Stomach

Question 1

Erosion

Answer 1

It’s the loss of superficial epithelium which produces a small defect in the mucosae that is limited to the lamina propria (do not penetrate the muscularis mucosae).

Question 2

Ulcer

Answer 2

Break in mucosal surface more than 5mm in size with depth to the submucosa i.e. they penetrate the muscularis mucosae.
Leads to a local defect or excavation due to active inflammation.
-GUs and DUs may be acute or chronic.

Question 3

Acute gastritis.

Answer 3

Transient inflammation of gastric mucosa.

Question 4

Etiopathogenesis of Acute Gastritis.

Answer 4

1. Drugs: Non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, cortisone, phenylbutazone, indomethacin, preparations of iron, chemotherapeutic agents.
2. Infections: -Bacterial e.g. Helicobacter pylori, diphtheria, salmonellosis, pneumonia, staphylococcal food poisoning. Viral e.g. viral hepatitis, influenzae infectious mononucleosis.
3. Diet and personal habits.
4. Reduced synthesis of mucin and bicarbonate secretion during old age.
5. Decreased oxygen supply at high altitudes.

Question 5

Gastric injury.

Answer 5

e.g. in uremia and with urease secreting H. pylori may be due to inhibition of gastric bicarbonate transporters.

Question 6

Gross morphology of acute gastritis.

Answer 6

The gastric mucosa is edematous with abundant mucus and hemorrhagic spots.

Question 7

Microscopic morphology of acute gastritis.

Answer 7

1. Depending upon the stage, there is a variable amount of edema (purulent exudate in lumen)
2. Infiltration by neutrophils in the lamina propria.

Question 8

Types of mucosal disease related to stress.

Answer 8

1. Stress ulcers.
2. Curling ulcers.
3. Cushing ulcers.

Question 9

Stress ulcers.

Answer 9

They occur with shock, sepsis or severe trauma.

Question 10

Curling ulcers.

Answer 10

They develop in the proximal duodenum with severe burns or trauma.

Question 11

Cushing ulcers.

Answer 11

They develop in stomach, duodenum and esophagus in patients with intracranial disease.
Highly prone for perforation.
They are probably due to the direct stimulation of vagal nuclei > causes increased secretion of gastric acid.

Question 12

Mucosal disease from Local Ischemia

Answer 12

1. Stress induced splanchnic vasoconstriction > Hypoxia and reduced blood flow.
2. Upregulation of inducible NO synthase and increased vasoconstrictor endothelin-1.

Question 13

Characteristic of ulcer due to mucosal disease related to stress.

Answer 13

• Margins are not indurated.
• Floors appears brown to black due to acid digestion of extravasated blood.

Question 14

Chronic gastritis, Type A

(Autoimmune gastritis)

Answer 14

• Involves mainly the body -fundic mucosa.
• Called the autoimmune gastritis because of the presence of circulating antibodies and is also associated with autoimmune diseases such as Hashimoto’s thyroiditis and Addison’s disease.

Question 15

Chronic gastritis, Type B

(H. pylori related)

Answer 15

• Involves the region of antral mucosa and is more common.
• Also called hypersecretory gastritis due to excessive secretion of acid.

Question 16

Chronic gastritis, Type AB

(Mixed, environmental, chronic atrophic gastritis)

Answer 16

• Affects the mucosal region of A as well as B types.
• Most common in all age groups.

Question 17

Host factors that play a role in the outcome of H. pylori infection.

Answer 17

1. Increased expression of pro-inflammatory cytokines: normally, H. pylori do not invade the cells/tissues. It causes increased production of pro-inflammatory cytokines [e.g. IL-1B, TNF] by mucosal epithelial cells.

Question 18

Decreased expression of anti-inflammatory cytokines.

Answer 18

IL-10

Question 19

H. pylori mechanism of action.

Answer 19

1. Produces urease, releases ammonia (strong alkali) from endogenous urea, raises the local gastric pH and enhances bacterial survival. Raised local gastric pH acts on the antral G cells and releases gastrin > hypergastrinemia result in hypersecretion of gastric acid.
2. Noninvasive.
3. Colonizes in the mucosal layer.
4. Cytotoxins: Products of two genes, namely cytotoxin-associated gene A (cag A) and vacuolating agent (vac A)
   gene involved in the progression of the disease and cause gastritis, peptic ulceration and cancer.
5. Flagella.

Question 20

H. pylori cause increased risk of?

Answer 20

• Gastric adenocarcinoma.
• Gastric MALT lymphoma.

Question 21

Demonstration of H. pylori.

Answer 21

• Giemsa stain and Diff-Quik.
• Warthin-starry stain (silver stain).

Question 22

Diagnostic tests for H. pylori.

Answer 22

• Catalase +
• Oxidase +
• Urease +
• Rapid urease test on gastric mucosal biopsy is 100% specific test.

Question 23

Morphologic features of various types of gastritis are:

Answer 23

1. Chronic superficial gastritis.
2. Chronic atrophic gastritis.
3. Gastric atrophy.
4. Chronic hypertrophic gastritis (Menetrier’s disease) (rare)

Question 24

Peptic Ulcer

Answer 24

Mucosal defect that is at least 0.5cm in diameter penetrates the muscularis mucosae.

Question 25

Prostaglandins protect gastric mucosa by:

Answer 25

1. Increasing secretion of bicarbonate.
2. Increasing vascular perfusion.
3. Inhibition of acid secretion.
4. Promoting synthesis of mucin.

Question 27

Peptic Ulcer Disease (PUD)

Answer 27

H. pylori infection and use of Anna seeds are the main cause of PUD.

Question 28

What infection is detected from the gastric antrum minimalist all patients with Duodenal ulcers?

Answer 28

Helicobacter pylori infection. 90% of duodenal ulcers and 65% of gastric ulcers are associated with H. pylori infection.

Question 29

In relation to peptic ulcer disease and acids and aspirin cause?

Answer 29

Direct chemical irritation of mucosa. Suppresses prostaglandin synthesis by mucosa. Reduces the HCO3 secretion.

Question 30

Chronic disorders Associated with peptic also disease?

Answer 30

Cirrhosis Alpha one antitrypsin deficiency Systemic mastocytosis Nephrolithiasis Chronic renal failure Chronic pulmonary disease

Question 31

Impaired defenses in peptic ulcer disease.

Answer 31

Ischemia: decreased oxygen delivery. Shock. Delayed gastric emptying. Host factors: reduced mucin synthesis in the elderly will increase susceptibility to gastritis.

Question 32

Most common sites of peptic ulcers:

Answer 32

Duodenal ulcer: first part of duodenum. Gastric ulcer: Lesser curvature along the incisura angularis. 

Question 33

In gastric ulcers,

Answer 33

And gastric ulcers size and location cannot differentiate between benign and malignant ulcers.

Question 34

Kissing ulcers

Answer 34

Kissing ulcers occur when peptic ulcers are on both posterior and anterior wall of the duodenum.

Question 35

Heaped up margins are more characteristic of which kind of cancer?

Answer 35

Gastric cancers.

Question 36

Gastric indoor general answers are microscopically similar. From the human outward followers gonna be identified and don’t known as Askenazi zones. What are the zones?

Answer 36

The most superficial zone is the necrotic soon. Superficial exudative zone: on it consists of fibrin no purulent exudate with predominantly neutrophilic inflammatory infiltrate. Granulation tissue zone: consist of granulation tissue infiltrated with mono nuclear leukocytes. Zone of cicatrization: it consists of fibrous tissue or collagen a scar which forms the base of the ulcer and may show chronic inflammatory cells.

Question 37

Complications of gastric ulcers.

Answer 37

1. Bleeding is the most most common complication of peptic also ulcer. Chronic get loss may lead to to iron deficiency anemia. Severe bleeding McLucas coffee ground vomitus or melena and may be life-threatening. 2. Perforation; develops in 5% of patients and is the most common complication of gastric ulcer. 3. Pyloric obstruction or gastric outlet instruction: is associated with ulcers in the pyloric region occurs in 10% of also patients. It is secondary to edema or scarring. 4. Rarely malignant transformation.

Question 38

Which is the most common type of tumor like lesion?

Answer 38

Hypo plastic or inflammatory polyps. The regenerative non-near plastic lesions. And they may be single or multiple other more often located in the pyloric antrum.

Question 39

Gross and microscopic anatomy of hyperplastic polyps?

Answer 39

Gross Anatomy: deletions BBC cellular pedunculated, 1 cm large in size, and smooth and soft. The surface may be ulcerated or hemorrhagic. Microscopy: composed of irregular hyperplastic glands, which may show cystic change. The lining epithelium is mostly superficial gastric type what antral glands, chief cells and parietal cells may be present.

Question 40

Hamartamatous Polyps.

Answer 40

Not true neoplasms but are malformations. There are various types for example gastric polyps of the Puetz-Jeghers syndrome, juvenile polyp, pancreatic heterotopia, heterotopia Bruners glands and inflammatory fibroid polyps.

Question 41

Gastrointestinal stromal tumors [GISTs]

Answer 41

Currently, the term gastrointestinal stromal tumours (GISTs) is used for a group of uncommon benign tumours composed of spindle cells or stromal cells but lacking the true phenotypic features of smooth muscle cells, neural cells or Schwann cells. They are uncommon but as compared to other sites in the GIT, are most common in the stomach.

Question 42

Tumor like lesions; give their types.

Answer 42

Hyperplastic polyps Hamartomatous polyps

Question 43

Gastric carcinoma incidence.

Answer 43

Carcinoma of the stomach comprises 90% of all gastric malignancies and is the leading cause of cancer related deaths in countries where is incidence is high. The highest incidence is between 4th to 6th decades of life and is twice as more common in men than women.

Question 44

Etiology of gastric carcinoma.

Answer 44

1. Studies have shown that a pseudo positivity with H. pylori is associated with 3 to 6 times higher risk of development of gastric cancer. 2. Dietary factors- occurrence of gastric cancer in the region of gastric canal where irritating foods exert their maximum affect -populations consuming certain food stuffs have a high risk of developing gastric cancer example ingestion of smoked foods, high and take of salt, pickles raw vegetables, high intake of carcinogens as nitrates in food and drinking water, nitrate in preservatives for certain meats etc. Tobacco smoke tobacco juice and consumption of alcohol have all been shown to have carcinogenic effects on gastric mucosa. 3. Incidence is higher in blacks, American Indians, Chinese in Indonesia, North Wales and other parts of Wales. 4. Not more than 4% of patients with gastric cancer have a family history of this disease. 5. Individuals with blood group A may have higher tendency to develop gastric cancer.

Question 45

How does gastric carcinoma appear on gross examination?

Answer 45

• Flat mucosal lesions: Early intramucosal carcinoma may present in the form of mucosal patches or a loss of rugae. Such early cancers are often not visible on macroscopic examination or endoscopy. Japanese physicians have pioneered early diagnosis of such tumors, which are discovered by screening high-risk people yearly with endoscopy and with cytologic examination of gastric brushings. Early intramucosal carcinoma has good prognosis.
• Exophytic tumors: These tumors protruding into the lumen of the stomach are usually described as polypoid or fungating (cauliflower-like).
• Ulcerating tumors: These tumors must be distinguished from benign peptic ulcers. Benign peptic ulcers have sharp regular margins, whereas ulcerated cancer has irregular margins and is not clearly demarcated from the normal mucosa. Ulcerated gastric carcinomas often have raised borders and are described as craterlike.
• Diffusely infiltrating tumors: Tumors that invade all layers of the gastric wall give the stomach a ‘‘leather-bottle’’ appearance and are called linitis plastica. Histologically, these infiltrating tumors often contain signet ring tumor cells filled with mucus.

Question 46

What is GIST?

Answer 46

GIST is an acronym for gastrointestinal stromal tumor. These tumors originate from stromal stem cells that are precursors of smooth muscle cells or GI fibroblasts. If a stromal tumor shows histologic signs of smooth muscle differentiation, it is called leiomyoma or leiomyosarcoma. If the cells retain the phenotype of undifferentiated stromal cells, the tumor is called GIST. It may be benign or malignant. Benign GISTs are small (2–5 cm) and have few dividing cells. Malignant GISTs are spindle cell sarcomas measuring more than 6 cm and showing the usual signs of malignancy (necrosis, hemorrhage, high mitotic activity, and anaplasia).

Question 47

Describe the histologic layers found in a typical chronic peptic ulcer.

Answer 47

Histologically, there are four layers, from top to bottom;

1. Superficial zone of necrosis composed of amorphous debris.
2. Acute inflammatory exudate full of neutrophils.
3. Granulation tissue rich in blood vessels and macrophages.
4. Scarring at the bottom (If the ulcer extends into the muscle layer, it may erode blood vessels and cause bleeding.)

Question 49

What is the most important developmental disorder of the stomach?

Answer 49

Congenital hypertrophic pyloric stenosis affects 1 in 400 to 600 infants. The disease shows a multifactorial pattern of inheritance, but it may also be associated with chromosomal developmental disorders (e.g., Turner syndrome). Typically, it presents with projectile vomiting. It is caused by hypertrophy of the smooth muscle in the pyloric portion of the stomach, which may be palpated through the abdominal wall. Surgical incision provides relief and is routinely performed with excellent results.