1
Q
What is the definition of Peptic Ulcer Disease (PUD)?
A
A disruption in the mucosal layer of the stomach or duodenum that extends through the muscularis mucosa (i.e., deeper than just the epithelium).
2
Q
What are the less common sites where peptic ulcers can occur?
A
1) Esophagus, 2) Jejunum (following gastrojejunostomy), 3) Ectopic gastric mucosa (e.g., in Meckel’s diverticulum).
3
Q
What is the most common complication of PUD?
A
Gastrointestinal bleeding (hemorrhage) – occurs more often in the elderly, likely due to NSAID use.
4
Q
Which gender and age group have the highest incidence of PUD?
A
Historically more common in men, but the gap has narrowed. Peak incidence is in the 60s and 70s. Women have a higher incidence of gastric ulcers; men have a higher incidence of duodenal ulcers.
5
Q
What is the annual incidence and lifetime prevalence of PUD?
A
Incidence: 0.1-0.3% per year. Lifetime prevalence: 5-10% of the general population [citation:1].
6
Q
How has the epidemiology of PUD changed over the past two decades?
A
The prevalence has declined substantially due to: 1) Declining H. pylori prevalence, 2) Widespread use of potent anti-secretory drugs (PPIs).
7
Q
What is the most common cause of PUD worldwide?
A
Helicobacter pylori infection – accounts for the majority of duodenal ulcers and a significant proportion of gastric ulcers.
8
Q
What are the three main etiologic/risk factors for PUD from the slides?
A
1) Helicobacter pylori infection, 2) NSAIDs, 3) Tobacco use.
9
Q
List the acid hypersecretory state that causes PUD.
A
Zollinger-Ellison syndrome (gastrinoma).
10
Q
List the physiologic stress conditions that can cause PUD.
A
Burns (Curling’s ulcers) and CNS trauma (Cushing’s ulcers).
11
Q
What genetic factors are associated with PUD?
A
Blood group O and family history.
12
Q
List the ‘other’ risk factors for PUD mentioned.
A
Alcohol, delayed gastric emptying, bile reflux, steroids, COPD, cirrhosis, CKD.
13
Q
What is the annual risk of upper GI bleeding in patients using NSAIDs?
A
Approximately 1-4% per year, but the risk increases with age, prior ulcer history, concomitant anticoagulant/antiplatelet use, and high-dose NSAID therapy.
14
Q
What is the pathophysiology of PUD?
A
PUD occurs when the balance between aggressive factors and protective factors in the GI wall is disrupted – an imbalance favoring mucosal injury.
15
Q
List the aggressive factors in PUD.
A
Acid, pepsin, H. pylori, NSAIDs, bile salts, tobacco, alcohol.
16
Q
List the protective factors in PUD.
A
Mucus, bicarbonate, mucosal blood flow, prostaglandins, epithelial renewal, hydrophobic layer, cellular restitution.
17
Q
Where is a gastric ulcer typically located?
A
Usually on the lesser curvature of the stomach, particularly at the incisura angularis.
18
Q
Where is a duodenal ulcer typically located?
A
Usually in the duodenal bulb (first part of the duodenum).
19
Q
How does gastric ulcer pain typically present?
A
Burning or gnawing epigastric pain that is AGGRAVATED by food and occurs SHORTLY AFTER a meal. Associated with nausea and weight loss.
20
Q
How does duodenal ulcer pain typically present?
A
Burning or gnawing epigastric pain that is RELIEVED by food or antacids and AGGRAVATED by hunger. Occurs 2-3 hours after a meal (may wake patient between midnight and 3 AM). Associated with hyperphagia and weight gain.
21
Q
What is the classic description of duodenal ulcer pain timing?
A
Pain occurs 2-3 hours after a meal, often waking the patient between midnight and 3 AM (nocturnal pain).
22
Q
What is the single most important prognostic factor in determining the likelihood of ulcer healing and recurrence?
A
H. pylori eradication status – successful eradication reduces recurrence rates from >60% to <10% per year.
23
Q
What is the most common complication of PUD and who is most affected?
A
Gastrointestinal bleeding (hemorrhage) – most common complication; occurs more often in the elderly (likely due to NSAIDs). Presents with hematemesis and/or melena.
24
Q
What is the second most common complication of PUD?
A
Perforation – also more common in the elderly (likely due to NSAIDs). Presents with sudden onset severe, sharp abdominal pain.
25
What is the presentation of gastric outlet obstruction?
New onset early satiety, projectile vomiting containing previous meals, increased post-prandial abdominal pain, weight loss.
26
Which complication of PUD is associated with gastric cancer?
Gastric ulcer (especially chronic, non-healing gastric ulcers) – requires biopsy to rule out malignancy.
27
List the 'alarm features' of PUD that warrant prompt gastroenterologist referral.
1) Bleeding or anemia, 2) Early satiety, 3) Unexplained weight loss, 4) Progressive dysphagia or odynophagia, 5) Recurrent vomiting, 6) Family history of GI cancer.
28
List the H. pylori-associated diseases.
1) Gastritis, 2) Peptic ulcer disease, 3) Gastric cancer (adenocarcinoma), 4) Gastric MALT lymphoma, 5) Gastrointestinal stromal tumor (possible association).
29
What percentage of gastric cancer cases are associated with H. pylori?
Approximately 90% of non-cardia gastric cancer cases are associated with H. pylori infection [citation:2].
30
What is the preferred diagnostic test for PUD?
Upper GI endoscopy (esophagogastroduodenoscopy – EGD) – highly sensitive for diagnosis of gastric and duodenal ulcers. Allows photographic documentation, tissue biopsy to rule out malignancy, and H. pylori testing.
31
List the invasive (endoscopic) tests for H. pylori.
1) Rapid urease test (e.g., CLOTest, Hpfast, Pyloritek), 2) Histology, 3) Culture.
32
List the non-invasive tests for H. pylori.
1) 13C or 14C urea breath test, 2) Stool antigen test, 3) Serology (antibody testing – cannot distinguish active from past infection).
33
What is the sensitivity and specificity of the urea breath test for H. pylori?
Sensitivity >95%, specificity >95% – the most accurate non-invasive test.
34
When is double-contrast barium meal used for PUD diagnosis?
Can detect ulcers >0.5 cm with diagnostic accuracy approaching endoscopy. However, it does NOT allow for tissue biopsy, so cannot rule out malignancy or test for H. pylori. Generally reserved for when endoscopy is unavailable.
35
What is the first-line test for H. pylori diagnosis in clinical practice?
Non-invasive tests (urea breath test or stool antigen test) are preferred for initial diagnosis. Endoscopic biopsy is preferred when endoscopy is already indicated.
36
What is the recommended H. pylori eradication regimen according to Maastricht VI/Florence consensus (2023)?
Bismuth-containing quadruple therapy is preferred over triple therapy due to increasing clarithromycin resistance [citation:2][citation:6].
37
What is the clarithromycin resistance threshold that determines empirical therapy choice?
Regions with clarithromycin resistance >15% should use bismuth quadruple therapy as first-line. Regions with resistance <15% may use triple therapy [citation:10].
38
What is the standard triple therapy regimen for H. pylori eradication?
PPI (e.g., omeprazole 20 mg bd or lansoprazole 30 mg bd) + clarithromycin (250-500 mg bd) + amoxicillin (500 mg tds) OR metronidazole (400 mg tds). Duration: 14 days.
39
What is the standard quadruple (bismuth) therapy regimen for H. pylori eradication?
PPI (omeprazole 20 mg daily or lansoprazole 30 mg daily) + bismuth subsalicylate (2 tablets qds) + metronidazole (400 mg tds) + tetracycline (500 mg qds). Duration: 14 days.
40
What is vonoprazan and when is it used?
A potassium-competitive acid blocker (P-CAB) – faster and more potent acid suppression than PPIs. Recommended as first-line for H. pylori eradication in some guidelines (e.g., JSGE 2020) [citation:5].
41
What is the success rate of first-line H. pylori eradication therapy with current regimens?
With 14-day bismuth quadruple therapy or concomitant therapy: >90% in compliant patients. With standard triple therapy in high-resistance regions: as low as 60-80%.
42
What is the recommended second-line therapy after failed H. pylori eradication?
Fluoroquinolone-based therapy (PPI + levofloxacin + amoxicillin) with or without bismuth, or repeat bismuth quadruple therapy if not used first-line [citation:10].
43
What is the role of PPIs in bleeding peptic ulcers?
PPIs reduce rebleeding rates, need for surgery, and mortality when given after endoscopic hemostasis. High-dose IV PPI (e.g., pantoprazole 80 mg bolus then 8 mg/hr for 72h) is standard.
44
What is the role of endoscopic therapy in bleeding peptic ulcers?
Endoscopic hemostasis (injection, thermal, or mechanical therapy) is indicated for high-risk stigmata (active bleeding, non-bleeding visible vessel, adherent clot). Combined with high-dose PPI.
45
What is the role of surgery in PUD?
Indicated for: 1) Perforation, 2) Bleeding not controlled endoscopically, 3) Gastric outlet obstruction, 4) Refractory disease, 5) Suspected or confirmed malignancy.
46
List the surgical procedures for PUD.
1) Vagotomy and drainage (e.g., pyloroplasty), 2) Highly selective vagotomy (no drainage needed), 3) Vagotomy with antrectomy, 4) Subtotal gastrectomy with Roux-en-Y esophago-gastro-jejunostomy.
47
List the acid-suppressing drugs used in PUD.
1) Proton pump inhibitors (PPIs): omeprazole, lansoprazole, rabeprazole, esomeprazole. 2) H2 receptor antagonists: cimetidine, ranitidine, famotidine, nizatidine. 3) Antacids (e.g., aluminum/magnesium hydroxide – Gaviscon).
48
List the mucosal protective agents used in PUD.
1) Sucralfate, 2) Misoprostol, 3) Bismuth subsalicylate.
49
List the antibiotics used in H. pylori eradication therapy.
Amoxicillin, tetracycline, clarithromycin, metronidazole.
50
How do PPIs work?
Irreversibly inhibit the H+/K+ ATPase (proton pump) on the apical membrane of gastric parietal cells – the final common pathway of acid secretion. Require activation in the acidic environment of the canaliculus.
51
How do H2RAs work?
Competitively block histamine at H2 receptors on gastric parietal cells – reducing acid secretion stimulated by histamine, gastrin, and ACh. Less potent than PPIs.
52
How does misoprostol work?
A synthetic prostaglandin E1 analogue – increases mucus and bicarbonate secretion, increases mucosal blood flow, and enhances epithelial repair. Also has cytoprotective effects.
53
What is the mechanism of sucralfate?
Forms a viscous adhesive barrier that binds to the ulcer base, protecting it from acid, pepsin, and bile. Does not reduce acid secretion.
54
What is the mechanism of bismuth compounds?
Multiple actions: 1) Direct bactericidal against H. pylori, 2) Forms protective coating on ulcer, 3) Stimulates mucus and bicarbonate secretion, 4) Adsorbs pepsin and bile acids.
55
What is the role of antacids in PUD?
Neutralize gastric acid – provide rapid but short-lived symptom relief. Do not heal ulcers effectively as monotherapy. Often used as adjunctive therapy.
56
What is the definition of refractory peptic ulcer?
An ulcer that fails to heal after 8-12 weeks of adequate therapy (PPI). Causes include: persistent H. pylori infection, NSAID continuation, non-adherence, Zollinger-Ellison syndrome, malignancy.
57
What is the first step in evaluating a refractory peptic ulcer?
Confirm medication adherence and ensure H. pylori eradication. If adherent and H. pylori negative, rule out NSAID/aspirin use, then consider Zollinger-Ellison syndrome or malignancy.
58
What is Zollinger-Ellison syndrome (ZES)?
A condition caused by a gastrin-secreting neuroendocrine tumor (gastrinoma) that causes gastric acid hypersecretion and severe, recurrent, or refractory peptic ulcers [citation:4][citation:8].
59
Where are gastrinomas typically located?
Most commonly in the duodenum (50-70%) or pancreas (20-40%). They are often small and may be multiple [citation:4][citation:8].
60
What is the association between ZES and MEN1?
Approximately 20-30% of ZES cases are associated with Multiple Endocrine Neoplasia type 1 (MEN1) – an autosomal dominant syndrome involving parathyroid, pituitary, and pancreatic neuroendocrine tumors [citation:4].
61
How is ZES diagnosed?
1) Fasting serum gastrin (markedly elevated >1000 pg/mL is diagnostic). 2) Gastric pH (<2 confirms hypersecretion). 3) Secretin stimulation test (paradoxical rise in gastrin). 4) Imaging to localize tumor (CT, MRI, somatostatin receptor scintigraphy) [citation:4].
62
What is the mainstay of treatment for ZES?
High-dose PPIs to control acid hypersecretion. Surgical resection if localized and not metastatic [citation:8].
63
What is the prognosis of ZES with complete surgical resection?">">90% 5-10 year survival. With metastatic disease: 43% 5-year survival and 25% 10-year survival [citation:8].
64
What is the role of H. pylori eradication in preventing gastric cancer?
Eradication of H. pylori reduces the risk of gastric cancer, especially if performed before the development of advanced premalignant changes (atrophy or intestinal metaplasia). Provides cancer prevention opportunity at any age in adults [citation:2].
65
What is the recommended PPI dosing for NSAID-induced ulcer prevention?
For high-risk patients (prior ulcer history, age >65, concomitant anticoagulant/antiplatelet, high-dose NSAIDs): PPI co-therapy with NSAID is recommended [citation:5][citation:9].
66
What is the preferred PPI for H. pylori eradication in terms of efficacy?
Newer PPIs (rabeprazole, esomeprazole) may achieve higher eradication rates due to more potent and consistent acid suppression, especially when given twice daily [citation:10].
67
What is the role of probiotics in H. pylori eradication?
Some evidence suggests adding certain probiotics (Lactobacillus, Saccharomyces boulardii) may reduce side effects and improve eradication rates, though not universally recommended [citation:10].
68
What is the significance of the Maastricht VI/Florence consensus?
A major international guideline (2023) updating H. pylori management. Key changes: 1) Emphasizes bismuth quadruple therapy over triple therapy, 2) Highlights H. pylori as always causing gastritis, 3) Reinforces cancer prevention benefits [citation:2][citation:6].
69
What is the recommended duration for H. pylori eradication therapy?
14 days – shorter durations (7 or 10 days) have lower eradication rates and are no longer recommended by most guidelines.
70
What is the management of a patient with PUD who is H. pylori negative and not on NSAIDs?
These are 'idiopathic' peptic ulcers – may have worse outcomes than H. pylori ulcers. Treatment: PPI for 8 weeks. Maintenance PPI often required due to high recurrence rates.
71
What is the role of smoking cessation in PUD?
Smoking impairs ulcer healing and increases recurrence rates. Smoking cessation is an important adjunctive measure.
72
What is the role of alcohol in PUD?
Alcohol can irritate the gastric mucosa and may contribute to ulcer formation, especially in high quantities. However, moderate alcohol is not a major independent risk factor compared to H. pylori and NSAIDs.
73
What is the difference between gastric and duodenal ulcer pathogenesis?
Gastric ulcers: often associated with impaired mucosal defense (NSAIDs, H. pylori-induced gastritis). Duodenal ulcers: primarily associated with increased acid load (H. pylori, ZES, high parietal cell mass).
74
What is the 'cascade' of H. pylori-induced duodenal ulcer formation?
H. pylori infection → antral-predominant gastritis → increased gastrin release → increased acid secretion → metaplasia in duodenal bulb → colonization of metaplastic epithelium → duodenitis → ulcer.
75
What is the management of a patient with upper GI bleeding from a peptic ulcer?
1) Resuscitation (IV fluids, blood transfusion if needed). 2) Urgent endoscopy. 3) Endoscopic hemostasis if high-risk stigmata. 4) High-dose IV PPI. 5) H. pylori testing and eradication. 6) Discontinue NSAIDs/aspirin if possible.
76
What is the Forrest classification for bleeding ulcers?
A classification system based on endoscopic stigmata: Ia (spurting bleeding), Ib (oozing), IIa (non-bleeding visible vessel), IIb (adherent clot), IIc (flat pigmented spot), III (clean base). High risk: Ia, Ib, IIa, IIb.
77
What is the rebleeding rate after endoscopic hemostasis without PPI?
Approximately 20-25% for high-risk lesions. High-dose IV PPI reduces rebleeding to 5-10%.
78
What is the mortality rate for bleeding peptic ulcers?
Approximately 5-10% – has not changed significantly despite advances in endoscopy and acid suppression, due to older, sicker patient population.
79
What is the management of perforated peptic ulcer?
1) Resuscitation (IV fluids, NG tube, broad-spectrum antibiotics). 2) Urgent surgical repair (primary closure with omental patch – Graham patch). 3) Laparoscopic approach if available. 4) Definitive ulcer surgery (vagotomy/drainage) may be added.
80
What is the mortality rate for perforated peptic ulcer?
Overall 10-30% – higher in elderly, those with delayed presentation (>24h), and those with significant comorbidities.
81
What is the management of gastric outlet obstruction due to PUD?
1) NG decompression, 2) IV fluids and electrolyte correction, 3) Endoscopic balloon dilation, 4) H. pylori eradication, 5) Surgery (gastrojejunostomy, vagotomy) if persistent.
82
What is the prognosis of PUD with appropriate treatment?
Excellent with H. pylori eradication and NSAID discontinuation. Recurrence rate <10% per year if H. pylori cured and NSAIDs stopped. Higher recurrence in idiopathic ulcers.
83
What is the lifetime risk of gastric cancer in patients with H. pylori infection?
Approximately 1-3% – significantly higher than uninfected individuals. The risk increases with the presence of gastric atrophy and intestinal metaplasia.
84
What is the role of surveillance endoscopy after gastric ulcer healing?
Recommended to confirm healing and rule out malignancy, especially for larger ulcers or those with atypical appearance. Repeat endoscopy after 8 weeks of PPI therapy.
85
What is the role of testing for H. pylori after eradication therapy?
Test of cure (using urea breath test or stool antigen) is recommended at least 4 weeks after completing therapy, especially in patients with complicated ulcers (bleeding, perforation) or persistent symptoms.
86
What is the first-line PPI for acute bleeding ulcer management?
High-dose IV PPI (e.g., pantoprazole 80 mg bolus followed by 8 mg/hour infusion for 72 hours) after successful endoscopic hemostasis. Oral high-dose PPI (e.g., omeprazole 40 mg bd) is an alternative if IV unavailable.
87
How does age affect the presentation of PUD?
Elderly patients are more likely to have: 1) NSAID-induced ulcers, 2) Bleeding as first presentation (without prior pain), 3) Silent ulcers, 4) Higher complication rates.
88
What is the role of COX-2 selective NSAIDs (coxibs) in reducing ulcer risk?
Coxibs (celecoxib, etoricoxib) have lower GI ulcer risk than non-selective NSAIDs, but do not eliminate risk, especially in high-risk patients. PPI co-therapy still recommended for high-risk patients on coxibs.
89
What is the recommended PPI for maintenance therapy in patients requiring long-term NSAIDs?
Any standard-dose PPI once daily (e.g., omeprazole 20 mg, lansoprazole 15 mg, esomeprazole 20 mg) co-prescribed with the NSAID. Continue for as long as NSAID is required.
90
What is the definition of 'complicated' peptic ulcer?
An ulcer that presents with: 1) Bleeding, 2) Perforation, 3) Gastric outlet obstruction, 4) Penetration into adjacent organ (e.g., pancreas).
91
What is the definition of 'refractory' peptic ulcer?
An ulcer that fails to heal after 8-12 weeks of adequate PPI therapy (usually 40 mg omeprazole equivalent daily).
92
What is the most common cause of refractory peptic ulcer?
Persistent H. pylori infection (clarithromycin resistance or poor adherence), followed by continued NSAID use, and then non-adherence to PPI.
93
What is the recommended third-line therapy for H. pylori eradication?
Rifabutin-based triple therapy (PPI + amoxicillin + rifabutin) – considered 'rescue' therapy when other regimens fail and antimicrobial susceptibility testing is unavailable [citation:10].
Internal Medicine
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