Cholestasis--defined as a reduction or stasis of bile flow with corresponding rise of bile substances in blood--can be caused by obstructive and non-obstructive mechanisms. Common pathomechanisms, manifesting mainly in centrolobular liver areas, can be classified with regards to the subcellular location of the cholestatic components: Impairment of sinusoidal and lateral hepatocyte membrane; disturbance of bonds, storage, transport and secretion of bile substances (particularly reduction of bile-acid dependent and non-dependent bile flow); impaired bile acid and drug metabolism as a result of hypoactive, hypertrophied endoplasmatic reticulum; impairment of the mitochondrial energy metabolism; alteration of the canalicular membrane; impairment of filaments and "tight junctions"; the building of precipitates resulting from disturbed micellar function; impairment of ductulus permeability with reabsorption of bile.--These pathomechanisms explain the behaviour of biochemical and cholestatic-specific symptoms in blood-plasma, inclusive the appearance of abnorm substances whose diagnostic values are illustrated.