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					Gastropathology
                       Helicobacter pillory




This microbe lives in stomach. It is main culprit of diseases like
   gastritis, ulcer disease of stomach and duodenum. This microbe
   products enzymes (ureaze, proteaze), which injure protect layer of
   stomach mucous, disorders of cell function, production of mucus
   metabolic processes and promotes arising of ulcer disease.
There are variants of diagnostic Helicobacter infection.
1.Biopsy of stomach mucous membrane. It is necessary to make
   gastroscopia for this method. The advantage and disadvantage of
   this method is gastroscopia. On the one hand, doctor can evaluate
   character of stomach and duodenal mucous membrane disorders, on
   the other hand, many children hate gastroscopia.
Respiratory test. Patient drinks solution of urea and 30 min. latter the
   concentration of CO2 in expired air is revealed. Positive result is
   painless.
Serologis test (determination of antibody in serum). If it is not indication
   to gastroscopy, serologic test is optimal method for identification of
   Helicobacter pillory. It is quickly, informative, painless.
            Scheme of Shay
Aggressive factors               Protective factors
Hyperproduction of HCL           Mucous barrier
                                 - mucin, sial acids;
- Vagotonia – increase
excitation of peptic cells       -bicarbonates         - back
                                 diffusion of         Н+ions
Irrational nutrition, drags      Regeneration
Disorders of blood circulation
                                 Proper blood circulation
of mucous membrane
Disorders of antroduodenal acid
                                Antroduodenal acid brake
brake
Bile acids and lisolecitin
      Main pathogenetical lincs of ulcer disease
Disorders of nervous and hormonal mechanisms
of stomach and duodenal regulation;
Local disorders of aggressive and protective
factors equilibrium in gastroduodenal system;
 Disfunction of nieropeptids in вAPUD-system;
  Regeneratory disorders of mucous membrane in
stomach and duodenum
                     CRITERIA OF GASTRODUODENITIS
                              IN CHILDREN
1. Anamnestic data – permanent bad feeding, drug and food poisoning, hereditary
  factors.
2. Clinical
painful syndrome
  In gastritis the pain is in epigastrium, left hypochondrium, round umbilican
region, often on empty stomach.
  In gastroduodenitis painful syndrome is marked, the pain is intensive, localized in
epigastrium or hypochondrium; on empty stomach or 1,5-2 hours after meal,
seasonal.
dyspeptic syndrome
  In gastritis there are heartburn, sour belching, thirst, constipation. Appetite is
usually preserved.
  In gastroduodenitis dyspeptic syndrome is similar to that one in gastritis with
hyperacidity.
intoxication syndrome (weekness, flaccidity, irritability, bad sleep, frequent
headaches, paleness, blue tint of skin under eyes, dryness of skin.
     CLINICAL CLASSIFICATION OF CHRONIC
            GASTRITIS IN CHILDREN
                                     Primary (exogenic)
 I. By origin:
                                     Secondary (endogenic)
 II. By prevalence & localization    Diffuse
of the pathologic process:           Focal (antral, fundal)
                                     Superficial gastritis
 III. By character of morphologic    Gastritis with lesion of the gland &
changes:                              without their atrophy
                                     Atrophic gastritis
                                     With normal secretory function
 IV. Character of gastric
                                     With decreased secretory function
secretion:
                                     With increased secretory function
                                     Exacerbation
 V. Phase of process:                Incomplete remission
                                     Remission
    CLINICAL CLASSIFICATION OF CHRONIC
          DUODENITIS IN CHILDREN
                                  Primary
 I. By origin (etiology)
                                  Secondary (concomitant)

                                  Superficial
 II. By character of
                                  Diffuse (moderately marked)
morphologic changes:
                                  Atrophic (marked)

                                  Exacerbation

 III. By phase of the disease:    Incomplete remission

                                  Remission
  CLINICAL CLASSIFICATION OF CHRONIC GASTRODUODENITIS

                               IN CHILDREN
                                    Primary
 I. By origin:
                                   Secondary (endogenic)
                                   gastritis (isolated, diffuse-
 II. By prevalence:                 pangastritis)
                                   duodenitis (isolated-bulbit; spread)
                                   Exacerbation
 III. By periods                   Incomplete remission
                                   Remission
                                   With normal secretory function
 IV. By character of gastric
                                   With decreased secretory function
secretion:
                                   With increased secretory function
                                   Superficial
 V. By character of                With lesion of the gland & without
morphologic changes:                their atrophy
                                   Atrophic
           ALGORITM OF DIAGNOSING OF
              GASTRODUODENITIS
1. Endoscopy (focal or diffuse hyperemia of mucosa, hypertrophy of folds.
2. Histological investigation (aspiration biopsy)
3. Evaluation of secretory function of the stomach:
   Gastric intubation is carried out on empty stomach by a thin tube
   with continuous suction. Four 15-minutes portion (basal fraction) are
   collected, than the stimulation (histamine, euphylline, pentagastrin) is
   introduced and the four 15 minutes portion are collected (stimulated
   fraction).
   Intragastral pH-measurement allows to evaluate pH in stomach by
   help of a specific probe with two incorporated electrodes.
        Normal pH in the body of stomach is – 1,7-2,5
   Rheogastrography allows to measure tissue resistance in several
   points of the stomach and esophagus
   Pepsinigen of plasma is normally – 70-100 pmol/h
   Electrogastroduodenoscopy – X-ray examination of motor function of
   the stomach and the duodenum with barium.
4. Diagnosing of Helicobacter pillory (histological, bacterioscopical,
   bacteriological, polymerase chain reaction, respiratory method
   (evaluation of increased urea metabolites under the influence of Hp).
              CRITERIA OF ULCER DISEASE
Anamnestic data: family predisposition,
irrational nutrition, prolonged intake of drags (salicylates,
      glucocorticoids), stress, endocrinological disorders.
 Clinical signs
Painful syndrome (pains are intensive, paroxysmal, 1,5-2 h
      after meal, often at night and on empty stomach. Food
      intake decrease pain. The pain is localized in
      epigastrium, umbilicus, right subcostal area.
 Dyspeptic syndrome: vomiting (usually remove pain),
      nausea, heartburn. Appetite is not changed.
 Intoxication syndrome: weakness, flaccidity, bad sleep,
      frequent headaches, irritability, tearfulness, increased
      disposition to perspiration, blue shadows under the
      eyes, possible emaciation.
Instrumental and laboratory data.
Endoskopy (fibrogastroduodenoscopy)
 Histological investigation (aspiration biopsy)
 Diagnosing of Helicobacter pillory
                   CLASSIFICATION OF ULCER DISEASE
                               I stage – fresh ulcer
                               II stage – beginning of epitelization of
                                ulcer defect
  I. Morphologic stage:        III stage – healing of ulcer defect of the
                                mucous membrane in duodenitis
                               IV stage – clinical & endoscopic
                                remission
                               Exacerbation
  II. Phase (period) of the
                               Incomplete clinical remission
disease:
                               Stable clinical remission
                               Stomach
                               Duodenum
  III. localization:           Bulb
                               Postbulb portion
                               Double localization
                              o Duodenum “hungry pain”– hunger-pain-
                                alleviation after food intake-hunger-pain-
       Rhythm of pain:          and so on
                              o Stomach “early pain”, arising after food
                                intake
                               Bleeding
                               Penetration
  IV. Form (without &
                               Perforation
  with complications)
                               Stenosis of the pylorum
                               Perivisceritis
                               increased
  V. Functional
                               decreased
characteristic of acidity:
                               normal
                               pancreatitis
                  TREATMENT
1. Atacids (almagel, maalox,            1. Gastrocitoprotectors
phospholugel)
2. Antisecretory remedies               2. Stimulants of mucus production
  -     M-cholinolitics (atropine)
  -     H2-histamine      receptors
        (ronitidine)
  -      Protone pump inhibitors
        (omeprazole,
        lansoprazole)
3. Antichelicobacter remedies           3.    Reparants       (metilurocil,
-antibiotics             (penicillin,   pentoxil)
macrolids),
- derivate of vismut subcitrate
(De-nol)

				
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posted:3/25/2012
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Description: Pediatrics Summaries