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pylori Infection
H. pylori infection
Weeks-moths
Chronic superficial gastritis Years-decades
Lymphoproliferative disease
ULCER
Acid
EROSIONS
Possible
Concomitant infection with H. pylori Cigarette smoking Alcohol consumption
Possible association
Hyperparathyroidism Coronary artery disease Polycythemia vera Chronic pancreatitis
SUMMARY OF POTENTIAL MECHANISMS BY WHICH H. PYLORI MAY LEAD TO GASTRIC SECRETORY ABNORMALITIES
Corpus IL-8+ Inflammatory cell
H. pylori D acid + D +
TNF-
IL-1 + + + G + SMS ECL +
Bacterial factors Structure Adhesins Ponns Enzymes (urease, vac A, cag A, etc)
Approximate Frequency, %
70 70 65 50 40 35-40 35-40 30 25 25
CLASSIFICATION OF GASTRITIS
I. Acute gastritis II. Chronic Atrophic Gasritis
A. Acute H. pylori infection A. Type A : Autoimmune, B. Other acute infectious gastritides body-predominant 1. Bacterial ( other than H. pylori ) B. Type B : H. pylori - related, 2. Helicobacter helmanni antral predominant 3. Phlegmonous C. Indeterminant 4. Mycobacterial 5. Syphilitic III. Uncommon Form of Gastritis 6. Viral A. Lymphocytic 7. Parasitic B. Eosinophilic 8. Fungal C. Crhns disease D. Sarcoidosis E. Isolated granulomatous gratritis
Cannaliculus Histamine H, K ATPase ECL cell Tubulovesicles Histamine ECL cell Somatostatin Somatostatin D cell Gastrin Blood vessel D cell ANTRUM Gastrin Somatostatin G cell
SCHEMATIC REPRESENTATION OF THE STEPS INVOLVED IN SYNTHESIS OF PROSTAGLANDIN E2(PGE2) AND PROSTACYCLIN (PGI2)
Membrane phospholipids
TXA2, PGI2, PGE2 Gastrointestinal mucosal integrity Platelet aggregation Renal function
HCI KCI Canaliculus H3 O + H+, K+ -ATPase CaGastrin Tubulovesicles Active pumps ACh Histamine KCI
Transmigration
H2 O 2
IL-8 PAF
P-selectin
Thrombin Histamine H2O2 LTC4 LTD4
E-selectin
Endothelial cells PAF PECAM-1 Endothelial injury Collagenase Elastase Activated PMN Oxygen radicals, Protease Tissue injury
Macrophage activation
ULCER SCAR
Catalase GSH-Px
H2 O
GSSG
H2O2 OCI-
Fe2+
HO
ROO-
H. pylori
NH2CI Urease NH3
TBA-RS
Apoptosis
Epithelial cell
LAP NAP Tissue injury Oxygen radicals
IL-8
Transmigration
Adhesion
Venule
LTC4, LTD4
LTB4
TNF-
Vasospasm
Neutrophil activation Endothelial cell activation (CD11b/CD18) (ICAM-1)
Ischemia-reperfusion
Oxygen radicals Elastase
Apoptosis
Ischemia
The black areas in the schematic of diffuse corporal atrophic gastritis and multifocal atrophic gastritis represent areas of focal atrophy and intestinal metaplasia
Reported Abnormalities in Gastric Acid Secretion and Acid Homeostasis in Peptic Ulcer Disease
Duodenal Ulcer
Increased Mass of gastric parietal cells Maximal acid output Peak acid output stimulated by meals* Duration of meal-stimulated acid secretion Basal acid output Daytime acid output Nocturnal acid output Fasting serum gastrin levels* Meal- and GRP-stimulated gastrin levels* Serum concentrations of pepsinogen I* Rate of gastric emptying for liquids Decreased Bicarbonate production by the proximal duodenum
Gastric Ulcer
Increased Serum levels of pepsinogen II Duodenogastric reflux Decreased Mass of gastric parietal cells Maximal acid output
*Evidence suggests that this abnormality may be a reersible consequence of exobacter pylori infection GRP, gastrin-releasing peptide
NSAID use
H. pylori infection
H. pylori infection
Duodenal
Gastric
Virulence Factors of Helicobacter pylori that Promote Colonization and induce Tissue Injury
Promote Colonization Flagella (for motility) Urease* Adherence factors Induce Tissue Injury Lipopolysaccharide Leukocyte recruitment and activating factors Vacuolating cytotoxin (VacA) Cytotoxin-associated antigen (CagA) Other membrane inflammatory protein (OipA) Heat shock proteins (HspA, HspB)
Acute Gastritis
Childhood
Old Age
FUNCTION
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 Early hydrolysis of dietary proteins Liberation of vitamin B12 from dietary protein Early hydrolysis of dietary triglyceride Binding of vitamin B12 for subsequentileal absorption Protection against noxious agents
Distribution of human gastric endocrine cells in glands from the oxyntic mucosa (left) and pyloric mucosa (right)
ECL 35%
EC 25%
G 49%
EC 29%
Other 14%
D 26%
Other 3%
D 19%
Oxyntic Mucosa
Pyloric Mucosa
ANATOMIC COUNTERPART
Proximal stomach just below esophagogastric junction Fundus and body
SECRETORY PRODUCTS
Mucin, PGII
Oxyntic (75%)
Mucus neck
Chief Parietal
Pyloric
Mucus neck
Mucin, PGI and PGII PGI and PGII, leptin HCI, intrinsic factor Mucin, PGII
*Pepsinogen I (PGI), includes Pg 1-5; PGII includes Pg6 and Pg7. Endocrine cells are also present within glands PGI and PGII are colocalized in zymogen granules and are secreted concurectly Some intrinsic factor may also be produced in chief cells and endocrine cells
GASTRIC GLAND
MSC MNC ECL CELL
D CELL PC
CC
Fundus
Body
Antrum
Pyloric gland mucosa