The thrombi which form in these individuals are unstable, tend to embolize, and may therefore lead to thromboembolic events such as pulmonary embolism. Both bleeding and thrombotic events can occur at separate times or even concurrently in the same individual with the disorder. Fibrinogen storage disease
All individuals with mutations causing fibrinogen storage disease have low blood fibrinogen levels but usually lack severe bleeding episodes, thrombotic episodes or liver disease. Individuals that do have fibrinogen storage disease often come to attention either because they have close relatives with the disease, are found to be hypofibrinogenmic during routing testing, or exhibit clinical (e.g. jaundice) or laboratory (e.g. elevated blood levels of liver enzymes) evidence of liver disease. Unlike other forms of congenital hypofibrinogenemia, a relatively high percentage of individuals with fibrinogen storage disease have been diagnosed in children of very young age. Pathophysiology
Fibrinogen is made and secreted into the blood by liver hepatocytes. The final secreted protein is composed of two trimers each of which is composed of three polypeptide chains, Aα (also termed α) encoded by the FGA gene, Bβ (also termed β) encoded by the FGB gene, and γ encoded by the FGG gene. All three genes are located on the long or "p" arm of human chromosome 4 (at positions 4q31.3, 4q31.3, and 4q32.1, respectively). The genes are ordered FGB, FGA, and FGG and are transcribed into messenger RNA in tight synchrony. The messenger RNAs associate with the endoplasmic reticulum, translated into polypeptides, and enter the endoplasmaic reticulum where they assembled together.
In cases where participants do not have or have minimal symptoms of anxiety or depression, antidepressants still have those effect.A limited study was presented at a conference in Berlin, suggesting opioid release differs in problem gamblers from the general population, but in a very different way from people who have a substance use disorder.The findings in one review indicated the sensitization theory is responsible. Dopamine dysregulation syndrome has been observed in the aforementioned theory in people with regard to such activities as gambling.Some medical authors suggest that the biomedical model of problem gambling may be unhelpful because it focuses only on individuals. These authors point out that social factors may be a far more important determinant of gambling behavior than brain chemicals and they suggest that a social model may be more useful in understanding the issue. For example, an apparent increase in problem gambling in the UK may be better understood as a consequence of changes in legislation which came into force in 2007 and enabled casinos, bookmakers, and online betting sites to advertise on TV and radio for the first time and which eased restrictions on the opening of betting shops and online gambling sites.Pathological gambling is similar to many other impulse-control disorders such as kleptomania. According to evidence from both community- and clinic-based studies, individuals who are pathological gamblers are highly likely to exhibit other psychiatric problems concurrently, including substance use disorders, mood and anxiety disorders, or personality disorders.Pathological gambling shows several similarities with substance use disorders.