Week 2: COPD Case Study: Part 1
NR-601 Primary Care of the Maturing and Aged Family
Name
Date
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
NR-601 Primary Care of the Maturing and Aged Family
Name
Date
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
