MINISTRY OF HEALTH OF UKRAINE

Zaporozhye state medical university

It is recomended
on a methodical conference
department of faculty pediatrics
________________________
Head of the chair professor Nedel'ska S.M.

METHODICAL RECOMMENDATIONS
FOR STUDENTS

Educational discipline Faculty pediatrics

Module 2 Widespread cardioreumatological diseases, illnesses of the
digestive and urinary systems in children

Substantial module 5 Gastroenterology in childhood

Topic of lesson 11 Functional diseases of gastrointestinal tract
Course 4
Faculty medical

Methodical recommendations are made Zhilenko I.A.

Zaporozhye 2015
Topicality.

Functional gastrointestinal (GI) and motility disorders are common among the pediatric
population that is, children from birth to age 18.

For example, the occurrence of irritable bowel syndrome (IBS) in children is similar to the rate
in adults (6% to 14%). Symptoms sufficient for a diagnosis of IBS were noted in 17% of high
school students and 8% of middle school students [Hyams J et al., Journal of Pediatrics, 1996].

Constipation and/or encopresis account for approximately 1025% of children who are referred
to a pediatric gastroenterologist (a doctor who specializes in digestive diseases or disorders).

Some gastrointestinal disorders in children are rare. For example, in the U.S. about 200 new
cases of intestinal psuedo-obstruction are diagnosed in children each year. Hirschsprung's disease
occurs in about 1 out of every 5,000 live births.

Regardless of whether common or rare, functional GI and motility disorders can be painful and
challenging to both the child and his or her family. A global approach to treatment, involving the
patient and family, as well as a team of health care professionals from different specialties is
sometimes called for and is often most effective.

2. The aims of the lesson

1. To determine the etiologic and pathogenetic factors of functional diseases of
gastrointestinal tract: functional dyspepsia, abdominal pain, irritable bowel syndrome,
functional constipation.
2. To classify and analyze the typical clinical picture of functional diseases of gastrointestinal
tract.
3. To determine the typical clinical features of widespread functional diseases of
gastrointestinal tract in elder children and put a previous clinical diagnosis.
4. To make the plan of examination and analyze data of laboratory and instrumental tests at
typical course of functional diseases of gastrointestinal tract: clinical and biochemical
blood tests; coagulogram; immunological data of 1 level; coprograme, stool analysis on
hidden blood and on helminth eggs, microflora examination, pH-metry, EGDS,
histological research of GI mucous, tests on revealing H.pylory .
5. To demonstrate the principles and skills of treatment, rehabilitation and prevention of the
main of functional diseases of gastrointestinal tract: functional dyspepsia, abdominal pain,
irritable bowel syndrome, functional constipation.
6. To make a final diagnose of the main of functional diseases of gastrointestinal tract:
functional dyspepsia, abdominal pain, irritable bowel syndrome, functional constipation
7. To conduct differential diagnostics of gastrointestinal pathology.
8. To make a prognosis of life in case of gastrointestinal tract pathology in children.
9. To demonstrate knowledge of moral and deontological principles and principles of
professional subordination in child's gastroenterology.

2. Base level of training, skills and knowledge.

DISCIPLINE Skills which must be got by students

Anatomy,
To know the anatomo-physiological features of gastrointestinal tract in
Physiology
children of different ages

Pat.anatomy, To determine the reaction of gastrointestinal tract on different irritants and

Pat.fiziology their connection with vegetative nervous system

Introduction to
To use research methods and to know semiotics of diseases of
the child's
gastrointestinal tract, to intrpretate clinical blood tests,
diseases
To draw the scheme of gastrointestinal tract structure, bile ways and
sphincter apparatus in normal.

To posses the methods of US and roentgenologic for diagnostics of hepato-

X-ray diagnostics
biliary and gastro-intestinal tract pathology , to evaluate US and X-ray data

To prescribe medications: cholagogue, vasodilatators, vitamins, antibiotics,

Pharmacology antiviral
To study indications, to prescribe and write recipes with the proper remedies

3. Task to write down in the copybook:

definition of functional GI diseases
definition of chronic gastritis
ethiology of functional disorders
classification of functional disorders
treatment of functional disorders

5. Main definitions

Chronic gastroduodenitis Chronic recurrent inflammatory disease which is

accompanied with nonspecific structural changes
of mucous and gland apparatus of stomach and
duodenum (distrophic, inflammatory,
regenerative) with secretion and motility
abnormalities
Chronic gastritis Chronic recurrent inflammatory disease of
stomach mucous, which affects also submucous
layer, is accompanied with cell infiltration,
abnormalities of regeneration, tendency to
progressive atrophy of glandular apparatus,
motility, secretion, incretion abnormalities
Irritable bowel syndrome
Functional intestinal abnormality, which is
characterized with abdominal pain and/or
disturbances of defecation and/or metheorism.
 1. Name anatomo-physiological features of gastrointestinal tract in children of different
ages
2. Write down the data of acid secretion in children of different age.
3. Write down factors that cause ulcer disease
4. Differentiate peptic ulcer disease, gastritis and functional dyspepsia, hyperkinetic variant
5. Types of functional dyspepsia
6. Indications for eradication of Hbp.
7. Scheme of Hbp-eradication therapy
8. Evaluation of its efficiency
9. Prescribe: omez, claritromycin, metronidazolum, pylobact, de-nolum, almagel, motilium
10. Classification of biliar dyscinesia
11. Gastroesophagus reflux disease, ethiology, clinical symptoms, principles of treatment
12. Irritable bowel syndrome ethyology, pathogenesis, clinic, treatment
13. Constipation in children, diet.

Practical skills
Curation of the patients
Making the diagnosis
To make a plan of investigation
A plan of treatment

Chronic gastritis

Chronic gastritis is a histopathological entity characterized by chronic inflammation of the

stomach mucosa. Gastritides can be classified based on the underlying etiologic agent (eg,
Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity,
allergic response) and the histopathological pattern, which may suggest the etiologic agent and
clinical course (eg, H pyloriassociated multifocal atrophic gastritis). Other classifications are
based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although
minimal inflammation is observed in some gastropathies, such as those associated with NSAID
intake, these entities are discussed in this article because they are frequently included in the
differential diagnosis of chronic gastritis.

Chemical or reactive gastritis is caused by injury of the gastric mucosa by reflux of bile
and pancreatic secretions into the stomach, but it can also be caused by exogenous substances,
including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol. These chemicals
cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia
detectable as foveolar hyperplasia, and damage to capillaries, with mucosal edema, hemorrhage,
and increased smooth muscle in the lamina propria. Inflammation in these lesions caused by
chemicals is minimal or lacking; therefore, the term gastropathy or chemical gastropathy is more
appropriate to describe these lesions than is the term chemical or reactive gastritis as proposed by
the updated Sydney classification of gastritis. Importantly, mixed forms of gastropathy and other
types of gastritis, especially H pylori gastritis, may coexist.
No single classification of gastritis provides an entirely satisfactory description of all types
of gastritis. However, an etiological classification provides a direct target towards which therapy
can be directed, and, for this reason, the etiological classification is used in this article. In many
instances, chronic gastritis is a relatively minor manifestation of diseases that predominantly
manifest in other organs or manifest systemically, such as gastritis in individuals who are
immunosuppressed.
Helicobacter gastritis is a primary infection of the stomach and is the most frequent cause
of chronic gastritis. Cases of histologically documented chronic gastritis are diagnosed as
chronic gastritis of undetermined etiology or gastritis of undetermined type when none of the
findings reflects any of the described patterns of gastritis and a specific cause cannot be
identified.
H pyloriassociated chronic gastritis
H pylori are gram-negative rods that have the ability to colonize and infect the stomach.
The bacteria survive within the mucous layer that covers the gastric surface epithelium and the
upper portions of the gastric foveolae. The infection usually is acquired during childhood. Once
the organism has been acquired, has passed through the mucous layer, and has become
established at the luminal surface of the stomach, an intense inflammatory response of the
underlying tissue develops.

The presence of H pylori is associated with tissue damage and the histological finding of
both an active and chronic gastritis. The host response to H pylori and bacterial products is
composed of T- and B-cell lymphocytes, denoting chronic gastritis, followed by infiltration of
the lamina propria and gastric epithelium by polymorphonuclear leukocytes that eventually
phagocytize the bacteria. The presence of polymorphonuclear leukocytes in the gastric mucosa is
diagnostic of active gastritis.
The interaction of H pylori with the surface mucosa results in the release of
proinflammatory cytokine interleukin (IL)-8, which leads to recruitment of polymorphonuclear
cells and may begin the entire inflammatory process. Gastric epithelial cells express class II
molecules, which may increase the inflammatory response by presenting H pylori antigens,
leading to further cytokine release and more inflammation. High levels of cytokines, particularly
tumor necrosis factor-a (TNF-a) and multiple ILs (eg, IL-6, IL-8, IL-10), are detected in the
gastric mucosa of patients with H pylori gastritis.
Leukotriene levels are also quite elevated, especially leukotriene B4, which is synthesized
by host neutrophils and is cytotoxic to gastric epithelium. This inflammatory response leads to
functional changes in the stomach, depending on the areas of the stomach involved. When
inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid
secretion. Continued inflammation results in loss of parietal cells, and the reduction in acid
secretion becomes permanent.
Antral inflammation alters the interplay between gastrin and somatostatin secretion,
affecting G cells (gastrin-secreting cells) and D cells (somatostatin-secreting cells), respectively.
Specifically, gastrin secretion is abnormal in individuals who are infected with H pylori, with an
exaggerated meal-stimulated release of gastrin being the most prominent abnormality. When the
infection is cured, neutrophil infiltration of the tissue quickly resolves, with slower resolution of
the chronic inflammatory cells. Paralleling the slow resolution of the monocytic infiltrates, meal-
stimulated gastrin secretion returns to normal.
Differences in virulence factors that characterize different strains of H pylori influence the
clinical outcome of H pylori infection. People infected with H pylori strains that secrete the
vacuolating toxin A (vacA) are more likely to develop peptic ulcers than people infected with
strains that do not secrete this toxin. Another set of virulence factors is encoded by the H pylori
pathogenicity island (PAI). The PAI contains the sequence for several genes and encodes the
CAGA gene. Strains that produce CagA protein (CagA+) are associated with a greater risk of
development of gastric carcinoma and peptic ulcer. However, infection with CagA- strains also
predisposes the person to these diseases.
H pyloriassociated chronic gastritis progresses with the following 2 main topographic
patterns that have different clinical consequences:
 Antral predominant gastritis is characterized by inflammation and is mostly limited to the
antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.
Multifocal atrophic gastritis is characterized by involvement of the corpus and gastric
antrum with progressive development of gastric atrophy (loss of the gastric glands) and partial
replacement of gastric glands by an intestinal-type epithelium (intestinal metaplasia). Individuals
who develop gastric carcinoma and gastric ulcers usually demonstrate this pattern of gastritis.

Most of the people who are infected with H pylori do not develop significant clinical
complications, and they remain carriers with asymptomatic chronic gastritis. Some individuals
who carry additional risk factors may develop peptic ulcer, gastric mucosaassociated lymphoid
tissue (MALT) lymphomas, or gastric adenocarcinomas.
An increased duodenal acid load may precipitate and wash out bile salts, which normally
inhibit the growth of H pylori. Progressive damage to the duodenum promotes gastric foveolar
metaplasia, resulting in sites for H pylori growth and more inflammation. This cycle results in
the increasing inability of the duodenal bulb to neutralize acid entering from the stomach until
changes in duodenal bulb structure and function are sufficient for an ulcer to develop. H pylori
can survive in areas of gastric metaplasia in the duodenum, contributing to the development of
peptic ulcers.

Autoimmune gastritis
This type of gastritis is associated with serum antiparietal and anti-intrinsic factor (IF)
antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients
may develop pernicious anemia.
The development of chronic atrophic gastritis limited to corpus-fundus mucosa and marked
diffuse atrophy of parietal and chief cells characterize autoimmune atrophic gastritis.
Autoimmune gastritis is associated with serum antiparietal and anti-IF antibodies that cause IF
deficiency, which, in turn, causes decreased availability of cobalamin and, eventually, pernicious
anemia in some patients.
Autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic
(microsomal-canalicular), and plasma membrane antigens. Two types of IF antibodies are
detected, ie, types I and II. Type I IF antibodies block the IF-cobalamin binding site, thus
preventing the uptake of vitamin B-12. Cell-mediated immunity also contributes to the disease.
T-cell lymphocytes infiltrate the gastric mucosa and contribute to epithelial cell destruction and
resulting gastric atrophy.

H pylori infection: Acute H pylori infection usually is not clinically detected, but
experimental infection results in a clinical syndrome characterized by epigastric pain, fullness,
nausea, vomiting, flatulence, malaise, and (sometimes) fever. The symptoms resolve in about a
week whether or not the organism is eliminated. Persistence of the organism causes H pylori
chronic gastritis, which usually is asymptomatic but may manifest as gastric pain or, rarely, with
nausea, vomiting, anorexia, or significant weight loss. Symptoms may occur with the
development of complications of chronic H pylori gastritis, which include peptic ulcers, gastric
adenocarcinoma, and MALT lymphoma.

The physical examination is of little contributory value in chronic gastritis. However,

some findings are specifically associated with the particular complications of H pylori
associated gastritis and autoimmune gastritis.

In uncomplicated H pyloriassociated atrophic gastritis, clinical findings are few and

nonspecific.
Epigastric tenderness may exist.
If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss.
 Bad breath (ie, halitosis) and abdominal pain or discomfort may occur, with bloating
associated with bacterial overgrowth syndrome.
Physical findings may result from the development of pernicious anemia and neurologic
complications in patients with autoimmune atrophic gastritis.
With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and
eyes. The pulse is rapid, and the heart may be enlarged. Auscultation usually reveals a systolic
flow murmur.

Non-invasive tests for the diagnosis of H. pylori infection include: the 13C-urea breath
test (UBT); stool antigen tests (polyclonal antibody, monoclonal antibody, and office based); and
immunological tests (laboratory and office based tests and tests on saliva and urine)
The rapid urease test can detect the presence of H pylori, within one hour with a
satisfactory accuracy (>90%).53 False negative results can occur in patients taking antisecretory
drugs. It is acceptable to initiate eradication therapy on the basis of a positive rapid urease test.
The stool antigen test is appropriate when multiple specimens are tested as a batch.
However, it is necessary to store stool samples at 20C before testing. The sensitivity of the
stool antigen test decreased to 69% after 23 days at room temperature. In a systematic review of
89 studies evaluating the stool antigen test the sensitivity and specificity were 91% and 93%,
respectively.37
Serology is a widely available and inexpensive non-invasive test, but the diagnostic
accuracy is low (8084%).38 Tests that detect active infection, although more expensive, are
preferable to serology as these reduce the number of patients inappropriately treated for
presumed H pylori infection.39,40 Some kits for serology with a high accuracy (>90%) are
recommended in validated settings.
Non-invasive tests should be employed for confirmation of eradication except in cases
where repeat endoscopy is indicated, for example in patients with gastric ulcer. Systematic
reviews of the studies performed in this context indicate that UBT is the best option, with a
sensitivity of 94% and a specificity of 95%.36,54 The accuracy of the stool antigen tests is less
than that of the UBT.5558 However, when a UBT is not available, a stool test can be used.
There are a number of stool tests available (one using monoclonal antibodies, laboratory and
office based and the other polyclonal antibodies). The sensitivity of the test is lower if polyclonal
antibodies59 or an office test is used. Confirmation of H pylori eradication should be performed
at least four weeks after treatment.

Performing an upper GI endoscopy is essential to establish a diagnosis of gastritis.

Although some studies have suggested that H pylori infection can be determined on the
basis of unique endoscopic features, particularly the presence of antral nodularity, a specific
relationship between H pylori and macroscopic features remains controversial. The endoscopic
findings in chronic H pylori infection may include areas of intestinal metaplasia. Sample
multiple biopsies. Tissue sampling from the gastric antrum, incisura, and corpus is essential to
establish the topography of gastritis and to identify atrophy and intestinal metaplasia, which
usually is patchy. It is recommended that biopsy samples of the gastric body and those from the
antrum and incisura are submitted in separate containers for pathological evaluation.

Accepted first-line treatments for H pylori are a 10- to 14-day course of proton pump
inhibitor (PPI), clarithromycin, and amoxicillin or metronidazole; or of PPI, bismuth,
tetracycline, and metronidazole.

In part because of increasing H pylori resistance to clarithromycin, rates of eradication

for first-line treatment with a PPI, clarithromycin, and amoxicillin have decreased to 70% to
85% worldwide. Seven-day regimens may have lower eradication rates than 14-day regimens.
 "The most important predictors of treatment failure following anti-H. pylori therapy
include poor compliance and antibiotic resistance," the study authors write. "It is critical for
clinicians to stress the importance of taking the medications as prescribed to minimize the
likelihood of treatment failure and development of antibiotic resistance.... There is limited
evidence to suggest that smoking, alcohol consumption, and diet may also adversely affect the
likelihood of successful eradication."

Another therapeutic option for first-line treatment is a 7- to 14-day course of bismuth-

containing quadruple regimens. Although sequential therapy for 10 days has appeared promising
in European trials, this regimen has not yet been validated in North America and therefore cannot
yet be recommended as a standard first-line treatment. Sequential treatment consists of a 5-day
course of a PPI and amoxicillin, followed by an additional 5 days of a PPI, clarithromycin, and
tinidazole.

Bismuth quadruple therapy is the most widely used salvage regimen for persistent H
pylori infection. Evidence from recent trials suggest that combination therapy with a PPI,
levofloxacin, and amoxicillin for 10 days is more effective and better tolerated than is bismuth
quadruple therapy for treatment of patients with persistent infection, but this has not yet been
validated in the United States.

Several recent trials studies have compared alternatives with bismuth-based quadruple
salvage therapy, such as rifabutin, with rates of eradication ranging from 38% to 91%;
furazolidone, with rates of eradication ranging from 52% to 90%; and levofloxacin-based triple
therapy.

If a patient was treated for H pylori infection, confirm eradication.

Evaluate eradication at least 4 weeks after the beginning of treatment.
The eradication may be assessed by noninvasive methods such as the urea breath test or
stool antigen test.
Follow-up may be individualized depending on findings during endoscopy. For example,
if dysplasia was found with endoscopy, increased surveillance is necessary.
For patients with atrophic gastritis and/or dysplasia, a follow-up endoscopy is
recommended after 6 months.

Five regimens are approved by the FDA for the treatment of H pylori infection. A
version of the traditional bismuth, metronidazole, tetracycline (BMT) triple therapy has been
approved and is available commercially as Helidac. The regimen combines a histamine 2 (H2)
receptor antagonist, bismuth subsalicylate, metronidazole, and tetracycline, which are
administered for 14 days. The antibiotics and bismuth are provided in a convenient dose pack
that is thought to enhance compliance. Three different combinations using clarithromycin have
been approved, including 2 dual therapies consisting of 500 mg of clarithromycin 3 times daily
plus either omeprazole or ranitidine bismuth citrate ([RBC] Tritec). The cure rates reported in the
packaging literature suggest that the 3 combinations are similarly effective. Clinical experience
has shown that the ranked order of effectiveness is the BMT triple therapy, RBC plus
clarithromycin, followed by omeprazole plus clarithromycin.
Because higher success rates can be achieved when a third drug is added to the
dual therapies, most authorities now recommend triple drug combinations. This recommendation
has been confirmed by the recent approval of the combination of a proton pump inhibitor (PPI),
lansoprazole (Prevacid), plus clarithromycin and amoxicillin. The cure rate with this
combination is greater than 85%. Lansoprazole plus amoxicillin was also approved, but the
tremendous variability with this dual therapy makes it a very poor choice.
 Currently, the most widely used efficient therapies to eradicate H pylori are triple
therapies, and they are recommended as first-line treatments; quadruple therapies are
recommended as second-line treatment when triple therapies fail to eradicate H pylori. In both
cases, the best results are achieved by administering therapy for 10-14 days, although some
studies have limited the duration of treatment to 7 days. The accepted definition of a cure is that
no evidence of H pylori exists for 4 or more weeks after ending the antimicrobial therapy.

Irritable bowel syndrome

In gastroenterology, irritable bowel syndrome (IBS) is a functional bowel disorder
characterized by abdominal pain and changes in bowel habits which are not associated with any
abnormalities seen on routine clinical testing.
Irritable bowel syndrome is a disorder characterized most commonly by cramping,
abdominal pain, bloating, constipation, and diarrhea. IBS causes a great deal of discomfort and
distress, but it does not permanently harm the intestines and does not lead to a serious disease,
such as cancer. Most people can control their symptoms with diet, stress management, and
prescribed medications. For some people, however, IBS can be disabling. They may be unable to
work, attend social events, or even travel short distances.
Other symptoms include rapid digestion of food, frequent defecation, bloating, headaches
and anxiety. Individuals with IBS may also burp frequently and suffer from bad breath, fatigue
and nausea.
The Manning criteria to distinguish IBS from organic disease are as follows:
Onset of pain associated with more frequent bowel movements
Onset of pain associated with looser bowel movements
Pain relieved by defecation
Visible abdominal bloating
Subjective sensation of incomplete evacuation more than 25% of the time
Mucorrhea more than 25% of the time
The Rome III criteria (2006) for the diagnosis of IBS require that patients must have
recurrent abdominal pain or discomfort at least 3 days per month during the previous 3 months
that is associated with 2 or more of the following:
Relieved by defecation
Onset associated with a change in stool frequency
Onset associated with a change in stool form or appearance

Supporting symptoms include the following:

Altered stool frequency
Altered stool form
Altered stool passage (straining and/or urgency)
Mucorrhea
Abdominal bloating or subjective distention

Four bowel patterns may be seen with IBS. These patterns include IBS-D (diarrhea
predominant), IBS-C (constipation predominant), IBS-M (mixed diarrhea and constipation), and
IBS-A (alternating diarrhea and constipation). The usefulness of these subtypes is debatable.
Notably, within 1 year, 75% of patients change subtypes, and 29% switch between constipation-
predominant IBS and diarrhea-predominant IBS.

Lab Studies
A comprehensive history, a physical examination, and tailored laboratory and
radiographic studies can establish a diagnosis of IBS in most patients.
Lab studies may include the following:
 CBC count with differential to screen for anemia, inflammation, and infection
A comprehensive metabolic panel to evaluate for metabolic disorders and to rule out
dehydration/electrolyte abnormalities in patients with diarrhea
Gastrointestinal bleeding should be ruled out. A hemoccult test may be useful.
Microbiologic studies to consider include the following stool examinations:
Ova and parasites: Consider obtaining specimens for Giardia antigen as well.
Enteric pathogens
Leukocytes
Clostridium difficile toxin
The following selected studies are directed by history:
Breath testing: Screen for lactose and/or fructose intolerance.
Thyroid function tests: Screen for hyperthyroidism or hypothyroidism.
Serum calcium: Screen for hyperparathyroidism.
Erythrocyte sedimentation rate or C-reactive protein: This is a nonspecific screening test
for inflammation.
Serologies or small bowel biopsy for celiac disease: Consider, especially in diarrhea-
predominant IBS.
H2 breath test to exclude bacterial overgrowth may be considered in patients with
diarrhea.
Imaging Studies
The following selected studies are directed by history:
Upper GI barium study with small bowel follow-through: Screen for tumor,
inflammation, obstruction, and Crohn disease.
Double-contrast barium enema: Screen for neoplasm and inflammation.
Gallbladder ultrasonography: Consider this test if the patient has recurrent dyspepsia or
characteristic postprandial pain.
Abdominal CT scan: Screen for tumors, obstruction, and pancreatic disease.
Other Tests
Direct a lactose-free diet for 1 week in conjunction with lactase supplements.
Improvement incriminates lactose intolerance, although the patient's clinical history and response
to a trial may be unreliable. Some gastroenterologists therefore recommend a formal hydrogen
breath test. Fructose intolerance must also be considered.
Direct a 48-hour fast. Persistent diarrhea suggests a secretory etiology.
Anal manometry may reveal spastic response to rectal distention or other problems.
Procedures
Endoscopy directed for many patients includes flexible sigmoidoscopy to determine
inflammation or distal obstruction.
The following selected studies are directed by history:
Esophagogastroduodenoscopy with possible biopsy - Indicated for a patient with
persistent dyspepsia or if weight loss or symptoms suggest malabsorption or if celiac disease is a
concern
Colonoscopy - Indicated for patients with warning signs such as bleeding; anemia;
chronic diarrhea; older age; history of colon polyps; cancer in the patient or first-degree
relatives; or constitutional symptoms such as weight loss or anorexia. A screening colonoscopy
should be performed according to published guidelines.
Histologic Findings
New research suggests that neuronal degeneration and myenteric plexus lymphocytosis
may exist in the proximal jejunum. Additionally, colonic lymphocytosis and enteroendocrine cell
hyperplasia has been demonstrated in some patients.

Treatment
Diet
 Fiber supplementation may improve symptoms of constipation and diarrhea.
Individualize the treatment because few patients experience exacerbated bloating and distention
with high-fiber diets. Polycarbophil compounds (eg, Citrucel, FiberCon) may produce less
flatulence than psyllium compounds (eg, Metamucil).
The data regarding the effectiveness of fiber are controversial because 40-70% of patients
improve with placebo.
Judicious water intake in patients who predominantly experience constipation is
recommended.
Caffeine avoidance may limit anxiety and symptom exacerbation.
Legume avoidance may decrease abdominal bloating.
Lactose and/or fructose should be limited or avoided in patients with these contributing
disorders. Take care to supplement calcium in patients limiting lactose intake.
laxative
For patients who do not adequately respond to dietary fiber, osmotic agents such as
polyethylene glycol, sorbitol, and lactulose can help avoid 'cathartic colon' which has been
associated with stimulant laxatives.[81] Among the osmotic laxatives, 17 to 26 grams/day of
polyethylene glycol (PEG) has been well studied.
The use of antispasmodic drugs (e.g. anticholinergics such as hyoscyamine or
dicyclomine) may help patients, especially those with cramps or diarrhea. A meta-analysis by the
Cochrane Collaboration concludes that if 6 patients are treated with antispasmodics, 1 patient
will benefit (number needed to treat = 6).Antispasmodics can be divided in two groups:
neurotropics and musculotropics. Neurotropics, such as atropine, act at the nerve fibre of the
parasympathicus but also affect other nerves and have side effects. Musculotropics such as
mebeverine act directly at the smooth muscle of the gastrointestinal tract, relieving spasm
without affecting normal gut motility. Since this action is not mediated by the autonomic nervous
system, the usual anticholinergic side effects are absent. Antispasmodic drugs are also available
in combination with tranquilizers or barbiturates, such as chlordiazepoxide and Donnatal. The
value of the combination therapies has not been established.
Drugs affecting serotonin (5-HT) in the intestines can help reduce symptoms. Serotonin
stimulates the gut motility and so agonists can help constipation predominate irritable bowel
while antagonists can help diarrhea predominant irritable bowel.
Probiotics
Probiotics are generally accepted to be potentially beneficial strains of bacteria and yeast,
often found in the human gut. One research study has shown a clear link between the ingestion
of Lactobacillus plantarum 299v (Lp299v) and sufferers of IBS who reported resolution of their
abdominal pain.[103] Another study showed the utility of B. infantis 35625, a strain of
Bifidobacteria, in normalizing bowel movement frequency in sufferers of IBS.[104] Some
practitioners of Integrative Medicine now recommend a strain of Lactobacillus rhamnosus
known commonly as "LGG" after its discoverers Gorbach and Goldin. This strain in particular
has shown an ability to endure the acidic environment of the stomach and survive until
presentation to the intestinal tract.
A prospective placebo-controlled study found patients with diarrhea predominant IBS
taking Saccharomyces boulardii, a probiotic yeast, had a significant reduction on the number and
improvement in consistency of bowel movements.
Prokinetics metoclopramid, motilium (domperidon)

Medical check-up is conducted all life. Each year an inspection of pediatrician and
gastroenterologist in polyclinic, blood and urine sample, coprogramme, feces analysis on
excrements.

Constipation in children
 Constipation, defined as a delay or difficulty in defecation, present for 2 or more weeks,
is a common pediatric problem encountered by both primary and specialty medical providers.
A normal pattern of stool evacuation is thought to be a sign of health in children of all
ages. Especially during the first months of life, parents pay close attention to the frequency and
the characteristics of their children's defecation. Any deviation from what is thought by any
family member to be normal for children may trigger a call to the nurse or a visit to the
pediatrician. Thus, it is not surprising that approximately 3% of general pediatric outpatient visits
and 25% of pediatric gastroenterology consultations are related to a perceived defecation
disorder (1). Chronic constipation is a source of anxiety for parents who worry that a serious
disease may be causing the symptom. Yet, only a small minority of children have an organic
cause for constipation. Beyond the neonatal period, the most common cause of constipation is
functional and has been called idiopathic constipation, functional fecal retention, and fecal
withholding.

In most cases the parents are worried that the child's stools are too large, too hard,
painful, or too infrequent. The normal frequency of bowel movements at different ages has been
defined (Table 1). Infants have a mean of four stools per day during the first week of life. This
frequency gradually declines to a mean average of 1.7 stools per day at 2 years of age and 1.2
stools per day at 4 years of age. Some normal breast-fed babies do not have stools for several
days or longer. After 4 years, the frequency of bowel movements remains unchanged.
Functional constipation-that is, constipation without objective evidence of a pathologic
condition-most commonly is caused by painful bowel movements with resultant voluntary
withholding of feces by a child who wants to avoid unpleasant defecation. Many events can lead
to painful defecation such as toilet training, changes in routine or diet, stressful events,
intercurrent illness, unavailability of toilets, or the child's postponing defecation because he or
she is too busy. Withholding feces can lead to prolonged fecal stasis in the colon, with
reabsorption of fluids and an increase in the size and consistency of the stools.
The passage of large hard stools that painfully stretch the anus may frighten the child,
resulting in a fearful determination to avoid all defecation. Such children respond to the urge to
defecate by contracting their anal sphincter and gluteal muscles, attempting to withhold stool.
They rise on their toes and rock back and forth while stiffening their buttocks and legs, or
wriggle, fidget, or assume unusual postures, often performed while hiding in a corner. This
dance-like behavior is frequently misconstrued by parents who believe that the child is straining
in an attempt to defecate. Eventually, the rectum habituates to the stimulus of the enlarging fecal
mass, and the urge to defecate subsides. With time, such retentive behavior becomes an
automatic reaction. As the rectal wall stretches, fecal soiling may occur, angering the parents and
frightening the child. After several days without a bowel movement, irritability, abdominal
distension, cramps, and decreased oral intake may result.
Etiology
Many things can contribute to constipation.
The most common cause in a child older than 18 months is their willful avoidance of the
toilet (for various reasons). For example, toddlers are often so involved in their play that they
lack time or patience for toilet breaks.
At school they may be concerned with lack of privacy or the cleanliness of the bathroom.
They may have had a prior painful or frightening experience that makes them want to
avoid the bathroom. Over time, their brain learns to ignore repeated urges by the colon to visit
the bathroom. As stool remains in the colon, the colon will absorb water out of the stool, making
it hard and dry. This hard stool is even more difficult or painful to pass, which causes the child to
continue "holding it."

Changes in diet, or a different diet affect bowel habits. In adults, high-fiber diets have
been shown to improve bowel function. In children, however, high-fiber diets have not been
proven to improve constipation. Infants and children who eat well-balanced meals typically are
not constipated.
Breastfed infants will generally have more stools per day. Their stools vary more in
frequency when compared to bottle-fed infants. For example, breastfed infants produce
anywhere from 5-40 bowel movements per week; whereas formula-fed infants have 5-28 bowel
movements per week. Switching the type of milk (or formula) can also cause constipation.
Teenagers and toddlers who eat a lot of sugar and desserts are prone to difficult passing of
their stools.
Any intense changes in a childsuch as illnesses causing fever, a long time in bed,
eating less, or dehydrationmay decrease frequency of stools or may harden stools.
A number of medical disorders can cause chronic constipation.
Hypothyroidism (lowered activity of the thyroid gland) is a condition that causes
decreased activity of the intestinal muscles along with many other symptoms. All newborns
should be tested for hypothyroidism as part of the newborn screening blood test (heel prick or
Guthrie test). This condition is usually diagnosed when a baby is very young but can occur at any
age.
True constipation in infants and children that has been present since birth may be from
Hirschsprung's disease. In this rare congenital condition, a segment of the colon lacks ganglion
cells (a type of nerve cell). The affected colon cannot receive directions from the brain to work
properly. Most infants with Hirschsprung disease display symptoms within the first few weeks of
life. They may be underweight or small for their age. They may vomit and pass small stools,
which are described as ribbon-like. Hirschsprung's disease is generally more common in boys
and in babies with Down syndrome. If Hirschsprung's disease is suspected, you need to take your
child to a specialist (gastroenterologist or pediatric surgeon) for further tests.
Diabetes is common medical problem associated with constipation.
Alterations in electrolytes levels, such as calcium or potassium, can changes bowel
habits.
Although other symptoms of lead poisoning will be more obvious, children with chronic
lead exposure may have constipation.
Cystic fibrosis, for many reasons, causes constipation in children by many mechanisms.
Children with disorders of the nervous system (such as cerebral palsy, mental retardation,
or spinal cord problems) display a high rate of constipation because they spend prolonged time in
one position, experience abnormal colon movement, or lack coordination in moving their
bowels.
Some medications can make children more likely to be constipated. Common
contributors include over-the-counter cold medications and antacids. Antidepressants,
anticonvulsants, chemotherapy medications, or narcotic pain medications (such as codeine) can
also constipate.
Other possible causes of constipation are depression, coercive toilet training, attention
deficit disorders, and sexual abuse.

Clinical symptoms.

Generally, if a child has fewer than three bowel movements per week and they are hard
and difficult to pass, he or she may have constipation.
Children often exhibit characteristic behaviors while trying to keep from having a bowel
movement.
Infants having painful bowel movements may extend their legs and squeeze their anal and
buttock muscles to prevent passage of stool.
Toddlers often rise up on their toes, rock back and forth, and hold their legs and buttocks
stiffly.
 Some medications can make children more likely to be constipated. Common
contributors include over-the-counter cold medications and antacids. Antidepressants,
anticonvulsants, chemotherapy medications, or narcotic pain medications (such as codeine) can
also constipate.
Other signs that children are constipated are these:
Vague abdominal pain around the navel (belly button) or even severe attacks of
abdominal pain
Decreased appetite, nausea, or vomiting
Urinary incontinence, frequent urination, or bedwetting
Reappearing urinary tract infections
Symptoms of persistent, severe constipation in children are:
being irritable,
loss of appetite,
soiling their clothes,
feeling sick, and
stomach pains.

Based on clinical experience, a thorough history is recommended as part of a complete

evaluation of a child with constipation (Table 3). There are no well-designed studies that
determine which aspects of a history are pertinent. Important information includes the time after
birth of the first bowel movement, what the family or child means when using the term
"constipation," (17) the length of time the condition has been present, the frequency of bowel
movements, the consistency and size of the stools, whether defecation is painful, whether blood
has been present on the stool or the toilet paper, and whether the child experiences abdominal
pain. Fecal soiling may be mistaken for diarrhea by some parents. A history of stool-withholding
behavior reduces the likelihood that there is an organic disorder. Medications are an important
potential cause of constipation

What is the treatment for chronic constipation in children?

A high fibre diet and lots to drink.
Definition

Food Sources
Vegetables, fruits (especially dried fruits) and some cereals (whole wheat, bran or oatmeal) are
excellent sources of fiber. It is easy to remember that the harder a vegetable is (like celery), the
more fiber it has. To reap the benefits of fiber, it is very important to drink an adequate amount
of water to help with the passage of stool in the intestines.
Recommendations
BABIES
Babies who are breastfed usually do not experience constipation. Bottle-fed infants often do.
Dietary changes that may help relieve constipation in infants are as follows:
1. Offer 1 - 2 ounces of apple or prune juice from the bottle or by spoon.
2. Babies who have advanced to solids may be offered more fruits and vegetables or small
amounts of bran sprinkled on top of cereal (about 1 teaspoon).
3. Babies age birth to 6 months should receive most of their fluids from breast milk or formula.
TODDLERS
The diets of older babies and toddlers should start to reflect the recommendations of the food
guide pyramid.
Offer fruits and vegetables with chunkier textures as opposed to strained. Begin to offer more
whole-grain breads and cereals as your child begins to tolerate a wider variety of foods. Be sure
your child is drinking adequate amounts of fluid -- pay attention to this as formula or breast milk
feedings decrease.
CHILDREN AND TEENS
The food guide pyramid is an excellent guide for choosing an appropriate diet. Choose whole
grains, and plenty of fruits and vegetables. Bran cereals can help as do prunes and prune juice.
Adequate fluid intake (8 - 10 cups a day) is also important in preventing constipation. Fluids
other than water are acceptable, because children need calories for growth. However, soft drinks
are not recommended. Juice should be limited to help avoid excessive caloric intake
Fluid requirements vary for children based on their size, activity level, and air temperature. To
assure adequate fluids offer water more frequently during exercise and in warm temperatures.

Laxatives.
Laxatives are usually prescribed if a child develops chronic constipation. The first aim is to clear
any impacted (stuck) stool. This can usually be done fairly quickly with a good dose of a strong
laxative. Sometimes a suppository or enema is needed to clear a large impacted stool. After the
impacted stool has been cleared, it is important to continue with 'maintenance' laxatives as
prescribed by your doctor. This can be for several months, even for up to two years. As the child
takes laxatives every day, what happens is that:
The child is likely go to the toilet and pass stools regularly. As they go to the toilet more often,
the stools will be smaller and softer. So, the stools will be passed more easily. Any fear of going
to the toilet to pass large and hard stools will ease.

The enlarged rectum can gradually get back to a normal size and function properly again.
Constipation is then unlikely to recur.

If laxatives are stopped too soon, a large stool is likely to recur again in the weakened 'floppy'
rectum which has not had time to get back to a normal size and strength.

Laxatives are recommended when:

Dietary measures fail
While dietary measures take effect
For drug-induced constipation
Where prolonged straining at stool may be dangerous e.g. angina or haemorrhoids
Before surgery and radiological procedures
To assist expulsion of parasites after anthelmintic treatment

There is little evidence on which to base recommendations for laxative selection. It is

reasonable to base individual choices on the severity of symptoms, stool consistency, patient
preference and cost. The lowest effective dose should be prescribed and reduced once symptoms
improve. Oral preparations should be used whenever possible but short courses of rectal
laxatives may be appropriate if oral treatments have failed or rapid relief of rectal loading is
required. Rectal laxatives should be avoided if haemorrhoids or anal fissures are present.4
Manual evacuation may be necessary if all pharmacological interventions fail.1
Laxatives can be divided into 4 main groups. An understanding of the basic mechanisms
of action assists in the selection of appropriate drugs.
Bulk-forming laxatives
Bulk-forming laxatives retain water within stools and increase faecal mass, thus
stimulating peristalsis, e.g. ispaghula, methylcellulose. An adequate water intake is necessary to
avoid worsening constipation and intestinal obstruction.6 Full effects may take several days so
they are inappropriate for acute relief of constipation.
Bulk-forming laxatives are useful in the management of patients with small, hard stools
and those with stomas, haemorrhoids, anal fissures, diverticular disease, irritable bowel
syndrome and as an adjunctive treatment of ulcerative colitis. Patients may complain of
flatulence, bloating and abdominal distension but side-effects usually settle with continued use.
 Stimulant laxatives
These drugs induce intestinal peristalsis by direct stimulation of the myenteric plexus e.g.
bisacodyl, docusate sodium, senna, danthron.1 Stimulant laxatives are popular because of
their rapid effect but will often cause abdominal cramps. Rectal preparations of stimulant
laxatives are useful for prompt evacuation of impacted stools. Bisacodyl suppositories are used
to evacuate soft stools from the lower rectum. Glycerol suppositories will eliminate soft or hard
stools from the lower rectum and docusate sodium enemas will clear faeces from the upper
rectum.4 Stimulant laxatives must be avoided in bowel obstruction as they may lead to
perforation. Long-term use of high-doses can cause diarrhoea with significant fluid and
electrolyte imbalances, however prolonged therapy is sometimes necessary.6 All preparations
containing danthron such as co-danthramer and co-danthrusate should be restricted to terminally
ill patients due to concerns regarding genotoxicity.4
Faecal softeners
Faecal softeners act by decreasing the surface tension of stools and facilitating infiltration
of intestinal fluid e.g. arachis oil, docusate sodium (which has stool-softening properties in
addition to its stimulant effects). These drugs are useful for oral administration in the
management of haemorrhoids and anal fissures as they will soften and lubricate faecal material.
Arachis oil enemas are also useful in the management of patients with hard, impacted
stools. Liquid paraffin is not recommended as it can cause anal seepage and irritation, lipoid
pneumonia and malabsorption of fat-soluble vitamins.
Osmotic laxatives
Osmotic laxatives act by increasing the amount of water in the large bowel e.g. lactulose,
polyethylene glycols, rectal phosphates.
Variable time is needed to achieve their full effects. An adequate fluid intake is necessary
to prevent dehydration and some preparations such as polyethylene glycols are administered with
fluid to avoid this problem. Phosphate enemas are useful for clearance of hard, impacted stools
and for bowel evacuation before surgery and radiological or endoscopic investigations. Osmotic
laxatives must not be used in bowel obstruction and polyethylene glycol should be avoided in
patients with severe inflammatory conditions of the gastrointestinal tract such as Crohn's disease
or ulcerative colitis.

Control questions
1. anatomo-fisiological features of organs of digestion depending on age.
2. Influence of the state of the nervous system and immune system on development of
defeats of upper organs of digestion.
3. Etiology and pathogenesis of functional diseases of stomach and duodenum.
4. Clinical features and methods of diagnostics.
5. Treatment of functional diseases of upper parts of organs of digestion.
6.Gastroesophageus reflux. Etiology, pathogenesis. Its role in forming of chronic
diseases of upper departments of GIT.
7. Etiology and pathogenesis of chronic gastritis. Clinic. Methods of diagnosis. Plan of
treatment, depending on the form of gastritis
8. Differential diagnosis of diseases of upper parts of GIT (chronic gastritis, ulcer,
functional diseases of stomach).
9. Estimation of efficiency of antihelicobakter therapy and methods of control of
eradication.
10. Features of abdominal pain syndrome in children.
11. Irritable bowel syndrome: etiology, pathogenesis, clinic, diagnostics.
12. Children have features of functional constipation. Differential diagnosis with the
organic diseases of GIT.
To prescribe: motilium, omeprazolum, lansap, ranitidine, lacidophil, lactulose
Reference
1.Piyush Gupta, V.V. Paul Essential pediatrics- Textbook for students and practitioners.- 6 Ed.-
New Delhi,2008.-719pp

2. Dr.Mayoor K. Chheda Practical aspects of Pediatrics.-4 Ed.-2006.-423pp

3. O.Tiazhka Pediatrics.-2011.- 575 pp

4.David Hull/Derek I Johnston Essential paediatrics.-4 Ed.-Churchill Livingstone,1999.-382 pp

5.www//E-medicine.com

6 Lecture material

Additional

1.Blaser MJ (1996). Role of vac A and the cag A locus of Helicobacter pylori in human disease. Aliment
Pharmacol Ther, 10, 7377. [Web of Science] [Medline]

2.Dorward S, et al. (2006). Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in
upper gastrointestinal bleeding. Cochrane Database Syst Rev, CD005415.

3.El-Omar EM, et al. (1997). Helicobacter pylori infection and chronic gastric acid hypo-secretion.
Gastroenterology, 113, 1524.[CrossRef] [Web of Science] [Medline]

4.European Helicobacter pylori Study Group. (1997). Current European concepts in the management of
Helicobacter pylori infection. The Maastricht Consensus Report. Gut, 41, 813.

5.Marmo R, et al. (2007). Dual therapy versus monotherapy in the endoscopic treatment of high-risk
bleeding ulcers: a meta-analysis of controlled trials. Am J Gastroenterol, 102, 27089.

6.Sung JJY, et al. (2010). Causes of mortality in patients with peptic ulcer bleeding: a prospective cohort
study of 10,428 cases. Am J Gastroenterol, 105(1), 849.[CrossRef] [Web of Science] [Medline]

Control tests
1. What properties of H. pylori sustain its existance in stomach?
A. Adherence to epithelium of antrum
B. The property of endocytosis
C. Spiral shape of microbe
D. Ability to convert urea into ammonia and carbohydrate and create alkaline invirement
of microbe
2. What medications from listed below is not H2 blocker?
A. Ranitidin
B. Famotidin
C. Nisatididn
D. Roxatidin
E.Gastrocepin
3. What type of cells is blocked by proton pump inhibitors?
A. Epithelium cells
B. Parietal cells
C. Chief cells
D. Polymorphonuclear cells
E. G-cells and D-cells ( gastrin and somatoststin secreted cells)
4. A 12 years old child has peptic ulcer disease. What test is proper to reveal H.Pylory?
 A. Fibrogastroscopy
B. X-ray imaging
C. Blood test
D. Urease test
E. Coprogramm
5. A 12 years old child has peptic ulcer disease (PUD). What pathogene can cause PUD?
A. Chlamidia
B. Streptococci
C. Mycoplasma
D. Helicobacter pylori
E. Viruses
6. What changes of stomach mucous cant be produced by H.Pylori?
A. No signs of inflammation
B. Superficial gastritis
C. Intestinal methaplasia
D. Severe gastritis with partial atrophy
E.Progressive atrophy with loss of parietal and chief cells
7. What symptoms are typical for PUD, except
A. Epigastric pain
B. Nausea
C. Vomiting
D. Diarrhea
E. Burnings
8. What medication isnt useful in PUD caused by
A. Omeprazol
B. Clarithromycine
C. Metronidazole
D.Kethoconazole
E. Bismuthi subsalicylatis
9. What drug us not proton pump inhibitor?
A. Omeprazol
B. Ketoconazol
C. Lansoprazol
D. Rabeprazol
E. Esomeprazol
10. What etiologic factor can cause development of gastritis, except
A. Tuberculosis
B. Cytomegaloviresus
C. Drugs (NSADs, steroids)
D. Streptococci
E. Radiation
11. A 10 years old child has been ill foe 3 years. His complaints are abdomen pain in right
part, subfebrile temperature. Palpation of abdomen reveal inlarged liver (+2 cm), positive Kera
symptom. Stool isnt regular and stable( intermittent diarrhea and constipation). Blood tests are
normal. What disease can produce such clinical picture?
A. Biliary tract dyskinesia
B. Chronic enterocolitis
C. Crohn disease
D. Chronic cholecystitis
E. Acute intestinal infection
 12. A 8 years old child has been ill for 3 years. His complaints are stool 5-6 times per day
with blood and mucus in it, weight deficit, fatigue. Pathologic microorganisms were not revealed
in stool. Blood tests show anemia, ESR 24 mm/h. What disease can you suspect?
A. Peptic ulcer disease
B. Acute gastritis
C.Crohn disease
D. Chronic pancreatitis
E. Biliary dyskinesia
13. A 15 years old boy complains to abdomen pains at night or hungry pains,
constipation, heartburn. He has been ill for 2 years. His grandfather has died because of
gastrointestinal bleeding. What diagnosis is not probable?
A. Chronic gastritis
B. Acute gastritis
C. Peptic ulcer disease of duodenum
D. Biliary dyskinesia
E. Chronic pancreatitis
14. A 13 years old boy has acute pancreatitis 3 years ago. For some month he has
complaints of epigastrium pain, positive Grotts, Kuch symptoms. What criteria is the most
accurate for pancreatic disease?
A. Hyperphosphatemia
B.Hyper amylaseaemia
C. Hyperbilirubinaemia
D. Elevated level of aspartattranspherase (AST)
E. Hyperproteinaemia
15. A 12 years old boy for 2 years periodically has pains in epigastrium 1-3 hours after
meals, gnawing and burning. Gastroduodenoscopy reveals signs of gastroduodenitis with ulcer
defect in duodenum mucous. What drug will be the most effective in this patient?
A. Papaverin
B. Almagel
C. Nospani
D. Atropin
E.De-nol ( Bismuthi subsalicylatis)
16. A 13 years old girl is under outpatient care because of chronic gastroduodenitis. for
the last 6 month she has regular night abdomen pains. What examination is necessary to be
done?
A. Ultrasound diagnostics of abdomen
B. Fecal test on blood presence in stool
C. Gastroduodenal endoscopic examining
D. Measurement of acid secretion
E. Colonoscopy.
17. A 11 years old child has attacks of pain in abdomen after meals and at night for 3
month. Endoscopic examining reveals ulcer defect in duodenum 5-7 mm in diameter surrounded
with inflammed edge. The bottom of erosion is filled with gray layer. H.pylory test is positive.
What treatment will you prescribe?
A. Omeprazole+clarithromycin+metronidazole
B. Omeprazole+amoxicylline
C. Cimetedin+ omeprazole
D. Bismuthi subsalicylatis+omeprazol
E. Almagel+ranitidin
18. A 10 years old boy complains on abdomen pain 20-30 min after taking meals,
burnings, gnawining. He has such complaints for 2 years. exacerbation is lasting for 1 week.
after examining the boy he is diagnosed chronic gastritis with elevated secretory function.
Choose the proper treatment.
A. Ganglioblocker+eubiatic+antibiotic
B. Antacid drug+antisecretory drug+antibiotic
C. Antiacid drug+spasmolytic+enzyme
D. Antisecretory+enzyme+antibiotic
E. Antiacid+spasmolytic+probiotic
19.A 7 years old girl complains on epigastrium pain at the morning, appetite loss. theese
complaints appear after school attendance for 1 mo. Symptoms can appear after stress and
irregular mealing. Palpation of abdomen find out tenderness in epigastrium. Blood tests,
biochemical tests, urinalysis are normal. endoscopy with pathologic signs. What is the diagnosis?
A. Functional dyspepsia
B. Peptic ulcer disease
C. Helmints
D. Chronic cholecystitis
E. Intestinal infection.
20 A boy has mumps. he begin complin of fever, loss of appetite, gnawing, vomiting,
attacks of pain in abdomen with irradiation to back, diarrhea. Amylase test is 48 IU. what is the
most probable diagnosis?
A. Intestinal infection
B. Disbacteriosis
C. Acute apendicitis
D. Acute cholecystitis
E. Acute pancreatitis

1. What from the noted diseases can cause violation of motility of the intestine?
A. chronic enteritis
B. chronic colitis
C. irritable bowel syndrome
D. Crown illness
E. all are incorrect
2. What from factors not important in pathogenesis of irritable bowel syndrome?
A. infectious
B. stress
C. alimentary
D. allergic
E. ptosis of inner organs
3. What clinical variant of irritable bowel syndrome is not present in classification?
A. mainly with a constipation
B. mainly with diarrhea
C. mainly with a stomach-ache and meteorism
D. mainly with the signs of chronic intoxication.
E. all are incorrect
4. What method of research allows to differentiate a chronic colitis
from a irritable bowel syndrome?
A. rectoromanoscopy
B. irigographya
C. histological research
D. electrogastrografy.
E. ultrasound
5. Method of treatment, which is not used in irritable bowel syndrome A. A.
psychoreflexoterapy
 B. diet
C. physiotherapy
D. antibacterial therapy
E. dufalak
6. Preparation which is not used for treatment of patients with an irritable bowel
syndrome which is accompanied with constipation:
A. motilium
B. root of licorice
C. carbolen
D. glaksena
E. dufalak

7. Preparation which is not used for treatment of patients with an irritable bowel
syndrome which is accompanied with diarrhea:
A. imodium
B. skinof pomegranate
C. tincture of john's-wort
D. tincture of pie plant.
E. all answers are incorrect
8. To confirm the diagnosis of chronic colitis we need a combination of typical
clinical symptoms with results of:
A. irrigoradiography
B. rectoromanoskopy
C. colonoskopy
D. hystological research
E. ultrasound research
9. For a chronic unulcerative colitis is not typical:
A. chronic intoxication
B. violation of defecation
C. pain during palpation of sigmoid colon
D. expressed and proved hemorrhagic colitis
E. all of answers are right
10. What medication is not a proton pomp inhibitor
A. Omez
B. Ornatolum
C. Losec
D. Axid
E. Lanzap
11. Data of pH in corpus of the stomach is 1,2. What type of acid secretion?
A. Hyperchlorhydria
B.Mean secretion
C.Normochlorhydria
D. Hypochlorhydria
E. Data is normal
12. Main clinical syndrome in peptic ulcer disease.
A. Pain
B. Dyspeptic
C. Astenovegetetive
D. Diencephalic
E. Regurhytation
13. What medication is not a prokinetic?
A. Cerucal
B. Buscopan
C. Motilium
D. Cizaprid
E. All listed above