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Flashcards in GI 2 Deck (25)
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1
Q

what is peptic ulcer disease?

A

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

2
Q

what is peptic ulcer disease usually associated with?

A

gastrits (inflammation)

3
Q

signs and symptoms of PUD

A

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
Q

major complications of PUD

A
penetration
obstruction
perforation
severe GI bleeding
death
5
Q

how is PUD diagnoses?

A

EGD- you can see and biopsy stomach and duodenum

6
Q

what stimulates parietal cells to produce acid?

A

G cells –> produce gastrin

7
Q

what produces HCl in the stomach?

A

parietal cells

8
Q

what protects the stomach from the acid it produces?

A

gastric mucous: rich in prostaglandin (PGE2) and bicarbonate

9
Q

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

A

H-Pylori - able to cross mucus layer of stomach

10
Q

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

A

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

11
Q

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

A
  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
Q

what is urease?

A

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
Q

5 year survival for early gastric cancer

A

85%

14
Q

5 year survival for advanced gastric cancer

A
15
Q

stages of gastric mucosa damage

A

gastritis –>metaplasia –> dyslasia –> cancer

16
Q

most common reasons for PUD injury/loss of protection

A

H-pylori and NSAIDS (local and systemic)

17
Q

local effect of NSAIDS and PUD

A

ASA accumulates in gastric cells causing cell death

18
Q

systemic effect of NSAIDS AND PUD

A

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
Q

what is PUD treatment based on?

A

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

20
Q

drugs used for acid neutralization, suppression or inhibition

A

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
Q

what do PPIs do?

A

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

22
Q

is anti acid/PPI treatment enough for PUD?

A

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

23
Q

how do you get H.pylori?

A

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
Q

treatment of H. Pylori

A

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
Q

treatment for PUD summary

A

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