The cardiovascular system
Blood circulates from the heart through the arteries to the capillaries to the veins and back to the heart.
Decrease in blood pressure as blood moves away from the heart.
Blood circulation
Blood flows away from the heart in arteries.
Arteries divide into smaller arterioles.
Blood flows through the smallest blood vessels
called capillaries.
Capillaries join to form small veins called venules.
These join to make veins which take blood back
to the heart
Direction of blood flow
The structure and function of arteries, capillaries and veins to include endothelium, central lumen, connective tissue, elastic fibres, smooth
muscle and valves.
The endothelium lining the central lumen of blood vessels is surrounded by layers of tissue.
Arteries have an outer layer of connective tissue containing elastic fibres and a middle layer containing smooth muscle with more elastic
fibres.
The elastic walls of the arteries stretch and recoil to accommodate the surge of blood after each contraction of the heart.
Arteries
Arteries carry blood away from the heart.
The diagram shows the structure of an artery
The outer layer of the artery wall is composed of connective tissue containing elastic
fibres.
The middle layer has smooth muscle and elastic fibres.
The central space of the artery through which blood flows is called the lumen.
The lumen in arteries is relatively small and is surrounded by a layer of cells called the
endothelium which lines the inside of the artery
outer layer of connective tissue
and elastic fibres
Middle layer of smooth
muscle and elastic fibres
endothelium
lumen
Pulse
The elastic walls of the arteries stretch as blood is forced through them when the heart contracts and recoil as the
heart relaxes – this can be felt as pulse in arteries near the skin surface.
The role of vasoconstriction and vasodilation in controlling blood flow.
The smooth muscle can contract or relax causing vasoconstriction or vasodilation to control
blood flow.
Vasoconstriction and vasodilation
Vasoconstriction = diameter of the lumen an artery
becoming smaller
Vasodilation = diameter of the lumen of an artery
increasing
Smooth muscles in the artery wall can contract causing vasoconstriction or relax causing vasodilation.
Vasoconstriction and vasodilation of arterioles (small arteries) allowing changes in blood flow depending on
the needs of different parts of the body.
For example during strenuous exercise, arterioles supplying the muscles dilate while those supplying the
organs of the digestive system constrict, resulting in blood being diverted to the muscles
Four layers are found in both arteries and veins:

central lumen
- blood flows through here
- much smaller in arteries
•
epithelium
made of epithelium cells, lines the lumen and reduces friction as the blood flows
through the vessel

middle layer
- middle layer of smooth muscle cells and elastic fibres
- much more strong and thick in arteries, allowing them to stretch and recoil to accommodate the surge
of blood after each contraction of the heart (creates the pulse)
- smooth muscle can contract or relax, causing vasoconstriction or vasodilation to control blood flow.

Outer layer
- outer layer consisting of connective tissue and some elastin fibres.
Veins have an outer layer of connective tissue containing elastic fibres but a much thinner muscular wall than
arteries.
Function of valves.
Veins
Veins (and venules) carry blood back to the heart.
Blood flows out of the capillaries into the smallest of
the veins – venules – which in turn reunite to
form larger veins.
The walls of veins are thinner than those of arteries as
blood pressure is far lower as it travels through
veins.
Because of this lower pressure, veins have valves to
prevent the back flow of blood.
Decrease in blood pressure as blood moves away from the heart.
Blood pressure
Blood pressure drops as blood flows through vessels
due to friction between blood and walls of vessels
Blood
pressure
Greatest drop in arterioles due to their large surface
area
Blood pressure low in veins - they have valves to
prevent backflow and contraction of muscles helps to
push blood along
Lowest BP is in the vena cava, the veins nearest the heart
Arteries arterioles capillaries venules veins
Capillaries allow exchange of substances with tissues.
Capillaries
Capillaries are tiny vessels where the exchange of
substances with the tissue occurs.
They also connect the arterioles to the venules.
Their walls are only one cell thick allowing
exchange of materials between the capillaries
and the cells.
Arteriole
Capillaries
(capillary
bed)
Venule
Capillary beds
Direction of
blood flow
arteriole
Lymphatic vessel
capillary
cells
venule
Blood plasma (except for the plasma proteins) is forced out of the capillaries at the arteriole
end to form the tissue fluid surrounding all body cells
Exchange of substances takes place between the tissue fluid and the cells
Tissue fluid returns to capillaries at the venule end of the capillary bed
Excess tissue fluid passes into the lymphatic vessels
Pressure filtration of fluids through capillary walls.
Tissue fluid supplies cells with glucose, oxygen and other substances.
Carbon dioxide and other metabolic wastes diffuse out of the cells and into the tissue fluid to be excreted.
Much of the tissue fluid returns to the blood.
Lymphatic vessels absorb excess tissue fluid and return the lymph fluid to the circulatory system
Direction of
blood flow
Lymphatic vessel
Pressure
filtration
venule
arteriole
Return of tissue
fluid to capillary
at venule end
Body cells
• Blood arriving at the arteriole end of the capillary bed is under higher pressure than blood in the capillaries.
• As blood is forced into the capillaries it undergoes pressure filtration – plasma apart from the plasma proteins is
forced out through the capillary walls and into the spaces between the body cells
• The fluid is now called tissue fluid.
• Glucose and oxygen from the tissue fluid pass into the body cells and carbon dioxide and other wastes produced by
the body cells diffuse into the tissue fluid
• Most of the tissue fluid returns to the capillary at the venule end of the capillary bed.
• Excess tissue fluid is absorbed by lymphatic vessels and eventually re-joins the blood.
Structure of the heart
Pulmonary artery
Aorta
Superior vena cava
Pulmonary vein
Right atrium
Inferior vena cava
Left atrium
Bicuspid valve
Tricuspid valve
Left ventricle
Right ventricle
Semi-lunar
valves
Tricuspid and bicuspid valves
are atrio-ventricular valves or
AV valves
Cardiac function and cardiac output.
Definition of cardiac output and its calculation.
The volume of blood pumped through each ventricle per minute is the cardiac output.
Cardiac output is determined by heart rate and stroke volume (CO = HR x SV).
The left and right ventricles pump the same volume of blood through the aorta and pulmonary artery.
The right and the left ventricle each pump the same volume of blood out of the heart when they contract.
The number of heart beats (contractions) per minute is called the heart rate.
The stroke volume is the volume of blood expelled by each ventricle on contracting.
The cardiac output is the volume of blood pumped out of a ventricle per minute.
cardiac output (CO) = heart rate (HR) X stroke volume (SV)
The cardiac cycle to include the functions atrial systole, ventricular systole, diastole.
Effect of pressure changes on atrio-ventricular (AV) and semi lunar (SL) valves.
During diastole blood returning to the atria flows into the ventricles.
Atrial systole transfers the remainder of the blood through the atrio-ventricular (AV) valves to the ventricles.
Ventricular systole closes the AV valves and pumps the blood out through the semi lunar (SL) valves to the aorta and pulmonary artery. In
diastole the higher pressure in the arteries closes the SL valve
Events in the cardiac cycle
During diastole blood enters the atria from the two vena cava
and the pulmonary veins
During diastole the higher pressure of blood in aorta and
pulmonary artery closes the semi-lunar valves
As the atria fill with blood, atrial pressure becomes greater
than in the ventricles and the AV valves are pushed open
Blood is pushed out of the ventricles into the aorta and
pulmonary arteries
The two atria contract (atrial systole) pushing blood into the
ventricles
Pressure of blood in the contracting ventricles is greater than
in the aorta and pulmonary artery forcing the SL valves open
The ventricles still in a relaxed state (ventricular diastole) fill
with blood, the semi-lunar valves are closed
Atrial systole is followed (about 0.1 seconds later) by
ventricular systole and closure of the AV valves
The structure and function of cardiac conducting system
Control of contraction and timing by cells of the sino-atrial node (SAN) and atrio-ventricular node (AVN).
The auto-rhythmic cells of the sino-atrial node (SAN) or pacemaker set the rate at which cardiac muscle cells contract.
The timing of cardiac cells contracting is controlled by the impulse from the SAN spreading through the atria and then travelling to
the atrio-ventricular node (AVN) and then through the ventricles.
These impulses generate currents that can be detected by an electrocardiogram (ECG).
Conducting system of the heart
An area in the wall of the right atrium called the pacemaker or
sino-atrial node (SAN) begins the electrical impulses that make
the heart muscle contract
Impulses begin in the SAN and spread through the two atria
making them contract (atrial systole)
Another area called the atrio-ventricular node (AVN) picks up
the impulses from the SAN and transmits them through a
network of fibres in the ventricles, making the two ventricles
contract (ventricular systole)
Electrocardiogram (ECG)
SA node generates electrical impulses which spread across the atrial walls
causing atrial systole
When they reach the atrio-ventricular node (AV node), at the base of the
atria, the AV node then sends the signal to contract down a bundle of
conducting fibres (bundle of His) in the central wall then upwards through
the ventricle walls via the purkinje fibres, causing the ventricles to contract
This electrical activity produces a pattern which can be
recorded as an electrocardiogram (ECG)
SAN sends impulses
through atria making
them contract
P wave caused by impulses from SAN
spreading through atria
QRS complex caused by impulses passing
through the ventricles
T wave results from electrical recovery of the
ventricles at the end of ventricular systole
1 heartbeat in 0.8 seconds
Heart rate = 60 divide by 0.8 = 75 beats per minute
0.8 seconds
AVN sends impulses
along fibres making
ventricles contract
Nervous and hormonal control of cardiac cycle
The heart beat originates in the heart itself but is regulated by both nervous and hormonal control.
The medulla regulates the rate of the SAN through the antagonistic action of the autonomic nervous system (ANS).
Sympathetic accelerator nerves release adrenaline (epinephrine) and slowing parasympathetic nerves release acetylcholine.
Effect of the nervous system and hormones on heart rate
Although the pacemaker initiates heart contractions, the rate of heartbeat is affected by the nervous system and the hormone adrenaline
from the adrenal glands.
Effect of the nervous system
The autonomic nervous system is that part of the nervous system that controls unconscious actions like breathing rate and heart rate.
The heart receives impulses from two nerves of the autonomic nervous system that are antagonistic (have opposite effects):
The sympathetic nerve sends impulses to the SAN that result in the heart rate increasing
The parasympathetic nerve (vagus nerve) sends impulses to the SAN that slow heart rate.
The control centre that regulates heart rate is found in a part of the brain called the medulla. The medulla sends impulses to the heart
through the sympathetic and parasympathetic nerves. Neurotransmitter substances are released by these nerves to cause the SAN to
increase or decrease heart rate. The sympathetic nerves release the neurotransmitter adrenaline (epinephrine), the parasympathetic nerves
release acetylcholine.
Effect of adrenaline
Adrenaline is a hormone released by the adrenal glands, e.g. in times of stress or during exercise.
This hormone causes the SAN to increase heart rate.
Blood pressure changes, in response to cardiac cycle, and its measurement.
Blood pressure changes in the aorta during the cardiac cycle.
Measurement of blood pressure using a sphygmomanometer.
An inflatable cuff stops blood flow and deflates gradually. The blood starts to flow (detected by a pulse) at systolic pressure. The
blood flows freely through the artery (and a pulse is not detected) at diastolic pressure.
A typical reading for a young adult is 120/70 mmHg.
Hypertension is a major risk factor for many diseases including coronary heart disease.
Blood Pressure
Blood pressure is the force caused by blood pushing against the vessels as it travels round your body. As the heart goes
through systole and diastole cycles, the blood pressure rises to a maximum and falls to a minimum. Blood pressure is
measured in millimetres of mercury (mmHg) using a sphygmomanometer.
Blood pressure results from contraction of the ventricles
During ventricular systole, blood pressure in arteries rises to a maximum and during diastole it falls to a minimum
Blood
pressure
Pressure at ventricular systole
Pressure at diastole
time
Measuring blood pressure
Blood pressure is measured using a sphygmomanometer
It is expressed as the systolic pressure over the diastolic, e.g. 120/80
Steps in measuring blood pressure
1. Cuff of sphygmomanometer is inflated until the
pressure it exerts stops blood flow in the arm artery
2. Cuff is deflated until the pressure is less than in the
artery – blood begins to flow through the artery again (this
can be heard using a stethoscope) and a pulse can be felt.
The pressure recorded at this point is the systolic pressure.
3. More air is released from the cuff until the sound of
spurting blood is not heard with the stethoscope and a
pulse can no longer be felt.
The pressure measured at this point is the diastolic blood
pressure.
Typical blood pressure for a healthy young adult is 120/70
The graph shows changes in average blood pressure as blood flows through different
blood vessels
Blood
pressure
Arteries arterioles capillaries venules veins
Little drop in pressure as blood flows through arteries because they have wide space inside
and elastic walls that stretch and so they don’t offer a great deal of resistance to blood flow
The greatest drop in blood pressure occurs as blood flows through the arterioles because
there are many of them and they have a small diameter so they have a large surface area drop in pressure occurs because of friction between the blood and the walls of the blood
vessels - since the walls of the arterioles have a large surface area, this increases the friction
Blood pressure is low in the veins - they have valves to prevent backflow of blood
Blood pressure is greatest in the aorta and lowest in the vena cava.
Hypertension (high blood pressure)
Hypertension is prolonged elevation of blood pressure
Hypertension is a major risk factor for stroke and coronary heart disease
Risk factors for hypertension
•
•
•
•
•
Being overweight
Lack of exercise
High fat (especially animal fat) diet
Too much salt
Stress
Cholesterol synthesis and its function in the cell membrane and in steroid synthesis.
Most cholesterol is synthesised by the liver from saturated fats in the diet. Cholesterol is a component of cell membranes and a precursor
for steroid synthesis.
Roles of high density lipoproteins (HDL) and low density lipoproteins (LDL).
HDL transports excess cholesterol from the body cells to the liver for elimination. This prevents accumulation of cholesterol in the blood.
LDL transports cholesterol to body cells. Most cells have LDL receptors that take LDL into the cell where it releases cholesterol.
The Role of Cholesterol
Cholesterol is a lipid which is a major component of all cell membranes and the precursor for the synthesis of all steroid
hormones.
Cholesterol is taken in from the diet but is mainly synthesised in the liver (from saturated fat in the diet). The liver is also
responsible for the elimination of cholesterol, as a component of bile.
There are two important types of cholesterol-carrying
proteins in the blood;
- low-density lipoproteins (LDL) or ‘bad’ cholesterol
- high-density lipoproteins (HDL) or ‘good’ cholesterol.
Type of
Cholesterol
LDL
Deliver cholesterol to body cells for
membrane and hormone synthesis via
LDL receptors controlled by negative
feedback.
HDL
Transports excess cholesterol from
body cells to liver for elimination.
Removal of cholesterol from
atheromas.
The summary table outlines the main differences
between these proteins in the body;
Most body cells make LDL receptors that become
inserted into their cell membranes. When an LDL
molecule transporting cholesterol attaches to a receptor,
the cell engulfs the LDL cholesterol and the cholesterol is
released to be used by the cell.
Function in Body
CHD risk
(ratio of
LDL:HDL)
Increased if
high levels
of LDL in
blood
compared
to HDL
Lowered if
high levels
of HDL in
blood
compared
to LDL
Process of atherosclerosis, its effect on arteries and blood pressure and its link to cardiovascular diseases (CVD). Atherosclerosis is the
accumulation of fatty material (consisting mainly of cholesterol), fibrous material and calcium forming an atheroma or plaque beneath the
endothelium.
As the atheroma grows the artery thickens and loses its elasticity.
The diameter of the artery becomes reduced and blood flow becomes restricted resulting in increased blood pressure. Atherosclerosis is the
root cause of various cardio vascular diseases including angina, heart attack, stroke and peripheral vascular disease.
Atherosclerosis
When a body cell has enough cholesterol, synthesis of new
LDL receptors is inhibited. Less LDL cholesterol is then
absorbed by the cells. Instead some is absorbed by
endothelium cells lining an artery and deposited in an
atheroma in the artery wall. This can happen when:
A person’s regular diet is high in saturated fat
A person suffers from familial hypercholesterolaemia
Atheromas build up over years from deposits of fatty cholesterol, fibrous material, calcium and more cholesterol as
shown in the diagram:
The main problems which the presence of atheromas cause;
Narrowing of the artery’s lumen
Restriction of blood flow
Loss of the artery’s elasticity
Increase in blood pressure
Atherosclerosis is the cause of various cardio vascular diseases including angina, heart attack, stroke and peripheral vascular
disease.
LDL receptors, negative feedback control and atheroma formation. Ratios of HDL to LDL in maintaining health, the benefits of physical activity and a
low fat diet. Reducing blood cholesterol through prescribed medications.
A higher ratio of HDL to LDL will result in lower blood cholesterol and a reduced chance of atherosclerosis.
Regular physical activity tends to raise HDL levels, dietary changes aim to reduce the levels of total fat in the diet and to replace saturated with
unsaturated fats. Drugs such as statins reduce blood cholesterol by inhibiting the synthesis of cholesterol by liver cells.
Once a cell has enough cholesterol a negative feedback system inhibits the synthesis of new LDL receptors and LDL circulates
in the blood where it may deposit cholesterol in the arteries forming atheromas
High density lipoproteins (HDL)
Some excess cholesterol is transported by high density lipoproteins (HDL). This prevents a high level of cholesterol from
accumulating in the bloodstream. HDL is not taken into the artery walls and does not contribute to atherosclerosis.
Lipoproteins and cardiovascular disease
Normally HDL molecules carry about 20 – 30 % of cholesterol and LDL about 60 – 70 %.
Higher HDL : LDL ratios reduce blood cholesterol and the chance of atherosclerosis and cardiovascular disease (CVD), the
opposite is true of low HDL : LDL ratios.
The concentration of HDL is normally higher and the risk of CVD lower for those who exercise regularly.
HDL levels may be increased by:


Reducing dietary fat
Replacing saturated fat with unsaturated fat
Statins
Statins are drugs that reduce cholesterol by inhibiting an enzyme needed for synthesis of cholesterol in the liver.
Thrombosis— Events leading to a myocardial
infarction (MI) or stroke.
Endothelium damage, clotting factors and the
role of prothrombin, thrombin, fibrinogen and
fibrin.
Atheromas may rupture damaging the
endothelium.
The damage releases clotting factors that activate
a cascade of reactions resulting in the conversion
of the enzyme prothrombin to its active form
thrombin.
Thrombin then causes molecules of the plasma
protein fibrinogen to form threads of fibrin.
The fibrin threads form a meshwork that clots the
blood, seals the wound and provides a scaffold
for the formation of scar tissue.
The formation of a clot (thrombus) is referred to
as thrombosis.
Formation of blood clots
It occurs to prevent loss of blood from the wound
Presence of damaged cells
leads to release of blood
clotting factors
Clotting factors cause the
enzyme prothrombin in the
blood to be converted to its
active form thrombin
Thrombin causes conversion
of the soluble plasma protein
fibrinogen into threads of
the insoluble protein fibrin
Fibrin fibres become interwoven
into a mesh that platelets stick to
forming blood clots which seal
the wound
Thrombus formation and effects of an embolus.
In some cases a thrombus may break loose forming an embolus and travel through the bloodstream until it blocks a blood
vessel.
A thrombosis in a coronary artery may lead to a heart attack (MI). A thrombosis in an artery in the brain may lead to a
stroke. Cells are deprived of oxygen leading to death of the tissues
Thrombosis
The plaque from atherosclerosis provides a roughened
surface that allows blood platelets to accumulate. The
platelets release clotting factors, which may result in the
formation of a blood clot or thrombus at the site of plaque
formation. If the thrombus grows large enough to obstruct
the artery completely,
a thrombosis occurs. For example, a coronary thrombosis
closes off a blood vessel in the heart.
Embolus
If the thrombus breaks loose from the site of formation (embolus), it travels along the blood stream until it reaches and
blocks an artery too narrow to allow it to get through.
If a thrombosis occurs in a coronary artery, the part of the heart supplied by the artery will be deprived of oxygen and
die – a heart attack or myocardial infarction (MI) results
An thrombosis occurring in an artery of the brain results in a stroke (cerebrovascular accident – CVA), the severity of
which depends on the area of brain tissue destroyed
•A blood clot formation = thrombus
•A large enough thrombus to completely
block an artery = thrombosis
•Embolus = thrombus that breaks loose
from site of formation
•If an embolus gets stuck in a narrow artery
esp. coronary, heart attack occurs
•Embolism in an artery of the
brain = stroke
Causes of peripheral vascular disorders including narrowing of arteries due to atherosclerosis, deep vein thrombosis (DVT) and
pulmonary embolism due to blood clots.
Peripheral vascular disease is narrowing of the arteries due to atherosclerosis of arteries other than those of the heart or brain.
The arteries to the legs are most commonly affected. Pain is experienced in the leg muscles due to a limited supply of oxygen. A
DVT is a blood clot that forms in a deep vein most commonly in the leg, and can break off and result in a pulmonary embolism.
Peripheral Vascular Disorders (PVD
Peripheral arteries are those OTHER THAN the aorta, coronary and carotid
arteries but most commonly affects vessels in the legs.
Atherosclerosis affects these arteries in much the same way and narrows
the central cavity as shown
Deep vein thrombosis
More commonly referred to as DVT, deep vein thrombosis is a common example of PVD which many people
associate with long haul flights. A thrombus forms in a vein (commonly in the calf of the lower leg) causing restricted
blood flow and symptoms which include swelling and pain due to the blockage.
Pulmonary embolism
A clot (now called an embolus) breaks free and travels to the lungs where it blocks arterial branches of the pulmonary
artery causing chest pains and breathing difficulties and untreated can lead to death
Genetic screening of familial hypercholesterolaemia (FH) and its treatments.
Familial hypercholesterolaemia (FH) due to an autosomal dominant gene predisposes individuals to developing high levels of
cholesterol. FH genes cause a reduction in the number of LDL receptors or an altered receptor structure. Genetic testing can
determine if the FH gene has been inherited and it can be treated with lifestyle modification and drugs.
Familial hypercholesterolaemia (FH)
FH is caused by an inherited autosomal dominant gene which decreases the number of LDL receptors present in the
cell membranes or changes their structures so that they do not function properly.
This means that cholesterol cannot be unloaded into cells properly by LDL resulting in extremely high levels of
cholesterol in the bloodstream which, if left untreated, the individual will suffer from cardiovascular problems at a
young age.
The condition can be screened for by a genetic test and treated through a modified lifestyle and use of medications such as statins.
Blood glucose levels
Chronic elevated blood glucose levels leads to atherosclerosis and blood vessel damage.
Chronic elevation of blood glucose levels leads to the endothelium cells taking in more glucose than normal damaging the
blood vessels. Atherosclerosis may develop leading to cardio vascular disease, stroke or peripheral vascular disease. Small
blood vessels damaged by elevated glucose levels may result in haemorrhage of blood vessels in the retina, renal failure or
peripheral nerve dysfunction.
Glucose and Microvascular Disease
If a person is suffering from untreated diabetes, their blood glucose levels may increase to an unusually
high level i.e. 30 mmol/l. This can cause severe damage to the endothelial cells which line the blood vessel
as they will absorb too much glucose causing their basement membrane to thicken and weaken, leaving
the vessel susceptible to haemorrhaging (burst and bleed).
Atherosclerosis can develop leading to increased risk of cardio-vascular disease, stroke or peripheral
vascular disease.
Microvascular disease (damage to small blood vessels) can cause severe damage to the retina, kidneys and
nerves therefore it is important to ensure that the blood glucose level is maintained within a narrow range
to avoid such internal damage.
Cell receptors and the role of hormones in negative feedback control of blood glucose through insulin, glucagon and adrenaline
(epinephrine).
Pancreatic receptors respond to high blood glucose levels by causing secretion of insulin. Insulin activates the conversion of glucose
to glycogen in the liver decreasing blood glucose concentration.
Control of blood glucose
Blood glucose is level is controlled by a negative feedback mechanism involving the hormones insulin and glucagon
Increase in blood glucose
When the blood glucose increases after eating food:
Increase in blood glucose
Increase detected by the receptor
cells in pancreas
Pancreas cells produce insulin
Insulin causes glucose to be changed
glycogen lowering blood glucose back
to normal
Insulin picked up by insulin receptors on
liver cells
Insulin transported in blood to the LIVER
Increase in blood glucose, e.g. after eating a meal
1. Detected by receptor cells in the pancreas
2. Receptor cells produce insulin
3. Insulin transported in the blood to the liver
4. Insulin picked up by insulin receptors on liver cells
5. Excess glucose is absorbed by liver cells and an enzyme is activated that converts
glucose to glycogen
6. Blood glucose decreases to normal level
Pancreatic receptors respond to low blood glucose levels by producing glucagon. Glucagon activates the conversion
of glycogen to glucose in the liver increasing blood glucose level.
Decrease in blood glucose
e.g. after fasting
Decrease in blood glucose
Glucagon causes glycogen to be
changed glucose increasing blood
glucose level
Decrease detected by the receptor
cells in pancreas
Glucagon picked up by receptors on
liver cells
Pancreas cells produce glucagon
Glucagon transported in blood to the LIVER
Decrease in blood glucose, e.g. after fasting
1. Decrease is detected by receptor cells in the pancreas
2. Pancreas cells produce glucagon
3. Glucagon is transported in the blood to the liver
4. Glucagon binds to receptors on liver cells
5. Liver cells convert glycogen to glucose
6. Blood glucose level increases back to normal level
During exercise and fight or flight responses glucose levels are raised by adrenaline (epinephrine) released from the
adrenal glands stimulating glucagon secretion and inhibiting insulin secretion.
Adrenaline (epinephrine)
During exercise or stress, increased levels of the hormone adrenaline (also called epinephrine) are
released from the adrenal glands.
Adrenaline overrides the normal mechanism for control of glucose by inhibiting release of insulin and
causing the conversion of glycogen to glucose.
This ensures that extra glucose is available to the muscles to contract and carry out the “fight or flight”
response.
Diagnosis, treatments and role of insulin in type 1 and type 2 diabetes
Vascular disease can be a chronic complication of diabetes. Type 1 diabetes usually occurs in childhood. Type 2 diabetes or adult onset diabetes
typically develops later in life and occurs mainly in overweight individuals. A person with type 1 diabetes is unable to produce insulin and can
be treated with regular doses of insulin. In type 2 diabetes individuals produce insulin but their cells are less sensitive to it. This insulin
resistance is linked to a decrease in the number of insulin receptors in the liver leading to a failure to convert glucose to glycogen. In both types
of diabetes individual blood glucose levels will rise rapidly after a meal and the kidneys are unable to cope resulting in glucose being lost in the
urine. Testing urine for glucose is often used as an indicator of diabetes.
Diabetes
People with this condition are unable to control blood sugar levels.
There are two types of diabetes; type 1 diabetes and type 2 diabetes
Feature
Type 1 diabetes
Type 2 diabetes
Stage at which condition normally occurs
childhood
Adult (also known as adult onset diabetes)
Associated with overweight/obesity
no
yes
Reason for the condition
Pancreatic cells unable to
produce insulin
Liver cells are less sensitive to insulin
(insulin resistant) due to decrease in
number of insulin receptors so glucose does
not enter cells to be changed to glycogen
Presence of glucose in urine indicates condition
yes
yes
Treatment
Insulin injections and
careful diet
Diet, exercise, weight loss (sometimes
insulin)
The glucose tolerance test is used to diagnose diabetes. The blood glucose levels of the individual are measured after
fasting and two hours after drinking 250–300 ml of glucose solution.
Glucose tolerance test
The blood glucose levels of the individual are measured after fasting and subsequently every two hours after drinking
250-300ml of glucose solution. The results are recorded as a glucose tolerance curve and analysed for diagnosis.
Diabetes is indicated by:
• A high level of blood glucose after fasting
• Glucose level continuing to rise for a long time after
ingesting glucose and failing to fall back to its initial
level
Obesity linked to cardiovascular disease and diabetes.
Definition and characterisation of obesity. Body fat, body density measurements and BMI calculations. Role of exercise in reducing CVD.
Obesity is a major risk factor for cardiovascular disease and type 2 diabetes. Obesity is characterised by excess body fat in relation to lean body
tissue (muscle). A body mass index (weight divided by height squared) greater than 30 is used to indicate obesity. Accurate measurement of
body fat requires the measurement of body density.
Obesity
Obesity is a condition in which excess fat has accumulated in the body to the extent that it begins to have an
adverse effect on health. It is largely a product of our modern 'Western' way of life and is rarely found in the
developing world however genetic, psychological and metabolic factors may also be contributors.
A person is generally classified as obese if they have an excess of body fat compared to their lean body tissues,
such as muscle.
The degree of obesity can be estimated by calculating the Body Mass Index (BMI) as:
BMI = mass (kg)
(height (m))2
BMI values can be used to assign people to body condition categories and associated health risks as shown below:
BMI range
Problems
< 18.5
18.5 - 24.9
25 - 29.9
30 - 40
40+
Category
underweight
normal
overweight
obese
very obese
Risk of Associated Health
Increased
Normal
Increased
Greatly Increased
Very Greatly Increased
The BMI method is not always an accurate measurement of body fat. For example, a bodybuilder would wrongly be
categorised as obese using this method and so there are some limitations to consider.
To ensure body fat is measured accurately, a measurement of body density is required using any one of the following methods:
densitometry, skin-fold callipers or waist/hip ratio.
Diet and exercise
Obesity is linked to high fat diets and a decrease in physical activity. The energy intake in the diet should limit fats
and free sugars as fats have a high calorific value per gram and free sugars require no metabolic energy to be
expended in their digestion. Exercise increases energy expenditure and preserves lean tissue. Exercise can help
to reduce risk factors for CVD by keeping weight under control, minimising stress, reducing hypertension and
improving HDL blood lipid profiles.