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Clinical Manifestation
Early onset of dyspnea on exertion (DOE) which progresses to continuous dyspnea. Rhonchi, crackles , accessory muscle breathing, Increased rate of breathing, prolonged expiratory phase, spontaneous exhibition of pursed-lip breathing, decreased FEV, and vital capacity with no response to bronchodilators.
Scanty sputum or absent.
Normal or mild hypoxemia-respiratory alkalosis; late stage hypoxemia respiratory acidosis.
Increased AP diameter (barrel chest), decreased lateral expansion, diaphragmatic - movement, complaint of epigastric fullness.
PFT shows increased residual volume, fuoctional residual capacity and total lung volume, decreased diffusing capacity, decreased forced expiratory volume (FEV), vital capacity may be normal or slightly reduced later in the disease, thus FEVII VC rate is decreased. Bronchodilators fail to show improvement is PFT(significant- differentiating findings)
ABG is often near normal
The holoenzyme is denatured by heat at very high temperature. It is found that two polypeptides, although denatured, contains chains that remain together as a unit, while two other
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Clinical Manifestation Early onset of dyspnea on exertion (DOE) which progresses to continuous dyspnea. Rhonchi, crackles , accessory muscle breathing, Increased rate of br
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