Thrombin (EC 3.4.21.5, fibrinogenase, thrombase, thrombofort, topical, thrombin-C, tropostasin, activated blood-coagulation factor II, blood-coagulation factor IIa, factor IIa, E thrombin, beta-thrombin, gamma-thrombin) is a serine protease, an enzyme that, in humans, is encoded by the F2 gene. Prothrombin (coagulation factor II) is proteolytically cleaved to form thrombin in the clotting process. Thrombin in turn acts as a serine protease that converts soluble fibrinogen into insoluble strands of fibrin, as well as catalyzing many other coagulation-related reactions. History
After the description of fibrinogen and fibrin, Alexander Schmidt hypothesised the existence of an enzyme that converts fibrinogen into fibrin in 1872.Prothrombin was discovered by Pekelharing in 1894. Physiology
Synthesis
Thrombin is produced by the enzymatic cleavage of two sites on prothrombin by activated Factor X (Xa). The activity of factor Xa is greatly enhanced by binding to activated Factor V (Va), termed the prothrombinase complex. Prothrombin is produced in the liver and is co-translationally modified in a vitamin K-dependent reaction that converts 10-12 glutamic acids in the N terminus of the molecule to gamma-carboxyglutamic acid (Gla). In the presence of calcium, the Gla residues promote the binding of prothrombin to phospholipid bilayers. Deficiency of vitamin K or administration of the anticoagulant warfarin inhibits the production of gamma-carboxyglutamic acid residues, slowing the activation of the coagulation cascade. In human adults, the normal blood level of antithrombin activity has been measured to be around 1.1 units/mL.
The scalp is the most common pulling site, followed by the eyebrows, eyelashes, face, arms, and legs. Some less common areas include the pubic area, underarms, beard, and chest. The classic presentation is the "Friar Tuck" form of vertex and crown alopecia. Children are less likely to pull from areas other than the scalp.People with trichotillomania often pull only one hair at a time and these hair-pulling episodes can last for hours at a time. Trichotillomania can go into remission-like states where the individual may not experience the urge to "pull" for days, weeks, months, or even years.Individuals with trichotillomania exhibit hair of differing lengths; some are broken hairs with blunt ends, some new growth with tapered ends, some broken mid-shaft, or some uneven stubble. Scaling on the scalp is not present, overall hair density is normal, and a hair pull test is negative (the hair does not pull out easily). Hair is often pulled out leaving an unusual shape. Individuals with trichotillomania may be secretive or shameful of the hair pulling behavior.An additional psychological effect can be low self-esteem, often associated with being shunned by peers and the fear of socializing, due to appearance and negative attention they may receive. Some people with trichotillomania wear hats, wigs, false eyelashes, eyebrow pencil, or style their hair in an effort to avoid such attention. There seems to be a strong stress-related component. In low-stress environments, some exhibit no symptoms (known as "pulling") whatsoever. This "pulling" often resumes upon leaving this environment.