Hematologic System Flashcards

1
Q

How are RBCs processed to reduce the chance of febrile transfusion reactions and alloimmunization?

A

leukoreduction

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2
Q

Why should sodium bicarbonate be given to treat an acute transfusion reaction due to ABO incompatibility?

A

to alkalinize the urine and prevent hemoglobin precipitation in the renal tubules

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3
Q

What alternative anticoagulants can be used in a patient with HIT? Which are better in patients with renal and/or hepatic failure?

A

fondaparinux - renal metabolism

argatroban - hepatic metabolism

bivalirudin

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4
Q

What is Humate-P?

A

factor VIII and vWF concentrate

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5
Q

Which drugs can cause a positive Coombs test (drug-induced hemolysis)?

A

penicillin

2nd and 3rd generation cephalosporins

alpha methyldopa

procainamide

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6
Q

How do you determine the volume of RBCs to transfuse to reach a target hct?

A

RBC volume = (Hctinitial - Hcttarget) x BV

HctRBC

BV: blood volume

HctRBC: 60% or 0.6

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7
Q

How are RBCs processed to reduce the chance of GVHD?

A

irradiation

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8
Q

Is activation of the extrinsic or intrinsic pathway usually the initiating step for fibrin formation?

A

extrinsic pathway

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9
Q

How much factor VIII activity is needed prior to surgery?

A

50% for minor surgery

100% for major surgery

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10
Q

Which factors are exposed/released upon platelet activation?

A

GP IIb/IIIa receptors are exposed on the platelet surface

Thromboxane A2 and platelet activating factor (PAF) are released

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11
Q

What is the “two-hit” hypothesis of TRALI?

A

hit 1: sequestration of neutrophils in the lung (causing transient leukopenia)

hit 2: activation of reipient neutrophils by donor antibodies

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12
Q

How can factor VIII levels be increased in a patient with hemophilia A?

A

Factor VIII concentrate: 40 u/mL

cryoprecipitate: 5-10 u/mL

FFP: 1 u/mL

ddAVP: increase production to 2-4x baseline levels

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13
Q

What is the target of the antibodies that cause HIT?

A

hepain – platelet GP 1b complexes

*causes thrombosis, platelet consumption, and thrombocytopenia

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14
Q

Which anticoagulant is recommended for patients with HIT who need CPB?

A

bivalirudin

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15
Q

What is the risk of infection due to blood transfusion for HIV? HepB? HepC?

A

HIV and HepC: 1 in 2,000,000

HepB: 1 in 200,000

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16
Q

What is the mechanism of febrile transfusion reactions?

A

recipient antibodies directed against donor leukocytes

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17
Q

Which are vitamin K-dependent clotting factors?

A

Factors 2, 7, 9, and 10

Protein C and S

18
Q

What are the classic lab findings in DIC?

A

low platelets

elevated PT/INR and PTT

decreased fibrinogen

increased D-dimer

19
Q

How much would transfusing one unit (a six-pack) of platelets increase the platelet count?

20
Q

What is the typical timecourse of TRALI?

A

onset within 2 hours of transfusion

resolution within 48 hours of transfusion

21
Q

Which receptor interaction causes platelets to adhere to a damaged vessel?

A

GP 1b on platelets adheres to vWF that is bound to exposed collagen on the damaged endothelium

22
Q

What are some common precipitating factors for DIC?

A

sepsis

cancer

retained placenta, fetal demise, amniotic fluid embolus

burns, trauma

transfusion reaction

MH

23
Q

How are RBCs process to reduce the chance of anaphylaxis in a patient with IgA deficiency?

24
Q

Which coagulation pathways are monitored with PT/INR? PTT? ACT?

A

PT/INR: extrinsic and common

PTT: intrinsic and common

ACT: intrinsic and common

25
Where is plasminogen made? tPA?
plasminogen is made in the liver and incorporated into fibrin clots tPA is made in the endothelium and released with endothelial damage
26
How do you calculate maximum allowable blood loss?
MABL = _(Hctinitial - Hctfinal) x BV_ Hctinitial BV: blood volume
27
Why are the intrinsic and extrinsic pathways so named?
Extrinsic refers activation of coagulation in the extravascular space (i.e., by exposed tissue factor on damaged endothelium) Instrinsic refers to activation of coagulation in the intravascular space
28
Why does massive transfusion often cause a metabolic alkalosis?
citrate in the blood products is converted to bicarbonate by the liver
29
What distinguishes the three type of von Willebrand Disease?
vWD type 1: low vWF -\> give ddAVP vWD type 2: mutant vWF -\> DON'T give ddAVP vWD type 3: VERY low vWF -\> ddAVP ineffective
30
What is contained in cryoprecipitate?
fibrinogen vWF factor 8
31
Which receptor interaction allow platlet aggregation?
GP IIb/IIIa receptors for extensive crosslinks with fibrin
32
Which anticoagulants are direct thrombin inhibitors?
bivalirudin argatroban dabigatran
33
Which anticoagulants are factor Xa inhibitors?
fondaparinux (binds to ATIII) rivaroxaban apixaban
34
How does clopidogrel affect platelet function?
blocks the ADP (P2Y12) receptor and prevents expression of GP IIb/IIIa on the platelet surface
35
How do abciximab and eptifibatide affect platelet function?
blocking GP IIb/IIIa receptors
36
Why are patients with sickle cell anemia anemic?
sickled cell are removed by the reticuloendothelial system after 10-20 days instead of the usual 120-day RBC lifespan
37
What are the crises of sickle cell anemia patients?
1. aplastic crisis: folate deficiency or viral infection affecting the bone marrow 2. sequestration crisis: hypotension due to massive blood accumulation in the spleen 3. hemolytic crisis: in patients with G6PD deficiency and sickle cell anemia 4. vaso-occlusive crisis: causing pain due to micro and macro infarcts (i.e., acute chest syndrome)
38
Which conditions promote sickling?
Anything that decreases SvO2 1. increased VO2: shivering, fever, increased metabolic rate 2. decreased CO 3. decreased SaO2 4. decreased Hgb (or right-shifted)
39
How does hydroxyurea help patients with sicke cell anemia?
as a long-term treatment, it increases fetal hemoglobin levels
40
How should hgb be optimized pre-operatively in sickle cell patients?
transfuse to a hgb of 30 (regardless of the SS fraction)
41
Which coagulation factors are not made exclusively in the liver?
factor III (a.k.a. tissue factor): endothelium vWF: endothelium factor VIII: endothelium and liver sinusoidal cells