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__NOTOC__
* Mixed Cryoglobulinemia is a combination of both types II and III.
* Mixed CGs is associated with following conditions:
** '''SLE (systemic lupus erythematous)'''
**  '''Sjögren's syndrome,'''
** '''HCV'''
** '''Lymphoproliferative disorders'''
* Al the above mentioned disorders can cause excessive production of B-cell which can further lead to selective expansion of Cryoglobulinemia producing B-cell clones.
* In HCV infected patients the HCV complexes such as HCV-IgG, HCV-lipoprotein cause B-cell hyper-proliferation through the CD81 leading to expansion of specific B-cell clones such as WA idiotype or V(H)1-69.
* HCV particles are often found in such patients' serum CG complexes, but, at the same time, CG development in hepatitis C infection does not directly require the HCV virion or its components [38]. In this sense, CG development may, in fact, reflect a normal, expected response to regulate immune complexes in states of chronic immune activation.
* Among patients with HCV infection, the number of circulating T cells with surface markers compatible with a suppressor phenotype may be a feature that differs between patients with cryoglobulinemic vasculitis and those with asymptomatic CG.
* This was illustrated in a study that compared the percentage of "regulatory" T cells in 69 patients with HCV infection who had symptomatic CG with others with asymptomatic HCV infection [39].
* The mean levels of regulatory T cells were significantly lower in those with symptomatic HCV-associated CG than asymptomatic subjects (2.6 versus 7.4 percent, respectively).
* Whether the diminished proportion of regulatory T cells plays a role in causing vasculitis is uncertain but warrants further exploration.


{{CMG}}; {{AE}} {{FT}}




==Overview==
=== Differentiating uremia from other diseases ===
 
Uremia and uremic encephalopathy must be differentiated from other diseases that cause [[personality changes]], altered level of [[consciousness]] and hand [[tremors]] ([[asterixis]]). The differentials include the following:<nowiki/><ref name="pmid20495225">{{cite journal| author=Meparidze MM, Kodua TE, Lashkhi KS| title=[Speech impairment predisposes to cognitive deterioration in hepatic encephalopathy]. | journal=Georgian Med News | year= 2010 | volume= | issue= 181 | pages= 43-9 | pmid=20495225 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20495225 }} </ref><ref name="pmid25013309">{{cite journal| author=Kattimani S, Bharadwaj B| title=Clinical management of alcohol withdrawal: A systematic review. | journal=Ind Psychiatry J | year= 2013 | volume= 22 | issue= 2 | pages= 100-8 | pmid=25013309 | doi=10.4103/0972-6748.132914 | pmc=4085800 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25013309  }} </ref><ref name="pmid12813481">{{cite journal| author=Roldán J, Frauca C, Dueñas A| title=[Alcohol intoxication]. | journal=An Sist Sanit Navar | year= 2003 | volume= 26 Suppl 1 | issue= | pages= 129-39 | pmid=12813481 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12813481 }} </ref><ref name="pmid21590619">{{cite journal| author=Seifter JL, Samuels MA| title=Uremic encephalopathy and other brain disorders associated with renal failure. | journal=Semin Neurol | year= 2011 | volume= 31 | issue= 2 | pages= 139-43 | pmid=21590619 | doi=10.1055/s-0031-1277984 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21590619  }} </ref><ref name="pmid6864698">{{cite journal| author=Handler CE, Perkin GD| title=Wernicke's encephalopathy. | journal=J R Soc Med | year= 1983 | volume= 76 | issue= 5 | pages= 339-42 | pmid=6864698 | doi= | pmc=1439130 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6864698 }} </ref><ref name="pmid23251840">{{cite journal| author=Kim Y, Kim JW| title=Toxic encephalopathy. | journal=Saf Health Work | year= 2012 | volume= 3 | issue= 4 | pages= 243-56 | pmid=23251840 | doi=10.5491/SHAW.2012.3.4.243 | pmc=3521923 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23251840 }} </ref><ref name="pmid2497395">{{cite journal| author=Hartmann A, Buttinger C, Rommel T, Czernicki Z, Trtinjiak F| title=Alteration of intracranial pressure, cerebral blood flow, autoregulation and carbondioxide-reactivity by hypotensive agents in baboons with intracranial hypertension. | journal=Neurochirurgia (Stuttg) | year= 1989 | volume= 32 | issue= 2 | pages= 37-43 | pmid=2497395 | doi=10.1055/s-2008-1053998 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2497395  }} </ref><ref name="pmid21590622">{{cite journal| author=Kumar N| title=Acute and subacute encephalopathies: deficiency states (nutritional). | journal=Semin Neurol | year= 2011 | volume= 31 | issue= 2 | pages= 169-83 | pmid=21590622 | doi=10.1055/s-0031-1277986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21590622  }} </ref><ref name="pmid23035103">{{cite journal| author=Chiu GS, Chatterjee D, Darmody PT, Walsh JP, Meling DD, Johnson RW et al.| title=Hypoxia/reoxygenation impairs memory formation via adenosine-dependent activation of caspase 1. | journal=J Neurosci | year= 2012 | volume= 32 | issue= 40 | pages= 13945-55 | pmid=23035103 | doi=10.1523/JNEUROSCI.0704-12.2012 | pmc=3476834 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23035103  }} </ref><ref name="pmid15284663">{{cite journal| author=Peate I| title=An overview of meningitis: signs, symptoms, treatment and support. | journal=Br J Nurs | year= 2004 | volume= 13 | issue= 13 | pages= 796-801 | pmid=15284663 | doi=10.12968/bjon.2004.13.13.13501 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15284663 }} </ref><ref name="pmid25821643">{{cite journal| author=Abdelhafiz AH, Rodríguez-Mañas L, Morley JE, Sinclair AJ| title=Hypoglycemia in older people - a less well recognized risk factor for frailty. | journal=Aging Dis | year= 2015 | volume= 6 | issue= 2 | pages= 156-67 | pmid=25821643 | doi=10.14336/AD.2014.0330 | pmc=4365959 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25821643 }} </ref>
Mesenteric ischemia is a type of intestinal ischemia primarily affecting the small intestine. It is one of the life-threatening gastrointestinal vascular emergencies which requires prompt surgical/medical intervention depending upon the underlying cause.
{|
 
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
It can be divided into occlusive/non-occlusive, arterial or venous, localized/generalized and superficial or transmural.<ref name="pmid24160929">{{cite journal| author=Corcos O, Nuzzo A| title=Gastro-intestinal vascular emergencies. | journal=Best Pract Res Clin Gastroenterol | year= 2013 | volume= 27 | issue= 5 | pages= 709-25 | pmid=24160929 | doi=10.1016/j.bpg.2013.08.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24160929 }} </ref>
! rowspan="2" |Diseases
 
! colspan="3" |History and Symptoms
== Pathophysiology ==
! colspan="4" |Physical Examination
==Overview==
! colspan="3" |Laboratory Findings
*The anatomy and physiology of the small intestine plays a vital role in the develpoment of mesenteric ischemia. Intestinal muscosa has a high metabolic rate and accordingly a high blood flow requirement. The majority of blood supply of the intestine comes from the superior mesenteric artery, with a collateral blood supply from superior and inferior pancreaticoduodenal arteries(branches of the celiac artery) as well as the inferior mesenteric artery. The splanchnic circulation(arteries supplying the viscera) receives 15-25% of the cardiac output, making it sensitive to the effects of decreased perfusion, The blood supply must be reduced by 50% of the original blood flow for the mesenteric ischemia to occur. Ischemia disrupts the mucosal barrier, allowing the release of toxins, bacteria and vasoactive mediators before the complete necrosis(which takes around 6 hours after the onset of ischemia). This further leads to myocaridal depression, sepsis, multiorgan failure and without prompt intervention, death.<ref name="pmid9146713">{{cite journal| author=Rosenblum JD, Boyle CM, Schwartz LB| title=The mesenteric circulation. Anatomy and physiology. | journal=Surg Clin North Am | year= 1997 | volume= 77 | issue= 2 | pages= 289-306 | pmid=9146713 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9146713 }} </ref>
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
!Personality changes
 
!Altered level of consciousness
OR
!Hand tremors (asterixis)
 
!Slurred speech
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
!Writing disturbances
 
!Voice monotonous
OR
!Impaired '''memory'''
 
!Elevated blood ammonia
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
!Hyponatremia
 
!hypokalemia
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Pathophysiology==
 
 
 
===Pathogenesis===
The pathophysiology of mesenteric ischemia can be explained on the basis of etiology:<ref name="pmid25689121">{{cite journal| author=Acosta S| title=Mesenteric ischemia. | journal=Curr Opin Crit Care | year= 2015 | volume= 21 | issue= 2 | pages= 171-8 | pmid=25689121 | doi=10.1097/MCC.0000000000000189 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25689121 }} </ref><ref name="pmid15729076">{{cite journal| author=Acosta S, Ogren M, Sternby NH, Bergqvist D, Björck M| title=Clinical implications for the management of acute thromboembolic occlusion of the superior mesenteric artery: autopsy findings in 213 patients. | journal=Ann Surg | year= 2005 | volume= 241 | issue= 3 | pages= 516-22 | pmid=15729076 | doi= | pmc=1356992 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15729076 }} </ref>
*'''Acute mesenteric arterial embolism''': Attributes to 50% cases of mesenteric ischemia.
*Mesenteric embolus can oringinate from the left atrium, associated with cardiac arrythmias such as atrial fibrillation.
*Recent myocardial infarction resulting in segmental wall motion abnormality leading to poor ejaction fraction and embolus formation.
*[[Infective endocarditis]]: vegetations on the cardiac valves resulting in turbulence in blood flow predisposing to formation of emboli into the blood stream.
*Embolus can typically lodge into points of normal anatomic narrowing, making [[superior mesenteric artery]] the most vulnerable because of its relatively large diameter and low take off angle from the aorta.
*The majority of emboli lodge 3-10cm distal to the origin of [[superior mesenteric artery]], classically sparing the proximal jejunum and colon.
*'''Acute mesenteric arterial thrombosis''':
*25% cases of mesenteric ischemia result from mesenteric arterial thrombosis.
*Most likely due to underlying atherosclerosis leading to stenosis.
*An underlying plaque in the superior mesenteric artery leads to critical stenosis over the years forming collaterals.OR
*It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
*The development of [disease name] is the result of multiple genetic mutations.
==Associated Conditions==
 
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==References==
{{Reflist|2}}
 
{{WH}}
{{WS}}
[[Category: (name of the system)]]
==Risk Factors==
===Common Risk Factors===
The following conditions pose a signifiacnt risk towards the development of mesenteric ischemia either by interrupting the blood flow through the artery or vein supplying the small intestine (e.g.thromboemboli) or by reducing the blood supply (e.g. vasoconstriction). Also, there are certain life-style related risk factors which predominantly cause mesenteric ischemia in the older age group. <ref name="pmid10917470">{{cite journal| author=Fitzgerald T, Kim D, Karakozis S, Alam H, Provido H, Kirkpatrick J| title=Visceral ischemia after cardiopulmonary bypass. | journal=Am Surg | year= 2000 | volume= 66 | issue= 7 | pages= 623-6 | pmid=10917470 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10917470 }} </ref><ref name="pmid9746774">{{cite journal| author=Martinelli I, Mannucci PM, De Stefano V, Taioli E, Rossi V, Crosti F et al.| title=Different risks of thrombosis in four coagulation defects associated with inherited thrombophilia: a study of 150 families. | journal=Blood | year= 1998 | volume= 92 | issue= 7 | pages= 2353-8 | pmid=9746774 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9746774 }} </ref><ref name="pmid16476108">{{cite journal| author=Acosta S, Ogren M, Sternby NH, Bergqvist D, Björck M| title=Fatal nonocclusive mesenteric ischaemia: population-based incidence and risk factors. | journal=J Intern Med | year= 2006 | volume= 259 | issue= 3 | pages= 305-13 | pmid=16476108 | doi=10.1111/j.1365-2796.2006.01613.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16476108  }} </ref>
{| class="wikitable"
!Risk factors
!
!
|-
| rowspan="13" |Occlusive
| rowspan="7" |Embolic
|[[Atrial fibrillation]]
|-
|[[Cardiac arrhythmia]]
|-
|[[Valvular heart disease]]
|-
|[[Infective endocarditis]]
|-
|Recent [[myocardial infarction]]
|-
|[[Ventricular aneurysm]]
|-
|Aortic atherosclerosis
|-
| rowspan="6" |Thrombotic
|Advanced age
|-
|Low cardiac output states
|-
|[[Peripheral arterial disease]]
|-
|Traumatic injury
|-
|Inherited thrombophilia-
* [[Factor V Leiden mutation|Factor V Leidin mutation]]
* [[Prothrombin G20210A mutation]]
* [[Protein S deficiency]]
 
* [[Antithrombin III deficiency]]
* [[Activated protein C resistance]]
* Anti-phospholipid syndrome
* [[Myeloproliferative neoplasm|Myeloproliferative disorders(JAK2 V617F) mutation.]]
|-
|Acquired thrombophilia- malignancy, oral contraceptives intake.
|-
|-
| colspan="2" rowspan="6" |Non-occlusive
|'''Hepatic encephalopathy'''
|Heart failure
| ++
| ++
| ++
|<nowiki>++</nowiki>
|<nowiki>++</nowiki>
|<nowiki>++</nowiki>
|<nowiki>++</nowiki>
|<nowiki>++</nowiki>
|<nowiki>++</nowiki>
|<nowiki>++</nowiki>
|-
|-
|[[Aortic insufficiency]]
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Alcohol intoxication]]'''
| 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;" | -/+
|-
|-
|[[Septic shock]]  
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Alcohol withdrawal]]'''
| 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;" | -/+
|-
|-
|Vasoconstrictive drugs:
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Uremia]]'''
* [[Digoxin]]
| style="background: #F5F5F5; padding: 5px;" | ++
* [[Alpha-adrenergic agonist|Alpha-adrenergic agonists]]
| 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;" |[[Hyperkalemia]]
|-
|-
|Cocaine abuse or ergot poisoning
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Wernicke encephalopathy]]'''
| 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;" | -
|-
|-
|[[Hemodialysis]]
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Toxic encephalopathy]] from drugs'''
| 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;" | -/+
|-
|-
| colspan="2" |Other causes
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''Altered [[intracranial pressure]]'''
|Lifestyle related risk factors:
| style="background: #F5F5F5; padding: 5px;" | +
* High cholesterol levels
| style="background: #F5F5F5; padding: 5px;" | -/+
* History of smoking
| style="background: #F5F5F5; padding: 5px;" | -
* Immobility
| style="background: #F5F5F5; padding: 5px;" | -/+
 
| style="background: #F5F5F5; padding: 5px;" | -/+
* Recent surgery
| style="background: #F5F5F5; padding: 5px;" | -
Less common risk factors:  
| style="background: #F5F5F5; padding: 5px;" | -/+
* Fibromuscular dysplasia
| style="background: #F5F5F5; padding: 5px;" | -
* Beta receptor blocking agents
| style="background: #F5F5F5; padding: 5px;" | -
* Hepatitis
| style="background: #F5F5F5; padding: 5px;" | -
|}
*Common risk factors in the development of mesenteric ischemia include:
**'''Occlusive causes'''
***'''Embolic causes''':<ref name="pmid10917470">{{cite journal| author=Fitzgerald T, Kim D, Karakozis S, Alam H, Provido H, Kirkpatrick J| title=Visceral ischemia after cardiopulmonary bypass. | journal=Am Surg | year= 2000 | volume= 66 | issue= 7 | pages= 623-6 | pmid=10917470 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10917470  }} </ref>
***Atrial fibrillation
***Cardiac arrhythmias
***Valvular heart diseases
***Infective endocarditis
***Recent myocardial infarction
***Ventricular aneurysm
***Aortic atherosclerosis 
***Aortic aneurysm
**'''Thrombotic causes''':<ref name="pmid9746774">{{cite journal| author=Martinelli I, Mannucci PM, De Stefano V, Taioli E, Rossi V, Crosti F et al.| title=Different risks of thrombosis in four coagulation defects associated with inherited thrombophilia: a study of 150 families. | journal=Blood | year= 1998 | volume= 92 | issue= 7 | pages= 2353-8 | pmid=9746774 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9746774  }} </ref>
***Advanced age
***Low cardiac output states
***Traumatic injury
***Peripheral artery disease
*'''Non-occlusive causes:'''<ref name="pmid16476108">{{cite journal| author=Acosta S, Ogren M, Sternby NH, Bergqvist D, Björck M| title=Fatal nonocclusive mesenteric ischaemia: population-based incidence and risk factors. | journal=J Intern Med | year= 2006 | volume= 259 | issue= 3 | pages= 305-13 | pmid=16476108 | doi=10.1111/j.1365-2796.2006.01613.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16476108  }} </ref>
**[[Heart failure]]
**[[Aortic insufficiency]]
**[[Septic shock]]
**Vasoconstrictive drugs(e.g. [[Digoxin]], [[Alpha-adrenergic agonist|alpha-adrenergic agonists)]]
 
**[[Cocaine abuse]] or ergot poisoning
 
**[[Hemodialysis]]
 
===Less Common Risk Factors===
*Less common risk factors in the development of mesenteric ischemia include:
**Fibromuscular dysplasia
**Hepatitis
**Beta recpetor blocking agents
**Polyarteritis nodosa
 
===Causes===
Narrowing of the arteries that supply blood to the intestine causes mesenteric ischemia. The arteries that supply blood to the intestines run directly from the aorta. Mesenteric ischemia is often seen in people who have hardening of the arteries in other parts of the body (for example, those with coronary artery disease or peripheral vascular disease). The condition is more common in smokers and in patients with high blood pressure or blood cholesterol. Mesenteric ischemia may also be caused by an embolus that suddenly blocks one of the mesenteric arteries. The emboli usually come from the heart or aorta. These clots are more commonly seen in patients with arrhythmias, such as atrial fibrillation. They can be broadly classified into four categories:<ref name="pmid2194948">{{cite journal| author=Reinus JF, Brandt LJ, Boley SJ| title=Ischemic diseases of the bowel. | journal=Gastroenterol Clin North Am | year= 1990 | volume= 19 | issue= 2 | pages= 319-43 | pmid=2194948 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2194948  }} </ref>
*[[Arterial thrombosis]]
*[[Arterial embolism]]
*[[Venous thrombosis]]
*[[Non-occlusive ischemia]]
 
{| class="wikitable"
! colspan="4" |Classification based on etiology
|-
|-
!Etiology
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''Intoxication by chemical agents'''
!Cause
| style="background: #F5F5F5; padding: 5px;" | -/+
!Incidence
| style="background: #F5F5F5; padding: 5px;" | -/+
!Examples
| 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;" | -/+
|-
|-
! rowspan="3" |Occlusive causes
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Malnutrition]]'''
|Aterial embolism
| style="background: #F5F5F5; padding: 5px;" | -/+
|50-70%
| style="background: #F5F5F5; padding: 5px;" | -
|
| style="background: #F5F5F5; padding: 5px;" | -
* Superior mesenteric artery obstruction (most common cause)
| style="background: #F5F5F5; padding: 5px;" | -
* [[Arrhythmia]]
| style="background: #F5F5F5; padding: 5px;" | -/+
* [[Myocardial infarction]]
| style="background: #F5F5F5; padding: 5px;" | -
* [[Infective endocarditis]]
| style="background: #F5F5F5; padding: 5px;" | -/+
* [[Valvular heart disease|Valvular heart diseases]]
| style="background: #F5F5F5; padding: 5px;" | -
* [[Ventricular aneurysm|Ventricular aneurysms]]
| style="background: #F5F5F5; padding: 5px;" | -/+
* History of embolic events
| style="background: #F5F5F5; padding: 5px;" | -/+
* Recent [[angiography]]
|-
|-
|Arterial thrombosis
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Hypoxic brain injury]]'''
|15-25%
| style="background: #F5F5F5; padding: 5px;" | -
|
| style="background: #F5F5F5; padding: 5px;" | -/+
* Atherosclerosis
| style="background: #F5F5F5; padding: 5px;" | -
* Advanced age
| style="background: #F5F5F5; padding: 5px;" | -/+
* Prlonged hypotension
| style="background: #F5F5F5; padding: 5px;" | -/+
* [[Hypercoagulability|Hypercoagulabilty]] states
| style="background: #F5F5F5; padding: 5px;" | -/+
* [[Peripheral arterial disease]]
| style="background: #F5F5F5; padding: 5px;" | -/+
* Traumatic injury
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
|-
|-
|Venous thrombosis
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Meningitis]] and [[encephalitis]]'''
|5%
| style="background: #F5F5F5; padding: 5px;" | -/+
|
| style="background: #F5F5F5; padding: 5px;" | -/+
* Right-sided heart failure
| style="background: #F5F5F5; padding: 5px;" | -
* Previous deep venous thrombosis (20-40% risk)
| style="background: #F5F5F5; padding: 5px;" | -/+
* Primary clotting disorder
| style="background: #F5F5F5; padding: 5px;" | +
* Pancreatitis
| style="background: #F5F5F5; padding: 5px;" | -
* Polycythemia
| style="background: #F5F5F5; padding: 5px;" | -
* Sickle cell anemia
| style="background: #F5F5F5; padding: 5px;" | -
* Recent abdominal surgery or infection
| style="background: #F5F5F5; padding: 5px;" | -/+
| style="background: #F5F5F5; padding: 5px;" | -
|-
|-
|Non-Occlusive causes
| style="background: #DCDCDC; padding: 5px; text-align: center;" |'''[[Hypoglycemia]]'''
|Non-occlusive ischemia
| style="background: #F5F5F5; padding: 5px;" | -/+
|20-30%
| style="background: #F5F5F5; padding: 5px;" | -/+
|
| style="background: #F5F5F5; padding: 5px;" | -
* Low cardiac output states(most commom cause)
| style="background: #F5F5F5; padding: 5px;" | -/+
* Hypovolemia
| style="background: #F5F5F5; padding: 5px;" | -/+
* Vasoconstrictive drugs (Digoxin, alpha-adrernergic agonists)
| style="background: #F5F5F5; padding: 5px;" | -
* Septic schock
| style="background: #F5F5F5; padding: 5px;" | -
* Aortic insufficiency
| style="background: #F5F5F5; padding: 5px;" | -
* Cocaine abuse or ergot poisoning
| style="background: #F5F5F5; padding: 5px;" | -/+
| style="background: #F5F5F5; padding: 5px;" | -/+
|}
|}
==References==
{{Reflist|2}}
{{WH}}
{{WS}}
[[Category: (name of the system)]]
==References==

Latest revision as of 19:56, 1 June 2018

  • Mixed Cryoglobulinemia is a combination of both types II and III.
  • Mixed CGs is associated with following conditions:
    • SLE (systemic lupus erythematous)
    • Sjögren's syndrome,
    • HCV
    • Lymphoproliferative disorders
  • Al the above mentioned disorders can cause excessive production of B-cell which can further lead to selective expansion of Cryoglobulinemia producing B-cell clones.
  • In HCV infected patients the HCV complexes such as HCV-IgG, HCV-lipoprotein cause B-cell hyper-proliferation through the CD81 leading to expansion of specific B-cell clones such as WA idiotype or V(H)1-69.
  • HCV particles are often found in such patients' serum CG complexes, but, at the same time, CG development in hepatitis C infection does not directly require the HCV virion or its components [38]. In this sense, CG development may, in fact, reflect a normal, expected response to regulate immune complexes in states of chronic immune activation.
  • Among patients with HCV infection, the number of circulating T cells with surface markers compatible with a suppressor phenotype may be a feature that differs between patients with cryoglobulinemic vasculitis and those with asymptomatic CG.
  • This was illustrated in a study that compared the percentage of "regulatory" T cells in 69 patients with HCV infection who had symptomatic CG with others with asymptomatic HCV infection [39].
  • The mean levels of regulatory T cells were significantly lower in those with symptomatic HCV-associated CG than asymptomatic subjects (2.6 versus 7.4 percent, respectively).
  • Whether the diminished proportion of regulatory T cells plays a role in causing vasculitis is uncertain but warrants further exploration.


Differentiating uremia from other diseases

Uremia and uremic encephalopathy must be differentiated from other diseases that cause personality changes, altered level of consciousness and hand tremors (asterixis). The differentials include the following:[1][2][3][4][5][6][7][8][9][10][11]

Diseases History and Symptoms Physical Examination Laboratory Findings
Personality changes Altered level of consciousness Hand tremors (asterixis) Slurred speech Writing disturbances Voice monotonous Impaired memory Elevated blood ammonia Hyponatremia hypokalemia
Hepatic encephalopathy ++ ++ ++ ++ ++ ++ ++ ++ ++ ++
Alcohol intoxication + + -/+ ++ + - + - -/+ -/+
Alcohol withdrawal + + - ++ + - + - -/+ -/+
Uremia ++ ++ + -/+ -/+ -/+ - ++ Hyperkalemia
Wernicke encephalopathy + + -/+ + + + ++ - - -
Toxic encephalopathy from drugs + + -/+ -/+ + -/+ + + -/+ -/+
Altered intracranial pressure + -/+ - -/+ -/+ - -/+ - - -
Intoxication by chemical agents -/+ -/+ -/+ -/+ -/+ - - - -/+ -/+
Malnutrition -/+ - - - -/+ - -/+ - -/+ -/+
Hypoxic brain injury - -/+ - -/+ -/+ -/+ -/+ - - -
Meningitis and encephalitis -/+ -/+ - -/+ + - - - -/+ -
Hypoglycemia -/+ -/+ - -/+ -/+ - - - -/+ -/+
  1. ↑ Meparidze MM, Kodua TE, Lashkhi KS (2010). "[Speech impairment predisposes to cognitive deterioration in hepatic encephalopathy]". Georgian Med News (181): 43–9. PMID 20495225.
  2. ↑ Kattimani S, Bharadwaj B (2013). "Clinical management of alcohol withdrawal: A systematic review". Ind Psychiatry J. 22 (2): 100–8. doi:10.4103/0972-6748.132914. PMC 4085800. PMID 25013309.
  3. ↑ Roldán J, Frauca C, Dueñas A (2003). "[Alcohol intoxication]". An Sist Sanit Navar. 26 Suppl 1: 129–39. PMID 12813481.
  4. ↑ Seifter JL, Samuels MA (2011). "Uremic encephalopathy and other brain disorders associated with renal failure". Semin Neurol. 31 (2): 139–43. doi:10.1055/s-0031-1277984. PMID 21590619.
  5. ↑ Handler CE, Perkin GD (1983). "Wernicke's encephalopathy". J R Soc Med. 76 (5): 339–42. PMC 1439130. PMID 6864698.
  6. ↑ Kim Y, Kim JW (2012). "Toxic encephalopathy". Saf Health Work. 3 (4): 243–56. doi:10.5491/SHAW.2012.3.4.243. PMC 3521923. PMID 23251840.
  7. ↑ Hartmann A, Buttinger C, Rommel T, Czernicki Z, Trtinjiak F (1989). "Alteration of intracranial pressure, cerebral blood flow, autoregulation and carbondioxide-reactivity by hypotensive agents in baboons with intracranial hypertension". Neurochirurgia (Stuttg). 32 (2): 37–43. doi:10.1055/s-2008-1053998. PMID 2497395.
  8. ↑ Kumar N (2011). "Acute and subacute encephalopathies: deficiency states (nutritional)". Semin Neurol. 31 (2): 169–83. doi:10.1055/s-0031-1277986. PMID 21590622.
  9. ↑ Chiu GS, Chatterjee D, Darmody PT, Walsh JP, Meling DD, Johnson RW; et al. (2012). "Hypoxia/reoxygenation impairs memory formation via adenosine-dependent activation of caspase 1". J Neurosci. 32 (40): 13945–55. doi:10.1523/JNEUROSCI.0704-12.2012. PMC 3476834. PMID 23035103.
  10. ↑ Peate I (2004). "An overview of meningitis: signs, symptoms, treatment and support". Br J Nurs. 13 (13): 796–801. doi:10.12968/bjon.2004.13.13.13501. PMID 15284663.
  11. ↑ Abdelhafiz AH, Rodríguez-Mañas L, Morley JE, Sinclair AJ (2015). "Hypoglycemia in older people - a less well recognized risk factor for frailty". Aging Dis. 6 (2): 156–67. doi:10.14336/AD.2014.0330. PMC 4365959. PMID 25821643.
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