WK10L4 - Stomach Pathology Flashcards
Pathology of the Stomach - Congenital Anomalies
Pancreatic heterotopic nodules where pancreatic tissue may be present in the gastric submucosa, muscle wall or at a subserosal location
Gastric heterotopia - where small patches of ectopic gastric mucosa occurs in the duodenum or in distal sites as a result of peptic ulceration
Diaphragmatic hernia - defective closure of the diaphragm leads to weakness, partial or total absence of a region of the diaphragm, usually the left side (resulting in diaphragmatic herniation)
Pyloric stenosis - encountered in infants as a disorder that affects males 3 to 4 times more than females
Acute Gastritis
Acute inflammatory process usually of a transient nature
- may be accompanied by haemorrhage into the mucosa
Pathogenesis unclear but associated with:
- heavy use of NSAIDS (esp. aspirin)
- excessive alcohol consumption
- heavy smoking
- tx with cancer therapeutic drugs
- uraemia
- bacterial infections
- ischaemia and shock
- gastric irradiation
Symptoms of Acute Gastritis
May be entirely asymptomatic May cause variable epigastric pain Nausea Vomiting Haematemesis (vomiting blood) - a major cause in alcoholics Melena (black tarry stools) Potentially fatal blood loss 25% of individuals who consume daily aspirin for RA develop acute gastritis
Morphology of Acute Gastritis
The surface epithelium is intact and scattered neutrophils are present within the surface epithelial cells
- presence of neutrophils above the basement membrane within the epithelial space is abnormal and signifies active inflammation
More severe mucosal damage, erosion and haemorrhage leads to loss of the superficial epithelium
This damage is accompanied by acute inflammation and extrusion of a fibrin containing purulent exudate into lumen
Haemorrhage generates punctate dark spots in hyperaemic mucosa assoc with erosion
Concurrent erosion and haemorrhage is referred to as erosive haemorrhagic gastritis
Chemical Gastritis
Commonly seen with bile reflux (toxic to cells)
Prominent hyperplastic response (inflammatory cells scanty)
With time => intestinal metaplasia
Chronic Gastritis
Defined as the presence of chronic mucosal inflammatory changes that lead eventually to mucosal atrophy and intestinal metaplasia, usually in the absence of erosions
Pathogenesis:
- H.pylori
- autoimmune association with pernicious anaemia
- alcohol and smoking
- radiation
- chemical damage (i.e. bile reflux, drugs)
- granulomatous conditions i.e. Crohn’s disease
Association Between Chronic Gastritis and H.pylori
H.pylori plays a critical role in both gastric and duodenal diseases
Peptic ulcers are a disease process caused by H.pylori in 90% of patients with chronic gastritis that affects the antrum
Following initial exposure to H.pylori, gastritis occurs in two patterns:
1. Predominantly antral gastritis with high acid production and increased risk for duodenal ulcers
2. Pan gastritis that follows multifocal atrophy with lower gastric acid secretion and higher risk for adenocarcinoma
Dx tests for H.pylori include:
- serologic test for Ab
- faecal bacterial detection
- urea breath test (gold standard)
Helicobacter Pylori
A non-sporing, gram-negative rod
Part of a genus that have adapted to gastric mucus, which is otherwise lethal to most bacteria
The traits that have enabled this association are:
- motility: flagella allows it to swim through viscous mucus
- elaboration of a urease, which produces ammonia and carbon dioxide from endogenous urea, which buffers gastric acid
- expression of bacterial adhesins, which bind to fucosylated Lewis B blood group Ag
- expression of bacterial toxins such as cytotoxin associated gene A and vacuolating cytotoxin gene A
Autoimmune Gastritis
Results from the presence of autoantibodies to gastric gland parietal cells including:
- acid producing enzymes H+, K+ATPase, gastrin receptor & intrinsic factor
- gland destruction and mucosal atrophy lead to loss of acid production
- severe cases, production of intrinsic factor is lost - leads to pernicious anaemia
- this form of AI gastritis is uncommon and seen in assoc with Hashimoto’s thyroiditis, Addison disease and type I diabetes
Patients with AI gastritis have an increased risk for developing gastric carcinoma and endocrine tumours
Morphology of Gastritis
Mucosa is reddened and has a coarser texture than normal
Inflammatory infiltrate may create a mucosa with thickened rugal folds, mimicking early infiltrative lesions
With long standing atrophic disease the mucosa may become thinned and flattened
See inflammatory infiltrate of lymphocytes and plasma cells within the LP
Peptic Ulcer Disease
Peptic ulcers are chronic, often solitary lesions that occur at sites exposed to the aggressive action of acid/peptic juices
Histologically these are defined as a breach in the mucosa of the alimentary tract that extends through the MM into the submucosa or deeper
- may occur anywhere along the GIT
- peptic ulcers occur in the duodenum and stomach
Acute gastric ulcers may appear under conditions of severe stress or ingestion of NSAIDS
- ulcers need to be differentiated from erosions where there is epithelial disruption within the mucosa but no breach of the MM
Symptoms of Peptic Ulcer Disease
Burning stomach pain
Vomiting or vomiting blood (Haematemesis)
Dark blood in stool or black tarry stools (Melena)
Feeling of fullness, bloating or belching
Fatty food intolerance
Heartburn
Nausea
Trouble breathing
Feeling faint
Pathogenesis of Peptic Ulcers
Peptic ulcers are the result of an imbalance between gastroduodenal mucosal defence mechanisms and the damaging forces (i.e. gastrin and pepsin)
H.pylori is a major contributor
- virtually seen in all patients with duodenal ulcers and in 70% of those patients with gastric ulcers
Mechanisms of action:
1. H.pylori - does not invade tissue, it induces an inflammatory and immune response
2. Increase in production of pro-inflammatory cytokines (IL1, IL-6, TNF and IL-8) produced by mucosal epithelial cells and activates neutrophils
3. Bacterial gene products are involved in cell injury and inflammation
4. H.pylori secrete urase that breaks down urea to form toxic ammonium chloride
Complications of Peptic Ulcers
Bleeding - occurs in 15-20% of patients - most frequent complication - may be life threatening - may be first indication of an ulcer Perforation (hole in stomach, intestines etc.) - occurs in ~5% of patients - accounts for 2/3 of ulcer deaths - rarely, is the first indication of an ulcer Obstruction from oedema or scarring - occurs in ~2% of patients - often due to pyloric channel ulcers - may occur with duodenal ulcers - causes incapacitating crampy abdominal pain
Gastric Tumours - Polyps
Uncommon Hyperplastic - response to damage Fundic gland - small hamartoma - hyperplastic and fundic gland polyps are not believed to have malignant potential Adenomatous - malignant potential
