GASTROINTESTINAL PHYSIOOGY

DR EZE EJIKE DANIEL

DEPARTMENT OF PHYSIOLOGY,

SEPTEMBER, 2022
OVERVIEW OF THE DIGESTIVE SYSTEM
• GI system is made up of the GIT and some associated glandular organs that
produced secretions that make the functions of the GIT possible.
• GIT consists of hollow tube that starts in the mouth and ends in the anus.
• Main functions of the GI system are:
– Digestion of nutrients
– Absorption of nutrients from the gut lumen into bloodstream
• In order to perform these functions, GI system carries out certain activities.
These activities can be broadly grouped into:
a) Motility
b) Secretion
c) Digestion and absorption
Motility
• Movements of the GIT which helps to mix and grind the contents of the tract
and propel it along the length of the tract in a proximal-distal direction i.e.
from the mouth to the anus.
Secretion
• Processes by which the glands associated with the GI system pour water and
other substances (enzymes, mucus, electrolytes etc) into the tract.
Absorption
• Processes by which nutrients molecules are transported from the gut
lumen into the blood stream.
• Digestive system consists of the following from above downwards:
1. Oral cavity (mouth)
2. Pharynx
3. Esophagus
4. Stomach
4. Small intestine (duodenum, jejunum & ileum)
5. Large intestine (colon, cecum, appendix, rectum & anal canal)
6. Anus
• Accessory associated glandular organs include :
1. Salivary glands
2. Liver
3. Gall bladder and the pancreas
 FUNCTIONAL ANATOMY OF THE GATRO-INTESTINAL SYSTEM

Structure of intestinal wall with intrinsic nerve plexus

• In general, wall of the GI tract is formed by four layers
which are from inside out:
1. Mucus layer
2. Submucus layer
3. Muscular layer
4. Serous or fibrous layer.
1. Mucus layer
• Innermost layer of the wall of GIT & faces the cavity of GIT.
• Also called GIT mucosa or mucus membrane.
• Has three layer of structures:
a) Epithelial lining- inner surface of mouth, tongue, pharynx &
esophagus have stratified squamous epithelial cells, while stomach,
small intestine & large intestine has columnar epithelial cells
b) Lamina propria- formed by connective tissues containing contain
fibro blasts, macrophages, lymphocytes and eosinophils.
c) Muscularis Mucosa- Thin layer of smooth muscle fibers. Absent in
mouth and pharynx. Present from esophagus onwards.
2. Submucus layer
• Present in all parts of GI tract, except the mouth and pharynx.
• Contains loose collagen fibers, elastic fibers, reticular fibers &
connective tissue.
• Blood vessels, lymphatic vessels and nerve plexus are present
3. Muscular layer
• Lips, cheeks and wall of pharynx contains skeletal muscle fibers.
• Esophagus has both skeletal and smooth muscle fibers.
• Wall of the stomach and intestine is formed by smooth muscle fibers.
• Smooth muscle fibers in stomach are arranged in three layers:
i. Inner oblique layer
ii. Middle circular layer
iii. Outer longitudinal layer.
• Smooth muscle fibers in the intestine are arranged in two layers:
i. Inner circular layer
ii. Outer longitudinal layer.
• Auerbach nerve plexus is present in between the circular and
longitudinal muscle fibers.
• Smooth muscle fibers present in inner circular layer of anal canal
constitute internal anal sphincter.
• External anal sphincter is formed by skeletal muscle fibers.
4. Serous or fibrous layer
• Outermost layer of the wall of GIT is either serous or fibrous in
nature.
• Formed by connective tissue and meso-epithelial cells.
• It covers stomach, small intestine and large intestine.
• It covers pharynx and esophagus.
Nerve Supply to GIT
•  GIT has two types of nerve supply:
I. Intrinsic nerve supply
• Controls all the secretions and movements of GI tract.
• Present within the wall of GIT from esophagus to anus.
• Nerve fibers of this system are interconnected and form two major
networks called
a) Auerbach Plexus
• Regulate the movements of GI tract.
• Called myenteric nerve plexus
• Located between the inner circular muscle layer and the outer
longitudinal muscle layer.
b) Meissner Nerve Plexus
• Situated in between the circular muscle and submucosal layer of GIT
• Regulation of secretory functions of GIT
II. Extrinsic Nerve Supply 
• Control the intrinsic nervous system
and are from autonomic nervous
system (ANS).
• Sympathetic and parasympathetic
divisions of ANS innervate the GIT .
Sympathetic Nerve Fibers
• Stimulation inhibit the movements &
decrease the secretions of GIT by
secreting the neurotransmitter
noradrenaline.
• Also causes constriction of
sphincters. 
Parasympathetic Nerve Fibers
• Stimulation accelerate the movements
and increase the secretions of GIT.
• Neurotransmitter secreted by the
parasympathetic nerve fibers is Ach.
General Structures of the GIT
Oral cavity
• Lips and cheeks are involved in facial expression, mastication
and speech
• Tongue is involved with speech, taste, mastication and
swallowing.
• Tooth types are : Molars, Canine, Pre molars, Incisors
• Tooth consists of a: Crown, Neck, Root
• Components of the tooth include: Dentin, Pulp cavity
(nerves, blood vessels ), Crown
• Teeth are held in the alveoli by peri-dontal ligaments
• Muscles mastication include: Masseter, Temporal, Medial
pterygoid and Lateral pterygoid
Temporalis muscle; Lateral (Externus) Pterygoid Muscle
Functions:: Elevation (anterior Fumctions:
part) and Retropulsion (posterior a) Bilateral contraction: propulsion
part)
b) Unilateral contraction:
lateropulsion
 .
lat
.
yg
er
pt
Med

Masseter muscle
Functions:
The superficial part: Bilateral contraction
(elevation and propulsion) Pterygoids Muscles
The deep portion: Unilateral contraction
(elevation and lateropulsion)
Esophagus
• Connects the pharynx to the stomach
• Upper and lower esophageal-sphincters regulate movement in
the esophagus and is approximately 25cm long, s
Esophagus consists of four layers:
a) Fibrous layer – outer
b) Muscular layer - circular and longitudinal
c) Submucosal layer
d) Stratified squamous epithelium (mucus layer)
• Position is as follows:
a) Lies in the mediastinum
b) Anterior to vertebra
c) Posterior to the trachea
d) Passes through the esophageal hiatus – opening
Structures of the stomach
• Include:
a) Opening into the esophagus
(gastro-esophageal) – cardiac
b) Opening into the duodenum
(pyloric )
Wall of the stomach includes:
c) External serosa
d) Muscle layer (circular,
longitudinal, oblique )
e) Sub-mucosa
f) Simple columnar (interior
mucosal)
g) Rugae: Folds in the stomach
when empty Stomach
f) Gastric pits: Are the
• Openings into the gastric
glands
• Within the gastric glands
are:
1. Mucosal neck cells –
secrete mucus
2. Parietal cells - Secrete
HCl
3. Chief cells- Zymogenic-
pepsinogen
4. Endocrine cells: secrete
some of the GIT hormones
Gastric glands
Continuation of the physiologic-anatomy of the stomach
Fundus/Body
• Includes the cardiac region, greater curvature, lesser curvature,
pyloric antrum, pyloric canal, pyloric orifice
Small intestine
• 20ft in length and divided into 3 portions:
a) Duodenum- 10 inches
b) Jejunum- 2/5
c) Ileum- 3/5
• Wall of the small intestine includes:
a) Villi and micro-villi increase surface area
b) Absorptive, goblet, and endocrine cells which develop in
intestinal glands, Crypts of Lieberkühn which secrete digestive
enzyme
c) Duodenal glands which produce mucus
Structure of the duodenum :
• Contains a 180 degree arc
• Bile and pancreatic ducts join this forms the hepato-
pancreatic ampulla opening: hepato-pancreatic ampullar
sphincter.
Mucosa of the duodenum
• Is simple columnar of three types:
• Contain absorptive cells (micro-villi)
• Contain also Goblet cells (produce mucus )
• Contain also endocrine cells (regulatory hormones)
Submucosa
• Contain cells called-the Brunner's glands these cells
produce mucus.
Jejunum and ileum
• Similar in structure to the duodenum, except that they:
a) Gradually decrease in diameter
b) Also decrease in thickness
c) As well as decrease in folds and villi.
• Jejunum and ileum are the site of most nutrient absorption
• Junction between the ileum and the large intestine is the
ileocecal junction and is regulated by a sphincter- ileocecal
sphincter.
Mechanical activities of the gastro-intestinal tract
• Some mechanical activities occur in different regions of the
GIT.
• These activities include the following :
– Chewing (Mastication)
– Swallowing (Deglutition)
– Gastric motility
– Motility of the small intestine
– Motility of the colon
– Defecation (Passage of feces)
Chewing
• Food taken into the mouth is broken down into smaller pieces by teeth
and mixed with saliva to make it easier to swallow and also make it
enjoyable. Thus releasing taste – producing substances
• Chewing ensures the food is mixed more readily with digestive
secretions of the stomach and duodenum
• Tongue and cheek muscles are used to keep the food mass between teeth
during mastication
• Its a well coordinated reflex but sometimes it can be carried out
voluntarily.
• Frequency of the chewing cycle (open-close cycle) is once per second,
but can also be faster depending on the consistency of the food
• Closure of the mouth during chewing is associated with pressure on the
teeth, gums, tongue and hard palate leading to a reflex relaxation of the
jaw
• In addition to up and down movement of the jaw, chewing also involves
forward and backward, side to side jaw movements that assist in grinding
the food
Swallowing or Deglutition
• Process by which food is propelled from the oral cavity into the
stomach
• Can be initiated voluntarily, but once it starts, it’s almost entirely
under reflex control and cannot be stop
• Receptors for the swallowing reflex are: touch receptors
(oropharyngeal receptors) -located mostly on the palate and near
the opening of the pharynx
• Sensory impulses (afferent fibres) from the these receptors are
transmitted in certain cranial nerves (glossopharyngeal nerve
fibers) to the Deglutition center in the medulla oblongata and lower
pons
• From the deglutition center (efferent fibres) motor impulses travel
through cranial nerves (glossopharyngeal and vagus nerves) and
reach the musculature of the pharynx, soft palate and upper
esophagus
• The esophagus muscles are the effectors of the reflex action
Stages of deglutition.

A. Preparatory stage

B. Oral stage

C. Pharyngeal stage

D. Esophageal stage

Swallowing or Deglutition
• Swallowing can be divided into 3 phases:
– The oral voluntary phase
– The pharyngeal phase
– The esophageal phase

Oral voluntary phase

• This phase is initiated by separating a bolus of food from the
quantity of food in the mouth with the tip of the tongue and moving
it into the mid-line of the tongue
• Bolus to be swallowed is moved upward and backward in the
mouth by first pressing the tip of the tongue and later the more
posterior portions of the tongue as well against the hard palate
• This propels the bolus into the pharynx where it stimulates the
touch (oropharyngeal) receptors that initiate the swallowing reflex
Pharyngeal Phase
• Pharyngeal stage is an involuntary stage.
• In this stage, the bolus is pushed from pharynx into the esophagus.
• Pharynx is a common passage for food and air & it divides into larynx
and esophagus.
• Larynx lies anteriorly and continues as respiratory passage.
• Esophagus lies behind the larynx and continues as GI tract.
• Since pharynx communicates with mouth, nose, larynx and esophagus,
during this stage of deglutition, bolus from the pharynx can enter into
four paths:
i. Back into mouth
ii. Upward into nasopharynx
iii. Forward into larynx
iv. Downward into esophagus.
• However, due to various coordinated movements, bolus is made to enter
only the esophagus.
• Entrance of bolus through other paths is prevented as follows:
Back into Mouth
• Return of bolus back into the mouth is prevented by:
i. Position of tongue against the soft palate (roof of the mouth)
ii. High intraoral pressure, developed by the movement of tongue.
Upward into Nasopharynx
• Movement of bolus into the nasopharynx from pharynx is prevented by
elevation of soft palate
Forward into Larynx
• Movement of bolus into the larynx is prevented by the following actions:
i. Approximation of the vocal cords
ii. Forward and upward movement of larynx
iii. Backward movement of epiglottis to seal the opening of the larynx (glottis)
• All these movements arrest respiration for a few seconds- called deglutition
apnea.
Deglutition apnea or swallowing apnea
• Refers to temporary arrest of breathing or the arrest of breathing during
pharyngeal stage of deglutition.
Entrance of Bolus into Esophagus
• As the other three paths are closed, the bolus has to pass only through
the esophagus by the combined effects of various factors:
i. Upward movement of larynx stretches the opening of esophagus
ii. Simultaneously, upper 3 to 4 cm of esophagus relaxes. This part of
esophagus is formed by the cricopharyngeal muscle and it is called
upper esophageal sphincter or pharyngoesophageal sphincter
iii. At the same time, peristaltic contractions start in the pharynx due to
the contraction of pharyngeal muscles
iv. Elevation of larynx also lifts the glottis away from the food passage.
• All the factors mentioned above act together so that, bolus moves
easily into the esophagus.
• Whole process takes place within 1 to 2 seconds and this process is
purely involuntary.
Oesophageal phase
• Is an involuntary stage and in this stage, food from esophagus enters the stomach.
• Esophagus forms the passage for movement of bolus from pharynx to the stomach.
• Movements of esophagus are specifically organized for this function and the
movements are called peristaltic waves
• Peristalsis means a wave of contraction, followed by the wave of relaxation of
muscle fibers of GI tract, which travel away from mouth.
• By this type of movement, the contents are propelled down along the GI tract.
• When bolus reaches the esophagus, the peristaltic waves are initiated.
• Usually, two types of peristaltic contractions are produced in esophagus:
I. Primary peristaltic contractions
• Start when bolus reaches the upper part of esophagus and it pass down through the
rest of the esophagus, propelling the bolus towards stomach.
• Pressure developed during the primary peristaltic contractions is important to propel
the bolus.
• Initially, the pressure becomes negative in the upper part of esophagus due to the
stretching of the closed esophagus by the elevation of larynx.
• But immediately, the pressure becomes positive and increases up to 10 to 15 cm of
H2O.
II. Secondary peristaltic contractions
• This start if the primary peristaltic contractions are unable to propel
the bolus into the stomach, the secondary peristaltic contractions
appear and push the bolus into stomach.
• Secondary peristaltic contractions are induced by the distention of
upper esophagus by the bolus.
• After origin, these contractions pass down like the primary
contractions, producing a positive pressure.
Role of Lower Esophageal Sphincter
• Distal 2 to 5 cm of esophagus acts like a sphincter - called lower
esophageal sphincter and It is constricted always.
• When bolus enters this part of the esophagus, this sphincter relaxes so
that the contents enter the stomach. After the entry of bolus into the
stomach, the sphincter constricts and closes the lower end of
esophagus.
• Relaxation and constriction of sphincter occur in sequence with the
arrival of peristaltic contractions of esophagus.
DEGLUTITION REFLEX
• Beginning of swallowing is a voluntary act, later it becomes involuntary and is carried out
by a reflex action called deglutition reflex.
• It occurs during the pharyngeal and esophageal stages.
Stimulus
• When the bolus enters the oropharyngeal region, the receptors present in this region are
stimulated.
Afferent Fibers
• Afferent impulses from the oropharyngeal receptors pass via the glossopharyngeal nerve
fibers to the deglutition center.
Center
• Located at the floor of the fourth ventricle in medulla oblongata of brain.
Efferent Fibers
• Impulses from deglutition center travel through glossopharyngeal and vagus nerves
(parasympathetic motor fibers) and reach soft palate, pharynx and esophagus.
• Glossopharyngeal nerve is concerned with pharyngeal stage of swallowing.
• Vagus nerve is concerned with esophageal stage.
Response
• Reflex causes upward movement of soft palate, to close nasopharynx and upward
movement of larynx to close respiratory passage so that bolus enters the esophagus.
• Now the peristalsis occurs in esophagus, pushing the bolus into stomach.
Gastric Motility
• Gastric motility is a spontaneous peristaltic movement of the
stomach that aid in digestion, moving of the food through the
stomach and out the pyloric sphincter into the duodenum.
• This sub-serves the following important functions:
1. It allows the stomach to serve as a reservoir for large
quantities of food ingested until it can be accommodated in the
lower segments of the GI tract
2. It helps in mixing the food inside it with gastric secretions so
that digestion can begin and mixing helps to form a semi-fluid
mixture called chime
3. It also helps in emptying gastric contents into the small
intestine at a rate suitable for proper digestion (this prevents
duodenal ulceration)
Structure of the stomach
 consists of the
following:
1. Fundus
2. Body
3. Antrum
Fundus and body
• Contractions of the fundus and body of the stomach are normally weak
• Walls are relatively thin and distensible
• Therefore, the fundus and body of the stomach can accommodate
volume increases as large as 1.5L without an appreciable increase in
intra-gastric pressure
• Hence serves as reservoir function of the stomach
Antrum
• Capable of vigorous contractions
• These contractions mix antral chyme thoroughly with gastric juice and
help in breaking the food particles into small bits
• Antral contractions also helps in emptying the stomach contents in
small quantities at a time into the duodenum.
Note:
• Rate of gastric emptying is well controlled so that chime is not
delivered into the duodenum too rapidly (preventing duodenal
ulceration)
Gastric motility
• Gastric contractions usually begin in the middle of the body of the
stomach and travel toward the pylorus.
• The contractions increase in force and velocity as they approach the
gastro-duodenal junction
• Hence the major mixing activity occurs in the antrum
• Unlike small intestine muscle which contracts only when action
potential spikes are generated
• The stomach contracts in response to slow waves, provided the waves
are above threshold value
• Action potential need not be generated before the stomach muscle
contracts
Note:
• Ach and hormone gastrin stimulate gastric contractility
• By increasing the amplitude and duration of the plateau phase gastric
slow wave.
• Noradrenaline has the opposite effect
Dr Juakali
• Stomach contents pass through the gastro-duodenal junction (pylorus) into
the first part of the duodenum
• Gastro-duodenal junction regulates the rate of gastric emptying into the
duodenum and prevents regurgitation of duodenal contents back into the
stomach
• Gastric mucosa is highly resistant to acid but may be damaged by bile
• Duodenal mucosa has the opposite properties i.e. it is highly resistant to bile
but may be damaged by acid
• Hence too rapid gastric emptying may lead to duodenal ulcers while
regurgitation of duodenal contents into the stomach may lead to gastric
ulcer
• Pylorus is innervated by both sympathetic and parasympathetic (vagus)
nerves
• Sympathetic stimulation increases the constriction of the pyloric sphincter
• Vagal stimulation is both excitatory and inhibitory to the pyloric smooth
muscle
• Stimulatory vagal fibres are cholinergic
• Inhibitory vagal fibres release VIP that relaxes the sphincter
Note:
• Cholecystokinin(CCK)
• Gastrin
• Gastric inhibitory polypeptide and secretin cause constriction of the
pyloric sphincter
Regulation of gastric emptying
• Rate of gastric emptying is regulated by signals from both:
A. Stomach
B. Duodenum
• Stomach signals are elicited by
1. Distension of the stomach by food leading to generation of nervous
signals
2. Presence of certain types of food in the stomach cause the hormone
(gastrin) to be released from the antral mucosa
• Both 1 and 2 increase the force of antral peristalsis i.e. pyloric pumping
• And at the same time inhibit the pyloric sphincter promoting stomach
emptying.
In the duodenum
• Excess volume of chyme or excess of certain types of chyme in the duodenum
initiates strong negative feedback signals which are both nervous and hormonal
• These signals depress the pyloric pump and increase pyloric sphincter tone
• The neural component of the duodenal signal is known as the enterogastric
reflex and the reflex can be elicited by:
1. The degree of distension of the duodenum
2. Irritation of the duodenal mucosa
3. Degree of acidity of the chyme reaching the duodenum. Duodenal pH < 3.5 to 4
elicits this reflex
4 . Osmolarity of the chyme (Hypo or Hypertonic) fluids especially hypertonic
fluids will elicit the reflex
5. Presence of certain breakdown products of proteins and probably fats
Note
• Cholecystokinin hormone
• Secretin hormone
• Gastric Inhibitory Peptide all can inhibit gastric emptying through the enter-
ogastric reflex
Gastric Motility Disorders
1. Delayed gastric emptying (Gastroparesis):
• Obstruction by an ulcer or tumour. Pyloric sphincter may not open
enough/ at the right times to allow food to pass through.
• Normally rhythmic 3/minute contractions of the lower part of the
stomach can become disorganised so that the contents of the
stomach are not pushed towards the pyloric sphincter.
2) Rapid gastric emptying(Damping syndrome);
• Happens when the upper end of the small intestine(jejunum) fills
too quickly with undigested food from the stomach.
3) Functional dyspepsia:
• Many patients have pain or discomfort that is felt at the centre of
the abdomen. Present with Fullness, Early satiety, bloating, nausea.
Motility of the small intestine
• The small intestine consists of the:
1. Duodenum
2. Jejunum
3. ileum
• The duodenum and the jejunum is the site of the digestion
and absorption in the GIT
• The movements of the small intestine mix chime with
digestive secretions
• And bring fresh chime into contact with the absorptive
surface of the microvilli and propel chime toward the colon
• There are two types of movement in the small intestine viz:
1. Mixing contraction or segmentation contractions
2. Propulsive movements or peristaltic movements
Movements of small intestine
This division into two types of movements is artificial because all movements of the
small intestine cause at least some degree of both mixing and propulsion
Note:
the contents of the ileum empty gradually into the colon through the ileo-caecal valve
1. Mixing or segmentation contractions
• Most frequent type of movement by the small intestine
• Occurs at a frequency of 8 to 12 times per minute
• The higher rates occur in the duodenum and the lower rates
in the ileum
• Several segmentation contractions occurs simultaneously
along the small intestine giving appearance of a sausages to
the intestine
• As one set of segmentation contractions end, a new set
begins but the sections between the previous contractions
are the ones that now contract
• Segmentation contractions depend mainly on reflex signals
generated in the myenteric plexus of the gut in response to
distention of the intestine
2. Propulsive movements or peristaltic movements
• Occurs less frequently than segmentation in the small intestine
• Waves travel only a short segment of the intestine-rarely more
than 10 cm leading to a relatively low rate of net propulsion
of chyme in the small intestine and allows time for digestion
and absorption
• Small intestine is about 5 m in length and chyme takes about
2 to 4 hours to move from the pylorus to the ileo-caecal valve
• Peristaltic movement of the intestine is greatly increased after
meal due partly to the entry of food into the duodenum, but
also by gastroenteric reflex or gastro-ileal reflex initiated by
stomach distension and conducted down to the intestine
through the myenteric plexus.
Motility of the colon
• The colon has the following functions:
1. Absorption of water and electrolytes from the chyme.
• Colon receives 500 to 1,500 ml of chyme per day from the ileum
• Feces normally contain 50 to 100 ml of water each day
• Hence most of the water and salts that enter the colon is absorbed
2. Storage of fecal matter until it can be expelled.
• Proximal half of the colon is concerned mainly with absorption
• Distal half is concerned with storage
• Intense movements are not required for these functions, movements
of the colon are normally sluggish
• Motility of the colon is similar to that of the small intestine and can
be divided into:
a) Mixing movements
b) Propulsive movements
Mixing movements
• During mixing movement, the circular muscles contract and
sometimes almost lead to occlusion of the gut lumen and at the same
time the tineae coli muscle contracts
• Combined contraction of the circular muscles and longitudinal
muscles (tineae coli) cause the un-stimulated part of the large to
bulge outward into bag-like sacs called haustrations
• Contractions last about a minute and then disappear, only for new
haustral contractions to occur a few minutes later in other areas near
the previous ones
• Haustral contractions bring the colonic contents close to the surface
of the large intestine and allow most of the water and salts to be
reabsorbed.
• Haustral contractions also result in slow propulsion of the colonic
contents especially in the caecum and ascending colon.
• From the transverse colon to the sigmoid colon, the propulsive
movements are called mass movements
• Mass movements involve powerful contraction of a large segment of
the colon
• (About 20 cm or more at a time)
• At the same time forcing the colonic contents down to the next
segment of the large intestine
• Mass movements can occur at any part of the colon, but they are more
frequent in the transverse or descending colon
• When mass movements have forced a mass of faeces into the rectum,
the desire to defecate is felt
• Mass movements are initiated in part by gastro-colic and duodenocolic
reflexes
• As in other segments of the GI tract, the intramural plexuses control
the contractile behavior of the colon While autonomic nerve reflexes
modify the response
• Mass movements is initiated by intense stimulation of the
parasympathetic nerves or by overdistension of a segment of the colon
DEFECATION
• Act of passing feces
• Complex behavior
involving both reflex and
voluntary actions
• Defecation center is
located in the sacral
segments of spinal cord
• The rectum is normally
empty
• When feces are pushed
into the rectum by mass
movements the urge to
defecate is felt
• Anal sphincter however
prevent escape of feces
unless the individual is
prepared for defecation Defecation reflex : 1. Afferent and efferent fibers of the reflex pass through pelvic (parasympathetic)
nerve
2. Voluntary control of defecation is by pudendal (somatic) nerve
• There are two anal sphincters viz:
1. Internal anal sphincter
• -Consists of circular smooth muscle that is in the anal wall
and supplied by parasympathetic nerves
2. External anal sphincter
• Consists of striated voluntary muscles surrounding the
internal anal sphincter and extends distally and supplied by
somatic nerves and is under voluntary control
• Process of defecation can be subdivided into two main
components:
1. The part under the defecation reflexes
2. The part under voluntary control
 The defecation reflexes
• There are two types of defecation reflexes:
1. Intrinsic defecation reflex
• Mediated through the myenteric plexuses
• Occurs when feces enter the rectum causing distension of the
rectal wall which initiate peristaltic waves.
• These peristaltic waves spread to the descending colon,
sigmoid colon and rectum forcing feces towards the anus
• As the peristaltic waves approach the anus, the internal anal
sphincter relaxes
• If the external anal sphincter is also relaxed, defecation occur
• Peristaltic waves produced by the intrinsic defection reflex is
normally weak and may not be effective in causing defecation
2. Parasympathetic defecation reflex
• Peristaltic waves produced by the intrinsic defecation reflex is
normally weak and may not be effective in causing defecation
• This weak contraction is often reinforced by contractions
mediated by the parasympathetic defecation reflex which
involves parasympathetic nerves in the sacral segment of the
spinal cord
• Distension of the rectum causes afferent parasympathetic
impulses to be transmitted into the spinal cord
• From the spinal cord, efferent parasympathetic impulses are
conducted through the nervi erigentes back to the descending
colon, sigmoid colon, rectum and anus
• These parasympathetic impulses augment the ineffectual weak
movements produced by the intrinsic defecation reflex so that
they become very powerful and effective in emptying the bowel
• Sometimes, the movements are so powerful that they cause emptying of
the large bowel in one movement all the way from the splenic flexure to
the anus
• In spite of the two reflexes above, defecation can only occur if the
circumstance is socially acceptable for the act
• For example, if a student feels the urge to defecate during a lecture, The
student will not give way to that urge, neither will any normal grown up
person give way to the urge to defecate in a public bus
• The ability not to defecate in such circumstances is due to the fact that the
conscious mind takes over voluntary control of the external anal sphincter
• Relaxation of the internal anal sphincter and forward movement of the
feces towards the anus normally cause an instantaneous contraction of the
external anal sphincter
• Impulses coming from the cerebral cortex which pass through the somatic
nerves to the external anal sphincter will either inhibit the sphincter
(relax) to allow defecation occur or further contract it if the environment
is not conducive for defecation to occur
• If the situation is not conducive for defecation to occur, after a few
minutes, the urge to defecate passes off and will not return until more
feces enter the rectum and another reflex is initiated
• When the situation is right for defecation to occur, the defecation
reflex is followed by relaxation of the external anal sphincter
• In addition, intra-abdominal pressure is elevated to aid in the
expulsion of feces
• Evacuation is normally preceded by a deep breath, so that the
diaphragm descends towards the abdominal cavity
• The glottis is closed is closed and contraction of the respiratory
muscles on full lungs raises the intra-thoracic and intra-abdominal
pressure
• Contraction of the muscles of the wall of the abdomen causes a
further increase in intra-abdominal pressure
• The additional pressure generated by this bearing down effort as well
as the strong contractions of the defecation reflex helps to force feces
out of the anus through the relaxed sphincter
GASTROINTESTINAL SECRETIONS
• The GIT from the mouth to the anus, produces secretions that
make it possible for the tract to perform its functions of:
i. Mixing
ii. Propulsion
iii. Digestion and absorption of nutrients
• Main secretions of the GIT are:
1. Saliva (secretion of salivary glands)
2. Gastric secretion
3. Pancreatic secretion
4. Secretion of bile by the liver
5. Secretions of the small intestine
6. Secretions of the large intestine
Secretion of Saliva
• Watery fluid secreted into the mouth.
• Produced by the major salivary glands as follows:
1. Parotid – Produces entirely serous type of secretion
2. Sublingual – Produces only the mucous
3. Submaxillary or submandibular glands-Secretes both serous and
mucous
Properties of saliva
1. Volume: 1000 to 1500 mL of saliva secreted per day & approximately
about 1 mL/minute. Under normal conditions, output of saliva is about
0.5 mL per minute. But during mastication, output can rise to about 4 mL
per minute. Rate of secretion of saliva varies with activities of the body
2. Reaction: Mixed saliva from all the glands is slightly acidic with pH
of 6.35 to 6.85
3. Specific gravity: Ranges between 1.002 and 1.012
4. Tonicity: Saliva is hypotonic to plasma. Saliva has a pH of about 7.0
Major salivary glands
Classification of Salivary Glands
• Classified into three types, based
on the type of secretion:
1. Serous Glands
• Made up of serous cells mainly.
• Secrete thin and watery saliva
rich in alpha amylase (ptylin)-
enzyme that digests starch
2. Mucus Glands
• Made up of mucus cells mainly.
• Secrete thick, viscous saliva rich
in mucin - for lubrication
purposes
3. Mixed Glands
• Made up of both serous and
mucus cells. Acini and duct system in salivary
glands
Composition of Saliva
• Saliva contains:
1. Water -Account for
99.5 % of the serous
secretion
2. Alpha amylase –
(ptylin)
3. Electrolytes -Na+, K+,
Ca+, Cl-, HC03-,
Thiocyanate, Iodide
4. Mucin
5. Lysozymes
6. Blood group factors
7. Carbonic anhydrase
8.Lingual lipase
Composition of saliva
Functions of saliva
1. Alpha-amylase helps in digestion of cooked starch
• Amount of cooked starch which the alpha-amylase in saliva can digest
depends upon how much the food is mixed with saliv.a
• Alpha-amylase is active until pH falls below 4 and up to 50% of the
starch may have been hydrolyzed before inactivation occurs
2. Aids speech by keeping the mouth moist so that the lips and tongue can
move easily to produce speech (Clear fluent speech facilitation)
3. It is important for taste
• Enables molecules to dissolve on the surfaces of the tongue, thereby
bringing the molecules in contact with the taste buds and this leads to
stimulation of the taste buds.
4. It keeps the teeth and the mouth clean
• Thereby preventing dental caries and unpleasant odour from the mouth
• Saliva helps to wash away oral pathogenic bacteria and the food particles
that provide metabolic support for the oral pathogens
• Dental caries is inhibited by salivary bicarbonates which
neutralizes residual acid either ingested acid or that produced by
oral bacterial (Buffering action)
5. Saliva is bactericidal
• Thiocyanate ions, immunoglobins and the proteolytic enzymes in
the saliva (lysozymes) help to kill oral bacteria
6. It prevent calcium from dissolving out of the teeth
• At its normal pH 7.0, saliva is saturated with Ca2+ which prevents
loss of Ca2+ ions from the teeth into saliva
7. It aids swallowing
• The mucin content act as a lubricant during swallowing
• Water in the saliva mixes with the food (e.g. dry biscuits) during
chewing converting it into a semi-solid consistency that can be
easily swallowed.
8. It provide optimal pH for the digestive action of salivary amylase
Secretion of Saliva
• Secretion of saliva occurs in two stages:
1. Acini of the salivary glands produce a primary secretion consisting of
i) Salivary amylase
ii) Mucus
iii) A watery fluid
• Whose composition is essentially the same as the ECF
2. Modification of the primary fluid by the salivary ducts
• As the primary fluid flows through the salivary ducts, there is active
secretion of bicarbonate into the duct lumen while Cl- ions are reabsorbed
• Bicarbonate secretion is catalyzed by carbonic anhydrase which speeds up
the conversion of CO2 and H20 to carbonic acid which then dissociates to
bicarbonate and H+ ions
• Also in the duct, Na+ are actively reabsorbed while K+ ions are actively
secreted in exchange for Na
• As a result the Na+ ion concentration in saliva is much lower than in the
ECF, while potassium is much higher in the saliva than in the ECF
Rate of salivary secretion
• When saliva secretion is maximal, rate of secretion can
increase up to 20 x the basal secretion rate.
• When rate of secretion is very high the primary secretion
flows so fast through the duct that modification of the
secretion in the duct is greatly reduced.
• As a result of this, the concentrations of sodium and chloride
in saliva rise because their reabsorption is greatly reduced.
• While that of potassium concentration is reduced to about 4X
that of the plasma
Nervous regulation of salivary secretion
• Salivary glands are stimulated by both the:
1. Sympathetic
2. Parasympathetic divisions of the ANS
Parasympathetic stimulation of nerve supply to salivary glands
• Results to copious watery secretion rich in Ptylin but poor in other
proteins
• There is also marked vasodilation, hence increased blood flow in the
gland
Sympathetic stimulation of nerves supply to salivary glands
• Causes vasoconstriction and scanty viscous secretion of saliva.
• Salivary secretion is also controlled by nervous control mechanisms
through:
1. Conditioned reflexes
2. Unconditioned reflexes
1. Conditioned reflexes
• Need previous experiences and learning
• Elicited by the presence of food in the mouth or taste of food
• Here afferent impulses from the mouth (pharynx and esophagus) are
conveyed to the salivatory centers in pons and medulla of the brain
stem.
• From salivary center efferent impulses are returned through the
parasympathetic pathway to salivary glands leading to reflex salivary
secretion.
• Smelling or hearing about food or even thinking of food impulses
from higher centers in the brain are sent to salivatory nuclei leading
to copious salivation.
Unconditioned reflexes
• Inborn reflexes that does not need previous learning
• Elicited by mechanical or chemical stimulation of the:
i. Taste buds in the tongue,
ii) Mucus membrane of the mouth
iii) Irritation of the lower part of the esophagus or stomach or
upper part of the intestine cause afferent impulses to salivatory
nuclei → reflex salivary secretion
iv) With nausea which precedes vomiting copious salivation also
occurs
Gastric secretion
Functional anatomy of the stomach
• Stomach is a muscular sac which is
divided into 4 parts:
1. The cardia
2. Fundus
3. Body
4. Pyloric antrum
1. Cardiac orifice:
• Opening of the esophagus into stomach
and kept closed by a cardiac sphincter
2. Pyloric orifice
• Connection of the pyloric antrum to the
duodenum
• Pyloric sphincter keeps this orifice
closed & controls the rate of gastric
emptying. Gastric Glands
• Gastric mucosa consists of simple branched tubular glands, packed
tightly together and arranged perpendicular to the surface
• Groups of glands open into gastric pits which in turn open into the
mucosa surface
• In the mucosa of the antrum, the gastric glands are lined by mucus-
secreting cells only
• While in the mucosa of the remaining parts of the stomach the glands are
lined with:
1. Mucus cells- produce mucus
2. Parietal cells – Produce HCl + intrinsic factor
3. Peptic (chief) cells - Pepsinogen 
• Tubular glands of the gastric mucosa secrets the gastric juice
• Gastric juice contains:
• HCl, pepsinogens, mucus, water, electrolytes (Na +, K+, HC03-), intrinsic
factor and other enzymes: gastric lipase, lysozymes, renin, urease,
carbonic anhydrase, gastric amylase &gelatinase (small qties)
Note:
1. The surface epithelial cells lying between the gastric pits produce –
HC03- rich secretion
2. HC03- + mucus from mucus producing cells = protect gastric mucosa
from damage by gastric acid and the pepsins
3. Gastric mucosa is protected from acid by a mucus layer (1 mm
thicker) which traps beneath it.
Blood supply to the stomach
• Stomach has a very rich blood and lymphatic supply
Nervous supply to the stomach
• Its parasympathetic nerves supply comes from - the vagus
• Sympathetic supply comes from – the celiac plexus
Blood supply to the stomach
• Blood flow to a resting stomach is about 0.5 % of the cardiac output
• Whereas in an active stomach it is about 20 % of the cardiac output
Functions of gastric HCl secretions
1. Provides the acid environment necessary for the activation and
optimum activity of the gastric proteolytic enzymes, the pepsins
2. Plays a protective role, destroying bacteria and other potential
pathogens
3. Pepsins have optimum proteolytic activities between pH 2 and 3.
• Formed from precursor (inactive) pepsinogens.
• Pepsinogens are activated by the action of acid or autocatalytic
action of the pepsins
• Once exposed to acid in the gastric lumen, the pepsinogen molecules
are cleaved and active pepsins are released.
• Pepsin act as auto-catalyst and thereby promote activation of more
pepsins
• Pepsins catalyze the hydrolysis of dietary proteins to form
polypeptide and few free amino acids
4. Mucus protects the mucosal cells from the gastric contents
• Mucus cells are stimulated by parasympathetic fibers in the
vagus nerves and directly by mechanical/chemical irritation
5. Intrinsic factor is a muco-protein produced by the oxyntic cells
• It is important for the absorption of vitamin B12 from diet.
• Intrinsic factor combines with free vitamin B12 and protects it
from digestion.
• Vitamin B12 is usually bound to protein in food and is released
from it either by cooking or by proteolytic enzymes
• Absorption of vitamin B12 occurs in the ileum and intrinsic
factor is required for this process
• Deficiency of intrinsic factor leads to pernicious anemia
• In the parietal cells CO2 from the ECF or
normal metabolism of the gastric cells.
• C02 combines with H20 to form carbonic
acid (H2C03) and in the presence of
carbonic anhydrase the H2C03 dissociates
into H+ ions and HC03-
• HC03- formed as a result of the
dissociation of H2C03 diffuses out of the
gastric cell into the ECF in exchange for
Cl- ion which is actively pumped into the
canaliculi.
• H+ are actively transported into the
canaliculi of the parietal cells
• Active transport of H+ and Cl- into the
canaliculi creates an osmotic gradient
which leads to diffusion of water into the
canaliculi resulting to formation of a HCl Mechanism of Secretion of HCl in
solution inside the canaliculus. the parietal cell of gastric gland
• This acid solution then passes into the
Note:
• Parietal cells are stimulated by:
1. Parasympathetic fiber in the vagus nerves
2. Gastrin hormone
3. Histamine (Exact role of histamine in acid secretion is not
known)
• However, if the histamine H2 receptors in the stomach are
blocked by the H2 receptor blocker (cimetidine), both
histamine and gastrin fail to stimulate acid secretion
• Suggesting that histamine is involved in the mechanism by
which gastrin stimulates gastric acid secretion
Control of gastric secretion
• Gastric secretion is controlled through:
1. Extrinsic or vagus nerves and the intrinsic nerves
• Nerve impulses arising from the vagi nuclei in the medulla oblongata
travel via the vagus to the intrinsic nerve plexus of the stomach wall
and from there to the gastric glands.
• And nervous stimulation results in production of large quantities of
acid, pepsin and mucus
• Vagal stimulation also causes the antral portion of the stomach to
secrete the hormone gastrin.
2. Gastrointestinal hormones
• Gastrin acts on the gastric glands to cause copious flow of highly acidic
juice
• Gastrin is produced by the gastrin cells or G-cells in the pyloric glands
• Small amount of gastrin is also produced by glands in the duodenum
• All these mechanisms are involved in the gastric response to a meal
 Control of gastric secretion is subdivided into 3 phases according to the
origin of the stimuli causing the secretion:
1. Cephalic phase
2. Gastric phase
3. Intestinal phase
• In real life, these 3 phases are not entirely discrete, they merge one into
the other
1. Cephalic phase of gastric secretion
• Accounts for about 10 % of the total secretion associated with meal
• Occurs due to stimulation of afferent/sensory nerves supplying the head
• Occurs even before the food enters the stomach and results from the
sight, smell, thought or taste of food and even hearing the bell that
signifies mealtime as in school boarding house can lead to gastric
secretion
• Afferent impulses from the organs of smell, sight, taste or sound relay to
cerebral cortex or appetite centers of the hypothalamus or amygdala
• From these centers impulses are sent to the dorsal nuclei of the vagi
from where vagal impulses are sent to the stomach which lead to
gastric secretion of acid in the stomach
Note: -
• There are two mechanisms involved in stimulating gastric secretion
1. Neural mechanism
• Vagal impulses stimulate the gastric glands directly-leading to
increased secretion of HCl, pepsinogen and mucus
• Vagal impulses also go to the pyloric glands causing release of
gastrin into the blood.
2. Hormonal mechanism
• Gastrin enters the venous goes to the heart and comes back to the
stomach in the arterial blood
• Gastrin then stimulates the gastric glands to produce more acid and
pepsinogen. Though the mechanism is no clear.
2. Gastric phase of gastric secretion
• Accounts for about 80 % of the total secretion of
gastric juice
• Initiated by the presence of food in the stomach
• As food enters the stomach, it stretches the
stomach wall and this distension stimulates the
gastric glands Via both the extrinsic (vagal) and
intrinsic (nerve plexuses) reflex pathways to
produce gastric juice
• Distension of the pyloric antrum also results in the
release of gastrin into the blood by an intrinsic
reflex
• Some substances in the food called secretagogues
such as (meat extracts, protein, digestion products,
alcohol, bile acids and caffeine) elicit release of
gastrin by the intrinsic reflex
• Histamine also stimulates gastric secretion It is
believed that histamine produced by gastric
mucosa is a pre-requisite for the stimulatory
function of gastrin
• If cimetidine which is an H2 – receptor blocker is
given, both histamine and gastrin fail to elicit acid Vago-vagal reflex
secretion
The intestinal phase of gastric secretion
• As long as food (products of gastric protein digestion) is present in the
duodenum
• It causes secretion of gastric juice above the basal rate
• This effect is mediated by intestinal gastrin from the duodenal mucosa
• However, fats, carbohydrates and acid in the duodenum inhibit gastric
acid and pepsin secretion and gastric motility
• This inhibition is mediated by enterogastric reflex
• Release of several intestinal hormones (secretin, cholecystokinin, &
gastric inhibitory peptide)-are some of hormones that inhibit gastric
secretion
Note:
• Secretin and CCK also stimulate secretion of copious amounts of
pancreatic and biliary secretion,
• Both secretions are alkaline (rich in bicarbonates)
• They neutralize the acidity of the chyme as they move into the
duodenum
Schematic diagram showing the regulation of gastric secretion CCKPZ =
Cholecystokinin pancreozymin, GIP = Gastric inhibitory peptide,
VIP = Vasoactive intestinal peptide.
PANCREATIC SECRETIONS
• The pancreas consists of two portions :
1. The exocrine – Pancreatic juice
2. The endocrine parts - Insulin
• For the purpose of this class, only the exocrine portion will be
considered here
• Bulk of the tissue of the pancreas is composed of exocrine cells
• Exocrine cells produce the pancreatic juice which conveyed into
the duodenum via the pancreatic duct.
• Exocrine portion of the pancreas secretes 1.5Ls of alkaline
pancreatic juice of PH 8 with high bicarbonate content
• Enzymes in pancreatic juice are very important for digestion of
various food materials
Functional anatomy of the pancreas
• Secretory unit of the pancreas is the acini
• Exocrine tissue is divided into lobules by connective tissue septa
• Within the lobules the cells are arranged to form acini around a central
intercalated duct
• Acini cells are responsible for the production of enzyme – rich
component of the pancreatic juice
• The cells of the first part of the ducts within the acini are called centr-
acinar cells & next to the centro-acinar cells are the intercalated ducts
which drain into interlobular ducts
• The interlobular ducts drain into the centrally located main pancreatic
duct which drains into the duodenum
• The other component of pancreatic juice is an alkaline – rich fluid
produced by the cells of smaller ducts (ductules)
• Pancreatic duct unites with common bile duct and both open into the
duodenum at the ampulla of bile duct (ampula of vater) and the opening
at the ampulla is guarded by a sphincter muscle called sphincter of oddi
Composition of the pancreatic juice
1. Water
2. Electrolytes [Na+, K+, Ca2+, Cl-, S042-, HC03-,
and P042-]
3. Enzymes:
• Trypsinogen
• Chymotrypsinogen =} these are
proteolytic enzymes for digestion of
protein into amino acids and Nucleotides
into sugar, phosphates and bases
• Ribonuclease
• Pro-elastase
• α – amylase [starch→maltose, maltoriose
and α-limit dextrin]
• Lipase [Neutral fat → fatty acids
+monoglycerides Connections of the bile cystic
• Cholesteryl esterase [Cholesterol esters and pancreatic ducts
→ cholesterol + fatty acids
Composition of pancreatic juice
• The digestive enzymes present in pancreatic juice include
enzymes that will break down food substances such as: Proteins,
carbohydrates, fats and nucleic acids.
• Proteolytic enzymes are secreted in an inactive form and this is
to prevent the enzymes from digesting the cells that produce
them
• In addition the epithelial lining of the pancreatic duct is weak
• Hence when enzymes are required for digestion, they are
activated by specific enzymes
Examples:
• Enzyme trypsinogen→ Active Trypsin by enterokinase present in
the intestinal villi
• Chymotrypsinogen → Active Chymotrypsins by trypsin
• Proelastase → Active Elastase by trypsin
• Procarboxypeptidase → Active Carboxypeptidases by trypsin
 Pancreatic enzymes and their actions
Enzyme Substrate Products
Trypsin Proteins &Large peptides Smaller peptides, Amino acids

Chymotrypsin Proteins Smaller peptides

Large peptides Amino acids

Elastase Elastin Peptides, Amino acids

Carboxypeptidase Proteins and peptides containing amino Acidic amino acids

acids

α- amylase Starch Maltose

Maltotiose&Dextrins

Lipase Triglycerides Monoglycerides

Free fatty acids

Ribonuclease RNA Nucleotides

Deoxy-ribonuclease DNA Nucleotides

Functions of the alkaline pancreatic juice
1. The alkaline pancreatic juice neutralizes gastric acid poured into the
duodenum
2. It provides an optimum pH for the action of pancreatic enzymes
3. CCK causes secretion of large quantities of digestive enzymes
Control of pancreatic secretion
• The exocrine pancreatic secretion is controlled by two mechanisms:
1. Nervous control
2. Hormonal control
1. Nervous control
• Occurs with cephalic and gastric phase secretion
• Vagal impulses to pancreas stimulate acini leading to secretion of
enzymes
• In this phase there is no flow of pancreatic juice into the duodenum
2. Hormonal control
i) Secretin
• Secreted by the S-cells in mucosa of the duodenum and jejunum
• Presence of HCl from stomach on the duodenal mucosa stimulate the release of this
hormone
• Stimulates secretion and flow of water, bicarbonate and electrolytes by centro-
acinar cells and pancreatic ductules.
• Contract pyloric sphincter and inhibits gastric acid secretion and motility
Note: All these reactions aim to protect the duodenum against the high acidity of
gastric chyme and provide optimum pH for the intestinal enzymes
ii) CCK
• Secreted from the duodenum and jejunum
• Presence of fat and fatty acids, amino acids and acids stimulates secretion of CCK
• Stimulates secretion and flow of enzymes from pancreatic acini and pancreatic
secretion rich in enzymes
• Stimulates contraction of the gall bladder and relaxation of the sphincter of oddi
• Increases the motility of the small intestine and colon
• Inhibits gastric secretion and motility by inhibition of gastrin hormone secretion
Schematic diagram showing the regulation of pancreatic secretion
SECRETION OF BILE
Functional anatomy of the biliary system
• Liver produces bile which has an
important role in lipid digestion in the
duodenum.
• Bile is initially secreted by the liver
cells in the bile canaliculi
• From the bile canaliculi, the bile passes
into the left and right hepatic ducts
• The two ducts unite to form the
common hepatic duct (CHD).
• CHD unite with cystic duct of the gall
bladder to form the CBD.
• CBD unites with the pancreatic duct just
before they enter the ampulla of bile
duct (The ampulla of vater) in the
duodenum Connections of the bile cystic and
• The opening into the duodenum is pancreatic ducts
guarded by the sphincter of oddi
Hepatic lobule
Bile flow
• About 1L of alkaline bile (pH 7.8) is secreted per day by the liver
• During rest the sphincter of oddi is tonically contracted and bile flow into
the gall bladder
• During digestion, the sphincter of oddi is relaxed and bile flows from gall
bladder and liver directly into the duodenum.
• While the bile is stored in the gall bladder, selective reabsorption of
some its constituents occurs
• Ions are absorbed, this is followed by water
• The organic components are not absorbed so that their concentration
increases
• The volume of bile may be reduced to just 10 % of its original value after
the re-absorptive processes
Properties of Bile
1. Volume : 800 to 1,200 mL/day; 2. Reaction : Alkaline
3. pH : 8 to 8.6 4. Specific gravity : 1.010 to 1.011
5. Color : Golden yellow or green.
Composition of Bile
• Bile is considered as secretion of (bile salts-made of cholesterol) and an
excretion of (bile pigments)
• Bile released from the gall bladder into the duodenum has the following
composition:
1. Water
2. Organic constituents [Bile salts, bilirubin,, fatty acids, lecithin and other lipds]
3.Inorganic constituents - Electrolytes [Na+, K+, Ca2+, Cl-, HC03-]
Formation of Bile
• Bile pigments (mainly bilirubin) are derived principally from the breakdown
of Hb, myoglobin and cytochromes which are waste products of these
breakdown
• Bile acids (cholic and chenodeoxycholic acids in man) are produced in the
liver from cholesterol
• These acids are conjugated with glycine or taurine in the liver
• The conjugated bile acid then combines with Na+ to from a bile salts:
i. Sodium glycocholate, sodium taurocholate and
ii. Sodium glycochenodeoxycholate and sodium taurochenodeoxycholate
Gall stones formation
• In the gall bladder an iso-osmotic electrolyte solution is reabsorbed leaving
behind a concentrated solution of bile salts, bile pigments, lecithin and
cholesterol
• Too much cholesterol or insufficient bile salts or lecithin in bile can result
in the precipitation of cholesterol → resulting to the formation of gall-
stones
Entero-hepatic circulation
• Bile is released by the contraction of the gall bladder and it enters the
duodenum after relaxation of the sphincter of oddi
• Bile salts travel along the small intestine and actively reabsorbed in the
terminal ileum where they enter the portal circulation and return to the
liver for recycling – called entero-hepatic circulation of bile salts
• This results to the bile salts being used over and over again (about 16 X)
• Bile salts emulsify fats thereby facilitating digestion
• Other substances which aid in the emulsification process include
cholesterol, lecithin, fat digestion products themselves (Monoglycerides&
fatty acids)
Factors affecting rate of bile secretion
1. Vagal stimulation
• During the cephalic phase of gastric secretion,
vagal impulses are transmitted leading to the
formation of bile by the liver and weak
contraction of the gall bladder
2. Secretin hormone
• Increases the bile flow by increasing
bicarbonate and water secretion by biliary
duct
3. Hepatic blood flow
• Rate of bile secretion is proportionate to the
hepatic blood flow
4. Bile salts
• Increase bile flow from the liver
• They don’t stimulate the formation of new
bile salts by the liver cells
• But when they reach the liver, they are rapidly
secreted, and so increasing the flow of bile Enterohepatic circulation
Gallbladder
• Bile secreted from liver is stored in gallbladder.
• The capacity of gallbladder is approximately 50 mL.
• Gallbladder is not essential for life and it is removed (cholecystectomy) in
patients suffering from gallbladder dysfunction.
• After cholecystectomy, patients do not suffer from any major disadvantage.
In some species, gallbladder is absent.
Functions of gallbladder
1. Storage of Bile
• Bile is continuously secreted from liver. But it is released into intestine only
intermittently and most of the bile is stored in gallbladder till it is required.
2. Concentration of Bile
• Bile is concentrated while it is stored in gallbladder.
• Mucosa of gallbladder rapidly reabsorbs water and electrolytes, except
calcium and potassium.
• But the bile salts, bile pigments, cholesterol and lecithin are not reabsorbed
and so, the concentration of these substances in bile increases 5 to 10 times.
3. Alteration of pH of Bile
• The pH of bile decreases from 8 – 8.6 to 7 – 7.6 and it becomes
less alkaline when it is stored in gallbladder.
4. Secretion of Mucin
• Gallbladder secretes mucin and adds it to bile. When bile is
released into the intestine, mucin acts as a lubricant for movement
of chyme in the intestine.
5. Maintenance of Pressure in Biliary System
• Due to the concentrating capacity, gallbladder maintains a
pressure of about 7 cm H2O in biliary system.
• This pressure in the biliary system is essential for the release of
bile into the intestine.
Filling and emptying of
gallbladder
• Sphincter of Oddi is closed
during fasting and the pressure
in the biliary system is only 7
cm H2O.
• Because of this pressure, the
bile from liver enters the
gallbladder.
• When chyme enters the
intestine, gallbladder contracts
along with relaxation of
sphincter of Oddi the pressure
increases to about 20 cm H2O.
• Because of the increase in
pressure, the bile from
gallbladder enters the intestine. Formation of bile from liver and changes taking
place in the composition of gallbladder bile
Functions of Bile salts
1. Facilitate lipid digestion
• Emulsification of fat: Detergent action of bile salts lower the
surface tension of fat globules leading to breaking of fat globules
into smaller ones that can make an emulsion with water
• Activation of pancreatic and intestinal lipases which secondary to
the emulsification effects on fats which increases the exposed
surface area for enzymatic action
2. Increase bile flow from the liver
• That is choleretic effect: when bile salts are absorbed in the
intestine and go to the liver (enterohepatic circulation)
• They are rapidly secreted and recirculated, thus increasing the bile
flow
3. Solvent action
• Bile salts help the dissolution of cholesterol and prevent its
precipitation and formation of cholesterol stones
4. Stimulate intestinal peristalsis
• This occurs through helping the digestion and absorption of fat because
accumulation of fat inhibits intestinal peristalsis
5. Prevent protein putrefaction
• This effect is secondary to digestion and absorption of fat
• Undigested lipids inhibit intestinal secretion and motility making good
amount of protein reaching the colon undigested and colonic bacteria
then act on protein causing its putrefaction
6. Facilitate lipid absorption
• Bile salts has a hydrotropic effect i.e. it makes lipid miscible with water
which form water soluble complex with phospholipids called micelles
• These micelles carry the insoluble FAs and cholesterol at the center and
ferry them across the unstirred water layer in the small intestine
• Near the villi, FFAs and cholesterol are liberated to be absorbed
• Without micelles the Fats and cholesterol cannot pass through the
unstirred water layer to reach the villi
Bile salts
• Bile salts are made up from cholesterol.
• There are two types of bile salts:
1. Primary bile salts
• Secreted by the liver.
• They are sodium glyco- and tauro-salts of cholic and
chenodeoxycholic acids i.e. sodium glycocholate, sodium
taurocholate, sodium glycochenodeoxycholate and sodium tauro-
chenodeoxycholate.
2. Secondary bile salts
• Derived from primary bile salts by the action of bacteria in the
large intestine.
• Secondary bile salts are the sodium glyco- and tauro-salts of
deoxycholic acid (i.e. derived from cholic acid) and lithocholic acid
(i.e. derived from chenodeoxycholic acid)
Formation of bile salts
Bile pigments
• Are the excretory products in bile.
• Formed during the breakdown of Hb released from the destroyed RBCs in the
reticuloendothelial system
• Bilirubin and biliverdin are the two bile pigments and bilirubin is the major bile
pigment in human beings
Formation and Excretion of Bile Pigments
1. Old RBCs are destroyed in reticuloendothelial system & Hb is released from them
2. Hb is broken into globin and heme
3. Heme is split into iron and the pigment biliverdin
4. Iron goes to iron pool and is reused
5. First formed pigment biliverdin is reduced to bilirubin.
6. Bilirubin is released into blood from the reticuloendothelial cells
7. In blood, the bilirubin is transported by the plasma protein, albumin.
Bilirubin circulating in the blood is called free bilirubin or unconjugated bilirubin
8. Free bilirubin is taken up by the liver cells
9. In the liver, it is conjugated with glucuronic acid to form conjugated bilirubin
10. Conjugated bilirubin is then excreted into intestine through bile.
Fate of Conjugated Bilirubin
1. In intestine, 50% of the conjugated bilirubin is converted into
urobilinogen by intestinal bacteria. First the conjugated bilirubin
is deconjugated into free bilirubin and reduced into urobilinogen.
2. Remaining 50% of conjugated bilirubin from intestine is
absorbed into blood and enters the liver through portal vein
(enterohepatic circulation). From liver, it is re-excreted in bile
3. Most of the urobilinogen from intestine enters liver via
enterohepatic circulation. Later, it is reexcreted through bile
4. About 5% of urobilinogen is excreted by kidney through urine.
In urine, due to exposure to air, the urobilinogen is converted into
urobilin by oxidation
5. Some of the urobilinogen is excreted in feces as
stercobilinogen. In feces, stercobilinogen is oxidized to
stercobilin.
Formation and circulation of bile pigments
APPLIED PHYSIOLOGY
1. JAUNDICE OR ICTERUS
• Condition characterized by yellow coloration of the skin, mucous
membrane and deeper tissues due to increased bilirubin level in blood.
• Normal serum bilirubin level is 0.5 to 1.5 mg/Dl and Jaundice occurs
when bilirubin level exceeds 2 mg/dL.
Types of Jaundice
1. Prehepatic or hemolytic jaundice
• Excessive destruction of RBCs results to an increased blood level of free
bilirubin.
• Excretory function of liver is normal but the quantity of bilirubin
increases enormously & liver cells cannot excrete that much excess
bilirubin rapidly.
• Free bilirubin is insoluble in water and is not excreted in urine, so it
accumulates in the blood resulting in jaundice.
• Formation of urobilinogen also increases resulting in the excretion of
more amount of urobilinogen in urine.
Causes
i. Condition that causes hemolytic anemia can lead to hemolytic jaundice
ii. Renal disorder
iii. Hypersplenism
iv. Burns
v. Infections such as malaria
vi. Hemoglobin abnormalities such as sickle cell anemia or thalassemia
vii. Drugs or chemical substances causing red cell damage
viii. Autoimmune diseases.
2. Hepatic or hepatocellular jaundice
• Occurs due to damage of hepatic cells and so the conjugated bilirubin from liver
cannot be excreted and it returns to blood.
Causes
i. Infection (infective jaundice) by virus, resulting in hepatitis (viral hepatitis)
ii. Alcoholic hepatitis
iii. Cirrhosis of liver
iv. Exposure to toxic materials.
3. Post-hepatic or Obstructive Jaundice
• Occurs because of the obstruction of bile flow at any level of
the biliary system hence bile cannot be excreted into small
intestine.
• So, bile salts and bile pigments enter the circulation. The
blood contains more amount of conjugated bilirubin
Causes
i. Gallstones
ii. Cancer of biliary system or pancreas.
Hepatitis
• Liver damage caused by many agents.
• Characterized by swelling and inadequate functioning of liver.
• Hepatitis may be acute or chronic. In severe conditions, it may
lead to liver failure and death.
Causes and Types
1. Viral infection
2. Bacterial infection like leptospirosis and Q fever
3. Excess consumption of alcohol
4. Excess administration of drugs like paracetamol
5. Poisons like carbon tetrachloride and aflatoxin
6. 8. Inheritance from mother during parturition.
Viral Hepatitis
• Caused by viruses and It is caused by two types of viruses, hepatitis A and
hepatitis B.
Causes of viral hepatitis
i. Mainly by intake of water and food contaminated with hepatitis virus
ii. Sharing needles with infected persons
iii. Accidental prick by infected needle
iv. Having unprotected sex with infected persons
v. Inheritance from mother during parturition
vi. Blood transfusion from infected donors.
• Hepatitis caused by hepatitis B virus is more common and
considered more serious because it may lead to cirrhosis and cancer
of liver.
Features of Hepatitis
1. Fever
2. Nausea
3. Vomiting, diarrhea and loss of appetite
4. Headache and weakness
5. In addition, chronic hepatitis is characterized by:
• Stomach pain
• Paleness of skin
• Dark colored
• urine and pale stool
• Jaundice
• Personality changes.
Cirrhosis of Liver
• Inflammation and damage of parenchyma of liver, resulting in degeneration of
hepatic cells and dysfunction of liver.
Causes
1. Infection
2. Retention of bile in liver due to obstruction of ducts of biliary system
3. Enlargement of liver due to intoxication
4. Inflammation around liver (perihepatitis)
5. Infiltration of fat in hepatic cells.
Features
1. Fever, nausea and vomiting
2. Jaundice
3. Increased heart rate and cardiac output
4. Portal hypertension
5. Muscular weakness and wasting of muscles
6. Drowsiness
7. Lack of concentration and confused state of mind
8. Coma in advanced stages
Gallstones
• Solid crystal deposit that is formed by cholesterol, calcium ions and bile
pigments in the gallbladder or bile duct.
Cholelithiasis
• Presence of gallstones in gallbladder.
Choledocholithiasis
• Presence of gallstones in the bile ducts.
Formation of Gallstones
• Cholesterol present in the bile combines with bile salts and lecithin, & make
the cholesterol soluble in water.
• Under some abnormal conditions, this water soluble cholesterol precipitates
resulting in the formation of gallstone.
• Initially, small quantity of cholesterol begins to precipitate forming many
small crystals of cholesterol in the mucosa of gallbladder.
• This stimulates further formation of crystals and the crystals grow larger and
larger.
• Later, bile pigments and calcium are attached to these crystals, resulting in
formation of gallstones.
Causes for Gallstone Formation
1. Reduction in bile salts and/or lecithin
2. Excess of cholesterol
3. Disturbed cholesterol metabolism
4. Excess of calcium ions due to increased concentration of bile
5. Damage or infection of gallbladder epithelium. It alters the
absorptive function of the mucous membrane of the
gallbladder. Sometimes, there is excessive absorption of water
or even bile salts, leading to increased concentration of
cholesterol, bile pigments and calcium ions
6. Obstruction of bile flow from the gallbladder.
Diagnosis of Gallstone
• Presence of gallstone is diagnosed by ultrasound scanning and
cholangiography. Cholangiography is the radiological study of
biliary ducts after the administration of a contrast medium.
Features
1. Pain in stomach area or in upper right part of the belly under the
ribs.
2. Nausea, vomiting, abdominal bloating and indigestion.
Treatment for Gallstone
3. Cholesterol gallstones can be dissolved over giving 1 to 1.5 gm of
chemo-deoxycholic acid daily. This increases the concentration of
bile acids. So, excessive concentration of bile does not occur.
4. In severe conditions, the gallbladder has to be removed
(cholecystectomy).
5. Laparoscopic surgery is the common method that may be
employed
Secretions of the Small Intestine
• Secretions of the small intestine consist of:
1. Large quantities of mucus secreted by the Brunner’s glands (1 st part of
duodenum)
2. Goblet cells (profusely distributed over the surface intestinal mucosa)
3. Additional mucus is secreted by the goblet cells located in the intestinal
pits called the crypt of Lieberkuhn
• Crypt of Liebarkuhn is located on the entire surface of the small intestine
except the Brunner’s gland area of the duodenum
• Intestinal secretions by crypt of Lieberkuhn is at the rate of about 2L per
day and once secreted, the secretions are rapidly reabsorbed by the villi
• Rapid movement of fluid from crypts to villi provides a watery medium
for the absorption of digested food substances that come into contact
with the small intestinal villi
• Secretion of mucus in the small intestine is in response to direct contact
or irritating stimuli of the intestinal mucosa by chyme, vagal stimulation
and intestinal hormone especially secretin.
`
Duodenal Ulceration
• ­Large quantity of mucus
produced by the Brunner’s
glands protect the duodenal
wall from digestion by gastric
juice
• Failure to produce adequate
mucus by the Brunner’s gland
can lead to development of
peptic ulcer in the first part of
the duodenum

Intestinal gland and villus

Enzymes of the small intestinal secretion
• Secretions of the small intestine with cellular debris contain no
enzymes
• However, epithelial cells of the small intestine mucosa contain
digestive enzymes e.g:
1. Aminopeptidase
2. Amylases (sucrase, maltase, and lactase)
3. Phosphatases
4. Intestinal lipase (small amount)
• Most of these enzymes are in the brush border of the epithelial
cells
• These enzymes at the brush border are not intestinal secretions, but
are released from desquamated intestinal cells.
Digestion and Absorption In the Gastrointestinal Tract
• Food eaten by man can be classified into three main groups:
1. Carbohydrates 2. Fats and 3. Proteins
• All these are complex molecules that cannot be absorbed in their natural
forms through the gastrointestinal mucosa
• Before they are made available for body use, they must be broken down
into smaller molecules which can be absorbed 
Digestion : Breaking down complex food molecules into smaller molecules
which can be absorbed by the body for use. End-products of the digestive
process, as well as water, electrolytes, vitamins and other substances are
then absorbed
Carbohydrates : Made up of monosaccharides joined together to form
disaccharides or polysaccharides of varying length
Proteins : Formed from amino acids joined by means of peptide bonds
Fats : Most of the fat in the diet consists of triglycerides (neutral fats)
which are combinations of three fatty acids molecules joined to a single
glycerol molecule
Digestion of carbohydrates
• The normal human diet contains 3 main types of carbohydrates:
1. Sucrose (a disaccharide known as cane sugar)
2. Lactose (a disaccharide in milk)
3. Starches (Large polysaccharides present in almost all foods especially in grains and
tubers e.g. yam

• Dietary carbohydrate is mainly amylopectin which consists of chains of glucose

molecules joined by 1-4α – linkages, with some branches linked by 1-6 α – linkages
• Amylose consists of straight chains with 1-4α – linkages
• Amylases (most important pancreatic amylase) →hydrolyze carbohydrate to produce
[disaccharides and oligosaccharides)
• Disaccharides and oligosaccharides are then hydrolyzed by the brush border
enzymes (oligosaccharides) to → monosaccharides
• Starch [Digested by Ptylin in saliva (20 - 40%) and pancreatic amylase (50 - 80%]
→Maltose and Isomaltose [digested by Maltase &Isomaltase in the intestine] to →
Glucose
• Lactose [Digested by lactase in the intestine] to → Glucose + Galactose
• Sucrose [Digested by sucrase] → to Glucose + Fructose
Digestion of carbohydrates
Metabolism of carbohydrate
Note:
• Glucose form about 80 % of the final products of carbohydrate
digestion.
• While galactose and fructose account for about 10 % each of
the products of carbohydrate digestion
Digestion of proteins
• Proteins in the diet are derived mainly from:
a) Meat
b) Fish and
c) Vegetables
• They are digested to amino acids by peptidases present at:
i. Brush border of the cells of intestinal villi.
ii. Succus entericus (intestinal secretions) which contain the enzyme
enterokinase/entero-peptidase which activates trypsinogen into trypsin.
iii. Cytoplasm of intestinal mucosal cells
• Protein digestion begins in the stomach by hydrolysis of protein by
pepsins to produce polypeptides plus few free amino acids
• Chyme in the duodenum is subjected to a variety of proteolytic enzymes
produced by the pancreas which releases free amino acids and small
peptides where it hydrolyzes single amino acids from the terminal end of
polypeptides.
• Although, pepsins have a pH of 2-3, appreciable activity persist in the
duodenum
• Once trypsinogen has been activated to trypsin by entero-peptidases
• Trypsin activate more trypsinogen → trypsin
• Chymotrypsinogens A and B are activated → chymotrypsins A and B
• These enzymes hydrolyze polypptides to oligopeptides 2-6 residues
• The pancreatic protease pro-carboxypeptidase is activated by trypsin →
carboxypeptidase in the duodenum
Summary of protein digestion
• Proteins [Activated by pepsin in the stomach] → Proteoses + Peptones +
Large polypeptides [In presence of Trypsin, Chymotrypsin, Carboxy-
peptidase] →Polypeptides + Amino acids → [Peptidases in Small
intestine] → Dipeptides + 2 Amino acids
Digestion of proteins
Metabolism of Protein
Digestion of Fats/Lipids
• The most common fats in the diet are:
1. Neutral fats – called triglycerides and each triglyceride molecule
is composed of 3 fatty acids and a glycerol nucleus
2. Phospholipids (small quantities)
3. Cholesterol: Has no fatty acid but exhibits some of the physical
& chemical properties of fats. It’s derived from fats and it is
metabolized like fats & for these reasons, cholesterol is considered
from the dietary point of view to be fat
4. Cholesterol esters : Contain fatty acids and can be regarded as
fats.
• Digestion of lipids starts in the stomach by the lingual lipase
secreted by the Ebner’s glands on the dorsal surface of the
tongue.
• Lingual lipase which is active in the stomach and can digest as
much as 30 % of the ingested lipids.
• Gastric lipase does not play any important role in lipids digestion
• Most important enzymes involved in the digestion of lipids is the
pancreatic lipase.
• Final digestion of lipids occurs in the small intestine.
• Action of these lipases is greatly helped by emulsifying action of:
1. bile salts,
2. lecithin and
3. Monoglycerides
• which occurs in the small intestine via mixing movements of the
intestine itself and fat digestion products themselves.
• Also the churning action of the stomach assists in the formation of
a coarse emulsion
Note:
• Problem in fat digestion and absorption is not the number of
enzymes involved (because its only one enzyme that is mainly
involved) or difficulty in absorption (because fat is relatively
transported through cell membrane).
• But the fact that fats and water do not mix and fats tend to form
a separate layer or large droplets in water
• Pancreatic lipase is a protein which is water soluble and
therefore can only act on the surface of fat droplet, thereby
breaking the fat droplets into large number of very small
droplets, so that the lipase has a sufficiently large surface area
on which to act.
• The bile salts produced by the liver carryout this emulsification
of fat, thereby facilitating its hydrolysis by digestive enzymes.
• Dietary fats are classified into two types:
1. Saturated fats
• Fats which contain triglycerides formed from only saturated fatty
acids (FAs).
• Fatty acids having maximum amount of hydrogen ions without any
double bonds between carbon atoms are called saturated fatty acids.
2. Unsaturated fats.
• Fats containing unsaturated fatty acids are known as unsaturated
fats.
• Unsaturated fatty acids are fatty acids formed by dehydrogenation
of saturated fatty acids.
• They are classified into 3 types:
i. Monounsaturated fats
ii. Polyunsaturated fats
iii. Trans fats.
i. Monounsaturated fats
• Contain one double bond between the carbon atoms.
ii. Polyunsaturated fats
• Contain more than one double bond between the carbon atoms and
belong to the family of essential fatty acids (required in diet).
• Polyunsaturated fats are of two types:
a) Omega-3 fats or omega3
• Have double bond in the third space from the end of the carbon chain
b) Omega-6 fats or omega6
• Have double bond in the sixth space from the end of the carbon chain.
• Both omega-3 and omega-6 FAs are beneficial to the body.
• However, consuming too much of omega 6 fatty acids s results in
hazards than benefits.
• So, the diet containing 3 : 1 ratio of omega-6 to omega-3 FAs is often
recommended by experts.
• Pancreas secretes 3 Lipolytic enzymes thus:
1. Pancreatic lipase (main Lipolytic enzyme)
• Hydrolyzes triglycerides to release the 2-monglyceride and 2- free
fatty acids molecules
2. Esterase
• Hydrolyzes 2-monoglyceride to glycerol and free fatty acids (FFA)
• Also hydrolyzes triglycerides provided they have been made soluble
by bile salts mixed micelles
3.Phospholipase
• Main enzyme for hydrolysis of phospholipids particularly lecithin
• It also hydrolyzes phospholipids that have been made soluble by
bile salt mixed micelles to lysolecithin and FFA
Digestion of lipids
Gastrointestinal Absorption
• End products of the digestion of the different types of food:
1. Ingested or secreted electrolytes
2. Vitamins
3. Large quantity of water secreted in the various digestive juice
• All the above mentioned must be moved from the lumen of the gut across the
epithelium to the intestinal fluid.
Absorption
• Process of transport of digested products from the gut lumen into the body interstitial
fluid
Note:
• Nature has provided the main absorptive portion of the gut (small intestine with a
large surface area
• This is achieved by the presence of mucosal in-folding called valvulae conniventes
(mucosal folds of small intestine starts from 2nd part of duodenum & are large and
thick at the jejunum & decrease considerably in size distally in the ileum)
• Millions of small villi which project about 1mm from the surface of the mucosa and
a brush border consisting of about 600 microvilli per cell
• Combination of the mucosal in folding, the villi and the microvilli increase the
absorptive surface area of the mucosa about 600 fold
• Absorption through the gastrointestinal mucosa occurs by:
1. Active transport
2. Diffusion
Glucose Absorption
• Glucose are rapidly absorbed across the wall of the small intestine
• Glucose molecules pass from the mucosal cells to the blood in the capillaries & drains
into the portal vein.
• Glucose in the small intestine enters the cells by secondary active transport using a
common symport carrier with Na+
• Transport of glucose is affected by the amount of sodium in the intestinal lumen
because glucose and sodium share the same co-transporter or symport- called the
SGLT(sodium-dependent glucose transporter) or sodium-glucose co-transporter
(SGLT1 and SGLT2).
• SGLT1 and SGLT2 are responsible for facilitated diffusion in that they cross the cell
membrane 12 times
• Since the intracellular concentration of Na+ is low in intestinal cell, Na+ moves into the
cell along its concentration gradient. Glucose moves with the Na + and is released in the
cell
• Na+ is transported into the lateral intercellular spaces and the glucose is transported
from the inside of the cell by GLUT 2 into the interstitium (ECF) and from there to the
capillaries
• Absorption of glucose is by secondary active transport in that the energy for
glucose transport is provided indirectly by the active transport of Na+ out of the
cell
• The removal of transported Na+ from the intracellular space ensures the
maintenance of the concentration gradient of Na+ across the luminal border of
the cell
• So that more Na+ and consequently more glucose can enter the cell
Note:
• Galactose utilizes the same mechanism as glucose
• Fructose utilizes a different mechanism
• Absorption of fructose is independent of Na+ unlike the transport of glucose
and galactose
• Fructose is transported by facilitated diffusion from the intestinal lumen into
the cell of the intestine by GLUT 5 and out of the cells into the interstitium by
GLUT 2
• Some fructose is converted to glucose in the mucosal cells
• All monosaccharides are absorbed into the portal blood draining the small
intestine
Absorption of proteins
• Amino acids (some small peptides) are absorbed in the duodenum and
jejunum into portal blood
• D-amino acids are absorbed passively and slowly across cell membrane
• L-amino acids are absorbed actively by secondary active transport with
Na+ in the same way as glucose
• There seems to be four different types of carriers for amino acids
absorption:
i. One for neutral amino acids
ii. One for basic amino acids
iii. One for acidic amino acids (Glutamic & aspartic acids)
iv. One for imino acids (proline,hydroxyproline & glycine sarcosine)
• Proteins and amino acids absorbed in the intestine come from -ingested
food (50%), proteins of digestive juices (25%) & proteins of
desquamated mucosal cells (25%).
• Almost all proteins are digested & absorbed in the small intestine.
• Proteins in the stools come from bacteria & colonic cellular debris.
• In infants absorption of whole protein occurs by endocytosis at the
luminal side and then by exocytosis at the basal side of the
intestinal mucosal cells.
• This enables the newly born to absorb the antibodies in the
maternal colostrum undigested.
• These antibodies induce passive immunity against many diseases at
this age.
Note:
• However, absorption of whole protein in the intestine declines with
age
• In subjects allergic to certain types of food, they retain the ability to
absorb the undigested antigenic proteins in this food, when these
food enter the blood stream they trigger the immune reactions that
lead to allergy
Absorption of Lipids
• Products of lipid digestion are: Fatty acids, cholesterol &
monoglycerides.
• Emulsifying action of bile salts is enhanced by lecithin and
monoglycerides.
• Bile salts combine with phospholipids to form a complex of water
miscible aggregates called micelles.
• Micelles carry the insoluble fatty acids, monoglycerides and
cholesterol at the center and ferry them across the unstirred water
layer to the brush border of the intestinal mucosal cells leading to the
release of monoglycerides, cholesterol and fatty acids by simple
diffusion through the cell membrane to the inside of cells of intestinal
mucosa.
• In the mucosal cells, most of the monoglycerides are converted into
triglycerides. Triglycerides are also formed by re-esterification of
fatty acids with > 10 to 12 carbon atoms.
• Some of the cholesterol is also esterified
• Triglycerides and cholesterol esters are coated with a layer of
protein, cholesterol and phospholipids to form the chylomicrons.
• Chylomicrons cannot pass through the membrane of the blood
capillaries because of the larger size and so, these lipid particles
enter the lymph vessels and then are transferred into blood from
lymph.
• Fatty acids containing < 10 to 12 carbon atoms enter the portal
blood from mucosal cells and are transported as free fatty acids or
unesterified fatty acids.
• Most of the fats are absorbed in the upper part of small intestine
and the presence of bile there is essential for fat absorption.
Lipid digestion and passage to
intestinal mucosa
• Fatty acids (FA) are liberated
by the action of pancreatic
lipase on dietary triglycerides
and, in the presence of bile
acids (BA), form micelles (the
circular structures), which
diffuse through the unstirred
layer to the mucosal surface.
• Not shown, colipase binds to
bile acids on the surface of the
triglyceride droplet to anchor
lipase to the surface and allow
for its lipolytic activity
Intracellular handling of the
products of lipid digestion
• Absorbed fatty acids (FA) and
monoglycerides (MG) are re-
esterified to form triglyceride
(TG) in the smooth
endoplasmic reticulum (ER).
• Apoproteins synthesized in the
rough ER are coated around
lipid cores, and the resulting
chylomicrons are secreted from
the basolateral pole of epithelial
cells by exocytosis
THE LIVER
Functional Anatomy
• Largest organ in the body and It’s a dual organ having both secretory
and excretory functions.
• Weighs about 1.8kg in the adult male and 1.4kg in the female
• Located in the upper and right side of the abdominal cavity immediately
beneath the diaphragm
• Divided into two parts – a large right lobe and a much smaller left lobe
Hepatic lobes
• Liver is made up of lobes
• Each lobe consists of many lobules called hepatic lobules
Hepatic lobules
• Structural and functional unit of the liver
• There are about 50,000-10,000 lobules in the liver
• The lobule is a honey comb-like structure and it is made up of liver
cells called hepatocytes
Hepatocytes and Hepatic plates
• Hepatocytes are arranged in
columns, which forms the
hepatic plates
• Each plate is made up of two
columns of cells
• In between the two columns of
each plate lies a bile
canaliculus
• In between the neighboring
plates, a blood space called
sinusoid is present
• Sinusoid is lined by the
endothelial cells
• In between the endothelial
cells some special
macrophages called kupffer Hepatic lobule
cells are found.
Portal Triads
• Each lobule is surrounded by many portal triads
• Each portal triad consists of three vessels
i) A branch of hepatic artery
ii) A branch of portal vein
iii) A tributary of bile duct
• Branches of the hepatic artery and portal vein open into the sinusoid
• Sinusoid opens into the central vein
• Central vein empties into hepatic vein
• Bile is secreted by hepatic cells and emptied into bile canaliculus
• From canaliculus, the bile enters the tributary of bile duct
• Tributaries of bile duct from canaliculi of neighboring lobule unite to
form small bile ducts
• These small bile ducts join together and finally form left and right
hepatic ducts, which emerge out of the liver
Blood supply to the
liver
• Liver is supplied by:
1. Hepatic artery
2. Portal vein
• Liver receives
maximum blood
supply of about
1,500mL/minute

Posterior surface of liver

Functions of the liver
• Has several important functions in the body
• Its functions can be divided into three main parts:
1. Vascular functions of storage and filtration of blood
• Act as a reservoir of blood
• Under normal conditions, the volume of blood in the liver is 450mL
• In conditions of increased right atrial pressure e.g congestive cardiac
failure, back pressure to the causes it to expand and 0.5 to 1L of extra
blood can be stored in the hepatic veins and sinuses
• When the precipitating condition is treated, this blood eventually goes
back into the circulation
• Also blood flowing through the GIT picks up many bacteria from
intestines
• These bacteria are passed through the hepatic portal vein to the liver,
the kupffer cells remove them from circulation thereby, cleansing the
blood
2. Metabolic functions – carbohydrate, fat, proteins, vitamins, blood
coagulation factors, iron, drugs, hormones and other substances
Carbohydrate metabolism
• Role of liver in –CHO metabolism are:
1.Storage of glycogen
2. Conversion of galactose and fructose to glucose
3. Gluconeogenesis
4. Formation of several important chemical compounds from the intermediate
products of carbohydrate metabolism
• Liver is very important for maintaining a normal blood glucose
concentration
• When the blood glucose rises above normal as occurs after digestion and
absorption of a carbohydrate meal, liver stores the excess glucose as
glycogen
• If blood glucose level falls below normal, as may occur in prolonged
starvation, the liver converts stored glycogen to glucose to raise the level of
glucose in the blood
• This is called glucose buffer function of the liver
Protein metabolism
• Most critical of the metabolic functions of the liver
• Failure of the liver in respect of protein metabolism for a few days can
lead to death
• Most important functions of the liver in protein metabolism are:
i. Deamination of amino acids
ii. Removal of ammonia from body fluids by formation of urea
iii. Formation of plasma proteins, except the gamma globulins
Fat metabolism
• Some aspects of fat metabolism occurs mainly in the liver include:
i. A high rate of oxidation of fatty acids to supply energy for other
functions in the body
ii. Formation of most of the lipoproteins
iii. Synthesis of large quantities of cholesterol and phospholipids
iv. Conversion of large quantities of carbohydrates s and proteins into fat
• After fat is synthesized in the liver, it is transported in the lipoproteins to
the adipose tissue for storage
Vitamins metabolism
• Liver stores many vitamins, especially vitamins A, D and B12
• The liver stores enough vitamin A to prevent vitamin A
deficiency
• Sufficient vitamin D can be stored to prevent deficiency for 3 to
4 months
• Enough vitamin B12 can be stored to prevent deficiency for at
least a year or sometimes several years
Heat production
• Enormous amount of heat is produced in the liver because of
metabolic reactions
Haemopoietic function
• In fetus (hepatic stage), liver produces the blood cells
• It stores vitamin B12needed for erythropoiesis and iron necessary
for synthesis of Hb
Iron storage
• Apart from the iron in the Hb of the blood, greater portion of iron in
the body is stored in the liver as ferritin.
• Liver cells contains large amounts of a protein called apoferritin
• When the level of iron is high in body fluids, the excess iron
combines with apoferritin to form ferritin which is stored in the
liver.
• When iron in the circulating body fluids fall below normal level, the
ferritin releases iron
• Thus, the apoferritin – ferritin system of the liver acts as a blood
iron buffer as well as an iron storage medium
• Liver is an important source of iron for RBC formation
Hemolytic function
• Senile RBCs after a life span of 120 days are destroyed by
reticuloendothelial cells called the kupffer cells of the liver
3. Secretory and excretory functions
Excretory function
• Liver is important for the removal or excretion of drugs, hormones,
heavy metals (lead, arsenic), bile pigments and other substances
• Liver excretes into bile many drugs e.g sulphonamides, penicillin,
ampicillin and erythromycin
• Several hormones are either chemically altered or excreted by the liver
• These include thyroxine, all steroid hormnes e.g estrogen, cortisol and
aldosterone
• Several other substances are secreted into bile and later released into gut
to be excreted with feces
Formation of bile and excretion of bilirubin
• Bile is formed by the liver cells and one of the many substances excreted
in the bile is the greenish yellow pigment called bilirubin
• Bilirubin is produced from the breakdown of Hb
• Excess bilirubin in the blood leads to jaundice