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**My Anesthesia ABA Advanced Study Cards > Hematologic System > Flashcards

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?

A

30-60k

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?

A

washed

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
Q

Where is plasminogen made? tPA?

A

plasminogen is made in the liver and incorporated into fibrin clots

tPA is made in the endothelium and released with endothelial damage

26
Q

How do you calculate maximum allowable blood loss?

A

MABL = (Hctinitial - Hctfinal) x BV

Hctinitial

BV: blood volume

27
Q

Why are the intrinsic and extrinsic pathways so named?

A

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
Q

Why does massive transfusion often cause a metabolic alkalosis?

A

citrate in the blood products is converted to bicarbonate by the liver

29
Q

What distinguishes the three type of von Willebrand Disease?

A

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
Q

What is contained in cryoprecipitate?

A

fibrinogen

vWF

factor 8

31
Q

Which receptor interaction allow platlet aggregation?

A

GP IIb/IIIa receptors for extensive crosslinks with fibrin

32
Q

Which anticoagulants are direct thrombin inhibitors?

A

bivalirudin

argatroban

dabigatran

33
Q

Which anticoagulants are factor Xa inhibitors?

A

fondaparinux (binds to ATIII)

rivaroxaban

apixaban

34
Q

How does clopidogrel affect platelet function?

A

blocks the ADP (P2Y12) receptor and prevents expression of GP IIb/IIIa on the platelet surface

35
Q

How do abciximab and eptifibatide affect platelet function?

A

blocking GP IIb/IIIa receptors

36
Q

Why are patients with sickle cell anemia anemic?

A

sickled cell are removed by the reticuloendothelial system after 10-20 days instead of the usual 120-day RBC lifespan

37
Q

What are the crises of sickle cell anemia patients?

A
  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
Q

Which conditions promote sickling?

A

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
Q

How does hydroxyurea help patients with sicke cell anemia?

A

as a long-term treatment, it increases fetal hemoglobin levels

40
Q

How should hgb be optimized pre-operatively in sickle cell patients?

A

transfuse to a hgb of 30 (regardless of the SS fraction)

41
Q

Which coagulation factors are not made exclusively in the liver?

A

factor III (a.k.a. tissue factor): endothelium

vWF: endothelium

factor VIII: endothelium and liver sinusoidal cells

**My Anesthesia ABA Advanced Study Cards (35 decks)

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