Exam 2-2 Flashcards
3 types of muscle
skeletal, cardiac, muscle
skeletal muscle ells
long multinucleated composed of many myofibrils is striated--from arrangement of protein fibers in cells voluntary contraction
Muscle cell life
born from merging of undifferentiated cells called myoblasts
once matured–no mitosis
Satellite cells
adult muscle stem cells, triggered to divide by injury– can repair some injured muscles (since muscles can’t fix themself–no mitosis)
hypertrophy
swelling of individual muscle cells– happens with exercise
sarcoplasmic reticulum
specialized endoplasmic reticulum that can sequester and store Ca.
It stores it in the ER and is will be used to spread signal throughout the muscle cell
T-tubules
invaginations of the plasma membrane that transmits the membrane depolarization into the cell
sarcoplasm
cytoplasm of a muscle cell
sarcoplasmic reticulum
endoplasmic reticulum of a muscle cell-stores Ca
Sarcolemma
the plasma membrane of a muscle cell
Sarcomere
contractile unit of a muscle cell
is the smallest functional unit of a muscle
consists of thick and thin filaments–myofilaments
1 sarcomere=z line to z line
Myosin
Thick filament
Have heads and tails– the heads are gathered and the tails are wrapped together
have 2 sites: ATP binding site and actin binding sites
What are the 2 sites on myosin
ATP site (binds and cleaves ATP-->ADP) Actin binding site
thin filament
Actin, troponin and tropomyosin
Tropomyosin
long- string like
hides myosin binding site, preventing myosin from binding to actin
Troponin
bound to tropomyosin, binds Ca which triggers a shape change that moves typopmyosin out of the way, revealing the myosin binding site and allowing actin and myosin to interact
During contraction, what is in high conc. in the sarcoplasm?
Ca
Sliding filament theory
filaments fo not get shorter, they slide across each other, shortening the length of the cell
Crossbridges
myosin binds to actin, pulling the actin framework closer together, Z lines get closer together and H and I zones are eliminated.
Requires ATP
Happens multiple times along the actin filament
Sarcomere shortens
Excitation contraction
- AP reaches motor neuron terminal
- AP opens Ca channels, Ach is released
- ACh binds receptors of sarcolemma of muscle cell
- Na channels open
- Na moves in to muscle fiber causing a small local depolarization
- If threshold is reached– a muscle AP occurs
Muscle AP travels along the sarcolemma and down T-Tubules - AP on t-tubules excited receptors on sarcoplasmic reticulum– opening Ca channels
- Ca is released into sarcoplasm
- Ca binds troponin causing s shape change, which moves tropomyosin out of the way.
- Myosin binds to actin– cross bridge
- Cross bridge formation triggers a shape change in myosin, cocking head to an abgle, sliding the filaments past each other
- ADP is released from myosin head, and a new ATP binds and releases the cross bridge
- Myosin binds to next available actin binding site
- ATP breaks down to ADP, energy is transfered to myosin head, cocks again and the filaments slide
- continues as long as intracellular Ca is high, and ATP is available
- In synapse- AChE is degradding ACh
- Chem gated Na channels close
- Ca pump in sarcoplasmic reticulum re-sequesters Ca
- Removal of Ca from troponin restores blocking of actins binding sites
- Cross bridge cycling stops, relaxation occurs
In muscles– do we use intra or extracellular Ca?
Intra cellular, while in normal AP in neurons we use extracellular Ca
What is ATPs role in filament binding?
ATP binds and releases the crossbridge.
Muscle motor units
functionally all the same– can’t contract q/o the others.
Helps control how much of a msucle you need to use– done by fine tuning the number of motor units
Neuromuscular junction overview
Only one NT: ACh
One form of NT clearance: AChE
Only excitatory
twitch
A response of a single muscle fiber to a single AP
latent period
can be different for different muscle fibers
depend on speed of Ca pump
Slow pump–> Ca stays longer->twitch lasts longer
Fast pump–>Ca removed faster–?twitch ends quickly
isotonic contraction
muscle contracts and creates enough force to move a load–> like lifting your keyys
Initiate as isometric contraction until the tension matches the load
Isometeri contraction
When you can’t move the load. Like pushing a wall thats not going to move no matter how hard you push
ATP is muscle contraction
- ADP–>ATP by creatine phosphate
- Oxidative phosphorylation of ADP in the mitochondria
- ADP–>ARP by anaerobic glycolysis in cytosol
Creatine phosphate
builds up in muscle
At start of contraction, CP can phosphorylate ADP to make ATP
Conversion is so fast that during intiial contraction, ATP rates barely change, while CP levels drop (aka ATP is being made as fast as its being used)
Oxidative phosphorylation/glycolysis for ATP
Glycolysis– 2 ATP/glucose
OP-36 ATP/glucose– needs O2
Both are slower than CP mediated ADP, OP is slower than glycolysis
myoglobin
can store oxygen for muscles
How long does glycogen storage last?What happens when you run out?
lasts for 5-10 minutes. After that circularory system must meet demands. Glycogen sfrom liver is broken down, adter 40 minutes, fatty acids begin to be broken down
Central fatigue
your CNS tells you to stop– deelings of tiredness, psychological factors
Peripheral fatigue
factors within muscle cells tell you to stop
includes conduction problems and lactic acid build up, inhibition of cross bridge formation
Conduction problems
K+ builds up in the t-tubules, no K+ gradient, no repolarization
Lactic acid buildup
lactic acid results from anaerobic glycolysis. It does not effect contractile proteins, but can slow re-sequestration of Ca, leading to prolonged contraction
Inhibition of cross bridge formation
an excess of ADP and Pi may inhibit formation od new cross bridges.Impaired full contraction and impaired relaxation may result.
How are skeletal muscle fibers classified?
Cross bridge cycling speed, based on ATPase on myosin
How they get most of their ATP, oxidative phosphorylation of anaerobic glycolysis
Fast v. Slow fibers
fast fiber cross bridge formation occurs 4X faster than slow fiber
force produced is the same
depends on ATPase
Oxidative Fibers
get ATP from oxidative phosphorylation–much more efficient
Requires lots of mitochondria
Myoglobin is the oxygen source
referred to as red fibers
Glycolytic Fibers
Gets ATP from glycolysis- less efficient, need more glucose, less oxygen
-few blood vessels
-few mitochondria
-much higher glycogen stores– since each glucose only gives 2 ATP
WHITE FIBERS
Type 1 Muscle
Slow oxidative
-low myosin ATPase, high oxidative capacity
Type IIa muscle
Fast oxidative glycolytic
high myosin ATPase, high oxidative capacity, intermediate glycolytic capacity
Type IIb
Fast glycolytic
high myosin ATPas, high glycolytic capacity
If looking at a dead body, with no ATP where will Ca be found?
In sarcoplasm, muscles will be contracted myosin can’t unbind from actin without binding a new ATP
If you block ACh in the NMJ what happens?
The cell would never have a graded potential
Slow oxidative fibers and fatigue
Slow use of ATP, can generate ATP
Doesn’t fatigue easily.
Used in muscles that are always on, back legs etc
Fast oxidative fibers and fatigue
Lasts a a while, then fatgues
fast ATP- can contract faster legs
Fast glycolytic fibers and fatigue
fast use of ATP minimal ability to replenish ATP, fatigues quickly.
In fingers and hands
Motor units
all the same fiber type, controled by one motor neuron.
Proportions of motor units vary based on need
Plasticity of skeletal muscle
- fiber type
- mitochondrial concentration
- capacity for glycogen storage
- local capillary concentration
- myoglobin concentration
- size of muscle cell
- concentration of actin and myosin microfilaments
- neural pathways
These changes can be gained OR lost
Soreness
exercising beyond capacity
- damage to muscles triggers inflammatory response
- lengthening muscle (going down stairs, lowering weights slowly) produces more soreness
NOT DUE TO LACTIC ACID BUILD UP
Cramps
persistent, high frequency AP
Elecytrolyte imbalance
Caused by overexercise, persistant dehydration
Changes with endurance exercise
Increased mitochondria
increase in capillary network feeding the muscles
slight decrease in fiber diameter and maximal strength
also leads to associated changes in the cardiovascular and repiratory system
Changes with strength exercise
Primarily affects fast twitch fibers–increase in diameter, increased synthesis of actin and myosin, increase in enzymes in glycolysis pathway.
Gain strength, but not endurance– fatigue rapidly
Sometimes fains in strength without gains in size
Poliomyelitis
Polio
A virus that infects motor neurons
90% of cases have no symptoms, 10% milkd disease, 1% paralysis
Muscular dystrophy
Genetic or autoimmune defects in costamere protein.
Progressive weakness, inability to walk by age 12 Death by 20-25
Atrophy
Use it or lose it
Muscle cell loss by decrease in nerve use, or decreased muscle use
Myasthenia gravis
Autoimmune activity against ACh receptors, muscle fatigue and weakness
Therapies:
AChE inhibitors, autoimmune drugs, removal of antibodies from plasma
Smooth muscle
no banding pattern
NO TROPONIN
innervation comes from autonomic– not voluntary
spindle shaped
contract as a sheet
uni-nuclear– can undergo mitosis and repair
in gut, uterus, blood vessels and pulmonary
Role of Ca in smooth muscl
CA binds to and activates calmodulin
Ca-calmodulin activates a kinase
The kinase phosphorylates myosin, activating it
Myosin binds actin and cross bridge cycling occures
as long as Ca is entering the cell, the contraction will occur.
Sources of Ca for smooth muscle
Can come from sarcoplasmic reticulum (inracellular) and from extracellular fluid
Smooth muscle cells have voltage gated and chemically gatedCa
There is NO ROLE for Na in smooth muscle contracition
Amount of Ca=amount of contraction
Removal of Ca in smooth muscle
removed by ATP dependent pumps
rate is very slow (3+ sec. compared to <1 sec. for skeletal muscle)
Smooth muscle gradation and tone
Ca channels only let in enough Ca to activate a portion of the cross bridges
more stimulus=stronger contraction
Can alter how much cystolic Ca is kept inside to maintain tone– helpful with always on muscles, like sphincters
The role of stretch in smooth muscle
Stretch does not effect force possible. Stretch can increase contraction because stretch can open mechanically gated ion channels
What do smooth muscle cells contract in response to?
autonomic inputs can be excitatory or inhibitory
- in response to depolarization from a neuron
- spontaneously
- spontaneously depolarize and contract without nueronal input– waves
Pacemaker cells
the tendancy to spontaneously depolarize at regular intervals.
Some smooth muscle cells work this way for regular contraction– like GI tract
Varicosities
string of NT filled bumbs of autonomic axons
Factors that indfluence smooth muscle cells
Hormones --ex. hormonal control over utering contraction --ex. epinepherine and gut motility Paracrine signalling Acidity O2 availability Extracellular ion composition
Single unit smooth muscle
gap junctions link the cells, many cells contract as a sheet stretching often induces contraction
ex. GI tract(full stomach=contraction), Uterus (braxton hicks), arterioles(high BP)
Multiunit smooth muscle
each cell responds on its own, no gap junctions
ex. Arteries, pulmonary system, haid associated muscle
Cardiac Muscle
- striated
- troponin AND tropomyosin
- T-tubules and SR
- single nucleated cells, forked
- specialized fused ends called intercalated disks
intercalated discs
in cardiac muscle
make stronger, and have gap junctions to quickly pass a contraction
So when one depolarizes, they all depolarize
Desmosomes
join cells tightly– at intercalated discs
Gap junctions
allow cytoplasmic flow of ions. So when one cell depolarizes, they all depolarize
Contraction in Cardiac muscle
-involves Ca and Na channels
Na channels provide initial depolarizeion (graded potential)
Voltage gated Ca channels open and Ca flows into the cell.
—these are called L-type channels, long lasting depolarization- elongates refractory period
Ca floods cytosol from SR and extracellular fluid
once in it binds to troponin and works the same way as skeletal muscle.
Ca pump redurns Ca to SR and exracellular fluid
Initiation of depolarization in cardiac muscle
Specialized cardiac muscle cells have pacemaker potential
These exist at only 2 plasces in the heard
Wave of depolarization spreads down through conducting fibers throughout the heard
Does skeletal muscle have striations?
yes
does cardiac muscle have striations?
yes
does smooth muscle have striations?
no
Does skeletal muscle have thick and thin filaments?
yes
Does cardiac muscle have thick and thin filaments?
yes
Does smooth muscle have thick and thin filaments?
yes
Is skeletal muscle control voluntary or involuntary?
voluntary
Is cardiac muscle control voluntary or involuntary?
involuntary
Is smoothmuscle control voluntary or involuntary?
involuntary
What shape are skeletal muscles cells
long and cylindrical
What shapre are cardiac muscle cells?
short and chubby
What shape are smooth muscle cells?
Spindle
Are skeletal muscle cells uni or multi nucleated?
multi
Are cardiac muscle cells uni or multi nucleated?
uni
Are smooth muscle cells uni or multi nucleated?
uni
What is the source of Ca for skeletal muscle?
Intracellular
What is the source of Ca for cardiac muscle?
intra and extracellular
What is the source of Ca for smooth muscle?
intra and extracellular
What is the site of Ca regulation in skeletal muscle?
troponin
What is the site of Ca regulation in cardiac muscle?
troponin
What is the site of Ca regulation in smooth muscle?
Myosin
What is the refractory period duration for skeletal muscle?
very short
What is the refractory period duration for cardiac muscle?
very long
What is the refractory period duration for smooth muscle?
short
What is the contraction control for skeletal muscle?
only somatic motor neurons
What is the contraction control for cardiacmuscle?
innervation, autorhythmc, endocrine
What is the contraction control for smooth muscle?
innervation, autorhythmic, endocrine
What is the effect of K+ channel blocker on NMJ?
Lots of ACh in the synapse
What happens if you leave ACh in the synapse?
Prolonged muscle contraction
What would adding an Ach antagonist to NMJ do?
no muscle contraction
Which type of muscle uses calmodulin?
Smooth
Tropic hormones
stimulate other glands to make and release hormones. Usually also trigger growth of the target gland
Hormone synthesis
most hormones are built in the cell as large inactive molecules
They are stored in their inactivated state and can be activated before release or activated in the blood or at the target tissue
In what ways can endocrine gands be stimulated to release a hormone?
- Monitor blood and release the hormone in response to a change
- Neuron stimulates the release of the hormone
- Controlled by a tropic hormone.
Humoral stimulus
When a hormone is released in response to a change in the blood..
Ex. insulin and glucose changes
hormones and allosteric inhibition
the presence of a hormone can inhibit the step of a pathway by acting as an allosteric nhibitor of an enzyme. This will turn off a pathway resulting in negative feedback
GnRH/testosterone feedback loop
GnRH–>LH–> testosterone. Testosterone then inhibits the release of more GnRH
Amines
derived from amino acids
help build thyroid hormones, epinephrine and norepinephrine
Are water soluble, so need transport into cells
Peptide hormones
larger than amine hormones
built from polypeptides
the majority of hormones are peptide hormones
they are typically water soluble, need transport into the cell
steroid hormones
lipid based, built from cholesterol
ex. corisol, aldosterone, tersosterone, estradiol, vitamin D
Are hydrophomic, so need plasma protein transporters, but easily diffure in and out of cells
Hyposecretion
When not enough hormone is secreted
Hypersecretion
too much hormone released
Hyporesponsiveness
not enough reception by target cells
Ex. type 2 diabetes
Hyperresponsiveness
More reception by target cells
Primary hyposecretion
- damage to gland=less hormone
- enzyme deficiency=less hormone
- dietary deficiency of iodine=less hormone produced
Secondary hyposecretion
too little tropic hormone produced/released. Results in reduction of hormone secretion
Primary hypersecretion
Endocrine cell tumor=produces hormone out of control
Secondary hypersecretion
excressive stimulation by tropic hormones
Roles of the hypothalamus
- influences hormone secretion activity of the anterior pituitary– with tropic hormones
- Produces hormones itself
- Oversees hormone secretion by the adrenal medulla
Anterior pituitary
hormone secretion from this is influenced by tropic hormones from the hypothalamus
releases 6 hormones
is regulated through secretion of hypophysiotropic hormones into the hypothalamo-pituitary portal system
posterior pituitary
stores hypothalamic hormones, then releases them into the local capillary network
Hypothalamus releases corticotropin releasing hormone (CRH)…
triggers release of adrenocoticotropic hormone from the anterior pituitary (ACTH)
Hypothalamus releases Growth hormone releasing hormone (GHRH)
which releases growth hormone (GH) from the anterior pituitary
Hypothalamus releases thyrotropin releasing hormone (TRH)
which releases thyroid stimulating hormone from the anterior pituitary
Hypothalamus releases gonadotropin releasing hormone (GnRH)
which releases Luteinizing hormone (LH) and follicle stimulatin hormone (FSH) from the anterior pituitary
Hypothalamus releases somatostatin (SS)
which INHIBITS the release of GH from anterior pituitary
,Hypothalamus releases dopamine (DA)
which inhibits the release of prolactin from the anterior pituitary
Thyroid stimualting hormone
anterior pituitary hormone
Is tropic
Stimulates the release of thyroid hormone from the thyroid gland
Prolactin
is an anterior pituitary hormone
regulates breast milk production, and is anti-libido released during stress
Adreocorticotropic hormone
is an anterior pituitary hormone
Stimulates the adrenal cortex to produce cortisol
Growth hormone
is an anterior pituitary hormone
Causes the growth of bones, muscles and most body cells
Follicle stimulating hormone and luteinizing hormone
anterior pituitary proteins
influence reproductive stuff by regulating hormone synthesis by the gonads
What regulates the hypothalamus?
CNS stimulation- stress, environmental influences, NT
Hormone levels in the blood
Oxytocin
Posterior pituitary hormone
positive feedback loop for cervical opening in labor and milk let-down in lactation.
plays a role in bonding an social stuff
Vasopressin
posterior pituitary protein
aka antidiuretic hormone
constricts smooth muscle cells around blood vessls, increasing blood vessels, increasing blood pressure and decreasing urine output
Thyroid gland
butterfly shaped gland in neck
secretes 2 hormones: Thyroid hormone and calcitonin
Thyroid hormone
released by thyroid gland
maintains metabolism/body temperature
iodine is an important part of TH production
There are 2 versions of TH: T4 and T3 (based on # of iodine molecules
Production and secretion is regulated by TSH`
TH production
TRH (hypothalamus)–>TSH (ant. pit.) –> TH (thyroid gland
TH then negative inhibits TSH and TRH
Hypothyroidism
low metabolic rate, weight gain, lethargy, feeling cold
Happens because
Goiter
due to low iodine in diet, thyroid can’t produce enough TH, but pituitary continues to make TSH
Action of thyroid hormone
- increase carb intake from intestine and fatty acid release by horone=more fuel in blood stream
- increase activity of Na/K pumps=increase use of calories and increase of heat
Symptoms of hypothyroidism
decrease in overall metabolism cold intolerance weight gain fatigue loss of concentration
Symptomes of hyperthyroidsim
overall metabolism increases heat tolerance weight loss twitchiness anxiety
Calcitonin
produced by thyroid glad
encourages calcium deposition into bone from blood
“calcium to the bone”
release is controlled by blood Ca levels
parathyroid hormone
released by parathyroid encourages less calcium to be deposited in blood stimulated formation of vt. D opposes the action of calcitonin regulated directly by blood Ca levels
Viamine
organic compound present in minute amounts in the diet that are essential to metabolism
Vit. D3
formed by action of UV light on a cholesterol molecules in the skin
Vit. D2
derived from plants
Vit. D function
targets the small intestine
increases uptake of Ca
Parathyroid hormone increases synthesis
is the most common deficiency in the US.
plays a role in reducing inflammation
Vitamin D and TB
vit. d helps to speed the recovery of TB patients, reducing markers of inflammation
increase in sun, decrease of TB symptoms.
Roles of Ca in the body
important in signalling pathways muscle function NT release BONES cardiac and smooth muscle function
Bones
rebuild 20% of our skeleto each year
is a type of connective tissue
Is a collagen matrix upon which calcium salts are deposited
Works as a bank-calcium is deposited and withdrawn as needed
growing bones contain cartilage connective tissue
epipheyseal growth plate
proliferating cartilage
bones can’t grow, cartilage at growth plates grow, then becomes bone
Osetoprogenitor cells
stem cells that become osteoblasts
osteoblasts
become new bone
osteocytes
mature bone cells in matrix
Osteoclasts
large multinuclearclls that eat/reabsorb bone
Bone growth
chondroblasts in epiphyseal plate generate new cartilage
osteoblasts at the shaft of the plate convert cartilage to bone
Growth rate
childre undergo 2 periods of intense growth
before 2 years, and during puberty
boys enter puberty 2 years later than girls, during puberty boys grow more due to the action of testosterone
factors that limit growth
persistent disease
lack of AA, fatty acids, vitamins, minerals
Physical or psychological stress
Growth hormone
stimulates maturation and mitosis of chondrocytes
elongates epiphyseal plates, more material for bone conversion
acromegaly
growth after plates fuse—just cartilage grows
IGF
insulin like growth factors
secreted by liver and osteoprogenitor cells
triggered by GH
autocrine, paracrin and hormonal functions to dive the mitosis of chondrocytes
Growth hormone stimuli
only secreted during exercise and 1-2 hours after sleep begins
Sex hormones and growth
At low levels: promote growth by increasing GH and IGF1
At high levels: promote ossification directly, cause ossification of epiphyseal plates
Testosterone
is an anaboilc steroid used to increase protein synthesis in muscles Side effects: liver damage prostate cancer infertility aggression
Cortisol
Antigrowth
inhibits DNA synthesis and bone growth
Use of cortisol in children to precent/treat asthma etc can temporarily stunt growth– have to take breaks to alow growth catch up
Stress and bone formation
high levels of cortisol (released when stressed) can temporarily hault growth
Gametes
cells that fuse with other cells to make an embryo
gametogenesis
making gametes
gonads
organs that produce gametes
Male reproductive goals
make gametes, get them to the egg
Female reproductive goals
make gametes, prepare place to receive gametes, prepare place to house the developing embryo, get give birth, feed offspring
leydig cells
in testes, secrete testosterone
sertoli cells
aid in spermatogenesis in semineferous tubules
filter nutrients for developing sperm
bind testosterone and transport it into the lumen
is triggered by FSH, make prosperm paracrine signaling molecules which help sperm mature
seminiferous tubules
unbroke ring of sertoli cells make blood-testes barrier sperm stem cells at periphery developing cells b/w sertoli cells are locked into place by tight junctions fully differentiated sperm at the lumen
how many sperm released in 1 ejaculation?
30-300 million
Items required for success of sperm
speed, envionmental conditions, direction, adequate digestion of egg coat
acrosome
on head of sperm. has enzyme that digests the coating of eggs
How does the egg prevent multiple sperm from entering?
once a sperm gets in , there is an exocytosis of the corticol granuales, the contents are released the the zona pellucida hardens so nothing else can pentrate it
testosterone functions
required for spermatogenesis
development and maintainance of male reproductive organs
required for maintenance of male secondary sex characteristics
opposes action ot estrogen on breat development
sex drive
muscle growth
what impact does endogenous testosterone have?
decrease in GnRH, LH and testosterone
production of testosteron
endocrine cells in testes have enzymes to convert:
Cholesterol–>androstenedione–>testosterone
androstenedione- is also found in the adrenal cortex
small amounts of testosterone are converted to estradiol
aromatase
converts testosterone to estradiol
semen
combination of sperm and secretions from accessory glands
takes 2 weeks to prepare
lives 48-72 hours once in the female reproductive tract
testosterone decline
occurs around age 40
slow and steady decline
Ovaries
make gametes
uterus
houses the fetus
fallopian tubes
transports egg to uterus, site of fertilization
vagina
entrance/exit to system
cervix
“doorway” from vagina to uterus
Gamete production
produce oocytes in the ovary during the fetal period
oocytes are encased in follicles
each month a few follicles mature, the one that matures the fastest is the one that releases the egg
ovulation
when the egg is released from the follivle and availabel for fertilization
corpus luteum
what the follicle is called after ovulation when it remains in the ovary (light body) , if pregnancy does not occur it dies and triggers menstruation
is an active endocrine gland- makes progesterone
perimetrium
outer membrane of uterus
myometrium
thick smooth muscle layer of uterus– is most powerful muscle in the body
endometrium
lining of the uterus composed of thick connective tissue, which is sloughed off and regrown every 28 days in menstruation
Preparing for pregnancy
- First half of ccyle: maturing an egg
- ovulation
- enriching uterine lining for implantation
- shedding lining if implantationdoes not occueqw
which cells release estrogen?
granulosa cells
what releases progesterone?
a small amount is made by theca cells, most is made by he corpus luteum
can also be made by the adrenal cortex
Progesterone synthesis location
made by corpus luteum and placenta in women, and in the adrenal cortex
progesterone functions
maintain uterine lining , water and ion balance, regulation of synaptic activity associated with mood, memory and immune functions, promotes schwann cells,
Progesterone and MS
progesterone promotes schwaan cells, so is helpful in relieving symptoms of MS
what triggers ovulation?
a surge in LH (which is released by anterior pituitary and controlled by estrogen levels)
What do birth control pills do with regard to LH
prevent the surge in LH this preventing ovulation
what triggers LH surge?
estrogen peak
what role does estrogen have in menstruation?
triggers LH secretion, builds endometrium and prepares for pregnancy
what role does progesterone have in menstruation/pregnancy?
progesterone prevents the shedding of the lining
menstruation occures when progesterone levels fall
how does progesterone based birth control pills work?
it inhibits LH surge
Basic role of FSH in female reproduction
stimulates development of follicles.
There is no role for this in the luteal phase
basic role of LH in female reproduction
triggers ovulation
There is no role for this in the luteal phase
basic role of estrogen in female reproduction
prepares uterine lining, breasts for lactation
SURGE IN ESTROGEN TRIGGERS THE LH SECRETION
basic role of progesterone in female reproduction
maintains uterine lining. Theres is no role for this in the follicular phase
How does the body make sure we only have one baby at a time?
Follicular phase and ovulation hormones are inhibited by the corpeus luteum
progesterone inhibits LH and GnRH
Mestruation
Corpeus lutum degrades–> decrease in estrogen and progesterone–>prostoglandin secreting in endometrium–>vasoconstriction and uterine contractions= menstruation
prostoglandins
triggers vasoconstriction and uterine contractions, released due to decrease in estrogen and progesterone.
Redues blood flow, causing endometrial tissue to die. and contractions trigger sloughing
In vitro
grow blastocyte in test tube, then implant it into uterine lining
fraternal twins
one egg ovulates from each ovary
Fertilization
occurs in fallopian tube
egg divides and develops as it travels to the uterus
if endometrium is primed, it implants and begins to grow.
tend and befriend
release oxytocin during stress events
oxytocin
promotes the resolution of stress by activating parasympathetic system
promotes bonding and social behavior during stress response to keep track to offspring and find friends
male hormanal profile during stress
epinephrine, corisol and testosterone
female hormonal profile during stress
epinephrine, cortisol and oxytocin
Needs in a stress situation
O2, blood to muscles, glucose
What physiologically changes in a stress event
Increase: breathing, hear rate, shift blood flow to skeletal muscles, mobilize glycogen, protein breakdown
Decrease: urine output, shift blood aaway from digestion, decrease inflammation and immunity, decease sex drive, decrease bone growth
Stress
real or perceived threats to our homeostasis
adrenal glands
pyramid shaped glands above the kidnesy–is the major stress gland
Release aldosterone, cortisol, androgens and epinepherine
Adrenal cortex
makes over 25 lipid based steroid hormones– the corticosteroids
(SALT, SUGAR, SEX)
mineralocorticoids
released by adrenal cortex,
are lipid based
regulate minerals/electrolytes (water salt balance)
released by the outer layers
glucocorticoids
released by middle section of adrenalcortex
regulate glucose levels in blood
lipid based
gonadocorticoids
regulate gonadal hormones (androgens)
made by inner section of adrenal cortex
lipid based
Epinephrine
dialiates airways to increase breathing rate
breakdown glycogen in liver/skeletal muscles, and breakdown fat in adipose tissues
shifts vlood away from digestive system– decreases the need to eat
Cortisol
Shifts bloodflow to skeletal muscles breakdown protein in bone and skeletal muscles and breakdown fat in adipose tissue turs everything off. decreases growth of immune system increases appetite to replenish stores increase prolactin to decrease sex drive breakdowns bone increases growth hormone (in order to break down protein)
Hyporthalamic pituitary adrenal axis
Hypothalmus releases CRH–>ant. pit. releases ACTH–>Adrenal cortex releases cortisol
cortisol has negative feedback on the other two
Stress and eating acute stress
Epi decreases the need to eat (ex. fen phen )
Stress and eating chronic stress
Cortisol increases the need to eat
to replenish energy storage.
Chronic stress and cardiovascular system
cort. causus systemic vasoconstriction and an increase in blood pressure
Chronic stress and immune system
Cort. decresases cytokine cross talk and decreases the immune cells, means system is vulnerabel and have increased risk of infection
need more glucose
decrease insulin, increase glucagon
decrease need to respond to injury
increase beta-endorphin– is a pain killer
decrease need to grow
decrease GH
decrease need to pee
increase ADH, increase blood volume– in case of hemmorrhaging
decrease need to have sex
increase prolactin
decrese sex drive
decrease gonadal hormones
decrease fertility
Benefits of cortisol
-circadian rhythm
-maintain BP –permissive for epi
-maintain glucose metabolism
brake on the immune system
Hyposecretion:Adrenal insufficiency
Causes
decreased cort.
decreased adrenal developmet
decreased enzyme synthesis
damage (addisons disease)
need more glucose
decrease insulin, increase glucagon
decrease need to respond to injury
increase beta-endorphin– is a pain killer
decrease need to grow
decrease GH
decrease need to pee
increase ADH, increase blood volume– in case of hemmorrhaging
decrease need to have sex
increase prolactin
decrese sex drive
decrease gonadal hormones
decrease fertility
Benefits of cortisol
-circadian rhythm
-maintain BP –permissive for epi
-maintain glucose metabolism
brake on the immune system
Hyposecretion:Adrenal insufficiency
Causes
decreased cort.
decreased adrenal developmet
decreased enzyme synthesis
damage (addisons disease)
Hyposecretion:Adrenal insufficiency
Symptoms
weakness,fatigue
decreased appetite and weight
decrease blood presure, decreased glucose
increase skin pigmentation (ACTH in blood is a precursor to melotoin
Hyposecretion:Adrenal insufficiency
Treatment
Hydrocortisone or prendisone for life
Hypersecretion: Cushing syndrome
Causes
exogenous therapies, increased cort adrenal tumors (increased cort) pituitary tumors (increased ACTH and cort)
Hypersecretion: Cushing syndrome
symptoms
osteoporosis decreased muscle mass odd body fat distribution hypertension hyperglycemia immunosuppression
Hypersecretion: Cushing syndrome
Treatment
stop exogenous therapy
surgery
prolonged heavy exercise
increase epi and cort decrease insulin, increase glucagon increase aldosterone and ADH increase endorphins increase prolactin
Fasting
increases epi and cort
decrease insulin, increase glucagon
increase aldosterone and ADH
Are neuromuscular junctions inhibitory?
No. Only excitatory
