Clotting Conditions Flashcards

1
Q

Clotting occurs in several steps:

A
  1. Vasoconstriction ← smooth muscle contraction
  2. Formation of platelet plug
  3. Clot reinforced by coagulation cascade→ Fibrin crosslinking
  4. Ends with fibrinolysis and restoration of blood flow
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2
Q

When a vessel is damaged- _____ is
exposed

A

collagen

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3
Q

Von Willebrand factor (vWF)

A

Forms a bridge between collagen of a damaged vessel and GPIb which is expressed on the surface of the platelet→ adhesion to the site

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4
Q

Platelet granules secret:

A

○ Adenosine diphosphate (ADP) released→ Activates nearby platelets
○ Arachidonic acid released which is converted to thromboxane A2

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5
Q

Eventually Factor X is activated by combination
of _____

A

IX and VIII and phospholipids

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6
Q

Measured with PT

A

Extrinsic pathway

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7
Q

Measured with aPTT

A

Intrinsic pathway

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8
Q

Intrinsic pathway is activated by ____

A

Activated by exposure to
collagen

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9
Q

Extrinsic pathway is activated by

A

Activated by presence of
tissue factor (III)

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10
Q

Ultimately both pathways lead
to activation of Factor ___

A

X

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11
Q

Factors that Inhibit Coagulation

A

○ Protein C
○ Protein S
○ Antithrombin III

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12
Q

Protein C and S are ____ dependent proteins

A

Vit K

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13
Q

_____ is a plasma protein which binds to
thrombin forming inert compound

A

Antithrombin III

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14
Q

Heparin acts to augment
____

A

Antithrombin III

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15
Q

What is Thrombophilia?

A

A condition where the blood has an increased tendency to form clots, potentially leading to life-threatening circumstances.

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16
Q

____ is a major cause of morbidity and mortality throughout the world

A

Thrombosis

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17
Q

_____ activates plasminogen into plasmin

A

tPA

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18
Q

The 19th century pathologist Rudolf Virchow proposed three independent processes which could increase the risk of abnormal thrombosis

A

○ Abnormal Flow / Stasis
○ Vessel Wall Injury
○ Hypercoagulability

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19
Q

Inherited Disorders of hypercoagulable state

A

○ Factor V Leiden Mutation
○ Prothrombin G20210A Mutation
○ Protein S Deficiency
○ Protein C Deficiency
○ Antithrombin III Deficiency

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20
Q

Acquired conditions of hypercoagulable states

A

○ Pregnancy-Related Hypercoagulability
○ Malignancy-Related Hypercoagulability
○ Antiphospholipid Antibody Syndrome
○ Heparin-Induced Thrombocytopenia

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21
Q

Factor V plays a crucial role in the conversion of Prothrombin to Thrombin and is normally inactivated by ____

A

Protein C (and S).

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22
Q

Factor V Leiden is ____ 10 times slower than
normal Factor V.

A

inactivated by Protein C
○ Leads to increased coagulation - more
Thrombin is created.

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23
Q

Factor V Leiden

A

Mutation of Factor V

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24
Q

____ is by far the most common
inherited risk factor for thrombophilia

A

Factor V Leiden mutation

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25
Q

The _____ triggers an overproduction of the Prothrombin protein (Factor II).

A

Prothrombin G20210A genetic mutation

26
Q

Normally, Protein C works to ____

A

inactivate Factors VIII and V
in an effort to slow down or inhibit coagulation
(anticoagulant).

27
Q

Antithrombin III normally inactivates several coagulation
factors, most importantly _____

A

Thrombin

28
Q

_____ are at an increased risk of
thrombosis (DVT and PE)

A

Pregnant women

29
Q

Antiphospholipid Syndrome

A

Antiphospholipid Antibody Syndrome is a condition in
which the body forms antibodies against proteins bound to
the phospholipids necessary for the coagulation cascade.

30
Q

Antiphospholipid Syndrome includes:

A

○ Lupus Anticoagulant
○ Anticardiolipin Antibody

31
Q

What is lupus anticoagulant

A

Those with Lupus Anticoagulant are at increased risk of venous thrombosis and recurrent miscarriage.

32
Q

Anticardiolipin Antibody

A

Those with Anticardiolipin Antibody are at increased
risk of arterial thrombosis, concerning for myocardial
infarction and peripheral arterial occlusions.

33
Q

Heparin-Induced TCP (HIT)

A

an adverse reaction to the medication
that occurs in 3% of those on
unfractionated Heparin and 0.6% of
those on LMWH.

34
Q

HIT results from

A

formation
of antibodies to the
Heparin-Platelet Factor
4 (PF4) complex.

35
Q

HIT usually occurs ____

A

5-10 days after initiation of Heparin.

36
Q

A decline in baseline platelet count of 50% or more is diagnostic for

A

HIT

37
Q

Treatment for HIT

A

○ Discontinue all forms of Heparin immediately.
○ Begin treatment with Direct Thrombin inhibitor (ie. Argatroban) or
Direct Factor Xa Inhibitor (ie. Rivaroxaban).
○ Check US Doppler of LEs and monitor Platelet count.
○ When platelet # recovers, can transition to Warfarin for at least 30
days

38
Q

Deep Vein Thrombosis S/S

A

○ Most commonly, patients present with…
■ Unilateral leg pain
■ Unilateral calf tenderness
■ Unilateral leg/ankle swelling

39
Q

DVT diagnostic testing

A

○ The use of a Clinical Prediction Tool is suggested.
■ Wells Score System for DVT
○ If low probability based on Prediction Tool:
■ Order High-Sensitivity D-Dimer (blood test)
● Negative D-Dimer rules out DVT
○ If moderate probability of DVT:
■ High-Sensitivity D-Dimer or Compression Ultrasound
○ If high probability of DVT:
■ Compression Ultrasound is diagnostic test of choice

40
Q

High-sensitive D-Dimer is very sensitive for ____

A

VTE

41
Q

The presence of D-Dimer
indicates that clotting
_____

A

has occurred

42
Q

Treatment and Management of DVT

A

○ Prevention in high-risk patients is critical!
○ Once diagnosed, Systemic Anticoagulation is treatment.

43
Q

Inpatient treatment for DVT recommended if…

A

● Massive DVT
● Symptomatic Pulmonary Embolism
● High risk of bleeding with anticoagulation
● Significant comorbid conditions

44
Q

Acute DVT treatment

A

○ Anticoagulation started immediately
○ Oral anticoagulant preferred for maintenance treatment
○ Anticoagulation is continued for at least 3 months.

45
Q

In the treatment of acute DVT, Recent studies have shown that____

A

early ambulation is safe and
recommended over bedrest

46
Q

If there is a high degree
of concern for a PE, an
_____ can be placed
endovascularly.

A

Inferior Vena Cava (IVC)
Filter

47
Q

_____ is the
most significant complication of
DVT.

A

Pulmonary Embolism

48
Q

Pulmonary Embolism

A

● If a DVT breaks loose, it can
travel through the heart and into
the lungs.

49
Q

Characteristic Signs and Symptoms of Pulmonary embolism

A

○ Sudden onset dyspnea
○ Tachypnea
○ Tachycardia
○ Pleuritic Chest Pain
○ Cough
○ Sometimes a fever
○ Symptoms of shock (massive PE)
○ Hemoptysis (not common)
○ Signs and symptoms of DVT are common

50
Q

Diagnostic testing for pulmonary embolism

A

○ Pulmonary Embolism Rule-out Criteria (PERC)
○ The use of a Clinical Prediction Tool is suggested.
○ Low probability, D-Dimer is used to rule out PE
● If positive advance to CT Angio
○ Moderate probability, D-Dimer or below imaging.
○ High probability of PE, D-Dimer is not indicated.

51
Q

Test of choice for pulmonary embolism

A

CT Pulmonary Angiography is test of choice

52
Q

Treatment for PE If patient is hemodynamically stable

A

■ SC LMWH (Lovenox) is preferred over IV UFH.
■ More common- DOACs-Rivaroxaban or Apixaban.

53
Q

Treatment for PE If massive PE with concern for shock

A

■ IV unfractionated Heparin is preferred.
■ IV Alteplase (a fibrinolytic called tPA) can also be used.
■ Endovascular pulmonary embolectomy is used as a measure of last resort
○ Long-term (at least 3-6 months) anticoagulation with an oral agent is recommended (Warfarin or NOAC ie. Novel oral anticoagulant)

54
Q

____ occurs when platelet aggregation
and the coagulation cascade are triggered by
disease of the artery

A

Arterial thrombosis

55
Q

Characteristic Presentation of arterial thrombosis

A

■ Myocardial Infarction
■ Unstable Angina
■ Ischemic Stroke
■ Acute Limb Ischemia of Peripheral Arterial Disease

56
Q

Risk factors of arterial thrombosis

A

smoking, obesity, diabetes,
hypertension, dyslipidemia, advancing age, atherosclerosis,
and positive family history.

57
Q

Treatment of Arterial thrombosis

A

○ Treatment specific to acute arterial thrombosis will be
discussed in the above listed courses.
■ Mostly uses antiplatelet drugs
○ Prevention of atherosclerosis (by addressing modifiable
risk factors) is critical to prevention of arterial
thrombosis.

58
Q

Virchow’s Triad

A

○ Venous Stasis
○ Vessel Wall Injury
○ Hypercoagulability

59
Q

Patient with a DVT are at very high risk
of ____

A

that clot breaking loose and traveling
to the lungs, causing a Pulmonary
Embolism.

60
Q

Prevention of _____ is critical to prevention of arterial thrombosis.

A

atherosclerosis (by addressing modifiable
risk factors)