Coag U4 - Thrombotic Disorders Flashcards

1
Q

thrombosis

A

inappropriate formation of a PLT or fibrin clot that obstructs a blood vessel

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2
Q

ischemia

A

loss of blood supply

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3
Q

necrosis

A

tissue death

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4
Q

thrombophilia

A

AKA hypercoagulability, predisposition to
thrombosis secondary to a condition

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5
Q

emboli

A

fragments of thrombi that move through the circulatory system and lodge in vasculature

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6
Q

pulmonary emboli (PE)

A

emboli that move through the heart and lodge in the arterial pulmonary vasculature

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7
Q

venous thromboembolism

A

prevalent in African Americans and women of childbearing age
symptoms of localized pain, sensation of heat, redness, edema

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8
Q

what are some examples of venous thrombosis?

A

PE and DVT

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9
Q

arterial thrombosis

A

activated PLTs, monocytes, and macrophages
embed fatty plaque within endothelial lining, suppress normal release of antithrombotic molecules (ex. NO, tissue factor) →
atherosclerotic plaque →
plaques rupture →
occlude arteries and trigger thrombotic events

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10
Q

what are some examples of arterial thrombosis?

A

MI and stroke

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11
Q

risk factors for thrombosis

A

age, immobilization, diet, pregnancy, smoking, inflammation, oral contraceptive use, hip/knee/prostate surgery

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12
Q

lupus anticoagulant

A

antiphospholipid antibody, the patient would clot which prolongs the result of PTT and therefore is more at risk for thrombosis

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13
Q

LAC testing

A

PTT – prolonged
mixing study – shortens prolonged PTT
DRVVT – ratio > 1.2
silica-based PTT – ratio < 1.2, difference of 8 seconds >

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14
Q

what are the 3 antiphospholipid antibodies?

A

LACs
ACL antibodies
anti-B2-GPI antibodies

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15
Q

APC resistance

A

factor V Leiden (R506Q) mutation gain of function renders factor V resistant to APC

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16
Q

prothrombin G20210A

A

mutation in prothrombin gene untranslated 3′ promoter region

moderate prothrombin activity elevation

17
Q

factor V leiden (FVL)

A

a mutation in the factor V gene

substitutes glutamine for arginine at position 506 of the factor V molecule (FV R506Q)

18
Q

what happens in FVL?

A

arginine substitution slows or resists APC hydrolysis

resistant factor Va remains active and raises production of thrombin, leading to thrombosis

19
Q

AT deficiency

A

enhanced by heparin, inhibits serine proteases IIa, IXa, Xa, and XIa

20
Q

PC deficiency

A

a serine protease that hydrolyzes factors Va and
VIIIa, requires protein S as a stabilizing cofactor

21
Q

PS deficiency

A

a stabilizing cofactor for activated protein C, 40% free, 60% circulates bound to C4bBP

22
Q

lipoprotein (a)

A

low-density lipoprotein that may predict
arterial thrombosis, contributes to thrombosis with antifibrinolytic property

23
Q

CRP

A

calcium-dependent pentameric ligand-binding member of pentraxin family
made in the liver

chronic CRP concentrations of 1.5 mg/L or greater =
atherosclerosis, low-grade inflammation → increased risk of MI or stroke

24
Q

FBG

A

increased fibrinogen = increased thrombosis

25
Q

homocysteine

A

amino acid intermediate in metabolism of dietary methionine

risk factor for arterial thrombosis

26
Q

disseminated intravascular coagulation (DIC)

A

consumption of coagulopathy, where generalized and uncontrolled hemostasis activation; bleeding and clotting at the same time

27
Q

DIC testings

A

PT and PTT – prolonged
FBG – decreased
PLT count and peripheral smear exam – confirms thrombocytopenia and schistocytes
D-dimer – increased

28
Q

acute DIC

A

associated with obstetric emergencies, intravascular hemolysis, septicemia, viremia, burns, acute inflammation, etc

29
Q

chronic DIC

A

associated with tissue necrosis

30
Q

Trousseau syndrome

A

tumor-induced chronic DIC that generates DVT and migrating thromboses causing ecchymoses and purpura fulminans

31
Q

heparin-induced thrombocytopenia (HIT)

A

an antiplatelet factor IV, consequence of an immune response to UFH and LMWH that is reflected in a reduced PLT count

32
Q

how does HIT affect hemostasis?

A

increases hemostasis