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MHD 1 > L34-35 Normal Hemostasis and Thrombosis > Flashcards

L34-35 Normal Hemostasis and Thrombosis Flashcards

1
Q

What is the difference between a thrombus and an embolus?

A

Thrombus: stationary clot Embolus: clot broken from a primary site that travels to a secondary site

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2
Q

What are the two parts of normal hemostasis?

A
  1. Ruptured vessels undergo changes which prevent blood loss. 2. Prevention of excessive loss of blood from a ruptured blood vessel
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3
Q

What is the major event of hemostasis?

A

Formation of a hemostatic plug that fills the leakage site in the injured vessel

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4
Q

What are the two parts of abnormal hemostasis?

A
  1. Formation of a clot within intact blood vessels 2. Loss of blood into surrounding soft tissues when a rupture occurs
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5
Q

Upon what three entities does hemostasis depend?

A
  1. Blood vessel wall (endothelium and sub-endothelial substances) 2. Platelets 3. Coagulation and fibrinolytic systems
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6
Q

What are the 4 hemostatic responses?

A
  1. Vasoconstriction 2. Primary hemostasis 3. Secondary hemostasis 4. Formation of platelet-thrombin plug
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7
Q

Vasoconstriction occurs immediately and briefly through reflex ___ mechanisms. It may also mediate ___ released from the endothelium. What is the primary purpose of vasoconstriction?

A

Neurogenic; humoral factors; reduce blood loss

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8
Q

___ is a potent vasoconstricting agent released from the endothelial cells in distress.

A

Endothelin

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9
Q

How is the extracellular matrix involved in vasoconstriction?

A

Contractile fibers

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10
Q

Describe the steps of primary hemostasis broadly.

A
  1. Platelets adhere to damaged vessels. 2. Platelets undergo a shape change. 3. Granule release from platelets. 4. Activated platelets recruit other platelets. 5. Aggregation/hemostatic plug formation
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11
Q

Describe the steps of secondary hemostasis broadly.

A
  1. Tissue factor is released from the site of injury; this promotes coagulation by combining with platelet factors to initiate the coagulation cascade. 2. Surface phospholipids are expressed; this also promotes coagulation (coagulation proteins form complexes on the platelet surface utilizing the phospholipids). 3. Thrombin is generated via the coagulation cascade 4. Fibrin polymerizes via Factor 13a
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12
Q

What happens during formation of the permanent plug?

A

Thrombin stimulates recruitment and activation of additional platelets. It also converts fibrinogen to fibrin. The clot forms a permanent plug; RBCs and WBCs become part of the thrombus.

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13
Q

Discuss the anti-platelet activity of the endothelium.

A

Intact endothelium prevents platelets and coagulation proteins from coming into contact with sub-endothelial collagen. They secrete prostacyclin and NO to prevent aggregation.

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14
Q

Discuss the anti-coagulant activity of the endothelium.

A
  1. Heparin-like molecules bind anti-thrombin III; this binds and inactivates thrombin. This can also inactive 10a and 9a. 2. Thrombomodulin binds thrombin. This activates protein C, which lyses 5a and 8a.
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15
Q

What does active protein C require to function?

A

Protein S

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16
Q

Discuss the fibrinolytic effect of the endothelium.

A

Endothelial cells secrete t-PA (plasminogen activators) which promote fibrinolysin. Plasminogen is converted to plasmin and dissolves the clot.

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17
Q

Discuss the prothrombotic effects of the endothelial cells.

A
  1. Secrete von Willebrand factor, which forms a molecular bridge between platelets and subendothelial collagen. 2. Synthesize and secrete tissue factor, which activates the extrinsic coagulation cascade (cytokines can stimulate cells to synthesize more TF)
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18
Q

What is the role of tissue factor?

A

Promotes generation of thrombin and formation of a clot

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19
Q

What are platelets?

A

Discoid, anuclear cells which play a major role in hemostasis

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20
Q

The plasma membrane contains many ___ receptors. What do they do?

A

Glycoprotein; play a role in the attachment of platelets to subendothelial proteins (via von Willebrand) and inter-adherence between platelets (via fibrinogen)

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21
Q

What is contained in the light (alpha) granules?

A
  1. Fibrinogen 2. Fibronectin 3. Factors 5 and 8 4. Platelet factor 4 (heparin-binding chemokine) 5. Growth factors (PDGF and TGF-beta)
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22
Q

What is contained in the dark (beta) granules)?

A
  1. ADP 2. ATP 3. Ionized Ca2+ 4. Histamine 5. Serotonin 6. Epinephrine
23
Q

What are the 5 platelet receptors?

A
  1. Glycoprotein 2b3a 2. Glycoprotein 1b 3. Thrombin 4. Serotonin 5. ADP
24
Q

With vessel injury, circulating proteins are exposed to subendothelial proteins which cause platelets to undergo what three reactions?

A
  1. Adhesion 2. Activation/Secretion 3. Aggregation
25
Q

Discuss the process of platelet adhesion.

A

Platelets attach to the subendothelial collagen through a molecular bridge. 1b attaches to von Willebrand factor, which attaches to collagen.

26
Q

Why is adhesion important?

A

It prevents the blood flow from dislodging the adherent platelets and unplugging the defect.

27
Q

Deficiency of Gp1b causes ___ syndrome.

A

Bernard-Soulier

28
Q

Deficiency of 2b3a causes ___.

A

Glanzmann thrombasthenia

29
Q

Discuss the process of platelet activation and secretion.

A

Activation is initiated by molecules binding with 2b3a. Upon activation, platelets release other granular content (coagulation factors, ADP, calcium, thromboxane A2). The phospholipid complex is activated when negatively charged phospholipids are exposed on the platelet surface.

30
Q

What is the purpose of the phospholipid complex?

A

The site on which coagulation factors combine with ionized calcium to activate the intrinsic pathway.

31
Q

Discuss the process of aggregation.

A

The release of ADP and thromboxane A2 from the platelet granules initiates a reaction which serves to recruit, activate, and aggregate platelets. Serotonin and thromboxane A2 vasoconstrict the vessel. Thrombin is formed by the activation of the intrinsic pathway. It also converts fibrinogen to fibrin.

32
Q

The blood coagulation system is comprised of a network of ___.

A

Proenzymes

33
Q

What is the ultimate goal of the coagulation system?

A

Formation of thrombin to convert fibrinogen to fibrin.

34
Q

What happens after fibrin is formed?

A

13a (and TAFIa) converted fibrin to stabilized fibrin.

35
Q

All of the coagulation cascade factors are ___ proteases except for 13a, which is a ___.

A

Serine; transamidase

36
Q

Draw the coagulation cascade.

A
37
Q

What is the test for measuring the extrinsic pathway?

A

PT test (prothrombin time)

38
Q

What is the test for measuring the intrinsic pathway?

A

PTT

39
Q

What is the central factor in the coagulation cascade?

A

10

40
Q

What are the factors in the fibrinogen group?

A

1, 5, 8 13

41
Q

What are the factors in the prothrombin group? What do they have in common?

A

2, 7, 9, 10; they all contain gamma-carboxy glutamic acid, which is needed for the binding of Ca2+; they are also all synthesized in the liver, require vitamin K, and are suppressed by warfarin.

42
Q

What are the factors in the contact group?

A

11, 12, Fletcher factor (prekallikrein), Fitzgerald factor (HMW kininogen)

43
Q

What are the inhibitors of the coagulation cascade?

A
  1. Antithrombin III (AT)
  2. Heparin cofactor II (HC II)
  3. Tissue factor pathway inhibitor (TFPI)
  4. Clotting factor inhibitors
  5. Lupus anti-coagulant and anti-phospholipid Ab
  6. Antibodies to coagulation factors
44
Q

Antithrombin is a plasma inhibitor which also mediates the anticoagulant actions of ___.

A

Heparin

45
Q

The ___ system is a network of enzymes that are responsible for the dissolution of a formed clot.

A

Fibrinolytic

46
Q

How is fibrin digested?

A

Plasmin

47
Q

___ is converted into plasmin. What can inhibit the fibrinolytic system?

A

Plasminogen; Plasminogen activator inhibitor (PAI), alpha-2-antiplasmin, alpha-2-macroglobulin, Thrombin activatable fibrinolytic inhibitor (TAFI)

48
Q

What is the pathologic transition of the state of blood from fluidity to non-fluidity?

A

Thrombosis

49
Q

True or false - the thrombogenic mechanisms are the same in the arterial and venous system.

A

False - they are not the same.

50
Q

What are the three hallmarks of thrombosis (Virchow’s triad)?

A
  1. Hypercoagulability (alterations in blood composition)
  2. Endothelial injury (release of tissue factor)
  3. Abnormal blood flow (stasis)
51
Q

What are the 3 types of thrombi?

A
  1. Arterial thrombi
  2. Venous thrombi and pulmonary emobli
  3. Microvascular thrombi
52
Q

What are some factors contributing to a hypercoagulable state?

A

Age, smoking, oral contraceptives, diet

Primary genetic conditions: molecular thrombophilias and inhibitor deficiences

Secondary acquired conditions: sepsis, cancer, trauma (all high risk); pregnancy, hyperlipidemia, drugs (all low risk)

53
Q

What are the three major molecular deficits contributing to thrombophilia?

A
  1. Factor V Leiden (APC resistance)
  2. Prothrombin 20210 (high production of prothrombin)
  3. Methylenetetrahydrofolate reductase (MTHFR mutation)

MHD 1 (58 decks)

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