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목차
pathophysiology
epidemiology
Clinical features
treatmentHistamine H2 receptor antagonist
Proton pump inhibitor(PPI)
pantoprazole
Antacid
sucralfate
Duodenal ulcer
Gastric ulcer
NSAIDs induced ulcer
Risk factor
treatment
NSAID사용시 위장관 부작용 예방
Refractory peptic ulcer disease
Helicobacter pylori
epidemiology
Pathology and pathogenesis
Natural history of H.pylori infection in humans
diagnosis
Urea breath test(UBT)
treatment
Definition of cure
H.pylori 재감염
Eradication failure
1.H.pylori의 초기박멸 후 추가적인 산억제제가 필요한가?
2.한국에서의 H.pylori박멸 현황
epidemiology
Clinical features
treatmentHistamine H2 receptor antagonist
Proton pump inhibitor(PPI)
pantoprazole
Antacid
sucralfate
Duodenal ulcer
Gastric ulcer
NSAIDs induced ulcer
Risk factor
treatment
NSAID사용시 위장관 부작용 예방
Refractory peptic ulcer disease
Helicobacter pylori
epidemiology
Pathology and pathogenesis
Natural history of H.pylori infection in humans
diagnosis
Urea breath test(UBT)
treatment
Definition of cure
H.pylori 재감염
Eradication failure
1.H.pylori의 초기박멸 후 추가적인 산억제제가 필요한가?
2.한국에서의 H.pylori박멸 현황
본문내용
Ulcer
: disruption of the mucosal integrity of the stomach /duodenum
: break in the mucosal surface > 5mm in size with depth to the submucosa
peptic ulcer disease
: ulcerations of the stomach, duodenum, or both, but peptic ulcers can develop in any portion of the gastrointestinal tract that is exposed to acid and pepsin in sufficient concentration and duration.
1910s no acid, no pepsin : no ulcer
1970s H2 receptor antagonist
1980s PPI(proton pump inhibitor)
1980s Helicobacter pylori, NSAIDs
pathophysiology
H.pylori
NSAIDs
Other ulcerogenic drugs
Chemotherapy(5-FU)
KCl solid preparation
crack cocaine bisphosphonate(alendronate,resedronate)
Hypersecretory condition
Gastrinoma
Systemic mastocytosis
MPD c basophilia (PV, basophilic CML)
Antral G cell hyperfunction
: disruption of the mucosal integrity of the stomach /duodenum
: break in the mucosal surface > 5mm in size with depth to the submucosa
peptic ulcer disease
: ulcerations of the stomach, duodenum, or both, but peptic ulcers can develop in any portion of the gastrointestinal tract that is exposed to acid and pepsin in sufficient concentration and duration.
1910s no acid, no pepsin : no ulcer
1970s H2 receptor antagonist
1980s PPI(proton pump inhibitor)
1980s Helicobacter pylori, NSAIDs
pathophysiology
H.pylori
NSAIDs
Other ulcerogenic drugs
Chemotherapy(5-FU)
KCl solid preparation
crack cocaine bisphosphonate(alendronate,resedronate)
Hypersecretory condition
Gastrinoma
Systemic mastocytosis
MPD c basophilia (PV, basophilic CML)
Antral G cell hyperfunction
소개글