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Auburn ECC > Coag/Transfusion > Flashcards

Coag/Transfusion Flashcards

1
Q

What are three alpha 2b beta 3 (GIIb/IIIIa) receptor antagonists?

A

Abciximab eptifibatide tirofiban

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2
Q

Thrombomodulin MOA? Where does it come from?

A

Binds thrombin > ACTIVATES PROTEIN C > inactivates Va and VIIIa (with cofactor protein S) & promotes fibrinolysis (inactivates PAI-1 & inhibits TAFI)Thrombomodulin from endothelium

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3
Q

What is the platelet receptor for collagen?

A

GPVI

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4
Q

Antiinflammatory effects of aPC

A

Inhibits apoptosis
Decrease NF-kB
Decrease inducible TF
Decrease adhesion molecules

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5
Q

What suppresses fibrinolysis?

A

PAI-1TAFI

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6
Q

PAI-1 upregulated by

A

TNF-a and CRP

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7
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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8
Q

What accumulates in stored blood?

A

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

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9
Q

TFPI MOA

A

inhibits EXTRINSIC pathwayTFPI from endothelium

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10
Q

How long can FWB be stored?

A

8h

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11
Q

How long can PC and PRP be stored?

A

5 d at 22C with gentle agitation

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12
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

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13
Q

Why should you not 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

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14
Q

Half life of factor II (in dogs)?

A

41 h

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15
Q

Half life of factor VII (in dogs)?

A

6.2 h

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16
Q

What is the platelet receptor for VWF?

A

GP 1b-IX-V

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17
Q

How can giving pRBCs help with 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
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18
Q

The platelet receptor alpha 2b beta 3 (GIIb/IIIIa) binds?

A

FIBRINOGENalso vWf

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19
Q

HES-induced hypocoagulability is due to?

A
  1. Reduced availability of alpha 2b beta 3 (GIIb/IIIIa) platelet receptors.
  2. Decreased vWF (and VIII)
  3. Altered FXIIIa fibrin crosslinking
  4. HES molecules coat surface of platelet limiting binding of ligands
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20
Q

LMWH MOA?

A

augments inhibitory effect of antithrombin on FXa.

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21
Q

What is the test of choice to monitor LMWH?

A

Anti-Xa activity

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22
Q

What is the test of choice to monitor warfarin?

A

Prothrombin time (PT) / INR

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23
Q

What is INR?

A

PT results vary from different manufacturers (different tissue factor properties), so INR developed to standardize results.

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24
Q

What is the test of choice to monitor unfractionated heparin?

A

activated partial thromboplastin time (aPTT) or anti-Xa activity

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25
Q

How many subunits must UFH have in order to bind AT and thrombin?

A

18

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26
Q

A patient with an increased risk of bleeding from LMWH overdose would have a low, normal, or high anti-Xa level?

A

high anti-Xa level

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27
Q

List 3 secondary agonists released by activated platelets to recruit additional platelets, amplifying the initial response

A

Thromboxane A2, ADP, and serotonin

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28
Q

Describe 2 mechanisms for platelet adhesion

A

Sub endothelial collagen via Platelet glycoprotein VI, or collagen bound vWF via glycoprotein 1b receptor

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29
Q

The final common pathway for all platelet agonists is the activation of?

A

Platelet integrin alphaIIbbeta3 receptor (aka glycoprotein IIbIIIa receptor); this induces a conformational change and exposes binding domains for fibrinogen

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30
Q

What factors does the PT test?

A

II, VII, X, V, and fibrinogen

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31
Q

What is tested with an aPTT?

A

Factors II, V, VIII, IX, X, XI, XII, prekallikrein, HMWK, or fibrinogen

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32
Q

What are FDP’s?

A

Fibrinogen degradation products, generated when fibrinogen, soluable fibrin, or cross-linked fibrin is lysed by plasmin.

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33
Q

List 10 causes of elevated FDPs

A

Neoplasia, sepsis, SIRS, DIC, hepatic dysfunction, heart failure, thromboembolism, IMHA, heat stroke, trauma, and GDV

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34
Q

What is a D-dimer?

A

Neo-epitope produced when soluable fibrin is crosslinked by fXIIIa. The epitope is exposed by plasmin-induced cleavage of cross-linked fibrin

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35
Q

How do D-dimers differ from FDPs?

A

D-dimers are specific for active coagulation and fibrinolysis; indicate the activation of thrombin and plasmin (not just plasmin like FDPs)

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36
Q

List 6 acquired causes of hypofibrinogenemia

A

Hemodilution, massive transfusion, hepatic dysfunction, DIC, sepsis, and after thrombolytic therapy

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37
Q

What is the thrombin time a measure of?

A

Tests functional fibrinogen via a measure of the time taken for a standardized thrombin solution to convert fibrinogen to fibrin

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38
Q

List 3 causes of a prolonged thrombin time

A

Hypofibrinogenemia, dysfibrinogenemia, or presence of factors (heparin, FSPs) that inhibit fibrin polymerization

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39
Q

What is R and what does it represent?

A

Reaction time; represents enzymatic portion of coagulation (secondary homeostasis)

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40
Q

What is K? What does it represent?

A

Clotting time; represents clot kinetics, largely determined by clotting factors, fibrinogen, and platelets

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41
Q

What is the angle? What does it represent?

A

The angle represents the rapidity of fibrin accumulation and cross-linking and depends largely on fibrinogen, as well as platelets and factors.

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42
Q

What is MA and what does it represent?

A

Maximum amplitude; it represents the ultimate strength of the fibrin clot, dependent primarily on platelet aggregation (number and function) and to a lesser extent, fibrinogen

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43
Q

What is G and what does it represent?

A

Clot shear elastic modulus; represents overall coagulant status

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44
Q

What is the formula to calculate G?

A

G= 5000XMA/(100-MA)

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45
Q

What is LY60 and what does it represent?

A

Extent of clot lysis at 60 minutes after MA determined by the percentage decrease in amplitude at that time after MA. Measures fibrinolysis

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46
Q

List 8 causes of thrombocytopenia from decreased platelet production

A

Drug induced, IM megakaryocytic hypoplasia, viral (FeLV/FIV), chronic rickettsial disease, estrogen secreting neoplasia, myelodysplasia, megakaryocytic leukemia, cyclic thrombocytopenia, radiation, idiopathic bone marrow aplasia, post vaccination

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47
Q

List 7 causes of consumption/sequestration thrombocytopenia

A

DIC, microangiopathies, splenic torsion/hypersplenism, sepsis, hepatic disease, severe acute hemorrhage, severe hypothermia, HUS

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48
Q

List 9 causes of acquired thrombopathia

A

Drugs, uremia, anemia, hepatic disease, hypothermia, colloid hemodilution, myeloproliferative disorders and paraproteinemias, erhlichiosis, snake venom, DIC

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49
Q

List 10 drugs associated with thrombocytopathia

A

NSAIDs (aspirin and non aspirin), carbenicillin, cephalothin, moxalactam, sulfonamides, CCB, methylxanthines, B blockers, barbiturates, heparin, HES

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50
Q

List 3 causes of acquired vascular disorders and 1 cause of inherited

A

Acquired- vasculitis, cushings, arteriosclerosis Inherited - Ehlers-Danlos syndrome

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51
Q

List 8 inherited causes of thrombopathia

A

vWD, signal transduction disorders, Glanzmann’s thrombasthenia, Chediak-Higashi syndrome, selective ADP deficiency, cyclic hematopoiesis, procoagulant expression disorders, macrothrombocytopenia

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52
Q

What is vWD, what breeds are affected?

A

Deficiency in vWF (type 1), decreased function of large proteins (type 2), or a complete absence of vWF (type 3). Affects many dog breeds (dobies!) rare in cats

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53
Q

What breeds have signal transduction disorders been reported in?

A

Bassett hound, Eskimo spitz

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54
Q

What is Glanzmann’s thrombasthenia and what breeds does it affect?

A

Otter hound, Great Pyrenees

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55
Q

What is Chediak-Higashi syndrome? Whom does it affect?

A

Grey Persian cats

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56
Q

Whom is affected by selective ADP deficiency?

A

American Cocker Spaniel

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57
Q

In what breed is cyclic hematopoiesis inherited?

A

Grey collie

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58
Q

In what breed is Scott syndrome reported, what is another name for this?

A

GSD, procoagulant expression disorder

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59
Q

In what breed is macrothrombocytopenia reported?

A

CKCS

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60
Q

List 8 causes of acquired secondary hemostasis disorders

A

Vit K deficiency, hepatic failure, DIC, pharmacologic anticoagulants, hemodilution, severe hypothermia, acidemia, shock, massive trauma

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61
Q

Hypofibrinogenemia and dysfibrinogenemia are caused by a deficiency in what factor and this is inherited in what breeds?

A

FI deficiency; Bernese, Borzoi, Lhasa Apso, Vizla, Saint Bernard among others

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62
Q

Factor II deficiency causes what and is inherited in what breeds?

A

Hypoprothrombinemia, boxer, otter hound, English cocker spaniel

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63
Q

Factor VII deficiency causes what and in what breeds?

A

Hypoproconvertinemia; beagle, malamute, boxer, bulldog, miniature schnauzer, mixed breeds

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64
Q

What is hemophilia A and what animals does it affect?

A

FVIII deficiency; GSD, mixed breed dogs, other breeds, cats; X linked, mostly males affected

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65
Q

What is hemophilia B and whom does it affect?

A

FIX deficiency; numerous dog breeds, cats

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66
Q

What is Stuart-Power trait and whom does it affect?

A

FX deficiency; American cocker spaniel, JRT, mixed breed dogs

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67
Q

FXI deficiency causes what and in what breeds?

A

Plasma thromboplastin antecedent deficiency; English springer Spanial, Kerry blue terrier, Great Pyrenees

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68
Q

What animals have an inherited Vit K dependent factor deficiency been reported in?

A

Devon Rex cats

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69
Q

What is Hageman factor deficiency, whom does it affect, and is it a pathological condition?

A

FXII deficiency, min poodle, standard poodle, GSP, Shar Pei, cats; no

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70
Q

What is Chediak-Higashi syndrome?

A

An intrinsic platelet storage pool deficiency. Patients with this have prolonged bleeding times with normal platelet concentrations. Also have altered lysosomal granule formation and abnormal degranulation in neutrophils and platelets so aggregation response to collagen is absent.

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71
Q

What is Glanzmann’s thrombasthenia?

A

Inherited intrinsic platelet functional defect which leads to a deficiency in alphaIIbbeta3 integrin and causes lack of fibrinogen binding. Corrected with experimental bone marrow transplantation and gene therapy

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72
Q

In what breed had a P2Y12 deficiency been reported and what does this cause?

A

Greater Swiss Mountain Dog; prevents activation via ADP induced outside in signaling for fibrinogen binding on the platelet surface at the alphaIIbBeta3 integrin

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73
Q

What is the mutation that alters protein signal transduction in inside out-outside in integrin signaling events in Landseers, Bassetts, and Spitz dogs?

A

Defect in the calcium-diacylglycerol guanine nucleotide exchange factor 1 gene (CalDAG-GEF1)

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74
Q

What is Canine Scott syndrome?

A

A defect so the phosphatidylserine is unable to be externalized for creation of a procoagulant surface. There is also decreased micro particle release. Diagnosis requires flow cytometry to show a difference in platelet function.

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75
Q

How is Canine Scott Syndrome treated?

A

Peri operative dimethylsulfoxide cryopreserved PRP transfusion plus a post operative antifibrinolytic

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76
Q

Thrombin has been shown to activate which members of the PAR family?

A

1,3,4

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77
Q

What does PAR mean?

A

Protease-activated receptors

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78
Q

According to The role of tissue factor in health and disease (JVECC 2009), what are the 4 coagulation proteases that activate PARs? PARs then mediate cell activation via what?

A

FVIIa, FXa, thrombin, TFG-proteins

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79
Q

TF activates what PAR receptor?

A

PAR 2

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80
Q

FXa activates what PAR receptor?

A

1, and 2

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81
Q

What are the 3 main endogenous anticoagulants?

A

TFPI, AT, and aPC

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82
Q

How does inflammation affect protein C production?

A

Down regulates PC pathway through inhibition of thrombomodulin and endothelial cell protein C receptor (EPCR) transcription so reduced ability to generate aPC. Neut elastases cleave TM from endothelial cells greatly reducing thrombomodulins activity. PC also dec in severe inflamm due to increased consumption and compromised ability to synthesize PC d/t hepatic dysfunction.

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83
Q

List the anti-inflammatory effects of TFPI

A

Decreased leukocyte activation and dampening expression of TNF alpha

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84
Q

Describe AT’s anti-inflammatory effects

A

AT binds to endogenous endothelial cell GAGs (heparin sulfate and dermatan sulfate) which causes increased prostacyclin formation, decreased NF KB activation and decreased leukocyte activation and adhesion to endothelial cells.

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85
Q

Thrombophilia is…

A

Hypercoagulability as a result of inherited or acquired causes

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86
Q

What are some causes of thrombophilia in humans?

A

Factor V Leiden mutation or protein C deficiency

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87
Q

What is Virchow’s triad?

A

Hypercoagulability, blood stasis/altered blood flow, endothelial dysfunction

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88
Q

What makes up the glycocalyx?

A

GAG’s, proteoglycans, and glycoproteins

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89
Q

Vascular endothelial cells can be activated by what?

A

TNF-alpha, bradykinin, histamine, thrombin, and vascular endothelial growth factor (VEGF)

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90
Q

What anticoagulants rely on the glycocalyx?

A

Thrombomodulin, protein C, tissue factor pathway inhibitor,heparin cofactor II

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91
Q

How does the glycocalyx function as a mechanoreceptor?

A

Sensing altered blood flow and releasing nitric oxide during conditions of increased sheer stress to maintain appropriate organ perfusion.

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92
Q

List 3 important effects nitric oxide has in relation to the glycocalyx

A

Inflammatory response, leukocyte adhesion to the endothelium, and inhibition of platelet aggregation

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93
Q

List 5 substances contained in Weibel-Palade bodies

A

Ultra large multimers of vWF, P-selectin, IL-8, tPA, fVIII

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94
Q

How are UL-vWF usually dealt with in health?

A

Quickly cleaved by ADAMTS13, a metalloproteinase and disintegrin-like with thrombospondin type 1 repeats

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95
Q

What is the function of UL vWF?

A

Bind platelet GP 1balpha receptors and initiate platelet tethering and activation; are more active for platelet adhesion and activation than smaller vWF multimers

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96
Q

How does tissue factor promote inflammation?

A

Through the activation of nuclear factor kB, leading to production of TNF-alpha

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97
Q

What happens to platelets upon activation?

A

Shuffle negatively charged phospholipids (phosphatidylserine and phosphatidylethanolamine) to the surface. These provide catalytic surface needed for tenase and prothrombinase complexes for the propagation phase of clot formation

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98
Q

With activation platelets greatly increase the number of copies of what on their surface?

A

Active fibrinogen receptor - glycoprotein IIbIIIa, aka integrin alphaIIb beta3

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99
Q

What are the contents of alpha and dense granules secreted when platelets are activated

A

Calcium, factor Va, serotonin, fibrinogen, P-selectin, and ADP. Feline alpha granules also release vWF

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100
Q

How does AT act?

A

To inhibit thrombin and fXa, lesser inhibitory effects on fIXa and the fVIIa-TF complex

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101
Q

How can AT activity be increased?

A

Heparins, or, in their absence, by binding to Thrombomodulin in the presence of thrombin

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102
Q

List the 3 mechanisms that can decrease AT in systemic inflammation

A

Consumption (due to thrombin generation), decreased production, degradation by neutrophil elastase

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103
Q

Where is TFPI found?

A

Endothelial cells, platelets, mononuclear cells, vascular smooth muscle, cardiac myocytes, fibroblasts and megakaryocytes

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104
Q

What is the function of the protein C system?

A

Important inhibitor of fVa and fVIIIa

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105
Q

How is protein C activated?

A

When trace amounts of thrombin bind TM located on the endothelium, predominantly in microcirculation; accelerated in presence of EPCR and cofactor protein S

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106
Q

What 3 electrolyte abnormalities might be expected with massive transfusion?

A

Hypocalcemia, hypomagnesemia, and hyperkalemia

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107
Q

What hemostatic defects might be associated with massive transfusion?

A

Thrombocytopenia, secondary dilutional coagulopathy, and hypofibrinogenemia

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108
Q

Other than electrolyte and hemostatic abnormalities, list 4 other abnormalities associated with massive transfusion

A

Metabolic acidosis, TRALI, hypothermia, immunosuppression, other transfusion reactions, transmission of infectious diseases

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109
Q

Describe how massive transfusion causes hypocalcemia and hypomagnesemia

A

Citrate (anticoag added to blood products) binds rapidly to Ca and Mg with equal affinity resulting in decreases in iCa and iMg. ICa reported to resolve quickly once perfusion is restored as citrate is rapidly metabolized by the liver

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110
Q

When is treatment with calcium glauconate indicated in regards to massive transfusion?

A

When hypocalcemia is severe or when hypotension, muscle tremors, arrhythmias, or prolonged QT interval are present

111
Q

What causes hyperkalemia associated with massive transfusion?

A

K levels rise over time d/t inactivation of Na-K-ATPase pumps by cold storage temperatures (less likely in dogs due to lower intracellular K stores). More likely K leakage from damaged tissues, extra cellular K shift secondary to acidosis, and reduced K excretion from oliguria

112
Q

What is the cause of thrombocytopenia associated with massive transfusion?

A

Blood loss and dilution (blood products devoid of platelets after 2 days due to cold storage temperatures causing cell oxidation and death

113
Q

Why is thrombocytopenia from dilution generally less severe than what would be predicted by the degree of dilution?

A

Platelets are released from stores in the lungs and spleen

114
Q

Other than dilution, list 2 other causes of thrombocytopenia related to MT

A

Consumption of platelets and clotting factors (secondary to shock, sepsis, SIRS, blunt trauma); platelet dysfunction resulting from acidosis or hypothermia

115
Q

Hemostasis is generally maintained as long as clotting factors are at least _____% of normal and PT and aPTT are not prolonged above ______.

A

30%; 1.5 times normal

116
Q

Loss and replacement of 1 blood volume removes ______% of circulating factors in plasma

A

Slightly less than 70%

117
Q

Acute coagulopathy of trauma is believed to result from what?

A

Altered coagulation enzyme activity, hyperfibrinolysis, and release of activated protein C secondary to tissue hypoperfusion, tissue injury, and acidosis.

118
Q

Ratios of FFP/platelet to RBC ratios of what have been associated with decreased mortality in human patients?

A

Increased (at least 2:1, up to 1:1)

119
Q

Describe 2 ways hypothermia can lead to coagulopathy in MT

A

Inactivates the enzymes that initiate the intrinsic and extrinsic coag cascades and to enhance fibrinolysis. Severe hypothermia can result in decreased platelet activity.

120
Q

What is the ‘bloody viscous cycle’ being recognized increasingly in human medicine as a leading cause of death after blunt trauma?

A

Progressive hypothermia, persistent acidosis, and inability to establish hemostasis

121
Q

What are the 3 definitions of massive transfusion?

A
  1. Transfusion of > 1 blood volume of blood or blood products within a 24 hour period2. Transfusion of 1/2 estimated blood volume in 3-4 hours3. Administration of 1.5 ml/kg/min of blood products over a period of 20 minutes
122
Q

List the factor numbers and their descriptive names

A

I-fibrinogenII-prothrombinIII-tissue factorV- labile factorVII- proconvertinVIII- antihaemophilic factorIX- Christmas factorX- Stuart prower factorXI- plasma thromboplastin antecedentXII- hageman factorXIII fibrin-stabilizing factor, prekallikrein (fletcher factor), HMWK (fitzgerald factor)

123
Q

What is the plasma half life of factor II?

A

65 hrs

124
Q

what is the half life of factor VII?

A

5 hrs

125
Q

what is the half life of factor IX?

A

25 hrs

126
Q

what is the half life of factor X?

A

40 hrs

127
Q

what is the half life of factor I?

A

90 hrs

128
Q

what is the half life of factor V?

A

15 hrs

129
Q

what is the half life of factor VIII?

A

10 hrs

130
Q

what is the half life of factor XI?

A

45 hrs

131
Q

what is the half life of factor XIII?

A

200 hrs

132
Q

which coagulation factors require vitamin K for synthesis and Ca2+ for activation?

A

II, VII, IX, X

133
Q

What is the role of endothelin?

A

It promotes vasoconstriction and decreases local blood flow

134
Q

What substances other than tissue plasmin activator, act as plasminogen activators?

A

urokinasebradykininkallikreinsoluble fibrin (non cross linked)

135
Q

When are D-Dimers produced?

A

Plasmin cleaves cross-linked fibrin into x-oligomers that are then broken down into D-dimers. They are only produced with active coagulation and subsequent fibrinolysis

136
Q

What are the three main mechanisms that limit thrombus formation?

A

Antithrombin
Protein C
Fibrinolytic system

137
Q

What anticoagulant substances are synthesized by the intact endothelium?

A

ThrombomodulinProtein SHeparan sulfateTissue factor pathway inhibitor

138
Q

Where is tissue factor pathway inhibitor synthesized?

A

LiverEndothelial cells

139
Q

Name 5 causes of endothelial disruption that may result in thrombus formation

A

SepsisSystemic inflammatory diseaseHeartwormNeoplasiaTraumaShockIV catheterizationReperfusion injury

140
Q

Name 5 conditions that may lead to abnormal blood flow and subsequent thrombus formation

A

Vascular obstructionCardiomyopathyEndocarditisCHFShockHypovolemiaProlonged recumbencyHyperviscosityHypoviscosityAnatomic abnormality

141
Q

Name 5 conditions that may lead to increased coagulability and subsequent thrombus formation

A

PLNCushingsIMHAPancreatitisPLESepsisNeoplasiaDICHeart disease

142
Q

Why are animals with PLE less prone to clot formation than animals with PLN?

A

PLE also causes loss of AT however they cause a concurrent loss of larger proteins maintains more of a balance between procoagulant and anticoagulant factors

143
Q

Other than obstructing flow in a vessel, what other local effects do thromboemboli have?

A

They release vasoactive substances (thromboxane A2 and serotonin) that induce vasoconstriction and compromise collateral blood flow development around the obstructed vessel

144
Q

Sonoclot ACT correlates with what on TEG

A

R time, K time, angle

145
Q

CR on sonoclot correlates with what on TEG

A

all parameters

146
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

147
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

148
Q

What 3 variables determined on Sonoclot

A

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

149
Q

What does CR measure on Sonoclot?

A

rate of fibrin formation

150
Q

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

A

T

151
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 VIIIathrombomodulin from endothelium

152
Q

MOA TFPI

A

inhibits extrinsic pathwayTFPI from endothelium

153
Q

What is the initiation stage of coagulation?

A

TF-VIIa makes a small amount of thrombin

154
Q

What is the prothrombinase complex?

A

Va-Xa

155
Q

What is the tenase complex?

A

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

156
Q

Antithrombin inhibits what factors?

A

2, 7, 9, 10, 11, 12

157
Q

What dramatically increases AT activity?

A

heparan sulfate from endothelial cells (or heparin exogenously)

158
Q

Effects of plasmin.

A

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

159
Q

What are inhibitors of plasmin generation

A

a2-antiplasmin, a-2 macroglobulin

160
Q

Heparin MOA

A

Facilitates AT-mediated inactivation of thrombin and factor Xa (also 7, 9, 11, 12)Facilitates release of TFPI from endothelial cellsPS binds to heparin-binding domain of endothelial cell matrix protein, thrombospondinInhibits complement and hemolysis induced thrombin generation

161
Q

How do you monitor heparin therapy?

A

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

162
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)

163
Q

How do you monitor LMWH (enoxaparin, dalteparin)?

A

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

164
Q

What is the vWF platelet receptor?

A

Gb1b-IX-V

165
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)

166
Q

How many platelets are in PRP and PC?

A

> 100 x 10^9/L

167
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

168
Q

Immunologic reactions to blood

A

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

169
Q

Virchows triad

A

blood stasis, hypercoagulable state, endothelial damage

170
Q

What coag factors increased in cushings?

A

5, 10, fibrinogen

171
Q

What IL stimulates TF?

A

6 - predominantly

172
Q

Where does heparan sulfate come from?

A

endothelial cells

173
Q

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

A

prostacyclin I2 and NF-kB

174
Q

Negatively charged proteins on platelet surfaces when activated.

A

phosphatidylserine and phosphatidylethanolamine

175
Q

What lives in Weibel Palade bodies

A

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

176
Q

What activates endothelial cells?

A

TNFa, bradykinin, thrombin, histamine, VEGF

177
Q

What is the prothrombinase complex?

A

Va and Xa and prothrombin (II)

178
Q

Feline platelet alpha granules have what that is special…

A

vWF (not in dog alpha granules)

179
Q

What supports decrease in fibrinolysis?

A

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

180
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

181
Q

G =

A

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

182
Q

Anticoagulant effects of aPC

A

inactivates Va and VIIIaenhances fibrinolysis

183
Q

Antiinflammatory effects of aPC

A

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

184
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

185
Q

PAI-1 upregulated by

A

TNF-a and CRP

186
Q

What is usually elevated with chronic end stage liver dz?

A

fVIII and vWF

187
Q

What does thrombomodulin do?

A

activates protein C

188
Q

Where is thrombomodulin at?

A

endothelial cells - its a transmembrane protein

189
Q

What converts plasminogen to plasmin?

A

fibrin

190
Q

What are antifibrinolytic drivers?

A

PAI-1, TAFI

191
Q

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

A
  1. Portal hypertension causing hemodynamic alterations2. Endothelial dysfxn3. Development of endogenous heparin-like substances from bacterial infection4. Renal failure
192
Q

What are the PAR receptors?

A

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

193
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

194
Q

TRALI

A

Occurs within 2-6 h of blood product, no pre-existing ALI, and no temporal relationship to alternative risk factors for ALIDue to anti-leukocyte antibodies, resolves rapidly, low mortality

195
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 riskRisk increased with transfusion of plasma-rich products, frozen plasma, and platelets, than transfusion with pRBC

196
Q

Massive tranfusion risk of…

A

ARDS/ALI

197
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)
198
Q

What accumulates in stored blood?

A

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

199
Q

Leukoreduction helps to prevent..

A

delayed TRALI

200
Q

Plateletpheresis yield

A

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

201
Q

DMSO cryopreserved platelets yield

A

50%, half life 2 days

202
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 donorReduces exposure of recipient to multiple donors

203
Q

Platelets in PC?

A

8 x 10^10 per PC unit

204
Q

Donor concern for plateletpheresis

A

citrate toxicity, hypocalcemia

205
Q

How long can FWB be stored?

A

8 h

206
Q

How long can PC and PRP be stored?

A

5 d at 22 C with gentle agitation

207
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

208
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 plateletGalactosylation decreases

209
Q

What is thrombosol?

A

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

210
Q

DMSO platelet half life

A

2 d, vs. 3.5 d for fresh platelets

211
Q

DMSO plt storage life

A

1 year

212
Q

pRBC mechanism for the role in hemostasis

A
  1. dispersion of platelets to periphery2. increase plt contact with endothelium3. release ADP4. scavenge NO (which inhibits plts)5. increase production of TXA2 by platelets at bleeding site
213
Q

FWB contains how many platelets?

A

10 x 10^9 /L

214
Q

Methods to decrease lymphocytotoxic antibodies.

A

leukoreductionultraviolet B irradiation

215
Q

What diseases are most common in cats with DIC

A

cancer, pancreatitis, sepsis

216
Q

What % cats have hemorrhage with DIC?

A

15%

217
Q

Other findings, DIC cats, JVIM 2009.

A

All DIC cats had high PTTMedian PT of nonsurivors * higher than survivorsNo effect of heparin or transfusion on outcomeMost cats died or euth (7% survival)

218
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.

219
Q

Half life of factor VII

A

6.2 h

220
Q

Half life of factor II (prothrombin)

A

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

221
Q

TFPI inhibits…

A

VIIa and XaTFPI lives in endothelial cells and platelets

222
Q

What effect does LPS have on monocytes related to coagulation?

A

De novo synthesis of TF on surface

223
Q

P-selectin

A

tethers platelets to surfaces
P-selectin + PSGL-1 (leukocytes binding)

224
Q

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

A

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

225
Q

vWF platelet receptor

A

GP 1b-V-IX

226
Q

collagen platelet receptor

A

GPVI

227
Q

thrombin platelet receptors

A

PAR-1 and PAR-4

228
Q

Alpha 2b Beta3 receptor antagonists

A

abciximabeptifibatidetirofiban

229
Q

Drug that blocks PAR1 receptor

A

vorapaxar and atopaxar

230
Q

Drugs that block P2Y12 receptor by blocking ADP from binding

A

thienopyridines (prodrugs): clopidogrel, prasugrel, ticlodipineirreversible: ticagrelorreversible: cangrelor

231
Q

Endothelial prostaglandins

A

PGD2, PGE2, PGF2, PGI2

232
Q

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

A

166Xvia acetylation of Ser529 preventing binding of AA to catalytic site on COX-1

233
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

234
Q

Clopidogrel action decreased by what drug?

A

PPIs - omeprazole

235
Q

Replacement of chlorine with ___ enhances prasugrels action.

A

fluorine

236
Q

What drug class is ticagrelor in?

A

cyclopentyltriazolopyrimidine

237
Q

Picotamide MOA

A

dual inhibitor of TxA2 receptors and TxA2 synthesis

238
Q

20% of blood content of FV is where

A

alpha granules

239
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

240
Q

Protease inhibitors TFPI and ATIII are always present bound to…

A

heparan sulfates on endothelial surfaces

241
Q

TFPI inhibits

A

Xa and VIIa

242
Q

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

A

VII (about 1% VIIa)

243
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 fibrinolysis2. activates Protein C which then binds cofactor Protein S to inactivate Va and VIIIa
244
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

245
Q

Recommended heparin levels for anticoagulation

A

0.35-0.7 U/ml

246
Q

aPTT goal with heparin

A

1.5-2 X baseline

247
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

248
Q

Extrinsic platelets disorders are characterized by a lack of a functional protein needed for what?

A

Platelet adhesion and aggregation

249
Q

Name the most common thrombocytopathy in dogs

A

Von Willebrands

250
Q

What contacts more von willebrand factor, platelets or endothelial cells?

A

endothelial cells (richest source of vwb)

251
Q

How many forms of von willebrands are there?

A

3

252
Q

describe type 1 von willebrands

A

quantitative reduction in vWF - all multimers are present. however the concentration is less than needed for hemostasis

253
Q

Describe type 2 von willebrands

A

measurable reductions in vWF, but the subset of large multimers is scant. This causes qualitative reduction in vWF because the large multimers are essentials for hemostasis

254
Q

Describe type 3 von willebrands

A

Absolute lack of vWF all together

255
Q

Clinical signs of vWF disease

A

Mucosal bleeding (epistaxis, melena, hematuria, gingival hemorrhage) or excessive cavity bleeding

256
Q

T/F - Petechia and ecchymosis in dogs with von willebrands is common

A

false

257
Q

What is the best in vivo diagnostic for primary hemostasis

A

buccal mucosal bleeding time BMBT

258
Q

Normal BMBT times are less than ______

A

3 minutes

259
Q

Which blood products are recommended to treat von willebrands

A

plasma containing VWF (fresh frozen plasma, cryoprecipitate or fresh whole blood)

260
Q

T/F - Patients with Chediak higashi syndrome have a normal number of platelets

A

true - these patients have prolonged bleeding time in the presence of normal platelet concentrations

261
Q

Describe the platelet defect in Chediak Higashi Syndrome

A

Patients with CHS have altered lysosomalgranuale formation, and abnormal degranulation in neutrophils/platelets. Because of this, aggregation to collagen is absent.

262
Q

Describe the primary defect in patients with Glanzmanns thrombasthenia

A

Primary defect leads to a deficiency in the number of the alpha 2b beta 3 integrin. Prolonged bleeding time occurs because of the lack of fibrinogen beinding to this integrin.

263
Q

Describe the mechanism behind the platelet membrane disorder in greater swiss mountain dogs

A

mutation is presnt on P2y12 receptor which prevents activation via ADP induced outside in signaling for fibrinogen binding on the platelet surface

264
Q

How does clopidogrel work

A

Clopidogrel blocks ADP from binding at the P2Y12 receptor - reducing platelet activation

265
Q

In which breed do we most often see Canine Scott Syndrome

A

German shepherd dogs

266
Q

Describe the mechansim behind Canine Scott Syndrome

A

Defect lies in the inability for phosphatidylserine to be externalied from the creation of a procoagulant surface

267
Q

Name the inherited autosomal recessive platelet defect seen in Cavaliers

A

Idiopathic asymptomatic macrothrombocytopenia

268
Q

Describe the mutation in idiopathic asymtopmatic macrothrombocytopenia

A

A mutation in B1 tubulin leads to altered proplatelet formation in megakaryocytes

269
Q

In humans, acquired von willebrands disease can occur through what mechanisms

A

autoimmune disease, increased shear-induced proteolysis of vWF (cardiovascualr lesions/pulmonary hypertension, etc), or increased binding of vWF to platelets on other cell surfaces

270
Q

In humans, name three drugs that can cause acquired von willebrands

A

ciprfloxacin, griseofulvin, valproic acid

271
Q

Name two molecules in the blood of uremic patients that become increased, resulting in altered vascualr tone and platelet function

A

nitric oxide and prostacylin

272
Q

Recommended dosing of cryoprecipitate for dogs with clinical bleeding secondary to von willebrands dsiease

A

1 unit/10 kg IV

273
Q

Recommended dosing of fresh frozen plasma

A

10-20mL/kg IV

Auburn ECC (26 decks)

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