South African Family Practice 2015; 57(4):13-19

S Afr Fam Pract

Open Access article distributed under the terms of the ISSN 2078-6190 EISSN 2078-6204
Creative Commons License [CC BY-NC-ND 4.0] © 2015 The Author(s)
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REVIEW

Gastric pain
Natalie Schellack,* Gustav Schellack, Nicolene van der Sandt, Bongiwe Masuku

Department of Pharmacy, Faculty of Health Sciences, Sefako Makgatho Health Sciences University
Corresponding author, email: natalie.schellack@smu.ac.za
*

Gastric pain may be generalised, diffused, specific to the right or left upper quadrant (or both), and may be attributed to a range of
possible causes. Types of gastric pain include dyspepsia and epigastric pain. The term “gastric pain” is not frequently encountered
in the literature. Therefore, the main focus of this review is on epigastric pain and dyspepsia, both of which are frequently
encountered in the clinical setting. For example, it is estimated that dyspepsia affects a quarter of the global population. Several
drugs and drug classes are also linked to a range of mechanisms through which the drugs induce mucosal injury in the upper
gastrointestinal tract. Therefore, this article provides an overview of the aetiology, classification, risk factors, diagnostic criteria and
management strategies aimed at gastric pain, and its two more distinct gastrointestinal-related manifestations, namely epigastric
pain and dyspepsia.

Keywords: gastric pain, epigastric pain, dyspepsia, peptic ulcer disease (PUD), GORD, proton-pump inhibitors

Introduction Table 1: Different areas of gastric pain and their associated causes6

The term “gastric pain” originates from the Greek word, gaster, Area Possible causes
and modern Latin term, gastrics, used in the mid-17th century,
General gastric pain • Stomach ulcers
which translates to “of the stomach”. Gastric pain is currently
• Heartburn and indigestion
commonly used to describe pain or discomfort in the upper • Pancreatitis
abdomen. It may be generalised, diffused, specific to the right or • Epigastric hernia
left upper quadrant (or both), and may be as a result of a range • Gallstones
of possible causes. Types of gastric pain include dyspepsia and
Diffuse gastric pain • Acute pancreatitis
epigastric pain. Epigastric pain is defined as pain that is localised • Diabetic ketoacidosis
in the upper-middle region of the abdomen.1-3 • Early appendicitis
• Gastroenteritis
Conversely, “dyspepsia” is the often recurring sensation of either • Intestinal obstruction
pain or discomfort in the area of the upper abdomen. The term • Mesenteric ischaemia
is used to refer to a variety of symptoms which are thought to • Peritonitis (any cause)
originate in the gastrointestinal tract. These include heartburn, • Spontaneous peritonitis
• Typhoid fever
epigastric pain, nausea, vomiting, a feeling of early fullness
• Sickle cell crisis
(satiety) and bloating.4 Dyspepsia is a complex disease. Numerous
potential mechanisms underlie its pathophysiology, including Right or left upper • Acute pancreatitis
abnormal intestinal motility and visceral hypersensitivity, as well quadrant pain • Herpes zoster
• Lower lobe pneumonia
as genetic, infectious, post-infectious and psychosocial factors.5
• Myocardial ischaemia
The term “gastric pain” is not frequently encountered in the • Radiculitis

literature. Therefore, the main focus of this review will be on Right upper quadrant • Cholecystitis and biliary colic
epigastric pain and dyspepsia. pain • Congestive hepatomegaly
• Hepatitis or hepatic abscess
Aetiology • Perforated duodenal ulcer
• Retrocecal appendicitis (rarely)
Epigastric pain has several different causes which are linked to
the localisation of gastric pain. Table 1 provides an exposition of Left upper quadrant • Gastritis
such causes, grouped according to the area of discomfort.6 pain • Splenic disorders (abscess and rupture)

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14 S Afr Fam Pract 2015;57(4):13-19

Risk factors for the development of epigastric pain Table 2: Diagnostic criteria for postprandial distress syndrome and
and dyspepsia epigastric pain syndrome8

The following factors increase the likelihood of significant Postprandial distress syndrome Epigastric pain syndrome
organic disease, and are trigger points for referral:7 Troublesome postprandial Pain or burning localised to the
fullness, after a standard-sized epigastrium of at least moderate
• Advancing age: Being 50 years of age or older at the first
meal, occurring several times per severity at a minimum of once
presentation. (The incidence of gastric cancer increases with week (at a minimum) per week
age) and
• A family history of gastric cancer, especially when the age of And/or Intermittent pain
and
onset is younger than 50 years Early fullness which prevents a Not generalised or localised to
• Severe or persistent dyspepsia regular meal from being finished, other abdominal or chest regions
• Treatment failure occurring several times per week and
(at a minimum) Not relieved by defecation or
• A history of peptic ulcer disease, particularly if complicated
passage of flatus
• The consumption of nonsteroidal anti-inflammatory drugs and
(NSAIDs), including aspirin Not fulfilling the criteria for
disorders of the gallbladder and/
• Severe, debilitating pain, or pain which wakes the patient at
or sphincter of Oddi
night
• Referred pain Supportive criteria

• Chronic gastrointestinal tract bleeding signs and symptoms, • Upper abdominal bloating, • The pain may be of a burning
including melena stools postprandial nausea or quality, but without a
excessive belching retrosternal component
• Iron-deficiency anaemia
• Epigastric pain syndrome may • The pain is commonly induced
• Dysphagia be coexistent or relieved by the ingestion of
• Persistent or protracted vomiting, with or without blood, or a meal, but may occur during
fasting
the persistent regurgitation of food
• Postprandial distress syndrome
• A palpable abdominal mass may be coexistent
• Coughing spells or nocturnal aspiration
• Unexplained weight loss • Bacterial overgrowth of the small intestine
• Continued changes in bowel habits. Table 3: Common causes of dyspepsia and their suggestive findings9

Criteria for the diagnosis of epigastric pain and Cause Suggestive findings
dyspepsia
Achalasia • Slowly progressive dysphagia
Because dyspepsia is a frequent clinical problem, the cornerstone • Early satiety, nausea, vomiting and
of the initial evaluation rests upon the identification of possible bloating
• Symptoms are exacerbated by food
causes. Heartburn and retrosternal pain are exceptions to • Occasional nocturnal regurgitation of the
the diagnostic criteria for dyspepsia. Heartburn is believed to undigested food
emerge from the oesophagus, which may be more indicative • Chest discomfort
of gastro-oesophageal reflux disease (GORD). However, it may Cancer, i.e. oesophageal • Chronic or vague discomfort
still occur as a coexistent condition. Conversely, non-cardiac or gastric • Later, dysphagia (oesophageal) or early
fullness (gastric)
chest pain should be differentiated from retrosternal pain, which
• Weight loss
originates from the oesophagus.8
Coronary ischaemia • Symptoms described as gas or
Furthermore, as per the Rome III criteria, symptoms are typically indigestion, rather than chest pain by
present for at least three months (symptoms may also classically some patients
• May have an exertional component
be sustained over six months or longer) in the case of functional • Cardiac risk factors
dyspepsia. Dyspepsia is also grouped by the Rome III criteria into
Delayed gastric Nausea, bloating and fullness
two separate categories, namely postprandial distress syndrome
emptying, caused by
(PDS) and epigastric pain syndrome (EPS) (Table 2).8 In addition, diabetes, viral illness or
the common causes of dyspepsia and their suggestive findings drugs
are outlined in Table 3. Oesophageal spasm Substernal chest pain, with or without
dysphagia for liquids and solids
A number of less probable causes should also be considered,
including the following:8 Gastro-oesophageal • Heartburn
reflux disease • Occasional reflux of acid or the stomach
• Pancreatic or hepatobiliary tract disease contents into the mouth
• Coeliac disease • Symptoms occasionally triggered by lying
down
• Infiltrative diseases of the stomach
• Relief with antacids
• Motility disorders
• Metabolic disturbances Peptic ulcer disease Burning or distressing pain, relieved by food
or antacids
• Intestinal angina
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Gastric pain 15

Dyspepsia causes Dyspepsia risk factors Dyspepsia characteristics

The majority of cases constitute functional The risk factors for dyspepsia are as The characteristics of dyspepsia are as
dyspepsia follows: follows:
Five major causes include: • A history of previous peptic ulcer • A feeling of postprandial fullness or
• GORD disease heaviness
• Chronic peptic ulcer disease • Age > 60 years • Early satiation
• Gastric cancer and other malignancies • High-dosage or prolonged use of • Acid heartburn (associated with GORD),
• Gallstones NSAIDs epigastric pain and epigastric burning
• Medication • Peptic ulcer disease that is associated • Non-cardiac chest pain
• Functional dyspepsia with Helicobacter pylori • Less specific symptoms include nausea,
• Chronic alcohol use vomiting, bloating, belching, gas and
• A smoking habit abdominal distension
• Stress and depression
(Patients who suffer from functional
dyspepsia usually experience intermittent
symptoms over the long term,
interspersed with periods of remission)

GORD: gastro-oesophageal reflux disease, NSAIDs: nonsteroidal anti-inflammatory drugs

Figure 1: Common risk factors, causes and characteristics of dyspepsia8,10-13

• Irritable bowel syndrome If a patient complains of indigestion, the healthcare professional

• Diabetic radiculopathy should contemplate all potential causative factors, including
• Intestinal hernia those originating from the oesophagus, stomach, heart, liver,
• Abdominal wall pain. gall bladder, pancreas and intestines, as well as the use of NSAIDs
and other medication.15
Classification of dyspepsia
Medication which may cause dyspepsia and epigastric
Dyspepsia can be classified as being either organic or non- pain
organic in nature.9-11
Medicine is commonly seen as a potential causative factor
Organic dyspepsia has a known underlying cause, such as gastric of dyspepsia. However, the symptoms experienced are often
cancer, peptic ulcer disease (PUD), chronic alcohol use and drug- assigned to a disease, rather than to drug therapy. Owing to the
induced gastric discomfort, or stress. Treatment of the underlying high occurrence of dyspepsia, it is troublesome to differentiate
cause may eliminate the symptoms. between spontaneous and true drug-related dyspepsia.4
Non-organic (functional or non-ulcer) dyspepsia is characterised The sensitivity of the patient is a considerable contributing factor
by the presence of dyspeptic symptoms originating in the to the experienced symptoms. Other contributing factors include
gastroduodenal region, but with no indicated abnormalities on dose-related side-effects, a history of pre-existing disease, e.g. a
physical examination and upper gatrointestinal endoscopy. peptic ulcer, and the intrinsic defects of the gastrointestinal tract,
e.g. gastric atrophy, coeliac disease and ageing.4
Figure 1 summarises the most common risk factors, causes and
characteristics of dyspepsia. Individual mechanisms are of significance in determining side-
effect profiles and accompanying individual susceptibility
Globally, approximately 25% of the population suffers from
factors. These include age, gender, genetic and physiological
dyspepsia, with rates ranging from 13–40% in different
factors, and underlying disease.4 Table 4 provides a list of
countries.14
medication which could cause dyspepsia and epigastric pain,
Red flags for dyspepsia together with the associated mechanisms of mucosal injury.

According to Greenberger, the following findings are of particular Management strategies for gastric pain
concern:9
The management of peptic ulcer disease
• Acute episodes accompanied by dyspnoea, diaphoresis or
tachycardia The treatment of chronic PUD varies, depending on the aetiology
of the ulcer (Helicobacter pylori or NSAIDs), whether the ulcer is
• Anorexia
initial or recurrent, and whether complications have occurred.
• Nausea or vomiting
The treatment goal is to relieve pain, heal the ulcer, and prevent
• Weight loss ulcer recurrence and to reduce ulcer-related complications.17
• Blood in the stools
The goal is to eradicate the organism, to heal the ulcer and to
• Dysphagia or odynophagia cure the disease for H. pylori-positive patients, who should be
• Failure to respond to therapy with H2-receptor blockers or initiated on a PPI-based, three-drug regimen which includes
proton-pump inhibitors (PPIs). the PPI once or twice a day, clarithromycin 500 mg twice daily,
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16 S Afr Fam Pract 2015;57(4):13-19

Table 4: Medication which could cause dyspepsia and epigastric pain4,16

Medication Mechanism of mucosal injury

Sustained-release medication and hygroscopic medication

Sustained-release medication • Non-specific, direct mucosal injury: Oesophageal injury can result from direct, prolonged mucosal contact with
and hygroscopic medication tablets or capsules due to insufficient clearance from the oesophagus in the supine position. The most common
reason is ingestion with an inadequate (< 100 ml) amount of fluid being consumed
• Contributing factors include acidity, alkalinity, the drug dissociation rate, osmolality, and intrinsic chemical
toxicity and hygroscopicity, which may result in a high ulcerogenic concentration, e.g. potassium chloride
• Sustained-release drugs may be more harmful to the oesophagus in the case of prolonged contact

Pain and fever, and These agents are gastric irritants which may cause damage throughout the gut. The major underlying mechanism
anti-inflammatory drugs of injury is thought to be due to direct cellular toxicity and disruption of the mucosal barrier (a local effect), rather
Examples of NSAIDs are: than by inhibiting prostaglandin synthesis (systemic effect)
• Indomethacin
• Meclofenamate
• Piroxicam

Acetylsalicylic acid More likely to cause gastric irritation

COX-2 inhibitors Cause less damage to the upper gastrointestinal mucosa than traditional NSAIDs, but dyspepsia remains a
significant problem

Sulphasalazine An intestinal anti-inflammatory agent, which may also cause dyspepsia

Corticosteroids • Dyspepsia occurs with all corticosteroids and is dose related to some extent, but is still dependent on individual
sensitivity, and is more common in patients with a history of previous ulcers
• Large dosages of glucocorticosteroids have been associated with the development of peptic ulcers due to the
suppression of the local immune response to Helicobacter pylori

Antimicrobial agents and drugs that act on the gastrointestinal tract

• Erythromycin directly stimulates the motilin receptors on the gastrointestinal smooth muscle, which may lead to
Macrolides, such as alterations in gastric motility
erythromycin, PPIs and • An induction of gastric acid rebound induces an increased (and paradoxical) capacity for gastric acid secretion.
H2-receptor antagonists, share The suggested mechanism of injury includes changes in gastrin secretion, which is induced by pH changes in
similar mechanisms of injury the gastric antrum due to prolonged acid inhibition
• Gastrin has a confirmed trophic effect on the oxyntic mucosa, which may induce hyperplasia or hypertrophy of
the enterochromaffin-like cells and the parietal cells. This rebound acid hypersecretion induces dyspeptic and
reflux symptoms in patients once the drugs which inhibit their acid secretion are stopped
• Newer macrolides, such as azithromycin, clarithromycin and roxithromycin, are better tolerated and cause fewer
adverse events

Tetracyclines • Mild gastrointestinal disturbances are common. Nausea, vomiting and epigastric burning are the most frequent,
but oesophageal ulcers may be the most dramatic
• An acute onset of a substernal burning pain and dysphagia has been described in cases where remaining parts
of ingested tetracycline capsules have been identified by endoscopy

Itraconazole, terbinafine, Cause gastrointestinal upset and may provoke dyspepsia

ribavirin, abacavir and
oseltamivir

Drugs that act on the central nervous system

Risperidone and the SSRIs Increased serotonergic activity in the gut is commonly associated with gastrointestinal upset, and may lead to
the induction of dyspepsia. However, adverse gastrointestinal effects tend to emerge early on in treatment, and
subsequently tend to improve after the first week of therapy

Drugs that act on the immune system

Oral methotrexate, tacrolimus, Mucositis is a frequent adverse effect of the immunosuppressive agents, and this leads to painful inflammation and
D-penicillamine and ulceration of the mucous membranes that line the digestive tract
mycophenolate sodium

Various other drugs

Iron • Dyspepsia can be seen with higher dosages

• Iron has a well-known reputation for poor gastric tolerance

Oral nicotinic acid, sildenafil May provoke GORD owing to the anticholinergic properties of these agents which facilitate the relaxation of the
and tadalafil, theophylline and lower oesophageal sphincter
the calcium-channel blockers

Bisphosphonates Generally associated with improper ingestion and inappropriate timing of the drug intake

Potassium chloride Is irritating to the gastrointestinal tract, which may lead to perforations of the gut and finally result in ulcer
formation
COX-2: cyclo-oxygenase-2, GORD: gastro-oesophageal reflux, H2-receptor antagonists: histamine type 2-receptor antagonists, NSAIDs: nonsteroidal anti-inflammatory drugs, PPIs: proton-pump
inhibitors, SSRIs: selective serotonin reuptake inhibitors

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Gastric pain 17

and amoxicillin 1 g twice daily (or metronidazole twice daily, if Acid suppression is the mainstay of therapy. The PPIs provide the
allergic to penicillin)17 (Table 5).18 greatest symptom relief and the highest healing rates, especially
in patients with complications, moderate to severe symptoms, or
Table 5: Recommended seven-day regimen for the eradication of
Helicobacter pylori 18 erosive disease.21

Rx: Nonpharmacological measures

A proton-pump inhibitor, e.g. omeprazole 20 mg, twice daily, for 7
Patients should be advised to refrain from indulging in foods
days
or
which trigger the onset of dyspeptic symptoms, such as chillies,
An H2-receptor antagonist, e.g. ranitidine 150 mg, twice daily, or 300
spices, fat, orange juice, tomato juice, coffee and alcohol.
mg at bedtime if proton-pump inhibitors are contraindicated Smaller meals should be taken more frequently, so as to avoid
plus unnecessary gastric distension. Patients are advised to avoid the
Two of the following antibiotics: use of NSAIDs and other medication with a strong link to the
• Clarithromycin 500 mg twice daily occurrence of dyspepsia, wherever possible. If a NSAID must be
• Amoxicillin 1 g twice daily
used, then the patient should also be given preventative therapy
• Metronidazole 400 mg twice daily
to avoid the uncomfortable dyspeptic symptoms.8,11,21,22
Rx: treatment

Additional measures include:21

Healing the ulcer as rapidly as possible is the specific goal of • Elevating the upper body when lying in bed or sleeping at
patients with NSAID induced-ulcers. Patients who are at risk of night, to facilitate oesophageal clearance
developing NSAID-induced ulcers should receive prophylactic
• Weight reduction in obese patients (reduces symptoms)
co-therapy or use a cyclo-oxygenase-2 (COX-2) inhibitor. PPI
• Additional dietary measures include avoiding foods which
co-therapy reduces the risk of NSAID-associated ulcers, is as
decrease lower oesophageal sphincter pressure or increase
effective as recommended dosages of misoprostol, and is
transient lower oesophageal sphincter relaxation, e.g. fats,
superior to H2-receptor antagonists. Standard PPI dosages and
chocolate, alcohol, peppermint and spearmint, and including
nonselective NSAIDs are as effective as selective COX-2 inhibitors
protein-rich meals in the diet to augment lower oesophageal
in reducing risk.17
sphincter pressure.
The intravenous administration of a PPI loading dosage, followed
Behavioural changes that may reduce oesophageal acid
by 72-hour continuous infusion, is the recommended treatment
exposure include:21
for severe peptic ulcer bleeding, after appropriate endoscopy
treatment. The goal is to maintain an intragastric pH of > 6.17 • Eating smaller meals more frequently, and avoiding sleeping
immediately after a meal
The management of dyspepsia
• Smoking cessation, if applicable
As already mentioned, the treatment approach to patients with • Avoiding wearing tight-fitting clothes
dyspeptic symptoms, as for acid heartburn and GORD, aims to19,20
• Always taking medication while in an upright or sitting
decrease the amount of stomach acid which enters the distal
position, and with a sufficient quantity of liquid.
oesophagus, usually by neutralising the stomach acid, decreasing
the production of hydrogen choloride (HCl), and increasing the Pharmacotherapy
rate at which the stomach empties into the duodenum, as well as
The following drug options may be used to treat dyspepsia.
relieving the discomfort caused by heartburn.
Simple antacids: Simple antacids, although very widely used in
The major drug targets in the current practice setting are the
the over-the-counter setting as symptom alleviators for acid
so-called proton pump (or the H+/K+-ATPase pump), the gastric
heartburn, may have very limited value in the management of
H2 receptor and the gastrointestinal 5-hydroxytryptamine 4
functional dyspepsia. Simple antacids, such as those containing
(5-HT4) receptor. These targets may be supported by simple
aluminium and magnesium, neutralise hydrochloric acid (HCl)
antacids and the prostaglandin analogues. The pharma-
in the stomach and are quite effective as pain relievers. The
cotherapeutic measures may be supported by basic, nonpharma-
magnesium-containing antacids cause diarrhoea, while the
cological intervention strategies.
aluminium-containing ones cause constipation. Therefore, a
Treatment is determined by the disease severity and includes:21 combination of magnesium and aluminium constitutes the
• Lifestyle changes and patient-directed therapy with an antacid of choice, e.g. a combination of aluminium hydroxide
antacid, non-prescription H2-receptor antagonist and/or non- and magnesium trisilicate.
prescription PPI However, the divalent cations, i.e. Al2+ and Mg2+, interact with
• Pharmacological treatment with prescription-strength acid- chelating agents, such as the tetracycline and fluoroquinolone
suppression therapy antimicrobial agents, and several other drug interactions are
• Anti-reflux surgery (a viable treatment alternative for patients possible. Combining an antacid with an alginate may actually
when long-term pharmacological treatment is undesirable, or prevent reflux in that the alginate literally forms a “floating gel”
when patients have refractory symptoms or complications). on top of the gastric contents. Calcium carbonate and sodium

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18 S Afr Fam Pract 2015;57(4):13-19

bicarbonate may also be used as a simple antacid. However, care to-mucus secretion favourably by increasing gastric mucus
should be taken with these agents since calcium carbonate may secretion, while decreasing acid secretion. However, care should
interfere with the normal acid base balance and cause metabolic be taken with this drug since PGE1 causes uterine contractions,
alkalosis, or may elicit rebound gastric acid secretion, making it may be used for the termination of pregnancy or the induction
suitable for short-term use only. Sodium bicarbonate should be of labour, and therefore should be avoided during pregnancy.
used with caution in patients who require a restricted sodium Bismuth compounds may also be used.19,20,23
intake. Dimethicone and simethicone may relieve a “bloated
Prokinetic agents: Metoclopramide acts as an agonist at the
feeling” by acting as an antiflatulent or defoaming agent. These
latter agents may also be of benefit in the management of gastrointestinal 5-HT4 receptors, thus increasing the rate of
intestinal colic in infants and children.19,20,23 gastric emptying and peristalsis. Domperidone has a similar
mechanism of action, but differs from metoclopramide in that it
The H2-receptor antagonists: Blocking the gastric H2 receptors does not cross the blood-brain barrier. Cisapride is another 5-HT4
of the parietal cells reduces stomach acid secretion. Ulcer receptor agonist, and is unrelated to the previously mentioned
healing rates are significant, but not nearly as good as those two drugs. It has the disadvantage of causing potentially serious
obtained through the use of PPIs, although these agents are cardiac side-effects, such as ventricular dysrhythmias by causing
good alternatives to PPIs in situations when the latter agents QTc interval prolongation, especially when its own metabolism
are contraindicated. Cimetidine, ranitidine, famotidine and is inhibited, for instance, through various drug interactions.
nizatidine are examples of selective H2-receptor blockers. Access to this drug has been restricted, and it should be used
Cimetidine has the disadvantage of sometimes producing with extreme caution. Bethanechol is a parasympathomimetic
unwanted anti-androgenic side-effects in male patients. (It has a drug which selectively stimulates the muscarinic receptors. This
fairly small affinity for androgen receptors). There is also a higher
causes smooth muscle contraction in the gastrointestinal tract,
likelihood of multiple drug interactions through its inhibition of
but produces relaxation of the sphincters. Therefore, bethanechol
the cytochrome P450 isozymes.11,19,20,23
stimulates the functional contraction of the gastrointestinal
Proton-pump inhibitors: PPIs enter the parietal cells of the gastric tract, i.e. it increases intestinal motility. The use of neostigmine
glands found in the gastric pits of the stomach lining, where they is a different approach and results in a similar outcome with
subsequently inhibit the H+/K+-ATPase pump, i.e. the “proton respect to the motility of the gastroinstesinal tract. Erythromycin
pump” that is specifically responsible for H+ secretion in the also has prokinetic properties.19,20,23
lumen of the gastric pits where these cations combine with the
Helicobacter pylori eradication: Similar to the management of
secreted Cl- from a separate pump to form HCl. This effectively
PUD, the eradication of H. pylori may be warranted in certain
prevents the secretion of gastric acid from the gastric pits into the
situations, or when a seeming case of functional dyspepsia has
lumen of the stomach. Therefore, these drugs are highly effective
not yet been fully evaluated. H. pylori damages the mucous
in increasing the stomach pH, rapidly relieving the symptoms
lining of the stomach and duodenum. This then exposes the
and achieving good cure rates. Well-known examples of PPIs
gastric tissue to damage by gastric acid and pepsin, and gastric
are omeprazole, esomeprazole (the S-isomer of omeprazole),
ulceration occurs. A seven-day regimen is used to eradicate
lansoprazole, pantoprazole and rabeprazole. The PPIs are widely
H. pylori in patients suffering from dyspepsia in South Africa
regarded as the first-line treatment option of choice and have
(Table 5).18
well-documented, superior efficacy levels compared to the other
acid-lowering drugs that are currently available. PPIs should Conclusion
preferably be taken 30-60 minutes before the first meal of the
day for optimal effectiveness.11,19,20,23 Epigastric pain and dyspepsia are two commonly occurring
types of gastric pain. It is most likely that dyspepsia originates
Cytoprotective agents: These drugs are referred to as from the gastrointestinal tract and encompasses a variety of
cytoprotective because they protect the cells of the stomach symptoms. These include heartburn, epigastric pain, nausea,
lining against the corrosive effects of stomach acid. In addition, vomiting, a feeling of early satiety and bloating. Dyspepsia may
misoprostol also promotes the perfusion of the gastric mucosa also be classified as being either functional or organic in nature,
because it is an analogue of prostaglandin E1 (PGE1). These and may manifest itself as either PDS or EPS according to the
agents may be more effective in the management of acid Rome III criteria. Conversely, epigastric pain, albeit one of the
heartburn than in that of functional dyspepsia. Sucralphate possible symptoms of dyspepsia, may also occur as a symptom
forms a protective layer that covers the exposed surface of the of several other conditions of the gastrointestinal system.
ulcer, and in so doing produces cure rates that are comparable
to those obtained with the H2-receptor antagonists. Preferably, Dyspepsia has no known, definitive, underlying patho-
sucralphate should be taken one hour before meals since it is physiological mechanism. It is a set of disorders that may even
activated by stomach acid. Wherever sucralphate is combined relate to co-morbidities such as malignancies and irritable
with any of the simple antacids, the antacid should be taken bowel syndrome. NSAID therapy is another well-known cause.
half an hour after taking the sucralphate, i.e. on an empty Physicians and healthcare professionals should be aware of
stomach as well. Misoprostol is of particular use in preventing dyspepsia and its treatment strategies since it constitutes a
the gastrotoxic effects of NSAIDs. It influences the ratio of acid- significant disease burden worldwide. Effective diagnosis and
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Gastric pain 19

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