Portal vein thrombosis pathophysiology: Difference between revisions

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===Pathogenesis===
===Pathogenesis===
*Ii is thought that vein thrombosis is caused by Virchow's triad which includes:
*It is thought that vein thrombosis is caused by Virchow's triad which includes:
**Reduced portal blood flow
**Reduced portal blood flow
**Hypercoagulable state  
**Hypercoagulable state  

Revision as of 17:27, 14 December 2017

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Portal vein thrombosis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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.

Structure

It is formed by the union of the

and divides into a right and a left branch before entering the liver.

Note that the portal vein drains blood into the liver, not from the liver. The blood entering the liver from the portal vein, after being cleaned by the liver, flows into the inferior vena cava via the hepatic veins. The inferior mesenteric vein usually does not directly connect to the hepatic portal vein; it drains into the splenic vein.


Portal vein branches into many generation of vessels that open into hepatic sinusoids. Blood is recollected into the hepatic vein and enters the inferior vena cava.

Tributaries

The tributaries of the hepatic portal vein include:

Pathophysiology

Pathogenesis

  • It is thought that vein thrombosis is caused by Virchow's triad which includes:
    • Reduced portal blood flow
    • Hypercoagulable state
    • Vascular endothelial injury
  • There are two mechanisms that contribute in loss of portal vein blood flow to liver:
    • Arterial rescue
      • Arterial rescue is the phenomenon of portal vein clamping during liver surgery.
      • It has role in preserving liver function in the acute stages of portal vein thrombosis.
    • Venous rescue
      • It consists development of collaterals to bypass the obstruction.
      • It starts a few days after portal vein obstruction, and finalizes within 3-5 weeks.
    • Thrombosed portal vein is replaced by a complex of collateral vessels which is called cavernoma and It connects the two obvious parts to the thrombus proximally and distally.
  • The original portal vein becomes a thin, fibrotic cord and visualizing is difficult.
  • Low systemic vascular resistance and high cardiac output, is characteristic findings of the development of a hyperkinetic circulation.

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

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