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achurch achurch
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Posts: 898
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6 years ago
1.   Julia won a lottery ticket and began to hyperventilation in her excitement. Explain how hyperventilation affects the partial pressure of carbon dioxide in her blood and her blood pH.

2.   Explain how smoking impairs the protective features of the epithelium of the respiratory tract.

3.   The partial pressure gradient for oxygen in the body is much steeper than that for carbon dioxide. Explain how equal amounts of these two gases can be exchanged (in a given time interval) in the lungs and at the tissues. What law describes this phenomenon?
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bio_manbio_man
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6 years ago
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6 years ago
1. Lucky for you, this question has already been asked. Check out this link:

https://biology-forums.com/index.php?topic=501620.0

2. The epithelium coating the upper respiratory tract acts as a first line of defense against invasive agents (pollutants, allergens, microorganisms), and it can cause upper airway symptoms and diseases when in contact with these agents.

Cigarette combustion produces a smoke with more than 4000 noxious components, including gas and particulate substances - among them we have acrolein, formaldehyde, carbon monoxide, nicotine, cotinin; acetaldehyde, phenol and potassium cianide8, and many of these components are provenly toxic to the respiratory epithelium. Thus, cigarette smoke causes important structural alterations to the respiratory epithelium.

studies have shown that cigarette smoke causes a reduction in cell viability and induction of apoptosis in respiratory hair cells, opposite mitogenic effects or pro-apoptotic depending on the cigarette smoke concentration or even an impairment on epithelial regeneration upon injury. Also, studies have shown that chronic and intermittent exposure to cigarette smoke cause morphological alterations to the epithelium of the entire respiratory tract, from hyperplasia in lower concentrations, all the way to loss of cilia and metaplasia with keratinization in higher concentrations, and also submucosal thickening and inflammation with neutrofilic and mononuclear inflammatory cells infiltrate. Which showed that the cigarette-induced respiratory mucosa inflammatory reaction persists even after seven months of recovery. Studies carried out with smokers have confirmed these findings in animal models, showing alterations in the respiratory epithelium as an enlargement of the naked epithelium, a greater prevalence of hyperplasia and cell atypias26 and ultrastructural cilia abnormalities.

Besides the alterations caused on the differentiated tissues,  cigarette smoke has a negative impact on the ciliogenesis process in a dose-dependent fashion to the respiratory epithelium in the maturation and differentiation phases. Using respiratory epithelium cell cultures obtained from the nasal septum of mice, they showed that the respiratory epithelium exposure to the particulate phase as well as the gas phase of cigarette smoke causes a significant reduction in the percentage of cilia development (Attached Figure 1 ), as well as reduction in their size (Figure 2). Therefore, these authors suggest that there must be more than one toxic substance in the cigarette smoke, particulate and gaseous phases, involved in ciliogenesis block.
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