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63 Cards in this Set
- Front
- Back
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What are problems with massive blood transfusion?
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PATCH:
P = Platelets (thrombocytopenia), Potassium (hyperkalemia), A = ARDS, Acid base changes (usually acidosis), T = temperature decreased C = Citrate intoxication leading to hypocalcemia (prolonged QT and hypotension), H = Hepatitis and other infections (AIDS, syphilis) |
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Why can you hold off on giving calcium to a patient with hypocalcemia after blood transfusion?
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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?
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It impairs platelet aggregation in 2 major ways
1. inhibits COX, an enzyme which converts arachadonic acid to protaglandin 2 2. prevents the formation of thromboxane, a potent platelet aggregator |
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What does ADP and fibrin do for platelet aggregation?
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- ADP is the most potent platelet aggregator
- fibrin stabilizes occlusive platelet plug |
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What are the advantages of preop transfusion?
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1. increasing 2,3-DPG
2. increased O2 carrying capacity |
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How do you treat DIC?
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1. treat cause
2. Give platelets, FFP, and cryo |
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What factors does PTT screen for?
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levels of V and VIII
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If PTT >1.5 x control what should you give?
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FFP
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How is the diagnosis of a hemolytic transfusion reaction confirmed?
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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?
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continue giving uncrossmatch blood or incompatabilities with the new blood will develop
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How often can patient's give autologous blood?
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1 unit per week for 4 weeks
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How does blood change as it sits on a shelf?
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1. PaCO2 increases leading to acidosis,
2. 2-3 DPG decreases, 3. platelets decreases, 4. factors deteriorate especially V and VIII, 5. potassium increases from hemolysis |
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Why can cigarette smokers have an anemia?
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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?
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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?
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in combination with 100% oxygen fluosol (20mg/kg) increases oxygen content and improves mixed venous oxygen saturation
- has a very short half life and may predispose to coagulopathies |
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When are cells savers likely to be used?
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1. when there is expected to be at least 1500mL of blood loss;
2. in the setting of difficult cross match problems when availability of enough cross matched blood is in doubt |
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When should cell savers not be used?
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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?
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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?
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-benefits:
1. reduce the need for allogenic blood, 2. improve blood viscosity and thus increased tissue perfusion, 3. reduced intraop red cell loss -risks: 1. decreased arterial O2 content, 2. increased HR and CO can lead to myocardial ischemia |
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Pt selection for acute normovolemic hemodilution is based on what factors?
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1. expected blood loss >1500 mL or 30% of blood volume
2. preop hemoglobin concentration 3. absence of significant heart, lung, kidney, or liver dz 4. free of infection |
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How do you know how much blood to withdraw for acute normovolemic hemodilution?
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Volume to be removed = EBV x ((Hi-Hf)/Ha),
Hi = initial hemoglobin, Hf = final hemoglobin, Ha is average of initial and final hemoglobin |
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How is blood that was withdrawn from a patient during acute normovolemic hemodiluation retransfused?
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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?
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8 hours
- If stored at 1-6 degrees 24 hrs |
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What is more often transmitted in blood transfusion, hep B or C?
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hep B
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Where are the A and B antibodies located?
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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?
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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
-the passively transfused anti-A and anti-B antibodies found in O PRBCs are seldom a problem |
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Laboratory workup of a bleeding problem.
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Hb/Hct
PT/PTT INR |
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What does an increased reticulocyte imply?
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Consumption of formed RBCs
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Formation of a platelet plug essential to normal clotting occurs in what 3 processes?
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1. Activation
2. Aggregration 3. Adhesion |
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Describe platelet activation
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When platelets contact
1. collagen, 2. tissue factor, or 3. thrombin they become activated |
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Describe platelet aggregation.
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-Activation from collagen contact stimulates platelets to aggregate, as well as fibronectin, prostaglandins, Ca, and ADP
-There are also important receptors that play a role in this process - most important is GP IIb/IIIa receptor |
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What do GP IIb/IIIa receptors allow? What are they also a receptor for?
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They allow fibrinogen to form bridges between platelets, triggering platelet aggregration
- it is a Ca-dependent aggregating receptor for fibrinogen, fibronectin, and vWF |
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What is the MOA of GP IIb/IIIa inhibitors?
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They inhibit platelet aggregation by blocking ADP binding to the IIb/IIIa receptor
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Describe platelet adherence.
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Platelets adhere via the GP Ia receptor
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Summarize platelet plug formation.
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-Once platelet activation occurs aggregation depends largely upon GP IIb/IIIa receptor and adhesion upon the GPIa receptor.
-Aggregation and Adhesion act together to form a platelet plug -Myosin and actin filaments in platelets are stimulated to contract during aggregation, further reinforcing the plug |
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What does procoagulant factor activation lead to?
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thrombin and then fibrin formation - the basic building block of a hemostatic plug
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2 coagulation pathways
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1. Primary tissue factor pathway - Extrinsic pathway
2. Secondary contact activation pathway - Intrinsic pathway -Both activate the final common pathway |
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What are the procoagulants of the final common pathway?
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Factor X
Thrombin Fibrin |
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What is the target for the anticoagulant Warfarin?
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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?
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1. After injury to the vessel wall, tissue factor is exposed on the surface of damaged endothelium.
2. The interaction of tissue factor with plasma factor VII activates the coagulation cascade and results in the conversion of Stuart factor (X) to Xa in the common pathway 3. Along with Va, Ca, and phospholipid, Xa then converts II (prothrombin) to IIa (thrombin) which converts fibrinogen (factor I) to a stable clot -> fibrin (Ia) |
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Other than convert fibrinogen to fibrin, what also does thrombin do?
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It also activates factors
V, VIII, and XI, as well as stimulating platelets |
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What factors are part of the common pathway?
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10, 2 (thrombin), 1 (fibrin)
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Which diseases effect the intrinsic pathway?
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Hemophilia A - factor 8 deficiency
Hemophilia B - factor 9 deficiency vWD - lack of protein important for the function of factor 8 as well as platelet function |
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PT measures the activity of which factors?
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1 - fibrinogen
2 - prothrombin 5 - proaccelerin 7 - proconvertin 10 - Stuart factor 12 - Hageman factor |
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Summarize intrinsic and common pathway.
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12 -> 11 -> 9 -> 10 -> 2 -> 1
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Summarize extrinsic and common pathway.
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7 -> 10 -> 2 -> 1
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What is the half life for factor 7? what is the significance of this?
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4-6 hrs
- makes PT useful in evaluating hepatic synthetic function, if liver function is compromised this is reflected quickly by factor 7 def - prolonged PT 2-3x normal generally indicates very severe liver dysfunction unless Vit K def is present |
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What is the importance of factor 7?
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It is the initiating event in coagulation.
- factor 7a binds with tissue factor producing a complex which activates factors 7, 9 and 10 |
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What does recombinant factor 7 do?
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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?
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- Found on X chromosome (sex linked)
- Manifested by prolonged PTT (intrinsic pathway) and a normal PT - Must be at least 30% normal factor 8 for clotting to occur - Can treat with factor 8 concentrate |
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Describe Hemophilia B's genetics, lab values, and tx.
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- Found on X chromosome (sex linked)
- Manifested by prolonged PTT (intrinsic pathway) and a normal PT - tx with human purified and recombinant factor 9 as well as FFP (2nd choice) |
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What is Humate P?
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virus deactivated purified factor 8 concentrate which is derived from plasma and has vW factor
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What is HIT?
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the development of thrombocytopenia due to the admin of various forms of heparin.
- predoses to thrombus formation and when thrombosis is ID'd it is called HITT (heparin induced thrombocytopenia and thrombosis) |
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What causes HIT?
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An abnormal interaction by heparin with the immune system which results in the formation of antibodies (Ig-G)
-this heparin-antibody complex activates platelets which results in intra-vascular clot formation and an overall reduction in systemic platelet count |
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What is strongly suggestive of HIT?
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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?
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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?
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Direct thrombin inhibitors lepirudin and argatroban
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How is lepirudin vs argatroban metabolized? Other characteristics?
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Lepirudin - Primary in the kidney, fatal anaphylaxis
Argatroban - in the liver, less immunogenic |
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MOA Warfarin. What are the lab findings?
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Interferes with the synthesis of vitamin K dependent factors 2,7,9, and 10
-Both PT and PTT are prolonged |
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What is Dabigatran (Pradaxa)?
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It is a direct thrombin inhibitor (DTI) approved for stroke prevention in AFib for use instead of Warfarin
-Does not require regular monitoring -In same family as lepirudin and argatroban |
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What are the factor 10a inhibitors?
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1. Rivaroxaban (Xarelto) - stroke prevention better in the setting of Afib than w/ Warfarin w/o increasing bleeding risk
2. Apixaban 3. Fondaparinux |
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What was the RE-LY trial? What were the results?
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- Randomized Evaluation of Long-term anticoagulant Therapy study which pitted 2 dosages of dabigatran against conventional warfarin for stroke convention
- Dabigatran was noninferior to warfarin at the lower dose (110mg) and superior to warfarin at the higher dose (150mg) decreasing stroke risk - The higher dose was associated with 75% drop in hemorrhagic stroke risk - Somewhat higher risk of MI, but the FDA felt the benefits outweigh the risk |
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Explain the fibrinolytic system.
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-Plasminogen is a protein normally found in the blood
- It is degraded into plasmin which begins with activation of the coagulation cascade - Plasmin acts upon fibrin to break down or degrade clot - forming fibrin split products Factor 12a -> Plasminogen -> Plasmin -> Fibrin -> Fibrin split products |
