Gas Exchange and Smoking

Human Gas exchange System

Trachea

Inner membrane covered in cilia, C-shaped rings of cartilage at the front and side which help protect the trachea and keep it open. Not complete circles due to oesophagus immediately behind the trachea - partially collapses to allow the expansion of the oesophagus when swallowing large pieces of food. Smooth muscle allows it to regain its shape.

Cartilage – stops the respiratory tract from collapsing

Cilia and goblet cells mucus traps solid particles cilia use periodic beating motion to move the trapped particles up for clearance.

Mucous glands Glands are abundant in the upper respiratory tract, but there are fewer lower down and they are absent starting at the bronchioles. The same goes for goblet cells, although there are scattered ones in the first bronchioles.

Smooth muscle and elastic tissue Smooth muscle starts in the trachea, where it joins the C-shaped rings of cartilage. It continues down the bronchi and bronchioles, which it completely encircles. Instead of hard cartilage, the bronchi and bronchioles are composed of elastic tissue.

Bronchi Irregular rings of cartilage surround the bronchi, and as the bronchi get smaller it forms small plates and islands Smooth muscle is present As the cartilage decreases, the amount of smooth muscle increases.

Bronchioles narrow tubes, less than 1 millimeter in diameter. No cartilage Change diameter to either increase or reduce air flow using smooth muscle.

An increase in diameter is called bronchodilation and is stimulated by either epinephrine or sympathetic nerves to increase air flow. A decrease in diameter is called bronchoconstriction and is stimulated by Histamine, parasympathetic nerves, cold air, chemical irritants and other factors to decrease air flow.

Alveoli Very thin walls of squamous epithelium for gas exchange Surrounded by a network of capillaries Approximately 3 million alveoli within an average adult lung.

Alveoli have elastic fibres in the walls to allow the alveoli to expand when breathing in but regain their shape when breathing out.

Process of gas exchange

Key features of respiratory surface Thin – one cell thick alveoli next to one cell thick capillaries. Therefore diffusion distance small so it will be quick. (0.3μm thick) Large – many alveoli and capillaries therefore large area for gas exchange. Moist – alveoli covered in a thin layer of moisture to allow gases to dissolve before moving.

Smoking

Tar and carcinogens 40 known carcinogens in tobacco smoke Causes mutations Tar stimulates mucus production

Lung Cancer Carcinogens cause mutations in the epithelial cells. It then spreads into the lymphatic system and will then spread around the body. Takes 20 – 30 years to develop. Symptoms include coughing up blood.

Chronic Bronchitis ≡ Damage and blocking of the airways. Tar stimulates goblet cells to produce more mucus. It also weakens and destroys cilia which stops the mucus from being removed. This leads to infections in the alveoli and blockage of the bronchioles. Infections like pneumonia develop.

Emphysema Inflammation of the lungs causes phagocytes to leave the blood and line the airways. To reach the lining they release elastase which destroys elastin in the alveoli walls so the phagocytes can fit through.

No recoil occurs in the alveoli and the bronchioles collapse trapping air and causing the alveoli to rupture. Air is not refreshed and the surface area decreases so gas exchange decreases. People with emphysema have a rapid breathing rate, and often need to move around with a cylinder of oxygen.

Chronic Obstructive Pulmonary Disease (COPD) When chronic bronchitis and emphysema occur together. Causes 30 000 deaths in the UK alone every year. Only noticeable once half the lung is destroyed so not reversible.

Nicotine The main drug Highly addictive Travels to brain in a few seconds Stimulates nervous system to reduce diameter of arterioles and to release adrenaline Heart rate and blood pressure increase Blood supply to the extremities decreases Increases stickiness of platelets increasing blood clots Damages lining of artery walls

Carbon Monoxide Joins with haemoglobin to form a stable compound carboxyhaemoglobin. Haemoglobin not fully saturated with oxygen. Strains the heart during exercise Carbon monoxide also damages lining of arteries

Cardiovascular diseases Smoking is one of the major risk factors for heart attack. The risk of developing coronary heart disease (CHD) increases with length and intensity of exposure to cigarette smoke. Among people less than 65 years of age, it is estimated that 36% of CHD in men and 33% in women is attributable to cigarette smoking. In all cases, risk increases with increased consumption.

Coronary Heart Disease (CHD) CHD has two principal forms - angina and heart attacks. Both occur because the arteries carrying blood to the heart muscle become blocked or narrowed, usually by a deposit of fatty substances, a process known as atherosclerosis. Angina is a severe pain in the chest brought on by exertion and relieved by rest. A heart attack is due to obstruction of a coronary artery either as a result of atherosclerosis or a blood clot: part of the heart muscle is deprived of oxygen and dies.

Atherosclerosis is a condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol. Smoking increases blood cholesterol levels. Cigarette smokers also have raised fibrinogen levels and platelet counts which make the blood more sticky. As the blockage progresses, blood flows less easily through rigid and narrowed arteries and the blood can form a thrombosis (clot). This sudden blockage of an artery may lead to a fatal heart attack, a stroke or gangrene of the leg.

Stroke When blood supply to part of the brain is blocked due to atherosclerosis then that part is starved of oxygen and it dies. Smokers are more likely to develop a cerebral thrombosis (stroke) than non-smokers. A form of cerebral haemorrhage (subarachnoid) is more common in smokers, especially among women who also take the contraceptive pill.

Epidemiological vs experimental evidence Epidemiologists collect data look for correlations in lifestyle Experimental Carry out experiments

Epidemiological evidence linking smoking to disease A survey started in 1951 in the UK Statistical facts: regular smoker 3 times more likely to die prematurely More cigarettes per day the earlier they die Pulmonary disease increases with number smoked 98% of emphysema sufferers are smokers Death rate from lung cancer 18x greater in smokers

Experimental evidence linking smoking and disease Dogs made to inhale smoke directly or through a filter. Dogs without filters developed lung cancer and pulmonary disease. Chemicals trapped in filters were then analysed Discovered tar contains carcinogens

Prevention of CHD Reduce risk by making lifestyle changes. Eg. stopping smoking eating more healthily doing regular exercise

Cure of CHD Coronary artery bypass surgery Expensive ($80 000 +) May not last more than 5 years Drugs taken after to keep blood from clotting

Heart Transplant A heart transplant is surgery to remove a damaged or diseased heart and replace it with a healthy donor heart High risk as body may reject it. Finding donor with tissue match Expensive ($145 000)