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Small Animal Final Year > Haemostatic Disease > Flashcards

Haemostatic Disease Flashcards

1
Q

What is the process of haemostasis?

A
  1. When a vessel is injured platelets adhere to collagen. Von Willebrand factor (vWF) is also important in platelet adhesion (primary haemostasis)
  2. Platelets change shape following adhesion with secretion of substances from granules which potentiate platelet aggregation and contraction of the platelet plug
  3. Stabilisation of the platelet plug is achieved by the deposition of fibrin, the end product of the coagulation cascade (secondary haemostasis)
  4. Tertiary haemostasis (certain breeds will have disorders – and will break down clots too quickly e.g. greyhound and sighthound)
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2
Q

Name clinical signs of primary haemostatic disease

A

•Petechiae/ecchymoses common

–Small bruise

•Bleeding from mucus membranes

–E.g. Von Willebands blled through

  • Often more than one site of bleeding
  • Haematomas rare
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3
Q

Name clinical signs of secondary haemostatic disorders

A

•Petechiae/ecchymoses rare

–Usually bigger bleeds

–Primary usually intact

  • Deep or cavity bleeds. Can bleed from mucus membranes
  • Sometimes single sites of bleeding
  • Haematomas common
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4
Q

What does this show?

A

Petechiae

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5
Q

What is this?

A

Ecchymoses

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6
Q

How can we tell if skin ecchymoses is present?

A

Press microscope against the skin and it wont disappear

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7
Q

What are the 3 causes of abnormal primary haemostasis?

A
  • Platelet numbers: Thrombocytopenia
  • Don’t have enough
  • Platelet function: Thrombocytopathia (thrombopathia)

–Don’t function well

•vWF: vWF deficiency

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8
Q

What is the signalment of primary haemostatic disorders?

A
  • Young animals more likely to have an inherited rather than acquired coagulopathy
  • Certain breeds are predisposed to inherited disorders of primary haemostasis
  • Certain breeds and female dogs prone to immune mediated thrombocytopenia
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9
Q

How can we test for primary haemostasis conditions?

A
  • Platelet count
  • Buccal mucosal bleeding time
  • von Willebrand factor antigen
  • Platelet function assays
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10
Q

Where should you take a blood sample from for haemostasis testing?

A

Peripheral e.g. cephalic or saphenous

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11
Q

What blood tube do we usually do for:

A) Haematology?

B) Cats and platelet?

A

A) EDTA

B) Citrate

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12
Q

How can we do a platelet (PLT) count?

A
  • EDTA sample
  • PLT counts should be performed as soon as possible to avoid clumping
  • Three methods can be used:

–estimated count from a blood smear

–automated cell count*

–haemocytometer

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13
Q

How do you interpret a platelet (PLT) count?

A
  • Scan for evidence of platelet clumps, before examining the monolayer of the film under oil immersion
  • Each platelet / hpf (1000x) equates to approximately 20 x109/l

–5-6 platelets per high power to ensure they wont bleed

•Assess morphology: large or shift platelets indicate increased platelet production

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14
Q

What are in the white circles?

A

Shift platelets

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15
Q

When is bleeding usually seen with a platelet (PLT) count?

A

Bleeding usually only seen if platelets <50 x109/l

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16
Q

Why should you not do a BMBT if platelets are low?

A

As it will be prolonged and can be dangerous

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17
Q

How do you interpret BMBT?

A

•An increased time to stop bleeding indicates defective primary haemostasis (vWF, platelets, vascular defects)

–Dog: 1.7–3.3 minutes (up to 4.2 if anaesthetised)

–Anaesthetised cat: <3.3 minutes

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18
Q

What is Thromboelastography (TEG) / ROTEM?

A
  • Provides dynamic global functional assessment of primary, secondary and tertiary haemostasis fibrinolysis
  • How the blood sample forms; rate of formation, strength off clot and how long it takes to break down
  • Looks at the whole process
  • Gold standard 0 £££. Unlikely in clinic.
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19
Q

What are the 3 causes of thrombocytopaenia?

A

1.Defective platelet production (severe)

–BM neoplasia e.g leukaemia

–Drug/chemical/toxin-induced BM suppression

–BM infections (especially viral and rickettsial)

1.Accelerated platelet removal (most severe)

–Immune-mediated destruction (ITP) (most common)

–Consumption in microangiopathic conditions (DIC)

1.Platelet sequestration or loss (not as severe)

–Splenomegaly / vascular pooling

–Acute ongoing haemorrhage

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20
Q

What is immune mediated thromcytopaenia and what is the signalment?

A
  • The most common acquired cause of primary haemostatic defects in the dog
  • Platelets are destroyed faster than they can be made
  • Primary (idiopathic) or secondary (e.g. drug-induced, infection, neoplasia related)
  • Young to middle-aged, female dogs

–Cocker spaniels, miniature / toy poodles and old English sheepdogs predisposed

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21
Q

How do you treat immune-mediated thrombocytopenia?

A

Suppress the immune system

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22
Q

Name 2 causes of Thrombocytopenia in cattle? (3)

A

•Bovine neonatal pancytopaenia (‘bleeding calf syndrome’)

–Related to the BVD vaccine…..

  • Bracken poisoning
  • Bovine Viral Diarrhoea Virus
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23
Q

When do we usually see inherited thrombopathias?

A

–Probably first suspect at vaccinations or neutering

–Haemophilia – severe secondary – vaccination or even with litter mates and injured themselves (end up with huge haemotoma)

–Primary e.g. VW - Dental eruptions or neutering – need more of a stimulus

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24
Q

What are the 3 causes of thrombocytopathia

A
  • Inherited thrombopathias
  • Drug induced defects of platelet function
  • Platelet dysplasia - Myeloproliferative disease and other forms of neoplasia
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25
Q

Name 3 inherited thrombopathias diseases (6)

A
  • Glanzmann’s thrombasthenia (adhesion defect)
  • Storage pool deficiency
  • Chediak Higashi syndrome (Persian cat)
  • Bassett hound thrombopathia
  • Scott syndrome in GSDs
  • Simmental cattle
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26
Q

How can we diagnose thrombocytopathia?

A

–Normal PLT count but prolonged BMBT

–Normal levels of vWF

–Diagnosis of exclusion?

–PLT function tests: aggregometry, adhesion assays, flow cytometry (expression of surface molecules)

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27
Q

How can you manage thrombocytopathia?

A
  • No specific therapy
  • Platelet transfusions not possible

–Platelet rich plasma – only last 24 hours so can only patch up short bleeding!!

–Only available from specialist hospitals

–Useful for surgery (normal secondary)

•Withdraw any drugs e.g. NSAIDs

–If we think its secondary to this

•Tx symptomatically e.g. blood transfusion if marked anaemia

28
Q

Discuss the 3 types of von Willebrand disease and the clinical severity of these.

A

Type

I

  • Abnormally low concentrations of structurally normal vWF
  • Milder / variable clinical severity

II

  • structurally abnormal vWF
  • Severe clinical severity

III

  • Essentially no plasma vWF
  • Diagnosed by ELISA
  • Severe clinical severity
29
Q

Name breeds predisposed to von Willebrans Disease

A
  • Dobermann pinschers
  • German shepherd dogs
  • German shorthaired pointer
  • Corgi
  • Golden retrievers
  • Shetland sheepdog
  • Standard poodle predispose
30
Q

What must you do in ll Dobermann pinschers which come to your practice?

A

Buccal mucosal bleeding

31
Q

Name clinical signs of Von Willebrands Disease

A

•Typical of a primary haemostatic defect

–Mucosal haemorrhage

–Cutaneous bruising

–Prolonged bleeding from surgical and traumatic wounds

•More profound bleeding including epistaxis, haematuria, gastrointestinal haemorrhage, prolonged oestral bleeding and gingival bleeding at tooth eruption reported

32
Q

How can we diagnose Von Willebrands Disease?

A
  • Platelet count normal
  • Buccal mucosal bleeding time is a useful screening test for vWD

–normal 2–4 min

–mild to moderate (type 1) 5–10 min

–severe forms of vWD >12 min

  • The diagnosis is confirmed by demonstration of low vWF antigen concentrations
  • ELISA for vWF antigen (vWF:Ag)

–Compare with species-specific plasma pool (100& or 100U/dL)

<50%=affected

>70%=normal

33
Q

What is the problem of vWF measuring the antigen?

A

Does not always accurately predict the risk of haemorrhage

34
Q

How can we use genetic testing for vWD?

A
  • Autosomal
  • Five mutations responsible for most vWD in dogs
  • Genetic testing available (VetGen) – not a diagnostic test
  • All recessive: clear, carrier or affected status
  • Not predictive of clinical bleeding (type 1)
35
Q

How can we treat vWD?

A

•Plasma

–stabilisation and cessation of active haemorrhage

  • Cryoprecipitate
  • Red cells

–if oxygen-carrying capacity compromised

36
Q

How do we treat type 1 vWD?

A

•Desmopressin

–1µg/kg BW SC in the dog

–acts by causing release of vWF from endothelial cells

–Synthetic vasopressin

–Might be enough to allow the secondary pathway

37
Q

What platelet numbers cause bleeding?

A

<50x10^9/l

38
Q

What is the most common cause of primary haemostatic disorder?

A

Immune-mediated destruction (ITP)

39
Q

Name signs of secondary haemostatic dosriders

A
  • Petechiae/ecchymoses rare
  • Deep or cavity bleeds. Can bleed from mucus membranes
  • Sometimes single sites of bleeding
  • Haematomas common
40
Q

What is this?

A

Haematoma

41
Q

What is this?

A

Melena

42
Q

What are the 2 cateories of secondary haemostasis?

Name a condition for each

A

•Congenital

–Haemophilia

•Acquired

–Vitamin K antagonism (coumarin/rat bait toxicity) – eaten rat poisoning

–Hepatic disease

43
Q

How do we test for secondary haemostasis?

A
  • Whole blood clotting time
  • (Activated clotting time)
  • One stage prothrombin time
  • Activated partial thromboplastin time
  • Specific factor assays
44
Q

How do you use whole blood clotting time?

A
  • Crude measure of intrinsic and common pathways
  • Will also be prolonged in severe thrombocytopenia
  • The WBCT is prolonged when a single factor is depleted to <5-10% of normal

Reported reference intervals:

  • Dogs: 3-13minutes
  • Cats: 8 minutes
45
Q

How is a one stage prothrombin time used?

A
  • Also known as prothrombin time
  • Measure of extrinsic and common pathways
  • OSPT is prolonged due to marked deficiency of a single factor (<30% of its normal concentration)

Reported reference intervals (but depends on the machine used):

  • Canine : 7 - 10 seconds *no need to learn this time*
  • Feline : 7 - 10 seconds *no need to learn this time*
46
Q

How is activated partial thromboplastin time used?

A
  • Also known as partial thromboplastin time
  • Measure of intrinsic and common pathways
  • APTT is prolonged due to marked deficiency of a single factor (<30% of its normal concentration)

Reported reference intervals (but depends on the machine used):

  • Dogs: 12-20 seconds *no need to learn this time*
  • Cats: 12-22 seconds *no need to learn this time*
47
Q

How can we diagnose haemophilia?

A

•Signalment/history

–signs present from a young age

  • Breed
  • Gender

–haemophilia A & B seen in male animals

48
Q

What is haemophilia A and how do we diagnose?

A

Factor VIII deficiency (Haemophilia A)

  • Sex-linked inherited; affected animals are males and suffer from spontaneous, life-threatening bleeding episodes
  • F.VIII is an essential cofactor in the intrinsic pathway and deficiencies result in prolongation of the APTT
  • The diagnosis is confirmed by a specific F.VIII assay
49
Q

What is haemophilia B and how do we diagnose?

A

Factor IX deficiency (Haemophilia B)

  • Factor IX deficiency is also a sex-linked inherited condition, which clinically is identical to F.VIII deficiency, since both factors are active at the same point in the coagulation cascade
  • The diagnosis is confirmed by a specific F. IX assay
50
Q

How do we manage/handle any animal with a coagulopathy?

A
  • Avoid subcutaneous injections
  • Do not use intramuscular injections

–Always have IV access

–If they go into circulatory collapse – you are doomed

  • Minimise invasive procedures
  • Handle gently
51
Q

How do we treat haemophilia?

A

•Small bleed contained by anatomical structures (e.g. haemarthrosis)

–pain relief is essential (care with drugs!)

–restrict movement

•Fresh plasma / FFP/ whole blood transfusion

–Giving whole blood might be too much – but like if its all you got its better than nothing

•Other options depending on availability

–Porcine factor VIII for haemophilia A

–cryoprecipitate (factor VIII) or
cryosupernatant (factor IX)

52
Q

What happens with coumarin poisoning?

A

Vitamin K antagonism

  • Depletion of clotting factors II, VII, IX and X
  • Clinical signs of poisoning may appear within <1 to 3 days
  • Haemorrhage may occur in a large number of sites, both externally and particularly into body cavities
  • Factors in both the intrinsic and extrinsic pathways become depleted
  • Since factor VII has a shorter half life than other factors, the prothrombin time (OSPT) is prolonged initially but later the activated partial thromboplastin time (APTT) also increases
53
Q

How can we treat vitamin K antagonism?

A

•+- Induce emesis, gastric lavage, enema, activated charcoal

–Acute rapid symptomatic therapy

•Therapy is Vitamin K

–Care about the route!!

–At the time of arrival – INJECT! S/C or I/M

  • DON’T GO IV – anaphylaxis
  • Several weeks to months of treatment may be required depending on type of coumarin
  • The OSPT promptly returns to normal with appropriate therapy, but if therapy is withdrawn too soon it will become prolonged again
54
Q

What do labatory tests of coagulation reveal in hepatic disease?

A

Elevation of both OSPT and APTT tests

55
Q

What confirms liver damage?

A

•Increased plasma concentrations of liver enzymes

56
Q

What confirms hepatic dysfunction?

A

Increased bile acid concentrations

57
Q

How can we test for tertiary haemostasis?

A

•Test for fibrinolysis

–fibrin(ogen) degradation products (FDPs)

–D-dimer

•Test for inhibitors (antithrombin)

–% of species-specific plasma pool

–healthy animals >80%

–<50% = risk of thrombosis

58
Q

What’s Virchow’s triad?

A
  • Endotelial injury
  • Abnormal blood flow
  • Hypercoagubility
59
Q

What is seen in thrombosis?

A
  • Decreased level of antithrombin III
  • Very marked increase ­ D-dimer, (FDPs)
60
Q

What happens in DIC?

A
  1. Primary and secondary haemostatic plugs form simultaneously in many small vessels

= multiple organ microthrombosis = ischaemic necrosis & organ failure

2.

Paradoxical bleeding

–Consumption of platelets = thrombocytopenia

–Consumption of clotting factors

–Consumption of anticoagulants

–Fibrinolysis = inactivation of clotting factors

= FDPs inhibit normal platelet function

61
Q

What are the possible mechanisms of DIC?

A

•Endothelial damage

–Electrocution, heat stroke, (sepsis)

–Sepsis via endothelial damage

•Platelet activation

–Mainly viral (e.g. FIP), endotoxaemia, platelets in dogs with cancer hyperaggregable

–Infection - common

•Release of tissue procoagulants

–Trauma, pancreatitis, bacterial infections, erythema multiforme and some neoplasms (e.g. haemangiosarcoma)

62
Q

Name 5 triggering conditions in dogs for DIC (7)

A

–Haemangiosarcoma

–Sepsis

–Pancreatitis

–Immune-mediated haemolytic anaemia

–Metastatic malignancies

–Erythema multiforme

–A. vasorum

63
Q

Name 3 triggering conditions for DIC in cats (5)

A

–Lymphoma (liver)

–Cholangiocarcinoma

–Pancreatic adenocarcinoma

–Sepsis

–Hepatic lipidosis

64
Q

What are the clinical features of DIC?

A

•Several presentations

–Chronic / silent / subclinical

–Acute / fulminant in dogs

•Profuse spontaneous bleeding (suggestive of primary and secondary bleeding)
& signs secondary to anaemia or parenchymal organ thrombosis (i.e. end organ failure)

65
Q

How do you diagnose DIC?

A
  • No single pathognomic test
  • An initiating disease

–Serum biochemistry & urinalysis

•Combination of haemostatic abnormalities

–thrombocytopenia

–prolonged clotting times (PT / aPTT)

–D-dimers (FDPs) raised

–antithrombin lowered (cant measure in clinica)

–hypofibrinogenaemia

•Shistocytes – blood cells pass through disturbed vascular network

66
Q

How do you treat DIC?

A

•Heparin treatment

–only effective if sufficient antithrombin

–acts to halt intravascular coagulation and decreases activity of the fibrinolytic system

  • Blood / blood products
  • Increase tissue perfusion
  • Prevent secondary complications
67
Q

What are the diagnostic tests for:

A) Primary disorders?

B) Secondary disorders?

C) Tertiary disorders?

A

A) Platelet count, BMBT, platelet function, vWf

B) WBCT, APTT, OSPT, (specific factors)

C) D-Dimers (FDPs)

Small Animal Final Year (317 decks)

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