MSCI 520RESEARCH PAPER: DISEASE PHARMACOLOGY ASSIGNMENT INSTRUCTIONS
OVERVIEW
The paper assignments in this course focus on diseases that highlight normal physiologic processes,
mechanisms of alterations to these processes that result in the diseases and the therapeutic manipulations
of molecular players in an attempt to restore homeostasis. In addition to exploring these processes, the
assignments are also aimed at helping students enhance their scientific inquiry skills including current
literature review and scientific communication. Theses afford students an opportunity to complete a
research journal-type of work that is relevant to a career in the field of biomedicine and healthcare.
INSTRUCTIONS
Paper Topic:
Your instructor will assign you a disease topic for your papers. Your references MUST include at least 5
recent primary research articles, 3 of which are from journals published by the American Physiological
Society (APS). There are 7 American Journal of Physiology (AJP) journals to choose from: Cell
Physiology; Endocrinology & Metabolism; Gastrointestinal & Liver Physiology; Heart & Circulatory
Physiology; Lung, Cellular & Molecular Physiology; Regulatory, Integrative & Comparative Physiology;
and Renal Physiology. In addition, there are a few other journals published by the APS that include
primary research that can be found on their website.
Writing the papers:
Research Paper: Disease Pharmacology
Start the body of the paper on a new page after the title page. You should review current research on at
least five (5) pharmacological management options for the disease you focused on in Research Paper:
Disease Physiology/Pathophysiology, including drugs in clinical trials. Your review should include these
components:
1) The physiologic rationale for using the drugs in treating your assigned disease.
2) The mechanisms of action of these drugs.
3) The side effects of these drugs and their contraindications.
4) The dosages and routes of administration of the drugs.
This section must include a minimum of 5 unique references that are recent and are cited in AMA format,
and the paper should be 3 pages long exactly.
Figures
Figures are allowed in any section, but do not count towards page count. These can be your original
figures/drawings or (if properly cited) from one of your sources. Place all figures at the end of the paper.
Page 1 of 2
MSCI 520
Formatting the paper:
1) The title page for each paper should include the title of the entire project; course name, number,
and section number; professor’s name; and date. Title page does not count toward the page count.
Please refer to the AMA sample paper.
2) Paper must be double-spaced, including between paragraphs. New paragraphs should be started
with a single tab.
3) Paper must have 1” margins on all sides.
4) Font must be 12 pt., Arial font (regular).
5) Minimum lengths refer to full pages; a full page is 23 lines of text. Do not use section headings for
“filler” as these will not count towards page count. Short or long papers will be penalized based on
the amount written/missing.
6) Direct quotations are not appropriate for this project; you are to write a paper, not copy and paste
from other papers.
7) All references must be professional peer-reviewed articles.
8) Your in-text citations and references need to be in current AMA format.
Failure to follow any of these formatting instructions will result in loss of points. (See rubrics.)
Each section will be graded on clarity and demonstration of mastery of topic. The information must be
accurate, and the writing must indicate thorough graduate-level work. The writing level and style should
be the same as the peer-reviewed professional articles you use for your sources.
Please review the Academic Honor Code to ensure you are following it when writing the paper. Penalties
for Academic Dishonesty can include failure of the assignment or the entire course.
Note: Your assignment will be checked for originality via the Turnitin plagiarism tool.
Page 2 of 2
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
1
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
Introduction
Millions worldwide suffer from chronic obstructive pulmonary disease (COPD), a
devastating respiratory ailment. According to Attaway et al.,1 due to ongoing airway
inflammation and lung tissue death, it is distinguished by prolonged airflow restriction.
With a focus on the epidemiology, etiology, classification, normal physiology, molecular
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
2
foundation, signs/symptoms, laboratory characteristics, differential diagnosis,
complications, and prognosis of COPD, this study seeks to provide an in-depth analysis
of its pathophysiology.
Epidemiology:
Being the third most common cause of mortality, COPD is a significant public
health concern on a global scale. Jurevičienė et al.,2 argues that males are more likely
to be affected than females by this progressive lung ailment, which typically affects
those over 40. Smoking causes an astounding 80–90% of COPD cases, making it the
main risk factor. Smoke from cigarettes causes’ lung and airway damage over time,
which restricts airflow and makes breathing harder.
Other than smoking, several environmental factors may have a role in the
development of COPD. Agustí et al.,3 notes that the risk of COPD rises with continued
exposure to air pollution, both inside and outside. Workplace dangers, including dust,
fumes, and chemicals, can exacerbate the illness. Additionally, as certain people may
be more prone to the ailment due to genetic abnormalities, genetics also plays a part in
COPD susceptibility.
Respiratory infections can damage lung health and raise the risk of developing
COPD, especially in youth or later in life. Jurevičienė et al.,2 suggests that effective
public health initiatives aimed at smoking cessation, pollution reduction, and early
identification are essential in reducing the burden of COPD on individuals and societies
because of its huge global impact and avoidable nature.
Etiology:
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
3
Chronic exposure to harmful gases and particles, most notably from cigarette
smoke, is the primary etiological cause of COPD. These irritants cause inflammation in
the lungs when inhaled by sensitive people. Attaway et al.,1 states that this inflammation
causes immune cells to activate and inflammatory mediators to be released, which
causes airways to reorganize and lung tissue to deteriorate gradually. This process
eventually results in typical COPD symptoms, including a persistent cough, shortness of
breath, and diminished lung function. According to research by Tang et al.,4 avoiding
exposure to hazardous substances and quitting smoking are important COPD
preventive practices, highlighting the need to address the disease’s root cause to lessen
its effects.
Types/Classification:
The two main categories of COPD are emphysema and chronic bronchitis.
Inflammation of the bronchial airways causes chronic irritation, increased mucus
production, and a persistent cough with sputum production in chronic bronchitis. It is
challenging to breathe because the inflammation narrows the airways5.
The deterioration of the alveolar walls, which are in charge of gas exchange in
the lungs, occurs due to emphysema, on the other hand. As a result, the air sacs lose
their suppleness and collapse during exhalation, decreasing the effectiveness of gas
exchange6. As a result, people with emphysema face breathing difficulties and low
blood oxygen levels. Both subtypes share symptoms like coughing, wheezing, and
dyspnea and are typically brought on by prolonged exposure to hazardous substances,
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
4
especially cigarette smoke. Improved diagnosis, care, and management are crucial to
raising COPD patients’ quality of life.
Normal Physiology and Homeostasis:
The alveoli and airways in a healthy respiratory system are remarkably elastic
and flexible, allowing for effective airflow into and out of the lungs. According to
Woldhuis et al.,7 cilia, tiny hair-like projections that coat the inside of these delicate
structures, are essential for filtering and getting rid of inhaled viruses and debris. By
doing this, they preserve a sterile environment and protect the lungs from potential
injury. The immune system is a watchful protector, quickly identifying and eliminating
invading germs to protect lung health and maintain general homeostasis. The smooth
exchange of oxygen and carbon dioxide is ensured by the harmonic interaction of the
respiratory and immune systems, which also reduces the risk of infections and
preserves the delicate balance necessary for healthy lung function.
Pathophysiology and Molecular Basis of the Disease:
Inducing a persistent inflammatory response in the airways due to repeated
exposure to noxious particles, especially from smoking, plays a role in the pathogenesis
of lung illnesses, including COPD. Inflammatory cells, including neutrophils and
macrophages, are drawn to the lungs in reaction to these damaging particles. These
immune cells cause damage to the lung tissue and start an inflammatory cycle by
releasing reactive oxygen species and proteolytic enzymes8. The balance between
tissue repair and degradation is gradually upset by this chronic inflammatory state,
resulting in the remodelling of the airways and the loss of the alveolar walls essential for
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
5
exchanging oxygen and carbon dioxide. As a result, lung function is compromised, and
patients report having trouble breathing and a lower activity tolerance. Treatment
solutions must consider the molecular underpinnings of this process to manage and
cure chronic respiratory disorders effectively.
Signs/Symptoms:
Exposure to irritants like smoke and pollution can lead to the progressive
respiratory disorder known as COPD. Long-lasting coughing up mucus, wheezing,
shortness of breath, and chest tightening are symptoms that get worse with time8. To
arrest progression and enhance the patient’s quality of life, early diagnosis and therapy
with bronchodilators, corticosteroids, and lifestyle modifications are essential. Essential
preventive actions include quitting smoking and avoiding lung irritants. The physical
limits, worry, and sadness that COPD can cause make prompt intervention essential.
Laboratory Features/Results:
Spirometry, which evaluates lung function and looks for airflow blockage, is a
crucial diagnostic tool for COPD. Reduced forced expiratory volume in one second
(FEV1) and forced vital capacity (FVC), which indicate decreased airflow, are
characteristics of COPD2. Blood gas analysis can also be used to identify hypoxemia,
low oxygen levels, hypercapnia, or high carbon dioxide levels, highlighting the severity
of respiratory failure in advanced COPD cases. These laboratory characteristics and
outcomes support medical practitioners in verifying the diagnosis of COPD, identifying
its stage, and directing suitable treatment approaches to enhance the patient’s
respiratory health.
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
6
Differential Diagnosis:
Due to the differences in their management and treatment modalities, it is crucial
to distinguish between COPD and other respiratory illnesses such as asthma,
bronchiectasis, and restrictive lung diseases. Asthma is characterized by reversible
airway blockage that is frequently brought on by allergens or irritants, whereas COPD is
characterized by persistent airflow limitation that is usually brought on by smoking.
Chronic infections can cause bronchial dilatation permanently in bronchiectasis, while
restrictive lung illnesses impede lung expansion3. The development of tailored treatment
strategies, such as bronchodilators and corticosteroids for COPD and asthma,
antibiotics for bronchiectasis, and addressing underlying causes in restrictive lung
disorders, is facilitated by accurate differential diagnosis. Patient outcomes are
enhanced by early detection and effective care.
Complications and Prognosis:
Exacerbations, respiratory failure, and cor pulmonale, or right heart failure, are
just a few serious problems resulting from COPD. Depending on the severity of the
condition, how well a patient responds to medication, and how well they adhere to
lifestyle changes like stopping smoking1, COPD patients have different outlooks or
prognoses. According to research10 the prognosis can be greatly improved by early
discovery, efficient management, and delaying the spread of the disease while
improving quality of life. The necessity of early intervention and continuous self-care
measures is highlighted because the prognosis may be less favourable for people with
advanced stages or poor adherence to treatment.
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
7
In conclusion, COPD is a dangerous respiratory ailment characterized by
persistent inflammation, structural alterations in the airways, and lung tissue harm. A
thorough knowledge of the disease’s underlying causes is essential for effective
treatment. For better patient outcomes, early detection and appropriate management
are essential. The main focus of prevention interventions should be lowering exposure
to risk factors, focusing on supporting quitting smoking. Furthermore, encouraging a
healthy lifestyle that includes regular exercise and a well-balanced diet will help lower
COPD’s prevalence and severity. By using these strategies, we may lessen the impact
of COPD on patients and healthcare systems.
Bibliography
1.Attaway A, Attaway A, Sekar J, et al. Prolonged intermittent hypoxia causes
mitochondrial dysfunction due to O-GlcNacylation of DRP1 in models of COPD
(chronic obstructive pulmonary disease). 2023;38(S1).
doi:https://doi.org/10.1152/physiol.2023.38.s1.5733211
2.Jurevičienė E, Burneikaitė G, Dambrauskas L, et al. Epidemiology of Chronic
Obstructive Pulmonary Disease (COPD) Comorbidities in Lithuanian National
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
8
Database: A Cluster Analysis. International Journal of Environmental Research
and Public Health. 2022;19(2):970. doi:https://doi.org/10.3390/ijerph19020970
3.Agusti A, Vogelmeier C, Faner R. COPD 2020: Changes and Challenges. American
Journal of Physiology-Lung Cellular and Molecular Physiology. 2020;319(5).
doi:https://doi.org/10.1152/ajplung.00429.2020
4.Tang K, Zhao J, Xie J, Wang J. Decreased miR-29b expression is associated with
airway inflammation in chronic obstructive pulmonary disease. American Journal
of Physiology-Lung Cellular and Molecular Physiology. 2019;316(4):L621-L629.
doi:https://doi.org/10.1152/ajplung.00436.2018
5.Nguyen JMK, Robinson DN, Sidhaye VK. Why new biology must be uncovered to
advance therapeutic strategies for chronic obstructive pulmonary disease.
American Journal of Physiology-Lung Cellular and Molecular Physiology.
2021;320(1):L1-L11. doi:https://doi.org/10.1152/ajplung.00367.2020
6.Lage VKS, Lacerda ACR, Neves CDC, et al. Cardiorespiratory responses in different
types of squats and frequencies of whole body vibration in patients with chronic
obstructive pulmonary disease. Journal of Applied Physiology. 2019;126(1):2329. doi:https://doi.org/10.1152/japplphysiol.00406.2018
7.Woldhuis RR, de R, Wim Timens, et al. Link between increased cellular senescence
and extracellular matrix changes in COPD. 2020;319(1):L48-L60.
doi:https://doi.org/10.1152/ajplung.00028.2020
8.Stine Nymand, Hartmann JP, Camilla Koch Ryrsø, et al. Exercise adaptations in
COPD: the pulmonary perspective. 2022;323(6):L659-L666.
doi:https://doi.org/10.1152/ajplung.00549.2020
9.Blackburn JB, Ngan Fung Li, Bartlett NW, Richmond BW. An update in club cell
biology and its potential relevance to chronic obstructive pulmonary disease.
2023;324(5):L652-L665. doi:https://doi.org/10.1152/ajplung.00192.2022
Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
10.Tsiligianni I, Kocks JWH. Daytime symptoms of chronic obstructive pulmonary
disease: a systematic review. npj Primary Care Respiratory Medicine.
2020;30(1). doi:https://doi.org/10.1038/s41533-020-0163-5
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