Pathophysiology

RISK FACTORS H. pylori Infection, Stress Habitual use of NSAIDs Cigarette Smoking Alcohol and Carbonated drinks Consumption
H. pylori Infection
Bile salts, aspirin, alcohol, ischemia

Urease Production Alkalosis Neutralization of acidity

Gastric Emptying

Serum Gastrin Levels Acid Secretion Pepsin

Damaged mucosal barrier

Bicarbonate

Function of mucosal cells Quality of mucus Loss of tight junctions between cells

Acid & Pepsin concentration in duodenum

Back diffusion of acid into gastric mucosa

Pepsin

Histamine Release Acid secretion

Penetration in the mucosal barrier

Mucosal injury
Further mucosal Erosion Destruction of blood vessels Bleeding

Local Vasodilation

ULCERATION

capillary permeability Loss of plasma proteins Mucosal Edema Loss of plasma into gastric lumen

Stimulation of cholinergic intramural plexus, causing muscle spasms

ULCERATION

Stimulation of Nociceptors

Destruction of Blood Vessels

Stimulation of Nerve Fibers (A & C Fibers)

Bleeding

Transmission of Impulses to the Brain

Blood Clotting (Risk for thrombisis)

Perception of

PAIN

Intestinal Blockage