Tashkent Medical Academy Peptic Ulcer Disease

Erect radiographic image of esophagus (lower portion), stomach and first part of duodenum after ingestion of contrast medium

Topography and internal surface of a stomach (blue line represent notional lines marking the parts of the stomach)

Microscopic section of a gastric gland

Cells THE PARIETAL CELLS – acid secretion THE CHIEF CELLS – pepsinogen secretion THE ENDOCRINE CELLS: The G-cells – gastrin secretion The D-cells – somatostatin secretion The ECL-cells – histamine production THE MUCOUS NECK CELLS – mucus secretion

Components involved in providing gastroduodenal mucosal defense and repair

Peptic ulcer disease Primary chronic recurrent disease of upper gastrointestinal tract associated with circumscribed ulcers within stomach and duodenum

Ulcer is disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation

1 – submucosa 2 – hard, undermined margin

Peptic Ulcers: Gastric & Dudodenal

Erosion A break in the mucosa not penetrating muscularis mucosa Peristalsis is not affected Heals rapidly

Epidemiology Duodenal ulcers (5x) > gastric ulcers ♂ (4x) > ♀ Urban resident > rural resident

Etiology Helicobacter pylori NSAIDs (aspirin)

H.pylori in GI diseases Healthy subjects 20-50% Chronic active gastritis 100% Duodenal ulcer >90% Gastric ulcer 50 - 80% Gastric adenocarcinoma 90% Gastric lymphoma 85%

Barry Marshal Robin Warran

Factors Predisposing factors Heredity Emotional stress Blood group Producing factors Active duodenitis or gastritis Gastric metaplasia

Aggravating causes of, and defense mechanisms against, peptic ulceration

Locations of ulcers Any area where pepsin and acid are present Prevailing locations Duodenum: duodenal bulb Stomach: over lesser curvature

Johnson’s classification (according to site, clinical manifestations) I type – ulcers of lesser curvature of stomach II type – combined ulcers of stomach and duodenum III type – ulcers of prepyloric part stomach IV type – ulcers of duodenum

Forms (according to severity) Mild 1 time/year Exacerbations Easily treated Few symptoms Medium-severe 2-3 times/year Treated by full course therapy Severe Frequent exacerbations Absence of stable remission Evident clinical manifestation

PAIN Clinical features LOCATION Gastric ulcer: in the centre of or left to epigastrium Duodenal ulcer: to the right of midline in epigastruim TIME Early: 0.5-1 h after meal, duration 1.5-2 hh, in gastric ulcers Late: 1.5-2 hh after meal, in duodenal and pyloric ulcers Nocturnal Pain of “hunger”: 6-7 hh after meal and ceased after meal CHARACTER Burning Gnawing Dull Cramplike IRRADIATION Cardiac area Left scapula Thoracic part of spinal column Lumbar region PAIN RELIEF Antacids Milk Meal After vomiting

DYSPEPSIA Clinical features HEARTBURN Related with gastroesophageal reflux After meal BELCHING More common in gastric ulcers NAUSEA & VOMITING At the peak of pain Pain relief after vomiting APPETITE Excessive

Clinical examination Vegetative dystonia: cold, damp palms, mottled skin, bradycardia, hypotension Palpation: tenderness Percussion: Mendel’s symptom, succussion splash (gastric outlet obstruction)

GP in Uzbekistan Non-complicated PUD – service of 1st category Complicated PUD – service of 2nd category Services of 3.1 category: Professional examination Interpretation of clinical and biochemical tests CBC Gastric lavage Diet prescription Services of 3.2 category: Analysis of gastric juice and duodenal contents Ultrasound Endoscopy Radiologic examination Biopsy Services of 4 category: Rational nutrition Struggle with harmful habits Personal hygiene

Laboratory and instrumental examination CBC ↑Hb ↑Erythrocyte Secretory function of stomach ↑BAO (N=5 mmol/h) ↑MAO (N=18-26 mmol/h) Occult blood feces analysis Latent PUD Exacerbation Stomach cancer Endoscopy Round or oval Edges: sharp, hyperemic, edematous (Barium meal) X-ray Niche sign Retention of barium meal Duodenogastric reflux Fold convergence Local spasm of stomach *BAO – basal acid output *MAO – maximal acid output Biopsy Test with Insulin Test with Histamine pH meter Gastrin concentration in serum

Diagnosis of Helicobacter pylori infection Invasive( through endoscopy) Gastric biopsy and staining Culture of biopsy specimen Tests using urease enzyme in biopsy specimens Non-invasive: Urea breath test H.pylori antibodies Stool antigen Salivary antigen

Radiology in PUD

Duodenal Ulcer

Peptic Ulcers: Gastric & Dudodenal

Gastric ulcer in endoscopy

Gastric ulcer

Gastric erosions

Duodenal ulcer

Duodenal ulcer

20% Complications Haemorrhage Perforation Penetration (pancreas, liver) Pyloric stenosis (due to scarring) Malignization 20%

Haemorrhage

Haemorrhage Hematemesis Melena Bergman’s symptom

Stages of bleeding by Forrest (endoscopy) I STAGE Actively bleeding ulcer II STAGE Signs of stopped fresh haemorrhage Thrombosed vessels at the bottom of ulcer Clot of blood III STAGE Absence of bleeding apparent signs

Ulcer perforation

Gastric outlet stenosis

Stages of stenosis Compensation 1-0.5 cm Subcompensation 0.5-0.3 cm Decompensation <0.3 cm

Differential Diagnosis Neoplasm of the stomach Pancreatitis Pancreatic cancer Diverticulitis Nonulcer dyspepsia (also called functional dyspepsia) Cholecystitis Gastritis MI—not to be missed if having chest pain

Treatment – Medical nutrition Diet №1: white stale bread, vegetable soups, softly boiled porridge, potato mash, fish, birds, mature fruits, berry and fruit juices, cottage cheese, milk, omelette, pudding Banned: spicy foods, marinated and smoked products Frequent small meals: 6-7 times a day

Treatment - Drugs H.pylori supressors: De-nol, Metronidazole, Furazolidone, Oxacillin, Amoxycillin Antisecretory drugs M-anticholinergic drugs: Nonselective: Atropine, Platyphyllin, Methacin Selective: Gastrozepine, Pirenzepine H2-histamine receptor blockers: Cimetidine, Ranitidine, Famotidine Proton pomp inhibitors: Omeprazole, Lansoprazole, Rabeprazole Antagonists of gastrin receptors: Milid, Proglumide Antacids: Magnesium hydroxide, Aluminum hydroxide, Almagel, Maalox

Treatment - Drugs Gastrocytoprotectors Cytoprotectors that stimulate mucus production: Carbenoxolone, synthetic prostaglandins (Enprostile, Misoprostole) Cytoprotectors that form protective film: Sucralfate, colloid bismuth (De-nol), Smecta Astringents: Vicaline, Vicair Drugs that normalize motor function of stomach and duodenum (Metoclopramide), spasmolytics (Papaverine, No-spa)

Side effects of drugs H2-blockers: gynecomastia, impotence Aluminum hydroxide: constipation Magnesium hydroxide: diarrhea

Therapy regimens MONOTHERAPY De-nol 1 tablet 3 times/day, 4-6 weeks Clarythromycin 250 mg, 2 times/day, 7-10 days Metronidazole 250 mg, 4 times/day, 14 days

Therapy regimens DOUBLE THERAPY De-nol [4-6 weeks] + Metronidazole [10-14 days] De-nol [4-6 weeks] + Tetracyclin OR Amoxycillin [10 days] Amoxycillin OR Clarythromycin [7- 10 days] + Omeprazole [40 mg, 4-6 weeks]

Therapy regimens TRIPLE THERAPY De-nol [4-6 weeks] + Metronidazole [10-14 days] Tetracyclin [7-10 days] Omeprazole + Amoxycillin OR Clarythromycin + Metronidazole Metronidazole [10-14 days] + Amoxycillin [10 days] + Ranitidine [150 mg, 10-14 days] A week

Therapy regimens QUADRUPLE THERAPY Omeprazole + De-nol+ Amoxycillin OR Clarythromycin + Metronidazole 10 days

Prophylaxy Primary Revelation and elimination of risk factors Sanitary and prophylactic measures Secondary Early diagnosis and timely treatment Screening, professional examination, questionnarires Tertiary Prevention of complications

To avoid sickness, eat less; to prolong life, worry less. Chu Hui Weng

THANKS FOR YOUR ATTENTION AND PATIENCE!!!