TRANSPORT IN ANIMALS

Why do simple organisms lack a specialized transport system?

Simple animals such as cnidarians and Platyhelminth lack specialized transport systems because the
organisms in this groups possess a large surface area to volume ratio; and so, diffusion of gases over its
whole-body surface is sufficient for all their needs. Internally, the distance materials have to travel is
small enough for them to move by diffusion; or cytoplasmic streaming or osmosis or active transport.
Why do large organisms need a specialized transport system?
As organisms increase in size and complexity, the surface area to volume ratio decreases, the quantity of
materials moving in and out of the body increases, and the distance materials have to travel within the
body increases; diffusion therefore becomes inadequate to distribute materials all over the body; but
rather mass flow;
The organs of which the organisms are made also become more specialized; and dependent on each other
making a transport system necessary;
Check point:
1. What is mass flow?
Is bulk movement of substances from one region to another due to difference in pressure. All materials
are swept along together at similar speeds unlike in diffusion; whereas mass flow occurs in specialized
transport systems, the systems are linked to specialized exchange systems; which maintain steep
concentration gradient.
There are two circulatory systems which rely on mass flow in animals, namely the vascular system and
lymphatic system;
Check point
2. What is a vascular system?
A vascular system is one which contains fluid filled vessels/tubes involved in transport; these systems
require a source of energy to function.
Transport systems in animals range from ciliated water filled canals in jelly fishes to blood vascular
system and lymphatic system in mammals.
Features of a transport system
Every transport system must have a
1. Suitable transport medium in which materials are carried. E.g. blood. This is normally a
liquid based on water since water readily dissolves substances and is easily moved from one
place to another.
2. Tubes through which the medium/ fluid circulates/ flows. E.g. veins, arteries, and
capillaries. Usually form a branching network with specific routes to distribute dissolve
materials to all parts of the body.
3. A form of mass flow transport in which the transport medium is moved around in bulk
over long distances.
 4. A mechanism for moving the medium within the vessels. This requires pressure difference
between on part of the system and another. This is achieved in two main ways;
 Animals use muscular contraction of either the body muscles or of specialized
pumping organs e.g. the heart to create pressure difference
 Plants rely on passive natural physical processes such as evaporation/ difference in
solute concentrations between two points.
5. A mechanism to maintain the mass flow movement in one direction. e.g. valves
6. A means of controlling the flow of the medium to suit the changing needs of the different
parts of the organism.
The blood vascular system provides the most important means of mass flow in mammals
Types of blood vascular systems
1. Open circulatory/ blood vascular system
2. Closed circulatory/ blood vascular system
Open blood vascular system
Description
Blood is pumped by the heart into an aorta which branches into a number of arteries; which open enter
into a series of blood-filled spaces collectively called haemocoel; the blood under low pressure moves
slowly between tissues and gradually percolates back into the heart through open ended veins;
distribution of blood to tissues is poorly controlled;
Examples of organisms with open blood vascular system
 Arthropods
 Cephalopod molluscs.
Advantages of open circulatory system
 Blood flows slowly under low pressure between tissues providing enough time for exchange of
materials with tissues
 Tissues are bathed in blood/ blood comes to direct contact with tissues shortening diffusion
distance for faster diffusion.
Disadvantages of open circulatory system
 Distribution of blood to different organs is poorly controlled hence less able to change to suit
the changing demands of different organs.
 Blood flows is slow and under low pressure therefore cannot carry materials to and from long
distances hence limiting organism’s size;
 Low pressure of blood reduces rate of diffusion;
 Blood flow is slow hence more time taken for materials to reach tissues for metabolism that
makes organisms sluggish.
Open circulatory system of insects
Insect have an open circulatory system in which the haemocoel is divided by a transverse pericardial
membrane into a pericardial cavity dorsally; and perivisceral cavity ventrally;
The tubular heart is suspended within the pericardial cavity by slender ligaments;
Heart is expanded in each segment of the body to form a small chamber;
Each chamber of the heart is pierced by a pair of tiny holes called ostia;
In the pericardial membrane is a series of alary muscles corresponding in position to the heart chambers;
Mechanism of blood circulation in insects

Systole
During systole, the heart ligaments are stretched with the result that they during diastole, they pull the
walls of the heart outwards;
The expansion of the heart is aided by contraction of alary muscles which increase tension on the
ligaments. The result is that blood is sucked into the heart via ostia;
The contraction of alary muscles also pulls the pericardial membrane downwards; decreasing pressure in
the pericardial cavity while at the same time increasing pressure within the perivisceral cavity; this forces
blood to flow form perivisceral cavity to pericardial cavity;
The ostia are equipped with valves that allow blood to enter the heart but not leave it.
Blood is propelled forward through the heart by waves of contraction which commence at the posterior/
rear end and work their way towards the anterior end. The blood then leaves the heart via aorta and enters
the haemocoel through which it flows.
Note that the circulatory system of insects is not directly involved in transport of respiratory gases.
Closed blood vascular system
Features of closed circulatory system
 Blood stays in blood vessels. It does not come into direct contact with tissues
 Blood is pumped by the heart rapidly under high pressure around the body and back to
the heart.
 Distribution of blood to body tissues can be adjusted, depending on demand. the only
entry and exit to the system are through walls of blood vessels.
Example of organisms with closed vascular system
 Cephalopod molluscs
 Echinoderms
  Annelids
 Vertebrates
For closed circulatory system within vertebrates, there are two ways of circulating the blood.
1. Single circulation;
Blood flows only once through the heart for every complete circuit of the body.
For example
In fish, deoxygenated is pumped from the heart to the gills, and then flows directly to the rest of the body
and then returns to the heart.

The pressure drops dramatically as blood leaves the gills, thus the blood flow to vital organs and venous
flow of blood back to the heart is both slower and at lower pressure.
The pressure problem in fishes has been overcome in different ways in different organisms e.g.
a) In fish, this has been overcome to some extend by replacing the veins large sinuses that offer
minimum resistance to blood flow.
b) Octopuses and squids have two hearts. i.e. the main heart which pumps blood to various parts
of the body; the blood from different parts of the body flows via a system of sinuses to a pair
of branchial hearts; the branchial hearts pump blood through the capillaries of the gills; for
oxygenation. The blood from gills then return to the main heart for distribution to the body.
This makes octopuses and squids as active as vertebrates

c) Mammals and frogs have a double circulatory system in which blood returns to the heart after
passing through the lungs to regain pressure from action of the heart muscles.
d) Organs are arranged in parallel rather than in series. If organs were arranged in series, blood
would pass from one organ to the other losing pressure, oxygen and nutrients and any damage
to one vessel connecting two organs would interrupt the whole circulation.
Check point
1. Explain why single circulation would not be a suitable transport system in mammals.
2. What are the advantages and disadvantages of single circulatory system?
2. Double circulation
Blood flows through the heart twice in each complete circuit of the body. Deoxygenated blood is pumped
to the lungs to pick oxygen and then returned to the heart to be pumped again before travelling around the
body. Blood loses pressure as it goes through capillaries of the lungs due to resistance of capillaries; and
so, the pressure is restored and boosted ensuring rapid circulation before the blood is circulated to the rest
of the body. This is made possible by the heart being divided into two halves; the left side pumping
deoxygenated blood to the lungs for oxygenation (pulmonary circulation), right side pumping oxygenated
blood to the rest of the body (systemic circulation). Division of the heart into two sides prevents
oxygenated and deoxygenated blood from mixing.
Double circulations sustain the high pressure of blood and ensures rapid circulation; for faster supply of
oxygen and nutrients and removal of wastes. This enables the organisms to sustain high metabolic rates.
Each organ has a major artery supplying it with blood and most have major veins taking blood back to the
heart except those with portal systems e.g. small intestine and stomach are linked to the liver by hepatic
portal vein.
The pressure of blood gradients of blood is maintained in the following ways
 By the pumping action of the heart
 By contraction of skeletal muscles squeezing blood along veins
 Inspiration movements of the thorax reducing pressure of the thoracic cavity which helps to draw
blood back to the heart which is within the thorax.
Check point
1. What are the advantages and disadvantages of closed double circulatory system?
2. Explain branchial hearts improve efficiency of single circulatory system?
Circulatory system of Annelids
Annelids are coelomate animals. Since internal structures are separated from body wall, internal
structures can move freely and independently. However, this means there is need for a specialized
transport system which connects the gut to the body wall.
Earthworms for example have a well-developed transport system which circulates blood around the body
through a system of blood vessels.
Two main blood vessels run the length of the body; one ventral and one dorsal. They are connected by
blood vessels in each segment. Near the front of the animal, five of these connecting blood vessels are
contractile and act as pumps. The main blood vessels can also pump blood. The blood contains
haemoglobin dissolved in blood rather than carried in red blood cells. The haemoglobin transports oxygen
round the body.
Blood vessels
General structure of blood vessels
Each artery and vein consist of three layers:
 Tunica intima/ The endothelium; an inner lining of squamous epithelium; has a single layer of
endothelial attached to a basement membrane.
 The tunica media (middle layer) which contains smooth involuntary muscles and elastic fibres;
the proportion of smooth muscles and elastic fibres varies depending on the type of blood vessel.
Elastic fibres vary most.
 The tunica externa (‘external coat’)/ tunica adventitia; an external layer consisting mainly of
inelastic white fibres (collagen fibres)
Comparison of blood vessels

Artery Vein Capillary

Transports blood away from the Transports blood towards the Blood changes from oxygenated
heart heart to deoxygenated
Thick tunica media Tunica media thin, with few No tunica media
elastic fibres and slightly
muscular
Thick muscular wall Thin muscular wall No muscle
Much elastic tissue Little elastic tissue No elastic tissue
No semilunar valves except in Valves throughout all veins No valves
aorta and pulmonary artery
Blood flows rapid Blood flows slowly Blood flow slowing
Low blood volume Much higher blood volume High blood volume
Blood oxygenated except in the Blood deoxygenated except Mixed oxygenated and
pulmonary artery pulmonary vein deoxygenated blood
Small lumen relative to diameter Large lumen relative to diameter Large lumen relative to diameter
Capable of constriction Not capable of constriction Not capable of constriction
Blood under high pressure Blood under low pressure Blood pressure reducing
Blood moves in pulses No pulses No pulses

Structure of artery Vein capillaries

Adaptations of arteries
Function of arteries is to transport blood rapidly, under high pressure form the heart to the tissues.
There structure is related to this function in the following ways;
  Tunica media is relatively thick to with stand the high pressure of blood flowing within it.
 Arteries close to the heart such as the aorta have high proportion of elastic fibres to allow
them expand rather than burst under pressure high pressure of blood from the ventricles
and to maintain pressure of blood high as a result of elastic recoil.
 In smaller arteries contraction of the smooth muscles causes the vessels to constrict,
narrowing the diameter of the lumen to allow regulation of blood flow to tissues.
 Tunica externa consists of collagen fibres which provide a tough outer covering for
protection and support
 Tunica externa also contains some elastic fibres to allow for stretching as blood flows
through.
 Overall thickness of the wall is large to prevent bursting under high pressure.
 Small lumen increases pressure of blood in them
 No valves except in arteries leaving the heart because blood is always constant high
pressure due to pumping action of the heart therefore blood tends not to flow backwards.
Adaptations of veins
Veins function in transporting blood, under low pressure, from the tissues to the heart. There structure is
related to this function in the following ways;
 The tunica media is thin as the low pressure of blood will not burst the blood vessel.
 There are very few elastic fibres because they do not need to stretch and recoil.
 There is less smooth muscle because veins carry blood away from tissues and therefore their
constriction and dilation cannot control the flow of blood to the tissues.
 Collagen fibres in tunica externa provide tough outer covering to prevent bursting of veins due to
external physical forces (near the skin surface).
 Large veins also have a small amount of smooth muscles that contract to regulate flow of blood.
 Overall thickness of wall is small because the blood pressure within veins too low to cause risk of
bursting.
 Overall thickness of wall is thin also to allow them to easily be flattened under pressure from
skeletal muscles to maintain flow of blood within them.
 The lumen is large to reduce resistance to blood flow/ allow blood flow at low pressure
 Has semi lunar valves to ensure blood does not flow backwards/ ensures that pressure of
contracting muscles directs blood in only one direction.
Adaptations of capillaries
The functions of capillaries is to exchange materials such as glucose, oxygen and carbon dioxide between
blood and the cells of the body. There structure is related to this function in the following ways;
 The walls are extremely thin/ made up of a single layer of cells this shortens diffusion distance
allowing for faster diffusion of materials between cells and blood.
 They are numerous and highly branched providing a large surface area for diffusion of materials
 Thay are thin/ have a narrow diameter hence can reach all body tissues reducing diffusion
distance further
 The lumen is very narrow making the red blood cells squeezed flat against the wall of capillaries
bringing them in to close contact with tissues to which they supply oxygen reducing further
diffusion distance.
  Spaces between endothelial cells/ endothelial spaces (except in the brain capillaries) allow white
blood cells to escape in order to combat infections within tissues and allows exchange between
tissue fluid and blood.
 Basement membrane has very fine pores forming a barrier for filtration of large blood
components.
Blood from the heart enters arteries, blood from arteries enters arterioles which pass blood into
capillaries. Blood from capillary beds enters the venules which pass blood to the veins that return blood to
the heart.
Check point
How does the structure of arterioles and venules relate to their functions?

Circulatory system of vertebrates

Blood vascular system of all vertebrates possess a muscular heart responsible for pumping blood rapidly
to all parts of the body. Oxygen is carried by haemoglobin in red blood cells
Circulatory system of fish.
Fish have a single circulatory system where blood flows only once through the heart for each complete
circuit of the body. Blood is pumped from the heart to the gills, and then flows directly to the rest of the
body. The resistance created by the fine network of capillaries in the gills causes blood pressure and
blood speed to drop significantly as it leaves the gills. After wards, this blood then meets more resistances
as it passes through capillaries of the body tissues and its pressure and speed is further reduced;
Circulatory system of mammals
Mammals are relatively large and highly organized, with different body regions adapted to perform
different functions. These specialized body regions depend on each other. This interdependence demands
an efficient transport system. Substances can diffuse across exchange surfaces and in and out of cells,
however mammals are too large to rely on diffusion alone to move materials throughout their body. Over
long distances, substances are transported more efficiently by mass flow based on pressure gradient.
Mammals therefore have a closed double circulatory system, with the heart completely divided into two
halves with 4 chambers.
General structure of the mammalian circulatory system.
A muscular heart pumps blood into a system of arteries; which split within tissues into capillaries; here,
exchange of materials between blood and cells takes place; from the capillaries, blood is collected up into
a series of veins; by which it returns to the heart. The heart is divided into 4 chambers;
Deoxygenated blood returning to the heart from the rest of the body enters the right atrium; then to the
right ventricle after which it passes via pulmonary artery to the lungs. As the blood passes through
capillaries of the lungs, it sheds its carbon dioxide into lungs and takes up oxygen from the lungs.
The oxygenated blood then returns to the left atrium via pulmonary vein. From here it passes to left
ventricle then to the dorsal aorta the main artery. From this, numerous veins convey blood to the capillary
systems in organs and tissues where exchange takes place. Some organs are directly connected by portal
systems, e.g. hepatic portal vein.
Refer to B.S 464, F.A. 168, A.B. 119.
Structure of the mammalian heart
The heart is situated between the two lungs, behind the sternum in the thorax. It is surrounded by a tough
sac called pericardium, the outer part of which is made up of inelastic white fibrous tissue.
The inner part is made up of two membranes; the inner membrane is attached to the heart while the outer
membrane is attached to the inelastic fibrous outer tissue.
A fluid called the pericardial fluid is secreted between the two membranes and reduces friction between
the heart and surrounding tissue while the heart is beating. The pericardium prevents the heart from over
expansion caused by elastic recoil when the heart is beating very fast/ over filling with blood.
There are 4 chambers in the heart, two upper thin-walled atria/ auricles, and two lower thick-walled
ventricles. The right side of the heart is completely separated from the left side by a septum which
becomes rigid just before the heart contracts to act as a fulcrum for action of heart muscles.
The right side of the heart receives deoxygenated blood from the general circulation and pumps it to the
lungs for oxygenation while the left side receives oxygenated blood from the lungs and pumps it to the
general circulation. The muscular wall of the left ventricle is thicker than the right ventricle. The
difference is due to the fact that the right ventricle has to pump blood to the lungs which are very near the
heart whereas the left ventricle pumps blood all-round the body.
Therefore, the blood entering the aorta from the left ventricle is at much higher pressure than blood
entering the pulmonary artery from the right ventricle. As atria contract, the ring of muscles surrounding
the venae cavae and pulmonary veins at their points of entry into the atria contract and close the veins to
prevent back flow of blood into the veins.
The left atrium is separated from the left ventricle by bicuspid valve and the right atrium is separated
from right ventricle by tricuspid valve. The two valves are jointly called atrioventricular valves. Attached
to the ventricle side of the flaps are fibrous cords which in turn attach to papillary muscles which are
extensions of the inner wall of the ventricles.
The valves open when the atria contract but close tightly when the ventricles contract. At the same time
the papillary muscles contract tightening the fibrous cords. This prevents the valves from being turned
inside out. Semi lunar valves are found at the point where the pulmonary artery and aorta leave the heart
to prevent blood flowing back to the ventricles. Just beyond the aortic valves are openings of coronary
artery which supply the heart wall with oxygenated blood.
The walls of the heart are made up of mainly specialized type of muscles called cardiac muscle. This
muscle never fatigues; however, it does immediately deprive it is deprived of oxygen and nutrients.
Check point
What is the advantage of supplying pulmonary circulation with blood at lower pressure than systemic
circulation?
Structure of a cardiac muscle
It consists of a network of branched interconnected muscle fibres
Each cell has one nucleus and many large mitochondria;
The cells are joined to each other by tight folded junctions called intercalated discs.
Each muscle fiber is made up of many contractile myofibrils.
Myofibrils contain actin and myosin filaments which bring about contraction.
They account for the striped nature of the muscle fibres
Adaptations of cardiac muscles
 Cardiac muscle fibres are branched and interconnected for faster spread of excitations/ action
potentials throughout the muscle
 Intercalated discs form tight junctions to reduce diffusion distance for faster spread of excitation
 Intercalated discs are folded to increase surface area for diffusion for faster spread of excitation
 Possess many large mitochondria to generate much ATP that provides energy for contraction on
hydrolysis
 Muscle fibres have many myofibrils that contain actin and myosin filaments to generate stronger
contractions
 Myogenic nature of cardiac muscles prevents reliance on external factors to generate contraction.
 Long absolute refractory periods/ slow contraction allow time for full recovery to avoid fatigue of
muscle.
Check point.
The figures show the record of contraction and the changes in the excitability of cardiac muscles.

a) Using the information on the graph, explain the meaning of the terms
i) Absolute refractory period. (03 marks)
A period of complete in excitability/ lowest excitability of a muscle/ unable to respond to another
stimulus; no matter the strength of the stimulus; when the muscle has begun to contract/ has already
been stimulated
ii) Relative refractory period. (03 marks)
Period of increasing excitability; when muscle only responds to strong stimulus; as the muscle
recovers after contraction;
b) Explain the importance of the nature of the refractory period of cardiac muscles to their
action.
Cardiac muscles have longer absolute refractory periods; to provide time for full recovery of the
muscle; during vigorous and rapid contraction; in order to prevent fatigue; tetanus/ sustained
prolonged contraction; and oxygen debt;

The Cardiac cycle/ heartbeat.

What is meant by the term cardiac cycle?
Is the sequence of events that take place during the completion of one heartbeat. It involves
contraction/ systole and relaxation/ diastole of cardiac muscles;
The events include the following.
Atrial systole.
Cardiac muscles of the walls of both atria contract simultaneously,
Pushing the blood remaining in the atria to the ventricles.
Via the atrioventricular valves which are forced open.
During this phase, the cardiac muscles of the ventricle walls remain relaxed (ventricular diastole).
Ventricular systole
After a short delay, the ventricles contract simultaneously. This increases the pressure within them,
forcing the atrioventricular valves to close preventing back flow of blood to the atria and producing the
first heart sound called ‘lub’.
With the atrioventricular valves closed, pressure within the ventricles rises. Once its higher than pressure
in the aorta and pulmonary artery, the semi-lunar valves are forced open. Blood is forced from ventricles
through the semi-lunar valves to the aorta and pulmonary artery.
Diastole.
The whole heart relaxes after ventricular systole, allowing blood from pulmonary vein and vena cava to
begin to fill the atria. As the ventricles relax, the pressure within them becomes lower than the pressure in
the atria and the atrioventricular valves open, allowing blood to pass into the ventricles. The cardiac
muscles of both the atria and ventricles are relaxed at this stage. The relaxation of the ventricle’s cardiac
muscles causes them to recoil, and reduces the pressure within the ventricles below that in the aorta and
pulmonary artery, so the semi-lunar valves in the aorta and pulmonary artery close producing the second
heart sound called ‘dub’
Control of heart beat (cardiac cycle)
The heart is myogenic, as the heartbeat is initiated from within the heart muscle itself.
Atrial systole.
The initial stimulus for heartbeat originates in a group of specialized cardiac muscle cells called the sino-
atrial node (SA node). The SA node generates waves of electrical impulses called cardiac impulses.
Waves of excitation spread out from the SA node slowly across both atria causing them to contract
gradually towards the ventricles simultaneously.
Contraction of atrial walls forces blood from atria into the ventricles via the atrioventricular valves which
are forced to open. During this phase, the ventricles remain relaxed (ventricular diastole).
When the impulses reach the junction between the atria and ventricles, they are delayed by the
atrioventricular septum, a layer of non-conducting tissue that completely separates the atria from
ventricles except for a region in the right atrium called the atrioventricular node (AV node). The delay
gives time for waves of contraction to pass over the whole of both atria.
Ventricular systole
The waves of cardiac impulses pass to the AV node after the short delay. The AV node passes a wave of
excitation between the ventricles along a series of specialized muscle fibres called the purkyne tissue. The
purkyne tissue conducts the excitation very rapidly to the base of the ventricles to allow near
instantaneous stimulation of cardiac muscles.
The wave of excitation is released from the purkyne tissue and passes more slowly across the cardiac
muscle causing the ventricles to contract from the apex (base) of the heart towards the aorta and
pulmonary artery.
Check point
How is simultaneous contraction of ventricles ensured?
The region of ventricle close to AV node have thin purkyne fibres which spread impulses more slowly
than thick purkyne fibres which supply distant parts of the ventricle.
Diastole
The whole heart relaxes after ventricular systole to allow the heart to refill with blood from the veins. No
waves of excitation sent from the SA node and AV node.
Innervation of the heart
The SA node receives two nerves: a sympathetic nerve which is part of the sympathetic nervous system
and a branch of the vagus nerve which is part of the parasympathetic system. These do not initiate the
heat beat but can modify it by slowing or speeding up the rate at which the heart beats. The two nerves are
antagonistic: if the sympathetic nerve is stimulated, the heart beat speeds up, if the vagus nerve is
stimulated, the heart beat slows down. This means that the speed at which respiratory gases are
transported around the body can easily be adjusted to suit the animals occasional demands.
Pressure, volume and electrical changes during the cardiac cycle on the left side of the heart.
Observations and possible explanations
Ventricular pressure low at first; then increases gradually as the ventricle fills with blood from atrium as
the atrium contracts. The bicuspid valve closes and the pressure rises rapidly in the ventricle as the thick
muscular walls of the ventricle contracts. The pressure in the ventricle rises above that in the aorta forcing
the semi-lunar valve. The pressure forces blood into the aorta via semi-lunar valve. Pressure of the
ventricles falls as it empties and the walls empty;
Ventricular volume
Ventricular volume rises as the atria contract and the ventricles fill with blood. The volume then falls
suddenly as the blood is forced into the aorta when semi-lunar valves are open. Volume increases again as
the ventricles fill with blood.
Atrial pressure
Atrial pressure is always relatively low because the thin walls of the atrium cannot create much force.
It is highest when they are contracted but drops when the atrioventricular valves close and its walls relax.
The atria then fill with blood which results into a gradual rise in pressure until a slight drop in pressure
when atrioventricular valve opens and some blood moves into the ventricle.
The maximum pressure of the left ventricle is higher than that of left atrium; since the muscular wall of
left ventricle is thicker to pump blood to all parts of the body except the lungs while muscular wall of left
atrium is thinner since it pumps blood only into the left ventricle.
Aortic pressure
Aortic pressure rises when ventricle contracts and forces blood into the aorta via the open semi-lunar
valve; it then drops as blood leaves the aorta to body tissues; the pressure in the aorta does not drop below
12kpa of the elasticity of its walls; which creates a recoil action; which produces a temporary rise in
pressure; at the start of the relaxation phase
Electrocardiogram
The P wave is caused by atrial systole; when waves of electrical impulses/ excitation spread slowly from
the SA node across the wall of the entire wall of atria; causing them to gradually contract simultaneously
towards the ventricle.
The QRS wave is caused by ventricular systole; when the AV node passes wave of electrical impulses
form atria via purkyne tissues to the apex of the ventricle; causing it to contract towards the aorta and
pulmonary artery; pushing blood into these vessels.
The T wave coincides with the start of ventricular diastole; when waves of excitation die off; the SA node
and AV node are not sending excitation to heart muscles.
NB: the heart rate can be calculated from the interval between one P wave and the next.
Check point
1. The table below shows the pressure in two heart chambers at different times during part of the
cardiac cycle. Use the data to answer the questions.

Blood pressure / kPa

Time/ s Left atrium Left ventricle
0.0 0.6 0.5
0.1 1.3 0.8
0.2 0.4 6.9
0.3 0.5 16.5
0.4 0.9 7.0
a) i) Calculate the percentage increase in left ventricular pressure between 0.0s and 0.3s. (03 marks)
ii) Explain the figure you have obtained in a(i) above. (07 marks)
b) Explain the significance of the difference in pressure between the left ventricle and left atrium at
different times during the cycle. (09 marks)
c) Between what times do the
i) Ventricles start to relax. (01 mark)
i) AV valves shut. (01 mark)
d) Explain how the following would differ
i) Pressure in left ventricle and right ventricle. (05 marks)
ii) Pressure in the aorta and pulmonary artery. (05 marks)
iii) Contraction of atria and ventricles. (03 marks)
2.
a) How is heartbeat initiated and controlled? (13 marks)
b) What role is played by blood vessels in circulation of blood. (07 marks)
3. The figure below shows the volume changes in the left ventricle of the heart.

a) Calculate the heart rate in beats per minute. (03 marks)

b) Explain the events represented by letters A, B, C, D. (12 marks)
c) Explain the significance of the volume changes represented by B to C. (05 marks)
d) Sketch on the same graph the curve for pressure changes within the same time range for the;
i) Left ventricle. (03 marks)
ii) Right ventricle. (03 marks)
iii) Aorta. (03 marks)
e) Explain the difference in pressure of blood pumped by the atria and ventricles. (04 marks)
4.
a) i) Explain the features of a closed double circulatory system in mammals. (06 marks)
ii) Discuss the advantages of a double circulatory system to mammals. (04 marks)
b) The figure below shows changes in pressure when a catheter, containing an instrument used
for measuring blood pressure was moved through the aorta into the left ventricle.
 i) Calculate the heart rate during the investigation. Show your working. (03 marks)
ii) Explain the difference in pressure as the catheter moves from the aorta into the left ventricle.
(06 marks)
iii) Of what importance are the pressure changes shown in the aorta. (03 marks)
Factors which modify heartbeat.
Changes to the cardiac output can be affected through the autonomic nervous system.
NB: Cardiac output is the amount of blood flowing from the heart over a given period of time. It
depends on the volume of blood pumped from the heart per beat (stroke volume) and the number of
beats per minute (heart rate)
Cardiac output is the volume of blood pumped at each beat multiplied by the number of beats in a
given time.
Cardiac output = stroke volume X heart rate
One way of controlling cardiac output is controlling heat rate.
The following factors affect heart rate/ modify heartbeat.
 Carbon dioxide concentration/ oxygen concentrations.
 pH
 blood pressure
 hormones e.g. adrenaline and neurotransmitters e.g. noradrenaline (sympathetic) and
acetylcholine (parasympathetic)
 concentration of potassium ions. High concentration of potassium ions in blood interferes with
impulses that control the pacemaker, causing the heart to slow down.
 High concentration of sodium levels in blood also slows down the heart because excess sodium
ions interfere with the action of calcium ions in muscle contraction.
 Emotional excitement also increases heart rate
 Rise in temperature causes heart rate to speed up
 Feelings of grief and depression may slow the heart rate down.
Nervous control of heart rate/ cardiac output.
Heart rate is controlled by cardiovascular centre in the medulla Oblongata of the hind brain.
The autonomic nervous system connects the cardiovascular centre of the brain to the heart.
The cardiac acceleratory centre is linked to the SA node and walls of ventricles by the sympathetic
nervous system/ fibres. Stimulation from these nerves increases cardiac output.
The cardiac inhibitory centre is linked to the SA node, AV node and bundle of His by the parasympathetic
fibres within the vagus nerve. Stimulation from these nerves reduces cardiac output.
Small receptors sensitive to stretching/baroreceptors are found in the walls of aortic arch, carotid sinuses,
the venae cavae and the right atrium. If blood pressure increases in any of these vessels, the baroreceptors
are activated and they send impulses to the cardiac centres.
Cardiac output varies with the volume of blood returning to the heart (venous return).
Under intense activity body muscles contract strongly and this increases the rate at which venous blood
returns to the heart. As a result, walls of the venae cavae are stretched by the large quantities of blood.
Under this condition, the cardiac acceleratory centre is stimulated and signals the SA node via
sympathetic fibres to increase heart rate (cardiac output).
When venous return is high, the walls of the right atrium are stretched and the heart beats faster.
At the same time increased blood flow to the heart places the cardiac muscles of the heart under
increased pressure. The Cardiac muscles respond automatically (no nerves are involved) to the pressure
by contracting more strongly during systole and pumping out an increased volume of blood (stroke
volume increases).
NB: a high venous return stretches the walls of the left ventricle causing the ventricles to contract
more strongly giving a greater stroke volume.
In turn, the Increased stroke volume/blood flow stretches the aorta and carotids, which in turn signals the
cardio inhibitory centre. The cardio inhibitory centre signals the SA node, AV node via vagus/
parasympathetic nerves to slow the heart rate (cardiac output).
Control of heart rate by blood pH/ blood carbon dioxide levels.
Under strenuous exercise, carbon dioxide concentration increases as a result of increased respiratory rate.
The pH of blood is lowered. Receptors in the carotid body are stimulated to send impulses to cardiac
acceleratory centre which increases heart rate, increasing the rate at which carbon dioxide is delivered to
the lungs for removal.
A fall in pH causes the carotid receptors to stimulate the cardiac inhibitory centre, thus reducing
heartbeat.
Hormonal control of heart rate
A number of hormones affect heart rate either directly or indirectly.
The following hormones affect the heart rate directly;
1. Adrenaline.
Secreted by the adrenal medulla (middle of adrenal gland), which also secretes smaller amount of
noradrenaline which has similar effects to adrenaline.
Both;
  Stimulate the heart though adrenaline is more effective.
 Increase heart rate
 Increases stroke volume
 Increase cardiac output
 Increase blood pressure
2. Thyroxine
Produced by the thyroid gland.
 Increases basal metabolic rate, which causes greater metabolic activity, with greater oxygen
demand and more heat production. As a result, vasodilation occurs followed by increased blood
flow, which causes increased cardiac output.
 Directly increases heart rate.
Blood pressure.
Is force exerted by blood on the walls of blood vessels. Blood pressure depends on several factors such
as;
 Heart rate
 Stroke volume- how much blood the ventricles pump in a given time.
 Resistance to blood flow by blood vessels (vasoconstriction and vasodilation)
 Strength of heart beat
 Total volume of blood in circulation.
NB: The above factors vary depending o the age, sex, state of health and physical activity of an
individual.
Blood pressure can be increased by;
 Increased cardiac output- increasing heart rate and stroke volume.
 Vasoconstriction- increased resistance to blood flow
 Increased blood volume- retention of more water in blood under influence of ADH
 Increased strength of contraction.
Blood pressure can be reduced by;
 Decreased cardiac output- decreasing stroke volume and heart rate
 Vasodilation- reduced resistance to flow of blood.
 Decreased blood volume- loss of much water from the blood in urine/ by bleeding.
 decreased strength of contraction.
Control of blood pressure
Blood pressure can be altered by changes in cardiac output already described. If blood pressure falls
below norm, cardiac acceleratory centre stimulates increased cardiac output in order to increase blood
pressure back to norm while when blood pressure rises above norm, cardiac inhibitory centre stimulates
decreased cardiac output.
Blood pressure is also controlled by the activity of the vasomotor centre in the medulla oblongata of the
hindbrain.
When blood pressure rises above norm, baroreceptors in the carotid artery detect rise in pressure and send
signals to vasomotor centre. The vasomotor centre sends impulses via parasympathetic nerves to
arterioles allover the body, causing them to dilate (vasodilation occurs) and so reducing blood pressure.
When blood pressure falls below norm, baroreceptors are less stimulated. The vasomotor centre sends
impulses along sympathetic nerves to the arterioles. The muscles in the arteriole walls contract, causing
vasoconstriction, which increases blood pressure.
A rise in carbon dioxide level also causes rise in blood pressure. This increases the speed with which
blood is delivered to the lungs for quick removal of carbon dioxide. Arise in carbon dioxide also causes
local vasodilation within the respiring tissues, while there is general vasoconstriction. This increases
supply of metabolites and removal of carbon dioxide from the affected respiring tissue.
Hormones like adrenaline also increase blood pressure by causing vasoconstriction and increased cardiac
output.

Chemical control of vasomotor centre.

When blood arriving at carotid body has a higher concentration of carbon dioxide than norm,
chemoreceptors in the carotid body are stimulated, to transmit impulses to the vasomotor centre.
NB: nerves leaving the chemoreceptors link with those from carotid sinuses by a synapse before
entering the vasomotor centre.
The vasomotor centre in turn sends impulses to the blood vessels to constrict/ causing contraction of
constrictor muscles rising blood pressure. This causes blood containing much carbon dioxide to be
delivered rapidly to lungs for quick removal and rapid oxygen uptake in exchange.
When carbon dioxide concentration lowers below norm, the chemoreceptors are less stimulated,
vasomotor centre sends impulses to the blood vessels causing general vasodilate, lowering blood pressure.
Reducing removal of carbon dioxide from blood.

Blood pressure within arteries, arterioles, capillaries and venules and veins.
When blood from left ventricle to the aorta, the high pressure of blood causes extension of the elastic
walls of the aorta; the pressure falls a little as a result of this extension. The elastic walls of the aorta
rebound in reaction as a result of elastic fibres in it. This is called recoil action. As the semi-lunar valves
are closed, this recoil action creates a new rise in pressure in the aorta. The process then continues along
the aorta and into the rest of the arterial system. The recoil therefore leads to regular fluctuation in
pressure of blood as it moves along the aorta and other major arteries. As the blood moves further from
the heart, its overall pressure decreases first slightly, then rapidly as volume of blood vessels increases
when arteries divided into arterioles. This fall in pressure is essential to prevent bursting of the one-cell-
thick walls of capillaries to which blood flows next. As blood gets further away from the heart, the pulse
becomes less and less pronounced until, in the capillaries and veins which have little/ no elastic fibres,
blood flows evenly.
Check point.
1. The figures show the changes in blood pressure, velocity, and cross-sectional area of blood
vessels in the systemic circulation as blood flows and returns to the heart.

a) Explain the relationship between velocity of blood and cross-sectional area of blood vessels. (05
marks)
b) i) Comment on the rate of blood flow through arteries and capillaries. (03 marks)
iii) Explain the importance of the above in bi) to the functioning of arteries and capillaries.
(07 marks)
c) Explain how the
i) velocity of blood in the arteries is maintained despite fluctuations in pressure. (03 marks)
ii) velocity of blood in veins is increases while pressure continues to decrease. (05 marks)
2. the table below shows the data for a well-trained endurance athlete and an untrained athlete
working at a standard rate.

Endurance Untrained
athlete individual
Oxygen uptake (dm3 per minute) 3.023 3.024

Volume of blood pumped per beat (dm3) 0.156 0.120

 Heart rate beats per minute 180

Cardiac output. (dm3 per minute) 19.5

a) Complete the table by calculating the missing values. Show your working. (04 marks)
b) What would be the cardiac output of each individual with a rate of 200 beats per minute?
i) Endurance athlete. (03 marks)
ii) Untrained individuals. (03 marks)
c) Explain the difference in cardiac output between the endurance athlete and untrained individual.
(05 marks)
d) Suggest ways in which the muscles of the endurance athlete obtain more oxygen from blood than
those of untrained individual. (03 marks)
Measurement of blood pressure.
Blood pressure is measured usually in the brachial artery in the arm by using a sphygmomanometer.
Systolic pressure is produced by contraction of the ventricles while diastolic pressure is produced by
relaxation.
Conditions that lead to narrowing and hardening of blood vessels such as atherosclerosis or damage of the
kidney may increase blood pressure, a condition known as hypertension.
Dangers of hypertension
 weakening and rupture of artery walls.
 Clogging of narrow blood vessels by blood clots/ thrombosis
NB: when these affect the heart it leads to coronary thrombosis
When it affects the brain arteries, it causes cerebral hemorrhage (stroke) and cerebral thrombosis.
Hypertension can also be caused by;
 Smoking, excessive alcohol intake, stress, obesity, lack of exercise, too much salt in the diet.
Effects of exercise on the cardiovascular and respiratory systems.
Short term effects on cardiovascular system.
 Increased blood pressure/ blood flow
 Increased heart rate / increased rate of contraction of muscular wall of ventricles
 Increased stroke volume/ more complete emptying of the ventricles.
 Vasodilation of blood vessels due to adrenaline and sympathetic nervous system in trained
athletes.
 Increased blood flow to muscles due to vasodilation.
 Vasodilation of heart and lung blood vessels.
 Dilation of veins in muscles leads to increased venous return to the heart increasing cardiac
output.
 Vasodilation of skin arterioles due to buildup of heat.
  Vasoconstriction of blood vessels supplying organs which are less in need for oxygen e.g. kidney,
gut, spleen.
Check point
Figure below shows effect of exercise on a marathon runner.

a) Explain the difference in the effect of exercise on stroke volume and heat rate. (05 marks)
From 5 to 15 dm3 per minute, stroke volume increases more rapidly than heart rate,
because trained athlete has large amount of heart muscles and large size of heart
chambers; so, increased venous return of blood to the heart caused by dilation of veins in
muscles; stretches the heart muscles; causing them to contract more strongly;

Long term effects on cardiovascular system.

 Heart gets stronger
 Chambers of the heart become larger
 Mass of muscles on heart wall increases
 Increased number of blood vessels in muscle fibres of the heart
 Increased number and size of mitochondria in cardiac muscles.
 Increased number of myofibrils in cardiac muscles.
 Decrease in resting heart rate. Because stroke volume increases while cardiac output
remains the same. The heart pumps more slowly but still pump the same volume of
blood.
 Decreased pressure of blood while at rest
 Increased total volume of blood.
 Increase in number of capillaries in the lungs and muscles.
Short term effects of exercise on respiratory system.
 Increased ventilation rate due to stimulation of chemoreceptors, and stretch receptors
in the muscles and tendons due to rapid limb movement.
  Increased metabolic/ respiratory rate due to increased energy demand, leading to
decrease in amount of ATP relative to ADP which stimulates breakdown of glucose.
 Increased oxygen supply to respiring tissues due to high carbon dioxide and
temperature within tissues,
Long term effects of exercise on respiratory system.
 Increased vascularization of lungs
 Increased strength of respiratory/ intercostal muscles and diaphragm
 Increased number and size of mitochondria in skeletal muscles to increase rate of
respiration.

Effect of temperature on the heart rate.

Temperature (oC) Heart rate

10 25.65
30 39.37
40 47.50
a) Explain the effect of temperature on heart rate. (06 marks)
o
Heart rate is highest at 40 C/ high temperature because of highest permeability of cardiac
muscle membranes to ions that control heart rate; accelerating self-excitation process/
activity of the SA node.
Heart rate is lowest at lowest temperature because of lowest permeability of cardiac muscle
membranes to ions; decreasing the self-excitation process.
b) Explain the significance of the relationship between temperature and heart rate. (05 marks)
Increase in temperature increases heart rate which increases blood pressure; hence increasing rate
of blood supply to the skin surface; encouraging heat loss by radiation, convection and conduction;
Low temperature decreases heart rate allowing more time for filling of the heart with blood causing
stronger and more powerful contractions; which increases stroke volume;
 Composition and function of Blood
Composition of blood
Blood comprises a watery plasma in which are a variety of different cells. The cells include red blood
cells/ erythrocytes, white blood cells/ leucocytes, and platelets.
Plasma
Plasma is mainly water containing a variety of dissolved and suspended substances which are transported
from one part of the body to another. For example, food materials e.g. glucose, lipids, and amino acids,
urea, hormones, mineral ions, plasma proteins, respiratory gases. These chemicals make the plasma
slightly alkaline.
NB: removal from blood of plasma proteins involved in clotting e.g. prothrombin and fibrinogen results
into a liquid called serum which does not clot.
Functions of plasma
 Transports dissolve/ suspended chemicals from where they are formed to where they are
absorbed/ excreted. These chemicals include; nutrients, waste products, mineral ions, hormones,
plasma proteins, and respiratory gases.
 Provides a medium of exchange between cells and blood.
Components of plasma and their functions

Component Function
Water  Provides cells with water
 Dissolves many materials for
transportation
 Water content regulates blood pressure
and blood volume
 Regulation of temperature
 Prevents freezing of blood
Serum albumins  Bind to and transport calcium
 Contribute to solute potential of blood
Serum globulins  Alpha globulins bind and transport the
hormone thyroxine, lipids and fat-soluble
vitamins.
 Beta globulins bind to and transport iron,
cholesterol and fat-soluble vitamins.
 Gamma globulins are antibodies produced
by lymphocytes important in immune
response.
Prothrombin  Involved in blood clotting
Fibrinogen  Produced by liver, takes part in blood
clotting.
Minerals ions Regulate solute potential and pH, etc
Red blood cells
Characteristics
 Are biconcave discs. Biconcave shape increases surface area to volume ratio, makes the cell
flexible allowing it to squeeze through narrow lumen of capillaries.
 Are numerous
 Are small in size.
 Have no nucleus, mitochondria, endoplasmic reticulum, Golgi apparatus when mature.
 Have short life span.
 They are very thin.
NB: because of the lack of nucleus and other organelles,
 They have short life span
 They are much thinner in the middle giving a biconcave shape which gives a large surface area to
volume ratio.
 They are can more easily change shape, allowing them to be flattened against the capillary walls
to reduce diffusion distance.
 Absence of mitochondria and nucleus provides more room for the pigment haemoglobin which
carries oxygen.
 Absence of mitochondria prevents utilization of oxygen while being transported, as red blood
cells respire anaerobically.
Adaptations of red blood cells.
 They are much thinner in the middle giving a biconcave shape which gives a large surface area to
volume ratio.
 They are can more easily change shape, allowing them to be flattened against the capillary walls
to reduce diffusion distance.
 Absence of mitochondria and nucleus provides more room for the pigment haemoglobin which
carries oxygen.
 Absence of mitochondria prevents utilization of oxygen while being transported, as red blood
cells respire anaerobically.
 Small size enables them squeeze through narrow capillary lumen
 Thin membrane reduces diffusion distance for faster diffusion.
 Numerous to increase blood oxygen carrying capacity
 Store large amounts of haemoglobin which combine with oxygen in areas of high partial
pressures and release them in areas of low partial pressure of oxygen.
 Contain carbonic anhydrase enzyme which catalyzes formation of carbonic acid from dissolution
of carbon dioxide gas.
 Biconcave shape increases surface area to volume for gaseous exchange.
White blood cells.
Characteristics
 Larger than red blood cells
  Fewer in numbers than red blood cells
 All nucleated
 All capable of amoeboid/ crawling movement. This allows them to squeeze through pores on
capillary walls to enter tissues and sites of infection
 Exist in a variety of forms
 Made in the marrow of the limb bones.

Adaptations of white blood cells

 Amoeboid movement enables them squeeze through pores on capillary walls to reach tissues and
sites of infection.
 Possess nucleus that controls activities of the cell.
 Numerous to increase surface area for fighting infections
 Exist in a variety of types which ensures varies means of combatting infections.
Types of white blood cells.
There two main groups of red blood cells;
1. Granulocytes (polymorphs/ polymorphonuclear leucocytes)
Characteristics
 Granular cytoplasm
 Lobed nucleus
 Made in the bone marrow
Types of granulocytes
a) Neutrophils (phagocytes)
Characteristics
 Actively phagocytotic, engulf and digest disease causing bacteria.
 Can move freely all over the body
 Make up the highest percentage of red blood cells present in blood.
Function
 Engulf bacteria
b) Eosinophils
Characteristics
 Have granules which are stained red by eosin dye.
 They possess antihistamine properties.
 Number in blood depends on hormones produced by adrenal cortex in response to stress.
 Their population increases in people with allergies
Function
 Allergic response and anti-histamine properties
c) Basophils
Characteristics
 Granules in their cytoplasm stain blue with methylene blue.
 The cells produce heparin, an anti-coagulant and histamine, a chemical found in damaged tissues
involved in inflammation. Inflammation stimulates repair of damaged tissues.
Function
 Produce histamine and heparin.
2. Agranulocytes

Characteristics
 Have non granular cytoplasm
 Have compact nucleus (oval/ bean shaped)
Types of agranulocytes
a) Monocytes
Characteristics
 Made in the bone marrow
 Have bean shaped nucleus
 Turn into macrophages while in tissues.
 Are phagocytotic
 Can move freely all over the body
 Non specific
Function
 Engulf bacteria
b) Lymphocytes
Characteristics
 They are produced in the thymus gland and lymphoid tissues from cells that originate from the
bone marrow.
 Cells are round and possess only a small quantity of cytoplasm. Amoeboid movement is limited
 Two types T cells and B cells.
 They are specific to pathogens.
Function
 Production of antibodies

Platelets
Characteristics
 Irregularly shaped membrane bound cell fragments.
  Usually lack nucleus
 Formed from large special bone marrow cells.
 Smaller in size than red blood cells.
 Numerous
Function
 blood clotting
FUNCTIONS OF BLOOD
Blood performs two main functions; transport/ distribution of materials and defense against disease.
Transport function of blood
Summary of transport functions of blood

Materials transported Examples Transported from Transported to Transported in

Respiratory gases Oxygen Lungs Respiring tissues Haemoglobin in
red blood cells.
Carbon dioxide Respiring tissues Lungs Haemoglobin in
red blood cells
Hydrogen
carbonate ions in
plasma
Organic digestive Glucose Intestines Respiring tissues/ Plasma
products liver
Amino acids Intestines Body tissues/ liver Plasma
Vitamins Intestines Body tissues/ liver Plasma
Mineral salts Calcium Intestine Bone/teeth Plasma
Iodine Intestine Thyroid gland Plasma
Iron Intestines/ liver Bone marrow Plasma
Excretory products Urea Liver Kidney Plasma
Hormones Insulin Pancreas Liver Plasma
Antidiuretic Pituitary gland Kidney Plasma
hormone
Heat Metabolic heat Liver and muscles All parts of the All parts of blood
body

Transport of respiratory gases

The solubility of oxygen in water (hence in blood) is low. Because of the high temperature of blood
(37oC), the solubility of oxygen is even lowered further.
Vertebrates and many invertebrates have evolved a group of Coloured proteins capable of loosely
combining with oxygen in order to increase the oxygen carrying capacity of their blood. These are known
as respiratory pigments.
With a few exceptions, pigments with large RMM are found in blood plasma while those with small
RMM are found within cells to prevent them from being lost by ultrafiltration in the kidney.
Necessity for a transport system in mammals.
Mammalian body is large and complex; therefore, has higher metabolic rate and hence higher oxygen
demands; which cannot be supplied by oxygen simply dissolved in plasma, and in addition, more carbon
dioxide is produced. This means it is necessary for organisms to possess respiratory pigments; which
readily combine with oxygen at respiratory surfaces where oxygen concentrations are high; increasing
blood oxygen carrying capacity; and to release oxygen readily in respiring tissues; where oxygen
concentrations are low;
The best-known respiratory pigment is haemoglobin.
Structure of haemoglobin
Haemoglobin is a conjugated protein;
It consists of a protein part called globin; consisting of four (4) polypeptide chains;
Two of the chains are alpha chains; the other two are beta chains; the two types of chains are about the
same lengths but have slightly different compositions.
Each chain is combined with a non-protein prosthetic group called Haem; Haem consists of an atom of
divalent iron enclosed in a ring structure.
Each haem group can combine with a molecule of oxygen in a process known as oxygenation.
Each molecule of human haemoglobin can therefore combine with a maximum of four molecules of
oxygen.
NB:
1. Different haemoglobins have different number of haem groups and so vary in their abilities to
carry oxygen.
2. oxygenation differs from oxidation in that the iron does not become loss any electron (is not
chemically oxidized)
3. plants such as leguminous plants also contain respiratory pigments. Root nodules of beans for
example contain a red oxygen binding pigment called leghaemoglobin which takes up oxygen in
the nodules maintaining anaerobic conditions for nitrogen fixing bacteria which are anaerobic.
Oxygen transport
An efficient respiratory pigment readily combines with oxygen at respiratory surfaces where oxygen
concentrations/ tensions/ partial pressures are high (readily loading) and readily dissociate from oxygen at
those tissues requiring it /respiring tissues (readily unloading).
When oxygen partial pressures are low such as in metabolically active tissues, the bonds holding oxygen
to haemoglobin become unstable and oxygen is released. This diffuses in solution into cells. The release
of oxygen from haemoglobin is called dissociation.
Oxygen dissociation curve
Is a graph that shows the relationship between the degree of saturation of haemoglobin (the saturation of
haemoglobin) with oxygen and the partial pressure of oxygen in the immediate surrounding.
The greater the oxygen partial pressures the more saturated haemoglobin becomes with oxygen. It might
be imagined that a simple straight-line/ linear relationship will be obtained on the oxygen dissociation
curve but this is not the case. Instead, an S shaped curve is obtained.

At partial pressures of oxygen (pO2) close to zero, there is no oxygen molecule bound to haemoglobin.
At low pO2 the percentage saturation of haemoglobin with oxygen rises gradually because polypeptide
chains of haemoglobin are tightly bound together; making it difficult for an oxygen molecule to gain
access to the iron atom;
At high partial pO2 the percentage saturation of haemoglobin with oxygen rises rapidly as one molecule
of oxygen becomes bound to one haem group; making the polypeptide chains to open up; exposing the
other three remaining haem groups to oxygen; this makes it much easier for them to become oxygenated
(allosteric effect)
At very high partial pressures of oxygen, the percentage saturation of haemoglobin with oxygen becomes
high and constant; because haemoglobin becomes saturated as most but not all the haemoglobin
molecules are completely loaded with oxygen molecules. There is never is never completely 100%
saturation because with many binding sites occupied; it is less likely that a single oxygen molecule will
find a free/ an empty binding site to bind.
Although it is much easier for the first three oxygen molecules to dissociate from haemoglobin as pO2
decreases, it much difficult for the final oxygen molecule to dissociate.
NB: the steep part of the curve corresponds to the range pO2 within tissues. Over this pO2, a small drop
in pO2 (in actively respiring tissues) brings about a comparatively large decrease in percentage saturation
i.e. when pO2 drops due to tissues utilizing oxygen at a faster rate, haemoglobin responds by giving up
more of its oxygen. And a small increase in pO2 (in the lungs/ respiratory surfaces) leads to a large
increase in saturation of haemoglobin with oxygen.
The Bohr effects
Unloading of oxygen in capillaries is aided by relatively high carbon dioxide concentrations produced by
the respiring tissues. Carbon dioxide reduces affinity of haemoglobin for oxygen at partial pressures in the
body. This therefore shifts the oxygen dissociation curve to the right. This is known as Bohr shift/ Bohr
effect.
Bohr effect is the reduction in haemoglobin’s affinity for oxygen in presence of high carbon dioxide
concentrations, which causes shifting of oxygen dissociation curve to the right.
For example

Curve A corresponds to conditions in the gaseous exchange surfaces like lungs, where carbon dioxide
partial pressures are low; as it diffuses across the exchange surface and it is expelled by exhalation from
the organisms. Haemoglobin’s affinity for oxygen is increased. Together with the high pO2 in the lungs,
this means haemoglobin readily binds to oxygen in the lungs. The carbon dioxide concentration shifts the
oxygen dissociation curve upwards to the left.
Curve C represents conditions in respiring tissues e.g. muscles, where carbon dioxide partial pressures are
high because of its production in aerobic respiration. Haemoglobins affinity for oxygen is reduced.
Together with the low concentration of oxygen in respiring tissues, this means that oxygen readily
dissociates from oxyhaemoglobin, The increased carbon dioxide concentrations shift the oxygen
dissociation curve downwards and to the right. This is important during exercise because the more carbon
dioxide is produced, the more readily oxygen is supplied from haemoglobin to meet the extra energy
demands of the exercise.
The Bohr effect is due to the acidic nature of dissolved carbon dioxide. It forms hydrogen ions and
hydrogen carbonate ions. The hydrogen ions lower the pH of blood and the affinity of haemoglobin for
oxygen. Low pH caused by other chemicals such as lactate also low affinity of haemoglobin for oxygen.
NB: the more the dissociation curve for a pigment is displaced to the right, the less readily it picks up
oxygen and the more readily it releases it.
The more the dissociation of a pigment is displaced to the left, the more readily it picks up oxygen but the
less readily it releases oxygen.
Haemoglobin found in different animals vary in their affinity for oxygen depending on a variety of factors
Factors which determine nature of haemoglobin in different animals.
1. Atmospheric pressure. Reduced atmospheric pressure makes it difficult to load oxygen.

Liama

Liama lives in areas of high altitudes with low atmospheric pressure and oxygen tensions; therefore their
haemoglobin has a high affinity for oxygen at low pO2 in order to load more rapidly with oxygen in the
lungs; than humans who live at low altitude with high oxygen partial pressure.
 2. Partial pressure of oxygen in the habitat. E.g. in muddy places

Arenicola

Arenicola lives in muddy water-logged burrows; with very low oxygen tensions; its haemoglobin has a
very high affinity for oxygen in order to obtain oxygen from this environment easily;
3. Level of activity
 Birds fly. Flight much energy hence birds have high metabolic rates. Thus, require rapid oxygen
supply. Therefore, their haemoglobin has lower affinity for oxygen in order to readily release
oxygen to respiring tissues; with oxygen tensions of 21kPa, the air still saturates the haemoglobin
with oxygen despite its low affinity.

4. Body surface area to volume ratio

5. Means of oxygen supply

Fetal haemoglobin has higher affinity for oxygen than adult haemoglobin to enable it obtain oxygen from
the mother’s haemoglobin in the placenta.
Different animals may also have different respiratory pigments. For example
1. Myoglobin vs haemoglobin.
Muscles of mammals contain a red pigment called myoglobin similar in structure to one of the four
polypeptide chains of haemoglobin.
It has a very high affinity for oxygen and unloads its oxygen only when blood is almost fully
deoxygenated.
Myoglobin readily takes up oxygen even when oxygen partial pressures are very low.
Myoglobin combines with one molecule oxygen to form oxymyoglobin which remains fully saturated
with oxygen at oxygen partial pressures low enough to cause unloading of haemoglobin. Myoglobin only
gives up its oxygen at partial pressures that are very low e.g. during muscle exertion/ strenuous exercise.
Muscles of active organisms such as birds that fly have more myoglobin than those of less active
organisms.
Carbon monoxide effect
Affinity of iron (II) in haemoglobin for carbon monoxide is very many times greater than for oxygen.
Therefore, haemoglobin will combine with any carbon monoxide available in preference to oxygen to
form a relatively stable compound called carboxyhaemoglobin. This prevents oxygen from binding to
haemoglobin, stopping transport of oxygen to tissues.
This effect can be solved by removing the victim from the area, and administering air containing almost
pure oxygen mixed with carbon dioxide. The pure oxygen is administered in order to quickly replace
carbon monoxide, since atmospheric pO2 are too low to replace it in the atmosphere. Carbon dioxide is
included to stimulate respiratory centre to increased ventilation rate.
the unfortunate thing about haemoglobin is its unusually high affinity for carbon monoxide, forming a
stable complex; which oxidizes the iron (II) to iron (III); preventing combination with oxygen.
NB: several other respiratory pigments are found in animals which differ from haemoglobin especially in
the nature of their prosthetic groups. E.g.
Haemoglobin, myoglobin, Chlorocruorin, haemoerythin both contain iron.
Haemocyanin contains copper.
Their affinities are almost similar though their total carrying capacity is lower
Carbon dioxide carriage
Carbon dioxide is more soluble than oxygen in water. However, its carriage In solution is still inadequate
to meet the needs of tissues. There are therefore three methods of carbon dioxide carriage.
1. In aqueous solution
Little carbon dioxide is carried in this way. Most of the carbon dioxide carried in this way is in physical
solution rather than dissolved.
2. Combined with haemoglobin (proteins)to form carbamino-haemoglobin.
Carbon dioxide combines with each of the free amino groups at the end of each polypeptide chain
of haemoglobin forming a neutral carbamino-haemoglobin. The amount of carbon dioxide
haemoglobin can combine depends on the amount of oxygen already being carried by
 haemoglobin. The less the amount of oxygen haemoglobin is already carrying the more carbon
dioxide is transported in this way.
Carbon dioxide + haemoglobin carbamino-haemoglobin
3. In form of hydrogen carbonate ions
Carbon dioxide from respiring tissues diffuses into blood stream and passes into red blood cells where it
combines with water to form weak carbonic acid. This process is catalyzed by enzyme carbonic
anhydrase found in red blood cells.
Some of the carbonic acid dissociates to form hydrogen ions and hydrogen carbonate ions.
The hydrogen ions displace oxygen from haemoglobin as already noted. The deoxygenated blood accepts
hydrogen ions forming haemoglobinic acid.
NB: by accepting hydrogen, haemoglobin acts as a buffer molecule, enabling large quantities of carbonic
acid to be carried to the lungs without causing major changes in blood pH.
The majority of hydrogen carbonate ions formed in red blood cells diffuses into blood plasma across the
thin membrane of red blood cells along a concentration gradient.
The hydrogen carbonate ions combine with sodium ions to form sodium hydrogen carbonate. The loss of
negatively charged hydrogencarbonate ions from red blood cells leaves them more positively charged.
This charge is balanced by chloride ions diffusing into red blood cells from the plasma. This phenomenon
is called chloride shift.
When red blood cells reach the lungs, hydrogen ions combine with hydrogen carbonate ions to form
carbonic acid which decomposes releasing carbon dioxide that diffuses into the lungs.
Adjustments to high altitudes/ acclimatization
The low partial pressures at high altitudes makes breathing and loading of haemoglobin with oxygen
difficult. If the ascent to high altitudes is slow, the body is given time to adjust. The following adjustments
occur.
1. increased red blood cell count to increase oxygen carrying capacity of blood.
2. Increased cardiac output by increased heart rate and stroke volume
3. Increased ventilation rate removes excess carbon dioxide and takes more oxygen.
4. Increased lung volume and flow of blood in lung capillaries. / increased oxygen uptake in
lungs
5. Increased concentration of haemoglobin in each red blood cell
6. Increase in level of myoglobin in muscles to increase oxygen storage
7. Change in pH of blood to alkaline due to excessive loss of carbon dioxide due to
increased ventilation rate. This is overcome by excretion of HCO3- in urine.
8. Oxygen dissociation curve shifts to right (in first few days) to facilitate release of oxygen
to tissues. In a long run, it shifts to left to increase oxygen uptake in lungs.

DEFENSIVE FUNCTION OF BLOOD

Immunity
Immunity is the ability of an organism to resist diseases. It involves the recognition of a foreign particle
and the mobilization of chemicals to help destroy them.
The immune system
 Enables us to withstand attack by pathogens.
 Removes foreign materials from the body.
Non-specific and specific immune system
Immune system has two components:
a) the non-specific immune system
Characteristics
 Present from birth
 Quickly responses to infection
 Responses to a very wide range of pathogens and foreign substances
 Non-specific/ gives the same type of response to every infection.
Examples
 Inflammation, phagocytosis (involving phagocytes and complement proteins), cytokines (small
proteins which inhibit reproduction of viruses)
Preventing entry of foreign materials/ withstanding attacks/ first line of defense.
 Skin forms a hard and keratinized outer layer forming a barrier for pathogens.
 Cilia lining the trachea and bronchi trap foreign particles and move them to throat for
swallowing
  Mucus secreted by goblet cells traps foreign particles.
 Coughing, sneezing and vomiting help to expel pathogens.
 Acid in the stomach kills many bacteria
 Clotting of blood prevents entry of pathogens
 Inflammation prevents spreading of infection
 Enzyme lysozyme in tears, nasal secretions and saliva destroy bacteria
 Environmental health and hygiene reduce exposure to pathogens.
 Hairy nasal/ eye lashes passages to trap foreign particles form entering the body
 Eye lids close the eye preventing entry of large pathogens
 Tears/ saliva clean dust/ foreign particles form the eye/ mouth
 Sphincter muscles and hair in the anus prevent entry of pathogens
 Sebum produced on skin by sebaceous glands has antibacterials that kill bacteria on skin surface.

Despite the body’s physical barriers/ first line of defense, pathogens still get into the body where
they multiply rapidly, attacking several cells and producing toxins into the blood stream.
However, they are dealt with by the second line of defense, the immune responses in two main
way; phagocytosis, and antibody formation brought about mainly by white blood cells.
The second line of defense functions to;
 Neutralize any toxins produced by the pathogens
 Prevent the pathogen from multiplying
 Kill the pathogens
 Remove any remains of the pathogen.
Immune responses by blood include the following;
1) clotting of blood
2) phagocytosis
3) antibody formation
Blood clotting
Damaged platelets or tissues release clotting factors which react with other blood factors (calcium
ions and factor III) to produce thromboplastin. Thromboplastin stimulates conversion of inactive
plasma protein prothrombin to active enzyme thrombin; this requires the presence of calcium ions and
K+ ions.
Thromboplastin in turn converts soluble plasma protein fibrinogen to insoluble protein fibrin.
The fibrin forms a meshwork of threads in which red blood cells become trapped. This dries to form a
clot beneath which repair of worn-out tissues takes place.
The clot prevents further blood loss and prevents entry of bacteria.
Burst pletelets also release a substance called serotonin. Serotonin causes vasoconstriction to stop loss
of blood from the damaged arterioles.
Fibrin inhibits excess fibrinogen conversion by negative feedback.
 NB: clotting of blood is prevented by substances such as oxalic acid which precipitates out calcium
ions as calcium oxalate and heparin which inhibits the conversion of prothrombin to thrombin. These
substances are known as anticoagulants.
Haemophilia results from a fault in one of the two genes. One of genes controls production of protein
factor VIII, the other gene is responsible for production of factor IX, both genes are located on the X
chromosome. This prevents conversion of prothrombin to thrombin.
Phagocytosis
Boths neutrophils and monocytes are capable of amoeboid movements. Both carry out phagocytosis
Phagocytosis is a process by which large particles are taken up by cells via cell membrane- derived
vesicles.
Why do white blood cells carry out phagocytosis
 To protect the organism against pathogens.
 To dispose of dead/ dying/ damaged cells and cellular debris.
The process of phagocytosis
 Antibodies attach themselves to the antigens on the cell surface membrane of the bacteria.
 Proteins found in the plasma, attach themselves to the antibodies.
 As a result of a series of reactions, the surface of the bacterium becomes coated with proteins
called opsonins. This process is called Opsonisation.
 Complement proteins and any chemical products of the bacterium acts as attractants, causing
neutrophils to move towards bacterium.
 Neutrophils attach themselves to the opsonins on the surface of the bacteria.
 Neutrophils engulf the bacterium to form a vesicle, known as phagosomes.
 Lysosomes move towards the phagosomes and fuse it.
 The enzymes within the lysosome’s breakdown the bacterium into smaller soluble materials.
 The soluble products from the breakdown of bacterium are absorbed into the cytoplasm of the
neutrophils and waste products are released from the cell.
NB: macrophages and Neutrophils make up the bodies reticulo-endothelial system.
One result of phagocytosis at a site of local infection may be inflammation.
Inflammation
When an area is wounded or injured, the tissue surrounding the wound becomes swollen, hot, red and
painful.
This results from release of histamine from the damaged tissues. Histamine causes local vasodilation of
capillaries in the area of infection.
This increases the amount of blood reaching the area and raises the temperature locally.
It also increases leakiness of capillaries in the area, increasing escape of plasma and white blood cells into
the surrounding tissues causing swelling of the area.
The plasma contains chemicals which inhibit growth of bacteria or kills them e.g. interferons produced by
macrophages which makes body cells resistant to infection by viruses. It also contains antibodies and
phagocytes which help to combat the spread of the infection. The phagocytes also engulf dubris and dead
cells.
The plasma also contains fibrinogen which is involved in blood clotting if required.
The excess tissue fluid tends to dilute and reduce the effects of toxins produced by the pathogens.
Neutrophils also pass through the walls of capillaries through a process known as diapedesis.
Histamine also makes the nerve endings more sensitive hence causing pain.
The pus formed contains dead bacteria and phagocytes.
Wound healing
BS. 485
b) the specific immune system
characteristics
 Involves and proteins within blood
 Responds slowly
 It is effective only against specific pathogens
 Response is speeded up on repeated infection.
 Able to distinguish between self and non-self-antigens
Antigens
Antigen is any molecule which can cause antibody production.
All cells possess antigens on their cell surface membranes that act as markers enabling cells to recognize
each other.
Antigens are usually proteins, glycoproteins or sometimes polysaccharides that make up the cell surface
membranes or the protein coat of viruses, microorganisms or diseased cells such as cancer cells.
Presence of an antigen triggers production of antibody. The body (lymphocytes) can distinguish its own
antigens (self-antigens) from foreign antigens (non-self-antigens). The body (lymphocytes) normally
makes antibodies against only non-self-antigens.
How does the body / lymphocytes distinguish between self and non-self-antigens?
There are more than 100 million lymphocytes, each capable of recognizing a different chemical shape/
antigen, and produce specific antibodies (B lymphocytes) form their cell surface membranes to act as
receptors.
In a fetus, these lymphocytes collide constantly with only other body cells, since infections are rare.
Those lymphocytes which have receptors that are complementary/ fit exactly on body’s own cells (self-
antigens) either die or are suppressed;
The only remaining lymphocytes will be those with receptors that are complementary/ fit to foreign
materials (non-self-antigens), therefore the only antibodies produced are those that respond to non-self-
antigens.
NB: occasionally B lymphocytes may fail to distinguish between self and non-self-antigens.
A disease which results from the immune system attacking its own cells and tissues is called autoimmune
disease. E.g. myasthenia gravis, in which antibodies act a against acetylcholine receptors on the cell
surface membrane of muscles, preventing muscle contraction.
Antibody/ immunoglobulins (Ig)
Antibodies are proteins synthesized by cells of the immune system known as plasma cells, a type of B
cells.
When the body is infected by non-self-antigens, a B lymphocyte produces antibodies which act against
the antigen on the surface of the foreign particle, by binding to them precisely as a key fit on a lock.
Antigens are therefore highly specific, each antigen having its own separate antibody.
General structure of antibody
Antibodies are made up of four polypeptide chains;
Consisting of two long chains called heavy chains (H chains) and two shorter chains called light chains (L
chains).
The chains are held together by disulphide bridges;
The hinge region is flexible allowing slight movement of the molecule when binding to antigens.
The antibody has two sights called binding sites, which fit precisely on to the antigen. The binding sites
are different on different antibodies and are therefore called variable regions.
They contain a specific sequence of amino acids that forms a specific three-dimensional shape which
binds directly to a single type of antigens.
The rest of the parts of the antibody are constant in all antibodies and is therefore known as the constant
region. This binds to the receptors on the phagocytes making phagocytosis of the pathogen easier.
Each antibody molecule has two antigen binding sites so can bind to two antigens on different pathogens.
Also, a pathogen can have a number of different antigens that bind to different antibodies. This leads to
clumping together of pathogens for phagocytosis.

Specific immune response/ system

Specific immune responses depend on the type of white blood cells called lymphocytes. There are two
types of lymphocytes, each with its own immune response. Namely
1. B lymphocytes (B cells) responsible for antibody mediated (Humoral immunity) involving antibodies
within body fluids (humours)
2. T lymphocytes (T cells) responsible for cell mediated immunity (involving cells)
Both types of lymphocytes are formed from stem cells in the bone marrow, however, develop and mature
from different regions of the body. For example
B lymphocytes mature in the Bone marrow
T lymphocytes mature in the Thymus gland
The maturation stage takes place in the fetus and produces different types of B cells each responsible for
specific antigen.

Immune response
Once a lymphocyte has attached to its complementary antigen, it multiplies/ divides/ proliferates rapidly
to form a clone of identical lymphocytes. This is known as primary response primary response. This is
the response the immune system to an antigen it meets for the first time.
Primary response is slow, taking long to recruit enough plasma cells to bring the infection under control.
During this time the invading pathogen multiplies and gives rise to symptoms of the disease. Some of the
lymphocytes in the clone change into cells known as memory cells. Unlike the other lymphocytes in the
clone which die within few days, memory cells survive longer. Further infection by the same pathogen
causes the memory cells to multiply immediately rapidly, causing their numbers to build up faster than for
the invading pathogen. Hence preventing symptoms from being induced. This is called secondary
response. This explains why we suffer some diseases once in a lifetime, despite continuous exposure.
Each time the pathogen enters the body, more and more memory cells are built up, making future
infections less likely. This progressive increase in level of immunity is known as adaptive or acquired
immunity.
HUMORAL IMMUNITY
When the body is invaded by foreign materials, these materials possess antigens that stimulate B cells to
produce antibodies into plasma, tissue fluid and lymph (body tissues/humor). The attack of pathogens also
takes place in the body fluids. There this type of response is known as humoral immunity.
Antibody production
When a B cell binds to a complementary antigen on an invading pathogen, it is activated to multiply
rapidly forming a clone of identical lymphocytes. The activation of B cell requires presence of specific
antigen and lymphokines secreted by T helper cells. Pathogens usually have many antigens on their cell
surfaces, therefore cause several types of B cells to multiply forming several clones, in order to produce
the specific antibodies for each antigen on the pathogen. This is known as polyclonal activation.
The process by which a particular antigen promotes production of a specific antibody is called clonal
selection.
For each clone, the cells produced develop/ differentiate into one of the two types of cells;
a) Plasma cells/ effector cells; which produce antibodies. Plasma cells survive for only few days but make
very many antibodies every second. The antibodies destroy the pathogens and any toxins produced by the
pathogen.
b) Memory cells. Memory cells live relatively longer than plasma cells. These cells do not produce
antibodies directly but rather remain in circulation (blood, tissue fluid, lymph and lymph nodes) until they
come across the same antigen at some future date. With the greater number of specific memory cells
present in the body, the chances of coming across the antigen more quickly than the first-time increases.
When they come across the pathogen, they divide rapidly; into many plasma cells; and more memory
cells.
The plasma cells secrete antibodies to destroy the pathogens. The memory cells remain in circulation and
are ready for further infection in the future. In this way, memory cells produce long term immunity
against the original infection. This is known as secondary response. It is both more rapid and of greater
intensity than primary response.
The graph shows relative amounts of antibodies in primary and secondary response.
a) shows primary response, during which one B cell is activated by binding to an antigen which has a
complementary shape to the immunoglobulin/ receptor protein/ antigen on its cell surface membrane; it
divides many times to produce a clone of identical B cells; all of which can produce identical antibodies
against the antigen. Some of the B cells formed become memory cells;
b) shows secondary response, during which the memory cells present in circulation in greater numbers
have greater chances of coming across antigens on second exposure; and multiply immediately rapidly
forming large population of B cells; each of which in turn can produce clones of B cells; which can
produce the same antibodies to destroy the pathogen;
Other ways B lymphocytes can be activated
Macrophages are often the first cells to come across pathogens and destroy the by phagocytosis.
Macrophages and some B cells can take up antigens and process them to form a complex with some cell
surface proteins known as major histocompatibility complex (MHC). This complex can be attached to the
cell surface membrane and the cell can act as an antigen presenting cell (APC). This involves the
following steps.
1. invading pathogen produces antigens. Some of the antigens are taken up by macrophages by
phagocytosis. Some attach to the receptors on B cells. Those attached to receptors on B cells are taken up
into the B cell for processing.
2. both macrophage cells and B cells process the antigens and bind them to MHC protein.
3. the MHC protein presents the processed antigen on the cell surface membranes of the cells now
referred to as antigen presenting cells.
4. A T helper cell binds to the processed antigen on macrophage and becomes activated. This makes it
capable of interacting with B cells.
5. The T helper cells binds to the MHC proteins with antigens on the surface of B cells.
6. the B cell is activated to divide mitotically to give a clone of plasma cells and specific memory cells.
7. the cloned plasma cells produce antibodies that exactly fit the antigen on the pathogen.
8. the antibodies attach to the antigens on the pathogen causing agglutination and lysis of the pathogen,
thereby destroying it. (primary response)
9. Some B lymphocytes develop into memory cells that survive for long periods. Future infection by the
same pathogen leads to rapid division of the memory cells, some of which develop into plasma cells that
produce antibodies. (secondary response).
NB: Once the antibody has reacted with the antigen, the destruction of the antigen bearing pathogen/
structure is brought about in several ways depending on the type of antibody bond to it e.g.
1. Agglutination caused by agglutinins. Some antibodies have many antigen binding sites and can bind to
same antigens (agglutinogens) on many different pathogens. In this way many different pathogens are
joined together in a clump; making them vulnerable to attack from other types of antigens and
phagocytes.
2. Precipitation caused by precipitins; Some antibodies bind together soluble antigens into large units
which are thus precipitated out of solution so that they are more vulnerable to phagocytosis.
3. Neutralization caused by antitoxins. Some antibodies bind to toxins produced by pathogens hence
neutralizing their harmful effects.
4. Lysis by lysins. Some antibodies bind to the pathogen and act as binding sites for complement proteins
which bring about rupture/ bursting of cells. Some of the complement proteins are enzymes that cause
breakdown of the pathogen.
5. Opsonization by opsonins. Some antigens coat bacteria with proteins known as opsonins. Phagocytes
cell membranes contain receptors that match opsonins enabling phagocytes to recognize, bid to and
engulf the bacteria.
Summary of humoral immunity
CELL MEDIATED RESPONSE
In cell mediated response, cells rather than antibodies are produced specific to the invading pathogen or
foreign substance. The cells are lymphocytes called T cells which mature in thymus gland then are
transported to lymph nodes in blood.
Role of thymus gland
The thymus gland is situated in the thorax just above the heart. It begins to function in the embryo and it
is most active at the time of and just after birth. After weaning, it decreases in size and soon ceases to
function.
Stem cells of the bone marrow which give rise to T lymphocytes must pass through the tissue of the
thymus gland before they can become fully functional. Within the thymus glands, they develop into cells
called thymocytes. At this point, any cells that recognize self-antigens are destroyed so that the body
cannot attack itself later. Some of the thymocytes mature into T cells. They leave the thymus gland in the
bloodstream. Some stay in blood, others migrate to lymph nodes, tissue fluids and spleen. Cell s of mature
lymphocytes possess a T4 molecule (T4 cells) or T8 molecules (T8 cells) which gives them different
functions.
NB: T lymphocytes are produced through out life in the lymph nodes from the lymphocytes which were
processed in the thymus.
The advantage of lymph nodes being the sites of sensitivity to foreign antigens is that the lymphatic
system drains lymph from all body tissues, therefore antigens from anywhere in the body can be detected.
Types of T cells
There are two main types of T cells.
1. T4 cells/ T helper cells. Which when attached to an antigen presenting cell secretes chemicals called
cytokines/ lymphokines/ interleukins. These cytokines;
 Stimulate macrophage cells to engulf the pathogen by phagocytosis.
 Stimulate B cells to divide and develop into antibody producing plasma cells.
 Activates T killer cells (T cytotoxic cells)
T helper cells produce chemicals called opsonins which mark the pathogen, labeling it ready for
phagocytosis.
2. T8 cells.
There are two types of T8 cells.
a) T killer cells/ Cytotoxic T cells.
That kill the body cell infected with pathogen by making holes on the cell surface membrane of the cell
using proteins called perforins. These holes allow water to rush into the cells causing them to burst. This
prevents viruses multiplying.
b) T suppresser cells. Once an infection has been eliminated, these cells suppress the activities of
lymphocytes and so maintain control of the immune system.
Cell mediated response
Unlike B cells (humoral response) which respond to foreign antigens (non-self-antigens) and toxins they
produce, T cells (cell mediated response) responds to the body’s own infected/invaded cells (body cells
invaded by viruses and bacteria), a cancer cell and a transplanted material/ organ/tissue which is
genetically different.
How do T cells distinguish between invaded cells and normal cells?
 Macrophage cells that have engulfed the pathogen and broken it down present some of the
proteins produced on their own cell surfaces;
 The body’s own cells invaded by pathogens/ viruses also manage to present some of the
viral/ pathogens proteins on their own cell surfaces, as a sign of distress.
 Cancer cells also displace non-self-proteins on their cell surface membranes.
The non-self-materials on the surfaces of these cells acts as antigens, hence these cells are
described as antigen presenting cells. There are many different versions of T helper cells and T
killer cells, each of which has different receptor proteins on its surface.
Although these receptors function in similar ways as antibodies, they are not antibodies as they
remain attached to the cell surface rather than being released into the blood plasma.
Since T cells only respond to antigens that are attached to a cell rather than those in body body
fluids, this response is known as cell mediated response.
Summary of the role of T cells in immune response/ cell mediated response
1. Viruses/ pathogens both invade body cells, and are engulfed by macrophage cells during phagocytosis.
2. Both the macrophage cells and invaded body cells process the pathogen/ virus; and bind antigen from it
to a MHC protein. The MHC protein presents the antigen on the surface of the cells; for recognition by,
and binding to specific T cells;
3. A T helper cell attaches to the antigen on the surface of the macrophage cells and is stimulated to divide
by mitosis (clonal expansion). Some of the new T helper cells develop into memory cells that survive
long periods and respond immediately to new infections by the same virus/ pathogen. Other T helper cells
produce cytokines that stimulate B cells to divide forming plasma cells that produce antibodies and
macrophages to engulf invaded cell/ carry out phagocytosis.
4. cytokines also cause T cytotoxic cells to divide by mitosis. Some of the T cytotoxic cells form memory
cells that survive for long periods and respond immediately to new infections by the same viruses/
pathogens.
5. the other T cytotoxic cells attach to any body cells presenting the viral antigen/ infected cells.
6. the attached T cytotoxic cells produce perforins to make holes in the cell surface membranes of the
infected cells. This causes influx of water, causing bursting of the cell and hence destruction of the
viruses.
NB: the activity of all other white blood cells, including phagocytes is decreased/ suppressed by
lymphokines/ cytokines produced by T suppresser cells; and increased by lymphokines produced by T
helper cells.
TYPES OF IMMUNITY
Immunity is the ability of an organism to resist infection. It may be naturally obtained (acquired) or
artificially induced (caused).
Type of immunity
1. Natural immunity; is immunity that is either inherited or acquired as part of normal life processes e.g.
as a result of having had a disease.
2. Artificial immunity is immunity acquired as a result of deliberate exposure of the body to antibodies or
antigen in a non-natural situation.
Both natural immunity and artificial immunity may be actively or passively acquired.
a) Passive immunity is immunity acquired by introduction of antibodies from another individual, rather
than one’s own immune system. It is generally short lived.
b) Active immunity is immunity acquired resulting from activity of one’s own system rather than an
outside source. It is generally long lasting.
Passive immunity
Natural passive immunity: occurs when an individual receives antibodies from the mother via the;
 Placenta as the fetus
  The mother’s milk during suckling (breast feeding)
Artificial passive immunity: occurs when antibodies from another individual are injected. E.g. in
treatment of diseases such as tetanus and diphtheria.
Active immunity
Naturally active immunity results from an individual being infected with a disease under normal
circumstances. The body produces its own antibodies and may continue to do so for many years. It is for
this reason that many people suffer diseases such as chicken pox only once in a lifetime. The immunity
results from the activity of B lymphocyte memory cells.
Artificially active immunity: involves inducing an immune response in an individual without them
having to suffer symptoms of the disease. This forms the basis for immunization. It involves introducing
the appropriate disease antigens into the body either by injection or by mouth. This process is called
vaccination. And the material introduced is called vaccine.
There are different forms of vaccines;
a) living attenuated microorganism. Which are microorganisms which have been treated, can’t cause
symptoms but can multiply.
b) Dead microorganisms.
c) Genetically engineered microorganisms. Genes for the antigens production are transferred to harmless
organisms.
Immunity in children is provided by
a) Antibodies acquired via placenta; short-lived
b) colostrum contains high concentration of antibodies that remain in babies’ gut/ get absorbed into the
bloodstream.
c) vaccination provides immunity.
Summary of types of immunity
Figure below shows changes in antibody concentration with time with passive and active immunity

BLOOD GROUPS
Blood groups are an example of antigen-antibody systems. The membrane of red blood cells contain
polysaccharides that can act as antigens. i.e. they may induce production of antibodies when introduced
into another individual.
The A BO system
In this system, there are just two antigens, A and B which determine blood group. For each of these
antigens there is a antibody which is given a corresponding lower case letter. Presence of an antigen and
its corresponding antibody causes immune response which causes agglutination/ clumping of red blood
cells together and their ultimate breakdown (haemolysis). For this reason, an individual does not produce
antibodies corresponding to the antigen they contain on red blood cells but can produce all others.
Therefore, in transfusing blood from one person, a Donor to another, the Recipient, it is important to
avoid bringing together corresponding antigens and antibodies. However, if only a small amount of blood
is to be transfused, the small amount of donor’s antibodies becomes diluted in the Recipients blood that
they are ineffective. It is therefore possible to add antibody a to antigen A, antibody b to antigen B in
small quantities without agglutination. For this reason, the blood group O is universal Donor, but can only
receive blood from their own. On the other hand, blood group AB can receive blood from all blood
groups (universal recipient).
The rhesus system
This is determined by rhesus antigen D called rhesus factor on the cell surfaces of red blood cells.
Individuals with rhesus antigen D are said to be rhesus positive. Individuals without rhesus antigen D are
said to be rhesus negative.
There is no naturally occurring antibody to antigen D. However, if blood with rhesus antigen is
transfused to a person without it (rhesus negative), antibody d production is induced.
One problem in line with rhesus system arises in pregnancy.
As blood groups are genetically inherited, it is possible for a fetus to inherit a different blood form the
father different from that of the mother. Incase the fetus for example is rhesus positive while the mother is
rhesus negative. Towards birth, fragments of blood cells may cross from the fetus to the mother.
The mother responds by producing antibody d, in response to the rhesus antigen D on fetal red blood
cells.
These antibodies cross the placenta. As the buildup of rhesus antibodies, and as the problem only arises
towards birth, the concentrations of rhesus antibodies are rarely sufficient to cause any effect on the first
child. The production of antibodies may continue for some months and the second child again induces the
process. This causes build up of greater concentrations of the antibodies and are subjected to greater
influx of antibodies. This breakdown the fetal red blood cells. (haemolytic diseases of the new born).
This may be fatal to the fetus if several blood transfusions are not done during pregnancy.
The problem however can be solved if the fathers and mother blood groups are known before birth. In this
case the father is rhesus positive and mother is rhesus negative, the mother is injected with rhesus
antigens immediately after first birth in order to destroy fetal cell fragments containing rhesus antigen
before it can induce the mother’s system to produce rhesus antibodies.
The injected antibodies are soon broken down by the mother. In absence of subsequent antibodies,
subsequent fetuses are not affected.