Week 3: Peptic ulcer disease Flashcards
1
Q
peptic ulcer disease definition
A
- gastric and duodenal ulcers
- break in lining due to loss of cells from mucosa extending through lamina propria to at least the depth of muscular mucosa
- gastric ulcers have malignant potential
2
Q
Clinical presentation of PUD
A
-abdominal pain: classically intermittent epigastric pain 2-3 hours after meals, relieved with food or antacids
COMPLICATIONS
-bleeding ulcer: hematemesis, melena, hematochezia. Rx with endoscopic therapy, IV PPI for high risk and oral PPI for low risks (clean base of ulcer)
-gastric outlet obstruction: postprandial nausea, vomiting. Succussion splash, large gastric volume. Rx: NPO, hydration, IV PPI or H2 blocker. dilation/surgery.
-penetration (pancreatitis)
3
Q
Pathogenesis of PUD
A
- imbalance of aggressive and defensive factors
- defensive factors: unstirred layer of mucus and bicarb, surface epithelial cells, cell renewal, alkaline “tide”, microcirculation-PGs, NO, protect cells from injury, sensory nerves, Prostaglandins working synergistically with NO
4
Q
Causes of ulcers
A
- H pylori: gram neg bacteria.
- contracted early on.
- produces locally toxic substances (urease -forming ammonia)
- induction of mucosal immune response: IL8, inflammatory cells
- increased gastrin, HCl secretion by decreasing astral somatostatin - NSAIDs
- acid hypersecretory state (zollinger-ellison syndrome)
5
Q
Diagnostic testing for H. pylori
A
- Invasive: endoscopy with biopsy
- rapid urease assay test: breakdown of urea into ammonia and bicarb results in pH increase
- histology
- culture: usually not done - Non invasive
- serology testing: IgG antibodies to HP. Less accurate than other tests.
- urea breath test: patients ingest urea, breath tested for labeled CO2
- stool antigen testing: enzyme immnoassay. high sensitivity and specificity for baseline screening.
6
Q
Treatment for H. pylori
A
- triple therapy PPI-A-C
-amoxicillin, clarithromycin, PPI - Quadruple therapy PPI-BMT
-metronidazole
-bismuth subsalicylate
-tetracycline
-PPI
Follow up with urea breath test or stool antigen test
7
Q
NSAIDs gastropathy
A
- regular NSAIDs users: dyspepsia, erosions, ulcers
- 4x increase in GI complications
- increased risk with hx of peptic ulcer, prior GI complication, use of steroids, anticoagulation drugs,
- pathophys: inhibition of mucosal prostaglandin synthesis->increased acid secretion, decreased bicarb,
- most important mechanisms of injury: decreased mucosal blood flow and neutrophil adherence to endothelium
8
Q
Treatment of PUD
A
- Relieve symptoms and heal ulcers: Acid suppression via PPI
- or H2 antagonist
- anticholinergics
- antacids - prevent ulcer recurrence: eliminate H pylori with triple or quad therapy, avoid NSAIDs, enhance mucosal defense