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Lymphoreticular and Haemopoietic > Disorders of Platelets and Coagulopathies > Flashcards

Disorders of Platelets and Coagulopathies Flashcards

1
Q

Define haemostasis

A

The interaction between blood vessels, platelets and coagulation factors that normally maintains blood in a fluid state and allows for formation of platelet plugs and clots vessels when injured

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2
Q

What does abnormal haemostatsis result in?

A

Haemorrhage

Thrombosis

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3
Q

What are the 4 components of haemostatsis?

A

Endothelium
Platelets
Coagulation factors
Fibrinolytic factors

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4
Q

Outline the role of endothelial cells…

A

Inhibit coagulation and platelet aggregation

Acts as a barrier to subendothelial collage

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5
Q

What produces vWF? What is its role?

A

Endothelium
Platelets
Responsible for platelet adhesion to collagen

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6
Q

Where are platelets produced from? What mediates their production?

A

Cytoplasm of megakaryocytes in bone marrow

Thrombopoietin

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7
Q

Outline the features/roles of platelet structure…

A

Outer membrane
Receptors for adhesion and aggregation

Cytoskeleton with actin and myosin
Allows shape change

Membrane bound granules
Contains vWF, fibrinogen, factors V and VIII, ADP and Ca

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8
Q

Name 3 surface receptors of platelets and their roles. What do defects in these lead to?

A

Glycoprotein Ib - binds to vWF
GP IIb and IIa - binds to fibrinogen and allows aggregation

Abnormal platelet function and clot formation

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9
Q

Define primary and secondary haemostasis and fibrinolysis..

A

Primary - Formation of primary platelet plug

Secondary - Activation of coagulation cascade and generation of insoluble fibrin, stabilises platelet plug

Fibrinolysis - Breakdown of fibrin and platelet plug

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10
Q

Outline the process of primary haemostasis…

A
  1. Damage to endothelium and exposure of collagen
  2. Endothelium releases vWF
  3. Platelet adhesion to collagen via GP Ib and vWF
  4. Platelets become spherical with filopodia (cytomplasmic projections), additional GP Ib and GPIIbIIIa receptors exposed
  5. Fibrinogen binds via GPIIbIIIa => aggregates of platelets
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11
Q

What factors are released by degranulating platelets during aggregation to increase further adhesion/coagulationi?

A 
ADP
Fibrinogen
vWF
Thromboxane A2
Factors V and VIII
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12
Q

Outline the process of secondary haemostasis…

A
  1. Endothelium releases tissue factors
  2. Extrinsic coagulation pathway is activated
  3. Coagulation pathway occurs
  4. Insoluble fibrin forms and stabilises platelet plug
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13
Q

What are the roles of the extrinsic and intrinsic pathway?

A

Extrinsic - initiation

Intrinsic - amplification

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14
Q

Outline the process of the extrinsic coagulation pathway…

A
  1. Tissue factors released from damaged tissue -> presence of Ca -> binds and activates FVIII
  2. TF-FVIII complex activates FX and FIX
  3. Common and intrinsic pathways activated
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15
Q

Outline the process of the intrinsic coagulation pathway…

A
  1. FXII activated by negatively charges surface
  2. FXI activated
  3. FIX activated
  4. FX of the common pathway activated
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16
Q

Outline the process of the common coagulation pathway…

A
  1. FX activated
  2. FV and Ca bind on platelet surface
  3. Prothrombin converts to thrombin
  4. Fibrinogen converts to fibrin
  5. FXIII cross links fibrin
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17
Q

What can inhibit coagulation?

A

Antithrombin III
Heparin (increases ATIII activity)
Protein C
Fibrinolysis

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18
Q

How can platelet numbers be estimated?

A

Machine count as CBC

Manual count from smear

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19
Q

What can cause inaccurate platelet counts by machine?

A

Similar size to RBC in cats, sheep and goat
Platelet clumps esp in cats
Giant platelets counts as RBCs in CKCS

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20
Q

What diagnostic tests can evaluate platelets? What does it measure?

A

Buccal mucosal bleeding time
Small incision in buccal mucous and blood is blotted until bleeding stopes

Length of time for a primary platelet plug to form

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21
Q

What is the main problem with the buccal mucosal bleeding time test?

A

V low sensitivity

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22
Q

What are possible platelet disorders?

A

Thrombocytopenia
Thrombocytosis
Platelet function disorders

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23
Q

What can a platelet disorder lead to? What would be the clinical signs?

A

Haemorrhage or thrombosis
Ecchymosis
Petchiae

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24
Q

What can cause thrombocytopenia?

A 
Immune-mediated destruction
Haemorrhage
DIC
Sequestration
Decreased production
Infections
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25
Q

What are the primary and secondary causes of IMTP?

A

Primary - antibodies produced against platelet antigens

Secondary - Immune disease, drugs/vacc, neoplasia, infections

26
Q

What are the clinical signs of IMTP?

A

Profound thrombocytopenia
Petchiae, ecchyosis
Bleeding from gums, mucosal surfaces, prolonged bleeding

27
Q

How is IMTP diagnosed?

A

Exclusion
Bone marrow exam
Anti-platelet antibodies test
Response to treatment

28
Q

What can decrease platelet production?

A

Bone marrow disease
Neoplasia
Drugs

29
Q

What infections can cause thrombocytopenia?

A

FeLV
BVDv
Ehrlichia
Leishmania

30
Q

Name 3 platelet function disorders and the breeds they affect…

A

Glanzmann’s thrombasthenia
(GPIIbIIIa defect) - Otter hounds, Great Pyrenees, Quarter Horses

Canine thrombopathia - Bassett Hounds

Bovine thrombopathia - Simmentals

31
Q

What mechanisms can cause thrombocytosis?

A

Physiological due to splenic contraction
Secondary to inflammation, haemorrhage, Fe deficiency
Myeloproliferative disorders

32
Q

What is vWF? Where is it produced? What clotting factors is it associated with?

A

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

  • Endothelial cells
  • Platelets
  • Megakaryocytes

FVIII

33
Q

What are the clinical signs of von Willebrand’s disease?

A

Mucosal bleeding
No petechiae
Prolonged buccal mucosal bleeding time with no thrombocytopenia
Normal/increased PTT

34
Q

Which species is vWF disease most commonly seen in?

A

Dogs

35
Q

Outline the characteristics of Type I vWF disease….

A

All multimers present but in low concentration
Most common
Dobermanns
M=F

36
Q

Outline the characteristics of Type II vWF disease….

A

Abnormal structure/function of vWF
Decreased conc of large multimers
Severe, uncommon
German pointers

37
Q

Outline the characteristics of Type III vWF disease…

A

All multimers absent

Scottish terriers, shetland sheepdogs

38
Q

How is vW disease diagnosed?

A

ELISA to measure vWF
Immunoelectrophoresis to separate different sized multimers
Genetic test for carriers

39
Q

Outline the results and diagnoses from a vWF ELISA…

A 
0% - Type III vWD
0-35% - vWD
0-50% - Suspected carriers
50-68% - Borderline, possible carriers
70-180% - Free from vWD
40
Q

How is vWD treated?

A

Cryoprecipitate, plasma or whole blood transfusion to supply vWF
Desmopressin (prophylactic before surgery)

41
Q

How should a blood sample be taken to assess platelets?

A

Plasma sample required
Do not sample through heparinised catheters
Minimise trauma to prevent platelet and coagulation activation

42
Q

What does the activated clotting time test evaluate? How is it carried out?

A

Intrinsic and common pathways of coagulation

  1. Collect 2ml blood into ACT tube
  2. Incubate for 1m at 37’
  3. Check for clot formation every 5-10s
43
Q

What does the partial thromboplastin time test evaluate? How is it carried out? What could interfere with the test?

A

Screening of intrinsic and common pathways of coagulation

  1. Incubate plasma with phospholipid, contact activator and calcium
  2. Measure time to clot formation

Lipaemia
Haemolysis
Oxyglobin treatments
Icterus

44
Q

What does a prolonged PTT indicate?

A

A defect in the intrinsic or common pathways

NOT thrombocytopenia

45
Q

What does the prothrombin test time evaluated? How is it carried out?

A

Screening of extrinsic and common pathways of coagulation

  1. Incubate plasma with tissue thromboplastin and calcium
  2. Measure time to clot formation
46
Q

How is fibrinolysis tested for?

A

Test serum for fibrin degradation products

47
Q

What can increase the concentration of fibrin degradation products?

A

DIC
Haemorrhage
Jugular vein thrombosis
Liver disease

48
Q

What can cause a vit K deficiency?

A

Rodenticide toxicity

Sweet clover ingestion (cattle)

49
Q

Which clotting factors are vit K dependent?

A

II
VII
IX
X

50
Q

Outline how rodenticide toxicity causes a coagulation disorder

A

Coumarin in rodenticide inhibits Vit K reductase

Vit K cannot be reduced

None available for Vit K dependent carboxylase

Factors II, VII, IX and X cannot be activated

Coagulopathy

51
Q

Which coagulation pathways are affected by Vit K deficiency? Which factor is affected first? How can it be diagnosed early on?

A

Intrinsic, extrinsic and common
Factor VII
Prolonged PT

52
Q

How is Vit K deficiency diagnosed?

A

Signs of haemorrhage
Prolonged PT and PTT
Normal platelet numbers and buccal mucosal bleeding time
Elevated FDPs

53
Q

How is vit K deficiency treated?

A

Emetics, cathartics, activated charcoal if rodenticide ingestion
Blood/plasma transfusion
Packed RBCs if anaemic
Vit K therapy PO/SQ

54
Q

How long does vit K therapy continue for?

A

<3weeks

Check PT after each dose

55
Q

What factors deficiencies can be inherited?

A 
VII
VIII (haemophilia A)
IX (haemophilia B)
XI
XII
56
Q

How are inherited coagulation defects treated?

A

Cryoprecipitates/plasma/blood transfusion

57
Q

What does DIC occur secondary to?

A

Neoplasia
Liver disease
Immune-mediated
Infections

58
Q

Outline the pathophysiology of DIC…

A

Excessive coagulation => widespread thrombosis => all clotting factors consumed => haemorrhage

59
Q

What diagnostic results indicate DIC?

A 
Thrombocytopenia
Prolonged PT and PTT
Elevated FDPs
Decreased fibrinogen
Decreased ATIII
60
Q

Is DIC acute or chronic?

A

Either!

61
Q

How is DIC treated? What is the prognosis?

A

Stop coagulation
Heparin
Transfusion of whole blood/plasma/cryoprecipitates
Aspirin

Poor prognosis

62
Q

Outline the approach to a bleed patient….

A
  1. Are haemorrhages ecchymotic or petechial? Age? Hx?
  2. CBC
  3. HCT and platelet numbers
  4. If thrombocytopenia, check clots/smears and recheck numbers
  5. If haemorrhages/ecchymosis check BMBT, vWF:Ag and clotting function
  6. PT and PTT, both prolonged => vit K deficiency or DIC
    PTT prolonged => defect in intrinsic pathway

Lymphoreticular and Haemopoietic (14 decks)

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