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Module 15 > Disorders of Hemostasis in Small Animals > Flashcards

Disorders of Hemostasis in Small Animals Flashcards

1
Q

what is hemostasis

A

stopping of a flow of blood

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2
Q

what is reduced hemostasis

A

bleeding

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3
Q

what is increased hemostasis

A

thrombosis

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4
Q

what are primary bleeding disorders (3)

A
  1. thrombocytopenia
  2. thrombocytopathia
  3. vWD
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5
Q

what are secondary bleeding disorders (3)

A
  1. rodenticide toxicity
  2. liver disease
  3. congenital factor deficiencies (hemophilia)
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6
Q

what are tertiary bleeding disorders

A

hyperfibrinolysis

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7
Q

what are mixed bleeding disorders

A
  1. DIC
  2. angiostrongylus vasorum
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8
Q

what are the steps in normal hemostasis

A
  1. primary
  2. secondary
  3. tertiary
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9
Q

what is primary hemostasis

A

formation of platelet plug

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10
Q

what is the secondary hemostasis

A

stabilization of the platelet plug –> fibrin formation

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11
Q

what is tertiary hemostasis

A

breakdown of platelet plug

aka fibrinolysis

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12
Q

what are the steps in primary hemostasis (4)

A
  1. vessel injury causes the release of tissue factor (TF) which is naturally found on the surface of the subendothelial collagen. Becomes exposed to the blood following injury
  2. blood vessel constricts in response to injury: slows the flow of blood
  3. platelets bind to exposed tissue factor using vWF as a bridge and become activated
  4. a loose plug of activated platelts is formed over the defect in vessel wall. This is only loosley held in place by vWF and interactions between platelets. Red cells are trapped amongst the platelets
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13
Q

what does primary hemostasis require to occur successfully (4)

A
  1. normal platelet number
  2. normal platelet function
  3. normal vWF activity
  4. normal vessel wall function (vasoconstriction)
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14
Q

what occurs during secondary hemostasis

A

clotting cascade (intrinsic, extrinsic, common pathways)

culminates in formation of fibrin –> cross linked into a mesh around the platelets

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15
Q

describe the clotting cascade pathway

A
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16
Q

what occurs in tertiary hemostasis

A

plasminogen is converted into plasmin which breaks down fibrin into fibrin degredation products (FDPs)

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17
Q

what other clinical diseases can cause epistaxis (5)

A
  1. hemostatic disorder
  2. hypertension
  3. nasal tumour
  4. aspergillosis
  5. nasal foreign body
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18
Q

what other clinical diseases can cause hemoabdomen (4)

A
  1. hemostatic disorder
  2. trauma
  3. post surgical
  4. neoplasia (splenic tumour, hepatic tumour, vena cava invasion)
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19
Q

what are 3 key things to diagnose a hemostatic disorder

A
  1. history
  2. clinical exam
  3. tests of hemostasis
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20
Q

what are specific primary hemostatic disorder clinical signs (8)

A
  1. petechiae
  2. echymoses
  3. oozing from wounds
  4. intraoperative bleeding
  5. capillary ooze
  6. epistaxis
  7. melena
  8. hematuria
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21
Q

what are the clinical signs for secondary hemostatic disorders (7)

A
  1. echymoses
  2. hematomas
  3. hemoarthrosis
  4. hemothorax
  5. hemoabdomen
  6. large body cavity bleeds
  7. subcutaneous hematomas
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22
Q

what are typical owner reported problems in primary hemostatic disorders

A
  1. melena
  2. bleeding from gums
  3. epistaxis
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23
Q

what are tests of primary hemostasis (4)

A
  1. buccal mucosal bleeding time
  2. platelet count
  3. platelet function
  4. vWF assays
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24
Q

what are tests of secondary hemostasis

A
  1. prothrombin time (PT)
  2. activated partial thromboplastin time (APTT)
  3. measure fibrinogen levels
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25
Q

what are tests of tertiary hemostasis

A
  1. fibrin degredation products (FDPs)
  2. D-dimers
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26
Q

what are mixed tests (viscoelastic tests)

A
  1. TEG
  2. TEM
  3. ROTEM
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27
Q

what is the first step when interpreting the platelet count

A

do you trust the hematology analyzer?

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28
Q

how do assess whether or not the platelet count is accurate

A

blood smear

check feathered edge for clumping

count # of platelets in 10 oil immersion fields and multiply by:

dogs 1.5 x 10^9/l

cats: 2 x 10^9/l

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29
Q

what is the reference range of platelet count in dogs and cats

A

dogs: 200 x 10^9/l
cats: 300-800 x 10^9/l

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30
Q

what platelet count value do you start to worry and what value does spontaneous bleeding occur at

A

worry at <50 x 10^9/l

spont bleeding: <30 x 10^9/l

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31
Q

what are common platelet count problems

A
  1. platelet clumping is present
  2. red cell platelet overlap
  3. large platelets in certain breeds (ex. CKCS have larger size than normal and fewer #)
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32
Q

what is thrombocytopenia

A

decreased platelet #

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33
Q

what are the causes of thrombocytopenia (5)

A
  1. decreased production (bone marrow disorder)
  2. increased destruction: immune mediated thrombocytopenia (IMTP), infectious disease (Ehrlichia)
  3. sequestration
  4. increased consumption: bleeding, DIC (angiostrongylus vasorum)
  5. breed idiosyncrasy (CKCS)
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34
Q

what does the platelet count need to be in order to be the primary cause of bleeding

A

<50

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35
Q

what are the 3 scenarios that lead to thrombocytopenia

A
  1. platelets are being destroyed
  2. severely used up
  3. failure of production
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36
Q

what should you look at if you think that there is a failure of production of platelets

A

look for other cytopenias (anemia, leukopenia, etc)

chemotherapy

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37
Q

what are the diagnostic work up for thrombocytopenia

A

look for causes of destruction

  1. rule out infectious diseases (anaplasma, ehrlichia, angiostrongylus vasorum)
  2. rule out neoplasia
  3. +/- bone marrow assessment?
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38
Q

how do you diagnose immune mediated thrombocytopenia (IMTP)

A

dx of exclusion if all secondary causes ruled out

39
Q

what is the signalment of immune-mediated thrombocytopenia (IMPT)

A

median age 4-5 years, but can be ANY

cocker spaniels seem predisposed

40
Q

what are the presenting signs of IMTP

A

primary hemostatic disorder: surface/capillary bleeding

41
Q

how is IMTP managed (3)

A

gentle handling

  1. blood transfusion only if anemia enough to CV compromised
  2. treatment of underlying trigger if secondary (infection, neoplasia?)
  3. immunosuppression: steroids (1-2mg/kg/24h), +/- second line agent
42
Q

can a transfusion replace platelet number

A

no you can’t give enough to increase the platelet number substantially and reduce risk of bleeding

even whole blood will not replace PLT

43
Q

if the platelet count is >50 but <200, why would that be?

A

this count isn’t low enough to cause spont bleeding

bleeding is causing PLT to be used up

44
Q

what is the workup if the PLT is >50 but <200 (3)

A
  1. is there bleeding? remember not all bleeding is a coagulopathy
  2. is there a secondary hemostasis disorder?
  3. is there a mixed disorder? DIC?
45
Q

what does prothrombin time (PT) test

A

extrinsic and common pathways

46
Q

what does activated partial thromboplastin time (APPT) test

A

intrinsic and common pathways

47
Q

what are common disorders of secondary homeostasis (3)

A
  1. vitamin K antagonism (rodenticide toxicity)
  2. vitamin K deficiency (hepatic/cholestatic disease)
  3. specific factor deficincies (hemophilia A and B, hageman effect factor XII)
48
Q

what is the cause of vitamin K antagonism

A

coumarin based rodenticides

first generation: warfarin

second generation brodifacoum, etc etc –> many types

inhibit enzymes that activates the vitmain K dependent factors –> II, VII, IX, X

49
Q

what are the clinical signs of vitamin K antagonism

A

secondary hemostatic: cavity bleeds

known intoxication: initally asymptomatic (~3 days)

50
Q

how is vitamin K antagonism diagnosed

A

history: any access?
testing: PT and APTT times

51
Q

what does vitamin K antagonism diagnosed using clotting times

A

PT: prolongs first (usually within 48 hours, before clinical bleeding starts –> factor VII has the shortest 1/2 life)

APTT: prolongs second

52
Q

how is vitamin K antagonism treated if there is a known recent ingestion

A

emesis, decontamination

monitoring PT (starting 48 hours post ingestion)

53
Q

how is vitamin K antagonism treated if there is increasing PT or active bleeding

A
  1. vitamin K: subcutaneous for 24-48h and then ongoing oral (several months)
  2. supportive care: thoracocentesis only if dyspnea with pleural effusion, transfusion (whole bood if CV unstable), fresh frozen plasma more specific to replace factors
54
Q

what are the casues of vitamin K deficiency (2)

A
  1. end stage liver disease: reduced production of clotting factors, reduced activation of vitamin K dependent factors
  2. severe cholestasis: reduced liver ability to recycle vitamin K dependent factors
55
Q

what are the clinical signs of vitamin K deficiency (3)

A
  1. secondary homeostasis: except cavity bleeds
  2. clinically spontaneous bleeding unlikely
  3. increased bleeding risk with surgery/biopsy
56
Q

how do you test between vitamin K antagonism or deficiency

A
  1. prolongation of both PT and APTT can be seen
  2. is there concurrent signs of liver/cholestatic disease? (increased liver enzymes, increased bilirubin, reduced albumin, reduced urea)
57
Q

what are the clotting factor deficiencies

A
  1. hemophilia A (factor VIII)
  2. hemophilia B (factor IX)
  3. factor XII deficiency (factor XII in cats)
  4. others: rare deficiency of factors II, VII, X, XI, XII
58
Q

what are the clinical signs in factor X deficiency

A

causes high neonatal mortality

59
Q

what are the clinical signs of hemophilia A and B

A

young animals: usually <1 year old

X-linked recessive: MALE animals

unexpectedly severe/spontaneous hemorrhage

prolonged APTT, normal PT

60
Q

what are the clinical signs of factor XII (hagemen trait)

A

asymptomatic

prolongs APTT

61
Q

when should a BMBT test not be done

A

not before you have done a platelet count

62
Q

when should bleeding stop in a BMBT

A

2-4 mins

63
Q

if there is a prolonged of BMBT

A

vWD

thrombocytopathia

64
Q

if there is a normal BMBT, clotting time and platelet count what could the cause be

A

angiostrongylus

hyperfibrinolysis

65
Q

what is von willebrand’s disease caused by

A

reduced vW factor concentration or function

congenital: breed predisposition (dobermann)

66
Q

what are the clinical signs of von willebrand’s disease

A

excessive hemorrhage with trauma or surgery

67
Q

how do you test for von willebrand disease

A

<50% vWF:Ag = affected

68
Q

what is the treatment of von willebrand disease

A

may be none needed

in the face of bleeding or prior to surgery –> desmopressin, cryoprecipitate

69
Q

what is thrombocytopathia

A

due to defective pseudopod formation and lack of spreading of platelets, i.e., defective adhesivity in contact with wettable surfaces.

70
Q

what are the clinical signs of thrombocytopathia

A

primary disorder

71
Q

what are the causes of thrombocytopathy (4)

A
  1. congenital
  2. infectious (Ehrlichia)
  3. systemic diseases (uremia/hepatic disease)
  4. drugs: NSAIDs, aspirin, clopidogrel
72
Q

how do you test for thrombocytopathy

A

difficult most commonly a diagnosis of exclusion

PFA/platelet aggregometry –> not available clinically

73
Q

how is thrombocytopathy managed

A

supportive

treat underlying disease

74
Q

what is hyperfibrinolysis

A

excessive breakdown of fibrin

75
Q

what are the causes of hyperfibrinolysis (4)

A
  1. liver disease
  2. angiostrongylus
  3. trauma
  4. congenital (suspected cause for increased bleeding in greyhounds ex. post dental extractions)
76
Q

how do you test for hyperfibrinolysis

A

FDPs, D-dimers

global tests –> TEG

77
Q

how do you manage hyperfibrinolysis

A

supportive

tranexamic acid

transfusion: fresh frozen plasma

78
Q

how does tranexamic acid work

A

inhibits the activation of plasminogen and prevents breakdown of fibrin

79
Q

what are the clinical signs of angiostrongylus vasorum

A
80
Q

how does angiostrongylus cause bleeding

A

can affect all parts of homeostasis

81
Q

how does angiostrongylus disrupt primary hemostasis (4)

A
  1. acquired vWF deficiency
  2. thrombocytopenia (immune mediated or consumptive)
  3. abnormal platelet function
  4. blood vessel endothelial disruption
82
Q

how does angiostrongylus disrupt secondary hemostasis (2)

A
  1. immune complex activation of clotting factors
  2. parasite secretes anticoagulant factors
83
Q

how does angiostrongylus disrupt tertiary hemostasis (2)

A
  1. reduced serum fibrinogen levels
  2. hyperfibinolysis
84
Q

how is angiostrongylus vasorum diagnosed

A
  1. fecal baermanns for L1 larvae
  2. in house ELISA: IDEXX angiodetect
85
Q

how is angiostrongylus vasorum treated

A

supportive care for hemorrhage

parasite kill

steroids: for worm kill immune side effects

86
Q

what medications kill the angiostrongylus parasites

A

imidacloprid/moxidectin and milbemycin

fenbendazole also effective but unlicensed

87
Q

how is angiostrongylus prevented

A

slug and snail control

prophylactic monthly parasite prevention

88
Q

how do you clinically judge if both platelet count and coagulation times are abnormal (3)

A
  1. if PT and APTT massively prolonged, PLT slightly low –> probably just consumption of PLT
  2. PLT <30, PT and APPT a second or two prolonged –> focus on thrombocytopenia
  3. both markedly abnormal –> concern for DIC
89
Q

what is DIC

A

disseminated intravascular coagulation

90
Q

what causes DIC

A

systemic coagulation and fibrinolysis together

91
Q

what are the effects of DIC

A

mix of thrombosis and bleeding: spectrum of signs over time

92
Q

what disorders can cause DIC and how

A

due to widespread endothelial damage/release of tissue thromboplastins

  1. inflammatory
  2. traumatic
  3. neoplasia
  4. angiostrongylus vasorum
93
Q

how do you test for DIC

A
  1. increased APTT (first) and PT
  2. thrombocytopenia (consumptive)
  3. decreased fibrinogen
  4. increased FDPs and D-dimer
  5. TEG/ROTEM: various curve shapes
94
Q

what are the treatment principles for DIC

A
  1. eliminating initiating cause
  2. ensuring adequate tissue perfusion
  3. supporting target organs usceptible to microthrombi, ischemia or hemorrhage
  4. replacement of blood components
  5. anticoagulants (heparin?)

Module 15 (27 decks)

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