Pathophysiology of Gastrointestinal tract

Pathophysiology of Gastrointestinal tract: the disordered physiological processes associated with gastrointestinal disorders and disease or injury.

2. Diseases of Mouth
-Sincemouthistheentrypointofvariouspathogensandmicroorganisms,
beitwithfoodorassuch,therearechancesofanumberofdiseasesto
occurinthemouth.
•Thrush(OralCandidiasis)
-ThrushacutefungalinfectioniscausedbytheyeastCandidaalbicans,
whichoccurswhenthecommensalmicrobegrowsinwhitepatchesonthe
tongueandoralmucosa.
-Causedby–Candidaalbicans(Yeast)
-Symptoms–Itchingandrashattheinfectedsite.
-Risks-Inadultsitcausesopportunisticinfectionmainlyinthosewhose
immunityisloweredby,e.g.,steroids,antibioticsorcytotoxicdrugs.In
childrenitoccursmostcommonlyinbottle-fedbabies.
-Diagnosis–Physicalexaminationofthelesionsinmouth;Bloodtest–
Candidaspecificantibodytestisusedtodetectedcandidiasis–IgM,IgA&
IgG.
-Treatment–Antifungals(Clotrimazole,Fluconazole,etc.),Antiseptics,
etc.

3. •Gingivitis
-Thisisinflammationofthegums.
-MaybeAcuteorChronic.
-Itoccursinresponsetoaccumulationofbacterialplaquearoundtheteeth.
-Itgraduallydestroysthetissuessupportingtheteeth.
-Symptoms–Swollengums,bleedinggums.
-Risks–Poororalhygiene,Smokingorchewingtobacco,Olderage,etc.
•DentalCaries
-Dentalcariescausedestructionofthecalcifiedtissuesoftheteeth.
-Ifuntreated-microorganismsmayinvadethepulp,causinginflammationandinfection.
-Bacteria-produceacidsthatdemineralizetheenamel.
-Dextran,astickypolysaccharideproducedfromsucrose,causesthebacteriatosticktothe
teeth.
-Massesofbacterialcells,dextran,andotherdebrisadheringtoteethconstitutedentalplaque.
-Rootcanaltreatmenthelpstotreatthedecayofpulpcausedduetotheinfection.

4. Diseases of Pharynx
•Tonsilitis
-Thisistheinflammationofpalatinetonsils,palatinearchesandwallsofthepharynx
causedbyVirusesandStreptococcuspyogenes.
-Theremaybeproductionofabscessatthesiteofinfection.
-Theinfection,ifuntreatedmayspreadtotheneckandcausecellulitis.
-Repeatedinfectionmayleadtochronicinflammation,fibrosisandpermanent
enlargement.
-Surgicalremovalofthetonsils(Tonsillectomy)canhelptoreducethepainand
inflammation.
-NSAIDs,analgesicsandantibioticscanbeused.

5. •Diphtheria
-Causativeagent-Corynebacteriumdiphtheriae
-Thisisabacterialinfectionofthepharynx–extendstothenasopharynx
andtrachea,causedbyabacteriainwhichthickfibrousmembrane
formsovertheareaandmayobstructtheairway.
-Themicrobeproducespowerfulexotoxinsthatmayseverelydamage
cardiacandskeletalmuscle,theliver,kidneysandadrenalglands.
-Itmaybetreatedbyusingantitoxintodiphtheriatoxin.
-Vaccinationwithdiphtheriatoxoidisthebestwaytopreventits
occurrence.

6. Diseases of Salivary Glands
•Mumps
-Causedby-Mumpsvirus
-Thisisanacuteinflammatoryconditionofthesalivaryglands,especiallytheparotids.
-Thevirusisspreadbyinhalationofinfecteddroplets.
-Virusesmultiplyelsewhereinthebodybeforespreadingtothesalivaryglands.
-Complicationsmayaffect:
a.thebrain,causingmeningitisormeningoencephalitis
b.thetestes,causingorchitis(testicularinflammation)
c.Pancreatitis,Heartproblems,miscarriage,etc.
Risks–Unvaccinatedindividualsareatahighrisk,childrenbetween2-12years,etc.
Symptoms–Painwhileswallowing,Fever,Lossofappetite,etc.

7. •TumorofSalivaryGlands
1.Salivaryadenoma
-Thisbenigntumoroccursmainlyintheparotidglandandisthe
mostcommontumorofthesalivaryglands.
-Asecondtumormaydevelopinthesameglandseveralyears-
malignanttype.
2.Carcinoma
-Malignanttumorsmostcommonlyaffecttheparotidglands.
-Someformshaveatendencytoinfiltratenervesinthe
surroundingtissues,causingseverepain.
•Symptoms–Swellingnearthejaworinneckormouth,
difficultyswallowing,numbnessinpartoftheface,etc.
•Causes–Geneticmutations(predominantly),smoking,
tobaccochewing,etc.

8. Diseases of Esophagus
•Gastro-esophageal reflux disease (GERD)
-This disease is characterised by the reflux of gastric juice and acids from
the stomach into the esophagus.
-It may be due to a fault in the lower esophageal sphincter to close and
prevent the gastric contents from entering intothe esophagus.
-It results in inflammation of the lower esophagus.
-It the reflux persists,fibrous tissues form at the site of inflammation.
-Reflux of gastric contents is associated with:
• increase in the intra-abdominal pressure, e.g.in pregnancy, constipation
and obesity.
• low levels of secretion of the hormone gastrin, leading to reduced sphincter
action at the lower end of the oesophagus.
• the presence of hiatus hernia.

9. Symptoms–Heartburn,nausea,regurgitation,discomfortinupper
abdomen,etc.
Cause–FailureofthelowerOesophagealsphinctertoconstrictproperly.
•Barrett’soesophagus
-ThisdiseaseisactuallyaconsequenceofRefluxOesophagitis.
-Inthisstratifiedsquamousepitheliumoftheloweroesophagusisreplaced
bycolumnarepithelium(columnarmetaplasia).
-Ifnottreatedontime,mayprogresstoCarcinomaofOesophagus
followedbyAdenocarcinoma.
-Symptoms–Difficultyinswallowingfood,Chestpain,heartburnand
regurgitation.
-Causes–Notknow,butisthoughttobeaconsequenceofRefluxdisease.
-Risk–Familyhistory,Gender(Menaremorelikelytodevelopit),Smoking,
GERD,Obesity,etc.

10. •Achalasia
-Achalasiaoftheoesophagusisaneuromusculardysfunction
duetowhichthecardiacsphincterfailstorelaxduring
swallowingandresultsinprogressivedysphagiaanddilatation
oftheoesophagus.
-Itoccurswhentheintramuralneuronsinthewallofthe
oesophagusaredamaged.
-Symptoms–Heartburn,regurgitationoffood,belching,chest
pain,vomiting,etc.
-Causes–Lossofnervecellsfromoesophagus.
-Risk–Allgrovesyndrome,Herpesinfection,Measles,
Autoimmunediseases,etc.

11. •OesophagealDiverticula
-Thesearetheprotrusionsorpouchesofoesophagealwallatthe
pointofweakness.
1.Congenitaldiverticulaoccureitherattheupperendofthe
oesophagusoratthebifurcationoftrachea.
2.Acquireddiverticulamaybeof2types:
a)Pulsion(Zenker’s)type—Itisseenintheregionofhypopharynxand
occursduetooesophagealobstructionsuchasduetochronic
oesophagitis,carcinomaetc.Themucosaandsubmucosaherniate
throughtheweakenedareaorthroughdefectinthemuscularispropria.
•b)Tractiontype—Itoccursinthelowerthirdofoesophagusfrom
contractionoffibroustissuesuchasfrompleuraladhesions,scartissue
ofhealedtuberculouslesionsinthehilum,silicosisetc.
•Complicationsofdiverticulaincludeobstruction,infection,perforation,
hemorrhageandcarcinoma.
Oesophageal
Diverticula
Congenital
Acquired

12. •CarcinomaofOesophagus
-Althoughexactetiologyofcarcinomaoftheoesophagusisnotknown,anumberofconditions
andfactorshavebeenimplicatedasunder:
1.Dietandpersonalhabits:
-i)Heavysmoking
-ii)Alcoholconsumption
2.Oesophagealdisorders:
-i)Oesophagitis(especiallyBarrett’soesophagusinadenocarcinoma)
-ii)Achalasia
-iii)Hiatushernia
-iv)Diverticula
3.Otherfactors:
-i)Familyhistory—associationwithtylosis(keratosispalmarisetplantaris).
-ii)Geneticfactors—predispositionwithcoeliacdisease,epidermolysisbullosa,tylosis.
-iii)HPVinfection—isarecentadditioninetiologicfactors.

13. -Abnormalityofp53tumorsuppressorgeneisfoundtobeassociatedwiththeonsetofthe
disease.
•Carcinomaoftheoesophagusismainlyof2types—
A.Squamouscellcarcinoma
-90%ofprimaryoesophagealcancersareofthistype.
-Majorityofthesquamouscellcarcinomaoccurinthemiddlethird,followedbylowerthird,
andtheupperthirdofoesophagusinthatorderoffrequency.
-3typesofpatternsarerecognized(Fig.18.4,B):
i)Polypoidfungatingtype—isthemostcommonform.Itappearsasacauliflower-like
friablemassprotrudingintothelumen.
ii)Ulceratingtype—isthenextcommonform.Itlooksgrosslylikeanecroticulcerwith
evertededges
iii)Diffuseinfiltratingtype—appearsasanannular,stenosingnarrowingofthelumendue
toinfiltrationintothewallofoesophagus.
Oesophageal
Carcinoma
Squamous cell
carcinoma
Adenocarcinoma

14. B.Adenocarcinoma
-10%ofprimaryoesophagealcancersareofthistype.
-Thecommonlocationsarelowerandmiddlethirdoftheoesophagus.
-Oesophagealadenocarcinomaappearsasnodular,elevatedmassinthelower
oesophagus.
-Threepatternsrecognized:
1.Intestinaltype—istheadenocarcinomawithapatternsimilartothatseenin
adenocarcinomaofintestineorstomach.
2.Adenosquamoustype—isthepatterninwhichthereisanirregularadmixtureof
adenocarcinomaandsquamouscellcarcinoma.
3.Adenoidcystictype—isanuncommonvarietyandshowsacribriformappearanceinan
epithelialtumour.

15. Diseases of Stomach
❖CongenitalandAcquiredCondition:-
•PyloricStenosis
-Inthisdisease,thereisnarrowingofthepyloricopening
especiallyinmalechildrenasacongenitaldefect
(infantilepyloricstenosis).
-Itisrarelyobservedinadults–maybeduetoacquired
inflammatoryfibrosisorbyinvasionoftumors
-Causes:
1.Forinfantilepyloricstenosis–Geneticand
environmentalfactorsresponsible.
2.Foradultpyloricstenosis–relatedtoantralgastritis,
andtumorsintheregion(gastriccarcinoma,
lymphoma,pancreaticcarcinoma,etc.)

16. -Inboththetypes,thereishypertrophyaswellashyperplasiaofthecircularlayerof
muscularisinthepyloricsphincteraccompaniedbymilddegreeoffibrosis.
-Symptoms–Vomitingafterfeeding/eating,Stomachcontractions,Dehydration,Changes
inbowelmovement,etc.
-Risks–Gender(Moreseeninmales),Prematurebirth,Familyhistory,Smokingduring
pregnancy,etc.
-Complications–Jaundice(rare),Stomachirritation,etc.
❖InflammatoryConditions:-
•Gastritis
-Itisaconditioninwhichtheliningofthestomachbecomesinflamedwhichmaybecause
upperabdominaldiscomfortlikeindigestionordyspepsia.
-Inworstcases,itmayprogresstopepticulcerorgastriccancer.

17. •Types:
A.AcuteGastritis
-Acutegastritisisatransientacuteinflammatoryinvolvementofthestomach,mainly
mucosa,andisusuallyaresponsetoirritantdrugs(NSAIDslikeAspirin,etc.)oralcohol.
-Causes-
1.Dietandpersonalhabits:-Highlyspicedfood,Excessivealcoholconsumption,
Malnutrition,Smoking.
2.Infections:-Bacterialinfectionse.g.Helicobacterpylori,diphtheria,salmonellosis,
pneumonia,staphylococcalfoodpoisoning,etc.
3.Drugs:-IntakeofdrugslikeNSAIDs,aspirin,cortisone,phenylbutazone,indomethacin,
preparationsofiron,chemotherapeuticagents.
Gastritis
Acute Chronic

18. 4.Severestress:-Emotionalfactors(likeshock,anger),Extensiveburns,Trauma,Surgery.
•MechanismofInjury:
B.ChronicGastritis
-Chronicgastritisisamilderbutlonger-lastingcondition.
-ItisusuallyassociatedwithHelicobacterpyloributissometimesduetoautoimmune
diseaseorchemicalinjury.
1. Reduced blood flow
2. Increased acid secretion and its accumulation
3. Decreased production of bicarbonate buffer.

19. 1.Helicobacter-associatedgastritis.
Helicobacterpyloriisabacteriumthatcansurviveinthegastricmucosa
andis
commonlyassociatedwithgastricconditions,especiallychronicgastritis
andpepticulcerdisease.
2.Autoimmunegastritis
-Itiscalledautoimmunegastritisduetothepresenceofcirculating
antibodiesandissometimesassociatedwithotherautoimmunediseases
suchasHashimoto’sthyroiditisandAddison’sdisease.
-Antibodiesagainstparietalcellsandintrinsicfactorareproduced,asa
resultthereisdepletionofparietalcellsandimpairedsecretionofintrinsic
factor.
-Mayleadtosignificantgastricatrophywhereintestinalmetaplasiamay
occur.
•Consequencesinclude:
-perniciousanemiaduetolackofintrinsicfactor
-increasedriskofcancerofthestomach

20. -Symptoms-Nausea,Vomiting,Burningacheorpaininupper
abdomen,etc.
-Risks–Bacterialinfection,Frequentuseofpainrelievers,Stress,
Excessivealcoholuse,Autoimmunedisease,etc.
-Complications–Ifleftuntreated,mayleadtostomachulcers
andbleeding.
-Prevention–Frequentwashingofhandswithsoapandwater,
consumingcompletelycookedfood.

21. •PepticUlcerDisease(PUD)
-Pepticulcersaretheareasofdegenerationandnecrosisof
gastrointestinalmucosaexposedtoacid-pepticsecretions.
-Thesearebasicallyopensoresthatdevelopontheinner
liningofthestomachandduodenum.
-TheycanoccurinanypartoftheGITwhichareexposedto
HClandPepsin,butmajorityoccurinStomachand
Duodenum.
A.AcutePepticUlcer
-Thesearearesultofseverestress.
-Thesearemultiple,smallmucosalerosions,seenmost
commonlyinthestomachbutoccasionallyinvolvingthe
duodenum.

22. -Causes-
B.ChronicPepticUlcer
-Ifnotspecified–chronicpepticulcerswouldmeangastricand
duodenalulcers–thetwomajorformsofpepticulcerdiseaseofthe
upperGItract.
-Morecommoninduodenumthaninstomach.
-H.pyloriinfectionisfoundassociatedin90%ofduodenaland70%of
stomachulcercases.
Causes
Physiological
stress
Severe
trauma
Extensive
burns
Septicaemia
Local irritants
(e.g. alcohol)
Psychological
stress

23. -ThreedistinctcausesofPUDarerecognized:
-thebacteriumHelicobacterpylori
-(2)nonsteroidalanti-inflammatorydrugs(NSAIDs)suchasaspirin
-(3)hypersecretionofHCl
-Causes-Helicobacterpylorigastritis,NSAIDs-inducedmucosalinjury,Psychological
factors,Geneticfactors,etc.
•Symptoms–Burningstomachpain,Bloating,Intolerancetofattyfood,Heartburn,etc.
•Risks–Smoking,Alcoholconsumption,Consumingspicyfood,Stress,etc.
•Complications-
1. Haemorrhage
2. Perforation
3. Anaemia
4. Gastric outflow obstruction
5. Gastric cancer

24. •Tumors
A.Polyps
1.Hyperplastic(Inflammatory)Polyps
-regenerative,nonneoplasticlesionswhicharethemostcommontype
(90%).
-Oftenlocatedinthepyloricantrum.
2.HamartomatousPolyps
-nottrueneoplasmsbutaremalformations.
B.BenignTumor
1.Adenomas
-truebenignepithelialneoplasmsandaremuchrareinthestomach
thaninthelargeintestine.
2.StromalTumors
-Firm,circumscribednodules,thatappearassubmucosalnodules.

25. B.BenignTumor
GastricCarcinoma
-Carcinomaofthestomachisresponsiblemorethan90%ofallgastric
malignancies.
•Causes-H.pyloriinfection,Geneticfactors,Pre-malignantchangesin
thegastricmucosa,etc.
•Symptoms-Digestion,Heartburn,Stomachpain,Difficulty
swallowing,Vomiting,etc.
•Risks–GERD,Obesity,Smoking,Stomachpolyps,Familialhistory,H.
pyloriinfection,etc.
•Prevention–Stopsmoking,consumelotsoffruitsandvegetables,
reducetheamountofsaltyfood,etc.

26. •Classification:-
1.Earlygastriccarcinoma(EGC)
Types:
TypeI:Polypoidtype
TypeIIa:Superficialelevated
TypeIIb:Superficialflat
TypeIIc:Superficialdepressed
TypeIII:Ulceratedtype
2.Advancedgastriccarcinoma
Types:
i)Ulcerativecarcinoma
ii)Fungating(Polypoid)carcinoma
iii)Scirrhouscarcinoma
iv)Colloid(Mucoid)carcinoma
v)Ulcer-cancer

27. Diseases of Small Intestine
❖CongenitalAbnormality:
•Meckel’sDiverticulum
-Meckel’sdiverticulumisanoutpouchingcontainingallthelayersof
theintestinalwallintheirnormalorientation.
-Itismorecommoninmales.
-Causes–Itoccursasaresultofincompleteabsorptionofthevitelline
ductbythefoetusduringthe7
th
weekofpregnancy.
-Symptoms–GIbleeding,Abdominalpain,Obstructionofthe
bowels,diverticulitis(swellingoftheintestinalwall),etc.
•Othercongenitalconditions:
1.Intestinalatresia(congenitalabsenceofintestinallumen)
2.Intestinalstenosis(congenitalnarrowingoftheintestinallumen)
3.Intestinalmalrotation(failureofnormalrotationofmidgut)

28. •Hernia
-Protrusionofanorganorpartofanorganthroughaweakpointorapertureinthe
surroundingstructures.
-Externalhernia-protrusionofthebowelthroughadefectorweaknessintheperitoneum.
-Internalhernia-herniationthatdoesnotpresentontheexternalsurface
-Mostcommontype–Inguinalhernias;followedbyfemoralandumbilicalhernias.
Factors involved in
formation of Hernia
Increased intra-
abdominal pressure
Local weakness

29. -Inguinalherniasmaybeof2types:
➢Directwhenherniapassesmedialtotheinferiorepigastricarteryandit
appearsthroughtheexternalabdominalring.
➢Indirectwhenitfollowstheinguinalcanallateraltotheinferiorepigastric
artery.
-Strangulatedhernia-bloodflowinthehernialsacisobstructed;resultsin
infarctionorgangreneoftheaffectedloopofintestine.
•SitesofHernias:-
1.Inguinalhernia–Inguinalcanal;occursmorecommonlyinmales.
2.Femoralhernia-femoralcanalthroughwhichthefemoralarterypasses.
3.Umbilicalhernia–umbilicus,wheretheumbilicalbloodvesselsfromthe
placentaenterthefetusbeforebirth.
4.Incisionalhernia-repeatedstretchingoffibrous(scar)tissueformed
afterpreviousabdominalsurgery.
5.Hiatushernia-protrusionofapartofthefundusofthestomachthrough
theesophagealopeninginthediaphragm.(Types–Rolling&Sliding)
(Figures:A.Commonsitesofherniation.B.Strangulatedherniaformation.)

30. -Causes–Congenital,Aging,Damagefrominjury,Pregnancy,
Previoussurgery,Obesity,etc.
-Symptoms–BulgeorLumpintheaffectedarea(which
disappearsonlyingdown),Pain,Heartburn,Difficultyin
swallowing,Chestpain(incaseofHiatushernia),etc.
-Risks–Familyhistory,Pregnancy,Smoking,Prematurebirth,
Cysticfibrosis,etc.
Figure: Hiatus hernia

31. •InflammatoryBowelDisease(IBD)
-Thisisatermusedtodescribedisordersthatinvolve
chronicinflammationofthedigestivetract.
-Itbasicallyincludes2conditions:
1.Crohn’sdisease
2.Ulcerativecolitis
A.Crohn’sdisease
-Itischaracterizedbyinflammationoftheliningofthe
digestivetract,ofteninvolvingdeeperlayersofthe
digestivetract.
-Thereischronicpatchyinflammationwithoedema–
causingpartialobstructionofthelumen–skiplesions.
-Complications-Fistulaformation,Malabsorption,
Developmentofmalignancy,Bowelobstruction,etc.

32. B.Ulcerativecolitis
-Involvesinflammationandulcersalongtheliningofthecolonand
rectum.
-Ulcerativecolitisbeginsintherectum,andextendsupwardsintothe
sigmoidcolon,descendingcolon,transversecolon,andsometimes
mayinvolvetheentirecolon.
•Complications-Fulminantcolitis(Toxicmegacolon),Perforatedcolon,
Perianalfistula,Coloncancer,Severedehydration,etc.
•Symptomsforboth:
-Diarrhoea,Bloodinstools,Reducedappetite,Weightloss,etc.
•Risksforboth:
-Smoking,Familialhistory,ExcessiveuseofNSAIDs,etc.
•Causes–MostlyIdiopathic;maybeduetoimmunesystem
malfunction,hereditary,etc.

33. •EntericFever(Typhoid&Paratyphoid)
-Causativeagents–Salmonellatyphi(Typhoid)andS.paratyphiAorB
(Paratyphoid).
Typhoid:
-Theincubationperiodisabout10–14daysduringwhichtimebacteriainvade
thelymphoidtissueofthesmallintestine,especiallytheaggregatedlymph
follicles(Peyer’spatches).
-Thebacilliinvadethebloodstreamcausingbacteremia,andthe
characteristicclinicalfeaturesofthediseaselikecontinuousrisein
temperatureandrosespotsontheskinareobserved.
-Eventually,thebacilliarelocalizedintheintestinallymphoidtissue,inthe
mesentericlymphnodes,intheliver,inthegallbladder,andinthespleen.
Paratyphoid:
-Paratyphoidfeverfollowsasimilarcoursebutisusuallymilderandofshorter
durationalthoughtheonsetcanbemoresudden;complicationsareless
frequent.

34. -Causes–IngestionoffoodorwatercontaminatedwithSalmonella
typhiandS.paratyphiAorB.
-Modeofspread-Throughtyphoidcarriers,Fecal-oraltransmission
route.
-Symptoms–Highfever,Stomachpain,ConstipationorDiarrhoea,
Rashes,etc.
-Risks–Closecontactwithaninfectedperson,Drinkingcontaminated
water,Travellingtoaffectedareas,etc.
-Complications-Myocarditis,Endocarditis,Pneumonia,Pancreatitis,
etc.
-Prevention–Washinghandsproperly,Avoiddrinkinguntreated
water,Avoidrawfruitsandvegetables,Consumptionofhotfood,
Gettingvaccinated,etc.

35. •Dysentery
-Thetermreferstoaconditioninwhichdiarrhoeaisaccompaniedwithabdominalcramps
andpassageofmucusinthestools.
-Types:
1.Bacillarydysentery
2.Amoebicdysentery
A.Bacillarydysentery
-Causativeagent-Shigellaspecies
-Vector-commonhousefly
-InfectioncausedbyShigellaspecies:S.dysenteriae,S.flexneri,S.boydiiandS.sonnei.
-Superficialtransverseulcerationsofmucosaofthebowelwalloccurintheregionof
lymphoidfollicles.
-Themucosaoverlyingthelymphoidfolliclesbecomenecrosedandthesurrounding
mucosashowscongestionandoedema.
Shigella dysenteriae

36. -Complications-Thecomplicationsofbacillarydysenteryarehaemorrhage,perforation,
stenosis.
B.Amoebicdysentery
-Causativeagent-Entamoebahistolytica
-Vector-commonhousefly,rodents,cockroaches
-Thediseaseprimarilyaffectsthelargeintestine.
-Infectionoccursfromingestionofcystformoftheparasite.
-Thecystwallisdissolvedinthesmallintestinefromwheretheliberatedamoebaepass
intothelargeintestine.
-Here,theyinvadetheepitheliumofthemucosa,reachthesubmucosaandproducethe
characteristicflask-shapedulcers.
-Complications-amoebicliverabscess,amoebichepatitis,perforation,haemorrhage.
Entamoeba histolytica

37. -Symptoms–Loosewaterstools,Bloodinstools,Fever,Mucusin
stools,Bloating,etc.
-Risks–Contaminatedfood,Poorhandwashing,Swimmingin
contaminatedwater-lakes,etc.
-Complications–Excessivethirst,Drymouth,Darkcoloured
urine,etc.
-Prevention–Washhandsfrequentlyandproperly,Usehand
sanitizer,etc.

38. Diseases of Large Intestine
•Appendicitis
-Itreferstoacuteinflammationoftheappendix(anarrow,worm-likepouchat
somedistanceawayfromthejunctionofileum–caecumi.e.ileocecal
junction).
-Adietwithlowbulkorcelluloseandhighproteinintakemoreoftencauses
appendicitis.
-Itcausesintensepaininthelowerrightabdomen.
-Itiscommonispeoplebetween10-30yearsofage.
-Causes–Blockageintheliningofappendix,Obstructive(Faecolith,Calculi,
Tumor,etc.),Lowbulkorcelluloseandhighproteinintakediet,Bacterial
infections,etc.
-Symptoms–Suddenpainintherightsideofthelowerabdomen,Nausea
andVomiting,Lossofappetite,ConstipationorDiarrhoea,Bloating,
Flatulence,etc.
-Complications–Rupturedappendix,Appendixabscess,Mucocele,etc.

39. •Hemorrhoids (Piles)
-These are varicosities of the hemorrhoidal veins in the anus and lower rectum.
-Internal piles -dilatation of superior hemorrhoidal plexus covered over by mucous
membrane; inside the rectum.
-External piles -involve inferior hemorrhoidal plexus; under the skin around the anus.
-Causes -Portal hypertension, Chronic constipation and straining at stool, Cardiac failure,
Venous stasis of pregnancy, Hereditary predisposition, Tumors of the rectum, Eating low
fiber diet, etc.
-Symptoms:
➢External hemorrhoids –Itching or irritation in anal region, Bleeding, Swelling around
anus, Pain, etc.
➢Internal hemorrhoids –Painless bleeding during bowel moment, Pain, Irritation, etc.
➢Thrombosed hemorrhoids –Severe pain, Swelling, Inflammation, Hard lump in anus,
etc.

40. -Risks–Aging,Pregnancy,etc.
-Complications–Anemia,Strangulatedhemorrhoid,
Bloodclot,etc.
-Prevention–Eathighfiberfoods,Drinkplentyof
fluids,Exercise,Avoidlongperiodsofsitting,etc.

41. Diseases of Liver
•Jaundice
-Itreferstotheyellowpigmentationoftheskinorscleraeoftheeyebybilirubin.
-BilirubinisderivedfromdegradationofhemoglobinfromthewornoutRBCs.
-Jaundiceistheresultofelevatedlevelsofbilirubininthebloodtermed
hyperbilirubinaemia(serumbilirubinexceeds2mg/dl).
-Types:
1.Pre-hepaticjaundice
-Occursasaresultofincreasedhemolysisofredbloodcellsthatresultsinproductionof
excessbilirubin.
-Becausetheexcessbilirubinisunconjugated(unconjugatedbilirubinisfatsoluble)it
cannotbeexcretedintheurine,whichthereforeremainsnormalincolour.
-Neonatalhaemolyticjaundice-highrateofhemolysiscoupledwithashortageof
conjugatingenzymesinthehepatocytesofthestillimmatureliverintheneonates.

42. 2.Intra-hepaticjaundice
-Thisistheresultofdamagetotheliveritselfby:Viralhepatitis,Toxic
substances,suchasdrugs,Amoebiasis,Cirrhosis,etc.
-Excessbilirubinaccumulatesintheliver.
-Becauseitismainlyintheconjugatedform,itiswater-solubleandexcretedin
theurinemakingurinedarkincolour.
3.Post-hepaticjaundice
-Causesofobstructiontotheflowofbileinthebiliarytractinclude:Gallstonesin
thecommonbileduct,Tumoroftheheadofthepancreas,Fibrosisofthebile
ducts,followingcholangitisorinjurybythepassageofgallstones.
-Inthissituationexcessbilirubinisalsoconjugatedandisthereforeexcretedin
theurine.
-Theeffectsofraisedserumbilirubininclude:Pruritus(itching),Palefecesdueto
absenceofstercobilin,Darkurineduetothepresenceofincreasedamountsof
bilirubin.

43. -Causes–Highrateofsynthesisofbilirubin,gallstones,Liver
damage,Alcoholism,etc.
-Symptoms–Fever,Chills,Abdominalpain.Darkcolouredurine,
Yellowingofskin,etc.
-Complications–Bloating,Stomachpain,Diarrhoea,Vomiting,
etc.
-Prevention–Avoidalcoholconsumption,Maintainhealthy
weight,Managecholesterollevels,etc.
-Risks-Liverinfectionslikehepatitis,cirrhosis,etc.

44. •Gilbert’sSyndrome
-Itisafamilial,genetically-determined,autosomaldiseaseoftheliver.
-Itischaracterisedbymild,benign,unconjugatedhyperbilirubinaemiawhichisnotdue
tohaemolysis.
-Itmaybeduetoreducedconjugationofbilirubinorimpairedhepaticuptakeof
bilirubin.
-Causes–Geneticallyinheriteddiseaseduetoanabnormalgene.
-Symptoms–Occasionalyellowingtingeoftheskinandwhitesoftheeyesdueto
slightlyelevatedlevelsofbilirubinasseeninJaundice,
-Risks–Gender(Malesareatahighrisk),Boththeparentscarrytheabnormalgene
forthedisorder.
-Complications–Lowlevelsoftheenzyme(UDP-glucuronosyltransferase)causing
Gilbert’ssyndromemayincreasethesideeffectsofotherdrugs(likeIrinotecan,etc.)
thataremetabolizedbythesameenzyme.

45. •Hepatic failure
-May develop from severe acute liver injury with massive necrosis of liver cells (acute
hepatic failure), or from advanced chronic liver disease (chronic hepatic failure).
-It occurs when liver function is markedly impaired.
-Liver failure has serious effects on other parts of the body.
-Manifestations:
1.Jaundice
2.Hepatic encephalopathy (Hepatic coma)
3.Hyperkinetic circulation
4.Hepatorenal syndrome
5.Hepatopulmonary syndrome
6.Oedema and ascites
7.Jaundice
8.Endocrine changes

46. -Causes–Certainmedicines(likeParacetamol),Viralhepatitis,Toxins,Certain
autoimmunedisease,etc.
-Symptoms–Lossofappetite,Jaundice,weightloss,bruisingorbleeding,
Itching,Edema,Ascites,etc.
-Complications–Cerebraledema,Bleedingdisorders,infections,Kidney
failure,etc.
-Prevention–GetvaccinatedforHBV,HAV,avoidalcoholconsumption,etc.

47. •ViralHepatitis
-Itreferstotheinfectionandinflammationoftheliverbyhepatotropic
viruses.
-Currentlythereare5mainvarietiesofthesevirusescausingdistinct
typesofviralhepatitis:
➢HepatitisAvirus(HAV)-causingafaecally-spreadself-limitingdisease.
➢HepatitisBvirus(HBV)-causingaparenterallytransmitteddisease
thatmaybecomechronic.
➢HepatitisCvirus(HCV)-involvedchieflyintransfusion-related
hepatitis.
➢Hepatitisdeltavirus(HDV)-associatedassuperinfectionwithhepatitis
Binfection.
➢HepatitisEvirus(HEV)-causingwater-borneinfection.
-OnlyHBVisaDNAvirus,allotherhumanhepatitisvirusesareRNA
viruses.

48. HepatitisA
-Itaffectsmainlychildren,causingamildillnessalthoughitisoften
asymptomatic.
-Infectionisspreadbythefecal–oralroute,e.g.viacontaminatedhands,
food,waterandfomites.
-HepatitisAisusuallyabenign,self-limitingdiseaseandhasanincubation
periodof15-45days.
-Mostfrequentlyaffectedagegroupis5-14years;adultsareofteninfectedby
spreadfromchildren.
-Serologicandviralmarkers:IgManti-HAVantibody,IgGanti-HAVantibody.
-Causes–InfectionfromHepatitisAvirus.
-Symptoms–Vomiting,Low-gradefever,Clay-colouredbowelmovement,
Darkurine,Yellowingofeyes,Intenseitching,etc.
-Risks–HIVpositive,Clottingfactordisorders,Physicalcontactwithinfected
person,etc.
-Complications–Lossofliverfunction,etc.
-Prevention–HepatitisAVaccine. Fig: Structure of hepatitis A virus

49. HepatitisB(serumhepatitis)
-Itistransmittedparenterally,suchasinrecipientsofbloodandbloodproducts,patients
treatedbyrenaldialysisandhospitalworkersexposedtoblood.
-Thevirushasalongerincubationperiod-30-180days.
-Theinfectioncausesmoresevereformofillnessthatincludes:acutehepatitisB,chronic
hepatitis,progressiontocirrhosis.
-Itleadstothedevelopmentofhepatocellularcarcinoma.
-Serologicandviralmarkers:
HBsAg
Anti-HBs
HBeAg
Anti-Hbe
HBcAg
Anti-HBc
HBV-DNA

50. -Causes–InfectionfromHepatitisBvirus.
-Symptoms–Abdominalpain,Darkurine,Fever,Lossofappetite,Weakness,Jaundice,etc.
-Risks–Unprotectedsexwithinfectedperson,Sharingofneedles,Infantborntoan
infectedmother,etc.
-Complications–Cirrhosis,Livercancer,Liverfailure,etc.
-Prevention–HepatitisBvaccine.
Fig: Structure of hepatitis B virus

51. HepatitisC
-Thisdiseaseisacquiredbybloodtransfusions,bloodproducts,
hemodialysis,parenteraldrugabuseandaccidentalcutsandneedle-pricks
inhealthworkers.
-AcuteHCVhepatitisismilderthanHBVhepatitisbutHCVhasahigherrate
ofprogressiontochronichepatitisthanHBV.
-Theinfectionisasymptomaticandinfectionisusuallydiagnosedlaterinlife
whencirrhosisorchronicliverfailurebecomesevident.
-Currently,HCVisconsideredmoreimportantcauseofchronicliverdisease
worldwidethanHBV.
-Serologicandviralmarkers:Anti-HCVantibodies,HCV-RNA.
-Causes–Infection from Hepatitis C virus.
-Symptoms–Dark urine, Fluid buildup in abdomen, Swelling of legs,
Bruising and bleeding easily, Jaundice, Poor appetite, etc.
-Risks–HIV, Piercing or tattoo, Infant born to an infected mother, etc.
-Complications–Cirrhosis, Liver cancre, Liver failure, etc.
-Prevention–Practice safe sex, Hepatitis C vaccine. Fig: Structure of hepatitis C virus

52. HepatitisD
-HDVisadefectivevirusforwhichHBVisthehelper;hepatitisDdevelops
whenthereisconcomitanthepatitisBinfection.
-Co-infection–HDVinfectionandhepatitisBoccursimultaneously.
-Superinfection–HDVinfectsachronicHBsAgcarrier.
-Serologicandviralmarkers:HDVidentificationinthebloodandinthe
livercell,HDAg,Anti-HDantibody.
-Causes–InfectionfromHepatitisDvirus
-Symptoms–Abdominalpain,Lossofappetite,Vomiting,Darkurine,
Fatigue,etc.
-Risks–Unprotectedsex,Infantborntoaninfectedmother,HVBinfected
individuals,etc.
-Complications–Cirrhosis,Livercancer,Liverdiseases,etc.
-Prevention–Getvaccinated,Practicesafesex,CautiousaboutPiercingor
tattoo,etc.
Fig: Structure of hepatitis D virus

53. Diseases of the Biliary Tract
•Gallstones(Cholelithiasis)
-Gallstonesconsistofdepositsoftheconstituentsofbile,most
commonlycholesterol.
-Manysmallstonesoroneormorelargestonesmayformbutthey
donotnecessarilyproducesymptoms.
-TypesofGallstones:
a.Puregallstones–Purecholesterolgallstones,Purepigment
gallstones,Purecalciumcarbonategallstones.
b.Mixedgallstones–containmorethan50%cholesterol
monohydrateplusanadmixtureofcalciumsalts,bilepigments
andfattyacids.
c.Combinedgallstones–hasapuregallstonenucleusandouter
shellofmixedgallstone;oramixedgallstonenucleuswithpure
gallstoneshell.

54. -Causes–Toomuchcholesterolinbile,Toomuchbilirubininbile,
obstructionofbileduct,etc.
-Symptoms–Suddenandrapidlyintensifyingpaininupperright
portionoftheabdomen,Paininrightshoulder,Backpainbetween
shoulderblades,etc.
-Risks–Gender(Femalesaremoreprone),Ageabove40,Lowfiber
diet,Familialhistory,Diabetes,Liverdisease,etc.
-Complications–Cholecystitis,Blockageofcommonbileduct,
Blockageofpancreaticduct,Gallbladdercancer,etc.
-Prevention–Don’tskipmeals,Consumehighfiberfood,etc.
Fig: Effects of gallstones in different locations

55. •Cholecystitis
-ThisisusuallyaccompaniedwithGallstones.
A.Acutecholecystitis
-Inthisthereisacuteinflammationofthegallbladderthatoccurswhenagallstone
becomesstuckinthecysticduct.
-Itdoesnotcausejaundicebecausebilefromthelivercanstillpassdirectlyintothe
duodenum.
-Itmaybecomplicatedbybacterialinfectionanddistensionofthegallbladder,which
carriestheriskofperforationandperitonitis.
B.Chroniccholecystitis
-Chroniccholecystitisisthecommonesttypeofclinicalgallbladderdisease.
-Theonsetisusuallyinsidious,sometimesfollowingrepeatedacuteattacks.
-Gallstonesarepresentandtheremaybeaccompanyingbiliarycolic.
-Thisconditionisassociatedwithcancerofthegallbladder.

56. -Causes–Gallstones,Tumor,Bileductblockage,Infection,etc.
-Symptoms–Severepaininupperrightabdomen,Tenderness
inabdomen,Vomiting,Fever,etc.
-Risks–Gallstones
-Complications–Infectionwithingallbladder,Necrosisor
gallbladder,etc.
-Prevention–Healthydiet,Maintainahealthywait,etc.

57. Diseases of Pancreas
•Pancreatitis
-Pancreatitisisinflammationofthepancreas.
-Proteolyticenzymesproducedbythepancreasaresecretedininactiveforms,
whicharenotactivateduntiltheyreachtheintestine–thisprotectsthe
pancreasfromdigestionbyitsownenzymes.
-Iftheseprecursorenzymesareactivatedwhilestillinthepancreas,pancreatitis
results.
A.Acutepancreatitis
-Theonsetissuddenandlastsforafewdays.
-Theseverityofthediseaseisdependentontheamountofpancreatictissue
involved.
-Theconditionoccursinadultsbetweentheageof40and70yearsandis
commonerinfemalesthaninmales.
-Thereiselevationofserumamylaselevelwithinthefirst24hoursandelevated
serumlipase(specificforpancreaticdisease)levelafter3to4days.

58. B.Chronicpancreatitis
-Theconditioniseitherduetorepeatedattacksofacutepancreatitis
ormayarisegraduallywithoutevidenceofpancreaticdisease.
-Itismorecommoninmen-associatedwithfibrosisanddistortionof
themainpancreaticduct.
-Proteinmaterialsecretedbytheacinarcellsblocksthetinyacinar
ducts.
-Thiseventuallyleadstotheformationofencapsulatedcysts,which
areafeatureofacuteandchronicpancreatitis.
-Causes–Infectionofpancreas,Injurytotheabdomen,Obesity,
Pancreaticcancer,Gallstones,Alcoholconsumption,etc.
-Symptoms–Upperabdominalpain,Rapidpulse,Tendernessinthe
abdomen,Abdominalpainthatworsensaftereating,etc.
-Risks–Excessivealcoholconsumption,Obesity,Familyhistoryof
pancreatitis,Smoking,etc.
-Complications–Pseudocyst,Kidneyfailure,Diabetes,Malnutrition,
Pancreaticcancer,etc.

59. References:-
1.Harsh Mohan, Textbook of Pathology,
Published by Jaypee Brothers Medical
Publishers Pvt. Ltd. , New Delhi, 7
th
Edition.
2.Ross and Wilson, Anatomy & Physiology
in Health and Illness by Anne Waugh and
Allison Grant Published by Churchill
Livingstone, 12
th
Edition.
3.Gerard J. Tortora & Bryan Derrickson,
Principles of Anatomy & Physiology,
Published by John Wiley and Sons, Inc.,
14th Edition.
4.www.mayoclinic.org
5.www.healthline.com
6.https://my.clevelandclinic.org