2. Mucous: Mucus, Pepsinogen IiChief: Pepsinogen I, IiParietal:
AcidEnteroendocrine: Histamine, Somatostatin,Endothelin 3.
StomachCondition CommentPyloric stenosis 1 in 300 to 900 live
births Male to female ratio 3:1 Pathology: muscular hypertrophy of
pyloric smooth muscle wall Symptoms: persistent, nonbilious
projectile vomiting in young infantDiaphragmatic hernia Rare
Pathology: herniation of stomach and other abdominal contents into
thorax through a diaphragmatic defect Symptoms: acute respiratory
embarrassment in newbornGastric heterotopiaUncommon Pathology: a
nidus of gastric mucosa in the esophagus or small intestine
("ectopic rest") (The Latin word for "nest) Symptoms: asymptomatic,
or an anomalous peptic ulcer in adult 4. Gastric heterotopia 6 5.
Inkeepingwiththelimitedsensoryapparatusofthe
alimentarytract,gastricdisordersgiveriseto
symptomssimilartoesophagealdisorders,primarily heartburnandvague
epigastric pain.Gastricmucosaandbleeding,hematemesisor
melenamayensue.Unlikeesophagealbleeding,however,bloodquickly
congealsandturnsbrownintheacidenvironment
ofthestomachlumen.Vomitedbloodhencehastheappearanceofcoffee
grounds. 6. Gastritis:includesamyriadofdisordersthatinvolve
inflammatorychangesinthegastricmucosa,including:Gastritis: is
simply defined as inflammation of the gastricmucosa. By far the
majority of cases are chronicgastritis, but occasionally, distinct
forms of acutegastritis areencountered.1. Erosive
gastritiscausedbyanoxiousirritant2. Reflux
gastritisfromexposuretobileandpancreatic fluids3. Hemorrhagic
gastritis4. Infectious gastritis5. Gastric mucosal atrophy 7. Acute
Gastritis Acute gastritis is an acute mucosal inflammatoryprocess,
usually of a transient nature. Theinflammation may be accompanied
by hemorrhage intothe mucosa and, in more severe circumstances,
bysloughing of the superficial mucosal
epithelium(erosion).Pathogenesis: The pathogenesis is poorly
understood, inpart because normal mechanisms for gastric
mucosalprotection are not totally clear. 8. H pylori (most common
cause of ulceration) NSAIDs, aspirin Gastrinoma (Zollinger-Ellison
syndrome) Severe stress (eg, trauma, burns), Curling ulcers Alcohol
Bile reflux Pancreatic enzyme reflux Radiation Staphylococcus
aureus exotoxin Bacterial or viral infection 9. 11 10. Suicide
attempts with acids and alkali Mechanical trauma (e.g., nasogastric
intubation)
Oneormoreofthefollowinginfluencesarethoughttobeoperativeinthesevariedsettings:
disruptionoftheadherentmucouslayer,
stimulationofacidsecretionwithhydrogenionback-diffusionintothesuperficialepithelium,
decreasedproductionofbicarbonatebufferbysuperficial
epithelialcells, reducedmucosalbloodflow,anddirectdamagetothe
epithelium. 11. 13 12. There is a spectrum of severity ranging
fromextremely localized (as occurs in NSAID-inducedinjury)todiffuse
andfromsuperficialinflammationtoinvolvement of the entire mucosal
thickness withhemorrhage and focal erosions.
Concurrenterosionandhemorrhageisreadilyvisibleby endoscopy and is
termed acute erosivegastritis. 14 13.
MORPHOLOGYAllvariantsaremarkedby:MucosaledemaInflammatoryinfiltrateof
neutrophilsandpossiblyby chronic inflammatory
cells.Regenerativereplicationof epithelialcellsinthegastricpitsis
usually prominent.Providedthatthenoxiouseventis
shortlived,acutegastritismay disappearwithindayswith
completerestitutionofthenormal mucosa. 14.
Freepowerpointtemplate:www.brainybetty.com 16 15. Histopathology
usually demonstratesincreased numbers of eosinophils17 16.
Dependingontheseverityoftheanatomicchanges,acutegastritismaybeentirelyasymptomatic,
Epigastric to left upper quadrant Frequently described as burning
May radiate to the back Usually occurs 1-5 hours after meals May be
relieved by food, antacids (duodenal), or vomiting(gastric)
Typically follows a daily pattern specific to patient
vomiting,ormaypresentasoverthematemesis,melena,andpotentiallyfatalbloodloss.
17.
Often,adiagnosiscanbemadebasedonthepatientsdescriptionofhisorhersymptoms,butothermethodsmaybeusedtoverify:
Blood tests: Bloodcellcount PresenceofH. pylori Pregnancy
Liver,kidney,gallbladder,orpancreasfunctions Urinalysis
Stoolsample,tolookforbloodinthestool X-rays
Endoscopy,tocheckforstomachlininginflammationandmucouserosion
Stomachbiopsy,totestforgastritisandotherconditions 19 18.
Malignancy Hemorrhage Perforation Obstruction 19. Chronic Gastritis
is defined as the presence of chronic mucosal inflammatory changes
leading eventually to mucosal atrophy and epithelial metaplasia. In
the western world, the prevalence of histologic changes indicative
of chronic gastritis exceeds 50% in thelaterdecadesofadultlife. 20.
Schematic presentation of the presumed action of H. pylori in
thedevelopment of chronic gastritis and peptic ulceration. The
histologicfeatures of the two disease conditions are depicted 21.
Aautoimmune Bbacterial(helicobacter) C-chemical Autoimmune chronic
gastritisAutoantibodiestogastricparietalcellsHypochlorhydria/achlorhydriaLossofgastricintrinsicfactorleadstomalabsorptionofvitaminB12withmacrocytic,megaloblasticanaemia
22. Commonlyseenwithbilereflux(toxictocells)
Prominenthyperplasticresponse(inflammatorycellsscanty) 23.
Commoninfection10%ofmen,4%womendevelopPUD*1stPartofduodenum>antrum>G-Ejunction.H.pylorirelateddisorders:
Chronicgastritis90% Pepticulcerdisease95-100% Gastriccarcinoma70%
Gastriclymphoma RefluxOesophagitis. Nonulcerdyspepsia 24.
ThemostimportantetiologicassociationischronicinfectionbythebacillusHelicobacter
pylori . Thisorganismisaworldwidepathogen.
Prevalenceofinfectionamongadultsmaybereachedto80%
itseemstobeacquiredinchildhoodandpersistsfordecades.
Mostindividualswiththeinfectionalsohavetheassociatedgastritisbutareasymptomatic.
25. H. pylori
isanoninvasive,non-spore-forming,S-shapedgram-negativerodmeasuringapproximately3.50.5m.
Causescelldamageandinflammatorycellinfiltration
Inmostcountriesthemajorityofadultsareinfected 26.
Pepticulcerdisease(Helicobacter) Adenocarcinoma(alltypes) 27.
Histological F. Regardless of the cause orhistological distribution
of chronicgastritis, theinflammatorychangesconsistofalymphocytic
and plasma
cellinfiltrateinthelaminapropria,occasionallyaccompaniedbyneutrophilicinflammationoftheneckregionofthemucosalpits.
A Steinersilverstain Theinflammationmaybe demonstrates the numerous
darkly stained H. pylori organisms
alongaccompaniedbyvariableglandlossthe luminal surface of the
gastricandmucosalatrophy.epithelial cells. Note that there is no
tissue invasion by bacteria. 28. In the autoimmune variant, loss of
parietal cells isparticularlyprominent. Intestinal
metaplasiareferstothereplacementofgastricepithelium with columnar
and goblet cells of intestinalvariety.
Gastrointestinal-typecarcinomasappeartoarisefromdysplasiaofthismetaplasticepithelium.
Second, H. pylori-inducedproliferationoflymphoid
tissuewithinthegastricmucosahasbeenimplicatedasaprecursorofgastriclymphomaFreepowerpointtemplate:www.brainybetty.com
30 29. Chronicinflammatorycell
infiltrationMucosalatrophyIntestinal(gobletcell)metaplasia Seen in
Helicobacter and autoimmune gastritis (not chemical) 30. Chronic
gastritis with lymphoid follicle formation in the gastric
mucosa(arrow)Some gastric glands are still found (arrowhead). 32
31. Chronic gastritis with chronic inflammatory cell infiltration
and lymphoidfollicle formation (arrowhead) in the gastric
mucosa.Atrophy of the gastric glands is seen.(arrow). (M: mucosa,
and SM:submucosa) 33 32. Clinical
FeaturesChronicgastritisusuallycausesfewornosymptoms;upperabdominaldiscomfort,nauseaandvomiting.
Hypochlorhydria or achlorhydria (referring to levels
ofgastricluminalhydrochloricacid)Hypergastrinemiaarecharacteristicallypresent.Most
important is the relationship of chronic gastritis to
thedevelopmentofpeptic ulcer and gastric carcinoma. 33. Normal
Acutegastritis
AtrophicgastritisChronicgastritisIntestinalDysplasiaCancermetaplasia
34. GASTRIC ULCERATION Ulcers are defined as a breach in the mucosa
of the alimentary tract that extends through the muscularis
mucosaintothesubmucosaordeeper. This is to be contrasted to
erosions, in which there is abreachintheepitheliumofthemucosaonly.
Erosions may heal within days, whereas healing of
ulcerstakesmuchlonger.
Althoughulcersmayoccuranywhereinthealimentarytract,noneareasprevalentasthepepticulcersthatoccurintheduodenumandstomach.
35. Focal, acutely developing gastric mucosal defects mayappear
after severe stress and are designated stressulcers. Generally,
there are multiple lesions located mainly in
thestomachandoccasionallyintheduodenum
Severetrauma,includingmajorsurgicalprocedures,sepsis,orgraveillnessofanytype
Extensive burns (the ulcers are then referred to asCurlingulcers)
Traumaticorsurgicalinjurytothecentralnervoussystemor an
intracerebral hemorrhage (the ulcers are thencalledCushingulcers)
Chronic exposure to gastric irritant drugs,
particularlyNSAIDsandcorticosteroids 36. Neurogenic or
catecholamine-induced vasoconstrictionMucosal ischemiaDamage the
mucosalDirectly injure mucosal cells bybarrier oxygen or metabolic
deprivation 37. Free powerpoint template: www.brainybetty.com40 38.
MORPHOLOGY Acute stress ulcers are usually circularand small (less
than 1 cm in diameter). The ulcer base is frequently stained adark
brown by the acid digestion ofextruded blood. They may occur
singly, but more oftenthey are multiple, located throughoutthe
stomach and duodenum Multiple stress ulcers of the Microscopically,
acute stress ulcers are stomach, highlighted by theabrupt lesions,
with essentially dark digested blood in theirunremarkable adjacent
mucosa.bases. 39. Anulcerisdistinguishedfromanerosionbyits
penetrationthroughthemuscularismucosaorthe
muscularcoatingofthegastricorduodenalwalloccurring asaresultofacid
and pepsin attackThelesionofpepticulcerdisease(PUD)isadisruption
inthemucosallayerofSites:Duodenum(DU)Stomach(GU)OesophagusGastro-enterostomystomaRelatedtoectopicgastricmucosa(e.g.inMeckelsdiverticulum)
40. Etiology of PUDNormalIncreased AttackHyperacidity,
ZollingerEllison syndrome.Weak defenseStress, drugs,
smokingHelicobacter pylori* 41.
Pepticulcerdiseaseresultsfromtheimbalancebetweendefensivefactorsthatprotectthemucosaandoffensivefactorsthatdisruptthisimportantbarrier.
Mucosalprotectivefactorsincludethewater-insolublemucousgellayer,localproductionofbicarbonate,regulationofgastricacidsecretion,andadequatemucosalbloodflow.
Aggressivefactorsincludetheacid-pepsinenvironment,infectionwithHelicobacter
pylori,andmucosalischemia Free powerpoint
template:www.brainybetty.com44 42.
Pepticulcersareremitting,relapsinglesionsthataremost
oftendiagnosedinmiddle-agedtoolderadults,butthey
mayfirstbecomeevidentinyoungadultlife.Theyoftenappearwithoutobviousprecipitatinginfluences
and may then heal after a period of weeks to months of
activedisease.Even with healing, however, the propensity to develop
pepticulcersremains.Genetic or racial influences appear to play
little or no role in the causation of peptic ulcers. Duodenal
ulcers are more frequent in patients with alcoholiccirrhosis,
chronic obstructive pulmonary disease, chronic
renalfailure,andhyperparathyroidism. 43. Pathogenesis
Therearetwokeyfacts. First, the fundamental requisite for peptic
ulceration ismucosalexposuretogastricacidandpepsin. Second, there
is a very strong causal association with H.pylori infection.
Despite the clarity of these two statements, the
actualpathogenesisofmucosalulcerationremainsmurky. 44. The array of
host mechanisms that prevent the
gastricmucosafrombeingdigestedlikeapieceofmeatincludethefollowing:
Secretion of mucus by surface epithelial cells Secretion of
bicarbonate into the surface mucus, to create abuffered surface
microenvironment Secretion of acid- and pepsin-containing fluid
from the gastric pitsas "jets" through the surface mucus layer,
entering the lumendirectly without contacting surface epithelial
cells Rapidgastricepithelialregeneration
Robustmucosalbloodflow,tosweepawayhydrogenionsthathave
back-diffused into the mucosa from the lumen and
tosustainthehighcellularmetabolicandregenerativeactivity Mucosal
elaboration of prostaglandins, which help maintainmucosalbloodflow.
45. Amongthe"aggressiveforces,"H. pyloriisvery
important,becausethisinfectionispresentin70%to
90%ofpatientswithduodenalulcersandinabout70%
ofthosewithgastriculcers.Thepossiblemechanismsareasfollows:
AlthoughH. pyloridontinvadethetissues,itinduces
anintenseinflammatoryandimmuneresponse. 46. Bacteria overepithelial
cells 47. H. pylori secretes a urease that breaks down urea
toformtoxiccompoundssuchasammoniumchlorideandmonochloramine.The
organisms also elaborate phospholipases that
damagesurfaceepithelialcells.Bacterial proteases and phospholipases
break down the glycoprotein-lipid complexes in the gastric mucus,
thusweakeningthefirstlineofmucosaldefense.Epithelial injury is also
caused by a vacuolating toxin(VacA). Another toxin encoded by the
cytotoxin-associatedgeneA(CagA)isapowerfulstimulusfortheproductionofIL-8bytheepithelialcells.
48. H. pylori enhances gastric acid secretion and impairsduodenal
bicarbonate production, thus reducingluminalpHintheduodenum.
TheBlymphocytesaggregatetoformfollicles.
TheroleofTandBcellsincausingepithelialinjuryisnotestablished, but
T-cell-driven activation of B cells may be
involvedinthepathogenesisofgastriclymphomas. 49.
Gramnegative,Spirochete. Doesnotinvadecells
ColonizeGastricmucosaonly* CommoncauseofDuodenalulcer*?
UreaseBreakdownureaammoniahighpHreflexacidprod
ProteaseBreakdownmucosaexposeepitheliumfordigestion.
Chronicinfl.GastricMetaplasiaUlceration.
Complications:Bleeding,perforation,stenosis,Carcinoma. 50. NSAIDs
are the major cause of peptic ulcer disease in patients who donot
have H. pylori infection. The gastroduodenal effects of NSAIDs
range from acuteerosive gastritis and acute gastric ulceration to
pepticulceration in 1% to 3% of users. Thus, those who take these
drugs for chronic rheumaticconditions are at particularly high
risk. 51. Inhibition of prostaglandin synthesis increases secretion
ofhydrochloric acid and reduces bicarbonate and mucinproduction.
Loss of mucin degrades the mucosal barrier that normallyprevents
acid from reaching the epithelium. Some NSAIDs can penetrate the
gut mucosal cells as well. By mechanisms not clear some NSAIDs also
impair angiogenesis, thus impeding the healing of ulcers. 52.
Allpepticulcers,whethergastric or duodenal, havean
identicalgrossandmicroscopicappearance.1. defects in the mucosa
that penetrate at least into the submucosa, and often into the
muscularis propria or deeper.2. Most are round, sharply punched-out
craters 2 to 4 cm in diameter.3. Those in the duodenum tend to be
smaller, and occasional gastriclesionsaresignificantlylarger.4.
Favoredsitesaretheanteriorandposteriorwallsofthefirst portion of
the duodenum and the lesser curvature of the stomach. 53. 5. The
base of the crater appears remarkably clean, owing topeptic
digestion of the inflammatory exudate and necrotictissue.6.
Infrequently, an eroded arteryis visible in the ulcer
(usuallyassociatedwithahistoryofsignificantbleeding).7.Iftheulcercraterpenetratesthroughtheduodenalorgastricwall,
a localized or generalized peritonitis may develop andadjacent
structure such as adherent omentum, liver, orpancreascouldbeaffect.
54. Histologic Appearanceo The histologicappearance
varieswiththeactivity,chronicity,anddegreeofhealing.o
Inachronic,openulcer,fourzonescanbedistinguished:o (1)
thebaseandmarginshaveathinlayerofnecroticfibrinoiddebriso (2)
azoneofactivenonspecificinflammatoryinfiltrationwithneutrophilspredominating,o
(3) granulationtissue,deeptowhichis--------------------------o (4)
fibrous,collagenousscarthatfansoutwidelyfromthemarginsoftheulcer. o
Vessels trapped within the scarred area are characteristically
thickened and occasionally thrombosed, but in some instances they
are widely patent. o With healing, the crater fills with
granulation tissue, followed by re- epithelialization from the
margins and more or less restoration of the normal architecture
(hence the prolonged healing times). o Extensive fibrous scarring
remains. 55. FIgure 2).( Four zones of active peptic ulcer. The
necrotic fibrinoid debris and nonspecific inflammatory infiltrate
are labeled by arrowhead. Figure 3). Necrotic fibrinoid debris
Beneath the necrotic and inflammatory zones, and inflammatory
infiltrate in thethere is granulation tissue (arrow). Below the
granulation tissue, fibrotic tissue is ulcer base.seen (F). 56.
Figure 4). Granulation tissue in the ulcerbase. New blood vessels
lined by plump(Figure 5). Fibrotic tissue beneathendothelial cells
(arrow). Edema and the ulcer baseinflammatory infiltrate are also
seen. 57. (Figure 7) Chronic gastritis with (Figure 8) Intestinal
metaplasia in chronicintestinal metaplasia (arrow) seen in
gastritis. The gastric foveolar epitheliumthe mucosa around the
peptic ulcer. (arrowhead) is replaced by intestinal typeThe
mucinous gastric foveolar of epithelium (arrow). The
intestinalepithelium (arrowhead) is replacedepithelium has goblet
cells. Chronicby intestinal type of epitheliuminflammatory cell
infiltration is also 58. Most peptic ulcers cause epigastric
gnawing, burning, or boring pain but a significant minority first
come to light with complications such as hemorrhage or perforation.
The pain tends to be worse at night and occurs usually1 to 3 hours
after meals during the day. Classically, the pain is relieved by
alkalis or food, butthere are many exceptions. Nausea, vomiting,
bloating, belching, and significantweight loss (raising the specter
of some hiddenmalignancy) are additional manifestations. Bleeding
is the chief complication, occurring in up toone third of patients,
and may be life-threatening. 59.
PainordiscomfortAfeelingoffullness--peoplewithseveredyspepsia
areunabletodrinkasmuchfluidaspeoplewithmildor
nodyspepsiaHungerandanemptyfeelinginthestomach,often1-
3hoursafteramealMildnausea(vomitingmayrelievesymptoms)Regurgitation(sensationofacidbackingupintothe
throat)Occasionally,symptomsofGERDarepresentObstruction of the
pyloric channel is rare.67 60.
Diagramofaggravatingcausesof,anddefensemechanismsagainst,pepticulceration.
61.
Sharpedges,convergingfoldsofmucosaintheupperhalf.Theulcerbediscoveredbyfibrinopurulentexudate.
62. Free powerpoint template: www.brainybetty.com70 63. (Figure 1)
Peptic ulcer of stomach (arrow). The whole mucosa and part
ofsubmucosa are denuded.(M: mucosa, SM: submucosa, MP: muscularis
propria) 64. as as a rereucosnc nc Pa PaM r lce U 65.
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