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Lymphoreticular and haematopoetic > Disorders of Platelets and Coagulation > Flashcards

Disorders of Platelets and Coagulation Flashcards

1
Q

What are endothelial cells?

A

Flattened cells that line blood vessels and have pro and anticoagulant properties

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2
Q

What are the functions of endothelial cells?

A

Normally anticoagulant inhibiting coagulation and platelet aggregation
Act as a barrier to sub-endothelial collagen which is procoagulant

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3
Q

What produced Von Willebrand’s Factor (vWF)?

A

Endothelium and platelets

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4
Q

Where is vWF stored?

A

Weibel Palade bodies

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5
Q

Where is vWF located?

A

On sub-endothelial surface

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6
Q

When is vWF released and what is its function?

A

Early in the haemostatic process and is responsible for platelet adhesion to collagen

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7
Q

What do platelets look like?

A

Small discoid anuclear cells found in the circulation, 3-5um, pale basophilic with small red granules

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8
Q

Where do platelets originate from?

A

Megakaryocytes in the bone marrow during a process called thrombopoiesis

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9
Q

What mediates platelet production?

A

Thrombopoietin

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10
Q

How long do platelets circulate for?

A

5-9 days in most species

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11
Q

What is the functional structure of platelets?

A

Outer membrane has receptors important for adhesion and aggregation
Cytoplasm has actin and myosin allowing shape change

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12
Q

What are the two different types of granules in platelets?

A 
Alpha granules (red) that contain vWF, fibrinogen and factors V and VII
Dense granules which contain ADP and calcium
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13
Q

What glycoprotein receptors are associated with platelet membrane?

A

GP Ib binds vWF

GP IIbIIIa binds fibrinogen on adjacent platelets and allows platelets to aggregate

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14
Q

What happens if there are defects in receptors?

A

Abnormal platelet function and clot formation occurs

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15
Q

What is primary haemostasis?

A

Formation of the primary platelet plug

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16
Q

What is the first step in primary haemostasis?

A

Damage to the endothelium and exposure of sub-endothelial collagen results in vWF release

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17
Q

What is the second step in primary haemostasis?

A

Platelet adhesion occurs and platelets bind to collagen via receptor GP Ib and vWF from the endothelium

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18
Q

What is the third step in primary haemostasis?

A

Platelets undergo shape change and become spherical with filipodia which exposes additional GP Ib and GP IIbIIIa

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19
Q

What is the fourth step in primary haemostasis?

A

Platelets bind fibrinogen via GP IIbIIIa between adjacent platelets forming a clump/aggregate of platelets

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20
Q

Where is fibrinogen generated from?

A

Coagulation cascade

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21
Q

What is the fifth step in primary haemostasis?

A

Aggregating platelets rapidly degranulate releasing ADP, fibrinogen and vWF as well as thromboxane A2 from the platelet membrane which increase platelet adhesion and aggregation

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22
Q

What is the final step in primary haemostasis?

A

Platelets release factors V and VIII which are involved in coagulation

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23
Q

What is secondary haemostasis?

A

Activation of the coagulation cascade simultaneously with platelet plug formation

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24
Q

What are the different pathways the coagulation cascade split into?

A

Intrinsic, extrinsic and common pathways but only for lab testing purposes not in vivo

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25
Q

What is the function of the extrinsic pathway of coagulation cascade?

A

Initiates coagulation cascade and is most important in vivo

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26
Q

What is the process of extrinsic pathway of coagulation cascade?

A

Tissue factor is released from damaged tissue binds to and activates FVII in the presence of calcium
TFFVII complex activates FX of the common pathway and FIX of the intrinsic pathway

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27
Q

What is the function of the intrinsic pathway of the coagulation cascade?

A

Amplifies the coagulation cascade

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28
Q

What is the process of intrinsic pathway of the coagulation cascade?

A

FXII is activated by contact with a negatively charged surface (co factor HMWK)
Activated FXII cleaves and activates FXI which in turn activates FIX which requires calcium
Activated FIX in turn activates FX of the common pathway

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29
Q

What is the process of the common pathway of the coagulation cascade?

A

Starts with activation of FX which binds activated FV and calcium on the platelet surface which converts prothrombin (FII) to thrombin (FIIa)
Thrombin converts fibrinogen (FI) to fibrin (FIa) and fibrin is cross-linked by activated FXIII

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30
Q

What is the importance of inhibitors of coagulation?

A

Required for a balanced clotting reaction only where it is required

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31
Q

What is the function of antithrombin III?

A

Inhibits thrombin and activated FX and is increased by heparin from the endothelium

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32
Q

What is the function of protein C?

A

Inactivates FV and FVIII

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33
Q

What is the process of fibrinolysis?

A

Enzymatic breakdown of fibrin by plasmin which is derived from plasminogen found in the platelet membrane and plasma

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34
Q

What does plasmin do?

A

Degrades both fibrinogen and fibrin to produce fibrin degredation products (FDPs)

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35
Q

How is platelet concentration calculated?

A

Automated count that can be done on platelets collected into EDTA as part of a CBC

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36
Q

In which species is platelet concentration inaccurate? Why?

A

Cats, sheep and goats as there is an overlap between RBC and platelet size

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37
Q

What other artefact can cause platelet concentration calculation inaccuracies?

A

Platelet clumps

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38
Q

In which species is an estimated platelet count from blood smear recommended?

A

Cats and CKCS

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39
Q

How few platelets indicate thrombocytopaenia?

A

< 100x10^9/L

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40
Q

How low do platelet numbers need to be for spontaneous haemorrhage to occur?

A

25x10^9/L

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41
Q

How many platelets do patients need to be diagnosed with thrombocytosis?

A

> 1000x10^9/L

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42
Q

What is the risk of thrombocytosis?

A

Increased risk of thrombi forming

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43
Q

What is measured in buccal mucosal bleeding time?

A

Length of time for a platelet plug to form evaluated primary haemostasis and platelet formation

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44
Q

How is a buccal mucosal bleeding time calculated?

A

Using a spring loaded cassette to make a small incision in the buccal mucosa and blood is blotted until bleeding stops

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45
Q

In which diseases is the buccal mucosal bleeding time altered?

A

Decreased in thrombocytopaenia

Prolonged with von Willebrands disease and disorders of platelet function

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46
Q

What can happen if platelet numbers are decreased or their function is impaired?

A

Haemorrhage in the form of eccymoses or petechiae

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47
Q

What can cause thrombocytopaenia?

A

Immune-mediated thrombocytopenia
Increased consumption
Decreased production due to bone marrow disease, neoplasia or drugs
Infection with FeLV, BVD, Ehrlichia and Leishmania
Sequestration is rare but may occur with splenomegaly/large cavitated mass

48
Q

What is the most common cause of thrombocytopaenia?

A

Immune-mediated thrombocytopaenia with numbers reaching below 10x10^9/L
Megakaryocytes in the bone marrow may also be affected

49
Q

What is Eva’s syndrome?

A

Concurrent immune-mediated thrombocytopaenia and anaemia

50
Q

What can cause immune-mediated thrombocytopaenia?

A

Primary, other immune disease, drugs, vaccine, neoplasia or infection

51
Q

What are the clinical findings of immune-mediated thrombosytopaenia?

A

Profound thrombocytopenia, petechial/eccymotic haemorrhage, beeding from gums/mucosal surfaces/prolonged bleeding from wounds

52
Q

How is immune-mediated thrombocytopaenia diagnosed?

A

Diagnosis of exclusion but can use bone marrow examination, anti-platelet antibodies and response to treatment

53
Q

What signs are seen if thrombocytopaenia due to haemorrhage?

A

Evidence of haemorrhage either into a cavity or out of the body
Numbers shouldn’t be lower than 100x10^9/L

54
Q

What is seen if thrombocytopaenia is due to DIC?

A

Numbers can be very low with concurrent signs of another coagulation defect so need to check PT, PTT to see if increased and see if FDPs are increased

55
Q

What is Glanzmann’s thrombasthenia?

A

Defect in GP IIbIIIa found in Otterhounds, Great Pyrenees and Quarter Horses causing defective platelet aggregation and abnormal clot retraction

56
Q

What is Canine thrombopathia?

A

Abnormal GP IIbIIIa exposure and impaired degranulation in Basset Hounds

57
Q

What is Bovine Thrombopathia?

A

Occurs in Simmentals causing mild to severe bleeding although the exact defect isn’t known

58
Q

What causes physiological thrombocytosis?

A

Transient increase due to epinephrine induced splenic contraction

59
Q

What is reactive thrombocytosis?

A

Secondary increase due to increased thrombopoietin/IL-6 or inflammation, haemorrhage or iron deficiency

60
Q

What is essential thrombocythemia?

A

Myeloproliferative disorder causing a marked persistent increase in platelets
Bone marrow megakaryocytes are increased and may have abnormal morphology
Function of platelets is variable as may see petechiae and eccymoses or thrombosis
TPO levels normal or increased

61
Q

What is vWF?

A

A plasma glycoprotein needed for platelet adherence to collagen and formation of primary haemostatic plug

62
Q

How does vWF circulate?

A

Bound to factor VII which is protective against accidental activation and can see concurrent disease in factor VII

63
Q

What are the different multimers of vWF?

A

There are three, small, medium and large with large being the most active in haemostasis

64
Q

What are the clinical signs of von Willebrands disease?

A

Mucosal bleeding as GI/epistaxis/haematuria, no petechiae (differentiates from other platelet disorders), prolonged buccal mucosal bleeding time without thrombocytopaenia, clotting times usually normal but PTT may be prolonged due to decrease in factor VII

65
Q

What animals has von Willedbrands disease been diagnosed in?

A

Most common in dogs and rare in cats, horses and pigs

66
Q

What is type I von Willebrands disease?

A

All multimers present but at decreased concentrations
Variable severity of bleeding but not until concentration of vWF are less than 20%
Accounts for 90% of cases especially in Dobermanns
Autosomal inheritance so equal males and females

67
Q

What is type II von Willebrands disease?

A

Qualitative abnormalities in vWF structure and function often with disproportionate decrease in large multimers
Severe and uncommon but seen in German shorthaired and wirehaired pointers with one horse case
Autosomal recessive

68
Q

What is type II von Willebrands disease?

A

Absence of all vWF multimers with less than 0.1%
Seen in Scottish Terriers, Chesapeake Bay retrievers, Shetland Sheepdogs and Dutch Kooiker
Autosomal recessive

69
Q

How do you perform a test to compare vWF:Ag ratio?

A

Collect blood into EDTA or citrate (dilution of 1:9)

Separate plasma immediately and send overnight with ice

70
Q

How is an ELISA used to diagnose von Willebrands disease?

A

Quantitative measurement of vWF using species specific antibodies with <50% considered decreased = carrier/affected

71
Q

How is immunophoresis used to diagnose von Willebrands disease?

A

Separates out relative amounts of different multimers and is required for diagnosis of type II disease

72
Q

How are carriers identified?

A

Genetic testing

73
Q

How is a vWF ELISA interpreted?

A

<35% = clinical disease
vWF:Ag 0% = type III disease
50-69% vWF:Ag = borderline, transmit but not affected
70-100% vWF:Ag = free from trait

74
Q

What is the treatment for vWF?

A

Transfusion to supply vWF using cryoprecipitate as 5-10 times greater concentration of vWF given at dose of 1U/10kg
Plasma given at 6-12 ml/kg if cryoprecipitate isn’t available and whole blood if anaemic as well

75
Q

What can be used prior to surgery to reduce risk of bleeding out?

A

Desmopressin for dogs with type I at a dose of 1ug/kg SQ 30 minutes prior to surgery
Also an intranasal preparation available

76
Q

What do most blood tests require blood to be collected in?

A

Citrated plasma with a ratio of anticoagulant:blood of 1:9 and filled up to the line

77
Q

Why should trauma whilst taking blood be reduced as far as possible?

A

Prevent activating platelets and coagulation

78
Q

How soon should serum be separated from blood?

A

Centrifuge within 1 hour and analyse within 4 hours or freeze it

79
Q

What colour are citrate tubes?

A

Blue, purple or green (always check for clots in lids and tubes)

80
Q

What is needed to calculate the activated clotting time (ACT)?

A

2ml of whole blood into an ACT tube containing diatomaceous earth and incubate for 60 seconds at 37C and check for clots every 5-10 seconds

81
Q

What does ACT test?

A

Intrinsic and common pathways

82
Q

How is the ACT interpreted?

A

ACT = time to initial signs of a clot

Similar to PTT but less sensitive and thrombocytopaenia will prolong

83
Q

What does PTT stand for?

A

Partial thromboplastin time

84
Q

What is it used to evaluate?

A

Intrinsic and common pathways of coagulation

85
Q

How is PTT performed?

A

Incubate citrated plasma with excess phospholipid, contact activator and calcium

86
Q

How is PTT interpreted?

A

Prolonged PTT indicates a defect in intrinsic (factors XII,XI,IX,VIII) or common pathways (X,V,II,fibrinogen)
Factor activity must be <30% of normal to prolong the PTT

87
Q

What causes a prolonged PTT?

A

Haemophilic (factors VIII or IX), factor XII deficiency, DIC, vitamin K deficiency and liver disease

88
Q

What pathology doesn’t affect the PTT?

A

Thrombocytopenia

89
Q

What does PT stand for?

A

Prothrombin time

90
Q

What does PT screen for?

A

Defects in extrinsic and common pathways of coagulation

91
Q

How is a PT performed?

A

Incubate citrated plasma with tissue thromboplastin (TF) and calcium and measure time to clot formation

92
Q

How is a PT interpreted?

A

Prolonged PT indicates defect in extrinsic (factor VII) or common pathways of coagulation
Factor activity must be <30% normal to prolong PT

93
Q

What causes a PT to be prolonged?

A

Factor VII deficiency, DIC, vit K deficiency and liver failure

94
Q

What test results are found in early vitamin K deficiency?

A

PT may be prolonged with a normal PTT

95
Q

What does specific factor analysis detect?

A

Specific factor deficiencies usually to detect hereditary deficiencies

96
Q

What does latex agglutination test evaluate? How is it performed?

A

Fibrinolysis

Special test kit using serum separated within 30 minutes and needs to be tested immediately or frozen

97
Q

What do increased FDPs indicate and what are they seen with?

A

Enhanced fibrinolysis and seen with DIC, haemorrhage, jugular vein thrombosis and liver disease

98
Q

What do D-dimers detect?

A

Plasmin mediated degradation of cross-linked fibrin = fibrinolysis

99
Q

What is the mechanism of vitamin K deficiency?

A

Factors II, VII, IX, and X produced in liver activated by vitamin K dependent carboxylase which requires reduced vit K which requires vit K reductase which is inhibited with coumarin = rodenticide
Lack of active FII, VII, IX, X so all pathways affected but FVII has shortest half life so PT prolonged first

100
Q

What are the clinical signs of vitamin K deficiency?

A

Mainly haemorrhage

101
Q

What do test results of animals with vitamin K deficiency show?

A

Prolonged PT and PTT
Mild thrombocytopenia is possible due to consumption associated with haemorrhage
FDPs may also be elevated
Same results if animal has coagulopathy secondary to hepatic disease

102
Q

What are the treatments for vitamin K deficiency?

A

Emetics, cathartics, activated charcoal if ingestion of rodenticide is recent
Transfusions of whole fresh blood/fresh frozen plasma and packed cells if severe anaemia
Vitamin K orally/SC with loading dose then lower doses every 8 hours

103
Q

How long will a patient with rodenticide poisoning need treatment for?

A

Warfarin/1st gen = 1 week treatment
2nd/3rd gen = 3-6 weeks
Check PT 24-48 hours after last dose

104
Q

What are some hereditary defects of coagulation?

A

Factor VII deficiency, Haemophilis A (Factor VIII), Haemophilia B (Factor IX), factor XI deficiency, factor XII deficiency

105
Q

What is the treatment for a hereditary defect of coagulation?

A

Transfusions of whole blood or plasma to replace factor deficiency and red cells
Fresh/frozen plasma gives a small amount of factor
Cryoprecipitate

106
Q

What is DIC?

A

Disseminated intravascular coagulation is a mixed haemostatic defect resulting from excessive coagulation leading to widespread thrombosis and haemorrhage eventually results as all coagulation factors are consumed
Can be secondary to other disease, acute or chronic

107
Q

What haemostatic abnormalities are seen in DIC?

A

Thrombocytopenia, prolonged PT and PTT, elevated FDPs, decreased fibrinogen, decreased antithrombin III

108
Q

What is the prognosis for DIC?

A

Poor

109
Q

What is the treatment for DIC?

A

Stop coagulation process using heparin/blood transfusion as a source of antithrombin III/asprin to stop platelet activation
Correct underlying abnormalities

110
Q

What is the first thing to do if presented with a patient with a bleeding abnormality?

A

Petechial/eccymoses - if yes then likely platelet defect if not coagulation defect
Check CBC and evaluate HCT and platelet numbers

111
Q

What do you do if a patient has thrombocytopenia?

A

Check for clots, check smear and recheck numbers
Assess degree of thrombocytopenia
If platelets 100x10^9/L consider haemorrhage as a cause but if below 25x10^9/L thrombocytopenia may be cause of haemorhage

112
Q

What diseases and tests should be considered if platelet numbers normal but haemorrhages/eccymoses/petechiae present?

A

vWD or platelet function defects

Check BMBT, vWF:Ag assay, clotting function

113
Q

What disease is likely if both PT and PTT are prolonged?

A

Vitamin K deficiency or DIC

114
Q

What disease is likely if PTT alone is prolonged?

A

Intrinsic pathways, haemophilia A or B

115
Q

What disease is likely if PT alone is prolonged?

A

Vitamin K deficiency, liver disease or early DIC

Lymphoreticular and haematopoetic (12 decks)

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