Problem 10 Flashcards
What are some of the complications for thromboembolie veineuse
postthrombotic syndrome (chronic venous insufficency, damage to the valves -> swelling and aching) pulmonary hypertension
What is the pathophysiology
- inflammation and platelet activation: Virchow’s triad leads to recruitment of activated platelets, which release microparticles. These microparticles contain proinflammatory mediators that bind neutrophils, stimulating them to release their nuclear material and form web-like extracellular networks called neutrophil extracellular traps. These prothrombotic networks contain histones that stimulate platelet aggregation and promote platelet-dependent thrombin generation. Venous thrombi form and flourish in an environment of stasis, low oxygen tension, and upregulation of proinflammatory genes.
- prothrombotic states: mutations and other risk factors
- embolization: deep venous thrombi detach -> vena cava -> right atrium -> right ventricle -> the pulmonary arterial circulation, thereby causing acute PE. Paradoxically, these thrombi occasionally embolize to the arterial circulation through a patent foramen ovale or atrial septal defect. Many patients with PE have no evidence of DVT because the clot has already embolized to the lungs.
What is the Virchow triad
venous stasis, hypercoagulability, and endothelial injury
What are some of the genetic risk factors
The two most common autosomal dominant genetic mutations are factor V Leiden, activated protein C (which inactivates clotting factors V and VIII), and the prothrombin gene mutation, which increases the plasma prothrombin concentration. Antithrombin, protein C, and protein S are naturally occurring coagulation inhibitors. Deficiencies of these inhibitors are associated with VTE but are rare.
What are some of the auto-immune syndromes that are risk factors
Antiphospholipid antibody syndrome is the most common acquired cause of thrombophilia and is associated with venous or arterial thrombosis.
What are some of the risk factors
cancer, obesity, cigarette smoking, systemic arterial hypertension, chronic obstructive pulmonary disease, chronic kidney disease, blood transfusion, long-haul air travel, air pollution, estrogen-containing contraceptives, pregnancy, postmenopausal hormone replacement, surgery, and trauma. Inflammation predisposes to thrombosis, and conditions such as psoriasis and inflammatory bowel disease have become recognized risk factors of VTE. Sedentary lifestyle.
What happens when a blood clot is in the lungs
The most common gas exchange abnormalities are arterial hypoxemia and an increased alveolar-arterial O2 tension gradient, which represents the inefficiency of O2 transfer across the lungs. Anatomic dead space increases because breathed gas does not enter gas exchange units of the lung. Physiologic dead space increases because ventilation to gas exchange units exceeds venous blood flow through the pulmonary capillaries.
Other pathophysiologic abnormalities include:
- Increased pulmonary vascular resistance due to vascular obstruction or platelet secretion of vasoconstricting neurohumoral agents such as serotonin. Release of vasoactive mediators can produce ventilation-perfusion mismatching at sites remote from the embolus, thereby accounting for discordance between a small PE and a large alveolar-arterial O2 gradient.
- Impaired gas exchange due to increased alveolar dead space from vascular obstruction, hypoxemia from alveolar hypoventilation relative to perfusion in the non-obstructed lung, right-to-left shunting, or impaired carbon monoxide transfer due to loss of gas exchange surface.
- Alveolar hyperventilation due to reflex stimulation of irritant receptors.
- Increased airway resistance due to constriction of airways distal to the bronchi.
- Decreased pulmonary compliance due to lung edema, lung hemorrhage, or loss of surfactant.
What happens to the heart
Pulmonary artery obstruction and neurohumoral mediators cause a rise in pulmonary artery pressure and in pulmonary vascular resistance. When RV wall tension rises, RV dilation and dysfunction ensue, with release of the cardiac biomarker, brain natriuretic peptide. The interventricular septum bulges into and compresses an intrinsically normal left ventricle (LV). Diastolic LV dysfunction reduces LV distensibility and impairs LV filling. Increased RV wall tension also compresses the right coronary artery, limits myocardial oxygen supply, and precipitates right coronary artery ischemia and RV microinfarction, with release of cardiac biomarkers such as troponin. Underfilling of the LV may lead to a fall in LV cardiac output and systemic arterial pressure, with consequent circulatory collapse and death.
What are the indicators of massive PE
Dyspnea, syncope, hypotension, and cyanosis
What are the characteristics of submassive PE
RV dysfunction despite normal systemic arterial pressure. The combination of right heart failure and release of cardiac biomarkers indicates a high risk of clinical deterioration.
Symptoms and signs of PE
dyspnee
Symptoms of TVP
cramps in the leg
Scors used to diagnose
geneva score
wells score
When do we use D-dimeres
if low or intermediate risk of PE
Diagnostics differentiels de TVP
Not all leg pain is due to DVT. Sudden, severe calf discomfort suggests a ruptured Baker’s cyst. Fever and chills usually herald cellulitis rather than DVT. Physical findings, if present, may consist only of mild palpation discomfort in the lower calf. However, massive DVT often presents with marked thigh swelling, tenderness, and erythema. Recurrent left thigh edema especially in young women raises the possibility of May-Thurner Syndrome, with right proximal iliac artery compression of the left proximal iliac vein. However, if a leg is diffusely edematous, DVT is unlikely. More probable is an acute exacerbation of venous insufficiency due to postthrombotic syndrome. Upper extremity venous thrombosis may present with asymmetry in the supraclavicular fossa or in the circumference of the upper arms.
