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General Pathology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What is Hemostasis?

A
  • The arrest of bleeding
    • Hemo = blood
    • Stasis = Halt, slow
  • A normal physiological response to localized vascular injury
  • It is a complex process
  • A balanced interaction between:
    • Blood vessels
    • Platelets
    • Coagulation factors
    • Tibrinolytic and thrombolytic factors
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2
Q

What is the goal of hemostasis?

A

Rapid return to norml blood flow and fluidity following vascular injury

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3
Q

What is the norml functino of blood vessels?

A
  • Provide unimpeded movement of blood to areas of need
    • Neur-chemical regulation of flow
  • Endothelium is a critical blood vessel component influencing vascular homeostasis
    • Multifunctional and complex:
      • Forms the vascular lining
      • Secretes mediators
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4
Q

What role does normal endothelium play in homeostasis?

A
  • Normal endothelium generally induces vascular relaxation and anti-clotting properties
    • Nitric oxide
    • Prostacyclin
    • Alpha-2-macroglobulin
    • Thrombomodulin
    • Protein S
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5
Q

What are the Anti-clotting characteritics and what do they do?

A
  • Prostacyclin
    • Enhanves vascular relaxation nd inhibis platelet adhesion and activation
  • Nitric oxide
    • Maintains vascular relaxation and inhibits platelet activation
    • Participates with Protein C and antithrombin to suppress thrombin production
  • Thrombomodulin
    • Binds thrombin to intitiate Protein C activation
  • Protein S
    • ​Cofactor in Protein C pathoway and independently inhibits activation of Factors VIII and X
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6
Q

What role does Damaged endothelium play in hemostasis

A
  • Damaged endothelium has predominately pro-clotting properties
    • Release of Tissue Factor from activted endothelium and subendothelial tissues
    • Exposure of underlying collagen and other subendothelil conponents provide sites for platelet adhesion
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7
Q

What are the Pro–clotting characteristics and their function?

A
  • Tissue Factor:
    • Released following endothelial injury, possibly by activated endothelium
  • Von willebrand Factor:
    • Forms bridges for platelet adhesion and aggresion
  • Plasminogen Activator Inhibitor-1:
    • Inhibits fibrinolysis
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8
Q

What is the normal function of platelets

A
  • Platelets
    • membrane-bound cytoplasmic fragments derived from megakaryocytes in the bone marrow
      • Trhombopoietin is the main regulator of production
      • Colony stimulating factors: IL-3, IL-6, IL-11 also participate
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9
Q

What is the platelets role in Primary Hemostasis?

A
  • Plaetlets are the principle mediators of primary hemostasis
  • Platelets bind to damaged endothelium or subendothelium to form a primary hemostatic platelet plug to Prevent blood loss
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10
Q

What is Primary Hemostasis?

A
  • The primary vascular and platelet response to vascular injury
    • Vascular contraction
    • Endothelial activation
      • Pro- and anti-clotting activity
    • Platelet plug formation
  • Most effective for minor vascular injury
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11
Q

What vascular changes occur during Primary Hemostais?

A
  • Contraction of mucsle layers of the blood vessle cause transient vasoconstriction
    • Neurogenic stimuli
    • Endotherlial and platelt products
  • Endothelial activation
    • Pro-coagulation to limit bleeding
    • Anti-coagulation to limit clotting
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12
Q

What happens with platelets during primary hemostasis?

A
  • Sequential activities in primary hemostasis
    1. Adhesion
    2. Aggregation​​
    3. Secretion
    4. Contraction
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13
Q

What happens during Adhesion of Platelets in Primary Hemostasis?

A
  • Platelets adhere to subendothelial substances at sites of vascular injury
  • Coating of subendothelial collagen by von willebrand factor acceleratesadhesion by a receptor-mediated process
    • Platelet GPIb binds to vWF on damaged surface
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14
Q

What happens to platelets during Aggregation in Primary Hemostasis

A
  • Platelets stick to each other to build up an adequate platelet mass for primary hemostasis
  • Conformational change induces expression of GPIIb-IIIa
    • Fibrinogen foms bridges between platelets
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15
Q

What happens to platelets during secretion in primary hemostasis?

A
  • Conformational change indued by adhesion/aggregtion results in granule release:
    • Platelet granules contain numerous preformed substances
  • Adhesions stimulates production of platelet membrane-associated substances involved in clotting
    • Thromboxane
    • Platelet Factor 3 (anionic membrane phospholipids including phosphatidylserine)
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16
Q

What is the content of a Platelet a-granule ?

A
  • Factor V
  • Fibrinogen
  • Thormbospondin
  • Fibronectin
  • Transforming growth factor-beta (TGF-beta)
  • Epidermal growth factor
  • Albuminn
  • B-Thromboglobulin
  • Platelet Factor 4
  • Platelet-derived growth factor (PDGF)
  • Endothelial cell growth factor (ECGF)
17
Q

What is the content of a Platelet Dense granule?

A
  • ATP
  • GTP
  • Calcium
  • Serotonin
  • ADP
  • GDP
  • Magnesium
  • 5’ hydroxytryptamine
18
Q

What happens to platelets during contraction in Primary Hemostasis?

A
  • Contraction minimizes the size of teh primary hemostatic plug
    • Platelet actin and myosin and interplatelet fibrinogen bridges are teh major mediators
  • This occurs during the resolution stages of primary hemostasis
    • Lysis of fibrin formed by secondary hemostasis (fibrinolysis) will occur concurrently
    • Contraction and fibrinolysis minimize the size of the platelet/fibrin plug and initiates vascular repair
19
Q

What is Coagulation?

A
  • A highly regulated cascde of reactions that form a variety of products involved in hemostasis
  • Participants include:
    • Enxymatic coagulation factors
    • Non-enzymtic co-factors
  • Described by severl different models:
    • Classical Coagulation pathways
    • Integrated model of coagulation
20
Q

What are the Enzymatic Coagulation Factors?

A
  • Proenzymes
    • Plasma proteins that circulate in inactive forms
      • Produced mainly in hepatocytes
    • Upon activation, they gin teh suffix “a”
      • Exception: Prekallikrein → Kallikrein
    • Include Factors II, VII, IX, X, XI, XII, XIII, Prekallikrein
21
Q

What are teh Non-enzymatic Coagulation Factors?

A
  • Cofactors
    • Non-enzymatic participants that are necessary for enxymatic coagulation reations
  • Cofacotrs include Factors I, III, V, VIII, High Molecular Weight Kininogen, Ca+2, and phospholipids
    • Ionized free calcium is required
22
Q

What are the Classical Coagulation pathways?

A
  • Extrinsic pathway
  • Intrinsic pathway
  • Common pathway
23
Q

What is the Coagulation Intrinsic Pathway?

A
  • Activation of Factor XII (Hageman Factor) is the key stp
    • Factor XIIa initiates the cascade leading to activation of Factor X
    • Factor XII initiates some important non-coagulant pathways
  • Contact factors (Factor XII, HMWK, and PK) initiate te pathway by binding negatively charged surfaces, like collagen
    • HMWK circulates in association with PK and Factor XI
      • Binding of HMWK brings reactants into close association on the activating surface
      • XIIa facilitates binding of HMWK to the activating surface
  • Probbly initiated secondary to extrinsic and common pathway activation
    • Propagates and amplifies thrombin formation initiated by the extrinsic pathway
  • Likely plays secondary role in vivo
    • individuals with deficiencies of Factor XII, HMWK, and PK don’t have bleeding tendencies
24
Q

What is the Coagulation Extrinsic Pathway?

A
  • Activated by the release of Tissue Factor (TF, Factor III) by damaged endothelial surfaces
    • “Tissue Factor Pathway”
  • Factor III reacts with Factor VII to cause the activation of Factor X
25
Q

What is the Coagulation Common Pathway?

A
  • This pathway is initiated by activated Factor X
    • Factor Xa can be generated by both intrinsic and extrinsic pathways
  • Major step in the pathway is the conversion of protrhombin (Factr II) to thrombin (Factor IIa)
    • Prothrobin (Factor II) is converted by the prothombinase complex
      • Complex consists of Factors Xa and Va, and cacium on a phospholipid surface
  • Fibrin monomers cleaved by trhombin from fibrinogen self-polymerize
    • Factor XIII helps to cross-link and stabilize the fibrin polymers
26
Q

What is the Integrated Model of Coagulation?

A
  • Many points of interaction between each of the classical pathways
  • A web-like integrated model may more appropriately demonstrate the integration and amplifcation that occur in vivo
  • Key Points:
    • TF-VIIa activates X (common) and IX (intrinsic)
    • Thrombin-initiated activation of Factors V, VIII, and XI amplifies intrinsic and common pathways
    • Activation of extrinsic Factor VII by Factors XIIa and IXa and kallikrein
27
Q

How is Hemostasis regulated?

A
  • Hemostasis is a fine balance between pro- and anti- clotting mechanisms
  • Major function of regulatory pathways is to confine hemostasis to only those locations it is needed
  • Factors that regulate hemostasis include:
    • Depletion of activted coagulation factors
    • Clearance of activaed coagulation factors
      • most are complexed by inhibitors and then cleared from teh circulation by hepatocytes orteh mononuclear/phagocyte system
    • Inactivation of activated coagulation factors or products
28
Q

What are the Coagulation inactivators/inhibitors?

A
  • Antithrombin (Antithrombin III)
  • Protein S: Protein C: Thrombomodulin
  • Tissue Factor Pathway Inhibitor
29
Q

What is Antithrombin?

A
  • The MAJOR circulating anti-coagulant
    • Antithrombin degrades all activated cogulation factors except fr Factor VIIa
    • It accounts for about 80% of the thrombin-activity of plasma
30
Q

What is Protein C?

A
  • A Vitamin K-dependent anti-coagulant and pro-fibrinolytic agent
    • Protein C is actvated by thrombin
    • Activated Protein C complexes with Protein S on phospholipid surfaces and inactivates factors Va and VIIa
31
Q

What is Fibrinolysis?

A
  • Dissolution of clots is important to maintain flow and fluidity of blood through the damaged area
    • It is ctivated simultaneously with coagulation
  • Plasmin is the major mediator of fibrinolysis
  • Must be well balanced and timed:
    • Too fast/excessive - clot may degrade before vascular repair occurs
    • Too slow/minimal - clot persistened may lead to permanent vessel alteration and reduce blood flow
32
Q

What are Fibrin Degradation Products?

A
  • Produce an anti-thrombotic, pro-hemorrhagic state
    • Major fragments include X, D, Y, and E
    • They impair platelet function
    • They compete with fibrinogen for binding sites on thrombin and platelets
    • They interfere with fibrin polymerization
    • They increase during coagulation, DIC, inflammation, hemorrhage, or drecreased clearance dur to lier or kidney disease
33
Q

What are the Fibrinolytic inactivators/inhibitors?

A
  • Plaminogen activator inhibitor - 1
  • Antiplamins
  • C1 inhibitor
34
Q

What does plaminogen activator inhibitor -1 do

A
  • inhibits tissue plaminogen activator and urokinaseto prevent conversion of plaminogen to plasmin
35
Q

What do antiplamins do?

A
  • Function cooperatively to prevent excessive plamin activity
    • a - 2 - antiplamin is the first to bind and neutralize plamsin
      • rapid inhibition of circulating plamin so fibrinolysis remains localized
    • a - 2- macrolobulin binds excess plasmin after a-2-antiplasmin becoes saturated
    • a-1-antitrypsin binds plasmin after a-2-macroglobulin becomes saturated
36
Q

What is C1 inhibitor

A
  • Modulated the complement, coagulatin, kinin, and fibrinolytic pathways
  • Inhibits:
    • Activation of C1
    • Cleavage of C2 and C4
    • Coagulation factors XIIa and XIa
    • Activation of plaminogen
    • Activation of kallikrein
37
Q

What is the endpoint of hemostasis?

A
  • When the damaged vessel is repared and the platelet/fibrin clot contracts and is lysed

General Pathology (34 decks)

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