- Created by: Laura McCartney
- Created on: 03-01-13 18:08
Into two catergories: Infectious-caused by microorganisms (harmful) called pathogens i.e. bacteria and viruses. non infectious-not caused by microorganisms but may be genetic or caused by lifestyle factors.
Can enter body through interfaces: Breaks in skin, gas exchange system, reproductive and urinary system, lining of digestive system (attach to cells that form this lining)
Digestive system consists of gut (tube extending from mouth to anus) Food is mixed with digestive juices made by gland cells and contains enzymes, secreted as squeezed through muscular walls of gut. Enzymes act on large insoluble molecules of protein, starch and fats. Protein--->amino acids, Starch--->glucose, fats--->fatty acids and glycerol. absorbed through walls of small intestine into blood and transported to body cells.
Cellulose cant be digested by human gut, it just passes out the anus with cells scraped from the gut lining, enzymes and bacteria, egested as faeces.
4 stages: Ingestion, digestion, absorption and egestion.
Carbohydrates and digestion
Carbohydrates, proteins, lipids-molecules organic, all contain carbon and can form 4 chemical bonds can form long straight or branched chains. Macromolceules are very large organic molecules made up of monomers, several monomers join together to form polymer.
Condensation reaction of two monomers (see notes for diagram) Condensation: removal of molecule of water. Hydrolysis: broken down with addition of molecule of water. Larger parts that remain are residues joining of lots of monomer residues form polymers.
Carbohydrate molecule contains carbon, hydrogen and oxygen. twice as many hydrogen atoms as oxygen (same as water). 3 main types of carbohydrates: monosaccharides: single sugars, contain different numbers of carbon atoms i.e. glucose, fructose and galactose, contain six carbon atoms. Disaccharides-contain two monosaccharide residues i.e. sucrose, maltose and lactose. Polysaccharides-very large molecules, contain many monosaccharide residues i.e. starch.
Glucose and other sugars
Glucose- monosaccharide-single sugar. C6H12O6
a-glucose: glucose, galactose, fructose-molecules arranged in different ways, gives slightly different properties.
(see notes for diagram of a-glucose bonding to form maltose) made by condensation reaction (H2O removed) held by glycosidic bond 1,4.
Lactose is formed by a-glucose and galactose, sucrose: a-glucose and fructose.
a-glucose boiled with benedicts solution, orange precipitate formed Cu(II) ions in the benedicts solution are reduced to orange Cu(I) ions. because of the way chemical groups are arranged. these are called reducing sugars. Fructose, maltose and galactose are reducing sugars. sucrose is a non-reducing sugar but if it is boiled with dilute acid, hydrolysed to monosaccharides so is split into a-glucose and fructose which are reducing sugars can be then tested with benedicts.
Starch and digesting carbohydrates
Starch test-drop of iodine if positive then will turn blue/black. mixtures of two substances=amylose and amlyopectin polymers made by large number of a-glucose molecules joined by condensation reaction.
Amylose-long chain of a-glucose residues, the joining together of the amino acids is the primary structure, linked by glycosidic bonds, the chain is soiled into a spiral. hydrogen bonds hold its shape. Amylopectin-branched chains of a-glucose residues.
digesting carbohydrates: glucose can be absorbed as soon as it reaches small intestine because they are small enough to pass through. starch---> broken down to maltose---> then glucose. starch--->maltose is by amylase, and by the reaction hydrolysis. maltose---> glucose is broken down by maltase also by hydrolysis. amylase and maltase are proteins that act as catalysts.
Proteins and protein structure
Proteins are made up of amino acids--> 20 different amino acids can be joined in any order. fibrin forms a mesh of threads over surface of a wound trapping red blood cells and forming a scab. Blood contains enzymes which are proteins, buiret reaction tests for proteins. NAOH added then few drops of copper sulphate if positive then will turn mauve.
Amino acid-general structure. Central carbon atom- a-carbon, attached to four groups of atoms, (-NH2)-amino group. (-COOH)-carboxyl group, (-H)-hydrogen atom, R-group this is the only group that differs in amino acids all others stay the same.
Amino acids join to form Dipeptide with peptide bonds by condensation reaction so H2O is released. (see notes for diagram) Many amino acids joined form an unbranched chain that is a polypeptide. Polypeptides can be broken down by hydrolysis into amino acids
Polypeptides and proteins
Protein, one or more polypeptide chains folded into a complex 3D shape. different proteins=different shapes. the shapes are determined by the order of the amino acids in the polypeptide chains. sequence of amino acids is the primary structure. Genes carry genetic code which enables cells to make polypeptides and ensures sequence is the same in all molecules of particular polypeptide. changing one amino acid in primary structure causes change in the shape of the protein this presents it carrying out its normal function.
parts of polypeptide chain fold in regular way, the way it is folded is its secondary structure. sometimes coils to produce spiral or a-helix. other parts of chain may form B-pleated sheet. two or more parts run parallel linked by hydrogen bonds. Ribonuclease-124 amino acids. Twisted/folded chain of secondary structure, may fold further to give whoole polypeptide molecule a globular shape-->tertiary structure is also determined by sequence of amino acids.
Different types of bond between different amino acids help to maintain shape of protein. hydrogen bonds-between R groups, not strong, easily broken, many of them. Disulphide bonds-formed between amino acids which have sulphur in their R-groups, quite strong, less easily broken than hydrogen bonds. Protein has quarternary structure if has more than 1 polypeptide chain. Haemoglobin has a quarternarry structure- 4 polypeptide chains.
How enzymes work
Activation energy is necessary to start a reaction (see notes for diagram of graph) Cells produce the enzyme catalase. Its substrate is hydrogen peroxide. Catalase lowers activation energy needed to breakdown the reaction of hydrogen peroxide.
Ribonuclease is an enzyme which breaks down RNA (ribonucleic acid) there are different forms of Ribonuclease, it has amino acids of cysteine-->contains sulphur, so disulphide bonds form between these.
Enzymes, substrates and products. If mix enzyme solution with biuret reagent it turns violet. Somewhere on the surface of the enzyme, amino acids form a pocket (active site for the enzyme) when ezyme catalyses particular chemical reaction, substrate molecule collides with active site binds and forms unstable, enzyme-substrate complex which then breaks down to form product molecules. Enzyme molecule is not used up in reaction, so it is now free to bind with another substrate molecule. (see notes for diagram of enzyme-substrate complex forming)
Enzymes and models
Enzymes are specific--> each one catalyses just one type of reaction with one type of substrate. i.e. Amylase can only hydrolyse its specific substrate, cant hydrolyse other substances. Emil Fischer produced the lock and key model. active site of enzyme like a lock and substrate is like the key. When you heat an enzyme it denatures it. Heat alters its shape, including shape of active site, so substrate no longer fits. A substance with molecules shaped like the substrate can stop activity of an enzyme. Similar shape of a molecule which is not the substrate could fit but a reaction doesnt happen, it blocks off the site, so substrate molecule cannot bind and react there. Molecules like this compete with the substrate molecules, this inhibiting reaction is called competitive inhibition.
Various parts of emzyme molecules move- some small, some not. this new model which shows this is called the induced fit model. (see notes for diagram) Substrate does not fit precisely until it binds with enzymes active site. Active site then changes shape and moulds round substrate. e.g. Hexokinase enzyme binds to glucose. Glucose+ATP---> glucose 6-phosphate + ADP
Properties of enzymes
High temperatures, each enzyme has an optimum temperature, rate of reaction is at maximum. If the temperature increases then it increases the kinetic energy of enzyme molecules, vibrate more, breaks chemical bonds of tertiary structure of enzyme molecules, enzyme changes shape/denatured, active site also changes shape, substrate no longer fits so no enzyme-substrate complex formed.
PH- PH of solution=measure of its hydrogen ion concentration, higher concentration of H+, lower PH, more acidic solution. Changing PH above or below optimum PH affects the rate at which enzyme works. Change alters concentration of H+ or OH- ions. Small change-alter charges of amino acids., substrate molecules no longer bind. Large change- breaks bond adn enzyme becomes denatured.
Inhibitors: slow down rate of enzyme-controlled reactions. Non-competitve inhibitors-doesnt fit into active site, binds somewhere else on enzyme. Active shape changes shape, so substrate molecules no longer fit, no enzyme-subsrate complex formed. (see notes for diagram)
Increased enzyme concentration-faster reaction, increased substrate concentration results in more successful collisions. Temperatures below optimum, increase can increase kinetic energy of enzyme and substrate molecules, as result move faster. increases probabilty enzyme and subsrate will collide. Rise of 10 degrees more or less doubles rate of reaction, provided temperature stays below optimum. (see notes for graph)
Light microscopes--> long wavelength can only see objects quite large. Electron microscopes--> shorter wavelengths can distinguish objects as close together as 0.1nm Magnification: Image= Actualxmagnification (Mske sure units of length are same) Convert to smallest e.g. mm-->nm 10,000,000nm--> 10mm
Resolution: Minimum distance apart can be in order to see them as seperate, depends on wavelength. light--> 0.2ym. Increase magnification=increase size of image not always resolution. 2
Electron microscope: 1930s, electrons negatively charged so beam focused by electromagnets. electrons absorbed by molecules in the air, near vacuum created within electron chamber for it to work. Two types: Transmission (TEM)--> whole system must be in vacuum, living organisms cant be observed, staining process required even then the image is in black and white, the specimen must be very thin. Scanning (SEM)--> same limitations as TEM but doesnt have to be thin.
Process where cells are broken up and different organelles seperated out. before fractionation, tissue placed in cold, isotonic, buffered solution. because: Cold-reduce enzyme activity. Isotonic-prevent bursting or shrinking. Buffered-maintain constant PH
2 stages of cell fractionation: allows detailed study of structure and function of organelles. 1.Homogenation: cells broken up by homogeniser (blender) releases organelles from cell. resultant fluid known as homogenate filtered to remove complete cells and large debris. 2. Ultracentrifugation: fragments in filtered homogenate seperated in ultracentrifuge. For animal cells: tube of filtrate spin at low speed--> heaviest organelles (nuclei) forced to bottom to form pellet. Fluid at top (supernatant) removed, leaving nuclei pellet. Supernatant placed in another tube spun at faster speed--> next heaviest (mitochondria) forced to bottom. Process continued Nuclei---> mitochondria---> Lysosomes---> ribosomes.
Structure of Epithelial cell
Eukaryotic cells: have distinct nucleus and membrane-bound organelles, function is to absorb and secrete.
Nucelus: Controls cell activities, nuclear envelope-double membrane surrounds nucleus often has ribosomes on surface, controls entry and exit of materials and contains reactions. Nuclear pores: allow passage of large molecules. Nuceloplasm: jelly-like material makes up bulk of nucleus. Chromatin: DNA found within nucleoplasm. acts as control centre through production of MRNA and hence protein synthesis, retain genetic material. Mitochondrion: rod-shaped, responsible for production of energy-carrier molecule ATP for carbs. Epithelial cells use lots of energy in process of absorbing substances from intestines by active transport. Endoplasmic Reticulum: Rough-has ribosomes, provide large surface area fo synthesis for proteins+glycoproteins. Provide pathway for transport of materials. Smooth-lacks ribosomes- synthesise, store and transport lipids and carbs. Golgi apparatus: Stack of membranes make up flattened sacs, proteins and lipids produced by ER passed through golgi, modifies these often adding non-protein components such as carb. sorts them, adds carb to proteins too form glycoproteins, produce secretory enzymes, secrete carbs, transport, modify and store lipids, form lysosomes. Lysosomes: break down material ingested by phagocytic cells, release enzymes to outside of cell, digest worn out organelles, completely break down cells. Ribosomes: 80s type-found in Eukaryotic cells 25nm, 70s type-found in prokaryotic cells, important in protein synthesis. Microvilli: Finger-like projections, increase surface area allow more efficient absorption. Lipids: contain carbon, hydrogen and oxygen, insoluble in water, soluble in organic solvents e.g. alcohols. Main groups: triglycerides, phospholipids and waxes. main role of lipids is in plasma membranes, 3 fatty acids combined with glycerol. over 70 fatty acids. no carbon double bond-saturated. single double bond- mono-unsaturated, more than one-polyunsaturated.
One fatty acid molecule replaced by phosphate molecule. Fatty acids are hydrophobic. Phosphate molecules are hydrophilic. Hydrophilic acid, hydrophobic tail. molecules like this are known as polar.
Test for lipids: emulsion test: 1. to 2cm3 of sample add 5cm3 ethanol. 2.shake to dissolve lipid 3. add 5cm3 water and shake 4.cloudy-white-presence of lipid. Cell-surface membrane:plasma membranes. Phospholipids form bilayer sheet, hydrophilic heads point inwards intereacting with water in cytoplasm. other layer pointing outwards reacting water surrounding cell. hydrophobic tails pointing in to centre of membrane (protected) functions of phospholipids allow lipid-soluble substances to enter and leave cell. Prevent water-soluble substances to enter and leave cell. membrane is flexible. Proteins: extrinsic proteins-on surface or embedded mechanical support or recpetors, intrinsic proteins-completely span bilayer-some act as carriers provide structural support, allow active transport by forming ion channels for Na, K etc...
individual phospholipid molecules move gives membrane flexible structure. Proteins embedded in bilayer vary in shape, size and pattern like a mosaic. Diffusion-passive transport high to low, concentration gradient steeper then faster the rate. large surface area faster rate, thinner pathway faster rate. polar faster rate.
Facilitated diffusion: Passsive, relies on kinetic energy of diffusing molecules. occurs down concentration gradient, occurs at special points on plasma membrane where there are special protein molecules. proteins form water-filled channels (protein channels) across membranes allow water-soluble ions to pass through. channels selective only specific ions pass through OR carrier proteins when molecule specific to protein it binds changes shape--> released into membrane. high--> low using KE
Osmosis: Passage of water--> high--> low through partially permeable when water potentials either side of plasma membrane are equal--> dynamic equilibrium (no net movement of water) Active transport: movement of molecules/ions from low--> high using energy and carrier molecules metabolic energy in form of ATP needed-directly to move molecules to transport. against concentration gradient. carrier proteins involved. very selective specific substances transported. ATP--> ADP+ Pi
recombines=ATP for use in respiration. Villi lined with epithelial cells, good blood supply, increase SA, this all accelerates rate of absorption. Situated interface between lumen and blood. increase SA, very thin walled, move=maintain concentration gradient, good blood supply. glucose+ sodium ions enter together. Na+ AT--> NaK pump into blood takes place byh protein carrier molecule.
Comparing Eukaryotic and Prokaryotic
Prokaryotic: No true nucleus, nuclear envelope, no chromosomes, no membrane-bound organelles, no chloroplasts, ribosomes smaller, no endoplasmic reticulum, golgi and lysosomes, or cell wall.
Eukaryotic: distinctive nucleus with envelope, chromosomes present, membrane-bound organelles, chloroplasts present, larger ribosomes, endoplasmic reticulum, golgi, lysosomes present, cell wall made mostly of chitin or fungi (cellulose)
outbreak in India 1826 then advanced westwards to Sunderland England in 1831 then it rapidly spread. Starts with severe muscle pain and stomach cramps, then vomitting and fever, then diarrhoea leads to huge loss of fluid. adults can lose upto 20dm3 per day. if no treatment then the person will die because loss of too much fluid makes the circulatory system fail. John Snow investigated as he already suspected that this was spread by dirty water. He took large sample of people (300,000) so the results were assumed to be reliable. He used experimental and control groups. the control didnt drink contaminated water, experimental did. 30 years later, Robert Koch isolated the chlorea bacteria. Magnification=length in photograph/real length. Real length=length in photograph/magnification.
Prokaryotes and their structure
Prokaryote means 'before the nucleus'. they are bacterial cells: have no nucleus, contains DNA as a loop in cytoplasm, doesnt form chromosomes in nucleus, some DNA they contain the genetic material is found in tiny circular strands called plasmids. Chlorea is surrounded by cell surface membrane. (see notes for diagram) Chlorea has flagellum used for locomotion, cell wall-muciaginous layer of slime, cell surface membrane, plasmid-small circular piece of DNA, ribosomes-small, nuclear material. How chlorea causes disease: almost all the vibrio chlorae is killed in the acidic conditions in the stomach, a few may survive though it PH is above 4.5. When the surviving bacteria reach small intestine, they use the flagella to propel themselves through the mucus lining of intestinal wall. Then they start to produce a toxic protein. protein hs two parts. one part binds to specific carbohydrate receptors on plasma membrane, only epithelial cells of small intestine have these receptors so chlorea toxin only affects this region of the body. the other (toxic) part enters epithelial cells, causes ion channels of cell-surface membrane to open, so chloride ions raises epithelial cells water potential, increase of chloride ions in lujmen lowers water potential. water therefore flows from cells to lumen. Loss of ions from epithelial cells establishes concentration gradient. ions move by diffusion into epithelial cells from surrounding tissues, including blood. establishes water potential which causes water to move by osmosis from blood and other tissues into intestine. Is this loss of water from blood and other tissues into intestine that causes symptoms of chlorea, diarrhoea and dehydration. treated by restoring water and ions that have been lost using oral rehydration therapy.
Diarrhoea and treatment
Causes of diarrhoea: Damage to epithelial cells lining intestine. loss of microvilli due to toxins, excessive secretion of water due to toxins e.g. chlorea toxin. Oral rehydration therapy: just drinking water is ineffective: water is not being absorbed from the intestine e.g. in chlorea water is actually being lost by cells. It does not replace the electrolytes (ions) that are being lost from epithelial cells. Can use drip but this requires trained personnel. there is more than one carrier protein in cell-surface membrane of epithelial cells that absorb sodium ions, need to develop rehydration solution that uses these alternative pathways. As sodium ions are absorbed, the water potential of cells falls and water enters the cells by osmosis.
A rehydration solution needs to contain: Water- to rehydrate tissues, sodium- to replace sodium ions lost from epithelial cells of intestine+ to make optimum use of alternative sodium-glucose carrier proteins. Glucose- to stimulate uptake of sodium ions from intestine + to provide energy. Potassium- replace lost K ions and stimulate appetite. other electrolytes- such as chloride and citrate ions help to prevent electrolyte imbalance.
Lungs and lung disease
All aerobic organisms require a supply of oxygen to release energy in the form of ATP during respiration. CO2 needs to be released. lungs are pair of lobed structures made up of series of highly branched tubules, called bronchioles, which end in tiny air sacs called alveoli. Trachea- flexible airway supported by rings of cartliage which prevents trachea from collapsing. walls of trachea are ciliated and made of muscle. also lined with goblet cells which produces mucus which traps dirt particles and bacteria. Bronchi- also produce mucus and have cilia. Bronchioles- series of branches off bronchi, walls made of muscle lined with epithelial cells. muscle allows them to constrict, so they con control flow of air in and out. Alveoli- minute air sacs at end of bronchioles. contain some collagen and elastic fibres and are lined with epithelium. the elastic fibres allow them to stretch as they fill with air.
Mechanism of breathing
Ventilation- constant movement of air in and out of lungs. inspiration (inhalation)- when air pressure of atmosphere is greater than air pressure inside lungs, air is forced into alveoli. expiration (exhalation)- when air pressure in lungs is greater than in atmosphere, air is forced out the lungs. Pressure changes brought about by movement of two sets of muscles: the diaphragm- sheet of muscle that seperates thorax from abdomen. intercostal muscles- lie between ribs two sets: Internal intercostal muscles (contraction leads to expiration) external intercostal muscles (contraction leads to inspiration) Inspiration: uses energy, external intercostal muscles contract, internal ones relax. ribs pulled upwards and outwards, increasing volume of thorax. diaphragm muscles contract causing it to flatten which also increases thorax volume. increased thorax volume results in reduction of pressure in lungs. atmospheric pressure now greater than lungs pulmonary pressure, so air is forced into lungs. Expiration: doesnt require much energy,, internal contract, external relax, ribs move downwards and inwards, decreasing volume of thorax. diaphragm muscles relax, returning to its upwardly domed position, decreasing volume of thorax. decreased thorax volume, increases pressure in lungs. pulmonary lung pressure now greater than atmosphere so air is forced out. Pulmonary ventiliation: total volume of air that is moved into lungs in one minute. Pulmonary ventilation (dm3 min-1) = tidal volume (dm3) x ventilation (min-1)
essential features of exchange surfaces: Large surface area- speed up rate, very thin- pathway short- speedy diffusion, partially permeable- diffuse easily. Diffusion= surface areaxdifference in concentration/ length of diffusion path. Red blood cells slowed to allow more time for diffusion. Breathing movements+ heart pumping + blood flow= steep concentration gradient.
Lung disease part 1
Pulmonary tuberculosis: infectious, mainly affects lungs which are firstg site of infection. caused by one or two species of rod-shaped bacteria: Mycobacterium tuberculosis or mycobacterium bovis. symptoms: persistent cough, tiredness, loss of appetite that leads to weight loss. then fever and coughing up blood may occur. Spread through air by droplets (cough, sneeze, laugh or talk) M.tuberculosis is resistant bacterium that can survive several weeks once droplets have dried. M.bovis affects cattle so can be spread from cows to humans via milk. Mycobacterium: the bacteria grows and divides within upper regions of lungs where there is a plentiful supply of oxygen. Bodys immune system responds and white blood cells accumulate at site of infection to ingest bacteria. leads to inflammation and enlargement of lymph nodes that drain that area of the lungs. called primary infection and usually occurs in children. In a healthy person, there are few symptoms, if any, and the infection is controlled within a few weeks, however some bacteria usually remain. many years later these bacteria can re-emerge to cause a second infection. called post-primary tuberculosis and typically occurs in adults. This infection also arises in upper region of lungs but is not so easily controlled. the bacteria destroy the tissue of lungs, resulting in cavities and scar tissue. Sufferer coughs up damaged lung tissue containing bacteria, along with blood. without treatment the TB spreads to the rest of body and can be fatal.
Lung disease part 2
Pulmonary fibrosis: when scars form on epithelial cells of lungs it arises. Lungs become too thick it needs thin wallls for effective diffusion of respiratory gases. reduces elasticy of lungs, makes it difficult to breathe out and ventilate lungs, shortness of breath , when excercising-volume of air space taken up by fibrous tissue, diffusion pathway increased, chronic, dry cough- fibrous tissue creates obstruction in airways of lungs bodys reflex is to cough up obstruction. tissue is more or less immoveable. nothing is expelled so cough is known as 'dry' Pain and discomfort in chest-pressure and hence damage from mass of fibrous tissue in the lungs and further damage and scarring due to coughing. weakness and fatigue- results from reduced intake of oxygen into the blood, this means that release of energy by cellular respiration is reduced, leading to tiredness.
Asthma: example of localised allergic reaction, caused by allergens, most common are: pollen, animal fur, faeces of house dust mites. Can be made worse by factors such as air pollutants (sulfur dioxide, nitrogen oxides and ozone), excercise, cold air, infection, anxiety and stress. one or more of these causes white blood cells on linings of bronchi and bronchioles to release chemical called histamine the effects of this are: linings of these airways become infamed, cells of epithelial lining secrete larger quantities of mucus then normal, fluid leaves capillaries and enters airways, muscle surrounding bronchioles contracts and constricts airway. There is much greater resistance to the flow of air in and out of alveoli. makes it difficult to ventilate lungs and maintain a diffusion gradient across exchange surface. Symptoms: diffculty breathing- constriction of bronchi and bronchioles their inflamed linings and additional mucus and fluid in them. wheezing sound when breathing- caused by air passing through very constricted bronchi and bronchioles. tight feeling in chest- consequence of not being able to ventilate lungs adequately because of constricted bronchi and bronchioles. coughing-reflex response to obstructed bronchi and bronchioles in an effort to clear them. Asthma tends to run in famililes. Asthma numbers are rising, could be because of: increase in air pollution, increase in stress, increase in variety of chemicals used in our food and manufactured products. Our 'cleaner' lifestyles mean we are less expposed to allergens as children so become sensitive to them in later life.
Lung disease part 3
Emyphysema: 1 in 5 smokers get this, it develops over period of about 20 years, virtually impossible to diagnose until lungs have been irreversibly damaged. healthy lungs contain large amounts of elastic tissue, mostly made of protein elastin, it stretches when we breathe in and springs back when we breathe out. Infected lungs, the elastin is permenently stretched and lungs no longer able to force out all the air from the alveoli. surface area of alveoli is reduced and they sometimes burst. as a result little or no gas is exchanged.
Symptoms: shortness of breath- difficulty in exhaling air due to loss os elasticity in lungs, tries to increase intake by breathing rapidly. Chronic cough - consequence of lung damage and bodys effort to remove damaged tissue and mucus that cannot be removed normally because cillia on the bronchi and bronchioles have been destroyed. Bluish skin colouration- due to low levels of oxygen in the blood as a result of porr gas diffusion. Lung function- to ventilate by inhalation- Asthma, to ventilate by exhalation-fibrosis and emphysema, to provide large surface area-emphysema, to provide short diffusion pathway-fibrosis.
Heart and heart disease
Heart-muscular organ that lies in thoratic cavity behind the sternum (breastbone) Human heart has two pumps lying side by side. pump on left= oxygenated blood from lungs. right= deoxygenated blood from body. Each pump has two chambers: atrium- thin walled and elastic+ stretches as it collects blood. It only has to pump blood the short distance to the ventricle, and therefore has only a thin muscular wall. Ventricle- much thicker muscular wall, as has to pump blood either to lungs or rest of body. The blood must pass through tiny capillaries in lungs in order to present a large surface area for exchange of gases, in doing so, there is large drop pressure and so with one pump, blood flow to the rest of the body would be very slow. Two pumps, returns blood to the heart to increase the pressure before it is sent to rest of body important to keep oxygenated blood on left side seperate from deoxygenated blood. Between each atrium and ventricle are valves that prevent backflow of blood into the atria when ventricles contract. There are two sets of valves: Left atrioventricular (bicuspid) valves, formed of two cup-shaped flaps on left side of heart. Right atrioventricular (tricuspid) valves, formed of three cup-shaped flaps on the right side of the heart. Each of the four chambers of the heart is served by large blood vessels that carry blood towards or away from heart. the ventricles pump blood away from the heart and into the arteries. The atria receive blood from the veins. Vessels connecting the heart to the lungs are called pulmonary vessels. The vessels connected to the four chambers are therefore as follows: Aorta- connected to left ventricle and carries oxygenated blood to all parts of body except lungs. Vena cava- connected to right atrium and brings deoxygenated blood back from tissues of the body. Pulmonary artery- connected to right ventricle and carries deoxygenated blood to the lungs where its oxygen is replenished and its CO2 removed. Pulmonary vein- connected to the left atrium and brings oxygenated blood back from lungs. unusually for a vein it carries oxygenated blood.
Suppying heart muscle with oxygen
Heart muscle is supplied by its own blood vessels called the coronary arteries, which branch off the aorta shortly after it leaves the heart. Blockage if these arteries e.g. by a blood clot, leads to myocardial infarction (heart attack) because an area of the heart muscle is deprived of oxygen and so dies. The cardiac cycle: =70bpm at rest. Known as cardiac cycle- sequence of events repeated, two phases of beating heart: contraction (systole) and relaxation (diastole). Contraction occurs seperately in ventricles and atria so is described in two stages. For some of the time relaxation takes place simultaneously in all chambers of the heart and is therefore treated as a single phase. The direction of blood flow through the heart is maintained by pressure changes and action of valves. Relaxation (diastole): Blood returns to the atria of the heart through the pulmonary vein (from the lungs) and the vena cava (from the body). As the atria fill the pressure in them rises, pushing open the atrioventricular valves and allowing blood to pass into the ventricles. The muscular walls of both the atria and ventricles are relaxed at this stage. Reduces pressure within ventricle, causes pressure to be lower than that in aorta and pulmonary artery, so semi-lunar valves in aorta and pulmonary close, accompanied by 'dub' sound of heart beat.
Contraction of the atria (atrial systole): Muscle of atrial wall contracts, forcing remaining blood that they contain (20%) into the ventricles. Blood only has to be pushed short distance, so muscular walls of atria are thin . During this, walls of ventricle wall are relaxed. Contraction of ventricles (ventricular systole) after short delay to allow ventricles to fill with blood, their walls contract simultaneously. Increases the blood pressure within them, forcing shut the atrioventricular valves and preventing back flow of blood into atria. The 'lub' sound of these valves closing is a characterisitic of the heart beat. With the valves closed the blood pressure rises forcing the semi-lunar valves open and pushing blood into the pulmonary artery and aorta. Walls of ventricles much thicker, as have to pump blood much further. Left ventricle thicker because pumps blood to extremeities but right ventricle only pumps to lungs.
Valves control blood flow: acheived this mainly by pressure created by heart muscle. Blood always moves from region of higher pressure to lower pressure. Are however different circumstances concerning pressure differences where blood could flow in opposite direction, so valves are used to prevent unwanted backflow of blood. When pressure differences are reversed, valves close. Atrioventricular valves: between left atrium and ventricle and right atrium and ventricle. Prevent backflow of blood when contraction of ventricles means ventricular pressure exceeds atrial pressure. closure of these valves ensures that, when the ventricles contract, blood within them moves to the aorta and pulmonary artery rather than back to the atria. Semi-lunar valves- in aorta and pulmonary artery. These prevent backflow of blood into ventricles when recoil action of elastic walls of these vessels creates greater pressure in the vessels than in the ventricles. Pocket-valves- in veins that occur throughout venous system. These ensure that when veins are squeezed e.g. when skeletal muscles contract, blood flows back to the heart rather than away. Valves are made up of number of tough, flexible flaps off fibrous tissue cusp-shaped. When pressure is greater on convex side of these cusps they move apart to let blood pass between them. When it isnt, blood collects within the 'bowl' of these cusps, this pushes them together to form a tight fit that prevents the passage of blood. The pressure can be so great within the ventricles that the atrioventricular valves are at risk of becoming inverted. To prevent this valves have string-like tendons attached to pillars of muscle in ventricle wall.
How its controlled
cardiac muscle is myogenic (contraction is initiated from within muscle itself, rather than by nervous impulses from outside (neurogenic), as is the case with other muscles) Within the wall of right atrium is a distinct group of cells known as the sinoatrial node (SAN) here the initial stimulus for contraction originates. Sinoatrial node has basic rhythm of stimulation that determines beat of heart. Is often referred to as pacemaker for this reason. Sequence of events that controls cardiac cycle is as follows: wave of electrical activity spreads out from SAN across both atria causing them to contract. Layer of non-conductive tissue (atrioventricular septum) prevents wave crossing to the ventricles. Wave of electrical activity allowed to pass through second group of cells (atrioventricular node (AVN)) which lies between atria. AVN after short delay conveys wave of electrical activity between ventricles along a series of specialised muscle fibres called 'bundle of His'. 'Bundle of His' conducts wave through atrioventricular septum to base of the ventricles, where bundle branches into smaller fibres. Wave of electricity activity released from these fibres causing ventricles to contract quickly at the same time, from apex of heart upwards. Mammals have closed circulatory system, the blood is confined to vessels, allows pressure within them to be maintained and regulated.
Coronary heart disease (CHD) affects pair of blood vessels (coronary arteries) which supply heart muscle wih glucose and oxygen for respiration. build up of fatty deposits in vessels known as atheroma impairs blood flow. If blood flow back to heart interrupted can lead to myocardial infarction (heart attack) An atheroma is a fatty deposit which forms within wall of artery, begins as fatty streaks-accumulations of white blood cells that have taken up low density lipoproteins. If the streaks enlarge= atheromatous plaque which is most common in larger arteries made up of cholesterol, fibres and dead muscle cells. Bulge into lumen of artery causes the blood vessel to narrow so blood flow is reduced. Atheromas increase the risk of thrombosis and an aneurysm.
Thrombosis: Is atheroma breaks through lining (endothelium) of the blood vessel, it forms rough surface--> interrupts smooth blood flow, may result in formation of blood clot or thrombus which may block blood vessel preventing supply of blood to tissues beyond it. Region of tissue often dies as a result of this (lack of oxygen, glucose and other nutrients) Thrombus is sometimes carried from its place of origin and lodges in another artery.
Aneurysm: Atheromas that lead to formation of a thrombus also weaken artery walls. weakened points swell to form balloon-like blood-filled structure called an aneurysm. Aneurysms frequently burst, leading to haemorrhage and therefore loss of blood to the region of the body served by that artery. Brain aneurysm known as Cerebrovascular accident (CVA) or stroke.
Refers to reduced supply of oxygen to muscle (myocardium) of heart. result of blockage of coronary arteries, if occurs close to junction of coronary artery and aorta, heart will stop beating because blood supply cut off. If blockage is further along coronary artery, symptoms milder because smaller area of muscle deprived. In britain, 500,000 people a year have a heart attack. Fewer than 1/3 die, almost all show signs of atheroma and many have coronary thrombosis.
Risk factors: smoking: 2-6 times more likely to suffer from heart disease. CO (Carbon monoxide) combines with haemoglobin in red blood cells to form carboxyhaemoglobin. reduces oxygen carrying capacity of blood. the heart therefore must work harder, raised blood pressure and raised risk of CHD and stroke. reduction of oxygen-carrying capacity means that heart may not be supplied with O2 during excercise so leads to chest pain (angina) or in severe cases myocardial infarction. Nicotine stimulates production of adrenaline which increases heart rate and blood pressure also makes platelets more 'sticky' leads to higher risk of thrombosis, strokes or myocardial infarction.
High blood pressure and cholesterol
High blood pressure can be genetic, caused by prolonged stress, from poor diets, lack of excercise. There are already high blood pressure in arteries, heart must work harder to pump blood into them therefore more prone to failure. High blood pressure more likely to develop aneurysm and burst causing haemorrhage. To resist high pressure walls of arteries may thicken and harden restricting blood flow.
Cholesterol: essential component of membranes, needs to be transported, carried in plasma as tiny lipoproteins, high density lipoproteins remove cholesterol from tissues and transport to liver for excretion. help protect against heart disease. Low density lipoproteins transport from liver, tissues and artery walls, infiltrate and lead to atheroma and heart disease.
Diet: high salt-raises blood pressure. High saturated fat- increase low density lipoproteins and blood cholesterol concentration. Antioxidants e.g. vitamin C reduce risk of heart disease and so does non-starch polysaccharide (dietary fibre)
Defence mechanisms: non-specific- do not distinguish between one pathogen or another, respond to all in same way. takes 2 forms: barrier to entry of pathogens, phagocytosis. Specific- do distinguish, responses less rapid but provide long-lasting immunity. Involves white blood cells called lympocyte and takes two forms again. a) cell meditated responses involving T-lympocytes b) humoral responses involving B lympocytes.
Recognising own cells: specific lymphocytes are not produced in response to an infection, they already exist. So many, that it is likely that when a pathogen enters the body there will be a lymphocyte with complementary protein ready. (lympocyte will 'recognise' pathogen) Right protein lympocyte is stimulated to build it up to a level where it can destroy the pathogen- why there is a time lag.
First line of defence is to form a physical or chemical barrier. Next is the white blood cells. Phagocytes: ingest, destroy pathogen by phagocytosis before it can cause harm. Lymphocytes-involved in immunity. Protective covering-skin covers body, providing physical barrier. Epithelia covered in mucus-pathogens stick to mucus then transported away by cilia up trachea to be swallowed into stomach. Acid in stomach-provides low PH enzymes of most pathogens denatured and organisms killed. Next line of defence-phagocytosis. Large particles i.e. bacteria are too big to cross cell membrane, by diffusion or active transport. so... must be engulfed by cells in form of vesicles formed from cell-surface-membrane- process called phagocytosis. type of white blood cells that carry out phagocytosis are phagocytes provide important defence against pathogens. Phagocytes can move out of blood vessels into tissues. Chemical products (chemoattractants) of pathogen act as attractants, causing phagocytes to move towards pathogen. Phagocytes attract themselves to surface of pathogen, engulf pathogen to form vesicle, known as phagosome. Lysosomes move towards the vesicle and fuse with it. Enzymes within lysosomes break down the pathogen. Soluble products absorbed into cytoplasm of phagocyte. Phagocytosis causes inflammation at site of infection this swollen area contains dead pathogens and phagocytes, known as pus. Inflammation is the result of the release of histamine which causes dilation of blood vessels this speeds up delivery of phagocytes to site of infection.
T-cells and cell-mediated immunity
Immunity is ability of organisms to resist infection by protecting against disease- causing micro organisms that invade their bodies, involves recognition of foreign material (antigens). Antigens- any part of an organism that is recognised as non-self (foreign) by immune system and so it stimulates an immune repsonse. Usually proteins part of cell-surface membrane, cell wall of invading cells.
Lympocytes: specific immune response depends on white blood cells called lympocytes. B lympocytes (Bcells)- associated with humoral immunity. i.e. immunity involving antibodies that are present in body fluids. T-lympocytes (T cells)- associated with cell-mediated immunity i.e. immunity involving body cells. Both types of lympocytes are formed from stem cells found in bone marrow. B lympocytes mature in the Bone marrow. T lympocytes mature inThymus gland.
T-lympocytes only respond to antigens. Attached to a body cell. T-lympocytes respond to organisms own cells that have been invaded by non-self material e.g. virus or cancer cell. Also repsond to transplanted material (genetically different) Because: Phagocytes that have engulfed and broken pathogen present some of pathogens antigens on own cell-surface membrane. Body cells invaded by a virus present some of viral antigens on own cell-surface membrane, as sign of distress. Cancer cells are likewise. these cells are called antigen-presenting cells. because can present antigens on own cell-surface membrane. 1. Pathogen invade body cells are taken in- phagocytosis. 2. Phagocytes place antigens from pathogen on cell-surface membrane. 3. Receptors on certain T-helper cells fit exactly on these 4.activates other T-cells to divide rapidly by mitosis and form a clone. 5. cloned T cells: a) develop into memory cells that enable rapid response to future infections by same pathogen. b) Stimulates phagocytes engulf pathogens by phagocytes. c) stimulates B cells to divide. d) Kill infected cells. Receptors on each T-cell respond to single antigen. so vast number of different T-cells to respond to different antigens. How kill infected cells: Do not kill by phagocytosis but produce a protein that makes holes in the cell surface membrane. holes means that cells become freely permeable to all substances so dies. T-cells most effective on viruses, because live inside cells.
B cell and humoral immunity
Involves antibodies- soluble in blood + tissue fluid (humour) Many different B cells, each produces different antibody. antibody is complementary to specific antigen. This type of B cell divides by mitosis to form clone of identical B cells all of which produce an antibody specific to the foreign antigen. Toxins also act as antigens. For each clone, cells produced develop into one or two types of cell. Plasma cells- secrete antibodies directly, survive only for few days. Antibodies produced destroy pathogens and toxins. Plasma cells responsible for immediate defence of body against infection. (primary immune response) Memory cell- live longer, dont produce antibodies directly, circulate in blood + tissue fluid. When encounter same antigen, divide rapidly + develop into plasma cells and more memory cells (provide long-term immunity (secondary immune response))
Role of B cells
1. surface antigens taken up by B cells 2. B cells process antigens and present them on their surfaces 3. T-helper cells attach to processed antigens on B cells thereby activating them. 4. B cells activated to divide by mitosis to give clone of plasma cells. 5.Cloned plasma cells produce antibodies that exactly fit antigens on pathogens surface. 6. Antibodies attach to antigens on pathogens and destroy (primary immune response) 7. Some B cells develop into memory cells. Can respond to further infections by same pathogen by dividing rapidly + developing into plasma cells that produce antibodies (secondary)
Antigenic variability: antigens of viruses such as flu is always changing, known as antigenic variability. Will not respond (memory cells wont remember) as changed. Only primary response can overcome infection. Body reacts as if infection is a new one o response much slower. In the meantime develop symptoms i.e. Sore throat, high temperature.
Antibodies: proteins synthesised by B cells, react with antigens on surface of non-self material by binding precisely, very specific made up of 4 polypeptide chains. one pair are long= heavy chains. Shorter= light chains, to help it bind to antigen, can change shape by moving. Antibodies have binding sites where antigens can bind to form antigen-antibody complex. Binding site different on different antibodies so called variable region. Each site consists of sequence of amino acids that form specific 3D shape that binds directly to single type of antigen. Rest of antibodies same= constant region. Binds to receptors on cells such as B-cells.
Each clone of B cell will produce a different antibody, collectively known as a polyclonal antibodies. Of considerable medical value to produce antibodies outside the body. Even better if single type of antibody isolated and cloned. Such antibodies known as monoclonal antibodies. Seperation of a chemical from a mixture. Immunoassy- calculating amount of substance in a mixture. used in pregnancy tests, urine drug tests, AIDS tests. Cancer treatment- can be made to attach only to cancer cells, activate cytotoxic drug (kills cells), cancer cells then destroyed. Transplant surgery- knock out T-cells which reject transplant organ.
Passive immunity- produced by introduction of antibodies not produced by individual, from outside source so short-lived immunity. Active immunity- stimulants production of antibodies by individuals own immune system long -lasting.
Suitable vaccine: economically available, few side effects, available transportation, production, and storing means. trained staff to adminster it, vaccinate vast majority, best done at one time so pathogen is not transmitted, known as herd immunity.
Failure: defective immune system, cant vaccinate certain people, may develop disease straight after vaccine so immune levels not high enough. Pathogen may mutate frequently, so many different types cant vaccinate against all, certain pathogen 'hide' from bodys immune system, conceal inside cells or in places out of reach i.e. intestines e.g. cholera. religious, ethical or medical reasons for not wanting vaccine.
Cholera: Oral treatment flushed out quick by diarrhoea, antigens of cholera change rapidly, mobile populations.
TB: HIV impairs immune system, overcrowded popualtion, mobile populations, lots of old people (poor immune system)