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Surgery_Schwartz_7302 | Surgery_Schwartz | with a curative intent. Am J Gastroenterol. 2008;103:2589-2597.Brunicardi_Ch25_p1009-p1098.indd 109601/03/19 6:06 PM 1097ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25McCort JJ. Esophageal carcinosarcoma and pseudosarcoma. Radiology. 1972;102:519-524.Medical Research Council Oesophageal Working Party. Surgi-cal resection with or without preoperative chemotherapy in oesophageal cancer: a randomized controlled trial. Lancet. 2002;359:1727-1733.Naunheim KS, Petruska PJ, et al. Preoperative chemotherapy and radiotherapy for esophageal carcinoma. J Thorac Cardiovasc Surg. 1992;103:887-893.Nicks R. Colonic replacement of the esophagus. Br J Surg. 1967; 54:124-128.Nigro JJ, Hagen JA, DeMeester TR, et al. Occult esophageal ade-nocarcinoma: extent of disease and implications for effective therapy. Ann Surg. 1999;230:433-438.Omloo JM, Lagarde SM, Hulscher JB, et al. Extended transtho-racic resection compared with limited transhiatal resection for adenocarcinoma of the mid/distal esophagus: | Surgery_Schwartz. with a curative intent. Am J Gastroenterol. 2008;103:2589-2597.Brunicardi_Ch25_p1009-p1098.indd 109601/03/19 6:06 PM 1097ESOPHAGUS AND DIAPHRAGMATIC HERNIACHAPTER 25McCort JJ. Esophageal carcinosarcoma and pseudosarcoma. Radiology. 1972;102:519-524.Medical Research Council Oesophageal Working Party. Surgi-cal resection with or without preoperative chemotherapy in oesophageal cancer: a randomized controlled trial. Lancet. 2002;359:1727-1733.Naunheim KS, Petruska PJ, et al. Preoperative chemotherapy and radiotherapy for esophageal carcinoma. J Thorac Cardiovasc Surg. 1992;103:887-893.Nicks R. Colonic replacement of the esophagus. Br J Surg. 1967; 54:124-128.Nigro JJ, Hagen JA, DeMeester TR, et al. Occult esophageal ade-nocarcinoma: extent of disease and implications for effective therapy. Ann Surg. 1999;230:433-438.Omloo JM, Lagarde SM, Hulscher JB, et al. Extended transtho-racic resection compared with limited transhiatal resection for adenocarcinoma of the mid/distal esophagus: |
Surgery_Schwartz_7303 | Surgery_Schwartz | Ann Surg. 1999;230:433-438.Omloo JM, Lagarde SM, Hulscher JB, et al. Extended transtho-racic resection compared with limited transhiatal resection for adenocarcinoma of the mid/distal esophagus: Five year survival of a randomized clinical trial. Ann Surg. 2007;246(6):992-1000.Orringer MB, Marshall B, Iannettoni MD. Transhiatal esopha-gectomy: clinical experience and refinements. Ann Surg. 1999;230:392.Orringer MB, Marshall B, Chang AC, et al. Two thousand tran-shiatal esophagectomies: changing trends, lessons learned. Ann Surg. 2007;246(3):363-372; discussion 372-374.Ott K, Herrmann K, Lordick F, et al. Early metabolic response evaluation by fluorine-18 fluorodeoxyglucose positron emis-sion tomography allows in vivo testing of chemosensitivity in gastric cancer: long-term results of a prospective study. Clin Cancer Res. 2008;14:2012-2018.Pacifico RJ, Wang KK, Wongkeesong LM, et al. Combined endo-scopic mucosal resection and photodynamic therapy versus esophagectomy for management of | Surgery_Schwartz. Ann Surg. 1999;230:433-438.Omloo JM, Lagarde SM, Hulscher JB, et al. Extended transtho-racic resection compared with limited transhiatal resection for adenocarcinoma of the mid/distal esophagus: Five year survival of a randomized clinical trial. Ann Surg. 2007;246(6):992-1000.Orringer MB, Marshall B, Iannettoni MD. Transhiatal esopha-gectomy: clinical experience and refinements. Ann Surg. 1999;230:392.Orringer MB, Marshall B, Chang AC, et al. Two thousand tran-shiatal esophagectomies: changing trends, lessons learned. Ann Surg. 2007;246(3):363-372; discussion 372-374.Ott K, Herrmann K, Lordick F, et al. Early metabolic response evaluation by fluorine-18 fluorodeoxyglucose positron emis-sion tomography allows in vivo testing of chemosensitivity in gastric cancer: long-term results of a prospective study. Clin Cancer Res. 2008;14:2012-2018.Pacifico RJ, Wang KK, Wongkeesong LM, et al. Combined endo-scopic mucosal resection and photodynamic therapy versus esophagectomy for management of |
Surgery_Schwartz_7304 | Surgery_Schwartz | study. Clin Cancer Res. 2008;14:2012-2018.Pacifico RJ, Wang KK, Wongkeesong LM, et al. Combined endo-scopic mucosal resection and photodynamic therapy versus esophagectomy for management of early adenocarcinoma of the esophagus. Clin Gastroenterol Hepatol. 2003;1:252-257.Pera M, Cameron AJ, Trastek VF, Carpenter HA, Zinsmeister AR. Increasing incidence of adenocarcinoma of the esoph-agus and esophagogastric junction. Gastroenterology. 1993;104(2):510-513.Pera M, Trastek VF, Carpenter HA, Allen MS, Deschamps C, Pairolero PC. Barrett’s esophagus with high-grade dysplasia: an indication for esophagectomy? Ann Thorac Surg. 1992;54:199-204.Pera M, Trastek VF, Carpenter HA, et al. Influence of pancreatic and biliary reflux on the development of esophageal carcinoma. Ann Thorac Surg. 1993;55:1386-1392.Peters JH, Clark GWB, Ireland AP, Chandrasoma P, Smyrk TC, DeMeester TR. Outcome of adenocarcinoma arising in Barrett’s esophagus in endoscopically surveyed and non-surveyed patients. J | Surgery_Schwartz. study. Clin Cancer Res. 2008;14:2012-2018.Pacifico RJ, Wang KK, Wongkeesong LM, et al. Combined endo-scopic mucosal resection and photodynamic therapy versus esophagectomy for management of early adenocarcinoma of the esophagus. Clin Gastroenterol Hepatol. 2003;1:252-257.Pera M, Cameron AJ, Trastek VF, Carpenter HA, Zinsmeister AR. Increasing incidence of adenocarcinoma of the esoph-agus and esophagogastric junction. Gastroenterology. 1993;104(2):510-513.Pera M, Trastek VF, Carpenter HA, Allen MS, Deschamps C, Pairolero PC. Barrett’s esophagus with high-grade dysplasia: an indication for esophagectomy? Ann Thorac Surg. 1992;54:199-204.Pera M, Trastek VF, Carpenter HA, et al. Influence of pancreatic and biliary reflux on the development of esophageal carcinoma. Ann Thorac Surg. 1993;55:1386-1392.Peters JH, Clark GWB, Ireland AP, Chandrasoma P, Smyrk TC, DeMeester TR. Outcome of adenocarcinoma arising in Barrett’s esophagus in endoscopically surveyed and non-surveyed patients. J |
Surgery_Schwartz_7305 | Surgery_Schwartz | JH, Clark GWB, Ireland AP, Chandrasoma P, Smyrk TC, DeMeester TR. Outcome of adenocarcinoma arising in Barrett’s esophagus in endoscopically surveyed and non-surveyed patients. J Thorac Cardiovasc Surg. 1994;108(5):813-821.Peters JH, Hoeft SF, Heimbucher J, et al. Selection of patients for cura-tive or palliative resection of esophageal cancer based on preopera-tive endoscopic ultrasound. Arch Surg. 1994;129:534-539.Peters JH. Surgical treatment of esophageal adenocarcinoma: con-cepts in evolution. J Gastrointest Surg. 2002;6:518.Rasanen JV, Sihvo EIT, Knuuti J, et al. Prospective analysis of accuracy of proton emission tomography, computed tomogra-phy and endoscopic ultrasonography in staging of adenocarci-noma of the esophagus and esophagogastric junction. Ann Surg Oncol. 2003;10:954-960.Ravitch M. A Century of Surgery. Philadelphia: Lippincott; 1981:56.Reed CE. Comparison of different treatments for unresectable esophageal cancer. World J Surg. 1995;19:828.Reid BJ, Weinstein WM, | Surgery_Schwartz. JH, Clark GWB, Ireland AP, Chandrasoma P, Smyrk TC, DeMeester TR. Outcome of adenocarcinoma arising in Barrett’s esophagus in endoscopically surveyed and non-surveyed patients. J Thorac Cardiovasc Surg. 1994;108(5):813-821.Peters JH, Hoeft SF, Heimbucher J, et al. Selection of patients for cura-tive or palliative resection of esophageal cancer based on preopera-tive endoscopic ultrasound. Arch Surg. 1994;129:534-539.Peters JH. Surgical treatment of esophageal adenocarcinoma: con-cepts in evolution. J Gastrointest Surg. 2002;6:518.Rasanen JV, Sihvo EIT, Knuuti J, et al. Prospective analysis of accuracy of proton emission tomography, computed tomogra-phy and endoscopic ultrasonography in staging of adenocarci-noma of the esophagus and esophagogastric junction. Ann Surg Oncol. 2003;10:954-960.Ravitch M. A Century of Surgery. Philadelphia: Lippincott; 1981:56.Reed CE. Comparison of different treatments for unresectable esophageal cancer. World J Surg. 1995;19:828.Reid BJ, Weinstein WM, |
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Surgery_Schwartz_7308 | Surgery_Schwartz | DB, Dowlatshahi KD, DeMeester TR. Potentially curable carcinoma of the esophagus. Cancer. 1982;50:2571-2575.Skinner DB, Little AG, Ferguson MK, Soriano A, Staszak VM. Selection of operation for esophageal cancer based on staging. Ann Surg. 1986;204:391-401.Smithers BM, Cullinan M, Thomas JM, et al. Outcomes from salvage esophagectomy post definitive chemoradiotherapy compared with resection following preoperative neoadjuvant chemoradiotherapy. Dis Esophagus. 2007;20:471-477.Sonnenberg A, Fennerty MB. Medical decision analysis of chemo-prevention against esophageal adenocarcinoma. Gastroenterol-ogy. 2003;124:1758-1766.Streitz JM, Jr, Ellis FH, Jr, Gibb SP, et al. Adenocarcinoma in Barrett’s esophagus. Ann Surg. 1991;213:122-125.Turnbull AD, Rosen P, Goodner JT, et al. Primary malignant tumors of the esophagus other than typical epidermoid carcinoma. Ann Thorac Surg. 1973;15:463-473.Urschel JD, Ashiku S, Thurer R, et al. Salvage or planned esophagectomy after chemoradiation for | Surgery_Schwartz. DB, Dowlatshahi KD, DeMeester TR. Potentially curable carcinoma of the esophagus. Cancer. 1982;50:2571-2575.Skinner DB, Little AG, Ferguson MK, Soriano A, Staszak VM. Selection of operation for esophageal cancer based on staging. Ann Surg. 1986;204:391-401.Smithers BM, Cullinan M, Thomas JM, et al. Outcomes from salvage esophagectomy post definitive chemoradiotherapy compared with resection following preoperative neoadjuvant chemoradiotherapy. Dis Esophagus. 2007;20:471-477.Sonnenberg A, Fennerty MB. Medical decision analysis of chemo-prevention against esophageal adenocarcinoma. Gastroenterol-ogy. 2003;124:1758-1766.Streitz JM, Jr, Ellis FH, Jr, Gibb SP, et al. Adenocarcinoma in Barrett’s esophagus. Ann Surg. 1991;213:122-125.Turnbull AD, Rosen P, Goodner JT, et al. Primary malignant tumors of the esophagus other than typical epidermoid carcinoma. Ann Thorac Surg. 1973;15:463-473.Urschel JD, Ashiku S, Thurer R, et al. Salvage or planned esophagectomy after chemoradiation for |
Surgery_Schwartz_7309 | Surgery_Schwartz | tumors of the esophagus other than typical epidermoid carcinoma. Ann Thorac Surg. 1973;15:463-473.Urschel JD, Ashiku S, Thurer R, et al. Salvage or planned esophagectomy after chemoradiation for locally advanced esophageal cancer: a review. Dis Esophagus. 2003;16:60-65.Vigneswaran WT, Trastek VK, Pairolero PC, et al. Extended esoph-agectomy in the management of carcinoma of the upper tho-racic esophagus. J Thorac Cardiovasc Surg. 1994;107:901-907.Walsh TN, Noonan N, Hollywood D, Kelly A, Keeling N, Hennessy TP. A comparison of multimodal therapy and surgery for esophageal adenocarcinoma. N Engl J Med. 1996;335:462-467.Watson WP, Pool L. Cancer of the cervical esophagus. Surgery. 1948;23:893.Benign Tumors and CystsBardini R, Segalin A, Ruol A, et al. Videothoracoscopic enucleation of esophageal leiomyoma. Am Thorac Surg. 1992;54:576-577.Bonavina L, Segalin A, Rosati R, Pavanello M, Peracchia A. Surgical therapy of esophageal leiomyoma. J Am Coll Surg. 1995;181:257-262.Esophageal | Surgery_Schwartz. tumors of the esophagus other than typical epidermoid carcinoma. Ann Thorac Surg. 1973;15:463-473.Urschel JD, Ashiku S, Thurer R, et al. Salvage or planned esophagectomy after chemoradiation for locally advanced esophageal cancer: a review. Dis Esophagus. 2003;16:60-65.Vigneswaran WT, Trastek VK, Pairolero PC, et al. Extended esoph-agectomy in the management of carcinoma of the upper tho-racic esophagus. J Thorac Cardiovasc Surg. 1994;107:901-907.Walsh TN, Noonan N, Hollywood D, Kelly A, Keeling N, Hennessy TP. A comparison of multimodal therapy and surgery for esophageal adenocarcinoma. N Engl J Med. 1996;335:462-467.Watson WP, Pool L. Cancer of the cervical esophagus. Surgery. 1948;23:893.Benign Tumors and CystsBardini R, Segalin A, Ruol A, et al. Videothoracoscopic enucleation of esophageal leiomyoma. Am Thorac Surg. 1992;54:576-577.Bonavina L, Segalin A, Rosati R, Pavanello M, Peracchia A. Surgical therapy of esophageal leiomyoma. J Am Coll Surg. 1995;181:257-262.Esophageal |
Surgery_Schwartz_7310 | Surgery_Schwartz | esophageal leiomyoma. Am Thorac Surg. 1992;54:576-577.Bonavina L, Segalin A, Rosati R, Pavanello M, Peracchia A. Surgical therapy of esophageal leiomyoma. J Am Coll Surg. 1995;181:257-262.Esophageal PerforationBrewer LA III, Carter R, Mulder GA, Stiles QR. Options in the management of perforations of the esophagus. Am J Surg. 1986;152:62-69.Bufkin BL, Miller JI, Jr, Mansour KA. Esophageal perfora-tion. Emphasis on management. Ann Thorac Surg. 1996;61: 1447-1451.Chang C-H, Lin PJ, Chang JP, et al. One-stage operation for treat-ment after delayed diagnosis of thoracic esophageal perforation. Ann Thorac Surg. 1992;53:617-620.Brunicardi_Ch25_p1009-p1098.indd 109701/03/19 6:06 PM 1098SPECIFIC CONSIDERATIONSPART IIEngum SA, Grosfeld JL, West KW, et al. Improved survival in chil-dren with esophageal perforation. Arch Surg. 1996;131:604-611.Gouge TH, Depan HJ, Spencer FC. Experience with the Grillo pleural wrap procedure in 18 patients with perforation of the thoracic esophagus. Ann Surg. | Surgery_Schwartz. esophageal leiomyoma. Am Thorac Surg. 1992;54:576-577.Bonavina L, Segalin A, Rosati R, Pavanello M, Peracchia A. Surgical therapy of esophageal leiomyoma. J Am Coll Surg. 1995;181:257-262.Esophageal PerforationBrewer LA III, Carter R, Mulder GA, Stiles QR. Options in the management of perforations of the esophagus. Am J Surg. 1986;152:62-69.Bufkin BL, Miller JI, Jr, Mansour KA. Esophageal perfora-tion. Emphasis on management. Ann Thorac Surg. 1996;61: 1447-1451.Chang C-H, Lin PJ, Chang JP, et al. One-stage operation for treat-ment after delayed diagnosis of thoracic esophageal perforation. Ann Thorac Surg. 1992;53:617-620.Brunicardi_Ch25_p1009-p1098.indd 109701/03/19 6:06 PM 1098SPECIFIC CONSIDERATIONSPART IIEngum SA, Grosfeld JL, West KW, et al. Improved survival in chil-dren with esophageal perforation. Arch Surg. 1996;131:604-611.Gouge TH, Depan HJ, Spencer FC. Experience with the Grillo pleural wrap procedure in 18 patients with perforation of the thoracic esophagus. Ann Surg. |
Surgery_Schwartz_7311 | Surgery_Schwartz | perforation. Arch Surg. 1996;131:604-611.Gouge TH, Depan HJ, Spencer FC. Experience with the Grillo pleural wrap procedure in 18 patients with perforation of the thoracic esophagus. Ann Surg. 1989;209:612-617.Jones WG II, Ginsberg RJ. Esophageal perforation: a continuing challenge. Ann Thorac Surg. 1992;53:534-543.Pate JW, Walker WA, Cole FH, Jr, Owen EW, Johnson WH. Spontaneous rupture of the esophagus: a 30-year experience. Ann Thorac Surg. 1989;47:689-692.Reeder LB, DeFilippi VJ, Ferguson MK. Current results of therapy for esophageal perforation. Am J Surg. 1995;169:615-617.Salo JA, Isolauri JO, Heikkilä LJ, et al. Management of delayed esophageal perforation with mediastinal sepsis. Esopha-gectomy or primary repair? J Thorac Cardiovasc Surg. 1993;106:1088-1091.Sawyer R, Phillips C, Vakil N. Shortand long-term outcome of esophageal perforation. Gastrointest Endosc. 1995;41:130-134.Segalin A, Bonavina L, Lazzerini M, De Ruberto F, Faranda C, Peracchia A. Endoscopic management of | Surgery_Schwartz. perforation. Arch Surg. 1996;131:604-611.Gouge TH, Depan HJ, Spencer FC. Experience with the Grillo pleural wrap procedure in 18 patients with perforation of the thoracic esophagus. Ann Surg. 1989;209:612-617.Jones WG II, Ginsberg RJ. Esophageal perforation: a continuing challenge. Ann Thorac Surg. 1992;53:534-543.Pate JW, Walker WA, Cole FH, Jr, Owen EW, Johnson WH. Spontaneous rupture of the esophagus: a 30-year experience. Ann Thorac Surg. 1989;47:689-692.Reeder LB, DeFilippi VJ, Ferguson MK. Current results of therapy for esophageal perforation. Am J Surg. 1995;169:615-617.Salo JA, Isolauri JO, Heikkilä LJ, et al. Management of delayed esophageal perforation with mediastinal sepsis. Esopha-gectomy or primary repair? J Thorac Cardiovasc Surg. 1993;106:1088-1091.Sawyer R, Phillips C, Vakil N. Shortand long-term outcome of esophageal perforation. Gastrointest Endosc. 1995;41:130-134.Segalin A, Bonavina L, Lazzerini M, De Ruberto F, Faranda C, Peracchia A. Endoscopic management of |
Surgery_Schwartz_7312 | Surgery_Schwartz | Vakil N. Shortand long-term outcome of esophageal perforation. Gastrointest Endosc. 1995;41:130-134.Segalin A, Bonavina L, Lazzerini M, De Ruberto F, Faranda C, Peracchia A. Endoscopic management of inveterate esophageal perforations and leaks. Surg Endosc. 1996;10:928-932.Weiman DS, Walker WA, Brosnan KM, Pate JW, Fabian TC. Noniat-rogenic esophageal trauma. Ann Thorac Surg. 1995;59:845-849.Whyte RI, Iannettoni MD, Orringer MB. Intrathoracic esophageal perforation. The merit of primary repair. J Thorac Cardiovasc Surg. 1995;109:140-144.Caustic InjuryAnderson KD, Rouse TM, Randolph JG. A controlled trial of cor-ticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990;323:637-640.Ferguson MK, Migliore M, Staszak VM, Little AG. Early evaluation and therapy for caustic esophageal injury. Am J Surg. 1989;157:116-120.Lahoti D, Broor SL, Basu PP, Gupta A, Sharma R, Pant CS. Corro-sive esophageal strictures. Predictors of response to endoscopic dilation. | Surgery_Schwartz. Vakil N. Shortand long-term outcome of esophageal perforation. Gastrointest Endosc. 1995;41:130-134.Segalin A, Bonavina L, Lazzerini M, De Ruberto F, Faranda C, Peracchia A. Endoscopic management of inveterate esophageal perforations and leaks. Surg Endosc. 1996;10:928-932.Weiman DS, Walker WA, Brosnan KM, Pate JW, Fabian TC. Noniat-rogenic esophageal trauma. Ann Thorac Surg. 1995;59:845-849.Whyte RI, Iannettoni MD, Orringer MB. Intrathoracic esophageal perforation. The merit of primary repair. J Thorac Cardiovasc Surg. 1995;109:140-144.Caustic InjuryAnderson KD, Rouse TM, Randolph JG. A controlled trial of cor-ticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990;323:637-640.Ferguson MK, Migliore M, Staszak VM, Little AG. Early evaluation and therapy for caustic esophageal injury. Am J Surg. 1989;157:116-120.Lahoti D, Broor SL, Basu PP, Gupta A, Sharma R, Pant CS. Corro-sive esophageal strictures. Predictors of response to endoscopic dilation. |
Surgery_Schwartz_7313 | Surgery_Schwartz | for caustic esophageal injury. Am J Surg. 1989;157:116-120.Lahoti D, Broor SL, Basu PP, Gupta A, Sharma R, Pant CS. Corro-sive esophageal strictures. Predictors of response to endoscopic dilation. Gastrointest Endosc. 1995;41:196-200.Popovici Z. About reconstruction of the pharynx with colon in extensive corrosive strictures. Kurume Med J. 1989;36:41-47.Sugawa C, Lucas CE. Caustic injury of the upper gastrointesti-nal tract in adults: a clinical and endoscopic study. Surgery. 1989;106:802-806.Wu M-H, Lai W-W. Surgical management of extensive corro-sive injuries of the alimentary tract. Surg Gynecol Obstet. 1993;177:12-16.Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modi-fied endoscopic classification of burns. Gastrointest Endosc. 1991;37:165-169.Techniques of Esophageal ReconstructionAkiyama H. Esophageal reconstruction. Entire stomach as esopha-geal substitute. Dis Esophagus. 1995;8:7-9.Banki F, Mason RJ, | Surgery_Schwartz. for caustic esophageal injury. Am J Surg. 1989;157:116-120.Lahoti D, Broor SL, Basu PP, Gupta A, Sharma R, Pant CS. Corro-sive esophageal strictures. Predictors of response to endoscopic dilation. Gastrointest Endosc. 1995;41:196-200.Popovici Z. About reconstruction of the pharynx with colon in extensive corrosive strictures. Kurume Med J. 1989;36:41-47.Sugawa C, Lucas CE. Caustic injury of the upper gastrointesti-nal tract in adults: a clinical and endoscopic study. Surgery. 1989;106:802-806.Wu M-H, Lai W-W. Surgical management of extensive corro-sive injuries of the alimentary tract. Surg Gynecol Obstet. 1993;177:12-16.Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modi-fied endoscopic classification of burns. Gastrointest Endosc. 1991;37:165-169.Techniques of Esophageal ReconstructionAkiyama H. Esophageal reconstruction. Entire stomach as esopha-geal substitute. Dis Esophagus. 1995;8:7-9.Banki F, Mason RJ, |
Surgery_Schwartz_7314 | Surgery_Schwartz | Endosc. 1991;37:165-169.Techniques of Esophageal ReconstructionAkiyama H. Esophageal reconstruction. Entire stomach as esopha-geal substitute. Dis Esophagus. 1995;8:7-9.Banki F, Mason RJ, DeMeester SR, et al. Vagal sparing esopha-gectomy: a more physiologic alternative. Ann Surg. 2002; 236:324-336.Burt M, Scott A, Williard WC, et al. Erythromycin stimu-lates gastric emptying after esophagectomy with gastric replacement. A randomized clinical trial. J Thorac Cardiovasc Surg. 1996;111:649-654.Cheng W, Heitmiller RF, Jones BJ. Subacute ischemia of the colon esophageal interposition. Ann Thorac Surg. 1994;57:899-903.DeMeester TR, Johansson KE, Franze I, Eypasch E, Lu CT, McGill JE, Zaninotto G. Indications, surgical technique, and long-term functional results of colon interposition or bypass. Ann Surg. 1988(4);208:460-474.DeMeester TR, Kauer WK. Esophageal reconstruction. The colon as an esophageal substitute. Dis Esophagus. 1995;8:20-29.Dexter SPL, Martin IG, McMahon MJ. Radical | Surgery_Schwartz. Endosc. 1991;37:165-169.Techniques of Esophageal ReconstructionAkiyama H. Esophageal reconstruction. Entire stomach as esopha-geal substitute. Dis Esophagus. 1995;8:7-9.Banki F, Mason RJ, DeMeester SR, et al. Vagal sparing esopha-gectomy: a more physiologic alternative. Ann Surg. 2002; 236:324-336.Burt M, Scott A, Williard WC, et al. Erythromycin stimu-lates gastric emptying after esophagectomy with gastric replacement. A randomized clinical trial. J Thorac Cardiovasc Surg. 1996;111:649-654.Cheng W, Heitmiller RF, Jones BJ. Subacute ischemia of the colon esophageal interposition. Ann Thorac Surg. 1994;57:899-903.DeMeester TR, Johansson KE, Franze I, Eypasch E, Lu CT, McGill JE, Zaninotto G. Indications, surgical technique, and long-term functional results of colon interposition or bypass. Ann Surg. 1988(4);208:460-474.DeMeester TR, Kauer WK. Esophageal reconstruction. The colon as an esophageal substitute. Dis Esophagus. 1995;8:20-29.Dexter SPL, Martin IG, McMahon MJ. Radical |
Surgery_Schwartz_7315 | Surgery_Schwartz | bypass. Ann Surg. 1988(4);208:460-474.DeMeester TR, Kauer WK. Esophageal reconstruction. The colon as an esophageal substitute. Dis Esophagus. 1995;8:20-29.Dexter SPL, Martin IG, McMahon MJ. Radical thoracoscopic esophagectomy for cancer. Surg Endosc. 1996;10:147-151.Ellis FH, Jr, Gibb SP. Esophageal reconstruction for complex benign esophageal disease. J Thorac Cardiovasc Surg. 1990; 99:192-199.Finley RJ, Lamy A, Clifton J, et al. Gastrointestinal function fol-lowing esophagectomy for malignancy. Am J Surg. 1995; 169:471-475.Fok M, Cheng SW, Wong J. Pyloroplasty versus no drainage in gas-tric replacement of the esophagus. Am J Surg. 1991;162:447-452.Gossot D, Cattan P, Fritsch S. Can the morbidity of esophagec-tomy be reduced by the thoracoscopic approach? Surg Endosc. 1995;9:1113-1115.Honkoop P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, van Blankenstein M. Benign anastomotic strictures after tran-shiatal esophagectomy and cervical esophagogastrostomy. Risk factors and | Surgery_Schwartz. bypass. Ann Surg. 1988(4);208:460-474.DeMeester TR, Kauer WK. Esophageal reconstruction. The colon as an esophageal substitute. Dis Esophagus. 1995;8:20-29.Dexter SPL, Martin IG, McMahon MJ. Radical thoracoscopic esophagectomy for cancer. Surg Endosc. 1996;10:147-151.Ellis FH, Jr, Gibb SP. Esophageal reconstruction for complex benign esophageal disease. J Thorac Cardiovasc Surg. 1990; 99:192-199.Finley RJ, Lamy A, Clifton J, et al. Gastrointestinal function fol-lowing esophagectomy for malignancy. Am J Surg. 1995; 169:471-475.Fok M, Cheng SW, Wong J. Pyloroplasty versus no drainage in gas-tric replacement of the esophagus. Am J Surg. 1991;162:447-452.Gossot D, Cattan P, Fritsch S. Can the morbidity of esophagec-tomy be reduced by the thoracoscopic approach? Surg Endosc. 1995;9:1113-1115.Honkoop P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, van Blankenstein M. Benign anastomotic strictures after tran-shiatal esophagectomy and cervical esophagogastrostomy. Risk factors and |
Surgery_Schwartz_7316 | Surgery_Schwartz | P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, van Blankenstein M. Benign anastomotic strictures after tran-shiatal esophagectomy and cervical esophagogastrostomy. Risk factors and management. J Thorac Cardiovasc Surg. 1996;111(6):1141-1148.Liebermann-Meffert DMI, Meier R, Siewert JR. Vascular anatomy of the gastric tube used for esophageal reconstruction. Ann Thorac Surg. 1992;54:1110-1115.Maier G, Jehle EC, Becker HD. Functional outcome following oesophagectomy for oesophageal cancer. A prospective mano-metric study. Dis Esophagus. 1995;8:64-69.Naunheim KS, Hanosh J, Zwischenberger J, et al. Esophagectomy in the septuagenarian. Ann Thorac Surg. 1993;56(4):880-884.Nishihra T, Oe H, Sugawara K, et al. Esophageal reconstruction. Reconstruction of the thoracic esophagus with jejunal pedicled segments for cancer of the thoracic esophagus. Dis Esophagus. 1995;8:30-39.Peters JH, Kronson J, Bremner CG, et al. Arterial anatomic con-siderations in colon interposition for esophageal | Surgery_Schwartz. P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, van Blankenstein M. Benign anastomotic strictures after tran-shiatal esophagectomy and cervical esophagogastrostomy. Risk factors and management. J Thorac Cardiovasc Surg. 1996;111(6):1141-1148.Liebermann-Meffert DMI, Meier R, Siewert JR. Vascular anatomy of the gastric tube used for esophageal reconstruction. Ann Thorac Surg. 1992;54:1110-1115.Maier G, Jehle EC, Becker HD. Functional outcome following oesophagectomy for oesophageal cancer. A prospective mano-metric study. Dis Esophagus. 1995;8:64-69.Naunheim KS, Hanosh J, Zwischenberger J, et al. Esophagectomy in the septuagenarian. Ann Thorac Surg. 1993;56(4):880-884.Nishihra T, Oe H, Sugawara K, et al. Esophageal reconstruction. Reconstruction of the thoracic esophagus with jejunal pedicled segments for cancer of the thoracic esophagus. Dis Esophagus. 1995;8:30-39.Peters JH, Kronson J, Bremner CG, et al. Arterial anatomic con-siderations in colon interposition for esophageal |
Surgery_Schwartz_7317 | Surgery_Schwartz | pedicled segments for cancer of the thoracic esophagus. Dis Esophagus. 1995;8:30-39.Peters JH, Kronson J, Bremner CG, et al. Arterial anatomic con-siderations in colon interposition for esophageal replacement. Arch Surg. 1995;130:858-863.Stark SP, Romberg MS, Pierce GE, et al. Transhiatal versus trans-thoracic esophagectomy for adenocarcinoma of the distal esophagus and cardia. Am J Surg. 1996;172:478-482.Valverde A, Hay JM, Fingerhut A, et al. Manual versus mechani-cal esophagogastric anastomosis after resection for carcinoma. A controlled trial. French Associations for Surgical Research. Surgery. 1996;120:476-483.Watson T, DeMeester TR, Kauer WK, Peters JH, Hagen JA. Esoph-agectomy for end stage benign esophageal disease. J Thorac Cardiovasc Surg. 1998;115(6):1241-1247.Wu M-H, Lai W-W. Esophageal reconstruction for esophageal strictures or resection after corrosive injury. Ann Thorac Surg. 1992;53:798-802.Brunicardi_Ch25_p1009-p1098.indd 109801/03/19 6:06 PM | Surgery_Schwartz. pedicled segments for cancer of the thoracic esophagus. Dis Esophagus. 1995;8:30-39.Peters JH, Kronson J, Bremner CG, et al. Arterial anatomic con-siderations in colon interposition for esophageal replacement. Arch Surg. 1995;130:858-863.Stark SP, Romberg MS, Pierce GE, et al. Transhiatal versus trans-thoracic esophagectomy for adenocarcinoma of the distal esophagus and cardia. Am J Surg. 1996;172:478-482.Valverde A, Hay JM, Fingerhut A, et al. Manual versus mechani-cal esophagogastric anastomosis after resection for carcinoma. A controlled trial. French Associations for Surgical Research. Surgery. 1996;120:476-483.Watson T, DeMeester TR, Kauer WK, Peters JH, Hagen JA. Esoph-agectomy for end stage benign esophageal disease. J Thorac Cardiovasc Surg. 1998;115(6):1241-1247.Wu M-H, Lai W-W. Esophageal reconstruction for esophageal strictures or resection after corrosive injury. Ann Thorac Surg. 1992;53:798-802.Brunicardi_Ch25_p1009-p1098.indd 109801/03/19 6:06 PM |
Surgery_Schwartz_7318 | Surgery_Schwartz | StomachRobert E. Roses and Daniel T. Dempsey 26chapterThe stomach stores and facilitates the digestion and absorption of ingested food and helps regulate appetite. Treatable dis-eases of the stomach are common, and it is accessible and rela-tively forgiving of surgical manipulation. To provide accurate diagnosis and rational treatment, the physician must under-stand gastric anatomy, physiology, and pathophysiology; this includes a sound understanding of the mechanical, secretory, and endocrine processes by which the stomach accomplishes its important functions and a familiarity with the common benign and malignant gastric disorders. Important historical milestones1-6 that influenced the contemporary understand-ing of gastric disease and surgical therapy are summarized in Table 26-1.ANATOMYAnatomic Relationships and Gross MorphologyThe stomach is the most proximal abdominal organ of the diges-tive tract (Fig. 26-1).7 The part of the stomach attached to the esophagus is called the | Surgery_Schwartz. StomachRobert E. Roses and Daniel T. Dempsey 26chapterThe stomach stores and facilitates the digestion and absorption of ingested food and helps regulate appetite. Treatable dis-eases of the stomach are common, and it is accessible and rela-tively forgiving of surgical manipulation. To provide accurate diagnosis and rational treatment, the physician must under-stand gastric anatomy, physiology, and pathophysiology; this includes a sound understanding of the mechanical, secretory, and endocrine processes by which the stomach accomplishes its important functions and a familiarity with the common benign and malignant gastric disorders. Important historical milestones1-6 that influenced the contemporary understand-ing of gastric disease and surgical therapy are summarized in Table 26-1.ANATOMYAnatomic Relationships and Gross MorphologyThe stomach is the most proximal abdominal organ of the diges-tive tract (Fig. 26-1).7 The part of the stomach attached to the esophagus is called the |
Surgery_Schwartz_7319 | Surgery_Schwartz | Relationships and Gross MorphologyThe stomach is the most proximal abdominal organ of the diges-tive tract (Fig. 26-1).7 The part of the stomach attached to the esophagus is called the cardia. Just proximal to the cardia at the gastroesophageal (GE) junction is the anatomically indistinct but physiologically demonstrable lower esophageal sphincter. At the distal end, the readily apparent pyloric sphincter con-nects the stomach to the proximal duodenum. The stomach is relatively fixed at these points, but the majority of the stomach is quite mobile with the shorter lesser curvature on the right and the longer greater curvature on the left.The superior-most part of the stomach is the distensible fundus, bounded superiorly by the diaphragm and laterally by the spleen. The angle of His is where the fundus meets the left side of the GE junction. Generally, the inferior extent of the fun-dus is considered to be the horizontal plane of the GE junction, where the body (corpus) of the stomach | Surgery_Schwartz. Relationships and Gross MorphologyThe stomach is the most proximal abdominal organ of the diges-tive tract (Fig. 26-1).7 The part of the stomach attached to the esophagus is called the cardia. Just proximal to the cardia at the gastroesophageal (GE) junction is the anatomically indistinct but physiologically demonstrable lower esophageal sphincter. At the distal end, the readily apparent pyloric sphincter con-nects the stomach to the proximal duodenum. The stomach is relatively fixed at these points, but the majority of the stomach is quite mobile with the shorter lesser curvature on the right and the longer greater curvature on the left.The superior-most part of the stomach is the distensible fundus, bounded superiorly by the diaphragm and laterally by the spleen. The angle of His is where the fundus meets the left side of the GE junction. Generally, the inferior extent of the fun-dus is considered to be the horizontal plane of the GE junction, where the body (corpus) of the stomach |
Surgery_Schwartz_7320 | Surgery_Schwartz | the fundus meets the left side of the GE junction. Generally, the inferior extent of the fun-dus is considered to be the horizontal plane of the GE junction, where the body (corpus) of the stomach begins. The body of the stomach contains most of the parietal (oxyntic) cells, some of which are also present in the cardia and fundus. At the angularis incisura, the lesser curvature turns rather abruptly to the right, marking the anatomic beginning of the antrum, which comprises the distal 25% to 30% of the stomach.Anatomy 1099Anatomic Relationships and Gross Morphology / 1099Arterial and Venous Blood Supply / 1100Lymphatic Drainage / 1100Innervation / 1101Histology / 1102Physiology 1105Acid Secretion / 1105Pepsinogen Secretion / 1108Intrinsic Factor / 1108Gastric Mucosal Barrier / 1109Gastric Hormones / 1109Gastric Motility and Emptying / 1110Diagnosis of Gastric Disease 1115Signs and Symptoms / 1115Diagnostic Tests / 1115Helicobacter Pylori Infection 1117Peptic Ulcer | Surgery_Schwartz. the fundus meets the left side of the GE junction. Generally, the inferior extent of the fun-dus is considered to be the horizontal plane of the GE junction, where the body (corpus) of the stomach begins. The body of the stomach contains most of the parietal (oxyntic) cells, some of which are also present in the cardia and fundus. At the angularis incisura, the lesser curvature turns rather abruptly to the right, marking the anatomic beginning of the antrum, which comprises the distal 25% to 30% of the stomach.Anatomy 1099Anatomic Relationships and Gross Morphology / 1099Arterial and Venous Blood Supply / 1100Lymphatic Drainage / 1100Innervation / 1101Histology / 1102Physiology 1105Acid Secretion / 1105Pepsinogen Secretion / 1108Intrinsic Factor / 1108Gastric Mucosal Barrier / 1109Gastric Hormones / 1109Gastric Motility and Emptying / 1110Diagnosis of Gastric Disease 1115Signs and Symptoms / 1115Diagnostic Tests / 1115Helicobacter Pylori Infection 1117Peptic Ulcer |
Surgery_Schwartz_7321 | Surgery_Schwartz | / 1109Gastric Hormones / 1109Gastric Motility and Emptying / 1110Diagnosis of Gastric Disease 1115Signs and Symptoms / 1115Diagnostic Tests / 1115Helicobacter Pylori Infection 1117Peptic Ulcer Disease 1120Pathophysiology and Etiology / 1121Clinical Manifestations / 1123Diagnosis / 1123Complications / 1124Medical Treatment of Peptic Ulcer Disease / 1125Surgical Treatment of Peptic Ulcer Disease / 1127Bleeding Peptic Ulcer / 1131Operation for Bleeding Peptic Ulcer / 1133Perforated Peptic Ulcer / 1134Obstructing Peptic Ulcer / 1136Intractable or Nonhealing Peptic Ulcer / 1136Zollinger-Ellison Syndrome / 1136Stress Gastritis and Stress Ulcer 1137Atrophic Gastritis 1138Malignant Neoplasms of the Stomach 1139Adenocarcinoma / 1139Pathology / 1143Gastric Lymphoma / 1149Gastrointestinal Stromal Tumor / 1149Gastric Neuroendocrine Tumors / 1151Benign Gastric Neoplasms 1152Leiomyoma / 1152Lipoma / 1152Gastroparesis / 1152Massive Upper Gastrointestinal Bleeding / 1152Isolated Gastric | Surgery_Schwartz. / 1109Gastric Hormones / 1109Gastric Motility and Emptying / 1110Diagnosis of Gastric Disease 1115Signs and Symptoms / 1115Diagnostic Tests / 1115Helicobacter Pylori Infection 1117Peptic Ulcer Disease 1120Pathophysiology and Etiology / 1121Clinical Manifestations / 1123Diagnosis / 1123Complications / 1124Medical Treatment of Peptic Ulcer Disease / 1125Surgical Treatment of Peptic Ulcer Disease / 1127Bleeding Peptic Ulcer / 1131Operation for Bleeding Peptic Ulcer / 1133Perforated Peptic Ulcer / 1134Obstructing Peptic Ulcer / 1136Intractable or Nonhealing Peptic Ulcer / 1136Zollinger-Ellison Syndrome / 1136Stress Gastritis and Stress Ulcer 1137Atrophic Gastritis 1138Malignant Neoplasms of the Stomach 1139Adenocarcinoma / 1139Pathology / 1143Gastric Lymphoma / 1149Gastrointestinal Stromal Tumor / 1149Gastric Neuroendocrine Tumors / 1151Benign Gastric Neoplasms 1152Leiomyoma / 1152Lipoma / 1152Gastroparesis / 1152Massive Upper Gastrointestinal Bleeding / 1152Isolated Gastric |
Surgery_Schwartz_7322 | Surgery_Schwartz | Stromal Tumor / 1149Gastric Neuroendocrine Tumors / 1151Benign Gastric Neoplasms 1152Leiomyoma / 1152Lipoma / 1152Gastroparesis / 1152Massive Upper Gastrointestinal Bleeding / 1152Isolated Gastric Varices / 1153Hypertrophic Gastropathy (Ménétrier’s Disease) / 1153Watermelon Stomach (Gastric Antral Vascular Ectasia) / 1154Dieulafoy’s Lesion / 1154Bezoars/Diverticula / 1154Foreign Bodies / 1154Mallory-Weiss Syndrome / 1155Volvulus / 1155Gastrostomy 1155Postgastrectomy Problems 1156Dumping Syndrome / 1156Diarrhea / 1157Gastric Stasis / 1157Bile Reflux Gastritis and Esophagitis / 1158Roux Syndrome / 1158Gallstones / 1159Weight Loss / 1159Anemia / 1159Bone Disease / 1159Laparoscopic Gastric Operations 1159Brunicardi_Ch26_p1099-p1166.indd 109901/03/19 7:11 PM 1100The liver, colon, spleen, pancreas, and occasionally the kidney, abut the stomach (Fig. 26-2). The left lateral segment of the liver usually obscures part of the anterior stomach. Infe-riorly, the stomach is attached to | Surgery_Schwartz. Stromal Tumor / 1149Gastric Neuroendocrine Tumors / 1151Benign Gastric Neoplasms 1152Leiomyoma / 1152Lipoma / 1152Gastroparesis / 1152Massive Upper Gastrointestinal Bleeding / 1152Isolated Gastric Varices / 1153Hypertrophic Gastropathy (Ménétrier’s Disease) / 1153Watermelon Stomach (Gastric Antral Vascular Ectasia) / 1154Dieulafoy’s Lesion / 1154Bezoars/Diverticula / 1154Foreign Bodies / 1154Mallory-Weiss Syndrome / 1155Volvulus / 1155Gastrostomy 1155Postgastrectomy Problems 1156Dumping Syndrome / 1156Diarrhea / 1157Gastric Stasis / 1157Bile Reflux Gastritis and Esophagitis / 1158Roux Syndrome / 1158Gallstones / 1159Weight Loss / 1159Anemia / 1159Bone Disease / 1159Laparoscopic Gastric Operations 1159Brunicardi_Ch26_p1099-p1166.indd 109901/03/19 7:11 PM 1100The liver, colon, spleen, pancreas, and occasionally the kidney, abut the stomach (Fig. 26-2). The left lateral segment of the liver usually obscures part of the anterior stomach. Infe-riorly, the stomach is attached to |
Surgery_Schwartz_7323 | Surgery_Schwartz | pancreas, and occasionally the kidney, abut the stomach (Fig. 26-2). The left lateral segment of the liver usually obscures part of the anterior stomach. Infe-riorly, the stomach is attached to the transverse colon by the gastrocolic omentum. The lesser curvature is tethered to the liver by the hepatogastric ligament, also referred to as the lesser omentum or pars flaccida. Posterior to the stomach is the lesser omental bursa and the pancreas.Arterial and Venous Blood SupplyThe stomach is the most richly vascularized portion of the ali-mentary tube with ample blood flow and a dense intramural vascular anastomotic network. The large majority of the gastric blood supply is from the celiac axis via four named arteries (Fig. 26-3). The left and right gastric arteries form an anasto-motic arcade along the lesser gastric curvature, and the right and left gastroepiploic arteries form an arcade along the greater gastric curvature. The left gastric artery is consistently the larg-est artery to | Surgery_Schwartz. pancreas, and occasionally the kidney, abut the stomach (Fig. 26-2). The left lateral segment of the liver usually obscures part of the anterior stomach. Infe-riorly, the stomach is attached to the transverse colon by the gastrocolic omentum. The lesser curvature is tethered to the liver by the hepatogastric ligament, also referred to as the lesser omentum or pars flaccida. Posterior to the stomach is the lesser omental bursa and the pancreas.Arterial and Venous Blood SupplyThe stomach is the most richly vascularized portion of the ali-mentary tube with ample blood flow and a dense intramural vascular anastomotic network. The large majority of the gastric blood supply is from the celiac axis via four named arteries (Fig. 26-3). The left and right gastric arteries form an anasto-motic arcade along the lesser gastric curvature, and the right and left gastroepiploic arteries form an arcade along the greater gastric curvature. The left gastric artery is consistently the larg-est artery to |
Surgery_Schwartz_7324 | Surgery_Schwartz | along the lesser gastric curvature, and the right and left gastroepiploic arteries form an arcade along the greater gastric curvature. The left gastric artery is consistently the larg-est artery to the stomach and usually arises directly from the celiac trunk and divides into an ascending and descending branch along the lesser gastric curvature. Approximately 20% of the time, the left gastric artery supplies an aberrant vessel that travels in the gastrohepatic ligament (lesser omentum) to the left side of the liver. Rarely, this is the only arterial blood supply to this part of the liver (replaced left hepatic artery), and inadvertent ligation may lead to clinically significant hepatic ischemia. The more common smaller accessory left hepatic artery may be ligated without significant consequences.The second largest artery to the stomach is the right gas-troepiploic artery, which consistently arises from the gastro-duodenal artery behind the first portion of the duodenum. The left | Surgery_Schwartz. along the lesser gastric curvature, and the right and left gastroepiploic arteries form an arcade along the greater gastric curvature. The left gastric artery is consistently the larg-est artery to the stomach and usually arises directly from the celiac trunk and divides into an ascending and descending branch along the lesser gastric curvature. Approximately 20% of the time, the left gastric artery supplies an aberrant vessel that travels in the gastrohepatic ligament (lesser omentum) to the left side of the liver. Rarely, this is the only arterial blood supply to this part of the liver (replaced left hepatic artery), and inadvertent ligation may lead to clinically significant hepatic ischemia. The more common smaller accessory left hepatic artery may be ligated without significant consequences.The second largest artery to the stomach is the right gas-troepiploic artery, which consistently arises from the gastro-duodenal artery behind the first portion of the duodenum. The left |
Surgery_Schwartz_7325 | Surgery_Schwartz | consequences.The second largest artery to the stomach is the right gas-troepiploic artery, which consistently arises from the gastro-duodenal artery behind the first portion of the duodenum. The left gastroepiploic artery arises from the splenic artery, and, together with the right gastroepiploic artery, forms the rich gastroepiploic arcade along the greater curvature. The right gastric artery usually arises from the hepatic artery near the pylorus and hepatoduodenal ligament and runs proximally along the distal stomach. In the fundus along the proximal greater curvature, the short gastric arteries and veins arise from the splenic circulation. There also may be additional vascular branches to the proximal stomach from the phrenic and splenic circulation.The veins draining the stomach generally parallel the arteries. The left gastric (coronary vein) and right gastric veins usually drain into the portal vein, though occasionally the coro-nary vein drains into the splenic vein. The right | Surgery_Schwartz. consequences.The second largest artery to the stomach is the right gas-troepiploic artery, which consistently arises from the gastro-duodenal artery behind the first portion of the duodenum. The left gastroepiploic artery arises from the splenic artery, and, together with the right gastroepiploic artery, forms the rich gastroepiploic arcade along the greater curvature. The right gastric artery usually arises from the hepatic artery near the pylorus and hepatoduodenal ligament and runs proximally along the distal stomach. In the fundus along the proximal greater curvature, the short gastric arteries and veins arise from the splenic circulation. There also may be additional vascular branches to the proximal stomach from the phrenic and splenic circulation.The veins draining the stomach generally parallel the arteries. The left gastric (coronary vein) and right gastric veins usually drain into the portal vein, though occasionally the coro-nary vein drains into the splenic vein. The right |
Surgery_Schwartz_7326 | Surgery_Schwartz | parallel the arteries. The left gastric (coronary vein) and right gastric veins usually drain into the portal vein, though occasionally the coro-nary vein drains into the splenic vein. The right gastroepiploic vein drains into the superior mesenteric vein near the inferior border of the pancreatic neck, and the left gastroepiploic vein drains into the splenic vein.The richness of the gastric blood supply and its many anastomotic connections have important clinical implications. At least two of the four named gastric arteries may be occluded or ligated without inducing gastric ischemia. This is done rou-tinely when the stomach is mobilized and pedicled on the right gastric and right gastroepiploic vessels to reach into the neck as an esophageal replacement (see Chapter 25) or during sleeve gastrectomy for weight loss when the gastroepiploic arcade is interrupted proximally and distally prior to gastric resection (see Chapter 27). Following radical subtotal gastrectomy dur-ing which the | Surgery_Schwartz. parallel the arteries. The left gastric (coronary vein) and right gastric veins usually drain into the portal vein, though occasionally the coro-nary vein drains into the splenic vein. The right gastroepiploic vein drains into the superior mesenteric vein near the inferior border of the pancreatic neck, and the left gastroepiploic vein drains into the splenic vein.The richness of the gastric blood supply and its many anastomotic connections have important clinical implications. At least two of the four named gastric arteries may be occluded or ligated without inducing gastric ischemia. This is done rou-tinely when the stomach is mobilized and pedicled on the right gastric and right gastroepiploic vessels to reach into the neck as an esophageal replacement (see Chapter 25) or during sleeve gastrectomy for weight loss when the gastroepiploic arcade is interrupted proximally and distally prior to gastric resection (see Chapter 27). Following radical subtotal gastrectomy dur-ing which the |
Surgery_Schwartz_7327 | Surgery_Schwartz | gastrectomy for weight loss when the gastroepiploic arcade is interrupted proximally and distally prior to gastric resection (see Chapter 27). Following radical subtotal gastrectomy dur-ing which the right and left gastric arteries and both gastroepi-ploic arteries are all ligated, the gastric remnant is adequately supplied by short gastric arteries as long as the splenic artery is patent and intact. Angiographic control of gastric bleeding from a deep ulcer or tumor often requires embolization of more than one feeding artery. Because of the rich venous interconnections in the stomach, a transjugular intrahepatic portosystemic shunt (TIPSS) can effectively decompress esophagogastric varices in patients with portal hypertension.8,9Lymphatic DrainageGenerally speaking, the gastric lymphatics parallel the blood vessels (Fig. 26-4).10 The cardia and medial half of the corpus commonly drain to nodes along the left gastric and celiac axis. The lesser curvature side of the antrum usually | Surgery_Schwartz. gastrectomy for weight loss when the gastroepiploic arcade is interrupted proximally and distally prior to gastric resection (see Chapter 27). Following radical subtotal gastrectomy dur-ing which the right and left gastric arteries and both gastroepi-ploic arteries are all ligated, the gastric remnant is adequately supplied by short gastric arteries as long as the splenic artery is patent and intact. Angiographic control of gastric bleeding from a deep ulcer or tumor often requires embolization of more than one feeding artery. Because of the rich venous interconnections in the stomach, a transjugular intrahepatic portosystemic shunt (TIPSS) can effectively decompress esophagogastric varices in patients with portal hypertension.8,9Lymphatic DrainageGenerally speaking, the gastric lymphatics parallel the blood vessels (Fig. 26-4).10 The cardia and medial half of the corpus commonly drain to nodes along the left gastric and celiac axis. The lesser curvature side of the antrum usually |
Surgery_Schwartz_7328 | Surgery_Schwartz | parallel the blood vessels (Fig. 26-4).10 The cardia and medial half of the corpus commonly drain to nodes along the left gastric and celiac axis. The lesser curvature side of the antrum usually drains to the right gastric and pyloric nodes, while the greater curvature half of the distal stomach drains to the nodes along the right gas-troepiploic chain. The proximal greater curvature side of the stomach usually drains into nodes along the left gastroepiploic or splenic hilum. The nodes along both the greater and lesser Key Points1 Whenever testing suggests Helicobacter pylori infec-tion, treatment should be initiated and eradication confirmed.2 Lifelong acid suppression should be considered in any patient admitted to a hospital because of peptic ulcer dis-ease. Acid suppressive medication may be equivalent to sur-gical vagotomy in preventing recurrent peptic ulcer or ulcer complications.3 If possible, gastric resection for peptic ulcer is avoided in the asthenic or high-risk | Surgery_Schwartz. parallel the blood vessels (Fig. 26-4).10 The cardia and medial half of the corpus commonly drain to nodes along the left gastric and celiac axis. The lesser curvature side of the antrum usually drains to the right gastric and pyloric nodes, while the greater curvature half of the distal stomach drains to the nodes along the right gas-troepiploic chain. The proximal greater curvature side of the stomach usually drains into nodes along the left gastroepiploic or splenic hilum. The nodes along both the greater and lesser Key Points1 Whenever testing suggests Helicobacter pylori infec-tion, treatment should be initiated and eradication confirmed.2 Lifelong acid suppression should be considered in any patient admitted to a hospital because of peptic ulcer dis-ease. Acid suppressive medication may be equivalent to sur-gical vagotomy in preventing recurrent peptic ulcer or ulcer complications.3 If possible, gastric resection for peptic ulcer is avoided in the asthenic or high-risk |
Surgery_Schwartz_7329 | Surgery_Schwartz | may be equivalent to sur-gical vagotomy in preventing recurrent peptic ulcer or ulcer complications.3 If possible, gastric resection for peptic ulcer is avoided in the asthenic or high-risk patient.4 Though less common in the United States, gastric cancer is a major cause of cancer-related morbidity and mortality worldwide.5 Diagnostic laparoscopy with peritoneal lavage should be considered in the evaluation of clinical stage 2 and 3 patients with gastric cancer.6 Multimodality therapy for gastric cancer, including resec-tion in combination with perioperative chemotherapy or adjuvant chemoradiotherapy is associated with a survival advantage compared to surgery alone.7 Most patients with primary gastric lymphoma can be treated without gastric resection.8 Localized gastrointestinal stromal tumors of the stomach are treated with full thickness excision. Adjuvant (or neo-adjuvant) imatinib is indicated for higher-risk lesions.9 Gastric neuroendocrine tumors may arise in the presence | Surgery_Schwartz. may be equivalent to sur-gical vagotomy in preventing recurrent peptic ulcer or ulcer complications.3 If possible, gastric resection for peptic ulcer is avoided in the asthenic or high-risk patient.4 Though less common in the United States, gastric cancer is a major cause of cancer-related morbidity and mortality worldwide.5 Diagnostic laparoscopy with peritoneal lavage should be considered in the evaluation of clinical stage 2 and 3 patients with gastric cancer.6 Multimodality therapy for gastric cancer, including resec-tion in combination with perioperative chemotherapy or adjuvant chemoradiotherapy is associated with a survival advantage compared to surgery alone.7 Most patients with primary gastric lymphoma can be treated without gastric resection.8 Localized gastrointestinal stromal tumors of the stomach are treated with full thickness excision. Adjuvant (or neo-adjuvant) imatinib is indicated for higher-risk lesions.9 Gastric neuroendocrine tumors may arise in the presence |
Surgery_Schwartz_7330 | Surgery_Schwartz | tumors of the stomach are treated with full thickness excision. Adjuvant (or neo-adjuvant) imatinib is indicated for higher-risk lesions.9 Gastric neuroendocrine tumors may arise in the presence (types 1 and 2) or absence (type 3) of hypergastrinemia. Type 3 gastric neuroendocrine tumors should usually be treated with subtotal gastrectomy and regional lymphadenectomy.10 Roux-en-Y gastrojejunostomy with a large (>50%) proxi-mal gastric remnant should be avoided because marginal ulceration and/or gastric stasis (Roux syndrome) may become problematic.Brunicardi_Ch26_p1099-p1166.indd 110001/03/19 7:11 PM 1101STOMACHCHAPTER 26curvature commonly drain into the celiac nodal basin. There is a rich anastomotic network of lymphatics that drain the stomach, often in a somewhat unpredictable fashion. Thus, a tumor aris-ing in the distal stomach may give rise to positive lymph nodes in the splenic hilum. The rich intramural plexus of lymphatics and veins accounts for the fact that there can be | Surgery_Schwartz. tumors of the stomach are treated with full thickness excision. Adjuvant (or neo-adjuvant) imatinib is indicated for higher-risk lesions.9 Gastric neuroendocrine tumors may arise in the presence (types 1 and 2) or absence (type 3) of hypergastrinemia. Type 3 gastric neuroendocrine tumors should usually be treated with subtotal gastrectomy and regional lymphadenectomy.10 Roux-en-Y gastrojejunostomy with a large (>50%) proxi-mal gastric remnant should be avoided because marginal ulceration and/or gastric stasis (Roux syndrome) may become problematic.Brunicardi_Ch26_p1099-p1166.indd 110001/03/19 7:11 PM 1101STOMACHCHAPTER 26curvature commonly drain into the celiac nodal basin. There is a rich anastomotic network of lymphatics that drain the stomach, often in a somewhat unpredictable fashion. Thus, a tumor aris-ing in the distal stomach may give rise to positive lymph nodes in the splenic hilum. The rich intramural plexus of lymphatics and veins accounts for the fact that there can be |
Surgery_Schwartz_7331 | Surgery_Schwartz | Thus, a tumor aris-ing in the distal stomach may give rise to positive lymph nodes in the splenic hilum. The rich intramural plexus of lymphatics and veins accounts for the fact that there can be microscopic evi-dence of malignant cells in the gastric wall at a resection margin that is several centimeters away from palpable malignant tumor. It also helps explain the not infrequent finding of positive lymph nodes, which may be many centimeters away from the primary tumor, with closer nodes that are uninvolved.Not surprisingly, extensive and meticulous lymphadenec-tomy is considered by many surgeons to be an important part of an operation for gastric cancer. Surgeons and pathologists have numbered the primary and secondary lymph node groups to which the stomach drains (see Fig. 26-4).11,12Innervation13The vagus nerves provide the extrinsic parasympathetic innerva-tion to the stomach, and acetylcholine is the most important neu-rotransmitter. From the vagal nucleus in the floor of the | Surgery_Schwartz. Thus, a tumor aris-ing in the distal stomach may give rise to positive lymph nodes in the splenic hilum. The rich intramural plexus of lymphatics and veins accounts for the fact that there can be microscopic evi-dence of malignant cells in the gastric wall at a resection margin that is several centimeters away from palpable malignant tumor. It also helps explain the not infrequent finding of positive lymph nodes, which may be many centimeters away from the primary tumor, with closer nodes that are uninvolved.Not surprisingly, extensive and meticulous lymphadenec-tomy is considered by many surgeons to be an important part of an operation for gastric cancer. Surgeons and pathologists have numbered the primary and secondary lymph node groups to which the stomach drains (see Fig. 26-4).11,12Innervation13The vagus nerves provide the extrinsic parasympathetic innerva-tion to the stomach, and acetylcholine is the most important neu-rotransmitter. From the vagal nucleus in the floor of the |
Surgery_Schwartz_7332 | Surgery_Schwartz | vagus nerves provide the extrinsic parasympathetic innerva-tion to the stomach, and acetylcholine is the most important neu-rotransmitter. From the vagal nucleus in the floor of the fourth cerebral ventricle, the vagus traverses the neck in the carotid sheath and enters the mediastinum, where it gives off the recur-rent laryngeal nerve and divides into several branches around the esophagus. These branches come together again above the esophageal hiatus and form the left (anterior) and right Table 26-1Historic milestones in gastric surgeryDATEEVENTDATEEVENT350 b.c.– 201 a.d. 1363 1586 1600–1700 16881737 1833 1869 1875 1879 1880 1880 1881 1884 1885Existence of gastric ulceration was acknowledged by Diocles of Carystos (350 b.c.), Celsus, and Galen (131–201 a.d.).Guy de Chauliac describes closure of gastric wound.Marcellus Donatus of Mantua describes gastric ulcer at autopsy.Reports of surgeons cutting stomach to remove foreign bodies.Muralto describes duodenal ulcer at | Surgery_Schwartz. vagus nerves provide the extrinsic parasympathetic innerva-tion to the stomach, and acetylcholine is the most important neu-rotransmitter. From the vagal nucleus in the floor of the fourth cerebral ventricle, the vagus traverses the neck in the carotid sheath and enters the mediastinum, where it gives off the recur-rent laryngeal nerve and divides into several branches around the esophagus. These branches come together again above the esophageal hiatus and form the left (anterior) and right Table 26-1Historic milestones in gastric surgeryDATEEVENTDATEEVENT350 b.c.– 201 a.d. 1363 1586 1600–1700 16881737 1833 1869 1875 1879 1880 1880 1881 1884 1885Existence of gastric ulceration was acknowledged by Diocles of Carystos (350 b.c.), Celsus, and Galen (131–201 a.d.).Guy de Chauliac describes closure of gastric wound.Marcellus Donatus of Mantua describes gastric ulcer at autopsy.Reports of surgeons cutting stomach to remove foreign bodies.Muralto describes duodenal ulcer at |
Surgery_Schwartz_7333 | Surgery_Schwartz | describes closure of gastric wound.Marcellus Donatus of Mantua describes gastric ulcer at autopsy.Reports of surgeons cutting stomach to remove foreign bodies.Muralto describes duodenal ulcer at autopsy.Morgagni describes both gastric and duodenal ulcer at autopsy.William Beaumont reports data recorded during his care of Alexis St. Martin who developed a gastric fistula from a left upper quadrant musket wound.Maury reportedly performs feeding gastrostomy to palliate esophageal stricture following consultation with Samuel D. Gross.Sidney Jones in London publishes the first successful gastrostomy for feeding.Paen performed distal gastrectomy and gastroduodenostomy. The patient died 5 d later.Rydygier resected a distal gastric cancer, and the patient died 12 h later.Billroth resects distal gastric cancer and performs gastroduodenostomy (Billroth I). Patient Therese Heller recovers and survives 4 mo.Anton Wolfler performs loop gastrojejunostomy to palliate an obstructing distal gastric | Surgery_Schwartz. describes closure of gastric wound.Marcellus Donatus of Mantua describes gastric ulcer at autopsy.Reports of surgeons cutting stomach to remove foreign bodies.Muralto describes duodenal ulcer at autopsy.Morgagni describes both gastric and duodenal ulcer at autopsy.William Beaumont reports data recorded during his care of Alexis St. Martin who developed a gastric fistula from a left upper quadrant musket wound.Maury reportedly performs feeding gastrostomy to palliate esophageal stricture following consultation with Samuel D. Gross.Sidney Jones in London publishes the first successful gastrostomy for feeding.Paen performed distal gastrectomy and gastroduodenostomy. The patient died 5 d later.Rydygier resected a distal gastric cancer, and the patient died 12 h later.Billroth resects distal gastric cancer and performs gastroduodenostomy (Billroth I). Patient Therese Heller recovers and survives 4 mo.Anton Wolfler performs loop gastrojejunostomy to palliate an obstructing distal gastric |
Surgery_Schwartz_7334 | Surgery_Schwartz | gastric cancer and performs gastroduodenostomy (Billroth I). Patient Therese Heller recovers and survives 4 mo.Anton Wolfler performs loop gastrojejunostomy to palliate an obstructing distal gastric cancer.Rydygier reports an unsuccessful gastrojejunostomy for benign gastric outlet obstruction.Billroth performs a successful distal gastrectomy and gastrojejunostomy (Billroth II) for gastric cancer.1886188818921902 1891–1913 1920–1950 1943 1952 1953 1955 1957 1980–2000 1990–current 1995–current2000–currentHeineke performs pyloroplasty.Mikulicz performs similar operation.Jaboulay describes bypassing the intact pylorus with gastroduodenostomy.Finney from Baltimore describes pyloroplasty technique.Different techniques of gastrostomy are described by Witzel (1891), Stamm (1894), and Janeway (1913).Subtotal gastrectomy grows popular as an operation for peptic ulcer. Von Haberer and Finsterer proponents.Dragstedt and Owen describe transthoracic truncal vagotomy to treat peptic | Surgery_Schwartz. gastric cancer and performs gastroduodenostomy (Billroth I). Patient Therese Heller recovers and survives 4 mo.Anton Wolfler performs loop gastrojejunostomy to palliate an obstructing distal gastric cancer.Rydygier reports an unsuccessful gastrojejunostomy for benign gastric outlet obstruction.Billroth performs a successful distal gastrectomy and gastrojejunostomy (Billroth II) for gastric cancer.1886188818921902 1891–1913 1920–1950 1943 1952 1953 1955 1957 1980–2000 1990–current 1995–current2000–currentHeineke performs pyloroplasty.Mikulicz performs similar operation.Jaboulay describes bypassing the intact pylorus with gastroduodenostomy.Finney from Baltimore describes pyloroplasty technique.Different techniques of gastrostomy are described by Witzel (1891), Stamm (1894), and Janeway (1913).Subtotal gastrectomy grows popular as an operation for peptic ulcer. Von Haberer and Finsterer proponents.Dragstedt and Owen describe transthoracic truncal vagotomy to treat peptic |
Surgery_Schwartz_7335 | Surgery_Schwartz | and Janeway (1913).Subtotal gastrectomy grows popular as an operation for peptic ulcer. Von Haberer and Finsterer proponents.Dragstedt and Owen describe transthoracic truncal vagotomy to treat peptic ulcer disease. By the early 1950s, it is well recognized that some patients developed gastric stasis after this procedure, and transabdominal truncal vagotomy and drainage (pyloroplasty or gastrojejunostomy) become a standard ulcer operation.Farmer and Smithwick describe good results with truncal vagotomy and hemigastrectomy for peptic ulcer.Edwards and Herrington (Nashville) describe truncal vagotomy and antrectomy for peptic ulcer.Zollinger and Ellison describe the eponymous syndrome.Griffith and Harkins (Seattle) describe parietal cell vagotomy (highly selective vagotomy) for the elective treatment of peptic ulcer disease.Japanese surgeons and other surgical groups from East Asia demonstrate that more aggressive lymphadenectomy may improve survival in patients with gastric | Surgery_Schwartz. and Janeway (1913).Subtotal gastrectomy grows popular as an operation for peptic ulcer. Von Haberer and Finsterer proponents.Dragstedt and Owen describe transthoracic truncal vagotomy to treat peptic ulcer disease. By the early 1950s, it is well recognized that some patients developed gastric stasis after this procedure, and transabdominal truncal vagotomy and drainage (pyloroplasty or gastrojejunostomy) become a standard ulcer operation.Farmer and Smithwick describe good results with truncal vagotomy and hemigastrectomy for peptic ulcer.Edwards and Herrington (Nashville) describe truncal vagotomy and antrectomy for peptic ulcer.Zollinger and Ellison describe the eponymous syndrome.Griffith and Harkins (Seattle) describe parietal cell vagotomy (highly selective vagotomy) for the elective treatment of peptic ulcer disease.Japanese surgeons and other surgical groups from East Asia demonstrate that more aggressive lymphadenectomy may improve survival in patients with gastric |
Surgery_Schwartz_7336 | Surgery_Schwartz | elective treatment of peptic ulcer disease.Japanese surgeons and other surgical groups from East Asia demonstrate that more aggressive lymphadenectomy may improve survival in patients with gastric cancer.Evolving role of laparoscopic techniques in the treatment of surgical gastric disease.Dramatic increase in bariatric operations.Development of natural orifice translumenal endoscopic surgery, such as transgastric appendectomy and peroral pyloromyotomy.Development of robotic gastrectomy.Brunicardi_Ch26_p1099-p1166.indd 110101/03/19 7:11 PM 1102SPECIFIC CONSIDERATIONS PART II(posterior) vagal trunks (mnemonic LARP). Near the GE junc-tion the anterior vagus sends a branch (or branches) to the liver in the gastrohepatic ligament, and continues along the lesser curvature as the anterior nerve of Latarjet (Fig. 26-5). Simi-larly, the posterior vagus sends branches to the celiac plexus and continues along the posterior lesser curvature. The nerves of Latarjet send segmental branches | Surgery_Schwartz. elective treatment of peptic ulcer disease.Japanese surgeons and other surgical groups from East Asia demonstrate that more aggressive lymphadenectomy may improve survival in patients with gastric cancer.Evolving role of laparoscopic techniques in the treatment of surgical gastric disease.Dramatic increase in bariatric operations.Development of natural orifice translumenal endoscopic surgery, such as transgastric appendectomy and peroral pyloromyotomy.Development of robotic gastrectomy.Brunicardi_Ch26_p1099-p1166.indd 110101/03/19 7:11 PM 1102SPECIFIC CONSIDERATIONS PART II(posterior) vagal trunks (mnemonic LARP). Near the GE junc-tion the anterior vagus sends a branch (or branches) to the liver in the gastrohepatic ligament, and continues along the lesser curvature as the anterior nerve of Latarjet (Fig. 26-5). Simi-larly, the posterior vagus sends branches to the celiac plexus and continues along the posterior lesser curvature. The nerves of Latarjet send segmental branches |
Surgery_Schwartz_7337 | Surgery_Schwartz | nerve of Latarjet (Fig. 26-5). Simi-larly, the posterior vagus sends branches to the celiac plexus and continues along the posterior lesser curvature. The nerves of Latarjet send segmental branches to the body of the stomach before they terminate near the angularis incisura as the “crow’s foot,” sending branches to the antropyloric region. There may be additional branches to the distal stomach and pylorus that travel near the right gastric and/or gastroepiploic arteries. In 50% of patients, there are more than two vagal nerves at the esophageal hiatus. The branch that the posterior vagus sends to the posterior fundus is termed the criminal nerve of Grassi. This branch typically arises above the esophageal hiatus and is easily missed during truncal or highly selective vagotomy (HSV). Vagal fibers originating in the brain synapse with neu-rons in Auerbach’s myenteric plexus and Meissner’s submu-cosal plexus. In the stomach, the vagus nerves affect secretion (including acid), motor | Surgery_Schwartz. nerve of Latarjet (Fig. 26-5). Simi-larly, the posterior vagus sends branches to the celiac plexus and continues along the posterior lesser curvature. The nerves of Latarjet send segmental branches to the body of the stomach before they terminate near the angularis incisura as the “crow’s foot,” sending branches to the antropyloric region. There may be additional branches to the distal stomach and pylorus that travel near the right gastric and/or gastroepiploic arteries. In 50% of patients, there are more than two vagal nerves at the esophageal hiatus. The branch that the posterior vagus sends to the posterior fundus is termed the criminal nerve of Grassi. This branch typically arises above the esophageal hiatus and is easily missed during truncal or highly selective vagotomy (HSV). Vagal fibers originating in the brain synapse with neu-rons in Auerbach’s myenteric plexus and Meissner’s submu-cosal plexus. In the stomach, the vagus nerves affect secretion (including acid), motor |
Surgery_Schwartz_7338 | Surgery_Schwartz | Vagal fibers originating in the brain synapse with neu-rons in Auerbach’s myenteric plexus and Meissner’s submu-cosal plexus. In the stomach, the vagus nerves affect secretion (including acid), motor function, and mucosal bloodflow and cytoprotection. They also play a role in appetite control and per-haps even mucosal immunity and inflammation.14,15 Most of the axons contained in the vagal trunks are afferent (i.e., carrying stimuli from the viscera to the brain).The extrinsic sympathetic nerve supply to the stomach originates at spinal levels T5 through T10 and travels in the splanchnic nerves to the celiac ganglion. Postganglionic sympa-thetic nerves then travel from the celiac ganglion to the stomach along the blood vessels.Neurons in the myenteric and submucosal plexuses consti-tute the intrinsic nervous system of the stomach. There may be more intrinsic gastric neurons than extrinsic neurons, but their function is poorly understood.The characterization of the vagus as the | Surgery_Schwartz. Vagal fibers originating in the brain synapse with neu-rons in Auerbach’s myenteric plexus and Meissner’s submu-cosal plexus. In the stomach, the vagus nerves affect secretion (including acid), motor function, and mucosal bloodflow and cytoprotection. They also play a role in appetite control and per-haps even mucosal immunity and inflammation.14,15 Most of the axons contained in the vagal trunks are afferent (i.e., carrying stimuli from the viscera to the brain).The extrinsic sympathetic nerve supply to the stomach originates at spinal levels T5 through T10 and travels in the splanchnic nerves to the celiac ganglion. Postganglionic sympa-thetic nerves then travel from the celiac ganglion to the stomach along the blood vessels.Neurons in the myenteric and submucosal plexuses consti-tute the intrinsic nervous system of the stomach. There may be more intrinsic gastric neurons than extrinsic neurons, but their function is poorly understood.The characterization of the vagus as the |
Surgery_Schwartz_7339 | Surgery_Schwartz | the intrinsic nervous system of the stomach. There may be more intrinsic gastric neurons than extrinsic neurons, but their function is poorly understood.The characterization of the vagus as the cholinergic system and the sympathetic system as the adrenergic system of innerva-tion is a misleading oversimplification. Although acetylcholine is an important neurotransmitter mediating vagal function, and epinephrine is important in the sympathetic nerves, both sys-tems (as well as the intrinsic neurons) have various and diverse neurotransmitters, including cholinergic, adrenergic, and pepti-dergic (e.g., substance P and somatostatin).HistologyThere are four distinct layers of the gastric wall: mucosa, sub-mucosa, muscularis propria, and serosa (Fig. 26-6).7 The inner layer of the stomach is the mucosa, which is lined with colum-nar epithelial cells of various types. Beneath the basement mem-brane of the epithelial cells is the lamina propria, which contains connective tissue, blood | Surgery_Schwartz. the intrinsic nervous system of the stomach. There may be more intrinsic gastric neurons than extrinsic neurons, but their function is poorly understood.The characterization of the vagus as the cholinergic system and the sympathetic system as the adrenergic system of innerva-tion is a misleading oversimplification. Although acetylcholine is an important neurotransmitter mediating vagal function, and epinephrine is important in the sympathetic nerves, both sys-tems (as well as the intrinsic neurons) have various and diverse neurotransmitters, including cholinergic, adrenergic, and pepti-dergic (e.g., substance P and somatostatin).HistologyThere are four distinct layers of the gastric wall: mucosa, sub-mucosa, muscularis propria, and serosa (Fig. 26-6).7 The inner layer of the stomach is the mucosa, which is lined with colum-nar epithelial cells of various types. Beneath the basement mem-brane of the epithelial cells is the lamina propria, which contains connective tissue, blood |
Surgery_Schwartz_7340 | Surgery_Schwartz | is the mucosa, which is lined with colum-nar epithelial cells of various types. Beneath the basement mem-brane of the epithelial cells is the lamina propria, which contains connective tissue, blood vessels, nerve fibers, and inflammatory cells. Beneath the lamina propria is a thin muscle layer called the muscularis mucosa, the deep boundary of the mucosal layer of the gut. The epithelium, lamina propria, and muscularis mucosa constitute the mucosa (Fig. 26-7).16 The epithelium of the gastric mucosa is columnar glandular. Scanning electron micrographs show a smooth mucosal carpet punctuated by the openings of the gastric glands or units. The gastric glands are lined with different types of epithelial cells, depending upon their loca-tion in the stomach (Fig. 26-8 and Table 26-2).17,18 There are also endocrine cells present in the gastric glands. Progenitor or stem cells in the isthmus and base of the glands differentiate and BodyFundusEsophagusCardiaPylorusDuodenumPyloric antrum | Surgery_Schwartz. is the mucosa, which is lined with colum-nar epithelial cells of various types. Beneath the basement mem-brane of the epithelial cells is the lamina propria, which contains connective tissue, blood vessels, nerve fibers, and inflammatory cells. Beneath the lamina propria is a thin muscle layer called the muscularis mucosa, the deep boundary of the mucosal layer of the gut. The epithelium, lamina propria, and muscularis mucosa constitute the mucosa (Fig. 26-7).16 The epithelium of the gastric mucosa is columnar glandular. Scanning electron micrographs show a smooth mucosal carpet punctuated by the openings of the gastric glands or units. The gastric glands are lined with different types of epithelial cells, depending upon their loca-tion in the stomach (Fig. 26-8 and Table 26-2).17,18 There are also endocrine cells present in the gastric glands. Progenitor or stem cells in the isthmus and base of the glands differentiate and BodyFundusEsophagusCardiaPylorusDuodenumPyloric antrum |
Surgery_Schwartz_7341 | Surgery_Schwartz | There are also endocrine cells present in the gastric glands. Progenitor or stem cells in the isthmus and base of the glands differentiate and BodyFundusEsophagusCardiaPylorusDuodenumPyloric antrum Lessercurvature GreatercurvatureFigure 26-1. Anatomic regions of the stomach. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Figure 26-2. Anatomic relationships of the stomach. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Liver (left lobe) Celiac trunk(splenic, gastric, hepatic)Gastrohepatic omentum Stomach(posterior wall)SpleenPancreasTransverse colonLesser omental spaceGastrocolic ligamentRight kidneyHepatoduodenal ligamentGallbladderT lictBrunicardi_Ch26_p1099-p1166.indd 110201/03/19 7:11 PM 1103STOMACHCHAPTER 26replenish | Surgery_Schwartz. There are also endocrine cells present in the gastric glands. Progenitor or stem cells in the isthmus and base of the glands differentiate and BodyFundusEsophagusCardiaPylorusDuodenumPyloric antrum Lessercurvature GreatercurvatureFigure 26-1. Anatomic regions of the stomach. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Figure 26-2. Anatomic relationships of the stomach. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Liver (left lobe) Celiac trunk(splenic, gastric, hepatic)Gastrohepatic omentum Stomach(posterior wall)SpleenPancreasTransverse colonLesser omental spaceGastrocolic ligamentRight kidneyHepatoduodenal ligamentGallbladderT lictBrunicardi_Ch26_p1099-p1166.indd 110201/03/19 7:11 PM 1103STOMACHCHAPTER 26replenish |
Surgery_Schwartz_7342 | Surgery_Schwartz | colonLesser omental spaceGastrocolic ligamentRight kidneyHepatoduodenal ligamentGallbladderT lictBrunicardi_Ch26_p1099-p1166.indd 110201/03/19 7:11 PM 1103STOMACHCHAPTER 26replenish sloughed cells on a regular basis. Genetic studies show that there are several different subpopulations of stem cells in the gastric glands and that during conditions of stress even chief cells exhibit the plasticity required to regenerate other types of gastric epithelial cells.19 Throughout the stomach, the luminal carpet consists primarily of mucus-secreting surface epithelial cells (SECs) that extend down into the gland pits for variable distances. These cells also secrete bicarbonate and play an important role in protecting the stomach from injury due to acid, pepsin, and/or ingested irritants. In fact, all epithelial cells of the stomach (except the endocrine cells) contain carbonic anhydrase and are capable of producing bicarbonate.In the cardia, the gastric glands are branched and | Surgery_Schwartz. colonLesser omental spaceGastrocolic ligamentRight kidneyHepatoduodenal ligamentGallbladderT lictBrunicardi_Ch26_p1099-p1166.indd 110201/03/19 7:11 PM 1103STOMACHCHAPTER 26replenish sloughed cells on a regular basis. Genetic studies show that there are several different subpopulations of stem cells in the gastric glands and that during conditions of stress even chief cells exhibit the plasticity required to regenerate other types of gastric epithelial cells.19 Throughout the stomach, the luminal carpet consists primarily of mucus-secreting surface epithelial cells (SECs) that extend down into the gland pits for variable distances. These cells also secrete bicarbonate and play an important role in protecting the stomach from injury due to acid, pepsin, and/or ingested irritants. In fact, all epithelial cells of the stomach (except the endocrine cells) contain carbonic anhydrase and are capable of producing bicarbonate.In the cardia, the gastric glands are branched and |
Surgery_Schwartz_7343 | Surgery_Schwartz | In fact, all epithelial cells of the stomach (except the endocrine cells) contain carbonic anhydrase and are capable of producing bicarbonate.In the cardia, the gastric glands are branched and secrete primarily mucus and bicarbonate, and little acid. In the fundus and body, the glands are more tubular, and the pits are deep. Parietal and chief cells are common in these glands (Fig. 26-9). Histamine-secreting enterochromaffin-like (ECL) cells and somatostatin-secreting D cells are also found. Parietal cells Figure 26-3. Arterial blood supply to the stomach. a. = artery; v. = vein. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)StomachCeliac a.Short gastric arteries(vasa brevia)SpleenDescending colonPancreasDuodenumTransverse colonPylorusSup. pancreatic duodenal a.Abdominal AortaInferior pancreatic duodenal a.Hepatic a.Left gastric a.Branchesto | Surgery_Schwartz. In fact, all epithelial cells of the stomach (except the endocrine cells) contain carbonic anhydrase and are capable of producing bicarbonate.In the cardia, the gastric glands are branched and secrete primarily mucus and bicarbonate, and little acid. In the fundus and body, the glands are more tubular, and the pits are deep. Parietal and chief cells are common in these glands (Fig. 26-9). Histamine-secreting enterochromaffin-like (ECL) cells and somatostatin-secreting D cells are also found. Parietal cells Figure 26-3. Arterial blood supply to the stomach. a. = artery; v. = vein. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)StomachCeliac a.Short gastric arteries(vasa brevia)SpleenDescending colonPancreasDuodenumTransverse colonPylorusSup. pancreatic duodenal a.Abdominal AortaInferior pancreatic duodenal a.Hepatic a.Left gastric a.Branchesto |
Surgery_Schwartz_7344 | Surgery_Schwartz | arteries(vasa brevia)SpleenDescending colonPancreasDuodenumTransverse colonPylorusSup. pancreatic duodenal a.Abdominal AortaInferior pancreatic duodenal a.Hepatic a.Left gastric a.Branchesto greateromentumSplenic a. & v.L. gastroepiploic a. Sup. mesenteric a. & v. Inferior mesenteric a.Ileocolic a.Jejunum21534a4b6128971011Figure 26-4. Lymph node stations draining the stomach according to the Japanese Research Society for Gastric Cancer. Stations 3 to 6 are commonly removed with D1 gastrectomy. Stations 1, 2, and 7 to 12 are commonly removed with D2 gastrectomy. (Reproduced with permis-sion from Hermanek P, Hutter RVP, Sobin LH, et al: TNM Atlas: Illustrated Guide to the TNM/pTNM Classification of Malignant Tumours, 4th ed. Berlin: Springer-Verlag; 1997.)Brunicardi_Ch26_p1099-p1166.indd 110301/03/19 7:11 PM 1104SPECIFIC CONSIDERATIONS PART IIRight vagus n.Hepatic br. left vagusCeliac br. rt. vagusNerve of LaterjetPyloric br.Left vagus n.Figure 26-5. Vagal | Surgery_Schwartz. arteries(vasa brevia)SpleenDescending colonPancreasDuodenumTransverse colonPylorusSup. pancreatic duodenal a.Abdominal AortaInferior pancreatic duodenal a.Hepatic a.Left gastric a.Branchesto greateromentumSplenic a. & v.L. gastroepiploic a. Sup. mesenteric a. & v. Inferior mesenteric a.Ileocolic a.Jejunum21534a4b6128971011Figure 26-4. Lymph node stations draining the stomach according to the Japanese Research Society for Gastric Cancer. Stations 3 to 6 are commonly removed with D1 gastrectomy. Stations 1, 2, and 7 to 12 are commonly removed with D2 gastrectomy. (Reproduced with permis-sion from Hermanek P, Hutter RVP, Sobin LH, et al: TNM Atlas: Illustrated Guide to the TNM/pTNM Classification of Malignant Tumours, 4th ed. Berlin: Springer-Verlag; 1997.)Brunicardi_Ch26_p1099-p1166.indd 110301/03/19 7:11 PM 1104SPECIFIC CONSIDERATIONS PART IIRight vagus n.Hepatic br. left vagusCeliac br. rt. vagusNerve of LaterjetPyloric br.Left vagus n.Figure 26-5. Vagal |
Surgery_Schwartz_7345 | Surgery_Schwartz | 110301/03/19 7:11 PM 1104SPECIFIC CONSIDERATIONS PART IIRight vagus n.Hepatic br. left vagusCeliac br. rt. vagusNerve of LaterjetPyloric br.Left vagus n.Figure 26-5. Vagal innervation of the stomach. br. = branch; n. = nerve; rt. = right. (Reproduced with permission from Menguy R: Surgery of Peptic Ulcer. Philadelphia, PA: Elsevier/Saunders; 1976.)Surface epitheliumGastric pitsLymphoid noduleLamina propria mucosaSubmucosaSmooth muscle layersSerosaMuscularis mucosaeFigure 26-6. Layers of the gastric wall. (Reproduced with permis-sion from Fawcett DW: Bloom and Fawcett’s Textbook of Histology, 11th ed. Philadelphia, PA: Elsevier/Saunders; 1986.)Figure 26-7. Gastric mucosa. (Used with permission from Emma Furth, MD.)Brunicardi_Ch26_p1099-p1166.indd 110401/03/19 7:11 PM 1105STOMACHCHAPTER 26secrete acid and intrinsic factor into the gastric lumen, and bicarbonate into the intercellular space. They have a character-istic ultrastructural appearance with secretory canaliculi | Surgery_Schwartz. 110301/03/19 7:11 PM 1104SPECIFIC CONSIDERATIONS PART IIRight vagus n.Hepatic br. left vagusCeliac br. rt. vagusNerve of LaterjetPyloric br.Left vagus n.Figure 26-5. Vagal innervation of the stomach. br. = branch; n. = nerve; rt. = right. (Reproduced with permission from Menguy R: Surgery of Peptic Ulcer. Philadelphia, PA: Elsevier/Saunders; 1976.)Surface epitheliumGastric pitsLymphoid noduleLamina propria mucosaSubmucosaSmooth muscle layersSerosaMuscularis mucosaeFigure 26-6. Layers of the gastric wall. (Reproduced with permis-sion from Fawcett DW: Bloom and Fawcett’s Textbook of Histology, 11th ed. Philadelphia, PA: Elsevier/Saunders; 1986.)Figure 26-7. Gastric mucosa. (Used with permission from Emma Furth, MD.)Brunicardi_Ch26_p1099-p1166.indd 110401/03/19 7:11 PM 1105STOMACHCHAPTER 26secrete acid and intrinsic factor into the gastric lumen, and bicarbonate into the intercellular space. They have a character-istic ultrastructural appearance with secretory canaliculi |
Surgery_Schwartz_7346 | Surgery_Schwartz | 26secrete acid and intrinsic factor into the gastric lumen, and bicarbonate into the intercellular space. They have a character-istic ultrastructural appearance with secretory canaliculi (deep invaginations of the surface membrane) and cytoplasmic tubulo-vesicles containing the acid-producing apparatus H+/K+-ATPase (proton pump) (see Fig. 26-9). There are numerous mitochon-dria; in fact, the parietal cell is the most mitochondria-rich cell in the body. When the parietal cell is stimulated, the cytoplasmic tubulovesicles fuse with the membrane of the secretory cana-liculus; when acid production ceases, the process is reversed. Arguably, parietal cells produce the only truly essential sub-stance made by the stomach (i.e., intrinsic factor). Parietal cells tend to occupy the midportion of the gastric glands found in the corpus of the stomach.Chief cells (also called zymogenic cells) secrete pep-sinogen I, which is maximally activated at a pH of 2.5. They tend to be clustered toward the | Surgery_Schwartz. 26secrete acid and intrinsic factor into the gastric lumen, and bicarbonate into the intercellular space. They have a character-istic ultrastructural appearance with secretory canaliculi (deep invaginations of the surface membrane) and cytoplasmic tubulo-vesicles containing the acid-producing apparatus H+/K+-ATPase (proton pump) (see Fig. 26-9). There are numerous mitochon-dria; in fact, the parietal cell is the most mitochondria-rich cell in the body. When the parietal cell is stimulated, the cytoplasmic tubulovesicles fuse with the membrane of the secretory cana-liculus; when acid production ceases, the process is reversed. Arguably, parietal cells produce the only truly essential sub-stance made by the stomach (i.e., intrinsic factor). Parietal cells tend to occupy the midportion of the gastric glands found in the corpus of the stomach.Chief cells (also called zymogenic cells) secrete pep-sinogen I, which is maximally activated at a pH of 2.5. They tend to be clustered toward the |
Surgery_Schwartz_7347 | Surgery_Schwartz | gastric glands found in the corpus of the stomach.Chief cells (also called zymogenic cells) secrete pep-sinogen I, which is maximally activated at a pH of 2.5. They tend to be clustered toward the base of the gastric glands and have a low columnar shape. Ultrastructurally, chief cells have the characteristics of protein-synthesizing cells: basal granular endoplasmic reticulum, supranuclear Golgi apparatus, and api-cal zymogen granules (Fig. 26-10). When stimulated, the chief cells produce two immunologically distinct proenzyme forms of pepsinogen: predominantly pepsinogen I and some pepsinogen II, most of which is produced by SECs. These proenzymes are activated in an acidic luminal environment.In the antrum, the gastric glands are again more branched and shallow, parietal cells are rare, and gastrin-secreting G cells and somatostatin-secreting D cells are present. A variety of hormone-secreting cells are present in various proportions throughout the gastric mucosa (Fig. 26-11).20 | Surgery_Schwartz. gastric glands found in the corpus of the stomach.Chief cells (also called zymogenic cells) secrete pep-sinogen I, which is maximally activated at a pH of 2.5. They tend to be clustered toward the base of the gastric glands and have a low columnar shape. Ultrastructurally, chief cells have the characteristics of protein-synthesizing cells: basal granular endoplasmic reticulum, supranuclear Golgi apparatus, and api-cal zymogen granules (Fig. 26-10). When stimulated, the chief cells produce two immunologically distinct proenzyme forms of pepsinogen: predominantly pepsinogen I and some pepsinogen II, most of which is produced by SECs. These proenzymes are activated in an acidic luminal environment.In the antrum, the gastric glands are again more branched and shallow, parietal cells are rare, and gastrin-secreting G cells and somatostatin-secreting D cells are present. A variety of hormone-secreting cells are present in various proportions throughout the gastric mucosa (Fig. 26-11).20 |
Surgery_Schwartz_7348 | Surgery_Schwartz | and gastrin-secreting G cells and somatostatin-secreting D cells are present. A variety of hormone-secreting cells are present in various proportions throughout the gastric mucosa (Fig. 26-11).20 Histologic analy-sis suggests that in the normal stomach, 13% of the epithelial cells are oxyntic (parietal) cells, 44% are chief (zymogenic) cells, 40% are mucous cells, and 3% are endocrine cells. In gen-eral, the antrum produces gastrin but not acid, and the proximal stomach produces acid but not gastrin. The border between the corpus and antrum migrates proximally with age (especially on the lesser curvature side of the stomach).Deep to the muscularis mucosa is the submucosa, which is rich in branching blood vessels, lymphatics, collagen, vari-ous inflammatory cells, and nerve fibers and ganglion cells of Meissner’s autonomic submucosal plexus. The collagen-rich submucosa gives strength to GI anastomoses. The mucosa and submucosa are folded into the grossly visible gastric rugae, which | Surgery_Schwartz. and gastrin-secreting G cells and somatostatin-secreting D cells are present. A variety of hormone-secreting cells are present in various proportions throughout the gastric mucosa (Fig. 26-11).20 Histologic analy-sis suggests that in the normal stomach, 13% of the epithelial cells are oxyntic (parietal) cells, 44% are chief (zymogenic) cells, 40% are mucous cells, and 3% are endocrine cells. In gen-eral, the antrum produces gastrin but not acid, and the proximal stomach produces acid but not gastrin. The border between the corpus and antrum migrates proximally with age (especially on the lesser curvature side of the stomach).Deep to the muscularis mucosa is the submucosa, which is rich in branching blood vessels, lymphatics, collagen, vari-ous inflammatory cells, and nerve fibers and ganglion cells of Meissner’s autonomic submucosal plexus. The collagen-rich submucosa gives strength to GI anastomoses. The mucosa and submucosa are folded into the grossly visible gastric rugae, which |
Surgery_Schwartz_7349 | Surgery_Schwartz | cells of Meissner’s autonomic submucosal plexus. The collagen-rich submucosa gives strength to GI anastomoses. The mucosa and submucosa are folded into the grossly visible gastric rugae, which tend to flatten out as the stomach becomes distended.Below the submucosa is the thick muscularis propria (also referred to as the muscularis externa), which consists of an incomplete inner oblique layer, a complete middle circular layer (continuous with the esophageal circular muscle and the circular muscle of the pylorus), and a complete outer longitudinal layer (continuous with the longitudinal layer of the esophagus and duodenum). Within the muscularis propria is the rich network of autonomic ganglia and nerves that make up Auerbach’s myen-teric plexus. Specialized pacemaker cells, the interstitial cells of Cajal (ICC), also are present.The outer layer of the stomach is the serosa, also known as the visceral peritoneum. This layer provides significant tensile strength to gastric anastomoses. | Surgery_Schwartz. cells of Meissner’s autonomic submucosal plexus. The collagen-rich submucosa gives strength to GI anastomoses. The mucosa and submucosa are folded into the grossly visible gastric rugae, which tend to flatten out as the stomach becomes distended.Below the submucosa is the thick muscularis propria (also referred to as the muscularis externa), which consists of an incomplete inner oblique layer, a complete middle circular layer (continuous with the esophageal circular muscle and the circular muscle of the pylorus), and a complete outer longitudinal layer (continuous with the longitudinal layer of the esophagus and duodenum). Within the muscularis propria is the rich network of autonomic ganglia and nerves that make up Auerbach’s myen-teric plexus. Specialized pacemaker cells, the interstitial cells of Cajal (ICC), also are present.The outer layer of the stomach is the serosa, also known as the visceral peritoneum. This layer provides significant tensile strength to gastric anastomoses. |
Surgery_Schwartz_7350 | Surgery_Schwartz | cells of Cajal (ICC), also are present.The outer layer of the stomach is the serosa, also known as the visceral peritoneum. This layer provides significant tensile strength to gastric anastomoses. When tumors originating in the mucosa penetrate and breach the serosa, microscopic or gross peritoneal metastases are common, presumably from shedding of tumor cells that would not have occurred if the serosa had not been penetrated. In this way, the serosa may be thought of as an outer envelope of the stomach.PHYSIOLOGYThe stomach stores food and facilitates digestion through a variety of secretory and motor functions. Important secretory functions include the production of acid, pepsin, intrinsic factor, mucus, and a variety of GI hormones. Important motor func-tions include food storage (receptive relaxation and accommo-dation), grinding and mixing, controlled emptying of ingested food, and periodic interprandial “housekeeping.”Acid SecretionHydrochloric acid in the stomach hastens both | Surgery_Schwartz. cells of Cajal (ICC), also are present.The outer layer of the stomach is the serosa, also known as the visceral peritoneum. This layer provides significant tensile strength to gastric anastomoses. When tumors originating in the mucosa penetrate and breach the serosa, microscopic or gross peritoneal metastases are common, presumably from shedding of tumor cells that would not have occurred if the serosa had not been penetrated. In this way, the serosa may be thought of as an outer envelope of the stomach.PHYSIOLOGYThe stomach stores food and facilitates digestion through a variety of secretory and motor functions. Important secretory functions include the production of acid, pepsin, intrinsic factor, mucus, and a variety of GI hormones. Important motor func-tions include food storage (receptive relaxation and accommo-dation), grinding and mixing, controlled emptying of ingested food, and periodic interprandial “housekeeping.”Acid SecretionHydrochloric acid in the stomach hastens both |
Surgery_Schwartz_7351 | Surgery_Schwartz | relaxation and accommo-dation), grinding and mixing, controlled emptying of ingested food, and periodic interprandial “housekeeping.”Acid SecretionHydrochloric acid in the stomach hastens both the physical and (with pepsin) the biochemical breakdown of ingested food. In an acidic environment, pepsin and acid facilitate proteolysis. Gastric acid also inhibits the proliferation of ingested patho-gens, which protects against both infectious gastroenteritis and intestinal bacterial overgrowth and helps to maintain a healthy gastrointestinal microbiome.21 Long-term acid suppression with proton pump inhibitors (PPIs) has been associated with an Surface mucous cellsParietal cellsMucous neck cellsArgentaffin cellChief cellsGastric pitIsthmusNeckBaseFigure 26-8. Mammalian gastric gland from the body of the stom-ach. (Reproduced with permission from Ito S, Winchester RJ: The fine structure of the gastric mucosa in the bat, J Cell Biol. 1963 Mar;16(3):541-577.)Brunicardi_Ch26_p1099-p1166.indd | Surgery_Schwartz. relaxation and accommo-dation), grinding and mixing, controlled emptying of ingested food, and periodic interprandial “housekeeping.”Acid SecretionHydrochloric acid in the stomach hastens both the physical and (with pepsin) the biochemical breakdown of ingested food. In an acidic environment, pepsin and acid facilitate proteolysis. Gastric acid also inhibits the proliferation of ingested patho-gens, which protects against both infectious gastroenteritis and intestinal bacterial overgrowth and helps to maintain a healthy gastrointestinal microbiome.21 Long-term acid suppression with proton pump inhibitors (PPIs) has been associated with an Surface mucous cellsParietal cellsMucous neck cellsArgentaffin cellChief cellsGastric pitIsthmusNeckBaseFigure 26-8. Mammalian gastric gland from the body of the stom-ach. (Reproduced with permission from Ito S, Winchester RJ: The fine structure of the gastric mucosa in the bat, J Cell Biol. 1963 Mar;16(3):541-577.)Brunicardi_Ch26_p1099-p1166.indd |
Surgery_Schwartz_7352 | Surgery_Schwartz | of the stom-ach. (Reproduced with permission from Ito S, Winchester RJ: The fine structure of the gastric mucosa in the bat, J Cell Biol. 1963 Mar;16(3):541-577.)Brunicardi_Ch26_p1099-p1166.indd 110501/03/19 7:11 PM 1106SPECIFIC CONSIDERATIONS PART IIincreased risk of community-acquired Clostridium difficile coli-tis and other gastroenteritis, presumably because of the absence of this protective germicidal barrier.22,23Parietal Cell. The parietal cell is stimulated to secrete acid (Fig. 26-12) when one or more of three membrane receptor types is stimulated by acetylcholine (from vagally stimulated enteric neurons), gastrin (from G cells), or histamine (from ECL cells).7,24,25 The enzyme H+/K+-ATPase is the parietal cell proton pump. It is stored within the intracellular tubulovesicles and is the final common pathway for gastric acid secretion. When the parietal cell is stimulated, there is a cytoskeletal rearrangement and fusion of the tubulovesicles with the apical membrane | Surgery_Schwartz. of the stom-ach. (Reproduced with permission from Ito S, Winchester RJ: The fine structure of the gastric mucosa in the bat, J Cell Biol. 1963 Mar;16(3):541-577.)Brunicardi_Ch26_p1099-p1166.indd 110501/03/19 7:11 PM 1106SPECIFIC CONSIDERATIONS PART IIincreased risk of community-acquired Clostridium difficile coli-tis and other gastroenteritis, presumably because of the absence of this protective germicidal barrier.22,23Parietal Cell. The parietal cell is stimulated to secrete acid (Fig. 26-12) when one or more of three membrane receptor types is stimulated by acetylcholine (from vagally stimulated enteric neurons), gastrin (from G cells), or histamine (from ECL cells).7,24,25 The enzyme H+/K+-ATPase is the parietal cell proton pump. It is stored within the intracellular tubulovesicles and is the final common pathway for gastric acid secretion. When the parietal cell is stimulated, there is a cytoskeletal rearrangement and fusion of the tubulovesicles with the apical membrane |
Surgery_Schwartz_7353 | Surgery_Schwartz | and is the final common pathway for gastric acid secretion. When the parietal cell is stimulated, there is a cytoskeletal rearrangement and fusion of the tubulovesicles with the apical membrane of the secretory canaliculus. The heterodimer assembly of the enzyme subunits into the microvilli of the secretory canalicu-lus results in acid secretion, with extracellular potassium being exchanged for cytosolic hydrogen. Although electroneutral, this is an energy-requiring process because the hydrogen is secreted against a gradient of at least 1 million-fold, which explains why the parietal cell is packed with energy producing mito-chondria. During acid production, potassium and chloride are also secreted into the apical secretory canaliculus through sepa-rate channels, providing potassium to exchange for H+ via the H+/K+-ATPase, and chloride to accompany the secreted hydrogen. At the basolateral membrane, the combined activity of various SCMTVFigure 26-9. Ultrastructural features of the | Surgery_Schwartz. and is the final common pathway for gastric acid secretion. When the parietal cell is stimulated, there is a cytoskeletal rearrangement and fusion of the tubulovesicles with the apical membrane of the secretory canaliculus. The heterodimer assembly of the enzyme subunits into the microvilli of the secretory canalicu-lus results in acid secretion, with extracellular potassium being exchanged for cytosolic hydrogen. Although electroneutral, this is an energy-requiring process because the hydrogen is secreted against a gradient of at least 1 million-fold, which explains why the parietal cell is packed with energy producing mito-chondria. During acid production, potassium and chloride are also secreted into the apical secretory canaliculus through sepa-rate channels, providing potassium to exchange for H+ via the H+/K+-ATPase, and chloride to accompany the secreted hydrogen. At the basolateral membrane, the combined activity of various SCMTVFigure 26-9. Ultrastructural features of the |
Surgery_Schwartz_7354 | Surgery_Schwartz | exchange for H+ via the H+/K+-ATPase, and chloride to accompany the secreted hydrogen. At the basolateral membrane, the combined activity of various SCMTVFigure 26-9. Ultrastructural features of the parietal (oxyntic) cell. SC = secretory canaliculus; M = mitochondria; TV = tubulovesicle. (Reproduced with permission from Ming S-C, Goldman H: Pathol-ogy of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.)ZGGAGERFigure 26-10. Ultrastructural features of the chief (zymogenic) cell. GA = Golgi apparatus; GER = granular endoplasmic reticu-lum; ZG = zymogen granule. (Reproduced with permission from Ming S-C, Goldman H: Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.)Table 26-2Epithelial cells of the stomachCELL TYPEDISTINCTIVE ULTRASTRUCTURAL FEATURESMAJOR FUNCTIONSSurface-foveolar mucous cellsApical stippled granules up to 1 μm in diameterProduction of neutral glycoprotein and bicarbonate to form a gel on the gastric | Surgery_Schwartz. exchange for H+ via the H+/K+-ATPase, and chloride to accompany the secreted hydrogen. At the basolateral membrane, the combined activity of various SCMTVFigure 26-9. Ultrastructural features of the parietal (oxyntic) cell. SC = secretory canaliculus; M = mitochondria; TV = tubulovesicle. (Reproduced with permission from Ming S-C, Goldman H: Pathol-ogy of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.)ZGGAGERFigure 26-10. Ultrastructural features of the chief (zymogenic) cell. GA = Golgi apparatus; GER = granular endoplasmic reticu-lum; ZG = zymogen granule. (Reproduced with permission from Ming S-C, Goldman H: Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.)Table 26-2Epithelial cells of the stomachCELL TYPEDISTINCTIVE ULTRASTRUCTURAL FEATURESMAJOR FUNCTIONSSurface-foveolar mucous cellsApical stippled granules up to 1 μm in diameterProduction of neutral glycoprotein and bicarbonate to form a gel on the gastric |
Surgery_Schwartz_7355 | Surgery_Schwartz | ULTRASTRUCTURAL FEATURESMAJOR FUNCTIONSSurface-foveolar mucous cellsApical stippled granules up to 1 μm in diameterProduction of neutral glycoprotein and bicarbonate to form a gel on the gastric luminal surface; neutralization of hydrochloric acidaMucous neck cellHeterogeneous granules 1–2 μm in diameter dispersed throughout the cytoplasmProgenitor cell for all other gastric epithelial cells; glycoprotein production; production of pepsinogens I and IIOxyntic (parietal) cellSurface membrane invaginations (canaliculi); tubulovesicle structures; numerous mitochondriaProduction of hydrochloric acid; production of intrinsic factor; production of bicarbonateChief cellModerately dense apical granules up to 2 μm in diameter; prominent supranuclear Golgi apparatus; extensive basolateral granular endoplasmic reticulumProduction of pepsinogens I and II, and of lipaseCardiopyloric mucous cellMixture of granules like those in mucous neck and chief cells; extensive basolateral granular endoplasmic | Surgery_Schwartz. ULTRASTRUCTURAL FEATURESMAJOR FUNCTIONSSurface-foveolar mucous cellsApical stippled granules up to 1 μm in diameterProduction of neutral glycoprotein and bicarbonate to form a gel on the gastric luminal surface; neutralization of hydrochloric acidaMucous neck cellHeterogeneous granules 1–2 μm in diameter dispersed throughout the cytoplasmProgenitor cell for all other gastric epithelial cells; glycoprotein production; production of pepsinogens I and IIOxyntic (parietal) cellSurface membrane invaginations (canaliculi); tubulovesicle structures; numerous mitochondriaProduction of hydrochloric acid; production of intrinsic factor; production of bicarbonateChief cellModerately dense apical granules up to 2 μm in diameter; prominent supranuclear Golgi apparatus; extensive basolateral granular endoplasmic reticulumProduction of pepsinogens I and II, and of lipaseCardiopyloric mucous cellMixture of granules like those in mucous neck and chief cells; extensive basolateral granular endoplasmic |
Surgery_Schwartz_7356 | Surgery_Schwartz | reticulumProduction of pepsinogens I and II, and of lipaseCardiopyloric mucous cellMixture of granules like those in mucous neck and chief cells; extensive basolateral granular endoplasmic reticulumProduction of glycoprotein; production of pepsinogen IIEndocrine cellsSee Figure 26-11 aBicarbonate is probably produced by other gastric epithelial cells in addition to surface-foveolar mucous cells.Reproduced with permission from Ming S-C, Goldman H: Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.Brunicardi_Ch26_p1099-p1166.indd 110601/03/19 7:11 PM 1107STOMACHCHAPTER 26cotransporters and ion exchangers accomplishes intracellular pH regulation and electrolyte homeostasis.24The normal human stomach contains approximately 1 billion parietal cells, and total gastric acid production is pro-portional to parietal cell mass. Almost all of the parietal cells are in the proximal 2/3 stomach, though there are some parietal cells found in gastric antral | Surgery_Schwartz. reticulumProduction of pepsinogens I and II, and of lipaseCardiopyloric mucous cellMixture of granules like those in mucous neck and chief cells; extensive basolateral granular endoplasmic reticulumProduction of glycoprotein; production of pepsinogen IIEndocrine cellsSee Figure 26-11 aBicarbonate is probably produced by other gastric epithelial cells in addition to surface-foveolar mucous cells.Reproduced with permission from Ming S-C, Goldman H: Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.Brunicardi_Ch26_p1099-p1166.indd 110601/03/19 7:11 PM 1107STOMACHCHAPTER 26cotransporters and ion exchangers accomplishes intracellular pH regulation and electrolyte homeostasis.24The normal human stomach contains approximately 1 billion parietal cells, and total gastric acid production is pro-portional to parietal cell mass. Almost all of the parietal cells are in the proximal 2/3 stomach, though there are some parietal cells found in gastric antral |
Surgery_Schwartz_7357 | Surgery_Schwartz | total gastric acid production is pro-portional to parietal cell mass. Almost all of the parietal cells are in the proximal 2/3 stomach, though there are some parietal cells found in gastric antral glands. The potent acid-suppressing PPI drugs irreversibly interfere with the function of the H+/K+-ATPase molecule. These agents must be incorporated into the activated enzyme to be effective and thus work best when taken before or during a meal (when the parietal cell is stimulated). When PPI therapy is stopped, acid secretory capability gradu-ally returns (within days) as new H+/K+-ATPase is synthesized.Gastrin, acetylcholine, and histamine stimulate the parietal cell to secrete hydrochloric acid (see Fig. 26-12). Gastrin binds to type B cholecystokinin (CCK2) receptors on ECL cells and stimulates ECL cell histamine release, which binds to H2 recep-tors on the parietal cell. This stimulates adenylatecyclase (via a G-protein–linked mechanism) and increases cAMP which acti-vates protein | Surgery_Schwartz. total gastric acid production is pro-portional to parietal cell mass. Almost all of the parietal cells are in the proximal 2/3 stomach, though there are some parietal cells found in gastric antral glands. The potent acid-suppressing PPI drugs irreversibly interfere with the function of the H+/K+-ATPase molecule. These agents must be incorporated into the activated enzyme to be effective and thus work best when taken before or during a meal (when the parietal cell is stimulated). When PPI therapy is stopped, acid secretory capability gradu-ally returns (within days) as new H+/K+-ATPase is synthesized.Gastrin, acetylcholine, and histamine stimulate the parietal cell to secrete hydrochloric acid (see Fig. 26-12). Gastrin binds to type B cholecystokinin (CCK2) receptors on ECL cells and stimulates ECL cell histamine release, which binds to H2 recep-tors on the parietal cell. This stimulates adenylatecyclase (via a G-protein–linked mechanism) and increases cAMP which acti-vates protein |
Surgery_Schwartz_7358 | Surgery_Schwartz | ECL cell histamine release, which binds to H2 recep-tors on the parietal cell. This stimulates adenylatecyclase (via a G-protein–linked mechanism) and increases cAMP which acti-vates protein kinases, leading to increased levels of phospho-proteins and activation of the proton pump. Gastrin also binds to CCK2 receptors on the parietal cell, but this is less important for acid secretion than the gastrin effect on ECL cells. Acetyl-choline from intrinsic neurons binds to M3 muscarinic recep-tors on the parietal cell, which (like gastrin binding to CCK2 receptors) stimulates phospholipase C via a G-protein–linked mechanism leading to increased production of inositol trispho-sphate from membrane bound phospholipids. Inositol trisphos-phate stimulates the release of calcium from intracellular stores, which leads to activation of protein kinases and activation of H+/K+-ATPase. Somatostatin released from mucosal D cells in the antral and oxcyntic mucosa in response to luminal acid binds to | Surgery_Schwartz. ECL cell histamine release, which binds to H2 recep-tors on the parietal cell. This stimulates adenylatecyclase (via a G-protein–linked mechanism) and increases cAMP which acti-vates protein kinases, leading to increased levels of phospho-proteins and activation of the proton pump. Gastrin also binds to CCK2 receptors on the parietal cell, but this is less important for acid secretion than the gastrin effect on ECL cells. Acetyl-choline from intrinsic neurons binds to M3 muscarinic recep-tors on the parietal cell, which (like gastrin binding to CCK2 receptors) stimulates phospholipase C via a G-protein–linked mechanism leading to increased production of inositol trispho-sphate from membrane bound phospholipids. Inositol trisphos-phate stimulates the release of calcium from intracellular stores, which leads to activation of protein kinases and activation of H+/K+-ATPase. Somatostatin released from mucosal D cells in the antral and oxcyntic mucosa in response to luminal acid binds to |
Surgery_Schwartz_7359 | Surgery_Schwartz | stores, which leads to activation of protein kinases and activation of H+/K+-ATPase. Somatostatin released from mucosal D cells in the antral and oxcyntic mucosa in response to luminal acid binds to SSTR2 receptors on parietal cells and inhibits acid release directly. Somatostatin also inhibits acid secretion in a paracrine fashion, binding to nearby ECL cells in the oxcyntic mucosa and decreasing histamine release, and binding to nearby antral G cells to inhibit gastrin release.26Physiologic Acid Secretion.27 Food ingestion is the physi-ologic stimulus for acid secretion (Fig. 26-13). The acid secre-tory response that occurs after a meal is traditionally described Oxyntic mucosaOther3%D19%G49%EC29%Other14%D26%EC25%ECL35%Pyloric mucosaFigure 26-11. Endocrine cells of the stomach—proportion by site. D = d cell (somatostatin); EC = enterochromaffin cell; ECL = enterochromaffin-like cell (histamine); G = g cell (gastrin). (Repro-duced with permission from Feldman M, Friedman LS, | Surgery_Schwartz. stores, which leads to activation of protein kinases and activation of H+/K+-ATPase. Somatostatin released from mucosal D cells in the antral and oxcyntic mucosa in response to luminal acid binds to SSTR2 receptors on parietal cells and inhibits acid release directly. Somatostatin also inhibits acid secretion in a paracrine fashion, binding to nearby ECL cells in the oxcyntic mucosa and decreasing histamine release, and binding to nearby antral G cells to inhibit gastrin release.26Physiologic Acid Secretion.27 Food ingestion is the physi-ologic stimulus for acid secretion (Fig. 26-13). The acid secre-tory response that occurs after a meal is traditionally described Oxyntic mucosaOther3%D19%G49%EC29%Other14%D26%EC25%ECL35%Pyloric mucosaFigure 26-11. Endocrine cells of the stomach—proportion by site. D = d cell (somatostatin); EC = enterochromaffin cell; ECL = enterochromaffin-like cell (histamine); G = g cell (gastrin). (Repro-duced with permission from Feldman M, Friedman LS, |
Surgery_Schwartz_7360 | Surgery_Schwartz | by site. D = d cell (somatostatin); EC = enterochromaffin cell; ECL = enterochromaffin-like cell (histamine); G = g cell (gastrin). (Repro-duced with permission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia, PA: Elsevier/Saunders; 2002.)Adenylate cyclaseATPHistamineInterstitiumLumenSomatostatinGi proteinGs proteinIP3PIP2Ca++K+ channelK+ClchannelCl-H+K+CCK8 receptorM3 receptorH+/K+-ATPaseGs proteinActivation ofother kinasescAMPActivatesprotein kinasesGastrinAcetylcholinePLCSomatostatinreceptorH2 receptorGs proteinFigure 26-12. Control of acid secretion in the parietal cell. ATP = adenosine triphosphate; cAMP = cyclic adenosine monophosphate; CCK = cholecystokinin; H2 = histamine 2; IP3 = inositol trisphosphate; PIP2 = phosphatidylinositol 4,5-bisphosphate; PLC = phospholipase C. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. | Surgery_Schwartz. by site. D = d cell (somatostatin); EC = enterochromaffin cell; ECL = enterochromaffin-like cell (histamine); G = g cell (gastrin). (Repro-duced with permission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia, PA: Elsevier/Saunders; 2002.)Adenylate cyclaseATPHistamineInterstitiumLumenSomatostatinGi proteinGs proteinIP3PIP2Ca++K+ channelK+ClchannelCl-H+K+CCK8 receptorM3 receptorH+/K+-ATPaseGs proteinActivation ofother kinasescAMPActivatesprotein kinasesGastrinAcetylcholinePLCSomatostatinreceptorH2 receptorGs proteinFigure 26-12. Control of acid secretion in the parietal cell. ATP = adenosine triphosphate; cAMP = cyclic adenosine monophosphate; CCK = cholecystokinin; H2 = histamine 2; IP3 = inositol trisphosphate; PIP2 = phosphatidylinositol 4,5-bisphosphate; PLC = phospholipase C. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. |
Surgery_Schwartz_7361 | Surgery_Schwartz | PIP2 = phosphatidylinositol 4,5-bisphosphate; PLC = phospholipase C. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Brunicardi_Ch26_p1099-p1166.indd 110701/03/19 7:11 PM 1108SPECIFIC CONSIDERATIONS PART IIin three phases: cephalic, gastric, and intestinal.28,29 The cephalic or vagal phase begins with the thought, sight, smell, and/or taste of food. These stimuli activate several cortical and hypotha-lamic sites (e.g., tractus solitarius, dorsal motor nucleus, and dorsal vagal complex), and signals are transmitted to the stom-ach by the vagal nerves which stimulate enteric submucosal neurons. Acetylcholine is released, leading to stimulation acid secretion from parietal cells. Vagal stimulation also leads to gas-trin release from antral G cells via CGRP, and sensitizes ECL cells to gastrin.30,31 Although the acid secreted per unit of time in the cephalic phase is | Surgery_Schwartz. PIP2 = phosphatidylinositol 4,5-bisphosphate; PLC = phospholipase C. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Brunicardi_Ch26_p1099-p1166.indd 110701/03/19 7:11 PM 1108SPECIFIC CONSIDERATIONS PART IIin three phases: cephalic, gastric, and intestinal.28,29 The cephalic or vagal phase begins with the thought, sight, smell, and/or taste of food. These stimuli activate several cortical and hypotha-lamic sites (e.g., tractus solitarius, dorsal motor nucleus, and dorsal vagal complex), and signals are transmitted to the stom-ach by the vagal nerves which stimulate enteric submucosal neurons. Acetylcholine is released, leading to stimulation acid secretion from parietal cells. Vagal stimulation also leads to gas-trin release from antral G cells via CGRP, and sensitizes ECL cells to gastrin.30,31 Although the acid secreted per unit of time in the cephalic phase is |
Surgery_Schwartz_7362 | Surgery_Schwartz | cells. Vagal stimulation also leads to gas-trin release from antral G cells via CGRP, and sensitizes ECL cells to gastrin.30,31 Although the acid secreted per unit of time in the cephalic phase is greater than in the other two phases, the cephalic phase is shorter. Thus, the cephalic phase accounts for no more than 30% of total acid secretion in response to a meal. Sham feeding (chewing and spitting) stimulates gastric acid secretion only via the cephalic phase, and it results in acid secretion that is about half of that seen in response to IV penta-gastrin or histamine.When food reaches the stomach, the gastric phase of acid secretion begins. This phase lasts until the stomach is empty and accounts for about 60% of the total acid secretion in response to a meal. The gastric phase of acid secretion has several compo-nents. Amino acids and small peptides directly stimulate antral G cells to secrete gastrin, which is carried in the bloodstream to the ECL and parietal cells, stimulating | Surgery_Schwartz. cells. Vagal stimulation also leads to gas-trin release from antral G cells via CGRP, and sensitizes ECL cells to gastrin.30,31 Although the acid secreted per unit of time in the cephalic phase is greater than in the other two phases, the cephalic phase is shorter. Thus, the cephalic phase accounts for no more than 30% of total acid secretion in response to a meal. Sham feeding (chewing and spitting) stimulates gastric acid secretion only via the cephalic phase, and it results in acid secretion that is about half of that seen in response to IV penta-gastrin or histamine.When food reaches the stomach, the gastric phase of acid secretion begins. This phase lasts until the stomach is empty and accounts for about 60% of the total acid secretion in response to a meal. The gastric phase of acid secretion has several compo-nents. Amino acids and small peptides directly stimulate antral G cells to secrete gastrin, which is carried in the bloodstream to the ECL and parietal cells, stimulating |
Surgery_Schwartz_7363 | Surgery_Schwartz | secretion has several compo-nents. Amino acids and small peptides directly stimulate antral G cells to secrete gastrin, which is carried in the bloodstream to the ECL and parietal cells, stimulating acid secretion in an endo-crine fashion. In addition, proximal gastric distention stimulates acid secretion via a vagovagal reflex arc, which is mitigated by truncal or highly selective vagotomy (HSV). Antral disten-tion also stimulates antral gastrin secretion. Finally, ongoing cephalic vagal input stimulates gastrin release, which in turn stimulates histamine release from ECL cells and acid secretion.The intestinal phase of gastric secretion is poorly under-stood. It is thought to be mediated by a hormone released from the proximal small bowel mucosa in response to luminal chyme. This phase starts when gastric emptying of ingested food begins, and it continues as long as nutrients remain in the proximal small intestine. It accounts for about 10% of meal-induced acid | Surgery_Schwartz. secretion has several compo-nents. Amino acids and small peptides directly stimulate antral G cells to secrete gastrin, which is carried in the bloodstream to the ECL and parietal cells, stimulating acid secretion in an endo-crine fashion. In addition, proximal gastric distention stimulates acid secretion via a vagovagal reflex arc, which is mitigated by truncal or highly selective vagotomy (HSV). Antral disten-tion also stimulates antral gastrin secretion. Finally, ongoing cephalic vagal input stimulates gastrin release, which in turn stimulates histamine release from ECL cells and acid secretion.The intestinal phase of gastric secretion is poorly under-stood. It is thought to be mediated by a hormone released from the proximal small bowel mucosa in response to luminal chyme. This phase starts when gastric emptying of ingested food begins, and it continues as long as nutrients remain in the proximal small intestine. It accounts for about 10% of meal-induced acid |
Surgery_Schwartz_7364 | Surgery_Schwartz | chyme. This phase starts when gastric emptying of ingested food begins, and it continues as long as nutrients remain in the proximal small intestine. It accounts for about 10% of meal-induced acid secretion.Interprandial basal acid secretion is 2 to 5 mEq hydrochlo-ric acid per hour, about 10% of maximal acid output (MAO), and it is greater at night. Basal acid secretion probably contrib-utes to the relatively low bacterial counts found in the stomach. Basal acid secretion is reduced 75% to 90% by vagotomy or continuous H2-receptor blockade.The pivotal role that ECL cells play in the regulation of gastric acid secretion is emphasized in Fig. 26-13. The acid stimulatory effect of gastrin is largely mediated by histamine released from mucosal ECL cells. H2-receptor knockout mice do not secrete acid in response to gastrin.24 This explains why the H2-receptor antagonists (H2RAs) are effective inhibitors of acid secretion, even though histamine is only one of three parietal cell | Surgery_Schwartz. chyme. This phase starts when gastric emptying of ingested food begins, and it continues as long as nutrients remain in the proximal small intestine. It accounts for about 10% of meal-induced acid secretion.Interprandial basal acid secretion is 2 to 5 mEq hydrochlo-ric acid per hour, about 10% of maximal acid output (MAO), and it is greater at night. Basal acid secretion probably contrib-utes to the relatively low bacterial counts found in the stomach. Basal acid secretion is reduced 75% to 90% by vagotomy or continuous H2-receptor blockade.The pivotal role that ECL cells play in the regulation of gastric acid secretion is emphasized in Fig. 26-13. The acid stimulatory effect of gastrin is largely mediated by histamine released from mucosal ECL cells. H2-receptor knockout mice do not secrete acid in response to gastrin.24 This explains why the H2-receptor antagonists (H2RAs) are effective inhibitors of acid secretion, even though histamine is only one of three parietal cell |
Surgery_Schwartz_7365 | Surgery_Schwartz | not secrete acid in response to gastrin.24 This explains why the H2-receptor antagonists (H2RAs) are effective inhibitors of acid secretion, even though histamine is only one of three parietal cell stimulants. The mucosal D cell, which releases somatosta-tin, is also an important regulator of acid secretion. Somatostatin inhibits histamine release from ECL cells and gastrin release from antral G cells. The function of D cells can be inhibited by Helicobacter pylori infection, resulting in an exaggerated acid secretory response (see “Helicobacter pylori Infection”).Proton pump inhibitors are potent suppressors of gastric acid secretion. This results in hypergastrinemia and conse-quent ECL stimulation. In patients on long-term PPI (median 5.5 years), the degree of hypergastrinemia does not appear to correlate with the length of treatment.32 Chronic PPI use has been associated with ECL hyperplasia and type 1 gastric neuro-endocrine tumor, but so far there has been no evidence linking | Surgery_Schwartz. not secrete acid in response to gastrin.24 This explains why the H2-receptor antagonists (H2RAs) are effective inhibitors of acid secretion, even though histamine is only one of three parietal cell stimulants. The mucosal D cell, which releases somatosta-tin, is also an important regulator of acid secretion. Somatostatin inhibits histamine release from ECL cells and gastrin release from antral G cells. The function of D cells can be inhibited by Helicobacter pylori infection, resulting in an exaggerated acid secretory response (see “Helicobacter pylori Infection”).Proton pump inhibitors are potent suppressors of gastric acid secretion. This results in hypergastrinemia and conse-quent ECL stimulation. In patients on long-term PPI (median 5.5 years), the degree of hypergastrinemia does not appear to correlate with the length of treatment.32 Chronic PPI use has been associated with ECL hyperplasia and type 1 gastric neuro-endocrine tumor, but so far there has been no evidence linking |
Surgery_Schwartz_7366 | Surgery_Schwartz | appear to correlate with the length of treatment.32 Chronic PPI use has been associated with ECL hyperplasia and type 1 gastric neuro-endocrine tumor, but so far there has been no evidence linking these agents to malignant gastric epithelial or neuroendocrine tumors. Gastrin levels return to normal within a few days of PPI cessation, but during this time, some patients may experience gastric hyperacidity and dyspeptic symptoms, which may lead to difficulty in getting patients off the medication.33,34 This is less likely to occur with short-term PPI use and may be amelio-rated by PPI dose tapering and/or initiation of H2 blockers prior to PPI cessation.Pepsinogen SecretionThe most potent physiologic stimulus for pepsinogen secre-tion from chief cells is food ingestion; acetylcholine is the most important mediator. Somatostatin inhibits pepsinogen secre-tion. Pepsinogen I is produced by chief cells in acid producing glands, whereas pepsinogen II is produced by chief cells and by SECs in | Surgery_Schwartz. appear to correlate with the length of treatment.32 Chronic PPI use has been associated with ECL hyperplasia and type 1 gastric neuro-endocrine tumor, but so far there has been no evidence linking these agents to malignant gastric epithelial or neuroendocrine tumors. Gastrin levels return to normal within a few days of PPI cessation, but during this time, some patients may experience gastric hyperacidity and dyspeptic symptoms, which may lead to difficulty in getting patients off the medication.33,34 This is less likely to occur with short-term PPI use and may be amelio-rated by PPI dose tapering and/or initiation of H2 blockers prior to PPI cessation.Pepsinogen SecretionThe most potent physiologic stimulus for pepsinogen secre-tion from chief cells is food ingestion; acetylcholine is the most important mediator. Somatostatin inhibits pepsinogen secre-tion. Pepsinogen I is produced by chief cells in acid producing glands, whereas pepsinogen II is produced by chief cells and by SECs in |
Surgery_Schwartz_7367 | Surgery_Schwartz | most important mediator. Somatostatin inhibits pepsinogen secre-tion. Pepsinogen I is produced by chief cells in acid producing glands, whereas pepsinogen II is produced by chief cells and by SECs in both acid producing and gastrin producing (i.e., antral) glands. Pepsinogen is cleaved to the active pepsin enzyme in an acidic environment and is maximally active at pH 2.5, and inactive at pH >5, although pepsinogen II may be activated over a wider pH range than pepsinogen I. Pepsin catalyzes the hydro-lysis of proteins and is denatured at alkaline pH. Serum levels of pepsinogen I and II are increased in helicobacter gastritis, so elevated pepsinogen I and II levels and positive helicobacter serology are presumptive evidence of active helicobacter infec-tion. Longstanding helicobacter infection may lead to atrophic gastritis, suggested by decreased pepsinogen I/II ratio (from chief cell loss) and hypergastriemia (from parietal cell loss and hypochlorhydria).35Intrinsic FactorActivated | Surgery_Schwartz. most important mediator. Somatostatin inhibits pepsinogen secre-tion. Pepsinogen I is produced by chief cells in acid producing glands, whereas pepsinogen II is produced by chief cells and by SECs in both acid producing and gastrin producing (i.e., antral) glands. Pepsinogen is cleaved to the active pepsin enzyme in an acidic environment and is maximally active at pH 2.5, and inactive at pH >5, although pepsinogen II may be activated over a wider pH range than pepsinogen I. Pepsin catalyzes the hydro-lysis of proteins and is denatured at alkaline pH. Serum levels of pepsinogen I and II are increased in helicobacter gastritis, so elevated pepsinogen I and II levels and positive helicobacter serology are presumptive evidence of active helicobacter infec-tion. Longstanding helicobacter infection may lead to atrophic gastritis, suggested by decreased pepsinogen I/II ratio (from chief cell loss) and hypergastriemia (from parietal cell loss and hypochlorhydria).35Intrinsic FactorActivated |
Surgery_Schwartz_7368 | Surgery_Schwartz | may lead to atrophic gastritis, suggested by decreased pepsinogen I/II ratio (from chief cell loss) and hypergastriemia (from parietal cell loss and hypochlorhydria).35Intrinsic FactorActivated parietal cells secrete intrinsic factor in addition to hydrochloric acid. Presumably the stimulants are similar, but MealVagusD-cellECLcellParietal cellGastrinSomatostatinHistamine++++–––++++AcetylcholineG-cellFigure 26-13. Physiologic control of acid secretion. ECL = enterochromaffin-like. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Brunicardi_Ch26_p1099-p1166.indd 110801/03/19 7:11 PM 1109STOMACHCHAPTER 26acid secretion and intrinsic factor secretion may not be linked. Intrinsic factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors. Vitamin B12 deficiency can be life threatening, and patients with total gastrectomy or | Surgery_Schwartz. may lead to atrophic gastritis, suggested by decreased pepsinogen I/II ratio (from chief cell loss) and hypergastriemia (from parietal cell loss and hypochlorhydria).35Intrinsic FactorActivated parietal cells secrete intrinsic factor in addition to hydrochloric acid. Presumably the stimulants are similar, but MealVagusD-cellECLcellParietal cellGastrinSomatostatinHistamine++++–––++++AcetylcholineG-cellFigure 26-13. Physiologic control of acid secretion. ECL = enterochromaffin-like. (Reproduced with permission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Brunicardi_Ch26_p1099-p1166.indd 110801/03/19 7:11 PM 1109STOMACHCHAPTER 26acid secretion and intrinsic factor secretion may not be linked. Intrinsic factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors. Vitamin B12 deficiency can be life threatening, and patients with total gastrectomy or |
Surgery_Schwartz_7369 | Surgery_Schwartz | factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors. Vitamin B12 deficiency can be life threatening, and patients with total gastrectomy or pernicious anemia (i.e., patients with no pari-etal cells) require B12 supplementation by a nonenteric route. Some patients develop vitamin B12 deficiency following gastric bypass, presumably because there is insufficient intrinsic fac-tor present in the small proximal gastric pouch and oral B12 intake may be decreased. Under normal conditions, a signifi-cant excess of intrinsic factor is secreted, and acid-suppressive medication does not appear to inhibit intrinsic factor production and release.Gastric Mucosal BarrierThe stomach’s durable resistance to autodigestion by caustic hydrochloric acid and active pepsin is intriguing. Some of the important elements of gastric barrier function and cytoprotection are listed in Table 26-3.36,37 When these defenses break down, ulceration occurs. A | Surgery_Schwartz. factor binds to luminal vitamin B12, and the complex is absorbed in the terminal ileum via mucosal receptors. Vitamin B12 deficiency can be life threatening, and patients with total gastrectomy or pernicious anemia (i.e., patients with no pari-etal cells) require B12 supplementation by a nonenteric route. Some patients develop vitamin B12 deficiency following gastric bypass, presumably because there is insufficient intrinsic fac-tor present in the small proximal gastric pouch and oral B12 intake may be decreased. Under normal conditions, a signifi-cant excess of intrinsic factor is secreted, and acid-suppressive medication does not appear to inhibit intrinsic factor production and release.Gastric Mucosal BarrierThe stomach’s durable resistance to autodigestion by caustic hydrochloric acid and active pepsin is intriguing. Some of the important elements of gastric barrier function and cytoprotection are listed in Table 26-3.36,37 When these defenses break down, ulceration occurs. A |
Surgery_Schwartz_7370 | Surgery_Schwartz | acid and active pepsin is intriguing. Some of the important elements of gastric barrier function and cytoprotection are listed in Table 26-3.36,37 When these defenses break down, ulceration occurs. A variety of factors are important in maintain-ing an intact gastric mucosal layer.38 The mucus and bicarbonate secreted by SECs form an unstirred mucous gel with a favorable pH gradient. Cell membranes and tight junctions prevent hydro-gen ions from gaining access to the interstitial space. Hydrogen ions that do break through are buffered by the alkaline tide cre-ated by basolateral bicarbonate secretion from stimulated pari-etal cells. Any sloughed or denuded SECs are rapidly replaced by migration of adjacent cells, a process known as restitution. Mucosal blood flow plays a crucial role in maintaining a healthy mucosa, providing nutrients and oxygen for the cellular func-tions involved in cytoprotection. During acid secretion, there is a tremendous gradient favoring the movement of | Surgery_Schwartz. acid and active pepsin is intriguing. Some of the important elements of gastric barrier function and cytoprotection are listed in Table 26-3.36,37 When these defenses break down, ulceration occurs. A variety of factors are important in maintain-ing an intact gastric mucosal layer.38 The mucus and bicarbonate secreted by SECs form an unstirred mucous gel with a favorable pH gradient. Cell membranes and tight junctions prevent hydro-gen ions from gaining access to the interstitial space. Hydrogen ions that do break through are buffered by the alkaline tide cre-ated by basolateral bicarbonate secretion from stimulated pari-etal cells. Any sloughed or denuded SECs are rapidly replaced by migration of adjacent cells, a process known as restitution. Mucosal blood flow plays a crucial role in maintaining a healthy mucosa, providing nutrients and oxygen for the cellular func-tions involved in cytoprotection. During acid secretion, there is a tremendous gradient favoring the movement of |
Surgery_Schwartz_7371 | Surgery_Schwartz | in maintaining a healthy mucosa, providing nutrients and oxygen for the cellular func-tions involved in cytoprotection. During acid secretion, there is a tremendous gradient favoring the movement of hydrogen ions from the lumen to the interstitium. This “back-diffused” hydrogen is buffered and rapidly removed by the rich blood supply. When “barrier breakers” such as bile or aspirin lead to increased back-diffusion of hydrogen ions from the lumen into the lamina propria and submucosa, there is a protective increase in mucosal blood flow. If this protective response is blocked, gross ulceration can occur. Important mediators of these protec-tive mechanisms include prostaglandins, nitric oxide, intrinsic nerves, and peptides (e.g., calcitonin gene-related peptide, gas-trin-releasing peptide [GRP], gastrin, and heat shock proteins). Sucralfate acts locally to enhance mucosal defenses. Protec-tive reflexes involve afferent sensory neurons, and they can be blocked by the application of | Surgery_Schwartz. in maintaining a healthy mucosa, providing nutrients and oxygen for the cellular func-tions involved in cytoprotection. During acid secretion, there is a tremendous gradient favoring the movement of hydrogen ions from the lumen to the interstitium. This “back-diffused” hydrogen is buffered and rapidly removed by the rich blood supply. When “barrier breakers” such as bile or aspirin lead to increased back-diffusion of hydrogen ions from the lumen into the lamina propria and submucosa, there is a protective increase in mucosal blood flow. If this protective response is blocked, gross ulceration can occur. Important mediators of these protec-tive mechanisms include prostaglandins, nitric oxide, intrinsic nerves, and peptides (e.g., calcitonin gene-related peptide, gas-trin-releasing peptide [GRP], gastrin, and heat shock proteins). Sucralfate acts locally to enhance mucosal defenses. Protec-tive reflexes involve afferent sensory neurons, and they can be blocked by the application of |
Surgery_Schwartz_7372 | Surgery_Schwartz | [GRP], gastrin, and heat shock proteins). Sucralfate acts locally to enhance mucosal defenses. Protec-tive reflexes involve afferent sensory neurons, and they can be blocked by the application of topical anesthetics to the gastric mucosa, or the experimental destruction of the afferent sensory nerves. In addition to these local defenses, there are important protective factors in saliva, duodenal secretions, and pancreatic or biliary secretions.Gastric Hormones13,39The stomach is quite an elegant endocrine organ. It is the source of important peptides which work in an autocrine (EGF and surface epithelial cells, TGF and parietal cells), paracrine (somatostatin), endocrine (gastrin), and/or neurocrine (ghrelin) fashion.Gastrin. Gastrin is produced by antral G cells and is the major hormonal stimulant of acid secretion during the gastric phase predominantly via an endocrine effect on histamine generating ECL cells and to a lesser extent via a direct effect on parietal cells. A variety of | Surgery_Schwartz. [GRP], gastrin, and heat shock proteins). Sucralfate acts locally to enhance mucosal defenses. Protec-tive reflexes involve afferent sensory neurons, and they can be blocked by the application of topical anesthetics to the gastric mucosa, or the experimental destruction of the afferent sensory nerves. In addition to these local defenses, there are important protective factors in saliva, duodenal secretions, and pancreatic or biliary secretions.Gastric Hormones13,39The stomach is quite an elegant endocrine organ. It is the source of important peptides which work in an autocrine (EGF and surface epithelial cells, TGF and parietal cells), paracrine (somatostatin), endocrine (gastrin), and/or neurocrine (ghrelin) fashion.Gastrin. Gastrin is produced by antral G cells and is the major hormonal stimulant of acid secretion during the gastric phase predominantly via an endocrine effect on histamine generating ECL cells and to a lesser extent via a direct effect on parietal cells. A variety of |
Surgery_Schwartz_7373 | Surgery_Schwartz | stimulant of acid secretion during the gastric phase predominantly via an endocrine effect on histamine generating ECL cells and to a lesser extent via a direct effect on parietal cells. A variety of molecular forms exist: big gastrin (34 amino acids; G34), little gastrin (17 amino acids; G17), and mini-gastrin (14 amino acids; G14). The large majority of gastrin released by the human antrum is G17. The biologically active pentapeptide sequence at the C-terminal end of gastrin is identical to that of CCK. Luminal peptides and amino acids are the most potent stimulants of gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion. The latter effect is predominantly mediated in a paracrine fashion by somatostatin released from antral D cells. Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that the principal media-tor of gastrin-stimulated acid production is histamine from mucosal ECL cells and not direct stimulation of | Surgery_Schwartz. stimulant of acid secretion during the gastric phase predominantly via an endocrine effect on histamine generating ECL cells and to a lesser extent via a direct effect on parietal cells. A variety of molecular forms exist: big gastrin (34 amino acids; G34), little gastrin (17 amino acids; G17), and mini-gastrin (14 amino acids; G14). The large majority of gastrin released by the human antrum is G17. The biologically active pentapeptide sequence at the C-terminal end of gastrin is identical to that of CCK. Luminal peptides and amino acids are the most potent stimulants of gastrin release, and luminal acid is the most potent inhibitor of gastrin secretion. The latter effect is predominantly mediated in a paracrine fashion by somatostatin released from antral D cells. Gastrin-stimulated acid secretion is significantly blocked by H2 antagonists, suggesting that the principal media-tor of gastrin-stimulated acid production is histamine from mucosal ECL cells and not direct stimulation of |
Surgery_Schwartz_7374 | Surgery_Schwartz | secretion is significantly blocked by H2 antagonists, suggesting that the principal media-tor of gastrin-stimulated acid production is histamine from mucosal ECL cells and not direct stimulation of parietal cells by gastrin (see Fig. 26-13). In fact, chronic hypergastrinemia is associated with hyperplasia of gastric ECL cells and, rarely, gastric type I gastric neuroendocrine tumors (type I gastric car-cinoid). Gastrin is trophic to gastric parietal cells and to other GI mucosal cells including gastric stem cells. It also is a regulator of gastric cellular proliferation, migration, invasion, apoptosis and angiogenesis.40 Mucosal biopsies of the gastric body from patients with gastrinoma show a thick mucosa with excess pari-etal cells, while similar biopsies in patients years after antrec-tomy (i.e., low gastrin state) show thin mucosa and decreased parietal cells. In animal studies, gastrin administration has been shown to stimulate the growth of established colon cancers and to cause | Surgery_Schwartz. secretion is significantly blocked by H2 antagonists, suggesting that the principal media-tor of gastrin-stimulated acid production is histamine from mucosal ECL cells and not direct stimulation of parietal cells by gastrin (see Fig. 26-13). In fact, chronic hypergastrinemia is associated with hyperplasia of gastric ECL cells and, rarely, gastric type I gastric neuroendocrine tumors (type I gastric car-cinoid). Gastrin is trophic to gastric parietal cells and to other GI mucosal cells including gastric stem cells. It also is a regulator of gastric cellular proliferation, migration, invasion, apoptosis and angiogenesis.40 Mucosal biopsies of the gastric body from patients with gastrinoma show a thick mucosa with excess pari-etal cells, while similar biopsies in patients years after antrec-tomy (i.e., low gastrin state) show thin mucosa and decreased parietal cells. In animal studies, gastrin administration has been shown to stimulate the growth of established colon cancers and to cause |
Surgery_Schwartz_7375 | Surgery_Schwartz | (i.e., low gastrin state) show thin mucosa and decreased parietal cells. In animal studies, gastrin administration has been shown to stimulate the growth of established colon cancers and to cause pancreatic acinar cell hyperplasia.41 Important causes of hypergastrinemia include pernicious anemia, acid-suppressive medication, gastrinoma, retained antrum following distal gas-trectomy and Billroth II surgery, and vagotomy.42,43Ghrelin. Ghrelin, first described in 1999, is a small peptide that is produced mainly in the stomach.44,45 It is produced by specialized P/D1 endocrine cells in gastric oxyntic glands. Ninety percent of the body’s ghrelin stores are in the stomach and duodenum. Ghrelin is a potent secretagogue of pituitary growth hormone and a weak secretogogue for ACTH and pro-lactin. It appears to be a major orexigenic regulator of appetite. Ghrelin crosses the blood brain barrier and stimulates appetite via hypothalamic receptors. It also stimulates appetite periph-erally by | Surgery_Schwartz. (i.e., low gastrin state) show thin mucosa and decreased parietal cells. In animal studies, gastrin administration has been shown to stimulate the growth of established colon cancers and to cause pancreatic acinar cell hyperplasia.41 Important causes of hypergastrinemia include pernicious anemia, acid-suppressive medication, gastrinoma, retained antrum following distal gas-trectomy and Billroth II surgery, and vagotomy.42,43Ghrelin. Ghrelin, first described in 1999, is a small peptide that is produced mainly in the stomach.44,45 It is produced by specialized P/D1 endocrine cells in gastric oxyntic glands. Ninety percent of the body’s ghrelin stores are in the stomach and duodenum. Ghrelin is a potent secretagogue of pituitary growth hormone and a weak secretogogue for ACTH and pro-lactin. It appears to be a major orexigenic regulator of appetite. Ghrelin crosses the blood brain barrier and stimulates appetite via hypothalamic receptors. It also stimulates appetite periph-erally by |
Surgery_Schwartz_7376 | Surgery_Schwartz | It appears to be a major orexigenic regulator of appetite. Ghrelin crosses the blood brain barrier and stimulates appetite via hypothalamic receptors. It also stimulates appetite periph-erally by stimulating vagal afferent fibers in the gastric wall. Table 26-3Important components and mediators of mucosal defenses in the stomachComponentsMucous barrierBicarbonate secretionEpithelial barrier Hydrophobic phospholipids Tight junctions RestitutionMicrocirculation (reactive hyperemia)Afferent sensory neuronsMediatorsProstaglandinsNitric oxideEpidermal growth factorCalcitonin gene-related peptideHepatocyte growth factorHistamineGastrin-releasing peptideBrunicardi_Ch26_p1099-p1166.indd 110901/03/19 7:11 PM 1110SPECIFIC CONSIDERATIONS PART IIWhen ghrelin is elevated, appetite is stimulated, and when it is suppressed, appetite is decreased. Typically, ghrelin levels are elevated before a meal and decreased postprandially. Levels are high during starvation and decreased during | Surgery_Schwartz. It appears to be a major orexigenic regulator of appetite. Ghrelin crosses the blood brain barrier and stimulates appetite via hypothalamic receptors. It also stimulates appetite periph-erally by stimulating vagal afferent fibers in the gastric wall. Table 26-3Important components and mediators of mucosal defenses in the stomachComponentsMucous barrierBicarbonate secretionEpithelial barrier Hydrophobic phospholipids Tight junctions RestitutionMicrocirculation (reactive hyperemia)Afferent sensory neuronsMediatorsProstaglandinsNitric oxideEpidermal growth factorCalcitonin gene-related peptideHepatocyte growth factorHistamineGastrin-releasing peptideBrunicardi_Ch26_p1099-p1166.indd 110901/03/19 7:11 PM 1110SPECIFIC CONSIDERATIONS PART IIWhen ghrelin is elevated, appetite is stimulated, and when it is suppressed, appetite is decreased. Typically, ghrelin levels are elevated before a meal and decreased postprandially. Levels are high during starvation and decreased during |
Surgery_Schwartz_7377 | Surgery_Schwartz | stimulated, and when it is suppressed, appetite is decreased. Typically, ghrelin levels are elevated before a meal and decreased postprandially. Levels are high during starvation and decreased during hyperglycemia. Obesity and insulin resistance is associated with low ghrelin levels, but resection of the primary source of this hormone (i.e., the stomach) may partly account for the anorexia and weight loss seen in some patients following gastric resection including sleeve gastrectomy (Fig. 26-14).46-48 The effect of RYGBP on ghrelin physiology is controversial. This very effective weight loss procedure has been shown by some investigators to be asso-ciated with suppression of plasma ghrelin levels (and appetite) in humans (Fig. 26-15A).49,50Other groups have failed to show a significant decrease in ghrelin levels following gastric bypass but have found such decreases following sleeve gastrectomy, another effective weight loss operation (Fig. 26-15B).50 Possibly, subtle differ-ences in | Surgery_Schwartz. stimulated, and when it is suppressed, appetite is decreased. Typically, ghrelin levels are elevated before a meal and decreased postprandially. Levels are high during starvation and decreased during hyperglycemia. Obesity and insulin resistance is associated with low ghrelin levels, but resection of the primary source of this hormone (i.e., the stomach) may partly account for the anorexia and weight loss seen in some patients following gastric resection including sleeve gastrectomy (Fig. 26-14).46-48 The effect of RYGBP on ghrelin physiology is controversial. This very effective weight loss procedure has been shown by some investigators to be asso-ciated with suppression of plasma ghrelin levels (and appetite) in humans (Fig. 26-15A).49,50Other groups have failed to show a significant decrease in ghrelin levels following gastric bypass but have found such decreases following sleeve gastrectomy, another effective weight loss operation (Fig. 26-15B).50 Possibly, subtle differ-ences in |
Surgery_Schwartz_7378 | Surgery_Schwartz | in ghrelin levels following gastric bypass but have found such decreases following sleeve gastrectomy, another effective weight loss operation (Fig. 26-15B).50 Possibly, subtle differ-ences in operative technique, patient selection, or experimental (including assay) conditions account for the disparate results of studies on the effect of bariatric surgery on ghrelin levels in obese patients. Interestingly the two common metabolites of ghrelin have different physiologic effects: acyl-ghrelin increases gastric emptying and appetite while deacyl ghrelin decreases gastric emptying and induces satiety.51 Obviously appetite con-trol is complex with redundant and overlapping orexigenic and anorexigenic pathways and signals.39,52Somatostatin. Somatostatin is produced by D cells located throughout the gastric mucosa. The predominant form in humans is somatostatin 14, though somatostatin 28 is present as well. The major stimulus for somatostatin release is antral acidification; acetylcholine | Surgery_Schwartz. in ghrelin levels following gastric bypass but have found such decreases following sleeve gastrectomy, another effective weight loss operation (Fig. 26-15B).50 Possibly, subtle differ-ences in operative technique, patient selection, or experimental (including assay) conditions account for the disparate results of studies on the effect of bariatric surgery on ghrelin levels in obese patients. Interestingly the two common metabolites of ghrelin have different physiologic effects: acyl-ghrelin increases gastric emptying and appetite while deacyl ghrelin decreases gastric emptying and induces satiety.51 Obviously appetite con-trol is complex with redundant and overlapping orexigenic and anorexigenic pathways and signals.39,52Somatostatin. Somatostatin is produced by D cells located throughout the gastric mucosa. The predominant form in humans is somatostatin 14, though somatostatin 28 is present as well. The major stimulus for somatostatin release is antral acidification; acetylcholine |
Surgery_Schwartz_7379 | Surgery_Schwartz | the gastric mucosa. The predominant form in humans is somatostatin 14, though somatostatin 28 is present as well. The major stimulus for somatostatin release is antral acidification; acetylcholine from vagal nerve fibers inhibits its release. Somatostatin inhibits acid secretion from parietal cells and gastrin release from G cells. It also decreases histamine release from ECL cells. The proximity of the D cells to these target cells suggests that the primary effect of somatostatin is mediated in a paracrine fashion, but an endocrine (i.e., blood-stream) effect also is possible.Gastrin-Releasing Peptide. GRP is the mammalian equiva-lent of bombesin, a hormone discovered more than two decades ago in an extract of skin from a frog. In the antrum, GRP stimu-lates both gastrin and somatostatin release by binding to recep-tors on the G and D cells. There are nerve terminals ending near the mucosa in the gastric body and antrum, which are rich in GRP immunoreactivity. When GRP is given | Surgery_Schwartz. the gastric mucosa. The predominant form in humans is somatostatin 14, though somatostatin 28 is present as well. The major stimulus for somatostatin release is antral acidification; acetylcholine from vagal nerve fibers inhibits its release. Somatostatin inhibits acid secretion from parietal cells and gastrin release from G cells. It also decreases histamine release from ECL cells. The proximity of the D cells to these target cells suggests that the primary effect of somatostatin is mediated in a paracrine fashion, but an endocrine (i.e., blood-stream) effect also is possible.Gastrin-Releasing Peptide. GRP is the mammalian equiva-lent of bombesin, a hormone discovered more than two decades ago in an extract of skin from a frog. In the antrum, GRP stimu-lates both gastrin and somatostatin release by binding to recep-tors on the G and D cells. There are nerve terminals ending near the mucosa in the gastric body and antrum, which are rich in GRP immunoreactivity. When GRP is given |
Surgery_Schwartz_7380 | Surgery_Schwartz | release by binding to recep-tors on the G and D cells. There are nerve terminals ending near the mucosa in the gastric body and antrum, which are rich in GRP immunoreactivity. When GRP is given peripherally, it stimulates acid secretion, but when it is given centrally into the cerebral ventricles of animals, it inhibits acid secretion, appar-ently via a pathway involving the sympathetic nervous system.Leptin. Leptin is a protein primarily synthesized in adipocytes. It is also made by chief cells in the stomach, the main source of leptin in the GI tract.39,53 Leptin works at least in part via vagally mediated pathways to decrease food intake in animals. Not surprisingly, leptin, a satiety signal hormone, and ghrelin, a hunger signal hormone, are both synthesized in the stomach, an organ increasingly recognized as central to the mechanisms of appetite control.39,52Autocrine Proteins. Gastric surface epithelial cells secrete a variety of proteins that are important regulators of SEC | Surgery_Schwartz. release by binding to recep-tors on the G and D cells. There are nerve terminals ending near the mucosa in the gastric body and antrum, which are rich in GRP immunoreactivity. When GRP is given peripherally, it stimulates acid secretion, but when it is given centrally into the cerebral ventricles of animals, it inhibits acid secretion, appar-ently via a pathway involving the sympathetic nervous system.Leptin. Leptin is a protein primarily synthesized in adipocytes. It is also made by chief cells in the stomach, the main source of leptin in the GI tract.39,53 Leptin works at least in part via vagally mediated pathways to decrease food intake in animals. Not surprisingly, leptin, a satiety signal hormone, and ghrelin, a hunger signal hormone, are both synthesized in the stomach, an organ increasingly recognized as central to the mechanisms of appetite control.39,52Autocrine Proteins. Gastric surface epithelial cells secrete a variety of proteins that are important regulators of SEC |
Surgery_Schwartz_7381 | Surgery_Schwartz | increasingly recognized as central to the mechanisms of appetite control.39,52Autocrine Proteins. Gastric surface epithelial cells secrete a variety of proteins that are important regulators of SEC health, including trefoil factor family proteins and heat shock pro-teins.38 Parietal cells may also be influenced by molecules they secrete including transforming growth factor-α.Gastric Motility and EmptyingGastric motor function has several purposes.43,54-56 Interprandial motor activity clears the stomach of undigested debris, sloughed cells, and mucus. When feeding begins, the stomach relaxes to accommodate the meal. Regulated motor activity then breaks down the food into small particles and controls the output into the duodenum. The stomach accomplishes these functions by coordinated smooth muscle relaxation and contraction of the various gastric segments (proximal, distal, and pyloric). Smooth muscle myoelectric potentials are translated into muscular activity, which is modulated by | Surgery_Schwartz. increasingly recognized as central to the mechanisms of appetite control.39,52Autocrine Proteins. Gastric surface epithelial cells secrete a variety of proteins that are important regulators of SEC health, including trefoil factor family proteins and heat shock pro-teins.38 Parietal cells may also be influenced by molecules they secrete including transforming growth factor-α.Gastric Motility and EmptyingGastric motor function has several purposes.43,54-56 Interprandial motor activity clears the stomach of undigested debris, sloughed cells, and mucus. When feeding begins, the stomach relaxes to accommodate the meal. Regulated motor activity then breaks down the food into small particles and controls the output into the duodenum. The stomach accomplishes these functions by coordinated smooth muscle relaxation and contraction of the various gastric segments (proximal, distal, and pyloric). Smooth muscle myoelectric potentials are translated into muscular activity, which is modulated by |
Surgery_Schwartz_7382 | Surgery_Schwartz | muscle relaxation and contraction of the various gastric segments (proximal, distal, and pyloric). Smooth muscle myoelectric potentials are translated into muscular activity, which is modulated by extrinsic and intrinsic innerva-tion and hormones. The mechanisms by which gastric distention is translated into a neurohormonal satiety signal have only been partially elucidated.39,52Intrinsic Gastric Innervation. The extrinsic parasympa-thetic and sympathetic gastric innervation was discussed pre-viously in “Innervation.” The intrinsic innervation consists of ganglia and nerves that constitute the enteric nervous system (Fig. 26-16).57 There are a variety of neurotransmitters that effect gastric smooth muscle; these are generally grouped as excitatory (augment muscular activity) and inhibitory (decrease muscular activity). Important excitatory neurotransmitters include acetylcholine, the tachykinins, substance P, and neu-rokinin A. Important inhibitory neurotransmitters include nitric | Surgery_Schwartz. muscle relaxation and contraction of the various gastric segments (proximal, distal, and pyloric). Smooth muscle myoelectric potentials are translated into muscular activity, which is modulated by extrinsic and intrinsic innerva-tion and hormones. The mechanisms by which gastric distention is translated into a neurohormonal satiety signal have only been partially elucidated.39,52Intrinsic Gastric Innervation. The extrinsic parasympa-thetic and sympathetic gastric innervation was discussed pre-viously in “Innervation.” The intrinsic innervation consists of ganglia and nerves that constitute the enteric nervous system (Fig. 26-16).57 There are a variety of neurotransmitters that effect gastric smooth muscle; these are generally grouped as excitatory (augment muscular activity) and inhibitory (decrease muscular activity). Important excitatory neurotransmitters include acetylcholine, the tachykinins, substance P, and neu-rokinin A. Important inhibitory neurotransmitters include nitric |
Surgery_Schwartz_7383 | Surgery_Schwartz | (decrease muscular activity). Important excitatory neurotransmitters include acetylcholine, the tachykinins, substance P, and neu-rokinin A. Important inhibitory neurotransmitters include nitric oxide (NO) and vasoactive intestinal peptide (VIP). Serotonin has been shown to modulate both contraction and relaxation. A variety of other molecules affect motility, including GRP, hista-mine, neuropeptide Y, norepinephrine, and endogenous opioids.Specialized cells in the muscularis propria also are impor-tant modulators of GI motility. These cells, called interstitial cells of Cajal, are distinguishable histologically from neurons and myocytes and appear to amplify both cholinergic excitatory 300200Plasma ghrelin (fmol/mL)100NormalcontrolsGastrectomizedpatients0*Figure 26-14. Ghrelin levels are decreased after gastrectomy. (Reproduced with permission from Ariyasu H, Takaya K, Tagami T, et al: Stomach is a major source of circulating ghrelin, and feed-ing state determines plasma ghrelin-like | Surgery_Schwartz. (decrease muscular activity). Important excitatory neurotransmitters include acetylcholine, the tachykinins, substance P, and neu-rokinin A. Important inhibitory neurotransmitters include nitric oxide (NO) and vasoactive intestinal peptide (VIP). Serotonin has been shown to modulate both contraction and relaxation. A variety of other molecules affect motility, including GRP, hista-mine, neuropeptide Y, norepinephrine, and endogenous opioids.Specialized cells in the muscularis propria also are impor-tant modulators of GI motility. These cells, called interstitial cells of Cajal, are distinguishable histologically from neurons and myocytes and appear to amplify both cholinergic excitatory 300200Plasma ghrelin (fmol/mL)100NormalcontrolsGastrectomizedpatients0*Figure 26-14. Ghrelin levels are decreased after gastrectomy. (Reproduced with permission from Ariyasu H, Takaya K, Tagami T, et al: Stomach is a major source of circulating ghrelin, and feed-ing state determines plasma ghrelin-like |
Surgery_Schwartz_7384 | Surgery_Schwartz | decreased after gastrectomy. (Reproduced with permission from Ariyasu H, Takaya K, Tagami T, et al: Stomach is a major source of circulating ghrelin, and feed-ing state determines plasma ghrelin-like immunoreactivity levels in humans, J Clin Endocrinol Metab. 2001 Oct;86(10):4753-4758.)Brunicardi_Ch26_p1099-p1166.indd 111001/03/19 7:11 PM 1111STOMACHCHAPTER 26Figure 26-15. A and B. Ghrelin secretion after bariatric surgery. Some investigators have suggested that ghrelin secretion is dramatically decreased after gastric bypass. Other groups have shown statistically insig-nificant changes in ghrelin levels after gastric bypass, (RYGBP) but significant decreases after sleeve gastrectomy (SG). A. green = gastric bypass; blue = obese controls; red = normal weight controls; B. blue = fasting; pink = postprandial. B. Top = RYGBP; B bottom = SG. (A, Repro-duced with permission from Cummings DE, Weigle DS, Frayo RS, et al: Plasma ghre-lin levels after diet-induced weight loss or gastric | Surgery_Schwartz. decreased after gastrectomy. (Reproduced with permission from Ariyasu H, Takaya K, Tagami T, et al: Stomach is a major source of circulating ghrelin, and feed-ing state determines plasma ghrelin-like immunoreactivity levels in humans, J Clin Endocrinol Metab. 2001 Oct;86(10):4753-4758.)Brunicardi_Ch26_p1099-p1166.indd 111001/03/19 7:11 PM 1111STOMACHCHAPTER 26Figure 26-15. A and B. Ghrelin secretion after bariatric surgery. Some investigators have suggested that ghrelin secretion is dramatically decreased after gastric bypass. Other groups have shown statistically insig-nificant changes in ghrelin levels after gastric bypass, (RYGBP) but significant decreases after sleeve gastrectomy (SG). A. green = gastric bypass; blue = obese controls; red = normal weight controls; B. blue = fasting; pink = postprandial. B. Top = RYGBP; B bottom = SG. (A, Repro-duced with permission from Cummings DE, Weigle DS, Frayo RS, et al: Plasma ghre-lin levels after diet-induced weight loss or gastric |
Surgery_Schwartz_7385 | Surgery_Schwartz | pink = postprandial. B. Top = RYGBP; B bottom = SG. (A, Repro-duced with permission from Cummings DE, Weigle DS, Frayo RS, et al: Plasma ghre-lin levels after diet-induced weight loss or gastric bypass surgery, N Engl J Med. 2002 May 23;346(21):1623-1630. B, Reproduced with permission from Karamanakos SN, Vagenas K, Kalfarentzos F, et al: Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: A prospec-tive, double blind study, Ann Surg. 2008 Mar;247(3):401-407.)Plasma ghrelin level (pg/mL)Detection limitTime6 a.m.8 a.m.10 a.m.noon2 p.m.4 p.m.6 p.m.8 p.m.10 p.m.080100200300400500600700800BreakfastLunchDinnerA1200P = 0.06P = 0.15P = 0.16P = 0.13P = 0.01P = 0.03P = 0.01P = 0.0310008006004002000PreGhrelin (pg/mL)Ghrelin (pg/mL)3Time (months)Time (months)612Pre36129008007006005004003002001000Band nitrergic inhibitory input to the smooth muscle of the stom-ach and intestine.58 They are | Surgery_Schwartz. pink = postprandial. B. Top = RYGBP; B bottom = SG. (A, Repro-duced with permission from Cummings DE, Weigle DS, Frayo RS, et al: Plasma ghre-lin levels after diet-induced weight loss or gastric bypass surgery, N Engl J Med. 2002 May 23;346(21):1623-1630. B, Reproduced with permission from Karamanakos SN, Vagenas K, Kalfarentzos F, et al: Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: A prospec-tive, double blind study, Ann Surg. 2008 Mar;247(3):401-407.)Plasma ghrelin level (pg/mL)Detection limitTime6 a.m.8 a.m.10 a.m.noon2 p.m.4 p.m.6 p.m.8 p.m.10 p.m.080100200300400500600700800BreakfastLunchDinnerA1200P = 0.06P = 0.15P = 0.16P = 0.13P = 0.01P = 0.03P = 0.01P = 0.0310008006004002000PreGhrelin (pg/mL)Ghrelin (pg/mL)3Time (months)Time (months)612Pre36129008007006005004003002001000Band nitrergic inhibitory input to the smooth muscle of the stom-ach and intestine.58 They are |
Surgery_Schwartz_7386 | Surgery_Schwartz | (pg/mL)Ghrelin (pg/mL)3Time (months)Time (months)612Pre36129008007006005004003002001000Band nitrergic inhibitory input to the smooth muscle of the stom-ach and intestine.58 They are thought to be the cell of origin for gastrointestinal stromal tumors (GISTs), which are the most common mesenchymal neoplasms in the GI tract.Segmental Gastric Motility.13,58,59 In general, the proximal stomach serves a short-term food storage function and helps regulate basal intragastric tone, and the distal stomach mixes and grinds the food. The pylorus helps the latter process when Brunicardi_Ch26_p1099-p1166.indd 111101/03/19 7:11 PM 1112SPECIFIC CONSIDERATIONS PART IIclosed, facilitating retropulsion of the solid food bolus back into the body of the stomach for additional breakdown. The pylorus opens intermittently to allow metered emptying of liquids and small solid particles into the duodenum.Most of the motor activity of the proximal stomach con-sists of slow tonic contractions and | Surgery_Schwartz. (pg/mL)Ghrelin (pg/mL)3Time (months)Time (months)612Pre36129008007006005004003002001000Band nitrergic inhibitory input to the smooth muscle of the stom-ach and intestine.58 They are thought to be the cell of origin for gastrointestinal stromal tumors (GISTs), which are the most common mesenchymal neoplasms in the GI tract.Segmental Gastric Motility.13,58,59 In general, the proximal stomach serves a short-term food storage function and helps regulate basal intragastric tone, and the distal stomach mixes and grinds the food. The pylorus helps the latter process when Brunicardi_Ch26_p1099-p1166.indd 111101/03/19 7:11 PM 1112SPECIFIC CONSIDERATIONS PART IIclosed, facilitating retropulsion of the solid food bolus back into the body of the stomach for additional breakdown. The pylorus opens intermittently to allow metered emptying of liquids and small solid particles into the duodenum.Most of the motor activity of the proximal stomach con-sists of slow tonic contractions and |
Surgery_Schwartz_7387 | Surgery_Schwartz | opens intermittently to allow metered emptying of liquids and small solid particles into the duodenum.Most of the motor activity of the proximal stomach con-sists of slow tonic contractions and relaxations, lasting up to 5 minutes. This activity is the main determinant of basal intra-gastric pressure, an important determinant of liquid empty-ing. Rapid phasic contractions may be superimposed on the slower tonic motor activity. When food is ingested, intragastric pressure falls as the proximal stomach relaxes. This proximal relaxation is mediated by two important vagovagal reflexes: receptive relaxation and gastric accommodation. Receptive relaxation refers to the reduction in gastric tone associated with the act of swallowing. This occurs before the food reaches the stomach and can be reproduced by mechanical stimulation of the pharynx or esophagus. Gastric accommodation refers to the proximal gastric relaxation associated with distention of the stomach.60 Accommodation is mediated | Surgery_Schwartz. opens intermittently to allow metered emptying of liquids and small solid particles into the duodenum.Most of the motor activity of the proximal stomach con-sists of slow tonic contractions and relaxations, lasting up to 5 minutes. This activity is the main determinant of basal intra-gastric pressure, an important determinant of liquid empty-ing. Rapid phasic contractions may be superimposed on the slower tonic motor activity. When food is ingested, intragastric pressure falls as the proximal stomach relaxes. This proximal relaxation is mediated by two important vagovagal reflexes: receptive relaxation and gastric accommodation. Receptive relaxation refers to the reduction in gastric tone associated with the act of swallowing. This occurs before the food reaches the stomach and can be reproduced by mechanical stimulation of the pharynx or esophagus. Gastric accommodation refers to the proximal gastric relaxation associated with distention of the stomach.60 Accommodation is mediated |
Surgery_Schwartz_7388 | Surgery_Schwartz | by mechanical stimulation of the pharynx or esophagus. Gastric accommodation refers to the proximal gastric relaxation associated with distention of the stomach.60 Accommodation is mediated through stretch recep-tors in the gastric wall and does not require esophageal or pha-ryngeal stimulation. Initially, as the meal enters the stomach, there is a drop in intragastric pressure mediated by nitric oxide. As the meal progresses, the intragastric pressure rises, parallel with the onset of satiety. Interestingly, satiety does not seem to be associated with any specific level of intragastric pressure. Obese patients have a delayed onset of satiety, so an obvious hypothesis to be tested is that a pharmacologic-induced increase in gastric tone leads to increased satiety and decreased food intake in this patient group.60 Because receptive relaxation and accommodation are mediated by afferent and efferent vagal fibers, they are significantly altered by truncal and highly selec-tive vagotomy. | Surgery_Schwartz. by mechanical stimulation of the pharynx or esophagus. Gastric accommodation refers to the proximal gastric relaxation associated with distention of the stomach.60 Accommodation is mediated through stretch recep-tors in the gastric wall and does not require esophageal or pha-ryngeal stimulation. Initially, as the meal enters the stomach, there is a drop in intragastric pressure mediated by nitric oxide. As the meal progresses, the intragastric pressure rises, parallel with the onset of satiety. Interestingly, satiety does not seem to be associated with any specific level of intragastric pressure. Obese patients have a delayed onset of satiety, so an obvious hypothesis to be tested is that a pharmacologic-induced increase in gastric tone leads to increased satiety and decreased food intake in this patient group.60 Because receptive relaxation and accommodation are mediated by afferent and efferent vagal fibers, they are significantly altered by truncal and highly selec-tive vagotomy. |
Surgery_Schwartz_7389 | Surgery_Schwartz | in this patient group.60 Because receptive relaxation and accommodation are mediated by afferent and efferent vagal fibers, they are significantly altered by truncal and highly selec-tive vagotomy. Both these operations result in decreased gastric compliance, shifting the volume/pressure curve to the left. Pre-sumably for any given amount of food ingested, the intragastric pressure is higher, and perhaps in some patients the onset of satiety is sooner. This may be one explanation for weight loss associated with vagotomy,61 and it also helps explain acceler-ated liquid gastric emptying postvagotomy, which likely con-tributes to dumping symptoms in some patients.NO and VIP are the principal mediators of proximal gas-tric relaxation. But a variety of other agents increase proximal gastric relaxation and compliance, including dopamine, gastrin, CCK, secretin, GRP, and glucagon. Proximal gastric tone also is decreased by duodenal distention, colonic distention, and ileal perfusion with | Surgery_Schwartz. in this patient group.60 Because receptive relaxation and accommodation are mediated by afferent and efferent vagal fibers, they are significantly altered by truncal and highly selec-tive vagotomy. Both these operations result in decreased gastric compliance, shifting the volume/pressure curve to the left. Pre-sumably for any given amount of food ingested, the intragastric pressure is higher, and perhaps in some patients the onset of satiety is sooner. This may be one explanation for weight loss associated with vagotomy,61 and it also helps explain acceler-ated liquid gastric emptying postvagotomy, which likely con-tributes to dumping symptoms in some patients.NO and VIP are the principal mediators of proximal gas-tric relaxation. But a variety of other agents increase proximal gastric relaxation and compliance, including dopamine, gastrin, CCK, secretin, GRP, and glucagon. Proximal gastric tone also is decreased by duodenal distention, colonic distention, and ileal perfusion with |
Surgery_Schwartz_7390 | Surgery_Schwartz | relaxation and compliance, including dopamine, gastrin, CCK, secretin, GRP, and glucagon. Proximal gastric tone also is decreased by duodenal distention, colonic distention, and ileal perfusion with glucose (ileal brake).The distal stomach breaks up solid food and is the main determinant of gastric emptying of solids. Slow waves of myo-electric depolarization sweep down the distal stomach at a rate of about three per minute. These waves originate from the proxi-mal gastric pacemaker, high on the greater curvature.62 The pac-ing cells appear to be the interstitial cells of Cajal, which have been shown to have a similar function in the small intestine and colon. Most of these myoelectric waves are below the thresh-old for smooth muscle contraction in the quiescent state and thus are associated with negligible changes in pressure. Neural and/or hormonal input, which increases the plateau phase of the action potential, can trigger muscle contraction, resulting in a peristaltic wave | Surgery_Schwartz. relaxation and compliance, including dopamine, gastrin, CCK, secretin, GRP, and glucagon. Proximal gastric tone also is decreased by duodenal distention, colonic distention, and ileal perfusion with glucose (ileal brake).The distal stomach breaks up solid food and is the main determinant of gastric emptying of solids. Slow waves of myo-electric depolarization sweep down the distal stomach at a rate of about three per minute. These waves originate from the proxi-mal gastric pacemaker, high on the greater curvature.62 The pac-ing cells appear to be the interstitial cells of Cajal, which have been shown to have a similar function in the small intestine and colon. Most of these myoelectric waves are below the thresh-old for smooth muscle contraction in the quiescent state and thus are associated with negligible changes in pressure. Neural and/or hormonal input, which increases the plateau phase of the action potential, can trigger muscle contraction, resulting in a peristaltic wave |
Surgery_Schwartz_7391 | Surgery_Schwartz | with negligible changes in pressure. Neural and/or hormonal input, which increases the plateau phase of the action potential, can trigger muscle contraction, resulting in a peristaltic wave associated with the electrical slow wave and of the same frequency (three per minute) (Fig. 26-17). There are measurable abnormalities in gastric slow wave activity in disor-ders of gastric motility such as gastroparesis, but reliable elec-trogastrogaphy to aid in the diagnosis and management of these problems is not yet a clinical reality. It is likely that implantable gastric pacemakers benefit some patients with gastroparesis by favorably impacting this myoelectric coupling, normalizing gas-tric slow wave patterns.During fasting, distal gastric motor activity is controlled by the migrating motor complex (MMC), the “gastrointesti-nal housekeeper” (Fig. 26-18). The purported function of the MMC is to sweep along any undigested food, debris, sloughed cells, and mucus after the fed phase of | Surgery_Schwartz. with negligible changes in pressure. Neural and/or hormonal input, which increases the plateau phase of the action potential, can trigger muscle contraction, resulting in a peristaltic wave associated with the electrical slow wave and of the same frequency (three per minute) (Fig. 26-17). There are measurable abnormalities in gastric slow wave activity in disor-ders of gastric motility such as gastroparesis, but reliable elec-trogastrogaphy to aid in the diagnosis and management of these problems is not yet a clinical reality. It is likely that implantable gastric pacemakers benefit some patients with gastroparesis by favorably impacting this myoelectric coupling, normalizing gas-tric slow wave patterns.During fasting, distal gastric motor activity is controlled by the migrating motor complex (MMC), the “gastrointesti-nal housekeeper” (Fig. 26-18). The purported function of the MMC is to sweep along any undigested food, debris, sloughed cells, and mucus after the fed phase of |
Surgery_Schwartz_7392 | Surgery_Schwartz | complex (MMC), the “gastrointesti-nal housekeeper” (Fig. 26-18). The purported function of the MMC is to sweep along any undigested food, debris, sloughed cells, and mucus after the fed phase of digestion is complete. The MMC lasts approximately 100 minutes (longer at night, shorter during daytime) and is divided into four phases. Phase I (about half the length of the entire cycle) is a period of relative motor inactivity. High-amplitude muscular contractions do not occur in phase I of the MMC. Phase II (about 25% of the entire MMC cycle) consists of some irregular, high-amplitude, gener-ally nonpropulsive contractions. Phase III, a period of intense, Figure 26-16. Enteric nervous sys-tem. (Reproduced with permission from Friedman SL, McQuaid KR, Grendell JH: Current Diagnosis and Treatment in Gastroenterology, 2nd ed. New York, NY: McGraw-Hill Education; 2003.)Parasympathetic (vagal) nerveMesenteryPerivascular sympathic nerveMuscularis externa (longitudinal)Muscularis externa | Surgery_Schwartz. complex (MMC), the “gastrointesti-nal housekeeper” (Fig. 26-18). The purported function of the MMC is to sweep along any undigested food, debris, sloughed cells, and mucus after the fed phase of digestion is complete. The MMC lasts approximately 100 minutes (longer at night, shorter during daytime) and is divided into four phases. Phase I (about half the length of the entire cycle) is a period of relative motor inactivity. High-amplitude muscular contractions do not occur in phase I of the MMC. Phase II (about 25% of the entire MMC cycle) consists of some irregular, high-amplitude, gener-ally nonpropulsive contractions. Phase III, a period of intense, Figure 26-16. Enteric nervous sys-tem. (Reproduced with permission from Friedman SL, McQuaid KR, Grendell JH: Current Diagnosis and Treatment in Gastroenterology, 2nd ed. New York, NY: McGraw-Hill Education; 2003.)Parasympathetic (vagal) nerveMesenteryPerivascular sympathic nerveMuscularis externa (longitudinal)Muscularis externa |
Surgery_Schwartz_7393 | Surgery_Schwartz | in Gastroenterology, 2nd ed. New York, NY: McGraw-Hill Education; 2003.)Parasympathetic (vagal) nerveMesenteryPerivascular sympathic nerveMuscularis externa (longitudinal)Muscularis externa (circular)Subepethelial plexusMuscularis mucosaSubmucosaVillusIntestinal lumenDeep muscularis plexusSerosaTertiary branchSecondary branchGanglionSubmucosal plexusMyenteric plexusBrunicardi_Ch26_p1099-p1166.indd 111201/03/19 7:11 PM 1113STOMACHCHAPTER 26regular (about three per minute), propulsive contractions, only lasts about 5 to 10 minutes. Most phase III complexes of the GI MMC begin in the stomach, and the frequency approximates that of the myoelectric gastric slow wave. Phase IV is a transi-tion period.Neurohormonal control of the MMC is poorly understood, but it appears that different phases are regulated by different mechanisms. For example, vagotomy abolishes phase II of the gastric MMC but has little influence on phase III that persists even in the | Surgery_Schwartz. in Gastroenterology, 2nd ed. New York, NY: McGraw-Hill Education; 2003.)Parasympathetic (vagal) nerveMesenteryPerivascular sympathic nerveMuscularis externa (longitudinal)Muscularis externa (circular)Subepethelial plexusMuscularis mucosaSubmucosaVillusIntestinal lumenDeep muscularis plexusSerosaTertiary branchSecondary branchGanglionSubmucosal plexusMyenteric plexusBrunicardi_Ch26_p1099-p1166.indd 111201/03/19 7:11 PM 1113STOMACHCHAPTER 26regular (about three per minute), propulsive contractions, only lasts about 5 to 10 minutes. Most phase III complexes of the GI MMC begin in the stomach, and the frequency approximates that of the myoelectric gastric slow wave. Phase IV is a transi-tion period.Neurohormonal control of the MMC is poorly understood, but it appears that different phases are regulated by different mechanisms. For example, vagotomy abolishes phase II of the gastric MMC but has little influence on phase III that persists even in the |
Surgery_Schwartz_7394 | Surgery_Schwartz | but it appears that different phases are regulated by different mechanisms. For example, vagotomy abolishes phase II of the gastric MMC but has little influence on phase III that persists even in the autotransplanted stomach, totally devoid of extrinsic neural input. This suggests that phase III is regulated by intrin-sic nerves and/or hormones. Indeed, the initiation of phase III of the MMC in the distal stomach corresponds temporally to elevation in serum levels of motilin, a hormone produced in the duodenal mucosa. Resection of the duodenum abolishes dis-tal gastric phase III in dogs, and resection of the duodenum in humans (e.g., with pancreaticoduodenectomy, the Whipple pro-cedure) commonly results in early postoperative delayed gastric emptying. There are clearly motilin receptors on gastric smooth muscle and nerves. Other modulators of gastric MMC activ-ity include NO, endogenous opioids, intrinsic cholinergic and adrenergic nerves, and duodenal pH. The onset of MMC phase III | Surgery_Schwartz. but it appears that different phases are regulated by different mechanisms. For example, vagotomy abolishes phase II of the gastric MMC but has little influence on phase III that persists even in the autotransplanted stomach, totally devoid of extrinsic neural input. This suggests that phase III is regulated by intrin-sic nerves and/or hormones. Indeed, the initiation of phase III of the MMC in the distal stomach corresponds temporally to elevation in serum levels of motilin, a hormone produced in the duodenal mucosa. Resection of the duodenum abolishes dis-tal gastric phase III in dogs, and resection of the duodenum in humans (e.g., with pancreaticoduodenectomy, the Whipple pro-cedure) commonly results in early postoperative delayed gastric emptying. There are clearly motilin receptors on gastric smooth muscle and nerves. Other modulators of gastric MMC activ-ity include NO, endogenous opioids, intrinsic cholinergic and adrenergic nerves, and duodenal pH. The onset of MMC phase III |
Surgery_Schwartz_7395 | Surgery_Schwartz | gastric smooth muscle and nerves. Other modulators of gastric MMC activ-ity include NO, endogenous opioids, intrinsic cholinergic and adrenergic nerves, and duodenal pH. The onset of MMC phase III signals the return of hunger in humans, but oddly ghrelin, a major orexigenic hormone, appears to have little to do with phase III.63Feeding abolishes the MMC and leads to the fed motor pattern. The fed motor pattern of gastric activity starts within 10 minutes of food ingestion and persists until all the food has left the stomach. The neurohormonal initiator of this change is unknown, but CCK and the vagus appear to play some role since sham feeding transiently induces antral motor activity resembling the fed motor pattern which is blocked by the CCK receptor antagonist loxiglumide. Gastric motility during the fed pattern resembles phase II of the MMC, with irregular but con-tinuous phasic contractions of the distal stomach. During the fed state, about half of the myoelectric slow waves | Surgery_Schwartz. gastric smooth muscle and nerves. Other modulators of gastric MMC activ-ity include NO, endogenous opioids, intrinsic cholinergic and adrenergic nerves, and duodenal pH. The onset of MMC phase III signals the return of hunger in humans, but oddly ghrelin, a major orexigenic hormone, appears to have little to do with phase III.63Feeding abolishes the MMC and leads to the fed motor pattern. The fed motor pattern of gastric activity starts within 10 minutes of food ingestion and persists until all the food has left the stomach. The neurohormonal initiator of this change is unknown, but CCK and the vagus appear to play some role since sham feeding transiently induces antral motor activity resembling the fed motor pattern which is blocked by the CCK receptor antagonist loxiglumide. Gastric motility during the fed pattern resembles phase II of the MMC, with irregular but con-tinuous phasic contractions of the distal stomach. During the fed state, about half of the myoelectric slow waves |
Surgery_Schwartz_7396 | Surgery_Schwartz | motility during the fed pattern resembles phase II of the MMC, with irregular but con-tinuous phasic contractions of the distal stomach. During the fed state, about half of the myoelectric slow waves are associated with strong higher frequency distal gastric contractions. Some are prograde and some are retrograde, serving to mix and grind the solid components of the meal. The magnitude of gastric con-tractions and the duration of the pattern are influenced by the consistency and composition of the meal.The pylorus functions as an effective regulator of gastric emptying and an effective barrier to duodenogastric reflux. Bypass, transection, or resection of the pylorus may lead to uncontrolled gastric emptying of food and the dumping syn-drome (see “Postgastrectomy Problems”). Pyloric dysfunction IntracellularrecordingTensionQuiescentStimulated0 mv0 5 g -70 1122Figure 26-17. The relationship between intracellular electrical activity and muscle cell contraction. Note that contractile | Surgery_Schwartz. motility during the fed pattern resembles phase II of the MMC, with irregular but con-tinuous phasic contractions of the distal stomach. During the fed state, about half of the myoelectric slow waves are associated with strong higher frequency distal gastric contractions. Some are prograde and some are retrograde, serving to mix and grind the solid components of the meal. The magnitude of gastric con-tractions and the duration of the pattern are influenced by the consistency and composition of the meal.The pylorus functions as an effective regulator of gastric emptying and an effective barrier to duodenogastric reflux. Bypass, transection, or resection of the pylorus may lead to uncontrolled gastric emptying of food and the dumping syn-drome (see “Postgastrectomy Problems”). Pyloric dysfunction IntracellularrecordingTensionQuiescentStimulated0 mv0 5 g -70 1122Figure 26-17. The relationship between intracellular electrical activity and muscle cell contraction. Note that contractile |
Surgery_Schwartz_7397 | Surgery_Schwartz | IntracellularrecordingTensionQuiescentStimulated0 mv0 5 g -70 1122Figure 26-17. The relationship between intracellular electrical activity and muscle cell contraction. Note that contractile activity is always associated with electrical activity, but the converse is not so. During mechanical quiescence, there are regular depolarizations that do not reach threshold. In the stimulated state, the threshold for contraction is reached, and motor activity is demonstrable. (Reproduced with permission from Kim CH, Malagelada JR: Electrical activity of the stomach: clinical implications, Mayo Clin Proc. 1986 Mar;61(3):205-210.)Figure 26-18. Migrating motor complex, the fasting pattern of GI activity. During phase III of the migrating motor complex, effective peri-staltic waves progress from the stomach to the distal small intestine. (Reproduced with permis-sion from Rees WD, Malagelada JR, Miller LJ, et al: Human interdigestive and postprandial gas-trointestinal motor and gastrointestinal | Surgery_Schwartz. IntracellularrecordingTensionQuiescentStimulated0 mv0 5 g -70 1122Figure 26-17. The relationship between intracellular electrical activity and muscle cell contraction. Note that contractile activity is always associated with electrical activity, but the converse is not so. During mechanical quiescence, there are regular depolarizations that do not reach threshold. In the stimulated state, the threshold for contraction is reached, and motor activity is demonstrable. (Reproduced with permission from Kim CH, Malagelada JR: Electrical activity of the stomach: clinical implications, Mayo Clin Proc. 1986 Mar;61(3):205-210.)Figure 26-18. Migrating motor complex, the fasting pattern of GI activity. During phase III of the migrating motor complex, effective peri-staltic waves progress from the stomach to the distal small intestine. (Reproduced with permis-sion from Rees WD, Malagelada JR, Miller LJ, et al: Human interdigestive and postprandial gas-trointestinal motor and gastrointestinal |
Surgery_Schwartz_7398 | Surgery_Schwartz | stomach to the distal small intestine. (Reproduced with permis-sion from Rees WD, Malagelada JR, Miller LJ, et al: Human interdigestive and postprandial gas-trointestinal motor and gastrointestinal hormone patterns, Dig Dis Sci. 1982 Apr;27(4):321-329.)AntrumProximal duodenumDistal duodenumJejunum1 min100 mm Hg100 mm Hg100 mm Hg100 mm HgPhase IIPhase IIIPhase IVPhase IBrunicardi_Ch26_p1099-p1166.indd 111301/03/19 7:11 PM 1114SPECIFIC CONSIDERATIONS PART IIor disruption may also result in uncontrolled entry of duode-nal contents into the stomach. Perfusion of the duodenum with lipids, glucose, amino acids, hypertonic saline, or hydrochloric acid results in closure of the pylorus and decreased transpylo-ric flow. Ileal perfusion with fat has the same effect. A variety of neurohumoral pathways are involved with these physiologic responses, and there is evidence that different pathways may be involved for different stimuli.The pylorus is readily apparent grossly as a | Surgery_Schwartz. stomach to the distal small intestine. (Reproduced with permis-sion from Rees WD, Malagelada JR, Miller LJ, et al: Human interdigestive and postprandial gas-trointestinal motor and gastrointestinal hormone patterns, Dig Dis Sci. 1982 Apr;27(4):321-329.)AntrumProximal duodenumDistal duodenumJejunum1 min100 mm Hg100 mm Hg100 mm Hg100 mm HgPhase IIPhase IIIPhase IVPhase IBrunicardi_Ch26_p1099-p1166.indd 111301/03/19 7:11 PM 1114SPECIFIC CONSIDERATIONS PART IIor disruption may also result in uncontrolled entry of duode-nal contents into the stomach. Perfusion of the duodenum with lipids, glucose, amino acids, hypertonic saline, or hydrochloric acid results in closure of the pylorus and decreased transpylo-ric flow. Ileal perfusion with fat has the same effect. A variety of neurohumoral pathways are involved with these physiologic responses, and there is evidence that different pathways may be involved for different stimuli.The pylorus is readily apparent grossly as a |
Surgery_Schwartz_7399 | Surgery_Schwartz | neurohumoral pathways are involved with these physiologic responses, and there is evidence that different pathways may be involved for different stimuli.The pylorus is readily apparent grossly as a thick ring of muscle and connective tissue. The density of nerve tissue in the pyloric smooth muscle is several folds higher than in the antrum, with increased numbers of neurons staining positive for substance P, neuropeptide Y, VIP, and galanin. Interstitial cells of Cajal are closely associated with pyloric myocytes, and the myoelectric slow wave of the pylorus has the same frequency as that seen in the distal stomach. The motor activity of the pylo-rus is both tonic and phasic. During phase III of the MMC, the pylorus is open as gastric contents are swept into the duodenum. During the fed phase, the pylorus is closed most of the time. It relaxes intermittently, usually in synchronization with lower-amplitude, minor antral contractions. The higher-amplitude, more major antral | Surgery_Schwartz. neurohumoral pathways are involved with these physiologic responses, and there is evidence that different pathways may be involved for different stimuli.The pylorus is readily apparent grossly as a thick ring of muscle and connective tissue. The density of nerve tissue in the pyloric smooth muscle is several folds higher than in the antrum, with increased numbers of neurons staining positive for substance P, neuropeptide Y, VIP, and galanin. Interstitial cells of Cajal are closely associated with pyloric myocytes, and the myoelectric slow wave of the pylorus has the same frequency as that seen in the distal stomach. The motor activity of the pylo-rus is both tonic and phasic. During phase III of the MMC, the pylorus is open as gastric contents are swept into the duodenum. During the fed phase, the pylorus is closed most of the time. It relaxes intermittently, usually in synchronization with lower-amplitude, minor antral contractions. The higher-amplitude, more major antral |
Surgery_Schwartz_7400 | Surgery_Schwartz | the fed phase, the pylorus is closed most of the time. It relaxes intermittently, usually in synchronization with lower-amplitude, minor antral contractions. The higher-amplitude, more major antral contractions are usually met with a closed pylorus, facilitating retropulsion and further grinding of food.Modulation of pyloric motor activity is complex. There is evidence for both inhibitory and excitatory vagal pathways. Some contractile vagal effects are mediated by opioid pathways because they are blocked by naloxone. Electrical stimulation of the duodenum causes the pylorus to contract, whereas electrical stimulation of the antrum causes pyloric relaxation. Nitric oxide is an important mediator of pyloric relaxation. Other molecules that may play a physiologic role in controlling pyloric smooth muscle include serotonin, VIP, prostaglandin E1, and galanin (pyloric relaxation); and histamine, CCK, and secretin (pyloric contraction).Gastric Emptying.13 The control of gastric emptying is | Surgery_Schwartz. the fed phase, the pylorus is closed most of the time. It relaxes intermittently, usually in synchronization with lower-amplitude, minor antral contractions. The higher-amplitude, more major antral contractions are usually met with a closed pylorus, facilitating retropulsion and further grinding of food.Modulation of pyloric motor activity is complex. There is evidence for both inhibitory and excitatory vagal pathways. Some contractile vagal effects are mediated by opioid pathways because they are blocked by naloxone. Electrical stimulation of the duodenum causes the pylorus to contract, whereas electrical stimulation of the antrum causes pyloric relaxation. Nitric oxide is an important mediator of pyloric relaxation. Other molecules that may play a physiologic role in controlling pyloric smooth muscle include serotonin, VIP, prostaglandin E1, and galanin (pyloric relaxation); and histamine, CCK, and secretin (pyloric contraction).Gastric Emptying.13 The control of gastric emptying is |
Surgery_Schwartz_7401 | Surgery_Schwartz | smooth muscle include serotonin, VIP, prostaglandin E1, and galanin (pyloric relaxation); and histamine, CCK, and secretin (pyloric contraction).Gastric Emptying.13 The control of gastric emptying is com-plex. In general, liquid emptying is faster than solid emptying. Osmolarity, acidity, caloric content, nutrient composition, and particle size are important modulators of gastric emptying. Stimulation of duodenal osmoreceptors, glucoreceptors, and pH receptors clearly inhibits gastric emptying by a variety of neurohumoral mechanisms. CCK has been consistently shown to inhibit gastric emptying at physiologic doses (Fig. 26-19). Recently, it has been noted that the anorexigenic hormone leptin, secreted largely by fat but also by gastric mucosa, inhib-its gastric emptying, perhaps through the same pathway as CCK (which also has properties of a satiety hormone). The orexigenic hormone ghrelin has the opposite effect.Liquid Emptying. The gastric emptying of water or isotonic saline follows | Surgery_Schwartz. smooth muscle include serotonin, VIP, prostaglandin E1, and galanin (pyloric relaxation); and histamine, CCK, and secretin (pyloric contraction).Gastric Emptying.13 The control of gastric emptying is com-plex. In general, liquid emptying is faster than solid emptying. Osmolarity, acidity, caloric content, nutrient composition, and particle size are important modulators of gastric emptying. Stimulation of duodenal osmoreceptors, glucoreceptors, and pH receptors clearly inhibits gastric emptying by a variety of neurohumoral mechanisms. CCK has been consistently shown to inhibit gastric emptying at physiologic doses (Fig. 26-19). Recently, it has been noted that the anorexigenic hormone leptin, secreted largely by fat but also by gastric mucosa, inhib-its gastric emptying, perhaps through the same pathway as CCK (which also has properties of a satiety hormone). The orexigenic hormone ghrelin has the opposite effect.Liquid Emptying. The gastric emptying of water or isotonic saline follows |
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