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Post Midterm Biochem > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Stages of hemostasis

A
  1. vascular spasm/vasoconstriction 2. platelet plug formation/1° hemostasis
  2. blood coagulation/2° homeostasis 5. disolution of fibrin clot/3° homeostasis
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2
Q

Vascular spasm

A
  • trauma to vessel wall results in smooth muscle contraction caused by:
  • local myogenic spasm
  • endothelin and serotonin released from vessel wall
  • nervous reflexes

-transient effect

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3
Q

Platelet adhesion (general)

A
  • first step in plug formation
  • normally prevented by negative charges on platelets and endothelial cells
  • mediated by platelet receipts glycoprotein Ib/Ia
  • receptors bind to components of exposed subendothelial matrix (basement membrane) eg: collagen, vWF
  • platelets change shape and release granule contents (ADP, Ca2+) that activate other platelets
  • binding of ADP to recepor facilitates release of Ca2+ adn decreases cAMP
  • increased intracellular Ca2+ activates PLA2 nd leads to TXA2 release
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4
Q

Platelet adesion steps

A
  1. Plately GpIa binds collagen-development of pseudopods promote platelet-platelet interactions
  2. vWF bind GpIb
  3. binding exposed GPIIb/IIa for binding of fibrinogen
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5
Q

von Willebran factor

A
  • bridge between GpIb and collagen fibbers
  • complexes with factor VIII
  • defect associated with platelet plug formation defect (1° homeostasis) and coagulation devect (low factor VIII, 2)
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6
Q

Platlet Aggregation

A
  • mediated by fibrinogen
  • binds to GpIIb/IIIa on adjacent platlets
  • GpIIb/IIIa defect: thrombastenia of Glanzman and Naegeli
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7
Q

Lab tests for platelet plug formation

A
  • bleeding time up–>defect leads to this
  • vWF down
  • platelet # down
  • GpIb down
  • GpIIb/IIIa down
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8
Q

Extrinsic Clotting Pathway

A

1e. Tissue injury—>release tissue factor (factor III)
2e. Tissue factor III: Factor ViII—>VIIa
3e. Factors III & VIIa & Ca2+ (IV): X—>Xa

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9
Q

Intrinsic Pathway

A

1i. Rough endothelial surface and exposure of collagen: XII–>XIIa
2i. XIIa: XI—>XIa; (also activates kallikrein for what its worth)
3i. XIa: IX—>IXa
4i. Thrombin (IIa): VIII—>VIIIa
5i. IXa, VIIIa, platelet phospholipids and Ca2+: X–>Xa

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10
Q

Common Pathway

A

1c. Thrombin (IIa): V–>Va
2c. Xa and Va and Ca2 form prothrombinase complex
3c. Prothrombinase complex: II–>IIa (prothrombin to thrombin)
4c. Thrombin (Ca2+): Fibrinogen (I)—>Fibrin (Ia) (soft clot as monomers aggregate linked by H-bonds)
5c. Thrombin (Ca2+): XIII—->XIIIa
6c. XIIIa: Crosslinks fibrin monomners (hard clot)

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11
Q

XIIIa

A
  • crosslinks fibrin to form hard clot

- highly specific transglutaminase

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12
Q

Actions of thrombin

A
  • Convert fibrinogen to fibrin
  • Activate XIII to XIIIa which crosslinks fibrin
  • Activation of factor V
  • Activation of factor VIII
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13
Q

Extrinic pathway uses;

A

III, VII (injury)

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14
Q

Intrinsic pathway uses:

A

XII, XI, IX, VII (pathological processeses like atherosclerosis)

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15
Q

Components of prothrombinase comples

A

Xa, Va, Phospholipid, Ca2+

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16
Q

Components reqiring phospholipids

A

prothombinase complex, intrinsic tenase complex

17
Q

Test for extrinsic coagulation pathway defect:

A
  • Increased prothrombin time (INR) (PT) (also in common pathway))
  • sensitive indicator of vitamin K deficiency (Factor VII very senstive to this)
18
Q

Test for intrinsic coagulation pathway defect:

A

Increased APTT (partial thromboblastin time)

19
Q

γ-Carboxylase

A
  • performs vitamin K depended carboxylation of Prothrombin (Factor II), VII, IX, X, and Proteins C, S, and Z
  • form mature clotting factors capable of activation, contain γ-carboxyglutamate
  • γ-carboxylation facilitates Ca2+ binding by introducing 2 adjacent negative charges to coordinate calcium ions and allows complex to bind to phospholipids on platelete membrane
  • factor VII (which is extrinsic) is most sensitive to Vit K deficiency
  • inibited by warfarin
20
Q

Warfarin

A

Inhibits epoxide reductase in liver, necessary for the regeneration of the active form of Vitamin K

(inhibits γ-Carboxylase, preventing production of mature Prothrombin (Factor II), VII, IX, X and Proteins C, S, and Z (but those are more anticoagulants))

21
Q

Fibrinolysis

A

Inactive plasminogen incorporated into developing clot

  • activated by tissue plasminogen activator, urokinase, or streptokinase to plasmin
  • can be inibited by plasminogen activator inhibitor 1 & 2
  • α2-antiplasmin inhibits Plasmin
  • fibrin broken down to fibrin degredation products/D-dimers–>elevated in DVT, measured to estimated rate of fibrinolysis and follow up on thrombosis patients
22
Q

Contorl of hemostasis

A
  • normal endothelia are anti-throbotic
  • put out PGI2 and NO that prevent platelet aggregation
  • PGI2-increases cAMP in platelets and hihibits platelet activation–>thromboxane antagonist
  • coagulation automatically initiates fibrinolysis
23
Q

Antithrombin III

A
  • bind and inhibits factor Xa and IIa (thrombin)
  • anticoagulent
  • activated by Heparin
24
Q

Heparin

A

Activates antithrombin III (bind and inhibits factor Xa and IIa (thrombin))

25
Q

Protein C and S

A
  • require vit K and γ-Carboxylase
  • inactivate cofactors Va and VIIIa
  • Protein C is activated by binding of thombomodulin to thrombin
  • S is a cofactor for C
26
Q

Streptokinase

A

Thrombolytic agent, activates plasminogen to plasmin to break down clots

27
Q

Hemophilia A

A
  • Inherited Factor VIII deficiency
  • X linked
  • Intrinsic pathway (increasted clotting time and increased APTT)
  • similar to hemophilia B
28
Q

Hemophilia B

A
  • Inherited Factor IX deficiency
  • X linked
  • Intrinsic pathway (increasted clotting time and increased APTT)
  • similar to hemophilia A
29
Q

Characteristic Hemophila lab findings/symptoms/signs

A
  • easy bruising
  • masvie hemorrhage after trauma and surgical procedure
  • spontaneous hemorrhages, particularly in the joints–>hemarthrosis
  • Bleeding time=normal (platelet plug)
  • Platelet count normal
  • clotting time increased (defect in intrinsic pathway)
  • PT/INR-normal (tests extrinsic and common)
  • APTT-increased
  • Assay indvidual factors to distiguish b/w the two
30
Q

Von Willebrand Disease

A
  • Deficiecny of vWF
  • most common inherited bleeidng disorder
  • defect in platelet plug formation
  • instability of factor VII (may lead to increased APTT)
  • clinical features similar to hemophila A
  • increased mucosal bleeding
  • epistaxis
  • post op bleeding
  • bleeding time prolonged
  • platelt count-normal
  • APTT-prolonged (factor VII levels low to normal)
  • vWF levels low
31
Q

Platelet defects

A
  • quatitative–>low platelet count and increased bleeding time–>thrombocytopenia
  • qualitative–>normal platelet count and increased bleeding time: Bernard soulier syndrome (GbIb defect) or Thrombastenia of Glanzman and Naegeli (defect of GpIIb/IIIa)
32
Q

Bernard soulier syndrome

A

normal platelet count and increased bleeding time: GbIb defect

33
Q

Thrombastenia of Glanzman and Naegeli

A

normal platelet count and increased bleeding time: (defect of GpIIb/IIIa)

Post Midterm Biochem (16 decks)

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