Peptic ulcer

What is the definition of a peptic ulcer?

A defect in the gastric or duodenal mucosa with a diameter of at least 0.5 cm and a depth that penetrates through the muscularis mucosae. Definitions 1

Where are gastric ulcers typically located?

Lesser curvature, between the corpus and antrum. Definitions 2

Where are duodenal ulcers typically located?

Anterior or posterior wall of the duodenal bulb. Definitions 3

How do erosions differ from ulcers?

Erosions are more superficial than ulcers. Ulcers extend beyond the muscularis mucosa. Definitions 4

What is the approximate incidence of PUD?

~1 case/1,000 person-years. Epidemiology 5

What is the approximate annual prevalence of PUD in the US?

~ 6 million cases. Epidemiology 6

Is the prevalence of PUD increasing or decreasing?

Decreasing. Epidemiology 7

How does the age of onset differ between duodenal and gastric ulcers?

Duodenal ulcers occur on average 10-20 years earlier than gastric ulcers. Epidemiology 8

What is the median age of diagnosis for PUD?

18-30 years. Epidemiology 9

How does the incidence of PUD differ by sex?

♂ = ♀ Epidemiology 10

What are the two major contributing factors to the development of PUD?

H. pylori infection and nonsteroidal anti-inflammatory drug (NSAID) use. Etiology 11

What percentage of duodenal ulcers are associated with H. pylori?

40-70%. Etiology 12

What percentage of gastric ulcers are associated with H. pylori?

25-50%. Etiology 13

Is the rate of H. pylori infection increasing or decreasing?

Decreasing. Etiology 14

How much does chronic NSAID use increase the risk of PUD?

Fourfold. Etiology 15

What other risk is associated with NSAID use and PUD?

Increased risk for PUD complications. Etiology 16

What medication should be considered for patients requiring chronic NSAID therapy to prevent ulcer formation?

Acid suppression medication. Etiology 17

What are some shared risk factors for PUD, GERD, and gastritis?

Smoking, heavy alcohol use, glucocorticoids, and caffeine. Etiology 18

Are diet or psychological factors associated with PUD?

Yes. Etiology 19

Name some rare causes of PUD?

Acid hypersecretory states, non-NSAID medications, infections, radiation, illicit drug use, systemic inflammatory diseases, mechanical factors. Etiology 20

Name some acid hypersecretory states.

Zollinger-Ellison syndrome (gastrinoma), systemic mastocytosis, hyperparathyroidism. Etiology 21

Name some non-NSAID medications associated with PUD.

Acetaminophen, bisphosphonates, sirolimus, mycophenolate, SSRIs, and chemotherapeutics (e.g., 5-FU). Etiology 22

Name some infections that are rare causes of PUD?

CMV, HSV-1, EBV, and Helicobacter heilmannii. Etiology 23

What is secreted by the cells of the gastric mucosa?

Gastric juice (an acidic fluid composed of HCl, pepsinogen, intrinsic factor, and mucus). Pathophysiology 24

What are some protective mechanisms in the gastric mucosa?

Secretion of mucus and HCO3- to form a protective barrier. Pathophysiology 25

When does ulcer formation occur?

Protective mechanisms are disrupted or there is excessive acid/pepsin secretion. Pathophysiology 26

What is secreted by parietal cells?

Hydrochloric acid (HCl) and intrinsic factor. Pathophysiology 27

What stimulates parietal cells?

Acetylcholine, histamine, and gastrin. Pathophysiology 28

What inhibits parietal cells?

Prostaglandins and somatostatin. Pathophysiology 29

What is secreted by mucosal cells?

Protective mucus. Pathophysiology 30

What stimulates mucosal cells?

Acetylcholine, prostaglandins, and secretin. Pathophysiology 31

What is secreted by chief cells?

Pepsinogen. Pathophysiology 32

What stimulates chief cells?

Acetylcholine, gastrin, secretin, and vasoactive intestinal polypeptide (VIP). Pathophysiology 33

How does H. pylori contribute to the development of gastric ulcers?

Secretes urease → conversion of urea to NH3 → alkalinization; colonization and cytotoxins disrupt mucosal barrier. Pathophysiology 34

How does H. pylori contribute to the development of duodenal ulcers?

Inhibits somatostatin → ↑ gastrin, direct spread to duodenum inhibits HCO3-. Pathophysiology 35

How do NSAIDs contribute to the development of PUD?

Inhibit COX-1 and COX-2 → ↓ prostaglandin production → erosion of mucosa, decrease mucosal blood flow and inhibit proliferation. Pathophysiology 36

How does acid hypersecretion contribute to the development of PUD?

↑ H+ secretion and parietal cell mass → delivery of excessive acid to the duodenum. Pathophysiology 37

Are most patients with PUD symptomatic or asymptomatic?

Asymptomatic, up to 70%. Clinical features 38

Are NSAID-induced ulcers likely to be symptomatic or asymptomatic?

Asymptomatic, more likely to present with complications. Clinical features 39

What is the most common symptom of PUD?

Abdominal pain. Clinical features 40

Where is the pain commonly located in PUD?

Epigastrium. Clinical features 41

What is the typical description of PUD pain?

"Gnawing" or "burning." Clinical features 42

Name some symptoms associated with PUD.

Belching, indigestion, gastrointestinal reflux, nausea/vomiting, and bloating/abdominal fullness. Clinical features 43

How does pain from a gastric ulcer correlate with eating?

Pain increases shortly after eating and causes weight loss. Clinical features 44

How does pain from a duodenal ulcer correlate with eating?

Pain is relieved with food intake, causing weight gain. Clinical features 45

When is pain from a duodenal ulcer most intense?

2-5 hours after eating. Clinical features 46

Are nocturnal pain more common in gastric or duodenal ulcers?

Duodenal ulcers. Clinical features 47

What are the first steps in the diagnostic approach of PUD?

Screen for common etiologies (e.g., NSAID use), consider CBC, BMP, FOBT if suspect occult bleeding. Diagnosis 48

When should noninvasive testing for H. pylori be done?

Patients ≤ 60 years of age without red flags for dyspepsia. Diagnosis 49

Name two noninvasive tests for H. pylori.

Urea breath test and H. pylori stool antigen test. Diagnosis 50

When should a patient be referred directly for EGD?

Patients > 60 years old or > 45 in areas with high gastric cancer, with red flags, or if unresponsive to empiric therapy. Diagnosis 51

When should specialized lab studies be considered?

Persistently uncertain etiology. Diagnosis 52

What are some alarm features warranting EGD?

Progressive dysphagia, odynophagia, rapid weight loss, persistent vomiting, suspected GI bleeding, and family history of upper GI malignancy. Diagnosis 53

What is the description and indication of Esophagogastroduodenoscopy (EGD)?

Description: Endoscopic procedure that allows visualization of the esophagus, stomach, and duodenum. Indication: Most accurate test to confirm PUD diagnosis, rule out malignancy, visualize lesions, obtain biopsy samples, invasive H. pylori testing, and for simultaneous therapeutic measures (e.g., hemostasis). Diagnosis 54

What are some typical endoscopic findings of peptic ulcers?

if benign pud u will see smooth ulcer base with rounded, regular edges and regular surrounding mucosa at typically location if Gastric ulcers: lesser curvature of the stomach, between the corpus and antrum

Duodenal ulcers: anterior or posterior wall of the duodenal bulb , . Diagnosis 55

What are some malignant endoscopic findings of peptic ulcers?

ulcerated mass with irregular, overhanging edges and nodular surrounding mucosa and usually at atypical locations

What type of ulcers have chronic inflammatory changes and active granulation on histology?

Benign ulcers. Diagnosis 56

What histopathological features indicate a malignant peptic ulcer?

Dysplasia, invasion of deeper layers. Diagnosis 57

What type of ulcers will have multiple ulcers and thick gastric folds?

Gastrinoma (Zollinger-Ellison syndrome). Diagnosis 58

When should biopsies be taken from gastric ulcers?

In most cases, multiple biopsies are recommended from the edge and base of the ulcer, and from different areas of the stomach lining including those not surrounding the ulcer. Diagnosis 59

When should biopsies be taken from duodenal ulcers?

Obtain biopsies from ulcers with endoscopic features that suggest malignancy. Diagnosis 60

What should be done with a suspicious gastric ulcer?

Follow-up EGD and histology until healed. Diagnosis 61

When should testing for rare causes of PUD be considered?

If the etiology remains unclear or the patient presents with recurrent ulcers. Diagnosis 62

What tests can be used to test for rare causes of PUD?

Fasting serum gastrin, secretin stimulation test and serum intact PTH level. Diagnosis 63

What lab study can be used to test for Zollinger-Ellison syndrome?

Fasting serum gastrin and secretin stimulation test. Diagnosis 64

What are the key differences between gastric and duodenal ulcers with regards to eating?

Pain increases shortly after eating in gastric ulcers causing weight loss, while pain is relieved with food intake causing weight gain in duodenal ulcers. Differential diagnoses 67

When is nocturnal pain more common?

In Duodenal ulcers. Differential diagnoses 68

What is the most accurate test to confirm the diagnosis of peptic ulcer disease?

Esophagogastroduodenoscopy (EGD). Differential diagnoses 69

What features of ulcers warrant multiple biopsies?

Gastric ulcers, or those with endoscopic features that suggest malignancy. Differential diagnoses 70

Are duodenal ulcers usually benign or malignant?

Usually benign. Differential diagnoses 71

Which type of ulcers have a higher risk of carcinoma?

Gastric ulcers. Differential diagnoses 72

What general measures are part of the treatment approach for PUD?

Nonpharmacological measures and follow-up to confirm treatment success. Treatment 73

What is done for H. pylori positive patients?

Eradication therapy with antibiotics and a PPI and acid suppression. Treatment 74

What is done for H. pylori negative patients?

Trial of acid suppression therapy (PPIs) for 4-8 weeks and reevaluation. Treatment 75

What should be considered in cases of treatment failure?

Elective surgery. Treatment 76

What is the initial management of overt GI bleeding in PUD?

Acute stabilization and immediate hemodynamic support for shock. Treatment 77

What should be done in patients with a perforated peptic ulcer?

Surgical emergency. Treatment 78

What should be done in patients with hemodynamic instability, peritonitis, and/or sepsis?

ICU admission or direct transfer to the OR. Treatment 79

What is the focus of medical treatment of uncomplicated PUD?

Symptom control, H. pylori eradication (if indicated), withdrawal of causative agents. Treatment 80

What should also be used for rapid symptom relief?

Antacids. Treatment 81

What is the recommended duration of acid suppression for duodenal ulcers?

≥ 4 weeks. Treatment 82

What is the recommended duration of acid suppression for gastric ulcers?

≥ 8 weeks. Treatment 83

What is the recommended duration of acid suppression if ulcer location is unknown?

8 weeks of empiric treatment. Treatment 84

When should maintenance acid suppression therapy be considered?

Select patients with idiopathic ulcers to prevent recurrence. Treatment 85

What is the description of Sucralfate?

Description: A sucrose sulfate-aluminum complex that reacts with HCl in an acidic environment to create a protective barrier. Acts as an acid buffer and promotes HCO3 production. Indication: Promote ulcer healing in patients with duodenal ulcers. Treatment 86

Should sucralfate be taken with a PPI or H2 blocker?

No. Treatment 87

When is Misoprostol indicated?

Indication: Consider as an alternative to PPIs for ulcer prophylaxis in patients at high risk of developing NSAID-induced GI toxicity (e.g., older individuals, those with a history of complicated peptic ulcer). Treatment 88

What is an example of a quadruple therapy for H. pylori?

Metronidazole, tetracycline, bismuth, and a PPI. Treatment 89

What are nonpharmacological measures recommended in PUD?

Restrict alcohol, smoking, and caffeine and avoid stress and medications that may worsen PUD and eating before bedtime. Treatment 90

When is elective surgical treatment considered in PUD?

Refractory symptoms or recurrence despite medical treatment, diseases that require NSAIDs, or inability to tolerate medical treatment. Treatment 91

What is a vagotomy?

Description: Surgical division of the anterior and posterior vagal trunk of the vagus nerve. Indication: To reduce acid production. Treatment 92

What are some complications of truncal vagotomy?

Delayed gastric emptying, postvagotomy diarrhea, postvagotomy hypergastrinemia, and dumping syndrome. Treatment 93

Name some drainage procedures that are combined with truncal vagotomy.

Pyloroplasty and antrectomy. Treatment 94

What does a Billroth I procedure involve?

Distal gastrectomy with end-to-end or side-to-end gastroduodenostomy. Treatment 95

What does a Billroth II procedure involve?

Resection of the distal two-thirds of the stomach with a blind-ending duodenal stump and end-to-side gastrojejunostomy. Treatment 96

What is the reconstruction technique used during total gastrectomy?

Roux-en-Y. Treatment 97

What should be done during the acute management of PUD?

Treat critical complications, evaluate underlying cause, and evaluate for occult bleeding, noninvasive tests for H. pylori, EGD for red flags/unsuccessful treatment, trial of acid suppression therapy, discontinue triggers and lifestyle modifications, specialized diagnostic studies if etiology unclear, ensure follow-up, and consider referral for elective surgery. Acute management checklist 98

What features of gastric ulcers warrant endoscopic follow up?

Refractory symptoms, ulcer of unknown etiology, ulcer that appears malignant in initial EGD, no biopsies taken in initial EGD, ulcer diagnosed by imaging. Follow-up 99

When is follow up endoscopy recommended for duodenal ulcers?

If symptoms persist after an appropriate course of antisecretory treatment. Follow-up 100