GIT pathology Flashcards
What are the 4 layers within a chronic peptic ulcer
- Exudate of fibrin, neutrophils and necrotic debris
- Narrow zone of fibrinoid necrosis
- Zone of cellular granulation tissue
- Zone of fibrosis
What are complications of chronic peptic ulcers
- Perforation leading to peritonitis
- Haemorrhage
- Aneamia
- Penetration and erosion of adjacent organs
- Stenosis from scarring
- Haemorrhage
What effects do PGE2 have on the gastric system (5)
inhibit acid secretion, stimulate HCO3- and mucus secretions, increase mucosal blood flow and modify local inflammation
What effects occur in response to histamine in acute gastritis
Can promote acute inflammation, oedema, neutrophil recruitment, fluid and blood into lumen, damage of muscosal and epithelial barriers (enterocytes). This can then lead to acid mediated damage, necrosis and superficial erosion (epithelial layer only).
How long do acute ulcers take to heal
Take around 3-4 days to heal after insult as the cells are able to be turned over very quickly. If not healed then can lead to superficial chronic gasrtitis
What can induce acute gastrritis
Alcohol, NSAIDs, bile, H.pylori and Aspirin. However can be caused by reduced bloodd flow that can be seen after shock, sepsis and trauma
How do acute peptic ulcers form
extension of erosions
What are the three types of chronic gastritis
Autoimmune, Bacterial and Chemicals
What are the targets in Autoimmune gastritis
parietal cells, H+/K+ pumps in the antrum and can lead to ECL hypertrophy and carcinodosis
Consequences of Autoimmune gastritis
Total atrophy of acid secreting cells, replaced by intestinal metaplasia accompanied by chronic inflammation. May cause development of cancer
Common chemicals that induce chroni gastritis
Aspirin, NSAIDs, refluxed bile and alkaline juice
What is the consequence of chemicals
Cause desruption of the mucousal layers of the stomach and gastric barriers causing direct damage to the enterocytes leading to epithelial desquamination. Leads to mucus cell hyperplasia with elongation and tortuosity of gastric pits, vasodilation, oedema and fibromuscular hyperplasia of LP and mild imflammatory infiltrate
Intestinal metaplasia and erosions can occur.
What are the bacterial causes of Chronic gastritis
H. pylori
How does H. pylori cause disease
invades into the mucosa layer and adheres to the enterocytes at their junctions leading to their breakdown. Muscus layer not as efective and breaksdown, leading to acid mediated damge of the enterocytes and below. This leads to a neutrophil response, and an acute inflammation
Histological changes seen in H/ Pylori infections
- Foveolar hyperplasia
- Intestinal metaplasia
- Neutrophil infiltrate
- Erosions and acute peptic ulcers
- Parietal cell hyperplasia
What is the Human gastric cancer sequence
Chronic gastritis atrophic gastritis Intestinal metaplasia dysplasia Adenocarcinoma
Long term complocations of H. Pylori infections
- Gastric mucosal atrophy and intestinal metaplasia leading to gastric adenocarcinoma
- Gastric Ulcer
- B-cell lymphoma of MALT
Why can the duodenum be invaded by H.pylori
HCl damage induces gastric foveolar cell metaplasia leading to colonisation as the D1 region now looks like body of stomach
What are the ratios of D1:Stomach body h pylori infections
4:1
What are the different classifications of peptic ulcers
erosion - superficual only
Acute ulcer - through the muscularis mucosae
Chronic ulcer - through the muscularis propria with associated fibrosis
What is the response of the omentum to perforation
Will aim to cover and prevent bleed
What gene is mutated in Signet ring cell carcinoma and who is predisposed
Adhesion proteins are mutated and most commonly seen in women under 45
What is the definition of acute gastritis
Acute gastritis is a transient mucosal inflammatory process that is caused by a deficiency in the mucosal protection of enterocytes
What is the definition of chronic gastritis
Is a less severe yet more persistent form of acute gastritis, most common cause if H.pylori
What is Peptic ulcer disease
Is a consequence of acute or chronic gastritis in which the integrity of enterocytes is compromised to acidic nature of the lumen and can result in intestinal metaplasia and adenocarcinoma formation
