Gastritis Bahasa Inggris

7/29/2019 Gastritis Bahasa Inggris

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ENGLISH ASSIGNMENT

ABOUT

FINDING ROOTS

Compiled By:

1. Anik yuliani (01.11.006)

2. Dwi abdul rohman (01.11.014)

3. Ratih Novia Sari (01.11.044)

4. Retno Wahyuningsih (01.11.047)

NURSING SCIENCE STUDY

HEALTH SCIENCE HIGH SCHOOL

MOJOKERTO

2013


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Gastritis: Terminology, Etiology, and Clinicopathological Correlations:

Another Biased View

HENRY D. APPELMAN, MD

The histological approach to gastritis, especially thechronic forms,has undergone a series of re-evaluations by differentexperts overthe past decade, mainly because of the recognition ofindividualdisease patterns that have specific clinical andepidemiological implications.The most spectacular of these was the discovery ofHelicobackrpylmi

and its common gastritis, its relation to almost all

duodenalpeptic ulcers and to most gastric peptic ulcers, itspotential as aprecursor of first multifocal atrophic gastritis andlater tubule-forminggastric carcinomas, and its status as a cause of gastricmucosallymphomas. During this same decade other classes ofgastric reactionand inflammations have been recognized, includingchemical injury

and lymphocytic gastritis. Also in the same decadethe importance ofnon-steroidal anti-inflammatory drugs (NSAIDs) hasemerged as acause of gastric mucosal injuries. To add emphasis toall these discoveries,

biopsies are being performed on stomachs in almostepidemicnumbers and each biopsy specimen has the potentialof having thefeatures of one or more of these injuries as well as

injuries thathave yet to be described. To cope with tbis rapidlyexpanding gastricinflammatory informational extravaganza,

pathologists need someway of dealing with the various entities comfortablyand some methodof cataloging them in ways that are understandable

both to them andto the endoscopists with whom they work. However,if emerging dataabout the chronic gastritides are correct, it isconceivable that the

need to diagnose them, from a strictly clinicalstandpoint, is limited.Either we may know what is in the biopsy specimen

before we see itor what we see may not be important, although it may

be intellectuallychallenging. HUM PATHOL 25:1006-1019.Copyright 0 1994 by W.B.Saunders Company

Gastritis should not be a nasty word, yet it hasbecome one. It is a word that often seems mysterious,a word with too many conflicting meanings, each ofwhich is dependent on who defines it. For the patientgastritis conjures up images of acute epigastric pepticulcer-type pain, sometimes accompanied by nauseaand vomiting, perhaps after an episode ofoverindulgencewith food and drink. Other patients gastritis accountsfor their constant low grade upper abdominalgnawing pain that only temporarily goes away with

overthe-counter antacids and then comes back. There isendoscopic gastritis, the erythematous, edematous,friable,slightly eroded mucosa found in stomachs of patientswho have the symptoms referred to above and,peculiarly, also in the stomachs of those who areasymptomatic.Finally, for the pathologist gastritis is anannoying collection of pits, glands, acute and chronicforms of inflammation, metaplasias, and bacteria, and

From the Department of Pathology, Univeuity ofMichigan, AnnArhw, MI. Accepted fol- publication April 18, 1994.Kq 7ourrl,:aastl-itis, helicohactel-. atrophic.lymphorytic. chemical.Address car-rcspontlcr~c and reprint xquests to HemyD. Appelman.MD, Dcpxtmrnt of. Patholc~h~. Univenity of.Michigan Hospitals,I.500 E Mdical Center- Dr. Ann Arbor. MI 48109-0054.Copyright 61 1994 hy W.B. Saundcr~


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these, in any combination or in no combination at all,may or may not have anything to do with the gastritisof. the patient and the gastritis of the endoscopist.-To

be perfectly frank the correlation betweenhistological

and endoscopic gastritis is terrible! When theendoscopistsees spectacular inflammatory changes, even witherosions, a biopsy specimen of such an area, even ofanerosion, is almost as likely to be normal asinflamed.,Whatever it is that the endoscopists see often has nohistological counterpart. Furthermore, a biopsyspecimenfrom an endoscopically normal antrum may be

intensely and actively inflamed. In contrast, theendoscopichistological correlation for lumps, masses, or bigulcers is very good. No wonder there have been a

bewilderingnumber of classifications ofgastritis, some ofwhich attempt to relate endoscopic and histologicalalterationsas well as others that make no pretense atcorrelation. Some classifications are named after

people,such as Whitehead, whereas others are named aftercities, such as Sidney.. Some use letters to designatetypes ofgastritis, giving us types A. B, AB, and C to

play with, whereas others skip letters and use wordsinstead., It is also no wonder that any clinicalclassificationof gastritis is likely to be of little value, consideringthe lack of correlation between symptoms, endoscopicfindings, and histological features.

Nevertheless, we pathologists must contend with

gastric inflammatory disease, much as we must dealwithinflammations of the esophagus and colon. Ourclinicalcolleagues continue to perform biopsies on stomachs,hoping that we will offer them some help with their

patients who have unpleasant upper gut symptoms orstriking endoscopic findings. To begin, we have todemystifythe word gastritis. This is best accomplished bydeveloping a classification system that is simple and

easily applicable to the types of inflammations that wesee regularly in our gastric biopsy specimens. In the

past 6 years several classifications for gastritis haveappearedin independent articles, chapters in books, andgastrointestinal pathology texts (Table 1). All of theminclude the common gastritides, although the namesvary.!-L Furthermore, much of the descriptive work

inhistological gastritis is still being published and, inaddition,it is critical that a classification scheme recognizethat there are inflammations that do not fit into

predeterminedcategories; in other words, there are gastritidesthat have not yet been named. Therefore, anyclassificationsystem must allow for periodic revisions. Sucha system also should recognize that more than one

typeof gastritis will occasionally occur in stomachs, sothatthere may be double or triple gdstritides.We have known for years that there are acute gastricinjuries and inflammations that include small super-1006

ficial ulcers. or erosions, with no plasma cells, scars,orgranulation tissue to indicate chronicity. Sometimes,these injuries lead to extensive superficial mucosalnecrosisaccompanied by hemorrhage. These reactionsare the acute types of gastritis, and they have beengivennames like acute erosive gastritis or acutehemorrhagegastritis. Precipitating injuries include alcohol,

steroids, .aspirin, and other non-steroidal anti-inflammatorydrugs (NSAIDs). Such acute processes have not

been part of the gastritis mystery unless theyweresuperimposedton a chronic inflammation. These will be discussedin more detail below.

It is the variety of inflammations with overtones ofchronicity that is the problem. In the past it wasassumed

that chronic gastritis was a single disease with acollectioir of- histological characteristics that were

prescnt


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in various combinations. Different forms of chronicgastritis differed only in the intensities of thesehistologicalcharacteristics and in their mix. Furthermore, thestomach was looked on as a single organ: yet weknow

that thcrr arc several distinctive mucosae, as differentIrom each other as the mucosa of the small intestinediffers from that of the colon. This approach wasaided

by the fact that no studies identified a precursor lesionand svstematically followed it with sequential

biopsiesthrough intermediate stages to the full-blown end-stagechronic gastritis. As a matter of fact. this giant hole inour knowledge and understanding persists because we

still have no proof of how each chronic gastritisevolvesand what the precursor or precursors are. A frequentsuggestion implicates a ubiquitous mild inflammationknown simply as superficial gastritis as thecommon

precursor. hut there is no proven support for thatcontention,Ionlv some questionable evidence based on

populationstuciies.~~ However, this should not deter us.Mc also havcb no idea of the histological evolutionofmost otl1c.r chronic inflammations of the gut,includingulcerative colitis. collagenous colitis, and Crohnsdisease.Recent discoveries, aided by the intense use ofupper endoscopy and the frequent biopsy specimensobtained by our endoscopic colleagues. have given~1s

insights into the intricacies of the chronic gastritides.We now recognize that several separate chronicentities

exist, although new discoveries seem to relate someofthem. Unfortunately, the more we know about thechronic gastritides, the more names we invent for thesame diseases. The practicing pathologist mustchoose

which names he or she will use routinely, and thatpathologistmust ensure that the endoscopists understand what

the names mean. It is silly to adopt a nomenclaturethathas no meaning for the very people on whose businesswe depend for our livelihood! The followingdiscussionis based on a simple, functional classification of

gastritis,concentrating mostly on the chronic fijrms, that has

proven useful in a busy endoscopic biopsy practice inalarge teaching hospital (Table 2). It incorporates manyattributes of other classifications, hopefully the hestones,and thus is not a fancifi4 invention of the author. Infact, it is really a simplified version of theclassifications

proposed by Correa and Yardley., It affirms the

existenceof several distinct entities, but it offers severalchoices of names for most entities, recognizing thatdif-

ferent names are used by different pathologists, all ofwhom are capable and accomplished. Thisclassificationsystem can be used easily when more than one type ofgastritis occurs in a single stomach, each of whichmayhave an independent cause or epidemiologicalassociation.The following discussion analyzes each item, notnecessarily in its order in the Table but in order of itsimportance in the evolution of the classificationsystem.HfL/CO5ACTfR PYLO/?/ AND ITS GASTRITISFor decades chronic gastritis was more of a painin the neck than in the stomach. Then approximately

10 years ago Marshall and Warren gave us the greatgastritis gift, their discovery that one type of chronicgastritis was an infectious disease, and theresponsibleorganism was a bacillus that now goes by the name ofHelirobarter pylo?-i (Fig 1A) ~ In fact. DrMarshall eveninfected himself with H p$on and developed an acutegastritis that began approximately a week afteringestion.At this time we are in the midst of an information

explosion about H pylon and its epidemiological,histological,genetic, and cancer-associated aspects. There


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are studies of prevalence in different populations andin different diseases, some using histologicaldiagnosisas proof of infection, whereas others use serumantibodiesas evidence of prior exposure, Whole books have

been dedicated to the organism and its praises havebeen sung during week-long symposia. Obviously, theinformation presented here must be an abbreviatedversionof what is known. However, even this shortenedversion of the H pylon story must by necessitydominatethis entire article because of the importance of theorganism.Briefly, H pyhri is a worldwide pathogen that hasdifferent infection rates in different populations, the

greatest rates occurring in developing countries whereinfection usually occurs in childhood. In developedcountries the infection rate increases with age, is more

common in lower socioeconomic populations, and isgreater in men than in women. Thus, there is a huge

population of asymptomatic infected individuals whonot only h:ave the infection but also have itsassociatedgastritis. Recent studies have cast doubt on adultacquisitionof the infection and suggest that now in Westernsocietises H fgh~ri is usually an infection acquired inchildhood and that it is decreasing in frequency.men, and in such cases some pathologists haveresortedto performing either Giemsa or Wdrthin-Starrv stainsroutinely on every gastric biopsy specimen.It was well known that duodenal peptic ulcers werealmost always accompanied by a significant chronicgastritis

that involved the antral mucosa.21 Furthermore,this gastril.is was characterized by three components:( 1) diffuse plasmacytosis of the superficial mucosa,(2)Iymphoid nodllles deep in the mucosa, and (3)neutrophilsinvading the proliferative zone of the mucosa,the neck Iregion (Figs 1B to lD)..)) In addition, pithyperplasia in which the pits were longer than normaland often mucin-depleted was common. This complexwas called hypersecretory gastritis by,Correa. It

alsoinvolved the body mLlCOS& especially if the ulcerswere

in the stomach instead of the duodenum. In such casesthe gastritis occurred proximally to the ulcer as wellasin the antrum so that the more proximal the ulcer, themore extensive the gastritis., It even can involve thecardia that has a mucosa much like antral.

Subseqtlently,this gastritis has been given several differentnames, including diffuse antral gastritis, type Bchronic gastritis. chronic active gastritis, andchronic nonspecific gastritis.,,The: lymphoid nodules and the plasma cells areprobably the result of chronic antigenic stimulation

bythe organisms. Genta et al found that all individualswith Hpyloti infection, with or without gastric 01duodenal

ulcers, had lvmphoid nodules that were more commonin the antrum than in the bodv, on the lesserrather than the greater curvature, and in ulcer patientsrather than in those without ulcers. Treatment of theH j?lllori infection resulted in gradual shrinkage of thenodules. It has been our experience that the density ofthe plasma cells also diminishes and there is gradualloss of those plasma cells deep in the mucosa.The organisms are found on the surface epithelialcells and less commonly on the superficial foveolarcells.In both locations they lie beneath the muco~ls coat,mostlv over intercellular junctions. They appear asslightly curved short rods. Ultrastructurally thevhavefour flagella at one pole. In almost all cases the

brganihmsare visible with hematoxylin-eosin (HE). The(iiernsa stain will darken them and silver stains, suchasthe Warthin-Starry, will both darken and thicken

them(Fig 1) . A. tissue &am stain also will make themmoreobvious. If all else fails there are commerciallvavailableantibodies for immunohistochemical de&on. Howfhstidious a pathologist should be in looking for H&hiis a matter of individual choice. Our approach has

beento use HE only because it has been our experiencethat a careful search of the HE-stained slide will

detectbacteria in almost every case; special stains add little,perhaps increasing the Yield by no more than 1%. If


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the gastritis is totally typical and if we cannot find thebacteria, then we use the Warthin-Starry stain. Thissituationoccllrs less than once a month, and we resort tothe special stain mostly out of f-rustration at notfinding

the bugs in the expected setting. Usually, theWarthin-Starry stain is also negative in these cases. In contrast,some studies have reported a significant infection ratein patients with normal antral biopsy specimens usingthe specinl stains or culture or both. We have noideawhat it means to have H p$ori with no disease, but

perhaps it indicates first infektion or a nonpathogenicstrain. In addition. pressures from outside the pathol-0~ department may dictate the intensity with which

wt.look for .Hpvlori. The gastroenterologists withwhom wework mav feel it is important for them to knowwhether

men, and in such cases some pathologists haveresortedto performing either Giemsa or Wdrthin-Starrv stainsroutinely on every gastric biopsy specimen.It was well known that duodenal peptic ulcers werealmost always accompanied by a significant chronicgastritisthat involved the antral mucosa.21 Furthermore,this gastril.is was characterized by three components:( 1) diffuse plasmacytosis of the superficial mucosa,(2)Iymphoid nodllles deep in the mucosa, and (3)neutrophilsinvading the proliferative zone of the mucosa,the neck Iregion (Figs 1B to lD)..)) In addition, pit

hyperplasia in which the pits were longer than normaland often mucin-depleted was common. This complexwas called hypersecretory gastritis by,Correa. Italsoinvolved the body mLlCOS& especially if the ulcerswerein the stomach instead of the duodenum. In such casesthe gastritis occurred proximally to the ulcer as wellasin the antrum so that the more proximal the ulcer, themore extensive the gastritis., It even can involve the

cardia that has a mucosa much like antral.Subseqtlently,this gastritis has been given several different

names, including diffuse antral gastritis, type Bchronic gastritis. chronic active gastritis, andchronic nonspecific gastritis.,,The: lymphoid nodules and the plasma cells areprobably the result of chronic antigenic stimulation

by

the organisms. Genta et al found that all individualswith Hpyloti infection, with or without gastric 01duodenalulcers, had lvmphoid nodules that were more commonin the antrum than in the bodv, on the lesserrather than the greater curvature, and in ulcer patientsrather than in those without ulcers. Treatment of theH j?lllori infection resulted in gradual shrinkage of thenodules. It has been our experience that the density ofthe plasma cells also diminishes and there is gradualloss of those plasma cells deep in the mucosa.

The organisms are found on the surface epithelialcells and less commonly on the superficial foveolarcells.In both locations they lie beneath the muco~ls coat,mostlv over intercellular junctions. They appear asslightly curved short rods. Ultrastructurally thevhavefour flagella at one pole. In almost all cases the

brganihmsare visible with hematoxylin-eosin (HE). The(iiernsa stain will darken them and silver stains, suchasthe Warthin-Starry, will both darken and thickenthem(Fig 1) . A. tissue &am stain also will make themmoreobvious. If all else fails there are commerciallvavailableantibodies for immunohistochemical de&on. Howfhstidious a pathologist should be in looking for H&hiis a matter of individual choice. Our approach has

beento use HE only because it has been our experiencethat a careful search of the HE-stained slide willdetect

bacteria in almost every case; special stains add little,perhaps increasing the Yield by no more than 1%. Ifthe gastritis is totally typical and if we cannot find the

bacteria, then we use the Warthin-Starry stain. Thissituationoccllrs less than once a month, and we resort tothe special stain mostly out of f-rustration at not

findingthe bugs in the expected setting. Usually, the Warthin-Starry stain is also negative in these cases. In contrast,


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some studies have reported a significant infection ratein patients with normal antral biopsy specimens usingthe specinl stains or culture or both. We have noideawhat it means to have H p$ori with no disease, but

perhaps it indicates first infektion or a nonpathogenic

strain. In addition. pressures from outside the pathol-0~ department may dictate the intensity with whichwt.look for .Hpvlori. The gastroenterologists with whomwework mav feel it is important for them to knowwhetherH @!cJ~? ii; present or absent in every gastric biopsyspeci-The neutrophils generally invade epithelium thatis mid-zone in the mucosa, at the level of the necks,

whereas the infection is colonizing the surface andSW

perficial pits. This fact is repeatedly- illustrated inessentially

every publication in which there is a microscopicpicture. The epithelium covered by the organisms isnever inflamed, whereas inflamed epithelium is nevercovered by organisms. This discrepancy in location

betweenbacteria and neutrophils has not been adequatcl)explained. Soluble chemotactic factors, either released

by the bacteria or by their interactions with hosttissues,have been suspected. In patients infected with H p$oritumor necrosis factor [TNF]-alpha production bvantralmucosa was higher when there was active gastritisthanwhen the gastritis was inactive. Tumor necrosisfactoralphacan activate neutrophils. Other neutrophilic

chemotacticfactors have been identified that appear tocome from the bacterium itself.7.xThere are modifications of the typical changes. Forinstance, the plasmacytosis may be accompanied bylymphocytosisand even ?.eosinophils, althongh when the)ale present the possibility of a second insult might beconsidered. The infiltrate in the lamina propria alsocommonly extends into the glandular compartmentfol

unpredictable distances, sometimes reaching themnscularismucosae. Perhaps this deep extension is an index

of severity. The combination of a deeply extendingor transmucosal infiltrate plus deep lymphoid nodulesresults in a histological lesion in which the glands arceither spread apart or else are destroyed bv theinflammation:in other words, there is loss of glands 01

atrophv. Unfortunately, we do not know which oftheseis the correct interpretation. It this is indeeddestructionof glands then we should have identified aglanddestructive

phase of the inflammation, yet such a phasehas not been found. The active epithelial damage withneutrophils involves the necks. Because this is thegenerativezone of the gastric mucosa from which both pits

and glands arisr, it is possible that darnnge to thiszoneresults in selective loss of regenerative capabilities forthe glandular compartment. If such is the case thengland loss may be attributed to attrition withoutreplaccment.H&cohmrtu?-infection also has been reported to beassociated with damage to the colonized surface andfoveolar cpithelial cells in patients with both duodenaland gastric peptic ulcers or with the tvpical activechronic gastritis without ulcers.-. Thc,se changesin-

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