Lesson 6: Nervous System Overview (167-182)
1. Describe the major components of the nervous system and the direction of information
flow within and among them.
2. Describe the basic anatomy of a neuron. Compare the functions of each part of a neuron,
and describe the types of ion channels located in each part. Describe the grouping of
neurons within the central nervous system and the peripheral nervous system.
3. Describe the structure and function of myelin.
4. Explain the ionic basis of the resting membrane potential.
5. Describe the various properties of graded potentials, including the direction of change in
a potential, the magnitude of change, and temporal and spatial summation. Explain how
graded potentials in neurons can trigger an action potential
Lesson 7: Action Potentials (182-193)
1. Explain the ionic basis of an action potential. Describe the gating mechanisms for voltagegated sodium and potassium channels.
2. Describe the propagation of action potentials from axon hillock to axon terminal and
compare propagation in myelinated and unmyelinated axons.
3. Describe refractory periods, including what causes the absolute and relative refractory
periods, and explain their physiological significance.
The refractory period is the period at which the cell membrane is less excitable then when it is at rest.
The absolute refractory period is all of the depolarization phase and most of the repolarization phase
of an action potential. It occurs because depolarization set in motion by the opening of sodium
channels will proceed regardless of a second stimulus and during the beginning of repolarization the
sodium channels are closed and in the incapable of opening state. The relative refractory period is
after the absolute and in it it is possible to generate an action potential but a stronger stimulus is
needed. It occurs because of the increased permeability of potassium in the repolarization phase.
Refractory period- the period at which the cell membrane is less excitable then when it is at rest
Absolute refractory period- all of the depolarization phase nd most of the repolarization phase of an
action potential. It occurs because depolarization set in motion by the opening of sodium channels
will proceed regardless of a second stimulus and during the beginning of repolarization the sodium
channels are closed and in the incapable of opening state.
Relative refractory period- after the absolute and in it it is possible to generate an action potential but a
stronger stimulus is needed. It occurs because of the increased permeability of potassium in the
repolarization phase.
Saltatory conduction- The type of conduction that happens in myelinated axons. The jumping of action
potentials between nodes is the saltatory conduction.
Lesson 8: Synapses and Neurotransmitters (197-213)
1. Understand the differences between chemical and electrical synapses.
2. Describe the communication across chemical synapses. Explain how neurotransmitters are
released, and describe their actions after release.
3. Compare fast and slow responses at synapses.
Fast responses- inotropic receptors channel linked receptors- cause PSPs
Slow response- G coupled- Metabotropic receptors- G proteins open or close channel
4. Describe the process of neural integration and the role of the axon hillock in this process.
5. Describe the major classes of neurotransmitters, including their chemical structures,
synthesis, degradation, and signal transduction mechanisms.
Electrical synapses- Linked by gap junctions and action potentials are directly transferred by means
of ions flowing through the gap junction. They allow rapid communication and are often
bidirectional.
Chemical synapses- These are much better understood and widely used in the nervous system. In
chemical synapses the presynaptic neuron releases neurotransmitters in response to an action
potential, triggering a response in the secondary cell.
Neural integration- The summation process of at the neuron that decides whether an action potential
will occur based off if threshold has been reached.
Frequency coding- Increases in the strength of a suprathreshold stimulus can cause the frequency of
action potentials to increase.
Presynaptic facilitation- When neurotransmitter release is enhanced.
Presynaptic inhibition- When neurotransmitter release is decreased.
Nicotinic cholinergic receptors- Ionotropic and have two binding sites for acetylcholine. Allow
sodium and potassium to come in and cause an EPSP
Muscarinic cholinergic receptors- metabotropic and operate through a G protein. This means many
enzymes or ion channels can be effected. These are found in some effector organs and are the
dominant cholinergic receptor in the CNS.
Adrenergic receptors- What norepinephrine and epinephrine bind to. Have beta and alpha subtypes
but both types bind both molecules with different affinities.
Lesson 9: CNS and Involuntary Control (216-238)
1. Describe the anatomy of the brain and spinal cord, and relate structure to function. Indicate
which structures protect the central nervous system and which are involved in neural
signaling.
2. Describe the anatomy, physiology, and consequences of the blood-brain barrier.
The blood brain barrier restricts the movement of hydrophilic molecules across the blood brain
barrier. It is due to tight junctions between the capillary endothelial cells which eliminate pores.
Astrocytes are critical as they signal to endothelial cells to develop tight junctions.
3. Describe the energy supplies of the brain, and explain why blood flow is so critical.
4. Define reflex arc. Describe the following reflex pathways: muscle spindle stretch reflex,
withdrawal reflex, and crossed-extensor reflex.
Astrocytes- most divers and numerous of glial cells
Cranium- bony skull that protects the brain
Vertebral column- bony column around spinal column
Meninges-The three connective tissue membranes that separate the soft tissues of the CNS from the
surrounding bone. The three plates are the dura mater, arachnoid mater, and pia mater.
Cerebrospinal fluid- Clear watery fluid that tbathes the CNS. Similar to plasma. Fills the ventricles
Blood-brain barrier- the movement of hydrophilic molecules across capillary walls is restricted by
the gap junctions between endothelial cells
Gray matter- the unmyelinated axons and dendrites
White matter- mylenated axons
Cerebral cortex- thin layer of gray matter that surrounds the brain
Spinal nerves- 8 cervical, 12 thoracic, 5 lumbar, 5 sacral nerves, 1 coccygeal
Dorsal horn- The dorsal part of the gray matter of the spinal cord. Sensory receptors terminate in the
dorsal horn.
Ventral horn- The ventral part of the gray matter of the spinal cord. Efferent neurons originate in the
ventral gray matter and synapse at the periphery.
Dorsal root ganglia- Where the cell bodies of the afferent fibers leading to the dorsal gorn are loated
in clusters.
Dorsal roots- Bundles of afferent axons
Ventral roots- bundles of efferent axons
Ascending tracts- info from spine to brain
Descending tracts- info from brain to spine
Cerebellum – inferior to the forebrain and dorsal to brain stem, it is responsible for coordination and
movement
Brain stem- composed of midbrain, pons, and medulla oblongata. Contains the processing center for
10 of the 12 pairs of cranial nerves. Also contains reticular formation which is important for sleep
wake cycles.
Thalamus- Sensory relay center, all go through here except for smell.
Hypothalamus- major lnk between endocrine and nervous system. Releases tropic hormones which
regulate anterior posterior hormone release.
Reflex-an automatic patterned response to sensory stimuli
Reflex arcs- all have five components. They are either spinal or cranial- somatic or autonomic- innate
or conditioned- and monosynaptic or polysynapitic. Five components:
1. Sensory receptor
2. Afferent neuron
3. Integration center
4. Efferent neuron
5. Efferent organ
Muscle spindle stretch reflex- only known monosynaptic reflex in the body. The muscle spindle is
the receptor. Tapping the patella tendon stretches the spindle in the quadricep. The efferent neuron
contracts the quad and relaxes the hamstring.
Withdrawal reflex- Painful reflex activates nociceptors. Afferent neurons bring this pain to the dorsal
horn and interneurons excite efferent neurons which activate muscles required for withdraw and relax
the ones necessary.
Crossed-extensor reflex- When painful stimuli trigger the withdrawal reflex, this reflex is initiated
simultaneously. Efferent neurons to the opposite leg are also activated that extend the opposite leg to
have support on the opposite leg.
Lesson 10: Sensory Perception and the Somatosensory System (254-269)
1. Describe the function of sensory receptors and explain how they perform that function.
The law of specific nerve energies states that a given sensory receptor is specific for a particular
modality. The modality to which a receptor responds best is called the adequate stimulus. Sensory
receptors preform transduction, which is the conversion of one form of energy into another. Visceral
receptors detect stimuli in the external environment. Somatosensory receptors detect stimuli
associated with receptors on the skin (somesthetic) and position of limbs (proprioception). Sensory
receptors have two forms. One is as a specialized structure at the peripheral end of an afferent
neuron. The receptor is depolarized to threshold and an action potential is propagated to the CNS.
The other form is as a separate cell that communicates with an afferent neuron through a chemical
synapse.
In sensory transduction, receptors convert the energy of a sensory stimulus into receptor potentials or
generator potentials. Receptor potentials are graded potentials caused by opening or closing of ion
channels.
2. Describe the neural pathways of the different sensory systems, from sensory receptor to
cerebral cortex.
Labeled lines are the specific neural pathways that transmit
information pertaining to a particular modality. A sensory
unit is a single afferent neuron and all the receptors associated
with it. Each afferent neuron has a receptive field in which it
can detect a stimulus. Sensory information enters a first-order
neuron, which synapses with an interneuron called a second
order neuron, which synapses with a third order neuron in the
thalamus and travels to the cerebral cortex.
Stimulus type is coded by the receptor and pathway activated
when the stimulus is applied. Stimulus intensity is coded by
the frequency of action potentials (frequency coding) and the
number of receptors activated (population coding). Stimulus
location is based on receptive fields.
Dorsal column-medial lemniscal pathway transmits
information from mechanoreceptors and proprioceptors to the
thalamus. First order neurons enter dorsal horn and terminate
in dorsal column nuclei, where the form synapses with second
order neurons that synapse with third order neurons in the
thalamus.
The spinothalamic tract transmits information from thermoreceptors and nociceptors to the thalamus.
Terms:
Visceral receptors – Receptors that detect stimuli from within the body. Visceral afferents are a class
of neurons that transmit information from visceral receptors to the CNS.
Somatosensory system – Controls perception of sensations associated with receptors in the skin and
limbs.
Somesthetic sensations – Sensation in the skin
Proprioception – Perception of position of limbs
Special senses – Vision, hearing, balance, taste, and smell
Sensory receptors – Specialized structures that detect a specific form of energy in the external
environment.
Modality – Energy form of a stimulus (light waves, sound waves, etc.)
Adequate stimulus – The modality to which a receptor responds best
Sensory transduction – Receptors convert the energy of a sensory stimulus into changes in membrane
potential
Receptor potentials – Changes in membrane potential. They resemble postsynaptic potentials in that
they are graded potentials caused by opening or closing of ion channels. They are triggered by
sensory stimuli.
Receptor adaptation – A decrease over time in the magnitude of the receptor potential in the presence
of a constant stimulus.
Tonic receptors – Slowly adapting receptors that can function in signaling intensity of a prolonged
stimulus.
Phasic receptors – Rapidly adapting receptors that can function in detecting changes in stimulus
intensity.
Labeled lines – Specific neural pathways that transmit information pertaining to a particular modality
Sensory unit – A single afferent neuron and all the receptors associated with it
Receptive field – The area over which an adequate stimulus can produce a response in the afferent
neuron
First order neuron – The afferent neuron that transmits information from the periphery to the CNS.
Second order neuron – Interneurons that transmit information to the thalamus
Third order neuron – Neurons in the thalamus that transmit information from second order neurons to
the cerebral cortex.
Acuity – The precision with which a stimulus is perceived. Larger receptor field means less acuity.
More overlap of receptor fields increases acuity. Lateral inhibition increases acuity.
Lateral inhibition – A stimulus that strongly excites receptors in a given location inhibits activity in
the afferent pathways of other nearby receptors. This increase acuity because it increases the contrast
of signals in the nervous system.
Two-point discrimination – The ability to detect 2 fine points pressed against the skin as 2 distinct
points; the points must be in different receptive fields.
Proprioceptors – Detect body position
Mechanoreceptors – Detect pressure, force, or vibration
Thermoreceptors – Free nerve endings tat contain ion channels called transient receptor potential
(TRP) channels that detect changes in skin temperature.
Nociceptors – Sensory receptors that perceive pain. There are three types: mechanical nociceptors,
thermal nociceptors, and polymodal nociceptors.
Lesson 11: Vision
1. Describe how light is focused on the retina
The lens focuses light on the retina. The lens and ciliary body separate the eye into two fluid-filled
chambers called the anterior segment and the posterior segment. The anterior segment contains aqueous
humor, which supplies nutrients to the cornea and lens. The posterior segment (aka vitreous chamber) is
filled with vitreous humor, which maintains the spherical structure of the eye.
The cornea and the lens are both convex
lenses, so light waves converge on the retina.
Accommodation is the ability of the lens to
change shape so that light converges at one
point on the retina. The shape of the lens is
controlled by ciliary muscles by applying
tension to zonular fibers. When the ciliary
muscle contracts, the lens becomes more round
(for close objects); when the ciliary muscle
relaxes, the lens becomes more flat (for far
objects). This process is controlled by the
parasympathetic nervous system, which
triggers contraction of the ciliary muscle to see
close objects.
2. Describe how the iris regulates the amount of light that enters the eye
Pupils are constricted in bright light and dilated in dark light. The size of the pupils are regulated by the
iris, which consists of two layers of smooth muscle called the circular muscle (constrictor muscle) and the
radial muscle (dilator muscle). The circular muscles form concentric rings around the pupil that constrict
the pupil when they contract. The radial muscles look like spokes of a wheel that dilate the pupil when
they contract. The muscles of the iris are controlled by the autonomic nervous system. Parasympathetic
neurons innervate the circular muscles; parasympathetic activity results in constriction. Sympathetic
neurons innervate the radial muscles; sympathetic activity results in dilation.
3. Explain the difference between the rods and cones in the eye
Rods and cones are the two types of
photoreceptors in the retina. Rods
allow for vision in low light
conditions, while cones allow for
color vision in bright light.
The retina consists of three layers:
the inner layer contains the ganglion
cells, the middle layer contains the
bipolar cells, amacrine cells, and
horizontal cells, and the outer layer
contains rods and cones.
Rods and cones preform phototransduction,
which is the conversion of light energy to
electrical signals. Both rods and cones consist of
outer and inner segments. The outer segment
contains membranous disks whose molecules
absorb light waves. The inner segment contains
the cell nucleus and synaptic terminal (similar to
an axon terminal). The membranous disks
contain photopigment, which consists of retinal
and one of four opsins: rhodopsin in rods and L
opsin, M opsin, or S opsin in cones. The disk
membrane contains a G protein called transducin
and the enzyme phosphodiesterase, which
catalyzes the degradation of cGMP.
Rods are responsible for scotopic vision, which is monochromatic vision. Cones are responsible for
photopic vision, which is color vision. Mesopic vision is a combination of scotopic and photopic vision in
intermediate levels of light.
Phototransduction in rods: in the dark, levels of cGMP are high. cGMP opens sodium channels in the
plasma membrane of the outer segment, which depolarizes the photoreceptor. The depolarization spreads
to the inner segment and opens calcium channels that are also present in the plasma membrane. Calcium
enters the cell, which triggers the release of a transmitter by exocytosis that communicates with bipolar
cells. In the light, rhodopsin absorbs light. Retinal changes conformation from cis to trans, which results
in dissociation from opsin and opsin is now called bleached opsin. Bleached opsin activates transducin,
which activates phosphodiesterase, which breaks down cGMP. Since cGMP opens sodium channels, a
decrease in cGMP results in more closed sodium channels, and transmitter is not released onto bipolar
cells (see figure 10.33).
Terms
Sclera – Tough connective tissue; the white of the eye (outer layer)
Cornea – Transparent structure that allows light to enter the eye (outer layer)
Choroid – Contains blood vessels that nourish the inner layer of the eye (middle layer)
Ciliary muscles – Muscles in the ciliary body attached to the lens by zonular fibers. These muscles change
the shape of the lens to focus light (middle layer)
Zonular fibers – Strands of connective tissue that connect the ciliary muscles to the lens (middle layer)
Lens – Focuses light on the retina (middle layer)
Iris – Consists of two layers of smooth muscle in front of the lens that regulates the diameter of the pupil
(middle layer)
Pupil – The hole in the center of the iris that allows light to enter the posterior part of the eye.
Retina – Consists of neural tissue and photoreceptors, which are cells that detect light waves (inner layer)
Photoreceptors – Cells that detect light; divided into rods and cones.
Fovea – Central region on the retina where light from the center of the visual field strikes.
Optic Disk – The portion of the retina where the optic nerve and blood vessels pass through the retina.
Blind spot – A region where light striking the retina cannot be transduced into neural impulses due to a
lack of photoreceptors in this area (because the optic nerve is there).
Aqueous humor – Clear, watery fluid in the anterior segment that supplies light and nutrients to the
cornea and lens. It is clear as to not obstruct light.
Vitreous humor – Jellylike material that maintains the spherical structure of the eye in the posterior
segment.
Reflection – A phenomenon in which light waves strike and bounce off of a surface.
Refraction – Bending of light waves as they pass through transparent materials of different densities.
Accommodation – The ability of the lens to increase its refractive power for viewing near objects.
Myopia – Near sightedness (cannot see distant objects clearly). Occurs because the lens or cornea is too
strong from the length of the eyeball and bends light rays too much so that light converges in front of the
retina.
Hyperopia – Far sightedness (cannot see near objects clearly). Occurs because the lens or cornea is too
weak for the length of the eyeball and does not bend light rays enough so that light converges behind the
retina.
Emmetropia – Normal vision.
Astigmatism – Irregularities on the surface of the cornea that cause erratic bending of light waves
Presbyopia – Hardening of the lens that occurs with aging; decreased elasticity means the lens cannot
become spherical, which makes accommodation for near vision more difficult.
Cataract – Opacification of the lens that decreases its transparency
Rods – Photoreceptors that allow for black and white vision in low light conditions
Cones – Photoreceptors that allow for color vision in bright light conditions
Ganglion cells – Cluster of neuron cell bodies that connect the retinal input to the visual processing
centers of the CNS.
Bipolar cells – Neurons that connect the outer retina to the inner retina.
Macula lutea – A depression in the center of the retina that allow for a clear path of light to the fovea by
displacing bipolar and ganglion cells.
Phototransduction – The conversion of light energy to electrical signals, which is carried out by rods and
cones.
Optic Nerve – Formed by the axons of ganglion cells. The two optic nerves exit each eye at the optic disk
and combine at the base of the brain just in front of the brainstem to form the optic chiasm. Axons travel
from the optic chiasm along the optic tract and terminate in a nucleus in the thalamus called the lateral
geniculate body. Pathways from the lateral geniculate body to the visual cortex are called optic radiations.
Lesson 12: Hearing, Taste, Smell (285-299)
1. Describe the two sensory systems of the ear.
Auditory system:
First the external ear channels sound to the tympanic membrane where the middle ear starts. The
middle ears purpose is to amplify sound. The ossicles connect the tympanic membrane to the oval
window, which leads to the inner ear. The ossicles amplify the sound like a series of levers. The
cochlea is the key in the inner ear. When the endolymph moves due to sound waves the vestibular
and basilar membranes move relative to each other. This causes the stereocilia to move which are
linked together by protein bridges, causing them to move together. At rest the there are K channels
that are open and closed, when moving towards the kinocilium the potassium channels open and the
cell depolarizes, causing more neurotransmitter to be released. When the hair moves the opposite
way the channels close, hyperpolarization occurs and no neurotransmitter is released. Low frequency
sounds are further from the oval window ( deeper in the curve of the cochlea)
Vestibular system:
Located in the inner ear
2. Describe the two chemical senses.
Taste:
Taste buds with pore and taste cells with microvilli that detect tastants.
 Salty- Na+ ions
 Sour- acid, tends to be unpleasant protects against excess acids
 Sweet- organic molecules such as sucrose. They are ligands in g coupled proteins
 Bitter- wide variety of N containing compounds. Several ways to affect, many include G couples
 Umami-response to amino acids most commonly mono sodium glutamate
90% of taste receptors respond to more then one primary taste and most respond to all four
Smell:
At the roof of the nasal cavity is the olfactory epithelium. Bipolar neurons with cilia detect the smells and
most involve Golf which activates adenylate cyclase, making cAMP. cAMP bind to cation chanells
allowing sodium and calcium to enter. One receptor cell responds to one type of odoront. Axons of
afferent neurons make up olfactory nerve.
External auditory meatus- the external ear canal
Tympanic membrane- also known as the ear drum
Ossicles- Three small bones in the middle ear. The malleus, incus, and stapes. The three ossicles connect
the tympanic membrane to the oval window.
Oval window- A thin membrane that connects the middle and inner ear.
Round window-another connection between the middle and inner ears
Eustachian tube- Connects middle ear with the pharynx to keep normal pressure in the middle ear
Cochlea- The organ at which sound transduction occurs. In it the vestibular and basilar membranes
separate the cochlea into the scala vestibuli, scala tympani, an scala media
Vestibular membrane- The upper membrane separating the cochlea
Basilar membrane- the bottom membrane separating the cochlea
Scala vestibuli-the upper cochlea chamber with the oval window attaching
Scala tympani-the lower cochlea chamber with the round window attaching
Scala media-the inner cochlea chamber which contains the organ of corti
Perilymph-Fluid in the scala vestibuli and scala tympani
Endolymph-fluid in the scala media. It is rich in potassium ions
Organ of corti-sensory organ for sound located on top of the basilar membrane. Contains hair cells and
the tectorial membrane
Hair cells- cells named for their hair like projections of stereocilia, the tips of which are embedded in the
tectorial membrane
Stereocilia-hair like projection from cells
Vestibular apparatus- The three semicircular canals, the utricle, and the saccule.
Semicircular canals- The canals that detect rotationals acceleration. Anterior does the “yes” movement.
Posterior detects ear to shoulder movement. Lateral detects “no”
Utricle -detects acceleration forward and backward
Saccule-detects acceleration up or down.
Ampulla- An enlarged area at the base of the semicircular canals, at the base has the cristae
Cupula- Gelatnous area separated from the endolymph by a membrane
Kinocilium- The largest hair in a hair cell in the semicircular canal
Otoliths- small calcium carbonate crystals that add mass to the gelatinous material
Taste buds- Where the chemoreceptors for taste are located. Each contains 50-150 receptor cells. At the
top is a pore that allws receptor cells to be exposed to saliva and dissolved food molecules. Taste cells are
modified epithelial cells with villi that reach into the pore
Tastants- Different chemicals that give foods their flavor. Interaction of tastant causes changes in the
membrane potential to change.
Olfactory epithelium- The roof of the nasal cavity which is the organ for smell. Two cell layers compose
it, the olfactory mucosa and the lamina propria
Olfactory binding proteins- proteins that bind to hydrophobic molecules to be transported across the
mucus to the cilia with receptors
Lesson 13: Autonomic and Motor System
1. Describe the anatomy of the somatic nervous system and the two branches of the autonomic
nervous system
Anatomy of Autonomic Nervous System:
Preganglionic and postganglionic neurons are arranged in series that bring information from the CNS
to the effector organ. The two neurons meet at synapses in peripheral structures called autonomic
ganglia.
Preganglionic neurons originate from the lateral horn, which is a region of gray matter in the spinal
cord.
The synapse between an efferent neuron and its effector organ is a neuroeffector junction.
Postganglionic neurons do not have discrete axon terminals. Neurotransmitters are released from
varicosities, which are numerous swellings along the axons. The membrane in the region of a
varicosity contains voltage-gated calcium channels that open when an action potential reaches them.
This allows neurotransmitters to be received throughout the entire effector organ.
Anatomy of the Sympathetic Nervous System:
There are three different possible arrangements of preganglionic and postganglionic neurons:
1 – Preganglionic neurons originate in the lateral horn of the thoracic or lumbar spinal cord, exit the
spinal cord and enter a sympathetic ganglion, where it synapses with several postganglionic neurons.
The postganglionic neuron travels to the effector organ.
2 – Group of long preganglionic nerves innervate the adrenal medulla instead of synapsing with
postganglionic neurons. Chromaffin cells are modified sympathetic postganglionic cells.
3 – Preganglionic neurons synapse with postganglionic neurons in collateral ganglia. Collateral
ganglia are found in pairs
Anatomy of the Parasympathetic Nervous System
Preganglionic neurons in the PNS originate in either the brainstem or the sacral spinal cord. They synapse
with postganglionic neurons in ganglia near the effector organ. In the cranial portion of the PNS,
preganglionic axons originate from cranial nerves in the brainstem and travel in cranial nerves. In the
spinal portion of the PNS, preganglionic neurons join together to form pelvic nerves (instead of traveling
with spinal nerves like in the SNS).
2. Describe the chemical messengers and receptor types associated with the peripheral nervous
system
Primary neurotransmitters in the peripheral nervous system are acetylcholine and norepinephrine.
Cholinergic neurons release acetylcholine. Adrenergic neurons release norepinephrine.
The two major classes of cholinergic receptors are nicotinic receptors, which are ionotropic receptors
(always excitatory because they are sodium and potassium channels), and muscarinic receptors, which are
metabotropic receptors (excitatory or inhibitory because they are GCPRs). Nicotinic receptors are in
postganglionic neurons of the SNS and PNS, chromaffin cells, and skeletal muscle cells. Muscarinic
receptors are in effector organs of the PNS.
The two major classes of adrenergic receptors are alpha receptors and beta receptors; both are GCPRs,
and both can be subdivided into three subtypes (alpha 1, alpha 2, alpha 3; beta 1, beta 2, beta 3).
Adrenergic receptors are located in effector organs of the SNS. Binding of norepi/epi to an alpha 1
receptor activates a G protein, which activates phospholipase C, which converts PIP2 to IP3 and DAG,
which triggers release of calcium from the ER, which causes a response. Binding of norepi/epi to an alpha
2 receptor activates an inhibitory G protein, which decreases the activity of adenylate cyclase. Binding of
norepi/epi to a beta receptor activates a stimulatory G protein, which increases the activity of adenylate
cyclase.
Alpha receptors have a greater affinity for norepinephrine and are generally excitatory. Beta 1 and 3
receptors have equal affinities and are generally excitatory. Beta 2 receptors have a greater affinity for
epinephrine and are generally inhibitory.
3. Explain the basic function of the two branches of the autonomic nervous system and the concept
of dual innervation
Dual innervation means that both branches of the autonomic nervous system (sympathetic and
parasympathetic) innervate most organs. Both the sympathetic and parasympathetic nervous systems
are active at all times, but one always dominates the other. The SNS is responsible for the fight-orflight response while the PNS is responsible for “rest and digest.”
4. Describe how the central nervous system regulates or controls the autonomic branch of the
peripheral nervous system
The CNS controls the ANS mainly through visceral reflexes, which are automatic changes in the
functions of organs due to changing conditions in the body. Major areas of the brain that regulate
autonomic function are the hypothalamus, pons, and medulla oblongata. The hypothalamus initiates
the fight or flight response and contains regulatory centers for body temperature, food intake, and
water balance. The medulla oblongata and pons regulate the heart and lungs.
Terms
Fight-or-flight – A set of physiological changes brought about by stimulation of the sympathetic nervous
system during periods of excitation or physical activity, which prepares the body to cope with threatening
conditions.
Preganglionic – Neurons that travel from the CNS to the ganglia
Postganglionic – Neurons that travel from the ganglia to the effector organs
Lateral Horn – Also known as the intermediolateral cell column. A region of gray matter that
preganglionic neurons originate from.
Sympathetic Chains – Links of sympathetic ganglia that run parallel to the spinal cord.
Collateral ganglia – Sympathetic ganglia independent of the sympathetic chain.
Vagus nerve – A cranial nerve that originates in the medulla and innervates much of the viscera (vital
organs).
Cholinergic – Neurons that release acetylcholine.
Adrenergic – Neurons that release norepinephrine.
Nicotinic receptors – Ionotropic cholinergic receptors
Muscarinic receptors – Metabotropic cholinergic receptors
Varicosities – Swellings along postganglionic neurons that function like axon terminals by releasing
neurotransmitters.
Visceral reflexes – Automatic changes in the functions of organs that occur in response to changing
conditions within the body.
*Lesson 14 was a lab
Lesson 15: Muscle I
1. Name the major structural features of a skeletal muscle cell, and briefly describe the relationship
between structure and function of each structural feature
Skeletal muscles are typically connected to at least 2 bones by tendons. Individual muscle cells are called
muscle fibers, which have many nuclei because each muscle fiber is formed by fused cells. The
membrane of a muscle cell is called the sarcolemma. The sarcoplasmic reticulum is a modified smooth
ER that surrounds myofibrils and stores calcium. Transverse tubules (T-tubules) are continuous with
the sarcolemma.
Myofibrils are made of myosin, which are thick filaments, and actin, which are thin filaments. Actin and
myosin are contractile proteins. Actin monomers are called G actin, and each has a myosin binding site.
Strands of G actin are called F actin. F actin is arranged in a double helix to form thin filaments. Myosin
molecules are dimers with heads called crossbridges, which can connect thin and thick filaments. The
heads of myosin have two sites: an actin-binding site (binds thin filaments) and an ATPase site (which
hydrolyzes ATP).
Tropomyosin and troponin are regulatory proteins that enable the start and stop of a contraction.
Tropomyosin blocks the myosin-binding sites of actin at rest. Troponin is a 3 protein complex: one
attaches to actin, one binds tropomyosin, and one that contains a calcium binding site.
Muscles are striated due to layers of thick and thin filaments, which run parallel along the length of a
muscle fiber. Sarcomeres are the individual units of a myofibril. The boundaries of the sarcomere are Z
lines, the middle is the M line. The A band is the center where actin and myosin overlap. The H zone
consists only of myosin. The I band consists only of thin filaments.
2. Describe the sequence of events that occurs in the crossbridge cycle, and relate this sequence to
the sliding-filament model of muscle contraction
Sliding filament model
Thin filaments slide past thick filaments, which means that the H zone shortens, the A band stays the
same size, and the I band shortens. The crossbridge cycle is the molecular mechanism that explains the
sliding filament model. Myosin molecules have 2 conformations (high energy form and low energy form),
and the crossbridge cycle is the oscillation between these 2 conformations. Steps of crossbridge cycle:
1. Binding of myosin to actin – myosin is bound to ADP and P. Myosin has a high affinity for actin
in this state. This step can only occur is calcium is present.
2. Power stroke – Binding of myosin to actin triggers release of P from the ATPase site. This causes
the myosin head to pivot towards the middle of the sarcomere, which pulls the thin filament.
3. Rigor – ADP is released from myosin so that myosin is in its low energy state. Myosin and actin
are tightly bound together in this state.
4. Unbinding of myosin and actin – A new ATP enters the ATPase site, which triggers a
conformational change that decreases the affinity of myosin for actin.
5. Cocking of the myosin head – ATP is split by hydrolysis into ADP and P, which releases energy
to bring myosin back to its high energy conformation.
During contraction, many cycles occur simultaneously but not in sync, which allows the muscle cell to
generate force continuously.
Excitation-contraction coupling is the process by which an action potential from a motor neuron
stimulates muscle contraction, which occurs at the neuromuscular junction. Each muscle fiber only
receives input from one motor neuron. The terminal buttons of the neuron fan out around the sarcolemma
onto boutons called the motor end plate, which has many acetylcholine receptors. The end-plate
potential is the depolarization on the motor end plate, which is a much greater than a normal
depolarization so that every action potential causes contraction. The action potential in a muscle cell
propagates down the entire sarcolemma down T tubules, then triggers release of calcium from the
sarcoplasmic reticulum. The release of calcium initiates the crossbridge cycle.
Binding of calcium to troponin causes tropomyosin to move away from the myosin-binding site of actin
so that the crossbridge cycle can occur.
Release of calcium from the sarcoplasmic reticulum occurs because dihydropyridine receptors (DHP
receptors) connect the action potential on a T tubule to the membrane of the sarcoplasmic reticulum. This
triggers a phenomenon called calcium-induced calcium release.
3. Identify the various factors that affect the force of muscle contraction
A motor unit is a motor neuron and all the muscle fibers it
innervates. A twitch is the mechanical response of an individual
muscle cell, a motor unit, or a whole muscle to a single action
potential. The latent period is the time between an action
potential reaching a muscle cell and the start of a contraction. The
contraction phase is the time between the start of the contraction
and the peak of muscular tension. The relaxation phase is the time
between peak tension and when tension returns to zero.
Repetitive stimulation of a muscle produces several twitches in a row, but each twitch is the same
magnitude and shape (like an action potential). Twitches vary from one muscle cell to another based on
diameter and whether the fiber is fast-twitch or slow-twitch.
Two variations of the twitch: isometric and isotonic. An isotonic twitch occurs when the muscle can
overcome the force placed on it, so the size of the muscle changes. An isometric twitch occurs when the
muscle cannot overcome the force placed on it, so the size of the muscle does not change because bones
do not move.
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Isotonic contraction – the muscle generates a constant tension barely greater than the force
opposing it, and muscle length changes. Measure by immobilizing one end of the muscle and
attaching it to a moveable load. Size and shape of the twitch depends on the size of the load
placed on the muscle.
o Concentric contraction – Muscle contraction involving shortening of the muscle
o Eccentric contraction – Muscle contraction involving lengthening of the muscle
Isometric contraction – Muscle generates tension but maintains the same length because the
load is greater than the force generated by the muscle. Measure by immobilizing both ends of the
muscle and electrically stimulate the muscle.
During an isometric contraction, sarcomeres shorten even though the entire muscle does not change
length because sarcomeres do not extend the entire length of the muscle fiber.
Force generated by a muscle depends on the force generated by individual muscle fibers (depends on
number of active crossbridges) and the number of muscle fibers contracting. The number of active
crossbridges depends on frequency of stimulation, fiber diameter (larger = more force), and changes in
fiber length (not too long or too short).
At high stimulation frequency, the rate of calcium release is greater than the rate of calcium reuptake, so
the amount of calcium in the cytosol continuously increases, which means more calcium is bound to
troponin so that more myosin-binding sites on actin are exposed, and peak tension increases. As
stimulation frequency increases, muscles move from twitch contractions → treppe → summation →
tetanus. Treppe occurs at a frequency of stimulation where individual twitches are not completely
separate so that peak tension rises in a stepwise fashion. Summation occurs at a frequency of stimulation
where twitches overlap because the muscle cannot fully relax between action potentials. Tetanus occurs
at high frequency of stimulation when troponin is saturated with calcium.
Recruitment is an increase in the number of active motor units. The size principle is the idea that smaller
motor units are recruited before larger motor units. This occurs because both motor units and the motor
neurons that control them vary in size.
Lesson 16 – Muscle II
Muscle cells contain small stores of ATP that can be used when it contracts. To ensure a steady supply of
ATP, muscles use creatine phosphate which donates a phosphate to ADP to make ATP (Catalyzed by
creatine kinase). This supplies ATP while metabolic reactions begin. Metabolic reactions first utilize
muscle glycogen stores, then glucose from the bloodstream, the fatty acids from the bloodstream.
1. Name the three types of skeletal muscle fibers, and describe the major differences among them
Fast twitch and slow twitch fibers differ in the type of myosin in their thick filaments. Fast myosin is able
to hydrolyze ATP at a faster rate than slow myosin so that it can complete more crossbridge cycles per
second.
White muscle consists of glycolytic fibers. Red muscle consists of oxidative fibers (red = more
mitochondria and myoglobin). Glycolytic fibers more easily preform glycolysis while oxidative fibers
more easily carry out oxidative phosphorylation (more mitochondria). Oxidative fibers have a smaller
diameter, better blood supply, and myoglobin.
Slow oxidative fibers contain slow myosin and have a high oxidative capacity (smallest diameter). Fast
glycolytic fibers contain fast myosin and have a high glycolytic capacity (largest diameter). Fast
oxidative fibers have a high oxidative capacity and contain fast myosin. The different types of fibers are
intermixed in skeletal muscle, but are not all utilized every time a muscle contracts.
Fatigue is a decline in a muscle’s ability to maintain constant force of contraction. Fatigue occurs because
of lactic acid production and compression of blood vessels. In low intensity exercise, fatigue occurs
because of glycogen depletion. Very high intensity exercise causes neuromuscular fatigue, which is when
acetylcholine is depleted.
Muscle spindles – receptors that detect muscle length
2. Describe the major characteristics of smooth and cardiac muscle, and compare these muscle types
to skeletal muscle
Smooth muscle is not striated. It is found in organs and blood
vessels and is under autonomic control. Differs from skeletal
muscle in that its filaments are not arranged in sarcomeres and
contracts occur along multiple axes. Calmodulin is the protein in
smooth muscle that calcium binds to stimulate contraction.
Myosin light chain kinase (MLCK) is an enzyme that catalyzes
the phosphorylation of myosin crossbridges after it is activated by
the calcium-calmodulin complex. Termination of the crossbridge
cycle requires removal of phosphate groups from myosin to
inactivate myosin and a removal of cytosolic calcium. It takes
longer to initiate and terminate smooth muscle contraction than in
skeletal muscle.
Smooth muscle is innervated by the sympathetic and/or parasympathetic nervous system, so stimulation
could be excitatory or inhibitory. Due to varicosities in autonomic neurons, the activity of smooth muscle
is more synchronized. Smooth muscle can have a level of resting tension called tone due to a base level of
calcium that is high enough to maintain crossbridge activity.
Multi-unit smooth muscle is when the cells are separate and the muscle has a dense supply of neurons
(ex: respiratory airways, large arteries). Single-unit smooth muscle is when the cells are linked by gap
junctions such that electrical signals originating in a few cells are transmitted to the rest of the cells.
Smooth muscle can exhibit spontaneous depolarizations of two types: Pacemaker potentials (slow
depolarizations caused by an increase in permeability to sodium, calcium, or a decrease in permeability to
potassium) and Slow-wave potentials (cyclic depolarizations and repolarizations caused by fluctuations
in sodium permeability).
Cardiac Muscle is similar to skeletal muscle in that it is striated, has the same sarcomere structure as
skeletal muscle, and has contractions that are regulated by the troponin-tropomyosin system. It is similar
to smooth muscle in that it has extensive gap junctions for more coordination. Cardiac action potentials
are long so that they are about the same length of time of a cardiac muscle contraction so that summation
of contraction cannot occur, even when the heart is beating rapidly.
Lesson 17 – Endocrine system I: Organs and Hormones
1. Name the primary and secondary endocrine glands, and the hormones associated with each
Primary endocrine glands have the primary function of secreting hormones, such as the hypothalamus.
Secondary endocrine organs are organs with separate functions that also secrete hormones. The secondary
endocrine organs are the heart (atrial natriuretic peptide), kidneys (erythropoietin), digestive organs
(gastrin, secretin, CCK), liver (IFGs), and skin (1,25-dihydroxy vitamin D3).
The Pineal gland regulates the circadian rhythm by secreting melatonin.
The thyroid gland regulates metabolism and development by secreting tetraiodothyronine (T4),
triiodothyronine (T3), and calcitonin. T4 and T3 regulate metabolism. Calcitonin decreases blood calcium
levels.
The parathyroid glands secrete parathyroid hormone, which increases blood calcium levels.
The thymus secretes thymosin, which regulates T-cell function.
The adrenal glands consist of the adrenal cortex and adrenal medulla. The
adrenal cortex secretes adrenocorticoids, which include mineralocorticoids
(such as aldosterone), glucocorticoids (such as cortisol), and sex hormones
(such as androgens). The adrenal medulla secretes catecholamines such as
epinephrine and norepinephrine.
The pancreas is an exocrine and endocrine organ. The endocrine pancreas
consists of islets of Langerhans, which produce insulin from beta cells and glucagon from alpha cells.
The gonads secrete sex hormones, primarily androgens in males and estradiol and progesterone in
females.
2. Describe the links between the hypothalamus with the anterior and posterior pituitary lobes
The hypothalamus and pituitary gland work together to regulate the body. The hypothalamus is a primary
endocrine gland because its primary functions is to secrete hormones. Some hormones from the
hypothalamus affect the pituitary gland, which is divided into the anterior lobe (epithelial tissue) and the
posterior lobe (neural tissue).
Axons from the hypothalamus terminate in the posterior pituitary that secrete ADH (vasopressin) and
oxytocin. ADH and oxytocin are
neurohormones because they are
secreted by neurons. The
neuroendocrine reflex is when ADH
and oxytocin are released from neurons
in response to neural stimulation.
The hypothalamus is connected to the
anterior pituitary by the hypothalamicpituitary portal system (arrangement of
blood vessels in series). Tropic
hormones from the hypothalamus
stimulate the release of other tropic
hormones from the anterior pituitary,
which then stimulate the release of
direct hormones in another endocrine
organ.
3. Describe the role of tropic hormones in regulating the release of other hormones including the
feedback loops involved in this process
Feedback loops regulate multistep pathways. Short loop negative feedback is when the anterior pituitary
hormones inhibit the respective hypothalamic hormone (Ex: TSH inhibits TRH). Short loop negative
feedback prevents the buildup of excess anterior pituitary hormone. Long loop negative feedback is when
the hormone at the end of the pathway inhibits the hypothalamic hormone (Ex: TH inhibits TRH).
The concentration of a hormone in the blood depends on the rate of hormone secretion, the amount of
hormone transported bound to carrier proteins, and the rate at which the hormone is metabolized.
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Endocrine cells alter hormone secretion in response to neural signals and humoral signals, which
can both be either excitatory or inhibitory. Humoral signals can be hormones, ions, or
metabolites. Many hormones are governed by circadian rhythm.
Only hormones that are unbound by carrier proteins can bind a receptor on a target cell. Carrier
proteins increase the half life of a hormone in the blood.
Hydrophobic hormones have a longer half life in blood than hydrophilic hormones because they
are bound to carrier proteins and they can be stored in fatty tissue.
4. Describe the types of interactions between hormones acting on the same target cell, including
additive, synergistic, and permissive interactions
Antagonism is when the effects of two hormones oppose each other, such as with calcitonin and
parathyroid hormone.
When two hormones produce the same response, their effects can either be additive or synergistic. They
are additive if the net effect equals the sum of the individual effects. They are synergistic if the net effect
is greater than the sum of the individual effects.
Permissiveness is when the presence of one hormone is needed for another hormone to act.
Lesson 18 – Cardio I
1. Identify the major components of the cardiovascular system, and briefly describe their functions.
The cardiovascular system consists of the heart, blood vessels, and blood.
The heart generates force that propels blood through blood vessels. It consists of two atria, which are the
upper chambers, and two ventricles, which are the lower chambers.
Vasculature is a system of blood vessels. As blood moves away from the heart, the blood vessels branch
and each branch is smaller in diameter; arteries branch into arterioles, which branch into capillaries.
Capillaries connect to venules, which connect to veins, which carry blood back to the heart.
Blood is ½ cells, ½ plasma. The cells in blood are erythrocytes and leukocytes. Blood also contains
platelets. The liquid portion of blood is called plasma.
2. Identify the major structures of the heart, and describe the path of blood flow through the heart
and vasculature.
The path of blood flow through the body can be divided into the pulmonary circuit and the systemic
circuit. The right heart supplies blood to the pulmonary circuit. The left heart supplies blood to the
systemic circuit. Capillary beds are dense networks of capillaries where gas exchange occurs.
The path of blood flow through the heart: left ventricle pumps oxygenated blood through the aortic
valve into the aorta, which leads blood to systemic circulation. Deoxygenated blood reenters the heart in
the venae cavae, which empty blood into the right atrium. Blood passes through the tricuspid valve
into the right ventricle, which pumps blood to the pulmonary arteries, which bring blood to pulmonary
circulation. Oxygenated blood enters the left atrium through the pulmonary vein. The blood from the
pulmonary vein goes through the mitral valve to enter the left ventricle.
Blood flow in the systemic circuit is called parallel flow because the path of blood is not sequential
(remember that vessels branch into smaller vessels). The heart works in parallel with the other organs in
the systemic circuit. This is important because it allows each organ to receive fully oxygenated blood, and
blood flow to each organ can be independently regulated.
The coronary arteries branch off the aorta and run through the heart muscle to deliver oxygen and
nutrients to the heart itself.
The cardiac cycle describes a heartbeat; the atria contracts before the ventricles. The heart has 4 valves
that prevent blood from flowing backwards. The atrium and ventricle are separated by atrioventricular
valves (AV valves) which allow blood to flow only from the atrium to the ventricle. The AV valves open
when atrial pressure is higher than ventricular pressure and close when ventricular pressure is higher than
atrial pressure. The AV valve on the left is called the bicuspid or mitral valve. The AV valve on the right
is called the tricuspid valve. Chordae tendineae are strands of connective tissue that prevent prolapse in
the AV valves, which is when the valves cannot completely seal. Semilunar valves are between the
ventricles and arteries. The aortic valve is the semilunar valve on the left. The pulmonary valve is the
semilunar valve on the right.
3. Trace the path action potentials through the conduction system of the heart and relate the heart’s
electrical activity to its pumping action.
Cardiac muscle uses myogenic contractile activity, meaning that it does not require external stimulation to
contract. Autorhythmicity is the ability of the heart to generate signals for contraction on a periodic basis.
Autorhythmic cells provide coordination of heart muscle cells to generate a heartbeat. Two types of
autorhythmic cells are pacemaker cells, which initiate action potentials, and conduction fibers, which
transmit action potentials through the heart. Pacemaker cells and conduction fibers make up the
conduction system of the heart. The cells that contract are called contractile cells.
Pacemaker cells are concentrated in the sinoatrial node (SA node) (wall of upper right atrium) and the
atrioventricular node (AV node) (near tricuspid valve). The SA node is the pacemaker of the heart.
Conduction fibers have a larger diameter, which means they can more quickly transmit action potentials.
Intercalated disks have a high density of gap junctions that can transmit electrical current in the form of
ions from one cell to the next.
Initiation and conduction of an impulse during a heartbeat:
1. An action potential is initiated in the SA node; impulses travel to the AV node by internodal
pathways, which are systems of conduction fibers that run through the walls of the atria.
2. AV node transmits action potentials more slowly (AV nodal delay)
3. Impulses travel from AV node to the bundle of His.
4. AV bundle splits into bundle branches, which conduct impulses to the right and left ventricles.
5. From bundle branches, impulses travel to Purkinje fibers, which spread through the ventricular
myocardium towards the valves.
The AV node can take over contraction if the SA node isn’t working, but the heart rate will be sloswer
because the AV node fires action potentials more slowly.
Pacemaker cells can fire action potentials spontaneously because they do not have a steady resting
potential. After an action potential, a pacemaker cell immediately begins to slowly depolarize until
reaching threshold. The slow depolarization is called pacemaker potential.
Increased permeability to sodium or calcium results in the cell becoming more positive. Increased
permeability to potassium results in the cell becoming more negative. Slow depolarization occurs due to
closing of potassium channels and opening of “funny channels.” Funny channels open after the cell
repolarizes to allow sodium and potassium ions to cross the membrane.
Contractile cells vary in the type and number of ion channels they process, which changes the speed of
propagation in different parts of the heart. Two important constants of cardiac action potentials:
1. Permeability to potassium decreases as a result of voltage-gated potassium channels that close
due to depolarization. Permeability to potassium increases during an action potential.
2. Depolarization causes opening of voltage-gated calcium channels, which trigger muscle
contraction.
Majority of ventricular muscle cells make up the bulk of the myocardium and have stable resting
potentials and longer-lasting action potentials.
Phases of cardiac action potential in ventricular muscle cells:
0. Depolarization of membrane triggers opening of
voltage-gated sodium channels, which increase sodium
permeability so that membrane potential becomes
more positive.
1. Sodium channels become inactivated so membrane
potential begins to fall. Voltage gated potassium
channels close so less potassium can leave the cell.
Calcium channels open so calcium enters the cell.
Both of these events prevent the membrane potential
from falling quickly.
2. Plateau phase – Most of the potassium channels that
were closed in phase 1 stay closed, and calcium channels remain open. The cell remains
depolarized.
3. Potassium permeability increases due to the slow opening of delayed rectifier channels so that
potassium leaves the cell and membrane potential falls.
4. Resting potential.
Current through gap junctions stimulates contraction of a cardiac muscle cell.
1. An action potential spreads through the plasma membrane and down T tubules
2. Voltage sensitive calcium channels on the sarcoplasmic reticulum open and calcium is released
into the cytosol
3. Action potential triggers opening of voltage gated calcium channels in the plasma membrane so
that calcium enters the cell.
4. Calcium that enters the cell triggers further opening of sarcoplasmic reticulum calcium channels
(calcium induced calcium release).
5. Calcium binds troponin, tropomyosin shifts off the myosin binding sites of actin, actin binds
myosin.
6. Crossbridge cycling occurs.
7. Calcium is removed from the cytosol so that the muscle relaxes.
8. The muscle fiber is relaxed.
The electrocardiogram (ECG, EKG) measures the electrical activity of the heart. Electrodes are placed in
Einthoven’s triangle. Shows 3 characteristic waveforms:
1. P wave – upward deflection due to atrial depolarization
2. QRS complex – series of sharp upward and downward
deflections due to ventricular depolarization
3. T wave – upward deflection caused by ventricular
repolarization.
Ventricular systole is the contraction of ventricles. It is estimated as the time between the outset of the
QRS complex and the end of the T wave.
Ventricular diastole is the relaxation of ventricles. It is estimated as the time between the end of the T
wave and the beginning of the QRS complex.
The R-R interval is the time between heart beats.
Lesson 19- Cardio II
Cardiac cycle and Control of Cardiac Output
Page 377-390
1. Explain the following events in the cardiac cycle: changes in ventricular, aortic, and atrial
pressure, changes in ventricular volume, and heart sounds
The cardiac cycle can be divide into
two major stages systole and
diastole. Systole is ventricular
contraction while diastole is
relaxation. Stages are written below
starting in mid-diastole.
Ventricular filling- Mid to late
diastole. Blood returning (from
systemic or pulmonary branches)
enters relaxed atria and passes
through AV valves into the
ventricles under its own pressure.
The return of blood from veins to
heart occurs because P of veins is
greater than that in the atria. The
pulmonary and aortic valves are
closed because the ventricular
pressure is lower than the aorta and
pulmonary arterias. Late in this
phase the aria contract driving more
blood to the ventricles. The entire
phase is called ventricular filling.
Isovolumetric contraction- At the
beginning of systole (ph 2) the
ventricles contract, raising the pressure. When pressure ventricle>atria the AV valves close and the
semilunar valves stay closed because pressure is not yet high enough to open them. It is called
isovolumetric contraction because the volume of blood in the ventricle is staying constant?
Ventricular ejection- In the remainder of systole (phase 3) blood is ejected out of the ventricles through
the semilunar valves and ventricular volume falls. During the exit of blood ventricular pressure peaks and
then declines, when it falls under aortic pressure the semilunar valves close ending both ventricular
ejection and systole.
Isovolumetric relaxation- at the onset of diastole the ventricular myocardium is relaxing. Some blood is
present in the ventricles. Ventricular pressure is spontaneously to low to open the semilunar valves and to
high for the AV valves to open resulting in isolvolumetric relaxation. Once the ventricular pressure
decreases past atrial, the AV valves open, allowing blood to enter the ventricles from the atria.
Diastole is the majority of a heart beat.
Heart sounds have a first soft low pitched lubb and a second louder and sharper dupp. They are caused by
the closing of AV valves and the closing of semilunar valves. The sounds are caused by the turbulent
rushing of blood.
2. Explain the difference between extrinsic control and intrinsic control and identify how these
terms relate to the regulation of the heart
Regulation by extrinsic control is done by things outside the organ. When the function of an organ or
tissue is within the organ itself it is under intrinsic control.
3. Explain how each of the following variables affect Cardiac output: sympathetic and
parasympathetic nervous activity, circulating epinephrine, afterload, preload, end-diastolic
volume, ventricular contractility, and filling time
Cardiac output = HR *SV.
Sympathetic neurons release norepinephrine which binds to B1 adregenic receptors on the SA node and
activate the cAMP messenger system. This leads to changes in the opening of funny channels and T type
calcium channels. The result is an increase in the slope of spontaneous depolarization and a decrease of
repolarization. Sympathetic stimulation also makes ventricles contract more quickly after atrial
contraction.
Hormonal control- Epinephrine is significant in the minute to mute regulation of function. The adrenal
medulla secretes it. It acts similarly to sympathetic arousal and increases action potentials at the SA node
while increasing the velocity of an action potential through muscle.
Stoke volume:
Stoke volume is also an important regulator of cardiac output. This is primarily controlled by
1. Ventricular contractility- the force of ventricular contraction at any given end diastolic volume.
a. Sympathetic control- autonomic control of SV is almost entirely sympathetic. As
sympathetic stimulation decreases ventricular contractility. Norepinephrine does this by
changing the open state of calcium channels, increasing calcium flow. They enhance the
release of calcium from the sarcoplasmic reticulum. They increase the rate of myosin
ATPase. They enhance the rate of Ca2+ ATPase activate in the sarcoplasmic reticulum,
increasing reuptake.
b. Hormonal control- epinephrine produces similar results to norepinephrine
2. End diastolic volume
a. Starling’s law of the heart: when the rate at which blood flows into the heart from the
veins changes, the stretch of the myocardium changes, causing the ventricle to contract
with changing force.
b. If an increase in end diastolic volume occurs the force of contraction rises, producing an
increase in SV and CO
c. Stretching in the myocardium increases contraction by :
i. Increasing the length of the muscle fiber close to its optimal length ( not its
resting length)
ii. Increased affinity of troponin for calcium in stretched fibers
d. Partly determined by end diastolic pressure- preload. Determined by
i. Filling time
ii. Atrial pressure
3. Afterload- arterial pressure places a load on the myocardium after contraction starts. Increases in
arterial pressure decrease stroke volume.
Lesson 20 – Cardio III Blood Flow and Blood Pressure and Liam’s B
1. Describe the physics of blood flow through blood vessels. Explain the concepts of pressure
gradient and resistance
Flow = change in pressure over resistance. The pressure gradient is the force that pushes liquid through a
pipe. The resistance is a measure of factors that hinder flow.
Fluid moves from higher pressure to lower pressure. Blood flow in the cardiovascular system is bulk flow
because the driving force is a pressure gradient. The heart increases mean arterial pressure by pumping
blood into the arteries, which creates a pressure gradient between arteries and veins.
Pressure gradients in the systemic circuit:
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Mean arterial pressure (MAP) = the average pressure in the aorta throughout the cardiac cycle (85
mm Hg)
Central venous pressure (CVP) – the pressure in the vena cava (2-8 mm Hg)
The difference between the MAP and the CVP drives blood through the cardiovascular system. Because
CVP is close to zero, the pressure gradient in the cardiovascular system approximately equals MAP.
Pressure gradient in the pulmonary circuit is the difference between the pressure in the pulmonary arteries
and in the pulmonary veins. This gradient is approximately 15 mm Hg.
To keep blood flow equal in systemic and pulmonary circulation despite their different pressure gradients,
the resistance is different. The pulmonary circuit has less resistance than the systemic circuit.
Factors that change resistance:
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Vessel radius – becomes smaller (more resistance) via vasoconstriction, or larger (less resistance)
via vasodilation.
Vessel length – Longer vessels have greater
resistance than shorter ones.
Blood viscosity – Resistance increases as
viscosity increases. The major factor that
changes viscosity is the concentration of
cells/proteins in the blood.
A network of blood vessels also has resistance (ex:
vasodilation anywhere within the network decreases
the total resistance of the network). Total peripheral
resistance (TPR) is the combined resistances of all the
blood vessels within a circuit.
Cardiac Output (CO) = (MAP)/(TPR).
2. Describe the anatomy of the vasculature, and
explain the basic functional properties of the
different types of blood vessels
Microcirculation = arterioles, capillaries, and venules.
Capillaries consist of a layer of epithelial cells and a basement membrane.
All other blood vessels have a layer of smooth muscle and fibrous and/or elastic connective tissue. The
fibrous connective tissue contains collagen,
elastic connective tissue contains elastin.
Arteries
The larger the artery, the more elasticity and
less resistance. Smaller arteries have less
elastic tissue and more smooth muscle which
enables better regulation of the radius.
Arteries are pressure reservoirs because they
can be stiff and flexible, ensuring continual
flow. During diastole, arterial walls passively
recoil inward, which propels blood forward.
Arteries have low compliance, which means
that a small increase in blood volume causes
a large increase in blood pressure, due to their
elasticity.
Arterial blood pressure is the pressure in the
aorta. Systolic pressure is the maximum
pressure, and diastolic pressure is the
minimum pressure. Pulse Pressure is the
difference between systolic pressure and
diastolic pressure.
Arterioles
Arterioles provide the greatest resistance to blood flow. The greatest pressure drop occurs in the
arterioles. Arterioles control blood flow to individual capillary beds and regulate MAP. Resistance is
regulated by contraction and relaxation of circular smooth muscle. Ateriolar tone is the resting level of
contraction (remember it’s smooth muscle).
Capillaries
Highly branched with overall surface area of over 600 square meters. Capillaries exist in capillary beds.
There are three types of capillaries:
-
-
Continuous capillaries: endothelial cells are joined by tight junctions. Highly permeable to small
water soluble substances that can move through the intercellular cleft and to lipid soluble
substances.
Fenestrated capillaries: Endothelial cells with pores that allow rapid diffusion of small watersoluble substances; can be large enough for proteins. Found in the kidneys and intestines.
Discontinuous capillaries: Transition from fenestrated capillaries to sinusoids so that proteins and
cells can cross the endothelium (ex: bone marrow). Sinusoids are large blood-filled spaces that
function as the exchange of substances between blood and tissue.
Venules
Slightly smaller than arterioles, very thin walls with little to no smooth muscle. Pores allow for fluid
exchange.
Veins
Larger than arteries but thinner walls because blood pressure in veins is lower than blood pressure in
arteries.
Contain one way valves that prevent backflow. Only peripheral veins (veins not in the thoracic cavity)
have valves; central veins (in the thoracic cavity) and veins in the CNS do not.
Veins are volume reservoirs because they are easily stretched and have high compliance. A small increase
in pressure causes a large degree of expansion and therefore an increase in volume.
3. Explain the role of arterioles in varying resistance. Describe how intrinsic control of vascular
resistance regulates blood flow to organs. Explain the role of extrinsic control of the arteriole
radius in determining the mean arterial pressure
Intrinsic controls include local metabolites that regulate blood flow to match the metabolic needs of the
cells in each region. Extrinsic controls include the autonomic nervous system and hormones. Each organ
has a different resistance, which accounts for the different volumes of blood flow to different organs.
Changes in distribution of blood flow result from changes in vascular resistance of individual organs.
Organs change their resistance by vasoconstriction or vasodilation of arterioles within that organ. Intrinsic
control mechanisms are especially important in regulating blood flow to the heart, brain, and skeletal
muscles.
Arterioles respond to changes in the concentration of various components in extracellular fluid. If the
changes are associated with increased metabolic activity, vasodilation occurs. If the changes are
associated with decreased metabolic activity, vasoconstriction occurs. When intrinsic control changes
resistance in individual capillary beds, extrinsic control has to ensure that mean arterial pressure stays the
same.
The sympathetic nervous system innervates smooth muscle of most arterioles. All arteriolar smooth
muscle has alpha receptors, while skeletal and cardiac muscle also have beta 2 receptors. Norepinephrine
released from sympathetic neurons bind to alpha receptors and cause vasoconstriction, which increases
MAP. At very high levels of sympathetic activation, epinephrine binds both alpha and beta 2 receptors.
Beta 2 receptors cause vasodilation so that blood flow to the heart and skeletal muscle increases while
overall blood pressure still increases due to vasoconstriction in the rest of the body.
Lesson 21- Cardio IV
Small Blood vessels, veins, and regulation of mean arterial pressure
Page 411-430
1. Explain how material is exchanged between blood and interstitium. Describe the forces that cause
bulk flow of fluid across capillary walls.
Precapillary sphincters regulate smooth muscle that surrounds capillaries on the arteriole end. Contraction
constricts the capillaries, which increases resistance. Precapillary sphincters relax and contract in response
to local metabolites.
Movement of materials across capillary walls allows for exchange of material between blood and cells
and normal distribution of extracellular fluid.
Filtration is movement of fluid from blood to interstitial fluid
Absorption is movement of fluid from interstitial fluid to blood
Edema is swelling of tissue resulting from a shift in fluid from plasma to interstitial fluid.
Starling Forces are the forces that determine direction of flow in a capillary:
-
-
Capillary hydrostatic pressure (Pcap) – hydrostatic pressure of fluid pushing out on capillary
walls
Interstitial fluid hydrostatic pressure (Pif) –
hydrostatic pressure of fluid pushing in on
capillary walls
Capillary osmotic pressure (πcap) – due to
presence of solutes in the capillary
Interstitial fluid osmotic pressure (πif) – due to
presence of nonpermeating solutes outside the
capillary
Capillary hydrostatic pressure and interstitial fluid
osmotic pressure both draw fluid out of the capillary
(filtration). Interstitial fluid hydrostatic pressure and
capillary osmotic pressure both push fluid into the
capillary (absorption).
Net filtration pressure determines the net direction of fluid movement. NEP = filtration pressure –
absorption pressure = (Pcap + interstitial osmotic) – (Cap osmotic + Pif)
Capillary hydrostatic pressure varies along the length of the capillary while the other Starling forces are
relatively constant. Capillary hydrostatic pressure is higher at the arteriole end and lower at the venous
end, so that net flow is out at the arteriole end and in at the venous end.
2. Explain how mean arterial pressure influences blood flow to individual organs and to the entire
systemic circuit and identify the factors that determine the mean arterial pressure.
MAP= CO x TPR = HR x SV x TPR
This equation is fairly straight forward to interpret- increases to any of these individual factors will
increase MAP.
Neural control- MAP is a regulated variable that is managed through negative feedback control. The
sensors for measuring MAP are arterial baroreceptors.
-Baroreceptors are found in the aortic arch and the carotid sinus of the carotid arteries. Stretching
induces depolarization for these neurons
The center for neural control is the Medulla Oblongata in the cardiovascular control center
The cardio vascular control center gets input from sensory receptors such as the low pressure
baroreceptors ( in the right atria and systemic veins) and brain input for the hypothalamus. This helps
coordinate the stress response
The center communicates with:
-
Sympathetic & Parasympathetic nerves to SA node (HR)
Sympathetic nerves to ventricles (contractility)
Sympathetic to arterioles and other resistance vessels (resistance)
Sympathetic nerves to veins (venomotor tone)
The main controller is sympathetic (parasympathetic really only has a role at the SA)
3. Describe what the arterial baroreceptor reflex is and explain how it regulates mean arterial
pressure
Baroreceptors are sensory receptors that respond to changes in pressure.
The baroreceptor reflex restores normal blood pressure. A fall in arterial pressure is detected by arterial
baroreceptors, which trigger an increase in sympathetic activity and a decrease in parasympathetic activity
so that heart rate, myocardial contractility, and vascular resistance all increase.
4. Describe how changes in arterial carbon dioxide level, body heat, and exercise affect
cardiovascular function and mean arterial pressure.
CO2-When Co2 rises, chemoreceptors stimulate breathing. The effects on the cardiovascular system are
difficult to predict as they can be changed by primary or secondary factors.
-
When CO2 Rises a decrease in heart rate and an increase in peripheral resistance occurs.
Decreasing heart rate decreases the hearts uses of oxygen. Increased resistance offsets changes in
MAP
Thermoregulation-Increased body temp decreases sympathetic activity in skin vessels, relaxing vascular
smooth muscle. Sweat glands produce bradykinin to vasodilate as well.
Lesson 22- Cardio V Blood
Pages 433-446
1. ID the major components of blood and describe their function
The blood is mostly plasma(3 L) and erythrocytes (2.5 L), but also contains leukocytes and platelets.
Plasma is least dense, then the leukocytes and platelets are a thin layer, than hemocrit is on the bottom.
Plasma is an aqueous solution with proteins, small nutrient molecules, metabolic waste products, gases,
and electrolytes. Plasma is very similar to interstitial fluid with respect to small solutes but is very
different with respect to proteins. The concentration of protein in plasma is much higher. Plasma proteins
have three main categories albumins, globulins, and fibrinogen. Albumins are made in the liver and the
most abundant- they make a large contribution to the osmotic pressure. The globulins are a wide range
and transport lipids, steroid hormones, and other substances, they also play an important role in clot
formation and defending against substances. Fibrinogen is made in the liver and is a key substance in
blood clots. Serum is plasma that has fibrinogen and other clotting proteins removed.
Erythrocytes major function is to transport oxygen and carbon dioxide. Their cytoplasm contains two
important proteins for this: hemoglobin and carbonic anhydrase.
2. Describe the life cycle of red blood cells
Once released into the blood stream
RBCs only stay about 120 days. They
have neither a nucleus or organellesthis means that RBCs cannot undergo
cell division. These are produced by a
process called erythropoiesis. In
this process the spleen removes old
RBCs.
Blood cells all come from
precursor hematopoietic cells in the
bone marrow. Erthrocytes and
leukocytes come to full maturity in
the bone marrow but T
lymphocytes must go to the thymus
gland. The HGF that stimutlates
erthrocyte production is
erthropoietin. Stimulants of leukocytes are colony stimulating factor and interleukins.
Erhtropoietin is released by the kidney in response to low ox in the blood. The last step before
differentiation is a reticulocyte which is a RBC with some ribosomes still present.
A shortage in the dietary elements for erthropoiesis can reduce the amount of hemoglobin per
cell or the amount of cells. Producing anemia. Iron causes iron deficiency anemia, pernicious
anemia is due to lack of B12.
Most old RBCs are engulfed by macrophages in the spleen. After Iron is removed, the resulting heme is
converted to bilirubin where it travels to the liver and is catabolized further. Iron is recycled however and
is transported in blood by transferrin. Iron is stored bound to ferritin.
3. ID the different classes of leukocytes, and explain their roles in the body’s defense against
pathogens
Neutrophils- 50-80% of all leukocytes and are capable of phagocytosis. Newly produced circulate 7-10
hours, migrate to tissues and live only a few days. Elevated neutrophils (neutrophilia) indicate bacterial or
viral infections.
Eosinophils- phagocytic but attack larger parasitic invades by attaching to them and releasing toxic
molecules
Basophils- nonphagocytic that defend against larger parasites. Basophils also release histamine, heparin,
and chemicals associated with allergic reactions.
Monocytes- important to phagocytotic defense. Circulate for few hours -> move to tissues -> enlarge.
Then they become macrophages. Macrophages can differentiate into dendritic cells. Typically, dendritic
cells are found in epithelial tissues Their roles are antigen presentation
Lymphocytes- three types. B lymphocytes, T lymphocytes, and null cells. Most null cells are large
granular lymphocytes known as natural killer cells. B lymphocytes differentiate into plasma cells that
secrete antibodies. T cells can destroy abnormal cells, helper T cells promote the action of leukocytes,
suppressor T cells serve to decrease the immune response.
4. Describe platelets and the mechanism of clot formation.
Platelets are colorless cell fragments that are broken off pieces of megakaryocytes. They are smaller than
RBCs and contain mitochondria, a smooth Er, and cytoplasmic granules with no nucleus. The process of
hemostasis occurs in three steps: vascular spasm, formation of a platelet plug, and formation of a blood
clot (thrombus).
Vascular spasm:
The internal mechanisms that cause contraction that resists blood flow. This also activates the
sympathetic- further causing vasoconstriction.
Platelet plug:
Platelets (thrombocytes) posses granules with substances for secretion such as ADP, serotonin,
epinephrine, an clot forming chemicals. The key protein is von Willebrand factor. The first step is platelet
adhesion. vWf binds to collagen in exposed subendothelial tissue and causes platelet binding to vWf. This
simultaneously activates platelets. Activated platelets secrete serotonin and epinephrine, causing
vasoconstriction. ADP is also secreted causing platelet aggregation; it does so by causing morphological
changes that allows them to adhere to one another. It also stimulates thromboxane A2 (TXA2) production
which further supports aggregation. TXA2 is formed from arachidonic acid and has many rolesvasoconstriction, ADP secretion, and platelet aggregation.
Healthy endothelial tissue releases prostacyclin and nitric
oxdie which inhibit aggregation. Prostacyclin is also made
from the conversion of arachidonic acid. Actin and myosin
are higher in platelets and act to contract and increase
tightness in a plug.
Blood clot:
Fibrin is the last necessary ingredient which is necessary to
convert the blood to a gel. Fibrin clot formation is secondary
because it requires activated platelets. It also requires the
coagulation cascade which involves the proteolytic
activation of coagulation factors. Coagulation factors are
largely numbered by roman numerals in the order of their
discovery.
The ultimate step is the conversion of fibrinogen to fibrin
catalyzed by thrombin- the active form of prothrombin.
Fibrin polymers adhere to one another causing a loose
meshwork. This is then stabilized by covalent linkages between strands (preformed by facto XIIIa).
Central to the stable fibrin meshwork is the activation of thrombin. This is performed by prothrombin
activation complex (Xa) with factor V, Ca 2+, and PF3. Thrombin converts fibrinogen to fibrin, activates
factor XIII, and positively enhances its own activation.
An intrinsic pathway, involving coagulation factors and chemicals already in the plasma, and an extrinsic
pathway, with coagulation factors present in damaged tissue, lead to thrombin activation.
The intrinsic pathway starts when circulation XII (Hageman factor) contacts substances in the subendothelium. Its activation leads to the activation of factor X, activation thrombin.
The extrinsic pathways starts when damage allow III (tissue factor) to contact plasma to react with VII
leading to VIIa and III complex which activates factor X.
Blood clotting cascade (simple): extrinsic pathway is when tissue factor is exposed. Instrinsic pathway is
when collagen is exposed. Both of these pathways ultimately lead to formation of factor X. Factor X
combines with factor V to become prothrombinase, which cleaves prothrombin into thrombin. Thrombin
cleaves fibrinogen into fibrin. Fibrin is what forms a clot.
Lesson 24- Respiratory I
Page 449-461
1. Compare internal to external respiration, describe the processes occurring in each.
Internal respiration is the process of using oxygen to generate ATP within mitochondria by oxidative
phosph with CO2 as a byproduct
External respiration is the exchange of ox and CO2 between the atmosphere and body tissues, which
involves both the respiratory and circulatory system. This encompasses:
a.
b.
c.
d.
Pulmonary ventilation- movement of air into the lungs and out of the lungs by bulk flow
Exchange of oxygen and CO2 between lung air spaces and blood by diffusion
Transportation of ox and CO2 between the lungs and body tissues by the blood
Exchange of ox and CO2 between the blood and tissue by diffusion
2. Describe the major structures of the respiratory system and list the functions of each.
The major organs are the lungs in the thoracic cavity. Right lung has three lobes, left has two.
Upper airways- air passages of the head and neck:
-
Air enters the nasal/ oral cavity which lead to the pharynx. The pharynx is used for food and air.
Air passes into first structure of the respiratory system, the larynx
Respiratory track – all passages leading from the pharynx to the lungs. It can be functionally divided into
the conducting and respiratory zone
-
Conducting – upper part of tract and conducts from larynx to lungs
Respiratory- lowermost part of tract and contains sites of gas exchange
Primary difference between the zones is the thickness of the walls.
Conducting zone
-
Starts with larynx (contains vocal cords)
Larynx’s opening, the glottis, is covered by the epiglottis to prevent food from entering (closes
during swallowing)
Then enters trachea- stays open constantly bc of cartilage unlike esophagus
Then enters bronchi which conduct air to lungs
Bronchi diverge into secondary bronchi. There are three secondary for the right lung and two for
the left
Then tertiary bronchi. These successively diverge, ultimately there will be about 8 million tubules
Tubules less than 1 mm in diameter are bronchioles ( these have no cartilage and can collapse).
To prevent this- there is elastic fiber in walls. These lead to terminal bronchioles
In conducting zone glovlet cells secrete mucus to catch foreign particles, The cilia beat and propel
the mucus towars the glottis, then to the pharynx where it is swallowed. This is the mucus
elevator
The respiratory zone-
-
Past the terminal bronchioles is where the respiratory zone begins
The first structure is the respiratory bronchioles, which terminate in alveolar ducts, which lead to
alveoli.
Most alveoli are arranged in alveolar sacs which resemble clusters of grapes
Adjacent alveoli are connected by alveolar pores, this equilibrates pressure
The walls of alveoli are primarily a single layer of type I alveolar cells, overlying a basement
membrane. In many places the basement membrane is fused with the capillary basement
membrane
Type II alveolar cells and alveolar macrophages engulf foreign paticles and pathogens that are
engales. The macrophages are free to move by amoeboid movement.
Thoracic cavity
3.
Chest wall is composed of structures to protect lungs
Internal/ extrernal intercostals
Diaphragm- muscle which seals off lower end of chest wall
Pleura- membrane that lines the interior surface of the chest wall and exterior surface of lungs
Pleural sac- surrounds each lung
Intrapleural space- between the two pleura
Describe the anatomy of the respiratory membranes, and explain how its structure facilitates the
exchange of gases between blood and air.
- Much surface area and blood expose encourage gas exchange with body. Thin membrane is also
an encourages.
4. Describe the anatomy of alveoli. Explain the roles of type I cells, type II cells, and alveolar
macrophages in respiratory function.
-
The walls of alveoli are primarily a single layer of type I alveolar cells, overlying a basement
membrane. In many places the basement membrane is fused with the capillary basement
membrane
-
Type II alveolar cells and alveolar macrophages engulf foreign particles and pathogens that are
enhaled. The macrophages are free to move by amoeboid movement.
5. Describe the mechanics of breathing and name the muscles of respiration. List the different
pulmonary pressures, and explain their roles in ventilation.
Four primary pressures:
1. Atmospheric- pressure of outside air.
2. Intra-alveolar- Pressure of air withing alveoli. At rest it is equal to atm pressure, thus is 0 mm Hg.
Varies during ventilation. The difference between it and atm pressure is what drives ventilation. If
atm is greater -> inspiration. If atm is lesser, expiration.
3. Intrapleural- Pressure inside the intrapleural space. Ut contains fluid not air. At rest it is -4 mm
Hg. It is always negative during negative breathing. At rest the chest wall is compressed an tends
to recoil outward. The lungs are stretched and tend to coul inward. These forces tend to move the
chest wall and lungs apart, but the fluid surface tension keeps them from pulling apart. To
maintain the negative pressure the sac must be air tight.
4. Transpulmonary-difference between intrapleural and intraalveolar. This represents the distending
fore across a wall so that the transpulmonary pressure indicates the distending force across the
lungs. An increase causes a larger distending pressure across the lungs, accompanied by greater
lung expansion.
Mechanincs:
-
Driven by boyles law
Intra-alveolar pressure is determined by their volume and the amount of air molecules in the
alveoli
Inspiration:
-
Contraction causes diaghpram to flatten and move down.
External intercostals cause ribs to pivot upward and outward
This causes the intrapleural pressure to decrease. This leads to an increase in trans pulmonary
pressure
This causes the aveoli to expand with the chest wall
Expiration:
-
There is passive- does not require contraction
Active- contraction does occur
Lesson 25- Respiratory II
Pg.461-469
Respiratory Volumes and Airflow
1. Describe the roles of lung compliance and airway resistance in ventilation.
Lung compliance is defined as the change in lung volume that results from a change in transpulmonary
pressure. A large compliance means that less of a change is needed for a given volume, so a higher one is
advantageous. As lungs expand work is required to stretch the elastic tissue but also expand the surface
area of the fluid layer. Surface tension therefore decreases compliance.
Airway resistance is the resistance of the entire system of airways in the respiratory tract. I tis determined
by the resistances of individual airways and is affected most by radius. Overall resistance in the
conducting zone is low, therefore the difference between lung pressures need not be overall large during
normal breathing. When resistance is increased, a larger pressure gradient is needed for airflow.
Bronchoconstriction-When smooth muscle contracts and decreases the radii of the bronchioles
Bronchodilation- wen smooth muscle relaxes, and bronchioles radii increases
Sympathetic causes dilation and parasympathetic causes constriction.
2. Explain the function of pulmonary surfactant.
Pulmonary surfactant decreases the surface tension in alveoli. It is secreted by type II alveolar cells in the
walls of the alveoli. Surfactant interacts with the hydrogen bonding between water molecules. This
increases lung compliance therefore decreasing the work necessary to expand the alveoli in breathing.
3. List the different lung volumes and capacities. Explain the clinical applications of lung volumes,
forced vital capacity, and forced expiratory volume
Using spirometry clinicians can measure three of the four nonoverlapping lung volumes which together
make up total lung capacity.
Tidal volume is the volume of air that moves in and out of the lungs during a single unforced breath.
Inspiratory reserve volume is the maximum volume of air that can be inspired from the end of a normal
inspiration. Expiratory reserve volume is the same for expiration.
Residual volume- the volume of air remaining in the lungs after max expiration
Lung capacity- the sums of two or more of the lung volumes described previously
Inspiratory capacity is the max volume of air that can be inspired after a resting expiration. (IC=
VT+IRV)
Vital capacity is the max volume of air that can be expired following a maximum inspiration.
(VC=Vt+IRV+ERV)
Total lung capacity is the volume of air in the lungs after the max inspiration
(TLC=VT+IRV+ERV+RV)
Forced vital capacity- the max amount of air a person can forcefully expire following a max inspiration
Forced expiratory volume- measure of the percentage of the forced vital capacity that can be exhaled
within a certain time frame
Peak expiratory flow rate- max rate a person can exhale
Minute ventilation is the total amount of air that flows into or out of the respiratory system in a minute
Minute ventilation can be calculates as the tidal volume times the respiratory rate.
The combined volume of the nonexchanging airways is the anatomical dead space
Lesson 26- Respiratory III
Pulmonary Circulation and Gas Exchange
Page 474-488
1. Describe the circulatory pathway for oxygenated and deoxygenated blood. Describe the exchange
of gas in the lungs and the systemic tissues.
The amount of carbon dioxide produced to the amount of oxygen consumed is the respiratory quotient.
Oxygen enters the alveoli and CO2 leaves the alveoli by bulk flow during ventilation. Pulmonary arteries
come from the right ventricle and oxygenated blood enters into the left atria through the pulmonary veins.
Oxygen and carbon dioxide follow concentration gradients.
2. List the normal partial pressures of oxygen and carbon dioxide in the arterial and mixed venous
blood and explain how they contribute to the exchange of gases.
Oxygen is about 21% of the partial pressure of ATM, which means at 760 torr it is about 160 torr. Carbon
dioxide is only .03% meaning it only has a pressure of about .21 torr. At a given partial pressure the
concentrations of the various dissolved gas particles vary between gases, CO2 for example is 20 times
more soluble than oxygen. When a gas and gas dissolved in a liquid reaches equilibrium the partial
pressures in the liquid and gas are said to be in equilibrium. This does not mean that the concentrations
are equal.
In a mixture of gases, a particular gas will go down its pressure gradient. This is how alveoli exchange
gases. Alveolar gas pressures differ from the atmospheric because exchange of das happens continually,
upon inspiration fresh air mixes with air in alveoli that is low in oxygen and high in co2, and air in the
alveoli is water saturated.
The blood in the pulmonary arteries has a pO2 of 40 mmHg and a PCO2 of 46 mmHg. In the alveoli the
pressure is pO2 100 mmHg and pCO2 of 40 mmHG. Blood in the pulmonary veins has the same partial
pressures as the alveolar air.
The blood in the pulmonary artery is mixed venous blood and the normal pressure of oxygen decreases in
it during exercise while pCO2 increases.
The appropriate increase in alveolar ventilation when the demands of the body change is called
hyperpnea. Hypoventilation means alveolar ventilation is insufficient, pCO2 rises and pO2 decreases.
Hyperventilation is too high of an alveolar ventilation and pCO2 decreases and pO2 increases.
3. Describe the mechanisms of transport of oxygen and carbon dioxide in the blood, including the
role of hemoglobin in the transport of both gases.
Hemoglobin allows oxygen to readily bind and leave. Every liter of blood has about 200 mL of oxygen,
of which only 3 mL are dissolved in plasma or erythrocytes. The rest is bound to hemoglobin.
Hemoglobin has four subunits which each have a globin and a heme group which contains iron. Each
hemoglobin can carry four oxygen molecules. Binding or release of O2 depends on the Po2 in the
surrounding fluid of oxygen. In mixed venous pooling hemoglobin is still about 75% bound to oxygen as
it bind more than normal body needs under resting conditions.
The hemoglobin disassociation curve. The ability to bind is sigmoidal as it is a cooperative process. The
steepest part demonstrates that when one oxygen binds the oxygen starts to bind rapidly.
Other factors affecting hemoglobin affinity:
1. Temperature- increases in temp decrease oxygens affinity for hemoglobin
2. pH- Bohr effect
a. Hb+O2Hb.O2+H+
3. When more CO2 is bound there is less oxygen affinity
4. 2,3 BPG decreases affinity of hemoglobin for oxygen
4. Explain the relationship between the PCO2 of blood and the pH of blood. Describe the actions of
carbonic anhydrase as blood passes through the systemic and pulmonary circulations.
Carbon dioxide is 5% freely dissolved, 5% heme bound, and 90% bicarbonate. The CO2 can bind to
the amino terminals of the heme, the Carbamino effect. Carbonic anhydrase catalyzes the conversion
of CO2 to carbonic acid. As bicarbonate levels rise, bicarbonate ions are moved into the plasma and
changed for chloride ions in the chloride shift. In the lung CO2 moves doewn its pressure gradient
from the blood to be exhaled. The decrease in CO2 causes the bicarbonate and Hydrogen ions to
combine and form carbonic acid which carbonic anhydrase then converts to CO2 and water. Most of
this new CO2 is exhaled, further driving the reaction. AS bicarbonate ions in the erythrocyte are used,
cell levels decrease, and bicarbonate ions in the plasma are transported in for chloride ions, this is the
reverse chloride shift. The Po2 of blood also affects heme affinity for CO2. At a given Pco2 the
carbon dioxide content of the blood falls at the PO2 rises, this is the Haldane effect.
Lesson 27- Respiratory IV
Respiratory system regulation and acid-base homeostasis
Page 489-499
1. Describe the neural mechanisms that establish the respiratory rhythm. Distinguish between the
respiratory centers that establish the rhythm and those that regulate the rhythm.
The signals that regulate whether or not respiration needs to change is the PCO2 and PO2 in the systemic
arterial blood (normal of 100 mm Hg O2 and 40 mm Hg CO2). Alveolar ventilation depends on the
frequency and volume of breaths.
The muscles of respiration are skeletal, so they are stimulated by somatic motor neurons - the phrenic
nerve, which innervates the diaphragm, and the intercostal nerves, which innervate the intercostals.
Central control of respiration is not fully understood, but the control centers are present in the medulla
and pons of the brain stem. Two general classes of neurons are found in these areas, inspiratory and
expiratory neurons. These neurons fire during their respective part of the respiration cycle.
Two respiratory control centers are on each side of the medulla- the ventral respiratory group and the
dorsal respiratory group. The VRG has two regions of primarily expiratory neurons and one region of
primarily inspiratory neurons. The inspiratory neurons show a ramp like frequency during inspiration.
The DRG contains primarily inspiratory neurons, although some expiratory neurons are present, the DRG
inspiratory pattern is more complex than those of the VRG as their firing pattern depends on the degree of
stretch of the lugs. VRG and DRG inspiratory neurons stimulate motor neurons in the phrenic and
external intercostal nerves which then cause inspiratory contraction.
The respiratory center of the pons is the pontine respiratory group, the PRG. It contains inspiratory and
expiratory neurons as well as mixed. This is thought to possibly explain the transition between inspiration
and expiration.
The Central pattern generator is a network of neurons that generate a regular and repeating rhythm which
is known as the respiratory rhythm. It is thought to be in the ventrolateral medulla and its mechanism of
action is unknown. One theory is that the neurons have pacemaker activity and another is that the rhythm
comes from the interactions between neurons.
Sensory, or peripheral, input can vary the central pattern generator. Chemoreceptors in the brain and
systemic arteries is especially important in this process. These are primarily responsible for control under
resting position. There is also info in the pulmonary stretch of smooth muscle. There are irritant receptors
in the tract. Arterial baroreceptors, nociceptors, and thermoreceptors also all regulate it.
Pulmonary stretch receptors seem not play a large role in humans but act against overinflation in other
animals. Irritant receptors sensors trigger bronchoconstriction, coughing and sneezing.
2. Explain the role of peripheral and central chemoreceptors in the control of ventilation.
Peripheral chemoreceptors are in the carotid body near the carotid sinus, others are in the arotic
arch in many animals but not humans.
Central chemoreceptors are in the medulla oblongata.
These differ in both their location and sensitivity. Peripheral chemoreceptors respond to changes in
arterial blood and communicate with afferent neurons to medullary respiratory control centers. Peripheral
can detect drops below 60 mmHg for Ox pressure. Low PO2 can cause increased sensitivity to CO2. The
primary stimulus is changes in H. The main source of these ions is the CO2 bc of the bicarbonate buffer
system.
Central chemoreceptors are neurons in the medulla that respond to changes In the H concentration of the
cerebrospinal fluid. The CO2 that moves into CSF is also converted by carbonic anhydrase. These are not
activated by low PO2. Increased brain activity and decreases in blood flow leads to increased H.
Peripherals are more rapid and critical to moment to moment while central are more important for the
steady state levels. In all cases activation of the chemoreceptors results in an increase of ventilation,
decreased activation results in decreased ventilation.
3. Describe how changes in PO2 and PCO2 in the lung tissues can alter ventilation. Explain the
ventilation-perfusion ratio.
In normal alveoli ventilation- the rate of air flow- is equal to the rate of blood flow-perfusion. The
relationship is the ventilation-perfusion ratio. It is Va/Q. When airways are obstructed Va decreases,
causing a decrease in PO2 and increase in PCO2 in the air and obstructed alveoli. Damage to pulmonary
capillaries decreases Q increasing PO2 and decreasing PCO2 in the alveoli, with little blood through these
areas. Gravity effects the ratio under normal conditions. Local control mechanisms operate to match
ventilation and perfusion. TO obtain a ventilation perfusion ratio of 1 areas with low perfusion require
high ventilation, and vice versa.
Importantly, the effects of carbon dioxide and oxygen
on the pulmonary circuit are the opposite of their
effects on the system arterioles.
4. Explain how the respiratory system regulates
the acid base balance of the blood by varying
the rate of carbon dioxide expiration.
Acidosis occurs when pH is 7.35 or lower. A pH
of 7.45 or grater is alkalosis. Acidosis is a CNS
depressor and alkalosis is a CNS exciter.
Hemoglobin is buffer because it can bind and
release H+. In the tissues, hemoglobin unloads O
and binds H+. This is important because the
tissues are producing CO2, which is quickly
converted to bicarbonate and H+. Some of these
H+ are buffered by heme, preventing acidosis. In
the lungs hemoglobin releases and loads oxygen
and the clearence of CO2 reduces the H+ ion
concentration.
Bicarbonate is the other major buffering system. If CO2 is allowed to increase, acidosis will result .
The Henderson-Hasselbalch equation for this is:
This means that at a normal range the bicarbonate to CO2 ratio must be about 20:1. Respiratory acidosis
is blood acidity due to increased CO2- such as in hypoventilation. Respiratory alkalosis is decrease in
acidity due to decreased CO2 such as during hyperventilation or at high altitues.
Lesson 28- Urinary I - WOOHOO!
KIDNEYSSSSSSSSSSSSSSSSSSSS
Anatomy and Renal Exchange Process
Page 504-515
1. Identify and describe the functions of the following structures in the urinary system: Nephron,
glomerulus, renal tubule, collecting duct, ureter, bladder, urethra
Kidneys filter blood and produce urine. The kidneys have many primary functions:
-
Regulation of plasma ionic composition
Regulation of plasma volume and blood pressure
Regulation of plasma osmolarity
Regulation of plasma pH
Removal of metabolic waste products and foreign substances from the plasma
Kidneys also have secondary functions, such as releasing erythropoietin in the endocrine system.
Urinary system consists of two kidneys, two ureters, the bladder, and the urethra (Fig 18.1).
The kidneys are retroperitoneal because they are located between the peritoneum and the wall of the
abdominal cavity.
Renal arteries supply the kidneys with blood. Kidneys receive 20% of cardiac output at rest. Renal veins
run parallel to the renal arteries.
The kidney is divided into the cortex (outside) and medulla (inside). The renal pelvis is the initial portion
of the ureter.
Nephrons are the functional units of kidneys. The renal tubule is part of the nephron and is a long, coiled
tube. The collecting ducts are common passageways that renal tubules drain into.
Each nephron consists of a renal corpuscle, which filters the blood, and a renal tubule, through which
filtrate travels to become urine.
Renal corpuscle consists of Bowman’s capsule and the glomerulus. Blood enters the glomerular
capillaries via an afferent arteriole, passes into Bowman’s capsule via glomerular filtration, then leaves
via an efferent arteriole. The afferent and efferent arterioles are arranged in series, forming a capillary
bed, which allows for greater regulation of filtration.
Renal tubule is where filtration occurs. Glomerular filtrate from Bowman’s capsule enters proximal
tubule, into the loop of Henle (descending limb, thin ascending limb, thick ascending limb), into the distal
convoluted tubule, then into the collecting duct of the renal corpuscle.
There are two classes of nephrons based on their location:
-
Cortical nephrons: located in the cortex with only the tip of the loop of Henle in the medulla
Juxtamedullary nephrons: The renal corpuscle is near the border between the cortex and medulla.
Unlike cortical neurons, they help maintain an osmotic gradient in the renal medulla.
o Juxtaglomerular apparatus connects the distal tubule to the afferent and efferent
arterioles. It regulates blood volume and blood pressure. It consists of the macula densa
(a cluster of epithelial cells) and granular cells (in the wall of afferent arterioles).
The renal artery branches into segmental arteries, which branch into interlobar arteries, which branch into
arcuate arteries, which branch into interlobar arteries. Each interlobar artery supplies a single nephron via
the afferent arteriole, which leads to glomerular capillary beds, then the efferent arteriole. There are two
types of capillary beds:
-
Peritubular capillaries: branch from efferent arterioles of cortical nephrons
Vasa recta: branch from efferent arterioles to juxtamedullary nephrons
2. Describe how the urinary excretion of solutes and water influences the volume composition of
plasma, and identify other processes that affect composition of plasma, and identify other
processes that affect plasma volume and composition
There are three exchange processes in renal nephrons: Glomerular filtration, reabsorption, and secretion.
Glomerular filtration: bulk flow of protein-free plasma from the glomerular capillaries into Bowman’s
capsule. Filtration is driven by Starling forces similar to in
capillaries. Filtrate is like plasma, but with no proteins.
-
To enter Bowman’s capsule, glomerular filtrate
passes through the glomerular membrane/filtration
barrier, which consists of the capillary endothelial
cell layer, the surrounding epithelial cell layer, and
the basement membrane. Epithelial cells that cover
glomerular capillaries have extensions called
podocytes. Fluid moves through slit pores, which
are gaps between podocytes.
-
Glomerular filtration pressure is the sum of starling forces in the renal corpuscle (analogous to net
filtration pressure). The 4 starling forces are:
o Hydrostatic pressure of glomerular capillaries: Favors filtration (push into Bowman’s
capsule)
o Hydrostatic pressure of Bowman’s capsule: Opposes filtration (push out of Bowman’s
capsule).
o Osmotic pressure in glomerular capillaries: Opposes filtration (pull out of Bowman’s
capsule). Presence of proteins in the plasma draws filtrate back into the glomerulus.
o Osmotic pressure in Bowman’s capsule: Favors filtration (pull into Bowman’s capsule).
This force is generated by proteins, because proteins are the only solute that cannot move
between plasma and Bowman’s capsule. This pressure is negligible under normal
conditions.
Reabsorption: selective transport of molecules from the lumen of renal tubules to the interstitial fluid
outside the tubules. Reabsorption is the movement of filtered solutes and water from the lumen of the
tubules back into the plasma
Secretion: selective transport of molecules from the peritubular fluid to the lumen of renal tubules.
Secretion can be by passive or active transport.
Excretion is the elimination of materials from the body as urine.
3. Define the following terms and how they relate to renal function: filtered load, glomerular
filtration rate, clearance, transport maximum, and renal threshold.
Glomerular filtration rate is the volume of plasma filtered per unit time (about 125 mL/min).
Filtration fraction is the fraction of the renal plasma volume that is filtered: Glomerular filtration
rate/renal plasma flow rate
Filtered load is the quantity of particular solute that is filtered per unit time. A freely filterable solute is
small enough to move across the glomerular membrane without restriction. Filtered load = GFR times
plasma concentration of specific solute.
Glomerular filtration rate is tightly regulated and is relatively constant under normal circumstances.
-
Intrinsic control: Three intrinsic control mechanisms allow kidneys to tolerate changes in MAP.
Changes in MAP alter GFR because arterial pressure affects glomerular capillary pressure, which
then affects glomerular filtration pressure. When arterial pressure rises, glomerular capillary
pressure also rises, so GFR rises.
o Myogenic regulation: Smooth muscle of the afferent arteriole is sensitive to stretch, so it
responds to stretch by contracting. When MAP rises, the pressure in the afferent arteriole
rises, so smooth muscle contracts to constrict the arteriole and increase resistance to flow.
The result is no net change in flow rate.
o
-
Tubuloglomerular feedback: A change in GFR causes a change in the flow of tubular
fluid past the macula densa, which alters secretion of paracrines from the macula densa.
These paracrines trigger contraction or relaxation of the afferent arteriole. This is an
example of negative feedback control to keep GFR constant.
o Mesangial cell contraction: Mesangial cells are modified smooth muscle cells around
glomerular capillaries. Contraction of mesangial cells decreases blood flow through
glomerular capillaries. An increase in blood pressure increases GFR and stretches
mesangial cells. In response, mesangial cells contract to keep GFR constant.
Extrinsic control mechanisms take over if MAP drops below 80 or above 180 mmHg. In response
to a drop in MAP, the sympathetic nervous system is activated by baroreceptor reflexes, causing
constriction of afferent and efferent arterioles. The decrease in GFR also decreases urine output to
help the body conserve water and keep blood pressure up.
Lesson 29 – Urinary II
Reabsorption and Micturition
515-527
Remember that basolateral membrane faces the blood and apical membrane faces the inside of the tubule.
1. Explain how the basic renal exchange process of filtration, secretion, and reabsorption affect the
rate at which materials are excreted in the urine
Reabsorption is selective transport of solutes and water from the lumen of the tubules back into the
plasma. Reabsorption of most solutes occurs in the proximal and distal convoluted tubules. When a
substance is reabsorbed, it has to move across the tubule epithelium and the capillary endothelium.
The epithelial cells lining renal tubules are connected by tight junctions, which restricts movement of
solutes. Plasma of epithelial cells facing the tubule lumen is the apical membrane, which has microvilli to
increase surface area. The plasma membrane facing the interstitial fluid is the basolateral membrane.
Active reabsorption of solute: A substance transported via active transport will be actively transported
across one membrane and passively transported across the other (Fig 18.14).
Water diffusion/reabsorption is based on osmolarity. Water resorption follows solute reabsorption.
Passive reabsorption of solute: For passive reabsorption, the concentration of the solute must be greater in
the tubular fluid the plasma, and it must be able to permeate the plasma membranes of the tubule
epithelium and the capillary endothelium.
Water movement follows the movement of solutes transported by active transport, then solutes
transported by passive transport follow the movement of water.
Transport maximum occurs when all carrier proteins and pumps are occupied. Renal threshold is the
concentration of a solute at which it is too high to be 100% reabsorbed. One example of this is glucose:
glucose is usually 100% reabsorbed, but if they concentration is so high that renal threshold is surpassed,
glucose will appear in the urine, which is characteristic of diabetes.
2. Describe the events that occur during micturition
Micturition is the elimination of urine from the bladder, it is also known as
urination. The wall of the bladder has smooth muscles connected by gap
junctions- this allows them to function as a unit known as the detrusor
muscle. In the neck of the bladder muscle fiber converge and overlap
forming a thicker wall called an internal urethral sphincter, forming a
valve that regulates urine flow. Skeletal muscle that surrounds the urethra
as it passes through the pelvic floor also controls this process and is
known as the external urethral sphincter.
Micturition has both voluntary and
involuntary control. It occurs when the
detrusor contracts, the internal urethral
sphincter relaxes, and the external
urethral sphincter relaxes. The detrusor
and internal sphincter are autonomically
innervated while skeletal is voluntary.
As stretch receptors in the bladder wall become activated as the kidney
continually adds urine to the bladder until the stretch becomes sufficient
to induce the micturition reflex. It is a spinal pathway that can be
overridden by voluntary control in trained individuals. In the pathway
stretch receptors are activated, info is transmitted to the spine, signals
are relayed on interneurons to three sets of neurons:
1) Parasympathetic neurons which innervate the detrusor muscle
2) Sympathetic neurons which innervate the internal urethral sphincter
3) Somatic motor neurons which innervate the external urethral sphincter
Stimulation of stretch receptors excites parasympathetic neurons that travel in the pelvic nerve and
stimulate the detrusor muscle to contract. Contraction of the detrusor muscle increases pressure in the
bladder, which cause the internal urethral sphincter to open. Stretch receptors also inhibit sympathetic
neurons to the internal sphincter and inhibit somatic motor neurons to the external urethral sphincter,
which allows for relaxation and opening of the sphincters. This reflex can be overridden by voluntary
control, in which the cerebral cortex inhibits parasympathetic neurons and excites sympathetic neurons so
that the sphincters remain closed. A person can also voluntarily initiate urination.
Lesson 30 -Urinary III
Balancing Water, Sodium, and Potassium
Pg. 532-549
1. Describe the different sources of body water input and output
Changes in water and solute content of the plasma affect plasma volume, which affects MAP. The solute
and water content of the plasma is controlled by movement of materials in and out of the body and
between different compartments within the body. Specifically, the plasma can gain or lose materials by
exchange with the lumen of the gastrointestinal tract, exchange with the lumens of the renal tubules, or
through sweating, bleeding, or respiration (Fig 19.1). Transport of materials across the gastrointestinal
tract amounts to a net gain of solutes and water by the body. Transport of materials across the renal
tubules amounts to a net loss of water and solutes from the body.
Positive balance is when a substance enters the body faster than it exits, so the concentration of that solute
in plasma increases. Negative balance is when a substance leaves the body faster than it enters, so the
concentration of that substance in the plasma decreases. For tightly regulated substances such as glucose,
a positive or negative balance does not cause a significant change in plasma concentration because of
regulatory mechanisms.
Intercalated cells regulate acid-base balance.
Principle cells in the distal tubule and collecting duct regulate water balance and osmolarity. To maintain
water balance, water intake plus metabolically produced water must equal water output plus water used in
chemical reactions.
Positive fluid balance is when more water is consumed than lost, resulting in hypervolemia. Negative
fluid balance is called hypovolemia. Normal blood volume is normovolemia. The kidneys regulate water
volume excretion by regulating water reabsorption in the late distal tubules and collecting ducts. This is
accomplished by establishing an osmotic gradient between the tubular fluid and peritubular fluid.
Plasma volume is directly related to blood pressure. Plasma volume can also affect osmolarity, because
changes in volume without changes in solute quantity change osmolarity. This affects the net movement
of water between fluid compartment, particularly between intracellular fluid and extracellular fluid.
The normal total solute concentration in both intracellular fluid and extracellular fluid (plasma and
interstitial) is 300 mOsm, which means there is no net movement of water into or out of cells. If a person
were to drink a lot of pure water and there was no regulatory mechanism, plasma volume would increase
and solute concentration would decrease, so water would move into cells and cells would swell. This does
not happen because the kidneys excrete more water under these conditions by reabsorbing
less water.
In the renal tubule, sodium is reabsorbed by several mechanisms across the apical
membrane of the epithelial cell, but always by active transport across the basolateral
membrane through the peritubular fluid and back into the plasma.
In the proximal and distal tubules, resorption of solutes increases
the osmolarity of peritubular fluid, which causes water to also be
resorbed. In the collecting ducts, the medullary osmotic gradient
drives water resorption. The medullary osmotic gradient refers to
the outer regions of the medullar having lower osmolarity than the
inner regions of the medulla. The descending limb of the loop of
Henle is permeable to water and impermeable to solutes, while the
ascending limb is impermeable to water and has active
transporters for solutes. This is called the countercurrent
multiplier, because fluid flowing through the descending and
ascending limbs move in opposite directions.
Urea is needed to maintain the osmotic gradient because it is
highly soluble and unable to permeate cell membranes without
transporters. UTB transporters are in endothelial cells of the descending limb of the vasa recta. UTA
transporters are in epithelial cells lining renal tubules. UTC transporters are in the proximal tubule and
collecting duct. Urea is most concentrated deep in the medulla.
The vasa recta capillaries prevent the diffusion of water and solutes in the renal capillaries to maintain the
osmotic gradient. It looks like the loop of Henle with a descending and ascending limb. The purpose of
the vasa recta is to keep the osmotic gradient in a steady state when working with the countercurrent
multiplier system. The descending limb of the vasa recta has urea transporters, and the ascending limb
does not.
70% of water resorption occurs in the proximal tubule, 20% in the distal tubule, and 10% in the collecting
ducts. Because the epithelial cells lining the tubules are connected by tight junctions, water diffusion
depends on aquaporins. Water will
be reabsorbed wherever it is
permeable due to the osmotic
gradient. Remember that only
principal cells contain aquaporins.
Aquaporin 3 is in the basolateral
membrane of principal cells and are
always present. Aquaporin 2 is in
the apical membrane and depend
on ADH. When the late distal
tubule is permeable to water, water
will be reabsorbed so that the
osmolarity of distal tubule fluid is
iso-osmotic to medullary interstitial
fluid, resulting in highly
concentrated urine.
2. Explain the control of water balance and osmolarity by antidiuretic hormone
Antidiuretic hormone (ADH) is a peptide hormone that varies the permeability of the late distal tubules
and collecting ducts to water. Without ADH, the principal cells of the apical membrane in the late distal
tubules and collecting ducts are impermeable to water. ADH stimulates synthesis and insertion of
aquaporin 2 into the apical membrane so that water reabsorption increases.
ADH secretion is regulated by changes in osmolarity of extracellular fluid, which are sensed by
osmoreceptors in the hypothalamus. The OVLT, where these osmoreceptors are located, is not protected
by the blood-brain barrier so that it can detect osmolarity. An increase in osmolarity stimulates ADH
secretion, while a decrease in osmolarity inhibits ADH secretion. Remember that ADH is released from
the posterior pituitary.
Plasma levels of ADH also depend on baroreceptors. Low blood pressure means that plasma volume is
low, which stimulates release of ADH to reabsorb more water and raise blood pressure.
ADH acts via a GPCR in the basolateral membrane of principal cells. The result is synthesis of aquaporin
2, which are inserted into the apical membrane via vesical fusion.
Changes in glomerular filtration rate also affect water resorption.
3. Describe the major mechanisms whereby water and sodium balance influence MAP
Sodium is the primary solute in extracellular fluid, so it has the greatest impact in establishing the osmotic
gradient that drives water reabsorption. Sodium levels are also important because they are required for
action potentials, and sodium is used in cotransport such as the glucose cotransporter. Hypernatremia is
too much plasma sodium; hyponatremia is too little. Sodium regulation occurs at the level of reabsorption
because it is not secreted. The two hormones that regulate sodium reabsorption are aldosterone and atrial
natriuretic peptide (ANP).
Sodium reabsorption always occurs by active transport, which is driven by sodium potassium pumps in
the basolateral membrane of renal tubule epithelial cells.
Proximal tubule: Sodium is actively transported across the basolateral membrane by the Na/K pump. This
causes a decrease in intracellular sodium, which drives reabsorption of sodium on the apical side. Sodium
movement from the tubular fluid across the apical membrane into the epithelial cell of the proximal tubule
occurs by cotransport or countertransport. Chloride ions follow sodium due to electrostatics.
Distal tubule: Sodium is actively transported across the basolateral membrane by the Na/K pump. Sodium
moves across the apical membrane by cotransport with chloride ions or through sodium channels. Sodium
resorption in the distal tubule is coupled potassium secretion to minimize changes in electric gradients.
Aldosterone is a steroid hormone from the adrenal cortex that regulates the reabsorption of sodium and
secretion of potassium.
To influence sodium reabsorption, aldosterone binds to cytosolic receptors in principal cells of the late
distal tubules and collecting ducts. The result is an increase in open sodium and potassium channels in the
apical membrane as well as synthesis of more Na/K pumps for the basolateral membrane. The result is
increased sodium resorption, which also increases potassium secretion (because they are coupled).
The renin-angiotensin-aldosterone system (RAAS) is a hormone axis that helps control aldosterone
release. Renin is a proteolytic enzyme released from granular cells of the macula densa into the
bloodstream. Renin converts angiotensin to angiotensin I. Angiotensin I is cleaved into angiotensin II by
angiotensin converting enzyme (abundant in the lungs). Angiotensin II increases MAP through several
mechanisms, including stimulation of ADH and aldosterone release. In addition to stimulating release of
ADH and aldosterone, angiotensin II also stimulates vasoconstriction of arterioles and the sensation of
thirst. Renin secretion is stimulated primarily by a decrease in MAP. Angiotensin secretes angiotensin.
Juxtaglomerular cells in the kidney release renin.
Intrinsic controls of renin secretion are afferent arteriolar pressure and MAP. An extrinsic control is the
sympathetic nervous system.
Atrial natriuretic peptide (ANP) is secreted by cells of the atria of the heart due to distension of the atrial
wall, which occurs when blood pressure rises. ANP increases sodium excretion by increasing GFR and
decreasing sodium resorption. ANP causes dilation of the afferent arteriole and constriction of the efferent
arteriole, which increases GFR. It also decreases the number of open sodium channels in the apical
membrane, and decreases secretion of renin and aldosterone.
4. Explain the role of aldosterone in potassium balance.
Hyperkalemia is an increase is plasma potassium. Hypokalemia is a decrease in plasma potassium. The
concentration of plasma potassium is regulated by changing the amount of potassium that is secreted into
renal tubules.
In principal cells in the late distal tubule, potassium is moved across the basolateral membrane by the
Na/K pump into principal cells. Potassium channels in the apical membrane allow passive movement of
potassium into the tubular fluid. Through this mechanism, potassium is regulated by secretion (movement
from blood to tubular fluid) rather than resorption (movement from tubular fluid to blood).
Aldosterone increases the number of Na/K pumps in the basolateral membrane in principal cells lining the
late distal tubules and collecting ducts. Aldosterone also regulates the number of potassium channels in
the apical membrane. Aldosterone thus increases potassium secretion. High potassium levels act directly
on secretory cells of the adrenal cortex to increase aldosterone secretion, which increases potassium
secretion.
WPR has 10-11 things to be labeled so find a figure in the book with 10ish labels
Lesson 31 – Urinary IV
Calcium and Acid-Base Balance
Page 549-561
Calcium is critical because it triggers exocytosis in neurons, stimulates secretion in various systems,
initiates the crossbridge cycle in muscle contraction, and controls contractility of the heart and blood
vessels. Hypercalcemia causes muscle weakness, atrophy, lethargy, hypertension, constipation, and
nausea. Hypocalcemia causes numbness, muscle cramps, exaggerated reflexes, and hypotension.
1. Describe the major hormone systems that regulate calcium balance
Plasma calcium levels are regulated by bone resorption, absorption from the gastrointestinal tract, or
removal from plasma by the kidneys. Bone resorption is when blood is broken down to increase bloodcalcium levels.
Calcium can travel in the blood as free ions or bound to carrier proteins. Calcium is filtered at the
glomerulus. Most of the filtered calcium is reabsorbed as the tubular fluid moves through the renal
tubules: 70% at the proximal tubules, 20% at the ascending limb of the LOH, and 10% in the distal
tubules.
Hormones that regulate calcium levels are parathyroid hormone, 1,25-dihydroxycholecalciferol, and
calcitonin. Parathyroid hormone is a peptide hormone produced by the parathyroid gland that increases
blood-calcium by stimulating bone resorption. 1,25-(OH2)D3 is a steroid hormone that increases bloodcalcium by stimulating calcium absorption from the digestive tract and resorption in the distal tubules of
the kidneys. Calcitonin lowers blood-calcium by stimulating uptake of calcium by bones.
Parathyroid hormone increases plasma calcium through three mechanisms: it stimulates calcium
reabsorption in the ascending limb of the LOH and the distal tubules. It stimulates activation of 1,25(OH2)D3, which stimulates calcium absorption in the digestive tract. It stimulates resorption of bone,
which increases plasma-calcium levels. 1,25-(OH2)D3 is synthesized from vitamin D3. Calcitonin is a
peptide hormone secreted by C cells of thyroid.
2. Describe venous factors that influence acid-base balance
Blood pH must be maintained between 7.38 and 7.42. If the pH moves outside of this range, the change in
H+ concentration causes varying protonation of proteins and changes their structure, nervous system
activity changes, potassium levels change, and cardiac arrhythmias occur.
Acid-base disturbances can occur due to changes in metabolism (Ex: ketoacidosis) or changes in
breathing (via bicarbonate buffer system).
Hydrogen ions are excreted by the kidneys in urine, while carbon dioxide is exhaled.
CO2 is produced during the citric acid cycle and causes a decrease in pH via the above reaction. The
respiratory system regulates blood pH by regulating the amount of exhaled CO2. PCO2 is maintained at
40 mmHg by chemoreceptor reflexes, which adjust alveolar ventilation (see lesson 27).
Metabolic acidosis and metabolic alkalosis are caused by something other than changes in PCO2, such as
the following factors:
-
High protein diet can cause acidosis by producing phosphoric acid and sulfuric acid
High fat diet can produce too many ketone bodies which causes acidosis
Intense exercise generates lactic acid
Excessive vomiting leads to large loss of H+ from the stomach which can cause alkalosis
Severe diarrhea can lead to loss of bicarbonate which leads to acidosis
Changes in kidney function can cause alkalosis or acidosis.
3. Explain how buffers in the blood, actions of the respiratory system, and the kidneys compensate
acid-base disturbances
There are three general mechanisms that compensate for pH changes (in order of fastest to slowest):
1) Buffering of hydrogen ions – binding or release of hydrogen ions into the blood. Examples are
the bicarbonate buffer system, phosphate buffers, and protein buffers. Buffer compensation is
controlled by the law of mass action (le Chatelier’s)
2) Respiratory compensation – change in exhalation rate of CO2 shifts the bicarbonate buffer
equation and thus changes pH. If pH decreases, alveolar ventilation increases so that more CO2 is
exhaled, and the bicarbonate buffer equation shifts left.
3) Renal compensation – changes in excretion rate of H+ and resorption rate of bicarbonate. If pH
decreases, kidneys increase H+ secretion and bicarbonate reabsorption and synthesis new
bicarbonate. CO2, H+, HCO3-, and HPO42- are also filtered at the glomerulus and are critical to
acid-base balance.
More on renal compensation: Bicarbonate resorption is coupled with hydrogen secretion in the proximal
tubule. Carbonic anhydrase on the apical membrane converts bicarbonate to water and CO2. The CO2
diffuses through the apical membrane and is converted back to carbonic acid and H+ by carbonic
anhydrase in the cytosol. The H+ is secreted by countertransport with sodium ions, while bicarbonate ions
are reabsorbed by cotransport with sodium ions and countertransport with chloride ions.
There are several carrier proteins in the epithelial cells of the proximal tubule that move hydrogen and
bicarbonate ions. The basolateral membrane has Na/K, Na/HCO3- cotransporters, and HCO3/Clcountertransporters. The apical membrane has Na/H+ countertransporters and H+ pumps. Generally, in
the proximal tubule, most bicarbonate is reabsorbed, H+ is secreted, and sodium is reabsorbed.
In intercalated cells of the late distal tubule and collecting duct, secretion of H+ is coupled to synthesis of
bicarbonate ions. The basolateral membrane has HCO3-/Cl- countertransporters that move bicarbonate
out of the cell into peritubular fluid and chloride into the cell. The basolateral membrane also has chloride
ions that allow chloride to diffuse back into the peritubular fluid. The apical membrane has H+ pumps
that actively transport H+ out of the cell into the tubular fluid. The apical membrane also has K+/H+
countertransporters that move potassium in and hydrogen out. Carbonic anhydrase is only in the
cytoplasm of intercalated cells (not the membrane).
H+ secreted into the tubular fluid is limited to a pH of 4.5 min. To minimize changes in urine pH, a
phosphate buffer exists in the distal tubules and collecting ducts.
Under conditions of severe acidosis, another renal mechanism kicks in to compensate. Glutamine is
transported from the tubular fluid and the peritubular fluid into epithelial cells. Glutamine is catabolized
to bicarbonate ions and ammonia. The bicarbonate is transported back into the peritubular fluid. The
ammonia binds with hydrogen ions to form ammonium, which is secreted by countertransport with
sodium ions.
Based on Henderson-Hasselbalch, the ratio of bicarbonate to CO2 must be 20:1 in plasma. During
acidosis, this ratio decreases. During alkalosis, this ratio increases.
If pH is disturbed due to respiratory changes, the renal system compensates. If metabolic
acidosis/alkalosis occurs, the respiratory system compensates.
Lesson 32- Gastrointestinal I
Gastrointestinal Anatomy
Page 566-578
1. Identify the major organs of the gastrointestinal system and describe the functions of each
Digestion is the chemical and mechanical breakdown of food so that it can be transported in the blood.
Absorption is transport into the bloodstream. Secretions are released from various organs to aid in
digestion. Motility is the movement of food through the digestive system. See figure 20.1.
The gastrointestinal system consists of the gastrointestinal tract and accessory glands. The gastrointestinal
tract are made of the pharynx, esophagus, stomach, small intestine, colon, and rectum.
-
-
-
Mouth: the beginning of the GI tract. Food enters the mouth; mechanical digestion occurs here.
Chemical digestion begins via salivary enzymes. Food passes from the mouth through the
pharynx.
Esophagus: Moves food from the pharynx to the stomach. It consists of both skeletal muscle and
smooth muscle. The upper esophageal sphincter is a ring of skeletal muscle that surrounds the
esophagus at its upper end. The lower esophageal sphincter is a ring of smooth muscle that
regulates flow of food into the stomach. Both are closed at rest.
Stomach: Stores food and continues digestion. The lining secretes gastric juice. Contractile
activity churns food to aid in mechanical digestion. Chyme is the mixture of food and gastric
-
-
-
juice. The stomach is divided into the fundus (top), body (middle) and antrum (bottom). The
fundus and the body contain gastric pits that have many secretory cells. The pylorus is the
connection between the stomach and the small intestine and is regulated by a ring of smooth
muscle called the pyloric sphincter.
o Neck cells secrete mucus
o Chief cells secrete pepsinogen
o Parietal cells secrete HCl and intrinsic factor
o G cells secrete gastrin
o The gastric mucosal barrier secretes bicarbonate to protect the stomach lining from HCl
Small intestine: The small intestine is divided into the duodenum, the jejunum, and the ileum.
Chyme is mixed with pancreatic juice in the duodenum, which contains bicarbonate to neutralize
the acidity of the stomach. The duodenum also receives bule from the liver, which contains bile
salts to aid in the digestion of fats. As digestion occurs via enzymes in chyme, the mucosal
epithelium simultaneously begins absorption. The small intestine is highly efficient due to villi,
which increase the surface area. Each villus contains capillaries and a lymphatic vessel called a
lacteal. The brush boarder on the mucosal surface is made of microvilli. Brush boarder enzymes
are digestive enzymes released from brush boarder. The hepatic portal vein connects blood supply
from the intestinal capillaries to the liver.
Colon: Divided into the ascending colon, transverse colon, descending colon, and sigmoid colon.
The first three segments absorb water and ions from chyme. The sigmoid colon stores waste until
it is excreted. The ileocecal sphincter is a ring of smooth muscle that regulates flow from the
ileum to the colon. The cecum, colon, and rectum together constitute the large intestine.
Rectum and Anus: controlled by the internal anal sphincter (smooth muscle) and external
sphincter (skeletal muscle).
Accessory glands: salivary glands (secrete saliva), liver (secretes bile), pancreas (pancreatic juice),
Acini ball-like clusters of epithelial cells located in the salivary glands and pancreas. They secrete a fluid
containing water, inorganic ions, and other solutes.
Salivary glands include the parotid glands, the sublingual glands, and the submandibular glands. They
secrete bicarbonate, mucus, salivary amylase, and lysozymes.
The pancreas has both exocrine and endocrine functions. Pancreatic juice contains bicarbonate, pancreatic
amylase, pancreatic lipase, nucleases, and proteases.
The liver has many functions. In the context of the GI system, the liver secretes bile, processes nutrients,
and eliminates toxins from the body. The functional unit of the liver is the liver lobule, which consists of
liver cells called hepatocytes. The hepatic artery and hepatic portal vein drain into liver sinusoids, which
are blood-filled cavities. Hepatocytes secrete bile into the bile canaliculi, which drain into bile ducts that
converge into the common hepatic duct. Kupffer cells are hepatic macrophages.
The gallbladder stores bile produced by the liver in between meals.
The sphincter of Oddi regulates flow of bile and pancreatic juice into the duodenum.
2. ID the various tissue layers that make up the wall of the intestinal track
The wall of the GI tract has four distinct
layers: mucosa, submucosa, muscularis
externa, and serosa.
-
-
-
-
Mucosa (from inside to outside):
mucous membrane, lamina propria,
muscularis mucosae. The mucous
membrane is made of epithelial cells
called enterocytes that line the inside
of the GI tract. Some enterocytes are
absorption cells and some are
exocrine cells (including goblet cells,
which secrete mucus). The lamina
propria is a layer of connective tissue underlying the mucous membrane. The muscularis mucosae
is a layer of smooth muscle that contracts the mucosa into folds
Submucosa: a layer of connective tissue that provides elasticity and blood supply. The enteric
nervous system consists of the myenteric plexus and the submucosal plexus. The enteric nervous
system regulates many GI functions independent of external influence. Input comes from
receptors located in the GI tract and autonomic neurons.
Muscularis Externa: Responsible for the motility of the GI tract. Consists of two layers of smooth
muscle: the inner circular muscle and the outer longitudinal muscle. The circular muscle
generates spontaneous slow-wave potentials. The longitudinal muscle depends on neural input for
contraction.
Serosa: Consists of connective tissue that provides structure and a layer of epithelial tissue called
mesothelium, which secretes a lubricating substance. The mesothelium is continuous with
mesenteries, which are membranes that interconnect abdominal organs. The peritoneum is a
membrane that lines the abdominal cavity.
Lesson 33 – Gastrointestinal II (578-599)
1. Describe the fundamental mechanisms involved in the absorption of carbohydrate, protein, and
lipid digestion products. Explain how the mechanism of lipid absorption is related to the
hydrophobic nature of fats.
Carbohydrates
Digestion: consumed as polysaccharides that must be broken down to monosaccharides. Cellulose cannot
be digested, so it passes through the entire intestinal track as a polysaccharide. Polysaccharides are
digested by amylases, which can be salivary amylase or pancreatic amylase. Salivary amylase is
inactivated by acid in the stomach, which is where pancreatic amylase dominates. Amylases cannot break
1,6 bonds at branch points, so they can reduce starch to either maltose (disaccharide) or limit dextrins.
Breakdown of disaccharides or limit dextrins is completed by brush boarder enzymes such as dextrinase
(breaks limit dextrins), glucoamylase (breaks straight-chain glucose), sucrase (hydrolyzes sucrose),
lactase (hydrolyzes lactose), and maltase (hydrolyzes maltose).
Absorption: Monosaccharides are absorbed by carrier-mediated transport across epithelial cells lining
intestinal villi. Glucose and galactose enter via cotransport with sodium. Fructose is absorbed by
facilitated diffusion.
Proteins
Digestion: Must be digested as tripeptides, dipeptides, or amino acids. Endopeptidases split polypeptides
at non-terminal bonds. Exopeptidases cleave polypeptides from the end working inward. Proteases are
stored as zymogens, which are inactive precursors to enzymes, to protect proteins in secretory cells. Once
in the lumen of the stomach, zymogens are activated via proteolytic activation. Protein digestion is
initiated by pepsin (from pepsinogen, secreted by chief cells), an endopeptidase. Pepsinogen is partially
activated by HCl (secreted by parietal cells) and is inactivated by the alkaline lumen of the small intestine.
The pancreas secretes trypsinogen, chymotrypsinogen, and procarboxypeptidase. Enterokinase cleaves
trypsinogen to trypsin, and trypsin cleaves chymotrypsinogen (to chymotrypsin) and procarboxypeptidase
(to carboxypeptidase). These are all endopeptidases. Aminopeptidase is an exopeptidase that finishes
digestion by cleaving the amino and carboxyl ends.
Absorption: Actively transported into intestinal epithelial cells by cotransport with sodium. There are at
least 4 distinct amino acid carriers. Dipeptides and tripeptides are also actively transported with different
transporters than the ones used for amino acids. Once in the epithelial cells, they are broken down into
amino acids. Amino acids are transported across the basolateral membrane by facilitated diffusion into the
blood.
Lipids
Digestion: Lipids are consumed primarily as triglycerides. Lipids are broken down by lipases, beginning
with lingual lipase in the saliva, and later by gastric lipase in the stomach. Pancreatic lipases in the small
intestine carry out the majority of lipid digestion. Bile salts (derived from cholesterol with several polar
groups) secreted by the liver into the duodenum carry out emulsification to increase the surface are of
lipids. Pancreatic lipase
2. In general terms, describe the role of short reflex pathways, long reflex pathways, and GI
hormones in control of digestive functions.
Conditions of the lumen of the GI tract are measured by mechanoreceptors, chemoreceptors, and
osomoreceptros. Control is exerted by smooth muscle or secretory cells.
Stimulus in the lumen of the GI tract without a response involvement in the CNS. This is the short
pathway; in this pathway stimulus goes straight from nerve plexus to effectors without CNS involvement.
In the long pathway, receptors go to the CNS then the intrinsic nerve plexuses which relay information to
effectors. Increased parasympathetic = increased muscle activity = increased product secretin.
Sympathetic does opposite.
The different phases are:
-cephalic-phase- always affected by CNS and involves stimuli in head (taste, thought, or smell of food)
-Gastric-phase- arising in stomach
-intestinal-phase- arising in intestines
One important factor for long term regulation is leptin. Adipocytes secrete leptin in a level propottional to
the amount of adipose. Leptin then acts to decrease the amount of hunger. Leptin itself is a satiety signal
but stimulates the release of others as well which coordinate responses to decrease fat stores and increase
sympathetic activity and TSH and ACTH, generally increasing metabolic rate. The oppisote of a satiety
factor is a orexigenic factor.
3. Describe the functions of saliva, stomach acid, pancreatic juice, and bile. Explain how the
secretion of each of these substances is regulated.
Saliva:
Neural input to salivary glands come from both branches of the autonomic system. This system is distinct
as saliva is secreted by both sympathetic and parasympathetic activation. Parasympathetic makes large
amounts of watery saliva and sympathetic makes a small amount of protein rich thick saliva. The saliva
center in the medulla oblongata controls it. Chemoreceptors relay information to the saliva center about
the taste of food. Food in the mouth activates the chemoreceptors which activate the parasympathetic
system, activating saliva secretion. The saliva center is also affected by input from the cerebral cortex
which gives information like the sight and smell of food.
Stomach acid:
The acid secreted by the stomach is generally made inside parietal cells by the carbonic anhydrase
catalyzed reaction. A proton pump uses ATP to pump out the H+ into the lumen in exchange for a K+
ion. Bicarbonate ions exit the cell across the basolateral membrane in exchange for chloride. The chloride
then moves to the lumen through channels. The net result is H+ and Cl- flow into the lumen and
bicarbonate to the interstitial. The secretion of acid is stimulated by parasympathetic nervous system,
gastrin, and histamine. Acid secretion is controlled by cephalic phase, gastric phase, and intestinal phase
stimuli. Pepsinogen and acid tend to rise and fall with each other. Cephalic phase stimuli and the act of
chewing or swallowing stimulate parasympathetic nerves which activate parietal, chief, and G cells.
Gastin from G cells enters the blood and further activates the parietal and chief cells. In the gastric phase,
mechanoreceptors sense stomach distension and chemoreceptors sense protein, and signals in the short
and long reflex increases chief, parietal, and G cells. After food leaves the stomach there is an absence of
the stimulates which increased acid and because proteins are not able to buffer the acid, the acid acts
stronger on G cells, suppressing the gastrin release. The distension and osmolarity increase in the
duodenum stimulate chemoreceptors, osmoreceptors, and mechanoreceptors which act via the short and
long reflex to decrease acid and pepsinogen secretion.
Pancreatic Juice:
In the pancreatic acini the cells produce a small volume of fluid with water, electrolytes, and digestive
enzymes. As this fluid flows through the ducts leading from the acini the duct cells secrete a larger
volume of bicarbonate rich fluid that is added. The regulatory mechanisms for the enzyme rich and
bicarbonate rich fluid are somewhat different despite simultaneous secretion. This means pancreatic juice
varies.
Intestinal-phase stimuli dominates pancreatic juice control. The strongest influences are CCK and secretin
which respond to food in the duodenum. CCK acts on acinar cells to stimulate enzyme secretion, and
secretin stimulates bicarbonate secretion. The effects of CCK and secretin are weak on their own but
strong when together, this amplification is known as potentiation. The release of secretin is strongly
affected by duodenal acidity which is measured by chemoreceptors. The secretion of CCK is regulated
primarily
4. Define peristalsis, segmentation, migrating motility complex, haustration, mass movement, and
basic electrical rhythm. Describe the role of each in digestion.
Peristalsis- propel the contents forward at a rate dependent on the basis of electrical rhythm
Segmentation- in the small intestine the muscularis externa can alternate contractions between the
segments to mix the chyme
Migrating motility complex- cyclical patterns of intense motility followed by relaxation in the stomach
and small intestine that clears the lumen of its contents
Haustration-mixing of the colon
Mass movement -peristaltic like wave in the colon that propels its contents forward. Its like peristaltic
wave except after contraction it remains contracted longer, propelling the luminal content forward.
Basic electrical rhythm – Is affected by neural activity and hormones. In general parasympathetic is
excitatory and sympathetic does the opposite. These influences reflect changes in the pattern of slowwave activity. Neural and hormonal signals affect amplitude of the slow wave rather than their frequency.
Lesson 35 – Endocrine System II
Pg. 603-616
1. Compare the metabolic pathways operating during energy mobilization of those operating during
energy utilization.
Absorptive state- 3-4 hours after typical meal. Absopation of nutrients after a meal.
Postabsorptive state- time between meals when nutrients are not absorbed.
2. Explain the concepts of negative energy balance and positive energy balance.
Positive energy balance- when energy input exceeds output
Negative energy balance- when energy output exceeds input
3. Describe the hormonal control of metabolism during absorptive and postabsorptive states.
Insulin- hormone secreted by beta cells in pancreas. Promotes the synthesis of storage molecules and
other molecules characteristic of the absorptive state.
Important to note that only GLUT4 is insulin sensitive and does facilitated diffusion of glucose.
Glucagon- peptide hormone made by alpha cells of pancrease. It is stimulated by drops in glucose, and
increase in symp activity and epinephrine. Its main goal is to mobilize energy stores.
Plasma glucose is tightly regulated by the effects of these gormones. Normal fasting glucose levels are
70-110 mg/dL.
Increases in plasma amino acids increases the release of both glucagon and insulin. This increases amino
acid intake by insulin, which also decreases blood glucose. If the meal was high protein low carb this can
dangerously drop blood glucose, necessitating the release of glucagon simultaneously to prevent negative
effects.
Lesson 36- Endocrine system III
Pg 616-628
1. Describe how the body regulates temperature
Negative heat balance, heat loss exceeds heat produced, fall in temp. Positive is the reverse. Heat is lost
generally lost by radiation, conduction, evaporation, and convection. When the environment is higher
temp than the body, heat transfers into the body by radiation and conduction, boosting the need for heat
loss.
The body’s efforts maintain the core temperature, the temp in the internal structures (CNS and abdominal
and thoracic cavity). This temp is normally about 37 C and is regulated in the hypothalamus at the
thermoregulatory center. Input about the core temp is transmitted by the central thermoreceptors. Other
thermoreceptors are peripheral thermoreceptors in the skin and are usually well below the core temp. Skin
temp is not regulated. Primary mechanism for regulating body temp is to vary the amount of blood flow
to the skin. Here thermal energy in the blood can be exchanged w that in the environment. Alterations in
the blood flow to skin can maintain body temp when within the thermoneutral zone (25-30 C).
When below 25 C, decrease in blood flow alone cannot prevent body temp falls. The heat promoting
center of the hypothalamus stimulates shivering and decreasing sweat production. As muscles contract
they generate heat. Infants and hibernating mammals can do non-shivering thermogenesis using brown
adipose tissye that generates heat by uncoupling the ETC from oxidative phosphorylation. The energy of
electrons is instead lost as heat instead of ATP.
The body produces sweat to evaporate excess heat. There are two types of sweat glands. Eccrine- all over
the body (especially in forehead, palms, soles). Apocrine- located primarily in arm pits and anal genital
region Apocrine empty into hair follicles. Apocrine sweat has proteins and fatty acids.
During fever, blood cells create pyrogens that induce fever. They act to adjust the tempt to be maintained
to ahigher level.
2. Explain how the growth hormone regulates growth
GH directly promotes growth in two ways: stimulates protein synthises (increasing cell size) and
stimulating cell division (increasing cell number). GH indirectly increases the plasma conc of glucose,
fatty acids, and glycerol. This makes the nutrients more available to growing tissues.
Many actions of Gh are caused my intermediate peptide insulin-like growth factors. GH is regulated by
GHRH and GHIH (somatostatin). Decreased GH is thought to be partially responsible for declines caused
by gaining
GH does:
a.
b.
c.
d.
Increase bone length
Insulin like growth factor
Increase muscle and amino acid uptake
Adipose tissues  lipolysis
3. Describe the synthesis and secretion of thyroid hormones. Distinguish between direct and
permissive actions of thyroid hormones.
Thyroid hormones show little variation throughout the course of a normal day. They therefore act to
maintain the status quo. The thyroid gland has numerous follicles that have a single outer layer of
follicular cells surrounding a central protein rich colloid secreted by the cells. In the interstitial space
between follicles are C cells, which make calcitonin. Thyroglobulin in the colloid is the precursor for TH.
Steps of TH synthesis and secretion:
1. Tyrosine residues TG are iodinated. One iodide= monoiodotyrosine, two is diiodotyrosine (DIT)
2. Two iodinated tyrosine residues on the same Tg are coupled. Changes in coupling make different
TH, T3 vs T4 for example. Two MIT groups cannot combine
3. Thyroid hormones are stored in the colloid bound to TG for up to three months
4. TSH arriving via the bloodstream binds to receptors on the follicular cells, cAMP second
messaging happens. The result is phosphorylation of necessary protein.
5. The follicular cells take in iodinated TG molecules from the colloid by phagocytosis
6. The phagasome containing the iodinated TG fuses w a lysosome
7. Lysosome breaks down the TG, freeing T3 and T4 into the follicular cell. They are passed into
the blood.
TH remains virtually constant. TSH is stimulated by TRH. Thyroid hormones are lipophilic and easily
cross membranes. The receptors of these hormones are found in the nuclei of target cells. They alter
protein synthesis. They take hours to days to take effect but last for days. The primary action is to raise
the BMR. It also promotes energy mobilization.
4. Describe the effects of glucocorticoids on whole body metabolism. Compare the physiological
effects of glucocorticoids to their pharmacological effects
At normal conc, these hormones maintain a wide variety of body functions, at higher levels, they help the
body adapt to stress. Secretion by the adrenal cortex is stimulated by ACTH, which is stimulated by
CRH. Cortisol is the primary glucocorticoid from the adrenal cortex. It is secreted in bursts and has a
circadian rhythm. The presence of glucocorticoids is essential to mobilize fuels in response from other
hormones. They act to maintain the normal conc of enzymes necessary for the breakdown of energy
sources. They are necessary for responding to fasting. They are also required for GH secretion, in
synergism with TH, and for the responsiveness of blood vessels to constriction and dilation. In high
concentration they enhance energy mobilization. Pharmacologically at high levels they inhibit
inflammation and allergic reactions, they also are given during transplants to reduce the risk of transplant
rejection.
5. Describe the stress response
Cortisol is important to helping the body adapt to stress. It mobilizes energy which is crucial to tissue
repair. Cortisol is still only one facet of the stress response. In general, if a stimulus is effective in
triggering an increased cortisol secretion it also triggers a pattern of other nueral and hormonal responses.
For example, stress increases the sympathetic response and epinephrine secretion. The combined general
adaption to stress is the general adaption syndrome.
Lesson 37 – Reproductive System I
Male and Female anatomy and Hormonal Regulation
Page 634-655
1. Describe the role of sex chromosomes and sex hormones in the development of sexual
characteristics
The gonads (testes or ovaries) are the primary reproductive organs bc they preform two functions that
govern reproduction- produce gametes and secrete sex hormones. Testes have angrogens and ovaries have
estogens and progesterone. The accessory reproductive organs are the tubes that are responsible for
moving the gametes from place to place, the reproductive tract, and the various glands which secrete fluid
into the reproductive tract.
The sex of the offspring is determined entirely by the genetic make up of the sperm, not the egg. XX is
female, XY is male. The genes themselves o not confer the full complement of sex related traits, they just
determine if the embryo will develop ovaries or testes. Initially the embryo has gonads that have the
potential to be overies or testes. Whether a fetus develops ovaries or testes is determined by the stY gene
which codes for the testis-determining factor on the Y chromosome. The srY gene causes testes
development, so in a way ovaries are the “default.”
In the first few weeks, the embryo is sexually indifferent with wolffian ducts and Mullerian ducts (male
and female respectively). These structures can give rise to all reproductive organs except the gonads. The
development of gonads in embryo sets stage for other sex characteristics. Whether these are male or
female depends on the presence of testosterone and Mullerian inhibiting substance. IF these are present,
the fetus develops as male, and when absent as female. Testosterone acts on wolffian ducts to promote the
development of male characteristics. MIS promotes the regression and disappearance of Mullerian ducts.
During puberty the body develops secondary sex characteristics, the external features that distinguish
sexes.
2. Describe the process of spermatogenesis and its hormonal regulation
Fully developed sperm have three distinct segments, a bulblike head, a short cylindrical midpiece, and a
long slender tail. Within the head are the chromosomes and a large vesicle called an acrosome which has
the enzymes necessary for fusion with the egg. The midpiece has the mitochondria necessary for motility.
Spermatogenesis starts near the basement membrane in the seminiferous tubules with undifferentiated
germ cells called spermatogonia. As spermatogenesis continues, the germ cell moves towards the lumen
of the tubule in the spaces between the Sertoli cells. At a certain point the developing germ moves to the
luminal compartment by passing through tight junctions which open temporarily to let the cells pass
through. Older more mature cells are found closer to the lumen, new younger ones are found near the
basement membrane.
Males are born w/ a finite # of spermatogonia but these cells undergo mitosis repeatedly, giving men the
capacity to produce sperm indefinitely. One of the split cells remains and the other differnetiates, meaning
the # of spermatogonia does not change. To become mature a spermatogonium must:
a. The chromosomes are replicated, and the cell differentiates to become a primary
spermatocyte, w/ 46 duplicated chromosomes
b. Go through meiosis I w/ two cells w/ 23 duplicated chromosomes (secondary
spermatocytes)
c. Secondary spermatocytes undergo meiosis II, to become spermatids, 23 single
chromosomes
d. Spermatids differentiate to become spermatozoa w/ a characteristic three segments.
Spermatids are released into the lumen of seminiferous tubules
Spermatids are immotile and remain so 20 days, they only acquire motility about 20 ays later when they
move to the epidymis to undergo further maturation. (remember SEVEn UP). Sperm are held in the vas
deferens until ejeaculation
S-seminiferous tubule
E-epididymus
Vas deferns
Ejaculatory duct
Nothing here
Urethra
penis
3. Explain the cyclic variation in plasma hormone levels that occur during the menstrual cycle.
Describe how these hormones regulate the ovarian and uterine changes that occur during this
cycle.
Hormones affect the cycle but the cycle also affects plasma levels of the hormones. The hormonal
changes during the menstrual cycle are shown below.
The early follicular phase has short lived declines in plasma estrogen and
progesterone levels. Estrogen and progesterone suppress the secretion of
gonadotropins by the anterior pituitary, so FSH and LH show a slight
increase. The rising FHS stimulates several follicles to develop and grow.
FSH binds to receptors on granulosa cells and causes proliferation, causing
them to increase in size. Under the influence of FSH the outer layer
differntiates into theca cells which then have LH receptors.LH then makes
the theca cells secrete androgens which travel to the granulosa and are
converted to estrogens. A dominant follicle emerges that secretes estrogens
at a high rate that causes plasma levels of these hormones to rise rapidly.
This in turn causes suppression of LH and FSH.
In the early to mid follicular phase estrogens promote a variety of physiological changes. Uterine changes
such as in the proliferative phase are included. Estrogens, with FSH, promote Oogenesis and follicular
growth. These hormones also prepare the body for subsequent events of the cycle. Estrogens also induce
progesterone receptors on endometrial cells.
In the late follicular phase, the rising estrogen triggers a fundamental change in the hypothalamus and
anterior pituitary secretion. Estrogens start to Stimulate the LH secretion. LH levels rise, which strimuates
more estrogen, creating a positive feedback loop. This is the LH surge. Estrogens stimulate granulosa
cells to express LH making them LH responsive. This causes the following in the dominant follicle:
a.
b.
c.
d.
e.
Granulosa cells secrete paracrine that stimulate the oocyte to complete meiosis I
Estrogen secretion by granulosa cells falls, causing plasma estrogen to decrease
Granulosa cells secrete progesterone, causing a small rise in plasma levels
Granulosa cells secrete enzymes and paracrine to break down the follicular wall
Granulosa cells and theca cells begin to differentiate into the cells forming the corpus luteum
Luteal phase. Early in this phase the corpus luteum is growing but not fully functional as an endocrine
organ. Plasma estrogen levels continue to fall bc the secretion by the corpus luteum cannot compensate
for the loss of the dominant follicle. This in turn terminates the LH surge. Progesterone secretion
increases bc of the corpus luteum. Estrogen and progesterone secretion continue to rise causing an
increase with a peak at the middle of the luteal phase. After the tenth day the corpus luteum begins to
degenerate and its activity declines. This causes a drop in estrogen and progesterone that triggers
menstruation. Below is the control during the luteal phase:
Lesson 38 – Reproductive System II
Fertilization to Parturition
Page 655-664
1. Describe the events that occur during fertilization, implantation, and early embryonic
development
Sperm can live for ~5 days in the female reproductive tract, and an oocyte is only viable for 12-24 hours
after release, so fertilization can only occur from 5 days before ovulation to 1 day after.
Capacitation is a process that makes sperm capable of fertilizing an oocyte. Capacitation occurs in the
first several hours after sperm is deposited in the female reproductive tract. It includes changes such as
faster movement and alteration of the plasma membrane so that fusion with an oocyte is possible.
Overview: Fertilization usually occurs in the uterine tubules. The fertilized egg then undergoes a series of
cell divisions and moves to the upper portion of the uterus. It undergoes implantation, during which it
adheres to and embeds in the uterine wall.
Specifics of fertilization:
-
Several sperm can work together to break down the corona radiata and zone pellucida, which
triggers the acrosome reaction.
The acrosome reaction includes the release of enzymes that digest the zona pellucida so that
sperm can access the oocyte’s surface.
One sperm binds to a receptor on the oocyte membrane, which precipitates transport of the head
of the sperm into the egg’s cytoplasm.
Fusion stimulates the oocyte to complete meiosis II and become an ovum.
-
Once in the ovum, the sperm’s plasma membrane disintegrates, and its chromosomes migrate
towards the center of the cell along with the oocyte’s chromosomes.
The two sets of chromosomes combine
The first DNA replication occurs, followed by the first mitotic division. Now called a zygote.
Polyspermy is when more than one sperm penetrates the egg, which is very rare due to several
mechanisms:
-
Fusion of the first sperm with the oocyte triggers inactivation of sperm-binding proteins.
The zona pellucida hardens and pulls away from the plasma membrane.
Morula = round ball of cells formed in the first few days after fertilization. Total volume of cytoplasm
does not increase, so that each cell division results in smaller cells. All of the cells in the morula are
totipotent. The morula has not yet implanted in the uterine wall; it is either still migrating to the uterus or
is floating in intrauterine fluid. Identical twins can form at this stage if the morula splits into two parts.
Blastocyst = A hollow structure that contains the trophoblast (spherical outer layer), the inner cell mass
(cluster of cells inside), and the blastocoele (fluid-filled cavity). Cells are no longer totipotent. The
blastocyst attaches to the uterine wall. This is 6-7 days after fertilization. Cells of the trophoblast initiate
the decidual response, which includes secretion of enzymes that digest adjacent endometrial cells to
nourish the embryo and an increase in the number of capillaries. The trophoblast eventually becomes the
placenta.
Development from embryo to fetus:
At about 7 weeks post
fertilization, the trophoblast
thickens into the chorion.
Chorion = a tissue derived
from the trophoblast that
eventually grows into a
tough envelope that protects
the embryo.
Inside the embryo, the
amniotic cavity grows
within the inner cell mass.
The surrounding cells
develop into the amnion
(AKA amniotic sac), which
eventually fuses with the
chorion.
Cells within the inner cell
mass begin to differentiate
into distinct tissues: heart,
brain, spinal cord, and GI
tract are developing by week
5. Heart is beating by week
6. All organ systems are developing at week 9. By the end of week 10, the embryo has a recognizable
human form and is called the fetus.
The placenta allows for exchange of gases,
nutrients, and other materials between the fetus
and mother. Placental development begins when
the chorion sends out chorionic villi, which
contain capillaries of fetal circulation and cells
that secrete paracrines. Maternal and fetal blood
come into close proximity without mixing so
that the mother’s immune system does not
attack the fetus. The umbilical cord contains the
uterine artery and uterine vein. The uterine
artery delivers maternal blood to fetal sinuses.
The uterine vein returns blood to the mother’s
circulation.
1st trimester is weeks 1-12, during which the
embryo develops into a fetus.
2nd trimester is weeks 13-28, during which the
liver and bone marrow produce red blood cells,
the heart beats, and the GI tract is active.
3rd trimester is weeks 29-40, during which the bones develop, the lungs function in gas exchange, and the
body can store ions and nutrients.
2. Describe the regulation of estrogen and progesterone secretion during pregnancy, and explain
how these hormones help maintain pregnancy an prepare the body for parturition
Human chorionic gonadotropin (hCG) maintains the corpus luteum during the first three months of
pregnancy. It is secreted by the chorionic portion of the placenta. It has similar effects as LH. In response
to hCG, the corpus luteum secretes estrogens and progesterone. Secretion of hCG begins at implantation
and falls off after about 2 months, causing the corpus luteum to disintegrate. At this point, the placenta
takes over secretion of estrogen and progesterone.
Effects of high estrogen levels on the mother:
-
Growth of duct tissue in breasts which prepares the breasts for lactation.
Prolactin secretion by the anterior pituitary, which promotes breast growth.
Growth and enhanced contractile responsiveness of uterine smooth muscle, which enables the
uterus to contract more forcefully. Also increases responsiveness to oxytocin, which stimulates
contractions during labor.
Effects of progesterone:
-
Growth of glandular tissue in the breasts. Glandular tissue secretes milk.
Suppression of contractile activity in uterine smooth muscle. Acts against estrogen to prevent
premature labor.
Maintenance of secretory-phase uterine conditions, which ensures good conditions for the fetus.
Progesterone exerts negative feedback on the hypothalamus and anterior pituitary to keep LH and FSH
secretion low so that no new follicles appear, and no LH surge occurs despite the high levels of estrogen.
The placenta secrets placental lactogen, which has similar effects to prolactin. It also mobilizes the
mother’s energy stores to provide nutrients to the fetus.
End of pregnancy:
Weak and infrequent uterine contractions occur in the last weeks of pregnancy. Estrogen stimulates
contractions while progesterone prevents contractions, and during the last few weeks of pregnancy,
estrogen levels are higher than progesterone levels.
The cervix undergoes ripening, during which is becomes softer and more flexible due to enzymatic
breakdown of collagen fibers and connective tissue. The fetus moves downward and comes into contact
with the cervix.
In the hours before parturition, the amniotic sac ruptures (“water breaks”). A series of strong uterine
contractions begin. Each contraction starts at the top of the uterus and travels downward through the
uterine smooth muscle as a wave. This pushes the uterus against the cervix, forcing the cervical canal to
open. Voluntary contractions of the mother’s abdominal muscles facilitate this process.
Uterine contractions are promoted by positive feedback mechanisms by stretch sensitivity of uterine
smooth muscle and by oxytocin.
Lactation: The decrease of estrogens and progesterone that occur
during parturition allow lactation to begin. For the first two days
after birth, the milk is called colostrum and contains man
y proteins but little nutrients. After this, the milk becomes enriched
with fats, lactose, growth factors, hormones, and antibodies. Milk is
produced in the mammary glands by a cluster of round glands
called alveoli. The alveoli are surrounded by myoepithelial cells,
which are epithelial cells with contractile ability. Suckling by the
infant stimulates contraction of these cells, which helps force milk
out. In more detail: suckling stimulates tactile receptors on the
nipples, which project to the hypothalamus and result in oxytocin
secretion by the posterior pituitary. Oxytocin causes myoepithelial
cells to contract. Suckling also stimulates milk production by
increasing release of prolactin releasing hormone and inhibiting the
release of prolactin inhibiting hormone (Fig 22.28).
Immune system I
Anatomy and Organization
Pg 669-685
1. Identify the lymphoid organs, and briefly describe their functions
The immune system consists of physical barriers (like skin), leukocytes
(white blood cells), and lymphoid tissues.
Central (primary) lymphoid tissues: sites of lymphocyte production and
maturation
-
Bone marrow: site where all leukocytes develop from
hematopoietic stem cells
Thymus: site of maturation of T cells (T cells migrate from the
bone marrow to the thymus to mature)
Fetal liver: site of lymphocyte development in a fetus
Peripheral (secondary) lymphoid tissues: sites where lymphocytes contact
pathogens and become activated
-
Spleen
Lymph nodes
Tonsils
Adenoids
Appendix
Lymph Nodules
Peyer’s patches
Physical barriers are the skin and mucous membranes that separate the internal and external
environments. Chemical barriers include lysozymes in saliva, HCl in stomach, acid in the urinary tract,
and fatty acids in sebaceous glands.
Leukocytes are all derived from hematopoietic stem cell sin the bone marrow. There are five types of
leukocytes divided into granulocytes and agranulocytes. The granulocytes are neutrophils, eosinophils,
and basophils. The agranulocytes are monocytes and lymphocytes.
-
Phagocytes = neutrophils, eosinophils, monocytes, macrophages, and dendritic cells.
Three types of lymphocytes: B cells, T cells, and null cells. Most null cells are granular. Natural
killer (NK) cells are null cells.
Precursors for mast cells and dendritic cells are also formed in bone marrow. Look at fig 23.2.
2. Identify the different pathogens that can invade the body causing disease
For different classes of pathogens
-
-
-
-
Viruses- Smallest pathogens and consist of RNA of DNA w/ a protein coat. These cannot survive
w/o a host. It can double itself every hour. Almost all viral infections result in disease. These
pathogens attack specific cell types.
Bacteria- Small prokaryotic cells, 1-5 microns. Do not have nucleus or organelles (Duh bc
prokaryotes). Bacteria cells cause disease by invasion of the tissue and release of toxins. On their
outer surface they have adhesin that can bind to certain receptors on eukaryotic cells, allowing
adhesion to epithelial cells. Bacteria release endotoxins or exotoxins to cause disease. Endotoxins
are located on the bacterial cell walls of all gram negative, and exotoxins are proteins secreted
primarily by gram positive bacteria.
Fungi- Fungi do not consume nutrients but absorb it from their environment. People tend to get
fungal infections on the skin or in the respiratory tract (spore exposure areas). Fungi grow slowly
and are normally constrained by good bacteria in the vagina or on the epithelium.
Parasites- organisms that invade the host in their quest to obtain nutrients. Two main classes,
protozoans, and metazoans. Protozoans range from 10 um to 20 cm, and metazoan are
multicellular animals with different tissue types (includes worms and arthropods). Often spread
through a vector or the fecal-oral route.
3. Explain events that occur during inflammation. Describe how the skin and mucous membranes,
inflammation, interferons, and natural killer cells contribute to the body’s nonspecific defenses.
Immune responses can be specific (adaptive) or nonspecific (innate). Nonspecific defenses are much
faster and do not involve pathogen recognition. The innate immune system consists of physical barriers,
chemical barriers, and pathogen-associated molecular patterns (PAMPs). PAMPs associate with proteins
called pattern-recognition receptors that help distinguish between self and non-self. Nonspecific responses
include inflammation, interferons, and the complement system.
Inflammation includes five major events. These steps occur regardless of the type of pathogen because
inflammation is nonspecific (fig 23.5):
1)
2)
3)
4)
5)
Nearby macrophages engulf debris and foreign matter
Nearby capillaries dilate and become more permeable to proteins and fluid
Foreign matter is contained
Additional leukocytes migrate into the region
Recruited leukocytes continue to help clear the infection
More detail on inflammation:
Macrophages already in affected tissues recognize bacteria and initiate phagocytosis. This stimulates the
macrophage to secrete cytokines. The cytokines have several effects including synthesis of adhesion
molecules by blood vessels and release of more neutrophils from bone marrow. Nearby blood vessels
dilate, and capillary walls become more permeable to increase local blood flow and allow more immune
cells to reach the area. These changes are induced by histamine. Mast cells and basophils release heparin,
which is an anticoagulant, in order to suspend clotting in the area. Clot formation eventually proceeds
normally as clotting factors leak from the plasma, which traps foreign particles in one area. Neutrophils
accumulate, then monocytes accumulate and develop into macrophages. Leukocytes are signaled to move
through blood vessel walls to a particular location through margination, attachment, diapedesis, and
chemotaxis. Margination is a weak interaction of leukocytes with endothelial cells lining the blood
vessels near the site of injury. Attachment and diapedesis are when the leukocytes move between
endothelial cells of the blood vessel wall through the basement membrane beneath. Chemotaxis is
movement towards chemical signals released from bacteria and the injured tissue.
4. Describe the complement system and its role in both innate and adapted immunity.
This system can act specifically or nonspecifically, which way it responds is dependent on the presence of
antibodies. Its name originates because it compliments or fulfills the actions of specific antibodies. It is
approximately 30 plasma proteins that act to destroy invade microorganisms, especially bacteria.
The complement cascade can be activated by:
a. Binding to antibodies that are already attached to bacterial cells (classical pathways)
b. By binding of a serum protein, mannose-binding lectin, to mannose-containing carbs on bacteria
or viruses (lectin pathway)
c. Binding directly to carbs on surface of a broad rang of bacterial cells (alternative pathway)
These pathways converge and make the same set of complement proteins. This protects against infection
by four pathways.
a.
b.
c.
d.
Covalently bond to pathogens and function as opsins
Recruiting more phagocytes to the site of infection
Triggering histamine secretion by mast cells
Development of a membrane attack complex, a pore forming protein that can pierce the bacterial
membrane.
Lesson 40-Immune System II
Adaptive immunity
Page 685-697
1. Describe humoral immunity, that is, how B cells, through the production of antibodies contribute
to the immune responses.
Many B lymphocytes w different specificities circulate, and when one binds with an antigen, the cell
proliferates (increasing the amount of cells w/ the same specificity) and the cell differentiates to create
some memory B cells and some short lived antibody producers. These short lived cells are known as
plasma cells.
The antigens that evoke production of memory cells are T-dependent antigens bc they require helper T
cells. When helper T cells respond to antigens they secret IL-2 and together these and T-dependent
antigens induce B cell proliferation. Without IL-2 all the proliferating cells differentiate into plasma cells.
Without T-dependent antigen production there will not be immune memory.
The way in which an antibody aids in antigen disposal depends on its class which is determined by the
tail.. All classes can mediate the simplest forms of attack, neutralization, and agglutination, whereas
specific classes deal with opsonization, complement activation, and NK stimulation.
Antibody methods:
-
Neutralization-antibody blocks antigen activity through binding alone.
Agglutination-the linking together of many antigens through the specific binding of many
antibodies.
Opsonization- once bound an antigen is effectively opsonized and therefore more susceptible to
phagocytosis.
Complement activation- IgM and IgG can activate the complement system which brings about
bacteria lysis
Enhanced activation of NK cells- IgG antibodies can enhance the nonspecific action of NK cells
2. Describe cell mediated immunity, that is, how helper T cells and cytotoxic T cells contribute to
immune responses.
T cells contact and respond to infected body cells. Because direct contact between targets are required it
makes this response “cell-mediated”
Three types of T cells:
-
Helper- The primary regulators of the immune response, operate indirectly by secreting cytokines
that enhance B Cells (remember IL-2?), Cytotoxic t cells, and suppresser T cell activity.
Cytotoxic t cells- are directly responsible for cell mediated immunity. They kill the cells infected
by viruses or intracellular bacteria.
Suppressor- are not well understood, thought to produce cytokines that suppress immune
activation
All these cells have antigen receptors that detect foreign antibodies. They only do so when these antigens
are w/ self-identifying proteins- major histocompatibility complex molecules (MHC). Essential in T cell
activation is antigen presentation. In this process MHC molecules bind to a foreign antigen present in a
body cell then transport it to the cell surface.Each persons MHC molecules are unique to themselves, it is
virtually impossible for the tissues of two people to have the same set. Interestingly blood has no MHCs
which is why this tissue is the least likely to be rejected.
MHC class I- glycoproteins on the surface of all nucleated cells. They present intracellular antigens to
CT-T cells
MHC class II- found on only a few specialized cells types (macrophages, dendritic cells, activated B cells,
cells on interior of thymus) these are all antigen presenting cells. They present to H T cells the
endogenous antigens
Each MHC molecule has a binding site. A newly
synthesized MHC molecule maked its way to the
surface of the cell. It can capture an antigen
fragment on it binding cite. How the MHC
molecule captures and presents the antigen and
which T cell recognizes caries between classes.
Class I MHC capture antigens w/in the infected
cells and transports them to the cell surface.
Class II are found in phagocytes and bind to
internalized antigen and transport it to the cell
surface.
T cells w/ different specialties normally circulate. Activation involves two events: 1. Helper t cells bind
w/ class II MHC, 2. Helper t cells receive signals from these cells in the form of IL-1. As a result they
proliferate and differentiate. Some of the daughter cells secrete cytokines and a small number become
long lived memory T cells. (this should sound similar to B cells ). Activated helper T cells secrete
cytokines that help stimulate and regulate the activities of other immune cells. This makes them the
central regulator of the immune response.
CT T cells become activated when: 1. The cell binds w/ I MHC, 2. Receives an inducing signal in IL-2.
When activated it releases perforins which cause the target cell to lyse by causing pores. They also secrete
fragmentins which can get into cells through perforins before inducing apoptosis.
3. Explain how immunization can lead to protection from infectious disease.
A safe form of a microorganism or a collection of its components that do not cause disease are introduced
to the body. It creates immunological memory. This is active immunity as it depends on the immunized
individuals body to mount a response.
4. Discuss the major immunological issues regarding blood transfusion and organ transplantation.
The body has a hostile response to foreign bodies. The blood is classified into different types. According
to the presence or absence of certain antigens. These are Type A or B antigens. It is important to consider
the antigens and both the antibodies in the blood of the donor in blood transfusions.
In tissue grafts- MHC molecules exist in many different forms. Thus HLA mismatches are responsible for
the rejections that occur in grafts and organ transplants. Tissue typing gets the closest match pssible.
5. Explain how immune dysfunction can result in allergy, autoimmunity, or immunodeficiency
Allergies are exagerted responses to environmental antigens. These common allergies involve IgE class
antibodies. The IgE tail goes into mast cells, then when pollen bind, the histamine in the mast cell is
released. In anaphalyictac shock it is not local dilations but widespread drops in TPR and MAP.
Epinephrine can counter these effects. Autoimmune is loss of self tolerance.