GI 2 Flashcards
what is peptic ulcer disease?
chronic, necrotic mucosal defect of stomach or duodenum which may cause pain, dyspepsia, nausea, vomiting, or bleeding
what is peptic ulcer disease usually associated with?
gastrits (inflammation)
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
major complications of PUD
penetration obstruction perforation severe GI bleeding death
how is PUD diagnoses?
EGD- you can see and biopsy stomach and duodenum
what stimulates parietal cells to produce acid?
G cells –> produce gastrin
what produces HCl in the stomach?
parietal cells
what protects the stomach from the acid it produces?
gastric mucous: rich in prostaglandin (PGE2) and bicarbonate
which bacteria is able to colonize in stomach despite gastric acidity?
H-Pylori - able to cross mucus layer of stomach
what 4 important qualities allow H-pylori to colonize in stomach
mobility (flagella)
penetration
adhesiveness (glycan receptors)
induction of inflammation
what 2 factors help H-pylori to survive despite gastric acid, cause injury, and induce cancer?
- urease: an active enzyme to reduce acid concentration and to protect H. pylori in its niche
- cytotoxin associated antigen (Cag A) causing DNA damage
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
5 year survival for early gastric cancer
85%
5 year survival for advanced gastric cancer
stages of gastric mucosa damage
gastritis –>metaplasia –> dyslasia –> cancer
most common reasons for PUD injury/loss of protection
H-pylori and NSAIDS (local and systemic)
local effect of NSAIDS and PUD
ASA accumulates in gastric cells causing cell death
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
what is PUD treatment based on?
pathogenesis- control of acid, eradication of H-pylori, discontinue NSAIDs to protect gastric mucosa
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
what do PPIs do?
inhibit acid secretion (and therefore heal ulcers and eliminate pain)
is anti acid/PPI treatment enough for PUD?
no, ulcers will come back unless we treat H-pylori and/or eliminate NSAIDs
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
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
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
