Peptic Ulcers and Gastric Cancer Flashcards
Where does gastrin come from?
G cells in the antrum
What does gastrin do?
Act on parietal cells to increase acid and pepsinogen and also increases motility
Stimulated by distention and peptides and amino acid in the stomach
Inhibited by decreased pH (<2) and PGs
What is a peptic ulcer?
Defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall
1 cause of GI bleed
Peptic ulcers
Etiology of PUD
#1 is helicobacter pylori #2 is NSAIDs Also non-NSAID and non-H pylori
What factors do not cause ulcers but can make them more difficult to heal?
Emotional stress, alcohol, spicy foods, caffeine and tobacco
some foods may cause dyspepsia but do not cause ulcer disease
What might a pt with h pylori be predisposed to?
Gastric cancer
Why is h pylori decreasing in developed countries?
Improved hygiene and decreased transmission
Correlates with decline in PUD
Increased rates of eradication
What does h pylori look like?
Gram negative rod
Motile flagella used to attach to mucosa
-disrupts protective properties by decreasing gastric mucus and mucosal bicarbonate secretion
Virulence factors of H pylori
Flagella
Urease (hydrolyze gastric urea to form ammonia to neutralize acid to penetrate)
Adhesins
Causes inflammation (cause G cells to secrete gastrin and increase HCl)
How is h pylori transmitted?
Oral-oral or fecal-oral to get to stomach
Why are NSAIDs not good for PUD?
They inhibit COX1 and 2 so there is no production of PGE2 which is important for a good environment in the stomach (stimulates mucin and inhibits gastrin to promote epithelial cell proliferation)
Factors that increase risk of PUD with use of NSAIDs
Prior history of PUD/ulcer complications Presence of H pylori infection Age >75 Increased dose, time and duration Concomitant use of steroids, other NSAIDs, anticoagulants, low dose ASA, SSRI and alendronate
Build up of what leads to formation of peptic ulcers?
H pylori
Gastric acid
Pepsin
NSAIDs
What are some protective factors of gastric mucosa?
Bicarbonate
PGs
Mucus production
Blood flow to mucosa
Most common sxs of PUD
Most are asymptomatic and of those that are symptomatic, they will have abdominal pain/ discomfort (burning/gnawing pain)
Other sxs of PUD
Belching, bloating, distention (dyspepsia-indigestion)
N/v, early satiety
Complications that cause hematemesis, melena, fatigue, dyspnea
Classic sxs of gastric ulcers
Pain worse after meals (30 min-1 hr)
Vomiting common
More likely to hemorrhage and cause hematemesis
Weight loss/ anorexia
Classic sxs of duodenal ulcers
Pain relieved by meals and worse 2-3 hrs after meal
Vomiting is uncommon
Less likely to hemorrhage but if does then melena
Weight gain
Alarm sxs of PUD
Bleeding (hematochezia is bad b/c these are upper and bleeding so fast that can't be digested) Unexplained iron deficiency anemia Early satiety Unintentional weight loss Progressive dysphagia/odynophagia Acute onset of intense upper abd pain Persistent vomiting Family hx of upper GI cancer
Most common complication of PUD
Bleeding/ hemorrhage
others are perforation, penetration and gastric outlet obstruction
Tx for bleeding due to PUD
Stabilize with IV fluids or PRBCs, start IV PPI and perform upper endoscopy/EGD (first thing you do after stabilize)
Standard tx to stop bleeding in PUD
Thermal coagulation
Hemoclip placement
Injection therapy
Presentation of perforation from PUD
Severe, diffuse, abdominal pain, tachycardia, weak pulse and n/v (may become board-like abd rigidity)