Edexcel

Unit 1

Structure of the Heart

Arteries and Veins

The Cardiac Cycle

Atherosclerosis

Estimating Risk

Identifying Health Risks

Prevention and Treatment of CVD

Blood Pressure

Carbohydrate Structure

Lipids

Energy Budget

Cholesterol

Caffeine affecting heart rate

Vitamin C

Dipole

Positive H

Negative O

Electrostatic attraction between water molecules forming Hydrogen bonds

Water molecules ‘stick together’

Components:

1. Plasma

2. Erythrocytes

3. Leucocytes

4. Platelets

Functions:

1. Transports; digested food to diff parts of the body, food molecules from storage areas to cells that need them, excretory products to e.g. kidneys or lungs, hormones

2. Keeps body temp regular

3. Acts as a buffer to pH changes

Thrombosis is used by the body to prevent lots of blood being lost when a blood vessel is damaged. A series or reactions occurs that leads to the formation of a blood clot.

1. Platelets releases two main substances; serotonin and thromboplastin.

2. Serotonin causes smooth muscle of blood vessels to contract. Blood flow cut off from damaged area.

3. Thromboplastin triggers the conversion of prothrombin (large protein) into thrombin (an enzyme)

4. Thrombin then catalyses the conversion of fibrinogen (soluble protein) to fibrin (solid insoluble fibres)

5. The fibrin fibres tangle together and form a mesh in which platelets and red blood cells get trapped – forms a blood clot.

Fibrin fibres have tangled together to form a mesh.

Learn the names of the different valves, arteries and veins for the exam.

Also known as Atrioventricular valve.

Arteries: Narrow lumen. Smaller the further

away from heart.

Smallest branches are ‘arterioles’

Thick muscular walls with elastic fibres

Near heart=more elastic fibres and collagen(for strength and flexibility)

Far from heart=more muscle tissue

Smooth lining allow easy blood flow

No valves

Pumps oxygenated blood to the body

Blood at high pressure

Veins Wide lumen

Thinner walls (less smooth muscle with few elastic fibres)

Less collagen than arteries, but outer tough layer of mainly collagen fibres

Has valves to stop backflow

Pumps deoxygenated blood to the heart

Blood at low pressure

Every time the heart contracts, blood is forced into arteries and their elastic wall stretch to accommodate the blood.

When the heart relaxes, the elasticity of the artery walls causes them to recoil behind the blood, helping to push the blood forward.

Pressure falls further away from heart

The heart has a less direct effect on the flow of blood through the veins.

In the veins, blood flow is assisted by the contraction of skeletal muscles during movement of limbs and breathing.

Backflow is prevented by semi lunar valves within the veins

The steady flow without pulses of blood means that the blood is under low pressure in veins

Valves preventing backflow

One cell thick

No collagen, smooth muscle or elastic fibres

Allows quick diffusion of gases

Phase 1: Atrial Systole

(Ventricles are relaxed) The atria contract, decreasing the volume of the chamber and increasing the pressure inside the chamber This pushes the blood into the ventricles. AV-valves are open

There is a slight increase in ventricular pressure and chamber volume as the ventricles receive the ejected blood from the contracting atria.

(The atria relax). The ventricles contract, increasing their pressure. The pressure becomes higher in the ventricles than the atria, which forces the atrioventricular valves shut to prevent back-flow.

The pressure in the ventricles is also higher than in the aorta and pulmonary artery, which forces open the semi-lunar valves and blood is forced out into the arteries.

Phase 2: Ventricular Systole

The ventricles and atria both relax. The higher pressure in the pulmonary artery and aorta closes the semi-lunar valves to prevent back-flow into the ventricles.

Blood returns to the heart and the atria fill again due to the higher pressure in the vena cava and pulmonary vein. This starts to increase the pressure of the atria.

As the ventricles continue to relax, their pressure falls below the pressure of the atria and the atrioventrivular valves open this allows blood to flow passively into the ventricles from the atria

The atria contract and the whole process starts again.

Phase 3: Diastole

Pulmonary vein

Or Atrioventricular valve

Or Atrioventricular valve

Vena Cava

Pulmonary Artery

Aorta

What is it?

Means ‘hardening of the arteries’

It is the disease process that leads to coronary heart disease and strokes.

Fatty deposits can either block an artery directly, or increase its chance of being blocked by a blood clot (thrombosis) – the blood supply can be blocked completely and cells can be permanently damaged.

The endothelium (smooth lining of blood vessel) becomes damaged. result from high blood pressure which puts an extra strain on the layer of cells, or from toxins in cigarette smoke in the bloodstream.

Then there is an inflammatory response once the inner lining of the artery is breached. White blood cells leave the blood vessel and move into the artery wall accumulates chemicals e.g. Cholesterol.

A fatty deposit builds up called an atheroma

A hard swelling called a plaque occurs as fibrous tissue and calcium salts build-up around the atheroma. Artery wall loses some of its elasticity. THIS IS ATHEROSCLEROSIS.

Plaques cause the artery to become narrower. This makes it more difficult for the heart to pump blood around the body and can lead to a rise in blood pressure.

Now there is a dangerous positive feedback plaques lead to raised blood pressure and raised blood pressure makes it more likely that plaques will form

Angina: gripping pain in the chest, breathless, narrowed coronary arteries (from a formation of a plaque) cannot supply enough oxygenated blood and heart muscle has to start anaerobically respiring.

Myocardial Infarction (Heart Attack): coronary artery becomes fully blocked, heart muscle starved of oxygen. Many as a result of atherosclerosis. A clot that forms in a blood vessels is known as a ‘thrombosis’

Interruption to normal blood supply in an area of the brain

Either from bleeding from damaged blood capillaries or blockage of blood vessel

Symptoms: FAST: face etc.

Risk – ‘the probability of occurrence of some unwanted event or outcome’

The statistical chance of something unfavourable happening is supported by scientific research e.g. The actual risk of dying from CVD is 60% higher for smokers than non-smokers.

People’s perception may be different from actual risk

May overestimate the risk e.g. May have known someone who smoked and died from CVD, therefore think if you smoke you will die of CVD. Articles and media give constant exposure which make people worry

Underestimate risk, could be due from lack of information making them unaware of the factors that contribute to diseases like CVD.

Lifestyle risk factors for CVD:

1. Diet – high in saturated fats increases blood cholesterol level leads to atheroma formation, which leads to blood clots and therefore heart attack or stroke. High is salt increases risk of high blood pressure.

2. High blood pressure – increases risk of damage to the artery walls, which increases risk of atheroma formation leads to CVD.

3. Smoking – CO combines with haemoglobin and reduces amount of oxygen transported in the blood.

4. Inactivity – lack of exercise increases risk of CVD as it increases blood pressure

Factors beyond your control

1. Genetics - inherit particular alleles that make them more likely to have high blood pressure or high blood cholesterol, more likely to suffer from CVD

2. Age – risk of developing CVD increases with age. Arteries lose some of their elasticity

3. Gender – men are 3 times more likely to suffer from CVD than pre-menopausal women

Antihypertensives Include diuretics, beta-blockers,

Sympathetic nerve inhibitors, ACE inhibitors

Reduce high blood pressure – less chance of damage to artery walls.

Benefits – different antihypertensives work in different ways, so can be given in combination. Blood pressure can be monitored at home

Risks – coughs, swelling of the ankles, impotence, tiredness, fatigue and constipation. Not serious compared to risks of high blood pressure

Reduce blood cholesterol level by reducing amount of cholesterol abosorbed by the gut

Block the enzyme in the liver that is responsible for making cholesterol

Benefits – reduce risk of developing CVD and atherosclerosis forming

Risks – muscle and joint aches, nausea, constipation, diorrhoea

Statins

Sold in spreads and yoghurts

Similar structure to cholesterol

Reduces amount of cholesterol being absorbed from your gut into your blood

Makes it easier for body to deal with cholesterol and reduces level of LDLs in your blood

Anticoagulants

E.g. Warfarin. Reduce blood clots (thrombosis) – blood clots are less likely to form at sites of damage in artery walls. Interferes with production of prothrombin

Benefits – used to treat people who already have blood clots or CVD or who have just had heart surgery. Prevent any existing blood clots from growing any larger and prevent any new blood clots from forming

Risks – if person is badly injured, the reduction of blood clotting can cause excessive bleeding, which can lead to fainting or even death. Other side effects are allergic reactions, osteoporosis and swelling of the tissues.

A type of anticoagulant

They work by making platelets less sticky so they don’t clump together to form a blood clot e.g. aspirin, clopidogrel

Benefits – can be used to treat people who already have blood clots or CVD, (but can’t get rid of existing blood clots)

Risks – side effects including, irritates stomach lining, rashes, diarrhoea, nausea, liver function problems and excessive bleeding

Platelet Inhibitory Drugs

Elevated blood pressure, known as hypertension, is considered to be one of the most common factors in the development of CVD.

Systolic pressure – pressure in the artery is at its highest, ventricles have contracted and forced blood into arteries

Diastolic pressure – pressure is at its lowest in the artery when the ventricles are relaxed

A sphygmomanometer is used to measure blood pressure

Blood pressure is reported in 2 measures

Systolic pressure, the max blood pressure when the hearts contracts

Diastolic pressure, the blood pressure when the heart is relaxed

What determines blood pressure?

Contact between blood and the walls cause friction, this impedes the flow of blood – peripheral resistance

If the smooth muscles in the walls of an artery contract, the vessels constrict , increasing resistance – blood pressure is raised.

If the smooth muscles relax, the lumen is dilated, so peripheral resistance is reduced and blood pressure falls.

Any factor that causes arteries or arterioles to constrict can lead to elevated blood pressure e.g. Natural loss of elasticity with age, adrenaline, high-salt diet.

Carbohydrates are the main energy supply in living organisms.

Most carbohydrates are large, complex molecules composed of long chains of monosaccharides

Glucose is a monosaccharide with 6 carbon atoms in each molecule

Structure of alpha- glucose.

Monossaccharides are joined together by glycosidic bonds in a condensation reaction

When 2 monosaccharides join together, they form a disaccharide

Names of disaccarides:

1. Maltose – glucose and glucose with a 1-4 glycosidic bond

2. Lactose – glucose and galactose, 1-4 glycosidic bond

3. Sucrose – glucose and fructose, 1-2 glycosidic bond

Two alpha glucose molecules can be joined together by a CONDENSATION REACTION in which a molecule of water is formed from two -OH groups in the two molecules

The remaining O atom forms a link between the carbon 1 of one glucose molecule and the carbon 4 of the other. This is called a 1,4 glycosidic link.

The disaccharide formed from two glucose molecules is MALTOSE.

Water is formed in this reaction

A polysaccharide is formed when more than 2 monosaccharide join together

Lots of glucose molecules are joined together by 1-4 glycosidic bonds to from amylose.

Animal cells get energy from glucose. Store excess glucose as glycogen. Lots of side branches – glucose can be released quickly. Very compact molecule. Insoluble in water, doesn’t cause cells to swell by osmosis. Large molecule, store lots of energy.

Starch is the main energy storage material in plants. Plants store excess glucose as starch Starch is a mixture of two polysaccharides; amylose & amylopectin.

Long, unbranched chain of glucose joined together with glycosidic bonds. Has a coiled structure to make it compact – good for storage as you can fit more in to a small space

Long branched chain of glucose . Side branches allow enzymes that break down molecules to get to the glycosidic bonds easily. Glucose can be released quickly

Triglycerides are a type of lipid

It is made up of one molecule of glycerol with 3 fatty acids attached to it. The fatty acid molecules have long tails made of hydrocarbons The tails are hydrophobic. These tails make lipids insoluble in water. All fatty acids consist of the same structure, but the hydrocarbon tail varies .

Triglycerides are formed by condensation reactions and broken up by hydrolysis reactions

Three fatty acids and a single glycerol are joined together by ester bonds

A hydrogen atom on the glycerol molecule bonds to a hydroxyl (OH) group on the fatty acid, releasing a molecule of water.

Reverse happens in hydrolysis – molecule of water added to each ester bond to break it apart, and the triglyceride splits up into 3 fatty acids and one glycerol molecule .

Saturated and unsaturated lipids

Saturated – animal fats (butter)

Unsaturated – plants (olive oil). Melt at a lower temp

The difference between these 2 types is their hydrocarbon tails.

Does not have double bonds between carbon atoms – every carbon is attached to at least 2 hydrogen atoms. ‘saturated’ with hydrogen.

Has double bonds between carbon atoms. Double bonds cause the chain to kink. If 2 or more, the lipid is called polyunsaturated.

You need a constant supply of energy to maintain your essential body processes which are ongoing, even when you are completely at rest.

Basal metabolic rate (BMR) is the name given to energy needed for essential processes.

Normal weight – equal energy input and output

Underweight - illness, diet, eating disorder. Excessive exercise, stress, high BMR

Overweight – overeating and low exercise

It is a lipid made in the body

Some is needed to function normally

Needs to be attached to protein to be moved around, do the body forms lipoproteins

High density lipoproteins (HDLs)

1. Mainly protein

2. Transport cholesterol from body tissues to the liver where it’s recycled or excreted.

3. Function is to reduce total blood cholesterol when level is too high

Low density lipoproteins (LDLs)

1. Mainly lipid

2. Transport cholesterol from liver to the blood, where it circulates until needed by cells

3. Function is to increase total blood cholesterol when level is too low.

A diet high in saturated fats increase the rick of CVD. This is because it increases blood cholesterol level. This increases atheroma formation which can lead formation of blood clots which can cause heart attacks and strokes.

Investigation: observe daphnia through a microscope to see the effect of caffeine on the heart rate.

1. Make up a range of caffeine solutions of different concentrations, with control solution with no caffeine

2. Transfer one daphnia into dimple of cavity slide

3. Place slide onto the stage of a light microscope and focus on bating of the heart

4. Place small drop of caffeine solution onto daphnia

5. Count number of heartbeats in 10 secs and multiply by 6 to calculate beats per min.

6. Repeat with all caffeine solutions, keeping all factors constant

7. Compare results to see how caffeine concentration affects heart rate.

Ethical Issues:

1. Studying animal allows scientists to study things unethical to study using humans

2. But using animals can also be seen as unethical – can’t give consent

3. Some believe more acceptable to perform experiments on invertebrates than on vertebrates – simpler organisms which have much less sophisticated nervous system

4. Could cause distress or suffering to living organism

Investigation to test how much vitamin C is in fruit juices:

1. Have about 6 different fruit juices of known concentrations

2. Measure out a set volume of DCPIP into a test tube

3. Add one of the fruit juices to the DCPIP, drop by drop, using a pipette.

4. Gently shake the test tube after each drop of fruit juice is added

5. When the solution turns colourless, record the volume of fruit juice that has been added

6. Repeat experiment twice more, with same solution to record an average

7. Make sure all other variables are kept constant

8. Use the results to make a line graph, showing volume of vitamin C solution against its concentration – calibration curve

9. This means an unknown solution can be tested in same way to find vitamin C content