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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
Q

What are the pharmacological inhibitors of secondary haemostasis and how do they act?

A

Heparin - potentiates AT activity
Warfarin - inhibits vitK recycling

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26
Q

Describe fibrinolysis

A

BSAVA Clin Path pg 100

27
Q

Where is plasminogen produced?

A

Liver

28
Q

What is the most potent activator of TPA and where is it produced?

A

FXIIa/kallikrein complex - weak plasminogen activators
- cleaves HMW kinogen => bradykinin

29
Q

What is the main physiological inhibitor of fibrinolysis?

A

Thrombin-activated fibrinolytic inhibitor (TAFI)
Plasminogen activator inhibitor-1
Antiplasmin

30
Q

What changes are seen on a CBC during active thrombopoeisis?

A

^ MPV

31
Q

What factors can cause an elevated MPV?

A

Storage (particularly at 4oC)
Clumping
Can be normal in cats
Inherited - CKCS, Norfolk Terrier, Cairn Terrier
BM neoplasia

32
Q

How if vWF:Ag interpreted?

A

> 70% - vWD unlikely
50-70% - vWD possible, bleeding unlikely
<50% - vWD likely
<35% - vWD likely, bleeding likely

33
Q

What are the normal BMBT ranges?

A

D - 1.7-3.3 mins (4.2 minutes if sedated or GA)
C - <3.3 mins

34
Q

What can lead to elevated BMBT?

A

Thrombocytopenia (inherited or acquired - aspirin/azotaemia), vWD, thrombopathia

35
Q

What can lead to an elevated closure time on a PFA-100?

A

Thrombocytopenia (weak correlation with plt count)
Drug - associated thrombopathia (not reliable)
vWD - severe only
Thrombopathia

36
Q

What factors can interfere with PFA-100 results?

A

Low hct - prolong
High hct - shorten
Citrate concentration

37
Q

What is assessed by the ACT?
How does it work?
What causes it to be elevated?

A

Intrinsic and common pathways
Contact with negatively charged surface activates FXII
Rodenticide, DIC, inherited defects (haemophilia A/B), severe thrombocytopenia (mild)

38
Q

What is assessed by the PT?
How does it work?
What causes it to be elevated?

A

Extrinsic and common pathways
Exogenous TF
Rodenticide, heparin, DIC, (angiostrongylus), liver failure, hypofibrinogenaemia (DIC/liver failure)
Activation of clotting during sampling

39
Q

What is assessed by the aPTT?
How does it work?
What causes it to be elevated?

A

Intrinsic and common pathways
Contact activators
Rodenticide, heparin, DIC, (angiostrongylus), liver failure, hypofibrinogenaemia (DIC/liver failure)
Activation of clotting during sampling

40
Q

What is assessed by the TCT?
How does it work?
What causes it to be elevated?

A

Fibrinogen => Fibrin
Thrombin
Hypofibrinogenaemia/afibrinogenaemia - DIC, liver failure
Dysfibrinogenaemia - reported with liver disease
Heparin
Elevated FDPs, monoclonal gammopathy

41
Q

Which test becomes abnormal first in rodenticide toxicity?

A

PT

42
Q

What can lead to reduced AT levels?

A

Liver failure
DIC
PLE/PLN
Inflammation (negative APP)
L-asparaginase
Heparin

43
Q

What is the action of protein C?

A

Inhibits the intrinsic tenase complex

44
Q

What can lead to low protein C?

A

Liver disease (failure, EHBO, PSS)
DIC
Vit K deficiency
Inflammation

45
Q

How is D-dimer interpreted?

A

Produced by cross-linked fibrin
Elevated levels = increased thrombin = hyper coagulability

46
Q

What can lead to increased D-dimer?

A

Pathological
- internal haemorrhage
- hepatopathies, EHBDO
- many diseases
- DIC, thrombosis, hyper coagulability

Physiological
- post surgery

False
- haemolysis

47
Q

Draw a normal TEG trace with parameters measured included

A

BSAVA Clin Path pg 111
Should include R time, K time, Alpha angle, MA, LY30, LY60

48
Q

What changes would be seen on a hypocoagulable TEG trace?

A

^ R, K
v alpha, MA

49
Q

What changes would be seen on a hypercoagulable TEG trace?

A

v R, K
^ alpha, MA

50
Q

What changes would be seen on a hyperfibrinolytic TEG trace?

A

^ LY30/60

51
Q

What can interfere with TEG?

A

Time to analysis
HCT - low = hypercoagulable, high = hypo
High blood viscosity = hypercoagulable

52
Q

What drives platelet production?

A

Thrombopoietin
Produced in liver, kidney and BM

53
Q

What are the possible causes of thrombocytosis?

A

Drugs - adrenaline/vinc/steroids
Reactive - inflammatory cytokines (IL-1/6/11)
Iron deficiency
Megakaryocytic neoplasia

54
Q

What are the features of type I vWD?
Which breeds are predisposed?

A

Decreased quantity, normal structure
Dobermans, Manchester Terriers, Airedales, Rottweilers

55
Q

What are the features of type II vWD?
Which breeds are predisposed?

A

Decreased quantity, abnormal structure
Pointers

56
Q

What are the features of type III vWD?
Which breeds are predisposed?

A

Absolute vWF deficiency
Scottish Terriers, Shetland Sheepdogs, Chesapeake Bay Retrievers, Dutch Kooiker Dogs

57
Q

What is the most common inherited disorder of secondary haemostasis in dogs and cats?

A

D - Haemophilia A
C - Hageman trait (FXII)

58
Q

Which factors are deficient in Haemophilia A and B?

A

A - VIII
B - IX

59
Q

What coagulation testing abnormalities are seen with Haemophilia A and B?

A

Prolonged aPTT

60
Q

How do rodenticide anticoagulants work?

A

Inhibit vitamin K epoxide reductase
Prevents recycling of Vit K - vit K epoxide accumulates => relative vit K deficiency

61
Q

What coagulation tests are abnormal with rodenticide anticoagulants?

A

PT - increases first
aPTT and ACT also elevated

62
Q

What confirmatory tests are available for rodenticide anticoagulant toxicity?

A

Toxicology
Vit K epoxide:it K ratio

63
Q

What is the mechanism of vitamin K deficiency in liver disease?

A

Vit K fat soluble - bile needed tor absorption, absent in cholestatic liver disease

64
Q

What is the abnormality in Scott syndrome?
How is it diagnosed?
How is it treated?

A

Inability to exteriorise PS
Flow cytometry for surface PS
Transfusion therapy

BSAVA Clin Path (25 decks)

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