Week 2: COPD Case Study: Part 1

NR-601 Primary Care of the Maturing and Aged Family

Susan Brown

January 2020

J.D. is a 62 y/o Caucasian male that presents to the office today with the CC of persistent

cough for the past 6 months with a recent onset of SOB. Cough is intermittent and frequent and

is noted to be worse in the AM. Cough is productive. The sx are aggravated by activity and are

relieved by rest. Tx has been Robitussin DM OTC without any relief of sx. Severity of sx; he is

unable to walk greater than 20ft w/o stopping to catch his breath. Pt states, “I routinely walked 1

mile a day without difficulty.”

Upon ROS the patient denies fever, chills, or weight loss. Denies any sx associated with

HEENT. He denies chest pain and LE edema. However, he reports a persistent productive cough

with white-yellowish phlegm; that is worse upon waking and SOB upon activity.

PMH is positive for primary HTN. He is currently taking Metoprolol succinate ER 50 mg

qd for HTN and a MV qd. PSH includes cholecystectomy and appendectomy. KDA PCN (hives).

He is married with 3 children and works at a risk management firm as a Senior accountant. He is

a former smoker with a 20 pack-year hx; denies ETOH or illicit drug use. FH is positive for

diabetes and HTN. Father deceased at age 59 of MI and CHF. Father was a smoker; pt quit “cold

turkey” at that time. Mother living and siblings all in good health.

Upon PE, J.D. appears his stated age, is A&O x4, NAD, and is able to speak in full

sentences. T. 98.1, P. 66, RR. 20, BP 156/94., O2 sat 94 % on RA, Ht. 68.9 “, Wt. 258, with BMI

of 38.2 (obese). Cardiopulmonary exam reveals S1 S2 with no murmurs or additional heart

sound, BBS clear to auscultation with faint forced expiratory wheezes in bilateral bases. R are

even and unlabored. No BLE edema noted. PE otherwise normal and unremarkable.

Differential Diagnosis in order of most likely:

1. Chronic Obstructive Pulmonary Disease (COPD)

2. Asthma

3. Heart Failure

COPD:

COPD is a progressive disease of the lungs that is characterized by airflow limitation

related to chronic obstruction that impedes normal breathing; this process is preventable as well

as treatable (Berg & Wright, 2016). As a result of repeated exposure to pollutants and inhaled

irritants, pathological changes in the airways and alveoli occur due to an increased inflammatory

response (Dunphy, Winland-Brown, Porter, & Thomas, 2019). The chronic inflammatory

response leads to irreversible structural changes, a narrowing of airways passages, and

parenchymal changes in the lung; the exaggerated inflammatory response in some individual is

thought to a certain degree to be related to a genetic predisposition. Overproduction and

hypersecretion of mucus is related to irritation of the goblet cells and permanent damage of the

airway specifically the cilia lead to chronic productive cough (GOLD, 2017). In the United

States, COPD is the third leading cause of death and the fourth leading cause of disability; and is

associated with exorbitant medical costs. 80 to 90 % of cases of COPD are caused by cigarette

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