Download Physiology Notes for Exam 4

Respiratory System
Chapter 23 p 806
Introduction
• All vertebrates (modern life forms) need O2 for energy metabolism
that releases energy from nutrient molecules and produces ATP.
• The by-product of oxidative energy metabolism is CO2 and H2O
and heat.
• CO2 can cause acid toxicity at high concentrations and must be
removed quickly.
• The cardiovascular and respiratory systems act together to
exchange these gasses between the body and environment.
• If either system fails, even for a short time, acute disruption of
homeostasis occurs with starvation of O2 and build up of waste
products, especially CO2.
Functions of the Respiratory System
1. Gas Exchange
• O2 into cells, CO2 out cells.
• Surface for exchange = tiny air sacs in the lungs surrounded by a dense
network of capillaries.
2. Protection
• Against foreign materials inhaled in air.
• Cleans air using:
o Alveolar macrophages found in the alveoli (smallest lung sac in lung),
and, fig 23.12 p 820
o Cilia that acts as an escalator to move foreign materials up and out.
Nicotine numbs the cilia!
• Warms and moistens air: prevents cold damage and drying of alveoli.
3. Sense of Smell
fig. 23.2b p.808
• Receptors for sense of smell are located in the olfactory epithelium
covering the superior nasal conchae.
4. Voice production
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• Bands of elastic ligaments in larynx can be stretched and made to vibrate
when air is directed over them.
5. pH regulation
• CO2 is an acid producing compound.
• pH must be maintained in narrow range because the 3D shape of proteins
changes with small changes in pH, thus disturbing their function.
• CO2 is quickly removed from the body primarily by exhaling, and can be
hastened by deep and rapid breathing.
Respiration
The term respiration is used in a number of ways in dealing with the exchange of
gasses.
We will differentiate between these using these terms:
1. Pulmonary Respiration (Ventilation): Moving air from environment to
and from lung space.
Fig 23.16 p 824
2 Phases:
1. Inhalation/Inspiration: intake (inhale)
2. Exhalation/Expiration: output (exhale)
3. External Respiration:
Respiratory organ (lungs)
O2 into blood, CO2 into alveoli.
Blood
3. Internal Respiration: Blood
Body Cells
4. Cellular Respiration: Metabolic process within tissue cells.
• Utilization of O2 in metabolic processes to make ATP, which gives off CO2
as an end product.
Components of the Respiratory System (in order)
2 Major Divisions:
1. Conduction Division
•
•
•
•
fig. 23.8 p.815
Function: conducts air and humidifies, cleanses, warms in the process.
Walls are too thick for exchange of gasses = dead air (nonexchangeable).
Anatomical dead space = about 150 ml air.
Consists of these structures in descending order:
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1.
2.
3.
4.
5.
Nasal Cavities
Pharynx (throat) pharyngitis
Larynx (voice box) laryngitis
Trachea (windpipe)
Bronchi branches into bronchioles
2. Respiratory Division
fig. 23.11 p.819
Function:
1. Cleans air using alveolar macrophages.
2. Gas diffusion.
a. Lungs with tiny thin walled alveoli. fig. 23.12 p.820
b. This is where the transfer of gasses occurs.
c. Human lung = 300 million alveoli with 70 m2 surface area for gas
exchange. 40x body area.
i. Draw a square meter on board for effect. Imagine 70 of these.
d. If alveoli are non functional in particular area = Physiological Dead
Space.
e. Maybe as high as 1-3 liters in conditions of asthma (smooth muscle
spasm) and emphysema (alveoli destroyed, elastic tissue destroyed).
Other Important Components of Respiratory System
fig. 23.14 p. 822
Muscles- Important for inspiration (air intake, inhalation).
• External Intercostals
o Located between ribs). Increase dimensions horizontally, by pulling
the ribs superiorly and the sternum anteriorly.
o fig.23.15 p.823 fig.23.16 p.824
• Diaphragm
o Increases size of thoracic cavity vertically.
o Diaphragm is naturally domed.
o When contracted it flattens out, about 1 cm in normal breathing (0.5 L
(tidal volume), creates a 1-3 mm Hg difference from atmospheric
pressure (760 mm Hg).
o Difference is up to 10 cm in strenuous breathing (2-3 L, 100mm
difference).
o Fig. 23.13 p. 821
o Boyle’s law states that when a container of gas increases in size the
pressure of the gas inside decreases.
o So atmospheric gas (now at a greater relative pressure) will move
into the container (the lungs).
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o The lungs adhere strongly to the expanding plural cavity the because
of subatmospheric pressure (756 mm Hg) and surface tension
created by their moist adjoining serous membranes.
o The intrapleural space is a closed sac and does not communicate
with the lung space.
o So, it maintains its subatmospheric pressure at all times.
o In this way the lungs become stretched and increase in volume as the
diaphragm is lowered.
o Accounts for 75% of air movement.
What happens when thoracic cavity punctured ?
• Lung collapses: called a pneumothorax.
So, inspiration is an active process.
Results from contraction of muscles.
Expiration (exhalation)
It is a passive process.
Requires no muscular activity.
A process called elastic recoil with 2 components:
1. Elastic tissue of the lung is stretched during inspiration and recoils
back to resting size.
• When the lung is easy to stretch it is termed ‘high compliance’.
2. Surface tension. This accounts for 2/3 of recoil.
• The inward pull on alveoli due to surface tension of alveolar fluid.
• Alveolar fluid consists of phospholipids and lipoproteins as well as water so
it doesn’t have as much surface tension as pure water. (secreted by type II
alveolar cells).
o The lipids get between water molecules and decrease the pull
between water molecules, so less tension. They are called
surfactants.
o If no surfactant then alveoli would collapse upon each expiration and
it takes great effort to reopen them during the next inspiration.
o **So, during expiration the alveoli become smaller but do not
collapse.
• The air left at this point is the residual volume that stays in the lungs and
airway.
o This decreases the volume of the lungs, which increases the
pressure of the gasses to about:
o 762 mm, so gasses move out into atmosphere (760 mm).
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• Premature infants tend to have less surfactant and have difficulty breathing
(respiratory distress syndrome (RDS) or hyaline membrane disease) due to
collapsing alveoli (not enough surfactant).
o Surfactant starts being made about week 25 and is complete by week
35 (6 weeks before normal delivery)
o This can be checked by amniocentesis.
o When baby is born with low surfactant, can introduce pharmaceutical
surfactant with assisted ventilation.
• Expiration may be active under conditions of rapid and forceful breathing.
o The internal intercostals depress the ribs and the abdominal muscles
(rectus abdominis, transverse abdominis, and int. and ext. obliques)
compress the abdomen to raise the diaphragm.
Exchange of Air
fig.23.17 p. 827
Lung Volumes and Capacities
Adult volumes (mls):
500 Tidal Volume (TV)
• The air entering or leaving the lungs during normal breathing in a single
breath.
3100 Inspiratory Reserve Volume (IRV)
• The extra volume of air that can be maximally inspired over and above the
typical resting tidal volume.
• It is caused by maximal contraction of the diaphragm, external intercostals,
and other accessory inspiratory muscles.
1200 Expiratory Reserve Volume (ERV)
• The extra volume of air that can be actively exhaled by maximal contraction
of the expiratory muscles beyond that passively expired in a typical tidal
volume.
1200 Residual Volume (RV)
• The minimum volume of air remaining in lungs even after maximal, forced
expiration. It includes the volume of the non collapsible airway plus slightly
inflated alveolar volume.
• This volume cannot be directly measured by a spirometer because it does
not move in and out of the lungs.
4800 Vital Capacity (VC)
• The maximum volume of air that can be moved out during a single breath
following a maximal expiration.
• VC represents the maximal volume change possible within the lungs.
o It is rarely used because the contractions involved are so exhausting.
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o It is useful to determine the functional capacity of the lungs.
• VC = Tidal volume (TC) + inspiratory reserve volume (IRV) + expiratory
reserve volume (ERV).
6000 Total Lung Capacity (TLC)
• The maximum volume of air that the lungs can hold.
• TLC = vital capacity (VC) + residual volume (RV).
• Total amount of air in lungs.
• Gives an idea of total lung size. If this was reduced, think of the effect of
running around the track breathing thru a straw!
Normal breathing rate = about 12 breaths/min.
• With a tidal volume of 500 ml = 12 x 500 = 6000 ml (6 L)/min of air =
respiration minute volume.
• Not all of this is available for exchange (only about 350 ml).
o About 150 ml/breath remains in anatomical dead space (conducting
airways= nose, pharynx, larynx, trachea, bronchi, bronchioles,
terminal bronchioles).
Alveolar Ventilation Rate
• 12 breaths/min x 350 ml (tidal volume (500) – anatomical dead space
(150)) = 4200ml/min.
• In maximal exercise, may increase to 50 breaths/min, > 200 L/min.
Composition Of Gases In The Atmosphere
Nitrogen (N2)
Oxygen (O2)
Carbon dioxide (CO2)
Rare gases
fig. 23.18 p.829
78%
21%
0.04%
0.9%
• Gas exchange in the lungs takes place by means of simple diffusion. No
ATP is used.
• Gasses are traditionally measured by their pressure rather than by their
percentage in the body or atmosphere.
• Dalton’s law states that the pressure created by a mixture of gasses is
determined by the sum of all the individual gasses present.
• So, the partial pressure of each gas (denoted by a ‘p’) can be easily
determined as follows:
Partial pressure in mm Hg = % of gas present in mixture x total pressure
Note: (760 mm Hg = atmospheric pressure at sea level)
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Examples:
pO2 =
0.21 x 760 mm Hg = 160 mm Hg of pressure
pN2 =
0.78 x 760 mm Hg = 593 mm Hg of pressure
pCO2 =
0.0004 x 760 mm Hg = 0.3 mm Hg pressure
The gasses diffuse according to the pressure found on each side of a membrane,
higher to lower.
Let’s see how this works out in the path of respiratory gasses in the body:
Fig. 23.18 p.829
O2 path
Atmosphere trachea
(pPressures)
160
150
alveoli arterial blood
(systemic)
105
100
Bulk flow by negative pressure
in thoracic cavity
tissues
Diffusion Diffusion
venous blood alveoli
40
40
105
No net diffusion
CO2 path
Atmosphere trachea
(pPressures)
0.3
0.3
Bulk flow
alveoli
40
venous blood
45
tissues
45
arterial blood
(systemic)
40
Diffusion
Major idea:
• Oxygen moves from lungs (alveoli) to blood to body tissues by diffusion.
• Carbon dioxide moves from body tissues to blood to lungs by diffusion.
• In blood, moves by bulk flow due to blood pressure.
• Then in/out of the lungs by bulk flow.
Henry’s law states that the ability of a gas to stay in a solution at a
constant temperature is due to its:
1. Partial pressure.
The higher the pressure, the more it will leave the solution.
2. Solubility.
The greater the chemical attraction for water (higher solubility coefficient), the
more gas will stay in solution.
Solubility coefficient
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CO2
0.57
O2
0.024
N2
0.012
• So, nitrogen does not dissolve in the blood easily and generally has no
physiological effect.
• However, as a diver moves deeper the pressure becomes greater and
more nitrogen dissolves in the blood and tissues.
• This may cause a narcosis ‘rapture of the deep’.
• If a diver comes up faster than the lungs can eliminate it, nitrogen gas
bubbles form in the blood and tissues = decompression sickness.
• Treat by using a decompression chamber.
A hyperbaric chamber
A high pressure O2 (3-4x atm, 2280-3040 mm Hg), is used to treat anaerobic
infection, crush injury, CO poisoning, burns, and others.
Transport Of The Gases By The Blood
fig. 23.19 p.833
Oxygen Transport
• O2 is transported by the hemoglobin molecule found in RBC’s.
• The O2 actually binds to the 4 iron (Fe) atoms found in the hemoglobin
molecule.
• When the binding takes place the hemoglobin molecule changes color.
• This accounts for the bright red vs. darkish red colors of the blood.
Formula p.831
Hb + O2
DeoxyHgb
HbO2
OxyHgb
98.5 % bound to Hb, 1.5 % dissolved O2 (low solubility)
Each 100 ml of blood carries 19.7 ml as HbO2 and 0.3 ml as dissolved O2.
O2 Saturation
fig. 23.20 p.833
•
•
•
•
•
The pO2 affects the amount of O2 bound to Hb.
As the pO2 increases, more O2 binds to Hb.
So, as blood goes through the lungs (pO2= 105), O2 is picked up by Hb.
In the tissue (pO2 = 40) the O2 is released.
Note that at 40 mm Hg, Hb is still 75% saturated so only 25% of circulating
O2 is normally available to tissues.
• In muscle during exercise, the pO2 may drop to 20 mm ,so then O2 sat
drops to 35% thus releasing large amounts of O2 for the tissues.
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(Optional material, not on exam) Skip to carbon dioxide transport.
pH and temperature are also important factors that affect the affinity of O2 to Hb.
pH fig. 23.21a
As pH lowers, O2 affinity for Hb decreases (more O2 available for tissues).
This is called the Bohr effect, as the binding of H+ ions changes the shape of Hb.
Temperature fig. 23.22 p.834
As temp rises, affinity of Hb for O2 decreases (more O2 for tissues).
Fetal Hgb (Hb-F) fig. 23.23 p. 834
Has a higher affinity for O2 than does maternal Hgb (Hb-A).
So the fetus will pick up O2 in the placenta readily.
Helps prevent hypoxia in fetus.
Oxygen toxicity
Occurs at about 2.5 – 3 atmospheres.
Huge amount of free radicals are formed which cause profound nervous disturbance
culminating in coma and death.
Carbon Dioxide Transport
CO2 is carried in 3 main forms in the blood:
1. Dissolved CO2 – 9%.
• This is the portion that can diffuse into the alveoli.
2. Carbaminohemoglobin HbCO2- 13%
• Binds to globin portion of Hb (terminal amino acids) not the heme portion!
• Amount bound is directly related to pCO2, so as blood enters alveoli, much
of the CO2 is released, and as blood enters tissue pCO2 is high so binding
is promoted.
3. Bicarbonate ions HCO3- 78%.
• An enzyme (called carbonic anhydrase) present in RBCs is responsible for
this reaction.
Fig. 23.24 p 836
formula p 835
CO2 + H2O
Carbonic anhydrase (CA)
H2CO3
H+ + HCO3Carbonic acid
bicarbonate ion
• *The reverse reaction occurs in the lungs.
• As CO2 is exhaled, the reaction is driven to the left.
• *Notice that CO2 and H+ concentrations can be regulated in the manner.
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o An increase in CO2 leads to an increase in H+ as the reaction moves
right.
o An increase in H+ can lead to more CO2 that is blown off in the lung
with H2O.
• What will this do to the pH of the blood as the lungs blow off CO2 + H2O?
o It raises the pH.
• ** The lung through its elimination of CO2 is a prime regulator of pH of the
blood.
Note
As bicarbonate is produced, a negative ion, it moves out of the RBC to plasma
(down its chemical concentration gradient).
And Cl- moves in to reestablish electrical balance (electrical gradient).
This is called the ‘chloride shift’.
Acid Base Balance
• A brief look at how the body gets rid of acids.
• The body produces acids during metabolism of glucose, fatty
acids, and amino acids, so a huge excess of H+ is produced that
would rapidly lead to death.
• The body has 3 mechanisms to remove H+ from body fluids and
then eliminate them:
1. Buffer systems.
• Buffers bind up reactive H+ to remove them from solution temporarily.
• Examples: Proteins are the most abundant buffer with both an amino and
acid group, carbonic acid we have already discussed, and phosphates.
• Hemoglobin is a good buffer.
2. Exhalation of CO2 and H2O .
• Increased ventilation will blow off CO2, which lowers the carbonic acid level
and raise the pH.
• Where does the H+ go if CO2 has no H? It blows off in the water vapor.
3. Kidney excretion
• Slow mechanism (hours to days) but only way to remove acids other than
carbonic acid.
• Death is caused quickly without the contribution of the kidney in removal of
these acids.
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Methods of compensation for acid imbalance.
Table 27.4 p.1005
Condition
Respiratory
acidosis
Common Cause
Hypoventilation due to emphysema,
airway obstruction, muscle
dysfunction, etc. >45mmHg CO2
Respiratory
alkalosis
Hyperventilation due to oxygen
deficiency, pulmonary disease,
anxiety, other causes. <35mmHg
CO2
Loss of bicarbonate ions due to
diarrhea, accumulation of acid
(ketosis), renal dysfunction.
<22 mEq/l HCO3Loss of acid due to vomiting,
gastric suctioning, diuretic use,
intake alkaline drugs. >26 mEq/l
HCO3-
Metabolic acidosis
Metabolic alkalosis
Compensatory Mechanism
Renal: increased excretion
of H+ with resorption of
bicarbonate. pCO2 stays
high.
Renal: decreased H+
excretion with decreased
bicarbonate resorption.
pCO2 low.
Respiratory:
hyperventilation, with loss
of CO2. HCO3- low.
Respiratory:
hypoventilation with less
CO2 loss. HCO3- high.
Control Of Breathing
(What determines rate and depth of breathing?)
fig. 23.28 p.839
Chemical Regulation
Fig. 23.27 p. 838
• ↑C02 (above 40mmHg), ↓pH, and ↓O2 (105-50 mmHg) will stimulate
breathing chemoreceptors to increase breathing rate.
o Central receptors: It is primarily the C02, and H+ (pH) in CSF that
determine breathing rate in the medulla oblongata.
o Peripheral receptors: Found in the aortic arch (via vagus (X)) &
carotid bodies (via glossopharyngeal nerve (IX)) respond to ↑C02 ,
↓pH, and ↓O2 levels.
• O2 levels below 50 mmHg actually decrease breathing rate, a very
dangerous situation.
• The chemoreceptors will send impulses to the respiratory center of the
medulla oblongata.
• The medulla will act mainly on diaphragm (via phrenic nerves) to increase
tidal volume (depth of breathing) and respiratory rate.
Other influences (cortical, limbic, temperature, pain, proprioceptor, etc.) affect the
respiratory center that we will not discuss.
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Pulmonary Disorders
p.844-846
• Pulmonary disorders are a major threat to 10% to 15% of persons over age
40.
• Especially to those individuals in a heavily polluted environment.
• Many chronic lung diseases share some degree of obstruction of the
airways.
p. 844
• The general term COPD (chronic obstructive pulmonary disease) is used to
refer to a patient’s condition when the airway is compromised.
• The Expiratory Reserve Volume will be reduced in these patients.
Black lung disease
• Exposure to air with various tiny dust particles: coal, silicates including
asbestos, grain, insulation.
• Originally named for coal miners lung disease.
• Very small dust particles accumulate and attract macrophages.
• The continual activation of macrophages causes local damage which
reduces diffusion through the alveolar walls (emphysema).
• The dust can be deposited in the walls of the alveoli and lead to inelasticity
of the alveolar walls.
• Bronchioles may become scarred and inflamed which cause airway
obstruction.
• Carcinoma may be an outcome depending on the type of dust (asbestos)
and coexistent risk (use of cigarettes) exposure.
Asthma
p.844
• Smooth muscles of the smaller bronchi and bronchioles undergo
contraction or spasm— it restricts and prevents alveolar ventilation as the
airway is partially or completely closed.
• Often mucous secretion is excessive that further compounds the problem
by clogging the respiratory airway.
• Asthma may be due to allergies, exercise, stress, pollutants, or cold air, all
of which causes spasms of bronchioles.
• These can act together, so on a smoggy day, exercise may need to be
avoided.
• Relief is achieved from inhaling muscle relaxants (epinephrine, ephedrine &
isoproterenol) or steroids (anti-inflammatory) or removing the patient from
the polluted environment.
Carbon Monoxide Poisoning
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• CO, a colorless odorless gas, is produced during combustion.
• It combines with the heme group of hemoglobin 200x stronger than O2, so
prevents O2 binding.
• A concentration of only 0.1% will combine with 50% of O2 binding sites,
which leads to hypoxia.
• Administration of 100% O2 will help recovery.
• So, get a CO detector in your home!
Emphysema
• Alveolar walls disintegrate producing larger air spaces that remain filled
with air during expiration.
• Elastic fibers are lost, so elasticity of lung alveoli is reduced with lack of
ability to recoil properly.
• Reduced surface area also reduces diffusion of O2 into capillaries.
• Although inhalation is easy, these individuals cannot exhale properly.
• They must voluntarily exhale to remove more air from the lungs.
• A ‘barrel chest’ may develop over time as chest cage is enlarged from
repeated exaggerated breathing
• Mild exercise leaves these people breathless as they cannot move enough
O2 into the body for metabolic needs.
Optional terms
Dyspnea: labored breathing
Eupnea: normal breathing
Assignment
What is a spirometer?
Define various lung volumes and capacities.
How is minute volume of respiration (MV) calculated?
What are alveolar ventilation rate and FEV1 ?
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The Digestive System
Chapter 24
Introduction
fig.24.1 p.853
Functions of the Digestive System (4 Basic Functions of Digestion)
1. Ingestion
• Food intake through the mouth.
2. Digestion
• Process of reducing foods to their constituent building blocks, from larger
molecules to smaller ones. To a form that can be used by the body.
• This requires a fairly hostile environment and active forces:
a. Mechanical: Tearing, mixing.
b. Chemical: strong acids, enzymes, bile.
• Digestion must take place in such a way as to not harm host cells and kill
any bacteria in the ingested food.
3. Absorption
• Taking in the nutrients that have been broken down.
• Nutrients will pass through the GI tract if not broken down to basic subunits.
4. Defecation (egestion)
• Elimination of unabsorbed residues of the digestive process and bacteria
that feed off these residues.
Components of the Digestive System
1. Alimentary Tract = muscular tube with various modifications from
mouth to anus.
• All digestion occurs in the tube or GI tract.
• This tube should be considered outside the body as it passes through the
body.
• All absorption occurs from this tube.
• Within wall of tract are muscles that serve to propel foods.
2. Accessory organs
•
•
•
•
Structures that lie outside of the alimentary tract.
These organs empty secretions into the digestive tract by way of ducts.
The secretions are necessary for digestion.
Examples: salivary glands, liver, gallbladder, pancreas.
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Theories of the Control of Feeding
Feeding is controlled by the hypothalamus. (remember homeostasis =
hypothalamus).
How the hypothalamus assesses we are hungry is not completely
understood. Several mechanisms are probably in place.
Here are some hypotheses:
1. Gastric sensation
•
•
•
•
Filling of stomach or stretching of abdominal wall.
Satiety (satiated)= not longer hungry. Tells us when to stop!
Some diet aids attempt to work on this manner- like a sponge that swells.
Recently a pacemaker device (Transneuronix Inc) for the stomach has
been tested with significant results. It works like a heart pacemaker
providing electrical stimulus to stomach muscle near nerves.
o Mechanism is not known yet but is an easy one hour procedure to
install and is reversible.
o Patients report feeling satiated and full sooner. Weight loss of 2540% of excess reported in clinical trials.
2. Glucostat
• Glucose uptake by liver cells influence vagus nerve and information is
transmitted to lateral hypothalamus (Glucose Receptors).
• Lesions of lateral hypothalamus and one may get obese.
o So, a measuring of glucose levels.
• Example:
o Problem: in diabetes mellitus there are high glucose levels and a
person eats like crazy.
o So, glucose must be made available to cells.
• Fatostat: a similar idea.
o Fat produces increase in fatty acids and release of leptin.
o Leptin is peptide hormone that promotes satiety signal to the
hypothalamus.
o It inhibits release of chemicals that stimulate hunger.
o It’s concentration is in direct proportion to amount of adipose tissue.
o Some obese persons have high levels of leptin but the receptors
don’t work.
3. Thermostat
• Intake of food associated with rise in metabolic activity.
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• Therefore, increase in heat.
• Closely tied to caloric need.
• Decreased temperature: the more food we eat.
4. General nutritional state
• Body can monitor usage of a particular nutrient (substance, vitamin,
minerals).
• Creates an appetite for a certain type of food.
• Nutrition: proteins, vitamins, cholesterol.
• Body needs these and can seek them out in food choice.
• Pica = craving for non food items of little or no nutritional value. e.g. ice,
clay, starch, paper, paint, etc. Also may crave ice (pagophagia) when Fe
deficient.
• E.g. lactating animals eat more ??? Women eat more calories during luteal
phase (time after ovulation) than follicular phase (time before ovulation),
about 90-500 kcal/day.
5. Intake of specific foods
• Body may be able to monitor presence of certain foods or food types.
6. Psychological status
• Sometimes we eat out of habit or boredom.
• Pleasure: food preferences, eat more in cafeteria, appetizers, dessert,
Pleasure Centers in Hypothalamus.
• Social factors: cultural demands to be thin...anxiety.
7. Neurotransmitter and hormones
• After food ingestion serotonin is released and animals appear satiated
(Carbohydrates increase serotonin levels in brain, so one may eat
carbohydrates when depressed).
• Use of fenfluramine (FenPhen is a combo drug. Biological Basis:
fenfluramine increases Serotoin levels, while phentermine is an
amphetamine mimic that promotes a sympathetic response. Both curb
appetite.) Taken off the market as heart failure occurred.
• Leptin- a new hormone released from fat cells to brain to cause feeling of a
saiety.
• PYY hormone from intestine seems to do the similar thing as leptin. Maybe
lead to new treatments for obesity.
One of these theories does not appear to suffice by itself.
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Feeding mechanisms are probably a combination of these.
Interesting note:
We tend to have appetite for different things at different times.
Apparently to satisfy nutritional need at that time.
Function and Control of Specific Digestive Organs (in order passed
by bolus of food).
I. Mouth
Fig 24.4 p 858
1. Ingestion begins
• Food put into the oral cavity to start the process.
2. Digestion: breakdown process of complex foodstuffs
• Mechanical digestion or chewing = mastication.
o Teeth, lips, cheeks, hard and soft palate, tongue.
o All these aid in slicing and tearing food.
• Chemical digestion
o Saliva: produced by the salivary glands (parotid, sublingual,
submandibular).
o 99.5% water, 0.5% proteins (amylase, mucus, lysozyme)
o 1-2 L/day under basal parasympathetic control.
o 4 Functions of Saliva:
1. Digestion
Begins breakdown of carbohydrates.
Starches broken down to disaccharides (maltose: 2 glucose
molecules) and other short chain glucose polysaccharides by
amylase.
Only 3-5% since food spends such short time in mouth.
2. Dissolves soluble foods.
3. Mucus moistens food or lubricates food for swallowing.
4. Cleanses and moistens mouth: lysozyme antibacterial and washing
effect helps to prevent tooth decay (dental caries). Note: Acidic waste
of bacteria promotes tooth decay.
3. Swallowing (deglutition): movement of bolus of food.
• A voluntary act.
• Tongue forces food against hard palate (roof of mouth).
• This triggers the involuntary stage in the pharynx
II. Pharynx
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Fig 24.8 p.864
• The bolus moves into the oropharynx and stimulates receptors that send an
afferent message to the swallowing center in the medulla oblongata.
• The involuntary returning motor impulses cause the soft palate and uvula to
be forced up and close off opening from the nose to pharynx.
• The tongue seals off the mouth by pressing on the hard palate.
• The larynx moves up under the tongue, the vocal cords come together, and
the epiglottis is forced over the glottis, which seals off the respiratory
passage.
• The bolus passes through the laryngopharynx and enters the esophagus in
1-2 seconds.
• This is an all or none, sequential reflex.
o Once triggered, you cannot stop.
• Have you ever swallowed a hard candy because you got it back too far in
the pharynx?
III. Esophagus
Histology: Fig. 24.9 p.865, peristalsis: fig. 24.10 p.865
1. Transportation of foods by pushing through the esophagus to
stomach by peristalsis.
• Wave like contraction of smooth muscle.
• Peristalsis is controlled by the medulla oblongata so is involuntary
response.
• Circular smooth muscle in muscularis layer above bolus contracts to
squeeze food inferiorly. The longitudinal smooth muscle below the bolus
contracts which opens the esophagus to receive the bolus.
• Takes about 4-8 seconds for bolus, 1 second for liquid to reach
gastroesophogeal sphincter. Liquid then waits for 5 seconds for peristaltic
wave to catch up and allow entry into the stomach.
• If bolus doesn’t make on first wave (peanut butter) a reflexive secondary
wave will occur and more mucus secreted.
2. Secretion of mucus by glandular cells acts as a lubricant of the
bolus.
• No digestion or absorption occurs in the esophagus.
3. Vomiting or reverse peristalsis.
• Usually stimulated by irritation and distention of the stomach.
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• Medulla oblongata vomit center causes abdominal wall muscles and
diaphragm to squeeze the stomach and expel its contents through the open
esophageal sphincters.
• Heartburn is due to HCl from the stomach contents entering the inferior part
of the esophagus causing burning and irritation.
o Don’t lie down after a meal. Prolonged exposure to acid pH can lead
to esophageal cancer.
IV. Stomach
Fig.24.11 p.867
J-shaped sac-like chamber connecting the esophagus and the small intestine.
Major functions:
1. Storage (reservoir).
• Mainly in the body with gas in the fundus.
2. Gastric mixing with chyme formation (saliva and gastric juice with
churning (every 15-20 seconds)).
• Occurs mainly in the antrum that holds about 30ml.
• Gastric emptying: A few mls enter the duodenum with each peristaltic
wave.
3. Protein digestion: HCl and pepsin.
• Some lipase activity.
4. Secretes gastrin, a digestive hormone.
• Hormone promotes secretion of gastric juice, closing of esophageal
sphincter, opening of pyloric sphincter.
Other Notes:
• Little absorption of food.
o Water, ions, some drugs, esp. lipid soluble (alcohol ‘candy is dandy
but liquor is quicker’, aspirin).
o Note: females have 60% less alcohol dehydrogenase than men in
their stomach, so get drunk with less. Liver is where most alcohol is
detoxified by same enzyme.
Digestion in the Stomach
table 24.3 p 871
The stomach contains many gastric glands that produce gastric juice.
Gastric juice = watery solution of HCl and pepsin, lipase, gastrin, and intrinsic
factor for B12 absorption.
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3 important types of cells in the stomach, each with different functions:
see histology in fig. 24.12 p.868
1. Parietal (oxyntic) cells
• Secretes HCl. Disassociates to H+ + Cl- to decrease pH to about 2.0.
• Kills microbes in food.
• Denature proteins.
• Converts pepsinogen to pepsin.
Other Notes: (not on exam)
• ACh from parasympathetic neurons and gastrin initiate H+ release from parietal cells in
the presence of histamine released from local mast cells. All 3 receptor types are found
on parietal cells.
• The histamine receptors on parietal cells are called H2 receptors.
• Tagamet, a widely popular drug, blocks the H2 receptors and relieves gastric upset by
inhibiting H+ release.
• Prilosec, another drug, directly inhibits active transport of H+ from parietal cells. Fig
24.13
• Before Tagamet and Prilosec were available, the vagus nerve was often cut to remove
the parasympathetic response that activated gastric secretion.
2. Chief (zymogenic) cells
• Secretes pepsinogen (inactive form) which is converted to pepsin in the
presence of HCl. Breaks certain peptide bonds in proteins.
• Secretes gastric lipase (breaks down triglycerides to fatty acids and
monoglycerides).
3. (Mucous) Neck cells
• Secretes mucus that forms a protective layer barrier that prevents digestion
of stomach wall (and absorption of materials).
• Gastrin is secreted by enteroendocrine (G) cells in pyloric area stimulates
the chief and parietal cells, increases stomach motility, and relaxes pyloric
sphincter.
Emptying of the Stomach
Normal time:
2-4 hours
Small amounts of chyme, about 10-15 mls, are squirted by a peristaltic
contraction through the pyloric sphincter into the duodenum.
Things that alter this time:
1. Type of food ingested:
a. Carbohydrate rich foods: the least time spent in stomach.
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b. Protein rich food: intermediate time spent in stomach.
c. Fat rich food: Longest time due to release of cholecystokinin (CCK) from the
receiving enteroendocrine cells of the small intestine.
• CCK is a hormone with many digestive function. Its effect on the stomach is
to inhibit emptying into the intestine.
• Decreased motility and secretions.
• May stay in stomach up to 6 hrs.
Note: alcohol will be absorbed into system slower with a meal high in fats (hamburger, pizza).
Stomach does not absorb alcohol as well as intestine and contains alcohol dehydrogenase
(breaks down alcohol).
2. Decreased vagal (parasympathetic) activity.
• Not relaxing after eating. Activation of sympathetic division.
3. Tonicity
• Chyme must be isotonic to plasma before emptying.
• Hypertonic chyme pulls water from the circulating plasma and if excessive
causes intestinal distention and circulatory disturbances.
• Digestion slows down when hypertonic conditions exist until absorption
catches up.
• Meals with more liquid will empty sooner.
4. Distension of stomach
• The more the stomach is stretched, the more gastric secretion and activity.
So empties sooner.
Stress factors:
5. Short term stress
• Decrease emptying time (shorter).
• By ACh production.
• Sometimes parasympathetic system gets activated in some stress
situations.
6. Long term stress
• Increase emptying time (longer).
By adrenal hormones. Sympathetic ANS response slows down digestion.
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The Small Intestine
Structure of Small Intestine
Fig 24.22 p 882
1. 3 sections of small intestine, in order:
Duodenum Jejunum
Ileum
2. Folds of Intestine
Fig. 24.23 p.883
• Plicae circularis of small intestine, permanent circular ridges about 10 mm
high.
o Causes chyme to move in a circular path rather than straight. Slows it
down for better absorption.
Histology Fig.24.24 p884. fig. 24.23 p.883.
• Villi- finger like projections of mucosa about ½ - 1 mm long. 20-40/mm2.
o Gives a velvety appearance.
o Contains blood and lymph capillaries that will carry the nutrients
away.
• Microvilli- absorptive simple columnar epithelium cell surface has a brush
border.
o Each microvilli is a 1 um long cylinder. 200 million/mm2 or 1700/cell.
o A massive area for absorption.
All these folds dramatically increase surface area, increases absorption area.
3. Structures associated with the small intestine.
All produce digestive secretions. These will be discussed later.
Fig. 24.17 p.875
Pancreas
• 5-6 inches long x 1 inch thick.
• Connects with 2 ducts (accessory and pancreatic) to the duodenum.
Liver
• A large organ about 3 lbs (second largest to skin).
• The common hepatic duct joins the cystic duct to form the common bile
duct that enters the duodenum.
Gallbladder
• 3-4 inch long pear shaped organ.
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• Cystic duct joins hepatic duct forming the common bile duct to enter the
duodenum.
• The main pancreatic duct joins just before entering the duodenum.
Function of Small Intestine
Fig 24.22 p 882
1. Primary in absorption of nutrients (microvilli is absorption unit).
• 90% of nutrients absorbed here.
2. Completes Digestion
• Many enzymes located in plasma membranes of intestine for final
breakdown of nutrients before entry into absorptive cells.
• These are found in the brush border of the intestine.
• table 24.5 p. 887 bottom = brush border section.
• Examples:
o Carbohydrates: 4: dextrinase (glucose), maltase (glucose), sucrase
(glucose + fructose), lactase (glucose + galactose).
o Protein: peptidases break down to amino acids.
o Nucleotides: nucleosidases, phosphatases. Products include
nitrogenous bases, pentoses, phosphates.
Note- Lactose intolerance due to lack of lactase causes problems typical of missing enzyme.
3. Secretion
• Secretes intestinal juice about 1-2 L/day. It is mostly reabsorbed under
normal conditions.
• Slightly alkaline (7.6) secretion of water, electrolytes, and mucus.
• Provides a vehicle for chyme to move through the intestine to be absorbed.
• Not much digestive activity in secretions.
4. Protection
• The submucosa contains lymphoid tissue (Peyer’s patches) especially
towards the end of the small intestine.
• The colon contains huge numbers of bacteria that must be kept in check.
Fig 24.23b p 883
• Paneth cells, deep in the mucosa, secrete lysosome, a bactericidal
enzyme, and are phagocytic.
Digestion in the Small Intestine
We shall take a look at digestion of the basic food groups:
Carbohydrates
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Proteins
Fats
We will see that the pancreas is:
Table 24.5 p 887 pancreatic juice section
1. An important source of digestive enzymes (carbohydrate, protein, triglyceride,
nucleic acid digesting enzymes) that act in the intestine.
Pancreatic juice ducted to duodenum, so an exocrine gland in this case.
2. Provides the alkalinity (bicarbonate) necessary for creating optimum pH for
enzyme activity in the small intestine.
Note- -ase on end of protein name indicates an enzyme that breaks down that chemical.
This diagram is in outline. Fig. 24.25 p. 888
from
Amylase
40% Saliva
60% Pancreas
Carbohydrates
(Starches)
from
Proteins
from
Fats
Pepsin
Stomach
Disaccharidase
from
Intestinal Cells
Mucosal Cells
Disaccharide
(Sucrose)
Trypsin
Chymotrypsin, others
from Pancreas
Polypeptides
Dipeptides
Bile Salts
Liver &
Lipase
Gall Bladder
from Pancreas
Emulsified Fats
Monosaccharides
(Glucose)
Peptidases
from
Intestinal
Mucosal Cells
Amino Acids
Fatty Acids & Glycerol
Other notes:
Bile (1 L/d) is produced in liver and stored in gallbladder.
• Greenish to brownish consisting of water, bile acids, phospholipids, bile
pigments.
• Gives stool its color (and urine too).
• Emulsifies large lipid globules into 1 mm droplets.
• This provides a large surface area for pancreatic lipase to perform a rapid
lipid digestion.
• Can also contain large amounts of bicarbonate to buffer intestinal fluid.
• Neutralizes the acidic chyme.
• If bile backs up due to liver injury or duct obstruction, bilirubin (from
breakdown of heme group in RBC) will back up and deposit in body
producing a yellow color.
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Absorption in Small Intestine
• Absorption of the end products of digestion takes place through epithelial
lining of small intestine.
• Microvilli offers increased surface area.
• Note: Any disruption of this lining will lead to discomfort, diarrhea, and
malabsorption.
o E.g., chemotherapy, radiation therapy, toxin, infection.
What are digestive products? Monosaccharides, amino acids, fatty acids
(glycerol).
fig. 24.25 p.888
Nutrient
Transport
Capillary Type in Villus
Monosaccharides
Facilitated Diffusion
Blood
Glucose transported as secondary active transport by riding along with active transport of Na+.
Amino Acids
Active Transport
Blood
Some are transported as secondary active transport by riding along with active transport of Na+.
Lipids & Vitamins A,D,E,K
Diffusion
Lacteal
Short lipids (10-12 carbons) diffuse into blood. Most (large) go through lacteals.
Water & Vitamins B**, C
Osmosis
Blood
Water absorption is dependent on the concentration gradient set up by the absorption of electrolytes and
nutrients. fig. 24.26 p.890 Notice large amounts of water secreted during digestion.
Ions
Active Transport, others
Blood
**Vitamin B12 combines with intrinsic factor (made in stomach) and is absorbed by receptor mediated
endocytosis.
Other notes:
• Oral Rehydration Therapy (ORT)
• Used to treat dehydration during diarrhea. Remember almost all Na is found in ECF and
is easily lost during secretory diarrhea. Major problems occur when Na and water are
lost in large amounts.
• You must give water, Na+, and glucose in a dilute solution. It works because of the co
transport of glucose and Na. Na and glucose are given in even molar amounts. If no
sugar is present, the salt will not be absorbed. It must not be too concentrated or the
solution will pull water out of the intestine, just the opposite of what is needed.
• A special formula was developed by the WHO and UNICEF to counteract dehydration.
• All in 1 liter:
o NaCl
3.5 g
o Sodium Bicarb
2.5 g
o KCl
1.5 g
o Glucose
20 g
• Bicarb ion is for pH control and K+ to replace loss in kidney and stool
• These formulations may be purchased at your local pharmacy. E.g., Pedialyte.
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Function of the Colon (large intestine)
Fig. 24.27 p.892
• No more digestion by you, but some by bacteria of indigestible foods.
• Can be beneficial (vitamins) or fun/embarrassing (gas).
Important for:
1. Water absorption.
2. Electrolyte absorption.
3. Vitamin absorption
• Bacterial products Vit. K, B complex (B1, B2) .
• Vitamin K is necessary for formation of clotting proteins in the liver.
• If given wide spectrum antibiotics that kills off bacteria, give Vit. K
injections.
4. Formation of feces (stool, solid waste (hopefully)).
• As feces enter and fill the rectum, stretch receptors initiate a defecation
reflex that empties the rectum to the anal canal.
• Once the reflex is triggered, only the voluntary external sphincter is holding
the feces back so voiding can be postponed until an appropriate time.
Functions of the Liver (other than bile formation)
Fig 24.21 p 879
1. Storage reservoir of blood in veins.
2. Cleanse blood from gut of bacteria. Phagocytic activity by Kupffer’s cells.
3. Produces blood in fetus.
4. Destroys old RBC. The heme portion is absorbed as bilirubin that is secreted
in the bile.
5. Detoxification: detoxifies alcohol, drugs, hormones, etc. that are secreted with
bile or removed in kidney.
6. Metabolism and storage of many substances.
• Examples:
• Carbohydrate: glycogen storage, makes glucose and glycogen.
o Manages blood sugar levels.
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• Protein: makes most plasma proteins. Coverts one a.a. to another.
o Deaminates a.a. for energy use.
• Lipids: stores triglycerides and breaks them down.
o Makes lipoproteins for lipid transport.
o Synthesizes cholesterol which is used to make bile salts.
• Stores vitamins: A, B12, D, E, K and minerals: Fe, Cu
Time for Food Passage
1-5 hours
End of pyloric
valve of
stomach
4.5 hours
Ileocecal valve
(end of small
intestine)
6.5 hours
End of
ascending
colon
9.5 hours
End of
transverse
colon
12-24 hours
End of colon to
anal canal
These are approximate times spent in each structure.
Intermediary Metabolism
fig. 25.16 p.926 table 25.2 p.927
• All the thousands of different chemical reaction in your cells.
• Mainly managing carbohydrates, proteins, and fats.
Anabolic Fig. 25.17, catabolic fig.25.18, table 25.2 p. 927
Carbohydrate metabolism
Catabolism = oxidation = cellular respiration = chief source of ATP.
To burn glucose, lipids, proteins, all use same reactions:
1. Glycolysis: converts glucose to pyruvate. Little ATP. Anaerobic.
2. Krebs cycle: ox-redox rxns, NAD+ and FAD are electron/hydrogen carriers.
Little ATP produced.
CO2, H20 are wastes.
3. Electron transport system (ETS): ox-redox rxns, electron energy is harvested
in steps, makes most of ATP, needs O2 (aerobic respiration).
If no O2 = anaerobic reactions = fermentation = lactic acid.
Anabolism
• Some glucose is converted to glycogen for storage.
• Can be reconverted to glucose for ATP.
• A.a., glycerol, lactic acid can be converted to glucose too.
Triglycerides
Catabolism
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• Broken down into glycerol and fatty acids.
• Burned for energy in Krebs-ETS .
• Ketone bodies appear in large amounts during a diabetic crisis.
Anabolism
• Synthesis of triglycerides from glucose and fatty acids = lipogenesis.
• Stored in adipose tissue.
Protein
Catabolism
• Amino acids oxidized through Krebs-ETS after deamination in liver, if
needed.
• Ammonia converted to urea in liver, excreted in urine.
• Can be converted to glucose, fatty acids, of ketone bodies.
Anabolism
• Protein synthesis is directed by DNA and carried out by RNA and
ribosomes.
Disorders of Digestive Tract
p.899-901
Diarrhea: defecation of liquid stool.
• Caused by increased motility and decreased absorption of water by the
intestines.
• Microbes (toxins or intestinal wall invasion), certain foods (some fruits
increase motility) (lactose intolerance, enzyme deficiency with increased
osmolarity in lumen), stress (anxiety increases parasympathetic activity to
lower bowel with increased motility).
• Dehydration and electrolyte imbalance may occur if prolonged.
• Can induce diarrhea with hyperosmol solutions such as Fleet’s enema
(sodium phosphate).
Constipation: infrequent or difficult defecation due to lack of motility.
• Feces remain in colon too long with excessive water absorption so feces
become dry and hard.
• Causes include lack of fiber in diet, improper bowel habits (failure to heed
the call), lack of exercise, emotional upset, lack of adequate fluid intake.
Ulcers
• PUD = peptic ulcer disease = a crater like lesion in the gastro/intestinal
membrane exposed to acidic gastric juice.
• Usually occurs in pyloric region (10%) or first part of duodenum (90%).
• Serious bleeding can occur (GI bleed) with anemia.
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• 3 causes:
1.Bacteria = Helicobacter pylori. Makes its own basic environment by splitting
urea.
2. Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin.
3. Hypersecretion of HCl, e.g. a gastrin producing tumor.
Food Poisoning
• Microbes can cause irritation of the intestines by direct invasion of the
mucosa or by secreted toxins.
• They find their way into foods where they multiple.
• Common causes are Salmonella, Shigella, Campylobacter, Staphylococcus
toxin.
Botulism
• Ingested toxin poisoning that is produced by Clostridium botulinum.
• Found in improperly cooked non acidic foods.
• The toxin inhibits ACh release so skeletal muscle flaccid paralysis results:
blurred vision, difficult breathing, swallowing, speech, general weakness.
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The Urinary System
Chapter 26 p 949
• The primary organ of the urinary system is the kidney.
• Life on land would not be possible without our kidneys.
o Sea animals live in a vast aqueous salty bath of constant
composition.
o We have to create our own private mini ‘sea’, our ECF.
• The ECF must remain in narrow limits for our cells to survive in the context
of a dry and ever changing environment.
• The kidney maintains the ECF indirectly by adjusting the plasma
composition.
• Therefore, the kidney plays a key role in maintaining this homeostasis by
controlling the composition, volume, and pressure of the blood in the
process of making urine.
• Each minute 1300 mls of blood enters the kidney via the renal arteries and
1298-9 leave by the renal veins, so only 1-2 mls/minute leave as urine.
We will look at what urine contains and why it is formed in this section.
The Functions of the Kidney
Fig 26.1 p 949
1. Regulates water balance by conserving or eliminating excess water.
• The kidney can handle excesses better than deficiencies.
• The kidney must put out about 500ml of water to accomplish the cleaning
of the blood even in the face of no water consumption.
2. Regulates salt concentration of the body.
• Examples: Na+, Cl-, K+, HCO3-, H+.
• Even minor fluctuations can be disastrous: K+ fluctuations can lead to
cardiac dysfunction.
Note: The first 2 functions help regulate blood volume, pressure, and
composition.
3. Eliminates Wastes
• There are many waste products that are formed as a byproduct of
metabolism in the body.
• Eliminates nitrogenous wastes that are toxic if retained. = wastes from the
breakdown of proteins. Ammonia changed to urea in liver, then excreted in
urine.
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• Other Examples: uric acid (nucleic acid metabolism), creatinine (muscle
origin), drugs.
• Most of these wastes are metabolized by the liver and made ready (water
soluble) for excretion by the kidney.
• Other organs in the body are responsible for getting rid of these wastes.
o Examples:
o Lungs:
CO2, water, heat
o Skin:
salts, urea, water, heat
o Kidney:
Excess H2O, ammonia, urea, uric acid, H+, salts, heat
4. Acid Base Balance
• Regulates H+ and HCO3- of the blood.
• Kidney actively excretes H+ as needed to maintain blood pH.
5. Kidney secretes erythropoietin (EPO) that stimulates RBC
production.
Water Balance in the Body
Fig. 27.1 p. 992
60% (male) of the body weight is water.
2/3 = Intracellular fluid (ICF)
1/3 = Extracellular fluid (ECF) = 80% Interstitial fluid, 20%Plasma
The kidney can effect all these fluid compartments by adjusting the plasma
compartment.
Total body water: content and concentration of the water (blood and ECF).
Fig. 27.2 p. 993 adult averages
Water is taken into body in 3 ways:
1. Food (water in food)
=
0.7 L/day
2. Drink
=
1.6 L/day
3. Metabolic production
=
0.2 L/day = water produced by chemical
reactions in the body (dehydration synthesis reactions, oxidation reactions).
Water is discharged from the body in 3 ways:
1. Sweating = 0.6 L/day
2. Lungs =
0.3 L/day
3. Urine =
1.5 L/day
Note: In both cases water lost and water uptake = about 2.5 L/day.
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These amounts will vary by ambient temperature (Taft in August vs. January)
and activity level. Job of kidney is to make sure water balance stays in balance
under varying environmental and intake conditions.
Component of the Urinary System
Gross Anatomy
Fig. 26.1 p.949
Or draw a diagram of the urinary system
Macroscopic Anatomy of the Urinary System
• The kidneys are above the waist and retroperitoneal to the peritoneal
cavity, partially protected by the 11th and 12th ribs.
• Blood supply = left and right renal arteries via abdominal aorta and enters
the hilus. Fig 26.3 p 952
• Blood leaves by renal veins to inferior vena cava.
• The ureter collects urine from the renal pelvis and delivers it to the bladder.
• The urine exits through a single urethra from the bladder.
Notes for anatomy
• 20-25% of resting cardiac output goes through kidneys via renal arteries.
• Kidneys serve to filter this blood of wastes and adjust constituents.
• Urination (micturition, voiding) = stretch receptors in the bladder fire when
bladder reaches certain volume (200-400 ml) to cause a micturition reflex in
the spinal cord.
• One gets the urge to urinate (a parasympathetic reflex) as the internal
sphincter relaxes and the bladder muscles contract.
• The external sphincter muscle is under voluntary control (cerebral cortex)
and will allow one to urinate at will.
Microscopic Inspection of the Kidney
Fig. 25.8b p.956
The functional unit (where the work gets done) of the kidney is the nephron.
It consists of:
• the renal corpuscle (glomerulus + glomerular (Bowman’s) capsule),
• the PCT (proximal convoluted tubule,
• loop of Henle,
• DCT (distal convoluted tubule), and
• collecting duct.
Each will be discussed below.
Draw diagram of a nephron.
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Microscopic notes
Blood supply
• Afferent arterioles deliver the first arterial blood to renal corpuscle and into
the glomerulus where filtration takes place. Note these are larger than the
efferent arterioles.
• The blood leaves via the efferent arteriole (an unusual situation to have
efferent arterioles).
• The efferent arterioles divide into a network of peritubular capillaries that
service the tubular portion of the nephron in the renal cortex.
• Some branches extend down into the medulla of the kidney, forming loop
shaped capillaries called the vasa recta that supply tubules in the medulla.
• The capillaries unite to progressively larger veins and ultimately leave the
kidney via the renal vein.
Urine flow
• The filtrate enters the glomerular capsule (located in the cortex of the
kidney) where it collects in a cup like space, the glomerular capsule
(Bowman’s capsule).
• It flows to the proximal convoluted tubule to the loop of Henle that
descends and then ascends in the medulla.
• Urine continues to the distal convoluted tubule in the cortex and then enters
the collecting duct that extends deep to the medulla.
• Now that urine is in its final form, it drains ultimately to the ureter and on the
bladder.
3 Basic Processes within the Nephron
fig. 26.7 p.959
1. Non-selective filtration (glomerular filtration) occurs in the renal corpuscle.
• Substances small enough to pass through the endothelial/capsular
membrane of the glomerulus filter into the renal tubule by the force of blood
pressure (bulk flow).
• This is basically a protein free and cell free filtrate.
2. Selective reabsorption into the blood
• As filtrate passes along renal tubule useful materials are returned to
peritubular capillaries (blood).
• In other words, there is movement of filtered substances from the tubular
lumen to the peritubular capillaries.
3. Secretion by tubule cells into urine
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• As fluid passes continues along the tubule, it also gains some material
(wastes, excess substances) from tubule cells and blood capillaries.
• In other words, movement of nonfiltered substances from the peritubular
capillaries into the tubular lumen.
Let’s look at these processes in more detail.
1. Non-selective Filtration (glomerular filtration)
draw a renal corpuscle or Fig.26.9 p.962
• Blood is filtered into capsule and through a membrane due to blood
pressure. p.962 for formula
• Net filtration Pressure = 10mm.
• Hydrostatic pressure = 55 mm Hg (large pressure in capillary due to large
afferent arteriole supply and small efferent arteriole drainage) and is
opposed by 15 mm back pressure from capsule and 30 mm of blood
osmotic pressure (due to pull on H2O by proteins left behind in plasma).
o See Starling’s law of capillaries, p.703-4 if you want to know more.
• About 16-20% of plasma volume becomes filtrate.
• GFR (glomerular filtration rate) = 120ml/min or 180L/day at net filtration
pressure (NFP) of 10mm Hg. This must be maintained to make urine.
• The JGA (juxtaglomerular apparatus cells) monitor GFR and release
vasoconstrictor substances to alter the diameter of the afferent arteriole to
maintain proper GFR. A method of local renal autoregulation. Fig 26.11 p
964
o Usually, the GFR is fairly constant when BP is between 80-180 mm
Hg.
• Under sympathetic stimulation during stress, sympathetic motor impulses
to all arterioles in kidney override autocontrol and restrict blood flow to
kidney, greatly reducing urine output, e.g. during heavy exercise.
• Everything in plasma is filtered into the glomerulus except formed elements
of blood and plasma proteins.
o Glomerular Filtrate =Glucose, amino acids, H2O, nitrogenous wastes:
urea (and uric acid, creatinine), ions (Na+, K+, Cl-).
o Similar in concentration to plasma.
• Filtrate moves next to the loop of Henle
2. Selective Reabsorption (tubular reabsorption)
• Returning most (99%) of the filtered water and solutes back to the blood
stream is a critical nephron function.
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• It is the reclamation of ‘valued substances’ while wastes continue along in
the tubule to form urine.
Let’s see how each portion of the nephron tubule reabsorbs substances.
a. PCT reabsorption fig 26.12 p.967
• Lined with cuboidal cells with microvilli. Highly permeable to H2O and many
solutes.
• Path of reabsorption = tubule lumen-transcellular- interstitial fluid – blood in
local capillary
• Reabsorbed substances:
o 100% glucose and amino acids
o 65% Na+ and water
o 50% urea
• Driving force of reabsorption = Na+ ion transport
o The active transport of Na+ via the sodium/potassium pump sets up
an osmotic, chemical and electrical gradients that promotes
reabsorption of the other solutes and water.
o Pumps are found in basolateral membranes next of interstitial fluid.
K+ is returned through a channel to interstitial fluid. Interstitial fluid
becomes concentrated with Na+.
o This requires a lot of ATP (6% of body total for renal tubules) made
by many mitochondria.
o Glucose uses a symporter protein to be carried along with Na+. Fig
26.12 p 967
b. Loop of Henle reabsorption
fig.26.15 p.969 or draw diagram of loop of Henle
• Reabsorbed substances:
o 20% Na+ (other ions K+ (30%), Cl+ (35%) come in with Na+)
o 15% water
• Most reabsorption occurs in ascending limb using a sodium pump that also
symports 2Cl- and 1K+ with each Na+.
o Na+ and Cl- move into interstitial space to increase saltiness.
o There is a 200 miliosmole difference between the tubule and
interstitial fluid at any level.
• Ascending loop has cuboidal cells with few microvilli.
o Luminal membrane lines with glycoprotein layer limits H2O passage.
o Many transporter proteins in membrane so permeable to solutes.
• The ascending portion of the loop is impermeable to water so no water can
be reabsorbed.
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o This increases the water concentration in the ascending limb (dilutes
the filtrate in the tubule, but increases solutes in the surrounding
medulla).
• Descending limb has simple squamous cells that are permeable to H2O but
not solutes. Not many protein transporters in membranes. No microvilli.
• Some water can leave the descending limb by osmosis due to the salty
medulla made so by the ascending limb and the urea from the collecting
duct.
c. DCT and collecting duct reabsorption
• DCT has 2 cuboidal cell types:
1. Principal cells with few microvilli.
i. Permeable to water and solutes (Na, K) under hormonal
control.
2. Intercalated cells with many microvili.
i. Secretes H+ into the urine from the surrounding capillaries for
acid base balance. See next section.
• 90% of solutes and water have been returned when entering this portion of
the tubule.
• The fine tuning of water reabsorption in the DCT/collecting duct will be
discussed in a few minutes.
Summing up:
• If it were not for reabsorption, plasma volume would be gone in 20 minutes.
• Plasma volume of average person = 3L.
• Total volume of plasma runs through kidney about 60 times/day.
• However, 99% is of fluid is reabsorbed.
3. Secretion (tubular secretion)
This is movement of materials from the blood (peritubular capillaries and vasa
recta) into the tubular fluid to become part of the urine.
Primarily functions:
1. H+ to control pH. This occurs as H+ is moved to the nephron (urine flow) from
the blood and HCO3- is reabsorbed to the blood flow. So this removes acid and
preserves the buffer in the body.
2. Some other important materials that are secreted are:
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• K+: to remove excess K+ ions to the urine from the capillaries. High levels
can damage heart contractions.
• Eliminate urea that has been reabsorbed.
• Dispose of some drugs that are not in filtrate.
We will not discuss the mechanisms of secretion.
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Let’s review what has happened during these 3 processes in the
nephron by reviewing this table of filtered substances.
This table is in the outline.
table 26.3 p. 965
Substance
Plasma (total)
Water
Proteins
Sodium ions
Bicarbonate ion
Glucose
Urea
Creatinine
3L
20g
9.7g
4.6g
3g
4.8g
0.03 g
Filtered (enters
glomerular
capsule/day)
180L
2g
580g
275g
180g
53g
1.6g
Reabsorbed
(returned to the
blood/day)
178.5L
1.9g
575g
275g
180g
28g
0
Urine
(excreted/day)
1.5L
0.1g
4.6g
0
0
25g
1.6g
Note: urea is secreted in addition to being filtered and reabsorbed.
The Regulation of Water Balance (control of water balance)
• As noted earlier, the kidney plays a main role and water balance.
• Bird and mammals (including man) have the ability to excrete hypertonic
urine (up to 4x that of blood, some desert mammals = 20x).
• hypertonic = urine that is more concentrated than their body fluids.
Fig. 26.19 p.974
Let's see how the production of hypertonic urine is accomplished in a nephron.
Draw diagram of nephron showing osmolarity at various points.
Fig. 26.18 p.973 = no ADH, 26.19 p. 974 = with ADH
• The diagram in the outline is similar to 26.19 p. 974 = with ADH
• Units = mOsm/L (milliosmoles/L) = 1/1000 of an osmole.
• Osmolarity = the number of moles of particles per Liter of water.
o It depends on the number of particles, not the kind.
o An osmole = the amount of substance that disassociates to produce
1 mole of particles in solution. (1 mole of NaCl = 2 Osm, 1 mole
glucose = 1 Osm)
o Body fluids are dilute, so we use mOsm/L, not Osm/l.
o In other words, the total number of dissolved particles per liter, or the
solute concentration (dissolved substances).
o Don't worry about units, just the magnitude.
• This will determine which way the water will move across a membrane.
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The loop of Henle is primarily responsible for this ability to concentrate
urine. fig. 26.19 p.974
An osmotic gradient is established in the medulla around the loop of Henle as
follows:
• The thick ascending limb cells establish the ionic gradient in the renal
medulla as follows:
• Na+ (and K+, 2Cl-) moves out of ascending limb by active transport but
water (impermeable cell membrane) continues up the ascending limb to the
distal tubule.
• This makes the medulla very salty with help by the slow moving vasa recta
blood carrying salt to the inner medulla.
• This makes ascending tubular fluid have more water and less solutes (100
mOsm).
• The opposite condition exists in the descending limb.
• Water moves out of the descending limb by diffusion (osmosis) but is
impermeable to salt. This makes the tubular fluid more concentrated as it
descends (1200 mOsm at bottom).
• H2O moves out of the distal convoluted tubule by osmosis near thick
portion of ascending limb. This makes medulla interstitial space near the
cortex more dilute (300- 400 mOsm).
• Urea diffuses from the collecting duct near the turn of the loop of Henle
(deep in the medulla) adding to the high concentration of solutes in the
interstitial space (1200 mOsm)
• The blood flow in the vasa recta is extremely sluggish and does not disturb
the gradient established by the loop of Henle.
• The osmotic gradient established in the medulla sets up the potential for
the collecting duct to fine tune the water balance.
• Permeability in collecting duct is controlled by increased antidiuretic
hormone (ADH) from pituitary.
This will be explained below.
How urine concentration is controlled.
Let’s see how this happens:
There are 2 hormones that regulate reabsorption in the kidney:
Aldosterone
ADH
1. Aldosterone
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• Aldosterone is a hormone produced by the adrenal gland (cortex).
o A mineralcorticoid (controls Na+ resorption and K+ excretion).
• Aldosterone increases Na+ reabsorption by the kidney.
• Aldosterone activates transport proteins (principal cells in collecting duct) to
move Na+ from the filtrate to the nearby peritubular capillaries.
• The water follows the sodium in the presence of ADH.
• This in turn increases amount of water being reabsorbed (water is
conserved).
• So, when low levels of aldosterone, more Na+ and therefore water are
removed from the body in the urine.
What triggers aldosterone to be produced?
2 things:
1. Drop in Na+ ion concentration, dehydration, or hemorrhage.
All these cause:
Fig 18.16 p 611 renin release with angiotensin II effects
2. Drop in blood pressure as measured by juxtaglomerular apparatus (Na+, Cl-,
H2O flow) located on afferent artery adjacent to the DCT.
• Causes kidney (JG cells) to produce renin, an enzyme that acts on
angiotensinogen (a protein produced in the liver).
• Note: Adequate blood pressure is necessary for filtration.
Fig. 18.16 p.611 renin-angiotensin-aldosterone combined effects
Drop in blood pressure
Liver
kidney produces renin.
kidney
renin
Bloodstream
angiotensinogen
lung
angiotensin I
= blood protein
angiotensin II
adrenal cortex
aldosterone
increased Na + reabsorption by kidney
• Renin from kidney transforms a blood protein angiotensinogen to
angiotensin I.
• Angiotensin I moves to lung and is converted to angiotensin II.
• Angiotensin II causes adrenal cortex gland to produce aldosterone.
• Angiotensin II also acts on brain to produce:
o Sensation of thirst in hypothalamus and constrict afferent arterioles to
increase BP.
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o In the kidney, it constricts afferent arterioles of glomerulus to slow
down filtration and enhances water and Na+ and Cl- reabsorption in
PCT.
• Aldosterone increases Na+/Cl- and water reabsorption in principal cells of
DCT and collecting duct with increased K+ secretion into urine so that blood
volume and osmolarity is increased.
o More Na+ pumps are put into membranes under aldosterone
influence.
See text box p.975
Diuretics = drugs that increase urine flow by inhibiting:
• Na+ transport (reabsorption) in ascending loop or collecting duct.
o So, water will also be lost in the urine.
• People taking them have to urinate often and also may lose more K+.
2. ADH (antidiuretic hormone) or vasopressin
fig. 18.9 p.602 or fig 26.17 p.971
• ADH is released by posterior pituitary gland (produced by cells in
hypothalamus).
• It works by controlling permeability of collecting duct to water.
• It is the main water regulator.
• It increases permeability to water by inserting channel proteins so water
leaves by osmosis to the blood.
• Therefore, decreases urine production.
• Urea passively follows the H2O into the medulla area maintaining the high
osmolarity in the lower medulla.
What triggers release of ADH by pituitary?
2 things:
1. Increased concentration of solutes in blood as monitored by the
hypothalamus.
• Example: Dehydration.
2. Decreased blood pressure.
• As monitored by stretch receptors in aorta and carotid arteries.
• Example: Hemorrhage.
Both act to cause ADH release.
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ADH increases water reabsorption.
• So, ADH decreases solute concentration in blood by dilution.
• In absence of ADH urine output rises: > 10X. Up to 20L/day.
• It also causes constriction of arterioles = BP increase, so called
vasopressin.
• So, ADH and Aldosterone work together to replace water, sodium, and
increase blood volume and pressure.
• Glomerular Filtration Rate is steady in the face of moderate BP changes for
short time periods via autoregulation of a local vasoconstrictor secreted by
JGA.
o Also affected by:
Hormones: Angiotensin II and ANP (atrial natriuretic peptide
from atria).
Neural regulation by sympathetic response that shuts down
afferent and efferent arterioles.
Why is urine yellow?
• Due to pigment created when old red cells are recycled.
• Hemoglobin breaks down and part of the heme portion becomes bilirubin
which is excreted as a similar pigment in the urine.
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The Regulation Of Water Balance
• Production Of Hypotonic Urine.
o No vasopressin (ADH) present.
o Collecting tubules impermeable to water.
o Therefore, large volume of dilute urine. Fig 26.18
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• Production Of Hypertonic Urine.
o Vasopressin (ADH) present.
o Collecting tubules permeable to water and water is conserved.
o Therefore, small volume of concentrated urine.
o Water picked up by the peritubular capillaries. Fig 26.19 Table 26.4
Effects of Drugs
Diuretics
• Substances that slow renal reabsorption of water and cause diuresis
(elevated urine flow rate) and therefore reduces blood volume.
o Prescribed to treat hypertension by lowering blood volume.
Prescription diuretics. These act by inhibiting reabsorption of filtered Na.
• Lasix (furosemide) act on ascending limb to inhibit Na 2K Cl symporters.
So more salt stays in tubule and water with it.
• Thiazide (e.g. chlothiazide Diuril) acts in DCT by inhibiting Na Cl
symporters.
• Excess K may be lost in DCT with above two examples.
o So, may need a K supplement.
• Spironolactone (Aldactone) acts to inhibit aldosterone by blocking Na
leakage channels. These are K sparing diuretics.
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Other diuretics
• Alcohol prevents release of ADH from pituitary, therefore greater urine
production.
o So you become dehydrated = hangover with thirst and headache.
• Caffeine inhibits Na+ reabsorption, so Na+ and water loss increases in
urine.
Antidiuretics
• Nicotine, morphine, barbiturates- all stimulate ADH release.
Creatinine Clearance
p.977-8
• Creatinine is produced in skeletal muscle from creatine phosphate at a
steady rate. So it remains in the blood at a steady value at about 0.5 – 1.5
mg/dl.
• It is cleared (filtered) by the kidney as fast as it is made. None is
reabsorbed. This makes it a good indicator of nephron filtration.
• So, if it blood level raises (>1.5 mg/dl) it is usually an indicator of poor renal
function.
• Better is a measure of renal creatinine clearance as expressed by how
effectively the kidneys remove it from the plasma in a 24 hour period.
Renal creatinine clearance = Urine creatinine level in 24 hr sample X urine volume in ml/min over 24 hrs
Plasma creatine level
Normal filtration = 140ml/min
Disorders of Kidney
p.985-6
Nephritis
• Bacterial infection of kidney.
• Usually see protein (proteinuria), white cells, bacteria, nitrate in urine.
• Nephritis is treated with antibiotics.
• If not successful use hemodialysis (machine performs function of kidney) or
kidney transplant.
Diabetes insipidus
• Loss of ability to secrete ADH, increased urine flow (5-20 L/day).
Renal failure
• Decrease or cessation of glomerular filtration.
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2 types:
1. Acute: abrupt stop. Less than 250 ml of urine/day.
• Causes: decreased CO, blood volume, damage to renal tubules (toxins,
drugs), kidney stones.
2. Chronic: progressive irreversible decline in glomerular filtration rate (GFR).
• Causes: glomerulonephritis, pyelonephritis, trauma to kidney.
• 75% of nephrons can be lost before noticeable (renal insufficiency).
Assign Q 20
Describe how the kidneys produce dilute or concentrated urine.
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The Reproductive System
Chapter 28 p. 1014
Introduction
• All of the systems we have studied so far have played a role in maintaining
homeostasis of the body.
• The normal functioning of the reproductive system is not necessary for
individual survival.
• But it is necessary for the survival of the species.
o At least for the time being, (e.g. human cloning, external wombs).
• Only through the reproductive process can the complex genetic blueprints
survive beyond the individual lives of the members of a species.
o Now we can even change the blueprints without sex using genetic
engineering! Changes maybe made in early stage embryos that will
affect every cell in the organism.
• The reproductive system strongly influences our psychological behavior
and social structures.
o Our feelings of maleness and femaleness and organization into family
units are examples.
o These behaviors are conducive for perpetuating our species.
• On the other hand, the population explosion of humans is putting pressure
on the earth’s dwindling resources and pollution is causing global damage.
o So, there is concern to provide the means to limit reproduction.
• Reproductive capability depends on an intricate relationship among the
hypothalamus, anterior pituitary, reproductive organs, and the target cells
of the sex hormones. These structures create an axis of control for
reproductive structures and behavior.
We will be discussing the details of these relationships.
For each of us life began with the fusion of 2 remarkable cells:
Sperm fror a male = spermatozoa
Egg from a female = ova
collectively known as gametes (sex cells)
• Union of the ova and sperm is called fertilization = time of conception.
• The resulting cell is known as a zygote.
• The zygote contains genetic material from each of the parents in a unique
combination.
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• This is due to recombination of chromosomes and independent assortment
of chromosomes, and, mutations that occur in the gamete of an individual.
o This gives rise to a unique individual with various characteristics
(traits).
o Some traits are from the mother, others from the father, some as the
result of both together (recessive traits).
• The organs that produce the sex cells (gametes) are known collectively as
the gonads.
• The gonads are the essential organs of reproduction:
o Testes = male = spermatozoa
o Ovaries = female = ova
The Components of the Male Reproductive System
Fig. 28.3 p.1017
Essential organs = testes
• Products:
o Sex cells = spermatozoa fig 28.8 p 1021
o Hormones (discussed later)
Accessory organs
Fig.28.11 p.1025
1. Genital Ducts = tubing. Functions to conduct or store of sperm.
2. Accessory Glands. Produce fluids, suspension, activation, nourishment
of sperm.
3. Penis = copulatory organ used for introduction of sperm into the vagina
of a female = insemination.
Formation of Sperm
fig. 28.7 p.1021
• Formation of sperm (average of several million/day) occurs from
adolescence (13-15 years) to old age. >90 years old. Viable? Defective?
• Sperm are first produced during puberty under the influence of an increase
of testosterone.
• Testosterone is produced by the Leydig cells (interstitial cells) located in
the CT between the seminiferous tubules under the influence of LH
(luteinizing hormone) from the anterior pituitary. Fig 28.6
• Testosterone also stimulates the growth and maturation of the external
genitals and reproductive tract.
• Sperm are formed within the testes in seminiferous tubules = seed bearing.
Fig. 28.5 p.1019.
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• Production of spermatozoa within seminiferous tubule takes about 74 days.
• Not all tubules show same stage of development at same time. (makes
sense or a male could only produce new crop every 74 days).
• So, sperm are available at most times for insemination.
• Sexually active male with self and/or partner could run out temporarily
(practice makes perfect!) and become infertile.
o Ejaculation 3-4x a week is about the limit before ‘running low’ on
sperm.
Spermatogenesis = sperm production.
• Gametogenesis = gamete production. Fig. 28.6 p.1020, fig. 28.7 p.1021
• Spermatogenesis (production of male gametes) takes place in a number of
steps within seminiferous tubules.
• Sperm begin as spermatogonium (stem cell: one daughter cell stays behind
undifferentiated as a reserve for more sperm) with full complement of
chromosomes = 2n or diploid.
• So
o 44 Somatic (=Autosomal) Chromosomes + 2 Sex Chromosomes X
+ Y = 46 total
o 23 pair or 46 = diploid chromosome # = 2n
• Review the following flow diagram of gamete development.
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1- Spermatogonium (stem cell) (2n)
Mitotic
Division
Stem cell
stays behind
25 days
Growth
GnRH (hypothalamus)
LH, FSH (pituitary)
w/ testosterone
1- Primary
Spermatocyte (2n)
16 days
Meiosis I = Reduction division
= Haploid or n = ½ total # chromosomes
22 chromosomes + X, ½ are this type
or 22 chromosomes + Y, ½ are this type
Autosomes maybe all maternal,
paternal, or combination (due to crossing
over). Independent assortment too.
2: Secondary
Spermatocyte (n)
16 days
4: Spermatids (n)
Meiosis II = Equatorial division
= no DNA replication, separation of 2
sister chromatids of same chromosome.
Sperm = haploid (n)
2 w/ 22 autosomes + X sex chromosome
2 w/ 22 autosomes + Y sex chromosome
16 days
4: Sperm (n)
Notes: fig 28.6
• An effective blood-testes barrier is maintained by the seminiferous tubule to
keep spermatogenic cells from interacting with the immune system.
o Sperm have antigens considered nonself by a man’s immune system.
o So, the sperm would be destroyed if this barrier were not intact. (This
can happen) Check for sperm antibodies in the male.
• Sperm do not appear until after puberty after the immune system has
developed.
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Differences in Sperm
Male promoting sperm characteristics
½ sperm produced =
Female promoting sperm characteristics
½ sperm produced =
22 autosomal chromosomes + Y chromosome
22 autosomal chromosomes + X chromosome
male producing sperm = androsperm
female producing sperm = gynosperm
Note- ova can only have:
22 autosomal chromosomes + X chromosome
22 chromosomes + X (from ova)
22 chromosomes + Y (from sperm)
22 chromosomes + X (from ova)
22 chromosomes + X (from sperm)
44 chromosomes + X + Y = 46 chromosomes
44 chromosomes + X + X = 46 chromosomes
male XY
Y chromosome smaller
female XX
X chromosome larger (2.8% more DNA per
sperm cell)
Small, rounded head
Large, oval shaped head
Greater in number at time of ejaculation
Fewer in number
Does poorly in acidic environment (vagina) Does better in acidic environment
Does best in alkaline environment
Does well in alkaline environment
Swims faster
Swims slower
Survives about 1 day in female
Survives about 2-3 days in female
Does best in high sperm count
Does best in low sperm counts
See handout on determining your baby’s sex. The Shettles method, an older
method. Not too reliable.
Today? More reliable methods. Cytoflow (mircrosort) method to separate andro
from gyno sperm! Then create embryo in vitro with desired sperm. Or, creation
and selection of male and female embryos in vitro, then select only embryos of
desired sex and implant in uterus. Remaining embryos may be frozen (saved),
donated, or destroyed.
Erection of the Penis
Fig.28.12 p.1027
Erection of the penis is an adaptation to ensure deposition of sperm in the female
reproductive tract near the cervix (inferior opening to the uterus) by penetrating
the vagina.
The Erection Reflex
Stimulus for erection:
Neural stimulus
• Mental (thinking about it), special senses detect erotic stimuli (seeing it,
hearing it, smelling it).
Mechanical stimulus of pressure receptors.
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• Tactile stimulation of genital area, especially the glans that caps the tip of
the penis.
• Stimulus leads to parasympathetic impulses (response) sent through sacral
segments (2-4) that innervate arteries of the penis.
o This parasympathetic reflex triggers release of NO (nitric oxide) leads
to relaxation of vascular smooth muscle, causing arterioles to dilate.
Note that this parasympathetic control of the arteriole
vasodilation is unusual in that arterioles are normally controlled
sympathetic innervation.
o This is where Viagra (sildenafil) is effective.
Viagra is an enzyme inhibitor of PDE5 (phosphodiesterase type
5). PDE5 stops turns off the trigger for erection by opposing the
action of the released nitric oxide (NO).
So as the man ages and less NO is released, Viagra allows
less NO to trigger the erection mechanism.
Viagra has no effect until sexual stimulation is present, it just
lowers the trigger mechanism.
• The vascular space of the erectile tissue fills with blood and becomes erect
(turgid).
• Expansion mechanically compresses the drainage veins so the erection is
maintained.
• Another parasympathetic response is stimulation (prior to ejaculation) of
the bulbourethral glands that has ducts to the spongy urethra that injects
mucus to lubricate the glans and alkaline substance to protect sperm from
the acidic vagina.
Ejaculation and the Formation of Sperm
• Ejaculation is the propulsion of semen from the male duct system.
• Ejaculation is under sympathetic control (L1-L2 level).
• After continued stimulation a massive discharge of nerve impulses leads to:
1. Contraction of smooth muscle in the genital ducts which delivers semen
into the urethra.
2. The urinary bladder sphincter closes (prevents urine flow and semen into
bladder).
3. Penis muscles undergo rapid contraction propelling sperm up to 200
inches/sec.
Summing up:
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• Sperm is forced from the epididymis, where it is stored, into the genital
ducts, to the urethra, and to the outside.
• Along the way secretions enter from the seminal vesicles and prostate
gland.
• This entire event is called a climax or orgasm.
• It results in intense pleasure, general muscle contraction, rapid heartbeat,
and elevated blood pressure.
• It is quickly followed by muscular and psychological relaxation and
vasoconstriction of penile arterioles (return to placid state).
• This latent period may last minutes to hours and increases with aging.
Semen (ejaculate) = mixture of sperm and seminal fluid.
• Seminal fluid is the liquid portion of the semen from the seminiferous
tubules, seminal vesicles, prostate and bulbourethral glands.
Constituents of Semen (Semen Analysis) p. 1026
1.Volume: 2.5 - 5 ml per emission.
2. Motility: at least 60% should show good forward motility within 3 hours.
3.Sperm count = 50-150 million/ml.
• If below 20 million, then infertility problems.
• Although only 1 sperm fertilizes the egg, many sperm are needed to
release hyaluronidase and proteinases (from acrosome) to digest materials
surrounding the oocyte (secondary).
• Sperm count may go down as a person ages, due to less testosterone.
• Environmental ‘estrogens’ are lowering sperm counts around the world.
• Tight fitting clothes and too many hot baths, or emissions too often may
lower count as well.
4. Liquefaction normally occurs within an hour or so.
• Delayed liquefaction greater than 2 hours indicates inflammation of
accessory glands.
5. Morphology
• No more than 30-35% should have abnormal shapes.
6. pH = 7.2 – 7.7
7. Fructose: absence indicates obstruction or congenital defect.
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Note: Absence of sperm and zero motility are key signs of sterility in the male.
Of the Total Semen Volume:
60% = from Seminal Vesicles. Sticky, viscous, consistency with yellow color.
p.1024
Contains:
• Fructose provides for ATP for motility.
• Prostaglandins causes of motility increase in sperm and reverse peristalsis
in uterus and uterine tubes.
• Clotting proteins (different from plasma)
• Alkaline pH protects from acids in vagina (pH = 3.5 – 4).
25% = from Prostate Gland. Milky white, slightly acidic (pH 6.5) fluid. p. 1025
Contains:
• Citrate (ionized citric acid)- used to make ATP
• Prostatic-specific antigen (PSA) and other proteolytic enzymes that liquefy
coagulated semen.
o PSA can be monitored annually to check for prostate cancer in men
over 50.
o It increases when a cancer grows.
• A DRE should be performed at the same time.
13% = from Seminiferous Tubules and Bulbourethral Gland. p. 1026
• For suspension of sperm and to lubricate penile urethra and glans penis.
2% = Sperm.
• So, a vasectomy in a male shows little difference in amount of ejaculate.
Role of Male in Reproduction
• Insemination of female where sperm is deposited in the vagina for easy
access to the cervical os (opening).
• Sperm must make its way via the cervix (with mucus plug present except
near ovulation) and uterus to uterine (fallopian) tubes where fertilization
occurs.
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The Female Reproductive System
Chapter 28 p 1012
Introduction
• The female reproductive system is more complex than that of the male.
• Unlike the male with constant release of gametes and testosterone, she
releases ova intermittently and secretion of female sex hormones is
characterized by wide cyclical swings.
o The tissues influenced by these sex hormones also undergoes
cyclical changes, the most obvious in the monthly menstrual cycle.
• She must produce gametes and prepare to nurture a developing embryo
each reproductive cycle.
o If pregnant, she must build the structures to maintain the fetus for 9
months.
• After pregnancy she continues her reproductive duties by producing milk
(lactation) for the baby’s nourishment.
Components of the Female Reproductive System
Fig. 28.13 and 14 p.1028-9
Essential organs = Ovaries. The ovaries have a dual function as in the male.
The ovary produces:
1. The sex cells or gametes = ova or secondary oocyte.
2. Hormones = Primary: progesterone and estrogens (the female sex hormones).
• Estrogen:
o Maturation and maintenance of the entire reproductive system and
secondary sexual characteristics.
o Similar to testosterone’s role in the male.
• Progesterone:
o Prepares the uterus as a suitable environment for a developing
embryo/fetus and contributes to the breasts’ ability to produce milk.
• Small amounts of others: inhibin (inhibits FSH secretion), relaxin (relaxes
uterus for implantation).
• Note: Ovarian cancer is the 6th most common cancer in females and is
quite deadly.
o Its onset is without symptoms or are mild and easily overlooked.
Cause is unknown.
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o It metastasizes beyond the ovaries easily, which makes a cure
difficult.
o CA 125 blood test can detect its presence but many false positives
and some false negatives occur.
Accessory organs
Uterine (Fallopian, Ovarian) tubes
• Receives the ova and provides site where fertilization (the sperm and ova
combine) generally occurs.
• Fertilization can only occur in a very limited time.
• The ovum begins to disintegrate in 12-24 hours and is subsequently
phagocytized.
• Sperm may live up to 5 days in the female.
Uterus (womb)
• Organ in which the zygote is implanted in the wall & the fetus develops.
• The inner lining of the uterus is called the endometrium.
o The endometrium becomes highly vascularized as it prepares for
implantation and is shed in each menstruation cycle when a zygote is
not received.
• The inferior tip of the uterus that communicates with the vagina is called the
cervix.
o The cervical mucosa provides some of the lubricant for the vagina
during intercourse.
o The mucous plug usually present is not present 3-4 days during
ovulation.
o The cervix is a common point of cancer development in women.
Cause is usually Human Papilloma Virus infection.
A Papanicolaou (Pap) smear is performed by scraping away
the epithelial cells of the tip of the cervix and placing them on a
glass slide.
The slide is stained and examined for abnormalities.
It is advised that annual Pap smears be performed to detect
these slow growing cancers.
A vaccine is available to the most common types of HPV that
cause this cancer as of 2006. Get it!!
Vagina
2 primary functions:
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1. Receptive organ for the penis of the male.
• Blood flow increases in the vagina are due to parasympathetic vasodilation
of arterioles during excitement.
o As in the male, this phase can be stimulated by either physical or
psychological stimulation in the female.
• Vasocongestion follows with fluid forced out of the capillaries into the
vaginal lumen.
• The lower 3rd of the vaginal reduces in diameter to better contact the penis
(the orgasmic platform) and the upper portion expands as the uterus raises
to create a space for the semen.
2. Passageway = the birth canal, and for menstrual flow with no pregnancy.
• Its mucosal lining contains large amounts of glycogen that is converted by
resident bacteria (lactobacilli) to fermented acid end products (pH 3-4) that
protect the vagina from infection but is hostile to sperm.
Various glands
• Provides secretions for lubrication for entry to vulva and vagina during
sexual intercourse.
• Plus, various other secretions for the maintenance of the reproductive tract.
External genitalia (vulva, pudendum)
• Protects the vaginal opening (labium majus, minus) and part of which is
erectile tissue (clitoris) important in sexual stimulation of the female
(analogous to the glans of male penis).
• The vulva and clitoris swell during sexual excitement as the inflow of blood
increases.
• Female orgasm differs in 2 respects from the male:
1. There is no ejaculate.
2. Females do not become as refractory following orgasm so can
immediately respond to continued erotic stimulation and possible
achieve multiple orgasms.
Mammary glands
• Produce milk to nourish the newborn baby, so are important after
reproduction has occurred.
• Breast feeding suppresses LH and FSH secretion (no ovulation) and helps
uterus involution via oxytocin. Suckling by infant stimulates release from
posterior pituitary.
• The baby receives antibodies, nutrients, promotes normal flora
establishment in the digestive tract.
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• Also the nipples become erect and the breasts enlarge during sexual
excitement.
• Note: 1 in 8 women will develop breast cancer in her lifetime.
• 70% have no known risk factor.
• 5% are associated with genetic mutations.
• Examples: BRCA1 and BRCA2
• Mammography is recommended every 2 years age 40-49, and every year
thereafter.
• Monthly self exam is important also every month after age 20. Look for
lumps, puckering, nipple retraction or discharge.
Formation Of Ova
see hand drawing- Oogenesis in Relationship to the Ovary
• The formation of ova is called oogenesis.
• Unlike the spermatozoa, the formation of ova does not begin at puberty.
o The process of oogenesis begins during the 3rd month of fetal
development.
o At birth, the female contains all the eggs she will ever have, about
200,000 to 2 million total for each ovary.
• The primary oocytes, as they are called at this time have undergone part of
the first division of meiosis (meiosis I). There are 46 replicated
chromosomes at this point.
• The primary oocytes remain in this stage of development (prophase of
meiosis I) until puberty (9 -12 years) when under the influence of certain
hormones (gonadotropins), the first meiotic division resumes.
• Of the 2 million primary oocytes, only 300 - 400 will reach maturity and
ovulate, usually 1 reaching maturity every 28 days after puberty and until
menopause is reached around age 50.
• Therefore, as many as 50 years may elapse between initial formation and
the end of the 1st meiotic division.
o This can lead to problems, e.g. Down syndrome, an extra
chromosome 21.
o Ova may be frozen early in life (before age 30?) so ‘young eggs’ may
be preserved for a later date of fertilization.
Oogenesis
Fig. 28.17 p.1032 or see oogenesis drawing.
• Like spermatogenesis, oogenesis takes place in a number of steps.
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• They begin as primitive ova (oogonia, stem cells) dividing by mitosis before
birth.
Reduction division = Meiosis I
• The primary oocyte arrests at prophase meiosis I before birth and until
puberty.
• Meiosis I completes, one primary oocyte each month (ovulation) after
puberty until menopause. There are 46 replicated chromosomes at this
point.
• So, this only occurs about 400 times in a women’s reproductive life.
• A secondary oocyte is produced that retains most of the cytoplasm and one
polar body.
• Polar bodies are nutrient poor cells and soon degenerate.
• There are 23 replicated chromosomes at this point: 22 autosomes and 1X
sex chromosome.
• The polar body may divide into 2 polar bodies.
Equatorial division = Meiosis II
• Meiosis II only completes if sperm are present and fertilization of the
secondary oocyte occurs.
• It degenerates if no sperm are present.
• An ovum and a polar body are produced if fertilization occurs.
• Chromosome number at this point is a single copy of 23 chromosomes.
• Note that only 1 ovum is produced for each of the four that starts meiosis 1,
the rest become polar bodies.
See drawing for further explanation.
Oogenesis In Relation To The Ovary
Fig.28.15 p. 1031 or see Oogenesis in Relation to the Ovary drawing in notes.
Primary Ovarian Follicle =oocyte + cells around it that serve to nourish oocyte &
secrete estrogens that initiate the build up of the endometrium.
• Stages from primordial follicle to secondary follicle are all in the arrested
meiosis I stage and are still diploid (2n).
• No new oocytes appear after birth.
• The 2 million or so primary follicles gives rise to an ongoing trickle of
developing follicles.
• These early follicles have 1 of 2 fates:
1. Reach maturity and ovulate.
2. Degenerate to form a scar tissue (atresia). Most follicles follow this route.
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• At menopause (early 50s), few if any primary follicles remain.
Mature (Graafian) Follicle
• Large fluid filled follicle that will soon rupture producing a secondary follicle.
• The secondary follicle is discharged into the abdomen space and quickly
assisted into the uterine tube.
• This cell is haploid (n) and is arrested in meiosis II until a sperm unites with
it.
• The developing follicles secrete increasing amounts of estrogen.
Corpus luteum
• Remaining cells of a ruptured (ovulated) follicle that remains behind in the
ovary.
• If fertilization does not occur, corpus luteum is resorbed in about 10 days.
• The corpus luteum secretes primarily progesterone.
• If fertilization does occur, corpus luteum continues production of estrogens
and progesterone which maintains the uterus during pregnancy for up to 3
months until placenta can take over.
Pathway of the Secondary Oocyte (Once Ovulated)
Fig. 28.18 p.1034
• Oocyte is discharged from the ovary (ovulation).
o A twinge of pain may felt as the ovarian wall is stretched.
o This has been is called mittelschmerz.
• Oocyte is swept into oviduct (fallopian tube) by movements of the fimbriae
and beating cilia as it moves down oviduct toward the uterus.
o Journey from oviduct to uterus for implantation of a zygote takes
about 7 days.
o The cells are indeterminate at this point so are the so called
‘omnipotent cell line’. These are the cells at issue for research use.
They can become any tissue at this point
• Note: If zygote stays in tube = tubal (or if in the abdomen ectopic)
pregnancy.
o Very dangerous so there is usually surgical intervention.
• Unfertilized oocyte only lives about 24 hours after ovulation, therefore, if
fertilization is to occur, it must happen in oviduct.
• Oviducts can become scarred by infections and interfere with ovum
passage
o May become completely blocked causing sterility.
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The Role of Hormones in the Female
Fig. 28.25 p.1042, fig.28.26 p. 1043
• During reproductive life, non pregnant females (not practicing hormonal
birth control) experience a cyclical sequence of ovaries (ovarian cycle) and
uterus (uterine cycle) called the female reproductive cycle.
• The hypothalamus and anterior pituitary, and ovaries act as a triad,
producing hormones that produce these events.
Let’s study these diagrams. Fig. 28.25 p. 1042 and 28.26 p.1025.
Draw ovarian, uterine, and hormonal cycle on board. Also, this flow diagram of hormones.
GnRH
Hypothalamus
Anterior Pituitary
Gonadotropic Hormones
FSH
Developing follicle
LH
Ovulation
Corpus luteum
Gonadal Hormones (Estrogens, Progesterone,)
Hormones
GnRH: Gonadotropic releasing hormone produced by the hypothalamus.
• Stimulates anterior pituitary to release LH and FSH.
FSH: Follicle stimulating hormone secreted by anterior pituitary.
• Gives initial stimulation to follicles to begin development.
LH: Luteinizing hormone secreted by anterior pituitary.
• Stimulates:
1. Further development of follicle
2. Triggers ovulation on 14th day.
Estrogen: primary gonadal hormone before ovulation.
• Produced by developing follicle until ovulation.
• Provides Feedback effects on pituitary and hypothalamus.
o Low levels: + GnRH, + LH, + FSH as exists in beginning of cycle (day
27 to day 5)
o Moderate levels: - GnRH, - LH, -FSH as exists day 5 to 11, day 15
to 26.
o High levels without progesterone: + GnRH, + LH, + FSH as exists
near ovulation day 11 to 14
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Fig 28.27 p. 1044
• Only a mature follicle can produce enough estrogen to trigger the LH spike
and therefore ovulation.
• The mature follicle is saying ‘I’m ready’.
Progesterone: Primary gonadal hormone present post ovulation.
• Produced by the corpus luteum.
• Feedback on pituitary and hypothalamus.
o Moderate to high levels: -GnRH, -LH, -FSH as in days 15 to 26, even
in the presence of estrogen.
o So, prevents ovulation as long as corpus luteum is functioning.
o Note: This is the basis for birth control pills. Given as Norplant or
Depro provera as a birth control method.
• If fertilization does not take place, ovum does not attach to uterine wall.
• Ovary (corpus luteum) stops producing estrogen and progesterone and
wall of uterus breaks down.
• Menstruation begins.
Fig 29.16 p. 1086
• If fertilization does occur, the zygote will start to release a hormone =
human chorionic gonadotropin (hCG) within 8-12 days.
o HCG maintains the corpus luteum until the placenta is developed and
can begin estrogen and progesterone production on its own.
o HCG may be detected within 7 days or so of conception. It is the
basis of a pregnancy test.
• Low amounts of gonadal hormone will stimulate production of
gonadotrophic hormones in the brain and cycle will begin again.
Estrogen and progesterone work the same on mammary glands, as on uterine
tissue:
Estrogen
Progesterone
proliferation of tissue development
glandular secretion in preparation for fertilized ovum.
Gonadal Hormone Functions
Fig. 28.25 p. 1042
Estrogen
1. Regulates gonadotropin secretion and helps regulate (with progesterone) the
ovarian cycle.
2. Development (proliferation) & maintenance of reproductive organs
(endometrium).
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3. Development of secondary sex characteristics: breast growth, adipose in
breasts, hips and abdomen, voice pitch, widen pelvis, pattern of hair growth.
4. Metabolic effects:
• Low cholesterol level protects against heart attacks until menopause.
• Increase protein anabolism is synergistic with human growth hormone.
Progesterone
1. Regulates gonadotropin secretion and helps regulate (with estrogen) the
ovarian cycle.
2. Prepares endometrium for implantation (secretion).
Other Hormone Notes
• Remember, the adrenal cortex secretes both male and female hormones in
small amounts. In normal functioning male adults, the gonad hormones
overwhelm these hormones.
• However in the female, the libido, axillary and pubic hair, and pubertal
growth spurt are maintained by the androgens in from the adrenal cortex.
o So, excessive secretion of adrenal androgens will primarily affect
women and pre puberty males and females.
The Role of Hormones in the Male
Testes function to produce:
1. Spermatozoa (seminiferous tubules)
2. Source of male hormones.
• Collectively known as androgens produced in interstitial cells.
• The principle androgen = testosterone.
Fig. 28.6 p.1020
Functions of Androgens
(Testosterone and DHT (dihydrotestosterone))
1. Development
• In the fetus: Male pattern development.
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o Important in development of external sex organs and descent of
testes. Without the influence of testosterone, a male would present
externally as appearing female like.
• At puberty: Enlargement of penis, testis, prostate gland, & seminal vesicles
2. Secondary Sexual Characteristics
• Androgens also effect body parts not included in sperm production
therefore they are called secondary sex characteristics.
• Secondary sex characteristics not directly involved with reproduction:
a. Growth of beard and body hair.
b. Growth of larynx with deepening of the voice.
c. Increase skeletal and muscular size.
d. Stimulates sweat glands, so increases production of sweat.
e. Stimulates oil secreting sebaceous glands. Overproduction can lead to
acne.
3. Sexual functions
• Spermatogenesis
• Contributes to sex drive (libido).
• In females too! From the adrenal cortex.
4. Metabolism
• Androgens are anabolic steroids that promote protein synthesis (protein
anabolism).
• This creates more muscle and bone mass.
• Stimulates closure of epiphyseal plates.
Regulation of Hormone Production on the Male
Fig. 28.9 p.1022, fig.28.10 p.1023
• Production of testosterone is regulated by gonadotropic hormone lCSH
(interstitial cell stimulating hormone) = LH (luteinizing hormone).
o LH is produced by the pituitary under influence of the hypothalamus
(GnRH).
o LH acts upon the interstitial cells of the testes stimulating them to
produce testosterone.
o Increased concentration of testosterone inhibits LH release by
pituitary = negative feedback.
• FSH is another pituitary gonadotropin (acts on testes).
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o It stimulates sperm production by the testes (seminiferous tubules) by
stimulating the release of ABP (androgen binding protein).
o It is also controlled by the hypothalamus.
• Testosterone is also required for sperm production as it binds with ABP to
stimulate spermatogenesis.
Prostaglandins
p. 618 (eicosanoids)
• These potent acting chemical messengers derived from plasma membrane
fatty acids act as local hormones (paracrine).
• Derived from 20 carbon phospholipids in cell membranes from arachidonic
acid.
• Originally thought that to be produced in prostate (‘prosta’) but later shown
to be produced in the seminal vesicles.
• They are now known to also be produced throughout the body for a variety
of functions.
Prostaglandins have hormone-like qualities but differ in 5 important ways.
1.
They are fatty acids- no other hormones are of fatty acid production.
(protein or cholesterol derivatives).
2.
Produced by enzymes in cell membrane from phospholipids instead of
cytoplasm activities.
3.
Target organ may be in the individual that produces prostaglandin or may
affect another individual (passed in semen).
4.
Found throughout the body but are produced and act locally (paracrine,
autocrine) instead of distribution through the bloodstream. Travels through
genital ducts causing local effects during reproduction activities.
5.
Produces marked effects in very low concentrations and but are degraded
before they can have systemic effects.
Effect of Prostaglandins in Reproduction
• Prostaglandins have many effects in the body: blood flow, platelet function,
inflammation mediation including fever, pain intensity and others.
• We will focus on smooth muscle contraction in the reproductive system.
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• Semen with prostaglandin causes contractions in uterus and oviducts of
female, therefore assisting sperm in route to oviduct and oocyte to the
uterus (females may have prostaglandins as well).
o The semen of some infertile men has been shown to be low in
prostaglandins.
o Some infertile women have been shown to be unresponsive to
prostaglandins.
• Prostaglandins are found in the menstrual flow of females.
o They are produced during low levels of ovarian hormones and first
cause disruption in blood supply to the endometrium causing its
death with sloughing.
o Females with severe menstrual cramps (dysmennorhea) have shown
2-3 times the normal amount of prostaglandins.
o An increase in prostaglandins causes stronger contractions of the
myometrium (muscular wall of the uterus) and more rapid
contractions that can lead to cramping.
• Prostaglandins produced by the placenta contribute significantly to labor by
stimulating contraction in the uterus and reinforcing oxytocin release from
the posterior pituitary.
o This is a positive feedback loop caused by increasing pressure on the
cervical opening that continues until birth.
o Taking aspirin like drugs may inhibit onset of labor.
o Aspirin inhibits prostaglandin activity by interfering with key enzyme in
its synthesis.
Aphrodisiacs
• An aphrodisiac is a food, drink, drug, scent, or device that promoters claim
can arouse or increase sexual desire, or libido. A broader definition
includes products that improve sexual performance.
o Named after Aphrodite, the Greek goddess of sexual love and
beauty, the list of aphrodisiacs has grown over the stretch of time.
• Although many aphrodisiacs have been suggested it is the consensus of
most biologists that none have been proven effective.
• The FDA in 1989 declared there is no scientific proof that over the counter
aphrodisiacs work to treat sexual dysfunction.
o However, people continue to be optimistic for a quest drug induced
sexual success.
Examples:
Law of Similarity: objects resembling genitalia
• Ginseng root
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• Rhinoceros horn
• Oysters
• Eating genitals: various animals testicles, uterus, etc. Romans ate all kinds
of genitailia: penises, wombs, testes.
Physiological effects observed during sex
• Chilies, curries, other spicy foods: raised heart rate and sweating.
• Chocolate may relieve some pain and make you feel better but not sexier.
Other substances
• Bear bile: bears poached for gallbladder (medicinal) and paws (for soup)
• Money! An observation made by a previous student.
Social lubricants
• Alcohol just lowers inhibitions to a point but then quickly starts to interfere
with performance if drink too much.
o Shakespeare’s Macbeth observed, it “provokes the desire, but it
takes way the performance”.
• Rohypnol, the ‘forget pill’ or flunitrazepam. Used as a date rape drug.
o Put in drink and in 10 minutes feel dizzy, disoriented, difficulty in
speaking.
o After 20-30 minutes, sedation occurs for 8 hours, with no recollection
of the events that occur under the drugs influence.
o Classified as a benzodiazepine, a central nervous system
depressant similar to Valium, Xanax, Halcion, and Librium.10x
stronger than valium.
o Drug is easy to get on the street or in Mexico and other countries with
little oversight on drugs.
o Use caution: never leave a drink unattended in any situation you
cannot control. Manufacturer is supposed to make drug so it leaves a
film on liquid. But street versions won’t be so accommodating.
Most effective stimulators:
1. The mind.
• Dr. Ruth Westheimer, Ed.D, says ‘The most important sex organ lies
between the ears’.
• So, the practice of erotic stimulation of one’s own imagination.
• Avoid stress, high blood pressure. Practice healthy living.
2. Physical stimulation.
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• A reliable method for centuries.
• Viagra, Levitra, Cialis: for men (not shown too be effective for women)
lowers the trigger for erectile tissues.
o Treatment for so call ED (erectile dysfunction).
o They all work by relaxing smooth muscle cells, thereby widening
blood vessels.
o None of the drugs automatically produce an erection. Rather, they
make an erection possible with sexual arousal.
o Resulting side effects are comparable and may include headaches,
heartburn, and flushing.
o The FDA advises against mixing these drugs with alpha blockers and
nitrate medications.
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