stress ulcer

1. Stress Ulcer Tianjin medical university general hospital Songtao shou

2. sex :male age: 75y chief complaints : cough,gasp and spitting for 10 days,fever for 3 days. lethargy for 1 day . past history : COPD for 10 years. After admission to ICU,we found his stools were dark stools. ( no history of peptic ulcer.) Symptoms :cough, expectoration, gasp and fever,without abdominal pain . laboratory examination : ABG:pH 7.40,PaO 2 50mmHg ,PaCO 2 80mmHg Chest x-ray : Diagnosis : COPD , respiratory failure, pneumonia

3. lung markings

4. What should we do next?

5. laboratory examination 1. BRT:WBC 15×10 9 /L,N 90%,Hb140g/L,PLT 300×10 9 /L . 2.ABG:pH 7.40,PaO 2 50mmHg ,PaCO 2 80mmHg 3.stool :OB(++++), WBC(-),RBC(3/hp) the occult blood is positive after admission for 24 hours.

7. Therapy? 1 . positively correct the primary disease. 2. Antiacides(Omeprazole) 3. Cytoprotection( Sucralfate) 4. H 2 recepter antagonist(cimetidine) 5. enteral feeding

10. fight or flight

11. LC-sympathetic nerve-adrenal medullar Stress neuroendocrine Cell fluid H-P-A system Other hormones AP HSP Cytokine enzyme

13. Change from gene to whole body Clinical expression of stress reaction

14. LC cerebrum brainstem Spinal cord adrenal kidney LC-Sympathetic-adrenal gland medullar

15. LC

19. stressor CRH↑ ACTH↑ GC↑ Cerebral cortex and limbic system 、 amygdaloid body 、 hippocamp Hypothalamus-pituitary-adrenal

24. Reaction of cell and body fluid Cell AP HSP Some enzymes Some cytokines stressors

25. stressors Sympathetic nerve-adrenal medullar  CA  H-P-A active  GC  ALD 、 ADH 、 Endopeptide,ect  Insulin  Neuroendocrine change AP  HSP  Metabolic change summary

27. Stress ulcer

35. Pathogenesis of stress ulcer stress ulcer syndrome appears to be mucosa ischemia resulting form splanchnic hypofusion in the setting of physiologic stress and an acid

36. （ 1 ） mucosa ischemia （ 2 ） H + diffuse to intramucosa （ 3 ） others : acidosis CA  Mucosa barrier  H + diffuse to intramucosa Blood flow  H + pump out  ulcer GC  stressor Mucosa ischemia

38. The mucosa is compromised by ischemia and attacked (mostly) by acid. It is injured, and, due to the presence of acid, cannot repair itself (hostile environment). The use of external agents to neutralize acid resolves this problem.

42. Differences between PU and SU Endoscopic barium meal and endoscope diagnose Abdominal pain, Bleeding and Perforation are unusual Abdominal pain,perforation and bleeding Signs and symptoms Multiple Single or two Ulceration cardia ,fundus and body antrum Location acute chronic Attack SU PU

43. The mucosa plica in the gastric body is smooth.

44. Before making gastroscope,we have to fulfill the stomach with enough air,so under gastroscope the mucosa is very smooth.pylorus is round and always in contraction.

45. Mucus lake

46. thrombosis Peptic ulcer + complication (Bleeding)

47. Minal clot

48. petechia

50. The goal of therapy Stress ulcers are not deep craters like those seen in peptic ulcer disease,but are superficial erosions confined to the surface of the mucosa.Therefore, the goal of therapy is not so much to prevent their appearance but to limit the incidence of troublesome bleeding.

54. Principle of enteral feeding 1. To neutralize gastric pH(to dilute the relatively acid enviroment) 2. To provide the cells of the gastric mucosa with a nutrient.the cells may use luminal nutrients as a source of energy to produce the protective surface lining. 3. It solves the problems of nutrition and stress ulcer prophylaxis.

58. SUS are often viewed as a primary illness instead of a signal for mucosal ischemia . The misconception has created some confusion about the appropriate therapy for stress ulcers and specifically about the role of gastric acid suppression therapy.through the chapter ,we know stress ulcers are a manifestation of mucosa ischemia and NOT a manifestation of gastric hyperacidity.

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