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Smoking and diseases

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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;
  • 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;
  • 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

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  • 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;

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