The Internet belongs to everyone. Let’s keep it that way.

Protect Net Neutrality
Loading presentation...

Present Remotely

Send the link below via email or IM

Copy

Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.

DeleteCancel

Physiology

Showing the details of physiology for AS, A2 and IBDP
by

Alex Van Dijk

on 4 February 2016

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Physiology

The Body
Digestive System
Nervous System
Circulatory System
Respiratory System
Absorption of monosaccharides in the small intestine.
Villi in the small intestine
Each epithelial cell in the small intestine is lined with microvilli, this forms the 'brush' border.
At the start of the small intestine the concentration of glucose will be much greater in the intestine than in the bloodstream.
The glucose will move across the membrane using facilitated diffusion.
Why can't diffusion remove all the glucose from the intestine?
Co-transport of sodium and glucose will move the remaining glucose from the small intestine.
Cholera interferes with your gut epithelial cells. The toxin causes a release of Cl- ions into the lumen. To balance this shift in water potential, water and Na+ ions will also flood into the lumen, causing diarrhea, loss of ions and dehydration.
Humoral Immunity
B lymphocytes:
are matured in the bone marrow
are involved in humoral immunity
respond to foreign material outside cells
respond to bacteria, viruses and toxins.
T helper cells will bind to the B cell and activate it. This causes a clonal expansion of the B cells using mitosis
Memory cells explain why vaccinations work (and we'll look in more detail at this later)

and also why you can only get certain diseases once.
However certain pathogens will have hundreds of different strains, all causing the same disease, but not necessarily having the same antigens. This is known as
antigenic variability.
The body will not develop immunity against strains of the disease it has not seen before.
These strains can arise through 2 different processes:
antigenic drift
antigenic shift (currently only known in influenza)
In antigenic drift, mutations in the gene coding for the protein that is recognised cause it to change shape and thus no longer be recognised by the memory cells
In an antigenic shift, influenza acquires the antigens from a related virus in a different species. This will usually happen in a 3rd species. For example, H1N1 "swine flu" strain was formed by combining a duck influenza strain with a human influenza strain in a pig that was infected by both. This dramatic change means that there will be little to no immunity in a population.
Homeostasis
Stimulus and Response
A
stimulus
is a detectable change in the environment (internal or external) of an organism that produces a response in this organism.
Why is it advantageous for organisms to respond to their environment?
Organisms that can detect stimuli and respond to them have an evolutionary advantage.
If you respond to the presence of food by moving towards it you get more food than if you do not.
If you respond to being touched by moving away, you are less likely to be eaten than if you do not.
Stimuli are detected by
receptors.
The response is carried out by
effectors.
As receptors and effectors might be some distance apart in a multicellular organism a message has to be sent from the receptor to the effector.
This can be done via hormones or by nervous impulses (in animals). Nervous impulses are usually coordinated by a centralised
coordinator.
A nervous response to stimuli can be summarised as:
stimulus
receptor
coordinator
effector
response
Taxes
Kineses
Tropisms
A
taxis
is a type of response whose direction is determined by the direction of the stimulus
A motile organism (or part of organism) will move towards a favourable stimulus and away from an unfavourable stimulus.
A positive taxis is a movement towards a stimulus.
A negative taxis is a movement away from a stimulus.
For example:
Algae and moths move towards light. This is positive phototaxis.
Earthworms and woodlice will move away from the light. This is negative phototaxis.
Some bacteria will move up a concentration gradient of food. This is positive chemotaxis.
In a
kinesis
the organism's response to the stimulus is non-directional.
The organism will move at a greater pace and change direction more often.
This movement is designed to bring it back into favourable conditions.
Woodlice moving from an area of low water concentration is an example of kinesis.
A
tropism
is the growth
movement

of part of a plant in response to a stimulus.
Tropisms are typically positive or negative in nature, causing growth towards or away from the stimulus.
Tropisms are controlled by hormones.
The shoots of plants will grow towards the light.
This is positive phototropism. This occurs as the cells that are away from the light elongate more than those close to the light.
The roots of a plant will grow away from light. This is negative phototropism.
The roots will grow towards the pull of gravity (positive gravitropism) and water (positive hydrotropism).
Organisation
Nervous System
Central Nervous System
Peripheral Nervous System
Brain
Spinal Cord
Motor nervous system
Sensory Nervous System
Voluntary Nervous System
Autonomic Nervous System
The nervous system is divided into two parts:
These are the coordinators
This contains the receptors and effectors, as well as the connecting neurones
Carry messages from receptor to the CNS
Carry messages from the CNS to the effectors
Carries impulses to body muscles and is under conscious control
carries messages to glands, smooth muscle and cardiac muscle and is not under conscious control
Reflex Arc
A Motor Neurone
The
cell body
contains a nucleus and lots of RER for protein synthesis and neurotransmitter production
A
dendron,
splitting into smaller branched fibres (
dendrites
), carries messages from nearby cells
The
axon
is a single long fibre that carries impulses far away from the cell body.
Schwann cell
s surround the axon in a thick layer, protecting it and providing insulation. They also carry out phagocytosis.
The membranes of the Schwann cells form the
myelin sheath
. Myelin is a type of lipid. Not all nerve cells have a myelin sheath but these
myelinated nerve cells
transmit nerve impulses faster than
unmyelinated nerve cells
.
The gap between adjacent Schwann cells are known as the
nodes of Ranvier
. The gaps are approx 2-3 micrometers wide and occur every 1-3 mm.
Motor neurones have many dendrites coming from the cell body and 1 long axon leading to the effector
Sensory neurones transfer information from a receptor to an intermediate or motor neurone. They have one dendron that carries information to the cell body and 1 axon that carries it away.
Intermediate neurones transmit impulses between neurones. They have lots of small dendrites, but no long axon.
The Nerve Impulse
A nerve impulse is self-propagating wave of electrical disturbance along the membrane of an axon.
It is not a current but rather a switch between two states, the
resting potential
and the
action potential.
Resting Potential
Na
+
Na
+
Na
+
Na
+
Na
+
3Na
+
Na
+
Na
+
Na
+
K
+
K
+
K
+
K
+
K
+
K
+
K
+
K
+
K
+
K
+
The resting potential is maintained by the control of certain membrane transport proteins as well as the membrane itself.
The phospholipid bilayer does not allow charged particles to pass through, including the ions involved in the nervous impulse, sodium and potassium.
Intrinsic proteins in the membrane can act as channels, gated channels or active transport pumps
The actions of these proteins cause a charge differential across the membrane. This is the resting potential. The inside of the axon is negatively charged compared to the outside. The value for this is 65mV. We say that the inside of the membrane has a charge of
-65mV
. The membrane is
polarised
.
The sodium-potassium pump protein will transport 3 sodium ions out of the cell for every 2 potassium ions it moves into the cell. This process occurs via active transport (uses ATP).
More positive ions are removed than enter the cell, resulting in a net movement of positively charged ions out of the cell.
2K
+
Outside axon
Cytoplasm of axon
Na
+
Pumping Na ions out of the cell results in a chemical gradient.
+
Sodium would normally diffuse back into the cell but most of the voltage-gated sodium channels are closed.
The pump also generates a concentration gradient for potassium, with more ions being in the cytoplasm rather than outside the cell.
Most of the potassium channels are open allowing diffusion of K ions out of the cell
+
Aside from chemical gradients, an electrical gradient is also created. Eventually this stops more K ions from diffusing out, and the cell reaches an equilibrium.
Action Potential
When a stimulus is received by a receptor or nerve ending the charge across the membrane is reversed. The inner membrane now has a charge of
+40mV
. This is the action potential. The membrane is now
depolarised
.
K
+
K
+
K
+
K
+
K
+
K
+
K
+
K
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
Na
+
1. At the resting potential some potassium channels are open but the voltage-gated sodium channels are closed.
2. The stimulus causes the gates on the sodium channels to open. This allows diffusion of sodium ions across the membrane.
3. The influx of sodium ions causes other sodium channels to open further down. Even more sodium ions move into the cell.
+40mV
4. Once the +40mV action potential has been established the sodium voltage-gated channels will close
5. At +40mV more potassium voltage-gated channels will open, and potassium ions will move out of the cell.
6. More and more potassium moves out of the cell,
repolarising
the axon.
7. This movement of potassium ions out of the cell will cause a temporary overshoot of the electrical gradient (past -65mV). This is known as
hyperpolarisation
. The gated potassium channels now close and the sodium-potassium pump will re-establish the resting potential.
In this graph the electrical changes as a result of the stimulus that generates an action potential are shown.

a. shows the cell at its resting
potential.
b. shows the depolarisation of the membrane due to the influx of Na ions.
+
c. shows the peak action potential at +40mV. At this point the sodium channels start to shut.
d. shows the hyperpolarisation as a result of the K ions leaving the cells
+
Line O is the threshold potential. The cell needs to reach this threshold (via the stimulus) to initiate the opening of the sodium voltage-gated channels and initiate the action potential.
Line X represents the refractory period during which the cell cannot be stimulated again.
Once an action potential has been established the change in electrical charge will "move" rapidly along the axon.
The depolarisation of one section of the axon acts as a stimulus to get the the next part up to the threshold and initiate its own action potential.
Those sections that have just depolarised will repolarise, and be in the refractory period where they cannot be stimulated again. This ensures that the wave only travels in one direction.
http://highered.mcgraw-hill.com/sites/0072943696/student_view0/chapter8/animation__action_potential_propagation_in_an_unmyelinated_axon__quiz_1_.html
+
+
+ +
- -
- -
+ + +
- - -
+ + +
- - -
+ + + +
+ + + +
- - - -
- - - -
Direction of impulse
The difference in charge causes a local current.
The area behind the current action potential has only just repolarised and is in its refractory period.
Refractory period
It cannot be stimulated again immediately.
The area to the front of the action potential can be stimulated and the sodium channels will start to open.
This continues down the axon, passing the message in one direction only.
Myelin Sheath
Myelin Sheath
Node of Ranvier
In a myelinated axon the charge differential will jump from one node of Ranvier to the next, as the myelin sheath stops the charge differential forming.
This process is known as
saltatory conduction
and is much faster than non-saltatory conduction.
The factors that can affect the speed of travel of an action potential are:
Myelination
. The presence of myelin sheath speeds up the rate of travel in a typical human neurone from 30ms-1 to 90ms-1.
Diameter
of axon. The greater the diameter of an axon the greater the speed of travel. This is because it is easier to maintain a concentration gradient in a larger volume.
Temperature
. An increase in temperature speeds up the speed of conduction, up to a certain point at which the enzymes and proteins are denatured. The heat energy is provided by respiration in endothermic animals.
Advantages of the control of the possible action potentials with the refractory period and the threshold potential are as follows:
Refractory period:
Ensures the action potential only travels in one direction along the axon.
Produces discrete impulses.
Limits the number of action potentials in a certain time frame.
All-or-nothing principle:
only a stimulus of a certain strength will induce an action potential.
Any stimulus below the threshold does not result in an action potential.
All stimuli above the threshold will result in identical action potentials.
A very strong stimulus will not result in a greater charge differential but rather in an increase of action potentials over time.
Different neurones will have different threshold potentials and are thus triggered at different intensities of stimulus (you might want to think about the difference in night vision for different people).
Synapse
A synapse is the point at which the axon of one neuron connects with the dendrite of another or an effector
Synaptic Cleft - Structure and Function
20-30nm
Synaptic Cleft - transmission of an impulse in a cholinergic synapse
1. The neuron that is carrying action potential is known as the
presynaptic neuron
.
2. The axon ends in a
synaptic knob
. This contains a large number of
mitochondria
as well as
smooth endoplasmic reticulum
.
These are needed to produce chemicals called
neurotransmitters
(e.g acetylcholine), which will transmit information across the
synaptic cleft
.
3. The neurotransmitter is stored in
synaptic vesicles
in the synaptic knob.
4. The neurotransmitter will be released via exocytosis into the synaptic cleft.
5. The presynaptic neuron also contains many Calcium ion channels.
The synaptic cleft is between 20-30nm wide
The post-synaptic neuron contains many sodium ion channels that will also act as receptors for the neurotransmitter.
Features of synapses:
Unidirectionality
. The impulse can only pass from the presynaptic neurone to the postsynaptic neurone.
Summation
. Low frequency action potentials often do not produce enough neurotransmitter to start a new action potential, but over time, or by different neurones working in concert they can induce an action potential in the postsynaptic neurone.
Inhibition
. Some postsynaptic neurones can make it harder to get above the treshold potential by hyperpolarisation of the membrane due to the added influx of Cl- ions into the cell.
Spatial Summation
In spatial summation a single presynaptic neurone releasing neurotransmitter does not cause the threshold potential to be exceeded, but more impulses working in concert will cause an action potential in the postsynaptic neurone
Temporal Summation
Low frequency action potentials do not release enough neurotransmitter for an action potential to be generated in the postsynaptic neurone. A higher frequency of action potential will cause enough neurotransmitter to be released to exceed the threshold potential.
1. The action potential reaches the end of axon at the synaptic knob
Ca
Ca
Ca
Ca
Ca
Ca
Ca
2+
2+
2+
2+
2+
2+
2+
The arrival of the action potential causes the calcium ion channels to open and calcium to flood into the cell
+
-
The influx of calcium ions causes synaptic vesicles to fuse with the presynaptic neurone's membrane, releasing the acetylcholine into the synaptic cleft.
Na
Na
Na
Na
Na
Na
Na
Na
+
+
+
+
+
+
+
+
The acetylcholine binds to the sodium channels on the postsynaptic nerve causing them to open and sodium ions to move into the postsynaptic nerve.
This causes the postsynaptic neurone to go past the threshold potential and generate a new action potential.
Acetylcholine is hydrolysed by acetylcholinesterase into choline and ethanoic acid.
These diffuse back into the presynaptic cell to be recycled. This also prevents a continuous generation of an action potential by leftover neurotransmitter.
When the acetylcholine has been hydrolysed the sodium channels will close again and the resting potential will be restored.
Many drugs act by interfering with synaptic processes.
some might create more action potentials in postsynaptic neurones, for example by mimicking a neurotransmitter, stimulating the release of neurotransmitter or inhibiting the breakdown of neurotransmitter
others will create fewer action potentials in postsynaptic neurones, for example by inhibiting the release of neurotransmitter or blocking the receptors.
For example opiates (morphine, codeine, heroin) bind to the endorphin receptor. Endorphin normally blocks the sensation of pain by binding to pain receptor sites.
The opiates do the same, and therefore block the feeling of pain.
The grey arrows show the route through the topic
A
reflex
is an involuntary response to a sensory stimulus. It bypasses the conscious areas of the brain completely.
A
reflex arc
is the pathway of neurones involved in a reflex action.
What are some examples of reflexes?
Receptor
Effector
Sensory Neuron
Intermediate (relay) neuron
Motor Neuron
Synapse
Synapse
Stimulus
Response
Spinal cord
Why are reflex arcs important?
Free up the decision making centres in the brain for more complex situations.
Protection from harmful stimuli, effective from birth and do not have to be learnt
Very fast, which is essential in many safety related reflexes.
Control of Heart Rate
We do not have conscious control over many parts of our nervous system as we saw in the reflex arc.
This part of the nervous system is called the
autonomic
nervous system.
The autonomic nervous system controls internal muscles and glands and consists of two parts:
the
sympathetic
nervous system
the
parasympathetic
nervous system
The sympathetic nervous system:
stimulates effectors
speeds up any activity
it helps us to cope with situations by heightening our awareness and preparing us for activity
The parasympathetic nervous system:
inhibits effectors and slows responses
controls activities under normal resting conditions.
It tries to conserve your energy and replenish your reserves.
The sympathetic and parasympathetic nervous systems are
antagonistic.
So if one stimulates an effector, the other inhibits it. The two systems balance.
In the control of heart rate these two systems coordinate whether the heart rate should go up, down or stay the same.
Why is it essential that your heart rate can change?
An area of your brain called the
medulla oblongata
controls changes to the heart rate.
It has two centres, one which speeds up heart rate by being linked to the SAN by the sympathetic nervous system, and the other which slows down the heart rate by linking the medulla to the SAN via the parasympathetic nervous system.
Which of these areas is activated depends on signals received by the medulla oblongata, particularly in relation to changes in blood pressure and changes in the pH of the blood.
Both sets of sensory receptors are located in the carotid artery.
Increased metabolic activity
Increased CO2 production, lowering blood pH
Chemical receptors in the carotid artery increase the frequency of impulses to medulla.
Medulla speeds up heart rate through stimulation of the SAN through the sympathetic nervous system
Increased blood flow results increased rate of CO2 removal in the lungs.
pH increases as carbon dioxide levels return to normal
The other sensors are pressure receptors.
If the pressure inside the carotid artery is too high they will cause the medulla to stimulate the SAN to reduce heart rate via the parasympathetic nervous system, and vice versa if it is too low.
Details on
Receptors
Pacinian Corpuscle
Rod and Cone Cells
A Pacinian corpuscle is a mechanical pressure receptor. You might find them on your hands, feet or any other pressure sensitive part of your skin.
All sensory receptors turn the stimulus into an action potential in the sensory neurone. This is known as the
generator potential
. The receptor acts as a
transducer
. This means it turns one form of energy into another.
A Pacinian corpuscle works because it has stretch-mediated sodium channels. These channels change their permeability to sodium ions depending on the pressure that acts on them.
In the resting state the channels are too narrow for sodium to pass through.
However when distorted by direct pressure, the sodium channels become wider and sodium ions can move through the channels into the cell.
This turns this area of the cell more positive than neighbouring areas, generating a local current and an action potential if the generator potential has been reached.
The eye contains two types of light-sensitive transducer cells.
These are the rod and cone cells
Rod cells are sensitive to the intensity of light, and allow you to see in dark situations. They don't give colour vision.
Cone cells are less sensitive to differences in the intensity of light but more sensitive to direction of the light.
Humans have many more rod cells than cone cells.
Many rod cells are attached to a single bipolar cell. This is known as retinal convergence and this allows for activation of a generator potential in the bipolar cells by spatial summation.
This also explains why rod cells have poor
visual acuity.
The generation of the generator potential is due to the breakup of a molecule called rhodopsin.
This breakup changes the messages that the rod cell sends to the bipolar cell and results in the activation of a generator potential and action potential.
There are three types of cone cell, each responding to a different colour of light. The proportion of cone cells of each colour that is activated results in us seeing colour (e.g if only red-sensing cone cells are activated we see red, but if a mixture of red and green cone cells are activated we will see yellow and orange colours).
Each cone cell is attached to its own bipolar cell, giving the cones a much greater visual acuity. However their stimulation cannot be combined to generate a generator potential.
This means that you need a higher intensity of light for the cone cells to start their bipolar cells firing.
Muscles
Muscles are effector organs that respond to nerve impulses by causing movement.
There are three types of muscle in the body:
Cardiac Muscle, which is found exclusively in the heart, is myogenic and not under our conscious control.
Smooth Muscle, which is found in the intestines and blood vessels, and is not under our conscious control.
Skeletal Muscle, which is attached to bones and generates conscious and unconscious movement.
You can imagine muscles as ropes in structure. It consists of many, individually weak, fibres, known as
myofibrils
, that together are strong.
These fibres are lined up in parallel to form larger fibres and these line up to form skeletal muscle.
The myofibrils are made up out of many cells, but these cells have fused together, resulting in a structure with many nuclei and a shared cytoplasm. This is known as the
sarcoplasm
.
The sarcoplasm also contains many mitochondria and endoplasmic reticulum.
The inside of the myofibril is divided into units called sarcomeres.
The myofibrils consist of two types of protein filament.
Actin - which is thinner and consists of two strands twisted around each other.
And myosin which is thicker, and consists of a long rod-shaped structure with bulbous heads on either side.
This area of the sarcomere where there are just actin fibres will look lighter under the microscope. The bands it forms are known as
isotropic bands
(or
I-bands
).
Myofibrils have different areas depending on how they look under a microscope.
The area where the actin and myosin fibres overlap will look darker under the microscope. They are known as
anisotropic bands
(or
A-bands
)
In the centre of the sarcomere is the
H-zone
. Here myosin fibres overlap without actin.
The lines forming the edge of each sarcomere are known as the Z-lines. The actin fibres are anchored here
There are two main types of muscle fibre:
Slow-twitch fibre
Fast-twitch fibre
Slow-twitch fibres contract slower and provide less powerful contractions over a longer time period.
They are adapted for aerobic respiration to avoid the build up of lactic acid. These adaptations include:
A large amount of myoglobin, a protein that can store oxygen in cells
A glycogen supply
A rich supply of blood vessels
large numbers of mitochondria.
Slow-twitch fibres are used in muscles that are used often and for long periods, such as your calves or your lower back. Marathon runners will have more slow-twitch than fast-twitch muscles.
Fast-twitch fibres contract rapidly and are more powerful, but can only function for short bursts of time.
They are adapted by having:
Thicker and more numerous myosin fibres
more enzymes involved in anaerobic respiration
a store of phosphocreatine, which can generate a rapid supply of ATP from ADP by donating a phosphate molecule.
Fast-twitch muscles are found in your biceps or in the quadriceps of sprinters.
The neuromuscular junction is where the nervous system interfaces with the effector organ (muscle). It is a cholinergic synapse as seen earlier.
There are many neuromuscular junctions along a muscle.
This ensures:
All muscle fibres can be stimulated at the same time resulting in a potentially fast and powerful movement when stimulated by all the action potentials at once.
Finer control by controlling the number of junctions that are stimulated. Fewer junctions will result in less force, more junctions in a greater force.
Sliding Filament Mechanism
The structure of the sarcomere allows it to contract. During contraction the myosin and actin filaments will slide over each other. This is known as the sliding filament mechanism.
Relaxed
Contracted
As you can see, the I-band becomes narrower (or nearly disappears).
The Z-Lines move closer together.
The H-zone becomes narrower.
The A band stays the same width. (the myosin fibres do not change in length)
Myosin is made of two proteins, a fibrous protein arranged into a filament and globular protein arranged into two bulbous structures at the end of a filament.
Actin and tropomyosin form intertwined threads to form the actin fibres.
The sliding filament mechanism works similarly to a ratchet. The myosin heads attach to the actin fibres and in doing so, change shape and pull themselves along in unison. ATP is used to restore the myosin fibre to its original state. It can then reattach further along the actin fibre and repeat the process.
In detail the following happens:
The muscle receives a stimulus:
Action potentials reach many neuromuscular junctions simultaneously
This causes an influx of Ca2+ ions which causes the release of acetylcholine into the synaptic cleft.
Acetylcholine binds to the muscle cells causing an influx of Na+ ions, causing depolarisation.
The muscle then starts its contraction:
The action potential travels down the tubules (T-tubules) through the sarcoplasm
The tubules are in contact with the sarcoplasmic reticulum (which has actively stored all the Ca2+ from the sarcoplasm).
The action potential causes the release of these ions into the sarcoplasm down a concentration gradient (voltage-gated channel)
The release of Ca2+ ions causes a change in the shape of the tropomyosin, causing it to move from binding sites on the actin fibre.
ADP is bound to the myosin head, and this allows it to now form a cross-bridge to the actin filament.
When it binds the head changes angle and moves the actin fibre along. It also releases the bound ADP.
A molecule of ATP can now bind to myosin head causing it to detach from the actin fibre.
The calcium ions activate an enzyme called ATPase, which breaks down the ATP into ADP and Pi. The energy released returns the myosin head to its original position.
The myosin with ADP attached can now form another cross-bridge.
This process keeps going as long as the calcium ions are around.
Muscle relaxation occurs when the stimulation ceases
The Ca2+ ions are actively transported back into the sarcoplasmic reticulum using energy from the hydrolysis of ATP.
The reduction in the concentration of Ca2+ ions changes the shape of tropomyosin back to its original shape, so that it once again blocks the binding sites on the actin filament.
Myosin can no longer bind and contraction stops.
This process takes a large amount of energy (in the form of ATP). This is used to:
Reabsorb calcium ions in relaxation
Move myosin heads in contraction
Most of it is created by mitochondria in aerobic respiration, but highly active muscle cells will have a store of phosphocreatine (made during periods of low intensity), which can phosphorylate ADP and recycle ATP quickly (without glycolysis).
Homeostasis is the maintenance of an organism's constant internal environment.
Why is it essential that an organism controls its internal environment?
The nervous system is mostly concerned with responding to external stimuli whereas the control of the internal environment is largely done by the endocrine system (hormonal system).
The internal environment of the organism is determined by the tissue fluid that surrounds each cell. The levels of nutrients, waste etc. as well as physical features such as temperature will affect the cells that bathe in it.
Homeostasis is the control of this environment and the process by which adjustments are made if the external environment causes a change in the internal environment.
Among some of the conditions controlled by homeostasis are:
Temperature
pH
Water potential
Ion and glucose concentrations.
The organism has a set ideal point to which homeostasis will return the internal environment if it changes (i.e. if the internal environment shifts to higher temperature, homeostasis will act to bring it back down again).
Why is it important to control pH?
Why is it important to control temperature?
Why is it important to maintain water potential?
One of the benefits of being able to maintain more aspects of your internal environment is that you are able to adapt to more extreme environments.
An example would be that you can find birds and mammals in the Arctic, but no reptiles or amphibians.
The process of homeostatic control can be shown in a flow diagram.
Input - causing a change to the system
Receptor - measuring the level of a factor.
Control Unit - Receives information and coordinates a response
Effector - causes changes in the system to return to the set point.
Output - system has returned to set point
Feedback loop (in this case negative) - turning the system off in response.
Information is often gathered from a variety of receptors and altered by a variety of effectors to allow for fine tuning of the output.
The various control mechanisms are coordinated to avoid the response from one system upsetting the set point of another system.
Temperature
Blood Glucose
Temperature control is important to organisms as too low a temperature results in reactions being too slow, and too high a temperature results in the denaturation of enzymes and other proteins.
Animals therefore control their body temperature. To do this they must control heat gain and heat loss.
Heat gain can be accomplished by:
Production of heat (through respiration)
Gain of heat from the environment (conduction, convection and radiation)
Heat loss can be accomplished by:
Evaporation of water (e.g. sweating, panting etc.)
Loss of heat to the environment (through conduction, convection and radiation)
Animals which gain most of their heat from their internal metabolic reactions are known as
endotherms
. These include mammals and birds.
Animals which gain most of their heat from the environment are known as
ectotherms
. These include reptiles, amphibians and fish.
Ectotherms
Endotherms
The body temperature of ectotherms fluctuates with their environment.
To control their body temperature they need to adapt their behaviour.
This manifests itself in a number of ways.
Exposure to the Sun
Hiding from the Sun
Pressing against hot soil or rocks
Ectotherms also generate some heat through metabolic reactions.
Their colour can also affect the amount of the heat they absorb, with ectotherms in colder environments generally being darker in appearance.
Endotherms gain most of their heat from internal metabolic activities. This gives them physiological as well as behavioural methods of responding to temperature changes.
A downside is that endotherms need to take in considerably more energy in the form of food.
Endotherms often make use of a small surface area to volume ratio in colder climates, but a larger ratio in warmer climates.
Many animals will decrease their SA:V by laying on fat for winter, which also aids as an insulator.
These changes are gradual at best and most have evolved over a very long period of time. An endotherm needs to be able to respond to more rapid changes in body temperature as well.
To conserve and gain heat endotherms will use:
Vasoconstriction
Shivering
Raising of hair
Increases in metabolic rate
A decrease in sweat production
Behavioural mechanisms
Vasoconstriction involves reducing the diameter of the arterioles near the skin. This reduce the blood flow near the skin and keeps most blood under the insulating layer of fat under your skin, reducing heat loss through radiation and convection.
Shivering involves involuntary rhythmic muscle contractions. Contracting these muscles requires metabolic activity (in particular ATP production in respiration), increasing the amount of heat produced by the endotherm.
Muscles in the skin called the hair erector muscles will contract and raise the hairs on the skin. This traps air within the fur, providing an insulating layer, reducing overall heat loss.
Hormones produced in your body (largely by your thyroid) can raise the metabolic rate above normal levels. This will increase heat production.
Endotherms use similar behavioural mechanisms to ectotherms such as huddling together, basking in the sun or sheltering from the wind.
Endotherms respond differently when trying to lose heat:
Vasodilation of skin arterioles, increasing blood flow.
Lowering of body hair, stopping air from being trapped.
Increased sweat production to increase energy loss through evaporation.
Behavioural mechanisms such as sheltering in burrows and nocturnal activity.
Control of body temperature
The control of body temperature in endotherms is an example of homeostasis, and follows the flow diagram we saw earlier.
The temperature is sensed by thermoreceptors. These thermoreceptors are mainly found in the skin and in hypothalamus, although some have been found in the intestines.
The messages from the thermoreceptors pass through the autonomous nervous system to the hypothalamus.
The hypothalamus contains an area known as the thermoregulatory centre.
This area consists of two parts:
A heat gain centre
A heat loss centre
Both parts respond to changes in body temperature.
Location of hypothalamus
When the thermoreceptors on the skin signal a change in ambient temperature, the thermoregulatory centre will anticipate a subsequent change in body temperature.
However the measurement of the core temperature in the hypothalamus is more important when initiating a response.
This results in the following homeostasis flow diagram
Normal temperature
Thermoreceptors in skin:
Increase in ambient temperature detected
Thermoreceptors in skin:
Decrease in ambient temperature detected
Increase
Decrease
Hypothalamus
Heat loss centre
Heat gain centre
Effectors:
Vasodilation of arterioles
Onset of sweat release
Relaxation of erector muscles
Decrease in metabolic rate
Effectors:
Vasoconstriction of arterioles
Onset of shivering
Contraction of erector muscles
Increase in metabolic rate
Feedback
Feedback
Hormones are chemical messengers that have certain characteristics in common:
They are produced by endocrine glands that secrete them straight into the bloodstream.
They act on specific target cells which can be identified by having a receptor for the hormone on their cell membrane.
They are effective in small quantities and often have long-lasting and widespread effects.
A significant number of hormones (including glucagon and adrenaline) work through a process known as the
second messenger model
.
Once the cyclic AMP has been produced it will activate other enzymes within the cell. For example when adrenaline acts this way it will activate the enzymes that will catalyse the breakdown of glycogen into glucose.
The pancreas is the main organ of the endocrine system that is involved in the regulation of blood glucose.
It is a gland that is situated in the upper left abdomen, behind and beneath the stomach.
A large part of the pancreas is taken up by exocrine cells producing digestive enzymes that are secreted into the duodenum.
However, between these cells are the Islets of Langerhans, which are group of hormone producing cells.
The two types of cell within the Islets of Langerhans are:
alpha cells
, which are larger and produce glucagon
beta cells,
which are smaller and produce insulin
As glucose is the main substrate for respiration it is essential that there is relatively constant supply of it in the blood stream of mammals
If the level drops too low, cells will not have enough energy and start to die (specifically brain cells which can only respire glucose).
If the level of glucose in the blood raises too high it will affect the water potential of blood causing water to move out of cells, potentially resulting in dehydration.
The normal level of blood glucose in humans is approximately 90mg per 100cm of blood.
3
There are three ways by which blood glucose levels can rise:
By absorption of the products of the breakdown of carbohydrates (be it starch, maltose, lactose or sucrose).
Glycogenolysis,
which is the breakdown (lysis) of glycogen, stored in liver and muscle cells.
Gluconeogenesis
, which is the production of glucose from sources other than carbohydrates (e.g. amino acids and lipids)
Because both uptake and use of glucose vary over time the body cannot rely on a steady rate of the mechanisms that increase/decrease glucose levels.
They must be controlled in response to changes through homeostasis.
The main hormones involved are
insulin, glucagon and adrenaline.
Beta cells act as receptors that detect a rise in blood glucose levels above 90mg per 100cm .
When this occurs, they secrete the polypeptide hormone insulin.
3
Most cells in the body have insulin receptors and when insulin binds to the receptors it will bring about a number of changes.
1. Change the tertiary structure of the glucose transport protein, causing them to open and allowing more glucose to flood into the cell.
2. Increase the transcription and translation of genes encoding glucose transport molecules. Once synthesised they move to the cell membrane and allow more glucose into the cell.
3. Activation of enzymes that convert glucose into glycogen and fat.
These actions result in the lowering of the blood glucose levels because:
the rate of absorption of glucose is vastly increased (especially in muscle cells)
the rate of respiration increases
the rate of glycogenesis (creation of glycogen) increases
the rate of conversion of glucose to fat increases (lipogenesis)
Negative feedback control will reduce the secretion of insulin when blood glucose levels have fallen sufficiently. The insulin already in the blood breaks down over time.
Glucagon is produced by the alpha cells in response to a fall in blood glucose level below normal levels.
Only liver cells have receptors for glucagon and they respond by carrying out glycogenolysis and increasing the amount of gluconeogenesis.
Once the glucose levels are sufficiently increased, negative feedback turns off the production of glucagon by the alpha cells.
One of the other hormones that can cause changes in blood sugar level is adrenaline.
Adrenaline will increase blood sugar levels to allow cells to generate enough energy to respond to a threatening situation.
It does by activating enzymes involved in glycogenolysis and inactivating enzymes in glycogenesis through a second messenger system.
Insulin
Glucagon
Feature
Hormone
Produced
Beta cells
Alpha Cells
Glycogen
Glycogenesis
Glycogenolysis
Cellular uptake
Increased
Decreased
Metabolic rate
Increased
Decreased
Gluconeogenesis
Decreased
Increased
Insulin and glucagon act antagonistically as can be seen in the following table.
Feedback Mechanisms
Once the effector has corrected any deviation and returned the system to the set point it is essential that this information is fed back to the receptor to avoid over-correction and deviation in the opposite direction.
Negative feedback is most commonly used in body systems. Once an effector causes a large enough change, the feedback mechanism will signal the receptor and cause the effector to be turned off.
Thinking about the control of body temperature we saw earlier, if the body cooled itself down too much through sweating, vasodilation etc. then we would run the risk of hypothermia.
Instead, when the cooler blood from near the skin flows through the hypothalamus, this change is noted and the various effectors are instructed through nervous impulses to turn themselves off.
A similar, but reverse, system prevents hyperthermia when trying to increase the body temperature.
Blood glucose is controlled in a similar fashion. Describe what feedback would be generated both for a correction of too high a blood glucose level as well as a blood glucose level that is too low.
Positive feedback occurs far less often in the body. The only way we have seen so far is the influx of sodium ions into a neurone as a result of a threshold being exceeded.
Certain diseases and conditions can cause a breakdown in the control systems, causing a serious imbalance.
For example typhoid can cause hyperthermia.
Hypothermia gives positive feedback resulting in ever colder core temperatures.
Control of the Oestrous Cycle
The oestrous cycle is the regular pattern of changes that takes place in the reproductive system of female mammals.
The oestrous cycle in humans starts at puberty and lasts until the menopause. The lining of the uterine wall is shed once during each cycle in primates, giving rise to the name menstrual cycle.
There are 4 hormones involved in the menstrual cycle:
Follicle-stimulating hormone (FSH), produced by the pituitary gland.
Luteinising hormone (LH), also produced by the pituitary gland
Oestrogen, produced by the ovaries
Progesterone, also produced by the ovaries.
FSH stimulates the development of follicles in the ovary, which contain eggs, and also stimulates these to produce oestrogen.
LH causes ovulation to occur and stimulates the production of progesterone from the corpus luteum (empty follicle left behind after ovulation).
Oestrogen causes the rebuilding of the lining of the uterus after menstruation and stimulates the pituitary gland to produce LH.
Progesterone maintains the lining of the womb so that it can receive the fertilised egg and also inhibits the production of FSH.
The cycle runs as follows:
It starts when the lining of the uterus is shed (days 1-5)
From day 1, FSH is released stimulating follicles in the ovary to grow and mature.
The growing follicles secrete some oestrogen, which inhibits the secretion of more FSH as well as LH. (negative feedback) This stops too many eggs from maturing at once.
The oestrogen stimulates the repair of the lining of the uterus.
As the follicles develop further, more oestrogen is produced.
At day 10, this increased level of oestrogen will stimulate the pituitary gland to release both FSH and LH (positive feedback)
The surge in LH causes the release of an egg from one of the follicles on day 14. This is ovulation.
After ovulation, LH stimulates the empty follicle to develop into a corpus luteum which secretes progesterone and lower levels of oestrogen.
Progesterone maintains the lining of the uterus and inhibits FSH and LH production (negative feedback)
If the egg is not fertilised the corpus luteum degenerates and stops producing progesterone.
A reduction in progesterone production results in lining of the uterus no longer being maintained and this starts to break down (menstruation).
FSH is also no longer inhibited, starting the cycle again.
If a fertilised egg implants into the lining, the corpus luteum is maintained and keeps secreting progesterone (positive feedback)
In non-primates the reduction in progesterone results in a reduction, rather than shedding, of the lining of the uterus.
Full transcript