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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
What are the primary and secondary causes of IMTP?
Primary - antibodies produced against platelet antigens Secondary - Immune disease, drugs/vacc, neoplasia, infections
26
What are the clinical signs of IMTP?
Profound thrombocytopenia Petchiae, ecchyosis Bleeding from gums, mucosal surfaces, prolonged bleeding
27
How is IMTP diagnosed?
Exclusion Bone marrow exam Anti-platelet antibodies test Response to treatment
28
What can decrease platelet production?
Bone marrow disease Neoplasia Drugs
29
What infections can cause thrombocytopenia?
FeLV BVDv Ehrlichia Leishmania
30
Name 3 platelet function disorders and the breeds they affect...
Glanzmann's thrombasthenia (GPIIbIIIa defect) - Otter hounds, Great Pyrenees, Quarter Horses Canine thrombopathia - Bassett Hounds Bovine thrombopathia - Simmentals
31
What mechanisms can cause thrombocytosis?
Physiological due to splenic contraction Secondary to inflammation, haemorrhage, Fe deficiency Myeloproliferative disorders
32
What is vWF? Where is it produced? What clotting factors is it associated with?
A plasma glycoprotein needed for platelet adherence to collagen and formation of primary platelet plug - Endothelial cells - Platelets - Megakaryocytes FVIII
33
What are the clinical signs of von Willebrand's disease?
Mucosal bleeding No petechiae Prolonged buccal mucosal bleeding time with no thrombocytopenia Normal/increased PTT
34
Which species is vWF disease most commonly seen in?
Dogs
35
Outline the characteristics of Type I vWF disease....
All multimers present but in low concentration Most common Dobermanns M=F
36
Outline the characteristics of Type II vWF disease....
Abnormal structure/function of vWF Decreased conc of large multimers Severe, uncommon German pointers
37
Outline the characteristics of Type III vWF disease...
All multimers absent | Scottish terriers, shetland sheepdogs
38
How is vW disease diagnosed?
ELISA to measure vWF Immunoelectrophoresis to separate different sized multimers Genetic test for carriers
39
Outline the results and diagnoses from a vWF ELISA...
``` 0% - Type III vWD 0-35% - vWD 0-50% - Suspected carriers 50-68% - Borderline, possible carriers 70-180% - Free from vWD ```
40
How is vWD treated?
Cryoprecipitate, plasma or whole blood transfusion to supply vWF Desmopressin (prophylactic before surgery)
41
How should a blood sample be taken to assess platelets?
Plasma sample required Do not sample through heparinised catheters Minimise trauma to prevent platelet and coagulation activation
42
What does the activated clotting time test evaluate? How is it carried out?
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
What does the partial thromboplastin time test evaluate? How is it carried out? What could interfere with the test?
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
What does a prolonged PTT indicate?
A defect in the intrinsic or common pathways | NOT thrombocytopenia
45
What does the prothrombin test time evaluated? How is it carried out?
Screening of extrinsic and common pathways of coagulation 1. Incubate plasma with tissue thromboplastin and calcium 2. Measure time to clot formation
46
How is fibrinolysis tested for?
Test serum for fibrin degradation products
47
What can increase the concentration of fibrin degradation products?
DIC Haemorrhage Jugular vein thrombosis Liver disease
48
What can cause a vit K deficiency?
Rodenticide toxicity | Sweet clover ingestion (cattle)
49
Which clotting factors are vit K dependent?
II VII IX X
50
Outline how rodenticide toxicity causes a coagulation disorder
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
Which coagulation pathways are affected by Vit K deficiency? Which factor is affected first? How can it be diagnosed early on?
Intrinsic, extrinsic and common Factor VII Prolonged PT
52
How is Vit K deficiency diagnosed?
Signs of haemorrhage Prolonged PT and PTT Normal platelet numbers and buccal mucosal bleeding time Elevated FDPs
53
How is vit K deficiency treated?
Emetics, cathartics, activated charcoal if rodenticide ingestion Blood/plasma transfusion Packed RBCs if anaemic Vit K therapy PO/SQ
54
How long does vit K therapy continue for?
<3weeks | Check PT after each dose
55
What factors deficiencies can be inherited?
``` VII VIII (haemophilia A) IX (haemophilia B) XI XII ```
56
How are inherited coagulation defects treated?
Cryoprecipitates/plasma/blood transfusion
57
What does DIC occur secondary to?
Neoplasia Liver disease Immune-mediated Infections
58
Outline the pathophysiology of DIC...
Excessive coagulation => widespread thrombosis => all clotting factors consumed => haemorrhage
59
What diagnostic results indicate DIC?
``` Thrombocytopenia Prolonged PT and PTT Elevated FDPs Decreased fibrinogen Decreased ATIII ```
60
Is DIC acute or chronic?
Either!
61
How is DIC treated? What is the prognosis?
Stop coagulation Heparin Transfusion of whole blood/plasma/cryoprecipitates Aspirin Poor prognosis
62
Outline the approach to a bleed patient....
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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