Download Peptic Ulcer Disease

Peptic Ulcer Disease
• A 52-year-old male presents with epigastric pain that
improves with meals. Endoscopy demonstrates a 2 Cm
ulcerated area located 3 cm distal to the pyloric
junction. Which of the following is most likely to have
made the strongest contribution to the development of
this disease?
A. Aspirin use
B. Chronic antacid use
C. Drinking alcohol
D. Helicobacter pylori infection
E. Smoking
Ulcer
1. Peptic ulcer
2. Stress ulcers (acute gastric ulcers)
Ulcer: a breach in the mucosa of the
alimentary tract extending through
muscularis mucosa into submucosa
or deeper.
Pathophysiology
Aggressive
Factors
Defensive
Factors
Pathophysiology
imbalance
Defensive Factors
Aggressive Factors
H. pylori
Drugs (NSAIDs)
Acid
pepsin
Bile salts
Aggressive
Factors
Defensive
Factors
Mucus
bicarbonate
Blood flow,
cell renewal
Prostaglandins
Phospholipid
Pathophysiology
imbalance
Defensive Factors
Aggressive Factors
H. pylori
Drugs (NSAIDs)
Acid
pepsin
Bile salts
Aggressive
Factors
Defensive
Factors
Mucus
bicarbonate
Blood flow,
cell renewal
Prostaglandins
Phospholipid
Acute peptic ulcers
Pathophysiology
• As part of an acute gastritis
• As a complication of a severe stress response
• As a result of extreme hyperacidity.
Pathophysiology
Acute peptic ulcers
• As part of an acute gastritis (acute response to an
irritant 'chemical' injury by drugs or alcohol
• As a complication of a severe stress response
(severe burns (Curling's ulcer), major trauma or
cerebrovascular accidents )
• As a result of extreme hyperacidity (ZollingerEllison syndrome).
Chronic peptic ulcer
Peptic Ulcer Disease
Locations
• May occur in any portion of the GI tract exposed to
acidic gastric juices
• 98% located in first portion of duodenum or
stomach, ratio = 4:1
• Esophagus……. as a result of GERD or acid secretion by
ectopic gastric mucosa.
• Gastric mucosa within a Meckel diverticulum can result in
peptic ulceration of adjacent mucosa.
Peptic Ulcer Disease
Gastric ulcers
Pathophysiology
 The mucosal defences against acid attack consist of:
1. Mucus-bicarbonate barrier
2. The surface epithelium.
Peptic Ulcer Disease
Gastric ulcers
Pathophysiology
 The mucosal defences against acid attack consist of:
1. Mucus-bicarbonate barrier
Duodeno-gastric reflux ( bile )
2. The surface epithelium.
1. NSAIDs (blocking the synthesis of the prostaglandins)
2. H. pylori infection, ( cytotoxins and ammonia)
Thus peptic ulcers in the stomach, breakdown of mucosal defence is much
more important than excessive acid production.
Peptic Ulcer Disease
Duodenal ulcers
Pathophysiology
Increased production of acid assumes more importance in the pathogenesis of
duodenal ulceration
H. pylori-infected individuals secrete 2-6 times as much acid as non-infected
controls
Helicobacter Pylori does not colonise normal duodenal epithelium
Helicobacter is involved in duodenal ulceration because there is gastric
metaplasia in response to excess acid. Gastric metaplasia paves the way for
colonisation by Helicobacter
+
Increased production of acid
Helicobacter P
=
Duodenal ulcers
Peptic Ulcer Disease
Pathophysiology
Duodeno-gastric reflux ( bile )
Gastric
ulcers
Hyperacidity
H. pylori
Duodenal
ulcers
NSAIDs
H pylori infection of the pyloric antrum is present in nearly all patients with chronic
duodenal ulcer and approximately 75% of patients with chronic gastric ulcer.
Although more than 70% of individuals with PUD are infected by H. pylori, fewer than
20% of H. pylori–infected individuals develop peptic ulcer.
Morphology
• Gross
• usually less than 20 mm in diameter but
they may > 100 mm in diameter.
• The classic peptic ulcer is a round to oval,
sharply punched-out defect
• In contrast, heaped-up margins are more
characteristic of cancers
• Microscopy
• the base consists of necrotic tissue and
polymorph exudate overlying inflamed
granulation tissue which merges with
mature fibrous (scar) tissue.
Clinical features
• Epigastric pain (the most common symptom)
– Gnawing or burning sensation
– Occurs 2-3 hours after meals
– Relieved by food or antacids
– Patient awakens with pain at night.
Some present with complications such as iron deficiency
anemia, frank hemorrhage, or perforation.
Therapy
Current therapies for PUD are aimed at
1. H. pylori eradication
2. Neutralization of gastric acid, primarily with proton
pump inhibitors
• A 52-year-old male presents with epigastric pain that
improves with meals. Endoscopy demonstrates a 2 Cm
ulcerated area located 3 cm distal to the pyloric
junction. Which of the following is most likely to have
made the strongest contribution to the development of
this disease?
A. Aspirin use
B. Chronic antacid use
C. Drinking alcohol
D. Helicobacter pylori infection
E. Smoking
• The correct answer is D. The patient has a duodenal
peptic ulcer. The strongest risk factor for duodenal
peptic ulcer is Helicobacter pylori infection, which is
found in almost 100% of these cases (contrast to 70%
Infection rate in gastric peptic ulcer).
• Aspirin use (choice A) and ethanol use (choice C) are
more strongly implicated in gastric ulcer disease than
duodenal ulcer disease.
• Chronic antacid use (choice B) is seen as a result of
peptic ulcer disease, not as a cause of it.
• Smoking (choice E) may also be a lesser contributing
factor to the development of peptic ulcer.
• All of the following are causes of acute peptic
ulcer except
1. Severe burns
2. Helicobacter pylori infection
3. Major trauma
4. Zollinger-Ellison syndrome
• All of the following are Defensive Factors against
gastric ulcer development except
A. Mucus
B. Bicarbonate
C. Bile salts
D. Prostaglandins
E. Phospholipid
A
1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
11)
H. pylori
Phospholipid
Drugs (NSAIDs)
Mucus
bicarbonate
Blood flow
Acid
pepsin
Bile salts
cell renewal
Prostaglandins
B
A. Aggressive Factors
B. Defensive Factors
Scenario
• 72-year-old man had multiple episodes
hematemesis. He was admitted to the hospital
with complaints of syncope, and abdominal pain.
• On admission, the patient's blood pressure was
96/72. His conjunctivae were pale. The
abdominal examination revealed mild epigastric
tenderness. The rectal and prostate examinations
were unremarkable; however, black stool, which
tested positive for fecal blood, was present.
• Hemoglobin : 4.1 gm/dL
• The patient was admitted to the Medical
Intensive Care Unit, where a nasogastric tube
lavage produced coffee-ground gastric
contents that tested positive for blood.
• He was transfused with six units of packed red
blood cells,
What is your next step?
• An upper GI tract endoscopy was performed,
which demonstrated a 5x5 cm gastric ulcer in
the antrum along the lesser curvature.
Biopsies were taken of the ulcers and
surrounding mucosa.
• The biopsy specimens showed necrotic debris
consistent with an ulcer, and the surrounding
mucosa showed acute and chronic
inflammation and organisms consistent with
Helicobacter pylori.
• The patient was treated with acid-suppressive
therapy and antibiotics, and was discharged
five days after admission. He was given
instructions not to take aspirin or drink
alcohol.