The most serious and common adverse side effect associated with<unk>  are increased risk of bleeding, both nonmajor and major bleeding events. Risk of bleeding is dependent on the class of<unk>  agent used, patient's age, and pre-existing health conditions. Warfarin has an estimated incidence of bleeding of 15-20% per year and life-threatening bleeding rate of 1-3% per year. Newer non-vitamin K antagonist oral<unk> s appear to have fewer life-threatening bleeding events compared to warfarin. Additionally, patients aged 80 years or more may be especially susceptible to bleeding complications, with a rate of 13 bleeds per 100 person-years. Bleeding risk is especially important to consider in patients with renal impairment and NOAC therapy due to the fact that all NOACs, to some extent, are excreted by the kidneys. Thus, patients with renal impairment may be at higher risk of increased bleeding. In people with cancer, a systematic review has found warfarin had no effect on death rate or the risk of blood clots. However it did increase the risk of major bleeding in 107 more people per 1000 population and minor bleeding in 167 more people in 1000 population. Apixaban had no effect on mortality, recurrence of blood clots in blood vessels or major bleeding or minor bleeding, however this finding comes only from one study. Nonhemorrhagic adverse events are less common than hemorrhagic adverse events but should still be monitored closely. Nonhemorrhagic adverse events of warfarin include skin necrosis, limb gangrene, and purple toe syndrome. Skin necrosis and limb gangrene are most commonly observed on the third to eighth day of therapy. The exact pathogenesis of skin necrosis and limb gangrene are not completely understood but are believed to be associated with warfarin's effect on inhibiting production of protein C and protein S. Purple toe syndrome typically develops three to eight weeks after initiation of warfarin therapy. Other adverse effects of warfarin are associated with depletion of vitamin K, which can lead to inhibition of G1a proteins and growth arrest-specific gene 6, which can lead to increased risk of arterial calcification and heart valve, especially if too much Vitamin D is present. Warfarin's interference of G1a proteins have also been linked to abnormalities in fetal bone development in mothers who were treated with warfarin during pregnancy. Long-term warfarin and heparin usage have also been linked to osteoporosis. Another potentially serious complication associated with heparin use is called heparin-induced thrombocytopenia (HIT). There are two distinct types of HIT 1) immune-mediated and 2) non-immune mediated. Immune-mediated HIT most commonly arises five to ten days after exposure to heparin. Pathogenesis of immune-mediated HIT is believed to be caused by heparin-dependent immunoglobulin antibodies binding to platelet factor 4/heparin complexes on platelets, leading to wide spread platelet<unk> tivation.
Anticoagulant
Decongestant
Anticonvulsant
Antipyretic
Cholagogue
Antiparasitic
Antipruritic
Abirritant