Materials for practical classes for 4-years student

Materials for practical classes for 4-years student

Gastritis

Acute gastritis (AG) - is an acute inflammation of stomach mucosa due to strong irritatants acting for a short period.

Thus it is divided into:

Primary (exogenous) AG

Secondary (endogenous) AG

The primary AG may be caused by:

Infectious factors directly affecting stomach mucosa. Usually it is connected with using of spoiled food. The most frequent agents are Staphylococci, Salmonella, Shigella, Iersinia, Klebsiella, and Esherichia.

Chemical irritatants and drugs. They are acids, alkalies, compounds of arsenic, iodine, phosphorus, salicylates, glycocorticoids, antibiotics, etc.

Food allergens. For the infants AG may be the result ofabrupt transition to formula feeding.

The secondary AG may develop in patients suffering from acute infectious diseases (diphtheria, influenza, measles, scarlet fever, exanthematous typhus, pneumonia, and viral hepatitis). In such situation stomach lesions may be caused either by action of toxins, or directly by viruses and microbes, spreading hematogenously.

Criteria of Acute Gastritis

/. Anamnestic data: acute onset, sudden transmission to formula feeding, intake of spoiled unfresh food or formulas, various allergens, chemical substances or drugs.

//. Clinical findings: excitement, decreasing of appetite, nausea, malaise, vomiting, stomach ache, then diarrhea, dehydration, intoxication, inflated abdomen, painful palpation in epigastric region and round umbilicus.

Differential diagnosis is provided with acute appendicitis, pancreatitis, and cholecystitis.

Chronic Gastritis, Gastroduodenitis (CGD) - chronic recurrent, inclinated to progressing, inflammatory-dystrophical damage of mucosa of stomach (and duodenum).

There are 3 groups of CG corresponding to main ethiological factors:

1) exogenous - infectious, associated with Hp (Helicobacter pylory), B-bacterial gastritis;

endogenous - autoimmune caused by production ofantibodies to stomach cells (accordingly autoimmune A-gastritis);

exogenous - endogenous, connected with irritation of stomach by drugs or expressed duodenogastral reflux (chemical or reactive C-gastritis).

Classification of gastroduodenitis in children (Sydney classification of 1990, adopted to pediatric practice by N.Shabalov, 1999)

Form Etiology Localization Endoscopv Histology Secretion Period Acute Hp(+) Antral Superficial Inflammation Normal Exacer- a)mild bation Chronic Hp(-) Fundal Erosive b)moderate Increased c)marked Subre- Special: Autoim- Pangast- Atrophic Decreased mission mune ritis Atrophy: Granulo- Reactive Duodenitis Hyper- a)mild Remis- matous plastic b)mode- sion rate Eosino- Idiopathic Antroduo- c)marked philous denitis Spread Intestinal gastroduo- methaplasia denitis

Criteria of CGD

/. Anamnestic data: permanent bad feeding, drug and food poisoning, hereditary factors and some other factors mentioned above.

//. Clinical:

a) painful syndrome;

In gastritis with preserved or increased acidity there are intensive pains in epigastrium, left hypochondrium, round umbilical region, often on empty stomach. They may cease after meal. In gastritis with hypacidity the pains are of small intensity, without accurate localization, more often after meal.

- In gastroduodenitis painful syndrome is marked, the painsare intensive, localized in epigastrium or hypochondrium; on empty stomach or 1,5-2 hours after meal, seasonal (spring or autumn).

b) dyspeptic syndrome;

In gastritis with preserved secretion or hypersecretion there are heartburn, sour belching, thirst, constipation. Appetiteis usually preserved.

In gastritis with hyposecretion appetite is decreased. There is feeling of weight and discomfort in epigastrium and left hypochondrium, gaseous, meteoric belching, and tendency to diarrheas.

In gastroduodenitis dyspeptic syndrome is similar to that one in gastritis with hyperacidity but it is more marked.

c) intoxication syndrome: weakness, flaccidity, irritability, bad sleep, frequent headaches, paleness, blue tint of skin under eyes, dryness of skin;

d) involvement of other digestive organs (the liver, the pancreas, the intestine) into pathological process.

- In the phase of remission the signs of the disease may be absent.

Algorithm of diagnosing of CGD

Analysis of anamnestic data, physical examination, endoscopy, USE of the abdominal cavity, functional methods of investigation, X-ray examination.

Endoscopy usually reveals focal or diffuse hyperemia of mucosa, edema, hypertrophy of folds. Lymphofollicular hyperplasia, plane or elevated erosion may be revealed. These changes are usually associated with Hp-infection.

Histological investigation of the stomach and the duodenal mucosa (by means of aspiration biopsy) is obligatory diagnostic method for CGD. It allows to estimate the degree of inflammatory, dystrophic or dysregenerative processes.

Evaluation of the secretory function of the stomach: a) gastric intubation is carried out on empty stomach by a thin tube with continuous suction. Four 15-minutes portions (basal fraction) are collected, then the stimulator (Histamine, Euphylline, Pentagastrin) is introduced and the next four 15-minutes portions are collected (stimulated fraction).

Normal values of stomach secretion (N. Shabalov, 1999)

IndicatorsBasalStimulated by brothStimulated by PentagastrinVolume (ml) 15-6027-6455-165Free hydrochloric acid (units) 10-3030-6030-85Common acidity (units) 20-4040-8045-135Acid production (hour output of HCI) (meq) 0,75-2,561,47-2,84,5-11,5

intragastrial pH-measurement allows to evaluate pH in vivo in the body and in the antral region of the stomach by help of a special probe with two incorporated electrodes. Normal pH in the body of the stomach on empty one is 1,7-2,5 for children over 5 years; after the stimulator (Histamine) is introduced pH is 1,5-2,5; pH of the antral secretion of the stomach is normallymore than 5. Thus the difference between pH of the body and the antrum is normally more than 2 units (compensated state). Lessening of this difference indicates the decrease of neutralizing ability of the antrum secretion and possible acidifying of the duodenum (decompensation).

rheogastrography allows, by help of a special probe, to measure tissue resistance in several points of the stomach and the esophagus: the level of tissue resistance makes it possible to evuluate acid-forming function with use of a special device or a computer. Acid-forming function is investigated before and after the introduction of histamine stimulator.

The secretory function is regarded to be decreased if all the values of basal and stimulated secretion are decreased. Secretory function is regarded to be increased if separate value even in one of the fractions is raised.

In children CGD is more often characterized by normal or increased secretory function.

pepsinogen of plasma is normally at the level of 70-100 pmol/h; excretion of uropepsinogen is normally 0,3-0,8 mg; proteolitic activity of uropepsinogen is 0,02-0,07 o.u. Examination of the above mentioned tests might be useful for indirect estimation of gastric enzymecreative function;

motor function of the stomach and the duodenum isinvestigated by means of electrogastroduodenoscopy, X-ray examination with barium and ultrasonic examination (after prior filling of the stomach with water). This can reveal sphincter disturbances, refluxes, etc.

diagnosing of Helicobacter infection is provided by meansof various methods: histological, bacterioscopical, bacteriological, PCR (polymerase chain reaction is examination of Hp in the stomach for DNA), respiratory method (evaluation of increased urea metabolites under the influence of helicobacter urease after prior intake of urea).

Functional stomach disorders (FSD) are the disturbances of motor and secretory functions of the stomach. They are not proceeded by the morphologic lesions of mucosa.

Primary (exogenous) FSD are caused by:

alimentary factors (irregular feeding, too quick changesof diets, dry food, overeating, abuse of refined food, pork and sheep fat, rude cellulose, mushrooms, spices, use of too hot or too cold food);

smoking;

helminthic and protozoan invasion, hard manual labor,vibration, noise, overheating;

- neuro-psychic disorders, stress, emotional and physical exertion.

Secondary FSD often accompanies:

chronic diseases of organs of digestive system (chronic cholecystitis, cholelithiasis, colitis, hepatitis);

vegetovascular dystonia;

diseases of the spinal column;

diseases of different organs - the kidneys, the heart, vessels, muscles, chronic foci of infection, etc.

FSD may be of 2 types:

Motor type in the forms of duodenogastric reflux, gastroesophageal reflux, cardiospasm.

Secretory type: the forms with increased or decreased secretory function.

Criteria of functional stomach disorders

/. Anamnestic data: connection between the stomach discomfort and the mentioned above causal factors (irregular feeding etc.)

//. Clinical signs:

pains in epigastrium or umbilical region often without accurate localization;

pains are irregular, changeable, without clear connection with food intake and its nature, gaseosus eructation, heartburn;

on palpation no local changes but painfulness in epigastrium which may quickly cease are usually found.

///. Instrumental and laboratory findings:

Endoscopy: sphincter spasms, hyperperistalsis, duodenogastric reflux (DGR), cardiac insufficiency and other motor disorders. Mucosa is usually intact.

Electrogastrography (EGG), USE may reveal motor and evacuative disorders.

Secretory function more often is increased, but it may be normal or decreased.

Peptic ulcer (PU) of the stomach and the duodenum (ulcer disease)

Helicobacter pylori is the commonest bacterial pathogen in humans, infecting more than 50% of the world's population. This infection (initially called Campylobacter pylori) was first described by Warren and Marshall in Perth, Australia in 1982, when they cultured the organism from the gastric antrum of adults with peptic ulcer disease. H. pylori as a paediatric infection is usually acquired in the first 2 years of life but the disease consequences

rarely arise in childhood. In 1999, the North American Society for Pediatric Gastroenterology and Nutrition convened an expert group to develop evidence based guidelines on H. pylori infection in children to address the issues of diagnostic tests, when testing is indicated, treatment indications and appropriate therapeutic regimens.

Epidemiology

In developing countries, up to 80% of children are infected by age 2 years, with a lower prevalence in breastfed infants. A similar pattern is seen in children in lower socioeconomic groups in developed countries. In developed countries, only 10% of all children are infected by age 10 years. The route of transmission is probably similar to other enteric pathogens, being faecal-oral, oral-oral or gastric-oral. H. pylori has been detected in vomitus, saliva, faeces and on children's dummies, and also in contaminated water and food prepared with contaminated water. The house fly has also been implicated as a vector. The spread of infection within families is most likely from infected mother to child, although there is some evidence of sibling to sibling spread. Risk factors for H pylori infection in children are shown in below.

Risk factors for H. py/or/infection

• Poor socioeconomic status

• Household crowding

• Ethnicity

• Migration from high prevalence areas

• Infected parent, particularly mother

• Contaminated water

The natural history of H. pylori infection in childhood remains obscure. A significant finding has been spontaneous clearing and reacquisition of gastric infections in preschool children, as spontaneous eradication does not appear to occur in adults.

According to N. Shabalov (1999) PU is a chronic recurring disease, which is characterized by the formation of ulceral lesion in the stomach or the duodenum, caused by breaking between balance of local protective and aggressive factors.

Ulcer disease is polyetiological: hereditary predisposition (several genetic factors have been proved), infectious factors (Helicobacter pylori), alimentary, neuropsychic (stress), bad habits are considered to be important causes of peptic ulcer.

Classification of ulcer disease in childhood (A.A.Baranov, 1986)

Localization Clinical phase and endoscopy stage Severity of course Complications Stomach: Exacerbation

1. Recent ulcer

2. Beginning

of epithelizaton

Subsiding of

exacerbation

3. Healing of ulcer

a) without cicatrix

b) cicatrical ulceral

deformation

Remission Mild Bleeding - medigastric Moderate Perforation - pyloroantral Severe Penetration Duodenum Stenosis Perivisceritis Criteria of Ulcer disease

/. Anamnestic data:

family predisposition;

exogenous factors: bad diet (as to regularity and quality of feeding), prolonged intake of drugs (salicylates, glucocorticoids, etc.);

endogenous - stress, endocrinological disorders etc.

//. Clinical signs:

- painful syndrome

Pains are intensive, paroxysmal, which occur 1,5-2 hrs after meal, more often at night and on empty stomach. Food intake releaves pain. The pain is localized in epigastrium, umbilicus, right subcostal area, sometimes irradiates to waist or has spread character. The pain is frequently connected with intake of coarse and plain food. Seasonal exacerbation of painful syndrome (spring and autumn) is remarked. There is tenderness on palpation in pyloroduodenal area, muscular defence, and hyperesthesia of skin in tender zones (Zakhariev-Ged), positive sign of Mendel.

- dyspeptic syndrome: vomiting, nausea, heartburn, vomiting frequently causes relief, removing pain. Sour, bitter, food, gaseous eructation. In case of pyloric stenosis belching with mustysmell is present.

Most patients’ appetite does not change, but some of the patients may have decrease of appetite.

The tongue is coated. Tendency to constipation (in patients with increased gastric acidity) or unstable stool (in patient with low gastric acidity) is present.

- intoxication syndrome: weakness, flaccidity, bad sleep, frequent headaches, irritability, tearfulness, increased disposition to perspiration, blue shadows under the eyes, possible emaciation;

- accompanied damages of other organs: the liver.

///. Instrumental and laboratory findings:

- Endoscopy investigations: fibrogastroduodenoscopy - reveals ulcer lesion;

X-ray signs of ulcer:

Direct signs:

niche with inflammatory elevation (roller);

convergence of folds;

cicatricial deformation of the stomach, the duodenal bulb.

Indirect signs:

hypersecretion on empty stomach;

strenuous segmentation.

Diagnostic tests for H. pylori infection

Diagnostic Tests for H. pylori

Endoscopic

Biopsy and histology

Rapid urease test

Bacterial culture

Indirect tests

Serum antibody (IgA, IgG)

Saliva antibody

Urine antibody

Stool culture/stool antigen

Urea breath test

The ideal test for H. pylori infection does not exist, but it should be non or minimally invasive, accurate, inexpensive, readily available and able to discriminate between past and present infection.

Endoscopy and biopsy is the only method that can provide evidence of disease activity such as gastritis or an ulcer. Urease testing of biopsy material gives indirect identification of infection but has only a 50% positive predictive value in children.

The urea breath test is currently the best non invasive test. It has a greater than 95% positive and negative predictive value for H. pylori infection. The principle of the test is outlined in Figure below.

Urea can be labelled with either radioactive I4C or stable isotope 13C. In children and women of child bearing age 13C-urea is recommended.

Serology, while commercially available, is frequently unreliable and cannot distinguish between past and present infection. All the other non invasive tests are still under trial or are not sufficiently sensitive.

The aim of testing is not to detect the presence of infection but to find the cause of clinical symptoms, and therefore the important question is who should be tested.

Treatment

The discovery of H. pylori as the cause of primary peptic ulceration and gastric ulcers has changed their management, as eradication of the organism cures the disease and prevents recurrence. If endoscopy is indicated to investigate organic disease and H. pylori is found, the child should receive treatment; however, if no ulcer is found the patient/parents should be informed that H. pylori eradication may not relieve the symptoms.

Who should be treated for H, pylori infection

• Histologically proven infection with gastrointestinal symptoms

• Duodenal/gastric ulcers

• Lymphoma

• Atrophic gastritis with intestinal metaplasia

The traditional treatments do not eradicate H. pylori infection and current treatment in children advocates a combined regimen using two antibiotics and a proton pump inhibitor, based on adult treatment regimens. At present there are no published peer reviewed controlled studies of treatment regimens in children. The currently recommended first line treatment is a combination of a proton pump inhibitor, clarithromycin and amoxycillin twice daily for 7 days. Metronidazole can be substituted for either amoxycillin or clarithromycin but there is a high resistance to this drug and its use may lead to treatment failure. Failure of eradication leads to the use of second line options, which usually include bismuth subsalicylate in a triple or quadruple therapy regimen.

The burden of illness caused by H. pylori is considerable, making the development of a prophylactic vaccine to prevent infection or a therapeutic vaccine to eliminate existing infection desirable but to date no vaccine is available.

MedicationsDosageFirst-Line Options1) Amoxicillin50 mg/kg/day up to 1g bidClarithromycin15 mg/kg/day up to 500 mg bidProton pump inhibitor: omeprazole (or comparable acid inhibitory doses of another PPI)1 mg/kg/day up to 20 mg bid2) Amoxicillin50 mg/kg/day up to 1g bidTinidazole (ornidazole)20 mg/kg/day up to 500 mg bidProton pump inhibitor: omeprazole (or comparable acid inhibitory doses of another PPI)1 mg/kg/day up to 20 mg bid3) Clarithromycin15 mg/kg/day up to 500 mg bidTinidazole (ornidazole)20 mg/kg/day up to 500 mg bidProton pump inhibitor: omeprazole (or comparable acid inhibitory doses of another PPI)1 mg/kg/day up to 20 mg bidSecond-Line Options1) Bismuth subcitrate1 tablet (120 mg) twice a dayTinidazole (ornidazole)20 mg/kg/day up to 500 mg bidProton pump inhibitor: omeprazole (or comparable acid inhibitory doses of another PPI)1 mg/kg/day up to 20 mg bidplus an additional antibiotic:Amoxicillin50 mg/kg/day up to 1g bidor Tetracycline50 mg/kg/day up to 1 g bidor Clarithromycin15 mg/kg/day up to 500 mg bid2) Ranitidine150 mg twice a day or Famotidine 20 mg twice a day Tinidazole (ornidazole)20 mg/kg/day up to 500 mg bidBismuth subcitrate1 tablet (120 mg) twice a dayplus an additional antibiotic:Amoxicillin50 mg/kg/day up to 1g bidor Tetracycline50 mg/kg/day up to 1 g bidor Clarithromycin15 mg/kg/day up to 500 mg bid

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Дата добавления: 2015-11-04