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

Intrinsic and Extrinsic Coagulation Pathways (choudhury) Flashcards

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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
fibrinogen (factor 1)
plasma protein produced by the liver "bridges" between platelets allows for platelet aggregation converted to fibrin by thrombin
22
calcium
without calcium would not be able to form any coagulation
22
what synthesizes vWF factor
endothelial cells
22
Endothelin
vasoconstrictor released by injured endothelium
22
Platelet process in primary homeostasis
Leads to formation of initial platelet hemostatic plug 1) Platelet adhesion 2) Shape change 3) Granule Release 4) Recruitment 5) Aggregation (plug)
22
How does the body keep the platelet plug in the specific site of injury
uninjured endothelium surrounding the injury site continues to release NO and Prostacyclin which inhibit platelet aggregation
22
what synthesizes vWF factor
endothelial cells
22
Thrombin (factor 2)
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
Fibrin (factor 1a)
Insoluble form, hold platelets together "cement" forms meshlike network at the site of vascular damage
22
How do platelets bind to vWF
via glycoprotein Ib (GpIb) receptors
22
TXA2
released by platelets vasoconstrictor and platelet aggregator
22
Delta Granules release....
SAC Serotonin- vasoconstrictor ADP-platelet activator and aggregator Calcium- activate coagulation factors
22
Alpha granules release....
CF- coagulating factors Fibrinogen PDGF- more platelets come/recruited
22
Initial vascular injury (what happens)
Transient vasconstriction and vasospasm ECM is exposed vWF produced by endothelial cells, acts as vital link "glue" for platelet adherence and activation
22
Secondary hemostasis
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
Fibrin
Insoluble form, hold platelets together "cement"
22
phospholipid platform
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
fibrinogen
"bridges" between platelets allows for platelet aggregation made into fibrin by coagulation cascade
22
Antithrombosis
Limitation and cessation of clot production
22
Coagulation cascade
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
Thrombin
Most important coagulation factor Converts fibrinogen (soluble) into fibrin (insoluble gel)
22
XIIIa (8)
Stabilizes and cross-links fibrin fibrin polymers
22
Intrinsic and extrinsic pathways converge on the activation of ....
factor X (10)
22
calcium
without calcium would not be able to form any coagulation
22
what does tissue factor activate
factor 7
22
what does factor seven activate
factor 9 as well as factor 10
22
Christmas factor
Factor 9 in the intrinsic pathway activated by factor 11 in the presence of Ca2+
22
Anti-hemophlic factor
Factor 8 (intrinsic) activated by Christmas factor (9) activates stuart factor (10)
22
Extrinsic pathway
Tissue factor--> factor 7---> factor 10
22
Stuart factor
``` Factor 10 (intrinsic) activated by antihemophilic factor- 8 ```
22
Hageman factor
Factor 12 (intrinsic) activated by exposed collagen activates Factor 11
22
Factor 11
intrinsic activates Christmas factor (9)
22
Accelerin (Factor V)
with factor X and the presence of calcium this helps form prothrombin
22
Prothrombinase
converts Prothrombin to thrombin
22
Thrombin in hemostasis
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
Plasminogen
Circulating non-enzymatic protein converted by t-PA into plasmin
22
Plasmin
Responsible for the enzymatic degradation of fibrin
22
t-PA
this is a protease secreted by endothelium that cleaves plasminogen to form plasmin it's activity is increased 500-fold by fibrin
22
u-PA
secreted by kidneys circulates in plasma and converts plasminogen into plasmin
22
thrombus
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
Thrombosis
results from impairment in ability to limit/terminate clot propagation
22
what activates the intrinsic pathway
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
how is the extrinsic pathway activated
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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