Midterm 1 Flashcards
transmembrane potential
definition and
3 factors contributing to it
Unequal distribution of ions across the plasma membrane because
1. ECF and ICF have different ionic composition
2. Cells have selectively permeable membranes
3. Membrane permeability varies by ion
Intracellular fluid (ICF)
fluid in the cytosol of cells, typically more negative than ECF due to greater amounts of K+ and negatively charged proteins
Extracellular fluid (ECF)
fluid outside the cells; includes intravascular and interstitial fluids, typically more positive than ICF
Passive forces acting across the membrane
chemical and electrical gradients
Common ions in the body
Na+, K+, Cl-, Ca2+
Potassium ion gradients
- K+ predominantly inside of cell
- Chemical Gradient tends to push K+ out of cell
- Electrical Gradient tends to push K+ out of cell
= Net Gradient (Electrochemical Gradient) - forces K+ outside of cell
Sodium ion gradients
-Na+ predominantly outside of the cell
- at the normal resting potential, chemical and electrical gradients combine to drive sodium ions into the cell
Why doesn’t more Na+ move into cell at rest?
There are very few Na+ leak channels into the cell
Resting potential of a nerve cell
-70 mV, with more sodium outside the cell and more potassium inside the cell with negatively charged proteins
Active force acting across the membrane
sodium-potassium ATPase (exchange pump)
Sodium-potassium exchange pump
for each ATP molecule used, 3 Na+ are pumped out of the cell while 2 K+ are pumped into the cell, helps to repolarize the membrane after an action potential, maintain the concentration of potassium and sodium ions across the PM
Why does the transmembrane potential exist across the plasma membrane?
because of a difference in ionic and chemical composition between the cytosol (ICF) and ECF due to locations of sodium and potassium and negatively charged proteins in the cell
Leak channels
channels that are always open and allow ions to move along their gradient
Gated channels
a transmembrane protein channel that opens or closes in response to a particular stimulus, ie. chemically-gated, voltage-gated and mechanically-gated
Chemically gated channels
open with binding of a specific neurotransmitter such as ACh
Voltage-gated channels
open and close in response to changes in transmembrane potential, is closed when membrane potential at resting potential of -70 mV, opens when membrane depolarizes to -60 mV, and is inactivated at +30 mV
Mechanically-gated channels
open and close in response distortion of the membrane
Graded potential
any stimulus that opens a gated channel, involve three steps: depolarization, repolarization and hyperpolarization
Graded potential in a neuron: steps
resting membrane potential is -70 mV with closed chemically-gated sodium ion channels -> membrane exposed to chemical that opes the sodium ion channels -> spread of sodium ions inside the PM produces a local current that depolarizes adjacent portions of the PM
Action potential
propagated changes in transmembrane potential that affect the entire membrane
Threshold for action potential
Level of stimulation needed to trigger a neural impulse, typically -60 mV
All-or-none principle
Refers to the fact that the action potential in the axon occurs either full-blown or not at all.
Axolemma
plasma membrane of an axon, contains both voltage-gated sodium channels and voltage-gated potassium channels that are closed when the membrane is at the resting potential
Depolarization to threshold
The stimulus that initiates an action potential is a graded depolarization large enough to open voltage-gated sodium channels, occurs at -60mV, the threshold.
Activation of sodium channels and rapid depolarization
When the sodium channels activation gates open, the PM becomes much more permeable to Na+. Driven by the large electrochemical gradient, sodium ions rush into the cytoplasm and rapid depolarization occurs. The inner membrane surface now contains more positive ions than negative ones and the transmembrane potential has changed from -60 mV to a positive value
Inactivation of sodium channels and activation of potassium channels
as the transmembrane potential approaches +30 mV, the inactivation gates of the voltage-gated sodium channels close, known as sodium channel inactivation, and it coincides with the opening of voltage-gated potassium channels. Positively charged potassium ions move out of the cytosol, shifting the transmembrane potential back toward resting levels. Repolarization now begins.
Closing of potassium channels step of action potential
The voltage-gated sodium channels remain inactivated until the membrane has depolarized to near threshold levels. At this time, they regain their normal status: closed but capable of opening. The voltage-gated potassium channels begin closing as the membrane potential reaches about -70 mV. Until all the potassium channels have closed, potassium ions continue to leave the cell, this produces a brief hyperpolarization.
Steps of an action potential
1.Depolarization to threshold -60 mv.
2.Activation of sodium channels and rapid depolarization.
3.Inactivation of sodium channels and activation of potassium channels +30 mV.
4.Potassium channels close greater than -70 mV.
Begins and ends with resting potential
Absolute refractory period
time during which another action potential is impossible; limits maximal firing rate, takes place when the voltage-gated sodium channels are open until the membrane starts to repolarize
Relative refractory period
the period of time following an action potential, when it is possible, but difficult, for the neuron to fire a second action potential and requires a larger than normal stimulus, due to the fact that the membrane is further from threshold potential (hyperpolarized)
Continuous propagation
action potentials along an unmyelinated axon, affects one segment of axon at a time
Saltatory propagation
- action potential along myelinated axon
- faster and uses less energy than continuous propagation
- myelin insulates axon, prevents continuous propagation
- local current “jumps” from node to node
- depolarization occurs only at nodes
Steps of continuous propagation
- Action potential develops at initial segment, depolarizes to +30 mV
- As sodium ions entering at initial segment spread away from open voltage-gated channels, a graded depolarization brings second segment to threshold
- An action potential now occurs at the second segment, while initial segment begins to repolarize
- As sodium ions entering second segment spread laterally, a graded depolarization quickly brings the third segment to threshold and the cycle is repeated
Steps of saltatory propagation
- An action potential occurs at the initial segment
- A local current produces a graded depolarization that brings the axolemma at the next node to threshold
- An action potential develops at node 2
- A local current produces a graded depolarization that brings the axolemma at node 3 to threshold
Factors affecting propagation speed
axon diameter and amount of myelination
Type A fibers
myelinated and large diameter fibers, highest conduction speed of up to 268 mph, rare
Type B fibers
myelinated and smaller diameter fibers, moderate conduction rate of 40 mph
Type C fibers
unmyelinated and small diameter fibers, conduction speed of 2 mph
Neural communication
presynaptic neuron -> synapse -> postsynaptic cell
Electrical synapse/gap junction
where two nerve cells are connected by connexons and action potentials move quickly and efficiently, found in heart and eye
Chemical synapse
a type of synapse at which a chemical (a neurotransmitter) is released from the axon of a neuron into the synaptic cleft, where it binds to receptors on the next structure (either another neuron or an organ), can have an excitatory or inhibitory effect
Cholinergic synapse
A synapse that uses acetylcholine as its neurotransmitter
Where are cholinergic synapses found?
- neuromuscular junctions (skeletal muscle)
- many CNS synapses
- all neuron-neuron PNS synapses
- all neuromuscular and neuroglandular junction in PNS
Steps of propagation at a cholinergic synapse
- an arriving action potential depolarizes the axon terminal of a presynaptic neuron
- Calcium ions (Ca2+) enters the cytosol of the axon terminal via voltage-gated Ca2+ channels, resulting in ACh release from the synaptic vesicles by exocytosis
- ACh diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane, chemically-gated sodium channel open producing a graded depolarization
- Depolarization ends as ACh is broken down by acetylcholinesterase into acetate and choline, the axon terminal reabsorbs choline from the synaptic cleft and uses it to resynthesizes ACh
information processing
integration of excitatory and inhibitory stimuli
excitatory postsynaptic potential (EPSP)
leads to depolarization of the cell membrane and action potential propagation
inhibitory postsynaptic potential (IPSP)
leads to hyperpolarization of the cell membrane and a larger than normal stimulus is needed to initiate an action potential
two types of summation
temporal and spatial
temporal summation
on a membrane that receives two depolarizing stimuli from the same source in rapid succession, the effects of the second stimulus are added to the first
1. first stimulus arrives
2. second stimulus arrives and is added to the first stimulus
3. action potential is generated
spatial summation
occurs when sources of stimulation arrive simultaneously but at different location, local currents spread the depolarizing effects and areas of overlap experience the combined effects
sympathetic nervous system nickname
fight or flight
parasympathetic nervous system nickname
rest and digest
organization of somatic nervous system
upper motor neurons located in primary motor cortex in precentral gyrus, somatic motor nuclei synapse directly onto brain and spinal cord, secondary motor neurons can be quite long as they span to reach their target
functions of sympathetic nervous system
- heightened alertness
- increased metabolic rate, respiratory rate, blood pressure and heart rate
- reduced digestive and urinary function
- activate of energy reserves and sweat glands
organization of sympathetic division
originate at T1-L2, ganglia are located adjacent to spinal cord except for the adrenal medulla where the ganglia synapses directly onto the medulla
organization of parasympathetic division
originate at brain stem and sacral vertebrae, ganglia are located very close to target organ
functions of parasympathetic division
- decreased metabolic rate, heart rate and blood pressure
- increased secretion by salivary and digestive glands
- increased motility and blood flow in digestive tract
- stimulation of urination and defecation
enteric nervous system
- digestive nervous system
- many local reflexes
- influenced by the sympathetic and parasympathetic nervous division
sympathetic nervous system neurotransmitters and receptors
- release ACh at central synapses
- releases norepinephrine (NE) at peripheral synapses
- have short preganglionic neurons and long postganglionic neurons
- leads to a releases of norepinephrine (NE) and epinephrine (E) from adrenal gland into bloodstream
- adrenergic receptors > alpha and beta receptors
parasympathetic nervous system neurotransmitters and receptors
- release ACh at all synapses
- have long preganglionic neurons and short postganglionic neurons
- cholinergic synapses > nicotinic and muscarinic receptors
effects of parasympathetic division
- eyes: constrict pupiles
- salivary glands: stimulate salivation
- heart: slows heartbeat
- lungs: constricts bronchi
- stomach: stimulates digestion
- liver: stimulates bile release
- intestines: stimulates peristalsis and secretion
- bladder: constricts bladder
effects of sympathetic division
- eyes: dilate pupils
- salivary glands: inhibit salivation
- heart: accelerates heartbeat
- lungs: dilates bronchi
- stomach: inhibits digestion
- kidneys: stimulates NE and E releases
- intestines: inhibits peristalsis and secretion
- bladder: dilates bladder
somatic vs sympathetic vs parasympathetic
- somatic NS has heavily myelinated axons and releases ACh, only has stimulatory effect
- sympathetic NS has lighter myelinated preganglionic axons that release ACh at ganglia and NE at effector, or ACh directly onto adrenal medulla
- parasympathetic NS has lightly myelinated preganglionic axons and release ACh at both ganglion and at effector
dual innervation
input from both sympathetic and parasympathetic divisions, can either have opposing or cooperative effects
autonomic tone
- the general degree to which both the sympathetic and parasympathetic divisions are always on
- allows an increase or decrease in activity levels
- provides a greater range of control, fine tuning
5 main sensory receptors
- mechanoreceptors
- chemoreceptors
- thermoreceptors
- photoreceptors
- nociceptors
mechanoreceptors
respons to touch + pressure stimuli
chemoreceptors
respond to chemical stimuli, smell and taste
thermoreceptors
respond to temperature stimuli
photoreceptors
respond to light for vision
nociceptors
respond to painful stimuli, most complex receptors and are tied to emotions
responses of sensory receptors to stimuli
- stimulus sensed by sensory receptors produce graded potentials aka receptor potentials
- receptor potentials give rise to action potentials (AP) that are responsible for sensory information
- sensory information is carried to the brain via sensory nerve tracts
graded potential
changes in membrane potential that are proportional to the size of the stimulus rather than all or none
sensory areas of cerebral cortex
- sensory pathways end up at specific regions of the brain called primary sensory areas found in post central gyrus
- sensory pathways > thalamus > appropriate sensory area
sensory homunculus
somatic sensory cortex is organized relative to the general plan of the body
motor homunculus
found in primary motor cortex located in precentral gyrus
hearing properties
- need to be able to discern volume, pitch, and location all using action potentials
auditory structures - external ear
auricle, external auditory meatus, tympanic membrane
auricle
“floppy” part of external ear, cartilaginous part, designed like a funnel to deflect sound into ear
external auditory meatus
entry part to internal portion of ear, passageway to tympanic membrane
tympanic membrane
separates outer ear from middle ear, also known as ear drum
auditory structures - middle ear
tympanic membrane, middle ear ossicles (malleus, incus, stapes), oval window
malleus
- 1st bone of middle ear ossicles, has a hammer like action
- has tensor tympani muscle attached for sound attenuation
incus
2nd bone of middle ear ossicles, shaped like an anvil
stapes
3rd bone of middle ear ossicles, shaped like a stirrup
oval window
separates middle and inner ear
auditory structures - inner ear
oval window, cochlea, round window, vestibule, semicircular canals
cochlea function
fluid-filled, spiral-shaped cavity found in the inner ear, plays a vital role in auditory transduction, sound waves are transduced into electrical impulses
round window
connects the middle ear with the lower half of the cochlea, functions to aid fluid motion within the cochlea and serve to equalize the hydraulic pressure
vestibule
sits between and connects the cochlea and semicircular canals and helps to maintain equilibrium, two regions lined by the membranous labyrinth; the utricle, which is closer to the semicircular canals, and the saccule, which is closer to the cochlea
semicircular canals
three tiny, fluid-filled tubes in the inner ear that help you keep your balance, when head moves liquid within the tubes bends hairs that line the canals
bony labyrinth
cochlea, vestibule, semicircular canals, has membranous labyrinth residing within
membranous labyrinth
group of ducts and chambers filled with endolymph, located within the bony labyrinth and can be subdivided into the vestibular labyrinth and cochlear labyrinth
perilymph
fills area between the bony labyrinth and membranous labyrinth
structures for balance
vestibule and semicircular canals
cochlea strucures (4)
scala vestibuli, scala tympani, helicotrema, and cochlear duct
scala vestibuli
superior most duct of cochlea, filled with perilymph
scala tympani
inferior most duct of cochlea, filled with perilymph
helicotrema
connects scala vestibuli and scala tympani, allows perilymph to move between the two regions
cochlear duct
also known as scala media, is an endolymph filled duct located between the scala vestibuli and scala tympani, lower membrane is the basilar membrane and middle membrane is tectorial membrane
basilar membrane
located on base of cochlear duct, holds base of hair cells, thickness determines pitch detection by hair cells, thinner area of membrane detect high frequency and thicker for lower frequency
tectorial membrane
located in centre of cochlear duct, support tips of hair cells to maintain them upright
hair cells
specialized inner ear cells found in cochlear duct, responsible for the transduction of sound waves into action potentials relayed to brain via afferent fibres which join to form the cochlear nerve, arranged in four long rows, cells for detection of high frequency located near oval window, cells for detection of low frequency located near round window
cochlear nerve
sensory nerve that transfers auditory information from the cochlea to the brain, formed from afferent fibres of hair cells
auditory function - sound
- sound travels in waves which are characterized by frequency and amplitude
- frequency range for humans is 20-20,000 Hz
- sounds louder than 125 db are painful
amplitude
determines the perceived volume of a sound, goes up in a logarithmic scale and is measured in db
frequency
determines the perceived pitch of a sound, measured in Hz, as we get older our ability to detect higher frequency sounds decreases, carried out by specific regions of hair cells on basilar membrane for specific frequency ranges
auditory function - outer ear
- auricle collect sound waves, collects info about pitch and volume
- external auditory meatus conducts the sound wave toward the tympanic membrane
auditory function - middle ear
- sound waves strike the tympanic membrane and cause it to vibrate
- vibration is transferred to three middle ear ossicles to oval window
sound attenuation reflex
helps protect inner ear from damage, involves tensor tympani muscle and stapedius muscle, when a loud stimulus is detected, the two muscles contract attenuating the vibration so it does not damage inner ear
auditory function - inner ear
- vibration of stapes > vibration of oval window > perilymph and endolymph
- vibration of endolymph causes distortion of basilar membrane
- as basilar membrane distorts, hair cells move relative to the tectorial membrane leads to depolarization
- increase in loudness leads to increase in frequency of action potentials (temporal summation)
order of structures for sound conduction
auricle > external auditory meatus > tympanic membrane > malleus > incus > stapes > oval window > cochlea > auditory nerve
auditory function - neural pathways
- hearing information travels along the vestibulocochlear nerve to thalamus
- the thalamus directs action potentials towards the auditory cortex in the temporal lobe
balance anatomy components
- two parts of inner ear responsible for balance: vestibule which contains saccule (up and down, closer to cochlea) and utricle (back and forth, closer to semicircular canals); semicircular canals (rotation)
- hair cells embedded in gelatinous mass containing otoliths
semicircular canals
- 3 canals corresponding to the three main planes of movement
- sagittal plane (forward roll), divides body into left and right
- frontal plane (cartwheel), divides body into front and back
- transverse plane (pirouette), divides body top and bottom
otoliths
a crystal structure in the saccule and utricle of the inner ear, specifically in the vestibular system
how do we detect movement using inner ear?
- by detecting which direction the hair cells bend tells the brain which way the head tilts in the semicircular canals
how does vertigo work?
caused by issues in semicircular canals, hair cells bend when there isn’t movement which confuses the brain
4 types of intercellular communication
- synaptic (neural)
- direct (gap junctions)
- paracrine (local effects)
- endocrine (whole body)
paracrine communication
allows communication between cells in the same tissue, occur when paracrine factor concentrations are relatively high, ie roll your ankle and leads to localized swelling
endocrine communication
-when cells communicate with target cells throughout the body using the bloodstream
-global communication
- target cells must have the appropriate receptors
similarities between nervous and endocrine systems
- rely on chemicals binding to specific receptors on target cells
- share many chemical messengers (epinephrine and norepinephrine)
- rely on negative feedback for regulation
- share a common goal of preserving homeostasis by regulating activities in cells, tissues, organs and systems
classes of hormones
- amino acid derivatives
- peptide hormones
- lipid derivatives
amino acid derivative hormones
- made up of amino acids, primarily tyrosine and tryptophan
- relatively small
- must bind to extracellular receptor
- ex. thyroid, dopamine, and melatonin
peptide hormones
- larger, multiple amino acids in structure, short polypeptides or glycoproteins
- must bind to extracellular receptor
ex. insulin, glucagon
lipid derivative hormones
- further divided into steroids and eicosanoids
- lipid membrane soluble, bind to intracellular receptors
secretion and distribution of hormones
- hormones are distributed throughout the body by the bloodstream
- hormones remain active for a couple of minutes to days
- hormones are inactivated by either the liver and kidneys or by enzymes in the plasma or interstitial fluid
mechanisms of hormone action
- hormones bind to specific receptors on or in the target cell
- presence or absence of receptors determines the cell’s hormonal sensitivity
- receptors are located either on the target cell membrane or inside the target cell
cell hormone sensitivity
- lots of receptors = high sensitivity
- few receptors = low sensitivity
membrane receptors up- or down-regulation
- when we want to increase number of receptors we up-regulate them
- when we want to decrease the number of receptors we down-regulate them
action of non-membrane permeable hormones
- for hormones such as peptide hormones or eicosanoids
- require second messenger to act within cell once the extracellular receptor has been bound
why do we want to up- or down-regulate receptors?
- circulating levels of hormone might be low, want to guarantee binding by increasing number of receptors
- circulating levels of hormone is too high so we reduce receptor quantities so we don’t have an overreacting system
method of receptor binding for extracellular receptors
first messenger (eg peptide hormone, catecholamine, or eicosanoid) binds to a membrane receptor and activates G protein > G protein becomes activated and functions as second messenger > modifies a component inside cell to continue cascade
GLUT-4
- stands for glucose transporter
- can either be activated by insulin or exercise to facilitate uptake of glucose into the cell
intracellular receptors
- necessary for steroid and thyroid hormones
- receptors are located in the cytoplasm or in nucleus
binding of steroid hormones
- steroid hormone diffuse through the PM and bind to receptors in the cytoplasm or nucleus
- the complex binds to DNA in the nucleus, activating specific genes
binding of thyroid hormones
- thyroid hormones enter the cytoplasm and bind to receptors in the nucleus to activate specific genes
- they also bind to receptors on the mitochondria and accelerate ATP production
endocrine reflexes and what they’re triggered by
- controls endocrine activity
- triggered by:
1. humoral (cell-mediated) stimuli (eg. insulin)
2. hormonal stimuli (eg. TSH)
3. neural stimuli (eg. epinephrine)
humoral stimuli
- anything that is in the body’s fluid, primarily blood
- eg. if blood glucose (BG) is high, triggers beta cells to produce insulin, if BG is low triggers alpha cells to produce glycogen
hormonal stimuli
- release hormones after another hormone tells it to be turned on
eg. TSH turning on production of T3 and T4
neural stimuli
- nervous system controls release
- eg. adrenal gland and sympathetic nerve synapses on adrenal medulla to innervate it
hypothalamus and hormones
- synthesizes two hormones: ADH and oxytocin
- secretes regulatory hormones which regulate anterior pituitary
- autonomic centre > adrenal medullae
- functions using negative feedback
ADH
- know as anti-diuretic hormone
- causes fluid retention to maintain blood pressure
- produced by hypothalamus
oxytocin
- promotes milk production in mammary glands for breast feeding
- produced by hypothalamus
negative feedback loop cycle
set point > stimulus/change (+/-) > sensor/detector senses change > comparator/ integrator initiates correction > effector promotes the correction and back to beginning
hormone production by the hypothalamus
- production of antidiuretic hormone (ADH) and oxytocin (OXY)
- secretion of regulatory hormones to control activity of the anterior pituitary gland
- control of sympathetic output to adrenal medullae leads to secretion of epinephrine (E) and norepinephrine (NE)
- hormones secreted by the anterior pituitary control other endocrine organs
anterior pituitary gland details
- anterior pituitary is controlled by regulatory hormones secreted by the hypothalamus, connected via blood vessels
- contains trophic hormone secreting cells, that produce 6 hormones
posterior pituitary details
- controlled neurally by the hypothalamus
- innervated by hypothalamus to release ADH and oxytocin where they are stored
pituitary gland functions
- often referred to as the ‘master gland’ as it helps control several glands
- produces hormones that control: blood pressure, stress response, bone growth and muscle mass, uterine contractions, breastmilk production and milk flow, and other glands
trophic hormones produced by anterior pituitary
- Adrenocorticotropic hormone (ACTH) which stimulates adrenal medullae to produce glucocorticoids (cortisol, corticosterone)
- thyroid stimulating hormone (TSH) which stimulates thyroid to produce T3 and T4
negative feedback in anterior pituitary
- hypothalamus produces regulatory hormone (thyroid regulating hormone, TRH or corticotrophin-releasing hormone, CRH) and sends it to anterior pituitary
- anterior pituitary releases stimulating hormone (TSH or ACTH)
- stimulation on target endocrine organ to release hormone which acts on target cells
- negative feedback from endocrine organ to anterior pituitary and hypothalamus
thyroid gland regulation
- controlled by TRH from hypothalamus and TSH from anterior pituitary
- produces hormones T3 and T4 to act on target cells
- key ion used is iodide ions
- binds to intracellular receptors since it is lipid soluble
thyroid hormone homeostasis
- hypothalamus releases TRH with acts on anterior pituitary to stimulate release of TSH
- TSH acts of thyroid gland to release T3 and T4
- T3 and T4 concentrations in blood increase
- normal T3 and T4 concentrations in blood, normal body temperature
- decreased T3 and T4 concentration in blood or low body temperature leads to stimulation of hypothalamus to release TRH and cycle continues
- if thyroid hormone levels rise too much, it is stopped by negative feedback to the hypothalamus or anterior pituitary
thyroid regulation problems: hypothyroidism
- if there is hypothyroidism, if you give TSH and problem is resolved, the problem is production in the anterior pituitary
- if you give TSH and still have a problem, then thyroid gland is the problem
thyroid gland functions
- affects nearly every cell in the body
- receptors for it are found inside target cell, lipid soluble
- metabolic hormone that readies the body for activity
- gets HR going, glycogen breakdown, increases oxygen consumption, stimulates RBC production
adrenal cortex
- exterior portion of adrenal gland with yellowish colour due to lipids, with medulla located in interior
- produces corticosteroids (aldosterone and cortisol)
- operates on same kind of programs as thyroid
- adrenal glands located on top of kidneys
adrenal cortex control for cortisol production
- hypothalamus secretes cortisol regulating hormone (CRH)
- CRH simulates anterior pituitary to produce adrenocorticotropic hormone (ACTH)
- ACTH acts to adrenal cortex to stimulate production of cortisol
- if levels rise too high, negative feedback loop to anterior pituitary and hypothalamus
aldosterone
helps body control sodium concentration, target kidneys
cortisol
- produced by adrenal cortex,
- stress hormone that helps breakdown glycogen, promote utilization of lipids and amino acids, has an anti-inflammatory effect
adrenal medulla
- pinkish due to high concentration of blood vessels and capillaries
- produces epinephrine and norepinephrine, work to activate fight or flight response, causing breakdown of glycogen into glucose, fat breakdown into fatty acids
pancreas
- exocrine and endocrine function due to islets of Langerhans
- islets of Langerhans contain alpha and beta cells
- alpha cells produce glucagon
- beta cells produce insulin
- cells acts as sensors for blood glucose and try to maintain homeostasis
insulin
- peptide hormone, so bind extracellularly and activates secondary messenger within cell, insulin-dependent cells have insulin receptor on cell membrane
- secreted by beta cells
- responds to elevated blood glucose levels, above 6.0 mmol/L, normal range in >4.0 - 6.0 mmol/L
- effects: increase glucose uptake and utilization and ATP generation, increased amino acid absorption and protein synthesis , stimulates glycogen formation, stimulates triglycerides formation in adipose tissue
diabetes mellitus main negative effects
- T2D
- poorly managed blood glucose leads to accumulation of glucose in tissues with high concentration of capillaries
- try to combat high concentration of glucose by increasing amount of fluid in tissues to dilute it, leads to high pressure in capillaries and hemorrhaging causing tissue damage
- can cause retinal damage, early heart attacks, peripheral nerve problems, and peripheral tissue damage, and kidney degeneration
glucagon
- peptide hormone, requires second messenger inside cell
- secreted by alpha cells
- responds to depressed blood glucose levels, below 4.0 mmol/L
- effects: stimulate glycogen breakdown in skeletal muscle and liver cells, stimulate production and release of glucose by the liver (gluconeogenesis), stimulate breakdown of triglycerides in adipose tissue
glycemic index
how quickly a source of glucose can move into cells
coordinated response of hormones
- cells often respond to more than one hormone at a time
antagonistic effect
- opposite effect on cell, if one goes up the other goes down, ie, insulin and glucagon
synergistic effect
- two hormones, if one is present nothing, need both to be present, ie. testosterone and FSH for sperm production
permissive effect
- if hormone needs to exert its effect, it needs a chaperone hormone to carry out effect, ie. childbirth, lactation
integrative effect
- tow hormones can function independently but function better together, common in digestion
hormone response to stress
- stress = threat to homeostasis
- stress response = general adaptation syndrome (GAS)
- made up of three stages: 1. alarm phase, 2. resistance phase, and 3. exhaustion phase
alarm phase of GAS
- immediate response to stress occurs
- sympathetic division of ANS directs this response
1. energy reserves are mobilize, mainly in the form of glucose
2. the body prepares to deal with the stress-causing factor by “fight or flight” response, epinephrine is the dominant hormone of alarm phase, its secretion is part of a generalized sympathetic activation
resistance phase of GAS
- if stress last longer than a few hours, the person enters the resistance phase of GAS
- glucocorticoids are the dominant hormones of resistance phase
- epinephrine, GH, and thyroid hormones are also involved
- energy demands in the resistance phase remain higher than normal, neural tissue has a high demand of energy, and requires a reliable supply of glucose, if BG levels fall too low, neural function deteriorates
- glycogen reserves can meet neural demand during the alarm phase but become depleted after several hours, hormones of the resistance phase mobilize lipids and amino acids as energy sources to conserve glucose for use by neural tissue
exhaustion phase of GAS
- body’s lipid reserves are sufficient to maintain the resistance phases for weeks or even months, but when the resistance phase ends, homeostatic regulation breaks down and the exhaustion phase begins
- unless corrective actions are taken almost immediately, the failure of one or more organ systems will prove fatal
- production of aldosterone throughout the resistance phase results in conservation of Na+ at the expense of K+, as content of K+ decrease, a variety of cells begin to malfunction
- underlying problem of exhaustion phase is the body’s inability to sustain the endocrine and metabolic adjustments of the resistance phase
type 1 diabetes (T1D)
- autoimmune disease
- destroys beta cells of pancreas
- body does not produce insulin
type 2 diabetes (T2D)
- body cells do not respond to insulin
- insulin insensitivity/resistance, common due to obesity and lack of exercise
- beta cells of pancreas work overtime
