Coronary Heart Disease |
- Arteries supplying the heart become narrowed and the blood supply to cardiac tissues is reduced
- Heart has to work harder to force blood through narrowed vessels / blood pressure increases
- Angina
- Chest pain due to severe shortage of blood to the heart muscle - cells do not die
- Pain only occurs during activity but not at rest
- Caused by narrowing of coronary arteries (atherosclerosis)
- Heart attack (myocardial infarction)
- When a coronary artery is totally blocked by a thrombus/embolus
- No blood supply to heart muscle and cells die - often fatal
- Heart failure
- Blockage leads to damage of heart muscle and to gradual weakening of muscle
- Less efficient pumping
- Often accumulation of blood on right side → enlargement of heart
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Causes of Coronary Heart Disease |
| The main cause is atherosclerosis |
- Often called hardening of the arteries
- Inner layer of artery wall thickens with deposits of
- Cholesterol
- Fibrous (scar) tissue
- Dead muscle cells
- Blood platelets
- Fats, in the form of lipoproteins, accumulate beneath the endothelium
- Form plaque on the wall of arteries, also called atheroma
- Arteries become less elastic and partially narrowed
- Accelerated by high blood pressure
- Arterial endothelium damage is more likely but also leads to further weakening
- Aneurysm: weak walls may burst leading to severe loss of blood (haemorrhaging)
- Brain aneurysm is called a stroke
- Atheroma increases the risk of blood clotting
- Thrombus (blood clot) may break away and lodge elsewhere in the circulation (e.g. brain, heart)
- Circulating thrombus is called an embolus
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Cholesterol and Atherosclerosis |
- Cholesterol has important functions and is needed for
- Vitamin D production in skin
- Sex hormone production in gonads and adrenal glands
- Making cell membranes
- Make bile acid (salts)
- Cholesterol is an alcohol, not a fat but has properties similar to fats - soft, waxy, and insoluble (difficult to remove if deposits form)
- Cholesterol is transported in the blood stream from the liver to tissues
- Safe transport is needed due to its insolubility
- This is achieved by lipoproteins, which are soluble fatty proteins
- These are wrapped around the cholesterol
- Usually, only small amounts of free cholesterol escape
- Fatty streaks adhere to wall of arteries - Atheroma/atherosclerosis/plaque forms
- Narrows lumen of artery
- Damages endothelium
- Can lead to formation of thrombus/blood clot
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Lipo-Proteins |
| Low density lipo-proteins LDL's |
- Carry cholesterol from the liver to the tissues
- Normal levels: some cholesterol 'leaks' from the lipoprotein and is absorbed to build cell membranes
- High levels: too much cholesterol leaks out
- Cholesterol is deposited on the arterial walls
- White blood cells are trapped within the cholesterol
- Free radicals are released by white blood cells and react with cholesterol
- This damages artery wall which allows further cholesterol deposits (i.e. Atherosclerosis)
- Blood platelets are activated and stick to damaged areas releasing clotting factors (thromboxanes)
- Healthy arteries produce anti-clotting factors (prostaglandins)
- Normally a balance between these two. Healthy vessels do not form clots
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High density lipo-protein HDL's |
- Carry cholesterol away from tissues, including artery walls
- Travels to liver, is broken down and removed with bile
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Smoking |
- Reduces levels of antitoxidants (vitamins), more damage due to release of free radials by phagocytes
- Nicotine constricts arteries causes platelets to stick together → vasoconstriction → heart must work harder to force blood through → increases blood pressure [EXAM]
- Raises conc. of fibrinogen (in blood) → increased risk of clotting
- Higher blood pressure causes damage to blood vessel lining/endothelium/collagen [EXAM]
- Leads to rise on blood platelets and makes them more sticky/form a plug/adhere to collagen fibres
- Release of thromboplastin/thrombokinase
- Fibrinogen converted to insoluble fibrin
- Platelet plug trapped by fibrin mesh
- Raises blood cholesterol by causing a rise in LDLs in blood
- Carbon monoxide reduces the efficiency of the blood in terms of carrying oxygen
- Haemoglobin combines with CO more readily than with oxygen → forms carboxyheamoglobin
- Associated with plaque formation
- Principle CHD = heart muscle receives inadequate amount of blood or oxygen/(coronary) blood supply reduced
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Cure of coronary heart disease |
- Lower blood pressure
- Drugs which regulate heart rate/beat - prevent abnormal rhythms (beta blockers)
- Drugs which prevent blood clotting making thrombosis less likely (warfarin)
If drugs fail:
- Heart by-pass
- Vein from the leg is used to by-pass the blocked region of the coronary artery
- Involves open heart surgery
- Angioplasty
- Deflated balloon-like device is passed up to the heart via the aorta
- Guided into damaged coronary artery and inflated to stretch the artery
- Transplant
- Need to find a suitable donor
- Need to prevent rejection → drugs that suppress immune system needed for rest of life
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Prevention is more cost effective then treatment |
| 1. Screen the population for |
- High blood pressure
- High cholesterol
- Stop smoking, healthier diet, more exercises
- Men over 35 are at highest risk
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2. Monitor the behaviour of the heart during exercise |
- Difficult but encouraging the population to adopt a more healthy lifestyle from an early age is important
- Often leads to changes in diet and weight management
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3. Giving up smoking and reducing alcohol intake |
- Reduces blood pressure
- Many people do not heed the advice until it is too late
- Coronary heart disease is a long-term degenerative disease, starts at birth
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Lung cancer |
- Tar in smoke contains several carcinogens (cancer causing agents)
- Cause mutations in the genes which control cell division (oncogenes)
- Divide uncontrollably to produce a mass of cells - tumour
- Tumour cells do not respond to signals from nerves and hormones
- Continue to grow
- No programmed cell death occurs
- A small group of tumour cells is called a primary growth. It may be
- Benign - does not spread from its origin
- Malignant - spread throughout the body invading other tissues and destroying them
- Cells breaking off malignant tumours from secondary growth cause cancer to spread - metastasis
- Hard to find and remove them in this state
- Tumour may take many years to develop with few or no real symptoms
- Well advanced when discovered
- If the respiratory system is involved:
- Symptoms like coughing up blood and blocked airways leading to diseases like pneumonia are common
- Removing a whole or part lung may be effective provided metastasis is not well advanced
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Smoking and lung cancer risk |
- Risk increases if
- Smokers start young
- Inhale deeply
- More cigarettes are smoked per day
- The cigarettes are high tar
- Smoking goes on over a long period of time
- Risk decreases if smoking stops
- Smokers 18x more likely to develop lung cancer than non-smokers
- One third of all deaths from cancer can be attributed to smoking
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Genes and Cancer |
- 3 types of evidence support a link
- Tendency to develop cancer seems to be inherited
- Tumour cells in some cancers have abnormal chromosomes
- There is a positive correlation between mutations and carcinogens
- Genes causing cells to become cancerous are called oncogenes (oncology = study of cancer)
- They are found when proto-oncogenes, normal versions of genes, mutate and become overactive
- The RAS proto-oncogene codes for plasma membrane proteins called G-proteins
- G-proteins enable cells to respond to growth factors
- These G-proteins are normally activated by one of their own enzymes GTPase
- The mutant ras gene produces GTPase deficient G-proteins / they remain active longer causing tumours
- Myc oncogenes (chromosome 8)
- Myc proto-oncogenes produce proteins needed for transcribing genes required for normal cell division
- Common mutation switches the myc proto-oncogenes to chromosome 14 where it acts as an oncogene / abnormal cell division / tumour
- When both ras and myc oncogenes are present together, malignant cells will result
- Tumour suppressor genes
- Associated with cell division
- Converted to oncogenes by mutation and reduce normal activity by inhibiting cell division
- Might inhibit transcription of the proto-oncogenes like myc
- May become overactive → tumour
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