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Peptic Ulcer Disease

Tashkent Medical AcademyDepartment of Treatment

TASHKENT - 2011

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

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

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Microscopic section of a gastric gland

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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

Cells

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Components involved in providing gastroduodenal mucosal defense and repair

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Primary chronic recurrent disease of upper

gastrointestinal tract associated with

circumscribed ulcers within stomach and duodenum

Peptic ulcer disease

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is disruption of the mucosal integrity of the stomach and/or

duodenum leading to a local defect or excavation due to active

inflammation

Ulcer

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1 – submucosa2 – hard, undermined margin

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Peptic Ulcers: Gastric & Dudodenal

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A break in the mucosa not penetrating muscularis mucosa

Peristalsis is not affected Heals rapidly

Erosion

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

Epidemiology

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Helicobacter pyloriNSAIDs (aspirin)

Etiology

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Healthy subjects 20-50% Chronic active gastritis 100% Duodenal ulcer >90% Gastric ulcer 50 - 80%

Gastric adenocarcinoma 90% Gastric lymphoma 85%

H.pylori in GI diseases

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Barry Marshal Robin Warran

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Heredity

Emotional stress

Blood group

Predisposing

factors

Active duodenitis or gastritis

Gastric metaplasia

Producing factors

Factors

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Aggravating causes of, and defense mechanisms against, peptic ulceration

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Any area where pepsin and acid are present

Prevailing locations◦ Duodenum: duodenal bulb◦ Stomach: over lesser curvature

Locations of ulcers

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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

Johnson’s classification (according to site, clinical manifestations)

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Mild

Exacerbations 1 time/year

Easily treated

Few symptoms

Medium-severe

Exacerbations 2-3 times/year

Treated by full course therapy

Severe

Frequent exacerbations

Absence of stable remission

Evident clinical manifestation

Forms(according to severity)

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Clinical features

•Gastric ulcer: in the centre of or left to epigastrium•Duodenal ulcer: to the right of midline in epigastruimLOCATION•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 mealTIME•Burning •Gnawing•Dull •Cramplike

CHARACTER

•Cardiac area•Left scapula•Thoracic part of spinal column•Lumbar region

IRRADIATION

•Antacids•Milk•Meal•After vomiting

PAIN RELIEF

PAIN

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Clinical features

•Related with gastroesophageal reflux•After mealHEARTBURN

•More common in gastric ulcersBELCHING

•At the peak of pain•More common in gastric ulcers•Pain relief after vomiting

NAUSEA & VOMITING

•Excessive APPETITE

DYSPEPSIA

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Clinical examination Vegetative dystonia: cold, damp palms,

mottled skin, bradycardia, hypotension Palpation: tenderness Percussion: Mendel’s symptom,

succussion splash (gastric outlet obstruction)

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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

GP in Uzbekistan

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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

X-ray(Barium meal)

•Niche sign•Retention of barium meal•Duodenogastric reflux•Fold convergence•Local spasm of stomach

Laboratory and instrumental examination

*BAO – basal acid output*MAO – maximal acid output •Biopsy

•Test with Insulin•Test with Histamine•pH meter•Gastrin concentration in serum

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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

Diagnosis of Helicobacter pylori infection

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Radiology in PUD

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Duodenal Ulcer

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Peptic Ulcers: Gastric & Dudodenal

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Gastric ulcer in endoscopy

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Gastric ulcer

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Gastric erosions

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Duodenal ulcer

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Duodenal ulcer

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

Complications

20%

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Haemorrhage

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HematemesisMelena Bergman’s symptom

Haemorrhage

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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

Stages of bleeding by Forrest(endoscopy)

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Ulcer perforation

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Gastric outlet stenosis

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Compensatio

n1-0.5 cm

Subcompensation

0.5-0.3 cm

Decompensat

ion<0.3 cm

Stages of stenosis

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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

Differential Diagnosis

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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 – Medical nutrition

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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

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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)

Treatment - Drugs

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H2-blockers: gynecomastia, impotence

Aluminum hydroxide: constipation

Magnesium hydroxide: diarrhea

Side effects of drugs

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De-nol1 tablet 3 times/day, 4-6 weeks

Clarythromycin250 mg, 2 times/day, 7-10 days

Metronidazole250 mg, 4 times/day, 14 days

Therapy regimensMONOTHERAPY

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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 regimensDOUBLE THERAPY

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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]

Therapy regimensTRIPLE THERAPY

A week

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Omeprazole + De-nol+

Amoxycillin OR Clarythromycin +Metronidazole

Therapy regimensQUADRUPLE THERAPY

10 days

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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

Prophylaxy

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

Chu Hui Weng

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THANKS FOR YOUR ATTENTION AND

PATIENCE!!!