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H&C Week 3-4 > 12-04 L3 Regulation of Coagulation > Flashcards

12-04 L3 Regulation of Coagulation Flashcards

1
Q

In platelets (define)

thromboxane A2

A
  • the potent mediator of platelet aggregation and vasoconstriction
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2
Q

In endothelial cells (define)

activation of endoperoxide PGI2

A
  • major inhibiotr of platelet aggregation and vasodilator
  • htus the endothelium counterbalances the release of thromboxan A2 (by the stimulated palatelets by basla secriont of PGI2)
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3
Q

Arachidonic acid metabolism is central to the counterbalancing effect of what?

A

central to the counterbalancing effect of PGI2 on Thromboxane A2

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4
Q

what is the main inhibitor of coagulant activity?

  • what does it contain?
  • what does it act on?
A
  • TFPI (tissue factor pathway inhibitor)
    • conatins kuntiz-type protease inhibitor domains
    • neurtalizes 7a and 10a by a feedback mechanism
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5
Q

MOA

Antithrombin III

_ _ enhanceds the activity (inhibition)of AT3 on a certain cofactor _ ._

A
  • 2a (thrombin), 9a, 10a, 11a, 12a, kallikrein
  • 2a inhibition is enchanced by heprain
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6
Q

Heparin

MoA

A
  • indirect effect on thrombin via AT
  • Acts like a catalyst in an enzymatic reaction
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7
Q

Anti-protein C inhibits what else?

A
  • activation of TAFI

(additional anti-coagulant/profibrinolytic effect)

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8
Q

Protein C

half-life

activated by what

A
  • Vit K dependent
  • half-life: 6 hours
  • activated by 2a (R169–>L170 cleavage) in complex with cell-surface cofactor TM, which can be modulated in part by EPCR
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9
Q

Protein C exerts irreversible proteolytic inactivation of what 2 compounds?

A
  • Va
  • VIIIa
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10
Q

Protein C

cofactors

A
  • PS, Phospholipids, V, HDL, glycosphingolipids
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11
Q

APc is inactivated by what?

A
  • protein C inhibitor (PAI-3)
    • alpha1-antitrypsin
    • alpha2-macroglobulin
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12
Q

Proetin S

serves as a co-factor for who?

possesse what unique attribute

A
  • co-factor for APC
  • possesses APC independent anticoagulant activity
    • direct & irreversible binding to Va
    • competition with Xa
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13
Q

TM

Thrombomodulin

A

non-enzymatic cofactor that accelerates PC activation by IIa

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14
Q

TM-bound IIa

A
  • loses its ability to cleave/clot fibrinogen and/or activate platelets
  • TM-bound 2a is inactivated by protease inhibitors more easily than free 2a
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15
Q

EPCR

(endothelial protein C receptor)

A
  • enhances the rate of PC activation by 2a/TM (by 5-fold)
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16
Q

Fibrin(ogen) degradation products

A
  • d-Dimers levels: an indirect measure of coagulation activation in the clinic,
  • helpful in diagnosiing DIC
17
Q

tPA (tissue-type plasminogen activator)

A
  • a major endogenous PA activator,
  • glycoprotein secreted mainly by endothelial cells
  • its assmebly with plasminogen is fibrin dependent
18
Q

12a-Kallikrein-HMWK system:

A
  • the second major endogenous PA activator
19
Q

u-PA (urokinase type PA)

A
  • a potent PA activator produced by renal epithelium mac and some tumor ells
  • has lower affinity to fibrin compared to t-PA
  • its activation of plasminogen is fibrin-independent
20
Q

streptokinase

A
  • an exogenous PA activator, product of hemolytic streptococci
    *
21
Q

Activation receptors

u-PAR

A
  • expressed on many cell types including endothelial cells
  • bound u-PA maintains its activation capability
22
Q

Activation

Annexin 2

A
  • possesses binding affinity for plasminogen and t-PA (but not u-PA)
23
Q

Name the 3 general inhibitors of Fibrinolysis

A
  • plasmin inhibitors
  • plasminogen activator inhibitors
  • Clearance receptors
24
Q

plasmin inhibitors

A

inhibitor of fibrinolysis

  • serpin: alpha2-plasmin inhibitor
  • non-serpin: alpha2-macroglobulin
  • Nexin: broad specificity protease
25
Q

Clearance receptors

A

inhibitors of fibrinolysis

  • LRP, mannose receptors play a major role in the clearance of ‘t-PA-PAI-1’ complex
26
Q

TAFI

Thrombin-activatable fibrinolysis inhibitor

  • what is it
  • actiavted by what
  • moa
A
  • Plasma carboxypeptidase: a potent inhibitor of fibrinolysis
  • actiavted via limited proteolysis by 2a
  • Down-regulates t-PA induced fibrinolysis (was shown to prolong endogenous clot lysis in vivo
27
Q

Name 4 disease that are hereditary resistance to APC

A
  • Factor V leiden (R506Q)
  • Factor V cambridge (R306T)
  • Factor V hong kong (R306C)
  • Primary pulmonary embolism (less freq)
28
Q

prothrombin G202010A gene alteration

  • MOA
  • clincial manifestaion
  • having _ _ increased likelihood of this disease
A
  • modified 3’-UTR of prothrombin mRNA leads to the mRNa increased stability and augments its translation
    • elevated synthesis and secretion of prothrombin
  • Clinical manifestaions: thrombosis in unusual sites (hepatic, portal, cerebral sinus)
  • arterial thrombosis incsreased likelihood of carring Prothrombin G20210A
29
Q

Protein C def

  • Type I
  • Type II
  • clinical features
A
  • Type I: low levels and activity
  • Type II: normal levels but altered/decreased activity
  • clinical features: _ superfical/deep venous thrombosis,_ unusal sites (cerebreal, mesentery)
30
Q

Protein S

  • Type I
  • Type II
  • Type III
  • clincal manifestations
A
  • Type I: low levels and activity
  • **Type II: **normal levels/imparied activity
  • Type III: low free levels, total protein levels in low-to-normal range)
  • clinical manifestations: DVT/PE (pulmonary embolism)
31
Q

Antithrombin def

  • Type I
  • Type II a,b,c
  • most common symptom
A
  • Type I: low antigen/activity in the presenc and absence of heparin
  • Type II: normal antigen/impaired activity
    • IIa: reactive site mutations
    • IIb: heparin binding site mutations
    • IIc: pleiotropic mutations
  • Most common symptom: venous thrombosis of the lower extremities at early age peaking at the 2nd decade of life.
32
Q

most common symptom of antithrombin def

A
  • venous thrombosis of the lower extremities
    • at early agepeaking at the 2nd decade of life

H&C Week 3-4 (12 decks)

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