Pathophysiology of Peptic Ulcer (Gastric Ulcer and Duodenal Ulcer)

Peptic Ulcer is any discontinuity or erosion of the GI mucosa. Various factors are involved in the mediation of ulcer and play direct and indirect role in the ulceration. However esophageal ulceration is generally kept in the separate category of GORD. This definition also exclude carcinoma and lymphoma which may also cause ulceration and also exclude Crohn,s disease, viral infections and amyloidosis. The prevalence of this disease is as common developed as in under developed countries, except the H Pylori mediated Ulcer, is more prevalent in Under-Developed countries.

Peptic Ulcer

Pathogenesis

Pathogenesis of Peptic Ulcer ( Word used for both Gastric and Duodenal ulcer) varies. Pathogenesis include factors like Halicobacter Pylori, NSAIDS, Stress and other factors previously excluded form the definition.

H Pylori

It is the most common cause of the Ulceration. About 80 Percent of Ulcers are due to this bacteria (one of the cancer causing bacteria).  The spread of this bacteria is possible through oral-oral, oro-fecal and other means like bad sharing, food sharing and congested areas. The pathogenesis cause by this bacteria is due to the cytotoxins like Cag A and other associated enzymes including urease, haemolysins, neuraminidase and fucosidase which digest the mucosal layer of the GI tract. In addition Hyper-acidity caused by H Pylori is due to the mediation on D cells decreasing D cell number which secrete Somatostatin. Somatostatin has inhibitory effect on the gastrin. So Low D cell low somatostatins and High level of Gastrin (Hypergastrinaemia) which leads toG receptor stimulation on parietal cells and also increase in Parietal cell mass (HCl secreting Cells).

NSAIDS

NSAIDS mediated ulcer follow three pattern of pathogenesis, including Superficial erosions, systemic effect due to COX inhibition and Hemorrhages which may exacerbate the ulcers. Superficial erosions mainly defined by the gastric acid mediate concentration of the weak acid like aspirin in the mucosal cells where it block COX and  also by increasing adherence of leucocytes to mucosal endothelia cells. Along with these one of the major effect is the  low production of systemic prostaglandin production.

Stress

Stress is also on of the common factors for GI ulceration.  Among potential mediators, several known behavioral risk factors for ulcers—smoking, alcohol abuse, and lack of sleep—have clear relations with real-life stress and are known to weaken wound healing through their effects on immune function, sleeplessness can also elevation of cortisol level.  A people under stress may also have increased use of NSAIDS.  Low blood flow to the stomach is one of the proposed mechanism due to which the mucosal secretion and synthesis decrease (one of the protective phenomenon of GI tract). Delayed gastric emptying in stress and increased Acid secretion are also included factors of stress. Similarly physiological stress as head injury, spinal cord injury and others may also contribute to Ulcers erosions.

Idiopathic Ulcers  

There are idiopathic tendencies of Ulcers. Confirmed by genetic and twin studies. It may run in families. Idiopathic ulcers is also connected with poor life style habits. However idiopathic ulcer is rare as compare to the factors induced one.