GastritisGastritis
Dr.Mohammad ShaikhaniAssistant professor
Sulaimanyah College of Medicine.
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 normal Endoscopic 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.
DefinitionDefinition “ “GastropathyGastropathy“: Epithelial cell damage /regeneration “: Epithelial cell damage /regeneration
without inflammation. without inflammation. Gastropathy may be referred without histological Gastropathy may be referred without histological
evidence, according to gross appearance in endoscopy or evidence, 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 &chronic NSAIDs& alcohol), bile reflux, hypovolemia &chronic congestion.congestion.
Gross–histologic Gross–histologic correlation?correlation?
ClassificationClassification
Acute: short term inflammation with neurophilic Acute: short term inflammation with neurophilic infiltrateinfiltrate
Chronic:long standing with mononuclear cell infiltrate Chronic:long standing with mononuclear cell infiltrate especially lymphocyte/maccrophagesespecially lymphocyte/maccrophages
Anatomical siteAnatomical site
ANTRUM
CARDIA
BODY
MUCOUS SECRETING ENDOCRINE
SPECIALISED SECRETORY: PARIETAL - ACID CHIEF - PEPSINOGEN
ENDOCRINEHIST, SOMASTATIN
MUCOUS SECRETING ENDOCRINE GASTRIN, 5HT
CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID
CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID
Acute hemorrhagic Acute hemorrhagic erosiveerosive
(NSAIDs, alcohol, or bile acids) (NSAIDs, alcohol, or bile acids) Mucosal hypoxia (trauma, burns [Curling's Mucosal hypoxia (trauma, burns [Curling's
ulcers],sepsis) ulcers],sepsis) Combination of factors as antineoplastic Combination of factors as antineoplastic
chemotherapychemotherapy Gastric/duodenal ulcers occurring during Gastric/duodenal ulcers occurring during
severe damage to CNS (Cushing's ulcers).severe damage to CNS (Cushing's ulcers).
Mucosal congestion, oedema, inflammation, ulceration & Bleeding.
ACUTE GASTRITIS - ACUTE GASTRITIS - MORPHOLOGYMORPHOLOGY
Acute hemorrhagic Acute hemorrhagic erosiveerosive
NSAID-induced acute hemorrhagic& erosive gastropathy NSAID-induced acute hemorrhagic& erosive gastropathy due to due to inhibition of prostaglandin productioninhibition of prostaglandin production. .
Prostaglandins protect mucosa by several mechanisms, as Prostaglandins protect mucosa by several mechanisms, as stimulation of mucus / bicarbonate secretion&maintenance stimulation of mucus / bicarbonate secretion&maintenance of mucosal blood flowof mucosal blood flow
Hemorrhagic or erosive gastropathy may be associated Hemorrhagic or erosive gastropathy may be associated with the development of gastric or duodenal ulcers. with the development of gastric or duodenal ulcers.
NSAID GI toxicity risk NSAID GI toxicity risk factorfactor
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 risk High (> 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.
HP/NSAIDHP/NSAID
If H/O uncomplicated or complicated peptic ulcers If H/O uncomplicated or complicated peptic ulcers (gastric, duodenal) (gastric, duodenal) should beshould be tested for H. pylori prior to tested for H. pylori prior to beginning a NSAID or low dose beginning a NSAID or low dose aspirinaspirin..
If present, H. pylori should be treated with appropriate If present, H. pylori should be treated with appropriate therapy, even if it is believed that the prior ulcer was due therapy, even if it is believed that the prior ulcer was due to NSAIDs.to NSAIDs.
NSAID-related GIT toxicity NSAID-related GIT toxicity prophylaxisprophylaxis
COX-2 selective inhibitor.COX-2 selective inhibitor. MisoprostolMisoprostol
PPI as PPI as lansoprazolelansoprazole..
Stress ulcer Stress ulcer pathophysiologypathophysiology
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 can patients, increased refluxed bile salts or uremic toxins can denude the glycoprotein mucous barrier denude 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.
Stress ulcer risk factorsStress ulcer risk factors 2 major risk factors for clinically significant bleeding due 2 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
Common type of Common type of gastritidesgastritides
CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID
H PyloriH Pylori A spiral shaped, microaerophilic, gram negative bacterium A 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 gastric urease 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 mucus Spiral shape, flagella facilitate its passage through the mucus
layerlayer Helicobacter pylori is the most common chronic bacterial Helicobacter 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 of The 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.
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/oral Person-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/ gastric Isolated from primates from domestic cats & in milk/ gastric
tissue of sheeptissue of sheep
Vac A & Cag AVac A & Cag A Vacuolating cytotoxin (VacA) causes cell injury in vitro & gastric Vacuolating 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 some All 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 tissue Strains producing VacA & CagA cause more intense tissue
inflammation&induce cytokine productioninflammation&induce cytokine production
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 not compared to 30-60% of infected patients who do not develop ulcersdevelop ulcers
CagA strains may be associated with a higher frequency of CagA strains may be associated with a higher frequency of precancerous lesions.precancerous lesions.
Host polymorphism of IL-1 betaHost polymorphism of IL-1 beta (&possibly IL-10) (&possibly IL-10) appears to determine the degree of inflammatory response appears to determine the degree of inflammatory response to infection, resulting alteration in acid secretion (hyper or to infection, resulting alteration in acid secretion (hyper or hypo secretion)&risk for subsequent gastric cancerhypo secretion)&risk for subsequent gastric cancer
HPHP The inflammation usually superficial, located in the The inflammation usually superficial, located in the
gastric pit & upper portion of the lamina propria, , gastric pit & upper portion of the lamina propria, , consists of mononuclear cells & polymorphonuclear consists of mononuclear cells & polymorphonuclear leukocytes, commonly termed leukocytes, commonly termed chronic active chronic active inflammationinflammation. .
The antrum consistently is involved, whereas The antrum consistently is involved, whereas inflammation in the acid-secreting gastric body inflammation in the acid-secreting gastric body &fundus is more variable. &fundus is more variable.
H. pyloriH. pylori is causally associated with gastritis, is causally associated with gastritis, duodenal &gastric ulcer, gastric duodenal &gastric ulcer, gastric adenocarcinoma&primary gastric B-cell lymphomas 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 Infected subjects have 1/6 lifetime risk of peptic ulcer; the lifetime risk of gastric cancer varies from ulcer; the lifetime risk of gastric cancer varies from 1-3% - > 12% in Japan.1-3% - > 12% in Japan.
DISTRIBUTION & PROGRESSION: Antral- DU& Pangastritis-GASTRIC CA.DISTRIBUTION & PROGRESSION: Antral- DU& Pangastritis-GASTRIC CA.
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 &gastric In 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 before Therapy may need to be discontinued for several weeks before
these tests become positive.these tests become positive.
HP:TrtHP:Trt H. pyloriH. pylori infection is typically latent. infection is typically latent. H. pyloriH. pylori gastritis is found more frequently, in patients with gastritis is found more frequently, in patients with
dyspepsia.dyspepsia. Cure of the infection resolves symptoms in only 10% of patients Cure of the infection resolves symptoms in only 10% of patients
with nonulcer dyspepsia. with nonulcer dyspepsia. Antibiotic therapy for Antibiotic 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 the Eliminates the individual as a carrier who can transmit the
infection.infection. H. pyloriH. pylori testing&treatment are appropriate for new-onset or testing&treatment are appropriate for new-onset or
previously undiagnosed dyspepsia without alarm featurespreviously undiagnosed dyspepsia without alarm features..
Bile reflux gastropathyBile reflux gastropathy Bile reflux gastropathy results from the regurgitation of Bile 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 to The effect of bile salts on gastric mucosa is comparable to
that seen after chronic NSAID usethat seen after chronic NSAID use
Chronic metaplastic Chronic metaplastic gastritidesgastritides
CLASSIFICATIONCLASSIFICATION
GASTRITIS
ACUTE COMMON CHRONIC
EMAG
AMAG
BILE HPSTRESS
NSAID
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
Metaplasia, especially intestinal type, is virtually a Metaplasia, especially intestinal type, is virtually a universal feature of atrophic gastritis.universal feature of atrophic gastritis.
Metaplasia is highly relevant to the pathogenesis of Metaplasia is highly relevant to the pathogenesis of atrophic gastritis & to its complications (eg, pernicious atrophic gastritis & to its complications (eg, pernicious anemia, gastric ulcer, gastric cancer).anemia, gastric ulcer, gastric cancer).
metaplastic atrophic metaplastic atrophic gastritisgastritis
AUTOIMMUNE METAPLASTIC ATROPHIC AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITIS (AMAG) is an inherited form that is GASTRITIS (AMAG) is an inherited form that is associated with an immune response in the oxyntic mucosa associated 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
SYNONYMS OF AMAGSYNONYMS OF AMAG TYPE A GASTRITISTYPE A GASTRITIS AUTOIMMUNE GASTRITISAUTOIMMUNE GASTRITIS DIFFUSE CORPORAL GASTRITISDIFFUSE CORPORAL GASTRITIS
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
The chronic inflammation, gland atrophy, epithelial The chronic inflammation, gland atrophy, epithelial metaplasia of AMAG are closely paralleled by elevated metaplasia 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.
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
The loss of parietal cell mass leads to profound The loss of parietal cell mass leads to profound hypochlorhydria, while the inadequate production of hypochlorhydria, while the inadequate production of intrinsic factor leads to intrinsic factor leads to vitamin B12vitamin B12 malabsorption& malabsorption& pernicious anemia. pernicious anemia.
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
Patients with AMAG are at increased risk for the Patients with AMAG are at increased risk for the development of gastric carcinoid tumors& development of gastric carcinoid tumors& adenocarcinoma.adenocarcinoma.
CANCER
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
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 be Removal of gastric polyps if possible; most of these polyps will be
benignbenign • • Frequent reinvestigation in patients whose polyps are not Frequent reinvestigation in patients whose polyps are not
removed or who have severe mucosal dysplasia; in the remaining removed or who have severe mucosal dysplasia; in the remaining patients follow-up endoscopies should be performed at patients follow-up endoscopies should be performed at approximately five-year intervals.approximately five-year intervals.
metaplastic atrophic metaplastic atrophic gastritisgastritis
Patients with AMAG are Patients 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. pylori Metaplastic epithelium is unsuitable for H. pylori colonization.colonization.
The associated hypochlorhydria encourages overgrowth by The associated hypochlorhydria encourages overgrowth by other bacterial speciesother bacterial species
EMAGEMAG Environmental metaplastic atrophic gastritis (EMAG) is Environmental metaplastic atrophic gastritis (EMAG) is
due to environmental factors, as diet (NITROSO due to environmental factors, as diet (NITROSO COMPOUNDS) & H. pylori infection, on the gastric COMPOUNDS) & H. pylori infection, on the gastric
mucosa.mucosa.
metaplastic atrophic metaplastic atrophic gastritisgastritis
Unlike AMAG, mucosal changes in patients with EMAG Unlike AMAG, mucosal changes in patients with EMAG affect both the corpus & antrum in a multifocal affect both the corpus & antrum in a multifocal distribution, but distribution, but with heaviest involvement of the antrum.with heaviest involvement of the antrum.
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
EMAG vs AMAGEMAG vs AMAG
• • Gastric acid production Gastric acid production does notdoes not disappear entirely disappear entirely • Serum gastrin • Serum gastrin is notis not elevated elevated • Parietal cell & intrinsic factor autoantibodies & pernicious • Parietal cell & intrinsic factor autoantibodies & pernicious anemia are anemia are absentabsent
Metaplastic atrophic Metaplastic atrophic gastritisgastritis
There is an increased risk for gastric ulcer compared to There is an increased risk for gastric ulcer compared to AMAG, presumably due to the accompanying AMAG, presumably due to the accompanying hypochlorhydria in the latter disorderhypochlorhydria in the latter disorder
CANCER
metaplastic atrophic metaplastic atrophic gastritisgastritis
Diagnosis of EMAG should not be made from biopsy Diagnosis of EMAG should not be made from biopsy specimens unless specimens unless at least 20 %at least 20 % of the available antral or of the available antral or transitional mucosa is replaced by metaplastic glands, or transitional mucosa is replaced by metaplastic glands, or there is unequivocal atrophy. there is unequivocal atrophy.
Hyperplastic Hyperplastic gastropathiesgastropathies
Proliferative, inflammatory, infiltrative conditions are associated with large folds due to excessive number of mucosal
epithelial cells
Large gastric folds > 1.0 Large gastric folds > 1.0 cm cm
Chronic gastritis/lymphoid hyperplasiaChronic gastritis/lymphoid hyperplasia Benign tumorsBenign tumors Gastric malignancy Gastric malignancy Zollinger-Ellison syndrome Zollinger-Ellison syndrome Menetrier's diseaseMenetrier's disease
Ménétrier's diseaseMénétrier's disease Epithelial hyperplasia Epithelial hyperplasia
involving the surface & involving the surface & foveolar mucous cells foveolar mucous cells
the oxyntic glands can be the oxyntic glands can be
normal or atrophic.normal or atrophic. Surgery has been Surgery has been
advocated for patients advocated for patients with intractable pain, with intractable pain, hypoalbuminemia with hypoalbuminemia with edema, hemorrhage, edema, hemorrhage, pyloric obstruction, & in pyloric obstruction, & in whom a malignancy whom a malignancy
cannot be excludedcannot be excluded
Zollinger-Ellison syndromeZollinger-Ellison syndrome
Increased numbers of parietal cells Increased numbers of parietal cells with no change in surface &foveolar with no change in surface &foveolar mucous cells. mucous cells.
Signs:Signs:
Multiple ulcersMultiple ulcersdiarrheadiarrheaulcer in atypical siteulcer in atypical siteresistant ulcerresistant ulcerenlarged foldsenlarged foldssevere esophagirtissevere esophagirtisFH of MEN1FH of MEN1
Hyperplastic Hyperplastic gastropathiesgastropathies
mixed-type in which both mucous mixed-type in which both mucous &oxyntic glandular cells show &oxyntic glandular cells show hyperplasia, may be seen in hyperplasia, may be seen in lymphocytic &H. pylori gastritis.lymphocytic &H. pylori gastritis.
Portal hypertensive Portal hypertensive gastropathygastropathy
Portal hypertensive gastropathy characteristically appears Portal hypertensive gastropathy characteristically appears as a fine white reticular pattern separating areas of pinkish as a fine white reticular pattern separating areas of pinkish mucosa on endoscopy, giving the gastric mucosa a mucosa on endoscopy, giving the gastric mucosa a ""snakeskinsnakeskin" appearance" appearance
Portal hypertensive Portal hypertensive gastropathygastropathy