GIT AND NUTRITION BLOCK 9

13 May 2018
WEEK 2
Objectives Discipline
Discuss the functional anatomy of the upper gastrointestinal tract Anatomy
(mouth to ligament of Treitz).

Discuss motility of the upper gastrointestinal tract. Physiology

Discuss gastric physiology. Physiology

Describe the mechanism involved in vomiting. Physiology

Explain the mechanisms involved in mucosal protection and injury. Anatomical Pathology

Explain the pathogenesis of mucosal ulceration. Anatomical Pathology

Explain the techniques used in the diagnosis of peptic ulcers. Internal Medicine

Explain the importance of a full blood count and the haemodynamic state Internal Medicine
in the setting of an acute upper gastrointestinal bleed.

Explain the rationale behind the comprehensive management of peptic Internal Medicine
ulcer in the presence of H. pylori.

Describe the complications of peptic ulcerations. Internal Medicine /

Surgery
Describe the follow up and preventative measures recommended for Internal Medicine
patients who are H .pylori positive and/or taking long term NSAIDs.

Describe the pharmacology of the drugs used in the management of Pharmacology

peptic ulcers and discuss the important role of proton pump inhibitors.

Describe the pharmacology of drugs used for nausea and vomiting. Pharmacology

Describe the mechanism of action of Helicobacter pylori in the Surgery

pathogenesis of PUD
Recognise the clinical presentation of perforated duodenal and gastric Surgery
ulcers

Learning Topics
LT 09.02.01. Upper Gastrointestinal Structures: Overview of Anatomy and Histology
LT 09.02.02. Motility – Upper GIT and GORD
LT 09.02.03. Vomiting
LT 09.02.04. Upper Gastrointestinal Haemorrhage – Variceal and Non-Variceal
LT 09.02.05. Investigations in Gastroenterology
LT 09.02.06. Pharmacology of Prostaglandins, Cyclo-oxygenase Inhibitors and the Gastric
System
LT 09.02.07. Approach to acute abdominal pain

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LT 09.02.01. Upper Gastrointestinal Structures: Overview of Anatomy and
Histology

Aim
To study the gross anatomical and histological structure of the organs found in the upper
gastrointestinal tract: oesophagus, stomach, liver, small intestine and pancreas.

Delivery Objectives
1. Describe the location of the organs of the gastrointestinal tract (GIT) and their relations
and their importance in clinical practice.
2. Describe the morphology of each of the organs in the upper GIT.
3. Describe the arterial supply, venous and lymphatic drainage and innervation of the organs
of the upper GIT and understand its clinical importance.
5. Describe the histological structure of the organs of the upper GIT.
6. Relate the structure (gross and histological) of the upper GIT organs to their functions.

Content
1. Digestive tract histological organisation

The digestive tract from the oral cavity to the anus forms a hollow tube of variable diameter
depending on the region of the tract. During embryonic development, the endoderm and
ectoderm form the epithelial lining of the tube while mesoderm forms muscle, connective
tissues and vessels (blood and lymphatic). The histological structure of the wall of this tube
has a similar layout in the different regions of the tract seen as four distinct layers. From
the lumen outwards these layers are mucosa, submucosa, muscularis externa and
adventitia/serosa.

a. Mucosa
It is found lining the lumen and is the most variable of all the layers due to the change in
epithelium and the functions performed by the epithelium. This layer can be further divided
into 3 layers viz. epithelium, lamina propria and muscularis mucosa.

Epithelium
It is a wet epithelial lining that

 undergoes abrupt changes at two regions viz. cardio-oesophageal junction and

recto-anal junction, where it changes from a stratified, squamous, non-keratinised to
a simple, columnar epithelium and from a simple columnar to stratified, squamous,
non-keratinised epithelium, respectively.
 performs various functions such as
o secreting mucous/mucin for lubrication of luminal contents
o protecting the underlying tissues (from abrasive substances, pathogens and
extreme temperatures)
o forming a selectively permeable barrier between luminal contents and body
tissues
o facilitating transport/digestion of food
o producing hormones that control digestive system activities
o lining the finger-like intestinal projections called villi and the deep tubular
intestinal invaginations called intestinal glands/crypts

Lamina propria
It is a loose/areolar and highly cellular connective tissue found below the lining epithelium.
It contains fibroblasts and wandering leukocytes, fibres (collagen type I, reticular and

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elastic), an extensive vascular network, lymphatic vessels and aggregations of lymphoid
tissue. It may contain glands depending on the organ.

Muscularis mucosa
It is formed by two layers of smooth muscle viz. an inner circular and outer longitudinal
layer. These layers are in fact spirals, with the inner circular forming a tight spiral and the
outer longitudinal forming a loose spiral of muscle fibres. It acts as a physical barrier
between the mucosa and underlying submucosa and promotes independent
movement/folding of the mucosa to increase the area of the mucosa in contact with luminal
contents. Its contractions in the small intestine alter the height of the villi/plicae circularis
and may relieve pressure on submucosal veins.

b. Submucosa
It is composed of a dense irregular and highly vascular connective tissue. It has within it
many arterioles and venules and a lymphatic plexus. Also found is a submucosal/Meissner’s
nerve plexus formed by aggregations of multipolar neurons from the autonomic nervous
system which generate/co-ordinate contractions of the muscularis mucosa. It may contain
glands and lymphoid tissue dependant on the region of the tract. The submucosa permits
mucosal mobility independent from muscularis externa.

c. Muscularis externa
It is made up of smooth muscle cells arranged in two or more layers depending on the
region of the tract. In the oesophagus and anal sphincter, however, the muscle fibres
present are skeletal due to the voluntary action of swallowing and defaecating, respectively.
The inner circular layer constricts the lumen (decreasing its diameter) while the outer
longitudinal layer shortens the tract and widens the luminal diameter.

Aggregations of multipolar neurons form small parasympathetic ganglia between the two
muscle layers and these form part of a plexus called the myenteric/Auerbach’s nerve
plexus. These ganglia will be most numerous in regions of greatest motility. Also found in
the loose connective tissue between the muscle layers are blood and lymphatic vessels.

The function of this muscle layer is to propel food by peristalsis. This is a distinctive pattern
of smooth muscle contractions that propels food distally through the oesophagus and
intestines and is coordinated by impulses from myenteric plexuses. Distension of the tube
by the bolus stimulates afferent enteric neurons that form synapses with interneurons
(containing acetylcholine, and substance P and K) which initiate contraction of the wall over
the bolus. Another set of interneurons initiate relaxation of the area below the bolus
mediated by vasoactive intestinal peptide, somatostatin etc.

d. Serosa/adventitia
This is the thin outermost layer of loose/areolar connective tissue containing adipose tissue
that covers the GIT. It is rich in blood and lymph vessels and is lined by a simple squamous
epithelium (mesothelium which is a reflected peritoneal covering) within the peritoneal
cavity. When lined by a mesothelium, this connective tissue layer is called a serosa, but
without the mesothelium (outside the peritoneal cavity) it is called an adventitia.

The structure of the organs (gross morphology and histology) discussed below will be
covered in the theme session (TS 09.02.01 BCS1).

2. Histology of the oesophagus

Mucosa
Has a stratified, squamous, non-keratinised epithelium that protects underlying tissues from
abrasion and friction of the food bolus. The epithelium is folded to allow for distention of the
lumen. The underlying lamina propria, which may have lymphoid follicles, is separated from

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the submucosa by a thick layer of longitudinally oriented bundles of smooth muscle
(muscularis mucosa).

Submucosa
This is a fibrous, dense, irregular connective tissue that is highly vascular and contains the
mucous secreting deep oesophageal glands.

Muscularis externa
This is a thick layer of inner circular and outer longitudinal muscle, which varies depending
on the region of the oesophagus. It is made up of only skeletal in the proximal 3 rd, smooth
inner circular and skeletal outer longitudinal in the middle 3rd and only smooth in the distal
3rd.

Adventitia
This is a loose connective tissue with lots of adipose tissue and blood vessels. It is not lined
by mesothelium in the thoracic cavity, though the distal portion, which lies in the abdominal
cavity, may be covered by a serosa.

3. Histology of the stomach

The four regions of the stomach can be differentiated histologically by the type of glands
they contain. The cardiac and pyloric regions contain simple branched coiled tubular glands
that secrete mucus and hormones. In the fundus and body of the stomach, the glands
(which secrete gastric juice, mucus and hormones) are simple branched tubular glands and
are called gastric glands. They contain various types of secretory cells viz. surface and neck
mucous secretory cells, stem cells, parietal (oxyntic) cells, chief (zymogenic) cells and
enteroendocrine cells.

Mucosa
It is lined by a simple, columnar epithelium, which invaginates to form closely packed
glands with slips of lamina propria between them. These glands open into v-shaped
foveolae/gastric pits. The mucosa is separated from the underlying submucosa by a thin
muscularis mucosa layer made up of inner circular and outer longitudinal layers of smooth
muscle.

Submucosa
This region contains many blood vessels in a fibrous, dense, irregular connective tissue.

Muscularis externa
In the cardia, fundus and body the muscularis externa is made up of inner oblique, middle
circular and outer longitudinal layers of smooth muscle. The circular layer thickens at the
cardia and pylorus to form the cardiac and pyloric sphincters, respectively; the pyloric
sphincter is much thicker than the cardiac sphincter.

Serosa
This is a loose connective tissue containing lots of adipose tissue, blood vessels and
lymphatics. It is lined on the outside by mesothelium.

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4. Histology of the small intestine

DUODENUM JEJUNUM ILEUM

Absorption Plicae circularis Plicae circularis Villi
adaptation Villi Villi Microvilli
Microvilli Microvilli
Intestinal Absorptive Absorptive columnar Absorptive columnar cells
glands columnar cells cells Goblet cells
Goblet cells Goblet cells Paneth cells
Paneth cells Paneth cells Enteroendocrine
Enteroendocrine Enteroendocrine Stem cells
Stem cells Stem cells
Lamina Fibres, Fibroblasts Fibres, Fibroblasts, Fibres, Fibroblasts, Migrating
propria Migrating Migrating leukocytes leukocytes
leukocytes Lymphoid tissue Lymphoid tissue (forms large
Lymphoid tissue (diffuse or nodular) Peyer’s patches which span
(diffuse or the mucosa and submucosa)
nodular)
Muscularis Smooth muscle Smooth muscle Smooth muscle forming an
mucosae forming an inner forming an inner inner circular and outer
circular and outer circular and outer longitudinal layer
longitudinal layer. longitudinal layer
It is discontinuous
because of the
ducts of glands
Submucosa Highly vascular Highly vascular and Highly vascular and fibrous
and fibrous dense fibrous dense dense irregular connective
irregular irregular connective tissue
connective tissue tissue
with duodenal
(Brunners') glands
Muscularis Thick layer of Thick layer of smooth Thick layer of smooth muscle
smooth muscle muscle forming an forming an inner circular and
forming an inner inner circular and outer longitudinal layer. The
circular and outer outer longitudinal inner circular layer forms the
longitudinal layer. layer. ileocaecal sphincter.
Serosa Loose connective Loose connective Loose connective tissue lined
tissue lined by tissue lined by by mesothelium
mesothelium mesothelium

5. Histology of the pancreas

The parenchyma is made up of an exocrine and an endocrine portion. The exocrine portion
contains 'pear' or alveolar shaped acini. Each acinus, which consists of 5-8 pyramidal cells,
is separated from other acini by a loose connective tissue that contains blood vessels,
lymphatics, nerves and intralobular ducts. The ducts that drain the acinus are called
intercalated ducts and form the centroacinar cells. The gland is separated into lobules by
connective tissue septae, which contain the larger branches of the ducts called interlobular
ducts.

Digestive enzymes produced by the exocrine portion

Proteolytic enzymes - trypsin, chymotrypsin

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Polypeptidases - carboxypeptidases
Nucleotidases - ribonucleases (RNAses) & deoxyribonucleases (DNAses)
Disaccharidase - pancreatic amylase
Lipidase - lipase and cholesterol esterase

Paper-based resources
1. Fawcett, DW. Bloom and Fawcett: A Textbook of Histology. Chapman and Hall.
2. Junqueira et al. Basic Histology. Prentice-Hall International.
3. Leeson et al. Text/Atlas of Histology. WB Saunders Company.
4. Ross, MH, Romrell, LJ and Kaye, GI. Histology: A text and Atlas. Williams and Wilkins.
5. Young and Heath. Wheater’s Functional Histology.
WHSL Homepage

LT 09.02.02. Motility – Upper GIT and GORD

Aim
To review the physiology of motility and its functions in the upper GIT.

Delivery objectives
1. Describe the process of swallowing, oesophageal motility and gastric motility.
2. Discuss the role of the lower oesophageal sphincter in GORD.

Content
General principles of GI motility

Motility refers to gastrointestinal movements that mix and circulate the GI contents and
propel them along the length of the tract. In addition, motility of the stomach contributes to
the physical component of the digestive process together with mastication.

Smooth muscle of the gut functions as a syncytium due to the presence of gap junctions
that allow electrical coupling of muscle fibres. Smooth muscle cells are long (500 µm) and
slender (5 µm in diameter). Smooth muscles are arranged in bundles (200 µm) that are
separated by connective tissue. Cells within each bundle are electrically connected.
Therefore the functional contractile unit of gut smooth muscle is the bundle. There are 2
types of contractions: phasic contraction - a transient twitch-like contraction and tonic
contractions during which contractile tension is maintained for prolonged periods.

Most of the GI tract (from the stomach onwards) does not show a set resting membrane
potential. Instead electrical slow waves (basic electrical rhythm - BER) due to rhythmic
cycles of depolarisation and repolarisation are observed. These occur spontaneously due to
“pacemaker” activity of GI muscle cells.

The frequency of this rhythm differs in different sections of the GI tract. Slow wave
frequency is:

Stomach 3/min; duodenum 12/min; ileum 9/min; colon variable.

Slow waves are always present. If the slow wave amplitude is large enough, then an action
potential (spike potential) is produced which translates into muscle contraction. If the slow
wave depolarisation does not reach threshold, then there is no corresponding muscle
contraction.

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Fig. 1. Showing basal electrical rhythm and superimposed spikes.

Excitation-contraction coupling. As in skeletal and cardiac muscle, the level of

intracellular Ca++ plays a central role in regulating the contraction of smooth muscle. Please
revise the mechanism of excitation-contraction coupling in smooth muscle (covered in nerve
and muscle physiology).

Types of motility are listed below:

Motility Site Function

Peristalsis Oesophagus Propulsive causes transport
Stomach
Small Non-propulsive causes mixing
intestine
Rhythmic Small and large Mixing
segmentation intestines
Tonic Sphincters Blocking passage
contraction Separation of compartments

Chewing and swallowing

Chewing (mastication) is the physical breakdown of food by the action of teeth. It prepares
food for swallowing by breaking it up, softening it, and mixing it with saliva.

Chewing makes food more accessible to the digestive action of enzymes it also stimulates
the production of saliva.

Chewing involves a large number of muscles coordinated by a chewing centre in the CNS. A
spinal reflex prevents the teeth from crushing together.

Swallowing (deglutition) - sending food to the stomach; it is an active process, best

illustrated by the fact that food, even liquids, can be swallowed while you are standing on
your head! Try it. It is divided into three phases; oral, pharyngeal and oesophageal.

The oral or voluntary phase is initiated by separating the bolus to be swallowed and
pressing it against the hard palate by the actions of the tongue. This forces the bolus into
the pharynx, where it stimulates the tactile receptors that initiate the swallowing reflex.

The pharyngeal phase involves a series of events that seal off the nasopharynx and the
trachea from the oropharynx with subsequent inhibition of respiration. The nasopharynx is
closed by upward movement of the soft palate combined with contraction of the dorsal

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constrictor muscles of the pharynx. Sealing of the trachea involves closure of the glottis
along with cranial displacement of the larynx by contraction of the laryngeal muscles. The
pharyngeal phase ends with propulsion of the bolus into the oesophagus by contraction of
pharyngeal constrictor muscles along with relaxation of the upper oesophageal sphincter.

The oesophageal phase propels the bolus from the pharynx to the stomach by peristalsis.
Two kinds of peristalsis occur in the oesophagus; primary and secondary. When the
oesophageal peristalsis is preceded by a pharyngeal phase, it is called primary peristalsis.
Secondary peristalsis is independent of the pharyngeal phase and occurs in response to
oesophageal distension if the primary peristaltic wave fails to empty the oesophagus.

A swallowing centre in the brainstem receives sensory inputs from the palate, pharynx, and
oesophagus. Pharynx and upper third of the oesophagus are comprised of skeletal muscle
which is innervated by the fibres of somatic nervous system.
The lower third of the oesophagus is comprised of smooth muscle whose motor activity is
controlled by the myenteric plexus which, in turn, receives parasympathetic input from the
vagus nerve.

Motility of the oesophagus

In the absence of food, the oesophagus is quiescent. Swallowing is initiated at will, but once
in the oesophagus, food is moved towards the stomach by an autonomic reflex by the
process of peristalsis. At rest, both ends of the oesophagus are normally closed by the
contraction of the upper oesophageal sphincter (UES), made of striated (skeletal) muscle,
and the lower oesophagus sphincter (LES), made of smooth muscle. Food bolus is propelled
along the oesophagus in the aborad (away from the mouth) direction by a progressive wave
of muscle contraction called peristalsis. The first wave initiated by the presence of food
bolus in the oesophagus is primary peristalsis. If a large food particle does not reach the
stomach during the initial peristaltic wave, the distension of the oesophagus is sensed by
stretch receptors which, by a reflex response, initiate another peristaltic wave called
secondary peristalsis – an oesophageal clearing wave. This reflex is mediated through
afferent signals to the brainstem swallowing centre and different signals to the oesophageal
muscles. A competent LES is required for normal filling of the stomach and for protection
against reflux of acid into the oesophagus.

Dysfunction of the LES

Achalasia - failure of LES to relax sufficiently to allow food to enter stomach results in
accumulation of food in oesophagus leading to mega-oesophagus - gross distension of the
oesophagus. Achalasia appears to be a degenerative disorder of inhibitory motor neurons in
which the level of inhibitory neurotransmitter VIP is diminished in the LES.

Reflux oesophagitis - If the LES does not remain closed, some of the contents are forced
into the oesophagus; the HCl from the stomach irritates the oesophagus walls causing a
sensation of ‘heartburn’.

Gastric (stomach) motility

The functions of gastric motility are to allow the stomach to serve as a reservoir for
ingested food, to physically break down food into smaller particles and mix it with gastric
secretions to aid digestion and to empty gastric contents (chyme) into the duodenum. The
fundus (top) and body middle have a thin muscularis externa and therefore the force of
contraction in this area is relatively weak. This part of the stomach serves a reservoir
function. Upon swallowing, as the food bolus reaches the LES, the fundus of the stomach

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relaxes to accommodate the incoming food. This type of motility is called receptive
relaxation. VIP and nitric oxide (NO) are involved in this response.

Between the fundus and the body of the stomach is a pacemaker zone - cells that undergo
spontaneous depolarisation at a rate of 3 slow waves/minute. Slow waves in different parts
of the stomach have this same frequency because of these pacemaker cells The antrum has
a thick layer of muscularis externa and can contract vigorously. Its functions include mixing
gastric contents and gastric emptying. The major motility pattern for the stomach is
peristalsis, which occurs at the frequency of the slow waves at maximum activity. Peristaltic
waves are propelled towards the pylorus. At the end of the wave, the antrum contracts
(antral systole) causing contents to be vigorously squirted back into the body - a process
called churning. This promotes the effective mixing of food with gastric juice and the
formation of chyme. After a meal, spike (action) potentials are increased therefore strength
of contraction is increased. The opposite is true during fasting. Ach, gastrin or CCK
increases strength of gastric contraction while adrenaline (epinephrine), noradrenaline
(norepinephrine), secretin, GIP or VIP decrease strength of gastric contraction.

Gastric emptying

This occurs when, at the time of the antral systole, the pyloric sphincter relaxes allowing a
small amount of gastric chyme to be squirted into the duodenum.

Particles greater than 7mm in diameter cannot pass the pylorus, preventing larger chunks
of food from entering the intestine. Gastric emptying is carefully adjusted to the capacity of
the intestine to digest and absorb food. High osmotic pressure of chyme, low pH and high
fat content slow down rate of gastric emptying. Liquids empty faster than solids. Driving
force for emptying is provided by wall motion of the churning process. A heavy meal with
lots of fat is released much lower than a light meal consisting of easily digestible
carbohydrates. Feedback control from chemical and physical (distension) receptors in the
duodenum regulates sphincter tone.
Paper-based resources
1. Core
1.1 Appropriate sections of Porth CM. Pathophysiology, Concepts of Altered Disease States.
Philadelphia, Lippincott, 6th Edition.
2. Supplementary
2.1 Appropriate sections of Sherwood L. Human Physiology. From Cells to Systems. Pacific Grove
USA, Brooks/ Cole, 4th Edition.
2.2 Appropriate sections of Ganong WF. Review of Medical Physiology. Lange Medical Books. USA,
20th Edition.
2.3 Appropriate sections of Guyton AC and Hall JE. Human Physiology and mechanisms of Disease.
WB Saunders Company. Philadelphia. 6th Edition.
WHSL Homepage

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LT 09.02.03. Vomiting

Aim
To review the physiology of vomiting.

Delivery objectives
1. Explain the triggers, mechanisms and consequences of vomiting.

Content
Vomiting/Emesis

Emesis is the expulsion of gastric (and duodenal) contents from the GIT via the mouth.
Emesis is a primitive reflex with afferent and efferent components (Figure 1). It is often
preceded by nausea, salivation, rapid irregular heart beat, dizziness, sweating, pallor, and
papillary dilation. Often it is preceded by retching in which gastric contents are forced into
the oesophagus but do not enter the pharynx. Reverse peristalsis empties the material from
the upper small intestine into the stomach. The glottis closes preventing aspiration of
vomitus into the trachea. The breath is held mid inspiration (intrathoracic pressure is
decreased), the muscles of the abdominal wall forcefully contract to increase intra-
abdominal pressure, the LES relaxes to receive gastric contents and the pylorus and antrum
contract to prevent orthograde flow of gastric contents. The rapid propulsion of gastric
contents into the oesophagus is accompanied by a reflex relaxation of the UES and gastric
contents are ejected.

Vomiting is integrated in the medulla. The vomiting centre is located in the reticular
formation of the medulla. Afferents for the reflex arise from the labyrinthine system (motion
sickness), diencephalon and limbic system (which may explain “nauseating smells” and
“sickening sights”). Triggers include gastric distension, tickling the back of the throat,
painful injury

to the genitourinary system, dizziness chemical stimulating the receptors in the stomach or
duodenum (ipecac), CNS stimulants and endogenously produced emetics. Chemoreceptor
cells in the medulla are located in the area postrema and are known as the chemoreceptor
trigger zone located in the floor of the fourth ventricle). It is stimulated by substances
such as apomorphine, digitalis glycosides, copper sulphate and urea.

Serotonin 5HT3 and dopamine D2 receptors in the area postrema, when antagonised by
specific drugs, ondansetron (5HT3 antagonist) and chlorpromazine and haloperidol (both D 2
antagonists), produce anti-emetic effects.

Integrative Physiology Question: What are the acute/chronic effects of severe vomiting
on acid-base, ionic and fluid balance?

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Fig. 1. Components of the emetogenic pathways in man. Neuroreceptors (dopamine, 5HT -
serotonin, His - histamine, Ach - acetylcholine) which are used as targets for emetics and
antiemetics are also shown. Modified from Mannix, K.A. Palliation of nausea and vomiting.
CME Cancer Medicine. 1 (1): 18-22.

Paper-based Resources
1. Core:
1.1 Appropriate sections of Porth CM. Pathophysiology, Concepts of Altered Disease States. Philadelphia,
Lippincott, 6th Edition.
2. Supplementary:
2.1. Appropriate sections of Sherwood L. Human Physiology. From Cells to Systems. Pacific Grove USA,
Brooks/ Cole, 4th Edition.
2.2 Appropriate sections of Ganong WF. Review of Medical Physiology. Lange Medical Books. USA, 20th
Edition.
2.3 Appropriate sections of Guyton AC and Hall JE. Human Physiology and Mechanisms of Disease. WB
Saunders Company. Philadelphia. 6th Edition.

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LT 09.02.04. Upper Gastrointestinal Haemorrhage – Variceal and Non-Variceal

Aim
To review the physiology and mechanisms of upper gastrointestinal haemorrhage.

Delivery objectives
1. Explain hypovolaemic shock and haemostasis.
2. Discuss causes of peptic ulceration and treatment thereof in an elective setting.
3. Discuss the complications of peptic ulcer.
4. Classify the causes of portal hypertension and explain the reasons for the classification.

Content
Upper gastrointestinal bleeding, by definition, originates in the GIT proximal to the
ligament of Treitz (the junction between fourth part of the duodenum and jejunum). This
bleeding may result in haematemesis which is extremely unlikely if the bleeding point is
distal to this point. Haematemesis is the vomiting of fresh or altered blood. Not all cases
with upper GIT bleeding have haematemesis. The blood passes distally through the GIT
and presents as malaena, which is characteristically thick, black, sticky and smells.
Malaena is due to the action of acid on haemoglobin, and therefore the blood usually
originates in the stomach or proximal duodenum. If GIT transit is very fast, which may
occur with a torrential upper GIT bleed, the patient may present with fresh bleeding
rectally. A lower GIT bleed is a more common cause of rectal bleeding (FRESH OR ALTERED
BLOOD, not MALAENA).

A lower GIT bleed occurs when the bleeding site is distal to the ligament of Treitz. This may
be due to a small bowel cause (uncommon, but must be excluded in young and middle
aged patients), or to a bleed from the colon or rectum. The commonest causes of large
lower GIT bleeding in the elderly are diverticular disease and angiodysplasia. Lower GIT
bleeds usually do not present with typical malaena, but it may be difficult to differentiate a
venous bleed from the right side of the colon from true malaena. Fresh rectal bleeding is
called haematochezia.

A GIT bleed is termed massive when it causes haemodynamic instability. An obscure GIT
bleed is defined as one where no obvious cause can be found despite routine investigations
e.g. gastroscopy and colonoscopy. Occult GIT bleeding occurs when the patient presents
with an iron deficiency anaemia and no history of overt GIT bleeding.

Upper gastrointestinal haemorrhage may be mild or severe but should always be

considered an ominous manifestation that deserves thorough evaluation. Bleeding is the
most common serious complication of peptic ulcer, portal hypertension and gastritis, and
these conditions taken together account for most episodes of major upper gastrointestinal
bleeding in the average hospital population.

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DIAGNOSIS OF CAUSE OF BLEEDING

Relative
Incidence
Common causes 95%

Peptic ulcer
Duodenal ulcer 25%
Gastric ulcer 20%
Oesophageal varices 20%
Gastritis 20%
Mallory-Weiss syndrome
10%
Uncommon causes 5%

Gastric carcinoma
Oesophagitis
Pancreatitis
Haemobilia
Duodenal diverticulum
Haemosuccus pancreaticus

Patients presenting with a history suggestive of an upper GIT bleed should be thoroughly
evaluated. The history and examination should help to establish a possible cause of
bleeding and the extent of the bleed. A history of vomiting preceding a haematemesis is
suggestive of a Mallory Weiss tear, features of portal hypertension suggests, but is not
diagnostic of, bleeding oesophageal varices (30% of patients with known oesophageal
varices bleed from another source); a prior history of peptic ulcer or NSAIDS abuse is
suggestive of a bleeding peptic ulcer.

Patients with massive bleeding and haemodynamic instability should be actively

resuscitated and monitored before any diagnostic tests are embarked upon. 80- 90% of
patients with an upper GIT bleed will stop spontaneously. However, a small percent will
continue to bleed actively, and some patients will rebleed, which, especially in the elderly,
carries a high mortality rate. The general status of the patient must be evaluated. Bloods
are sent for Hb and platelet estimation, U and E and PI/PTT. Blood is ordered if deemed
necessary. The aims of initial management are resuscitation and then determination of the
source of the bleeding. It is important to differentiate between bleeding oesophageal
varices and non-variceal causes of bleeding, as management and prognosis differ in these
two groups.

Early upper GIT endoscopy is a vital component of this early diagnostic workup. However,
the patient must be stabilised beforehand and the stomach vigorously washed out with
warm tap water using a large bore stomach washout tube. This washout is now omitted by
many experienced endoscopists. Precautions against aspiration must be taken. If the bleed
is non-haemodynamically significant and upper endoscopy reveals an innocuous source of
bleeding, the patient may be discharged, thus saving a costly admission.

Variceal bleeding

This may be suspected after careful history taking and examination. These patients rarely
exsanguinate. The cause of death is usually hepatic failure due to the hypotension and
increased protein load in the GIT (blood), and multi-organ failure. The aims of treatment

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are to stop the bleeding and to optimise liver function. Methods of stopping the bleeding
are the following:

 Variceal sclerotherapy. This is done at the time of initial flexible endoscopy.

Ethonolamine oleate (EO) or STD are usually injected para- or intra-variceally.
Oesophageal banding using a flexible endoscope has recently been introduced
with good results.
 Intravenous infusions to decrease portal pressure. Initially vasopressin was used but
this is no longer available in South Africa. Somatostatin at 50 micrograms per hour
is now used. It has been shown to be effective, and can be used during transport of
patients to specialist centres, where these patients should be managed.
 If these measures fail, balloon tamponade using a Sengstaken Blakemore tube
can be attempted but this is time consuming and may lead to complications.
 Emergency surgery, either in the form of a shunt or an oesophageal transection, has
been used if the above measures fail.
 Transjugular, Intrahepatic Portosystemic Shunts (TIPS) using expandable metallic
stents are deployed by radiologists to tide patients over who are candidates for a
hepatic transplant.

These patients should ideally be treated in an ICU setting. Multiple system failure is
common and support e.g. ventilation and dialysis is commonly needed. Once the patient
has been stabilised, further management to prevent rebleeding is commenced (See lecture
on portal hypertension).

Non-variceal upper GIT bleeding

The causes of upper GIT bleeding are shown in the Table. Commoner causes of massive
non-variceal bleeding are bleeding duodenal and gastric ulcers, gastritis and Mallory Weiss
tears. After initial resuscitation and gastric lavage, upper flexible endoscopy is performed.
Before about 1988, upper endoscopy was diagnostic and prognostic, but not therapeutic in
this context. However since then, various methods of endoscopic haemostasis have
evolved. These include injection of 1/10 000 adrenaline, sclerotherapy of dilute adrenaline
+/- sclerosant, heater probes, laser, bipolar electrocautery and application of metallic clips
endoscopically.

As mentioned earlier, rebleeding in these patients is a major cause of morbidity and

mortality. Most patients will not bleed again (80%). Attempts have been made to identify
those patients at high risk of rebleeding. Factors identified include:

 Shock on admission
 Admission Hb < 8g/dl
 Haematemesis as opposed to malaena
 Concomitant medical illness
 Age > 65 years
 Endoscopic features (Foster’s criteria)
o bleeding vessel in base of ulcer
o clot in base of ulcer
o visible vessel in base of ulcer
 Location of ulcer( duodenal and lesser curve)

Prior to endoscopic haemostasis, elderly patients at high risk of rebleeding were taken to
the operation theatre for emergency surgery. The use of endoscopic therapy has decreased
the need for emergency surgery and has probably decreased mortality rates. With the
advent of Helicobacter eradication as a treatment (cure?) for most peptic ulcer disease,
indications for elective operation for peptic ulcer disease have decreased. Endoscopic

14
therapy has decreased the amount of emergency surgery as well. If endoscopic therapy is
used, patients must be closely monitored for rebleeding. If they do rebleed, operation is
usually indicated, but repeat endoscopic therapy is recommended by some clinicians.

INTRAVENOUS PROTON PUMP INHIBITORS

Omeprazole and pantoprazole are now available in intravenous form. There are a number
of prospective trials that have shown that a bolus of 80 mg and then a constant infusion of
8 mg/hr of iv PPI for 72 hours significantly decreases the risk of rebleeding in those
patients who have undergone endoscopic therapy for acute non variceal upper GIT
bleeding. Although expensive and not freely available, this would now be regarded as
standard of care.

Keeping the pH in the stomach above 6 increases platelet aggregation, decreases clot lysis
and promotes coagulation. This in turn prevents rebleeding. The effect on patient mortality
remains controversial. The use of iv H2 blockers has not been effective. There is some
evidence that high dose oral therapy might be effective (for example, omeprazole 80mg BD
po).

CONCLUSION

All GIT bleeding must be treated seriously. Neoplasms often cause occult bleeding and
present with small amounts of bleeding or anaemia.
Haemodyamically significant GIT bleeding is often life threatening. Such patients are best
treated in specialised units.
Upper GIT bleeds present with haematemesis, malaena or both. Haematemesis is not
always present. Initial resuscitative steps are required. Early endoscopy is essential as it
helps triage patients and identifies patients at risk of rebleeding. Early endoscopy also
helps differentiate non variceal from variceal bleeding.

Endoscopic therapy is used for those patients who have endoscopic stigmata and clinical
predictors of a high risk of rebleeding. Intravenous PPI bolus followed by infusion is now
standard of care for such high risk patients with non variceal bleeds. Patients with variceal
bleeds are best treated with banding. Somatostatin infusions are often used as well. Lower
GIT bleeds often present dramatically but almost always stop spontaneously. Massive
upper GIT bleeding masquerading as a lower GIT bleed needs to excluded (most reliably by
upper endoscopy). Semi elective visualisation of the colon is mandatory in these cases. The
occasional patient who continues to bleed from a lower GIT cause presents a diagnostic and
therapeutic challenge

LT 09.02.05. Investigations in Gastroenterology

Aim
To review the imaging techniques involved in gastroenterology.

Delivery objectives
1. Explain the principles of radiology, endoscopy, manometry, tests for H.pylori and other
imaging modalities.

Content
A) Radiology – Contrast
B) Endoscopy
C) Manometry
D) Other Imaging:
i) Ultrasonography

15
 ii) Computed Tomography (CT)
iii) Magnetic Resonance Imaging

A) RADIOLOGY

 Alimentary radiology has undergone great changes with the introduction of cross
sectional computer-assisted techniques, which have been complementing the
barium single- and double-contrast studies. Because of the competition of
endoscopy, the need for rigorous controls over the accuracy of radiologic studies
has made great advances.
 Plain radiography of the abdomen is mandatory as it serves as scout films which
identify e.g. gas patterns, possible free gas in the cavity or retroperitoneal and
calcifications.
 Radiographic contrast media for alimentary canal studies include:
o Water insoluble – barium sulphate
o Water soluble – gastrograffin
o Amipaque
o Hexabrix
 Pharmacoradiology – refers to the agents used to modify tone, peristalsis and
secretions of the alimentary tract and includes spasmolytics and motility enhancers.
 Single-contrast or double-contrast (contrast and air insuffation) studies with
preference for double-contrast.

I) UPPER GASTROINTESTINAL TRACT

a. Barium Swallow: Oesophagus

b. Barium Meal: Stomach and duodenum
c. Follow through: Upper small intestine
Enteroclysis: Small intestine

II) LOWER GASTROINTESTINAL TRACT

a. Barium enema – viewing the colon

b. Defecography
Abnormalities of anorectal functions, such as incontinency and incomplete
evacuation of the rectum, are examined by defecography.

III) TRANSIT STUDIES- During the investigation of constipation, motility and transit
abnormalities may be suspected.

B) ENDOSCOPY

 Endoscopy has revolutionised clinical gastroenterology. In 1961, Basil Hirschowitz

(South African) published the first flexible endoscopic examination of the stomach
and duodenal bulb. Since then endoscopy has moved on to video and computerised
electronic signals.
 Endoscopes are now used to examine the entire gastrointestinal tract from
oesophagus to rectum, including the biliary and pancreatic ductal systems. Targeted
endoscopic biopsy offers rapid and precise diagnosis. Endoscopic ultrasound is of
unsurpassed accuracy in staging gastrointestinal tumours, in assessing pancreatic
and biliary disease, and disorders of the rectum and anal canal. Endoscopic
therapies such as stopping bleeding, removing polyps and foreign bodies, placing of

16
 stents and other prosthesis and removing stents, still remain its most useful clinical
benefit.

I) UPPER ENDOSCOPY

1. Indications

Heartburn, regurgitation
Retrosternal or upper abdominal pain
Odynophagia or dysphagia
Persistent nausea and/or vomiting; dyspepsia
Haematemesis and/or malaena
Unexplained anaemia
Anorexia and weight loss
Accidental or deliberate ingestion of caustic substances

2. Complications

a. Hospital morbidity 0.14% and mortality 0.04%.

b. Cardiopulmonary complications
c. Perforations
d. Haemorrhage

II) ERCP (Endoscopic Retrograde Cholangio Pancreatography)

1. Indications

Suspected biliary disorders

Suspected pancreatic disorders
Prior to therapeutic endoscopic procedures
Preoperative mapping
Additional procedures

2. Complications

Pancreatitis 0.7-7.4%
Cholangitis 0.6-0.8%
Abscess of pancreas 0.5-1.3%
Side-effect of drugs 0.1-0.6%
Injury to gastrointestinal tract 0.07-0.4%
Mortality 0.001-0.8%

III) COLONOSCOPY

1. Indications

If X-ray examination does not reveal an easily identifiable abnormality.

If diagnosis and the therapeutic policy to be followed are determined by

histology (e.g. villous or carcinomatous). The abnormality can be biopsied
endoscopically or possibly even removed completely.

17
 May also be necessary for differentiation of inflammatory disorders. Is one
dealing with ulcerative colitis or Crohns? Severity? Extension?

Rectal blood loss.

Colonoscopy can also be carried out as a screening procedure, e.g. in cases of

familial colon carcinoma or familial polyposis coli. Others prefer an adequate
double-contrast X-ray investigation of the colon combined with sigmoidoscopy.

2. Complications

Perforation 0,2%
Haemorrhage 0,4%

Hypotension and cardiac/respiratory failure from over sedation.

After polypectomy – bleeding, perforation.

IV) OTHER

Laparoscopy

This technique is an important diagnostic tool in hepatogastroenterology.

1. Indications

Liver biopsy in specific circumstances.

Macroscopic assessment for diseases affecting the peritoneal cavity.

Macroscopic and microscopic assessment of the spleen.

2. Complications

In a review of 148 086 procedures, Henning et al found a 0.79% incidence of

complications and a 0.051% fatality rate. Following liver biopsy – bleeding; biliary
peritonitis, bleeding from the abdominal wall; leaking of ascitic fluid, respiratory
distress and shock.

C. MANOMETRY

 The alimentary canal relies on motor function and contractions to propel the bolus
of food from the pharynx to the anus.
 Besides mechanical obstructions, motor abnormalities are common in causing
gastrointestinal symptoms.
 The common areas of investigations are:
o Oesophagus
o Stomach and duodenum
o Sphincter of Odi
o Anorectal
 Functional manometry – using electrodes that transmit both pressure and electrical
activity, to computer software, provides information regarding intrinsic motor
function.

18
 1. Oesophagus

Indications
Swallowing disorders
Non obstructive dysphagia
Consequence of oesophagitis on body function.
Upper and lower sphincters; reflux.
Primary Oesophageal motility disorders.
NCCP (non cardiac chest pain)

2. Stomach and Duodenum

Indications
Gastroparesis (delayed gastric emptying)
Functional dyspepsia

3. Sphincter of Odi

Obstruction of flow through the sphincter of Odi may lead to biliary symptoms.
Sphincter of Odi dyskinesia can be investigated by manometry.

4. Colonic and Anorectal disorders

 Constipation - non organic - functional

- spastic pelvic floor syndrome – anismus
- Hirschsprung’s disease
- descending perineum syndrome

 Irritable bowel syndrome

D) OTHER IMAGING

I) ULTRASONOGRAPHY

 Conventional
 Endoscopic

II) CT SCANNING

III) MAGNETIC RESONANCE IMAGING

E) TESTS FOR H.PYLORI

a. INVASIVE – BIOPSY SAMPLE (OF STOMACH MUCOSA)

i. Rapid urease test (CLO)
ii. Histology

b. NON INVASIVE
i. C 13/14 urea breath test (Radio Nuclear Labelled Carbon)
ii. Serum antibodies

F) IMAGES (Check the website to view the images)

19
LT 09.02.06 Pharmacology of Prostaglandins, Cyclo-oxygenase Inhibitors
and the Gastric System

(PDF document is available on the google drive)

LT 09.07.07. Approach to Acute Abdominal Pain

Aim
To study the mechanism of causation of abdominal pain and the associated neural pathways,
to emphasise that there are medical, surgical and psychological causes of acute abdominal
pain and to stress that the cause of abdominal pain may be systemic or the result of
pathology above the diaphragm or pathological processes in the abdomen and pelvis or in
the scrotum.

Delivery objectives
1. Describe the neural pathways that transmit pain sensation from both the parietal and
visceral peritoneum.
2. Describe the various processes that may cause irritation of the peritoneal surfaces (both
medical and surgical causes) and discuss conditions requiring urgent surgery.
3. Explain how pathological processes in the chest may mimic an acute abdomen.
4. Explain how pathological processes in the scrotum may cause an acute abdominal pain.
5. Describe the possible systemic (medical) causes of acute abdomen.
6. Demonstrate a systematic way of taking a history and examining the patient with special
emphasis on the abdomen.

Content
Acute abdominal pain is a common presenting symptom. Pain is a symptom and should be
differentiated from the sign which is elicited on examination (palpation) which is
tenderness.

Abdominal pain may be localised or diffuse colicky or constant.

Diffuse pain implies that there is inflammation of the visceral peritoneum or that there is
widespread inflammation of the parietal peritoneum. Visceral type pain is usually poorly
localised (e.g. the initial phase of acute appendicitis). If there is widespread inflammation
of the parietal peritoneum, the patient often presents with a surgical “acute abdomen”
with board like rigidity on palpation. This is mostly due to a variety of surgical conditions.
A careful history, clinical examination and relevant investigations often results in a correct
diagnosis and treatment. However, it is not unusual for the cause to be identified only at
operation. It should be remembered that there are systemic (medical) causes of an acute
abdomen. These are listed in surgical texts. It may, however, be difficult to manage a
patient who has a pre-existing medical condition which may cause acute abdominal pain
who has in fact got a surgical cause for their abdominal pain.

Acute intestinal ischaemia is a rare event and is seldom diagnosed timeously. The patient
complains of severe diffuse abdominal pain (visceral pain). Characteristically in the initial
stages, there are minimal signs on abdominal examination. By the time there is
inflammation of the parietal peritoneum, there is often irreversible ischaemia of the bowel.

It should also be noted that blood and non-infected bile do not cause peritonism. A
haemoperitoneum due to a ruptured spleen will cause shock before it causes diffuse
peritonitis.

20
Localised abdominal pain mostly implies inflammation of the parietal peritoneum in that
area. It is often preceded by vague, diffuse visceral pain (usually central). This is typical in
acute appendicitis where vague periumbilical pain (and nausea) moves to the right iliac
fossa. The position of localised pain helps in narrowing down the possible causes e.g. right
upper quadrant pain may be due to biliary disease, hepatic disease or a localised
complication of a duodenal ulcer. However, uncommon causes such as a right lower
pneumonia (a supra-diaphragmatic cause of abdominal pain must be excluded.

Colicky abdominal pain implies that the pain is always present but that it gets worse
intermittently. This is typical of obstruction in an organ which has peristalsis such as the
ureter (ureteric calculus causing renal colic) or a small bowel (intestinal colic). Biliary colic
is a misnomer as the bile duct and gallbladder do not have peristaltic activity.

Intermittent pain implies that the pain disappears and then recurs.

Approach to the patient presenting with acute abdominal pain

Whenever possible, a thorough history should be taken. The onset, duration, site and
nature of the pain should be obtained. Relieving and aggravating factors may be helpful.
Radiation of the pain e.g. the pan of pancreatitis is felt in the epigastrium but often
radiates to the back. Associated visceral symptoms such as vomiting, constipation,
obstipation etc should be specifically asked for. A careful past surgical and medical history
is essential. Current medication use is often helpful.

If after initial contact, it is apparent that the patient has a life threatening condition, the
necessary basic and advanced life support measures should be instituted.

A careful systemic examination should be carried out before examination of the abdomen.
The abdomen should be examined in the normal sequence (inspection, auscultation,
palpation and percussion). Examination of the scrotum, groin hernia sites, vaginal and
rectal examination when appropriate is essential. Palpation of the area of maximum pain
should be left to last. Careful monitoring of the patient’s facial response to palpation is
necessary to prevent undue infliction of pain which may compromise the rest of the
examination. Peritonism may be elicited by gentle percussion. There is no place for
eliciting ‘rebound tenderness’.

After a careful history and examination a differential diagnosis will be arrived at.

If there is still diagnostic uncertainty, further investigations are necessary. Simple tests
such as an erect chest radiograph (to check for air under the diaphragm and possible
chest pathology), WCC and CRP, an abdominal radiograph or sonar may suffice.
Occasionally more sophisticated and expensive tests such as a CT scan may be necessary.
It should be remembered that a period of in hospital observation by an experienced
clinician can sometimes be valuable in making a diagnosis.

If it is clear that the patient has an acute surgical abdomen, few if any further
investigations are required to make a diagnosis. However, tests to help with
resuscitation/stabilisation before surgical intervention are commonly required.
Paper-based resources
1. Further Reading
1.1 Most standard surgical texts have lists of the common and unusual causes of
abdominal pain. They include the common surgical and gynaecological causes. Medical
conditions which may mimic an acute abdomen are also listed and discussed.
WHSL Homepage

21
Lectures
L 09.02.01. Anatomy of the Upper GIT
L 09.02.02. Gastric Physiology
L 09.02.03. Pathology of upper GIT I, II & III
L 09.02.04. Peptic Ulcer, H.Pylori and Complications
L 09.02.05. Pharmacology of Anti-Ulcer Drugs
L 09.02.06. Pharmacology of drugs used for nausea & vomiting
L 09.02.07. Reflux
L 09.02.08. Perforated peptic ulcers

L 09.02.01. Anatomy of the Upper GIT

Aim
This lecture covers the clinically relevant anatomy of the abdominal part of the oesophagus,
stomach, small intestines and pancreas.

Delivery objectives
1. Describe the clinically relevant anatomy of the oesophagus, stomach, small intestine and
pancreas.
2. Describe relations of these organs that may have clinical implications.
3. Describe the functions of each of these organs
4. Describe arterial supply and venous and lymphatic drainage.

Content
This lecture covers the following:

 Oesophagus
o Extent
o Cardiac sphincter and anatomical reasons for hernias
o Clinical anatomy
 Stomach
o Clinical anatomy of the stomach
 Small intestine
o Clinical anatomy of the small intestine with special emphasis on
the duodenum

L 09.02.02. Gastric Physiology

Aim
To study the substances secreted by the stomach.

Delivery objectives
1. List the secretory glands/cells of the stomach.
2. Describe the functions of the substances secreted by the stomach.
3. Explain the process of HCl secretion and the mechanism by which it is regulated.

Content
Stomach secretions

The secretory glands in the stomach can be delineated into 3 regional divisions:

1. Cardiac glands: mucus secreting found primarily in proximal stomach.

2. Gastric or oxyntic glands of the fundus and body:
a. Parietal (oxyntic) cells secrete HCl and Intrinsic factor
b. Chief (peptic) cells secrete mucus and HCO 3-

22
 3. Pyloric glands of the antrum region near the pyloric sphincter:
a. Goblet cells secrete mucus into stomach
b. G-cells secrete gastrin into the blood

Functions

1. Hydrochloric acid - produces an acid environment which helps to kill bacteria and to
activate pepsin, solubilises connective tissue and reduces iron to ferrous form for
absorption.
2. Pepsin - proteolytic enzyme secreted in an inactive form (pepsinogen) and
converted by stomach acidity or by autocatalysis to pepsin. Active at pH < 5.0.
3. Mucus - Soluble mucus secreted by neck cells in response to Ach, functions to
lubricate gastric chyme.
Insoluble mucus secreted by surface mucus cells in response to chemical and
physical stimulation by gastric contents, produces a barrier along the walls of the
stomach to protect the stomach from the acid and from physical and chemical
damage.
4. Intrinsic factor - a glycoprotein essential for normal absorption of vitamin B12 in the
ileum. Without intrinsic factor, pernicious anaemia will develop.
5. Gastroferrin - binds Fe++ preventing formation of insoluble iron salts and
phosphates.

The gastric secretions into the stomach lumen form the gastric juice (2-3l/day). At low
secretion rates, gastric juice contains a large amount of NaCl and small amounts of H+ and
K+. When the rate of secretion increases, the concentration of Na + decreases while that of
H+ increases. Coupled with the increase in gastric secretion is an increase in Cl - secretion.

Mechanism of HCl secretion

The driving force of H+ secretion is the H+/K+ pump found on the apical membrane of the
parietal cell. The pump hydrolyses one ATP molecule for each hydrogen ion pumped out of
the cell (primary active transport). K+ pumped into the cell is recycled via an epical K +
channel. The K+ efflux creates an electrical potential gradient which, in turn, promotes the
efflux of Cl- through an epical Cl- channel. HCO3- leaves the cell in exchange for Cl-.
Hydrogen ions and bicarbonate are supplied by the dissociation of carbonic acid, a reaction
that is catalysed by carbonic anhydrase (CA). In the resting cell, acid accumulates in
apical vesiculo-tubular structures within the cell. Upon stimulation, the vesicular
membrane fuses with the apical cell membrane and acid secretion begins. During active
secretion of acid, the pH of venous blood leaving the stomach is elevated by HCO3- ions.
This phenomenon is called the alkaline tide. The mucosal surface of the stomach is
protected by mucus. The surface epithelial cells also secrete HCO3- which is entrapped
within the mucus layer. The mucus gel protects the mucosa from mechanical damage from
chunks of food and the alkaline fluid it entraps protects the mucosa against damage by
HCl and pepsin. The mucus and alkaline secretions form the gastric mucosal barrier that
prevents damage to the mucosa by gastric contents.

Regulation of acid secretion

Acid response to a meal can be divided into 3 phases: The cephalic phase, the gastric
phase and the intestinal phase.

23
Stimuli Pathways to the parietal cell Result
Cephalic phase(central
anticipatory signals) Vagus nerve (Ach) ↑ HCl secretion

Sight G-cells (Gastrin)

Smell Histamine
Taste
Chewing
Hypoglycaemia
Gastric phase Long and short enteric nervous
system reflexes
Stomach distension Gastrin ↑ HCl secretion
H+ concentration
Peptides
Intestinal phase Long and short enteric nervous
system reflexes
Distension ↓ HCl secretion
H+ concentration Secretion
Osmolarity Cholecystokinin (CCK)
Nutrient concentration GOP
Other hormones

Cephalic phase of acid stimulation is neuronal. The CNS sends messages for increased
acid secretion via the vagus nerve that synapses on neurons in the stomach wall enteric
nervous system. Stimulatory postganglionic fibres (Ach) then synapse on parietal cells to
stimulate acid secretion. Some neurons also synapse on G-cells in the antrum to stimulate
gastrin release into the blood. Circulating gastrin will also act on parietal cells to stimulate
acid secretion (40% of acid secretion).

During a meal, the rate of acid secretion increases markedly. Once food enters the
stomach, the meal is considered to be in its gastric phase. Before food entered the
stomach, the luminal H+ concentration was high. Once food enters H+ ions are diluted by
the food. The consequent decrease in concentration triggers more gastrin release (N.B.
acid in the stomach inhibits the release of gastrin; lack of acid stimulates gastrin
secretion). Distension of the stomach walls due to increased contents stimulates stretch
receptors on G-cells, stimulating gastrin secretion. Peptides (in diet and products of pepsin
hydrolysis) stimulates gastrin secretion. Caffeine also stimulates gastrin secretion.

The more gastrin is secreted, the more acid is secreted (50% of acid secretion) As a
feedback protective mechanism, when gastric pH falls below 3, acid secretion is inhibited
by stimulation of D-cells in the antrum which release somatostatin, which acts on G-cells
to inhibit secretion and, thus, gastric acid secretion is inhibited. Once the stomach begins
to empty its contents into the duodenum, the intestinal phase of the meal begins.
During this phase, there is an initial stimulation of acid secretion before pH of duodenal
lumen falls below 3

(10% of acid secretion). Overall, this phase involves inhibition of gastric acid secretion
which occurs when duodenal pH falls below 3. When this happens, secretin, and a number
of other peptides collectively known as enterogastrones are released that inhibit gastrin
secretion. Presence of high concentrations of digestive products (fatty acids, amino acids),
osmolarity stimulate the release of hormones CCK, GIP to inhibit gastrin secretion.
Distention of the intestine stimulates long and short enteric nervous system reflexes
(ileogastric reflex) to inhibit gastrin secretion.

24
 Paper-based Resources
1. Core
1.1 Hard copies of diagrams will be handed out in the lecture.
2. Supplementary
2.1 Appropriate sections of Porth CM. Pathophysiology, Concepts of Altered Disease States. Philadelphia,
Lippincott, 6th Edition.
2.2 Appropriate sections of Ganong WF. Review of Medical Physiology. Lange Medical Books. USA, 19th Edition.
2.3 Appropriate sections of Guyton AC. and Hall JE. Human Physiology and Mechanisms of Disease. WB
Saunders Company. Philadelphia. 6th Edition.
WHSL Homepage

L 09.02.03. Peptic Ulcer, H.pylori and Complications

Aim
To review the role of H. pylori in the pathogenesis of stomach diseases.

Delivery objectives
1. Describe the biology of H. pylori
2. Describe the immunological responses to H. pylori
3. Explain histopathological changes in the stomach mucosa
4. Discuss diseases associated with H. pylori.

Content
The purpose of this lecture will be to study the role of a bacterium i.e. Helicobacter
pylori in the pathogenesis of stomach diseases e.g. gastritis, peptic ulcer disease,
gastric cancer and Ipsid-Malt lymphoma.

1. Historically, gastric acid was thought to be the main culprit for disordered
stomach function. In recent years, a bacterial pathogen has been incriminated.
2. In July 1994, the International Agency for Research on Cancer (part of the
World Health Organisation) determined that there was sufficient evidence to
class H. pylori as a Group 1 carcinogen - an agent that is carcinogenic for
humans. A group 1 carcinogen is the most potent type of carcinogen. H. pylori
has also been declared an important cause of duodenal and gastric ulcers.
3. Patients with duodenal ulcers have a decreased risk of gastric cancer (Harrison
et al N. Engl J Med 1996; 335:242-9), whereas those with gastric ulcers have
an increased risk. The incidence of gastric cancer correlates positively with the
incidence of gastric ulcer but negatively with duodenal ulcer (Correa et al
Aliment Pharmacol Ther 1995; 9: Supp; 2:13-19)
4. Epidemiological evidence suggests that most, but not all, individuals infected
with H. pylori acquire the infection at an early age.
5. Eradication of H. pylori leads to permanent cure of peptic ulcer disease and
anti-H. pylori treatment is appropriate for all patients with duodenal and gastric
ulcers. Triple therapy with bismuth, tetracycline, and metronidazole for 14 days
provides the highest cure rates.
6. Ulcers can result from medications such as nonsteroidal anti-inflammatory agents,
(NSAIDS), which include aspirin and are often used to treat chronic arthritis.

25
L 09.02.04. Pathology of upper GIT I & II

Aim
An overview of the most common non-neoplastic and neoplastic pathologies of the
oesophagus, stomach and small intestine with particular emphasis on chronic / reflux
associated oesophagitis, Barrett’s oesophagitis, chronic gastritis and peptic ulcer disease.

Delivery objectives
1. A few common oral cavity disorders that are specific to this site and may explain
other symptoms from other parts of the gastro-intestinal tract.
2. The causes of acute oesophagitis.
3. The aetiology and pathogenesis of chronic / reflux associated gastritis, the
pathological findings and complications with particular reference to Barrett’s
oesophagitis.
4. The complications of Barrett’s oesophagus.
5. The aetiology of squamous cell carcinoma of the oesophagus and the pathological
features.
6. The mechanisms of gastric mucosal protection and the causes of gastritis and peptic
ulcer disease, emphasizing the role Helicobacter pylori.
7. The pathological features of gastritis.
8. The pathological features of a peptic ulcer.
9. The complications of peptic ulcers.
10. The normal histology of the small bowel and morphological changes of injury.
11. The aetiology of coeliac disease, the macroscopic and microscopic features.
12. Describe some common infections of the small bowel.
13. Discuss the commonest, but overall uncommon, tumours of the small bowel.

Content
a. Oral: Pleomorphic adenoma, oral Candidia and oral hairy leukoplakia.
b. Oesophagus: acute and chronic oesophagitis, Barrett’s oesophagus, and
adenocarcinoma and squamous cell carcinoma.
c. Stomach: acute and chronic gastritis, peptic ulcer disease and adenocarcinoma.
d. Small bowel: coeliac disease, specific infections and common tumours.

L 09.02.05. Pharmacology of Anti-Ulcer Drugs

Aim
Understand the pharmacological principles of drugs used in the prevention and treatment of
peptic ulcers.

Delivery objectives
1. List the different drug groups used in the treatment of peptic ulcers.
2. Discuss the agents used in the treatment of peptic ulcers associated with Helicobacter
pylori.
3. Describe their pharmacological properties (mechanism of action, kinetics, adverse effects,
contraindications and possible drug interactions).

Content

26
In the management of peptic ulcers, initial therapy should include advising patients to
avoid ulcerogenic agents (e.g. NSAIDs) and to stop smoking or drinking alcohol. Patients
should also be informed about other health education and lifestyle modifications such as
an altered diet or stress management.

If this does not alleviate the problem, then drug therapy would include those agents which
raise intragastric pH or enhance mucosal cytoprotection. These drugs include:

 Antacids (aluminium hydroxide, magnesium trisilicate)

 Histamine-2 receptor antagonists (cimetidine, ranitidine)
 Proton pump inhibitors (omeprazole, pantoprazole)
 Cytoprotective agents (misoprostol, sucralfate, bismuth)
 Antimicrobial agents (clarithromycin, amoxicillin, tetracycline, metronidazole)

Thus, the aim of this lecture would be to understand the pharmacological principles of
each drug group used in the prevention and treatment of peptic ulcers. Including:

 Mechanism of action
 Pharmacokinetics
 Adverse effects
 Contraindications
 Drug interactions

Paper-based resources
1. McQuaid KR. Chapter 63: Drugs used in the Treatment of Gastrointestinal
Diseases. Katzung BG. Basic and Clinical Pharmacology. 2004 Lange Medial
Books/McGraw-Hill, New York, Ninth Edition. PP 1034-1044
2. DF Altman. Chapter 63: Drugs used in the Treatment of Gastrointestinal
Diseases. Katzung BG. Basic and Clinical Pharmacology. 2001 Lange Medial
Books/McGraw-Hill, New York, Ninth Edition, PP 1064-1068.

L 09.02.06. Pharmacology of drugs used for nausea & vomiting

(PDF document is available on the google drive)

L 09.02.07. Gastro Oesophageal Reflux Disease

Delivery objectives and Content

 To be discussed at the lecture.

L 09.02.08. Perforated peptic ulcers disease (PUD)

Delivery objectives
 At the end of the lecture the learner will:
 Be able to list the various forms of peptic ulcer
 Be able to list the possible complications of PUD
 Know the common causes of and predisposing factors for peptic ulcer disease (PUD)
 Be able to describe the mechanism of action of Helicobacter pylori in the
pathogenesis of PUD
 Be able to describe how non-steroidal anti inflammatories (NSAIDS) predispose to
PUD

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  Be able to recognise the clinical presentation of perforated duodenal and gastric
ulcers
 Be able to list the conditions that can present in a similar way (differential diagnosis)
 Be able to list the possible neoplasms of the stomach that may perforate
 Be able to describe the intraperitoneal and systemic consequences of a perforated
peptic ulcer
 Be able to list the possible diagnostic tests used to diagnose a perforated peptic ulcer
 Be able to list the possible therapeutic modalities to treat patients with perforated
ulcers and the characteristics of the patient that affect the choice of treatment
 Be able to list the possible long term interventions to prevent ulcer recurrence
 Understand the mechanism of action of H2 blockers and Proton Pump Inhibitors

Theme Sessions

TS 09.02.01. Clinical Anatomy of the upper GIT

TS 09.02.02. Pathology of the upper GIT
TS 09.02.03. Moving bowels – investigations

TS 09.02.01. Clinical Anatomy of the upper GIT

Aim
This theme session covers the clinical anatomy of the oesophagus, stomach, small intestine
and pancreas. The histological structure and function of these structures is also outlined.

Delivery Objectives
1. Describes the clinically relevant anatomy of the oesophagus, stomach, small intestine
and the pancreas.
2. The relations of these organs that may have clinical implications are detailed.
3. Describes the histological structure of each of these.
4. Describes how the structure is adapted to perform its functions.
5. Congenital and mechanical abnormalities are highlighted.

Content

Divisions of the GIT & basic histological structure

1. Oesophagus: Structure & Functions

a. Macroscopic and microscopic appearance

b. Oesophageal hiatus
c. Clinical anatomy

2. Stomach
a. Macroscopic divisions
b. Sphincters
c. Histological structure & secretions
d. Blood supply and lymphatic and venous drainage
e. Clinical anatomy

3. Small intestine
a. Extent & divisions
b. Histological changes in the 3 parts
c. Function
d. Blood supply
e. Innervation
f. Clinical anatomy

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 4. Pancreas
a. Parts of the pancreas
b. Ductal system (including common variations)
c. Exocrine histological structure
d. Blood supply
e. Clinical anatomy

See worksheet

TS 09.02.02. Pathology of the Upper GIT

Aim
To ensure that the student is able to relate the aetiology and pathogenesis of the important
diseases that affect the gastrointestinal tract, including the pancreas, with the identification
of their gross and microscopic features.

Delivery Objectives

1. To identify the common and important diseases of the gastro-intestinal tract and
understand the pathogenetic mechanisms that accompany these changes.
2. To relate these diseases to their broad morphological features.

Content

The pathology of the gastrointestinal tract comprises inflammatory and infective lesions and
neoplasms, as well as a small group of disorders of miscellaneous origin. The approach to
these specific pathological changes is best served by their identification within the specific
anatomical sub-divisions of the system.

Furthermore, certain of these pathological entities are of special importance in South Africa,
including AIDS-related infections and neoplasms including oesophageal and colorectal
carcinoma.

The aetiology, pathogenesis and complications of these specific diseases will be presented as
they are best understood by referral to the gross macroscopy and broad microscopic
features thereof.

TS 09.02.03. Moving bowels – Investigations

Aim
Understand how imaging and endoscopy is used to examine the GI tract and abdomen.

Delivery Objectives
1. Learn clinically relevant gross anatomy of the GI tract and abdomen.
2. Show how imaging and endoscopy is used to examine the GI tract and abdomen.

Content

Learn clinically relevant gross anatomy of the GI tract and abdomen. Understand how
imaging and endoscopy is used to examine the GI tract and abdomen.

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Viseral Organs Imaging Modalities
Oesophagus Barium – Radiology
Endoscopy
Ultrasonography
Stomach Gastroscopy
Radiology: Plain and Contrast (e.g. Barium meal)
Ultrasonography: Endoscopic Ultrasound (EUS)
Nuclear medicine: Gastric emptying study

Small Intestine
Duodenum (four parts) Push enteroscopy (to mid jejunum)
Jejunum Radiology: Plain
Contrast (small bowel series, small bowel enema)
Ileum Angiogram
CT scan
Nuclear medicine: transit study
Large Intestine
Colon Colonoscopy
Radiology: Plain; Contrast (Barium enema)
Angiogram
CT scan
Magnetic Resonance Imaging (MRI)
Nuclear medicine: transit study, RBC scan
Rectum Ultrasonography (Rectal)

Extra-intestinal gastrointestinal organs

Liver Radiology: Plain
CT Cholangiogram
Angiogram
Biliary Tracts & Pancreas Endoscopic Retrograde Cholangio-Pancreaticogram (ERCP)
MRI
Ultrasonograghy/ Doppler studies
Endoscopic Ultrasound (EUS)
Nuclear medicine: Liver/ spleen scan

4. Discuss the interaction of these factors in providing optimal care for the child in hospital.

5. Discuss the importance of the patient / doctor relationship.

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 Theme session: Anatomy of the oesophagus, stomach, small intestine and pancreas

STATION 1 ANSWER
The GIT is conveniently divided into 3 regions based on the different arteries that supply it. Study the
diagrams and answer the following questions
1 Name the constituents of each division of the GIT
2 Name the 3 unpaired branches of the aorta. What does each of these supply?
3 How does gradual occlusion of the abdominal aorta, produced by atherosclerosis
present? Why?
4 Name the three veins that drain each of the divisions of the GIT.
Study the diagram showing the basic/ common histological pattern of the wall of the GIT.
5 What are the different layers that form the wall of the GIT?
6 Identify the features of these layers.
STATION 2 ANSWER
Study the diagrams of the oesophagus.
1 Where does the oesophagus begin and end?
2 Name the important relations of the thoracic part of the oesophagus.
3 At what vertebral level does the oesophagus pierce the diaphragm?
4 Through which part of the diaphragm does the oesophagus pass?
5 What is the gastro-oesophageal sphincter? Explain how this sphincter works.
The oesophagus is accompanied through the oesophageal hiatus by the right and left vagal trunks.
6 Why are these trunks referred to as anterior and posterior trunks in the abdomen?
STATION 3 ANSWER
Study the barium swallow radiograph of a normal oesophagus and of achalasia.
1 Identify the three normal constrictions of the oesophagus and name the anatomical
reason for their presence.
2 Why are these constrictions clinically important?
3 What is achalasia? What is its likely anatomical cause?
Study the slides of the oesophagus.
4 What is the function/s of the oesophagus?
5 How is the wall of the oesophagus adapted for these functions?
6 What features of the wall protect it from developing ulcers?
7 Identify the changes in the mucosal and submucosal layers in the transition from the
oesophagus to the stomach.
STATION 4 ANSWER
Study the diagrams and radiographs of the stomach.
1 Identify the following regions of the stomach: fundus, body, pylorus, angular notch,
cardiac orifice, pyloric sphincter, greater and lesser curvatures.
2 Identify the greater and lesser omentum. Where do these structures attach?
3 Name the structures on which the stomach lies (stomach bed).
4 What are hiatal hernias? Differentiate between the 2 types.
5 Pylorospasm sometimes occurs in infants between 2-12 weeks. Discuss the anatomical
reasons for this.
STATION 5 ANSWER
Study the diagrams, endoscopic images and slides of the stomach.
1 Describe the macroscopic appearance of the internal surface of the stomach.
2 List the functions of the stomach.
3 Describe the histological structure of gastric glands and name their secretions.

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 4 In which part of the stomach are these glands located?
5 Describe the features of the wall of the stomach that prevent it from developing peptic
ulcers.
6 Study the radiographs of gastric and duodenal ulcers and note their features.
7 When, where and why is pain from the peptic ulcer referred to the back?
8 Why is selective vagotomy indicated in the treatment of unresponsive gastric ulcers?
STATION 6 ANSWER
Study the diagrams of the blood supply to the stomach.
1 Identify the coeliac trunk and its branches. Which of these contribute to the arterial
anastomosis around the stomach?
2 Where does venous blood from the stomach drain to?
3 Why do surgeons use the prepyloric vein to identify the pylorus?
4 Describe the arterial supply and venous drainage of the oesophagus.
5 Why is it possible to ligate one or more arteries that supply the stomach during
gastrectomy?
6 Where does lymph from the stomach drain to?
STATION 7 ANSWER
Study the diagram and table of the duodenum
1 Identify the different parts of the duodenum
2 What are the relations of each part of the duodenum? Note the peritoneal relationship.
3 Name the structures which open into the major and minor duodenal papillae. Where are
these papillae situated?
4 What is the suspensory muscle of the duodenum (ligament of Treitz)? What is the effect
of contraction of this structure?
5 Note the position of the duodenal recesses. Why are these clinically important?
STATION 8 ANSWER
Study the radiograph and diagram of the duodenum.
1 Where is the most common location of duodenal ulcers?
2 What are the consequences of a perforated duodenal ulcer?
3 What is the function/s of the duodenum?
4 How is the structure of the wall adapted for these functions?
5 Name the submucosal glands found in the duodenum.
STATION 9 ANSWER
Study the diagram and slides of the small intestine.
1 Describe the root of the mesentery of the jejunum and ileum.
2 Identify the structures that the mesentery crosses in its attachment.
3 Name the structures that are found between the 2 layers of the mesentery.
4 Name the main arterial supply to the small intestine. What is the result of occlusion to
this vessel?
5 Briefly describe the venous drainage of the small intestine.
6 Describe the structure of the villi and intestinal glands in the wall of the jejunum.
7 What is the function of Peyer’s patches in the ileum?
8 Describe the change in the concentration of goblet cells from the duodenum to the ileum.
What is the significance of this change?
STATION 10 ANSWER
Study the diagrams and slides of the pancreas.
1 Identify the different parts of the pancreas and review the relations.
2 Describe the macroscopic and microscopic structure of the ductal system of the
pancreas.

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3 Describe the histology of the exocrine pancreas.
4 Describe the features of the acinar cells.
5 Name the functions of the gland.
6 Revise the histological structure of the endocrine pancreas.
7 Where does the pancreas derive its arterial supply from?
8 What is an annular pancreas? How is this caused and what are the clinical implications?

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