Download Sierra College Bio 6 Human Physiology Lecture Outline

Sierra College
Bio 6 Human Physiology
Lecture Outline
Keri Muma
SPRING 2016
2
TABLE OF CONTENTS
Homeostasis
4
Chemistry
12
Cells & Membrane Transport
24
DNA Replication
31
Mitosis
31
Protein Synthesis
38
Energy Concepts
43
Cell Metabolism
51
Cell Communication
58
Neurophysiology
63
Sensory
73
Central Nervous System
80
Control of Body Movement
91
Autonomic Nervous System
93
Muscle Physiology
101
Endocrine System
114
Blood
126
Cardiac Physiology
131
Blood Pressure
140
Body Defenses / Immunology
146
Respiratory Physiology
156
Digestive Physiology
169
Renal Physiology
185
Reproductive Physiology
197
3
Homeostasis
Study Objectives:
1. Define physiology and apply the definition to examples.
2. Distinguish between the teleological approach and the mechanistic approach to
physiology. Be able to recognize examples of each.
3. Describe the six levels of organization found in the human body from simplest to most
complex.
4. Define homeostasis and define the components of the homeostatic control
mechanisms (variable, stimulus, receptor, input, control center, output, effector,
compensatory response). Be able to identify examples of each component.
5. Discuss the “law of the maximum and minimum” and how it applies to maintaining
homeostasis.
6. Distinguish between intrinsic (local control) and extrinsic control of homeostasis. Be
able to recognize if an example would be considered intrinsic or extrinsic.
7. Compare and contrast negative feedback and positive feedback mechanisms and give
examples of each.
4
Homeostasis Outline
I.
Physiology – the study of body functions; how the body carries out its lifesustaining activities. Physiology primarily focuses on the cellular and
molecular levels.
Example: how the stomach digests food and the chemical reactions taking
place within the cell or organ.
a. Associated Areas of Physiology
i. Anatomy - structure determines function
1. Physiological mechanisms are only possible through
structural design
2. A slight change in anatomy can have a significant effect on
physiology For example if you have a ventricular septal
defect (basically a hole between the chambers of the heart)
it will no longer function properly as a pump. Therefore a
change in structure will lead to a problem with the function.
ii. Physics
1. Electrical currents
2. Blood pressure
3. Flow rates
4. Gas Laws
iii. Chemistry
1. Acid / Bases
2. Osmolarity
3. Biochemistry
II.
Homeostasis - state of balance in which the body’s internal environment
remains relatively stable despite changes in the internal and external
environments.
a. Mainly controlled by a process called negative feedback - the output or
response of the effector counteracts the original stimulus, returning the
variable to normal limits.
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i. Internal values within the body may vary within narrow limits (for
example: body temperature, pH, blood glucose levels, etc.) These
are called variables.
ii. However, a stimulus can cause these variables to deviate from
their stable condition. This will trigger a sequence of events
(compensatory responses) that will counteract the change caused
by the stimulus to bring the variable back into its normal limits.
iii. Tends to be stabilizing
iv. Can be a short-term immediate response to a stimulus or a longterm adaptation to a constant stimulus.
a. Example: Heart’s response to exercise
i. Short term response: increased heart rate
ii. Long term adaptation: increased stroke
volume
b. Law of Maximum and Minimum – affects of various conditions on the
functional efficiency of body processes. Refers to the value or range of the
variable.
i. Optimal range – range in which the body functions most
efficiently
ii. Range of tolerance –body can still function just may not be as
efficient
iii. Minimum or Maximum condition that the body can function at
iv. Moving past the max or min condition may result in death
v. PH example giving in lecture: The body functions most efficiently
when blood pH is in the range of 7.38-7.42. The range of tolerance
would be between 7.0 – 7.8. The body may still function but less
efficiently. For example acidosis can depress the nervous system
and the individual can become disorientated or comatose.
Alkalosis can cause hyperexcitability of the nervous system
resulting in muscle spasms and tetany. The minimum value would
be around 7.0 and maximum would be 7.8 which moving beyond
these values could result in death.
c. Components of Homeostatic Control Mechanisms - Let’s look at some
of the components involved in controlling homeostasis. I will define these
components below and then I will apply these components of negative
feedback to the example of maintaining a stable body temperature.
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i. Components:
1. Variable: factor being regulated (in this example it would
be body temperature)
2. Stimulus: produces a change in the variable (exercise
could be one stimulus that would cause body temperature
to increase)
3. Receptor: detects change in the variable. (in this example,
thermoreceptors in your body monitor body temperature
and they would detect that temperature is increasing)
4. Input: communicates the information from the receptor to
the control center. (in this example your thermoreceptors
and control center are both located within the same place
the hypothalamus. Therefore, there isn’t a distinct input.
However, if the receptors are in a different location then
the control center your input would usually be the afferent
nervous system but it depends on the example.)
5. Control Center: analyzes the information from the
receptor and determines the appropriate response to the
change. (in this example the control center would be a part
of your brain called the hypothalamus that regulates
temperature. It will decide that body temperature needs to
be lowered and will send the information to the effector.)
6. Output – sends/communicates the response instructions
from the control center to the effector. (in this example the
output would be the efferent (motor) nervous system. It
would be specifically the autonomic nervous system
traveling to smooth muscle in the blood vessels and sweat
glands.)
7. Effector: are organs or glands that carry out the response
from the control center. (in this example the effector would
be the sweat glands and the blood vessels in the skin.
8. Compensatory response: The action of the effector that
will counteract the stimulus and bring the variable back to
its normal value. (in this example it would be producing
sweat to help cool the body and the dilation of the blood
vessels in the skin that allow more heat to radiate away
from the body. Both these responses will cool the body and
bring the temperature back to normal).
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**Listen to your audio lecture for other examples and in your post
lecture assignment you will have an opportunity to apply these
components to your own example.
d. Sources of Homeostatic Controls – homeostasis can be controlled from
outside the organ or tissue through a reflex or it could be controlled
completely within the organ/tissue where the change occurs.
i. Extrinsic control - from outside the organ/tissues
1. Accomplished by the nervous and endocrine systems. This
is also called reflex control.
2. It involves several systems working towards a common
goal
3. For example, let’s stick to our control of body temperature.
This would be considered a reflex or extrinsically
controlled because the change is detected in one part of the
body (the hypothalamus) and than the response involves
other areas such as the blood vessels of the skin and sweat
glands which are located elsewhere and are controlled by
the nervous system. In the audio lecture I also went over
the sympathetic regulation of blood pressure.
ii. Intrinsic control - from within the organ/tissue (a.k.a local
control)
1. Self-serving the organ it occurs in
2. Example given in lecture: Decreased oxygen levels
detected within skeletal muscle tissue can causes
vasodilation of local blood vessels so that more blood flows
into the active tissue. The low oxygen levels are detected
and the response occurs all within the skeletal muscle
tissue. Therefore, it is considered locally controlled and
does not involve the nervous or endocrine communicating
systems.
iii. Positive Feedback - output of effector is amplified or the original
stimulus is intensified
1. Variable moves further from set value
2. Tends to be destabilizing if it is not self limiting
3. Examples of Positive Feedback: Childbirth
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iv. Feed forward mechanism– reflex that starts the response loop in
anticipation of the stimulus or change
1. Examples of Feed forward mechanisms: Thought or smell
of food triggers salivation and increased respiratory rate in
anticipation of exercise
III.
Approaches to explaining physiology
a. Teleological – explanation is based on purpose, meeting body needs
i. Does not consider how it occurs. Focus on why.
ii. Example: Why do we sweat? Answer: To cool down
b. Mechanistic – in terms of cause and effect, sequence of events
i. Example: Why do we sweat? Answer:
1. Thermoreceptors in hypothalamus detect temperature
change
2. Motor pathways activated to stimulate sweat glands
3. As sweat evaporates it takes heat with it and the body
temperature decreases
c. Activity: Why do red blood cells transport oxygen?
i. Write down a teleological explanation to this question:
ii. Write down a mechanistic explanation to this question:
IV.
Physiology as an integrative science - integrates function across many levels
of organization and information from different body systems
a. Levels of Organization
i.
ii.
iii.
iv.
v.
vi.
Chemical level
Cellular level
Tissue level
Organ level
Organ system level
Organism
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b. Emergent properties – properties that cannot be predicted based only on
the knowledge of individual systems
i. Important to look at the human body as a whole and how the
different systems work together and affect each other
1. Example: how blood pressure influences kidney function
ii. Physiological responses depend on numerous factors both internal
and external.
1. Example: Think of all the factors that can affect just blood
pressure. Diet, exercise, genetics, temperature, dehydration,
loss of blood, and the list can go on and on!
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Post-lecture Practice
Homeostasis
The purpose of this exercise is to give you an opportunity to see if you can apply the
concepts of homeostasis you learned about in lecture to a real life example. You may find
it helpful to discuss your assignment with your classmates but each individual should try
to come up with their own example written in their own words.
 In this assignment you will pick a specific example of negative feedback
in our body and describe how it maintains homeostasis.
 You can use your book, the internet or other sources to find an example of
a negative feedback loop. The only exception is you cannot pick body
temperature.
 Define negative feedback and homeostasis in your own words.
 You need to define the role of all the components of a homeostatic
control mechanism and then identify theses components in your specific
example. Components to include:
o Variable
o Stimulus
o Receptor
o Input
o Control center / integrator
o Output
o Effector
o Compensatory response
 Hypothetically, describe how the “laws of maximum and minimum”
apply to your variable?
o Define optimal range, range of tolerance, max and min value and
how it specifically applies to your variable.
o You may have to do some research to find these specific values.
11
Chemistry
Study Objectives:
1. Define the terms matter, elements, and atoms
2. Differentiate between ionic, covalent, and hydrogen bonds
3. Differentiate between polar and non-polar molecules: how do they interact?
4. Describe the unique properties of water and their importance to the human body
5. Distinguish between inorganic and organic compounds
6. Describe acids and bases, and explain the concept of the pH scale
7. Explain the importance of buffer systems and how they work
8. Describe the building blocks, structure, and functions of carbohydrates:
monosaccharide, disaccharides, and polysaccharides
9. Describe the building blocks, structure, and functions of lipids: neutral fats,
phospholipids, steroids, and eicosanoids
10. Describe the building blocks, structure, and functions of proteins: fibrous and
globular
11. Explain how acidity and high temperature affect the functioning of globular proteins
12. Describe the building blocks, structure, and functions of nucleic acids: DNA and
RNA
12
Chemistry Outline
I.
Matter - anything that occupies space and has mass
a. Elements are substances that cannot be broken down into other substances
b. Atoms - the smallest unit of matter that still retains the properties
i. Structure of atoms - composed of subatomic particles
1. Protons - that are positively charged and are found in the
nucleus (center) of an atom
2. Neutrons - are neutral or have no charge; are also found in
the nucleus
3. Electrons - are negatively charged and exist in the
orbits/shells around the nucleus.
a. Maximum number of electrons per shell = 2 in the
first shell; 8 in the other shells
b. Number of electrons on the outer shell determines
the atoms chemical behavior
c. Chemical Bonds
i. Ionic Bonds - formed between oppositely charged ions
1. When an atom loses or gains electrons, it becomes
electrically charged
2. Ions are charged atoms
ii. Covalent Bonds - form when electrons are shared between atoms
1. non-polar covalent bonds – electrons shared equally
2. polar covalent bonds – electrons are NOT shared equally
iii. Hydrogen bonds – interaction between a hydrogen atom bound to
an electromagnetic atom and another electromagnetic atom.
1. The polarity of water results in hydrogen bonds between
neighboring water molecules
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2. Gives water some unique vital properties:
a. High heat capacity - requires a lot of energy to
increase in temperature, and releases a lot of energy
when it cool
b. High heat of vaporization - as water evaporates it
takes large amounts of heat with it
c. Good solvent properties –dissolves chemicals,
making it a good medium for transporting
biological molecules
i. Solution - is a liquid consisting of two or
more substances evenly mixed
1. Solvent: is the dissolving agent
2. Solute: is the substance being
dissolved
ii. Hydrophilic – water soluble (likes water)
1. Polar molecules
iii. Hydrophobic – does not dissolve in water
(water fearing)
1. Non – polar molecules
iv. Amphiphilic – molecules that is both
hydrophilic and phobic
1. Polar and non-polar ends
d. Chemical reactivity
i. Hydrolysis – water breaks bond apart
ii. Dehydration – removing water to form
bonds
e. Cohesion - stickiness of water molecules
f. Cushioning
II.
Acid and Base Concepts
a. Acid – a chemical compound that donates H+ ions to solutions
i. HCl  H+
+
Cl-
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b. Base - a compound that accepts H+ ions and removes them from solution
i. NaOH  Na+ +
OH-
c. pH scale - measures concentration of hydrogen ions
i. Logarithmic scale – each pH unit is a tenfold change in H+
concentration
1. pH 7 = neutral
2. pH below 7 = acidic
3. pH above 7 = basic
d. Buffers - substances that resist pH change
i. They accept H+ ions from the solution when they are in excess
ii. They donate H+ ions to the solution when they are depleted
III.
Biochemistry
a. Organic molecules – large molecules containing carbon
(macromolecules)
i. Have a unique three-dimensional shape that defines its function in
an organism
ii. The molecules of your body recognize one another based on their
shapes
iii. Most macromolecules are polymers. Polymers are made by
stringing together many smaller molecules called monomers
(subunits)
b. Four types of macromolecules found in cells
i. Carbohydrates - includes sugars and starches
1. Contain carbon, hydrogen, and oxygen (1:2:1 ratio)
2. Monomer = monosaccharide
3. Classified according to size:
a. Monosaccharides – one sugar, referred to as simple
sugars
b. Disaccharide - a double sugar
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c. Polysaccharides - complex carbohydrates formed
by long chains of monosaccharides
i. Starch, cellulose (plants), glycogen
(animals)
ii. Lipids
1. Carbon and hydrogen outnumber oxygen
2. Lipids are hydrophobic
3. Functions:
a. Energy storage
b. Cushioning
c. Insulation
4. Types of lipids:
a. Neutral fats – mostly triglycerides
i. A combination of glycerol and three fatty
acids
ii. Found in fat deposits (adipose tissue)
iii. Source of stored energy and insulation
iv. Cushions organs
v. Unsaturated fatty acids - have less than the
maximum number of hydrogen bonded to
the carbons
1. Examples: Most plant oils;
vegetable or corn oil
vi. Saturated fatty acids - have the maximum
number of hydrogen bonded to the carbons
1. Example: Most animal fats
vii.
What is trans fat then???
16
b. Phospholipids – composed of phosphate head
(hydrophilic) and two lipid tails (hydrophobic)
i. Forms cell membranes and the myelin
sheaths of neurons
c. Eicosanoids – a 20 carbon fatty acid with a 5 or 6
carbon ring
i. Examples: prostaglandins, leukotrienes,
thromboxanes
d. Steroids - the carbon skeleton is bent to form four
fused rings
i. Cholesterol is the “base steroid” from which
your body produces other steroids
ii. Example: testosterone, estrogen, cortisol,
bile salts
iii. Protein - a polymer constructed from chains of amino acid
monomers
1. Contains C, H, O, N, and sometimes S
2. Monomer = Amino Acids
a. There is 20 different amino acids
b. The arrangement and combination of amino acids
makes each protein different
c. Amino acids are held together by peptide bonds
3. Types of Proteins
a. Fibrous proteins
i. Provides for construction materials for body
tissues
ii. Important role in structure
iii. Examples: collagen, elastic fibers, myosin
and actin
17
b. Globular Proteins
i. Relies on complex folded structure to
function
ii. Plays a vital role in cell function
iii. Act as enzymes, hormones, transport
proteins or antibodies
iv. Protein Shape - protein’s shape is sensitive
to the surrounding environment
1. Primary structure – order of amino
acids
2. Secondary structure -polypeptide
folded into a helix or a sheet
3. Tertiary structure- sheets and helices
folded into a 3-D globule
4. Quaternary structure - several
tertiary units put together
5. A slight change in the primary
structure of a protein affects its
ability to function
a. Example: sickle cell anemia
6. Denaturation - unfavorable
temperature and pH changes can
cause a protein to unravel and lose
its shape
iv. Nucleic Acids - information storage molecules
1. Monomer = nucleotides
a. 5 carbon sugar
b. Phosphate group
c. Nucleic base
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2. Types of Nucleic Acids
a. Deoxyribonucleic Acid
i. Composed of 4 types of nucleotides
1. Purines – Adenine (A) and Guanine
(G)
2. Pyrimidines – Thymine (T) and
Cytosine (C)
ii. Organized by complimentary base pairing to
form a double stranded helix
1. A = T
2. C = G
iii. The nucleotides of the two stands are joined
by hydrogen bonds
iv. Contains a sugar-phosphate backbone
b. Ribonucleic acid
i. RNA is different from DNA in that:
1. Its sugar is ribose instead of
deoxyribose
2. It has the base uracil (U) instead of
thymine (T)
3. It’s single stranded
c. Some other nucleotides:
i. ATP used for cellular work
ii. NAD and FAD, used as electron carriers in
cellular respiration
iii. GTP, cyclic AMP, ADP in cell signaling
19
Chemistry
Post-Lecture Practice
1. List at least four vital properties of water and describe why this is important to the
human body.
2. Draw two or three water molecules interacting with each other by accurately depicting
where the hydrogen bonds would take place in your illustration.
3. Bicarbonate ions, HCO3- is an important ion in the body. It reacts in the following
way:
HCO3- + H+  H2CO3
a. Are bicarbonate ions acids or bases? _________________
b. Why?
20
4. HNO3 reacts in the following way when dissolved in water:
HNO3  H+ + NO3a. Is HNO3 an acid or a base? ___________
b. Why?
5. How much more H+ is in a solution that has a pH of 3 when compared to a pH of 6?
6. How much OH- is in a solution with a pH of 11 when compared to a pH of 7?
21
Organic Molecules
Name
Monomers (subunits) List examples of:
Monosaccharide
biological function
Carbohydrates
Disaccharide
Polysaccharide
Neutral Fats
Lipids
Phospholipids
Steroids
Eicosanoids
22
Name
Monomers (subunits) List examples of:
Fibrous
biological function
Proteins
Globular
DNA
Nucleic acids
RNA
23
Cell Physiology & Membrane Transport
Study Objectives:
Cell Physiology
1. Explain the structure and functions of nucleus structures: nuclear envelope, nucleolus,
and nuclear pores
2. Describe the structure and function of the following cell structures: cytoplasm,
mitochondria, rough ER, smooth ER, golgi apparatus, lysosomes, peroxisomes,
ribosomes, cytoskeleton, centrioles, cilia, flagella, microvilli.
Membrane Transport
1.Describe the general structure of the plasma membrane and its overall functions:
phospholipid bilayer, proteins (peripheral, integral), cholesterol, and glycocalyx
2. Explain Fick’s law and the factors that affect the rate of diffusion
3. Define these terms, be able to recognize examples of each, and apply them: passive
transport vs. active transport, simple diffusion, facilitated diffusion, osmosis,
hypertonic, hypotonic, isotonic, filtration, solute pumping (primary transport,
secondary transport) exocytosis, and endocytosis (phagocytosis, pinocytosis,
receptor mediated)
4. Explain the effects of hypertonic, hypotonic, and isotonic solutions would have on
cells and the direction solutes and water would diffuse.
24
Cells & Membrane Transport Outline
I.
Cell Theory
a. Cells are the smallest structural and functional units of life
b. All living organisms are composed of one or more cells
c. Cells arise from other cells
II.
Plasma Membrane - separates the living cell from its nonliving surroundings
a. General Functions
i. Barrier – separates extracellular fluid from intracellular fluid
ii. Selective permeability – controls what enters and exits the cell
iii. Cell markers and receptors – cell recognition, binds hormones, cell
communication
iv. Adhesion – between other cell membranes or extracellular
materials
b. Structure – fluid mosaic model (see figure 3-3 in textbook)
i. Phospholipid bilayer
1. Hydrophilic heads orientate themselves towards the
extracellular and intracellular fluid
2. Hydrophobic tails orientate themselves inward, away from
the fluid
3. Sketch the arrangement of the phospholipid bilayer:
ii. Cholesterol – stabilizes the membrane
iii. Glycocalyx – serve as biological markers
iv. Proteins
1. Peripheral – attach to inner or outer surface of the
membrane
2. Integral – embedded in or span the membrane
3. Functions of membrane proteins:
a. Transport
i. Channel proteins – water filled pathways
that allow select ions in/out of the cell
ii. Carrier proteins- transport select substances
across the membrane
25
b. Cell adhesion molecules – play a role in anchoring
cells to each other and the cytoskeleton, responsible
for stickiness of cells
c. Receptors– cell recognition, cell signaling, binding
of hormones
d. Enzymes – facilitate chemical reactions on inner
and outer membrane surfaces
III.
Plasma Membrane Transport – two types of transport passive vs. active
a. Passive transport – does not require energy to move solutes across a
membrane
i. Diffusion – solutes move down their concentration gradient until
evenly distributed throughout the solution
1. Simple diffusion – solutes diffuse across the membrane
unassisted
a. Small non-polar and lipid-soluble solutes
b. Examples given in lecture: oxygen or carbon
dioxide
2. Facilitated diffusion – proteins carry or assist solutes
across the membrane
a. Charged ions move through protein channels
b. Large molecules such as glucose or amino acids are
carried across by carrier proteins
c. Carrier proteins (see figure 3-14 in textbook and
watch the carrier-mediated animation posted on
Canvas)
i. Transports a specific substance (for example
you have specific glucose transporters in the
membrane of some cells)
ii. Can reach saturation when all binding sites
are occupied (Transport maximum)
iii. Competitive inhibitor - other closely related
compounds can compete for the same
binding sight
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3. Fick’s law of diffusion –factors that affect the rate of
diffusion
a. the magnitude of the concentration gradient
i. if you increase the concentration gradient
then would the rate of diffusion increase or
decrease?
b. the permeability of the plasma membrane to a
substance.
i. if you increase the permeability of the
membrane to a substance then would the
rate of diffusion increase or decrease?
c. the surface area of the membrane across which
diffusion takes place
i. if you increase the surface area of the
membrane to a substance then the rate of
diffusion would increase or decrease?
d. the molecular weight of a substance
i. if you increase the molecular weight of a
substance then would the rate of diffusion
increase or decrease?
e. the distance through which diffusion takes place
i. if you increase the distance a substance
must diffuse then would the rate of diffusion
increase or decrease?
f. Temperature
i. if you increase the temperature then would
the rate of diffusion increase or decrease?
•
See Table 3-1 in your textbook for a summary of factors influencing rate of
diffusion.
ii. Osmosis – diffusion of water across a membrane down its
concentration gradient
1. Tonicity – ability of a solution to change the shape of a cell
by altering its internal water volume, depends on
concentration of non-penetrating solutes
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a. Isotonic solution – contains equal concentration
solutes as the cell
i. What effect would this solution have on cell
volume?
b. Hypertonic solution – contains more solutes than
the cell
i. What effect would this solution have on cell
volume?
c. Hypotonic solution – contains less solutes than the
cell
i. What effect would this solution have on cell
volume?
*See figures 3-10, 3-11, 312, and 3-13 in your textbook to support these osmotic
concepts.
iii. Filtration – water and solutes are pushed across a membrane from
an area of higher pressure to an area of lower pressure
1. Non-selective process, only large molecules cannot pass
iv. Summary: Types of passive transport
1. Diffusion: simple or facilitated
2. Osmosis
3. Filtration
b. Distribution of Solutes In Fluid Compartments
i. Osmotic equilibrium – total amount of solutes per volume of fluid
is equal
ii. Chemical disequilibrium – some solutes are more concentrated in
one fluid compartment than another (requires input of energy)
c. Active transport – movement of solutes across the membrane requires
energy (ATP). Occurs during movement of solutes against their
concentration gradient or very, very large molecules
i. Solute pumping – proteins use ATP to transport solutes against
concentration gradient
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1. Cotransporters – carrier proteins that transport two or more
substrates across a membrane (See figure 3-17)
a. Symport: moves two substrates in same direction
b. Antiport: moves two substrates in opposite
directions
2. Types of solute pumping:
a. Primary active transport – energy is provided
directly by the hydrolysis of ATP
i. Example: Sodium-Potassium pump
maintains a higher concentration of
potassium inside the cell and a higher
concentration of sodium outside the cell.
Pumps 3 Na+ out and 2 K+ in. (See figure 316 for illustration)
b. Secondary active transport – primary transport of
one molecule creates an ion gradient used to drive
another molecule against its concentration gradient
(See figure 3-18 for illustration)
ii. Exocytosis - moves material from cell interior to the extracellular
space (Figure 2-5a)
1. Vesicles fuse with the plasma membrane expelling the
contents out of the cell
iii. Endocytosis- moves material from extracellular space into the
interior of the cell (Figure 2-5b)
1. Phagocytosis – “cell eating”
2. Pinocytosis – “cell drinking”
3. Receptor mediated endocytosis – receptors bind specific
substances and initiates endocytosis (See figure 2-8b)
iv. Summary of Types of Active Transport:
1. Solute Pumping: primary or secondary
2. Exocytosis
3. Endocytosis: phagocytosis, pinocytosis, or receptor
mediated
*There is a helpful summary of membrane transport methods in Table 3-2 of your
textbook.
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Membrane Transport
Post-lecture Practice
1. Circle all of the following factors that would increase a solute’s diffusion rate:
a. Increasing temperature
b. Decreasing surface area for diffusion
c. Increasing the distance
d. Lower molecular weight
2. Look at the following illustrations of solutions whose solute is indicated by small
circles.
A
B
C
D
E
a. Solution A is hypertonic to solution(s) __________.
b. Solution A is hypotonic to solution (s) ___________.
c. Solution A is isotonic to solution(s) ____________.
3. A cell containing 4% NaCl is suspended in a solution that consists of 15% NaCl.
Assume the sac is permeable to all substances:
a. Which direction will water initially move?
i. Into the cell
ii. Out of the cell
iii. It will not move
b. Which direction will NaCl initially move?
i. Into the cell
ii. Out of the cell
iii. It will not move
Cell
4% NaCl
Solution
15% NaCl
4. List four examples of active transport:
30
DNA Replication & Mitosis
Study Objectives:
1. Describe the structure of DNA and where it is found.
2. Explain complimentary base pairing: A-T and C-G
3. Describe the steps involved in DNA replication. Include the enzymes involved and
their functions.
4. Compare the replication of the leading strand vs. the lagging strand.
5. Explain why DNA replicates and when during the cell cycle it happens.
6. Describe the structure and function of a eukaryote chromosome.
What is a chromosome? How many do you have?
What are homologous chromosomes?
7. Explain why cells undergo mitosis.
8. Briefly describe the events that occur in each phase of interphase: G1, S, G2
9. Briefly describe the events that occur in each phase of mitosis: prophase, metaphase,
anaphase, telophase. What is the final result of mitosis? Which types of cells
undergo mitosis?
10. Define cytokinesis.
11. Compare and contrast the characteristics of normal cells vs. cancer cells
12. Describe factors that control cell division and the role they play in the development of
cancer: proto-oncogenes, tumor suppressor genes, apoptosis (cell death),
telomeres
31
DNA Replication Outline
I.
Review of DNA Structure
a. Double stranded
i. The chemical side groups of the nitrogen bases form hydrogen
bonds, connecting the two strands.
1. Adenine forms two hydrogen bonds with thymine
2. Guanine forms three hydrogen bonds with cytosine
ii. Sugar-Phosphate Backbones run antiparallel to each other
1. Each DNA strand has a 3’ end with a free hydroxyl
group and a 5’ end with a free phosphate group (See figure
14- 6 in textbook)
2. One strand runs 5’ to 3’ and the other runs 3’ to 5’
3. Sketch two DNA strands running antiparallel to each other
and label the 5’ and 3’ ends.
II.
DNA Replication
a. Purpose - before a cell divides it must replicate its DNA so each daughter
cell has a full set of DNA
b. Mechanism: Semiconservative – the two parent strands serve as a template
for the synthesis of the new complementary strands (See figure 14.7 and
14.8)
c. Steps in replication:
i. Replication Origin - begins at special sites called origins of
replication
1. There may be hundreds or thousands of origin sites per
chromosome.
2. Strands separate forming a replication “bubble” with
replication forks at each end.
3. The replication bubbles elongate as the DNA is replicated
and eventually fuses with other replication bubbles
4. Enzymes Involved
a. Helicase – unwinds and unzips the DNA helix at the
replication forks
b. Topoisomerases – relieves the torque from the
unwinding DNA
32
ii. Elongation of new strand
1. Primase – constructs RNA primer complementary to the
DNA templates
2. After formation of the primer, DNA polymerase III –
elongates the new strand by adding nucleotides to the 3’end
(~50 per second)
3. Replication always occurs in the 5’ to 3’ direction
a. Leading strand – elongates toward the replication
fork, continuous
b. Lagging strand – elongates away from the
replication fork
i. Results in Okazaki fragments:
discontinuous short segments
c. Sketch your original template strands and then add
your leading and lagging strands. Label your 5’
and 3’ ends on your template strands so you can
determine your leading and lagging strand:
4. DNA polymerase I – replaces RNA primers with DNA
nucleotides
5. Ligase – enzyme that joins fragments into a single DNA
strand
III.
Proofreading and Repair
a. Replication is extremely accurate
i. 1 error per billion nucleotides
b. DNA polymerase proofreads each nucleotide against the template and
fixes any mismatches
c. Causes of mistakes
i. replication errors
ii. physical and chemical agents
**Note: DNA replication only occurs when the cell is preparing to divide. When the cell
is NOT dividing DNA is used as a blueprint for protein synthesis.
33
Cell Division – Mitosis
Outline
I.
Why do cells divide?
a. To grow
b. To repair damaged cells
c. To replace lost cells
d. To reproduce
II.
Chromosomes in Eukaryotes -long threads of DNA wrap around proteins
called histones
a. Chromatin -when a cell is not dividing the DNA is loose & unwound
b. Chromosomes - when the cell divides the chromatin condenses into
tightly
c. Chromosome number – humans have 46 chromosomes (23 pairs)
i. “n” is the number of different types of chromosomes
1. in humans n =23
ii. Humans are diploid (2n) therefore each somatic cell has two sets of
chromosomes
1. in humans 2n = 46
iii. Homologous chromosomes - are matching pairs of chromosomes
1. 22 pairs of homologous (matching) chromosomes,
called autosomes
2. 1 pair of sex chromosomes, XY or XX
d. Before a cell divides, it must duplicates all of its chromosomes so that
each new cell gets a complete copy of DNA
i. A duplicated chromosome consists of 2 sister chromatids, which
are identical molecules of DNA
III.
Phases of Cell Division
a. The cell cycle consists of two phases:
i. Interphase – cell carrying out daily functions or preparing to
divide
ii. Mitosis- division of the nucleus
b. Phases of Interphase
i. G1 phase – cell spends 90-95% of its time in this phase growing
and carrying out its everyday functions
ii. S-phase - DNA is replicated
iii. G2 phase - final “check point”: make sure everything is ready for
mitosis
34
c. Phases of Mitosis
i. Prophase
1. Chromatin condenses into chromosomes
2. Centrioles migrate to opposite poles
3. Nuclear membrane breaks down
4. Mitotic spindles form
ii. Metaphase
1. Sister chromatids are aligned in the center of the mitotic
spindle
iii. Anaphase
1. Mitotic spindles shorten pulling chromosomes to opposite
poles
2. Sister chromatids separate becoming daughter
chromosomes
3. The cell begins to elongate
iv. Telophase
1. Chromosomes uncoil into chromatin
2. Spindle breaks down
3. Nuclear membrane reforms
d. Cytokinesis – division of the cytoplasm
i. Original cytoplasmic mass divides resulting in two identical
daughter cells
IV.
Cell division out of control!!!!
a. Cell division is usually under strict control in order to ensure appropriate
proportions. When cell cycle regulation fails, cells start dividing
uncontrollably and result in abnormal masses of dividing cells called
tumors.
b. Types of Tumors
i. Benign – does not invade adjacent tissues, encapsulated
ii. Malignant – invades adjacent tissues
1. Metastasize – cells break away from primary tumor and
travel to other areas of the body
c. Normal cells vs. Cancerous cells
i. Characteristics of Normal Cells
1. Stop dividing after a certain # of divisions
2. Have contact inhibition
3. Differentiated (have a job)
4. Undergo apoptosis if DNA is damaged
35
ii. Characteristics of Cancer cells
1. Immortal, divide indefinitely
2. No contact inhibition, pile up on each other
3. Non differentiated (no job)
4. Large abnormal nuclei or chromosome numbers
d. Factors that control cell division
i. External signals from neighboring cells
1. Proto-oncogenes – produce proteins that turn on cell
division
a. Mutations in proto-oncogenes (now called
oncogenes) may cause these genes to stay turned on
and produce excess growth stimulating proteins
resulting in uncontrolled cell division
2. Tumor suppressor genes – code for proteins that receive
stop signals from neighboring cells. If mutated they cannot
suppress cell division
ii. Apoptosis – programmed cell death, back up system for cells with
damaged DNA
iii. Telomeres – regions at the end of chromosomes that become
shorter each time the cell divides
1. Keeps cells from becoming immortal
2. Cancer cells have enzyme telomerase which repairs
telomeres
*Optional reading to better understand how cells become cancerous: the article “How
Cancer Arises” posted on Canvas.
36
Mitosis
Post-Lecture Practice
1. Draw and label the events occurring in the stages of cell division for a cell that is 2n
= 4 and give a brief description for each event. Include the phases of interphase,
mitosis (prophase, metaphase, anaphase, telophase), and cytokinesis. Other things
you should include somewhere in your drawing is the labeling of chromatin,
homologous chromosomes, sister chromatids, and daughter chromosomes.
37
Protein Synthesis
Study Objectives:
1. Define what a gene is.
2. Describe the steps involved in transcription: initiation, elongation, and termination.
Include enzymes involved and where the process occurs in the cell.
3. Describe the roles of mRNA, rRNA, and tRNA in protein synthesis.
4. Describe the post-transcriptional modifications of mRNA, rRNA, and tRNA
5. Describe the steps involved in translation: initiation, elongation, and termination
Include enzymes involved and where in the cell the process occurs.
6. Describe the post-translational modifications of polypeptides
7. Define mutation and explain how the following mutations may affect the final protein:
silent, point, and frame-shift mutations
38
Protein Synthesis Outline
I.
Gene Expression
a. What is a gene?
i. Gene = a segment of DNA coding for a RNA segment. These
RNA segments will be used to produce a polypeptide
(structural or enzymatic protein)
ii. Each strand of DNA can contain thousands of genes
iii. Each gene has a beginning and an end
b. DNA is used as the blueprint to direct the production of certain proteins
c. Genetic Code
i. The DNA nucleotide sequence codes for the order in which amino
acids are put together to form proteins
ii. Every three nucleotides (codon) on the mRNA codes for a
specific amino acid
iii. There are 20 different amino acids but 64 possible codons
iv. Some redundancy - more then one codon codes for the same amino
acid
v. The genetic code is universal in almost all organisms (See figure
15.5 for a copy of the code)
II.
Protein Synthesis
a. Transcription - information is transferred from DNA to RNA
i. Occurs in the nucleus
ii. All three types of RNA are transcribed from DNA
1. Messenger RNA – carries the coded message from the DNA
to the ribosome in the cytoplasm
2. Ribosomal RNA – reads the mRNA
3. Transfer RNA – transfers the correct amino acid to the
ribosome
iii. Overview of Transcription: the segment of DNA that contains the
gene for a specific protein or RNA that the cell wants to produce
will unwind and the complementary RNA strand will be made by
incorporation the complementary RNA nucleotides
39
iv. Stages in Transcription
1. Initiation
a. Each gene has a precise beginning known as the
promotor region and an end known as the
termination sequence
b. Transcription factors bind to the promoter region
(TATA box) of the DNA.
c. RNA polymerase then initiates transcription by
binding to the transcription factor. It:
i. Unwinds the DNA
ii. Elongates the RNA segment
2. Elongation of the RNA transcript
a. RNA nucleotides are added in the 5’ to 3’ direction
by RNA polymerase
b. RNA nucleotides form temporary hydrogen bonds
with the DNA template
c. As the DNA helix reforms the RNA peels away
3. Termination
a. At the end of the gene the termination sequence
causes transcription to end
b. The pre-RNA segment dissociates from the DNA
4. Post-transcriptional Modifications to mRNA
a. 5’ cap – a guanine triphosphate is added that signals
for ribosomal attachment in the cytoplasm
b. 3’ poly A tail – polyA polymerase adds ~250 “A”
nucleotides to the end. Protects RNA from being
degraded by nucleases.
c. Splicing - introns are cleaved out by snRNPs, and
exons are spliced together
i. Exons – coding region
ii. Introns – noncoding region
5. Post-transcriptional modifications rRNA
a. rRNA associates with proteins to form two subunits
(40s and 60s)
b. Leaves the nucleus and enters the cytoplasm
6. Post-transcriptional Modifications tRNA
a. Folds into a three dimensional structure (clover
shaped)
40
b. Translation - going from the mRNA nucleotide code to amino acid code
i. Occurs in the cytoplasm
ii. Overview: mRNA is read by a ribosome (rRNA) to determine the
sequence of amino acids to produce a polypeptide
iii. Players in Translation
1. mRNA strand
2. ribosomes (rRNA)
a. rRNA has a mRNA binding site and three tRNA
binding sites:
i. A site (amino-acyl binding site)
ii. P site (peptidyl binding site)
iii. E site
3. tRNA
a. Has an anticodon - three base sequence that is
complementary to a codon on the mRNA
b. 3’ end of the tRNA contains a binding site for the
specific amino acid the tRNA carries
iv. Stages of Translation
1. Initiation
a. mRNA binds to the 40s ribosome subunit
b. The initiator tRNA binds to the mRNA start codon
(AUG) at the P site on the ribosome
c. The anticodon on the tRNA matches with the codon
on the mRNA strand
d. The arrival of the 60s subunit completes the initiator
complex
2. Elongation – of the polypeptide chain
a. The next tRNA enters at the A site
b. The enzyme peptidyl transferase forms a peptide
bond between the amino acid on the P site and the
new amino acid on the A site
c. The ribosome then moves down the mRNA (this is
called translocation)
d. The tRNA that was at the A site is now at the P site
and the empty tRNA that was at the P site now exits
at the E site
e. Charging of tRNA
i. Amino acids are floating freely in the
cytoplasm
ii. The enzyme amino-acyl tRNA synthetase
attaches the amino acids to the 3’end of the
tRNA
iii. Requires ATP
41
3. Termination of translation
a. Elongation continues until a stop codon on the
mRNA is reached (UAA, UAG, UGA)
b. The polypeptide is then released from the ribosome
by a release factor
v. Polysomes - several ribosomes can simultaneously translate the
same mRNA strand to make multiple copies of the same
polypeptide
vi. Post-translational modifications to the polypeptide
1. The start methionine is removed by the enzyme
aminopeptidase
2. Proteins will under go folding or modifications
a. Cleavage into smaller fragments or joined with
other polypeptides
b. Chemical modifications: addition of carbohydrates
or lipids
c. Transport to its final destination
III.
Mutations and their consequences
a. Mutation = a change in the sequence of bases within a gene
b. Caused by a mistake during DNA replication (rare) or due to
environmental factors called mutagens
c. Mutations can be somatic or germinal
d. Types of Mutations
i. Point mutations (substitutions) – change in a single nucleotide
1. Due to redundancy of the genetic code it may change the
amino acid, it may not “wobble”
2. Silent mutations do not change the protein
ii. Frame-shift mutation – caused by insertion or deletion of a
nucleotide
1. Changes the reading frame of the codons, usually results in
a non-functional protein
e. Are all mutations bad? Although mutations are sometimes harmful…..
i. They are also the source of the rich diversity of genes in the world
ii. They contribute to the process of evolution by natural selection
42
Energy Concepts
Study Objectives:
1. Define energy
2.Describe the 1st law of thermodynamics
Compare kinetic and potential energy, be able to give or recognize examples of
each
3. Describe the major forms of energy and explain how energy flows from one
type to another: radiant, electrical, mechanical, chemical, and heat (2nd
law of thermodynamics)
4. Describe the structure of ATP and explain the role of ATP in the body. How is it
recycled? What organelle produces ATP?
5. Define the following terms: metabolism, catabolism, anabolism, synthetic reactions,
decomposition reactions, reversible reactions
6. Describe the characteristics and function of enzymes. How do they work?
7. Describe the various factors that effect enzyme activity: concentrations, temperature,
pH, inhibition, and allosteric regulation
43
Energy Concepts Outline
I.
Energy -the ability to do work or to put matter into motion
A. 1st Law of Thermodynamics - conservation of energy
i. Energy is not created or destroyed, it is only converted from one
form to another
B. Types of energy
i. Kinetic- energy doing work, energy of motion
ii. Potential- inactive or stored energy
C. Forms of Energy
i. Radiant - travels in waves
Example: Light waves are essential for photosynthetic
organisms; vision in animals
ii. Electrical - flow of charged particles
Example: Nerve impulses are created by the
movement of Na+ and K+ ions
iii. Mechanical - directly involved in moving matter
Example: Muscle contraction
iv. Chemical – potential energy stored in chemical bonds and is
released when bonds are broken
1. Found in food, fuel, ATP
II. Types of Reactions
A. Synthesis reaction (A+BAB)
i. Atoms or molecules combine to form larger molecules
ii. Endergonic – reaction absorbs energy into the chemical bonds
B. Decomposition reaction (ABA+B)
i. Larger molecule is broken down into smaller molecules
ii. Exergonic - chemical energy is released
44
C. Reversible reaction: (A + B  C + D)
i. Chemical reaction that can proceed in either direction
ii. Direction of the reaction will shift depends on the concentration of
the reactants and products
III. Energy Conversions
A. 2nd Law of Thermodynamics - Heat is a product of all energy
conversions
i. Heat= the kinetic energy contained in the random motion of
molecules
ii. Entropy = measure of disorder or randomness
1. Therefore, all energy transformations increase the entropy
of the universe.
2. Living things are organized, therefore they have low
entropy
3.
To maintain low entropy, constant input of energy is
needed
4. Where do we get this energy???
IV. ATP and Cellular Work
A. The chemical energy in food is released in cellular respiration to make
ATP in the mitochondria
B. ATP is used to drive different types of cell work:
i. active transport
ii. muscle contraction
iii. impulse conduction
iv. we use 10 million ATP molecules per second
45
C. The Structure of ATP
i. ATP (adenosine triphosphate) - chemical energy used by all cells
ii. Consists of adenosine plus a tail of three phosphate groups
iii. Energy is released by breaking high energy phosphate bond (-7.3
kcal/mol)
D. ATP is always recycled…
i. ATP  ADP + P + Energy
ii. Cellular work uses (spends) ATP so more must be made
iii. ATP is recycled from ADP and phosphate through cellular
respiration
V. Metabolism - the sum of all the chemical reactions that occur in the body
A. Two types of metabolic reactions
i. Catabolic – breaking down molecules, releases energy which is
captured in the bonds of ATP
ii. Anabolic – uses energy from ATP to synthesize large molecules
B. Enzymes
i. Few metabolic reactions occur without the assistance of specialize
proteins called enzymes
ii. Enzymes are protein molecules that speed up the rate of chemical
reactions (biological catalyst)
iii. Enzymes lower the activation energy for chemical reactions
1. Activation energy is the energy required to trigger a
chemical reaction
iv. Characteristics of Enzymes
1. Each enzyme is very selective – it catalyzes specific
reactions
2. Each enzyme recognizes a specific substrate
3. Enzymes can function over and over again (can be reused)
46
v. How an enzyme works
1. Each enzyme binds a specific reactant molecule (substrate)
at its active site.
2. After the reactants are converted, the products are released
and the enzyme remains unchanged.
3. Enzyme + Substrate  Enzyme-substrate complex 
Product + Enzyme
vi. Factors Affecting Enzyme Activity
1. Concentration
a. Increase in substrate or enzyme concentration will
increase the rate
b. At some substrate concentrations, the active sites on
all enzymes are engaged and has reached saturation
2. Temperature
a. Increase in temperature, increases the rate of
enzymatic reactions by increasing kinetic energy of
molecules
b. However, at a point the rate will drop off sharply
due to denaturing of the enzyme at high
temperatures
3. pH – enzymes work best at an optimal pH
a. If it is more acidic or basic than the optimal pH the
rate of enzymatic activity will decrease
4. Enzyme inhibitors or activators- can inhibit or activate a
metabolic reaction
a. Competitive inhibition - binds to the active site, as
substrate impostors
i. Can be reversible or irreversible
47
b. Noncompetitive - bind at a different site
(allosteric), changing the shape of the enzyme’s
active site
5. Allosteric Regulation
a. Feedback inhibition – the accumulation of the end
product turns off the metabolic pathway
b. Most allosterically regulated enzymes are
constructed of two or more polypeptide chains.
c. The whole protein oscillates between two
conformational shapes, one active, and one inactive.
d. Binding of regulatory molecules can either inhibit
or stimulate enzyme activity.
48
Post – Lecture Practice
1. Review Energy Concepts PowerPoint slides #1-10. Describe in your own words in a
short paragraph what is happening in the diagram below. Include the specific types of
energy and how the First and Second Law of Thermodynamics apply. (Act like I don’t
know anything about this drawing and you are teaching me about the flow of energy )
49
2. Explain how ATP is used as a source of energy for cellular processes. You can draw
and describe a diagram OR use words to get your point across. Include in your answer:
a. the general structure of ATP
b. how is it used and recycled during cellular processes
c. give examples of two specific mechanisms that you have learned about so far
that use ATP
3. Describe the role enzymes play in living organisms. Include in your answer:
a. Define enzyme, substrate, and product
b. Describe the characteristics of an enzyme
c. Give an example of two variables that can affect the activity of an enzyme and
explain why these variables change the course of an enzymatic reaction.
50
Cell Metabolism
Study Objectives:
1. Define oxidation and reduction.
2. Describe the mechanisms of ATP synthesis: substrate level phosphorylation vs.
oxidative phosphorylation
3. Write the overall general equation for cellular respiration.
4. Describe the role of dehydrogenases and coenzymes NAD and FAD in cellular
respiration.
5. Distinguish between anaerobic (lactic acid fermentation) and aerobic respiration in
terms of when they occur and the total number of ATP produced per glucose
molecule.
6. Describe the basic stages of aerobic respiration: glycolysis, transitional stage, Krebs
cycle and Electron Transport System. For each stage include:
What goes into each stage and what is produced in each stage?
Where does each stage occur in the cell?
Is it anaerobic or aerobic?
7. Define lipolysis and explain how glycerol and fatty acids are used for cellular
respiration.
8. Define beta-oxidation, ketogenesis, ketosis, and ketoacidosis
9. Describe protein metabolism. Explain the role of proteases, deamination, and organic
acids in utilizing proteins for cellular respiration.
10. Define glycogenolysis and gluconeogenesis.
51
Cell Metabolism Outline
I.
The big picture:
a. The sun provides the energy that powers all life
b. Animals depend on plants to convert solar energy to chemical energy
c. This chemical energy is in the form of organic molecules which animals
then eat to convert into ATP through cellular respiration
II.
Cellular Respiration
a. Overview
i. Cell respiration is the main way that chemical energy is harvested
from organic molecules and converted to ATP
ii. It involves a series of catabolic reactions
iii. This is an aerobic process —it requires oxygen
iv. OVERALL EQUATION: (write it below)
b. Oxidation-Reduction Reactions (review these types of reactions on page
103 of your textbook).
i. Reactions transferring electrons from one molecule to another
ii. Molecules that lose electrons are said to be oxidized
iii. Molecules that gain electrons are said to be reduced
iv. Movement of electrons is usually associated with movement of
hydrogen atoms
v. Look at the overall equation above: which molecule is oxidized
and which is reduced during cellular respiration?
c. Enzymes Involved
i. Dehydrogenases - enzymes that catalyze redox reactions by
removing hydrogen
ii. Most require coenzymes that are able to accept and carry the
electrons (electron carriers)
1. Nicotinamide adenine dinucleotide (NAD+) – derived
from niacin
2. Flavin adenine dinucleotide (FAD) – derived from
riboflavin
52
d. Three overall stages of cellular respiration
i. Glycolysis
ii. Krebs Cycle (a.k.a. Citric Acid Cycle)
iii. Electron Transport Chain
e. Mechanisms of ATP Synthesis
i. Substrate-level phosphorylation
1. Enzymes transfer a phosphate group from a substrate to
ADP
2. Occurs during glycolysis and Krebs cycle
ii. Oxidative phosphorylation
1. The phosphorylation of ADP is powered by a series of
redox reactions that transfer electrons from organic
molecules to oxygen
2. Produces the majority of the ATP molecules
3. In electron transport system
III.
Stage 1: GLYCOLYSIS
a. Overview
i. Occurs in the cytoplasm
ii. Does not require oxygen (anaerobic)
iii. Six carbon glucose molecule is broken down into 2 three carbon
molecules of pyruvic acid
iv. Produces 2 net ATP and 2 NADH (electron carrier)
v. See figure 2-11 in your textbook for reaction
b. The Fate of Pyruvic Acid (see figure 2-16)
i. Depends on the availability of oxygen
ii. In aerobic conditions pyruvic acid is converted to acetyl-CoA and
enters the Krebs cycle
iii. In anaerobic conditions NADH + H+ reduces pyruvic acid to form
lactic acid
c. Lactic Acid Fermentation
i. Produces 2 ATP per glucose (less efficient)
ii. When oxygen becomes available again lactic acid is oxidized back
to pyruvic acid and enters the Krebs cycle
IV.
Stage 1½ : TRANSITION
a. Pyruvic acid enters the mitochondrial matrix through facilitated diffusion
b. There it is converted to Acetyl-Coenzyme A to enter Krebs cycle
c. 1 CO2 and 1 NADH is produced in this stage per pyruvate
53
V.
Stage 2: KREBS CYCLE
a. Overview
i. Occurs in the matrix of the mitochondria
ii. Requires oxygen (aerobic)
iii. Completes the breakdown of glucose to CO2 and harvests the
energy as:
1. 2 ATP
2. 6 NADH
3. 2 FADH2
(Numbers based on per one glucose molecule)
b. Events (see figure 2-12):
i. Acetate joins the four carbon compound oxaloacetate to form the 6
carbon compound citrate
ii. 2 decarboxylation events release 2 CO 2
iii. Four oxidation events generate 3 NADH and 1 FADH2
iv. 1 molecule of ATP is formed via substrate-level phosphorylation
VI.
Stage 3: Electron Transport Chain
a. The hydrogen being delivered to the ETC by the coenzymes are split into
electrons and H+ ions
b. Electrons from NADH and FADH2 are passed down a chain of protein
complexes embedded in the inner membrane of the mitochondria
c. Electrons fall to lower energy levels as they are passed down the chain
(releases energy)
d. Oxygen is the final electron acceptor
e. The negative oxygen binds to 2 H+ to form water
f. Chemiosmosis (see figure 2-13)
i. The energy released by electrons moving down the chain is used to
pump H+ from the matrix to the intermembrane space
ii. This creates a proton gradient (potential energy)
iii. This gradient drives protons back in through a protein called
ATPsynthase
iv. This creates kinetic energy that ATPsynthase harnesses to catalyze
ADP + P  ATP (oxidative-phosphorylation)
VII.
Metabolic pool concept: any organic molecule can be used in respiration
a. Lipid Metabolism
i. Lipolysis – the hydrolysis of triglycerides into glycerol and fatty
acids
1. Catalyzed by the enzyme lipase
54
ii. The glycerol
1. is converted into glyceraldehyde phosphate a glycolysis
intermediate
2. then enters into Krebs cycle
3. complete oxidation of glycerol yields 18 ATP molecules
iii. The fatty acid chains
1. Are broken apart into 2 carbon acetic acid fragments (Betaoxidation)
2. Coenzyme A is attached to the acetic acid fragments
forming Acetyl CoA
3. Enters the Krebs cycle
4. Complete oxidation yields ~54 ATP
iv. Ketogenesis
1. If Acetyl CoA production exceeds the capacity of the Krebs
cycle to process it, the liver will convert it to ketone bodies
which are released into the blood
2. Ketones can be used as an energy source in skeletal and
cardiac muscle
a. Examples of ketones: acetoacetic acid, Bhydroxybutyric acid, acetone
3. Ketosis - an increase in circulating ketone bodies
a. Occurs when lipids are the primary energy source
(starvation and diabetes mellitus)
b. May lead to ketoacidosis – decreased blood pH
c. Depresses nervous system, may become comatose
d. Compensatory response to ketosis: increased
ventilation and large amounts of ketones excreted in
urine
b. Protein Metabolism
i. Proteins are hydrolyzed into individual amino acids by proteases
ii. Amino acids are deaminated in the liver (amine group is removed)
iii. Amine group is removed as ammonia
iv. Combined with CO2 to form urea which is excreted by the kidneys
v. Generates organic acids which can be converted to glucose or enter
Krebs cycle to be oxidized for energy
55
c. Glucose Synthesis
i. Aerobic metabolism of glucose is the most efficient way for cells
to make ATP
ii. It is the primary source of energy in cells and normally the ONLY
source neurons prefer
iii. There is multiple metabolic pathways for producing glucose to
ensure that there is a continuous supply for the brain
iv. Synthesis of Glucose
1. Glycogenolysis – the breakdown of glycogen to glucose
a. The liver and skeletal muscle contains high
concentrations of glycogen
2. Gluconeogenesis - synthesis of glucose from noncarbohydrates
a. Can start with glycerol, lactic acid or various amino
acids
b. Occurs in the liver and kidneys
56
Post-lecture Practice
Cell Respiration Worksheet
1. Overall equation for cellular respiration:
+
What you
eat.
+
What you
inhale.
What you
exhale.
+
What your
cells use
for energy!
2. Fill out the table below to organize the main ideas of cellular metabolism.
(Assume per glucose molecule for number of electron carriers and ATP):
Aerobic or
Anaerobic?
Location in
cell
Starting
Molecule
Ending
Molecules
# of Electron
Carriers
made
Number
of ATP
made
Glycolysis
Transition
stage
Krebs Cycle
(citric acid
cycle)
Electron
Transport
Chain
Fermentation
57
Cell Communication
Study Objectives:
1.
Describe the different mechanisms of cell communication: direct contact vs.
extracellular messengers.
2.
Compare and contrast paracrine, autocrine, neurotransmitters, hormonal, and
neurohormonal communication.
3.
Discuss the general mechanism of hormone action and list the effects they can
have on cellular activity
4.
Distinguish between lipid soluble and water soluble hormones. Describe how
they are transported in the blood and the type of receptors they bind to at the
target cells.
5.
Define and give examples of secondary messengers.
6.
Describe the general mechanism of the cyclic AMP signal transduction
pathway.
7.
Describe the general mechanism of the calcium signal transduction pathway.
58
Cell Communication Outline
I.
Types of Cellular Communication (See figure 4-20)
a. Direct contact between cells
i. Gap junctions – cells are connected by tunnels formed by
connexons
1. Allows ions and small water soluble chemicals to pass
between cells
2. Examples: cardiac and smooth muscle
ii. Cell to cell recognition – interaction of cell-surface molecules
1. Example: immune cells – recognize self vs. non-self
b. Through extracellular chemical messengers - cells release ligands that
bind to receptors on target cells to initiate a desired cellular response
i. Local regulators
1. Paracrine – through diffusion, ligands affect cells in the
local vicinity
a. Examples: histamine, cytokines, prostaglandins
2. Autocrine – chemicals act on the cell that produced it
3. Neurotransmitters – secreted by neurons
a. Diffuse across the synaptic cleft and target the
adjacent cell (neuron, gland, muscle)
b. Short-lived
ii. Long-range (distant) regulators
1. Hormones – secreted into the blood by endocrine glands to
travel to distant target cells
2. Neurohormones – neurons secretes hormones into the
blood
II.
Cellular Effects of Chemical Signals
a. Example of various effects chemical signals may have on the target cell
i. Activate or inhibit enzymes
ii. Direct protein synthesis through activation of transcription factors
iii. Stimulate cell division
iv. Alter membrane permeability – membrane potential or
opening/closing of ion channels
59
b. How do hormones work?
i. Hormones are chemical substances that travel through the blood to
a target cell
ii. Target cells must have specific receptors to which the hormone
binds
iii. These receptors may be intracellular or located on the plasma
membrane
iv. They trigger a change in cellular activity
c. Types of Hormones/Chemical Signals
i. Amines – amino acid derivatives
1. Examples: catecholamines (NE and E), T3, T4, serotonin,
melatonin
ii. Peptides – proteins
1. Examples: vasopressin (ADH), insulin
iii. Steroids – cholesterol based
1. Examples: cortisol, aldosterone, estrogen, testosterone
iv. Eicosanoids –derived from arachidonic acid
1. Prostaglandins, leukotrienes
d. Transport of Hormones
i. Hydrophilic (water-soluble) hormones – transported dissolved in
the plasma
1. Examples: peptide and catecholamines
ii. Lipophilic (lipid-soluble) hormones – circulate bound to plasma
proteins such as albumin
1. Examples: steroids and thyroid hormones
e. Mechanism of Signaling Molecules
i. Lipid soluble hormones (see figure 4-28)
1. Move through the plasma membrane and bind to an
intracellular receptor in the nucleus
2. Binding of the hormone receptor complex to the DNA
triggers transcription of a specific gene and the synthesis of
a protein that initiates a cellular response
ii. Water soluble hormones- utilize a membrane bound receptor
1. Binding of hormone causes a conformational change in the
receptor
2. Affects of ligands binding to membrane bound receptors
(see figure 4-22):
a. Triggers the opening or closing of ion channels
OR
b. Transfers the signal to a secondary messenger
within the cell which triggers a cascade of
biochemical events
60
III.
Signal Transduction
a. Secondary Messenger Pathways
i. Signaling pathways amplify the cells response to signals
ii. G-protein linked receptor – spans the membrane and is
associated with a G protein on the cytoplasmic side (see figure 422c)
1. Ligand binds to the receptor
2. Receptor then activates a G protein
iii. G proteins are considered relay proteins that cycle between an
inactive and active form
b. Types of secondary messenger pathways
i. Cyclic AMP Secondary Messenger Pathway (see figure 4-25)
1. G protein activates the enzyme adenylyl cyclase (the
effector)
2. Converts ATP to cyclic AMP
3. Activates protein kinase A which phosphorylates other
proteins
4. Trigger cellular responses
ii. Calcium Secondary Messenger Pathway (see figure 4-26)
1. Binding of extracellular messenger to a G protein linked
receptor or a tyrosine kinase receptor
2. Activates phospholipase C which converts PIP2 to DAG
and IP3
3. DAG will activate protein kinase C in another signaling
pathway
4. IP3 binds to calcium channels triggering the release of
calcium from the ER into the cytoplasm
5. Calcium binds to and activates calmodulin which can alter
other proteins to bring about a cellular response
61
Cell Communication
Post-lecture Practice
1. When a ligand triggers a secondary messenger pathway a cascade of events
occurs. Place the following events of the calcium signaling pathway in the proper
sequence 1 being the first event and 9 being the last.
_____ IP3 binds to an IP3 receptor on the smooth endoplasmic reticulum
_____ G-protein is activated
_____ the effector phospolipase C is activated
_____ ligand binds to G-linked protein receptor
_____ calcium is released from the smooth ER and dumped into the cytosol
_____ transcription factors are activated
_____ cellular response occurs
_____calcium activates calmodulin
_____ PIP2 is converted into DAG and IP3
2. Categorize the following signaling molecules as local regulators or distant
regulators:
Chemical signaling through gap junctions
Paracrine
Neurotransmitters
Hormones
Neurohormones
Cell to cell recognition
Autocrine
62
Neurophysiology
Study Objectives:
1.
Describe the functions of the nervous system.
2.
List the types of neuroglia and describe their general functions.
3.
Describe the general anatomical structure of a neuron and their function: cell
body, dendrites, axon hillock, axon, telodendrites, axon terminals, Schwann
cells, and nodes of Ranvier
4.
Classify neurons according to function: afferent, efferent, and interneuron
5.
Define resting membrane potential and describe its electrochemical basis.
6.
Define depolarization, threshold potential, repolarization, and
hyperpolarization.
7.
Compare ligand gated, voltage gated, and leaky channels.
8.
Compare and contrast graded potentials and action potentials
9.
Explain how action potentials are generated and propagated along axons.
10.
Distinguish between absolute and relative refractory periods
11.
Describe the structure and function of a synapse: presynaptic neurons, synaptic
cleft, and postsynaptic neurons.
12.
Describe the transmission of an impulse across a synapse.
13.
Distinguish between how excitatory and inhibitory postsynaptic potentials are
generated.
14.
Define presynaptic inhibition and presynaptic facilitation.
15.
Define temporal summation and spatial summation.
16.
Describe how neurotransmitters can be inactivated.
17.
Identify factors that influence the speed of a nerve impulse and define
salutatory conduction.
18.
Categorize neurotransmitters by chemical structure, function, and receptor
mechanism.
19.
Define types of neural circuits.
63
Neurophysiology Outline
I.
The Nervous System
a. The master controlling and communicating system of the body
b. Cells communicate by electrical signals that are rapid and cause
immediate responses
c. Functions
i. Sensory input – monitoring stimuli occurring inside and outside
the body
ii. Integration – interpretation of sensory input
iii. Motor output – response to stimuli by activating effector organs
d. Overall Organization
i. The two principal cell types of the nervous system are:
1. Neuroglial – cells that surround and support neurons.
(descriptions found in figure 5.3 and table 5.1 of your
textbook)
a. Oligodendrocytes
b. Astrocytes
c. Ependymal cells
d. Microglia
e. Schwann cells
f. Satellite cells
2. Neurons – excitable cells that transmit electrical signals
a. Anatomy of Neurons
i. Cell body – contains nucleus and organelles
ii. Dendrites – branching extensions
1. Receptive to neurotransmitters from
pre synaptic neurons and transmit
graded potential towards cell body
iii. Axon hillock – where cell body tapers into
the axon, site where action potential
originate
iv. Axon – single process extending from the
cell body, transmits action potential away
from cell body
v. Myelin sheath – formed by schwann cells
wrapping around the axon resulting in
concentric layers of plasma membrane
vi. Nodes of Ranvier – gaps in the myelin
sheath
vii. Telodendrites – distant branches of the axon
viii. Axon terminals – enlarged distal ends
containing secretory vesicles filled with
neurotransmitters
64
b. Synapses – junctions between neurons (see figure
4-14 and 4-15)
i. Function as a control or decision point since
they can be excitatory or inhibitory
ii. Occurs between axon terminals and a cell
body, dendrite, axon hillock, muscle or
gland
iii. Structure of chemical synapse
1. Presynaptic neuron – transmits
impulse towards the synapse, axon
terminal with vesicles containing
neurotransmitters
2. Synaptic cleft – fluid filled space
between pre and post synaptic
neuron
3. Postsynaptic neuron - transmits
impulse away from synapse, contains
receptors for neurotransmitters
II.
Neurophysiology
a. Principles of Electricity
i. Electricity = when opposite charges are separated they contain
potential energy and when they come together energy is released
ii. In cells, the separation of charges by the plasma membrane is
referred to as the “membrane potential”
iii. Voltage – the measurement of potential energy created by charge
separation
1. In neurons voltage is measured in millivolts (1 mV =
1/1000 V)
2. The voltage depends on the quantity of charges and the
distance between the charges
* More information on the general principles of electricity and the resting membrane
potential can be found in Chapter 3 pages 79-86.
b. Types of Ion Channels found in Neurons
i. Ligand-gated channels – chemically gated, open when
neurotransmitters bind. Found on dendrites, cell bodies, and axon
hillocks
ii. Mechanically gated channels – open in response to physical
forces
iii. Voltage-gated channels – open or close in response to changes in
membrane potential. Found along axon
iv. Leaky channels – always open, non-gated, found everywhere
65
c. Membrane Potentials
i. Resting Membrane Potential – potential difference across the
membrane in a resting neuron (-70mV)
1. Chemical gradient – higher concentration of Na+ in the
extracellular fluid and a higher concentration of K+ in the
intracellular fluid
2. Electrical gradient – the inside of the membrane is
negatively charged and the outside is slightly positive
3. Factors contributing to the resting membrane potential
a. Membrane is 50 – 75X more permeable to K+ so
K+ ions leak out faster than Na+ leak in
b. Intracellular proteins - fixed anions inside the cell
c. Sodium-Potassium pump maintains the gradient – 3
Na+ out for every 2 K+ in
4. Stimuli will trigger a disruption in RMP
ii. Graded potential – a localized change in membrane potential (see
figure 4-2 and 4-3 in your textbook)
1. Short lived and dissipates as it travels
2. Can be stimulated by neurotransmitters binding to ligand
gated channels, mechanical stress, or temperature change
3. Examples: receptor potentials, post-synaptic potentials,
motor-end plate potentials
4. If the stimulus is excitatory it will cause depolarization of
the membrane
5. Magnitude of the stimuli depends on how many Na+
channels open
a. This determines the distance that the graded
potential will travel
b. Magnitude and duration depends on:
i. Frequency of stimuli – summation
ii. Amplitude of stimuli – strength
iii. Depolarization – the membrane potential becomes less negative
1. When neurons are stimulated Na+ channels open and Na+
rushes into the cell down its electrochemical gradient
iv. Threshold potential = -55mV the critical level the membrane
potential must reach to open voltage-gated Na+ channels on the
axon to produce an action potential
1. Strong graded potentials can initiate action potentials if the
threshold potential is reached at the trigger zone (axon
hillock)
66
v. Action Potential – brief reversal of the membrane potential (see
figures 4-4 and 4-7)
1. Propagated away from the cell body down the entire length
of the axon without diminishing (all or none)
2. Wave of depolarization followed by repolarization
3. Frequency of axon potentials increases to reflect stronger
stimuli
vi. Repolarization - the membrane returns to its resting membrane
potential
1. Voltage gated Na+ channels close
2. Voltage gated K+ channels fully open and K+ efflux
restores the resting membrane potential
3. Membrane potential becomes more negative as K+ rushes
out
vii. Hyperpolarization - the inside of the membrane becomes more
negative than the resting potential
1. Voltage gated K+ channels are sluggish to close
2. K+ permeability lasts longer and membrane potential dips
below resting potential
viii. Restoring the Resting Membrane Potential:
1. Repolarization restores the electrical gradient
2. Na/K pump restores resting ionic concentrations
d. Refractory Period - amount of time required for a neuron to generate
another action potential
i. Absolute Refractory Period - when another AP cannot be
generated (See figure 4-10)
1. From the opening of the Na+ activation gates until the
resetting of the activation gates
2. Ensures that each action
potential is separate
3. Enforces one-way transmission of nerve impulses
ii. Relative Refractory Period (See figure 4-11)
1. The interval following the absolute refractory period
2. Threshold is raised so only exceptionally strong stimuli will
trigger another action potential :
a. Sodium gates are reset
b. Potassium gates are still open
c. Hyperpolarization is still occurring
67
e. Factors Influencing Conduction Velocity
i. Myelination of axon – increases impulse rate by acting as an
insulator preventing charge leakage
1. Saltatory conduction – voltage gated channels are
concentrated at the nodes so electrical impulses jump from
node to node instead of having to travel down the entire
axon (see figure 4-13)
ii. Diameter of the axon – the larger the diameter the quicker the
impulse travels, less resistance to current flow so adjacent
membranes depolarize quicker
iii. Alcohol, sedatives, and anesthetics – slow or block nerve impulses
by reducing permeability to Na+.
iv. Insufficient blood flow – slows impulses, caused by cold or
pressure
f. Transmission Across the Synapse (see figure 4-15)
i. Action potential reaches the axon terminal
ii. Voltage-gated Ca2+ channels open and Ca2+ floods into the
terminal
iii. Synaptic vesicles fuse with the plasma membrane and release
neurotransmitters into the synaptic cleft
iv. Neurotransmitters diffuse across the synaptic cleft and bind to
receptors on chemical gated channels initiating a postsynaptic
potential
g. Neurotransmitter effects on Postsynaptic Potentials
i. Binding of neurotransmitters cause a graded potential (localized
change in the membrane)
ii. Depending on how the neurotransmitter affects the membrane
potential determines if it will excite or inhibit the postsynaptic
neuron
iii. Types of Postsynaptic Potentials (graded potentials)
1. Excitatory postsynaptic potentials (EPSP) – binding of
neurotransmitter opens Na+ channels and causes
depolarization (See figure 4-16a)
a. Membrane potential becomes less negative and
closer to reaching threshold potential therefore
closer to firing an action potential
68
2. Inhibitory Postsynaptic Potentials (IPSP) – binding of
neurotransmitters cause hyperpolarization of the membrane
therefore moving away from threshold and reducing the
ability to initiate an action potential (See figure 4-16b)
a. Causes K+ or Cl- channels to open
b. K+ rushes out or Cl- rushes in, both causing the
inside to become more negative
iv. Summation - a single EPSP cannot induce an action potential but
they can be summed. The axon hillock keeps score of all graded
potentials received (See figure 4-17)
1. Temporal summation – a presynaptic neuron increases the
frequency of impulses and more neurotransmitters are
released in quick succession
2. Spatial summation – postsynaptic neuron is stimulated by
multiple presynaptic neurons at the same time
3. IPSPs and EPSPs can also be summed and cancel each
other out
4. Modulator Neurons -the effectiveness of the presynaptic
input can be affected by another neuron (see neuron B in
figure 4-18). Allows for the selective inhibiting/enhancing
of a specific presynaptic neuron without affecting the input
from other neurons or effecting all targets
a. Presynaptic inhibition – the amount of
neurotransmitter released from neuron “A” is
decreased by neuron “B”
b. Presynaptic facilitation – the amount of
neurotransmitter released from neuron “A” is
enhanced by neuron “B”
v. Effects of Neurotransmitters
1. Neurotransmitter receptors mediate changes in membrane
potential according to:
a. The amount of neurotransmitter released
b. The amount of time the neurotransmitter is bound to
receptors
c. Neurotransmitters will affect the membrane
potential as long as they are bound so they must be
deactivated
69
vi. Mechanisms for deactivation of neurotransmitters
1. Inactivated by enzymes
a. Example: Acetylcholine
b. Degraded by the enzyme acetylcholinesterase found
in the synaptic cleft
i. Ach  Acetate + Choline
c. Choline is actively transported back into the
presynaptic terminal and recycled
i. Choline + acetyl CoA  Ach
2. Reuptake by presynaptic axon terminals or astrocytes
a. Examples: Norepinephrine, dopamine, serotonin
b. Taken back up by presynaptic terminal
c. Repackaged or broken down by monoamine oxidase
(MAO)
d. Catechol-O-methytransferase is used by liver and
kidney cells to break down NE & E in the
circulation
3. Diffuse away from synapse
h. Classification of Neurotransmitters by Chemical Structure
i. Acetylcholine (ACh)
ii. Biogenic amines – catecholamines, serotonin
iii. Amino acids – glutamate, glycine, GABA
iv. Peptides – endorphins, substance P
v. Messengers: ATP and dissolved gases NO
i. Classification of Neurotransmitters by Function
i. Excitatory neurotransmitters (e.g., glutamate)
ii. Inhibitory neurotransmitters (e.g., GABA and glycine)
iii. Some neurotransmitters have both excitatory and inhibitory effects
1. Determined by the receptor type of the postsynaptic neuron
2. Example: acetylcholine
a. Excitatory at neuromuscular junctions with skeletal
muscle (nicotinic receptor)
b. Inhibitory in cardiac muscle (muscarinic receptor)
j. Classification of Neurotransmitters by Receptor Mechanisms
i. Direct: neurotransmitters that open ion channels
1. Promote rapid responses “fast synapses”
2. Examples: ACh and amino acids
ii. Indirect: neurotransmitters that act through second messengers
1. Promote long-lasting effects, “slow synapses”
2. Examples: biogenic amines, peptides, and dissolved gases
70
k. Types of Circuits in Neuronal Pools (See figure 4-19)
i. Divergent – one incoming fiber stimulates ever increasing number
of fibers, often amplifying circuits
ii. Convergent – opposite of divergent circuits, resulting in either
strong stimulation or inhibition
iii. Reverberating – chain of neurons containing collateral synapses
with previous neurons in the chain
iv. Parallel after-discharge – incoming neurons stimulate several
neurons in parallel arrays
71
Neurophysiology
Post-lecture Practice
1. Which type of neuroglial cell forms the myelin sheath in the central nervous
system?
a. astrocytes
b. Schwann cells
c. oligodendrocytes
d. microglial
e. ependymal
2. Depolarization:
a. Results in a negative charge on the inside of the cell, positive on the
outside
b. Involves sodium ions flooding into the cell causing the membrane
potential to become less negative
c. Involves potassium ions flooding out of the cell causing the membrane
potential to become more negative
d. Triggers hyperpolarization
3. A change in a membrane potential from +30 mV to – 70 mV is an example of:
a. Repolarization
b. Depolarization
c. Hyperpolarization
d. Absolute refractory
4. When an action potential arrives at the axon terminals:
a. Is weaker than it was when it originated at the axon hillock
b. It causes the release of neurotransmitters from synaptic vesicles into the
synaptic cleft
c. Causes potassium (K+) channels to open
d. Turns into a graded potential
5. Explain the events that are involved in the conduction of a nerve impulse. In your
answer, include the events involved in the generation of an EPSP graded
potential, the propagation of an action potential and how transmission across
the synapse occurs.
6. Explain the events that happen during an IPSP and how this decreases the chance
of a neuron generating and action potential.
72
Sensory Physiology
Study Objectives:
1. Describe the organization of the afferent sensory division.
2. Describe the different types of somatic receptors and the type of stimuli they
detect: types of free nerve endings, mechanoreceptors, chemoreceptors
3. Define sensation, perception, adequate stimulus, and law of specific nerve energies.
4. Compare receptor potential and generator potential.
5. Compare and contrast tonic and phasic receptors.
6. Discuss cortical processing of sensory information and perception of stimuli.
Coding of sensory stimuli
Determining type, location, intensity, and duration of stimuli
7. Distinguish between fast and slow pain pathways.
8. List the chemicals that stimulate the pain pathways.
9. List the two neurotransmitters involved in the pain pathway.
10. Describe the analgesic pathway and the role of endorphins.
73
Sensory Physiology Outline
I.
Sensory
a. Function – specialized cells that monitor internal and external conditions
b. Two types of senses:
i. General – receptors are distributed throughout the body
1. Afferent impulses are sent to the somatosensory cortex
ii. Special – receptors are concentrated in sense organs
1. Afferent impulses are sent to special sense cortexes
c. Afferent (sensory) division – carries sensory info from receptors to the
CNS
i. Somatic afferent fibers – carries impulses from skin, skeletal
muscles and joints
ii. Visceral afferent fibers – carries impulses from organs within
ventral body cavities
iii. Special sense afferent fibers – eyes, ears, taste, smell
d. Anatomy of Sensory Neurons
i. Pseudounipolar neuron
1. Cell body lies in the dorsal root ganglia
2. Action potential is initiated at the peripheral end of the
neuron
II.
Sensory Receptors - found on the peripheral end of sensory neurons. Act as
transducers to change an incoming stimulus of one type into an electrical
impulse.
a. Adequate stimulus - receptors are specific for the type of stimulus it is
sensitive to and can transduce
b. Receptors can respond to other types of stimuli if strong enough
c. “Law of Specific Nerve Energies” – regardless of the type of stimulus
the sensation is perceived as what the receptor is specific for
d. Sensory Transduction (See figure 6-1)
i. A stimulus alters the membrane permeability of the receptor. This
leads to the production of a graded receptor potential
ii. Receptors that are modified endings of the afferent neuron produce
generator potentials
iii. Receptors that are separate cells from the afferent neuron produce
receptor potentials
iv. Release chemicals that open ligand gated channels on the afferent
neuron
74
e. Types of Receptors:
i. Free nerve endings
1. Nociceptors – activation causes the sensation of pain
a. Free nerve endings found in the skin, joints, bones,
and blood vessels
b. Sensitive to chemicals, tissue damage, and extreme
temperatures
2. Themoreceptors – react to changes in temperature
a. Free nerve endings in the dermis,
hypothalamus, and liver
b. You have 3X more cold receptors than
warm receptors
ii. Mechanoreceptors – stimulated by physical change such as
pressure or movement
1. Merkel cells – cells in the stratum basale associated with
free nerve endings, detect fine touch
2. Hair root plexus – free nerve endings associated with hair
follicles, detect movement of hair
3. Meissner’s corpuscles –detect touch, found in dermal
papillae
4. Ruffini corpuscles – sensitive to stretch and distortion,
found in the dermis
5. Pacinian corpuscles – deep pressure receptors found in the
dermis
(See figure 6-5 for an illustration of all the
mechanoreceptors described above)
6. Baroreceptors – sensitive to internal pressures. Monitors
blood pressure in vessels (carotid sinus and aorta), lungs,
bladder, intestines
7. Proprioceptors – monitors position and stretch of muscles,
tendons, ligaments, and joint capsules. Helps maintain
posture and sense of body position
iii. Chemoreceptors – detect chemicals dissolved in solution.
Olfactory, taste, osmolarity, pH, CO2, O2
75
III.
Organization of the Somatosensory System
a. Ascending tracts – a bundle of axons transmitting impulses towards the
brain. Usually involves three successive neurons (three levels of
processing) (See figure 5-28):
i. Receptor level - Primary neuron running from the receptor to the
posterior horn of the spinal cord or medullary nuclei
ii. Circuit level – Secondary neuron synapses with the first and
transmit impulses to the thalamus
iii. Perception level – Tertiary neuron running from the thalamus to
the primary somatosensory cortex or a special senses cortex. The
cerebral cortex is responsible for:
1. Sensation - the awareness of the stimuli
2. Perception – the interpretation of the stimuli
b. Each sensory fiber is a “labeled line” - the type, location, strength, and the
intensity of the stimuli is encoded in the area of the cortex it travels to and
the frequency of the impulse
i. Determining type of stimulus or receptor activated
1. Depends on the pathway it takes and the area of the
cerebral cortex it travels to
2. The area of the cortex devoted to each region is related to
the regions sensitivity (# of receptors)
3. Messing with perception:
a. Referred pain (defined in chapter 5 pg 178) - some
visceral pathways are shared with somatosensory so
the brain perceived it as the more frequently
stimulated pathway
b. Phantom pain – caused by nerve endings are
irritated or remodeling of the cortex
ii. Localization of the stimulus
1. Also based on area of cerebral cortex (See figure 5-11b)
2. Accuracy of localization depends on the size of the
receptor field. The smaller the receptor field the more
accurate. (See figure 6-6)
3. Accuracy also depends on lateral inhibition. Only the
most intensely stimulated pathway is excited. Less excited
pathways surrounding the stimulated area are inhibited.
(See figure 6-7)
76
iii. Intensity of the stimulus
1. Number of receptors stimulated – stronger stimuli
usually affect larger areas
2. Frequency of action potentials – stronger stimuli generate
larger receptor potential, therefore a greater frequency of
action potentials (see figure 6-3)
iv. Duration of the stimulus
1. Adaptation – receptors change their sensitivity in the
presence of constant stimulus (See figure 6-4)
a. Phasic receptors – fast adapting
i. Report changes in the environment
ii. Burst of firing at the beginning
and end of stimulus
iii. Examples: temperature, smell,
touch
b. Tonic receptors – slow adapting or not at all
i. Constant firing rate
ii. For situations were continuous information
about a stimulus is valuable
iii. Examples: proprioceptors
pain, muscle stretch
IV.
Pain
a. The perception of pain is subjective
b. Influenced by past and present experiences
c. Unlike other senses pain is coupled with behavioral and emotional
responses
d. Types of pain pathways
i. Fast pain pathways – myelinated
1. Immediate sharp pain
2. Easy to localize
ii. Slow pain pathways – unmyelinated
1. Dull aching pain
2. Persists longer and hard to localize
e. What stimulates the pain pathways?
i. Nociceptors are sensitized to stimuli by chemicals released in
damaged tissues
1. Prostaglandins – which are inhibited by aspirin
2. Bradykinins –chemicals activated by enzymes released by
damaged tissue
3. Histamine – triggers itching
4. Capsaicin – chemical in chili peppers, stimulates pain and
thermoreceptors
77
ii. Primary neuron releases neurotransmitter substance P or glutamate
to stimulate ascending pathway. Carried to the thalamus then to the
somatosensory cortex for perception. Also sent to the reticular
formation which increases level of alertness and the hypothalamus
(limbic system) which triggers behavioral and emotional responses
to pain (See figure 6-9a)
iii. Analgesic Pathway (See figure 6-9b)
1. The CNS has a descending analgesic pathway that can
inhibit the pain pathway
2. By presynaptic inhibition, the release of endorphins or
enkephalins blocks the release of substance P
3. Endorphins bind to opiate receptors on the axon terminal
and block the release of substance P
4. Morphine binds to these opiate receptors to inhibit pain
f. Gate control theory (See figure in PowerPoint lecture)
78
Sensory
Post-lecture Practice
1. Proprioreceptors monitor:
A. limb and muscle position
B. taste perception
C. arterial blood pressure
D. A and C
2. The intensity of a sensory stimulus is coded by _____.
A. the amplitude of action potentials
B. which receptors are activated
C. the frequency of action potentials
D. the duration of each action potential
E. how rapidly the receptor adapts
3. Primary sensory neurons and secondary sensory neurons would synapse with each
other in the:
A. Spinal cord
B. Brain stem
C. Thalamus
D. Cerebral cortex
E. Either A or B
4. Tonic receptors are:
A. fast adapting
B. slow adapting
C. fire rapidly and then stop firing even in the presence of constant stimulus
D. touch receptor
E. both A and D
5. The descending analgesic pathway can inhibit the pain pathway by releasing:
A. substance P
B. glutamate
C. prostaglandins
D. endorphins
E. histamine
79
Central Nervous System
Study Objectives:
1. Identify the major brain regions: cerebral hemispheres, diencephalon, brain stem, and
cerebellum
2. Describe the structure, function, and location of the three meningeal layers
3. Describe the functions of cerebrospinal fluid
4. Explain the role of the blood brain barrier in protecting the brain
5. List the major lobes and functional areas of the cerebral cortex
6. Define gray and white matter and describe their locations in the CNS
7. Define the types of tracts: projection, association (arcuate), and commissural
8. Explain the general roles of the limbic system
9. Distinguish between short term and long term memories. Describe the factors that
affect the transfer of short term to long term memory.
10. Compare and contrast declarative and procedural memory.
11. Define long term potentiation and describe how they modify synapses during memory
formation.
12. Describe the function of the reticular formation systems. List factor that activate or
inhibit it.
13. Describe the stages of sleep: NREM and REM
14. Define dynamic equilibrium and circadian rhythms.
15. Discuss the cause and effect of desynchronosis.
16. Describe the general structure and main functions of the following regions: medulla
oblongata, pons, midbrain, cerebellum, thalamus, and hypothalamus
80
Central Nervous System Outline
I.
Overall organization of the central nervous system (CNS)
a. Central Nervous system – integration and command center
i. Brain
ii. Spinal cord
b. Neural Tissue Organization
i. Gray matter – non-myelinated material (cell bodies, dendrites,
telodendrites)
1. Nuclei – in the CNS
2. Ganglia – in the PNS
ii. White matter – myelinated axons
1. Nerves – bundles of axons in the PNS
2. Tracts – axons in the CNS
a. Types Of Tracts - axons running to or from
i. Projection – vertical tracts, responsible for
the communication between the cerebral
cortex and lower CNS
ii. Association (arcuate) – connect gyri within
the same cerebral hemisphere
iii. Commissural – connects gyri between left
and right hemispheres
c. Protection of CNS
i. Bones of the skull and vertebral column
ii. Meninges – three CT membranes surrounding the brain
1. Dura Mater – superficial layer, consists of two layers of
fibrous CT
2. Arachnoid Mater – loose middle layer
3. Pia Mater – deepest, clings tightly to the brain following
every convolution.
iii. Cerebrospinal fluid -found in the ventricles and the subarachnoid
space around the brain and spinal cord
1. Gives buoyancy to the brain and spinal cord – keeps it from
being damaged by its own weight
2. Cushions and protects
3. Transports materials
81
iv. Blood Brain Barrier - capillaries are less permeable due to tight
junctions between endothelial cells and between astrocytes
1. Helps maintain a constant environment for the brain
2. Very selective- fat soluble materials, glucose, and select
ions and amino acids are allowed to pass, others are not
d. Metabolic Requirements of the CNS
i. Neurons rely on a constant supply of oxygen and glucose to
produce ATP for active transport of ions and neurotransmitters.
ii. Oxygen diffuses across the BBB
iii. Under normal circumstances glucose is the only energy source for
neurons
iv. Glucose is transported from the plasma into the interstitial fluid by
insulin independent membrane transporters
v. Hypoglycemia leads to confusion, unconsciousness and death
e. Regions Of CNS (See table 5-2)
i. Cerebrum – integration of sensory/motor, higher functions
ii. Diencephalon – innate drives and emotions
1. Epithalamus
2. Thalamus
3. Hypothalamus
iii. Cerebellum
iv. Brainstem –basic functions to maintain life
1. Midbrain
2. Pons
3. Medulla oblongata
v. Spinal cord – reflexes
II.
Cerebrum
a. Structure (Anatomy Review)
i. Right and Left cerebral hemispheres – divided by longitudinal
fissure and connected by the corpus callosum
ii. Cerebral cortex is the outer gray matter
iii. Inner region is white matter with basal nuclei (gray matter)
iv. Lobes of the Cerebrum (see figure 5-9)
1. Frontal
2. Parietal – central sulcus separates frontal and parietal
3. Temporal – outlined by lateral sulcus
4. Occipital
5. Insula – deep to the temporal lobe
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b. Plasticity of the Brain
i. The architecture of the cortex is determined by genetic and
developmental processes but it can be modified due to “usedependent competition” for cortical space
ii. Formation of new neural pathways and connections between
existing neurons
iii. Some cortical regions can be remodeled throughout life while
other can be for only a limited time
c. Functional Areas of the Cortex
i. Sensory areas – process afferent impulses, interpret sensations
ii. Motor areas – involved in planning and initiating muscular
movement
iii. Association areas – involve combining information from multiple
areas and processing them together, involved in higher functions
d. Sensory areas of the cerebral cortex
i. Primary somatosensory area – postcentral gyrus in the parietal
lobe. Receives impulses involved in touch, pain, pressure, stretch
ii. Somatosensory association – integrates sensory input into
understanding by analyzing sensory based on past experiences.
Lies posteriorly to primary somatosensory
iii. Primary visual cortex – receives sensory input from the retina to
the occipital lobe. Data only.
iv. Visual association area – interprets the raw data and puts it into
context. Surrounds the primary.
v. Primary auditory – receives sensory input from the
vestibulocochlear nerve. Temporal lobe.
vi. Auditory association area – lies posterior to primary, interprets
sound into context
vii. Olfactory cortex –found on medial aspect of temporal lobe.
Sensory input from olfactory nerves. Linked limbic system – tied
to emotions and memories
viii. Gustatory cortex – perception of taste, found in the insula
e. Motor areas of the cerebrum
i. Primary motor cortex – controls somatic motor neuron output.
Lies in the precentral gyrus of the frontal lobe
1. Output is usually controlled by higher motor areas and
input from the cerebellum
2. Amount of cortex devoted to each area relates to which
regions have the most precise control.
3. Control is contra lateral
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ii. Premotor cortex – anterior to the primary motor cortex in the
frontal lobe. Responsible for coordinating learned motor skills
1. Examples: typing, driving, playing the piano
iii. Basal Nuclei (basal ganglia)
1. Adjust the stopping, starting and intensity of movements
after receiving input from cerebral cortex and substantia
nigra (midbrain)
2. Lesions of nuclei lead to increase motor output leading to
increased muscle tone, difficulty initiating movement, and
involuntary muscle movement
f. Other association areas of the cerebrum
i. Prefrontal cortex – involved with intellect, recall, reasoning,
judgment, concern for others, personality traits, and management
of emotions
1. Develops later in life and is impacted by social
environment
2. Linked to emotions (limbic system)
ii. Language areas – surrounds lateral sulcus in the left hemisphere
only. Receives input from auditory and visual senses. Coordinates
with the motor cortex to carry out motor skills involved in speech
and writing. (see figure 5-12)
1. Language involves both expression and comprehension
2. Two cortical areas specializing in language are:
a. Wernicke’s area – language comprehension and
formulation of coherent patterns of speech
b. Broca’s area – speech production and word
formation, associated with motor cortex
g. Cerebral lateralization - distribution of functional areas are not always
symmetrical.
h. Limbic system – emotional brain, consists of tracts and nuclei of the
medial cerebrum, anterior thalamus, and hypothalamus
1. Functions:
a. Establishes emotional state and behavioral drive
b. Linked to prefrontal cortex, sometimes logic
overrides emotion or vice versa
c. Long term memory storage and retrieval
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2. Limbic system structures (see figure 5-16)
a. Amygdala – recognizes angry or fearful expressions
and assesses danger
b. Cingulate gyrus – role in expressing emotion and
resolving mental conflicts
c. Hippocampus – role in memory along with
amygdale
3. Emotions can influence physiological functions
ii. Memory - is the storage and retrieval of information
1. The three principles of memory are:
a. Storage – occurs in stages and is continually
changing (stored in regions that need them)
b. Processing – accomplished by the hippocampus and
surrounding structures
c. Memory traces – chemical or structural changes that
encode memory
2. Stages of Memory - short-term memory and long-term
memory
a. Short-term memory (working memory)
i. STM lasts seconds to hours and is limited to
7 or 8 pieces of information
ii. Only 5% of sensory input is transferred to
STM
b. Long-term memory (LTM) has limitless capacity
i. Factors that affect transfer of memory from
STM to LTM include:
1. Emotional state – we learn best when
we are alert, motivated, and aroused
2. Rehearsal – repeating or rehearsing
material enhances memory
3. Association – associating new
information with old memories in
LTM enhances memory
4. Automatic memory – subconscious
information stored in LTM
85
3. Two categories of memory
a. Fact (declarative) memory:
i. Entails learning explicit information (names,
dates)
ii. Is related to our conscious thoughts and our
language ability
iii. Is stored with the context in which it was
learned
b. Skill (procedural) Memory
i. Is less conscious than fact memory and
involves motor activity (example: riding a
bike)
ii. It is acquired through practice
iii. Skill memories do not retain the context in
which they were learned
iv. Hard to unlearn
v. Stored in the premotor cortex
4. How Memories are Formed
a. Long-term potentiation (LTP) - prolonged
increase in synaptic strength (See figure 5-18)
i. Repetitive stimulation results in
modification of synapses that increase the
ability of pre-synaptic neurons to stimulate
post-synaptic neurons
ii. Necessary for memory trace formation
b. Aspects of Long-term potentiation
i. Synaptic modifications that can occur as a
result of LTPs
ii. Number and size of presynaptic terminals
may increase
iii. More neurotransmitter is released by
presynaptic neurons
iv. Dendritic spines change shape
v. Extracellular proteins are deposited at
synapses
86
III.
Diencephalon (see figure 5-15)
a. Thalamus – forms lateral walls of the 3rd ventricle
i. Acts as a relay station for all incoming sensory impulses except
olfactory
ii. Screens sensory impulses and decides if it should be passed onto
the cortex and where it should be sent
iii. Crude awareness of sensation
b. Hypothalamus – slightly anterior and inferior to the thalamus. Important
in maintaining body homeostasis
i. Functions
1. Autonomic control center – controls ANS centers in the
brain stem and spinal cord, BP, HR, digestive tract,
respiration rate, pupil size
2. Emotions – heart of limbic system, basic primitive drives
such as fear, anger, pleasure
3. Regulates body temperature – thermostat, initiates
cooling or heating mechanisms
4. Sleep-wake cycles – acts with pineal gland to set cycles in
response to light and dark
5. Food intake – responds to changes in levels of nutrients
and hormones. Contains satiety and feeding centers.
6. Water balance and thirst – osmoreceptors that detect
concentrations of body fluids, triggers anti-diuretic
hormone (ADH) and thirst centers
7. Hormones - produces releasing or inhibiting factors which
controls the release of hormones from the anterior pituitary.
Produces posterior pituitary hormones, ADH and oxytocin
IV.
Brain Stem
a. Midbrain – superior portion of the brain stem
i. Corpora quadrigemina – four protrusions on the dorsal surface,
contain sensory nuclei
1. Superior colliculi – visual reflexes
2. Inferior colliculi – auditory reflexes
ii. Substantia nigra – axons linked to cerebral basal nuclei, release
dopamine, controls motor output. Degeneration of these neurons
causes Parkinson’s disease
b. Pons – bulging region between midbrain and medulla, anterior to
cerebellum
i. Pontine nuclei – relay station for tracts between motor cortex and
cerebellum
ii. Pneumotaxic and apneustic respiratory center – works with
medulla to maintain rhythmic breathing
87
c. Medulla Oblongata – base of brain stem, blends inferiorly with the spinal
cord
i. Pyramids – longitudinal ridges on the ventral surface. Contains
motor tracts that cross over (decussation) before they continue
down the spinal cord
ii. Autonomic Nuclei
1. Cardiovascular center – adjusts force and rate of heart
contraction and blood pressure
2. Respiratory center – controls rate and depth of breathing,
works with pons for rhythm
3. Vomiting, swallowing, coughing, sneezing, hiccups
d. Reticular Formation – loose cluster of neurons extending through the
brain stem to the thalamus, hypothalamus, cerebellum and spinal cord.
Responsible for the arousal (alertness) of the brain
i. Reticular Activation System (RAS) - neurons sending constant
impulses to the cortex via the thalamus to keep the cortex
conscious and alert. (See figure 5-21)
1. Inhibited by the hypothalamus sleep center, adenosine,
alcohol, and tranquilizers
2. Damage suffered by a jolt to the brain stem may result in
permanent unconsciousness (coma)
V.
Types of Sleep
a. There are two major types of sleep
i. Slow-wave or non-rapid eye movement (NREM)
ii. Paradoxical or rapid eye movement (REM)
b. One passes through four stages of NREM during the first 30-45 minutes of
sleep
c. REM sleep occurs after the fourth NREM stage has been achieved
d. A typical sleep pattern alternates between REM and NREM sleep
e. Characteristics of REM sleep
i. Vital signs increase
ii. Neuronal activity is high
iii. Skeletal muscles (except ocular muscles) are inhibited
iv. Most dreaming takes place
f. Sleep Patterns
i. Alternating cycles of sleep and wakefulness reflect a natural
circadian rhythm
ii. The suprachiasmatic and preoptic nuclei of the hypothalamus
regulate the sleep cycle
iii. Adenosine appears to be a sleep inducing chemical that
accumulates in the brain
1. Inhibits RAS neurons
2. Caffeine blocks adenosine receptors
88
g. Importance of Sleep
i. NREM sleep is presumed to be the restorative stage
ii. REM sleep may be a reverse learning process where superfluous
information is purged from the brain (one hypothesis)
iii. Those deprived of REM sleep become moody and depressed
iv. Daily sleep requirements decline with age
h. Sleep Disorders
i. Narcolepsy – lapsing abruptly into REM sleep from the awake
state
ii. Insomnia – chronic inability to obtain the amount or quality of
sleep needed
iii. Sleep apnea – temporary cessation of breathing during sleep
VI.
Physiological Rhythms (See chapter 18 pgs. 679 - 682)
a. Dynamic Equilibrium – variables are continuously fluctuating within their
narrow limits
i. These fluctuations tend to be in wave patterns called biorhythms
ii. If they fluctuate in a cycle every 24 hours they are referred to as
circadian rhythms
iii. Controlled by the suprachiasmatic nucleus (SCN) in the
hypothalamus
b. List examples of Circadian Rhythms given in lecture:
c. Suprachiasmatic Nucleus (see figure 18-13)
i. Secretes clock proteins.
ii. Cyclic changes in their concentration throughout the day changes
the neural output from the SCN.
iii. This neural output produce cyclic changes in effector organs
through the day
iv. The SCN cycle is a little longer than 24 hours
v. Internal clock must be reset daily by external cues in order to stay
in sync.
1. Light and dark cycle
2. Melatonin secreted from the pineal gland keeps the SCN in
tune with the environment and regulates sleep/wake cycles
89
d. Desynchronosis – internal clock is out of synchronization with the external
environment
i. Jet lag, work rotations, change in sleep schedule
1. Effects: decreased cognitive function, depression, foggy
head, can’t sleep or wake up
ii. Seasonal affective disorder: depression during short winter days
due to decreased sunlight
1. Can be treated with bright light or melatonin
VII.
Cerebellum (see figure 5-19)
a. Maintains posture, balance, and plays a role in learning and executing
skilled motor movements
b. Body map – sensory and motor maps of the body so it is aware of what
each skeletal muscle is doing
c. Functions of the Cerebellum
i. Monitors intended movements from the motor cortex and basal
nuclei
ii. Monitors current movements – receiving input from proprioceptors
and the vestibule (equilibrium)
iii. Compares intended movements, sensory input, and the actual
movement and placement of muscles at that time
iv. Sends corrective feedback to the upper motor centers if there is a
discrepancy between the intended movement and the actual
movement
d. Ataxia- disruption of muscle coordination resulting in inaccurate
movements
i. Caused by damage to the cerebellum through trauma or genetic
disease
ii. Abnormal walking movements, uncoordinated speech, overshoot
objects
No Post-Lecture Practice for this lecture
90
Control of Body Movement
Study Objectives:
1. Describe descending motor pathways
2. Distinguish between flaccid and spastic paralysis.
3. Define a reflex and list the components of the reflex arc. Distinguish between
somatic and autonomic reflexes.
Control of Body Movement Outline
VIII. Motor Output
a. Descending tracts – axons carrying motor commands from the brain to
the PNS, majority are anterior and lateral, usually involve two neurons
(See figure 5-28b)
i. Upper neuron – extends from motor cortex or motor nuclei in the
cerebrum to the anterior horn
ii. Lower neuron – lie in anterior horn and travel to the effectors in
the periphery
b. Spinal Cord Trauma: Paralysis– loss of motor function
i. Flaccid paralysis – severe damage to the ventral root or anterior
horn cells
1. Lower motor neurons are damaged and impulses do not
reach muscles
2. There is no voluntary or involuntary control of muscles
ii. Spastic paralysis – only upper motor neurons of the primary motor
cortex are damaged
1. Spinal neurons remain intact and muscles are stimulated
irregularly
2. There is no voluntary control of muscles
3. Exaggerated reflexes
91
I.
Reflexes – rapid predictable motor response to a stimulus
a. Occur at the spinal cord or brain stem
b. May be inborn or learned
c. May be somatic or autonomic
d. May be monosynaptic or polysynaptic
e. Important clinically, exaggerated or absence of reflex responses may
indicate neurological problems
f. Reflex Activity
i. Components of a reflex arc
1. Receptor – detects stimulus
2. Sensory neuron – relays info to CNS
3. Integration – may be monosynaptic or polysynaptic
4. Motor neuron – carries response away from the CNS to the
effector
5. Effector – muscle or gland
g. Examples of somatic reflexes mediated by the spinal cord
i. Stretch reflexes – muscle spindles are stretched and excited,
afferent impulse is sent to the spinal cord where it synapses
directly with a motor neuron that triggers the muscle to contract
(serial). The sensory neuron also synapses with an interneuron that
inhibits the motor neurons of antagonist muscles, this is called
reciprocal inhibition.
ii. Flexor (withdrawal) reflex – initiated by painful stimulus and
causes withdrawal of the body part. Examples: touch something
hot, abdominal reflex (see figure 5-31)
iii. Superficial reflexes – initiated by cutaneous stimulation.
Example: plantar reflex
h. Autonomic reflexes mediated by the brain or spinal cord
No Post-Lecture Practice for this lecture
92
Autonomic Nervous System
Study Objectives:
1.Compare the somatic and autonomic nervous systems relative to their effectors,
structure, functions, and neurotransmitters.
2. Compare and contrast the roles of the parasympathetic and sympathetic divisions.
3. Describe the origin, location of ganglia, length of pre and postganglionic fibers, and
neurotransmitters used for the parasympathetic and sympathetic divisions
4. Describe dual innervation and explain exceptions to dual innervation such as
sympathetic tone.
5. Define cholinergic and adrenergic fibers and list the different types and subtypes of
cholinergic and adrenergic receptors and their locations
6. Explain the clinical significance of drugs that mimic or inhibit parasympathetic or
sympathetic effects.
7. Contrast the localized effects of the parasympathetic system versus the wide spread
effects of the sympathetic system
93
I.
Efferent (motor) Division –consists of two divisions, somatic and autonomic
a. Somatic Nervous System
i. Voluntary control
ii. Effector = skeletal muscles
iii. Muscle fibers must be excited by a motor neuron or they are
inactive (On or off)
iv. One motor neuron extends from the CNS all the way to the
effector muscle
b. Autonomic Nervous System
i. Involuntary control
ii. Effectors = glands, smooth and cardiac muscles
iii. Two neuron chain between the CNS and the effector (see figure
7-1)
1. Preganglionic neuron – before the ganglia
2. Postganglionic neuron – after the ganglia
iv. Two divisions
1. Sympathetic – fight or flight
2. Parasympathetic – rest and digest
II.
Anatomy of the Autonomic Nervous system (see figure 7-2 and 7-3 for a
summary)
a. Anatomy of the Sympathetic System
i. Origin sites
1. Thoracolumbar - emerges from thoracic and lumbar
regions T1-L2
ii. Length of neurons
1. Short preganglionic
2. Long postganglionic
iii. Location of Sympathetic Ganglia - close to vertebral column
1. Paravertebral ganglia – chain running parallel to the
vertebral column, extends from C3 to S4
2. Collateral (prevertebral) ganglia – lie anterior to the
vertebral column
iv. Path of Sympathetic Neurons
1. Cell bodies are located in the lateral gray horns of spinal
segments T1 – L2
2. White ramus communicans – pre neuron passes from the
spinal nerve to the paravertebral ganglia
3. Gray ramus communicans – post neuron exits the
paravertebral ganglia
94
4. Three different routes the preganglion neuron can take once
it enters the paravertebral ganglia
a. Synapse with post at the same level
b. Synapse with post at a different level
c. Travel through splanchnic nerve and synapse with
post in collateral ganglia
5. The sympathetic nervous system triggers the release of
epinephrine from the adrenal medulla
a. Some preganglion fibers travel to the adrenal
medulla where they synapse with hormone
producing cells
b. These cells release epinephrine into the blood
stream
b. Anatomy of the Parasympathetic System
i. Origin sites
1. Craniosacral - emerges from brainstem and sacral regions
ii. Length of neurons
1. Long preganglionic
2. Short postganglionic
iii. Location of Parasympathetic Ganglia - ganglia close to target
organ
1. Terminal ganglia – very close to target organ
2. Intramural ganglia – within the walls of the target organ
III.
Functions of the ANS
a. General regulatory functions
i. Cardiovascular activities
1. Cardiac output, heart rate, blood pressure and distribution
ii. Body fluid chemistry
1. pH, osmolarity, thirst, water content
iii. Pulmonary activities
1. Breathing rate, bronchiole diameter, O2 and CO2 content
iv. Gastrointestinal activities
1. Motility along digestive tract, mechanical and chemical
digestion
v. Visceral reflexes
1. Micturation, defecation, sexual reflexes
vi. Stress
1. Stimulates various hormones to cope with situation
95
b. Functions of the Sympathetic division – fight or flight
i. Enables body to cope rapidly during emergency situations
ii. Dominant when excited, frightened, or during exercise
1. Increase heart rate and blood pressure
2. Increase respiratory rate, dilates bronchioles
3. Blood shunted to skeletal muscles, brain, and heart away
from digestive organs and skin
4. Dilates pupils
5. Liver releases glucose to meet increased energy needs
6. Increased cellular metabolism
7. Initiates sweating to lower body temperature
8. Increased RBC production and clotting ability
9. Na+ absorption / K+ secretion, decreased urine production
c. Functions of the Parasympathetic division – rest and digest
i. Dominant in non-stressful situations
ii. Conserves energy and directs maintenance activities such as
digestion and excretion
1. Blood shunted to visceral organs
2. Constricts pupils
3. Increased digestive glandular secretions and activity
4. Respiratory and lacrimal secretions
5. Blood pressure, heart rate, respiratory rates at low normal
levels
*See table 7-2 in your textbook and the handout posted on Canvas for additional effects
the two divisions of the ANS have on various organs/tissues.
d. Dual Innervation - most internal organs are innervated by both
autonomic divisions
i. Antagonistic control – the divisions counterbalance each other by
continuously making adjustments. The ANS either further excites
or inhibits the organs.
ii. There are exceptions to dual innervation:
1. Most blood vessels, sweat glands, and arrector pili muscles
are controlled by sympathetic fibers only
2. Sympathetic Tone: the sympathetic division controls
blood pressure and keeps the blood vessels in a continual
state of partial constriction
a. Increased sympathetic activity constricts blood
vessels
b. Decreased sympathetic activity dilates blood vessels
96
3. Some sympathetic metabolic effects are not reversed by the
parasympathetic division
a. Increases the metabolic rate of body cells
b. Raises blood glucose levels
c. Mobilizes fat as a food source
d. Stimulates the reticular activating system (RAS) of
the brain, increasing mental alertness
IV.
ANS Neurotransmitters & Receptors
a. Acetylcholine (ACh) and norepinephrine (NE) are the two major
neurotransmitters of the ANS
i. Neurons that release ACh are cholinergic fibers:
1. All parasympathetic pre and postganglionic neurons
2. All sympathetic preganglionic neurons
3. Sympathetic postganglionic that innervate sweat glands and
arrector pili muscles
ii. Neurons that release NE are adrenergic fibers:
1. Most sympathetic postganglionic neurons (except sweat
glands and arrector pili)
b. Types of Receptors - neurotransmitter effects can be excitatory or
inhibitory depending upon the receptor type they bind to. Two types of
receptors are cholinergic and adrenergic.
i. Cholinergic receptors – bind Ach
1. Nicotinic receptors
a. Nicotinic receptors are found on:
i. Motor end plates (somatic targets)
ii. All postganglionic neurons of both
sympathetic and parasympathetic divisions
iii. The hormone-producing cells of the adrenal
medulla
iv. The effect of ACh binding to nicotinic
receptors is always excitatory
2. Muscarinic
a. Muscarinic receptors are found on all effectors
stimulated by postganglionic cholinergic fibers:
i. Parasympathetic effectors
ii. Sweat glands and arrector pili
b. The effect of ACh binding to muscarinic receptors
can be either inhibitory or excitatory depending on
the receptor subtype of the target organ
i. Examples – slows cardiac muscle:
inhibitory; smooth muscle of digestive:
excitatory
97
ii. Adrenergic receptors – binds NE and/or E
1. Alpha Receptors - greater sensitivity to NE
a. α 1 – binding of NE is stimulatory. Example:
constriction of blood vessels serving the skin and
abdominal viscera
b. α 2 – binding of NE is inhibitory. Example: inhibits
insulin secretion from the pancreas
2. Beta Receptors
a. β 1 – found primarily in the heart, binding of NE and
E is excitatory. Example: increases cardiac output,
release of renin from kidneys to increase BP
b. β 2 – binding of E is generally inhibitory. Example:
dilates coronary blood vessels and bronchioles in
the lungs, relaxes digestive and urinary smooth
muscle
c. β 3 – found in adipose tissue. Example: stimulates
lipolysis
*See table 7-3 for a nice summary of which fibers are cholinergic and adrenergic and the
receptor types.
V.
Localized vs. Wide Spread Effects
a. Parasympathetic – localized and short lived effect
i. Preganglionic synapse with one or a few postganglionic
ii. ACH is quickly destroyed
b. Sympathetic – longer lasting and body wide mobilization
i. Preganglionic synapse with many posts at different levels
ii. NE is inactivated slower than ACH
iii. NE and E are indirect neurotransmitters, using a second-messenger
system
iv. Epinephrine is released into the blood and remains there until
destroyed by the liver
VI.
Effects of Drugs on the ANS - drugs are designed to obtain an inhibitory or
excitatory effect on a target organ by either blocking or initiating desired
effects of neurotransmitters
a. Types of drugs:
i. Sympathomimetic agents – enhance sympathetic response
ii. Sympatholytic agents – decrease sympathetic response
iii. Parasympathomimetic agents – enhance parasympathetic
response
iv. Parasympatholytic agents – decrease parasympathetic response
98
b. Examples of Drugs:
i. Atropine – blocks muscarinic receptors therefore blocks
parasympathetic effects, increase heart rate and fecal and urinary
retention. Would be parasympatholytic.
ii. Tricyclic antidepressants – prolong the activity of NE on
postsynaptic membranes. Would be sympathomimetic.
iii. Over-the-counter drugs for colds, allergies, and nasal congestion –
stimulate α-adrenergic receptors. Would be sympathomimetic.
iv. Beta-blockers – blocks cardiac B1 receptors, decreases HR and
BP. Would be sympatholytic.
v. Alpha-blockers - interfere with vasomotor fibers and are used to
treat hypertension. Would be sympatholytic.
vi. Salbutamol – activates B2 receptors, dilates bronchioles (asthma
treatment). Would be sympathomimetic.
c. Age and the ANS
i. In old age, ANS efficiency decreases, resulting in constipation, dry
eyes, and orthostatic hypotension.
ii. Orthostatic hypotension is a form of low blood pressure that occurs
when sympathetic vasoconstriction centers respond slowly to
positional changes.
99
Autonomic Nervous System
Post-Lecture Practice
3. Catagorize the following ANS fibers as cholinergic or adrenergic.
a. Parasympathetic preganglionic
b. Parasympathetic postganglionic
c. Sympathetic preganglionic
d. Sympathetic postganglionic that innervate arrector pili and sweat glands
e. Majority of sympathetic postganglionic
4. Match the following structures with the type of ANS receptors you would find
on them.
a. Nicotinic receptor
b. Muscarinic receptor
c. Adrenergic receptor (either alpha or beta)
____ Parasympathetic postganglionic
____ Sympathetic postganglionic
____ Parasympathetic targets
____ Majority of sympathetic targets
____ Arrector pili and sweat glands
____ Skeletal muscle (remember however this is a somatic target not an
autonomic target)
5. Autonomic Nervous System
a. Randomly pick 6 different tissues off the top of your head and write them
down
b. Now compare and contrast the effects of the sympathetic and
parasympathetic on these different tissues: will the effects be excitatory or
inhibitory?
c. Give 3 reasons why the sympathetic response has longer lasting effects on
the body than the parasympathetic response
100
Muscle Physiology
Study Objectives:
1. List the functions of skeletal muscle
2. Describe the four functional properties of muscle tissue
3. Identify and describe the connective tissue sheaths: epimysium, perimysium, and
endomysium
4. Describe the microscopic anatomy of muscle fibers. Include the structure and function
of the sarcolemma, sarcoplasmic reticulum, terminal cisternae, transverse tubules,
myofibrils, sarcomeres, and myofilaments (actin, tropomyosin, troponin, myosin,
titin)
5. Describe the structure and function of the neuromuscular junction: axon terminal,
synaptic cleft, and motor end plate
6. Describe the events of muscle cell contraction:
Steps involved in the transmission of nerve impulses to muscle
Excitation-contraction coupling events
Steps of the sliding filament theory
Explain the role of myosin, actin, sarcoplasmic reticulum (terminal
cisternae), transverse tubules, troponin-tropomyosin complex, calcium and
ATP in the sliding filament theory
7. Define motor unit, muscle tension, recruitment, isotonic contraction (concentric vs.
eccentric), isometric contraction, muscle tone, graded response, and “all or none”
response
8. Describe the following factors and how the contribute to muscle tension: frequency of
stimulation (wave summation), intensity of stimulation (motor unit summation),
treppe, size of muscle, and optimal operating length
9. Describe three ways ATP is generated during muscle activity: direct phosphorylation,
aerobic respiration, anaerobic glycolysis
10. Describe muscle fatigue
11. Define oxygen debt and explain why it must be repaid
12. Distinguish between fast glycolytic, fast oxidative, and slow oxidative muscle fibers,
explain the characteristics of each
101
13. Compare the effects of aerobic vs. resistance exercise on muscles
14. Compare and contrast skeletal muscle and smooth muscle based on their innervation,
structure, and contraction mechanisms.
15. Describe the characteristics of single unit and multi unit smooth muscle.
16. Describe the stress-relaxation response in smooth muscle.
Muscle Physiology Outline
I.
Functions of Skeletal Muscle
a. Movement – muscles attach directly or indirectly to bone, pull on bone or
tissue when they contract
b. Maintain posture / body position – muscles are continuously contracting to
make adjustments to maintain posture
c. Stabilize joints – tendons crossing joints and muscle tone
d. Thermogenesis - generate heat when contracting
II.
Properties of Muscle Tissue
a. Excitable – respond to nerve stimulus
b. Contractible – shorten when stimulated
c. Extensible – can stretch beyond resting length when relaxed
d. Elastic – can recoil/rebound to original resting length after contraction or
stretching
III.
Gross Anatomy of Skeletal Muscle (See figure 8-2)
a. Endomysium – surrounds individual muscle fibers
b. Perimysium – surrounds bundles of muscle fibers called fascicles
c. Epimysium – dense irregular CT, surrounds the entire muscle
IV.
Microscopic Anatomy of Skeletal Muscle (See figure 8-2, 8-3, 8-4)
a. Sarcolemma – plasma membrane surrounding muscle fiber
b. Sarcoplasm
i. Contains a lot of mitochondria, glycogen, myoglobin, and
contractile organelles called myofibrils
c. Myofibril
i. Long fiber-like organelle that fills the sarcoplasm of the cell
ii. Runs parallel to muscle fiber
d. Sarcomere
i. Aligned end to end along the length of the myofibril
ii. Z-line – boundary at the end of each sarcomere
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iii. Myofilaments - contractile proteins in the sarcomere and
arrangement gives muscle its striations
1. Myosin (thick) filaments
a. Tail with split head
b. Arranged in bundles
c. Heads contain:
i. ATP binding site
ii. ATPase enzyme which splits ATP to
provide energy during contraction
iii. Actin binding site
2. Actin (thin) filament
a. Attached to Z – line and extends towards the center
of the sarcomere
b. Contains active binding site for myosin heads
3. Regulatory proteins - proteins that regulate the binding of
myosin to actin
a. Tropomyosin – spirals around actin, blocks active
site when muscle is relaxed
b. Troponin – contains three binding sites
i. Binds to actin
ii. Binds to tropomyosin and controls its
position on active binding site
iii. Contains calcium binding site
4. Titin (elastic) filaments
a. Large protein attached to z-line and runs through
the center of thick filaments
b. Gives muscle elastic property; uncoils when muscle
stretches yet stiffens to avoid over extension, and
recoil when muscle relaxes
e. Sarcoplasmic reticulum (SR) – specialized smooth endoplasmic
reticulum.
i. Surrounds each myofibril.
ii. Terminal cisternae – expanded ends of SR. Stores and releases
calcium when muscle fiber is stimulated to contract
f. Transverse Tubules (T-tubule) – deep indentations of the sarcolemma
into the muscle fiber
i. Lies between two terminal cisternae
ii. Conducts electrical impulse from the sarcolemma into the muscle
fiber
iii. Coordinates muscle contraction by triggering calcium release from
the terminal cisternae
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V.
Skeletal Muscle Contraction
a. In order to contract, a skeletal muscle must:
i. Be stimulated by a somatic motor neuron
ii. Propagate an electrical current, or action potential, along its
sarcolemma
iii. Have a rise in intracellular Ca2+ levels, the final trigger for
contraction
b. Excitation-contraction coupling -linking the electrical signal to the
contraction
i. The neuromuscular junction is formed from:
1. Axon terminals, which have synaptic vesicles that contain
acetylcholine (ACh)
2. Synaptic cleft
3. The motor end plate, which is a specific part of the
sarcolemma that contains ACh receptors
ii. Excitation-contraction coupling events (See figure 8-11):
1. When a nerve impulse reaches the end of an axon at the
neuromuscular junction:
a. Voltage-regulated calcium channels open and allow
Ca2+ to enter the axon
b. Ca2+ inside the axon terminal causes vesicles to fuse
with the axon membrane and release ACh into the
synaptic cleft by exocytosis
c. ACh diffuses across the synaptic cleft to ACh
receptors on the motor end plate
d. Binding of ACh to its receptors initiates an action
potential in the muscle
e. ACh bound to ACh receptors is quickly destroyed
by acetylcholinesterase
2. Once generated, the action potential:
a. Is propagated along the sarcolemma
b. Travels down the T tubules
c. Triggers Ca2+ release from terminal cisternae
3. Ca2+ binds to troponin and causes:
a. A conformational change in troponin
b. Tropomyosin rolls off the actin active binding sites
allowing them to be exposed for myosin to attach
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c. Sliding Filament Theory (See figure 8-12):
i. Events of contraction:
1. Cross bridge formation – myosin cross bridge attaches to
actin filament
2. Working (power) stroke – myosin head pivots and pulls
actin filament toward M line
3. Cross bridge detachment – ATP attaches to myosin head
and the cross bridge detaches
4. “Cocking” of the myosin head – energy from hydrolysis of
ATP cocks the myosin head into the high-energy state
ii. Muscle Relaxation
1. When the nerve stimulation ceases:
a. Ca2+ is removed and actively transported back into
the SR (requires ATP)
b. Tropomyosin roles back over the binding sites, and
the muscle fiber relaxes
d. Tension – force muscle exerts on an object when contracted
i. Load or resistance is the opposing force exerted on the muscle
ii. Muscle tension must over come the force of the load in order to
shorten
e. Phases of a Muscle Twitch (See figure 8-13)
i. Latent period – first few milliseconds, excitation-contraction
coupling
ii. Period of contraction – cross bridge cycling, tension increases
iii. Period of relaxation – calcium transported back into SR, cross
bridge cycling ends, tension decreases
f. Graded Muscle Response - individual muscle fiber contraction is an “all
or none” response, but whole muscles can vary in tension produced and
length of contraction
i. Factors Effecting Tension
1. Intensity of stimulus – number of motor units
a. Motor unit – a single motor neuron and all the
muscle fibers it supplies (See figure 8-18)
b. Recruitment – calling additional motor units,
therefore stimulating more fibers and increasing
muscle tension
c. Threshold stimulus – minimal stimulus needed to
invoke visible muscle contraction
d. Maximal stimulus – all motor units are recruited,
strongest contraction produced
e. Asychronous recruitment of motor units – alternates
motor units
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2. Frequency of stimulation (See figure 8-20)
a. Twitch – single impulse, contraction followed by
relaxation
b. Wave summation – when impulses are delivered in
succession the second twitch will be stronger then
the first
c. Complete tetanus – rapid stimulation results in
sustained smooth contraction without periods of
relaxation
i. Refractory Period in Skeletal Muscle
1. Contractile response lasts longer, far
beyond the refractory period of the
action potential
2. This is important in skeletal muscle’s
ability to produce tetanus
d. Treppe: The Staircase Effect – increased
contraction in response to multiple stimuli of the
same strength.
i. Different than summation because relaxation
occurs.
ii. Contractions increase because:
1. There is increasing availability of
Ca2+ in the sarcoplasm
2. Reduced slack of the elastic series
component
3. Muscle enzyme systems become
more efficient because heat is
increased as muscle contracts
3. Size of Muscle
a. Number of muscle fibers per muscle
b. Size of individual muscle fibers – fibers produce
more myofilaments in response to demands placed
on them. Fibers hypertrophy.
4. Optimal operating length – the resting length in which
maximum contraction can be generated (70 -130%)
a. Occurs when the muscle is slightly stretched and
filaments barely overlap (see figure 8-21)
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g. Types of Contractions
i. Isotonic – same tension
1. Muscle tension remains constant during contraction
2. Muscle length changes during contraction, shortens or
lengthens
3. Types of isotonic contractions:
a. Concentric - muscle shortens and does work
i. Examples: pick up pencil, kick soccer ball
b. Eccentric – muscle contracts as it lengthens
i. Helps counter act gravity or prevent joint
injury “muscle braking”
ii. Example: squats – quadriceps stretch but are
contracted to counter act gravity and control
movement
ii. Isometric – same length
1. Tension increases but muscle length remains the same
2. Muscle is unable to produce enough force to overcome the
load
3. Example: pushing against a stationary wall
h. Muscle Tone
i. Constant low level of tension in relaxed muscles
ii. Maintained by spinal reflexes that activate alternating motor units
iii. Keeps muscles firm and ready to respond to stimuli
VI.
Muscle Metabolism (See figure 8-22)
a. Role of ATP - muscles need a constant supply of ATP to carry out
contractions
i. For cross bridge formation and power stroke
ii. For disconnecting of cross bridges
iii. For active transport of calcium back into the terminal cisternae
iv. For Na-K pump
v. Muscles only have enough ATP stored for 4-6 seconds worth of
contraction. Therefore ATP must be constantly regenerated.
vi. Three pathways that supply additional ATP:
1. Creatine phosphate (direct phosphorylation)
2. Oxidative phosphorylation
3. Glycolysis
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vii. Creatine phosphate (direct phosphorylation)
1. Creatine phosphate, transfers energy and a phosphate to
ADP forming ATP
2. Creatine phosphate + ADP  Creatine + ATP
3. Creatine phosphate is stored in the muscle fibers
4. Provides a rapid source of energy for 10 – 15 seconds of
contraction
viii. Oxidative Phosphorylation - Aerobic Respiration
1. Occurs in the mitochondria
2. Main source when O2 is present
3. Fueled by glycogen stores and glucose and fatty acids
delivered by the blood
4. Can provide hours of muscle contraction for prolonged
moderate activity
5. Slower because it requires the delivery of oxygen and
glucose
6. There is cardiovascular limits to the amount of nutrients
that can be delivered to muscle
a. CV system cannot keep up with O2 demands
b. Blood vessels in the muscle are compressed during
maximal contraction
c. Oxidative phosporylation may not be able to
produce enough ATP quick enough to keep up with
the demands
ix. Glycolysis – anaerobic
1. Glucose is broken down to pyruvic acid and produces
2ATP
2. In the absence of O2 pyruvic acid is converted to lactic acid
3. Produces minimal amounts of ATP but occurs quickly
4. Provides 30-60 seconds of high level activity
b. Muscle Fatigue - decline in muscle tension as a result of previous activity
i. Muscles are unable to contract despite being stimulated
1. Results from a deficit of ATP (not a total absence)
2. Anaerobic respiration becomes less efficient as lactic acid
accumulates and pH drops in the muscle fiber
3. Muscle fibers lose K+ as the Na-K pump is unable to
restore ion balance since it requires ATP
ii. Neuromuscular fatigue – caused by a shortage of
neurotransmitters at the NMJ
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c. Oxygen Debt - the amount of extra oxygen the body must take in to
restore muscle chemistry back to resting state
i. The liver converts lactic acid in the blood to pyruvic acid which
can be converted to glucose or enter aerobic respiration now that
O2 is available
ii. Glycogen stores are replenished in muscles and liver
iii. Creatine is re-phosphorylated into creatine phosphate and stored in
muscles
iv. O2 rebinds to myoglobin
d. Types of Muscle Fibers (See table 8-1 and figure 8-23)
i. Muscle fibers differ in their methods of metabolism based on:
1. Pathways they use to produce ATP
2. Duration of muscle contraction
3. How quickly their ATPases work
4. Speed (velocity) of contraction
ii. Muscle Fiber Types
1. Slow – oxidative (red)
a. Slow to contraction but most resistant to fatigue
b. Good for endurance and continuous contraction
c. Better equipped for oxidative phosphorylation:
i. Numerous mitochondria and rich supply of
capillaries
ii. Small in diameter
iii. High myoglobin content
d. Slow myosin ATPase activity
2. Fast – oxidative (pink)
a. Fast to contraction but resistant to fatigue
b. Also equipped for oxidative phosphorylation
c. Fast myosin ATPase activity
3. Fast glycolytic fibers (white)
a. Fast to contract but fatigue quickly
b. Good for power and speed for short durations
c. High glycogen reserves and relies mainly on
glycolysis
d. Fatigue quickly due to lactic acid build up
e. Large fibers generate more force but poor nutrient
diffusion
f. Light in color due to reduced myoglobin
g. Fewer capillaries and mitochondria
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e. Effects of Exercise on Muscle Fibers
i. Aerobic Exercise
1. Results in more efficient muscle metabolism and resistance
to fatigue
2. Increases capillaries, mitochondria and myoglobin
3. Also increases efficiency of the heart, lungs, body
metabolism, and neuromuscular coordination
ii. Resistance – weight lifting and isometric contractions
1. Fibers produce more myofilaments and myofibrils causing
muscle fibers to hypertrophy
2. Increases glycogen stores
3. Results in increased muscle size and strength
VII.
Smooth Muscle Tissue
a. Structure and Location
i. Composed of spindle-shaped fibers
ii. Organized into two layers (longitudinal and circular)
iii. Found in walls of hollow organs (except the heart)
b. Innervation of Smooth Muscle
i. Smooth muscle lacks neuromuscular junctions
ii. Innervating nerves have bulbous swellings called varicosities that
release neurotransmitters
iii. Some neurotransmitters are excitatory and some are inhibitory,
depending on the receptor
c. Structural Characteristics (see figure 8-29)
i. SR is less developed than in skeletal muscle and lacks a specific
pattern
ii. T tubules are absent
iii. Thin filaments only contain tropomyosin (NO troponin)
iv. Thick and thin filaments are arranged diagonally, causing smooth
muscle to contract in a corkscrew manner
d. Contraction Mechanism (see figure 8-30 and 8-31)
i. Actin and myosin interact according to the sliding filament
mechanism
ii. Calcium influx from the extracellular space triggers Ca2+ release
from the SR
iii. The trigger for contractions is a rise in intracellular Ca2+
110
iv. Role of Calcium Ion
1. Ca2+ binds to calmodulin
2. Activated calmodulin activates the myosin light chain
kinase enzyme which transfers phosphate from ATP to
myosin cross bridges
3. Phosphorylated cross bridges interact with actin to produce
shortening
v. Smooth muscle relaxes when intracellular Ca2+ levels drop
e. Types of Smooth Muscle
i. Single Unit
1. Visceral smooth muscle is autonomous
2. Smooth muscle pacemaker cells display rhythmic,
spontaneous variations in membrane potentials known as
slow wave potentials. (See figure 8-32)
3. Self-excitable (myogenic) – can produce spontaneous
action potentials without external stimulation
4. Cells are electrically coupled to one another via gap
junctions and contract rhythmically as a unit
5. Pacemaker smooth muscle cells (Interstitial cells of Cajal)
membrane potential oscillates closer and further away from
threshold
a. If threshold is reached a burst of action potentials is
triggered causing rhythmic smooth muscle
contractions
i. Drive several digestive processes
(e.g., peristalsis and segmentation)
6. Hormones, paracrines, mechanical stress, and nerve stimuli
determines the starting point of the slow wave potentials.
Example:
a. Food in the GI tract – closer to threshold
b. Empty GI tract – further away from threshold
7. Response to Stretch
a. Smooth muscle exhibits a phenomenon called
stress-relaxation response in which:
i. Smooth muscle responds to stretch only
briefly, and then adapts to its new length
ii. The new length, however, retains its ability
to contract
iii. This enables organs such as the stomach and
bladder to temporarily store contents
111
ii. Multiunit
1. Multiunit smooth muscles are found:
a. In large airways to the lungs, large arteries, arrector
pili muscles, attached to hair follicles, and in the
internal eye muscles
2. Their characteristics include:
a. Rare gap junctions
b. Structurally independent muscle fibers
c. A rich nerve supply, forms motor units
d. Graded contractions in response to neural stimuli
112
Muscle Physiology
Post-Lecture Practice
1. View “Neuromuscular Junction” and “Sliding Filament Theory” animations on
Canvas or you can go to Google video and type these topics in to find numerous
animations depicting these processes.
2. Give a brief description of the events happening in the 4 steps of the sliding
filament theory. (use your physiology terminology)
3. Compare and contrast skeletal and smooth muscle by listing at least three
physiological distinctions for each type of muscle tissue. (hint: think about how
they differ in innervation, structure, and contraction mechanisms)
Skeletal
Smooth
__
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Endocrine System
Study Objectives:
1. Define endocrine gland, hormones, and target cell/organ
2. Describe the factors affecting target cell activation.
3. Define humoral, neural, and hormonal stimuli. Be able to recognize examples of each.
4. Discuss how the hypothalamus and the pituitary gland are structurally and functionally
related.
5. Describe the structural and functional differences between the anterior and posterior
pituitary gland.
6. List the major endocrine organs and the hormones they secrete. Then for each
hormone, discuss what stimulates its release, the target cells, and its effect on the target
cells. (this is where your optional endocrine worksheet may be handy.)
7. Describe the role of the renin-angiotensin-aldosterone pathway in the maintenance of
blood pressure and volume.
8. Describe the general stress responses that accompany the General Adaptation
Syndrome. What hormones are involved?
9. Compare and contrast the events of the alarm reaction, resistance reactions, and the
exhaustion phase of G.A.S.
10. Describe the consequences of long term stress on the physiology of the body.
11. Distinguish between the absorptive state and the postabsorptive state. Which
hormones are dominate in each state?
12. Distinguish between insulin dependent and insulin independent glucose transporters.
Give examples of where they are found.
13. Distinguish between the causes of type 1 diabetes and type 2 diabetes.
14. Describe the three cardinal signs of diabetes mellitus. What are the common long
term complications caused by the disease?
114
Endocrine System Outline
I.
What is the Endocrine System?
a. Composed of glands that secrete hormones
b. Responsible for continuous processes such as growth, cell metabolism, &
reproduction
II.
What do Hormones Do?
a. Hormones are chemical substances that travel through the blood to a target
cell
i. Target cells must have specific receptors to which the hormone
binds
ii. These receptors may be intracellular or located on the plasma
membrane
iii. They trigger a change in cellular activity
b. Target cell activation depends on three factors:
i. Blood levels of the hormone
ii. Relative number of receptors on the target cell
1. Up-regulation – target cells form more receptors in
response to the hormone
2. Down-regulation – target cells lose receptors in response to
the hormone
iii. The affinity of those receptors for the hormone
c. Control of Hormone Release
i. Hormones are synthesized and released in response to humoral,
neural, and hormonal stimuli:
1. Humoral stimuli - secretion of hormones in response to
changing blood levels of ions and nutrients. Examples:
a. Concentration of calcium ions in the blood and the
release of PTH
b. Concentration of blood glucose and the release of
insulin
2. Neural stimuli – nerve fibers stimulate hormone release.
Example: preganglionic sympathetic fibers stimulate
adrenal medulla to release catacholamines
3. Hormonal stimuli – release of hormones in response to
hormones produced by other endocrine organs. Example:
The anterior pituitary gland secretes hormones that
stimulate other endocrine glands
115
IV.
Hypothalamus – Pituitary Axis
a. Hypothalamus
i. Regulatory hormones from the hypothalamus control the release
of hormones from the anterior pituitary
1. Releasing hormones stimulate the release of hormones
from the anterior pituitary
2. Inhibiting hormones shut off release of hormones from the
anterior pituitary
ii. Produces oxytocin and antidiuretic hormone that is secreted by the
posterior pituitary
b. Pituitary gland – two-lobed endocrine gland that secretes nine major
hormones
i. Posterior lobe - neurohypophysis, made up of neural tissue
1. The posterior lobe is a down growth of hypothalamic
neural tissue and has a neural connection with the
hypothalamus (see figure18-4)
2. Nuclei of the hypothalamus synthesize oxytocin and
antidiuretic hormone (ADH)
3. These hormones are transported to the posterior
pituitary where they are stored and released.
4. Posterior pituitary hormones:
a. Antidiuretic Hormone (ADH) (a.k.a Vasopressin)
i. Function: triggers increased water
reabsorption in the kidney tubules
ii. Release of ADH is stimulated by:
1. Increase in osmolarity detected by
the hypothalamus
2. Decrease in blood pressure and
volume
b. Oxytocin – causes contractions of uterus smooth
muscle during labor
ii. Anterior lobe - adenohypophysis, made up of glandular tissue
1. The anterior lobe of the pituitary and the hypothalamus are
connected by the hypophyseal portal system (see figure
18-7)
116
2. Anterior pituitary hormones (figure 18-5):
a. Tropic hormones – regulates the release of
hormones from other endocrine glands
i. Thyroid-stimulating hormone (TSH)
ii. Adrenocorticotropic hormone (ACTH)
iii. Follicle-stimulating hormone (FSH)
iv. Luteinizing hormone (LH)
v. Growth hormone (GH)
b. Additional non-tropic hormones released by the
anterior pituitary
i. Prolactin (PRL)
ii. Melanocyte-stimulating hormone (MSH)
c. Growth Hormone (GH) (see figure 18-10)
i. Targets most cells, especially bone and
skeletal muscle when young
ii. Growth promoting actions:
1. stimulates bone and soft tissue
growth.
2. increases protein synthesis, cell
growth, and cell division.
iii. Metabolic actions:
1. mobilizes fat stores and increases
fatty acid levels in the blood
2. increases blood glucose
a. through glycogenolysis the
breakdown of glycogen
b. inhibits glucose uptake in
skeletal muscle
d. Adrenocorticotropic hormone (ACTH)
i. Targets the adrenal cortex
ii. Stimulates the release of glucocorticoids
V.
Adrenal glands – paired, pyramid-shaped organs atop the kidneys
a. Structurally and functionally, they are two glands in one (see figure 19-7):
i. Adrenal medulla – nervous tissue that acts as part of the
sympathetic nervous system
ii. Adrenal cortex – glandular tissue derived from embryonic
mesoderm
b. Adrenal Cortex - synthesizes and releases steroid hormones called
corticosteroids
117
i. Regions of the adrenal cortex and hormone secreted (see figure 197):
1. Zona reticularis – gonadocorticoids (mainly androgens)
2. Zona fasciculate – glucocorticoids (mainly cortisol)
3. Zona glomerulosa – mineralocorticoids (mainly
aldosterone)
ii. Hormones released by Adrenal Cortex:
1. Glucocorticoids (Cortisol) - helps the body resist stress
by:
a. Increasing blood glucose levels
b. Cortisol has the following effects :
i. Promotes gluconeogenesis - formation of
glucose from non-carbohydrates
ii. Enhances lipolysis
iii. Triggers protein catabolism in skeletal
muscle
iv. Suppresses the immune system
v. See figure 19-9
2. Mineralocorticoids (Aldosterone)– regulate the
electrolyte concentrations of extracellular fluids.
a. Regulates blood pressure, blood volume, and Na+
and K+ levels in the blood
i. Stimulates reabsorption of Na+ by the
kidneys
ii. Causes secretion of K+
b. Aldosterone secretion is stimulated by:
i. Low blood Na+
ii. Rising blood levels of K+
iii. Decreasing blood volume or pressure
iv. Stress
c. The Four Mechanisms of Aldosterone Secretion:
i. Plasma concentration of sodium and
potassium – directly influences the zona
glomerulosa cells
ii. ACTH – causes small increase in
aldosterone during stress
118
iii. Renin-angiotensin mechanism – kidneys
release renin in response to decreased BP,
stimulates aldosterone release. Reninangiotensin-aldosterone pathway:
1. Is triggered when the kidneys release
renin
2. Renin converts the plasma protein
angiotensinogen into angiotensin I
3. Angiotensin I is converted into
angiotensin II by ACE (angiotensin
converting enzyme)
4. Angiotensin II:
a. Causes systemic arteriole
vasoconstriction
b. Stimulates the adrenal cortex
to release aldosterone
5. Results in increased blood pressure
and volume
iv. Atrial natriuretic peptide (ANP) –
produced by the heart in response to
increased pressure, inhibits the release of
aldosterone
VI.
Long term stress
a. What is stress?
i. Stress = any factor that disrupts our natural balance (homeostasis)
ii. Stressor = anything that causes us to adjust
1. Can be emotional, physical, environmental
2. Can be an immediate response to a threat or a response to
prolonged exposure to stress
iii. Stress stimulates the hypothalamus to initiate a chain of reactions
that results in general adaptation syndrome (see figure 19-13)
b. General Adaptation Syndrome (G.A.S)
i. Definition: “the sum of all non-specific systemic reactions of the
body to long continued exposure to stress” (Hans Selye)
ii. Phases of G.A.S.
1. Alarm reaction – mobilize resources
2. Resistance reaction – cope with stress
3. Exhaustion – deplete reserves
119
iii. Alarm Reaction
1. Immediate response to stress triggers the sympathetic
nervous system “fight or flight” through the hypothalamus
2. Mobilizes the body for immediate physical activity
3. Short-lived
iv. Resistance Reaction
1. If stress persists longer than a few hours then the resistance
reaction is initiated
2. Prepares the body for long term protection, slow to start but
longer lasting
3. The hypothalamus triggers the pituitary gland to secrete
hormones that will allow the body to continue to survive
the stress until homeostasis is returned
4. Overall goal of resistance reaction is to:
a. Maintain blood pressure and volume
b. Increase ATP production
c. Prevent water loss
d. Prevent inflammation from causing tissue damage
5. Maintained by ADH, aldosterone, cortisol, growth
hormone, and thyroid hormones
v. Exhaustion Phase
1. If the resistance reaction fails to overcome the stress
eventually the body reserves are exhausted and the
resistance reaction cannot be sustained
2. The adrenal cortex cannot produce aldosterone and cortisol
3. “Link between the breakdown of the hormonal adaptation
mechanism and fatal diseases” Hans Selye
a. Results in illness or death
b. Cancer, heart disease, depression, hypertension,
diabetes
vi. Prolonged exposure to stress hormones:
1. Depresses cartilage and bone formation
2. Depresses the immune system
3. Promotes changes in the cardiovascular, neural, muscular,
and gastrointestinal function (usually due to hypokalemia =
potassium deficiency)
a. Cardiac arrhythmias
b. Muscle wasting
c. Fatigue, concentration loss, irritability
120
c. Some Stress is Good!
i. We all need a little stress
ii. Norepinephrine which is a neurotransmitter released during stress
plays a role in:
1. Creating and retrieving memories
2. Improves moods (feel good chemical)
VII.
Pancreas – controls blood glucose levels
a. Anatomy Review (see figure 22-8 19-15)
i. Located behind the stomach
ii. Has both exocrine and endocrine functions
1. Acinar cells – exocrine cells that produce digestive
enzymes that are secreted into the duodenum
2. The endocrine cells are organized into the islets of
Langerhans. Contain both:
a. Alpha (α) cells that produce glucagon
b. Beta (β) cells that produce insulin
b. Control of Blood Glucose
i. Insulin and glucagon act as antagonistic hormones to control
blood glucose levels. Most of the time both of these hormones are
found in the blood, it is the ratio of the two that determines which
is dominant. (See figure 19-20)
1. Absorptive State – occurs when ingested nutrients are
being absorbed into the blood from the digestive tract
a. Metabolic fuels are stored during the absorptive
state (fed state).
b. Circulating glucose is used for energy or is stored as
glycogen in the liver and skeletal muscles.
c. Excess circulating fatty acids are stored into
triglycerides, mainly in adipose tissue.
d. Excess amino acids not needed for protein synthesis
and excess glucose are converted to fatty acids and
stored as triglycerides in adipose tissue.
2. Postabsorptive State – fasting state that occurs between
meals
a. When blood glucose drops during the
postabsorptive state glycogen is broken down into
glucose
b. Many body cells will burn fatty acids to spare
glucose for the brain. To supply the brain, amino
acids can be converted to glucose by
gluconeogenesis.
121
ii. Insulin - lowers blood glucose, fatty acid, and amino acid levels
and promotes their storage. Dominate during the absorptive state.
1. Insulin’s effects:
a. Enhances transport of glucose into body cells
b. Stimulates glycogenesis in skeletal muscle and liver
cells
c. Promotes the transport of amino acids into cells for
protein synthesis.
d. Promotes the transport of fatty acids into adipocytes
e. Inhibits metabolic activity that would increase
blood glucose levels such as: glycogenolysis,
gluconeogenesis, and lipolysis
f. (See figure 19-18)
2. Glucose Transporters - plasma membrane carriers that
facilitate the passive diffusion of glucose into cells.
a. Some are insulin independent – do not require
insulin for transporters to be present in the
membrane
i. Brain, working muscles, liver, digestive
mucosa, pancreas B-cells
b. Most are insulin dependent – present in the
membrane when insulin binds to cell receptors
i. The case in most cells especially resting
muscle and adipose tissue
c. Insulin promotes up regulation of GLUT 4
i. Glucose transporters are contained in
intracellular vesicles and are inserted into
the plasma membrane when insulin is
present. Triggers a 10 – 30X increase in
glucose uptake
iii. Glucagon – increases blood glucose levels
1. Glucagon secretion increases when the blood concentration
of glucose is too low. Dominate during the postabsorptive
state.
2. Its major target is the liver, where it promotes:
a. Glycogenolysis – the breakdown of glycogen to
glucose
b. Gluconeogenesis – synthesis of glucose from lactic
acid and noncarbohydrates
c. Promotes fat metabolism (lipolysis)
122
iv. Summary of hormones controlling blood glucose:
1. Growth hormone, cortisol, epinephrine, and glucagon all
increase blood glucose
2. Insulin is the only hormone that decreases blood glucose
v. Diabetes Mellitus - inadequate insulin action resulting in
hyperglycemia.
1. Type I diabetes mellitus is due to an insulin deficiency
a. Cause is usually autoimmune - destruction of Beta
cells
2. Type II diabetes mellitus is due to the reduced sensitivity
of target cells to the presence of normal or increased insulin
a. Cause can be genetic predisposition and/or lifestyle,
diet, exercise, ect.
3. The three cardinal signs of DM are:
a. Polyuria- increased urine output due to glucosuria
and osmotic diuresis. Can lead to dehydration and
circulatory and renal failure.
b. Polydipsia – excessive thirst
c. Polyphagia – excessive hunger and food
consumption
4. Consequences of Diabetes (See figure19-19)
a. Liver use of fatty acids leads to ketosis. Acidosis
develops and can depress brain function.
b. Increase in protein degradation can reduce growth
and leads to the wasting of skeletal muscles.
c. Long-term complications include degenerative
disorders of the vascular and nervous systems.
VIII. Control of Blood Calcium Levels
a. Blood calcium levels affect many physiological events including:
i. neural and muscular excitability
ii. excitation-coupling in skeletal, cardiac, and smooth muscle
iii. cell signaling
iv. blood clotting
b. Controlled by two hormones calcitonin and parathyroid hormone.
i. Parathyroid Glands - tiny glands on the posterior side of the
thyroid (see figure 19-22)
1. Secretes parathyroid hormone which increase blood
calcium levels
123
2. Effects of parathyroid hormone:
a. Stimulates osteoclasts to digest bone matrix
b. Enhances the reabsorption of Ca2+ and the secretion
of phosphate by the kidneys
c. Stimulates calcitriol synthesis (vitamin D) by the
kidneys which increases absorption of Ca2+ by
intestinal mucosal cells (see figure 19-27)
3. Rising Ca2+ in the blood inhibits PTH release
ii. Thyroid gland
1. Secretes the hormone calcitonin which lowers blood
calcium levels
a. Produced by the parafollicular, or C cells in the
thyroid gland
b. Antagonist to parathyroid hormone (PTH)
2. Calcitonin targets the skeleton and kidneys, where it:
a. Inhibits osteoclast activity thus the release of
calcium from the bone matrix
b. Increase renal Ca2+ excretion
iii. Calcium disorders
1. Hypocalcemia - deficient PTH secretion
a. Nervous system becomes hyperexcitable
b. Causes muscle tetany
c. Caused by autoimmune disease
2. Hypercalcemia - excess PTH secretion
a. This reduces the excitability of muscle and nervous
tissue
b. Other effects are the thinning of bones and the
development of kidney stones.
c. May be caused by a tumor
IX.
Additional Endocrine Glands and the Hormones they secrete
a. Thymus
i. Thymosin – matures T-cells
b. Ovaries
i. Estrogen – female characteristics
ii. Progesterone- works with estrogen to maintain uterine cycle
c. Testes
i. Testosterone– male characteristics
124
d. Adipocytes
i. Leptin – decreases food intake by acting as a satiety factor
e. Stomach
i. Ghrenlin – increases hunger
**Optional - read more about leptin and ghrenlin in chapter 17 pgs 638 – 641
and see figure 17-2 if you are interested in factors influencing food intake.
Endocrine
Post Lecture Assignment:
Complete the Endocrine Worksheet posted on Canvas. This worksheet is not for
points but it will be a good study resource when it comes to learning the functions
of all the hormones we discussed. It focuses you on the endocrine gland, the
hormones it releases, the target of the hormones and their effect.
125
Blood
Study Objectives:
1. List the functions of blood
2. Describe the composition of whole blood
3. Describe the structure and function of the cell types making up the formed elements of
blood: erythrocytes, types of leukocytes, platelets
4. Define erythropoiesis and describe where erythrocyte production and destruction take
place.
5. Define hematopoiesis and where does it occur?
6. Define hemostasis. Describe the processes of vascular spasm and platelet-plug
formation.
7. Describe the stages involved in the coagulation process (intrinsic and extrinsic clotting
pathways).
8. Name the factors that promote and inhibit blood clotting.
9. Define and know possible causes for the following disorders: anemia, polycythemia,
leukocytosis, thromboembolism, thrombocytopenia, and hemophilia
126
Blood Outline
I.
Functions of Blood
a. Transport
i. Oxygen and nutrients to the cells
ii. Waste away from cells
iii. Hormones
b. Regulation
i. Maintain body temperature by absorbing and distributing heat
c. Protection
i. WBC fight infection
ii. Blood clotting prevents blood loss
II.
Composition of Blood (see figures 11-1 & table 11-1)
a. Plasma – 90% water along with dissolved compounds
i. Proteins – albumin, antibodies, clotting proteins. Proteins help
maintain osmotic pressure.
1. Albumin – 60% of plasma proteins
a. Transports substances such as bilirubin and bile
salts
2. Globulins
a. α , β – transports hormones, cholesterol, and iron;
angiotensinogen and clotting factors
b. Gamma globulins – antibodies
3. Fibrinogen
a. Precursor for the clotting protein fibrin
ii. Electrolytes – sodium, potassium, calcium, magnesium, chloride,
bicarbonate
b. Formed elements – erythrocytes, leukocytes, platelets
i. Erythrocytes (red blood cells)
1. Biconcave shape
2. Contains no nucleus or organelles
3. Enzymes in cytoplasm:
a. Glycolytic enzymes to carry out glycolysis
b. Carbonic anhydrase – converts CO2 to HCO34. Last ~120 days and are then destroyed by the spleen or
liver
5. Function – to transport oxygen and to a lesser extent carbon
dioxide
6. Contains hemoglobin – protein that binds and carries
oxygen (see figure 11-2)
a. Made of 4 globin polypeptides and 4 heme groups
127
7. Erythropoiesis – production of new erythrocytes (~3
million per second)
a. Occurs in the red bone marrow
b. Rate of production is controlled by erythropoietin
produced by the kidneys in response to blood
oxygen levels (see figure 11-4)
8. Anemia - decrease in oxygen carrying ability of the blood.
Causes:
a. Decreased number of RBC (low hematocrit)
b. Deficient or abnormal hemoglobin
c. Deficiency in iron or vitamin B12
d. Kidney disease, decrease in EPO
e. Blood loss
f. Malaria
g. Sickle-cell anemia
9. Polycythemia – increased numbers of erythrocytes /
hematocrit
a. Causes: cancer, high altitudes, lung and heart
disease, dehydration
ii. Leukocytes – white blood cells
1. Functions
a. Protect against infection and initiates inflammation
b. Destroy cancerous cells
c. Tissue repair
2. Types of Leukocytes (see figure 11-8)
a. Granulocytes – granule containing cells with lobed
nuclei
i. Neutrophils (60 – 70%)
1. Phagocytes
2. First on the scene of infection
and triggers inflammation
ii. Eosinophils (1-4%)
1. Associated with allergies and
parasite infections
iii. Basophils (< 1%)
1. Contain and release histamine
b. Agranulocytes – without granules
i. Monocytes (2 - 6%)
1. Travel into the tissue and mature
into macrophages
128
ii. Lymphocytes (25 – 33%)
1. Specific immune defenses
2. B cells & T cells
3. Hemopoiesis - all blood cells arise from a common stem
cell found in the red bone marrow (see figure 11-9).
iii. Thrombocytes – platelets
1. Irregular shaped cell fragments from megakaryocytes (see
figure 11-10)
2. Play a role in blood clotting
3. Hemostasis –prevents the loss of blood when blood vessels
are damaged
a. 3 phases:vascular spasm, platelet plug formation,
coagulation
b. Platelet plug formation (see figure 11-11)
i. Broken or damaged blood vessels cause
platelets to become sticky and cling to the
site
ii. Release chemicals that attract other platelets
(ADP)
iii. Release chemicals that cause
vasoconstriction: serotonin, epinephrine,
thromboxane A2
iv. Normal endothelial cells release prostacyclin
and NO to inhibit platelet aggregation
c. Vascular spasms
i. Blood vessels constrict to diminish blood
flow and loss
d. Coagulation -formation of a network of fibers
that seals the blood vessel. Involves a clotting
cascade.
i. Clotting cascade (see figure 11-14):
1. Involves 12 clotting factors
2. Requires the presence of Ca2+ and
platelet factor 3 (PF3) produced by
aggregating platelets
3. Summary of events:An initial
inactive clotting factor, found in the
plasma, is activated by exposed
collagen. This activates the next
factor and so on….. Until thrombin
converts fibrinogen into fibrin
129
a. Intrinsic Pathway - initiated
when Hageman factor is
activated by exposed
collagen
b. Extrinsic Pathway - Factor
X is activated by
thromboplastin released by
damaged tissues
ii. Role of Thrombin (see figure 11-13)
1. Converts fibrinogen to fibrin
2. Activates stabilizing factor (XIII)
3. Enhances conversion of more
thrombin from prothrombin
4. Enhances platelet aggregation
iii. Clot retraction - platelets trapped in the clot
contract and squeeze serum out
iv. Vessel repair - platelets attract fibroblasts
that repair blood vessel
v. Clot dissolution - thrombin and tissue
plasminogen activator (tPA) converts
plasminogen into plasmin which breaks
down fibrin (see figure 11-15)
vi. Clotting disorders
1. Thromboembolism – clots forming
in intact vessels
2. Imbalance in clotting – anticlotting
mechanisms
3. Slow moving blood
4. Release of thromboplastin from
damaged tissue
5. Hemophilia – deficiency in one of
the clotting factors (usually VIII),
excessive bleeding
6. Thrombocytopenia – deficiency in
platelets
7. Impaired liver
8. Lack of vitamin K
No Post-Lecture Practice for this lecture
130
Cardiac Physiology
Study Objectives:
1. Describe the location of the heart in the body
2. Identify the major anatomical areas of the heart: chambers, valves, and greater vessels
3. Trace the path of blood flow through the heart
4. Describe the intrinsic conduction system and explain the electrical pathway through
the heart. Explain the initiation and conduction of impulses through the intrinsic
conduction system.
5. Describe the conduction of impulses through the contractile myocardial cell and the
events leading to cardiac muscle contraction.
6. Describe the phases of the cardiac cycle and explain the following as they relate to the
cardiac cycle:
Atrial and ventricular systole and diastole
Operation of the heart valves and heart sounds
Pressure changes associated with blood flow through the heart
P, QRS, T deflections of a normal ECG
7. Define cardiac output and describe the factors that affect it:
Factors influencing heart rate
Factors influencing stroke volume: intrinsic and extrinsic
8. Contrast the effects of sympathetic and parasympathetic stimulation of the heart.
9.Define: systole, diastole, inotropic, chronotropic, electrocardiogram, bradycardia,
tachycardia, arrhythmia, fibrillation
131
Cardiac Physiology Outline
I.
The Cardiovascular System
a. Cardiovascular system is composed of:
i. The heart and blood vessels
ii. Functions in transportation of blood:
1. delivers oxygen and nutrients to tissues
2. removes carbon dioxide and waste
products from tissues
b. Gross Anatomy of the Heart (review anatomy on figure 9-4)
c. Microscopic Anatomy of Heart Muscle
i. Cardiac muscle is striated, short, fat, branched, and interconnected
ii. Intercalated discs anchor cardiac cells together and allow free
passage of ions through gap junction
d. Cardiac Tissue
i. Myocardial cells:
1. 99% of the heart is made of contractile cardiac muscle cells
2. Generates the force of contraction produced by the heart
ii. Autorhythmic cells:
1. 1% of cells that are self-excitable
2. Generate action potentials spontaneously without neural
stimuli
e. Intrinsic Conduction System
i. Autorhythmic cells composed the intrinsic conduction system of
the heart
ii. Coordinates the rhythmic excitation and contraction of the cardiac
muscle to ensure efficient pumping
iii. The action potential generated by autorhythmic cells travel through
the conduction system and to surrounding myocardial tissue by gap
junction
iv. Sequence of Excitation (see figure 9-8)
1. Sinoatrial (SA) node –pacemaker, generates impulse (70
times/minute)
2. Atrioventricular (AV) node (40-60 times/minute), delays
the impulse about 0.1 second
3. Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)
4. AV bundle splits into two pathways in the interventricular
septum (bundle branches)
5. Bundle branches carry the impulse toward the apex of the
heart (35 times/minute)
6. Purkinje fibers carry the impulse from the heart apex to the
ventricular walls (30 times/minute)
132
v. Ectopic focus – abnormal overly excitable area begins to
depolarizes faster than the SA node (see figure 9-9)
1. Can lead to a premature heartbeat (extrasystole) and/or
accelerated heart rate
2. Can be caused by heart disease, anxiety, lack of sleep, to
much caffeine, nicotine
vi. What gives autorhythmic cells the unique ability to
spontaneously generate action potentials? (see figure 9-7)
1. They have an unstable membrane potentials called
pacemaker potentials
2. Their membrane gradually depolarizes and drifts towards
threshold due to slow Na+ entry
3. When threshold is reached they fire an action potential
4. Calcium influx (rather than sodium) causes the
depolarization phase of the action potential
5. Repolarization is cause by K+ efflux
vii. Electrocardiography (see figures 9-13 & 9-14)
1. EKG – tracing of the electrical currents created by the
intrinsic conduction system. Test to screen for a variety of
cardiac abnormalities
a. P wave – atrial depolarization
b. QRS complex – ventricles depolarization
c. T wave – ventricles repolarization
2. Cardiac Abnormalities (see figure 9-15)
a. Bradycardia - <60 BPM
b. Tachycardia - >100 BPM
c. Arrhythmias – uncoordinated atrial and ventricular
contractions
i. Damaged SA node – pace set by AV node ~
50 BPM
ii. Heart block – damage to the AV node,
ventricles contract at ~30 BPM
d. Fibrillation – irregular chaotic twitching of the
myocardium
II.
Cardiac Muscle Contraction
a. Contraction of cardiac muscle cells:
i. Must be stimulated by autorhythmic cells to contract
ii. Have a long absolute refractory period (see figure 9-12)
1. Prevents summation and tetany
2. Ensures filling of the chambers
133
b. Action potentials in Cardiac Muscle Cells (see figure 9-10)
i. Contractile myocardial cells have a stable resting membrane
potential
ii. Depolarization wave travels through the gap junctions and opens
fast voltage gated Na+ channels in the contractile cell
iii. Triggers an action potential
iv. Na+ channels close and slow Ca2+ channels and K + channels
open causing the plateau phase
v. Plateau phase – Ca2+ influx from the ECF
prolongs the action potential and
prevents rapid repolarization
vi. Ca2+ close and K+ channels remain open causing repolarization
due to K+ efflux
c. Contraction of Cardiac Muscle (see figure9-11)
i. Cardiac muscle contraction is similar to skeletal muscle
contraction
ii. The action potential traveling down the T-tubules triggers the
influx of Ca2+ from the ECF
iii. The Ca2+ influx induces the release of additional Ca2+ from the
SR
iv. Ca2+ binds to troponin allowing sliding of the myofilaments
d. Metabolism of Cardiac Muscle
i. Relies almost exclusively on aerobic respiration
ii. Constant and adequate blood supply is critical
iii. Adaptive to multiple fuel sources: glucose, fatty acids, lactic acid)
III.
Cardiac Physiology
a. Cardiac Cycle
i. Contraction of the myocardium must occur in a coordinated
rhythm to ensure proper pumping of blood
ii. Atrial excitation and contraction must be completed before
ventricular contraction occurs
iii. Cardiac cycle refers to all events associated with one complete
heart beat
1. Systole – contraction of heart muscle
2. Diastole – relaxation of heart muscle
iv. Phases of the Cardiac Cycle (see figure 9-16)
1. Mid-to-late diastole – ventricular filling
a. Blood passively flows into ventricles from atria
b. Atria contract (atrial systole)
c. AV valves open, SL valves closed
134
2. Ventricular systole
a. Atrial diastole
b. Rising ventricular pressure results in closing of AV
valves
c. Isovolumetric contraction phase
d. Ventricular ejection phase opens semilunar valves
3. Early diastole - isovolumetric relaxation
a. Ventricles relax
b. Backflow of blood in aorta and pulmonary trunk
closes semilunar valves
c. Atria re-filling
d. Atria pressure increases, AV valves open and cycle
repeats
v. Heart Sounds - (lub-dup) are associated with closing of heart
valves
1. First sound occurs as AV valves close and signifies
beginning of systole
2. Second sound occurs when SL valves close at the
beginning of ventricular diastole
b. Cardiac Output (CO) - the amount of blood pumped by each ventricle in
one minute
i. CO = (heart rate [HR]) x (stroke volume [SV])
1. HR is the number of heart beats per minute
2. SV is the amount of blood pumped out by a ventricle with
each beat
ii. Cardiac Output: Example
1. CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) CO =
5250 ml/min (5.25 L/min)
iii. Cardiac reserve is the difference between resting and maximal CO
c. Regulation of Heart Rate (see table 9-3 & figure 9-20)
i. Heart rate is modulated by the autonomic nervous system
1. Parasympathetic activity –slows HR down via Ach
a. Increases K+ permeability, hyperpolarization
2. Sympathetic activity–increases HR via NE/E
a. Increases Na+, and Ca2+ channels, speeds up
depolarization
ii. Chronotropic agents – affect heart rate
1. Positive chronotropic factors increase heart rate
135
2. Negative chronotropic factors decrease heart rate
iii. Other factors that affect HR
1. Hormones - Epinephrine and Thyroxine increase HR
2. Ions
a. Elevated K+ and Na+ – decrease HR
3. Physical factors
4. Age – decreases HR
5. Exercise – increases HR
6. Temperature – increases HR
d. Regulation of Stroke Volume
i. Stroke volume = end diastolic volume (EDV) minus end systolic
volume (ESV)
1. EDV = amount of blood collected in a ventricle during
diastole
2. ESV = amount of blood remaining in a ventricle after
contraction
ii. Factors Affecting Stroke Volume (see figure 9-21 through 9-25)
1. Internal Factors:
a. Preload – amount ventricles are stretched by
contained blood, dependent on EDV
i. Frank-Starling’s Law: increased stretch =
increased contraction strength
ii. Affected by volume of venous return and
ventricular filling time
iii. Factors that would increase preload:
1. Exercise
2. Slower heart beat
iv. Factors that would decrease preload
1. Blood loss
2. Rapid heart beat
b. After load – back pressure exerted by blood in the
large arteries leaving the heart
i. Increase in after load decreases stroke
volume
ii. Atherosclerosis, arteriosclerosis,
hypertension, loss of elasticity of
blood vessels
136
2. Extrinsic Factors:
a. Contractility – cardiac cell contractile force due to
factors independent of stretch and EDV
i. Inotropic agents – effect contractility
1. Positive inotropic increases
contractility
2. Negative inotropic decreases
contractility
ii. Increase in contractility comes from:
1. Increased sympathetic stimuli
2. Hormones – thyroxine, epinephrine
a. Sympathetic stimulation
releases norepinephrine and
initiates a cyclic AMP
second-messenger system
(see figure 14-30 pg. 503)
3. Increased ECF Ca2+ and some drugs
like digitalis
iii. Agents/factors that decrease contractility
include:
1. Acidosis
2. Increased extracellular Na+ and K+
3. Calcium channel blockers
*See figure 9-25 for a summary of controlling cardiac output by adjusting heart rate and
stroke volume.
137
Cardiac Physiology
Post-Lecture Practice
1. Compare and contrast skeletal, smooth, and cardiac muscle by listing three
distinctions for each type of muscle tissue. (hint: think about how they differ in
innervation, structure, and contraction mechanisms and then pick two for each)
Skeletal
Smooth
Cardiac
2. Describe / contrast the changes in membrane potential for a cardiac autorhythmic cell
verses a contractile myocardial cell by labeling what happens in each phase. Use graphs
from your textbook as a reference.
138
3. Fill out this chart below. Determine if the following factors would increase, decrease,
or have no effect on heart rate, stroke volume, and cardiac output.
Factor
Affect on Heart Rate
Affect on Stroke
Volume
Affect on Cardiac
Output
Increased Sympathetic
Stimulation
Increased
Parasympathetic
Stimulation
Increased Venous
Return
Slow Heart
Rate
Extremely Fast
Heart Rate
Exercise
Sudden Drop in
Blood Pressure
Rising Blood
Pressure
Sudden Drop in
Blood Volume
Excess Calcium
Chart was adapted from InterActive Physiology CD, ©2006 Pearson Education.
139
Blood Pressure
Study Objectives:
1. Compare and contrast the structure and function of arteries, arterioles, capillaries,
venules, and veins.
2. Discuss the factors that affect blood flow and how they relate to blood pressure:
a. Blood flow = pressure gradient / resistance.
b. Discuss the factors that affect resistance: viscosity, length, elasticity, and
peripheral resistance
3. Define blood pressure. Explain the clinical significance of systolic, diastolic, and
pulse pressures.
4. Describe, in detail, the major factors which affect mean arterial blood pressure.
a. Relate the importance of cardiac output, blood volume, and peripheral
resistance, to blood pressure.
b. Distinguish between intrinsic and extrinsic controls of arteriole diameter.
c. Describe the effects of epinephrine, ADH, angiotensin II, histamine, and
kinins on blood pressure.
5. Describe the role of the baroreceptor reflex in regulating blood pressure.
6. Define ultrafiltration and reabsorption and describe the process of net filtration in
the capillaries.
7. Explain how the return of lymph through lymph vessels maintains blood volume
and pressure.
8. Describe the factors that play a role in venous return.
140
Blood Pressure Outline
I.
Types of Blood Vessels
a. Capilaries Venules Veins Heart Arteries Arterioles
b. Review histology of blood vessels
II.
Blood Flow
a. Flow rate – volume of blood per unit time.
Flow rate = Pressure gradient / Resistance. Depends on:
i. Pressure gradient – difference in pressure between the beginning
and ending of a vessel (see figure 10-2)
ii. Vascular resistance – hindrance or opposition to blood flow
through a vessel
1. As resistance increases flow rate decreases
2. Factors affecting resistance:
a. Viscosity – friction between molecules increases
resistance (# of circulating RBC)
b. Length – increased surface area increases resistance
(remains constant in body)
c. Elasticity
d. Peripheral resistance – friction between the blood
and the vessel wall (see figure 10-3)
i. Radius the main determinant of resistance
1. Increased surface area exposed to
blood increases resistance
2. Flow is faster in larger vessels than
smaller
III.
Arteries
a. Elastic arteries – offer little resistance due to their large diameter and
elastic properties
i. Function – maintain constant flow of blood through capillaries
despite ventricular systole and diastole
ii. Arteries distend during systole
iii. Recoils pushing blood forward during diastole (see figure 10-6)
IV.
Blood Pressure - force exerted by the blood on the vessel wall (see figures
10-7 through 10-9)
a. Systolic pressure – maximum pressure during ventricular systole
b. Diastolic pressure – minimum pressure following ventricular diastole and
blood moving forward into arterioles
c. Pulse pressure – difference between the two
141
d. Mean arterial pressure – average pressure in the vessel throughout the
cardiac cycle
i. MAP = DP + 1/3 (pulse pressure)
ii. MAP = cardiac output (CO) x total peripheral resistance (TPR)
1. CO = stroke volume x HR
2. TPR = radius and viscosity
e. Arterioles – small radii, have more resistance
i. Can adjust diameter to:
1. Vary distribution of blood to organs
2. Regulate arteriole pressure
ii. Arteriole smooth muscle always displays a state of vascular tone
(partial constriction). Maintained by:
1. Myogenic activity of smooth muscle cells
2. Sympathetic fibers
iii. Factors influencing the level of smooth muscle contraction /
arteriole radius (see figure10-10):
1. Intrinsic (local) controls – determines distribution of
cardiac output
a. Chemical
i. Increased metabolic activity triggers
vasodilation
1. Decreased O2
2. Increased CO2
3. Increased adenosine
4. Increased NO
ii. Histamine and prostaglandins – vasodilation
b. Physical influences
i. Temperature
1. Heat – vasodilation
2. Cold – vasoconstriction
ii. Myogenic response to stretch
1. Increased perfusion – increases
stretch triggers vasoconstriction
2. Decreased perfusion – decreased
stretch triggers vasodilation
2. Extrinsic controls – regulates systemic blood pressure
a. Sympathetic Nervous System
i. Maintains overall MAP for the system but
local regulation can over ride it for tissues
that need increased blood flow
142
b. Hormones
i. ADH (a.k.a vasopressin) – vasoconstriction
ii. Angiotensin II –vasoconstriction
iii. NE / Epinephrine
1. α receptors – vasoconstriction
2. Β receptors – vasodilation (skeletal
and coronary blood vessels)
iv. Atrial Natriuretic Peptide – vasodilation
**See figure 10-14 for a nice summary of how these intrinsic and extrinsic factors affect
total peripheral resistance.
f. Blood pressure regulation
i. Short term regulation – adjustments occur within seconds.
Involves the Baroreceptor Reflex:
1. Baroreceptors monitor MAP and initiate reflex responses to
maintain BP homeostasis
a. Receptors - found in the carotid sinus and aortic
arch
b. Sent to cardiovascular control center in the medulla
c. Response – adjusts parasympathetic/ sympathetic
activity (see figures 10-35 through 10-38)
ii. Long term regulation – minutes to days. Involves adjusting blood
volume.
1. Hormones
a. Renin – angiotensin II – aldosterone pathway
b. ADH
V.
Capillaries
a. Site for exchange of materials between the blood and the tissues
b. Precapillary sphincters control the flow of blood through the capillary
beds (see figure 10-19)
i. Smooth muscle that respond to local controls (see figure 10-20)
c. Factors that influence diffusion in capillary beds
i. Minimal diffusion distance
ii. Maximized surface area for exchange (600m2)
iii. Maximized time for exchange (slow velocity of flow)
d. Exchange of solutes across capillary wall (see figure 10-18)
i. Fat soluble solutes pass through endothelial cells
ii. Small water soluble solutes pass through pores
iii. Plasma proteins are too large to pass
iv. Protein hormones cross by vesicular transport
143
e. Movement of fluid across the capillary wall occurs because of
differences in hydrostatic and osmotic pressures (see figure 10-22)
i. Plasma hydrostatic pressure – exerted on the vessel wall due to
pushing of blood
ii. Plasma osmotic pressure – created by movement of water as it is
pulled down its concentration gradient
iii. Net Filtration Pressure - determines if there is a net gain or net
loss of fluid from the blood
1. Takes into account all hydrostatic and osmotic forces on
the capillary
2. Bulk flow – movement of fluid across the capillary walls.
Involves (see figure 10-23):
a. Ultrafiltration – movement out of the capillary into
the interstitial fluid, occurs at the arteriole end
b. Reabsorption – movement into the capillary from
the interstitial fluid, occurs at the venule end
VI.
Lymphatic Vessels (see figure 10-24 &10-25)
a. More fluid is filtered into the ECF that reabsorbed
b. This extra fluid is picked up by lymph capillaries
i. Fluid leaks into lymph capillaries when interstitial pressure is high
and one-way flap-like valves prevent lymph from leaking back out
ii. Fluid is returned back to the blood by the lymph system
iii. Pump-less one way system -lymph moves towards the heart
iv. Flow is accomplished by:
1. Valves
2. Milking action of skeletal muscle
3. Contraction of smooth muscle in vessel walls
4. Pressure changes in the thorax
VII.
Veins - carry blood back to heart
a. Large diameter, little resistance, low pressure
b. At rest contains more than 60% of the total blood volume (see figure 1027)
c. Factors affecting venous return (see figure10-28):
i. Pressure gradient
ii. One-way valves
iii. Skeletal muscle contraction
iv. Respiratory pump
v. Cardiac suction
vi. Sympathetic activity
**see figure 10-34 for a nice summary of the numerous factors that influence MAP
144
VIII.
Cardiovascular Disease (see figures 9-29 through 9-31 & table 9-4)
a. Cardiovascular disease accounts for over half of all deaths in the United
States
i. Myocardial infarction - heart attack
ii. Atherosclerosis – hardening of the arteries
iii. Arteriostenosis – narrowing of the arteries
b. Treatments for Cardiovascular Disease
i. Life style changes and drugs
ii. Angioplasty – use balloon or laser to remove the blockage from the
artery
1. Or insert a stent to keep artery open
iii. Coronary bypass surgery – use another blood vessel from another
part of the body as a bridge to get around the blockage
Blood Pressure
Post Lecture Assignment:
On Canvas I have posted a Blood Pressure Concept Map. It contains numerous terms that
all relate to mean arterial pressure. You can print these terms, cut them out, and then
arrange them in various ways to show relationships between them and how they affect
mean arterial blood pressure. If you don’t want to spend the time cutting them up you
could just write your own flow chart using these terms and making relationships. For
example which factors would increase BP, which factors decrease BP, etc.
145
Body Defenses / Immunology
Study Objectives:
1. List the organs in the lymphatic system and describe their functions.
2. Distinguish between innate and acquired (adaptive) immunity.
3. List the non-specific defenses of the body.
a. Describe the characteristics, chemicals and cells involved in the
inflammatory response.
b. List the body’s antimicrobial proteins
i. Explain the roles of interferon and the complement system
c. Explain how the release of pyrogens help protect the body against
invading bacteria
4. Compare and contrast the origins, maturation process, and general functions of B
and T lymphocytes.
5. Define the following: immunity, antigens, and antibodies
6. Describe the process of (humoral) antibody mediated immunity
a. Describe the process of clonal selection of a B cells
b. Describe the role of plasma cells and memory cells
c. Explain the functions of antibodies
d. Compare and contrast active and passive immunity
7. Describe the events of cell-mediated immunity
a. Describe the role of antigen presenting cells, T helper cells and cytotoxic
T cells in the cell-mediated response
b. Describe the function of perforins and granzymes released by cytotoxic T
cells
8. Distinguish between primary and secondary immune responses
9. Describe and give examples of the following immunological disorders: immediate
and delayed hypersensitivities, immunodeficiencies, and autoimmune diseases.
146
Body Defenses / Immunology Outline
I.
Lymphoid Organs
a. Lymphoid tissues and organs –provide defense against disease by:
i. Function:
1. Housing and facilitating the maturation of lymphocytes
2. Cleansing the lymph of pathogens
ii. Organs/tissues (see figure 12-1):
1. Lymph nodes
2. Tonsils
3. MALTs (mucus associated lymph tissue)
4. Spleen
5. Thymus
6. Bone marrow
II.
Body Defenses
a. Body defense mechanisms are aimed at eliminating abnormal cells or any
foreign materials that are not self
i. Invading pathogens (viruses, bacteria, ect.)
ii. Removal of worn out cells, damaged tissue
iii. Identification and destruction of abnormal or cancerous cells
iv. Rejection of foreign tissue
v. Inappropriate responses can lead to allergies or autoimmune
diseases
b. The body has two defense systems – that differ in timing and specificity
yet are interactive and interdependent
i. Innate immunity
ii. Adaptive or Acquired immunity
III.
Innate (nonspecific) system responds quickly and consists of:
a. First line of defense – physical barriers; intact skin and mucosa prevent
entry of microorganisms
b. Second line of defense – antimicrobial proteins, phagocytes, and other
cells
i. Inhibit spread of invaders throughout the body
ii. Inflammation is its hallmark and most important mechanism
c. Engulfing and Destroying Pathogens
i. Neutrophil and macrophage destruction of bacteria
ii. Phagocytosis:
1. Engulfs foreign material into a vacuole
2. Enzymes from lysosomes digest the material
147
d. Inflammation - the inflammatory response is triggered whenever body
tissues are injured (see figure 12-2)
i. Purpose:
1. Prevents the spread of damaging agents to nearby tissues
2. Disposes of cell debris and pathogens
3. Sets the stage for repair processes
ii. The four cardinal signs of acute inflammation (see figure 12-3)
1. Redness
2. Heat
3. Swelling
4. Pain
iii. Inflammation is mediated by phagocytes
1. Toll-like receptors (TLRs) present on phagocytes recognize
and bind to foreign microbes and microbes that have been
marked by an opsonin (complement proteins or antibodies)
(see figure 12-4).
2. Activated TLRs triggers the phagocyte to:
a. Engulf and destroy the pathogen
b. And/or release chemicals that promote
inflammation (cytokines)
c. Inflammatory chemicals are released into the
extracellular fluid by injured tissue, phagocytes,
lymphocytes, and mast cells
3. Inflammatory chemicals:
a. kinins, histamine, prostaglandin, complement, and
cytokines, bacterial toxins
b. Cause local blood vessels to dilate, resulting in
hyperemia (heat and redness)
c. Capillaries become “leaky” (edema and pain)
d. Attract other WBCs to the area
4. Additional neutrophils are released from the bone marrow
in response to leukocytosis-inducing factors released by
injured cells
5. Mobilization of WBC – leukocytes emigrate from the
blood into the tissues
a. Margination – neutrophils cling to the walls of
capillaries in the injured area
b. Diapedesis – neutrophils squeeze through capillary
walls
c. Chemotaxis – inflammatory chemicals attract
neutrophils to the injury site and they begin
phagocytosis
148
e. Other Secreted Chemicals
i. Pyrogens – secreted by macrophages
1. Cause hypothalamus to elevate the body’s set temperature
(fever)
2. Moderate fever can be beneficial, as it causes:
a. The liver and spleen to sequester iron and zinc
(needed by microorganisms to grow and divide)
b. Increase rate of chemical reactions which speeds up
tissue repair
ii. Antimicrobial Proteins
1. Enhance the innate defenses by:
a. Attacking microorganisms directly
b. Hindering microorganisms’ ability to reproduce
2. The most important antimicrobial proteins are:
a. Interferon (see figure 12-5)
i. Released by virus infected cells and binds to
receptors on neighboring healthy cells
ii. Interferon protects these neighbors by
activating genes for PKR (an antiviral
protein)
iii. PKR nonspecifically blocks viral
reproduction in the cell if it becomes
infected
iv. Also slows division of tumor cells
v. Enhances natural killer cells
1. Lyse and kill cancer cells and virusinfected cells on first exposure to
them
2. Immediate and nonspecific response
3. Immunosurveillance
b. Complement proteins
i. 25 or so proteins that circulate in the blood
in an inactive form
ii. Forms membrane attacking complex that
punch holes in foreign cell’s membrane and
causes the cell to lyse (see figure 12-6b)
iii. Also acts as opsonins and chemotaxins
iv. Activated by:
1. Exposure to carbohydrate chains on
the surface of micro-organisms
2. Exposure to antibodies produced by
the acquired immune response
against the micro-organism
149
IV.
Acquired or Adaptive (specific) defense system
a. Third line of defense – mounts attack against particular foreign substances
i. Takes longer to react than the innate system
ii. Targets invaders that the body has previously been exposed to
iii. Involves lymphocytes
iv. Works in conjunction with the innate system
b. Characteristics of Acquired Immunity
i. The acquired immune system is:
1. antigen-specific - requires the production of specific
lymphocytes and antibodies against a specific antigen
2. systemic - not restricted to the initial infection site
3. has memory -second encounter causes a more rapid and
vigorous response
ii. Antigens - any substance capable of provoking an immune
response. Antigens include foreign protein, nucleic acid, some
lipids, and large polysaccharides
iii. It has two separate but overlapping branches:
1. Humoral, or antibody-mediated immunity
2. Cellular, or cell-mediated immunity
iv. Lymphocytes - originate from stem cells in the red bone marrow
1. Each lymphocyte is equipped with:
a. a unique receptor that binds a specific antigen
b. and a MHC receptor that distinguishes self
2. Immunocompetent – cells display a unique type of receptor
that responds to a distinct antigen (based on genetic
variance)
a. Become immunocompetent before they encounter
antigens they may later attack
b. Are exported to secondary lymphoid tissue where
encounters with antigens occur
c. Mature into fully functional antigen-activated cells
upon binding with their recognized antigen
3. B lymphocytes become immunocompetent in the bone
marrow
a. Responsible for antibody-mediated immunity
b. Defend against extracellular pathogens by
producing antibodies
150
4. T lymphocytes become immunocompetent in the thymus
a. Responsible for cell-mediated immunity
b. Defend against intracellular pathogens and cancer
c. Maturation of T Cells
i. T cells mature in the thymus under negative
and positive selection pressures
ii. Negative selection – eliminates T cells that
are strongly anti-self
iii. Positive selection – selects T cells with a
weak response to self-antigens, which thus
become both immunocompetent and selftolerant
c. Antibody-Mediated Response
i. Triggered when B-cells with specific receptors bind to a specific
antigen
ii. The binding event activates the lymphocyte to multiply (clonal
selection) (see figure 12-12)
1. Most B cells become plasma cells that produce antibodies
to destroy antigens
2. Some B cells become long-lived memory cells that will
remain in the body to respond to the antigen if exposed
again
iii. Antibodies (immunoglobulins) – proteins that travel in the plasma
and combine with a specific antigen.
1. Function: mark the antigens for destruction by specific or
nonspecific mechanisms
2. Structure: Y shaped molecules with variable region on the
tips of each arm that binds a specific antigen (12-10)
3. Antibodies inactivate antigens in a number of ways (see
figure 12-11):
a. Complement fixation – bind and lyse cell,
inflammation
b. Opsonization – mark antigen for phagocytosis
c. Neutralization – block harmful effects of toxins
d. Agglutination – clumping of foreign cells
e. Precipitation – clumping of antigens
f. Attract natural killer cells
d. Cell Mediated Response
i. T cells can only recognize and bind antigens that are presented to
them by antigen presenting cells (APC). APCs are macrophages
that engulf pathogens and then present pieces of the antigen to
lymphocytes. (See figure 12-18 and 12-20)
151
ii. Antigens must be presented by APC to a THelper cell which triggers
the cell to release cytokines that stimulate division of various cells:
1. Enhances proliferation of B-cells
2. and Cytotoxic T-cells which specialize in killing cancer and
virus infected cells
iii. Mechanisms of Cytotoxic T cell (see figure12-14)
1. Cytotoxic T cells bind to virus infected and cancerous cells
and destroy them by releasing:
a. Perforins that punch holes in the target cells
membrane (see figure 12-15)
b. Granzymes that cause the cell to undergo apoptosis
**Table 12-3 summarizes the immune’s response to extracellular bacteria and table
12- 2 summarizes the immune response to intracellular pathogens such as viruses.
These figures do a nice job of distinguishing between the antibody and cell mediated
responses while also showing the overlap that occurs between the innate and
acquired defense when an immune response is initiated.
V.
Immunological Memory
a. Immunity – ability to defend against specific invaders
b. Immune Responses (see figure 12-13)
i. Primary immune response – cellular differentiation and
proliferation, which occurs on the first exposure to a specific
antigen
1. Lag period: 3 to 6 days after antigen challenge
2. Peak levels of plasma antibody are achieved in 10 days
3. Antibody levels then decline
ii. Secondary immune response – re-exposure to the same antigen
1. Sensitized memory cells respond within hours
2. Antibody levels peak in 2 to 3 days at much higher levels
than in the primary response
3. Antibodies bind with greater affinity, and their levels in the
blood can remain high for weeks to months
c. Mechanisms for acquiring immunity
i. Active Immunity - B cells encounter antigens and produce
antibodies against them
1. Naturally acquired – response to a bacterial or viral
infection
2. Artificially acquired – response to a vaccine of dead or
attenuated pathogens
a. Vaccines – spare us the symptoms of disease, and
their weakened antigens provide antigenic
determinants that build our immunity
152
ii. Passive Immunity -differs from active immunity in that:
1. B cells are not challenged by antigens
2. Immunological memory does not occur
3. Protection ends when antigens naturally degrade in the
body
4. Naturally acquired – from the mother to her fetus via the
placenta or IgA antibodies in breast milk
5. Artificially acquired – from the injection of serum that
contains the immunoglobulins
VI.
Immune Disorders
a. Hypersensitivity - abnormal, vigorous immune responses (overzealous
immune system) (Table 12-5)
i. Immediate hypersensitivity – occurs within seconds to 20
minutes
1. Allergies and Asthma (see figure 12-24)
a. Plasma cells produce IgE antibodies which attach to
mast cells
b. Mast cells release histamine – which causes
inflammation and itching
c. Also releases a leukotriene called slow reactive
substance – causes smooth muscle contraction in air
ways
d. Treated with anti-histamines and newer drugs that
block leukotrienes such as Singular
2. Anaphylactic Shock - systemic allergic response that is
life-threatening
a. Allergen directly enters blood
b. Systemic histamine and SRS releases may result in:
i. Constriction of bronchioles
ii. Sudden vasodilation and fluid loss from the
bloodstream
iii. Hypotensive shock and death
c. Treated with epinephrine
ii. Delayed hypersensitivity - symptoms appear after 1-3 days
1. Inflammation caused by cytotoxic T-cells release of
lymphokines
2. Treated with corticosteroids
153
b. Immunodeficiency - production or function of immune cells is lacking or
abnormal
i. Severe combined immunodeficiency disease (SCID)
1. Deficiency of B and T-cells
ii. Acquired Immune Deficiency Syndrome (AIDS)
1. HIV destroys THelper cells
c. Autoimmune diseases - the immune system does not distinguish between
self and non-self
i. The body produces antibodies and cytotoxic T-cells that attack its
own tissues
ii. Possible causes:
1. Inefficient lymphocyte programming
2. Appearance of new self-antigens
3. Antibodies produced against foreign antigens react with
self-antigens (streptococcus and rheumatic fever)
154
Body Defenses
Post-Lecture Practice
1.Which of the following is NOT considered a lymphoid organ/tissue?
a. Liver
b. Spleen
c. Tonsils
d. Peyer’s patches in the intestinal mucosa
e. Thymus
2. All of the following are part of the innate immune system EXCEPT:
a. production of complement proteins
b. inflammation
c. production of antibodies
d. phagocytosis by neutrophils
3. Which type of lymphocyte would physically destroy cells infected by an intracellular
pathogen?
a. B-cell
b. Plasma cell
c. T-helper cell
d. Cytotoxic T cell
4. Which cell type produces antibodies?
a. plasma cells
b. T-helper cells
c. memory cells
d. macrophages
e. all of the above
5.Where do T-lymphocytes mature?
a. Thymus
b. Spleen
c. Lymph nodes
d. Bone marrow
e. Tonsils
155
Respiratory Physiology
Study Objectives:
1. List the functions of the respiratory system
2. Identify the organs of the respiratory system and a general function of each.
3. Describe the structure and function of the mucus membrane (ciliated
pseudostratified with goblet cells), the respiratory membrane, and the pleural sac.
4. Describe the mechanism of pulmonary ventilation.
a. Describe the changes in pressure, volume and events involved in
inspiration and expiration.
b. Describe the factors that affect ventilation: lung compliance, elasticity,
surface tension, and resistance
5. Compare the volumes and capacities of air exchanged during ventilation.
6. Distinguish between obstructive and restrictive pulmonary disorders
7. Explain how the following gas principles apply to respiration: Dalton’s Law,
Boyle’s Law, and Henry’s Law.
8. Explain how blood transports both oxygen and carbon dioxide.
9. Describe the factors that affect the binding of oxygen to hemoglobin thus
affecting the loading and unloading mechanisms.
10. Explain the differences between “external” and “internal” respiration.
11. Explain the roles of the medulla and pons in the regulation of respiration.
12. Describe the factors that affect respiratory center activity: chemical factors (CO2,
O2, pH), reflexes, hypothalamic controls (emotions), and cortical controls
(voluntary)
13. Compare and contrast the roles of peripheral and central chemoreceptors in the
regulation of respiration.
156
Respiratory Outline
I.
Functions of the Respiratory System
a. Gas exchange – between the external environment and the blood
b. Filters, humidifies, and warms inspired air
c. Production of sound
d. Smell
e. Maintains pH homeostasis
II.
Anatomy Review
a. Structures (see figure 13-2)
i. Nose
ii. Pharynx
iii. Larynx
iv. Trachea
v. Bronchi
vi. Bronchioles
vii. Alveolar ducts
viii. Alveoli
ix. Respiratory Membrane
1. Site of gas exchange between the alveoli and the blood
2. Formed by the alveolar wall and the capillary wall
x. Pleural membrane (serous membranes) (see figure 13-5)
1. Pleural Sac – double walled membrane surrounding the
lungs
2. Visceral pleura - covers the lung surface
3. Parietal pleura - lines the walls of the thoracic cavity
4. Pleural fluid fills the area between layers to allow gliding
and resist separation
III.
Respiratory Pressures (see figure 13-6 & 13-7)
a. Respiratory pressures are described relative to atmospheric pressure @ sea
level:
i. Patm = 760 mm Hg
ii. Negative pressure: -1mm Hg = 759 mm Hg
iii. Positive pressure: + 1 mm Hg = 761 mm Hg
iv. 0 mm Hg = 760 mm Hg
b. Intrapulmonary pressure (a.k.a alveolar pressure) – pressure within the
alveoli
c. Intrapleural pressure – pressure within the pleural cavity
157
d. Transpulmonary pressure – difference between the intrapulmonary and
intrapleural pressures
i. Intrapleural pressure is always less than
intrapulmonary pressure ( -4 mmHg )
ii. Keeps the airways open
e. Pneumothorax – occurs when intrapleural pressure equals atmospheric
pressure, causes lungs to collapse (see figure 13-3)
IV.
Respiration Events
a. Events in Respiration
i. Pulmonary ventilation
ii. External respiration
iii. Gas transport
iv. Internal respiration
b. Pulmonary ventilation – moving air in and out of the lungs
i. Mechanical process that depends on volume changes in the
thoracic cavity
1. Caused by the contraction/relaxation of intercostal muscles
and the diaphragm
2. ∆ Volume → ∆ Pressure → flow of gases
a. Boyle’s law – the relationship between the
pressure and volume of gases P1V1 = P2V2
i. P = pressure of a gas in mm Hg
ii. V = volume of a gas in cubic millimeters
iii. See figure 13-9
ii. Phases of Ventilation
1. Intrapulmonary pressure and intrapleural pressure fluctuate
with the phases of breathing
2. Two phases (see figure 13-11):
a. Inspiration – flow of air into lung.
i. Intrapulmonary P decreases as thoracic
cavity expands (volume increases); air
moves into lungs from the higher pressure to
lower pressure
b. Expiration – air leaving lung.
i. Intrapulmonary P increases as lungs recoil
(volume decreases); air moves out of lungs
from the higher pressure to the lower
pressure
158
iii. Factors Affecting Ventilation
1. Lung Compliance - the ease with which the lungs can be
expanded
a. Reduced by factors that produce resistance to
distension of the lung tissue and surrounding
thoracic cage
i. Pulmonary edema, fibrosis, surface tension
of the alveoli
2. Elasticity – how readily the lungs recoil after stretching
a. Elastic CT and surface tension of the alveoli
3. Surface tension -the attraction of liquid molecules to one
another in the alveolus (see figure 13-5)
a. The liquid coating is always acting to reduce the
alveoli to the smallest possible size
b. Surfactant, a detergent-like complex, reduces
surface tension and helps keep the alveoli from
collapsing
4. Airway Resistance
a. Friction is the major source of resistance to airflow
i. The relationship between flow (F), pressure
(P), and resistance (R) is: F = Pressure
gradient / Resistant
ii. Affected by:
1. Autonomic Nervous System –
controls diameter of bronchioles (see
table 13-1)
a. Sympathetic –
bronchodilation decreases
resistance
b. Parasympathetic –
bronchoconstriction increases
resistance
2. Chronic Obstructive Pulmonary
Diseases: asthma, bronchitis,
emphysema (see figure 13-14)
c. Testing Respiratory Function
i. Respiratory capacities are measured with a spirometer
ii. Spirometer – an instrument consisting of a hollow bell inverted
over water, used to evaluate respiratory function
159
iii. Spirometry can distinguish between:
1. Obstructive pulmonary disease – increased airway
resistance
2. Restrictive disorders – reduction in lung compliance and
capacity from structural or functional lung changes
iv. Respiratory Volumes (see figure 13-16)
1. Tidal volume (TV) – air that moves into and out of the
lungs during normal breathing (~ 500 ml)
2. Inspiratory reserve volume (IRV) – air that can be inspired
forcibly beyond the tidal volume (2100–3200 ml)
3. Expiratory reserve volume (ERV) – air that can be
evacuated from the lungs after a tidal expiration (1000–
1200 ml)
4. Residual volume (RV) – air left in the lungs after strenuous
expiration (1200 ml)
5. Dead space volume - air that remains in conducting zone
and never reaches alveoli ~150 ml
6. Functional volume - air that actually reaches the respiratory
zone ~350 ml
v. Respiratory Capacities – two or more volumes added together
1. Inspiratory capacity (IC) – total amount of air that can be
inspired after a tidal expiration (IRV + TV)
2. Expiratory capacity (EC) - total amount of air that can be
expired after a tidal inspiration (ERV + TV)
3. Functional residual capacity (FRC) – amount of air
remaining in the lungs after a tidal expiration (RV + ERV)
4. Vital capacity (VC) – the total amount of exchangeable air
(TV + IRV + ERV)
5. Total lung capacity (TLC) – sum of all lung volumes
(approximately 6000 ml)
6. Forced vital capacity (FVC) – gas forcibly expelled after
taking a deep breath
a. Forced expiratory volume (FEV) – the amount of
gas expelled during specific time intervals of the
FVC
vi. Total ventilation – total amount of gas flow into or out of the
respiratory tract in one minute
1. (respiratory rate X tidal volume)
vii. Restrictive vs. Obstructive diseases
1. Obstructive disease - increases in RV, decrease in ERV
2. Restrictive disease -reduction in VC, TLC, and IRV
3. See figure 13-17
160
d. External Respiration – gas exchange between pulmonary blood and
alveoli across the respiratory membrane
i. Oxygen movement from the alveoli into the blood
ii. Carbon dioxide movement out of the blood into the alveoli
iii. Factors influencing external respiration:
1. Partial pressure gradients and gas solubility
a. Dalton’s Law – partial pressure gradients.
i. Total pressure exerted by a mixture of gases
is the sum of the pressures exerted
independently by each gas in the mixture.
ii. The partial pressure of each gas is directly
proportional to its percentage in the mixture
(see figure 13-21)
b. Oxygen movement into the blood from the alveoli
i. The alveoli have a higher PO2 than the
blood
ii. Oxygen moves by diffusion towards the area
of lower partial pressure
c. Carbon dioxide movement out of the blood to the
alveoli
i. Blood returning from tissues has a higher
PCO2 than the air in the alveoli
ii. See figure 13-22
d. Henry’s Law – gas solubility
i. Gas will dissolve into liquid in proportion to
its partial pressure.
ii. The amount of gas that will dissolve in a
liquid also depends upon its solubility
iii. Various gases in air have different
solubilities:
1. Carbon dioxide is the most soluble;
20X more soluble than oxygen
2. Nitrogen is practically insoluble in
plasma
iv. Hemoglobin acts as a “storage depot” for O2
by removing it from the plasma as soon as it
is dissolved. (See figure 13-25)
1. This keeps the plasma’s PO2 low
and prolongs the partial pressure
gradient between the plasma and the
alveoli
2. Leads to a large net transfer of O2
161
2. Matching of alveolar ventilation and pulmonary blood
perfusion
a. Ventilation and perfusion are matched for efficient
gas exchange
i. Ventilation – the amount of gas reaching
the alveoli
ii. Perfusion – the blood flow reaching the
alveoli
b. Changes in PCO2 and PO2 in the alveoli cause
local changes:
i. When alveolar CO2 is high and O2 is low:
Bronchioles will dilate and arterioles
constrict
ii. When alveolar CO2 is low and O2 is high:
Bronchioles will constrict and arterioles will
dilate
iii. See figure 13-19
3. Structural characteristics of the respiratory membrane:
a. Are only 0.5 to 1 µm thick, allowing for efficient
gas exchange
b. Have a total surface area (in males) of about 60 m2
(40 times that of one’s skin)
c. Thickening causes gas exchange to be inadequate:
inflammation, edema, mucus, fibrosis
d. Decrease in surface area with emphysema, when
walls of adjacent alveoli breakdown (see figure 1323)
* See table 13-5 for a summary of some of the factors influencing external respiration.
e. Gas Transport in the Blood
i. Oxygen transport in the blood
1. 98% of oxygen is transported attached to hemoglobin
(oxyhemoglobin [HbO2])
2. A small amount is carried dissolved in the plasma (~2%)
3. Each Hb molecule binds four oxygen atoms in a rapid and
reversible process
4. Hemoglobin Saturation/Dissociation Curve (See figure
13-24)
a. The % hemoglobin saturation depends on the PO2
of the blood
i. In the alveoli – 98% saturation
ii. In the tissues - ~75% saturation
iii. In an exercising muscle the PO2 equals ~ 20
mmHg
162
b. Factors Affecting Saturation of Hemoglobin (See
figure 13-26)
i. Increases in the following factors
decreases hemoglobin’s affinity for
oxygen:
1. Temperature
2. H+ (acidity)
3. PCO2
4. 2,3-biphosphoglycerate (BPG)
ii. These factors modify the structure of
hemoglobin and alter its affinity for oxygen
and enhances oxygen unloading from Hb
iii. These parameters are higher in systemic
capillaries supplying tissues, where oxygen
unloading is the goal
ii. Carbon dioxide is transport in the blood
1. CO2 is transported in three forms:
a. Dissolved in plasma – 7%
b. Bound to hemoglobin – 23% is carried in RBCs as
carbaminohemoglobin, at a different binding site
than oxygen
c. Most is carried as bicarbonate ions in plasma –
70% is transported as bicarbonate (HCO3–)
i. Carbon dioxide diffuses into RBCs and
combines with water to form carbonic acid
(H2CO3), which quickly dissociates into
hydrogen ions and bicarbonate ions
2. Exchange of Carbon Dioxide (See figure 13-27)
a. At the tissues:
i. Bicarbonate quickly diffuses from RBCs
into the plasma
ii. The chloride shift – to counterbalance the
outrush of negative bicarbonate ions from
the RBCs, chloride ions (Cl–) move from
the plasma into the erythrocytes
b. At the lungs:
i. Bicarbonate ions move into the RBCs and
bind with hydrogen ions to form carbonic
acid
ii. Carbonic acid is then split by carbonic
anhydrase to release carbon dioxide and
water
iii. Carbon dioxide then diffuses from the blood
into the alveoli
163
f. Internal Respiration - exchange of gases between blood and body cells
i. Oxygen diffuses from blood into tissue
ii. Carbon dioxide diffuses out of tissue into blood
V.
Control of Respiration
a. Medullary centers (see figure 13-29):
i. The dorsal respiratory group (DRG), or inspiratory center:
1. Appears to be the pacesetting respiratory center
2. Excites the inspiratory muscles and sets eupnea (12-15
breaths/minute)
3. Becomes dormant during expiration
ii. The ventral respiratory group (VRG) is involved in forced
expiration
b. Pons centers – pneumotaxic and apneustic areas
i. Influence and modify activity of the medullary centers
ii. Smoothes out inspiration and expiration transitions
c. Depth and Rate of Breathing
i. Cortical controls are direct signals from the cerebral motor cortex
that bypass medullary controls (conscious control)
1. Examples: voluntary breath holding, taking a deep breath
ii. Hypothalamic controls act through the limbic system to modify
rate and depth of respiration
1. Example: breath holding that occurs in anger,
hyperventilation from anxiety
iii. Three chemical factors affecting ventilation:
1. Carbon dioxide levels- main regulatory chemical for
respiration
a. ↑ CO2 = ↓ blood pH
b. Increased CO2 increases respiration. A rise in
PCO2 levels (hypercapnia) increases ventilation.
c. Changes in CO2 act on central chemoreceptors in
the medulla oblongata (See figure 13-31))
i. Carbon dioxide in the blood diffuses into the
cerebrospinal fluid where it is hydrated
ii. Resulting carbonic acid dissociates,
releasing hydrogen ions (decreases pH)
d. Hyperventilation – increased depth and rate of
breathing that:
i. Quickly flushes carbon dioxide from the
blood
ii. Occurs in response to hypercapnia
164
e. Hypoventilation – slow and shallow breathing due
to abnormally low PCO2 levels
i. Apnea (breathing cessation) may occur until
PCO2 levels rise
f. See figure 13-28 Hyperventilation vs.
hypoventilation
2. Oxygen levels
a. Peripheral chemoreceptors in the aorta and carotid
artery detect oxygen concentration changes
b. Substantial drops in arterial PO2 (to 60 mm Hg)
are needed before oxygen levels become a major
stimulus for increased ventilation
c. Information is sent to the medulla oblongata via the
vagus nerve
d. If carbon dioxide is not removed (e.g., as in
emphysema and chronic bronchitis),
chemoreceptors become unresponsive to PCO2
chemical stimuli
i. In such cases, PO2 levels become the
principal respiratory stimulus (hypoxic
drive)
3. Arterial pH levels
a. Changes in arterial pH can modify respiratory rate
even if carbon dioxide and oxygen levels are normal
b. Increased ventilation in response to falling pH is
mediated by peripheral chemoreceptors in the aorta
and carotid body (see figure 13-30)
c. Acidosis may reflect:
i. Carbon dioxide retention
ii. Accumulation of lactic acid
iii. Excess fatty acid metabolism in patients
with diabetes mellitus
d. Respiratory system controls will attempt to raise the
pH by increasing respiratory rate and depth
*See table 13-8 for a summary of chemical factors effect on peripheral and central
chemoreceptors.
iv. Other Reflexes
1. Pulmonary irritant reflexes – irritants promote reflexive
constriction of air passages
165
2. Inflation reflex (Hering-Breuer) – stretch receptors in the
lungs are stimulated by lung inflation
a. Upon inflation, inhibitory signals are sent to the
medullary inspiration center to end inhalation and
allow expiration
d. Respiratory Adjustments to High Altitude
i. Quick movement to high altitude (above 8000 ft) can cause
symptoms of acute mountain sickness – headache, shortness of
breath, nausea, and dizziness
1. A more severe illness is high-altitude pulmonary edema
caused by high pulmonary arterial pressure from
constriction of pulmonary arteries in response to low PO2
2. High-altitude cerebral edema – increased cerebral blood
flow and permeability of cerebral endothelium when
expose to hypoxia
ii. Acclimatization to the hypoxia – respiratory and hematopoietic
adjustments to altitude include:
1. Increased ventilation – 2-3 L/min higher than at sea level
2. Chemoreceptors become more responsive to PCO2
3. Substantial decline in PO2 stimulates peripheral
chemoreceptors
4. Kidneys accelerate production of erythropoietin (slower
response ~4 days)
166
Respiratory
Post-Lecture Assignment
1.
List four factors that affect ventilation:
2.
List at least four factors that affect external respiration:
3.
During inspiration the thoracic cavity volume ________ causing a
________in intrapulmonary pressure.
a. increases; decrease
b. decreases; increase
c. increase; increase
d. decrease; decrease
4.
All of the following factors directly affect ventilation EXCEPT:
a. Lung compliance
b. Elasticity
c. Surface tension
d. Air flow resistance
e. Perfusion
5.
The volume of air moving into and out of the lungs during a normal breath is
the:
a. tidal volume
b. vital capacity
c. residual volume
d. inspiratory reserve volume
e. inspiratory capacity
167
6.
Most carbon dioxide is transported through the blood as_________.
a. Bicarbonate
b. Carbaminohemoglobin
c. Carbon monoxide
d. Carbonic acid
e. Oxyhemoglobin
7.
In a healthy individual the main stimulus to breath is:
a. decreasing carbon dioxide levels
b. decreasing oxygen levels
c. increasing carbon dioxide levels
d. increasing oxygen levels
e. alkaline pH
168
Digestive Physiology
Study Objectives:
1. Identify the organs of the alimentary canal and accessory organs.
2. Describe the overall functions of the digestive system.
3. Be able to recognize examples of mechanical and chemical digestion.
4. List the factors that regulate digestive tract activity: autonomous smooth muscle,
mechanical and chemical receptors, hormones, intrinsic nerves, and extrinsic
nerves
5. Describe the structure and general activities of each digestive system organ.
6. Describe the composition and the function of saliva in digestion.
7. Describe the composition and function of bile in digestion.
8. Describe the four phases of gastric motility: filling, mixing, storing, and emptying
9. Describe the function of the parasympathetic nervous system and the following
hormones in the digestive processes: gastrin, secretin, and cholecystokinin
10. List the major digestive enzymes, which digestive or accessory organ produces it,
the substrate it works on and products produced: amylase, pepsin, trypsin,
chymotrypsin, carboxypetidase, lipase, brush border enzymes
11. Describe the mechanisms of absorption of vitamins, electrolytes, sugars,
aminoacids, and lipids in the small intestines.
169
Digestive Outline
I.
Anatomy of the Digestive System
a. Organs of the Alimentary Canal
i. Mouth
ii. Pharynx
iii. Esophagus
iv. Stomach
v. Small Intestines
vi. Large Intestines
b. Accessory organs – assist with digestion
i. Salivary glands
ii. Teeth
iii. Pancreas
iv. Liver
v. Gallbladder
c. Histology of the Alimentary Canal (see figure 16-2)
i. Mucosa – innermost layer lining the lumen, mucus membrane
epithelium
ii. Submucosa – areolar CT layer
iii. Muscularis externa – inner circular and outer longitudinal layer of
smooth muscle
iv. Serosa – outermost layer lining the external surface
II.
Functions of the Digestive System
a. Ingestion – taking food in
b. Propulsion – movement of food along the digestive tract
i. Peristalsis
1. Involuntary waves of contraction and relaxation of muscles
in the organ walls
2. Propel digestive material forward through the digestive
tract
ii. Segmentation
1. Contractions that churn and break apart digestive material
c. Digestion – breaking down food into smaller molecules
i. Mechanical – changing physical structure
ii. Chemical – changing chemical structure
d. Absorption – transport of nutrients from the lumen of the gastrointestinal
tract to the blood
e. Defecation – elimination of indigestible substances from the body
170
III.
Regulation of Digestive Tract Activity
a. Regulation of digestion involves:
i. Autonomous smooth muscle
ii. Mechanical and chemical stimuli – stretch receptors, osmolarity,
and presence of substrate in the lumen
iii. Gastrointestinal hormones
iv. Extrinsic nerves control by CNS centers
v. Intrinsic nerves control by local centers (Enteric Nervous System)
vi. See figure 16-3
b. Autonomous Smooth Muscle
i. Visceral smooth muscle is autonomous
ii. Smooth muscle pacemaker cells display rhythmic, spontaneous
variations in membrane potentials (slow wave potential) (review
this topic in chapter 8, figure 8-32)
iii. Hormones, mechanical stress, and nerve stimuli determines the
starting point of the slow wave potentials
c. Nervous Control of the GI Tract
i. Long reflexes
1. Stimulus may be within or outside the GI tract
2. Involves integration in CNS (usually in the medulla) and
output sent via autonomic nerves to GI tract
3. Extrinsic control
a. Can alter muscle and gland activity
b. Can alter levels of hormone secretions
c. Modify intrinsic activity
d. Coordinate different parts of the GI tract
i. Example: chewing food causes increased
gastric secretions in stomach (feed forward
mechanism)
ii. Short reflexes
1. Involves the enteric nervous system - myenteric and
submucous plexus within the digestive tract wall
2. Intrinsic control - entire reflex arc is carried out within the
GI tract (responds to local stimuli)
a. Coordinates local activity, can work independently
of the CNS or it can be influenced by extrinsic
nerves because it is linked to long autonomic reflex
arcs
d. Gastrointestional hormones
i. Gastrointestinal peptides can act as digestive hormones and
paracrine signals
171
ii. Released into the blood or ECF by cells of the digestive tract
iii. Can act on digestive organs and accessory organs to excite or
inhibit motility or secretions
iv. Can also act on the brain to trigger hunger or satiety
IV.
Digestive Activities
a. Mouth
i. Chewing begins mechanical digestion by breaking food into
smaller pieces and mixing food with saliva
ii. Compacts food into a bolus
iii. The salivary enzyme amylase begins the chemical digestion of
carbohydrates
1. Polysaccharides  Maltose
iv. Saliva
1. Secreted from serous and mucous cells in the salivary
glands
2. Composition of saliva
a. 97-99.5% water
b. Digestive enzyme – salivary amylase
c. Mucus – moistens food and holds bolus together
d. Lysozyme and IgA – antibacterial action
3. Control of Salivation
a. Salivary secretion is enhanced by two reflexes:
i. Simple reflex - ingested food stimulates
chemoreceptors and pressoreceptors that
trigger the salivary center in the medulla
ii. Acquired reflex - the thought
of food, cortex triggers the
salivary center in the medulla
iii. See figure 16-4
b. ANS control
i. Parasympathetic – larger volume of saliva,
watery and rich with amylase
ii. Sympathetic – smaller volume, more mucus,
results in dry mouth
b. Deglutition (Swallowing) see figure 16-5
i. Involves the coordinated activity of the tongue, soft palate,
pharynx, and esophagus
1. Buccal phase (a.k.a. oropharyngeal)– bolus is forced into
the oropharynx (voluntary)
2. Pharyngeal-esophageal phase – controlled by the medulla
and lower pons (involuntary)
ii. Peristalsis moves food through the pharynx and the esophagus
172
c. Stomach
i. Food enters stomach from the esophagus through the
gastroesophageal sphincter
ii. Functions of the stomach:
1. Mixes and stores food until it can be emptied into the small
intestines
2. Degrades the bolus both physically and chemically
a. Food is mixed with gastric juices to produce chyme
(mechanical)
b. Enzymatically digests proteins with the enzyme
pepsin (chemical)
3. Secretes intrinsic factor required for absorption of vitamin
B12
iii. Four phases of gastric motility
1. Gastric filing
2. Storage
3. Mixing
4. Emptying
iv. Gastric filling
1. Stomach relaxes as it fills, rugae flatten out
2. Stomach dilates in response to gastric filling (1L)
v. Gastric storage
1. Peristaltic contractions are weak in the body of the
stomach, so little mixing occurs
vi. Gastric mixing
1. Takes place in the muscular antrum
2. Occurs as chyme is propelled forward against the closed
pyloric sphincter by peristaltic contractions
3. Gastric Secretions
a. Types of secretions (See table 16-3)
i. Exocrine
1. Mucous cells – produce mucus to
protect stomach wall from harsh
acids
2. Parietal cells – produce HCL and
intrinsic factor
3. Chief cells – produce pepsinogen, an
inactive form of the protein digesting
enzyme pepsin
173
a. Chemical digestion of
proteins begins in the
stomach
b. Pepsinogen is converted into
pepsin by HCl
c. Pepsin breaks down proteins
into peptide fragments
d. Proteins 
Peptides
ii. Endocrine
1. G cells – produce the hormone
gastrin which stimulates gastric acid
secretion
iii. Paracrine
1. ECL cells – secrete histamine,
stimulates secretion from parietal
cells
2. D cells – secrete somatostatin,
inhibits secretions from parietal,
ECL cells, and G cells
b. Regulation of Gastric Secretion
i. Neural and hormonal mechanisms regulate
the release of gastric juices
ii. Excitatory and inhibitory events occur in
three phases:
1. Cephalic phase – prior to food entry
a. Excitatory events include:
i. Sight or thought of
food
ii. Stimulation of taste,
smell, pressure
receptors; chewing
iii. Vagal stimulation
releases ACh –
stimulates parietal, G
cells, and ECL cells
b. Inhibitory events include:
i. Loss of appetite or
depression
ii. Decrease in
stimulation of the
parasympathetic
division
174
2. Gastric phase: once food enters the
stomach
a. Excitatory events include:
i. Stomach distension activation of stretch
receptors (neural
activation)
ii. Activation of
chemoreceptors by
peptides, caffeine, and
alkaline pH
iii. Triggers release of
gastrin into the blood
b. Inhibitory events include:
i. An acidic pH lower
than 2 - triggers
release of
somatostatin
3. Intestinal phase: as partially
digested food enters the duodenum
a. Mostly inhibitory
b. Inhibitory phase – distension
of duodenum, presence of
fatty, acidic, or hypertonic
chyme in the duodenum
c. Initiates local reflexes and
vagal nuclei
i. Closes the pyloric
sphincter
d. Release of hormones that
inhibit gastric secretion
i. Cholecystokinin and
Secretin – decrease
gastric secretions and
slows gastric motility
ii. Gastric inhibitory
peptides (GIP) (a.k.a
glucose-dependent
insulinotropic
peptide)– inhibits
gastric acid secretion,
also promotes insulin
release from pancreas
* Tables 16-4 and 16-5 summarize factors that stimulate and inhibit gastric secretions.
175
vii. Gastric emptying
1. A strong enough peristaltic wave can push a small amount
of chyme through the pyloric sphincter before it closes
tightly
2. The rate of gastric emptying is controlled by both
gastric and duodenal factors
a. Gastric factors that increase gastric emptying
i. Amount of chyme in the stomach – the
stomach empties at a rate that is proportional
to the volume of chyme
ii. Distention – triggers smooth muscle and
intrinsic plexuses
iii. Fluidity of chyme
iv. Signaling by the vagus nerve (extrinsic
control)
v. The hormone gastrin
b. The duodenum controls gastric emptying by
reducing peristaltic activity in the stomach until it is
ready to accommodate more chyme
c. Duodenal factors that decrease gastric emptying
i. Fatty chyme – digested and absorbed slower
than other nutrients in the duodenum
ii. Acidity – chyme must be completely
neutralized
iii. Hypertonicity – need time for absorption of
nutrients to catch up with digestion
iv. Distention – needs to cope with volume
before receiving more
3. Gastric emptying is regulated by:
a. The neural enterogastric reflex -when the
duodenum fills stretch receptors are stimulated and
the pyloric sphincter closes
b. Hormonal mechanisms:
i. Cholecystokinin and secretin – released by
duodenal endocrine cells into the blood; will
inhibit gastric motility
d. Small Intestines
i. Extends from the pyloric sphincter to the ileocecal valve
ii. Main function is chemical digestion and absorption of nutrients
176
iii. Three regions:
1. Duodenum – first part
a. Chemical digestion, absorption
2. Jejunum – middle
a. Absorption
3. Ileum – last part, joins the large intestines
iv. Surface area for absorption is increased by villi and microvilli
v. Substances must pass through an epithelial cells and then diffuse
through the interstitial fluid in the underlying CT into a capillary or
lacteal
vi. Chyme enters the duodenum where it is mixed with bile from the
liver and digestive enzymes from the pancreas
1. Liver
a. Functions of the Liver
i. Produces bile to aid in the digestion of fats
ii. Stores excess nutrients and releases them
when needed
iii. Detoxifies drugs and metabolites
iv. Produces plasma proteins
b. Production of Bile by the Liver
i. Hepatocytes produce bile and secrete it into
bile ducts that empty into the common
hepatic duct.
ii. The sphincter of Oddi at the base of the
common bile duct prevents bile from
entering the duodenum between meals
iii. Bile will back up into the gallbladder where
it is concentrated and stored
iv. Function of Bile
1. Bile is secreted into the duodenum to
emulsify fats (see figure 16-16)
2. Bile increases the surface area for
lipase to work on fats
v. Bile is composed of:
1. Aqueous alkaline solution
2. Bile salts
a. Nonpolar portion –
cholesterol based steroid
b. polar portion
3. Cholesterol
4. Lecithin – a phospholipid
5. Bilirubin – byproduct of
RBC destruction
177
c. Regulation of Bile Release
i. Acidic, fatty chyme causes the duodenum
to release:
1. Cholecystokinin (CCK) and secretin
into the bloodstream
a. Secretin transported in blood
stimulate the liver to produce
bile
b. Cholecystokinin causes the
gallbladder to contract and
the sphincters to relax
ii. Vagal stimulation causes weak contractions
of the gallbladder
d. Recycling of Bile Salts (see figure 16-15)
i. Most bile salts are reabsorbed back into the
blood in the ileum are returned by the
hepatic portal system
ii. About 5% of bile escapes in feces
2. Pancreas
a. Secretes pancreatic juices into the duodenum that
break down all categories of food
i. Acini cells secrete digestive enzymes
ii. Duct cells secrete NaHCO3– which
neutralizes acidic chyme
b. Regulation of Pancreatic Secretion
i. When chyme enters the duodenum CCK and
secretin enter the bloodstream. Upon
reaching the pancreas:
1. CCK induces the secretion of
enzyme-rich pancreatic juice
2. Secretin causes secretion of
bicarbonate-rich pancreatic juice
3. See figure 16-12
ii. Vagal stimulation also causes release of
pancreatic juice
c. Pancreatic Enzymes
i. Proteolytic enzymes are released in an
inactive form and are activated in the
duodenum
178
1. Each breaks different peptide bonds
resulting in short peptides and amino
acids
2. Proteolytic enzymes:
a. Enterokinase
Trypsinogen  Trypsin
b. Trypsin
i. Chymotrypsinogen 
Chymotrypsin
ii. Procarboxypeptidase
Carboxypeptidase
ii. Amylase – hydrolyzes polysaccharides into
disaccharides
iii. Nucleases – hydrolyzes nucleic acids into
nucleotides
iv. Lipase – hydrolyzes triglycerides into
monoglycerides and fatty acids
v. Brush Border Enzymes - final chemical
digestion is carried out by brush border
enzymes found in the plasma membrane of
the small intestine’s mucosal cells
1. Sucrase, Maltase, Lactase
Disaccharides Monosaccharides
2. Aminopeptidase
Peptides amino acids
*Table 16-6 in your textbook summarizes the digestive enzymes discussed above
vii. Absorption in the Small Intestines
1. Most electrolytes, nutrients and vitamins are completely
absorbed
2. Vitamins
a. Fat soluble vitamins such as A, D, E, and K are
absorbed along with lipids
b. Water soluble vitamins such as C and B are
passively absorbed with water
c. Vitamin B12 is combined with intrinsic factor and
absorbed by receptor mediated endocytosis in the
ileum
179
3. Minerals
a. Ca2+ and iron are absorbed on an as needed basis
mostly by active transport
i. Ca2+ absorption:
1. Depends on blood levels of ionic
calcium
2. Is regulated by vitamin D and
parathyroid hormone (PTH)
ii. Iron (see figure 16-26)
1. Absorbed iron is stored in the
epithelial cells as ferritin until
needed
2. If blood iron levels are low it is
released into the blood
3. Carried in the blood by transferrin to
the bone marrow to be used for RBC
production
4. Nutrient Absorption
a. Electrolytes
i. Cl-, H20, glucose, and amino acids
absorption depends on active transport of
Na+ into the interstitial fluid
ii. Active transport of Na+ creates a
concentration gradient
iii. Water follows the osmotic gradient and
anions passively follow the electrical
gradient established by sodium
b. Absorption of sugars and amino acids are
facilitated diffusion via cotransport with Na+. (See
figures 16-23 & 16-24)
1. Na+ re-entry through a cotransporter
can drive solutes against the
concentration gradient
2. Driven by secondary active transport
3. Enter the capillary bed in the villi
4. Transported to the liver via the
hepatic portal vein
c. Absorption of lipids (See figure 16-25)
i. When micelles get close to the absorptive
surface lipids are released and diffuse into
intestinal cells where they are:
180
1. Synthesized into triglycerides in the
SER
2. Combine with proteins to form
chylomicrons in the golgi apparatus
3. Released by exocytosis
4. Enter lacteals and are transported to
systemic circulation via lymph
viii. Motility in the Small Intestine
1. Segmentation is the most common motion of the small
intestine
a. It is initiated by intrinsic pacemaker cells (Cajal
cells)
b. Mixes chyme with digestive juices and exposes it to
the absorptive surface of the small intestines
c. Moves contents steadily toward the ileocecal valve
d. Factors enhancing the intensity of segmentation
contractions:
i. Distention
ii. Gastrin
iii. Extrinsic nerve
2. After nutrients have been absorbed:
a. A series of peristaltic waves called the migrating
motility complex begins with each wave starting
distal to the previous
b. Sweeps remnants of the previous meal, bacteria,
mucosal cells, and debris into the large intestine
c. Regulated by the hormone motilin which is
released during the postabsorptive state by mucosa
endocrine cells
3. Ileum empties into the cecum through the ileocecal valve
a. The gastroileal reflex – ileocecal sphincter relaxes
and allows chyme to pass into
the large intestine
i. Triggered by food entering stomach
ii. Gastrin and increased motility of the
small intestines
e.
Large Intestines
i. Frames the small intestines
ii. Extends from the ileocecal valve to the anus
181
iii. Functions:
1. Absorb remaining water, electrolytes, vitamin K
2. Eliminated indigestible food from the body
iv. Motility of the Large Intestines
1. Segmentation in the large intestines occurs less frequently
(3 to 4 times a day)
2. Gastrocolic reflex – contraction of the ascending and
transverse colon results in mass movement of content
forward into the rectum
a. Triggered by gastrin and extrinsic nerves when food
enters the stomach
3. Defecation Reflex
a. Distention of the rectum triggers stretch receptors
causing the internal sphincter to relax (involuntary)
b. When the external sphincter is voluntarily relaxed
defecation occurs
182
Digestive
Post-Lecture Practice
Complete the following practice questions:
1.
Regulation of digestive activities involve:
a. Autonomous smooth muscle
b. Gastrointestinal hormones
c. Extrinsic nerves
d. Enteric nervous system
e. All of the above
2.
Bile is produced by the:
a. Liver
b. Gallbladder
c. Pancreas
d. Duodenum
e. Gastric glands
3.
The sight or smell of food will trigger the _______phase of gastric secretions.
a. Gastric
b. Intestinal
c. Cephalic
d. Active
e. Inhibitory
4.
Which of the following digestive enzymes is CORRECTLY matched with its
substrate?
a. Lipase- carbohydrates
b. Maltase – sucrose
c. Amylase – nucleic acids
d. Trypsin – peptides
e. Pepsin – lipids
5.
Parietal cells in the gastric pits produce:
a. HCl
b. Gastrin
c. Pepsinogen
d. Bile
e. Sodium bicarbonate
6.
Parasympathetic innervation of the digestive tract occurs primarily through the
vagus nerve.
a. True
b. False
183
7.
Chemical digestion of carbohydrates begins in the:
a. Mouth
b. Esophagus
c. Stomach
d. Small intestineså
e. Large intestines
8. Chemical digestion of proteins begins with:
a. Chewing
b. Amylase in the mouth
c. Pepsin in the stomach
d. Trypsin in the duodenum
e. Lipase in the duodenum
9. Which of the following is NOT produced in the stomach?
a. HCL acid
b. Cholecystokinin
c. Gastrin
d. Mucus
e. Pepsinogen
10. Which of the following conditions would decrease the rate of gastric emptying?
a. Chyme high in fat in the doudenum
b. Large volume of chyme in the stomach
c. Vagal stimulation of the stomach
d. Gastrin secretion
11. Pancreatic enzymes for digestion are secreted into the:
a. Duodenum
b. Mouth
c. Large intestines
d. Gallbladder
e. Stomach
12. The absorption of all of the following nutrients rely on the active transport of
sodium in the small intestines EXCEPT:
a. Chloride
b. Glucose
c. Amino acids
d. Water
e. Iron
184
Renal Physiology
Study Objectives:
1. List the functions of the kidneys.
2. Describe the anatomy of the kidneys.
3. Describe the structure and function of the nephron.
4. Describe the structure and function of the juxtaglomerular apparatus.
5. Define glomerular filtration, tubular reabsorption, and tubular secretion.
6. Define the forces (pressures) involved in glomerular filtration.
7. Describe the mechanisms that function in the autoregulation of the glomerular
filtration rate (GFR): myogenic and tubuloglomerular feedback mechanism
8. Describe the extrinsic controls regulating the glomerular filtration rate:
sympathetic nervous system and renin-angiotensin-aldosterone pathway
9. Discuss the tubular reabsorption of sodium, glucose, water, and amino acids.
10. List the substances that are normally reabsorbed in the nephron and those that are
not.
11. Compare the role of aldosterone and atrial natriuretic peptide in sodium and water
balance.
12. Compare obligatory and facultative reabsorption of water.
13. Describe the role of ADH in water retention
14. Describe the role of aldosterone in K+ secretion.
15. Describe the processes in the renal regulation of pH balance by explaining how
the kidneys regulate hydrogen and bicarbonate ion concentrations in the blood.
16. Describe the mechanism responsible for establishing the medullary osmotic
gradient.
17. Contrast the mechanisms in formation of dilute urine verses concentrated urine.
18. Explain the physiology of the micturition reflex.
185
Renal Physiology
I.
Functions of the Urinary System
a. Kidneys – eliminate unwanted plasma constituents through the urine while
conserving materials of value to the body
i. Excrete nitrogenous waste – urea, uric acid, creatinine
ii. Regulate blood volumes – by regulating H2O balance and release
of erythropoietin
iii. Regulates blood pressure – releases renin which triggers
vasoconstriction and aldosterone secretion
iv. Regulates chemical composition of the blood – regulating ions and
osmolarity
v. Stabilizes pH – balances acids and bases
vi. Converting Vitamin D into its active form
b. Ureters, bladder, and urethra – transport and store urine
II.
Anatomy of the Kidney (see figure 14-1 through 14-3)
a. Regions
i. Cortex – outer region
ii. Medulla – deep to the cortex
iii. Renal pelvis – flat funnel shaped cavity
b. Microscopic Anatomy
i. Nephron – structural and functional unit of the kidneys
1. Composed of vascular and tubular components
2. Responsible for the filtration of blood and urine formation
3. Tubular Component
a. Bowman’s capsule – cup surrounding the
glomerulus, collects filtrate
b. Proximal convoluted tubule – extends from the
Bowman’s capsule
c. Loop of Henle – hairpin loop
d. Distal convoluted tubule – leads away from the
ascending loop of Henle to the collecting duct
e. Collecting duct – receives filtrate from DCT of
numerous nephrons
4. Vascular Component
a. Afferent arterioles – supply glomerulus
b. Glomerulus – capillary knot
c. Efferent arterioles – drains the glomerulus
d. Peritubular capillaries – surround tubular portions
of the nephron in the cortex
e. Vasa recta – surround tubular portions of the
nephron in the medulla
186
5. Types of Nephron
a. Cortical nephron – majority of the nephron is within
the cortex with a short loop of Henle
b. Juxtamedullary nephron – glomeruli is deep in the
cortex and have a long loop of Henle that extends
deep into the medulla
ii. Juxtaglomerular Apparatus (JGA) (see figure 14-11)
1. Region between the beginning of the DCT and the afferent
arteriole
2. Contains cells that regulate the rate of filtration and blood
pressure
a. Macula densa – in the DCT, contain osmoreceptors
that monitor solute concentration and flow rate of
filtrate
b. Granular cells (JG) – smooth muscle cells in the
afferent arteriole, act as mechanoreceptors to
monitor BP, synthesize and secrete renin
III.
Renal Processes
a. The four basic processes of the nephrons are:
i. glomerular filtration
ii. tubular reabsorption
iii. tubular secretion
iv. excretion
b. Glomerular filtration
i. Plasma is filtered from the glomerulus into the Bowman’s capsule.
ii. Solutes and fluid are forced through the filtration membrane by
hydrostatic pressure
iii. Blood cells and plasma proteins normally do not enter the filtrate
iv. The glomerulus is more efficient at filtration than other capillary
beds because:
1. Its filtration membrane is significantly more permeable to
solutes and water due to capillary pores
2. Glomerular blood pressure is higher due to a larger afferent
arteriole than efferent arteriole
3. It has a higher net filtration pressure
v. Glomerular Filtration Rate (GFR) - the total amount of filtrate
formed per minute by the kidneys. 125mL/min or 180L/day!
1. Factors governing filtration rate at the capillary bed are:
a. Net filtration pressure
b. Total surface area available for filtration
c. Filtration membrane permeability
187
2. Forces Involved in Glomerular Filtration (see table 14-1)
a. The glomerular capillary pressure (55 mm Hg) is
the result of the blood pressure pushing on the
inside of the capillary wall
b. The plasma-colloid osmotic pressure (30 mm Hg)
is due to the retention of plasma proteins in the
blood of the glomerulus.
i. The concentration of water is higher in the
capsule, because proteins are absent there.
Water tends to return to the glomerulus by
osmosis
c. There is also a hydrostatic pressure (15 mm Hg)
tending to move fluid from the Bowman’s capsule
into the glomerulus
d. From the previous examples: The net pressure =
glomerular blood pressure - (plasma-colloid
osmotic pressure + Bowman’s capsule hydrostatic
pressure)
i. 55 - (30 +15) = 10
ii. The net filtration pressure is 10 mm Hg by
this example.
vi. Regulation of Glomerular Filtration Rate
1. Uncontrolled shifts in the GFR can lead to fluid and
electrolyte imbalances
a. If the GFR is too high:
i. Needed substances cannot be reabsorbed
quickly enough and are lost in the urine
b. If the GFR is too low:
i. Everything is reabsorbed, including wastes
that are normally disposed of
2. Changes in GFR primarily result from changes in
glomerular capillary blood pressure.
3. Three mechanisms controlling the GFR:
a. Renal autoregulation (intrinsic control)
b. Sympathetic NS (extrinsic control)
c. Hormonal mechanisms (the RAA system)
4. Intrinsic Controls
a. Autoregulation - regulates the GFR by factors
within the kidneys.
i. Under normal conditions, it prevents
inappropriate changes in the GFR
188
ii. Autoregulation entails two types of control:
1. Myogenic – responds to changes in
pressure in the renal blood vessels. (see
figure 14-9)
a. Controlled by arteriole smooth
muscle cells
i. If the arterial pressure
increases, the afferent
arterioles constrict to lower
GFR.
ii. If the arterial pressure
decreases the afferent
arterioles dilate to increase
GFR.
iii. Tubuloglomerular feedback mechanism senses changes in flow rate in the nephron’s
tubular component (see figure 19-10)
1. Involves the cells of the JGA
2. Macula densa cells – detect change
in flow-rate and osmolarity
a. Increase in flow rate –
releases vasoactive chemicals
that cause vasoconstriction of
afferent arteriole
b. Decrease in flow rate –
inhibits release of vasoactive
chemicals causing
vasodilation of afferent
arteriole
5. Extrinsic Controls
a. Sympathetic Nervous System
i. When the sympathetic nervous system is at
rest or low levels autoregulation
mechanisms prevail and afferent arteriole is
dilated
ii. However, the sympathetic nervous system
can override the autoregulatory mechanisms
to carry out long term adjustments for blood
pressure if blood volume drops (see figure
14-12)
189
iii. If arterial blood pressure severely drops, the
baroreceptor reflex triggers vasoconstriction
of systemic arterioles
1. The afferent arterioles constrict by
sympathetic innervation. Less blood
flows through the glomeruli,
lowering the blood pressure in these
capillaries.
2. The decrease in the GFR reduces
urine volume.
3. This helps to conserve plasma
volume, increasing blood pressure.
iv. The sympathetic nervous system also
stimulates the renin-angiotensin-aldosterone
mechanism
b. Renin-angiotensin-aldosterone pathway (see
figure 14-16)
i. Renin release is triggered by the following:
1. Reduced stretch of the granular JG
cells
2. Stimulation of the JG cells by
activated macula densa cells
3. Direct stimulation of the JG cells via
β1-adrenergic receptors by renal
nerves
ii. Is triggered when the JG cells release renin
1. Renin acts on angiotensinogen to
produce angiotensin I
2. Angiotensin I is converted to
angiotensin II
3. Angiotensin II:
a. Causes systemic arteriole
vasoconstriction
b. Stimulates the adrenal cortex
to release aldosterone
4. As a result, both systemic blood
pressure and blood volume increase
c. Tubular Reabsorption - is the selective transfer of substances needed by
the body from the filtrate back into the peritubular capillaries
i. Reabsorption rates are high: 124 of 125 ml of filtered fluid per
minute, 99% for water, 100% for glucose, and 99.5% for Na+
190
1. By transepithelial transport a reabsorbed substance must
cross the tubule wall, enter the interstitial fluid, and pass
through the wall of the peritubular capillaries, entering the
blood.
2. Epithelial cells of the nephron tubule have a luminal
membrane and a basolateral membrane (see figure 14-14)
ii. Sodium Reabsorption (see figure 14-15)
1. Sodium reabsorption is mostly driven by active transport
a. Na+ enters the tubule cells at the luminal membrane
by diffusion
b. Then it is actively transported out of the tubules by
a Na+-K+ pump at the basolateral membrane
2. 67% of sodium reabsorption occurs in the proximal tubule
at a constant rate
3. The reabsorption of sodium in the loop of Henle plays a
role in the production of varying concentrations and
volumes of the urine
4. In the distal tubule, reabsorption of sodium is variable and
depends on aldosterone. More or less is reabsorbed,
depending on the needs of the body.
a. Aldosterone increases Na+ absorption in the DCT
and collecting ducts by promoting the insertion of:
i. Additional Na+ channels in the luminal
membrane
ii. Additional Na-K+ pumps into the
basolateral membranes
b. About 8% of the filtered Na+ is dependent on
aldosterone for reabsorption. If aldosterone is
absent it is lost in the urine
5. Atrial Natriuretic Peptide Activity (see figure 14-17)
a. ANP inhibits Na+ reabsorption which:
i. Decreases blood volume
ii. Lowers blood pressure
b. ANP lowers blood volume and pressure by:
i. Acting directly on collecting ducts to inhibit
Na+ reabsorption
ii. Inhibits RAA pathway
iii. Dilates afferent arteriole triggering an
increase in GFR which reducing water and
sodium reabsorption
191
iii. Reabsorption of water, glucose, amino acids, and anions - linked to
the active reabsorption of Na+
1. Active pumping of Na+ drives reabsorption of:
a. Water by osmosis, aided by water-filled pores
called aquaporins
b. Anions following by diffusion
c. Glucose and amino acids by secondary active
transport
2. Reabsorption of Water
a. The accumulation of sodium in the lateral spaces
produces an osmotic gradient and hydrostatic
pressure that pushes the water into the peritubular
capillaries. (see figure 14-19)
b. 80% of water reabsorption is obligatory in the
proximal tubule and loop of Henle. Occurs by
osmosis, no control.
c. 20% of water reabsorption is facultative in the distal
tubule and collecting duct. Based on the secretion of
ADH (vasopressin), depends on body’s needs,
i. ADH works on tubule cells through a cyclic
AMP mechanism
ii. Promotes the insertion of aquaporins on the
luminal membrane thus increasing water
reabsorption (see figure 14-26 & 14-27)
iii. Produces concentrated urine
3. Reabsorption of glucose and amino acids are reabsorbed
by secondary active transport and cotransported with
sodium on the luminal membrane
4. Oppositely-charged chloride ions follow sodium
iv. Nonreabsorbed Substances
1. A transport maximum (Tm):
a. Reflects the number of carriers in the renal tubules
available
b. Exists for nearly every substance that is actively
reabsorbed
c. When the carriers are saturated, excess of that
substance is excreted
192
2. Substances are not reabsorbed if they:
a. Lack carriers
b. Are not lipid soluble
c. Are too large to pass through membrane pores
d. Urea, creatinine, uric acid and other nitrogen
containing wastes are excreted
d. Tubular secretion - a selective process by which substances from the
peritubular capillaries enter the lumen of the nephron tubule.
i. Provides a mechanism to speed up the elimination of substances
from the blood
ii. Tubular secretion is important for:
1. Disposing of substances not already in the filtrate
2. Eliminating undesirable substances such as urea and uric
acid
3. Ridding the body of excess potassium ions
4. Controlling blood pH
iii. Tubular Secretion of K+
1. K+ is almost completely reabsorbed in the proximal tubule
2. Aldosterone stimulates the tubular cells to secrete
potassium if plasma levels are elevated
3. K+ secretion occurs in the distal tubule
4. As the basolateral pump transports sodium into the lateral
spaces, it pumps potassium into the tubular cells where it
diffuses into the lumen for elimination. (see figure 14-21)
iv. Acid-Base Balance
1. Concentration of hydrogen ions is regulated sequentially
by:
a. Chemical buffer systems – act within seconds
b. The respiratory center in the brain stem – acts
within 1-3 minutes
c. Renal mechanisms – require hours to days to effect
pH changes
2. Renal Mechanisms of Acid-Base Balance
a. The most important renal mechanisms for
regulating acid-base balance are:
i. Conserving (reabsorbing) or generating new
bicarbonate ions
ii. Excreting bicarbonate ions
iii. Losing a bicarbonate ion is the same as
gaining a hydrogen ion; reabsorbing a
bicarbonate ion is the same as losing a
hydrogen ion
193
b. Reabsorption of Bicarbonate (see figure 15-9)
i. Secreted hydrogen ions form carbonic acid
with filtered bicarbonate
ii. Carbonic acid dissociates to release carbon
dioxide and water
iii. Carbon dioxide then diffuses into tubule
cells, triggering further hydrogen ion
secretion and bicarbonate reabsorption
iv. Thus, bicarbonate disappears from filtrate at
the same rate it is reabsorbed
c. Generating New Bicarbonate Ions (see figure 151)
i. Dietary hydrogen ions must be counteracted
by generating new bicarbonate
ii. Two mechanisms generate new bicarbonate
ions:
1. Both involve renal excretion of acid
via secretion and excretion of
hydrogen ions or ammonium ions
(NH4+)
2. The excreted hydrogen ions must
bind to buffers in the urine
(phosphate buffer system)
iii. In response to acidosis:
1. Hydrogen Ion Excretion
a. Kidneys generate bicarbonate
ions and add them to the
blood
b. An equal amount of hydrogen
ions are added to the urine
c. H+ binds with buffers in the
filtrate (monohydrogen
phosphate)
2. Ammonium Ion Excretion
a. This method uses ammonium
ions produced by the
metabolism of glutamine in
PCT cells
b. Each glutamine metabolized
produces two ammonium
ions and two new bicarbonate
ions
194
c. Bicarbonate moves to the
blood and ammonium ions
are excreted in urine
d. Bicarbonate Ion Secretion (see figure 15-10)
i. When the body is in alkalosis, type B cells:
1. Exhibit bicarbonate ion secretion
2. Reclaim hydrogen ions and acidify
the blood
IV.
Varying Urine Concentration
a. Kidneys excrete varying concentrations and volumes of urine depending
on the body’s needs
i. Can produce urine ranging from 0.3ml/min at 1200 mosm/L to 25
ml/min at 100 mosm/L
b. This variation in reabsorption is made possible by a large, vertical
osmotic gradient in the interstitial fluid of the medulla from 300 to
1200 mosm/liter. (see figure 14-24)
i. This increase follows the juxtamedullary nephron’s loop of Henle
deeper and deeper into the medulla.
ii. The gradient is established by means of the countercurrent system
c. Countercurrent – the movement in opposite directions of filtrate through
the ascending and descending limbs of the loop of Henle. Also applies to
the flow of blood through the vasa recta.
i. Countercurrent multiplier – refers to the ability to increase the
osmolarity of the interstitial fluid (see figure 14-25)
1. Due to the properties in the two limbs of the loop:
a. The descending loop of Henle:
i. Is relatively impermeable to solutes
ii. Is permeable to water
b. The ascending loop of Henle:
i. Is permeable to solutes
ii. Is impermeable to water
2. The ascending limb actively transports NaCl out of the
tubular lumen into the surrounding interstitial fluid. It is
impermeable to water. Therefore, water does not follow
the salt by osmosis.
3. The ascending limb produces an interstitial fluid that
becomes hypertonic to the descending limb. This attracts
the water by osmosis for reabsorption.
195
ii. Countercurrent exchanger - The hairpin structure of the vasa
recta allows the blood of the vasa recta to equilibrate with the
interstitial fluid (see figure 14-28)
1. Prevents the dissipation of the medullary osmotic gradient
2. Blood is isotonic when it enters and when it leaves the
medulla
d. Formation of Concentrated Urine
i. ADH is the signal to produce concentrated urine
1. Allowing the distal and collecting ducts to become
permeable to water (see figure 14-27)
2. In the presence of ADH, 99% of the water in filtrate is
reabsorbed
e. Diuretics – large volume of dilute urine
i. Osmotic diuretics include:
1. High glucose levels – carries water out with the glucose
2. Alcohol – inhibits the release of ADH
3. Caffeine and most diuretic drugs – inhibit sodium ion
reabsorption
4. Lasix and Diuril – inhibit Na+-associated symporters
V.
Transport and Storage of Urine
a. Urine Excretion – elimination of what remains in the tubular lumen. The
unwanted filtrate material.
i. Urine is transported from the kidney to the bladder by the ureters.
Due to gravity or peristaltic waves.
ii. The bladder temporarily stores urine
1. Micturition Reflex (see figure 14-29) - act of emptying the
bladder
a. The filling of the bladder activates stretch receptors
which trigger reflex contractions of the bladder and
relaxation of the internal sphincter
b. Urine is forced past the internal sphincter
c. Must voluntary relax external sphincter to void the
bladder of urine
*No post-lecture practice for this lecture.
196
Reproductive Physiology
Study Objectives:
1. List the functions of the reproductive system.
2. List the bipotential tissues and what they will become in males or females during
embryonic development.
3. Describe the role of the SRY gene in embryonic development in males.
4. Describe the role of testosterone, DHT, and anti-mullerian hormone in the
embryonic development in males. Also know which cells secrete these hormones.
5. Describe how the lack of the SRY gene leads to the embryonic development of
females.
6. Briefly describe the events that occur during meiosis in respect to number of
nuclear divisions and number of chromosomes present in the daughter cells. What
types of cells undergo meiosis? What is the final result of meiosis?
7. Define: gametes, sister chromatids, homologous chromosomes, tetrads,
autosomal chromosomes vs. sex chromosomes.
8. Define: spermatogonia and oogonia, primary gametes and secondary gametes.
9. Define spermatogenesis and discuss the role of GnRH, FSH, LH, testosterone, and
inhibin in spermatogenesis. (Know who secretes each hormone, their target cell,
and their effect.)
10. Define oogenesis and discuss the role of GnRH, FSH, LH, estrogen, and inhibin in
oogenesis. (Know who secretes each hormone, their target cell, and their effect.)
11. Describe the function of the corpus luteum and progesterone in maintenance of the
endometrial lining.
12. Explain the effects of fertilization and hCG on the corpus luteum.
13. Describe the roles of FSH, LH, estrogen and progesterone in the female
reproductive cycle.
a. Describe the three stages of the ovarian cycle: follicular, ovulation,
luteal phase
b. Describe the three stages of the uterine cycle: menstrual, proliferation,
secretory
197
Reproductive Physiology Outline
I.
Functions of the Reproductive System
a. Secretion of sex hormones – influence growth and development of organs
and tissues
b. Production of gametes – sperm and ova
i. Male gonads  testes  sperm
ii. Female gonads  ovaries  eggs
c. Produce offspring
i. Male – deliver sperm to the female reproductive tract
ii. Female – provide an environment for fetus development
II.
The human life cycle
a. Sexual reproduction in humans involves:
i. Meiosis:
1. Stem cells within the gonads are diploid 2(n) = 46
Contain two sets of chromosomes
2. Gametes are haploid (n) = 23 having only one set of
chromosomes
ii. Fertilization
1. Is the fusion of sperm and egg
2. Creates a zygote (2n), or fertilized egg that will develop
into a new organism
III.
Sex Determination
a. Inheritance of X and Y chromosomes
i. XX = female
ii. XY = male
b. Bipotential stage: during the first 6 weeks of fetal development the
internal reproductive organs have the potential to develop into male or
female structures
i. Bipotential tissues:
1. Gonads
a. Testis or ovary
2. Wolffian duct - remains in males
3. Mullerian duct – remains in females
198
c. Embryonic Development: Males
i. Role of SRY gene in male development – gene found on the Y
chromosome
1. Produces the SRY protein that causes the gonad medulla to
differentiate into the testes
a. Sertoli cells – secrete anti-Mullerian hormone,
cause the Mullerian duct to degrade
b. Leydig cells – secrete testosterone and
dihydrotestosterone (DHT) leading to the
development of the Wolffian duct and external male
genitalia
d. Embryonic Development: Females
i. Females do not have the Y chromosome so they lack the SRY gene
to produce SRY proteins
ii. Gonadal cortex becomes the ovaries
iii. Wolffian ducts degenerates in absence of testosterone
iv. Mullerian ducts become
1. Superior portion of vagina
2. Uterus
3. Fallopian tubes
v. In the absence of testosterone and DHT the external genitalia
develops as females
IV.
Meiosis (information can be found in supplemental chapter 11pgs 219-228 in
back of textbook)
a. Chromosome Review
i. Humans have 23 pairs of chromosomes
ii. Each somatic cell has two sets of chromosomes (one maternal, one
paternal) and is said to be diploid (2n)
iii. Each pair of homologous chromosomes carry equivalent genes
which determine particular traits
iv. There are alternative forms of each gene which are called alleles
v. Gametes only have 23 chromosomes and are said to be haploid (n)
b. Purpose of Meiosis
i. Meiosis is a type of cell division that produces gametes (sperm and
ova) from stem cells in the reproductive tissue
1. Reduces the original number of chromosomes in half in
preparation for fusing with another gamete
2. Recombination (scrambling) of parents’ genomes to create
a unique set of chromosomes in each gamete
199
c. Stages of Meiosis
i. Overview
1. In meiosis there is two rounds of division which results in 4
haploid cells See figure 11-2
a. 1st round separates duplicated homologous
chromosomes
b. 2nd round separates sister chromatids
ii. Interphase
1. Occurs prior to Prophase I of meiosis
2. G1 phase
3. S-phase homologous chromosomes replicate into sisters
4. G2 phase – checkpoint
iii. Meiosis I –first division
1. Prophase I
a. Duplicated homologous chromosomes pair up
(tetrads)
b. Crossing over occurs: homologous chromosome
exchange equivalent segments
c. Occurs between non-sister chromatids
i. How are non-sister chromatids different
from sister chromatids?
2. Metaphase I
a. Homologous chromosomes line up in pairs along
the central plane in tetrads
b. Independent assortment: which side each
chromosome lines up on is independently of the
other pairs
3. Anaphase I
a. Homologous chromosomes are separated and move
to opposite poles
4. Telophase I and Cytokinesis
a. Results in two haploid cells with 23 duplicated
chromosomes
iv. Meiosis II
1. Prophase II
2. Metaphase II
a. Sister chromatids (duplicated chromosomes) line up
along midline
3. Anaphase II
a. Sister chromatids separate and are pulled towards
opposite poles
4. Telophase II and Cytokinesis
a. Results in 4 haploid gametes
200
d. Three factors contributing to genetic recombination
i. Crossing over during prophase and metaphase I (see figure 11.6)
1. Additional mixing of alleles produces further variation in
offspring
ii. Independent assortment of chromosomes in Metaphase I & II
1. Total # of chromosome combinations = 2n
2. Humans 223 = 8 million combinations
iii. Random fertilization - egg is fertilized randomly by one sperm
1. 8 million x 8 million = 64 TRILLION possibilities (not
considering crossing over)
V.
Gametogenesis – production of gametes (see figure 20-15)
a. Begins in utero and resumes during puberty
i. Mitotic divisions in embryonic gonads increases number of
spermatogonia or oogonia
ii. DNA replication (S-phase)  primary gametes with 46
duplicated chromosome
iii. Meiosis I  secondary gametes with 23 duplicated chromosomes
iv. Meiosis II  egg (ova) or spermatid with 23 chromosomes
b. Spermatogenesis -production of sperm cells (see figure 20-8)
i. Begins at puberty and continues throughout life
ii. Occurs in the seminiferous tubules
iii. Regulation of Spermatogenesis
1. GnRH  LH  Leydig cells  testosterone  sex
characteristics
2. GnRH  FSH  Sertoli cells  spermatocyte maturation
3. Inhibin triggers negative feedback loop for FSH secretion
4. Testosterone triggers negative feedback loop through the
kiss1 neurons for LH and GnRH secretion
5. See figure 20-10
c. Oogenesis – production of ova
i. The total supply of primary follicles are present at birth
ii. Ability to release eggs begins at puberty
iii. Refer to figure 20-14 for detail on when the first and second
meiotic division occur
201
VI.
Menstrual Cycle in Females
a. Ovarian cycle –changes that occur in the ovaries, divided into three
phases (see figures 20-16 – 20-19):
i. Follicular phase – follicular growth in ovary
1. Low levels of FSH and LH, increased sensitivity to FSH
2. Granulosa cells producing increasing amounts of estrogen
through positive feedback.
3. Moderate levels of estrogen selectively inhibits FSH and
LH secretion.
4. High levels of estrogen late in the follicular stage
stimulates the production of GnRH thus triggering
increased production in FSH and the LH surge.
ii. Ovulation – ova released from ovary, triggered by surge in LH
iii. Luteal phase – corpus luteum produces hormones to prepare for
pregnancy
1. Estrogen and progesterone being produced
2. High levels of progesterone during the luteal phase inhibits
LH and FSH production.
3. Corpus luteum – remnants of the ovulated follicle,
produces increasing amounts of progesterone and some
estrogen for about two weeks after ovulation
a. If fertilization does not occur –it degenerates into
scar tissue and drop in hormones triggers
menstruation
b. If fertilization occurs – the oocyte secretes human
chorionic gonadotropin (hCG) which causes the
corpus luteum to persist so the menstrual cycle will
not be initiated
b. Uterine cycle – changes in the endometrial lining of the uterus, also
divided into three phases:
i. Menses- shedding of the lining
1. Triggered by drop in progesterone and estrogen
ii. Proliferation phase – endometrial lining adds new layers
1. Stimulated by increasing estrogen levels
iii. Secretory phase – increased blood flow to endometrium, increased
glandular secretions
1. Stimulated primarily by increased progesterone
c. Summary of Hormonal Control of the Menstrual Cycle – see figure 20-18
202
Reproductive
Post-lecture Practice
Draw and label the events occurring in the stages of meiosis for a cell that is 2n = 4 and give a
brief description for each event. Include the phases of meiosis I and meiosis II. Other things you
should include somewhere in your drawing is the labeling of chromatin, homologous
chromosomes, sister chromatids, daughter chromosomes. For an additional challenge show
crossing over and independent assortment of chromosomes.
203
204
Name:_________________
Lab Section:_________________
REPRODUCTION HOMEWORK
Instructions: Use your textbook or other reference sources to answer the questions
below. All answers must be in your own words! This assignment will be worth up to
11 points and is due by midnight after your last lecture exam. No late work will be
accepted.
1. Briefly summarize how the cortical reaction that occurs during fertilization
prevents polyspermy. (1 pt)
2. When the developing embryo reaches the uterus and capable of implanting it is
called a ______________________(a hollow ball of cells). (1/2 pt)
3. What is the function of the following membranes? (1 pt)
a. Chorion (chorionic tissue)
b. Amnion
4. Through what process does nutrients, gases, and waste move across the placenta?
(1/2 pt)
5. At about what week does the placenta take over progesterone production from the
corpus luteum? (1/2 pt)
6. What hormone produced by the placenta is responsible for altering the mother’s
glucose and fatty acid metabolism? (1/2 pt)
a. How does this hormone specifically affect the mother’s glucose levels and
fatty acid metabolism? (1 pt)
205
7. Between what weeks does normal parturition (labor and delivery) occur? (1/2 pt)
8. In the days leading up to parturition estrogen levels soar. List three ways high
estrogen levels prepare the uterus and cervix for labor and delivery. (1.5 pts)
9. In your own words, write a brief summary of the positive feedback loop
responsible for parturition. (2 pt)
10. During lactation, the primary hormone responsible for milk production/secretion
is __________________and the ejection of milk from the mammary glands is
stimulated by the hormone ________________. (1 pt)
11. The absence of the hormone ___________________leads to symptoms in
postmenopausal women. List two or three symptoms below (1pt):
206