PATHOLOGY OF

STOMACH 02
DR KISHORE
PEPTIC ULCER DISEASE

• Defined as disruption of the mucosal integrity of

the stomach and/or Duodenum leading to a local
defect or excavation due to Active inflammation.
RESULTS DUE TO IMBALANCE BETWEEN
GASTRODUODENAL MUCOSAL DEFENCES
& DAMAGING FORCES THAT OVERCOME
THESE DEFENCES
KEY CONCEPT
GASTRODUODENAL MUCOSAL DEFENCE

• The gastric epithelium is under constant assault by a series

of endogenous noxious factors , including hydrochloric acid ,
pepsinogen/ pepsin and bile salts.
• A highly intricate biologic system is in place to provide
defence from mucosal injury and to repair any injury that
may occur.
MUCOSAL DEFENCE SYSTEM

• 03 level barrier.
• Preepithelial , Epithelial & Sub-epithelial elements
1ST LINE OF DEFENCE IS MUCOUS-
BICARBONATE-PHOSPHOLIPID
BILAYER
Serves as a Physiochemical barrier to multiple molecules; including hydrogen ions.
MUCOUS IS SECRETED IN REGULATED
FASHION BY GASTRODUODENAL
SURFACE EPITHELIAL CELLS.
Mucous is mostly made of Water (95%), phospholipids and glycoproteins.
PUD

• Surface epithelial cells provide the next line of defence through

several factors
• Mucous Production
• Epithelial regenerative capacity
• Bicarbonate production
AN ELABORATE MICRO VASCULAR SYSTEM
WITHIN GASTRIC SUB MUCOSAL LAYER IS
THE KEY COMPONENT OF SUB EPITHELIAL
DEFENCE / REPAIR SYSTEM.
Bicarbonate
PROSTAGLANDINS PLAY A CRUCIAL
ROLE IN GASTRIC EPITHELIAL
DEFENCE/ REPAIR.
DEFENCE MECHANISM
NITRIC OXIDE IS IMPORTANT IN
MAINTENANCE OF GASTRIC MUCOSAL
INTEGRITY.
Key concept
PUD ENCOMPASSES BOTH GASTRIC &
DUODENAL ULCERS.
PUD
DUODENAL ULCERS MOST OFTEN IN
1ST PART OF DUODENUM
PUD
H. PYLORI INFECTION AND NSAID USE ARE
THE PRIMARY UNDERLYING CAUSES OF
PUD.

Key concept
PUD USUALLY DEVELOP IN THE
BACKDROP OF CHRONIC GASTRITIS.
Key concept
PUD

• H. pylori infection and NSAID use are the primary underlying causes of
PUD.
• More than 70% of PUD cases are associated with H. pylori infection and
in these individuals PUD generally develops on a background of chronic
gastritis.
• Because only 5% to 10% of H. pylori–infected individuals develop ulcers,
it is probable that host factors as well as variation among H. pylori strains
also contribute to the pathogenesis.
MORPHOLOGY:

• Peptic ulcers are solitary in more than 80% of patients.

• Lesions less than 0.3 cm in diameter tend to be shallow,
whereas those over 0.6 cm are likely to be deeper.
• The classic peptic ulcer is a round to oval, sharply punched-
out defect
PUD : GROSS & MICROSCOPY
PEPTIC ULCER DISEASE

• Peptic ulcers are chronic, recurring lesions that occur most often in
middle-aged to older adults without obvious precipitating conditions,
other than chronic gastritis
• . A majority of peptic ulcers come to clinical attention after patient
complaints of epigastric burning or aching pain, although a significant
fraction manifest with complications such as iron deficiency anemia,
frank hemorrhage, or perforation.
ZE SYNDROME : UNCONTROLLED
RELEASE OF GASTRIN BY TUMOR
(“GASTRINOMA”) & RESULTING MASSIVE
ACID PRODUCTION.
Key concept :Zollinger Ellison Syndrome :multiple peptic ulcerations in the
stomach,duodenum , and even jejunum.
ACUTE GASTRITIS IS A TRANSIENT
MUCOSAL INFLAMMATORY PROCESS.
It could be Asymptomatic OR present with nausea, pain and vomitting.
GASTRITIS & GASTROPATHY

• Gastritis results from mucosal injury. When neutrophils are

present, the lesion is referred to as acute gastritis.
• When cell injury and regeneration are present but
inflammatory cells are rare or absent, the term gastropathy
is applied.
WHAT IS THE MOST COMMON CAUSE
OF CHRONIC GASTRITIS??
Key concept
CHRONIC GASTRITIS

• The most common cause of chronic gastritis is infection with

the bacillus Helicobacter pylori. Autoimmune gastritis,
typically associated with gastric atrophy, represents less
than 10% of cases of chronic gastritis but is the most
common cause in patients without H. pylori infection.
Chronic NSAID use is a third important cause of gastritis in
some populations,
MICROSCOPY

• Chronic gastritis
04 FEATURES ARE LINKED TO H PYLORI
VIRULENCE
• FLAGELLA
• UREASE , which generates ammonia from endogenous Urea , thereby elevating local
gastric pH around the organism & protecting the bacteria from acidic pH of the
stomach.
• ADHESINS
• TOXINS
H PYLORI GASTRITIS TYPICALLY
AFFECTS THE ANTRUM.
Key concept
AUTOIMMUNE GASTRITIS

• Accounts for less than 10 % cases of Chronic gastritis.

• Antibodies to parietal cell & intrinsic factor
• Defective gastric acid secretion :Achlorhydria
• In contrast with gastritis caused by H. pylori , autoimmune gastritis typically spares the
antrum and induces hypergastrinemia.
• Antral endocrine cell hyperplasia seen.
• Vitamin B12 deficiency