Pathology of GIT

Question 1

What are the protective factors in the stomach?

Answer 1

1. Surface mucous production (bicarbonate rich)
2. Mucosal blood flow
3. Epithelial barrier function
4. Epithelial regeneration
5. Elaboration of prostaglandins

Question 2

What are the features of acute erosive gastritis?

Answer 2

• Neutrophils present (acute inflammation) with fibrin exudate
• Loss of epithelium resulting in a mucosal defect
• Can be due to direct irritant, NSAIDs and alcohol

Question 3

What are the features of stress induced ulcers?

Answer 3

• Related to local ischemia (patients that have been through shock, sepsis or trauma)
• Cushings ulcers: gastric, duodenum, oesophagus (due to intracranial disease and high acid)
• Curling ulcers: proximal duodenum (associated with burns and trauma)
• Borders are clearly demarcated
• Surrounded by oedema and erythma

Question 4

What are the features of chronic H. pylori gastritis?

Answer 4

• Caused by spiral, flagellated GN rods
• Leads to antral gastritis -> can progress to body or fundus
• Leads to mucosal erythema and erosions, granularity and nodularity
• Lamina propria heavily infiltrated with lymphocytes, plasma cells and (occasional neutrophils) - acute + chronic infiltrate
• Formation of lymphoid follicles in superficial lamina propria
• Acute inflammation more prominent in gastric pits

Question 5

What are the features of autoimmune gastritis?

Answer 5

• Antibodies are produced against parietal cells (secrete acid and intrinsic factor)
• Absence leads to hypergastremia
• G cells over secrete gastrin and proliferate
• Leads to chronic inflammatory cells in the lamina propria
• Intestinal metaplasia: globlet cells within the stomach epithelium

Question 6

What are the complications of gastritis?

Answer 6

1. Peptic ulcer disease
   - Well markated borders
   - Can lead to bleeding (submucosa has large vessels) or perforation
2. Increased risk of gastric cancer
   - MALToma in H. pylori
   - Adenocarcinoma in autoimmune

Question 7

What zone in the liver is most vulnerable to damage?

Answer 7

• Zone 3 (next to central vein)
• Lowest oxygen (damaged by hypoxia)
• Highest toxins (area where detoxificaiton occurs)
• Zonal necrosis can occur (necrosis + inflammatory infiltrate)

Question 8

What is zonal, bridging and lobular necrosis

Answer 8

1. Zonal:
   - Perferential death of one zone e.g. zone 3 in paracetemol toxicity
2. Bridging:
   - Necrosis extends across from hepatic vein to portal triad
   - Extensive damage (zone 1, 2 and 3)
3. Lobular:
   - Almost no surviving hepatocytes in an entire area of liver
   - Parenchyma collapses and is replaced by chronic inflammatory cells

Question 9

What changes occur in injured hepatocytes?

Answer 9

• Ballooning
• Steatosis
• Mallory hyaline bodies
• Impaired bile excretion (cholestasis)

Question 10

Describe the pattern of damage seen in paracetemol induced liver necrosis:

Answer 10

• Preferential death of zone 3 hepatocytes (CYP2E1 present there)
• Causes coagulati ve necrosis
• Minimal inflammation