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Angiodysplasia physical examination

2018-10-18T16:16:16Z

Aishwarya Taneja: /* Physical Examination */

__NOTOC__
{{Angiodysplasia}}
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==Overview==

==Physical Examination==
[[Fecal occult blood]] testing is positive when bleeding is active.

If bleeding is intermittent the test may be negative at times.

==References==
{{Reflist|2}}

[[Category:Gastroenterology]]

{{WS}}
{{WH}}

Angiodysplasia history and symptoms

2018-10-18T15:00:26Z

Aishwarya Taneja: /* Symptoms */

__NOTOC__
{{Angiodysplasia}}
{{CMG}}

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==Overview==

==History==
* Many patients with angiodysplasia lack symptoms. Others present with GI bleeding or its consequences.
* The incidence of active GI bleed in patients with angiodysplasia is less than 10%. However, because these lesions may be located throughout the GI tract and because the rate of bleeding may be variable, presentation ranges from bloody vomiting or rectal bleeding to occult iron deficiency anemia.
* Bleeding is usually chronic or recurrent and, in most cases, low grade and painless because of the venous source.
* GI bleeding from small bowel lesions has occurred in as many as 22% of patients. In 50% of patients with gastric/stomach and duodenal angiodysplasia have multiple lesions / EGD with colon lesions associated in 20%. Lesions in the colon are more frequently multiple than single.
* Bloody vomit frequently is observed in patients with angiodysplasia of the upper GI tract. Presentation with low grade chronic bleeding is typical and may have had bleeding from days to years. Bleeding from colon lesions most often is chronic and low grade, but as many as 15% of patients present with acute massive hemorrhage.
* Patients may present with rectal bleeding (0-60%), melena (passing black tarry bloody stool) (0-26%), occult blood positive stool (4-47%), or iron deficiency anemia (0-51%).
* Spontaneous cessation of bleeding (90%) is the rule for lesions located in any part of the GI tract

==Symptoms==
* Hematochezia ( 60%)
* Melena ( 26%)
* Hematemesis observed in angiodysplasia of the upper GI tract.

==References==
{{Reflist|2}}

[[Category:Gastroenterology]]

{{WS}}
{{WH}}

Angiodysplasia screening

2018-10-18T14:53:13Z

Aishwarya Taneja: /* Screening */

__NOTOC__
{{Angiodysplasia}}
{{CMG}} {{AE}}

{{PleaseHelp}}

==Overview==

==Screening==
No specific screening indications has been mentioned.

==References==
{{reflist|2}}

[[Category:Gastroenterology]]

{{WS}}
{{WH}}

Angiodysplasia risk factors

2018-10-11T00:36:30Z

Aishwarya Taneja: /* Risk Factors */

__NOTOC__
{{Angiodysplasia}}
{{CMG}} {{AE}}- -

Please help WikiDoc by adding more content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing.

==Overview==

==Risk Factors ==
[[Category:Gastroenterology]]
{{WS}}
{{WH}}

The conditions most commonly associated with Angiodysplasia are:

=== 1.Aortic stenosis (AS) ===
- Heyde ''et al'' and then Schwartz ''et al'' were the first to report a possible association between AS and bleeding from AD in 1958. This was called ‘Heyde's Syndrome’.

- A retrospective case–control study of 1443 patients found that the incidence of AS in patients with OGIB was much higher (25.5%) compared with controls (4.4).

- Further support for this hypothesis comes from evidence of improvement or cessation of chronic GI bleeding in the vast majority of patients with AS after aortic valve replacement (AVR). This effect was sustained for up to 12 years after surgery in the largest case series of 91 patients.

- This observation has led to the hypothesis that abnormal von Willebrand factors (vWF) could provide the explanation to the increased risk of bleeding in patients with AS or aortic sclerosis and otherwise ‘silent’ AD.

=== Von Willebrand disease (vWD) ===
- Patients with certain subtypes of vWD are at an increased risk of GI bleeding from colonic AD. These patients have low levels of the high molecular weight (HMW) multimers of vWF, which is either hereditary (type 2a vWD) or acquired (AS).

=== Chronic renal failure (CRF) ===
- AD is more common in patients with CRF . Prevalence is related to the duration and severity of the kidney disease.

- AD accounts for 19–32% of Lower GI bleeding episodes in patients with CRF compared with 5–6% of episodes in the general population.

- Likewise, gastric and small bowel AD are reportedly the most common causes of upper GI bleeding and OGIB in these patients, respectively.

- Patients with CRF are at an increased risk of bleeding due to several mechanisms including uraemic platelet dysfunction75, 76 and use of anti‐coagulants.77 The causes of platelet dysfunction (aggregation and adhesion) are thought to be due to both intrinsic and extrinsic factors.76, 78 Intrinsic factors include reduced levels of agonists like adenosine diphosphate, serotonin, epinephrine, thrombin and collagen leading to impaired platelet function.79 It has also been noted that levels of platelet cyclic adenosine mono‐phosphate –which causes platelet dysfunction by mobilizing calcium – were high in patients with CRF. Extrinsic factors include release of toxins and increased nitric oxide, which inhibits platelet‐to‐platelet interaction and affects platelet to vessel wall interaction.

- AD is therefore an important cause of GI bleeding in patients with CRF. Other factors, which contribute to abnormalities in haemostasis, include reduced production of erythropoietin and effect of drugs.79

Angiodysplasia epidemiology and demographics

2018-10-11T00:21:00Z

Aishwarya Taneja: /* Epidemiology and Demographics */

__NOTOC__
{{Angiodysplasia}}
{{CMG}} {{AE}}

<sup>[44]</sup>{{PleaseHelp}}

==Overview==

==Epidemiology and Demographics==

[[Category:Gastroenterology]]
AD is the most common vascular malformation of the GI tract in the general population.

=== United States statistics ===
The incidence of colonic diverticular and angiodysplasia bleeding per 100 000 person-years increased over time. Recent recorded drug intake showed an increased frequency of anticoagulants with colonic diverticular and angiodysplasia bleeding, whereas NSAID and low-dose aspirin use were more prevalent in peptic ulcer bleeding and colonic diverticular bleeding, respectively.

The prevalence of angiodysplasia is 0.8% in healthy patients older than 50 years who are undergoing screening colonoscopy.

Foutch et al noted the prevalence of angiodysplasia to be 0.83% from 3 prospective studies in which screening colonoscopies were performed in 964 asymptomatic individuals (mean age, 62 y). Angiodysplasia is the most common reason (50%) for occult GI bleeding. The pooled completion rate was 84%. The pooled retention rates were approximately 2%.

Angiodysplasia accounts for 20-30% of GI bleeding episodes in patients with end-stage renal disease and up to 50% of recurrent GI bleeding in this patient population. Patients with Von Willebrand disease may have an increased incidence of GI bleeding from colonic angiodysplasia.

=== International statistics ===
No widespread studies to determine the international incidence of angiodysplasia have been conducted, but the incidence probably is similar to that in the United States.

Colonic angiodysplasia in Japanese patients is predominantly located in the left colon, whereas in Western patients it is mainly located in the right colon.

The percentage of colonic lesions with a size of more than 5 mm or elevated type detected in Japanese patients was significantly higher than in Western patients.

=== Race-, sex-, and age-related demographics ===
No racial predilection exists in cases of angiodysplasia of the colon.

Angiodysplasia of the colon occurs with equal frequency in men and women.

Most patients found to have angiodysplasia are older than 60 years; of these patients, most are older than 70 years. However, case reports exist of occurrence in young people.

=== Location wise statistics: ===

=== Upper GI tract ===
AD is reportedly the cause in 4–7% of patients presenting with nonvariceal upper GI bleeding. In the largest study, 676 patients underwent endoscopy for suspected UGIB over a 40‐month period. AD was found in 4% of patients, of whom 77% had experienced at least one episode of overt upper GI bleeding (hematemesis or melena) and the rest had features of occult GI bleeding. Multiple lesions were found in 63% of cases and colonic AD was detected 50% of those who had a colonoscopy performed.

=== Small bowel ===
In patients under 50 years of age with obscure GI bleeding (OGIB), small bowel tumors are commonly identified as the cause in 5–7%. However, in patients older than 50 years, the source is likely to be small bowel AD.

Liao ''et al''. performed a systematic review of all original articles relevant to wireless capsule endoscopy (WCE) for the evaluation of patients with small bowel signs and symptoms published between 2000 and 2008. A total of 227 studies involving 22 840 procedures were included. OGIB (overt and occult) was the most common indication (66.0%) and AD was the most common cause (50.0%) of bleeding in those patients. In another study, small bowel AD lesions were the most common cause of severe life‐threatening overt OGIB.

=== Colon ===
The colon is the most frequent site of AD in the GI tract. In western patients, lesions are predominantly located in the caecum and ascending colon (54–81.9%), while lesions diagnosed in Japanese patients are more likely to be in the descending colon (41.7%). The prevalence of colonic AD in healthy asymptomatic adults was estimated to be 0.83% and none of these individuals developed bleeding over a mean follow‐up duration of 3 years.

Therefore, treatment of nonbleeding lesions is generally not recommended. The frequency of colonic AD as a cause of lower GI haemorrhage varies between 3% and 40%. Bleeding from colonic AD can be mild, chronic, recurrent and can stop spontaneously in up to 90% of patients; nonetheless, it can also be life threatening.

Approximately 40–60% of patients with upper or lower GI AD have more than one lesion and 27% of patients with colonic AD had multiple lesions involving two or more segments of the large bowel.28 Moreover, while AD is usually present in the same part of the GI tract, synchronous lesions elsewhere can occur in approximately 20% of patients.

These findings suggest that local factors may be important in the pathogenesis of nonhereditary AD. It also highlights the importance of evaluating both the upper and lower GI tract in patients with symptomatic AD. AD can only be confidently diagnosed as the cause of blood loss if it was actively bleeding at the time of endoscopy.

{{WS}}
{{WH}}

Angiodysplasia differential diagnosis

2018-10-11T00:08:07Z

Aishwarya Taneja: /* Overview */

__NOTOC__
{{Angiodysplasia}}
{{CMG}} {{AE}}

==Overview==
Angiodysplasia must be differentiated from other diseases that cause hematochezia, melena, and iron deficiency anemia , such as hemorrhoids, diverticular disease and colon cancer.

==Differentiating Angiodysplasia from other Diseases==

Angiodysplasia must be differentiated from Diverticulosis, Colon cancer, and Hemorrhoids.
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Diseases
| colspan="6" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! colspan="7" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold standard'''
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Additional findings
|-
| colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
! colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical examination
|-
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab Findings
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Imaging
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Histopathology
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptom 1
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptom 2
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptom 3
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical exam 1
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical exam 2
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical exam 3
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab 1
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab 2
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab 3
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Imaging 1
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Imaging 2
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Imaging 3
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Diverticular Disease
| style="background: #F5F5F5; padding: 5px;" |Abdominal Cramps
| style="background: #F5F5F5; padding: 5px;" |Bloating
| style="background: #F5F5F5; padding: 5px;" |diarrhoea
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |colonoscopy
| style="background: #F5F5F5; padding: 5px;" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Hemorrhoids
| style="background: #F5F5F5; padding: 5px;" |hematochezia
| style="background: #F5F5F5; padding: 5px;" |anal pain
| style="background: #F5F5F5; padding: 5px;" |anal protrusion
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |anoscopy
| style="background: #F5F5F5; padding: 5px;" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Colon cancer
| style="background: #F5F5F5; padding: 5px;" |tenesmus
| style="background: #F5F5F5; padding: 5px;" |bowel habits change
| style="background: #F5F5F5; padding: 5px;" |weight loss
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |colonoscopy
| style="background: #F5F5F5; padding: 5px;" |
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!Diseases
!Symptom 1
! colspan="1" rowspan="1" |Symptom 2
!Symptom 3
!Physical exam 1
! colspan="1" rowspan="1" |Physical exam 2
!Physical exam 3
!Lab 1
!Lab 2
!Lab 3
!Imaging 1
!Imaging 2
!Imaging 3
!Histopathology
|'''Gold standard'''
!Additional findings
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Differential Diagnosis 4
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
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| style="background: #F5F5F5; padding: 5px;" |
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| style="background: #F5F5F5; padding: 5px;" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Differential Diagnosis 5
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
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| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Differential Diagnosis 6
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
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| style="background: #F5F5F5; padding: 5px;" |
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| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
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| style="background: #F5F5F5; padding: 5px;" |
| style="background: #F5F5F5; padding: 5px;" |
|}

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Angiodysplasia causes

2018-10-10T23:51:54Z

Aishwarya Taneja: /* Causes */

__NOTOC__
{{Angiodysplasia}}
{{CMG}}
Please help WikiDoc by adding more content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing.

==Overview==

==Causes==

The exact cause of angiodysplasia is unknown, but there are different theories:

1.Degenerative changes of small blood vessels associated with aging (most widely accepted theory)

2. long-term local hypo-oxygenation of the microcirculation from cardiac, vascular, or pulmonary disease.

==References==
{{Reflist|2}}

[[Category:Gastroenterology]]

{{WS}}
{{WH}}

Angiodysplasia pathophysiology

2018-10-10T23:44:41Z

Aishwarya Taneja: /* Pathophysiology */

__NOTOC__
{{Angiodysplasia}}
{{CMG}}

Please help WikiDoc by adding more content here. It's easy! Click [[Help:How_to_Edit_a_Page|here]] to learn about editing.

==Overview==

==Pathophysiology==
The most widely quoted hypothesis in literature is the one by Boley et al in a study using resected colon specimens from patients with angiographic and clinical evidence of cecal vascular lesions. Histological evaluation revealed dilated and tortuous veins in the submucosa even without obvious mucosal lesion. It was suggested that those lesions develop with aging due to chronic low‐grade intermittent obstruction of submucosal veins as a result of increased contractility at the level of muscularis propria. This leads to congestion of the capillaries and failure of the pre‐capillary sphincters, resulting in the formation of small arterio‐venous collaterals.

It is a degenerative lesion, acquired, probably resulting from chronic and intermittent contraction of the colon that is obstructing the venous drainage of the mucosa. As time goes by the veins become more and more tortuous, while the capillaries of the mucosa gradually dilate and precapillary sphincter becomes incompetent. Thus is formed an arteriovenous malformation characterized by a small tuft of dilated vessels. This hypothesis accounts for the high prevalence of these lesions in the right colon and is based on the Laplace law.

Dilated submucosal veins have been one of the most consistent histologic findings and may represent the earliest abnormality in colonic angiodysplasia. This histologic feature supports the theory of chronic venous obstruction in the genesis of Angiodysplasia.

Investigators have observed that patients with AD are more likely to have underlying cardiac, vascular or pulmonary diseases and therefore suggested that mucosal ischemia from chronic hypoxia or hypo‐perfusion may contribute to the development of AD; however, these were small observational case–control studies with no histological correlation. This has led to the suggestion that the increased incidence of bleeding AD in patients with AS could be due to reduced cardiac output and tissue perfusion in this subgroup.

Increased expression of angiogenic factors, like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), is also believed to play a role in the pathogenesis of colonic angiodysplasia as the expression of VEGF is higher in patients with hypoxia than normoxia.

There is a role of VWF in regulating angiogenesis which has been studied recently. The link between the mechanical disruption of high molecular-weight multimers of von Willebrand factor, due to the turbulent blood flow through a narrowed valve in patients with aortic stenosis, and colonic angiodysplasia has been formed.

==References==
{{Reflist|2}}

[[Category:Gastroenterology]]

{{WS}}
{{WH}}

Angiodysplasia classification

2018-10-10T23:15:33Z

Aishwarya Taneja: /* Overview */

__NOTOC__
{{Angiodysplasia}}
{{CMG}} {{AE}}

{{PleaseHelp}}

==Overview==
There is no established system for the classification of [disease name].

OR

Angiodysplasia may be classified according to Endoscopic appearance into 4 subtypes: Type 1, Type 2, Type 3, and Type 4.

OR

[Disease name] may be classified into [large number > 6] subtypes based on [classification method 1], [classification method 2], and [classification method 3]. [Disease name] may be classified into several subtypes based on [classification method 1], [classification method 2], and [classification method 3].

OR

Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

OR

If the staging system involves specific and characteristic findings and features: According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

OR

The staging of [malignancy name] is based on the [staging system].

OR

There is no established system for the staging of [malignancy name].

Classification

There is no established system for the classification of [disease name].

OR

[Disease name] may be classified according to [classification method] into [number] subtypes/groups:

[Group1]

[Group2]

[Group3]

[Group4]

OR

[Disease name] may be classified into [large number > 6] subtypes based on:

[Classification method 1]

[Classification method 2]

[Classification method 3]

[Disease name] may be classified into several subtypes based on:

[Classification method 1]

[Classification method 2]

[Classification method 3]

OR

Based on the duration of symptoms, [disease name] may be classified as either acute or chronic.

OR

If the staging system involves specific and characteristic findings and features:

According to the [staging system + reference], there are [number] stages of [malignancy name] based on the [finding1], [finding2], and [finding3]. Each stage is assigned a [letter/number1] and a [letter/number2] that designate the [feature1] and [feature2].

OR

The staging of [malignancy name] is based on the [staging system].

OR

There is no established system for the staging of [malignancy name].

==Classification==
Type 1: Angioectasias: Punctate erythema with/ without oozing

Type 2: Dieulafoy's lesions: Punctate lesions with pulsatile bleeding

Type3: AV malformations : Pulsatile red protrusion, without surrounding venous dilation

Type 4: Unclassifiable : Lesions that cannot be classified in one of the above categories.

==References==
{{Reflist|2}}

[[Category:Gastroenterology]]

{{WS}}
{{WH}}

Angiodysplasia historical perspective

2018-10-10T01:23:21Z

Aishwarya Taneja: /* Discovery */

__NOTOC__
{{Angiodysplasia}}
{{CMG}} {{AE}}
{{CMG}}; {{AE}}

==Overview==

==Historical Perspective==

===Discovery===
*Angiodysplasia was first discovered by Philips], in 1839 as a vascular abnormality that causes bleeding.
*In 1958 Heyde was the first to discover the association between Aortic Stenosis and the development of Angiodysplasia

==Landmark Events in the Development of Treatment Strategies==
In , [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].

==Impact on Cultural History==

==Famous Cases==
The following are a few famous cases of [[disease name]]:

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Angiodysplasia (patient information)

2018-10-06T23:42:40Z

Aishwarya Taneja: /* Overview */

__NOTOC__

'''For the WikiDoc page for this topic, click [[Angiodysplasia|here]]'''

{{CMG}} {{CP}}
{{Angiodysplasia (patient information)}}

==Overview==
Angiodysplasia of the colon is swollen, fragile blood vessels in the colon that occasionally result in blood loss from the gastrointestinal (GI) tract

==What are the symptoms of angiodysplasia==
In elderly patients, the symptoms of anemia are often seen.

These include: - Shortness of Breath

- Tiredness/ Weakness

- Pale skin

- Light Headedness/dizziness

- Fast heartbeat

- Mild or severe bleeding episodes with bright red blood coming from the rectum.

- Painless Bleed

==What causes angiodysplasia?==
Angiodysplasia of the colon is mostly related to the aging and degeneration of the blood vessels.

It usually occurs in older adults. It is almost always seen on the right side of the colon.

Reasons:

1.Age related weakening of the blood vessels.

2. Normal spasms of the colon lead to enlargement of blood vessels in the area. This swelling becomes so severe that a small direct passageway develops between a very small artery and vein. This is called an arteriovenous fistula. It is in this area of the colon wall that the patient is at risk for bleeding.

3. Angiodysplasia should not be confused with diverticulosis, which is the most common cause of bleed in elderly. Diverticulosis occurs due to outpouching of the bowel wall due to increased pressure during the normal bowel movements. For example, in cases of constipation.

==Who is at highest risk?==

- Persons over the age of 60 years old are in the highest risk age group.

- Patients on anticoagulants

- Patients with heart condition like Aortic stenosis

==Diagnosis==
Tests that may be done to diagnose this condition include:
*[[Angiography]] (only useful if there is active bleeding into the colon)
*[[Complete blood count]] (CBC) to check for anemia
*[[Colonoscopy]]
*[[Stool test]] for occult (hidden) blood (a positive test result suggests bleeding from the colon)

==When to seek urgent medical care?==
- Call your health provider if rectal bleeding occurs.

- If the patient BP drops called as hemodynamic instability.

==Treatment options==
It is important to determine what is causing the bleeding in the colon and how fast blood is being lost. You may need to be admitted to a hospital. Fluids may be given through a vein, and blood products may be required. Other treatment may be needed once the source of bleeding is found. Most patients stop bleeding on their own without any treatment.

If treatment is needed, it may involve:

Angiography to help block the blood vessel that is bleeding or to deliver medicine to help cause the blood vessels to tighten to stop the bleeding
Burning (cauterizing) the site of the bleed with heat or a laser using a colonoscope

In some instances, surgery is the only option. Removal of the entire right side of the colon (right hemicolectomy) is the treatment of choice for someone with this condition who continues to bleed at a dangerously quick rate, despite several treatments by angiography and colonoscopy. Medications (thalidomide and estrogens) may be used to reduce bleeding and the number of angiodysplasias in certain patients.

==Prevention==
There are no known preventative measures for angiodysplasia.

==What to expect (Outlook/Prognosis)?==

Patients who have bleeding related to this condition despite having had colonoscopy, angiography, or surgery are likely to have more bleeding in the future. The outlook remains good if the bleeding is controlled.

==Possible complications==
*Anemia
*Death from excessive blood loss
*Side effects from treatment
*Severe loss of blood from the GI tract

==Sources==
http://www.nlm.nih.gov/medlineplus/ency/article/000238.htm