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A Level OCR Biology A CGP Book Summary, Units 5 to 8 (Post 2015 Spec)
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BIOLOGY A2Homeostasis
Stmuli, Receptors and Efectors
Changes in External Environment: Animals and plants increase their chances of survival by
responding to changes in external environment as could be harmful. E.g. light intensity and
external temperature.
Changes in Internal Environment: Animals and plants respond to changes in internal
environment so conditons are optmal for metabolism. E.g. blood glucose conc, internal temp,
water potental and cell pH.
Stimulus: Any change in internal OR external environment is called stmulus.
Receptors: Stmuli are detected by receptors. Some receptors are cells e.g. photoreceptors.
Some receptors are proteins on cell surface membranes e.g. glucose receptors in pancreatc
cells.
Effectors: Efectors are cells that bring about a response to stmulus. Examples are muscle cells
and cells in glands e.g. pancreas.
Communicaton
Cell Signalling: Receptors, efectors and other cells communicate via cell signalling so body cells
and systems coordinated to work efectvely. Cell signalling can occur between adjacent or
distant cells. For example…
Cells in nervous system- they communicate by secretng neurotransmiters, which send nerve
impulses to adjacent nerve or muscle cells.
Cells in hormonal system- they communicate by secretng hormones, which travel in blood to
distant cells. Hormones soluble in blood.
Both nervous and hormonal system are communicaton systems.
Cell- Surface Receptors: Cell- surface receptors allow cells to recognise chemicals involved in
cells signalling.
,Homeostasis
Homeostasis: Homeostasis is the maintenance of a constant internal environment- ensures cells
functon and do not damage.
Temperature: Important to maintain core body temperature. Highest rate of enzyme actvity is
37C, the optmum temperature in humans.
Too High Temperature: If temperature too high, enzymes denature- enzyme’s vibrate more, so
hydrogen bonds break, so shape of actve site changed. So enzymes no longer work as catalysts
and metabolic reactons less efcient.
Too Low Temperature: If temperature too low, enzyme actvity reduced, which slows rate of
metabolic reactons.
Glucose: Important to maintain correct concentraton of glucose in blood, so enough for
respiraton.
Negatve and Positve Feedback
Homeostatic System: Homeostatc systems involve receptors, communicaton system and
efectors.
Receptors: Receptors detect when level is too high or too low. Informaton is communicated via
the nervous or hormonal system to efectors.
Effectors: Efectors respond by counteractng change.
Negative Feedbaac Mechanism: Mechanism that restores level to normal is negatve feedback
mechanism. E.g. temperature. Negatve feedback has certain limits, for example if change is too
big, efectors may not be able to counteract.
Positive Feedbaac Mechanism: Efectors respond to certain stmuli to further increase level
away from normal level is positve feedback. Positve feedback isn’t homeostasis as doesn’t keep
internal environment constant.
Platelet Example: A blood clot afer injury- Platelets become actvated and release chemical.
This triggers more platelets to be actvated and so on. Platelets form blood clot.
Control of Body Temperature
Animals either ectotherms or endotherms…
Ectotherms: Examples are reptles and fsh.
- Can’t control body temperature internally. Change their behaviour instead e.g. reptles gain
heat by basking in sun.
- Their internal temperature depends on external temperature.
- Their actvity level depends on external temperature. More actve at higher temperature.
- Have variable metabolic rate and generate litle heat themselves.
Endotherms: Examples are mammals and birds.
- Control their body temperature internally by homeostasis. Also control temperature by
behaviour e.g. fnding shade.
- Internal does not depend on external.
- Actvity level does not depend on external temperature.
- Constantly high metabolic rate and generate lot of heat from metabolic reactons.
Mammals Mechanisms to Reduce Body Temperature… WHEN HOT.
, - Sweating: Sweat secreted from sweat glands. Water evaporates in sweat from skin, takes
heat from the body, which cools skin.
- Hairs Lie Flat: Erector pili muscles relax, so hairs lie fat. Less air trapped, skin less insulated
and heat lost more easily.
- Vasodilation: Arterioles near surface of skin dilate- vasodilaton. More blood fows through
capillaries in surface layers of dermis. More heat lost by radiaton, temperature lowered.
Mammals Mechanisms to Increase Body Temperature… WHEN COLD.
- Shivering: Muscles contract in spasms, makes body shiver, more heat produced from
increased respiraton.
- Less Sweat: Less sweat secreted from sweat glands, reduces heat loss.
- Hairs Stand Up: Erector pili muscles contract, hairs stand up, traps more air, insulates, so
prevents heat loss.
- Vasoconstriction: Arterioles near surface of skin constrict- vasoconstricton, less blood fows
through capillaries in surface layers of dermis. Reduces heat loss.
- Hormones: Body releases adrenaline and thyroxine. Increases metabolism, more heat
produced.
Hypothalamus: The hypothalamus keeps body temperature at constant level in mammals.
Thermoreceptors: Thermoreceptors in the hypothalamus detect internal temperature (the
blood). Thermoreceptors in the skin, called peripheral temperature receptors, detect external
temperature (temperature of skin).
Homeostasis: Hypothalamus receives informaton about temperature from thermoreceptors
(temp receptors) via sensory neurone. Then impulse sent along motor neurone to efectors e.g.
skeletal muscles, sweat glands or erector pili muscles in skin. Restores body temperature back to
normal.
Control of Blood Glucose
Blood Glucose Concentration: All cells need constant energy supply so blood glucose
concentraton must be controled.
Lifestyle: Blood glucose concentraton rises afer eatng carbohydrates. Blood glucose
concentraton falls afer exercise, as more glucose used in respiraton.
Glucose Too High: Insulin lowers blood glucose concentraton when too high. Insulin binds to
specifc receptors on cell membranes of hepatocytes and muscle cells.
- This increases permeabaility of cell membranes to glucose, so cells takes up more glucose.
- Insulin also actvates enzymes to convert glucose to glycogen so cell can store glycogen in
cytoplasm for energy/ ATP- called glycogenesis.
- Insulin also increases rate of respiration of glucose.
Glucose Too Low: Glucagon raises blood glucose concentraton when too low. Glucagon binds to
specifc receptors on cell membranes of hepatocytes.
- Glucagon actvates enzymes that break down glycogen to glucose- glycogenolysis.
- Glycagon also forms glucose from faty acids and amino acids. The process of forming
glucose from non- carbohydrates called gluconeogenesis.
- Glucagon decreases rate of respiraton of glucose.
Homeostasis:
- Pancreas detects blood glucose concentraton too high/ low.
, - Beta cells secrete insulin OR alpha cells secrete glucagon.
- Insulin/ glucagon binds to receptors.
- Responses above- the efectors. Causes less glucose/ more glucose in blood- back to normal
level.
- Negatve feedback mechanism.
Process of Beta Cells Secreting Insulin… Insulin stored in vesicles of beta cells.
- When blood glucose concentraton high, more glucose enters beta cells by facilitated
difusion through channel proteins.
- This causes rate of respiraton in beta cell to increase, making more ATP since glucose enters
glycolysis pathway.
- Rise in ATP triggers potassium ion channels in beta cell plasma membrane to close, so
positvely charged potassium ions build up in cell.
- Makes inside of beta cell less negatve, so beta cell is depolarised.
- Depolarisaton triggers calcium ion channels to open and calcium ions difuse into beta cell.
- This causes vesicles to fuse with beta cell plasma membrane, releasing insulin by exocytosis.
Diabetes
Diabaetes: Diabetes mellitus is when blood glucose concentraton can’t be controlled properly.
Type 1 Diabaetes: Type 1 diabetes is an auto- immune disease. Body destroys beta cells in islets
of Langerhans. So body can’t produce any insulin. Afer eatng, blood glucose concentraton
stays high, which can result in death.
Kidney can’t reabsorb all this glucose, so some excreted in urine. Develops in children. Risk of
developing is increased if family history of disease.
Treatment of Type 1…
Insulin Therapy: Type 1 diabetes treated with insulin therapy. Need regular insulin injectons
throughout day. Some use insulin pump- it contnuously delivers insulin into body via tube
inserted beneath skin.
Islet Cell Transplantation: Some people treated with islet cell transplantaton. Receive healthy
islet cells from donor so their pancreas can produce insulin.
Lifestyle: As well as treatment, suferers need to eat healthy diet to reduce amount of insulin
needed to be injected. Need to do regular exercise to also reduce amount of insulin injected by
using up blood glucose.
Stem Cells: Stem cells are unspecialised. Stem cells could be grown in beta cells. Beta cells then
implanted into pancreas of person with Type 1 diabetes. Person would make insulin as normal.
This treatment stll being developed but could cure Type 1 diabetes and permanent/ no
repeated treatments.
Type 2 Diabaetes: Type 2 diabetes occurs when beta cells don’t produce enough insulin. Or
occurs when insulin receptors don’t respond as well to insulin. Means blood glucose
concentraton higher than normal.
Type 2 diabetes acquired later in life than Type 1. Linked with obesity. Risk of type 2 increased in
certain ethnic groups (African/ Asian) and with family history of disease.
Treatment of Type 2…
Lifestyle: Type 2 diabetes initally managed by lifestyle changes. Eatng healthy diet, regular
exercise and losing weight.
, Medication: If blood glucose concentraton not being controlled by lifestyle, medicaton
prescribed. For example metformin- acts on liver cells to reduce amount of glucose they release
into blood. Also increases sensitvity to insulin to cells so more glucose taken up. Sulfonylureas-
pancreas produces more insulin.
Insulin Therapy: If medicaton not enough to control blood glucose concentraton, insulin
therapy used.
Genetically Modified Bacteria: Now human insulin can be produced by genetcally modifed
bacteria. Insulin used to be extracted from animal pancreases to treat Type 1. GM bacteria
beter because…
- GM cheaper than extractng from animal pancreases.
- Larger supply can be produced with GM.
- GM makes human insulin. Less likely to trigger allergic response or be rejected by immune.
- GM beter ethically and religiously. Vegetarians may object the use of animals and religious
people object insulin from pigs.
Neuronal Communicaton
Nervous System
Nervous System: Nervous system made of neurons, which send informaton as nerve impulses
aka acton potentals. Nerve impulses are electrical impulses.
3 Types of Neurons: Relay neurons transmit acton potentals between sensory neutrons and
motor neutrons in CNS (the brain and spinal cord).
Energy of Stmulus and Potentals
Sensory Receptors: Sensory receptors are specifc to single type of stmulus. Examples are
mechanoreceptors, chemoreceptors, thermoreceptors and photoreceptors (light). Diferent
stmuli have diferent forms of energy e.g. light or chemical energy.
Conversion of Energy: Sensory receptors convert energy of stmulus into electrical energy/
generator potental. Sensory receptors therefore act is transducers- conversion of one energy
form into another.
Resting Potential: When nervous system receptors in restng state, there’s diference in charge
between inside and outside of cell, so a voltage aka potental diference across the membrane.
This is caused by ion pumps and ion channels. The potental diference when cell at rest is called
its restng potental.
Stimulation: When stmulus detected, cell membrane of neurone becomes more permeable.
This allows ions to move in and out, altering potental diference. Causes depolarisaton.
Generator Potential: The change in potental diference caused due to this stmulus is called
generator potental. A bigger stmulus, causes greater excitaton of membrane, bigger
movement of ions, bigger change in potental diference so bigger generator potental produced.
Action Potential: An acton potental (nerve impulse) only triggered stmulus strong enough so
generator potental reaches threshold potental. If threshold not reached, no acton potental-
‘all or nothing’ principle.
, Strength of Stimulus: No mater how big stmulus is, acton potental will fre same magnitude.
However will fre acton potental more frequently, which brain will interpret as big stmulus.
Pacinian Corpuscles: Pacinian corpuscles are mechanoreceptors- detect mechanical pressure
and vibratons. Found in skin. Pacinian corpuscles contain end of sensory neurone called sensory
nerve ending, which is wrapped in layers of connectve tssue/ lamellae.
Process when Pacinian Corpuscle Stimulated…
- When Pacinian corpuscle stmulated, lamellae/ corpuscle changes shape and press on
sensory nerve ending.
- Cell membrane of sensory neurone stretches, stretch-
mediated sodium channels widen. Causes to sodium ion
difuse into cell. Causes depolarisaton.
- This creates generator potental. If generator potental
reaches threshold, it triggers acton potental.
Types of Neurons
Cell Body: All neurons have cell body which contains nucleus and organelles such as ER and
mitochondria for producing neurotransmiters.
Extensions: Cell body has extension... Dendrons which divide into dendrites. Dendrons carry
nerve impulse from receptor to cell body. Axons- singular, elongated nerve fbre. They carry
impulse away from cell body to CNS.
Sensory Neurons: Sensory neurons have short dendrites. One dendron and one axon. Cell body
in middle.
Motor Neurons: Motor neurons have short dendrites. One long axon. Cell body in CNS. Cell body
at end. No dendron.
Relay Neurons: Relay neurons have many short dendrites. Many short axons.
Myelinated Neurones: Schwann cell produces myelin sheath, an electrical insulator. These
neurones are myelinated. Depolarisaton only happens at nodes of Ranvier. Faster transmission.
Saltatory conducton means impulse ‘jumps’ from node to node. The top one in right pic.
Label as Schwann cell and not myelin sheath.
Nodes of Ranvier: Between the Schwann cells are patches of bare membrane called nodes of
Ranvier. Sodium ion channels are concentrated at the nodes.
Non- Myelinated Neurone: In non- myelinated neurone, impulse travels as wave along whole
length of axon membrane. Slower than saltatory conducton. The botom one in right pic.
Acton Potentals
, Process of Resting Potential/ Polarisation…
- -70mV is the resting potential.
- Sodium- potassium pumps actvely transport (ATP) sodium ions out of neurone, but sodium
ions can’t diffuse back in as membrane impermeable to sodium ions. Creates a sodium ion
electrochemical gradient.
- Sodium- potassium pumps actvely transport potassium ions into neurone. Potassium ions
however can diffuse back out through potassium ion
channels using facilitated difusion down concentraton
gradient.
- This makes outside of cell positively charged compared to
inside as more positve ions outside cell than inside when
neuron at restng state (not stmulated).
- Membrane polarised- diference in charge, inside negatve.
- POP.
- SO PO PI (sodium out, potassium out, potassium in).
Process of Action Potential…
- When stimulated, neurone cell membrane excited, causing sodium ion channels to open. So
sodium ions difuse into neurone down sodium ion electrochemical gradient. Makes inside
of neurone less negative.
- Depolarisation- if potental diference reaches the threshold (-55 mV), voltage gated
sodium ion channels open (voltage gated open at certain voltage). More sodium ions difuse
into neurone. This is positve feedback.
- Repolarisation- at potental diference +30 mV, sodium ion channels close and voltage-
gated potassium ion channels open. So potassium ions difuse out of neurone down
potassium ion concentraton gradient. This starts to get membrane to restng potental.
Negatve feedback.
- Hyperpolarisation- potassium ion channels are slow to close so slight ‘overshoot’ where too
many potassium ions difuse out. Potental diference more negative than restng potental.
- Resting Potential- ion channels reset. Sodium- potassium pump returns membrane to
restng potental and maintains untl another stmulus.
- SS SP (sodium IC open, sodium VG open, sodium IC close + potassium VG open).
- Depolarised- inside less negatve (so outside and inside positve).
Refractory Period: Afer acton potental, neurone cell membrane can’t be excited again straight
away. Because ion channels are recovering and can’t be made to open. Called refractory period.
Process of Action Potential along Neurone...
- When acton potental occurs, some of the sodium ions that difuse into neurone, difuse
sideways along neurone.
- This causes sodium ion channels in next region of neurone to open and allow sodium ions to
difuse in- a wave of depolarisaton to travel along neurone.
- The wave moves away from the parts of the membrane in refractory period because these
can’t fre an acton potental.
,Synapse
Synapse: A synapse is a juncton between a neurone and another neurone/ efector cell.
Synaptic Clef: A synaptc clef is gap between the cells at a synapse.
Presynaptic Neurone: The presynaptc neurone has synaptc knob. This contain synaptc vesicles
with neurotransmiters.
Process of Nerve Impulse baetween Synapse…
- An acton potental arrives at synaptc knob of presynaptc neurone, which stmulates
voltage- gated calcium ion channels to open. Calcium ions difuse into synaptc knob.
- This causes synaptic vesicles to move and fuse with the presynaptc membrane. Vesicles
release neurotransmiter into synaptc clef by exocytosis.
- Neurotransmiter diffuses across synaptc clef and binds to specifc receptors on
postsynaptc membrane.
- This causes sodium ion channels to open so sodium ions difuse into postsynaptc neurone.
- This causes depolarisation. Action potential on postsynaptc membrane generated if
threshold reached, which can cause muscle contracton or hormone secreton.
- Neurotransmiters are baroen down (by enzymes) in synaptc clef so response doesn’t keep
happening. Or neurotransmiters may be taken back into presynaptc neurone.
Cholinergic Synapses: Acetylcholine (ACh) is a type of neurotransmiter. Synapses that use ACh
are cholinergic synapses and ACh binds to cholinergic receptors. ACh common in CNS and
neuromuscular junctons.
- Acetylcholine broken down/ hydrolysed by enzyme acetylcholinesterase (AChE) to give
choline and ethanoic acid- which are taken into presynaptc knob to be reformed.
Two types of Neurotransmiter…
- Excitatory: These neurotransmiters result in depolarisaton of postsynaptc neurone. If
threshold reached, acton potental triggered. ACh an example.
- Inhibaitory: These neurotransmiters result in hyperpolarisaton of postsynaptc neurone.
Prevents acton potental being triggered. Gamma- aminobutyric acid (GABA) an example,
found in brain.
, Drugs: Drugs may bind to receptors on postsynaptc neurone. This blocks neurotransmiter from
binding. Sodium ion channels do not open so Na+ cannot enter. No/ insufcient depolarisaton-
does not reach threshold potental.
Some poisons cause constant depolarisaton/ constant fring of acton potentals.
Importance of Junctions- ensures that only stmulaton that is
strong enough will be passed on. Also stuf below works due to
junctons.
Synaptic Divergence: When one neurone connects to many
neurones, informaton dispersed to around body- synaptc
divergence. Single stmulus creates number of simultaneous
responses.
Synaptic Convergence: When many neurons connect to one neurone, informaton amplifed-
synaptc convergence. Diferent receptors produce same response.
Summaton is about building up amount of neurotransmiter, as amount of neurotransmiter
from single impulse not enough to reach threshold level and trigger acton potental.
Spatial Summation: Spatal summaton is when many presynaptc neurones converge, small
amount of neurotransmiter released from each neurone. All together this reaches threshold in
a single postsynaptc neurone and triggers acton potental. Multple stmuli would give single
response.
Temporal Summation: Temporal summaton is where a number of nerve impulses arrive in
quick succession from single presynaptc neurone. Neurotransmiter builds in synaptc clef and
if reaches threshold, acton potental triggered. It is high frequency of weak impulses.
One Direction: Receptors for neurone transmiters only on postsynaptc membranes so acton
potental only travel in one directon. Only presynaptc neurone releases neurotransmiter and
has calcium ion channels. Also neurotransmiter broken down at postsynaptc neurone so only
one directon.
Hormonal Communicaton
Hormonal System
Hormonal System: The hormonal system aka endocrine system.
Endocrine Glands: Endocrine glands are groups of cells that are specialised to secrete hormones
when stmulated. Glands can be stmulated by change in concentraton of a substance OR by
electrical impulses.
Hormones: Hormones are chemical messengers. Many are proteins or peptdes. Some are
steroids. Hormones difuse into blood and travel around body via circulatory system.
Receptor: Hormones bind to a specifc receptor- complementary shape. Receptors found on
membranes of target cells in target tssue. Cell receptors are glycoproteins and glycolipids.
Effector: Hormones trigger a response in target cells (the efectors).
Some medicinal drugs/ poisons work because they’re complementary to certain cell receptor
sites. Some drugs may block hormones to prevent response. Others mimic hormones.
, Steroid Hormones: Steroid hormones are lipid soluble. Pass through cell membrane and bind to
steroid hormone- receptor complex in cytoplasm or nucleus. Steroid hormone- receptor
complex acts as transcripton factor so facilitates/ inhibits transcripton of gene, steroid
hormones interact with DNA. Example is oestrogen.
Non- Steroid Hormone: Peptide hormone. They are hydrophilic so cannot pass directly through
cell membrane. Instead bind to cell surface membrane of target cell, uses secondary messenger
to trigger a cascade etc. Examples are adrenaline and hCG.
Cell Signalling
Hormone: Hormone is called frst messenger because carries chemical message for frst part-
gland to receptor.
Enzyme: When hormone binds to receptor, actvates an enzyme in cell membrane. Enzyme
catalyses producton of signalling molecule inside the cell.
Signalling Molecule: Signalling molecule signals to other parts of cell to change how cell works,
actvate a cascade (chain of reactons) inside the cell. Signalling molecule called second
messenger because carries chemical message for second part.
Adrenaline: This is one of the efects of adrenaline in fght or fight response. Adrenaline is frst
messenger. Adrenaline does not pass through cell membranes. It binds to specifc receptors in
cell membranes of many cells e.g. in this case liver cells.
This actvates enzyme adenylyl cyclase in membrane, which catalases producton of ATP into
cyclic adenosine monophosphate (cAMP), the second messenger. cAMP actvates a cascade of
enzyme reactons to catalyse breakdown of glycogen into glucose (glycogenolysis) for increased
respiraton for energy for muscle contracton in liver cells.
Diferent tssues have diferent receptors for adrenaline so produces diferent efects in diferent
target tssue. As secondary messenger diferent or secondary messenger actvates diferent
enzymes in the diferent target cells.
Overexpression of Gene: Overproducton of a hormone means overexpression of the gene. So
more protein synthesised.
Adrenal Glands
Adrenal Glands: Adrenal glands are endocrine glands. Found above kidney. Each adrenal gland
has outer part- cortex. And also inner part- medulla.
Adrenal Cortex: Cortex secretes steroid hormones such as…
- Cortisol: A glucocortcoid. Regulates metabolism by controlling conversion of fats, proteins
and carbohydrates into glucose for energy. In response to stress, regulates blood pressure.
- Corticosterone: Another glucocortcoid. Works with cortsol to regulate immune response
and supress infammatory reacton. Controlled by hypothalamus.
- Aldosterone: A mineralocortcoids. Controls blood pressure by maintaining balance of salt
and water concentratons in blood and body fuids. Triggered by kidney.
- Androgens: Male and female sex hormones.
Adrenal Medulla: Stmulated by sympathetc nervous system. Medulla secretes catecholamine
hormones- adrenaline and noradrenaline when stressed/ fght or fight- see topic. Hormones act
short term.
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