Session 20-Gastritis and Pud

Gastritis and Peptic ulcer
disease
CMT 05102: INTERNAL MEDICINE I
Learning objectives
• Definition of gastritis and PUD
• Classification of gastritis and PUD
• Etiologies of gastritis and PUD
• Clinical features and complications of gastritis and PUD
• Provisional and differential diagnosis
• Investigations of gastritis
• Treatment, referral, follow up and prevention of gastritis
Gastritis
Definition
• The term gastritis should be reserved for histological
documented inflammation associated with the gastric
mucosa injury.
• Epithelial cell damage and regeneration without associated
inflammation is referred as gastropathy
• Gastritis is not the mucosal erythema seen during endoscopy
and is not interchangeable with ‘dyspepsia.
Etiologies of gastritis
• The etiologic factors leading to gastritis are broad and heterogeneous
• Acute infection with H. pylori induces gastritis
• Infectious causes, Pyogenic bacteria(phlegmonous
gastritis),mycobacterial, syphilitic, CMV, Fungal
• Other causes of acute gastritis
• o NSAIDS
• o Alcohol
• o Drugs-Iron
• o Bile
• o Severe psychological stress
• o Uremia
Classification of gastritis
Gastritis has been classified based on time course
Acute
Chronic
Acute Gastritis
• This is a term covering a broad spectrum of entities that induce
inflammatory changes in the gastric mucosa for less than 2 weeks.
• Acute inflammation is represented by neutrophilic infiltration.
• The inflammation may involve the entire stomach (e.g. pan gastritis)
or a region of the stomach (e.g. antral gastritis).
Types of acute gastritis
• Acute gastritis can be broken down into 2 categories
Erosive (eg, superficial erosions, deep erosions, hemorrhagic
erosions)
Non-erosive (generally caused by Helicobacter pylori)
• The most common causes of acute gastritis are infectious
• Acute infection with H. pylori induces gastritis
Types of acute gastritis
• Other infection include: Helicobacter helmanni,
Phlegmonous(bacterial infection of stomach that characterized by
necrosis of stomach wall), Mycobacterial, Syphilitic, Viral(herpes
simples and CMV), Parasitic, Fungal.
• Other causes of acute gastritis : NSAIDS, Alcohol, Drugs-Iron, Bile
Severe psychological stress, Uremia .
Clinical features of acute gastritis
Reported as presenting with sudden onset of
Epigastric pain
Nausea
Vomiting
Chronic gastritis
• Chronic gastritis is identified histologically by an inflammatory cell
infiltrate consisting primarily of lymphocytes and plasma cells, with
very scant neutrophil involvement.
• This form of gastritis increases with age.
• Chronic gastritis may progress into gastric atrophy in which the
mucosa is thin and the infiltrate sparse with subsequent metaplasia,
this may ultimately lead to development of gastric adenocarcinoma
Chronic gastritis
• H. pylori infection is now considered an independent risk
factor for gastric cancer.
• Infection with H. pylori is also associated with development
of a low grade B cell lymphoma, Gastric MALT (mucosa-
associated lymphoid tissue) lymphoma.
Differential diagnosis
• Peptic ulcer
• Esophagitis
• Gastric carcinoma
• Dyspepsia
Complications of gastritis
• Pernicious anemia
• Lymphoma(MALT)
• Peptic ulcer disease
• Esophagitis
Investigations
Laboratory tests
• Stool for h. pylori
• Positive urease test :breath test, on endoscopic biopsy.
• CBC count to assess for anemia, as acute gastritis can cause
gastrointestinal bleeding
• Stool for occult blood
• Gastric biopsy for histopathology
Imaging studies.
• Barium meal
• Endoscopy(esophagogastroscopy)
Treatment of gastritis
• Administer fluids and electrolytes as required, particularly if
the patient is vomiting.
• Discontinue the use of drugs known to cause gastritis (e.g.
NSAIDs, alcohol).
• For non h. pylori gastritis: omeprazole 20 mg od for 8 weeks
Treatment of gastritis
• Triple therapy, with indicated adult dose (eradication of H.
pylori) for 14 days then continue acid suppression to complete
4-8 weeks.
Proton pump inhibitors (PPI) - Lansoprazole 30 mg PO once a
day OR Omeprazole 20 mg PO twice a day for 4 – 8 weeks
 PLUS
Clarithromycin 500 mg PO bid OR Amoxicillin 500 mg PO 12

hourly for 2 weeks
 PLUS
metronidazole 400mg PO 12 hourly for 2 weeks

Continue
• The treatment of Candida albicans includes a variety of
agents, including nystatin, oral clotrimazole, itraconazole,
fluconazole, amphotericin B, and ketoconazole
• No effective antiviral therapy exists for the treatment of
human cytomegalovirus (HCMV) infection, though 2 agents
(i.e. ganciclovir, foscarnet) have been shown to be virostatic.
Treating vomiting : injections metoclopramide 10mg bid as
required for a patient with intractable vomiting.
Treatment of chronic gastritis
• Treatment in chronic gastritis is aimed at the sequelae and
not the underlying inflammation.
• Patients with pernicious anemia will require parenteral
vitamin B12 supplementation on a long-term basis.
• Eradication of H. pylori is not routinely recommended unless
PUD or a low-grade lymphoma is present.
Referral plan
• Refer to next level service with adequate expertise and
facilities for complicated case with alarm features (anemia,
vomiting blood and weight loss.
Follow up
• After 2 weeks for PPI refill and monitoring progression of
symptoms
PREVENTION
• Reduce the use of drugs known to cause gastritis (e.g.,
NSAIDs, alcohol)
• Stop smoking
• Reduce fatty, spicy and deep-fried foods
• Prompt treatment of H.pylori infections
• Counselling on adherence to medications
PEPTIC ULCER DISEASE(PUD)
Peptic ulcer disease (PUD)
• Peptic ulcer also known as gastric ulcer is a circumscribed loss
or Break in the mucosa (of esophagus, Stomach, duodenum)
• After exposure to acid‐peptic activity they extends deep into

the muscularis and are associated with an acute or chronic
inflammatory cell infiltrate.
• But an ulceration which doesn’t reach the muscularis mucosa is
called erosion.
Peptic ulcer disease (PUD)
• Peptic ulcers (gastric and duodenal) are defects in the GI
mucosa that extend through the muscularis mucosa.
• PUD results when “aggressive” factors (gastric acid, pepsin)

overwhelm “defensive” factors involved in mucosal
resistance (gastric mucus, bicarbonate, microcirculation,
prostaglandins, mucosal “barrier”), and from effects of
Helicobacter pylori
Etiologies of PUD
• Main causes of Peptic ulcer disease (PUD) are;
• Helicobacter Pylori infection:
• Cause 90% of all duodenal ulcers,
• Cause 70% of all gastric ulcers,
• NSAID use, inhibit prostaglandin production, which leads to
impaired mucosal defenses
• Acid hyper secretion (Gastrinoma / Zollinger‐ Ellison),
• Alcohol and Smoking
• Malignancy,
• Stress related (ICU patients, stroke, ventilator dependence,
immunocompromised)
Peptic ulcer disease
• Types
• • PUD encompasses both
• o Gastric ulcers (GU)
• o Duodenal ulcers (DU)
Types of PUD
• Gastric Ulcers (GU)
• Occur later in life than duodenal lesions, with a peak incidence
reported in the sixth decade, commonly GUs occurs in males.
• Are less common than DUs,due to the higher likelihood of GUs
being silent and presenting only after a complication develops.
• GUs can represent a malignancy, benign GUs associated with
H. pylori are associated with antral gastritis.
• Gastric Ulcers (GU)
• Gastric acid secretory rates are usually normal or reduced,
possibly reflecting earlier age of infection by H. pylori than in
DU pts. Gastritis due to reflux of duodenal contents
(including bile) may play a role
• NSAID use may account for 15–30% of GUs and increase risk
of associated bleeding, perforation
Types of PUD
• Duodenal Ulcers (DU)
• DUs are estimated to occur in 6 to 15% of the western population.
• Before the discovery of H. pylori, the natural history of DUs was
typified by frequent recurrences after initial therapy.
• Eradication of H. pylori has greatly reduced these recurrence rates.
• DUs occur most often in the first portion of duodenum (>95%), with
~90% located within 3 cm of the pylorus.
• Malignant duodenal ulcers are extremely rare
Clinical Features
• Epigastric pain Aching or OR burning in nature, radiating to the
back
• Burning epigastric pain made worse by or unrelated to food;
anorexia, food aversion, weight loss related to GUs.
• Burning epigastric pain 90 min to 3 h after meals, often
nocturnal, relieved by food related to DUs.
• May be complicated by upper GI bleeding

• Other symptoms: nausea/vomiting, early satiety, and weight
loss
• Dyspepsia, Heartburn, bloating, abdominal distention,
Chest discomfort
• Hematemesis or melena resulting from gastrointestinal
bleeding.
• Symptoms consistent with anemia (eg, fatigue, dyspnea)
• Sudden worsening of symptoms may indicate perforation.
Complications of PUD
1. Obstructed peptic ulcer disease
• fullness and bloating associated with nausea and emesis
that occurs several hours after food intake.
• Succussion splash positive
• Early satiety
2. Bleeding peptic ulcer disease
• Hematemesis or melena, rarely hematochezia.
• Anemia (eg, fatigue, dyspnea) may be present
Complications of PUD
• 3. Perforated peptic ulcer.
• Features of peritonitis; rebound tenderness, lie still in the
bed, generalized pain, sudden onset of sharp pain
• 4. Gastric malignancy
weight loss
• 5.Obstruction
• 6. penetration causing acute pancreatitis, perforation,
intractability
Differential diagnosis of peptic ulcer disease.
• Pancreatitis –back pain, • Aortic aneurysm
radiating to the back,
relieved on bending foward; • Cholangitis
(Mohammedi sign) • Cholecystitis
• Gastric malignancy – • Gastritis
aversion to meat • Gastroenteritis
• Myocardial infarction • Gastroesophageal reflux
• Esophagitis Disease(GERD)
• Hepatitis
Investigations
Basing on medical history and symptoms the following investigation should be
done
H pylori test
• Breath urease tests–reported as positive
• Urea breath test generally used to confirm eradication of H. pylori
• Fecal antigen test for H pylori
• Oesophageal gastro duodenoscopy(OGD)

• Histopathology
• Blood Culture and sensitivity
• Full blood picture and differential
• Haemoglobin level
Management of PUD.
• There are two modalities of treating PUD of H pylori;
1. PPI‐based triple therapy regimens for H pylori consist of a PPI,
amoxicillin, and clarithromycin for 14 days.
• Omeprazole : 20 mg PO twice daily
• Metronidazole : 500 mg PO twice daily
• Amoxicillin : 1 g PO twice daily
OR
• Lansoprazole (PO) 30mg twice daily
• Clarithromycin : 500 mg PO twice daily
• Tinidazole (PO) 500mg twice daily
• Then omeprazole for 8 weeks
Management of PUD.
• Quadruple treatment includes the following drugs, administered for 14
days.
• PPI, standard dose, or ranitidine 150 mg, PO twice daily
• Bismuth 525 mg PO four times daily
• Metronidazole 500 mg PO four times daily
• Tetracycline 500 mg PO four times daily
• NOTE; Quadruple therapies for H pylori infection are generally reserved

for patients in whom the standard course of treatment has failed.
Complication treatment
• Obstructed PUD
Surgery
• Bleeding PUD
Iron sulphate(hematinics)
• Perforated PUD
Surgery and laparotomy
Referral plan
• For further investigations incase of suspected malignancy
• For further treatment
Follow plan
• H.pylori diagnostic tests should be repeated 5 weeks after the last
dose of eradication therapy,
• PPI should be stopped 2weeks before testing the H.pylori stool
antigen test to confirm eradication.
Prevention of PUD
• Avoid NSAIDS use
• Avoid cigarette
• Stop or reduce alcohol consumption
• Preventive therapy in stress associated PUD
• Early detection and treatment
References
• Davidson 24th Edition
• Harrisons principle of internal medicine 16th edition
• Harrisons Manual of Medicine 18th edition.
• STG&NLMT 2021
• UptoDate
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Gastritis and Peptic ulcer

Clarithromycin 500 mg PO bid OR Amoxicillin 500 mg PO 12

metronidazole 400mg PO 12 hourly for 2 weeks

• After exposure to acid‐peptic activity they extends deep into

• PUD results when “aggressive” factors (gastric acid, pepsin)

• May be complicated by upper GI bleeding

• Oesophageal gastro duodenoscopy(OGD)

• NOTE; Quadruple therapies for H pylori infection are generally reserved

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