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'''Emphysema''' is a form of [[Chronic obstructive pulmonary disorder|Chronic obstructive pulmonary disorder]] '''(COPD). '''It is carachterised by a loss of elasticity in the [[Lungs|lungs]] and severe shortness of breath. There  are two forms of emphysema; familial and non-familial. Familial emphysema is a result of a [[Genetic mutation|genetic mutation]] of a common respiratory protein [[Alpha-1-antitrypsin|Alpha-1-antitrypsin]] (ATT). Non-familial emphysema is more common and is generally caused by smoking. When smoking, noxious particles enter the lungs and irritate the [[Alveoli|alveoli]], they stimulate an increased production of the [[Enzyme|enzyme]] [[Elastase|elastase]], which breaks down elastin; an important structural component of the lung walls. ATT inhibits elastase function however, there is an imbalance of the two [[Proteins|proteins]] when smoking and  in familial emphysema it is defective and cannot stop the break down of elastin. The alveoli are very delicate, one cell thick sacks that allow for efficient gas exchange into the [[Blood stream|blood stream]]. When elastin is broken down the alveoli become more susceptible to tearing and scar tissue forms. The scar tisue results in a smaller surface area for gas exchange and the alvoli can not inflate to their full capacity, so the prosses becomes inefficient. The patient therefore is forced to take rapid shallow breaths, and the damage is irreversible so the disease progresses with time.
Emphysema is a form of Chronic obstructive pulmonary disorder ([[COPD|COPD]]). The disease has two forms; familial and non-familial. Familial emphysema is a result of a [[Genetic mutation|Genetic mutation]] of a common respiratory protein Alpha-1-antitrypsin (AAT) which protects tissues from [[Enzymes]] of [[Inflammation|inflammatory]] response. For patients with a lack of AAT protein, the enzyme which is normally kept regulated in check, is allowed to attack the lungs – a form of autoimmune response. Non-familial emphysema is more common and is generally caused by smoking, in fact between 80% and 90% of all cases of emphysema are caused by smoking. When smoking, particles of [[Carbon monoxide|Carbon monoxide]] enter the lungs and irritate the [[Alveoli]] causing large amounts of damage.  
 
Alveoli are small spherical sacs of [[Epithelial Cells|epithelial cells]] (one cell thick) that allow for efficient gas exchange into the bloodstream. They are extremely compact which allows 300 million of each alveolus to fit into each lung, resulting in an enormous surface area – the key to the efficiency of gaseous exchange in the lungs. Alveoli expand in size when the air is inhaled and recoil during exhalation, this process is enabled by the protein elastin.
 
In emphysematous lungs, there is a much larger concentration of carbon monoxide (due to smoking) which in turn leads to an increased production of the enzyme elastase, which breaks down elastin. Without this key protein, the alveoli become permanently stretched leaving the lungs unable to expel all of the air during exhalation. Each alveolus also becomes more susceptible to tearing and therefore scar tissue forms. This scar tissue results in a smaller surface area for gas exchange making the process far less efficient.
 
There are several typical symptoms associated with this disease which include:
 
*Shortness of breath – this is due to the reduced efficiency of the alveoli and therefore the lungs as a whole. As the lungs cannot expel air it becomes increasingly difficult to inhale fresh air containing oxygen making the patient often feel breathless.  
*Chronic cough – due to scar/damaged tissue and mucus of the lungs that the body is constantly trying to remove but faces difficulty as the [[Cilia|cilia]] on the bronchi have been destroyed.
*Fatigue – with a reduced intake of oxygen, there is less available for energy-yielding processes such as the [[Citric Acid Cycle]] and oxidative phosphorylation, leaving the patient with a considerably smaller amount of energy than a healthy individual.
*Bluish Skin Colouration - due to low levels of oxygen in the blood as a result of poor gas [[Diffusion]] in the lungs<ref>Toole, G., Toole, S., 2008. AQA Biology, Cheltenham: Nelson Thornes</ref><ref>Cleveland Clinic. (2011) Emphysema. Available at: http://my.clevelandclinic.org/health/diseases_conditions/hic-emphysema (last accessed 26/11/2014)</ref><ref>Patient.co.uk (2012) Alpha-1-Antitrypsin Deficiency. Available at: http://www.patient.co.uk/health/alpha-1-antitrypsin-deficiency-leaflet (last accessed 26/11/2014)</ref>.
 
=== References  ===
 
<references />

Latest revision as of 17:22, 23 October 2018

Emphysema is a form of Chronic obstructive pulmonary disorder (COPD). The disease has two forms; familial and non-familial. Familial emphysema is a result of a Genetic mutation of a common respiratory protein Alpha-1-antitrypsin (AAT) which protects tissues from Enzymes of inflammatory response. For patients with a lack of AAT protein, the enzyme which is normally kept regulated in check, is allowed to attack the lungs – a form of autoimmune response. Non-familial emphysema is more common and is generally caused by smoking, in fact between 80% and 90% of all cases of emphysema are caused by smoking. When smoking, particles of Carbon monoxide enter the lungs and irritate the Alveoli causing large amounts of damage.

Alveoli are small spherical sacs of epithelial cells (one cell thick) that allow for efficient gas exchange into the bloodstream. They are extremely compact which allows 300 million of each alveolus to fit into each lung, resulting in an enormous surface area – the key to the efficiency of gaseous exchange in the lungs. Alveoli expand in size when the air is inhaled and recoil during exhalation, this process is enabled by the protein elastin.

In emphysematous lungs, there is a much larger concentration of carbon monoxide (due to smoking) which in turn leads to an increased production of the enzyme elastase, which breaks down elastin. Without this key protein, the alveoli become permanently stretched leaving the lungs unable to expel all of the air during exhalation. Each alveolus also becomes more susceptible to tearing and therefore scar tissue forms. This scar tissue results in a smaller surface area for gas exchange making the process far less efficient.

There are several typical symptoms associated with this disease which include:

  • Shortness of breath – this is due to the reduced efficiency of the alveoli and therefore the lungs as a whole. As the lungs cannot expel air it becomes increasingly difficult to inhale fresh air containing oxygen making the patient often feel breathless.
  • Chronic cough – due to scar/damaged tissue and mucus of the lungs that the body is constantly trying to remove but faces difficulty as the cilia on the bronchi have been destroyed.
  • Fatigue – with a reduced intake of oxygen, there is less available for energy-yielding processes such as the Citric Acid Cycle and oxidative phosphorylation, leaving the patient with a considerably smaller amount of energy than a healthy individual.
  • Bluish Skin Colouration - due to low levels of oxygen in the blood as a result of poor gas Diffusion in the lungs[1][2][3].

References

  1. Toole, G., Toole, S., 2008. AQA Biology, Cheltenham: Nelson Thornes
  2. Cleveland Clinic. (2011) Emphysema. Available at: http://my.clevelandclinic.org/health/diseases_conditions/hic-emphysema (last accessed 26/11/2014)
  3. Patient.co.uk (2012) Alpha-1-Antitrypsin Deficiency. Available at: http://www.patient.co.uk/health/alpha-1-antitrypsin-deficiency-leaflet (last accessed 26/11/2014)