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GERD
Functional dyspepsia
Chronic gastritis
lecture
.
Lykhatska G.V.
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.
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 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 < 5 mm in maximal length
Grade B - one or more mucosal breaks > 5mm, but without continuity
across mucosal folds
Grade C - mucosal breaks continuous between > 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).
Signs and symptoms
Signs and symptoms
Signs and symptoms
Heartburn (during physical
exertion, in a prone position,
after meals)
Belching air, food, sour, bitter,
vomiting(appears due to
retrograde flow of gastric
contents into the esophagus
and mouth)
Chest pain(occurs due to
spasm of the esophagus in
response to acid-peptic
aggression)
Dysphagia. (feeling of
difficulty passing food
through the esophagus)
Increased salivation, hiccups,
feeling of clutter in the throat,
pain in jaw, etc.
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.
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 <4.0 during the day is> 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.
Internally esophageal
manometry
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.
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).
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.
Barrett esophagus
Barrett esophagus
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).
X-ray study
X-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 modifications
to avoid horizontal
position during sleep
raising the head end of
the bed by 15 sm);
Lifestyle modification
giving up smoking and alcohol abuse;
weight loss in case of excess;
Dietary recommendations
exclusion of overeating
avoidance horizontal body position for 3-4 hours
after a meal;
refusal of food overnight
limit foods that reducing lower esophageal
sphincter tone (coffee, strong tea, chocolate,
mint, milk, fatty meats, spices);
Pharmacological arsenal
l Proton pump
inhibitors(to
effectively eliminate
the symptoms of
GERD and treatment
of inflammatory and
erosive changes)
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
Procinetics(to reinforce tone and reduce lower
esophageal sphincter)
Selective(domidon, motilium)
Nonselective(metoclopramide)
Antacids(to neutralize the hydrochloric acid
and pepsin)
-almagel
-fosfalyugel
-Maalox
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
Erosive form: Level C,
Level D
PPIs at standard doses
1t / day in the morning
30 minutes before
breakfast
for 4 weeks
PPIs in the double
standard dosage 2t / day
(30 min. before breakfast
and 30 min. before
dinner) for 8-12 weeks
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.
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.
36
Mechanism of development
Classification
FGIDs ( classified by anatomic region)
(A) Esophageal
(B) Gastroduodenal (B1: FD)
(C) Bowel (C1: IBS)
(D) Functional abdominal pain
(E) Biliary
(F) Anorectal.
38
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
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
40
Rome III diagnostic criteria for functional
dyspepsia.
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
Dyspepsia subgroup classification
-
based on the predominant single symptom
Ulcer-like dyspepsia (pain centered in the upper
abdomen is the predominant (most bothersome)
symptom).
2. Dysmotility-like dyspepsia (An unpleasant or
troublesome non-painful sensation (discomfort)
centered in the upper abdomen
is the predominant symptom)
3. 3. Unspecified (non-specific) dyspepsia
(symptomatic patients whose symptoms do not fulfill
the criteria for ulcer-like or dysmotility-like
dyspepsia)
1.
43
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
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
45
Management of Dysmotility-like Functional Dyspepsia
Dysmotility-like Symptoms Dominant
Educate/lifestyle modification
Trial of prokinetic
medication
Success
Failure
Continue with
cyclic therapy
Investigate
Test H. pylori
Gastroscopy or UGI
+
-
Eradicate
Success
Failure
Consider H2
antagonists, tricyclics
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Chronic gastritis
Normal
Stomach
Anatomy of the stomach
The stomach is divided into five
regions:
• cardia
• fundus
• body
• antrum
• pylorus
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.
Types of gastritis
Etiology.
Leading role in the development of chronic gastritis plays
Hp..
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).
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
Intestinale metaplasia in chronic gastritis
Type A (autoimmune gastritis).
Acute gastritis with superficial erosions.
Endoscopic picture antral gastritis
Chronic Gastritis in the gastric body caused
by Helicobacter pylori
a | Multifocal atrophic gastritis is caused by long-standing Helicobacter pylori infection
and is characterized by antrum-predominant or pangastritis and various degrees of
metaplastic atrophy (blue patches) that invariably involve the antrum and might extend
into the corpus. b | In autoimmune gastritis, the inflammatory atrophic process involves
exclusively the corpus (grey discoloration) and patches of intestinal, pseudopyloric and
pancreatic metaplasia are found throughout the gastric body and fundus.
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).
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),
endoscopy with biopsy
Definition Hp
chromoendoscopy - for early detection areas dysplasia
of the gastric mucosa
Intragastric pH-metry - for evaluation of gastric acidity
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)
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
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
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 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.
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, gastrofarm)
Physiotherapy treatment (ultrasound therapy, galvanization,
electrophoresis,diadynamic, paraffin,);
Thank you for attention