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Unit 2 Physiology and Health
Summary Notes
Physiology and health
Reproduction
Testes
 Gametes are produced from germline cells
 Testes produce sperm in the seminiferous
tubules
(Seminiferous tubules = tiny tubules in the
testes)
Seminiferous tubules
 Link up into coiled tubes that connect to the sperm duct
 Sperm leave the testis through the sperm duct
Interstitial cells
 Are found between the
seminiferous tubules
 Produce testosterone = which
into the bloodstream
passes
Motility of sperm
 Sperm are said to be motile = this
motility requires a fluid and a
source
of energy
 Fertilisation is dependent on this
motility as the sperm must be able to make their way up into the uterus, along the oviducts to a
potential egg
Prostate gland and seminal vesicles
Secrete fluids that maintain the mobility and viability of the sperm
Seminal vesicles
 Secrete a liquid high in fructose = this sugar provides the sperm with the energy needed for
motility after ejaculation
 This liquid also contains hormone-like compounds that stimulate contractions of the female
reproductive tract = these movements help the sperm to reach the oviduct faster than swimming
along would
Prostate gland
 Secretes a thin lubricating liquid that contains enzymes = these enzymes maintains the optimum
viscosity of the fluid which allows the motility of the sperm
Semen
 Semen = the name given to the mix of all of these liquids = milky liquid released in ejaculation
Ovaries
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Female gamete eggs (ova) are
produced in the ovaries by germline
cells
Contain immature ova in various stages of
development
Each ovum is surrounded by a follicle which
o protects the developing ovum
o secretes hormones (oestrogen)
Once the ova has matured it is released (ovulation)
into the oviduct where it may be fertilised by sperm
to produce a zygote
The follicle then develops into a corpus luteum = this
structure releases the hormone progesterone
Hormonal control of reproduction
Hormones control the onset of puberty, sperm production and the menstrual cycle
Hormonal onset of puberty
 The hypothalamus releases a hormone that stimulates the pituitary gland to release 2 hormones
1. FSH = follicle-stimulating hormone
2. In men = ICSH = interstitial cell-stimulating hormone or in women = LH = luteinising hormone
These hormones which are released at puberty
trigger
 Sperm production in men

Menstrual cycle in women
Hormonal control of sperm production
 FSH and ICSH are produced by the
pituitary and travel in the bloodstream to
the testes
 FSH = promotes sperm production in the
seminiferous tubules
 ICSH = promotes interstitial cells to produce testosterone
 Testosterone also = stimulates sperm production and activates the prostate gland and seminal
vesicles to produce secretions (see previous page!)
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Negative feedback control of testosterone by FSH and ICSH
As the concentration of testosterone increases it reaches a level where it starts to inhibit the
secretion of FSH and ICSH
The decrease in FSH and ICSH will lead to a decrease in testosterone
This will then allow the pituitary gland to produce FSH and ICSH again = which will then stimulate
production of testosterone
This self-regulating mechanism is known as negative feedback
Hormonal control of the menstrual cycle
Menstrual cycle
 Lasts for ~28days (this can vary from woman to woman)
 The first day of menstruation is regarded as day one of the cycle
 Every cycle is continuous with the cycle before and the cycle after
 Has 2 phases
1. Follicular phase
2. Luteal phase
Follicular phase
 Is the first half of the cycle
 FSH from the pituitary stimulates
o Development of a follicle
o The production of oestrogen by the follicle
 Oestrogen stimulates proliferation of the endometrium = preparing it for implantation
 Oestrogen also affects the consistency of cervical mucus = making it more easily penetrated by
sperm
 This high concentration of oestrogen (peak levels) stimulates a surge in the secretion of LH (by
the pituitary)
 This surge of LH causes ovulation = release of the ovum
 Which is now moved slowly along the oviduct
 During a period ~3-4 in the oviduct is where fertilisation may take place
 Fertilisation is when the nuclei of the gametes fuse to produce a zygote
Luteal phase
 Is the second half of the cycle
 LH stimulates the follicle (which remains inside the ovary after ovulation) to become the corpus
luteum = this is a gland-like structure that secretes progesterone and oestrogen
 Progesterone concentration will increase and promotes further development and vascularisation
(increase in blood vessels) of the endometrium = becomes thick and spongy
 This prepares the endometrium to receive a blastocyst (formed after repeated rounds of mitosis
of the zygote) if fertilisation occurs
 The high concentrations of oestrogen and progesterone inhibit the production of FSH and LH by
the pituitary gland = this means that no new follicles will develop at this time
o Negative feedback
 If fertilisation doesn’t occur the lack of LH leads to the degeneration of the corpus luteum by
~day 22
 This leads to a rapid drop in progesterone (and oestrogen)
 By day 28 the progesterone (and oestrogen) levels are at such a low concentration that the
endometrium is no longer maintained and menstruation begins = loss of the inner layer of
endometrium, this is accompanied by a small volume of blood
 This continues for a few days and the cycle starts again
Influence of pituitary hormones on the ovaries
 FSH and LH are produced by the pituitary gland and travel in the bloodstream to the ovaries
 FSH = stimulates the development and maturation of each follicle and stimulates tissue in the
ovary to secrete the sex hormone oestrogen
 LH = stimulates ovulation and it also stimulates the corpus luteum to secrete the sex hormone
progesterone
 Oestrogen and progesterone are called ovarian hormones
Influence of ovarian hormones
on uterus and pituitary gland
Oestrogen
 Stimulates proliferation (cell division) of the lining of the uterus = endometrium
 This allows the repair of the endometrium after menstruation which would then allow
implantation of a blastocyst
 It also stimulates the secretion of LH by the pituitary gland
Progesterone
 Promotes further development and vascularisation of the endometrium = endometrium becomes a
spongy layer which has lots of blood vessels
 This ready’s the endometrium for implantation of the blastocyst
 It also inhibits the secretion of FSH and LH (by pituitary gland)
Biology of controlling fertility
Is used in the design of treatments for infertility and producing contraception
Fertile periods
 Men are continuously fertile
Due to the negative feedback effect of testosterone
This maintains a relatively constant concentration of FSH and ICSH in the bloodstream = which
means a fairly constant concentration of testosterone is secreted and thus sperm produced
 Women show cyclical fertility
The interaction of pituitary and ovarian hormones results in a period of fertility which is restricted
to ~1-2 days immediately after ovulation
Calculation of the fertile period
Temperature
 During the menstrual cycle menstruation and ovulation are separated by ~ 2 weeks
 ~1 day after ovulation (LH surge that causes the egg to be released) progesterone produced causes
in increase in body temperature of ~0.2-0.5°C
 This increase in temperature continues for the rest of the luteal phase
 The period of fertility only lasts for ~1-2 days after ovulation
 After this the infertile phase is resumed
 After the 3rd daily recording of the higher temperature = the unfertilised egg will have
disintegrated
Mucus
 Cervical mucus is secreted into the vagina during the fertile period = it is thin and watery = this
allows the sperm easy access to the uterus
 After ovulation the mucus gradually increases in viscosity (thickness) = this is due to the action of
progesterone
 This indicates the return to the infertile phase
Use of indicators
 Women can use body temperature and viscosity of mucus as an indicator to calculate her fertile
period = this is useful for couples who are trying to get pregnant
 If the couple can identify the fertile period and have sex within this period it is more likely to result
in fertilisation
Treatments for infertility
Stimulating ovulation
 Some women may not ovulate due to an underlying factor
 e.g. the pituitary gland fails to produce enough FSH or LH
 In these cases ovulation can be stimulated by drugs that prevent the negative feedback effect of
oestrogen on FSH secretion (during the luteal phase) or drugs that mimic the action of FSH and LH
 Sometimes these drugs can cause ‘super-ovulation’ = this can lead to multiple births
 These drugs can also be used to promote the release of eggs that can then be used in IVF
Artificial insemination
 Natural insemination = introduction of semen into the female reproductive tract by sexual
intercourse
 Artificial insemination = introduction of semen into the female reproductive tract by some other
means e.g. sperm in a syringe
 This can be used if a man has a low sperm count = several samples of semen can be collected over
some time and preserved by being frozen
 The samples can then be defrosted and combined for release together into his partners
reproductive tract
 This is done during her fertile period
 This can also be used to insert semen from a sperm donor (e.g. women who don’t have a partner or
who’s partner is sterile)
ICSI = intra-cytoplasmic sperm injection
 Used if mature sperm are defective or very
low in number
 The head of the sperm is drawn into a needle
and injected directly into the egg to achieve
fertilisation
 Is quite commonly used in IVF
In vitro fertilisation = IVF
 Can be used if a woman has a blocked oviduct
so is unable to become pregnant without help
 The woman is given hormone treatment = this
stimulates multiple ovulation
 These eggs are then removed surgically using
a special syringe
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The eggs are then mixed with sperm in a culture dish (can also use ICSI) and fertilisation takes
place
The zygotes (fertilised eggs) are then incubated in nutrient medium for 2-3 days = this is to allow
cell division = when it is ~8 or more cells it can then be used
2 or 3 embryos are picked and inserted into the woman’s uterus (via the vagina) for implantation
The hormone treatment will also have made the endometrium ready for implantation
The remaining embryos are frozen and stored = can be used in a 2nd attempt
Before embryos are implanted pre-implantation genetic screening (PGS) is done
o Checks each embryo for single gene mutations and common chromosomal abnormalities
o This is a non-specific broad screening
 Pre-implantation genetic diagnosis (PGD) can also be carried out
o Specific screening that can be used to check for a known chromosomal abnormality or gene
mutation
Ethics
 Many people strongly agree with PGS and PGD as people who are at high risk of having a child with a
genetic disorder are reassured that they can have a child who will not suffer from the specific
genetic disorder
 Many of these people without IVF would simply choose to not have children due to the risk to the
child
 Some people argue that this doesn’t only help these specific families but society on the whole as it
reduces the frequency of these mutations in the gene pool
 Other people disagree with PGS and PGD as they believe it is morally wrong to interfere with the
process of conception by making it selective
 These people argue that these procedures are the start of eugenics = humans selectively breeding to
‘improve quality’
 They also argue that this is the doorway to ‘designer’ children = where people would start to select
characteristics and not just select for health e.g. genetic defects
Contraception
Is when pregnancy/conception is prevented
Physical methods of contraception
Barrier methods
Physically blocks sperm
 Condom
 Diaphragm
o Dome shaped rubber cap inserted into the
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woman’s vagina
o This blocks the cervix
o Inserted before sex
Cervical cap
o Rubber structure that fits tightly round the cervix
o Can be left in for a few days
Intra-uterine devices (IUD)
 IUD is a T-shaped structure fitted into the uterus to prevent the implantation of a blastocyst into
the endometrium
 Lasts months or even years
Sterilisation procedures
 Vasectomy
o Doctors cut and tie the two sperm ducts
o This prevents sperm being released during sex
o After a man has a vasectomy the sperm that are produced but can’t travel down the sperm
ducts are destroyed by phagocytes
 Tubal ligation
o Doctors cut and tie the two oviducts
o This prevents eggs meeting sperm
 Sterilisation is highly effective but is usually irreversible
Chemical methods of contraception
Chemical contraceptives are based on combinations of synthetic
hormones that
 Mimic negative feedback preventing the release of FSH/LH =
combination pill
 Prevent implantation = ‘morning after pill’
 Cause thickening of cervical mucus = ‘mini-pill’
Combination pill
 Pills containing a combination of hormones
 Oral contraceptive pills usually contain synthetic progesterone and
synthetic oestrogen
 Usually a pill is taken every day for 3 week from the final day of
the previous menstrual period
 This increases the concentration of progesterone and oestrogen =
causing negative feedback
 This means that FSH and LH production by the pituitary is inhibited
 This low concentration of FSH and LH means that follicle
maturation is inhibited and ovulation doesn’t occur
 During the 4th week of no pills the oestrogen and progesterone concentrations fall and allow
menstruation to occur (e.g. bleeding)
Mini-pill
 Only contain synthetic progesterone and not oestrogen
 Cause thickening of the cervical mucus
 This reduces the chance of the sperm ever reaching the uterus
‘Morning after’ pills
 This is also known as an emergency hormonal contraception pill
 Usually contain higher does of progesterone and oestrogen
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Taken after unprotected sex = ideally should be taken soon, however can be taken up to 72 hours
after
These pills prevent implantation from occurring if fertilisation has occurred
Ante-natal
 A variety of techniques can be used to monitor the health of the mother and developing fetus
 Also known as prenatal
 Identifies risk of disorder so that further tests and prenatal diagnosis can be offered
 Include blood pressure, blood types, ultrasound, biochemical tests, diagnostic testing as well as
routine blood and urine tests
Ultra-sound imaging
 Ultra-sound scanner used
 Picks up high-frequency sounds that bounce off the fetus
which are then converted to an ultrasound image on a
computer screen
 A dating scan at 8-14 weeks determines the stage of
pregnancy and due date
 An anomaly scan at 18-20 weeks may detect serious physical
problems
 Dating scans are used with tests for marker chemicals which
vary normally during pregnancy (measuring a substance at the
wrong time could lead to a false positive result – see later)
Biochemical tests
 Detect the normal physiological changes of pregnancy
 Medical conditions can be detected by a range of marker
chemicals that indicate a condition but need not necessarily be
part of the condition
 HCG = human chorionic gonadotrophin
o (one of it’s jobs is to stimulate progesterone production = this thickens the endometrium and
makes it rich in blood vessels = extremely important for a growing fetus)
o Detection of HCG in blood and urine is used in early pregnancy tests
 A chemical marker AFP is used in assessing the risk of Down’s syndrome, the mother’s age is also
taken into account
False positives and false negatives
 Some chemical markers vary in concentration depending on the time in the pregnancy measuring the
substance at the wrong time could lead to a false positive result
HCG concentration
 Is high during weeks 6-10
 It then decreases
 However in Down’s syndrome it remains at a high concentration
 If HCG was measured at 10 weeks this result would mean nothing as normal and Down’s syndrome
pregnancy would both be high
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If a marker is measured at the wrong time in a pregnancy this can lead to a false positive result =
would show the fetus to have a condition when it doesn’t
Measuring a marker at the wrong time can also give a false negative = marker measured and found to
be low when during a normal pregnancy it is also low = suggest a fetus doesn’t have a condition when
it actually does
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To avoid false positives and negatives chemical testing is used carefully in conjunction with scans so
as to date the pregnancy and do chemical test at the correct times
Diagnostic testing
 Is a screening test that is used to detect signs and symptoms of a specific condition or disorder
 If signs are found then the probability of the fetus having the condition is assessed as a degree of
risk
 However a diagnostic test tells us whether or not the fetus has the condition without doubt
 Diagnostic tests are offered to pregnant woman if
o Screening test has indicated a potential problem
o Family history of genetic disorder
o Belongs to t high-risk category e.g. women over 35 have higher chance of fetus having Down’s
syndrome
 In deciding to proceed with these tests, the element of risk will be assessed as will the decisions the
individuals concerned are likely to make if a test is positive
 Diagnostic tests use the fetus’s karyotype = picture of chromosome complement (chromosomes
arranged in their matching pairs)
 Examples amniocentesis and chorionic villus sampling (CVS)
Amniocentesis
 Done at ~14-16 weeks
 A needle removes a little amniotic fluid containing fetal cells
 These cells are then cultured, stained and examined
 Chromosome complement is photographed
 The chromosomes are then arranged in their matching pairs to give
the karyotype
 Allows chromosomal abnormalities to be detected e.g. extra
chromosome 21 = Down’s syndrome
 Some people may then decide to terminate the pregnancy
 Small risk associated with miscarriage = ~ 1 in 100 women
Chorionic villus sampling (CVS)
 One advantage is that it can be done
as early as 8 weeks = earlier than amniocentesis
 Fine tube is inserted through the vagina
 Takes a tiny sample of placental cells
 Karyotyping can be performed on the fetal cells immediately
 If there was something genetically wrong with the fetus many people find a termination at this stage
less traumatic than at ~14-16 weeks with the amniocentesis
 However there is a slightly higher risk of miscarriages
Rhesus antibody testing
 Generally mother show no immune response to their fetus
 If a Rhesus-negative woman is pregnant with a Rhesus-positive fetus this can cause huge problems
 The Rhesus antigens on the fetus’s red blood cells are recognised as foreign by the mother’s immune
system if the cells come into contact e.g. during birth = the mother is said to have been ‘sensitised’
 The mother would produce antibodies against the antigen and retain some of the immune cells
involved as memory cells
 If the woman was to get pregnant with another Rhesus-positive fetus she would mount an immune
response against the antigen = the memory cells would produce antibodies which could cross the
placenta and attack the fetus
 After the first birth the mother is given antiRhesus antibodies = these destroy any Rhesus
antigens left behind by the baby before the mothers
immune system has time to respond
 If a woman is Rhesus-negative it is detected very
early in the pregnancy so that these measures can
be put in place
Post-natal (after birth)
Diagnostic testing for metabolic disorders
Test for PKU = phenylketonuria
 Gene mutation that leads to the incorrect production
of an enzyme in a metabolic pathway being produced
 Individuals who suffer from PKU cannot metabolise phenylalanine into tyrosine
 Suffers placed on a restricted diet = low in phenylalanine
 This is called an inborn error of metabolism
Genetic screening and pedigree charts
 Pedigree charts are also known as family trees
 Shows the pattern of inheritance
 Gives information about a specific characteristic
 Most of the members genotypes can be deduced from the phenotypes
 Genetic counsellors can construct pedigree charts and counsel families who are worried about the
risk/possibility of passing on an inherited genetic disorder (that exists in their family) to their
children
Patterns of inheritance
Autosomal recessive inheritance
 Autosomes = chromosomes that are not sex
chromosomes
 Trait expressed relatively rarely
 Trait skips generation
 Trait is expressed in some of the offspring
of consanguineous marriage e.g. cousins
 Males and females are equally affected
 Geneticist can then deduce that
o Sufferes of the trait are homozygous
recessive
o Non-sufferers are either homozygous
dominant or heterozygous
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ex = cystic fibrosis
Autosomal dominant inheritance
 Trait expressed in every generation
 Each person with the condition has a parent with
the condition
 If a branch of the family tree doesn’t have the
condition it doesn’t reappear in future
generations
 Males and females are equally affected
 Geneticist can then deduce that
o Non-sufferers are homozygous recessive
o Sufferers are homozygous dominant or
heterozygous
 ex = Huntington’s disease
Autosomal incomplete dominance
 Fully expressed form of the disorder is relatively rare
 Partially expressed form of the disorder occurs more frequently
 Someone who has the fully expressed form has both parents suffering from the partially expressed
form
 Males and females are equally affected
 Geneticist can then deduce that
o Non-sufferers are homozygous for one incompletely dominant allele
o Sufferers of the fully expressed form are homozygous for the other incompletely dominant
allele
o Sufferers of the partially expressed form are heterozygous for the two alleles
 ex = sickle-cell disease
Sex-linked recessive trait
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Far more
males
affected
than
females
Trait
carried
on the X
chromosome
An affected male cannot pass the condition onto his sons as he passes on the Y chromosome that
doesn’t carry the trait
If a mother is affected (it can happen rarely) or if the mother is a carrier she can pass the condition
onto her son
If an affected male and an unaffected female have a son and a daughter
o Daughter will be a carrier
o Male will be unaffected
o The daughter may then go on to produce sons who are affected
The geneticist can deduce that
o Sufferers of the trait are homozygous recessive
o Non-sufferers are homozygous dominant or heterozygous carrier females
Cardiovascular system
Blood circulates from the heart through the arteries to the capillaries, to the veins and back to the
heart. There is a decrease in blood pressure as blood moves away from the heart
Structure and function of blood vessels
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The lumen is the central cavity of a blood vessel
The lumen is lined with a thin layer of epithelial cells = called the endothelium
The endothelium lining the central lumen of blood vessels is surrounded by layers of tissue that
differ between arteries, capillaries and veins
Arteries
 Carry blood away from the heart
 Have a thick middle layer of muscle
 This middle layer of muscle is found in between an outer and inner layer of elastic fibres
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The elastic walls of the arteries stretch and recoil to accommodate the surge of blood after each
contraction of the heart
Have a narrow lumen
Vasoconstriction and vasodilation
o Arterioles are small arteries
o The smooth muscle in the walls of arterioles can contract or relax to control blood flow,
depending on the body’s needs at a particular time
o During strenuous exercise arterioles that connect to the muscles working go through
vasodilation = this increases blood flow to these muscles
o Whereas the arterioles that connect to organs involved in digestion go through
vasoconstriction = this reduces blood flow to these parts during this period of strenuous
exercise
Capillaries
 Allow exchange of substances with tissues
 Made of epithelium that is only one cell thick
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Have a
muscle
inner
The wall
along a
Have a
Have
backflow
Veins
 Carry blood back to the heart
thin middle layer of
between an outer and
layer of elastic fibres
is thinner as blood flows
vein at low pressure
wide lumen = reduces
resistance of blood flow
valves to prevent the
of blood
Exchange of materials
 Blood contains red blood cells, white blood cells, platelets all suspended in plasma
 Plasma is a yellow substance that contains many dissolved substances – glucose, amino acids,
respiratory gases, plasma proteins etc.
 Blood arrives at the capillary bed from an arteriole = so the blood is at high pressure
 The blood is forced into the narrow capillary vessels and goes through pressure filtration
 Pressure filtration results in a lot of the plasma being squeezed out through the one cell thick
epithelium
 This liquid is now called tissue fluid
 The difference between plasma and tissue fluid is that the tissue fluid contains little/no plasma
proteins
 Tissue fluid has a high concentration of dissolved food molecules and dissolved oxygen which will
diffuse from a high concentration in the tissue fluid to the low concentration in the tissue cells down
the concentration gradient
 CO2 and other metabolic waste products will diffuse from a high concentration in the tissue cells to
a low concentration in the tissue fluid to be excreted
 Most of the tissue fluid returns to the capillaries by osmosis = water moves from high water
concentration (tissue fluid with no plasma proteins) to low water concentration (blood plasma rich in
plasma proteins)
 CO2 and other metabolic waste products diffuse into the blood in the capillaries
 Lymphatic vessels absorb excess tissue fluid = this fluid is now called lymph
 The lymph fluid is then returned to the circulatory system by the lymphatic vessels
 Lymphatic system = specialised part of the cardiovascular system
o Carries lymph fluid – collected all over the body
o System of vessels that returns the lymph to the bloodstream
o Disorders of lymphatic systems ex. Kwashiorkor and Elephantiasis
Structure and function of the heart
Structure
 4 chambers
 2 atria and 2 ventricles
 Deoxygenated blood is taken to the heart by 2 main veins called the venae cavae
 Blood enters the right atrium
 Flows through the atrio-ventricular (AV) valve to the right ventricle
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Blood is pumped through the semi-lunar (SL) valve into the pulmonary arteries to be taken to the
lungs
Oxygenated blood returns to the heart in the pulmonary veins
Blood enters the left atrium
Flows through the AV valve into the left ventricle
Blood is pumped through the SL valve into the aorta (largest artery in the body) to be taken all over
the body
The left ventricle wall is thicker than the right ventricle wall as the left has to pump blood all round
the body whereas the right only has to pump blood to the lungs
AV and SL valves prevent backflow of
blood
Cardiac function
 The left and right ventricles pump the
same volume of blood through the aorta
and pulmonary artery

Heart rate (pulse) (HR)
 Number of heartbeats per minute
Stoke volume (SV)
 Volume of blood pumped out by each
ventricle on contraction
 The stronger the contraction the greater
the stoke volume
Cardiac output (CO)
 The volume of blood pumped through each ventricle per minute is the cardiac output
 CO = HR x SV
Cardiac cycle
 Is the pattern of contraction (systole) and relaxation (diastole) by the heart in one heartbeat
Diastole
 Blood returning to the atria
 Volume of blood in atria increases
 This increases atrial pressure, the AV valves are pushed open and blood begins to enter the
ventricles
Atrial systole
 The right and left atria contract at the same time and pump blood into the ventricles through the
open AV valves
Ventricle systole
 The ventricles contract
 The AV valves close
 This increases pressure = pressure of blood in the ventricles is higher than the blood in the arteries
 The SL valves are pushed open
 Blood is pumped out of the hear and into the aorta and pulmonary arteries
Diastole
 The higher pressure in the arteries closes the SL valves
 The next cardiac cycle begins
AV and SL valves
 Responsible for the heart sounds
heard with a stethoscope
Cardiac conducting system
 The heartbeat originates in the heart
itself but is regulated by both
nervous and hormonal control
 The pacemaker and conducting system
of
the heart bring about the heartbeat
 The pacemaker is also known as the
sino-atrial node (SAN)
 SAN is found in the wall of the right atrium
 SAN is made of autorhythmic cells
 The SAN sets the rate at which cardiac muscle cells contract
 It does this by emitting an electrical impulse that spreads out from the SAN through the atria,
making them contract simultaneously = atrial systole
 Then travelling to the atrioventricular node (AVN) = found in the middle at the base between the
two atria
 Then into a bundle of conducting fibres which branches into the left and right ventricle
 The stimulation of the conducting fibres by the impulse causes the simultaneous contraction of the
ventricles = ventricular systole
 This cardiac conducting system ensures that ventricular systole occurs just after atrial systole =
allows time for
the ventricles to
completely fill
with blood before
contracting
 These impulses
generate currents
that can be
detected by an
electrocardiogram
(ECG)
ECG
See diagram of normal ECG pattern
 P wave shows the electrical impulse from the SAN spreading through the atria
 QRS complex shows the electrical impulse stimulating the AVN and passes down through the
ventricles
 T wave shows the electrical recovery (relaxation) of the ventricles = happens towards the end of
ventricular systole
See diagram of atrial flutter
 The waves occur in the same way as the normal ECG however they occur much more rapidly
See diagram of ventricular fibrillation
 Heart muscle cells contracting at different times = not coordinated
 If the heart doesn’t resume coordinated contraction the person will die
See diagram of ventricular tachycardia
 Abnormal cells in ventrical walls act like pacemakers = causes the ventricles to beat rapidly and not
in coordination with atria
 No P wave and QRS waves are not normal
Emergency situations
 A defibrillator gives an electric shock to patients heart = can allow the muscle cells to start
contracting in coordination again
Regulation
 The medulla regulates the rate of the SAN
 It does this through two different parts of the autonomic nervous system (ANS) that act
antagonistically = they have opposite effects on the heart
 Cardio-accelerator centre sends nerve impulses to the heart via a sympathetic accelerator nerve
 Impulses arriving at the SAN from the sympathetic nerve results in an increase in heart rate
 Due to the release of the neurotransmitter norepinephrine (noradrenaline)
 Cardio-inhibitor centre sends impulses to the heart via a slowing parasympathetic nerve
 Impulses arriving at the SAN from the parasympathetic nerve results in a decrease in heart rate
 Due to the release of the neurotransmitter acetylcholine
 The actual heart rate depends on part of the ANS exerts the greater influence
Hormonal control
 During stress and exercise the sympathetic nervous system stimulates the adrenal gland to release
the hormone epinephrine
 Epinephrine also
Blood pressure
 Is the force exerted by the blood against the walls of blood vessels
 Measured using a sphygmomanometer in millimetres of mercury (mmHg)
 Blood pressure changes, in response to cardiac cycle, and its measurement
 Blood pressure is generated by the ventricles contracting
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This means blood pressure will be highest in arteries e.g. aorta and pulmonary artery
Blood pressure changes in the aorta during the cardiac cycle
As the heart goes through systole and diastole arterial pressure rises and falls
During ventricular systole = blood pressure in the aorta rises e.g. 120
During ventricular diastole it drops e.g. 80
A typical reading for a young adult is 120/70 mmHg
Hypertension = also called high blood pressure
Usually ~ 140/90 mmHg
Hypertension is a major risk factor for many diseases including
coronary heart disease and strokes
Risk factors of hypertension
o Being overweight
o Not exercising regularly
o Eating a diet rich in fat/salt
o Drinking too much alcohol
o Continued stress
Cardiovascular disease (CVD), diabetes and obesity
Atherosclerosis
 Formation of plaques called atheromas
 These plaques form underneath the endothelium in the wall of an
artery
 The plaques start of as fatty material = cholesterol
 As the plaques become larger fibrous material, calcium and more
cholesterol are added
 Atheromas lead to
o Diameter of the artery’s lumen is reduced
o Blood flow to the capillary bed the artery supplies is reduced/restricted
o Blood pressure increases
 When large atheromas become hardened by calcium this causes the artery wall to become thicker =
which reduces elasticity
 This is also known as hardening of the arteries
 Atherosclerosis can lead to
o Coronary heart disease (including angina)
o Strokes
o Heart attacks (myocardial infarctions)
o Peripheral vascular disease
Blood clotting
 Usually occurs to prevent blood loss at the site of a wound
 Damage of cells leads to blood clotting factors being released
 Prothrombin inactive enzyme present in plasma, is converted
into the active form thrombin
 Thrombin promotes conversion of fibrinogen (soluble plasma protein) into threads of fibrin (insoluble
protein)
 Fibrin threads are interwoven = this allows platelets to adhere and form a blood clot
 The wound is now sealed = scar tissue begins to be formed
Thrombosis
 Formation of a blood clot (thrombus) in a vessel = see events above!
 This can happen if an atheroma enlarges to a point where it causes damage e.g. bursts through the
endothelium
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Embolus
Thrombus breaks loose = called an embolus
Embolus is carried in the blood stream until it blocks a narrow vessel = this will cause blood flow to
be extremely restricted or stopped altogether
If this occurs in a coronary artery = coronary thrombosis
This could then deprive part of the heart muscle of oxygen = leads to a myocardial infarction (heart
attack)
 If a thrombus/embolus causes a blockage in an
artery in the brain = leads to a stroke
 Stroke normally results in death of some of the
tissues that are supplied by that artery due to
oxygen deprivation
Peripheral vascular disorders
 Peripheral arteries = any artery that is not the;
aorta, coronary and carotid arteries
 When peripheral arteries have an atheroma and are
narrowed
 Most commonly affects the legs
Blood flow is restricted = leads to pain in leg muscles due to oxygen deprivation
Deep vein thrombosis
 Also known as DVT
 Thrombus formed in a vein
 Most commonly in calf muscles
 Leads to swelling and pain
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Pulmonary embolism
Embolus carried vena cava to the heart and subsequently to the
lungs in the pulmonary artery
Blocks a branch of the pulmonary artery in the lungs = pulmonary
embolism
Symptoms = chest pains, breathing difficulties and palpitations
Treatment = antigoagulant
If untreated can lead to collapse and sudden death
Cholesterol
 Lipids are a huge group of organic compounds which include
o Saturated and unsaturated fats
o Steroids
 Cholesterol is produced by liver cells from saturated fats in the diet
 Cholesterol is extremely important as it’s a component of cell membranes and is a precursor for
steroid synthesis
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Transport of cholesterol
High-density lipoprotein (HDL) transports excess cholesterol from the body cells to the liver for
elimination
This prevents accumulation of cholesterol in the blood = prevents it from being taken into artery
walls and contributing to atherosclerosis
Low-density lipoprotein (LDL) transports cholesterol to body cells
Most cells have LDL receptors that take LDL into the cell where it releases cholesterol
Once a cell has sufficient 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
A higher ratio of HDL to LDL will result in lower blood cholesterol and a reduced chance of
atherosclerosis and CVD
People who exercise regularly usually have a higher
concentration of HDL in the blood and so have decreased risk
of CVD
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A diet with saturated fat
swapped for unsaturated fat
and less fat in general may
also result in a higher
concentration of HDL
Medicine
Statins are prescribed drugs that can reduce blood cholesterol
They inhibit an enzyme that is involved in the synthesis of cholesterol by liver cells
Familial hypercholesterolaemia (FH)
 Inherited disorder = autosomal dominant
 Gene mutation that causes a decrease in number of LDL receptors or a change in LDL receptor
structure so that it no longer functions
 LDL carrying cholesterol are unable to deposit cholesterol inside cells
 This causes a very high concentration of LDL-cholesterol in the blood
 If untreated large quantities of cholesterol are deposited inside artery walls in a young age
 This means individuals suffering from FH will be more likely to suffer from CVD at a much younger
age than normal
 If FH runs in a family genetic screening can determine if they have inherited the gene mutation and
start treatment
 Treatment = healthy lifestyle e.g. low fat diet and regular exercise AND medication e.g. statins
Blood glucose levels and obesity
Blood glucose levels
Regulation
 Blood glucose concentration is regulated by insulin and glucagon = negative feedback
 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
 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
concentration
Adrenaline/epinephrine
 In exercise and fight or flight responses adrenal glands release adrenaline/epinephrine
 Adrenaline/epinephrine stimulates glucagon secretion and inhibits insulin secretion = increasing blood
glucose concentration
Diabetes
 A diabetic is unable to control their glucose concentration
 Can result in chronic elevation of blood glucose concentration
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Type 1 diabetes
Usually occurs in childhood
Person unable to produce insulin
Can be treated with regular doses of insulin
Type 2 diabetes
Sometimes referred to as adult onset diabetes
Usually develops later in life
Occurs mainly in overweight individuals
Person is able to produce insulin but their cells are less sensitive to it = sometimes referred to as
insulin resistance
This insulin resistance is linked to a decrease in the number of insulin receptors in the liver
Leads to a failure to convert glucose to glycogen
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In both cases blood glucose concentration rise rapidly after a meal
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
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
250-300ml of glucose solution
Vascular disease can be a chronic complication of diabetes = see next page
Vascular disease
 Complication associated with diabetes
 Chronic elevation of blood glucose concentrations leads to the endothelium cells in blood vessels
taking in more glucose than normal = damages the blood vessels
 This damage can then lead to atherosclerosis which can cause = CVD, stroke or peripheral vascular
disease
 Small blood vessels damaged by elevated glucose concentrations may result in
o Haemorrhage of blood vessels in the retina = the blood vessels burst and bleed
o Renal failure
o Peripheral nerve dysfunction
Obesity
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Characterised by excess body fat in relation to lean body
tissue (muscle)
Is a major risk factor for cardiovascular disease, type 2
diabetes, kidney failure and osteoarthritis
Body mass index =
weight divided by
height squared
See table
Limitations = if a person has an unusually high percentage of
muscle e.g. a body builder they could be wrongly classified as
obese if BMI was used
To measure body fat accurately = measure body density
Body density
Can be measured in the following ways
Densitometry
 Individuals are weighed in air and while submerged in a tank
 Researchers use formulas to estimate body volume, body density, and
body fat percentage
 Fat is more buoyant (less dense) than water, so someone with high body
fat will have a lower body density than someone with low body fat
 This method is typically only used in a research setting
Skin-fold thickness
 Use a special calliper to measure the thickness of a “pinch” of skin and the
fat beneath it in specific areas of the body e.g. back of upper arm
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Equations are used to predict body fat percentage based on these measurements
Waste/hip ratio
 Is used to measure abdominal obesity
 It’s calculated by measuring the waist and the hip (at the widest diameter of the buttocks), and then
dividing the waist measurement by the hip measurement
 This is used as distribution of fat is important in measuring health risks
 ‘Apple-shaped’ people = carry excess fat round their abdominal area
 ‘Pear-shaped’ people = carry excess fat round their hips
 ‘Apple-shaped’ people are at greater risk of type 2 diabetes and CVD
than ‘pear-shaped’ people
Bioelectrical impedance
 BIA equipment sends a small, imperceptible, safe electric current
through the body, measuring the resistance
 The current faces more resistance passing through body fat than it does passing through lean body
mass and water
 Equations are used to estimate body fat percentage and fat-free mass
Causes of obesity and treatments
 Linked to genetic, physiological, environmental, metabolic and dietary
factors
 Most common cause = diet rich in fat and sugar AND a decrease in
physical activity
 The energy intake in the diet should limit fats and free sugars
 Fats have a high calorific value per gram
 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
o Keeping weight under control
o Minimising stress
o Reducing hypertension
o Increasing HDL levels in the blood