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Bleeding & clotting disorder & their assessment |Pathology|Physiology


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 the cells 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. These
causes are decreas in platelet count, then if there is problem
with platelet adhesion, even if platelet count is normal for example in Von Willebrand Disease and GP 1B receptor problem.. Then if there is problem
with platelet aggregation like in GP2 B 3A problems. Even with aspirin
overdose there can be abnormal platelet plau formation because aspirin
inhibits thromboxane which is important for these steps -platelet activation and
platelet aggregation. Similarly other drug overdose: like ADP receptor
antagonist ,GP2b3a receptor antagonists- they will lead to decreased
platelet plug formation. Disorders of platelet plaque formation manifests as
appearance of petechiae and purpura on skin and mucous membranes. So these
spontaneous appearance of small-small red dots due to bleeding in capillaries
appear on skin and mucous 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- there will be decreased platelet plug formation.
Second is bleeding time which is 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 relook at the clotting pathway- so one limb is the
intrinsic pathway and other side is extrinsic pathway and from factor 10th
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 decrease
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 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 – deficiency of
clotting factors due to any cause may lead to bleeding disorders. Second cause
may be presence of inhibitors of clotting factors -so concentration of
for clotting factors will be normal but there may be certain inhibitors which
inhibit its activity. The problems of clotting pathways have prolonged
clotting times. So clotting time is prolonged.
Further assessment needs to be done to pinpoint which pathway is involved and
which clotting factor is involved. Now extrinsic and common pathways can be
assessed by a simple method – taking blood and adding tissue thromboplastin into
it and then by finding out how much time it takes the clot.
This is known as prothrombin time- In this we are adding this factor 3 that is
tissue thromboplastin and activating extrinsic pathway. So if any of these
clotting factors factor 7, 10, 5, 2, 1 are deficient or are inhibited- they will be
prolonged prothrombin time. Intrinsic pathway is assessed by activating factor
12 and this is known as activated partial thromboplastin
time. So any of the factors of intrinsic and common pathway if they’re affected- APTT
will be prolonged. So we can deduce from 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 assays. 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 : 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 patient’s 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 prothombin 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
assays. So these are the major assessment strategies for various bleeding
disorders

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