topic 1

1.1 - limitations of diffusion

• All organisms require transport systems for absorbion and waste disposal
• multicellular organisms require a more complex transportation system as they cant rely on diffusion
• Larger organisms have larger Surface area to volume ratios and so a specialised transport system os required
• For example an elephant has a very small surface area compared to its volume, so unlike and single celled organism, cant rely on diffusion from the air, so instead it must use another method for the distribution of oxygen and other substances to its cells - for an elephant this could be a circulatory system. 

1.2 - properties of water

• water is a dipole = it has two charges
• Ionic substances dissolve easily in water as their positive elements are attracted to the negative ends of the water molecule and the negative elements to the positive ends of the water - making them hydrated (surrounded by water)
• Polar molecules also dissolve easity as they are hydrophilic (water loveing)
• Non polar molecules do not dissolve in water as they are hydrophobic (water hating) e.g; lipids (to enable transport in blood, lipids combine with proteins to form lipoproteins)
• Thermal properties:
• heats and cools slowly
• high BP due to lots of hydrogen bonds

1.3 - structure of blood vessles and their function

Arteries:

• Thick muscle + elastic fibres = allows elastic recoil to prevent damage and maintain high BP
• Narrow lumen = high BP

Veins:

• Thin walls + less muscle = under lower pressure
• have valves to prevent backflow
• wider lumen

Capillaries:

• wall of single cells (endothelial cells) = quick diffusion pathway
• very small lumen 

1.4i - cardiac cycle

• systole of the mycocardium (heart muscle tissue) generates pressure changes which result in movement of blood
• blood flows from high to low pressure
• Events on the left and right side of the heart are the same, just at different pressures
• STAGE 1 - ATRIAL SYSTOLE AND VENTRICULAR FILLING:
• The ventricles relax and blood flows into them through the atrio-ventricular valves (whoch open due to high pressure) from the atria as they contract
• STAGE 2 - VENTRICULAR SYSTOLE:
• The atria relax the ventricles contract, and blood is pumped from the ventricles into the aorta and pulmonary artery. This pressure forces the atrio-ventricular valves shut and opens the semi-lunar valves. The start of ventricular contraction coincides with the first heart sound.
• STAGE 3 - DIASTOLE:
• The ventricles relax, their pressure falling below that of the arteries. The semi-lunar valves close to prevent backflow into the ventricles due to their high pressure. The cycle begins again and blood from the vena cava and pulmonary veins enter the atria

1.5 - Atherosclerosis cycle

• Stage 1 - Damage: 

• The first step and so the cause of atherosclerosis is damage to the endothelium of an artery.

• The endothelium is a very thin layer of cells that lines the inside of an artery and thus is quite vulnerable to damage from the high pressure blood flow that an artery (the blood vessel that carries blood away from the heart) has to deal with.

• Damage to the endothelium can also occur from the toxins that are found in cigarette smoke and therefore it is said that smokers are more at risk from atherosclerosis (and so heart attacks and stroke) than other people.

1.5 - atherosclerosis cycle

• stage 2 Inflammatory response:

• After the endothelium has been damaged, an inflammatory response occurs.

1.5 athrosclerosis 

• Stage 3 - sclerosis

• Fibrous tissue and calcium salts add themselves to the atheroma formed.
• This creates a hard plaque (hard swelling of the aterial wall)

• As a result, elasticity of the artery is lost.

1.5 atherosclerosis 

• Stage 4 - positive feedback

• Since the plaques make the artery narrower (by taking up space in the lumen), blood pressure is raised.

• Higher blood pressure increases the chance of atherosclerosis and therefore as atherosclerosis increases, the chance of acquiring further atherosclerosis increases (positive feedback).
• Atherosclerosis can lead to heart attacks and strokes, so the more that form, the higher the risk of irreversable damage.

1.6 clotting cascade 

• platelets, vitamin K and calcium ion form a plug on the wound
• This stimulates the protein thromboplastin to be released
• Thromboplastin turns prothrombin into its active state, thrombin
• Thrombin recruits soluable fibrinogen out of the blood
• Fibrinogen is then converted into insoluble fibrin.
• The fibrin can then reinforce the plug on the wound and seal the wound, stopping bleeding.

1.7 CVD risk factors

• High blood pressure - Hypertension inreases the chances of atherosclerosis as a higher systolic blood pressure can cause damage to the arteries, this activates the positive feedback. 
• Obesity - obesity comes with an increased risk of CVD as being obese is linked to a hightened blood pressure, this makes atheromas more likely.
• Blood cholesterol - High levels of LDL cholesterol (lipids) can lead to atherosclerosis as the lipids build up in arteries, forming plaque, which reduces the size of the lumen, increasing the pressure within the artery.
• Smoking - Smoking damages the lining of arteries, leading to the formation of an atheroma, which increases blood pressure and the chance of getting further atheromas (positive feedback)which inturn increases the chance of getting heart attacks or strokes.
• Inactivity - Inactivity can mean there is a 30-50% greater risk of developing high blood pressure, which can lead to atherosclerosis and further damage.
• Genetic inheritance - if there is inheritance of high blood pressure or other factors that effect ones cardiac health, the risk of CVD increases.
• Age - CVD is most common among people over 50, and men have a higher chance of developing it.

1.11 i - Energy budgets and diet

• Carbohydrates, lipids and proteins provide energy in our diet
• Energy is measured in calories:
• one calorie is the quantity of heat required to raise the temperature of 1cm3 of water by 1 degree 
• normally they are displayed as kilocalories
• 4.18 joules (j) of energy = 1 calorie
• 1kj = 1000j

1.11 ii - Consequences of energy imbalance

• There are daily energy requirements for men and women called EAR's (estimated energy requirements) 
• If you consume more energy than you are using, there is risk of weigh gain and over time becoming obease, which can in turn lead to more serious health problem such as CVD.
• If you consume less energy than you are using, your body takes energy from your fat stores, meaning you loose weight, however, your body can become depleted of all fat stores, and weightloss becomes unhealthy and you may no longer have the energy to maintain essential body proccesses e.g; heart pumping breathing and body temp.
• If your energy intake is the same as your output, assuming no other factors are acting, your mass should stay the same, maintaining a healty diet ensures this. 

1.12 i - the different saccharides:

• monosaccharides:
• single sugar units e.g: glucose, galactose and fructose
• general formula of (CH2O)n, where n is the number of carbon atoms in the molecule
• hexose sugar have 6 carbon atoms
• disaccharides:
• Two single sugar units e.g: Surcrose, maltose and lactose
• join in a condensation reaction
• forms glycosidic bond

• carbons are numbered anticlockwise from the oxyge
• Polysaccharides:
• polymers made up of simple sugar monomers
• joined by glycosidic bonds into long chains
• they can be branched and unbranche
• e.g; starch, cellulose and glycogen.

1.12 ii - roles of the saccharides

• monosaccharides = Organisms can store these simple sugars after eating them to be used for energy later. When in the presence of oxygen, glucose and the rest of the monosaccharides can be broken down into their constituent parts. This releases energy, which is why monosaccharides are used primarily as a source of energy
• Disaccharides = After people eat foods containing disaccharides, the stomach and small intestine break them apart. The small intestine absorbs the resulting monosaccharides, sending them into the bloodstream and ultimately to the liver, which converts them all to glucose.
• Polysaccharides = Polysaccharides, sometimes called “glycans”, have two roles: some, like starch or glycogen, help store the energy we gain from consuming food. Others help with cell structure.

1.13 - saccharide bonding

• disaccharides = two single sugar units can bond in a condensation reaction releasing a water molecule - the bond between sugars is known as a glycosidic bond
• Maltose (disaccharide) has a 1-4 glycosidic bond
• Polysaccharides = polymers made up of simple sugar monomers joined by glycosidic bonds into long chains by a condensation reaction. 
• Starch, cellulose and glycogen are all polymers of glucose. 

1.14 i - synthesis of triglycerides

• Triglycerides are made up of three fatty acids and one glycerol molecule linked by condensation reactions

• The Bond that forms between the fatty acid and the glycerol is known as an ester bond 
• There are three ester bonds formed in a triglyceride 

• each bond formation is a condensation reaction that releases a water molecule

1.14 ii - saturated and unsaturated lipids

• If the fatty acid chains in a lipid contain the maximum number of hydrogen atoms they are saturated
• in saturated lipid the hydrocardon chain is long and straight
• There are no carbon to carbon double bonds in saturated fatty acid chains so no more hydrogen can be added
• the hydrocarbon chains can pack closely together as there are strong intermolecular bonds between triglycerides made up of saturated fatty acids - so they are solid at room temperature.
• Unsaturated fats:
• monounsaturated fats have one double bond between two of the carbon atoms in each fatty acid chain
• polyunsaturated fats have a larger number of double bonds
• A double bond causes a kink in the hydrocarbon chain
• these kinks prevent the hydrocarbon chains from packing closely together 
• the increased distance between chains weakens the intermolecular forces

1.15 i - cholesterol 

• Cholesterol is a short lipid molecule wich is a vital component of cell membranes - with roles in thwir organisation and functioning
• LDL - Low density lipoprotein = LDL's circulate in our bloodstream and bind to receptor sites on the cell membrane
• LDL's are involved in the synthesis and maintenance of cell membranes
• Excess LDL's overload the receptor sites, reulting in high blood cholesterol levels - the LDl's are sometimes then deposited in the artery walls forming atheromas.
• HDL's have a higher percentage of protein and less cholesterol compared to LDL's 
• HDL's are made when triglycerides from fats combine with cholesterol and protein
• HDL's transport cholesterol from the body tissues to the liver where it is broken down
• this lowers blod cholesterol levels and helps remove the fatty plaques of atherosclerosis.

1.18 - treatments of CVD

• antihypertensives = reduce blood pressure:
• ACE inhibitors = reduce the hormone which causes vasocontriction - can cause dizziness and abnormal heart rhythm
• Calcium channel Blockers = blocks calcium from muscles so the muscles dont constrict - can cause swollen ankles and headaches
• Diuretics = increase the volume of urine produced which decreases cardiac output - can cause dizziness and muscle cramps
• statins = Reduce cholesterol levels:
• Statins = inhibits the enzyme which produces LDl's - can cause vomiting and weak muscles
• anticoagulants = reduces the risk of clotting
• Warfin = interfeers with the production og vitamin K and so effects the synthesis of clotting factors - can cause bleeding
• platelet inhibitors = reduces the clotting factors of platelets
• clopidogrel = reducess the stickiness of platelets - can cause severe bleeding in high ammounts
• Asprin = reduces the stickiness of platelets - can cause bleeding in gastointestinal track.