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Coagulation Flashcards

1
Q

A balance between clot generation, thrombus formation, and regulatory mechanisms that inhibit uncontrolled thrombogenesis is called?

A

Hemostasis

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2
Q

What are the goals of hemostasis?

A
  • Limit blood loss from vascular injury
  • Maintain intravascular blood flow
  • Promote revascularization after thrombosis
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3
Q

What is Primary Hemostasis?

A

Immediate platelet deposition at the endovascular injury site (adhesion, activation, and aggregation)

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4
Q

What role do vascular endothelial cells play in hemostasis?

A

Antiplatelet, anticoagulant, and fibrinolytic effects to inhibit clot formation

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5
Q

Are endothelial cells pro or anti clot?

A

Anti-clotting

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6
Q

Endothelial cells are ___ charged to repel ______

A

Negatively charged; Repel platelets

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7
Q

Endothelial cells produce platelet inhibitors such as (2)

A

Prostacyclin and nitric oxide

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8
Q

What are platelets derived from? What is their lifespan?

A

Derived from bone-marrow megakaryocytes
Lifespan: 8-12 days

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9
Q

How many platelets are consumed and formed daily?

A

10% consumed to support vascular integrity and 150 billion formed daily

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10
Q

Damage to the endothelium exposes the underlying

A

Extracellular matrix (ECM)

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11
Q

What is contained within the ECM?

A

Collagen
vWF (von Willebrands Factor)
Glycoproteins

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12
Q

Platelets undergo which three phases of alteration?

A

Adhesion
activation
aggregation

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13
Q

What occurs upon exposure to ECM proteins?

A

Adhesion

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14
Q

This is stimulated when platelets interact with collagen and tissue factor (TF), causing the release of granular contents.

A

Activation

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15
Q

What are the two types of storage granules in platelets?

A

Alpha Granules & Dense Bodies

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16
Q

What do alpha granules contain?

A

Fibrinogen, factors V & VIII, vWF

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17
Q

What do dense bodies contain?

A

ADP, ATP, calcium, serotonin, histamine, and epinephrine

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18
Q

What occurs when released granular contents activate additional platelets, propagating plasma-mediated coagulation?

A

Aggregation

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19
Q

Each stage of the clotting cascade requires assembly of membrane-bound activated ____?

A

Tenase-complexes

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20
Q

What is each tenase complex composed of?

A
  1. Substrate (inactive precursor)
  2. Enzyme (activated coagulation factor)
  3. Cofactor (accelerator or catalyst)
  4. Calcium
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21
Q

The extrinsic pathway of coagulation starts off with what?

A

Endothelial injury, exposing tissue factor to the plasma

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22
Q

Tissue Factor forms an active complex with what other factor?

A

VIIa (TF-VIIa Complex)

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23
Q

TF/VIIa complex binds to and activates what factors?

A

Factor X –> Xa
Factor 9 –> 9a (in the intrinsic pathway)

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24
Q

From the intrinsic pathway, which 2 factors convert Factor X to Xa?

A

Factor 9a and Calcium

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25
Q

which factor initiates the final common pathway?

A

Factor Xa

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26
Q

What does Factor 10 do?

A

Augments the intrinsic pathway (via factor 9)

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27
Q

What is the role of factor XIIIa in coagulation?

A

Factor XIIIa stabilizes the fibrin clot by cross-linking.

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28
Q

The extrinsic pathway is the initiation phase of what type of homeostasis?

A

Plasma-mediated homeostasis

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29
Q

Activated thrombin (IIa) activates which factors to amplify thrombin generation and activate platelets?

A

5, 7, 8, 11

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30
Q

In the common pathway, Factor Xa binds with Factor _____ to form which complex?

A

Factor Xa binds with Va to form Prothrominase complex

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31
Q

Prothrombinase Complex converts ___ to ____

A

Prothrombin (II) to Thrombin (IIa)

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32
Q

Thrombin attaches to the _____ and converts _____ to ______

A

Thrombin attaches to platelets and converts fibrinogen (I) to fibrin (Ia)

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33
Q

Thrombin cleaves ________ from fibrinogen to generate _______ which polymerizes into strands to form a basic clot

A

Fibrinopeptides; Fibrin

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34
Q

Factor ____ crosslinks the fibrin strands to stabilize and make an insoluble clot that is resistant to fibrinolytic degredation

A

13a

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35
Q

Platelets adhere to _____ to become activated and recruit additional platelets

A

collagen

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36
Q

Fibrin molecules _______ to form a mesh that stabilizes the clot

A

crosslink

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37
Q

The intrinsic pathway begins with which factor?

A

Factor 12a

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38
Q

Initially, the intrinsic pathway was thought to occur due to endovascular contact with _____ _____ substances

A

negatively charged (glass, dextran)

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39
Q

Now we know that the intrinsic pathway plays a minor role in initiation of hemostasis and is more of an _____ ______ for thrombin generation intitiated by the ______ ______

A

Amplification system; extrinsic pathway

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40
Q

Most thrombotic events follow which pathway?

A

Extrinsic pathway

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41
Q

Lab coag studies rely on which pathway to activate the pathway?

A

Intrinsic pathway

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42
Q

Contact with what surface causes Factor 12 to be activated?

A

Negatively charged surface

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43
Q

Factor 12a converts ____ to _____

A

Factor 11 to 11a

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44
Q

4 Things convert Factor X to Xa, what are they?

A
  1. Factor 9a
  2. Factor 8a
  3. Platelet membrane phospholipid
  4. Calcium
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45
Q

What is the common pathway in coagulation?

A

In the common pathway, factor X becomes Xa and binds with Va to form the prothrombinase complex, converting prothrombin into thrombin.

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46
Q

Both intrinsic and extrinsic tenase complexes facilitate formation of

A

Prothrombinase complexes

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47
Q

The intrinsic Tenase complex is made up of

A
  1. an activator (the catalyst)
  2. Factor 9a
  3. Factor 8a
  4. Calcium
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48
Q

The extrinsic tenase complexes are made up of

A
  1. Injury (the catalyst)
  2. TF
  3. Factor 7a
  4. Calcium
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49
Q

What are the four major coagulation counter-mechanisms?

A
  • Fibrinolysis
  • Tissue factor pathway inhibitor (TFPI)
  • Protein C system
  • Serine Protease Inhibitors (SERPINs)
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50
Q

Fibrinolysis: endovascular TPA and urokinase convert ___ to ___

A

plasminogen to plasmin

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51
Q

During Fibrinolysis,_____ breaks down clots enzymatically, and degrades Factors 5 and 8

A

Plasmin

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52
Q

Protein C system inhibits which factors? (3)

A
  1. Factor 2
  2. Factor 5a
  3. Factor 8a
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53
Q

Tissue factor pathway inhibitor (TFPI) forms a complex with Xa that inhibits _____ complex along with Xa; thereby ________ the extrinsic pathway

A

Inhibits TF/7a complex; thereby downregulating the extrinsic pathway

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54
Q

Serine protease inhibitors (SERPIN) consist of what 3 things

A
  1. Antithormbin
  2. Heparin
  3. Heparin cofactor II
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55
Q

Antithrombin inhibits (5)

A

Thrombin, Factors 9a, 10a, 11a, 12a

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56
Q

What is the mechanism of Heparin?

A

Binds to antithrombin causing a conformational change that accelerates AT activity

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57
Q

What is the mechanism of action of Heparin cofactor II?

A

Inhibits thrombin alone

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58
Q

What is the most effective predictor of bleeding?

A

Careful bleeding history

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59
Q

What should you ask about in pre-op assessment?

A

History of:
nose bleeds
bleeding gums
easy bruising
excessive bleeding during dental extraction
surgery
trauma
childbirth and blood transfusions

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60
Q

vWF is the most common inherited bleeding disorder which leads to defective ____ ______

A

Platelet adhesion

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61
Q

How does vWF help with platelet adhesion?

A

Prevents degradation of Factor 8

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62
Q

What are common laboratory findings in von Willebrand’s disease?

A

Platelets and PT will be normal
aPTT might be prolonged depending on the level of factor VIII.

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63
Q

What are better tests to asses for vWF?

A

Factor 8 level, Plt function assay

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64
Q

What drug increases vWF?

A

Desmopressin (DDAVP)

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65
Q

What do you give for intraop bleeding?

A

vWF and Factor 8 concentrates

66
Q

What characterizes hemophilia A?

A

Factor VIII (8) deficiency

67
Q

What characterizes hemophilia B?

A

Factor 9 deficiency

68
Q

What fraction of hemophilia is genetically inherited?

69
Q

Hemophilia presents in childhood as spontaneous hemorrhage in the

A

joints and muscles

70
Q

What do hemophilia labs show?

A

Normal PT, platelets, bleeding time
Prolonged PTT

71
Q

What should you do if your patient shows up and has hemophilia?

A

Consult hematologist
Consider DDAVP and Factor 8/9 before surgery

72
Q

What is the most significant cause of intra-op bleeding?

A

Anticoagulation medication

73
Q

What factors does the liver produce?

A

Factors: 5,7,9,10,11,12
Protein C & S
Antithrombin

74
Q

Liver disease leads to what implication on hemostasis?

A
  1. Impaired synthesis of coagulation factors
  2. Quantitative and qualitative platelet dysfunction
  3. Impaired clearance of clotting and fibrinolytic proteins
75
Q

What do labs show in liver disease?

A

Prolonged PT and possible prolonged PTT

76
Q

Lab values only reflect the lack of _____ ______ factors, and do not account for the lack of _______ _____Factors

A

Pro-coagulation; Anticoagulation

77
Q

Liver Disease patients have sufficient amounts of _____ production

78
Q

CKD patients have anemia due to: (2)

A
  1. Lack of EPO
  2. Platelet dysfunction (d/t uremic environment)
79
Q

Treatment of CKD platelet dysfunction includes:

A
  1. Cryo (rich in vWF)
  2. DDAVP (tachyphylaxis)
  3. Conjugated estrogens (give 5 days preop)
80
Q

What is pathological hemostatic response to ______ causing excessive activation of the extrinsic pathway, which generates intravascular _____

A

DIC
TF/7a Complex; Thrombin

81
Q

What triggers Trauma-Induced Coagulopathy (TIC)?

A

Trauma, Amniotic fluid embolism, malignancy, sepsis, incompatible blood transfusion

82
Q

DIC Labs?

A

Decreased Platelets
Prolonged: PT/PTT/Thrombin time
Increased soluble fibrin & Increased FDP

83
Q

What are causes of coagulopathies?

A

Acidosis
Hypothermia
Hemodilution

84
Q

Trauma induced coagulopathy (TIC) is thought to be related to ..?

A

Activated protein C decreasing thrombin generation

85
Q

What is the driving factor for Protein C activation in TIC?

A

Hypoperfusion

86
Q

In TIC, the endothelial glycocalyx degrades which might result in

A

Auto-heparinization

87
Q

The most common inherited prothrombin diseases are caused by mutations in which 2 factors?

A

Factor 5 and 2 (Prothrombin)

88
Q

Factor V Leiden mutation leads to ______ ______ resistance, present in 5% of the Caucasian population.

A

Activated Protein C

89
Q

Prothrombin mutation causes increased ____ concentration, leading to hypercoagulation

90
Q

Thrombophilia is an inherited or acquired predisposition for

A

Thrombotic events, generally manifesting as a venous thrombus

91
Q

Thrombophilia pt. are highly susceptible to

A

Virchow’s triad

92
Q

Antiphospholipid syndrome is an AI disorder that creates antibodies against

A

Phospholipid binding proteins in the coagulation system
-Characterized by recurrent thrombosis and pregnancy loss
-Requires lifetime anti-coagulants

93
Q

What greatly increases the risk of thrombosis in pro-thrombotic prone patients?

A

Oral contraceptives
Pregnancy
immobility
infection
trauma
Surgery

94
Q

HIT is associated with _______ occurring _____ days after heparin treatment

A

Thrombocytopenia; 5-14 days (*for the first time you experience it), can be within 1 day if seen heparin prior

95
Q

Who is at a high risk for HIT?

A

Women
High-dose patients (Cardiopulmonary bypass)
Unfractionated heparin over LMWH

96
Q

What drug is contraindicated in HIT?

A

Warfarin (decreases Protein C and S synthesis)

97
Q

How long does it take the HIT antibodies to clear from the circulation?

98
Q

What are the laboratory tests used to assess coagulation?

A
  • Prothrombin Time (PT)
  • Activated Partial Thromboplastin Time (aPTT)
  • Anti-factor Xa activity assay
  • Platelet Count
  • Activated Clotting Time (ACT)
99
Q

What does Prothrombin Time (PT) assess and how is the test performed?
What does it monitor?

A

Plasma mixed with TF and number of seconds to clot is measured
-Assesses the integrity of the extrinsic and common pathways, reflecting deficiencies in factors 1,2,5,7,10
Monitors: Vitamin K antagonists (Warfarin)

100
Q

What does Activated Partial Thromboplastin Time (aPTT) measure?

A

aPTT measures seconds until clot formation after mixing plasma with phospholipid, Ca², and an activator of the intrinsic pathway.
-Assesses integrity of the intrinsic and common pathway
-more sensitive for 8 & 9 deficiency
-May be used to measure heparin

101
Q

How is Xa activity assay performed?

A

Plasma mixed with Xa and an artificial substrate that releases a signal after Xa is cleaved
-Functional assessment of Heparin’s effect
-Also used to test LMWH, Fondapurinux, Factor Xa inhibitors

102
Q

What is the normal platelet count?

A

> 100,000 platelets /microliter

103
Q

What does Activated Clotting Time (ACT) measure?

A

Measures responsiveness to heparin
-Variation to whole blood clotting time, adds a clotting activator to accelerate the time
-Addresses intrinsic and common

104
Q

What is the normal range for Activated Clotting Time (ACT)?

A

107 +/- 13 seconds

105
Q

What does Heparin Concentration Measurement estimate?

A

Estimates preoperative plasma heparin concentration

106
Q

1 mg protamine will inhibit ____ mg of heparin

A

1 mg heparin

107
Q

What do Viscoelastic Coagulation Tests measure?

A

All aspects of clot formation from early fibrin generation to clot retraction & fibrinolysis

108
Q

Name two types of Viscoelastic Coagulation Tests.

A
  • TEG (Thromboelastogram)
  • ROTEM (Rotational Thromboelastometry)
109
Q

What are the three main classes of Antiplatelet Agents?

A
  • Cyclooxygenase Inhibitors
  • P2Y12 receptor antagonists
  • Platelet GIIb/IIIa Receptor antagonists
110
Q

What is the mechanism of action for Cyclooxygenase Inhibitors?

A

Block Cox 1 from forming TxA₂ (which is important in platelet aggregation)
-ASA and NSAIDS

111
Q

How long do the anti-platelet effects of Aspirin last after discontinuation? NSAIDs?

A

Aspirin: 7-10 days
NSAIDs: 3 days

112
Q

What is the mechanism of action for P2Y12 Receptor antagonists?

A

Inhibit P2Y22-R preventing GIIb/IIIa expression
-Clopidogrel, Ticlopidine, Ticragrelor, Cangrelor

113
Q

How long do the anti-platelet effects of ____ last after discontinuation?
Clopidogrel
Ticlopidine
Ticagrelor & Cangrelor

A

Clopidogrel: 7 days
Ticlopidine: 14-21 days
Ticagrelor & Cangrelor: < 24 hours

114
Q

MOA for Platelet GIIb/IIIa -R Antagonists?

A

Prevent vWF and fibrinogen from binding to the GIIb/IIIa -R
-Abciximab, Eptifibatide, Tirofiban

115
Q

What are the main types of Anticoagulants?

A
  • Vitamin K antagonists
  • Heparin
  • Direct Thrombin Inhibitors
  • Direct Oral Anticoagulants (DOACs)
116
Q

What is the most common Vitamin K antagonist? MOA?

A

Warfarin - inhibits synthesis of vit. K dep. clotting factors (2,7,9,10, Protein C & S)

117
Q

What is the DOC for Afib and Valve replacements?

118
Q

What is the half-life of Warfarin? What labs do you use to monitor warfarin?

A

40 hours, can take 3-4 days to reach goal INR (2-3)
Lab: PT/INR, requ. frequent monitoring

119
Q

MOA of Heparin?

A

Binds to antithrombin and inhibits soluble thrombin and Xa

120
Q

What is a key characteristic of Low Molecular Weight Heparin (LMWH)?

A

NO coagulation testing needed, longer half-life
-protamine is only partially effective

121
Q

What is the main difference between Unfractionated Heparin and LMWH?

A

Unfractionated Heparin has a short half-life and requires close monitoring

122
Q

What is the MOA of Fondaparinux and Half life?

A

Direct Xa inhibitor
Long Half-life (17-21 hrs)
-Protamine is not effective

123
Q

Name some direct thrombin inhibitors and the drug class MOA

A

MOA: Bind/block thrombin in both soluble and fibrin-bound states
Hirudin, Argatroban, Bivalirudin, Dabigatran

124
Q

Which direct thrombin inhibitor is found in leeches

125
Q

Which direct thrombin inhibitor reversibly binds to thrombin with a half life of 45 min?

A

Argatroban (measure intraop with PTT and ACT)

126
Q

Which direct thrombin inhibitor has the shortest half life and is the drug of choice for renal or liver impairment?

A

Bivalirudin

127
Q

Which direct thrombin inhibitor is the first DOAC approved for CVA prevention and non-valvular Afib?

A

Dabigatran (Pradexa)

128
Q

What is beneficial about DOAC?

A

New class with predictable PK properties, fewer drug interactions, dosed daily with NO lab monitoring, shorter half life than warfarin, fewer: thrombotic events, ICH, and lower mortality than warfarin

129
Q

What are the DOAC that are DIrect Xa inhibitors?

A
  1. Rivaroxaban (Xarelto)
  2. Apixaban (Eliquis)
  3. Edoxaban (Savaysa)
130
Q

What is the primary use of Thrombolytics?

A

To dissolve blood clots via serine proteases that convert plasminogen to plasmin, breaking down fibrinogen to fibrin

131
Q

Name a Fibrin-Specific Thrombolytic.
Non-specific?

A

Altepase (tPA)
Non-specific: Streptokinase (allergic reactions)

132
Q

Surgery is contraindicated within ____ days of receiving a thrombolytic

133
Q

What are Procoagulants used for?

A

To mitigate blood loss
-Antifibrinolytics and Factor replacements

134
Q

Name two types of antifibrinolytics that are lysine analogues. MOA?

A
  • Epsilon-amino-caproic acid (EACA)
  • Tranexamic Acid (TXA)
    MOA: Bind and inhibit plasminogen from binding to fibrin impairing fibrinolysis
135
Q

TXA is used for what surgery frequently?

A

ortho surgery

136
Q

Factor replacements such as Recombinant 7a increase _____ generation via intrinsic and extrinsic path

137
Q

Prothrombin Complex Concentrates contain _____ Factors

A

vitamin-K factors

138
Q

Fibrinogen concentrates are derived from _____

A

pooled plasma at a standard concentration

139
Q

Cryo and FFP contain _____ coagulation factors, but ______ specific composition

A

more; less specific
(cheaper though)

140
Q

What should be done with Warfarin in low risk patients before surgery?
High risk patients?

A

Low risk: Stop 5 days prior to surgery & restart 12-24h postop
High risk: Stop 5 days prior and bridge UFH/LMWH

141
Q

UFH should be discontinued ____ hours prior to surgery and resumed with no bolus ____ than 12 hours postop

A

Discontinue heparin 4-6 hours before surgery
start no sooner than 12 hours postop

142
Q

Discontinue LMWH ____ hours prior to surgery and resume ___ hours postop

A

24 hours and 24 hours

143
Q

Current recommendations from the AHA suggest that moderate to high risk patients _____ their aspirin thru the periop period

143
Q

Post-bare metal stent, delay elective surgery
Drug eluding stent?

A

Bare metal: 6 weeks after placement
Drug eluding: 6 months

144
Q

What is the emergency reversal agent for Warfarin?

A

Prothrombin Complex Concentrates (PCC) - works fast, but short half life so also give Vitamin K to restore liver carboxylation of factors

145
Q

What is the emergency reversal agent for direct thrombin inhibitors

A

No reversal but they have a short half life (besides dabigatran)

146
Q

What is the antidote for Dabigatran (Pradaxa)?

A

Idarucizumab

147
Q

True or False: Surgery is contraindicated within 10 days of thrombolytic treatment.

148
Q

Fill in the blank: Direct Oral Anticoagulants (DOACs) have ______ pharmacokinetics/dynamics.

A

more predictable

149
Q

What is a characteristic of Direct Thrombin Inhibitors?

A

Bind/block thrombin in both soluble & fibrin-bound states

150
Q

What is the effect of adding protamine to heparinized blood?

A

Time to clot decreases until protamine concentration > heparin concentration

151
Q

What is the key action of P2Y12 receptor antagonists?

A

Prevent GIIb/IIIa expression

152
Q

What is the main function of Factor Replacements?

A

Increase thrombin generation via intrinsic & extrinsic pathways

153
Q

What is the half-life of Argatroban?

A

45 minutes

154
Q

What is secondary hemostasis?

A

Clotting factors activated, stabilizing the clot with crosslinked fibrin

155
Q

Adenosine Diphosphate (ADP) is a ________

A

Platelet activator

156
Q

Endothelial cells excrete this enzyme which degrades ADP

A

Adenosine diphosphatase (inactivating platelets)

157
Q

Endothelial cells increase ______ which is an anticoagulant

158
Q

Tissue Factor Pathway Inhibitor (TFPI) inhibits which factors?

A

Factor Xa and TF-7a complex

159
Q

Endothelial cells synthesize what “clot buster”

A

t-PA (tissue plasminogen activator)

160
Q

DOAC Factor Xa inhibiors might be reversed by _____, a derivative of Factor Xa

Assessment (9 decks)

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