2013-11-1 Thrombophilia/Hypercoag States Flashcards

1
Q

acquired thrombophilias (just list ‘em)

A

—obesity
—HIT
—estrogens, cancer, pregnancy, surgery, inflamm
—hyperhomocysteinemia
—hemato d/o: PNH, myeloprolif
—APA (anti-phospholipid abs): lupus anticoag
—elevated coag fators (also familial)

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2
Q

hereditary thrombophilias (just list ‘em)

A
—Factor V Leiden
—Prothrombin Gene Defects
—Herid Prot C def
—Herid Prot S def
—Herid Antithrombin Def
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3
Q

how does obesity cause hypercoaguable state?

A

increases F8
—2° to inflamm cytokines made by adipose
—increased PAI-1 (Plasminogen activator inhib-1)

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4
Q

HIT (Heparin-induced thrombocytopenia)

A

poor name
—triggers antibodies Heparin-PF4* complex
—get removed by splpeen BUT THEN
—HO SHIT fragments of plts escape—> activate other platelets and you get GOD DAMN CLOTS MOTHAFUCKERRRRRRRRRR
—Shistocytes
—DON’T GIVE WARFARIN

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5
Q

Lupus Anticoag

A

Another stupid ass name; causes THROMBOSIS
—also not specific to lupus
—Abs against prothrombinase (Va-Xa)

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6
Q

Factor V Leiden

A

—most common herid thrombophilia
—causes resistance of FV to APC
—can be acquired (preg, thalidomide, OCPs, lupus anti-coag)
—more a polymorph (15% N euros)

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7
Q

Prothrombin Gene Defects

A

—herid incr in prothrombin

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8
Q

Herid Protein C Def

  • inheritance
  • associated complicaitons
A

-autosomal dominant

–incr RR of VTE =7; warfarin skin necrosis b/c Prot C is vit-k dep

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9
Q

Herid Prot S Def
-major comp
—types?

A

homozygous lethal
—VENOUS, thrombosis; warfarin-indcued skin necrosis
-three types:
-I: consumpation of prot S, vit k def, liver dz, hiv
-II: acquired?
-III: incr complement prot C46BP

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10
Q

Herid Antithrombin def

  • inheritance
  • comps?
  • acquired forms?
A
autosomal dom (homozygous lethal)
—also VENOUS, but worse than PC/PS def
—can also be acquired: liver dz, consumption (acute clot, DIC, heparin, preg), proteinuria, 1-asparaginase tx for leukemia
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