Peptic Ulcer Disease

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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
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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
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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
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1 – submucosa
2 – hard, undermined margin
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


A break in the mucosa not penetrating
muscularis mucosa
Peristalsis is not affected
Heals rapidly
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Duodenal ulcers (5x) > gastric ulcers
 ♂ (4x) > ♀
 Urban resident > rural resident

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 Helicobacter
pylori
 NSAIDs (aspirin)
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Healthy subjects
 Chronic active gastritis
 Duodenal ulcer
 Gastric ulcer
 Gastric adenocarcinoma
 Gastric lymphoma

20-50%
100%
>90%
50 - 80%
90%
85%
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Barry Marshal
Robin Warran
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Predisposing
factors
Producing
factors
Heredity
Active
duodenitis
or gastritis
Emotional
stress
Gastric
metaplasia
Blood group
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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
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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
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PAIN
LOCATION
TIME
CHARACTER
IRRADIATION
PAIN RELIEF
•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
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DYSPEPSIA
HEARTBURN
BELCHING
NAUSEA &
VOMITING
APPETITE
•Related with gastroesophageal reflux
•After meal
•More common in gastric ulcers
•At the peak of pain
•More common in gastric ulcers
•Pain relief after vomiting
•Excessive
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


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:

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
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CBC
• ↑Hb
• ↑Erythrocyte
Secretory function
of stomach
Occult blood feces
analysis
Endoscopy
X-ray
(Barium meal)
• ↑BAO (N=5
mmol/h)
• Latent PUD
• Round or oval
• Niche sign
• Exacerbation
• ↑MAO (N=18-26
mmol/h)
• Stomach cancer
• Edges: sharp,
hyperemic,
edematous
• 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
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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
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Haemorrhage
 Perforation
 Penetration (pancreas, liver)
 Pyloric stenosis (due to scarring)
 Malignization

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 Hematemesis
 Melena
 Bergman’s
symptom
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I STAGE
II 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
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Compensation
Subcompensation
Decompensation
1-0.5 cm
0.5-0.3 cm
<0.3 cm
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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

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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
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
H.pylori supressors: De-nol, Metronidazole,

Antisecretory drugs
Furazolidone, Oxacillin, Amoxycillin
• 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
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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)
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
H2-blockers: gynecomastia,
impotence

Aluminum hydroxide:
constipation

Magnesium hydroxide:
diarrhea
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 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
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 De-nol [4-6 weeks]
Metronidazole
+
[10-14 days]
 De-nol [4-6 weeks]
+
Tetracyclin OR Amoxycillin
 Amoxycillin
+
Omeprazole
[10 days]
OR Clarythromycin [7-
10 days]
[40 mg, 4-6 weeks]
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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]
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Omeprazole +
De-nol+
Amoxycillin OR Clarythromycin +
Metronidazole
10 days
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• Revelation and elimination of risk factors
PRIMARY
• Sanitary and prophylactic measures
• Early diagnosis and timely treatment
• Screening, professional examination,
SECONDARY
questionnarires
• Prevention of complications
TERTIARY
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