AceMed Universities MU Plovdiv Medicine Year 4 Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) Topic 16
Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) · MU Plovdiv
11. Pulmonary embolism
Inside: 19 sections · 2 labelled pictures · 10 tables · 13 flashcards · 27 min
Topic 16 of 68 in the MU Plovdiv syllabus for Internal Diseases – Part 1 (Rheumatology, Pulmonology, Phthisiatrics, Cardiology, Haematology) (Medicine, Year 4). The free AceMed note covers it in 16 sections, about 3,227 words (27 min of reading), with 13 flashcards .
In this note Essay 11- Pulmonary embolism Definition Etiology Risk factors of PTE Pathophysiology Types of PTE Symptoms Physical exam Signs Diagnosis Management of large pulmonary embolism Risk factors Classification Clinical presentation Treatment Complications and prognosis
Definition Entity of peripheral vein thrombosis followed by embolisation of the thrombus into a branch of the pulmonary artery leading to hypertension and necrosis of pulmonary parenchyme! Etiology Most often appears as a result of acute PTE Sources of thrombi include: Pelvic and abdominal veins DVT Hypercoagulable states Amniotic emboli Fat emboli from long bones ARDS Risk factors of PTE Acquired - age, immobilization, traumas, estrogens, weight, COPD, HF, sepsis, neoplasms, polychemotherapy, nephrotic syndromeGenetic - deficiency of antithrombine, protein C and S, hyperhomocysteinemia, high conc of factors VIII, IX, XIPathophysiology The deep venous thrombi of legs and pelvis are the most usual origin of pulmonary thromboemboli They embolise into the pulmonary arteries and cause hemodynamic and gas exchange disturbances Sudden increase of RV afterload can cause RV dilation and hypokinesia, tricuspid regurgitation and then RV failure The decreased RV output and septal shift to left in diastole impedes LV filling Changes of coronary circulation are due to a reduced transcoronary pressure gradient (which is due to aortic hypotension and increased RA pressure)This reduces myocardial blood flow and hypoperfusion of RV endocardium Lung perfusion is decreased but perfusion is the same Increased dead space and impaired gaseous exchange After some hours, the non-perfused lung no longer produces surfactant so alveolar collapse occurs
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