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Flashcards in GI 2 Deck (25):
1

what is peptic ulcer disease?

chronic, necrotic mucosal defect of stomach or duodenum which may cause pain, dyspepsia, nausea, vomiting, or bleeding

2

what is peptic ulcer disease usually associated with?

gastrits (inflammation)

3

signs and symptoms of PUD

vague or just discomfort
fullness, postprandial pain and or pre-prandial pain (hunger pain)
anorexia, weight loss
epigastric pain
nausea, vomiting, and signs of gastric obstruction
hematemesis and/or melena
anemia - iron deficiency anemia

4

major complications of PUD

penetration
obstruction
perforation
severe GI bleeding
death

5

how is PUD diagnoses?

EGD- you can see and biopsy stomach and duodenum

6

what stimulates parietal cells to produce acid?

G cells --> produce gastrin

7

what produces HCl in the stomach?

parietal cells

8

what protects the stomach from the acid it produces?

gastric mucous: rich in prostaglandin (PGE2) and bicarbonate

9

which bacteria is able to colonize in stomach despite gastric acidity?

H-Pylori - able to cross mucus layer of stomach

10

what 4 important qualities allow H-pylori to colonize in stomach

mobility (flagella)
penetration
adhesiveness (glycan receptors)
induction of inflammation

11

what 2 factors help H-pylori to survive despite gastric acid, cause injury, and induce cancer?

1. urease: an active enzyme to reduce acid concentration and to protect H. pylori in its niche
2. cytotoxin associated antigen (Cag A) causing DNA damage

12

what is urease?

enzyme produced by H-Pylori that regulates the conversion of urea into CO2 and ammonia, which reduced gastric acidity so other HPs come in

13

5 year survival for early gastric cancer

85%

14

5 year survival for advanced gastric cancer

15

stages of gastric mucosa damage

gastritis -->metaplasia --> dyslasia --> cancer

16

most common reasons for PUD injury/loss of protection

H-pylori and NSAIDS (local and systemic)

17

local effect of NSAIDS and PUD

ASA accumulates in gastric cells causing cell death

18

systemic effect of NSAIDS AND PUD

DISRUPTING PROSTAGLANDIN SYNTHESIS AND DESTROYING GASTRIC BARRIER TO ACID WHICH CAUSES ULCER

NSAIDS block the production of PGE2 which is essential for gastric mucosa protection

19

what is PUD treatment based on?

pathogenesis- control of acid, eradication of H-pylori, discontinue NSAIDs to protect gastric mucosa

20

drugs used for acid neutralization, suppression or inhibition

aluminum hydroxide, magnesium hydroxide, bicarbonates- neutralize acid for a short time: H+ neutralizers (minor drugs)

H2 blockers: block the histamine effect on parietal cell and work for 4-6 hours and reduce acid (medium effect)

PPI: block formation of acid by inhibiting ATPase activity in parietal cells (most effective): PPI (omperazol)

sucralfate, bismuth, misoprostal: protection of mucosa

21

what do PPIs do?

inhibit acid secretion (and therefore heal ulcers and eliminate pain)

22

is anti acid/PPI treatment enough for PUD?

no, ulcers will come back unless we treat H-pylori and/or eliminate NSAIDs

23

how do you get H.pylori?

water or fecal contamination, so this infection should be prevented by better hygiene and education

*in any EGD referral for PUD, dyspepsia, anemia or NSAIDs induced ulcer or GI bleeding look for H-pylori

24

treatment of H. Pylori

most common: triple therapy (PPI + amoxicillin + claithromycin) 7-10 days

best!!: quadruple therapy (PPI +bismuth + metronidazole + tetracycline) for 14 days
PPI twice daily for 8 weeks
bismuth 2 tablets QID x 2 weeks
metronidazol 250 mg TID for 2 weeks
tetracycline 500 mg QID, for 2 weeks or levofloxacin; levaquin 500 mg daily

most recent: levofloxacin + amoxicillin + tinidazole + simvastatin 20 mg for 7-5 days

25

treatment for PUD summary

treat for 8 weeks with PPI, repeat EGD only in GU
if you find h-pylori: treat for 10-14 days with antibiotics combination based on patient's allergy and resistance history

eliminate NSAIDs
check stool h-pylori antigen 4 weeks after all drug treatments are stopped