A 56-year-old woman presents to your office with chronic cough. She says that the cough is dry and affects quality of her life significantly. She denies chest pain, hemoptysis and shortness of breath. Her past medical history is significant for long-standing hypertension, diabetes and myocardial infarction experienced two months ago. She does not smoke or consume alcohol. Her blood pressure is 130/70 mmHg and heart rate is 70/min. Which of the following is the best next step in the management of this patient?
With a history of hypertension, diabetes, and coronary heart disease, the likelihood that this patient is on standard ACE inhibitor therapy is very high. A dry, nonproductive, and persistent cough is one of the most well-known side effects of ACE inhibitor therapy.
The mechanism of ACE inhibitor induced cough is believed to involve increased bradykinin, substance P, or prostaglandins. ACE is a very nonspecific enzyme responsible for the breakdown of many substrates. By blocking ACE, ACE inhibitors block degradation of bradykinin and substance P. Bradykinin and substance P accumulation can cause inflammation and stimulate lung irritation.
Because angiotensin receptor blockers (ARBs) do not affect ACE activity, they theoretically should not cause cough.
(Choice A) Chronic cough is one of the early signs of cancer. Screening family history will allow risk assessment for cancer, but since patient does not complain of any other symptoms of cancer (unexplained fatigue, weight loss, change in bowel habits, etc.), suspicion for cancer is low.
(Choice B) Although cough can occur secondary to post nasal drip in patients with allergies, the patient describes no other allergy type symptoms (itchy and watery eyes, runny nose, sneezing, etc.).
(Choice D) Diet and physical activity are not linked to causing cough.
(Choice E) Cough may be linked to pulmonary infection or disease. Chest x-ray would be helpful in diagnosis if suspicion for pneumonia, TB, bronchitis, or emphysema were high. However, patient has no symptoms associated with any infection and her risk for emphysema is low since she does not smoke.
Educational Objective:
Cough is a very well recognized side effect of ACE inhibitor therapy. Cough secondary to ACE inhibitor therapy is characterized as dry, nonproductive, and persistent. The mechanism behind ACE inhibitor induced cough is accumulation of bradykinin, substance P, or prostaglandins. Because angiotensin receptor blockers (ARBs) do not affect ACE activity, they theoretically should not cause cough.