![]() In some cases, the gene mutation occurs sporadically (out of the blue), with no family history of clotting disorders. Unless there have been other affected boys in the family there may be no way of knowing whether the mother is a carrier, as most carriers remain healthy. 25 per cent chance of the child being an affected boy.25 per cent chance of the child being an unaffected boy.25 per cent chance of the child being an unaffected carrier girl.25 per cent chance of the child being an unaffected non-carrier girl.This means that only boys are affected by x-linked disorders and the mother is a carrier of the disease. However, in males, who only have one ‘X’, there is not another ‘X’ to provide a functioning gene. As females have two ‘X’ chromosomes, a fault on this chromosome can be completely or partially overcome by the other healthy ‘X’ in the pair. The chromosome that determines the gender of the child will either contain ‘XX’ (female) or ‘XY’ (male). ![]() Platelets only live for just over a week, then the body destroys them and new ones are released. Megakaryocytes (large bone marrow cells) are formed, mature and then die, which is when they release platelets. Over half of the new platelets circulate in the bloodstream and the rest remain in storage in the spleen. Platelets – also called thrombocytes – are formed in the bone marrow from stem cells. This complicated chemical reaction always follows a strict pattern – with each clotting protein (known as a coagulation factor) turned on in order. When all of the factors are turned on, the blood forms a clot which stops the injury site bleeding any further. They also start off a complicated chemical reaction to form a mesh made of a substance called fibrin. When a blood vessel is injured, platelets clump together to block the injury site. ![]() Blood is made up of different types of cells (red blood cells, white blood cells and platelets) all suspended in a straw-coloured liquid called plasma. Platelets are the cells responsible for making blood clot.
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