1.2.3 Approach to Gastritis & Peptic Ulcer Disease in Clinical Practice.pdf

Clinical Officer General Programme
Target: Intermediate & Finalist Students
2022 Version
Unit: Gastroenterology PBL Series
Lecture: Approach to Gastritis & Peptic Ulcer Disease
INTERNAL MEDICINE II PREP PACK
ML LUBUNDI
Dip, BSc CM,PgCert.ME,DPH,PgCert.HPE,mZMLPA,mANCP,mIAPAE,APGD TMSI (IP)
CERTIFIED HEALTH PROFESSION EDUCATOR-UNZA SoM (DMED)
INTERNATIONAL FACULTY MENTOR (MEDICINE)-IFPACS 1
MEDSUPA REVISION INITIATIVE

Sayings of the Wise
 To study the phenomena of disease without books is to
sail an uncharted sea,
 To study books without patients is not to go to sea at all.
Sir William Osler (1849-1919)
Monday, December 26, 2022 Lubundi K MLP 2022-Bye Bye!!!!!!!!!! 2

SSBT
 Define gastritis and peptic ulcer diseases (PUD).
 List the aetiologies of gastritis and PUD
 Describe the epidemiology of PUD
 Explain the pathogenesis gastritis and PUD
 Describe the clinical features of gastritis and PUD
 List the common complications gastritis and PUD
 Describe the most commonly used methods for the diagnosis
of gastritis and PUD
 Make an accurate diagnosis of gastritis and PUD
 Treat gastritis and PUD at the primary care level with
appropriate drugs
 Refer those presenting with complications of gastritis and PUD
to the next level of healthcare 3

Epidemiology
Incidence: ∼ 1
case/1,000
person-years
Prevalence: ∼ 6
million cases
annually in the
US
The prevalence of
PUD is
decreasing
Duodenal ulcers
occur on average
10–20 years
earlier than
gastric ulcers
Age: The median
age of diagnosis
is 18–30 years.
Sex: M = F

The Stomach & Duodenum

 The stomach is a muscular pouch continuous from the
esophagus (the cardia) to the pylorus.
 It consists of the cardia, an upper region (the fundus, under the
left diaphragm), the mid-region or body and the antrum, which
extends to the pylorus.
The cardia is lined by mucin
Secreting foveolar cells that form shallow glands.
The fundus contains parietal cells and chief cells.
The body also contains parietal and chief cells.
The antrum contains G-cells and D cells.
The pylorus has a sphincter separating the stomach from the
duodenum Lubundi K MLP 2022-Bye Bye!!!!!!!!!! 6

Lubundi K MLP 2022-Bye Bye!!!!!!!!!! 7

 It serves as a reservoir where food can be retained (Stomach
capacity=1500- 3000ml) and broken up before being actively
expelled into the proximal small intestine.
 The stomach is innervated by the vagus nerve.
 The smooth muscle of the wall of the stomach has 3 layers:
Outer longitudinal
Inner circular
Innermost oblique
Lubundi K MLP 2022-Bye Bye!!!!!!!!!! 8

 There are 2 sphincters,the gastro-esophageal sphincter and the
pylorc sphincter.
 The pyloric sphincter is largely made up of a thickening of the
circular muscle layer and controls the exit of gastric contents
into the duodenum.
 The duodenum has outer longitudinal and inner smooth muscle
layers, it is C-shaped and the pancreas sites in the concavity.
 It terminates at the duodenojejunal flexure where it joins the
duodenum.
 The mucosal lining of the stomach can stretch in size with
feeding. The greater curvature of the undistended stomach has
thick fold or rugae.
 The mucosa of the upper 2/3 of the stomach contains:
 Parietal cells which secrete hydrochloric acid and intrinsic factor.
 Chief cells these secrete pepsinogen (which initiates proteolysis)
9

 There is a color change at the junction between the body and
the antrum of the stomach that can be seen macroscopically
and confirmed by measuring surface pH.
 The antral mucosa contains
 G- cells which secretes gastrin which stimulates acid
production.
• There are 2 major forms of gastrin G17 and G34,depending on
the number of amino acid residues.
• G17 is the major form found in the antrum.
D-cells which secrete somatostatin, a suppressant of acid
secretion.
Mucus secreting cells which produce mucus and bicarbonate.
The mucus is made of glycoproteins called mucins
10

 The wall of the stomach also contains enterochromaffin cells
which produce histamine that promotes acid secretion.
 The ‘mucosal barrier’ made up of the plasma membrane of
mucosal cells and the mucus layer protects the gastric
epithelium from damage by acid and for example, alcohol,
aspirin, NSAIDs and bile salts.
 Prostaglandins stimulate secretion of mucus and their synthesis
is inhibited by aspirin and NSAIDs which inhibit cyclo-
oxygenase.
 The duodenal mucosa has villi like the rest of the small bowel
and also contains Brunner’s glands that secrete alkaline
mucus.
 This along with pancreatic and biliary secretions,helps to
neutralize the acid secretion from the stomach when it reaches
the duodenum.
11

 Gastric acid secretion:
 The apical membrane contains H+ -K+ ATPase as well as Chloride
channels.
 The basolateral membrane contains Na+ -K+ ATPase and Cl—HCO-3
exchanger
 The parietal cell also contains the enzyme carbonic anhydrate.
 Carbon dioxide in the cell reacts with water in the presence of carbonic
anhydrase to form carbonic acid which dissociates into hydrogen and
bicarbonate ions.
 The hydrogen ions are secreted along with chloride ions into the lumen of
the stomach while the bicarbonate is absorbed into the blood.
 At the apical membrane hydrogen ions are exchanged for potassium ions.
 Potassium ions leave via a potassium channel found on the apical
membrane.
 At the basolateral side of the cells chloride is exchanged for bicarbonate
ions (Responsible for the alkaline tide observed in gastric venous blood after
a meal)
12

Monday, December 26, 2022 14

Monday, December 26, 2022 15
 Acid is not essential for digestion but does prevent some food-
born infectious.
 It is under neural and hormonal control and both stimulate acid
secretion through the direct action of histamine on the parietal
cell.
 Acetylcholine and gastrin also release histamine via the
enterochromaffin cells.
 Somatostatin inhibits both histamine and gastrin release
therefore acid secretion.

 Other major functions are:
Reservoir for food
Emulsification of fat and mixing of gastric contents
Secretion of intrinsic factor
Absorption (of only minimal importance)
 Gastric emptying depends on many factors.
 There are osmoreceptors in the duodenal mucosa that control
gastric emptying by local reflexes and the release of gut
hormones.
 In particular, intraduodenal fat delays gastric emptying by
negative feedback through duodenal receptors.

Gastritis

Gastritis.
 Gastritis is defined as the inflammation of the gastric mucosa
secondary to the abnormal level of acid production in the
stomach.
 It starts usually from the pyloric antrum and can spread to the
rest of the stomach.

Aetiology/Risk Factors.
 Drugs: NSAIDs and Steroids-long term use.
 Life style: Alcohol,Smoking,Stress and Anxiety, spicy foods.
 Infectious agents: Helicobacter Pylori, CMV and Herpes
simplex.
 Autoimmune disorders.
 Mechanical trauma.-e.g: Nasogastric intubation

Types of Gastritis
 Acute gastritis: This is commonly caused by Helicobacter
pylori.
 It is often erosive and hemorrhagic due to chemical injury
(drugs, alcohol).
 Other infections e.g. virus (CMV, Herpes simplex),
mycobacterium and syphilis
 Other causes:
Drugs e.g. ASA, NSAIDs
Alcohol in high doses
Severe stress

Types of Gastritis
 Acute gastritis:
 Patients are usually asymptomatic but at times may present
with:
 Sudden onset of epigastric pain
Nausea & vomiting (with or without diarrhea)
Upper GIT bleeding (melena and haematesis)
 Indigestion with neutrophilic infiltration
Oedema and hyperemia of the gastric mucosa.
 If not treated, H. pylori gastritis may progress to one of the
chronic gastritis.
 No specific treatment of acute gastritis is indicated.
 Removal of the offending agents may be adequate

Types of Gastritis
 Chronic gastritis: This is defined as a histological
demonstration of lymphocytic and plasma cell infiltration of
gastric mucosa.
 Course: Superficial gastritis is followed by atrophic gastritis
(characterized by distortion and destruction of gastric glands)
progressing to gastric atrophy (with loss of gastric glands)
which then undergo intestinal metaplasia (replacement of
gastric mucosal cells by intestinal cells) and finally progressing
to gastric carcinoma.
 It is characterized by increased lymphocytes and plasma cells
in gastric mucosa.
 It is caused by H. Pylori and autoimmunity conflicts

Types of Gastritis
 Chronic gastritis:
 Chronic gastritis is classified into 3 types:
Type A (autoimmune) gastritis (chronic fundal gastritis)
√ The inflammation is limited to the gastric fundus and body with
antral sparing.
√ Associated with pernicious anemia, with circulating
autoantibodies to parietal cells (AKA Autoimmune gastritis)
24

Types of Gastritis
 Chronic gastritis is classified into 3 types:
Type B (Bacterial) Gastritis (chronic antral gastritis)
√ It is the more common type
√ It commonly involves the antrum and mostly associated with
H. pylori infection. However, the inflammation may progress to
involve the gastric fundus and body causing Pangastritis
usually after 15-20 years.
√ Histology improves with eradication of H. pylori.
Type C (chemical) gastritis
√ Is due to repeated injury with bile reflux (duodenal-gastric
reflex) or chronic ingestion of NSAIDs
25

Types of Gastritis
 Most chronic gastritis is asymptomatic.
 Treatment:
Lifelong parenteral Vitamin B12 is recommended for patients
with pernicious anemia.
There is no need to treat H. pylori unless there is ulcer or
MALT Lymphoma.
26

Pathophysiology
 The mucosal barrier which protects the gastric epithelium from
being damaged by acid products, is made of mucosal cells and
mucus.
 The secretion of that mucus is stimulated by the prostaglandins.
 The chemical substances (drugs like Aspirin and other NSAIDS)
exercise their effects through inhibition of cyclooxygenase
(COX),an enzyme responsible for the production of
prostaglandins.
 The depletion of mucosal prostaglandins leads to a reduction in
gastric mucus.
 The autoimmune reaction directs its response towards the
parietal cells and intrinsic factor; this leads to the increased level
of Gastrin,the hormone that stimulates the gastric acid secretion.

Pathophysiology
 Alcohol in high concentration damages the gastric mucosal
barrier.
 Smoking impairs the gastric mucosal layer.
 Stress/Anxiety increases the acid production by stimulating the
CNS.

Clinical Features
 Abdominal pain in the epigastric region, burning in nature.
 The pain is postprandial or appearing at night with radiation to
the left shoulder.
 Nausea and Vomiting.
 Heart burn and Haematemesis.
 Bloating and excessive belching.
 Backache.
 On examination, the patient is in pain, walking bending the
waist forward and tenderness is noted in the epigastric region
or the right hypochondrium.

Differential Diagnosis
 Peptic Ulcer Disease.
 Gastro-esophageal reflux disease.
 Cholecystitis.
 Gastric carcinoma.
 Pancreatitis.
 Appendicitis.

Investigations.
 Generally the diagnosis of gastritis is clinical.
 However Endoscopy and Biopsy may be necessary to exclude
peptic ulcer or gastric cancer.
 Urease breath test (serology): quick way of detecting the
presence of H. Pylori.

Principles of Treatment.
 Identification and elimination of underlying cause: NSAIDS,
Alcohol, Smoking…
 Triple therapy made of:
 Clarithromycin tab 500mg TDS for 7 days.
 Metronidazole tab 400mg TDS for 7 days.
 Omeprazole cap 20mg BD (Proton pump inhibitors)
 Antiemetic drugs:e.g: Domperidone tab 10mg BD or
Metoclopramide (Plasil) injection.
 Antispasmodic drugs:e.g: Butylbromide (Buscopan) IM 20mg.
 Painkillers: Paracetamol tab 500mg TDS for 5 days.
 H2 antagonists: Cimetidine 200mg TDS/Ranitidine IV 25mg BD
 Antibiotics against H. Pylori: Amoxicillin cap 500mg TDS.
 IV Fluids if signs of dehydration.

Complications
 Bleeding.
 Anaemia.
 Dehydration.
 Mallory Weiss syndrome.
 Gastric ulcers.
 Gastric perforation.
 Malignancy.

PEPTIC ULCER DISEASE (PUD)

Peptic Ulcer Disease (PUD)
 Peptic ulcer: a defect in the gastric or duodenal mucosa with a diameter of
at least 0.5 cm
 A Peptic ulcer is an erosion or break in the tissues of the digestive tract
that comes in contact constantly with gastric juices.
 A Peptic ulcer can also be defined as an ulceration involving the mucosa of
the upper gastro-intestinal tract and it is due to the action of the gastric
juice.
 Gastric ulcer: a peptic ulcer of the gastric mucosa located along the lesser
curvature in the transitional portion between the corpus and antrum
 Duodenal ulcer: a peptic ulcer of the duodenal mucosa located on the
anterior or posterior wall of the duodenal bulb

PUD

Types of Peptic Ulcers
*According to the location (Anatomical classification):
 Esophageal ulcers: they affect the lower portion of the
oesophagus and they are due to the weakness of the
esophageal sphincter which allows the gastric contents to
escape into the esophagus.
 Gastric ulcers: these occur in the stomach mainly in the lesser
and greater curvatures and pyloric antrum.
 Duodenal ulcers: they are the commonest seen in the first
portion of the duodenum.
They result from high secretion of the hydrochloric acid.

Types of Peptic Ulcers
*According to the degree (Clinical classification):
 Acute peptic ulcers: they are multiple usually located in the
fundus of the stomach.
They are superficial and stress related.
 Chronic ulcers: they are more common than acute, they occur
as a single lesion and tend to cause extensive scarring.

Aetiology and Pathophysiology
The two major contributing
factors to the development
of PUD are:
Helicobacter pylori
infection
Associated with 40–70% of
duodenal ulcers and 25–
50% of gastric ulcers
The rate of H. pylori
infection (and, therefore, the
development of PUD) is
decreasing
Chronic NSAID use
Associated with a 4x
risk of developing PUD
Increases the risk for
complications of PUD

 The erosion or ulceration of the gastro-intestinal mucosa is
caused by the digestive action of hydrochloric acid and pepsin
secondary to the imbalance between the aggressive factors
and the defensive factors.
 This reduces the resistance of the gastro-intestinal mucosa to
pepsin and acid injury.
 That imbalance may be due to:
Gram negative bacteria Helicobacter pylori which is present in
70% of patients with gastric ulcers and 95% of patients with
duodenal ulcers.
Zollinger Ellison’s syndrome: Condition characterized by
excessive production of hydrochloric acid which erodes the
gastric mucosa.

 Protective forces:
Surface mucus
Presence of bicarbonate
Rapid epithelial regeneration
Normal mucosal blood flow
Normal mucosal prostaglandin secretion
 Aggressive forces:
H. pylori o NSAIDs
Corticosteroids o ASA
Smoking
Alcohol
Psychological stress
Zollinger-Ellison syndrome
Pepsin
Hydrochloric Acid
PUD
PF
AF
PUD
AF PF

 Emotional Factors: emotional tension, anxiety, frustration
and stress may cause an imbalance in the autonomic
nervous system, resulting in increased vagal stimulation
of gastric secretion.
 Hereditary: gastric ulcers are common in people with type
A blood while duodenal ulcers are common in people with
type O blood.
Duodenal ulcers are three times more common in first-
degree relatives of duodenal ulcers patients than in the
general population.
 Trauma: Conditions such as severe burns, shock, etc.
may lead to peptic ulceration.

 Prolonged use of irritants: certain drugs including Non-
Steroidal Anti-inflammatory Drugs (NSAIDs) may predispose to
peptic ulcer disease (e.g. Acetylsalicylic acid (Aspirin), adrenal
steroids, indomethacin and Phenylbutazone).
 Alcohol and smoking: Alcohol inhibits prostaglandin secretion.
 Nicotine in cigarette inhibits pancreatic secretion of
bicarbonate, it also may accelerate the emptying of gastric acid
into the duodenum and promote mucosal breakdown.
 Bile reflux: the reflux of bile and pancreatic enzymes into the
stomach due to an incompetent pyloric sphincter may lead to a
gastric ulcer.
 The bile salts damage the gastric mucosa, predisposing it to
ulceration.

Summarized Pathophysiology
• H. pylori secretes urease → conversion of urea
to NH3 → alkalinization of acidic environment →
survival of bacteria in gastric lumen
• Bacterial colonization and attachment to
epithelial cells → release of cytotoxins →
disruption of the mucosal barrier and damage to
underlying cells
Gastric
ulcers
• H. pylori inhibits somatostatin secretion → ↑
gastrin secretion → ↑ H+ secretion → excess
H+ delivery to the duodenum
• Direct spread of H. pylori to the duodenum →
inhibition of duodenal HCO3- secretion→
acidification and insufficient neutralization of
duodenal contents
Duodenal
ulcers
• Inhibit COX-1 and COX-2 → decrease in
prostaglandin; production → erosion of
the gastric mucosa
• Decrease mucosal blood flow
• Inhibit mucosal cell proliferation
NSAIDs

Signs and Symptoms
 Epigastric pain: burning pain, related to food, radiating to the
back.
 Heartburn (pyrosis) and chest discomfort.
 Anorexia and Vomiting.
 Weight loss especially in gastric ulcers.
 Dyspepsia including belching, bloating, distention.
 Hematemesis resulting from gastro-intestinal bleeding from
eroded small blood vessels.
 Melena stool: passing out black tarry stool. This is more
common in duodenal ulcers.

Differential Diagnosis
 Functional dyspepsia: a diagnosis of exclusion made in patients
with chronic persistent epigastric pain in whom a thorough
evaluation shows no organic disease.
 The differential diagnosis of PUD consists of other causes of
dyspepsia and includes:
GERD- affects mainly the esophagus, while ulcers are
usually an issue in the stomach or intestine. GERD irritates
the tissue lining, while ulcers wear away the tissue lining
Biliary disease eg cholecystitis
Gastric malignancy
Less commonly, chronic pancreatitis.
*These conditions can be excluded from peptic ulcer disease by
upper endoscopy.

Investigations
 Endoscopy:
Esogastroduedonoscopy
to visualize and identify
the inflammatory
changes and ulcers.
 Biopsy for
histopathology.
 Special radiology:
Barium swallow and
Barium meal.
 Full blood count in case
of severe bleeding.

Approach to MGT-Acute
Approach to PUD: Stop
NSAIDs, Acid
neutralization, H. pylori
eradication, and Quit
smoking
Identify and treat critical
complications, e.g., GI
bleeding,
gastrointestinal
perforation, secondary
peritonitis
Evaluate for underlying
cause (e.g., NSAID use)
Consider evaluation for
occult bleeding (e.g.,
CBC, BMP, FOBT
H. pylori test-and-treat
strategy: A management
strategy for H. pylori infection
in patients with dyspepsia
without risk factors for gastric
malignancy
Consists of noninvasive
testing and, if results are
positive, treatment with
antibiotics and acid
suppression medications.
This strategy reduces the
need for endoscopy and the
prolonged use of
antisecretory medications

Approach to MGT-Acute
Provide
trial of
acid
suppress
ion
therapy
with PPI
01
Discontinue
underlying
triggers (e.g.,
NSAIDs,
alcohol,
tobacco,
caffeine) and
counsel on
lifestyle
modifications.
02
Consider
specialized
diagnostic
studies if
the
etiology
remains
unclear.
03
Ensure
appropriate
follow-up
e.g., EGD,
H. pylori
eradication
confirmation
04
Consider
referral for
elective
surgery for
refractory or
complicated
cases.
05

Principles of Treatment
 Proton pump inhibitors (PPI): Omeprazole 20mg BD or
Rabeprazole 40mg BD for 4 to 8 weeks.
 H2 antagonists: Ranitidine 150mg BD or Cimetidine 400mg
BD for 4 to 6 weeks.
 Antibiotics to eradicate the H. Pylori: Clarithromycin tab 500mg
TDS or Amoxicillin cap 500mg TDS.
 Painkillers
 Antispasmodic drugs.
 Anticholinergic drugs can also be given to decrease the vagal
stimulation.(action of the vagus nerve).
 Change of life-style.

Management: Elective surgical treatment
 Refractory symptoms or
recurrence of disease despite
appropriate medical treatment
 Diseases that require the
continuation of NSAIDs e.g.,
ankylosing spondylitis
 Inability to tolerate medical
treatment

Complications
 Hemorrhage
 Anaemia
 Penetration to other organs e.g. pancreas, liver
 Perforation
 Gastric outlet obstruction
 Pyloric stenosis
 Malignant Transformation (Stomach Cancer)
 Fistula Formation

IEC
Diet and Lifestyle
 Avoid : smoking, alcohol, fried, greasy, acidic, or spicy, dairy, caffeine, fast
foods, processed food
 Aim to have a diet high in fibre and rich in vegetables, fruits, and whole
grains.
 Try for a minimum of seven servings of vegetables and fruits each day, and
a minimum of five servings of whole grains
S/E of Medications
 Metronidazole (Flagyl) or Clarithromycin (Biaxin). These medications can
cause a metallic taste in the mouth and nausea.
 Alcoholic beverages (eg, beer, wine) should be avoided while taking
Metronidazole; the combination can cause skin flushing, headache, nausea,
vomiting, sweating, and a rapid heart rate.
 Bismuth, which is contained in some of the regimens, causes the stool to
become black and may cause constipation.

Summary
 Define gastritis and peptic ulcer diseases (PUD).
 List the aetiologies of gastritis and PUD
 Describe the epidemiology of PUD
 Explain the pathogenesis gastritis and PUD
 Describe the clinical features of gastritis and PUD
 List the common complications gastritis and PUD
 Describe the most commonly used methods for the diagnosis
of gastritis and PUD
 Make an accurate diagnosis of gastritis and PUD
 Treat gastritis and PUD at the primary care level with
appropriate drugs
 Refer those presenting with complications of gastritis and PUD
to the next level of healthcare 58

Resource and Further Reading
 Edwards C, et al (2021) Davidson’s Principles and Practice
of Medicine 23rd Ed. Edinburgh: Churchill Livingstone
 Kumar P, Clark M (2021) Kumar and Clark’s Clinical
Medicine 10th ed. London: Elsevier Saunders.
 Munro JF, Campbell IW (2021) Macleod’s Clinical
Examination 14th ed. Edinburgh: Churchill Livingstone
 Swash M, Glynn M (2020). Hutchison’s Clinical Methods: An
Integrated Approach to Clinical Practice 25th ed. London:
Elsevier Saunders
Monday, December 26, 2022 Lubundi K MLP 2020 59

End of the Lecture

Post-Lecture Assessment 1
A peptic ulcer is an erosion in the stomach or the first few
centimeters of the duodenum. Nearly all ulcers are caused
by Helicobacter pylori infection or use of nonsteroidal anti-
inflammatory drugs. Several risk factors exist for the development
of ulcers and their complications. Which of the following risk
factors impairs healing and increases the incidence of
recurrence?
A. Alcohol use
B. Cigarette smoking
C. Family history of ulcers
D. History of gastrinoma

Post-Lecture Assessment 2
A 32-year-old woman comes to the office because she has had
abdominal pain for the past 2 months. She describes the pain as
a burning or gnawing sensation in her stomach. Which of the
following additional characteristics of this patient’s pain is most
likely to suggest duodenal ulcer as the diagnosis?
A. Awakens the patient at night
B. Intermittent throughout the day
C. Is not relieved by food
D. Is present immediately upon awakening

Thank You
Seen by SML Lubundi
06/09/2022
14:00 hrs
C/O
-Chest pain x 3/7
-Weakness x 1/52
-Sweating x 2/52
-painful sores on
hands x 2/52
Roots of education are bitter, but the fruit is Sweet

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