Gastro-esophageal reflux disease. Chronic gastritis. Lykhatska G.V.

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

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• 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.

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• Classification of GERD
• (According to unified clinical and statistical
  classification of diseases of the digestive
  system (HCD of Ukraine, 2004)
• -Endoscopic "-" GERD (without esophagitis)
• -Endoscopic "" GERD (with esophagitis)
• Clinical forms of GERD
• Nonerosive GERD (is defined as those who have
  typical reflux symptoms without evidence of
  erosive changes in their lower esophageal mucosa
  observed in approximately 60 of patients with
  GERD)
• Erosive GERD (erosive changes of esophageal
  epithelium in varying degree, found in 37 of
  patients)
• Grade A - one or more mucosal breaks lt 5 mm in
  maximal length
• Grade B - one or more mucosal breaks gt 5mm, but
  without continuity across mucosal folds
• Grade C - mucosal breaks continuous between gt 2
  mucosal folds, but involving less than 75 of the
  esophageal circumference
• Grade D - mucosal breaks involving more than 75
  of esophageal circumference
• Complications of GERD (Barrett's esophagus,
  peptic esophageal ulcer, stricture, bleeding)
  (defined in 3 of patients).

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Signs and symptoms

• Heartburn
• Belching air, food, sour, bitter, vomiting
• Chest pain
• Dysphagia.
• Increased salivation, hiccups, feeling of clutter
  in the throat, pain in jaw, etc.

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Signs and symptoms

• Belching air, food, sour, bitter, regurgitation
  occurs because of retrograde reflux of gastric
  content into the esophagus and mouth (more than
  50 of patients)
• Chest pain. Less frequently observed arises from
  spasm of the esophagus in response to acid-peptic
  aggression. Localization and irradiation are
  similar to symptoms in angina. In these patients,
  excluding cardiac etiology is important prior to
  labeling the pain as noncardiac chest pain
  secondary to GERD.

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METHODS OF DIAGNOSIS GERD

• pH-metry (one-stage and daily pH monitoring)
• Normal esophageal pH - 5,5-7,0.
• Total time of lowering intraesophageal
• pH lt4.0 during the day isgt 4 hours in
• patients with GERD.
• Internally esophageal manometry
• (is a test to assess motor function of the Upper
  Esophageal Sphincter (UES), Esophageal body and
  Lower Esophageal Sphincter (LES). An EMS is
  typically done to evaluate suspected disorders of
  motility or peristalsis of the esophagus. These
  include achalasia, diffuse esophageal spasm,
  nutcracker esophagus and hypertensive lower
  esophageal sphincter.

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METHODS OF DIAGNOSIS GERD

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

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METHODS OF DIAGNOSIS GERD

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

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METHODS OF DIAGNOSIS GERD

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

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METHODS OF DIAGNOSIS GERD

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

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Pharmacological arsenal

• Proton pump inhibitors
• Prokinetics
• Antacids

• Proton pump inhibitors
• Omeprazole - 20 mg 2 / d
• Lansoprazole - 30 mg 2 / d
• Pantoprazole (Kontrolok) - 40 mg 1-2 / d
• Rabeprazole (Pariet) -
• 20 mg 1-2 / d
• Esomeprazole (Neksium) - 20 mg 1-2 / d

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Treatment Guidelines-2008 Latin American
Consensus - 2010 "The best strategy in the
treatment of GERD - appointment PPI"

• Not erosive form
• Erosive form Level A, Level B
•  PPIs at standard doses 1t / day in the morning
  30 minutes before breakfast
• for 4 weeks

• Erosive form Level C, Level D
•  PPIs in the double standard dosage 2t / day (30
  min. before breakfast and 30 min. before dinner)
  for 8-12 weeks

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Functional dyspepsia (FD)

• Functional dyspepsia (FD) usually indicates
  abdominal discomfort or pain with no obvious
  organic cause that could be identified by
  endoscopy.
• FD - is a diagnosis of exclusion. necessary is
  to perform full examination of the patient and to
  exclude organic disease, occurring with similar
  clinical signs.

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Definition

• Persistent or recurrent pain or discomfort
  centered in the upper abdomen
• including pain,  early satiety, nausea,
  vomiting, abdominal distension, bloating, and
  anorexia
• Evidence of organic disease likely to explain the
  symptoms is absent.

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Classification

• FGIDs ( classified by anatomic region)
• (A) Esophageal
• (B) Gastroduodenal (B1 FD)
• (C) Bowel (C1 IBS)
• (D) Functional abdominal pain
• (E) Biliary
• (F) Anorectal.

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Classification of dyspepsia

• Organic dyspepsia
• PUD, GERD, Pancreatico-billiry disease
• Functional dyspepsia
• Ulcer-like dyspepsiea
• Pain
• Dysmotility-like dyspepsia
• Discomort nausea, vomiting, postprandial
  fullness and upper abdominal bloating
• Reflux-like dyspepsia
• Heartburn but not the predominant symptom

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Definitions of the symptom

• Pain a subjective, unpleasant sensation
• Discomfort a subjective, unpleasant sensation
  or feeling that is not interpreted as pain
  according to the patient, including upper
  abdominal fullness, early satiety, bloating, or
  nausea
• centered in the upper abdomen the pain or
  discomfort is mainly in or around the midline

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Rome III diagnostic criteria for
functionaldyspepsia.

• At least 3 months, with onset at least 6 months
• previously, of one or more of the following
• bothersome postprandial fullness
• early satiation
• epigastric pain
• epigastric burning
• AND
• no evidence of structural disease
• (including upper endoscopy) that is likely
• to explain the symptoms

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Dyspepsia subgroup classification -based on
the predominant single symptom

• Ulcer-like dyspepsia (pain centered in the upper
  abdomen is the predominant (most bothersome)
  symptom).
• Dysmotility-like dyspepsia (An unpleasant or
  troublesome non-painful sensation (discomfort)
  centered in the upper abdomen
  is the
  predominant symptom)
• 3. Unspecified (non-specific) dyspepsia
  (symptomatic patients whose symptoms do not
  fulfill the criteria for ulcer-like or
  dysmotility-like dyspepsia)

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Pharmacological therapies

• H. pylori therapy - controversial
• Acid suppression and prokinetic agents (digestive
  agents) - may help
• Gut analgesics - relaxants of the nervous system
  of the gut may be beneficial
• Antidepressant - may help

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Management of Ulcer-like Functional Dyspepsia
Ulcer-like Symptoms Dominant
Education/lifestyle modification
Test Hp

-
Eradicate Hp
Trial of acid suppression
Reassess
Success
Failure
Investigate
Trial of prokinetic
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Management of Dysmotility-like Functional
Dyspepsia
Dysmotility-like Symptoms Dominant
Educate/lifestyle modification
Trial of prokinetic medication
Success
Failure
Investigate
Continue withcyclic therapy
Test H. pylori
Gastroscopy or UGI

-
Eradicate
Consider H2antagonists, tricyclics
Success
Failure
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Chronic gastritis
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Normal Stomach
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Anatomy of the stomach

• The stomach is divided into five regions
  cardia fundus body
  antrum pylorus

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

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• Chronic gastritis is a widespread disease of the
  digestive system, in which worldwide affects
  about 20-30 of the total adult population.

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Etiology.

• Leading role in the development of chronic
  gastritis plays Hp. These microorganisms by
  enzyme activity (urease, phospholipase, etc.)
  produce cytotoxin, which penetrate into the
  intercellular spaces that results in damage of
  gastric mucose and trigger a cascade of
  immunoinflammatory reactions.
• Etiologic factors of endogenous origin include
  genetic predisposition, chronic infections,
  autoimmune and endocrine diseases, food
  allergies.
• Major risk factors violation diet, smoking,
  alcohol, stress, medications (NSAIDs).

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Pathogenesis.

• There are different mechanisms of pathogenesis of
  chronic gastritis depending on the form of the
  disease distinguish.
• Chronic gastritis caused by Helicobacter pylori
  (Hp) is the most common form, affects antral
  part, but may be diffuse

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• Autoimmune gastritis (type A) is characterized by
  production of autoantibodies to the cells of the
  gastric mucosa. There is a progressive atrophy of
  the gastric mucosa, development B12-deficiency
  anemia. Its characterized by the prevalence of
  atrophic processes of inflammation, hypoacidity,
  affectes mainly fundal part of the stomach.

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Pathogenesis.

• Chemical chronic gastritis (reactive reflux
  gastritis) affects antrum associated with
  alcohol, bile reflux (after gastrectomy,
  pyloroplasty, blending gastroduodenoanastomosis),
  use of nonsteroidal anti-inflammatory agents.
  Damaging effect of chemical substances on gastric
  mucosal barrier leads to degranulation of mast
  cells, increased vascular permeability and edema.

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Pathogenesis.

• Lymphocytic chronic gastritis often causes damage
  fundus of the stomach, may be pangastritis .
  Observed in immune disorders, celiac disease.
  Etiologic this form of chronic gastritis may be
  associated with helicobacterial infection. In
  such cases, the reaction of the mucous membrane
  of the stomach may be caused by abnormal immune
  response to the presence of Hp. Lymphocytic
  gastritis may be one sign of the phases of
  development or progression Menetrier's disease.
• For hypertrophic gastritis (Menetrier's disease)
  is characterized by proliferation of mucosa,
  which leads to the formation of giant folds of
  the type of "brain convolutions replacement
  glands of mucose by adenomatous cysts.

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Pathogenesis.

• Noninfectious granulomatous chronic gastritis
  more common in Crohn's disease (about 50 of all
  cases of granulomatous gastritis), sarcoidosis.
• Eosinophilic chronic gastritis (allergic) is
  rare, often caused by food allergies, can occur
  in case of vasculitis, connective tissue
  diseases, combined with marked eosinophilia in
  the peripheral blood. Its characterized by the
  appearance of eosinophilic infiltrates in the
  gastric mucosa, epithelial damage, including
  necrosis. Often in the pathological process
  involves the esophagus, small and large
  intestine.

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• Autoimmune gastritis (type A) is characterized by
  production of autoantibodies to the cells of the
  gastric mucosa. There is a progressive atrophy of
  the gastric mucosa, development B12-deficiency
  anemia. Its characterized by the prevalence of
  atrophic processes of inflammation, hypoacidity,
  affectes mainly fundal part of the stomach.

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Clinical features

• The main clinical syndromes
• 1. Pain - pain in the epigastric region after
  eating, especially spicy, rough, fried smoking
• 2. Gastric dyspepsia a feeling of heaviness and
  discomfort in the epigastrium after eating,
  belching, and sometimes heartburn, regurgitation,
  nausea, vomiting.
• 3. Intestinal dyspepsia bloating, rumbling and
  transfusion in abdominal disorders emptying
• 4. Asthenic syndrome increased irritability,
  emotional lability, sleep disorders
• 5. Anemic syndrome pale skin, bleeding gums,
  brittle nails, hyperkeratosis, premature hair
  loss (only in patients with autoimmune gastritis,
  which is associated with pernicious anemia).

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Laboratory analysis and other studies

• Complete blood count (pernicious anemia -
  patients with autoimmune gastritis, eosinophilia
  in chronic eosinophilic gastritis)
• Stool sample, to look for blood in the stool
• Determination of antibodies to parietal cells
  (autoimmune gastritis)
• Definition of blood bilirubin, total protein
  (hypoproteinemia) protein fractions in serum
  (dysproteinemia with hypergamma-globulinemia in
  autoimmune gastritis),

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• ? endoscopy with biopsy (if superficial gastritis
  endoscopically detected inflammatory edema and
  hyperemia of the stomach mucosa, hypertrophic
  gastritis is characterized by swelling and
  redness of the mucosa, the presence of small
  hemorrhages, mucosal folds thickened, rigid,,
  atrophic gastritis (autoimmune gastritis)
  manifested smoothing wrinkles and thinning of the
  stomach mucosa, through which rayed blood
  vessels, hemorrhagic gastritis characterized
  polymorphic spots hemorrhage against the backdrop
  of the inflammatory edema and hyperemia of the
  gastric mucosa to the presence of layers of
  fibrin
• ? morphological study of biopsy (advantage in the
  preparation of neutrophils infiltrating own plate
  gastric mucosa indicates activity chronic
  gastritis, infiltration of predominantly
  lymphocytes and plasma characterizes the severity
  of chronic inflammation). Diagnosis chronic
  gastritis is the morphological, this installation
  is only possible after confirmation of changes in
  the gastric mucosa by morphological study of
  biopsies in accordance with the recommendations
  of the Sydney system.

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• ? Definition Hp
• ? chromoendoscopy - for early detection areas
  dysplasia of the gastric mucosa
• ? Intragastric pH-metry - for evaluation of
  gastric acidity

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Differential diagnosis

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

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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
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Treatment

• 1. Disclaimer patients from drinking alcohol,
  smoking, compliance regime food, work and rest
• 2. Diet (secretory deficiency-table?2)
• In chronic gastritis with increased secretion
  table?1

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• 3. Drug treatment
• Principles of treatment ChG type A
• a) Anti-inflammatory therapy
• ? includes treatment for one of the schemes in
  accordance with the recommendations of the
  Maastricht-2000, 2005 (with the exception of
  antisecretory drugs). Among the antibiotics used
  amoxicillin, clarithromycin, metronidazole,
  tetracycline, bismuth subcitrate.
• ? Gastrocytoprotective therapy (sucralfate
  (Venter) and 1 g 3 times / day for 40-60 minutes
  before eating, de-nol 120 mg 4 times / day),
  stimulants of prostaglandins synthesis
  (misoprostol 200 mcg 3 times / day, mukogen 100
  mg 3 times / day before meals)
• b) drugs that stimulate the secretory function of
  the stomach plantahlyutsyd 1 g 3 times a day
  before meals, plantain juice 15 ml 2-3 times a
  day for 15 minutes before eating.
• c) replacement therapy - natural gastric juice 1
  tbsp. spoon, 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
  meals.

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• d) Correction of digestion in the gut
  pancreatin, mezim forte, Creon, pangrol, Festal,
  panzinorm.
• e) Correction of motor function prokinetic
  (primer, domperidone ,metoclopramide 10 mg 3
  times a day for 15-20 minutes before meals and at
  bedtime)
• f) Stimulation of regenerative and reparative
  processes in the gastric mucosa (Methyluracilum, )

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Principles of treatment ChG type B

• a) Eradication of Hp
• b) Anti-inflammatory therapy (gastrocytoprotectors
  , stimulators of prostaglandin synthesis)
• c) Antisecretory drugs
• ? PPIs (omeprazole, lansoprazole, pantoprazole,
  rabeprazole, esomeprazole)
• ? H2 histaminoblocks (ranitidine, famotidine)
• ? antacids (almagel, Maalox)
• ? cholineblocks (gastrotsepin, platifillin)
• d) motor disorders correction (primer,
  domperidon. metoclopramide)
• e) Reparative Therapy (Solcoseryl, hastrofarm)
• Physiotherapy treatment (ultrasound therapy,
  galvanization, electrophoresis,diadynamic,
  paraffin,)

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Thank you for attention