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Surgery > Chapter 2 > Flashcards

Chapter 2 Flashcards

1
Q

How does the endothelium prevent propagation of a clot?

A

Thrombomodulin production results in activation of protein C and subsequent inhibition of factors Va and VIIIa, while local TFPI release reversibly inhibits factor Xa
Endogenous heparin and dermatan sulfate expression results in antithrombin III binding- thus inactivating thrombin and preventing propagation of clot

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2
Q

What is an early mediator of primary hemostasis during endothelial injury?

A

Vasoconstriction, as a result of neuromyogenic reflexes within the vascular smooth muscle

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3
Q

How is vascular contraction further augmented?

A

Paracrine signaling via ADP, thromboxane A2 and serotonin from nearby adherent platelets

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4
Q

What provides an avenue for platelet and leukocyte adhesion

A

Exposure of subendothelial tissue factor and collagen

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5
Q

What improves coagulation protein and platelet binding?

A

Increased endothelial cell production of vWF
Expression of cellular TF and platelet-activating factor (PAF)
Reduced thrombomodulin activity

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6
Q

Origin of platelets and lifespan

A

Derived from bone marrow megakaryocytes

Lifespan of 9-12 days

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7
Q

What percentage of the body’s platelet pool is stored in the spleen?

A

1/3

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8
Q

How is platelet adhesion further strengthened?

A

Presence of vWF, which mediates the binding of collagen with glycoprotein Ib/IX

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9
Q

When does platelet plug formation occur?
When does clot stabilization occur?
What is clot stabilization aided by?

A

Within 1-3 mins of injury
Within 10 mins of injury
Aided in part by negative feedback from endothelial cell PGI2 release

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10
Q

What occurs after platelet plug formation?

A

Procoagulant protein complexes (i.e, prothrombinase, tenase) form on platelet phospholipid surfaces and augment the production of thrombin via the coagulation cascade

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11
Q

What is responsible for the production of all coagulation factors with the exception of VIII and vWF?

A

Liver

VIII and vWF are produced by endothelial cells

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12
Q

How are factors II, VII, IX and X formed

A

Through vit K-dependent reactions

They are of particular importance in pharmacologic anticoagulation

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13
Q

Traditional coagulation pathway

A

Extrinsic (PT/INR) and intrinsic (aPTT) merge into a common pathway

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14
Q

More recent discovery of the coagulation pathway

A

Described in cell-based phases:
Initiation
Amplification
Propagation

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15
Q

Process of initiation

A

TF is released by the injured vascular endothelium
Binds to factor VII to form TF-VIIa complexes
Complex activates factors X and IX to form Xa and IXa
Factors Xa and Va form the Xa-Va complex (prothrombinase complex)
Prothrombinase complex converts small amts of factor II (prothrombin) to factor IIa (thrombin)

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16
Q

Process of amplification

A

Thrombin produced from initiation activates additional factor V, VIII, XI, and platelets through a pos feedback loop

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17
Q

Process of propagation

A

Factors IXa and VIIIa form the factor IXa-VIIIa complex (tenase complex)
Tenase complex converts additional factor X to Xa, which then forms more prothrombinase complexes
Large amts of thrombin are generated, leading to the formation of fibrin from fibrinogen
Fibrin weaves throughout the platelet plug to form a stable fibrin clot

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18
Q

What are important natural anticoagulants?

A

ATIII
Protein C
Protein S

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19
Q

What does ATIII do?

A

Directly inhibits factors IIa (thrombin), IXa, Xa, and XIa

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20
Q

What is protein C?

A

A vit-K dependent natural anticoagulant, which is activated by thrombin-thrombomodulin complexes on the endothelial cell surface following the formation of a clot

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21
Q

What is protein S?

A

A vit-K dependent cofactor in the formation of APC

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22
Q

What are important regulatory and precursor proteins necessary for fibrin degradation?

A

Plasminogen
tPA
a2-antiplasmin

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23
Q

What does tPA do?

A

Acts to convert plasminogen to plasmin, which in turn binds fibrin and degrades the polymer into soluble split products

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24
Q

What does a2-antiplasmin do?

A

Serves as a negative regulator of plasmin and binds and inactivates circulating excess plasmin
Binds continuously secreted plasmin, allowing early clot formation during vascular injury without immediate degradation

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25
Q

What is a nl platelet count?

A

150-450K/microL of blood

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26
Q

What occurs with a platelet count <50,000?

A

Pts are subject to easy bruising and bleeding?

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27
Q

When does spontaneous bleeding occur?

A

Does not typically occur unless platelet counts are <20K

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28
Q

What is considered a nl bleeding time?

A

Between 2-10 mins

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29
Q

What does bleeding time measure?

A

Qualitative platelet dysfunction

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30
Q

What is an abnormal bleeding time?

What is it associated with?

A

Between 10-15 mins
Associated with low-mod risk for bleeding
>15 mins is serious risk for spontaneous bleeding and severe platelet dysfunction or thrombocytopenia

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31
Q

What does prothrombin time (PT) measure?

A

The function of the extrinsic and common pathways of the ex vivo coagulation cascade
Measures the function of VII, V, X, II and I

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32
Q

What is a nl INR?

A

1.0

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33
Q

What prolongs INR? Why?

A

Warfarin

Due to depletion of vit K-dependent factors II, VII, IX, and X

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34
Q

What does aPTT measure?

A

The ex vivo intrinsic coagulation cascade, compromising high molecular weight kininogen, prekallikrein, and factors XI, IX, VIII, V, X, II, and I

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35
Q

What is activated clotting time?

A

ACT is a test similar to aPTT but used in clinical situations requiring high-dose heparin administration (cardiopulmonary bypass, endovascular interventions, ECMO)

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36
Q

What is TEG?

A 
Thromboelastography
Provides a quantitative measure of all aspects of hemostasis, including:
Platelet aggregation
Clot strengthening
Fibrin cross-linking
Fibrinolysis
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37
Q

Advantages of TEG

A

Quantification of thrombodynamics
Ability to differentiate between platelet and plasma coagulative disorders
Rapidity of its results

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38
Q

What is the MC congenital bleeding disorder?

A

vWD

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39
Q

Lab findings of vWD

A

Prolonged bleeding time
Mildly prolonged aPTT
Abnl platelet binding as measured by a depressed ristocetin cofactor assay

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40
Q

Type I vWD inheritance pattern

A

Autosomal dominant

Characterized by quantitative reduction in vWF levels with nl protein structure and function

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41
Q

Type II vWD

A

Variable inheritance pattern

Characterized by abnl qualitative protein function

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42
Q

Type III vWD

A

Autosomal recessive inheritance pattern

Associated with severe bleeding with absent vWF production

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43
Q

First-line therapy for type I and II vWD

A

DDAVP

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44
Q

Tx for type III vWD

A

Surgical prophylaxis or bleeding

Transfusion with cryoprecipitate or factor VIII: vWF concentrate

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45
Q

What is Glanzmann’s thrombasthenia?

A

A rare congenital platelet disorder that is a result of defective or decreased synthesis of glycoprotein IIb/IIIa
Platelets are unable to bind fibrinogen and lack the ability to form platelet aggregates

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46
Q

Why does platelet dysfunction occur in renal dz?

A

It’s a result of numerous changes to protein function and intraluminal fluid dynamics

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47
Q

What bleeding problems are found in uremic pts?

A

Dysfunctional vWF
Decreased thromboxane A2
Altered platelet granules

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48
Q

What does anemia cause in renal dz pts?

A

Decreased platelet adhesion and aggregation

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49
Q

Tx of uremic pts

A

Depends on severity of sx/bleeding risk
Dialysis
Epo
DDAVP/cryoprecipitate

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50
Q

What is extracorporeal circuitry?

What does it give rise to?

A

Cardiopulmonary bypass, ECMO

Abnl platelet activation in part d/t fibrinogen accumulation within the oxygenation membrane

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51
Q

What does consumption and loss of platelets from the circulating pool result in?

A

Thrombocytopenia as well as qualitative dysfunction

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52
Q

How are therapeutic anticoagulation levels maintained with extracorporeal circulation?

A

Systemic unfractionated heparin given IV and intermittently into the extracorporeal circuit

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53
Q

Type I HIT

A

May occur in as many as 10% of pts receiving unfractionated heparin
Typically resolves spontaneously within 96 hrs of heparin cessation

54
Q

Type II HIT

A

Unusual immunologic complication affecting 1-3% of pts

55
Q

Pathology of HIT

A

Heparin binds with PF4, which is released from platelet alpha granules normally.
in HIT, IgG antibodies form against the heparin-PF4 complex within 5-10 days of exposure that in turn, strongly activates platelet adhesion and aggregation

56
Q

When should you raise clinical concern for HIT?

A

When platelet counts decrease by >50% from preheparin levels

57
Q

What does massive platelet activation and platelet plug formation predispose the pt to?

A 
Venous thrombosis
Thromboembolism
Limb ischemia
Stroke
MI
58
Q

Labs for HIT

A

Serotonin release assay (SRA)
Heparin-induced platelet aggregation assay (HIPA)
ELISA

59
Q

What is one of the more common screening tests in clinical use for HIT?

A

ELISA

60
Q

Tx of HIT

A

Immediate cessation of all heparin therapies
Non-heparin-based anticoagulation strategies unless clinical CI
Avoidance of platelet transfusion is appropriate to help propagation of white clot

61
Q

Idiopathic thrombocytic purpura (ITP)

A

An acquired d/o rising from pathologic destruction of platelets d/t autoantibody formation

62
Q

When does ITP commonly occur?

A

Time of infection (often viral) OR

altered immune homeostasis (malignancy, lymphoproliferative d/os, concurrent autoimmune dz)

63
Q

Dx of ITP

A

Clinical and one of exclusion

64
Q

Tx of ITP

A

With platelet count of <30K, initially prevention of bleeding
Include glucocorticoids and IVIG
2nd line is splenectomy
If surgery is CIed, rituximab

65
Q

Pathology of hemophilia A/B

A

A is deficiency of factor VIII
B is deficiency of factor IX
Impaired formation of tenase (VIII-IXa) complex, impacting the amplification phase of coagulation and leading to decreased factor Xa and thrombin creation

66
Q

Sx of hemophilia A/B

A

Mucosal bleeding
Excessive bleeding during circumcision
Hemarthrosis
Intracranial hemorrhage

67
Q

Labs for hemophilia A/B

A

Elevated aPTT

Decreased factor VIII or IX levels

68
Q

Tx of hemophilia A

A

Recombinant factor VIII
Cryoprecipitate transfusion
Desmopressin

69
Q

Tx of hemophilia B

A

Recombinant factor IX

FFP or cryoprecipitate transfusion

70
Q

DIC

A

Results from unchecked activation of the normal coagulation response with loss of localization
Sepsis is the MCC of DIC

71
Q

Pathophys of DIC

A

Stems from systemic microvascular activation of platelets, diffuse activation of clotting factors, deposition of fibrin with microangiopathic thrombosis, and subsequent fibrinolytic pathway inactivation

72
Q

Dx of DIC

A

Clinical dx of exclusion

Schistocytes on peripheral blood smear

73
Q

Tx of DIC

A

Maintain an INR <1.5 and platelet count >50K

74
Q

Tx of bleeding secondary to hepatic failure

A

Correction of factor and platelet deficiencies with blood component management

75
Q

When is hypothermia commonly seen?

A

Altered coagulation as a result of:
Trauma
Massive resuscitation
Extended exposure to open body cavities during procedures
Iatrogenic hypothermia for cerebral or myocardial protection

76
Q

What is hypothermia associated with?

A

Impaired platelet function

Decreased collagen-induced platelet aggregation

77
Q

Tx of hypothermia

A

Treat underlying cause
Limit evaporative heat loss
Mild (>34 degrees Celsius)- passive rewarming techniques
Moderate (30-34 Celsius)- active rewarming
Severe (<30 Celsius)- External passive and active rewarming, internal rewarming

78
Q

Definition of massive transfusion

A

Replacement of a pts blood volume with packed RBCS (pRBCs) in a 24-hr period or acute transfusion of over half the pt’s blood volume per hr

79
Q

What is the massive transfusion protocol?

A

1:1:1 ratio of pRBC, FFP and platelet administration

80
Q

What is the MC hereditary procoagulant d/o?

A

Factor V Leiden

81
Q

Pathology of factor V Leiden

A

Mutation of the factor V protein prevents APC-mediated inactivation, thereby increasing risk for uncontrolled clot formation

82
Q

Dx of factor V Leiden

A

aPTT with and without APC

83
Q

Tx of factor V Leiden

A

No lifelong anticoagulation, only in thromboembolic events

84
Q

What does ATIII do?

A

Inactivates thrombin and factors Xa, IXa, and XIa

85
Q

What is the MC site of thrombosis in an ATIII deficiency?

A

Iliofemoral DVT

86
Q

Dx of ATIII deficiency

A

ATIII-heparin cofactor assay

87
Q

Tx of ATIII deficiency

A

FFP transfusion or ATIII concentrate

88
Q

Dx of protein C/S deficiency

A

Serum protein C and S levels below the nl limits

89
Q

What is the MC clinical manifestation of C/S deficiency?

A

Venous thromboembolism

90
Q

What is a known RF for pts with decreased protein C and S levels d/t a transient procoagulant state during initiation of the drug?

A

Warfarin-induced skin necrosis

91
Q

When should postponement of surgery occur?

A

Postpone beyond 6 wks for bare-metal stenting and 6 mos for drug-eluting stenting for noncardiac surgery pts
If not possible, continue dual antiplatelet therapy

92
Q

MOA of ASA

A

NSAID that irreversibly inhibit clyclooxygenase isoforms (COX-1 and COX-2)
Maintains its effects for the lifespan of the platelet

93
Q

MOA of ticlopidine, prasugrel and clopidogrel

A

Irreversibly inhibit activity of the ADP-P2Y receptor on the platelet membrane, which in turn impairs glycoprotein IIb/IIIa-mediated platelet cross-linking and aggregation

94
Q

When to use clopidogrel

A

ACS
Recent MI or CVA
Established PAD

95
Q

When to use prasugrel

A

ACS during PCI

It is found to inhibit platelet aggregation more rapidly and consistently compared to clopidogrel

96
Q

When to use cilostazol

A

Intermittent peripheral arterial claudication
Prevents vasoconstriction and smooth muscle proliferation
May require up to 1 yr before symptomatic relief is noticeable

97
Q

CIs of cilostazol

A

Dx of heart failure

98
Q

What are abciximab, eptifibatide, and tirofiban used for?

A

Adjuncts to heparin and ASA therapy

99
Q

What do heparin and LMWH do?

A

Increase ATIII activity

Primarily affects intrinsic and common pathways of in vitro coagulation

100
Q

How do you measure heparin and LMWH efficacy?

A

aPTT needs to be 1.5-2.5x the baseline aPTT value

101
Q

What is the onset of therapeutic warfarin anticoagulation

A

Takes at least 24-72 hrs

Principally affects extrinsic and common pathways of in vitro coagulation

102
Q

How to measure effect of warfarin

A

PT and INR

103
Q

MOA of direct thrombin inhibitors (DTI)

Examples of DTI

A

Inactivates circulating and clot-bound thrombin
Argatroban and bivalirudin
Dabigatran

104
Q

When to use argatroban

A

Those with contraindication to heparin

105
Q

Monitoring of argatroban

A

aPTT

106
Q

What is bivalirudin approved for?

A

Pts with ACS undergoing PCI

107
Q

What is dabigatran used for?

A

Tx/prevention of DVT, PE, non-valvular atrial fibrillation-associated stroke

108
Q

What are apixaban, roxaban, and edoxaban approved for?

A

VTE and nonvalvular a fib

109
Q

Measurement of apixaban, roxaban, and edoxaban

A

Anti-factor Xa activity

110
Q

What is r-tPA approved for?

A

Acute STEMI
Acute ischemic stroke
Acute massive PE

111
Q

Use of oxidized regenerated cellulose products

A

Frequently used as topical mesh placed on sites of bleeding to promote coagulation

112
Q

Use of gelatin matrix products

A

Can absorb blood up to 40x their weight and serve as the foundation of a hemostatic plug

113
Q

Use of topical thrombin and fibrin sealants

A

Commonly used bioactive topicals that augment hemostasis via directed factor II (topical thrombin) or fibrinogen (fibrin) application

114
Q

MOA of aminocaproic acid

A

Interferes with fibrinolysis by competitively blocking the fibrin-binding site on plasminogen, thereby preventing conversion to plasmin

115
Q

Use of aminocaporic acid

A 
Prevention of fibrinolytic bleeding d/t:
Cardiac surgery
Congenital hematologic dz
Cirrhosis
Malignancy
116
Q

Use of tranexamic acid

A

Hemophiliac pts undergoing dental procedures

Tx of menorrhagia

117
Q

Uses of desmopressin

A

DI
Nocturia
Management of bleeding secondary to hemophilia A, type I and 2 vWD, and prevention of surgical bleeding in hemophiliac pts

118
Q

Dosing of desmopressin in perioperative vWD and hemophilia A pts

A

30 mins IV or 2 hrs IN prior to the procedure

119
Q

What does protamine sulfate do?

A

Reverses the effects of heparin

120
Q

What does phytonadione (vit K) do?

A

Antagonizes the effects of warfarin

121
Q

What does each unit of pRBCs contain?

A

200 mL of RBC concentrate and an additional 100 mL of preservation solution

122
Q

What do pRBCs do?

A

Raise the recipient hematocrit approximately 3-4%

123
Q

Derivation of FFP and FP-24

A

Donor whole blood that has been separated and frozen within 8 (FFP) and 24 (FP-24) hrs

124
Q

When are FFP and FP-24 indicated?

A

Tx of multiple coagulation factor deficiencies, massive transfusion protocols, and when specific factor concentrates are not available

125
Q

What are components of cryoprecipitate?

A

Fibrinogen
Factor VIII
Factor XIII
vWF

126
Q

Indications of cryoprecipitate

A

Massive transfusion protocols
Hypofibrinogenemia
Factor VIII deficiencies when factor concentrates are not available
Bleeding associated with vWD when factor concentrates or DDAVP are not available

127
Q

Platelet concentration dose and efficacy

A

Contain around 7 x 10 to the 6th platelets per 50 mL

Each unit should increase platelet levels by at least 5K

128
Q

Indications for platelet transfusions

A 
Massive transfusion
Hereditary platelet dysfunction
Drug-induced platelet dysfunction
Cardiopulmonary bypass surgery-related platelet destruction
Platelet underproduction
129
Q

What should platelet counts be in preparation for surgical procedures?

A

> 50K

130
Q

What are isolated and recombinant factors currently available?

A 
Fibrinogen concentrate
Recombinant thrombin
Recombinant factors VIII and IX
vWF concentrate
Antithrombin concentrate
Of particular note in surgical populations: prothrombin complex concentrates (PCCs) and recombinant factor VIIa

Surgery (30 decks)

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