Ficks law= S.

A x difference in concentration/length of diffusion path

Magnification
Magification = size of image/size of object
Remember the 1micrometer=1000nanometers units...1m=1000mm, 1mm=1000micrometers,

Ficks Law
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Pulmonary ventilation
Pulmonary ventilation = tidal vol. x ventilation rate
(dm3min-1) (dm3) (min-1)

(dm3min-1) (min-1) (dm3)

Cardiac output = heart rate x stroke volume

Cardiac output
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Differences between microscopes 1

Light microscope: poor resolution (long wavelength of light) Electron microscopes: very short wavelength, therefore high resolution power 2 types of electron microscope: Transmission electron microscope (TEM) Scanning electron microscope (SEM) TEM: consists of an electron gun, fires a beam of electrons focused on specimen (by condenser magnet) The beam passes through a small part of the specimen, which absorbs and appears dark. It gives a phoomicrograpf of 0.1 nm SEM:directs a beam of electrons onto the specimen from above (rather than penetrating from below). The beam is passed back and forth across a portion of specimen in a regular pattern. A 3D image can be made from is pattern. SEM has a lower resolving power than TEM, approx 20nm.

Limitations of electron microscopes: whole system must be in a vaccum, therefore livig species cannot be observed, a complex staining process required and even then image only in black and white, for TEM the specimen has to be very very thin, images may contain artefacts (things that result due to the way the specimen has benn prepared.

Differences between microscopes 2

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e.g if a red blood cell was put into a hypotonic solution it would burst (lysis) due to gain in osmotic pressure, if the same red blood cell was put into a hypertonic solution it would shrink (crenulation)

Extrinsic and intrinsic protiens-how are they different

Extrinsic protiens: occur on the surface or partially embedded (never extended fully across phospholipid bilayer). They gave mechanical support to the membrane, and they act as cell receptors for molecules such as hormones. Intrinsic protiens: Completely span phospholipid bilayer from one side to the other. Some act as carriers to transport water-soluble material across the membrane while others are enzymes.

Hypertonic=not much water Hypotonic=full of water

Difference between hypotonic and hypertonic

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Pathogens points of entry

2 main points of entry: digestive system and respiratory system Defences the bodt has to prevent pathogens entering: 1. Skin: sebum, commensal, epidermis 2. Eyes: tears 3. Lungs and digestive: epithelial tissue, cillia, stomach acid, phagocytic cells 4. Vagina: vaginal acid.

Eukaryotes: Nucleus, complex membrane bound organelles, can be large Prokaryote: No nucleus, No membrane bound organelles, very small

Prokaryotes and Eukaryotes

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Nucleus
Most prominant featuire of eukaryotic cell It contains the hereditary materrial and controlls the cell It controlls throught the production of MRNA(hence protien synthesis) It manufactures ribosomal RNA and ribosomes When a cell is dividing, DNA takes the form of chromatin insdie the nucleus.

Functions of its structure: nuclear envolope: double membrane, the outer membrane continuous with endoplasmic rectiliumof the cell and often ribosomes on its surface. It controls entry and exit to the cells Pores: allow the passage of large molecules such as messanger RNA out of the nucleus. Nucleoplasm: Jell-like mterial that makes up the bulk of the nucleus. Nucleolus:makes ribosomal RNA and assembles the ribosomes

Specific: mechanisms that do distinguich between different pathogens, these responses are less rapid, but provide long lastin immunity. These responses invole a white blood cell called a lymphocyte and again takes two forms: a) Cell-mediated responses involving T cells b) Humoral responses involving B lymphocytes Non-specific: mechanisms that dont distinguish between one type of pathogen and another, responds to all in the same way. These mechanisms immediatley take 2 forms: a) a barrier to entry of pathogens b) phogocytosis

Defence mechanisms:specific and non-specific

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Mitochondria
Functions of its structure: Inner membrane:greater S.A than outer membrane due to cristae Outer membrane:controls exit an entry into the cells Cristae:provide S.A for the attachment of enzymes incvolved in respiration. More ATP reactions Matrix:contains protien, lipids and traces of DNA that allows the control to the production of their own protiens. You would find lots of mitochondria in: Muscle cells-because mitochondria are responsible for carrying the energy carrier ATP, this energy would go th muscles to hepl thwm contract. Sperm cells-ATP, energy to move (travel), Epithelial cell-uses ATP in the process of absorbing substances

They occur in the cytoplasm of the rough endoplasmic rectilium. 2 types: 80s type-found in eykaryotic cells, 70s type-found in prokaryotic cells. Large cytoplasmic granuals found in all cells.

Ribosomes
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Lysosomes
Lysosomes are formed when vesicles produced by the golgi apparatus contain enzymes such as proteases and lipases. Functions of lysosome: break down material ingested by phagocytic cells, such as white blood cells release enzymes to the outside of the cell (exocytosis) in order to destroy material around the cell. Digest worn-out organelles so that the useful chemicals they are made of can be re-used. completely break down cells after they have died (autolysis) Lysosomes break down bacteria that has been taken into the cell by: releasing enzymes to the outside of the cell to destroy to material around. Lysosomes are important for protecting the cell: because they isolate potentially harmful enzymes from the rest of the cell before releasing outside, or into a phagocytic vesicle in the cell.

In cells that need to manufacture and store lrage quantities of carbs, protiens and lipids have ver extensive ER. SER's functions: To synthesise, stroe and transport lipids, and to synthesis, store and transport carbohydrates. RER's functions: To provide a large S.A for the synthesis of protiens and glycoprotiens, and to provide a pathway for trnsport of materials (especially protiens). There are 2 types of ER: Rough RER-(has ribosomes on its surface), and smooth SER (lacks ribosomes on its surface) ER is an elaborte 3-D system of sheet like membranes speading through the cytoplasm of the cells. It continuous witht eh outer membrane.

Endoplasmic recticulum
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Fluid-mosaic model (of cell surface)

FLUID because: individual phospholipid molecules can move relative to one another. This gives; the membrane a flexible structure thats constantly changing shape. MOSAIC because: protiens that are embedded in phospholipid bilayer vary in shape, size and patter (in same way as tiles on a mosaic tiles).

Roles of lipids: Main groups: Triglycerides (fats and oils), phospholipids, and waxes. Properties: They are insoluble in water, soluble in organic solvents such as alcohols and acetones What do they contain: carbon, hydrogen + oxygen

Lipids

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An energy source waterproofing insulation protection

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Lungs
Lungs are a pair of lobes tissue made of branched bronchioles and their tiny alveoli. Structure of human gas-exchange system: Trachea: has cartilage surrounding it-to prevent the trachea from collapsing as the air pressure inside falls when breathing in. Trachea walls made of muscle lined with epithelium and goblet cells-producing mucus (cillia moves the mucus). Bronchi: has cartilage plates Bronchioles: are branched off the bronchi, made of muscle which allows them to constrict so that they can control the flow of air in and out of the alveoli. Alveoli:made of collagen and elastic fibres lined with epithelium. elastic fibres allow alveoli to stretch as they fill with air when breathing in and spring back when breathing out.

Respiratory graphs

Tidal volume: volume of air normally taken in at each breath when body at rest, usually 0.5dm3 Ventilation: breathing rate (no. of breaths per min, usually 12-20 in healthy adult) Pulmonary ventilation: total volume of air moved the lungs in one minute Vital capacity: max amount if air which can be exhaled after max inhaled (inspiration) Residual volume: amount of air left in lungs after max exhalation.
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People at greater risk: close contact with the infected, work or reside in long-term care facilities where large no. of people live in close contact, countries where TB is common, reduced immunity-(AIDS, v.young, v.old, medical condition, malnourished, alcoholics, injecting drug users, homeless). Transmission: spread throught the air by droplets, released when the infected: cough, sneeze or talk. Bacterium can survive several weeks once dried. Usually transmitted over a long period of tim with close contact. TB also spread from cows to humans, cows contract the M.Bovis bacterium.

Lung disease
3 main ones in the exam: Pulmonary fibrosis, asthma, Emphysema. Pulmonary fibrosis;arises when scars form on the epithelium of the lungs, causing them to be irreversibly thickened. Meaning that diffusion pathway lengthened, the volume the lungs can contain reduced. Resulting in: shortness of breath (due to less O2 in lungs), chronic dry cough (the fibrous tissue an obstruction in airways), pain and discomfort in chest (pressure and damage from mass of fibrous tissue), weakness and fatigue (from reduced intake of O2 into the blood-release of energy by cell respiration reduced) Asthma;is an example of a localized allergic reaction. Asthma: inflames the lining of the airways, epithelial lining secrete more mucus, fluid leaves capillaries and enters airways, muscle surrounding bronchioles contracts and restricts. Made worse by: pollutants, exercise, clod air, stress. Symptoms: difficulty breathing, wheezing sound, tight feeling in chest, coughing (reflex response to obstructed bronchioles). Emphysema;develops over a period of approx. 20 years. In emphysema lungs elastin has become permanently stretched and lungs no-longer able to force air out of alveoli (the alveoli can also burst). Symptoms: shortness of breath, chronic cough (body tries to remove damaged tissue-that cannot be removed), blushes skin coloration (reduction in levels of O2)

Symptoms: persistent cough, tiredness and loss of apetite. As disease develops fever and coughing up blood can occur. Caused by 1 of 2 species: mycobacterium tuberculosis or mycobacterium bovis An infectious disease that can affect any part of the body-though usually found in lungs as they are the first site of infection. It kills approx 2 million a year.

Pulmonary tuberculosis
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Heart components
4 chambers: Atrium: thin walled and elastic and stretches as it collects. Only pumps short distance. Ventricle: much thicker muscular walls as it has to push blood some distane (either to lungs or all around the body) Heart is built of 3 layers: Epicardium-thin and slippery to reduce friction Myocardium-muscluar layer Endocardium-thin and smooth to reduce friction Division of oxygenated an deoxygenated blood maintained by double circulation. LEFT SIDE = OXYGENATED RIGHT SIDE = DEOXYGENATED Valves: between atrium and ventricle prevents back-flow of blood into atria. There's the; left atrioventricular (bicuspid) valves and right atrioventricular (tricuspid) valves

Risk factors for lung disease

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Smoking: 90% of sufferers of COPD are/have been heavy smokers Air pollution: pollutant particles e.g sulpher dioxide Genetic make-up:more genetically likley to get diseased, some less so;explaining why some life smokers never get lung disease and others die early. Infections:people who frequently get chest infections have a higher incidence of COPD Occupation: working with harmful chemicals, gases and dusts that can be inhaled.

Supplying heart muscle with O2=supplied by its own blood vessels coronary arteries which branch of the aorta. Blockage may cause myocardial infarction.

Heart disease
Coronary arteries: carry blood away from the heart. Their function is to carry oxygenated and nutrient filled blood to the heart muscle. Right coronary artery-supplies O2 blood to walls of ventricles and right atrium Left main coronary artery-directs O2 blood to left descending artery and circumflex Left descending artery-supplies O2 blood to walls of ventricles and left atrium Left circumflex artery-supplies O2 blood to walls of ventricles and left atrium (back of the heart)

Atheroma: an accumulation and swelling in artery walls. Its a fatty deposit in the walls of the arteries, commonly referred to as atheromatous plaques. Thrombosis: the clotting of blood within a blood vessel, when the clot obstructs a vein or artery it obstructs the flow of blood. Arterial thrombosis is a blood clot within an artery-in most case follows a rupture causing an atheroma. This can be followed by a stroke, or myocardial infarction. Aneurysms: a localized, blood-filled dilation of a blood vessel caused by disease or weakening of the vessel wall. Weakness usually at branch points. Risk of having an aneurysm-rupture and clotting, rupture leads to drop in blood pressure and rapid heart rate. Blood clot can travel downstream and suffocate tissue. Myocardial infarction: occurs when blood supply to the heart is interrupted. Commonly a blockage of coronary artery following a rupture of plaque in wall of artery. This results in reduced blood supply and O2 shortage can damage heart

Pulmonary vein connected to left atrium and brings oxygenated blood back from the lungs. Pulmonary artery connected to right ventricle and carries deoxygenated blood to lungs where its oxygen is replenished and carbon dioxide removed Vena Cava connected to right atrium and brings deoxygenated blood back from tissues of the body Aorta is connected to left ventricle and carries oxygenated blood to whole body (except blood) Vessels connecting heart to lungs=pulmonary vessels

Blood vessels
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Angioplasty and stenting

Angioplasty: is a minimally invasive procedure performed to improve blood flow. The procedure is a technique used to guide a balloon-tipped catheter, along with thin plastic tube into an artery/vein where vessel narrow/blocked then inflated to open vessel then deflated and removed. Vascular stent performed with angioplasty is a small wire mesh tube permanently placed in newly opened artery/vein ti help remain opened.

Aortic pressure>ventricular=semi-lunar valve shut Ventricular pressure>aortic pressure=semi-lunar valve shut Ventricular pressure>atrial pressure=valve closing Atrial pressure>ventricle pressure=valve opens

pressure and volume changes in the heart

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Non-communicable diseases are in 5 groups: 1. Cardiovascular disease e.g stroke 2. Respiatory disease e.g bronchitis 3. Genetic diseases e.g cistic fibrosis 4. Cancers e.g Leukemia 5. Life style e.g emphysema

How do microorganisms get into the body?

They have to penetrate one of the organisms interfaces with the environment.
Interfaces of the body + common points of entry: respiratiory+digestive system How we are protected: Skin:

fatty acid-->makes skin greasy-->less moisture=less hospitable Epidermis-->dead (keratonised)-->bacteria can't stay on
Eyes:

Tears-->contain lysozyme, digests bacteria and washes away

Lungs and digestive system: Epithelial tissue-->closely packed fiberous cells Cilla-->move mucus Stomach acid-->kill microorganisms Phygocytic cells-->macrophags-->freelance white cells

Vagina:

Pathogenics diseases are communicable Microorganisms/microbes can be classed as pathogens. To be classed as pathogens they have to: Disease suggests a malfunction of the body/mind which has an adverse effect on good health.

Causes of disease

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Gain entry to the host Colonise tissues of the host Resist defences of the host Cause damage to the host tissues
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Major parts of the digestive system

Mouth: saliva-amylase, teeth Tounge: helps to swallow Oesphagus:muscles contract, moving down food Stomach: muscular wall, hydrochloric acid (pH2) Small intestine: secretes enzymes (intestinal juice), pancreatic duct brings in material, bile duct nueutralises acid (alkeline), 2nd part of intestine=absorption from villi (increasing S.A+microvilli firther incresing S.A) Large intestine: absorbs water 2 types of digestion: physical digestion, and chemical digestion Digestive enzymes: Carbohydrases-breaking carbs into monosccharides Lipases-break down lipids into glycerol+fatty acids Proteases-break down proteins into amion acids.

Producing toxins:most bacterial pathogens produce toxins. The cholera bacterium produces a toxin that leads to excessive water loss from lining of intestines. Damaging host tissues:sometimes sheer no. of pathogenscauses damage by preventing tissues functioning properly. Viruses inhibit synthesis of DNA, RNA and proteins of the host cells. Many pathogens break down the cell walls of the host cells.

How do pathogens cause disease?

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Carbohydrates
Carbohydrates are made up of a long chain of molecules. Each of the individual molecules that make up the chain are known as monomers. Carbon atoms of these monomers join to form longer chains, called polymers In carbohydrates the basic monomer is a sugar (saccharide), a single monomer=monosaccharide. Pair of monosaccharides=disaccharide. Monosaccharides general formula (CH2O)n Best known monosacharide is glucose=C6H12O6 Disacharide examples: glucose+glucose=maltose glucose+fructose=sucrose glucose+galagtose=lactose

Non-reducing sugars-some disaccharides Reducing sugars-all monosaccharides and some disaccharides (e.g maltose) When water is added to a disaccharide under suitable conditions, it breaks the glycosidic bond releasing the constituent monosaccharides. This is HYDROLYSIS. When monosaccharides join, a molecule of water is removed, this is a CONDENSATION REACTION. The bond formed is a glycosidic bond.

Glycocidic bond
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However in some people there is little, no lactase produced. This means that there is undigested lactose in large intestine, microorganisms break it down-->giving large vol. of gas=bloating, nausea, diarrohea and cramps.

Disaccharide digestion
Sucrose-must physically broken down to release it. Sucrose passes through stomach into small intestine whose lining secreats the enzyme sucrase. Sucrase hydrolyses the single glycocidic bond in sucrose molecule producing 2 monosaccharides that make up sucrose:glucose+fructose Lactose-sugar found in milk. lactose is digested in the small intestine , whose epithelial lining secreates lactase. Lactase hydrolyses the glycocidic bond that links glucose and galactose (the monosaccharides)

As baby, milk is only source of milk, so lots of lactase is produced. In adult life less milk milk in consumed therefore less lactase produces.

Lactose intolerance
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Proteins
They differ greatly from species to species. Each protein has its own unique sequence of amino acids (20 different types commonly occurring in proteins) and unique shape. Functions of proteins:

Primary structure: through a sequence of condensation reactions many amino acid monomers joined together (in a process of polymerisation). Resulting chain of hundreds of amino acids=polypeptide. The primary structure decides the ultimate shape and hence function. Proteins shape specific to function. Secondary structure: hydrogen bonds form between the -NH and -C=O groups (-NH has an overall +ive charge, -C=O overall -ive charge). This causes the long polypeptide chain to be twisted into a 3-D shape, such as the coil known as an alpha helix.

Amino acids are basic monomers which combine to make a polymer (polypeptide)-polypeptides form proteins.
structural (growth+repair) e.g collagen Enzymes (digest proteins) e.g trypsin Hormones e.g insulin Transport e.g haemoglobin Protective e.g antibodies Contractile e.g muscles storage e.g casein Toxins e.g bacterial toxins

COOH the carboxyl group H2N-the amino group R group-a range of chemical groups different in each amino acid
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H H2N C COOH R

Amino acids
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Factors affecting enzyme action

For an enzyme ot work it has to:

come into physical contact with its substrate have an active site which fits the substrate
Measuring enzyme catalyzed reactions-usually by its time-course, how long it takes forn event to run its course. The 2 most commonly measured: vol. of formation of products, disappearence of substrate e.g reduction in conc. EFFECT OF TEMPERATURE: Rise in temperature increases the kinetic energy of molecules = molecules moving around more and collide more often = increased rate of reaction. Enzyme and substrate come together more often. However at some point-usually 60 degrees enzymes is denatured (so disrupted it stops working altogether). Its permanent change. Our body temp is 37 degrees. EFFECT OF pH ON ENZYME ACTION: The pH sol. is a measure of its hydrogen ion concentration. each enzyme has an optimum pH. A change in pH reduces effectiveness of an enzyme + may eventually atop it working all together. Change in pH affects in the following ways: change the amount of amino acids that make up active site of an enzyme-as result substrate can no longer become attached to active site so enzyme-substrate complex isn't formed. Change in pH can also cause the bonds that maintain enzymes tertiary structure to break. Enzyme changes shape=changing shape of the active site=substrate no-longer fitting. Enzyme has denatured

and consequently lowers activation energy needed to break the bond. As the enzyme changes shape the enzyme puts a strain on the substrate molecule. This strain distorts a particular bond a glove fit a hand. The enzyme actually changes slightly to fit the profile of the substrate. The enzyme is flexible and can mould itself like Induced fit However substrate doesnt have the 'same shape' as active site, it has a complementary shape. they catalyse. Substrate will only fit the active site of one particular enzyme, supported by the fact enzymes are specific in reactions Lock and key model The molecule on which the enzyme fits is the substrate. This fits in to form an enzyme-substrate complex. much larger enzyme molecule. site and is made up of a relatively small no. of amino acids. The active site forms a small hollow depression within the Enzyme structure-although enzyme molecules are large overall only a small region of it is functional, known as the active more likley. Enzymes are gobular protiens that act as catalysts. They lower the activation energy of a reaction-making the reaction

Enzyme action
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Non-competitive: Attach to an area that isn't the active site, shape of active site, upon attaching itself the shape of the active site is altered in such a way that the substance no longer fits making the enzyme not fit and not function. As its not competing for same space increase in conc. wont affect the inhibitor.

Defence mechanisms
Non-specific: mechanisms that don't distinguish between one type of pathogen and another but respond to all in the same way. They take 2 forms: Barrier to entry of pathogens Phagocytosis Specific mechanisms that do distinguish between different pathogens. The response is less rapid but provides long lasting immunity. Involves a white blood cell called a lymphocyte and again takes 2 forms: Cell mediated response using T lymphocytes Humoral responses involving B lymphocytes Recognising your own cells, self and non-self: to defend body from foreign material, lymphocytes must be able to tell the difference between their own cells and chemicals and those that are foreign. If they couldn't they would destroy their own organisms and tissues.

Competitive: Bind to active site. They're competitive because compete with substrate molecule, similar shape, which allows them to occupy space, inhibiter not permanent, it doesn't stop the a reaction but slows it down. Enzyme inhibitors interfere directly or indirectly with witht the function of the active ite of an enzyme and so reduce its activity. 2 types: competitive and non-competitive.

Enzyme inhibition
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Antibodies
Antibodies are made up of 4 polypeptide chains. Heavy chains, and light chains Antibodies have a binding site where antigen fits precisely known as a antigen-antibody complex. Monoclonal antibodies: when antigens induce different B cells to multiply itself, each of these clones will produce a different antibody, known as polyclonal antibodies. If a single type of antibody can be isolated and cloned they are known as monoclonal antibodies. Function of monoclonal antibodies: separation of a chemical from a mixture immunoassay method of calculating amount of substance in a mixture, used in pregnancy testing kits and athletic drug testing kits cancer treatment-can be made to attach themselves to cancer cells, then used to activate a cytotoxic drug transplant surgery-even with close matching, a transplanted organ normally suffer some rejection because of action of t cells. produced outside the body

Feature of successful vaccination program: 2 types of immunity: Passive immunity + Active immunity

Vaccination

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Passive immunity-->produced by introduction of antibodies into individuals from as outside source. As the antibodies are not being produced by individual themselves, they're not replaced when broken, so immunity short lived. Active immunity-->produced by stimulating production of antibodies by individuals own immune system. Generally long-lasting

few side effects suitable vaccine-economical available in sufficient quantities to immunize vunerable pop. producing, storing and transporting vaccine must be avaliable possibility of vaccinating all the population-->herd immunity
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vaccination 2
why it doesn't eliminate disease: fails to immunise certain individuals individual may develop disease immediately after vaccination before immunity levels can prevent it.Many varieties of pathogen certain pathogens 'hide' from body's immune system. individuals may have objections to vaccination mobile populations poverty, wars =refugees=over crowded camps proportion of elderly on increase Ethics of vaccination: animals Side-effects who should they be tested on? Is it acceptable to trial new vaccination of health risks in a country where targeted disease common, on basis population has most to gain Majority vaccinated individual risks

Pellet-bottom of centrifuge (heaviest particles) Supernant-liquid portion of mixture 6. spun in ultracentrifuge at high speed 5. spun in ultracentrifuge at medium speed 4. Result of being spun of 10 mins at low speed=some sediment and supernant 1. 3. Homogenized tissue spun in ultracentrifuge at low speed for 10 mins 2.cut-up tissue further broken down in homogenizer 1. tissue cut up + left in cold isotonic buffered solution (cold-reduce enzyme activity, isotonicprevent cells bursting/shrinking, buffered-to maintain constant pH)

Ultracentrifugation
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Golgi apparatus
Receives protiens from ER Passes into a strict sequence It modifies proteins often adding non-protein components such as carbs and labels them adding carbs changes proteins to form glycoproteins produce secretory enzymes transport store and modify lipids form lysosomes

glycerol + 3 fatty acids ---> triglyceride + water The bond formed between them is a condensation reaction, water is removed. 3 fatty acids

Formation of triglyceride
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Diffusion
'Net movement of molecules/ions from a region where more highly concentrated ti one where their concentration is lower' all particle constantly in motion due to kinetic energy they posses Motion random, no set pattern Particles constantly bouncing off one another What affects it? conc. gradient area over it takes place thickness of barrier nature of membrane size and nature of diffusing molecule

6. control repeat using water not sample 5. Cloudy white indicates presence of lipid 4. add 5cm3 of water + shake gently 3. shake tube thourghly to dissolve any lipid in sample 2. 2cm3 of sample and 5cm3 of ethanol 1.take grease free tube Known as emulsion test:

Test for lipids

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Osmosis
'passage of ester from a region where it has a higher water potential to a region where it has lower water potential through a partially permeable membrane' Solutions and water potential-->a solute is a substance that is dissolved in a solvent. Water potential, measured in KPa Hypotonic=dilute, less negative-->bursts (lysis) Hyertonic=concentrated, more negative-->crenultion (shrinks) Isotonic=equal water potential Water moves from higher water potential to lower water potential. O-->pure water is the highest water potential.

4. other facilitated diffusion method is with protein channels across the membrane. Protein channels allow water-soluble ions+molecules to pass 3. Change in shape causes the particles to be released on the other side of the membrane 2. particles taken up by carrier proteins which as a result changes shape 1. facillitated diffusion by carrier protiens A passive process, but NO external input of energy. Not against conc gradient.

Facilitated diffusion
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Absorption into small intestine

villi+microvilli-->glucose absorbed through walls of small intestine. Villi are folded and posses finger-like projections. On the other side of villi is a rich network of blood capillaries. Villi increase S.A of small intestine and therefore accelerate rate of absorption. Villi situated at the interface between lumen and blood They increase rate of absorption: increase S.A for diffusion very thin walled therefore reducing the distance over which diffusion takes place able to move to maintain conc. gradient well supplied with blood vessels so blood can carry away absorbed molecules and hence maintain a diffusion gradient.

Role of diffusion in absorption carbs continuously digested greater conc of glucose in intestine than in blood. blood continuously moving + glucose removed by respiring cells-maintaining conc gradient also villi contain muscles that regularly contract+relax mixing contents of small intestine, ensures glucose is absorbed again maintaining conc gradient and therefore allowing diffusion to continue.

Direct active transport: Uses ATP in 2 ways: different to passive transport in these ways: 'movement of molecules or ions into or out of a cell from a region of lower concentration to a region of higher conc. using energy and carrier molecules'

Active transport

carrier proteins span cell surface molecules bind to receptors on channels of carrier proteins On inside of cell ATP bind to protein causing it to split. As result protein molecule changes shape and open to opposite side of membrane. Directly to move molecules using conc. gradient thats already there , known as co-transport
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metabolic energy in form of ATP needed Materials moved against conc. gradient Carrier proteins molecules which act as pumps are involved Process is very selective
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Cholera (vibro cholerae)

How Cholera infects the body: most bacteria killed by stomach acid Surviving bacteria reach small intestine+use their flagella to propel themselves in corkscrew fashion through mucus lining they produce a toxin protein, this protein has 2 parts 1 part binds to specific carb receptors on cell-surface membrane 2nd part enters epithelial cells which causes ion channels of cell surface membrane to open, chlorine ions that are are normally contained flood into lumen loss of chloride ions from epithelial cells raises water pot and increase of chloride ions in lumen lowers water pot. water therefore flows from cells into lumen loss of ions from epithelial=conc gradient. ions therefore move by diffusion into epithelial cells from surrounding tissues. This establishes water pot that causes water to move by osmosis from blood+tissues into intestine causes severe diarrhea+dehydration.

Drinking just water is inefficient , water not absorbed, and electrolytes (ions) that are lost. What it needs to contain:

Oral rehydration therapy

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water sodium glucose potassium electrolytes

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inspiration and expiration

Inspiration: contraction of external intercostals this pulls ribcage up and out diaphragm flattens and lowers this creates negative pressure causes lungs to inflate, drawing air from eternal environment

Expiration: contraction of intercostals while external intercostals relax ribs move down and in decreasing vol of thorax diaphragm muscles relax retuning to upwardly domed position decreasing vol in thorax positive pressure in lungs Pulmonary pressure is now greater than that of lungs, air forced out

diffusion is rapid: gas exchange:

Exchange of gas into lungs

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red blood cells slowed as pass through capillaries=more time distance between alveolar air and red blood cell is reduced (flattened against capillary wall) walls very thin alveoli have large S.A steep conc gradient by constant breathing blood flow maintains conc gradient large S.A vol ratio very thin movement of internal medium semi-permeable movement of environmental medium
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course of infection after TB bacterium inhaled

1. Bacteria grow and divide within upper regions of lungs where plentiful supply of O2 2. Body's immune system responds, white blood cell accumulate at site of infection 3. Leading to inflamation and enlargement of the lymph. This is known as primary infection 4. in a healthy person few symptoms and controlled within a few weeks howev usually some bacteria remain 5. Many years later bacteria may re-emerge and cause 2nd infection of TB, post-primary tb 6.thin infection arises in upper regions of lungs but not easily ontrolled=scar tissue 7. sufferer coughs up damaged lung tissue containing bacteria with blood. If TB spreads to rest of body can be fatal Prevention of TB: better education about TB more+better housing improved health fcilities better nutrition-immune system not weakened

contraction of ventricles: contraction of atria: Relaxation: 2 phases of beating of heart:contraction (systole) and relaxtion (diastole)

cardiac cycle

short delay to allow ventricles to fill this increases pressure within them this forces shut atrioventricular valves preventing back flow into atria muscle in atria walls contact forcing the blood they contain into ventricles blood pushed short distance during this muscle of ventricle walls relaxed
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as atria fill pressure in them rises, pushing open atrioventricular valves allowing blood to pass into ventricles Muscle walls relaxed relaxation of ventricle walls reduces pressure in ventricle causes pressure to be lower than aorta and pulmonary artery so semilunar valves in aorta lose
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How the cardiac cycle is controlled

cardiac muscle is myogenic-contraction form within itself, How it works: wave of electrical activity spreads out from SAN (sinoatrial node) across both atria, causing them to contract layer of non-conductive tissue prevents wave crossing the ventricles wave of electrical activity is allowed to pass through 2nd group of cells called AVN (atrioventricular node) then short delay conveys a wave of electrical activity along series of specialised fibersthe bundle of his Bundle of his conducts wave through atrioventricular septum to base of ventricles into smaller fibers wave of electrical activity is released from these fibers, causing ventricles to contract quickly at same time from apex of heart upwards.

Blue=none green=v.low yellow=low orange=medium red/orange=high 4. if reducing sugar turns orange/brown 3.heated in water bath 2.equal vol. of benedicts reagent 1. food sample dissolves in water 2cm3 Benedicts test!

Reducing sugars test

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Non-reducing sugars
Do benedicts test, if turns out colourless... add another 2cm3 of food sample to 2cm3 of dilute hydrochloric acid in test tube, heat for 5 mins, dilute hydrochloric acid will hydrolyse and disaccharides. slowly add sodium hydrogenate sol. to neutralise acid, test pH to check Re-test resulting sol. by heating with 2cm3 benedicts reagentin boiling water. If non-reducing present in original shape=orange/brown

if starch is present turns iodine blue/black colour 2 drops of iodine added to test solution

Test for starch

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starch digestion
enzymes are specific, usually more than 1 enzyme for a large molecule. Process as follows: 1. food taken into mouth and chewed by teeth, breaking into small pieces-large S.A 2. Saliva enters mouth from salivary glands and is throughly mixed with food during chewing 3. Saliva contains amylase=hydrolyzing any starch into maltose also contains mineral salts that maintain pH at neutral 4. food swallowed and enter stomach-->acidic conditions denaturesa amylase and prevents further hydrolysis of starch 5. After food passed into small intestine it mixes with secrection from pancreas 6. pancreatic juice contains pancreatic amylase this continues hydrolysis of remaining starch to maltose. salts produced maintain pH so amylase can function 7. muscles in intestinal walls push food along . Its lining produces the enzyme maltase. Maltase hydrolyses maltose from stach breakdown into alph glucose

3. Bond broken by hydrolysis 2. linked by a new peptide bond 1.The process is the removal of water, condensation reaction, combining an OH from a carboxylgroup of 1 amino acid and H from other amino group.

Peptide bond
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phagocytosis
process of phagocytosis: chemical products of pathogen acts as attractants causing phagocytes ti move to pathogen phagocytes attach themselves to surface of pathogen engulf pathogen forming vesicle known as phagosome lysosomes move towards vesicle and fuse with it enzymes within lysosome break down pathogen. the process is the same as digestion of food in intestine namely hydrolysis of larger insoluble molecules into smaller soluble ones. soluble products from the breakdown of the pathogen are absorbed into cytoplasm into cytoplasm of phagocyte.

Biruet test:

test for proteins

place sample sol. in test tube and add equal vol of sodium hydroxide sol. at room temp add few drops of dilute copper sulphate and mix purple colouration=presence of peptide bond and hence protein. nif no protein remains blue
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How T cels kill-not by phagocytosis, but by producing protein that making holes in the cell surface membrane 4. Activate other T cells to divide rapidly by mitosis and form clone-->t cells produce memory cells, stimulates B cells, stimulate phagocytosis, kills infected cells.

lymphocytes 2
Humoral immunity B-cells respond to antibodies in the blood and tissue fluid HOW: 1. surface antigens if invading pathogen taken up by B cells 2. B cells process the antigens and present them on their surfaces 3. T helper cells attach to processed antigens on B cells therefore activating them 4. B-cell activated to divide by mitosis to give a clone of plasma cell 5. Cloned plasma cells produce antibodies that exactlly fit antigens on pathogens surface 6. Antibodies attach to antigens on the pathogen and destroy them. This is primary immune 7. B cells develop into memory cells-->readiness to respond to a future infection by same pathogen by dividing and developing into plasma cells-produce antibodies

3. Receptors on certain T helper fits onto antigens 2. phagocyte places antigens from the pathogen on its cell-surface membrane 1. pathogens invade body cells or taken in by phagocytes Respond to organisms own cells that have been invaded by non-self. HOW FORMED: Cell mediated T lymphocytes, cell-mediated -mature in thymus gland B lymphocytes, humoral immunity-mature in bone marrow Lymphocytes are the specific response.

lymphocytes 1
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