Acute Renal Failure and Cirhosis

Posted by e-Medical PPT
Involves complex Pathophysiologic changes in body.
Ascites-most common complication
Hydraulic and Oncotic pressures determine net capillary pressure and Ascites formation
Portal Pressure >12 mmHg required for Ascites formation
Redution in Systemic Vascular Resistance
Lower mean arterial pressure
Increased cardiac output
Hyperdynamic Circulation
Reduced SVR is more prominent in the Splanchnic circulation- Ascites formation

Mechanisms of Vasodilation in CIRHOSIS
Increased circulation of vasodilators
Vasoactive  intestinal peptide
Substance P
Platelet Activating factor
Nitric Oxide – most important

Increased NO synthesis is possibly because of,
 Increased endotoxin absorption from GI tract.
 Decreased clearance by liver because of Portasystemic shunts.
 Decreased Reticuloenthelial Cell Function
NO concetration higher in Portal vein than peripheral veins

Consequences of Vasodilation
Increased endogenous Vasoconstrictors.
Sodium retention
Water retention
Renal vasoconstrition

Hepatorenal Syndrome- is a diagnosis of exclusion
Classically charaterised by Oliguria, Benign Urine sediments,Low Urine Sodium, Rise in creatinine

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