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Chronic Gastritis
• Definition
• CG – is a chronic inflammation of the gastric mucosa with the restructuring of its structure and progressive atrophy,
disorders of secretory, motor and endocrine functions, with different clinical manifestations .
• CG is the most common diseases among diseases of the digestive system. Its prevalence among adult population is
50-80%.
• Etiology
The most common cause of chronic gastritis is infection with the bacillus Helicobacter pylori - 90%.
Other causative factors:
- heavy use of NSAIDS, especially aspirin;
- excessive alcohol consumption;
- heavy smoking;
- severe stress, that is trauma, burns, surgery;
- Ischemia;
- systemic infection;
Imbalanse between the protection factor and aggression factor.5%
Pathogenesis
• H.Pylory produces urease;
• Under the influence of urea, urease is converted into ammonia and carbon dioxide, 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);
• Excess hydrochloric acid enters the initial part of duodenum (bulb) and strongly acidifies its contents. Under the
influence of hydrochloric acid the cells of epithelium of the bulb of duodenum undergo metaplasia. While creating
favorable conditions for the colonization of HP. This leads to the development of chronic duodenitis, more
precisely gastroduodenitis according to the above scheme;
• 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.
Classification Chronic gastritis
• Type A (autoimmune) characterized by the presence of antibodies to parietal cells, a high level of
gastrin in the blood and a predominant lesion of the body of the stomach;
• Type B develops as a result of infection of the gastric mucosa of HP and bacterial inflammation,
mainly the antrum of the stomach, a normal or reduced level of gastrin in the blood and the
absence of immune disorders;
• Type C develops as a result duodenal gastric reflux or influence on mucosa of some medical
product, more often non-steroid anti inflammatory agents or chemical substances;
• Pangastrite (mixed type A and B).
Clinical manifestation:-
The symptoms are not specific.
With chronic gastritis and duodenitis the following syndromes are revealed:
• Pain syndrome (a dull, aching pain in the epigastric region);
• Dyspeptic syndrome (heartburn, belching, eructation, sometimes nausea and vomiting, which
usually occurs when the errors in the diet, bloating, flatulence);
• Asthenovegetative syndrome (general weakness, fatigue).
Methods of investigation of CG and CD
• During inspection we can not find specific signs of CG and CD
• At palpation can detect pain and tenderness in epigastric region
• Since clinical studies do not reveal any specific changes in the diagnosis of CG and CD, great
important is played by additional methods of investigation:
Diagnosis of HP
X-ray
Upper-endoscopy
Modern methods of diagnosing HP
• Bacteriological method – is a specific method of directly determining the sensibility of
HP to antibacterial drugs. Limitations: the need for
special laboratory equipment, adherence to fens rules transportation, selection of
special media.
• Histological method – reveals the degree of dissemination of HP.
• Cytological method – simple, fast and sensitive way of diagnosis; parietal mucosa is
obtained with a brush included in the endoscope.
• Maastricht IV (2012) recommends non invasive methods for diagnosis of HP – urease
respiratory test, study feces for the presence of antigens, with the use monoclonal
antibodies.
Urease respiratory test (URT)
• Urease respiratory test (URT) based on
the definition of 13C urea, is the best
of all HP diagnostic tests, as it is a fast
and highly accurate method. URT can
be used for both - primary diagnosis of
HP and for evaluation eradication of
HP.
Upper-endoscopy (UE)
• UE is performed on an empty stomach in the
morning. In normally the mucosa of the
stomach and duodenum smooth, pale pink in
color and is covered with a thin layer of
mucus.
• In case of CG and CD on UE is revealed
redness, swelling and erosion of mucosa of
stomach and duodenum
X-ray
At the X-ray examination of stomach and
duodenum, the following structural
changes can be detected:
broad and exaggerated folds of gastric
mucosa,
or the small, inconspicuous creases,
or absence of gastric mucosa.
Complications of CG and CD
• Ulcer of stomach and duodenum
• Cancer of stomach and
duodenum
• Types of anemia
Treatment of CG and CD
• Treatment includes non-pharmacological and drug therapy.
• Non – pharmacology therapy includes diet-therapy:
- 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 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.
HP eradication therapy regimens recommended by the Maastricht
Consensus V (Florence 2010)
• Clarithromycin (josamycin) 500 mg 2 times per day + amoxicillin 1000 mg 2 times per day. The duration
of treatment is 10-14 days.
• Clarithromycin (josamycin) 500 mg 2 times per day + amoxicillin 1000 mg 2 times per day + bismuth
tricalcium dicitrate – 120 mg 4 times per day or 240 mg 2 times per day. This increase the efficiency of
eradication by 15-20% and supplemented by the anti - inflammatory action of bismuth. The duration
of treatment is 10-14days.
• PPI + bismuth tricalcium dicitrate + metronidazole + tetracycline
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)
Choice of therapy for some other conditions
Patients with chronic atrophic gastritis
Bismuth tricalcium dicitrate 240 mg 2 times per day or 120 mg 4 times per day +
clarithromycin 500 mg 2 times per day + amoxicillin 1000 mg 2 times per day
(duration 10-14 days)
Elderly patients with situation when high – great anti HP therapy impossible
Bismuth tricalcium dicitrate 240 mg 2 times per day or 120 mg 4 times per day
+PPI (omeprazole or lansoprazole 2 times per day) + amoxicillin 1000 mg 2 times
per day (duration 14 days) or bismuth tricalcium dicitrate 120 mg 4 times per
day (duration 28 days)
In the presence of pain syndrome – a short course of PPI
The eradication of HP to pregnant women is not indicated

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Chronic gastritis and duodenitis

  • 1. Chronic Gastritis • Definition • CG – is a chronic inflammation of the gastric mucosa with the restructuring of its structure and progressive atrophy, disorders of secretory, motor and endocrine functions, with different clinical manifestations . • CG is the most common diseases among diseases of the digestive system. Its prevalence among adult population is 50-80%. • Etiology The most common cause of chronic gastritis is infection with the bacillus Helicobacter pylori - 90%. Other causative factors: - heavy use of NSAIDS, especially aspirin; - excessive alcohol consumption; - heavy smoking; - severe stress, that is trauma, burns, surgery; - Ischemia; - systemic infection; Imbalanse between the protection factor and aggression factor.5%
  • 2. Pathogenesis • H.Pylory produces urease; • Under the influence of urea, urease is converted into ammonia and carbon dioxide, 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); • Excess hydrochloric acid enters the initial part of duodenum (bulb) and strongly acidifies its contents. Under the influence of hydrochloric acid the cells of epithelium of the bulb of duodenum undergo metaplasia. While creating favorable conditions for the colonization of HP. This leads to the development of chronic duodenitis, more precisely gastroduodenitis according to the above scheme; • 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.
  • 3. Classification Chronic gastritis • Type A (autoimmune) characterized by the presence of antibodies to parietal cells, a high level of gastrin in the blood and a predominant lesion of the body of the stomach; • Type B develops as a result of infection of the gastric mucosa of HP and bacterial inflammation, mainly the antrum of the stomach, a normal or reduced level of gastrin in the blood and the absence of immune disorders; • Type C develops as a result duodenal gastric reflux or influence on mucosa of some medical product, more often non-steroid anti inflammatory agents or chemical substances; • Pangastrite (mixed type A and B). Clinical manifestation:- The symptoms are not specific. With chronic gastritis and duodenitis the following syndromes are revealed: • Pain syndrome (a dull, aching pain in the epigastric region); • Dyspeptic syndrome (heartburn, belching, eructation, sometimes nausea and vomiting, which usually occurs when the errors in the diet, bloating, flatulence); • Asthenovegetative syndrome (general weakness, fatigue).
  • 4. Methods of investigation of CG and CD • During inspection we can not find specific signs of CG and CD • At palpation can detect pain and tenderness in epigastric region • Since clinical studies do not reveal any specific changes in the diagnosis of CG and CD, great important is played by additional methods of investigation: Diagnosis of HP X-ray Upper-endoscopy
  • 5. Modern methods of diagnosing HP • Bacteriological method – is a specific method of directly determining the sensibility of HP to antibacterial drugs. Limitations: the need for special laboratory equipment, adherence to fens rules transportation, selection of special media. • Histological method – reveals the degree of dissemination of HP. • Cytological method – simple, fast and sensitive way of diagnosis; parietal mucosa is obtained with a brush included in the endoscope. • Maastricht IV (2012) recommends non invasive methods for diagnosis of HP – urease respiratory test, study feces for the presence of antigens, with the use monoclonal antibodies.
  • 6. Urease respiratory test (URT) • Urease respiratory test (URT) based on the definition of 13C urea, is the best of all HP diagnostic tests, as it is a fast and highly accurate method. URT can be used for both - primary diagnosis of HP and for evaluation eradication of HP.
  • 7. Upper-endoscopy (UE) • UE is performed on an empty stomach in the morning. In normally the mucosa of the stomach and duodenum smooth, pale pink in color and is covered with a thin layer of mucus. • In case of CG and CD on UE is revealed redness, swelling and erosion of mucosa of stomach and duodenum
  • 8. X-ray At the X-ray examination of stomach and duodenum, the following structural changes can be detected: broad and exaggerated folds of gastric mucosa, or the small, inconspicuous creases, or absence of gastric mucosa.
  • 9. Complications of CG and CD • Ulcer of stomach and duodenum • Cancer of stomach and duodenum • Types of anemia
  • 10. Treatment of CG and CD • Treatment includes non-pharmacological and drug therapy. • Non – pharmacology therapy includes diet-therapy: - 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 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.
  • 11. HP eradication therapy regimens recommended by the Maastricht Consensus V (Florence 2010) • Clarithromycin (josamycin) 500 mg 2 times per day + amoxicillin 1000 mg 2 times per day. The duration of treatment is 10-14 days. • Clarithromycin (josamycin) 500 mg 2 times per day + amoxicillin 1000 mg 2 times per day + bismuth tricalcium dicitrate – 120 mg 4 times per day or 240 mg 2 times per day. This increase the efficiency of eradication by 15-20% and supplemented by the anti - inflammatory action of bismuth. The duration of treatment is 10-14days. • PPI + bismuth tricalcium dicitrate + metronidazole + tetracycline 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. Choice of therapy for some other conditions Patients with chronic atrophic gastritis Bismuth tricalcium dicitrate 240 mg 2 times per day or 120 mg 4 times per day + clarithromycin 500 mg 2 times per day + amoxicillin 1000 mg 2 times per day (duration 10-14 days) Elderly patients with situation when high – great anti HP therapy impossible Bismuth tricalcium dicitrate 240 mg 2 times per day or 120 mg 4 times per day +PPI (omeprazole or lansoprazole 2 times per day) + amoxicillin 1000 mg 2 times per day (duration 14 days) or bismuth tricalcium dicitrate 120 mg 4 times per day (duration 28 days) In the presence of pain syndrome – a short course of PPI The eradication of HP to pregnant women is not indicated