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33 Cards in this Set
- Front
- Back
3 roles in platelet plug formation
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adhesion (vWF on collagen, then GPIb-IX on platelet)
aggregation (via fibrinogen bridges) secretion |
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Fibrinogen bridges form between what?
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GP IIb-IIIa
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Collection of mucocutaneous bleeding locations?
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epistaxis, gum, heavy menses, bruising, GI/GU bleeding
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Where do petechiae tend to occur? What is going on with platelets?
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legs, LE; low platelets
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too few platelets
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thrombocytopenia
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too many platelets
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thrombocytosis
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Describe pseudothrombocytopenia (platelet clumping)
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EDTA-anticoagulation, certain pts have a change that causes platelets to clump together (otherwise no bleeding consequence)
check peripheral blood smear |
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levels of platelets that need tx or risk for hemorrhage
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<20,000
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three broad causes of thrombocytopenia
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underproduction (don't make them)
peripheral destruction (make before destroyed) splenic sequestration (hiding out) |
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Causes of underproduction of thrombocytopenia
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marrow failure (myelodysplasia, aplastic anemia, vitamin def.)
marrow infiltration (tumors) marrow toxins (chemo, radiation, infections, alcohol) |
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Non-immune mechanisms of peripheral destruction
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DIC, TTP
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process of abnormal generation of thrombin, consumption of clotting factors, destruction of platelets, and activate fibrinolysis
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DIC
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Components of DIC diagnosis
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elevated PT (using up FVII)
low platelets low/falling fibrinogen Inc fibrin degradation (D-Dimer) maybe schistocytes |
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Etiologies of DIC
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gram- sepsis, severe burns, obstetrical disasters, certain leukemias, shock, insect/snake venoms
regardless, treat underlying cause -can support with platelets, clotting factors, or fibrinogen |
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Process with abnormal activation of platelets with vWF and fibrin deposition in microvasculature & peripheral destruction of platelets and RBCs
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thrombotic thrombocytopenic purpura
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Pentad of Thrombotic thrombocytopenic purpura
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MAHA(microangiopathic hemolytic anemia)(MUST HAVE)
-inc LDH, inc bilirubin, schistocytes present low platelets (MUST HAVE) fever neurologic manifestations renal manifestations |
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Underlying Cause of TTP
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antibody against protease (ADAMTS-13)
-can measure activity levels of ADAMTS-13 or presence of inhibitor to ADAMTS-13 |
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When can TTP occur?
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Drugs (ticlopidine, quinine, cyclosporine, tacrolimus, gemcitabine)
inc incidence with pregnancy or AIDS |
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Tx of TTP
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plasma exchange (avoid platelet transfusions, fuels the fire)
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Common HUS manifestations
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fewer neuro than TTP, more renal manifestations
post diarrheal illness (shiga toxin) Tx with plasma exchange or supportive care |
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Drugs that can cause thrombocytopenia immune mechanism
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B-lactam antibiotics
Trimeth-sulfa drugs quinine/quinidine heparin |
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What occurs with heparin-induced thrombocytopenia?
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about 7-10d after heparin starts, platelets drop by 30-50%.
STOP heparin immediately (can lead to thrombosis) |
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Diagnosis of immune/idiopathic thrombocytopenic purpura
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dx of exclusion (unlike Coombs test in hemolytic a)
-megakaryocytes should be present in marrow |
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When is ITP treated?
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Not in children, usually resolves
In adults, treat below 30,000 w/ corticosteroids |
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Tx protocol for ITP
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2/3 resolve on steroids
1/3 have splenectomy 2/3 respond to splenectomy 1/3 have immunosuppression |
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Differences between ITP and TTP
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TTP has schistocytes; ITP had normal RBCs
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How many platelets are normally in spleen?
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1/3; if spleen enlarges, platelet count drops
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When are platelet transfusions used?
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when bleeding or prevent bleeding
NOT TTP |
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Describe secondary thrombocytosis
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working at appropriate reactive responses
inflammation, infection, bleeding, iron deficiency |
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Describe diseases causing primary thrombocytosis
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essential thrombocythemia, polycythemia vera, CML, and myelofibrosis
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Qualitative bleeding disorders marked by...
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prolonged bleeding time
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2 congenital qualitative platelet disorders
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Glanzmann's thrombaesthenia (defect in IIb/IIIa)
Bernard-Soulier (defect in Ib/IX) |
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4 main sources of acquired qualitative platelet disorders
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uremia
drugs (ASA, NSAIDs) Herbs Myeloproliferative diseases |