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LectureLecture
PEPTICPEPTIC ULCERULCER
DISEASEDISEASE
SponsoredSponsored
Medical Lecture Notes –Medical Lecture Notes – All SubjectsAll Subjects
USMLE Exam (America) –USMLE Exam (America) – PracticePractice
DefinitionDefinition
PepticPeptic ulcerulcer diseasedisease isis
diseasedisease ofof thethe stomachstomach oror duodenum,theduodenum,the
mainemaine signsign ofof wichwich isis anan excoriatedexcoriated
segmentsegment ((ulcerulcer defect)defect) onon gastrointestinalgastrointestinal
mucosamucosa..
About 10% of the populatione in differentAbout 10% of the populatione in different
countryes are suffered this disease.countryes are suffered this disease.
EthiologyEthiology

TheThe mainemaine causescauses of Peptic ulcer disease areof Peptic ulcer disease are
**AcidAcid hypersecretionhypersecretion
* Bacteria H-pylori* Bacteria H-pylori
 Predisposing factors:Predisposing factors:
--hereditaryhereditary predispositionpredisposition ((0(1)blood0(1)blood groupgroup,,
quatityquatity parietcellsparietcells numbernumber,, factorsfactors ofof locallocal immunity,other)immunity,other)
--StresStres,, psychogenicpsychogenic overexertionoverexertion
--NSAIDsNSAIDs ((decreasedecrease mucosalmucosal defensedefense andand repairrepair))
--Smoking, alcochol, sharp dietSmoking, alcochol, sharp diet
PathogenesisPathogenesis
 The traditional theories regarding pathogenesThe traditional theories regarding pathogenes
of peptic ulcer focus on acid hypersecretion.of peptic ulcer focus on acid hypersecretion.
Accodig to this theories,Accodig to this theories, hydrochlorichydrochloric acidacid
is the maine case of damage gastrointestinumis the maine case of damage gastrointestinum
mucosae, in situation,when local defensmucosae, in situation,when local defens
factors is decreases.This findings is notfactors is decreases.This findings is not
universal anduniversal and
it is now known that hypersecretion is not theit is now known that hypersecretion is not the
primary mechanism ulcerogenesis.primary mechanism ulcerogenesis.
PathogenesisPathogenesis
 InfectiousInfectious theoriestheories nownow isis veryvery impotentimpotent..
Accoding this theories the main cause ofAccoding this theories the main cause of
ulcerogenesis isulcerogenesis is H.pylori,wichH.pylori,wich producedproduced
enzymeenzyme –– ureaseurease andand cytotoxins, whichcytotoxins, which
may erode the mucous barrier, leading to epithelialmay erode the mucous barrier, leading to epithelial
damage.Mucolitic enzymes (eg,bacterialdamage.Mucolitic enzymes (eg,bacterial
proteases,lipase) apper to be involved in degradationproteases,lipase) apper to be involved in degradation
of the mucouse layer,making the epithelium moreof the mucouse layer,making the epithelium more
susceptible to acid damage.susceptible to acid damage.
Clinical findingsClinical findings
 Complans:Complans:
 *Attac of epigastric paine, which arise after*Attac of epigastric paine, which arise after
food from 30-60 min (ulcer stomach) or 1,5-2food from 30-60 min (ulcer stomach) or 1,5-2
houres and fasting or in the night (ulcerhoures and fasting or in the night (ulcer
duodenum) and relieved by vomiting, alkaliduodenum) and relieved by vomiting, alkali
food and medicines. Paine may be near thefood and medicines. Paine may be near the
xiphoid process or in the epigastrium to thexiphoid process or in the epigastrium to the
left of the midl line and may radiation to theleft of the midl line and may radiation to the
back near the angle of the left scapula.back near the angle of the left scapula.
Clinical findingsClinical findings

NauseaNausea
 VomitingVomiting is once(solitare), on height of theis once(solitare), on height of the
paine and is afferented reliefpaine and is afferented relief
 ConstipationConstipation
 Hematemesis (Hematemesis (vomitingvomiting withwith blood, blacblood, blac
color)color)
 Melena (blac, water stool)Melena (blac, water stool)
Clinical findingsClinical findings
 On examination:On examination:
 Usually low weight, tongue is furredUsually low weight, tongue is furred
 Tenderness and cutaneous hyperalgesia in theTenderness and cutaneous hyperalgesia in the
epigastriumepigastrium
 Mendel symptom’s positive (tenderness in oneMendel symptom’s positive (tenderness in one
poit on midl line due to percassion)poit on midl line due to percassion)
 Muscular rigidity of the upper rectus muscleMuscular rigidity of the upper rectus muscle
due to free perforationdue to free perforation
Diagnostics methodsDiagnostics methods
 FIBEROPTICFIBEROPTIC
ENDOSCOPY is a powerfulENDOSCOPY is a powerful
method for the diagnosismethod for the diagnosis
and menegement of pepticand menegement of peptic
ulcer disease.ulcer disease.
 Signs of the peptic ulcerSigns of the peptic ulcer
disease aredisease are
* ulcer defect on mucousa* ulcer defect on mucousa
* hyperemia and oderma* hyperemia and oderma
mucousa membrane aroundmucousa membrane around
ulcer defectulcer defect
Ulcer duodenum is covered fibrinUlcer duodenum is covered fibrin
Fiberoptic methodFiberoptic method
Diagnostic methodsDiagnostic methods
 Double-contrastDouble-contrast bariumbarium X-rayX-ray::
* projecting mass of barium in the lesser* projecting mass of barium in the lesser
curvaturecurvature
** nicheniche - symptom or permanent filling- symptom or permanent filling
defect in the stomach walldefect in the stomach wall
* pyloric spasm may be present with juxta-* pyloric spasm may be present with juxta-
pyloric ulcerationpyloric ulceration
* Forefinger-symptoms or symptom gastrica plica* Forefinger-symptoms or symptom gastrica plica
convergenceconvergence
Diagnostic methodsDiagnostic methods
 Diagnostic tests in order to detection H-Diagnostic tests in order to detection H-
PyloryPylory
* Morfological method* Morfological method
* Ureasa-test or “Campi” test* Ureasa-test or “Campi” test
* Respiratory test* Respiratory test
* Immunologycal blood test* Immunologycal blood test
^ PH- Metria (method for tetermination pH in^ PH- Metria (method for tetermination pH in
the stomach)the stomach)
Morphologycal methodMorphologycal method
Bacteria H- pyloryBacteria H- pylory
ComplicationComplication
 HemorrhageHemorrhage (vomiting of”coffe-ground”material -(vomiting of”coffe-ground”material -
hematemesis, black tarry stools - melena, syncope, anemia)hematemesis, black tarry stools - melena, syncope, anemia)
 PerforationPerforation and local or general peritonitisand local or general peritonitis
(extrimity pane in abdomen, rectum muscle(extrimity pane in abdomen, rectum muscle
tension, X-ray- freedom gas in abdomen)tension, X-ray- freedom gas in abdomen)
 Penetration (Penetration (paine is encrease and may be beltingpaine is encrease and may be belting
character,low grade fever,pancreatitis)character,low grade fever,pancreatitis)
 GastricGastric stenosisstenosis (vomiting with food, took in the(vomiting with food, took in the
day before, lose weight, desorders electrolits change)day before, lose weight, desorders electrolits change)
** CarcinomaCarcinoma stomach (stomach (lose weight, anemia,constant paine,other)lose weight, anemia,constant paine,other)
TreatmentTreatment
 Regim comfortableRegim comfortable
 DietDiet N1 with exclusion acute, rich, roasted(fried) food, coffe,N1 with exclusion acute, rich, roasted(fried) food, coffe,
tea, alcochol,tomatous,smoked sausage and fishtea, alcochol,tomatous,smoked sausage and fish
EthiologyEthiology treatmenttreatment
**AntibioticAntibiotic drugs for H.pylory is evolving:drugs for H.pylory is evolving:
Amoxicillin 0,5g 4 time per day 5days orallyAmoxicillin 0,5g 4 time per day 5days orally
Clarithromycin 0,5g 2 time per day 7days poClarithromycin 0,5g 2 time per day 7days po
Metronidasol 250mg 4 time per day 10 days poMetronidasol 250mg 4 time per day 10 days po
*Drugs are normalased functions*Drugs are normalased functions nervousnervous systemsystem::
Phenasepam, t-ra Valerianae or AmitriptylinPhenasepam, t-ra Valerianae or Amitriptylin
TreatmentTreatment
 PathogeneticPathogenetic treatmenttreatment
Antisecretory drugs:
* Proton pump inhibitors (blocked enzyme
H+,K+ - ATPase and intracellular syntes HCl
of the parietal cells):
Omeprasol 20 mg/day 2-4wk
Lansoprasol 30mg/day 2-4 wk
Rabeprasol 20 mg/day 2-4 wk
TreatmentTreatment
 H2-blockersH2-blockers::
Ranitidin 150mg 2 time per day 3-5 wkRanitidin 150mg 2 time per day 3-5 wk
Famotidine 20mg 2 time per day 3-5 wkFamotidine 20mg 2 time per day 3-5 wk
Nizatidin 40 mg/day 3-5wkNizatidin 40 mg/day 3-5wk
 Antacids:Antacids:
Aluminium hydroxideAluminium hydroxide
Magnesium hydroxideMagnesium hydroxide
Bismuthum nitratum or cytratum (de-nol)Bismuthum nitratum or cytratum (de-nol)
““Almagel”,”Maalox”,”Fospholugel”,otherAlmagel”,”Maalox”,”Fospholugel”,other
TreatmentTreatment
 DrugsDrugs areare enhanceenhance mucosalmucosal defencedefence::
ProstaglandinE (Misoprostol 400mg/dayProstaglandinE (Misoprostol 400mg/day
Sucralfat 0,5-1,0g 3 time per day 3-5wkSucralfat 0,5-1,0g 3 time per day 3-5wk
Venter 1,0g 2 time per day 3-5wkVenter 1,0g 2 time per day 3-5wk
De-nol 120 mg 3time per day 3-5 wkDe-nol 120 mg 3time per day 3-5 wk
Tribimol 120mg 3 time per day 3-5 wkTribimol 120mg 3 time per day 3-5 wk
TreatmentTreatment
TreatmentTreatment
 OptimalOptimal schemsschems treatmenttreatment PUPU
* Schem dual therapy* Schem dual therapy
PantoprasolPantoprasol ++ AmoxicillinAmoxicillin
RabeprozolRabeprozol ++ ClaritromycinClaritromycin
* Schem triplet therapy PU:* Schem triplet therapy PU:
Pantoprazol+Amoxicillin+MetranidazolPantoprazol+Amoxicillin+Metranidazol
* Schem quadri therapy PU* Schem quadri therapy PU
Pantoprasol+Amoxicillin+De-nolPantoprasol+Amoxicillin+De-nol+ M+ Metronidasoletronidasol
TreatmentTreatment
 SurgerySurgery methods treatmentmethods treatment
may be using, if patient has complication.may be using, if patient has complication.
IndicationsIndications::
PerforationPerforation
HemorrageHemorrage
Stenosis (gastric outlet obstraction)Stenosis (gastric outlet obstraction)
Malignization (stomach cancar)Malignization (stomach cancar)
If the patient hasn’t complication,surgery methodsIf the patient hasn’t complication,surgery methods
not indication.not indication.
Thank you for attention !Thank you for attention !

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Peptic Ulcer Diseases

  • 2. SponsoredSponsored Medical Lecture Notes –Medical Lecture Notes – All SubjectsAll Subjects USMLE Exam (America) –USMLE Exam (America) – PracticePractice
  • 3. DefinitionDefinition PepticPeptic ulcerulcer diseasedisease isis diseasedisease ofof thethe stomachstomach oror duodenum,theduodenum,the mainemaine signsign ofof wichwich isis anan excoriatedexcoriated segmentsegment ((ulcerulcer defect)defect) onon gastrointestinalgastrointestinal mucosamucosa.. About 10% of the populatione in differentAbout 10% of the populatione in different countryes are suffered this disease.countryes are suffered this disease.
  • 4. EthiologyEthiology  TheThe mainemaine causescauses of Peptic ulcer disease areof Peptic ulcer disease are **AcidAcid hypersecretionhypersecretion * Bacteria H-pylori* Bacteria H-pylori  Predisposing factors:Predisposing factors: --hereditaryhereditary predispositionpredisposition ((0(1)blood0(1)blood groupgroup,, quatityquatity parietcellsparietcells numbernumber,, factorsfactors ofof locallocal immunity,other)immunity,other) --StresStres,, psychogenicpsychogenic overexertionoverexertion --NSAIDsNSAIDs ((decreasedecrease mucosalmucosal defensedefense andand repairrepair)) --Smoking, alcochol, sharp dietSmoking, alcochol, sharp diet
  • 5. PathogenesisPathogenesis  The traditional theories regarding pathogenesThe traditional theories regarding pathogenes of peptic ulcer focus on acid hypersecretion.of peptic ulcer focus on acid hypersecretion. Accodig to this theories,Accodig to this theories, hydrochlorichydrochloric acidacid is the maine case of damage gastrointestinumis the maine case of damage gastrointestinum mucosae, in situation,when local defensmucosae, in situation,when local defens factors is decreases.This findings is notfactors is decreases.This findings is not universal anduniversal and it is now known that hypersecretion is not theit is now known that hypersecretion is not the primary mechanism ulcerogenesis.primary mechanism ulcerogenesis.
  • 6. PathogenesisPathogenesis  InfectiousInfectious theoriestheories nownow isis veryvery impotentimpotent.. Accoding this theories the main cause ofAccoding this theories the main cause of ulcerogenesis isulcerogenesis is H.pylori,wichH.pylori,wich producedproduced enzymeenzyme –– ureaseurease andand cytotoxins, whichcytotoxins, which may erode the mucous barrier, leading to epithelialmay erode the mucous barrier, leading to epithelial damage.Mucolitic enzymes (eg,bacterialdamage.Mucolitic enzymes (eg,bacterial proteases,lipase) apper to be involved in degradationproteases,lipase) apper to be involved in degradation of the mucouse layer,making the epithelium moreof the mucouse layer,making the epithelium more susceptible to acid damage.susceptible to acid damage.
  • 7. Clinical findingsClinical findings  Complans:Complans:  *Attac of epigastric paine, which arise after*Attac of epigastric paine, which arise after food from 30-60 min (ulcer stomach) or 1,5-2food from 30-60 min (ulcer stomach) or 1,5-2 houres and fasting or in the night (ulcerhoures and fasting or in the night (ulcer duodenum) and relieved by vomiting, alkaliduodenum) and relieved by vomiting, alkali food and medicines. Paine may be near thefood and medicines. Paine may be near the xiphoid process or in the epigastrium to thexiphoid process or in the epigastrium to the left of the midl line and may radiation to theleft of the midl line and may radiation to the back near the angle of the left scapula.back near the angle of the left scapula.
  • 8. Clinical findingsClinical findings  NauseaNausea  VomitingVomiting is once(solitare), on height of theis once(solitare), on height of the paine and is afferented reliefpaine and is afferented relief  ConstipationConstipation  Hematemesis (Hematemesis (vomitingvomiting withwith blood, blacblood, blac color)color)  Melena (blac, water stool)Melena (blac, water stool)
  • 9. Clinical findingsClinical findings  On examination:On examination:  Usually low weight, tongue is furredUsually low weight, tongue is furred  Tenderness and cutaneous hyperalgesia in theTenderness and cutaneous hyperalgesia in the epigastriumepigastrium  Mendel symptom’s positive (tenderness in oneMendel symptom’s positive (tenderness in one poit on midl line due to percassion)poit on midl line due to percassion)  Muscular rigidity of the upper rectus muscleMuscular rigidity of the upper rectus muscle due to free perforationdue to free perforation
  • 10. Diagnostics methodsDiagnostics methods  FIBEROPTICFIBEROPTIC ENDOSCOPY is a powerfulENDOSCOPY is a powerful method for the diagnosismethod for the diagnosis and menegement of pepticand menegement of peptic ulcer disease.ulcer disease.  Signs of the peptic ulcerSigns of the peptic ulcer disease aredisease are * ulcer defect on mucousa* ulcer defect on mucousa * hyperemia and oderma* hyperemia and oderma mucousa membrane aroundmucousa membrane around ulcer defectulcer defect
  • 11. Ulcer duodenum is covered fibrinUlcer duodenum is covered fibrin
  • 13. Diagnostic methodsDiagnostic methods  Double-contrastDouble-contrast bariumbarium X-rayX-ray:: * projecting mass of barium in the lesser* projecting mass of barium in the lesser curvaturecurvature ** nicheniche - symptom or permanent filling- symptom or permanent filling defect in the stomach walldefect in the stomach wall * pyloric spasm may be present with juxta-* pyloric spasm may be present with juxta- pyloric ulcerationpyloric ulceration * Forefinger-symptoms or symptom gastrica plica* Forefinger-symptoms or symptom gastrica plica convergenceconvergence
  • 14. Diagnostic methodsDiagnostic methods  Diagnostic tests in order to detection H-Diagnostic tests in order to detection H- PyloryPylory * Morfological method* Morfological method * Ureasa-test or “Campi” test* Ureasa-test or “Campi” test * Respiratory test* Respiratory test * Immunologycal blood test* Immunologycal blood test ^ PH- Metria (method for tetermination pH in^ PH- Metria (method for tetermination pH in the stomach)the stomach)
  • 17. ComplicationComplication  HemorrhageHemorrhage (vomiting of”coffe-ground”material -(vomiting of”coffe-ground”material - hematemesis, black tarry stools - melena, syncope, anemia)hematemesis, black tarry stools - melena, syncope, anemia)  PerforationPerforation and local or general peritonitisand local or general peritonitis (extrimity pane in abdomen, rectum muscle(extrimity pane in abdomen, rectum muscle tension, X-ray- freedom gas in abdomen)tension, X-ray- freedom gas in abdomen)  Penetration (Penetration (paine is encrease and may be beltingpaine is encrease and may be belting character,low grade fever,pancreatitis)character,low grade fever,pancreatitis)  GastricGastric stenosisstenosis (vomiting with food, took in the(vomiting with food, took in the day before, lose weight, desorders electrolits change)day before, lose weight, desorders electrolits change) ** CarcinomaCarcinoma stomach (stomach (lose weight, anemia,constant paine,other)lose weight, anemia,constant paine,other)
  • 18. TreatmentTreatment  Regim comfortableRegim comfortable  DietDiet N1 with exclusion acute, rich, roasted(fried) food, coffe,N1 with exclusion acute, rich, roasted(fried) food, coffe, tea, alcochol,tomatous,smoked sausage and fishtea, alcochol,tomatous,smoked sausage and fish EthiologyEthiology treatmenttreatment **AntibioticAntibiotic drugs for H.pylory is evolving:drugs for H.pylory is evolving: Amoxicillin 0,5g 4 time per day 5days orallyAmoxicillin 0,5g 4 time per day 5days orally Clarithromycin 0,5g 2 time per day 7days poClarithromycin 0,5g 2 time per day 7days po Metronidasol 250mg 4 time per day 10 days poMetronidasol 250mg 4 time per day 10 days po *Drugs are normalased functions*Drugs are normalased functions nervousnervous systemsystem:: Phenasepam, t-ra Valerianae or AmitriptylinPhenasepam, t-ra Valerianae or Amitriptylin
  • 19. TreatmentTreatment  PathogeneticPathogenetic treatmenttreatment Antisecretory drugs: * Proton pump inhibitors (blocked enzyme H+,K+ - ATPase and intracellular syntes HCl of the parietal cells): Omeprasol 20 mg/day 2-4wk Lansoprasol 30mg/day 2-4 wk Rabeprasol 20 mg/day 2-4 wk
  • 20. TreatmentTreatment  H2-blockersH2-blockers:: Ranitidin 150mg 2 time per day 3-5 wkRanitidin 150mg 2 time per day 3-5 wk Famotidine 20mg 2 time per day 3-5 wkFamotidine 20mg 2 time per day 3-5 wk Nizatidin 40 mg/day 3-5wkNizatidin 40 mg/day 3-5wk  Antacids:Antacids: Aluminium hydroxideAluminium hydroxide Magnesium hydroxideMagnesium hydroxide Bismuthum nitratum or cytratum (de-nol)Bismuthum nitratum or cytratum (de-nol) ““Almagel”,”Maalox”,”Fospholugel”,otherAlmagel”,”Maalox”,”Fospholugel”,other
  • 21. TreatmentTreatment  DrugsDrugs areare enhanceenhance mucosalmucosal defencedefence:: ProstaglandinE (Misoprostol 400mg/dayProstaglandinE (Misoprostol 400mg/day Sucralfat 0,5-1,0g 3 time per day 3-5wkSucralfat 0,5-1,0g 3 time per day 3-5wk Venter 1,0g 2 time per day 3-5wkVenter 1,0g 2 time per day 3-5wk De-nol 120 mg 3time per day 3-5 wkDe-nol 120 mg 3time per day 3-5 wk Tribimol 120mg 3 time per day 3-5 wkTribimol 120mg 3 time per day 3-5 wk
  • 23. TreatmentTreatment  OptimalOptimal schemsschems treatmenttreatment PUPU * Schem dual therapy* Schem dual therapy PantoprasolPantoprasol ++ AmoxicillinAmoxicillin RabeprozolRabeprozol ++ ClaritromycinClaritromycin * Schem triplet therapy PU:* Schem triplet therapy PU: Pantoprazol+Amoxicillin+MetranidazolPantoprazol+Amoxicillin+Metranidazol * Schem quadri therapy PU* Schem quadri therapy PU Pantoprasol+Amoxicillin+De-nolPantoprasol+Amoxicillin+De-nol+ M+ Metronidasoletronidasol
  • 24. TreatmentTreatment  SurgerySurgery methods treatmentmethods treatment may be using, if patient has complication.may be using, if patient has complication. IndicationsIndications:: PerforationPerforation HemorrageHemorrage Stenosis (gastric outlet obstraction)Stenosis (gastric outlet obstraction) Malignization (stomach cancar)Malignization (stomach cancar) If the patient hasn’t complication,surgery methodsIf the patient hasn’t complication,surgery methods not indication.not indication.
  • 25. Thank you for attention !Thank you for attention !