PAT 20A/B Lecture Notes - Lecture 11: Chronic Obstructive Pulmonary Disease, Viscosity, Perfusion

• School: Ryerson University
• Department: Pathotherapeutics
• Course: PAT 20A/B
• Professor: Susan Bishop

Document Summary

Asthma = acute inflammation of the airways & hyper-responsiveness of the bronchioles. Copd = inflammation of the airways/bronchioles; destruction of the lung tissue (parenchyma), alveoli, & the capillaries/capillary bed surrounding each alveolus. [not fully reversible only partially reversible] ((chronic disease)) Elastase eats away the alveoli walls and capillary beds less blood vessels to move same amount of blood through to the lungs & capillary vasoconstriction pulmonary htn. Many things can increase elastase & decrease aat creating imbalance start to constrict capillaries near non- functioning alveoli (partly adaptive) & supplying blood to functioning alveoli instead pulmonary htn. Rv pushes blood up into lungs to be oxygenated over years consistently pushing against resistance d/t. Pulmonary htn r-side of heart hypertrophies = cor pulmonale && pulmonary arterial hypertrophy can develop into r-sided hf; muscle wasting; polycythemia (excess rbcs b/c body is starving for oxygen hypoxic/hypoxemic) = adaptive but increases viscosity of blood.