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IPC CARDIOLOGY 2 JEN > Physiology of Hemostasis > Flashcards

Physiology of Hemostasis Flashcards

1
Q

What is the Coagulation System?

A

Highly complex, regulated interaction of cells and plasma proteins

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2
Q

What does the coagulation system provide?

A

Immediate activation when hemostasis is required and confines its activity to the site of blood loss

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3
Q

End result of the Coagulation System?

A

Complex of cross linked fibrin molecules and platelets that terminate a hemorrhage

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4
Q

Components of the Coagulation System

A

Platelets
Endothelial Cells
Tissue-Factor Bearing Cells
Coagulation Factors
Antithrombotic Factors

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5
Q

What are platelets?

A

-Fragments of megakaryocytes
-Creation is stimulated by cytokines and thrombopoietin (TPO)
-Important source of phospholipids which are required for the function of the coagulation system proteins

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6
Q

What do platelets intracellularly contain?

A

Dense granules and alpha granules

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7
Q

What is platelet activation called?

A

Degranulation

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8
Q

What are endothelial cells?

A

Cells that line blood vessels

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9
Q

What are tissue-factor bearing cells?

A

Principle initiator of BLOOD COAGULATION

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10
Q

What do activated forms of factors have at the end?

A

“a”

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11
Q

What are protein C and S?

A

natural anticoagulants that are also vitamin K dependent

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12
Q

Which factors are dependent on gammacarboxylase?

A

II, VII, IX, X (2,7,9,10)

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13
Q

Antithrombin inactivates…

A

Serine proteases IIa, IXa, XIa, Xlla (2,9,11,12)

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14
Q

Primary Hemostasis

A

Vasoconstriction
Platelet: Adhesion, Activation, Aggregation

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15
Q

Which line of hemostatic defense is primary hemostasis?

A

First

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16
Q

How does primary hemostasis work?

A

Begins within seconds of vessel injury and is mediated by circulating platelets.
Involves vasoconstriction, platelet adhesion and activation.
Collagen and thrombin activate platelets –> increase in intracellular Calcium –> secretion of platelet granules

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17
Q

The role of platelets: Adhesion

A

Adhere to collagen in the vascular subendothelium.
Exposed collagen releases von willebrand factor

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18
Q

The role of platelets: Activation

A

Granules release ADP, calcium, and thromboxane A2 to activate further platelets
-GP llb/llla receptors are exposed on the platelet

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19
Q

The role of platelets: Aggregation

A

Changes shape from discord –> spherical with extensions and then a flat shape to cover the injury

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20
Q

Secondary Hemostasis

A

Formation of fibrin via initiation, amplification, and propagation

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21
Q

Where does initiation occur?

A

the SURFACE of INJURED CELLS

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22
Q

What is released first in initation?

A

Tissue factor (TF) by the injured cells

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23
Q

Which factors does TF activate? (initiation)

A

Factor VII (7)

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24
Q

Which factors does Factor VII activate? (initation)

A

Factors IX and X (9 and 10)

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25
Q

What does the activation of factors IX and X catalyze? (initiation)

A

The conversion of factor II to IIa (activates it)

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26
Q

What is factor II?

A

Thrombin

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27
Q

What does factor IIa do? (initiation)

A

cleaves fibrinogen to fibrin

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28
Q

What is fibrin?

A

Small insoluble proteins that polymerize to form the complex fibrin

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29
Q

The amount of fibrin generated during initiation is…

A

Insufficient to stabilize the platelet plug

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30
Q

Where does amplification occur?

A

the SURFACE of PLATELETS

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31
Q

Thrombin is generated in initiation activates…

A

platelets and coagulation factors V, VIII, and XI (found on platelet surface) (5, 8, 11)

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32
Q

Factor VIII is activated by… (amplification)

A

releasing it from Von Willebrand Factor

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33
Q

Factor XIa catalyzes… (amplification)

A

activation of IX and IXa

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34
Q

What is propagation?

A

Activated platelets recruit other circulating platelets to the site of injury

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35
Q

What are the two main complexes formed in propagation?

A

Tenase and Prothrombinase

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36
Q

What is tenase?

A

factors VIIIa and IXa with phospholipids and calcium (8,9)

37
Q

What does tenase activate?

A

factor X on the platelet surface

38
Q

What is prothrombinase?

A

factors Xa and Va with phospholipids and calcium (5,10)

39
Q

What does the prothrombinase complex catalyze?

A

The cleavage of factor II to IIa

40
Q

The cleavage of factor II to IIa is…

A

prothrombin –> thrombin

41
Q

Thrombin activates _____ fibrin to stabilize platelet plug

A

enough

42
Q

Thrombin activates factor XIIIa which…

A

solidifies the fibrin polymer

43
Q

What is fibrinolysis?

A

Process of breaking down fibrin into degradation products

44
Q

Plasmin is a serum protease that cleaves fibrin, which leads to…

A

the breakdown of clot and creation of fibrin degradation products

45
Q

Thrombin catalyzes formation of…

A

plasmin from its inactive precursor plasminogen which functions as its own negative feedback loop

46
Q

Coagulation Cascade: Platelets initiate here

A

Vascular Injury

47
Q

Coagulation Cascade: This pathway amplifies and propagates the cascade

A

Surface Activation

48
Q

Coagulation Cascade: Which has to do with amplification (thrombin activates V, VIII, and XI on platelet surface?

A

Thrombin

49
Q

Why does a clot form to begin with?

A

Virchow’s Triad!
Hypercoagulable state, Vascular injury, circulatory stasis

50
Q

Risk factors for clotting: Hypercoagulable State…

A

Malignancy, Pregnancy, Inflammatory state, Factor V Leiden, Protein C/S deficiency, Oral contraceptives

51
Q

Risk factors for clotting: Circulatory Stasis…

A

Hospitalizations, surgery, obesity, long distance travel

52
Q

Risk factors for clotting: Vascular Injury…

A

Orthopedic Surgery, trauma, venous catheters, smoking

53
Q

Risk factors for clotting: Multiple Components…

A

History of VTE, Age (older = increase risk)

54
Q

Other risk factors: Metabolic syndrome…

A

especially in presence of abdominal obesity

55
Q

Other risk factors: inflammatory disorders…

A

Crohn’s disease, ulcerative colitis, rheumatoid arthritis, infections

56
Q

What is VTE?

A

Venous Thromboembolism
clot occurring in the VENOUS circulation

57
Q

What are the two types of VTE?

A

Deep Vein Thrombosis (DVT)
Pulmonary Embolism (PE)

58
Q

Deep Vein Thrombosis (DVT)

A

Usually occurs in a lower extremity
Due to blockage (thrombosis= clot in diseases vessel)
Rarely fatal

59
Q

Pulmonary Embolism (PE)

A

Occurs in the lung
Usually due to dislodged blockage (embolism= mobile clot)
Can be fatal (usually the more serious VTE)

60
Q

Embolus

A

traveling clot (usually more serious)

61
Q

Thrombus

A

located in the spot where it started to form

62
Q

Signs and Symptoms of DVT?

A

Unilateral leg pain, redness, swelling, and/or warmth
Positive Horman’s sign (dorsiflexes foot)
Elevated D-dimer (byproduct of thrombin generation)

63
Q

What % of DVTs are proximal?

A

70-80%

64
Q

Location of proximal DVTs?

A

Knee and above! Closer to the heart

65
Q

What % of DVTs are distal?

A

20-30%

66
Q

Location of distal DVTs?

A

Isolated in veins under the knee! Further from the heart

67
Q

Why do we care about proximal vs distal DVT?

A

Distal DVT is unlikely to lead to PE

68
Q

What is Pulmonary Embolism (PE)?

A

Most commonly thromboembolism (>95%) but can be made of other material

69
Q

What test is used for DVT?

A

Duplex ultrasound with doppler flow
Usually diagnosed through this, it allows the radiologist to see blood flow, relatively quick and easy

70
Q

In PE, the lungs possess…

A

Excess functional capacity and redundant vascular supply allowing them to filter a significant amount of emboli within minimal impact on lung function or hemodynamics

71
Q

Large thrombi or an accumulation of smaller ones can cause…

A

Substantial impairment of cardiac and respiratory function/death

72
Q

Where does PE never usually originate from?

A

The pulmonary circulation

73
Q

Signs and Symptoms of PE?

A

The Classic Triad (dyspnea, pleuritic chest pain, hemoptysis)
Dyspnea most common
Cough, tachypnea, tachycardia, elevated D-dimer

74
Q

Where are symptoms of DVT usually identified?

A

Legs

75
Q

Creation of ‘dead space’ ventilation is…

A

When there is oxygen in the area but there is no perfusion (no blood flow)
Limits the ability to eliminate carbon dioxide

76
Q

How does the body usually overcompensate for ‘dead space’ ventilation?

A

It increases minute ventilation which blows off extra carbon dioxide, which can lead to respiratory alkalosis
(little to no impact on oxygenation- oxygen saturation is normal or moderately reduced)

77
Q

Testing for PE…

A

Multiple options
Ventilation/perfusion scan
CT pulmonary angiography

78
Q

Severity of PE is dependent on…

A

Clot burden, neurohormonal reflexes, pre-existing cardiopulmonary disease

79
Q

Without cardiopulmonary disease: can accommodate….

A

an occlusion up to about 1/3 of their pulmonary circulation
Adapts to diverted blood flow through the recruitment and dilation of compliant pulmonary arterial vessels

80
Q

Without cardiopulmonary disease: hemodynamic compromise occurs when…

A

larger emboli occur or vasoconstricting mediators are elaborated

81
Q

In patients with cardiopulmonary disease: the size of the emboli,,,

A

does not correlate with the level of hemodynamic compromise
Normal adaptive mechanisms are ineffective

82
Q

PE Severity Classification: Low Risk

A

PE not meeting other criteria

83
Q

PE Severity Classification: Intermediate Risk

A

Right ventricular strain:
On ECHO, (+) troponin, (+) BNP

84
Q

PE Severity Classification: High Risk

A

Systolic BP < 90 mmHg or decrease of 40 mmHg from baseline

85
Q

PE Severity Classification: High Risk…what does it require?

A

Vasopressors, Pulseless

86
Q

Provoked VTE

A

Caused by a known event

87
Q

Some known events for Provoked VTE?

A

Long-distance travel, surgery, hospitalization, other elements of Virchow’s Triad!

88
Q

Unprovoked VTE

A

No identifiable factor causing VTE

IPC CARDIOLOGY 2 JEN (6 decks)

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