NR 507 Week 3 case study: Pathophysiology & Clinical Findings of The Disease 

NR 507 Week 3 case study: Pathophysiology & Clinical Findings of The Disease

1. Are the spirometry results consistent with obstructive or restrictive pulmonary disease? What is the most likely pulmonary diagnosis for this patient?

The spirometry results are consistent with obstructive pulmonary disease. The forced expiratory volume in one second (FEV1) result of this patient is decreased below 80%, which is typical for obstructive pulmonary disease (Haynes, 2018). The ratio of FEV1 against forced vital capacity (FVC), FEV1/FVC, is reduced below 70%, with the pre-bronchodilator prediction being 69% and the post-bronchodilator prediction being 64%. The correct diagnosis of this patient is chronic pulmonary disease (COPD). The normal FEV1/FVC is above 80%, and with this patient, the figures pre- and post-bronchodilator prediction are below 80%, justifying the diagnosis of COPD.

2. Explain the pathophysiology associated with the chosen pulmonary disease.

COPD is a progressive lung disease caused by inhalation of toxic particles and smoking of cigarettes (Alfahad et al., 2021). With persistent exposure to the toxins, abnormal inflammatory responses develop within the airways leading to permanent respiratory damage and pathological changes that are irreversible. COPD results from oxidative stress and imbalance of proteases and antiproteases (Agarwal et al., 2022). Alpha-1 antitrypsin deficiency is implicated in the pathophysiology of emphysema since deficiency of antiproteases and imbalances cause the lung parenchyma to be predisposed to protease-mediated damage. The two entities of COPD are emphysema and chronic bronchitis. Emphysema encompasses structural changes associated with COPD where the alveolar air sacs become damaged and causes obstructive physiology. Irritants such as smoking cause inflammatory responses in emphysema (Agarwal et al., 2022). With the inflammatory responses, there is the recruitment of neutrophils and macrophages and the release of structural changes associated. With oxidants and excess proteases being released, air sacs become destroyed. Due to inflammation and airway obstruction, there is a decrease in FEV1 and destruction of tissues leading to limitation of airflow and impairment of gaseous exchange (Agarwal et al., 2022). This will cause lung hyperinflation upon imaging studies because air is trapped due to the collapse of airways during exhalation. With the advancement of the disease, impairment of gaseous exchange takes place. Patients will present with chronic progressive difficulty breathing, cough, and production of sputum. There may also be complaints of wheezing and chest tightness. Chronic bronchitis is associated with a productive cough occurring for more than three months over a span of two years.

3. Identify at least three subjective findings from the case which support the chosen diagnosis.

Increasing dyspnea for three months, 35 pack-year smoking history, history of evaluation for acute bronchitis, and a dry, non-productive cough. Agarwal et al. (2022) cite that patients with COPD will report chronic and progressive dyspnea, cough, and sputum production. In most circumstances, there is a history of smoking. In the absence of a smoking history, there is a family history, occupational exposure, or second-hand smoke exposure.

4. Identify at least three objective findings from the case which support the chosen diagnosis.

On lung exam, the patient has bilateral wheezes with forced exhalation along with a prolonged expiratory phase. On performing a chest X-ray, the lungs are bilaterally hyperinflated, and the diaphragm is flattened. The spirometry results are consistent with COPD. The FEV1/FVC, FEV1, and TLC figures are appropriate for COPD. According to Agarwal et al. (2022), upon evaluating the chest of patients with COPD, wheezes are auscultated; X-ray shows hyperinflation of the lungs due to trapping of air secondary to airway collapse during exhalation.

Management of the Disease

*Utilize the required Clinical Practice Guideline (CPG) to support your treatment recommendations.

1. Classify the patient’s disease severity. Is this considered stable or unstable?

The COPD of this patient is stage I. According to the GOLD classification for COPD, in patients whose FEV1/FVC is less than 70%, GOLD 1 is classified as mild, and the FEV1 value is equal to or more than 80% of the predicted value. A.C. has a predicted value of 81%; therefore, his severity is classified as mild. His condition is unstable since the patient has had progressive difficulty breathing over three months, and pre-existing medical conditions such as hypertension, hyperlipidemia, and atherosclerotic coronary disease may worsen his COPD. Cor-pulmonale is a complication of COPD and is associated with heart failure.

2. Identify two (2) “Evidence A” recommended medication classes for the treatment of this condition and provide an example (drug name) for each.

Medication classes are bronchodilators and include drug groups like antimuscarinic agents, selective B2-agonists, anticholinergics, and methylxanthines. B2-agonists include albuterol, salmeterol, and formoterol. Methylxanthines include theophylline and aminophylline. Anticholinergics include ipratropium bromide (GOLD, 2023).

Another medication class is glucocorticoids which can be inhaled or systemic. Inhaled corticosteroids include budesonide and beclomethasone, while systemic corticosteroids include prednisolone (GOLD, 2023).

3. Describe the mechanism of action for each of the medication classes identified above.

Bronchodilators: B2-agonists cause bronchodilation by stimulating the enzyme adenylyl cyclase that, leads to increased formation of cyclic adenosine monophosphate, which subsequently mediates the relaxation of bronchial smooth muscles, ultimately achieving bronchodilation. This also improves mucociliary clearance. Anticholinergics lead to bronchodilation through competitive inhibition of cholinergic receptors found in bronchial smooth muscles. On the other hand, methylxanthines cause phosphodiesterase inhibition, prevent the influx of calcium ions into smooth muscles, and antagonize adenosine receptors. The overall effect is the achievement of bronchodilation (Fazleen & Wilkinson, 2020).

Glucocorticoids cause a reduction in capillary permeability, leading to a decrease in mucus production. They also prevent the release of proteolytic enzymes from leukocytes and inhibit the release of prostaglandins. Glucocorticoids help limit inflammatory activity, which is a major factor implicated in the pathophysiology of COPD (Fazleen & Wilkinson, 2020).

4. Identify two (2) “Evidence A” recommended non-pharmacological treatment options for this patient.

Non-pharmacological treatment options include oxygen supplementation, cessation of cigarette smoking, nutritional support, among others. A.C. has already undergone smoking cessation counseling as part of managing his condition. A combination of the other options, like the provision of oxygen concentrators and supporting on his nutrition, will lead to a positive response regarding his COPD.

 References

Agarwal, A., Raja, A., & Brown, B. (2022). Chronic Obstructive Pulmonary Disease. StatPearls. https://www.statpearls.com/articlelibrary/viewarticle/26083/

Alfahad, A. J., Alzaydi, M. M., Aldossary, A. M., Alshehri, A. A., Almughem, F. A., Zaidan, N. M., & Tawfik, E. A. (2021). Current views in chronic obstructive pulmonary disease pathogenesis and management. Saudi Pharmaceutical Journal, 29(12), 1361–1373. https://doi.org/10.1016/j.jsps.2021.10.008

Fazleen, A., & Wilkinson, T. (2020). Early COPD: current evidence for diagnosis and management. Therapeutic Advances in Respiratory Disease, 14(1), 175346662094212. https://doi.org/10.1177/1753466620942128

GOLD. (2023). Clinicians. Global Initiative for Chronic Obstructive Lung Disease – GOLD. https://goldcopd.org/clinicians/

Haynes, J. (2018). Basic spirometry testing and interpretation for the primary care provider. Canadian Journal of Respiratory Therapy, 54(4), 92–98. https://doi.org/10.29390/cjrt-2018-017

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 Preparing the Assignment

Requirements

Content Criteria:

Read the case study listed below.

Refer to the rubric for grading requirements.

Utilizing the Week 3 Case Study TemplateLinks to an external site., provide your responses to the case study questions listed below.

You must use at least one scholarly reference to provide pathophysiology statements. For this class, use of the textbook for pathophysiology statements is acceptable. You may also use an appropriate evidence-based journal.

You must use the current Clinical Practice Guideline (CPG) for the management and prevention of COPD (GOLD Criteria) to answer the classification of severity and treatment recommendation questions. The most current guideline may be found at the following web address: https://goldcopd.org/Links to an external site.. At the website, locate the current year’s CPG and download a personal copy for use. You may also use a medication administration reference such as Epocrates to provide medication names.

Proper APA format (in-text citations, reference page, spelling, English language, and grammar) must be used.

Case Study Scenario

Chief Complaint

A.C., is a 61-year old male with complaints of shortness of breath.

History of Present Illness

A.C. was seen in the emergency room 1 week ago for an acute onset of mid-sternal chest pain. The event was preceded with complaints of fatigue and increasing dyspnea for 3 months, for which he did not seek care. He was evaluated by cardiology and underwent a successful and uneventful angioplasty prior to discharge. Despite the intervention, the shortness of breath has not improved. Since starting cardiac rehabilitation, he feels that his breathlessness is worse. The cardiologist has requested that you, his primary care provider, evaluate him for further work-up. Prior to today, his last visit with your practice was 3 years ago when he was seen for acute bronchitis and smoking cessation counseling.

Past Medical History 

Hypertension 

Hyperlipidemia 

Atherosclerotic coronary artery disease

Smoker

Family History

Father deceased of acute coronary syndrome at age 65

Mother deceased of breast cancer at age 58. 

One sister, alive, who is a 5 year breast cancer survivor.

One son and one daughter with no significant medical history. 

Social History

35 pack-year smoking history; he has cut down to one cigarette at bedtime following his cardiac intervention. 

Denies alcohol or recreational drug use 

Real estate agent  

Allergies

No Known Drug Allergies 

Medications

Rosuvastatin 20 mg once daily by mouth 

Carvedilol 25 mg twice daily by mouth

Hydrochlorothiazide 12.5 mg once daily by mouth

Aspirin 81mg daily by mouth

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Review of Systems

Constitutional: Denies fever, chills or weight loss. + Fatigue.

HEENT: Denies nasal congestion, rhinorrhea or sore throat.  

Chest: + dyspnea with exertion. Denies productive cough or wheezing. + Dry, nonproductive cough in the AM.

Heart: Denies chest pain, chest pressure or palpitations.

Lymph: Denies lymph node swelling.

General Physical Exam  

Constitutional: Alert and oriented male in no apparent distress.  

Vital Signs: BP-120/84, T-97.9 F, P-62, RR-22, SaO2: 93% 

Wt. 180 lbs., Ht. 5’9″

HEENT 

Eyes: Pupils equal, round and reactive to light and accommodation, normal conjunctiva. 

Ears: Tympanic membranes intact. 

Nose: Bilateral nasal turbinates without redness or swelling. Nares patent. 

Mouth: Oropharynx clear. No mouth lesions. Dentures well-fitting. Oral mucous membranes dry. 

Neck/Lymph Nodes 

Neck supple without JVD. 

No lymphadenopathy, masses or carotid bruits. 

Lungs 

Bilateral breath sounds clear throughout lung fields. + Bilaterally wheezes noted with forced exhalation along with a prolonged expiratory phase. No intercostal retractions.

Heart 

S1 and S2 regular rate and rhythm, no rubs or murmurs. 

Integumentary System 

Skin cool, pale and dry. Nail beds pink without clubbing.  

Chest X-Ray 

Lungs are hyper-inflated bilaterally with a flattened diaphragm. No effusions or infiltrates.

Spirometry

Title Predicted Pre-bronchodilator % Predicted Post-bronchodilator % Predicted Change

FVC (L)

5.64

5.23

93

5.77

102

9%

FEV1 (L)

4.57

2.92

64

3.01

66

2%

FEV1/FVC (%)

81

56

69

52

64

-5%

TLC

5.5

6.9

125

6.9

125

0%

Case Study Questions

Pathophysiology & Clinical Findings of the Disease

Are the spirometry results consistent with obstructive or restrictive pulmonary disease? What is the most likely pulmonary diagnosis for this patient?

Explain the pathophysiology associated with the chosen pulmonary disease.

Identify at least three subjective findings from the case which support the chosen diagnosis.

Identify at least three objective findings from the case which support the chosen diagnosis.

Management of the Disease

*Utilize the required Clinical Practice Guideline (CPG) to support your treatment recommendations.

Classify the patient’s disease severity. Is this considered stable or unstable?

Identify two (2) “Evidence A” recommended medication classes for the treatment of this condition and provide an example (drug name) for each.

Describe the mechanism of action for each of the medication classes identified above.

Identify two (2) “Evidence A” recommended non-pharmacological treatment options for this patient.