Lower gastrointestinal bleeding pathophysiology: Difference between revisions

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**The [[Intestinal wall|colonic wall]] weakens with age and results in the formation of sac-like protrusions known as [[Diverticulum|diverticula]].<ref name="pmid20011269">{{cite journal |vauthors=Hobson KG, Roberts PL |title=Etiology and pathophysiology of diverticular disease |journal=Clin Colon Rectal Surg |volume=17 |issue=3 |pages=147–53 |year=2004 |pmid=20011269 |pmc=2780060 |doi=10.1055/s-2004-832695 |url=}}</ref><ref name="pmid20011276">{{cite journal |vauthors=Maykel JA, Opelka FG |title=Colonic diverticulosis and diverticular hemorrhage |journal=Clin Colon Rectal Surg |volume=17 |issue=3 |pages=195–204 |year=2004 |pmid=20011276 |pmc=2780065 |doi=10.1055/s-2004-832702 |url=}}</ref><ref name="pmid17468551">{{cite journal |vauthors=Comparato G, Pilotto A, Franzè A, Franceschi M, Di Mario F |title=Diverticular disease in the elderly |journal=Dig Dis |volume=25 |issue=2 |pages=151–9 |year=2007 |pmid=17468551 |doi=10.1159/000099480 |url=}}</ref><ref name="pmid20676256">{{cite journal |vauthors=Matrana MR, Margolin DA |title=Epidemiology and pathophysiology of diverticular disease |journal=Clin Colon Rectal Surg |volume=22 |issue=3 |pages=141–6 |year=2009 |pmid=20676256 |pmc=2780269 |doi=10.1055/s-0029-1236157 |url=}}</ref>
**The [[Intestinal wall|colonic wall]] weakens with age and results in the formation of sac-like protrusions known as [[Diverticulum|diverticula]].<ref name="pmid20011269">{{cite journal |vauthors=Hobson KG, Roberts PL |title=Etiology and pathophysiology of diverticular disease |journal=Clin Colon Rectal Surg |volume=17 |issue=3 |pages=147–53 |year=2004 |pmid=20011269 |pmc=2780060 |doi=10.1055/s-2004-832695 |url=}}</ref><ref name="pmid20011276">{{cite journal |vauthors=Maykel JA, Opelka FG |title=Colonic diverticulosis and diverticular hemorrhage |journal=Clin Colon Rectal Surg |volume=17 |issue=3 |pages=195–204 |year=2004 |pmid=20011276 |pmc=2780065 |doi=10.1055/s-2004-832702 |url=}}</ref><ref name="pmid17468551">{{cite journal |vauthors=Comparato G, Pilotto A, Franzè A, Franceschi M, Di Mario F |title=Diverticular disease in the elderly |journal=Dig Dis |volume=25 |issue=2 |pages=151–9 |year=2007 |pmid=17468551 |doi=10.1159/000099480 |url=}}</ref><ref name="pmid20676256">{{cite journal |vauthors=Matrana MR, Margolin DA |title=Epidemiology and pathophysiology of diverticular disease |journal=Clin Colon Rectal Surg |volume=22 |issue=3 |pages=141–6 |year=2009 |pmid=20676256 |pmc=2780269 |doi=10.1055/s-0029-1236157 |url=}}</ref>
**These protrusions generally occur at the junction of [[blood vessel]] penetrating through the [[mucosa]] and circular [[muscle fibers]] of the [[colon]].
**These protrusions generally occur at the junction of [[blood vessel]] penetrating through the [[mucosa]] and circular [[muscle fibers]] of the [[colon]].
**[[Hemorrhage]] results from rupture of the intramural branches ([[vasa recta]]) of the [[marginal artery]] at the dome of a diverticulum and can give rise to a massive, life-threatening LGIB.
**[[Hemorrhage]] results from rupture of the intramural branches ([[vasa recta]]) of the [[marginal artery]] at the dome of a [[diverticulum]] and can give rise to a massive, life-threatening LGIB.
**Despite the majority of [[Diverticuli|diverticula]] being on the left side of the colon, diverticular bleeding originates from the right side of the [[colon]] in 50% to 90% of instances.
[[Image:Sigmoid diverticulum (diagram).jpg|thumb|center|400px|Diagram of sigmoid diverticulum<br>Source:By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons]]
[[Image:Sigmoid diverticulum (diagram).jpg|thumb|center|400px|Diagram of sigmoid diverticulum<br>Source:By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons]]
*'''<u>Anorectal disease</u>'''
*'''<u>Anorectal disease</u>'''
:*[[Hemorrhoids]] are engorged [[Blood vessel|vessels]] in the normal [[anal]] cushions. When swollen, this [[tissue]] is very friable and susceptible to [[trauma]], which leads to painless, bright red bleeding.<ref name="pmid22563187">{{cite journal |vauthors=Lohsiriwat V |title=Hemorrhoids: from basic pathophysiology to clinical management |journal=World J. Gastroenterol. |volume=18 |issue=17 |pages=2009–17 |year=2012 |pmid=22563187 |pmc=3342598 |doi=10.3748/wjg.v18.i17.2009 |url=}}</ref><ref name="pmid22379400">{{cite journal |vauthors=Sanchez C, Chinn BT |title=Hemorrhoids |journal=Clin Colon Rectal Surg |volume=24 |issue=1 |pages=5–13 |year=2011 |pmid=22379400 |pmc=3140328 |doi=10.1055/s-0031-1272818 |url=}}</ref><ref name="pmid22563187">{{cite journal |vauthors=Lohsiriwat V |title=Hemorrhoids: from basic pathophysiology to clinical management |journal=World J. Gastroenterol. |volume=18 |issue=17 |pages=2009–17 |year=2012 |pmid=22563187 |pmc=3342598 |doi=10.3748/wjg.v18.i17.2009 |url=}}</ref>
:*Hemorrhoids are defined as [[Swelling (medical)|swelling]] and [[inflammation]] of [[veins]] in the [[Rectum|rectal]] and [[Anus|anal region]]
:*[[Anal fissures]] are defined as a tear in the anal mucosa. With the passage of [[stool]], the [[mucosa]] continues to tear and leads to bright red bleeding. <ref name="pmid3140330">{{cite journal |vauthors=Holland RA, Rimes AF, Comis A, Tyndale-Biscoe CH |title=Oxygen carriage and carbonic anhydrase activity in the blood of a marsupial, the Tammar wallaby (Macropus eugenii), during early development |journal=Respir Physiol |volume=73 |issue=1 |pages=69–86 |year=1988 |pmid=3140330 |doi= |url=}}</ref>
:*Hemorrhoids can be either internal or external based on their relation to dentate line.
:*The first step in the pathogenesis of either type of hemorrhoids is weakening of the surrounding connective tissue and vein wall.<ref name="pmid22563187">{{cite journal |vauthors=Lohsiriwat V |title=Hemorrhoids: from basic pathophysiology to clinical management |journal=World J. Gastroenterol. |volume=18 |issue=17 |pages=2009–17 |year=2012 |pmid=22563187 |pmc=3342598 |doi=10.3748/wjg.v18.i17.2009 |url=}}</ref><ref name="pmid22379400">{{cite journal |vauthors=Sanchez C, Chinn BT |title=Hemorrhoids |journal=Clin Colon Rectal Surg |volume=24 |issue=1 |pages=5–13 |year=2011 |pmid=22379400 |pmc=3140328 |doi=10.1055/s-0031-1272818 |url=}}</ref><ref name="pmid22563187">{{cite journal |vauthors=Lohsiriwat V |title=Hemorrhoids: from basic pathophysiology to clinical management |journal=World J. Gastroenterol. |volume=18 |issue=17 |pages=2009–17 |year=2012 |pmid=22563187 |pmc=3342598 |doi=10.3748/wjg.v18.i17.2009 |url=}}</ref>
:*Weakening of blood vessels can result in bleeding under pressure.
:*An anal fissure can be defined as disruption or tear in the mucosal surface of the skin.
:*During defecation, due to increased pressure which can exaggerate the tears may  present as bright red rectal bleeding with severe periodic pain.<ref name="pmid3140330">{{cite journal |vauthors=Holland RA, Rimes AF, Comis A, Tyndale-Biscoe CH |title=Oxygen carriage and carbonic anhydrase activity in the blood of a marsupial, the Tammar wallaby (Macropus eugenii), during early development |journal=Respir Physiol |volume=73 |issue=1 |pages=69–86 |year=1988 |pmid=3140330 |doi= |url=}}</ref>
*'''<u>[[Mesenteric ischemia|Mesenteric Ischemia]]</u>'''
*'''<u>[[Mesenteric ischemia|Mesenteric Ischemia]]</u>'''
:*[[Mesenteric ischemia]] results when there is inadequate blood supply at the level of the [[small intestine]].<ref name="pmid9146726">{{cite journal |vauthors=Krupski WC, Selzman CH, Whitehill TA |title=Unusual causes of mesenteric ischemia |journal=Surg. Clin. North Am. |volume=77 |issue=2 |pages=471–502 |year=1997 |pmid=9146726 |doi= |url=}}</ref><ref name="pmid21326562">{{cite journal |vauthors=Walker TG |title=Mesenteric ischemia |journal=Semin Intervent Radiol |volume=26 |issue=3 |pages=175–83 |year=2009 |pmid=21326562 |pmc=3036494 |doi=10.1055/s-0029-1225662 |url=}}</ref><ref name="pmid18625147">{{cite journal |vauthors=Berland T, Oldenburg WA |title=Acute mesenteric ischemia |journal=Curr Gastroenterol Rep |volume=10 |issue=3 |pages=341–6 |year=2008 |pmid=18625147 |doi= |url=}}</ref><ref name="pmid26909235">{{cite journal |vauthors=Mastoraki A, Mastoraki S, Tziava E, Touloumi S, Krinos N, Danias N, Lazaris A, Arkadopoulos N |title=Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities |journal=World J Gastrointest Pathophysiol |volume=7 |issue=1 |pages=125–30 |year=2016 |pmid=26909235 |pmc=4753178 |doi=10.4291/wjgp.v7.i1.125 |url=}}</ref>
:*[[Mesenteric ischemia]] results when there is inadequate blood supply at the level of the [[small intestine]].<ref name="pmid9146726">{{cite journal |vauthors=Krupski WC, Selzman CH, Whitehill TA |title=Unusual causes of mesenteric ischemia |journal=Surg. Clin. North Am. |volume=77 |issue=2 |pages=471–502 |year=1997 |pmid=9146726 |doi= |url=}}</ref><ref name="pmid21326562">{{cite journal |vauthors=Walker TG |title=Mesenteric ischemia |journal=Semin Intervent Radiol |volume=26 |issue=3 |pages=175–83 |year=2009 |pmid=21326562 |pmc=3036494 |doi=10.1055/s-0029-1225662 |url=}}</ref><ref name="pmid18625147">{{cite journal |vauthors=Berland T, Oldenburg WA |title=Acute mesenteric ischemia |journal=Curr Gastroenterol Rep |volume=10 |issue=3 |pages=341–6 |year=2008 |pmid=18625147 |doi= |url=}}</ref><ref name="pmid26909235">{{cite journal |vauthors=Mastoraki A, Mastoraki S, Tziava E, Touloumi S, Krinos N, Danias N, Lazaris A, Arkadopoulos N |title=Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities |journal=World J Gastrointest Pathophysiol |volume=7 |issue=1 |pages=125–30 |year=2016 |pmid=26909235 |pmc=4753178 |doi=10.4291/wjgp.v7.i1.125 |url=}}</ref>
:*2 or more vessels ([[Celiac artery|celiac]], [[Superior mesenteric artery|SMA]], or [[Inferior mesenteric artery|IMA]]) must be involved for bleeding to occur.
:*2 or more vessels ([[Celiac artery|celiac]], [[Superior mesenteric artery|SMA]], or [[Inferior mesenteric artery|IMA]]) must be involved for bleeding to occur.
:*Non occlusive [[mesenteric ischemia]] affects critically ill patients who are [[vasopressor]]-dependent.
:*Decreased blood supply can occur due to obstruction of blood vessel either by emobolus or due to vasoconstriction effect of drugs.
:*[[Venous thrombosis]] of the [[visceral]] [[vessels]] can also precipitate an [[acute]] [[ischemic]] event.
:*Decreased blood supply initiates necrosis of mucosal surface of intestine.
:*Decreased blood flow leads to transmural [[infarction]] with [[necrosis]] and [[perforation]].
:*unopposed blood deprivation leads to trans-mural necrosis and ultimately sloughing of the tissues with associated bleeding.
:*Associated [[mucosal]] sloughing results in bleeding.
*'''<u>[[Ischemic colitis|Ischemic Colitis]]</u>'''
*'''<u>[[Ischemic colitis|Ischemic Colitis]]</u>'''
:*[[Ischemic colitis]] is caused by poor [[perfusion]] of the [[colon]], which results in the inability of that area of the [[colon]] to meet its [[metabolic]] demands.<ref name="pmid26034405">{{cite journal |vauthors=FitzGerald JF, Hernandez Iii LO |title=Ischemic colitis |journal=Clin Colon Rectal Surg |volume=28 |issue=2 |pages=93–8 |year=2015 |pmid=26034405 |pmc=4442720 |doi=10.1055/s-0035-1549099 |url=}}</ref><ref name="pmid19109863">{{cite journal |vauthors=Theodoropoulou A, Koutroubakis IE |title=Ischemic colitis: clinical practice in diagnosis and treatment |journal=World J. Gastroenterol. |volume=14 |issue=48 |pages=7302–8 |year=2008 |pmid=19109863 |pmc=2778113 |doi= |url=}}</ref><ref name="pmid25504381">{{cite journal |vauthors=Rania H, Mériam S, Rym E, Hyafa R, Amine A, Najet BH, Lassad G, Mohamed TK |title=Ischemic colitis in five points: an update 2013 |journal=Tunis Med |volume=92 |issue=5 |pages=299–303 |year=2014 |pmid=25504381 |doi= |url=}}</ref>  
:*Ischemic colitis is a condition in which injury of the [[large intestine]] results from decreased blood supply.<ref name="pmid26034405">{{cite journal |vauthors=FitzGerald JF, Hernandez Iii LO |title=Ischemic colitis |journal=Clin Colon Rectal Surg |volume=28 |issue=2 |pages=93–8 |year=2015 |pmid=26034405 |pmc=4442720 |doi=10.1055/s-0035-1549099 |url=}}</ref><ref name="pmid19109863">{{cite journal |vauthors=Theodoropoulou A, Koutroubakis IE |title=Ischemic colitis: clinical practice in diagnosis and treatment |journal=World J. Gastroenterol. |volume=14 |issue=48 |pages=7302–8 |year=2008 |pmid=19109863 |pmc=2778113 |doi= |url=}}</ref><ref name="pmid25504381">{{cite journal |vauthors=Rania H, Mériam S, Rym E, Hyafa R, Amine A, Najet BH, Lassad G, Mohamed TK |title=Ischemic colitis in five points: an update 2013 |journal=Tunis Med |volume=92 |issue=5 |pages=299–303 |year=2014 |pmid=25504381 |doi= |url=}}</ref>  
:*It can be [[gangrenous]] or nongangrenous, acute or chronic, transient or permanent.
:*The [[Colon (anatomy)|colon]] is most commonly involved due the presence of water shed areas ( splenic flexure and hepatic flexure).
:*The [[Colon (anatomy)|left colon]] is predominantly affected, with the [[splenic flexure]] having increased susceptibility.
:*Similar to mesentric ischemia bleeding occurs due to necrosis and sloughing of mucosal membrane.
:*Intraluminal [[hemorrhage]] occurs as the [[mucosa]] becomes [[necrotic]], sloughs, and bleeds.
:*Damage to the tissue is caused both with the [[ischemic]] insult as well as [[reperfusion injury]].
*'''<u>Inflammatory Bowel Disease</u>'''<ref name="pmid28261018">{{cite journal |vauthors=Kim DH, Cheon JH |title=Pathogenesis of Inflammatory Bowel Disease and Recent Advances in Biologic Therapies |journal=Immune Netw |volume=17 |issue=1 |pages=25–40 |year=2017 |pmid=28261018 |pmc=5334120 |doi=10.4110/in.2017.17.1.25 |url=}}</ref><ref name="pmid11781268">{{cite journal |vauthors=Hendrickson BA, Gokhale R, Cho JH |title=Clinical aspects and pathophysiology of inflammatory bowel disease |journal=Clin. Microbiol. Rev. |volume=15 |issue=1 |pages=79–94 |year=2002 |pmid=11781268 |pmc=118061 |doi= |url=}}</ref>
*'''<u>Inflammatory Bowel Disease</u>'''<ref name="pmid28261018">{{cite journal |vauthors=Kim DH, Cheon JH |title=Pathogenesis of Inflammatory Bowel Disease and Recent Advances in Biologic Therapies |journal=Immune Netw |volume=17 |issue=1 |pages=25–40 |year=2017 |pmid=28261018 |pmc=5334120 |doi=10.4110/in.2017.17.1.25 |url=}}</ref><ref name="pmid11781268">{{cite journal |vauthors=Hendrickson BA, Gokhale R, Cho JH |title=Clinical aspects and pathophysiology of inflammatory bowel disease |journal=Clin. Microbiol. Rev. |volume=15 |issue=1 |pages=79–94 |year=2002 |pmid=11781268 |pmc=118061 |doi= |url=}}</ref>
**'''[[Crohn's disease]]'''
**'''[[Crohn's disease]]'''
***In [[Crohn's disease]], [[T cell]] activation stimulates [[Interleukin 12|interleukin (IL)-12]] and [[Tumor necrosis factor alpha|tumor necrosis factor (TNF)-α]], resulting in [[chronic]] [[inflammation]] and tissue injury.<ref name="pmid4447044">{{cite journal |vauthors=Woźniak-Parnowska W, Werakso B |title=[Comparative studies of microbiological purity of ointments by the direct culture method and use of membrane filters] |language=Polish |journal=Acta Pol Pharm |volume=31 |issue=6 |pages=819–23 |year=1974 |pmid=4447044 |doi= |url=}}</ref><ref name="pmid24395894">{{cite journal |vauthors=Mazal J |title=Crohn disease: pathophysiology, diagnosis, and treatment |journal=Radiol Technol |volume=85 |issue=3 |pages=297–316; quiz 317–20 |year=2014 |pmid=24395894 |doi= |url=}}</ref><ref name="pmid2694136">{{cite journal |vauthors=Jewell DP |title=Aetiology and pathogenesis of ulcerative colitis and Crohn's disease |journal=Postgrad Med J |volume=65 |issue=768 |pages=718–9 |year=1989 |pmid=2694136 |pmc=2429831 |doi= |url=}}</ref><ref name="pmid16819502">{{cite journal |vauthors=Sartor RB |title=Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis |journal=Nat Clin Pract Gastroenterol Hepatol |volume=3 |issue=7 |pages=390–407 |year=2006 |pmid=16819502 |doi=10.1038/ncpgasthep0528 |url=}}</ref><ref name="pmid15656711">{{cite journal |vauthors=Head K, Jurenka JS |title=Inflammatory bowel disease. Part II: Crohn's disease--pathophysiology and conventional and alternative treatment options |journal=Altern Med Rev |volume=9 |issue=4 |pages=360–401 |year=2004 |pmid=15656711 |doi= |url=}}</ref><ref name="pmid24415861">{{cite journal |vauthors=Zhang YZ, Li YY |title=Inflammatory bowel disease: pathogenesis |journal=World J. Gastroenterol. |volume=20 |issue=1 |pages=91–9 |year=2014 |pmid=24415861 |pmc=3886036 |doi=10.3748/wjg.v20.i1.91 |url=}}</ref>
***In [[Crohn's disease]], [[T cell]] activation stimulates [[Interleukin 12|interleukin (IL)-12]] and [[Tumor necrosis factor alpha|tumor necrosis factor (TNF)-α]], resulting in [[chronic]] [[inflammation]] and tissue injury.<ref name="pmid4447044">{{cite journal |vauthors=Woźniak-Parnowska W, Werakso B |title=[Comparative studies of microbiological purity of ointments by the direct culture method and use of membrane filters] |language=Polish |journal=Acta Pol Pharm |volume=31 |issue=6 |pages=819–23 |year=1974 |pmid=4447044 |doi= |url=}}</ref><ref name="pmid24395894">{{cite journal |vauthors=Mazal J |title=Crohn disease: pathophysiology, diagnosis, and treatment |journal=Radiol Technol |volume=85 |issue=3 |pages=297–316; quiz 317–20 |year=2014 |pmid=24395894 |doi= |url=}}</ref><ref name="pmid2694136">{{cite journal |vauthors=Jewell DP |title=Aetiology and pathogenesis of ulcerative colitis and Crohn's disease |journal=Postgrad Med J |volume=65 |issue=768 |pages=718–9 |year=1989 |pmid=2694136 |pmc=2429831 |doi= |url=}}</ref><ref name="pmid16819502">{{cite journal |vauthors=Sartor RB |title=Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis |journal=Nat Clin Pract Gastroenterol Hepatol |volume=3 |issue=7 |pages=390–407 |year=2006 |pmid=16819502 |doi=10.1038/ncpgasthep0528 |url=}}</ref><ref name="pmid15656711">{{cite journal |vauthors=Head K, Jurenka JS |title=Inflammatory bowel disease. Part II: Crohn's disease--pathophysiology and conventional and alternative treatment options |journal=Altern Med Rev |volume=9 |issue=4 |pages=360–401 |year=2004 |pmid=15656711 |doi= |url=}}</ref><ref name="pmid24415861">{{cite journal |vauthors=Zhang YZ, Li YY |title=Inflammatory bowel disease: pathogenesis |journal=World J. Gastroenterol. |volume=20 |issue=1 |pages=91–9 |year=2014 |pmid=24415861 |pmc=3886036 |doi=10.3748/wjg.v20.i1.91 |url=}}</ref>
***Initially, [[inflammation]] starts focally around the [[Crypts of Lieberkühn|crypts]], followed by superficial [[ulceration]] of the [[mucosa]].
***TNF-alpha induces expression of adhesion factors that allow for inflammatory cells to infiltrate and activates macrophages resulting in granuloma formations
***The deep [[mucosal]] layers are then invaded in a noncontinuous fashion, and noncaseating [[granulomas]] form, which can invade through the entire thickness of the bowel wall and into the [[mesentery]] and surrounding structures resulting in bleeding.
***The inflammatory response invades through the entire thickness of the bowel wall weakening the surrounding blood vessels resulting in bleeding.
:* '''<u>Ulcerative colitis</u>'''
:* '''<u>Ulcerative colitis</u>'''
:** In [[ulcerative colitis]], [[T cells]], [[cytotoxic]] to the colonic epithelium, accumulate in the [[lamina propria]], accompanied by [[B cells]] that secrete [[immunoglobulin G]] ([[Immunoglobulin G|IgG]]) and [[Immunoglobulin E|IgE]].<ref name="pmid16819502">{{cite journal |vauthors=Sartor RB |title=Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis |journal=Nat Clin Pract Gastroenterol Hepatol |volume=3 |issue=7 |pages=390–407 |year=2006 |pmid=16819502 |doi=10.1038/ncpgasthep0528 |url=}}</ref><ref name="pmid27914657">{{cite journal |vauthors=Ungaro R, Mehandru S, Allen PB, Peyrin-Biroulet L, Colombel JF |title=Ulcerative colitis |journal=Lancet |volume=389 |issue=10080 |pages=1756–1770 |year=2017 |pmid=27914657 |doi=10.1016/S0140-6736(16)32126-2 |url=}}</ref><ref name="pmid11830216">{{cite journal |vauthors=Farrell RJ, Peppercorn MA |title=Ulcerative colitis |journal=Lancet |volume=359 |issue=9303 |pages=331–40 |year=2002 |pmid=11830216 |doi=10.1016/S0140-6736(02)07499-8 |url=}}</ref><ref name="pmid1516252">{{cite journal |vauthors=Rönnblom LE, Janson ET, Perers A, Oberg KE, Alm GV |title=Characterization of anti-interferon-alpha antibodies appearing during recombinant interferon-alpha 2a treatment |journal=Clin. Exp. Immunol. |volume=89 |issue=3 |pages=330–5 |year=1992 |pmid=1516252 |pmc=1554468 |doi= |url=}}</ref>
:** In [[ulcerative colitis]], [[T cells]], [[cytotoxic]] to the colonic epithelium, accumulate in the [[lamina propria]], accompanied by [[B cells]] that secrete [[immunoglobulin G]] ([[Immunoglobulin G|IgG]]) and [[Immunoglobulin E|IgE]].<ref name="pmid16819502">{{cite journal |vauthors=Sartor RB |title=Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis |journal=Nat Clin Pract Gastroenterol Hepatol |volume=3 |issue=7 |pages=390–407 |year=2006 |pmid=16819502 |doi=10.1038/ncpgasthep0528 |url=}}</ref><ref name="pmid27914657">{{cite journal |vauthors=Ungaro R, Mehandru S, Allen PB, Peyrin-Biroulet L, Colombel JF |title=Ulcerative colitis |journal=Lancet |volume=389 |issue=10080 |pages=1756–1770 |year=2017 |pmid=27914657 |doi=10.1016/S0140-6736(16)32126-2 |url=}}</ref><ref name="pmid11830216">{{cite journal |vauthors=Farrell RJ, Peppercorn MA |title=Ulcerative colitis |journal=Lancet |volume=359 |issue=9303 |pages=331–40 |year=2002 |pmid=11830216 |doi=10.1016/S0140-6736(02)07499-8 |url=}}</ref><ref name="pmid1516252">{{cite journal |vauthors=Rönnblom LE, Janson ET, Perers A, Oberg KE, Alm GV |title=Characterization of anti-interferon-alpha antibodies appearing during recombinant interferon-alpha 2a treatment |journal=Clin. Exp. Immunol. |volume=89 |issue=3 |pages=330–5 |year=1992 |pmid=1516252 |pmc=1554468 |doi= |url=}}</ref>
:** This results in [[inflammation]] of the [[crypts of Lieberkuhn]], with [[abscesses]] and [[pseudopolyps]] along with rupturing of minute [[blood vessels]] in [[mucosa]] resulting in bleeding.
:** This results in [[inflammation]] of the [[crypts of Lieberkuhn]], with [[abscesses]] and [[pseudopolyps]] along with  
:** rupturing of minute [[blood vessels]] in [[mucosa]] resulting in bleeding.
*'''<u>Neoplasia</u>'''
*'''<u>Neoplasia</u>'''
:*[[Mutations]] of multiple [[genes]] are required for the formation of [[Colon cancer|adenocarcinoma]], including the [[APC (gene)|APC gene]], [https://en.wikipedia.org/wiki/KRAS Kras], [https://en.wikipedia.org/wiki/DCC DCC], and [[P53 (protein)|p53]].<ref name="pmid12702969">{{cite journal |vauthors=Itzkowitz S |title=Colon carcinogenesis in inflammatory bowel disease: applying molecular genetics to clinical practice |journal=J. Clin. Gastroenterol. |volume=36 |issue=5 Suppl |pages=S70–4; discussion S94–6 |year=2003 |pmid=12702969 |doi= |url=}}</ref><ref name="pmid21530747">{{cite journal |vauthors=Ullman TA, Itzkowitz SH |title=Intestinal inflammation and cancer |journal=Gastroenterology |volume=140 |issue=6 |pages=1807–16 |year=2011 |pmid=21530747 |doi=10.1053/j.gastro.2011.01.057 |url=}}</ref><ref name="pmid19589728">{{cite journal |vauthors=Kraus S, Arber N |title=Inflammation and colorectal cancer |journal=Curr Opin Pharmacol |volume=9 |issue=4 |pages=405–10 |year=2009 |pmid=19589728 |doi=10.1016/j.coph.2009.06.006 |url=}}</ref>  
**Colon cancer arises mostly due to sporadic mutations that originates from the [[epithelial cells]] of [[colon]] or [[rectum]].
:*Certain [[hereditary]] syndromes are also classified by defects in [[DNA]] [[mismatch repair]] genes and [[microsatellite]] instability.
**Genetic instability/mutation results in [[Epigenetic|epigenetic alteration]], [[chronic inflammation]], [[oxidative stress]], and intestinal [[microbiota]].<ref name="pmid12702969">{{cite journal |vauthors=Itzkowitz S |title=Colon carcinogenesis in inflammatory bowel disease: applying molecular genetics to clinical practice |journal=J. Clin. Gastroenterol. |volume=36 |issue=5 Suppl |pages=S70–4; discussion S94–6 |year=2003 |pmid=12702969 |doi= |url=}}</ref><ref name="pmid21530747">{{cite journal |vauthors=Ullman TA, Itzkowitz SH |title=Intestinal inflammation and cancer |journal=Gastroenterology |volume=140 |issue=6 |pages=1807–16 |year=2011 |pmid=21530747 |doi=10.1053/j.gastro.2011.01.057 |url=}}</ref><ref name="pmid19589728">{{cite journal |vauthors=Kraus S, Arber N |title=Inflammation and colorectal cancer |journal=Curr Opin Pharmacol |volume=9 |issue=4 |pages=405–10 |year=2009 |pmid=19589728 |doi=10.1016/j.coph.2009.06.006 |url=}}</ref>
:*As [[tumor]] grows it invades the surrounding tissue disrupting the normal [[vasculature]] along with it
**As [[tumor]] tends to grow slowly it invades the surrounding tissue disrupting the normal blood vessels along with it.
:*Therefore tumors tend to bleed slowly, and patients present with hemoccult positive stools and [[Microcytic anemia|microcytic anemia.]]
**This is responsible for slow occult bleeding that is found positive on FOBT.
 
*'''<u>AV Malformation/Angiodysplasia</u>'''
*'''<u>AV Malformation/Angiodysplasia</u>'''
:*In [[Arteriovenous malformations|AV malformation]] direct connections between [[arteries]] and [[veins]] occur in the colonic [[submucosa]].<ref name="pmid8389094">{{cite journal |vauthors=Foutch PG |title=Angiodysplasia of the gastrointestinal tract |journal=Am. J. Gastroenterol. |volume=88 |issue=6 |pages=807–18 |year=1993 |pmid=8389094 |doi= |url=}}</ref><ref name="pmid9048468">{{cite journal |vauthors=Dodda G, Trotman BW |title=Gastrointestinal angiodysplasia |journal=J Assoc Acad Minor Phys |volume=8 |issue=1 |pages=16–9 |year=1997 |pmid=9048468 |doi= |url=}}</ref><ref name="pmid1744847">{{cite journal |vauthors=Kheterpal S |title=Angiodysplasia: a review |journal=J R Soc Med |volume=84 |issue=10 |pages=615–8 |year=1991 |pmid=1744847 |pmc=1295562 |doi= |url=}}</ref><ref name="pmid311247">{{cite journal |vauthors=Athanasoulis CA, Galdabini JJ, Waltman AC, Novelline RA, Greenfield AJ, Ezpeleta ML |title=Angiodysplasia of the colon: a cause of rectal bleeding |journal=Cardiovasc Radiol |volume=1 |issue=1 |pages=3–13 |year=1977 |pmid=311247 |doi= |url=}}</ref><ref name="pmid24138285">{{cite journal |vauthors=Sami SS, Al-Araji SA, Ragunath K |title=Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management |journal=Aliment. Pharmacol. Ther. |volume=39 |issue=1 |pages=15–34 |year=2014 |pmid=24138285 |doi=10.1111/apt.12527 |url=}}</ref>
:*In [[Arteriovenous malformations|AV malformation]] abnormal connections occur between [[arteries]] and [[veins]].<ref name="pmid8389094">{{cite journal |vauthors=Foutch PG |title=Angiodysplasia of the gastrointestinal tract |journal=Am. J. Gastroenterol. |volume=88 |issue=6 |pages=807–18 |year=1993 |pmid=8389094 |doi= |url=}}</ref><ref name="pmid9048468">{{cite journal |vauthors=Dodda G, Trotman BW |title=Gastrointestinal angiodysplasia |journal=J Assoc Acad Minor Phys |volume=8 |issue=1 |pages=16–9 |year=1997 |pmid=9048468 |doi= |url=}}</ref><ref name="pmid1744847">{{cite journal |vauthors=Kheterpal S |title=Angiodysplasia: a review |journal=J R Soc Med |volume=84 |issue=10 |pages=615–8 |year=1991 |pmid=1744847 |pmc=1295562 |doi= |url=}}</ref><ref name="pmid311247">{{cite journal |vauthors=Athanasoulis CA, Galdabini JJ, Waltman AC, Novelline RA, Greenfield AJ, Ezpeleta ML |title=Angiodysplasia of the colon: a cause of rectal bleeding |journal=Cardiovasc Radiol |volume=1 |issue=1 |pages=3–13 |year=1977 |pmid=311247 |doi= |url=}}</ref><ref name="pmid24138285">{{cite journal |vauthors=Sami SS, Al-Araji SA, Ragunath K |title=Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management |journal=Aliment. Pharmacol. Ther. |volume=39 |issue=1 |pages=15–34 |year=2014 |pmid=24138285 |doi=10.1111/apt.12527 |url=}}</ref>
:*The lack of [[capillary]] buffers causes high pressure blood to enter directly into the venous system, making these [[vessels]] at high risk of rupture into the bowel lumen.
:*This connections results in blood flow from high pressure arteries to low pressure veins without buffering effects of capillaries.
:*In [[Angiodysplasia]], over time, previously healthy blood vessels of the [[cecum]] and [[ascending colon]] [[degenerate]] and become prone to bleeding.
:*The lack of [[capillary]] buffers makes the [[vessels]] weak due to increased blood flow and ultimately bleeding.
:*In [[Angiodysplasia]], with age the connective tissue of the blood vessels become weak.
:*With mild increase in pressure leads to disrupture of vessels leading to painless bleeding.


==Associated Conditions==
==Associated Conditions==
Line 140: Line 144:
* [[Pagetoid]] dyskeratosis  
* [[Pagetoid]] dyskeratosis  
|-
|-
|Mesenteric ischemia <ref name="pmid1731389">{{cite journal |vauthors=Mitsudo S, Brandt LJ |title=Pathology of intestinal ischemia |journal=Surg. Clin. North Am. |volume=72 |issue=1 |pages=43–63 |year=1992 |pmid=1731389 |doi= |url=}}</ref>
|[[Mesenteric ischemia]] <ref name="pmid1731389">{{cite journal |vauthors=Mitsudo S, Brandt LJ |title=Pathology of intestinal ischemia |journal=Surg. Clin. North Am. |volume=72 |issue=1 |pages=43–63 |year=1992 |pmid=1731389 |doi= |url=}}</ref>
|
|
* Hemorrhagic infarctions
* [[Hemorrhagic]] [[Infarction|infarctions]]


* [[Ulcerations]]
* [[Ulcerations]]
* [[Strictures]]
* [[Strictures]]
|
|
* Hemorrhage in lamina propria  
* [[Hemorrhage]] in [[lamina propria]]
* [[Necrosis]] of superficial epithelial   
* [[Necrosis]] of superficial [[epithelial cells]]  
* Deep crypts
* Deep crypts
* [[Fibrosis]]  
* [[Fibrosis]]  
|-
|-
|Ischemic colitis<ref name="pmid1731389">{{cite journal |vauthors=Mitsudo S, Brandt LJ |title=Pathology of intestinal ischemia |journal=Surg. Clin. North Am. |volume=72 |issue=1 |pages=43–63 |year=1992 |pmid=1731389 |doi= |url=}}</ref>
|[[Ischemic colitis]]<ref name="pmid1731389">{{cite journal |vauthors=Mitsudo S, Brandt LJ |title=Pathology of intestinal ischemia |journal=Surg. Clin. North Am. |volume=72 |issue=1 |pages=43–63 |year=1992 |pmid=1731389 |doi= |url=}}</ref>
|
|
* Discrete or serpiginous ulcerations  
* Discrete or [[serpiginous]] [[ulcerations]]
* [[Pseudopolyps]]
* [[Pseudopolyps]]
* Hemorrhagic infractions
* [[Hemorrhagic]] [[Infarction|infarctions]]
* Frank blood or dark mucus in lumen
* Frank blood or dark mucus in lumen
* [[Strictures]]
* [[Strictures]]
|
|
* Necrotizing phlebitis  
* [[Necrotizing]] [[phlebitis]]
* Multiple thrombi  
* Multiple thrombi  
* [[Ulcerations]]
* [[Ulcerations]]
* [[Granulation tissue]] extending into surrounding [[submucosa]] and smooth muscle fibers.
* [[Granulation tissue]] extending into surrounding [[submucosa]] and smooth muscle fibers.
|-
|-
|Crohn's disease<ref name="pmid1089084">{{cite journal |vauthors=Price AB, Morson BC |title=Inflammatory bowel disease: the surgical pathology of Crohn's disease and ulcerative colitis |journal=Hum. Pathol. |volume=6 |issue=1 |pages=7–29 |year=1975 |pmid=1089084 |doi= |url=}}</ref><ref name="pmid9537465">{{cite journal |vauthors=Wright CL, Riddell RH |title=Histology of the stomach and duodenum in Crohn's disease |journal=Am. J. Surg. Pathol. |volume=22 |issue=4 |pages=383–90 |year=1998 |pmid=9537465 |doi= |url=}}</ref> 
|[[Crohn's disease]]<ref name="pmid1089084">{{cite journal |vauthors=Price AB, Morson BC |title=Inflammatory bowel disease: the surgical pathology of Crohn's disease and ulcerative colitis |journal=Hum. Pathol. |volume=6 |issue=1 |pages=7–29 |year=1975 |pmid=1089084 |doi= |url=}}</ref><ref name="pmid9537465">{{cite journal |vauthors=Wright CL, Riddell RH |title=Histology of the stomach and duodenum in Crohn's disease |journal=Am. J. Surg. Pathol. |volume=22 |issue=4 |pages=383–90 |year=1998 |pmid=9537465 |doi= |url=}}</ref> 
|
|
* Creeping fat
* Creeping fat
* Thick/rubbery intestinal wall  
* Thick/rubbery [[intestinal wall]]
* [[Strictures]] (string sign on barium enema)
* [[Strictures]] (string sign on barium enema)
* Skip areas
* Skip areas
* [[Aphthous ulcers|Aphthous mucosal ulcers]]
* [[Aphthous ulcers|Aphthous mucosal ulcers]]
|
|
* Superficial or deep ulcerations  
* Superficial or deep [[ulcerations]]
* [[Granulation tissue]] extending into surrounding [[submucosa]] and smooth muscle fibers.
* [[Granulation tissue]] extending into surrounding [[submucosa]] and smooth muscle fibers.
* Transmural inflammation with lymphoid aggregates
* Transmural inflammation with lymphoid aggregates
* [[Goblet cells]]  
* [[Goblet cells]]  
* Focal neutrophils in epithelium
* Focal [[neutrophils]] in [[epithelium]]
* Lymphoid aggregates  
* [[Lymphoid]] aggregates  
* [[Plasmacytosis]]
* [[Plasmacytosis]]
* Edematous mucosa and submucosa  
* Edematous [[mucosa]] and [[submucosa]]
|-
|-
|Ulcerative colitis<ref name="pmid24942757">{{cite journal |vauthors=DeRoche TC, Xiao SY, Liu X |title=Histological evaluation in ulcerative colitis |journal=Gastroenterol Rep (Oxf) |volume=2 |issue=3 |pages=178–92 |year=2014 |pmid=24942757 |pmc=4124271 |doi=10.1093/gastro/gou031 |url=}}</ref>
|[[Ulcerative colitis]]<ref name="pmid24942757">{{cite journal |vauthors=DeRoche TC, Xiao SY, Liu X |title=Histological evaluation in ulcerative colitis |journal=Gastroenterol Rep (Oxf) |volume=2 |issue=3 |pages=178–92 |year=2014 |pmid=24942757 |pmc=4124271 |doi=10.1093/gastro/gou031 |url=}}</ref>
|
|
* Deep fissuring ulcerations
* Deep fissuring [[ulcerations]]
* Hemorrhagic mucosa  
* [[Hemorrhagic]] [[mucosa]]
* [[Pseudopolyps]]  
* [[Pseudopolyps]]  
|
|
* Mononuclear inflammatory infiltrate in lamina propria
* [[Mononuclear cells|Mononuclear]] inflammatory infiltrate in [[lamina propria]]
* Crypt abscesses   
* [[Crypt (anatomy)|Crypt]] [[abscesses]]  
* [[Granulation tissue]] extending into surrounding [[submucosa]] and smooth muscle fibers.
* [[Granulation tissue]] extending into surrounding [[submucosa]] and smooth muscle fibers.
* Submucosal fibrosis  
* [[Submucosal]] [[fibrosis]]
* Schwann cell proliferation
* [[Schwann cell]] [[proliferation]]
|}
|}


Latest revision as of 22:47, 28 December 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Superior mesenteric artery and inferior mesenteric artery are the two major blood vessels that supply lower gastrointestinal tract. Disruption of blood vessel junction, formed by these two vessels, by any of the disease process results in bleeding. Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by ano-rectal disease, ischemia of bowel, inflammatory bowel disease (IBD), neoplasia, and arteriovenous (AV) malformations. The characteristic gross and microscopic findings of lower gastrointestinal tracts depends upon the underlying pathology.

Pathophysiology

Blood supply

Lower GI Tract Arterial Supply Venous Drainage
Midgut
Hindgut
ɸ -Except lower rectum, which drains into the systemic circulation.
Blood supply to the intestines includes the celiac artery, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the internal iliac artery (IIA).
Source: By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons

Pathogenesis

The pathogenesis of lower gastrointestinal bleeding can be discussed based on the etiology. Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by anorectal disease, ischemia, inflammatory bowel disease (IBD), neoplasia, and arteriovenous (AV) malformations.

Diagram of sigmoid diverticulum
Source:By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons
  • Anorectal disease
  • Hemorrhoids are defined as swelling and inflammation of veins in the rectal and anal region
  • Hemorrhoids can be either internal or external based on their relation to dentate line.
  • The first step in the pathogenesis of either type of hemorrhoids is weakening of the surrounding connective tissue and vein wall.[8][9][8]
  • Weakening of blood vessels can result in bleeding under pressure.
  • An anal fissure can be defined as disruption or tear in the mucosal surface of the skin.
  • During defecation, due to increased pressure which can exaggerate the tears may present as bright red rectal bleeding with severe periodic pain.[10]
  • Mesenteric ischemia results when there is inadequate blood supply at the level of the small intestine.[11][12][13][14]
  • 2 or more vessels (celiac, SMA, or IMA) must be involved for bleeding to occur.
  • Decreased blood supply can occur due to obstruction of blood vessel either by emobolus or due to vasoconstriction effect of drugs.
  • Decreased blood supply initiates necrosis of mucosal surface of intestine.
  • unopposed blood deprivation leads to trans-mural necrosis and ultimately sloughing of the tissues with associated bleeding.
  • Ischemic colitis is a condition in which injury of the large intestine results from decreased blood supply.[15][16][17]
  • The colon is most commonly involved due the presence of water shed areas ( splenic flexure and hepatic flexure).
  • Similar to mesentric ischemia bleeding occurs due to necrosis and sloughing of mucosal membrane.
  • AV Malformation/Angiodysplasia
  • In AV malformation abnormal connections occur between arteries and veins.[32][33][34][35][36]
  • This connections results in blood flow from high pressure arteries to low pressure veins without buffering effects of capillaries.
  • The lack of capillary buffers makes the vessels weak due to increased blood flow and ultimately bleeding.
  • In Angiodysplasia, with age the connective tissue of the blood vessels become weak.
  • With mild increase in pressure leads to disrupture of vessels leading to painless bleeding.

Associated Conditions

Other diseases that are commonly associated with lower gastrointestinal bleeding include:

Gross and Microscopic Pathology

Disease Gross Pathology Microscopic Pathology
Diverticulosis[37]
Angiodysplasia[38]
Hemorrhoids[8]
  • Tortuous superficial dilatations of multiple blood vessels.
Mesenteric ischemia [39]
Ischemic colitis[39]
Crohn's disease[40][41] 
Ulcerative colitis[42]

References

  1. ↑ Geboes K, Geboes KP, Maleux G (2001). "Vascular anatomy of the gastrointestinal tract". Best Pract Res Clin Gastroenterol. 15 (1): 1–14. doi:10.1053/bega.2000.0152. PMID 11355897.
  2. ↑ Granger DN, Holm L, Kvietys P (2015). "The Gastrointestinal Circulation: Physiology and Pathophysiology". Compr Physiol. 5 (3): 1541–83. doi:10.1002/cphy.c150007. PMID 26140727.
  3. ↑ "The Gastrointestinal Circulation - NCBI Bookshelf".
  4. ↑ Hobson KG, Roberts PL (2004). "Etiology and pathophysiology of diverticular disease". Clin Colon Rectal Surg. 17 (3): 147–53. doi:10.1055/s-2004-832695. PMC 2780060. PMID 20011269.
  5. ↑ Maykel JA, Opelka FG (2004). "Colonic diverticulosis and diverticular hemorrhage". Clin Colon Rectal Surg. 17 (3): 195–204. doi:10.1055/s-2004-832702. PMC 2780065. PMID 20011276.
  6. ↑ Comparato G, Pilotto A, Franzè A, Franceschi M, Di Mario F (2007). "Diverticular disease in the elderly". Dig Dis. 25 (2): 151–9. doi:10.1159/000099480. PMID 17468551.
  7. ↑ Matrana MR, Margolin DA (2009). "Epidemiology and pathophysiology of diverticular disease". Clin Colon Rectal Surg. 22 (3): 141–6. doi:10.1055/s-0029-1236157. PMC 2780269. PMID 20676256.
  8. ↑ 8.0 8.1 8.2 Lohsiriwat V (2012). "Hemorrhoids: from basic pathophysiology to clinical management". World J. Gastroenterol. 18 (17): 2009–17. doi:10.3748/wjg.v18.i17.2009. PMC 3342598. PMID 22563187.
  9. ↑ Sanchez C, Chinn BT (2011). "Hemorrhoids". Clin Colon Rectal Surg. 24 (1): 5–13. doi:10.1055/s-0031-1272818. PMC 3140328. PMID 22379400.
  10. ↑ Holland RA, Rimes AF, Comis A, Tyndale-Biscoe CH (1988). "Oxygen carriage and carbonic anhydrase activity in the blood of a marsupial, the Tammar wallaby (Macropus eugenii), during early development". Respir Physiol. 73 (1): 69–86. PMID 3140330.
  11. ↑ Krupski WC, Selzman CH, Whitehill TA (1997). "Unusual causes of mesenteric ischemia". Surg. Clin. North Am. 77 (2): 471–502. PMID 9146726.
  12. ↑ Walker TG (2009). "Mesenteric ischemia". Semin Intervent Radiol. 26 (3): 175–83. doi:10.1055/s-0029-1225662. PMC 3036494. PMID 21326562.
  13. ↑ Berland T, Oldenburg WA (2008). "Acute mesenteric ischemia". Curr Gastroenterol Rep. 10 (3): 341–6. PMID 18625147.
  14. ↑ Mastoraki A, Mastoraki S, Tziava E, Touloumi S, Krinos N, Danias N, Lazaris A, Arkadopoulos N (2016). "Mesenteric ischemia: Pathogenesis and challenging diagnostic and therapeutic modalities". World J Gastrointest Pathophysiol. 7 (1): 125–30. doi:10.4291/wjgp.v7.i1.125. PMC 4753178. PMID 26909235.
  15. ↑ FitzGerald JF, Hernandez Iii LO (2015). "Ischemic colitis". Clin Colon Rectal Surg. 28 (2): 93–8. doi:10.1055/s-0035-1549099. PMC 4442720. PMID 26034405.
  16. ↑ Theodoropoulou A, Koutroubakis IE (2008). "Ischemic colitis: clinical practice in diagnosis and treatment". World J. Gastroenterol. 14 (48): 7302–8. PMC 2778113. PMID 19109863.
  17. ↑ Rania H, Mériam S, Rym E, Hyafa R, Amine A, Najet BH, Lassad G, Mohamed TK (2014). "Ischemic colitis in five points: an update 2013". Tunis Med. 92 (5): 299–303. PMID 25504381.
  18. ↑ Kim DH, Cheon JH (2017). "Pathogenesis of Inflammatory Bowel Disease and Recent Advances in Biologic Therapies". Immune Netw. 17 (1): 25–40. doi:10.4110/in.2017.17.1.25. PMC 5334120. PMID 28261018.
  19. ↑ Hendrickson BA, Gokhale R, Cho JH (2002). "Clinical aspects and pathophysiology of inflammatory bowel disease". Clin. Microbiol. Rev. 15 (1): 79–94. PMC 118061. PMID 11781268.
  20. ↑ Woźniak-Parnowska W, Werakso B (1974). "[Comparative studies of microbiological purity of ointments by the direct culture method and use of membrane filters]". Acta Pol Pharm (in Polish). 31 (6): 819–23. PMID 4447044.
  21. ↑ Mazal J (2014). "Crohn disease: pathophysiology, diagnosis, and treatment". Radiol Technol. 85 (3): 297–316, quiz 317–20. PMID 24395894.
  22. ↑ Jewell DP (1989). "Aetiology and pathogenesis of ulcerative colitis and Crohn's disease". Postgrad Med J. 65 (768): 718–9. PMC 2429831. PMID 2694136.
  23. ↑ 23.0 23.1 Sartor RB (2006). "Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis". Nat Clin Pract Gastroenterol Hepatol. 3 (7): 390–407. doi:10.1038/ncpgasthep0528. PMID 16819502.
  24. ↑ Head K, Jurenka JS (2004). "Inflammatory bowel disease. Part II: Crohn's disease--pathophysiology and conventional and alternative treatment options". Altern Med Rev. 9 (4): 360–401. PMID 15656711.
  25. ↑ Zhang YZ, Li YY (2014). "Inflammatory bowel disease: pathogenesis". World J. Gastroenterol. 20 (1): 91–9. doi:10.3748/wjg.v20.i1.91. PMC 3886036. PMID 24415861.
  26. ↑ Ungaro R, Mehandru S, Allen PB, Peyrin-Biroulet L, Colombel JF (2017). "Ulcerative colitis". Lancet. 389 (10080): 1756–1770. doi:10.1016/S0140-6736(16)32126-2. PMID 27914657.
  27. ↑ Farrell RJ, Peppercorn MA (2002). "Ulcerative colitis". Lancet. 359 (9303): 331–40. doi:10.1016/S0140-6736(02)07499-8. PMID 11830216.
  28. ↑ Rönnblom LE, Janson ET, Perers A, Oberg KE, Alm GV (1992). "Characterization of anti-interferon-alpha antibodies appearing during recombinant interferon-alpha 2a treatment". Clin. Exp. Immunol. 89 (3): 330–5. PMC 1554468. PMID 1516252.
  29. ↑ Itzkowitz S (2003). "Colon carcinogenesis in inflammatory bowel disease: applying molecular genetics to clinical practice". J. Clin. Gastroenterol. 36 (5 Suppl): S70–4, discussion S94–6. PMID 12702969.
  30. ↑ Ullman TA, Itzkowitz SH (2011). "Intestinal inflammation and cancer". Gastroenterology. 140 (6): 1807–16. doi:10.1053/j.gastro.2011.01.057. PMID 21530747.
  31. ↑ Kraus S, Arber N (2009). "Inflammation and colorectal cancer". Curr Opin Pharmacol. 9 (4): 405–10. doi:10.1016/j.coph.2009.06.006. PMID 19589728.
  32. ↑ Foutch PG (1993). "Angiodysplasia of the gastrointestinal tract". Am. J. Gastroenterol. 88 (6): 807–18. PMID 8389094.
  33. ↑ Dodda G, Trotman BW (1997). "Gastrointestinal angiodysplasia". J Assoc Acad Minor Phys. 8 (1): 16–9. PMID 9048468.
  34. ↑ Kheterpal S (1991). "Angiodysplasia: a review". J R Soc Med. 84 (10): 615–8. PMC 1295562. PMID 1744847.
  35. ↑ Athanasoulis CA, Galdabini JJ, Waltman AC, Novelline RA, Greenfield AJ, Ezpeleta ML (1977). "Angiodysplasia of the colon: a cause of rectal bleeding". Cardiovasc Radiol. 1 (1): 3–13. PMID 311247.
  36. ↑ Sami SS, Al-Araji SA, Ragunath K (2014). "Review article: gastrointestinal angiodysplasia - pathogenesis, diagnosis and management". Aliment. Pharmacol. Ther. 39 (1): 15–34. doi:10.1111/apt.12527. PMID 24138285.
  37. ↑ West AB, Losada M (2004). "The pathology of diverticulosis coli". J. Clin. Gastroenterol. 38 (5 Suppl 1): S11–6. PMID 15115923.
  38. ↑ Stamm B, Heer M, Bühler H, Ammann R (1985). "Mucosal biopsy of vascular ectasia (angiodysplasia) of the large bowel detected during routine colonoscopic examination". Histopathology. 9 (6): 639–46. PMID 4029903.
  39. ↑ 39.0 39.1 Mitsudo S, Brandt LJ (1992). "Pathology of intestinal ischemia". Surg. Clin. North Am. 72 (1): 43–63. PMID 1731389.
  40. ↑ Price AB, Morson BC (1975). "Inflammatory bowel disease: the surgical pathology of Crohn's disease and ulcerative colitis". Hum. Pathol. 6 (1): 7–29. PMID 1089084.
  41. ↑ Wright CL, Riddell RH (1998). "Histology of the stomach and duodenum in Crohn's disease". Am. J. Surg. Pathol. 22 (4): 383–90. PMID 9537465.
  42. ↑ DeRoche TC, Xiao SY, Liu X (2014). "Histological evaluation in ulcerative colitis". Gastroenterol Rep (Oxf). 2 (3): 178–92. doi:10.1093/gastro/gou031. PMC 4124271. PMID 24942757.

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