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General Pathology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Hemostasis

A

Arrest of bleeding. A normal physiological response to localized vascular injury

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2
Q

What are the factors of hemostasis

A

-Blood vessels
-Platelets
-Coagulation
-Fibrinolytic and thrombolytic factors (Regulating factors)

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3
Q

Anti-coagulant factos made by endothelium

A

-Prostacyclin
-NO
-Thrombomodulin
-Protein S

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4
Q

Prostacyclin

A

Ehance relaxation and inhibits platelet adhesions and activation

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5
Q

NO

A

Maintains vascular relaxation and inhibits platelet activation. Participates with Protein C and antithrombin to suppress thrombin production

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6
Q

Thrombomodulin

A

Binds tothrombin and activates protein C

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7
Q

Protein S

A

Cofactor in Protein C pathway and independently inhibits activation of factors VIII and X

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8
Q

Endothelium in hemostasis

A

Damage to endothelium produces pro clotting properties like Tissue factor
-Exposure of underlying collagen and other components activates coagulation and platelet adhesion

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9
Q

Pro clooting endothelial mediators

A

-Tissue Factor (Factor III)
-Von willebrand Factor
-Plasminogen Activator Inhibitor-1

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10
Q

Platelets

A

Come from bone marrow
-Membrane bound cytoplasmic fragments
-Get pinched off megakaryocytes
-Bind to damaged endothelium or subendothelium to form hemostatic plug to prevent blood loss (primary hemostasis)

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11
Q

Main regulator of platelet production

A

Thrombopoietin

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12
Q

Primary Hemostasis

A

Primary vascular and platelet response.
-Best for minor injuries
-Vascular contraction and endothelial activation of pro and anticlotting activity
-Platelet plug formation

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13
Q

Vascular changes in primary hemostasis

A

Contraction of muscle layers to prevent blood loss
-Neurogenic stimuli
-Endothelial and platelet products
Endothelial activation
-Pro and anti-coagulation to get clotting but not too much

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14
Q

Platelets in primary hemostasis

A

Sequential activities
-Adhesion
-Aggregation
-Secretion
-Contraction

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15
Q

Platelet adhesion

A

-Coat to subendothelial collagen
-Von Willebrand factor accelerates adhesion
-GPlb binds to vWF on damaged surface

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16
Q

Platelet aggregation

A

Build up of plaque allows for conformational change which induces GPIIb-IIIa binds fibrinogen forms bridges between platelets

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17
Q

Platelet secretion

A

Induced by adhesion and aggregation start to release granules. Things like Factor V, fibrinogen, fibronectin, growth factors, and platelet factors to enhance coagulation and start healing. Most are preformed

18
Q

Why is calcium an important co factor

A

Want a lot of calcium at the site of wound so released by platelets

19
Q

Thromboxane and platelets

A

Part of COX pathway enhances platelet aggregation and vasoconstriction. TBX synthase is in higher concentrations in platelets

20
Q

Platelet Factor 3

A

Substrates for coagulation to happen

21
Q

Contraction of platelets

A

Want to minimize size in vessel so blood can flow through
-Use actin and mysoin
-Get concurrent fibrinolysis to minimize size and initiate repair

22
Q

Contraction of platelets

A

Want to minimize size in vessel so blood can flow through
-Use actin and myosin
-Get concurrent fibrinolysis to minimize size and initiate repair

23
Q

Enzymatic coagulation

A

All are proenzymes. Once activated add an a at the end. Produced mainly by hepatocytes

24
Q

Non-enzymatic coagulation factors

A

Non enzymatic participants for enzymatic coagulation reaction. Calcium is the mediator of the binding of these factors to the phospholipids of the platelets

25
Q

Types of coagulation models

A

-Classical coagulation
-Integrated model of coagulation

26
Q

Intrinsic pathway

A

Activation of Factor XII->XIIa which initiates the cascade leading to factor X
-Also get contact factors (XII, HMWK, and PK) these are involved in binding to activating surfaces

27
Q

Intrinsic pathway role

A

Usually secondary to extrinsic and amplify thrombin when everything is formed and extrinsic gets going. Can have deficiencies here and not a huge issue

28
Q

Extrinsic pathway

A

Activated by the release of Tissue Factor (Factor III) by damaged endothelial surfaces-> get activation of Factor X
-Works most invivo

29
Q

Common pathway

A

Starts with Factor X and gets activated-> Get conversion of prothrombin ( factor II) into thrombin (IIa) by prothrombinase complex-Thrombin cleaves fibrinogen to fibrin monomers and form polymers
-Facter XIII stabilizes with cross linking of the fibrin polymers

30
Q

Prothrombinase complex

A

Factor Xa and Va and calcium on phospholipid surface

31
Q

Integrated model

A

Many points of interaction between each of the classical pathways

32
Q

Key points of integration

A

-TF-VIIa activates X and IX (intrinisic)
-Thrombin-initiated activation of factors V, VIII, and XI amplifies intrinsic and common pathways
-Activation of extrinsic Factor VII by XIIa and IXa and kallikrein

33
Q

Regulation of hemostasis

A

Need balance between pro and anti coagulation
-Deplete
-Clear
-inactivate activated coagulation factors

34
Q

Antithrombin

A

major circulating anticoagulant
-Degrades all activated coagulation factors except for Factor VIIa

35
Q

Protein C

A

Vitamin K dependent
-Pro-fibrinolytic agent
-Activated by thrombin
-Complexes with Protein S on phospholipid surfaces and inactivates Factors Va and VIIa

36
Q

Fibrinolysis

A

Dissolution of clots to maintain homeostasis
-Plasmin (from plasminogen) is important to break the fibrin monomer
-Needs to be timed not too slow or too fast

37
Q

FDPS

A

Fibrin degradation products produce anti-thrombotic and pro hemorrhagic
-Compete with fibrinogen for binding sites
-Impair platelet function
-Used as a landmark for coagulopathies

38
Q

Plasminogen activator inhibitor-

A

Inhibits plasminogen activators so you don’t get plasmin

39
Q

Antiplasmins

A

-Prevent excessive plasmin activity
-Alpha 1 and 2

40
Q

C1 inhibitor

A

Modulates complement, coagulation, kinin, and fibrinolytic pathways

General Pathology (30 decks)

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