Factor V Leiden mutation: This is the most common inherited cause of hypercoagulability, leading to an increased risk of deep vein thrombosis and pulmonary embolism due to its effect on the coagulation pathway, making it resistant to activated protein C.

Prothrombin G20210A mutation: Another inherited condition that increases the production of prothrombin, leading to a hypercoagulable state.
Antithrombin III deficiency: A deficiency in this anticoagulant protein increases the risk of thrombosis.
Protein C deficiency: Similar to Factor V Leiden, a deficiency in protein C leads to decreased regulation of the coagulation cascade, resulting in a hypercoagulable state.
Protein S deficiency: Acts as a cofactor for protein C, and its deficiency also leads to an increased risk of thrombosis.
Antiphospholipid syndrome: An autoimmune disorder characterized by the presence of antiphospholipid antibodies, which can lead to both arterial and venous thrombosis.

Cancer: Certain types of cancer, such as pancreatic cancer, can lead to a hypercoagulable state (Trousseau’s syndrome), making it crucial not to miss this diagnosis due to its severe implications.
Nephrotic syndrome: The loss of anticoagulant proteins in the urine can lead to a hypercoagulable state.
Pregnancy and postpartum state: Both conditions are known to increase the risk of thrombosis due to changes in coagulation factors and venous stasis.

Homocystinuria: A genetic disorder that affects the metabolism of the amino acid methionine, leading to elevated levels of homocysteine, which can cause thrombosis.
Disseminated intravascular coagulation (DIC): A condition characterized by both widespread clotting and bleeding, which can be life-threatening if not recognized and treated promptly.
Heparin-induced thrombocytopenia: A rare but serious condition where the use of heparin triggers an immune response, leading to thrombocytopenia and a hypercoagulable state.