Info
🌱 來自: Huppert’s Notes
Stomach🚧 施工中
Stomach
Peptic ulcer disease (PUD)
• Pathophysiology: Ulcers that develop in the stomach or duodenum. Common risk factors include H. pylori infection, NSAID use
• Clinical features: Asymptomatic (70%), abdominal pain, bleeding. Features differ based on the ulcer location:
- Gastric ulcer: NSAIDs, H. pylori, high malignant potential (always biopsy!), eating does NOT help
- Duodenal ulcer: H. pylori 90%, low malignant potential (don’t need biopsy), eating relieves pain
• Diagnosis:
- Endoscopy: Low-risk gastric ulcers (e.g., young person on NSAIDs) and duodenal ulcers do not typically require follow-up; high-risk patients (including gastric ulcers with inadequate-quality biopsy) require repeat endoscopy in 8–12 weeks
- H. pylori testing:
• H. pylori IgG antibody test: Positive if any prior exposure (i.e., cannot differentiate active vs. prior infection); however, a negative result is very helpful. Highest-yield clinical use is if never tested or treated before and high pre-test probability for infection; no role if known prior H. pylori infection.
• Urea breath test: Identifies active infection. Costly. Used to confirm infection if pre-test probability low, to confirm eradication (eradication should be confirmed for all patients, approximately 4 weeks after treatment), or to assess for reinfection. Less accurate in patients taking a PPI, bismuth, or antibiotics, or during active PUD bleeding.
• Fecal antigen test: Identifies active infection. Less expensive. Used to confirm infection if pre-test probability low, to confirm eradication (eradication should be confirmed for all patients, approximately 4 weeks after treatment), or to assess for reinfection. Less accurate in patients taking a PPI, bismuth, or antibiotics; the impact on accuracy of active bleeding may depend on the assay used.
• EGD with biopsy: Gold standard, identifies active infection. Less accurate in patients taking a PPI, bismuth, or antibiotics, or during active UGIB.
• Treatment:
- Supportive care: Stop ASA, NSAIDs, restrict alcohol use, smoking cessation
- Acid suppression: PPIs (first line; more rapid at promoting ulcer healing); H2 blockers, antacids
- Eradicate H. pylori, if present. Guidelines now recommend triple therapy only in regions where H. pylori clarithromycin resistance is known to be <15% and in patients with no previous history of macrolide exposure. Quadruple therapy is an appropriate first-line treatment, and the paradigm is shifting toward quadruple therapy as first line for most patients due to resistance.
• Triple therapy: PPI BID + clarithromycin 500 mg BID + amoxicillin 1000 mg BID or metronidazole 500 mg BID for 14 days
• Quadruple therapy: PPI BID + bismuth 420 mg QID + metronidazole 500 mg QID + tetracycline 500 mg QID for 10–14 days
• Key association: H. pylori infection is also associated with gastric MALT lymphoma. First-line treatment is H. pylori treatment, followed by serial endoscopies.
Gastritis
• Atrophic gastritis: Two forms 1) H. pylori associated (treat H. pylori); 2) Autoimmune (not curable; can lead to pernicious anemia requiring lifelong vitamin B12 replacement).
• Metaplasia (chronic) atrophic gastritis: Precancerous lesion of the gastric mucosa associated with H. pylori. Treat H. pylori. Risk factor for adenocarcinoma; unclear if H. pylori eradication can affect the natural history of gastric intestinal metaplasia/progression to gastric cancer.
• Eosinophilic gastritis/gastroenteritis: Rare inflammatory disorder characterized by eosinophilic infiltration of the stomach and/or duodenum (most commonly). Treatment: Elimination diet, steroids.
• Lymphocytic gastritis: Rare, benign, chronic inflammatory condition, associated with H. pylori and Celiac disease. Treat H. pylori.
Gastroparesis
• Clinical features: Delayed stomach emptying; early satiety, postprandial fullness, nausea/vomiting, pain, bloating, weight loss
• Diagnosis: Perform EGD and upper GI barium radiography first to rule out an obstruction. Then perform a gastric emptying study while off all medications that can affect motility (e.g., opiates). Evaluate for the cause of gastroparesis with work-up such as: HgA1c, TSH, +/− ANA or additional testing for neuroautonomic etiologies based on the clinical context.
• Treatment: Dietary changes, diabetes control, metoclopramide (side effects: parkinsonism, tardive dyskinesia), erythromycin, prucalopride (off-label). For refractory symptoms, consider PEG placement for decompression and feeding or gastric pacemaker for diabetic gastroparesis.
Gastric outlet obstruction
• Pathophysiology: Obstruction of the gastric outlet by malignancy, PUD, strictures, caustic injury
• Clinical features: Nausea/vomiting, epigastric pain, early satiety; “succussion splash” on physical exam
• Diagnosis: EGD to diagnose and identify cause
• Treatment: Depends on the cause of obstruction; sometimes need nasogastric tube placement, PPI, endoscopic dilation, stenting or surgery
Bariatric surgery
• Indication: Can be offered to patients with an elevated BMI (typically >35) despite diet/exercise and lifestyle interventions
• Procedure: Surgical procedure. There are several different types/approaches.
• Potential complications:
- Restrictive complications: Band slippage, staple-line leakage
- Malabsorptive complications: Cholelithiasis, nephrolithiasis (due to increased urine oxalate excretion), dumping syndrome, short bowel syndrome, SBO, fistulas, stricture
- Nutritional complications: Micronutrient deficiencies
- Bleeding-related complications: Marginal ulcers