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SIU SOM: CRR > hemostasis > Flashcards

hemostasis Flashcards

1
Q

define hemostasis

A

cessation of bleeding from a severed blood vessel

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2
Q

define thrombosis

A

intravascular clot formation

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3
Q

list stages of hemostasis

A
  1. vasoconstriction
  2. platelet plug formation
  3. blood coagulation
  4. fibrinolysis
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4
Q

describe adhesion step in plug formation

A
  1. adhesion: Von Willebrand factor binds subendothelial collagen which facilitates platelet adhesion through its platelet receptors (GPIb-IX-V) which initiates tethering. collagen’s platelet receptor (GPVI) binds FcRgamma on platelet and this activates alpha2beta1 a2b3 receptors
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5
Q

describe activation/secretion step in platelet plug formation

A
  1. activation/secretion: receptor activation activates PIP2 –> IP3 –> Ca+ and PIP2 –> DAG –> PKC, phospholipid –> pLA2 –> arachindonic acid –> PGG2, PGH2 (via COX-1) –> thromboxane A2 (via TXA2 synthase)
    these reactions cause an accumulation of thromboxane A, ADP and thrombin which stimulate GCPRs which acts as positive feedback
    the granules are released due to increased cytoplasmic calcium
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6
Q

alpha granules of platelets

A 
coagulants/anticoagulants: V, XI, ATIII
adhesion proteins: fibrinogen, vWF
integral membrane proteins: GPIIb-IIIa
growth factors: EGF, TGFbeta
angiogenic factors/inhibitors: VEGF, PDFG
chemokines and immune mediators
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7
Q

dense granules of platelets

A

ADP
Ca2+
polyphosphate
serotonin

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8
Q

describe the aggregation step of platelet plug formation

A

after morphological changes through the inside out signlaing of platelet activation GPIIbIIIIa is able to bind fibrinogen or vWF which other platelets are bind to which allows clumping GPIIbIIIa binding to fibrinogen also causes outside in signaling which further accelerates the aggregation process

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9
Q

what is vWF bound to as it travels in the blood

A

factor VIII

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10
Q

which antiplatelet drug(s) block COX-1

A

aspirin and other NSAIDs

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11
Q

which antiplatelet drug(s) block ADP receptor on platelet

A

clopidogrel
prasurgrel
ticagrelor
cangrelor

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12
Q

which antiplatelet drug(s) blocks thrombin recptor (PAR-1) on platelets

A

vorapaxar

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13
Q

which antiplatelet drug(s) block fibrinogen and vWF binding to activated GPIIb/IIIa

A

abciximab
eptifibatide
tirofiban

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14
Q

prostacyclin and platelet plug formation

A

prostacyclin activates adenylyl cyclase –> cAMP which blocks platelet responses

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15
Q

factors that can activate phospholypase C

A

vWF, TxA, thrombin

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16
Q

function of phospholupase C in platelet plug formation

A

PIP2 –> DAG and IP3
IP3 –> Ca+
DAG –> PKC

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17
Q

function of Ca+ in platelet plug formation

A 
initaite platelet responses
activate PLA2 (--> aa -->TxA)
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18
Q

what initiates the intrinsic pathway vs the extrinsic pathway

A

intrinsic: contact activation pathway, everything needed is already in plasma
extrinsic: needs TF (on subendothelium)

19
Q

intrinsic pathway coagulation steps

A

XII –> XIIa –> kalikrein/high molecular weight kininogen a –> XIIa –> XIa –> IXa –> compelx forms: IXa + VIIIa + X + Ca
when X binds this complex it becomes Xa

20
Q

extrinsic pathway coagulation steps

A

VII + TF –> complex: VIIa, TF, X, Ca+

when X binds to complex it becomes activated

21
Q

common pathway coagulation steps

A

complex: Xa, Va, prothrombin, Ca+ –> thrombin –> fibrin –> soft clot
thrombin –> XIIIa –> fibrin cross-linked

22
Q

steps that are enhanced by thrombin

A 
XI-->XIa
VIII --> VIIIa
V-->Va
VII --> VIIa
fibrinogen --> fibrin
fibrin --> soft clot
XIII-->XIIIa
23
Q

TFPI

A

tissue factor pathway inhibitor
acts as anticoagulant in stopping early phase responses
blocks Xa and TF

24
Q

antithrombin III

A

increased by heparin
blocks thrombin and therefore K/HMWK, XIIa, XIa, IXa, Xa
most importantly: blocks thrombin and X

25
Q

thrombomodulin

A

changes specificity of thrombin so it cleaves protein C

protein C and protein S block VIIIa and Va

26
Q

Leiden V mutation

A

resistant to APC (activated protein C) mediated activation so there is an increased risk of thrombosis

27
Q

warfarin

A

competitively inhibits vitamin k epoxide reductase which reduces vitamin k-dependent gamma-carboxyglutamic acid modifications essential to biological function
reduces hepatic production of vitamin k-dependent coagulation factors: II, VII, IX, X, and the anticoagulation proteins C and S

28
Q

how is VII membrane bound

A

Ca+ binds gamma carboxyglutamate residues on factor VII which facilitates interaction with anionic phospholipid membrane

29
Q

heparin

A

unbranched anionic glycosaminoglycan composed of alternating variations of sulfated and or acetylated glucosamine and sulfated uronic acid
unfractionated heparin: increases antithrombin III activity to inhibit factor X and thrombin
low molecular weight heparin inhibits factor X more than thrombin

30
Q

bivalirudin

A

competitive inhibitor which binds active site and anion binding exosite of thrombin (bivalent)

31
Q

dabigatran

A

competitive inhibitor that binds only active site of thrombin

32
Q

apixaban

A

competitive inhibitor for factor Xa

33
Q

prothrombin time (PT) and INternationalized normalization ratio (INR)

A

evaluates the extrinsic and common pathways: fibrinogn, prothrombin, V, VII, and X
PT = time elapsed before clotting
INR= (PTtest/PTcontrol)^ISI

34
Q

partial thromboplastin time (PTT) or activated partial thromboplastin time (APTT)

A

evaluates intrinsic pathway and common pathhways
normal PTT requires: fibrinogen, prothrombin, factors V, VIII, IX,X,XI, and XII (does not require factor VII)
partial bc no tissue factor is present in assay
PTT= time elapsed before clotting

35
Q

function of plasmin

A

in fibrinolysis: breaks down fibrin

36
Q

how is plasminogen activated into plasmin

A

t-PA and u-PA which is released from injured endothelium

factors XIa, XIIa, and kallikrein also weakly activate

37
Q

PAI-1 and PAI-2

A

plasminogen activator inhibitors

block t-PA and u-PA

38
Q

alpha2-antiplasmin

A

blocks free plasmin (reduces fibrinolysis)

39
Q

TAFI

A

thrombin activatable fibrinolysis inhibitor
inhibits fibrinolysis by removing C-terminal lysine residues of fibrin that facilitate plasminogen binding and activation

40
Q

thrombolytics

A

plasminogen activators

ex. alteplase, reteplase, tenectaplase, urokinase, streptokinase

41
Q

aminocaproic acid (amicar)

A

inhibits plasmin

42
Q

D-dimer test

A

antibodies detect the neoepitope that arises upon covalently cross-linking two D domains from saparate molecules of fibrin
does not detect fibrin or fibrinogen

43
Q

how do NO and prostacyclin affect hemostasis

A

they are secreted by healthy endothelial cells and promote vasodilation and inhibit platelet aggregation

44
Q

how does thrombomodulin affect hemostasis

A

healthy endothelial cells express thrombomodulin which converts thrombin from pro-coagulant to anti-coagulant. thrombins specificity changes upon binding thombomodulin, leading to activation of anti-coagulant proteins such as activated protein C and TAFI

SIU SOM: CRR (15 decks)

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