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This set of flashcards covers the etiology, pathophysiology, and pharmacological risks associated with peptic ulcer disease and nonvariceal upper gastrointestinal bleeding as described in the lecture.
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Peptic ulcer disease
The most common cause of nonverastal upper GI bleed, responsible for approximately 50 to 70% of cases globally.
Principal causes of peptic ulcer disease
h pylori infection and NSAIDS use, with additional contributors including burns, head injury, smoking, and alcohol abuse.
Posterior wall of the duodenum
Anatomical location where associated nerves and the erosion of the gastroduodenum, or rarely the left gastric artery, cause significant bleeding.
Nonvericile upper GI bleed causes
Conditions like gastritis and duodenitis resulting from NSAIDs and antiflucentral angioplasty, especially in elderly and cardiovascular patients.
Drug induced mucosa in GFD
Mucosal injury particularly from NSAIDs and antiplatelets that has become a prominent cause of bleeding as h pylori eradication protocols have increased.
Cyclooxygenase one (COX-1)
An enzyme always present in the gastric mucosa that produces prostaglandin, which is essential for protecting the mucosa.
Suppression of COX-1
A process that reduces mucus and bicarbonate secretions, hampers mucosal barthrow, and impairs epithelial repair, creating vulnerability to acid related damage.
P two y one two inhibitors
Antiplatelet drugs such as flopidogrel and ticagrelor that further increase bleeding risk by impairing primary hemostasis.
Combined antithrombotic therapy risk
The risk of major gastrointestinal bleeding following marketinous coronary intervention can be 2 to 3 times a prior than with monotherapy.
Low dose aspirin
A common cause of occult or overt gastritis and bleach, particularly at doses of hundred percent.