Tashkent Medical Academy Peptic Ulcer Disease 1 2

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Tashkent Medical Academy Peptic Ulcer Disease 1

Tashkent Medical Academy Peptic Ulcer Disease 1

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

Erect radiographic image of esophagus (lower portion), stomach and first part of duodenum after ingestion of contrast medium 3

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

Topography and internal surface of a stomach (blue line represent notional lines marking the parts of the stomach) 4

Microscopic section of a gastric gland 5

Microscopic section of a gastric gland 5

Cells �THE PARIETAL CELLS – acid secretion �THE CHIEF CELLS – pepsinogen secretion �THE

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 6

Components involved in providing gastroduodenal mucosal defense and repair 7

Components involved in providing gastroduodenal mucosal defense and repair 7

Peptic ulcer disease Primary chronic recurrent disease of upper gastrointestinal tract associated with circumscribed

Peptic ulcer disease Primary chronic recurrent disease of upper gastrointestinal tract associated with circumscribed ulcers within stomach and duodenum 8

Ulcer is disruption of the mucosal integrity of the stomach and/or duodenum leading to

Ulcer is disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation 9

1 – submucosa 2 – hard, undermined margin 10

1 – submucosa 2 – hard, undermined margin 10

Peptic Ulcers: Gastric & Dudodenal 11

Peptic Ulcers: Gastric & Dudodenal 11

�A Erosion break in the mucosa not penetrating muscularis mucosa � Peristalsis is not

�A Erosion break in the mucosa not penetrating muscularis mucosa � Peristalsis is not affected � Heals rapidly 12

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

Epidemiology �Duodenal ulcers (5 x) > gastric ulcers �♂ (4 x) > ♀ �Urban resident > rural resident 13

Etiology �Helicobacter pylori �NSAIDs (aspirin) 14

Etiology �Helicobacter pylori �NSAIDs (aspirin) 14

H. pylori in GI diseases �Healthy subjects �Chronic active gastritis �Duodenal ulcer �Gastric adenocarcinoma

H. pylori in GI diseases �Healthy subjects �Chronic active gastritis �Duodenal ulcer �Gastric adenocarcinoma �Gastric lymphoma 20 -50% 100% >90% 50 - 80% 90% 85% 15

Barry Marshal Robin Warran 16

Barry Marshal Robin Warran 16

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

Factors Predisposing factors Producing factors Heredity Active duodenitis or gastritis Emotional stress Gastric metaplasia Blood group 17

Aggravating causes of, and defense mechanisms against, peptic ulceration 18

Aggravating causes of, and defense mechanisms against, peptic ulceration 18

� Any Locations of ulcers area where pepsin and acid are present � Prevailing

� Any Locations of ulcers area where pepsin and acid are present � Prevailing locations ◦ Duodenum: duodenal bulb ◦ Stomach: over lesser curvature 19

Johnson’s classification (according to site, clinical manifestations) �I type – ulcers of 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 20

Forms (according to severity) Mild Exacerbations 1 time/year Medium -severe Severe Exacerbations Frequent exacerbations

Forms (according to severity) Mild Exacerbations 1 time/year Medium -severe Severe Exacerbations Frequent exacerbations 2 -3 times/year Absence of stable remission Easily treated Few symptoms Treated by full course therapy Evident clinical manifestation 21

Clinical features LOCATION TIME CHARACTER IRRADIATION PAIN RELIEF PAIN • Gastric ulcer: in the

Clinical features LOCATION TIME CHARACTER IRRADIATION PAIN RELIEF PAIN • Gastric ulcer: in the centre of or left to epigastrium • Duodenal ulcer: to the right of midline in epigastruim • 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 • Burning • Gnawing • Dull • Cramplike • Cardiac area • Left scapula • Thoracic part of spinal column • Lumbar region • Antacids • Milk • Meal • After vomiting 22

Clinical features DYSPEPSIA HEARTBURN • Related with gastroesophageal reflux • After meal BELCHING •

Clinical features DYSPEPSIA HEARTBURN • Related with gastroesophageal reflux • After meal BELCHING • More common in gastric ulcers NAUSEA & VOMITING • At the peak of pain • More common in gastric ulcers • Pain relief after vomiting APPETITE • Excessive 23

Clinical examination � Vegetative dystonia: cold, damp palms, mottled skin, bradycardia, hypotension � Palpation:

Clinical examination � Vegetative dystonia: cold, damp palms, mottled skin, bradycardia, hypotension � Palpation: tenderness � Percussion: Mendel’s symptom, succussion splash (gastric outlet obstruction) 24

GP in Uzbekistan � Non-complicated PUD – service of 1 st category � Complicated

GP in Uzbekistan � Non-complicated PUD – service of 1 st category � Complicated PUD – service of 2 nd category � Services of 3. 1 category: � Services of 3. 2 category: � Services of 4 category: ◦ ◦ ◦ Professional examination Interpretation of clinical and biochemical tests CBC Gastric lavage Diet prescription ◦ ◦ ◦ Analysis of gastric juice and duodenal contents Ultrasound Endoscopy Radiologic examination Biopsy ◦ Rational nutrition ◦ Struggle with harmful habits ◦ Personal hygiene 25

Laboratory and instrumental examination X-ray CBC • ↑Hb • ↑Erythrocyte Secretory function of stomach

Laboratory and instrumental examination X-ray CBC • ↑Hb • ↑Erythrocyte Secretory function of stomach • ↑BAO (N=5 mmol/h) • ↑MAO (N=1826 mmol/h) *BAO – basal acid output *MAO – maximal acid output Occult blood feces analysis • Latent PUD • Exacerbation • Stomach cancer Endoscopy • Round or oval • Edges: sharp, hyperemic, edematous (Barium meal) • Niche sign • Retention of barium meal • Duodenogastric reflux • Fold convergence • Local spasm of stomach • Biopsy • Test with Insulin • Test with Histamine • p. H meter • Gastrin concentration in serum 26

Diagnosis of Helicobacter pylori infection � Invasive( through endoscopy) ◦ Gastric biopsy and staining

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 27

Radiology in PUD 28

Radiology in PUD 28

Duodenal Ulcer 29

Duodenal Ulcer 29

Peptic Ulcers: Gastric & Dudodenal 30

Peptic Ulcers: Gastric & Dudodenal 30

Gastric ulcer in endoscopy 31

Gastric ulcer in endoscopy 31

Gastric ulcer 32

Gastric ulcer 32

Gastric erosions 33

Gastric erosions 33

Duodenal ulcer 34

Duodenal ulcer 34

Duodenal ulcer 35

Duodenal ulcer 35

Complications �Haemorrhage �Perforation �Penetration (pancreas, liver) �Pyloric stenosis (due to scarring) �Malignization 20% 36

Complications �Haemorrhage �Perforation �Penetration (pancreas, liver) �Pyloric stenosis (due to scarring) �Malignization 20% 36

Haemorrhage 37

Haemorrhage 37

Haemorrhage �Hematemesis �Melena �Bergman’s symptom 38

Haemorrhage �Hematemesis �Melena �Bergman’s symptom 38

Stages of bleeding by Forrest (endoscopy) I STAGE III STAGE Signs of stopped fresh

Stages of bleeding by Forrest (endoscopy) I STAGE III STAGE Signs of stopped fresh haemorrhage Actively bleeding ulcer Thrombosed vessels at the bottom of ulcer Absence of bleeding apparent signs Clot of blood 39

Ulcer perforation 40

Ulcer perforation 40

Gastric outlet stenosis 41

Gastric outlet stenosis 41

Stages of stenosis Compensation 1 -0. 5 cm Subcompensation 0. 5 -0. 3 cm

Stages of stenosis Compensation 1 -0. 5 cm Subcompensation 0. 5 -0. 3 cm Decompensation <0. 3 cm 42

Differential Diagnosis �Neoplasm of the stomach �Pancreatitis �Pancreatic cancer �Diverticulitis �Nonulcer dyspepsia (also called

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 43

Treatment – Medical nutrition � Diet № 1: white stale bread, vegetable soups, softly

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 44

Treatment - Drugs q H. pylori supressors: De-nol, Metronidazole, q Antisecretory drugs Furazolidone, Oxacillin,

Treatment - Drugs q H. pylori supressors: De-nol, Metronidazole, q Antisecretory drugs Furazolidone, Oxacillin, Amoxycillin • M-anticholinergic drugs: • Nonselective: Atropine, Platyphyllin, Methacin • Selective: Gastrozepine, Pirenzepine • H 2 -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 45

Treatment - Drugs q • • • q Gastrocytoprotectors Cytoprotectors that stimulate mucus production:

Treatment - Drugs q • • • q 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) 46

Side effects of drugs � H 2 -blockers: impotence gynecomastia, � Aluminum hydroxide: constipation

Side effects of drugs � H 2 -blockers: impotence gynecomastia, � Aluminum hydroxide: constipation � Magnesium diarrhea hydroxide: 47

Therapy regimens MONOTHERAPY �De-nol 1 tablet 3 times/day, 4 -6 weeks �Clarythromycin 250 mg,

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 48

Therapy regimens DOUBLE THERAPY �De-nol [4 -6 weeks] Metronidazole + [10 -14 days] �De-nol

Therapy regimens DOUBLE THERAPY �De-nol [4 -6 weeks] Metronidazole + [10 -14 days] �De-nol [4 -6 weeks] + Tetracyclin OR Amoxycillin �Amoxycillin + Omeprazole 10 days] [10 days] OR Clarythromycin [7[40 mg, 4 -6 weeks] 49

Therapy regimens TRIPLE THERAPY � De-nol [4 -6 weeks] + Metronidazole [10 -14 days]

Therapy regimens TRIPLE THERAPY � De-nol [4 -6 weeks] + Metronidazole [10 -14 days] Tetracyclin [7 -10 days] A + Amoxycillin OR Clarythromycin + Metronidazole � Omeprazole � Metronidazole [10 -14 days] + we e k Amoxycillin [10 days] + Ranitidine [150 mg, 10 -14 days] 50

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

Therapy regimens QUADRUPLE THERAPY Omeprazole + De-nol+ Amoxycillin OR Clarythromycin + Metronidazole 10 days 51

Prophylaxy PRIMARY SECONDARY TERTIARY • Revelation and elimination of risk factors • Sanitary and

Prophylaxy PRIMARY SECONDARY TERTIARY • Revelation and elimination of risk factors • Sanitary and prophylactic measures • Early diagnosis and timely treatment • Screening, professional examination, questionnarires • Prevention of complications 52

To avoid sickness, eat less; to prolong life, worry less. Chu Hui Weng 53

To avoid sickness, eat less; to prolong life, worry less. Chu Hui Weng 53

THANKS FOR YOUR ATTENTION AND PATIENCE!!! 54

THANKS FOR YOUR ATTENTION AND PATIENCE!!! 54