Git 4th 5th Gastritis.
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Git 4th 5th Gastritis.

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Medical college lectures: GIT 4th year.

Medical college lectures: GIT 4th year.

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Git 4th 5th Gastritis. Git 4th 5th Gastritis. Presentation Transcript

  • Gastritis Dr.Mohammad Shaikhani Assistant professor Sulaimanyah College of Medicine.
  • Definition
    • Inflammation associated with mucosal injury
    • A histological term that needs biopsy to be confirmed.
    • Usually due to infectious agents (As H pylori) , autoimmune & hypersensitivity reactions.
    • Endoscopic mucosal changes of gastritis, 27% had a normal endoscopic biopsy specimen& a normal endoscopic appearance, 63 % had histological evidence of gastritis.
  • Definition
    • “ Gastropathy “: Epithelial cell damage /regeneration without inflammation.
    • Gastropathy may be referred without histological evidence, according to gross appearance in endoscopy or radiology.
    • Gastropathy usually caused by irritants as drugs (eg, NSAIDs& alcohol), bile reflux, hypovolemia &chronic congestion.
  • Gross–histologic correlation?
  • Classification
      • Acute: short term inflammation with neurophilic infiltrate
      • Chronic:long standing with mononuclear cell infiltrate especially lymphocyte/maccrophages
  • Anatomical site ANTRUM CARDIA BODY MUCOUS SECRETING ENDOCRINE SPECIALISED SECRETORY: PARIETAL - ACID CHIEF - PEPSINOGEN ENDOCRINE HIST, SOMASTATIN MUCOUS SECRETING ENDOCRINE GASTRIN, 5HT
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  • CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID
  • CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID
  • Acute hemorrhagic erosive
    • (NSAIDs, alcohol, or bile acids)
    • Mucosal hypoxia (trauma, burns [Curling's ulcers],sepsis)
    • Combination of factors as antineoplastic chemotherapy
    • Gastric/duodenal ulcers occurring during severe damage to CNS (Cushing's ulcers).
  • ACUTE GASTRITIS - MORPHOLOGY Mucosal congestion, oedema, inflammation, ulceration & Bleeding.
  • Acute hemorrhagic erosive
    • NSAID-induced acute hemorrhagic& erosive gastropathy due to inhibition of prostaglandin production .
    • Prostaglandins protect mucosa by several mechanisms, as stimulation of mucus / bicarbonate secretion&maintenance of mucosal blood flow
    • Hemorrhagic or erosive gastropathy may be associated with the development of gastric or duodenal ulcers.
  • NSAID GI toxicity risk factor
    • H/O adverse GI event (ulcer, hemorrhage) *5 increases.
    • Age >60 increases risk *6.
    • High (> twice normal) dosage of a NSAID increases risk *10.
    • Concurrent use of glucocorticoids increases risk *5.
    • Concurrent use of anticoagulants increases risk *10- 15.
  • HP/NSAID
    • If H/O uncomplicated or complicated peptic ulcers (gastric, duodenal) should be tested for H. pylori prior to beginning a NSAID or low dose aspirin .
    • If present, H. pylori should be treated with appropriate therapy, even if it is believed that the prior ulcer was due to NSAIDs.
  • NSAID-related GIT toxicity prophylaxis
    • COX-2 selective inhibitor.
    • Misoprostol
    • PPI as lansoprazole .
  • Stress ulcer pathophysiology
    • Hypersecretion of acid –head trauma.
    • Defects in gastric glycoprotein mucus –In critically ill patients, increased refluxed bile salts or uremic toxins can denude the glycoprotein mucous barrier
    • Ischemia – Shock, sepsis, trauma can lead to impaired perfusion of the gut.
  • Stress ulcer risk factors
    • 2 major risk factors for clinically significant bleeding due to stress ulcers are:
    • Mechanical ventilation for > 48 hours & coagulopathy .
    • • Shock • Sepsis • Hepatic failure • Renal failure • Multiple trauma • Burns >35% total body surface area • Organ transplant recipients • Head or spinal trauma • H/O peptic ulcer disease or upper GI bleeding
  • Common type of gastritides
  • CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID
  • H Pylori
    • A spiral shaped, microaerophilic, gram negative bacterium measuring 3.5 length* 0.5 microns in width
    • urease forms ammonia & bicarbonate that neutralize gastric acid& form a protective cloud around the organism
    • Urease appears to be vital for its survival & colonization.
    • Spiral shape, flagella facilitate its passage through the mucus layer
    • Helicobacter pylori is the most common chronic bacterial 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 bacterial acquisition during childhood years &affected by:
    • Density of housing.
    • Overcrowding
    • Number of siblings.
    • Sharing a bed.
    • Lack of running water.
  •  
  •  
    • The route by which infection occurs remains unknown.
    • Person-to-person transmission by either fecal/oral or oral/oral exposure seems most likely
    • Humans appear to be the major reservoir of infection
    • Isolated from primates from domestic cats & in milk/ gastric tissue of sheep
  • Vac A & Cag A
    • Vacuolating cytotoxin (VacA) causes cell injury in vitro & gastric tissue damage in vivo .
    • All H. pylori contain the gene coding for VacA; but, only some strains have cytotoxin-associated gene A (cagA)
    • Strains producing VacA & CagA cause more intense tissue inflammation&induce cytokine production
    • 85-100% with duodenal ulcers have CagA+ strains, compared to 30-60% of infected patients who do not develop ulcers
    • CagA strains may be associated with a higher frequency of precancerous lesions.
    • Host polymorphism of IL-1 beta (&possibly IL-10) appears to determine the degree of inflammatory response to infection, resulting alteration in acid secretion (hyper or hypo secretion)&risk for subsequent gastric cancer
  • HP
    • The inflammation usually superficial, located in the gastric pit & upper portion of the lamina propria, , consists of mononuclear cells & polymorphonuclear leukocytes, commonly termed chronic active inflammation .
    • The antrum consistently is involved, whereas inflammation in the acid-secreting gastric body &fundus is more variable.
    • H. pylori is causally associated with gastritis, duodenal &gastric ulcer, gastric adenocarcinoma&primary gastric B-cell lymphomas of mucosa-associated lymphoid tissue (MALT)
    • Infected subjects have 1/6 lifetime risk of peptic ulcer; the lifetime risk of gastric cancer varies from 1-3% - > 12% in Japan.
    • DISTRIBUTION & PROGRESSION: Antral- DU& Pangastritis-GASTRIC CA.
  • HP: diagnosis
    • Serology with ELISA for IgG or IgA antibodies, 13C-urea or 14C-urea breath tests, or stool antigen testing.
    • Tests requiring endoscopy&biopsy include histologic exam , urease testing of antral biopsy specimens, or culture.
    • The optimal method depends on circumstances, local expertise, /availability.
    • All tests have good sensitivity/specificity, but false-positive/false-negative determinations occur.
    • In tests that depend on the No of organisms (breath &gastric biopsy specimens for urease activity, histology& culture), false-negative occur esp when the organism suppressed by antibiotics, PPI, or bismuth.
    • Therapy may need to be discontinued for several weeks before these tests become positive.
  • HP:Trt
    • H. pylori infection is typically latent.
    • H. pylori gastritis is found more frequently, in patients with dyspepsia.
    • Cure of the infection resolves symptoms in only 10% of patients with nonulcer dyspepsia.
    • Antibiotic therapy for H. pylori is recommended because:
    • Less expensive & safer than additional diagnostic studies & long-term continuous antacid therapy.
    • Cure of the inf reduces the risk of subsequent PUD &gastric ca.
    • Eliminates the individual as a carrier who can transmit the infection.
    • H. pylori testing&treatment are appropriate for new-onset or previously undiagnosed dyspepsia without alarm features .
  • Bile reflux gastropathy
    • Bile reflux gastropathy results from the regurgitation of bile into the stomach because of:
    • An operative stoma.
    • An incompetent pyloric sphincter
    • Abnormal duodenal motility
    • The effect of bile salts on gastric mucosa is comparable to that seen after chronic NSAID use
    • Chronic metaplastic gastritides
  • CLASSIFICATION GASTRITIS ACUTE COMMON CHRONIC EMAG AMAG BILE HP STRESS NSAID
  • Metaplastic atrophic gastritis
    • Metaplasia, especially intestinal type, is virtually a universal feature of atrophic gastritis.
    • Metaplasia is highly relevant to the pathogenesis of atrophic gastritis & to its complications (eg, pernicious anemia, gastric ulcer, gastric cancer).
  • metaplastic atrophic gastritis
    • AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITIS (AMAG) is an inherited form that is associated with an immune response in the oxyntic mucosa directed against parietal cells &intrinsic factor.
    • AMAG is inherited as an autosomal dominant disorder
  • SYNONYMS OF AMAG
    • TYPE A GASTRITIS
    • AUTOIMMUNE GASTRITIS
    • DIFFUSE CORPORAL GASTRITIS
  • Metaplastic atrophic gastritis
    • The chronic inflammation, gland atrophy, epithelial metaplasia of AMAG are closely paralleled by elevated serum antibodies to parietal cells & intrinsic factor, reflecting its autoimmune origin.
  •  
  • Metaplastic atrophic gastritis
    • The loss of parietal cell mass leads to profound hypochlorhydria, while the inadequate production of intrinsic factor leads to vitamin B12 malabsorption& pernicious anemia.
  • Metaplastic atrophic gastritis
    • Patients with AMAG are at increased risk for the development of gastric carcinoid tumors& adenocarcinoma.
    CANCER
  • Metaplastic atrophic gastritis
    • surveillance strategy for patients diagnosed with pernicious anemia
    • • Upper endoscopy soon after diagnosis
    • • Removal of gastric polyps if possible; most of these polyps will be benign
    • • Frequent reinvestigation in patients whose polyps are not removed or who have severe mucosal dysplasia; in the remaining patients follow-up endoscopies should be performed at approximately five-year intervals.
  • metaplastic atrophic gastritis
    • Patients with AMAG are less likely to be infected by H. pylori than aged-matched controls:
    • Metaplastic epithelium is unsuitable for H. pylori colonization.
    • The associated hypochlorhydria encourages overgrowth by other bacterial species
  • EMAG
    • Environmental metaplastic atrophic gastritis (EMAG) is due to environmental factors, as diet (NITROSO COMPOUNDS) & H. pylori infection, on the gastric mucosa.
  • metaplastic atrophic gastritis
    • Unlike AMAG, mucosal changes in patients with EMAG affect both the corpus & antrum in a multifocal distribution, but with heaviest involvement of the antrum.
  • Metaplastic atrophic gastritis
    • EMAG vs AMAG
    • • Gastric acid production does not disappear entirely • Serum gastrin is not elevated • Parietal cell & intrinsic factor autoantibodies & pernicious anemia are absent
  • Metaplastic atrophic gastritis
    • There is an increased risk for gastric ulcer compared to AMAG, presumably due to the accompanying hypochlorhydria in the latter disorder
    CANCER
  • metaplastic atrophic gastritis
    • Diagnosis of EMAG should not be made from biopsy specimens unless at least 20 % of the available antral or transitional mucosa is replaced by metaplastic glands, or there is unequivocal atrophy.
  • Hyperplastic gastropathies Proliferative, inflammatory, infiltrative conditions are associated with large folds due to excessive number of mucosal epithelial cells
  • Large gastric folds > 1.0 cm
    • Chronic gastritis/lymphoid hyperplasia
    • Benign tumors
    • Gastric malignancy
    • Zollinger-Ellison syndrome
    • Menetrier's disease
  • Ménétrier's disease
    • Epithelial hyperplasia involving the surface & foveolar mucous cells
    • the oxyntic glands can be normal or atrophic.
    • Surgery has been advocated for patients with intractable pain, hypoalbuminemia with edema, hemorrhage, pyloric obstruction, & in whom a malignancy cannot be excluded
  • Zollinger-Ellison syndrome Increased numbers of parietal cells with no change in surface &foveolar mucous cells. Signs: Multiple ulcers diarrhea ulcer in atypical site resistant ulcer enlarged folds severe esophagirtis FH of MEN1
  • Hyperplastic gastropathies
    • mixed-type in which both mucous &oxyntic glandular cells show hyperplasia, may be seen in lymphocytic &H. pylori gastritis.
  • Portal hypertensive gastropathy
    • Portal hypertensive gastropathy characteristically appears as a fine white reticular pattern separating areas of pinkish mucosa on endoscopy, giving the gastric mucosa a " snakeskin " appearance
  • Portal hypertensive gastropathy