Effects of tar in tobacco smoke on the gaseous exchange system

• stimulates extra cell division +thickening of the epithelium;
• which may develop into a tumour;
• tar coats the epithelium lining of the breathing tubes;
• causing irritation of the epithelial cell;
• epithelia replaced by scar tissue;
• production of excess mucus by the goblet cells;
• paralysis of cilia;
• build up of pathogens + mucous;
• smoker‘s cough/emphysema;
• reduced surface area for gaseous exchange;

 

Effects of tar and carcinogens in tobacco smoke on the gaseous exchange system

• paralyses/destroys cilia;
• stimulates over secretion of mucus by goblet cells;
• growth of scar tissue;
• leads to development of bronchitis/emphysema;
• epithelial lining coated with tar;
• carcinogens;
• combine with DNA/chromosomes of cells in the bronchial epithelium/lining;
• leading to tumour growth/growth in the epithelium/lining;
• bronchial carcinoma;
• malignancy;
• metastasis/secondary tumours;

 

The effects of nicotine and carbon monoxide on the cardiovascular system

Nicotine

• causes constriction of arterioles;
• stimulates release of adrenaline;
• increase heart rate/blood pressure;
• reduced peripheral blood flow;
• less blood flows to the skin/hands/feet (blood supply to extremities reduced);
• increased stickiness of blood platelets;
• increases cholesterol levels;
• which may lead to atherosclerosis;
• due to formation of atheromas
• increases likelihood of thrombosis;

 

Carbon monoxide

• combines with haemoglobin;
• to form a stable compound;
• haemoglobin has a greater affinity for carbon monoxide than oxygen;
• decreases oxygenation of blood/lead to shortage of oxygen;
• increases strain on the cardiovascular system to supply oxygen to all tissues;
• blood vessels more vulnerable to the development of atherosclerosis; – may lead to CHD/stroke;

 

Describe how atherosclerosis develops.

• onset may be caused by damage to lining of artery;
• smooth muscle cells proliferate at site of damage;
• phagocytes invade breaks and release growth factors and stimulate the growth of smooth muscle cells/accumulation of cholesterol/slow down passage of LDLs back into the blood which therefore deposit more cholesterol)
• usually large arteries;
• deposit is called atheromas;
• (uneven) patches develop called plaques/atheromatous plaques;
• causes walls of artery to thicken/lumen narrow;

 

Explain how atherosclerosis may lead to death

• plaques roughen the lining of artery;
• may lead to slow development of a blood clot/thrombus over the plaque;
• causes cessation or restriction of blood flow to affected area;
• if in coronary artery can cause coronary thrombosis heart muscles starved of oxygen (myocardial infarction) and becomes damaged/dies/heart attack;
• if in brain can cause cerebral thrombosis/stroke; if clot breaks away can travel through blood vessels and jam at a narrower vessel (embolism);
• narrowing of arteries causes rise in blood pressure;
• may weaken wall of artery;
• wall may stretch/balloon out to form aneurysm, causing bursting of wall/hemorrhage; – cerebral hemorrhage causes strokes;

 

Link between atherosclerosis and coronary heart disease

• atherosclerosis is the main cause of CHD;
• coronary arteries become narrower;
• therefore blood pressure increases;
• can damage walls of arteries/cause aneurysm, causing wall to burst;
• atheromas roughen lining of arteries causing blood clots/thromboses;
• clot can block coronary artery;
• clot may break away and lodge where artery narrows/embolism; – heart muscle is deprived of oxygen and diets;

 

Evaluate the epidemiology and experimental evidence linking smoking to lung cancer and early death

Epidemiology

• more smokers died of cancer;
• number of woman developing cancer increased with number of women smoking
• number of cigarettes smoked per day increased per day linked with death rate;

 

Experimental

• carcinogen identified in tar;
• dogs exposed to cigarette smoke developed tumours; rate of tumour development reduced when filter tipped brands used;

 

Discuss the epidemiological and experimental evidence which links smoking with disease.

• more new diseases in smokers;
• compared to non-smokers
• the higher the number of smokers the higher the number of sufferers
• experimental animals exposed to smoke developed diseases;
• compared to those not exposed to smoke;
• animals exposed to smoke have higher chances of developing disease – filtered vs. unfiltered

 

Why sporting performance is lowered by smoking

• carbon monoxide combines with hemoglobin;
• to from carboxyhaemoglobin;
• up to 10% decrease in oxygen transport by blood/slight anemia;
• reduces endurance activities;
• nicotine stimulates sympathetic nervous system;
• release adrenaline/epinephrine;
• increase in heart rate;
• raised blood pressure;
• reduced appetite;
• dust not removed from lungs;
• reduced lung efficiency;

 

How cigarette smoking can lead to coronary heart disease

• main cause of CHD is atherosclerosis;
• carbon monoxide/nicotine in smoke responsible;
• cholesterol deposited in inner layers/linings of artery walls form plaques which lead to restriction of blood flow/clotting which can block vessels; smoking increases blood cholesterol/fat level;
• nicotine causes constriction of coronary arteries/arterioles;
• rise in blood pressure makes damage to walls more likely;
• increases number of platelets stimulating formation of blood clots;
• nicotine makes platelets more sticky;
• smoking causes rise in ratio of VLDLs/LDLs, to HDLs in blood so more atherosclerosis/cholesterol deposited;
• decrease concentration of antioxidants/Vitamin C/vitamin E, so increasing damage to artery walls by free radicals;

 

The difficulty in achieving a balance between prevention and cure of coronary heart diseases.

• due to life style;
• such as smoking/diet/lack of exercise most causes can be avoided;
• government could take steps to encourage change of life;
• a few patients are victims of their own genetic;
• cure is expensive;
• g. heart transplants/coronary by-pass/drug treatment;
• ethical problems of who to treat, suitable example;
• since donors are few;
• problems associated with tissue rejection;
• should patient change their life style before treatment is made available

 

Arguments for diverting funds from the treatment of coronary heart disease to its prevention

• cure is expensive;
• g. heart transplant, coronary by-pass, drug treatment;
• difficult to find enough donor hearts;
• ethical problems of who to treat e.g. father with young family; many of the risks are avoidable; associated with life style –  change will make people less  susceptible;

 

Discuss the factors that should be taken into account when deciding how to share limited resources between prevention and treatment of coronary heart disease

• treatment is expensive due to technology and professional expertise of surgeons;
• after – care also expensive (immunosuppressant drugs, e.t.c.);
• NHS working on tight/limited budget;
• preventive measures cheaper;
• not so dependent on expensive equipment/manpower;
• very expensive to advertise/train/employ health educators;
• difficulty in disseminating information;
• prevention saves a lot of suffering for potential victims;
• and families;
• g. may cause financial difficulties if wage earner affected/fatherless family/e.t.c;
• in terms of years of healthy life gained preventive measures may be better;
• great demand for treatment because heart disease so common;
• moral dimension – if a treatment is available should we not make resources available to use it; – more lives can be saved by preventative measures;

 

Global distribution of CHD

• mainly confined to developed/affluent countries;
• due to lifestyle + sedentary work;
• fatty diets;
• high saturated fats;
• cigarette smoking;
• alcohol intake;
• obesity; high blood pressure; lack of exercise; fast foods;

 

Reasons why coronary heart disease is so common in developed countries.

• caused by many factors most of which are common in developed countries;
• smoking s common risk factor;
• carbon monoxide and nicotine are the components responsible;
• carbon monoxide reduces oxygen carrying capacity;
• increasing strain on the cardiovascular system;
• nicotine increases stickiness of platelets, raising risk of clotting;
• diets tend to be rich in saturated fats;
• increased blood cholesterol and hence atherosclerosis;
• cause rise in ratio of LDLs to HHDLs;
• hypertension/high blood pressure common which puts arteries under strain; – lack of exercise is a risk factor and life style/ occupations often sedentary

 

Common categories of diseases which could be applied to coronary heart disease.

• physical;
• non-infectious;
• self – inflicted;
• degenerative;
• social;
• links with diet/lifestyle of developed countries;
• inherited;