Unit 3 & 4 Exam Notes
Year 12 2023
The Endocrine System
A chemical messenger system
consisting of hormones, the group of
glands of an organism that secrete
those hormones directly into
circulation system to regulate function
of target organs. And the feedback
loop which modulate hormone release
so that homeostasis is maintained.
Exocrine
= duct
that
carries
secretion
to the
surface.
E.g.
sweat
Endocrine = ductless, secretes directly
into extracellular fluid into capillaries
and transported by blood.
Hypothalamus
 Regulates basic body
functions. E.g. body temp,
heart rate
 Located at base of brain
above the pituitary gland
 The “coach” – receives
information about hormone
levels in the body, then sends
hormones of its own (called
releasing/inhibiting factors)
to increase or decrease
production.

The hypothalamus is
connected to the pituitary
gland by the infundibulum
Pituitary Gland
Regulates many bodily activities (e.g.
growth/metabolism)
Made up of 2 divisions/lobes.
1.POSTERIOR LOBE
 Connected to the
hypothalamus by nerves
 Hyp. Synthesizes posterior
lobes’ hormones and stores
them in posterior until release
is signaled.
 Hormones transported down
axons.
 Hormones released into
bloodstream.
2.ANTERIOR LOBE
 Has no nerves connecting to
hyp. only blood vessels
 Makes own hormones
 Releasing/inhibiting factors of
hypothalamus tell anterior
lobe when to secrete into
blood stream.
Hormones secreted from lobes:
Posterior Lobe
1.Oxytocin (OT)
2.Antideuretic
Hormone (ADH)
Anterior Lobe
1.Follicle-Stimulating
Hormone(FSH)
2.Luteinising
Hormone(LH)
3. Growth
Hormone(GH)
Uterus/mammary glands –
contraction in birth or milk
release
Kidneys – reabsorption of
water
Ovaries – growth of follicles
or
Testes – sperm prod.
Ovaries – ovulation/maintain
corpus luteum or Testes –
testosterone secretion
All cells – growth & protein
synthesis
4.Adrenocorticotrophic
Hormone(ACTH)
5.Thyroid Stimulating
Hormone (TSH)
6. Prolactin (PRL)
Adrenal cortex- secretion of
hormones from adrenal
cortex
Thyroid – hormone secretion
from thyroid
Mammary Glands – milk
production
*posterior lobe is
usually in front of
anterior.
Thyroid Gland
The largest endocrine gland, located in
the neck below the larynx. It is divided
into a left and right lobe.
Main hormone released:
THYROXINE;
 Controls metabolic rate (how
quickly molecules broken
down: catabolism, or
produced: anabolism)
 Many metabolic processes
produce heat; therefore,
thyroxine plays a role in body
temp. (e.g. shivering)
 Thyroxine is secreted when
TSH is released by anterior
lobe
- iodine is important in the
production of thyroxine; diet
mainly through salt.
Parathyroid Gland
Embedded in the rear surface of the
thyroid and there are usually 4, the
size of small peas. Acts on bone/kidne
 Secrete Parathyroid hormone
(PTH) which control calcium
and phosphate levels in blood
Thymus Gland
Located in the chest above the heart,
behind the sternum.
 Secretes thymosins which
influence maturation of
disease-fighting cells (T-cells).
The Gonads
They are the testes and ovaries.
 Androgens; male, prod. by
testes, development and
maintenance of male sex
characteristics.
 Oestrogen and Progesterone;
female, produced by ovaries.
stimulate development and
maintenance of female
characteristics. Also involved
in regulating menstrual cycle
and changes in pregnancy.
Pineal Gland
Located deep inside brain. Secretes
melatonin, involved in regulation of
sleep cycles, production is stimulated
by darkness.
Adrenal Glands
Inner: Adrenal Medulla
 Adrenaline; prepare body for
threatening situation
 Noradrenaline; increases rate
and force of heartbeat
Outer: Adrenal Cortex
 Aldosterone; acts on kidney,
decrease sodium and increase
potassium in urine
 Cortisol; promotes normal
metabolism, help with stress
& repair of damaged tissues
Hormones – Types of Action
Hormones can be proteins, steroids or
amines. They’re transported through
blood.
Paracrines = communicate with cells in
the same tissue, moving through
extracellular fluid.
Hormones can only influence cells
that have the correct receptor;
SPECIFIC.
Protein/Amine Hormones
-Active
-Work quickly within seconds/minutes
1. Hormone binds to specific
receptor on cell membrane of
target cell, it stays outside of
cell (not lipid soluble)
2. The combination activates a
particular enzyme inside
membrane to convert ATP
into a secondary messenger
3. Effect in the body occurs
E.g. Insulin binds to receptor protein
and causes increase in glucose
absorption
There’s a limited number of receptors
on cells so there can be no further
increase in the rate of cell’s activity
when all receptors and being used.
Different cells have different types and
numbers of receptors, that’s why
there is a variation in the sensitivities
of cells to different hormones.
Steroid Hormones
-Slower effect, Passive (hours or days)
1. Enter target cells via diffusion
through lipid soluble
membrane.
2. Combines with receptor
protein found floating in
cytoplasm or connected to
organelle, depending on
hormone.
3. Hormone-receptor complex
activates genes directly
controlling particular proteins
in cell’s DNA.
Hormones can:
 Activate certain genes in the
nucleus so a particular
enzyme of protein is prod.
 Change shape or structure of
enzyme to turn on or off
 Change prod. rate of an
enzyme or structural protein,
by changing rate of
transcription or translation.
E.g. oestrogen, testosterone. An
imbalance of hormones can cause
mood swings, cramps etc.
Nervous System
2 division:
Central Nervous System
Consists of the brain and spinal cord
and is the control center.
Peripheral Nervous System
Consists of all the nerves and ganglia
(groups of nerve cell bodies) that
connect the CNS with the
receptors, muscles and glands.
The main function of the PNS is to
carry info to and from the CNS.
 12 pairs of nerve fibres
arise from the brain –
cranial nerves
 31 pairs arise from the
spinal cord – spinal
nerves. They are all mixed
nerves, each is joined to
spinal cord by two roots;
ventral root and dorsal root.
Motor/efferent neurons, that carry
impulses away from the CNS, go
through the ventral root. The impulses
are subdivided into the somatic
division; takes impulses from skeletal
muscles. And autonomic division;
impulses from involuntary muscles,
the ANS is subdivided further in to the
parasympathetic and sympathetic NS.
Sensory/afferent neurons, which
carry impulses to the CNS, go through
the dorsal root (have cell bodies in a
small swelling called dorsal root
ganglion). Impulses carried by sensory
nerve cells from receptors in skin and
around muscles and joints, these
nerve cells are somatic sensory
neurons. Impulses from internal
organs are called visceral sensory
neurons.
SOMATIC NERVOUS SYSTEM
Carries messages to the voluntary
skeletal muscles.
 Only has one nerve fibre
leading from CNS
 Neurotransmitter released is
always acetylcholine
AUTONOMIC NERVOUS SYSTEM
The ANS controls the involuntary
activities of smooth muscles and
glands.
Divided into two subdivisions:
1.Sympathetic pathway – prepares the
body for a threatening situation
2.Parasympathetic pathway – slows
body processes to homeostasis
 Each pathway within the ANS
has two: a preganglionic
neuron and postganglionic

neuron. A synapse is between
them
The neurotransmitter
released at the effector for
sympathetic NS:
noradrenaline. Whereas for
parasympathetic NS:
acetylcholine.
Effect: Sympathetic VS
Parasympathetic
Fight-flight-or-freeze response;
sympathetic NS becomes dominant
and increases body activity. This
reaction occurs when you feel fear,
stress, anger or danger e.g.
The parasympathetic, rest-anddigest, maintains the body during
quiet conditions.
Parts of the Brain
The two pathways work together with
opposing actions: antagonistic.
CONTRASTING SOMATIC AND
AUTONOMIC NS
Characteristic
Effectors
General
function
Efferent
pathway
Neurotransmitter
Control
Nerves to
target organ
Effect on
target organ
Autonomic
Heart muscle, involuntary
muscles, glands
Adjustment of internal
environment (homeostasis)
Two nerve fibres from CNS
to effector with synapse of
a ganglion
Acetylcholine/noradrenaline
Somatic
Skeletal muscles
Involuntary
Two sets: sympathetic /
parasympathetic
Excitation or inhibition
Voluntary
One set
Response to external
environment
One nerve fibre from
CNS to effector; no
synapse, no ganglion
Acetylcholine
Always excitation
Sensory areas: receive
and process nerve
impulses from afferent
pathway
Motor areas: send
impulses to effectors via
efferent pathway
Association areas:
interpret information
from senses and make it
useful.
Structure
Heart
Eyes
Lungs
Lungs
Bladder + anus
Saliva prod.
Liver/gall bladder
Sympathetic
Increased cardiac output
Dilates pupils (for more light)
Dilates bronchioles (more air intake)
Increased breathing rate (more oxygen to muscles)
Contracts sphincters
Decreased prod. (dry mouth)
Liver – increased glycogen breakdown to glucose
Gall – inhibited action
Stomach/intestines
Adrenal medulla
Inhibited movement (stops peristalsis)
Stimulates hormone secretion of noradrenaline and
adrenaline
Greater sweat prod. to cool body
Vasoconstriction of blood vessels
Vasodilation of blood vessels
Vasoconstriction (all except heart + lungs)
Sweat glands
Skin
Skeletal muscles
Internal organs
Cerebrum:
 biggest part of brain
 high order functions: thinking,
reasoning, memory, learning
etc.
 grey matter (outer 2-4mm
surface) called cerebral cortex
 basal ganglia = deepest part of
cerebrum
 two hemispheres joined by
corpus callosum (nerve-fibre
network) which allows
communication between them.
 Cerebrum is folded into
convolutions or gyri to increase
surface are. Between folds are
grooves (gaps); shallow – sulci;
deep – fissures: deepest fissure
is between hemispheres and
called longitudinal fissure
 Bundles of nerve fibres = tracts
which are myelinated (aka
white matter).
Parasympathetic
Decreased cardiac output
Constricts pupils
Constricts bronchioles
Decreased breathing rate
Relaxes sphincters
Increases saliva prod.
Liver – increases conversions of glucose
to glycogen
Gall – stimulated
Stimulates movement
No obvious effect
No obvious effect
Little effect
No effect
Little effect
Cerebellum
 Under rear of cerebrum
 Folded into parallel ridges
 Complex association areas
concerned with muscle/body
posture
 Fine coordination of voluntary
muscle movement
 Receives sensory info from
skeletal muscles and stretch
receptors in inner ear
 Doesn’t initiate movement,
only COORDINATES it
 Any damage means
jerky/uncontrolled movement
Hypothalamus
 Main controlling region for ANS
 Controls complex patterns
(feeding/ sleeping)
 Mostly concerned with
homeostasis
Medulla Oblongata
 Continuation of spinal cord
(3cm)





Cardiac center: regulates rate
and force of heart beat
Respiratory center: regulates
rate and depth of breathing
Vasometer center: regulates
diameter of blood vessel
Everything influenced and
regulated by higher centers of
the brain
Plays role in automatically
adjusting body functions
Spinal Cord
 A dorsal cylinder of nervous
tissue from bottom of brain,
through opening (foramen
magnum) at base of skull to
second lumbar vertebrae
(44cm long)
 2 sections:
- grey matter – composed of
cell bodies and unmyelinated
nerve fibres (found in center) –
center is the central canal
containing spinal cord and CSF
-white matter – composed of
myelinated fibres. Arranged
into bundles knowns as:
Ascending tracts – sensory
axons carrying impulses to
brain
Descending tracts – motor
axons that conduct impulses
away from brain
 main functions are to carry
impulses to/from brain and
integrate certain reflexes.
Reflexes
A rapid, automatic response to a change
in the external/internal environment.

There are 4 important properties:
1. a stimulus is required to
trigger a reflex
2. involuntary
3. rapid – small number of
neurons involved
4. stereotyped – occurs in same
way each time
its coordinated by the spinal cord
hence the spinal reflex. The message is
not carried to the brain because it
delays reaction time. It’s carried by
motor neurons.
The impulses are sent to the brain
AFTER reflex response.
Basic components of reflex arc:
 Receptor: reacts to change &
initiates nerve impulse in
sensory neurons
 Sensory neurons: carries
impulses from receptor to
spinal cord
 Synapse: ad least one
between interneuron and
motor neuron
 Motor neuron: impulse to
effector
 Effector: receives and carries
out appropriate response (e.g.
muscle/secretory cells)
Protection of CNS:
1. Bone
Cranium protects brain and vertebral
canal protects spinal cord.
2. Meninges
Three layers of connective tissue that
cover the entire CNS. Made up of tough
fibrous tissue.
First layer: DURA MATER – thick,
durable membrane. It is attached to
cranium but not vertebral canal, instead
there’s a space filled with fat,
connective tissue and blood vessels, to
allow cord to bend with spine. Dura
mater is a fibro elastic layer of cells. It
contains larger blood vessels that split
into capillaries in the pia mater.
Second layer: ARACHNOID MATER –
has spider web like appearance.
Cushions CNS. Thin, transparent which is
thought to be impermeable to fluid.
Third layer: PIA MATER – firmly sticks to
surface of brain and spinal cord, like a
fibrous glove. Very thin fibrous tissue,
Punctuated by blood capillaries to brain
and spinal cord. They allow CNS to be
nourished.
Inflammation of these layers is
called meningitis, caused by
virus, bacteria or protozoan.
This places dangerous pressure
on the brain.
3.Cerebrospinal fluid
clear, watery fluid containing few cells,
glucose, protein, urea, salts and
occupies inner and middle layers of
meninges.
It circulates through cavities (or
ventricles) providing nutrients to CNS
while also removing waste products
Its formulated through blood and after
circulating around and through CNS It
returns to blood capillaries
CSF also acts as a shock absorber,
cushioning CNS from any blows or
shocks.
NERVE CELLS
NEURONS
o
o
o
o
o
The basic units of whole
nervous system.
Nerve fibre = axon
Most axons have a myelin
sheath – myelinated, if not –
unmyelinated
Grey matter – nerve cell
bodies & unmyelinated
White matter – myelinated
fibres
Myelin Sheath:
formed by
Schwann cells,
which wrap
around axon.
There’s gaps or intervals along the
sheath called “Nodes of Ranvier”.
Outermost coil of Schwann cell =
neurilemma, which helps repair of
injured fibres.
Structural Types
1. Multipolar: one axon, multiple
dendrites. Most common, most
interneurons and motor neurons.
2. Bipolar: one axon, one dendrite.
Occur in eye, ear, nose etc. (where
they take impulses from receptors to
other neurons.)
3. Unipolar: one extension – one axon,
cell body to one side. Most sensory
neurons.
Synapse
the junction between axon terminals
and dendrites when transmitting
messages. – chemical messengers –
neurotransmitters.
- Action potentials are transmitted
between neurons across junctions
called synapses.
- Chemical synapses are the most
common synapse in the NS.
- The axon terminal is a swollen knob
and a small gap separates it from
receiving neuron.
- The synaptic knobs are filled with
tiny packets (vesicles) of chemicals
called neurotransmitters.
-Transmission involves the diffusion of
the neurotransmitter across the
synaptic cleft (gap), where it interacts
with the receiving membrane and
causes an electrical impulse.
- The neurotransmitter causes a
membrane depolarization and the
generation of an action potential
- Some neurotransmitters have
opposite effect and cause inhibition
(e.g. slowing heart rate)
5. the neurotransmitter is deactivated
by enzymes located on the membrane
(until impulse comes).
Neurotransmitter examples:
Acetylcholine, noradrenaline,
serotonin, Gamma-aminobutyric acid
(an inhibitory)
*when in neuron it is electricity, when
crossing synaptic cleft, it is chemical.
Transmission of a Nerve Impulse
Nerve impulse = involves movement
of an action potential along a neuron
as a series of electrical depolarization
events.
Polarization: + - (opposite)
across the synaptic cleft:
1. The arrival of a nerve impulse at the
end of the axon causes an influx of
Ca2+ and causes the vesicles to release
their neurotransmitters into the
synaptic cleft.
2. the neurotransmitter diffuses across
the synaptic cleft to receptors on the
receiving membrane. Diffusion across
the cleft delays the impulse
transmission by about 0.5 milliseconds
3. the neurotransmitter binds to the
receptor proteins on the receiving
membrane
4. Ion channels in the membrane
open, causing an influx of Na+ ions.
This response may or may not reach
the threshold required to generate
nerve impulse


the cell membrane of cells,
including neurons, contain
SODIUM POTASSIUM ION
PUMPS which actively pump
sodium out of the cell and
potassium inside.
This action causes a
POTENTIAL DIFFERENCE or
VOLTAGE. This is due to the
separation of charge.
+ + + + + + + +
Resting state
Types of Neurons
Functional Types
1. Sensory: carries msgs from
receptors in skin/organs to CNS
2. Motor: carries msgs from CNS to
muscles/glands – effectors
3. Interneurons: located in CNS and
are the link between sensory and
motor neurons.
- - - - - - - - - - - -
Na+
(x3)
K+
(x2)
- - - - - - - - - - - - -
+ + + + + + + +
Cell Membrane

-
The difference in charge
makes the cells electrically
excitable. It is this that allows
neurons to transmit electrical
impulses
 Resting state = + outside –
inside
Resting at -70mV (membrane
potential) – a nerve impulse is
only then possible
 When a nerve is stimulated, a
brief increase in membrane
permeability to Na+,
temporarily reverse the
membrane polarity.
+ + + + + - - - - + + + + + +
- - - - - + + + + - - - - -- - - - - + + + + - - - - -+ + + + + - - - - + + + + + +
DEPOLARISATION
*the nerve impulse (like Mexican
wave)


After nerve impulse passes,
the Na/K pump restores the
resting potential
Electrical impulse = 340 m/s
Action Potential
Resting State: voltage activated Na+, K+ channels
closed.
Depolarization: voltage activated Na+ channels
open and Na+ floods in. Interior becomes + and
exterior becomes –
Repolarization: voltage activated Na+ channels
close, K+ moves out of cell restoring interior –
charge
Refractory period: returning to resting state
-Depolarization in the axon can be
shown as a change in membrane
potential (in millivolts)
-A stimulus must be strong enough to
reach threshold potential before an
action potential is generated.
-This is the voltage at which
depolarization of the membrane
becomes unstoppable (-50mV)
-The action potential is all-or-nothing
in its generation and because of this,
the impulse once generated will
always reach threshold and more
along the axon without it being
reduced
- the time it takes to return to a
resting state formed is the refractory
period
- during this time, the nerve cannot
respond.
All or nothing response
The size of a nerve impulse is always
the same. A weak stimulus is the same
as a strong stimulus, providing they
both exceed the threshold.
Two things enable us to distinguish
stimuli of different intensity:
1. More nerve fibres get
depolarization in a strong
stimulus than a weak one.
2. Strong stimuluses produce
more nerve impulses in a
given time than a weak one.
Conduction
Along unmyelinated fibres:
 Depolarization occurs
immediately adjacent to
neighboring areas.
 Repeats along whole way
(Mexican wave)
 Action potential doesn’t
travel, it is the impulse
 Prevented from going
backwards due to refractory
period – can’t be generated
because not at resting state.
 Speed = 2m/s
Along myelinated fibres:
 Insulated except at nodes of
Ranvier
 Therefore, ions can’t flow
between inside/outside of
membrane and action
potential can’t perform
 So the action potential jumps
from one node to the next =
SALTATORY CONDUCTION
 Speed = 140m/s
RECEPTORS
-A structure that is able to detect
change in the body’s internal or
external environment.
-Sense organ= a group of same type of
receptors (e.g. eye for light)
- other receptors may be simple nerve
endings and spread throughout (e.g.
pain/temp)
TYPES
1. THERMORECEPTORS
respond to heat and cold and relay
info to hypothalamus and cerebrum.
(makes us aware).
These receptors are nerve endings in
skin and respond to either hot or cold
but not both.
Internal body temp is monitored by
thermoreceptors within hypothalamus
which detect temp of blood flowing
through brain, and with this info it can
help regulate body temp.
2.OSMORECEPTORS
sensitive to changes in osmotic
pressure (the ability to gain water)
and are located in hypothalamus.
OP is determined by concentration of
substances dissolved in water of blood
plasma; needs to be maintained
within very narrow limits.
3.TOUCH RECEPTORS
mainly on surface of skin and sensitive
to light touches. They’re attached on
skin and to hairs and adapt rapidly. In
greater concentration on lips, fingers,
eyelids etc. other receptors located
deeper in skin and sensitive to
pressure and vibrations.
4.PAIN RECEPTORS
stimulated by damage to tissues,
poor blood flow or excessive
exposure.
Located in skin and mucous
membranes, most organs but not
brain.
They’re essential to warn us that
damage is occurring and to take action
or immediate help.


FEEDBACK SYSTEMS
-a circular situation in which the body
responds to a change or stimulus with
the response
altering
the
Stimulus –
change occurs
in the
environment
Feedback–
pos/neg
Excretion
Is the removal of waste products of
metabolism. Most are toxic and must
be removed.
LUNGS; excretion of CO2. Produced by
all body cells in cellular
respiration, cannot be
Receptor –
used so carried in blood
stimulus
until reaches lungs and
detected by
sensory cells
exhaled.
SRMERF
Response –
effector bring
about
appropriate
reaction
original
Modulator
– a control
center
processes the
msg received
Effector–
muscle or gland
receives
message
stim.
HOMEOSTASIS
the process of keeping the internal
environment fairly constant
 homeostatic mechanisms
help us be independent to
external env.
 a dynamic equilibrium in
which most input and output
of materials and energy are
balanced
Fluid Balance
-fluid gain must equal fluid loss.
-water is lost via kidneys, skin, lung
surface, alimentary canal. Typically
2.5L lost and gained per day.
NS and endocrine system are
main SENSORY and
CONTROLLING systems
Operate through feedback
systems
Negative feedback = when change is
opposite to original stimulus. Keeps
internal env. at fairly steady state
Positive feedback =
reinforces/intensifies original
stimulus. Plays no role in homeostasis.
SWEAT GLANDS; excrete
water with by-products such as salts,
urea, lactic acid to cool body.
ALIMENTARY CANALS; passes
out bile pigments that entered
small intestine with bile. These are
breakdown of
haemoglobin.
(not including undigested products)
KIDNEYS; the principal excretory
organ: responsible for maintaining
constant concentration of materials in
body fluids. Removed urea, produced
by liver during liver breakdown.
KIDNEYS
 60% fluid lost by kidneys
 only water loss from kidneys
can regulate constant conc. of
dissolved substances in fluid.


Ureter leaves each kidney to
urinary bladder and emptied
through urethra
Contains 1.2 million nephrons
Blood enters glomerulus under high
pressure. Filtration then occurs
because high blood pressure forces
water and small molecules into
capsule. Large molecules and blood
cells retained in blood.
Reabsorption of water into
peritubular capillaries.
Secretion of materials that need to be
removed secreted into kidney tubule
from capillaries.
CONTROL OF WATER LOSS BY KIDNEYS
Volume and urine composition
produced depends on how much
water in fluids.
Reabsorption of water occurs through
walls of tubules along entire length,
however at PCT and LOH it is by
osmosis.
 At DCT it is active
reabsorption controlled by
the antidiuretic hormone
(ADH) produced by
hypothalamus, released by
posterior.

ADH controls permeability of
DCT walls and Collecting
duct. When ADH is increased
in plasma, tubules are very
permeable hence reduces
water volume and increases
concentration of materials in
tubules and vice versa.
Dehydration and Water Intoxication
An excessive loss of water from the
body accompanied by loss of salts
results in dehydration.
 Often occurs during exercise
when a lot of water lost
through sweat or during
illness from vomiting or
diarrhea.
 Most people can cope with
mild dehydration which is
about 3-4% loss of total body
water, but greater than this
result in fatigue and dizziness.
 Greater than 10% causes
physical and mental
detoriation
 15% = death.
 Mild dehydration is restored
with oral rehydration
 Care is needed when
rehydrating because it is
possible to drink too much,
whilst not replacing the salts
that have also been lost. Salt
and other electrolytes need to
be replaced as well.
 Drinking too much is called
water intoxication. It is rare.
 The first symptom is
sensation of light headedness.
Headaches, vomiting and
collapse may follow. Initial
treatment involving restricting
fluids then with fluids with
electrolytes to replenish those
lost.
This is a feedback system goes as
follows:
Dehydration
Lower water
content in blood
plasma
Water conc. of
blood plasma
increases in
osmotic pressure
Water
intoxication
Higher water
content in blood
plasma
Water conc. of
blood plasma
decreases
osmotic pressure
Osmoreceptors
in hypothalamus
detect increase
in OP
Osmoreceptors in
hypothalamus
detect decrease
in OP
Modulator
Hypothalamus
stimulates the
posterior lobe of
pituitary via
nervous
conduction to
release more
Antidiuretic H.
Hypothalamus
stimulates
posterior lobe of
pituitary via
nervous
conduction to
release less
Antidiuretic H.
Effector
Permeability of
walls of DCT and
collecting ducts
is increased
(through a
greater number
of channels
opened)
Permeability of
walls of DCT and
collecting duct is
decreased
Response
More water is
reabsorbed. Less
urine is
produced and it
is more
concentrated
Less water is
reabsorbed. More
urine produced
and less
concentrated
Stimulus
Receptor
Feedback
There’s a
decrease in water
There’s an
increase in water
conc. of blood
therefore the OP
is decreased. The
result is a
negative
feedback as this
eliminates or
reduces original
stimulus.
conc. in blood. OP
is increased and a
negative
feedback is
accomplished due
to elimination or
reduce of original
stimulus.
Thermoregulation
Human body constant around 36.8
degrees Celsius – gained heat must
equal lost heat.
 heat is produced by metabolic
activity
 increased heat can cause
nerve malfunction, change in
protein structure, death
Heat Production:
o carbohydrates, proteins, lipids
contain energy which is
released in cellular respiration
o rate at which energy is
released by breakdown of
food = metabolic rate
o greatest effect on MR is
exercise (up to 40x more, also
stress from noradrenaline and
body temp in fever)
Thermoreceptors provide information
to hypothalamus about body
temperature which sends nerve
impulses to control temp. (2 types:
cold and hot receptors)
The Skin and Temperature Regulation:
o skin can speed up or slow
down heat loss rate by
conduction, convection,
radiation and evaporation.
o
Controlled by blood
Heat In:
Heat Out:
vessels that carry heat to skin
-body processes
-radiation, conduction,
-gained from
and convection to
that change diameter (by
surroundings by
surroundings
ANS) to increase or decrease
radiation and
-evaporation of water
heat loss from skin.
conduction
from skin and lungs,
……warm air breathed
Vasoconstriction or
out, warm urine &
Vasodilation.
faeces
when diameter at max,
 variation occurs at different
sweating occurs and cools
parts of day or changes to
body when heat is removed
external env. Also high temps
when it evaporates.
in second half of menstrual
To prevent temperature falling:
cycle.
(5 ways)
1. Vasoconstriction
2. Adrenaline – increase cellular
respiration = increase heat
production
3. Shivering – increase in
skeletal muscle tone which
leads to oscillating (under
hypothalamus control)
4. Increase in thyroxine
production – increases MR,
slow effect but long lasting
5. Behavioural response –
putting on jacket or curling
into ball.
To prevent temperature rising:
1. Vasodilation – increase flow
to skin, turn red, surface temp
rises, loss through radiation
and convection
2. Humidity and high temp = no
sweat evaporation
Low humidity and high temp =
sweating (to cool down)
3. Long term - decrease in MR =
less heat produced
4. Behavioural response –
turning on AC
IN COLD CONDITIONS
Decrease Heat
Increase Heat Prod
Loss
-Vasoconstriction
-reduction in sweating
-reduction of surface
area (curling)
-behavioural
- shivering
- increase in voluntary
activity
- increase in MR (long
term)
IN HOT CONDITIONS
Increase Heat Loss Decrease Heat
Prod
-vasodilation
-sweating
-decrease in voluntary
activity
- decreased metabolic
rate (long term)
-increase surface area
(spread out)
-behavioural
Hypothalamus controls temperature of
blood and receives impulses from
peripheral thermoreceptors. Through
negative feedback loops, involving
Autonomic Nervous System, control of
diameter of blood vessels, sweating,
shivering for maintaining body
temperature.
Receptors = central (in hyp.) and
peripheral (in skin) thermoreceptors
Temperature Tolerance:
Heat Exhaustion:
If our thermoregulatory mechanisms
do NOT work – death can occur
quickly. If we lose too much water and
do not replace it, heat exhaustion may
result.
 Dehydration leads to reduced
blood volume and a fall in
blood pressure
(High BP= dilate, Low BP=constrict)
 Normally the Vasomotor area
in the medulla would
normally compensate for this
by vasoconstriction blood
vessels
 In this case the Vasomotor
center is in conflict with the
thermoregulatory center.
*thermoregulatory center wants to
dilate vessels to release more heat
through radiation but vasomotor
center wants to constrict due to
falling blood pressure through
sweating.

In the beginning the
thermoregulatory is able to
override the need to correct
BP so sweating continues.
 So person may feel nauseous,
headache, confused and may
collapse.
 Prevented by drinking fluids
and resting
Heat Stroke
 If this does not happen, heat
stroke can occur
 When the person’s body temp
rises about 41 degrees which
causes failure of the heat loss
center, causing sweating to
stop and skin becomes hot
and dry
 The temp continues to rise to
seriously affecting enzyme
action. (denature)
 Unless temperature can be
brought down, they will fall
into a coma and die.
Hypothermia
Starts when the core body temp falls
below 35 degrees Celsius.
 Causes their metabolism to
slow down and vital body
processes will get slower
 Warning signs = lethargy,
weakness and loss of
coordination,
 If core temp falls to 24-26
degrees, the heart may stop
beating and the person will
die unless body temp can be
quickly brought back to
normal.
Fever
The abnormal elevation of body temp.
Can result from trauma, infections,
drug reactions, brain tumors, etc.
When people let their fevers run their
course, people recover more quickly
and are less infective than people who
use fever reducing drugs (e.g. aspirin).
Benefits:
1. Improves reduction of
bacteria and viruses
2. Increases metabolic rate and
accelerates tissue repair
3. Promotes interferon activity
(a substance, protein that
fights viruses)
When the body’s defenses attack the
invading bacterial viruses it causes
release of pyrogens – fever causing
substance.
This causes the body’s thermostat to
raise to set point to reset, controlled
by hypothalamus.



When set point it raised, the
person shivers to generate heat
and vasoconstriction helps
reduce heat loss
This stage of fever is termed
ONSET- a person has chills,
feels cold and clammy to touch
and has raising body temp.
In the next stage the person’s
body temp osculates around
the new set point until the



pathogen is eliminated –
STADIUM stage.
When the infection ends the set
point is returned to normal.
This activates heat losing
mechanisms, vasodilation,
sweating and skin is warm and
flushed.
We say the fever has broken.
Fevers above 40.5, person can
become delirious, convulsions
(vomit, fits), coma can occur at
higher temp or lead to death or
irreversible brain damage (4446 degrees).
there can be periods of time when the
bloodstreams don’t receive any
glucose from the small intestine.
However, cells need a constant
supply.
- to this end the liver plays a key role
in maintaining a constant supply, by
adding glucose to the blood in one of
two ways:
1. Glycogenolysis – breakdown
of glycogen to glucose
2. Gluconeogenesis – conversion
of other substances
(fats/amino acids) to glucose
HOMEOSTASIS OF BLOOD
SUGAR AND GAS
CONCENTRATIONS
Glossary:
Glucose comes from our diet in the
form of carbohydrates.
- carbs pass through bloodstream in
the form of glucose
- all metabolizing cells require glucose
in order to function, as it is the main
respiratory substance.
Hormones:
Insulin: decrease BGL
Glucagon: increase BGL
Glucose + O2 = CO2 + water + energy
- The Nervous System is especially
sensitive to any reduction in Blood
glucose levels.
- The set point of glucose is:
90mg glucose/100mL blood
- During a 24-hour period, the conc. of
glucose in blood fluctuates at
different meal times, each containing
varying glucose amounts. Therefore,
Glucose = energy source from food
Glycogen = storage in liver/muscles
To increase BGL processes:
Glycogenolysis: breakdown
(stimulated by glucagon + cortisol)
Gluconeogenesis: build-up of sugar
molecules from fats and amino acids
(stimulated by glucagon)
Decrease BGL:
Glycogenesis (chemically combined
in long chains), stimulated by insulin
Role of the Liver:
The liver is able to convert glucose into
glycogen for storage, or glycogen to
glucose for release into the blood.
The blood supply comes
through the hepatic portal vein
directly from the stomach,
spleen, pancreas and
intestines. Thus, has the first
chance to absorb nutrients
from digested food.
(short-term storage)
 Glucose is absorbed
into blood capillaries
of villi of small
intestine and the
hepatic portal vein
carries the glucose to
the liver, where a
number of things may
occur:
- Provide energy for liver
functioning
- converted into glycogen for
storage
- continue to circulate in blood,
for cells to absorb and use as
energy
- excess is converted into fat
for long-term storage
HYPERGLYCAEMIA
HYPOGLYCAEMIA
STIMULUS
After a meal, there is
an increase in
amount of glucose
entering blood from
small intestine.
When not eating,
respiration still
occurs so BGL start
to fall below set
point
RECEPTORS
Detected by B cells
Detected by A cells
MODULATOR
B cells of islets of
Langerhans secrete
INSULIN into blood
EFFECTOR
-Glucose is taken up
by the cells (mainly
of liver + skeletal
muscles)
-glucose is
converted to
glycogen
(glycogenesis)
-some is converted
to fat in adipose
tissue
- protein synthesis
increase in some
cells.
Lowers blood
glucose levels
The initial stimulus
has been
eliminated/reduced,
so the B cells are no
longer stimulated to
release insulin.
Feedback is
negative.
Alpha cells of islets
of Langerhans
secrete GLUCAGON
into blood
-stored glycogen in
the liver is
converted to
glucose
(Glycogenolysis)
-new glucose
molecules are
formed from fats
and amino acids
(gluconeogenesis)
RESPONSE
FEEDBACK
Role of the Pancreas:
Islets of Langerhans, clusters of
hormone secreting cells, have
two types:
1.
Alpha Cells – secrete
glucagon
2. Beta cells – secrete insulin
These are secreted into bloodstream to
control blood sugar levels.
Insulin causes a decrease in BGL in two
ways: first, accelerates conversion of
glucose into glycogen. Secondly,
Increase blood
glucose levels
Initial stimulus has
been
eliminated/reduced
so the a cells are no
longer stimulated
to release
glucagen. Feedback
is negative.
stimulates conversion of glucose into fat
in adipose tissue, and causes an increase
in protein synthesis in some cells.
Glucagon stimulates Glycogenolysis. It
also stimulates liver to produce new
sugar molecules from fats and amino
acids – Gluconeogenesis.



If the supply of glycogen in the liver becomes
exhausted, glucose may be formed by other
means. Once the low level is detected by
hypothalamus, it stimulates anterior lobe to
release Adrenocorticotrophic hormone.
Which stimulates cortisol releases in adrenal
cortex. This stimulates conversion of
glycogen to glucose, and conversion of
amino acids into glucose.
The phrenic nerve stimulates
muscles in diaphragm to
contract, causing ribs to move
up and out
This increases volume of
thoracic cavity and decreases
pressure inside lungs so air
enters
The concentration of gases
influences the rate this occurs
at resulting in the rate and
depth of inspiration.
Regulation of Gas Concentrations
The Breathing Mechanism
 Within medulla oblongata,
there is a respiratory center
 The ventral (underside) of the
RC is called the inspiratory
center, and the rest controls
breathing out, the expiratory
center
 Also control relies upon
chemoreceptors in the carotid
and aortic bodies of the blood
system which are sensitive to
slight changes in gas
concentrations, mainly CO2.
Expiration
 The expansion of lung causes
stretch receptors in their walls
to be stimulated
 This results in nerve impulses
travelling along the vagus
nerve, which prevents further
stimulation by inspiratory
center so the diaphragm and
intercostal muscles relax,
causing diaphragm to its dome
shape and ribs to move in and
down.
 The stretch receptors are no
longer stimulated and the
expiratory center is no longer
stimulated so the inspiratory
center can be stimulated again,
resulting in taking next breath.
Inspiration
 Nervous impulses from the
chemoreceptors stimulate the
inspiratory center of the
medulla oblongata
 This stimulates nerve impulses
to pass along the phrenic and
intercostal nerves
Breathing can be controlled to some
extent by conscious thought from the
forebrain.
However, whilst this allows us to control
speech and hold our breaths, we cannot
stop breathing consciously forever.
Eventually we will be FORCED to take a
breath.
Carbon Dioxide has the greatest effect
on rate of breathing.
PROTECTION AGAINST
INVADORS
Pathogens: bacteria and
viruses/something that causes disease/
infection.
Bacteria:
 Most are harmless
(nonpathogenic)
 Many are essential, e.g. food
flavour or role in decomposing
organic material
 Many live on our skin and have
major part of digestion
processes, have no ill effect
 Bacteria consist of a single cell
Viruses:
 Small and contain genetic
material, either DNA or RNA
 Virus induces it’s DNA/RNA into
living cell to manufacture more
virus particles, then able to
leave host and infect others. If
multiply in bacteria:
bacteriophage
 Not all are harmful and being
used for science to insert new
genes into organisms
Types of White Blood Cells (Leucocytes)
and internal Non-specific Defenses.
WBC
SUB-CLASS
FUNCTION
MONOCYTES
-dendritic cells
-macrophage
(some develop from
WBC, some wonder
through blood
looking for
pathogens. Others
are ‘fixed’ in one
place dealing with
pathogens coming
to them.)
-antigen
presenting cell
-phagocytic
cells which are
larger and
survive longer
than
neutrophils
LYMPHOCYTES
-B-cells
-involved in
humoral
mediated
immunity
-involved in
cell mediated
immunity
-T-cells
Disruptions to Homeostasis
Insulin: stimulates cells to take in
glucose from the blood, also stimulates
conversion of glucose into glycogen by
liver and muscle cells. A person with
diabetes has an abnormally high BGL, a
condition called hyperglycaemia.
If a diabetic skips a meal, exercises
heavily or takes too much insulin,
BGL will fall and can lead to
hyperglycemic reaction: dizziness,
sweating, headache etc. it can be
quickly remedied with a boost of
sugar.
(Blood Glucose Levels is the disrupted
homeostatic mechanism)
Type 1 Diabetes
Causes:
 Occurs at birth, due to fault in
immune system which causes
destruction of beta cells in islets of
Langerhans of the pancreas.
 Beta cells produce insulin, therefore
those with type 1 does not produce
insulin and therefore BGL remain
high in blood as there’s no insulin to
take it in.
 The body recognizes this and tries
to provide body with other sources
of fuel, such as fat.
Diagnosis:
o Taking blood test to measure BGL
Types:
Fasting test; checked ever 12 hours
Random blood test; throughout day
Oral glucose tolerance test (high
glucose drink); checked every 2hrs
Symptoms:
 Excessive thirst
 Frequent urination
 Weight loss
 Fatigue
 Visual disturbances
 Itchy skin
 Nausea and vomiting
Treatment:
o No cure
o Can be treated by giving injected
insulin or programmable pump
o Regulating diet so intake is matched
to insulin and exercise
o Increasing amount of ‘slow carbs’ in
the body e.g. fruit
Synthetic Hormones:
 Insulin used to be obtained from
pancreas of cows and pigs and was
expensive and limited. Also had to
be purified and some patients
suffered allergic reactions or
infection
 Gene for human insulin is now
inserted into bacterial DNA and the
bacteria are cultured to make
human insulin. It is marked as
HUMULIN. Yeast is also now made
in a similar way to make insulin.
Future Treatments:
Gene therapy:
Investigated replacing beta cells as a
means of eradicating type 1 diabetes.
o tired and lethargic
o slow healing wounds
o itching and skin infections
o blurred vision
Treatents:
 no cure but earlier the better
 if it remains untreated, condition
increases complications such as
heart disease, stroke, kidney
disease, eye problems etc
 can improve lifestyle and diet
synthetic hormones same as type 1
Type 2 Diabetes
Causes:
 A lifestyle disease; often occurs
over age of 45
 Able to produce insulin but their
cells do not respond to it
 Increasing lifestyle risks:
Lack of exercises
Overweight
High fat, sugar, salt diet and low in
fiber
High blood pressure
High blood cholesterol
Smoking
Also:
Relatives with type 2
Other health concerns e.g.
cardiovascular disease
People taking certain medication
Thyroxin (T4): affects nearly every tissue
in the body by stimulating
carbohydrates, protein and fat
metabolism; thus regulates basal
metabolic rate.
It can maintain body heat, (because heat
released from chemical reactions).
Thyroxin secretion is controlled by
thyroid-stimulating hormone (TSH),
secreted by anterior lobe of pituitary,
but it’s release is controlled by
hypothalamus of brain.

Unhealthy lifestyles are increasing
numbers of diagnosis.
Diagnosis:
 same as type 1
 also glycosylated haemoglobin:
gives average BGL over 10 weeks
Symptoms:
o thirst
o frequent urination
1. HYPOTHYROIDISM
Disrupted homeostatic mechanism:
Metabolic rate Occurs due to too little thyroxine being
released, due to either the thyroid
gland, pituitary gland or hypothalamus.
Thyroxine contains iodine which is
needed to produce adequate levels of
thyroxine.
Causes of disruption:
 IODINE DEFICIENCY DISORDER: lack
of iodine prevents thyroid gland
from making enough thyroxin. The
thyroid gland then in effort to
comply for the pituitary glands
constant chemical messages to
produce more hormones. This
enlargement is called a goitre.
 HASHIMOTO’S DISEASE: most
common cause, an attack of white
blood cells and antibodies of
immune system on cells of the
thyroid gland. Without treatment,
death can occur within 10-15 years.
 SURGERY: primary treatment for
thyroid cancer that involves
removal of all or part of the thyroid
gland, therefore produces
decreases hormone levels
 PARTICULAR DRUGS: such as
lithium, can interfere with normal
processing of iodine and thyroxin
production
 PITUITARY GLAND DYSFUNCTION: if
it doesn’t produce enough TSH to
prompt the thyroid
 HYPOTHALAMIC DYSFUNCTION:
hypothalamus influences pit. Gland
through thyrotropin-releasing
hormone, problems with
hypothalamus can affect secretions.
Diagnosis and symptoms:
Involves physical examinations and
blood tests to measure TSH and/or
thyroxin levels. Also ultrasounds or
radioactive iodine scans to check
internal structure of thyroid.
Slow heart rate
Unexplained weight gain
Fatigue or lack of energy
Depression
Hair loss
Dry, coarse skin
Cold intolerance
Swelling of face and goitre
Treatment:
There is no cure, medication taken for
rest of life with careful monitoring
because too little won’t relieve
symptoms, too much cane result in
hyperthyroidism.
Now compulsory addition of iodine
into most breads with iodized salts
Adequate iodine important during
pregnancy because iodine
deficiency can affect development
of baby’s brain and body.
(cretinism)
Synthetic Hormones:
Used to be treated with tablets from
dried and powdered thyroid glands of
animals (pigs, sheep) but is not as
effective as human thyroid. Most tablets
are now made with synthetic hormones
e.g. LEVOTHYROXINE: daily dose which
restores adequate hormone levels,
lowers cholesterol levels and reverses
signs and symptoms. Is inexpensive an
has no symptoms.
2. HYPERTHYROIDISM
An overactive metabolic rate, from too
much thyroxine being produced.
Causes:
 Grave’s Disease: most common. An
abnormality in immune system,
when antibodies manufactured
behave like TSH and stimulate
thyroid uncontrollably, rather than
attacking foreign pathogens.
 What causes grave’s? possible
stress levels can show to impact
onset of autoimmune conditions.
Autoimmune conditions have a
distinct genetic element; some
inheritance can predispose them to
grave’s. another cause is excessive
intake of iodine.

Presence of thyroid stimulating
antibodies in a blood test
Diagnosis and Symptoms:
with blood test that measures thyroid
hormone levels, a person will have high
thyroxine levels but low TSH.
Rapid heartbeat
Weight loss
Increased appetite
Heat intolerance
Protruding eyeballs (grave’s only)
Treatment:
o no cure
o medication: anti-thyroid drugs to
interfere with gland’s ability to use
iodine. Side effects include skin
rashes and joint pain. Drugs can
suppress immune system.
o Radioiodine therapy: taken as a
drink which iodine is taken up by
active cells in thyroid and then
killed, it is not absorbed by other
cells. It is then excreted through
urine with no side effects
o Surgery: some or all of thyroid gland
is removed.
Future Treatment
Cell replacement therapy: Coaxing
genetically modified embryonic stem
cells from mice to develop into thyroid
cells.
Transmission of Disease
- Pathogens passed on in number of
ways
Mode of Description
Transmission
Contact:
Direct and
Indirect
1.0Transfer
of Body
Fluids
1.1Infection
by droplets
1.2 Airborne
Transmission
Ingestion of
food/water
- Direct = spread of
pathogen by physical
contact by touching
- Indirect = touching
object that was touched
by infected individual
e.g skin infections, STI’s
- From one person to
another; when
blood/bodily fluids from
infected person come
into contact with mucous
membranes
(nose/genitals etc) or
bloodstream of
uninfected. E.g. HIV,
Hepatitis B & C
- tiny droplets of moisture
holding pathogenic
organisms are emitted
when breathing/
coughing etc. can be
settled on utensils or food
E.g. influenza, measles
- exhaled moisture
droplets evaporate,
bacteria is killed but
viruses remain viable and
can be inhaled e.g.
influenza
- contaminated food or
drinks with pathogens
E.g. dysentery, typhoid,
salmonella
Transmission
by Vectors
- transfer of pathogens by
other animals.
- some directly, others
through food/water
- many vector-borne
diseases are spread by
specific vectors
e.g. malaria + dengue
fever by mosquitoes,
lyme disease by ticks
Defenses against disease
Non-specific defenses: work against all
pathogens. They’re the body’s first line
of defense
Specific Defenses: Directed at particular
pathogens
EXTERNAL DEFENSE MECHANISMS
- all are non-specific
Skin
 Stops entry of micro-organisms,
provided not broken by
cuts/abrasions
 has numbers of “normal”
bacteria occupying skin that
fight pathogens for area
 oil glands produce sebum,
which contains substances that
kill pathogenic bacteria
 sweat contains salts and fatty
acids that prevent growth of
many micro-organisms
Digestive + Reproductive Tract
 mucous membranes:
- line body cavities open to
exterior
- secrete mucous which inhibits
entry of micro-organisms to
organs of body
Urogenital Tract
 Acids:
Stomach juices kill many bacteria
(acidity)
Vagina also has acid secretions that
reduce growth of micro-organisms
 Flushing action of body fluids
 Urine through urethra has cleansing
effect: prevents bacterial growth to
bladder and kidneys (women have
shorter urethra and tend to suffer more
bladder infections)
Respiratory system
 Hairs:
In nose cavity with mucous to trap
up to 90% of particles when
breathing
 Cilia:
Tiny hair-like projections from cells
that do a beating motion, when
containing trapped particles, they
motion towards to throat where it
is coughed or swallowed
Ear
 Hairs
 Cerumen (ear wax)
Protects outer ear against infection
Slightly acidic containing lysozyme
(kills bacteria)
Eye
 Eyes protected by flushing
action of tears with lysozyme
Protective Reflexes
1. Sneezing: irritation of nasal cavity
stimulates forceful explosion from lungs
carrying foreign particles and mucous
2. Coughing: irritation in lower
respiratory tract forces air from lungs
and drives particles up
3. Vomiting: excessive stomach
stretching and bacterial toxins stimulate
muscles of abdomen and diaphragm to
expel contents
4. Diarrhoea: irritation of intestines
increases muscle contractions of walls to
remove irritant. Material is watery
because doesn’t stay in intestine long
enough for water to be absorbed.
Pathogens that enter the body are
targeted by non-specific immune
responses of inflammation and fever.
Phagocytes, leucocytes and
macrophages are body’s internal nonspecific defense and the second line of
defence.
HISTAMINE: increases blood flow to the
site of the injury and causes capillaries
in area to become permeable. With
more blood flow there is an increases in
metabolic heat and the area becomes
hotter and redder. Also with more fluid
being filtered from blood, the site
becomes swollen.
HEPARIN: prevents blood clotting in
localized area. This allows flow of blood
to the injury to allow phagocytes to be
attracted to chemicals released by mast
cells. Blood clots form around the
damaged area, slowing blood flow so
any pathogens present spread less
quickly.
o
The inflammatory Response
o A response that occurs when
tissue is damaged. Usually a
breach to the skin, the
damaged part becomes RED,
SWOLLEN and HOT. Often
accompanied by PAIN.
o It is aimed at reducing the
spread of infection, destroying
any microbes and reducing
further risk by reducing
opportunity for more
pathogens to enter.
o During response, cell debris is
removed and repair begins on
tissue
o Mechanical damage results in
localized chemical change
whereby Mast cells stimulate
the production of histamine
and heparin into tissue fluid.
Phagocytes are attracted to site by
chemicals released. Macrophages
and Leucocytes carry out
phagocytosis.
Often pain receptors are impinged
during this process so the person
feels pain
Phagocytic cells filled with
pathogens and debris begin to die
and together with tissue fluid form
a yellow liquid called pus
Over time new cells are formed by
mitosis and repair of damaged
tissues take place.
The immune system
Immunity = the resistance to infection
by invading microbes.
Once the first line of defence is
breached + the second line of defence is
activated.
Antigen Presentation occurs in the
lymph system, which results in a specific
immune system.
The Lymphatic System
(non- specific defence)
works by collecting escaped fluid from
blood capillaries and returning to
circulatory system.
Lymph: contains cell debris, foreign
particles and micro-organisms that
penetrated external defence.
Lymph Nodes: occur at intervals along
lymphatic vessels, contain masses of
lymphoid tissues, cells of which are criscrossed by network of fibres.
 The larger particles (e.g.
bacteria) are trapped in the
mesh; destroyed by
macrophages
 During infection, lymphocyte
formation increases and nodes
are swollen and sore
Antigen = any substance capable of
producing a specific immune response.
On the surface of ALL cell
membranes; often proteins, but can
be carbohydrates of lipids
Those belonging/produced by the
individual are self/non-foreign
antigens
An autoimmune disorder is caused
by the body not recognizing selfantigens and attacking its own
tissues
Macrophages are involved in both nonspecific and specific immunity. T-cells
and B-cells are involved in the specific
immune response.
2 types of SPECIFIC immune response:
1.
HUMORAL RESPONSE
(antibody-mediated)
Sensitized B-cells are produced and
mature in bone marrow.
B-cells (lymphocytes) are stimulated by
a foreign substance (an antigen) which
reaches lymphoid tissue. This is called
antigen presentation.
Once stimulated, they rapidly divide by
mitosis to produce plasma and memory
cells.
Plasma cells produce antibodies –
specialized proteins produced in
response to a non-self-antigen – which
are released into the bloodstream.
Antibodies inactivated or destroy nonself-antigens by:
 Binding to viral binding sites or
to bacterial antigens
 Agglutination: clumping nonself-particles together
 Reacting with soluble antigens
and making them insoluble
 Coat bacteria enhancing
phagocytosis
 Inhibiting reactions with other
cells or compounds by
breakdown of non-self cell
This is a primary response. It takes time
to develop the antibodies, and so the
individual usually suffers symptoms of
the disease caused by the pathogen.
Memory cells result in a much faster
response should the same non-self
antigen invade the body again.
2.
CELL-MEDIATED RESPONSE
Produced in bone marrow, mature in
thymus gland.
This provides resistance to intercellular
phase of bacterial and viral infections.
When foreign antigens reach lymphoid
tissue, T-cells (lymphocytes) are
sensitized and undergo rapid mitosis.
Most produced are Killer T-cells, which
destroy the antigen. Others become
Helper T-cells, which sensitize
lymphocytes to intensify response and
promote phagocytosis. Or Suppressor Tcells, which inhibit B and T-cells to slow
down immune response once infection
has been dealt with effectively. Some
become Memory cells which initiate a
faster response secondary response
should the same antigen reenter the
body.
NATURAL
ARTIFICAL
PASSIVE
- occurs without
human
intervention
- body gets
antibodies
produced by
someone else
- not long lasting
- e.g. antibodies
enter bloodstream
across the
placenta or in
breast milk
- occurs when
someone is
given antibodies
produced by
someone else
- not long lasting
- e.g. influenza
antibodies
injected into
bloodstream
ACTIVE
- Occurs without
human
intervention
- body makes it’s
own antibodies in
response to nonself antigen
long-lasting
immunity due to
memory cells
- e.g. contracting
chicken pox +
produces
antibodies for it
- occurs when
Why are secondary responses always faster
than primary?
Secondary responses are always faster
than primary responses, because there
are a few memory cells moving around
in the blood; plasma. When the same
non-self antigen attacks the body again,
antibodies are produced rapidly and
remain in the plasma for a lot longer.
Consequently, the symptoms of the
disease are not normally experienced.
Types of Immunity
Can be natural – no human intervention
– or artificial – a result of being given
antibody/antigen.
Passive immunity: receives antibodies
from another source
Active immunity: when body processes
its own antibodies as a response
someone is
given antigens
- body makes
it’s own
antibodies in
response to a
non-self antigen
long-lasting due
to memory cells
-e.g. antigens
given by
vaccination
(living
accentuated
MMR injected:
treated with
heat –
weakened)
Vaccines
Immunization: means programming
immune system to respond rapidly to
infecting micro-organisms
(naturally/artificially)
Vaccination: artificial introduction of
pathogenic organisms so that the ability
to produce appropriate antibodies is
acquired without person suffering.
Vaccine: an antigen preparation used in
artificial immunization (result of needle)
4 types of vaccines:
Type of
vaccine
1. Living
attenuated
microbes
Explanation & examples



2. Dead
microbes



3. Toxoids

4. Sub-unit


My helpful hints:
Passive
Active
natural
Baby
Sickness
artificial
Injections
Given
antigens
Passive: always not long-lasting, always from
someone else
Active: always long-lasting, always made by
own body
Natural: never synthetic
Artificial: synthetic

Reduced virulence (less
ability to produce
disease)
Can be produced by
recombinant DNA tech.
E.g. rabies,
poliomyelitis
Microbe killed before
injected
Not as long lasting, but
can result in an
immune response
E.g. cholera, bubonic
plague
The toxins produced by
bacteria can be
inactivated so that
don’t make the person
ill
Diphtheria, tetanus
A fragment of the
microbe is used to
provoke an immune
response
E.g. hepatitis B, human
papilloma virus – hpv
-usually delivered by injection, but may
be delivered by sugary syrup or other
methods. Research into nasal sprays,
skin patches and food supplements
being conducted
Vaccination of Populations
 use of vaccinations in mass
immunization programs has
eradicated or greatly reduced the
incidence of certain diseases
HERD IMMUNITY: a high proportion
of the population being immunized
so those who are not immune are
protected e.g. influenza in winter
good herd immunity depends on all
people being on board with
program and not being complacent,
otherwise its less effective.
Gives less chance of disease
transmitted between people
 One problem in all countries: as
incident of infectious diseases
decline, people become complacent
and may decide risk of side effects
from vaccine is higher than risk of
disease itself. – outbreaks
 Parents must decide if they will
vaccinate their children in infancy
Vaccines shouldn’t be given too
early (<2 months) because child’s
blood still contains antibodies from
its mother via placenta/breast milk
If a newborn is given a vaccine, it
will be eliminated by original
antibodies. This occurs before
child’s immune response becomes
activated
 One shot is sometimes not enough
 When someone is vaccinated, the
immune system will activate a
certain number of B-cells, they will
multiply and some will produce
antibodies, others become memory
cells, these can last for decades.
 In most cases, the first dose of
vaccine doesn’t enable enough Bcells. Booster shots are required

Timing of booster: too soon = it’ll be
eliminated before more B-cells can
be activated (approx. 2 months)
Ethical Concerns
Major concern is how the vaccine was
manufactured, how it was tested and
risks associated with its use.
As viruses can only reproduce in living
cells, the manufacture of viral vaccines
require host cells – chicken, embryos,
mice etc. – some people are concerned
about treatment of animals.
Many vaccines require human tissue as
it grows better from same species and
prevents cross species infections
Testing of vaccines:
 Most produced in developing
countries, but also mostly for them.
 E.g. genetically distinct subtypes of
HIV have been identified, mostly in
developing regions. Trialing of
vaccines, therefore in these regions
where education is low and
population may not be aware of
risks. People are concerned for the
selected trial group that are open to
exploitation.
 Before clinical trials, there are
animal trials. Usually mice
 People are concerned they suffer
and too many sacrificed for science
 Arguments are based on the
contention that causing pain to
another creature is not morally
acceptable, claiming all lives have
value.
 Discontinuing testing on animals
would benefit them but result in
serious consequence for humans.
End of semester 1
Semester 2
Mutations & Gene Pools
Alleles: alternative forms of a gene, the
pairs of alleles inherited control and
determine characteristics.
Species: a group of individuals that
share many characteristics and able to
interbreed under natural conditions to
produce fertile offspring.
Gene Pool: a sum of all alleles in a given
population
Allele frequency: how often an allele
occurs in a gene pool. These may change
overtime due to migration, natural
selction etc.
E.g. Scandinavians more likely to have
blue eyes over brown eyes like in Africa.
Mutations
Variations in offspring that do not
resemble any characteristic
occurred before in family history.
Occur during replication of DNA
molecule (mitosis, meiosis)
Two types:
1. Gene Mutations: changes
within a single gene
 Each 3 bases codes for an amino
acid, a change in one base – point
mutation – could alter a protein or
have no effect, or prevent it from
being produced
 Examples:
Albinism: result of a missing protein
that code for pigmentation
Duchenne Muscular Dystrophy:
mutation arise in mother inherited
by sons
-
Cystic Fibrosis: mutation on
chromosome 7 (recessive)
2.
Chromosomal Mutations: all or
part of a chromosome is
affected.
Can be:
 Deletion – part is lost
 Duplication – part occurs twice
 Inversion – breaks, joins back wrong
way (changes order)
 Translocation – breaks off, joins to
wrong chromosome
 Non-disjunction – change in
chromosome number during
meiosis
Chromosomal mutations cause severe
abnormalities so severe that miscarriage
often occurs.
Examples:
Down Syndrome: has 3 of Ch.21
Patau Syndrome: has 3 of Ch.13 –
small head, cleft palate etc
Klinefelters Syndrome: has 3 of
Ch.16 – in males, small testes,
enlarged breasts (xxy or xyy)
Cri-du-chat: missing Ch.5
Turner’s: missing X Ch. - females
SOMATIC: mutations that occur in body
cells, only that individual is affected and
once they die the mutation is lost.
GERMLINE: those that affect the
reproductive cells, can be passed on to
the next and subsequent generation.
E.g. PKU
Mutagens: agents that increase the
likelihood/rate that mutations occur.
e.g. mustard gas, sulfur dioxide, ionizing
radiation
not all mutations are harmful and can
have little effect or provide a survival
advantage – natural selection.
Lethal Recessives
If two recessive mutations are
reproduced and appears in their
offspring – not masked by a dominant
allele, can be lethal and cause death of
foetus. If they are born the usually die
before passing it on.
E.g. Tay Sachs: missing enzyme resulting
in fatty substance in nervous system.
Techniques in Human Biotechnology
Human Genome Project: the entire set
of genetic info of a person. Giving the
order of nucleotide bases. Helps check
for faulty sequence of bases – e.g.
Huntington’s disease.
DNA SEQUENCING:
Determines the sequence of nucleotide
bases in a DNA sample.
o In building a sequence, each new
nucleotide is bonded to a hydroxyl
group (OH) of the previous.
o A method for determining the
sequence is adding synthetic
nucleotides lacking the OH group to
the growing strand.
Dideoxynucleotide.
o This stops the elongation of the
sequence because there is no OH
group to bond to. The result is a
series of DNA fragments of different
lengths and can be compared.
o Gel electrophoresis used to
separate and order the bases. The
actual template will be
complementary to that in the gel.
DNA PROFILING
A technique to distinguish between
individuals
 99% of our DNA is identical but
there are sections called core
sequences with short tandem
repeats (STR).
 The exact number of repeats varies
greatly from person to person.
 The pattern of bands on gel
electrophoresis can be used to
determines someone’s DNA profile.
Only identical twins have identical
profiles
Used for forensics
POLYMERASE CHAIN REACTION (PCR)
To amplify the amount of a sample of
DNA, producing thousands of identical
copies and to do so quickly.
Steps:
1. denaturing
2 template strands of DNA are
separated (broken hydrogen bonds)
by heating DNA up to 96C
at this temp, DNA polymerase is
destroyed so a more heat stable
one is required, called Taq
Polymerase; bacterium from hot
springs
2.
-
3.
-
-
-
-
Annealing
Once dna has been cooled to 4865C, a primer (short fragment of
DNA that provides a starting point
for DNA replication) is attached to
each strand. This is a section with a
known sequence, which attaches to
a specific part of a single DNA chain
Elongation
PCR only amplifies a certain region
of the DNA not the whole template.
Primers act as a starting point for
the Taq Polymerase to start adding
complimentary DNA nucleotides
which are added to the process.
The bases are added one at a time
in a single direction to the singlestranded DNA.
This takes place at 72C in a
thermocycler and doubles the
number of DNA molecules.
(2,4,8,16,32,64 etc)
The process is repeated several
times to produce thousands of
copies with exact sequences.
Due to the compounding amplification it
is known as chain reaction.
*note never just say polymerase, specify
if it’s DNA or Taq etc.
Restriction Enzymes:
Occur naturally in bacteria and
work to protect bacterial cells from
infection of foreign DNA (viral DNA)
but cutting DNA into smaller pieces.
 Cuts dna at specific base
sequence recognition sites (4-8
base pairs long)
 Between two specific bases =
blunt ends
 In a staggered manner = sticky
ends. These allow it to bind to
complementary sticky ends on
other dna, cut by the same
restriction enzyme, to produce
matching sticky ends.
RECOMBINANT DNA TECHNOLOGY
(rDNA)
 Dna is universal and restriction
enzymes can therefore be used to
cut dna in other species.
 Sticky ends become complimentary
and so the cut out section can be
inserted into other organisms.
 DNA ligase is used to glue these
pieces of DNA together

An organism is called
Transgenic when a gene it is
moved from one organism into
another, in such a way that it is
expressed in the new host.
Plasmids:
 Small, circular, double-stranded
pieces of DNA separate from main
chromosome.
 Found in bacteria and some yeast
 Self-replication and have a point of
origin where it starts.
 May vary in size –can be one
plasmid of hundreds
 Contain recognition sites, where
restriction enzymes cut the plasmid,
this allows matching DNA
sequences to be inserted.
 May be used as vectors to transfer
genes from one chromosome to
another.
 May be used to make multiple
copies by allowing plasmids to
reproduce inside growing bacteria
Examples of use of rDNA
1.
INSULIN

Messenger RNA is extracted from
human pancreatic tissue
Complementary strands of DNA (cDNA)
are produced using viral enzyme –
reverse transcriptase
The single-stranded mRNA is made into
double-stranded by allowing enzyme,
DNA polymerase to make second strand
of complementary nucleotides. (PCR)







The human insulin gene is identified and
isolated on cDNA using restriction
enzymes
The insulin gene is inserted into a
plasmid using, DNA Ligase.
The plasmid with the human gene =
vector. The plasmid is closed and placed
into a culture of plasmid-free bacteria,
these bacteria take up the vector and
multiply.
Transcription and translation of the
genes in the plasmid occur, resulting in
the production of human insulin.
This is then purified.
*can also use example with Human
Growth hormone. Instead mRNA is
derived from human Pituitary Gland
tissue and using E.coli bacteria.
GEL ELECTROPHORESIS
Used to match DNA fragments with
others – for crime scenes, matching
fossils with closes organism etc.
 DNA samples are placed in wells on
one side of a gel where an electric
current is passed through the agar
gel to separate fragments of
different sized DNA.
 DNA is negatively charged, so it
moved towards the positive
electrode. Larger fragments move
slower than smaller fragments so
they don’t travel as far through the
gel. This is seen as a series of bands
 Restriction enzymes cut the DNA
when they come across specific
sequences, therefore they are of
different lengths of nucleotides. In
this way bands are formed in the
gel at different points.
 Each band represents a group of the
same sized fragments


Comparisons can be made between
DNA from different individuals as
long as the SAME restriction
enzyme has been used.
The banding pattern formed during
gel electrophoresis forms a DNA
profile/fingerprint for that
individual.
Gene Therapy: replacing faulty genes
with healthy ones – cystic fibrosis,
Huntington’s disease
Cell replacement therapy: specializing
undifferentiated stem cells into specific
cells – Parkinson’s, Alzheimer’s
Evolutionary Mechanisms
Law: evolution requires variation!
Every organism is different, brought
about by a number of factors:
crossing over of chromosomes in
meiosis
independent assortment
random choice of mates and
Fertilisation (sperm and ovum)
Mutations (required for variation
with asexual organisms)
Darwin concluded: due to excessive
birth rates and limited resources there
must be a struggle for existence. And
due to variation, the organisms with the
most favourable characteristics
survived, while the others with
unfavourable traits died before being
able to reproduce.
Factors affecting allele frequency:
NATURAL SELECTION
Process where a selective agents of the
environment favour alleles at the
expense of others, to become better
adapted.
6 main factors:
1. Variation: the diversity in genetic
and phenotypic traits within and
between species and passed onto
offspring.
There must be variation, within a
population there are slight
differences. Some may give
individuals a selective advantage
over others.
2. Over-production: more individuals
produced than can be sustained by
the available resources. The
ecosystem can only support a
certain number so if the climate
changes faster than the population
of a species, then it will die out.
3. Struggle for existence: due to
excessive birth rates and limited
resources, there’s a struggle
between individuals.
4. Survival of the fittest: only the best
adapted individuals survive to reach
maturity and reproduce. They pass
on their favourable traits.
5. Like produce Like: favoured
characteristics are passed onto the
next generation
6. Overtime gene pool changes: the
proportion of the favourable allele
increases and the less favourable
will eventually die out.
RANDOM GENETIC DRIFT
(Sewell-wright effect)
In small populations there can be
random, non-directional differences in
the allele frequency, which are not
representative of the population as a
whole. This means that in isolated
populations, an allele which is rare in
the larger population may, purely by
chance, become more prevalent.
e.g. Dunkers – from Pennsylvania, didn’t
marry outside the religious community.
And constituted an isolated population,
containing higher or lower allele
frequencies for certain traits – blood
group, handedness, earlobe type.
These small, isolated communities exist
WITHIN the larger population, so
changes in allele frequency within these
gene pools are as a result of random
changes between phenotypes.
FOUNDER EFFECT
The gene pool of a newly established
pioneer population, carrying only a small
portion of the total genetic variation of
the larger population – not
representative.
This occurs when a small group moves
away from its homeland to a totally new
area and establishes an expanding
community.
If a dominant allele codes for an
adaptive feature, then it could kick-start
evolution as they are only a few original
members to pass on the traits.
These random traits can be further
enhanced by RGD – from premature
death of differential reproductive
success, some certain traits can be
totally lost from pioneer populations.
On the other hand, unusual traits not
commonly found in the parental
population can become quickly
established.
(note- isn’t always obvious in the
phenotype)
e.g high frequency of Huntington’s
disease in Afrikaner population from
Dutch population.
In what once was 50:50 ratios of orange
and purple balls, now becomes 9:1.
Founder effect = different ratio of a trait
in comparison to the larger population
for a small, isolated group that moved
away.
Random genetic drift = the random
chance of the trait being expressed as it
does not contribute to survival.
MIGRATION
flow of genes from one population
to another
Changes in allele frequency can be
caused by gene flow. i.e. where alleles
are introduced into a gene pool due to
migration. Can come from immigrants.
E.g. Mongols have higher proportion of
allele IB because they invaded Europe in
12th-13th centuries.
Barriers between gene flow:
> Ecological: different food locations
> Behavioural: different mating calls
> Geographical: mountain ranges
> Socio-cultural: mate selection within
ethnic/religious groups only
Barriers can keep populations apart and
prevent interbreeding. When separated,
allele frequencies develop and overtime
generations become less alike as they
develop different characteristics.
TAY SACH’S DISEASE (TSD)
 a hereditary disorder of lipid
metabolism
 occurred most commonly in people
of Jewish descent from Eastern
Europe (Ashkenazi Jews). It is
caused by a missing enzyme which
results in the accumulation of fatty
substances in the nervous system.
 Death usually occurs by age 4 or 5.
 Incidence worldwide: 1 in 500 000
Ashkenazi jews: 1 in 2500 births
Two theories have been proposed: jews
often lived in isolated groups, those who
were heterozygous for the condition are
less susceptible to Tuberculosis (TB).
Therefore, in overcrowded, isolated
conditions that would increase the the
threat of TB
Those who got TB would die and those
who got TSD would die, but carriers
would survive, therefore the allele
remains in the population. It is selected
by the environment, which acts as a
selective agent.
Geographical isolation allows different
groups within a species to adapt
according to the environment they are
in. this is called ADAPTIVE RADIATION
e.g. birds down south are larger than in
north Australia to contain more heat.
Selective agent = a factor that causes
death of organism’s with certain
characteristic, but which has no effect
on individuals without those
characteristics.
Genetic Diseases
the result of mutations
most are eradicated over time
because people die before they
reach reproductive age and so allele
isn’t passed on. However, some still
remain in the population:
SICKLE CELL AMENIA
When RBC’s (erythrocytes) fold into
a sickle shape and stick together. It
is fatal and don’t carry as much
oxygen as normal RBC’s. they also
stick together and block small blood
vessels
 Occurs mainly in black Africans
 a recessive mutation
 individuals with one allele for sickle
cell show no ill effects unless in
short supply of oxygen
 it provides a degree of immunity to
malaria, therefore allele is
maintained in areas where malaria
is present.
Speciation
NOT A MECHANISM OF EVOLUTION, IT’S
THE RESULT OF THE MECHANISMS
speciation is the process by which
new species are formed from
existing species
the process relies on groups of
individuals within a species being
isolated from eachother in some
way. Then, based on the selection
pressure at work, these groups or
demes, tend to interbreed with
individuals more often within this
groups then with other separate
groups of the same species.
If the flow of genes between the
groups becomes less frequent, and
eventually ceases, the groups are
likely to evolve along separate
pathways.
1.
2.
3.
4.
Variation within population exists
Barrier separates into two groups
exposed to different environmental
factors. Eventually have different
gene pools. No interbreeding occurs
Environmental differences provide
different selection pressures,
resulting in a change in gene
frequency within the two separate
gene pools
Sub-species develop – isolated but
can still interbreed
5.
Over prolonged period, gene
frequency changes make it
impossible for two groups to
produce fertile offspring therefore
are 2 new species.
Evidence for Evolution
DNA
All living organisms use the same DNA
code (A,C,T,G) – which means all living
things are related to each other and
have evolved from a common ancestor.
Although they have the same code, the
sequence varies. New genes gained by
mutations; others lost by natural
selection etc.
When speciation occurs, they’d have
very similar DNA however, over a
prolonged period they accumulate more
and more differences. Hence, species
more closely related share a greater
portion of their DNA.
E.g. 98% of human dna shared with a
gorilla




Chromosomes contain non-coding
sequences of bases (junk dna) as
they serve no purpose/function.
More closely relates species have
more junk dna in common – which
would only make sense if they
evolved from a common ancestor.
ENDOGENOUS RETROVIRUSES (ERV)
– a viral sequence that has become
part of an organism’s genome. They
store their genetic info as RNA.
Upon entering a cell, a retrovirus
copies its RNA genome into DNA:


reverse transcriptase. The dna is
then inserted into a chromosome
host cell.
Endogenous = inherited
(ovum/sperm cell)
Offspring will have a copy of this
ERV in all their cells, and then all
subsequent generations in same
location.
Mitochondrial DNA (mtDNA)
Protein Sequences
Comparative Genomics
Proteins consist of long chains of amino
acids in precise sequences. The degree
of difference enables estimated amount
of evolution taken place since two
species developed from a common
ancestor.
Ubiquitous proteins: amino acids that
appear to be in all species, performing
basic but essential tasks for life.
-
In the form of a small, circular molecule.
About 5-10 in each mitochondrion.
Involved with tRNA and cellular
respiration.
mtDNA is a lot easier to find and
extract due to large numbers of
copies in mitochondria – so smaller
samples can be used

INHERITANCE OF MTDNA
 eggs have hundreds of
mitochondria but sperm have
enough for energy to swim –
mtDNA is inherited from the mother
 mutations have a higher rate in
mtDNA than nuclear DNA so it has
been slowly diverging from our
original female ancestor; amount of
mutation roughly proportional to
amount of time passed.
 Similarity between individuals of
mtDNA can estimate closeness of
their relationship.
e.g. used to track migration routes of
ancient people. Most Europeans
descended from hunter-gatherers rather
than farmers from middle east.



Cytochrome C is an example of a
ubiquitous protein.
Carries function in cellular energy
and appeared to have changed very
little. 37 have been found in same
location regardless the species.
Therefore, suggests descent from
ancestral cytochrome C molecule
found in primitive microbe.
Gorillas and chimpanzee’s
comparison differ by one
cytochrome C.
-
Comparing genome sequences of
different species
Allows to identify similarities and
differences
Comparative Anatomy
Comparing structural features of
related animals to a certain degree of
similarity
Embryology: comparing early stages of
organism development.
 More difficult to distinguish
between embryos. In vertebrates
(animals with spinal cord covered
by cartilage or bone) there’s
massive similarity.
 Embryonic gill pouches appear in all
species – hint evolutionary series
began with fish – in humans, they
develop into Eustachian tube.
Bioinformatics
-
-
The use of computers to describe
the molecular components of living
things
Used in evolutionary mechanisms
by measuring changes in their DNA
Allows comparison of entire
genomes
Annotation: identifying these
genomes, which are long and need
to be computerized. They are
possible by the fact genes have stop
and start codons.
Homologous Structures: forelimbs of
vertebrates have same bones that
appear in various forms. They’re
arranged in similar ways with different
functions. These called homologous
organs, because of similar structure.
Likely to have common ancestor
Vestigial Organs: functionless organs for
original role, some may retain lesser
functions or develop new ones.
In humans:
Appendix
Male nipples
Wisdom teeth
Body hair
Nictitating membrane
Evolutionary mechanisms explain
existence of structures that appear to
have no function. Over time, they were
no longer essential to survival and
gradually reduced to vestigial remnants.
Natural selection reduced organs to
non-functional remnants because it
would’ve been a waste of energy and
resources to maintain it. Will disappear
completely as there is no selection
pressure to maintain it.
Fossil Evidence
Any trace or remains of an organism
that lived in the past.
Important in allowing an idea of
what extinct species were like.
The surrounding rock can provide
the age of the fossil
Fossil Formation:
1. In shallow lakes; marshes and
swamps. Organism is quickly
covered by sediment and decay
stopped.
2. Marine Habitats: organisms are
buried and preserved on ocean
floor – occurs quickly
3. Dry Cave Deposits: where soft parts
decay leaving hard parts
undisturbed
4. Trapped in Ice: low temps stop
decay process. Whole bodies with
soft parts can be preserved
5. Amber: insects and spiders can be
trapped in fossilized tree resin
preserved intact
6. Traces of Organisms: include
footprints, tracks, burrows, nests,
hardened dung etc.
SMDTAT
The chance of fossilization is very small
due to decay by microbes. However, if
rapid burial occurs, conditions may not
be favourable for decay.
In wet, acid soils decay occurs rapidly,
but in soils with no oxygen (and usually
low temp) decay is slowed or prevented.
Alkaline soils provide the best fossils,
because minerals in bone survive and
deposits of new minerals, such as lime,
are deposited in the pores of bone
Petrification = bone turned to rock.
Carbon-14 Method
Based on the decay of the radioactive
isotope of carbon-14 nitrogen
 Is produced in the upper
atmosphere by cosmic radiation on
nitrogen, at the same rate it decays
 Ration of 1 atom of carbon -14 for
every trillion atom of carbon-12
 Therefore 1:trillion absorbed by
plants during photosynthesis,
should an animal eat the plant, it
becomes part of their tissues.
 When it dies, the carbon-14 decays
at a fixed rate
 “Half-life” – every 5730 +/- 40
years, the number of carbon-14
atoms will be halved. (changes to
Nitrogen-14)
 When the halved number gets so
low, aging fossils becomes
inaccurate
 Hence the ratio of N-14 to C-14 can
be used to measure the age of an
organisms
 Can be measured with accelerator
mass spectrometry
Artefacts = objects deliberately made by
humans and often found in association
with human fossils.
DATING OF FOSSILS
1. Absolute Dating:
-
Founding out actual age of
specimens in years and arranging
the historical specimen in order of
their ages.
Limitations:
Radiocarbon dating cannot date
back more than 60 000 years
Organism must contain organic
compounds
-
Amount of C-14 in atmosphere
fluctuates
Potassium-Argon Technique
Based on decay of radioactive potassium
to form calcium and argon – used to
calculate age of ROCKS
 The isotope potassium-40 is
radioactive and decays very
slowly at constant rate to form
calcium-40 and argon-40
 Hence ration of K-40 to A-40
Limitations:
Not all rock types suitable for this
method
Can only date rocks older than 100
000 – 200 000 years
Younger rocks would have only a
tiny % of K-40 already decayed and
pushes limits of detection devices.
*to use this method for fossils, some
suitable rock of same age must be
available e.g. when rocks produced in
volcanic eruptions bury bones.
Dendrochronology – not in wace
syllabus
Tree ring dating – each ring represents
one year’s growth, differing in width
according to how favourable the
growing season was. Certain rings
produced in years of exceptional
weather conditions used as MARKER
RINGS.
 Can correlate marker rings from
ancient human structures with
living trees
 Counting tings on living trees
determines age. Wider rings may e
near middle of trunk (good season),
this marker ring could be found
near the outside of a piece of tree
trunk used in ancient structure.
Hence dates can be determined
 Bristle cone pines help date back
dead pines as far back as 8600 years
Limitations:
Conditions necessary for use of
method don’t occur often
Timber is rarely preserved for more
than a few thousand years
Limitations for accurate dating occur
because each depend on the occurrence
of a particular set of circumstances.
2. Relative Dating:
-
When not possible to determine
actual age, these techniques can be
used to determine if it is younger or
older than another sample
Stratigraphy
Study of layers/strata
Two ways:
1. Principle of Superposition
o In layers of sedimentary rock, top
layers are younger, bottom layers
are older. Thus anything found
inside the sediment can order age.
Limitations:
Distortions of the earth’s crust do
occur – rocks turned upside down
Can be buried by animals/early
humans after deposition of
sediment



2. Correlation of Rock Strata
Matching layers of rock from
different areas
Rocks containing same fossils
assumed to be of same age
INDEX FOSSILS – of great value,
because they’re widely distributed
and were present on earth for a
limited time
Fossilized pollen grains: index fossils
useful to construct images of type and
amount of vegetation at the time – also
gives idea of climatic conditions.
Fluorine Dating
 when a bone left in soil, the fluoride
ions in water of soil replace some
ions in the bone itself
 all bones in particular deposit
should contain same amount of
fluorine so any displaced can be
detected
 older fossils = more fluoride so
relative ages can be detected

However, concentration of fluoride
in ground water caries from place to
place and time to time.
Phylogenetic Trees/Dendragram
Reflect the historical, evolutionary
relationships between different
organisms/species/groups of organisms
(taxa’s)
 As more is discovered these
diagrams may change
 The end of the branches is
represented by different
organism or species. The node
where the branches are formed
represent a common ancestor
 Useful for showing the
relationships between closely
related organism and possible
evolutionary pathways
Limitations:
Don’t necessarily accurately
represent the evolutionary history
of specific groups or oganisms.
Problems if is based on one set of
data only
Problems with the Fossil Record
Type of
problems
Explanation
1. few
organisms
become fossils
Poor probability of an
organism becoming a fossil. It
relies on quick burial of the
material, the presence of hard
part, an absence of decay
microbes and a long period of
stability
2. incomplete
fossil record
Fossils need to be found.
Dynamic earth movement and
cycling of rock materials mean
many fossils have been
destroyed or located in
inaccessible sites or areas yet
to be explored. Also it is
unusual to find fossil of a
complete organism.
Human activities e.g.
agriculture and industry may
destroy fossils or potential
fossil sites.
Also animals can disturb earth
through burrowing etc.
Hard to apply principles of
interbreeding to produce
fertile offspring to determine
classification of species on
extinct species. Classification
can depend on number of
fossils recovered to determine
range of variation for each
fossil type.
3.
classification
of species
Primate Evolution
4. different
interpretations
of the same
evidence
Different scientists will use
same evidence to support
different theories.
5. dating
methods
cannot be used
Some dating methods have
limited time periods. Some
methods also rely on material
present in the sample, and if
not it can’t be used.
FICID
Fat iguanas cry in diapers 
Homo Sapiens (humans), Pan
troglodytes (chimpanzees), Pan piniscus
(Bonobos) and Gorilla gorillas (Gorillas)
are all classified at the ORDER level of
grouping PRIMATES
*hint: genus spelt with upper case and
species spelt with lower case!! E.g.
Homo sapiens
Primate features:
 Arboreal – fingerprints for hands
gripping branches
 Body is non-specialized
 Shoulders/hips – at back for
flexibility when swinging
 Hands/feet – can grip well –
pentadactyl and opposable thumbs
 Eyes – stereoscopic vision
 Sense of smell – poor
 Teeth – 4 incisors and lower jaw
 Brain – large + complex – cerebrum
increases
 Reproduction – no restricted
breeding season
 Nails- instead of claws – efficient in
arboreal life
Adaptations for an Erect Posture
Erect = upright
Adaptation = any characteristic that
helps an organisms survive and
reproduce in its natural environment.
Erect posture helped our human
ancestors to survive
magnum are of equal weight.
(minimizes muscular effort)
VERTEBRAL COLUMN
DENTITION
FORAMEN MAGNUM




Located centrally in the base of the
cranium but further back in apes +
earlier ancestors
Gradually moved forward so it
appears on top of vertebral canal
As weight of skull is carried by v.c,
large neck muscles are not required
anymore, whereas apes require
much stronger neck muscles to
keep head forward-facing (sagittal
crest)


Dentition has evolved so canine
teeth don’t project and now look
more like incisors. This resulted in a
more U-shaped jaw
The large canines had a distinct gap
called the DIASTEMA to slide them
in when the jaw shut
Teeth size reduced and diastema
lost


PELVIS


FEMURS
Striding gait =
walking in a
straight line
allowing knee
and hip to be
fully extended
Carrying angle
= ensures
weight
distributes
close to central axis to allow a striding
gait when walking bipedally





Small + reduced prognathism so
that it enables the skull to balance
on the v.c.
Flatter, less protruding face means
skull balances on top of spine
because the sides of the foramen

CHEST AND RIB CAGE
JAW BONE



The lumbar
vertebrae are
wedge-shaped
producing an Sshape curve (double
curvature)

This brings
the spine directly
under the centre of
the skull and
contributes to
upright stance
Apes have C-shaped spine (single
curvature) which forces them on all
fours (quadrupedal)
Head balances on top of the neck
due to s-shape
Cervical curve in neck brings spine
directly under centre of gravity of
the skull

Broad, flatter chest from front to
back, places the centre of gravity
closer to the spine
Apes have rounder, broader-shaped
chest so the centre of gravity is
further away from the spine,
therefore less stable in upright
stance
C.O.G at pelvis level for humans





Short + broad: shallow from top to
bottom
Sacrum is wider, providing a wider
base for support
Bowl-shaped: provides support for
abdominal organs
In females, have wider pelvis for
support developing foeteus
Attachment of femurs wide apart
contribute to the carrying angle
Broad hip bones provide
attachments for large buttock
muscles which move legs and keep
body erect
Broader pelvis provides stability
when walking upright as weight is
transferred directly to the legs
A long and narrow pelvis found in
apes doesn’t provide the broad
base of stability needed for bipedal
walking


Acetabulum: socket of pelvis in
which femur fits- contributes to
carrying angle
Femur converges towards knees
forming an angle to the vertical and
ensures weight distribution remains
close to central axis of body when
walking.
Results in greater stability so
humans have striding gait instead of
swaying side to side like apes,
Apes have vertical angle from hips
to knee and doesn’t converge
inwards, resulting in less stability
when walking bipedally
KNEE JOINT
 Outer hinge joints are larger and
stronger to take the weight of the
body, as there is greater support
 Allows knee to be straightened
 Prevents leg from bending
backwards because ligaments in
joints resist this
 The degree of movement in humans
is less than apes because it is
designed to provide strength and
requires no energy to support body

LEGS
 Legs longer than arms, especially
femur, contributing to a lower
centre of gravity and stability
 Carrying angle allows weight of
body to be kept close to central axis
 Ankle: body weight transferred
through talus to the other tarsal
bones, then to metatarsals and
phalanges via the arches in the foot
Muscle tone:
o Essential for maintaining upright
stance e.g. back neck muscles to
keep head erect
o Arms also assist in natural rotation
of pelvis when walking. Swinging of
arms keeps shoulders at right
angles to direction of travel and
reduces energy use
o If arms didn’t swing, energy would
be wasted in reversing rotation of
body after each stride
FOOT

Large heel bone and aligned big toe
form a pedestal in which the body is
supported



Foot has longitudinal arch and
transverse arch, only transverse
arch unique to humans
Both arches allow humans to carry
out perfect bipedal motion using
the striding gait.
Arches allow energy and weight to
run down longitudinal, through
transverse and pushed off with the
big toe
The big toe has lost its opposability
in order to serve as a weight-bearer.
Relative size of the cerebral cortex:
Humans have large brains
(1350cm3) in contrast with apes
(450cm3)
Outer portion of cerebrum is the
cerebral cortex (greatest
development)
Frontal lobe increased due to more
complex thinking – e.g. strategic
hunting
Cranium changed shape to house
the brain so the brow is more
vertical and lacks prominent brow
ridge like in apes
Shortening of the snout and brow
ridge gives human a flat face
-
Note: bipedalism evolved before
any increase in brain size –
australopithecines had small brain
like apes
Endocasts:
Impressions of inside of skulls made
from rock/solid material.
Determining shape of brain surface,
can occur naturally or synthetically
Endocasts can reveal increase in
convolutions
*note that Neanderthals actually had
bigger brains – thought to be due to
control increased amount of muscle
Hominin
Australopithecus
afarensis
Australopithecus
africanus
Paranthropus
robustus
Homo habilis
Homo erectus
Homo
neanderthalensis
Homo sapiens
Cranial capacity
(cm3)
430
457
542
590
1004
1485
1350