Portal hypertension pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Portal venous pressure is determined by portal blood flow and portal vascular resistance. Increased portal vascular resistance is often the main factor responsible for it. The consequences of portal hypertension are due to blood being forced down alternate channels by the increased resistance to flow through the portal system. Due to formation of alternate channels initially some of the portal blood and later most of it is shunted directly to the systemic circulation bypassing the liver.
Pathophysiology
- Portal hypertension is caused by conditions classified as pre-hepatic, hepatic, and post-hepatic disorders.
- The exact pathogenesis in portal hypertension is disturbance in normal physiology of portocaval circulation.
Physiology
- Ohm's law in vascular system defines the pressure gradient in blood vessels as equal to product of blood flow (Q) and vascular resistance (R):<math display="block">\Delta P =P2-P1= Q\times R</math>
- Vascular resistance (R) has to be measured through Pouseuille’s law formula:<math display="block">R = {8 \eta L\over \pi r^4}</math>η= Viscosity; L= Length of vessel; r= Radius of vessel
- When the (R) measurement formula is integrated in Ohm's law it becomes as the following:
<math display="block">\Delta P= P_2-P_1 = {Q\times 8 \eta L\over \pi r^4}</math>
- Length of blood vessels (L) never differs in normal physiologic condition.
- Blood viscosity (η) does not change, unless dramatic changes in hematocrit happen.
- Thus, the main factors that affect the pressure gradient in blood vessels are blood flow (Q) and vessel radius (r) in a direct and inverse way, respectively.
| • Anatomical (irreversible component) • Functional/vascular tone (reversible component) | • Opening of pre-existing vascular channels • Formation of new vascular channels | • Systemic vasodilation (r) • Increasing plasma volume (Q) | |||||||||||||||||||||||||||||||||||||
| lntra-hepatic resistance (r) | Portosystemic collaterals (Q) | ||||||||||||||||||||||||||||||||||||||
| Increased resistance to portal blood flow (R) | Increased systemic/splanchnic blood flow (Q) (hyperdynamic circulation) | ||||||||||||||||||||||||||||||||||||||
| Elevated portal pressure (P) | |||||||||||||||||||||||||||||||||||||||
| Portal hypertension | |||||||||||||||||||||||||||||||||||||||
Pathogenesis
- 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].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
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].