Gastrointestinal

System

Module 2

MOTILITY OF THE
GASTROINTESTINAL TRACT

Oct, 2010
Module 2. Gastrointestinal Motility
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Module 2. Motility of the Gastrointestinal Tract

CONTENT

1. Introduction to GI motility

2. Musculature of the GIT

2.1. Muscles of the GIT wall
2.2. Sphincters of the GIT

3. Types of GIT motility

4. Oral and esophageal motility (Ingestion, Mastication, Swallowing and

Peristalsis)
4.1. Ingestion
4.2. Mastication
4.3. Deglutition
4.4. Peristalsis
4.5. Clinical conditions associated with esophagus

5. Gastric motility
5.1. Normal gastric functions
5.2. Slow waves in the stomach
5.3 The actions of the stomach on eating
5.4. Migrating motor complex
5.5. Control of gastric emptying

6 Intestinal motility
6.1. Motility of the small intestine
6.2. Motility of the large intestine

7 Colonic motility and defecation

8 Vomiting

9 Disorders of gastric motility

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 Content Pg Comments on mastery
i Abstract
ii Learning resources
iii Background knowledge
iv Terms to know
v Objectives
vi Learning activities
1 Introduction to GI motility
ACTIVITY 2.1: GIT processes
2 Musculature of the GIT
2.1 Muscles of the GIT wall
ACTIVITY 2.2: Musculature of the GIT
2.2 Sphincters of the GIT
ACTIVITY 2.3: Sphincters of the GIT
3 Types of GIT motility
ACTIVITY 2.4: Types of GIT contraction
4 Oral and esophageal motility (Ingestion,
Mastication, Swallowing and Peristalsis)
4.1 Ingestion
ACTIVITY 2.5: Factors regulating food intake
4.2 Mastication
ACTIVITY 2.6: Mastication
4.3 Deglutition
ACTIVITY 2.7: Deglutition
4.4 Peristalsis
ACTIVITY 2.8: Peristalsis
4.5 Clinical conditions associated with esophagus
ACTIVITY 2.9: Disturbances in the esophagus
5 Gastric motility
5.1 Normal gastric functions
5.2 Slow waves in the stomach
ACTIVITY 2.10: Slow waves and spike potentials
5.3 The actions of the stomach on eating
5.4 Migrating motor complex
5.5 Control of gastric emptying
ACTIVITY 2.11: Control of gastric emptying
6 Intestinal motility
6.1 Motility of the small intestine
ACTIVITY 2.12: Motility of the small intestine
6.2 Motility of the large intestine
ACTIVITY 2.13: Intestinal motility

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7 Colonic motility and defecation
ACTIVITY 2.14: Colonic motility
ACTIVITY 2.15: Control of defecation
8 Vomiting
ACTIVITY 2.16: Control of vomiting
9 Disorders of gastric motility
vii Summary
ACTIVITY 2.17: GI reflexes
viii Conclusions
ix Assessment

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I. Abstract

All of the gastrointestinal processes (ingestion, propulsion, secretion, digestion,

absorption, defecation) are designed to provide optimal opportunity for conversion of
macromolecular foodstuff to micromolecular nutrients to be absorbed into the
circulatory system and delivered to the entire body cells. The physical process of
motility that occurs throughout the GIT relates directly to muscle contraction. It is
important in propelling the food through the entire tract, churning and mixing the
luminal content for optimal digestion and absorption, and controlling the movement
from one compartment to another via sphincters. In this module, we’ll discuss the
movement of food materials along the entire GIT due to muscle contraction that
produces motility of the GIT, focusing on the regulatory mechanisms. In addition,
we’ll also look at sphincter muscle contraction and relaxation that controls the flow of
food materials from one segment of the GIT to another. The GIT processes that
depend on muscle contraction include ingestion, propulsion and defecation.

II. Learning resources

1. Notes in this Module
2. Boron and Boulpaep, Ch. 41
3. Widmaier, Raaf and Strang (Vander’s Human Physiology) Ch. 15
4. Marieb. Ch. 24
5. Tortora and Derrickson. Ch. 24
6. Guyton and Hall. Ch. 62
7. Ganong. Ch.25 and 26

III. Background knowledge

1. Principles of homeostasis
2. Principles of the nervous system
3. Principles of the endocrine system
4. Mechanism of smooth muscle contraction
5. Module 1: Introduction to the GI System: Functional Anatomy and Basic GI
Processes

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IV. Terms to Know
Please list down the terms you should know in this module and write in your own words
what the terms mean.

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V. Objectives
On completion of this Module, you should be able to:

1. List and describe the GI processes that involve muscle contraction and state their
significance in terms digestion of foods and absorption of nutrients.
2. Describe the musculature of the GIT including the sphincters and explain the
mechanisms that control contraction of the muscles. Deduce the significance of
contraction of the GIT muscles.
3. Compare and contrast between “peristalsis”, “segmentation” and “tonic
contraction” and discuss their significance.
4. Describe the processes involved in oral and esophageal motility (ingestion,
mastication, swallowing and peristalsis) and give examples of clinical conditions
arising from abnormal oral and esophageal motility.
5. Describe the processes involved in stomach motility and give examples of clinical
conditions arising from abnormal stomach motility.
6. Describe the processes involved in intestinal motility and give examples of
clinical conditions arising from abnormal intestinal motility.
7. Describe the processes involved in motility and defecation.
8. Describe the processes involved in vomiting and explain how anti-emetic drugs
work.
9. Describe the common disorders of GI motility.

Extra objectives

1. Describe the musculature of the GIT and its innervation

2. Describe the sequence of events in swallowing
3. Describe the origin and consequence of the high basal tone found in the upper esophageal
sphincter (UES) and lower esophageal sphincter (LES).
4. State the stimulus that initiates the swallowing sequence. Identify the point at which the
swallowing sequence becomes automatic (independent of voluntary control).
5. Contrast the patterns of external and internal innervations of the upper, middle, and lower
esophagus.
6. Describe the pressure changes that occur in the esophagus as a bolus of food moves from the
pharynx to the stomach, including the pressures immediately oral and aboral to the bolus, and the
pressures in the upper and lower esophageal sphincters.
7. Contrast primary and secondary peristalsis based on initiating event, voluntary control, reflex
propagation, and regions of the pharynx and esophagus involved.
8. Contrast the lower espohageal tone, innervation, and motility defects that lead to heartburn with
those leading to achalasia.
9. Describe the storage, digestion, and motility roles of the stomach.
10. Define receptive relaxation of the stomach and state mechanism and consequence.
11. Describe origin and form of electrical activity and the progression of peristaltic waves across the
body and antrum of the stomach. Include their role in mixing and propulsion of gastric contents
and how the frequency is altered by the volume of gastric contents.
12. Predict the effects of a) meal content (osmolarity, fat content, etc.), b) particle size, and c) volume
on the rate of gastric emptying, including duodenal feedback.

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1. Describe the characteristics of the basic electrical rhythm (BER) of the small intestine and its
relation to smooth muscle contractile activity.
2. Describe the role of “interstitial cells of Cajal” in generation of electrical slow waves, and predict
the consequence of the frequency gradients of electrical slow waves occurring within the intestinal
tract.
3. Explain the functional significance of ongoing activity of enteric inhibitory motor neurons to
intestinal circular muscle.
4. Contrast the patterns of intestinal motility seen during the absorptive phase (segmentation) with
that of the post-absorptive phase between meals [the migrating motility complex (MMC)].
5. Contrast the effects of parasympathetic and sympathetic nervous activity in modulating small
intestinal motility.
6. Describe the effects of distension on small intestinal motility.
7. State effects of increased pressure in the ileum and cecum on the ileocecal sphincter, including
defining the term “gastroileal reflex.”
8. Compare colonic motor activity with the motor activity in the small intestine.
9. Contrast the colonic motor activity during a “mass movement” with that during haustral shuttling
and the consequence of each type of colonic motility.
10. Describe the sequence of events occurring during reflexive defecation, differentiating those
movements under voluntary control and those under intrinsic control

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VI. Learning Activities

1. Introduction to GI motility

Objective 1: List and describe the GI processes that involve muscle contraction
(motility) and state their significance in terms digestion of foods and absorption of
nutrients.

We know that the following processes occur in the GIT (Module 1):
• Ingestion
• Propulsion
• Secretion
• Digestion
• Absorption
• Defecation

The above processes are all geared towards providing optimal opportunity for conversion of
foodstuff to nutrients to be absorbed into the circulatory system and delivered to the entire
body cells. After ingestion, GIT motility helps in the propulsion of food materials from
mouth to anus, during which digestion, secretion and absorption take place. The undigested
materials are removed from the GIT via defecation.

In this module, we’ll discuss the movement of food materials along the entire GIT due to
muscle contraction that produces motility of the GIT, focusing on the regulatory
mechanisms. In addition, we’ll also look at sphincter muscle contraction and relaxation that
controls the flow of food materials from one segment of the GIT to another. The GIT
processes that depend on muscle contraction include ingestion, propulsion and defecation.

• Ingestion is the process of taking a substance into the body through the mouth.
• Propulsion is the antegrade (forward) movement of GIT content due to contraction of
muscles in the wall of the GIT.
• Defecation is the removal of fecal materials via the anus.

Activity 2.1: GIT processes

• List down all the GIT processes. Which of the processes involve muscle contraction?
Explain how muscle contraction is involved in these processes.

• Describe the basic mechanism of regulation of smooth muscle contraction. Relate it to

the above processes.

We will first look at the structures that are involved in the propulsion of materials along
the GIT viz. the musculature and sphincters.

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2. Musculature of the GI tract

Objective 2: Describe the musculature of the GIT including the sphincters and
explain the mechanisms that control contraction of the muscles. Deduce the
significance of contraction of the GIT muscles.

2.1. Muscles of the GIT wall

Motility is directly related to the action of muscles. The vast majority of the muscle in
the GI tract is smooth muscle (Refer to Fig. 1.3, Module 1), with two important
exceptions, the top part of oesophagus and the external anal sphincter. Areas of the gut
which have striated muscle are those areas under conscious rather than autonomic
control.

Contraction of the GIT muscles that results in motility is controlled by both humoral and
neural mechanisms. Innervation of the GIT has been discussed in Module 1. The
extrinsic nervous system, via its parasympathetic neurons that release Ach increases
contraction, whereas the sympathetic neurons that release NE inhibits contraction. In
addition, the intrinsic nervous system also induces contraction when it is stimulated by
the mechanoreceptors and chemoreceptors. The only hormones known to have
physiological effect on motility are motilin (increased gastric motility) and CCK
(decreased gastric emptying).

Activity 2.2. Musculature of the GIT

• Draw a cross section of the GIT to show the location of the muscle layers and how
they are innervated by the extrinsic and intrinsic nerves.
• List the stimuli that can initiate muscle contraction in the GIT.
• How do longitudinal and circular muscles work in propelling the food materials along
the GIT?
• Explain the regulation of muscle contraction that produces peristalsis, segmentation
and tonic contraction.
• Explain how the muscles are involved in ingestion, propulsion, and defecation.

2.2. Sphincters of the GIT

A sphincter is a structure, usually a circular muscle, which normally maintains

constriction of a natural body passage or orifice and which relaxes as required by normal
physiological functioning. Thus, sphincters
• separate two adjacent hollow organs
• function as barriers to flow by maintaining a positive resting pressure
(contraction) between the organs, in which lower pressure prevails.

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 • regulate both antegrade (forward) and retrograde movement (reverse)
movement.

E.g. the resting pressure of the pyloric sphincter controls, in part, the emptying of gastric
contents in to the duodenum. On the other hand, the resting pressure of the lower
esophageal sphincter (LES) serves to prevent gastric contents from refluxing back into
the esophagus and causing gastroesophageal reflux disease (GERD).

Generally, stimuli proximal to the sphincter

cause sphincteric relaxation, whereas stimuli
distal to a sphincter induce sphincteric
contraction.

Six sphincters are present in the GIT, each

with different resting pressure and different
responses to various stimuli (Fig. 2.1). An
additional sphincter, the sphincter of Oddi,
regulates the movements of the contents of
the common bile duct into the duodenum.

Upper esophageal sphincter (UES)

• Consists of striated muscle
• Has highest resting pressure of all
the GI sphincters
• Involves in swallowing
mechanism

Lower esophageal sphincter (LES)

• Consists of smooth muscle which
is anatomically and
pharmacologically distinct from Fig. 2.1. Various sphincters of the GIT
adjacent smooth muscle in the
distal end of the esophagus and proximal portion of the stomach.
• Controls entry of food into stomach and prevents reflux of gastric content into
esophagus.

Pyloric sphincter
• Separates stomach from duodenum
• Regulates gastric emptying and prevents duodenal-gastric reflux

Ileocecal sphincter
• Separates ileum from caecum
• Regulates ileal flow into the colon
• Under control of vagus nerve, sympathetic nerves and the ENS

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Internal and external anal sphincter
• The internal sphincter has longitudinal and circular smooth muscle and under
involuntary control.
• The external sphincter, which encircles the rectum, contains only striated
muscle but is controlled by both voluntary and involuntary mechanisms.
• The high resting pressure of the overall anal sphincter predominantly reflects
the resting tone of the internal anal sphincter.
• The sphincters are involved in defecation reflex (Section 7)

Activity 2.3: Sphincters of the GIT

• With the aid of a diagram, list down all the sphincters of the GIT and state their functions.
Which of these sphincters are made of

smooth muscle?

skeletal muscle?
• Compare and contrast between smooth muscle sphincter and skeletal muscle sphincter.
• How is contraction of sphincters controlled? Please include receptors, control centres and
effectors in your explanation.
• Case on GERD

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3. Types of GIT motility

Objective 3: Compare and contrast between “peristalsis”, “segmentation” and “tonic

contraction” and discuss their significance.

There are three types of muscle contraction in the GIT:

• peristalsis
• rhythmic segmentation
• tonic contraction.

Peristalsis is used to propel chyme from proximal to distal and consists of coordinated
contractions with relaxation ahead which moves as a wave pushing the chyme ahead of it.
Occasionally reverse peristalsis occurs in the small intestine, but the enteric nervous
system, which controls the contraction through local reflexes or intestinointestinal
reflexes, seems to be polarised so peristalsis in the ‘wrong’ direction peters out rapidly.

Segmentation contractions are the most common in the small intestinal and serve to mix
the chyme with the various secretions of the intestines, and also to ensure that the chyme
comes into the maximum contact with the gut wall so that nutrients can be absorbed.
Segmentation consists of several contractions occurring in a piece of gut at any one time,
but several centimetres apart. This serves to segment the gut and makes it look a little like
a chain of sausages. As the contractions fade, a new set begins and this chops the chyme
up and mixes it. Contractions occur at the frequency of the slow waves that is about 12
per minute in the duodenum.

Tonic contractions are contractions which can last for minutes or hours. This is not
related to the slow waves but is independent of it. The most obvious example of tonic
contractions are the sphincters which are found at intervals along the GI tract, most of
which are contracted and therefore closed to passage of chyme under normal conditions.

Activity 2.4: Types of GIT contraction

• Using examples, compare and contrast between peristalsis, segmentation, and tonic
contraction. What is the significance of these processes?
• Where does each occur in the GIT? How are they regulated?

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 4. Oral and Esophageal Motility (Ingestion, Mastication,
Swallowing and Peristalsis)

Objective 4: Describe the processes involved in oral and esophageal motility

(ingestion, mastication, swallowing and peristalsis) and give examples of clinical
conditions arising from abnormal oral and esophageal motility.

4.1. Ingestion

Ingestion is the process of taking a substance into the body through the mouth.

Food ingestion is determined by the sensation of hunger. The regulation of food intake is
coordinated by neurons in 2 areas of the brain: feeding centre (central hypothalamus)
and satiety centre (ventromedial nuclei of the hypothalamus). The satiety centre
operates primarily by inhibiting the feeding centre. These areas are under the influence
of the higher cortical centres (Fig. 2.2).

Activity 2.5: Factors Psychological factors External stimuli (sight, smell)

regulating food intake +/-
•
Cortex
List down the various
stimuli and receptors
+/- +/-
involved in regulation of

•
food intake.
Describe the afferent Feeding centre - Satiety centre
pathways and the
destinations of afferent + +
signals from the
receptors. + GIT sensation
• Describe the role of the Feeding (distension, chemical) +
feeding centre and satiety
centre in the regulation of
food intake.
• What are the effectors Increase in blood
involved in food intake? + nutrients (glucose, amino
• Describe the efferent
pathways from the acids, fat metabolites)
feeding centre to the
effectors.
Fig. 2.2. Factors involved in regulation of food intake
ors
Role of the mouth: mastication (chewing), salivary secretion & swallowing.

Food is taken into the mouth in small quantities and mixed with saliva while being
chewed. This serves 2 purposes:

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 1. To begin breakdown of the food, both mechanically by chewing and chemically
by enzymes in saliva

2. To mix the food bolus with a lubricant i.e. saliva. However, food can be
digested without either chewing or the contribution of the amylases found in
saliva.

4.2. Chewing (Mastication)

The process of chewing or mastication requires coordination of the chewing muscles, the
cheeks, the palate and the tongue. Chewing is normally a reflex action:

• Stimulus: food in the mouth (taste, texture, Activity 2.6: Mastication

temperature)
• Receptor: mechanoreceptor (touch, pressure) in • Explain the importance of mastication.
oral mucosa and periodontum and stretch and
other receptors in the masticatory muscles. • Draw a “box diagram” and describe
• Afferent pathway: lingual nerve, trigeminal nerve the process and control of
• Integration centre: chewing centre (brain stem) mastication.
• Efferent pathway: trigeminal nerve (cranial verve
V) • Is chewing completely voluntary?
• Effector: masseter and temporalis (powerfully Justify your answer.
bring the lower jaw up against the upper jaw) and
the pterygoids (open the jaw, keep them aligned, • How is mastication related to taste of
and moves them sideways, and backwards and the food? Explain how the sensation
forwards for grinding) of taste is accomplished.

A single bite is a voluntary process involving the cerebral cortex. However, chewing
appears to be a programmed pattern of movements organised at a rather low level in the
CNS, involving neurons of the fifth cranial nerve (trigeminal). The chewing centre is
built into the organisation of this group of neurons. Bursts of electrical activity produced
by the cortical masticatory centre are associated with jaw opening and jaw closing.
Afferent information from the receptors to the brain stem inhibit jaw closing when the
biting force rises, and therefore regulate the force applied.

The forces involved in grinding and cutting the food are enormous, and sufficient to
fragment cellulose membranes. Finally, the food is mixed with saliva and formed into a
bolus. The bolus is pushed back into the pharynx, when the tongue is pressed against the
hard palate.

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4.3. Swallowing (deglutition)

Swallowing consists of 3 phases:

1. buccal phase (voluntary)
2. pharyngeal phase
3. esophageal phase

Once the bolus has been adequately chewed, it is moved to the back of the mouth by a
forward to back contraction of the tongue. This is the voluntary phase. Once
swallowing is initiated it cannot be stopped voluntarily. It becomes a classic all-or-none
reflex.

In the pharyngeal phase when the food enters the pharynx, pressure receptors in the
palate and anterior pharynx are activated. This initiates the swallowing reflex:
• Afferent pathway: trigeminal and glossopharynx nerves
• Control centre: swallowing centre in the brain stem
• Efferent pathway:
• Effectors: 25 different skeletal muscles. E.g. Soft palate (elevated  seals
nasal cavity preventing food entry), muscles of respiration inhibited, larynx
raised, glottis closed  prevent food from entering the trachea; tongue forces
food further back into the pharynx; opening of upper esophageal sphincter,

In the esophageal phase, the food is moved along the esophagus by peristalsis. This is
involuntary as sequential contractions of the oesophagus carry the bolus down the
oesophagus into the stomach. The transition of the oesophageal muscle from striated to
smooth reflects the transition from the voluntary to reflex control of swallowing.

Fig. 2.3. The process of swallowing

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In summary, the sequence of events in swallowing is as follows:

1. Tongue sweeps hard palate moving food backward into oropharynx

2. Nasopharynx closes (superior pharyngeal sphincters)
3. Respiration inhibited
4. Laryngeal muscle contract to close glottis and elevate larynx
5. Peristalsis initiated by superior pharyngeal constriction and continued by middle
and inferior pharyngeals
6. Upper oesopharyngeal sphincter (UES) relaxes
7. Peristaltic wave proceeds down oesophagus
8. Receptive relaxation occurs in the stomach
9. Lower oesophageal sphincter (LES) dilates just prior to contraction wave

Vagal stimulation relaxes both sphincters.

The upper third of the oesophagus is composed of striated muscle, the middle third
contains mixed smooth and striated muscle, and the lower third contains only smooth
muscle.
Swallowing is controlled by brainstem neurons. They form a swallowing centre (Fig.
2.3). The vagus nerve contains both somatic motor neurons (originate in the nucleus
ambiguus) that form motor endplates on striated muscle fibres, and visceral,
preganglionic motor neurons (from the dorsal motor vagal nucleus to the myenteric
plexus). The swallowing reflex coordinates motor signals from both oesophageal striated
and smooth muscles as well as signals to the upper and lower oesophageal sphincters.

Disruption of swallowing can also cause major problems, with regurgitation of food, or
passage of food into the nose of the lungs, either of which can cause problems.
Swallowing problems can be either due to a constriction or blockage of the oesophagus,
or due to a nervous dysfunction which prevents coordinated contraction of the
oesophagus.

Activity 2.7. Swallowing

• Explain the importance of swallowing.

• Draw a “box diagram” and describe the process and control of swallowing.

• Is swallowing completely voluntary? Justify your answer.

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 4.4. Peristalsis

Peristalsis comprises a coordinated wave of contraction behind the bolus of food, with
relaxation ahead of it, propelling the food bolus forward. It is involuntary, resulting from
intrinsic neuromuscular reflexes, independent of extrinsic innervation. However, external
stimuli modify the frequency and strength of peristaltic activity throughout the intestine.
Very strong peristaltic contractions can cause pain.

• Stimulus: distension
• Receptors: mechanoreceptors
• Afferent pathway: vagal afferents
• Control centre: dorsal vagal complex
• Efferent pathway: vagal efferents
• Effector: striated muscle in the upper third of the esophagus or smooth muscle
of the GIT via nerves of the ENS
• Net effect: bolus is moved aborally

Fig. 2.4. Control of peristalsis by the enteric nervous Fig. 2.5. Control of peristalsis by vago-vagal reflexes in
system. the lower esophagus.

Activity 2.8: Peristalsis

Refer to Fig. 2.4 and Fig. 2.5.

• Explain the importance of peristalsis.

• Draw a “box diagram” and describe the process and control of peristalsis.

• Is peristalsis completely voluntary? Justify your answer.

• Describe the mechanism of regulation of peristalsis via the vago-vagal reflex and via the
enteric nervous system

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4.5. Clinical conditions associated with the esophagus

a. Disorders affecting skeletal muscle

Primary diseases of skeletal muscle musculature (e.g. myasthenia gravis, myotonic

dystrophy) or primary diseases of the nervous system involving the somatic motor nerves
(e.g. amyotrophic lateral sclerosis, poliomyelitis) affect the striated muscles of the tongue
and pharynx, the upper esophageal sphincter, and the wall of the upper esophagus.
Consequence? Dysphagia (difficulty in swallowing) and loss of propulsive force of the
upper esophagus. Lesions of the stem (e.g.in stroke) can also interfere with the
movements of the tongue and pharynx.

b. Disorders affecting smooth muscle

1. Cricopharyngeal spasm, characterized by swallowing difficulty, appears to be due

to increased fibrosis of the cricopharyngeal muscle.
2. Achalasia due to failure of peristalsis or defective relaxation of the lower
esophageal sphincter impedes the flow of materials into the stomach.
3. Abnormality in the function of the smooth muscle in the lower two-thirds of the
esophagus whereby the coordinated control of peristalsis is lost.

Heartburn is a burning, unpleasant retrosternal sensation that may be caused by acid

reflux from the stomach into the esophagus.

Activity 2.9: Disturbances in the esophagus

A 42-year-old policeman has been seen by his family physician for heartburn of 5 years
duration. He has been intermittently taking ranitidine, a histamine-2 blocking agent, with
some relief. An upper endoscopic examination that was performed recently revealed some
reddish discoloration and friability of the lower esophageal region. A biopsy of the lower
esophagus was performed, and the microscopic examination revealed columnar cells
containing goblet cells.

• What is the most likely diagnosis?

• What is a long-term complication of this process?
• What is the most likely mechanism of this process?

Certain drugs can be absorbed across the oral mucosa and may be prescribed
sublingually. In this way, the need to swallow is avoided and the absorbed drug
bypasses the liver and avoids hepatic first-pass metabolism. Glycerine trinitrate
(GTN) is one of the most common drugs administered this way.

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5. Gastric Motility

Objective 5: Describe the processes involved in gastric motility and give examples of
clinical conditions arising from abnormal stomach motility.

5.1. Normal gastric functions

The stomach has three major functions:

1. Storage of food
2. Mixing and breakdown of the food into chyme.
3. Slow emptying into the duodenum at a rate suitable for digestion and absorption
to occur.

The fundus and upper body of the

stomach are the storage areas. They
have little musculature in the walls,
and show little contraction. This
means this area of the stomach is
very compliant or easily stretched.
Receptive relaxation occurs in
response to swallowing and
entrance of food.

The body of stomach contains

pacemaker cells for origin of
peristaltic contraction. The
frequency and force of contraction
increase with feeding. Maximal rate
of contraction is about 3/min.
Contractions last from 2 to 20
seconds, break up contents, mix and
propulse. Contractions migrate from Fig. 2.6. Parts of the stomach
point of origin toward pylorus. The
velocity of contraction increases as
contraction moves distally.

In the antral region, contractile wave overrides the contents and pushes most of it
proximally (retropulsion). The rate and force of contraction are modulated by gastrin
and motilin (increase) and by GIP, secretin and somatostatin (decrease).

The pylorus is a thickened area of muscle which is in a tonic state of contraction. It

remains contracted although it can be modulated. This means that only small volumes of
liquid can usually pass through the pylorus into the duodenum.

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5.2. Slow waves in the stomach

Normal gastrointestinal motility results from coordinated contractions of smooth muscle,

which in turn derive from two basic patterns of electrical activity across the membranes
of smooth muscle cells - slow waves and spike potentials.

Like other excitable cells, gastrointestinal smooth muscle cells maintain an electrical
potential difference across their membranes. The resting membrane potential of smooth
muscle cells is between -50 and -60 mV. In contrast to nerves and other types of muscle
cells, the membrane potential of smooth muscle cells fluctuates spontaneously.

Activity 2.10. Slow

waves and spike
potentials

Describe the formation of

the slow wave and relate it
to the GI motility.

Compare and contrast

between slow waves and
spike potentials.

Fig. 2.7. Intestinal smooth muscle potentials and contraction

Because the cells are electrically coupled, these fluctuations in membrane potential
spread to adjacent sections of muscle, resulting in what are called "slow waves" - waves
of partial depolarization in smooth muscle that sweep along the digestive tube for long
distances. These partial depolarizations are equivalent to fluctuations in membrane
potential of 5 to 15 mV.

The frequency of slow waves depends on the section of the digestive tube - in the small
intestine, they occur 10 to 20 times per minute and in the stomach and large intestine 3 to
8 times per minute. Slow wave activity appears to be a property intrinsic to smooth
muscle and not dependent on nervous stimuli.

Importantly, slow waves are not action potentials and by themselves do not elicit
contractions. Rather, they coordinate or synchronize muscle contractions in the gut by
controlling the appearance of a second type of depolarization event - "spike potentials"
- which occur only at the crests of slow waves.

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Spike potentials are true action potentials that elicit muscle contraction. They result when
a slow wave passes over an area of smooth muscle that has been primed by exposure to
neurotransmitters released in their vicinity by neurons of the enteric nervous system. The
neurotransmitters are released in response to a variety of local stimuli, including
distension of the wall of the digestive tube and serve to "sensitize" the muscle by making
its resting membrane potential more positive.

Fig. 2.8. Slow waves

One can now step back and understand how a particular pattern of motility is achieved.
Think for a moment about what happens when a large bolus of ingested food enters the
small intestine:

• The bolus distends the gut, stretching its walls.

• Stretching stimulates nerves in the wall of the gut to release neurotransmitters into
smooth muscle at the site of distension - the membrane potential of that section of
muscle becomes "more depolarized."
• When a slow wave passes over this area of sensitized smooth muscle, spike
potentials form and contraction results.
• The contraction moves around and along the gut in the coordinated manner
because the muscle cells are electrically coupled through gap junctions.

Slow wave frequency and height are modulated by body temp & metabolic activity,
intrinsic & extrinsic nerves (increased by Ach, SP; decreased by noradrenaline, NO,
VIP), and circulating hormones (esp CCK, motilin).

The stomach is the only part of the gut where the slow waves can generate contractions
without generating action potentials. The slow waves are generated by the myenteric
plexus and occur in the stomach with a frequency of 3 per minute. They have a specific,
characteristic 'peak and plateau' appearance when the electrical activity in the muscle is
measured.

5.3. The actions of the stomach on eating

On eating the fundus relaxes to accommodate the food. This is controlled by a vagovagal
reflex whereby the vagus sends signals to the brainstem, and back which cause relaxation
of the musculature.

22
The body and antrum begin strong contractions which are stimulated by the presence of
food in the stomach causing distension and initiating activity in the myenteric plexus. The
results are strong contractions which move parts of the stored food down towards the
pylorus.

The food is mixed with gastric juices by retropulsion, where contractions of the antrum
crush the food against the closed pyloric sphincter. This results in very small amounts of
liquid chyme being squirted through the pylorus, but the vast amount of food being
squeezed back into the stomach.

About 20% of the time the contractions in the stomach get stronger and sweep the chyme
through the pylorus into the duodenum, a small amount at a time

The contractions in the stomach are entirely dependent on an intact myenteric plexus,
they do not need any other stimuli to maintain adequate contractions. The rate is usually
set by the rate of slow wave activity, and slow waves themselves initiate contractions
without the need for action potentials. The extrinsic nervous system can modulate gastric
contractions in the usual ways, parasympathetic stimulation causes increased frequency
and strength of contraction and sympathetic has the opposite effect.

5.4. Migrating motor complex

On fasting i.e. after digestion and absorption of last meal (when the stomach is empty), a
motor event called the migrating motor complex is initiated every 90 minutes or so. It
is due to peristaltic contractions that sweep down the whole of the GIT. The function is
to clear the undigested food particles. It is thought to be controlled by motilin. However,
it is still not conclusively proven that motilin causes the MMC, but its secretion coincides
with the motor complex and occurs at about the same frequency in the fasting state, and
eating inhibits its release.

5.5. Control of gastric emptying

It’s fairly easy to work out that because the pylorus maintains a high resting tone, it is
much easier for liquids to be squeezed through than solids. Liquids empty from the
stomach very rapidly; actually about 80% of liquids can leave the stomach within about
an hour, whereas solids take up to 3 hours to be 80% emptied.

There are several factors which control gastric emptying and we can divide them into two
sections:
• signals from the stomach
• signals from the duodenum

In general the signals from the stomach that stimulate emptying are weak in comparison
to control exerted by the duodenum. Particularly strong contractions occur in the stomach
while mixing is going on, which serve to sweep the chyme down to the pylorus. This
results in more liquid being forced through the pylorus than during retropulsion. These

23
 strong contractions occur in response to distension of the stomach i.e. the presence of
food.

Activity 2.11. Control of

gastric emptying

• What are the stimuli that

cause gastric emptying?
Where are these stimuli
acting?
• What are the receptors for
these stimuli?
• What is the nature of the
afferent information?
• Where is the integrating
centre?
• What is the nature of the
efferent information?
• What are the effectors
involved? How do they
respond to the efferent
information?

Fig. 2.9. Regulation of gastric emptying

Gastrin is secreted in the stomach in response to food and acid and this peptide also
exerts a stimulatory effect on stomach emptying.

The duodenum primarily controls the rate of stomach emptying as efficient digestion and
absorption is dependent on emptying chyme into the duodenum at an appropriate rate.
When food enters the duodenum sensory receptors in the wall are stimulated which cause
reflexes to feedback onto stomach activity and inhibit emptying. These receptors are
stimulated by distension, and constituents of food such as lipids. If the stimulus is
powerful enough for example something extremely irritating stomach emptying can be
completely stopped.

The reflexes can be extremely rapid, particularly those mediated by the enteric nervous
system, and are particularly sensitive to irritants and acid of pH < 4.

Humoral factors primarily cholecystokinin (CCK) are released by the presence of

peptides, amino acids and importantly fats in the jejunum. CCK is particularly effective
at decreasing gastric emptying by blocking the effect of gastrin on stomach motility.

The strong inhibitory stimuli from the intestine i.e. the enterogastric reflexes and the
humoral factors act together to control the rate of gastric emptying so that efficient
absorption and digestion can occur. These mechanisms are activated when there is either

24
too much chyme in the duodenum, by distension and food products, or if the chyme is
unprocessed i.e. it is too acid, has too much unbroken down fat or protein or is irritating.

6. Intestinal motility

Objective 6: Describe the processes involved in intestinal motility and give examples
of clinical conditions arising from abnormal intestinal motility.

6.1. Motility of the small intestine

Again in the small intestine the major types of contraction are peristaltic, which we’ve
dealt with and shows the same features as peristalsis elsewhere in the gut, i.e. a
coordinated wave of contraction preceded by a wave of relaxation pushing chyme
forward. The circular and longitudinal muscles function to mix contents with secretions
and to expose all contents to mucosal surface so that it is contact with mucosal cell
enzymes and with absorptive surface.

The nervous control of intestinal motility is primarily down to the myenteric plexus.
Although the contractions occur at the rate of the slow waves which are generated in
muscle, if the nerve transmission is blocked the contractions become weak, suggesting
that the slow waves also need a further contribution to excitation from the myenteric
plexus.

Peristalsis is controlled by reflexes which serve to increase intestinal motility after a meal
called the gastro-enteric reflex. This is initiated by distension of the stomach wall and is
transmitted through the myenteric plexus.

GI motility is controlled by the action of stimulatory and inhibitory effectors on muscle

slow wave activity.

Motor contractions serve to mix and move chyme along the GI tract by coordinated
contraction and relaxation. Various controls are exerted on this by either neural
(generally the myenteric plexus) or humoral means.

25
Activity 2.12: Motility of the small intestine

• What are the stimuli that cause motility of

the small intestine?
• What are the receptors for these stimuli?
• What is the nature of the afferent
information?
• Where is the integrating centre?
• What is the nature of the efferent
information?
• What are the effectors involved? How do
they respond to the efferent information?
• Why is motility of the small intestine
important?

6.2. Motility of the large intestine

The large intestine is a tube 6 cm in diameter and about a meter long. Its first portion, the
caecum, forms a blind–ended pouch from which extends the appendix, a small fingerlike
projection having no known essential function. The colon consists of the ascending,
transverse, and descending portions. The last segment is the rectum that ends at the
anus.

The large intestine secretes mucus and fluid containing bicarbonate and K+, but does not
secrete digestive enzyme. Its primary function is to store and concentrate fecal material
before defecation.

Chyme enters the caecum through the ileocaecal sphincter. This sphincter is normally
closed, but after a meal, when the gastroileal reflex increases ileal contraction, it relaxes
each time the terminal portion of the ileum contracts, allowing chime to enter the large
intestine. Distension of the large intestine, on the other hand, produces a reflex
contraction of the sphincter, preventing fecal material from moving back into the small
intestine.

About 1500 ml of chyme enters the large intestine from caecum each day. Fluid
absorption by the large intestine normally accounts for only a small fraction of the fluid
absorbed by the GIT each day. The primary absorptive process in the large intestine is
the active transport of Na+ from lumen to blood, with accompanying osmotic absorption
of water. If fecal material remains in the large intestine for a long time, almost all water
is absorbed, leaving behind hard fecal pellets.

Activity 2.13. Intestinal motility

Describe the control of ileocaecal sphincter.

Describe the motility in the large intestines.
What is ileocaecal reflex and gastro-enteric reflex?

26
7. Colonic motility and defecation

Objective 7: Describe the processes involved in motility and defecation.

Fig. 2.10. Parts of the large intestine and the anus

Activity 2.14. Colonic motility

Label the parts of the large intestine (Fig. 2.10) and describe the control of movement of
materials in the large intestine.

The circular smooth muscle of the colon thickens distally to form internal anal sphincter.
The external anal sphincter is made up of skeletal (striated) muscle.

Contractions of the circular smooth muscle in the large intestine produce a segmentation
motion with a rhythm considerably slower (one every 30 min) than that in the small
intestine. Thus, materials in the large intestine remain there for about 18-24 h. This
provides time for bacterial growth and multiplication. Three to four times a day,
generally following a meal, a wave of intense contraction, known as a mass movement,
spreads rapidly over the transverse segment of the large intestine toward the rectum. The
smooth muscle of the large intestine remains contracted for some time after a mass
movement. The large intestine is innervated by sympathetic (decreases colon
contraction) and parasympathetic nerves (increases colon contraction).

The anus is normally closed by the internal anal sphincter (smooth muscle) and external
anal sphincter (skeletal muscle). The defecation reflex is initiated by the increase in

27
volume (thus distension) in the rectum. This stimulates the mechanoreceptors which
sends message to the control centre (the medulla and the higher centre). The efferent
information causes contraction of the rectum, relaxation of the internal sphincter, and
contraction of the external sphincter (initially), and increased peristaltic activity in the
sigmoid colon. Eventually, a pressure is reached in the rectum that triggers reflex
relaxation of the external anal sphincter, allowing the feces to be expelled.

Brain centres can, however, via descending pathways to somatic nerves to the external
anal sphincter, override the reflex signals that eventually would relax the sphincter,
thereby keeping the external sphincter closed and allowing a person to delay defecation.
Voluntary control of the external anal sphincter is learned during childhood. Spinal cord
damage can lead to a loss of voluntary control over defecation.

Defecation is normally assisted by a deep breath, followed by closure of the glottis and
contraction of the abdominal and thoracic muscles, producing an increase in abdominal
pressure that is transmitted to the contents of the large intestine and rectum. This
maneuver (termed the Valsalva maneuver) also causes a rise in intrathoracic pressure,
which leads to a transient rise in blood pressure followed by a fall in pressure as the
venous return to the heart is decreased. The cardiovascular changes resulting from
excessive strain during defecation may precipitate a stroke or heart attack, especially in
constipated elderly people with cardiovascular disease.

Activity 2.15: Control of

defecation

With reference to Fig. 2.11

describe the mechanism of
defecation reflex. Name the
stimuli, receptors, nature of
afferent pathway, control
centre, nature of efferent
pathway, and the effector.

Differentiate between the

defecation reflex in babies and
in adults.

Describe the effect of

“straining” on defecation. What
is this maneuver called? How
may it cause a stroke or heart
attack?

How do you treat a constipated

patient?

Fig. 2.11. The process of defecation

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8. Vomiting

Objective 8: Describe the processes involved in vomiting and explain how anti-
emetic drugs work.

Vomiting or emesis is part of the protective role of the stomach as it protects the body
from ingested toxic substances. What are other protective mechanisms of the stomach?
(acid against ingested bacteria; mucin protects columnar epithelium).

Factors that can trigger vomiting:

1. Stimulation of sensory nerve endings in the stomach and duodenum (e.g. by
solutions of copper sulphate and hypertonic sodium chloride)
2. Cytotoxic drugs (e.g. Cisplatin used in the treatment of cancer)
3. Endogenous substances produced as a result of radiation damage, infections, or
disease
4. Touch receptors at the back of the throat
5. Disturbances of the vestibular apparatus (known as motion sickness)
6. Stimulation of the sensory nerves of the heart and viscera (uterus, renal pelvis,
bladder, testicles)
7. A rise in intracranial pressure
8. Nauseating smells, sights, and emotional factors acting through higher central
nervous system centres
9. Endocrine factors (e.g. Increase in estrogen concentration in morning sickness)
10. Migrane
11. Circulatory syncope

Neural control of vomiting

The vomiting centre (VC) in the medulla oblongata is the main site of neural control of
vomiting. It receives and coordinates signals from a number of other centres, and
coordinates the output (Fig. 2.12). E.g.
1. the chemical trigger zone (CTZ) in the floor of the fourth ventricle lies outside the
blood brain barrier and therefore senses blood-borne chemical stimuli that induce
vomiting, such as drugs like morphine and digoxin. The CTZ in turn stimulates
VC to induce vomiting.
2. motion sickness and diseases of the inner ear cause vomiting by sending nerve
signals from the nucleus of the vestibulocochlear (VIII cranial) nerve to the VC,
possibly via the CTZ.
3. other areas of the brain, such as cortex, thalamus, and hypothalamus, also signal
to the VC, mediating vomiting associated with pain, emotional upset, fever, and
serous physical illness.
4. sensory inputs from the GIT and other viscera, carried by the vagal and
splanchnic autonomic nerves, also stimulate the VC, so that gastrointestinal
distension, infection and inflammation can all induce vomiting.

29
Duodenal contents can be forced into the stomach by anti-peristalsis (Fig. 2.12). During
the expulsion of gastric contents, the person takes a deep breath, the pylorus is closed,
the glottis is closed so respiration stops, and the stomach is squeezed between the
diaphragm and the abdominal muscles, causing rapid emptying. Vomiting is co-
ordinated by the vomiting centre in the medulla.

Drugs (opiates) Pharyngeal Gastric mucosa Pain, sight, Motion

chemotherapy,
hormones
stimulation (5-HT receptors) anticipation sickness

Chemical trigger centre Nucleus tractus Higher centres Vestibular

(CTZ) solitarius (NTS) nuclei
(D2 & 5-HT3 receptors) (H1 and muscarinic
receptors)

Vomiting Centre (VC)

(muscurinic receptors)

Programmed vomiting
response

Fig. 2.12. Vomiting co-ordinated by the vomiting centre.

Activity 2.16: Control of vomiting

List down the factors that can cause vomiting. Explain how each of these factors causes
vomiting.
Describe the vomiting reflex.
Explain how anti-emetic drugs work.

30
During deep anaesthesia the swallowing mechanisms are paralysed. Any patient must
abstain from food and water for at least six hours before deep anaesthesia is administered.
Otherwise, the patient may vomit into the pharynx, and suck his own vomit into the
trachea. Over the years, many patients have choked to death due to this mechanism. The
survivors develop aspiration pneumonia. Such events are clearly malpractice.
An acute loss of H+ from the extracellular fluid (ECF) by vomiting creates a metabolic
alkalosis (high pH with high Base Excess).

Anti-emetic drugs and their actions

Receptor involved Drugs Used against vomiting induced by

Histamine H1 receptor Piperazine derivatives Motion, morphine

Muscarinic (Ach) receptor Hyoscine Motion, copper sulphate
Dopamine receptor (D2) Phenothiazines Apomorphine, GI infections,
cancer chemotherapy (cisplatin),
oestrogen (morning sickness),
narcotics
5-hydroxytryptamine Ondensetron Cancer chemotherapy (cisplatin)
(5-HT3) receptor (serotonin)
Cannabinoids Nabilone Cancer chemotherapy (cisplatin)

Efferent pathways and effectors?

31
9. Disorders of GI motility

Objective 9: Describe the common disorders of GI motility.

Disorders of motility affect all major regions of the GI tract. Because GI tract motility is
a complex result of smooth muscle contraction under neural and hormonal control,
abnormal motility of the GI tract can occur through damage to GI smooth muscle or to
the neural and hormonal mechanisms by which it is controlled, or both. An example of
muscle damage leading to abnormal motility is seen in esophageal stricture as a result of
caustic ingestions or gastroesophageal reflux disease (GERD). Abnormal neural control
of motility is seen in esophageal achalasia. Esophageal motility disorders are typically
characterized by dysphagia and odynophagia. An example of a neural defect that affects
motility is Hirschsprung's disease, in which a loss of myenteric neurons in the colon
inhibits motility.
In the esophagus the most common disorders are reflux esophagitis (due to exposure of
the lower esophagus to gastric acid regurgitating upwards from the stomach) and
carcinoma, both squamous and adenocarcinoma being important. In children, esophageal
atresia and abnormal developmental links with the trachea are important congenital
malformations.

Motility disorders of the stomach include gastroparesis, a complication of diabetes

mellitus, and dysmotility as a consequence of stomach surgery, from either resection of
part of the stomach or vagotomy. Vagotomy entails surgical transection of the vagus
nerve trunks, which prevents vagus-stimulated acid secretion and regulation of gastric
motility. Before the availability of histamine H2 receptor antagonists and proton pump
inhibitors, selective vagotomy of the stomach was used as a treatment for the
hypersecretion of gastric acid. Vagotomy is still sometimes performed as treatment for
Zollinger-Ellison syndrome (ie, acid hypersecretion and severe peptic ulcer disease
caused by a gastrin-secreting tumor).
The symptoms and signs of motility disorders in the stomach depend on their cause.
Because vagotomy cuts fibers influencing the enteric nervous system as well as the
intended fibers that influence acid secretion, a classic complication of vagotomy is
disordered gastric motility. This may present clinically as either partial outlet obstruction
or as too-rapid emptying of gastric contents into the duodenum, with resulting fluid shifts
and vasomotor symptoms ("dumping syndrome"). Sometimes, however, patients may
develop symptoms of stomach distention, nausea, early satiety, and vomiting suggestive
of partial gastric outlet obstruction. To ameliorate the latter symptoms, pyloroplasty
(severing the fibers of the pyloric sphincter) is done to render the sphincter less
competent, so that food can pass more easily into the duodenum. Intrinsic neuropathy
(eg, in diabetes mellitus) results in delayed gastric emptying, nausea, vomiting, and
constipation rather than the classic dumping syndrome. The pathophysiologic basis for
these differences is not known.

32
In the small intestine and colon, disordered motility occurs in irritable bowel syndrome.
Irritable bowel syndrome is characterized by recurrent episodes of abdominal pain,
bloating, and diarrhea alternating with constipation in the absence of detectable organic
disease or structural abnormalities.

The stomach is an important site of peptic ulceration, the ulceration being due to breakdown of
the normal mechanisms which protect the stomach mucosa from its own acid. The recent
increase in the use of endoscopy has shown that chronic gastritis is a frequent and important
condition with a number of different causes, and may play an etiological role in the eventual
development of adenocarcinoma of the stomach. The small intestine is the major site of
absorption of the basic food materials, and diseases of small intestinal mucosa may lead to
malabsorption syndromes; an important cause is celiac disease (gluten enteropathy) which is an
immune process leading to destruction of the small intestinal mucosa. The small intestine,
particularly ileum, is the most common site for the chronic inflammatory disease called Crohn’s
disease. Acute inflammatory disorders of the small bowel are common but transient, being due to
bacterial or viral infection. The stomach and colon are usually also involved (infective
gastroenteritis).

Probably the most common inflammatory disease of the entire alimentary tract which requires
surgical treatment is acute appendicitis, mainly in children and young adults, but occasionally in
mature adults and the elderly where the diagnosis may be missed.

The colon may also be involved in the chronic inflammatory condition Crohn’s disease, but is the
main site of the chronic intermittent inflammatory disease called ulcerative colitis. This disease
is a known predisposing factor to the development of colorectal adenocarcinoma which is
extremely common.

Other predisposing factors to colonic cancer include the development of benign neoplastic polyps
in the colonic mucosa (adenomatous polyps). In colorectal carcinoma there is a well-recognized
sequence of changes from benign polyp to invasive adenocarcinoma. Other important conditions
in the colon are the mechanical abnormalities diverticular disease and volvulus. Disorders of
the anus are a frequent source of medical consultations in family practice, but the disorders are
mainly trivial, though with distressing symptoms (hemorrhoids, pruritus ani, anal fissure); the only
life-threatening disease of the anus is squamous carcinoma.

The alimentary tract is generally susceptible to bacterial and viral infection, producing acute
vomiting and diarrhea, the main source for the infection being contaminated or infected food
items (‘food poisoning’).

Vascular diseases affecting the alimentary tract are uncommon, with the exception of arterial
infarction of the small bowel due to thrombotic or embolic occlusion of the mesenteric vessel,
and acute venous infarction of small or large bowel due to some mechanical obstruction to
normal venous drainage. The most common examples of venous infarction of the bowel are
strangulation of a loop of small bowel in a hernial sac and volvulus of the large bowel.

33
VII. Summary
Motility is a very important process in the GIT. Without it, food cannot be moved down
the GIT to be digested and absorbed. Motility is mainly controlled by the nervous
system.

Activity 2.17: GI reflexes

For each of the reflexes listed on the

right, explain how it operates via the
receptor, control centre, and effector.
Draw box diagrams to illustrate the
flow of information.

Describe the significance of each of

the reflexes.

How could these reflexes

malfunction? What would be the
consequence? How would you treat
such disturbances?

34
VIII. Conclusion
Make sure you have achieved all the objectives in this Module.

Objectives Achievement
1. List and describe the GI processes that involve
muscle contraction and state their significance
in terms digestion of foods and absorption of
nutrients.
2. Describe the musculature of the GIT including
the sphincters and explain the mechanisms that
control contraction of the muscles. Deduce the
significance of contraction of the GIT muscles.
3. Compare and contrast between “peristalsis”,
“segmentation” and “tonic contraction” and
discuss their significance.
4. Describe the processes involved in oral and
esophageal motility (ingestion, mastication,
swallowing and peristalsis) and give examples
of clinical conditions arising from abnormal
oral and esophageal motility.
5. Describe the processes involved in stomach
motility and give examples of clinical
conditions arising from abnormal stomach
motility.
6. Describe the processes involved in intestinal
motility and give examples of clinical
conditions arising from abnormal intestinal
motility.
7. Describe the processes involved in motility and
defecation.
8. Describe the processes involved in vomiting
and explain how anti-emetic drugs work.
9. Describe the common disorders of GI motility.

35
APPENDIX

TOP SIX CAUSES OF VOMITING

1. Stomach flu – by far the most common cause.

2. Food poisoning – relax, this doesn't really mean "poison", it simply means there were
some bad bacteria in the food your child ate.

3. Other intestinal illnesses – there are a variety of other viral and bacterial intestinal
illnesses besides the flu that can cause vomiting. Most are not serious.

4. Severe cough and cold – children can often vomit after a big coughing fit. This isn't
really considered a vomiting problem but rather a coughing problem. Click on Coughs,
Colds & Sinus Infections for more info.

5. Bladder infection – if your child has had a high fever for several days with occasional
vomiting, and the urine burns or smells foul, consider this cause.

6. Intestinal obstruction – now DON'T PANIC. This is by far the least common cause,
but it is also the most serious and is considered a surgical emergency. See below.

HOW TO DETERMINE THE CAUSE

The top four causes are very difficult to distinguish at the onset because they all start out
the same – profuse vomiting every 5 to 30 minutes for the first 1 to 12 hours.
Understanding the various causes and expected course of these three will help you
determine the cause.

1. Stomach flu – this is a virus that causes sudden onset of vomiting, high fever and
stomach pain. Diarrhea usually begins during the first or second day. The length of
vomiting varies from the "12 hour flu" to the dreaded "72 hour flu". There is no blood or
stool test to diagnose this.

2. Food poisoning – this is caused by bad bacteria that is present in spoiled food. The
onset usually comes 2 to 12 hours after eating the food. Common food sources are:
spoiled mayonnaise, chicken, fish, beef, or salad dressing. Some clues that it may be food
poisoning are:

• Often there is no fever

• Usually occurs within a few hours after eating an identifiable source of bad food such as a
questionable restaurant or a picnic.
• Vomiting usually does not last more than 12 hours.
• Therefore, if there is a high fever, you can't think of any bad food your child ate, and the vomiting
lasts beyond 12 hours, it probably is not food poisoning. Diarrhea may or may not develop.

36
3. Other intestinal viruses or bacterial illnesses – there are a variety of these. Some
examples include Rotavirus, Salmonella, and E-Coli. The initial vomiting pattern,
stomach pain and fever of these illnesses is the same as the stomach flu and therefore
difficult to distinguish from the flu. However, in the initial period of vomiting, it is not
really necessary to determine which of all these illnesses is causing it. Instead, you
simply need to know how to handle the vomiting.

4. Intestinal obstruction – this occurs when the intestines become twisted and is
considered a medical emergency that demands immediate medical attention. The key
symptom here is actually SEVERE abdominal pain. If there is only moderate or no
pain, it's probably not an obstruction. Here are the symptoms:

• Sudden onset of abdominal pain

• Persistent dark-green vomiting (bile), not just light-green mucus
• Usually, but not always, projectile
• Agonizing pain that may be constant, but may also come and go
• No bowel movements
• Pale and sweaty skin
• Child is overall worsening rather than staying the same or improving

37