Here are proper answers to your questions based directly on your lecture notes:
1. Briefly discuss the defence mechanisms of stomach.
The stomach protects itself from acid damage through several mechanisms:

A mucin layer forms a barrier between acid and the stomach wall.

Bicarbonate ions neutralize any acid that reaches the epithelium.

Prostaglandins promote mucus and bicarbonate production and improve blood flow.

A rich blood supply removes harmful substances and supports tissue repair.

Rapid cell regeneration replaces damaged epithelial cells.
These defences work together to maintain mucosal integrity and prevent ulceration.
2. Briefly discuss about H. pylori.
Helicobacter pylori is a Gram-negative, spiral-shaped bacterium found in the stomach. It produces
urease, which neutralizes acid, and enzymes like proteases and phospholipases that damage the
mucosal lining. It spreads via oral-oral, fecal-oral, or environmental routes and is linked to poor hygiene
and overcrowding. This organism is associated with gastritis, peptic ulcers, and gastric cancer due to its
ability to cause chronic inflammation.
3. List diseases caused by H. pylori.
1. Helicobacter pylori infection can
cause atrophic gastritis, which
involves the thinning and
inflammation of the stomach lining.
2. It is a major cause of peptic ulcer
disease, affecting both the stomach
and the duodenum.
3. It is linked to the development of
MALT (mucosa-associated lymphoid
tissue) lymphoma, a type of cancer
that arises from lymphoid tissue in
the stomach.
4. H. pylori infection also increases the
risk of gastric carcinoma, a malignant
tumor of the stomach lining.
1. Atrophic gastritis
2. Peptic ulcer disease (stomach and
duodenum)
3. MALT (mucosa-associated lymphoid
tissue) lymphoma
4. Gastric carcinoma
4. List various aetiologies of PUD (Peptic Ulcer Disease).
1. Infection with Helicobacter pylori is
one of the most common causes of
both gastric and duodenal ulcers.
2. Non-steroidal anti-inflammatory
drugs (NSAIDs) contribute by
chemically irritating the mucosa and
inhibiting protective prostaglandins.
3. Hypersecretion of gastric acid and
pepsin leads to increased mucosal
damage.
4. Chronic gastritis often coexists with
PUD and impairs mucosal defences.
5. Local irritants, including smoking,
alcohol, and spicy foods, can damage
the mucosal lining or increase acid
production.
6. Dietary factors, such as poor nutrition
or excessive caffeine intake, may play
a contributing role.
7. Psychological stress, anxiety, and
personality factors can exacerbate
ulcer formation.
8. Genetic factors, including blood
group O and specific HLA types, have
been associated with increased risk.
9. Hormonal causes, such as gastrinsecreting tumors in Zollinger-Ellison
syndrome, or hyperparathyroidism,
can lead to excessive acid production.
10. Other systemic conditions, like
alcoholic cirrhosis, chronic kidney
disease, and bile reflux, can also
contribute to PUD development
1. H. pylori infection
2. NSAIDs (e.g. aspirin, ibuprofen)
3. Gastritis
4. Acid-pepsin over-secretion
5. Local irritants: smoking, alcohol,
spicy foods
6. Dietary factors (e.g. caffeine,
nutritional deficiencies)
7. Psychological factors: stress, anxiety
8. Genetic predisposition (blood group
O, HLA-B5)
9. Hormonal disorders (e.g. gastrinsecreting tumors like Zollinger-Ellison
syndrome)
10. Miscellaneous: alcohol-related
cirrhosis, chronic renal failure, bile
reflux
5. Briefly discuss various complications of PUD.
PUD can result in several complications:
1. Obstruction occurs when ulcers cause scarring near the pylorus or duodenum, leading to
narrowing and delayed gastric emptying.
2. Hemorrhage happens when ulcers erode blood vessels, causing chronic anemia, melena,
or even massive bleeding (hematemesis).
3. Perforation is a serious emergency where the ulcer creates a hole, leading to peritonitis,
shock, and air under the diaphragm.
4. Malignant transformation is rare, but long-standing ulcers may undergo cancerous
changes, especially gastric ulcers.
6. Briefly discuss IBD (Inflammatory Bowel Disease).
Inflammatory bowel disease (IBD) refers to chronic inflammation of the bowel due to inappropriate
immune responses. It includes two main conditions: Crohn’s disease and ulcerative colitis.
The exact cause is unknown, but contributing factors include genetics, immune system dysfunction,
microbial exposure, and psychological stress.
IBD can affect people at any age, especially in the 2nd–3rd decades, and may involve other systems (e.g.
joints, skin, eyes).
Common symptoms include diarrhea, abdominal pain, blood or mucus in stool, and malabsorption.
7. Briefly discuss Crohn’s disease.
Crohn’s disease is a form of IBD that can affect any part of the gastrointestinal tract, most commonly
the terminal ileum and colon.
It causes transmural inflammation (affecting all layers of the bowel) and forms non-caseating
granulomas.
The disease shows skip lesions—normal segments between inflamed areas.
Grossly, the bowel wall becomes thick and hard, with cobblestone appearance and deep fissures.
Complications include malabsorption, fistulas, strictures, and increased cancer risk.
8. Briefly discuss ulcerative colitis.
Ulcerative colitis is another form of IBD that affects the rectum and colon, spreading continuously
without skip lesions.
It involves only the mucosal layer, causing ulcers, pseudopolyps, and loss of normal haustral folds
(“garden-hose appearance”).
Sometimes inflammation extends into the terminal ileum (back-wash ileitis).
Microscopically, active disease shows crypt abscesses, ulcers, and mucosal regeneration.
Long-standing disease may lead to carcinoma, especially after 10+ years.
Complications include toxic megacolon, perianal fistulas, and colorectal cancer.
9. Classify the tumours of GIT.
Benign:
1. Polyps
2. GIST (Gastrointestinal Stromal Tumors)
Malignant:
1. Adenocarcinoma (most common)
2. Squamous Cell Carcinoma (oral cavity, esophagus, anal canal)
3. Lymphomas
4. Carcinoid tumors (neuroendocrine origin)
5. Malignant GIST
10. List various diagnostic methods for PUD.
1. Endoscopy with biopsy (Gold
standard)
2. Radiological: Barium meal X-ray
3. Lab Investigations:
o
Blood tests (anemia, infection)
o
H. pylori detection:

Urea breath test

Stool antigen test

Serology (antibodies)

PCR
 The most accurate method is
endoscopy with biopsy, which allows
direct visualization and tissue sampling
of the ulcer site.
 Radiological investigations, such as a
barium meal X-ray, can help identify
ulcerations or structural deformities.
 Laboratory tests may include routine
blood work to detect anemia or
infection.
 For identifying H. pylori, several
specific tests are available:
a. The urea breath test, which
detects urease activity from H. pylori
metabolism.
b. The stool antigen test, which
identifies bacterial antigens in feces.
c. Serological tests for antibodies
against H. pylori.
d. PCR tests, which detect
bacterial DNA.
11. Briefly discuss lab diagnosis of H. pylori infection.
histological examination of gastric biopsy, where special stains
such as Giemsa or Silver stain are used to visualize the bacteria.
blood tests can detect antibodies against H. pylori, indicating exposure or infection.
stool antigen test identifies the presence of H. pylori antigens in the patient’s feces.
carbon urea breath test involves ingestion of labeled urea, which is metabolized by the bacteria,
releasing labeled carbon dioxide that is measured in the patient’s breath.
rapid urease test detects bacterial urease activity during endoscopy using a gastric
biopsy sample.