4.3.5: Haemostatic disorders - Thrombosis and DIC Flashcards

1
Q

What does thrombosis result from? (Physiology)

A

3 abnormalities:
* Endothelial injury
* Alterations in blood flow (either stasis or turbulence, stasis probs more important)
* Hypercoagulability

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2
Q

What is hypercoagulability and what might it result from?

A

Hypercoagulability: defined as an abnormally activated haemostatic system that predisposes a patient to thrombosis. This can result from:
* Hyperfunctional platelets
* Activation of coagulation with generation of excessive thrombin
* Deficiency of inhibitors

Hypercoagulability is a characteristic feature of DIC. It occurs in conditions known to initiate DIC e.g. severe inflammation, sepsis, cancer, IMHA (dogs), GI disorders associated with endotoxaemia e.g. strangulating obstructions, colitis in horses

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3
Q

How do you test tertiary haemostasis?

A

Tertiary haemostasis: breakdown of the clot.
* Test for fibrinolysis by testing levels of fibrinogen and its degradaton products, FDPs, e.g. D-dimer
* High D-dimers = lots of clots being broken down
* Can also theoretically test for levels of inhibitors e.g. antithrombin III -> if this is low, there is a risk of thrombosis

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4
Q

When might D-dimers be elevated?

A

When the animal is in a pro-thrombotic state
Examples
* Feline thromboembolic disease
* Protein-losing nephropathy/ enteropathy -> clotting factors are being lost
* Hyperadrenocorticism -> steroids cause a thromboembolic state

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5
Q

1

A

Platelet count, BMBT, platelet function, vWF

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6
Q

2

A

WBCT, APTT, OPST (PT), specific factors

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7
Q

3

A

D-dimers (FDPs)

FDP: fibrinogen degradation products

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8
Q

Describe the pathogenesis of DIC

A

Disseminated intravascular coagulation (DIC)
* a.k.a. death is coming
* This occurs when there is excessive activation of the haemostasis pathways (this has been triggered by something)
* At the start, you are more prone to making clots
* Then, you have no clotting factors and platelets because you used them all up, so then you bleed
* This all happens subclinically until it doesn’t because it’s catastrophic

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9
Q

Describe the clinical presentations of DIC and species differences

A
  • Cats like to clot (they favour thrombotic disease)
  • Dogs like to bleed

DIC can present in various ways:
* Chronic/ silent/ subclinical
* OR acute/ fulminant in dogs -> there is profuse spontaeous bleeding (primary and secondary haemostasis suggested) with possible signs secondary to anaemia or parenchymal organ thrombosis i.e. end organ failure

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10
Q

True/false: DIC always occurs secondary to an inciting cause.

A

True
Examples of inciting causes:
* Endothelial damage e.g. electrocution, heat stroke, sepsis
* Platelet activation often viral e.g. FIP, endotoxaemia, neoplasia
* Release of tissue procoagulants e.g. trauma, pancreatitis, bacterial infections, erythema multiforme and some neoplasia (haemangiosarcomas)
* Basically anything

If a neoplasia is the cause of something, going for either haemangiosarcoma or lymphoma is often a good idea. They cause most things so usually a safe bet.

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11
Q

What is overt DIC and what clinical signs might you see?

A

Overt DIC: the disease is clinically detectable.
* Widespread microvascular thrombosis decreases blood flow to vital tissues causing hypoxic injury, cell death, and organ failure -> high morbidity and mortality
* Sometimes there is only the overt phase of DIC, if the inciting cause is bad and acute enough

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12
Q

How can you test for DIC?

A

No single pathognomonic test for DIC
* Confirm and identify an intiating disease e.g. infectious cause
* Identify haemostatic abnormalities:
* Thrombocytopaenia / dropping platelet count
* Prolonged clotting time (PT/ aPTT)
* Low antithrombin III
* Hypofibrinogenaemia as coagulation factors get used up
* High FDPs/ D-dimers
* Schistocytes, keratocytes, acanthocytes - although this is non-specific

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13
Q

Treatment of DIC

A
  • Must identify and treat underlying cause, otherwise is hopeless
  • Supportive care: fluid therapy to increase tissue perfusion, and for shock, correction of acidosis etc.
  • Could do transfusion but limited evidence for this
  • Could give heparin -> this acts to halt intravascular coagulation and decreases activity of the fibrinolytic system, but only works if you have sufficient antithrombin
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14
Q

Which virus in rabbits can cause DIC?

A

Rabbit haemorrhagic disease virus (RHD2)
* Incubation period 3-9 days
* Some animals remain subclinical and may shed the virus for several weeks
* Less virulent and lower mortality than RHDV classical form

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15
Q
A

b) PCV and coag is most appropriate
* PCV willl tell us whether we need to transfuse/ what our starting point pre-transfusion is
* Coagulation profile will show us where the cascade is failing -> in this case we are considering a genetic coagulopathy
* A blood smear and manual platelet count are always good but will not save you here

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16
Q

True/false: BMBT will increase with disorders of secondary haemostasis.

A

False
BMBT tests primary haemostasis

17
Q

Which of the following tests would be abnormal with thrombocytopathia?
a) PLT count
b) BMBT
c) Platelet function assay

A

b) BMBT will be increased
c) Platelet function assay will be abnormal

18
Q

When will you see raised D-dimers?

A

When the animal is in a prothrombotic state
May see with inflammatory disease BUT NOT ALWAYS.