NURS 6501: Advanced Pathophysiology

Sample Answer for NURS 6501: Advanced Pathophysiology Included After Question

What’s Happening This Module? 

Module 2: Cardiovascular and Respiratory Disorders is a 2-week module, Weeks 3 and 4 of the course. In this module, you will examine fundamental concepts of cellular processes and the alterations that lead to various cardiovascular and respiratory diseases and disorders. You will evaluate the genetic environment and its impact on these diseases. You will also evaluate the impact of patient characteristics, including racial and ethnic variables, on physiological functioning.  

NURS 6501: Advanced Pathophysiology
NURS 6501: Advanced Pathophysiology
What do I have to do?      When do I have to do it?     
Review your Learning Resources  Days 1–7, Weeks 3 and 4 
Knowledge Check: Cardiovascular and Respiratory Disorders  Complete by Day 7 of Week 3 
Module 2 Case Study Analysis  You are encouraged to work on your Module 2 Assignment throughout the module. However, this Assignment is not due until Day 7 of Week 4. 

A Sample Answer For the Assignment: NURS 6501: Advanced Pathophysiology

Title: NURS 6501: Advanced Pathophysiology

Case Study Analysis 

The assigned case study demonstrates a middle age female patient with chief complaints of dyspnea, fever, and cough with thick green sputum production for 3 days. The patient also reports a history of chronic cough and COPD. She claims that the cough has worsened in the past few days. Examination findings reveal a flattened diaphragm and increased AP diameter. The patient also has hyper resonance with rhonchi and coarse rales in all the lung fields. The purpose of this discussion is to provide an analysis of the patient described above and the cardiovascular and cardiopulmonary pathophysiologic processes that contributed to the patient’s symptoms.  

Pathophysiologic Processes 

The patient presents with a history of COPD and chronic cough with thick green sputum. The current symptoms of dyspnea, cough, and fever indicate exacerbation of COPD with complications of a respiratory infection (Hikichi et al., 2018). The patient’s shortness of breath resulted from the obstructed airways secondary to inflammation, sputum hypersecretion, and airway remodeling. Elastic recoil reduction in the lungs following obstruction of the airways and emphysema causes partial air expelling and active hyperinflation (Santus et al., 2019). Accumulation of the mucus leads to coughing by the patient as an attempt to try and clear the airways. The increased production of thick green sputum and fever are signs of bacterial infection in COPD exacerbation. 

Racial/Ethnic Variables 

There is limited evidence on the racial/ethnic variables in the characteristics and progress of COPD. Non-Hispanic whites have however been reported to have the highest burden associated with symptoms of chronic bronchitis and cardiovascular diseases as comorbidities of COPD (Park et al., 2021). African Americans on the other hand, have reported the highest incidences of dyspnea due to lifestyle habits like smoking and reduced exercise capacity (Lee et al., 2018). Korean patients on the other hand were more likely to be underweight as compared to other ethnic groups, hence reduced COPD symptoms and complications (D’Cruz et al., 2020). Generally, the ethnic variables in COPD are due to sociodemographic differences in lifestyle habits, education, and cultural beliefs among other factors.  

How Processes interact to Affect the Patient 

As discussed above, the pathophysiology of COPD involves the interaction of both cardiovascular and cardiopulmonary processes. Impairments in the cardiopulmonary functioning leading to COPD are associated with several risk factors including smoking, exposure to chemicals, race, age, and history of asthma (Hikichi et al., 2018). The above risk factors have the potential of resulting in pathological changes within the peripheral bronchioles, parenchyma of the lungs, and central airways. Structural changes in the airways include ciliary abnormalities, focal squamous metaplasia, atrophy, inflammation, airway smooth muscle hyperplasia, and bronchial wall thickening leading to chronic bronchitis (Santus et al., 2019). When the air spaces enlarge permanently distal to the bronchial on the terminals, the alveoli surface area that is available for gaseous exchange is usually reduced leading to emphysema. The above mechanisms contribute to the patient’s symptoms such as shortness of breath, chronic cough, increased sputum production, and fever. 


The middle-aged patient in the provided case study presents with symptoms indicating COPD exacerbation. Several cardiopulmonary processes contribute to the development of the patient’s condition such as the small (peripheral) bronchioles, large (central) airways, and the lung parenchyma. However, with a comprehensive understanding of the pathophysiology of the patient’s condition, it will be easier for the clinician to develop the most effective treatment plan.  



D’Cruz, R. F., Murphy, P. B., & Kaltsakas, G. (2020). Sleep-disordered breathing and chronic obstructive pulmonary disease: a narrative review on classification, pathophysiology and clinical outcomes. Journal of Thoracic Disease, 12(S2), S202–S216. 

Hikichi, M., Hashimoto, S., & Gon, Y. (2018). Asthma and COPD overlap the pathophysiology of ACO. Allergology International, 67(2), 179–186. 

Lee, H., Shin, S. H., Gu, S., Zhao, D., Kang, D., Joi, Y. R., Suh, G. Y., Pastor-Barriuso, R., Guallar, E., Cho, J., & Park, H. Y. (2018). Racial differences in comorbidity profile among patients with chronic obstructive pulmonary disease. BMC Medicine, 16(1). 

Park, H. Y., Lee, H., Kang, D., Choi, H. S., Ryu, Y. H., Jung, K.-S., Sin, D. D., Cho, J., & Yoo, K. H. (2021). Understanding racial differences of COPD patients with an ecological model: two large cohort studies in the US and Korea. Therapeutic Advances in Chronic Disease, 12, 204062232098245. 

Santus, P., Pecchiari, M., Tursi, F., Valenti, V., Saad, M., & Radovanovic, D. (2019). The Airways’ Mechanical Stress in Lung Disease: Implications for COPD Pathophysiology and Treatment Evaluation. Canadian Respiratory Journal. 

A Sample Answer 2 For the Assignment: NURS 6501: Advanced Pathophysiology

Title: NURS 6501: Advanced Pathophysiology

The case scenario depicts a 16-year-old male patient who presents with a chief complaint of a sore throat for three days. Positive physical findings include temp of 99.6 F, erythematous posterior pharynx with white exudate on enlarged tonsils 3+. The patient has positive anterior and posterior cervical adenopathy, and a Rapid strep test was positive. He was prescribedAmoxicillin 500 mg orally q and upon taking the first capsule, he reported tongue and lips swelling and difficulty breathing with audible wheezing. He was taken to the ED and treated for an allergic reaction.

The Role Genetics Plays In the Disease

Individuals with penicillin allergies may have genetic variations on an immune system gene that enables the body to differentiate between the body cells and harmful bacteria and viruses (Lteif & Eiland, 2019). A major histo-compatibility on the complex gene HLA-B is thought to cause penicillin allergies, as seen in the patient in the case study.

Why the Patient Is Presenting With the Specific Symptoms Described

The patient experienced an acute allergic reaction, which occurs immediately or abruptly within minutes to an hour or two. It includes abrupt anaphylaxis with hypotension, angioedema, bronchospasm, and urticaria (Shenoy et al., 2019). Acute reactions are due to reaction with preformed IgE to penicillin from previous exposure. This results in the release of histamine and other mediators from mast cells, which produces the patient’s specific symptoms of tongue and lips edema, difficulty breathing, and audible wheezing.

Physiologic Response to the Stimulus Presented In the Scenario

The allergic reaction to penicillin occurs when antigen-specific IgE is present on mast cells. Systemic exposure to antigen transpires and cross-links the IgE, resulting in concurrent degranulation of many mast cells (Maker et al., 2019). The allergic reaction to penicillin occurred after a sudden release of histamine and other vasoactive mediators by the mast cells. This was due to an IgE-mediated anaphylactic reaction resulting in the hypersensitivity symptoms.

Cells Involved In This Process

Cells involved in the hypersensitivity reaction include IgE, which mediates Type I hypersensitivity reactions. Penicillin-specific IgE binds to Fc-epsilon-RI receptors on mast cells and basophils, releasing histamine and vasoactive mediators (Maker et al., 2019).

How another Characteristic Would Change the Response

Studies have proposed a genetic influence on penicillin allergy (Lteif & Eiland, 2019). Thus, if the patient has a close relative with a history of penicillin allergy, the condition would have been attributed to genetics.


Lteif, L., & Eiland, L. S. (2019). The Basics of Penicillin Allergy: What A Clinician Should Know. Pharmacy (Basel, Switzerland)7(3), 94.

Maker, J. H., Stroup, C. M., Huang, V., & James, S. F. (2019). Antibiotic Hypersensitivity Mechanisms. Pharmacy (Basel, Switzerland)7(3), 122.

Shenoy, E. S., Macy, E., Rowe, T., & Blumenthal, K. G. (2019). Evaluation and Management of Penicillin Allergy: A Review. JAMA321(2), 188–199.