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Peptic Ulcer

The term gastritis should be reserved for histologically documented inflammation of the gastric mucosa.
Table 293-9 Classification of Gastritis (Ref. Hari. 18th ed., Pg-2457, Table-293.9)
  1. Acute gastritis
    1. Acute H. pylori infection
    2. Other acute infectious gastritides
      1. Bacterial (other than H. pylori)
      2. Helicobacter helmanni
      3. Phlegmonous
      4. Mycobacterial
      5. Syphilitic
      6. Viral
      7. Parasitic
      8. Fungal
  2. Chronic atrophic gastritis
    1. Type A: Autoimmune, body- predominant
    2. Type B: H. pylori–related, antral-predominant
    3. Indeterminant
  3. Uncommon forms of gastritis
    1. Lymphocytic
    2. Eosinophilic
    3. Crohn's disease
    4. Sarcoidosis
    5. Isolated granulomatous gastritis
Acute Gastritis
  1. The most common causes of acute gastritis are infectious.
  2. Acute infection with H. pylori induces gastritis.
  3. Hypochlorhydria lasting for up to 1 year may follow acute H. pylori infection.
  4. The highly acidic gastric environment may be one reason why infectious processes of the stomach are rare.
  5. Elderly individuals, alcoholics, and AIDS patients may be affected.
Type A Gastritis
  1. It involves primarily the fundus and body, with antral sparing is seen. 
  2. This form of gastritis pernicious anemia in the presence of circulating antibodies against parietal cells and IF; thus, it is also called autoimmune gastritis.
Type B Gastritis
Type B, or antral-predominant, gastritis is the more common form of chronic gastritis. H. pylori infection is the cause of this entity. 
Diseases caused by H. pylori (It does not cause leiomyoma)
  1. DU
  2. Gastric ulcer
  3. Gastric carcinoma
  4. Atrophic gastritis (Type B)
  5. Mucosa associated lymphoid tissue (MALT) lymphoma.
Peptic Ulcer
  1. Duodenal ulcers (DU) (Most common site = 1st part due) are much commoner than GU.
    Duodenal ulcers are always benign but 1 to 2% of gastric ulcer can being malignant.
    In India ratio of DU to GU is 95% to 5%.
Risk factors:
  1. H. pylori (-90%);
  2. Drugs (aspirin; NSAIDs; steroids).
  3. Blood group OQ 
  4. Smoking.
  5. ZES,
  6. Hyperparathyroid
  7. Cushing disease
  8. Cirrhosis of liver
  9. Polycythemia vera
Epigastric pain typically before meals or at night, (Hunger pain) relieved by eating, or drinking milk. 50% are asymptomatic; others experience recurrent episodes.
Signs: Epigastric tenderness, melena can be there.
  1. Upper GI endoscopy. (Biopsy not needed) most common site is 1st part of duodenum
  2. Test for H. pylori.
    1. Urea breath test
    2. Rapid urease test.
    3. Gastric biopsy to see H. pylori by staining.
  3. Measure gastrin concentrations if Zollinger-Ellison syndrome is suspected.
Extra Edge
  1. H. pylori are gram negative bacteria. Only toxicogenic strain cause peptic ulcer.
  2. Best Epidemiological marker is H. pylori Serology.
  3. The most sensitive and most specific tests for H.pylori is rapid urease test (invasive).PNQ 
  4. In non invasive, urea breath tests is the most sensitive and most specific. Overall rapid urease test is the best. 
  1. Gastric ulcer (Most common site prepyloric area (Ref. Hari. 18th ed., Pg - 2441), Gastric acid output is normal or decreased!!! (Ref. Hari. 18th ed., Pg - 2441)
    1. NSAIDs
    2. Reflux of duodenal contents (Bile acid reflux)
    3. Delayed gastric emptying
    4. Stress, eg neurosurgery (Cushing's ulcers) or burns (Curling's ulcers).
  1. Asymptomatic or epigastric pain (Pain increases on taking meals relieved by antacids) 
  2. Weight loss. 
  3. They are rare in fundus but usually occur in antrum.
  1. Upper GI endoscopy biopsy is mandatory to exclude malignancy because It may be premalignant and repeat endoscopy after treatment is also mandatory. 

Misoprostol is use as a preventive drug for NSIAD induce gastric ulceration. It is not use in acute BD.


Treating peptic ulcers
Table 293-4 Regimens Recommended for Eradication of H. Pylori Infection (Ref. Hari. 18th ed., Pg- 2449)
  1. Triple Therapy
    1. Bismuth subsalicylate plus
      1. Metronidazole plus
      2. Tetracycline
    2. Ranitidine bismuth citrate plus
      1. Tetracycline plus
      2. Clarithromycin or metronidazole
    3. Omeprazole (lansoprazole) plus
      1. Clarithromycin plus
      2. Metronidazole or
      3. Amoxicillin
  2. Quadruple Therapy
    1. Omeprazole (lansoprazole)
    2. Bismuth subsalicylate
    3. Metronidazole
    4. Tetracycline
H. pylori eradication therapy
Triple therapy is 80-85% effective at eradication. 
  1. Drugs to reduce acid:
  2. Antibiotic: Any of the two – Ampicillin or Amoxicillin + Erythromycin or Clarithromycin + Metronidazole or Tinidazole + Ciprofloxacin or Ofloxacin.
  3. Coating agent: Bismuth colloid or Sucralfate
  4. NSAID-associated ulcers: Stop NSAID if possible (if not, use H2RA, PPI, or misoprostol for prevention).
    1. PPls are the most effective, eg lansoprazole.
    2. H2RAs eg ranitidine
S/E of sucralfate - ↓ PO4, constipation gastric Bezoar formation.
Complications of peptic ulcer
  1. Bleeding (M/C is from gastroduodenal artery)
  2. Perforation
  3. Malignancy (in GU)
  4. Gastric outflow obstruction
Extra Edge
  1. In a patient of new onset dyspepsia, anti H .pylori therapy is to be given only if noninvasive H pylori testing is positive.
  2. In patients without cardiovascular risk factors but with a high potential risk (prior GI bleeding or multiple GI risk factors) for NSAID-induced GI toxicity, cautious use of a selective COX-2 inhibitor and co-therapy with misoprostol or high-dose PPI is recommended.
  3. Once an ulcer (GU or DU) is documented, the main issue at stake is whether H. pylori or an NSAID is involved. With H. pylori present, independent of the NSAID status, triple therapy is recommended for 14 days.


Ménétrier's Disease
  1. Ménétrier's disease is characterized by large, tortuous gastric mucosal folds.
  2. The differential diagnosis of large gastric folds includes ZES, malignancy, infectious etiologies (CMV, histoplasmosis, syphilis), and as sarcoidosis.
  3. The mucosal folds in Ménétrier's disease are often most prominent in the body and fundus.
  4. Histologically, massive foveolar hyperplasia (hyperplasia of surface and glandular mucous cells) is noted, which replaces most of the chief and parietal cells.
  5. Patients develop a protein-losing gastropathy accompanied by hypoalbuminemia and edema.
  6. Gastric acid secretion is usually reduced or absent because of the replacement of parietal cells.
  7. Large gastric folds are readily detectable by either radiographic (barium meal) or endoscopic methods.
  8. Endoscopy with deep mucosal biopsy (and cytology) is required to establish the diagnosis and exclude other entities that may present similarly.
  9. Ménétrier’s Disease: Treatment
    1. Anticholinergic agents,
    2. Prostaglandins, PPIs,
    3. Prednisone,

Pernicious anemia causes gastric atrophy.

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