Platelets drop in the blood stream when
1. you don't make enough of them. This can happen when a. there is damage to the stem cells that eventually make platelets . We aren't exactly sure who this happens but we know that in some children this appears to be congenital. Sometimes it happens as a result of a viral infection and recovers over time. There is some sense that maybe part of the virus' infective ability damages primitive cells such as stem cells. No test is available. b. there is not enough thrombopoietin (the hormone that stimulates platelet production (similar to erythropoietin for red cells). Apparently this can happen in any number of people who have damaged bone marrow cells since thrombopoietin is made there. No test is available in the routine laboratory. There is a research level test similar to that of EPO but it is not a great test.. c. there is enough thrombopoietin and enough stem cells but somehow they don't work well together . This is really new since we are still trying to find out a lot about those pesky markers. But it does have a logic here. If the TPO receptor is somehow damaged, then it wouldn't make any difference how much TPO you had, the cells wouldn't recognize it. No test is available.
2. you make enough but they are removed from the circulation a. you make an antibody (either specifically directed against the platelets or an antibody that mistakes your platelets for something else) that "coats" the platelet making it an easy target for the splenic macrophages to remove them. [ITP] There are several infectious agent (Mycoplasma is one) for which you make a really good set of antibodies. The problem is that the antibody frequently thinks that the "i" antigen on your red cells is the antigen against which it was made so it binds to the red cell membrane. It appears that many antibodies against viruses work the same way against platelets. To further confuse the issue, there are several antimirobials which, when they are present in therapeutic amounts in the blood stream will passively coat the platelets. Regardless of how they get coated, the spleen recognizes the antibody/goo coated cell and the splenic macrophages (who were made for just this sort of job) phagocytize the cell. We actually have a test that might pick this condition up. b. your spleen is hyperactive and eliminates normal stuff like platelets and red cells indiscriminately (hypersplenism) This can be either primary (the spleen decided to do this for its own reasons) or secondary to another disease (such as CLL). You usually don't need a test for this other than a CT scan since the spleen gives itself away.
c. something has gone awry in your microcirculation (capillaries). When the vessel walls become "different", they stimulate platelets to clump together - with or without the rest of the coagulation cascade becoming activated. 1. DIC - disseminated or diffuse intravascular coagulation This is classically a secondary condition. It cannot be initiated by itself. There must be damage to the capillaries. (The list of potential causative agents or activities is literally pages long.) The damage causes the collagen on the inside membrane of the capillary to change its chemical charge. The charged collagen activates the coagulation cascade which involves the platelets. As these microclots build in the capillaries, there are inadequate amounts of the coagulation factors and platelets in the major circulation (arteries and veins). So, bleeding becomes an issue. The only way to control DIC is to stop the primary event or to stop the blood from wanting to clot so heparin will be used. We have great tests for this (D-Dimer, fibrin degradation products, CBC, etc.)
2. TTP - thrombotic thrombocytopenic purpura. Purpura means bruising, Thrombocytopenic means inadequate numbers of platelets and thrombotic means that there are clumped platelets forming thrombi. Again, for reasons that are not clear, there is some stimulation of the platelets to aggregate in the small vessels. The platelets can randomly clump and "unclump" so a person can have TIA's or migraines or big stuff. while the clumping is going on. In TTP, the organs in which the platelets prefer to clump are the lungs, the brain, and the kidneys. There have never been any antibodies identified with this disease but, one day about 15 years ago, a patient with muscular dystrophy was admitted with this. She was already using the apheresis process for the MD and so when she was hooked up to it for that, she made a remarkable recovery from the TTP. So the theory is that maybe there is a something floating in the blood stream (does n't have to be an antibody) that irritates the capillary lining. So, if you remove the patient's plasma,then you are removing the irritant. One potential culprit is immunosuppression . For example, when you bush your teeth, you cause oral bacteria to enter the blood stream. Your wbc's can clear them out of the system within 20 minutes. BUT, supposing they are left to wander around your blood stream for a couple of hours, then they could alter the vessel wall. Another potential culprit (who is going to sound familiar) suppose you took a medication that killed off a number of cells. The - ah "dead bodies" are left floating around your blood stream and as they disintegrate they cause irritation in the vessels. Treatment is continually removing the plasma until you remove all of the debris and then you have to allow the vessel walls to un-irritate themselves. After that, she can go home. There are no specific tests for TTP but the combination of signs and symptoms and the result of the CBC are quite clear.