The platelet count and PT And APTT
in a person suffering from frequent
nasal and gastrointestinal bleeds
were seen to be normal. He was also
not taking any medication of any sort,
can you explain why he could still be
having bleeding ddisorders
Answers
Answer: mark me as brainlist
Explanation:
Broadly speaking, if there is no evidences of other cytopenias in the face of a low platelet count, the cause is either medication, platelet antibodies, hypersplenism, infection, or a bone marrow production defect. Methods for measuring platelet antibodies are not within the capability of most laboratories, so other tests should be performed to exclude the aforementioned disorders. These tests would include an antinuclear antibody test of lupus erythematosus, a direct Coombs test for antibodies on red cells, and a bone marrow aspiration and biopsy for myelophthisic processes. Timely observation after omission of medications has been previously described.
When the platelet count is normal but the patient has a qualitative platelet defect with an abnormal Simplate bleeding time, the most likely causes are medication, the myeloproliferative disorders, chronic renal failure, or an inherited platelet function defect. Further tests, which include platelet aggregation studies, are necessary to define acquired or inherited platelet function defects.
Coagulation Protein Deficiencies
The hemorrhagic disorders, von Willebrand's disease (VWD), and hemophilia A are most frequently encountered inherited coagulation factor deficiencies. In order to understand and manage these disorders, it is mandatory to have some knowledge of the macromolecular structure of the factor VIII complex, which is a multimer of a basic molecule. Most agree that the basic molecule can be regarded as having two subunits: one is of lower molecular weight and contains factor VIII coagulant activity (VIII:C); the other is of higher molecular weight and contains factor VIII, von Willebrand factor (VIII:VWF), and VIII:VWF antigen (protein). It may be seen that varying quantities or activities of these two subfractions can be present, thereby causing variabilities in the hemostatic test results that check VIII:C and VIIIrVWF. In most laboratories these tests are the activated partial thromboplastin time (aPTT) for VIII:C and the Simplate bleeding time for VIII:VWF. The major problem that complicates the diagnosis of VWF is that the levels of VIII:C and VIII:VWF may not be reduced in activity enough to produce the classic pattern of laboratory abnormalities such as an abnormal PTT and bleeding time. Hence, other solutions are needed to diagnose the variant forms of VWD. Von Willebrand factor causes the aggregation of platelets in vitro when ristocetin is added. In the absence of von Willebrand factor, ristocetin will not induce platelet aggregation. So, too, if the larger subunits of the factor VIII molecule containing VII1:VWF are reduced, then the antigen level of this subfraction is reduced. Measurements of ristocetin aggregation and VIII von Willebrand factor antigen levels are helpful in sorting out the various forms of VWF and may be required for diagnosis. This is of extreme importance because one of the pitfalls that the clinician must avoid in VWF is to be fooled into thinking that he is dealing with a qualitative or functional platelet defect in a patient who has epistaxis and purpura when only the bleeding time is abnormal. Platelet transfusion will not correct the problem. Von Willebrand's disease should be treated by transfusion of factor VIII cryoprecipitate to correct a qualitative deficiency or by infusing desmopressin acetate for a quantitative deficiency.