Download Part 4 Physiology Notes

Part 4 Physiology Notes
Neural Communication
- Instantaneous cut on
- Instantaneous cut off
Endocrine System
- cell secrete messengers into blood stream
- Which then goes throughout the body to target
- Doesn’t usually involve cells that are close to each
Characteristics that differ from Neural
- Takes much longer to get to target
- When it gets there, it doesn’t get there abruptly
- Takes awhile to reach full amplitude
- When stop secreting; it lasts in blood stream for awhile
- The message is diffused- some hormone acts on many different cells
Hormones- messenger chemicals secreted by endocrine system; which is secreted straight into
bloodstream
 therefore, the Endocrine Glands are also called “ductless glands”
- there are instances when the Neural System releases into bloodstream instead of target cells,
and they are known as Neuroendocrine and the hormones that release are called
Neurohormones.
Basic Principles
Endocrine Physiology Topics:
1.) what controls secretion
2.) what effects they have
- They are practically important in things that have to be maintained, over long periods of
time.
 this is important because in Neural System receptors fatigues or adapts, so they are not
good choices for maintaining things
 Things that are under endocrine control- (total body water; blood/glucose level)
- Things that make up endocrine system consists of glands that are not connected or
anatomically disconnected, but work as a group because they are held together by
circulation.
 there are hormones that are released, just to control other secretion of other hormones,
are called Tropic Hormones
 Hormones that mainly on things outside endocrine system, called Nontrophic
Hormone
 some endocrine glands, that have more than one cell in them, so they secrete more
than one type of hormone.
 Very common for a hormone to have effect on more than one type of cell
Hormone Classes:
- Determined by Chemical Structure
1.) Peptides
2.) Steroids
3.) Amines
 Useful grouping because, each class have similarities in how:
a.) they are synthesized
b.) what its stored in, if it is
c.) how they get secreted
d.) how they are transported
e.) what it does when it gets there
Peptide Hormones
-
basically small proteins
synthesized for export from cell
synthesis happens on ribosomes, as in active precursors
Get transported through cell in ER
When arrive at Golgi, they get enclosed in membrane, and get stored
When it is stimulated, the packages get released (somewhere between last one and here, get
turned into hormones)
- All water soluble- they dissolve in plasma with no trouble, and that’s how they travel in
blood
 they do not get into cells because large water soluble
- When they get to target cell, there have to be structures on the external surface of the target
cells, called receptors, that the hormone can interact with it, and cause cell to do its trick.
 any cell that doesn’t have receptor, won’t be effected.
- If gave a peptide orally, it would be destroyed in stomach, meaning you can’t use them
orally, as therapeutic devices.
Steroid Hormones
- Unlike peptides, they are fat (lipid) fat soluble, meaning they can get into cell; can diffuse
right across
- There is no way for cell to synthesize and store them; so there is not step of storage to wait
for stimulus
- Instead, when cell gets stimulated then it starts producing steroid, and release them.
- When they get to target cell, the membrane doesn’t stop them, so they diffuse in , get to
nucleus, get to proteins, that bind to steroids to steroid, which get in DNA, which activate
genes.
- Have specific carrier proteins in plasma, which steroid bind tightly to them, it behaves as if
proteins didn’t exist hormones would end up in the walls of gland. (used like taxies)
- Remains tied to proteins, until it encounters a place that causes them to release from protein
- Because steroid cross membrane easily, and they are not destroyed in stomach, they can be
given orally.
Amines
- Fairly diverse group, so not able to produce a list of properties
Characteristics of all Hormones
1.) Effective at very low concentrations(10-8 M to 10-12 M)- much more potent, unlike
other systems (10-3 to 10-1)
 Many times more potent
- Concentration of hormone in blood stream represents a balance in it bring added of
subtracted to blood stream
- it almost never means that one is acting more than another
 one goes up, the other goes up too
Endocrine Disorders
- include situation in which blood concentrations are pathologically high-secrete too much
- Plasma levels are low- secrete too little
- Target cell responses abnormal- some effects are if concentrations were low.
- When plasma level is too low, give them hormone
- When too high, depends on reason why it is too high
 Tumor is not subject to same regulations as endocrine gland
 When gland secreting too much, have to find out why it is not regulating
Hypothalamus
- secretes tropic hormones; have cells that secrete through the posterior
- Infundibulum
- Pituitary  Hormone
- Anterior = Adenohypophysis
- Posterior = Neurohypophysis
- An endocrine gland that has function mechanism in brain
- Many animals have MSH = Melonocyte Stimulating Hormone- in intermediate lobe
 has no function in humans
 Pathological case in which skin color darkens
- there is a connection or identity to the posterior and hypothalamus- relationship close;
hypothalamus is main link between neural and endocrine
- Blood Flow arteries, capillaries, hypothalamus
- Blood in Pituitary have already been in hypothalamus
- Hypothalamus in good position to secrete things that influences the pituitary, where it can
exert its action
Posterior Pituitary
- Secretion made in hypothalamus
- Produces 2 hormones- both neural hormones- polypeptides- made on ribosomes
1.) ADH = (Vasopressin) has two names because have 2 known effects- ADH increasing
water permeability in collecting ducts; Vaso- constricts the blood vessels, increasing
resistance, the BP up, increasing arteriole pressure
2.) Oxytocin- stimulated by reflexes or mechanical stimulation; major effect is it
stimulates contractions during childbirth, and promotes release of milk in breasts.
- they get synthesized in hypothalamus
- migrate down the axons, eventually reaching axon terminals
- action potentials release transmitters, but don’t terminate on target cell, but instead into
circulation.
Anterior Pituitary
- once called master gland, but now obsolete because hypothalamus controls the pituitary
- makes the thing it secretes in gland
- makes 6 hormones:
1.) somatotropin = growth hormone = GH- promotes growth
2.) thyrotropin- thyroid stimulating hormone= (TSH)- stimulates thyroid
3.) Adrenocorticotropin- adrenocortical stimulating hormone (ACTH)- stimulates adrenal
cortex
4.) Follicle Stimulating (FSH)- stimulates ovary
5.) Luteinizing Hormone = LH(female) ovary or ICSH(male) testes both have effects on
other endocrine glands
6.) Prolactin(PRL)- stimulates milk
Mechanism of Control
1.) Feedback from target organ
2.) Secretion of all pituitary hormones under control of at least one hormone from
hypothalamus, causing their rate of secretion controlled.
- all hormones of hypothalamus are peptides
Hypothalamus Hormones
- difference in these and posterior are where axons are; hypo is a endocrine organ, in brain;
very busy.
1.) GHRH (stimulates), GHIH (inhibits) growth hormone in pituitary
2.) TRH (stimulates) thyroid stimulation
3.) CRH controls secretion of ACTH
4.) Since both FSH and LH stimulates gonads, GNRH in hyp controls both FSH and LH
5.) PRH (stimulates), PIH (inhibits) protection
- at least nine hormones synthesized by hypothalamus
Hypothalamus- gets excitatory and inhibitory stimulus from lots of other parts of brain
 can have great endocrine change (secretion) from physiological stress
Growth Hormone
- makes you grow
- this is the one, of the anterior pituitary hormones, that is secreted the most, even in adults
- stimulates protein synthesis
- inhibits protein breakdown
- tends to increase the net amount of protein
 which leads to secondary effect, which is it stimulated cell division
- has particular influence on long bones
- in adults, has metabolic process, which decreases glucose uptake by muscle, therefore
increases plasma glucose
 as a result, muscles metabolize fat
 fat stores decrease- fat-mobilizing effect
 many tissues will show incease cell size under increase of growth hormone
- tip of long bone covered with cartilage, the growing region is here
- In adolescence, the cartilage ossifies  bone growth ends
- Hypothalamic hormones secretes growth hormone inhibitor hormone(GHIH)- depresses
amount of growth hormone released, GHIR stimulates GH release.
Growth Hormone Defiency
- can come from a depression in secretion in pituitary gland
- if your hypothalamus isn’t producing adequate amount of GHRH
- In adults, not real dramatic, results in lack of muscle strength and bone density be reduced
- In children, it is known as dwarfism, and will not get to average stature, usually have under
developed muscluatur, and have rather large fat deposits
Excess Growth Hormone
- very different in kids and adults
- leading cause is pituitary tumor
- Children- great heigh, but normal body proportions- gigantism
 can grow to heights of 7 or 8 feet.
- When the growing ends, they can’t get any taller, but there is still continued thickening to
other bones
- Hands become abnormally large, jaw, chin, eyebrow got very prominent- AcromegalyAndre the Giant
- These people die young
- Adult effects can happen to people that didn’t have it as kids
Thyroid
- consists on two lobes on each side of trachea and one thin bridge
- arrangement of secretory cells, called thyroid follice- cells that make up boundary called
follicular cell, and sac inside colloid
 Colloid given name because historical throughout that their were 2 types of chemicals;
ones that could be crystallized and these can’t. colloid means “glue-like”;
uncrystalizable.
- Colloid- consists of solution with high protein solution, in which they produce
Thyroglobulin
- Follicular cells produce two types of hormone:
1.) Thyroxine = T4- 90%
2.) Triiodothyronine = T3- 5 times as powerful
 many years before they were known as 2 difference things, so are referred to as
thyroid hormone, but actually consists set 2 hormones
 Elicit some effects, but one more potent
Major Effect
 Increase metabolic rate
Follicular Cells are good at:
1.) Remove Iodine- concentration of cell is so big, that it diffuses into colloid
2.) Remove Tyrosine- use some of this in the synthesis of thyroglobulin- which has high
amounts of tyrosine because they were made on ribosomes, of which the tyrosine was
taken in.
 Iodine spontaneously attaches itself to Tyrosine
 some tyrosine have iodine attached- Monoiodotyrosine
 some have 2 iodine- Diiodotyrosine
 this happens to tyrosine even when they are in thyroglobulin
 Diiodotyrosine- is much more reactive than monoidotyrosine
 when these things react, you usually get two tied together you get Thyrosine
 When a dio and mono react, you get triidothyronine
 all this happens when stimulates part of protein structure
 next step is follicular cell takes up thyroglobulin
 lysosomes digest thyroglobulin
 you have these compounds in free state
 these hormones are fat soluble
 diffuse out of cell
 get carried off
 when it receives secretory stimulus it increases most of its activities
 about 90% or what gets synthesized is T4
 T3 is 5 times more powerful
 Liver and kidneys convert T4 to T3, so after short time, majority in blood
stream, majority of effects (response) is
due to T3.
 Most important thing T4 does is to be a source for T4
 Almost all of these things are bound to protein
 One called thyroxine binding protein- protein that binds the most; binds T3 and
T4
Thyroid Hormone Regulation
- Calorigenic Effect- burns calories
- Sympathomimetic effect- mimics sympathetic nervous system
-
Increase blood pressure and heart rate (reason it is no longer used for weight loss)
Necessary for normal growth
Essential for development of nervous system
Essential for proper function of the nervous system in adults
Major regulator is TSH from Pituitary
When there are deficiencies of TSH; thyroid gland atrophies
When there is too much TSH; thyroid gland hypertrophies
Control of TSH secretion comes from feedback in Thyroid and stimulation by Hypothalamus
TRH
Hypothalamus controlled by many aspects of the Nervous System
Hypothyroidism can have many different causes
Salt is iodized, so that there isn't a deficiency in dietary aid.
Thyroid deficiences are easy and cheap to treat.
Hypothyroidism Effect
- Reduced metabolic rate
- Weight gain
- Always have poor tolerance for cold
- Sympathomimetic is reduced, so act like they are getting sympathetic stimulation
 Blood pressure goes down and tire easily
 slows reflexes
 Mentally sluggish
- In Adults, hypothyroidism is called Myxedema because there is fluid accumulation in tissues
 round face, bone structure obscured, poke skin leaves dent
- In Newborns, called Cretinism
 at serious risk if not treated early, growth retarded
 has profound mental retardation.
Hyperthyroidism
- In Adults, hyperthyroidism called Grave's Disease
 Produces antibody that acts like TSH, fools thyroid and is not subject to feedback
control
 most common cause of adult hyperthyroidism
 greatly increases metabolic rates
 lose weight
 muscle mass reduced
 have elevated heart rate and BP
 makes them irritable and anxious
 on edge; easily startled
 poor emotional control
 easy to identify symptom: Exopthalmos- eyes pop out of head, as a result of
accumulation of fluid behind eye.
~ this is only a symptom of Grave's Disease; not all hyperthyroidism
Goiter
- Enlarged thyroid gland
 looks like a fat lower neck
 doesn't tell you whether it is hypo or hyper thyroidism
 can have thyroid problem without goiter
 anything that hyperstimulates thyroid, will cause goiter
 a hyper secreting thyroid gland with goiter is hyperthyroidism
 when a person has a tumor will cause a change
 when iodine deficiency,pituitary secret lots of TSH, thyroid enlarging,but can't make
thyroid hormone,so hypothyroidism
Adrenal Cortex
- Adrenal glands are 2 little pyramids on top of kidneys
- Gland has two parts:
1.) Adrenal Medulla- (Inner) derived from nervous tissue; part of the sympathetic nervous
system, for the most part.
2.) Adrenal Cortex- has 3 layers and make 3 kinds of hormones (layers don't specify
hormone)
Hormones:
a.) Mineralocorticoid- involved in regulating electrolyte balance; help to
maintain composition of ECF
b.) Glucocorticoid- have to deal with metabolism of fats
c.) Adrenal Sex Hormone- similar in nature and effect to hormones produced
in gonads; not terribly important; exception DHEA- effects same as
testosterone, so insignificant in males, but in women, it is the only male
sex hormone, important in puberty
- All Hormones are Steroids and do all the things Steroids do.
Mineralocorticoid
- Aldosterone
 most important effect is promotion of sodium reabsorption and Potassium Secretion
 it osmotically increases amount of water retained
 help to maintain blood pressure
Glucocorticoid
- Cortisol
 Stimulates liver to produce glucose from amino acids
 Stimulates the breakdown into amino acids from protein
 Increase plasma levels of glucose and amino acids go up; while protein goes down.
 Inhibits glucose uptake- except in brain
 Fat mobilization- use this as a fuel
 Permissive effects- almost every hormone that have effects has to have a little Cortisol
 Extremely important for body to deal with stress
 Anti-inflammatory and immunosuppressive- reduces it, but not at a physiological level
~ Secretion under control of Pituitary; secretes when Pituitary releases ACTH.
 also stimulates hypertrophy with high levels of ACTH
~ ACTH is stimulated by the Hypothalamus, which releases CRH
~ Cortisol inhibits ACTH and LRH; Feedback System
Too Much
- Hyper levels of Aldosterone:
 Blood Pressure goes up
 Sodium level goes up
 Potassium level goes down
 usually caused by Aldosterone secreting tumor.
- Hyper levels of Cortisol:
 called Cushing's Syndrome
 Elevated blood glucose levels
 Protein loss- muscle weakness and loss
 Development of fatty deposits usually in face (moon face)
 Protein loss causes patient much less able to heal wounds because ability to make
collagen decreases
- Hyper levels of DHEA:
 has no effect in men because they have so much testosterone
 In women:
1.) Hirsutism- develop facial hair
2.) Pattern of hair growth is more masculine
3.) Develop other male characteristic (body muscles)
4.) Depress secretion of female hormones:
a.) decrease breast size
b.) causes menstruation problems
 Young boys do not have testosterone, so if they have hypersecretion of DHEA, they
have Precocious Puberty- artificial
puberty. Grow hair and voice changes, but do not start producing sperm.
Inadequate Amounts
- Addison's Disease- Adrenal Cortex Atrophy
 reduced levels of all adrenal cortical hormones
 reduced Cortisol doesn't allow good stress management
 causes hypoglycemia- tired all the time; headaches
 lives not threatened
 reduced levels of Aldosterone is life threatening
 due to large amount of sodium, which causes loss of blood, which causes shock.
 Pretty easy to treat- high salt diet or medications
 Untreated will die in about a week
Adrenal Medulla
- Inside Adrenal Cortex where releases noroepinephrine
 Part of the Sympathetic Nervous System- begin in CNS; preganglionic neuron forms
synapes forms ganglion and then post
ganglionic neuron projects to target cell.
 cells are basically post ganglionic cells, but they release transmitters directly into target;
release epinephrine
 Epinephrine is very similar to noroepinephrine
 these cells synthesize 4 times as much Epinphrine as noroepinphrine; 80% epi to 20%
noro
 Store in granules- they stain very easily, called Chromaffin Granules
 Cells of Adrenal Medulla called Chromaffin Cells
 Effects of Epinephrine is very similar to Noroepinephrine
 Noro and epi have different receptors
- Important Effects:
 make stimulation last longer
 mobilizes stored carbos and fat
 stimulates synthesis of glucose
 there is no such thing as disorder of lacking adrenal medulla parasympathetic would
take care of loss.
 Was originally called Adrenaline.
- Pheochromocytoma- tumor that releases epinephrine and noroepinephrine spontaneously
 chronic high levels
 Rapid Pulse
 High BP
 High blood glucose
General Rule: able to synthesize lower level precursors of fat, carbohydrates, proteins to each
other.
Ways to make ATP
- Major Producers:
1.) glucose
2.) glycerol
3.) fatty acid
- Stored as glycogen in glucose
- Fatty acid glycerol stored as fat
- Not much storage of glycogen
- Lots of storage of fat
- Glucose is the only thing that the brain can use as fuel
 Reason why the blood glucose regulated closely; blood glucose = 100mg/dL;
100mg%; 1 mg/mL
 Reason we regulate, is that we switch metabolism, in everything except in brain, to fat
as fuel.
Gluconeogensis- conversion of other things into glucose
- Because we eat periodically instead of constantly, we have 2 separate metabolisms:
1.) Fed = Absorptive State
2.) Starving = Postabsorptive State
 These exist at different times
 When in Absorptive State, absorbing digested food, during state burning glucose as fuel
everyone here.
 Postabsorptive- not absorbing digested food, during state, burning fattry acids, except in
brain.
 These flip flop back and forth
 Which one of these states that a person is in is controlled by Endocrine System
 Epinephrine, Cortisol, growth hormone have effects on the control
 The Dominant control:
Islets of Langerhaus (Pancreatic Islets)- endocrine organ in pancreas
- 2 Hormones Produced:
1.) Beta- Insulin
2.) Alpha- Glucagan
 The balance between these two determine which metabolic state person is in.
Insulin
- Created by beta hormones; released into blood stream, NOT pancreatic duct
- Promotes the conversion of glucose to glycogen in liver and muscle
- Promotes uptake of fatty acid
- Promotes uptake of amino acids
- Promotes these conversions to glucose
- Promotes uptake of glucose
- Reduce level of fatty acids
- Reduce level of amino
- Reduce level of glucose in plasma
- Increase glucose levels in cells
- Convert amino acid in glucose increase glucose in cells
- Convert fatty acid in glucose increase glucose in cells
- Increase the amount of glycogen stored
- Inhibits glycogen breakdown
- In presence of elevated insulin removing nutrients from plasma, storing glycogen
- Does this when digested food is being absorbed
- Major stimulus is elevated blood glucose levels
- When Insulin goes up, liver and muscles take up fatty acids, inhibit breakdown of glycogen
- Neural control also factors into control:
 sympathetic fibers that terminate on Islets of Langerhaus, and inhibits secretion of
insulin
 parasympathetic stimulates insulin secretion
 when digesting meal, parasympathetic stimulation is high
 Reason tired after a meal because blood is being reduced elsewhere, and taken to gut.
Diabetes Insipidous- ADH deficiency, tasteless urine produced
Diabetes Mellitus- means production of honey sweet urine
 Most common endocrine disorder
 Result of insulin defiecency
 High rate of urnation, and attracts bees
 Urine has no toxic effects; can be used as a sterile irrigation in war.
 Cause of sweetness is there is glucose in it
 There is a max rate kidneys can reabsorb- 100% for glucose
 That works til plasma glucose levels get too 300mg/dL high, gets saturated and can
not be reabsorbed.
 Proximal tubules can’t absorb all, so glucose is released urine
 Urine volume is osmotically expanded- meaning large urine volume
Two types of Diabetes:
1.) Type 1- Low insulin levels
2.) Type 2- Low insulin sensitivity- can have normal plasma insulin level, but his cells
don’t respond to it.
 Sometimes referred to as “Starvation in the Midst of Plenty”
 Cells behave as though they are starving because cells don’t respond to
nutrients
 This means that the plasma has elevated levels of nutrients in it.
Symptoms:
- Hyperglycemia- pathologically high glucose levels in the blood
 Breaking down protein, and using it as a fuel because can’t use glucose
~ suffers muscle wasting
 Expanded urine level
- The high levels of fluid loss, due to an expanded urine loss, causes effects:
 Always dehydrated
 Extra fluid intake doesn’t compansate for fluid loss, so never takes back to
normal level, so he gradually
dehydrates anyway.
~ One of the most severe effects because:
1.) Reduced BP
2.) Reduced Perfusion, which results:
a.) Renal Failure
b.) Wounds heal badly
- Assortment of Neural Complications:
 Pain in extermeties reduced
 Pathology in eyes- leads to blindness
- Always feels hungry, so increase food supply
 continues to lose weight
- Burns fat as metabolic fuel
 gives breath a distinct smell, caused by keytone; doctors can use this as
diagnostic tool.
 Makes them Acidotic- producing more acids than CO2 , so that lungs can’t
keep pH level
~ Usually leads to diabetic coma
~ Can Cause Death
- Type 1- usually treated with insulin injection
- Type 2- usually treated with drugs that increase the production of insulin
- Sometimes can be controlled by changing diet
- Diabetic is always helped by exercise because exercise stimulates glucose uptake, so
helps hyperglycemia
Glucagan
- Everything that is true for insulin is opposite for glucagan
- It is the balance between glucagan and insulin that determines whether we are in fed or
starving state.
- *** Insulin and Glucogan are both peptides ***
Regulation of Blood Calcium Levels
- closely regulated
Three Hormones Involved:
1.) Parathyroid Hormone
2.) Calcitonin
3.) Vitamin D
- Regulation of Ca++ automatically regulates PO4
Distribution of Calcium in Body
- 99% in teeth and bones
- 0.9% Soft Tissues
- 0.1% ECF (half free, half bound)
 ** Free is what we can regulate 0.05%
- Level of calcium in plasma reflects the amount of calcium intaken into plasma and the
amount being taken out
- Renal exceretion removes calcium
- Calcium absorbed through gut- goes to body
- Amount absorbed is not necessarily the amount eaten
- When loss of calcium exceeds the rate of intake, body immoblizes it from bone
- In additino to endocrine regulation of calcium release from teeth and bone there is endocrine
regulation of intake and output
- When changes in plasma levels of calcium, rapid but not precise adjustments involve
adjustments of moving calcium back and forth from bones.
- The long term precise adjustments, occur in kidneys
- Primary regulator is Parathyroid Hormone
Effects:
1.) Bone
2.) Kidney
3.) Amount of absorption from gut
-- overall effect is that it increases plasma calcium levels
Bone
- Bone is metabollically active
- Matrix- made up of collagen and CaPO4- what makes it hard
- Is constantly reabsorbed and reformed
 way that happens is the reabsorption and reformed
 the laying down new stuff is most rapid in areas of stress
- While this is happening, CalciumPhosphate is being released by bones, the collagen is being
removed and laid back down again. Collagen goes where stress is and calciumphosphate
forms on collagen
- Parathyroid Hormone
1.) induces loss of calcium from fluid within bones into plasma
2.) Accelerates the disolution of bone
 all extra calcium ends up in plasma
- major effect is it raises calcium levels in plasma
- give you less dense bones
- Control of Parathyroid Hormone
 Direct Response to plasma calcium levels- level goes down, hormone released
Kidneys
- when remove calcium from bones, brings Phosphate with it
- if nothing happened, would form crystals in plasma
- Parathyroid hormone causes kidneys to release more phosphate into renal excretion
Absorption from Gut
- Parathyroid hormone doesn’t do anything directly
- Effects Vitamin D
Calcitonin
- thyroid gland also produces
- decreases rate of reabsorption of bone
- not very physiologically important
Vitamin D
- derivitive of cholesterol
- cannot absorb calcium in intestine, without Vitamin D
Two Sources:
1.) can synthesize it in skin- when exposed to sunlight
 hardly ever adequate source (clothes, hair block sun)
2.) Diet- gets added to milk
- Doesn’t do anything until it goes through 2 steps:
1.) Liver- transformed; then goes to
2.) Kidneys- converted to Activated Vitamin D- what promotes calcium absorption in gut
-- In absence of Activated Vitamin D no calcium absorbed
- Parathyroid Hormone accelerates the conversion of Vitamin D into Activated Vitamin D
- When plasma levels of calcium falls, parathyroid increase bone and kidney, and increases
conversion of Vitamin D into Activated Vitamin D.
- Will lose bone deficiency by calcium or Vitamin D defciency
Disorders
- Hyperparathyroid usually caused by tumor
 symptoms all related to loss of bone density;
1.) muscle weakness
2.) depresses neural activity
3.) depresses activity of the heart
- Hyperparathyroid people have bad memory, depression, kidney stones, and increasing
fragility
- Hypoparathyroid is very rare
 Get spasms, twitches, tingling sensations
- Complete lack of parathyroid hormone can cause death, by spasms in Respiratory System
- Vitamin D deficency has reduced capacity to absorb calcium
 In adults, loss of bone density
 In kids, causes Ricketts- legs bowed
- Osteoporisis- bone density decreases
- After 50, there is change in rate of matrix
- More common in women
- Normal levels of plasma calcium and phosphate levels
- Symptoms include being bent over
Reproductive System
Gonads
- Testes  testosterone
- Ovaries  Estrogen, Progestorone
Male
- Scrotal temp.  92 F
 Important because sperm doesn't develop at normal body temp.
- Scotal muscles under reflexive control
 when cold, bring testes up
 when warm, relax them away from body
- A way of birth control was that guy would sit on steam radiator before sex
- Descent of testes from body cavity to scrotum happens around 2 months before birth
 testosterone starts this descent
 if boy baby has testes that aren't descended- give testorterone
- Undescended testes in adult called Cryptochidism  sterile
Testes
- 75%- Seminiferous Tubules  sperm development
- 25%- Interstitial or Leydig Cells  secrete testosterone
 Seminifersous Tubles embedded in Interstitial Cells
 place where there is the most testosterone in the body
 testosterone is a steroid; diffuses into S.T. and promotes production of sperm
 also gets into blood stream and has other target cells
- In absence of testosterone, in fetus, will develop into a femal characteristics.
 testosterone gives male characteristics
 secretion usually ends at birth and then doesn't start again until puberty
- Average of 13, testosterone starts again
 S.T. starts producing sperm
- Testosterone is important for growth and maturation of reproduction system and continued
supply of testosterone is important for its maintence.
- A male that is castrated before puberty is called Eunuch- never develops sex characteristics
of a male
 Used as the keepers of the wives of the wealthy
 Used to keep young soprano voices high, in Europe; Mozart came about 15 minutes
from being castrated
- Testosterone promotes protein synthesis and bone growth
 Protein synthesis most striking in muscle- promotes muscle growth
 Bone growth- reason why boys have growth spurts come from spurts of testosterone
 Causes the ossification at the ends of the growth plates
Functions of Testes controlled by Pituitary Hormones
- LH & ICSH- effects the Interstitial or Leydig cells- makes them secrete testosterone
- FSH- stimulates the generation of new sperm cells
 both produced by anterior pituitary
 in hypothalamus- GNRH stimulates the 2 pituitary glands
 before puberty, hypothalamus produce very little GNRH, so LH & FSH don't secrete,
so don't make sperm
- At 13, hypothalamus discovers it's time to secrete GNRH, which makes other stuff happen,
and this continues throughout life.
Female
- Women have Ovarian Cycle
 once girls begin puberty, oscilate between 2 phases:
1.) Follicular phase
2.) Luteal Phase
 this cycle is usually around 28 days
 interrupted during pregnancy
ended at menopause
- Every ovary has a Primary Follicle
 consists of egg and follicular hairs
 granulosa cells proliferate
 a little follicle filled with fluid with egg embedded inside
 follicular cells produce estrogen
 fluid in follicles is estrogen- primarily estradiol
 some of this gets into blood stream
 one of the follicles grows faster than all other, called the Graafian Follicle
 about 14 days into cycle, graafian follicle ruptures and edd is released and estrogen
fluid
 ** This defines the end of the follicular phase!!! **
 after G.F. ruptures, the follicular cells are left on surface of ovary, start to turn yellow,
producing progesterone- called
Corpus Luteum
 they are reason second half is called luteal phase
 if oven doesn’t get fertilized or doesn’t get embedded into uterine wall, this phase lasts
for about 14 days.
 Follicular- estrogen
 Luteal- progesterone
 If fertilization occurs, remains in luteal phase for pregnancy
 Except for these interruptions, cycles like this until menopause.