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THE ENDOCRINE SYSTEM
A.
ENDOCRINE GLANDS
Compare exocrine with endocrine glands.
The body contains two types of glands:
Exocrine glands secrete their products into ducts or directly onto
epithelial surfaces.
Endocrine glands secrete their products called hormones, into the
extracellular fluid around the secretory cells. The secretion then
diffuses into the blood for distribution throughout the body.
Which organs are endocrine only?
There are a number of specific organs whose sole function is endocrine:
pituitary gland
thyroid gland
parathyroid glands (4)
adrenal glands (2)
pineal (epithalamus)
thymus gland
Name other organs that have some endocrine function.
pancreas
gonads (2)
kidneys
stomach
small intestine
liver
heart
placenta
B.
COMPARISON OF NERVOUS AND ENDOCRINE SYSTEMS
Together, the nervous and endocrine systems coordinate the functions of all
body systems. How does the nervous system achieve this?
The nervous system achieves this through the use of nerve impulses and
the secretion of neurotransmitter substances that either excite or inhibit
the effector.
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How does the endocrine system achieve this control?
The endocrine system, in contrast, regulates body functions by releasing
chemical messengers called hormones (“to urge on” or “to set in motion”)
into the bloodstream for delivery throughout the body.
Compare the types of effectors the two systems utilize to maintain homeostasis.
The nervous system causes muscles to contract and glands to secrete.
The endocrine system regulates metabolic activities, growth and
development, and reproduction.
Compare the time frame the two systems need to accomplish their actions.
The nervous system tends to act in milliseconds. The endocrine system
acts in seconds, minutes, hours, weeks, months, even years, depending
upon the hormone.
Compare how long the effects of the two systems persist.
Nervous effects are brief; endocrine effects are much longer lasting.
C.
HORMONES
1.
HORMONE RECEPTORS
What is an endocrine target cell?
Although a given hormone travels throughout the body in the blood
and is “seen” by all cells of the body, it only affects specific cells
called target cells.
Like neurotransmitters, hormones influence their target cells by
chemically combining to protein receptors on the target cell surface.
Only target cells for a particular hormone bear receptors for that
hormone, bind to it, and respond to it.
Receptors, like other cellular proteins, are constantly synthesized
and broken down as part of routine cellular maintenance.
What is down-regulation of a target cell’s hormone receptors?
Down-regulation occurs when the hormone is present in excess
and the cell reduces the number of available receptors for it.
This causes a decrease in cellular responsiveness to the
hormone.
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What is up-regulation of a target cell’s hormone receptors?
Up-regulation occurs when the hormone is present in less than
normal amounts and the cell increases the number of
available receptors for it. This causes an increase in cellular
responsiveness to the hormone.
2.
CIRCULATING AND LOCAL HORMONES
Define each of the following:
Circulating hormones – Hormones that pass into the blood and act
on distant target cells are called circulating hormones or
endocrines.
Local hormones – Hormones that act on target cells close to their
site of release are called local hormones. They are further
subdivided into either paracrine or autocrine.
Paracrine hormones – Paracrines are local hormones that act on
neighboring cells.
Autocrine hormones – Autocrines are local hormones that act on
the same cell that secreted them.
D.
MECHANISMS OF HORMONE ACTION
Various target cells may respond differently to the same hormone (Ex: insulin in
the liver causes glycogen formation, but in adipose cells it causes lipid
formation). Give a brief discussion for how this is possible.
The response of a target cell to a hormone depends on both the hormone
and the target cell. In part, these varied effects of hormones are possible
because there are different mechanisms of hormone action. Hormones
bind to and activate their specific receptors in different ways.
Where are the receptors for lipid-soluble hormones?
Lipid-soluble hormones, which can diffuse freely through the cell
membrane, use target cell receptors that are found in the cytoplasm or
nucleus of target cells.
157
Where are the receptors for water-soluble hormones?
Water-soluble hormones, which cannot cross the cell membrane, use
target cell receptors, integral proteins found on the cell surface of target
cells.
1.
ACTIVATION OF INTRACELLULAR RECEPTORS
Name the lipid-soluble hormones and give a brief description of their
mechanism of action at the target cell.
Steroid hormones and thyroid hormones are lipid-soluble and easily
pass through cell membranes.
Upon entering a target cell, the hormone binds to and activates an
intracellular receptor, located within the nucleus.
The activated hormone-receptor complex than alters gene
expression by turning specific genes of the nuclear DNA either on
or off.
This usually involves the synthesis of new enzymes that alter
cellular metabolism in the way specific for that hormone, and in that
way alters some function.
2.
ACTIVATION OF PLASMA MEMBRANE RECEPTORS
Name the water-soluble hormone and give a brief description of their
mechanism of action at the target cell.
Catecholamine, peptide, and protein hormones are water-soluble,
cannot diffuse through the cell membrane, and therefore must
utilize receptors on the target cell surface.
Since the hormone can only bring the physiological message to the
cell membrane of the target cell, rather than the nucleus, the
hormone is called the first messenger.
A second messenger is needed to relay the message from the
receptor, through the cell membrane, and into the cytoplasm where
the hormone-stimulated response can take place.
The best known second messenger is cyclic 3’, 5’-monophosphate
(cyclic AMP or camp).
158
The receptor is attached on its inner side to the enzyme adenylate
cyclase. The enzyme is stimulated to convert intracellular ATP to
cyclic AMP when the hormone binds to the receptor.
Increased levels of intracellular cyclic AMP acts as a second
messenger within the cell, directing a specific response that is celltype dependent.
The increased cyclic AMP within the cell is transient, however,
because of the intracellular enzyme phosphodiesterase, which
quickly degrades cyclic AMP to 5’-AMP.
5’-AMP has no biological activity (therefore, the hormonal effect on
the cell is tightly regulated) within the cell and is used to regenerate
ATP.
E.
CONTROL OF HORMONAL SECRETIONS
In general, how are hormone secretions controlled?
Most endocrine glands secrete their product(s) in short bursts, with little or
no secretion in between stimulations.
Regulation of secretion depends on homeostasis and prevents over- or
underproduction.
Hormone secretion is stimulated and inhibited by signals from the nervous
system, chemical changes in the blood, and other hormones.
Most often, negative feedback systems maintain homeostasis for
hormonal secretions.
F.
HYPOTHALAMUS AND PITUITARY GLAND (HYPOPHYSIS)
What is the role of the hypothalamus in endocrine control?
The hypothalamus serves as the master control for many of the hormones
secreted by the endocrine system, and serves as the major integrator
between the nervous and endocrine systems. In particular, the
hypothalamus controls the secretions of the pituitary gland, also known as
the hypophysis.
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What is the anatomical relationship between the pituitary gland and the
hypothalamus?
The pituitary gland is a pea-sized organ lying within the sella turcica of the
sphenoid bone. It is suspended from the base of the hypothalamus by the
infundibulum, a stalk-like structure.
Describe the pituitary gland by describing its embryologic formation.
The pituitary gland has two anatomically and functionally distinct portions
due to its embryological formation.
The anterior pituitary gland (adenohypophysis) (about 75% of the total
gland) is derived from an outpouching of the roof of the developing mouth,
called Rathke’s pouch.
Rathke’s pouch breaks off from the mouth and migrates as a unit to make
contact with the forming posterior pituitary gland associated with the
hypothalamus.
The posterior pituitary gland (neurohypophysis) forms as an outgrowth of
the base of the hypothalamus and remains attached to it via the
infundibulum.
The posterior pituitary gland contains axons and axon terminals of about
5,000 neurons whose cell bodies are located in nuclei in the
hypothalamus.
The nerve fibers that terminate in the posterior pituitary gland are
associated with neuroglial-like support cells called pituicytes, which are
secretory.
Regardless of origin, both the anterior and posterior pituitary glands are
wholly dependent upon the hypothalamus for regulation of hormonal
secretion.
Describe the anatomical mechanism by which the hypothalamus controls
hormonal secretions from the anterior pituitary gland.
The anatomical pituitary gland (adenohypophysis) secretes seven
hormones that regulate a wide variety of bodily functions.
Release of these hormones is dependent upon chemicals secreted by the
hypothalamus called releasing and inhibiting factors (hormones).
160
These hypothalamic hormones reach the anterior pituitary gland through a
system of blood vessels that connect the two regions.
This system of vessels, called the hypophyseal portal system, consists of
several superior hypophyseal arteries that enter the lower hypothalamic
region and divide into the primary plexus of capillaries.
The primary plexus is recollected into hypophyseal veins that pass down
the infundibulum, enter the anterior pituitary gland, then divide into the
secondary plexus of capillaries.
The secondary plexus is then recollected into the anterior hypophyseal
veins that exit the anterior pituitary gland and return the blood to the
general circulation.
The releasing and inhibiting factors secreted by hypothalamic neurons
diffuse into the blood of the primary plexus and are carried by the portal
system into the anterior pituitary.
The factors diffuse out of the blood of the secondary plexus and into the
interstitial fluid of the anterior pituitary, where they interact with their
specific target cells.
In response, the cells of the anterior pituitary may secrete specific
hormones that diffuse into the blood of the secondary plexus and
ultimately are distributed throughout the body.
1.
ANTERIOR PITUITARY GLAND (ADENOHYPOPHYSIS)
Name the seven hormones secreted by the anterior pituitary gland.
growth hormone (GH)
thyroid-stimulating hormone (TSH)
follicle-stimulating hormone (FSH)
luteinizing hormone (LH)
prolactin (PRL)
adrenocorticotropic hormone (ACTH)
melanocyte-stimulating hormone (MSH)
Tropic hormones (tropins) are those hormones that influence other
endocrine glands to secrete their hormone (s). Name them.
FSH
LH
TSH
ACTH
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a.
GROWTH HORMONE
Growth hormone (somatotropin or GH) stimulates protein
synthesis, increased lipolysis, and the decreased use of
glucose for ATP production, promoting hyperglycemia (the
diabetogenic effect.
GH causes cells to increase their rate of amino acid uptake
from the blood, especially during childhood and
adolescence, thus promoting increased protein anabolism.
Control of GH secretion is via GH-Inhibiting Factor and GHReleasing Factor from the hypothalamus and is related to
blood glucose concentration.
Hypoglycemia inhibits GH-IF secretion, allowing GH-RF
secretion and GH blood levels to rise.
Hyperglycemia inhibits GH-RF secretion, allowing GH blood
levels to fall. this promotes normoglycemia.
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GROWTH HORMONE
increased blood glucose
(hyperglycemia)
decreased blood glucose
(hypoglycemia)
(stimulates)
(stimulates)
increased hypothalamic secretion
secretion
of GH-IF
increased hypothalamic
of GH-RF
(inhibits)
(stimulates)
anterior pituitary gland
secretion of GH
increased anterior pituitary gland
secretion of GH
(has the following effects)
decreased blood glucose
anabolism
1.
increased protein
2.
3.
increased lipolysis
increased
glycogenolysis
(lead to)
increased blood glucose
normoglycemia
(Normoglycemia feeds back to turn off both the hypothalamus and anterior pituitary
gland so that both GH-IF and GH-RF secretions are inhibited)
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b.
THYROID-STIMULATING HORMONE
HYPOTHALAMIC-PITUITARY-THYROID AXIS
decreased basal metabolic rate
(stimulates)
increased hypothalamic secretion of TSH-RF
(stimulates)
increased anterior pituitary gland secretion of TSH
(stimulates)
increased thyroid gland secretion of T3 and T4 (thyroxine)
(has the following effects))
1.
2.
3.
increasing carbohydrate catabolism
increasing fat catabolism
increasing protein anabolism
(lead to)
increased basal metabolic rate
(This feeds back to turn off both the hypothalamus and anterior pituitary gland so that
TSH-RF and TSH blood levels decline)
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c.
FOLLICLE-STIMULATING HORMONE
HYPOTHALAMIC-PITUITARY-GONADAL AXIS
(male – follicle stimulating hormone)
decreased blood levels of inhibin
(stimulates)
increased hypothalamic secretion of gonadotropin-RF
(stimulates)
increased anterior pituitary gland secretion of FSH
(stimulates)
1.
2.
increased spermatogenesis
increased activity of Sertoli cells
(leading to)
increased secretion of inhibin by Sertoli cells
(Inhibin feeds back to turn off both the hypothalamus and anterior pituitary gland so that
Gn-RF and FSH blood levels decline)
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HYPOTHALAMIC-PITUITARY-GONADAL AXIS
(female – follicle stimulating hormone)
decreased blood levels of estrogen
(stimulates)
increased hypothalamic secretion of gonadotropin-RF
(stimulates)
increased anterior pituitary gland secretion of FSH
(stimulates)
development of ovarian follicles
(has the following effects))
1.
2.
increasing blood levels of estrogen
maturation of an egg for ovulation
(leads to)
increased blood estrogen
(This feeds back to turn off both the hypothalamus and anterior pituitary gland so that
Gn-RF and FSH blood levels decline)
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d.
LUTEINIZING HORMONE
HYPOTHALAMIC-PITUITARY-GONADAL AXIS
(male – luteinizing hormone)
decreased blood levels of testosterone
(stimulates)
increased hypothalamic secretion of gonadotropin-RF
(stimulates)
increased anterior pituitary gland secretion of LH
(stimulates)
increased secretion of testosterone
(has the following effects))
support of all male secondary sex characteristics
(Testosterone feeds back to turn off both the hypothalamus and anterior pituitary gland
so that Gn-RF and FSH blood levels decline.)
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HYPOTHALAMIC-PITUITARY-GONADAL AXIS
(female – luteinizing hormone)
increased blood levels of estrogen
(stimulates)
increased hypothalamic secretion of gonadotropin-RF
(stimulates)
increased anterior pituitary gland secretion of LHH
(stimulates)
1.
2.
directly stimulates ovulation,
which leads to formation of the corpus luteum
(has the following effects))
ovulation
(leads to)
formation of the corpus luteum
(After ovulation, blood estrogen falls below the level necessary ot stimulate the anterior
pituitary gland. Therefore, this is not really inhibition of LH secretion. The anterior
pituitary gland cannot secrete LH without sufficient blood estrogen.)
168
e.
PROLACTIN
PROLACTIN
(female only)
increased estrogen during
initiated by
last half of menstrual cycle
nipple
neuroendocrine reflex
suckling of postpartum
(stimulates)
increased hypothalamic secretion
of PRL-IF
(stimulates)
increased hypothalamic secretion
of PRL-RF
(inhibits)
anterior pituitary gland
secretion of PRL
(stimulates)
increased anterior pituitary gland
secretion of PRL
has the following effects)
decreased blood PRL
by mammary
increased milk synthesis
gland cells (not secretion)
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f.
MELANOCYTE-STIMULATING HORMONE
MELANOCYTE STIMULATING HORMONE
increased hypothalamic
secretion ofsecretion of MSH-IF
(inhibits)
anterior pituitary gland
secretion of MSH
increased hypothalamic
MSH-RF
(stimulates)
increased anterior pituitary gland
secretion of MSH
(stimulates)
increased skin pigmentation by
stimulation of melanocytes
gland cells (not secretion)
(This hormone is poorly understood.)
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g.
ADRENOCORTICOTROPIC HORMONE
HYPOTHALAMIC-PITUITARY-ADRENAL AXIS
increased stress or decreased blood levels of glucocorticoids
(stimulates)
increased hypothalamic secretion of corticotropin-RF
(stimulates)
increased anterior pituitary gland secretion of ACTH
(stimulates)
increased adrenal cortex gland secretion of glucocorticoids (cortisol)
(has the following effects))
1.
promote normal metabolism and ensure glucose availability by:
increasing protein catabolism
increasing gluconeogenesis
increased lipolysis
2.
provide resistance to stress by:
increased mental alertness
increased energy
increased blood pressure
3.
increased anti-inflammatory activity by:
stabilizing cell membranes
depressing phagocytosis
decreased capillary permeability (decreased swelling)
(lead to)
decreased stress
(This feeds back to turn off both the hypothalamus and anterior pituitary gland so that CRF and ACTH blood levels decline)
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2.
POSTERIOR PITUITARY GLAND (NEUROHYPOPHYSIS)
Describe the posterior pituitary gland and the way it is controlled by the
hypothalamus.
The posterior pituitary gland (neurohypophysis), in a strict sense, is
not an endocrine organ at all since the hormones released from the
gland are actually synthesized by neurons in the hypothalamus.
In the axon terminals of the neurons that pass down the
infundibulum and terminate among the pituicytes are synaptic
vesicles filled with one of two hormones: oxytocin and antidiuretic
hormone (ADH).
An action potential in one of these neurons causes the release of
the hormone into the extracellular fluid of the posterior pituitary,
where it will diffuse into the blood for distribution throughout the
body.
These axons passing from the hypothalamus are collected together
as the hypothalamo-hypophyseal tract.
a.
OXYTOCIN
What are the functions of oxytocin?
Oxytocin stimulates the contraction of uterine smooth muscle
during delivery of the baby and placenta. After birth,
oxytocin stimulates contraction of the myoepithelial cells of
the mammary glands, causing milk ejection (letdown) from
the breast.
How is oxytocin secretion controlled?
Both events are controlled by a neuroendocrine reflex in
which stretch of the cervix or tactile stimulation of the nipple
initiates sensory impulses that terminate on the appropriate
neurons of the hypothalamus. Stimulation of these neurons
results in the release of oxytocin into the posterior pituitary
gland.
What is the role of oxytocin in males and nonpregnant females?
In the nonpregnant and postpartum nonnursing female and
in the male, the role of oxytocin is unknown.
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OXYTOCIN
(female only)
increased stretch of the
postpartum
pregnant cervix
tactile stimulation of
areola and nipple
(stimulates)
(stimulates)
increased activity of
hypothalamic neurons
increased activity of
hypothalamic neurons
(stimulates)
(stimulates)
posterior pituitary gland
neurosecretion of oxytocin
posterior pituitary gland
neurosecretion of oxytocin
(stimulates)
(stimulates)
contraction of uterine smooth
muscle during labor and delivery
contraction of mammary gland
myoepithelial cells, resulting I
milk letdown
(This system requires the hormones of pregnancy to properly prime the uterus and
mammary gland cells so that they are responsive to oxytocin.)
b.
ANTIDIURETIC HORMONE
What is an antidiuretic?
An antidiuretic is any chemical substance that prevents
excessive urine formation.
What are the functions of ADH?
The principal effect of ADH is to cause the kidneys to
remove water from the forming urine and return it to the
blood, thus conserving it. ADH also causes decreased
perspiration and vasoconstriction of blood vessels. All
efforts of ADH are related to maintaining normal blood
pressure.
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How is ADH secretion controlled?
The neurons of the hypothalamus that secrete ADH are
osmoreceptors and detect high osmotic pressure in the
extracellular fluid. Increased osmolarity stimulates the
neurons to create an action potential that results in the
release of ADH. Decreased osmolarity inhibits ADH
secretion.
What is diabetes insipidus?
Diabetes insipidus results when there is too little ADH
secretion. As a result, the kidneys conserve much less
water than usual and daily urine output may be as much as
10-fold normal.
ANTIDIURETIC HORMONE
(VASOPRESSIN)
increased extracellular fluid osmolarity
(stimulates)
hypothalamic neurosecretory osmoreceptors
(leading to)
posterior pituitary gland secretion of ADH
(has the following effects)
1.
2.
increased water reabsorption by kidney tubule cells
increased thirst
(leading to)
increased extracellular fluid volume and therefore decreased body osmolarity
(Decreased extracellular fluid osmolarity feeds back to turn off the hypothalamic
osmoreceptors and blood levels of ADH decline.)
174
G.
THYROID GLAND
Describe the thyroid gland.
The thyroid gland is located just below the larynx in the anterior neck,
consisting of a right and left lateral lobe, and a central portion called the
isthmus. The gland itself consists of microscopic spherical sacs or follicles
formed by the follicular cells.
Name the hormones secreted by the follicular cells.
Follicular cells secrete two hormones that are closely related:
1.
triiodothyronine (T3), with three iodine atoms, and
2.
tetraiodothyronine (T4 or thyroxine), with four iodine atoms
What are parafollicular cells?
Between the follicles, lying in small nests, are the parafollicular (C-) cells
that secrete the hormone calcitonin.
1.
FORMATION, STORAGE, AND RELEASE OF THYROID HORMONES
Describe the synthesis pathway for thyroxine.
The thyroid gland is the only endocrine gland that stores its
secretory product in large quantity, normally about a 10-day supply.
In essence, the thyroid gland captures iodide ions, which are then
stored in the cytoplasm of the follicular cells until needed.
The follicular cells synthesize a glycoproteins called thyroglobulin,
which has tyrosine molecules along its length, and secrete it into
the center of the follicle.
The iodide ions are moved out of the cells and into the center of the
follicle to iodinate the tyrosine residues, forming colloid, the storage
form of T3 and T4.
When stimulated by TSH from the anterior pituitary gland, the
follicular cells remove colloid from the follicle center and
enzymatically remove the T3 and T4 molecules from the
thyroglobulin.
The follicular cells then secrete the T3 (triiodothyronine) and T4
(tetraiodothyronine or thyroxine) molecules, into the extracellular
space around the follicle so they can diffuse into the blood.
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2.
3.
ACTIONS OF THYROID HORMONES
CONTROL OF THYROID HORMONE SECRETION
Describe the functions of thyroxine and the control of its secretion.
The major action of thyroxine is to regulate all metabolic processes
of the body cells by stimulating the following:
1.
increased carbohydrate catabolism
2.
increased fat catabolism
3.
increased protein anabolism
The net result is an increase in catabolism, thereby increasing the
basal metabolic rate (BMR) and raising body temperature (the
calorigenic effect).
In addition, thyroxine is required for normal growth and
development of children, particularly of the nervous system
(cretinism results from too little thyroxine during development).
Thyroxine secretion is controlled by TSH secretion from the anterior
pituitary, which is itself controlled by TSH-RF from the
hypothalamus, which is controlled by the BMR, the blood glucose
level, and the T4 concentration.
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HYPOTHALAMIC-PITUITARY-THYROID AXIS
decreased basal metabolic rate
(stimulates)
increased hypothalamic secretion of TSH-RF
(stimulates)
increased anterior pituitary gland secretion of TSH
(stimulates)
increased thyroid gland secretion of T3 and T4 (thyroxine)
(has the following effects))
1.
2.
3.
increasing carbohydrate catabolism
increasing fat catabolism
increasing protein anabolism
(lead to)
increased basal metabolic rate
(This feeds back to turn off both the hypothalamus and anterior pituitary gland so that
TSH-RF and TSH blood levels decline)
4.
CALCITONIN
Describe the role of calcitonin in calcium homeostasis.
The second major cell population of the thyroid gland is the
parafollicular (C-) cell. These cells are located between the thyroid
follicles. They secrete the hormone calcitonin.
Calcitonin works antagonistically with parathyroid hormone (PTH)
to maintain blood calcium levels between 9.5 – 10.5 mg%.
177
The C-cells have receptors that monitor extracellular fluid calcium
concentration. They are stimulated to secrete calcitonin when
blood calcium levels exceed 10.5 mg% (hyperglycemia).
Calcitonin works to decrease serum calcium by:
1.
inhibiting osteoclasts
2.
stimulating osteogenesis
3.
decreasing calcium reabsorption by the kidneys
When blood calcium levels drop back below 10.5 mg%, the C-cells
are inhibited and no longer secrete calcitonin.
CALCITONIN
blood calcium > [10.5 mg%]
(hypercalcemia)
(stimulates)
parafollicular cells of the thyroid gland
(leading to)
increased secretion of calcitonin
(has the following effects)
1.
2.
3.
decreased bone resorption
increased bone formation
decreased calcium reabsorption by kidneys
(leading to)
decreased blood calcium concentration (normocalcemia)
(Blood calcium < [10.5 mg%] feeds back to turn off calcitonin secretion.)
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H.
PARATHYROID GLANDS AND PARATHYROID HORMONE
Describe the parathyroid glands and the role of parathyroid hormone (PTH) in
calcium homeostasis.
There are four parathyroid glands embedded into the posterior surface of
the thyroid gland.
The glands consist of two cell types:
1.
chief cells that secrete parathyroid hormone (PTH)
2.
oxyphil cells – function unknown
PTH works antagonistically with calcitonin to regulate the blood
concentration of calcium and is secreted by chief cells under conditions of
PTH works antagonistically with calcitonin to regulate the blood
concentration of calcium and is secreted by chief cells under conditions of
hypocalcemia (<9.5 mg%).
PTH works to increase blood calcium levels by:
1.
activating osteoclasts
2.
increasing calcium reabsorption by the kidneys
3.
increasing calcium absorption by the gut
4.
stimulating secretion of vitamin D (similar effects as PTH)
When blood calcium levels rise above 9.5 mg%, the chief cells are
inhibited and no longer secrete PTH.
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PARATHYROID HORMONE
blood calcium < [9.5 mg%]
(hypocalcemia)
(stimulates)
chief cells of the parathyroid glands
(leading to)
increased secretion of PTH
(has the following effects)
1.
2.
3.
increased bone resorption
decreased bone formation
increased calcium reabsorption by kidneys
(leading to)
increased blood calcium concentration (normocalcemia)
(Blood calcium > [9.5 mg%] feeds back to turn off PTH secretion.)
I.
ADRENAL (SUPRARENAL) GLANDS
Describe the adrenal glands.
The paired adrenal (suprarenal) glands, each lying just superior to each
kidney, are structurally and functionally divided into two separate glands:
the adrenal cortex and the adrenal medulla.
What are steroids?
All hormones secreted by the adrenal cortex are called steroid hormones,
lipid molecules whose chemical structure is derived from cholesterol.
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1.
ADRENAL MEDULLA, EPINEPHRINE, AND NOREPINEPHRINE
Describe the adrenal medulla and its hormones.
The adrenal medulla, the inner portion of the gland, consists of
chromaffin cells that secrete the catecholamines epinephrine and
norepinephrine.
These cells receive direct innervation from sympathetic
preganglionic neurons. In response, they secrete these
catecholamines and add to the fight-or-flight response.
2.
ADRENAL CORTEX
Name the three zones of the adrenal cortex.
The adrenal cortex is subdivided into three zones, each of which
has a different cellular arrangement and secretes a different class
of steroids.
a.
MINERALOCORTICOIDS
What are the mineralocorticoids?
The mineralocorticoids are the class of steroids produced by
the outermost zone of the adrenal cortex, the zona
glomerulosa.
Aldosterone is the primary mineralocorticoid and, like all the
steroids of this class, work to control water and electrolyte
balance, particularly by controlling sodium and potassium
concentrations.
Under normal conditions, aldosterone secretion is in
response to high potassium ion concentration in the
extracellular fluid.
Aldosterone stimulates kidney cells to lose potassium ions
into the forming urine, while at the same time conserving
sodium ions and, by osmosis, water.
Describe control of aldosterone secretion by the renin-angiotensin
system and its role in homeostasis.
During times of dehydration, hemorrhage, or sodium
deficiency, aldosterone secretion may be stimulated via the
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renin-angiotensin system. This is related to blood pressure
control.
Decreased blood volume causes decreased blood pressure,
which in turn causes the kidneys to secrete renin.
Renin converts the inactive plasma protein angiotensinogen
to angiotensin I. As angiotensin I passes through the lungs
in the blood it is converted to angiotensin II.
Angiotensin II stimulates aldosterone secretion, which
causes increased sodium reabsorption and therefore water
reabsorption. As a result, blood volume increases and
therefore blood pressure rises.
This is an important long-term compensatory mechanism for
blood pressure control. It will be discussed in greater detail
with the kidneys
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MINERALOCORTICOIDS
(RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM)
dehydration
sodium deficiency
hemorrhage
Above the dashed line represents
compensatory changes in response to
decreased blood pressure.
(leading to)
Below the dashed line shows the normal
physiologic control mechanism for
aldosterone secretion
decreased blood volume
(leading to)
increased blood pressure
decreased blood pressure
(leading to)
increased renin secretion from kidney
(converts)
angiotensinogen
angiotensin I
(converted in
lungs to)
increased blood volume
angiotensin II
(effects)
increased water retention
by kidneys
1.
2.
3.
systemic vasoconstriction
increased thirst
increased ADH secretion
increased sodium reabsorption
4.
increased aldosterone
by kidneys
secretion
--------------------------------------------------------------------------------------------------------------------decreased K+
(stimulates)
reabsorption by kidneys
(inhibits)
increased K+ in blood
(leads to)
loss of potassium into urine
decreased K+ in blood
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b.
GLUCOCORTICOIDS
What are glucocorticoids?
The glucocorticoids are the class of steroids produced by the
middle zone of the adrenal cortex, the zona fasciculate. The
predominant glucocorticoids are hydrocortisone, cortisone,
and corticosterone.
What controls their secretion?
Glucocorticoids are secreted in response to ACTH from the
anterior pituitary, which is controlled by corticotropic-RF from
the hypothalamus.
C-RF secretion is in response to stress. Reduction in stress
inhibits C-RF and therefore ACTH and the glucocorticoids.
What are their principal effects?
Glucocorticoids have the following effects:
1.
increased gluconeogenesis, thus increasing
available glucose for body cells for normal
metabolism and to combat stress
2.
inhibition of the inflammatory response
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HYPOTHALAMIC-PITUITARY-ADRENAL AXIS
increased stress or decreased blood levels of glucocorticoids
(stimulates)
increased hypothalamic secretion of corticotropin-RF
(stimulates)
increased anterior pituitary gland secretion of ACTH
(stimulates)
increased adrenal cortex gland secretion of glucocorticoids (cortisol)
(has the following effects))
1.
promote normal metabolism and ensure glucose availability by:
increasing protein catabolism
increasing gluconeogenesis
increased lipolysis
2.
provide resistance to stress by:
increased mental alertness
increased energy
increased blood pressure
3.
increased anti-inflammatory activity by:
stabilizing cell membranes
depressing phagocytosis
decreased capillary permeability (decreased swelling)
(lead to)
decreased stress
(This feeds back to turn off both the hypothalamus and anterior pituitary gland so that CRF and ACTH blood levels decline)
185
c.
GONADOCORTICOIDS
Briefly describe the gonadocorticoids.
The gonadocorticoids are the class of steroids produced by
the innermost zone of the adrenal cortex, the zona
reticularis. these steroids are the male androgens and the
female estrogens.
During reproductive left, the concentration of these
hormones from the adrenal cortex is of little importance
because of gonadal secretion. their secretion during
development, childhood, and after menopause does
contribute to normal metabolism.
J.
PANCREAS
Describe the pancreas.
The pancreas is both an exocrine organ related to digestion and an
endocrine gland. It is a flattened organ located posterior and just inferior
to the stomach. Scattered throughout the exocrine portion of the gland are
small islands of cells called the islets of Langerhans.
Describe the cell types of the islets of Langerhans?
Islets are composed of four cell types:
1.
alpha cells that secrete glucagon
2.
beta cells that secrete insulin
3.
delta cells that secrete somatomedin (GH-IF)
4.
F-cells that are related to digestion
1.
GLUCAGON
Describe the role of glucagon in maintaining glucose homeostasis.
Glucagon works antagonistically with insulin to maintain blood
glucose levels within homeostatic range (90 – 110 mg%).
The alpha cells of the islets of Langerhans bear receptors for
glucose that monitor the extracellular fluid for glucose
concentration.
Under conditions of hypoglycemia (<90 mg%), the alpha cells are
stimulated to secrete glucagon.
186
Glucagon works to raise blood glucose by:
1.
increasing glycogenolysis (glycogen breakdown)
2.
increasing gluconeogenesis (formation of glucose
from other sources, such as amino acids).
When blood glucose concentration rises above 90 mg%, the alpha
cells are inhibited and glucagon secretion stops.
GLUCAGON
blood glucose < [90 mg%]
(hypoglycemia)
(stimulates)
alpha cells of the islets of Langerhans in the pancreas
(leading to)
increased secretion of glucagon
(has the following effects)
1.
2.
increased glycogenolysis
increased gluconeogenesis
(leading to)
increased blood glucose concentration (normoglycemia)
(Blood glucose > [90 mg%] feeds back to turn off glucagon secretion.)
2.
INSULIN
Describe the role of insulin in maintaining glucose homeostasis.
Insulin works antagonistically with glucagon to maintain blood
glucose levels within homeostatic range (90 – 110 mg%) or
normoglycemia.
Beta cells of the islets of Langerhans bear receptors for glucose
that monitor the extracellular concentration for conditions of
hyperglycemia (>110 mg%).
187
When blood glucose levels exceed 110 mg%, the beta cells are
stimulated to secrete insulin.
Insulin decreases blood glucose by:
1.
increasing cell uptake of glucose
2.
increasing glycogenesis
3.
decreasing glycogenolysis
4.
decreasing gluconeogenesis
5.
increasing lipogenesis
When blood glucose levels fall back into the normoglycemic range
(<110 mg%), the beta cells are inhibited and insulin secretion is
stopped.
INSULIN
blood glucose > [110 mg%]
(hyperglycemia)
(stimulates)
beta cells of the islets of Langerhans in the pancreas
(leading to)
increased secretion of insulin
(has the following effects)
1.
2.
3.
4.
increased cellular uptake of glucose from the blood
(particularly liver, skeletal muscle, and adipose cells)
increased glycogenesis
increased lipogenesis
increased protein anabolism
(leading to)
decreased blood glucose concentration (normoglycemia)
(Blood glucose < [110 mg%] feeds back to turn off insulin secretion.)
188
K.
THE GENERAL ADAPTATION SYNDROME
Review the stages and events of the general adaptation syndrome.
Three phases:
1.
Alarm phase – immediate short-term responses to stressors,
causing fight-or flight, which might lead to the
2.
Resistance phase – long-term metabolic adjustments to
provide resistance to the stressors, which might lead to
3.
Exhaustion phase – collapse of vital systems as resistance
efforts fail to counteract stressors.
In the alarm phase, stress stimulates the hypothalamus, leading to general
sympathetic action and activation of the adrenal medulla. This leads to
secretion of norepinephrine and epinephrine, causing fight-or-fight.
During the resistance phase, a number of hormones cause the following
effects:
1.
mobilization of remaining energy reserves from lipid and
muscle
2.
conservation of glucose
3.
elevation of blood glucose level
4.
decreased inflammatory response
5.
conservation of sodium and water
6.
increased blood pressure
Continued use of resistance phase to counter the effects of stress
eventually leads one into the exhaustion phase. Causes of multisystem
collapse may be due to:
1.
exhaustion of lipid (energy) reserves
2.
depressed immune response
3.
failure of electrolyte balance
4.
cardiac and/or renal failure
The net result of the exhaustion phase is death.
189