Portal vein thrombosis pathophysiology

Jump to navigation Jump to search
https://www.youtube.com/watch?v=RKxoYs3mDew%7C350}}

Portal vein thrombosis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Portal vein thrombosis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Portal vein thrombosis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Portal vein thrombosis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Portal vein thrombosis pathophysiology

CDC on Portal vein thrombosis pathophysiology

Portal vein thrombosis pathophysiology in the news

Blogs on Portal vein thrombosis pathophysiology

Directions to Hospitals Treating Portal vein thrombosis

Risk calculators and risk factors for Portal vein thrombosis pathophysiology

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:[1]
    • Arterial rescue
      • Arterial rescue is the phenomenon that occurs after portal vein clamping during liver surgery.[2]
      • It is a vascular reflex present in organs with both arterial and venous supply.
      • It has a role in preserving liver function in the acute stages of portal vein thrombosis.
    • Venous rescue
      • Venous rescue is the phenomenon of neovascularization by forming collateral vessels.
      • It helps to bypass the obstruction.
      • It is a rapid process and takes a few days to start and 3-5 weeks to complete after portal vein obstruction.[3]
      • Collateral vessel joins to form cavernoma which connects the proximal and distal part of thrombosed portal vein.
      • Finally, the portal vein becomes fibrosed, thin cord.[4]
  • All these events leads to low systemic vascular resistance and high cardiac output. These are the characterstic findings of hyperkinetic circulation.[5]

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

  1. Zhang WW, Churchill S, Churchill P (1989). "Developmental regulation of D-beta-hydroxybutyrate dehydrogenase in rat liver and brain". FEBS Lett. 256 (1–2): 71–4. PMID 2806552.
  2. Henderson JM, Gilmore GT, Mackay GJ, Galloway JR, Dodson TF, Kutner MH (1992). "Hemodynamics during liver transplantation: the interactions between cardiac output and portal venous and hepatic arterial flows". Hepatology. 16 (3): 715–8. PMID 1505914.
  3. De Gaetano AM, Lafortune M, Patriquin H, De Franco A, Aubin B, Paradis K (1995). "Cavernous transformation of the portal vein: patterns of intrahepatic and splanchnic collateral circulation detected with Doppler sonography". AJR Am J Roentgenol. 165 (5): 1151–5. doi:10.2214/ajr.165.5.7572494. PMID 7572494.
  4. Hoekstra J, Janssen HL (2009). "Vascular liver disorders (II): portal vein thrombosis". Neth J Med. 67 (2): 46–53. PMID 19299846.
  5. Wang JT, Zhao HY, Liu YL (2005). "Portal vein thrombosis". HBPD INT. 4 (4): 515–8. PMID 16286254.

Template:WH Template:WS