The top 3 differential diagnoses for Ms. Johnson are asthma, chronic bronchitis, and emphysema. Data that supports the diagnosis of asthma for Mr. Johnson are shortness of air especially upon exertion (“can’t keep up during walk”), respiratory wheezes, productive white sputum, tachycardia, decreased force expiratory volume in one second (FEV1), which is 56% as listed in the case study. Supporting data for chronic bronchitis are that Ms. Johnson has risk factor of extensive history of tobacco smoking, works as a cook, chronic smoker’s cough with occasionally production of white sputum, scattered respiratory wheezes, dyspnea (“can’t keep up during walk”), decreased force expiratory volume in one second (FEV1), which is 56% as listed in the case
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Johnson presented in relation to the pathophysiology of asthma are that the antigen exposure from tobacco smoke and other irritants to the bronchial mucosa activates B cells, which produce IgE, together cause cell degranulation on the mast cells’ surface which cause inflammatory mediators to be released. Inflammatory mediators cause vasodilatation, increase capillary permeability, mucosal edema, bronchial smooth muscle contraction, and mucus secretion. Other inflammatory cytokines cause increase level of acetylcholine, which in turn causes bronchial smooth muscle contraction and mucus secretion (which is mentioned in the case that Ms. Johnson has occasionally productive white sputum secretions). The reduced flow rate and increase resistance to airflow caused by airway obstruction leads to air trapping in the lungs, which cause hyperinflation of the distal obstructions, and increase breathing effort. Ms. Johnson’s respiratory rate was 26, increased respiratory rate is triggered by the lung receptors due to airway obstruction and increase lung volume. Asthma is a potential reversible disease (Brashers, 2012a). Data from the case study did not show significant improvement with bronchodilator use. FEV1 was1.29 pre-bronchodilators, however post bronchodilator the FEV1 was not scientifically changed. FVC was slightly decreased post bronchodilator. No significant reversible effect was seen from the …show more content…
Johnson presented in relation to the pathophysiology of chronic bronchitis are that the inhaled irritants most likely from tobacco smoking and biomass fuel used for cooking cause inflammation, which may lead to the neutrophils, macrophages and lymphocytes penetrating the bronchial wall. The inflammation leads to bronchial swelling, hypertrophy and hyperplasia of mucous glands and goblet cells. Mucus is produced, and dysfunctional ciliary also cannot clear the mucus. The airway defense mechanisms are interrupted, which may lead to potential infection and injury risk. Bronchospasm, shortness of breath, and productive cough can be signs and symptoms of infection. Obstruction due to hypertrophied bronchial smooth muscle especially during expiration are noted, which is reflected in Ms. Johnson’s FVC and FEV1, which are below predicated (Brashers,
Johnson presented in relation to the pathophysiology of asthma are that the antigen exposure from tobacco smoke and other irritants to the bronchial mucosa activates B cells, which produce IgE, together cause cell degranulation on the mast cells’ surface which cause inflammatory mediators to be released. Inflammatory mediators cause vasodilatation, increase capillary permeability, mucosal edema, bronchial smooth muscle contraction, and mucus secretion. Other inflammatory cytokines cause increase level of acetylcholine, which in turn causes bronchial smooth muscle contraction and mucus secretion (which is mentioned in the case that Ms. Johnson has occasionally productive white sputum secretions). The reduced flow rate and increase resistance to airflow caused by airway obstruction leads to air trapping in the lungs, which cause hyperinflation of the distal obstructions, and increase breathing effort. Ms. Johnson’s respiratory rate was 26, increased respiratory rate is triggered by the lung receptors due to airway obstruction and increase lung volume. Asthma is a potential reversible disease (Brashers, 2012a). Data from the case study did not show significant improvement with bronchodilator use. FEV1 was1.29 pre-bronchodilators, however post bronchodilator the FEV1 was not scientifically changed. FVC was slightly decreased post bronchodilator. No significant reversible effect was seen from the …show more content…
Johnson presented in relation to the pathophysiology of chronic bronchitis are that the inhaled irritants most likely from tobacco smoking and biomass fuel used for cooking cause inflammation, which may lead to the neutrophils, macrophages and lymphocytes penetrating the bronchial wall. The inflammation leads to bronchial swelling, hypertrophy and hyperplasia of mucous glands and goblet cells. Mucus is produced, and dysfunctional ciliary also cannot clear the mucus. The airway defense mechanisms are interrupted, which may lead to potential infection and injury risk. Bronchospasm, shortness of breath, and productive cough can be signs and symptoms of infection. Obstruction due to hypertrophied bronchial smooth muscle especially during expiration are noted, which is reflected in Ms. Johnson’s FVC and FEV1, which are below predicated (Brashers,