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Foundations of Anesthesia 1 > Blood and Coagulation > Flashcards

Blood and Coagulation Flashcards

1
Q

What is the formula for the Maximal Allowable Blood Loss (MABL)

A

EBV x (initial Hct - lowest acceptable Hct) / Initial Hct

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2
Q

What is the estimated blood volume (EBV) for obese patients?

A

60mL/kg

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3
Q

What is the estimated blood volume (EBV) for adult male patients?

A

70mL/kg

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4
Q

What is the estimated blood volume (EBV) for adult female patients?

A

65mL/kg

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5
Q

What is the estimated blood volume (EBV) for preemie patients?

A

95-105mL/kg (more blood volume per kg body weight)

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6
Q

What is the estimated blood volume (EBV) for term infant patients?

A

85mL/kg

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7
Q

What is the estimated blood volume (EBV) for infants under one year?

A

80mL/kg

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8
Q

What is the estimated blood volume (EBV) for children ages 1-6 years old?

A

70-75 mL/kg

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9
Q

What is the lowest acceptable Hct based on?

A

Based on the patient’s comorbidities. The general number is 20-21%.

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10
Q

Which substance is responsible for adhering the platelet to the damaged vessel?

A

von Willebrand Factor

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11
Q

Which substances are associated with platelet activation and aggregation with?

A

The endothelium releases collagen which activates platelets to release ADP and Thromboxane A2.

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12
Q

The 4 steps of Hemostasis

A
  1. Vascular Spasm
  2. Formation of the platelet Plug (primary hemostasis)
  3. Coagulation and Fibrin formation (secondary hemostasis)
  4. Fibrinolysis when the clot is no longer needed
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13
Q

What and Where are platelets produced?

A

Megakaryocytes produce platelets in the bone marrow

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14
Q

What is the lifespan of platelets?

A

8-12 days (1-2 weeks)

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15
Q

What removes platelets?

A

Cleared by macrophages

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16
Q

Normal lab value for platelets?

A

150,000-300,000
(some texts say 100,000)

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17
Q

In the absence of vascular injury, the endothelium inhibits platelet function by :

A

Prostaglandin I2, NO, and ADP: inhibit platelet aggregation

Thrombomodulin: Binds thrombin and interferes with Protein C activation. This stops the inactivation of factors 5 and 8, which promotes thrombosis.

Releases t-PA: activates fibrinolysis

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18
Q

What is the function of Actin in platelets?

A

Helps the platelet contract to form a platelet plug

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19
Q

What is the function of the GpIIb/IIIa receptor complex compared to the GpIb receptors?

A

The GpIIb/IIIa receptor complex links activated platelets together to form a primary platelet plug on the platelet surface.

The GpIb emerges from the surge of the platelet to attach vWF and attract platelets to the endothelial lining.

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20
Q

What are the 2 functions of Vascular Spasm?

A
  1. reduces blood flow to area to minimize blood loss
  2. Helps procoagulants remain in the affected area so that they can do their job
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21
Q

During vasular injury, platelets adhere to collagen via?

A

Glycoprotein Ib of platelets to VWF. vWF functions as an adhesion bridge between subendothelial collagen and the GpIb receptor on platelets.

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22
Q

How does Von Willebrand factor (vWF) adhere to platelets?

A

vWF is synthesized and released from the endothelium. Binds the Glycoprotein 1b receptor on platelets and anchors them to the subendothelium

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23
Q

Activated platelets release? These substances do what?

A

Release ADP and Thromboxane A2. They recruit nearby platelets and facilitate platelet aggregation

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24
Q

Activated platelets release the contents of their alpha granules, this includes:

A

Fibrinogen, Fibronectin, vWF, platelet factor 4, platelet growth factor

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25
Q

Activated platelets express two glycoproteins on their surface, they are?

A

Gp IIb and Gp IIIa

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26
Q

What are the 3 steps of Primary Hemostasis (Platelet Plug Formation)

A
  1. Adhesion
  2. Activation
  3. Aggregation
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27
Q

What receptor complex links activated platelets together to form the platelet plug

A

Gp IIb/IIIa

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28
Q

What is required for Gp IIb/IIIa to accept fibrinogen?

A

Thromboxane A2 and ADP configure the receptor complex to accept fibrinogen

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29
Q

Do micro-injuries require a clot or only a platelet plug

A

Only a platelet plug. The more significant vascular injury requires a clot

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30
Q

The primary purpose of the coagulation cascade is to produce?

A

Fibrin (to form a clot)

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31
Q

Two distinct coagulation pathways arrive at the same endpoint to form the final common pathway. What point in the cascade is this?

A

Thrombin Activation - 2a

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32
Q

The extrinsic pathway is activated when?

A

Coagulation is initiated outside the intravascular space

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33
Q

The intrinsic pathway is activated when?

A

Coagulation is initiated inside the intravascular space

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34
Q

What coagulation factors are Vitamin K dependent?

A

Factors 2, 7, 9, 10

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35
Q

Factor 1 is _____ and is synthesized in the _____. Its function is?

A

Fibrinogen and Liver
Clot formation

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36
Q

Factor 2 is _____ and synthesized in the _____. Its function is?

A

Prothrombin and Liver
When in active form (Thrombin), it activates Factors 1, 5, 8, 11,13, platelets, and Protein C

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37
Q

Factor 3 is _____ and synthesized in the _____. Its function is?

A

Tissue Factor

Vascular Wall + Extravascular Cell Membranes; released from traumatized cells

Cofactor for Factor 7

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38
Q

Factor 4 is _____ and synthesized in the _____. Its function is?

A

Calcium Ions and Diet
Promotes clotting reactions

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39
Q

Factor 5 is _____ and synthesized in the _____. Its function is?

A

Proaccelerin (Labile Factor) and Liver

Cofactor for Factor 10. Forms prothrombinase complex

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40
Q

Factor 7 is _____ and synthesized in the _____. Its function is?

A

Proconvertin (Stable Factor) and Liver

Activates Factor 9 and 10

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41
Q

Factor 8 is _____ and synthesized in the _____. Its function is?

A

Antihemophilic Factor and Liver
Cofactor to Factor 9

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42
Q

Factor 9 is _____ and synthesized in the _____. Its function is?

A

Christmas Factor and Liver
Activates Factor 10

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43
Q

Factor 10 is _____ and synthesized in the _____. Its function is?

A

Stuart-Prower Factor and Liver
Activates Factor 2, forms prothrombinase complex with Factor 5

44
Q

Factor 11 is _____ and synthesized in the _____. Its function is?

A

Plasma Thromboplastin Antecedent and Liver

Activates Factor 9

45
Q

Factor 12 is _____ and synthesized in the _____. Its function is?

A

Hageman Factor and Liver

Activates Factor 11

46
Q

Factor 13 is _____ and synthesized in the _____. Its function is?

A

Fibrin Stabilizing Factor and Liver

Cross Links Fibrin

47
Q

What two factors are not blood proteins?

A

Factor 3 - Tissue Factor
Factor 4 - Calcium Ions

48
Q

The Intrinsic Pathway is measured by?

A

PTT (more letters - intrinsic longer than extrinsic)

49
Q

The Extrinsic Pathway is measured by?

A

PT (less letters - shorter than intrinsic)

50
Q

The extrinsic pathway is activated by?

A

Tissue Factor - factor 3

51
Q

Which coagulation factor has the shortest half-life? What is the implication of this?

A

Factor 7 - shortest half-life of about 4-6hrs.
It will be the first factor to become deficient in patients with liver failure, Vitamin K deficiency, and those on warfarin

52
Q

How fast is the extrinsic pathway?

A

Fast - requires only about 15 seconds

53
Q

What factors are specific to the extrinsic pathway

A

Factor 7 (Stable Factor)
Factor 3 (Tissue Factor)

54
Q

What factors are specific to the intrinsic pathway

A

12 (Hageman Factor)
11 (Plasma Thromboplastic Antecendent)
9 (Christmas Factor)
8 (Antihemophilic Factor)

55
Q

How long does it take the intrinsic pathway to form a clot?

A

Up to 6 minutes

56
Q

A deficiency of what factor causes Hemophilia A?

A

Factor 8 (Antihemophilic Factor)

57
Q

What is the role of thrombin

A

Converts fibrinogen to fibrinogen monomer
Activates or is a cofactor for 1, 13, 5, 8, 11

58
Q

What must be present to convert fibrinogen monomer to fibrin fibers?

A

Calcium (factor 4)

59
Q

Once a clot is degraded, how does the body turn off the fibrinolytic process?

A

tPA inhibitor (TPAI) inhibits the conversation of plasminogen to plasmin

Alpha-2 antiplasmin inhibits the action of plasmin on fibrin

60
Q

What is plasmin?

A

A proteolytic enzyme that degrades fibrin into fibrin degradation products.

61
Q

How is Plasmin activated?

A

Injured tissue releases tissue plasminogen activator (tPA) over a period of days (major mechanism)

Urokinase is produced by the kidneys and releases into the circulation (minor mechanism)

62
Q

What are 4 mechanisms that counterbalance clot formation?

A
  1. Vasodilation and washout of ADP and TxA2
  2. Antithrombin inactivating thrombin
  3. Tissue factor pathway inhibitor neutralizes tissue factor
  4. Release of proteins C and S
63
Q

What are 2 enzymes that convert plasminogen to plasmin

A

tPA and urokinase

64
Q

What 2 enzyme inhibitors turn off the fibrinolytic process?

A

tPA inhibitor (TPAI)
Alpha-2 antiplasmin

65
Q

How are plasmin activators used therapeutically?

A

They help dissolve thrombi to restore blood flow

66
Q

The contemporary cell-based cascade consists of three phases. They are?

A
  1. Initiation
  2. Amplification
  3. Propagation
67
Q

What is the end result of the initiation phase within the contemporary cell-based cascade?

A

A small amount of Thrombin (2a) is produced but not enough to activate fibrin.

68
Q

Why do thrombin levels remain low in the first phase of the contemporary coagulation model?

A

Because tissue factor pathway inhibitor (TFPI) limits the amount of tissue factor released

69
Q

What phase are platelets activated in the contemporary coagulation model?

A

Amplification

70
Q

Chapter 10 Apex Left Off

A
71
Q

How does Tissue Factor (3) not continually activate the extrinsic pathway?

A

When Tissue Factor activates Factor 7, it is immediately inhibited by TF Inhibitor so only a predetermined amount of factor becomes activated.

72
Q

Going from Extrinsic Pathway to Common, after Factor 7 is activated, it then activates?

A

Activates Factor 10 (X) of the common pathway

73
Q

What 3 factors are needed to activate Thrombin from Prothrombin?

A

Factor 10a, 5a, and Factor 4

(Stuart Power, Proaccelerin, and Calcium)

74
Q

What 2 factors form the Prothrombinase Complex?

A

Factor 10a and 5a

75
Q

Thrombin (2a) + Calcium (4) =?

A

Convertes Fibrinogen to Fibrin

76
Q

The Intrinsic Pathway (Contact Activation Pathway) is initiated when?

A

Damage occurs to the blood vessels themselves.

77
Q

The Extrinisic Pathway (TF Pathway) becomes activated when?

A

By the release of TF when injury occurs outside the vessel wall (organ trauma or crushing injuries)

78
Q

What is the first factor to become activated in the Intrinsic Pathway?

A

Factor 12 (Hageman)

79
Q

Thrombin ASSISTS with the activation of which Factors?

A

5, 8, 1, 11 and 13
And influences the recruitment of platelets to the injured area

80
Q

How does Thrombin act as an anticoagulant?

A
  1. Prevents continuous clot formation by releasing Tissue Plasminogen Factor (tPA)
  2. Stimulates Protein C and S to inhibit clot formation
  3. Forms a relationship with AntiThrombin III to interfere with coagulation.
81
Q

AntiThrombin III collects/distrupts which factors to disrupt clot formation?

A

12, 11, 10, 9, and 2

Which influences Factor 2 (prothrombin)

82
Q

Plasminogen is activated to Plasmin by?

A

tPA (tissue plasminogen activator) and Urokinase

83
Q

What are 2 important fibrinolytic mediators that stop the process of fibrinolysis once a clot has been digested / fully broken down?

A

Alpha-Antiplasmin and Tissue Plasminogen Activator Inhibitor

84
Q

How and where does Aspirin and NSAIDS affect coagulation?

A

Within the phospholipid bilayer. Aspirin (irreversible) and NSAIDS (reversible) inhibit cyclooxygenase (COX). COX converts arachidonic acid to prostaglandins which in turn releases/excites Thromboane A2, responsible for platelet aggregation.

So - Aspirin and NSAIDS decrease platelet function

85
Q

Plt levels: 100,000 , 50,000 , and 20,000 what is the risk of spontaneous bleeding

A

Plt levels under 100,000 is considered thrombocytopenic.

50,000 - spontaneous bleeding is rare but you should suspect prolonged bleeding under surgical conditions

20,000 - spontaneous bleeding is likely to occur. Considered a critical level.

86
Q

What are 2 key functions of vWF

A
  1. Mediates adhesion of platelets at sites of vascular injury
  2. Binds and stabilizes factor 8. Carries inactivated factor 8 in plasma.
87
Q

Lab values expected in DIC

A

Reduced platelet count : At least less than 100.
Decreased Fibrinogen: Less than 1g/L

Increased PT/PTT: At least greater than 3sec
Increased D-Dimer:

88
Q

Pt is in DIC and needs to go to OR. What would you give?

A

FFP
Platelets
In some cases Cryo or AntiThrombin III

89
Q

Your patient has an X-Linked coagulation disorder and needs surgery. What can you give them if indicated?

A

Hemophilia A - Factor 8 deficient
Hemophilia B - Factor 9 deficient

Factor 8 concentrate can be given prior to surgery
Factor 7 can be given intraoperatively
Desmopressin can also be given in increase vWF and Factor 8 plasma levels

90
Q

A Sickle Cell Crisis can be triggered by?

A

Hypoxemia
Hypothermia
Infection
Dehydration
Venous Stasis
Acidosis

91
Q

What is one of the most common surgeries needed by people with Sickle Cell Disease and why?

A

Cholecystectomy for gall stones.
Because of excess bilirubin resulting from the rapid breakdown of sickle erythrocytes

92
Q

What are some intraoperative management strategies for patients with sickle cell?

A

Adequate hydration
Avoid hypoxemia
Maintain normothermia
Maintain normal-acid base balance
Provide adequate perioperative pain management
Caution using vasoocclusive devices such as tourniquets

93
Q

What is Heparin Induced Thrombocytopenia (HIT)?

A

An immune response to herparin that can progress to severe thrombosis, amputation, and in some cases death

94
Q

Describe HIT type I
(immune or nonimmune, onset, degree of thrombocytopenia, tx, long term effects)

A

-Nonimmune Mediated. Thrombocytopenia is mediated by direct heparin-induced platelet aggregation
-Onset is typically 1-4 days after start of heparin therapy
-Mild thrombocytopenia (<100,000)
-Thrombocytopenia often resolves even with continued heparin therapy
-typically occurs with high-dose heparin administration
-Not associated with thrombosis and serious sequelae

95
Q

Describe HIT type II
(immune or nonimmune, onset, degree of thrombocytopenia, tx, long term effects)

A
  • Immune mediated. thrombocytopenia mediated by heparin, platelet factor 4, and IgG expression
  • Onset usually 5-14 days after start of heparin therapy
    -Severe thrombocytopenia (<60,000)
  • Thrombocytopenia does not resolve spontaneously. must stop heparin.
    -Associated with thrombosis and serious sequelae
96
Q

What are 2 anti-platelet drugs whose MOA are COX-1 nonspecific inhibitors?

A

Aspirin (ASA) COX-1 Inhibitor (irreversible)

NSAIDS COX-1 inhibitor (reversible)

97
Q

What are 2 anti-platelet drugs whose MOA are ADP receptor antagonist?

A

Clopidogrel
Ticagrelor

98
Q

What are 3 anti-platelet drugs whose MOA are Glycoprotein IIb/IIIa receptor antagonists?

A

Abiximab
Eptifibate
Tirofiban

99
Q

What anticoagulant medication is a Factor Xa indirect antagonist? (indirect - antithrombin cofactor)
What lab monitors?

A

Fondaparinux
Antifactor Xa assay

100
Q

What 2 anticoagulant medication is a Factor IIa AND Xa indirect antagonist? (indirect - antithrombin cofactor)
What lab monitors? What is the reversal?

A

LMWH and Heparin (unfractionated)

LMWH - Antifactor Xa assay
*partial reversal with protamine
Heparin - aPTT
*Protamine

101
Q

What anticoagulant drug has an MOA that is a Vitamin K epoxide reductase antagonist?
What lab monitors? What is the reversal?

A

Warfarin
PT
Vitamin K (phytonadione), FFP, PCC

102
Q

What anticoagulant drug has an MOA that is a Factor IIb direct antagonist?
What lab monitors? What is the reversal?

A

Dabigatran (Pradaxa)
Dilute Thrombin Time
Idarucizumab

103
Q

What 4 anticoagulant drugs have an MOA that is a Factor Xa direct antagonist?
What lab monitors? What is the reversal?

A

Rivaroxaban (Xarelto)
Apixaban (Eliquis)
Edoxaban
Betrixaban (Portola)
-Antifactor Xa Assay
-Andexanet alfa

104
Q

What are 2 Fibrinolytic drugs whose MOA are Tissue Plasminogen Activators?
What lab values monitor?
What is the reversal?

A

t-PA
Streptokinase
(Tenecteplase could also be included)
PT/aPTT
-Antifibrinolytics

105
Q

Some drugs have secondary anti-platelet activity. What are two Direct Thrombin Inhibitors that do that?

A

Bivalrudin
Dabigatran

106
Q

What is the most common comordbidity in patients with SCD?

A

Asthma. Occurs in about 50% of SCD patients

Foundations of Anesthesia 1 (17 decks)

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