 stoppage of bleeding occurs in three steps after vessel injury. So in case of bleeding disorders, we need to assess each of the steps. If vessels are too fragile, that is, there is some problem in their connective tissue support, then there will be excessive bleeding. But there are many causes for that also, like vitamin C deficiency, connective tissue disorders, which make blood vessels very fragile. If there is any problem in platelet plug formation, that will also lead to bleeding disorders. Some of these causes are decrease in platelet count, then there is if there is problem with platelet addition, even if platelet count is normal. For example, in 1-villagrant disease and GP1B receptor problem, then if there is problem with platelet aggregation, like in GP2B 3A receptor problems, even with aspirin overdose, there can be abnormal platelet plug formation, because aspirin inhibits thromboxin, which is important for these steps, platelet activation and platelet aggregation. Similarly, other drug overdose like ADP receptor antagonist, GP2B3A receptor antagonist, they will lead to decreased platelet plug formation. Disorders of platelet plug formation manifest as appearance of Pettici and Papura on skin and mucus membranes. So these spontaneous appearance of small small red dots due to bleeding in capillaries appear on skin and mucus membranes. The disorders of platelet plug formation can be assessed by various tests. One is platelet count. So if there is decrease in number of platelet counts, there will be decreased platelet plug formation. Second is bleeding time, which assess the time taken for bleeding to stop after an injury. Bleeding disorders can also occur due to disorders of clotting mechanisms. So we need to re-look at the clotting pathway. So one limb is the intrinsic pathway and other side is extrinsic pathway and from pattern 10 onwards, it's a common pathway, which is common to both intrinsic and extrinsic pathway. So deficiency of any of these clotting factors can lead to decreased clot formation and bleeding. Very important cause is hemophilia, which occurs due to factor 8 and factor 9 deficiency. So factor 8 deficiency is known as hemophilia A and factor 9 deficiency is known as hemophilia B. Then there can be liver diseases, which lead to decreased formation of clotting factors as these are proteins and we know proteins are synthesized in liver. More importantly, liver disease also lead to vitamin K deficiency because vitamin K is a fat soluble look and for its absorption, it requires presence of bile. So liver diseases lead to vitamin K deficiency, which is responsible for regeneration of factors 2, 7, 9 and 10. So these causes will lead to deficiency of clotting factors. Second cause may be presence of inhibitors of clotting factors. So concentration of clotting factors will be normal, but there may be certain inhibitors, which inhibit its activity. All the problems of clotting pathways have prolonged clotting time. So clotting time is prolonged. Further assessment needs to be done to pinpoint with pathways involved and which clotting factor is involved. Now extrinsic and common pathways can be assessed by simple method taking blood and adding tissue thromboblastin to it and then finding out how much time it takes to clot. This is known as pro thrombin time. In this, we are adding this factor 3 that is tissue thromboblastin and activating extrinsic path. So if any of these clotting factors, factors 7, 10, 5, 2, 1 are deficient or are inhibited, they will be prolonged pro thrombin time. Intrinsic pathways are assessed by activating factor 12. This is known as activated partial thromboblastin time. So any of the factors of intrinsic and common pathway if they are effective, APTT will be prolonged. So we can deduce from that that when common pathway factors are affected both APTT and PT will be prolonged. Now another assessment known as thrombin time assesses the function of thrombin that is time taken for conversion of fibrinogen to fibrin after addition of thrombin. Further assessment involves specific factor assesses. Presence of inhibitors of clotting factors is assessed by mixing studies. The principle is simple that when we are suspecting any clotting factor disorders, these can be corrected by replacing that specific clotting factors. However, if there is presence of inhibitors, they will block the function of that transfused clotting factor. So in mixing studies patients plasma is mixed with normal plasma. So this normal plasma will have that deficient clotting factor. If our assessment is corrected that PT and PTT which were abnormal before if they are corrected that means clotting factors present in normal plasma have corrected the problem. However, if there is no improvement that means these clotting factors are not able to correct the problem. Now this is due to the presence of inhibitors in the patients plasma. So whatever normal clotting factors are there they are also inhibited by these inhibitors. So we have discussed a lot of assessment strategies for platelet function we talked about bleeding time, platelet count then for clotting factors we talked about thrombin time for extrinsic pathway, activated partial thromboplastin time for intrinsic pathway, clotting time prolonged in both. We talked about thrombin time taken for conversion of fibrinogen to fibrin and we also spoke about specific factor assess. So these are the major assessment strategies for various bleeding disorders.