Hemostasis And Transfusion Medicine

Front 1

most common causes of ABO incompatibility

Back 1

clerical error

Front 2

The three leading causes of transfusion-related death

Back 2

ABO incompatibility, transfusion-related acute lung injury, and sepsis caused by bacterial infections.

Front 3

In the setting of massive transfusion, assuming maintenance of isovolemia and the absence of a consumptive coagulopathy, critical dilution of clotting factors and platelets is likely to occur when?

Back 3

after an average replacement of 140% and 230% of blood volume, respectively

Front 4

infection w/ which virus poses the greatest risk w/ transfusion?

Back 4

Hepatitis B

Front 5

greatest risk of sepsis w/ platelets or w/ blood products?

Back 5

The incidence of sepsis is substantially greater with platelet than RBC administration because the former are stored at room temperature.

Front 6

antibodies that fix complement and commonly produce immediate intravascular hemolysis

Back 6

those against A, B, Kell, Kidd, Duffy, and Ss antigens. Rh antibodies (i.e., anti-D, anti-Cc, and anti-Ee), although typically not complement binding, are also capable of causing serious acute hemolytic reactions

Front 7

what happens when ABO incompatible blood enters the blood stream?

Back 7

antigen-antibody complexes activate Hageman factor (factor XII), which in turn acts on the kinin system to produce bradykinin. The release of bradykinin increases capillary permeability and dilates arterioles, both of which contribute to hypotension. Activation of the complement system results in the release of histamine and serotonin from mast cells, resulting in bronchospasm. Thirty to 50% of patients develop DIC.

Front 8

What happens to released Hb from ABO incompatibility rx?

Back 8

Initially it is bound to haptoglobin and albumin. When those binding sites are saturated, it circulates unbound until it is excreted by the kidneys.

Front 9

why does renal damage occur w/ incompatibility rxns?

Back 9

Blood flow to the kidneys is reduced in the presence of systemic hypotension and renal vasoconstriction. Free Hb in the form of acid hematin or red cell stroma may damage renal tubules. Antigen-antibody complexes may be deposited in the glomeruli. If the patient develops DIC, fibrin thrombi will also be deposited in the renal vasculature, further compromising perfusion and/or causing acute cortical necrosis, which is frequently irreversible

Front 10

signs and symptoms of acute hemolytic rxn?

Back 10

fever, chills, nausea and vomiting, diarrhea, and rigors. The patient is hypotensive and tachycardic (bradykinin effects) and may appear flushed and dyspneic (histamine). Chest and back pains occur and have been attributed to cytokine release. The patient is often restless, has a headache, and a sense of impending doom

Front 11

at which point does hemoglobinuria occur?

Back 11

Hemoglobinuria will occur if plasma Hb rises above the renal threshold (about 25 mg/dL).

Front 12

what to do w/ acute hemolytic rxn in OR?

Back 12

stop infusion, check the administered blood, take blood sample and check for hemolysis. maintenance of systemic blood pressure, preservation of renal function, and the prevention of DIC.
Serum haptoglobin level, plasma, and urine Hb and bilirubin assays. Determine coagulation status of the patient

Front 13

what is a delayed hemolytic rxn?

Back 13

occurs in days following transfusion, due to anamnestic rxn to RBCs or de-novo alloimmunization, antibody-coated RBC is sequestered extravascularly and lysis occurs in the spleen and reticuloendothelial system. Less severe sx.

Front 14

which antibodies are responsible for delayed hemolytic rxn?

Back 14

antibodies against Kell, Kidd, and Rhesus antigens

Front 15

sings and symptoms of delayed hemolytic rxn?

Back 15

low-grade fever, increased indirect bilirubin with or without mild jaundice, and/or an unexplained reduction in Hb concentration. Serum haptoglobin may also be decreased

Front 16

test for delayed transfusion rxn?

Back 16

positive direct antiglobulin test (Coombs test) and the identification of a new antibody in the patient's plasma.

Front 17

treatment of delayed transfusion rxn?

Back 17

mild and self-limiting and the clinical manifestations resolve as the transfused cells are removed from the circulation. Supportive care includes monitoring of Hb, maintenance of hydration, and provision of compatible blood if necessary.

Front 18

minor allergic rxns to transfusion, symptoms, how often do they occur?

Back 18

urticarial reactions in 0.5 to 4% of all transfusions, itching, swelling, and a rash (histamine release).

Front 19

anaphylactic rxns to transfusions often occur in?

Back 19

patients with hereditary immunoglobulin (Ig) A deficiency who have been sensitized by previous transfusions or pregnancy are exposed to blood with foreign IgA protein

Front 20

Patients who receive multiple transfusions of RBCs or platelets commonly develop antibodies (alloimmunization) to ?

Back 20

the human leukocyte antigens (HLAs) on the passenger leukocytes in these products - febrile reaction.

Front 21

what is a febrile rxn due to?

Back 21

ab to leukocytes

Front 22

describe febrile transfusion rxn?

Back 22

patient experiences a temperature increase of more than 1°C within 4 hours of a blood transfusion and defervesces within 48 hours. The fever is sometimes accompanied by chills, respiratory distress, anxiety, headache, myalgias, nausea, and a nonproductive cough

Front 23

what is TRALI?

Back 23

is a noncardiogenic form of pulmonary edema occurring after blood product administration

Front 24

TRALI occurs more often w/ which blood product ?

Back 24

associated with all plasma-containing blood components, with platelet concentrates and FFP being implicated much more commonly than PRBCs or other products.

Front 25

why does TRALI occur?

Back 25

TRALI occurs when mediators present in the plasma phase of donor blood activate leukocytes in the host. the activated leukocytes are sequestrated in the lung and the mediators they release cause capillary endothelial damage and increased permeability.

Front 26

Criteria for diagnosis of TRALI?

Back 26

Acute onset of hypoxemia (within 6 hours of conclusion of transfusion)
Bilateral CXR infiltrates consistent with ALI
Absence of evidence of left atrial hypertension
Absence of other temporally related causes of ALI

Front 27

Transfusion related GVHD, how does it occur?

Back 27

the donor lymphocytes may become engrafted, proliferate, and establish an immune response against the recipient

Front 28

patients at risk from GVHD?

Back 28

organ transplant recipients, neonates who have undergone a blood-exchange transfusion, and patients immunocompromised by many other disease processes (but not AIDS

Front 29

which blood products cause GVHD?

Back 29

GVHD has been reported only after the transfusion of cellular blood components. It has not occurred following transfusion of FFP or cryoprecipitate.

Front 30

most effective way to stop GVHD?

Back 30

Irradiation remains the only effective means for preventing GVHD.

Front 31

benefits of leukoreduction?

Back 31

Confirmed benefits

Decreased alloimmunization/platelet refractoriness in multiply transfused leukemics
Prevention of febrile reactions to RBC transfusions
Reduction of CMV transmission
Reduced inflammatory mediator accumulation during storage

Front 32

Hazards of massive transfusion?

Back 32

Hypothermia
Volume overload
Dilutional coagulopathy
Reduced oxygen-carrying capacity (decreased 2,3-DPG)
Metabolic acidosis
Hyperkalemia
Citrate intoxication
c

Front 33

risks of hypothermia due to cold blood product administration?

Back 33

cogaulopathy, decreased enzymatic processes, increased PT and aPTT, decreased platelets by up to 40%, shivering incrases oxygen demand

Front 34

which coagulopathy develops first in massive PRBC transfusion? which initial factors will be first to decrase?

Back 34

factor deficiencies develop before thrombocytopenia.
The most common initial factor deficiencies in the setting of trauma are FV and FX

Front 35

changes in pH of stored blood, explain?

Back 35

citrate-phosphate-dextrose (CPD) solution is added to a unit of freshly drawn blood, pH decreases to approximately 7.0 to 7.1 . Further reduction of pH will occur during storage as a consequence of ongoing metabolism of glucose to lactate. At the end of 21 days, the pH may be as low as 6.9, but much of this is the result of the production of CO2 that is rapidly eliminated following the transfusion.

Front 36

why is there a need for washing blood prior to administration to neonates?

Back 36

due to hyperkalemia
and typically therefore receive either fresh (<8 day old), plasma-reduced, or washed PRBCs if rapid transfusion (>10 to 15 mL/kg per 2 hours) is required.

Front 37

citrate intoxication is due to?

Back 37

Ca depletion

Front 38

signs of citrate intoxication?

Back 38

include hypotension, narrow pulse pressure, and elevated intraventricular end-diastolic pressure and central venous pressure, prolonged QT interval, widened QRS complexes, and flattened T waves.

Front 39

at which hematocrit does extraction ratio of oxygen increase?

Back 39

25%

Front 40

what is P50?

Back 40

the PO2 at which the Hb molecule is 50% saturated with oxygen at 37°C and a pH of 7.4, is 27 mm Hg

Front 41

when Hb curve shifts to left, what happens to P50?
what is the result of this?

Back 41

P50 is reduced
The Hb molecule is more “stingy” and requires lower PO2 to release oxygen to the tissues; that is, the Hb molecule does not release 50% of its oxygen until an ambient PO2 <27 mm Hg is reached. This may impair tissue oxygenation.

Front 42

when Hb curve shifts to the right what happens to P 50?

Back 42

increase of P50, decreased Hb affinity for the oxygen molecules and release of oxygen to tissues at higher partial pressures of oxygen.

Front 43

factors that shift Hb curve to the right?

Back 43

high temp, pCO2, 2,3 BPG
low PCO and low pH

Front 44

at what Hb level is synthesis of 2,3 BPG increased?

Back 44

at 9.0

Front 45

One apheresis unit will increase platelet count by

Back 45

30,000 to 60,000/µL

Front 46

platelets of a single unit of blood will increase platelet count by?

Back 46

5-10 k

Front 47

indications for FFP administration?

Back 47

Correction of multiple coagulation factor deficiencies (e.g., DIC) with evidence of microvascular bleeding and PT and/or aPTT >1.5 times normal
Correction of microvascular bleeding during massive transfusion (more than one blood volume) when PT/aPTT cannot be obtained in a timely manner
Urgent reversal of warfarin therapya
Heparin resistance (antithrombin III [AT] deficiency) in a patient requiring heparin when AT concentrate is not available
Thrombotic thrombocytopenic purpura or hemolytic uremic syndrome
Correction of single coagulation factor deficiencies for which specific concentrates are not available (principally factor V)
? Formula management of trauma/massive blood loss

Front 48

indications for giving cryo?

Back 48

Microvascular bleeding when there is a disproportionate decrease in fibrinogen, such as DIC and very massive transfusion,a with fibrinogen <80–100 mg/dL (or assay result not available)
Fibrin sealant (if virus-inactivated concentrate is unavailable)
Bleeding due to uremia that is unresponsive to DDAVP
Prophylaxis before surgery or treatment of bleeding in hemophilia A and vWD (if virus-inactivated concentrates are unavailable or ineffective)
Prophylaxis before surgery or treatment of bleeding in patients with congenital dysfibrinogenemias
FXIII deficiency

Front 49

what percentage of factors is needed for normal coagulation?

Back 49

Normal coagulation can be achieved with clotting factor levels of 20 to 30% of normal. Those levels can usually be achieved by administration of 10 to 15 mL/kg of FFP.

Front 50

what is in cryoprecipitate?

Back 50

factor VIII, the von Willebrand factor (vWF), fibrinogen, fibronectin, and factor XIII.

Front 51

one unit of PRBCs will increase the Hb and Hct by?

Back 51

The administration of one unit of PRBCs will increase the Hb and Hct of a 70-kg adult by approximately 1 g/dL and 3%, respectively.

Front 52

what tem should platelets be stored?

Back 52

22 deg C

Front 53

how long can platelets be stored?

Back 53

5 days due to potential bacterial growth.

Front 54

when platelets are given is ABO compatibility required?

Back 54

no, it is ideal, but not required

Front 55

does FFP have to be abo compatible?

Back 55

yes

Front 56

what is thawed plasma?

Back 56

It is obtained from thawed FFP that is maintained at 6°C for a maximum of 5 days. Its advantage is immediate availability (and reduction of wastage of thawed FFP not administered within 24 hours).

Front 57

factors in FFP

Back 57

FFP is efficacious for treatment of deficiencies of factors II, V, VII, IX, X, and XI

Front 58

is abo compatibility required for cryo?

Back 58

ABO compatibility is not essential because of the limited antibody content of the associated plasma vehicle (10 to 20 mL).

Front 59

at which temp is cryo stored?

Back 59

- 20 deg C

Front 60

vWF deficiency causes which defects?

Back 60

1) a defect in primary hemostasis because of a failure of platelet adhesion to the sites of vascular injury, and (2) the clinical equivalent of hemophilia A because of deficiency of circulating factor VIII:C

Front 61

vit K dependent factors?

Back 61

. Factors II, VII, IX, and X require vitamin K for completion of their synthesis in the liver. Each undergoes a final enzymatic addition of a carboxyl group that requires the presence of vitamin K.

Front 62

how does warfarin act?

Back 62

vitamin K is displaced by warfarin and the vitamin K-dependent factors are not carboxylated.

Front 63

which factors are labile factors and why/

Back 63

Factors V and VIII are also referred to as the labile factors because their coagulant activity is not durable in stored blood. While PRBCs contain some residual plasma with clotting factors, massive transfusion with stored blood will nonetheless lead to a dilutional coagulopathy because of diminished activity of factors V and VIII.

Front 64

action of TPA

Back 64

converts plasmin to plasminogen

Front 65

how is tPA released?

Back 65

Activated protein C (APC) stimulates the release of tPA. tPA is also released from the endothelium in response to venous occlusion, physical activity, stress, or vasoactive drugs (such as epinephrine, vasopressin, and DDAVP

Front 66

Platelet count decreased (normal aPTT and PT), DDx?

Back 66

decreased platelet production (see later discussion), excess consumption, platelet destruction, or sequestration in the spleen

Front 67

Prolonged BT DDX

Back 67

Differential diagnosis: antiplatelet drug ingestion (e.g., nonsteroidal anti-inflammatory drugs, acetylsalicylic acid, clopidogrel), uremia, vWD (although factor VIII:C levels may be decreased with vWD [type 1], only 25 to 30% of VIII:C coagulant activity is necessary to produce a normal aPTT).

Front 68

Prolonged aPTT , DDx

Back 68

heparin, the lupus anticoagulant or other antiphospholipid antibodies such as anticardiolipin and anti-B2-GPI antibodies,186 deficiency of FXII, HMWK, or prekal-likrein, hemophilia A or B, vWD, acquired factor inhibitors, and poor collection technique.

Front 69

Prolonged PT Ddx

Back 69

vitamin K deficiency, warfarin administration, early liver dysfunction, FVII deficiency, and acquired coagulation factor inhibitors

Front 70

Prolonged PT and aPTT (normal platelet count). DDx

Back 70

vitamin K deficiency, warfarin, and heparin.

Front 71

Prolonged PT, aPTT, and TT (normal platelet count).

Back 71

heparin, DTIs, FDPs, hypofibrinogenemia, and dysfibrinogenemia.

Front 72

Prolonged PT, aPTT, TT, decreased platelet count. Ddx

Back 72

DIC, dilution by massive transfusion, liver disease, and heparin therapy.