Search results
Results from the WOW.Com Content Network
LAM cells appear to arise from an extrapulmonary source and migrate to the lung. [21] Increased LAM cell migration and invasiveness is rescued by TSC2 re-expression. [49] The cellular and molecular mechanisms of neoplastic transformation and lung parenchymal destruction by LAM cells remain unknown.
Local venous pressure falls to -5 at the apexes and rises to +15 mmHg at the bases, again for the erect lung. Pulmonary blood pressure is typically in the range 25–10 mmHg with a mean pressure of 15 mmHg. Regional arterial blood pressure is typically in the range 5 mmHg near the apex of the lung to 25 mmHg at the base.
Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), [3] is a group of respiratory diseases affecting the interstitium (the tissue) and space around the alveoli (air sacs) of the lungs. [4] It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, and perivascular and perilymphatic tissues. It ...
Underexpansion can also cause interstitial markings due to parenchymal crowding, which can mimic the appearance of interstitial lung disease. Enlargement of the right descending pulmonary artery can indirectly reflect changes of pulmonary hypertension , with a size greater than 16 mm abnormal in men and 15 mm in women.
In most DIPNECH cases, upon examination of the lung tissue, the overgrowth of pulmonary neuroendocrine cells is seen along the small airways, with extension through the basement membrane of the bronchiolar epithelium leading to formation of carcinoid tumorlets. When the tumorlets become greater than 5mm in size they are considered bronchial ...
In chronic thromboembolic pulmonary hypertension, or CTEPH (WHO Group IV), the initiating event is thought to be blockage or narrowing of the pulmonary blood vessels with unresolved blood clots; these clots can lead to increased pressure and shear stress in the rest of the pulmonary circulation, precipitating structural changes in the vessel ...
They are present wherever red blood cells encounter macrophages, such as pulmonary hemorrhage. In left heart failure, the left ventricle can not keep pace with the incoming blood from the pulmonary veins. The resulting backup causes increased pressure on the alveolar capillaries, and red blood cells leak out.
It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure to the lungs. This can be treated with inotropic agents or by intra-aortic balloon pump , but this is regarded as temporary treatment while the underlying cause is addressed ...