DIC Flashcards

1
Q

diagnostic value of schistocytes on peripheral smear for DIC diagnosis

A

this finding is neither sensitive nor specific for DIC

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2
Q

Indications for cryo in DIC

A

critical bleeding AND

fibrinogen level <50 mg/dL

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3
Q

Why d-dimer is commonly elevated in metastatic cancer

A

Systemic activation of hemostasis is common in metastatic cancer, even in the absence of thrombosis. Moreover, it has been implicated in tumor progression, angiogenesis and metastatic spread.

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4
Q

how is DIC diagnosed

A
  • Clinical + laboratory diagnosis (labs + inciting factor)
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5
Q

How does normal hemostasis work?

A

Blood clot forms at the site of vessel injury –> clot is resolved to allow tissue repair.

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6
Q

WHy is thrombocytopenia associated with DIC?

A

Microthrombi include platelets

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7
Q

Cancers highly associated with DIC

A

1) acute promyelocytic leukemia (APML)
2) mucinous tumors (eg, pancreatic, gastric, ovarian)
3) brain tumors

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8
Q

Thrombotic vs. bleeding risk of DIC

A
  • acute DIC is much more likely to present with bleeding (consumption of fibrinogen and other procoagulant factors and the disruption of normal fibrin formation and platelet function by the large amount of fibrin degradation products)
  • chronic DIC (more likely to present with thromboembolic complications because production of procoagulant factors keeps pace with ongoing generation of thrombi).
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9
Q

complication of chronic DIC in cancer patients

A

non-bacterial thrombotic endocarditis (marantic endocarditis, Libman-Sacks endocarditis, verrucous endocarditis)

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10
Q

organ dysfunction that can result from DIC

A

Mostly from vascular damage and hypoperfusion.
(basically everything)
- Acute renal failure
- Hepatic dysfunction
- Acute lung injury (damage to vascular endothelium)
- Neurologic dysfunction
- Adrenal failure

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11
Q

what is purpura fulminans?

A

Rare, life-threatening condition characterized by DIC, with extensive tissue thrombosis and hemorrhagic skin necrosis.

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12
Q

Laboratory differences between acute and chronic DIC

A
  • Prolonged PT and PTT and hypofibrinogenemia + thrombocytopenia more common in acute setting (clotting factor consumption)
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13
Q

Key principle in treatment of DIC

A

Treat underlying cause (eliminate the stimulus)

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14
Q

why you can’t give TXA to counteract fibrinolysis

A

It will increase risk of thrombosis

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15
Q

Risk of thrombosis with DIC generally speaking

A

Low, it’s still rare, more common if underlying trigger is infection
*more common in chronic

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16
Q

When to expect coagulation abnormalities to resolve after underlying issue is treated

A

There’s a LAG. DIC does not resolve immediately once the inciting factor is corrected. Resolution generally requires synthesis of coagulation factors, which are produced at different rates; clearance of anticoagulant factors and fibrin degradation products from the circulation, which depend on hepatic function; and production of new platelets from the bone marrow, which may take several days.

17
Q

Rule of thumb for cryo dosing and response in fibrinogen level

A

Each 10 units will increase fibrinogen by roughly 100

18
Q

pathophysiology of DIC

A
  • abnormally and massively activation of hemostasis and fibrinolysis
19
Q

when chronic DIC is typically seen

A

advanced malignancy (pancreatic, gastric, ovarian, brain tumors)