edexcel a2 biology unit 4 revision cards [autosaved]

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How you can use these notes:

Write them again and again- every day & memorise them.

Write out/ Print in A4 and stick on your wall- read before sleep.

Print out as A5 flashcards and revise from them.

All of the above because youre serious about that grade.

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PHOTOSYNTHESIS

Light- dependant reactions (in the thylakoid membrane) [Produces ATP and reduced NADP]

Energy from sunlightraises two electrons in

chlorophyll to a higher

energy level.

6CO2 + 6H2O C6H12O6 + 6O2

Definition: Using energy from sunlight to split apart the strong bonds in water molecules. Storing the hydrogen in a fuel

(glucose) by combining it with CO2 and releasing oxygen gas to the atmosphere as a waste product.

Light- independent reactions (The Calvin Cycle) (in the stroma) [Produces GALP]

Energy lost by the electrons are used

to produce ATP in

photophosphorylation (P(i) added to

ADP using energy from sunlight.)

The two electrons pass through carrierproteins in the electron transport chain. They

gain and lose energy through a series of

oxidation and reduction reactions.

In the thylakoid space, an

enzyme catalyses the photolysis

of water into H+ , electrons andO2 (waste product.)

Electrons from photolysis of water replace

those emitted by the chlorophyll molecule

(so it is no longer positively charged).Photolysis raises H+ concentration in the

thylakoid space.

The electrons passed through

the electron transport chain

combine with H+ and thecoenzyme NADP to make

reduced NADP.

CO2 combines with (5C) RuBP

(Ribulose Biphosphate). Thisreaction is catalysed by the

enzyme RUBISCO (Ribulose

Biphosphate Carboxylase.)

This forms an unstable (6C)

compound which immediatelybreaks down into two (3C)

compounds called GP (Glycerate 3-

phosphate.)

GP is reduced using the ATP and

reduced NADP from L-dependantreactions, regenerating coenzyme NADP.

This produces (3C) GALP

(Glyceraldehyde 3-phosphate.)

2/12 GALP used to synthesise a (6C) sugar-

this is used to make biological molecules e.g.

amino acids, lipids, nucleic acids &polysaccharides.

10/12 GALP used to regenerate RuBP to continue the Calvin

cycle. The 10 GALP rearrange to form 6 (5C) compounds which

are phosphorylated using ATP to form RuBP.

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ESTIMATING TIME OF DEATH

Body temperatureHuman core body temperature is around 37oc.

Immediately after death, the temperature starts to fall-

in the absence of heat-producing chemical reactions.

Core temperature is measured via the rectum or usingan abdominal slab.

Rigor mortisAfter death muscles totally relax, then stiffen.

-After death, the body is starved of oxygen so oxygen-dependant

reactions stop.

-Respiration is now anaerobic which produces lactate.-Lactic acid decreases the pH of cells which inhibits enzymes so

anaerobic respiration stops.

-The ATP required for muscle contraction is not available- this

causes bonds between muscle proteins to become fixed.

-The proteins can no longer move over one another to shorten

the muscle- fixing muscles and joints.

-Rigor mortis eventually passes off as muscle tissue starts tobreak down, in the order in which it was formed.

Factors that affect post-mortem cooling-Body size -Body position

-Clothing -Movement of air

-Humidity -Temperature

-Whether the corpse was immersed in water

Signs of decompositionPutrefaction- Greenish colouration of the lower abdomen as a

result of a formation on sulphaemglobin. Gas or liquid blisters

appear on skin.

Stages of successionThe population of organisms on a corpse changes over

time as the body decays. There is a succession of

species. The community of species found on the body

can give an estimate of T.O.D. by allowing the stage of

succession to be determined.

Forensic entomologyThe stage of development of any insect on the corpse, though its lifecycle can help work outT.O.D. The stage of development of maggots can be considered with reference to the life cycle of a fly- to give estimate of

maggot age. Determining age of insects- can estimate when eggs were laid on the body= estimate T.O.D. assuming eggs

were laid soon after death. Other factors e.g. toxins will affect results (cocaine will affect development.)

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NON- SPECIFIC IMMUNITYPathogens enter the body through:-Cuts on skin

-Digestive system via food & drink

-Respiratory system via being inhaled

-Other mucosal surfaces.

But the body has BARRIERS to infection- Skin: physical barrier. However, if the skin is damaged,

pathogens can enter the blood stream. Blood clots to

prevent this but pathogens may enter before clotting.

- Stomach acid: Pathogens in your food & drink will

mostly be killed by stomach acid. Those that survive

pass into intestines, invade the gut wall and causedisease.

- Gut and skin flora: The intestines and skin are covered

with billions of harmless microbes. These compete with

pathogens for nutrients and space, keeping their

numbers down.

- Lysozyme: Enzyme present in secretions produced by

mucosal surfaces (eyes, mouth, nose.) These kill bacteria

by damaging their cell walls> causes cell lysis> causescell death.

Inflammation at the infection siteSite at which pathogens enter becomes red, swollen, warm

and painful.

Immune system cells recognise foreign antigens and release

molecules that trigger inflammation.-Molecules cause vasodilation around site.

-Increases blood flow to site> molecules increase permeability

of blood vessels> lots of blood cells, these destroy the

pathogen.

Interferon: anti-viral proteinCells infected with viruses produce protein interferon's.

-These prevent viruses spreading to uninfected cells by:(1) Preventing viral replication by inhibiting production of viral

proteins.

(2) Activate cells of specific immunity to kill infected cells.

(3) Activate other non-specific mechanisms e.g. inflammation.

Phagocytosis: engulfment of pathogens

Phagocytes are found in the blood and tissues, they are thefirst cells in the body to respond to pathogens. Phagocyte

recognises antigen on pathogen as foreign> cytoplasm of

phagocyte moves around the pathogen, engulfing it. The

pathogen is now in a phagocytic vacuole.

-A lysosome (organelle) which contains digestive enzymes,

fuses with the phagocytic vacuole and the enzymes break

down the pathogen. The pathogen then becomes and

Antigen Presenting Cell (APC.)

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Antigens:

Protein or polysaccharide markers found on the surface

of all cells- helps to identify them e.g. as self cells or

foreign cells.

APCs show antigens on the surface membranes toactivate other immune cells. Macrophages are a type

of phagocyte (White Blood Cell) that can become an

APC (Antigen Presenting Cell) after engulfing a

pathogen.

Antibodies:

Plasma cells make antibodies to a specific antigen.

Antibodies then bind to antigens on the surface of

pathogens to produce lots of antigen- antibody complexes.

The variable regions form antigen binding sites that are

complementary to the shape of the antigen.

Hinge regions allow flexibility when an antigen binds.

Disulphide bridges hold polypeptide chains together.

What antibodies do:

1) Agglutinating pathogens- each antibody can bind to twopathogens and make them clump together so phagocytes

can engulf many pathogens at once.

2) Neutralising toxins- antibodies bind to toxins produced by

pathogens, forming antibody-toxin complexes which get

engulfed.

3) Prevents pathogens binding to human cells- by blocking

the cell surface receptors that pathogens need to bind to

host cells. This happens when the antigen-antibody

complex is made. This means that these pathogens cannot

affect human cells.

Antigen-antibody complex:Antigen

Variable

region

Constantregions

Heavy

chain

Hinge

protein

Light

chain

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Activation of T-helper cells:Bacterium is covered in antigens. Macrophages engulf the

bacterium, becoming APCs (Antigen-Presenting Cells.) T-

helper cells with complementary CD4 receptors binds to the

APC. This binding activates the T-helper cell so it

divides and differentiates into (a) Clones of T-helper memorycells and (b) Clones of active T-helper cells.

Role of T-killer cellsBacterium infects the host cell which becomes an APC. The

complementary receptors on a T-killer cell bind to the APC.

This, as well as chemicals (cytokines) released by T-helper

cells activates the T-killer cell so that it divides and

differentiates into (a) Clones of T-killer memory cells and (b)

Clones of active T-killer cells. The active T-killer cells bind to

the APC and secrete chemicals which cause pores to form onthe APC, leading to cell lysis and cell death.

T-CELLS: activated by phagocytes

-Surface is covered in receptors.

-Receptors bind to antigens presented by phagocytes.

-Each T-cell has different receptors so each T-cell will bind to

a different complementary antigen. The binding activates

the T-cell so it divides into two different types with different

functions:

- T-helper cell: releases substances to activate T-killer

cells, macrophages and B-cells.

- T-killer cell: attaches to antigens on an APC and kills the

cell.

- T-memory cell: divides into the correct type of T-cell to

kill the cell presenting the non-self antigen.

B-cell clonal selection:Bacterium has antigens on it s surface. Antigens bind to

complementary antibodies on the surface of the B-cell. The

B-cell becomes an APC. A T-helper cell with complementary

receptors binds to the APC and release protein cytokines

which activate the B-cell. The B-cell divides anddifferentiates into (a) B- memory cells and (b) B-effector

cells. The B-effector cells further differentiate into plasma

cells which release the antigen-specific antibodies.

Antibodies bind to antigens on pathogens, making them

easily identifiable for destruction.

B-CELLS: activated by T-helper cells

-Surface is covered in antibodies.

-Each antibody binds to an antigen on the surface of a

pathogen, forming an antigen-antibody complex.

-Each B-cell has a different type of antibody on its surface

so it will bind to a different complementary antigen.

This binding, and chemicals released by T-helper cells

(cytokines) activates the B-cell so that it divides by mitosis

into:

-B effector cells/plasma cells: secrete the correct antibody

to the pathogens antigen.

-B memory cells: can later divide into plasma cells.

Memory cells remain in the body for months/years- givingthe person IMMUNITY to that pathogen.

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TB (Tuberculosis)HIV & AIDS

-The Human Immunodeficiency Virus causes AIDS.

-The virus infects and destroys immune system cells.

-AIDS is a condition where the immune system

deteriorates and eventually fails. People with HIV are

classed as having AIDS when symptoms of their failingimmune system starts to appear.

-AIDS sufferers generally develop opportunistic

infections- which would not cause serious problems to

someone with a healthy immune system.

-The length of time between infection with HIV and

development of AIDS varies but is usually 8-10 years.

The disease then progresses through a series of

symptoms:

-Mycobacterium Tuberculosis causes TB- a lung disease.

-The bacterium infects phagocytes in the lungs.

-Most people dont develop TB straight away- their immune

system seals off the infected phagocytes in the lung in

structures called tubercules.-The bacteria is dormant inside the tubercules and the

person shows no obvious symptoms.

-The bacteria can become reactivated, overcoming the

immune system and causing TB. This is more likely in people

with weakened immune systems e.g. AIDS sufferers.

-The length of time between infection with the bacteria and

the development of TB varies- from weeks to years.

-TB then progresses through a series of symptoms.

Initial symptoms: Minor infections of mucus

membranes and recurring respiratory infections-caused

by lower than normal number of immune system cells.

Progression: Number of immune system cells further

decreases. More serious infections e.g. Chronicdiarrhoea, severe bacterial infections, Tuberculosis.

Later stages: Very low immune system cell count at this

point. Suffers a RANGE of serious infections e.g.

Toxoplasmosis of the brain, Candidiasis of the

respiratory system. It is the serious infection that kills

the person, not the HIV itself.

Initial symptoms: fever, general weakness, severe

coughing- caused by inflammation of lungs.

Progression: TB progression damages the lungs. If its left

untreated, it can cause respiratory failure which can cause

death.-Also, TB can spread from the lungs to other parts of the

body e.g. the brain and kidneys. If this is left untreated, it

can cause organ failure and can lead to death.