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27 Cards in this Set

  • Front
  • Back
where does the ulcer usually form?
wall of GI tract in duodenum or stomach
what are three common peptic ulcers?
Helicobacter pylori - associated - chronic

NSAID - induced (chronic)

Stress ulcers/SRMD (acute)
HP infection usually occurs where?

NSAIDs ulcer usually occurs where?
HP - duodenal ulcers

NSAIDs - stomach
Helicobacter pylori transmission is?
fecal-oral transmission

more common in developing countries

colonization does not mean active infection
-need cellular invasion to cause infection
What percentage of regular NSAID users get ulcers?
15-30%
What are some risk factors for NSAID-induced upper GI complications?
age > 60
history of PUD
history of upper GI bleed
concomitant corticosteroid therapy
Duration of NSAID use
high dose NSAID use
Nsaid related dyspepsia
anticoagulant or coagulopathy
CVD & other comorbid conditions
What are other factors attributed to NSAID induced PUD?
Cigargettes
-may impair healing of ulcers

Stress

Diet
-coffee, tea, cola, beer, spicy food
What is the pathophysiology attributing to ulcer formation?
Lack of balance between factors that break down food (gastric acid and pepsin)

Factors that promote epithelial helaing (bicarbonate, mucus secretion, and prostaglandins)
Gastric acid and pepsin secreation is normal or slightly eleveated in PUD, T/F?
T

NSAIDs do not effect acid secretion

HP infection causes slight increase in acid secretion
What does pepsin do?
initiates protein digestion and proteolysis of collagen

proteolytic activity may cause ulcer formation
How does mucosal defense work?

what effect do prostaglandins have on the GI environment?
mucosal gel
buffering action
allows acidic environment in lumen but near neutral pH on epithelial lining

Prostaglandins
inhibit gastric secretion
stimulate mcus and phospholipid production
promote bicarbonate secretion
increase mucosal cell turnover
Helicobactor pylor is gram-negative microaerophilic rod?

How does HP cause direc mucosal injury?
yes, it is also S shaped with flagella

causes gastroduodenal injury through:

direct mucosal damage
alterations to host inflammatory response
hypergastrinemia causing increased acid secretion
How do NSAIDs work and cause GI damage?
inhibit both COX-1 and COX-2 inhibition causes irritation

also is weakly acidic so it is a topical irritant

systemic pharmacologic action is promary cause of PUD
Why is it bad to inhibit COX-1?
becasue COX-1 leads to the production of PGs that are GI protective

produces productive prostaglandins that regulate GI mucosal integrity, renal fx, platelet homeostasis
Why are COX-2 good to inhibit?
theres cyclooxygenases lead to inflammation

these PGs are related to pain, fever, and inflammation
What are some complications of PUD?
- bleeding - erosion of ulcer into artery

- obstruction - scarring or inflammation near peripyloric region leading to gastric retention and early Satiety
What are some symptoms of PUD?
epigastric pain, abdominal pain, nocturnal pain, pain severity fluctuates, pain often 1-3 hrs after meals, heartburn, belching, bloating, N/V
Signs of PUD?
weight loss - associated with N/V
complications - bleeding, perforation, obstruction
alarm signs = bleeding, anemia, tarry stools, coffee ground emesis, weight loss
What are some desired out comes of treatment?
resolve symptoms
decrease acid secretion
promote epithelial healing
prevent ulcer related complications
prevent ulcer recurrence
if HP, then eradicate
What are some lifestyle modifications for PUD?
What are some HP eradication regimens?
Prevent NSAID-Induced Ulcer