This document discusses gastritis and Helicobacter pylori (H. pylori) infection. It defines gastritis as inflammation of the stomach lining and notes that it is usually caused by infectious agents like H. pylori, autoimmune issues, or hypersensitivity reactions. H. pylori is described as a common chronic bacterial infection that can lead to gastritis. Strains of H. pylori that produce vacuolating cytotoxin and cytotoxin-associated gene A are associated with more severe inflammation and increased risk of ulcers and precancerous lesions. The document provides classifications of gastritis and risk factors for conditions like stress-related gastric ulcers.

1. GastritisGastritis
Dr.Mohammad Shaikhani
Assistant professor
Sulaimanyah College of
Medicine.

2. DefinitionDefinition
 Inflammation associated with mucosal injuryInflammation associated with mucosal injury
 A histological term that needs biopsy to be confirmed.A histological term that needs biopsy to be confirmed.
 Usually due to infectious agents (As H pylori) , autoimmune &Usually due to infectious agents (As H pylori) , autoimmune &
hypersensitivity reactions.hypersensitivity reactions.
 Endoscopic mucosal changes of gastritis, 27% had a normalEndoscopic mucosal changes of gastritis, 27% had a normal
endoscopic biopsy specimen& a normal endoscopic appearance,endoscopic biopsy specimen& a normal endoscopic appearance,
63 % had histological evidence of gastritis.63 % had histological evidence of gastritis.

3. DefinitionDefinition
 ““GastropathyGastropathy“: Epithelial cell damage /regeneration“: Epithelial cell damage /regeneration
without inflammation.without inflammation.
 Gastropathy may be referred without histologicalGastropathy may be referred without histological
evidence, according to gross appearance in endoscopy orevidence, according to gross appearance in endoscopy or
radiology.radiology.
 Gastropathy usually caused by irritants as drugs (eg,Gastropathy usually caused by irritants as drugs (eg,
NSAIDs& alcohol), bile reflux, hypovolemia &chronicNSAIDs& alcohol), bile reflux, hypovolemia &chronic
congestion.congestion.

4. Gross–histologic correlation?Gross–histologic correlation?

5. ClassificationClassification
 Acute: short term inflammation with neurophilicAcute: short term inflammation with neurophilic
infiltrateinfiltrate
 Chronic:long standing with mononuclear cell infiltrateChronic:long standing with mononuclear cell infiltrate
especially lymphocyte/maccrophagesespecially lymphocyte/maccrophages

6. Anatomical siteAnatomical site
ANTRUM
CARDIA
BODY
MUCOUS
SECRETING
ENDOCRINE
SPECIALISED SECRETORY:
PARIETAL - ACID CHIEF -
PEPSINOGEN
ENDOCRINE
HIST, SOMASTATIN
MUCOUS SECRETING
ENDOCRINE
GASTRIN, 5HT

9. CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID

10. CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID

11. Acute hemorrhagic erosiveAcute hemorrhagic erosive
 (NSAIDs, alcohol, or bile acids)(NSAIDs, alcohol, or bile acids)
 Mucosal hypoxia (trauma, burns [Curling's ulcers],sepsis)Mucosal hypoxia (trauma, burns [Curling's ulcers],sepsis)
 Combination of factors as antineoplastic chemotherapyCombination of factors as antineoplastic chemotherapy
 Gastric/duodenal ulcers occurring during severe damageGastric/duodenal ulcers occurring during severe damage
to CNS (Cushing's ulcers).to CNS (Cushing's ulcers).

12. Mucosal congestion, oedema,
inflammation, ulceration & Bleeding.
ACUTE GASTRITIS -ACUTE GASTRITIS -
MORPHOLOGYMORPHOLOGY

13. Acute hemorrhagic erosiveAcute hemorrhagic erosive
 NSAID-induced acute hemorrhagic& erosive gastropathyNSAID-induced acute hemorrhagic& erosive gastropathy
due todue to inhibition of prostaglandin productioninhibition of prostaglandin production..
 Prostaglandins protect mucosa by several mechanisms, asProstaglandins protect mucosa by several mechanisms, as
stimulation of mucus / bicarbonate secretion&maintenancestimulation of mucus / bicarbonate secretion&maintenance
of mucosal blood flowof mucosal blood flow
 Hemorrhagic or erosive gastropathy may be associatedHemorrhagic or erosive gastropathy may be associated
with the development of gastric or duodenal ulcers.with the development of gastric or duodenal ulcers.

14. NSAID GI toxicity risk factorNSAID GI toxicity risk factor
 H/O adverse GI event (ulcer, hemorrhage) *5 increases.H/O adverse GI event (ulcer, hemorrhage) *5 increases.
 Age >60 increases risk *6.Age >60 increases risk *6.
 High (> twice normal) dosage of a NSAID increases riskHigh (> twice normal) dosage of a NSAID increases risk
*10.*10.
 Concurrent use of glucocorticoids increases risk *5.Concurrent use of glucocorticoids increases risk *5.
 Concurrent use of anticoagulants increases risk *10- 15.Concurrent use of anticoagulants increases risk *10- 15.

15. HP/NSAIDHP/NSAID
 If H/O uncomplicated or complicated peptic ulcersIf H/O uncomplicated or complicated peptic ulcers
(gastric, duodenal)(gastric, duodenal) should beshould be tested for H. pylori prior totested for H. pylori prior to
beginning a NSAID or low dosebeginning a NSAID or low dose aspirinaspirin..
 If present, H. pylori should be treated with appropriateIf present, H. pylori should be treated with appropriate
therapy, even if it is believed that the prior ulcer was duetherapy, even if it is believed that the prior ulcer was due
to NSAIDs.to NSAIDs.

16. NSAID-related GIT toxicity prophylaxisNSAID-related GIT toxicity prophylaxis
 COX-2 selective inhibitor.COX-2 selective inhibitor.
 MisoprostolMisoprostol

PPI asPPI as lansoprazolelansoprazole..

17. Stress ulcer pathophysiologyStress ulcer pathophysiology
 HypersecretionHypersecretion of acid –head trauma.of acid –head trauma.
 Defects in gastric glycoprotein mucusDefects in gastric glycoprotein mucus –In critically ill–In critically ill
patients, increased refluxed bile salts or uremic toxins canpatients, increased refluxed bile salts or uremic toxins can
denude the glycoprotein mucous barrierdenude the glycoprotein mucous barrier
 IschemiaIschemia – Shock, sepsis, trauma can lead to impaired– Shock, sepsis, trauma can lead to impaired
perfusion of the gut.perfusion of the gut.

18. Stress ulcer risk factorsStress ulcer risk factors
 2 major risk factors for clinically significant bleeding due2 major risk factors for clinically significant bleeding due
to stress ulcers are:to stress ulcers are:
 Mechanical ventilationMechanical ventilation for > 48 hours &for > 48 hours & coagulopathycoagulopathy..
 •• ShockShock
• Sepsis• Sepsis
• Hepatic failure• Hepatic failure
• Renal failure• Renal failure
• Multiple trauma• Multiple trauma
• Burns >35% total body surface area• Burns >35% total body surface area
• Organ transplant recipients• Organ transplant recipients
• Head or spinal trauma• Head or spinal trauma
• H/O peptic ulcer disease or upper GI bleeding• H/O peptic ulcer disease or upper GI bleeding

19. Common type ofCommon type of
gastritidesgastritides

20. CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID

21. H PyloriH Pylori
 A spiral shaped, microaerophilic, gram negative bacteriumA spiral shaped, microaerophilic, gram negative bacterium
measuring 3.5 length* 0.5 microns in widthmeasuring 3.5 length* 0.5 microns in width
 urease forms ammonia & bicarbonate that neutralize gastricurease forms ammonia & bicarbonate that neutralize gastric
acid& form a protective cloud around the organismacid& form a protective cloud around the organism
 Urease appears to be vital for its survival & colonization.Urease appears to be vital for its survival & colonization.
 Spiral shape, flagella facilitate its passage through the mucusSpiral shape, flagella facilitate its passage through the mucus
layerlayer
 Helicobacter pylori is the most common chronic bacterialHelicobacter pylori is the most common chronic bacterial
infection in humans ;50% of the world's population is affected.infection in humans ;50% of the world's population is affected.
 The frequency of H.P for any age in any locality reflects rate ofThe frequency of H.P for any age in any locality reflects rate of
bacterial acquisition during childhood years &affected by:bacterial acquisition during childhood years &affected by:
 Density of housing.Density of housing.
 OvercrowdingOvercrowding
 Number of siblings.Number of siblings.
 Sharing a bed.Sharing a bed.
 Lack of running water.Lack of running water.

23. 

24.  The route by which infection occurs remains unknown.The route by which infection occurs remains unknown.
 Person-to-person transmission by either fecal/oral or oral/oralPerson-to-person transmission by either fecal/oral or oral/oral
exposure seems most likelyexposure seems most likely
 Humans appear to be the major reservoir of infectionHumans appear to be the major reservoir of infection
 Isolated from primates from domestic cats & in milk/ gastricIsolated from primates from domestic cats & in milk/ gastric
tissue of sheeptissue of sheep

25. Vac A & Cag AVac A & Cag A
 Vacuolating cytotoxin (VacA) causes cell injury in vitro & gastricVacuolating cytotoxin (VacA) causes cell injury in vitro & gastric
tissue damage in vivo .tissue damage in vivo .
 All H. pylori contain the gene coding for VacA; but, only someAll H. pylori contain the gene coding for VacA; but, only some
strains have cytotoxin-associated gene A (cagA)strains have cytotoxin-associated gene A (cagA)
 Strains producing VacA & CagA cause more intense tissueStrains producing VacA & CagA cause more intense tissue
inflammation&induce cytokine productioninflammation&induce cytokine production

26.  85-100% with duodenal ulcers have CagA+ strains,85-100% with duodenal ulcers have CagA+ strains,
compared to 30-60% of infected patients who do notcompared to 30-60% of infected patients who do not
develop ulcersdevelop ulcers
 CagA strains may be associated with a higher frequency ofCagA strains may be associated with a higher frequency of
precancerous lesions.precancerous lesions.

27.  Host polymorphism of IL-1 betaHost polymorphism of IL-1 beta (&possibly IL-10)(&possibly IL-10)
appears to determine the degree of inflammatory responseappears to determine the degree of inflammatory response
to infection, resulting alteration in acid secretion (hyper orto infection, resulting alteration in acid secretion (hyper or
hypo secretion)&risk for subsequent gastric cancerhypo secretion)&risk for subsequent gastric cancer

28. HPHP
 The inflammation usually superficial, located in the gastric pit &The inflammation usually superficial, located in the gastric pit &
upper portion of the lamina propria, , consists of mononuclearupper portion of the lamina propria, , consists of mononuclear
cells & polymorphonuclear leukocytes, commonly termedcells & polymorphonuclear leukocytes, commonly termed chronicchronic
active inflammationactive inflammation..
 The antrum consistently is involved, whereas inflammation in theThe antrum consistently is involved, whereas inflammation in the
acid-secreting gastric body &fundus is more variable.acid-secreting gastric body &fundus is more variable.
 H. pyloriH. pylori is causally associated with gastritis, duodenal &gastricis causally associated with gastritis, duodenal &gastric
ulcer, gastric adenocarcinoma&primary gastric B-cell lymphomasulcer, gastric adenocarcinoma&primary gastric B-cell lymphomas
of mucosa-associated lymphoid tissue (MALT)of mucosa-associated lymphoid tissue (MALT)
 Infected subjects have 1/6 lifetime risk of peptic ulcer; the lifetimeInfected subjects have 1/6 lifetime risk of peptic ulcer; the lifetime
risk of gastric cancer varies from 1-3% - > 12% in Japan.risk of gastric cancer varies from 1-3% - > 12% in Japan.
 DISTRIBUTION & PROGRESSION: Antral- DU& Pangastritis-GASTRICDISTRIBUTION & PROGRESSION: Antral- DU& Pangastritis-GASTRIC
CA.CA.

29. HP: diagnosisHP: diagnosis
 Serology with ELISA for IgG or IgA antibodies, 13C-urea or 14C-Serology with ELISA for IgG or IgA antibodies, 13C-urea or 14C-
urea breath tests, or stool antigen testing.urea breath tests, or stool antigen testing.
 Tests requiring endoscopy&biopsy include histologic exam ,Tests requiring endoscopy&biopsy include histologic exam ,
urease testing of antral biopsy specimens, or culture.urease testing of antral biopsy specimens, or culture.
 The optimal method depends on circumstances, local expertise,The optimal method depends on circumstances, local expertise,
/availability./availability.
 All tests have good sensitivity/specificity, but false-positive/false-All tests have good sensitivity/specificity, but false-positive/false-
negative determinations occur.negative determinations occur.
 In tests that depend on the No of organisms (breath &gastricIn tests that depend on the No of organisms (breath &gastric
biopsy specimens for urease activity, histology& culture), false-biopsy specimens for urease activity, histology& culture), false-
negative occur esp when the organism suppressed by antibiotics,negative occur esp when the organism suppressed by antibiotics,
PPI, or bismuth.PPI, or bismuth.
 Therapy may need to be discontinued for several weeks beforeTherapy may need to be discontinued for several weeks before
these tests become positive.these tests become positive.

30. HP:TrtHP:Trt
 H. pyloriH. pylori infection is typically latent.infection is typically latent.
 H. pyloriH. pylori gastritis is found more frequently, in patients withgastritis is found more frequently, in patients with
dyspepsia.dyspepsia.
 Cure of the infection resolves symptoms in only 10% of patientsCure of the infection resolves symptoms in only 10% of patients
with nonulcer dyspepsia.with nonulcer dyspepsia.
 Antibiotic therapy forAntibiotic therapy for H. pyloriH. pylori is recommended because:is recommended because:
 Less expensive & safer than additional diagnostic studies & long-Less expensive & safer than additional diagnostic studies & long-
term continuous antacid therapy.term continuous antacid therapy.
 Cure of the inf reduces the risk of subsequent PUD &gastric ca.Cure of the inf reduces the risk of subsequent PUD &gastric ca.
 Eliminates the individual as a carrier who can transmit theEliminates the individual as a carrier who can transmit the
infection.infection.
 H. pyloriH. pylori testing&treatment are appropriate for new-onset ortesting&treatment are appropriate for new-onset or
previously undiagnosed dyspepsia without alarm featurespreviously undiagnosed dyspepsia without alarm features..

31. Bile reflux gastropathyBile reflux gastropathy
 Bile reflux gastropathy results from the regurgitation ofBile reflux gastropathy results from the regurgitation of
bile into the stomach because of:bile into the stomach because of:
 An operative stoma.An operative stoma.
 An incompetent pyloric sphincterAn incompetent pyloric sphincter
 Abnormal duodenal motilityAbnormal duodenal motility
 The effect of bile salts on gastric mucosa is comparable toThe effect of bile salts on gastric mucosa is comparable to
that seen after chronic NSAID usethat seen after chronic NSAID use

32. Chronic metaplasticChronic metaplastic
gastritidesgastritides

33. CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID

34. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
 Metaplasia, especially intestinal type, is virtually aMetaplasia, especially intestinal type, is virtually a
universal feature of atrophic gastritis.universal feature of atrophic gastritis.
 Metaplasia is highly relevant to the pathogenesis ofMetaplasia is highly relevant to the pathogenesis of
atrophic gastritis & to its complications (eg, perniciousatrophic gastritis & to its complications (eg, pernicious
anemia, gastric ulcer, gastric cancer).anemia, gastric ulcer, gastric cancer).

35. metaplastic atrophic gastritismetaplastic atrophic gastritis
 AUTOIMMUNE METAPLASTIC ATROPHICAUTOIMMUNE METAPLASTIC ATROPHIC
GASTRITIS (AMAG) is an inherited form that isGASTRITIS (AMAG) is an inherited form that is
associated with an immune response in the oxyntic mucosaassociated with an immune response in the oxyntic mucosa
directed against parietal cells &intrinsic factor.directed against parietal cells &intrinsic factor.
 AMAG is inherited as an autosomal dominant disorderAMAG is inherited as an autosomal dominant disorder

36. SYNONYMS OF AMAGSYNONYMS OF AMAG
 TYPE A GASTRITISTYPE A GASTRITIS
 AUTOIMMUNE GASTRITISAUTOIMMUNE GASTRITIS
 DIFFUSE CORPORAL GASTRITISDIFFUSE CORPORAL GASTRITIS

37. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
 The chronic inflammation, gland atrophy, epithelialThe chronic inflammation, gland atrophy, epithelial
metaplasia of AMAG are closely paralleled by elevatedmetaplasia of AMAG are closely paralleled by elevated
serum antibodies to parietal cells & intrinsic factor,serum antibodies to parietal cells & intrinsic factor,
reflecting its autoimmune origin.reflecting its autoimmune origin.

39. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
 The loss of parietal cell mass leads to profoundThe loss of parietal cell mass leads to profound
hypochlorhydria, while the inadequate production ofhypochlorhydria, while the inadequate production of
intrinsic factor leads tointrinsic factor leads to vitamin B12vitamin B12 malabsorption&malabsorption&
pernicious anemia.pernicious anemia.

40. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
 Patients with AMAG are at increased risk for thePatients with AMAG are at increased risk for the
development of gastric carcinoid tumors&development of gastric carcinoid tumors&
adenocarcinoma.adenocarcinoma.
CANCER

41. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
surveillance strategy for patients diagnosed with pernicious anemiasurveillance strategy for patients diagnosed with pernicious anemia
•• Upper endoscopy soon after diagnosisUpper endoscopy soon after diagnosis
•• Removal of gastric polyps if possible; most of these polyps will beRemoval of gastric polyps if possible; most of these polyps will be
benignbenign
•• Frequent reinvestigation in patients whose polyps are notFrequent reinvestigation in patients whose polyps are not
removed or who have severe mucosal dysplasia; in the remainingremoved or who have severe mucosal dysplasia; in the remaining
patients follow-up endoscopies should be performed atpatients follow-up endoscopies should be performed at
approximately five-year intervals.approximately five-year intervals.

42. metaplastic atrophic gastritismetaplastic atrophic gastritis
 Patients with AMAG arePatients with AMAG are less likely to be infected by H.less likely to be infected by H.
pyloripylori than aged-matched controls:than aged-matched controls:
 Metaplastic epithelium is unsuitable for H. pyloriMetaplastic epithelium is unsuitable for H. pylori
colonization.colonization.
 The associated hypochlorhydria encourages overgrowth byThe associated hypochlorhydria encourages overgrowth by
other bacterial speciesother bacterial species

43. EMAGEMAG
 Environmental metaplastic atrophic gastritis (EMAG) isEnvironmental metaplastic atrophic gastritis (EMAG) is
due to environmental factors, as diet (NITROSOdue to environmental factors, as diet (NITROSO
COMPOUNDS) & H. pylori infection, on the gastricCOMPOUNDS) & H. pylori infection, on the gastric
mucosa.mucosa.

44. metaplastic atrophic gastritismetaplastic atrophic gastritis
 Unlike AMAG, mucosal changes in patients with EMAGUnlike AMAG, mucosal changes in patients with EMAG
affect both the corpus & antrum in a multifocalaffect both the corpus & antrum in a multifocal
distribution, butdistribution, but with heaviest involvement of the antrum.with heaviest involvement of the antrum.

45. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
 EMAG vs AMAGEMAG vs AMAG
•• Gastric acid productionGastric acid production does notdoes not disappear entirelydisappear entirely
• Serum gastrin• Serum gastrin is notis not elevatedelevated
• Parietal cell & intrinsic factor autoantibodies & pernicious• Parietal cell & intrinsic factor autoantibodies & pernicious
anemia areanemia are absentabsent

46. Metaplastic atrophic gastritisMetaplastic atrophic gastritis
 There is an increased risk for gastric ulcer compared toThere is an increased risk for gastric ulcer compared to
AMAG, presumably due to the accompanyingAMAG, presumably due to the accompanying
hypochlorhydria in the latter disorderhypochlorhydria in the latter disorder
CANCER

47. metaplastic atrophic gastritismetaplastic atrophic gastritis
 Diagnosis of EMAG should not be made from biopsyDiagnosis of EMAG should not be made from biopsy
specimens unlessspecimens unless at least 20 %at least 20 % of the available antral orof the available antral or
transitional mucosa is replaced by metaplastic glands, ortransitional mucosa is replaced by metaplastic glands, or
there is unequivocal atrophy.there is unequivocal atrophy.

48. Hyperplastic gastropathiesHyperplastic gastropathies
Proliferative, inflammatory,
infiltrative conditions are
associated with large folds due
to excessive number of mucosal
epithelial cells

49. Large gastric folds > 1.0 cmLarge gastric folds > 1.0 cm
 Chronic gastritis/lymphoid hyperplasiaChronic gastritis/lymphoid hyperplasia
 Benign tumorsBenign tumors
 Gastric malignancyGastric malignancy
 Zollinger-Ellison syndromeZollinger-Ellison syndrome
 Menetrier's diseaseMenetrier's disease

50. Ménétrier's diseaseMénétrier's disease
 Epithelial hyperplasiaEpithelial hyperplasia
involving the surface &involving the surface &
foveolar mucous cellsfoveolar mucous cells
 the oxyntic glands can bethe oxyntic glands can be
normal or atrophic.normal or atrophic.
 Surgery has beenSurgery has been
advocated for patientsadvocated for patients
with intractable pain,with intractable pain,
hypoalbuminemia withhypoalbuminemia with
edema, hemorrhage,edema, hemorrhage,
pyloric obstruction, & inpyloric obstruction, & in
whom a malignancywhom a malignancy
cannot be excludedcannot be excluded

51. Zollinger-Ellison syndromeZollinger-Ellison syndrome
Increased numbers of parietal cellsIncreased numbers of parietal cells
with no change in surface &foveolarwith no change in surface &foveolar
mucous cells.mucous cells.
Signs:Signs:
Multiple ulcersMultiple ulcers
diarrheadiarrhea
ulcer in atypical siteulcer in atypical site
resistant ulcerresistant ulcer
enlarged foldsenlarged folds
severe esophagirtissevere esophagirtis
FH of MEN1FH of MEN1

52. Hyperplastic gastropathiesHyperplastic gastropathies
mixed-type in which both mucousmixed-type in which both mucous
&oxyntic glandular cells show&oxyntic glandular cells show
hyperplasia, may be seen inhyperplasia, may be seen in
lymphocytic &H. pylori gastritis.lymphocytic &H. pylori gastritis.

53. Portal hypertensive gastropathyPortal hypertensive gastropathy
 Portal hypertensive gastropathy characteristically appearsPortal hypertensive gastropathy characteristically appears
as a fine white reticular pattern separating areas of pinkishas a fine white reticular pattern separating areas of pinkish
mucosa on endoscopy, giving the gastric mucosa amucosa on endoscopy, giving the gastric mucosa a
""snakeskinsnakeskin" appearance" appearance

54. Portal hypertensive gastropathyPortal hypertensive gastropathy