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10조 Case Presentation 10조 이현경
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백O기 71/M Chief complaints Hematemesis, 2회 Melena Onset : 6.17
Vector : spontaneous (최근 음주량 증가)
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Present illness 상기 71세 남자환자는 6월 17일 오후에 발생한
Hematemesis, melena 주소로 ER 내원하여 시행한 GFS 상 Dieulafoy’s Ulcer 소견보여 Hemoclipping 시행 후 입원함
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Past History ‘95 gastric ulcer Dx & Tx
No known DM,HTN, pul Tb, hepatitis
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Personal history Family history Smoking (-)
Alcohol (+), 소주 1병/회, 주 3~4회 Allergy (-) Family history Non-specific
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Review of system Fever/ Chills/Weight loss (ㅡ /ㅡ/ ㅡ)
Cough/Coryza/Sputum (ㅡ/ㅡ/ ㅡ) Anorexia/Nausea/ Vomiting /Constipation/ Diarrhea (ㅡ/ㅡ/ㅡ/ㅡ/ㅡ)
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Vital sign
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Physical Examination General Appearance Head/Neck Chest
Relatively well appearance Head/Neck No anemic conjunctiva Anicteric sclera Chest Regular heart beat without murmur Clear breathing sound without rale
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Abdomen Extremities Soft & Flat Usual bowel sound No DT & RT
No pretibial pitting edema
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Lab - CBC
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Lab - Chemistry
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CXR FINDING - Rt lower lung에 2.2cm 크기의 nodular lesion이 calcification과 함께 보임 - Enhancement는 미약함 CONCLUSION Tuberculoma R/O Hamartoma
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Abdomen FINDING Normal range of bowel gas patterns. No abnormal calcific density. CONCLUSION Nonspecific findings
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GFS(6/18) [Esophagus] Non-specific [Stomach]
Deep ulcerative lesion with basal exposed vessel was noted at the pylorus.-hemoclipping done (*2) [Duodenum] Circular opening with outpouching of the mucosa at the 2nd portion
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Impression Acute gastric ulcer with exposed vessel
Anemia due to gastric ulcer bleeding
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Plan Diagnostic plan GFS F/U CBC F/U
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Therapeutic plan GI bleeding
Volume replacement(crystalloid solution or plasma expander) Transfusion(Packed RBC, peniramine, albumin) NPO Ulcer : IV PPI therapy + endoscopic therapy Pantoloc, Macool(metoclopromide)
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Radiology 폴리클 10조 44번 민현준
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6/20 (HD #2) S O A P General weakness WBC: 4740 Hb: 9.4 PLT: 108000
Upper gastroendoscopy A Acute gastric ulcer with exposed vessel P Ulcermin(sucralfate): 항pepsin제 Dulanta(Boehmite), Lamina G sol(sodium Alginate): GU & DU Upper gastroendoscopy F/U CBC F/U Sip's diet start , liquid 증량
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Upper Gastroendoscopy (6/20)
Known dieulafoy ulcer with bleeding at p-ring LC side -previous two hemoclip state -near completed healing state Reflux esophagitis Acute erosive gastritis
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6/22 (HD #4) S O A P Melena(+), hematemesis(-) WBC: 7500 Hb: 9.0
PLT: F/U GFS due to bleeding A Known dieulafoy ulcer c bleeding Reflux esophagitis, acute erosive gastritis P NPO, PPI Tx CBC F/U PRC transfusion
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Endoscopic Hemostasis (6/22)
Large exposed vessel without difinite ulceration was noted at upper portion of pyloric ring- hemoclipping Dieulafoy ulcer
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6/23 (HD #5) O A P WBC: 4200 Hb: 9.4 PLT: 158000
Known dieulafoy ulcer c bleeding, near complete healing stage Reflux esophagitis, acute erosive gastritis P CBC F/U
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6/25 (HD #7) O A P WBC: 5080 Hb: 9.6 PLT: 230000
Upper Gastrointestinal endoscopy A Known dieulafoy ulcer c bleeding, near complete healing stage Reflux esophagitis, acute erosive gastritis P CBC F/U Diet start
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Upper gastrointestinal endoscopy (6/25)
Just below pyloric channel-linear ulcer was noted. Pyloric channel- two hemoclips without bleeding Duodenal ulcer P-channel ulcer
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6/26 (HD #8) S O A P Melena (+), hematemesis (-) WBC: 5700 Hb: 8.2
PLT: GFS시행 Angiography, TAE A Known dieulafoy ulcer c bleeding, near complete healing stage Duodenal Ulcer, P-channel ulcer Reflux esophagitis, acute erosive gastritis P High dose PPI PRC transfusion CBC F/U NPO
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Upper gastrointestinal endoscopy (6/26)
Duodenum bulb에서 active한 arterial ejection관찰 UGI bleeding due to Duodenal ulcer with exposed vessel Angiographic embolization recommended
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Transarterial Embolization (6/26)
Retroduodenal A’ br’에서 bleeding focus가 보여 microcatheter를 이용하여 superselection 한 후 emblization함. Successful TAE due to GI bleeding
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6/28 (HD #10) S O A P Melena (+), hematemesis (-) WBC: 4540 Hb: 12.2
PLT: A Known dieulafoy ulcer c bleeding, near complete healing stage Duodenal Ulcer, P-channel ulcer Reflux esophagitis, acute erosive gastritis P PRC transfusion CBC F/U Sip’s water
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Peptic ulcer disease 10조 김경민
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Definition Ulcers defined as a break in the mucosal surface >5mm in size, with depth to the submucosa. PUD encompasses both gastric and duodenal ulcers.
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Epidemiology Duodenal ulcers (DU) Gastirc ulcers (GU)
Occur in 6~15% of the western population Incidence has steadily declined from 1960 to 1980 and has remained since than. This is related to decreasing frequency of H.pylori Gastirc ulcers (GU) Tend to occur later in life than duodenal ulcers Peak incidence in the sixth decade.
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Pathology Duodenal ulcers Gastric ulcers
DUs occur most often in the first portion of duodenum (>95%) Usually < 1 cm in diameter Gastric ulcers GUs are most often found in the antrum (60%)
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Pathophysiology A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic inflammation due to H.pylori that colonizes the antral mucosa. The bacterium can cause a chronic active gastritis resulting in a defect in the regulation of gastrin production Gastrin secretion is increased. gatrin, in turn, stimulates the production of gastric acid by parietal cells. The acid erodes the mucosa and causes the ulcer.
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Pathophysiology Another major cause is the use of NSAIDs.
The gastric mucosa protects itself from gastric acid with a layer of mucous, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cycloxygenase 1 (cox-1), which is essential for the production of these prostaglandins.
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Symptoms Epigastirc pain Duodenal ulcers Gastric ulcers
Occurs 90 min to 3hr after a meal Relieved by antacid or food. Pain that awakes the patient from sleep is the most discriminating symptom. Gastric ulcers Discomfort precipitated by food. Nausea and weight loss occur more commonly in GU patient.
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Symptoms Bloating and abdominal fullness Nausea, vomiting
Loss of appetite and weight loss Hematemesis Melena
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PUD - related complication
Gastrointestinal bleeding Most common complication in PUD. Occurs in 15% of patients and more often in > 60 years old. Perforation Second most common ulcer-related complication. Reported as many as 6~7% of PUD patients.
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PUD - related complication
Penetration Form of perforation in which the ulcer bed tunnels into adjacent organs. DUs tend to penetrate posterioly into pancreas, leading to pancreatitis. GUs tend to penetrate into the left hepatic lobe.
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PUD - related complication
Gastric outlet obstruction The least common complication, occuring in 1~2% of patients. Relative obstruction due to inflammation and edema in the peripyloric region. Mechanical obstruction secondary to scar formation.
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Treatment Acid neutralizing / inhibitory agent Cytoprotective agents
Antacid H2 receptor antagonist Cimetidine, ranitidine, famotidine Proton pump inhibitors Omeprazole, esomeprazole, lansoprazole Cytoprotective agents Sucralfate Bismuth – containing preparations Prostaglandin analogues misoprostal
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Treatment Eradication of H.pylori infection Triple therapy
Bismuth + Metronidazole + Tetracyclin Ranitidine + Tetracyclin + Clarithromycin or Metronidazole Omeprazole + Clarithromycin + Metronidazole or Amoxicillin Quadruple therapy Omeprazole + Bismuth + Metronidazole + Amoxicillin
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Treatment NSAID – related gastric or duodenal injury Active ulcer
NSAID discontinued : H2 blocker or PPI NSAID continued: PPI Prophylactic therapy Misoprostol PPI Selective COX-2 inhibitor
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