Emphysema: Detailed Overview of Causes, Pathophysiology, and Treatment

This report provides a detailed overview of emphysema, a chronic lung condition characterized by shortness of breath due to damage to the air sacs in the lungs. It explores the various causes of emphysema, including tobacco smoke, marijuana smoke, chemical fumes, dust, and air pollution, as well as the associated risk factors such as smoking, age, and occupational exposures. The report delves into the pathophysiology of emphysema, explaining the inflammatory processes involving macrophages, neutrophils, and T lymphocytes, along with the role of oxidative stress and protease-antiprotease imbalance in the destruction of lung tissue. It also discusses airway remodeling and the role of vascular endothelial growth factor (VEGF). Furthermore, the report examines the pharmacology of emphysema, including short-acting and long-acting bronchodilators, long-acting beta agonists, long-acting muscarinic agonists, phosphodiesterase inhibitors, anti-inflammatory therapy, antibiotics, mucolytic agents, and proton pump inhibitors. It details the mechanisms of action, pharmacokinetics, and side effects of these medications. Finally, the report highlights the relevance of this knowledge to nursing practice, emphasizing how understanding the pathophysiology and pharmacology of emphysema enables nurses to better understand and manage the symptoms of the disorder, ultimately leading to improved patient care.

EMPHYSEMA

Emphysema:
• the condition of the lung that results in occurrence of shortness of breath
in patients
• air sacs in the lungs are damaged
• the inner walls of the air sacs are seen to get weaken
• reduction of the surface area of the lungs (Steiger et al. 2017)
• amount of oxygen that reaches the bloodstream is reduced
• old air is seen to get trapped which thereby gives no space to the fresh,
oxygen rich air to enter

Causes
Main symptom:
• shortness of breath
Causes
• marijuana smoke, (Klooster et al. 2015)
• tobacco smoke,
• chemical fumes and
• dust and
• even air pollution
risk factors
• Smoking
• Age
• occupational exposure
• exposure to different indoor as well as outdoor pollution

Pathophysiology: Macrophages
• invading foreign antigens infiltrate the innate respiratory defenses
• the inflammatory responding immune cells take active participation in the
transportation of the antigens to different bronchial associated lymphatic
tissue layer
• inflammatory immune cells are the eosinophils, polymorphonuclear cells,
macrophages as well as cd4 and cd8 positive lymphocytes
• huge amount of release of the neutrophilic chemotactic factors
• results in the destruction of the epithelial barrier of the lungs

neutrophils
• neutrophils also take an active part in this procedure
• responsible for the secretion of the proteases along with the
free radical hydrogen peroxide
• add up to the ruination procedures of the epithelial cells
• neutrophils are seen to take an active part in the
pathogenesis

T lymphocyte cells
• t lymphocyte cells mainly cd8 positive cells in the sputum
• cells are seen to release a number of the chemotactic factors
• recruiting more cells like the pro-inflammatory cytokines
• amplify the procedures of inflammation
• promotion of the structural changes (Pinto-Plaster 2018).

oxidative stress
• Cigarette smoke mainly produces the oxidants and inflammatory cells
mainly release the oxidants
• inflammatory macrophages as well as epithelial cells are seen to produce
proteases
• protease-antiprotease imbalance
• elastin destruction
• elastase is responsible for the destruction of the fragile elastic lamina of
the lungs

airway remodeling cases
• vascular endothelial growth factor (VEGF) are mainly seen to
be expressed in the airway smooth muscles
• neovascularisation as well as the expression of the fibroblastic
developments
• changes in structures of the bronchiolar edema, mucus
hyperplasia, and smooth muscle hypertrophy and fibrosis in
the airways
• narrowing of the small airways (Rabinvioch et al. 2016)

Pharmacology of emphysema:
• short acting bronchodialators,
• long acting bronchodialators,
• long acting beta agonists,
• long-acting muscarinic agonist,
• Phosphodiesterase inhibitors,
• Anti-inflammatory therapy,
• antibiotics,
• mucolytic agents,
• Proton pump inhibitors (Kinose et al. 2016)

Short acting bronchodialators comprise of
• beta 2 agonists
• as well as the anticholinergic agents

Mechanism of action
• Mechanism of action of beta 2 agonist: increasing of the cyclic
adenosine monophosphate called the camp which ultimately
results in bronchodialation.
• Mechanism of action of anticholinergic agent: helps by
blocking the M2 and M3 cholinergic receptors. This ultimately
results in bronchodialation

Pharmacokinetics:
• aerosol as well as capsule formulation
• not a substrate for the cellular uptake procedures like
that of the COMT as well as the catecholamines
• does not cross blood brain barrier
• bronchodialation takes place maximally in the 15
minutes approximately and stays for 3 to 4 hours