Emphysema Research and Comparative Studies

The provided assignment involves a comprehensive review of emphysema research, focusing on comparative studies between different types of emphysema, such as panlobular and centrilobular emphysema. The document includes references to several scientific articles and presentations, providing detailed information on the inflammatory immune cell infiltration associated with lung tissue destruction in alpha-1 antitrypsin deficiency and smoking-related emphysema. It also touches upon endobronchial valves for emphysema without interlobar collateral ventilation and the associations between emphysema-like lung on CT and incident airflow limitation. The assignment aims to analyze and compare different aspects of emphysema research, providing valuable insights for researchers and professionals in the field.

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

Other characters
• Route of administration: inhaled route
side effects:
• tachycardia symptoms
• tremors
• Hypokalemia (Oelsner et al. 2017)
• Hypertension

Relevance to practice
• Developing detailed idea about the pathophysiology as well as
pharmacology of the disorder, nurses can be able to
understand the rationale of the occurrence of the symptoms
of the disorder in the patients
• prescribe the patients with the proper type of drugs

Conclusions and considerations
• Emphysema can therefore be described as the loss of lung elasticity
• Irritants cause release of proteolytic enzymes from polymorphonuclear
leukocytes and alveolar macrophages
• Irritants destroy their activity and make lungs expose to the protease
causing symptoms of emphysema
• short-term bronchodialators help in treating the disorder
• nurses can develop this knowledge for providing effective care

references
• Davey, C., Zoumot, Z., Jordan, S., McNulty, W.H., Carr, D.H., Hind, M.D., Hansell, D.M., Rubens, M.B., Banya, W., Polkey, M.I. and
Shah, P.L., 2015. Bronchoscopic lung volume reduction with endobronchial valves for patients with heterogeneous emphysema
and intact interlobar fissures (the BeLieVeR-HIFi study): a randomised controlled trial. The Lancet, 386(9998), pp.1066-1073.
• Kinose, D., Vasilescu, D.M., Hackett, T.L., Elliott, W.M., Chu, F., Verleden, S., Vanaudenaerde, B.M., Cooper, J.D. and Hogg, J.C.,
2016. A Comparison Of The Inflammatory Immune Cell Infiltration Associated With Lung Tissue Destruction In Panlobular
Emphysema In Alpha-1 Antitrypsin Deficiency And Centrilobular Emphysema Associated With Smoking. In B31. ALPHA-1
ANTITRYPSIN DEFICIENCY (pp. A3139-A3139). American Thoracic Society.
• Klooster, K., ten Hacken, N.H., Hartman, J.E., Kerstjens, H.A., van Rikxoort, E.M. and Slebos, D.J., 2015. Endobronchial valves for
emphysema without interlobar collateral ventilation. New England Journal of Medicine, 373(24), pp.2325-2335.
• Oelsner, E.C., Smith, B.M., Hoffman, E.A., Folsom, A.R., Kawut, S.M., Kaufman, J.D., Manichaikul, A., Lederer, D.J., Schwartz, J.E.,
Watson, K.E. and Enright, P.L., 2017. Associations between emphysema-like lung on CT and incident airflow limitation: a
general population-based cohort study. Thorax, pp.thoraxjnl-2017.
• Pinto-Plata, V., 2018. Emphysema and extrapulmonary tissue loss in COPD: a multi-organ loss of tissue phenotype.
• Rabinovich, R.A., Miller, B.E., Wrobel, K., Ranjit, K., Williams, M.C., Drost, E., Edwards, L.D., Lomas, D.A., Rennard, S.I., Agustí, A.
and Tal-Singer, R., 2016. Circulating desmosine levels do not predict emphysema progression but are associated with
cardiovascular risk and mortality in COPD. European Respiratory Journal, 47(5), pp.1365-1373.
• Steiger, D., Filopei, J., Siddiqi, M., Yip, R., Yankelevitz, D. and Henschke, C., 2017. Evidence Of Emphysema In A Cohort Of
Participants Without Symptoms Undergoing Low Dose Chest CT Screening For Lung Cancer. In C30. Lung Cancer Screening:
Who, Why, Where, And How Much (Pp. A5177-A5177). American Thoracic Society.
• Wysham, N., Ekstrom, M., Mathews, A., Xie, J., Qin, X. and MacIntyre, N., 2017. Mechanisms Of Hypercapnea In Advanced
Chronic Obstructive Pulmonary Disease: A Secondary Analysis Of The National Emphysema Treatment Trial. In C80-B. Multi-
Modality Assessment Of Copd, Asthma, And Asthma-Copd Overlap SYNDROME (pp. A6485-A6485). American Thoracic Society.