Angiodysplasia overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Exact etiology of angiodysplasia is unclear. Various theories appear in the literature. According to one theory, ageing and intermittent, low-grade obstruction of submucosal veins in the muscularis propria layer leads to the formation of small arterio-venous collaterals. Another theory states that due to chronic hypoxia | Exact etiology of angiodysplasia is unclear. Various theories appear in the literature. According to one theory, ageing and intermittent, low-grade obstruction of submucosal veins in the muscularis propria layer leads to the formation of small arterio-venous collaterals. Another theory states that due to chronic hypoxia angiogenic factors like vascular endothelial growth factor (VEGF) and basic fibroblast growth factor increase which contribute to the development of angiodysplasia. <ref name="pmid31210709">{{cite journal| author=García-Compeán D, Del Cueto-Aguilera ÁN, Jiménez-Rodríguez AR, González-González JA, Maldonado-Garza HJ| title=Diagnostic and therapeutic challenges of gastrointestinal angiodysplasias: A critical review and view points. | journal=World J Gastroenterol | year= 2019 | volume= 25 | issue= 21 | pages= 2549-2564 | pmid=31210709 | doi=10.3748/wjg.v25.i21.2549 | pmc=6558444 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31210709 }} </ref> A proposed mechanism that may lead to the development of angiodysplasia in aortic stenosis is the development of acquired von Willebrand disease (VWD) from mechanical disruption of von Willebrand factor multimers during their passage from the stenosed aortic valve. | ||
==Differentiating {{PAGENAME}} from Other Diseases== | ==Differentiating {{PAGENAME}} from Other Diseases== | ||
<br /> | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
==Risk Factors== | ==Risk Factors== | ||
The risk factors | |||
==Screening== | ==Screening== | ||
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Overview
In medicine (gastroenterology), angiodysplasia is a small, acquired vascular malformation of the gut. It is a common cause of otherwise unexplained gastrointestinal bleeding and anemia, especially after sixth decade of life. Lesions are often multiple, and frequently involve the cecum or ascending colon, although they can occur at other places. Treatment may be with endoscopic interventions, medication, or occasionally surgery.
Historical Perspective
The first case of angiodysplasia was described in a letter to the London Medical Gazette by Phillips as a vascular abnormality causing bleeding from the large bowel in 1839. However, the term "Angiodysplasia" was coined by Galdabini in 1974. Due to the unknown etiology of these lesions, multiple terms have been used, like arteriovenous malformation, telangiectasia, angioma, and hemangioma.[1]
Classification
One system of classification is based on location, size, and number of angiodysplasias. [2]
| Location | Size | Number of lesions |
|---|---|---|
| Gastric | Minute (<2 mm in diameter) | Unique (n = 1) |
| Duodenal | Intermediate (2 to 5 mm) | Multiple (n = 2 to 10) |
| Jejunal | Large (>5 mm) | Diffuse (n > 10) |
| Colonic | ||
| For example, "D-S2-N3" signifies multiple angiodysplasias of intermediate size in the duodenum. | ||
Another system of classification uses endoscopic techniques to classify angiodysplasia depending on size, bleeding and surrounding venous dilatation. [3]
Type 1: Angioectasias:
Type 1 a - punctulate erythema (< 1 mm), with or without oozing
Type 1 b - patchy erythema (a few mm), with or without oozing
Type 2: Dieulafoy's lesions:
Type 2 a - punctulate lesions (< 1 mm), with pulsatile bleeding
Type 2b - pulsatile red protrusion, without surrounding venous dilatation
Type 3 - pulsatile red protrusion, with surrounding venous dilatation
Type 4 - other lesions not classified into any of the above categories.
Pathophysiology
Exact etiology of angiodysplasia is unclear. Various theories appear in the literature. According to one theory, ageing and intermittent, low-grade obstruction of submucosal veins in the muscularis propria layer leads to the formation of small arterio-venous collaterals. Another theory states that due to chronic hypoxia angiogenic factors like vascular endothelial growth factor (VEGF) and basic fibroblast growth factor increase which contribute to the development of angiodysplasia. [4] A proposed mechanism that may lead to the development of angiodysplasia in aortic stenosis is the development of acquired von Willebrand disease (VWD) from mechanical disruption of von Willebrand factor multimers during their passage from the stenosed aortic valve.
Differentiating Angiodysplasia overview from Other Diseases
Epidemiology and Demographics
Risk Factors
The risk factors
Screening
Natural History, Complications, and Prognosis
Natural History
Complications
Prognosis
Diagnosis
Diagnostic Criteria
History and Symptoms
Physical Examination
Laboratory Findings
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ Athanasoulis, C. A.; Galdabini, J. J.; Waltman, A. C.; Novelline, R. A.; Greenfield, A. J.; Ezpeleta, M. L. (1978). "Angiodysplasia of the colon: A cause of rectal bleeding". Cardiovascular Radiology. 1 (1): 3–13. doi:10.1007/BF02551967. ISSN 0342-7196.
- ↑ Schmit A, Van Gossum A (1998). "Proposal for an endoscopic classification of digestive angiodysplasias for therapeutic trials. The European Club of Enteroscopy". Gastrointest Endosc. 48 (6): 659. doi:10.1016/s0016-5107(98)70080-x. PMID 9852467.
- ↑ Yano T, Yamamoto H, Sunada K, Miyata T, Iwamoto M, Hayashi Y; et al. (2008). "Endoscopic classification of vascular lesions of the small intestine (with videos)". Gastrointest Endosc. 67 (1): 169–72. doi:10.1016/j.gie.2007.08.005. PMID 18155439.
- ↑ García-Compeán D, Del Cueto-Aguilera ÁN, Jiménez-Rodríguez AR, González-González JA, Maldonado-Garza HJ (2019). "Diagnostic and therapeutic challenges of gastrointestinal angiodysplasias: A critical review and view points". World J Gastroenterol. 25 (21): 2549–2564. doi:10.3748/wjg.v25.i21.2549. PMC 6558444 Check
|pmc=value (help). PMID 31210709.