Sunday, 28 February 2010
The Effects Of Smoking
In the essay I will explore the contents of cigarettes while looking at the diseases that they can cause and how smoking links to those diseases.
Cigarette contents
Carbon Monoxide
Carbon monoxide is a colourless, odourless gas and is produced by the partial oxidisation of carbon containing compounds. Smokers are at an increased risk of carbon monoxide poisoning due to the cigarette smoke containing it. Carbon monoxide combines with the haemoglobin in the blood, displacing the oxygen meaning that less oxygen can be transported. The carbon monoxide that combines with haemoglobin to form COHb and this cannot be reversed back to oxyhaemoglobin. While smokers have a much higher level of COHb, non smoker’s levels can be high through second-hand smoke through smoking partners or friends. This is a reason why smokers are often associated with loss of breath during exercise. Exposure to carbon monoxide could lead to fatigue, vomiting and mental confusion. It is harmful at any level and can kill you, long term exposure of lower levels can cause heart problems.
Tar
Tar a brown substance which is left behind after a cigarette. It is the reason why smokers characteristically have yellowy brown teeth and fingers. The tar also paralyses the cilia in our airways preventing them from sweeping mucus and bacteria out of our throats preventing infect. The paralysis of the cilia causes lung diseases such as emphysema, bronchitis and lung cancer. The tar coats your lungs with a layer which for an average 20 a day smoker could fill up a 210ml cup full of tar. Tar can be deposited in the bronchiole tube blocking them up near to the air sac. This causes the smoker to cough in order to try and remove the blocked bronchioles. The constriction of the airways is another reason why smokers have difficulty breathing. When the lungs can’t clear the tar out of the air sacs the air sacs can collapse. When the collapse the tar can be cleared out and after this occurs they can reinflate. However, when this is a regular occurrence sometimes the walls of the alveoli will fuse with the walls of other alveoli. This decreases the surface area, which reduces the area for gaseous exchange to occur causing emphysema.
Nicotine
Nicotine as well as being the substance smokers get addicted to is also a vasoconstrictor. It is believed that Nicotine is as addictive as heroin or cocaine which explains why people become so addicted. The nicotine travels in your bloodstream and can reach ones brain in 10 seconds, giving the smoker an instant effect of euphoria. Nicotine has an average half life of around 40 minutes. This means after this smokers feel the urge to have another cigarette. This means that it reduces the diameter of the blood vessels while present in the blood. This puts an additional strain on the heart as it has to pump harder to get blood through the body. The constriction of the airways means that it reduces gaseous exchange. It is also thought that nicotine also paralyses cilia as well as tar. Nicotine stimulates the adrenal glands to release the hormone adrenaline.
Cardiovascular disease
Cardiovascular disease is defined as any disease that affects the circulatory system, including the heart and blood vessels. Smoking is one of the main causes of cardiovascular disease specifically chronic heart disease. Smoking causes the levels of fibrinogen causing the blood to clot, making the blood thicker. Studies have shown that smokers have a 50% higher chance of getting CHD than non smokers, 75% in heavy smokers and mortality from any cardiovascular disease is 60% higher in smokers than non smokers and in heavy smokers this is as much as 85% higher. This is why cardiovascular disease is the second biggest killer from smoking in the UK.
Atherosclerosis
Carbon monoxide and high blood pressure can cause serious damage to the endothelium. This damage is repaired by the action of the phagocytes which encourages the growth of a layer of smooth muscle and the deposition of fatty substances. The deposits otherwise known as atheromas include cholesterol from low density lipoproteins, fibres, dead blood cells and platelets. The process of deposition is called atherosclerosis. Atheromas can eventually lead to a build up of plaque in the lumen of the artery, meaning that reduces blood flow but also it makes the artery less flexible and leaves the walls a lot rougher than that of a healthy artery.
Thrombosis
Blood flowing past the plaque which has been built up through atherosclerosis cannot flow as smoothly increasing the chances of it clotting. Nicotine is a big contributor to this as it causes the platelets to become ‘sticky’ which increases the chance that the blood will stick. The plaque is covered with a thin, delicate membrane which if ruptured causes the red blood cells to also stick to the plaque. This causes the blood to clot, and a clot is called a thrombus. Clots in arteries are very dangerous and is potentially life threatening. The clot reduces the lumen but more serious damage occurs when part of the clot breaks off and lodges itself in a narrower artery preventing blood flow through it.
Coronary Heart Disease
The heart has its own supply of blood through the coronary artery which is branched off the aorta. The blood travels through it at a high blood pressure and is at risk of atherosclerosis. A build up of plaque of thrombosis in the coronary artery can lead to a lack of blood flow to the heart and therefore the heart receives an inadequate supply of oxygen which is need for respiration. This can lead to coronary heart disease which can be in the form of angina, myocardial infarction (heart attack) or heart failure. Angina is a severe chest pain which may spread up your neck and down your left arm, it is often confused with myocardial infarction. Myocardial infarction however is the death of the heart muscle usually caused by a thrombosis (clot) in the coronary artery. This blocks blood and oxygen getting to the heart muscle. Finally heart failure is when the heart has problems pumping blood due to a blockage in the coronary artery.
Stroke
A stroke is the death of part of the tissue in the brain. It is caused by a loss of blood flowing to the brain and is caused in two ways. The first is by part of a thrombus breaking and getting stuck in a smaller artery leading to the brain preventing any blood flowing to it. Secondly and artery which is leading to the brain bursts, this is called a haemorrhage.
Evidence Linking Smoking To Diseases
Studies done across the world in countries such as Japan and USA have shown us that 9 out of every 10 cases of lung cancer are due to smoking. IN 2002, 33,600 people were killed due to lung cancer meaning roughly 4 an hour died because of it. It was first discovered that smoking caused lung cancer in 1950 when a study found that people smoking between 15 and 24 cigarettes a day were 26 times more likely to have lung cancer than people who didn't smoke. Even people smoking less than 15 a day still were 8 times more likely to develop lung cancer. However it’s not just lung cancer that smoking can cause. It also contributes towards bladder, cervix, kidney, larynx (voice box), mouth, oesophagus , pancreas, stomach, liver and some types of leukaemia. Smokers are 7 times more likely to die of cancer than non smokers. The reason for all these cancers being caused is due to the poisons in the cigarettes. Benzene is a known cause of leukaemia and one study suggests that it can be accounted for 10 – 50% of the deaths due to leukaemia.
Reference
http://www.carbonmonoxidekills.com/carbon_monoxide_in_cigarettes.htm
http://quitsmoking.about.com/b/2006/06/20/tar-in-cigarettes.htm
http://www.allsands.com/health/smokingeffects_srw_gn.htm
http://www.heartstats.org/datapage.asp?id=3851
http://info.cancerresearchuk.org/healthyliving/smokingandtobacco/howdoweknow/
OCR Biology AS Frank Sochacki and Peter Kennedy
By Alexander Ewing
The Effects of Smoking
The following essay contains information pertaining to the biological effects of smoking. In particular it examines the effects of tar, nicotine and carbon monoxide on the respiratory and circulatory system. In addition to this it looks at some of the diseases linked with smoking, such as chronic bronchitis, emphysema, lung cancer and coronary heart disease; the latter of which is looked into in greater detail. The information for the essay, along with the statistics which are dispersed throughout, has been obtained from the point of referance cited at the end of the essay.
The Effects of Smoking;
Smoking kills around 114,000 people in the UK each year. Of these deaths, about 42,800 are from smoking-related cancers, 30,600 from cardiovascular disease and 29,100 die slowly from emphysema and other chronic lung diseases. Cigarettes contain more than 4000 chemical compounds, over 400 of these are toxic substances and at least 60 are known to be carcinogenic. These substances are taken into the body via the smoke that the smoker inhales, through the filter, and the smoke breathed in from the burning end; this smoke can also affect nearby non-smokers (termed passive smoking). It is thought that the most dangerous of the chemicals present are tar, nicotine and carbon monoxide.
Tar is a combination of chemicals, which settles on the lining of the airways and alveoli. Its presence can cause an allergic reaction, in which the smooth muscles in the walls of the airway contract; narrowing the lumen and thus restricting the flow of air to the alveoli. In addition to this the tar stimulates the goblet cells in the airway, to secrete more mucus; this traps viruses and bacteria as usual. However as the tar also paralyses or destroys the cilia that line the surface of the airway, preventing them from wafting layers of mucus to the back of the throat, the mucus collects in the airway; where the pathogens can multiply, blocking the bronchioles. This makes the lungs more susceptible to infection; meaning that smokers are more likely to catch diseases such as influenza or pneumonia. This is part of the reason why smokers take 25 per cent more sick days a year than non-smokers. Over time the continual irritation of the airways by these pathogens, leads to the smoker developing what is known as a smokers cough, this is the bodies attempt to remove the mucus from the lungs. However this has numerous detrimental side effects on the respiratory system. The delicate lining of the airways and alveoli can be damaged; this will then be replaced by scar tissue, which is thicker and has less elasticity. Whilst the layer of smooth muscle in the walls of the bronchioles thickens. This combination permanently narrows the lumen of the airway, further impeding the flow of air to the alveoli.
The recurring infections produced by the presence of bacteria and viruses in the mucus, inflames the lining of the airways; this damages the epithelium and attracts white blood cells to the area, to combat the pathogens. In order to get into the airways, they must leave the blood; they do this by releasing enzymes such as elastase, which digest parts of the lining of the lungs, allowing them to pass into the air spaces. This reduces the elasticity of the alveolus wall, so when we exhale they do not recoil pushing air out; thus the bronchioles collapse and this can cause the alveoli to burst as the pressure in the lungs increases. The above factors contribute to cause diseases such as chronic bronchitis, Emphysema and Chronic obstructive pulmonary disease which is a combination of the two. Furthermore tar is also known to contain the carcinogenic compound Benzopyrene (in the United States, 87% of lung cancer cases have been linked to smoking) and also damages the mouth by rotting, teeth, damaging gums and taste buds.
Nicotine and Carbon monoxide both enter the lungs, where they are quickly absorbed into the blood stream (within 30 seconds of entering the body nicotine reaches the brain); where they cause changes to the circulatory system, which lead to an increased risk of cardiovascular disease. This is shown by the fact that Smokers tend to develop coronary thrombosis 10 years earlier than non-smokers, and make up 9 out of 10 heart bypass patients. Nicotine is a highly addictive drug, but with repeated use, tolerance develops rapidly. For example, non-smokers can absorb (by tablet) only 4 mg of nicotine before symptoms of nausea, vomiting, diarrhoea and weakness begin. While the average smoker can tolerate twice as much nicotine, without any immediately noticeable effects. However Nicotine does have a variety of effects on the body. It mimics the action of transmitter substances, at the synapses between nerves, making the nervous system more sensitive and the smoker feel more alert. It stimulates the adrenal glands to release the hormone adrenaline; this increases the heart rate and breathing rate, and causes the constriction of the arterioles; together these raise the blood pressure in the arterioles. Nicotine also affects the platelets, making them sticky, increasing the risk that a blood clot or thrombus may form. Carbon Monoxide is a toxic gas (the gas that kills people when they commit suicide, by turning on their car engine and closing the garage door) which diffuses into red blood cells where it combines, more readily that oxygen, with haemoglobin, forming carboxyhaemoglobin. This reduces the amount of oxygen that can be carried in the blood, and heart rate may increase as a result of this. It also damages the lining of the arteries.
These changes all contribute to causing diseases such as coronary heart disease, roughly 120,000 people in the UK die each year from heart disease; making it the most common form of death in the UK. Coronary heart disease is caused by a build up of lipid plaques (often referred to as atheroma) on the inner walls of the coronary arteries that supply blood to the heart muscle, narrowing the vessel’s lumens. This is known as atherosclerosis. The development of arthrosclerosis is a response of the blood vessel to damage to the endothelial cells lining the lumen of the vessel by toxins such as carbon monoxide. Once the lining is damaged, cells known as foam cells enter the vessel and absorb the cholesterol and fat from the blood stream. Accumulation of foam cells forms a fatty streak on the side of the vessel; this is the earliest sign of arthrosclerosis. Next is the formation of intermediate lesions (a section of abnormal tissue) consisting of foam cells and lipid pools. Smooth muscle cells also gather at the site of plaque formation and die. Together these cells form fibrous plaques which often impede blood flow and can rupture; causing the blood to clot forming a thrombus, blocking the artery, or it can break free and be carried around in the blood until it reaches a narrow artery, where it will lodge, preventing blood flow through that artery. The chance of a thrombus forming is increased by the presence of nicotine; which makes the platelets sticky and thus more likely to clot and constricts the arterioles, making it easier for a clot to block them. The restriction of the blood supply and hence the supply of oxygen for respiration, caused by atherosclerosis, reduces the hearts ability to function and can lead to coronary heart disease in three forms; Angina, a severe pain in the chest which may extend down the left arm or up the neck, often experienced during exercise. A heart attack or myocardial infarction, the death of part of the heart muscle. Finally heart failure, when the heart cannot sustain its pumping action. It can also lead to a stroke. This occurs when the blood flow to part of the brain is lost, causing the death of a part of the brain tissue. If the thrombus blocks an artery leading to part of the brain or an artery leading the brain bursts (haemorrhages). However it should be remembered that coronary heart disease is a multifactoral disease, and that other factors such as age, sex and diet all contribute to the risk of a person developing CHD as well.
Ultimately it is quite clear, from the information above, that smoking cigarette’s increases the risks of an early death. This is supported by epidemiological data links; such as the fact that up to 50% of smokers may die of smoking-related diseases. One third of cancer deaths are as a result of cigarette smoking, and a quarter of smoker’s die of lung cancer. Chronic obstructive pulmonary disease is very rare in non smokers, less than 10% of victims are non-smokers, and less than 2% of people with emphysema are non-smokers. One fifth of smokers suffer from emphysema, and as a result deaths from pneumonia and influenza are twice as high amongst smokers.
References;
1.http://www.netdoctor.co.uk/health_advice/facts/smokehealth.htm
2.http://www.patient.co.uk/health/Smoking-The-Facts.htm
3.http://www.nlm.nih.gov/medlineplus/smoking.html
4.http://americanheart.mediaroom.com/index.php?s=43&item=897
5.http://ezinearticles.com/?Tar-Smoking---How-it-Works-in-Ruining-Your-Health&id=2362076
6.Ocr Biology for AS, by Pete Kennedy and Frank Sochacki, published by Heinemann.
By Marcus Ghosh
Thursday, 14 January 2010
CHD
Coronary Heart Disease
Total
Coronary heart disease 91,458
Stroke 53,186
Other CVD 48,643
Lung cancer 34,552
Colo-rectal cancer 16,025
Breast cancer 11,995
Other cancer 96,739
Respiratory disease 78,330
Injuries and poisoning 20,371
All other causes 115,852
In the
Atherosclerosis is the cause of CHD, where deposits of fat and inflammatory cells build up in the walls of the coronary arteries. Gradual increase in these deposits or “plaques” reduces blood flow and will often present as angina. Angina is the painful sensation described by the patient due to a restriction in coronary blood flow. Angina typically occurs when the patient undergoes exercise, as the supply of oxygen and glucose is restricted. If the plaque in a coronary artery ruptures, the flowing blood around it clots which can block the artery- leading to a heart attack (or myocardial infarction - MI). Typical symptoms of an MI include, crushing chest pain, often radiating to the jaw or down the left arm, shortness of breath, nausea and vomiting.
Diet plays a relatively small role in promoting CHD, although a ‘healthy’ diet includes low quantities of saturated fat, and adequate supplies of fruit and vegetables. Additional vitamins, minerals and health food supplements do not confer any benefit. Nevertheless, recent studies have shown that fruit and vegetables can play a role as anti-oxidants, oxidation occurring as the deposits form within the artery wall. They also contain potassium which may help to control blood pressure and the aid the regulation of the heartbeat. Leafy and root vegetables also contain a lot of folate, essential for the formation of blood cells and to maintain levels of homocysteine; additionally, links have been established that high levels of homocysteine can contribute to the risk of CHD.
However, high salt levels in a typical diet have been proven to increase blood pressure. Increased blood pressure causes the heart muscle to work harder, causing them to grow larger- this causes some vessels to be obstructed and impairs the function of the heart. High blood pressure has also been linked to the accelerated development of plaques, further increasing the risk of myocardial infarction.
In contrast, the level of cholesterol in the blood increases the risk of MI greatly. High levels of low density lipoprotein cholesterol (or LDL) mean that cholesterol builds up in the coronary arteries quicker. This enhances the plague build up, narrowing the lumen of the artery itself and increasing the risk of plague rupture and heart attack In contrast, high density lipoprotein cholesterol protects the vessels from CHD. The role of dietary cholesterol’s in CHD however is slight, as only 25% of cholesterol in our bodies comes from diet. Nevertheless, when LDL is too high, it can be treated with drugs that reduce LDL levels, such as statins, which also restore HDL to a more normal level.
Since 1994 diabetes has doubled in men and increased more than two and a half times in women. .Men who have type 2 diabetes have a between a two and fourfold increase risk of CHD, with that risk raises to three to fivefold in women. Diabetes plays a relatively large role in the build up of plagues, as the increased levels of glucose within the bloodstream accelerate the plague build up leading to high chance of incident. Diabetes also increases the production of certain cholesterols which are then deposited in the walls of the arteries which also leads to plague growth acceleration.
CHD and genetics is a developing field and very little is known about the genetic links between the two. The genes which actually cause CHD are unknown, but in recent years defective genes have been found which increase production of body cholesterol, which code for faulty cholesterol synthesis or uptake. Family history is a very important factor and a patient being treated for chest pain with a family history of heart failure often signals heart problems above anything else.
In 2007, a third of all premature deaths in men were from CHD and a fifth in women, and a 60 year old woman with CHD and a 50 year old man in the same development on CHD as the woman potentially have the same chance of death. Part of the reason why women are less affected by CHD or have it set on later is the role of oestrogen. Due to the higher levels of oestrogen in the female body, it provides protection to the heart, not much is known about what is done exactly.
There are numerous risk factors for CHD, so there are multiple treatments depending on which risk factors are the most applicable. When blood pressure is too high, drugs called Beta Blockers are given which reduce blood pressure and also offer some protection to the heart. Statins act to reduce cholesterol and slow plaque build up, reducing the risk of another heart attack. After a heart attack, the area surrounding the coronary artery is often dead or damaged due to nutrient starvation (oxygen, glucose etc). The heart’s own function will have also been damaged, making it less efficient due to the scarring of the muscle- ACE (angiotensin converting enzyme) inhibitors work to restore the heart and improve its function. On the other hand, if a patient is admitted as an emergency they are given aspirin, an anti-platelet agent, which prevents the possibility of a clot forming again as it reduces platelet coagulation. Thrombolysis can also be used, where a drug such as Tissue Plasminogen Activator is injected intravenously to dissolve the clot and does so quickly. Angioplasty can also be used, where a wire with a small balloon is placed into the artery and inflated, widening the lumen and allowing blood to flow through the vessel again.
In terms of prevention, the best method of prevention of CHD is to stop smoking, estimates vary but smoking related deaths from CHD per year stand at approximately 25,000 deaths a year and regular exposure to second hand smoke increases the risk of CHD by 25%. Smoking contributes to existing plaques and will quicken Atherosclerosis further increasing the risk of episode. Following stopping smoking is a chance in diet and lifestyle, with little exercise and large amounts of fatty foods a change in diet can slow the growth of plaques. However, as stated before, diet plays a relatively small role and this can only do so much as the damage is already done
Sources
· http://www.ehow.com/how-does_5151206_high-pressure-cause-heart-disease.html
· http://www.bhf.org.uk/publications/publications_search_results.aspx?m=simple&q=chd+statistics
· Professor Martin Bennett
By Jonathan Bennett