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Anesthesiology > Hematology, Transfusions, & Fluids > Flashcards

Hematology, Transfusions, & Fluids Flashcards

1
Q

What is GP IIb/IIIa responsible for in hemostasis?

A

Aggregation of platelets by binding a crosslink, glue-like pattern of fibrinogen with the GP IIb/IIIa receptors

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2
Q

What are the vitamin K dependent clotting factors?

A

2, 7, 9, 10 Protein C, Protein S

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3
Q

How does plasminogen play a role in coagulation?

A

During crosslinking of fibrin, plasminogen is incorporated; with endothelial damage, tPA is also released to activate plasminogen into plasmin which degrades cross-linked fibrin, releasing D-dimers (keeps thrombosis in check)

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4
Q

What does activated clotting time (ACT) measure?

A

Intrinsic and common pathway coagulation cascades

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5
Q

Hemophilia A: what factor is missing and hereditary pattern?

A

Factor 8 deficiency, X-linked recessive disorder

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6
Q

How does DDAVP work for clotting?

A

Up-regulates natural production of Factor 8 and vWF (increasing levels by 2-4 times)

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7
Q

What is Type 1 von-Willebrand Disease? Does DDAVP help?

A

Less vWF (quantitative defect), DDAVP increases levels.

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8
Q

What is Type 2 von-Willebrand Disease? Does DDAVP help?

A

Weird vWF (paradoxical thrombosis), DDAVP produces more weird vWF

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9
Q

What is Type 3 von-Willebrand Disease? Does DDAVP help?

A

Extremely low vWF, DDAVP doesn’t increase it enough to make a difference

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10
Q

Does von-Willebrand Disease increase PTT and bleeding time?

A

Does not routinely rise PTT but does increase BT

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11
Q

Would you place an epidural in a patient with von-Willebrand Disease?

A

Use DDAVP prior to epidural placement (no official guidelines though)

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12
Q

What is Humate-P?

A

Factor 8 and vWF concentrate

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13
Q

How do you expect the following lab values to change in DIC: Platelets, D-dimer, fibrinogen, INR, PTT

A

Decreased Plt (consumptive), increased INR/PTT (consumptive), increased D-Dimer (increased fibrin breakdown by plasmin), decreased fibrinogen

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14
Q

What is the pathophysiology behind Idiopathic Thrombocytopenic Purpura (ITP)?

A

IgG antibodies towards platelet antigens leading to platelet destruction

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15
Q

What should the platelet count be for major surgeries?

A

> 100,000

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16
Q

How much do you expect a pack of plasmapheresis platelets to increase the platelet count?

A

60,000 increase (6-pack)

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17
Q

What blood type is the universal donor for FFP?

A

AB, Rh + (since FFP contains no antibodies while O, Rh- has antibodies against A, B, and Rh)

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18
Q

What is found in cryoprecipitate?

A

Fibrinogen, vWF, Factor 8

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19
Q

What factors are found in Factor 9 Complex?

A

Factors 2,7,9, 10 (recall that’s the same as the vitamin K factors!)

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20
Q

What does washing RBCs do?

A

Remove IgA to avoid anaphylactic reactions in IgA deficient patients

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21
Q

What does leukodepletion of RBCs do?

A

Reduction of febrile reactions and alloimmunization

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22
Q

What does irradiation of RBCs do?

A

Destroys DNA to prevent graft vs host disease

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23
Q

When do you normally see a delayed hemolytic transfusion reaction?

A

Typically in lesser antigens (Kidd, Kell, Duffy, etc.), appears a few days to weeks as an unconjugated hyperbilirubinemia and low serum haptoglobin

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24
Q

What is the underlying cause of febrile reactions to transfusions?

A

Due to recipient antibodies towards donor WBCs

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25
Q

Do you stop a transfusion for a febrile transfusion reaction?

A

No, treat conservatively

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26
Q

What are the two major transfusion related causes of morbidity and mortality?

A

Transfusion related acute lung injury (TRALI) and Transfusion associated circulatory overload (TACO)

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27
Q

What is TRALI? Onset of symptoms?

A

Capillary leak syndrome causing significant non-cardiogenic pulmonary edema (donor WBC Ab that bind recipient WBC antigens); starts within 2 hours and resolves within 48 hours

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28
Q

What is negative pressure pulmonary edema?

A

Forceful inspiratory pressure against a closed glottis -> large (-) intrathoracic pressure pulls water from interstitium to alveolus

29
Q

What is transfusion associated circulatory overload?

A

TACO: fluid overload from products that cause a cardiogenic pulmonary edema

30
Q

Transfusing a pediatric patient 4 cc/kg of pRBCs will raise hemoglobin levels by how much?

A

1 g/dL

31
Q

What are the average blood volumes for each age group: adult, infant, full term neonate, premature neonate

A

Adult: 60-70 cc/kg
Infant: 75 cc/kg
Full term neonate: 85 cc/kg
Premature neonate: 100 cc/kg

32
Q

What is the risk of HIV transmission with transfusions? Hep B? Hep C?

A

HIV: 1 in 2 million
Hep C: 1 in 2 million
Hep B: 1 in 200,000

33
Q

Why would you see a slight mild hyperkalemia with massive transfusions?

A

Potassium levels in pRBCs increase with shelf time

34
Q

What metabolic changes do you see with massive transfusions and why?

A

Metabolic alkalosis: citrate binds to calcium leading to hypocalcemia + citrate is converted to bicarbonate in the liver

35
Q

What product should NOT be warmed?

A

Platelets

36
Q

Which blood product is associated with the highest rate of bacterial contamination?

A

Platelets (stored at room temperature for 5 days)

37
Q

Warfarin with an active episode of heparin induced thrombocytopenia can cause what?

A

Limb gangrene (worsens thrombosis)

38
Q

If a patient has a history of heparin-induced thrombocytopenia, what would you use as an alternative for coronary bypass surgery?

A

Argatroban (direct thrombin inhibitor)

39
Q

Mechanism of action for warfarin?

A

Inhibits synthesis of vitamin K dependent factors

40
Q

Mechanism of action for heparin and lovenox?

A

Accelerates anti-thrombin 3 activity (inhibits thrombin, factor 9 and 10)

41
Q

Mechanism of action for fondaparinux?

A

Factor X inhibitor

42
Q

Mechanism of action for argatroban and lepirudin?

A

Direct thrombin inhibitors

43
Q

Mechanism of action for clopidogrel?

A

ADP receptor antagonist

44
Q

Mechanism of action for eptafibatide and abciximab?

A

GP IIb/IIIa inhibitor

45
Q

Mechanism of action of protamine?

A

Binds ionically to heparin to reverse its actions

46
Q

Why are sickle cell patients anemic?

A

Sickled cells are removed from the reticuloendothelial system -> lots of RBC production needs -> increasing need for folate -> aplastic crisis -> need for transfusion

47
Q

What are common crises for sickle cell patients?

A

Splenic sequestration crisis (autosplenectomy), hemolytic crisis (if G6PD deficient), aplastic crisis, vaso-occlusive crisis

48
Q

What conditions increase sickling in sickle cell patients?

A

Anything that decreases mixed venous sats: Hypoxia, acidosis, increased 2,3 DPG, hypotension, hypovolemia, vasoconstriction, hyperviscosity, increased VO2 (shivering, fever)

49
Q

What is a complication from transfusions in sickle cell patients?

A

Hemachromatosis from iron overload

50
Q

What makes up lactated ringers?

A

Na (130 mEq/L), Cl (109 mEq/L), K (4 mEq/L), Ca (2.7 mEq/L), lactate (28 mEq/L, converted to bicarb in liver)

51
Q

What makes up normal saline?

A

Na (154 mEq/L), Cl (154 mEq/L)

52
Q

What are some side effects noted with Hetastarch?

A

Increases PT, aPTT, and clotting time, may interfere with platelet function + indirect hyperbilirubinemia + temporary elevated amylase

53
Q

What are some side effects noted with Pentastarch?

A

Increased PT, aPTT, and clotting time, may interfere with platelet function + temporary elevated amylase

54
Q

What is a Type, a Screen, and a Crossmatch?

A

Type: ABO and RhD determination (patient’s RBCs are mixed with anti-A, anti-B, and anti-D antibodies)
Screen: Detection of Ab (patient’s serum mixed with O RBCs with known antigen panel)
Crossmatch: determination of compatibility (trial transfusion)

55
Q

What changes do you see in a pRBC with storage?

A

Intracellular acidosis, extracellular hyperkalemia, and decreased 2,3-DPG

56
Q

In patients with chronic anemia, what makes O2 transport more efficient?

A

Increased 2,3-DPG (right shift in the oxyhemoglobin dissociation curve)

57
Q

What is the formula for oxygen carrying capacity?

A

CaO2 = (1.36 * Hgb) * SaO2 + (0.003 * PaO2)

58
Q

What is the formula for oxygen delivery?

A

DO2 = CO * CaO2

59
Q

Do you need to ABO match for platelets?

A

No; that being said, we do match only to Rh (to decrease risk of alloimmunization)

60
Q

What is the treatment for an acute transfusion reaction?

A
  1. Stop transfusion
  2. Pharmacologic support of circulation (i.e. fluids, pressors, etc.)
  3. Sodium bicarbonate to alkalinize urine to prevent precipitation of hematin and RBC in renal tubules
  4. Send samples and return blood to check compatibility
61
Q

What is the pH of normal saline?

A

5.5

62
Q

What is the pH of a pRBC?

A

6.5

63
Q

What product carries the greatest risk of transfusion-related lung injury?

A

FFP

64
Q

What product carries the greatest risk of hemolytic transfusion reactions?

A

pRBCs

65
Q

What is the classic triad of an acute hemolytic transfusion reaction?

A
  1. Fever
  2. Flank pain
  3. Red-brown urine
66
Q

In an acute hemolytic transfusion reaction, what is the cause of the renal failure?

A

Acute tubular necrosis (thought to be from renal vasoconstriction and hypotension leading to ischemic renal failure)

67
Q

What is the mechanism of action for an anaphylactic transfusion reaction?

A

Typically in IgA deficiency -> antibodies against donor IgA) causing an anaphylactic response

68
Q

What is the leading cause of transfusion-related deaths in the US?

A

TRALI (mortality rate just under 10%)

69
Q

How does hypothermia affect coagulation?

A

Coagulopathy secondary to decrease in thrombin and other coagulation activation factors

Anesthesiology (21 decks)

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