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1. AlimentaryTractandPancreatic
disease
•Lecture6

2. 2-Juvenilepolyposis.
*Tenstohundredsofmucus-filledHamartomatous
polypsarefoundinthecolon,stomachandrectum.
*One–thirdofcasesareinheritedinanautosomal
dominantmannerandupto20%ofpatientsdevelop
colorectalcancerbeforetheageof40.
Screening
*ColonoscopyandOGDusuallybeginsafter15years
ofage.Ifsymptomshavenotoccurredalready.
Asymptomaticrelativesalsoshouldbescreened
Treatmentiswithendoscopicpolypectomy.

3. 3-Cronkhite-Canadasyndrome
Thisisarare,non-familialsyndromeofgastrointestinal
hamartomatouspolyposis
Clinicalfeatures
skinpigmentation,alopecia,,naildystrophy,diarrhea,
weightloss,andabdominalpain.
TheetiologyofCronkhite-CanadaSyndromeisunclearbut
couldbeimmune-mediated.
Itisassociatedwithahighmortalityrateduetomalnutrition
andgastrointestinalcomplications.
Thereisanincreasedriskofgastricandcoloncancer.
Treatment:nutritionalsupport(TPN).Steroidsand
azathioprine

4. 4-Cowden'sdisease
Autosomaldominantinheritance.Characterizedbythe
presenceofcolonic,Esophageal,smallintestineand
gastricpolypswithextraintestinalfeatureslike
congenitalanomalies,oral,cutaneoushamartomats,
thyroidandbreasttumors

5. ColorectalCancer
Etiology
•Environmentalfactors
•dietaryriskfactorsincolorectalcancer
•Non-dietaryriskfactorsincolorectalcancer
Geneticfactors
Pathology
ClinicalPresentation
Examination
Investigations
Treatment

6. ColorectalCancer
Colorectal cancer is the second most common internal malignancy
-increasingly after the age of 50.
-90% are Adenocarcinoma.
Etiology
Important factors are
*Environmental factors
Dietary with Increased risk include
-Red meat and saturated animal fat.
Probably because
*carcinogenic amines formed during cooking,
*High fecal bile acid and fatty acid levels May affect colonic prostaglandin turnover].

7. Dietarywithdecreasedriskinclude–
Dietaryfiber.probablybecause–
*Shortenedtransittime.
*bindingofbileacidsandEffectonbacterialflora.
-Fruitandvegetables.
probablybecauseGreenvegetablescontainanticarcinogens.
-Calcium.probablybecausecalciumBindsandprecipitatesfecalbileacids.
-Folicacid. ProbablybecausefolicacidReversesDNAhypomethlytion.

8. •Non-dietaryriskfactorsincolorectalcancer
Medicalconditions
-Colorectaladenomas
-Long-standingextensiveulcerativecolitis
-Acromegaly
-Pelvicradiotherapy
-Obesityandsedentarylifestyle-mayberelatedtodietaryfactors
-Alcoholandsmoking

9. *Geneticfactors
Severalimportanthereditaryformsofcoloncancerare
*Hereditarynon-polyposiscoloncancer.
*Familyhistoryofcolorectalcancer.
*Familialadenomatouspolyposis(FAP).
Hereditarynon-polyposiscoloncancer[HNPCC]alsoknown
as[Lynchsyndrome] isanautosomaldominantdisorders.
Thesepatientshavegerm-linemutationsinmismatchrepairgenes
involvedintherepairoferrorswhichnormallyoccurduringDNA
replication.
.

10. Criteriaforthediagnosisofhereditarynon-polyposis
coloncancer[Lynchsyndrome]
1-Threeormorerelativeswithcoloncancer(atleast
onefirst-degree)
2-Colorectalcancerintwoormoregenerations.
3-Atleastonememberaffectedunder50yearsofage
4-Familialadenomatouspolyposis(FAP)excluded

11. Pathology
Mosttumorsarisefrommalignanttransformationofabenignadenomatous
polyp.
Adenocarcinomaalmostalwaysarisefrompreexisting
adenomatouspolypsexceptinUC,orCrohn’scolitis.
Over50%ofcolorectalcanceroccursintherectosigmoidand
synchronoustumoursarepresentin2-5%ofpatients.

12. Distribution of sporadic colorectal cancer. Only 60% are in the range of flexible sigmoidoscopy.

13. Macroscopicallycolorectalcancermaybe
[Polypoid,‘Fungating’,annularorconstricting].
Spreadoccursthroughthe
*bowelwall
*Lymphatic
*portalandsystemiccirculationstoreachtheliverand thelungs

14. ClinicalPresentation
•Rightcolonictumor
•*Patientpresented with symptomsofirondeficiency
anemia*Anorexia,weightloss
•*Palpablemass
•*Obstructionuncommonbecauseofthelarger
diameterofthececumandascendingcolon.

15. Leftcolonictumor
*Colickyabdominalpainoccursin2/3ofpatientdueto
partialobstruction,spasmorinvasion
*Freshbleeding perrectum,mucusdischargeor
feelingofincompleteevacuation..
*Alteredbowelhabitmorecommonindistaltumors
*Emergencypresentationincluding[obstruction,
perforationleadingtoperitonitis,localizedabscessor
fistulaformation].

16. Examination
1-Theremaybeapalpablemass,
2-Signsofanemiaorweightloss
3-Hepatomegalyduetometastases.
4-Lowrectaltumorsmaybepalpableondigitalexamination.

17. Investigations
*Bloodtest-Anemiamaybetheonlyfeatureofcaecal
tumors.
-RaisedALPmayeduetohepaticmetastases.
•*MeasurementsofCEA duringfollow-upandcan
helptodetectearlyrecurrence.

18. *Colonoscopyistheinvestigationofchoice
because*itismoresensitiveandspecificthan
bariumenema.*lesionscanbebiopsiedand
polypsremoved
*Bariumenema
Radiologicalfeaturesofcancerarestrictures
withshoulderingorirregularfillingdefectin
thebowel.
*CTColonography[virtualcolonoscopy]non
invasivetechniquefordiagnosingtumourand
largepolyps.

19. Forpreoperativestaging
*AbdominalUS.
*Endo-analultrasound.Forrectalcancers.
*PelvicMRIforrectaltumorstaging
*Computedtomographyisvaluablefor
detectinghepaticmetastases,although
intraoperativeultrasoundisbeingused
increasinglyforthispurpose
*CXR

20. Dukesstagingofcolorectalcancer.
StageATumorconfinedwithinbowelwall.
StageBTumorExtensionthroughbowelwall.
Butthereisnocancerinthelymphnodes.
StageCExtensionthroughbowelwallWithlymphnodeinvolvement.
StageDtumorhasspreadoutsidethecolontootherpartsofthebodysuch
asliverorthelung.
5yearsurvivaldependonthestage.
stageA >90%,stageB65%,stageC30-35%,
stageD <5%.

22. •Surgery
Thetumorisremovedwithadequateresectionmarginsandpericolic
lymphnodes.
Carcinomaswithin5cmoftheanalvergemayrequireabdomeno-perineal
resectionandformationofacolostomy.Solitaryhepaticmetastasesare
sometimesresectedatalaterstage.
Post-operatively,patientsshouldundergocolonoscopyafter6-12months

23. Adjuvanttherapy
Two-thirdsofpatientshavelymphnodeordistantspread(dukes
stageCorD]atpresentationandare,therefore,beyondcurewith
surgeryalone.
-Adjuvantchemotherapywith5-fluorouracilandfolinicacid(to
reducetoxicity)improvesbothdisease-freeandoverallsurvival
inpatientswithdukesCcoloncancer.
-Thiscombinationalsoprovidesusefulpalliationforpatientswith
metastaticdisease.
•-InpatientswithdukesBorCrectaltumours,post-operative
radiotherapyincombinationwith5-fluorouracil,reduceslocal
•recurrenceandmortality

24. Screening
Aimstodetectcancerattreatablestage
Include
*RegularFecaloccultblood(FOB)testingreducescolorectalcancer
mortalityby15-20%andincreasestheproportionofearlycancers
detected.
*AnnualFOBscreeningaftertheageof50years.
*FlexibleSigmoidoscopy.every3-5yearsafter50yearsofage.
*Colonoscopyremainsthegoldstandardmethod.
*Moleculargeneticanalysis

25. InflammatoryBowelDisease
• Definition
• Types
Factorsareimplicated inthedevelopmentofIBD
Pathogenesis
Pathology
Clinicalfeatures
Investigations
Complications
Treatment

26. Inflammatoryboweldisease(IBD)isan
idiopathicandchronicintestinalinflammation,
whichcharacterizedbyrelapsingandremitting
courseusuallyextendingoveryears.Ulcerative
colitis(UC)andCrohn'sdisease(CD)arethe
twomajortypesofIBD.
Thediseaseshavemanysimilaritiesanditis
sometimesimpossibletodifferentiatebetween
them

27. *Ulcerativecolitis
*Isanidiopathicchronicinflammatorydisorderofthe
colonicmucosawiththepotentialforextra-intestinal
inflammation.
*Thediseaseextendsproximallyfromtheanalvergein
anuninterruptedpatterntoinvolveallorpartofthe
colon.

28. *Crohn’sdisease
*isanidiopathicchronicinflammatorydisorderofthe
fullthicknessoftheintestine,withthepotentialto
involvethegastrointestinaltractatanylevelfromthe
mouthtotheanusandperianalregion
*Mostcommonlyintheileumandthecolon,
*Thereisalso thepotentialforextra-intestinal
inflammation.
*Typically,thereisPatchydiseaseinthegastrointestinal
tract,withinterveningareasofnormalmucosa

29. ThepeakageofonsetofUCandCDisbetween 15and30years.
*Asecondpeakoccursbetweentheagesof60and80.*Themaleto
femaleratioforUCis1:1andforCDis1.1to1.8:1.

30. Bothgeneticandenvironmentalfactorsareimplicated inthedevelopment
ofIBD
Geneticfactorsinclude.
*MorecommoninJews
*10%haveafirstdegreerelativeoratleastonecloserelativewithIBD.
*Highconcordancebetweenidenticaltwins.
*AssociatedwithautoimmunethyroiditisandSLE.
*UCandCDpatientwithHLA-B27commonlydevelopankylosing
spondylitis.

31. Environmentalfactorsinclude.
*UC-morecommoninnon-smokerorex-smokers
*CD-mostpatientsaresmokers.
*Associatedwithlow-residue,highrefinedsugardiet.
*AppendectomyprotectsagainstUC.

32. Pathogenesisofinflammatoryboweldisease
(1)Dietary or bacterial antigens either are taken up by specialized M cells, pass
between leaky epithelial cells or enter the lamina propria through ulcerated
mucosa.
(2)After processing these antigens they are presented to CD4+ T cells by
antigen-presenting cells (APC) in the lamina propria.
APCs secrete pro-inflammatory cytokines such as tumour necrosis factor-α
(TNF-α), interleukin 12 (IL-12) and interleukin-18 (IL-18).
(3)T-cell activation and differentiation results in a Th1T cell-mediated
cytokine response with secretion of interleukin-2 (IL-2) and gamma
interferon (IFN-γ).

34. •TheregulatoryIL10andtransforminggrowth
factor-B[TGF]producedby macrophagesand
matureTlymphocytes
*Thesecytokinesdownregulateinflammatory
processesinnormalindividual exposedtoan
inflammatoryinsult.
•Ingeneticallypredisposedpersonsdysregulation
ofthesestepsleadstochronicIBD

35. PATHOLOG
UC

36. Crohnsdisease

37. ClinicalfeaturesofUlcerativecolitis
The first attack is usually the most sever and thereafter the disease is followed by relapses and
remissions
The severity of symptoms correlates with the site and activity of the disease.
Emotional stress, intercurrent infection, gastroenteritis, AB ,NSAID therapy may provoke a relapse.
PatientsWithProctitisusuallycomplainof rectalbleeding,mucous
dischargeandtenesmus.
Patientmaypresentwithconstipation.[Becauseofspasms,thepelvic
floordoesn'trelax.Thisinterfereswithnormalbowelactivity,
makingitdifficulttopassstools].
Whenthediseaseextendsbeyondtherectum,presentationinclude
*bloodydiarrhea,anorexia,nausea,vomiting,fever,andweightloss.
*lowerabdominalpainbefore bowelmovementandtemporarilyrelived
bydefecations.

38. diseaseseverityassessmentinulcerativecolitis

39. Physicalsigns
*Ulcerativecolitis
-Withextensivedisease,patientshaveabdominaltendernesstopalpation
directlyoverthecolon.
-Patientswithatoxiccolitishaveseverepain,bleeding,feverand
tachycardia.
Thosewithmegacolonhavehepatictympani.
•-Patientwithproctitishave atenderanalcanalandbloodonrectal
examination

40. ClinicalFeaturesof Crohn'sdisease
Presentation of Small intestine Crohn's disease include
-Diarrheawhichis wateryanddoes not containbloodor mucus.
-Abdominal pain[due tosubacute intestinal obstruction,inflammation,biliary
or renal stone] ,
-Weight lossdue toMalabsorptionor patient avoids foodsince eating
provokes pain.
-Fever,malaise,anorexia andvomiting[from jejunal obstruction].
-Aphthous ulcer,Post bulbar DUwhichis difficult toheal
Presentation of Crohn's Colitis
Bloodydiarrhea,passage of mucus
Constitutional symptoms includinglethargy,malaise andanorexia.
Manypatient present withsymptoms of bothsmall bowel andcolonic disease.
Few have isolatedperianal disease

41. ClinicalFeaturesof Crohn'sdisease
Presentation of Small intestine Crohn's disease include
-Diarrheawhich is watery and does not contain blood or mucus.
-Abdominal pain[due to sub acute intestinal obstruction, inflammation,
biliary or renal stone] ,
-Weight lossdue to Malabsorption or patient avoids food since eating
provokes pain.
-Fever, malaise, anorexia and vomiting[from jejunal obstruction].
-Aphthous ulcer,Post bulbar DUwhich is difficult to heal
Presentation of Crohn's Colitis
Bloody diarrhea, passage of mucus
Constitutional symptoms including lethargy, malaise and anorexia.
Many patient present with symptoms of both small bowel and colonic
disease.
Few have isolated perianal disease

42. Physical examination
-Evidence of wt loss
-Anemia, glossitis and angular stomatitis
-Abdominal tenderness.
-Abdominal massdue to matted loops of thickened bowel or intra-
abdominal abscess.
-Perianal skin tags, fissures or fistulae

43. Investigations of IBD
*Blood tests
-Elevated sedimentation rate and C-reactive protein.
-Hypo-albuminemia as a consequence of protein losing Enteropathy.
-Anemia results from iron, folic acid or Vit. B12 Malabsorption.
-Leukocytosis.
-ASCA[anti‐Saccharomycescerevisiaeantibodies].
40-60%positiveinCDand 5%inUC
-PANCA[Perinuclearantineutrophilcytoplasmic
antibodies].
positivein60-65%inUCand20-25inCD

44. *Bacteriology
*Stoolculturestoexcludesuperimposedentericinfection
inpatientwhopresentwithexacerbationofIBD.
*ElevatedfecalCalprotectinandlactoferin
indicatesthemigrationofneutrophilstothe
intestinalmucosa,
whichoccursduringintestinalinflammationcaused
byinflammatoryboweldisease
*BloodcultureforpatientwithcolitisorCrohn'sdisease

45. Endoscopy
Endoscopical appearance in UC
include
-the disease is continues and more
sever in the distal colon and rectum.
-The mucosa is erythematous, loss of
vascular patterns and contact bleeding
and in more sever disease a fine
granular surface, petechial
hemorrhages, spontaneous bleeding,
discrete ulcers and purulent exudates,
inflammatory polyps (pseudo polyps).
-The mucosa may appear normal in
remission but in patients with many
years of disease it appears atrophic
and featureless and the entire colon
becomes narrowed

46. Endoscopicalappearancein
Crohn’scolitisinclude
Theendoscopicalfinding
includeAphthousulcer,
skiplesions,strictures
anddeeplongitudinal ulcers.
*

47. *Bariumstudies.
Islessensitiveinvestigationthancolonoscopyforthe
investigationofcolitis.
-InlongstandingUCthecolonisshortenedandlossof
haustratobecometubularandpseudopolypsareseen.
-ContraststudyofsmallbowelisnormalinUC
-ContraststudyofsmallbowelinCD[Affectedareasare
narrowedandulcerated,multiplestricturesare
common.].

48. *Plainradiographs
Showcolonicdilatation,mucosaledema[thumb-
printing]orevidenceofperforation.
InsmallbowelCrohn'sdiseasetheremaybeevidence
ofintestinalobstructionordisplacementofbowelloop
byamass.
*Radionuclidescans
Radio-labelledwhitecellscansshowareasofactive
inflammation.
*MRI
Isveryaccurateindelineatingpelvicorperineal
involvementbyCrohn'sdisease

49. ComplicationsofIBD
1-Intestinal
Toxicmegacolon
•definedasacutecolonicdilatation
withatransversecolondiameter
of>6cm(onimaging
examination).
•Developasaresultoftheextension
of theinflammatoryprocesstothe
muscularispropriaandserosa
causingatonyleadingtothe
accumulationofgasandfluid
withinthelumenandsubsequent
colonicdilatation,perforationand
peritonitis.

50. •This complicationoccursinbothUCandCDmost
commonlyduringthefirstattackofcolitis.
•Predisposingfactorsforthedevelopmentoftoxicmegacolon
include
•AdministrationofNSAID,narcotics,anticholinergic.
•Toxicmegacolon maycomplicateanyseverinflammatory
conditionofthebowellike bacterial
colitis,pseudomembranouscolitis.

51. Perforationofthesmallintestineorcolonmayoccurwithoutthe
developmentoftoxicmegacolon.
*Fistulaandperianaldisease.Fistulousconnectionsbetween
loopsofaffectedbowelorbetweenbowelandbladderorvagina
arespecificcomplicationofCrohn'sdiseaseanddonotoccurin
UC.
-Entero-entericfistulae.CausesdiarrheaandMalabsorptiondueto
blindloopsyndrome.
-Entero-vesiclefistulae.Causesrecurrenturinarytractinfections
andpneumaturia.
-Entero-vaginalfistulae.Causesafeculentvaginaldischarge.
-fistulationfromthebowelmayalsocauseperianalorischiorectal
abscess,fissuresandfistulae

52. *Cancer
•BothchronicUCandCDpredisposesto
adenocarcinomaofthecolon.
•Theriskofcancerisdirectlyrelatedwithtotheextent
ofcolonicinvolvementanddurationofdisease
•Patientwithextensivecolitis areatincreasedriskof
coloncancer.
•Patientwithlongstandingextensivecolitisare
thereforeenteredintosurveillancecolonoscopy
programbeginning8-10yafterdiagnosisand
•patientwithleftsidecolitisafter10-15years.

53. Surveillance istoperformcolonoscopy with Multiple
randombiopsies.
patientswhohavenoevidenceofdysplasiaoronlylow
gradedysplasiaarescreenedevery1-2years.
Whilethosewithhighgradedysplasiashouldbe
consideredforproctocolectomybecauseofthehighrisk
ofcoloncancerdevelopment.

54. 2-ExtraIntestinalmanifestations[EIMs] thatParallel
diseaseactivity include
*Conjunctivitis,Iritis,Episcleritis
*Mouthulcers
*Portalpyaemia,Liverabscess
*Mesentericorportalveinthrombosis
*Venousthrombosis
*Arthralgiaoflargejoints.Itisasymmetric,
polyarticular,migratoryandmostoftenaffectslarge
jointsoftheupperandlowerextremities

55. *Erythemanodosum[EN].Thetenderlnodulesrangeinsizefrom1to
5centimeters.mostcommonlylocatedinthefrontofthelegsbelowthe
knees

56. *Pyodermagangrenosum[PG].
These arehot,redandtendernodulesfoundontheanteriorsurfaceof
thelowerlegs,ankles,calves,thighsandarms.Measuring1to5cmin
diameter

57. 3-TheExtraintestinal[EIMs]thatrunacourse
independentofdiseaseactivityinclude
*Autoimmunehepatitis.
*Sclerosingcholangitis,Cholangiocarcinoma.
*Gallstones.
*Sacroilitis/Ankylosingspondylitis.
*Metabolicbonedisease.
*Amyloidosis.
•*Oxalatecalculi

59. DifferentialdiagnosisofIBD
*Conditions which can mimic UC or CD.
Infective
-Bacterial. Salmonella, shigalla, campylobacter, enteropathic.Ecoli, gonococal proctitis,
pseudo membranous colitis.
-Viral. Herpes simplex and Chlamydia proctitis
-Protozoa. Amoebiasis
Non-infective
-Vascular. Ischaemic colitis, Radiation proctitis
-Idiopathic .Collagenous colitis, Behcets disease
-Drugs. NSAID
-Colonic carcinoma
-Diverticulitis
*Differential diagnosis of small bowel Crohn's disease
-Other causes of right iliac fosse mass .Caecal carcinoma and Appendix abscess
-Infection. [TB, yersinia, actinomycosis]
• -Mesenteric adenitis

60. drugsusedintreatmentofIBD
Glucocorticoidsareusedtoinduceremissioninmild‐to‐severe
UCandCD.
*Prednisolone[30-40mg/dayorally]for2wandthenreduced
slowlyover8W.
SeveractivecolitiscanbetreatedbyIVmethyl-Prednisolone
[60mgdaily]byinfusion,onceimprovementoccursthepatient
isconvertedtooralsteroid.
*Steroidfoamorliquidretentionenemasforprocto-sigmoditis
Patientwithveryactiveprocto-sigmoditisthosewhoare
unabletoretainenemasneedsoralsteroids
*Systemicandlocal steroidcanbeusedforextensivedisease.

61. *5-aminosalicylicacid[5-ASA]
*Sulfasalazine[sulfapyridineboundto5‐ASA]
whichactsbymodulatingintestinalinflammatoryactivity.
Highconcentrationof5-ASAaredeliveredtothecolon
usingthepreparationsmesalazineorolsalazine.
Dose2-4.8g/d..Dosesof1.5-4g/dmaintainremissionin
50to75%ofpatientswithUCandCD
*.liquidorfoamretentionenemasareusedfortreating
activeproctitis.[500mgtwiceaday]
*oralandlocalformoreextensivedisease.
aminosalicylates,areconsideredfirst‐lineagents

62. • immunomodulators drugs
•ForPatientwhorelapsefrequentlyaftercoursesofsteroidsorwhorequire
maintenancesteroidtherapy
Azathioprine[1.5-2mg/kgdaily] isaprodrugthatisconvertedto6‐MPBoth
areusedtomaintainremissioninUCandCD.Thisimmunosuppressantdrug
exertsitsmaximaleffectonlyafter6-12Wandsteroidtherapyshould
continueuntilthistime.Sideeffects are bonemarrowsuppression,nausea,
vomitingoracutepancreatitis.
•*MethotrexateforCD15-25MgWeeklySCorIV
•*Cyclosporine4mgkgIV forinductionofremissioninUC

63. •Biologicaltherapy
•Anti‐TNFagents[monoclonalantibodyagainstTNF]
include
•infliximab,adalimumab,certolizumabforseverUCand
CDwithrefractoryperianalandEntero-cutaneous
fistulasorUC
*Infliximab[5mg/kg)0,2,6 andthenevery8W]-
Sideeffects includesepsis,reactivationoftuberculosis,
fungalinfectionandT‐celllymphoma.
Infusionreactions,characterized bychestpain,shortness
ofbreath,rash,andhypotension,aremorecommon

64. •Anti-adhesionmolecules
•Natalizumab
•monoclonalantibodiesagainstlymphocyteadhesion
moleculesindicatefor CD unresponsivetobiological
therapy
•agentstargetingIL-12/23

65. • Induction therapy for UC Based on Disease Severity
*Mild Disease
5-Aminosalicylates
*Topical (distal colitis)
*Oral (distal/extensive colitis)
*Combination
*Moderate Disease
1-5-Aminosalicylates
*Topical (distal colitis)
*Oral (distal/extensive colitis)
*Combination
2-Glucocorticoids
• 3-Azathioprine or 6-mercaptopurine

66. *Severe Disease
*IV glucocorticoids
*Cyclosporine
*Infliximab, adalimumab, or vedolizumab

67. •MaintenancetherapyforUCUC
•*5-Aminosalicylates
•Topical(distalcolitis),Oral(distal/extensivecolitis
OrCombination
•*Azathioprineor6-mercaptopurine
•*Infliximaboradalimumab

68. • Drug treatment of Small Bowel Crohn's Disease include
• *Corticosteroids[Prednisolone 30-40 mg/day] reducing over 6-8
weeks
• *Azathioprine[1.5-2 mg/kg] for patient who relapses after stopping
steroids or who are steroid dependent.
• *Budesonide[this is a potent synthetic corticosteroid which reduces
mucosal inflammation9 mgequivalent to30mg of Prednisolone.
following absorption the drug undergoes first pass metabolism in
the liver, adrenocortical suppression is minimized and steroid side
effects are reduced

69. -Metabolic bone disease
Patient should encourage exercising, adequate calcium intake and
bisphosphonate should be given if osteoporosis is documented.
Nutritional therapy
The best advice for the majority of patient is to eat a well balanced
diet with protein, mineral and Vit, supplements.
Patient with small bowel stricture should avoid nuts, raw fruit and
vegetable which may precipitate intestinal obstruction
Patient with proctitis and constipation needs dietary fibers

70. indications for surgery in ulcerativecolitis
1-Impaired quality of life
-Loss of occupation or education
-Disruption of family life
2-Failure of medical therapy
-Corticosteroids dependence.
-Complication of drug therapy
3-Fulminant colitis
4-Disease complication unresponsive to medical therapy
-Arthritis
-Pyoderma gangrenosum
5-Colon cancer or Sever dysplasia
• Surgery involves removal of the colon and the rectum with ileostomy or
ileal anal pouch

71. The indications for surgery in Crohn’s Disease
Are similar to those for UC and for fistulae, abscesses, perianal
disease and small or large bowel obstruction. Because CD is
chronic and recurrent with no clear surgical cure, as little intestine
as possible should be resected

72. *Fulminant colitis
This is a life threatening complication needs intensive medical and surgical
management
-Patient should be monitored for clinical signs of peritonitis, fever, tachycardia,
stool frequency and volumes and abdominal x-ray are taken daily for
evidence of toxic dilatation or perforation.
Steps in the management of fulminant UC are
*IV fluids
*Blood Transfusion if Hb<10 gr.
*IV methylprednisolone [60mg daily] or hydrocortisone.
*Antibiotic for infection
*Nutritional support
*SC heparin for prophylaxis of thromboembolism
*Avoidance of opiates and Antidirrhoeal agents
If improvement has not occurred within 5-7 days or if the patient deteriorates
urgent colectomy should be under-taken.

73. Perianal disease
-Ciprofloxacin (500 mg bid).
-Metronidazole dose is 15 to 20 mg/kg per day in three divided doses; it is
usually continued for several months
-Abscess requires drainage.
Infliximab may induce remission in resistant cases.
Prognosis
-90%of UC patients have intermittent disease activity.
-10% have continuous symptoms
-1/3 of those with pancolitis under go colectomy within 5 y of diagnosis.
-80% of CD undergoes surgery at some stage
• -70% of these require more than one operation during their lifetime

74. MicroscopicColitis[MC]
•Definition
•Types
•Riskfactures
•Clinicalfeatures
•Diagnosis
•Treatment

75. •DefinitionofMC
Itisadiseaseofthecolon
Characterized
Clinicallybyintermittentwatery
diarrhea
Endoscopicallybythepresenceof
normalcolonicmucosa .
Histopathologybythepresenceof
chronicinflammationinthe
absenceofcryptarchitectural
distortion.

76. Typesofmicroscopiccolitisare
-Lymphocyticcolitis.Characterizedbyanincreased
numberofintraepitheliallymphocytes.
-Collagenouscolitis.characterizedbyasubepithelial
collagenband>10micrometerthick.
Thediseasemorecommoninfemaleandassociatedwith
rheumatoidarthritis,Thyroiddisease,DMandCeliac
disease.
Riskfactors–Smoking,
MedicationsPPI,Ranitidine,Statins,NSAID,Acarbose
Ticlopidine
ClinicalManifestation
Chronicwaterydiarrhea,abdominalpain
PresentationmaymimicIBS-D

77. Treatment
Stopsmokingand medicationsthatcouldbe
relatedtoMC
Firstlinetreatmentissteroid,.
2
nd
linetreatment Mesalamine
othertreatmentoptionsinclude
Antidiarrhealdrugs,bismuth,subsalicylate

78. Endofthelecture
Thankyou