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From Flashcardlet > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Sonoclot ACT correlates with what on TEG

A

R time, K time, angle

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2
Q

CR on sonoclot correlates with what on TEG

A

all parameters

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3
Q

What does the Sonoclot do?

A

Measures changes in blood viscosity by detecting a change in mechanical impendance of a tubular, disposable, plastic probe oscillating vertically in a cuvette containing whole blood or plasma

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4
Q

How is platelet function determined on Sonoclot?

A

Not directly, calculated value based on both teh time it takes for the signature to peak, as well as degree of clot retraction

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5
Q

What 3 variables determined on Sonoclot

A

ACT, clot rate (CR), and platelet function (indirectly)

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6
Q

What does CR measure on Sonoclot?

A

rate of fibrin formation

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7
Q

Sonoclot correlated to several TEG parameters, platelet count, and fibrinogen, but not to other commonly used coagulation tests. T/F

A

T

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8
Q

MOA thrombomodulin

A

binds thrombin changing its substrate specificity and becomes an anticoagulant by activating protein C, with its cofactor, protein S, inactivates Va and VIIIa

thrombomodulin from endothelium

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9
Q

MOA TFPI

A

inhibits extrinsic pathway

TFPI from endothelium

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10
Q

What is the initiation stage of coagulation?

A

TF-VIIa makes a small amount of thrombin

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11
Q

What is the prothrombinase complex?

A

Va-Xa

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12
Q

What is the tenase complex?

A

VIIIa-IXa

Fxn: activates X to Xa which then binds with Va on platelet surface forming the prothrombinase complex to create thrombin burst

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13
Q

Antithrombin inhibits what factors?

A

2, 7, 9, 10, 11, 12

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14
Q

What dramatically increases AT activity?

A

heparan sulfate from endothelial cells (or heparin exogenously)

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15
Q

Effects of plasmin.

A

cleaves fibrin creating FDPs
inactivates 5, 8, 9, 11, cleaves complement C3, enhances conversion of 12 to 12a and conversion of prekallikrein to kallikrein

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16
Q

What are inhibitors of plasmin generation

A

a2-antiplasmin, a-2 macroglobulin

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17
Q

Heparin MOA

A

Facilitates AT-mediated inactivation of thrombin and factor Xa (also 7, 9, 11, 12)

Facilitates release of TFPI from endothelial cells

PS binds to heparin-binding domain of endothelial cell matrix protein, thrombospondin

Inhibits complement and hemolysis induced thrombin generation

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18
Q

How do you monitor heparin therapy?

A

anti-factor Xa (gold standard) or APTT (want 1.5-2.5 x normal)

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19
Q

What can affect APTT measurement with heparin therapy?

A

reagent used, high fibrinogen levels, antiphospholipid antibodies, increased circulating VIII, steroids, more low molecular weight multimers (can still have anti-factor Xa activity, but reduced ability to complex with thrombin, so APTT may appear subtherapeutic when it really is)

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20
Q

How do you monitor LMWH (enoxaparin, dalteparin)?

A

anti Xa only - b/c they are LMW do not complex to thrombin

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21
Q

What is the vWF platelet receptor?

A

Gb1b-IX-V

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22
Q

What’s the difference between platelet rich plasma and platelet concetrate?

A

PRP is made by a soft spin at 1000 x 4 min of FWB (200 mls). If you spin again (hard spin, 2000 x 10 min), get platelet concentrate (40-70 mls)

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23
Q

How many platelets are in PRP and PC?

A

> 100 x 10^9/L

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24
Q

Non immunologic complications of blood transfusion

A

pyrogen-mediated fever (most common), transmission of infectious agents, vomiting, mechanical hemolysis, CHF, hypothermia, citrate toxicity, pulmonary complications

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25
Q

Immunologic reactions to blood

A

acute and delayed hemolytic transfusion reactions manifesting as urticaria, anaphylaxis, graft vs host dz

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26
Q

Virchows triad

A

blood stasis, hypercoagulable state, endothelial damage

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27
Q

What coag factors increased in cushings?

A

5, 10, fibrinogen

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28
Q

What IL stimulates TF?

A

6 - predominantly

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29
Q

Where does heparan sulfate come from?

A

endothelial cells

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30
Q

When AT bound to heparan sulfate on endothelium, stimulates what factors regarding inflammation?

A

prostacyclin I2 and NF-kB

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31
Q

Negatively charged proteins on platelet surfaces when activated.

A

phosphatidylserine and phosphatidylethanolamine

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32
Q

What lives in Weibel Palade bodies

A

vWF, VIII, p-selectin, IL-8, TPA

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33
Q

What activates endothelial cells?

A

TNFa, bradykinin, thrombin, histamine, VEGF

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34
Q

What is the prothrombinase complex?

A

Va and Xa and prothrombin (II)

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35
Q

Feline platelet alpha granules have what that is special…

A

vWF (not in dog alpha granules)

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36
Q

What supports decrease in fibrinolysis?

A

decreased tPA, increased a2 antiplasmin, PAI-1, TAFI

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37
Q

What is MPC on Advia 120?

A

mean platelet component - granularity of platelets, activated platelets will have released their granules, so decreased MPC may indicate hypercoagulable state

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38
Q

G =

A

5000 x MA / (100-MA); higher = more hypercoagulable

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39
Q

Anticoagulant effects of aPC

A

inactivates Va and VIIIa

enhances fibrinolysis

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40
Q

Antiinflammatory effects of aPC

A

Inhibits apoptosis, decreases NF-kB, decreases inducible TF, decreases adhesion molecules

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41
Q

How does inflammation alter the protein C pathway?

A

Inhibits thrombomodulin and endothelial cell protein C receptor transcription resulting in a decreased ability to generated APC

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42
Q

PAI-1 upregulated by

A

TNF-a and CRP

43
Q

What is usually elevated with chronic end stage liver dz?

A

fVIII and vWF

44
Q

What does thrombomodulin do?

A

activates protein C

45
Q

Where is thrombomodulin at?

A

endothelial cells - its a transmembrane protein

46
Q

What converts plasminogen to plasmin?

A

fibrin

47
Q

What are antifibrinolytic drivers?

A

PAI-1, TAFI

48
Q

Underlying conditions that explain the bleeding tendency in patients with decompensated chronic liver disease.

A
  1. Portal hypertension causing hemodynamic alterations
  2. Endothelial dysfxn
  3. Development of endogenous heparin-like substances from bacterial infection
  4. Renal failure
49
Q

What are the PAR receptors?

A

PAR1 binds TFVIIa, Xa, thrombin
PAR2 binds TF-VIIa, Xa, trypsin
PAR 3 and 4 bind thrombin

50
Q

Bentley, JVECC, 2013 on coagulation with septic peritonitis, findings?

A

Preop PC >60% and AT >41.5% sensitive predictors of survival.

TEG survivors were more hypercoagulable

51
Q

TRALI

A

Occurs within 2-6 h of blood product, no pre-existing ALI, and no temporal relationship to alternative risk factors for ALI

Due to anti-leukocyte antibodies, resolves rapidly, low mortality

52
Q

Delayed TRALI

A

Occurs w/i 6-72 h after transfusion, occurs in 25% of critically ill transfused patients, mortality up to 40%

Trauma, burns, sepsis increased risk

Risk increased with transfusion of plasma-rich products, frozen plasma, and platelets, than transfusion with pRBC

53
Q

Massive tranfusion risk of…

A

ARDS/ALI

54
Q

TRALI theories:

A
  1. Donor antibodies to antigens on recipient leukocytes, or less likely the other way around (in humans at least)
  2. mediated by an interaction b/t biologically active mediators in banked blood products and the lung (classic 2 hit theory - lung endothelium of recipient primed with neutrophils from critical dz, then transfuse blood with inflammatory mediators causing endothelial damage, capillary leak, and TRALI)
55
Q

What accumulates in stored blood?

A

IL-1, IL-6, IL-8, bactericidal permeability increasing protein, phospholipase A2, TNF-a

56
Q

Leukoreduction helps to prevent..

A

delayed TRALI

57
Q

Plateletpheresis yield

A

3-4.5 x 10^11 vs. <1 x 10^11 for whole blood derived platelets

58
Q

DMSO cryopreserved platelets yield

A

50%, half life 2 days

59
Q

What is plateletpheresis?

A

selective removal of platelets from the donor’s blood via an automated cell separator with return of RBCs and plasma to the donor

Reduces exposure of recipient to multiple donors

60
Q

Platelets in PC?

A

8 x 10^10 per PC unit

61
Q

Donor concern for plateletpheresis

A

citrate toxicity, hypocalcemia

62
Q

How long can FWB be stored?

A

8 h

63
Q

How long can PC and PRP be stored?

A

5 d at 22 C with gentle agitation

64
Q

What are platelet storage lesions?

A

Change in shape from discoid to spherical, generation of lactate from glycolysis with decrease in pH, release of platelet granules, decrease in fxn, reduction in posttransfusion recovery and survival

65
Q

Why can’t you chill platelets?

A

chilling causes vWF receptors (GP1balpha-IX complex) on platelet surface. The integrin receptor alphaMbeta2 (C3R) of hepatic macrophages recognizes the receptor and eats the platelet

Galactosylation decreases

66
Q

What is thrombosol?

A

mixture of amiloride, adenoseine, and sodium nitroprusside to inhibit platelets - used with DMSO to improve platelet survival

67
Q

DMSO platelet half life

A

2 d, vs. 3.5 d for fresh platelets

68
Q

DMSO plt storage life

A

1 year

69
Q

pRBC mechanism for the role in hemostasis

A
  1. dispersion of platelets to periphery
  2. increase plt contact with endothelium
  3. release ADP
  4. scavenge NO (which inhibits plts)
  5. increase production of TXA2 by platelets at bleeding site
70
Q

FWB contains how many platelets?

A

10 x 10^9 /L

71
Q

Methods to decrease lymphocytotoxic antibodies.

A

leukoreduction

ultraviolet B irradiation

72
Q

What diseases are most common in cats with DIC

A

cancer, pancreatitis, sepsis

73
Q

What % cats have hemorrhage with DIC?

A

15%

74
Q

Other findings, DIC cats, JVIM 2009.

A

All DIC cats had high PTT
Median PT of nonsurivors * higher than survivors
No effect of heparin or transfusion on outcome
Most cats died or euth (7% survival)

75
Q

Incidence of prolonged PT in dogs following GI decontamination for acute anticoagulant rodenticide ingestion. JVECC, 2008, Pachtinger, findings….

A

Dogs presenting w/i 6 ingestion, then PT done w/i 2-6 days. Only 8.3% developed prolonged PT needing treatment (none had bleeding or needed transfusion). No diff in age, wt, time elapsed b/t treated and untreated patients found.

No assc’n w/ type of anticoagulant.

Trend towards smaller dogs needing vitamin K.

76
Q

Half life of factor VII

A

6.2 h

77
Q

Half life of factor II (prothrombin)

A

41 h

Should take a minimum of 2 prothrombin half lives, or 3.5 days, to express the antithrombotic effect in patients

78
Q

TFPI inhibits…

A

VIIa and Xa

TFPI lives in endothelial cells and platelets

79
Q

What effect does LPS have on monocytes related to coagulation?

A

De novo synthesis of TF on surface

80
Q

P-selectin

A

tethers platelets to surfaces

P-selectin + PSGL-1 (leukocytes binding)

81
Q

Firm adhesion of plts to neuts is fibrinogen binding, which couples the platelet…

A

alpha2b beta3 to CD11b/CD18 counterreceptor (MAC-1)

82
Q

vWF platelet receptor

A

GP 1b-V-IX

83
Q

collagen platelet receptor

A

GPVI

84
Q

thrombin platelet receptors

A

PAR-1 and PAR-4

85
Q

Alpha 2b Beta3 receptor antagonists

A

abciximab
eptifibatide
tirofiban

86
Q

Drug that blocks PAR1 receptor

A

vorapaxar and atopaxar

87
Q

Drugs that block P2Y12 receptor by blocking ADP from binding

A

thienopyridines (prodrugs): clopidogrel, prasugrel, ticlodipine

irreversible: ticagrelor
reversible: cangrelor

88
Q

Endothelial prostaglandins

A

PGD2, PGE2, PGF2, PGI2

89
Q

Acetylation of COX-1 is ___ more effective than COX-2 by aspirin

A

166X

via acetylation of Ser529 preventing binding of AA to catalytic site on COX-1

90
Q

Other effects of aspirin besides inhibition of COX-1

A

stimulates NO release via 15-epoxylipoxin A4 and inhibiting leukocyte endothelial reactions, enhances fibrin clot permeability and lysis by acetylating lysine residues on fibrin

91
Q

Clopidogrel action decreased by what drug?

A

PPIs - omeprazole

92
Q

Replacement of chlorine with ___ enhances prasugrels action.

A

fluorine

93
Q

What drug class is ticagrelor in?

A

cyclopentyltriazolopyrimidine

94
Q

Picotamide MOA

A

dual inhibitor of TxA2 receptors and TxA2 synthesis

95
Q

20% of blood content of FV is where

A

alpha granules

96
Q

What is the protein C/protein S/thrombomodulin (TM) system?

A

thrombin binds thrombomodulin, which activates protein C which binds with its cofactor, protein S, and intactivates any factors Va and VIIIa

97
Q

Protease inhibitors TFPI and ATIII are always present bound to…

A

heparan sulfates on endothelial surfaces

98
Q

TFPI inhibits

A

Xa and VIIa

99
Q

What is the only coagulation protein that routinely circulates in its active form?

A

VII (about 1% VIIa)

100
Q

What two effects does thrombin bound thrombomodulin have?

A
  1. activates TAFI which modifies fibrin molecules by removing their terminal lysine residue making them more resistant to fibrinolysis
  2. activates Protein C which then binds cofactor Protein S to inactivate Va and VIIIa
101
Q

How does the Sonoclot work?

A

Measures changes in blood viscosity using a vertically oscillating probe immersed in a cuvette of whole blood. Glass beads in the cuvette activate coagulation. Results are Sonoclot Signature graphically and quantitative results are ACT, clot rate, and platelet function

102
Q

Recommended heparin levels for anticoagulation

A

0.35-0.7 U/ml

103
Q

aPTT goal with heparin

A

1.5-2 X baseline

104
Q

Babski, JVIM, 2012. Sonoclot evaluation of UFH dogs

A

ACT prolonged, CR decreased, aPTT correlated well with AXA; however, aPTT ratio did not correlate as strongly with AXA, Sonoclot equivalent to aPTT

From Flashcardlet (19 decks)

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