Rheumatoid arthritis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*[[Rheumatoid arthritis]] is mediated by the combination of a predisposing genotype upon which genetic factors, environmental and microorganism resulting in the inflammatory and destruction of the synovial membrane. | *[[Rheumatoid arthritis]] is mediated by the combination of a predisposing genotype upon which genetic factors, environmental and microorganism resulting in the inflammatory and destruction of the synovial membrane. | ||
'''Environmental factors''': It causes repeated activation of innate immunity at mucosal surfaces. | |||
**Smoking interacts with genes to increase susceptibility up to 20- to 40-fold. | |||
***Smoking causes increased expression of peptidyl arginine deiminase (PAD) in alveolar macrophages. | |||
***Peptidyl arginine deiminase convert arginine to citrulline in the airway which further creates neoantigens that can be recognized by the adaptive immune system. | |||
'''Microrganism''' | |||
**Genetics factors like class II major histocompatibility complex (MHC), most common human leukocyte antigen (HLA)-DR | **Genetics factors like class II major histocompatibility complex (MHC), most common human leukocyte antigen (HLA)-DR | ||
Revision as of 16:01, 23 March 2018
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Rheumatoid arthritis Microchapters | |
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Diagnosis | |
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Treatment | |
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Case Studies | |
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Rheumatoid arthritis pathophysiology On the Web | |
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American Roentgen Ray Society Images of Rheumatoid arthritis pathophysiology | |
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Risk calculators and risk factors for Rheumatoid arthritis pathophysiology | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
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].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
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
- Rheumatoid arthritis is mediated by the combination of a predisposing genotype upon which genetic factors, environmental and microorganism resulting in the inflammatory and destruction of the synovial membrane.
Environmental factors: It causes repeated activation of innate immunity at mucosal surfaces.
- Smoking interacts with genes to increase susceptibility up to 20- to 40-fold.
- Smoking causes increased expression of peptidyl arginine deiminase (PAD) in alveolar macrophages.
- Peptidyl arginine deiminase convert arginine to citrulline in the airway which further creates neoantigens that can be recognized by the adaptive immune system.
- Smoking interacts with genes to increase susceptibility up to 20- to 40-fold.
Microrganism
- Genetics factors like class II major histocompatibility complex (MHC), most common human leukocyte antigen (HLA)-DR
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].