Peptic ulcer disease is a condition that causes sores, or ulcers, in the lining of the stomach or duodenum. The main causes are acid hypersecretion and infection with the bacteria H. pylori. Common symptoms include a burning pain in the upper abdomen that occurs hours after eating and is relieved by food or antacids. Diagnosis is typically made through endoscopy or imaging tests. Treatment involves lifestyle changes, medications to reduce acid production or kill H. pylori, and sometimes surgery for complications.

1. LectureLecture
PEPTICPEPTIC ULCERULCER
DISEASEDISEASE

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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

12. Fiberoptic methodFiberoptic method

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)

15. Morphologycal methodMorphologycal method

16. Bacteria H- pyloryBacteria H- pylory

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

22. TreatmentTreatment

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 !