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LCB2 > Haemostatic disorders > Flashcards

Haemostatic disorders Flashcards

1
Q

Describe the process of primary haemostasis

A
  • Injury to vessel
  • Platelets adhere to collagen
  • Von Willbrand’s factor released from endothelium
  • Platelets change shape following adhesion with secretion of substances from granules which potentiate platelet aggregation and contraction of the platelet plug
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2
Q

Describe the process of secondary haemostasis

A

Stabilisation of the platelet pug by deposition of fibrin

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3
Q

Describe the process of tertiary haemostasis

A
  • Formation of plasmin from plasminogen
  • Fibrinolysis to break down fibrin clot
  • Predominantly by action of plasmin
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4
Q

Describe hyperfibrinolysis

A
  • Breakdown of clots too quickly leading to bleeding
  • Sight and Greyhounds predisposed
  • Can bleed badly from minor wounds or surgical sites
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5
Q

What are the 2 pathways of clotting activation?

A

Intrinsic, extrinsic

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6
Q

Briefly outline the intrinsic pathway of clotting activation

A
  • Damaged surface
  • Activation of cascade
  • Production of FXa
  • FXa converts prothrombin to thombin, which converts fibrinogen to fibrin
  • Clot forms from cross linked fibrin
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7
Q

Briefly outline the extrinsic pathway of clotting activation

A
  • Trauma/tissue factor activates cascade
  • Production of FXa from FVII
  • FXa activates prothrombin to thrombin, which converts fibrinogen to fibrin
  • Clot forms from cross linked fibrin
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8
Q

Describe the clinical signs of disorders of primary haemostasis

A
  • Petechiae (<3mm), echymosis (>1cm)/purpura (3-10mm)
  • Bleeding from MM
  • often more than one site of bleeding
  • Haematomas rare-
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9
Q

Describe what is meant by diascopy

A
  • Using glass slide to determine if a wheal is from a bite, reaction or if a haemorrhage
    Press slide against skin - if haemorrhage will not blanche
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10
Q

What sign may be seen at the teeth in Von Willebrand’s disease?

A

Bleeding from gingiva as teeth come through

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11
Q

Describe the clinical signs of disorders of secondary haemostasis

A
  • Petechiae/echymoses rare
  • Deep or cavity bleeds, can bleed from mucous membranes
  • Sometimes single sites of bleeding
  • Haematomas common
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12
Q

Describe the clinical signs of Von Willebrands disease

A
  • Typical primary haemostatic defect: mucosal haemorrhage, cutaneous bruising, prolonged bleeding from surgical and traumatic wounds
  • More profound bleeding incl. epistaxis, haematuria, GI haemorrhage, prolonged oestral bleeding and gingival bleeding at tooth eruption
  • Classically seen around first events e.g. first season, first tooth
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13
Q

What are potential causes of disorders of primary haemostasis?

A
  • Thrombocytopaenia
  • Thrombocytopathia
  • von Willebrand factor deficiency
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14
Q

Describe the typical signalment for disorders of primary haemostasis

A
  • Young animals more likely to have inherited vs acquired
  • Certain breeds predisposed to inherited disorders of primary haemostsis
  • Certain breeds and female dogs prone to immune mediated thrombocytopaenia
  • Acquired immune mediated thrombocytopaenia is the most common cause for haemostatic disorder
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15
Q

What may cause thrombocytopaenia?

A
  • Defective platelet production
  • Accelerated platelet removal
  • Platelet sequestration or loss
  • Thrombocytopaenia in cattle: BVD, bracken, alloantibodies
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16
Q

Outline potential causes for defective production of platelets

A
  • Bone marrow neoplasia
  • Drug/chemical/toxin induced bone marrow suppression
  • Bone marrow infections (esp. viral and rickettsial)
  • Less severe
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17
Q

List the potential causes of accelerated platelet removal

A
  • Immune mediated destruction

- Consumption in microangiopathic conditions (DIC)

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18
Q

What is the most common acquired cause of primary haemostatic defects in the dog?

A

Immune mediated thrombocyte destruction

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19
Q

Explain how immune mediated destruction of platelets leads to thrombocytopaenia

A
  • Platelets destroyed faster than they are produced

- Can be primary (idiopathic) or secondary (e.g. drug induced, infection, neoplasia related)

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20
Q

Describe the signalment for idiopathic immune mediated destruction of platelets

A
  • Young to middle aged female dogs

- Cockers, miniature/toy poodles, Old English sheepdogs predisposed

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21
Q

List the potential causes of platelet sequestration or loss

A
  • Splenomegaly/vascular pooling

- Acute ongoing haemorrhage (rare)

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22
Q

List the potential causes of thrombocytopaenia in cattle

A
  • Bovine neonatal pnacytopaenia (bleeding calf syndrome)
  • Bracken poisoning
  • Bovine viral diarrheoa virus
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23
Q

Describe the pathogenesis of bovine neonatal pancytopaenia

A
  • Caused by alloantibodies absorbed form colostum of particular cows
  • Commercial BVD vaccine is likely source of alloantigens eliciting BNP associated antibodies
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24
Q

Describe the pathogenesis of bone marrow toxicity

A
  • Leads to decreased platelets = bleeding = non-regenerative anaemia
  • Decreased erythrocyte production leads to non-regenerative anaemia
  • Decreased leukocytes leads to secondary bacterial infection
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25
Q

List the potential causes of thrombocytopathia

A
  • Inherited thrombopathias
  • Drug induced defects of platelet function
  • Platelet dysplasia
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26
Q

Describe the common presentation of inherited thrombopathias

A
  • Age important part of diagnosis
  • First suspicion at vacc or neuter or dental eruption - stimulus required for bleeding
  • Secondary haemostatic disorders when still with litter mates e.g mild trauma = huge bleeds
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27
Q

Outline von Willebrands factor deficiency

A
  • Most common of the inherited bleeding disorders
  • Wide range of dog breeds
  • Very rare in cats
  • 3 classification sbased on severity and abnormality of the vWF protein
  • Variable bleeding tendency
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28
Q

List the breeds prediposed to von Willbrand factor deficiency

A
  • Doberman pinschers
  • GSD, German shorthaired pointer
  • Corgi
  • Golden retrievers
  • Shetland Sheepdog
  • Standard poodle
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29
Q

Describe the plasma vWF and clinical severity of type I von Willebrand Factor deficiency

A
  • Abnormally low concentration of structurally norma vWF

- Milder/variable

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30
Q

Describe the plasma vWF and clinical severity of type II von Willebrand factor defiency

A
  • Structurally abnormal vWF

- Severe

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31
Q

Describe the plasma vWF and clinical severity of type III von Willebrand factor deficiency

A
  • Essentially no plasma vWF, diagnosed by ELISA

- Severe

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32
Q

LIst tests that are used to investigate disorders of primary haemostasis

A
  • Platelet count
  • Buccal mucosal bleeding time
  • Von Willebrand factor antigen
  • Platelet function assays
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33
Q

What methods can be used to perform a platelet count?

A
  • Estimated ocunt from blood smear
  • Automated cell count
  • Haemocytometer
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34
Q

Describe the use of a platelet count in the investigation of disorders of primary haemostasis

A
  • Do first to rule out thrombocytopaenia
  • Perform as soon as possible to avoid clumping once sampled
  • Scan for evidence of platelet clumps before examining the monolayer of the film under oil immersion
  • assess morphology
  • Care with breeds: e.g. cavvies have lower numbers of larger paltelets
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35
Q

Which sample tube may be best for performing a platelet count?

A

Citrated

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36
Q

How many platelets per high power field would indicate no risk of bleeding?

A

5-6 platelets per high power filed (each platelet/hpf = 20x10^9/L)

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37
Q

Describe the morphology of platelets that would be suggestive of increased platelet production

A

Large or shift platelets

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38
Q

If the platelet concentration is normal, but the animal is bleeding, what does this suggest?

A

Thrombocytopathia

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39
Q

Evaluate the use of buccal mucosal bleeding time to investigate disorders primary of haemostasis

A
  • If platelet count low on smear, do not perform BMB as it will be prolonged and can be dangerous
  • Can be difficult
  • Usually performed sedated, but some sedatives can interfere with platelet function
  • Very subjective
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40
Q

Describe the method for a buccal mucosal bleeding time

A
  • Use simplate devide
  • Makes 2 parallel cuts into mucosa
  • Assess and time the clot formation
  • Remove blood coming out without disturbing any potential clots that may be forming
  • Increased time to stop bleeding indicates defective primary haemostasis
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41
Q

What is a normal buccal mucosal bleeding time in dogs and cats?

A
  • Dogs: 1.7-3.3 mins (up to 4.2 if anaesthetised)

- Cat: up to 3.3. minutes

42
Q

Outline the use of platelet function assays in the investigation of disorders of primary haemostasis

A
  • Thromboelastography/ROTEM
  • Provides dynamic global functional assessment of primary, secondary and tertiary haemostasis fibrinolysis
  • Investigates interaction of coagulation factors, their inhibitors, anticoagulant drugs, blood cells, specifically platelets
43
Q

Where should samples for the investigation of disorders of primary haemostasis be taken from and why?

A
  • Peripheral veins e.g. cephalic, saphenous

- Can be pressure bandaged to prevent animal bleeding out until secondary haemostasis takes place

44
Q

Outline the diagnosis of thrombocytopathia

A
  • Normal PLT but prolonged BMBT
  • Normal vWF levels
  • Diagnosis of exclusion
  • PLT function tests (not first opinion practice)
45
Q

Give examples of platelet function tests

A
  • Aggregometry
  • Adhesion assays
  • Flow cytometry
46
Q

What methods are used in the diagnosis of von Willebrands disease?

A
  • Platelet count
  • Buccal mucosal bleeding time
  • ELISA for vWF antigens
47
Q

Outline the buccal mucosal bleeding time in the diagnosis of von Willebrands disease

A
  • Useful screening test for vWD
  • Normal: 2-4 min
  • Mild to moderate (type I): 5-10 min
  • Severe vWD: >12 min
48
Q

Outline the use of ELISA for vWF antigens in the diagnosis of von Willebrands disease

A
  • Diagnosis confirmed by demosntration of low vWF antigen concentrations
  • ELISA shows vWF:Ag ratio
  • Compare with species specific plasma pool
  • <50% = affected, >70% = normal
49
Q

Evaluate the use of ELISA in the diagnosis of von Willebrands disease

A
  • Does not always accurately predict risk of haemorrhage
  • May need repeat if clinical signs are present but not seen on ELISA
  • Can wax and wane depending on how much vWF released from endothelium at time of testing
50
Q

What condition may be mistaken as vWD and why?

A

Haemophilia A due to low factor VIII

51
Q

Describe the genetic testing available for von Willebrands disease

A
  • 5 mutations responsible for most vWD in dogs
  • Autosomal
  • Is not a diagnostic test
  • 3 possible results: clear, carrier or affected status
  • Not predictive of clinical bleeding (type I)
52
Q

Outline the treatment of immune mediated thrombocytopaenia

A
  • Suppress immune system
  • Avoid subcut injections
  • Do not use IM injections
  • Minimise invasive procedures
  • Gentle handling
  • Poor surgical candidates
  • Will often get intracranial bleeds which are fatal but can do very little about
53
Q

OUtline the management of thrombocytopathia

A
  • No specific therapy
  • Platelet transfusions not possible
  • Withdraw any durgs
  • Treat symptomatically e.g. blood transfusion if marked anaemia
54
Q

Discuss the use of platelet rich plasma transfusion in the treatment of acute short term bleeding

A

Platelets only last 24 hours, but good if animal needs surgery as will be able to clot for this period of time until secondary haemostasis can take over

55
Q

Outline the treatment of vWD

A
  • Plasma: stabilisation and cessation of active haemorrhage
  • Cryoprecipitate
  • Red cells if oxygen carrying capacity is compromised, whole blood may be required
  • Administer demospressin 1ug/kg BW SC to patient
56
Q

Describe how the use of plasma in the treatment of vWD can be optimised

A
  • If donor dog, administer DDAVPs before taking blood to elevate vWF in the donor
  • Supplements vWF of patient even more
57
Q

Describe the clinical signs of disorders of secondary haemostasis

A
  • Deep or cavity bleeds
  • Petechiae/echymoses rare
  • Haematomas comon
  • radiographs may show areas of increased opacity (identify if are solid soft tissue masses or fluid)
  • Melena and epistaxis common
58
Q

How can you differentiate between a solid soft tissue mass or fluid in the thorax on a radiograph?

A

Solid soft tissue masses generally lead to displacement of the trachea, not the case for fluid

59
Q

What are the potential aetiologies of disorders of secondary haemostasis?

A
  • Congenital (haemophilias)

- Acquired

60
Q

What factor is affected in:

1) haemophilia C?
2) haemophilia B?
3) haemophilia A?

A

1) Factor XI
2) factor IX
3: Factor VIII

61
Q

Describe the history for disorders of secondary haemostasis

A

Signs present from young age e.g. bruises, lame (haemarthroses), subcut haematoma from playing

62
Q

Discuss the importance of factor XII in haemophilia

A
  • Clinically irrelevant, not required for activation of intrinsic pathway but can be seen in cats
  • Occasionally seen in cats, asymptomatically carried, in vitro artefact
63
Q

What gender is susceptible to haemophilia A and B?

A

Males

64
Q

Describe haemophilia A

A
  • Factor VIII deficiency
  • Sex linked inherited in males
  • Suffer from spontaneous life threatening bleeding episodes
65
Q

Outline the pathogenesis of haemophilia A

A

Factor VIII is essential cofactor in the intrinsic pathway and deficiencies result in prolingation of the APTT

66
Q

What is the APTT?

A

Activated Partial Thromboplastin Time

67
Q

How is haemophilia A diagnosed?

A

Confirmation by a specific FVIII assay

68
Q

Describe haemophilia B

A
  • Sex-linked inherited condition
  • Clinically identical to F VIII deficiency
  • Active at same point in coagulation cascade
69
Q

How is haemophilia B diagnosed?

A

Specific F. IX assay

70
Q

What should samples being tested for haemophilia be tested for? Why?

A

Haemophilia A and B as these are clinically identical

71
Q

Describe the clinical signs of vitamin K antagonism/coumarin toxicity

A
  • Clinical signs may appear within 1-3 days (variable onset of signs)
  • Haemorrhage may occur in large number of sites externally and into body cavities
  • Can occur without major clinical signs, esp. if bleeds into cavity rather than epistaxis or coughing up blood
72
Q

Explain the pathogenesis of coumarin toxicity

A
  • Inhibit vit K epoxide reductase with normally reactivates vit K in the liver
  • Vit K needed to activate factors II, VII, IX, X
  • VII has the shortest half life so is quickest to become abnormal (but also quickest to normalise)
  • Depletion of intrinsic and extrinsic pathway factors
73
Q

Describe the OSPT and APPT in coumarin toxicity

A
  • OSPT prolonged initially

- Then later APTT increases

74
Q

What is the OSPT?

A

One stage prothrombin time

75
Q

Outline the treatment of coumarin toxicity

A
  • Induce emesis, gastric lavage, enema, activated charcoal (aim to remove 80% f ingested rat bait to decrease clinical risk dramatically)
  • Vitamin K supplementation initially subcut
  • Several weeks to months of treatment may be required depending on type of coumarin
  • OSPT promptly returns to normal with appropriate therapy, but if withdrawn too soon will become prolonged again
76
Q

Why shoudl vit K be given subcut?

A

IV associated with systemic anaphylaxis and shock

77
Q

Explain why hepatic disease can lead to disorders of secondary haemostasis

A
  • Many clotting factors and inhibitors of coagulation are synthesised in the liver
  • Vit K dependent factors activated in the liver
78
Q

Describe the signs that may indicate disorders of secondary haemostasis are secondary to hepatic disease?

A
  • Elevated OSPT and APTT
  • Increased plasma concentrations of liver enzymes showing liver damage
  • Increased bile acid concentrations showing hepatic dysfunction
  • Jaundice
  • rarely spontaneously bleed
79
Q

What is the main risk regarding disorders of secondary haemostasis secondary to hepatic disease?

A

Bleeding during liver biopsy so liver disease diagnosis is difficult

80
Q

Outline the treatment of hepatic disease leading to disorders of secondary haemostasis

A
  • If coagulation parameters prolonged, provide vit K parenterally
  • Some animals may require plasma therapy
81
Q

List appropriate tests for the investigation of disorders of secondary haemostasis

A
  • Whole blood clotting time
  • Activated clotting time
  • One stage prothrombin time
  • Activated partial thromboplastin time
  • Specific factor assays
82
Q

Describe the use of whole blood clotting time in the investigation of disorders of secondary haemostasis

A
  • Crude measure of intrinsic and common pathways

- Will be prolonged in severe thrombocytopaenia

83
Q

Describe the interpretation of whole blood clotting time in the investigation of disorders of secondary haemostasis

A
  • Prolonged when single factor depleted to <5-10% of normal
  • Normal values: dogs 3-13 mins, cats 8 mins
  • Collect in a warmed glass tube
84
Q

What does one stage prothrombin time assess?

A

Extrinsic and common pathways, becomes prolonged due to marked deficiency of a single factor <30% of its normal concentration)

85
Q

Describe the interpretation of one stage prothrombin time (PT/OSPT)

A
  • Reference intervals depend on machine used
  • May have normal values on APTT
  • If signs suggestive but results say normal, run again
86
Q

What does activated partial thromboplastin time assess (APTT)?

A

Intrinsic and common pathways

87
Q

Describe the interpretation of the activated partial thromboplastin time

A
  • Prolonged due to marked deficiency of a single factor (<30% of its normal concentration but can be significantly lower)
  • Reference intervals depend on machine used
  • Haemophilia: 18019% of factor VIII but may give normal APTT occasionally, care regarding clinical signs and results
88
Q

Outline the use of specific factor assays for the investigation of disorders of secondary haemostasis

A
  • Level of individual clotting factors can be measured

- Most commonly indicated in the investigation of inherited coagulation disorders

89
Q

Give an important consideration when taking samples for specific factor assays for the investigation of disorders of secondary haemostasis

A
  • Ensure are not using up clotting factors by slow sampling, or old blood in needle/hub from previous sampling attempts
  • Clotting will use up factors
90
Q

List the fibrinogen degradation products that are produced in tertiary haemostasis

A

Fragments X, Y, D, E

91
Q

List the fibrin degradation products that are produced in tertiary haemostasis

A

X-oligomers, D-dimer

92
Q

List the tests used to asses fibrinolysis

A
  • Fibrin(ogen) degradation products (FDPs)

- D-dimer (not used alone as diagnostic tool)

93
Q

Outline the process of tertiary haemostasis

A
  • Formation of plasmin from plasminogen

- Carries out fibrinolysis to break down fibrin clot

94
Q

How can tertiary haemostasis be assessed?

A
  • Test for fibrinolysis

- Test for inhibitors (antithrombin)

95
Q

Outline the testing of inhibitors in the investigation of tertiary haemostasis

A
  • Antithrombin III in particular is measured

- % of species specific plasma pool

96
Q

What antithrombin value would be expected in a healthy animal?

A

> 80%

97
Q

What antithrombin value indicates that an animal is at risk of thrombosis?

A

<50%

98
Q

What is the consequence of decreased level of antithrombin III and very marked increased D-dimer (FDPs)

A

Thrombosis - clot forms due to reduced resistance to clot formation

99
Q

Give examples of conditions that may lead to thrombosis

A
  • Feline thromboembolic disease
  • Protein losing nephropathy
  • Hyperadrenocorticism
  • Hypertrophic cardiomyopathy in cats
100
Q

Explain how hyperadrenocorticism may lead to thrombosis

A
  • Increase in factors V, VIII, IX, X, fibrinogen and plasminogen
  • Decrease in antithombin from hypertension induced urinary loss
  • Obesity and hypercholestreolaemia may also contribute to thrombus formation

LCB2 (14 decks)

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