Lower gastrointestinal bleeding pathophysiology: Difference between revisions

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:*[[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 mesenetric ischemia affects critically ill patients who are vasopressor-dependent.
:*Non occlusive [[mesenteric ischemia]] affects critically ill patients who are [[vasopressor]]-dependent.
:*[[Venous thrombosis]] of the visceral vessels can also precipitate an acute ischemic event.
:*[[Venous thrombosis]] of the [[visceral]] [[vessels]] can also precipitate an [[acute]] [[ischemic]] event.
:*Decreased blood flow leads to transmural infarction with [[necrosis]] and [[perforation]].
:*Decreased blood flow leads to transmural [[infarction]] with [[necrosis]] and [[perforation]].
:*Associated mucosal sloughing results in 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 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>  
:*It can be [[gangrenous]] or nongangrenous, acute, transient, or chronic.
:*It can be [[gangrenous]] or nongangrenous, acute or chronic, transient or permanent.
:*The [[Colon (anatomy)|left colon]] is predominantly affected, with the [[splenic flexure]] having increased susceptibility.
:*The [[Colon (anatomy)|left colon]] is predominantly affected, with the [[splenic flexure]] having increased susceptibility.
:*Intraluminal [[hemorrhage]] occurs as the [[mucosa]] becomes [[necrotic]], sloughs, and bleeds.
:*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]].
:*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]], which causes 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]].
***Initially, [[inflammation]] starts focally around the [[Crypts of Lieberkühn|crypts]], followed by superficial [[ulceration]] of the [[mucosa]].
***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 and into the mesentery and surrounding structures resulting in bleeding
***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.
:* '''<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]], Kras, 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>  
:*Mutations of multiple genes are required for the formation of [[Colon cancer|adenocarcinoma]], including the [[APC (gene)|APC gene]], Kras, 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>  

Revision as of 17:08, 21 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
  • Neoplasia
  • Mutations of multiple genes are required for the formation of adenocarcinoma, including the APC gene, Kras, DCC, and p53.[29][30][31]
  • Certain hereditary syndromes are also classified by defects in DNA mismatch repair genes and microsatellite instability.
  • As tumor grows it invades the surrounding tissue disrupting the normal vasculature along with it
  • Therefore tumors tend to bleed slowly, and patients present with hemocult positive stools and microcytic anemia.
  • AV Malformation/Angiodysplasia

Associated Conditions

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

Gross and Microscopic Pathology

Disease Gross Pathology Microscopic Pathology
Diverticulosis[37]
  • Numerous visible flask like protrusions along the intestinal wall.
  • Thick and corrugated circular muscle fibers with mucosal folds.
Angiodysplasia[38]
  • Tortuous dilation of multiple small submucosal and mucosal blood vessels.
  • Clusters of numerous dilated and thin-walled vessels in mucosa and submucosa.
  • Erosion of surrounding mucosa.
Hemorrhoids[8]
  • Tortuous superficial dilations of multiple blood vessels.
  • Dilated, thick-walled, congested submucosal vessels
  • Papillary endothelial hyperplasia
  • Superficial ulcerations
  • Pagetoid dyskeratosis
Mesenteric ischemia [39]
  • Hemorrhagic infarctions
  • Hemorrhage in lamina propria
  • Necrosis of superficial epithelial
  • Deep crypts
  • Fibrosis
Ischemic colitis[39]
  • Discrete or serpiginous ulcerations
  • Pseudopolyps
  • Hemorrhagic infractions
  • Frank blood or dark mucus in lumen
  • Strictures
Crohn's disease[40][41] 
  • Superficial or deep ulcerations
  • Granulation tissue extending into surrounding submucosa and smooth muscle fibers.
  • Transmural inflammation with lymphoid aggregates
  • Goblet cells
  • Focal neutrophils in epithelium
  • Lymphoid aggregates
  • Plasmacytosis
  • Edematous mucosa and submucosa
Ulcerative colitis[42]
  • Mononuclear inflammatory infiltrate in lamina propria
  • Crypt abscesses
  • Granulation tissue extending into surrounding submucosa and smooth muscle fibers.
  • Submucosal fibrosis
  • Schwann cell proliferation

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.
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  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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