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419 Coagulation > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Healthy blood vessels - prevent clotting

A
  • Prostacyclin
  • Nitric oxide
  • Tunica intima: smooth flow and barrier between collagen and pro-coagulant proteins
  • Smooth internal surface: endothelium, subendothelium, internal elastic lamina
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2
Q

Damaged blood vessels - promote clotting

A
  • Vascular spasm (vasoconstriction)
  • Collagen fibers exposed
  • vWF secreted by endothelium –> bind PTL and collagen
  • Tissue factor from subendothelium –> Coagulation cascade
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3
Q

Platelets granules

A
  • Alpha granules (large protein): vWF, fibrinogen, albumin, PF4, Factor V, Factor VIII, Proteins S
  • Delta granules (small molecular): Calcium, ADP/ATP, serotonin
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4
Q

Primary hemostasis

A
  • Vessel injury
  • Adhesion
  • Aggregation
  • Activation (Platelet)
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5
Q

Adhesion of PTL

A

Platelet binds to

  • Collagen via GP1a receptor
  • vWF via GP1b/IX/V (vWF links PTL & collagen/endothelial cell)
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6
Q

Aggregation of PTL

A

Platelet binds to fibrinogen via PTL receptor: GPIIb/IIIa

Requires Ca

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7
Q

Activation of (more) PTL

A
  • TXA2 (thromboxane A2) bind to TXA2 receptor: get more Ca from bone, increases receptor GPIIb/IIIa
  • ADP binds to P2Y12 receptor: active more PTL, change PTL shapes, form more TXA2
  • Thrombin (factor II): initiate intracellular signal events
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8
Q

PTL aggregometry

A
  • ADP and collagen: via GPIIb/IIIa
  • Ristocetin: via vWF
  • Arachidonic acid: via COX/endoperoxidase/TXA2 stimulation
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9
Q

Mechanism of aspirin

A
  • Aspirin irreversibly block the COX enzyme
  • Low dose: inhibit COX-1 –> reduce TXA2 –> reduce aggregation
  • High dose: inhibit COX-2 –> reduce prostacyclin –> increase blood clot
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10
Q

Secondary hemostasis

A

Fibrin clot is formed

Extrinsic + Intrinsic + Common

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11
Q

Factors involved in 2nd hemostasis

A

Extrinsic: TF –> VIIa
Intrinsic: XII –> XI –> IXa + VIIIa
Both ways activate X –> Xa
Common:
1. Xa + V –> activate Prothrombin to Thrombin (IIa)
2. Thrombin activate Fibrinogen to Fibrin (Ia)

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12
Q

Enzymatic coagulation factors

A

II, VII, IX, X, XI

Usually inactive and must be activated

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13
Q

Non-enzymatic coagulation factors

A

TF, V, VII

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14
Q

Zymogens

A

Inactive enzymes circulated in the bloodstream

Become serine proteases when activated

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15
Q

Clot forming

A
  • Thrombin converts solube fibrinogen to insolube fibrin
  • Link with PTL via GPIIb/IIIa
  • Factor XIIIa cross-link fibrin
  • Level of fibrinogen in blood: 200-400 mg/dL
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16
Q

PT test (Prothrombin time)

A
  • Measure extrinsic pathway
  • Measure 3 of 4 vit K dependent factors (II, VII, X)
  • Add: pt’s plasma, TF, Ca
  • PT prolong with: warfarin, deficiency of factor: I, II, V, VII, X; liver disease, some antibiotics
17
Q

aPTT test (Activated partial thromboplastin time)

A
  • Measure intrinsic pathway
  • Add: Activator (surface), Ca, pt’s plasma, phospholipids
  • Prolong with: All factors (except VII, XIII), presence of inhibitors for VIII and IX, some drugs (heparin, anticoagulant)
18
Q

Hemophilia

A
  • Genetic disorders on X chromosome
  • Hemophilia A: factor 8
  • Hemophilia B: factor 9
  • Bleeding from mild to severe
19
Q

Vitamin K dependent factors

A

II, VII, IX, X

Protein S, C

20
Q

Thrombophilia

A

Imbalance in naturally occurring clot factors

21
Q

Protein C and S

A

Activated Protein C: inhibits V and VIII –> inhibits clotting cascade
Protein S: cofactor for protein C

22
Q

Factor V Leiden

A

The point mutation in factor V –> Protein C unable to bind –> Super active –> More clot

23
Q

Heparin - Anticoagulant drugs

A
  • Blood thinner
  • Given IV
  • Can be produced by basophils and mast cells
  • Treat and prevent vein thrombosis, pulmonary embolism
24
Q

6 functions of thrombin

A
  • Activating V
  • Activating VIII
  • Activating XI
  • Activating XIII for cross-link
  • Combine with thrombomodulin to activate protein C
  • Activate TAFI to suppress fibrinolysis
25
Q

Fibrinolysis

A

Fibrin clot degraded after bleeding stops

26
Q

Steps of fibrinolysis

A
  • Tissue plasminogen activator (t-PA) released from site
  • t-PA comes to fibrin clot and convert plasminogen to plasmin
  • Plasmin cleaves fibrin to fibrin degradation products
  • Macrophage clear the product
  • Plasmin also digest: fibrinogen, V, VIII, prothrombin, and XII
27
Q

Products of plasmin cleavage

A
  • Cleave fibrinogen to form E & D fragments

- Cleave fibrin to form E and D-dimer fragments

28
Q

D-dimers role

A
  • Presence of D-dimers –> occurrence of thrombosis and ongoing fibrinolysis
  • Normal level: 2ng/mL
29
Q

Testing of D-dimer to

A

Diagnosis of Disseminated intravascular coagulation (DIC) - Blood clot in small vessels throughout the body

30
Q

Inhibitors of fibrinolysis

A
  • Plasminogen activator inhibitor (PAL-1):
  • Alpha2-antiplasmin (A2AP):
  • Thrombin-activatable fibrinolysis inhibitor (TAFI):.
31
Q

PAL-1

A

Store in PTL, inactivate t-PA –> inhibits plasminogen activation

32
Q

A2AP

A

Made by the liver, inactivate plasmin

33
Q

TAFI

A

Not a serpin, keep plasminogen from binding to fibrin

419 Coagulation (8 decks)

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