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ANESTHESIA PRACTICE 2 > HEMOSTASIS > Flashcards

HEMOSTASIS Flashcards

1
Q

define hemostasis

A

a complex physiological process that balances the opposing forces of coagulation and anticoagulation to protect the vasculature from uncontrolled bleeding on the one hand and excessive clotting on the other

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2
Q

what are the three phases of hemostasis?

A
  • primary hemostasis – formation of platelet plug
  • secondary hemostasis – coagulation
  • tertiary hemostasis – fibrinolysis
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3
Q

what are the three actions of platelet plug formation?

A
  • platelet adhesion
  • platelet activation
  • platelet aggregation
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4
Q

what is von Willebrand factor?

A
  • large, heterogenous multimeric glycoprotein that protects coagulation factor VIII from rapid inactivation
  • binds platelets vial the glycoprotein Ib receptor complex
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5
Q

what makes vWF bind to platelets?

A

change in shear rate

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6
Q

platelet adhesion requires two components – what are they?

A
  • tissue factor - vWF via the glycoprotein Ib receptor

* collagen from the sub endothelial matrix – via the glycoprotein VI receptor and the a2b1 integrin

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7
Q

what is von Willebrand’s disease?

A
  • deficiency in vWF
  • most common in congenital bleeding disorder
  • manifests as impaired platelet function
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8
Q

what is the treatment for von Willebrand’s disease?

A

DDAVP or transfusion of FFP or cryoprecipitate or vWF/FVIII concentrate

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9
Q

how are platelets activated?

A

platelets become activated by agonists at the site of injury – collagen, thrombin, ADP, epinephrine

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10
Q

describe the process of platelet activation

A
  • platelets change morphology
  • release contents of alpha granules and dense granules – ADP, serotonin, factor V, factor VIII, vWF, fibrinogen
  • release thromboxane A2 into environment
  • express new negatively-charged receptors on their surface membrane
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11
Q

name the three platelet surface receptors

A
  • thrombin –> protease-activated receptors (PAR1 and PAR4)
  • ADP –> P2Y1 and P2Y12 : blocked by thienopyridines (ticlopidine and clopidogrel)
  • fibrinogen –> glycoprotein IIb/IIIa : blocked by antagonists (abciximab and tirofiban)
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12
Q

how is platelet aggregation mediated?

A

platelet surface receptor – glycoprotein IIb/IIIa receptor

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13
Q

what are the primary adhesive molecules of primary adhesion?

A

fibrinogen and vWF – form bridges between platelets to create a platelet plug

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14
Q

what is the function of factor XIII?

A

fibrin stabilizing factor

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15
Q

how does aspirin affect clot formation?

A

aspirin acetylates fibrinogen – clot structure is looser and easier to lyse

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16
Q

formation of the platelet plug is coordinated with what?

A

formation of the platelet plug is coordinated with activation of the blood coagulation system leading to the generation of thrombin and the formation of a fibrin clot

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17
Q

how are most coagulation factors found in the circulation?

A

most coagulation factors circulate in an inactive form – “pro-enzyme” or “zymogen”

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18
Q

how are coagulation factors activated?

A

a portion of the pro-enzyme must be cleaved off or modified to activate the coagulation factor

19
Q

what is required for the proper interaction of coagulation factors?

A

the proper interaction of coagulation factors requires the presence of a negatively-charged phospholipid membrane

20
Q

where are most coagulation factors synthesized?

A

in the liver

  • contact activation factors = FXII and FXI
  • vitamin K-dependent factors = FII, FVII, FIX and FX
21
Q

which coagulation factor has an extra-hepatic origin?

A

FVIII

  • high molecular weight portion = carrier
  • small molecular weight portion = coagulant activity
22
Q

what is the function of vitamin K in coagulation?

A
  • catalyzes the carboxylation of glutamic acid –> carboxyglutamic acid
  • possible for the factor to bind calcium
23
Q

what effect does coumadin have on coagulation?

A

coumadin inhibits carboxylation of vitamin K-dependent factors by vitamin K

24
Q

which coagulation factor has the shortest half-life?

A

FVII has the shortest half-life of the vitamin K-dependent factors

25
Q

define hemophilia A and hemophilia B

A
  • hemophilia A – FVIII deficiency

* hemophilia B – FIX deficiency

26
Q

describe the cascade model of coagulation in three steps

A
  • overall structure is a series of proteolytic reactions
  • protein coagulation factors direct and control the process
  • cells serve as surface on which coagulation complexes are assembled
27
Q

describe the interdependence of the intrinsic and extrinsic coagulation pathways

A
  • (extrinsic) TF/VIIa ––> FX; TF/VIIa ––> FIX (intrinsic)

* thrombin ––> FXI (intrinsic)

28
Q

describe the three overlapping stages of the cell-based model of coagulation

A
  1. initiation: a procoagulant stimulus generates enough thrombin to initiate the coagulation process
  2. amplification: latelets and coagulation factors are activated
  3. propogation: large amounts of thrombin are generated on the activated platelet surface
29
Q

what is the function of thrombin in coagulation?

A
  • cleavage of fibrinogen to fibrin

* activates factor XIII to cross-link fibrin

30
Q

how does the tissue factor pathway inhibitor (TFPI) regulate coagulation?

A

inhibits the (extrinsic) TF/FVIIa complex and TF/FVIIa/FXa complex

31
Q

how does antithrombin (AT) regulate coagulation?

A

inhibits FXa and thrombin

32
Q

how does protein C (PC) regulate coagulation?

A

with co-factor protein S (PS), inhibits FVa and FVIIIa (intrinsic)

33
Q

how does heparin inhibit coagulation?

A
  • primary anticoagulation action: inhibits thrombin activity

* binds to AT causing conformational change, transforming AT from a slow to a rapid inhibitor of thrombin

34
Q

name three quantitative age-related coagulation changes?

A
  • VitK-dependent factors
  • contact activation factors
  • coagulation inhibitors
35
Q

name there qualitative age-related coagulation changes?

A
  • platelets
  • fibrinogen
  • plasminogen
36
Q

how do neonate platelets compare to adult platelets?

A
  • neonatal platelet counts = 100% adult values
  • neonatal platelet membrane glycoprotein expression is fully developed
  • contents of platelet dense granules = 50% adult contents
  • neonatal platelet aggregation is impaired in response to ADP, epinephrine, collagen and thrombin
37
Q

how does neonatal platelet aggregation in response to collagen and thrombin compare to adults?

A

platelet aggregation is almost 2x slower in neonates than adults in response to both collagen and thrombin

38
Q

despite longer response times to collagen and thrombin, neonates show efficient platelet function. How is that?

A
  • increased concentration of vWF

* increased number of large vWF factor multimers

39
Q

how long does the fetal form of fibrinogen exist?

A

until approximately 1yo

40
Q

how do neonatal and infant fibrin clots differ from adults?

A

fibrin clots are less dense

41
Q

how does neonatal plasminogen differ from adults?

A

less fibrinolytic activity secondary to quantitative and qualitative deficiencies in plasminogen

  • lower concentration (50% adult values)
  • decreased functional activity (bind poorly to cellular receptors, activation/inhibition kinetics are slower)
42
Q

what are the FDA-approved uses for recombinant activated factor VII?

A
  • patients with hemophilia A an dB with inhibitors against FVIII and FIX
  • patient with congenital FVII deficiency
  • Treatment/prevention of bleeding for surgical interventions or invasive procedures
43
Q

what are the thrombolitic event risks associated with rFVIIa?

A

CVA, MI, other arterial thromboses, PE, other venous thrombosis, and clotted devices

ANESTHESIA PRACTICE 2 (5 decks)

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