Excessive bleeding due to a lack of clotting factors
Excessive bleeding can result from the lack of any clotting factor. The three most common types that will be discussed here are (1) vitamin K deficiency, (2) haemophilia and (3) thrombocytopenia.
Decreased prothrombin, factor VII, IX, and X due to lack of vitamin K
Almost all clotting factors are synthesized in the liver. As a result, liver diseases such as hepatitis, cirrhosis, and acute yellow atrophy (with hepatocellular degeneration caused by toxins, infections, or other factors) sometimes impair the system. The coagulation system is numerous and the patient is bleeding from a severe lack of factors.
Another cause of a decrease in the synthesis of coagulation factors in the liver is a lack of vitamin K. Vitamin K is an essential element for liver carboxylation (adding the carboxyl group to the tail of the glutamic acid structure) to form into 5 important clotting factors: prothrombin, factor VII, factor IX, factor X, and protein C. In this reaction, vitamin K is oxidized and converted to its inactive form. One enzyme is vitamin K epoxide reductase (vitamin K epoxide reductase complex 1VKOR c1) that converts vitamin K back into its active form.
Lack of vitamin K leads to a lack of clotting factors in the blood, which can lead to severe bleeding.
Vitamin K is continuously synthesized in the intestine by bacteria, so vitamin K deficiency rarely occurs in healthy people even when food is deficient in vitamin K (except for infants without intestinal lice bacteria). However, in patients with gastrointestinal disease, vitamin K deficiency often occurs due to fat malabsorption because vitamin K is oil-soluble and is usually absorbed into the bloodstream along with the fat.
One of the most common causes of vitamin K deficiency is that the liver does not excrete bile into the digestive tract (due to obstruction of the bile duct or disease of the liver). Lack of bile prevents the absorption of fat thereby reducing vitamin K absorption. Thus, liver disease is often the cause of decreased prothrombin production and some other coagulation factors due to both reasons: vitamin malabsorption. K and due to damage to liver cells. Therefore, vitamin K is injected before surgery for surgical patients with liver disease or obstruction, usually 4 to 8 hours before surgery so that liver cells can produce coagulation factors with at least 1 / 2 normal capacity, from which there is enough clotting factor to avoid the risk of bleeding too much during surgery.
Hemophilia is a bleeding disease whose patients are mostly men. In 85% of cases, it is due to a lack of factor VIII, which is known as hemophilia A or classic hemophilia. One in every 10,000 men in the United States has hemophilia A. The other 15 percent are due to a deficiency of factor IX.
Both of these factors are inherited on the X chromosome.
So, women almost never get hemophilia because at least one of their two X chromosomes will not carry the disease gene. If one of their chromosomes carries a disease gene, they become a hemophilia carrier, transmitting the disease to half of the boys and passing the carrier state to half of the girls.
There are several levels of bleeding depending on the genetic deficiency. Bleeding usually occurs after trauma, but in some patients, severe and prolonged bleeding can occur after a small, barely noticeable wound, such as bleeding for days after tooth extraction.
Factor VIII is made up of two components, a large particle with a molecular weight of up to millions and a small particle with a molecular weight of only about 230,000.
Small particles play a very important role in the endogenous coagulation pathway, if there is a lack of this sub-particle will cause hemophilia A. In the absence of large particles will cause von Willebrand disease.
When a hemophilia A patient develops severe bleeding, the only truly effective treatment is injected with pure factor VIII. Factor VIII is very expensive because it is synthesized from human blood and is obtained only in very small amounts. However, the production and use of recombinant factor VIII has enabled this treatment to reach more hemophilia A patients.
Thrombocytopenia means a low platelet count in the circulation.
Patients with thrombocytopenia tend to bleed like hemophilia, except that bleeding usually occurs from more small veins or capillaries than from large blood vessels such as in hemophilia. As a result, there are numerous small, dot-like hemorrhages throughout the entire body tissue. Skin appears many small petechiae, purple-red in color, hence the disease is called thrombocytopenic purpura. As noted earlier, platelets are especially important for repairing small damage to capillaries and other small blood vessels.
Normally, bleeding will not occur until the platelet count falls below 50,000 / µl with normal amounts between 150,000 and 300,000. When platelets fall to 10,000 cells / l, the patient usually dies.
Sometimes there is no need for a blood platelet count test and it is still possible to predict thrombocytopenia if the person's blood clot is not contracting.
This is considered an early sign because normal clot contraction depends on the release of clotting factors from a large number of platelets trapped in the fibrin network in the clot.
The majority of people with thrombocytopenia have idiopathic thrombocytopenia ITP (idiopathic thrombocytopenia ITP). In the majority of these patients, there is a reason for which special antibodies are formed, reacting against and destroying platelets. Whole fresh blood containing large amounts of platelets may be administered to these patients. Splenectomy is also an effective remedy because the spleen normally removes a large number of platelets from the circulation.