A client in an urgent care clinic is complaining of heart palpitations, fatigue, and shortness of breath. A 12-lead electrocardiogram (ECG) shows no discernable P-waves, and an irregular ventricular rate. The nurse should understand that this finding represents which of the following conditions?

A. Barrel chest is a physical finding commonly associated with COPD due to hyperinflation of the lungs. It results from chronic air trapping and enlargement of the chest. While barrel chest is not directly caused by cor pulmonale, it is a characteristic feature of advanced COPD.
B. Clubbing of the fingers is not directly caused by cor pulmonale. It is typically associated with chronic hypoxia, which can occur in advanced lung diseases like COPD. Clubbing involves changes in the shape and texture of the nails and fingertips due to chronic lack of oxygen in the blood.
C. Destruction of the alveoli is a hallmark of emphysema, which is a type of COPD. Emphysema leads to loss of lung tissue elasticity and surface area, contributing to chronic airflow limitation. While emphysema is a risk factor for developing cor pulmonale, destruction of alveoli itself does not directly cause cor pulmonale.
D. Peripheral edema is a manifestation caused by cor pulmonale. When the right side of the heart fails (cor pulmonale), it leads to increased pressure in the pulmonary circulation, which can eventually cause fluid to leak out into the tissues, resulting in peripheral edema. This is a consequence of the right heart's inability to effectively pump blood forward due to pulmonary hypertension and subsequent right ventricular failure.

A. Dopamine is primarily associated with other neurodegenerative disorders such as Parkinson's disease, not Alzheimer's disease. In Alzheimer's disease, the focus is on changes related to beta-amyloid plaques and neurofibrillary tangles rather than alterations in dopamine levels.
B. Glial cells, including astrocytes and microglia, play a role in the brain's immune response and support of neurons. In Alzheimer's disease, there is evidence of increased activation and proliferation of glial cells in response to neuroinflammation and the presence of beta-amyloid plaques and neurofibrillary tangles. This reactive gliosis is a secondary response to the underlying pathology.
C. Glutamate is an excitatory neurotransmitter involved in various brain functions, including memory and learning. In Alzheimer's disease, there is evidence of dysregulation in glutamate metabolism and

signaling pathways. This dysregulation can lead to excitotoxicity, which contributes to neuronal damage and cell death seen in the disease.
D. Neurofibrillary tangles are one of the hallmark pathological features of Alzheimer's disease. These tangles are aggregates of hyperphosphorylated tau protein that accumulate inside neurons, disrupting their normal functioning and eventually leading to cell death. Neurofibrillary tangles, along with beta- amyloid plaques, contribute to the progressive cognitive decline observed in Alzheimer's disease.