H. pylori Infection
H. pylori infection
Weeks-moths
Chronic superficial
gastritis
Years-decades
Gastric
adenocarcinoma
Risk Factors for NSAIDs Induced
Gastroduodenal Ulceration
Established Possible
Advanced age Concomitant infection with
History of ulcer H. pylori
Concomitant use of glucocorticoids Cigarette smoking
High-dose NSAIDs Alcohol consumption
Multiple NSAIDs
Concomitant use of anticoagulants
Serious or multisystem disease
Disorders Associated with Peptic
Ulcer Disease
Acetylcholine
Cannaliculus
Histamine
H, K ATPase ECL cell
Tubulovesicles
Histamine –
– –
ECL cell Somatostatin
Somatostatin
Gastrin D cell
Phospholipase A2
Arachidonic acid
Stomach Macrophages
Kidney COX-1 COX-2 Leukocytes
Platelets housekeeping inflammation Fibroblasts
Endhothelium Endothelium
Oxygen radicals
IL-1
TNF IL-8 Activation
Macrophage Neutrophil
Chemotaxis
Transmigration
Adhesion
Venule
CONDITIONS ASSOCIATED WITH
PEPTIC ULCER
H. pylori H. pylori
infection infection
Duodenal Gastric
Physiologic Functions of Gastric
Exocrine Secretions
PRODUCT FUNCTION
Hydrochloric acid Provides optimal pH for pepsin and gastric lipase
(see below)
Facilitates duodenal inorganic iron absorption
Negative feedback of gastrin release
Stimulation of pancreatic HCO3- secretion
Supression of ingested microorganisms
Pepsins Early hydrolysis of dietary proteins
Liberation of vitamin B12 from dietary protein
Gastric lipase Early hydrolysis of dietary triglyceride
Intrinsic factor Binding of vitamin B12 for subsequentileal ab-
sorption
Mucin/HCO3- Protection against noxious agents
Exocrine Cells within Gastric Glands and
Their Secretory Products*,†
GLAND EXOCRINE
AREA CELLS
% OF ANATOMIC WITHIN SECRETORY
TOTAL COUNTERPART GLANDS PRODUCTS
Cardiac Proximal stomach Mucus neck Mucin, PGII
(<5%) just below esoph-
agogastric junc-
tion
Oxyntic Fundus and body Mucus neck Mucin, PGI and
(75%) PGII‡
Chief PGI and PGII, ‡
leptin
Parietal HCI, intrinsic
factor§
Pyloric Antrum and pylorus Mucus neck Mucin, PGII