Pepticulcersofstomachandduodenum(PUD)
• Ulcersarechronic,oftensolitarylesions,thatoccurinanypartofGITthatisexposedtoaggresivefactorsofthe
gastricfluids
• Ulceration–disruptionofmucosaatleasttothe
muscularismucosaelayerduetosecretionofHCl
andactivationofpepsinogen
• Erosion–superficialdamage(mucosa)
• 10%ofpopulationhaveorwilldevelopanulcer
Pepticulcersofstomachandduodenum(PUD)
• Occurduetodysbalanceofgastro-duodenalprotectivemechanismsandaggressivefactors,whiletheeffectsare
furtherenhancedbyexternalorimmunologicalfactors
Pepticulcersofstomachandduodenum(PUD)
Protectivefactors• normal
compositionandproductionofmucin
• Alk.secretionofHCO3-
• intactmicrocirculation
• regenerationofgastricmucosa
• secretionofendogenousprostaglandins
Agressivefactors
• Helicobacterpylori• drugswith
ulcerogenouseffects(NSAIDs)
• deleteriouseffectsofduodenalfluids
• smoking,alcohol• disruptionsof
microcirculationinthemucosaandsubmucosa
PUD–H.pyloriinfection
• colonizationofgastricmucosa
• Doesnotentercells,onlymucosa(extracellularpathogens)
• Urease→ammonium→acidneutralization→reflexive
productionofacid
• Proteases→disruptionofmucouslayer
• Weakresistanceofthemucosa
• Digestionofthemucosabyacidandpepsin
• Chroniculcerations
PUD–Otherfactors
• Zollinger–Elissonsyndrome(gastrinoma)
• Meckel´sdiverticulumandectopicgastric
mucousmembrane
PUD–symptomes
• Epigastricpain(heatburn)• Painworseatnightand1-3hoursaftermeal
• Nauseas,vomiting,lossofweight
• Complications:anemia,bleeding,perforation
• Cancerdevelopmentisrareandconnectedtogastritis
Gastriculcer• Moreinmen,5th-6thdecade• Similartoduodenalulcerbutsurroundedbygastritis• Moreacid,moreprobability–usuallyattheborderofcorpusandantrum
• Productionofacid– Normalordecreased– Sometimesachlorhydria(absenceofHCl)
• 10-20%haveduodenalulcer• Damageofmucusbarrierdominates• Epigastricpain–themostoftensymptom• Healsbutappearsagainonthesamespot
Duodenalulcer
• 4xmoreoftenthangastric• Chronic,recurrent• Oval,1cm,• Intosubmucosisandmuscularispropria• Bottom–bloodorexsudatewitherythrocytesandcellinfiltration,inflammation
• Acidsecretion–normaltoincreased,sometimesincreasedsecretionofpepsin– 50%haveincreasedpepsinogeninserum
• Oftenhereditary• Increasedincidence– HLA-B5antigens
• Connectedtosmokingßdecreasedmicrocirculation– Bicarbonatessecretioninhibition– Quickemptyingofgastertoduodenum
• Incidence– Chronickidneydisease– Alcoholiccirrhosis– COPD
• 80-100%-H.pyloriàbadhealing• Epigastricpain90min-3hoursafterfood• Penetrationsometimes
Pancreatitis
• Inflammationofthepancreasconnectedwithedema,
differentdegreeofautodigestion,necrosisand
haemorrhagia
• 5thdecade
• Acute(reversible)vschronic(irreversibledamage)
Acute-etiology
• Gallstones• Alcohol• Idiopathic• Diseasesofduodenum
• Endocrineormetabolic
disease
• Immunologicalfacotors
• Hereditaryfactors• Drugs• Infections
Othercauses:
• Drugsandtoxicsubstances
• hypercalciemia
• Renalfailure• Viralinfections
• Cysticfibrosis• Trauma,operations
• ERCP• hyperlipidemia
Alcohol
• Directtoxiceffectonpancreaticcells• Alcoholismetabolizedbypancreasandcausesoxidativestress
• Promotessynthesisofdigestiveenzymes• Destabilizesintracellularmembranes
• Predisposestoautodigestion
Pancreatitis
Autodigestion
• Proteolyticenzymesareactivated
inpancreasinsteadofduodenum
• Endotoxines,viruses,ischemia...
etc.
• Activatedproteolyticenzymes
mayactivateother
• Proteolysis,edema,interstitial
bleeding,vasculardamage,
necrosis
Acute-pathophysiology• Abnormalactivationofdigestiveenzymeswithinthepancreas(trypsinogen–trypsin)
• Celldeath–apoptosisandnecrosis
2typesbasedonpredominantresponsetocellinjury1. Mild–Inflammationandedema2. Severe–Necrosis- Nocapsuleoverpancreas–spreadingofinflammationandnecrosis
Acute-symptoms• Severeupperabdominalpain• Nauseaandvomiting• Lossofappetite• Feverandchills• Shock• Tachycardia• Respiratorydistress• Peritonitis• Hiccup
Acute–lesscommonsigns
• Grey-Turner'ssign(hemorrhagicdiscolorationoftheflanks)
• Cullen'ssign(hemorrhagicdiscolorationoftheumbilicus)
• Körte'ssign(painorresistanceinthezonewheretheheadofpancreasislocated)
• Kamenchik'ssign(painwithpressureunderthexiphoidprocess)
Differentialdiagnosis
• Perforatedpepticulcer• Ciliarycolic• Acutecholecystitis• Pneumonia• Peuriticpain• Myocardialinfarction
BalthazarscoreBalthazargrade AppearanceonCT CTgradepoints
GradeA NormalCT 0points
GradeB Focalordiffuseenlargementofthepancreas 1point
GradeC Pancreaticglandabnormalitiesandperipancreaticinflammation 2points
GradeD Fluidcollectioninasinglelocation 3points
GradeE Twoormorefluidcollectionsand/orgasbubblesinoradjacenttopancreas 4points
Necrosispercentage Points
Nonecrosis 0points
0to30%necrosis 2points
30to50%necrosis 4points
Over50%necrosis 6points
Acute-treatment
• Fluidreplacement• Paincontrol• Bowelrest• Nutritionalsupport• Antibiotics• ERCP• Surgery
Chronic-causes
• Alcohol• Autoimmunedisorders• Intraductalobstruction• Tumors• Ischemia• Calcificstones• Idiopathic
Chronic-symptoms
• Upperabdominalpain–increasesafterdrinkingandeating
• Nauseaandvomiting• Steatorrhea• Weightlossevenwheneatinghabitsandamountsarenormal
• Type1diabetes
Ileus
• intestinaldistensionandslowerornomovementofstoolintheintestinallumen–failureofperistalsis
• Laparotomy,metabolic/electrolytichypokaliemia
• Hyponatremia,hypomagnesemia,uremia,diabeticcoma,abdominalinfection,retroperitonealbleeding,intestinalischemia,sepsa,spinalcordinjuries
• Drugs–opiates,psychotropics,anticholinergics
Ileus• Mechanical–obstruction(volvulus,gallstone,adhesion)
• Paralytic–bowelparalysis(surgery,medications,muscleandnervedisorders,cancer,Crohndisease)
• Signsandsymptoms:– Abdominalpainthatcomesandgoes– Lossofappetite– Constipation– Vomiting– Swellingofabdomen
Ileus
• Complications:– Necrosis– Peritonitis
• Treatment– Obstruction–diet,surgery– Paralysis–identifyingthecause,surgery