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SCC > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What are examples of DOACs?

A

Factor Xa inhibitors; endoxaban, rivaroxaban, apixaban

Direct thrombin inhibitors; dabigatran

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2
Q

Reversal agents for DOACs?

A

Factor Xa inhibitors (apixaban, rivaroxaban)—-> andexanet Alfa

Direct thrombin inhibitors (dabigatran)—-> idarucizumab

PCC (3 factor & 4 factor) can be used when a-Alfa and idarucizumab not available

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3
Q

3 factor PCC v 4 factor PCC:

A

3 PCC; contains factors 2, 9, 10

4 PCC: contains factor 2, 7, 9, 10—> this is recommended over 3 factor PCC

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4
Q

What is idarucizumab;

A

Monoclonal antibody used for reversal of direct thrombin inhibitor dabigatran

5 g IV

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5
Q

Citrate associated hypocalcemia;

A

Every unit of blood contains 3 g of citrate which binds with calcium (FFP and platelets are also stored in citrate; something to consider when giving balanced resuscitation)

Whole blood has 50% less citrate than individual products

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6
Q

Symptoms of hypocalcemia associated with citrate binding calcium during massive transfusion?

A

Hypotension
QT prolongation
Decreased ventricular contraction

Tx—> CaCl

No real protocolized recommendations on giving Ca; some recommend 1 g calcium after first unit of blood and repeating after every 4th unit

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7
Q

Primary v secondary hemostasis’

A

Primary; vasoconstriction; platelet aggregation/adhesion, platelet plug formation (platelets bind to exposed VWF via GP1B receptors and to neighboring platelets via GP2B/3A)

Secondary; involves coagulation factors via intrinsic/extrinsic pathway

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8
Q

Extrinsic coagulation pathway activation;

A

Vessel damage release Tissue Factor

Tissue Factor then bind to Factor VII and activates it; forming a complex; TF-Factor VIIa complex

TF-Factor VIIa then activated IX and X ——> IXa + Xa

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9
Q

Intrinsic coagulation pathway activation;

A

Factor XII (Hagemon factor) is exposed to a negative charge and gets activated to Factor XIIa

Factor XIIa then binds to High-molecular-weight-kininogen (HMWK)

Factor XIIa-HMWK complex converts XI to XIa—-> leads to activation of factor IX + VIII

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10
Q

Common pathway?

A

Begins of activation of Factor X to Xa

Xa then forms complex with Factor V, Calcium and phospholipid to create prothrombinase complex
This then converts prothrombin to thrombin

Thrombin then converts fibrinogen to fibrin

Generation of fibrin forms framework of mature clot

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11
Q

What are some intrinsic mechanism that prevent clot propagation as secondary hemostasis is going on?

A

Thrombin that’s not used at the site of injury gets bound to thrombomodulin downstream

This activates thrombomodulin which then activates Protein C

Activated protein C then binds to Protein S on vessel wall and together they destroy activated Va + VIIIa

Antithrombin III (ATIII) can inactivate the enzymes in the coagulation cascade

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12
Q

ABC criteria to activate massive transfusion?

A

Penetrating mechanism
SBP <90
HR >120
+ FAST

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13
Q

What does PT measure?

A

Extrinsic pathway; II, VII, X

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14
Q

What does PTT measure?

A

Intrinsic and common pathways

Factors: II, VIII, IX, X, XI, XII

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15
Q

Drawbacks to PT/INR testing ?

A

Assess a separate arm each of the coagulation cascade

Do not account for the cellular component of the coagulation cascade, such as platelet function

Take time to process; not practical in a real trauma situation

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16
Q

Difference between PT/INR and TEG-ROTEM?

A

PT/INR use platelet free plasma samples

TEG-ROTEM use whole blood

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17
Q

R-time in TEG?

A

Initiation of clot formation

Assess clotting factor activity

Tx—> FFP

18
Q

K time in TEG?

A

Measure of clot firmness

Tx—-> Cryo

19
Q

Alpha angle in TEG?

A

Assesses rate of clot formation and functionality of clotting factors

Tx—-> cryo

20
Q

MA in TEG?

A

Maximum strength of clot

Tx—> plts

21
Q

Ristocetin test can be used to dx?

A

VWD

22
Q

What does FFP contain?

A

Coagulation factors

23
Q

What does cryoprecipitate contain?

A

VWF
Fibrinogen
Fibronectin
Factors VIII/XIII

24
Q

PROPR trial?

A

Early balanced resuscitation with 1:1:1 of plasma/platelets/pRBCS vs 1:1:2 reduced death within 24 hrs

25
Q

Old definition of massive transfusion?

A

> 10 units pRBCs within 24 hrs but this is outdated

26
Q

What is CAT?

A

Critical administration threshold used to active MTP

transfusion of >3 pRBCs in 1 hr period

27
Q

TRICC trial?

A

Compared transfusing patients with a cutoff of hgb of 7 vs 10

Restrictive blood transfusion strategy preferred

28
Q

Advantages of whole blood vs separated components?

A

Less blood transfused at 24 hrs (although no mortality benefit)
Use of single bag product storage
Decreased human error when administering 1 bag vs 3 for component products
Decreased transfusion reaction
Decreased transfused volume, additives, anticoagulants

29
Q

What do we need to classify TRALI after a transfusion?

A

B/l infiltrates (w/absence of left atrial HTN)
P/F ratio of <300
Absence of acute injury before transfusion

Must have occurred within 6 hrs of last transfusion

30
Q

What causes TRALI?

A

Donor antibodies in the transfused blood

Tx is supportive

31
Q

This is a synthetic derivative of lysine which inhibits fibrinolysis by blocking the lysine binding site on plasminogen:

A

TXA

Must be given within 3 hrs

32
Q

CRASH2 trial;

A

Trauma pts with significant bleeding demonstrated significant reduction in all cause mortality when TXA given within 3 hrs

Little evidence exists for use in children

33
Q

Normal MA?

A

50-70 mm

If MA decreased; give plts

34
Q

Advantages of TEG in setting of trauma?

A

Results available within 10 mins
Helps use fewer blood products
Dynamic measure

**Survival benefit has not been demonstrated

35
Q

What LY30 > 3-5% mean?

A

Hyperfibrinolysis

Give TXA

36
Q

Pros and Cons of ABC score for activating MTP?

A

Has a great negative predictive value 5%

Has a poor positive predictive value 50-55% (meaning that 45-50% of pts in whom MTP is activated will not need a massive transfusion)

37
Q

Apharesis platelets vs pooled platelets:

A

Apharesis come from 1 donor; thus less risk of bacterial/viral contamination

No difference in survival between the two and no difference in TRALI or hemolytic transfusion rxns

38
Q

Sxs of hypocalcemia seen with MTP>?

A

Prolonged QT

Hypotension
Decreased myocardial contractility
PEA/Vfib

39
Q

Characterized by widespread microvascular thrombosis with activation of the coagulation system and impaired protein synthesis; leading to exhaustion of clotting factors and platelets;

A

DIC

40
Q

MOA of argatroban:

A

Direct thrombin inhibitor (IIa)

Used as an alternative in pts with HIT when heparin discontinued

41
Q

How does hypothermia cause coagulopathy?

A

Causes platelet and clotting factor dysfunction

42
Q

What type of blood can we use in emergency situation?

A

Type O positive blood safe in most patients; men and women

Type O negative blood usually reserved for pregnant women

SCC (9 decks)

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