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IHL Exam 1 Me > Intrinsic and Extrinsic Coagulation Pathways (choudhury) > Flashcards

Intrinsic and Extrinsic Coagulation Pathways (choudhury) Flashcards

1
Q

hemostasis

A

regulated process that maintains blood in a fluid state

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2
Q

thrombosis

A

pathological counterpart of hemostasis, results in clot within vessels

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3
Q

5 major events in physiological clotting

A

1) Initial vascular injury
2) Primary hemostasis
3) Secondary hemostasis
4) Antithrombosis
5) Fibrinolysis

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4
Q

What properties do endothelial cells exhibit normally

A

Antiplatelet
Anticoagulant
fibrinolytic

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5
Q

Antiplatelet properties of endothelial cells

A

NO
PGI2
Adenosine Diphosphatase

make sure platelets don’t stick

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6
Q

Anticoagulant properties of endothelial cells

A

Heparin Sulfate
Thrombomodulin
Protein S
TFPI

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7
Q

Fibrinolytic properties of endothelial cells

A

t-PA
this is a protease secreted by endothelium that cleaves plasminogen to form plasmin

plasmin then cleaves fibrin into FDP, essentially degrading thrombi

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8
Q

Hemostasis and thrombosis involves

A

Endothelium (vascular wall)
Platelets
Coagulation cascade
Fibrinolysis

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9
Q

NO

A 
vasodilator
antiplatelet aggregator (platelets don't stick to endothelial membrane)
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10
Q

Layers of normal endothelium

A 
Innermost
Endothelial cells
ECM
Smooth muscle layer
outer connective tissue layer
outermost
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11
Q

PGI2

A

Prostacyclin
anti platelet component of endothelial cells

vasodilator in lungs/blood vessels

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12
Q

ADP phosphatase

A

degrades ADP and inhibit platelet adhesion and aggregation

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13
Q

Heparin Sulphate (HS)

A

Anticoagulant of endothelial cells

HS hooks onto antithrombin III (AT III) and activated AT III

AT III inactivates Thrombin, Factor 10, Factor 9a

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14
Q

Thrombomodulin (TM)

A

Anticoagulant property

binds to thrombin and converts it form procoagulant into anticoagulant via thrombin’s ability to activate protein C

Protein C activated inhibits factors 5 and 8

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15
Q

What does Protein C require

A

Cofactor protein S

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16
Q

Protein S

A

Cofactor for Protein C

necessary for anticoagluant effects of protein C

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17
Q

TFPI

A

Tissue factor pathway inhibitor
anticoagulant property of endothelial

directly inhibits factor 7 and 10

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18
Q

when is a platelet plug formed

A

primary homeostasis

this is a temporary patch formed at endothelial injury site

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19
Q

what occurs during homeostasis

A

the initial platelet plug is enlarged and stabilized by adding a structural matrix of fibrin (coagulation) to form a coagulum or “clot”

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20
Q

Antithrombosis

A

Once a stable and effective clot forms then additional clot formation has to cease

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21
Q

Fibrinolysis

A

last major step in hemostasis to remove clot and restore normal blood flow through the vessel

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22
Q

phospholipid platform

A

Formed during secondary hemostasis

activated platelets undergo conformation change exposing a phospholipid-rich portion of the platelet surface cell membrane

this platform dramatically accelerates fibrin production by bringing in close proximity the enzymatic rxns of the intrinsic/common pathways

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22
Q

Thrombosis

A

results from impairment in ability to limit/terminate clot propagation

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22
Q

Initial vascular injury (what happens)

A

Transient vasconstriction and vasospasm

ECM is exposed

vWF produced by endothelial cells, acts as vital link “glue” for platelet adherence and activation

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22
Q

fibrinogen (factor 1)

A

plasma protein produced by the liver

“bridges” between platelets
allows for platelet aggregation

converted to fibrin by thrombin

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22
Q

calcium

A

without calcium would not be able to form any coagulation

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22
Q

what synthesizes vWF factor

A

endothelial cells

22
Q

Endothelin

A

vasoconstrictor released by injured endothelium

22
Q

Platelet process in primary homeostasis

A

Leads to formation of initial platelet hemostatic plug

1) Platelet adhesion
2) Shape change
3) Granule Release
4) Recruitment
5) Aggregation (plug)

22
Q

How does the body keep the platelet plug in the specific site of injury

A

uninjured endothelium surrounding the injury site continues to release NO and Prostacyclin which inhibit platelet aggregation

22
Q

what synthesizes vWF factor

A

endothelial cells

22
Q

Thrombin (factor 2)

A

Most important coagulation factor

Converts fibrinogen (soluble) into fibrin (insoluble gel)

also activates fibrin-stabilizing factor (factor XIII) which in the presence of Ca2+ stabilizes fibrin polymer through covalent bonding of fibrin monomers

22
Q

Fibrin (factor 1a)

A

Insoluble form, hold platelets together

“cement”
forms meshlike network at the site of vascular damage

22
Q

How do platelets bind to vWF

A

via glycoprotein Ib (GpIb) receptors

22
Q

TXA2

A

released by platelets

vasoconstrictor and platelet aggregator

22
Q

Delta Granules release….

A

SAC

Serotonin- vasoconstrictor
ADP-platelet activator and aggregator
Calcium- activate coagulation factors

22
Q

Alpha granules release….

A

CF- coagulating factors
Fibrinogen
PDGF- more platelets come/recruited

22
Q

Initial vascular injury (what happens)

A

Transient vasconstriction and vasospasm

ECM is exposed

vWF produced by endothelial cells, acts as vital link “glue” for platelet adherence and activation

22
Q

Secondary hemostasis

A

Clot propagation and stabilization by coagulation (fibrin production)

Tissue factor released by platelets activates coagulation cascade
This results in fibrin formation “cementing” that is put on top of primary plug
Forms the secondary hemostatic plug (5-10 min)

Also forms Phospholipid platform

22
Q

Fibrin

A

Insoluble form, hold platelets together

“cement”

22
Q

phospholipid platform

A

Formed during secondary hemostasis

activated platelets undergo conformation change exposing a phospholipid-rich portion of the platelet surface cell membrane

this platform dramatically accelerates fibrin production by bringing in close proximity the enzymatic rxns of the intrinsic/common pathways

22
Q

fibrinogen

A

“bridges” between platelets
allows for platelet aggregation

made into fibrin by coagulation cascade

22
Q

Antithrombosis

A

Limitation and cessation of clot production

22
Q

Coagulation cascade

A

Part of secondary hemostasis

amplifying series of enzymatic conversions

each step proteolytically cleaves and inactive prenzyme into activated enzyme–> leading to thrombin formation

process where soluble fibrinogen is converted to fibrin (insoluble)

22
Q

Thrombin

A

Most important coagulation factor

Converts fibrinogen (soluble) into fibrin (insoluble gel)

22
Q

XIIIa (8)

A

Stabilizes and cross-links fibrin fibrin polymers

22
Q

Intrinsic and extrinsic pathways converge on the activation of ….

A

factor X (10)

22
Q

calcium

A

without calcium would not be able to form any coagulation

22
Q

what does tissue factor activate

A

factor 7

22
Q

what does factor seven activate

A

factor 9 as well as factor 10

22
Q

Christmas factor

A

Factor 9

in the intrinsic pathway
activated by factor 11 in the presence of Ca2+

22
Q

Anti-hemophlic factor

A

Factor 8 (intrinsic)

activated by Christmas factor (9)
activates stuart factor (10)

22
Q

Extrinsic pathway

A

Tissue factor–> factor 7—> factor 10

22
Q

Stuart factor

A 
Factor 10 (intrinsic)
activated by antihemophilic factor- 8
22
Q

Hageman factor

A

Factor 12 (intrinsic)
activated by exposed collagen
activates Factor 11

22
Q

Factor 11

A

intrinsic

activates Christmas factor (9)

22
Q

Accelerin (Factor V)

A

with factor X and the presence of calcium this helps form prothrombin

22
Q

Prothrombinase

A

converts Prothrombin to thrombin

22
Q

Thrombin in hemostasis

A

makes fibrin by cleaving fibrinogen

activates XIII with Ca2+

induces platelet aggregation and TxA2 production and activates EC’s to express adhesion molecules, t-PA, NO, PGI2 and PDGF

activates leukocytes

VERY IMPORTANT

22
Q

Plasminogen

A

Circulating non-enzymatic protein converted by t-PA into plasmin

22
Q

Plasmin

A

Responsible for the enzymatic degradation of fibrin

22
Q

t-PA

A

this is a protease secreted by endothelium that cleaves plasminogen to form plasmin

it’s activity is increased 500-fold by fibrin

22
Q

u-PA

A

secreted by kidneys

circulates in plasma and converts plasminogen into plasmin

22
Q

thrombus

A

produced if a clot size becomes progressively larger than needed

can cause:
vascular obstruction (altered blood flow)
framgentation and movement in direction of flow (embolism)

22
Q

Thrombosis

A

results from impairment in ability to limit/terminate clot propagation

22
Q

what activates the intrinsic pathway

A

when hageman factor (XII) is activated by contact with exposed collagen at a damaged vessel surface or by contact with a foreign surface

brings about clotting within damaged vessels and clotting of blood samples in test tubes

22
Q

how is the extrinsic pathway activated

A

initiated when factor X is activated by tissue factor released from damaged tissue

the extrinsic pathway causes clotting of blood that escapes from blood vessels into the surrounding tissue

IHL Exam 1 Me (11 decks)

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