brief discussion on Peptic ulcer, types and there Pathogenesis

1. Presented To: Presented By:
Sir Tabish Ali Zeeshan Ali
Usama Naushahi
Daniyal Khan
Hasanat Ahmed

2. Definitions:
• Peptic ulcer can also be defined “as a hole in a mucous of any portion
of GIT exposed to acid-pepsin secretion”
• Peptic ulcer is a chronic solitary mucosal lesion that occur in any level
of gastrointestinal tract exposed to acid-pepsin secretion.

3. In order of frequency peptic ulcer occur in:
• Duodenum 75%
• Stomach 20%
• Barret's esophagus 1%
• Gastroenterostomy stroma
• Duodenum, stomach and jujenum (in Z.E syndrome)
• Meckel's diverticulum (ectopic gastric mucosa)

4. Etiology:
• Peptic ulcers are believe to be produced by some imbalance between
some gastroduodenal mucosal defensive and aggressive forces.

5. Defensive Forces:
• Secretion of surface mucosal layer
• Secretion of bicarbonate into the mucus layer.
• The specialized apical surface of the gastric mucosal cell
• Regenerative capacity of mucosal epithelial cell
• Mucosal elaboration of prostaglandin's

6. Aggressive Forces:
• Acid secretion
• Peptic activity derived from pepsinogen
• Helicobacter pylori infection of the gastric antrum
• NSAIDS and ulcerogenic
• Impaired inhibition of stimulator mechanism

7. Symptoms:
• dull pain in the stomach
• weight loss
• not wanting to eat because of pain
• nausea or vomiting
• bloating
• feeling easily full
• burping or acid reflux
• heartburn (burning sensation in the chest)
• pain that may improve when you eat, drink, or take antacids
• anemia (symptoms can include tiredness, shortness of breath, or paler skin)
• dark, tarry stools
• vomit that’s bloody or looks like coffee grounds

8. Types:
Major types of peptic ulcers are:
• Duodenal ulcers: ulcers that develop
in the upper section of the small
intestines, called the duodenum.
• gastric ulcers: ulcers that develop
inside the stomach.
• esophageal ulcers: ulcers that
develop inside the esophagus.

12. Sites
•Gastric and duodenal – 98 %
•Ratio of 1:4
•Duodenum:1st st part >95%
•Gastric:junction b/w antrum &acid secr. mucosa

13. Causes
• Gram-negative bacteria (H. Pylori)
• NSAIDS
• Excessive secretion of HCL in the stomach due to ingestion
of CAFFEINATED BEVERAGES, SPICY FOODS, SMOKING and
ALCOHOL.
• Regular use of pain relievers
• Stress
• Decreased duodenal mucosal bicarbonate

14. Pathophysiology
• In most people H. pylori causes antral gastritis associated with
depletion of somatostatin (from D cells) and gastrin release
from G cells. cells).
• The subsequent hypergastrinaemia stimulates acid production
by parietal cells, but majority of cases this has no clinical
consequences.
• In a minority of patients (perhaps those who inherit a large
parietal cell mass) this effect is exaggerated, leading to
duodenal ulceration.

16. Pathophysiology

19. • In Gastric ulcers , there is some primary defects in gastric mucosal
resistance.
• Patients have low to normal levels of gastric acid but not true
achlorhydria.

20. Major influences for GU are
1. An increased tendency for back diffusion of hydrogen ions, suggesting some
derangement in the gastric mucosal barriers.
2. GU is frequently associated with chronic antral gastritis( Bile and lysolecithin
reflux into the stomach, which occurs in gastritis , damages the mucosal barrier
and impairs gastric mucosal defenses).
3. Gastric mucosa may be deficient due to decreased mucus secretion or decreased
mucosal HCO3 secretion.
4. Exogenous agents that damage the mucosa(unbuffered aspirin, alcohol, tobacco)
are more likely to cause gastric ulcers than duodenal ulcers.
5. Helicobacter pylori breaks down the glycoproteins within the gastric mucus and
favors the production of gastritis and ulcerations.

21. Phases of ulcer:
• During the active phase ,four zones can be distinguished in an ulcer.
1. The base and margins have a thin layer of necrotic fibrinoid debris .underlain is
2. A zone of active nonspecific inflammatory infiltrate with neutrophils. Deep to
this layer is
3. Active granulation tissue followed by
4. Fibrous collagenous scar
• Trapped vessels in the ulcerated area are thickened and thrombosed or widely
patent.
• In GU, the surrounding mucosa show chronic atrophic gastritis and intestinal
metaplasia of glands.

23. Healing phase of ulcer:
• In hemorrhagic erosions and acute peptic ulcers, the crater is filled up by
granulation tissue . Then there occurs reepithelization and restoration of normal
architecture.
• In subacute and chronic peptic ulcers, extensive fibrous scarring hampers
reparative process leading to contraction and obstruction.

25. It includes;
 Acute complications
 Late complications

26. ACUTE COMPLICATIONS
It may includes;
 Hemorrhage
 Perforation
 Intractable pain

27. Hemorrhage
Due to unchecked ulceration, destruction of blood vessels in GIT takes place in the
affected area which may lead to;
 Hematemesis: vomiting of blood.
 Melena: Black tarry stools, occur as a result of upper GIT bleeding. It has a
characteristic tarry color and offensive smell, and is often difficult to flesh out,
which is due to the alteration and degradation of blood by intestinal enzymes.

29. Perforation
 A condition in which an untreated ulcer can burn through the wall of the stomach,
allowing digestive juices and food to leak into the abdominal cavity.
 It may lead to acute peritonitis; inflammation of peritoneum.
 Treatment generally requires immediate surgery.
 Ultimately results in dead of victim if remain untreated.

31. Intractable Pain
 In case of gastric ulcer, pain in the chest cavity.
 But in case of duodenal ulcer, severe, unbearable pain in the right lateral chest
region.

32. LATE COMPLICATIONS
It includes;
 Pyloric obstruction
 Penetration
 Malignant transformation
 Abscess Formation

33. Pyloric Obstruction
In gastric ulcer, stomach (gastric) outlet obstruction is an infrequent complication of
peptic ulcer. Such obstruction may produce large losses of acid gastric secretions by
vomiting.

35. Penetration
• Penetration is only reported in 20% cases.
• Ulcer usually penetrates in the gastroduodenal region and left gastric arteries.
• Penetration in the splenic artery is a very rare condition.
• And it may penetrate to the nearby organ i.e., pancreas.

36. Malignant Transformation
 It is the most serious complication of the gastric ulcer.
 Lead to the ulcer-carcinoma.
 It is reported in 1% cases.

38. Abscess Formation
It results in the formation of abscess in the affected area.

39. REFERENCES
 Gross pathology by Jawad Ahmed Special Pathology Chapter 5 page no
305— 310
 https://www.healthline.com/health/stomach-ulcer#symptoms
 Robbins & Cotran Pathologic Basis of Disease