Acute Gastritis Flashcards
What is gastritis?
More generalised inflammation of the stomach tissue
*it may occur as short episode or long duration
NB: clinically it is very difficult to differentiate from PUD (both have epigastric pain, and worsened and caused by overlap of things)
Aetiological causes of gastritis
a. Helicobacter pylori infection*
b. NSAIDs* or alcohol
c. Chemical induced
d. Bile reflux
e. Autoimmune gastritis or Crohn’s
f. Stress induced (Cushings - raised ICP with stim vagal nuclei inc gastric acid secretion, Curling - burns leads to hypovol -> isch -> necrosis of gastric mucosa)
g. Phlegmonous gastritis: suppurative gastritis
h. B12 deficiency
What is erosive gastritis?
Discrete foci of surface necrosis due to damage to mucosal defenses
Acute gastritis can be broken down into 2 categories: erosive and non-erosive. What are the causes of each?
Non erosive refers to:
- H pylori infection
NB: chronic H pylori infection predisposes to atrophic gastritis and autoimmune gastritis
Erosive (superficial, deep, haemorrhagic) “reactive gastritis”:
- NSAIDs chronic use
- Alcohol use
- Cocaine
- Stress ulcers from severe physiology stress (Cushing’s, Curling’s)
- Reflux of bile salts into the stomach due to pyloric dysfunction (e.g. after gastric surgery)
- Radiation
Pathophysiology of H pylori causing gastritis
- Starts as an acute gastritis in the antrum, and over time it may extend to involve the entire gastric mucosa resulting in chronic gastritis
- intense inflammation can result in loss of gastric gland leading to atrophic gastritis (acid prod’n drops)
a. Imbeds itself into mucous layer
b. Protected from acidity through urease prod’n to b’down urea into alkaline ammonia to neutralise HCl
c. Flagella to move and penetrate mucous layer to gastric epithelial cell, its toxins and enzymes stimulate inflammation
H pylori infection is usually symptomatic or asymptomatic?
Asymptomatic
Pathophysiology of NSAIDs and alcohol causing gastritis
NSAIDs and alcohol decrease gastric mucosal blood flow with loss of the mucosal protective barrier.
NSAIDs inhibit prostaglandin production, whereas alcohol promotes depletion of sulfhydryl compounds in gastric mucosa
Pathophysiology of autoimmune gastritis
anti-parietal cell antibodies stimulate a chronic inflammatory, lymphocytic infiltrate involving the oxyntic mucosa, leading to loss of parietal and chief cells
Pathophysiology of phlegmonous gastritis
Low pH of the gastric fluid normally does not allow bacterial growth, but when the gastric mucosa is damaged (e.g., gastric ulcer or carcinoma, ingestion of caustic materials, ingestion of foreign bodies), ingested bacteria may become invasive resulting in phlegmonous gastritis.
The suppurative process involves primarily the submucosa and muscularis.
Hx of acute gastritis
- Gnawing or burning epigastric distress
- N/V
- Pain may worsen or improve with eating
- Previous mucosal injury (PUD, gasritis, endoscopic injury)
- Noxious drugs including coritcosteroids
- Routine use of aspirin, NSAIDs
DDx of acute gastritis
Cholecystitis Cholelithiasis Crohn Disease Gastric Cancer Gastroenteritis, Viral Lymphoma, B-Cell Peptic Ulcer Disease Sarcoidosis
Ix lab studies of acute gastritis
- FBC count to assess for anemia, as acute gastritis can cause gastrointestinal bleeding
- Liver and kidney function tests
- Gallbladder and pancreatic function tests
- Pregnancy test
- Stool for blood
Ix imaging studies for acute gastritis
AXR: 4 radiological signs (regardless of aetiology):
- thick folds (>5mm), inflam nodules (bumpy), coarse area gastrica, erosions
CT: thickening of gastric wall
What are the three non-endoscopy based H pylori tests?
- HpSA: H pylori stool antigen test
- Urea breath test
- Serum Ab H pylori
What are the three endoscopy based H pylori tests?
- Rapid urease test: test biopsy specimen immediately
- Bacterial culture H pylori (rarely used)
- Histological detection in biopsy
