Causes of Peptic Ulcer | Acute Peptic Ulcer | Duodenal Ulcer
Peptic ulcers are divided into acute and chronic ulcers -
- Acute peptic ulcers
- Etiology
- Half of the patients give history of ingestion of aspirin or anti-inflammatory drugs.
- Sometimes these acute ulcers may occur following stress, when they are called ‘stress ulcers’. This may occur following hypotension from hemorrhage, endotoxin shock or cardiac infarction.
- Sepsis is an important etiological factor. Un-drained pus may be responsible for acute stress ulcers. Upper gastrointestinal bleeding from these ulcers may be seen in critically ill patient and should be a signal of search for pus.
- These acute ulcers are seen after cerebral trauma or neurological operations.
- After major burns acute ulcers may be seen (Curling’s ulcer). Within first 48hrs multiple erosions may develop anywhere in the body and fundus of the stomach. During convalescent period of such burn cases, acute duodenal ulcer may occur which often become chronic.
- Patients on steroids may develop acute ulcers, known as ‘steroid ulcers’.
Chronic peptic ulcers are divided into gastric ulcer and duodenal ulcer -
- Gastric ulcer
- Diminished mucosal resistance – due to lowering of the ability to resist the effect of acid pepsin digestion causes gastric ulcer.
- Pyloro-duodenal reflux – Regurgitated bile and other duodenal juices have been taken to be the prime cause of pre-ulcerative superficial gastritis. Such biliary reflux may account for a large number of gastric ulcer cases.
- Deficient mucous barrier – A surface layer of mucus protects normally from the digestive effect of the hydrochloric acid and pepsin. When this mucous barrier becomes deficient gastric ulcer may develop. Most cases of gastric ulcers produce large quantities of mucus.
- Mucosal trauma – 85% of gastric ulcers occur along the lesser curve of the stomach. This part of the stomach is exposed to injurious effects of heat and trauma.
- Local ischemia – arterio-venous shunts which are present in the sub-mucosa of the stomach are under control of sympathetic nervous system and excessive stress and strain may cause diminution of blood supply to the mucous membrane of the stomach leading to ulcer formation.
- antral stasis – As the gastric ulcer patients have low acid content some factor such as injury to the gastric mucosa which renders it more susceptible to acid peptic damage may lead to ulcer formation.
- Non-steroidal anti-inflammatory drugs (NSAIDs) – ingestion of these drugs in patient suffering from arthritis as a long term basis are a significant etiologic factor at present time. The drugs of this group are often called as ulcerogenic drugs.
- Helicobacter pylori – it is a spirochetal bacterium which exits in the deep mucosal layer of the antrum mainly and duodenum rarely is associated with ulcer disease.
- Duodenal ulcers
- Acid hyper-secretion – Duodenal ulcer is seemingly simplified at first sight by a clear relationship to over-production of hydrochloric acid by the stomach.
- Genetic factors – in a great number of cases the acid production may be within the high side of the normal range and in these cases ulceration cannot be explained except the diminished mucosal resistance to normal acid secretion. Diminished power of resistance of the mucosa has also been incriminated to cause duodenal ulcer. There is a significant relationship between blood group ‘O’ and the development of duodenal ulcer.
- Endocrine organ dysfunction – There are various endocrine dysfunction (Cushing’s syndrome, Zollinger-Ellison syndrome, parathyroid tumor etc) can cause duodenal ulcer.
- Liver disease – Ulceration of both stomach and duodenum has co-existed with disease of the liver particularly cirrhosis. It may be due to increase in blood supply to the gastric mucosa and over-production of histamine in the stomach wall to stimulate the partial cells.
- Emotional factors – Anxiety, stress and strain have always been incriminated to cause peptic ulcer.
- Diet and smoking – Irregular diet, spicy food and excessive drinking tea and coffee have always provoked ulcer formation. Smoking does appear to predispose ulcer formation. The exact cause is not yet clearly understood, but it seems that smoking diminishes mucosal defense mechanism almost similar to NSAIDs.
- Helicobacter pylori – it has been isolated in 100% of duodenal ulcer cases. Its eradication has definitely has definitely led to decrease in recurrence rate and this clearly indicates its importance in the etiology of duodenal ulcer.
