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The paper "Pathophysiology of the Respiratory System" states that smoking, alcohol abuse, and a high-fat diet are all significant health risk factors that imply the possibility of chronic diseases, including cardiovascular diseases, diabetes, hypertension, cancer, and associated organ failure…
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Extract of sample "Pathophysiology of the Respiratory System"
What will kill you first: smoking, a high fat diet or alcohol abuse? I. General Background/Introduction A. General Introduction There are various health problems which have emerged in the past 50 or so years, and most of these diseases seem to be attributed to lifestyle choices and preventable health issues. These health problems also represent chronic illnesses which eventually translate to overwhelming health costs and high mortality as well as morbidity rates. Issues relating to lifestyle choices include high cholesterol diet, high sodium and high sugar content in foods, low rates of exercise and activity among the general population, smoking, unprotected sex, alcohol, and drug abuse. These lifestyle choices and unfavourable habits are risk factors for diseases including coronary heart disease, diabetes, HIV-AIDS, cancer, and other related chronic illnesses. These diseases represent shorter life spans and significant health as well as economic costs, not just for the individuals concerned but for the government as well.
The health impact of these diseases in terms of life span has generally translated to shorter life spans. For health issues like smoking, high fat diet, and alcohol abuse, the precise number of years shaved off an individual’s life cannot exactly be determined because of varying elements and individual qualities present for each patient. This study will seek to establish which among the following health issues would likely kill an individual first: smoking, a high fat diet, or alcohol abuse.
B. Statistics/Prevalence
In the global scene, about 80,000 to 100,000 children start smoking every day, and about a quarter of children in the Western Pacific region will likely die from smoking (Martin, 2012). According to the World Health Organization (WHO, 2008) about a third of the male adult global population are considered smokers and smoking-related illnesses kill about one in 10 adults worldwide, causing four million deaths annually. If these trends persist, by 2030, smoking will likely kill one in six people worldwide (Centers for Disease Control, 2012). In terms of health effects, long-term smokers are likely to die from smoking, with every cigarette smoked cutting at least five minutes of one’s life (CDC, 2012). It is also a significant health risk factor in heart disease, stroke, and chronic lung disease; and it has been known to cause cancer of the lungs, larynx, oesophagus, mouth, and bladder. The cancer risk has mostly been associated with the carcinogenic chemicals found in tobacco smoke (CDC, 2012).
High fat diet has been associated with obesity and overweight. The rates for obesity have doubled since the 1980s (WHO, 2012). In 2008 alone, about 1.4 billion adults have been classified as overweight, and out of these numbers, over 200 million and 300 million were in the obese category. In 2011, 40 million under the age of five were considered overweight. This obesity problem has mostly been attributed to high fat foods and decreased physical activity due to sedentary lives. Health risk factors related to obesity include cardiovascular diseases, diabetes, musculoskeletal disorders, and some cancers (WHO, 2012).
In relation to alcohol abuse, the Global Information System on Alcohol and Health (2012) declares that the negative results of alcohol have been known to cause the death of 2.5 million individuals yearly. There are about 60 different kinds of diseases wherein alcohol has been considered the primary cause. Alcohol has also been known to impact on the well-being and the health of the people around the drinker (Global Information System on Alcohol and Health, 2012). In 2005, the global consumption of alcohol reached 6.13 litres of alcohol per individual 15 years and above. This would not even include the unrecorded consumption of alcohol in about 30% of the worldwide adult population (Global Information System on Alcohol and Health, 2012)
II. Pathophysiology and pathology
A. Smoking
Active elements of tobacco and cigarettes enter the body through the burning of the leaves and through the inhalation of the vaporised gases (Gately, 2004). This process immediately causes the entry of substances into the bloodstream via the alveoli in the lungs. Not all the smoke is inhaled and some active substances may be lost through pyrolysis (Gilman and Xun, 2004). The pipe and cigar smoke are usually not inhaled due to their high levels of alkalinity, which can be irritating to the lungs and the trachea. However due to its higher level of alkalinity, much higher than cigarette smoke, non-ionised nicotine is usually absorbed faster into the mucous membranes of the mouth (Gilman and Xun, 2004).
The substances inhaled cause chemical reactions in the nerves. The cholinergic receptors are usually stimulated by the neurotransmitter acetylcholine. Acetylcholine along with nicotine leads to chemical similarities which then causes the nicotine to stimulate the receptor (Wigand, 2006). The nicotinynic acetylcholine receptors are found in the central nervous system as well as the nerve-muscle points of the skeletal muscles. Their activity causes the heart rate to increase and causes alertness as well as increased reaction times (Wigand, 2006). The nicotine acetylcholine stimulation is not necessarily an addictive process, however as there are numerous dopamine-releasing neurons on the nicotine receptors, the dopamine is soon released (Chandra and Chaloupka, 2003). The release of dopamine which usually triggers feelings of pleasure would be reinforcing (Gilman and Xun, 2004).
When smoke is inhaled, damage is already caused to the tissues of the airways and the lungs. Chemicals including nitrogen oxide can cause the narrowing of the airways prompting the lungs to work more, making breathing more difficult (Cancer Research, 2012). Hydrogen cyanide, carbon monoxide, and ammonia cause the natural cleaning mechanisms of the lungs. As a result, the chemicals, bacteria, as well as viruses inhaled are usually not eliminated and instead fester in the lungs, making the smoker more vulnerable to respiratory tract infections and other diseases. Years of smoking can also cause cell mutation and differentiation which can later lead to the development of cancer cells (Proia, et.al., 2006). Radioactive polonium-210 is also deposited on the airways usually at the areas where the airways split before entering the lungs (Cancer Research, 2012). As a result, the local cells are exposed to more radiation than is safe for them to experience. The carcinogens and other poisonous toxins in the smoke also enter the bloodstream and transported to the different parts of the body.
The tobacco poisons, including arsenic and hydrogen cyanide causes damage to the lining of the blood vessels and the heart (Cancer Research, 2012). Nicotine and carbon monoxide narrows the blood vessels and the smoke can also increase cholesterol levels, thereby prompting bigger risks in the development of blood clots. Carbon monoxide and nitrogen oxide can also decrease the transport of oxygen to the different cells of the body (Cancer Research, 2012). This then decreases the amount of oxygen transported to the brain and the organs of the body; as a result, the energy levels of the individual are also decreased.
Studies also support the fact that based on the mechanisms by which smoking leads to disease, there is no specific or risk-free exposure level to tobacco smoke (Berlin, et.al., 2003). The inhalation of the complicated mixture of combustion compounds in tobacco smoke leads to unfavourable health outcomes, including cancer and cardiovascular diseases caused by processes like DNA damage, inflammation, and oxidative stress (Chandra, et.al., 2007). With various and specific mechanisms, the risk and impact of negative health outcomes related to smoking are founded on the period as well as exposure to tobacco smoke. The persistent use and long-term exposure to smoking are based on the addictive impact of tobacco chemicals and products, mostly affected by the actions of nicotine and other chemicals, at varying levels of nicotine receptors of the nervous system (West and Shiffman, 2007). A low level of exposure, which usually includes exposure to second-hand smoke, causes a sharp elevation in the endothelial dysfunction and inflammation; this is akin to the body’s reaction seen in acute cardiovascular incidents as well as thrombosis (CDC, 2012).
B. Alcohol abuse
Various neurobehavioral elements relating to alcohol has been related to the manifestation of alcohol dependence (British Medical Journal, 2013). The favourable and stimulating impact of alcohol is mediated by a dopaminergic pathway coming from the ventral tegmental aspect into the nucleus accumbens (BMJ, 2013). Persistent and excessive alcohol intake causes the hypersensitivity of the pathway which then leads to dependence. Long-term exposure to alcohol intake leads to changes in the neurotransmitters, which includes the down-regulation of inhibitory neuronal gamma-aminobutyric acid receptors, the up-regulation of glutamate receptors, as well as the elevated norepinephrine activity (BMJ, 2013).
Ceasing alcohol intake causes the excitatory condition to be unopposed, leading to the nervous system being hyperactive and dysfunctional; this characterises alcohol withdrawal. Withdrawal symptoms can also increase with withdrawal episodes being exacerbated through the phenomenon known as kindling (BMJ, 2013). The alcohol-dependent individuals are also likely to manifest craving, a strong urge to drink more alcohol. Such craving has been associated with dopaminergic, serotonergic, and opioid systems which support positive reinforcement (BMJ, 2013).
Long-term alcohol abuse can lead to numerous physical effects, with cirrhosis being one of the primary diseases often reported (Blondell, 2005). Pancreatitis, epilepsy, polyneuropathy, alcohol dementia, heart disease, nutritional imbalance, and peptic ulcers, as well as sexual dysfunction are also risks associated with alcohol abuse, and these diseases can eventually prove to be fatal health risks (Heilig, et.al., 2010). There is also an elevated risk for the development of cardiovascular diseases, alcohol liver disease, and cancer. The central and peripheral nervous system may also suffer damage after prolonged alcohol abuse (Testino, 2008). Immunologic imbalances can also be seen, alongside generalized skeletal fragility, as well as an acknowledged propensity towards accidents, including bone fractures and physical injuries from falls.
Women have also been known to develop long-term complications resulting from alcohol dependence faster than their male counterparts. Moreover, women have also registered higher mortality rates from alcohol abuse as compared to men (Walter, et.al., 2003). Long-term complications which have manifested among alcohol abusers include organ damage, specifically, the brain, heart, and liver (Moore, et.al., 2007) as well as an elevated risk for the development of breast cancer. Furthermore, prolonged alcohol abuse has been seen to impact negatively on the reproductive functions of women. This has been known to cause reproductive dysfunction including anovulation, reduced ovarian mass, issues in the regulation of the menstrual cycle as well as early menopause (Stavro, et.al., 2012). Alcoholic ketoacidosis is also a major risk for alcoholics, especially those who have a history of binge drinking (Sibai and Eggimann, 2005).
A study in the UK revealed that in general, alcohol abuse was considered the most harmful drug, affecting the drinker as well as other individuals. When combined with other substances, alcohol has also been known to lead to serious effects (Thompson, 2013). Moderate alcohol intake has also been known to have a lesser risk for cardiovascular diseases. Drinking patterns also impact differently in terms of cardiovascular risks. Meals taken with alcohol has been known to reduce risks, but binge drinking, even among moderate drinkers has been known to imply a greater risk for cardiovascular incidents (Thompson, 2013). Moderate alcohol consumption has also been known to cause an elevated risk for breast cancer among women. The total mortality risk is decreased with moderate alcohol intake, but not for heavy alcohol drinkers. Any reduced cardiovascular risk for moderate drinkers however is offset by the presence of cirrhosis and cancer (Thompson, 2013). The level of alcohol associated with the lowest mortality rates is 2 drinks a day for men and 1 drink per day for women. Moderate alcohol intake has also been known to reduce the possibility of developing diabetes; however heavy alcohol intake has been known to increase the risk (Thompson, 2013).
C. High fat intake
Stored fat is needed in order to ensure survival in times of deprivation, including starvation. During persistent periods of abundance in food however, efficient fat storage causes excess stored fats, which later causes obesity (Redinger, 2007). The storage of fatty acids is labelled as triacylglycerol within adipocytes which then helps prevent fatty acid toxicity; in any case, the free fatty acids travel freely in the blood vessels and cause oxidative stress via dissemination in the body (Redinger, 2007). However, the elevated levels of fat storage lead to obesity which then leads to the release of excessive fatty acids with enhanced lipolysis, triggered by the improved sympathetic state seen in obesity. The manifestation of the excessive free fatty acids causes lipotoxicity, with lipids and metabolites cause oxidant stress to the endoplasmic reticulum and mitochondria (Redinger, 2007). This affects adipose and nonadipose tissue, being credited for the pathophysiology in various organs, including the liver and pancreas (Evans, et.al., 2004). The free fatty acids seen with the excessive levels of triacylglycerol stored also prevent lipogenesis, thereby preventing the clearance of serum triacylglycerol levels which impact on hypertriglyceridemia. The free fatty acids released by the endothelial lipoprotein lipase leads to lipotoxicity which then causes insulin-receptor dysfunction (Evans, et.al., 2004). The resultant insulin-resistant state causes hyperglycemia along compensated hepatic gluconeogenesis. Gluconeogenesis causes higher hepatic glucose secretion worsening hyperglycemia triggered by insulin resistance. The free fatty acids also reduce the utilization of insulin-stimulated muscle glucose, adding to the issue of hyperglycaemia (Hutley and Prins, 2005). Lipotoxicity caused by excessive free fatty acids also reduces the release of pancreatic B-cell insulin, which later leads to B-cell exhaustion (Niswender, et.al., 2004).
High fat content in food is the major cause for obesity, and obesity is one of the leading causes of death in the world. Mortality risks are lowest for those who are not overweight, but are high among those with a BMI of 32 kg/m2 (Charlton, 2004). In the US, it is said to cause about 111,000 to 365,000 deaths a year. In general, obesity reduces life expectancy by six to seven years, with severely obese experiencing up to a 10 year reduction in their expected life expectancy. Various risks are also seen with high fat diet, with diseases like diabetes, high blood pressure, high cholesterol levels manifesting often within this population (Kawanami, et.al., 2004). Other issues also include osteoarthritis, obstructive sleep apnoea, diabetes, cancer, cardiovascular disease, and liver disease.
III. Prehospital/medical management
A. Smoking
For smoking, the best recommended medical management for the habit is to end it. For various smokers, there may be different ways by which they can end their habit with the option of entirely quitting being the highly recommended option (WHO, 2008). Other medical practitioners also recommend gradually cutting back on the number of cigarettes smoked a day until the individual reaches the point where he totally quits his habit. Regular diagnostic tests and chest x-rays for smokers is recommended in order to detect cancer cells, bacterial growth, and similar unfavourable health effects on the patient (WHO, 2008). Early detection and early management of possible health issues arising from smoking seems to be one of the better options in this case.
B. Alcohol abuse
For alcohol abuse, the assistance of psychiatric therapy is crucial to these patients. Entering a rehabilitation program can help these patients recover from their alcoholism and manage the withdrawal symptoms they are bound to face as they quit their habit (Walden, et.al., 2004). A rehabilitation period in a treatment facility is important for alcoholics, including the use of medications which would help them reduce or end their excessive alcohol intake. Disulfiram is the recommended drug of choice for these alcoholics (Krampe, et.al., 2006). The management of health issues manifesting due to alcohol abuse is also crucial. Where diagnostic tests reveal liver affectations or any other organ affectations, the proper medical management is essential.
C. High fat diets
For individuals with high fat diets, the medical management includes a diet plan which would reduce the intake of fats and which would increase the patient’s diet in fruits, vegetables, and a general balanced diet and portions for protein, carbohydrates, mineral, vitamins, water, and also fat (Levy-Navarro, 2008).
D. Comparison of impact
In comparing the overall impact of these risk factors on mortality and morbidity, the risk for death is highest for binge drinking among alcoholics and moderate drinkers. As was mentioned above, binge drinking can cause alcoholic ketoacidosis which can lead to death (Thompson, 2013). No other risk factors or elements need to be present for alcoholic ketoacidosis to cause death. When compared to smoking, the mortality risk is usually accumulated, mostly seen after years of smoking. The unfavourable health effects of smoking including lung cancer take years to manifest (Martin, 2012). This is the same situation for high fat diets which usually take years to manifest any significant effects on the health of the individual. In general however, the longer years when the unhealthy habits are seen indicate the greater risk for patients. In effect, the longer the years that an individual is considered obese, alcoholic, or smoker, the greater the risk is to his life (Heinz, et.al., 2005). Moreover, when combined with various unhealthy habits including sedentary lifestyle, drug abuse, and a family history of cancer, diabetes, and cardiovascular diseases, the patient is likely to manifest health issues earlier than others.
IV. Summary and Conclusions
Based on the above discussion, smoking, alcohol abuse, and high fat diet are all significant health risk factors which imply the possibility of chronic diseases, including cardiovascular diseases, diabetes, hypertension, cancer, and associated organ failure. It is important to note that alcoholic binges can immediately cause an individual’s death, especially with the associated risk of alcohol ketoacidosis. Without such element however, these three risk factors can equally have a significant impact on one’s mortality. Differences however would likely be seen based on the years the person has been smoking, has been abusing alcohol, or has been having a high fat diet. The chemicals found in cigarettes cause deposits in the lungs which can constrict the blood vessels and make the lungs and eventually the heart to work faster. It can also lead to cell mutation and differentiation, eventually to the development of cancer cells. High fat diets can cause the development of fat deposits in the blood vessels also causing strain on the heart’s pumping and circulatory action. Alcohol can cause reactions with the chemicals and hormones in the body, causing elevated heart rates and coronary affectations. With years of strain on the heart, the blood vessels, and the organs, various health effects manifest in the form of coronary artery disease, hypertension, and eventual cell differentiation leading to cancer.
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