Chronic Obstructive Pulmonary Disease ( Copd )

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Mr Johns, a 60-year-old male with a history of heavy smoking and a productive cough, presents with increasing shortness of breath on exertion and now at rest. His vital signs convey a normal temperature, low blood pressure, and an elevated pulse and respiration rate. There are abnormities in his routine blood results. Physical examination highlights bilateral neck vein distension and pitting oedema at his extremities, as well as peripheral cyanosis and a swollen abdomen. On auscultation there is a loud second heart sound, and an additional heart can be heard. Examination of the chest reveals coarse crackles and wheezes. Mild hepatomegaly is also noted. Such findings are consistent with a differential diagnosis of right heart failure (Cor…show more content…
This disease may be characterised by abundant thick, green/yellow sputum daily (months to years duration) and episodic haemoptysis. A risk factor is recurrent bronchopneumonia. Alternatively, increased mucus production suggests asthma, as increased mucus secretion contributes to the viscid mucous plugs that occlude asthmatic airways (Frieri, 2005). A further differential diagnosis is pulmonary oedema, where acute left ventricular failure (LVF) with pulmonary venous hypertension and alveolar flooding which causes blood-tinged sputum (Kelly, 1999). If LV filling pressure increases suddenly, plasma fluid moves rapidly from pulmonary capillaries into interstitial spaces and alveoli (Kelly, 1999). The haemoptysis/purulent sputum may also be caused by chronic lung abscesses. Mr. Johns has been chronically ill, exhibiting airway inflammation symptoms over the last 15 years with exacerbations every two years. Chronicity is a feature of COPD and recurrent infections and chronic mucous hypersecretion are risk factors (Johnston et al., 2012). This patient has had chronic viral/bacterial infections, which contribute to the inflammation. Respiratory tract viruses in asthmatics lead to an increase in airway inflammation with increased numbers of eosinophils and neutrophils (Frieri, 2005). Mr John’s was a heavy smoker, therefore Cytotoxic T Cell lymphocyte and eosinophil
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