Pulmonary Embolism Flashcards
(87 cards)
T/F: DVT can be located only in the lower extremities
F: It can be in either upper or lower extremities
It is a condition characterized by the presence of a clot in the deep venous sytem
Deep Vein Thrombosis (DVT)
What is the pathway of the clot causing pulmonary embolism?
Vena cava -> right atrium -> right ventricle -> pulmonary artery -> clot lodges at PA -> pulmonary embolism
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
b. Chronic Thromboembolic pulmonary Hypertension (CTEPH)
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. Post-PE Syndrome
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. Post-PE Syndrome
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
c. Post-thrombotic syndrome
T/F: The most severe form of post-PE syndrome could cause deep skin ulcerations
F: it’s the most severe form of post-thrombotic syndrome
Trigger of acute PE and DVT
Inflammation
T/F: Type 2 DM can trigger PE or DVT
T
Most common autosomal dominant genetic mutations
Factor V Leiden and Prothrombin gene
How do Factor V Leiden and prothrombin gene influence DVT/PE?
Factor V Leiden causes resistance to activated anticoagulant protein C
Prothrombin gene increases plasma prothrombin concentration -> increased coagulation
T/F: Factor V Leiden and Prothrombin gene mutations do NOT appear to increase the risk of RECURRENT VTE
T
T/F Antiphospholipid antibody syndrome is a genetic thrombophilic disorder that predisposes to venous and arterial thrombosis
F: it is ACQUIRED
What are the three contributing factors in the formation of thrombosis (Virchow’s Triad)?
Venous stasis, hypercoagulability, endothelial injury
T/F Low oxygen tension promote venous thrombi formation
T
How does the virchow’s triad form venous thrombi?
The vascular injury and venous stasis will stimulate activated platelets (increased by hypercoagulability)»_space; activated platelets will release microparticles, which contain proinflammatory mediators that bind to neutrophils»_space; bound neutrophils will release materials and form “neutrophil extracellular traps (NET)”»_space; NET contains histones that would further stimulate platelet aggregation and promote platelet-dependent thrombin generation»_space; formation of venous thrombi
T/F: Patients suffering from VTE are more than 2x likely to have future MI or stroke
T
Since VTE, stroke, and acute coronary syndrome share similar risk factors and pathophysiology involving inflammation, endothelial injury, hypercoagulation
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»_space; circulatory collapse and death
F
The RV experiences Pressure overload
the LV gets compressed
Types of pulmonary embolism
Low-risk
Submassive (Intermediate-risk)
Massive (high-risk)
Hallmarks of massive PE
Dyspnea, hypotension, syncope, cyanosis
This type of PE has RV dysfunction despite having normal systemic arterial pressure
Submassive
Types of DVT
Lower Extremity
Upper Extremity
Superficial Venous Thrombosis (primarily not a DVT)
Most common symptom of pulmonary embolism
Unexplained breathlessness
