Pulmonary Embolism Flashcards

1
Q

T/F: DVT can be located only in the lower extremities

A

F: It can be in either upper or lower extremities

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2
Q

It is a condition characterized by the presence of a clot in the deep venous sytem

A

Deep Vein Thrombosis (DVT)

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3
Q

What is the pathway of the clot causing pulmonary embolism?

A

Vena cava -> right atrium -> right ventricle -> pulmonary artery -> clot lodges at PA -> pulmonary embolism

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4
Q

This medical condition occurring after DVT/PE is characterized by symptoms of breathlessness, especially with exertion

a. Post-PE Syndrome
b. Chronic Thromboembolic pulmonary Hypertension (CTEPH)
c. Post-thrombotic syndrome

A

b. Chronic Thromboembolic pulmonary Hypertension (CTEPH)

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5
Q

This medical condition occurring after DVT/PE could present with right ventricular dysfunction after PE diagnosis

a. Post-PE Syndrome
b. Chronic Thromboembolic pulmonary Hypertension (CTEPH)
c. Post-thrombotic syndrome

A

a. Post-PE Syndrome

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6
Q

This medical condition occurring after DVT/PE may subsequently cause CTEPH

a. Post-PE Syndrome
b. Chronic Thromboembolic pulmonary Hypertension (CTEPH)
c. Post-thrombotic syndrome

A

a. Post-PE Syndrome

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7
Q

This medical condition occurring after DVT/PE damages the venous valves of the leg, causing ankle/calf swelling and leg aching after prolonged standing

a. Post-PE Syndrome
b. Chronic Thromboembolic pulmonary Hypertension (CTEPH)
c. Post-thrombotic syndrome

A

c. Post-thrombotic syndrome

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8
Q

T/F: The most severe form of post-PE syndrome could cause deep skin ulcerations

A

F: it’s the most severe form of post-thrombotic syndrome

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9
Q

Trigger of acute PE and DVT

A

Inflammation

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10
Q

T/F: Type 2 DM can trigger PE or DVT

A

T

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11
Q

Most common autosomal dominant genetic mutations

A

Factor V Leiden and Prothrombin gene

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12
Q

How do Factor V Leiden and prothrombin gene influence DVT/PE?

A

Factor V Leiden causes resistance to activated anticoagulant protein C

Prothrombin gene increases plasma prothrombin concentration -> increased coagulation

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13
Q

T/F: Factor V Leiden and Prothrombin gene mutations do NOT appear to increase the risk of RECURRENT VTE

A

T

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14
Q

T/F Antiphospholipid antibody syndrome is a genetic thrombophilic disorder that predisposes to venous and arterial thrombosis

A

F: it is ACQUIRED

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15
Q

What are the three contributing factors in the formation of thrombosis (Virchow’s Triad)?

A

Venous stasis, hypercoagulability, endothelial injury

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16
Q

T/F Low oxygen tension promote venous thrombi formation

A

T

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17
Q

How does the virchow’s triad form venous thrombi?

A

The vascular injury and venous stasis will stimulate activated platelets (increased by hypercoagulability)&raquo_space; activated platelets will release microparticles, which contain proinflammatory mediators that bind to neutrophils&raquo_space; bound neutrophils will release materials and form “neutrophil extracellular traps (NET)”&raquo_space; NET contains histones that would further stimulate platelet aggregation and promote platelet-dependent thrombin generation&raquo_space; formation of venous thrombi

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18
Q

T/F: Patients suffering from VTE are more than 2x likely to have future MI or stroke

A

T
Since VTE, stroke, and acute coronary syndrome share similar risk factors and pathophysiology involving inflammation, endothelial injury, hypercoagulation

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19
Q

T/F: In PE, pressure overload in the left ventricle increases its wall tension, leading to left ventricle ischemia and dysfunction. It also dilates, compressing the adjacent normal right ventricle, resulting to its decreased CO and systemic arterial pressure&raquo_space; circulatory collapse and death

A

F
The RV experiences Pressure overload
the LV gets compressed

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20
Q

Types of pulmonary embolism

A

Low-risk
Submassive (Intermediate-risk)
Massive (high-risk)

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21
Q

Hallmarks of massive PE

A

Dyspnea, hypotension, syncope, cyanosis

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22
Q

This type of PE has RV dysfunction despite having normal systemic arterial pressure

A

Submassive

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23
Q

Types of DVT

A

Lower Extremity
Upper Extremity
Superficial Venous Thrombosis (primarily not a DVT)

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24
Q

Most common symptom of pulmonary embolism

A

Unexplained breathlessness

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25
Q

Most common symptom of deep vein thrombosis

A

Cramp or “Charley horse” in the lower calf that persists and intensifies over several days

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26
Q

This help estimate clinical likelihood of DVT and PE

A

Wells point Scoring

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27
Q

T/F: In High DVT/PE, Blood test such as D-dimer test should be skipped

A

T
Should undergo diagnostic imaging tests instead

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28
Q

T/F In low and low-moderate PE, there are no obligatory imaging tests

A

T

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29
Q

T/F Age-adjusted dimer is NOT applicable to patients suspected of acute DVT

A

T

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30
Q

Age adjusted D Dimer is applicable to more than ___ yo and with ______ clinical probability of PE

A

> 50 yo; low or moderate

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31
Q

Standard upper limit in ng/mL of age-adjusted D dimer

A

500 ng/mL
formula: age x 10

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32
Q

Most cited ECG abnormality aside from sinus tachycardia

A

S1Q3T3 sign (specific but NOT sensitive)

s wave in lead I, Q wave, and an inverted T wave

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33
Q

Most common ECG abnormality

A

T wave inversion in leads V1 to V4 due to RV myocardial strain and ischemia

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34
Q
A
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35
Q

Principal diagnostic test for suspected DVT

A

Venous Ultrasonography

36
Q

Primary diagnostic criterion for DVT in venous ultrasound

A

Loss of vein compressibility

37
Q

3 Well-established xray abnormalities in PE

A

Westermark’s sign, Hampton’s hump, Palla’s Sign

38
Q

This Xray abnormality in PE shows reduction in the pulmonary volume

A

Westermark’s sign

39
Q

This xray abnormality in PE shows wedge-shaped density usually at the pleural base

A

Hampton’s Hump

40
Q

This is the sign of sausage appearance in chest xray of PE due to enlarged right descending pulmonary artery

A

Palla’s Sign

41
Q

What is the enlarged structure seen in Palla’s Sign?

A

(Right) descending pulmonary artery

42
Q

This imaging modality is the principal imaging test for PE diagnosis

A

Chest CT

43
Q

T RV Enlargement indicates an increase likelihood of death in 7 days

A

F: 30 days

44
Q

Second-line diagnostic test for PE

A

Lung Scan (Ventilation-Perfusion Scan) for patients who cannot tolerate intravenous contrast

45
Q

90% certain of PE if the ff are seen in lung scan:

A

Two or more segmental perfusion defects with normal ventilation (VQ Mismatch)

46
Q

T/F Contrast-enhanced MRI can be used to detect large proximal, and smaller segmental/subsegmental PE

A

F
Unreliable for smaller segmental and subsegmental PE

47
Q

Abnormal chest CT but without PE could have the following alternative diagnoses:

A

Pneumonia, emphysema, pulmonary fibrosis, pulmonary mass, aortic pathology

48
Q

Possible other differentials in lung scan with abnormal ventilation

A

Asthma, COPD

49
Q

T/F Echocardiography can be used in diagnosing PE

A

F : it would have normal results

50
Q

What diseases can mimic PE in Echo?

A

Acute MI, pericardial tamponade, aortic dissection

51
Q

Best known indirect sign of PE on transthoracic echocardiography

A

McConnel’s Sign - hypokinesia of RV free wall with normal or hyperkinetic RV Apex

52
Q

If there’s an unsatisfactory chest CT results or plans for catheter-directed thrombolysis, this diagnostic modality is indicated

A

Pulmonary Angiography

53
Q

T/F: Venous ultrasound is also used when lung scan for PE diagnosis is unsatisfactory

A

T

54
Q

Chest CT: What contrast is the primary diagnostic modality for PE?

A

Iodine Contrast

55
Q

Primary therapy for DVT

A

Clot dissolution that uses iodine contrast

56
Q

Secondary prevention for DVT

A

Anticoagulation or placement of an inferior vena cava filter

57
Q

Which anticoagulant is useful when hour to hour control of intensity of anticoagulation is desired?

a. UFH
b. LMWH
c. Fondaparinux
d. Warfarin

A

a. UFH

58
Q

T/F Lab monitoring is needed when taking UFH

A

T
Lab monitoring is needed to target apTT of 60-80s

59
Q

T/F UFH has pleiotropic effects that may decrease systemic and local inflammation

A

T

60
Q

T/F No lab monitoring or dose adjustment is needed in using LMWH, except if obese or with CKD

A

T

61
Q

dosing of this weight-based anticoagulant must be adjusted downwards for patients with renal dysfunction

a. UFH
b. LMWH
c. Fondaparinux
d. Warfarin

A

Fondaparinux

62
Q

Daily therapy for at least _______ days is required for the full effect of warfarin

A

5 days

63
Q

T/F Fondaparinux has suspected or proven heparin-induced thrombocytopenia

A

F
DTI (Argatroban and Bivalirudin) has HIT

64
Q

This LMWH has a dosage of 1 mg/kg twice daily with normal renal function

a. Enoxaparin
b. Dalteparin
c. Tinzaparin

A

A. enoxaparin

65
Q

This LMWH has a dosage of 200U/kg daily or 100U/kg twice daily with normal renal function

a. Enoxaparin
b. Dalteparin
c. Tinzaparin

A

b. Dalteparin

66
Q

This LMWH has a dosage of 175U U/kg once daily with normal renal function

a. Enoxaparin
b. Dalteparin
c. Tinzaparin

A

c. Tinzaparin

67
Q

This anticoagulant is taken 15mg twice daily for 3 weeks, followed by 20 mg once daily with dinner meal thereafter

a. Rivaroxaban
b. Apixaban
c. Dabigatran
d. Edoxaban

A

a. Rivaroxaban

68
Q

This anticoagulant is taken 10mg twice daily for 1 week, followed by 5mg twice daily

a. Rivaroxaban
b. Apixaban
c. Dabigatran
d. Edoxaban

A

b. Apixaban

69
Q

This is taken at 150mg twice daily after having 5 days of unfractionated heparin/LMWH/fondaparinux.

a. Rivaroxaban
b. Apixaban
c. Dabigatran
d. Edoxaban

A

c. Dabigatran

70
Q

This is taken at 60mg once daily after having 5 days of unfractionated heparin/LMWH/fondaparinux.

a. Rivaroxaban
b. Apixaban
c. Dabigatran
d. Edoxaban

A

d. Edoxaban

71
Q

Usual start dose of warfarin

A

5 mg

72
Q

Antidote for heparin/LMWH hemorrhage

A

Protamine Sulfate

73
Q

Antidote for dabigatran

A

Idarucizumab

74
Q

Antidote for antiXa anticoagulants complications (Rivaroxaban/Apixaban)

A

Andexanet

75
Q

Antidote for major bleeding from warfarin

A

Prothrombin complex concentrate

76
Q

Antidote for less serious bleeding from warfarin

A

Fresh frozen plasma or IV Vitamin K

77
Q

Minor bleeding from wrfarin or excessively high INR in the absence of bleeding

A

Oral vitamin K

In order of severity (antidotes)
Oral vitamin K&raquo_space; Fresh frozen plasma or IV Vitamin K&raquo_space; Prothrombin complex concentrate

78
Q

T/F LMWH is prescribed as monotherapy for px with cancer and VTE

A

T

79
Q

2 principal indications for IVC filter insertion

A

For active bleeding that precludes anticoagulation

For recurrent venous thrombosis despite intensive anticoagulation

80
Q

First line vasopressor agent for treatment of PE-related shock

A

Norepinephrine

81
Q

First line inotropic agent

A

Dobutamine

82
Q

Fibrinolysis: administration of ____ mg rtPA as a continuous peripheral intravenous infusion over ___ hrs

A

100 mg; 2 hrs

83
Q

This combines physical fragmentation of thrombus and catheter-directed low-dose thrombolysis

A

Pharmacomechanical catheter-directed therapy

84
Q

Aside from fibrinolysis, ________ is an option to avert risk of major hemorrhage

A

Pulmonary embolectomy

85
Q

Indicated for patients with CTEPH (Chronic Thromboembolic Pulmonary Hypertension)

A

Pulmonary Thromboendarterectomy

86
Q

In-hospital prophylaxis offered for hospitalized patients to avoid VTE

A

low dose UFH or LMWH

87
Q

This is approved as continuing prophylaxis after discharge

A