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2H SystemicPatho GIT > Chapter 17: GIT- STOMACH-Acute Gastritis > Flashcards

Chapter 17: GIT- STOMACH-Acute Gastritis Flashcards

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1
Q

What is Acute gastritis?

A

Acute gastritis is a transient mucosal inflammatory process that may be asymptomatic or cause
variable degrees of epigastric pain,nausea, and vomiting.

In more severe cases there may be
mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or, rarely, massive blood loss.

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2
Q

What is the pH of the gastric lumen?

A

strongly acidic with pH close to 1, more than a million times more acidic than the blood.

This harsh environment contributes to digestion but also has the potential to
damage the gastric mucosa.

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3
Q

Multiple mechanisms have evolved to protect the gastric mucosa (
Fig. 17-11 ).

A
  • Mucin secreted by surface foveolar cells forms a thin layer of mucus that prevents large food particles from directly touching the epithelium.
  • The mucus layer also promotes formation of an “unstirred” layer of fluid over the epithelium that protects the mucosa and has a neutral pH as a result of bicarbonate ion secretion by surface epithelial cells.
  • Finally, the rich vascular supply to the gastric mucosa delivers oxygen, bicarbonate, and nutrients while washing away acid that has back-diffused into the lamina propria.
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4
Q

What is the pathology of acute gastritis?

A

Acute or chronic gastritis can occur following disruption of any of these protective mechanisms.

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5
Q

How go elderly acquire acute gastritis?

A

For example, reduced mucin
synthesis in the elderly has been suggested as one factor that may explain their increased
susceptibility to gastritis.

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6
Q

How can NSAIDS contribute to acute gastritis?

A

Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with cytoprotection normally provided by prostaglandins or reduce bicarbonate secretion, either of which increases the susceptibility of the gastric mucosa to injury.

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7
Q

How can gastric injury occur in uremeic patients and those with urease secreting H.pylori?

A

due to
inhibition of gastric bicarbonate transporters by ammonium ions.

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8
Q

Ingestion of harsh chemicals,
particularly acids or bases, either accidentally or as a suicide attempt, also results in severe gastric injury, predominantly as a result of what?

A

direct injury to mucosal epithelial and stromal cells.

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9
Q

Direct cellular injury is also implicated in gastritis due to what factors?

A
  • excessive alcohol consumption,
  • NSAIDs,
  • radiation therapy,
  • and chemotherapy.
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10
Q

How can cancer therapy caused generalized mucosal damage?

A

Since the entire gastric mucosal surface is

replaced every 2 to 6 days, mitotic inhibitors, including those used in cancer chemotherapy,

cause generalized mucosal damage due to insufficient epithelial regeneration.

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11
Q

What is the reason for acute gastritis in high altitudes?

A

Finally,

decreased oxygen delivery may explain increased incidence of acute gastritis at high altitudes.

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12
Q
A

FIGURE 17-11 Mechanisms of gastric injury and protection. This diagram illustrates the progression from more mild forms of injury to ulceration that may occur with acute or chronic gastritis.

Ulcers include layers of necrosis (N), inflammation (I), and granulation tissue (G), but a fibrotic scar (S), which takes time to develop, is only present in chronic lesions

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13
Q

What are the Normal secretion in the stomach?

A
  • Gastric Acid
  • Peptide enzymes
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14
Q

What are defensive forces in the stomach?

A
  • Surface mucus secretion
  • Bicarbonate secretion into mucus
  • Mucosal blood flow
  • Apical surface
    • membrane transport
  • Epithelial regenerative capacity
  • Elaboration of prostaglandins
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15
Q

What are the factors the cause injury in the stomach?

A
  • H.pylori infection
  • NSAIDS
  • Aspirin
  • Cigarettes
  • Alcohol
  • Gastric Hyperacidity
  • Duodenal-gastric reflux
  • INCREASE DAMAGED or DECREASED DEFENSIVE FACTORS
  • Ischemia
  • Shock
  • Delayed Gastric emptying
  • Host factors
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16
Q

What is the apperance of acute gastritis histologically?

A

Histologically, mild acute gastritis may be difficult to recognize, since the lamina propria shows only moderate edema and slight vascular congestion.

  • surface epithelium is intact
  • active inflammation may be present
  • , erosions
  • acute erosive hemorrhagic gastritis.
  • The surface epithelium is intact, although scattered neutrophils may be present among the epithelial cells or within mucosal glands.
    • In contrast, an abundance of lymphocytes or plasma cells suggests chronic disease.
    • The presence of neutrophils above the basement membrane in direct contact with epithelial cells is abnormal in all parts of the GI tract and signifies active inflammation. This term is preferred over acute inflammation, since active inflammation may be present in both acute and chronic disease states.
  • With more severe mucosal damage, erosions and hemorrhage develop. It is accompanied by a pronounced neutrophilic infiltrate within the mucosa and a fibrin-containing purulent exudate in the lumen.
  • Hemorrhage may occur and cause dark punctae in an otherwise hyperemic mucosa. Concurrent erosion and hemorrhage is termed acute erosive hemorrhagic gastritis.
  • Large areas of the gastric surface may be denuded, although the involvement is typically superficial.
  • When erosions extend deeply, they may progress to ulcers, as
    described below
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17
Q

In acute gastritis the surface epithelium is intact, what cell are seen scattered among the epithelial cells or within mucosal glands.?

A

neutrophils may be present

(In contrast, an abundance of lymphocytes or plasma cells suggests chronic disease)

18
Q

What does it signifis when there is the presence of neutrophils above the basement membrane in direct contact with epithelial cells?

A

abnormal in all parts of the GI tract and signifies active
inflammation.

This term is preferred over acute inflammation, since active inflammation may be present in both acute and chronic disease states.

19
Q

Why is active inflammation preffered over acute inflammation?

A

This term is preferred over acute inflammation, since active inflammation may be present in both acute and chronic disease states.

20
Q

With more severe mucosal damage in acute gastritis what eventually develops?

A

erosions and hemorrhage

​

NOTE :

An erosion denotes loss of the superficial epithelium,
generating a defect in the mucosa that is limited to the lamina propria. It is accompanied by a
pronounced neutrophilic infiltrate within the mucosa and a fibrin-containing purulent exudate in the lumen.

Hemorrhage may occur and cause dark punctae in an otherwise hyperemic mucosa.

Concurrent erosion and hemorrhage is termed acute erosive hemorrhagic gastritis.

Large areas of the gastric surface may be denuded, although the involvement is typically superficial.

When erosions extend deeply, they may progress to ulcers, as
described below.

21
Q

What is denoted by erosion in acute gastritis?

A

An erosion denotes loss of the superficial epithelium,
generating a defect in the mucosa that is limited to the lamina propria.

It is accompanied by a
pronounced neutrophilic infiltrate within the mucosa and a fibrin-containing purulent exudate in the lumen.

22
Q

When hemorrhage may occurs in Acute gastritis it causes what?

A

dark punctae in an otherwise hyperemic mucosa.

23
Q

What is the term for Concurrent erosion and hemorrhage in acute gastritis?

A

acute erosive hemorrhagic gastritis.

24
Q

ACUTE GASTRIC ULCERATION

Focal, acutely developing gastric mucosal defects are a well-known complication of therapy with what?

A

NSAIDs.

25
Q

ACUTE GASTRIC ULCERATION

Focal, acutely developing gastric mucosal defects are a well-known complication of therapy with
NSAIDs.

They may also appear after severe physiologic stress. Some of these are given specific names, based on location and clinical associations. For example:

A
  • • Stress ulcers
  • Curling ulcers.
  • Cushing ulcers
26
Q

Stress ulcers are most common in individuals with what conditions?

A
  • shock,
  • sepsis, or
  • severe trauma.
27
Q

What are Curling ulcers?

A

Ulcers occurring in the proximal duodenum and associated with severe burns or trauma
are called Curling ulcers.

Curly hairs looked BURNED!

28
Q

What are Cushing ulcers?

A

Gastric, duodenal, and esophageal ulcers arising in persons with intracranial disease
are termed Cushing ulcers and carry a high incidence of perforation.

Cushion for the HEAD!!!

29
Q

What is the pathogenesis of Acute Gastic Ulceration with regards to NSAID-induced ulcers?

A

The pathogenesis of acute ulceration is complex and incompletely understood.

NSAID-induced ulcers are related to cyclooxygenase inhibition.

This prevents synthesis of prostaglandins, which enhance bicarbonate secretion, inhibit acid secretion, promote mucin synthesis, and increase vascular perfusion.

30
Q

What is the pathogenesis in ACUTE GASTRIC ULCERATION associated with intracranial injury ?

A

Lesions associated with intracranial injury are thought to becaused by direct stimulation of vagal nuclei, which causes hypersecretion of gastric acid.

31
Q

What is the pathogenesis in ACUTE GASTRIC ULCERATION associated with systemic problems ?

A

Systemic acidosis, a frequent finding in intracranial injury, may also contribute to mucosal injury by
lowering the intracellular pH of mucosal cells.

  • *Hypoxia and reduced blood flow** caused by stressinduced
  • *splanchnic vasoconstriction** also contribute to the pathogenesis of acute ulcers.
32
Q

What is the morphology of acute gastric ulcers?

A

Morphology.

  • Lesions described as acute gastric ulcers range in depth from shallow erosions caused by superficial epithelial damage to deeper lesions that penetrate the depth of the mucosa.
  • Acute ulcers are rounded and less than 1 cm in diameter.
  • The ulcer base is frequently stained brown to black by acid digestion of extravasated blood and may be associated with transmural inflammation and local serositis.
  • Unlike peptic ulcers, which arise in the setting of chronic injury, acute stress ulcers are found anywhere in the stomach.
  • The gastric rugal folds are essentially normal, and the margins and base of the ulcers are not indurated. While they may occur singly, more often there are multiple ulcers throughout the stomach and duodenum.
33
Q

What is the microscopic apperance of Acute Gastric Ulcers?

A

Microscopically, acute stress ulcers are sharply demarcated, with essentially normal adjacent mucosa.

Depending on the duration of the ulceration, there may
be a suffusion of blood into the mucosa and submucosa and some inflammatory reaction.

Conspicuously absent are the scarring and thickening of blood vessels that characterize chronic peptic ulcers.

Healing with complete re-epithelialization occurs after the injurious factors are removed. T

he time required for healing varies from days to several weeks

34
Q

Most critically ill patients admitted to hospital intensive care units have histologic evidence of
what?

A

gastric mucosal damage.

35
Q

What are the clinical features of Acute Gastric Ulceration?

A
  • Bleeding from superficial gastric erosions or ulcers that may require transfusion develops in 1% to 4% of these patients
  • . Other complications, including perforation, can also occur ( Table 17-2 ).
36
Q

What can blunt the impact of stress ulceration ?

A

Prophylactic H2 histamine receptor antagonists or proton pump inhibitors

37
Q

What is the most important determinant of
clinical outcome in Acute Gastric Ulceration?

A

ability to correct the underlying conditions.

The gastric mucosa can
recover completely if the patient does not succumb to their primary disease.

38
Q

TABLE 17-2 – Complications of Gastric Ulcers

A
  • Bleeding
  • Perforation
  • Obstruction
39
Q

TABLE 17-2 – Complications of Gastric Ulcers

Bleeding

A
  • Occurs in 15% to 20% of patients
  • Most frequent complication
  • May be life-threatening
  • Accounts for 25% of ulcer deaths
  • May be the first indication of an ulcer
40
Q

TABLE 17-2 – Complications of Gastric Ulcers

Perforation

A
  • Occurs in up to 5% of patients
  • Accounts for two thirds of ulcer deaths
  • Is rarely first indication of an ulcer
41
Q

TABLE 17-2 – Complications of Gastric Ulcers

Obstruction

A
  • Mostly in chronic ulcers
  • Secondary to edema or scarring
  • Occurs in about 2% of patients
  • Most often associated with pyloric channel ulcers
  • May occur with duodenal ulcers
  • Causes incapacitating, crampy abdominal pain
  • Can rarely cause total obstruction and intractable vomiting

2H SystemicPatho GIT (34 decks)

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