Response to question 1
In outlining similarities and differences between chronic bronchitis and emphysema in terms of anatomical/cellular, chemical, and functional changes, inevitably it would be highlighting differentiations between two conditions affecting the respiratory system.
Major differerences are that there are primary and secondary types of emphysemas classified as panacinary and centroacinary. In panacinary emphysema there is expansion of the entire respiratory acinus beginning from the respiratory bronchiole towards the alveoli. The changes commonly appear at the lower lobes of the lungs and the anterior walls (McCance , Huether, Brashers, & Rote, 2010). Centroacinary emphysema expresses changes in the upper lobe anatomy. There are no changes in the distal acinus or alveoli, but the respiratory bronchioles are expanded (Nazari, 2002). Bronchitis, however, is inflammation of the mucous membranes covering the bronchioles and not lung fields and alveoli as in emphysema. Precisely, it relates to the passage or airway through which air travels from the trachea to the lungs and not absorption and transference of oxygen as in emphysema.
Like emphysema, bronchitis is classified as acute and chronic. Acute stages are usually due to bacterial or viral infection and sequels an upper respiratory tract infection. Chronic bronchitis is more described as chronic obstructive pulmonary disease and like emphysema is due to the bronchioles reacting to toxic substances entering lung fields. Chemical changes are similar to emphysema, but can be more fatal due to the airway obstruction (Cohen & William, 2004).
In describing functional changes in the alveoli, absorption of oxygen and transference to the blood become compromised in emphysema. Also, when toxic substances enter the alveoli they are trapped creating a localized inflammatory response expressed as breathing difficulties and shape alterations of the rib cage. (McCance , Huether, Brashers, & Rote, 2010). Chemicals are released during this exchange among toxins/ blood/ oxygen and carbon dioxide which can initiate the alveoli septum to disintegrate and rupture (Webb & Higgins, 2005).
Response to question 11
In explaining the concept of alveolar remodeling and its consequences to efficient ventilation and external respiration a brief discourse on the impacts of alveolar remolding on tissue and peripheral gas exchange will be undertaken.
Studies conducted by Peter Jeffery (2004) confirmed that the concept of alveolar remodeling, especially, when related to respiratory conditions is not an abnormal undertaking. More importantly, it is altering the size/ mass of the amount of structural tissue component found within the lung due to bacterial, viral disease or inflammation. It occurs naturally as a compensatory mechanism for conditions such as chronic obstructive pulmonary disease as seen in bronchitis and emphysema (Jeffery, 2004). This mechanism continues the process of efficient ventilation and external respiration, which would have otherwise been halted and the patient would ultimately die from respiratory failure (McCance , Huether, Brashers, & Rote, 2010).
Basically, gas exchange in the lungs consists of the diffusion of O2 from the alveoli into the pulmonary capillary, and the diffusion of CO2 from the pulmonary capillary into the alveoli. Alveolar ventilation and alveolar gas equations are used to mathematically describe gas exchange in the lungs. Such derivations are perceived from the concept of mass conservation, whereby the amount of a particular gas that is either consumed or produced by the body must equal the net amount that either enters or leaves the lungs (Nilsson, 2010). Alveoli remodeling helps this process to continue.
References
Jeffery, Patrick (2004). Remodeling And Inflammation Of Bronchi In Asthma And Chronic
Obstructive Pulmonary Disease” Proc Am Thorac Soc. 1(3):176-183
McCance, K.L., Huether, S.E., Brashers, V.L. & Rote, N.S. (2010). Pathophysiology: The biologic basis for disease in adults and children. Philadelphia: Mosby
Nazari S. (2002) “Mechanical Events In Physiopathology Of Idiopathic Pulmonary Emphysema: A Theoretical Analysis.” The Internet Journal of Thoracic and Cardiovascular Surgery. 5(2)
Nilsson, Goran E. (2010). Respiratory Physiology of Vertebrates. Cambridge: Cambridge
Webb WR, Higgins CB (2005). Thoracic Imaging. Lippincott, Williams & Wilkins
