The document discusses peptic ulcers, which occur in the stomach or duodenum when acid and pepsin exposure damages the gastrointestinal mucosa. It describes the normal stomach anatomy and layers. Peptic ulcers are classified as acute (stress-related) or chronic. Chronic ulcers have multiple potential causes like H. pylori infection, NSAIDs, diet, and genetics. Duodenal ulcers are linked to excess acid secretion while gastric ulcers involve impaired mucosal defenses. The pathogenesis of each involves disruption of mucosal barriers by factors such as inflammation, toxins, and hyperacidity.

1. PEPTIC ULCER
RVS Chaitanya
Koppala

2. NORMAL STRUCTURE
The stomach is ‘gland with cavity’, extending from its junction with
lower end of the oesophagus (cardia) to its junction with the duodenum
(pylorus).
The stomach has 5 anatomical regions:
1. Cardia is the oesophagogastric junction and lacks the sphincter.
2. Fundus is the portion above the horizontal line drawn across the
oesophagogastric junction.
3. Body is the middle portion of the stomach between the fundus and
the pyloric antrum.
4. Pyloric antrum is the distal third of the stomach.
5. Pylorus is the junction of distal end of the stomach with the
duodenum. It has powerful sphincter muscle. The mucosal folds in the
region of the body and the

4. Histologically, thewall of thestomachconsists of 4layers—
SEROSA, MUSCULARIS, SUBMUCOSA ANDMUCOSA.
1. Serosa is derived from the peritoneum which is deficient in the region
of lesser and greater curvatures.
2. Muscularis consists of 3 layers of smooth muscle fibres the outer
longitudinal, the middle circular and the inner oblique (Nerve plexuses
and ganglion cells)
3. Submucosa is a layer of loose fibroconnective tissue binding the
mucosa to the muscularis loosely and contains branches of blood
vessels, lymphatics and nerve plexuses and ganglion cells.

5. i) Superficial layer. It co nsists o f a sing le laye r o f surface epithelium
composed of regular, mucin-secreting, tall columnarcells with basal
nuclei. Cardiac mucosa, O xyntic m uco sa, Antralm uco sa .
ii) Deep layer:
Glands of cardia
Glands of body fundus (parietal cell, chief cells, mucin secreting
neck cells, enterochromaffin cells)
Glands of pylorus: gastrin producing G- cells

6. GASTRIC JUICE
The secretory products of the gastric mucosa are the g astric juice
and the intrinsic facto r, re q uire d fo r abso rptio n o f vitamin B12
Gastric juice consists of hydrochloric acid, pepsin, mucin and
electrolytes like Na +, K+ , HCO’3 and Cl-
Hydrochloric acid is produced by the parietal (oxyntic) cells by the
interaction of Cl’ ions of the arterial blood with water and carbon
dioxide in the presence of the enzyme, carbonic anhydrase.
Injection of histamine can stimulate the production of acid component
of the gastric juice,
while the pepsin-secreting chief cells do not respond to histamine.
Physiologically, the gastric secretions are stimulated by the food
itself.

7. CONTROL OF GASTRIC
SECRETIONS
chieflyoccurs inoneof thefollowing 3 ways:
Cephalic phase—is stimulated by the sight, smell, taste or
even thought of food. A neural reflex is initiated via branches of
the vagus nerve that promotes the release of hydrochloric acid,
pepsinogen and mucus.
Gastric phase—is triggered by the mechanical and chemical
stimuli. Me chanicalstim ulatio n co m e s fro m stre tching o f the
wallof the stomach and conveying neural messages to the
medulla for gastric secretion.
Che m icalstim ulatio n is by dig e ste d pro te ins, am ino acids, bile
salts and alcohol which act on gastrin-producing G cells.
Gastrin then passes into the blood stream and on return to the
stomach promotes the release of gastric juice.
Intestinal phase—is triggered by the entry of protein rich food
in the small intestine. An intestinal hormone capable of

10. PEPTIC ULCERS
Peptic ulcers are the areas of degeneration and necrosis of
gastrointestinal mucosa exposed to acid-peptic secretions.
Though they can occur at any level of the alimentary tract that is
exposed to hydrochloric acid and pepsin, they occur most
commonly (98-99%) in either the duodenum or the stomach in the
ratio of 4:1.
Each of the two main types may be acute or chronic.

11. ACUTE PEPTIC (STRESS)
ULCERSAcute peptic ulcers or stress ulcers are multiple, small mucosal
erosions, seen most commonly in the stomach but occasionally
involving the duodenum.
ETIOLOGY. These ulcers occurfollowing severe stress. The causes
are as follows:
i) Psycho lo g icalstre ss
ii) Physio lo g icalstre ss as in the fo llo wing :
Shock
Severe trauma
Septicaemia
Extensive burns
Intracranial lesions.
Drug intake (e.g. aspirin, steroids, indomethacin).

12. PATHOGENESIS.
It is not clearhow the mucosal erosions occur in stress ulcers
because actual hypersecretion of gastric acid is demonstrable in only
Cushing’s ulcers occurring from intracranial conditions such as due to
brain trauma, intracranial surgery and brain tumours.
In all other etiologic factors, gastric acid secretion is normal or below
normal. In these conditions, the possible hypotheses for genesis of
stress
ulcers are as under:
1. Ischaemic hypoxic injury to the mucosal cells.
2. Depletion of the gastric mucus ‘barrier’ rendering the mucosa
susceptible to attack by acid-peptic secretions.

13. CHRONIC PEPTIC ULCERS
(Gastric and Duodenal Ulcers) If not specified, chronic peptic ulcers
would mean gastric and duodenal ulcers.
Peptic ulcers are common in the present-day life of the
industrialised and civilised world.
Gastric and duodenal ulcers represent two distinct diseases as far
as their etiology, pathogenesis and clinical features are concerned.
However, morphological findings in both are similar and quite
diagnostic.

14. ETIOLOGY.
The immediate cause of peptic ulcer disease is disturbance in
normal protective mucosal ‘barrier’ by acid pepsin, resulting in
digestion of the mucosa.
However, in contrast to duodenal ulcers, the patie nts o f g astric
ulce r have lo w-to -no rm al g astric acid se cre tio ns, tho ug h true
achlo rhydria in re spo nse to stim ulants ne ve r o ccurs in be nig n g astric
ulce r.
Besides, 10-20% patients of gastric ulcer may have coexistent
duodenal ulcer as well.
These factors are discussed below but the first two—H. pylo ri

15. Helicobacterpylori gastritis
NSAIDS induced mucosa injury.
Acid pepsin secretions
Gastritis
Other local irritants (alcohol, cigarette smoking, unbuffered
aspirin)
Dietary factors
Psychological factors ( stress)
Genetic factors (blood group of o are more prone to ulcers
association with HLA-B5 antigen.)
Hormonal factors (gastrin by islet-cell tumour in Zollinger-Ellison
syndrome, endocrine secretions in hyperplasia and adenomas of
parathyroid glands, adrenal cortex and anterior pituitary)
Miscellaneous (alcoholic cirrhosis, chronic renal failure,
hyperparathyroidism, chronic obstructive pulmonary disease, and

18. PATHOGENESIS.
Although the role of various etiologic factors just described is well
known in ulcerogenesis, two most important factors in peptic ulcer
are as under:
Exposure of mucosa to gastric acid and pepsin secretion.
Strong etiologic association with H. pylo ri infe ctio n.
There are distinct differences in the pathogenetic mechanisms
involved in duodenal and gastric ulcers as under:

19. Duodenal ulcer.
There is conclusive evidence to support the role of high acid-pepsin
secretions in the causation of duodenal ulcers. Besides this, a few
other noteworthy features in the pathogenesis of duodenal ulcers
are as follows:
1. There is generally hype rse cre tio n o f g astric acid into the fasting
stomach at night which takes place under the influence of vagal
stimulation.
2. Patients of duodenal ulcer have rapid e m ptying o f the stomach
so that the food which normally buffers and neutralises the gastric
acid

20. 3. Helicobacter gastritis cause d by H. pylo ri is se e n in 9 5-1 0 0 %
ases of duodenal ulcers. The underlying mechanisms are as under:
i) Gastric m uco salde fe nse is bro ke n
ii) Ho st facto rs: H. pylo ri-infe cte d m uco sal e pithe lium re le ase s
pro inflam m ato ry cyto kine s such as IL-1 , IL-6 , IL-8
iii) Bacte rial facto rs: Epithe lial injury is also induce d by cytotoxin-
associated gene protein (Cag A), while vacuo lating cytotoxin (VacA)
induce s e labo ratio n o f cyto kine s.

21. GASTRIC ULCER.
The pathogenesis of gastric ulcer is mainly explained on the basis of
impaired gastric mucosal defenses against acid-pepsin secretions.
Some other features in the
pathogenesis of gastric ulcer are as follows:
1. Hyperacidity may occur in gastric ulcer due to incre ase d se rum
g astrin le ve ls in re spo nse to ing e ste d fo o d in an ato nic stomach.
2 Ulcerogenesis in such patients is explained on the basis of damaging
influence of o the r facto rs such as gastritis, bile reflux, cigarette smoke
etc.
3. The normally protective g astric m ucus ‘barrie r’ ag ainst acid-pepsin
is deranged in gastric ulcer.
One of the mechanisms for its depletion is colonisation of the gastric
mucosa by H. pylo ri se e n in 7 5-8 0 % patie nts o f g astric ulce r.