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2.b. Biochemistry II > Blood Coagulation > Flashcards

Blood Coagulation Flashcards

1
Q

Steps in hemostasis

A
  1. Vascular spasm / vasoconstriction
  2. Platelet plug formation / primary hemostasis
  3. Blood coagulation / secondary hemostasis
  4. Dissolution of the fibrin clot / tertiary hemostasis
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2
Q

Vascular spasm

A

Trauma to vessel wall results in smooth muscle contraction

Cannot cause long term bleeding cessation.

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3
Q

Primary Hemostasis

A

Platelet plug formation

Stages:
Platelet adhesion to damaged tissue
Activation of platelet aggregation

-Defects in platelet plug formation result in increased bleeding time.

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4
Q

Steps in platelet adhesion

A
  1. Platelet glycoprotein Ia (GPIa) binds to subendothelial collagen
  2. Von Willedrand factor (vWF) binds to platelet glycoprotein Ib (GPIb) resulting in changes to the platelet membrane
  3. Membrane changes expose GPII/IIIa for binding of fibrinogen.
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5
Q

Von Willebrand Factor

A

vWf acts as a bridge between specific glycoproteins(GPIb) on the surface of platelets and collagen fibres –Facilitates platelet adhesion to the vessel wall and platelet aggregation

Carries and stabilized Factor VIII in the intrinsic pathway.

Deficiency is associated with a defect in the formation of the platelet plug (primary hemostasis) and a defect in coagulation (due to low levels of factor VIII)

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6
Q

Platelet Aggregation

A
  1. Adhesion platelets release granule contents (ADP, Ca++) that activate other platelets.

ADP binding facilitates cellular release of Ca++ and decreases cAMP.

  1. Ca++ activates phospholipase A2 which cleaves PIP2 to arachidonic acid. COX then forms prostaglandins (G2, H2) then finallly Thromboxane A2 which induces platelet aggregation and vasoconstriction.
    - Platelets aggregation is maintained mainly by fibrinogen which binds to GPIIb/IIA receptors.
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7
Q

Secondary Hemostasis

A

Blood Coagulation

Converts blood from liquid form to a solid, gel-like state.

Converts fibrinogen to insoluble fibrin (requires thrombin)

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8
Q

Production of thrombin

A

Coagulation cascade via 2 pathways

  1. intrinsic
  2. extrinsic
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9
Q

Extrinsic Pathway

A

Tissue Injury —> release of tissue factor (Factor III)
Tissue factor activates VIII to VIIIa

VIIIa and tissue factor (in the presence of Ca++ and platelet phospholipids) activates X to Xa.

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10
Q

Intrinsic Pathway

A

Rough endothelial surface –> Exposure to collagen
Activation of XII to XIIa.

XIIa activates XI to XIa.

XIa activates IX to IXa.

Thrombin activates VIII to VIIIa.

IXa and VIIIa, (in the presence of platelet phospholopids and Ca++) activates X to Xa.

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11
Q

Common Pathway

A

Thrombin (IIa.) acts on V —> Va.

Xa and Va. (in the presence of Ca++ and platelet phospholipids) form Prothrombinase Complex

Prothrombinase complex splits prothrombin to thrombin

Thrombin forms fibrin from fibrinogen

Thrombin activates XIII to XIIIa.

XIIIa establishes covalent cross-links in fibrin

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12
Q

Actions of Thrombin in coagulation

A
  1. Activates Factor VIII in the intrinsic pathway (needed for Factor X activation)
  2. Activates Factor V in the common pathway
    (along with activated factor X cleaves (activates) factor II (prothrombin to thrombin))
  3. Activates Factor XIII in the common pathway
    (required for fibrin cross-linkages)
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13
Q

Fibrinogen

A

Plasma protein synthesized by the liver

Thrombin cleaves the fibrinopeptides of fibrinogen to form the fibrin monomer

fibrin monomers aggregate and are linked to each other via hydrogen bonds, forming the fibrin polymer (soft clot)

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14
Q

Vitamin K

A

Cofactor for gamma-carboxylase that forms mature clotting factors II, VII, IX, X as well as protein C and protein S

Gamma-carboxylase is inhibited by warfarin

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15
Q

Tertiary Hemostasis

A

Fibrinolysis

Dissolution of the fibrin clot

Inactive Plasminogen gets incorporated into the developing clot.

A tissue plasminogen activator, urokinase, or strptokinase activates plasminogen to plasmin which degrades fibrin.

  • Plasminogen activator inhibitor 1&2 inhibits activation to plasmin.
  • Antiplasmin inhibits plasmin activity.
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16
Q

Control of hemostasis

A

Normal endothelial cells are anti-thrombic

PGI2 and NO are released by healthy endothelial cells to prevent platelet aggregation

Coagulation automatically initiates fibrinolysis

17
Q

Antithrombin III

A

Anti-coagulation factor

Binds and inhibits Factor Xa.

Activated by Heparin

18
Q

Proteins C and S

A

Anti-coagulation factors

Act together to inhibit Factors Va. and VIIIa.

Protein C binds throbomodulin to thrombin. Protein S is a cofactor for this reaction

19
Q

Warfarin

A

Blocks epoxide reductase in liver preventing the regeneration of the active form of Vitamin K.

Inhibits the synthesis of the mature vitK dependent clotting factors II, VII, IX, X

20
Q

Streptokinase

A

Drug

thrombolytic agent; plasminogen activator; converts plasminogen to plasmin enabling the dissolution of clots

21
Q

Bleeding Time

A

Tests the time from initial injury to platelet plug formation.

Prolonged bleeding time is an indicator of

  • Low platelet count
  • vWF deficiency
  • Platelet receptor defects (GPIIb/IIIa)
22
Q

Clotting Time

A

Time to formation of stable fibrin

Prolonged clotting time is an indicator of defects in the coagulation pathway

Specific defects of the extrinsic/ intrinsic pathways are indicated by prothrombin time & Activated partial thromboplastin time (APTT) respectively

23
Q

Prothrombin time

A

or International normalized ratio (INR)

Test extrinsic and common pathway factors:
III - Tissue factor
VII

II - Prothrombin
I - Fibrinogen
V
X

24
Q

Activated Partial Thromboplastin Time

A

APTT

Tests intrinsic and Common Pathway Factors:
XII
XI
IX
VIII

V
X

25
Q

Hemophilia

A

Inherited coagulation disorder of the intrinsic pathway.

Increased clotting time and APTT

X-linked recessive

Type A- Factor VIII
Type B - Factor IX

Characterized by:
Tendency toward bruising
Spontaneous hemorrhage especially in joints

26
Q

Von Willebrand Disease

A

Defect in platelet plug formation

Instability of Factor VIII (carried and stabilized vWf)

Most common inherited bleeding disorder

Clinical features:
Presents with the clinical features similar to hemophiliaA
-Increased mucosal bleeding
-Epistaxis
-Increased post-operative bleeding
27
Q

Bernard-Soulier syndrome

A

Glycoprotein Ib deficiency

results in deficient platelet plug formation and increased bleeding time.

28
Q

Thrombasthenia of Glanzman and Naegeli

A

GpIIb/IIIa deficiency

results in deficient platelet plug formation and increased bleeding time

29
Q

Thrombocytopenia

A

Low platelet count

results in deficient platelet plug formation and increased bleeding time

2.b. Biochemistry II (17 decks)

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