Explain about peptic ulcer mbbs 2nd year for exam

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Peptic Ulcer Disease - MBBS 2nd Year Exam Guide

Definition

A peptic ulcer is an excoriated (mucosal break extending through the muscularis mucosae) area of the stomach or intestinal mucosa caused principally by the digestive action of gastric acid (HCl) and pepsin. In the absence of acid, peptic ulcers do not occur.

Guyton & Hall Textbook of Medical Physiology, p. 825

Sites (Common Locations)

Causes and sites of peptic ulcer - from Guyton & Hall Textbook of Medical Physiology

Peptic ulcers occur wherever mucosa is exposed to acid-pepsin:

Duodenum - First part (D1), most common overall
Stomach - Lesser curvature (especially incisura angularis), antrum
Lower esophagus - Due to acid reflux (GERD)
Meckel's diverticulum - Contains ectopic gastric epithelium
Stomal/marginal ulcer - At gastrojejunostomy site

The ulcer tends to occur at the junction between different epithelial types, in the mucosa least resistant to acid damage.

Epidemiology

PUD affects >4 million people annually in the US
Lifetime risk: ~10% in males, ~4% in females
Duodenal ulcers are more common than gastric ulcers (DU:GU = ~4:1)
Gastric ulcers: equal sex incidence, tend to occur in older patients and lower socioeconomic groups

Pathogenesis - The Key Concept

"Imbalance between mucosal protective factors and damaging factors"

Protective Factors

Factor	Mechanism
Mucus layer	Forms gel barrier between lumen and epithelium
HCO3- secretion	Trapped in mucus; neutralizes any H+ that penetrates
Prostaglandin E2	Stimulates mucus + HCO3- secretion; maintains mucosal blood flow
Mucosal blood flow	Delivers O2 and nutrients; removes back-diffused H+
Epithelial tight junctions	Prevent luminal H+ from entering mucosa
Growth factors	Aid mucosal repair

Damaging Factors

Factor	Mechanism
H. pylori	Destroys mucosal barrier via urease (NH3), cytotoxins (CagA), phospholipases
NSAIDs/Aspirin	Inhibit COX → suppress prostaglandin synthesis → loss of mucosal protection
Excess HCl + Pepsin	Direct erosive action on unprotected mucosa
Smoking	Reduces mucosal blood flow; impairs healing
Alcohol	Breaks down mucosal barrier directly
Corticosteroids	Suppress prostaglandin synthesis; impair healing
Stress	Increases acid secretion via vagal stimulation

Etiology

1. Helicobacter pylori (Most Important - 70-75% of PUD)

Gram-negative, microaerophilic, spiral bacterium
Urease splits urea → NH3, which neutralizes local acid, allows survival in gastric lumen
NH3 and NH4+ are cytotoxic to epithelial cells
Virulence factors: CagA toxin (breaks mucosal barrier), VacA (vacuolating cytotoxin)
In gastric ulcer: directly colonizes antral mucosa, releases cytotoxins, destroys protective mucous barrier
In duodenal ulcer (indirect mechanism):
- H. pylori in gastric antrum → inhibits somatostatin from D cells → somatostatin normally inhibits gastrin → "inhibition of inhibition" = excess gastrin secretion → excess HCl
- H. pylori spreads to duodenum → inhibits duodenal HCO3- secretion → inadequate neutralization of H+
Only 5-10% of H. pylori-infected individuals develop ulcers (host factors + bacterial strain variation matter)

2. NSAIDs / Aspirin

Inhibit COX-1 and COX-2 → reduced prostaglandin E2 synthesis
Loss of mucosal protection (mucus, HCO3-, blood flow) → gastric ulcers more than duodenal
Becoming the most common cause of gastric ulcers as H. pylori infection rates fall

3. Zollinger-Ellison Syndrome

Gastrinoma (usually pancreatic islet cell tumor) secretes gastrin constitutively
Massive, unregulated HCl secretion overwhelms all buffering
Multiple peptic ulcers in stomach, duodenum, and even jejunum
Gastrin is not feedback-inhibited by H+ (unlike physiologic G-cell secretion)
Steatorrhea occurs because excessive H+ inactivates pancreatic lipase in the duodenum

4. Other Contributing Factors

Hyperparathyroidism, CRF - hypercalcemia stimulates gastrin production
Cirrhosis, COPD, CKD - associated with increased PUD risk
Parietal cell hyperplasia - increased secretory capacity

Gastric Ulcer vs Duodenal Ulcer - High-Yield Comparison

Feature	Gastric Ulcer	Duodenal Ulcer
Frequency	Less common	More common (4x)
Age	Older patients (50-60s)	Younger patients (30-50s)
Sex	Equal	More in males
Acid secretion	Normal or low (H+ leaks into damaged mucosa)	High (increased parietal cell mass)
Gastrin level	Increased (due to reduced H+ feedback)	Baseline normal; meal-stimulated increased
H. pylori role	Direct mucosal barrier destruction	Indirect via excess H+ delivery to duodenum
Pain and food	Eating may worsen (or no relief)	Eating relieves pain (food buffers H+)
Night pain	Less characteristic	Characteristic (2-3 am - awakens patient)
Malignancy risk	YES - must biopsy to exclude (up to 10x biopsies)	NO - duodenal ulcers almost never malignant
Site	Lesser curvature, incisura angularis, antrum	Anterior wall of D1 (most common)
Blood group	Group A	Group O

Costanzo Physiology 7th Edition, p. 370; Bailey & Love Surgery 28th Ed.

Morphology (Pathology - Robbins)

Gross:

Usually solitary (multiple suggest Zollinger-Ellison)
Round to oval, sharply "punched out" defect
Size: Usually <2 cm (rarely >4 cm); size does NOT differentiate benign from malignant
Margins: flat, overhanging edges (benign); rolled-up edges suggest malignancy
Base: Clean, smooth (benign) vs irregular hemorrhagic (malignant)
Surrounding mucosa shows mucosal folds radiating to the ulcer edge (benign)

Microscopic:

Zone of necrotic fibrinoid debris (superficial)
Active inflammatory exudate (neutrophils)
Granulation tissue with dilated capillaries and fibroblasts
Fibrous/collagenous scar at the base - endarteritis obliterans (thickened vessel walls at the base)

Note: healing epithelium can mimic invasion - must not be mistaken for carcinoma

Clinical Features

Symptoms

Epigastric pain - gnawing, burning, or aching
May radiate to the back (especially if posterior penetration into pancreas)
Periodicity - symptoms for weeks → remission for months → recurrence (due to spontaneous healing and relapse)
Seasonality - worse in spring and autumn
Vomiting - not prominent unless gastric outlet obstruction occurs
Weight loss or gain possible; patients with gastric ulcers often underweight

Examination

Epigastric tenderness is the main finding
Otherwise examination may be unremarkable in uncomplicated PUD

Investigations

Investigation	Findings
OGD (upper endoscopy)	Gold standard - directly visualizes ulcer; allows biopsy
Barium meal (Ba meal)	"Niche" = ulcer crater; gastric ulcer appears as barium pool projecting outside lumen
CLO test (Campylobacter-like organism)	Rapid urease test for H. pylori at endoscopy
Urea breath test (13C-UBT)	Patient drinks 13C-urea → H. pylori urease converts it → 13CO2 expired in breath; non-invasive
H. pylori serology	Detects IgG antibodies; cannot distinguish active from past infection
Stool antigen test	Active H. pylori infection
Serum gastrin	Elevated if Zollinger-Ellison syndrome suspected
Hemoglobin/FBC	Microcytic anemia if chronic blood loss

Complications (Mnemonic: PBS-H)

1. Perforation

Most commonly anterior DU perforates (duodenal ulcers more likely to perforate)
Presents with: sudden severe epigastric pain → generalized peritonitis
Board-like rigidity, shoulder tip pain (phrenic nerve irritation by subphrenic air)
X-ray: Free air under diaphragm (pneumoperitoneum)
Treatment: Emergency surgery (Graham's patch repair)

2. Bleeding (Most Common Complication)

May be chronic (presenting as microcytic iron-deficiency anemia) or acute (hematemesis + melena)
Posterior DU erodes into gastroduodenal artery (most dangerous)
Treatment: Endoscopic hemostasis (adrenaline injection, clips, thermal coagulation), PPIs IV; surgery if endoscopy fails

3. Stenosis / Gastric Outlet Obstruction (GOO)

Chronic DU → fibrosis and scarring → pyloric stenosis
Features: projectile, non-bilious vomiting; visible peristalsis; succussion splash
Metabolic consequence: Hypochloraemic, hypokalaemic metabolic alkalosis (from loss of HCl in vomit)
Treatment: Endoscopic balloon dilatation; surgery (pyloroplasty)

4. Penetration

Ulcer erodes through wall into adjacent structure without free perforation
Posterior GU → pancreas (raised serum amylase)
GU → splenic artery (rare but fatal hemorrhage)
Change in pain character: becomes constant, no longer relieved by food/antacids

5. Malignant Transformation (Gastric Ulcers Only)

Gastric ulcers can harbor carcinoma or undergo malignant change
ALL gastric ulcers require biopsy (minimum 6-10 biopsies from margin and base)
Duodenal ulcers do NOT become malignant

Treatment

Medical (Mainstay)

Step 1: Acid Suppression

Drug	Class	Mechanism
Omeprazole, Pantoprazole, Rabeprazole	Proton Pump Inhibitors (PPIs)	Irreversibly block H+/K+ ATPase (proton pump) on parietal cells
Ranitidine, Famotidine	H2-receptor antagonists	Block histamine H2 receptors on parietal cells → 70-80% reduction in acid
Vonoprazan	Potassium-competitive acid blocker (PCAB)	Binds K+-binding region of proton pump; more rapid, sustained acid suppression

Step 2: H. pylori Eradication

Standard Triple Therapy (7-14 days):

PPI (twice daily) + Amoxicillin + Clarithromycin

Quadruple Therapy (if clarithromycin resistance):

PPI + Bismuth + Metronidazole + Tetracycline

Confirm eradication with urea breath test 4 weeks after completing therapy.

Additional Measures

Misoprostol (prostaglandin E1 analogue) - protects gastric mucosa; used for NSAID-induced ulcers
Sucralfate - coats ulcer base; forms a protective barrier
Antacids - neutralize HCl; symptomatic relief
Lifestyle: Stop smoking, avoid NSAIDs and alcohol, stress reduction

Surgical (Rarely Indicated Now)

Performed only for complications (perforation, uncontrolled bleeding, obstruction) or refractory disease.

Vagotomy (truncal or selective) - cuts vagal supply to parietal cells → reduces acid
Partial gastrectomy (Billroth I or II) - removes ulcer-bearing mucosa
Pyloroplasty - relieves GOO

Zollinger-Ellison Syndrome (ZES) - Special Topic

Feature	Detail
Cause	Gastrinoma (most commonly in pancreatic head or duodenum)
Gastrin levels	Very high (>1000 pg/mL)
Ulcers	Multiple, unusual sites (jejunum), recurrent
Diarrhea + Steatorrhea	Excess H+ inactivates pancreatic lipase
Diagnosis	Secretin stimulation test (gastrin paradoxically rises in ZES); CT/MRI to locate tumor
Treatment	High-dose PPI + surgical resection of tumor; if metastatic, somatostatin analogues

Key Exam Points to Remember

"No acid, no ulcer" - Schwartz's Surgery principle
H. pylori causes DU indirectly (inhibits somatostatin → excess gastrin) and GU directly (mucosal barrier destruction)
Urease test principle: H. pylori urease + 13C-urea → 13CO2 (expired in breath)
Gastric ulcers: biopsy is mandatory to exclude malignancy; duodenal ulcers do not require biopsy
Metabolic complication of GOO: hypochloraemic hypokalaemic metabolic alkalosis
The most common complication of PUD is bleeding; the most dangerous is perforation
Posterior DU erodes into gastroduodenal artery → bleeding; posterior GU erodes into pancreas → penetration
PPIs work better than H2 blockers because they act at the final common pathway of acid secretion
NSAIDs cause ulcer by COX-1 inhibition → loss of prostaglandin → less mucus, less HCO3-, less blood flow
Zollinger-Ellison: multiple ulcers + diarrhea + high gastrin; secretin test is diagnostic

Sources

Guyton & Hall Textbook of Medical Physiology, Chapter 67 (Peptic Ulcer)
Robbins & Kumar Basic Pathology, Chapter 13 (Peptic Ulcer Disease)
Costanzo Physiology 7th Edition, Chapter 8 (Table 8.4)
Bailey & Love's Short Practice of Surgery 28th Edition, Chapter 67

Can you show diagram of the lesion with label

Finding Sources

Generating Image

Medical textbook-style labeled cross-section diagram of a peptic ulcer showing all four microscopic zones from surface to base: Zone 1 - Fibrinoid necrotic debris (superficial), Zone 2 - Acute inflammatory infiltrate with neutrophils, Zone 3 - Granulation tissue with new capillaries and fibroblasts, Zone 4 - Fibrotic scar with endarteritis obliterans at base. Show the surrounding intact gastric mucosa (mucus layer, epithelium, lamina propria, muscularis mucosae, submucosa, muscularis propria) on either side of the ulcer crater. Include a blood vessel at the base with thickened wall (endarteritis obliterans). Label each zone clearly with arrows. Clean white background, educational anatomy illustration style.

Generating Image

Medical diagram of stomach and duodenum showing labeled sites of peptic ulcer disease. Show a clear anatomical outline of the stomach and proximal duodenum with labels pointing to: 1) Lesser curvature of stomach, 2) Incisura angularis (most common gastric ulcer site), 3) Gastric antrum, 4) First part of duodenum D1 (most common duodenal ulcer site), 5) Pylorus / pyloric channel, 6) Cardia / lower esophagus (GERD-related), 7) Meckel's diverticulum (ectopic gastric mucosa). Mark duodenal ulcer sites in blue and gastric ulcer sites in red. Add a small inset showing benign ulcer features: punched out edges, flat margins, radiating mucosal folds. Clean educational medical illustration style, white background, clear labeled arrows.

Here are two labeled diagrams for your exam preparation:

Diagram 1 - Cross-Section / Histological Zones of a Peptic Ulcer

Labeled cross-section of peptic ulcer showing four histological zones

The Four Microscopic Zones (Surface → Base):

Zone	Contents	Key Feature
Zone 1 (Surface)	Fibrinoid necrotic debris	Dead tissue sloughing off
Zone 2	Acute inflammatory exudate	Neutrophil infiltration
Zone 3	Granulation tissue	New capillaries + fibroblasts
Zone 4 (Base)	Fibrous/collagenous scar	Endarteritis obliterans - thickened, obliterated vessel walls

Exam tip: The four zones are sometimes asked as a short answer. Endarteritis obliterans at the base is a classic histology MCQ point. The healing epithelium can mimic invasion - do NOT misinterpret as carcinoma.

Diagram 2 - Anatomical Sites of Peptic Ulcers

Labeled anatomical diagram showing sites of peptic ulcer in stomach and duodenum

Sites Summary:

Site	Type	Notes
D1 (first part duodenum)	Duodenal ulcer	Most common overall; anterior wall perforates, posterior wall bleeds (gastroduodenal artery)
Incisura angularis	Gastric ulcer	Most common gastric site
Lesser curvature	Gastric ulcer	Benign; malignant ulcers more on greater curvature
Pyloric channel	Similar to DU	Requires biopsy - can be malignant
Lower esophagus	Peptic (GERD)	Acid reflux related
Meckel's diverticulum	Marginal ulcer	Ectopic gastric mucosa
Gastrojejunostomy stoma	Stomal ulcer	Post-surgery; on jejunal side

Bonus - Gross features of a BENIGN peptic ulcer (exam favourite):

Round/oval, punched-out crater

Flat, overhanging edges (NOT rolled-up - that suggests malignancy)

Mucosal folds radiate toward the ulcer margin

Clean, smooth base

Usually <2 cm (though size alone cannot confirm benign vs malignant)

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