Git 4th 5th Gastritis

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


GASTRITIS


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


GASTRITIS


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


GASTRITIS


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


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.


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.


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


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.


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.


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.


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


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


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

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Git 4th 5th Gastritis