Gastritis is an inflammation of the stomach lining that can be caused by infection, autoimmune disorders, bile reflux, or pernicious anemia. Chronic gastritis refers to a wide range of disorders including those induced by H. pylori infection, NSAIDs, Crohn's disease, and more. H. pylori bacteria are able to attach to and invade the stomach lining, producing toxins that cause cell death and allow the bacteria to access nutrients while evading the immune system. Over time, prolonged H. pylori infection can potentially lead to gastric atrophy, intestinal metaplasia, and intestinal-type gastric cancer due to epigenetic changes. Gastric cancer staging evaluates the primary

1. Stomach and duodenum
Teaching slides
Stefano Fiorucci, MD
University of Perugia
Department of Surgery and Biomedical Sciences

4. Istologia

5. Radiologia

6. Gastric Glandular Morphology

7. Composition of the Gastric Juice
p.282

8. Gastric HCl Secretion
Proton Pump
(H,K-ATPase)
Na+ Pump
(Na,K-ATPase)
ATP

9. p.282A protective role for mucus

10. Gastritis
Gastritis is an inflammation of the stomach
lining.
can be caused by infection, irritation, autoimmune
disorders (where the body' s immune system
mistakenly attacks the stomach), or backflow of bile
into the stomach (bile reflux). Gastritis can also be
caused by a blood disorder called pernicious anemia.

11. Gastritis
Gastritis is an inflammation of the stomach lining.
• Infections can be caused by:
• Bacteria (usually Helicobacter pylori)
• Virus (including herpes simplex virus)
• Parasite
• Fungus
• Long term use of NSAIDs, such as ibuprofen or naproxen
• Alcohol use
• Cigarette smoking
• Chronic vomiting
• Coffee and acidic beverages
• Too much stomach acid (such as from stress)
• Eating or drinking caustic or corrosive substances (such as poisons)

12. Gastritis
Acute
• Erosive gastritis is a gastric mucosal erosion caused by
damage to mucosal defenses.Alcohol erodes the
mucosal lining of the stomach; low doses of alcohol
stimulate hydrochloric acid secretion. High doses of
alcohol do not stimulate secretion of acid.
• NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme
responsible for the biosynthesis of eicosanoids in the
stomach, which increases the possibility of peptic
ulcers forming. Also, NSAIDs, such as aspirin, reduce
prostaglandin.

14. Gastritis
• Chronic
• Chronic gastritis refers to a wide range of
disorders of the stomach including:
- Autoimmune gastritis
- Reflux (bile) induced gastritis
- Helicobacter pylori associated gastritis
- NSAIDs induced gastritis
- Crohn’s gatsritis

15. The Nobel Prize in Physiology or Medicine 2005
Barry J. Marshall, J. Robin Warren

16. Helicobacter pylori
• Attachment:
• The Helicobacter pylori enter the stomach and attach to
the protective mucus lining of the stomach wall. The
bacteria are able to survive in the strongly acid
environment of the stomach because they excrete the
enzyme urease which neutralized the acidic
environment of the stomach by converting urea into the
basic ammonia and buffer bicarbonate. Inside the
mucus lining of the stomach wall, the bacteria cannot be
killed by the bodies immune system.
• Toxin production:
• The Helicobacter pylori produce toxins such as
vaculating cytotoxin A (VAC A) that cause the cells in the
lining of the stomach to die. This allows the bacteria to
better access of nutrients as it decreases the
competition from stomach lining cells.
• Cell Invasion:
• The bacteria invade the protective inner lining of the
stomach so that they can be protected from immune
system. The bacteria then kill the cells that they invade
which creates holes in the mucus lining of the stomach,
causing the formation of ulcers. Additionally, the
substances released by the bacteria during the invasion,
hurt the stomach cells ability to absorb calories from
food in the stomach.

17. Consequences of H. pylori infection

18. Fig. 2 Progression of <ce:italic> H. pylori</ce:italic> -related diseases in stomach and duodenum as related to life stages. Clinical appearance of
diseases occurs in mid-life resulting in severe degenerative conditions only in advanced age in a ...

19. Diagnosi
Biopsia gastrica
Breath test
Ricerca anticorpi (sangue o campioni fecali)

23. Terapia eradicante
• Terapia antibiotica e IPP
Omeprazolo/pantoprazolo/esomeprazolo
Claritromicina
Amoxicillina
Levofloxacina
metronidazolo

24. Progression to intestinal-type gastric cancer. H. pylori infection leads to superficial
gastritis over a period of weeks. The presence of proinflammatory host
polymorphisms and the H. pylori cag pathogenicity island increase the risk of
developing gastric atrophy, intestinal metaplasia, and gastric adenocarcinoma.
Epigenetic inactivation of E-cadherin via promoter hypermethylation may also
contribute to intestinal-type gastric cancer.

26. Gastric cancer staging
• Primary tumor (T):
Tis = carcinoma in situ: intraepithelial tumor without invasion of lamina propria
T1 = tumor invades lamina propria or submucosa
T2 = tumor invades muscularis propria or subserosa
T3* = tumor penetrates serosa (visceral peritoneum) without invasion of adjacent structures
T4**,*** = tumor invades adjacent structures
• *A tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic
ligaments or into the greater or lesser omentum without perforation of the visceral peritoneum.
**Structures adjacent to the stomach include the spleen, transverse colon, liver, diaphragm,
pancreas, abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
***Intramural extension to the duodenum or esophagus is classified by the depth of greatest
invasion in any of these sites, including the stomach).
• Regional lymph nodes (N):
Include the perigastric nodes along the lesser and greater curvatures, and the nodes along the left
gastric, common hepatic, splenic, and celiac arteries.
N0 = no regional lymph node metastasis
N1 = metastasis to 1–6 regional lymph nodes
N2 = metastasis in 7–15 regional lymph nodes
N3 = metastasis in more than 15 regional lymph nodes
• Distant metastasis (M):
M0 = no distant metastasis
M1 = distant metastasis

27. Endoscopic treatment

28. Gastric cancer surgery

30. Chemotherapy
•
ADENOCARCINOMA of the stomach is relatively sensitive to
chemotherapy
• Fluorouracil (5-FU) is the most commonly used drug in the
treatment of gastric cancer, with a response rate around 21%. In an
attempt to improve this rate, drug combinations have been tried;
the most common is 5-FU, doxorubicin, and mitomycin C (FAM)
with a response rate of 33% and an acceptable degree of toxicity
.Other drug combinations have been tried, although the response
duration and overall survival, when compared with 5-FU alone,
were not significantly different. In addition, the combination groups
had a higher toxicity rate. Newer investigational modalities employ
tumor antigen-specific immunochemotherapy. Antibodies to tumor
antigens are conjugated with chemotherapeutic drugs; in this way,
the drugs can be delivered to the tumor directly.

31. Endoscopic palliation