Sandbox:Hamid: Difference between revisions

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__NOTOC__
__NOTOC__


{{CMG}}; {{AE}} {{SMP}}, {{USAMA}}
{{CMG}}; {{HQ}}


==Ovreview==
==Overview==
There are no established risk factors for [disease name].


==Pathophysiology==
OR
 
The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
 
OR
 
Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
 
OR
 
Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
==Risk Factors==
*There are no established risk factors for [disease name].
OR
*The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
 
*Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
===Common Risk Factors===
*Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
*Common risk factors in the development of [disease name] include:
**[Risk factor 1]
**[Risk factor 2]
**[Risk factor 3]
 
===Less Common Risk Factors===
*Less common risk factors in the development of [disease name] include:
**[Risk factor 1]
**[Risk factor 2]
**[Risk factor 3]


===Life cycle===


====Type 1====
*1
**1.1 [[Fever]]<ref name="pmid28343553">{{cite journal| author=Murina F, Graziottin A, Felice R, Gambini D| title=Alpha Lipoic Acid Plus Omega-3 Fatty Acids for Vestibulodynia Associated With Painful Bladder Syndrome. | journal=J Obstet Gynaecol Can | year= 2017 | volume= 39 | issue= 3 | pages= 131-137 | pmid=28343553 | doi=10.1016/j.jogc.2016.12.035 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28343553  }} </ref>
**1.2 [[Pain]]<ref name="pmid15630106">{{cite journal| author=Scholes D, Hooton TM, Roberts PL, Gupta K, Stapleton AE, Stamm WE| title=Risk factors associated with acute pyelonephritis in healthy women. | journal=Ann Intern Med | year= 2005 | volume= 142 | issue= 1 | pages= 20-7 | pmid=15630106 | doi= | pmc=3722605 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15630106  }} </ref>
**1.3 [[Jaundice]]
*2
*3
*4


====Type 2====
{| class="wikitable"
!1
!2
!3
!4
|-
|a
|
|
|
|-
|b
|
|
|
|-
|c
|
|
|
|}


Coagulation necrosis, characterized by hypereosinophilia and nuclear pyknosis followed by karyorrhexis, karyolysis, total loss of nuclei, and loss of cytoplasmic cross-striations, is generally first visible in the period from 4-12 hours following infarction. Necrotic myocytes may retain their striations for a long time. Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours, but generally closer to 12 hours. The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages who phagocytose or eat the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue: Which will replace the infarct with a fibrous or collagenous scar (which are typical steps in wound healing). The interstitial space or the space between cells, outside of blood vessels, may be infiltrated with red blood cells. Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts, and capillaries begins around the periphery at 3-10 days. Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an Infarct or with reperfusion, for example with thrombolytic therapy.


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

Revision as of 22:54, 12 December 2017


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Hamid Qazi, MD, BSc [2]

Overview

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.

Risk Factors

  • There are no established risk factors for [disease name].

OR

  • The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
  • Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

Common Risk Factors

  • Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
  • Common risk factors in the development of [disease name] include:
    • [Risk factor 1]
    • [Risk factor 2]
    • [Risk factor 3]

Less Common Risk Factors

  • Less common risk factors in the development of [disease name] include:
    • [Risk factor 1]
    • [Risk factor 2]
    • [Risk factor 3]



References

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