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    Gastritis

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    Sri Wahyuni Harli
    This document discusses gastritis and Helicobacter pylori infection. It defines gastritis as inflammation of the stomach and notes that it increases in frequency with age. It then discusses various types of gastritis including acute, chronic, and specific types. Chronic gastritis is often caused by H. pylori infection, which can lead to ulcers and increases cancer risk long-term. The document outlines the pathophysiology, clinical presentation, diagnosis, and treatment of H. pylori infection.

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    Gastritis

    Uploaded by

    Sri Wahyuni Harli
    189 views17 pages
    This document discusses gastritis and Helicobacter pylori infection. It defines gastritis as inflammation of the stomach and notes that it increases in frequency with age. It then discusses various types of gastritis including acute, chronic, and specific types. Chronic gastritis is often caused by H. pylori infection, which can lead to ulcers and increases cancer risk long-term. The document outlines the pathophysiology, clinical presentation, diagnosis, and treatment of H. pylori infection.

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    This document discusses gastritis and Helicobacter pylori infection. It defines gastritis as inflammation of the stomach and notes that it increases in frequency with age. It then discusses various types of gastritis including acute, chronic, and specific types. Chronic gastritis is often caused by H. pylori infection, which can lead to ulcers and increases cancer risk long-term. The document outlines the pathophysiology, clinical presentation, diagnosis, and treatment of H. pylori infection.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    189 views17 pages

    Gastritis

    Uploaded by

    Sri Wahyuni Harli
    This document discusses gastritis and Helicobacter pylori infection. It defines gastritis as inflammation of the stomach and notes that it increases in frequency with age. It then discusses various types of gastritis including acute, chronic, and specific types. Chronic gastritis is often caused by H. pylori infection, which can lead to ulcers and increases cancer risk long-term. The document outlines the pathophysiology, clinical presentation, diagnosis, and treatment of H. pylori infection.

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    © All Rights Reserved
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    You are on page 1of 17

    Level of

    competent : 4

    GASTROPATHY/ GASTRITIS

    Definition : any disease or inflammation of the


    stomach
    Increased frequency with age

    Gastric carcinoma
    Surgery/chemothera
    py

    Gastric lymphoma
    Chemo/debulking
    agent

    Specific gastritis
    Eosinophilic gastritis :
    corticosteroid
    Granulomatous gastritis
    Portalhypertensive
    gastropathy : BB, nitrate,

    Hypertropic folds
    Zollinger-Ellison Syd

    Nonspesific gastritis
    Nonerosive gastritis :
    Type A & B
    Erosive gastritis : H.pylori

    GASTRITIS

    Acute gastritis is a term


    covering a broad spectrum of
    entities that induce
    inflammatory changes in the
    gastric mucosa
    Chronic gastritis is a
    histopathological entity
    characterized by chronic
    inflammation of the stomach The inflammation may involve the
    mucosa.
    entire stomach (eg, pangastritis) or
    a region of the stomach (eg, antral
    gastritis).

    Causes
    CHRONIC GASTRITIS :

    ACUTE GASTRITIS : certain


    drugs; alcohol; bacterial,
    viral, and fungal
    infections; acute stress
    (shock); radiation; allergy
    and food poisoning; bile;
    ischemia; and direct
    trauma.

    Infectious gastritis (bacterial,


    viral, and fungal infections)

    Noninfectious gastritis

    Chronic gastritis of
    undetermined etiology or
    gastritis of undetermined type

    H pylori infection - is the most common cause of


    chronic gastritis.

    Pathophysiology
    Acute/stress gastropathy
    NSAID, alcohol, corticosteroids
    Stress gastritis : any critical illness under perfusion, within 24 hours,
    GI bleeding 30% (respiratory failure, liver/renal disease with
    coagulopathy, sepsis, surgery/trauma(Cushings ulcer), burns
    (Curlings ulcer), CNS insult)

    Chronic gastritis

    Chronic Antral gastritis (Type B): H.pylori


    Chronic Fundal gastritis (Type A) : autoantibody against intrinsic factor
    & parietal cell loss intrinsic factor & achlorhydria

    Congestive gastropathy
    Cirrhosis & portal hypertension

    Clinical manifestation

    Many asymptomatic
    Dyspepsia (epigastric
    discomfort), N/V,
    postprandial fullness,
    bloating, occasionally
    GI bleeding

    Diagnostic study

    EGD : scattered
    mucosal erosion
    or foci of
    intramucosal
    hemorrage

    Treatment

    Increased stomach
    pH>4 (pepsin is
    inactivated & blood
    coagulation is
    enhanced) : Proton
    pump inhibitor
    drugs & supportive
    measures

    Helicobacter pylori (Hp)

    Flagellated gram negative bacilli


    with urease activity :
    hydrolyzes urea >> ammonia
    (NH3) & CO2 (help resist
    stomatch acid)
    Transmission : fecal-oral, oral-oral
    and most infection acquired in
    childhood
    Natural habit :
    gastric mucosa of the antrum,
    if found in duodenum,
    associated with metaplastic
    gastric epithelium

    90% duodenal ulcer and


    70% gastric ulcer

    Pathophysiology

    Inflammation
    Toxin : vacuolating
    cytotoxin (VacA),
    cytotoxin-associated
    gene A (CagA)
    Acid

    Moayyedi P. In Clinical Gastroenterology and Hepatology. 2005; p.2

    Clinical
    presentation

    Majority individuals
    (app. 80%) remain
    asymptomatic
    Small subset patients
    : dyspeptic
    symptoms (epigastric
    pain, fullness, early
    satiety & nausea)

    Diagnostic
    methods
    Performed only if treatment
    intended
    INVASIVE TEST
    Endoscopic
    Rapid urease/CLO (>95%)
    Biopsy/histology using HE
    (>95%)
    Biopsy/culture ( highly
    spesific only)

    NON-INVASIVE TEST

    UBT = urea breath test


    (> 90%)
    Serology IgG Anti-Hp
    serum (85-90%), urine
    (85%), saliva +IgA (7085%)
    Stool test Ag Hp= HpSA
    (>95%)

    Treatment

    Complication

    In 1994, WHO classified


    H.pylori as group I
    carcinogen3-6 fold higher
    incidence of gastric ca.
    Strong association with
    mucosal associated
    Lymphoid tumors (MALT) :
    treatment Hp
    regression/cure 90%
    patient

    With acid hyposecretion (left),


    the main effect of H pylori
    gastritis affecting the gastric
    body is to suppress parietal cells,
    leading to low acid secretion,
    which is associated with gastric
    cancer. With acid hypersecretion
    (right), antral H pylori gastritis
    increases acid secretion by
    suppressing somatostatin and
    elevating gastrin release,
    increasing the risk of duodenal
    ulceration. Orange areas indicate
    extent and location of gastritis

    Autoregulation of acid
    secretion. Food stimulates
    release of gastrin from antral
    G cells (G). Gastrin stimulates
    enterochromaffin-like cells
    (ECL) to release histamine,
    which stimulates parietal cells
    (P) in the gastric corpus to
    secrete acid. Acid stimulates
    release of somatostatin from
    somatostatin cells (S) in the
    antrum, inhibiting further
    gastrin release

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