and absorption
(piecemeal evacuation).
(4) Digestion of fats and proteins
(5) Red blood cell formation*
(6) Initiates certain reflexes that besides controlling gastric functions, regulates other functions
in the GIT e.g. gastrocolic reflex, gastroileal reflex, vomiting and gastro-salivary reflex.
Atrophy of gastric mucosa is called achylia gastrica. This could cause pernicious anaemia, reduced
appetite, weakly developed bones, susceptibility to gastritis, digestion will be almost normal
because the better part of digestion occurs in the intestines.
Gastric Motility
 The stomach musculature is relatively inactive
 There are continuous mild contractions in the fundus and body (tonic rhythm)
 When food enters the stomach, the stomach wall relaxes (receptive relaxation) and the
contractions stop
 Peristalsis mixes the food with gastric juice then empties the food in the duodenum
 If the stomach is empty for an extended period, hunger contractions appear
Receptive Relaxation
A reflex triggered by movements of the pharynx and oesophagus and increases when food enters
the stomach. It is mediated by vagal reflexes and occurs mainly in the fundus and body, preparing it
for reception of food. It allows the stomach to receive about 1.5 L of food and fluid. There is only a
slight increase in intra-gastric pressure because:
i. the gastric wall has the property of plasticity, yielding to stretch with a little increase in
tension
ii. it obeys Laplace’s law, P=T/r. The distending pressure in a hollow organ equals the tension
in its wall divided by its radius
Gastric Relaxation
Occurs mainly in the distal part of the stomach after food intake. It is coordinated by the basic
electric rhythm (BER) of the stomach. When well developed, the wave of contractions occurs at a

16. 16
rate of three contractions per minute. It starts in the middle of the stomach by contraction of the
circular muscle and proceeds towards the antrum where the peristalsis becomes stronger and
continues to the pyloric canal and upper duodenum. The consequences are:
 Propulsive movement: evacuates 9squirts0 content into the duodenum one bit at a time
through the pylorus which allows only small particles to pass through.
 Retropulsive movement
 Grinding
Hunger Contractions
Intense rhythmic peristaltic contractions that occur in the body of the stomach when it is empty.
These fuse together and form a tetanic contraction that lasts for about 2-3 minutes. Sometimes they
can be painful and during starvation they appear after 12-24 hours and reach a peak of 3-4 days. It is
caused by strong vagal stimulation.
After hours of starvation, there is hypoglycaemia leading to stimulation of the feeding centre which
in turn stimulates the vagal nerve in the medulla. Hunger is not a result of hunger contractions, its is
a sensation.
Factors Affecting Gastric Emptying
A) Type of Food
Foods rich in carbohydrates leave the stomach in a few hours. Foods rich in proteins leave
the stomach slowly and fatty foods leave the stomach the slowest. Peristaltic waves cause
contraction of the antrum and a reduction in size of the stomach
B) Gastric Factors
i) Degree of distension: the greater the volume of gastric content, the more rapid the
emptying rate. Local enteric reflex and vagovagal reflex will be initiated and gastrin
secretion is stimulated.
ii) Consistency of gastric content: fluids are evacuated more rapidly than solids
C) Duodenal Factors
i) Degree of duodenal distension: excessive distension delays gastric emptying through the
enterogastric reflex.

17. 17
ii) Type of food in the duodenum: presence of excess fat delays gastric emptying through
stimulating release of hormones that inhibit gastric motility.
Iii) Duodenal acidity: a increase in the acidity (pH<4) delays gastric emptying by both
stimulating the release of inhibitory factors and initiating the enterogastric reflex.
Effects of Complete Gastrectomy
1) Loss of storage function of stomach
2) Pernicious anaemia due to loss of intrinsic factor that helps absorb vitamin B12
3) Iron deficiency anaemia due to lack of conversion of ferric iron to the absorbable ferrous
form. The reaction requires HCl.
4) Weak bones due to lack of absorption of Ca2+
5) Normal digestion continues but with some difficulty because it reaches the duodenum in
solid form
6) Dumping Syndrome: a distressing syndrome that sometimes occurs after a heavy meal,
characterised by;
a) abdominal discomfort
b) nausea and vomiting as a result of abnormal sudden distension or stretch of the duodenum
c) hyperglycaemia due to rapid absorption of glucose then hypoglycaemia two hours later
due to to increased released of insulin
d) weakness, dizziness and sweating due to hypoglycaemia and partly due to withdrawal of
water to the gut by the hypertonic meal.
Vomiting (Emesis)
This is the reflex expulsion of gastric content through the mouth. It starts with a sensation of nausea
and is mostly preceded by retching. Retching is the reverse movement of gastric and oesophageal
contents without vomiting.
Mechanism of Vomiting
It is controlled by the vomiting centre located in the medulla oblongata. Excitation of the centre
produces several effects leading to expulsion and this occurs through CN V, VII, X, XI and XII,
spinal nerves that supply the diaphragm and abdominal muscles.

18. 18
i. Forced expiration, the diaphragm is moved downwards and breath is held there
ii. Closure of the glottis and elevation of the soft palette to prevent the vomitus from entering
the trachea and nasal cavity
iii. Body of stomach and cardiac sphincter relax completely while the pyloric antrum
powerfully at the incisura angularis
iv. The abdominal wall muscles contract increasing intra-abdominal wall pressure (downward
movement of diaphragm)
v. The raised intra-abdominal pressure squeezes the relaxed stomach leading to the raising of
the cardiac part into the thorax and ejection of its contents into the mouth and outwards
N.B Nausea is associated with pallor, excessive salivation and sweating. Vomiting is anti-peristaltic
in the small intestine. During retching, intermittent contractions of the diaphragm and abdominal
wall and withdrawing of the abdominal part of the oesophagus into the thorax but the cardiac
sphincter is kept contracted.
Types of Vomiting
1) Reflex Vomiting: as a result of conditioned and unconditioned reflexes. Conditioned
reflexes occur after observing something sickening, unconditioned reflexes occur when
conditions initiate signals that are discharged via nerves to the medulla oblongata and
stimulate the vomiting centre e.g.
a) gastric irritation, peritonitis and intestinal obstruction
b) irritation of posterior part of tongue and oropharynx
c) motion sickness impulsively discharged from the semi-circular canals in the ears
2) Central Vomiting: certain drugs e.g. apomorphine, digitalis and nervous diseases such as
meningitis, migraines, intra-cranial tension induce vomiting by exciting the vomiting centre.
These emetics stimulate a nearby area in the medulla oblongata (chemoreceptor trigger zone
[CTZ]) which then stimulates the vomiting centre. Stimulation of semi-circular canals and
other conditions stimulate the vomiting centre through CTZ. Stimulation of CTZ is what
happens in early pregnancy, in uraemia and diabetic ketoacidosis.
Vomiting due to nervous causes is often sudden, projectile, strong and not preceded by nausea.
Functions of Vomiting

19. 19
In case of irritation of the upper GIT vomiting provides rest and helps drive out the irritant.
In many conditions such as pregnancy, motion sickness, vomiting plays no role.
Negative Effects of Excessive Vomiting
 Dehydration
 Loss of electrolytes (K+
, Na+
, H+
) leading to a development of metabolic alkalosis due to a
loss of H+
Treatment of Vomiting
Treat the cause
Anti-emetics e.g. chlorpromazine
Effects of vomiting are corrected by giving fluids, electrolytes and acidifying salts
The Pancreas
This is a gland that consists of an exocrine part and an endocrine part.
Exocrine Part
Compound acinar gland secretes pancreatic juice that collects in ducts that coalesce into the
pancreatic duct that opens into the duodenum through the ampulla of Vater guarded by the sphincter
of Oddi. It is supplied by the vagal nerve (parasympathetic) and the greater splanchnic nerve
(sympathetic).
Pancreatic Juice
Pancreatic juice, bile and intestinal juice are involved in the conclusion of digestion. Pancreatic
juice is the most important digestive juice and the daily volume produced is 1500 ml. It is alkaline
(pH=8, due to rich HCO3
-
content) and formed of two parts:
(a) Aqueous: watery part and has HCO3
-
secreted from ductule cells. Contains K+
, Na+
, Ca2+
,
Mg2+
, H+
, K+
, PO4
3-
, Cl-
and SO4
2-
. The bicarbonate from pancreatic juice and bile help
neutralise chyme for enzyme activity and it protects duodenal mucosa from the harshness of
the acidic chyme.
(b) Enzymatic: secreted from pancreatic acini. Enzymes include:
i) Proteolytic enzymes secreted as inactive pro-enzymes.

20. 20
-Trypsinogen: activated into trypsin in small intestines by an enzyme secreted by duodenal
mucosa called enterokinase or enteropeptidase. Trypsin also auto-activates and is an
endopeptidase.
-Chymotrypsinogen
-Proelastase
-Procarboxypeptidases
ii) Lipolytic enzymes
- Pancreatic lipase: secreted as an active enzyme that hydrolyses triglycerides into
monoglycerides and fatty acids. Its activity is enhanced by the presence of bile salts
(emulsification of fats). The pancreas secretes an enzyme called pro-colipase that is
activated by trypsin to co-lipase. Co-lipase facilitates the action of pancreatic lipase (which
acts only on emulsified fats) by displacing the emulsifying bile salts.
- Prophospholipase A2: an inactive enzyme that is activated to phospholipase A2 by trypsin.
It acts on phospholipids leading to formation of fatty acids and lysophospholipids
Example: converts lecithin to lysolecithin
converts cephalin to lysocephalin
- Cholesterol ester hydrolase: it hydrolyses cholesterol free esters in the intestinal lumen
leading to the liberation of free cholesterol.
(c) Pancreatic α-amylase
It requires Cl-
for its activation and it converts starch to maltose, maltotriose and α-limit
dextrins. It completes the action of salivary amylase.
(d) Pancreatic Nucleases: include ribonucleases and deoxyribonucleases
N.B All pancreatic proteolytic enzymes are produced in their inactive forms to prevent auto-
digestion of the pancreas. Activation occurs in the small intestine. The pancreas keeps enzymes in
their inactive form by the trypsin inhibitor which blocks any activity of trypsin in the pancreas.
Acute Pancreatitis
Inflammation of the pancreas and it is fatal if not treated. It occurs as a complication in obstruction
of the main pancreatic duct. Levels of activated trypsin increase and this activates other proteolytic
enzymes and phospholipase A2.

21. 21
Consequences
1. Auto-digestion accompanied by haemorrhage and severe pain.
2. Activated phospholipase A2 converts lecithin to the toxic substrate lysolecithin causing
further damage and necrosis.
3. Blood level of pancreatic amylase increases and this is a diagnostic feature of acute
pancreatitis.
Control of Exocrine Pancreatic Function
(1) Neural Control
Controlled primarily by parasympathetic supply (vagal nerve). Vagal impulses stimulate
pancreatic acinar cells producing a secretion rich in digestive enzyme and poor in fluid
causing little or no flow of pancreatic fluid.
The enzymes remain temporarily stored in the acini and ducts till more fluid is secreted to
take them to duodenum. Sympathetic stimulation decreases pancreatic pancreatic secretion
by acting on α adrenergic receptors and normally there is no role in control of secretion. On
taking a meal, pancreatic secretion increases upon vagal stimulation and passes through two
phases:
a) Cephalic Phase: the gastric cephalic phase accompanies the cephalic phase of pancreatic
secretion as a result of conditioned and unconditioned reflexes.
b) Gastric Phase: the gastric phase of pancreatic secretion accompanies the gastric phase of
gastric secretion as a result of the vagovagal reflex. Gastrin release stimulates pancreatic
secretion.
(2) Hormonal Control
a) Secretin: produced in S cells of duodenal mucosa and stimulates the secretion of the
aqueous part of pancreatic juice. It now flushes the secretion stored in acini and is essential
to neutralise the acidic chyme.
b) Cholecystokinin-pancreozymin: produced in the duodenum in response to products of
digestion. It stimulates secretion of the enzyme part of pancreatic juice from the acinar cells.
Kinins are potent vasodilators and may be the reason for a marked increase in blood flow to
the pancreas that accompanies pancreatic secretion.

22. 22
Effect of Extirpation/Damage to the Pancreas
 Diabetes mellitus
 Digestive and nutritional imbalances
The various constituents are not properly digested leading to deficient absorption. Loss of
considerable amounts of proteins and fats in the stool (steatorrhoea, fatty diarrhoea). The
faeces become bulky, pale, loose and this leads to under nutrition.
Effects of Loss of Pancreatic Juice
This occurs secondary to severe diarrhoea.
 Marked digestive and nutritional disturbances
 Dehydration
 Metabolic acidosis
Bile and the Gall Bladder
The Biliary Tree
Biliary system or extra-hepatic biliary apparatus is formed by gallbladder and extra-hepatic bile
ducts (bile ducts outside the liver). Right and left hepatic bile ducts which come out of liver join to
form common hepatic duct. It unites with the cystic duct from gallbladder to form common bile
duct. All these ducts have similar structures. Common bile duct unites with pancreatic duct to form
the common hepato-pancreatic duct or ampulla of Vater, which opens into the duodenum. There is a
sphincter called sphincter of Oddi at the lower part of common bile duct, before it joins the
pancreatic duct. It is formed by smooth muscle fibres of common bile duct. It is normally kept
closed; so the bile secreted from liver enters gallbladder where it is stored. Upon appropriate
stimulation, the sphincter opens and allows flow of bile from gallbladder into the intestine.
Bile is secreted from the liver and stored in the gall bladder . It is an important digestive juice.
Hepatocytes secrete bile into biliary canaliculi which coalesce to give the right and left hepatic
ducts that drain each lobe of the liver. These two ducts join outside the liver to form the common
hepatic duct which joins the cystic duct from the gall bladder to form the common bile duct and this
joins the main pancreatic duct at the ampulla of Vater.
Composition of Liver Bile

23. 23
Liver bile is golden, yellow alkaline fluid (pH 7.8-8.6). 600-1200 ml produced per day. It is
composed of H2O and organic and inorganic concentrates and alkaline phosphatase enzyme. The
constituents are: bile salts and bile pigments together with small amounts of cholesterol, lecithin,
fatty acids and fat, K+
, Na+
, Ca2+
, Cl-
and bicarbonate. These are actively transported across the cell
membrane into biliary canaliculi.
Bicarbonate is primarily secreted by the biliary duct cells and initiates the neutralisation of gastric
HCl in duodenum. The hormone that stimulates this secretion is secretin.
Functions of Gall Bladder
1) Storage of bile
Bile from the liver moves in retrograde to be stored in the gall bladder in between meals
because the sphincter of Oddi is tonically contracted.
2) Concentration of bile
The storage capacity of the gall bladder is 20-60 ml and bile produced in the liver is about
600-1200 ml. For storage it must be concentrated. The mucosa of the gall bladder actively
reabsorbs Na+
followed by passive re-absorption of H2O and other electrolytes except Ca2+
.
Due to this, the concentration of bile salts in the gall bladder bile increases 5-10 times that in
the liver and its water concentration is about 87% instead of 97% found in the liver.
3) Acidification of bile
As a result of bicarbonate re-absorption during bile concentration, the pH of bile in the
bladder decreases to 7-7.4. This prevents the precipitation of calcium and formation of gall
stones.
4) Decreasing the pressure in the bile ducts
When the sphincter of Oddi is contracted there is stasis of fluid in the liver hence a pressure
builds up in the bile ducts. The gall bladder helps relive this pressure because it contains a
considerable part of liver bile secreted between meals. A rise in pressure in the biliary ducts
causes bile secretion to stop thus impairing liver function.
5) Secretion of mucus
Secreted by mucus glands in the gall bladder mucosa
Functions

24. 24
- protects gall bladder mucosa against highly concentrated bile salts
- gives bile a semi-fluid consistency
- in the small intestine it acts as a lubricant and a buffer
6) Evacuation
Evacuation of bile into the small intestine by contraction of gall bladder wall and relaxation
of the sphincter of Oddi.
Factors Affecting Bile Flow
1) Hepatic blood flow
Bile secretion and flow is directly proportional to hepatic blood flow within physiologic
reason. The moer blood flow to the liver, the more bile secreted.
2) Vagal Stimulation
Increases bile flow through liberating acetylcholine which produces vasodilation and
increases hepatic blood flow. Acetylcholine also helps in gall bladder emptying.
3) Bile salts
90-95 % of bile salts upon reaching the intestines are actively reabsorbed at the terminal
ileum into the portal vein, This portal vein carries it back to the liver where they are rapid;y
secreted.
4) Hormones
Secretin stimulates secretion of bicarbonate and water from the biliary duct cells. It has a
hydrocholeretic effect.
5) Gall Bladder Emptying
Emptying contents of the gall bladder occurs under two mechanisms:
a) Nervous Control: stimulation of vagus nerve causes weak contraction of of the gall
bladder, facilitating its evacuation and increasing bile flow into the duodenum. Vagal
stimulation is caused by food intake.
b) Hormonal Control: CCK causes strong contractions of the gall bladder wall and weak
relaxation of the sphincter of Oddi leading to evacuation of its contents into the duodenum.

25. 25
CCK production is stimulated by presence of protein digestion and is released by mucosa
cells.
Choleretics and Cholagogues
These are substances that increase bile flow into the duodenum but each exert its effect in a
different mechanism.
A) Choleretics
Increase bile flow by increasing its formation by the liver. The natural choleretics include
bile salts (most potent) and secretin. Certain drugs also act as choleretics e.g. drugs that
cause vasodilation and increase hepatic blood flow.
B) Cholagogues
Cause contraction of the gall bladder wall leading to evacuation of its contents. Natural
cholagogue is CCK and certain drugs such as magnesium sulphate relax the sphincter of
Oddi.
Functions of Bile
The importance of bile as a digestive juice is due to the presence of bile salts. Bile also performs the
following functions:
i. Alkaline content shares in the neutralisation of HCl in the duodenum
ii. Mucin content serves as a lubricant and buffer in the small intestine
iii. It is an excretory route for bile pigments which exert no meaningful function, certain heavy
metals, cholesterol, lecithin and alkaline phosphatase enzyme.
iv. It helps in fat digestion by:
a) Reducing surface tension of fats and together with phospholipids and monoglycerides
they lead to fat emulsification. This exposes a larger area of fats for the action of lipase
enzymes. It activates lipase enzymes in the small intestine.
b) They are essential for fat absorption by their hydrotropic effect. They combine with lipids
to form water soluble compounds called micelles from which fats are more easily
absorbable.
c) Essential for absorption of fat soluble vitamins A, D, E, K

26. 26
d) Most potent choleretic substances.
e) Exert a laxative action by stimulating intestinal peristalsis probably secondary to
facilitation of lipid digestion and absorption
f) Essential for keeping cholesterol dissolved in bile thus preventing its precipitation and
formation of cholesterol stones. Stones can be prevented or treated physiologically by giving
high doses of chenodeoxycholic acid.
Chemical Nature and Formation Bile Salts
Bile salts are the Na+
and K+
salts of bile acids conjugated with glycine and taurine. In humans there
are 4 bile acids, two are synthesised in the liver from cholesterol and are called primary bile acids
(cholic acid and chenodeoxycholic acid). The secondary acids are formed in the colon from the
primary acids by bacterial action (cholic acid----> deoxycholic acid, chenodeoxycholic acid---->
lithocholic acid). Conjugation of primary bile acids with glycine and taurine occurs in the liver cells
and the conjugates (glycocholic and taurocholic) form Na+
and K+
salts in hepatic bile.
Bile Pigments
Bile pigments are excreted while bile salts are secreted.
Bilirubin is then excreted into plasma and picked up by albumin as free unconjugated bilirubin.
When it goes to the liver, substance P helps to transfer it to hepatocytes where about 80% of it is
conjugated with glucuronic acid via the enzyme UDP glucuronyl transferase. About 10% is
conjugated with sulphates. This conjugated bilirubin (yellow) is excreted in bile and goes to the
small intestine. In large intestines, bacteria acts on it to form urobilinogen. In stool, this is converted
to stercobilinogen and when it comes in contact with air it forms stercobilin (brown). Some
urobilinogen is moved to the kidney (about 5%) and is converted to urobilin, this is excreted in
urine and gives it a yellow colour.
Haemoglobin
Haeme Globin Amino acid pool
Porphyrin Iron Transported by transferin and stored as
ferritin/haemosiderin
Biliverdin
Bilirubin

27. 27
Jaundice
Jaundice is a yellow discolouration of the skin and sclera of the eyes due to accumulation of either
free or conjugated bilirubin. It can be physiologic or pathologic. Physiologic jaundice is observed in
newborns due to the fact that UDP glucuronyl transferase is synthesized slowly after birth and this
leads to an accumulation of unconjugated bilirubin. It is also observed when people from high
altitudes come down to sea level due to the increased breakdown of red blood cells (at high altitudes
the body increases erythropoiesis).
Pathologic jaundice is of three types:
(1) Pre-Hepatic Jaundice (Haemolytic)
This caused by conditions that raise the blood’s rate of haemolysis such as SCA, anaemia,
G6PD deficiency, sulphonilamides, tetracyclines.
(2) Hepatic Jaundice
Caused by dysfunctional liver tissue as in hepatitis, liver cirrhosis, biliary cirrhosis, puridine
glucuronide transferase enzyme deficiency.
(3) Post-Hepatic Jaundice (Obstructive)
Occurs when bilirubin cannot be drained properly into the ducts or digestive tract because of
a blockage as in liver cirrhosis, biliary atresia, cholesterol stones and iatrogenic causes.
Questions
1. Briefly summarise control of the motor and secretory functions of the GIT by the enteric
nervous system and sympathetic and parasympathetic innervation.

28. 28
2. What are slow waves and what are the relationships among slow waves, action potential and
contraction of GIT muscle.
3. Describe the regulation of gastric emptying by chemical stimuli in the duodenum.
4. Contrast the contractile activity of the small intestine of a fed individual that of a fasted
person.
5. Summarise the control of gastric acid secretion during cephalic, gastric and intestinal
phases.
6. Describe haemoglobin metabolism, add a note on jaundice.
7. Describe how parietal cells secrete HCl.
8. What are the mechanisms for absorption of monosaccharides by intestinal epithelial cells.
9. Write short notes on:
a) Incompetence of the lower oesophageal sphincter.
b) Enterogastric reflex.
c) Functions of saliva.
d) Protective reflexes during deglutition.
e) Oesophageal peristalsis
f) Dysphagia.
g) Mechanisms of protection of the gastric mucosa.
h) Basic Electric Rhythm.
10. Write an essay on control of HCl secretion. Add a note on functions of HCl.
11. Write a detailed essay on the physiology of vomiting.
12. Write short notes on:
a) Histamine test.
b) Acute pancreatitis.
c) Effects of partial gastrectomy.
d) Functions of the gall bladder.
e) Choleretics and cholagogues.
13. Describe how vitamin B12 is absorbed and how is the stomach involved.