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Gastritis final
Aamir Sharif,
      BEMS 4th Professional
Department of Eastern Medicine & Surgery
Stomach
   3 muscle layers
     Oblique
     Circular
     Longitudinal
   Regions
       Cardiac sphincter
       Fundus
       Antrum (pylorus)
       Pyloric sphincter
   Vascular
   Inner surface thrown into
    folds – Rugae
   Contains enzymes that work
    best at pH 1-2                    3
Normal Stomach Anatomy
Stomach - Normal
Stomach - Normal
Stomach
   Functions                       Absorbs
     Mix food                         Alcohol
     Reservoir                        Water
     Start digestion of
                                       Lipophilic acid
           Protein
                                       B 12
           Nucleic acids
           Fats
     Activates some enzymes
     Destroy some bacteria
     Makes intrinsic factor – B
      12 absorption
     Destroys some bacteria


                                                          7
Inflammatory
Disease of Stomach
Definition
 The    term gastritis is used to denote
    inflammation associated with
    mucosal injury.
 Gastritis is mostly a histological term that
  needs biopsy to be confirmed.
 Gastritis is usually due to infectious
  agents (such as Helicobacter pylori) and
  autoimmune and hypersensitivity
  reactions.
Definition
   Epithelial cell damage and regeneration
    without associated inflammation is
    properly referred to as "gastropathy.―
   Gastropathy may be referred without
    histological evidence and just according to
    gross appearance in endoscopy or radiology
   Gastropathy is usually caused by irritants such
    as drugs (e.g., nonsteroidal anti-inflammatory
    agents and alcohol), bile reflux, hypovolemia,
    and chronic congestion.
Sex:

   Male-to-female ratio of gastritis is approximately1:1

   Male-to-female ratio of PUD is approximately 2:1
Pathophysiology
    The mechanisms of mucosal injury in gastritis is thought
    to be an imbalance of
           aggressive factors

    acid production or pepsin

and
          defensive factors

    mucus production
   bicarbonate
   and blood flow
Protective factors vs. hostile factors
Gastritis



Acute     Chronic
Acute & Chronic Difference


 Acute refers to short term inflammation
 Acute refering to neurophilic infiltrate

 Chronic referring to long standing forms
 Chronic referring to mononuclear cell
  infiltrate especially lymphocyte and
  macrophages
Acute Gastritis

 Definition

   An acute mucosal inflammatory
    process, with neutrophilic infiltrate,
    that is usually transient.
   There may be hemorrhage into the
    mucosa or sloughing of the mucosa.
   Severe erosive form is an important
    cause of severe GI bleeding
 Etiology
  Frequently associated with, among others:
    heavy use of NSAIDS, especially aspirin

    excessive alcohol consumption

    heavy smoking

    severe stress e.g. trauma, burns,
     surgery
    Ischemia

    Systemic infection

  Often, idiopathic
NSAIDs

 NSAIDs   and aspirin also
 interfere with the protective
 mucus layer by inhibiting
 mucosal cyclooxygenase activity,
 reducing levels of mucosal
 prostaglandins
Smoking
       Promotes gastritis & ulcer occurrence
       Increases the likelihood of
                ulcer complications

       Mechanisms
         Stimulate gastric acid secretion
         Stimulate bile salt reflux
         Causes alteration in mucosal blood flow
         Decrease mucus secretion
         Reduces prostaglandin synthesis
         Decrease pancreatic bicarbonate secretion
Effects of Diet and Stress

 Diet and Stress                    Action

Diet               Dyspepsia, may pain - not believed
                   to cause ulcer or assist healing


Physiologic        ↓ mucosal blood flow, tissue hypoxia,
stress             mucosal lining degradation; e.g. ICU,
                   sepsis, burn, trauma. Associated with
                   multiple erosions & significant bleeding
Etiology of
Gastritis
A) Normal
B) Increased
Attack
*Hcl
*Pepsin.
*NSAIDs.
C) Weak defense
*Helicobacter pylori
*Stress, drugs, smoking
Acute Gastritis - Pathogenesis


                             Acid secretion    +    Bicarbonate
All above Factor
                            + back diffusion           buffer


                                                       +

    Direct              Disruption
   Mucosal         +        of                     Blood flow
    Injury             Mucus layer




                         Acute Gastritis
Stages of Acute Gastritis

    Acute superficial           Acute erosive
         gastritis                   gastritis
    Inflammation of         Destruction of multiple
     superficial gastric         small zones of
         mucosa.              superficial mucosa.




              Acute Gastric Ulceration
              

      Destruction of full thickness of mucosa
ACUTE GASTRITIS -
  MORPHOLOGY
Mucosal congestion ,edema
 inflammation & ulceration
Acute Gastritis - Morphology
Ranges from edema with neutrophil infiltration, vascular congestion,&
an intact epithelium, to erosion (mucosal defect that does not cross
the muscularis mucosa) and hemorrhage.
Acute Gastritis




   Gastric mucosa
    demonstrates
    infiltration by
    Neutrophils
Acute Gastritis



   diffusely hyperemic
    gastric mucosa
   causes for acute
    gastritis
     alcoholism
     drugs
     infections, etc.
Acute Gastritis
   Clinical Features
     broad range of signs and symptoms that depend
      on the severity of the condition
        Asymptomatic

        Epigastric pain, nausea & vomiting
        Hemorrhage, massive hematemesis, melena, or
         fatal blood loss
     One of the major causes of massive
      hematemesis, particularly in alcoholics.
     ~25% patients taking aspirin for rheumatoid
      arthritis will develop acute gastritis, and some
      will bleed
Complications:

   Malignancy

   Hemorrhage

   Perforation

   Obstruction
Chronic Gastritis
   Definition

     Chronic mucosal inflammatory changes leading
      to atrophy and metaplasia (usually without
      erosions)



   Dysplasia and ultimate neoplasia are
    complications.
Chronic
            Gastritis



Type B                Type A
 Antral             Autoimmune
Gastritis             gastritis
Type B (Antral Gastritis)
     90% of patients with antral chronic gastritis:
      Helicobacter pylori infected
        Motile, gram negative curvilinear rods that
         elaborate urease (buffers gastric acid) & toxins
         and have adhesins to bind to the epithelium.
   Pathogenesis
     H. pylori (urease   NH4+ + toxins) + Host (acid
      + peptic enzymes)     Chronic Inflammation
     Antibodies     Gland destruction + Mucosal
      atrophy        acid   intrinsic factor (which can
      lead to pernicious anemia)
Helicobacter gastritis
   2 patterns of infection
     Diffuse involvement of body and antrum (―pan
      gastritis‖ associated with diminishing acid
      output)
     Infection confined to antrum (antral gastritis,
      associate with increased acid output)
Helicobacter pylori

   Adapted to live in
    association with
    surface epithelium
    beneath mucus barrier
   Causes cell damage
    and inflammatory cell
    infiltration
   In most countries the
    majority of adults are
    infected
H. pylori Gastritis - Morphology




        H. pylori organisms along
        superficial mucus layer of
        antral biopsy

                                     Web Path
Bile reflux gastropathy
   Bile reflux gastropathy typically results from the
    regurgitation of bile into the stomach because
    of an operative stomach, an incompetent
    pyloric sphincter, or abnormal duodenal motility.



   The effect of bile salts on gastric mucosa is
    comparable to that seen after chronic NSAID
    use
Chemical gastritis

   Commonly seen with bile
    reflux (toxic to cells)
   Prominent hyperplastic
    response (inflammatory
    cells scanty)
   With time – intestinal
    metaplasia
Clinical Features
Usually only a few symptoms:

   nausea, vomiting, upper abdominal discomfort


   Most  infected person have gastritis, but
    are asymptomatic
   Hypochlorhydria, but NOT achlorhydria
    and pernicious anemia (parietal cells
    never completely destroyed)
   Gastrin normal to slightly elevated
   Antibiotics are treatment of choice
Clinical Complications
 H. pylori
   H. pylori predisposes to peptic ulcers
    in duodenum and stomach—Most
    patients with a peptic ulcer are
    infected.
   Risk of gastric carcinoma and
    lymphoma
Type A (Auto immune)
 Etiology


   Autoimmune - antibodies to parietal cells,
    gastrin receptor, intrinsic factor, and H+,K+
    ATPase
     <10% of cases of chronic gastritis

     Possible autosomal dominant
      inheritance
Morphology of chronic gastritis

 Chronic inflammatory cell
  infiltration
 Mucosal atrophy

 Intestinal (goblet cell)
  metaplasia
Seen in Helicobacter and
  autoimmune gastritis (not
  chemical)
Autoimmune gastritis


   Autoimmune gastritis -
    pernicious anemia
   Chronic atrophic
    gastritis is associated
    with Ab’s
    - intrinsic factor
    - patietal cell
   bright green IF- in the
    parietal cells of the
    gastric mucosa.
Autoimmune Gastritis -Morphology
Diffuse mucosal damage of the body and fundic
mucosa. Antrum less involved.




                    PJ Goldblatt, MD
Chronic Gastritis
   Clinical Features
     Usually only a few symptoms: nausea,
      vomiting, upper abdominal discomfort

     Autoimmune
       Hypo to achlorhydria (severe loss of
        parietal glands)
       Hypergastrinemia
       10% have pernicious anemia
Clinical Complications

 Autoimmune:
   Often seen in association with other
    autoimmune disorders (Hashimoto
    thyroiditis, Addison disease, and type I
    diabetes)
   Significant risk for the development of
    gastric carcinoma (2-4%) and
    endocrine tumors (carcinoid tumor)
Chronic Gastritis
 Morphology
  Varying degrees of mucosal damage
   possible
  Mucosal lesions are reddened, with
   thickened rugae
  Atrophied rugae in long-standing cases
  Lymphocytes and plasma cell infiltrate;
   neutrophils indicate ―active‖ inflammation
   (may or may not be present)
 Regeneration - constant feature
 Metaplasia - mucosa of antral and
  body-fundic regions converts to
  columnar absorptive cells and goblet
  cells (intestinal metaplasia)
 Atrophy - marked loss of glands
 Dysplasia – precursor lesion to
  gastric cancer in atrophic gastritis
Hypertrophic gastritis
     Three variants are recognized

   Menetrier’s disease

   Hypersecretory gastropathy

   Gastric gland hyperplasia
    [the Zollinger-Ellison syndrome]
Hyperplastic gastropathies

proliferative,
inflammatory, and
infiltrative
conditions are
associated with
large folds due to
excessive number
of mucosal
epithelial cells
Ménétrier's disease
   Epithelial hyperplasia
    involving the surface
    and foveolar mucous
    cells (i.e., foveolar
    hyperplasia); the
    oxyntic glands can be
    normal or atrophic.
Zollinger-Ellison syndrome


Increased numbers
of parietal cells
with no change in
surface and
foveolar mucous
cells.
Hyperplastic gastropathies
mixed-type in which
both mucous and
oxyntic glandular
cells show
hyperplasia, may be
seen in as
lymphocytic and H.
pylori gastritis.
   Stomach
   Acute Gastritis= inflammation of gastric mucosa
     acute – presence of neutrophils
     Chronic –lymphocytes and plasma cells
   Caused by ingestion of strong acids or alkalies, NSAIDs,
    cancer chemotherapy, irradiation, alcohol, uremia, severe
    stress & shock states
   Proposed mechanisms: ↑ acid production with ↓ surface
    bicarbonate buffer
   Morphology: Mucosal edema, hyperemia, PML infiltration,
    erosions (not deeper than muscularis mucosa) &
    hemorrhages
   Stomach
   Chronic Gastritis = Chronic mucosal inflammation
   Leading to mucosal atrophy, intestinal metaplasia &
    dysplasia.
   Pathogenesis:
   Chronic infection by Helicobacter pylori (90%): MCC of
    chronic gastritis, Elaboration of urease  produces
    ammonia that buffers gastric acid, protecting organism from
    acid
   Other diseases associated with H. pylori Infection
     Peptic ulcer disease
     Gastric carcinoma
     Gastric lymphoma
   Autoimmunity (>10%): Antibodies to parietal cells cause
    parietal cell destruction (HCl & intrinsic factor)
   Stomach
   Chronic Gastritis
   Morphology:
      Autoimmune diffuse mucosal damage of the body-fundic
       mucosa
      H. pylori affect antral mucosa
   Histology: Lymphocytic & plasma cell infiltrate of the lamina propria
      atrophy, regeneration, metaplasia (to intestinal type mucosa) &
       dysplasia.
      H. pylori detected on the mucosal surface
   Clinically:
      Mild abdominal discomfort, nausea, vomiting; hypochlorhydria,
       hypergastrinemia & rarely
      Overt pernicious anemia (in autoimmune) gastritis).
   Long-term risk of cancer is 2-4%
Gastritis final
Gastritis final

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Gastritis final

  • 2. Aamir Sharif, BEMS 4th Professional Department of Eastern Medicine & Surgery
  • 3. Stomach  3 muscle layers  Oblique  Circular  Longitudinal  Regions  Cardiac sphincter  Fundus  Antrum (pylorus)  Pyloric sphincter  Vascular  Inner surface thrown into folds – Rugae  Contains enzymes that work best at pH 1-2 3
  • 7. Stomach  Functions  Absorbs  Mix food  Alcohol  Reservoir  Water  Start digestion of  Lipophilic acid  Protein  B 12  Nucleic acids  Fats  Activates some enzymes  Destroy some bacteria  Makes intrinsic factor – B 12 absorption  Destroys some bacteria 7
  • 9. Definition  The term gastritis is used to denote inflammation associated with mucosal injury.  Gastritis is mostly a histological term that needs biopsy to be confirmed.  Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.
  • 10. Definition  Epithelial cell damage and regeneration without associated inflammation is properly referred to as "gastropathy.―  Gastropathy may be referred without histological evidence and just according to gross appearance in endoscopy or radiology  Gastropathy is usually caused by irritants such as drugs (e.g., nonsteroidal anti-inflammatory agents and alcohol), bile reflux, hypovolemia, and chronic congestion.
  • 11. Sex:  Male-to-female ratio of gastritis is approximately1:1  Male-to-female ratio of PUD is approximately 2:1
  • 12. Pathophysiology The mechanisms of mucosal injury in gastritis is thought to be an imbalance of aggressive factors  acid production or pepsin and defensive factors  mucus production  bicarbonate  and blood flow
  • 13. Protective factors vs. hostile factors
  • 14. Gastritis Acute Chronic
  • 15. Acute & Chronic Difference  Acute refers to short term inflammation  Acute refering to neurophilic infiltrate  Chronic referring to long standing forms  Chronic referring to mononuclear cell infiltrate especially lymphocyte and macrophages
  • 16. Acute Gastritis  Definition  An acute mucosal inflammatory process, with neutrophilic infiltrate, that is usually transient.  There may be hemorrhage into the mucosa or sloughing of the mucosa.  Severe erosive form is an important cause of severe GI bleeding
  • 17.  Etiology  Frequently associated with, among others: heavy use of NSAIDS, especially aspirin excessive alcohol consumption heavy smoking severe stress e.g. trauma, burns, surgery Ischemia Systemic infection  Often, idiopathic
  • 18. NSAIDs  NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins
  • 19. Smoking  Promotes gastritis & ulcer occurrence  Increases the likelihood of ulcer complications  Mechanisms  Stimulate gastric acid secretion  Stimulate bile salt reflux  Causes alteration in mucosal blood flow  Decrease mucus secretion  Reduces prostaglandin synthesis  Decrease pancreatic bicarbonate secretion
  • 20. Effects of Diet and Stress Diet and Stress Action Diet Dyspepsia, may pain - not believed to cause ulcer or assist healing Physiologic ↓ mucosal blood flow, tissue hypoxia, stress mucosal lining degradation; e.g. ICU, sepsis, burn, trauma. Associated with multiple erosions & significant bleeding
  • 21. Etiology of Gastritis A) Normal B) Increased Attack *Hcl *Pepsin. *NSAIDs. C) Weak defense *Helicobacter pylori *Stress, drugs, smoking
  • 22. Acute Gastritis - Pathogenesis Acid secretion + Bicarbonate All above Factor + back diffusion buffer + Direct Disruption Mucosal + of Blood flow Injury Mucus layer Acute Gastritis
  • 23. Stages of Acute Gastritis  Acute superficial  Acute erosive gastritis gastritis Inflammation of Destruction of multiple superficial gastric small zones of mucosa. superficial mucosa. Acute Gastric Ulceration  Destruction of full thickness of mucosa
  • 24. ACUTE GASTRITIS - MORPHOLOGY Mucosal congestion ,edema inflammation & ulceration
  • 25. Acute Gastritis - Morphology Ranges from edema with neutrophil infiltration, vascular congestion,& an intact epithelium, to erosion (mucosal defect that does not cross the muscularis mucosa) and hemorrhage.
  • 26. Acute Gastritis  Gastric mucosa demonstrates infiltration by Neutrophils
  • 27. Acute Gastritis  diffusely hyperemic gastric mucosa  causes for acute gastritis  alcoholism  drugs  infections, etc.
  • 28. Acute Gastritis  Clinical Features  broad range of signs and symptoms that depend on the severity of the condition  Asymptomatic  Epigastric pain, nausea & vomiting  Hemorrhage, massive hematemesis, melena, or fatal blood loss  One of the major causes of massive hematemesis, particularly in alcoholics.  ~25% patients taking aspirin for rheumatoid arthritis will develop acute gastritis, and some will bleed
  • 29. Complications:  Malignancy  Hemorrhage  Perforation  Obstruction
  • 30. Chronic Gastritis  Definition  Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions)  Dysplasia and ultimate neoplasia are complications.
  • 31. Chronic Gastritis Type B Type A Antral Autoimmune Gastritis gastritis
  • 32. Type B (Antral Gastritis)  90% of patients with antral chronic gastritis: Helicobacter pylori infected  Motile, gram negative curvilinear rods that elaborate urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium.  Pathogenesis  H. pylori (urease NH4+ + toxins) + Host (acid + peptic enzymes) Chronic Inflammation  Antibodies Gland destruction + Mucosal atrophy acid intrinsic factor (which can lead to pernicious anemia)
  • 33. Helicobacter gastritis  2 patterns of infection  Diffuse involvement of body and antrum (―pan gastritis‖ associated with diminishing acid output)  Infection confined to antrum (antral gastritis, associate with increased acid output)
  • 34. Helicobacter pylori  Adapted to live in association with surface epithelium beneath mucus barrier  Causes cell damage and inflammatory cell infiltration  In most countries the majority of adults are infected
  • 35. H. pylori Gastritis - Morphology H. pylori organisms along superficial mucus layer of antral biopsy Web Path
  • 36. Bile reflux gastropathy  Bile reflux gastropathy typically results from the regurgitation of bile into the stomach because of an operative stomach, an incompetent pyloric sphincter, or abnormal duodenal motility.  The effect of bile salts on gastric mucosa is comparable to that seen after chronic NSAID use
  • 37. Chemical gastritis  Commonly seen with bile reflux (toxic to cells)  Prominent hyperplastic response (inflammatory cells scanty)  With time – intestinal metaplasia
  • 38. Clinical Features Usually only a few symptoms: nausea, vomiting, upper abdominal discomfort  Most infected person have gastritis, but are asymptomatic  Hypochlorhydria, but NOT achlorhydria and pernicious anemia (parietal cells never completely destroyed)  Gastrin normal to slightly elevated  Antibiotics are treatment of choice
  • 39. Clinical Complications  H. pylori H. pylori predisposes to peptic ulcers in duodenum and stomach—Most patients with a peptic ulcer are infected. Risk of gastric carcinoma and lymphoma
  • 40. Type A (Auto immune)  Etiology  Autoimmune - antibodies to parietal cells, gastrin receptor, intrinsic factor, and H+,K+ ATPase <10% of cases of chronic gastritis Possible autosomal dominant inheritance
  • 41. Morphology of chronic gastritis  Chronic inflammatory cell infiltration  Mucosal atrophy  Intestinal (goblet cell) metaplasia Seen in Helicobacter and autoimmune gastritis (not chemical)
  • 42. Autoimmune gastritis  Autoimmune gastritis - pernicious anemia  Chronic atrophic gastritis is associated with Ab’s - intrinsic factor - patietal cell  bright green IF- in the parietal cells of the gastric mucosa.
  • 43. Autoimmune Gastritis -Morphology Diffuse mucosal damage of the body and fundic mucosa. Antrum less involved. PJ Goldblatt, MD
  • 44. Chronic Gastritis  Clinical Features  Usually only a few symptoms: nausea, vomiting, upper abdominal discomfort  Autoimmune Hypo to achlorhydria (severe loss of parietal glands) Hypergastrinemia 10% have pernicious anemia
  • 45. Clinical Complications  Autoimmune: Often seen in association with other autoimmune disorders (Hashimoto thyroiditis, Addison disease, and type I diabetes) Significant risk for the development of gastric carcinoma (2-4%) and endocrine tumors (carcinoid tumor)
  • 46. Chronic Gastritis  Morphology  Varying degrees of mucosal damage possible  Mucosal lesions are reddened, with thickened rugae  Atrophied rugae in long-standing cases  Lymphocytes and plasma cell infiltrate; neutrophils indicate ―active‖ inflammation (may or may not be present)
  • 47.  Regeneration - constant feature  Metaplasia - mucosa of antral and body-fundic regions converts to columnar absorptive cells and goblet cells (intestinal metaplasia)  Atrophy - marked loss of glands  Dysplasia – precursor lesion to gastric cancer in atrophic gastritis
  • 48. Hypertrophic gastritis Three variants are recognized  Menetrier’s disease  Hypersecretory gastropathy  Gastric gland hyperplasia [the Zollinger-Ellison syndrome]
  • 49. Hyperplastic gastropathies proliferative, inflammatory, and infiltrative conditions are associated with large folds due to excessive number of mucosal epithelial cells
  • 50. Ménétrier's disease  Epithelial hyperplasia involving the surface and foveolar mucous cells (i.e., foveolar hyperplasia); the oxyntic glands can be normal or atrophic.
  • 51. Zollinger-Ellison syndrome Increased numbers of parietal cells with no change in surface and foveolar mucous cells.
  • 52. Hyperplastic gastropathies mixed-type in which both mucous and oxyntic glandular cells show hyperplasia, may be seen in as lymphocytic and H. pylori gastritis.
  • 53. Stomach  Acute Gastritis= inflammation of gastric mucosa  acute – presence of neutrophils  Chronic –lymphocytes and plasma cells  Caused by ingestion of strong acids or alkalies, NSAIDs, cancer chemotherapy, irradiation, alcohol, uremia, severe stress & shock states  Proposed mechanisms: ↑ acid production with ↓ surface bicarbonate buffer  Morphology: Mucosal edema, hyperemia, PML infiltration, erosions (not deeper than muscularis mucosa) & hemorrhages
  • 54. Stomach  Chronic Gastritis = Chronic mucosal inflammation  Leading to mucosal atrophy, intestinal metaplasia & dysplasia.  Pathogenesis:  Chronic infection by Helicobacter pylori (90%): MCC of chronic gastritis, Elaboration of urease  produces ammonia that buffers gastric acid, protecting organism from acid  Other diseases associated with H. pylori Infection  Peptic ulcer disease  Gastric carcinoma  Gastric lymphoma  Autoimmunity (>10%): Antibodies to parietal cells cause parietal cell destruction (HCl & intrinsic factor)
  • 55. Stomach  Chronic Gastritis  Morphology:  Autoimmune diffuse mucosal damage of the body-fundic mucosa  H. pylori affect antral mucosa  Histology: Lymphocytic & plasma cell infiltrate of the lamina propria  atrophy, regeneration, metaplasia (to intestinal type mucosa) & dysplasia.  H. pylori detected on the mucosal surface  Clinically:  Mild abdominal discomfort, nausea, vomiting; hypochlorhydria, hypergastrinemia & rarely  Overt pernicious anemia (in autoimmune) gastritis).  Long-term risk of cancer is 2-4%