Which type of pulmonary disease requires more force to expire a volume of air?

A. Left heart failure: COPD primarily affects the lungs and increases pulmonary vascular resistance, leading to right-sided heart strain rather than left heart failure. Left heart failure is more commonly associated with conditions such as hypertension, myocardial infarction, and valvular diseases, which impair the heart’s ability to pump blood systemically.

B. Restrictive cardiomyopathy: Restrictive cardiomyopathy is a condition where the heart muscle becomes stiff and loses its ability to relax and fill properly, often due to infiltrative diseases such as amyloidosis or sarcoidosis. COPD does not directly lead to restrictive cardiomyopathy, as its primary cardiovascular complication is increased pulmonary resistance causing right heart strain.

C. Hypertrophic cardiomyopathy: Hypertrophic cardiomyopathy is characterized by abnormal thickening of the heart muscle, usually due to genetic mutations. It primarily affects the left ventricle and impairs diastolic filling. COPD does not cause hypertrophic cardiomyopathy, as its cardiovascular effects are due to pulmonary hypertension and right ventricular overload rather than structural abnormalities of the myocardium.

D. Right heart failure: Chronic COPD leads to persistent pulmonary hypertension due to hypoxic vasoconstriction and remodeling of pulmonary vessels. This increased pulmonary vascular resistance forces the right ventricle to work harder to pump blood into the lungs, leading to right ventricular hypertrophy and eventual right heart failure, also known as cor pulmonale. Symptoms include peripheral edema, jugular vein distention, and hepatomegaly due to systemic venous congestion.

A. Injury to the endothelial cells that line the artery walls: The development of atherosclerosis begins with damage to the endothelial cells of the arterial wall. This injury can be caused by various factors, including hypertension, smoking, high cholesterol, and diabetes. Once the endothelium is injured, it becomes more permeable, allowing lipids and inflammatory cells to penetrate and accumulate, leading to the formation of atherosclerotic plaques.

B. Release of the platelet-derived growth factor: While platelet-derived growth factor (PDGF) plays a role in the proliferation of smooth muscle cells and the progression of atherosclerosis, it is not the initiating event. PDGF is released in response to endothelial injury and inflammation but does not cause the initial damage itself.

C. Macrophages adhere to vessel walls: The adherence of macrophages to the vessel walls occurs after the initial endothelial injury. Once the endothelium is damaged, macrophages migrate to the site and contribute to the inflammatory response and plaque formation, but this is not the initiating event.

D. Release of inflammatory cytokines: Inflammatory cytokines are part of the response that follows endothelial injury and play a role in the progression of atherosclerosis. However, the release of these cytokines is a consequence of the initial injury rather than the initiating event.