Gastrointestinal Pathologies
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Gastrointestinal Pathologies

Created by
@FrugalCamellia

Questions and Answers

What is the result of mast cell degranulation in the development of gastrointestinal ulcers?

Histamine release that perpetuates further gastric acid secretion

What is the role of COX-2-specific NSAIDs in reducing gastrointestinal ulceration?

They increase the production of protective prostaglandins

What is the effect of corticosteroids on mucosal damage?

They decrease cell mucus production

What is the result of grain overload in ruminants?

<p>Rumen hypomotility to atony</p> Signup and view all the answers

What is the association between hepatic disease and gastrointestinal ulceration?

<p>Hepatic disease increases gastric acid secretion</p> Signup and view all the answers

What is the primary cause of gastrointestinal ulceration in dogs?

<p>NSAID administration</p> Signup and view all the answers

What is the primary factor contributing to the development of grain overload in ruminants?

<p>Access to large quantities of readily digestible carbohydrates</p> Signup and view all the answers

What is the association between neoplasia and gastrointestinal ulceration in cats?

<p>Neoplasia has been associated with gastrointestinal ulceration, but the cause is often unknown</p> Signup and view all the answers

What is the effect of NSAIDs on the GI mucosa?

<p>They cause direct topical damage to the GI mucosa</p> Signup and view all the answers

What is the effect of hepatic disease on mucosal blood flow?

<p>It decreases mucosal blood flow</p> Signup and view all the answers

Study Notes

Gastrointestinal Ulcers

  • Expanding stomach can compress thoracic cavity, leading to respiratory distress
  • Gastric mucosal barrier protects normal mucosa from harsh chemical environment of gastric luminal contents
  • pH of gastric luminal contents is 2, while mucous layer maintains a pH of 4-6
  • GI barrier is maintained by protective layer including mucosal cells, tight junctions, prostaglandins, and mucus
  • Prostaglandins help maintain GI mucosal blood flow and integrity, increase mucus and bicarbonate secretion, and decrease acid secretion
  • Defect in GI mucosal barrier leads to self-perpetuating cycle of mucosal damage, injury, and inflammation

Inflammatory Bowel Disease

  • Inflammatory Bowel Disease (IBD) is a group of GI diseases characterized by persistent clinical signs and histologic evidence of inflammatory cell infiltrate of unknown etiology
  • IBD includes granulomatous enteritis (GE), lymphocytic-plasmacytic enterocolitis (LPE), multisystemic eosinophilic epitheliotropic disease (MEED), and idiopathic focal eosinophilic enterocolitis (IFEE)
  • Disease is characterized by infiltration of small and large intestine with inflammatory cells, including lymphocytes, plasma cells, macrophages, and eosinophils
  • Several factors may be involved, including GI lymphoid tissue, permeability defects, genetic, ischemic, biochemical disorders, infectious and parasitic agents, dietary allergens, and drug reactions

Etiology and Pathogenesis of Gastrointestinal Ulcers

  • Mast cell degranulation occurs, causing histamine release that perpetuates further gastric acid secretion
  • NSAID administration, neoplasia, and hepatic disease are the most common causes of GI ulcers in dogs
  • NSAIDs can cause direct topical damage to GI mucosa and inhibition of COX-1, leading to decreased production of protective prostaglandins
  • Corticosteroids potentiate the effects of mucosal damage by decreasing cell mucus production and stimulating acid production

Grain Overload in Ruminants

  • Grain overload is an acute disease of ruminants characterized by rumen hypomotility to atony, dehydration, acidemia, diarrhea, and in severe cases, death
  • The disease is most common in cattle that accidentally gain access to large quantities of readily digestible carbohydrates, particularly grain

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Description

This quiz covers gastrointestinal disorders, including stomach compression, respiratory distress, and gastrointestinal ulcers. It explores the consequences of drugs and diseases on the GI mucosal barrier and the gastric mucosal defense mechanism.

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