Chapter 17: GIT- STOMACH- Chronic Gastritis

Question 1

In contrast to acute gastritis, the symptoms associated with chronic gastritis are what?

Answer 1

typically less severe but more persistent.

Nausea and upper abdominal discomfort may occur, sometimes with vomiting, but hematemesis is uncommon.

Question 2

What is the most common cause of chronic gastritis?

Answer 2

infection with the bacillus Helicobacter pylori.

Question 3

What are the other chronic irritants contributing to primary causes of chronic gastritis?

Answer 3

• psychologic stress,
• caffeine,
• alcohol, and
• tobacco

Question 4

What is the most common cause of atrophic gastritis,represents less than 10% of cases of chronic
gastritisand is themost common form of chronic gastritisin patientswithout H. pylori infection?

Answer 4

. Autoimmune gastritis

Question 5

What are the Less common etiologies of chronic gastritis?

Answer 5

• radiation injury,
• chronic bile reflux,
• mechanical injury, and
• involvement by systemic disease such as
  
  • Crohn disease,
  • amyloidosis, or graft-versus-host disease.

Question 6

Chronic Gastritis

Answer 6

• Helicobacter pylori
• chronic irritants, including
  
  • psychologic stress,
  • caffeine,
  • alcohol, and
  • tobacco
• Autoimmune gastritis
• radiation injury,
• chronic bile reflux,
• mechanical injury, and
• involvement by systemic disease such as
  
  • Crohn disease,
  • amyloidosis,
  • or graft-versus-host disease.

Question 7

What is H. pylori?

Answer 7

These spiral-shaped or curved bacilli are present in gastric biopsy specimens of almost all patients
with duodenal ulcers and the majority of individuals with gastric ulcers or chronic gastritis. [13]

TRIVIA:

In a now-famous experiment, the Nobel laureate Barry Marshall ingested H. pylori cultures and
developed mild gastritis. While not a recommended approach to infectious disease investigation, this experiment did demonstrate the pathogenicity of H. pylori.

Question 8

How does H.pylori produce sufficient symptoms?

Answer 8

Acute H. pylori
infection does not produce sufficient symptoms to require medical attention in most cases; _it is
the chronic gastritis that ultimately causes the individual to seek treatment._

H. pylori organisms
are present in 90% of individuals with chronic gastritis affecting the antrum.

Question 9

In addition, H. pylori has important roles in other gastric and duodenal diseases.

Answer 9

For example, the increased acid
secretion that occurs in H. pylori gastritis may result inpeptic ulcer disease, and H. pylori
infection also confers increased risk of gastric cancer

Question 10

What is the epidemiology of H. pylori?

Answer 10

In the United States, H. pylori infection is associated with poverty, household crowding, limited
education, African-American or Mexican-American ethnicity, residence in rural areas, and birth
outside of the United States.

Colonization rates exceed 70% in some groups and vary from less than 10% to more than 80% worldwide. In high-prevalence areas infection is often acquired in
childhood and then persists for decades, explaining the direct correlation between colonization
rate and patient age

Question 11

What is the mode of transmission of H.pylori?

Answer 11

The mode of H. pylori transmission is not well defined, but humans are the only known host,
making oral-oral, fecal-oral, and environmental spread the most likely routes of infection.

The
related organism Helicobacter heilmannii causes similar disease and has reservoirs in cats,
dogs, pigs, and nonhuman primates.

While the morphologic differences between H. pylori and H. heilmannii organisms are subtle, recognition of H. heilmannii infection can be important since
it may prompt treatment of household pets to prevent re-infection of the human companion

Question 12

What is the presentation of H.pylori?

Answer 12

H. pylori infection is the most common cause of chronic gastritis.

The disease most often
presents as a predominantly antral gastritis with high acid production, despite hypogastrinemia .

The risk of duodenal ulcer is increased in these patients and, in most, gastritis is limited to the
antrum with occasional involvement of the cardia.

In a subset of patients the gastritis
progresses to involve the gastric body and fundus.

This pangastritis is associated with
multifocal mucosal atrophy, reduced acid secretion, intestinal metaplasia, and increased risk of
gastric adenocarcinoma.

Question 13

H. pylori organisms have adapted to the ecologic niche provided by gastric mucus.

Although H.
pylori may invade the gastric mucosa, this is not evident histologically and the contribution of invasion to disease is not known.

Four features are linked to H. pylori virulence:

Answer 13

• Flagella
• Urease
• Adhesins
• Toxins

FUTA

Question 14

How does the flagella of the H.pylori contribute to chronic gastritis?

Answer 14

Flagella, which allow the bacteria to be motile in viscous mucus

Question 15

When H.pylori release urease, what does it do to contribute to chronic gastritis?

Answer 15

Urease, which generates ammonia from endogenous urea and thereby elevates local
gastric pH

Question 16

How can the virulence factor of H.pylori adhesins contribute to chronic gastritis?

Answer 16

Adhesins that enhance their bacterial adherence to surface foveolar cells

Question 17

How do Toxins, such as cytotoxin-associated gene A (CagA) of H.pylori can contribute to chronic gastritis>

Answer 17

, that may be involved in ulcer or
cancer development by poorly defined mechanisms

Question 18

Although the mechanisms by which H. pylori cause gastritis are incompletely defined, it is clear
that infection results in what?

Answer 18

increased acid production and disruption of normal gastric and duodenal protective mechanisms, as described earlier (see Fig. 17-11 ).

H. pylori gastritis is,
therefore, the result of an imbalance between gastroduodenal mucosal defenses and damaging
forces that overcome those defenses

Question 19

What is the underlying mechanisms contributing to chronic antral H.pylori

Answer 19

Over time chronic antral H. pylori gastritis may progress to pangastritis, resulting in multifocal
atrophic gastritis.

The underlying mechanisms contributing to this progression are not clear, but
interactions between the host and bacterium seem to be critical.

For example, particular
polymorphisms in the gene encoding the pro-inflammatory cytokine interleukin-1β (IL-1β)
correlate with the development of pangastritis after H. pylori infection.

Polymorphisms in TNF
and a variety of other genes associated with the inflammatory response also influence the
clinical outcome in H. pylori infection. [14]

Severity of disease may also be influenced by
genetic variation among H. pylori strains. For example, the CagA gene, a marker for a
pathogenicity island of approximately 20 genes, is present in 50% of H. pylori isolates overall
but in 90% of H. pylori isolates found in populations with elevated gastric cancer risk.

Question 20

H.pylori is concentrated on whic location?

Answer 20

Gastric biopsy specimens generally demonstrate H. pylori in infected individuals.

The organism is concentrated within the superficial mucus overlying epithelial
cells in the surface and neck regions.

The distribution can be irregular, with areas of heavy
colonization adjacent to those with few organisms.

In extreme cases, the organisms carpet
the luminal surfaces of foveolar and mucous neck cells, and can even extend into the gastric
pits.

Organisms are most easily demonstrated with a variety of special stains ( Fig. 17-12A ).

Question 21

H. pylori shows tropism for gastric epithelia and is generally not found in association with
gastric intestinal metaplasia or duodenal epithelium.

T or F

Answer 21

True

However, H. pylori may be present in

• *foci of pyloric metaplasia** within chronically injured duodenum or gastric-type mucosa within
• *Barrett esophagus**

Question 22

Within the stomach where is H.pylori typically found?

Answer 22

Within the stomach, H. pylori are typically found in the antrum ( Table 17-3 ).

Although there
is a good concordance between colonization of the antrum and cardia, infection of the cardia
occurs at somewhat lower rates.

H. pylori are uncommon in oxyntic (acid-producing)
mucosa of the fundus and body except in heavy colonization.

Remember: Antrum is where there is mucus prodution. So dba pathogenesis include imbalance with protective factors ( mucin )

Question 23

Why is antral biopsy is preferred for evaluation of H. pylori gastritis?

Answer 23

H. pylori are uncommon in oxyntic (acid-producing)
mucosa of the fundus and body except in heavy colonization.

Question 24

When viewed endoscopically, what is the apperance of H. pylori–infected antral mucosa?

Answer 24

• erythematous and has a coarse or even nodular appearance.
• The inflammatory infiltrate generally includes
  variable numbers of neutrophils within the lamina propria, including some that cross the basement membrane to assume an intraepithelial location ( Fig. 17-12B ) and accumulate in the lumen of gastric pits to create pit abscesses.
• In addition, the superficial lamina propria includes large numbers of plasma cells, often in clusters or sheets, and increased numbers of lymphocytes and macrophages.
• Intraepithelial neutrophils and subepithelial plasma cells are characteristic of H. pylori gastritis.
• When intense, inflammatory infiltrates may create thickened rugal folds, mimicking early infiltrative lesions.
• Long-standing H. pylori gastritis may extend to involve the body and fundus, and the mucosa can become atrophic.
• Lymphoid aggregates, some with germinal centers, are frequently present ( Fig. 17-12C ) and represent an induced form of mucosaassociated lymphoid tissue, or MALT, that has the potential to transform into lymphoma.

Question 25

In what instance where you can find H.pylori in the oxyntic mucosa of the fundus and body?

Answer 25

H. pylori are uncommon in oxyntic (acid-producing)
mucosa of the fundus and body except in heavy colonization.

In addition, the superficial lamina propria includes large numbers of plasma cells, often in
clusters or sheets, and increased numbers of lymphocytes and macrophages.

Question 26

When viewed endoscopically, H. pylori–infected
antral mucosa is usually has an appearnace of what?

Answer 26

erythematous and has a coarse or even nodular appearance.

Question 27

How does the H.pylori assume an intraepithelial
location?

Answer 27

The inflammatory infiltrate in H.pylori generally includes variable numbers of neutrophils within the lamina propria, including some that cross the basement membrane to assume an intraepithelial
location ( Fig. 17-12B ) and accumulate in the lumen of gastric pits to create pit abscesses.

Question 28

What is in characteristic of H.pylori in its histological morphology?

Answer 28

Intraepithelial neutrophils and subepithelial plasma cells are characteristic of H. pylori
gastritis.

Question 29

What happens to the inflammatory infiltrates when there is intense H.pylori?

Answer 29

When intense, inflammatory infiltrates may create thickened rugal folds, mimicking
early infiltrative lesions.

Question 30

What happens when there is a long standing H.pylori gastritis?

Answer 30

Long-standing H. pylori gastritis may extend to involve the body and fundus, and the mucosa can become atrophic.

Lymphoid aggregates, some with germinal
centers, are frequently present ( Fig. 17-12C ) and represent an induced form of mucosaassociated
lymphoid tissue, or MALT,that has the potential totransform into lymphoma

Question 31

Answer 31

FIGURE 17-12 Helicobacter pylori gastritis

• . A, Spiral-shaped H. pylori are highlighted in this Warthin-Starry silver stain. Organisms are abundant within surface mucus.
• B, Intraepithelial and lamina propria neutrophils are prominent.
• C, Lymphoid aggregates with germinal centers and abundant subepithelial plasma cells within the superficial lamina propria are characteristic of H. pylori gastritis

Question 32

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Location

Answer 32

• H. pylori–Associated :Antrum
• Autoimmune :Body

Question 33

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Inflammatory
infiltrate

Answer 33

• H. pylori–Associated : Neutrophils, subepithelial plasma cells
• Autoimmune : Lymphocytes, macrophages​

Question 34

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Acid production

Answer 34

• H. pylori–Associated : Increased to slightly decreased
• Autoimmune : Decreased

Question 35

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Gastrin

Answer 35

• H. pylori–Associated : Normal to decreased
• Autoimmune: Increased

Question 36

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Other
lesions

Answer 36

• H. pylori–Associated : Hyperplastic/inflammatory polyps
• Autoimmune: Neuroendocrine hyperplasia

Question 37

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Serology

Answer 37

• H. pylori–Associated : Antibodies to H. pylori
• Autoimmune: Antibodies to parietal cells (H+ , K + -
  ATPase, intrinsic factor)

Question 38

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Sequelae

Answer 38

• H. pylori–Associated : Peptic ulcer, adenocarcinoma
• Autoimmune : Atrophy, pernicious anemia,
  adenocarcinoma, carcinoid tumor

Question 39

TABLE 17-3 – Characteristics of Helicobacter pylori –Associated and Autoimmune
Gastritis

Associations

Answer 39

• H. pylori– Associated : Low socioeconomic status, poverty, residence in rural areas
• Autoimmune : Autoimmune disease; thyroiditis, diabetes mellitus, Graves disease

Question 40

What are the diagnostic modalities for H.pylori?

Answer 40

• histologic identification of the organism,
• noninvasive serologic test for antibodies to H. pylori,
• fecal bacterial detection,
• and the urea breath test based on the generation of ammonia by the bacterial urease.
• Gastric biopsy specimens can also be analyzed by
  
  • the rapid urease test,
  • bacterial culture, or
  • bacterial DNA detection by PCR.

Question 41

What are the Effective treatments for H. pylori infection?

Answer 41

• combinations of antibiotics and
• proton pumpinhibitors.

Individuals with H. pylori gastritis usually improve after treatment, although relapses can occur after incomplete eradication or re-infection.

Prophylactic and therapeutic vaccine
development is still at an early stage of development.

Peptic ulcer disease, a complication of
chronic H. pylori gastritis, is described later.

Question 42

Autoimmune gastritis accounts for less than 10% of cases of chronic gastritis.

What is the difference of autoimmune gastritis regarding on area affected?

Answer 42

spares the antrum and includes
hypergastrinemia (see Table 17-3 ).

Question 43

Autoimmune gastritis is characterized by:

Answer 43

• Antibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions
• • Reduced serum pepsinogen I concentration
• • Antral endocrine cell hyperplasia
• • Vitamin B12 deficiency
• • Defective gastric acid secretion (achlorhydria)

NOTE:

Why reduced pepsinogen I?

• *Chief or zymogenic cells** are filled with secretory granules that contain the proenzyme
• *pepsinogen, an inactive precursor of pepsin**.

Release of pepsinogen during gastric secretion
into the acidic environment of the stomach converts the inactive pepsinogen into a highly
active, proteolytic enzyme pepsin.

e dba nga decrease acid prod kasi autantibodies against parietal cells so dec acid hence dec conversion of pepsinogen to pepsin

Question 44

What is the responsible for the loss of secretion of gastric acid and intrinsic factor in Autoimmune gastritis?

Answer 44

Autoimmune gastritis is associated with loss of parietal cells, which are responsible for secretion
of gastric acid and intrinsic factor.

Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12 deficiency and a slow-onset
megaloblastic anemia (pernicious anemia).

Question 45

Why is there a hypergastrinemia and hyperplasia of antral gastrin-producing G cells in autimmune gastritis?

Answer 45

The absence of acid production stimulates gastrin release, resulting in hypergastrinemia and hyperplasia of antral gastrin-producing G cells.

Question 46

Why is H.pylori not associated with achlorhydria or pernicious anemia in contrast with autoimmune gastritis?

Answer 46

The reduced serum pepsinogen I concentration
results from chief cell destruction.

In contrast, although H. pylori can cause hypochlorhydria, it is not associated with achlorhydria or pernicious anemia because the parietal and chief cell
damage is not as severe as in autoimmune gastritis

Question 47

What is the pathogenesis in autoimmune gastritis?

Answer 47

It was initially thought that the autoantibodies to parietal cell components, most prominently the
H+ ,K + -ATPase, or proton pump, and intrinsic factor were involved in the pathogenesis of
autoimmune gastritis.

However, this is unlikely because neither secreted intrinsic factor nor the luminally oriented proton pump are accessible to circulating antibodies, and passive transfer of these antibodies does not produce gastritis in experimental animals.

It is more likely that C_D4+ T cells directed against parietal cell components,** _including the **H+ ,K + -ATPase,** are the **principal agents of injury.

This is supported by the observation that transfer of H+ ,K + - ATPasereactive CD4+ T cells into naive mice results in gastritis and production of H+ ,K + -
ATPase autoantibodies.

There is no evidence of an autoimmune reaction to chief cells, suggesting that these are lost through gastric gland destruction during autoimmune attack on
parietal cells. If autoimmune destruction is controlled by immunosuppression, the glands can repopulate, demonstrating that gastric stem cells survive and are able to differentiate into
parietal and chief cells.

Question 48

What is more likely the principal agents of injury in autoimmune gastritis?

Answer 48

It is more likely that CD4+ T cells directed against parietal cell components, including the H+ ,K + -ATPase, are the
principal agents of injury.

Question 49

What are the important things to remember regarding the autoimmune gastritis morphology?

Answer 49

• damage of the oxyntic (acid-producing) mucosa
• diffuse atrophy
• intestinal metaplasia
• antral endocrine cell hyperplasia

Question 50

Autoimmune gastritis is characterized by what damages on the cell of the stomach?

Answer 50

diffuse mucosal damage of the oxyntic (acid-producing) mucosa within the body and fundus.

Damage to the antrum and
cardia is typically absent or mild.

Question 51

With diffuse atrophy in autoimmune gastritis what is the appearance of the oxyntic mucosa of the body and fundus?

Answer 51

,the oxyntic mucosa of the body and fundus appears markedly thinned, and rugal folds are lost.

If vitamin B12 deficiency is severe,
nuclear enlargement (megaloblastic change) occurs within epithelial cells.

Question 52

What are the cells present in autoimmune gastrtitis?

Answer 52

Neutrophils may be present, but the inflammatory infiltrate is more often composed of lymphocytes, macrophages, and plasma cells.

Lymphoid aggregates may be present.

The superficial lamina propria
plasma cells of H. pylori gastritis are typically absent, and the inflammatory reaction is most often deep and centered on the gastric glands ( Fig. 17-13A ).

Loss of parietal and chief cells
can be extensive.

Question 53

Why is there an appearance of multiple small polyps or nodules in autoimmune gastritis?

Answer 53

When atrophy is incomplete residual islands of oxyntic mucosa may give the appearance of multiple small polyps or nodules.

Question 54

What correlates metaplasia in Autoimmune gastritis?

Answer 54

Small surface elevations may be
apparent, and these correlate with areas of intestinal metaplasia, characterized by the
presence of goblet cellsandcolumnar absorptive cells ( Fig. 17-13B ).

The antral
endocrine cell hyperplasia that develops in most patients can be difficult to appreciate on H&E-stained sections, since the endocrine cells, which are also referred to as enterochromaffin-like (ECL) cells, are not easily recognized.

This hyperplasia *parallels the
degree of mucosal atrophy and is a physiologic response to decreased acid production*.

Over time, hypergastrinemia can stimulate endocrine cell hyperplasia in the fundus and body.
Rarely, this may progress to form small, multicentric, low-grade neuroendocrine, or carcinoid,
tumors.
Chronic Gastritis
1483

Question 55

Answer 55

FIGURE 17-13 Autoimmune gastritis.

• A, Low-magnification image of gastric body demonstrating deep inflammatory infiltrates, primarily composed of lymphocytes, and glandular atrophy.
• B, Intestinal metaplasia, recognizable as the presence of goblet cells admixed with gastric foveolar epithelium.

Question 56

What is the clinical course in autoimmune gastritis?

Answer 56

• Antibodies to parietal cells and to intrinsic factor are present early in the disease course.
• Progression to gastric atrophy probably occurs over 2 to 3 decades, and anemia is seen in only a few patients.

Question 57

Why are patients of autoimmune gastritis diagnosed only after being affected for many years?

Answer 57

Because of the slow onset and variable progression, patients are generally diagnosed only after being affected for many years.

Question 58

What is the median age at diagnosis of autoimmune gastritis?

Answer 58

the median age at diagnosis is 60 years.

Question 59

Which gender is more affected in autoimmune gastritis?

Answer 59

Slightly more women than men are affected.

Question 60

Pernicious anemia and autoimmune gastritis are
often associated with other autoimmune diseases including

Answer 60

• Hashimoto thyroiditis,
• insulindependent (type I) diabetes mellitus,
• Addison disease,
• primary ovarian failure,
• primary hypoparathyroidism,
• Graves disease,
• vitiligo,
• myasthenia gravis, and
• Lambert-Eaton syndrome.

NOTE :

These associations, along with concordance in some monozygotic twins and clustering of
disease in families, support a genetic predisposition. In general, about 20% of relatives of individuals with pernicious anemia also have autoimmune gastritis, although they may be
asymptomatic.

Despite this strong genetic influence, autoimmune gastritis stands apart from
other autoimmune diseases in that there is little evidence of linkage to specific HLA alleles.

Question 61

What are the clinical presentations of autoimmune gastritis?

Answer 61

Clinical presentation may be linked to symptoms of anemia. [15]

• In addition, vitamin B12deficiency may cause
  
  • atrophic glossitis, in which the tongue becomes smooth and beefy red,
  • epithelial megaloblastosis, and
  • malabsorptive diarrhea.
  • Vitamin B12 deficiency may also cause peripheral neuropathy,
    
    • The most frequent manifestations of peripheral neuropathy are paresthesias and numbness.
  • spinal cord lesions, and
  • cerebral dysfunction.
  • Neuropathic changes include:
    
    • demyelination,
    • axonal degeneration,
    • and neuronal death.
  • The spinal lesions may be associated with a mixture of :
    
    • loss of vibration and position sense,
    • sensory ataxia with positive Romberg sign,
    • limb weakness,
    • spasticity, and
    • extensor plantar responses.
  • Cerebral manifestations range from mild personality changes and memory loss to psychosis.

In contrast
to anemia, neurologic changes are not reversed by vitamin B12 replacement therapy

Question 62

UNCOMMON FORMS OF GASTRITIS

Answer 62

• Reactive Gastropathy
• Eosinophilic Gastritis
• Lymphocytic Gastritis
• Granulomatous Gastritis

Question 63

What is Reactive Gastropathy?

Answer 63

This group of disorders is marked by :

• foveolar hyperplasia,
• glandular regenerative changes,
• and mucosal edema.
• Neutrophils are not abundant.

Question 64

Causes of reactive gastropathy include what?

Answer 64

• chemical injury,
• NSAID use,
• bile reflux, and
• mucosal trauma secondary to prolapse.

Question 65

reactive gastropathy and bile reflux are common after what?

Answer 65

Notably,

gastric surgeries that bypass the pylorus.

Question 66

What is GAVE?

Answer 66

**Gastric antral trauma induces a grossly characteristic** lesion referred to as **gastric antral
vascular ectasia ( dilatation) (GAVE)**

. Endoscopy shows longitudinal stripes of edematous erythematous mucosa alternating with less severely injured mucosa that is sometimes referred to as
watermelon stomach.

Histologically, the antral mucosa shows reactive gastropathy with dilated
capillaries containing fibrin thrombi

Question 67

What is Eosinophilic Gastritis?

Answer 67

As indicated by the name, this form of gastritis is characterized by tissue damage associated
with dense infiltrates of eosinophils in the mucosa and muscularis, usually in the antral or
pyloric region.

The lesion is often present in other areas of the GI tract as well and is associated with peripheral eosinophilia and increased serum IgE levels.

Question 68

What is the causesof eosinophilic gastritis?

Answer 68

• Allergic reactions are one cause of eosinophilic gastritis.
• In children, the allergens include cow’s milk and soy protein, while drugs are common allergens in children and adults.
• Eosinophilic gastritis can also occur in association with systemic collagen-vascular disease, such as systemic sclerosis and polymyositis.
• Parasitic infections and H. pylori infection are other causes of eosinophilic gastritis.

Question 69

What is Lymphocytic Gastritis?

Answer 69

• preferentially affects women and
• produces nonspecific symptoms such as abdominal pain, anorexia, nausea, and vomiting.
• It is idiopathic, but approximately 40% of cases are associated with celiac disease, suggesting an immune-mediated pathogenesis.
• also referred to as varioliform gastritis based on the distinctive endoscopic appearance (thickened folds covered by small nodules with central aphthous ulceration). [17]
• entire stomach is affected in most cases, but disease is occasionally limited to the body.

Question 70

What is the etiology of Lymphocytic Gastritis?

Answer 70

It is idiopathic, but approximately 40% of cases are associated with celiac disease, suggesting an immune-mediated pathogenesis.

Question 71

Why is lymphocity gastritis also referred to as varioliform gastritis?

Answer 71

based on the distinctive endoscopic appearance (thickened folds covered by small nodules with central aphthous ulceration). [17]

entire stomach is affected in most cases, but disease is occasionally limited to the body.

Question 72

What is histologically seen in Lymphocytic gastritis?

Answer 72

Histologically there is a marked increase in the number of intraepithelial T lymphocytes, mostly
CD8+ cells, within surface and pit regions.

Question 73

What is Granulomatous Gastritis?

Answer 73

This descriptive term is applied to any gastritis that contains granulomas, or aggregates of
epithelioid histiocytes (tissue macrophages).

It encompasses a diverse group of diseases with
widely varying clinical and pathologic features.

Correlation with clinical, endoscopic, radiologic,
and serologic data is generally necessary for diagnosis.

Question 74

In Western populations, what is the most common specific cause of granulomatous gastritis?

Answer 74

gastric involvement by Crohn disease

Question 75

what is the second most common specific cause of granulomatous gastritis.

Answer 75

[18] Sarcoidosis is the second most common cause,

followed by a variety of infections
including:

• mycobacteria,
• fungi,
• CMV, and
• H. pylori.

Question 76

In addition to the presence of histologically

evident granulomas in granulomatous gastritis, what else can be seen?

Answer 76

narrowing and rigidity of the gastric antrum may occur secondary to
transmural granulomatous inflammation