Peptic ulcer

Peptic Ulcer

1. Definition
Peptic ulcer is a loss of continuity of the gastric or duodenal mucosa that extends beyond the muscularis mucosae and is usually accompanied by local inflammation.
It represents a breach in the protective barrier of the upper gastrointestinal tract.

2. Synonyms (if any)

• Gastric ulcer – ulcer located in the stomach.
• Duodenal ulcer – ulcer located in the first part of the duodenum.
  Both terms specify the anatomical site of the same pathological process.

3. Causes / Etiology

• Helicobacter pylori infection – the organism adheres to the mucosa, produces urease and toxins, and provokes chronic gastritis that weakens the mucosal defence. It is the most common cause worldwide.
• Non‑steroidal anti‑inflammatory drugs (NSAIDs) – inhibit cyclo‑oxygenase → ↓ prostaglandin synthesis → reduced mucus and bicarbonate secretion, and impaired mucosal blood flow. Long‑term use markedly raises ulcer risk.
• Stress (physiological or psychological) – increases catecholamines and gastric acid secretion, and may cause mucosal ischemia. Seen especially in severe illness or trauma.
• Smoking – nicotine causes vasoconstriction, reduces mucosal blood flow and impairs healing. Smokers have higher recurrence rates.
• Alcohol excess – irritates the mucosa and may potentiate acid secretion. Acute binge drinking can precipitate bleeding.
• Genetic predisposition – family history of ulcer disease suggests inherited variations in mucosal defence or acid regulation. Important in younger patients with no other risk factors.

Each factor either enhances aggressive forces or weakens protective mechanisms.

4. Types / Classification

All types share the same underlying mucosal breach but differ in location, precipitating factors and symptom timing.

5. Pathophysiology / Pathology

1. Aggressive factors – gastric acid, pepsin, bile salts, H. pylori toxins, NSAID‑induced prostaglandin loss.
2. Defence mechanisms – mucus–bicarbonate layer, mucosal blood flow, cell regeneration, prostaglandins, bicarbonate secretion.
3. Imbalance – when aggressive forces exceed defence, epithelial cells are damaged, exposing the underlying lamina propria.
4. Inflammation – neutrophils and lymphocytes infiltrate, releasing cytokines that further impair healing.
5. Ulcer crater formation – continued acid attack enlarges the defect, creating a visible ulcer crater.
6. Healing or complication – with restored balance, granulation tissue forms and ulcer heals; if imbalance persists, complications such as bleeding, perforation or fibrosis develop.
   The process is dynamic; any factor that tips the balance can initiate or perpetuate ulceration.

6. Clinical Features

General features – epigastric discomfort, nausea, loss of appetite, weight loss, occasional vomiting of blood (hematemesis) or black stools (melena).
Specific to gastric ulcer – pain 30 min after meals, may be relieved by antacids, early satiety, possible vomiting of food.
Specific to duodenal ulcer – pain 2–4 h after meals or at night, relieved by food or antacids, may have a “hunger pang” pattern.
Acute presentation – sudden severe epigastric pain, signs of peritonitis (rigidity, rebound), hypotension if bleeding.
Chronic presentation – recurrent, dull‑burning pain with a predictable pattern, may be intermittent for years.
These features help differentiate ulcer type and indicate possible complications.

7. Complications

• Acute
  • Perforation: ulcer erodes full thickness → free air under diaphragm, acute abdomen, surgical emergency.
  • Massive hemorrhage: erosion into a submucosal artery → hematemesis, melena, hypovolemic shock.
• Chronic
  • Gastric outlet obstruction: scarring and fibrosis at pylorus or duodenal bulb → vomiting of undigested food, weight loss.
  • Penetration: ulcer extends into adjacent organ (pancreas, liver) → localized pain, possible fistula formation.
  • Malignant transformation: long‑standing gastric ulcer may evolve into gastric carcinoma (rare).

Early detection and treatment are essential to avoid these life‑threatening outcomes.

8. Investigations / Diagnosis

• Upper gastrointestinal endoscopy – visualises ulcer size, location, depth; allows biopsy to exclude malignancy. Gold standard for diagnosis.
• Barium meal/upper GI series – outlines ulcer crater when endoscopy unavailable; useful for detecting perforation. Provides radiographic confirmation.
• H. pylori testing – urea breath test, stool antigen, rapid urease test on biopsy, or serology. Guides eradication therapy.
• Complete blood count – assesses anemia from chronic blood loss. Helps gauge severity of bleeding.
• Serum gastrin level – elevated in Zollinger‑Ellison syndrome, a rare cause of refractory ulcer. Used when hyper‑acidic ulcer suspected.
• Abdominal X‑ray (erect) – detects free air under diaphragm in perforation. Rapid bedside test for acute perforation.

Each test contributes specific information for confirming ulcer, identifying cause, and planning management.

9. Differential Diagnosis

1. Gastro‑oesophageal reflux disease (GERD) – heartburn and regurgitation dominate; endoscopy shows oesophagitis rather than ulcer crater. Distinguished by oesophageal symptoms and lack of ulcer scar.
2. Acute gastritis – diffuse mucosal inflammation without a discrete crater; pain often less localized and improves rapidly with antacids. Biopsy shows inflammatory infiltrate without ulceration.
3. Pancreatitis – epigastric pain radiating to back, elevated serum amylase/lipase, often associated with alcohol use. Imaging shows pancreatic inflammation, not ulcer.
4. Biliary colic/cholelithiasis – right upper quadrant pain after fatty meals, ultrasound shows gallstones. Pain pattern and imaging differentiate from ulcer.

Accurate history, examination and targeted investigations separate ulcer from these mimics.

10. Management / Treatment

• General management

  • Discontinue NSAIDs and other ulcerogenic drugs.
  • Counsel on smoking cessation and alcohol moderation.
  • Reduce stress through relaxation techniques and adequate sleep.
    These measures remove aggravating factors and support mucosal healing.

• Modern medicine treatment

  • H. pylori eradication – triple therapy (clarithromycin + amoxicillin + PPI) for 14 days or quadruple therapy (metronidazole + tetracycline + bismuth + PPI). Eradication heals most ulcers and prevents recurrence.
  • Acid suppression – Proton‑pump inhibitors (omeprazole, pantoprazole) 20–40 mg twice daily for 4–8 weeks; H2‑receptor antagonists (ranitidine, famotidine) as alternatives. Reduces acid to allow ulcer repair.
  • Cytoprotective agents – sucralfate (forms protective coating) or misoprostol (prostanoid analogue) when NSAID use cannot be stopped. Enhances mucosal defence.
  • Management of complications – urgent surgery for perforation; endoscopic hemostasis or angiographic embolisation for bleeding; dilatation or surgery for obstruction. Targeted intervention based on complication severity.

• Diet and lifestyle advice

  • Eat small, regular meals; avoid large, fatty or highly spiced dishes that stimulate acid.
  • Limit caffeine and carbonated drinks; they may increase gastric secretions.
  • Maintain adequate hydration; water dilutes gastric acid.
  • Encourage a balanced diet rich in fruits, vegetables and lean protein to promote healing.
    Lifestyle modification reduces recurrent irritation and supports overall health.

11. Homeopathic Therapeutics (7–8 remedies, each with 7–8 bullet points)

For each remedy the bullets are written in simple sentences as a student would note them.

Nux vomica

• Causation: over‑use of stimulants (coffee, tea, alcohol) and NSAIDs; stress from over‑work.
• Characteristic symptoms: burning epigastric pain that is worse after eating, especially rich food.
• Modalities: pain worsens from the first bite, improves a little after vomiting; better from warm drinks.
• Mental state: irritable, impatient, feels “under pressure” and “rushed”.
• Thirst and appetite: great thirst for warm water; appetite reduced, especially for meat.
• Discharges/secretions: may have sour taste in mouth, occasional nausea with retching.
• Physical generals: pale, restless, often with headache over the temples.
• Suitable constitution: busy professionals, students pulling all‑nighters, people with a “hard‑working” temperament.
  Helps by addressing the irritant‑induced hyper‑acidity and stress component of the ulcer.

Lycopodium clavatum

• Causation: hereditary tendency, poor digestion of heavy foods, anxiety about performance.
• Characteristic symptoms: bloating, flatulence, epigastric pain that improves when lying on left side.
• Modalities: worse in the evening, after cold drinks; better after warm milk.
• Mental state: self‑critical, fear of being judged, low confidence in public speaking.
• Thirst and appetite: prefers warm drinks; appetite irregular, often craves sweets.
• Discharges/secretions: may have sour belching, occasional constipation.
• Physical generals: low‑grade fever, cold hands and feet, tendency to feel chilly.
• Suitable constitution: people with a “shy” or “introverted” nature, often thin‑built.
  Balances the digestive weakness and emotional inhibition that predispose to ulcer formation.

Pulsatilla pratensis

• Causation: emotional upset, changeable moods, sudden grief or disappointment.
• Characteristic symptoms: epigastric pain that shifts location, feels better in open air.
• Modalities: worse in warm, stuffy rooms; better in fresh, cool air.
• Mental state: tearful, seeks consolation, feels “weary” and “indifferent”.
• Thirst and appetite: little thirst, appetite variable, often prefers cold drinks.
• Discharges/secretions: thin, bland stool; occasional mild diarrhoea.
• Physical generals: pale, soft skin, tendency to feel chilly, especially in the evenings.
• Suitable constitution: young women, people who are “people‑pleasers” and easily upset.
  Relieves the fluctuating emotional stress that can aggravate ulcer pain.

Carbo veg (Carbo vegetabilis)

• Causation: excessive intake of raw vegetables, over‑eating, prolonged fasting periods.
• Characteristic symptoms: gnawing epigastric pain that is worse on an empty stomach.
• Modalities: worse when lying on back, better when sitting up and breathing fresh air.
• Mental state: apathetic, feels “heavy” and “sluggish”.
• Thirst and appetite: great thirst for cold water; appetite poor, especially for solids.
• Discharges/secretions: may have foul‑smelling flatulence, occasional vomiting of mucus.
• Physical generals: pallor, cold extremities, weak pulse.
• Suitable constitution: people with a “low‑energy” disposition, often thin and frail.
  Provides a gentle, nutritive stimulus to restore mucosal vitality.

Kali mur (Kali muriaticum)

• Causation: chronic irritation from acidic foods, alcohol, or long‑term NSAID use.
• Characteristic symptoms: burning pain that is relieved by antacids but returns quickly.
• Modalities: worse after eating sour or spicy foods; better after lying on left side.
• Mental state: irritable, impatient, feels “tight‑chested”.
• Thirst and appetite: thirst for cold water; appetite moderate, prefers bland foods.
• Discharges/secretions: may have sour taste in mouth, occasional sour vomiting.
• Physical generals: dry skin, tendency to develop eczema, weak digestion.
• Suitable constitution: individuals with a “hard‑working” lifestyle, often middle‑aged men.
  Targets the acidic environment and mucosal irritation that maintain the ulcer.

Natrum mur (Natrum muriaticum)

• Causation: emotional suppression, grief, and a tendency to retain “salt” (fluid) in the body.
• Characteristic symptoms: dull, lingering epigastric ache that worsens at night.
• Modalities: worse from salty foods, better from fresh air and light exercise.
• Mental state: withdrawn, prefers solitude, often “holds back” tears.
• Thirst and appetite: thirst for small sips of water; appetite reduced, especially for meat.
• Discharges/secretions: dry mouth, scanty urine, occasional constipation.
• Physical generals: dry skin, brittle nails, tendency to develop headaches.
• Suitable constitution: introverted, emotionally restrained persons, often with a history of “unexpressed” sorrow.
  Helps by releasing emotional tension and correcting the salt‑water imbalance that can aggravate ulcer pain.

Arsenicum album

• Causation: prolonged use of irritating chemicals, alcohol, or chronic stress.
• Characteristic symptoms: burning epigastric pain that is relieved by warm drinks, worse at night.
• Modalities: worse from cold, dry weather; better from warmth and rest.
• Mental state: anxious, fearful of death, constantly “checking” symptoms.
• Thirst and appetite: great thirst for cold water; appetite poor, prefers light, dry foods.
• Discharges/secretions: may have watery diarrhoea, occasional vomiting of clear fluid.
• Physical generals: trembling, restlessness, dry skin, thin build.
• Suitable constitution: people who are “over‑anxious”, often with a history of chronic illness.
  Addresses the anxiety‑driven hyper‑acidity and the drying effect of chronic irritants.

12. Prognosis
With appropriate eradication of H. pylori, cessation of NSAIDs, and adequate acid suppression, most peptic ulcers heal within 6–8 weeks and recurrence is low.
Factors that worsen prognosis include continued smoking, ongoing NSAID use, delayed diagnosis of complications, and poor compliance with therapy.

13. Prevention

• Avoid unnecessary NSAID use; use the lowest effective dose with gastro‑protective agents if needed.
• Test and treat H. pylori infection in high‑risk individuals.
• Quit smoking and limit alcohol intake.
• Manage stress through regular exercise, adequate sleep, and relaxation techniques.
  These measures markedly reduce the incidence of new ulcers and prevent relapse.

14. Diet