300 Deep Venous Thrombosis and Pulmonary Thromboembolism

Question 1

Nr. of deaths in the states for pulmonary embolism.

Answer 1

100,000 to 180,000 deaths annually from PE

Question 2

Postthrombotic syndrome

Answer 2

damages the venous valves of the leg and causes ankle or calf swelling and leg aching, especially after prolonged standing. In its most severe form, postthrombotic syndrome causes skin ulceration

Question 3

What are the two most common thrombophilic autosomal dominan genetic mutations?

Answer 3

factor V Leiden and prothrombin

Question 4

Most common acquired cause of thrombophilia

Answer 4

Antiphospholipid antibody syndrome

Question 5

Name the 5 pathophysiologic abnormalities in PE.

Answer 5

pathophysiologic abnormalities include:

1. Increased pulmonary vascular resistance
2. Impaired gas exchange
3. Alveolar hyperventilation
4. Increased airway resistance
5. Decreased pulmonary compliance

Question 6

Massive PE accounts for which % of cases?

Answer 6

5–10%

Question 7

Submassive PE accounts for which % of patients?

Answer 7

20–25%

Question 8

Low-risk PE constitutes which % of cases.

Answer 8

70–75%

Question 9

Clinical presentation of Massive and Submassive PE?

Answer 9

Dyspnea, syncope, hypotension, and cyanosis are hallmarks of massive PE. Patients with massive PE may present in cardiogenic shock and can die from multisystem organ failure.
Submassive PE is characterized by RV dysfunction despite normal systemic arterial pressure. The combination of right heart failure and release of cardiac biomarkers indicates an increased likelihood of clinical deterioration.

Question 10

Relation between leg DVT and arm DVT?

Answer 10

Leg DVT is about 10 times more common than upper

extremity DVT.

Question 11

Nonthrombotic PE etiologies

Answer 11

Fat embolism after pelvic or long bone fracture, tumor embolism, bone marrow and air embolism. Cement embolism and bony fragment embolism in total hip or knee replacement. Intravenous drug users
may inject themselves with hair, talc, and cotton. Amniotic fluid embolism.

Question 12

What is the sensitivity of the d-dimer test?

Answer 12

The sensitivity of the d-dimer is more than 80% for DVT (including isolated calf DVT) and more than 95% for PE.

Question 13

Diseases that can elevate D-Dimers?

Answer 13

Myocardial infarction, pneumonia, sepsis, cancer, and the postoperative state and those in the second or third trimester of pregnancy.

Question 14

What is the ECG abnormality more specific por PE?

Answer 14

In addition to sinus tachycardia, is the S1Q3T3 sign

Question 15

Changes in the ultrasonography of DVT?

Answer 15

Ultrasonography of the deep venous system relies on loss of vein compressibility as the primary criterion for DVT. The thrombus can be visualized, it appears homogeneous and has low echogenicity. The vein itself often appears mildly dilated, and collateral channels may be absent.

Question 16

Changes in the chest x-ray of PE?

Answer 16

focal oligemia (Westermark’s sign), a peripheral wedged-shaped density above the diaphragm (Hampton’s hump), and an enlarged right descending pulmonary artery (Palla’s sign)

Question 17

What is the principal imaging test for the diagnosis of PE?

Answer 17

CT of the chest with intravenous contrast.

Question 18

VPP of Lung scanning for PE?

Answer 18

About 90% certain in patients with high-probability scans

Question 19

False negatives of Lung scanning for PE?

Answer 19

As many as 40% of patients with high clinical suspicion for PE.

Question 20

What is the use of MR pulmonary angiography in PE?

Answer 20

May detect large proximal PE but is not reliable for smaller segmental and subsegmental PE.

Question 21

McConnell’s sign

Answer 21

hypokinesis of the RV free wall with normal or hyperkinetic motion of the RV apex.

Question 22

Definitive diagnosis of PE in Pulmonary Angiography?

Answer 22

Visualization of an intraluminal filling defect in more than
one projection. Secondary signs of PE include abrupt occlusion (“cutoff”) of vessels, segmental oligemia or avascularity, a prolonged arterial phase with slow filling, and tortuous, tapering peripheral vessels.

Question 23

open vein hypothesis postulate

Answer 23

patients who receive primary therapy will sustain less long-term damage to venous valves, with consequent
lower rates of postthrombotic syndrome. Still not confirmed.

Question 24

Alternatives for effective anticoagulation.

Answer 24

(1) parenteral therapy “bridged” to warfarin, (2) parenteral therapy “bridged” to a novel oral anticoagulant such as dabigatran (a direct thrombin inhibitor) or edoxaban (an anti-Xa agent), or (3) oral anticoagulation with rivaroxaban or apixaban (both are anti-Xa agents) with a loading dose followed by a maintenance dose as monotherapy without parenteral anticoagulation.

Question 25

Dosage of UFH

Answer 25

target activated partial thromboplastin time (aPTT) of 60–80 s. The most popular nomogram uses an initial bolus of 80 U/kg, followed by an initial infusion rate of 18 U/kg per h.

Question 26

Warfarin Dosage

Answer 26

Requires 5–10 days of administration to achieve effectiveness as monotherapy (Unfractionated heparin, low-molecular-weight heparin, and fondaparinux
are the usual immediately effective “bridging agents” used when initiating warfarin)
Usual start dose is 5 mg
Titrate to INR, target 2.0–3.0
Continue parenteral anticoagulation for a minimum of 5 days and until two sequential INR values, at least 1 day apart, achieve the target INR range

Question 27

Approved treatment for PE and DVT?

Answer 27

Rivaroxaban, a factor Xa inhibitor, is approved
for treatment of acute DVT and acute PE as monotherapy, without a parenteral “bridging” anticoagulant. Apixaban is likely to receive similar approval for oral monotherapy. Dabigatran, a direct thrombin inhibitor, and edoxaban, a factor Xa inhibitor, are likely to be approved for treatment of VTE after an initial course of parenteral anticoagulation.

Question 28

What is the most serious adverse effect of anticoagulation?

Answer 28

hemorrhage

Question 29

What are the two principal indications for insertion of an IVC filter?

Answer 29

(1) active bleeding that precludes anticoagulation and (2) recurrent venous thrombosis despite intensive anticoagulation.

Question 30

1st therapeutic measure in patients with massive PE and hypotension?

Answer 30

500 mL of normal saline

Question 31

Action of fibrinolytic therapy?

Answer 31

(1) dissolving much of the anatomically obstructing pulmonary arterial thrombus, (2) preventing the continued release of serotonin and other neurohumoral factors that exacerbate pulmonary hypertension and (3) lysing much of the source of the thrombus in the pelvic or deep leg veins, thereby decreasing the likelihood of recurrent PE.

Question 32

What is the preferred fibrinolytic regimen?

Answer 32

100 mg of recombinant tissue plasminogen activator (tPA) administered as a continuous peripheral intravenous infusion over 2 h. The sooner thrombolysis is administered, the more effective it is.

Question 33

what is the overall major bleeding rate with alteplase 100 mg/2 h? And the risk of intracranial hemorrhage?

Answer 33

overall major bleeding rate is about 10%, including a 1–3% risk of intracranial hemorrhage.

Question 34

Is there a benefit to using thrombolytic agent tenecteplase?

Answer 34

Death or hemodynamic collapse within 7 days of randomization was reduced by 56% in the tenecteplase group. However, hemorrhagic stroke occurred in 2% of tenecteplase patients versus 0.2% in patients who only received heparin.

Question 35

% of patients with acute PE that develop chronic thromboembolic pulmonary hypertension?

Answer 35

2–4%

Question 36

What is the mortality rate of pulmonary thromboendarterectomy?

Answer 36

approximately 5%

Question 37

Computerized reminder systems can increase the use of preventive measures and, at Brigham and Women’s
Hospital, have reduced the symptomatic VTE rate by how much?

Answer 37

more than 40%

Question 38

What is the ongoing trial novel oral anticoagulant for extended-duration VTE prophylaxis?

Answer 38

betrixaban

Question 39

How long is prophylaxis for patientes with hip replacement or extensive cancer surgery?

Answer 39

the duration of prophylaxis is usually at least 1 month

Question 40

% of patients that will develop a disease very similar

clinically and pathologically to PAH after resection of the proximal thrombus in group IV of PH?

Answer 40

10-15%

Question 41

Name other diseases that causa PH.

Answer 41

Sarcoidosis; sickle cell disease and schistosomiasis

Question 42

What are the available pharmacologic therapies for PH?

Answer 42

prostacyclin analogues, phosphodiesterase-5 inhibitors, a soluble guanylyl cyclase stimulator, and endothelin receptor antagonists

Question 43

Available prostanoids?

Answer 43

Epoprostenol delivered as a continuous intravenous infusion (6 min.); Treprostinil subcutaneous (4 h); Inhaled iloprost and treprostinil

Question 44

Available Phosphodiesterase-5 (PDE5) inhibitors for PH?

Answer 44

Sildenafil, tadalafil. Recently, the oral soluble guanylyl cyclase stimulator, riociguat, was approved for the treatment of both PAH and CTEPH.

Question 45

What is the median survival for a person with PAH?

Answer 45

It is only 5–6 years.