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How do you differentiate between thrombocytopenia vs coag defect

1. low platelets versus low clotting factors 2. PT and PTT time will be elevated in coag defect but not thrombocytopenia 3. Thrombocytopenia usually results in superficial bleeds like petechiae and epistaxis

How does bone marrow examination help you to distinguish between a thrombocytopenia due to a production defect versus increased destruction?

Accelerated destruction = a compensatory increase in the number of megakaryocytes

What is the MOST common hematologic manifestation of AIDS?

Thrombocytopenia; it tends to occur early in HIV infection

Idiopathic Thrombocytopenic Purpura

A subset of Immune Thombocytopenic Purpura in which there is no underlying disease/risk factor;

Does ITP in children tend to be acute or chronic? and what is it associated with?

Acute. Upper Respiratory viral infections. Spontaneously resolves and is self-limited

What population of people get chronic ITP?

Women 20-40 years of age

What antibodies are seen in chronic version of ITP?

Autoantibodies against platelets (antiplatelet antibodies) that bind to GpIIb/IIIa or GpIb in 80% of the cases

What is an important organ in the body that mediates platelet removal in ITP?

Spleen- seems to be important in both the clearance of antibody-coated platelets, and in the production of the antiplatelet antibodies in the first place; splenectomy is indicated in ITP

Is there splenpmegaly in ITP?

No, if there is splenomegaly noticed then you should consider another diagnosis than ITP

Findings in ITP?

Petechiae, ecchymoses, easy bruising, epistaxis, gum bleeding, hemorrhages after minor trauma

What drug interestingly leads to thrombocytopenia?

Heparin; Heparin-Induced Thrombocytopenia

What % of patients on heparin develop HIT?


What form of heparin causes HIT? How many weeks after administration does it occur?

Unfractionated heparin. 1-2 weeks

What should you do if you patient on heparin develops a drop in thrombocytes?

Stop the heparin drips immediately; may be an indication of imminent HIT

Pathophysiology of HIT?

Antibodies form against Platelet factor IV-heparin complexes on platelet surfaces. This causes the activation of platelets and they degranulate causing thrombosis (both venal and arterial thromboses occur) and death and thrombocytopenia

What are the three causes of microangiopathic hemolytic anemia?


What is the cause of TTP?

Thrombotic Thrombocytopenic Purpura is caused by a defect in ADAMTS13 which is a metalloprotease that digests large multimers of vWF circulating in the blood. If there is no ADAMTS13 activity then there is no degradation of the vWF multimers

Is TTP more associated with mutations in ADAMTS13 or with functional inactivation of ADAMTS13?

Functional inactivation due to the presence of an acquired antibody

Symptoms of TTP?

Fever, Thrombocytopenia, transient neurologic symptoms, micrangiopathic hemolytic anemia, renal failure

How can HUS be distinguished from TTP?

Absence of neurologic symptoms in HUS and the predominance of the kidney failure in HUS.

Are there abnormal ADAMTS13 levels in HUS?


What is normally associated with HUS?

Infection wth E. coli O157:H7 and bloody diarrhea normally precede this condition in children; perhaps the Shiga-like toxin released by the E. coil strain causes endothelial damage which then leads to activation of coagulation

Is the coagulation system normal in TTP or in HUS"

Yes. not a problem with coagulation cascade itself

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