[DOWNLOAD] Chapter 20 Tobacco Test Answers | HOT
The last reigning queen of the Hawaiian Islands , she ascended the throne in As queen, she fought for the independence of Hawaii. She was deposed by US marines in and formally renounced her royal claim in Although the Open Door is generally...
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In it became a commonwealth in voluntary association with the US with full powers of local government. The islands were settled, mainly in the 17th century, by British and Danish sugar planters. The US islands include about 50 islands; pop. They...
Glencoe Biology
Inhaled tobacco smoke moves from the mouth through the upper airway, ultimately reaching the alveoli. As the smoke moves more deeply into the respiratory tract, more soluble gases are adsorbed and particles are deposited in the airways and alveoli. The substantial doses of carcinogens and toxins delivered to these sites place smokers at risk for malignant and nonmalignant diseases involving all components of the respiratory tract including the mouth. Consider, for example, the lungs of a year-old person with a pack-year 1 smoking history starting at age 20 years. By age 60 years, this person will have inhaled the smoke from approximately , cigarettes and will bear a substantial risk for chronic obstructive pulmonary disease COPD and lung cancer. The dose of inhaled toxic particles and gases received from each of these cigarettes varies depending on the nature of the tobacco, the volume and number of puffs of smoke drawn from the cigarette, the amount of air drawn in through ventilation holes as the smoke is inhaled, and local characteristics within the lung that determine the diffusion of toxic gases and the deposition of particles.
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Health Effects Of Tobacco
This chapter addresses the mechanisms by which tobacco smoke causes diseases other than cancer in the lower respiratory tract: the trachea, bronchi, and lungs. Department of Health, Education, and Welfare [USDHEW] , cigarette smoking has been causally linked to multiple diseases and to other adverse effects on the respiratory system Table 7. In addition to causing lung cancer and COPD , smoking increases the risk of death from pneumonia and causes chronic bronchitis U. Typically, the lungs of smokers show evidence of diffuse changes affecting the lining of the airways, the epithelium, and the structure of the bronchioles, which are the smaller air-conducting tubes.
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Table 7. Previous reports of the Surgeon General have also addressed the effects of smoking on the respiratory tract. In discussing the plausibility of associations of cigarette smoke with chronic bronchitis and emphysema, the report gave full consideration to the nature of tobacco smoke and its effects on the respiratory tract USDHEW The principal nonmalignant respiratory diseases caused by cigarette smoking— COPD , emphysema, chronic bronchitis, and asthma—are defined in Table 7. The definitions indicate that chronic bronchitis is a specific set of symptoms, whereas emphysema refers to a particular pattern of lung damage. COPD comprises a clinical syndrome characterized by limitation in airflow; persons with COPD often have chronic bronchitis as well, and their lungs typically display emphysema. Other nonmalignant respiratory diseases that have been linked to smoking include asthma and idiopathic pulmonary fibrosis USDHHS , but the evidence has not reached a level of certainty sufficient to warrant a conclusion of cause and effect.
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FindTestAnswers.com
The nonmalignant respiratory diseases caused by smoking contribute substantially to the burden of morbidity and mortality attributable to smoking in the United States Table 7. In , the Centers for Disease Control and Prevention CDC estimated that an average of , deaths per year could be attributed to lung cancer caused by smoking for the period — CDC Great advances have been made in our understanding of how smoking causes these diseases. Research has been facilitated by methods that directly assess changes in the lungs.
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Chapter 20. Population, Urbanization, And The Environment
Methods for obtaining biologic material from human lungs include bronchoalveolar lavage BAL , a technique that allows recovery of cellular and noncellular components of the epithelial surface of the lower respiratory tract Cantrell et al. BAL is of value in the study of immune and inflammatory mechanisms in the lower airways, because most of the cells recovered are believed to be derived from both air spaces and lung interstitium. Lung tissue obtained by biopsy or autopsy procedures can be used for cellular, protein, and nucleic acid assays. Exhaled breath condensate provides information about the composition of epithelial lining fluid ELF that can be used to detect inflammation and redox disturbance Paredi et al.
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Physical Assessment, Part II, 50 Questions
Blood samples may be used to assess systemic inflammatory responses, and blood cells serve as a source of nucleic acids. Characteristics of Tobacco Smoke Tobacco smoke, which comprises an aerosol a mixture of solid and liquid particles and gases, has thousands of chemical components, including many well-characterized toxins and carcinogens International Agency for Research on Cancer [IARC] Many of these components are in the gas phase, and others are components of the particles. Nicotine, for example, is bound to particles in mainstream smoke. Numerous components of the smoke have the potential to injure the airways and alveoli. Components of tobacco smoke with the potential to injure the lungs through a variety of mechanisms are listed in Table 7. Some components adversely affect host defenses; others act through specific or nonspecific mechanisms.
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Alcohol, Tobacco And Other Drugs: Clinical Guidelines For Nurses And Midwives
Notably, cigarette smoking has very strong oxidant potential in that both the gas and tar phases contain high concentrations of free radicals Repine et al. Many of the components of cigarette smoke are the targets of regulations because of their toxic effects: these include nitrogen dioxide, carbon monoxide, and various metals. For information on the toxic effects of components, see reports of the U. Assessment of toxic effects of cigarette smoke in the respiratory tract requires consideration of the complexity of the mixture inhaled and the possibility of synergistic interactions among its many components.
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Although it is little studied, the possibility of numerous interactions has great plausibility because of the myriad components of cigarette smoke and the interlocking pathways of lung injury. Dosimetry of Tobacco Smoke in the Respiratory System To protect the lungs from injury, the respiratory tract has an elegant set of mechanisms for handling the particles and gases in inhaled air Figure 7. These defenses include physical barriers, reflexes and the cough response, the sorptive capacity of the epithelial lining, the mucociliary apparatus, alveolar macrophages, and immune responses of the lung Schulz et al. These defenses are critical because of the substantial volume of air inhaled daily: about 10, liters per day are inhaled by an adult. Even harmful substances present at low concentrations may eventually achieve a toxic dose after sustained exposure.
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Cigarette smoke, for example, contains components that impair mucociliary clearance Table 7. Figure 7. Source: Cook The size of particles in the smoke inhaled directly from a cigarette mainstream smoke has been studied in a variety of systems. These studies indicate that the mass median aerodynamic diameter of particles is 0. Particles of this size penetrate to and are deposited in the deep lung. Large particles e. Small particles, with a mean aerodynamic diameter less than about 2. About 60 percent of the particles inhaled in mainstream smoke are deposited. Although these particles are subject to handling by the mucociliary apparatus and alveolar macrophages, removal is not complete because of their very high numbers in the lungs of long-term smokers, which show evidence of a substantial burden of retained particles. Similarly, evidence shows that smokers clear these particles at a reduced rate Cohen et al. Figure based on data from the International Commission more The removal of gases in the respiratory tract is accomplished through sorption by the liquid that lines the epithelial layer Kreyling and Scheuch Both the site and the efficacy of removal of gases depend on the solubility of the gas.
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Passive Smoking
Highly soluble gases are removed high in the respiratory tract, but insoluble gases e. These dosimetric considerations indicate a high potential for lung injury in active smokers, who inhale a rich mixture of gases and particles that penetrates throughout the lungs, with deposit of particles and sorption of gases in the two anatomic sites most critical to respiration, the airways and alveoli. Major Pulmonary Diseases Caused by Smoking This section provides a brief overview of the principal diseases of the lung that are caused by smoking. A brief description of pathophysiology and pathogenesis is provided as background for the more comprehensive discussions of mechanisms. These topics are covered in great detail elsewhere Mason et al. Chronic Bronchitis The symptom complex of chronic bronchitis has been investigated for decades. In the s, the British Medical Research Council suggested that a diagnosis of chronic bronchitis was warranted when the symptoms of chronic cough and production of sputum were present on most days of the month for at least three months in two consecutive years without any other explanation BMJ This proposal is reflected in the current definition of chronic bronchitis Table 7.
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Earlier, Reid had used the size of the mucous gland layer as a predictor for the postmortem diagnosis of this condition but did not implicate the inflammatory process in the pathogenesis of either enlargement of the gland or the production of excess mucus. Subsequent studies of lung tissue surgically removed from cancer patients Figure 7. In addition, longitudinal studies of chronic bronchitis in persons with normal lung function have clarified that its presence does not predict future progression to more severe obstructive lung disease Fletcher et al. Presence of chronic bronchitis in persons who already have limited airflow, however, is predictive of a more rapid decline in lung function and a higher risk of hospitalization than are seen with a similar limitation of airflow but no chronic bronchitis Saetta et al. Source: Hogg Note: A Histology of bronchus with epithelial lining more This chronic inflammation, consisting of enlargement of the mucous glands and remodeling of the walls of both large and small bronchi reflects a deregulated healing process in tissue persistently damaged by the inhalation of tobacco smoke Hogg However, this inflammatory process has little influence on airflow limitation unless it extends to the small conducting airways that account for much of the increase in airway resistance in COPD.
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Studies reported from the laboratory of Snider and associates in Israel Breuer et al. Later, Nadel and other investigators Takeyama et al. This step is followed by phosphorylation of the intracellular component of this receptor and stimulation of downstream signaling pathways that activate the expression of the MUC5AC gene and lead to the production of mucus Takeyama et al. Nadel has also shown that reactive oxygen species ROS can bypass the extra-cellular sphere of influence of this regulatory axis. More recent work in transgenic mice has found that overexpression of epithelial sodium ion channels resulted in excess reabsorption of epithelial sodium and volume depletion of periciliary fluid Mall et al.
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Download American Pageant Chapter 20 Test Answers:
The depletion of the periciliary fluid layer interferes with the frequency of ciliary beats and results in decreased clearance and adherence of mucus to the airway surface. Results of this study showed that depletion of the periciliary fluid in animals is associated with the accumulation of mucus in the lumen of both large and small airways, leading to greater susceptibility to infection of the lower respiratory tract and early death. Chronic Obstructive Pulmonary Disease The hallmark of COPD is chronic airflow obstruction demonstrated with spirometry and the accompanying dyspnea and limitation of activity.
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Chapter Test Practice
Maximum expiratory flow is determined by the product of the resistance to flow in the small conducting airways centimeters of water [ H 2O ] per liter per second and the elastic recoil of the lung parenchyma that drives expiratory flow liters per centimeter of H2O. The product of these two variables, the time constant, characterizes the rapidity with which the lung fills and empties during respiration. Surprisingly, the time constant of the lung remains stable over a wide range of breathing frequencies in healthy lungs, but if disease increases either the compliance as in emphysema or the resistance as in obstruction of small airways, the time required to empty the lung is prolonged Otis et al.
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Physical Assessment, Part II, 50 Questions - ProProfs Quiz
The classic cohort study of the natural history of chronic bronchitis and emphysema performed by Fletcher and colleagues Lancet ; Fletcher used this type of measurement to test the hypothesis of a sequence beginning with tobacco smoking and then moving to symptoms of chronic bronchitis or recurrent chest infections and, finally, chronic limitation of airflow. The natural history of the decline in FEV developed by Fletcher and colleagues to summarize findings of a six-year longitudinal study of men working in West London is illustrated in Figure 7. Note: Adapted from Fletcher et al. Fletcher and colleagues observed that only 15 to 25 percent of the smokers in the study developed air-flow limitation, and they showed that smoking cessation slowed the rate of decline in FEV1 in those who stopped smoking permanently. In subsequent studies of various populations, only a minority of smokers developed COPD.
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This repeated finding indicates a role for genetic factors that may determine susceptibility to cigarette smoke. These investigators rejected the hypothesis of a pathogenetic continuum from smoking to obstructive bronchitis. Most persons who developed airflow limitation during the study had no evidence of chronic bronchitis, a finding that was not consistent with the hypothesis of a continuum from smoking to bronchitis to obstruction. Subsequent studies have confirmed that the presence of chronic bronchitis in persons with normal lung function GOLD stage 0 does not predict progression of disease Vestbo and Lange Using data from the Copenhagen City Heart Study, however, Vestbo and colleagues found that the symptoms of chronic bronchitis were associated with an accelerated decline in FEV1.
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Acute exacerbations, a concern in treatment of COPD , are attributed to viral infections Monto et al. Although Fletcher and colleagues found that these exacerbations had no effect on the rate of decline of FEV1 in the working men in West London, the U. Lung Health Study showed that such exacerbations were associated with a more rapid decline in persons with mild disease who continued to smoke Kanner et al. Subsequently, other investigators found that frequent exacerbations in patients with more severe COPD, especially those resulting from a higher bacterial load, were associated with more accelerated decline in FEV1 Donaldson et al.
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Chapter Tobacco | General Health Quiz - Quizizz
Collectively, these data suggest that when lung defenses become compromised in the later stages of COPD, chronic infection might play a role in the pathogenesis of the airflow limitation. This obstruction is related to an inflammatory process that thickens the airway wall, fills the lumen with exudates containing mucus, and narrows the airway by depositing connective tissue in the airway wall Figure 7. McLean and Leopold and Gough recognized that an inflammatory process was present in the small bronchi and bronchioles of lungs affected by centrilobular emphysema.
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APUSH Chapter 20 Terms Test Answers | 1medicoguia.com
An overall introduction to any type of hypothesis test. A specific focus on conducting a hypothesis test for proportions. Sharpen that pencil and get ready. This is where the fun begins. Eventually we will look at testing claims about proportions, means, the differences between proportions, the differences between means, and more. This part of the flipped lecture will focus on the structure of any hypothesis test. Some of the specifics, like formulas or conditions, will change depending on the parameter being tested, but the structure stays the same. For this class, we will use an acronym to remember the steps needed to conduct a hypothesis test. Keep in mind that these will all make more sense, once you see some examples. You won't know what all of these mean right away, but for now we want to become familiar with the process. P - Parameter Statement - After reading the problem, define the parameter you are going to test. Another way to describe this step is to state the claim that is being tested in sentence form.
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H - Hypotheses - Write your null and alternative hypotheses. Keep in mind that the claim could be in either, but the null must always have and equal sign, greater than or equal sign, or less than or equal sign. N - Name the Test - Is this a left tail, right tail, or two-tail test? Are you using a normal model z or a student's t-model t? T - Test Statistic - Make sure to use the correct test statistic formula. Once you have the correct formula, it's just plug and chug. O - Obtain the P-Value - The p-value is the area under the curve that is created by your test statistic. This is the probability that your results just happened by chance.
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M - Make a Decision about the Null Hypothesis - If your p-value is less than or equal to your level of significance alpha , then reject the null hypothesis. If the p-value is greater than alpha, then fail to reject the null. S - State Your Conclusion About the Claim - Write a sentence or two giving the conclusion you can make according to the decision you made in the previous step. Again, we should emphasize that you really won't know what all of this means until you see some examples and work through some problems yourself.
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Glencoe Health Book Chapter 20 Assessment Answers
Writing the Hypotheses Every hypothesis test starts with a claim of some kind. The claim does NOT always have to be the null hypothesis. The following video gives instructions about how to write your null and alternative hypotheses. Even though this chapter will focus on hypothesis tests for proportions, this video demonstrates how to write a null and alternative hypothesis using both means and proportions. The test statistic formula is slightly different depending on whether you are working with proportions or means as your population parameter, but every test statistic is similar to a z-score. And the p-value is used to decide if you will reject the null hypothesis or fail to reject the null hypothesis. By the way, "retaining the null hypothesis" is the same as "failing to reject the null hypothesis".
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Assumptions and Conditions The assumptions and conditions for a hypothesis test for proportions are the same as the assumptions and conditions for creating a confidence interval for proportions. Plausible Independence Condition - Is there any reason to believe that the data values somehow effect each other? This is a condition that depends on your knowledge of the situation. Randomization Condition - Were the data sampled at random or generated from a properly randomized experiment? If so, you're ok, if not then your sample size is too big. An Example of a Hypothesis Test for Proportions This video gives you one example of how to conduct a full hypothesis test for a proportion.
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You should note that this example is a two-tailed test. In a two-tailed test, you must double your p-value in order to compare to alpha. HT for Proportions Two-Tailed The previous video showed an example of a two-tailed test, the next video shows an example of a one-tailed test. In a one tailed test, you do not double the p-value. Don't base your null hypothesis on what you see in the data. You are not allowed to look at the data first and then adjust your null hypothesis so that it will be rejected. Don't always make your null hypothesis your claim. Once you decide on the claim that is to be tested, don't assume that it is always going to be the null hypothesis. Don't make the assumption that you are "proving" anything. You can reject the null hypothesis, but you can never "accept" or "prove" the null. The evidence either supports the claim or does not support the claim. Don't forget to check the conditions. The reasoning of inference depends on randomization.
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APUSH Chapter 20 Terms Test Answers
No amount of care in the calculating a test result can recover from a biased sample. The probabilities we compute depend on the independence assumption. And our sample must be large enough to justify our use of a Normal model. Ask a question or answer a question. Google Moderator.
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7.1 States Of Consciousness
Comparing these four countries reveals that in Afghanistan, there are more men than there are women, whereas the reverse is true in Canada, Sweden, and the United States. Afghanistan also has significantly higher fertility and mortality rates than any of the other three countries have. Do these statistics surprise you? How do you think the population makeup impacts the political climate and economics of the different countries? What factors lead to a sex ratio in which men outnumber women? Demographic Theories Sociologists have long looked at population issues as central to understanding human interactions.
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Free Flashcards About Chapter 20 Tobacco
Below we will look at four theories about population that inform sociological thought: Malthusian, zero population growth, cornucopian, and demographic transition theories. He identified these factors as war, famine, and disease Malthus Thinking practically, Malthus saw that people could only produce so much food in a given year, yet the population was increasing at an exponential rate. Eventually, he thought people would run out of food and begin to starve. They would go to war over the increasingly scarce resources, reduce the population to a manageable level, and the cycle would begin anew. Of course, this has not exactly happened. So what happened? Why did we not die off? There are three reasons that sociologists suggest we continue to expand the population of our planet. First, technological increases in food production have increased both the amount and quality of calories we can produce per person. Second, human ingenuity has developed new medicine to curtail death through disease.
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John Howard Northrop | Biographical Memoirs: Volume 63 | The National Academies Press
Finally, the development and widespread use of contraception and other forms of family planning have decreased the speed at which our population increases. But what about the future? His ideas suggest that the human population is moving rapidly toward complete environmental collapse, as privileged people use up or pollute a number of environmental resources, such as water and air.
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He advocated for a goal of zero population growth ZPG , in which the number of people entering a population through birth or immigration is equal to the number of people leaving it via death or emigration. While support for this concept is mixed, it is still considered a possible solution to global overpopulation. Cornucopian theory scoffs at the idea of humans wiping themselves out; it asserts that human ingenuity can resolve any environmental or social issues that develop.
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Chapter 20 Tobacco Test Answers
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