L27: Disseminated Intravascular Coagulation Flashcards

1
Q

What is DIC

A

Complex & acquired disorder of haemostats that commences with widespread activation of blood coagulation within microcirculation and may progress to sustained fibrinolysis and haemorrhage!!!

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2
Q

Is DIC a bleeding or clotting disorder?

A

Initially a clotting disorder that leads to haemorrhage

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3
Q

Is DIC a primary dz?

A

nah –> there are triggers for it!

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4
Q

What are some brief examples of pathologies that can trigger DIC

A

Pancreatitis, tissue trauma, snake envenomation, trauma, malignant neoplasia, foetal membrane retention, tumours releasing proteases, bacteraemia, widespread vascular endothelial injury, heart worm, widespread hepatic necrosis, GDV, shock, stagnant blood flow following prolonged anaesthesia etc.

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5
Q

Which major mechanisms trigger DIC?

A

large release of TISSUE FACTOR (factor III aka thromboplastin) which activates the extrinsic coagulation system

Wide endothelial injury

G- endotoxin release

tumours releasing proteolytic enzymes

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6
Q

What occurs during phase 1 of DIC (compensated)

A

Hypercoagulability

Primary disease –> procoagulants released –> counterbalanced (antithrombin III etc.)

Clin signs= of primary disease

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7
Q

Why does phase 2 of DIC occur?

A

run out of anticoagulants!!!

ECs change to procoagulant phenotype, fibrinolysis is suppressed

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8
Q

What happens n DIC phase 2?

A

run out of anticoagulants –> congestion/ oedma/ haemorrhage –> microthrombosis

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9
Q

What clinical signs are evident in DIC phase 2?

A

coughing, in RR, cyanosis, shock, pallor, prolonged CRT, organ failure, coma

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10
Q

What is microangiopathic haemolytic anaemia?

A

fragmented trauma to circulating erythrocytes –> schistocytosis

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11
Q

What happens during phase 3 of DIC?

A

Haemorrhage!

Platelets and coagulation factors have been exhausted –> thrombocytopenia –> haemorrhage

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12
Q

why are systemic inflammatory responses and cytokine cascades activated in DIC?

A

systemic inflammatory response
Cytokine cascades
*activated coagulation factors are generally pro-inflammatory

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13
Q

Why do DIC animals go into shock?!

A

Clotting factors generate kinins e.g. bradykinin –> mass vasodilation + increased vascular permeability –> systemic hypotension

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14
Q

What stage of DIC is associated with the highest morbidity and mortality?

A

2

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15
Q

What post mortem lesions might you find from an animal that has died from DIC?

A

Microscopic thrombi in tissues,

Large volume bleeds

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16
Q

How does DIC evolve?

A

changes from a thrombotic disorder to a widespread haemorrhage dx (due to thrombocytopenia etc.)

17
Q

Which coagulation cascade is activated in early DIC?

A

extrinsic