Duodenal ulcer presentation. Peptic ulcer

Slide 2: Definition

Peptic ulcer of the stomach and duodenum (PU) is a chronic disease of the gastrointestinal tract, the main manifestation of which is the formation of a fairly persistent ulcerative defect in the stomach and/or duodenum (DU). In the International Classification of Diseases (ICD-10), ulcer disease is called peptic ulcer disease. Peptic ulcer is a chronic and recurrent disease, prone to progression and involvement in the pathological process, except for the stomach, other digestive organs and the whole body. Inadequate treatment of ulcer leads to complications that threaten the patient’s life.

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Slide 5: Etiology and pathogenesis

the presence of the microbe Helicobacter pylori on the gastric mucosa; decreased mucosal resistance to stomach acid; increased production of stomach acid (for example, the effect of caffeine); smoking; regular use of non-steroidal anti-inflammatory drugs, such as, for example, aspirin, ibuprofen, diclofenac and naproxen (Emox, Nalgesin) and glucocorticoid hormones (prednisolone, etc.), which directly damage the mucosa; stress.

Slide 6: Genetic factors that contribute to the occurrence of ulcers:

high level of maximum secretion of hydrochloric acid; an increase in the number of parietal cells and their increased sensitivity to gastrin; trypsin inhibitor deficiency; fucomucoprotein deficiency; increased pepsinogen content in blood serum and urine; excess gastrin production in response to stimulation; gastroduodenal dysmotility - prolonged retention of food in the stomach; increased pepsinogen formation; insufficiency of secretory Ig A and prostaglandin production; serological blood markers: reduce the resistance of the gastric mucosa blood group 0(1), positive Rh factor; hereditary histocompatibility markers for duodenal ulcer - HLA B5 (in the Ukrainian population - B15, in the Russian population - B14); congenital antitrypsin deficiency; absence of secretion of ABO system factors with gastric juice (the risk of ulcer increases 2.5 times).

Slide 7: Classification according to A.V. Mazurins et al. (1984), with additions on the etiological factor

1. Clinical and endoscopic stage: acute ulcer; the beginning of epithelization; healing of an ulcerative defect of the mucous membrane with existing gastroduodenitis; clinical and endoscopic remission. 2. Phases: exacerbation; incomplete clinical remission; clinical remission. 3. Localization: stomach; duodenum (bulb; bulbous section); dual localization. 4. Form: without complications; with complications (bleeding, penetration, perforation, pyloric stenosis, perivisceritis). 5. Functional characteristics: acidity of gastric contents and motility (increased, decreased, normal). 6. Etiological characteristics: Helicobacter pylori associated; Helicobacter pylori non-associated.

Slide 8: Clinical manifestations of ulcer

Asymptomatic ulcers also exist, but this is not the traditional situation (ulcers resulting from medication often occur without complaint). The most common symptoms are: 1. dull aching or burning pain in the abdomen, primarily in the central area of ​​the upper abdomen. Stomach ulcers often hurt while eating, while duodenal ulcers hurt a couple of hours after eating or on an empty stomach, and eating is more likely to relieve symptoms; 2. nausea and/or vomiting; 3. pain that is relieved by eating or taking medications that reduce the acidity of gastric contents (antacids); 4. pain that intensifies a couple of hours after eating or sometimes also before eating; 5. pain that causes you to wake up at night; 6. weight loss, lack of appetite. If the ulcer bleeds, you may experience; 7. vomiting; the vomit may contain bright red blood or brown blood resembling coffee grounds; 8. black stool.

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Slide 10: Clinical manifestations of complicated ulcer

Complicated course of ulcer is observed in 10-15% of cases, twice as often in boys. Bleeding is the most common complication of ulcer (80% of complications). Clinical signs of acute bleeding in PU: vomiting “coffee grounds”, vascular collapse and signs of anemia in the body – pallor, general weakness. Often, as bleeding develops, a weakening of the pain syndrome is observed, which can lull the doctor’s vigilance. Perforation. (7-8%); Perforation of an ulcer usually begins with an attack of acute “dagger pain”, which is accompanied by a clinical picture of an acute abdomen, tension in the epigastric region, abdominal wall, and symptoms of peritoneal irritation. Note the weakening or absence of peristalsis. The clinic data is confirmed by an x-ray examination - the presence of free gas under the liver during an x-ray examination of the abdominal organs. Penetration. (1-1.5%). Ulcers of the duodenum penetrate into the head of the pancreas, liver, bile ducts, and hepatoduodenal ligament. Gastric ulcers penetrate into the lesser omentum and the body of the pancreas. The main clinical manifestations are sharp pain that radiates to the back, vomiting that does not bring relief, and heartburn. Penetration is characterized by constant pain and loss of a clear connection with food intake. A characteristic radiological symptom of penetration is an additional shadow of a contrast agent next to the examined organ. Deformity and pyloroduodenal stenosis. (10-12%). Patients feel fullness of the stomach, nausea, and belching. In severe cases, vomiting of stagnant stomach contents is observed. The patient can provoke vomiting himself to obtain a feeling of relief. The patient is losing weight. In typical cases, hourglass-type peristalsis and a splashing phenomenon during palpation in the epigastric zone are observed.

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Slide 12: Paraclinical examination methods for ulcerative disease

1. Laboratory research. 1.1 Mandatory (at the present stage of development of gastroenterology): General clinical blood test. General clinical urine analysis. Analysis of stool for worm eggs. Coprocytogram. Total protein into protein fractions of blood. Histological (cytological) examination during endoscopy. Tests for HP: rapid urease, bacteriological, respiratory urease test, serological (IFA), ELISA analysis of the concentration of HP antigen in stool, polymerase chain reaction (PCR). Intragastric pH-metry. 1.2. According to indications: Fecal occult blood test (Gregersen reaction). Blood test for hormone levels to detect hypergastrinemia, hypersomatotropinemia. Immunogram.

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2. Instrumental studies and diagnostic criteria: Study of gastric secretion: Intragastric pH-metry. Fractional study of gastric juice (detection of hyperacidity, increased proteolytic activity). Fibroesophagogastroduodenoscopy (FGDS) with targeted biopsy, diagnosis of HP infection is carried out for diagnostic purposes and 3-4 weeks after the start of treatment with complete epithelization of the ulcer.

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Slide 14: Endoscopic criteria for ulcer stages

1. Exacerbation phase. a) Stage I - acute ulcer. Against the background of pronounced inflammatory changes in the coolant and duodenum - a round-shaped defect (defects), surrounded by an inflammatory shaft; pronounced swelling. The bottom of the ulcer is layered with fibrin. b) Stage II - the beginning of epithelization. Hyperemia decreases, the inflammatory shaft is smoothed out, the edges of the defect become uneven, the bottom of the ulcer begins to clear of fibrin, and convergence of folds towards the ulcer is noted. 2. Phase of incomplete remission. c) Stage III - healing of the ulcer. At the site of reparation there are remains of granulations, red scars of various shapes, with or without deformation. Signs of gastroduodenitis activity remain.

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Slide 15

3. Remission Complete epithelization of the ulcerative defect (or “quiet” scar), there are no signs of concomitant gastroduodenitis. When performing a targeted biopsy, rapid diagnosis of HP is performed; histological and microbiological diagnosis of HP; histological (cytological) verification of the diagnosis, differential diagnosis with acute ulcers. X-ray examination is currently of an auxiliary nature. It is used primarily for the diagnosis of motor-evacuation disorders, duodenostasis, cicatricial and ulcerative deformities of the stomach and duodenum. For diagnostic purposes in case of absolute contraindications to endoscopy. X-ray criteria for ulcers: “niche” symptom, convergence of folds, etc. are rare in children.

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Slide 16

Ultrasound examination of the abdominal organs. The examination is carried out once to screen for the diagnosis of concomitant pathologies.

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Slide 17: Treatment of ulcers

The scope of therapeutic measures depends on the location of the ulcer (stomach or duodenum), the phase of the disease, the severity of the course, the presence of complications, the connection with HP, the leading pathogenetic mechanisms and the clinical and endoscopic symptom complex. According to the tradition that has developed in domestic pediatrics, treatment of a patient with newly diagnosed ulcer and its exacerbation is carried out in a hospital. At the same time, many foreign pediatricians are more reserved in recommending inpatient treatment. In case of exacerbation, the average duration of inpatient treatment is about 1 month. 1. Mode. In the first weeks of hospital stay, bed or semi-bed rest. 2. Nutrition. Diet tables No. 1a, 1b, and then N5 are assigned sequentially. Considering the low caloric content of the N1 diet options, the choice of motor mode depends on the duration of its administration. The basis of dietary therapy for ulcers is the principle of preventing thermal, chemical and mechanical irritating effects on the ulcer. That is, very hot or cold foods, extractive, spicy dishes, and roughage foods rich in dietary fiber are excluded. When PU is complicated by bleeding, the Meulengracht diet is prescribed, which includes purees enriched with proteins, salts and vitamins. For HP-associated peptic ulcer disease in Ukraine, the following treatment regimens are officially recommended, which are based on the provisions of the 2nd Maachtricht Consensus of 2000. In the treatment of HP-associated forms of gastritis and peptic ulcer in children, first- and second-line combination therapy is consistently used.

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Slide 18: The main drugs used to eradicate HP

1. Bismuth preparations. Denol in a single dose of 4 mg per 1 kg of body weight twice a day, or 120 mg 2 times a day (up to 7 years), 240 mg 2 times a day (after 7 years). An analogue of Denol is the Ukrainian drug Gastro-norm 2. Antibiotics: Amoxicillin (flemoxin-solutab) in a single dose of 25 mg per 1 kg scale (the maximum dose should not exceed 1.0 g); For children under 7 years old 500 mg 2 times a day, after 7 years 1000 mg 2 times a day. Clarithromycin (erythromycin) at a dose of 7.5 mg per 1 kg of body weight per day in 2 divided doses (the maximum daily dose should not exceed 500 mg). Roxithromycin 5-8 mg per 1 kg of body weight per day in 2 doses (maximum dose - up to 300 mg). 3. Nitroimidazole: metronidazole 250 (up to 7 years) 500 mg (after 7 years) 2 times a day or 20-40 mg per 1 kg scale. 4. Nitrofurans: furazolidone 0.05-0.1 g 4 times a day, up to 20 mg per 1 kg scale per day. 5. Histamine H2 receptor blockers: famotidine 20-40 mg per day or ranitidine. 6. Proton pump inhibitors: omeprazole in a single dose of 0.5 mg per kg scales 1-2 times a day.

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Slide 19: Schemes of rational anti-Helicobacter therapy for peptic ulcer disease in children

Options for first-line triple therapy for children (treatment duration 7 days). I. Bismuth-based circuits. 1. Dn+Fl+Me. 2. Dn+Fl+Fur. 3. Dn+Fl+Cl. 4. Dn+Fl+Er. II. Schemes based on histamine H2 receptor blockers. 1. Fa+(Ra)+ Fl+Fur. 2. Fa+Fl+Me.

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Slide 20

III. Proton pump inhibitor regimens. 1. Ohm+Fl+Cl. 2. Ohm+Cl+Fur. IV. Second-line quadruple therapy options for children (treatment duration 7 days). 1. Dn+Fa+Fl+Fur. 2. Dn+Fa+Cl+Fur. 3. Dn+Fa+Fl+Me. 4. Dn+Fa+Fl+Me. 5. Dn+Ohm+Fl+Fur. 6. Dn+Ohm+Cl+Fur. 7. Dn+Ohm+Fl+Me. 8. Dn+Ohm+Cl+Me. List of drug name abbreviations: Dn - Denol Er - erythromycin. Cl – clarithromycin. Om - ompeprazole. Ra - ranitidine. Fa – famotidine. Fl - flemoxin - solutab.

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Slide 21

Care: 1. carefully follow the treatment prescribed by your doctor; 2. come regularly for follow-up; 3. don't smoke; 4. If you have had a stomach or duodenal ulcer or if you have the symptoms described above: Avoid medicines that irritate the stomach, such as aspirin, ibuprofen, diclofenac and naproxen. Take paracetamol instead; 5. eat healthy. Several small meals a day are better than 2-3 large meals. Follow the diet prescribed by your doctor; 6. Avoid coffee, including decaffeinated coffee, alcohol, cola drinks, and all foods and drinks that may irritate the stomach. 7. rest and sleep enough time; 8. Be physically active and follow your doctor's recommendations. If complaints persist or worsen, consult your doctor

chronic, cyclical
a disease characterized
occurring during an exacerbation
ulcerative defect of the mucous membrane
stomach and duodenum
(ICD-10: K25 gastric ulcer,
K26 - duodenal ulcer, K28 gastrojejunal ulcer)

Factors predisposing to the development of ulcer.

Hereditary predisposition
Acute and chronic stress
situations
Nutritional factor
Abuse of alcohol, coffee,
smoking
Effect of drugs
Infection N.R.

H. pylori

electron microscopic image of a section of the gastric mucosa infected with Helicobacter pyloricus. The picture shows the undersides

electron microscopic image of a section of the gastric mucosa,
infected with Helicobacter pyloric bacteria. Visible in the picture
upward projections of mucous cells and rounded sections
Helicobacter, located both on the surface and in the intercellular

PATHOGENESIS.

Aggressive factors.
1.
2.
3.
4.
5.
Helicobacter pylori infection.
Hyperproduction of hydrochloric acid.
Proulcerogenic nutritional factors.
Reverse diffusion of hydrogen ions.
Gastroduodenal dysmotility, GDR
Acceleration of motor-evacuation function of the stomach
Decreased gastric motor function and prolonged
gastric retention
Endogenous factors of aggression: HCl, pepsin,
lipase, bile.
Exogenous factors: ethanol, NSAIDs,
components of tobacco smoke.

PROTECTIVE FACTORS.

1.
2.
3.
4.
5.
6.
A layer of visible insoluble mucus and
bicarbonates.
Layer of epithelial cells of the stomach,
enterocytes that produce mucus and
bicarbonates.
Microcirculatory bed of the gastroduodenal
mucous membrane, optimal blood supply to the coolant and
12pcs. Ischemia for about 30 minutes causes necrosis
cells.
Active regeneration of the surface epithelium.
Coolant cells are renewed every 3-5 days.
Local synthesis of protection mediators. coolant
synthesizes prostaglandins and growth factors:
epidermal and alpha transforming.
Anti-ulcerogenic nutritional factors.

"Libra Neck"

Classification of peptic ulcer.

Etiology.
Associated with Helicobacter pylori.
Not associated with Helicobacter pylori.
Localization of stomach ulcer.
1.
2.
3.
4.
Cardial and subcardial sections.
Bodies.
Antrum.
Pyloric canal.
Ulcers of the 12 duodenum.
1.
2.
Bulbs (anterior, posterior).
Extrabulb ulcers.
Gastrojejunal ulcer, including peptic ulcer
anastomosis of the stomach, afferent and efferent loops
small intestine, anastomosis with the exception of a primary ulcer
small intestine.

Clinical course.
Typical
Atypical (with atypical pain
syndrome).
Level of gastric secretion.
With increased secretion
With normal secretion
With reduced secretion
The nature of the current.
1.
2.
Newly diagnosed peptic ulcer
Recurrent course
WITH
WITH
WITH
rare exacerbations (once every 2-3 years or less)
annual exacerbations
frequent exacerbations (2 times a year or more often)

1.
2.
Exacerbation
Remission:
Stages of the disease.
Clinical
Anatomical: epithelization, scarring (stage
red scar 4-6 weeks, white scar stage 3-6
months).
Functional.
Bleeding
Penetration
5.
Complications.
3.
Perforation
4.
Stenosis
Malignization.
Duration of scarring of ulcers.
The usual time frame for scarring (ulcer 12 PCs - 3-4 weeks,
stomach ulcer – 6-8 weeks)
Long-term non-scarring, resistant (ulcer 12 PCs
more than 8 weeks, stomach ulcer more than 12 weeks).

Type of ulcers
Singles
Multiple
Size of ulcers
Small, diameter up to 0.5 cm.
Medium, diameter up to 0.5-1 cm.
Large, diameter 1.1-2.9 cm in the stomach and 0.7 cm in
onion 12 pcs.
Giant, diameter 3 cm or more for stomach ulcers,
more than 2 cm for ulcers 12 PCs.
Superficial up to 0.5 cm deep from level
gastric mucosa.
Deep more than 0.5 cm in depth from level
gastric mucosa.

Clinic depending on the location of the ulcers

peculiarities:
- atypical clinic
- late diagnosis
- high percentage of bleeding
localization of pain behind the sternum, under the xiphoid process
burning or pressure feeling
irradiation to the left shoulder, heart area, left scapula
20 minutes after eating
treated with antacids
cardiac and subcardial ulcers
mediogastric ulcers
features: more often malignant (especially greater curvature)
epigastric pain, to the left of the midline
moderate intensity, aching
1 – 1.5 hours after eating
disappear on their own
severe dyspeptic symptoms

antral ulcers
features: age less than 40 years, frequent complication –
bleeding
intense hungry, late (after 1.5 – 3
hours after eating) and night pain in the epigastrium
vomiting at the height of pain with stomach contents
constipation
seasonality
pyloric ulcers
Features: frequent complications – stenosis, bleeding
pain is localized in the right half of the epigastrium
strong, paroxysmal, 20 – 40 min,
repeatedly during the day, poorly relieved
eating, soda, injections M -
anticholinergics, analgesics
nausea, vomiting

bulbar ulcers
features: age less than 40 years, male, rare
becomes malignant
late, hungry, night pain
relieved with food and soda
localization - near the navel
intense, cutting
constipation
seasonality
postbulbar ulcers
feature: men over 40 years old, anatomical proximity to
head of pancreas, right kidney, bile duct
right upper quadrant of the abdomen
irradiation to the back, spine, right shoulder blade
2 – 3 hours after eating
resembles renal, hepatic colic

DIAGNOSTICS.

1.
2.
3.
4.
5.
6.
7.
8.
9.
Clinical criteria, features
clinical picture depending on gender,
age and location of the ulcer.
Blood test, determination of blood group,
Rh.
Examination of feces for occult blood.
Serum iron.
Ultrasound of the abdominal organs.
Study of gastric secretion.
FGDS with targeted biopsy.
R-scopy of the stomach and 12 PCs.
Definition of N.r.

ALGORITHM FOR DIAGNOSIS AND TREATMENT OF Helicobacter pylori INFECTION.

1.
2.
3.
4.
5.
6.
7.
ALGORITHM FOR DIAGNOSIS AND TREATMENT
Helicobacter pylori INFECTIONS.
Determination of H. pylori is necessary
carried out if
eradication therapy is planned.
Indications for mandatory
eradication therapy for infection
H. pylori serve:
BU 12 PC and stomach (in the stage of exacerbation and remission;
complicated forms after emergency measures,
aimed at eliminating complications).
MALT lymphoma.
Atrophic gastritis.
Condition after gastric resection for cancer.
Persons who are closely related to patients
stomach cancer.
At the request of the patient after comprehensive
examinations.
An acceptable treatment option for functional
dyspepsia.

DIAGNOSTIC METHODS. Before starting treatment, it is necessary to confirm the presence of H. pylori by at least one method.

DIAGNOSTIC METHODS.
Before starting treatment, it is necessary to confirm the presence of H. pylori
.
at least oneInvasive
method
Non-invasive methods
methods
(not related to
(necessary
carrying out endoscopy)
carrying out endoscopy)
1.
Breath test with
1.
Rapid urease test
urea, labeled with 13C
2.
Histological
2.
PCR diagnostics in stool
research (drugs
Giemsa and Gram stained
3.
Antigen determination
and other methods; smears of H. pylori in stool (available in
prints
scientific purposes)
3.
PCR diagnostics in
4.
Antibody determination
biopsy
H. pylori in blood serum
(for serological
4.
Bacteriological
research most often
research (available in
used
scientific purposes).
immunoenzyme
analysis).

All proton pump inhibitors affect results
diagnosis of infection N.r., leading to
false negative results. Therefore, before
carrying out diagnostic tests for N.R., preferably
refrain from prescribing PPIs.
Strictly mandatory control of eradication of N.r.
Methods for diagnosing infection eradication
N.r.
Conducted at least 4 weeks after the course
anti-helicobacter treatment,
When using invasive methods, be sure to
examination of several biopsies and from the antrum
department, and from the body of the stomach.
For complicated peptic ulcer
flow (bleeding, etc.) decreases
sensitivity of all methods for detecting N.r..

Indications for hospitalization of patients with peptic ulcer disease (O.N. Minushkin, 1995)

Newly diagnosed ulcer (to exclude symptomatic
ulcers, differential diagnosis with tumor
process in gastric localization of ulcers, definitions
nature of the course of ulcer 12PK.
Gastric localization of ulcer
Postbulbar localization of the ulcer
Frequent relapses
Complicated course of the disease
Large (more than 2 cm) and/or deep ulcers
Persistent and severe pain syndrome lasting
more than 7 days
Long-term (more than 4 weeks) non-scarring ulcer
The need for further examination and individual selection
medicinal and non-medicinal treatments
Weakened patients
Severe concomitant diseases.

Symptomatic gastric ulcers and 12 PCs.

1. Drug-induced ulcers
2. Stress ulcers
Cushing's ulcers in patients with severe central nervous system pathology
Ulcers developing after severe traumatic surgery
Ulcers in acute MI, various types of shock
3. Endocrine ulcers
Zollinger-Ellison syndrome
Ulcers due to hyperparathyroidism
4. Gastroduodenal ulcers in diseases of internal organs
Atherosclerosis of the abdominal aorta, hypertension, rheumatoid arthritis
Liver cirrhosis, chronic pancreatitis, Crohn's disease
COPD, diabetes mellitus, erythremia
Chronic glomerulonephritis, chronic pyelonephritis, chronic renal failure
Elderly patients (“senile ulcers”)
Tuberculosis, syphilis

Maastricht Consensus 2005. Schemes for eradication therapy of infection N.R.

First line therapy
Proton pump inhibitors (omez, pariet, nexium) in
standard dose 2 times a day
+ clarithromycin 500 mg 2 times a day
+ amoxicillin 1000 mg 2 times a day
Triple therapy is prescribed for 10-14 days
If treatment fails
Second line therapy is prescribed:
Proton pump inhibitors in a standard dose 2 times a day
day
+ bismuth subsalicylate/subcitrate 120 mg 4 times a day
+ metronidazole 500 mg 3 times a day
+ tetracycline 500 mg 4 times a day.
Quadruple therapy is prescribed for 10-14 days.

H2-histamine blockers should not be used in
triple regimens with metronidazole.
Replacement of amoxicillin and clarithromycin
other antibiotics are unacceptable.
7-day regimens cannot be used
eradication N.R., but only 10-14 days.
Treatment is then continued for 5 weeks
for duodenal and 7 weeks for gastric
localization of ulcers with a single dose
proton pump inhibitor at 14-16 hours.

Treatment of gastroduodenal
ulcers not associated with N.r.
Antisecretory drug + antacid
drug or sucralfate (Venter).
FGDS control for gastric ulcers and
gastrojejunal ulcer after 8 weeks, with
duodenal ulcer after 4 weeks.
Treatment of resistant ulcers.
1.
2.
3.
Analyze the rationality of therapy
Repeat additional examination
(exclude complications, other diseases)
Correction of treatment (increase dose,
add cytoprotective agents,
antacids, non-drug therapy,
local therapeutic effect through
endoscope).

Prevention of peptic ulcer disease.

To prevent relapses of ulcers, two types are used
therapy.
1.
2.
Continuous maintenance therapy
antisecretory drug in half
dose up to a year for several months.
Indications:
Ineffectiveness of therapy
Complications of ulcer,
Erosive and ulcerative reflux esophagitis,
Concomitant diseases requiring use
NSAIDs,
Patients over 60 years of age with annual relapses.
On-demand therapy. Taking ASP in
full daily dose for 3 days, then
at half for 3 weeks is indicated
patients with healed ulcers and
reliable eradication of N.r.

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• Number of slides: 70

Description of the presentation Presentation Modern methods of diagnosis and surgical treatment of gastric ulcer and 12-p on slides

Saratov State Medical University Department of Hospital Surgery, Faculty of Medicine. Head The department is headed by Honored Scientist of the Russian Federation, Professor R. Z. Losev. Modern methods of diagnosis and surgical treatment of gastric and duodenal ulcers.

Peptic ulcer (PU). Definition of the concept. Peptic ulcer is a chronic relapsing disease characterized by the formation of a persistent defect in the mucous membrane of the stomach or duodenum due to a disorder of the general and local mechanisms of nervous, hormonal, immune regulation, the main functions of the gastroduodenal system, trophic disturbances and the development of proteolysis in the mucous layer.

Predisposing factors 1. 1. Heredity 2. 2. Prolonged psycho-emotional stress 3. 3. Errors in nutrition 4. 4. Bad habits (alcohol, smoking) None of the existing theories fully reveals all the secrets of ulcer formation - this is evidenced by the multiplicity hypotheses. YaB. Etiology and pathogenesis

1. 1. Vascular theory (R. Virchow) Anatomical changes in blood vessels in the area of ​​the ulcer (thrombosis, embolism, stenosis) 2. 2. Mechanical theory (L. Aschoff) Food bolus injuries of the gastric mucosa in the area of ​​the lesser curvature (“gastric track” ) 3. 3. Inflammatory theory (V. Konechny) Gastritic origin of ulcers 4. 4. Peptic theory (E. Rigel) 5. 5. Acidosis theory (P. Balint) 6. 6. Neurovegetative theory (G. Bergmann) Hypersecretion and hypermotility of the stomach in persons with constitutional parasympathetic hypertonicity. 7. 7. Immune theory of ulcers. Etiology and pathogenesis

YaB. Etiology and pathogenesis 8. 8. Neuro-reflex theory (I. Grekov, N. Strazhesko) Reflex effect on the stomach of other abdominal diseases (appendicitis, pancreatitis, cholelithiasis, etc.) 9. 9. Cortico-visceral theory (K. Bykov , I. Kurtsyn) The role of the central nervous system and subcortical centers in dysregulation of the functions of the stomach and 12-pc. 10. Hormonal theory The influence of TSH and ACTH on gastric secretion 11. Impaired motility Duodenostasis and insufficiency of the pyloric sphincter cause reflux and destruction of the mucous membrane by bile acids and lysolecithin. Hypotonicity of the stomach causes stagnation, hypersecretion and gastric ulcers. Hypertonicity causes rapid evacuation, 12-pk acidification and 12-pk ulceration. 12. Infectious theory Waste products of H. pylory destroy the mucosal barrier.

YaB. Etiology and pathogenesis. Pathogenetic mechanisms Factors of aggression and defense Proteolysis Trophic state. Bicarbonate buffer Quantity and quality of mucus Regenerative capacity of the epithelium. Glycosaminoglycans and glycoproteins containing fucose State of blood supply and innervation. Neurohumoral influences Impaired motor skills Immune disorders. Increased activity of TSH and ACTH Waste products of H. pylory

YaB. Clinical picture, course of the disease 1. 1. Pain syndrome Localization in the epigastrium, possible irradiation to the back, hypochondrium, chest Relationship with the nature and time of food intake Seasonal frequency Local (point) pain on palpation in the epigastric region 2. 2. Dyspeptic syndrome Heartburn Belching Nausea Vomiting, which brings relief Possible bowel disturbances

YaB. Clinical picture, course of the disease 3. 3. Neurasthenic syndrome Irritability Sleep disorder Sweating hypochondria 4. 4. General condition disorder syndrome Fatigue Weakness Loss of appetite Weight loss 5. 5. Syndrome of dysfunction of other organs Pancreas Liver Gallbladder Intestines Cardiovascular system

Gastritis phase (absence of ulcerative defect, symptoms of chronic gastritis) penetrating ulcer. JJJAB. . Clinical picture, course of the disease. Phases of the clinical course of peptic ulcers Ulcerative-gastric phase (unstable mucosal defect, quickly resolving picture of peptic ulcer) Visceropathic phase (persistent ulcerative defect with a pronounced clinical picture, dysfunction of other organs) Dystrophic phase (physical and mental asthenia, cachexia. Observed in decompensated stenoses )bleeding ulcer perforation stenosis

YaB. Clinical picture, course of the disease. Diagnostics Complaints Hypothesis of diagnosis History Examination Laboratory data Confirmation of the hypothesis Clin. differential diagnostics Radiologist. study Confirmation of the diagnosis FGDS with biopsy

X-ray of the stomach Direct projection for an ulcer of the lesser curvature, the arrow indicates retraction of the greater curvature of the stomach caused by local spasm

Sight radiographs of the duodenal bulb Profile or contour niche on the posterior wall of the bulb (indicated by an arrow) with an inflammatory shaft in the form of a clearing

Endoscopic picture of the stomach Ulcer of the anterior wall of the antrum of the stomach: a longitudinal irregularly shaped ulcerative defect covered with white fibrin is visible (indicated by an arrow); the edges of the ulcer are hyperemic; there is a convergence of folds of the mucous membrane to the edges of the ulcer

Sight radiographs of the duodenal bulb Relief niche, or fasal niche (indicated by an arrow) with convergence of mucosal folds to it

Endoscopic picture of the stomach Ulcer of the lesser curvature of the stomach (indicated by an arrow) with a tendency to scarring: convergence of the folds of the mucous membrane to the edges of the ulcer is visible

YaB. Clinical picture, course of the disease. Differential diagnosis 1. 1. Diseases of the abdominal organs (liver, gall bladder, pancreas, intestines) 2. 2. Diseases of the esophagus (esophagitis), heart (IHD), lungs (thoracoabdominal syndrome), spine (osteochondrosis) 3. 3. Symptomatic ulcers

Differential diagnostic criteria for peptic ulcer disease and symptomatic gastroduodenal ulcers. Main criteria for diagnosing ulcers Symptomatic ulcers Age Predominantly young and middle-aged More often elderly and senile Gender More common in men Occurs with approximately equal frequency in men and women Hereditary predisposition Frequently detected Uncharacteristic Clinical picture In most cases typical with severe symptoms Often low-symptomatic, often masked symptoms of another (main) disease Duration of ulcer history As a rule, several years There is no long-term ulcer history; often acute onset Pre-existing diseases Not typical; only random combinations of peptic ulcer with other diseases can occur. The ulcerative process often develops against the background of another (main) disease (extensive burns, myocardial infarction, pulmonary heart failure, liver cirrhosis, hyperparathyroidism, etc.) or diseases for which long-term therapy with anti-inflammatory drugs was carried out , including steroid drugs (rheumatoid arthritis) and a number of other ulcerogenic drugs (for example, reserpine)

Differential diagnostic criteria for peptic ulcer disease and symptomatic gastroduodenal ulcers. Seasonality of exacerbations Expressed Not typical Localization of the ulcer Most often in the duodenal bulb, less often in the stomach Mostly in the stomach, less often in the duodenal bulb Number of ulcers In most cases, a single ulcerative defect Often 2-3 or more ulcers, which are often combined with erosions of the mucous membrane Frequency of complications (bleeding, perforation) Up to 15-20% Frequent, can reach 40-70% Average time for scarring of ulcers with conservative treatment 30-35 days - if the ulcer is localized in the duodenal bulb, 40-45 days - if the ulcer is localized in the stomach Duration of scarring ulcers last longer and depend largely on the effectiveness of treatment of the underlying disease

YaB. Treatment. For the convenience of choosing treatment tactics for uncomplicated duodenal ulcers, the following classification was used: GASTRITIC phase (no ulcerative defect or remission)) Drug treatment ULCER-GASTRITIC phase (open ulcer, no complications)) Drug treatment, laparoscopic vagotomy is possible VISCEROPATHIC phase (Complicated course or unsuccessful drug treatment )) Surgical treatment DYSTROPHIC phase Symptomatic treatment

The main goals of drug treatment of gastric and duodenal ulcers Relief of pain Healing of ulcers Sanitation of the mucous membrane of the stomach and duodenum from H. pylori in order to prevent relapses

The main goals of rational surgical treatment for gastroduodenal ulcers: Mandatory elimination of the pathological substrate (ulcer removal) - a source of complications and antigenic stimulation; Correction of the secretory function of the stomach; Creation of optimal conditions for adequate evacuation of the contents of the stomach or its stump; eradication of H. pylory is not excluded.

YaB. Treatment. Uncomplicated duodenal ulcer Despite the revolution in the treatment of ulcers, the recorded incidence of gastric and 12 peptic ulcers does not decrease. The number of patients with perforated ulcers is increasing. The number of patients with bleeding from the upper gastrointestinal tract is increasing, but ulcerative bleeding in this group of patients heterogeneous in etiology is about 50%. At the same time, the number of gastric resections for peptic ulcer disease decreases. 15-20% of patients with duodenal ulcer are operated on due to its serious complications and the same number require planned surgical treatment V. I. Onopriev, 1995; A. S. Balalykin, 1996; A. G. Khasanov et al. ,

YaB. Treatment. Uncomplicated duodenal ulcer According to international statistics, the number of operations for uncomplicated duodenal ulcers has decreased by 75–80%. The question is: is this situation desirable for all patients and is it justified in all cases? The last decade is characterized by an increase in the number of emergency operations for perforated (2 times) and bleeding ulcers (3 times), which was reflected in an increase in mortality during this period by 20 - 25%. But is long-term drug treatment really an equivalent alternative to surgical treatment? Anyone who has and still has too much hope for conservative treatment will be disappointed by the high rate of relapses and expected complications.

YaB. Treatment. Uncomplicated duodenal ulcer, the overall mortality rate for peptic ulcer disease, despite the possibilities of drug treatment, remained the same and has no tendency to decrease; in surgical clinical observations, the rate of emergency interventions due to complications is growing, the number of emergency operations compared to planned ones has increased disproportionately, which negatively affects the results of operations; The age median of patients with complications of peptic ulcer disease has increased significantly over the past 20 years.

YaB. Treatment. Uncomplicated duodenal ulcer Theoretically, patients with uncomplicated duodenal ulcer have two options for treating the disease. With such competition, elective surgery must be weighed against the risk factors of drug treatment. - Mortality rate in the natural course of duodenal ulcer after 5 years was 1.6%; with drug therapy - 1%; with early surgical treatment - 0.1%.

YaB. Treatment. Uncomplicated duodenal ulcer Addiction to conservative methods of treatment for frequently recurrent and long-lasting ulcers does not cure the disease, but postpones the development of its complications V. I. Petrov et al. , 1995; E. M. Blagitko,

YaB. Treatment. Uncomplicated duodenal ulcer Surgical treatment K Absolute indications include perforation of the ulcer, profuse gastrointestinal bleeding, decompensated pyloric stenosis, malignancy of the ulcer. Relative indications include deeply penetrating gastroduodenal ulcers, callous ulcers of the stomach, severe scar-ulcerative deformities of the stomach and duodenum, accompanied by a violation of the evacuation function of the stomach, as well as repeated gastrointestinal bleeding. Relative indications are the visceropathic stage, penetration, multiple ulcers, combined ulcers, recurrence of ulcers after suturing, a history of bleeding, age over 50 years.

YaB. Treatment. Uncomplicated duodenal ulcer Surgical treatment In addition, surgery is indicated in the following cases: Ulcers that are refractory to therapeutic methods of treatment (15 - 20%). Negative attitude of some patients towards frequently repeated and expensive courses of treatment. The presence of social and ethical problems that make it difficult to carry out appropriate courses of treatment.

YaB. Treatment. Surgical treatment Due to the advent of minimally invasive surgical technologies, indications for surgical treatment are expanding - surgical interventions are possible already in the second ulcerative gastric phase

YaB. Surgical treatment Arsenal of surgical interventions for ulcerative stenosis Gastroenterostomy, Gastric resection with removal of the ulcer or “off”, Antrumectomy with vagotomy, Vagotomy with pyloroplasty or gastroduodenoanastomosis, PPV with duodenoplasty.

YaB. Treatment. Surgical treatment. Classification of resection methods 1. 1. By the volume of the removed part Subtotal Hemiresection Antral 2. 2. By the localization of the removed part Distal Median proximal 3. 3. By the method of completion Gastroduodenal anastomosis (method B-II)) Gastrojejunostomy (method B-IIII)) Gastrojejunostomy on a disconnected loop (according to Ru)

Schematic representation of distal gastrectomy 1. 1. Billroth method-II 2. 2. Billroth method-III modified by Hoffmeister-Finsterer 3. 3. Billroth method-III modified by Balfour

YaB. Treatment. Surgical treatment Currently, indications for gastric resection have narrowed due to the risk of developing PGRS and the relatively high mortality rate. Resection according to B-II and modification of Roux is recognized as the most physiological. It is used mainly for stomach ulcers. Indications for economical resections in combination with vagotomy and other organ-saving operations have been expanded. Their advantages are physiological and minimal lethality. SPV is recognized as the most optimal.

Schematic representation of vagotomy 1. 1. Stem 2. 2. Selective gastric 3. 3. Selective proximal

Scheme of extended selective proximal vagotomy (Kuzin M.I. et al., 1980) Institute of Surgery named after. A. V. Vishnevsky RAMS 1. 1. crossed secretory fibers of the vagus nerves along the lesser curvature of the stomach; 2. 2. “crow’s foot” of the vagus nerve; 3. 3. skeletonized cardia and lower part (4-5 cm) of the esophagus; 4. 4. denervated greater curvature of the stomach from the antrum to the short arteries of the stomach; 5. 5. anterior and posterior trunk of the vagus nerve.

Schematic representation of pyloroplasty. The dotted lines indicate the dissection lines 3. 3. According to Finney (anastomosis between the antrum of the stomach and the duodenum)

Schematic representation of pyloroplasty The dotted line indicates the dissection lines 1. 1. According to Heineke-Mikulich (the pyloric part of the stomach and duodenum are dissected lengthwise, the resulting hole is sutured in the transverse direction) 2. 2. According to Judd (diamond-shaped excision of the anterior semicircle of the pylorus along with the ulcer)

YaB. Treatment. Surgical treatment Pathogenetically based organ-saving operations can be performed laparoscopically (vagotomy), as well as combined - laparoscopic vagotomy + drainage surgery from a mini-access.

A good treatment result is determined primarily not by the type of surgical intervention, but by the correct choice in each specific case, especially in case of duodenal ulcer

YaB. Treatment. Surgical treatment The choice of surgical method is determined depending on many factors: 1. 1. Phase of the disease 2. 2. Localization of the ulcer 3. 3. Type of gastric secretion 4. 4. Presence of complications 5. 5. Predisposition to PGRS 6. 6. Condition of the patient

YaB. Treatment. Surgical treatment When choosing a surgical method, it is necessary to take into account that vagotomy affects the first phase of gastric secretion, and drainage operations affect the second. Trunk and selective vagotomy can only be performed in combination with a drainage operation (due to pyloric spasm), and SPV - in an isolated form

Types of gastric secretion Type of secretion Debit-hour of hydrochloric acid (mmol) 1st phase 2nd phase Normal 1. 1-4. 1 1. 1-5. 9 Asthenic More than 4.1 5.9 and less Excitable More than 4.1 More than 5.9 Inert 4.1 and less More than 5.9 Inhibitory Less than 1.

YaB. Treatment. Surgical treatment of PWS has an advantage when it is necessary to act only on the first phase of secretion (asthenic type). For the excitable type of secretion, SV is most often used in combination with antral resection or pyloroplasty. For inert and inhibitory types, gastric resection is indicated, which performs the task of removing the ulcer together with an area of ​​the stomach with impaired trophism Vagotomy and drainage operations provide minimal mortality, but the number of relapses reaches 10%

Surgeries for ulcer perforation account for about 30% of all surgical interventions for duodenal ulcers, with mortality ranging from 3 to 12%. In 15-20%, gastroduodenal ulcers are complicated by bleeding ulcers. Complications. Perforation

YaB. Complications. Perforation. Pathogenesis In perforated ulcers, an autoimmune conflict similar to the Arthus phenomenon is recognized as the most reliable cause.

YaB. Complications. Perforation. Symptoms and diagnosis Clinical course I. I. The period of “acute abdomen”, shock is the easiest for diagnosis, the most pleasant for healing. Characteristic symptoms: Main “dagger” pain (90%) Plank-like tension of the muscles of the abdominal wall (90%) Ulcerative history (80%) Pneumoperitoneum (85%) (with pneumogastrography increases to 96%) Auxiliary Preperforative conditions Difficulty breathing Anxiety, fear Forced positions Vomiting Hyperleukocytosis Fluid in the abdominal cavity Shchetkin's symptom is not caused

YaB. Complications. Perforation. Symptoms and diagnosis II. A period of imaginary well-being. Signs of shock disappear. The intensity of pain decreases. The abdomen becomes softer (although tension in the epigastrium is almost always preserved) III. Period of diffuse peritonitis Difficulties in diagnosis are most likely in the second period, as well as with covered and atypical perforations

YaB. Complications. Perforation. Differential diagnosis Differential diagnosis is carried out with other acute diseases of the abdominal organs, most often with acute pancreatitis

YaB. Complications. Perforation. Differential diagnosis No. Signs Weight values ​​11 Woman 33 22 Age 40 years and older 11 33 Radiation of pain to the lower back 44 44 Error in diet 11 55 Absence of gastric history 22 66 Repeated attack 33 77 Increased nutrition 22 88 No forced position 33 99 No motor restlessness 11 1010 The abdomen is involved in breathing 44 1111 Peristalsis is heard 33 1212 Absence of dullness in the sloping parts of the abdomen 22 1313 Absence of tension in the muscles of the abdominal wall 44 1414 Hepatic dullness is preserved 33 1515 Shchetkin’s symptom is negative 33 If the sum of the weights of symptoms is 19 or more, a diagnosis of acute pancreatitis is made that

YaB. Complications. Perforation. Diagnostic algorithm for perforated gastroduodenal ulcer. Perforation of an ulcer? X-ray examination Presence of gas Absence of gas EGD Presence of an ulcer Absence of an ulcer. Operation Laparoscopy

YaB. Complications. Perforation. Treatment of perforated ulcers of the gastroduodenal zone 1. If there are indications and conditions (in combination with stenosis, bleeding, penetration, ulcers of the body of the stomach) - economical gastrectomy + sel. vagotomy. 2. ulcers of the duodenum against the background of CDN - economical gastrectomy + sel. vagotomy, Jabulei or Finney operation + sel. Vagotomy. 3. Excision of a perforated ulcer (Judda operation) + sel. vagotomy. Before the development of purulent peritonitis: With purulent peritonitis: 1. Suturing the perforation, toilet and drainage of the abdominal cavity. 2. Excision of the perforated ulcer and suturing (Judd operation), toilet and drainage of the abdominal cavity. In case of a serious condition of the patient (stroke, heart attack, etc.) 1. Conservative method of treatment: constant aspiration of gastric contents, intensive antibacterial and detoxification therapy, laparoscopic drainage of the abdominal cavity is possible

The choice of surgical method for perforated gastroduodenal ulcers according to mathematical modeling of long-term results No. Signs Weight values ​​11 Age over 30 years 2828 22 Presence of gastric history 1818 33 Duration of gastric history over 1 year 2525 44 Localization of the ulcer in the body of the stomach 3131 55 Ulcerative infiltrate more than 1 cm in diameter 4040 66 Hard edges of the ulcer 4848 77 The size of the perforated hole is more than 0.5 cm 4343 88 Concomitant chronic diseases of the respiratory and cardiovascular systems 2424 If the total weight is less than 73, the prognosis for suturing surgery is favorable

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Peptic ulcer or peptic ulcer is a complex pathological process, which is mainly based on inflammation of the mucous membrane of the gastroduodenal zone, in most cases of infectious origin, with the formation of local damage to the mucous membrane of the upper parts of the alimentary canal as a response to a violation of the endogenous balance of local factors of “aggression” and “defense” .

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The etiological involvement of the nutritional factor is not as significant as previously thought, since epidemiological studies have not confirmed the predominant prevalence of BU in those regions where hot and spicy foods are common. Smoking causes ischemia and has a direct cytotoxic effect on the mucosa. Gastric secretion directly depends on the functional state of the nervous system, and therefore sedatives are widely used in the treatment of peptic ulcers

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Technology

The high prevalence of peptic ulcers is observed among people who, due to their professional characteristics, are exposed to psycho-emotional and physical overload in combination with inadequate rest and poor diet (doctors, telephone operators, dispatchers, managers, railway and water transport workers). Among the drugs that contribute to the development of ulcers are NSAIDs (aspirin, indomethacin, etc.) and corticosteroids, antibacterial agents, digoxin, theophylline, reserpine, iron and potassium preparations.

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The hereditary factor is important in 30-40% of patients. In the first degree of relationship, duodenal ulcers occur approximately 3 times more often than in persons with uncomplicated heredity, and a predisposition to them is more often transmitted through the male line. It has been established that the following signs are genetically determined: increased number and density of parietal cells per unit surface of the gastric mucosa, increased content of pepsinogen 1 (increases the risk of ulcers by 8 times).

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Duodenal ulcers occur 1.5 times more often and are more severe in individuals with blood group 0(I)Rh+, with the presence of HLA antigens B5, B15, B35. The ratio of men to women is 4:1. It is believed that female sex hormones to some extent protect against ulcer formation. After menopause, the ratio of ulcers in men and women equalizes. At a young age, duodenal ulcers occur 13 times more often than gastric ulcers, and in older age groups, gastric ulcers predominate. In recent years, the structure of age-related morbidity has changed and the age range for peptic ulcer disease has expanded due to an increase in the number of “youthful” and “senile” ulcers.

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Today, the leading factors in the formation of ulcerative lesions are overproduction of hydrochloric acid and Helicobacter pylori infection. Researchers B. Marshall and D. Warren in 1983 did not suspect that they had opened a new era in the study of gastric diseases when they opened the incubator after a vacation week and discovered the growth of a culture of spiral-shaped bacteria from biopsies of the gastric mucosa obtained from a patient with gastritis. Today we already know that this microorganism causes gastritis in more than half of the world's population, being also the etiological factor in more than 95% of all duodenal ulcers and pustules and 90% of benign non-medicinal gastric ulcers.

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Perhaps N.R. plays a causal role in the occurrence of 60-70% of cases of stomach cancer and other diseases. A prerequisite for the existence of bacteria N.R. – a certain optimal pH level of 3-6, the presence of urea in gastric juice and the presence of gastric epithelium. All strains of N.R. produce large amounts of the enzyme urease, which hydrolyzes urea in gastric juice, resulting in the formation of carbon dioxide and ammonia. The diagnostic methods of N.R. are based on this fact. (urease test). Increased production of hydrochloric acid is important in the development of duodenal and gastric ulcers. In most patients with duodenal ulcers, basal production of hydrochloric acid is approximately three times higher than in healthy people.

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The mechanisms for regulating the secretion process are diverse. Central stimulation of secretion is initiated by thoughts about food, the sight, smell, and taste of food and begins with the activation of the hypothalamic nuclei of the efferent fibers of the vagus. Next, the excitation is transmitted through the nerve plexus of the stomach wall to many cells of the mucous membrane. Distension of the stomach by food and stimulation by food components, amino acids, and proteins of the G-cells of the antrum leads to the release of gastrin. Increasing serum gastrin levels is key to endocrine acid stimulation because... it activates the -cells located around the parietal cells in the lower third of the gastric glands and are rich in histamine.

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Gastrin binds to the surface receptors of ECL cells, as a result of which the release of histamine is stimulated, which, in turn, binds to the H2 receptor and triggers the entire intracellular biochemical chain, the result of which is the release of hydrochloric acid into the lumen of the glands and stomach. At the end of the gastric secretion phase, when the pH in the antrum reaches a value below 3, reverse processes of inhibition of gastric secretion begin. This is primarily due to the release of antral somatostatin from D-cells, which inhibits not only the function of G-cells of the antrum and the production of gastrin according to the “feedback” type, but also is a “universal brake fluid” for other hormones and biologically active substances.

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During the intestinal secretion phase, when gastric contents with a pH below 4 enter the duodenum, secretin is released from the cells of the intestinal mucosa, which inhibits both gastric secretion and the release of gastrin. Prostaglandins, which act on the parietal cell through a special receptor, also have an inhibitory effect on gastric secretion.

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But along with aggressive factors (overproduction of hydrochloric acid and pepsin, H. pylori bacteria, trauma to the gastroduodenal mucosa, impaired evacuation-motor function of the stomach and duodenogastric reflux, drugs with an ulcerogenic effect), there are also protective factors. These are the surface epithelium and the mucous-bicarbonate barrier covering it, active cellular regeneration, sufficient blood flow in the mucous membrane, and cytoprotective substances.

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It is traditionally believed that in the pathogenesis of pyloroduodenal ulcers, the strengthening of aggressive factors is of greater importance, and in the case of mediogastric ulcers, the weakening or failure of protective factors is of greater importance. That is why in the treatment of gastro-duodenal ulcers many medications are used with a variety of application points.

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Localization of peptic ulcers: gastric ulcer, duodenal ulcer (bulb, postbulbar), combined gastric and duodenal ulcers, gastrojejunal ulcer.

Classification of ulcers (according to V.G. Perederi).

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With an ulcer of the cardia or posterior wall of the stomach, the pain is localized behind the sternum and radiates to the left shoulder, resembling angina. Pain from an ulcer of the pyloroduodenal zone radiates to the back, right hypochondrium, under the right shoulder blade. Pain from a gastric ulcer is localized in the epigastric region on the left near the xiphoid process and does not radiate anywhere.

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Characteristic is the rhythm of pain and the connection with food intake. When the ulcer is localized in the cardiac region or on the back wall of the stomach, pain appears immediately after eating. An ulcer of the antral (prepyloric) stomach is indicated by hunger pain that occurs 2-3 hours after eating or late at night. The pain lasts until the stomach is emptied.

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The main symptom is pain in the epigastric region 1.5-3 hours after eating. This is a hungry, night pain that goes away after eating food or alkalis. Patients with concomitant duodenitis experience persistent night pain. Sometimes the pain is not related to food. The seasonality of pain with periods and exacerbations in autumn and spring is very characteristic.

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In addition to pain, patients are bothered by nausea and vomiting, which occurs at the height of pain and, as a rule, brings relief. Heartburn is a burning sensation in the lower third of the sternum; it can be the equivalent of pain and can intensify with changes in body position or bending downwards. The occurrence of heartburn is caused by reflux, i.e. reverse flow of stomach contents into the esophagus due to a decrease in the tone of the cardiac contactor and an increase in intragastric pressure. In addition to reflux, esophagitis plays a role in the development of heartburn. In addition, sour belching, bloating, and persistent constipation with sheep stool may occur.

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A physical examination reveals: autonomic dysfunction syndrome (increased sweating, red and white dermographism, sleep disorders, increased irritability), local soreness and muscle tension in the epigastric region and pyloroduodenal zone, increased peristalsis of the stomach and spastic condition of the colon.

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The ulcer is verified endoscopically - gastrofibroduodenoscopy. Each endoscopy must be accompanied by a biopsy to solve 3 problems: conducting a CLO test for the purpose of rapid diagnosis of Helicobacter pylori infection, collecting biopsy material for subsequent inoculation on selective media, obtaining a culture of N.R. and determining its sensitivity to various antibacterial drugs, conducting a histological examination of biopsy material to exclude rare causes of duodenal ulcers and clarify the severity of chronic gastritis.

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Urea breath test. Currently the most sensitive and easy to perform. The method is based on the fact that after oral administration of a solution of urea labeled with 13C or 14C, urease N.R. metabolizes labeled urea and releases labeled carbon dioxide, which is determined in exhaled air within 10-30 minutes. In contrast to serological reactions, the test is positive for current infection with N.R. .

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Pyloric ulcer. It is characterized by an atypical clinical syndrome, attacks of nausea, rapid loss of body weight, the pain loses its frequency, is constant, and the aching intensifies immediately after eating. Bleeding is typical (sometimes this is the first sign of the disease). Indicators of gastric secretion remain normal; diagnosis is confirmed by x-ray and endoscopic examination of ulcerative defects along the lesser curvature, most often on the posterior wall of the pylorus.

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Giant ulcers. More often detected in elderly people, they measure at least 3 cm in diameter. They are located on the lesser or greater curvature of the stomach, in the duodenal bulb. They are characterized by an atypical clinical picture - pain may resemble renal colic or pancreatitis. Giant ulcers are asymptomatic for a long time and manifest themselves as bleeding or penetration.

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Peptic ulcers should be differentiated from symptomatic ulcers, Mallory-Weiss syndrome, and Zollinger-Ellison syndrome. Acute ulcerations of the mucous membrane of the stomach and duodenum include stress, aspirin-induced, glucocorticoid-induced, heparin, and non-steroidal anti-inflammatory drugs. They can occur with acute coronary syndrome, liver cirrhosis, chronic renal failure, thyroid diseases, burns (Carling's ulcer), abuse of alcohol and other toxicants, etc.

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They are most often localized in the fundus and body of the stomach. Patients experience pain in the epigastric region, heartburn, nausea, belching, dry mouth, general weakness, and tachycardia. FGDS, Treatment - abolition of ulcerogenic drugs, prescription of H2-himstamin blockers or proton pump blockers, sucralfate.

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Mallory-Weiss syndrome is cracks and ruptures in the mucous membrane of the cardial part of the stomach, their immediate cause is repeated vomiting. Spasms of the lower esophageal closure. Cracks-ruptures are localized along the longitudinal axis of the stomach, occasionally affecting the submucosal and muscular layers. Clinic: bloody vomiting. Treatment is to stop bleeding, prescribe proton pump blockers.

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Mallory-Weiss syndrome Cracks are ruptures in the mucous membrane of the cardial part of the stomach, their immediate cause is repeated vomiting. Spasms of the lower esophageal closure. Cracks-ruptures are localized along the longitudinal axis of the stomach, occasionally affecting the submucosal and muscular layers. Clinic: bloody vomiting. Treatment is to stop bleeding, prescribe proton pump blockers.

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Zollinger-Ellison syndrome. Ulcerogenic gastrinoma (gastric secreting neuroendocrine tumor), clinically manifested by recurrent duodenal ulcerations, diarrhea (inactivation of pancreatic lipase). Acid-forming function – panhyperchlorhydria. The concentration of gastrin in the blood is increased. Treatment is proton pump inhibitors.

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Medical nutrition Diets No. 1a and 1b are prescribed in the acute phase for 2-3 days, after which they are transferred to diet No. 1, which stimulates the repair processes of the mucous membrane, prevents the development of constipation, and restores appetite. The goal is mechanical, thermal and chemical sparing of the mucous membrane. Food is given boiled, but not pureed, 5-6 times a day. The diet includes white stale bread, soups from cereals, vegetables, well-cooked porridge, mashed potatoes, and poultry meat. There is an opinion that the purpose of tables 1, 1a and 1b is only suitable for persons with complicated ulcers.

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* The essence of gastric and duodenal ulcers These are chronic recurrent diseases, prone to progression and manifested by disorders of the mucous and submucosal layers of the stomach and duodenum.

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* ETIOLOGY 1. Genetic predisposition. 2. The presence of chronic gastritis and duodenitis. 3. Infection with Helicobacter pylori and candida. 4. Dietary disorders and unbalanced nutrition. 5. Abuse of drugs with ulcerogenic effects (NSAIDs, corticosteroids) 6. Smoking and drinking alcohol.

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* PATHOGENESIS Under the influence of meteorological factors, the functional state of the cerebral cortex is disrupted, as a result, the activity of the parasympathetic nervous system increases, the motility of the stomach and duodenum is disrupted, the secretion of gastric juice is increased, and the formation of mucus and a protective film on its surface is inhibited. A dystrophic process develops in the stomach and duodenum. This is promoted by Helicobacter pylori.

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* Classification of diseases General characteristics of diseases: I. Gastric ulcer a) damage to the cordial part of the stomach; b) small curvature; c) pyloric part of the stomach. II. Duodenal ulcer a) bulb ulcer; b) post-bulb ulcer; c) ulcer of unspecified localization.

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Clinical forms: 1. Acute or newly identified. 2. Chronic Course: 1. Latent. 2. Rarely recurrent (once every 4–5 years). 3. Moderately recurrent (once every 2–3 years). 4. Often recurrent (once a year or more often).

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* Phases of exacerbation of peptic ulcers 1. Aggravated. 2. Incomplete remission. 3. Remission. Types of ulcers: Acute. 2. Scarring. 3. Non-scarring. 4. Chronic. According to the level of gastric secretion: 1. Increased. 2. Normal. 3. Reduced.

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* Complications of peptic ulcers: Bleeding. Perforation. Penetration (germination). Malignization. Stenosis. Reactive hepatitis. Reactive pancreatitis.

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* Clinic of gastric ulcer Pain in the epigastrium of varying intensity. With ulcers of the cardiac region, pain behind the sternum; occur immediately after eating and can radiate to the left shoulder. With an ulcer in the lesser curvature, pain occurs within an hour after eating. With an ulcer of the antrum and pylorus, pain occurs 1.0 - 1.5 hours after eating (late pain). With an ulcer, vomiting brings relief.

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Clinic of duodenal ulcer 1. Pain occurs 1.5 - 2 hours after eating (late pain) or on an empty stomach, i.e. hunger and night pain. 2. Typically, pain subsides after eating food or alkalis. 3. Vomiting occurs at the height of pain and brings relief. 4. Heartburn, sour belching after eating 5. Constipation is typical. 6. Increased appetite.

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* Diagnosis of peptic ulcers: Gastroduodenoscopy reveals ulcerative defects, their location, depth, nature, clarifies the presence of complications, and so on. X-ray examination of the stomach using a suspension of barium sulfate. Examination of feces for occult blood. Examination of gastric juice (does not have much diagnostic value). Examination of general blood and urine tests. Uriase tests for Helicobacter pylori.

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