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SNAB A2 Revision Notes Unit 4: Environment and

Topic 5: On the wild side
A particular species can be identified using the features (the phenotype) which are characteristic to only that species. Species with similar phenotypes are likely to be related to each other. A key of characteristics is used to identify the species Organisms are classified into families according to similarity of features. The families start of large, but rapidly become smaller. This is the basis of a hierarchical classification system Kingdom Phylum Class Order Family Genus Species There are 5 kingdoms Animals, Plants, Fungi, Protoctists, Prokaryotes You need to know the main characteristics of each kingdom

Taxonomy: the science of classifying living things. Biodiversity: the variety of life on our planet, measurable as the variety within species, between species, and the variety of ecosystems If two organisms can interbreed to produce fertile offspring they are the same species. If not, they are different species Binomial System: (2 names)

Felix catus

Italics in print Underlined in hand

Genus: tells you what group the species is from (has a capital letter)

species: tells you the exact species (small case letter)

Distinguishing Characteristics of the Kingdoms


Microscopic prokaryotic cells (2 - 5 m long rather than 10-100 m) Lack of a nucleus (DNA in cytoplasm) and possibly plasmids Lack of membrane-bound organelles Presence of 70s ribosomes No cytoskeleton

Protoctists Eukaryotic cell structure Simple body form, either unicellular, filamentous (chains), colonial (ball) or macroscopic (large and visible)

The Proctoctists kingdom tends to be full of organisms that do not fit into any other Kingdom e.g. algae and yeast Fungi Heterotrophic nutrition (get food from eating, unlike plants) Made of a network of Hyphae, which form a 3D structure called a Mycelium. (look up Module 1 notes) Call walls containing chitin

Plants The distinguishing features of the Plants are; Multicellular with eukaryotic structure Cell walls containing cellulose Complex body form Photoautotrophic nutrition (make food themselves through P/S) Presence of photosynthetic cells with chloroplasts 2 stages in the life cycle: a diploid spore-producing stage and a haploid gamete-producing stage.

Animals The distinguishing features of the Animals are; Multicellular with eukaryotic cell structure Cells without cell walls Heterotrophic nutrition


Highly organised organs and tissues including Genetic diversity nervous co-ordination The only haploid cells they have are gametes

Individuals in the same species look different (have different phenotypes). This is called variation Variation is caused by; The genotype of the individual (i.e. which alleles they have) 2. The environment

Genetic diversity describes the range of different genotypes within a species. If there are few genotypes the genetic diversity is small. If there are lots of genotypes the genetic diversity is large.
Advantages of little genetic diversity

Advantages of wide genetic diversity

Less chance of genetic disease Less chance of extinction when faced with disease (i.e. some individuals will have a phenotype that allows them to survive) Environment has less effect on phenotype Species more likely to survive environment change Species more likely to colonise Allows access to more niches, therefore less interspecific competition Natural selection & speciation can occur

All individuals have a preferential phenotype

Causes of Genetic Diversity: 1. Independent Assortment

Mutation 3. Random fusion 4. Crossing Over Independent Assortment = which allele of each pair goes into which gamete. This is caused by the orientation of homologous pairs of chromosomes during metaphase 2 of meiosis

Changes in the sequence of bases in codons (mutation) cause genetic variation. This usually occurs by DNA being improperly copied or damaged. Chemicals (mutagens) and radiation can do this. Each gamete is different. Therefore, by combining different gametes new variation occurs (random fusion). During meiosis sections of DNA are swapped between homologous chromosomes (pairs of chromosomes). This creates more variation by creating new combinations of alleles (crossing over)


Dihybrid Cross
Dihybrid Crosses are for crosses involving two different genes (2 loci).
A = Purple stem, a = Green Stem, D = Big Leaves, leaves Purple stem & Big Leaves AaDd Purple Stem & Big Leaves AaDd d = little

Parents Phenotype: Parents Genotype: Gametes:





aD F1 Genotype: AD






















ad F1 Phenotype:





9:3:3:1 A_B_ : A_bb : aaB_ : aabb Purple & Big : Purple & Little : Green & Big : Green & Little


Ecological Sampling Techniques

Biotic Factor: A living variable within the ecosystem, which affects the survival of organisms. Examples include predation, competition, and pollution from excreted waste. Abiotic Factor: A non-living variable within the ecosystem, which affects the survival of organisms. Examples include temperature, light, and water. Random Sampling (quadrats placed at randomly generated intervals) Used where habitat is uniform Removes observer bias Used in a large area Used if time is limited Systematic Sampling (quadrats placed at regular intervals) Used to show zonation Used where there is continuous variation Used to sample linear habitats (e.g. a roadside) 2 types of systematic sampling technique; Line Transect: Used where time is limited Used to visually illustrate how species change along a line Belt Transect: Produces more data, gives detail about species abundance down the line as well as range Shows species dominance down the line What interval should be used? Transects can either be continuous with the whole length of the line being sampled, or samples can be taken at particular points along the line For both line and belt transects, the interval at which samples are taken will depend on the individual habitat, as well as on the time and effort which can be allocated to the survey.

Too great an interval may mean that many species actually present are not noted, as well as obscuring zonation patterns for lack of observations.


Too small an interval can make the sampling time consuming, as well as yielding more data than is needed.

An example of a Named Environment Is the British Rocky Seashore

Abiotic Factors have more effect going up the beach

Biotic Factors have more effect going down the beach

Abiotic Factors include; dessication, salinity, wave action, temperature, water availability, substrate, aspect, pH etc Biotic Factors include; interspecific competition, intraspecific competition, predation, food availability, presence of excreted wastes

Species living in the Rocky Sea shore

Splash Zone: Lichen can survive dessication & temp variation, requires little nutrient Upper Shore: Black Tar Lichen can survive long periods without water, grows slowly, but is less tolerant to dessication than lichen. Middle Shore: Eggwrack More water availability, less temp range, but more predation from herbivores and carnivores Lower Shore: Kelp constant environment, usually submerged, lower light levels, intense competition from same and other species

Dont learn this case study if your teacher gave you notes on a different habitat. Learn this study if youre desperate

4.5.6 Adaptations of Species in trophic levels

Micro-algae Limpet Dogwhelk Crab
1. 2.



Micro-algae (Bladderwrack):

3. 4. 5.

Has bladders of N2 that allow it to float (to reach light) Tolerates fresh water Has specialised gonads (resceptacles) which release lots of sperm into the sea Has a specialised holdfast that anchors it to rocks Has fucoxanthin pigments that absorb more light than chlorophyll

3. 4.

Has a mantle organ that makes the shell Has a radula covered in teeth that grind the microalgae off the rock Has gills and breathes through a hole in its head As the limpet clamps to the rock it grinds its shell, creating a perfect fit with the rock Have no sex for their 1st year then change into males / females

Dogwhelk: Has a adapted radula that bores through barnacle shells 2. Has a grove in its shell that allows it to breath whilst boring 3. Vary in colour across species 4. Has a very muscular foot to stop the effect of wave action

Common Shore Crab: Has antennal glands, which allows it to osmoregulate (it can cope with varying salinity) 2. Can bubble air through its gills and breathe out of water 3. Strong claws for snapping open dogwhelk shells 4. Carries eggs to be released in optimum conditions

Blenny: Retains water in its gill cavity, so can survive out of water 2. Powerful jaws crush crabs 3. Has a pair of canine teeth behind main teeth 4. Young mature off-shore and then move back when mature

Oystercatcher: Long pointed beak for opening shells and picking fish out of the water 2. Can shut down the circulation in its legs to stop them cooling the whole bird 3. Has natural anti-freeze in its blood to stop the legs from freezing 4. Is intelligent and can learn techniques for opening shells


Dont learn this case study if your teacher gave you notes on a different habitat. Learn this study if youre desperate

Light Dependent Step of Photosynthesis

Light Dependent Step:


Chlorophyll absorbs light (remember chlorophyll is the trap in the bottom of the photosystem)

2. Chlorophyll emits electrons


Electrons are received by electron carrier proteins in the thylakoid membrane (electron transport chain) Electron transport chain uses high energy electrons to power the following conversions; ADP + Pi ATP and NADP + H+ + eNADPH Water is split (photolysis) to produce replacement electrons for the photosystems, H+ for the reduction of NADP and O2 which is excreted.



The purpose of the light dependent step is to produce ATP and NADPH. ATP provides the energy for converting CO2 into glucose and NADPH provides the H for glucose.


Light Independent Step of Photosynthesis



GALP Glucose

There are three steps in the Calvin Cycle;


Carboxylation: RuBP fixes CO2to form GP. This reaction is catalysed by the enzyme Rubisco Reduction: In a series of reactions GP reacts with ATP and NADPH reduced GP to form GALP (by reducing GP the NAHPH itself is oxidised, reverting to NADP) Regeneration: Some GALP is converted back into RuBP so the Calvin Cycle can continue. The rest of GALP is converted into glucose in a series of reactions.



A glucose molecule is generated every 6 turns of the Calvin Cycle


4.5.10 Thylakoid membrane = location of photosystems & electron transport chain

Stroma = site of Calvin Cycle & photolysis of water Grana provide large surface area for absorbtion of light

NPP = Net Primary Productivity (amount of stored chemical energy the plant has to use for growth. This is directly proportional to biomass) GPP = Gross Primary Productivity (amount of stored chemical energy the plant earns through photosynthesis) R = Respiration (amount of energy lost through respiration, i.e. heat, lost as CO2 etc) Best analogy is a salary. GPP is the amount of stored chemical energy the plant earns through photosynthesis. R is like income tax. The plant has to pay respiration tax because it cant photosynthesis at night & not all parts of the plant are capable of photosynthesis. NPP = disposable income: what the plant has to spend after paying tax.

Energy in Primary Consumer Lost energy NPP in plant Lost energy

Energy in Sunlight

Energy is lost between trophic levels. Energy is lost in the following ways; in respiration (mostly lost through heat), energy still present in egested food, through movement, through digestion, energy still present in excreted materials etc Of the 100% sunlight energy that reaches plants, ~3% is converted into NPP. Energy is lost in the following ways; reflected light, light of wavelengths not useful to plants, passes through leaves, lost in respiration, lost as heat etc

Evolution: the idea that one species changes into another over time Natural Selection: Darwins suggestion for the process by which evolution might occur Evolution by Natural Selection (Darwinian Evolution) 1. There is variation in a species 2. More individuals are born than the environment can sustain, so some individuals must die.

The individuals that survive tend to be those that have alleles which give them a selective advantage in their environment (i.e. they are the best adapted to their environment, e.g. camouflaged). These are the fittest

4. The fittest survive long enough to reproduce and pass their alleles onto the next generation. 5. Over a few generations the frequency of fit alleles increases and the frequency of unfit alleles decreases 6. Soon all / most individuals have the fit phenotype and the unfit phenotype is eradicated

This process continues over many generations

8. Over this time new mutations occur, which give new even better alleles


Over time the mutations accumulate in the phenotype until the organism is unable to reproduce (i.e. produce fertile offspring) with the original organisms. At this point a new species has been produced (speciation)

This process is speeded up by isolation (see 4.5.14) because this stops the influx of alleles from outside and allows new mutations to accumulate in the genotype more quickly

1798 Malthus publishes paper on population growth. Malthus noticed that the human population was expanding exponentially. He thought that the human population would outgrow its resources and that this would lead to famine and war. Darwin was influenced by this idea, because he noticed that animal populations grow exponentially and then plateau when they reach the limits the environment can sustain (i.e. the population size is determined by the environment)

1809 Lamarck publishes a mechanism for evolution based on two laws Law 1: Organs / structures grow if they are used. This means that the environment determines the phenotype of an organism Law 2: Changes are passed on to the next generation So a blacksmith, who uses his muscles all day, will grow bigger muscles. This works! But, will the bigger muscles be passed onto his children? No, so Lamarcks theory is easy to falsify.

1859 Darwin publishes the Origin of species by means of Natural Selection. He publishes with Wallace who wrote to Darwin to discuss his own ideas about evolution. They were very similar to Darwins and this prompted Darwin to publish.

Isolation is important for evolution because it decreases the size of the gene pool. This stops new alleles coming in from breeding with original alleles and speeds the accumulation of new mutations (which is what leads to speciation) The different types of isolation.

Method of isolation Ecological isolation Temporal isolation Behavioural isolation Physical incompatibility Hybrid inviability Hybrid sterility

Description The species occupy different parts of the habitat The species exist in the same area, but reproduce at different times The species exist in the same area, but do not respond to each others courtship behaviour Species coexist, but there are physical reasons which stop them from copulating In some species, hybrids are produces but they do not survive long enough to breed Hybrids survive to reproductive age, but cannot reproduce

Evolution is a theory, not a fact. Many people believe that species were created (creationism). Other people believe in evolution, but by mechanisms other than Natural Selection. You shouldnt respect the opinions of other people who have no evidence to support a theory.

Primary succession is the first stage of the ecological succession of plant life from abiotic land with no soil to fully support plant ecosystems (e.g., a forest). In primary succession, pioneer plants like mosses and lichen, start to "normalize" the habitat, creating rudimentary soil from their dead matter. These pioneer plants create conditions for the start of plant growth and so more complex plants like grasses and shrubs begin to colonise the area.

Over time the grass area is colonised by small woody plants, which give way to small trees and finally, after a few hundred years, large trees take over. The large trees represent the climax community because succession stops at this point. A good example of primary succession takes place after a volcano has erupted. The barren land is first colonised by simple pioneer plants which pave the way for more complex plants, such as hardwood trees by creating soils and other necessities. Unlike secondary succession, which refers to succession after an environmental disaster (such as a forest Parents Phenotype: Red Red fire) primary succession occurs on the geologic timescale, over thousands Parents Genotype: Rr Rr of years


Zoos can play a large role in conserving endangered species by; 1. Conducting research 2. Running captive breeding programmes

F1 Genotype:

3. Reintroducing species into the wild 4. Educating people

Research enables scientists to understand the role of a species in an ecosystem. By understanding the niche, food web, reproductive behaviour, habitat, feeding relationships etc scientists can suggest effective methods of conserving species. Captive breeding programmes are used to reintroduce species to the wild, build up population numbers and maintain genetic diversity. In a small population many alleles are lost between generations because an individual only passes on 50% of their alleles. E.g.

R = Red,

r = white

F1 Phenotype:

9:3:3:1 A_B_ : A_bb : aaB_ : aabb Purple & Big : Purple & Little : Green & Big : Green & Little

If the parents only have 2 children and they are both Red (RR) then the r allele has been lost. This is genetic drift and is a big cause of the loss of genetic diversity in an endangered species. To avoid this studbooks are kept (basically, a family tree for the captive animals) so that only non-related animals are bred with each other. This decreases the change of genetic drift and also decreases the change of genetic disease. Wild animals are often introduced to captive breeding programmes to avoid these problems Reintroducing species into the wild has some success, but depends greatly on the species. As a general rule of thumb, the more advanced the species the more difficult reintroduction is. This is because animals need to learn specific behaviours e.g. how to hunt, how to reproduce, how / where to find shelter, group behaviours. Breeding animals in captive environments that mimic the wild has more success because it allows some of these behaviours to be learned in captivity. Feeding the animals in the wild also helps survival rates. Educating people is essential to conservation. Often just doing something slightly differently will have a big impact on conserving a species e.g. building roads with tunnels under them for badgers.

If you get a question on this in the exam youll need to think. There are no set facts to learn.

If you get a question on this in the exam youll need to think. There are no set facts to learn.

SNAB A2 Revision Notes

Unit 4: Environment and Survival
Topic 6: Infection, Immunity & Forensics
Time of death can be measured using the following factors;

o o o o

Body temperature Extent of rigor mortis Level of decomposition Forensic entomology

Body temperature: A body cools following an S-shaped (sigmoid) curve. The initial plateau at 37C lasts 30 60 min, then the body cools quickly to ambient temperature. After 24hrs a body has usually finished cooling and temperature is no longer useful. Temperature is measured using a long thermometer with a wide range. Temperature is usually taken rectally or using an abdominal stab.

The rate of cooling depends on the situation the body is found in e.g. Clothing slows cooling Found in water speeds cooling Found indoors slows cooling Air movements speed cooling Extent of rigor mortis: Temperature of body Warm Warm Cold Cold Stiffness of body Not stiff Stiff Stiff Not stiff Approx time since death No more than 3 hrs 3 8hrs 8 36hrs > 36 48hrs

Rigor mortis is the stiffening of joints and muscles. Small muscles stiffen first and unstiffen last. Muscles stiffen because they run out of ATP, causing the actin and myosin muscle fibres to stick permanently to each other. Muscles unstiffen because the muscle fibres begin to break down. On page 80 of your text book is a little more detail about the sequence of events that causes muscles to run out of ATP. Level of decomposition: Autolysis is the break down of body tissues using the bodys own enzymes from the digestive system and from lysosomes After this, bacteria from the gut invade tissues and release more enzymes. This tends to happen in anaerobic conditions, which favours the growth of anaerobic bacteria Greenish discolouration of abdomen (36hrs) Spreads across rest of body (36 72hrs) Discolouration darkens to reddish green (36 72hrs) Discolouration darkens to purple-black (72hrs) Body becomes bloated with gas (one week) Gas is released, body deflates & shrinks (one week +)

Autolysis is increased by mild heat and slowed by intense heat. Humidity has a big involvement as well dry conditions slow autolysis and, in some cases (e.g. mummies) stop it completely. The presence of wounds, the clothing the person was wearing and the combination of gases released during decomposition also have an effect. Forensic entomology: The insects found in a dead body can help identify time of death in 3 ways;

If the temperature of the body has remained relatively constant the age of the maggots growing in it can be determined by their starting length and the temperature of the part of the body they grew in.

Corpse succession:

e.g. a maggot 3mm long found growing at 28C will be roughly 0.3 days (8 hrs old)

Using the life-cycle of the maggot to identify age

3. If maggots are taken from the body, allowed to grow and the time taken to pupate is recorded; it is sometimes possible to work backwards from the pupation date and work out hold the maggots

must have been when they were taken from the body. This works because maggots of different species usually take a fixed number of days to pupate.

The identity of a dead person can be ascertained by; 1. Identity papers 2. Fingerprints 3. Dental records 4. Genetic Fingerprint Identity Papers: This is very obvious, think about it. Fingerprints: The skin on fingers, toes etc is ridged into specific patterns (arches, tented arches, whorls & loops). Sweat and sebum oil is left behind from our fingers on the things we touch. Using aluminium powder or protein stain (e.g. ninhydrin) fingerprints are revealed. Fingerprints are unique and can be used to identify people. Dental Records: Can be used to identify age and to identify a person based on their dentists record of their teeth. This is usually used when the body is damaged (e.g. a corpse from a fire) Genetic Fingerprint: Used because DNA is unique to individuals (except identical twins and clones grown by mad scientists). Genetic fingerprinting looks for the presence of repeated sequences of bases in the non-coding sections of DNA (introns). The repeated sequences are called satellites and can be 2 4 bases long (Micro-satellite) or 5 20 bases long (Minisatellite). The satellites are repeated anything from 5 500 times and this produces a unique DNA signature. Fingerprinting process: 1. A sample of DNA is copied using PCR 2. Sample is cut using a restriction enzyme


Sample is run on an electrophoresis gel, often using a DNA sample of known length to act as a standardization.

4. A southern blot is taken


DNA is labeled using a DNA probe specific to the satellite

6. An X-ray is taken to reveal the location of the bands of DNA The fingerprint is the pattern of bands on the electrophoresis gel. Assuming the original DNA sample has not been contaminated (by e.g. a hair from the pathologist) the fingerprint will be exact.

Succession on corpses: The idea that as each organism or group of organisms feeds on a body, it changes the body. This change in turn makes the body attractive to another group of organisms, which changes the body for the next group, and so on until the body has been reduced to a skeleton. This is a predictable process, with different groups of organisms occupying the decomposing body at different times. This technique allows you to tell, by the age and specific species living on a corpse, how old the corpse is. Succession and forensic entomology also show if the body has been moved.


A typical prokaryote

Ribosomes. Same function as eukaryotic cells (protein synthesis), but are smaller (70s rather than 80s). Nuclear Zone. The region of the cytoplasm that contains DNA. There is no nuclear membrane. DNA. Always circular, and not in chromosome form. Plasmid. Very small circles of DNA, containing non-esential genes. Can be exchanged between different bacterial cells. Cell membrane. made of phospholipids and proteins, like eukaryotic membranes. Mesosome. Tightly-folded region of the cell membrane containing all the proteins required for respiration and photosynthesis. Cell Wall. DIFFERENT from plant cell wall. Made of murein (a protein). There are two kinds of cell wall, which can be distinguished by a Gram stain: A: Gram positive bacteria have a thick cell wall and stain purple B: Gram negative bacteria have a thin cell wall with an outer lipid layer and stain pink. Capsule (or Slime Layer). Thick polysaccharide layer outside of the cell wall. Used for; 1. Sticking cells together

2. As a food reserve 3. As protection against desiccation (drying out) and chemicals, and as protection against phagocytosis (being broken down by a white blood cell).

Flagellum. A rotating tail used for propulsion.

Prokaryotic Cells
Small cells (< 5 mm) Always unicellular No nucleus or any membrane-bound organelles DNA is circular, without proteins Ribosomes are small (70S) No cytoskeleton Cell division is by binary fission Reproduction is always asexual

Eukaryotic cells
Larger cells (> 10 mm) Often multicellular Always have nucleus and other membrane-bound organelles DNA is linear and associated with proteins to form chromatin Ribosomes are large (80S) Always has a cytoskeleton Cell division is by mitosis or meiosis Reproduction is asexual or sexual

A typical virus

Viruses have a wide range of different structures. Some viruses are about 100nm in diameter, whilst others can range from 20 3000nm. All viruses have a protein coat (the capsid), which contains genetic material. The genetic material is either DNA or RNA, and can be single or double-stranded. The virus genetic material (the viral genome) contains only a few genes, from about 20 in the polio virus to more than 200 in the herpes virus (human genome contains ~80,000 genes). The viral genome codes for the proteins required to manufacture the virus. The protein capsid is made from identical subunits (called capsomeres). The capsomeres can be arranged into an icosahedral shape (e.g. polio & herpes), or a cylindrical shape (e.g. TMV & rabies) or a loose containment structure (e.g. measles & influenza).

In addition, some viruses also have an outer membrane envelope, which allows the virus to penetrate the host cell membrane by endocytosis. Influenza, HIV and measles virus all have membrane envelopes.


Viral Damage What do Viruses actually do to us?

Like bacteria, viruses have protein ligands on their capsid that attach to ligand receptors on eukaryotic cells. After a virus ligand attaches to a host cell ligand receptor it becomes anchored to the host cell. The virus attempts to get its viral genome into the host cell, usually through endocytosis using its lipid membrane. Viruses without lipid membranes may have specialised proteins designed to help inject the viral genome into the cell cytoplasm. (i) (ii) (iii) Virus RNA enters host cell Virus may also inject RNA Polymerase into host cell as well. Viral RNA and RNA Polymerase enter host cell nucleus via nuclear pores (iv) Viral RNA is copied in nucleus (v) Viral RNA is transcribed using viral RNA Polymerase (vi) Viral mRNA is translated in the cytoplasm (vii) New Virus proteins formed (viii) Viral proteins associate with copied RNA forming new complete viruses (ix) New viruses leave host cell to infect other cells Viruses that have a DNA code instead of an RNA code often insert their viral DNA into the host cells DNA. Other RNA viruses inject the enzyme Reverse Transcriptase, which makes a cDNA copy of the viral RNA. The cDNA copy is then inserted into the host cells DNA. Other viruses (e.g. HIV) also inject the enzyme integrase, which helps insert the viral cDNA into the hosts DNA Be sure you can recall what the 3 viral enzymes do; DNA Polymerase: RNA Transcriptase: Integrase: Some viruses target specific tissues (e.g. Poliomyelitis virus targets motor neurones, HIV targets helper T cells, Influenza targets epithelial cells & rabies virus targets specific brain cells). If lots of new virus is being made, these host cell may lyse (burst) and die.

4.6.5 & 4.6.6

Course of infection for Tuberculosis: Tuberculosis (TB) is caused by the Mycobacterium tubercolusis bacterium. Mycobacterium tuberculosis is inhaled into the lungs in droplets of water & mucus from another persons lung (droplet infection) 2. TB begins to reproduce in the lungs. 3. The bacteria produce toxins, which damage lung tissue & cause coughing, increasing the transmission of the disease. 4. The body launches an immune response to the TB bacterium. 5. Histamine release and inflammation occur (see 4.6.7) 6. Macrophages enter the lungs in large numbers. 7. The macrophages engulf the TB bacteria in large groups, forming a mass of tissue called a granuloma. The inside of the granuloma is starved of oxygen, which kills the bacteria. 8. Once the bacteria are dead, the lung heals

BUT TB bacteria can survive inside macrophages as the cell wall of the bacterium is very thick and waxy and is resistant to the macrophage enzymes. 10.The bacterium can survive and reproduce inside the macrophage for many years without causing infection. When the immune system is weakened (by stress, malnutrition, or another disease HIV is a common cause) the TB bacterium breaks out and re-infects the body. 11. The bacteria reproduce too rapidly for the body to destroy 12. The lungs are progressively damaged, which eventually leads to death. 13. TB can also spread to the lymph nodes in the body, where it reproduces causing the disease scrofula

Course of infection for Tuberculosis:

HIV is the Human immunodeficiency Virus, which eventually leads to Acquired Immunodeficiency Syndrome (AIDS) HIV is spread by direct contact i.e. through sexual intercourse, blood-to blood transfer (tattoos, needle sharing, piercing & cut-tocut transfer). Once inside the bloodstream an HIV infection occurs in 3 distinct phases;

The acute phase. HIV virus has a ligand (GP120), which attaches to a receptor (CD4) on the membrane of a type of white blood cell called a Helper T cell. HIV rapidly infects Helper T cells and the virus population increases quickly. At the same time the population of Helper T cells falls rapidly. The acute phase ends when the Killer T cells begin to recognise infected Helper T cells and kill them, which slows the replication of the virus. The chronic phase. This can last for many years. The virus continues to replicate, but the Killer T cells keep the numbers in check. However, because the immune system is weakened other bacteria and viruses are more likely to infect the person (TB may reactivate at this point) The disease phase. As the numbers of virus increase and the numbers of Helper T cell fall the immune system becomes weaker and weaker. Eventually a second pathogen will infect the person (an opportunistic infection) which cannot be fought off. The person will die quickly from the secondary infection and this is the AIDS disease state.



The huge problem with HIV is that it mutates very quickly. Once inside the body the viral antigens change and the (already damaged ) immune system cant keep pace with the changes. Another problem is that HIV attacks Helper T cells, which are crucial for activating the B cells and also play a role in activating

Killer T cells. With low numbers of Helper T cell, the immune system cannot communicate effectively and this increases the ability of HIV to survive in the body.

Non-specific immune responses: Inflammation: damaged white blood cells and mast cells release histamine at the site of infection. Histamine causes local arterioles to vasodilate, increasing the blood supply to the area. It also causes holes to open between endothelial cells in capillary walls. This causes local oedema (the swelling associated with inflammation). It allows monocytes and neutrophils into the infected area, which engulf and destroy foreign bodies and pathogens. Eventually phagocytes arrive and complete the job. Dead monocytes and pathogen form pus. Lysozyme: an enzyme that breaks down bacterial cell walls, causing them to lyse and die. Lysozyme is made in lysosomes inside phagoctyes and is responsible for digesting engulfed bacteria. Lysozyme is also made by the skin, epithelial cells, and is present in tears Interferon: a protein made by virus-infected cells. It blocks RNA synthesis and therefore stops virus replication Phagocytosis: the process in which a pathogen is engulfed and destroyed. Macrophages engulf pathogens using pseudopodia (fake feet). The bacterium is taken into the macrophage by endocytosis and enters the macrophage inside a vacuole. Lysosomes containing lysozyme fuse with the vacuole and digest the bacterium inside.

Pathogens have proteins on their surface that our immune system has learned to recognise as foreign. These proteins are called antigens. T cells, B cells & Macrophages all have the ability to recognise an antigen and once this has happened, they will trigger an immune response. In addition to this, macrophages have the ability to present foreign antigens to T and B cells. Once a pathogen has been engulfed and destroyed MHC proteins inside the Macrophage stick to the pathogenic antigen. They are then incorporated into the cell membrane of the Macrophage, so it can present the foreign antigen and activate the T and B cells responses. Antibodies (also called Immunoglobulins) are proteins produced by B cellls. They are found in blood plasma, lymph, tissue fluid, tears, mucus and milk.

Antigen-binding site

Variable Region

Disulphde Bridges Constant Region

Each B cell produces a different immunoglobulin molecule which recognises and binds to a specific antigen. There are over a million different B cells in your body, therefore you have the ability to recognise and react to a million different antigens. The variable region of the immunoglobulin protein is what recognises & binds to the antigen. Each variable region is different, hence the name. There are 5 different families of immunoglobulin molecule in the human body (G, M, A, D & E. IgG - also known as -globulin). The families can be distinguished from each other by slight differences in the constant region of the protein Each antobody molecule contains two pairs of proteins; - Two heavy chains - Two light chains Each pair of chains is held together by disulphide bridges (hydrogen bonds would be too weak).

Each immunoglobulin molecule has 2 antigen binding sites and can, therefore, bind 2 antigens at one time. This means that a single antibody molecule can bind to 2 pathogens at the same time, which causes pathogens to clump together and form the Antibody-Antigen Complex.

Antibody Pathogen


The formation of the Antibody-Antigen Complex is important because it; - Isolates pathogens so they cannot infect other host cells - Makes it easier for macrophages to engulf & destroy the pathogens. - Stops the pathogen from entering a host cell - Makes it easier for T cell activation as more antigens are presented in one area

There are two different types of Immune Response; A B Cell-mediated Immune Response Antibody-mediated Immune Response.


Isolated viruses do not present antigens and therefore do not trigger either the Cell- or Antibody-mediated immune Response. However, when viruses invade host cells, viral proteins are expressed which become incorporated into the host cell surface membrane via MHC. These proteins are recognised as antigens.

Cell-Mediated Immune Response:


Competent T Cells recognise a specific foreign antigen using its T cell receptor.

2. Activated T Cell undergoes rapid mitosis forming a large number of identical clone T

Cloned T Cells differentiate into Killer, Helper, Memory or Suppressor T Cells.

4. Killer and Helper Cells migrate to the site of infection Killer T Cells: attach to the infected / foreign cell and release the enzyme Perforin, which makes holes in the pathogens cell membrane causing it to die Helper T Cells: stimulate B cells to start producing antibody and attract macrophages to the site of infection Memory T Cells: remain in the lymph nodes. They will respond rapidly if the same pathogen invades the body again, because they have the right T cell receptor to recognise the pathogen. This means that the body can mount an immune response before infection becomes serious Suppresor T Cells: stop the immune reaction after about a week Antibody-mediated Immune Response:

1. B cells are recognise a specific foreign antigen using the antibody molecules on their surface. B cells can also be activated by macrophages & Helper T cells. When a macrophage digests a pathogenic cell antigens from the cell membrane get stuck in the macrophages membrane; any B Cells which come into contact with the antigen will then be activated 2. The activated B cell undergoes rapid mitosis and lots of clone B cells are produced

Cloned B Cells differentiate into either Plasma or Memory cells Plasma Cells Memory Cells is Memory Cells continue to secrete antibody for many years, so that if the body is infected by the same pathogen the Memory B cells can produce an instant supply of antibody before the infection becomes serious

a) Plasma cells antibody, which specific for one antigen only

b) Antibody is transported via the lymph to the site of infection c) Antibody attaches to the specific antigen

An antigen-antibody formed

complex is

Negative feedback systems aim to keep something (e.g. blood [glucose] or body temperature) at a constant level. Negative feedback works as follows; 1. Signal causes action 2. Action has effect 3. Effect removes original

E.g. 1. High [glucose] in blood causes insulin release 2. insulin stimulates liver to take up glucose & convert it into glycogen stores 3. [glucose] falls

Homeostasis is the maintenance of the bodys internal environment. This is carefully controlled by a series of systems, which aim to keep conditions at a stable controlled level. Body Temperature: Body temperature is carefully regulated to maintain a steady 37.5C, which is the optimum temperature for human enzymes. Sensors (thermoreceptors) in the hypothalamus continually monitor blood temperature and activate warming / cooling processes to keep the temperature as stable as possible.

Body temperature is normal


Body temperature rises

Detected by thermoreceptors in hypothalamus

Hair erector muscles cause body hairs to lie flat

Peripheral arterioles vasodilate

Sweat glands release sweat onto skin

Less insulating air trapped next to skin

More heat radiated away from skin

Sweat evaporates carrying heat away

Body temperature returns to normal

Tuberculosis bacterium (Mycobacterium tuberculosis) causes fever. How does fever work? All white blood cells communicate with each other and the rest of the immune system using a class of hormones called cytokines. The cytokines have hundreds of different roles and many more are yet to be discovered. One class of cytokine is the hormone interleukin, which causes fever. Fever can be induced by many factors. The general class of hormones that lead to fever are called pyrogens (interleukin is a natural pyrogen). However, bacterial toxins, viral proteins and substances produced by necrotic tissue may also trigger fever. Pyrogens travel in the blood to the hypothalamus in the brain. They bind to receptors there and trigger a complex set of reactions that lead to the production of PGE2 hormone, which elevates the thermoregulatory set point, i.e. it re-sets the bodys natural thermostat to a higher temperature. The hypothalamus now thinks body temperature is too low and triggers a system of responses which aim to generate heat (thermogenesis) and raise body temperature. These mechanisms include; shivering, increased muscle tone, vasoconstriction and the

production of thyroxine hormone (which makes respiration less efficient, therefore producing more heat).

4.6.12 Barrier Mechanisms include; Skin Stomach Acid Normal Flora Epithelial cells
Skin Adaptations for defence:

The skin is made from 2 layers; - Outer epidermis layer - Inner dermis layer The epidermis provides a physical barrier to invading pathogens. There are 2 layers in the epidermis;

Outer cornified layer, composed of compacted dead dry cells filled with indigestible keratin protein (which also forms nails and hair) Inner Malpighian layer, site of rapid mitosis and keratinisation.

The skin also has chemical defence mechanisms;


sweat & sebaceous glands secrete sebum, which is an oil with pH 3 5. This makes the skin acidic sebaceous glands also secrete the enzyme lysozyme, which is a natural antibiotic. Lysozyme destroys bacterial cell walls.

Stomach Acid: Is made from HCl at pH 1 2. it is a very effective barrier. Normal Flora: The skin, respiratory tract and gut are covered with commensual bacteria, which are part of the normal flora of the body. Commensual bacteria are adapted to live the environment of the skin and the gut and the and compete with invading pathogens for the limited supply of nutrients.

Epithelial cell Adaptations for defence: 1. Epithelial cells are closely packed & connected by tight junctions forming a continuous impermeable layer 2. Epithelial cells have cilia, which form a direct physical barrier preventing pathogen attachment

3. Cilia beat in waves, which helps clear bacteria out of the lungs and into the throat, where they are swallowed. Ingested bacteria are quickly killed by the low stomach pH and digestive proteases. Cilia also beat in the GI tract. 4. Epithelial cells secrete mucus, which is trapped by cilia. Mucus also directly prevents pathogen attachment 5. Mucus contains lysozyme

Both T and B Cells differentiate into Memory Cells, which remain in our lymph nodes and wait until we are re-exposed to the same pathogen. When the Memory B cell is activated by the old antigen it makes large quantities on antibody quickly and kills the pathogen before it can infect us properly. The memory cells provide active immunity. When we are exposed to a new antigen it takes us about a week to be able to make new antibody. However, a second exposure to antigen produces a much faster response, and several orders of magnitude higher levels of antibody are produced.

Plasma B cells make lots of antibody on re-exposure Antibody made by memory B cells provides active immunity

Without immunity the level of antibody produced by plasma cells is much less

Passive Immunity is immunity to a pathogen without Memory cells. It can occur through antibody injection or from drinking breast milk (breast milk contains high [antibody]) Active Natural Immunity the process above Passive Natural Immunity beastfeeding (antibody in milk) Artificial Active Immunity - vaccination Artificial Passive Immunity antibody injection

We have evolved a very effective immune system, consisting of barriers, non-speficif defence mechanisms and specific ones. If were so good at fighting infections, why do we still get ill? Answer: pathogens are evolving as well.
So how has TB evolved to beat us? 1. It is spread by droplet infection, which is the most effective method of infection 2. It specifically targets epithelial cells, which means that, when inhaled, it is exactly where it wants to be 3. It does not kill immediately. This means that it has a large window of opportunity to spread to others 4. It has a very thick waxy cell wall, which means it is partially protected against lysozyme

5. It can survive inside macrophages and lie dormant until the immune system is weakened, when it can re-infect. So how has HIV evolved to beat us? 1. It weakens the immune system to increase its chance of survival 2. It stays in the body for years, so it can spread 3. It specifically targets Helper T cells 4. It is spread by sexual contact, so it is easily spread

Antibiotics work by targeting prokaryotic features not found in eukaryotic cells, e.g. penicillin targets the cell wall and breaks it down. Penicillin can be taken in large doses by humans because it has no effect on our cells (we have no cell walls). Bacteriostatic antibiotics stop bacteria reproducing, they do not kill bacteria Bacteriocidal antibiotics kill bacteria

4.6.16 The effectiveness of antibiotics can be measured using a disc diffusion technique.

A bacterial lawn is grown on an agar plate (either by spreading the bacteria over the plate, or by using a pour plate).

2. A disc of blotting paper is soaked in antibiotic of known concentration and placed in the centre of the plate. 3. A clear circle of dead bacteria will form around the disc 4. The diameter / radius of the circle of dead bacteria is proportional to the effectiveness of the antibiotic 5. This can be compared to other antibiotics, as long as the same concentration of antibiotic is used. In addition, one can also compare the effectiveness of an antibiotic with a disinfectant or sanitiser (e.g. Phenol coefficient) 4.6.17
Bacteria are becoming resistant to antibiotics. Bacteria develop resistance through mutation. A bacteria can mutate and develop resistance by; 1. Having an enzyme that breaks the antibiotic down 2. Having a protein which pumps antibiotic out of the cell 3. Mutating the structure of the bacterium so that the antibiotic no longer works

This problem is very serious. Bacteria become resistant because;


Bacteria mutate very easily. One in every million bacteria contains a mutation. That might sound like a small amount, but consider that one E coli bacterium can reproduce to form a colony of 2 million bacteria in two hours. Over weeks, months and years thats a lot of mutations, some of which will be beneficial

2. Bacteria reproduce very quickly (they divide every 20min) so a bacterium with a beneficial mutation will spread quickly


Bacteria have the ability to pass copies of plasmids from one to another (conjugation). So a mutation in one bacterium can quickly be copied to others, even others in different species.

4. The use of antibiotics speeds the rise of immunity. If a bacterial population is continually exposed to antibiotic all bacteria will die. As soon as a bacterium mutates the rest of the bacteria will be killed off by the latest dose of antibiotic; now the field is open for the mutated bacterium to grow without competition. 5. Humans have been reckless with use of antibiotics. They are often given to people who dont need them (i.e. they have viral infections) or to people who dont bother to complete the course of antibiotic.

The evolutionary arms race between bacteria and drug developers is, at the moment, tipped against humans. There are over 100 different types of antibiotic and in the 40years since their development 4 species of bacterium have developed resistance against all of them. E.g. Methicillin Resistant Staphyloccus Aureus (MRSA) has been named the Superbug, because we have do drugs left that can kill it. Unless drug developers discover another branch of antibiotics were not currently using (i.e. another way of targeting prokaryotic

structures without damaging eukaryotic ones) there may well be a global pandemic of resistant bacteria.

SNAB A2 Revision Notes

Unit 5: Energy, Exercise and Coordination

Topic 7: Run for your life

Cartilage: a tissue made from collagen, which protects bone ends A muscle: an organ that produces movement by contraction A joint: the junction between two bones A tendon: joins muscle to bone A ligament: joins bone to bone to stabilise a joint Muscles work in pairs. One muscle produces the opposite movement from the other muscle, therefore, the pairs are called antagonistic pairs. Muscles which cause a joint to extend are called extensors, muscles which cause a limb to retract are called flexors. A Synovial Joint
Bone Ligament Muscle Cartilage Synovial Fluid Synovial membrane


Muscles are made from muscle fibres arranged into bundles. Each fibre is made from bundles of myofibrils, which are extremely long, cylindrical muscle cells. Arrangement of myofibrils into a muscle fibre Muscle cells (Myofibrils)


A nerve impulse arrives at the neuromuscular junction

Muscle Fibre

2. The muscle cell is depolarised


Ca2+ is released from the sarcoplasmic reticulum inside muscle cells Ca2+ bids to Troponin protein in the thin filament.


Troponin protein and Tropomyosin protein move position in the The functional unit of contraction is the sarcomere. Muscle cells thin filament

contain many sarcomeres arranged in parallel. The muscle cell takes on a characteristic banded appearance 6. Myosin binding sites are exposed because of the regular on the thin arrangement of the sarcomeres. This is called striation.filament

7. Myosin heads of the thick filament stick to actin

A 8.sacromere. Note to the striated ATP (already bound the myosin appearance is hydrolysed causing the head) of the muscle
myosin head to pivot forwards in the powerstroke

Cross-Bridge Cycling:

The sarcomere contains overlapping 9. As the head pivots the thick actin and myosin. The myosin is often filament moves across the thin called filament muscle contraction the the thick filament because myosin heads make it appear thick. occurs The actin is, therefore, the thin 10. ADP diffuses away from the filament
myosin head leaving the ATPbinding site empty & causes the myosin head to detach from the actin.

The process by which the thin filaments are pulled in towards each other by 11. New ATP contract. the myosin is called cross-bridge cycling. It is how musclesbinds & the myosin head

12. The myosin head re-cocks 13. The head rebinds further up the myosin.

Repeat stages 7 to 13 until the [Ca2+] falls too low, when contraction stops

Key Point: ATP is required to release myosin from actin. If ATP levels drop (assuming Ca2+ is present) the myosin stays attached to the actin and the muscle stays permanently 5.7.3 contracted. This is what causes rigor mortis Adenosine TriPhosphate (ATP) is made from three components;

Ribose (the same sugar that forms the basis of DNA). A base (a group consisting of linked rings of carbon and nitrogen atoms); in this case the base is adenine. Ribose Adenine base

3 x phosphate

Up to 3 phosphate groups. These phosphates are the key to the activity of ATP

The energy used in all cellular reactions comes from ATP. By breaking the 3rd phosphate from the ATP molecule energy is released, which can be used to power intracellular reactions. The ATP is then regenerated by recombining the phosphate and ADP in respiration (or another process e.g. photosynthesis). The recycling of ATP is crucial for life. For example a runner uses ~84kg of ATP in a marathon (more than their total body weight), yet there are only 50g of ATP in the entire body! This means each that each molecule of ATP has been recycled 1676 times during the race!


ATP + H2O ADP + Pi

ATP = one adenosine molecule with 3 phosphate groups attached

Energy rich bond Less energy rich bond(30.6kJ/mol) (13.8kJ/mol)

Energy rich bond (30.6kJ/mol)

How the energy in ATP is liberated: + P ADP + H2O AMP i Energy Adenosine

AMP + H2O Adenosine + Pi

Energy Adenosine

Energy Adenosine

Normally, as soon as ATP has been converted into ADP + Pi it is converted back into ATP using energy from respiration. However, during exercise ADP may be converted into AMP or even Adenosine to provide energy.

Respiration: a process in which the chemical bond energy in
glucose molecules is used to convert 38 ADP molecules into 38 ATP molecules. Oxygen is required and Carbon Dioxide and Water are produced as waste products. Respiration occurs in 4 distinct steps;

1. Glycolysis (cytoplasm) 2. Link Reaction (mitochondria matrix) 3. Krebs Cycle (mitochondria matrix)

1 x Glucose 2 x ATP

2 x Pyruvate 4 x ATP 2 x NADH

A 6C glucose molecule is split into two 3C pyruvate molecules. Some ATP is used to split the glucose molecule in the first part of glycolysis 3C Pyruvate is split into a 2C molecule, which is attached to a CoA enzyme to form Acetyl CoA. The remaining carbon atom is used to form CO2 CoA enzyme gives its 2C atoms to a 4C molecule to form a temporary 6C molecule. In a series of steps the 6C molecule releases the two C atoms as CO2 eventually re-forming the starting 4C compound. The cycle is then ready to repeat itself. As the cycle turns ATP, NADH & FADH2 are formed

1 x Pyruvate 1 x CoA

1 x Acetyl CoA 1 x CO2 1 x NADH

1 x Acetyl CoA

1 x CoA 1 x ATP 2 x CO2 3 x NADH 1 x FADH 2

4. Oxidative Phosphorylation


10 x NADH 2 x FADH2 6 x O2

(mitochondria christae)

The electron transport chain uses the NADH and FADH2 made in previous steps to make lots of 2ATPs are required ATP Respiration: Step 1 - Glycolysis

34 x ATP 6 x H2O


2ATPs are made (4 overall) Glyceraldehyde Phosphate Glyceraldehyde Phosphate 1 NADH is made (2 overall)



Glycolysis takes place in the cytoplasm of a cell

In Glycolysis a Glucose molecule (6C) is split into 2 molecules of Glyceraldehyde Phosphate (3C). 2ATPs are required for this to happen. Then, each 3C Glyceraldehyde Phosphate molecule is converted into a 3C Pyruvate molecule. In the process of converting one Glyceraldehyde Phosphate to one Pyruvate, enough energy is released to convert one NAD molecules into one NADH molecules and also to make two ATP molecules. Overall; 4ATP are made, 2NADH are made and 2ATPs are used. Net gain: 2ATP and 2NADH

In anaerobic conditions [H+] rises in the mitochondria as there are no available oxygen molecules to mop it up with and form water. This leads to saturation of the electron transport chain and a build-up of NADH and FADH2. This means [NAD] falls, which stops the Krebs Cycle. Acetyl CoA levels build-up, [CoA] falls and the Link Reaction stops. Pyruvate levels start to rise Muscle cells turn pyruvate into lactate to stop rising [pyruvate] from stopping Glycolysis (remember, enzyme controlled reactions are reversible and depend on [reactants] and [products]). NADH Pyruvate NAD Lactate

In the liver the lactate is converted back into pyruvate. This requires oxygen, which is the basis of the Oxygen Debt

Respiration: Step 2 Link Reaction

Pyruvate 1 NADH is made (2 overall) 1 CO2 is made (2 overall) CoA enzyme Acetyl CoA

Link Reaction takes place in the matrix of the mitochondria

In the Link Reaction a Pyruvate molecule (3C) is split into a 2C molecule and a CO2. The 2C molecule is attached to a CoA enzyme, forming Acteyl CoA. Remember, two molecules of Pyruvate were made at the end of Glycolysis, therefore the Link Reaction happens twice. Overall; 2NADH and 2 CO2 are made. Net gain: 2NADH


Respiration: Step 3 Krebs Cycle

CoA enzyme 2 NADH are made (4 overall) 1 ATP is made (2 overall) 1 FADH2 is made (2 overall) 2 CO2 are made (4 overall)

Krebs Cycle takes place in the matrix of the mitochondria

In the Krebs Cycle the Acetyl CoA gives its 2C atoms to a 4C molecule (Oxaloacetate) forming an unstable 6C molecule (Citric Acid). The 6C molecule breaks down into a 4C compound (Succinyl CoA) releasing enough energy to make one NADH. The two spare C atoms are released as two CO2 molecules. Succinyl CoA is converted back into Oxaloacetate and this releases enough energy to make one NADH, one FADH2 and one ATP. The Oxaloacetate can then be used in the cycle again. Remember, two molecules of Acetyl CoA were made at the end of the Link Reaction, therefore the Krebs Cycle happens twice. Overall; 4NADH, 2FADH2, 2CO2 and 2ATP are made.


Respiration: Step 4 Oxidative Phosphorylation

Oxidative Phosphorylation uses the NADH and FADH2 produced in the previous steps of respiration to make ATP. Each NADH makes 3ATP and each FADH2 makes 2 ATP.





H+ Carrier

H+ Carrier

e- Carrier

e- Carrier

e- Carrier


O2 + 2H+ 2e

Oxidative Phosphorylation takes place using enzymes embedded in the inner membrane of cristae of the mitochondria
Hydrogen atoms from the NADH and the reduced FADH2 are passed onto 2 the first 2 enzymes of the Electron Transport Chain. These enzymes are Hydrogen Carriers and they accept the H atoms from the NADH and the FADH2. Electrons, which made up the chemical bond between the hydrogen atoms and the NADH / FADH2 are passed onto 3 Electron Carrier enzymes further down the Electron Transport Chain.

At the end of the Electron Transport Chain, the electrons are recombined with the H+ atoms and oxygen, to form water. This is the only, but crucial, part of respiration to involve oxygen. NADH starts at the first Hydrogen Carrier and has enough energy to phosphorylate 3ADP. FADH2 has less energy and starts at the second Hydrogen Carrier, it generates 2 ATPs

Where does the 38 ATP come from?

Glycolysis produces; Link Reaction produces; Krebs Cycle produces; 2ATP Total 4 ATP 2ATP 2NADH 2NADH 6NADH 2 FADH2 10NADH 2 FADH2

Each NADH produces 3ATP total production is 30ATP from NADH Each FADH2 produces 2ATP total production is 4ATP from FADH2

Grand Total

4ATP +

30ATP + 4ATP

= 38ATP

Chemiosmosis of H+ ions from the mitochondrial envelope into the matrix through ATP Synthetase proteins is what actually generates the ATP in respiration

The electron transport chain uses the process of chemiosmosis (the diffusion of ions across a membrane). H+ ions are actively pumped into the mitochondrial envelope. This is done by the proteins in the electron transport chain, using the energy stored in NADH and FADH2. The [H+] builds up to very high levels in the envelope. However, H+ cannot escape because it is charged (hydrophilic) and therefore cannot move through the phospholipid bilayer in the envelope membranes. Special proteins called ATP Synthetase do allow H+ to pass through them and escape into the mitochondrial matrix. Whenever an H+ ion moves through the ATP Synthetase protein an ADP is phosphorylated by the ATP Synthetase. In summary;
1. 2.

NADH and FADH2 contain stored chemical energy The energy is used to pump H+ into the mitochondrial membrane against the concentration gradient H+ trapped in one place represents a store of potential energy H+ ions leave the envelope through ATP Synthetase proteins. The potential energy of the H+ is used to phosphorylate ATP as the H+ moves out of the envelope




In anaerobic respiration lactate is taken via the blood to the liver, where it is broken down into pyruvate using oxygen and NADH.

c h e m o r e c e p t o r s in c h e m o r e c e p s o t rr es t ci n h t r e c e p t oc r o s r t e x a o r t ic a n d c a r o t i d m e d u l la in m u s c l e s( v o l u n t a r y b o d ie s

c o

n t r o


R in

E S P I R A T O C E N T R E m e d u l la o f

b r a in

in t e r c o s t a l p h r e n i nc e r v e v a g u s n e r v e n e r v e

s t r e t cnh t e r c o s t a l i r e c e p m t o u r ss c l e s d ia p h r a g m

p r e s s u r e c h e m o r e c e p t o t er s m i p e r a t u r e n r e c e p t o r s i n a o r t ic s t r e t c h r e c e p t o a o r t ic a n d c a r r o e t ci d e p t o r s i n a n d c a r o t id in m u s c le s b o d ie s m u s c le s b o d ie s

C in

R D I O V A S C U L A C E N T R E m e d u l la o f b r a in t ic m p a t h e t i c e r v e c c e le r a t o r ) t r ia l

p a r a s y m p a t h e s y n e r v e n ( in h ib it o r ) ( a

s in o a n o d e

v a s o c o n s t r ic t io n a n d v a s o d il a t io n



A spirometer is used to plot breathing patterns Vital Capacity: The maximum amount of air a person can exhale after inhaling the maximum possible volume of air The volume of air inhaled & exhaled in one breath The rate of respiration

Tidal Volume: Basal Metabolic Rate:

The spirometer can be used to plot VC and TV directly. BMR can be worked out if a CO2 scrubber is used. The spirometer has fixed volume and is filled with 100% O2 before the experiment begins. As the person respires, O2 is replaced proportionally with CO2. The total volume should stay constant. However, if CO2 is removed, the total volume will slowly fall as O2 is used. The rate at which the volume decreases is proportionaly to BMR. You are not expected to know how the spirometer works although its not very difficult to understand.

5.7.10 & 5.7.11

Sprinters need lots of fast twitch muscle, joggers need slow twitch. Therefore, the muscle type of a cheetah or a gazelle will be predominantly fast twitch, whereas the muscle of a camel or an elephant will be predominantly slow twitch. Muscle type in humans is predominantly one or the other due to inherited alleles. However, different training programmes can cause the % of either type to change slightly.

Slow twitch fibres Red (lots of myoglobin) Many mitochondria Little sarcoplasmic reticulum Low glycogen content Numerous capillaries Fatigue resistant 5.7.12

Fast twitch fibres White (little myoglobin Few mitochondria Lots of sarcoplasmic reticulum Lots of glycogen Few capillaries Fatigue quickly

See 4.6.11 for mechanisms of thermoregulation. The thermoregulatory process (and most homeostatic systems) are controlled by negative feedback processes. If a system changes, it is detected, a homeostatic response is activated, which aims to return the system to its original level. Negative feedback, therefore, holds systems at a set point, in this case 37.5C.


A moderate level of exercise improves health & well-being. However, over-training can result in the opposite effect. This is the phenomenon known as burn-out

Positive effects of exercise include; Increased BMR 1. Decreased blood pressure 2. Increased HDL 3. Decreased LDL

4. Maintaining healthy BMI 5. Decreased risk of diabetes 6. Increased bone density 7. Improved well being 8. Decreased adrenaline levels 9. Less stress 10.Decreased risk of CHD 11. Moderate exercise increases levels of Natural Killer cells, which secrete apoptosis-inducing chemicals in response to non-specific viral or cancerous threat Negative effects of exercise (over-training) include; Decreased levels of Natural Killer Cells, Phagoctyes and B & T Cells. This decreses immune response. 1. Increased muscle inflammation 2. Muscle tears and sprains 3. Increased adrenaline levels 4. Increased cortisol levels, which also decreases the immune response 5. Increased stress 6. Damaged cartilage 7. Tendinitis 8. Ligament damage 9. Swollen bursae

Key-hole surgery is a technique which allows doctors to conduct surgery with the minimum possible damage to the patient. The surgeon makes a small incision (a key-hole) and uses a fibre-optic camera to view the damaged area. If required, the surgeon can make a second incision and use a number of small, remote operated tools to repair the damage. Because the incisions are small and only the damaged area is targeted, the patient recovers quickly. There is also less chance of infection.

Unfortunately, the procedure requires a high degree of training, expensive equipment and can only be used on certain types of surgery. Prosthetics allow people with amputations to participate in many activities, including sports.

Drug Effect on physiology Effect on performance Side-effects Increased haemocrit increases blood viscosity. This causes strain on the heart and can lead to infarction Diarrhoea , vomiting, liver damage and kidney damage.

Erythropoietin EPO causes the bone marrow Extra blood cells mean the (EPO) to generate extra red blood blood can carry extra oxygen. cells. This increases the level of work the body can sustain through aerobic respiration (aerobic threshold). Creatine Creatine combines with Because ATP is re-generated phosphate to form Creatine without using the respiratory Phosphate (CP). CP can pathways, theoretically it phosphorylate ADP, re- should increase the maximum generating ATP. power of muscles and decrease recovery time Testosterone Binds to androgen receptors Muscle mass increases, which in target cells and increases makes the athlete more transcription of anabolic powerful. It also decreases proteins (growth proteins) recovery time. such as actin & myosin.

Agression, decreased sex drive, infertility, skin problems, acne, shrunken testicles

Why should we allow use of drugs; Gives people a chance to be as good as their potential allows Removes unfair genetic advantages Controlled use of drugs is less risky People should have the right of choice Legalising drugs makes their distribution controllable (no use by under-age, infirm etc)

Arguments for not using drugs; Dangerous (obviously) May be pushed onto athletes by trainers Effects are permanent

Not used under doctors supervision Often cut with other drugs Exposes athletes to criminals (danger of using other drugs) The list goes on, just think for yourself in the context of the question. You can argue the toss either way, but make sure you can back up your opinion with some sensible, logical arguments.

SNAB A2 Revision Notes Unit 5: Energy, Exercise and

Topic 8: Grey matter
Sensory nerve: Motor nerve: Relay nerve: Schwann cells: carries electrical message from receptor to spine carries electrical message from spine to effector connects sensory and motor nerves. Also relays message to the brain. wrap around the axon of the long nerves, creating a thick layer of membrane, which insulates the nerve and allows for much faster conduction speed. The thick layer of membrane has gaps in it between adjacent Schwann cells, these are called Nodes of Ranvier.


High light intensity Circular muscles: contracted Radial muscles: relaxed Pupil diameter: small

Low light intensity Circular muscles: relaxed Radial muscles: contracted Pupil diameter: large

5.8.3 The Action Potential

Voltage-Gated K+ Channels open

Voltage-Gated Na+ Channels open

Nerve is hyperpolarised and inactive (refractory period)

Sequence of events in an action potential;

1. Nerve is at resting membrane potential (-70mV)

2. 3.

A stimulus depolarises the nerve to threshold (-50mV) Voltage-gated Na+ Channels open

4. Sodium floods into the cell and the membrane potential depolarises to +30mV

Voltage-gated K+ Channels open

6. Potassium floods out of the cell and the membrane potential falls to -90mV 7. The nerve is in the refractory period and cannot conduct another action potential

The 3Na+/2K+ ATPase (Na+/K Pump) restores the ion concentrations

9. The nerve is ready to fire again As one part of the nerve fires off, Na+ diffuses into the next section of the nerve, which depolarises the nerve to threshold. This sequence is repeated like a tiny Mexican wave down the axon of the nerve. Nodes of Ranvier speed this conduction process up. When one node depolarises it induces the next section of the nerve to depolarise by forming a mini-circuit between nodes. This causes the action potential to jump between nodes of ranvier, making conduction speed much faster.

A synapse is the junction between two nerves. It is also a verb, i.e. one nerve synapses with another (meaning, passes a message to another). The neurotransmitter on your syllabus is Ach, but over 2000 other transmitters have been discovered

3 1 2

5 7 6


The wave of depolarisation arrives at the synaptic knob. The membrane in the presynaptic neuron is depolarised to 50mv (threshold potential) and the voltage-gated Na+ channels open, letting Na+ into the cell. The membrane is depolarised to +30mV and voltage-gated K+ channels open. The membrane potential falls to 90mV and the cell goes into its refractory period, where the 3Na+/2K+ATPase restored the ion concentrations. Unlike axons, presynaptic nerves also contain a Voltagegated Ca2+ channel. As the presynapstic membrane depolarises these channels open and let Ca2+ into the cell. The Ca2+ causes vesicles in the presynaptic nerve to migrate and fuse with the presynaptic membrane, where they spill neurotransmitter chemical into the synaptic cleft.





The neurotransmitter (Acetyl Choline) diffuses across the cleft and binds to receptors on the postsynaptic membrane. The receptors let a little Na+ into the postsynaptic neuron, which is enough to initiate another action potential in the postsynaptic nerve. The ACh is broken down by an enzyme called Acetyl Choline Esterase (AchE), which allows the postsynaptic receptors to be freed ready for a second synapse.



In a neuromuscular junction the sequence of events in the synapse is exactly the same. The only difference is that the posysynaptic nerve is a muscle cell and, instead of being flat, the postsynaptic membrane has deep grooves (t tubules) which allow the depolarisation to spread quickly through the muscle so all parts of the muscle contract at the same time. Some neurotransmitters can hyperpolarise postsynaptic nerves, which essentially switches them off. An example of this type of inhibitory neurotransmitter is GABA 5.8.5
Visual transduction is the process by which light initiates a nerve impulse. The structure of a rod cell is:

The detection of light is carried out on the membrane disks in the outer segment. These disks contain thousands of molecules of

rhodopsin, the photoreceptor molecule. Rhodopsin consists of a membrane-bound protein called opsin and a covalently-bound prosthetic group called retinal. Retinal is made from vitamin A, and a dietary deficiency in this vitamin causes night-blindness (poor vision in dim light). Retinal is the light-sensitive part, and it can exists in 2 forms: a cis form and a trans form: In the dark retinal is in the cis form, but when it absorbs a photon of light it quickly switches to the trans form. This changes its shape and therefore the shape of the opsin protein as well. This process is called bleaching. The reverse reaction (trans to cis retinal) requires an enzyme reaction and is very slow, taking a few minutes. This explains why you are initially blind when you walk from sunlight to a dark room: in the light almost all your retinal was in the trans form, and it takes some time to form enough cis retinal to respond to the light indoors. Rod cell membranes contain a special sodium channel that is controlled by rhodopsin. Rhodopsin with cis retinal opens it and rhodopsin with trans retinal closes it. This means in the dark the channel is open, allowing sodium ions to flow in and causing the rod cell to be depolarised. This in turn means that rod cells release neurotransmitter in the dark! However the synapse with the bipolar cell is an inhibitory synapse, so the neurotransmitter stops the bipolar cell making a nerve impulse. In the light everything is reversed, and the bipolar cell is depolarised and forms a nerve impulse, which is passed to the ganglion cell and to the brain.

Summary for light; 1. Photon hits rhodopsin

2. 3.

Bleaching occurs and trans retinal is formed Trans retinal blocks Na+ channels

4. The rod is hyperpolarised and stops releasing inhibitory neurotransmitter 5. The bipolar cell is no longer inhibited and depolarises 6. The ganglion cell is activated, which carries the message to the brain Cones work in exactly the same way, except that they contain the pigment Iodopsin, which is found in 3 different forms; redsensitive, blue-sensitive and green-sensitive. This gives us colour vision.

Homeostasis is the maintenance of the internal environment. - Nerve reflexes give immediate responses - Hormone responses give responses over weeks months

Hormones are released from glands, which release hormone into the blood. The hormone is carried all over the body. It binds to hormone receptors on cell membranes and initiates responses in those cells.


Midbrain Cerebrum

Cerebellum Medulla Brainstem

Brainstem Uppermost part of the spine, where the spine joins the brain Medulla - controls vital housekeeping functions, such as heartbeat, blood pressure and peristalsis.

Cerebellum - controls muscle co-ordination & learns motor programmes (e.g. like how to ride a bike, or write).

Thalamus a relay station that carries sensory information from the sense organs to the correct part of the cortex and hypothalamus. The thalamus contains the Superior Collicului, which control the initial processing of visual information. The Superior Colliculi control object tracking, spatial position and partial recognition (i.e. whether a stimulus is food or a threat) Hypothalamus receives sensory information from the thalamus. Contains homeostatic centres, which control factors like body temperature and blood osmolarity. The hypothalamus is connected to the Pituitary gland and therefore the hypothalamus can stimulate the release of a great number of pituitary hormones

Cortex processes sensory information and controls the bodys voluntary behaviour, i.e. learning, personality and memory. This is the part of the brain that actually thinks. The cortex is very large in humans and is folded to increase the surface area further. Other animals have roughly similar size hind- and midbrains. However, their cortex is much, much smaller.


(Speech motor Auditory area)association area

Somatosensory Visual association area


What it allows us to see The patient can tell the doctor what he/she is feeling as the doctor stimulates parts of Surgery his/her brain. This can tell us a lot about the function of the brain. (Understanding language) Thousands of narrow-beam X- CT Scans show brain structures, rays pass through the patients not brain activity. They also only head from a rotating interprets information still Occipital lobe - processes & source. give frozen from theimages. eyes The rays are collected on the However, they are very useful other side of the head and for picking up diseases, such as their strength measured. The cancer, stroke and oedema. Temporal lobe - processes & interprets information from the C T Scan density of the tissue the Xray ears and processes language and the meaning of words passes through decreases the strength of the signal, and Parietal lobe processes work interprets information about therefore, lets us and out touch, taste,type of tissue is in the cold. Also initiates motor what pressure, pain, heat and commands. brain. Magnetic fields are used to By recording the energy given Frontal lobe - planswater organises thought, is involved with up a align protons in and molecules out by protons we can build in the patients brain. When the sequence short term memory and puts speech together. of thin pictures of the fields are switched off, the types of tissues inside the brain. MRI Scan 5.8.8 protons give out a little energy, This can be fed into a computer, which can be detected. which uses the picture to build up a 3D image of the inside of the head Very similar to above, except that the magnetic fields are tuned to excite deoxygenated haemoglobin. This shows up all the areas in the brain where oxygen is being used As above, but the doctor not only knows what the tissues look like, but whether they are active. This is the only technique, that shows brain activity.

How it works During brain surgery a local anaesthetic is often used. This allows the surgeon to ask the patient questions as he operates on their brain

fMRI Scan

How to process stimuli correctly must be learned. The cortex is split into column of cells. When we are born, the columns overlap and are tangled. As we learn to process stimuli, the cells organise themselves into discrete columns, which no longer overlap. There is a critical window for this to happen (usually before puberty,

younger for visual processing). If we miss the window, our brains will become fixed with tangled columns and wont be able to process stimuli properly. Hubel & Wiesels experiments prove this.

The Muller-Lyer illusion;

Lines A and B are the same length, yet look different why? The answer is that you have learned to process this kind of stimuli in a certain way. We live in a carpentered world of straight lines and we interpret line B as a corner (therefore larger than it appears, because it must be far away) and line A as a corner (therefore, smaller than it appears, because it must be close). These optical illusions do not work on Zulus, which proves the illusion is caused by learned visual processing, rather than an innate function of the eye / brain.

Association (classical conditioning): US UR (Food Salivation)

Over time, if a neutral stimulus (CR) is played with the US, it becomes associated with the US and begins to elicit the same response. Eventually, the animal learns CS CR (Bell Salivation)

Pavlovian conditioning occurs by synapses between nerves growing together. This means that the sensory nerve carrying the message of the CS will always lead to the firing of the motor nerve, which triggers the CR. Operant Conditioning: This is very similar to classical conditioning except the animal learns by doing something i.e. it learns that an action has a certain outcome A O Habituation: If the neutral stimulus is continuously present (not just before the US), but all the time, the animal learns to ignore the CS. The animal learns the bell signals nothing and it ignores the CS totally. This is called habituation. If a nerve is frequently stimulated, the amount of Ca2+ that enters the pre-synaptic nerve gradually diminishes, until it is no longer enough to trigger vesicles to fuse with the pre-synaptic membrane. This means no neurotransmitter is released, which results in no post-synaptic depolarisation. The effect is, essentially, that the stimulus is ignored. Insight Learning: In the early 1900s, Wolfgang Kohler performed insight experiments on chimpanzees. Kohler showed that the chimpanzees sometimes (pushing a level food)

used insight instead of trial-and-error responses to solve problems. When a banana was placed high out of reach, the animals discovered that they could stack boxes on top of each other to reach it. They also realized that they could use sticks to knock the banana down. In another experiment, a chimp balanced a stick on end under a bunch of bananas suspended from the ceiling, then quickly climbed the stick to obtain the entire bunch intact and unbruised (a better technique than the researchers themselves had in mind). Kohler's experiments showed that primates can both see and use the relationships involved to reach their goals. This type of learning is very difficult to explain using the Pavlovian model of conditioning. It is also difficult to explain using neuronal models of learning (i.e. synapses growing together through use) developed through studies on Aplysia. How insight learning occurs is unknown at the moment.

Pavlovs Dogs Pavlov had observed that an unconditioned stimulus causes an unconditioned response, i.e. food causes salivation. This is not learned and is, therefore, unconditioned. What Pavlov discovered was that if a neutral stimulus, such as a bell is rung just before the food is given for a few occasions, the dog will salivate every time the bell is rung, even if no food is presented. In this case, the dog has learned that the bell signals food. The food is, therefore, a conditioned stimulus and it prompts a conditioned response. US UR US + CS UR Eventually, CS CR Hubel & Wiesel

Permanently blind monkeys?

Hubel & Wiesel investigated the critical window. They used monkeys and kittens in their studies Their work permanently blinded some animals and can be argued to be unethical.

Hubel & Wiesels Method:

1. 2.

Raise monkeys from birth in three groups for 6 months Group 1 are the control (no blindfold), Group 2 are blindfolded in both eyes, Group 3 are blindfolded in one eye (monocular deprivation)

3. Test the monkeys to see whether they can see using each eye 4. Test the sensitivity of retinal cells 5. Test the activity of nerves in the visual cortex in response to stimuli The results:

Monkeys in Group 2 (both eyes blindfolded) had impaired vision Monkeys in Group 3 (monocular deprivation) were blind in the deprived eye Retinal cells were responsive in all groups Cortical activity was reduced in parts of the brain that process information from the deprived eye Adults undergoing the same tests showed no difference between groups. All could see.

The Conclusion: There is a critical window for visual neural development, which requires stimulus from the eye. If this window is missed the monkey is blind, because of events happening in the brain, not the eye. You need to know about these experiments because they all use animals


Arguments For

Arguments Against

Clinical Trials Stage 1 involves animals.Why not use computer simulations in Without animals we would not be ableClinical trials instead? to discover new drugs Animal physiology is different to human Animal testing is better than nothingphysiology. Animal testing is, therefore, and does, in some cases, avertunhelpful potential loss of human life Utilitarian argument: Animal testingAnimals have rights too. is for the greater good Animals have no informed consent Machines like the MRI were unvested using animals. Testing on animals when the potential side-effects are unknown is immoral. Animal testing has advanced our understanding of human physiology Animals cant tell you when they are suffering


Animals are often poorly cared for in labs In Parkinsons disease neurons in the brain die. All these neurons secrete dopamine neurotransmitter, which causes difficulty in movement and limb shaking. In depression neurons in the brain that secrete serotonin neurotransmitter stop working properly and serotonin levels fall.

In both cases treatments that increase the levels of neurotransmitter might prove successful in relieving the symptoms of these diseases

Drugs that affect synapses can drastically alter the functioning of the brain; MDMA: Active ingredient in ecstasy. This binds to protein pumps on the pre-synaptic membrane of nerves that secrete serotonin. The pumps would normally take serotonin up after it had been released, therefore reducing firing in post-synaptic nerves. BUT, when these channels are blocked, serotonin builds up in the cleft, giving greater post-synaptic activation and a sense of euphoria. L-Dopa: This is a precursor of dopamine. When given to Parkinsons sufferers it is turned into dopamine, which helps alleviate some of the symptoms of the disease.

Continuous variation: there is a wide range of phenotypes (e.g. height) Discontinuous variation: phenotypes fall into discrete categories (e.g. blood type) Discontinuous variation tends to be coded for by one gene with a few different alleles. However, continuous variation is more complex. This is usually coded for by many genes (polygenes), with many alleles, which produces the much greater range of possible phenotypes.

Polygenes can give rise to susceptibility to disease, usually with an environmental trigger. Diseases that are both genetic and environmental are called multifactorial

Brain development is a combination of nature and nurture.

Courtesy of Wellington College