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63 Cards in this Set
- Front
- Back
What are problems with massive blood transfusion? |
PATCH: |
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Why can you hold off on giving calcium to a patient with hypocalcemia after blood transfusion? |
serum ca often returns to normal rapidly after transfusion because citrate is metabolized by the liver and calcium is mobilized from endogenous source |
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How does aspirin affect platelet aggregation? |
It impairs platelet aggregation in 2 major ways |
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What does ADP and fibrin do for platelet aggregation? |
- ADP is the most potent platelet aggregator |
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What are the advantages of preop transfusion? |
1. increasing 2,3-DPG |
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How do you treat DIC? |
1. treat cause |
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What factors does PTT screen for? |
levels of V and VIII |
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If PTT >1.5 x control what should you give? |
FFP |
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How is the diagnosis of a hemolytic transfusion reaction confirmed? |
presence of free hemoglobin in spun plasma with a direct coombs test |
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In a patient that required an O- emergency transfusion what should you do after giving 2 or more units of uncrossmatch blood? |
continue giving uncrossmatch blood or incompatabilities with the new blood will develop |
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How often can patient's give autologous blood? |
1 unit per week for 4 weeks |
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How does blood change as it sits on a shelf? |
1. PaCO2 increases leading to acidosis, |
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Why can cigarette smokers have an anemia? |
They have an effective anemia due to binding of hemoglobin by carbon monoxide which creates carboxyhemoglobin |
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Why do patients with poor LV function or ischemic heart disease require higher hematocrits? |
it optimizes O2 delivery and does not predispose to compensatory cardiovascular changes like tachycardia, which increases oxygen consumption |
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What is fluosol-DA? |
in combination with 100% oxygen fluosol (20mg/kg) increases oxygen content and improves mixed venous oxygen saturation |
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When are cells savers likely to be used? |
1. when there is expected to be at least 1500mL of blood loss; |
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When should cell savers not be used? |
risk of contaminated blood is high (infection, gut perforation, malignancy-risk of systemic spread) |
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What is contained in blood salvaged by a cell saver? |
red blood cells and saline (coagulation factors, platelets, and calcium are not salvaged) |
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What are benefits and risks of acute normovolemic hemodilution? |
-benefits: |
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Pt selection for acute normovolemic hemodilution is based on what factors? |
1. expected blood loss >1500 mL or 30% of blood volume |
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How do you know how much blood to withdraw for acute normovolemic hemodilution? |
Volume to be removed = EBV x ((Hi-Hf)/Ha), |
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How is blood that was withdrawn from a patient during acute normovolemic hemodiluation retransfused? |
blood should be transfused in the reverse order of removal - 1st unit has the highest hematocrit and should be given last |
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How long can you keep blood that was removed during acute normovolemic hemodilution at room temperature? |
8 hours |
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What is more often transmitted in blood transfusion, hep B or C? |
hep B |
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Where are the A and B antibodies located? |
in the serum and not in the plasma |
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When a patient receiving uncrossmatched O- PRBCs receives multiple units of O- uncrossmatched PRBCs can you switch back to their actual type specific blood? |
they can be switched back to their type specific blood after further testing by the blood bank indicates that it is safe to do so |
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Laboratory workup of a bleeding problem. |
Hb/Hct |
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What does an increased reticulocyte imply? |
Consumption of formed RBCs |
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Formation of a platelet plug essential to normal clotting occurs in what 3 processes? |
1. Activation |
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Describe platelet activation |
When platelets contact |
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Describe platelet aggregation. |
-Activation from collagen contact stimulates platelets to aggregate, as well as fibronectin, prostaglandins, Ca, and ADP |
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What do GP IIb/IIIa receptors allow? What are they also a receptor for? |
They allow fibrinogen to form bridges between platelets, triggering platelet aggregration |
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What is the MOA of GP IIb/IIIa inhibitors? |
They inhibit platelet aggregation by blocking ADP binding to the IIb/IIIa receptor |
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Describe platelet adherence. |
Platelets adhere via the GP Ia receptor |
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Summarize platelet plug formation. |
-Once platelet activation occurs aggregation depends largely upon GP IIb/IIIa receptor and adhesion upon the GPIa receptor. |
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What does procoagulant factor activation lead to? |
thrombin and then fibrin formation - the basic building block of a hemostatic plug |
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2 coagulation pathways |
1. Primary tissue factor pathway - Extrinsic pathway |
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What are the procoagulants of the final common pathway? |
Factor X |
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What is the target for the anticoagulant Warfarin? |
Vitamin K epoxide reductase (VKORC) which reduces Vit K back to its active form |
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Describe the steps of thrombin formation. What converts prothrombin to thrombin? |
1. After injury to the vessel wall, tissue factor is exposed on the surface of damaged endothelium. |
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Other than convert fibrinogen to fibrin, what also does thrombin do? |
It also activates factors |
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What factors are part of the common pathway? |
10, 2 (thrombin), 1 (fibrin) |
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Which diseases effect the intrinsic pathway? |
Hemophilia A - factor 8 deficiency |
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PT measures the activity of which factors? |
1 - fibrinogen |
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Summarize intrinsic and common pathway. |
12 -> 11 -> 9 -> 10 -> 2 -> 1 |
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Summarize extrinsic and common pathway. |
7 -> 10 -> 2 -> 1 |
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What is the half life for factor 7? what is the significance of this? |
4-6 hrs |
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What is the importance of factor 7? |
It is the initiating event in coagulation. |
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What does recombinant factor 7 do? |
It increases factors 10a and 9a on the surface of platelets with subsequent increases in thrombin. It reduces clot lysis and bleeding. |
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Describe Hemophilia A's genetics, lab values, and tx. How much must be present for clotting to occur? |
- Found on X chromosome (sex linked) |
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Describe Hemophilia B's genetics, lab values, and tx. |
- Found on X chromosome (sex linked) |
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What is Humate P? |
virus deactivated purified factor 8 concentrate which is derived from plasma and has vW factor |
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What is HIT? |
the development of thrombocytopenia due to the admin of various forms of heparin. |
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What causes HIT? |
An abnormal interaction by heparin with the immune system which results in the formation of antibodies (Ig-G) |
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What is strongly suggestive of HIT? |
Drop in platelet count >30-50% (acutely or over several days) in those receiving heparin |
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What is the hallmark of HITT? |
A massive thrombin burst triggering thrombosis which then actives the fibrinolytic system producing consumptive coagulopathy |
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What is the tx of HIT and HITT? |
Direct thrombin inhibitors lepirudin and argatroban |
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How is lepirudin vs argatroban metabolized? Other characteristics? |
Lepirudin - Primary in the kidney, fatal anaphylaxis |
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MOA Warfarin. What are the lab findings? |
Interferes with the synthesis of vitamin K dependent factors 2,7,9, and 10 |
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What is Dabigatran (Pradaxa)? |
It is a direct thrombin inhibitor (DTI) approved for stroke prevention in AFib for use instead of Warfarin |
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What are the factor 10a inhibitors? |
1. Rivaroxaban (Xarelto) - stroke prevention better in the setting of Afib than w/ Warfarin w/o increasing bleeding risk |
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What was the RE-LY trial? What were the results? |
- Randomized Evaluation of Long-term anticoagulant Therapy study which pitted 2 dosages of dabigatran against conventional warfarin for stroke convention |
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Explain the fibrinolytic system. |
-Plasminogen is a protein normally found in the blood |