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BSAVA Clin Path > Chapter 6 > Flashcards

Chapter 6 Flashcards

1
Q

What are the initiators of haemostasis?

A

Tissue factor (FIII)
Extracellular matrix proteins (collagen)

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2
Q

What are the 3 stages of haemostasis and what do they involve?

A

Primary - platelet plug
Secondary - formation of fibrin
Tertiary - fibrinolysis

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3
Q

What are the main cells, facilitators and inhibitors of primary haemostasis?

A

Platelets
F - vWF, collagen, fibrinogen
I - ADPase, prostacyclin, NO

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4
Q

What are the main cells, facilitators and inhibitors (initiation and progression) of secondary haemostasis?

A

Initiation
Fibroblasts
F - tissue factor, FVII
I - tissue factor pathway inhibitor

Progression
Platelets
F - Thrombin, intrinsic and common pathway factors
I - Antithrombin, protein C, protein S

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5
Q

What are the main cells, facilitators and inhibitors of tertiary haemostasis?

A

Endothelial cells
F - plasminogen, tissue plasminogen activator
I - TAFI, antiplasmin, plasminogen activator inhibitor-1

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6
Q

Where is vWF produced/stored?

A

Endothelial cells, stored in Weibel-palade bodies

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7
Q

Explain primary haemostasis

A

BSAVA Clin Path pg 95

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8
Q

What are the tests of primary haemostasis?

A

Platelet count, BMBT, PFA

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9
Q

Explain secondary haemostasis

A

BSAVA Clin path pg 98

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10
Q

What are the 3 stages of secondary haemostasis?
What cells are responsible for each step?

A

Initiation (fibroblasts), amplification (platelets), propagation (platelets)

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11
Q

What activates the extrinsic pathway?

A

TF - binds FVII (requires Ca and PS)

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12
Q

What activates the intrinsic pathway?

A

Surface contact - activates FXII

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13
Q

What activates the common pathway?

A

Intrinsic tenase - FIXa-FVIIIa-PS-Ca
Extrinsic tenase - TF-VIIa-PS-Ca

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14
Q

What is the prothrombinase complex?

A

FXa-FVa-PS-Ca

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15
Q

What is FXIII? What activates it?

A

Cross links fibrin
Activated by thrombin

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16
Q

What are the vit K - dependent coagulation factors?

A

FII, VII, IX, X
Protein C+S

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17
Q

What is the ‘alternative’ pathway

A

TF-FVII complex of extrinsic pathway can activate FIX of intrinsic pathway

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18
Q

What are the roles of thrombin in coagulation?

A

Fibrin formation
Amplification - activates FXI and intrinsic pathway
Activates FXIII and cross linking of fibrin
Activates TAFI - prevents fibrinolysis

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19
Q

What are the anti-platelet medications and their mechanisms of action?

A

Aspirin/NSAIDs - inhibit COX - prevents thromboxane A2 production
Clopidogrel - ADP receptor antagonist

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20
Q

What are the major physiological inhibitors of secondary haemostasis?

A

AT and protein C (intrinsic and common)
TFPI (extrinsic)

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21
Q

What are antithrombins targets?

A

FXa and thrombin

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22
Q

What activates protein C?

A

Thrombin binding to thombomodulin

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23
Q

What is protein S role in coagulation?

A

Cofactor - supports protein C and TFPI

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24
Q

Where are AT, protein C, protein S and TFPI produced?

A

Liver

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25
What are the pharmacological inhibitors of secondary haemostasis and how do they act?
Heparin - potentiates AT activity Warfarin - inhibits vitK recycling
26
Describe fibrinolysis
BSAVA Clin Path pg 100
27
Where is plasminogen produced?
Liver
28
What is the most potent activator of TPA and where is it produced?
FXIIa/kallikrein complex - weak plasminogen activators - cleaves HMW kinogen => bradykinin
29
What is the main physiological inhibitor of fibrinolysis?
Thrombin-activated fibrinolytic inhibitor (TAFI) Plasminogen activator inhibitor-1 Antiplasmin
30
What changes are seen on a CBC during active thrombopoeisis?
^ MPV
31
What factors can cause an elevated MPV?
Storage (particularly at 4oC) Clumping Can be normal in cats Inherited - CKCS, Norfolk Terrier, Cairn Terrier BM neoplasia
32
How if vWF:Ag interpreted?
>70% - vWD unlikely 50-70% - vWD possible, bleeding unlikely <50% - vWD likely <35% - vWD likely, bleeding likely
33
What are the normal BMBT ranges?
D - 1.7-3.3 mins (4.2 minutes if sedated or GA) C - <3.3 mins
34
What can lead to elevated BMBT?
Thrombocytopenia (inherited or acquired - aspirin/azotaemia), vWD, thrombopathia
35
What can lead to an elevated closure time on a PFA-100?
Thrombocytopenia (weak correlation with plt count) Drug - associated thrombopathia (not reliable) vWD - severe only Thrombopathia
36
What factors can interfere with PFA-100 results?
Low hct - prolong High hct - shorten Citrate concentration
37
What is assessed by the ACT? How does it work? What causes it to be elevated?
Intrinsic and common pathways Contact with negatively charged surface activates FXII Rodenticide, DIC, inherited defects (haemophilia A/B), severe thrombocytopenia (mild)
38
What is assessed by the PT? How does it work? What causes it to be elevated?
Extrinsic and common pathways Exogenous TF Rodenticide, heparin, DIC, (angiostrongylus), liver failure, hypofibrinogenaemia (DIC/liver failure) Activation of clotting during sampling
39
What is assessed by the aPTT? How does it work? What causes it to be elevated?
Intrinsic and common pathways Contact activators Rodenticide, heparin, DIC, (angiostrongylus), liver failure, hypofibrinogenaemia (DIC/liver failure) Activation of clotting during sampling
40
What is assessed by the TCT? How does it work? What causes it to be elevated?
Fibrinogen => Fibrin Thrombin Hypofibrinogenaemia/afibrinogenaemia - DIC, liver failure Dysfibrinogenaemia - reported with liver disease Heparin Elevated FDPs, monoclonal gammopathy
41
Which test becomes abnormal first in rodenticide toxicity?
PT
42
What can lead to reduced AT levels?
Liver failure DIC PLE/PLN Inflammation (negative APP) L-asparaginase Heparin
43
What is the action of protein C?
Inhibits the intrinsic tenase complex
44
What can lead to low protein C?
Liver disease (failure, EHBO, PSS) DIC Vit K deficiency Inflammation
45
How is D-dimer interpreted?
Produced by cross-linked fibrin Elevated levels = increased thrombin = hyper coagulability
46
What can lead to increased D-dimer?
Pathological - internal haemorrhage - hepatopathies, EHBDO - many diseases - DIC, thrombosis, hyper coagulability Physiological - post surgery False - haemolysis
47
Draw a normal TEG trace with parameters measured included
BSAVA Clin Path pg 111 Should include R time, K time, Alpha angle, MA, LY30, LY60
48
What changes would be seen on a hypocoagulable TEG trace?
^ R, K v alpha, MA
49
What changes would be seen on a hypercoagulable TEG trace?
v R, K ^ alpha, MA
50
What changes would be seen on a hyperfibrinolytic TEG trace?
^ LY30/60
51
What can interfere with TEG?
Time to analysis HCT - low = hypercoagulable, high = hypo High blood viscosity = hypercoagulable
52
What drives platelet production?
Thrombopoietin Produced in liver, kidney and BM
53
What are the possible causes of thrombocytosis?
Drugs - adrenaline/vinc/steroids Reactive - inflammatory cytokines (IL-1/6/11) Iron deficiency Megakaryocytic neoplasia
54
What are the features of type I vWD? Which breeds are predisposed?
Decreased quantity, normal structure Dobermans, Manchester Terriers, Airedales, Rottweilers
55
What are the features of type II vWD? Which breeds are predisposed?
Decreased quantity, abnormal structure Pointers
56
What are the features of type III vWD? Which breeds are predisposed?
Absolute vWF deficiency Scottish Terriers, Shetland Sheepdogs, Chesapeake Bay Retrievers, Dutch Kooiker Dogs
57
What is the most common inherited disorder of secondary haemostasis in dogs and cats?
D - Haemophilia A C - Hageman trait (FXII)
58
Which factors are deficient in Haemophilia A and B?
A - VIII B - IX
59
What coagulation testing abnormalities are seen with Haemophilia A and B?
Prolonged aPTT
60
How do rodenticide anticoagulants work?
Inhibit vitamin K epoxide reductase Prevents recycling of Vit K - vit K epoxide accumulates => relative vit K deficiency
61
What coagulation tests are abnormal with rodenticide anticoagulants?
PT - increases first aPTT and ACT also elevated
62
What confirmatory tests are available for rodenticide anticoagulant toxicity?
Toxicology Vit K epoxide:it K ratio
63
What is the mechanism of vitamin K deficiency in liver disease?
Vit K fat soluble - bile needed tor absorption, absent in cholestatic liver disease
64
What is the abnormality in Scott syndrome? How is it diagnosed? How is it treated?
Inability to exteriorise PS Flow cytometry for surface PS Transfusion therapy

BSAVA Clin Path (25 decks)

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