Category: V

In the circulatory system, veins (from the Latin vena) are blood vessels that carry blood toward the heart. Most veins carry deoxygenated blood from the tissues back to the heart; exceptions are the pulmonary and umbilical veins, both of which carry oxygenated blood to the heart. In contrast to veins, arteries carry blood away from the heart. Veins are less muscular than arteries and are often closer to the skin. There are valves in most veins to prevent backflow.

A venous thrombus is a blood clot (thrombus) that forms within a vein. Thrombosis is a term for a blood clot occurring inside a blood vessel. A common type of venous thrombosis is a deep vein thrombosis (DVT), which is a blood clot in the deep veins of the leg. If the thrombus breaks off (embolizes) and flows towards the lungs, it can become a life-threateningpulmonary embolism (PE), a blood clot in the lungs.

When a blood clot breaks loose and travels in the blood, this is called a venous thromboembolism (VTE). The abbreviation DVT/PE refers to a VTE where a deep vein thrombosis (DVT) has moved to the lungs (PE or pulmonary embolism).

An inflammatory reaction is usually present, mainly in the superficial veins and, for this reason this pathology is called most of the time thrombophlebitis. In fact, the inflammatory reaction and the white blood cells play a role in the resolution of venous clots.

Vitamin K refers to a group of structurally similar, fat-soluble vitamins the human body needs for complete synthesis of certain proteins that are required for blood coagulation. Without vitamin K, blood coagulation is seriously impaired, and uncontrolled bleeding occurs. Low levels of vitamin K also weaken bones and promote calcification of arteries and other soft tissues.

Vitamin K1 is active as a vitamin in animals and performs the classic functions of vitamin K, including its activity in the production of blood-clotting proteins.

Vitamin K deficiency is a form of avitaminosis resulting from insufficient vitamin K1 or vitamin K2 or both.

Vitamin K1 Deficiency

Vitamin K1-deficiency may occur by disturbed intestinal uptake (such as would occur in a bile duct obstruction), by therapeutic or accidental intake of a vitamin K1-antagonist such as warfarin, or, very rarely, by nutritional vitamin K1 deficiency. As a result, Gla-residues are inadequately formed and the Gla-proteins are insufficiently active.

Von Willebrand disease (vWD) is the most common hereditary coagulation abnormality described in humans, although it can also be acquired as a result of other medical conditions. It arises from a qualitative or quantitative deficiency of von Willebrand factor (vWF), a multimeric protein that is required for platelet adhesion. It is known to affect humans and dogs (notably Doberman Pinschers), and rarely swine, cattle, horses, and cats. There are three forms of vWD: hereditary, acquired, and pseudo or platelet type. There are three types of hereditary vWD: vWD Type I, vWD Type II, and vWD Type III. Within the three inherited types of vWD there are various subtypes. Platelet type vWD is also an inherited condition.

vWD Type I is the most common type of the disorder and those that have it are typically asymptomatic or may experience mild symptoms such as nosebleeds although there may be severe symptoms in some cases. There are various factors that affect the presentation and severity of symptoms of vWD such as blood type.

vWD is named after Erik Adolf von Willebrand, a Finnish pediatrician who first described the disease in 1926.

Von Willebrand factor (vWF) is a blood glycoprotein involved in hemostasis. It is deficient or defective in von Willebrand disease and is involved in a large number of other diseases, including thrombotic thrombocytopenic purpura, Heyde’s syndrome, and possibly hemolytic-uremic syndrome. Increased plasma levels in a large number of cardiovascular, neoplastic, and connective tissue diseases are presumed to arise from adverse changes to the endothelium, and may contribute to an increased risk of thrombosis.