Gastrointestinal Physiology: Department of Physiology Faculty of Medicine Hasanuddin University Makassar

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GASTROINTESTINAL

PHYSIOLOGY
DEPARTMENT OF PHYSIOLOGY
FACULTY OF MEDICINE
HASANUDDIN UNIVERSITY
MAKASSAR
STRUCTURE
Structure of gastrointestinal
system
– Gastrointestinal tract; oral cavity,
pharynx, esophagus, stomach, small
intestine, large intestine, rectum,
and anal canal
– Accessory organs; tounge, teeth,
salivary glands, liver, and gall
bladder
FUNCTION
Breaking down food and supplying
the body with the water, electrolytes,
and nutrients to sustain life.
Before can be used, food must be:
– ingested
– digested
– absorbed
All of these processes involve
coordinated movement of muscle and
secretion of various substances
INGESTION

Placing food into the mouth


Chewing the food into smaller
pieces (mastication)
Moistening the food with salivary
secretions
Swallowing the food (deglutition)
DIGESTION

 Food is broken down into small particle


by grinding action
 Food is degraded by digestive enzymes
into usable nutrient
– Starches are degraded by amylase into
monosaccharides
– Proteins are degraded by variety of enzymes
(pepsin, trypsin) into dipeptides and amino
acids
– Fats are degraded by lipases and esterases
into monoglyserides and free fatty acids
LEARNING CONCEPT
ORAL CAVITY
PHARYNX
ESOPHAGUS
GI TRACT STOMACH
SMALL INTESTINE
LARGE INTESTINE
RECTUM
STRUCTURE ANAL CANAL

TONGUE
TEETH
ACCESSORY SALIVARY GLANDS
ORGANS PANCREAS
LIVER
GALL BLADDER

INGESTION
SECRETION
FUNCTION DIGESTION
MOVEMENT
ABSORPTION
MOTILITY OF GI TRACT
 The basic mechanisms of GI movement is
peristaltis. Peristaltis is a coordinated pattern of
smooth muscle contraction and relaxation
 Peristaltis helps move food through the pharynx
and esophagus and within the stomach.
Peristaltis plays a minor role in propelling food
through the intestine
 During peristaltis, contraction of small section
of proximal muscle is followed immediately by
relaxation of the muscle just distal to it. The
resulting wavelike motion.
Electrical Activity and
Regulation of Motility
 The smooth muscle of GI tract has spontaneous
rhytmic fluctuations (basic electrical rhytm; BER)
which is initiated by the interstitial cells of Cajal
 The rate of BER is 4/min in the stomach, 12/min
in duodenum and fall to about 8/min in distal
ileum
 Spike potensials playing important role in BER
 Ionic basis of spike potentials is due to Ca2+ influx,
and K+ efflux
 Many neurotransmitter and hormone affect the
BER. Acetylcholine increases BER and
Epinephrine decrease BER
Basic Electrical Activity (BER) of
Gastrointestinal Sooth Muscle
Migrating Motor Complex
 Modification of motor activity during fasting
between periods of digestion
 Each cycle of this activity starts with quiescent
period (phase I), continues with period of
irregular activity (phase II), and ends with a
burst of regular activity (phase III)
 MMCs migrate at a rate of about 5 cm/min,
with interval of 90 minutes
 The function of MMC is to clear the stomach
and small intestine luminal contents in
preparation of the next meal
 MMC immediately stopped by ingestion
Migrating Motor Complexes
III
Stomach Meal
II
I
Propagatian
rate 5cm/min

Distal
Ileum
90 minute
MASTICATION
Function of Mastication

 Breaks food into smaller pieces, which:


– Makes it easier for the food to be
swallowed
– Breaks off the undigestible cellulose
coatings of fruits and vegetables
– Making easier for food to be digested
by digestive enzymes
MASTICATION
Function of Mastication

 Mixes the food with salivary gland


secretions, which:
– Initiates the process of starch digestion
by salivary amylase
– Initiates the process of lipid digestion
by lingual lipase
– Lubricates and softens the bolus of
food, making it easier to swallow
MASTICATION
Function of Mastication

 Brings food into contact with taste


receptors and release odors that
stimulate the olfactory receptors
 The sensations generated by these
receptors increase the pleasure of
eating and initiate gastric secretions
MASTICATION
Mastication Reflex
 Although mastication is a voluntary act, it is
coordinated by reflex centers in he brain stem
that facilitate the opening and closing of the jaw
– When the mouth opens, stretch receptors in the jaw
muscle initiate a refkex contraction of the masseter,
medial pterygoid, and temporal muscle, causing
mouth to close
– When the mouth closes, food comes into contact with
buccal receptors eliciting a reflex contraction of
digastric and lateral pterygoid muscles, causing the
mouth to open
– When the jaw drops, the stretch reflex causes the
entire cycle to be repeated
DEGLUTITION
(SWALLOWING)
 Deglutition or swallowing consists of three
phase:
– Oral (voluntary) phase. During this phase, the
tongue forms a bolus of food and forces it into
the oropharynx by pushing up and back against
the hard palate
– Pharyngeal phase. This phase coordinated by a
swallowing center in the medulla and lower
pons
– Esophageal phase. After reaching the
esophagus, food is propelled into stomach by
peristaltis
Pharyngeal Phase
 This phase begins when the food reaches the
oropharynx and progresses as follows:
– The nasopharynx is closed by the soft palate,
preventing regurgitation of food in to nasal
cavities
– The palatopharyngeal folds are pulled medially,
forming a passageway for the food to move into
the pharynx
– The glottis and vocal cords are closed and the
epiglottis swing down over the larynx, guiding
the food toward the esophagus
 Respiration is inhibited for the duration of
the pharyngeal phase (1-2 seconds)
Esophageal Phase
 Sphincters involved in esophageal peristaltis:
– The upper esophageal sphincter (striated muscle)
– The lower esophageal sphincter (smooth muscle)
 Types of esophageal peristaltis:
– Primary esophageal peristaltis is initiated by
swallowing
– Secondary peristaltis is initiated by the presence of
food within the esophagus
 Coordination of esophageal peristaltis:
– Primary esophageal peristaltis is coordinated by
vagal fibers
– Secondary esophageal peristaltis is coordinated by
the intrinsic nervous system
Esophageal Muscle
Swallowing Mechanism and Regulation
Disorders of Swallowing
 Esophageal reflux, may occur if the intragastric
pressure rise high enough to force the lower
esophageal sphincter open
– During pregnancy
– Reflux of stomach acid causes esophageal pain
 Belching (eructation), following a heavy meal
or ingestion of large amount of gas (e.g., from
carbonated beverages)
 Achalasia, is a neuromuscular disorder of the
lower two-thirds of the esophageal that leads to
absence of peristaltis and failure of the lower
esophageal sphincter to relax
MOTILITY OF STOMACH
Functional components
 The three functional parts of the stomach
are the fundus, corpus, and antrum
 Gastric contents are isolated from other
parts of the GI tract by the lower
esophageal sphincter proximally and by the
pylorus distally
 The antrum and pylorus are anatomically
continous and respond to nervous control as
a unit
MOTILITY OF STOMACH
Musculature
 Each muscle layer forms a functional
syncytium and therefore acts as a unit
 In the fundus, where the layers are
relatively thin, strength of contraction is
weak; in the antrum, where the muscle
layers are thick, strength of contraction is
strong
 The stomach and duodenum are divided by
a thickened muscle layer called the pyloric
sphincter
MOTILITY OF STOMACH
Innervation
 Intrinsic innervation directly responsible for
peristaltis
– The myenteric plexus (Auerbach’s) is located
between the layers of the circular and
longitudinal muscles of the stomach
– The submucosal plexus (Meissner’s) is located
between the layers of the circular muscle and
mucosa on the luminal surface of the stomach
 Extrinsic through autonomic nervous
system:
– Sympathetic, via the celiac plexus (inhibits
motility)
– Parasympathetic, via the vagus nerve (stimulates
motility)
Function of Motility
Gastric motility serves three basic function
 Storage. When food enters the stomach, the
upper region - primarily fundus - enlarges to
accommodate the food by receptive
relaxation
 Mixing. Combination of peristaltis and
retropulsion mixes the food with acid and
enzymes. When the food is mixed into pasty
consistency, it is called chyme
 Emptying. When the chyme is broken down
into small enough particles, it is propelled
through the pyloric sphincter into intestine
Function of Motility
Receptive relaxation
 Initiated as apart of the peristaltic process
causing swallowing and esophageal motility
or in response to food entering the stomach
 Strecth receptors in the upper portion of
stomach detect the presence of food and
initiate a vago-vagal reflex producing
relaxation
 This process regulate by postganglionic
fibers within the enteric nervous system
release a noncholinergic nonadrenergic
transmitter, may be ATP or VIP
Function of Motility
Peristaltis

 Produced by periodic change in BER


originate in a pace maker within longitudinal
muscle
 BER or slow wave occur at a rate of
approximately 3-4/min and velocity is 1
cm/sec at the corpus and increase to 3-4
cm/sec in the antrum
 Ca2+ play an important role in BER, and the
force of peristaltis contractions is regulated
by gastrin and acetylcholine
Function of Motility
Retropulsion

 Is the back and forth movement of the


chyme caused by the forceful propulsion of
food against the closed pyloric sphincter
 The forward and backward movement of the
chyme (caused by peristaltis and
retropulsion) breaks the chyme into smaller
and smaller pieces and mixes it with the
gastric secretions present within stomach
Function of Motility
Gastric emptying
 Each time the chime pushed against the
pyloric sphincter, a small amount (2-7 ml)
may escape into duodenum
 The amount of chyme passing the pylorus
depends on the size of the particles
 Liquids empty much faster than solids. The
rate of liquids emptying is proportional to
pressure within the upper portion of
stomach, which increase slowly during the
digestive period
Functional Disorder of Motility
Vomiting or emesis
 Initiation
– The vomiting center. Directly activated by
afferent fibers or by irritation due to injury or
increases in intracranial pressure
– Chemoreceptor trigger zone. Activated by
afferent nerves originating within the GI tract
or by circulating emetic agents
 Mechanical sequence of vomiting
– Begins with deep inspirasion followed by the
closing of the glottis
– Intestine propels chyme into upper region of
stomach
– Increase in abdominal pressure forces the
chyme into esophagus and out of the mouth
Vomiting Reflex
INTESTINAL MOTILITY
Contractile activity

 Contractile activity of the smooth muscle


lining the small intestine serve two functions:
– Mixing the chyme with digestive enzymes and
bile to facilitate digestion and absorption
– Propelling the chyme from the duodenum to the
colon
 It usually takes about 2-4 hours for the
chyme to move from one end of the small
intestine to the other
INTESTINAL MOTILITY
Types of movements

Segmentation is the most common type


of intestinal contraction
Peristaltic contractions is not
considered to be an important
component of intestinal transit
MMC spreads over the intestine during
interdigestive period
INTESTINAL MOTILITY
Segmentation contractions
 During segmentation, about 2 cm of the
intestinal wall contracts, forcing the chyme
throughout the digestive period
 When the muscle relaxes, the chyme returns
to the area from which it was displaced
 This back-and-forth movement enables the
chyme to become mixes with digestive
enzymes and to make contact with the
absorptive surface of the intestinal mucosa
 Segmentation occur about 12 times/min in the
duodenum and 8 times/min in the ileum. The
contraction last for 5-6 seconds
INTESTINAL MOTILITY
Regulation of intestinal motility
 Segmentation occur only if the slow waves
produce spikes potentials which is controlled by
pacemaker cells within the wall of the intestine
and is not infuenced by neural activity or
circulating hormones
 The frequency of segmentation is directly
related to the frequency of the slow wave
 The strength of segmentation is proportional to
the frequency of the spike potentials generated
by slow wave
 Slow wave amplitude is increased by gastrin,
CCK, motilin, and insulin; and decreased by
secretin and glucagon

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