Great video! We should emphasize more pathophysiological mechanisms when learning radiology. More on the why than on the what. By the way, any idea why a UIP pattern of IPF most commonly affects the lower lungs?
Thank you for the great question. In order to answer, I will need to borrow some talking points from my advanced version of this talk (the version I've uploaded here on RUclips is the basic version). 1. I mentioned there is a superoinferior blood perfusion gradient that favors the lower lungs. There is ALSO a radial blood perfusion gradient that favors the central lungs over the peripheral lungs. Pulmonary vessels in peripheral lung are, on average, smaller in caliber than those in the central lung, which means that pulmonary vascular resistance is higher in peripheral lung than central lung. Higher pulmonary vascular resistance results in slower vascular transit time. Slower transit times are why we see greater deposition of things like septic emboli and metastases in the peripheral vascular bed of the lung than its central vascular bed. 2. There is a FOURTH factor that influences the geographic distribution of diseases in the lungs, besides blood perfusion, lymphatic flow, and ventilation. This fourth factor is mechanical stress. Mechanical stress is greatest in the upper lung and the peripheral lung. Imagine you're hanging off the ledge of a cliff by just your hands, and someone below you is hanging on to your ankles... that's sort of like how the upper lung feels. The upper lung "carries" the weight of the lower lung, which results in more connective tissue strain and alveolar distention in the upper lungs. Surface tension keeping the visceral and parietal pleural surfaces adherent to each together result in more connective tissue strain in the peripheral lungs. UIP/IPF have a BASAL predominance because: (1) higher blood perfusion in the lower lungs results in greater deposition of substances that may contribute to the development of UIP/IPF (e.g. chemotherapy agents, inflammatory mediators, etc.) and (2) alveoli are smaller in the lower lungs at end-expiration, which means higher surface tension inside the alveolar sac, greater possibility of alveolar collapse, and subsequently traction on adjacent bronchioles. UIP/IPF have a PERIPHERAL predominance because: (1) mechanical stress is higher in the peripheral lungs, and (2) vascular transit time is slower, resulting in greater deposition of substances that may contribute to the development of UIP/IPF. Hope that helps!
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Very simple but elegant explanation of radiographic changes. I have not come across any book that does it so succinctly thank you.
Glad it was helpful!
Great video! We should emphasize more pathophysiological mechanisms when learning radiology. More on the why than on the what. By the way, any idea why a UIP pattern of IPF most commonly affects the lower lungs?
Thank you for the great question. In order to answer, I will need to borrow some talking points from my advanced version of this talk (the version I've uploaded here on RUclips is the basic version).
1. I mentioned there is a superoinferior blood perfusion gradient that favors the lower lungs. There is ALSO a radial blood perfusion gradient that favors the central lungs over the peripheral lungs. Pulmonary vessels in peripheral lung are, on average, smaller in caliber than those in the central lung, which means that pulmonary vascular resistance is higher in peripheral lung than central lung. Higher pulmonary vascular resistance results in slower vascular transit time. Slower transit times are why we see greater deposition of things like septic emboli and metastases in the peripheral vascular bed of the lung than its central vascular bed.
2. There is a FOURTH factor that influences the geographic distribution of diseases in the lungs, besides blood perfusion, lymphatic flow, and ventilation. This fourth factor is mechanical stress. Mechanical stress is greatest in the upper lung and the peripheral lung. Imagine you're hanging off the ledge of a cliff by just your hands, and someone below you is hanging on to your ankles... that's sort of like how the upper lung feels. The upper lung "carries" the weight of the lower lung, which results in more connective tissue strain and alveolar distention in the upper lungs. Surface tension keeping the visceral and parietal pleural surfaces adherent to each together result in more connective tissue strain in the peripheral lungs.
UIP/IPF have a BASAL predominance because: (1) higher blood perfusion in the lower lungs results in greater deposition of substances that may contribute to the development of UIP/IPF (e.g. chemotherapy agents, inflammatory mediators, etc.) and (2) alveoli are smaller in the lower lungs at end-expiration, which means higher surface tension inside the alveolar sac, greater possibility of alveolar collapse, and subsequently traction on adjacent bronchioles.
UIP/IPF have a PERIPHERAL predominance because: (1) mechanical stress is higher in the peripheral lungs, and (2) vascular transit time is slower, resulting in greater deposition of substances that may contribute to the development of UIP/IPF.
Hope that helps!
@@radiologyframeworks Thank you very much, were could we find the advanced version of this lecture?
Thank you very much for this talk . Great video
Glad you liked it!
Superb