Gastric Pathology Flashcards

1
Q

What are the normal damaging forces in the gastric mucosa?

A
  • Gastric acidity

- Peptic enzymes

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2
Q

What are the normal defensive forces in the gastric mucosa?

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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3
Q

What are causes of increased damage or injury to the gastric mucosa?

A
  • H. pylori infection
  • NSAID
  • Aspirin
  • Cigarettes
  • Alcohol
  • Gastric hyperacidity
  • Duodenal-gastric reflux
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4
Q

What are causes of impaired defenses in the gastric mucosa?

A
  • Ischemia
  • Shock
  • Delayed gastric emptying
  • Host factors
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5
Q

What do ulcers and chronic lesions contain?

A

Ulcers: Necrosis, Inflammation, Granulation tissue but a fibrotic scar takes time to develop and is only present in chronic lesions

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6
Q

What is Acute Gastritis?

A

Acute neutrophillic inflammation of the mucosa, often with hyperemia (increased redness) and hemorrhage (acute hemorrhagic gastritis). These inflammatory changes can be complicated by gastric mucosal erosion or an acute ulceration.

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7
Q

What is Gastric Mucosal Erosion?

A

Loss and necrosis of surface epithelium, confined to the lamina propria, i.e. mucosa

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8
Q

What is Acute Ulceration?

A

Necrotizing process extends beyond the mucosa into the submucosa and even into and through the muscle wall.

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9
Q

What are the main causes of Acute Gastric Ulceration?

A
  • Acute infection with Helicobacter organisms
  • First time use of large doses of NSAIDs and aspirin (COX inhibition)
  • Ingestion of large quantities of alcohol (direct toxic effect)
  • Patients with shock, trauma, sepsis, uremia, severe burns, and intracranial disease can get acute stress ulcers (burns - curling’s ulcers in duodenum; CNS injury - Cushing’s ulcers)
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10
Q

What is the most common pathologic finding in H. pylori gastritis?

A

Active chronic gastritis which typically begins in the antrum and can progress to involve the fundus.

  • Gastric atrophy can also be present
  • Patient can have high acid production and can get mucosal erosions and peptic ulcers.
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11
Q

What are complications of H. pylori infection?

A

MALT-lyphoma and gastric adenocarcinoma.

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12
Q

How does someone typically acquire H. helmannii gastritis?

A

Dogs or cats licking people’s faces. Helicobacter helmannii can also cause disease similar to H. pylori and reservoirs in cats, dogs, pigs, and nonhuman primates.

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13
Q

What H. pylori diagnostic tests indicate active infection?

A

Stool antigen and urea breath test indicate active infection. (also Rapid Urease testing according to Dr. Zimmer)

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14
Q

What are all the diagnostic tests for H. pylori?

A

Diagnostic tests include H. pylori stool antigen, urea breath test, serology, and rapid urease test on fresh tissue biopsy.

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15
Q

What is the pathogenesis of Autoimmune Gastritis?

A

Due to autoimmune CD4+ T-cell mediated destruction of parietal cells; chief cells are also lost during destruction of the gastric glands (“bystander damage”). Antibodies to parietal cells and intrinsic factor are also produced as part of the autoimmune response, but are not pathogenic (can be used as a diagnostic test)

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16
Q

What does the autoimmune damage in Autoimmune Gastritis result in?

A
  • Decreased gastric acid secretion (achlorhydria)
  • Compensatory hypergastrinemia and hyperplasia of antral gastrin-producing G cells, along with endocrine cell hyperplasia in the fundus and body of the stomach
  • Vitamin B12 deficiency due to loss of secreted intrinsic factor (pernicious anemia with increased RBC MCV)
  • Reduced serum pepsinogen I concentration
  • Inflammatory mucosal damage and atrophy of the gastric mucosa in the body and fundus with paring of the antrum and cardia
17
Q

What are the complications or clinical findings many years after development of Autoimmune Gastritis?

A
  • Megaloblastic anemia (macrocytic anemia)
  • Atrophic glossitis
  • Malabsorptive diarrhea
  • Peripheral neuropathy: Secondary to subacute combined degeneration of the dorsal and lateral spinal columns. Patients can present with paresthesias and ataxia associated with loss of vibration and position sense, and can progress to sever weakness, spasticity, clonus, paraplegia and fecal and urinary incontinence.
  • CNS alterations can also occur, including mild personality changes, memory loss, and psychosis
18
Q

What is Chronic Reactive Gastropathy?

A

Pattern of chronic gastric injury characterized by foveolar hyperplasia, mucin depletion, vascular congestion, edema and lamina propria fibrosis.

19
Q

What are common causes of Chronic Reactive Gastropathy?

A

Changes are due to chemical mucosal injury, associated with use of NSAIDs, aspirin, bile reflux, and alcohol ingestion. Patients can get gastric erosions and ulceration.