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GK F3 E6 Heme/Onc > Clotting Disorders > Flashcards

Clotting Disorders 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

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18
Q

PT and PTT MIxing study:

deficiencies caused by what?

A

supratherapeutic warfarin or rat poison

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19
Q

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

A

LAC

nonspecific factor inhibitors

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20
Q

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

A

lymphoproliferative d/o

monoclonal protein d/o

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21
Q

Warfarin:

What can supratherapeutic INR lead to?

A

elevated PTT

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22
Q

every 1.0 increase of PT is what of PTT?

A

16-17 sec PTT

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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

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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

AT III deficiency

41
Q

essential cofactor to allow conversion of prothrombin to thrombin, which then converts fibrinogen to fibrin –> clot

This is inactivated by protein C

What Factor?

A

Favtor Va

42
Q

single AA substituted allowing resistance to inactivation or activated protein C resistance so continues to clot d/t high levels of prothrombin –> thrombin (factor IIa)

WHat mutation?

A

Mutation Arg506Gln

43
Q

Mutation of nucleotide substitution in 3’-untranslated region of prothrombin gene which results in greater function of prothrombin (factor II)

What mutation?

A

Prothrombin Gene G20210A Mutation

44
Q

High levels of homocysteine lead to what?

A

Vascular injury

Intimal thickening

Elastic lamina disruption

Platelet aggregation

Smooth muscle hypertrophy

Impairs nitric oxide activity

45
Q

MTHFR deficiency- alanine to valine substitution at 677 amino acid position

Deficiencies of vitamins B6, B12 and folic acid

Fibrates and nicotinic acid increase

What condition?

A

Hyperhomocysteinemia

46
Q

What do you treat Hyperhomocysteinemia with?

A

Vit B12 & folate

47
Q

Recurrent arterial or venous thrombosis, pregnancy morbidity/fetal loss and presence of antiphospholipid antibodies including

Lupus anticoagulant (LAC)

Anticardiolipin antibody

Anti-Beta 2 glycoprotein

What dz?

A

Antiphospholipid Ab Syndrome (APS)

48
Q

body forms IgG or IgM antibodies against phospholipids

Phospholipids are involved in coag cascade

More arterial clotting

Sneddon syndrome (livedo reticularis and neurologic abnormalities)

What dz?

A

LAC and Anticardiolipin Ab

49
Q

Best test to evaluate VTE?

A

Doppler US: can be falsely negative with DVT below the knee

fi high suscpicion = repeat in 2-3 day

50
Q

Dx test for PE

A

CT angiogram

51
Q

If pt has renal insufficiency, pregnancy or anaphylaxis to iodine, what dx test would you do if they have VTE?

A

VQ scan

52
Q

How do you approach a pt with VTE?

A
  1. Find out if they have risk factors: Surgery, pregnancy, cancer, HRT, travel
  2. Start UFH or LMWH first and then warfarin: Sounds paradoxical but warfarin initially will drop protein c & s levels placing pt. at higher risk of VTE before actually taking effect to “thin” blood out

Can start with DOAC

If pt. started on UFH, LMWH, or warfarin, recommended not to run hypercoagulable panel because some tests will be falsely low

_Wait until off warfarin for at lease 3 weeks before running tests**_

53
Q

VTE & AC duration:

1st VTE

A

AC for 3-6 mos

54
Q

VTE & AC duration:

1st VTE and hypercoagulable

A

no need for lifelong AC

55
Q

Recurrent VTE & hypercoagulable

A

lifelong AC

56
Q

Who is tPA indicated for?

A

pts who have extensive clot burden

PE causing significant hemodynamic instability & RV strain

57
Q

When would you use an IVC filter?

A

pts who cannot take AC and have or are at risk for lower extremity DVT to prevent propogation of clot.

pt that had a BIG PE to avoid possible future lung injury

pts with high risk of bleeding complications

58
Q

SF thrombophlebitis TX

A

NSAIDS/ASA + warm compresses

Consider AC if:

>5cm

very symptomatic

clot is within 2 cm of where SF vein enters the deep vein

if pt had SF vein thrombosis while on ASA

59
Q
A

GK F3 E6 Heme/Onc (6 decks)

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