“Peptic ulcers are chronic, most often solitary, lesions that occur in any portion of the gastrointestinal tract exposed to the aggressive action of acid-peptic juices.”
Each of the two main types may be acute or chronic.
A.] Acute Peptic (Stress) Ulcers:
Acute peptic ulcers or stress ulcers are multiple, small mucosal erosion, seen most commonly in the stomach but occasionally involving the duodenum.
It is not clear how the mucosal erosion occurs in stress ulcer because actual hypersecretion of gastric acid is demonstrable in only Cushing’s ulcers occurring intracranial conditions such as due to brain trauma, intracranial surgery and brain tumor. In these conditions, the possible hypotheses for genesis of stress ulcers are as under:
- Ischemic hypoxic injury to the mucosal cells
- Depletion of the gastric mucus ‘barrier’ rendering the mucosa susceptibility to attack by acid-peptic secretion.
The ulcers occur following severe stress. The causes are as follows:
1.] Psychological stress
2.] Physiological stress as follows:
- Severe trauma
- Extensive burn
- Intracranial lesions
- Drug intake like aspirin, butazolidine, indomethacin.
- Local irritants
B.] Chronic Peptic Ulcers (Gastric and Duodenal Ulcers):
Chronic peptic ulcer would mean gastric and duodenal ulcers, the two major forms of ‘peptic ulcer disease’ of the upper GI tract in which the acid-pepsin secretion are implicated in their pathogenesis. Peptic ulcers are common in the present-day life.
In both gastric and duodenal ulcer morphological findings are similar for quick diagnostic.
There are distinct differences in the pathogenetic mechanisms involved in duodenal and gastric ulcers as under:
1.] DUODENAL ULCER:
- There is generally hypersecretion of gastric acid into the fasting stomach at night which takes place under the influence of vagal stimulation.
- Patients with duodenal ulcer have rapid emptying of the stomach so that the food which normally buffers and neutralizes the gastric acid, passes down into the small intestine, leaving the duodenal mucosa exposed to the aggressive action of gastric acid.
2.] GASTRIC ULCER:
- Hyperacidity may occur in gastric ulcer due to increased serum gastrin levels in response to ingested food in an atonic stomach.
- Many patients of gastric ulcer have low to normal gastric acid levels. Ulcerogenesis in such patients is explained on the basis of damaging influence of other factor such as gastrisis, bile reflex, cigarette smoke etc.
Following are the treatment given to a peptic ulcer patient:
1.] Patients with PUD should eliminate or reduce psychological stress, cigarette smoking,
and use of NSAIDs (including aspirin). If possible, alternative agents such as
acetaminophen or a nonacetylated salicylate (eg, salsalate) should be used for pain
2.] Although there is no need for a special diet, patients should avoid foods and beverages
that cause dyspepsia or exacerbate ulcer symptoms (eg, spicy foods, caffeine,
3.] Elective surgery is rarely performed because of highly effective medical management.
Emergency surgery may be required for bleeding, perforation, or obstruction.
MULTIPLE CHOICE QUESTIONS: –
1.] Which of the following receptor is closed by drug during a peptic ulcer?
c. Proton Pump
d. H1 and Proton Pump
2.] Which of the following drug are ulcer protective?
3.] All are true about amoebic ulcer except?
a. Flask shaped ulcers
b. Commonest site in ascending colon and cecum
c. Perforation is common
d. Paucity of inflammatory cells
4.] Transverse ulcers are seen in?
d. Ulcerative colitis
5.] Aphthous ulcers are also known as?
a. Canker sores
b. Marjolijn’s ulcer
c. Curling ulcer
d. Cushing’s ulcer
6.] All are complications of typhoid ulcer except?
b. Structure formation
7.] Most ulcers are due to the result of M. pylori?
8.] Which of the following correctly defines a peptic ulcer?
a. When the esophagus starts getting thinner
b. A benign lesion of gastric mucosa
c. Both (a) and (b)
d. None of the above
9.] Which of the following drug is an antacid?
c. Mg hydroxide
10.] What are causes of GERD?
a. Overproduction of acid
b. Over relaxation of lower esophagus sphincter
c. Both (a) and (b)
d. None of the above
1.] (d) H1 and Proton Pump
2.] (c) Sucralfate
3.] (c) Perforation is common
4.] (c) Tuberculosis
5.] (a) Canker sores
6.] (b) Structure formation
8.] (b) A benign lesion of gastric mucosa
9.] (c) Mg hydroxide
1.] Textbook of Pathology by Harsh Mohan; 7th edition; Page no.533 – 537.
2.] Robbin’s Basic Pathology; 5th edition; Page no.773 – 778.