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Izatty Lim
0308188
Batch 4

 defined as having one or more symptoms of
epigastric pain, burning, postprandial fullness, or
early satiety.
 Bloating
 Nausea
 Loss of appetite
Dyspepsia

PUD

 Type I
 typically located near the angularis incisura on the lesser
curvature, close to the border between the antrum and the
body of the stomach. Patients with type I gastric ulcers
usually have normal or decreased gastric acid secretion.
 Type II
 a combination of stomach and duodenal ulcers and are
associated with normal or increased gastric acid secretion.
 Type III
 prepyloric and are associated with normal or increased
gastric acid secretion.
 Type IV
 occur near the gastroesophageal junction, and gastric acid
secretion is normal or below normal.
Types of Gastric Ulcer
 Etiology:
 H. pylori bacterium
 NSAID
Gastric Ulcer
 H. pylori
 70% of gastric ulcer patients are infected with H. pylori.
Majority of colonised people remain healthy and
asymptomatic.
 uses adhesin molecules (BabA) to bind to Lewis b antigen on
epeithelial cells.
 induces an intense inflammatory and immune response
 IL-1, IL-6, tumor necrosis factor, IL-8
 Production of ammonia by the enzyme urease
 Toxic to epithelial cell
 Increase gastrin release from G cells
 Negative feedback loop for gastrin release is halted
 stimulates increased acid production by parietal cells.
Pathophysiology

 NSAID
 Direct chemical irritation & COX enzyme inhibition,
which prevent prostaglandin synthesis
 increases secretion of hydrochloric acid and reduces
bicarbonate and mucin production
 Damage gastric and duodenal mucosal barrier
 increased risk of upper gastric ulcer, bleeding
&perforation.
Pathophysiology

 Smoking
 Increased risk of gastric ulcer and duodenal ulcer to a
lesser extent.
 more likely to causing complication and less likely to
heal if the patient continues to smoke.
Pathophysiology

 recurrent abdominal pain
 localisation to the epigastrium
 Relation to food
 Episodic occurrance
 Occasional vomiting
 Anorexia & nausea
 Completely ‘silent’
 presented with anaemia for the first time
 Recurrent acute bleeding without ulcer pain
 Gnawing or burning sensation
 occurs shortly after meals with gastric ulcer and 2-3 hours afterward
with duodenal ulcer.
 Diagnostic value of individual symptoms for PUD is poor.
Clinical Features

 Upper GI endoscopy
 Rapid urease tests
 Fecal antigen testing
 detecting the presence of H pylori antigens in stools
 Urea breath test
 testing for the enzymatic activity of bacterial urease.
 Antibodies (IgG)
 X- ray
 detect free abdominal air when perforation is suspected.
 upper GI contrast study
 extravasation of contrast indicates gastric perforation
Investigation

 H. pylori eradication
 proton pump inhibitor (PPI)–based triple therapy.
 PPI, amoxicillin, and clarithromycin for 7-14 days.
 Amoxicillin should be replaced with metronidazole in penicillin-
allergic patients only  high rate of metronidazole resistance
 NSAID
 American College of Gastroenterology (ACG ) guideline: test
for H pylori done in patients who started long-term NSAID
therapy
 NSAIDs should be immediately discontinued in patients with
positive H pylori test results if clinically feasible
 Patient with known history of ulcer and in whom NSAID use is
unavoidable, the lowest possible dose and duration of the
NSAID and co-therapy with a PPI or misoprostol are
recommended.
Treatment

 Surgical
 Rarely required
 Choice for a chronic non-healing gastric ulcer
 partial gastrectomy to exclude an underlying cancer.
Treatment

 Duodenal ulcer and gastric ulcer both belong to the
family of peptic ulcer disease.
 H. pylori infection is the major cause of duodenal
ulcer followed by NSAID
 They share almost the same clinical features.
Duodenal Ulcer

 Gastric Ulcer
 Symptoms do not
follow a consistent
pattern
 Eating sometimes
exacerbates rather
than relieves pain
Gastric Ulcer vs Duodenal Ulcer
 Duodenal Ulcer
 Tend to cause more
consistent pain.
 Pain can awaken the
patient at night.
 Pain is relieved by
food, but recurs 2 to
3 hours after a meal

Complication
Stricture
•Gastric outlet
obstruction
•Abdominal distension
•Nausea, vomiting
•Diagnosis by visible
gastric peristalsis
Perforation
•Sudden severe pain then
become generalized
•Irritation of diaphragm
leading to shoulder tip
pain
Peritonitis
•Paralytic ileus
•Absent bowel sound
•Abdominal guarding

 Harmon RC, Peura DA. Evaluation and Management of
Dyspepsia [Internet]. Medscape. [cited 2015 May 24]. Available
from: http://www.medscape.com/viewarticle/721062_1
 Robbins basic Pathology. 9th Ed.
 BS Anand. Peptic Ulcer Disease Treatment & Management
[Internet]. [cited 2015 May 24]. Available from:
http://emedicine.medscape.com/article/181753-
treatment#aw2aab6b6b1aa
 Davidson’s Principle & Practice of Medicine. 22nd Ed.
References

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Dyspepsia- Peptic Ulcer Diseases

  • 2.   defined as having one or more symptoms of epigastric pain, burning, postprandial fullness, or early satiety.  Bloating  Nausea  Loss of appetite Dyspepsia
  • 4.   Type I  typically located near the angularis incisura on the lesser curvature, close to the border between the antrum and the body of the stomach. Patients with type I gastric ulcers usually have normal or decreased gastric acid secretion.  Type II  a combination of stomach and duodenal ulcers and are associated with normal or increased gastric acid secretion.  Type III  prepyloric and are associated with normal or increased gastric acid secretion.  Type IV  occur near the gastroesophageal junction, and gastric acid secretion is normal or below normal. Types of Gastric Ulcer
  • 5.  Etiology:  H. pylori bacterium  NSAID Gastric Ulcer
  • 6.  H. pylori  70% of gastric ulcer patients are infected with H. pylori. Majority of colonised people remain healthy and asymptomatic.  uses adhesin molecules (BabA) to bind to Lewis b antigen on epeithelial cells.  induces an intense inflammatory and immune response  IL-1, IL-6, tumor necrosis factor, IL-8  Production of ammonia by the enzyme urease  Toxic to epithelial cell  Increase gastrin release from G cells  Negative feedback loop for gastrin release is halted  stimulates increased acid production by parietal cells. Pathophysiology
  • 7.   NSAID  Direct chemical irritation & COX enzyme inhibition, which prevent prostaglandin synthesis  increases secretion of hydrochloric acid and reduces bicarbonate and mucin production  Damage gastric and duodenal mucosal barrier  increased risk of upper gastric ulcer, bleeding &perforation. Pathophysiology
  • 8.   Smoking  Increased risk of gastric ulcer and duodenal ulcer to a lesser extent.  more likely to causing complication and less likely to heal if the patient continues to smoke. Pathophysiology
  • 9.   recurrent abdominal pain  localisation to the epigastrium  Relation to food  Episodic occurrance  Occasional vomiting  Anorexia & nausea  Completely ‘silent’  presented with anaemia for the first time  Recurrent acute bleeding without ulcer pain  Gnawing or burning sensation  occurs shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer.  Diagnostic value of individual symptoms for PUD is poor. Clinical Features
  • 10.   Upper GI endoscopy  Rapid urease tests  Fecal antigen testing  detecting the presence of H pylori antigens in stools  Urea breath test  testing for the enzymatic activity of bacterial urease.  Antibodies (IgG)  X- ray  detect free abdominal air when perforation is suspected.  upper GI contrast study  extravasation of contrast indicates gastric perforation Investigation
  • 11.   H. pylori eradication  proton pump inhibitor (PPI)–based triple therapy.  PPI, amoxicillin, and clarithromycin for 7-14 days.  Amoxicillin should be replaced with metronidazole in penicillin- allergic patients only  high rate of metronidazole resistance  NSAID  American College of Gastroenterology (ACG ) guideline: test for H pylori done in patients who started long-term NSAID therapy  NSAIDs should be immediately discontinued in patients with positive H pylori test results if clinically feasible  Patient with known history of ulcer and in whom NSAID use is unavoidable, the lowest possible dose and duration of the NSAID and co-therapy with a PPI or misoprostol are recommended. Treatment
  • 12.   Surgical  Rarely required  Choice for a chronic non-healing gastric ulcer  partial gastrectomy to exclude an underlying cancer. Treatment
  • 13.   Duodenal ulcer and gastric ulcer both belong to the family of peptic ulcer disease.  H. pylori infection is the major cause of duodenal ulcer followed by NSAID  They share almost the same clinical features. Duodenal Ulcer
  • 14.   Gastric Ulcer  Symptoms do not follow a consistent pattern  Eating sometimes exacerbates rather than relieves pain Gastric Ulcer vs Duodenal Ulcer  Duodenal Ulcer  Tend to cause more consistent pain.  Pain can awaken the patient at night.  Pain is relieved by food, but recurs 2 to 3 hours after a meal
  • 15.  Complication Stricture •Gastric outlet obstruction •Abdominal distension •Nausea, vomiting •Diagnosis by visible gastric peristalsis Perforation •Sudden severe pain then become generalized •Irritation of diaphragm leading to shoulder tip pain Peritonitis •Paralytic ileus •Absent bowel sound •Abdominal guarding
  • 16.   Harmon RC, Peura DA. Evaluation and Management of Dyspepsia [Internet]. Medscape. [cited 2015 May 24]. Available from: http://www.medscape.com/viewarticle/721062_1  Robbins basic Pathology. 9th Ed.  BS Anand. Peptic Ulcer Disease Treatment & Management [Internet]. [cited 2015 May 24]. Available from: http://emedicine.medscape.com/article/181753- treatment#aw2aab6b6b1aa  Davidson’s Principle & Practice of Medicine. 22nd Ed. References

Notes de l'éditeur

  1. Although H. pylori does not invade the tissues, it induces an intense inflammatory and immune response. There is increased production of proinflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor, and, most notably, IL-8. IL-8 is produced by the mucosal epithelial cells, and it recruits and activates neutrophils.Several bacterial gene products are involved in causing epithelial cell injury and induction of inflammation. Epithelial injury is mostly caused by a vacuolating toxin called VacA, which is regulated by the cytotoxin-associated gene A (CagA). This gene is a component of the Cag pathogenicity island, a cluster of 29 genes, some of which encode pro-inflammatory proteins. In addition, H. pylori secretes a urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine. The organisms also elaborate phospholipases that damage surface epithelial cells. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucus, thus weakening the first line of mucosal defense.H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum. This altered milieu seems to favor gastric metaplasia (the presence of gastric epithelium) in the first part of the duodenum. Such metaplastic foci provide areas for H. pylori colonization.Several H. pylori proteins are immunogenic, and they evoke a robust immune response in the mucosa. Both activated T cells and B cells can be seen in chronic gastritis caused by H. pylori. The B lymphocytes aggregate to form follicles. The role of T and B cells in causing epithelial injury is not established, but T-cell-driven activation of B cells may be involved in the pathogenesis of gastric lymphomas
  2. Suppression of mucosal prostaglandin synthesis, which increases secretion of hydrochloric acid and reduces bicarbonate and mucin production