This document summarizes information about peptic ulcer disease (PUD), including its causes, symptoms, complications, diagnosis, and treatment. Key points: - Helicobacter pylori (HP) infection is the primary cause of PUD and is present in 95% of duodenal and 70% of gastric ulcers. Non-steroidal anti-inflammatory drugs can also increase risk. - Common symptoms include abdominal pain, nausea, loss of appetite, and weight loss. Complications can include bleeding, perforation, and stenosis. - Diagnosis is typically made through endoscopy, which allows visualization of ulcers. Treatment involves eradicating HP with antibiotic therapy in combination with proton pump

1. Peptic ulcer of stomach and duodenum :-
 Peptic ulcer is a chronic, recurrent disease, the main morphological
manifestation of which is a stomach ulcer or duodenum ulcer, usually
developing against a background of chronic gastritis associated with HP.
 Epidemiology :-
 Peptic ulcer disease is very prevalent in various countries and covers about
8% of the adult population. Among residents of cities the disease is more
prevalent, than among residents of the village.
 Men are ill with peptic ulcer, especially the duodenum, more often 7-8
times compared to women.
 In the past few decades, develop countries have been experiencing a global
decline in morbidity and mortality from peptic ulcer, which can be
attributed to the active introduction of anti HP – therapy.

2. Etiology
Peptic ulcer of the duodenum is diagnosed 3-4 times more often than peptic ulcer
of the stomach. Among the reasons for the development of peptic ulcer are:
 Infection (Helicobacter pylori). HP is found in 95% of patients with peptic ulcer of
duodenum, and in 70% of patients with peptic ulcer of stomach.
 hereditary predisposition;
 neuropsychiatric factors;
 alimentary factors;
 bad habits (smoking significantly increase the risk of developing peptic ulcer,
reduces the effectiveness of treatment and increases mortality; the use of strong
alcohol leads to a decrease in the production of mucus, a violation of capillary
blood flow, slowing the recovery of the epithelium);
 uncontrolled administration of non-steroidal anti-inflammatory drugs suppress the
production of mucus secretions and prostaglandins.

3. Pathogenesis
 H.Pylory produces urease;
 Under the influence of urea, urease is converted into ammonia and carbon dioxcide,
create an alkaline environment, with is favorable for the existence of HP;
 HP penetrates into the layer of protective mucus, while violating the protective
properties of mucus (reduces its viscosity);
 HP after passing through a protective layer of mucus, destroys the epithelium, producing
mucus, and endocrine cells, producing gastrin and somatostatin;
 Ammonia strengthens the secretion of gastrin, suppresses the secretion of somatostatin.
Somatostatin limits the secretion of hydrochloric acid. This leads to increased secretion
of hydrochloric acid, increased acidity of gastric juice, which is the most important factor
of aggression.
 The activity of inflammation can increases when exposed to adverse factors
(stress, alcohol);
 Non-steroidal anti-inflammatory drugs (including acetylsalicylic acid) interfere with the
synthesis of prostaglandins, reducing the formation of protective alkaline mucus, thereby
increasing the risk of ulcers especially in the stomach.

4. Classification of PUD
I. General characteristics of PUD:
- Ulcer of stomach;
- Ulcer of duodenum;
- Peptic gastroejunal ulcer after gastrectomy.
II. Clinical forms:
- Acute or the first time identify;
- Chronic.
III. Flow:
- Latent flow;
- Easy flow with rarely recurrent (relaps less than once a year);
- Moderate flow with more frequent recurrent (1-2 relapses during a year);
- Severe flow (3 relapses and more during a year).
IV. Phase
- exacerbation (relapse);
- fading exacerbation (incomplete remission);
- remission.

5. V. Characteristics of the morphological substrate of the disease:
1. Types of ulcers:
- acute;
- chronic.
2. Dimensions of the ulcer:
- small ulcer - less 0,5 cm;
- medium ulcer - 0,5-1,0 cm;
- large ulcer - 1,1 - 3,0 cm;
- giant ulcer - more 3,0 cm.
3. Stage of ulcer development:
- active stage;
- cicatrizing stage;
- stage of “red scar”;
- stage of “white scar”.
4. Localization of the ulcer:
4.1 Stomach: a) cardia, subcardia, body of the stomach, antrum of the stomach, pyloric department;
b) front wall, back wall, low curvature, great curvature.
4.2 Duodenum: a) bulb, postbulbar part

6. Clinical manifestation
Diagnosis of PUD still begins with the study of anamnesis, complaints and the
results of physical examination (palpation, percussion).
 One of the main manifestations of peptic ulcer in the phase of exacerbation is pain,
which is localized in the upper half of the abdomen.
 Distinguish the following types of abdominal pain:
- “early pain” – pain appear after the meal immediately or 15-30 minutes after meal.
Its characteristic for stomach ulcer.
- “late pain” - pain in 1,5-2 hours after meal; its characteristic for duodenum ulcer.
- “hungry pain” – pain appears on an empty stomach and disappears after eating;
- “night pain” - repeatedly awakens the patient;
 Nausea, Violation of appetite. Heartburn;
 Constipation in peptic ulcer is more often due to spastic dyskinesia of the colon;
 Melena is a specific sign of the syndrome of gastrointestinal bleeding;
 Loss of weight.

7. Complications of PUD
 Gastrointestinal bleeding is the most common complication. Sudden large bleeding can
be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as
the gastroduodenal artery. Gastroduodenal bleeding ulcerous nature account 44-55% of
gastrointestinal bleeding. Clinically gastrointestinal bleeding is manifested by bloody
vomiting, tarry stool and symptoms of acute blood loss.
 Perforation is a serious complication of peptic ulcer, requiring urgent surgical
intervention. This complication occurs in 5-20% of causes of PUD and in men 10-20
times more often than in women.
 Penetration is a spread of the ulcer beyond the walls of the stomach and duodenum
into surrounding tissues and organs Stenosis of pyloric stomach is a narrowing of the
pyloric canal by scarring and swelling of the gastric antrum and duodenum due to peptic
ulcers.
 Gastric ulcer can degenerate into a malignant tumor (malignancy), this complication
occurs frequently - in 5-15% of patients.

8. Methods of investigation of PUD
 X-ray examination is performed if
the patient refuses from
endoscopic examination or if there
are absolute contraindications to
endoscopic examination.
Ulcer niche is a direct symptom of
the PUdisease on X-ray.

9. Treatment of PUD
 Treatment includes non-pharmacologic and drug therapy.
 Non – pharmacologic therapy includes diet-therapy, rejection of bad habits:
 Food should be full, varied and corresponds the conditions of chemical, thermal and
mechanical sparing of the mucous membrane of the stomach and duodenum;
 It is advisable to exclude from the diet only food that this patient causes discomfort,
for example fried dishes, fruit juice, coffee, spices, alcohol;
 Eating should be regular with the a frequency of at least four times a day, dinner
should not be later than two hours before bedtime;
 Contraindicated large breaks between meals, overeating and dry eating;
 Studies have shown that a strict diet not significantly affect the outcome of the
disease;
 Cessation of smoking – increases the effectiveness of eradication therapy

10. Eradication therapy
 When prescribing anti-Helicobacter drugs (antibiotics), resistance to
antibiotics is taken into account.
The following antibiotics included WHO experts and they are used in anti-
Helicobacter pylori therapy:
- Clarithromycin 500 mg 2 times per day;
- Amoxicillin 1000 mg 2 times per day;
- Levofloxacin 500 mg 2 times per day;
- Tetracycline 1000 mg 2 times per day;
- Furazolidone 200 mg 2 times per day;
- Metronidazole 500 mg 2 times per day;

11. PPI – antisecretory therapy
 PPI include:
- omeprazole 20 mg 2 times per day;
- lansoprazole 30 mg 2 times per day;
- pantoprazole 40 mg 2 times per day;
- esomeprazole 20 mg 2 times per day;
- rabeprazole 20 mg 2 times per day.
 Quadrotherapy based on bismuth preparations:
PPI + metronidazole + tetracycline + bismuth tricalcium dicitrate
 Quadrotherapy without bismuth preparations:
PPI + clarithromycin + amoxicillin + metronidazole
 Sequential therapy:
PPI + amoxicillin (first 5 days) + PPI + clarithromycin + metronidazole (the next 5 days)

12. HP eradication therapy
 The first line:
- triple therapy:
proton pump inhibitors (PPI) + clarithromycin + amoxicillin or metronidazole;
- quadrotherapy:
proton pump inhibitors + clarithromycin + amoxicillin or metronidazole + bismuth
preparations.
The second line of anti HP – therapy:
PPI + levofloxacin + amoxicillin;
PPI + levofloxacin + amoxicillin + bismuth preparations.
The third line of anti HP – therapy:
Individual selection of drugs based of the result of testing the resistance of HP to
antibiotics
“Salvage” therapy
PPI + clarithromycin + levofloxacin