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3154 Haematology > IC2 Hemostasis > Flashcards

IC2 Hemostasis Flashcards

1
Q

3 phases of hemostasis

A
  1. Vasoconstriction (immediate)
  2. Platelet plug (seconds)
  3. Fibrin clot (minutes)
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2
Q

Describe vasoconstriction/vascular spasm phase

A

Initiated by sympathetic nerves (e.g., serotonin) and mediated by vascular smooth muscle cells

May last 30min - hours

Process:

  • endothelial cells of opposite side stick together, and reduce blood loss
  • the cells contract and expose basal lamina
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3
Q

Describe platelet plug phase

A

1)

Damage to the endothelial wall exposes collagen, which binds and activates platelets. Platelet adhesion to exposed collagen is mediated by Von Willebrand’s Factor (vWF), a plasma protein produced by the platelets

vWF binds platelets to exposed collagen via glycoprotein receptor

Adhesion activates platelets and induces morphological change (flat inactivated => branched activated)

2)

Activation of platelets triggers release of granules that secrete chemical mediators (ADP and TXA2)

ADP: released from mitochondria attracts and activates more platelets

TXA2: promotes aggregation and further vasoconstriction

Fibrinogen (produced in the liver), links platelets through GP IIb/IIIa receptors

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4
Q

What do platelets contain and what are their roles?

A
  • Contractile proteins (actin and myosin)
  • Organelles: Mitochondria - release ADP, ER and Golgi - stores Ca2+ and synthesizes enzymes
  • Express COX-1 which produces TXA2
  • Growth factors (PDGF, VEGF)
  • Factor XIII (fibrin-stabilizing factor)
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5
Q

Describe the fibrin clot phase

A

Factor XIII (fibrin stabilizing factor) produced by the platelets, is activated by thrombin to factor XIIIa

Factor XIIIa crosslinks fibrin strands to form a stable fibrin meshwork

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6
Q

What are the factors involved in the extrinsic pathway?

A

VII

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7
Q

Extrinsic pathway
- speed of response
- triggered by

A

Short and fast within seconds, triggered by external tissue damage that release tissue factor/thromboplastin

*Tissue factor is factor III
*Note that platelet aggregation further enhances secretion of tissue factor as well which further leads to downstream coagulation cascade

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8
Q

What are the factors involved in the intrinsic pathway?

A

XII, XI, IX

*VIIIa along with IXa and Ca2+ is involved in activating factor X to Xa

*Ca2+ is factor IV

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9
Q

Intrinsic pathway
- speed of response
- triggered by

A

Slower as more factor activation is involved

Occurs due to exposure to collagen fibers or contact activation due to exposure to foreign surface (e.g., glass) => occurs within the blood circulation

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10
Q

What are the factors involved in the common pathway?

A

I - fibrinogen
II - prothrombin
V - involved with Xa and Ca2+ in activating prothrombin to thrombin
X
XIII - fibrin stabilizing factor

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11
Q

What are the 4 roles of thrombin?

A
  1. Enhance its own activation from prothrombin to thrombin (positive feedback)
  2. Cleave and activate conversion of fibrinogen to fibrin
  3. Activates factor XIII to XIIIa which will stabilize fibrin into fibrin mesh
  4. Enhance platelet activation/aggregation (positive feedback)

FYI: platelet aggregation will further cause release of PF3 from platelets

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12
Q

What occurs after hemostasis?

A
  1. Clot retraction (20min-1h)
  • mediated by platelets
  • stabilization of clot by squeezing serum from clot (serum is plasma without fibrinogen)
  • closure of leak, retraction of clot
  • clot dissolved in a few hours (action of plasmin)
  1. Healing (1-2w)
  • fibrous tissue replaces blood clot
  1. Repair
  • involvement of PDGF (stimulate vascular smooth muscle cell to build new vessel wall) and VEGF (endothelial cells multiply and restore inner endothelial lining)
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13
Q

What are the mediators involved in regulation of blood clotting?

A

Intact endothelial cells release:

  • Nitric oxide - inhibits platelet activation and aggregation
  • Prostacyclin - inhibits platelet activation and aggregation

Others:

  • Serotonin - inhibits ADP at high concentrations
  • Blood clot itself may limits the spread of thrombin
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14
Q

List the body’s procoagulants

A
  • Tissue factor (extrinsic pathway)
  • Collagen (exposure to collagen activates factor XII of intrinsic pathway)
  • Collagen (platelet plug)
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15
Q

List the body’s endogenous anticoagulants

A
  • Antithrombin III (AT III)
  • Heparin - potentiates action of AT III, inactivates thrombin
  • Thrombomodulin - inhibits procoagulant functions of thrombin
  • Tissue plasminogen activator (tPA) - breaks down clots, catalyzes plasminogen to plasmin conversion
  • Protein C
  • Protein S

Other mechanisms:

  • Smoothness of endothelial surface (prevent collagen fiber exposure) - platelet-repellent property of the endothelium
  • Fluidity of normal blood flow also helps to dilute small amounts of thrombin that form spontaneously (vs decreased flow or stagnation of blood may incr risk for thrombosis - e.g., in immobility, AFib)
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16
Q

Disruptions in the self-regulatory anticoagulant system can lead to?

A

Hypercoagulability and thrombotic complications

17
Q

What are some artificial anticoagulants?

A
  • VKA (warfarin, coumarins)
  • DOAC (dabigatran, rivaroxaban)
  • Chelators (citrate, EDTA)
18
Q

Describe the process of fibrinolysis

  • what is involved in dissolution of the clot
  • what happens to remains of the clot
A

Fibrinolysis - dissolution of clot

  • plasminogen is a plasma protein and protease precursor made by the liver
  • surrounding tissue and vascular endothelial cells release tissue plasminogen activator (tPA) which cleaves plasminogen to protease plasmin
  • plasmin digests fibrin, thereby dissolving the clot
  • macrophages remove the remains of the clot
19
Q

What are some heritable blood clotting disorders that result in excessive bleeding (insufficient clotting)

A

Hemophilia (genetic linked)

  • primarily affects males
  • hemophilia A: deficiency of factor VIII (common pathway)
  • hemophilia B: deficiency of factor IX (intrinsic pathway)
  • hemophilia C: deficiency of factor XI (intrinsic pathway)

Von Willebrand disease

  • deficiency of VWF

Platelet disorders

  • defects in platelet receptors
20
Q

Why might liver disease be associated with clotting defect?

A
  • Inability to synthesize procoagulants (since most clotting factors are produced in the liver - e.g., factor II, VII, IX, X, fibrinogen)
  • Inability to produce bile
  • Inability to produce bile and absorb fat and Vit K (active Vit K => essential for activating clotting factors for coagulation)
21
Q

Vitamin K deficiency can cause inability to clot because Vit K is essential for the activation of which of the following clotting factors?

A

II, VII, IX, X

22
Q

What is the name of a clotting disorder that results in low platelet counts?

A

Thrombocytopenia

23
Q

What are some conditions that may arise due to inappropriate clotting?

A

Thrombosis
Thromboembolism
Stroke due to AFib

24
Q

Blood coagulation tests
- PTT

A

Partial thromboplastin time

  • measures efficacy of intrinsic + common coagulation pathways (factors I, II, V, X, VIII, IX, XI, XII)
  • consist: citrated plasma + calcium + phospholipid + kaolin
  • citrate: anticoagulant
  • phospholipid: involved in conformational change/activation of platelets in the intrinsic pathway
  • used to monitor heparin therapy (factors II, IX, X, XII, XI)
  • Normal range: 25-39s
25
Q

Blood coagulation tests
- PT

A

Prothrombin time

  • measures efficacy of extrinsic and common coagulation pathways (factors I, II, V, X, VII)
  • consists: citrated plasma + calcium + tissue factors
  • used to monitor warfarin therapy (factors II, X, VII, IX - does not monitor IX)
  • Normal range: 12-15s
26
Q

Blood coagulation tests
- INR

A

Ratio of: PT of pt / PT of healthy person

Normal range: 0.9-1.3

Warfarin therapy: 2-3

3154 Haematology (14 decks)

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