What are the cross question asked in viva on topic of peptic ulcer disease in ward ?

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Viva Questions on Peptic Ulcer Disease (PUD) - Ward

Below is a structured set of cross-questions typically asked in clinical viva, organized by topic area.

1. Definition & Basic Concepts

Q: What is a peptic ulcer? A peptic ulcer is a breach in the mucosa of any part of the GI tract exposed to acid-pepsin secretion, penetrating through the muscularis mucosae. Despite the name, pepsin plays a secondary role - in the absence of acid, peptic ulcers do not occur. - Bailey & Love's Surgery, p.1179

Q: What are the common sites?

First part of the duodenum (most common site overall)
Lesser curve of the stomach
Prepyloric region / pyloric channel
Stoma following gastric surgery
Oesophagus (GERD-related)
Meckel's diverticulum (ectopic gastric mucosa)

Ulcers occur at the junction between different types of epithelia, in the epithelium least resistant to acid damage. - Bailey & Love's, p.1179

Q: Which is more common - gastric or duodenal ulcer? Duodenal ulcers are more common than gastric ulcers. However, symptoms are indistinguishable between the two. - Bailey & Love's, p.1179

2. Etiology & Risk Factors

Q: What are the two most common causes of PUD?

H. pylori infection - accounts for >70% of PUD cases
NSAID/aspirin use - increasing in prevalence, especially in the elderly

Other risk factors:

Cigarette smoking (doubles the risk; delays healing, promotes recurrence)
Zollinger-Ellison syndrome (gastrinoma causing massive acid secretion)
Corticosteroids (suppress prostaglandin synthesis)
Alcohol-related cirrhosis, COPD, chronic renal failure, hyperparathyroidism (hypercalcemia stimulates gastrin) - Robbins & Kumar, p.795; Washington Manual, p.681

Q: How does H. pylori cause ulcers? H. pylori infects the gastric antrum, causing chronic active gastritis. It increases gastrin secretion, reduces somatostatin (loss of acid inhibition), and damages the mucosal protective barrier (reduces mucus, bicarbonate). Only 5-10% of those infected develop ulcers - host factors and H. pylori strain variation also contribute. - Robbins & Kumar

Q: Why do NSAIDs cause peptic ulcers? NSAIDs inhibit COX-1, reducing prostaglandin (PGE2) synthesis. Prostaglandins normally stimulate mucus and bicarbonate secretion, maintain mucosal blood flow, and inhibit acid secretion. Their reduction leaves the mucosa unprotected. Complications like hemorrhage and perforation are much more common with NSAID use. - Schwartz's Surgery, p.2857

3. Pathophysiology

Q: What is the balance that governs ulcer formation? PUD arises from an imbalance between mucosal aggressive forces and defensive forces:

Aggressive: Gastric acid, pepsin, H. pylori, NSAIDs, bile reflux
Defensive: Mucus-bicarbonate layer, mucosal blood flow, prostaglandins, epithelial restitution

Q: Why are duodenal ulcer patients hypersecretors of acid, but gastric ulcer patients are not? Duodenal ulcer patients often have parietal cell hyperplasia and reduced somatostatin inhibition, leading to increased acid output. Gastric ulcer patients typically have relatively normal acid levels - the problem is primarily a defective mucosal barrier (from H. pylori or NSAIDs). - Bailey & Love's

4. Clinical Features

Q: What are the typical symptoms?

Epigastric pain - gnawing, burning; may radiate to the back
Pain with eating (gastric ulcers - pain worsened by food; duodenal ulcers - food/antacids relieve pain, pain returns 2-3 hours later - "food-pain-relief" vs. "food-relief-pain" pattern)
Periodicity - symptoms disappear for weeks or months and recur
Nausea, vomiting (especially if outlet obstruction)
Weight loss or gain
Chronic GI bleeding presenting as iron deficiency anemia

Q: Are duodenal and gastric ulcer symptoms distinguishable? No - the clinical features of gastric and duodenal ulceration cannot be reliably differentiated on symptoms alone. Demographics differ (duodenal more common in younger men, gastric in older patients) but this does not allow discrimination. - Bailey & Love's, p.1180

Q: What alarm symptoms warrant urgent endoscopy?

Weight loss
Early satiety
GI bleeding / hematemesis / melena
Anemia
Persistent vomiting
Epigastric mass
Lack of response to PPI therapy - Washington Manual, p.681

5. Investigations

Q: What is the gold standard for diagnosis of PUD? Upper GI endoscopy (OGD/EGD) - gold standard. Allows direct visualization, tissue biopsy (especially important for gastric ulcers to exclude malignancy), CLO test, and histology. - Washington Manual

Q: What tests are available for H. pylori diagnosis? Which is best for confirming eradication?

Test	Type	Note
CLO (rapid urease) test	Invasive (endoscopic biopsy)	May be false-negative on PPIs
Histopathology of biopsy	Invasive	Standard; may be false-negative on PPIs
Urea breath test (UBT)	Non-invasive	Most accurate; sensitivity & specificity ~95%; best for confirming eradication
Stool H. pylori antigen	Non-invasive	Good sensitivity/specificity; also used to confirm eradication
Serum IgG antibody	Non-invasive	Cannot confirm eradication (antibody persists up to 18 months post-treatment)

Washington Manual, p.681

Q: When is a barium meal useful? Barium meal can show a duodenal ulcer crater or deformed duodenal cap. However, it cannot allow biopsy, so endoscopy is preferred - especially for gastric ulcers which may be malignant.

Q: What does an erect CXR show in perforation? Free gas under the diaphragm (pneumoperitoneum) - seen in >50% of perforated peptic ulcers. CT scan is now more commonly used and more accurate. - Bailey & Love's, p.1186

6. Complications (key viva area)

Q: What are the complications of PUD? The classic triad:

Hemorrhage - most common complication
Perforation - surgical emergency
Obstruction (Gastric outlet obstruction) - due to scarring/fibrosis

Additional: Penetration into adjacent structures (e.g., pancreas causing back pain).

Q: Anterior vs. posterior duodenal ulcer - what is the clinical significance?

Anterior ulcers tend to perforate (into the peritoneal cavity)
Posterior ulcers tend to bleed, by eroding the gastroduodenal artery

"Kissing ulcers" = both anterior and posterior ulcers present simultaneously. - Bailey & Love's, p.1179

Q: What is the Rockall Score? When is it used? The Rockall Score is used to risk-stratify patients with upper GI bleeding. Variables include age, pulse rate, systolic BP, comorbidities, endoscopic diagnosis, and stigmata of recent hemorrhage. Score ≥8 carries 41% rebleeding rate and 41% mortality. - Sleisenger & Fordtran

Q: What is the classic presentation of a perforated peptic ulcer?

Sudden-onset severe generalized abdominal pain
Shock with tachycardia (initially; pyrexia develops later)
Board-like rigidity - abdomen does not move with respiration
Patient is still, disinclined to move
Bacterial peritonitis supervenes over hours - Bailey & Love's, p.1186

Q: How is perforated peptic ulcer managed?

Resuscitation (IV fluids, analgesia - do NOT withhold analgesia)
NBM, NG tube, urinary catheter
IV antibiotics
Surgery: Laparotomy via upper midline incision; most commonly Graham patch repair (omental patch closure of perforation), followed by H. pylori eradication

Q: What is gastric outlet obstruction (GOO) and how does it present? GOO results from scarring/fibrosis from chronic duodenal or pyloric ulceration. Presents with:

Projectile, non-bilious vomiting (large volume, undigested food)
Succussion splash
Weight loss, dehydration
Metabolic alkalosis with hypokalemia (loss of HCl and K+)
"Tetany of the stomach" (hypochloremic, hypokalemic metabolic alkalosis)

7. Treatment

Q: What is the medical management of PUD?

Acid suppression is the mainstay: PPIs are preferred over H2 blockers
- Gastric ulcers: 12 weeks of PPI
- Duodenal ulcers: 8 weeks of PPI
H. pylori eradication if positive (H. pylori is classified as a carcinogen and must be eradicated)
Stop NSAIDs, smoking, alcohol

Q: What is the H. pylori eradication regimen?

First-line (current standard): Quadruple therapy - PPI + bismuth + metronidazole + tetracycline (14 days)
- Replaced clarithromycin-based triple therapy due to rising clarithromycin resistance
Clarithromycin triple therapy (PPI + amoxicillin + clarithromycin): used only if no prior macrolide exposure
Avoid clarithromycin if prior macrolide exposure; avoid levofloxacin if prior fluoroquinolone exposure
Confirm eradication with stool antigen test or UBT (wait 4 weeks after completing antibiotics, 2 weeks after stopping PPI) - Washington Manual, p.681

Q: What is the role of surgery in PUD today? Elective surgery is very rarely performed - reserved for:

Refractory ulcers not responding to medical therapy
Malignancy suspected Emergencies remain the main surgical indication (perforation, hemorrhage not controlled endoscopically, obstruction). Formerly used operations include Billroth I (gastroduodenostomy), Billroth II/Polya gastrectomy, and vagotomy procedures. - Bailey & Love's, p.1182

8. Gastric Ulcer vs. Cancer - Crucial Viva Point

Q: Can a gastric ulcer be malignant? How do you differentiate? Yes - a gastric ulcer can be malignant, and an ulcerated gastric cancer may mimic a benign ulcer. Therefore:

All gastric ulcers must be biopsied at endoscopy (multiple biopsies from edges and base)
Features suggesting malignancy: irregular edges, heaped-up margins, abnormal mucosal folds
Benign ulcers: round/oval, smooth, clean base, radiating folds
Duodenal ulcers: malignancy is extremely uncommon here - biopsies are less mandatory but still common practice - Bailey & Love's, p.1179

Q: What is the CLO test / rapid urease test? A biopsy from the gastric antrum is placed in a urea-containing medium with a pH indicator. H. pylori's urease splits urea into ammonia + CO2, raising the pH and changing the indicator color (yellow to pink/red). Result within 30-60 minutes. May be falsely negative in patients on PPIs. - Washington Manual

9. Zollinger-Ellison Syndrome

Q: What is Zollinger-Ellison (ZE) syndrome? A condition caused by a gastrin-secreting tumor (gastrinoma), usually in the pancreas or duodenum. Massive gastrin secretion leads to extreme acid hypersecretion, causing multiple peptic ulcerations in the stomach, duodenum, and even the jejunum. Associated with MEN-1 syndrome. Suspect if: multiple ulcers, unusual locations, recurrence despite treatment, secretory diarrhea. Diagnose with fasting serum gastrin levels (>1000 pg/mL highly suggestive). - Robbins & Kumar

10. Quick-Fire Viva Points

Question	Answer
Most common site of PUD	First part of duodenum
Vessel eroded in posterior DU hemorrhage	Gastroduodenal artery
Best non-invasive test for H. pylori	Urea breath test (95% sensitivity/specificity)
Test to confirm H. pylori eradication	Stool antigen test or UBT (NOT serology)
Why must gastric ulcers be biopsied?	To exclude malignancy
Complication of chronic DU scarring	Pyloric stenosis / gastric outlet obstruction
Metabolic disturbance in GOO	Hypochloremic hypokalemic metabolic alkalosis
Sign of perforation on erect CXR	Free gas under diaphragm
Why is PPI better than H2 blocker?	More effective acid suppression; renders patient near achlorhydric
H. pylori status as carcinogen	Group I carcinogen (associated with gastric adenocarcinoma and MALT lymphoma)

Key Sources:

Bailey and Love's Short Practice of Surgery 28th Ed., Chapter 67
Washington Manual of Medical Therapeutics, Chapter 18
Robbins & Kumar Basic Pathology, Chapter 13
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, Chapter 20

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