INTRODUCTORY

GASTROINTESTINAL TRACT
PHYSIOLOGY

A.H. UMAR

DEPARTMENT OF HUMAN PHYSIOLOGY

AHMADU BELLO UNIVERSITY, ZARIA
OUTLINE
 INTRODUCTION
 PHYSIOLOGIC ANATOMY OF GIT
 NERVE SUPPLY TO GIT
 GIT MOTILITY
 GIT REFLEEXES
 MOUTH AND SALIVARY SECRETION
 MASTICATION AND SWALLOWING (CONTROL AND DISORDERS)
 STOMACH AND GASTRIC SECRETION
 PATHOPHYSIOLOGY OF ULCER AND ITS MANAGEMENT
 PANCREAS
 INTESTINE
 DIGESTION AND ABSORBTION IN THE GIT
 RECTUM AND PHYSIOLOGY OF DEFECATION
 GIT HORMONES
NOTES

 Gastrointestinal physiology encompasses:

 movement of food through the alimentary

tract.
 secretion of digestive juices and digestion of
food.
 absorption of digestive products, water,
electrolytes, and vitamins.
 circulation of blood to carry away absorbed
Substances.
 nervous and hormonal control of GI functions
 The gastrointestinal tract (GI tract/GIT)
 is a system responsible for digestion of
food and absorption of nutrients.

 It includes the esophagus, stomach, small

intestine and large intestine.

 It provides the body with a continual supply

of water, electrolytes, vitamins, and
nutrients.

 Understanding the dynamics of the GIT is

crucial for maintaining overall health and
well-being.
 Each of the distinct structures of
the GIT have specific functions.

 The esophagus transports food to the

stomach

 The stomach is where gastric juices

aid in digestion.

 The small intestine is where most

nutrient absorption occurs

 The large intestine is responsible for

water reabsorption and waste
elimination.
 Various enzymes play a
critical role in breaking down
food in the GIT.
 Amylase breaks down
carbohydrates
 Lipase acts on fats
 Proteases break down proteins

 These enzymes are secreted

by the pancreas and intestines
to facilitate digestion and
nutrient absorption.
 The GIT is home to a diverse
microbiota, which aids in
digestion and nutrient
processing.

 These beneficial bacteria help

ferment fibre, produce
vitamins, and protect against
harmful pathogens.

 Maintaining a healthy balance

of gut microbiota is essential
for overall digestive health.
Gut-Brain Connection
 The GIT and the brain communicate
bidirectionally through the gut-brain
axis.

 This connection influences appetite

regulation, mood, and overall well-
being.

 The enteric nervous system in the

gut plays a crucial role in this
connection, thus, highlighting the
impact of gut health on mental and
emotional states.
 Several common GI disorders can
impact digestive function, including

 Irritable bowel syndrome (IBS)

 Gastroesophageal reflux disease (GERD)
 Inflammatory bowel disease (IBD)

 These conditions can lead to

symptoms such as abdominal pain,
bloating, and diarrhea

 It is thus important to understand

GI dynamics for effective
management of these disorders.
Diet and GI Health

 A balanced diet plays a crucial role

in maintaining optimal GI health.

 Consumption of fibre-rich foods,

probiotics, and staying hydrated
supports a healthy digestive system.

 Conversely, a diet high in processed

foods and saturated fats can
contribute to GI issues and disrupt
the dynamics of the GIT
 Chronic stress and smoking can
negatively affect the GIT

 Lifestyle factors such as physical

activity, stress management, and
smoking cessation can
significantly impact GI dynamics.
 Regular exercise promotes
healthy digestion

 Making positive lifestyle choices is

essential for maintaining optimal
GI function.
 In cases of severe GI disorders, clinical
interventions such as medication,
surgery, and nutritional support may
be necessary.

 Endoscopic procedures and biopsies

are also used to diagnose and treat GI
disorders

 Understanding the physiology of the

GIT is crucial for healthcare
professionals in providing effective
interventions.
 Understanding the dynamics of
the GIT is essential for
maintaining overall health and
well-being.

 From the anatomy and function

of the GIT to the impact of
lifestyle and dietary choices,
this knowledge is crucial for
promoting optimal digestive
health and managing GI
disorders.
 INTRODUCTION
What is the GI System?
 A hollow tube from
mouth to anus +
accessory glands and
organs.

 Hollow organs are

separated from each
other at key
locations by
sphincters.
Functions of the GI System

 The sedentary human body requires ≈ 30

kcal/Kg BW per day.

 This nutrient requirement is acquired through

the GI system.

 Some of the food we consume is not in a form

that can be directly absorbed by the small
intestine, thus, the need for digestion
 • The GI system processes consumed food
mechanically & chemically to facilitate
absorption.

Dietary nutrient Consumed form Absorbed form

Fat (lipids) Triglycerides Fatty acids

Monoglycerides

Proteins Proteins Amino acids

Large peptides

Carbohydrates Starch monosaccharides

Glycogen
 Excretion of waste material.
 Non-digested non-absorbed dietary products.
 Colonic bacteria & their products.
 Heavy metals (iron & copper).
 Organic cations & anions (e.g. drugs)

 Regulation of water & electrolyte balance.

 Immunity.
Digestive functions of digestive system:

 Ingestion.
 Secretion.
 Mixing & Propulsion.
 Digestion
 Absorption.
 Defecation
 Digestive system:
 made of the gastrointestinal
tract (GIT; alimentary canal)
and secondary/accessory
digestive organs (liver, gall
bladder, salivary glands and
exocrine pancreas)

 Gastrointestinal tract (GIT):

 Muscular tube of about 5m long
 Stretches from mouth to anus
 Serves as portal where nutrients
can be absorbed into the body
 The GIT is made of
 mouth, oesophagus, stomach,
intestine, rectum and anal canal

 Digestion mostly occur in stomach

and small intestine

 Absorption mainly in jejunum and

ileum
Physiologic Anatomy of GIT
 Wall of GIT is made of four layers; from the lumen
outward:
 mucosa, submucosa, musculosa and serosa.

Cross section of GIT wall

Mucosa (mucus layer)
 Innermost layer of the GIT wall

 Also called gastrointestinal mucosa or mucus

membrane.

 It is made of the epithelium (mucus membrane), lamina

propria and muscularis mucosa.

 Epithelium range from stratified squamous in mouth,

pharynx and oesophagus, to columnar in the stomach
and intestine.
 The epithelium in the mouth, pharynx, esophagus, and
anal canal is mainly nonkeratinized stratified squamous
epithelium that serves a protective function
 Wall of stomach and intestine are lined by simple
columnar epithelium.
 The epithelial cells are joined by tight junctions that
restrict leakage between cells.
 The epithelial cells are replaced every 5 to 7 days
 Located among the epithelial cells are exocrine cells
that secrete mucus and fluid into the lumen of the
tract
 There are also endocrine cells, collectively called
enteroendocrine cells, that secrete hormones.
 Beneath the epithelium is the lamina
propria, a thin layer of connective tissue
containing blood and lymphatic vessels, as
serves as the layer through which nutrients
are absorbed into the blood.
 The lamina propria contains the majority of
the cells of the mucosa associated
lymphatic tissue (MALT).
 The MALT nodules contain immune cells
that protect against diseases.
 The muscularis mucosa is a thin layer of
smooth muscle fibres present beneath
lamina propria, from the oesophagus
onwards.
 Itis responsible for various degrees of
infoldings in the mucosa, which greatly
increase the surface area for absorption.
Submucosa

 Layer of loose collagen fibres, elastic fibres, reticular

fibres and connective tissue cells.

 Also contain blood vessels, lymphatics and nerve

plexuses.
Musculosa
 Layer of smooth muscle fibres made of outer
longitudinal and inner circular muscle layers.
 Pharynx and upper part of oesophagus contain skeletal
muscle, while lower part of the oesophagus, stomach
and the intestine contain smooth muscle.
 In the stomach, the musculosa is made of outer
longitudinal, middle circular and inner oblique muscle
layers
 The myenteric plexus is located between the muscle
layers in musculosa
 Involuntary contractions of the smooth muscle help to
break down food, mix it with digestive secretions, and
propel it along the GI tract.
Serosa
 Serous layer/serous membrane is the outermost layer
of the GIT wall and is formed by connective tissue and
simple squamous mesoepithelial cells.

 It is present in stomach, small intestine and large

intestine.

 Pharynx and oesophagus are covered by fibrous

adventitia.

 The serosa forms portion of the peritoneum called the

visceral peritoneum.
Nerve Supply to GIT
 Both intrinsic (enteric nervous system) and extrinsic
(from ANS)

The Enteric Nervous System

 Called brain of the gut.
 A system of about 100 million neurons (motor, sensory
and inter-neurons) that control gastrointestinal motility
and secretions.
 Lies in the wall of the GIT, from the oesophagus to the
anus
 Though independent, it is regulated by the extrinsic
autonomic nervous system.
 Composed of two main plexuses:
 Outer myenteric/Auerbach’s plexus that lie in
the musculosa, between the longitudinal and
circular muscle layers. It control GIT motility

 Innersubmucosa/Meissner’s plexus, which lies in

the submucosa. It control GIT secretions

Neurotransmitters in enteric NS include

acetylcholine, norepinephrine, serotonin,
dopamine, somatostatin, enkephalin, GABA, VIP,
ATP, NO, CO, and many different peptides and
polypeptides.
Enteric nervous system
The Myenteric plexus Stimulation
cause:

 Increased intensity of rhythmical contraction

 Increased rate of contraction

 Increased velocity of conduction

 Inhibiting the pyloric sphincter which controls

emptying
Submucosal plexus:

 Controls function within small

segments of the Gastrointestinal wall.

 Helps control local intestinal

secretions, absorption, blood flow
and local contraction of the
muscularis mucosa
 Myenteric vs Submucosal
Plexus
Myenteric plexus Submucosal plexus
 Located in the muscle  Located in the
layer between submucosa.
longitudinal & circular
muscle layers.
 Controls GI secretion &
 Controls GI movement. local blood flow.
 Found throughout the  Only in the small & large
GIT. intestine.
 Extrinsic nerve supply (ANS)
Extrinsic nerve supply to GIT is
from the ANS
 Post-ganglionic sympathetic
nerve fibres arise from thoracic
and upper lumber segments of
the SC (from T5 to L2) and are
distributed throughout the GIT.

 They inhibit motility, decrease

secretions and cause
constriction of sphincters.

 Emotions such as anger, fear,

and anxiety may slow digestion
via sympathetic stimulation.
 Parasympathetic nerve fibres to
mouth and salivary glands pass
through facial and
glossopharyngeal nerves.
 To oesophagus, stomach, small
intestine and upper part of large
intestine pass through vagus
nerve
 To lower part of large intestine
arise from S2, S3 and S4
segments of spinal cord and pass
through pelvic nerve.
 Parasympathetic system
increase motility, stimulate
secretions and cause relaxation
of sphincters.
GIT Motility
 Two types of movements occur in the GIT
 Peristalsis, a propulsive movement which cause food to
move forward along the tract
 mixing movements, which help in mixing of food with
digestive juice.

 Peristalsis
 Contractile ring that appears around the gut and move
forward, in caudal (anal) direction
 Propels contents of the lumen forward.
 Stimulated by stretch of gut wall
 Controlled by myenteric plexus
 Can be affected by autonomic input to the gut, but its
occurrence is independent of the extrinsic innervation.
Mixing movements
 A segmentation contraction designed to retard
the movement of the intestinal contents along
the length of the intestinal tract to provide
time for digestion and absorption.

 Helps in ample mixing of intestinal content

(chyme) with digestive juice.

 A segment of the bowel contracts at both ends,

and then a second contraction occurs in the
centre of the segment to force the chyme
backward and forward.
 Motor activity of
the GIT

Propulsive movement Mixing movement

“Peristalsis” “Segmentation”

Progressive wave of contraction & Non-propulsive segmental

relaxation. contractions.
Move GI content in a caudal direction. Cause mixing and chopping of
intestinal content.
“Law of the Gut”
Due to contraction of circular
Distension of bowel → contraction of muscle + relaxation of
circular muscle & relaxation of receiving segment.
longitudinal muscle in upstream segment
+ the opposite in the downstream
segment.
Regulation of GIT motility

 Regulated by nervous and hormonal factors

 Sympathetic stimulation ͢ Decrease

 Parasympathetic ͢ Increase

 Motility in the GIT is also controlled by some important

hormones such as gastrin, CCK, secretin, GIP and
motilin
 During fasting, the GIT contraction is
initiated by the migrating motor
complexes (MMC).

 It is a tonic contraction

 Occurs every 90-120min.

Reflexes in the GIT

 Gastrointestinal reflexes are classified into

local enteric, ganglionic and central nervous
reflexes.

Local enteric reflex: controlled by the enteric

nervous system.
These include reflexes that control much
gastrointestinal secretions, peristalsis, mixing
contractions, etc.
Local ganglionic reflex:
 Reflexes from the GIT to the prevertebral sympathetic
ganglia and then back to the GIT.
 They transmit signals from one part of the GIT to another.
 They include the gastrocolic reflex (signals from the
stomach to cause evacuation of the colon), enterogastric
reflex (signals from the colon and small intestine to
inhibit stomach motility and stomach secretion) and
colonoileal reflex (reflexes from the colon to inhibit
emptying of ileal contents into the colon).
Central nervous reflex: Reflexes from the GIT to the
spinal cord or brain and then back to the GIT.

 Include reflexes from the stomach and duodenum to the

brain stem and back to the stomach by way of the vagus
nerves (vago-vagal reflex) to control gastric motility and
secretion
 Defecation reflexes that travel from the colon and
rectum to the spinal cord and back to the colon to
produce the powerful colonic, rectal, and abdominal
contractions required for defecation
 GI Reflexes

3 types of reflexes

Integrated Integrated
Integrated
at at spinal
within the
Sympatheti cord/brain
ENS
c ganglia stem
Control local effects; Gastro-colic reflex Pain reflexes
GI secretion Entero-gastric reflex Defecation reflex
Peristalsis Colono-ileal reflex
Mixing movement
The Mouth (Oral/Buccal Cavity)
 It is initial part of GIT that
encloses the teeth, tongue and
lingual glands
 Digestive juice in the mouth is
saliva
 Saliva is slightly alkaline and
hypotonic, contain 99.5% water
and 0.5% solid (organic and
inorganic).

 It contains ptyalin, an alpha-

amylase enzyme that converts
starch to maltose.

 Also contains mucins (mucous

glycoproteins) Kallikrein and
Immunoglobulins
Saliva & Salivary Glands

Are exocrine glands.

The secretory unit is

made up of acini
and ducts.
 About 800 – 1500ml of saliva is secreted per day
(average 1L).
 pH of saliva = 6.0-7.0
 Functions of saliva
 Digestion: due to presence of digestive enzymes; amylase (convert starch to
maltose, maltotriose and α-dextrin) and lingual lipase (digests milk fats)
 Lubrication.
 Cleansing.
 Swallowing: Mucin of saliva lubricates the bolus and facilitates swallowing.
 Protection
 Proteolytic enzymes.
 Antibodies (IgA).
 Lactoferrin

 Other functions include: cleansing, speech, regulation of body temperature,

excretion, regulation of water balance, appreciation of taste, etc.
 The salivary gland consist of blind
end pieces (acini) that produce the
primary secretion

 Composition of saliva is modified as

it flows from the acini out into ducts
that eventually coalesce and deliver
the saliva into the mouth.

 Na+ and Cl– are extracted and K+ and

bicarbonate are added.

 Saliva Contains low Concentrations

of potassium and Bicarbonate Ions
and high Concentrations of sodium
and chloride Ions.
Types of salivary gland
 Serous Glands:
 Acini contain mainly serous cells that
secrete thin and watery saliva.
 They include Parotid glands and lingual
serous glands.

 Mucus Glands:
 Acini contain mainly mucus cells that
secrete thick, viscous saliva with high
mucin content.
 They include Lingual mucus glands,
buccal glands and palatal glands.

 Mixed Glands:
 Made up of both serous and mucus cells.
 Submaxillary, sublingual and labial
glands are mixed glands.
 Based on type of secretion
they are classified into

Serous Mucus Mixed

Clear, salty, Thick slimy A mixture of

watery secretion of both
containing mucus (mucin).
ptyalin (α- e.g.
amylase). e.g. tiny Submandibular
buccal glands &
e.g. Parotid sublingual
gland
Saliva is secreted by three major
pairs of salivary glands

 Parotid Gland:
 They are the largest of all salivary glands and
contribute 25% of salivary secretion.
 They are serous in nature.
 Secretions are emptied into the oral cavity by
Stensen duct.

 Submaxillary (submandibular) Glands:

 mixed salivary glands located in submaxillary
triangle, medial to mandible.
 They form 70% of salivary secretion.
+ Many tiny
 Their secretions empty into the oral cavity by
Wharton duct buccal
glands
 Sublingual Glands:
 mixed glands that contribute 5% of total secretion.
 They are situated in the mucosa at the floor of the
mouth.
Phases of salivary secretion
 Cephalic phase-- before food enters the stomach
(conditioned reflex)

 Buccal phase– when the food is in the buccal cavity

(unconditioned/inborn reflex)

 Intestinal phase – after the food has been swallowed

Mechanism of salivary secretion

1st stage → Acini

Two stage process

Isotonic
concentration of major
ions similar to that in
plasma

2nd stage → Ducts

Secondary secretion
Hypotonic to plasma
Control of salivary secretion
 Controlled by nervous mechanism (conditioned and
unconditioned reflexes)

 Regulated by the Autonomic nervous system.

 Submandibular and sublingual glands receive

parasympathetic supply from chorda tympani branch of
facial nerve (which arise from superior salivatory
nucleus in pons)

 Parotid gland receives from glossopharyngeal nerve

(from inferior salivatory nucleus in medulla oblongata).
 Parasympathetic stimulation increases salivary
secretion
 When food is placed in the
mouth, the chemicals in the food
stimulate receptors in taste buds
on the tongue

 Impulses are conveyed from the

taste buds to salivary nuclei in
the brain stem (superior and brain stem
inferior salivatory nuclei).

 Efferent parasympathetic
impulses return in fibres of the
facial (VII) and glossopharyngeal
(IX) nerves, and stimulate the
secretion of saliva.
 Sympathetic preganglionic fibres to salivary glands
arise from T1 and T2 and synapse in superior cervical
ganglion of the sympathetic chain.

 Postganglionic fibres are distributed to the salivary

glands along the nerve plexus, around the arteries
supplying the glands.

 Sympathetic stimulation act on mucous cells and

produce small amount of viscous secretion.
 Cause vasoconstriction.
Disorders
 Hyposalivation: Reduction in the secretion of saliva.
 It could be due to obstruction of salivary duct (Sialolithiasis),
congenital absence of salivary glands, or Bell palsy (paralysis of facial
nerve).
 Hypersalivation: Excess secretion of saliva (ptyalism, sialorrhea,
sialism or sialosis).
 It can occur during pregnancy, tooth decay, cerebral palsy, nausea,
vomiting, etc.
 Xerostomia: Dry mouth due to hyposalivation or absence of
salivary secretion (aptyalism).
 It may occur due to dehydration, renal failure, Sjögren syndrome
(autoimmune disorder in which the immune cells destroy exocrine
glands such as lacrimal glands and salivary glands), radiotherapy, or
trauma.
 causes difficulties in mastication, swallowing and speech. It also
causes bad breath (halitosis).
 Chorda tympani syndrome: condition characterized by sweating while
eating.
 During the regeneration of some parasympathetic nerves to salivary gland,
some of the nerve fibres which run along with chorda tympani branch of facial
nerve may deviate and join with the nerve fibres supplying sweat glands.
 When the food is placed in the mouth, salivary secretion is associated with
sweat secretion.

Mumps
 Mumps is an inflammation and enlargement of the parotid glands
accompanied by moderate fever, malaise (general discomfort), and
extreme pain in the throat, especially when swallowing sour foods or
acidic juices.
 Mumps virus (paramyxovirus) typically attacks the parotid glands.
 In about 30% of males past puberty, the testes may also become
inflamed;
 Since a vaccine became available for mumps in 1967, the incidence of
the disease has declined dramatically.
 Mastication (Chewing)
 A mechanical process by which food
substances are torn or cut into small
particles and crushed or ground into a soft
bolus by the teeth.
 Helps to breakdown the foodstuffs into
smaller particles
 mix them with saliva
 lubrication and moistening of dry food
 appreciation of taste of the food.
 Food is ground by the teeth, mixed with
saliva and reduced to a soft, flexible,
easily swallowed mass called a bolus
 Muscles involved include masseter,
temporal, pterygoid and buccinators
muscles.
 Teeth perform cutting and Food in mouth
grinding action.
Reflex inhibition to
 Chewing is largely a reflex muscles of
 Centre is located at the
mastication
medulla oblongata and the
information travel via
mandibular branch of Jaw drops
trigeminal nerve (CN V).

 It is important in The drop initiates a

breaking and grinding stretch reflex in jaw
the food to increase muscles
surface area for
enzymatic action
Rebound contraction
Swallowing (Deglutition)
 Process by which food moves from
the mouth, through the
oesophagus into the stomach.
 It is a reflex response that is
triggered by afferent impulses in
the trigeminal, glossopharyngeal,
and vagus nerves.
 Centre for swallowing is located in
the nucleus of tractus solitarius
and nucleus ambiguous in the
medulla oblongata.
 Efferents pass via the trigeminal,
facial, and hypoglossal nerves
Swallowing occurs in three stages:
 Oral stage:
 a voluntary stage initiated by collecting the oral contents
on the tongue and propelling them backward into the
pharynx.

 Pharyngeal stage:
 an involuntary stage in which the bolus is pushed from
the pharynx into the oesophagus, guided by High intraoral
pressure and elevation of the tongue against the soft
palate

 Oesophageal stage:
 an involuntary stage that guides food from the
oesophagus into the stomach, by peristalsis.
 The peristaltic waves cause relaxation of the lower
oesophageal sphincter (LES), which otherwise is tonically
active/contracted.
 Stage Changes Nervous control
Food is “squeezed”
Oral/voluntary posteriorly into the
pharynx by the
stage
tongue

Soft palate-up
Larynx – anterior & Food stimulates
up. touch receptors in

Swallowing reflex
Pharyngeal Epiglottis –down pharynx
stage Esopahgus opens Afferent via CN V
UES –relaxes & IX
Respiration inhibited Swallowing center
A wave of peristalsis Motor efferent via
starts
CN V, IX, X, & XII
Esophageal Primary peristalsis
stage Secondary peristalsis
Myenteric plexus
LES- relax
Vagus
Disorders
 Dysphagia: Difficulty in swallowing
 May be caused due to mechanical obstruction of
oesophagus by tumor, strictures or diverticular hernia
(out pouching of the wall), neurological disorders that
cause decreased movement of oesophagus (e.g.
parkinsonism), or muscular disorders.

 Esophageal Achalasia:
 a neuromuscular disease characterized by accumulation
of food substances in the oesophagus.
 It is due to the failure of LES to relax during swallowing.
 The accumulated food substances cause dilatation of
oesophagus.
 Gastroesophageal Reflux Disease (GERD)

A disorder characterized by regurgitation of

acidic gastric content through oesophagus, due
to the weakness or incompetence of LES.

 GERD is characterised by heart burn or pyrosis

(painful burning sensation in chest due to
regurgitation of acidic gastric content into
oesophagus), oesophagitis (inflammation of
oesophagus), dysphagia and oesophageal ulcers.
STOMACH
 Receives, stores, breaks down and
partially digests food prior to its
gradual release into the small
intestine.
 Wall has three layers of smooth
muscle (outer longitudinal, middle
circular and inner oblique).

 In an empty stomach, the mucosa

lies in large folds called rugae
 It has two curvatures; a lesser
curvature on the right and a
greater curvature on the left.
 Functional Anatomy of the
Stomach
 Anatomically:
 Fundus
 Body
 Antrum
 Physiologically:
 Orad region
 Caudad region
 It is divided into four regions:
 cardiac region, fundus, body
(corpus) and pylorus.
 The cardia surrounds the
opening of the esophagus into
the stomach

 The pylorus communicates with

the duodenum via the pyloric
sphincter

 As a result of repeated cycles of

propulsion and retropulsion of
food in the stomach, the food is
mixed with gastric juice and
become transformed to a soupy
liquid called chyme
Functions of stomach Stomach is a poor
absorptive area of GIT
It lacks the villous
 Storage of food until the food can type of absorptive
be processed in the duodenum membrane
It has tight junctions
between epithelial
cells
 Mixing of food with gastric Only a few highly-lipid
secretions until it forms a soluble substances can
be absorbed such as:
semifluid mixture called chyme. Alcohol
 Digestion of food by gastric Aspirin
enzymes

 Emptying of food into the small

intestine at a rate suitable for
proper digestion and absorption.
 3 main functions

Storage of food

• Entrance of food
• ↓ muscular tone of the body of stomach
• Allowing stomach to accommodate food
• ≈ 0.8-1.5L

Mixing food

• Weak peristaltic waves start from mid upper portion of

stomach
• “constrictor/mixing waves” move toward antrum
• ↑ intensity against a tight pylorus will result in “retropulsion”

Emptying into duodenum

• Movement of chyme into duodenum is achieved by “Pyloric

pump”
Gastric secretion

Types of Gastric glands

gastric
glands

Mucus- Oxyntic
Pyloric
secreting (parietal)
glands
glands glands
Secrete; Secrete; Secrete;
mucus HCl Gastrin
HCO3 Pepsinogen Mucus
IF Pepsinogen
Found in; Mucus
Cardia Found in;
Found in; Antrum
Body & fundus
Distal 20% of stomach
Proximal 80% of stomach
 Gastric glands are tubular glands
made of numerous gastric pits
 They secrete acidic gastric juice
(HCl, pepsinogen, mucus, intrinsic
factor)
 Cells in gastric gland include:
 Stem cells: they lie in the neck
region and continuously replenish
other cell types of the gastric
gland
 Mucous neck cells: also present in
the neck region and secrete
mucus  Enterochromaffin – like cells:
scattered throughout the gland.
 Chief (peptic) cells: lie deep
Secrete histamine
within the gland and secrete
digestive enzymes (pepsinogen,  D-cells: secrete somatostatin
renin, gastric lipase, etc)  G cell: located mainly in the pyloric
 Parietal (oxyntic) cells: lie close antrum and secretes the hormone
to the gland opening and secrete gastrin
HCl and intrinsic factor
 Pepsinogen is synthesized
in chief cells and packed
into zymogen granules

 When zymogen granule is

secreted into stomach
from chief cells, the
granule is dissolved and
pepsinogen is released
into gastric juice, where
it is activated into pepsin
by HCl.
Gastric gland Parietal cell
HCl secretion by parietal cell
 Secretion of HCl is an active process.
 It takes place in the canaliculi of parietal cells in
gastric glands
 Control of HCl Secretion

Control of HCl Secretion

Neural Endocrine Paracrine

Via parasympathetic stimulation
Ach Gastrin Histamine →
Direct Indirect activates H2
effect effect receptor
(parietal
On Parietal cells
cells) 
↑ HCl secretion
By + G cells By + ECL increases acid
secretion
Gastrin ↑ HCl Histamine↑
secretion HCl secretion H2
Blockers
 The primary stimuli for gastric secretion are gastrin,
histamine and Ach.
 Gastrin binds to receptors on parietal cells and
stimulates them directly to activate secretion.

 It also stimulates the enterochromaffin-like cells (ECL

cells) that release histamine which also triggers
parietal cell secretion, via binding to H2 histamine
receptors.

 Parietal cells can also be stimulated by acetylcholine.

 PGs inhibit gastric acid secretion
Other Gastric Secretions

Optimum pH for pepsin = 1.8-3.5

pH > 5 inactivates pepsin

 The Mucus Layer of the
Stomach
Bicarbonate –rich mucus layer protects the stomach mucosa
Vagal stimulation affects
many gastric cells
Phases of gastric secretion
Gastric secretion occurs in three phases:

 Cephalic phase: It is regulated by nervous

mechanism (conditioned and unconditioned
reflexes).
 Conditioned reflex - Impulses from the special sensory
organs (eye, ear and nose) → cerebral cortex →dorsal
nucleus of vagus → stomach wall → acetylcholine →
gastric secretion

 Unconditioned reflex - Presence of food in the mouth

(stimulation of receptors in the mouth) → Sensory
impulses (via afferent nerve fibres of glossopharyngeal
and facial nerves to amygdala and appetite centre
present in hypothalamus) → dorsal nucleus of vagus →
vagal efferent nerve fibres to the wall of the stomach →
acetylcholine → gastric secretion
 Gastric phase: Secretion of gastric juice due
to presence of food in the stomach.
 Itis regulated by both nervous and hormonal
mechanisms (local myenteric reflex, vagovagal
reflex and gastrin hormone).

 Intestinal phase: Is the secretion of gastric

juice due to presence of chyme in the
intestine.
 Gastric secretion initially increase due to gastrin
hormone, and later decrease as a result of
enterogastric reflex and inhibitory GI hormones
(secretin, CCK, GIP, VIP, peptide YY).
Disorders
 Gastritis: inflammation of gastric mucosa with atrophy of
gastric gland.
 May be caused by bacterial infection, excess alcohol and NSAIDs.
 It may lead to gastric atrophy, Achlorhydria (no acid),
Hypochlorhydria (decreased acid), pernicious anaemia
 It is characterised by nausea, vomiting, anorexia and loss of
weight.

 Peptic ulcer disease: It refers to erosion of the wall of

stomach or duodenum, caused by digestive action of gastric
juice.
 It occurs as a result of imbalance between the rate of secretion of
gastric juice and the degree of protection afforded by the mucosal
barrier and neutralization of the gastric acid by duodenal juices.
 Common causes of PUD include stress, spicy food,
smoking, longterm use of NSAIDs and chronic
inflammation due to Helicobacter pylori.

 Is associated with severe burning pain in epigastric

region (heart burn).
 The pain occurs while eating or drinking in gastric ulcers,
or 1 to 2 hours after food intake (and during night) in
duodenal ulcer.
 Other symptoms include nausea, vomiting,
hematemesis (vomiting blood), anorexia and loss of
weight.
 PUD can be treated by histamine H2 blockers (e.g.
cimetidine), proton pump inhibitors (e.g. omeprazole)
or prostaglandin agonists (e.g. misoprostol).
 Antibiotics may be used in H. pylori induced ulcers.

 Zollinger-Ellison syndrome: Secretion of excess

hydrochloric acid in the stomach due to large quantity
of gastrin.
 May be caused by tumour of pancreas or stomach which
produces a large quantity of gastrin.
 It is associated with abdominal pain, diarrhoea and
hematemesis (vomiting blood).
PANCREAS
 It is a dual organ having both
endocrine and exocrine functions.
 Endocrine part (Islet of
Langerhans) is concerned with
production of hormones
 Exocrine part (pancreatic acinar
and ducts) is concerned with
production of digestive juice
(pancreatic juice).

 The pancreatic acinus/alveolus has

a single layer of acinar cells
surrounding a lumen (as in salivary
gland).
 The acinar/alveolar cells contain
zymogen granules, which possess
digestive enzymes.
 The pancreas

Exocrine Endocrine

95% of pancreas 1-2% of pancreas

Secretes digestive Secretes hormones.

enzymes, HCO3-
and water. Into blood

Into duodenum Made of Islets of

Langerhan’s.
Made of acinar &
ductal cells.
 Ducts from several acinus unite to form intralobular
duct.

 All the intralobular ducts unite to form the main

pancreatic duct which joins common bile duct to form
ampulla of Vater that opens into duodenum.

 About 500 mL is secreted per day

 It is highly alkaline with a pH of 8 to 8.3

COMPOSITION OF PANCREATIC JUICE
 99.5% water and 0.5% solids (organic and inorganic).

 Bicarbonate content is very high in pancreatic juice.

 Proteolytic enzymes are secreted in inactive form (e.g.

trypsinogen and chymotrypsinogen). They are activated
in the duodenum.

 Enterokinase in intestinal juice activate trypsin, which

inturn activate the other enzymes.
 Pancreatic Juice

 Refers to the final combined product secreted

by the exocrine pancreas.

 It contains;
1. An electrolyte solution rich in HCO3-
2. Digestive enzymes

Pancreatic digestive enzymes

For
For proteins For lipids carbohydrat For DNA &
es RNA

Trypsin P. Lipase P. Amylase Nucleases

Chymotrypsin Esterase
Carboxypeptidase Phospholipase
 Pancreatic secretion

Acini provide the primary

secretion → organic
constituents (digestive
juices) in a solution with
similar composition to
plasma.

Ducts dilute & alkalinize

the pancreatic juice.
Regulation of pancreatic secretion
 By both nervous and hormonal factors.
 It is regulated in three phases:
 Cephalic phase: a nervous phase regulated by both
conditioned and unconditioned reflexes.
 Gastric phase: a hormonal phase regulated by gastrin due
to presence of food in the stomach.
 Gastrin from stomach is transported to pancreas through
blood, and stimulates secretion of enzyme rich pancreatic
juice.
 Intestinal phase: due to presence of chyme in the
intestine.
 Itis under the influence of intestinal hormones. Secretin
and CCK stimulate while Pancreatic polypeptide,
Somatostatin, Peptide YY, ghrelin and leptin inhibit.
Applied physiology
 Pancreatitis: Is the inflammation of pancreatic acini. It
is associated with abdominal pain, nausea and
vomiting, anorexia and loss of weight.
 May be caused by alcohol consumption, obstruction of
ampulla of Vater, congenital abnormalities of pancreatic
duct, malnutrition.
 Steatorrhea: is the formation of bulky, foulsmelling,
and claycolored stools with large quantity of
undigested fat. It is due to impairment in digestion and
absorption of fat.
 It may be caused by Lack of pancreatic lipase, liver
disease affecting secretion of bile or celiac disease.
SMALL INTESTINE
 Longest part of the GIT that extends from pyloric
sphincter to ileo-cecal valve.
 made of the duodenum, jejunum and ileum.
 Final digestion and maximum absorption of food
products takes place in the small intestine.
 The mucosa is highly folded and covered by minute
finger-like projections called villi, which contain blood
vessels and a central lacteal (lymphatic vessel).
 The columnar epithelial cells of the villi (enterocytes;
secrete enzymes) give rise to hair-like projections
called microvilli. Villi and microvilli increase surface
area for absorption.
Intestinal secretion
 Intestinal secretion (succus entericus) is secreted by
intestinal glands.
 Intestinal glands (crypts of Lieberkuhn) are simple
tubular glands that open into the lumen between the
villi.
 Cells found in crypts of Lieberkuhn include
 argentaffin cells that secrete intrinsic factor,
 goblet cells that secrete mucus
 paneth cells that secrete cytokine (defensin).

Enzymes in succus entericus are secreted by enterocytes of the

villi.
 About 1500 mL is secreted per day

 It is alkaline with pH of 8.3 (due to high bicarbonate

content)

 Enzymes found in intestinal secretion act on partially

digested food and convert them to final end products.
They include:
 Proteolytic enzymes (peptidases that convert peptides to amino acids)
 Amylolytic enzymes (sucrose, lactase, maltase, dextrinase) that
convert disaccharides to monosaccharides
 lipolytic enzyme (Intestinal lipase) that acts on triglycerides and
converts them into fatty acids and glycerols.
 Enterokinase present in intestinal juice activate trypsinogen into
trypsin.
Regulation of intestinal secretion
 Secretion of succus entericus is regulated by both nervous
and hormonal mechanisms.

 The enteric nervous system plays an important role the

secretion of intestinal juice.

 Stimulation of parasympathetic nerves causes vasodilatation

and increases the secretion of succus entericus.

 Stimulation of sympathetic nerves causes vasoconstriction

and decreases the secretion of succus entericus.

 Secretin and cholecystokinin promote the secretion of succus

entericus by stimulating the intestinal glands.
APPLIED PHYSIOLOGY
ENTERITIS (CROHN’S DISEASE):
 Is an inflammatory bowel disease (IBD), characterized
by inflammation of small intestine.
 It causes malabsorption and diarrhea.
 It develops because of abnormalities of the immune
system.
 The immune system reacts to pathogens and results in
inflammation of the intestine.
 It is characterised by malabsorption, weight loss,
abdominal pain, diarrhea, rectal bleeding
CELIAC DISEASE:
 It is an autoimmune disorder characterized by the
damage of mucosa and atrophy of villi in small
intestine, resulting in impaired digestion and
absorption.

 It is caused by gluten, a protein present in grains

(gluten-sensitive enteropathy).

 Features include diarrhea, steatorrhea, abdominal

pain, weight loss, depression.
LARGE INTESTINE
 It is also called colon.

 The outermost layer (serosa) is formed by peritoneum.

 The longitudinal muscles in large intestine are arranged

in three long bands called tenia coli.

 Because tenia coli is shorter than the colon, the large

intestine is made into pouches called haustra.
 Large intestinal glands secrete watery
secretion rich in bicarbonate.
 Villi are absent and mucosa contains only
mucus glands. No digestive enzymes.

 Functions of large intestine include

absorption of water and electrolytes,
formation of feces and synthesis of folic
acid, vit k and vit B12
Applied physiology
DIARRHEA:
 Frequent and profuse discharge of watery stool.
 It occurs due to the increased intestinal motility.

 Severe diarrhea results in loss of excess water and

electrolytes, causing dehydration and electrolyte
imbalance.

 Chronic diarrhea results in hypokalemia and metabolic

acidosis.
CONSTIPATION:
 Difficulty in voiding of faeces, or passage of hard stool
 It is due to impairment in movements necessary for
defecation.
 Faeces remain in the large intestine for a long time,
resulting in absorption of fluid.

 It may be caused by lack of fibre or lack of liquids in

diet, irregular bowel habit, drugs like diuretics,
narcotics, antihypertensive drugs (calcium channel
blockers), antiparkinson drugs, antidepressants and the
anticonvulsants.
MEGACOLON:
 Is a condition characterized by distension
and hypertrophy of colon due to absence
or damage of ganglionic cells in myenteric
plexus (aganglionic megacolon).

 It is associated with constipation and

leads to accumulation of large quantity of
faeces in colon.

 Congenital development of megacolon is

known as Hirschsprung disease.
DIGESTION, ABSORBTION AND METABOLISM
OF FOOD

 Before complex ingested food can

be utilised by the body, it must
first of all be digested and
absorbed from the GIT.

 Digestion is an enzymatic process by

which complex organic food
substances are mechanically and
chemically broken down into simple
chemical compounds that can be
absorbed and utilized by the body.
 Absorption is the net passage of
substances from the lumen of the gut,
across the epithelium into the blood.

 Metabolism (anabolism or catabolism) is

the process by which food substances
undergo chemical and energy
transformation.
 It is the utilisation of absorbed nutrients
for energy, development, growth and
repair of tissues.
Carbohydrate
 Carbohydrate is a major constituent of diet

 Three major sources of carbohydrates in diet

 Sucrose (disaccharide) also known as cane sugar
or table sugar
 Lactose (disaccharide) in milk
 Starches (polysaccharides) present in almost all
non animal foods especially in the grains.

 Other carbohydrates ingested to a slight extent

are glycogen, alcohol, lactic acid, pyruvic acid,
pectins, dextrins, and others.
 End products of carbohydrate digestion are
monosaccharides (glucose, fructose and galactose).
 Enzymes involved in digestion of carbohydrate are
known as amylolytic enzymes (amylases).

In the mouth
 Digestion of carbohydrate begins in the mouth,
under the influence of ptyalin (salivary amylase)

 The food remains for short time in the mouth, and

only 3 - 5% of all starches that have been eaten will
have become digested.
 Enzyme α-amylase (ptyalin) hydrolyzes starches
into the disaccharide maltose, dextrose and other
small polymers of glucose.
In the stomach
 Gastric juice in the stomach contains a
weak gastric amylase, but its role in
carbohydrate digestion is negligible.

 Salivary amylase can continue for an hour

after the food has entered the stomach

 Activity of the salivary amylase is blocked

by the acid in gastric juice
 30 - 40% of the starches will be
hydrolyzed mainly to maltose.
In the duodenum

 pancreatic amylase breaks down

undigested starch and
polysaccharides to maltose and
dextrin.
Small intestine

• Final digestion of carbohydrate takes place in

the small intestine, under the influence of
intestinal amylases (maltase, dextrinase,
sucrase, lactase) bound to brush border of
intestinal epithelial cells.
 Maltase → maltose to glucose
 Dextrinase → dextrin to glucose
 Sucrase → sucrose to glucose and fructose
 Lactase → lactose to glucose and galactose
 Absorption of carbohydrates
(monosaccharides) occurs in
the small intestine. Na+

 Glucose and galactose are

actively transported from the
lumen into the epithelial cell
by means of sodium-glucose
co-transport, with the aid of a
carrier protein called sodium
glucose-linked transporter
(SGLT). Na+

 Sugar: uphill (against conc.

grad).
K+
 Na+ : downhill (along conc.
grad).
 The SGLT is activated by
binding with sodium and
glucose, and transports them
from the lumen of intestine
into the epithelial cell.
 The Na+-K+ pump in the basolateral border keeps the
intracellular Na+ concentration low, thus maintaining the
Na+ gradient across the luminal membrane.
 Absorption of fructose is by facilitated diffusion through
glucose transporter 5 (GLUT5), which is independent of
sodium
 It is mainly converted into glucose inside the epithelial cell
before entering the portal blood.

 The absorbed monosaccharides leave through the

basolateral membrane through GLUT2 and enter blood
capillaries

 Absorbed glucose is used to release energy through the

process of glycolysis and in the citric acid cycle
 Excess glucose is converted to glycogen and stored in liver
and muscles.
 Deficiency of disaccharidase leads to
diarrhoea, bloating, and flatulence after
ingestion of sugar.

 Diarrhea is due to the increased number

of osmotically active oligosaccharides
molecules that remain in the intestinal
lumen, causing the volume of the
intestinal contents to increase.

 Bloating and flatulence are due to the

production of gas (CO2 and H2) from
disaccharide residues which are
metabolized by intestinal flora in the
lower small intestine and colon.
♦ Lactose intolerance is the most common
cause of carbohydrate malabsorption.

♦ It results from the inability of the goblet cells

to produce lactase.

♦ In infants, the diarrhea-induced dehydration

can be life threatening.

♦ it is hereditary disorder, affecting 5-15% of

Europeans and 80-90% of Asians and
Africans.
Protein
 Dietary proteins are formed by long chains of
amino acids, bound together by peptide
linkages.
 Enzymes responsible for the digestion of
proteins are called proteolytic enzymes
(proteases).
 Proteolytic enzymes break proteins to peptides
and amino acids.
 Digestion of protein begins in the stomach,
under the influence of pepsin in gastric juice.
 Pepsin
converts ingested proteins into Proteoses,
peptones, large polypeptides.
 Digestion of proteins in the stomach
 Pepsin
 secreted by chief (peptic) cells.
 It is active at pH 2-3 and inactive at pH 5.
 Initiateprotein digestion (10-20% of protein
digestion).

 Hydrochloric acid
 secreted by parital (oxyntic) cells.
 Digestion of proteins occurs mostly in the duodenum
and jejunum by the proteolytic enzymes of the
pancreatic juice and succus entericus.
 Pancreatic juice contains endopeptidases (trypsin and
chymotrypsin) and carboxypeptidases.
 Proteolytic enzymes in succus entericus include tripeptidases,
dipeptidases and aminopeptidases.

 Absorption of amino acids from intestinal lumen is also

by means of carrier proteins (transporters). Levo
rotatory amino acids are absorbed by co transport with
sodium, while dextro rotatory amino acids are absorbed
by facilitated diffusion.
 Di- and tri- peptides are absorbed by H ion dependent
peptide transporters. They are hydrolysed to amino
acids within the epithelial cells by cytosolic peptidases.
 The amino acids diffuse through the basolateral border
into blood capillaries.

 Amino acids may be taken up by the liver and used to

form glucose (gluconeogenesis) or plasma proteins
(anabolism).

 It may also be used for growth and repair in other

tissues.

 Catabolism of amino acid leads to formation of

ammonia and urea, which are excreted by the kidney.
Lipids
 About 150g of dietary lipids is ingested per day, in the
form of triglycerides (neutral fats), phospholipids,
cholesterol and plant sterols.
 Dietary fats are classified into saturated and
unsaturated fats (e.g. omega-3 fats or omega-6 fats).

 Saturated fats increase blood cholesterol, while

unsaturated fats help to decrease blood cholesterol
level.

 Very little digestion of fat occur by Lingual and gastric

lipase. Essentially most fat digestion occurs in the small
intestine
In the stomach

 Gastric lipase and lingual lipase (from

saliva) liberate mostly short chain and
unsaturated fatty acids.
In the duodenum
 Fats are insoluble in water due to their high surface tension,
and thus cannot be digested by lipolytic enzymes.

Emulsification
 The first step in fat digestion is to break the fat globules into
small sizes so that the water soluble digestive enzymes can
act on the globule surfaces.
 This process is called emulsification and it is achieved under
the influence of bile salts and aided by lecithin in the bile.

 The fat globules are broken down by bile salts into minute
droplets and made into emulsion (Emulsification).
 Because bile salts are amphipathic (have both
hydrophobic and hydrophilic regions), they
emulsify fats by reducing their surface tension
due to their detergent action, thus, increasing
their surface area.

 Pancreatic lipase, cholesterol esther hydrolase,

phospholipase and intestinal lipase act on the
emulsified fat with the aid of colipase (pancreatic
co-enzyme), and convert it to cholesterol, fatty
acids and glycerol.

 The cholesterol, fatty acids and glycerol,

together with bile salts, lecithin and fat soluble
vitamins form small aggregations called micelles.
 As micelles come in contact with the brush
border microvilli → These fat products
leave the micelles and are absorbed
across the epithelial cell membranes

 The micelles can pick up more fat

products which have been produced from
digestion of other TG molecules in the fat
emulsion
 Bile salts continuously repeat their fat-
emulsifying function down the length of
the small intestine until all fat is
absorbed.

 Then the bile salts themselves are

reabsorbed in the terminal ileum by a Na+
- dependent active transport process.
 Final products of fat digestion diffuse into the
intestinal epithelial cell through the luminal border.
 They are esterified in the epithelial cell into
triglycerides.
 The triglycerides, cholesterol esters and fat soluble
vitamins are now coated with a layer of protein,
cholesterol and phospholipids to form particles called
chylomicrons.
 The chylomicrons are released across the basolateral
membrane by exocytosis and enter lymphatic lacteals
in the villi, and to the systemic circulation via thoracic
duct.
Absorption of Fats

Figure 14.14
 When chylomicrons are traveling through capillaries of
adipose tissue or liver, the enzyme called lipoprotein
lipase present in the capillary endothelium hydrolyzes
triglycerides of chylomicrons into free fatty acids and
glycerol, which enter the fat cells (adipocytes) of the
adipose tissue or liver cells, where they are again
converted into triglycerides and stored.

 The other contents of the chylomicrons (cholesterol

and phospholipids) are released into the blood and
combine with proteins (beta globulins called
apoproteins) in the liver to form lipoproteins, the form
which lipids are transported in the blood.
 Free fatty acids are transported in
combination with albumin.

 Lipoproteins may be either low density

lipoproteins (LDL) or high density
lipoproteins (HDL).
 LDL contains low concentration of protein
and high concentration of cholesterol and
phospholipids (bad cholesterol).
 HDL contains high concentrations of
proteins with low concentration of
cholesterol and phospholipids (good
cholesterol).
 Primary function of lipoproteins is transport of lipids.

 LDL (bad cholesterol) transport cholesterol and phospholipids
from the liver to different areas of the body, viz. muscles,
other tissues and organs such as heart.
 It is responsible for deposition of cholesterol on walls of
arteries causing atherosclerosis.
 High level of LDL in the blood increases the risk of coronary
heart disease.

 HDL (good cholesterol) transport cholesterol and

phospholipids from tissues and organs back to the liver for
degradation and elimination.
 It prevents deposition of cholesterol on the walls of arteries,
thereby reducing the risk of atherosclerosis.
 High level of HDL is a good indicator of a healthy heart,
because it reduces the blood cholesterol level and the risk of
coronary heart disease.
DEFEACATION

 Normally, the rectum is empty of faeces.

 This is due to presence of a functional sphincter and sharp
angulation at the juncture between the sigmoid colon and the
rectum.
 Entry of faeces into the rectum by mass movement of the
colon causes the desire for defecation, including reflex
contraction of the rectum and relaxation of the internal anal
sphincter.
 The external anal sphincter is controlled by nerve fibres in
the pudendal nerve, which is part of the somatic nervous
system and therefore is under voluntary, conscious control.
 The external anal sphincter is usually kept continuously
constricted unless conscious signals from higher centres
inhibit the constriction.
Defecation reflex
 The desire for defecation occurs when faeces enters rectum due to
the mass movement of the colon.
 Usually, the desire for defecation is elicited by an increase in the
intrarectal pressure.
 When rectum is distended due to the entry of faeces by mass
movement of the colon, stretch receptors in the rectum are
stimulated.
 Impulses from the nerve endings are transmitted via afferent fibres
of pelvic nerve to the defecation centre, situated in sacral
segments of spinal cord.
 Motor impulses are sent to the descending colon, sigmoid colon
and rectum via efferent nerve fibres of pelvic nerve to cause
strong contraction of descending colon, sigmoid colon and rectum
and relaxation of internal anal sphincter.
 Simultaneously, voluntary relaxation of external anal sphincter
occurs due to the inhibition of pudendal nerve, by impulses arising
from cerebral cortex.
Incontinence

 In newborn babies and in some people

with transected spinal cords, the
defecation reflexes cause automatic
emptying of the lower bowel at
inconvenient times because of lack of
conscious control exercised through
voluntary control of the external anal
sphincter by higher brain centres.
Hormonal control of GI function