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Lecture : ULCERAL DISEASE

Lecture : ULCERAL DISEASE. Gastric antral and body mucous helikobakterial contamination degree determination. a) smears stained by the method of Romanovsky - Giemsa and study of spiral or S - like bacteria in the microscope field of view with increasing 360.

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Lecture : ULCERAL DISEASE

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  1. Lecture: ULCERAL DISEASE

  2. Gastric antral and body mucous helikobakterial contamination degree determination • a) smears stained by the method of Romanovsky - Giemsa and study of spiral or S - like bacteria in the microscope field of view with increasing 360. They diagnose with three degrees of contamination. • - Up to 20 germs in sight - a faint degree (+) • - 20 to 50 - the average degree (+ +) • - 50> - high (+ + +)

  3. Diagnosis of HP • a) diagnosiscontaminationof HP canbeperformedwith SLO - test (firmDelta), whichis a specialplatewiththereagentinthecenter, oneofwhichfitsbiopsyandtochangethecolorofthecentralringofbiopsiesjudgedontheavailabilityof HP.b) forthesamepurposethe de-nol-tests (by "Yamanouchi").c) ureabreathtest, basedonthereceptioninthemiddleofurealabeledcarbon (C13, C14).

  4. Diagnosis of HP

  5. Histological examination They are:-severity of inflammation,- activeness of the process- atrophy (decrease in the number of glands) - intestinal metaplasia - degree of mucous HP insemination.

  6. Histological examination determine the type of intestinal metaplasia. There are 3 types of intestinal metaplasia.Type I - entericType II - incomplete colonType III - colon with secretion sulfomutsyniv.

  7. Intragastric pH - metry allows you to set the concentration of free hydrogen ions on the surface of the body and pyloric stomach • pHintherange 0.1 -1.3 indicateshiperacidity, • 1,3-2,0 of normo-, • 1,7-3,0 - hipoacidity, • andpH 3.0 andmoreaboutanacidity.

  8. † Normal stomachshell mucose Chronic gastritis Atrophic gastritis ~ 30 лет Intestinal metaplasia Dysplasia Gastric adenocarcinoma

  9. Peptic ulcer. • Definitions. Pepticulcer - a commonchronicrelapsingdiseasewith a tendencytoprogressionofpolycycliccourse, themeofwhichisseasonalexacerbation, accompaniedbytheappearanceoftheulcerintheliningofthestomachorduodenum, andthedevelopmentofcomplicationsthatthreatenthelifeofthepatient. (I.I.Degtyarev, N.V.Kharchenko, 1996).

  10. Being a fairlycommondisease, pepticulcerdiseaseleadsto 20% ofallcasesoforganicnaturedyspepsia. IntheEuropeanpopulationincidenceofpepticulceris 10% amongmenand 5% amongthefemalepopulation. InUkraineulcerdiseaseaffectedabout 5 millionpeople. A characteristicfeatureofourtimeissexualdyzmorfizm.Inrecentyearstherehasbeenincreasingincidenceamongwomen 2-3. Themale / femaleis 1 to 2.3 forduodenalulcerand 1 to 4.8 forgastriculcer. Theincidenceofstomachulcersarealmostidenticalamongtheelderly. Epidemiology.

  11. Etiology: • Pyloricontaminationofthegastricmucosa; • Featuresgastricacid production (decreasethepHofgastriccontents, decreasedactivityofalpha 1-antitrypsin) deficiencymukohlikoproteinis gastricmucus, excessivepostprandialreleasehastrin; • Hereditaryfactor (thepresenceofbloodgroup I (0), HLA B5 antigen); • Stressfulfactors; • Dyzbalanshormones (sex, thyroid, parathyroidglands); • Tobacco; • Reception "ulcerogenic" ofdrugs (especiallyNSAIDs

  12. pathogenesis • Thepredominanceof "aggressionfactors" (hyperatsidity, increasepepsyccomponentofgastriccontents, dysmoty, microcirculationdisturbances) over "protectionfactor" (theformationofmucusandbicarbonate, prostaglandin, regenerativeprocessesinthestomachmucosa) ("weightSheya").

  13. Localizationoftheulcer:Gastriculcers:-cardia-body-stomach, small and large curvature (mediogastral) -antral-pyloric channel Duodenalulcer (DU): -bulbar -postbulbarni Multipleulcers (stomachorduodenum) Combinedulcers course:firstdetectedrecurrentcourse Phase:        -active phase (exacerbation)        nonaktyv-phase (remission: clinical, endoscopic, eradicationofHp) Gravityflow: -Light-sharpening every 1-2 years;-Mild-2 times a year;-Severe-more than 3 timesordifficult. classification

  14. classification Thepresenceof H. pyloricontaminationofthegastricmucosa:- HP - associated- HpP- notassociatedConditionatsydnostigastriccontents:- Statusnormaciditas- Status hyperaciditas- Status hypoaciditas- Statusanaciditas Presenceofcomplications:-bleeding (intermsofthesourceofbleedingandseverityofclinicalandendoscopic (by J. Forest) features)-perforation- Penetration (intermsoftheobject / bodypenetration)-pyloric stenosis (intermsofthedegreeforradiographicfeatures)-malignancy (forstomachulcers)Pepticulcerisalwaysaccompaniedbygastritis, duodenitis

  15. Diagnosis of peptic ulcer provides next volume clinical examination: • Anamnestic examination (identification of etiologic factors, comorbidities, genetic predisposition to debutants, determine the number and rate of relapse, the effectiveness of antiulcer therapy and metafilaktyky). • Physical examination (local palpation pain in the area of ​​the projection of the ulcer, positive symptom of Mendel at peryviscerytis), presence of pylori-bulbar shaft. • Endoscopic examination, diagnostic accuracy which reaches 95%, has advantages over X-ray only when localising duodenal ulcer. The optimal method of monitoring the effectiveness of antiulcer therapy (duodenal ulcer uncomplicated, if full clinical remission endoscopic control is optional).

  16. HP and duodenal ulcer

  17. X-ray examination • is superior to endoscopic where gastric ulcer localization, because it allows to assess the state of gastric motility, convergence of folds of mucous membrane, which is valuable in the differentiation of ulcer-cancer. In addition, X-ray method is leading in the assessment of cardiac and pyloric sphincter and to establish the extent of their dysfunction

  18. pH Acidic condition 7,0 – 7,5 3,6 – 6,9 2,3 – 3,5 1,6 – 2,2 1,3 – 1,5 0,9 – 1,2 anacidityexpressedhypoaciditymoderatehypoaciditynormaciditymoderatehyperacidityexpressedhyperacidity Interpretation of pH data (V.M.Chernobrovyy, 1998):

  19. Treatment. At the present stage ulcer requires the use of combinations of the means that can affect the basic pathogenetic links ulceration. Featured Maastricht 2-2000 consensus, 2003-2005. modern concept of treatment of infections associated with H. Pylory, provide mandatory Helicobacter therapy in cases of duodenal ulcer and gastric ulcer (active or inactive, complicated oruncomplicated).Two component circuits are inefficient (low percentage of eradication). Optimum is currently schema triple and quadro therapy based on proton pump inhibitor

  20. Nowrecommendseradicationof H. Pylori withcoronaryarterydisease (levelofscientificevidence B) immunethrombocytopenia (level B) unexplainedirondeficiencyanemia (level B). Inaddition, theMaastricht2003-2005 necessarilyrecommended (level A) toeradicate H. Pyloriindyspepsia, andinallcasesapplythestrategy «Testandtreat atMaastricht2003-2005 expandedindicationsforeradicationof H. pyloribyekstragastricdiseases

  21. III line-for patients with newly diagnosed ulcer-the absence of anamnestic instructions on receiving macrolides, including erythromycin II line- If first-line therapy did not lead to eradication H.pylory- In relapse- In the long history of ulcerative -Proton pump blockers (only the means with proven high antisecretory activity: Loseke, Ultop, Pariet, Oprazol, Kontralok, Esomeprazole) - Omeprazole 20 mg twice a day to 3 weeks- Clarithromycin (klatsyd) 500 mg twice a day- Amoxicillin (Flemoksyn, Osmamoks) 1000 mg twice a day The duration of treatment 7 days -Proton pump blockers (only the means with proven high antisecretory activity: Loseke, Ultop, Pariet, Oprazol, Kontralok, Esomeprazole) - Omeprazole 20 mg twice a day to 3 weeks- Bismuth subcitrate * (de-nol) or subsalitsylat- Metronidazole 500 mg three times a day- Tetracycline 500 mg 4 times a day The duration of treatment 7 days Treatment *minimum inhubuyucha bismuth subcitrate concentration is 4 times higher than in subsalits илату

  22. THANKS FOR ATTENTION!!!

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