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Hematology Block 2 > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What are the 3 broad sides of Virchow’s Triad?

A

Endothelial Injury

Venous stasis

Hypercoagulable state

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2
Q

What is included in the common methods of “endothelial injury” in Virchow’s triad?

A

Surgery

Prior DVT

Venous access

Trauma

Sepsis

Vasculitis

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3
Q

What is included in the common methods of “venous stasis” in Virchow’s triad?

A

Advancing age

Immobilization (e.g. bed-ridden, long plane flights)

Stroke, cord injury

Anesthesia

Heart or lung failure

Hyperviscosity (e.g. in Sickle cell patients)

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4
Q

What is included in the common methods of developing a hypercoagulable state in Virchow’s triad?

A

Protein C, S or AT III deficiency

Activated protein C resistance (Leiden)

Hyperhomocysteinemia

Antiphospholipid antibody

Prothrombin 20210 mutation

Sickle Cell

Cancer

Estrogen

Pregnancy

HIT

MPN

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5
Q

What is the differential diagnosis of a painful, red, swollen leg?

A

Clot

Baker’s cyst (a buildup of synovial joint fluid) that forms a cyst behind the knee

Soft tissue infection (cellulitis)

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6
Q

What are some important risk factors for developing a clot?

A
  • Prior hx of VTE
  • Family hx of clot
  • Surgical procedures
  • Hospitalization
  • Trauma
  • Pregnancy
  • Heart failure
  • Immobility
  • oral contraceptives or hormone replacement therapy
  • obstetric history
  • Cancer?
  • Other illnesses
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7
Q

The best option for diagnosing a DVT is _____ for a patient with a moderate or high probability of having a first episode of a DVT.

What are other good options?

A

Duplex ultrasound

can also do a contrast venography, MRI venography, or impedance plethysmography

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8
Q

In a person with a low pretest probability, a NEGATIVE ____ test can rule OUT a clot, but a POSITIVE test is less helpful - why?

A

In a person with a low pretest probability, a NEGATIVE D-dimer test can rule OUT a clot, but a POSITIVE test is less helpful because there is a long list of things that could cause a positive result.

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9
Q

How does a D dimer test work?

A

A D dimer is a fragment of crosslinked fibrin clot that has undergone fibrinolysis.

Indicates a clot has formed somewhere.

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10
Q

Why do we treat DVTs?

A
  • To prevent further clot extension
  • To prevent acute pulmonary embolism - 50% of untreated proximal DVT will lead to PE.
  • To reduce the risk of recurrent thrombosis
  • To relieve the symptoms of massive iliofemoral thrombosis with acute lower limb ischemia and/or venous gangrene (ie, phlegmasia cerulea dolens)
  • To limit the development of late complications, such as the post-thrombotic syndrome, chronic venous insufficiency, and chronic thromboembolic pulmonary hypertension.
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11
Q

How is a DVT treated?

A
  • Everyone should have a CBC and PT/INR and aPTT drawn at baseline. Kidney and liver function tests help determine which drugs can be used most safely
  • Everyone (almost) goes on an anticoagulant for at least three months
  • At three months, we’ll evaluate for necessity of continuing anticoagulation therapy.
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12
Q

What types of clots aren’t treated with blood thinners? Why?

A

Superficial venous clots

Distal DVTs

Because these rarely embolize or cause long-term symptoms, and anticoagulants increase the risk of bleeding—so if the risks outweigh the benefits. . .don’t treat

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13
Q

Superficial Femoral Vein:

A

IS actually a deep vein and NOT a superficial vein. A clot in the SFV is a DVT and needs to be treated as a DVT.

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14
Q

Which arm veins are superficial and which are deep?

A

Superficial: radial, basilic, cephalic (clots here usually result from IVs and do NOT need anticoagulation)

Deep arm veins: brachial, axillary, subclavian

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15
Q

How do most patients get PEs?

A

From a clot (often DVT) that fragments and lodges in a pulmonary artery.

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16
Q

What symptoms are commonly associated with a clot that lodges in a major branch of the pulmonary artery?

A

Hypotension, right heart failure, syncope, and death (from lack of cardiac output)

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17
Q

If a PE lands in a more peripheral branch artery of the lungs, what symtoms are commonly found?

A

SOB, cough, and chest pain that is pleuritic (hurts more to breathe, especially deep breathing due to ischemia of outer portion of lobes and pleural lining)

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18
Q

What is included in a differential diagnosis for acute chest pain?

A

PE

Pneumonia

MI

Costochondritis

Muscle strain

Panic attack

Trauma

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19
Q

How is a PE diagnosed?

A

•CT angiography:

  • CT scan with addition of contrast
  • Can see the clot or sometimes another reason for the pulmonary symptoms

•V/Q scanning:

  • A nuclear medicine study, looking at areas of ventilation and trying to match them with areas of perfusion
  • A V/Q mismatch indicates a clot (something that’s ventilated but not perfused)

•Pulmonary angiography – the gold standard (but CT w/ angio is quickest, cheapest)

•Echocardiography:

  • Can sometimes see the clot
  • Can see the effect of the clot on the right side of the heart
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20
Q

What is indicated in this image?

A

This is a CT angio that shows a bilobed PE called a “saddle PE”

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21
Q

What does this image indicate?

A

This is a V/Q mismatch test, which shows the difference in ventilation vs. perfusion of an area. In this photo, the patient has a PE in the R lobe.

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22
Q

How is a PE treated?

A
  • Mainstay is anticoagulation for at least three months
  • Can sometimes consider giving thrombolytic therapy for massive PE with right heart collapse
  • Supportive care (oxygen, blood pressure support)
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23
Q

What are IVC filters used for?

A
  • Interrupt the IVC (inferior vena cava) to “catch” clots arising from the lower extremities—preventing further PEs
  • Indicated in patients who are unable to safely use anticoagulation, such as someone who just had neurosurgery 12 hours ago with a new DVT or in someone with recurrent PEs despite therapeutic anticoagulation
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24
Q

What problems are associated with IVC filters?

A

They only work for a year, then they get clotted off and lead to worsening lower extremity symptoms

They can migrate and perforate

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25
Q

What are the consequences of an unprevented VTE?

A
  • Symptomatic DVT or PE
  • Fatal PE
  • Increased spending for investigating symptomatic patients
  • Increased risk of recurrence
  • Chronic post-thrombotic syndrome
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26
Q

What are the two categories of VTE prophylaxis?

A

-Mechanical:

  • Graduated Compression Stockings (GCS)
  • Intermittent Pneumatic Compression Devices (IPC)

-Pharmacologic (drugs given at lower doses than full “treatment” doses)

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27
Q

Thrombophilias are inherited states that predispose patients to _____.

A

blood clotting

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28
Q

Thrombophilias typically lead to ___ clots rather than ___ clots

A

Thrombophilias typically lead to venous clots rather than arterial clots

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29
Q

Describe the Protein C system:

A

Thrombin can act as both a pro and anti coagulant. When bound to thrombomodulin on an in-tact endothelial surface, thrombin acts as an anti-coagulant.

Here, it doesn’t activate platelets or fibrinogen or Factors 5 and 9 like it does when it is pro-coagulating in the serum. Instead, it activates Protein C. Activated protein C has a cofactor called protein S. These two inactivate Factor VIIIa and Va.

This turns off the coagulation cascade.

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30
Q

How is the aPTT changed when Activated protein C is added to a normal patient’s serum?

A

The aPTT gets longer, because it slows the coagulation cascade.

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31
Q

Factor V Leiden (FVL) is a mutation in the factor V molecule, rendering it resistant to cleavage by ______. Factor V remains a procoagulant and thus predisposes the carrier to ____ formation.

A

Factor V Leiden (FVL) is a mutation in the factor V molecule, rendering it resistant to cleavage by activated protein C. Factor V remains a procoagulant and thus predisposes the carrier to clot formation.

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32
Q

What is the mutation responsible for Factor V Leiden? What populations is this disease prevalent in?

A

Mutation: FV R506Q

Found in 5% of Caucasians

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33
Q

What are the symptoms associated with Factor V Leiden and why?

A

The deficiency in this disorder is due to a mutation in the factor V molecule, which makes it resistant to cleavage by Activated Protein C. As a result, the coagulation cascade can’t be properly turned off.

Patients thus experience an increased risk for their first episode of a DVT 5 fold.

HOWEVER, has no effect on VTE recurrence.

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34
Q

Many proteases cleave at ___ (amino acid). Why is this important in Factor V Leiden?

A

Cleave at arginines

Mutation in FV is R506Q, changing an arginine to a glutamate, thus abolishing the major cleavage site by APC.

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35
Q

The prothrombin G20210 mutation is a ____ mutation in the 3’ untranslated region of the ___ gene.

A

The prothrombin G20210 mutation is a gain of function mutation in the 3’ untranslated region of the Factor II gene.

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36
Q

Patients with the Prothrombin G20210 mutation have higher ___ levels, resulting in ____.

A

Patients with the Prothrombin G20210 mutation have higher Factor II levels, resulting in mild thrombophilia.

(increased risk for DVT 4 fold, no effect on VTE recurrence)

**factor II is prothrombin

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37
Q

What inherited thrombophilias are gain of function vs loss of function?

A

Gain of function:

  • Prothrombin G20210

Loss of function:

  • Factor V Leiden
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin deficiency
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38
Q

Among patients with thrombosis, what is the most common genetic disorder found?

A

Factor V Leiden

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39
Q

What is Antiphospholipid Syndrome and how is it characterized?

A

A clinico-pathologic diagnosis characterized by the presence of antibodies that can lead to an increased risk for clotting.

Requires BOTH clinical symptoms AND lab abnormalities

Clinical findings:

  • Thrombosis – venous or arterial
  • Recurrent pregnancy loss

Lab abnormalities—antiphospholipid antibodies:

  • Lupus anticoagulant or/and
  • Anticardiolipin antibodies
  • Beta-2- glycoprotein I antibodies

Mechanism of clots–unclear

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40
Q

How is Antiphospholipid Syndrome diagnosed?

A

These antibodies can occur as a reaction to a clot OR they can be the reason behind the clot.

We make sure that the antibodies are present at least twice—antibodies measured at least 12 weeks apart.

41
Q

What are common environmental risk factors for a VTE?

A
  • Estrogens - pregnancy, combined OCP, HRT
  • Surgery - abdomen/pelvis, orthopedic to back, pelvis, lower extremities
  • Trauma - back, pelvis, lower extremities
  • Prolonged immobilization - 3+ days bed rest, stroke
  • Long distance airline travel (6+ hours)
  • Indwelling venous catheters
  • Cancer (“Trousseau’s syndrome”)
42
Q

Why screen for a thrombophilia?

A
  • Because it might impact the length of anticoagulation
  • Because patients want to know why they had a clot
  • Because it may have impact on other family members in terms of OCPs, etc.
43
Q

Why NOT screen for a thrombophilia?

A
  • Because it’s expensive
  • Because at the time of a clot, some of the measurements of proteins can be abnormally low due to consumption
  • Because in a provoked event, it won’t change management
  • Because some of the mild thrombophilias may never produce symptoms,
  • Asymptomatic family members with the thrombophilia may not be able to get life/disability insurance
44
Q

What events might prompt a clinicial to consider screening for thrombophilia

A

NOT with a provoked VTE

Maybe if:

age <50

Clot in a weird place

Family history of clot

Recurrent clots

45
Q

How is Thrombophilia managed?

A

In asymptomatic carriers, consider prophylaxis in high risk situations

After a patient’s first clot, use standard 3-6 mo anticoagulation

Consider indefinite anticoagulation under the following circumstances:

  • Cancer
  • Antiphospholipid antibodies
  • Compound thrombophilias
  • Recurrent unprovoked VTE
46
Q

At low doses, aspirin produces an antithrombotic effect by irreversibly acetylating ___, thus inhibiting platelet generation of ______. Higher doses also inhibit _____.

A

At low doses, aspirin produces an antithrombotic effect by irreversibly acetylating COX-1, thus inhibiting platelet generation of thromboxane A2. Higher doses also inhibit COX-2.

47
Q

____ is used for both primary and secondary prevention of arterial blockages (MI, stroke, PVD)

A

aspirin

48
Q

List important adverse effects associated with aspirin use:

A

•GI upset

•GI bleeding—inflammation and peptic ulcer disease

•Can provoke asthma in atopic patients

•Contra-indicated in children and teenagers with chickenpox or flu symptoms (Risk of Reyes syndrome)

•Kidney damage by renal papillary necrosis

•At high doses, salicylate toxicity and tinnitus

49
Q

What is the mechanism of action of warfarin?

A

Warfarin is a vitamin K antagonist (interferes with the vitamin K cycle)

Warfarin interacts with the Vitamin K epoxide reductase enzyme so that oxidized Vitamin K cannot be recycled back to normal, functional reduced vitamin K (KH2), which is used to gamma-carboxylate the vitamin K-dependent factors.

This leads to a depletion of vitamin KH2, thereby limiting the γ- carboxylation of the coagulation factors (II, VII, IX, X, Protein C and S).

Factors like prothrombin are thus not gamma-carboxylated, and cannot effectively bind to phospholipid membranes. Thus blood coagulation is limited.

50
Q

Warfarin acts to block ___ synthesis of the vitamin K-dependent factors. Why is this important?

A

Warfarin acts to block NEW synthesis of the vitamin K-dependent factors.

SO there are still some pre-formed factors left, and thus Warfarin’s anticoagulant effect isn’t immediate.

51
Q

For the first three days of “warfarinization,” the levels of _____ drop faster than ______

A

For the first three days of “warfarinization,” the levels of protein C and S (anticoagulation factors) drop faster than procoagulation proteins (Factor II, VII, IX, X)

52
Q

What are bridging anticoagulant therapies and why are they used?

A

These are anticoagulant therapies that act quickly, such as heparin, that are used to reverse the temporary hypercoagulable state characteristic of the first 3 days of “warfarinization.” The hypercoagulable state is worse in patients with Protein C or underlying vitamin K deficiency. Additionally, patients are not fully anticoagulated until levels of factor II drop to 20% or so.

53
Q

What vitamin K-dependent clotting factor has the shortest half-life?

A

Factor VII

54
Q

What is warfarin used for?

A

•Treatment of VTE

•Prevention of thrombosis on mechanical heart valves and artificial hearts

•Prevention of embolic stroke in patients with atrial fibrillation

55
Q

How do we measure the effect of warfarin?

A

Measure the effect on the INR - in most cases, we want this value between 2-3

56
Q

What needs to happen when a patient begins warfarin?

A
  • Start dose (usually 5 mg)—check INR in 2 days
  • Lower dose in those with underlying Vit K deficiency
  • Bridge!!—and don’t stop the bridge for at least 5 days
57
Q

What is important for maintaining warfarin treatment?

A
  • Drug-food interactions - maintain steady amount of Vit-K containing foods
  • Drug-Drug interactions:
  • Drugs that interfere with CYP enzymes
  • Antibiotics - kill gut bacteria that make vitamin K

•Constant INR monitoring – weekly to start, then at least monthly

58
Q

What lab values do we test/expect to see while monitoring warfarin patients?

A
  • At therapeutic levels, we follow the PT/INR
  • At toxic levels, the aPTT will also be prolonged.
  • No effect on the PFA-100
59
Q

Possible side effects of warfarin:

A
  • Alopecia
  • Osteoporosis
  • Bleeding

•Warfarin Skin Necrosis

  • When warfarin is started in someone who is vitamin K deficient or who has protein C deficiency without bridging
    • Microvascular thrombosis
    • Fatty tissues
60
Q

Discuss warfarin use during pregnancy:

A
  • Warfarin is a teratogen (5-30% risk of birth defects)
  • Warfarin embryopathy
  • 1st trimester, especially between weeks 6-12
  • Bone/cartilage abnormalities
    • stippled epiphyses and nasal and limb hypoplasia

•Other—CNS abnormalities reported with warfarin use throughout pregnancy.

•OK for lactating women, since it’s not excreted into breast milk

61
Q

How is warfarin reversed?

A

-Vitamin K

-Plasman (not super helpful because you have to give a lot and it takes a while to thaw)

-Prothrombin complex concentrates (PCC)

  • Pharmacologic concentrate, plasma derived, virally inactivated
  • KCentra is a Mixture of Factor II, VII, IX, X
  • Fast, effective, and only a small amount needed to reverse effects.
62
Q

Heparin is a ________ containing variable amounts of a disaccharide-repeating unit of either iduronic acid or glucuronic acid residues linked to a glucosamine residue.

A

polysaccharide

63
Q

Heparin is composed of variable amounts of either iduronic acid or glucuronic acid residues, each of which is _______

A

variably sulfated

64
Q

Both the variation in polysaccharide sequence and length and the variation in the degree of sulfation results in a(n) ____ population of molecules that collectively is called heparin

A

heterogenous

65
Q

All of heparin’s effects require binding to ____. The resulting complex will then inactivate __, __, and __.

A

All of heparin’s effects require binding to antithrombin. The resulting complex will then inactivate Xa, IXa, and XIa.

66
Q

Full length heparin (at least ___ long) will form a ternary complex with ____ and ___, which accelerates the action of antithrombin to inactivate thrombin by 10,000 fold.

A

Full length heparin (at least 18 sugars long) will form a ternary complex with thrombin and antithrombin, which accelerates the action of antithrombin to inactivate thrombin by 10,000 fold.

67
Q

Unfractionated heparin:

A
  • Must be given intravenously (for treatment) or subcutaneously (for prophylaxis)
  • UFH has variable binding to plasma proteins, endothelium, and macrophages, So there is not a fixed dose for therapeutic anticoagulation.

•Must be monitored and administered in the hospital (generally)

68
Q

What is heparin used for?

A
  • VTE
  • Both treatment and prophylaxis (different doses)
  • Arterial occlusions—acutely
  • MI, stroke, peripheral arterial disease
  • Angioplasty
  • Vascular and cardiac surgery
  • Hemodialysis
  • Flushes to keep IV catheters patent
69
Q

How is heparin monitored?

A
  • Follow the aPTT (prolonged)
  • Follow the anti-Xa level (prolonged) (either directly measured or derived from the aPTT). Xa activity is measured by the rate of conversion of a substrate into a colored byproduct.
  • The TCT will be prolonged
  • The PT will be prolonged with very large doses of heparin, but normal otherwise
  • Why?? Because the PT reagent mix also contains heparinase to degrade any stray amounts of heparin around
70
Q

How is the anti-Xa level measured?

A
  • The lab activates FX to FXa using a snake venom.
  • Xa activity is measured by the rate of conversion of a substrate into a colored byproduct.
  • We then add the patient’s plasma to the reagent mix and see if it slow the conversion of colorless solution into a colored solution.
  • The decrease in rate is the Anti-Xa level
71
Q

Heparin side effects:

A
  • Bleeding
  • Osteoporosis with long-term use
  • Some patients can develop hyperkalemia
  • Development of HIT
  • 5% of patients treated with UFH
  • Can paradoxically lead to thrombosis
72
Q

What is the antidote to heparin?

A

Protamine sulfate

(positively charged—neutralizes the negatively charged heparin)

73
Q

Low Molecular Weight Heparin:

A
  • Made from UFH by further chemical or enzymatic processing.
  • Smaller—about 1/3 the size of UFH lengths
  • Multiple formulations, all a little different
  • Enoxaparin = Lovenox
  • Dalteparin
  • Tinzaparin
74
Q

How/when is LMWH administered and monitored?

A
  • Given Subcutaneously – best if given twice daily (bid)
  • Immediately bioavailable
  • Can use to bridge warfarin
  • Weight based dosing—very reliable anticoagulation
  • Cleared by the kidneys
  • No need to follow levels except in:
  • Children
  • Very obese
  • Renal insufficiency
  • Pregnant
75
Q

What is the mechanism of action of low molecular weight heparin?

A

Remember enoXaparin is the drug

  • Binds to AT using the pentasaccharide sugar motif
  • But the LMWH-AT complex cannot inactivate thrombin

•It ONLY inactivates Xa

76
Q

What levels are measured during LMWH monitoring?

A

•NO effect on the PT or aPTT

•I know—it doesn’t make sense—since it’s blocking FXa—which is needed to make a normal PT and aPTT. But trust me—it doesn’t prolong these tests. And no one I know can explain why.

•Need to follow Anti–Xa levels (order this as a LMWH level)

NO ANTIDOTE

77
Q

What is LMWH used for?

A

•VTE:

  • Treatment
    • Can be done at home if patients are taught to give themselves SQ injections
    • Especially in pregnant women
  • prophylaxis

•VTE associated with Cancer:

  • This should NOT be treated with warfarin
  • LMWH has been shown to be better
  • Treat indefinitely

•Acute coronary syndromes

78
Q

Side effects of LMWH:

A
  • Bleeding
  • Pain at injection site

•Renally cleared, so may not use in dialysis or ESRD

•Can cause HIT (but less commonly than UFH)

  • If HIT occurs, then CANNOT use LMWH
  • Cost - one month’s supply about $1000
79
Q

What is Fondaparinux composed of/generated from?

A
  • Chemically synthesized
  • made from JUST the pentasaccharide part of heparin
80
Q

What is the mechanism of action of Fondaparinux?

A
  • Contains the pentasaccharide part of heparin
  • Binds to antithrombin and inactivates Xa
  • Does not cause HIT, but may potentiate HIT once it has occurred
81
Q

Can Fondaparinux be used in patients with renal failure?

A

No - cleared renally

82
Q

How is fondaparinux administered?

A

SQ administration

Once daily dosing

83
Q

What is the antidote for Fondaparinux?

A

Tricked ya

there’s not one

84
Q

What is Fondaparinux used for?

A

Used for treatment and prophylaxis of VTE

85
Q

What is Dabigatran and what is its mechanism of action?

A

•The first US approved DOAC (direct oral anticoagulant)

•Directly binds and inactivates IIa (thrombin)

•No need for antithrombin as a mediator

86
Q

What is Dabigatran used for?

A
  • Use for prevention of stroke in Atrial Fibrillation and also for treatment of VTE
  • May NOT use for heart valves
87
Q

Important considerations for Dabigatran use:

A

Renally cleared

Variable dose effect

prolongs the thrombin time

88
Q

Side effects of dabigatran:

A

Bleeding

GI upset (1/3 need to stop drug)

Renal clearance - so increased bleed risk in patients with renal impairment

89
Q

What is the antidote for Dabigatran?

A

Idarucizumab

  • Trade name is Prax-bind (trade name for dabigatran is Pradaxa)
  • Humanized monoclonal antibody fragment (Fab)
  • Specifically binds to dabigatran and its metabolites and reverses their anticoagulant effect immediately after administration
90
Q

What is Argatroban?

A
  • An intravenous direct thrombin inhibitor
  • Currently, only used in hospital for patients with HIT
91
Q

How is argatroban metabolized?

A

hepatically

92
Q

What will coagulation time tests look like with argatroban use?

A

•Prolongs the aPTT, the PT/INR, and the TCT

•Monitor using the aPTT

93
Q

What is the mechanism of action of Rivaroxaban, apixaban, and endoxaban?

A

Bind and inactivate Factor Xa

94
Q

How are Rivaroxaban, apixaban, and endoxaban cleared by the body?

A

cleared by both the kidney and by chemical degradation

95
Q

What are Rivaroxaban, apixaban, and endoxaban indicated for use for?

A

VTE treatment and prophylaxis

Stroke prevention in A fib

96
Q

What is the antidote to Xa inhibitors (rivaroxaban, apixaban, and endoxaban)?

A

Andexanet

  • Synthetic analog of Xa
  • Binds the Xa inhibitor competitievely with Xa
  • GLA domain removed to prevent anticoagulant effect
  • Catalytic domain mutated to prevent thrombin generation
  • Currently limited in distribution
  • Cost is at least $27000 per dose
97
Q

Why use a DOAC instead of warfarin?

A

More convenient to administer

Fewer intracranial bleeds

98
Q

What are the disadvantages of using DOACs instead of warfarin?

A

•NOT effective in preventing stroke in patients with mechanical heart valves

  • Dabigatran-treated patients had slightly more MIs than warfarin-treated patients
  • Dabigatran and Rivaroxaban caused more GI bleeds in the elderly

Hematology Block 2 (7 decks)

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