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IPC Cardiology 2 > Anticoagulation, Hemostasis and Venous clotting(Patho) > Flashcards

Anticoagulation, Hemostasis and Venous clotting(Patho) Flashcards

1
Q

These are the componenets of the Coagulation of system

A
  • Platelets
  • Endothelial Cells
  • Tissue-Factor Bearing Cells
  • Coagulation factors
  • Antithrombotic factors
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2
Q

Platelets

A
  • Fragments of megakaryocytes
  • Creation is stimulated by cytokines and thrombopoietin
  • Important source of phospholipids which are required for the function of the coagulation system proteins
  • Intracellularly contain dense granules and alpha granules
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3
Q

Endothelial Cells

A

Cells that line blood vessels

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4
Q

Tissue-Factor Bearing Cells

A

Principle initiator of blood coagulation

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5
Q

Coagulation Factors

Plasma proteins that are enzymes(serine proteases)
Activated forms of factors have an “a” at the end
Most are created by the liver

A

Factors II,VII,IX,X are dependent on gammacarboxylase which is dependent on Vitamin K

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6
Q

Antithrombotic factors

A
  • Protein C and S (natural anticoagulants that are also vitamin K dependent)
  • Antithrombin(inactivates serine proteases IIa,IXa,XIa and XIIa)
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7
Q

Primary Hemostasis

Vasoconstriction

A
  • Adhesion
  • Activation
  • Aggregation
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8
Q

Secondary Hemostasis

Formation of fibrin

A
  • Initiation
  • Amplification
  • Propagation
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9
Q

Fribrinolysis

Natural negative feedback loop

A

Breaks down fibrin clots

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10
Q

PrimaryHemostasis (Adhere)

A
  • Adhere to collagen in the vascular subendothelium
  • Exposed collagen releases von willebrand factor
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11
Q

Primary Hemostasis(Activation)

A
  • Granules release ADP, calcium and thromboxane A2 to activate further platelets
  • GP IIb/IIa receptors are exposed on the platelet
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12
Q

Primary Hemostasis(Aggregate)

A
  • Changes shape from discord–> spherical with extensions and then a flat shape to cover the injury
  • Forms a “platelet plug”
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13
Q

Secondary Hemostasis(Initiation)

A
  • Begins with release of tissue factor (TF) by the injured cells
  • TF directly activates factor VII which activates factor IX and X
  • Activation of IX and X catalyzes conversion of pro-thromnin to thrombin
  • Thrombin cleaves fribrinogen to fibrin(stable clot)

The amount of fibrin generated during initiation is insufficient to stabilize the platelet plug

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14
Q

Secondary Hemostasis(Amplification)

A
  • Thrombin generated in intiation activates platelets and coagulation factors V,VIII and XI(found on plate[let surface)
  • Factor VIII is activated by releasing it from von willebrand factor
  • Factor XIa catalyzes activation of IX to IXa
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15
Q

Fibrinolysis

A
  • Process of breaking down fibrin into degradation products
  • Thrombin catalyzes formation of plasmin from its inactive precursor plasminogen

Plasmin is a serum protease that cleaves fibrin–>breakdown of clot and creation of fibrin degradation products

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15
Q

Secondary Hemostasis(Propagation)

A

Two major complexes are formed:
1.Tenase–> Factors VIIIa and IXa with phopholipids and calcium (this activates factor X on the platelet surface)
2.Prothrombinase–>Factors Xa and Va with phospholipids and calcium(catalyzes prothrombin => thrombin)
3.Activated thrombin stabilizes the platelet plug
4.Thrombin activates factor XIIIa which stabilizes the fibrin polymer

16
Q

Virchow’s Triad

A

Hypercoagulable state <–> Vascular injury<—>Circulatory Stasis

17
Q

Risk factors Hypercoagulable state

A
  • Malignancy
  • Pregnancy
  • Inflammatory state
  • Factor V Leiden
  • Protein C/S deficiency
  • Oral contraceptives
18
Q

Risk factors of Circulatory stasis

A
  • Hospitilization
  • Surgery
  • Obesity
  • Long distance travel
19
Q

Risk factors of Vascular injury

A
  • Orthopedic surgery
  • Trauma
  • Venous catheters
  • Smoking
20
Q

Risk factors of Multiple Components

A
  • History of VTE
  • Age(older=increased risk)
21
Q

Other risk factors of the Virchow’s triad

A
  • Metabolic syndrome
  • Inflammatory disorders: Crohn’s diseas, ulcerative colitis, RA, infections
22
Q

What is Venous Thromboembolism(VTE)?

A

Clot occuring in the VENOUS circulation

23
Q

Types of VTE

A
  • Deep vein thrombosis(DVT)
  • Pulmonary Embolism(PE)
24
Q

Deep Vein Thrombosis (DVT)

A
  • Usually occurs in the lower extremity
  • Due to blockage (thrombosis—>clot in diseased vessel)
  • Rarely fatal
25
Q

Pulmonary Embolism(PE)

A
  • Occurs in the lung
  • Usually due to a dislodged blockage (embolism= mobile clot)
  • Can be fatal
26
Q

Types of Clots

A
  • Arterial clot (Platelet rich)
  • Venous clot (Fibirn rich)
27
Q

Signs and symptoms of DVT

A
  • Unilateral leg pain, redness,swelling, and/or warmth
  • Positive Homan’s sign
  • Elevated D-dimer(by product of thrombin generation)
28
Q

Proximal DVT

A

70-80% of DVTs are proximal, ,ost commonly the popliteal and superficial femoral vein

29
Q

Distal DVT

A

20-30% of DVTs are isolated in veins of the calf: the anterior, tibial, peroneal, and posterior

30
Q

Testing for DVT

A

Usually diagnosed through a duplex ultrasound with doppler flow

31
Q

Pulmonary Embolism

A

Large thrombi or an accumulation of smaller ones can cause substantial impairment or cardiac and respiratory function/death

32
Q

Signs and symptoms of PE

A
  • Cough
  • Tachypnea
  • Tachycardia
  • Often identify signs/symptoms of DVT in the leg
  • Elevated D-dimer
33
Q

Testing for PE

A
  • Ventilation/perfusion scan
  • CT pulmonary angiography
34
Q

PE severity classification

A
  • Low risk(PE not meeting other criteria)
  • Intermediate risk(Right ventricular strain-> ECHO,->(+) troponin, ->(+) BNP)
  • High risk (systolic BP<90mmHG of decrease of 40 mmHG from baseline,requiring vasopressors, pulseless)
35
Q

Provoked vs Unprovokes VTE

A
  • Provoked(caused by a known event)
    1. Long-distance travel
    2. Surgery
    3. Hospitilization
    4. other elements in VIrchow’s Triad
  • Unprovoked(no identifiable factor cause VTE)

IPC Cardiology 2 (6 decks)

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