Cirrhosis differential diagnosis: Difference between revisions
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== Differentiating Cirrhosis from other Diseases == | == Differentiating Cirrhosis from other Diseases == | ||
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|style="height:100px"; style="width:10%" border="1" bgcolor="LightSteelBlue" | Condition | |||
|style="height:100px"; style="width:45%" border="1" bgcolor="Beige" | Differentiating Signs and Symptoms | |||
|style="height:100px"; style="width:45%" border="1" bgcolor="Beige" | Differentiating Tests | |||
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| '''Type I IgE mediated''' | |||
|bgcolor="Beige"|Immediate onset caused by [[IgE]] binding to [[mast cells]] causing [[degranulation]] and release of [[histamine]]. | |||
|bgcolor="Beige"|[[Urticaria]], [[anaphylaxis]], [[angioedema]], [[bronchospasm]]. | |||
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| '''Type II antibody mediated cell destruction/ cytotoxic''' | |||
|bgcolor="Beige"|Delayed onset reaction caused by [[IgG]] or [[IgM]] [[antibodies]], directed at drug-hapten coated cells. | |||
|bgcolor="Beige"|[[Thrombocytopenia]], [[anemia]], [[cytopenia]]. | |||
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| '''Type III immune complex deposition''' | |||
|bgcolor="Beige"|Delayed in onset and caused by [[IgG]] [[immune complex]] formation and deposition, and [[complement]] activation. | |||
|bgcolor="Beige"|[[Vasculitis]], [[serum sickness]], [[arthralgia]], [[fever]], [[rash]]. | |||
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| '''Type IV cell mediated/ delayed-type hypersensitivity reaction''' | |||
|bgcolor="Beige"|The presentation of drug molecules by major histocompatability complexes to [[T cells]], causing the release of [[cytokines]] and other [[inflammatory]] mediators. Also associated with the activation of [[eosinophils]], [[monocytes]], and [[neutrophils]]. | |||
|bgcolor="BeigeSkin [[rashes]], organ tissue damage, contact sensitivity. | |||
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Revision as of 15:33, 7 September 2012
Cirrhosis Microchapters |
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Cirrhosis differential diagnosis On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Overview
Differentiating Cirrhosis from other Diseases
Condition | Differentiating Signs and Symptoms | Differentiating Tests |
Type I IgE mediated | Immediate onset caused by IgE binding to mast cells causing degranulation and release of histamine. | Urticaria, anaphylaxis, angioedema, bronchospasm. |
Type II antibody mediated cell destruction/ cytotoxic | Delayed onset reaction caused by IgG or IgM antibodies, directed at drug-hapten coated cells. | Thrombocytopenia, anemia, cytopenia. |
Type III immune complex deposition | Delayed in onset and caused by IgG immune complex formation and deposition, and complement activation. | Vasculitis, serum sickness, arthralgia, fever, rash. |
Type IV cell mediated/ delayed-type hypersensitivity reaction | The presentation of drug molecules by major histocompatability complexes to T cells, causing the release of cytokines and other inflammatory mediators. Also associated with the activation of eosinophils, monocytes, and neutrophils. | bgcolor="BeigeSkin rashes, organ tissue damage, contact sensitivity. |
Differentiating Cirrhosis from other Diseases Based on Ascitic Fluid
Ascites may be caused by portal hypertension due to cirrhosis of liver or due to other causes like malignancies etc.,
Ascitic fluid analysis should be done to broadly categorize the cause of ascites.
Ascites is broadly classified as two types based on the serum-ascites albumin gradient (SAAG):
- Transudate - SAAG > 1.1 g/dL (indicates the ascites is due to portal hypertension).
- Exudate - SAAG < 1.1 g/dL (indicates the ascites is due to non-portal hypertension etiology).