{"id":4663,"date":"2019-10-22T09:50:21","date_gmt":"2019-10-22T09:50:21","guid":{"rendered":"https:\/\/endoscopiaterapeutica.net\/pt\/uncategorized\/novo-gastropatias\/"},"modified":"2022-05-26T23:48:54","modified_gmt":"2022-05-26T23:48:54","slug":"novo-gastropatias","status":"publish","type":"post","link":"https:\/\/endoscopiaterapeutica.net\/pt\/assuntosgerais\/novo-gastropatias\/","title":{"rendered":"GASTROPATIAS"},"content":{"rendered":"<p>Depois de muitas tentativas de padronizar a classifica\u00e7\u00e3o histol\u00f3gica das gastropatias, hoje ainda vemos diverg\u00eancias de opini\u00f5es. A classifica\u00e7\u00e3o de Sydney atualizada tem se mostrado a mais reconhecida e amplamente utilizada na atualidade. Ela classifica as les\u00f5es em termos de morfologia, topografia e poss\u00edveis etiologias (aguda, cr\u00f4nica ou espec\u00edfica).<\/p>\n<p>Gastropatia refere-se a dano e regenera\u00e7\u00e3o de c\u00e9lulas epiteliais, sem ou com m\u00ednimo processo inflamat\u00f3rio. Para avaliar a etiologia, uma hist\u00f3ria completa \u00e9 necess\u00e1ria, avaliando o uso de medicamentos, hist\u00f3rico de cirurgias pr\u00e9vias e fatores de risco. As causas de maior destaque s\u00e3o:<\/p>\n<p>&nbsp;<\/p>\n<p><img fetchpriority=\"high\" decoding=\"async\" class=\"alignnone size-medium wp-image-8026\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-1-186x300.png\" alt=\"\" width=\"186\" height=\"300\" srcset=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-1-186x300.png 186w, https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-1.png 303w\" sizes=\"(max-width: 186px) 100vw, 186px\" \/><\/p>\n<p>Gastropatias erosivas hemorr\u00e1gicas agudas s\u00e3o caracterizadas por desenvolvimento de hemorragia e eros\u00e3o ap\u00f3s\u00a0 exposi\u00e7\u00e3o da mucosa a algum agente agressor ou por baixa perfus\u00e3o.<\/p>\n<p>As les\u00f5es na superf\u00edcie do epit\u00e9lio costumam estar associadas a uma perda na barreira mucosa que pode ocorrer por dano direto: refluxo biliar, uso de AINE, abuso de \u00e1lcool, alendronato, sais de ferro; por isquemia da mucosa com hip\u00f3xia do tecido: sepse, queimaduras, uso de coca\u00edna, trauma ou pela associa\u00e7\u00e3o das duas condi\u00e7\u00f5es como em alguns agentes antineopl\u00e1sicos. Nos casos de TCE pode ocorrer um aumento na produ\u00e7\u00e3o de gastrina, o que aumentaria a secre\u00e7\u00e3o \u00e1cida causando les\u00e3o direta.<\/p>\n<p>A ruptura da barreira de prote\u00e7\u00e3o g\u00e1strica permite que o fator agressor penetre at\u00e9 a l\u00e2mina pr\u00f3pria causando danos a vasculatura, estimulando nervos, liberando histamina e outros mediadores inflamat\u00f3rios. O dano tecidual aumenta ap\u00f3s a reperfus\u00e3o com libera\u00e7\u00e3o de radicais livres e infiltra\u00e7\u00e3o de neutr\u00f3filos. Nos casos espec\u00edficos de AINE o dano ainda \u00e9 aumentado pela diminui\u00e7\u00e3o das prostaglandinas (que atuariam na estimula\u00e7\u00e3o da barreira protetora de muco e bicarbonato).<\/p>\n<p>Clinicamente pode se apresentar como dor abdominal, pirose, n\u00e1usea, v\u00f4mito e <a href=\"https:\/\/endoscopiaterapeutica.net\/pt\/assuntosgerais\/hda-guia-resumido-de-condutas-desde-admissao-a-alta-hospitalar\/\">hemat\u00eamese<\/a>. O sangramento pode ocorrer de 3 a 10 dias do evento agressor e pode variar de sangue oculto nas fezes at\u00e9 a sangramento massivo. Na endoscopia pode se visualizar, geralmente, hemorragia petequial difusa e aparecimento de pequenas eros\u00f5es vermelhas ou pretas.<\/p>\n<p><img decoding=\"async\" class=\"alignnone size-full wp-image-8028\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/FIGURA-1-300x235-1.png\" alt=\"\" width=\"300\" height=\"235\" \/><\/p>\n<p>\u00dalceras de estresse usualmente ocorrem geralmente no corpo e fundo g\u00e1strico, pr\u00f3ximo a transi\u00e7\u00e3o esofagog\u00e1strica. Costumam ser m\u00faltiplas, rasas e o tamanha varia de 0,5 a 2cm de di\u00e2metro.<\/p>\n<p>As les\u00f5es por AINE e \u00e1lcool envolvem todo o est\u00f4mago desde o in\u00edcio, apesar das altera\u00e7\u00f5es ficarem mais evidentes em antro. As eros\u00f5es nessas condi\u00e7\u00f5es costumam ser mais facilmente reepitelizadas que nas gastropatias isqu\u00eamicas.\u00a0 Algumas outras condi\u00e7\u00f5es tem suas particularidades como exposto na tabela.<\/p>\n<p><img decoding=\"async\" class=\"alignnone wp-image-8029\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-2-768x342-1-300x134.png\" alt=\"\" width=\"443\" height=\"198\" srcset=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-2-768x342-1-300x134.png 300w, https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-2-768x342-1-585x261.png 585w, https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/TABELA-2-768x342-1.png 768w\" sizes=\"(max-width: 443px) 100vw, 443px\" \/><\/p>\n<p>O tratamento das gastropatias hemorr\u00e1gicas erosivas agudas deve incluir o afastamento do fator agressor\/ condi\u00e7\u00e3o desencadeante; o uso de IBP e terap\u00eautica espec\u00edfica para les\u00e3o focal.<\/p>\n<p>&nbsp;<\/p>\n<h2><strong>GASTROPATIA REATIVA<\/strong><\/h2>\n<p>A exposi\u00e7\u00e3o por longos per\u00edodos a agentes agressores da mucosa pode levar a altera\u00e7\u00f5es da mesma (discreta inflama\u00e7\u00e3o, graus variados de hiperplasia foveolar, edema, prolifera\u00e7\u00e3o de musculatura lisa da l\u00e2mina pr\u00f3pria, congest\u00e3o e dilata\u00e7\u00e3o vascular). O uso cr\u00f4nico de AINE, alendronato ou refluxo biliar s\u00e3o as principais causas desta condi\u00e7\u00e3o.<\/p>\n<ul>\n<li>\n<h3>Associada a Refluxo Biliar<\/h3>\n<\/li>\n<\/ul>\n<p>Incompet\u00eancia do piloro, motilidade duodenal alterada ou estoma podem acarretar refluxo biliar levando a dor abdominal, v\u00f4mito bilioso e perda de peso;\u00a0 conhecido como gastropatia do refluxo biliar. Podem sofrer altera\u00e7\u00f5es adaptativas na maioria dos casos, por\u00e9m em alguns casos pode acarretar eros\u00f5es e \u00falceras. O tratamento definitivo geralmente \u00e9 cir\u00fargico (revis\u00e3o de Y de Roux), que melhora os sintomas em 50-90% dos casos.<\/p>\n<ul>\n<li>\n<h3>Associada a AINE<\/h3>\n<\/li>\n<\/ul>\n<p>O uso cr\u00f4nico de AINE obedece ao mesmo padr\u00e3o de adaptabilidade na maior parte dos usu\u00e1rios, reduzindo o sangramento e as eros\u00f5es; no entanto, quando ocorre falha na adapta\u00e7\u00e3o ao AINE o paciente pode apresentar sangramento por eros\u00f5es ou \u00falceras. Essa falha costuma ser mais prevalente em pacientes com H. pylori.<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<h2><strong>VASCULAR<\/strong><\/h2>\n<ul>\n<li>\n<h3><strong>Gastropatia hipertensiva portal (GHP)<\/strong><\/h3>\n<\/li>\n<\/ul>\n<p>Ocorre geralmente associada a cirrose ou trombose de veia porta. A hipertens\u00e3o portal nessas situa\u00e7\u00f5es geram um aumento do fluxo sang\u00fc\u00edneo que irrigam os vasos g\u00e1stricos.<\/p>\n<p>A gravidade da GHP est\u00e1 relacionada a press\u00e3o portal, o grau de resist\u00eancia vascular hep\u00e1tica e o grau de redu\u00e7\u00e3o da perfus\u00e3o hep\u00e1tica. \u00c9 comum que o diagn\u00f3stico da GHP ocorra durante endoscopia de rastreio para varizes de es\u00f4fago. No entanto pode ocorrer sangramento cr\u00f4nico em 3-60% dos casos e sangramento agudo em 2 -12%.<\/p>\n<p>Os achados endosc\u00f3picos s\u00e3o caracterizados por enantema associado a fino rendilhado branco sobreposto dando a apar\u00eancia de pele de cobra, pode tamb\u00e9m ocorrer red spots \u00a0ou black\/brown spots. Sua localiza\u00e7\u00e3o costuma ser em fundo e corpo proximal mas pode se estender para antro.<\/p>\n<p><a href=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/09\/FIGURA-6.png\" data-rel=\"penci-gallery-image-content\" ><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-10345\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2021\/08\/FIGURA-6.png\" alt=\"\" width=\"217\" height=\"184\" \/><\/a><\/p>\n<p>Casos de GHP leve podem mimetizar outras condi\u00e7\u00f5es e ent\u00e3o a realiza\u00e7\u00e3o de bi\u00f3psias poderia ajudar no diagn\u00f3stico (sempre atentar a coagulopatia). Casos mais graves costumam cursar com hemorragias subepiteliais e aumento da vasculatura semelhante a angioma.<\/p>\n<p>O tratamento na profilaxia prim\u00e1ria consiste em beta bloqueador n\u00e3o seletivo para manter uma freq\u00fc\u00eancia card\u00edaca (FC) em torno de 50-55 bpm. Em casos de sangramento cr\u00f4nico deve-se repor ferro e se houver uma queda de hemoglobina abaixo de 7 deve ser realizada transfus\u00e3o.<\/p>\n<p>Nos casos de sangramento agudo deve ser lan\u00e7ado m\u00e3o de droga vasoativa (Octreotide por 2 dias, ou Somatostatina por 3 dias, ou Terlipressina 2-5 dias), ressuscita\u00e7\u00e3o vol\u00eamica, manter a hemoglobina entre 7-8 nos cirr\u00f3ticos, os portadores de cirrose tamb\u00e9m devem receber antibi\u00f3tico profilaxia para PBE. Em pacientes refrat\u00e1rios pode ser lan\u00e7ado m\u00e3o de TIPS, shunt cir\u00fargico ou transplante hep\u00e1tico.<\/p>\n<p>&nbsp;<\/p>\n<ul>\n<li>\n<h3><strong>Ectasia vascular antral g\u00e1strica (GAVE)<\/strong><\/h3>\n<\/li>\n<\/ul>\n<p>Ocorre devido a dilata\u00e7\u00e3o de pequenos vasos da regi\u00e3o antral.\u00a0Na histologia nota-se <strong><a href=\"https:\/\/endoscopiaterapeutica.net\/pt\/lesoes-vasculares-em-intestino-delgado\/\">ectasia<\/a><\/strong> vascular, al\u00e9m de trombos, prolifera\u00e7\u00e3o celular e fibro-hialiniza\u00e7\u00e3o. Apresenta-se com enantema petequial e que por vezes podem ser lineares, podendo ter apar\u00eancia de est\u00f4mago em melancia.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-8030\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/Imagem6-300x225-1.png\" alt=\"\" width=\"300\" height=\"225\" \/> <img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-medium wp-image-8031\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/Imagem2-300x225-1.png\" alt=\"\" width=\"300\" height=\"225\" \/> <img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-medium wp-image-8032\" src=\"https:\/\/endoscopiaterapeutica.net\/pt\/wp-content\/uploads\/2019\/10\/Imagem1-300x225-1.png\" alt=\"\" width=\"300\" height=\"225\" \/><\/p>\n<p>Apesar de sua etiologia n\u00e3o ser bem definida pode estar associada a cirrose, doen\u00e7as autoimunes, insufici\u00eancia renal cr\u00f4nica, cardiopatia isqu\u00eamica ou transplante de medula \u00f3ssea. Pode levar a anemia e\u00a0raramente a hemorragia digestiva. O tratamento consiste na abla\u00e7\u00e3o das les\u00f5es com plasma de arg\u00f4nio ou heater probe.<\/p>\n<p>&nbsp;<\/p>\n<h2><strong>Refer\u00eancias<\/strong><\/h2>\n<p>1.\u00a0\u00a0\u00a0 Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996; 20:1161.<br \/>\n2.\u00a0\u00a0\u00a0 Carpenter HA, Talley NJ. Gastroscopy is incomplete without biopsy: clinical relevance of distinguishing gastropathy from gastritis. Gastroenterology 1995; 108:917.<br \/>\n3.\u00a0\u00a0\u00a0 Marrone GC, Silen W. Pathogenesis, diagnosis and treatment of acute gastric mucosal lesions. Clin Gastroenterol 1984; 13:635.<br \/>\n4.\u00a0\u00a0\u00a0 Silen W. The clinical problem of stress ulcers. Clin Invest Med 1987; 10:270.<br \/>\n5.\u00a0\u00a0\u00a0 Franke A, Teyssen S, Singer MV. Alcohol-related diseases of the esophagus and stomach.<br \/>\nDig Dis 2005; 23:204.<br \/>\n6.\u00a0\u00a0\u00a0 Kvietys PR, Twohig B, Danzell J, Specian RD. Ethanol-induced injury to the rat gastric mucosa. Role of neutrophils and xanthine oxidase-derived radicals. Gastroenterology 1990; 98:909.<br \/>\n7.\u00a0\u00a0\u00a0 Minalyan A, Gabrielyan L, Scott D, et al. The Gastric and Intestinal Microbiome: Role of Proton Pump Inhibitors. Curr Gastroenterol Rep 2017; 19:42.<br \/>\n8.\u00a0\u00a0\u00a0 Haig A, Driman DK. Iron-induced mucosal injury to the upper gastrointestinal tract. Histopathology 2006; 48:808.<br \/>\n9.\u00a0\u00a0\u00a0 Nam SY, Choi IJ, Park KW, et al. Risk of hemorrhagic gastropathy associated with colonoscopy bowel preparation using oral sodium phosphate solution. Endoscopy 2010; 42:109.<br \/>\n10. Petras RE, Hart WR, Bukowski RM. Gastric epithelial atypia associated with hepatic arterial infusion chemotherapy. Its distinction from early gastric carcinoma. Cancer 1985; 56:745.<br \/>\n11. Gourgoutis G, Das G. Gastrointestinal manifestations of cocaine addiction. Int J Clin Pharmacol Ther 1994; 32:136.<br \/>\n12. Dixon MF, O&#8217;Connor HJ, Axon AT, et al. Reflux gastritis: distinct histopathological entity? J Clin Pathol 1986; 39:524.<br \/>\n13. Sobala GM, King RF, Axon AT, Dixon MF. Reflux gastritis in the intact stomach. J Clin Pathol 1990; 43:303.<br \/>\n14. Graham DY, Malaty HM, Goodgame R. Primary amino-bisphosphonates: a new class of gastrotoxic drugs&#8211;comparison of alendronate and aspirin. Am J Gastroenterol 1997; 92:1322.<br \/>\n15. Weinstein WM, Buch KL, Elashoff J, et al. The histology of the stomach in symptomatic patients after gastric surgery: a model to assess selective patterns of gastric mucosal injury. Scand J Gastroenterol Suppl 1985; 109:77.<br \/>\n16. Shafique K, Araujo JL, Veluvolu R, et al. Mitochondrial Iron Accumulation in Parietal and Chief Cells in Iron Pill Gastritis Following Billroth II Gastrectomy: Case Report Including Electron Microscopic Examination. Ann Clin Lab Sci 2017; 47:354.<br \/>\n17. Cheli R, Giacosa A, Marenco G, et al. Chronic gastritis and alcohol. Z Gastroenterol 1981; 19:459.<br \/>\n18. Oddsson E, Binder V, Thorgeirsson T, et al. A prospective comparative study of clinical and pathological characteristics in Icelandic and Danish patients with gastric ulcer, duodenal ulcer, and X-ray negative dyspepsia. II. Histological results. Scand J Gastroenterol 1978; 13:489.<br \/>\n19. Uppal R, Lateef SK, Korsten MA, et al. Chronic alcoholic gastritis. Roles of alcohol and Helicobacter pylori. Arch Intern Med 1991; 151:760.<\/p>\n<p>20. Roth SH, Bennett RE. Nonsteroidal anti-inflammatory drug gastropathy. Recognition and<br \/>\nresponse. Arch Intern Med 1987; 147:2093.<br \/>\n21. Shorrock CJ, Rees WD. Mucosal adaptation to indomethacin induced gastric damage in man&#8211;studies on morphology, blood flow, and prostaglandin E2 metabolism. Gut 1992; 33:164.<br \/>\n22. Konturek SJ, Brzozowski T, Majka J, et al. Adaptation of the gastric mucosa to stress. Role of prostaglandin and epidermal growth factor. Scand J Gastroenterol Suppl 1992; 193:39.<br \/>\n23. Silvoso GR, Ivey KJ, Butt JH, et al. Incidence of gastric lesions in patients with rheumatic disease on chronic aspirin therapy. Ann Intern Med 1979; 91:517.<br \/>\n24. Larkai EN, Smith JL, Lidsky MD, Graham DY. Gastroduodenal mucosa and dyspeptic symptoms in arthritic patients during chronic nonsteroidal anti-inflammatory drug use. Am J Gastroenterol 1987; 82:1153.<br \/>\n25. Davenport HW. Salicylate damage to the gastric mucosal barrier. N Engl J Med 1967; 276:1307.<br \/>\n26. Sloan JM. Acute haemorrhage gastritis and acute infective gastritis, gastritis caused by physi cal agents and corrosives, uraemic gastritis. In: Gastrointestinal and Oesophageal Patholog y, Whitehead R (Ed), Churchill Livingstone, Edinburgh 1989. p.385.<br \/>\n27. Hernandez LA, Grisham MB, Twohig B, et al. Role of neutrophils in ischemia-reperfusion- induced microvascular injury. Am J Physiol 1987; 253:H699.<\/p>\n<p>Confira tamb\u00e9m: <a href=\"https:\/\/endoscopiaterapeutica.net\/pt\/artigoscomentados\/iv-consenso-brasileiro-sobre-infeccao-pelo-helicobacter-pylori\/\">H. pylori<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Depois de muitas tentativas de padronizar a classifica\u00e7\u00e3o histol\u00f3gica das gastropatias, hoje ainda vemos&hellip;<\/p>\n","protected":false},"author":3971,"featured_media":5321,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_lmt_disableupdate":"","_lmt_disable":"","footnotes":""},"categories":[151],"tags":[],"ano":[145],"tipo":[153],"volume":[147],"class_list":["post-4663","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-assuntosgerais","ano-145","tipo-endoscopia-digestiva-alta","volume-volume-ii"],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v27.2 (Yoast SEO v27.2) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>GASTROPATIAS &#8226; Endoscopia Terapeutica<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/endoscopiaterapeutica.net\/pt\/assuntosgerais\/novo-gastropatias\/\" \/>\n<meta property=\"og:locale\" content=\"pt_BR\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"GASTROPATIAS\" \/>\n<meta property=\"og:description\" content=\"Depois de muitas tentativas de padronizar a classifica\u00e7\u00e3o histol\u00f3gica das gastropatias, hoje ainda vemos diverg\u00eancias de opini\u00f5es. 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