GERDGERD

Functional dyspepsia Functional dyspepsia

Chronic gastritisChronic gastritislecturelecture

Lykhatska G.V. Lykhatska G.V. .

Gastroesophageal reflux disease (GERD) - Gastroesophageal reflux disease (GERD) - a a chronic relapsing disease with the development chronic relapsing disease with the development of characteristic symptoms (heartburn, of characteristic symptoms (heartburn, regurgitation, etc.) and / or inflammatory lesions regurgitation, etc.) and / or inflammatory lesions of the distal part of esophagus due to periodic of the distal part of esophagus due to periodic regurgitation into the esophagus of gastric and / regurgitation into the esophagus of gastric and / or duodenal contents.or duodenal contents.

Cause of disease

axial hiatal hernia

intense physical exertion

Stress

gastroduodenal pathology(peptic ulcer, duodenostasis)

irrational food

medications that decrease lower esophageal sphincter tonus

increased intra-abdominal pressure

The main symptom (GERD) - Heartburn - daily experience of 7 to 11% of the adult population,

at least 1 time per week - 12%

at least 1 time per month - 40-50%.

  In this pregnancy symptom is observed in 48% of women.

Mechanism of development

Classification of GERDClassification of GERD(According to unified clinical and statistical classification of diseases of (According to unified clinical and statistical classification of diseases of

the digestive system (HCD of Ukraine, 2004)the digestive system (HCD of Ukraine, 2004)-Endoscopic "-" GERD (without esophagitis)-Endoscopic "-" GERD (without esophagitis)-Endoscopic "+" GERD (with esophagitis)-Endoscopic "+" GERD (with esophagitis)Clinical forms of GERDClinical forms of GERDNonerosive GERD (Nonerosive GERD (is defined as those who have typical reflux is defined as those who have typical reflux

symptoms without evidence of erosive changes in their lower symptoms without evidence of erosive changes in their lower esophageal mucosaesophageal mucosa; observed in approximately 60% of patients with ; observed in approximately 60% of patients with GERD);GERD);

Erosive GERD (erosive changes of esophageal epithelium in varying Erosive GERD (erosive changes of esophageal epithelium in varying degree, found in 37% of patients);degree, found in 37% of patients);

Grade A - one or more mucosal breaks < 5 mm in maximal lengthGrade A - one or more mucosal breaks < 5 mm in maximal length

Grade B - one or more mucosal breaks > 5mm, but without continuity Grade B - one or more mucosal breaks > 5mm, but without continuity across mucosal foldsacross mucosal folds

Grade C - mucosal breaks continuous between > 2 mucosal folds, but Grade C - mucosal breaks continuous between > 2 mucosal folds, but involving less than 75% of the esophageal circumferenceinvolving less than 75% of the esophageal circumference

Grade D - mucosal breaks involving more than 75% of esophageal Grade D - mucosal breaks involving more than 75% of esophageal circumferencecircumference

Complications of GERD (Barrett's esophagus, peptic esophageal ulcer, Complications of GERD (Barrett's esophagus, peptic esophageal ulcer, stricture, bleeding) (defined in 3% of patients).stricture, bleeding) (defined in 3% of patients).

Signs and symptomsSigns and symptoms

Signs and symptomsSigns and symptoms

Signs and symptomsSigns and symptomsHeartburnHeartburn ( (during physical during physical exertion, in a prone position, exertion, in a prone position, after meals)after meals)

Belching air, food, sour, bitter, Belching air, food, sour, bitter, vomitingvomiting((appears due to appears due to retrograde flow of gastric retrograde flow of gastric contents into the esophagus contents into the esophagus and mouthand mouth))Chest painChest pain((occurs due to occurs due to spasm of the esophagus in spasm of the esophagus in response to acid-peptic response to acid-peptic aggressionaggression))Dysphagia. Dysphagia. ((feeling of feeling of difficulty passing food difficulty passing food through the esophagusthrough the esophagus))Increased salivation, hiccups, Increased salivation, hiccups, feeling of clutter in the throat, feeling of clutter in the throat, pain in jaw, etc.pain in jaw, etc.

Signs and symptomsSigns and symptomsBelching air, Belching air, food, sour, bitter, food, sour, bitter, regurgitation occurs because of regurgitation occurs because of retrograde reflux of gastric content into retrograde reflux of gastric content into the esophagus and mouth (more than the esophagus and mouth (more than 50% of patients);50% of patients);

Chest pain. Chest pain. Less frequently observed Less frequently observed arises from spasm of the esophagus in arises from spasm of the esophagus in response to acid-peptic aggression. response to acid-peptic aggression. Localization and irradiation are similar to Localization and irradiation are similar to symptoms in angina. In these patients, symptoms in angina. In these patients, excluding cardiac etiology is important excluding cardiac etiology is important prior to labeling the pain as noncardiac prior to labeling the pain as noncardiac chest pain secondary to GERD. chest pain secondary to GERD.

METHODS OF DIAGNOSIS GERDMETHODS OF DIAGNOSIS GERDpH-metry (one-stage and daily pH monitoring)pH-metry (one-stage and daily pH monitoring)

Normal esophageal pH - 5,5-7,0.Normal esophageal pH - 5,5-7,0.Total time of lowering intraesophagealTotal time of lowering intraesophagealpH <4.0 during the day is> 4 hours in pH <4.0 during the day is> 4 hours in patients with GERD.patients with GERD.

Internally esophageal manometryInternally esophageal manometry(is a test to assess motor function of the Upper Esophageal (is a test to assess motor function of the Upper Esophageal

Sphincter (UES), Esophageal body and Lower Esophageal Sphincter (UES), Esophageal body and Lower Esophageal Sphincter (LES). An EMS is typically done to evaluate Sphincter (LES). An EMS is typically done to evaluate suspected disorders of suspected disorders of motility or or peristalsis of the esophagus. of the esophagus. These include These include achalasia, , diffuse esophageal spasm, , nutcracker esophagus and and hypertensive lower esophageal sphincter. .

Internally esophageal Internally esophageal manometrymanometry

METHODS OF DIAGNOSIS GERDMETHODS OF DIAGNOSIS GERD

Endoscopy with analysis Endoscopy with analysis of biopsy specimens of biopsy specimens obtained during obtained during endoscopy endoscopy Endoscopically "+" signs Endoscopically "+" signs of GERD are reflux of GERD are reflux esophagitis: hyperemia esophagitis: hyperemia and friability of mucose and friability of mucose (catarrhal oesophagitis), (catarrhal oesophagitis), erosion (erosive reflux erosion (erosive reflux esophagitis varying esophagitis varying degrees of severity) and degrees of severity) and ulcerative reflux ulcerative reflux esophagitisesophagitis..

METHODS OF DIAGNOSIS GERDMETHODS OF DIAGNOSIS GERD

Chromoscopy broadly Chromoscopy broadly refers to the use of refers to the use of contrast agents to contrast agents to accentuate surface accentuate surface topography (contrast topography (contrast staining), and/or identify staining), and/or identify specific epithelia by vital specific epithelia by vital staining (absorptive staining (absorptive staining), or chemical staining), or chemical reactions (reactive reactions (reactive staining). staining).

METHODS OF DIAGNOSIS GERDMETHODS OF DIAGNOSIS GERD Vital staining could be used to identify specific Vital staining could be used to identify specific epithelia, ie, intestinal metaplasia or dysplasia epithelia, ie, intestinal metaplasia or dysplasia that are associated with the carcinogenic that are associated with the carcinogenic pathway in Barrett's esophagus, or conversely pathway in Barrett's esophagus, or conversely identifying areas unstained that may represent identifying areas unstained that may represent early malignancy. early malignancy.

Barrett esophagusBarrett esophagus

Barrett esophagusBarrett esophagus

METHODS OF DIAGNOSIS GERDMETHODS OF DIAGNOSIS GERD

X-ray study of the X-ray study of the esophagus and stomach esophagus and stomach (detects reflux, esophageal (detects reflux, esophageal stricture, diffuse stricture, diffuse esophageal spasm. This esophageal spasm. This study used for screening study used for screening diagnosis GERD).diagnosis GERD).

X-ray studyX-ray study

X-ray studyX-ray study

Test with PPI

PPI in the standard dose

duration of 7-14 days

positive with the disappearance or reduction of symptoms of GERD

if symptoms disappear(GERD )

lifestyle modificationslifestyle modifications

to avoid horizontal

position during sleep

(raising the head end of

the bed by 15 sm);

Lifestyle modificationLifestyle modification

giving up smoking and alcohol abuse;giving up smoking and alcohol abuse;

weight loss in case of excess;weight loss in case of excess;

Dietary recommendationsDietary recommendations

exclusion of overeatingexclusion of overeating

avoidance horizontal body position for 3-4 hours avoidance horizontal body position for 3-4 hours after a meal;after a meal;

refusal of food overnightrefusal of food overnight

limit foods that reducing lower esophageal limit foods that reducing lower esophageal sphincter tone (coffee, strong tea, chocolate, sphincter tone (coffee, strong tea, chocolate, mint, milk, fatty meats, spices);mint, milk, fatty meats, spices);

Pharmacological arsenalPharmacological arsenal

l Proton pump Proton pump inhibitors(inhibitors(to to effectively eliminate effectively eliminate the symptoms of the symptoms of GERD and treatment GERD and treatment of inflammatory and of inflammatory and erosive changes)erosive changes)

Proton pump inhibitorsOmeprazole - 20 mg 2 / dLansoprazole - 30 mg 2 / dPantoprazole (Kontrolok) - 40 mg

1-2 / dRabeprazole (Pariet) -20 mg 1-2 / dEsomeprazole (Neksium) - 20 mg

1-2 / d

Procinetics(Procinetics(to reinforce tone and reduce lower to reinforce tone and reduce lower esophageal sphincteresophageal sphincter))

Selective(domidon, motilium)

Nonselective(metoclopramide)

Antacids(to neutralize the hydrochloric acid and pepsin)

-almagel

-fosfalyugel

-Maalox

Treatment Guidelines-2008 Latin American Treatment Guidelines-2008 Latin American Consensus - 2010 "The best strategy in the Consensus - 2010 "The best strategy in the

treatment of GERD - appointment PPI"treatment of GERD - appointment PPI"

Not erosive formNot erosive form

Erosive form: Level A, Erosive form: Level A, Level BLevel B

  PPIs at standard doses PPIs at standard doses 1t / day in the morning 1t / day in the morning 30 minutes before 30 minutes before breakfastbreakfast

for 4 weeksfor 4 weeks

Erosive form: Level C, Erosive form: Level C, Level DLevel D

  PPIs in the double PPIs in the double standard dosage 2t / day standard dosage 2t / day (30 min. before breakfast (30 min. before breakfast and 30 min. before and 30 min. before dinner) for 8-12 weeksdinner) for 8-12 weeks

Functional dyspepsia (FD)Functional dyspepsia (FD)

Functional dyspepsia (FD) usually indicates Functional dyspepsia (FD) usually indicates abdominal discomfort or pain with no obvious abdominal discomfort or pain with no obvious organic cause that could be identified by organic cause that could be identified by endoscopy.endoscopy.

FD - is a diagnosis of exclusion. necessary is to FD - is a diagnosis of exclusion. necessary is to perform full examination of the patient and to perform full examination of the patient and to exclude organic disease, occurring with similar exclude organic disease, occurring with similar clinical signs.clinical signs.

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Persistent or recurrent pain or discomfort Persistent or recurrent pain or discomfort centered in the upper abdomen:centered in the upper abdomen:

including pain,including pain,   early satiety, nausea, vomiting,early satiety, nausea, vomiting,

abdominal distension, bloating, and anorexia abdominal distension, bloating, and anorexia

Evidence of organic disease likely to explain the Evidence of organic disease likely to explain the symptoms is absent.symptoms is absent.

Mechanism of developmentMechanism of development

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ClassificationClassification

FGIDsFGIDs ( classified by ( classified by anatomic regionanatomic region))

(A) Esophageal(A) Esophageal

(B) (B) Gastroduodenal (B1: FD)Gastroduodenal (B1: FD)

(C) (C) Bowel (C1: IBS)Bowel (C1: IBS)

(D) Functional abdominal pain(D) Functional abdominal pain

(E) Biliary(E) Biliary

(F) Anorectal. (F) Anorectal.

Classification of dyspepsiaClassification of dyspepsiaOrganic dyspepsiaOrganic dyspepsiaPUD, GERD, Pancreatico-billiry diseasePUD, GERD, Pancreatico-billiry diseaseFunctional dyspepsiaFunctional dyspepsiaUlcer-like dyspepsieaUlcer-like dyspepsiea

PainPain

Dysmotility-like dyspepsiaDysmotility-like dyspepsiaDiscomort; nausea, vomiting, postprandial fullness Discomort; nausea, vomiting, postprandial fullness

and upper abdominal bloatingand upper abdominal bloating

Reflux-like dyspepsiaReflux-like dyspepsiaHeartburn but not the predominant symptomHeartburn but not the predominant symptom

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Definitions of the symptomDefinitions of the symptom

Pain:Pain: a subjective, unpleasant sensationa subjective, unpleasant sensation

Discomfort: Discomfort: a subjective, unpleasant a subjective, unpleasant sensation or feeling that is not interpreted sensation or feeling that is not interpreted as pain according to the patient, including as pain according to the patient, including upper abdominal fullness, early satiety, upper abdominal fullness, early satiety, bloating, or nauseabloating, or nausea

centered in the upper abdomen: centered in the upper abdomen: the pain or the pain or discomfort is mainly in or around the discomfort is mainly in or around the midlinemidline

Rome III diagnostic criteria for functionalRome III diagnostic criteria for functionaldyspepsia.dyspepsia.

At least 3 months, with onset at least 6 monthsAt least 3 months, with onset at least 6 months

previously, of one or more of the following:previously, of one or more of the following:

bothersome postprandial fullnessbothersome postprandial fullness

early satiationearly satiation

epigastric painepigastric pain

epigastric burningepigastric burning

ANDAND

no evidence of structural diseaseno evidence of structural disease

(including upper endoscopy) that is likely(including upper endoscopy) that is likely

to explain the symptomsto explain the symptoms

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Dyspepsia subgroup classification -Dyspepsia subgroup classification -based on the predominant single symptombased on the predominant single symptom

1.1. Ulcer-like dyspepsia (Ulcer-like dyspepsia (ppain centered in the upper ain centered in the upper abdomenabdomen is the predominant (most is the predominant (most bothersome) symptom).bothersome) symptom).

2.2. Dysmotility-like dyspepsia (Dysmotility-like dyspepsia (An unpleasant or An unpleasant or troublesome non-painful sensation (discomfort) troublesome non-painful sensation (discomfort) centered in the upper abdomen centered in the upper abdomen is the predominant symptom) is the predominant symptom)

3.3. 3. Unspecified (non-specific) dyspepsia 3. Unspecified (non-specific) dyspepsia (symptomatic patients whose (symptomatic patients whose symptoms do not fulfill symptoms do not fulfill the criteriathe criteria for ulcer-like or dysmotility-like for ulcer-like or dysmotility-like dyspepsia)dyspepsia)

Pharmacological therapiesPharmacological therapiesH. pylori therapyH. pylori therapy - - controversial controversial

Acid suppression and prokinetic Acid suppression and prokinetic agentsagents (digestive agents) - (digestive agents) - may helpmay help

Gut analgesicsGut analgesics - - relaxants of the nervous relaxants of the nervous system of the gut may be beneficialsystem of the gut may be beneficial

Antidepressant - Antidepressant - may helpmay help

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Management of Ulcer-like Management of Ulcer-like Functional DyspepsiaFunctional Dyspepsia

Ulcer-like Symptoms Ulcer-like Symptoms DominantDominant

Ulcer-like Symptoms Ulcer-like Symptoms DominantDominant

Education/lifestyle Education/lifestyle modificationmodification

Education/lifestyle Education/lifestyle modificationmodification

Test Test HpHpTest Test HpHp

++++ ----

Eradicate Eradicate HpHp

Eradicate Eradicate HpHp

SuccessSuccessSuccessSuccess FailureFailureFailureFailure

Trial of acid Trial of acid suppressionsuppressionTrial of acid Trial of acid suppressionsuppression

InvestigatInvestigatee

InvestigatInvestigatee

Trial of Trial of prokineticprokinetic

Trial of Trial of prokineticprokinetic

ReassesReassesss

ReassesReassesss

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Management of Dysmotility-like Functional Management of Dysmotility-like Functional DyspepsiaDyspepsia

Dysmotility-like Symptoms Dominant Dysmotility-like Symptoms Dominant

Dysmotility-like Symptoms Dominant Dysmotility-like Symptoms Dominant

Educate/lifestyle Educate/lifestyle modificationmodification

Educate/lifestyle Educate/lifestyle modificationmodification

Test Test H. pyloriH. pyloriTest Test H. pyloriH. pylori

++++ ----

Continue withContinue withcyclic therapycyclic therapyContinue withContinue withcyclic therapycyclic therapy

SuccessSuccessSuccessSuccess FailureFailureFailureFailure

InvestigateInvestigateInvestigateInvestigate

Trial of prokinetic Trial of prokinetic medicationmedication

Trial of prokinetic Trial of prokinetic medicationmedication

EradicateEradicateEradicateEradicate

Gastroscopy or UGIGastroscopy or UGIGastroscopy or UGIGastroscopy or UGI

SuccessSuccessSuccessSuccess FailureFailureFailureFailureConsider HConsider H22

antagonists, antagonists, tricyclicstricyclics

Consider HConsider H22

antagonists, antagonists, tricyclicstricyclics

Chronic gastritis

Normal Normal StomachStomach

Anatomy of the stomachAnatomy of the stomach

The stomach is divided into five The stomach is divided into five regions:regions:

• cardia• cardia• fundus• fundus

• body• body• antrum• antrum

• pylorus• pylorus

Chronic gastritis Chronic gastritis - a morphological concept for - a morphological concept for which is characterized by inflammatory and which is characterized by inflammatory and degenerative processes in the gastric mucosa degenerative processes in the gastric mucosa that is accompanied by breach of the that is accompanied by breach of the processes of cell regeneration, progressive processes of cell regeneration, progressive atrophy of the glandular epithelium, a violation atrophy of the glandular epithelium, a violation of the secretory, motor and incretory functions of the secretory, motor and incretory functions of the stomach.of the stomach.

Types of gastritisTypes of gastritis

Etiology.Etiology.

Leading role in the development of chronic gastritis plays Leading role in the development of chronic gastritis plays Hp..Hp..

Etiologic factors of endogenous origin include genetic Etiologic factors of endogenous origin include genetic predisposition, chronic infections, autoimmune and predisposition, chronic infections, autoimmune and endocrine diseases, food allergies.endocrine diseases, food allergies.

Major risk factors: violation diet, smoking, alcohol, stress, Major risk factors: violation diet, smoking, alcohol, stress, medications (NSAIDs).medications (NSAIDs).

Pathogenesis.Pathogenesis.

There are different mechanisms of pathogenesis There are different mechanisms of pathogenesis of chronic gastritis depending on the form of the of chronic gastritis depending on the form of the disease distinguish.disease distinguish.

Chronic gastritis caused by Helicobacter pylori Chronic gastritis caused by Helicobacter pylori (Hp) – is the most common form, affects antral (Hp) – is the most common form, affects antral part,part, but may be diffusebut may be diffuse

Intestinale metaplasia in chronic gastritisIntestinale metaplasia in chronic gastritis

Type A (autoimmune gastritis). Type A (autoimmune gastritis). 

Acute gastritis with superficial erosions.Acute gastritis with superficial erosions.

Endoscopic picture antral gastritisEndoscopic picture antral gastritis

Chronic Gastritis in the gastric body caused Chronic Gastritis in the gastric body caused by Helicobacter pyloriby Helicobacter pylori

aa |  | Multifocal atrophic gastritis is caused by long-standing Multifocal atrophic gastritis is caused by long-standing Helicobacter pyloriHelicobacter pylori infection  infection and is characterized by antrum-predominant or pangastritis and various degrees of and is characterized by antrum-predominant or pangastritis and various degrees of

metaplastic atrophy (blue patches) that invariably involve the antrum and might extend metaplastic atrophy (blue patches) that invariably involve the antrum and might extend into the corpus. into the corpus. bb | In autoimmune gastritis, the inflammatory atrophic process involves  | In autoimmune gastritis, the inflammatory atrophic process involves exclusively the corpus (grey discoloration) and patches of intestinal, pseudopyloric and exclusively the corpus (grey discoloration) and patches of intestinal, pseudopyloric and

pancreatic metaplasia are found throughout the gastric pancreatic metaplasia are found throughout the gastric body and fundus.body and fundus.

Clinical featuresClinical featuresThe main clinical syndromes :The main clinical syndromes :

1. Pain - pain in the epigastric region after eating, especially 1. Pain - pain in the epigastric region after eating, especially spicy, rough, fried; smoking;spicy, rough, fried; smoking;

2. Gastric dyspepsia: a feeling of heaviness and discomfort in the 2. Gastric dyspepsia: a feeling of heaviness and discomfort in the epigastrium after eating, belching, and sometimes heartburn, epigastrium after eating, belching, and sometimes heartburn, regurgitation, nausea, vomiting.regurgitation, nausea, vomiting.

3. Intestinal dyspepsia: bloating, rumbling and transfusion in 3. Intestinal dyspepsia: bloating, rumbling and transfusion in abdominal disorders emptying;abdominal disorders emptying;

4. Asthenic syndrome : increased irritability, emotional lability, 4. Asthenic syndrome : increased irritability, emotional lability, sleep disorderssleep disorders

5. Anemic syndrome: pale skin, bleeding gums, brittle nails, 5. Anemic syndrome: pale skin, bleeding gums, brittle nails, hyperkeratosis, premature hair loss (only in patients with hyperkeratosis, premature hair loss (only in patients with autoimmune gastritis, which is associated with pernicious autoimmune gastritis, which is associated with pernicious anemia).anemia).

Laboratory analysis and other Laboratory analysis and other studies:studies:

Complete blood count (pernicious anemia - patients with Complete blood count (pernicious anemia - patients with autoimmune gastritis, eosinophilia in chronic eosinophilic autoimmune gastritis, eosinophilia in chronic eosinophilic gastritis)gastritis)

Stool sample, to look for blood in the stoolStool sample, to look for blood in the stool

Determination of antibodies to parietal cells (autoimmune Determination of antibodies to parietal cells (autoimmune gastritis)gastritis)

Definition of blood bilirubin, total protein (hypoproteinemia) Definition of blood bilirubin, total protein (hypoproteinemia) protein fractions in serum (dysproteinemia with protein fractions in serum (dysproteinemia with hypergamma-globulinemia in autoimmune gastritis), hypergamma-globulinemia in autoimmune gastritis),

endoscopy with biopsyendoscopy with biopsy

Definition HpDefinition Hp

chromoendoscopy - for early detection areas dysplasia chromoendoscopy - for early detection areas dysplasia of the gastric mucosaof the gastric mucosa

Intragastric pH-metry - for evaluation of gastric acidityIntragastric pH-metry - for evaluation of gastric acidity

Differential diagnosisDifferential diagnosis

The differential diagnosis make with: The differential diagnosis make with: peptic ulcer, stomach cancerpeptic ulcer, stomach cancer,,chronic chronic pancreatitis, chronic cholecystitis, biliary pancreatitis, chronic cholecystitis, biliary dyskinesia, functional dyspepsia, between dyskinesia, functional dyspepsia, between different types of chronic gastritis (type A different types of chronic gastritis (type A and type B)and type B)

sign Chronic gastritis type A Chronic gastritis type B

Leading syndrome dyspeptic pain

Characterization of stool Tendency to diarrhea constipation

appetite reduced saved

Expressed gastrin emia there is not There are

Acid-producing function of the stomach reduced Normal or increased

Development of B12-deficiency anemia typical Not typical

Malignization often Very rarely

Localization of lesions The bottom of the body of the stomach

Antrum

Inflammatory reaction mild expressed

Development of atrophy of the epithelium primary secondary

The presence of erosions rarely often

The presence of Hp not always There are

Antibodies to parietal cells There are there is not

Antibodies to intrinsic factor Castle There are there is not

TreatmentTreatment1. 1. Disclaimer patients from drinking alcohol, Disclaimer patients from drinking alcohol, smoking, compliance regime food, work andsmoking, compliance regime food, work and restrest

2. Diet (secretory deficiency-table2. Diet (secretory deficiency-table№2)№2)

In chronic gastritis with increased secretionIn chronic gastritis with increased secretion ––tabletable№1№1

3. Drug treatment:3. Drug treatment:

Principles of treatment ChG type APrinciples of treatment ChG type Aa) Anti-inflammatory therapya) Anti-inflammatory therapy

includes treatment for one of the schemes in accordance with the includes treatment for one of the schemes in accordance with the recommendations of the Maastricht-2000, 2005 Among the recommendations of the Maastricht-2000, 2005 Among the antibiotics used amoxicillin, clarithromycin, metronidazole, antibiotics used amoxicillin, clarithromycin, metronidazole, tetracycline, tetracycline, bismuthbismuth subcitrate. subcitrate.

Gastrocytoprotective therapy (sucralfate (Venter) and 1 g 3 times / Gastrocytoprotective therapy (sucralfate (Venter) and 1 g 3 times / day for 40-60 minutes before eating, de-nol 120 mg 4 times / day), day for 40-60 minutes before eating, de-nol 120 mg 4 times / day), stimulants of prostaglandins synthesis (misoprostol 200 mcg 3 stimulants of prostaglandins synthesis (misoprostol 200 mcg 3 times / day, mukogen 100 mg 3 times / day before meals);times / day, mukogen 100 mg 3 times / day before meals);

b) drugs that stimulate the secretory function of the stomach: b) drugs that stimulate the secretory function of the stomach: plantahlyutsyd 1 g 3 times a day before meals, plantahlyutsyd 1 g 3 times a day before meals, plantainplantain juice 15 ml juice 15 ml 2-3 times a day for 15 minutes before eating.2-3 times a day for 15 minutes before eating.

c) replacement therapy - natural gastric juice 1 tbsp. spoon, c) replacement therapy - natural gastric juice 1 tbsp. spoon, previously dissolved in 100 ml of water, atsydyn-pepsin on 1 tab. 3 previously dissolved in 100 ml of water, atsydyn-pepsin on 1 tab. 3 times / day during a meal, abomin 200 mg 3 times / day during times / day during a meal, abomin 200 mg 3 times / day during meals.meals.

Principles of treatment ChG Principles of treatment ChG type B:type B:

a) Eradication of Hpa) Eradication of Hp

b) Anti-inflammatory therapy (gastrocytoprotectors, stimulators of b) Anti-inflammatory therapy (gastrocytoprotectors, stimulators of prostaglandin synthesis)prostaglandin synthesis)

c) Antisecretory drugs:c) Antisecretory drugs:

PPIs (omeprazole, lansoprazole, pantoprazole, rabeprazole, PPIs (omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole)esomeprazole)

H2 histaminoblocks (ranitidine, famotidine)H2 histaminoblocks (ranitidine, famotidine)

antacids (almagel, Maalox)antacids (almagel, Maalox)

cholineblocks cholineblocks ((gastrotsepingastrotsepin, , platifillinplatifillin))

d) motor disorders correction (primer, domperidon. d) motor disorders correction (primer, domperidon. metoclopramide)metoclopramide)

e) Reparative Therapy (Solcoseryl, gastrofarm)e) Reparative Therapy (Solcoseryl, gastrofarm)

Physiotherapy treatment (ultrasound therapy, galvanization, Physiotherapy treatment (ultrasound therapy, galvanization, electrophoresis,diadynamic, paraffin,);electrophoresis,diadynamic, paraffin,);

Thank you for attention