Circulating Inhibitors

106 flashcardsby CHRISTY
Study these flashcardsFree · spaced repetition · iPhone, Android, Mac & web

All cards

1
Laboratory detection finding characteristic of acquired circulating inhibitors of coagulation is
Prolongation of PT or APTT NOT corrected by the addition of normal (fresh) plasma
2
Target structures against which specific circulating inhibitors are directed are
Specific coagulation factors
3
Clinical outcome primary associated with specific circulating inhibitors is
Bleeding
4
Most common specific circulating inhibitors observed clinically are
Antibodies to factors VIII and IX
5
Antibody classes associated with lupus anticoagulant non-specific inhibitors include
IgG, IgM, IgA
6
Prevalence rate of lupus anticoagulant in systemic lupus erythematosus (SLE) patients is
Found in 10% of SLE patients
7
General PT and APTT screening pattern seen with lupus anticoagulant is
Normal or slightly increased PT and increased APTT
8
Target structure of lupus anticoagulant antibodies and associated clinical bleeding tendency are
Directed against phospholipids and generally not associated with bleeding
9
Laboratory tests used to evaluate non-specific inhibitors like lupus anticoagulant include
Substitution test, Platelet neutralization test, dRVVT
10
Examples of non-specific circulating inhibitors in plasma include
Lupus anticoagulant, Paraproteins, Fibrinogen degradation products
11
Thrombin complex component responsible for activating Protein C in the body is
Thrombin bound to thrombomodulin (TM)
12
Target factors inactivated by Activated Protein C (APC) in the anticoagulant pathway are
Factors Va and VIIIa
13
Role of Protein S in the Protein C anticoagulant system is
Co-factor to Protein C
14
Main serine protease inhibitor in the plasma serine protease inhibitor (SERPIN) system is
Antithrombin (formerly antithrombin III)
15
Enzymes and factors inhibited by Antithrombin (AT) in coagulation include
IIa (thrombin), IXa, Xa, XIa, kallikrein, XIIa
16
Definition of fibrinolysis in the coagulation system refers to
Final stage of coagulation and dissolution of the formed clot
17
Timeline when fibrinolysis initiates after fibrin cross-linking is
Starts a few hours after fibrin polymerization and cross-linking
18
Two plasminogen activators released in response to inflammation and coagulation are
TPA and UPA
19
Proteins of the fibrinolysis pathway that accumulate on fibrin during clotting are
Plasminogen, plasmin, TPA, UPA, PAI-1
20
Primary action of TPA and UPA on fibrin-bound plasminogen hours after clot formation is
Activate fibrin-bound plasminogen, degrading fibrin and reestablishing normal blood flow
21
Site of synthesis and transport cell type for the zymogen plasminogen are
Produced by the liver; stored and transported in eosinophils
22
Enzymatic nature of plasmin and its function on bound fibrin are
Serine protease that digests clot and restores blood vessel patency
23
Plasma proteins degraded by free plasmin in primary fibrinolysis if uninhibited include
Plasma fibrinogen, factor V, factor VIII, fibronectin
24
Plasma inhibitor that rapidly binds and inactivates free plasmin in circulation is
α2-antiplasmin
25
Secreting cell source and function of Tissue Plasminogen Activator (TPA) are
Secreted by activated endothelium; activates plasminogen
26
Circulating inhibitor bound to TPA in plasma prior to clearance is
PAI-1
27
Secreting cell sources for Urokinase Plasminogen Activator (UPA) include
Urinary tract epithelial cells, monocytes, and macrophages
28
Fibrin binding capability and physiologic role of UPA compared to TPA are
Does NOT bind firmly to fibrin and has a relatively minor physiologic effect
29
Primary role of Plasminogen Activator Inhibitor 1 (PAI-1) in fibrinolysis is
Principal inhibitor of plasminogen activation
30
Enzymatic activators inhibited by PAI-1 to prevent plasminogen conversion are
Both TPA and UPA
31
Organ site of synthesis and main role of α2-antiplasmin are
Synthesized in the liver; primary inhibitor of free plasmin
32
Pharmacologic antifibrinolytic agents that inhibit the proteolytic activity of plasmin are
ε-aminocaproic acid and tranexamic acid
33
Site of synthesis and activating complex for Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) are
Synthesized in the liver; activated by thrombin-thrombomodulin complex
34
Functional role of activated TAFI in the fibrinolytic system is
Functions as an antifibrinolytic enzyme
35
Fibrin degradation product containing D-dimer is generated when
Plasmin lyses the fibrin
36
Diffentiation in D-dimer production between fibrin lysis and fibrinogen lysis is
Plasmin lyse fibrinogen, but will NOT produce the D-dimer
37
Diagnostic implication of D-dimer presence in plasma is
Indicates that a stable fibrin clot has been lysed
38
Combination of FDP/FSP and D-dimer results specific for Pathological Fibrinolysis is
FDP(+), D-dimer (-)
39
Combination of FDP/FSP and D-dimer results specific for Disseminated Intravascular Coagulation (DIC) is
FDP(+), D-dimer (+)
40
Condition under which euglobulin proteins precipitate in the Euglobulin Lysis Time test is
Precipitate when plasma is diluted with water and acidified (1% acetic acid)
41
Components included in the precipitated euglobulin fraction are
Plasminogen, plasmin, fibrinogen, and plasminogen activators
42
Sample preparation steps prior to redissolving and clotting in Euglobulin Lysis Time are
Citrated PPP diluted with water, acidified, and refrigerated
43
Typical normal value for Euglobulin Lysis Time is
Typically longer than 2 hours
44
Diagnostic interpretation when euglobulin clot lysis occurs in less than 2 hours is
Increased fibrinolytic activity
45
Alternative name and location of G proteins in platelet activation are
Guanine nucleotide-binding proteins located at the inner membrane surface
46
Two major internal platelet signaling pathways stimulated by G proteins are
Eicosanoid synthesis pathway and IP3-DAG pathway
47
Alternative names for the eicosanoid synthesis pathway are
Prostaglandin, cyclooxygenase, or thromboxane pathway
48
Origin precursor molecule of eicosanoids is
20-carbon atom arachidonic acid (20 in Greek is "eicosa")
49
Examples of lipid mediators classified as eicosanoids include
Prostacyclin, thromboxane
50
Enzyme activated when collagen, ADP, thrombin, and epinephrine bind platelet membrane receptors is
Phospholipase A2
51
Substrate cleaved by Phospholipase A2 to release arachidonic acid is
Membrane phosphatidylinositol
52
Sequential enzymes acting on arachidonic acid to synthesize TXA2 in platelets are
Cyclooxygenase, peroxidase, and thromboxane synthase
53
Intracellular effect of TXA2 on adenylate cyclase and cyclic AMP in platelets is
Suppresses adenylate cyclase and reduces cyclic AMP concentration
54
Organelle from which ionic calcium is released due to reduced cAMP during TXA2 action is
Dense tubular system (DTS)
55
Key difference in eicosanoid pathway enzymes between endothelial cells and platelets is
Prostacyclin synthase replaces thromboxane synthase in endothelial cells
56
End product of the eicosanoid pathway in endothelial cells is
Prostaglandin I2 (prostacyclin)
57
Membrane receptor to which prostacyclin binds on the platelet surface is
IP receptor
58
Effect of prostacyclin on adenylate cyclase, cyclic AMP, and ionic calcium in platelets is
Accelerates adenylate cyclase, increases cyclic AMP, and sequesters ionic calcium to the DTS
59
Net effect of intact endothelial cell eicosanoid pathway on platelets is
Suppresses platelet activation
60
Enzyme activated directly by G-protein in the IP3-DAG pathway is
Phospholipase C
61
Substrate cleaved by Phospholipase C to generate IP3 and DAG is
Membrane phosphatidylinositol 4,5-bisphosphate
62
Primary function of IP3 in the IP3-DAG pathway is
Promotes release of ionic calcium from the DTS to activate actin microfilament contraction
63
Secondary enzyme that IP3 may activate in platelet signaling is
Phospholipase A2
64
Enzyme activated by DAG in the IP3-DAG pathway is
Phosphokinase C
65
Protein phosphorylated by Phosphokinase C to regulate actin microfilament contraction is
Pleckstrin
66
Three primary factors exposed or released upon blood vessel injury to initiate hemostasis are
Exposes collagen, releases VWF, and releases tissue factor
67
Definition of platelet adhesion is
Platelets adhering to a foreign surface
68
Subendothelial matrix structure that initiates platelet adhesion upon vessel injury is
Subendothelial collagen
69
Source organelle from which damaged endothelial cells release VWF is
Cytoplasmic storage organelles (Weibel-Palade bodies)
70
Conformational change of VWF upon binding exposed matrix at the injured site is
Unrolls (similar to a carpet) from globular to fibrillar form
71
Specific subunit portion of platelet GP Ib/IX/V complex that binds unrolled VWF is
GPIbα portion
72
Physical nature of the initial VWF-GPIbα interaction is
Reversible binding process that "tethers" or decelerates the platelet
73
Enzyme that regulates localized platelet-VWF interactions by digesting unused VWF is
ADAMTS-13
74
Platelet surface receptor required to bind exposed collagen and halt rolling is
GP VI
75
Agonist molecules released internally when collagen binds platelet GP VI receptor are
TXA2 and ADP
76
Platelet surface receptors bound by TXA2 and ADP to increase α2β1 affinity are
TPα/TPβ for TXA2; P2Y1/P2Y12 for ADP
77
Integrin receptor whose affinity for collagen is increased by TXA2 and ADP signaling is
α2β1 (GP Ia/IIa)
78
Combined effect of GP Ib/IX/V, GP VI, and α2β1 binding during adhesion is
Causes platelet to become firmly attached, lose its discoid shape, and spread
79
Inside-out activation target stimulated by TXA2 and ADP on adjacent platelets is
αIIbβ3 (GP IIb/IIIa)
80
Definition of platelet aggregation is
Platelets adhering to other platelets
81
Thrombin receptors on platelets activated by tissue factor generation are
PAR1 and PAR4
82
Specialized platelet phenotype generated by collagen and thrombin co-activation is
COAT platelet ("collagen and thrombin activated")
83
Membrane assembly subunits that form functional αIIbβ3 integrin are
Resting membrane units αIIb and β3
84
Bridge molecules that bind αIIbβ3 receptors to support platelet-to-platelet aggregation are
Fibrinogen and VWF
85
Morphologic change occurring in thrombocytes during aggregation is
Lose their shape and extend pseudopods
86
Membrane phospholipid rearrangement occurring on aggregating platelets is
Phosphatidylserine flips to the outer layer
87
Purpose of phosphatidylserine exposure on the outer platelet membrane is
Establishing a surface for assembly of coagulation factor complexes
88
Ultimate fate of aggregated platelets as cytoplasmic integrity is lost is
Syncytium of platelet cytoplasm forms
89
Internal structural movement triggering granule compression during platelet secretion is
Activation triggers actin microfilament contraction and intermediate filament contraction inward
90
Phospholipid surface on which tenase and prothrombinase complexes assemble is
Phosphatidylserine
91
Required ion that supports assembly of tenase and prothrombinase on phosphatidylserine is
Ionic calcium
92
Key coagulation factors stored in and secreted from α-granules include
Fibrinogen, Factor V, Factor VIII, and VWF
93
Canalicular system through which α-granule and lysosome contents flow during secretion is
Surface-connected canalicular system (SCCS)
94
Destination route for dense granules during platelet secretion is
Travel to the plasma membrane
95
Hemostatic functional role of α-granule contents is
Proteins that participate in secondary hemostasis
96
Hemostatic functional role of dense granule contents is
Vasoconstrictors and platelet agonists that intensify primary hemostasis
97
In vivo digestive role of platelet lysosomal contents is
Digest vessel wall matrix components and autophagic debris
98
Clinical definition of Bleeding Time is
Length of time a standard wound bleeds
99
Hemostatic parameters screened using Bleeding Time testing are
Disorders of platelet function and VWD
100
Hemostatic system that does NOT affect Bleeding Time results is
Coagulation mechanism
101
Four major physiological/pathological factors that affect Bleeding Time results are
Platelet count and function, skin thickness and vascularity, blood vessel quality, medications
102
Discontinuation timeframe for Aspirin or aspirin-containing products prior to Bleeding Time is
Avoid 7 days before bleeding time test
103
Discontinuation timeframe for NSAIDs (ibuprofen, tolmetin sodium, naproxen) prior to Bleeding Time is
Discontinued 24 hours before the test
104
Puncture site and instrument used in the Duke method for Bleeding Time are
Finger punctured using a sterile lancet
105
Blotting paper material and time interval specified for Duke method Bleeding Time are
Filter paper every 30 secs (must not touch wound)
106
Normal value range for Duke method Bleeding Time is
2 to 4 mins
Study all 106 cards for free