Vitamin K deficiency thus activate) certain enzymes involved in coagulation: Factors II, VII, IX, X, and protein C and protein S. Inability to activate the clotting cascade via these factors leads to the bleeding symptoms mentioned above. Notably, when one examines the lab values in Vitamin K deficiency [see below] the prothrombin time is elevated, but the partial thromboplastin time is normal or only mildly prolonged. This may seem counterintuitive given that the deficiency leads to decreased activity in factors of both the intrinsic pathway (F-IX) which is monitored by PTT, as well as the extrinsic pathway (F-VII) which is monitored by PT.
Vitamin A deficiency and lymphocytes. Suppression of these result in a lack of immune reaction if pathogens become present in the body and consequently a greater susceptibility to incubation of disease. VAD and infections aggravate each other, so with infection, vitamin A levels are depleted, which in turn reduces intestinal absorption of vitamin A. Very often seen with VAD is protein energy malnutrition, in which the synthesis of retinol binding protein (RBP) is decreased, consequently the uptake of retinol is reduced. This leads to an inability to use any vitamin A present as the RBP is absent, so the retinol cannot be transported