Introduction as ?1-Antitrysin deficiency due to the

Introduction to COPD

COPD (Chronic Obstructive Pulmonary Disease) is an obstructive lung disease that is often characterized by chronic bronchitis and emphysema. While both chronic bronchitis and emphysema has their distinct clinical and anatomical presentation, in COPD, they exist together as evident in this patient.

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1Symptoms of a typical COPD includes chronic cough, presence breathlessness, sputum production initially and at later stages, chest pain, wheeze and fatigue could possibly develop. During winter, bronchitis in the COPD patient may also worsen. All these symptoms are seen in the patient.

 

2 It is suggested that tobacco smoke from smoking is the primary cause of COPD. Other causes can include air pollution which may come from pollutant from motor and industries (3In fact, it is suggested in the Danish Diet, Cancer, and health cohort study that shows correlation between COPD and nitrogen dioxide level) or 4from burning of biomass with poor ventilation indoor especially in rural areas. 5Genetic factor such as ?1-Antitrysin deficiency due to the mutation in the SERPINA 1 also contributes to COPD. Genetic factor will still be discussed in this essay although, it is important to take note that the primary cause of the patient’s COPD could be the patient’s smoking history for the last 40 years. Furthermore, no genetic test was done since ?1-Antitrysin deficiency tends to present early in the patient.

 

Emphysema

6’Emphysema is characterized by abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without significant fibrosis’.

7Taking cigarette smoke as a cause, emphysema caused by so is a two-way process. Cigarette smoke releases toxic substances and pollutant that stimulate the activation of macrophage present in the alveoli. Activation of macrophage causes the release of cytokines, proteases and other mediators. Cytokines such as IL-8, LTB4, GRO? further activates neutrophils. Protease such as elastase, matrix metalloproteinases, cathepsins and proteinases are released. Other mediators such as CXCR3, Mig and IP-10 are also released activating CD8+ lymphocytes. Release of these mediators lead to the breakdown of connective tissue such as collagen and elastin in the lungs and extra cellular matrix, leading to elastic fiber damage.

Oxidative stress caused by cigarette smoking also plays a part. Oxidative stress refers to the imbalance between the manifestation of reactive oxygen species in the body system and the body system’s ability to detoxify or repair the damage. 8It is suggested that oxidative stress activates the transcription factor nuclear factor -kB which starts the cytokine transcription that encourages inflammation. Furthermore, cigarette smoke could also inhibit histone deacetylase ,whose function is to stop histone in pro-inflammatory gene from being unwind for transcription,  further encouraging inflammation.

9 ?-1 antitrypsin deficiency , a genetic factor, also plays a part. ?-1 antitrypsin is first produced in the liver. Its main function is to protect the lung against proteolytic damage from neutrophil elastase. Mutation in the SERPINA 1 gene ( which provides instruction for making ?-1 antitrypsin) reduces the concentration of ?-1 antitrypsin by retaining polymerised molecules inside liver cells.

 

In prevailing hypothesis, under normal condition, there is a balance between the protease that breaks down the alveoli and the anti-protease that inhibits its function. However, in emphysema, this balance is tilted10 towards the protease. This increases the amount of alveoli destruction caused by the protease, resulting in emphysema.

 

Furthermore, 11studies from shown that elastin fragments from the destruction of the alveoli wall acts as chemoattractant to monocytes, precursor to macrophage. This suggests that the end product of the alveoli destruction actually serves to start the destruction by the macrophage, creating a cycle of alveoli destruction.

 

Chronic Bronchitis

12’Chronic Bronchitis is defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.’

13Irritants from tobacco smoke also induce hypertrophy and hyperplasia of mucous cells in the trachea and main bronchi and an increase in mucin secreting goblet cells in the surface epithelium of the peripheral bronchioles. 14Long term smoking also causes an impairment in abnormal cilia cells whose function is to clear the mucus along the bronchi and the thickening of the epithelial layer on the airway lumen. Coupled with respiratory muscle weakness and reduced peak expiratory flow, there is inability to clear the excess mucus form, leading to airway obstruction.

Context of the patient

Shortness of breath is evident in the patient. This is due to emphysema that results in the loss of the alveoli wall that causes the alveoli to lose its elasticity. In normal circumstances, during expiration, the elastic recoil of alveoli takes place, helping to expel gas from the lungs. However, in COPD, the loss of alveoli elasticity means more effort is needed to breathe out. Loss of alveoli walls also means that the smaller alveoli has reform into larger alveoli. The loss of alveoli elasticity and formation of larger alveoli result in the hyperinflation of the lungs, further contributing to the difficulty for alveoli to collapse hence expiration is impaired. Also, the narrowing of the lumen caused by the swelling of the inflamed airway and hypersecretion of mucus makes it harder for air to flow through hence more it harder to breathe in. Both contributes to shortness of breath.

 

15Due to the loss of alveoli wall, pulmonary capillaries bed and the narrowing of the airway lumen, the physiological dead space has increased, ventilation fell and hence V/Q ratio fell. This would suggest that the arterial partial pressure of oxygen will fall. In the context of this patient, this Is seen by the lower than normal SpO2 of 80%.

 

Hypersecretion of mucus in the trachea and main bronchi resulted in more mucus produced than usual. As a means to clear the additional mucus produced, the body reacts by coughing to clear the mucus to breathe easier. This is evidenced the productive cough with white sputum as seen in this patient before the exacerbation.

 

Wheezing could also be heard. This is due to the opening of small airway due to the expulsion of air through the narrowed lumen of those airway, being heard as popping sound known as wheezing. 

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