Clotting GK Flashcards

1
Q

Platelets and clotting factors circulate normally in an _________ form.

A

Platelets and clotting factors circulate normally in an inactive form.

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2
Q

Vascular injury disrupts endothelium and leads to what 3 things?

A
  1. Vascular spasm
  2. Platelet adhesion mediated by Von Willebrand factor
  3. Coagulation cascade
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3
Q

What does PT represent?

A

time in seconds for plasma to clot after addition of calcium and an activator of extrinsic pathway (thromboplastin)

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4
Q

What leads to a prolonged PT?

A

Deficiencies or inhibitors of clotting factors within extrinsic or final common pathways

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5
Q

Why was INR created?

A

PT results for identical patients vary with different labs

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6
Q

What is INR?

A

mathematical conversion of patient’s PT compared to geometric mean of PT of at least 20 healthy subjects of males and females at THAT lab

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7
Q

What does PTT (Partial Thromboplastin Time) measure?

A

integrity of intrinsic and final common pathways of coag cascade

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8
Q

What does PTT represent?

A

time in seconds for patient’s plasma to clot after the addition of phospholipid, an intrinsic pathway activator- calcium

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9
Q

if clotting times remain prolonged what should you think?

A

inhibitor

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10
Q

if clotting times normalize or decrease to near-normal what should you think?

A

factor-deficiency

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11
Q

What does PTT correct?

A

Factor DEFICIENCY of intrinsic pathway like factors VIII, IX, XI, or XII

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12
Q

How can you determine which clotting factor is involved with an abnormal PTT?

A

clotting factor assay

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13
Q

PTT stays prolonged with what?

A

an inhibitor: heparin, LMWH, AIH/Factor 8 inhibitor

Lupus anticoagulant

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14
Q

What do you see in pts w/LAC (lupus anticoag)?prolonged PTT

A

prolonged baseline PTT

Seen more in young females

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15
Q

When would you suspect LAC?

A

pt w/no bleeding hx

pt w/clot w/baseline prolonged PTT before Ant-coag was started

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16
Q

What should you think if a PT corrects with normal PTT?

A

DEFICIENCY of factors II, VII, and X or fibrinogen (2, 7, 10)

Liver dz (prolonged PT)

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17
Q

What should you think if PT is still prolonged with prolonged PTT?

A

Factor 5 inhibitor

18
Q

PT and PTT MIxing study:

deficiencies caused by what?

A

supratherapeutic warfarin or rat poison

19
Q

what inhibitors will you see in lymphoproliferative d/o or monoclonal protein d/o?

A

LAC

nonspecific factor inhibitors

20
Q

Pts with what 2 disorders can develop antibodies against self (have autoimmune characteristics)?

A

lymphoproliferative d/o

monoclonal protein d/o

21
Q

Warfarin:

What can supratherapeutic INR lead to?

A

elevated PTT

22
Q

every 1.0 increase of PT is what of PTT?

A

16-17 sec PTT

23
Q

3 MC reasons to use Warfarin

A

1) A-Fib INR 2-3
2) VTE INR 2-3
3) Mechanical valve replacement- INR 2.5-3.5

24
Q

Warfarin interferes with what factors and proteins?

A

factors VII, IX, X and proteins C & S

25
Q

Can you use warfarin in pregnancy?

A

No: Preggo X

26
Q

UFH inhibits which factors?

A

IIa (thrombin)

Xa

27
Q

UFH PK and risk

A

PK: large molecule: 30 units long and not well absorbed subcutaneously

risk of HIT

28
Q

What does LMWH inhibit?

A

More of Xa

some of IIa

29
Q

LMWH benefits

A

smaller so well absorbed subcutaneously

predictable 1/2 life

Ex: Enoxaparin, Dalteparin

Risk of HIT

Can give with preggos

30
Q

T/F: No need to draw blood tests to see if anticoag is therapeutic unless pt. is very obese or very thin

What would you draw if you had to?

A

TRUE

anti-factor Xa levels 3-4 hrs post LMWH administered

31
Q

synthetic pentasaccharide that inhibits factor Xa and binds to antithrombin III causing antithrombin III to go through conformational change inhibiting coag cascade

Half-life 17 hrs. long and NO reversal agent

Which med?

A

Fondaparinux

32
Q

Direct Xa inhibitors

A

Rivaroxaban

Apixaban

33
Q

ex of DOAC

A

dabigatran

34
Q

what are fondaparinux, rivaroxaban/apixaban and dabigatran used for?

A

A-fib & VTE

35
Q

What agents should be used to reverse overdose in the following meds?

  1. Heparin
  2. Enoxaparin
  3. Pradaxa
  4. Xarelto
  5. Fondaparinux
A
  1. Heparin: Protamine
  2. Lovenox/Fragmin: Protamine
  3. Pradaxa: Dialysis (if bleeding in brain) or Idarucizumab (if no bleeding)
  4. Xarelto/Eliquis- PCC
  5. Fondaparinux (Arixtra)- Novo 7, DDAVP
36
Q

RF for VTE & hypercoagulable state

A

stasis

recent trauma/surgery and hypercoagulable state

increased risk for venous thromboembolism (VTE)

CA (Trousseau’s syndrome)

pregnancy

smoking

estrogen

37
Q

Protein C & S along with antithrombin III deficiencies

Factor V Leiden mutation

Prothrombin gene mutation

Lupus anticoagulant

Hyperhomocysteinemia

Anticardiolipin antibody

Paroxysmal nocturnal hemoglobinuria

These are all…

A

hypercoagulable states

38
Q

what 3 things prevent overclotting?

A

Protein C, Protein S, and Antithrombin III

39
Q

Both are vitamin K dependent proteins

Both can be low in nephrotic syndrome

A

Protein C &S

40
Q

Can be low d/t liver disease, nephropathy or heparin

Mutations reduce levels or decrease its functional capacity

A

Antithrombin III deficiency

41
Q
A