could you explain it for the rest of us? 🙂
Of course - sorry I deleted my post! Reply coming right up!
So... First, bleeding time has to do with platelet aggregation. The 1st process in stopping a bleed is the platelets start adhering. So for a BT, they cut the pt & see how long it takes for that initial platelet plug to form. Anything that inhibits platelets from adhering to each other or to the collagen underneath the endothelial cells will increase bleeding time.
PTT & PT are tests for the coagulation cascade/clotting factors. PT is for the extrinsic pathway (mnemonic: the EX-PresidenT) which tests the stability of factor VII and everything downstream. PTT is for the intrinsic pathway which tests factors XII, XI, IX, VIII and everything downstream.
"Bleeding" disorders can affect either or both.
For example, Hemophilia A, a deficiency of factor VIII. Factor VIII is involved in the upstream part of the intrinsic pathway, so PTT will be prolonged. PT will be fine b/c VII and everything downstream is fine. Bleeding time will be fine b/c the platelets are happy clams. Same goes for Hemophilia B, but with factor IX.
In the case of something like Bernard-Soulier (which I think of as mini-VWD), your Gp1b receptors are jacked. Platelets adhere to the exposed collagen through their Gp1b receptors which bind vWF which binds the collagen forming a bridge. If Gp1b receptors are jacked, the whole adhering to collagen is jacked -platelets just whizz by. Your BT will be increased, but those coagulation factors are just fine - so if you take that pt plasma & put it in a test tube & initiation coag, everything will be just peachy. For some reason (unknown to me) you also have thrombocytopenia in Bernard-Soulier compounding the problem (think: B-S is 2 words, we have 2 problems in this scenario).
But what about vWD? vWD is special - first, it messes up your vWF, which we said above is involved in platelets adhering to the exposed collagen. Without it, platelets whizz by, BT is increased.
But importantly, vWF hugs your factor VIII and keeps it safe. W/o vWF, it's like a functional factor VIII deficiency - now you can have prolonged PTT (extrinsic pathway). PT will be fine, cuz nothing over there is jacked.
In the case of Glanzmann, we have messed up GpIIa/IIIb receptors. This time, our platelets have trouble adhering to each other b/c they use their GpIIa/IIIb receptors to form bridges connecting each other using fibrinogen. W/o the receptors, no bridges, no aggregating platelets, no sticking & plugging up our open wound. So BT is increased.
DIC. In DIC we've generally damaged our endothelium so we initiate the coagulation cascade and make all these thrombi everywhere that suck up our coagulation factors & platelets. Without coag factors of all kinds, PT & PTT go up. Without platelets circulating, platelet count goes down & BT increases.
One last thing: Vitamin K. Vitamin K is involved in the gamma-carboxylation of factors II, VII, IX, X (and protein C & S). When we have a Vit K deficiency, we lack all these factors. Notice they belong to both pathways so we have prolonged PTT & PT. Interestingly, when we take warfarin, we're creating essentially a vitamin K deficiency - which affects both pathways - but someone figured out that measuring PT was better for Warfarin. So, BOTH PT & PTT increase in Warfarin therapy, but we only monitor PT. The same is true for heparin - it affects both pathways, but someone figured out PTT was better for monitoring therapy, so we use PTT for heparin even though both PT & PTT are increased (b/c heparin increases degredation of II, IX, X, XI & XII, both pathways involved)
Hopefully this helps
🙂 Obviously, I'm a med student, not an expert so if there are mistakes above, apologies in advance
🙂
