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week 4- coagulation and hemostasis Flashcards

1
Q

blood within an animals vessels must be maintained in a _____ state

A

fluid

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2
Q

flowing blood does what:

A
  1. moves platelets along
  2. doesnt allow platelets to contact the endothelial cells
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3
Q

endothelial cells aid in _________

A

prevention of blood clot formation

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4
Q

what do endothelial cells secrete

A

-proteins that help prevent activation of platelets and proteins that participate in blood clot formation
-proteins that break down blood clots

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5
Q

what is hemostasis

A

process the body utilizes to stop blood from escaping damaged vessels

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6
Q

hemostasis relies on interactions between:

A

the blood vessel, platelets, and coagulation factors

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7
Q

defects in hemostatic process results in

A

hemorrhage

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8
Q

what is hemorrhage

A

the escape/loss of blood from the vascular space

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9
Q

what is physiologic hemostasis?

A

goes on constantly

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10
Q

thrombosis (pathologic hemostasis)

A

the same processes can occur in contexts where formation of blood clot is pathologic and detrimental to downstream tissue

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11
Q

when can thrombosis occur

A
  1. when factors promoting coagulation are inc.
  2. actions of inhibitors/fibrinolysis are dec
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12
Q

what is fibrinolysis

A

enzymatic breakdown of blood clots

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13
Q

when are blood clots pathologic

A

when they are not localized to a site of injury, form in an uncontrolled manner, or fail to resolve over time

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14
Q

2 types of hemostasis:

A

primary - provided by platelet
secondary- provided by soluble coagulation factors

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15
Q

major components of hemostasis

A
  • blood vessels
    -platelets
    -coagulation factors
    -inhibitors
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16
Q

general steps of hemostasis:

A
  1. vasoconstriction
  2. primary hemostasis
  3. secondary hemostasis
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17
Q

what is vasoconstriction the result from?

A

local sympathetic pain response

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18
Q

what is primary hemostasis

A

-platelet plug
-physically bridges the defect
-platelets also provide the surface for secondary hemostasis
-secrete cofactors to aid in secondary

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19
Q

what are platelets

A

anucleate cells that form when megakaryocytes in bone marrow break off pieces of their cytoplasm

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20
Q

what are platelets made of

A
  1. alpha granules (adhesion, GFs)
  2. dense granules (activators, co-factors, GFs)
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21
Q

main steps of platelet plug formation;

A

-Adhesion
-Shape change
-Secretion
-Aggregation
-Contraction

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22
Q

platelet plug formation detailed:

A
  1. injury causes the endothelial cell layer to be unattached and expose vWF and collagen
  2. platelets bind to vWF and hold them weakly via GPIb
  3. platelets also bind to collagen via GPVI that activates platelets and change its shape
  4. form platelet plug and stable adhesion
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23
Q

what is the blood vessel subendothelial matrix rich in

A

-vWF
-collagen

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24
Q

what are vWF produced by

A

produced mainly by endothelial cells

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25
Q

what are vWF stored in?

A

Weibel palade bodies in endothelial cells and platelets

26
Q

what does vWF do?

A

coats subendothelial collagen
-facilitates binding of PLT via GPIb
-stabilizes FVIII
-also binds GPIIb-IIIa

27
Q

what are some platelet activators

A
  1. collagen
  2. thrombin via secondary hemostasis
    -PAF
    -ADP
28
Q

glycoproteins vs integrins

A

-glycoproteins: weaker: tether
-integrins: stronger adhesion
-similar to leukocyte transmigration

29
Q

what receptor is the most important in platelet aggregation

A

fibrinogen receptor

30
Q

what happens when platelets stick to the underlying matrix ?

A
  1. conformation change in GPIIb-IIIa
  2. secrete mediators
  3. aggregate
  4. support activation of secondary hemostasis
31
Q

what forms bridges between platelets

A

fibrinogen

32
Q

what does activation of platelets cause

A

platelets to secrete granules that contain substances that activate additional platelets

33
Q

first platelet aggregation is

A

reversible

34
Q

once thrombin is generated, the platelet plug is

A

stabilized

35
Q

platelet plug is stabilized because thrombin:

A
  1. binds to receptors on platelets that cause the platelets cytoskeleton to contract
  2. thrombin leads to fibrin generation which glues platelets together
36
Q

secondary hemostasis overal goal:

A

to create the fibrin lattice via coagulation factors, zygomens, and co factors

37
Q

a series of proteolytic cleavages produces

A

active thrombin

38
Q

what does active thrombin do?

A

cleaves fibrinogen into fibrin

39
Q

what does fibrin do?

A

forms the meshwork that holds cells within the clot and gives the clot its tensile strength

40
Q

proteolytic cleavage can be achieved via

A
  1. extrinsic pathway
  2. intrinsic pathway
  3. common pathway
41
Q

which is the primary pathway that activates coagulation in vivo

A

extrinsic

42
Q

mechanism of extrinsic pathway:

A
  1. TF 3 exposed to factor VIIa
  2. TF-VIIa complex cleaves factor X to Xa
  3. starts common pathway
43
Q

TF/VIIa complex requires

A
  1. negatively charged phospholipids and Ca
44
Q

intrinsic pathway mechanism:

A
  1. Factor XII is exposed to thrombogenic surface
  2. activated to XIIa
  3. activates XI
  4. activates IX
  5. activates X with factor VIIIa
  6. common pathway
45
Q

what is the intrinsic pathway known as

A

amplification pathway

46
Q

what is the common pathway:

A

where intrinsic and extrinsic converge

47
Q

mechanism of common pathway

A
  1. X is activated to Xa via intrinsic and extrinsic pathway
  2. Xa cleaves prothrombin to thrombin
  3. thrombin cleaves fibrinogen to fibrin
48
Q

Main activators of the extrinsic pathway:

A

Tissue factors: via monocytes, endothelial cell damage, and VSMCS
TF VI+ Ca that activates factor X

49
Q

what are the hemophilia TFs?

A

VIII and IX

50
Q

lack of factor XII or XI causes

A

no bleeding

51
Q

lack of factor VIII or IX leads to

A

hemophiliacs
bleeding

52
Q

which factors are vit K dependent?

A

IX, X, VII, prothrombin (II)

53
Q

What does thrombin do?

A
  1. cleave fibrinogen
  2. activates FXIII
  3. activates FV and VIII
  4. enhances XI activation
  5. activates protein C
  6. activates platelets
54
Q

coagulation must be ______ to be effective

A

localized

55
Q

localization is provided by:

A
  1. TF expressing cells
  2. cell membranes rich in neg charged phospholipids (PS)
56
Q

cell based model of coagulation steps

A
  1. activation
  2. amplification
  3. propagation
57
Q

initiation of Cell based model of coagulation

A
  1. TF exposed to VIIa in blood and extrinsic pathway is activated
  2. generates a little bit of thrombin
    activity of Xa is restricted to cell surface
    -thrombin acts on platelets which cause their activation/aggregation
    -platelets can only interact in injury/endothelial cell compromise/firmly adhered
58
Q

how does amplification occur ?

A

-activated platelets flip their membranes and expose large amounts of PS which adds more fuel to coagulation
-thrombin activates more FV, FVIII, FXI
-whole process is amplified as thrombin diffuses from initial site and activates more nearby platelets and coag factors

59
Q

how is propagation occur?

A

-critical threshold of activated platelets and coag factors is reached
-large burst of thrombin occurs
-burst is sufficient for cleavage of fibrinogen and formation of fibrin meshwork

60
Q

thrombin generated during burst ___

A

can promote clot formation but is a signaling molecule that initiates feedback systems to dampen coagulation and activate fibrinolysis

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