Clotting Flashcards

1
Q

Polycythemia vera sx?

A

vertigo, tinnitus, TIA, splenomegaly, clotting, thrombocytosis

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2
Q

EPO in PCV?

A

decreased

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3
Q

secondary polycythemia EPO level?

A

increased

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4
Q

causes of secondary Polycythemia?

A

RCC, OSA, COPD

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5
Q

level of platelet in secondary polycythemia?

A

not increased

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6
Q

clinical findings of APS?

A

arterial or venous thrombosis, recurrent pregnancy losses

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7
Q

other symtpoms of APS?

A

livedo reticularis, migraines, chorea, TIA

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8
Q

Labs for APS?

A

thrombocytopenia, hemolysis, coombs postivie, B2 glycoprotein, lupus anticoagulant, anticardiolipin

Elevated PTT

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9
Q

treatment of APS?

A

anticoagulation, steroids, pharesis if MAHA

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10
Q

factor V leiden mutation mechanism?

A

prevents protein C from braking down coagulation cascade therefor thrombophilic

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11
Q

high risk sites for DVT?

A

iliac, fem, pop 50% will travel

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12
Q

protein C deficiency genetics?

A

AD

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13
Q

protein C typically inhibits what?

A

factor V, VIII

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14
Q

thrombotic complication of PC vera?

A

mesenteric vein thrombosis

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15
Q

mechanism of polycythemia vera?

A

Jak2 mutation

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16
Q

how is vitamin K synthesized?

A

gut bacteria

17
Q

what can lead to a vitamin K deficiency?

A

chronic abx use depleting gut bacteria

18
Q

patients with APS and lupus can have a false positive for what disease?

A

syphillis (RPR), react with anticardiolipin ab

19
Q

ATIII deficiency presentation?

A

AD hypercoagulable disease

20
Q

resistance to what drug in ATIII deficiency?

A

heparin- PTT will remain normal because ATIII needed to achieve effect

21
Q

cryoglobulinemia association?

22
Q

cryoglobulinemia labs?

A

low complement,

23
Q

cryoglobulinemia presentation

A

hyperviscosity syndrome

24
Q

tx for HCV associated cryo?

A

ribavirin or direct hepatitis meds

25
how does heparin work?
potentiates ATIII binding to factor X and thrombin
26
ATIII deficiency?
clotting and heparin resistance- no increase in PTT with heparin
27
protein C deficiency?
prothrombotic AD dz with overactivity of V and VIII which are normally inhibited by protein C