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Overview of the Endocrine System

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22 views12 pages

Overview of the Endocrine System

chapter summary

Uploaded by

lamayoguene
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

THE ENDOCRINE SYSTEM i.

Change plasma membrane permeability or


I. A major controlling system of the body. membrane potential (electrical state) by
Through hormones, it stimulates such opening or closing ion channels
long-term processes as growth and ii. Activate or inactive enzymes
development, metabolism, reproduction, and iii. Stimulate or inhibit cell division
body defense. iv. Promote or inhibit secretion of a product
II. Endocrine organs are small and widely v. Turn on or turn off transcription of certain
separated in the body. Some are part of genes (such as those encoding proteins or
mixed glands (both endocrine and exocrine in regulatory molecules)
function). Others produce only hormones.
a. Exocrine – has ducts (an exit) IV. HORMONE CHEMISTRY AND ACTION
b. Endocrine – ductless, releases into the a. Target cells/organs – a given hormone affects
bloodstream only certain tissue cells or organs.
b. Hormones fall into three chemical classes:
i. Steroids – lipids synthesized from
cholesterol
ii. Monoamine – small molecules, bearing an
amino group, synthesized from the amino
acids, tyrosine and tryptophan
iii. Peptides – chains of about 3 to 200 amino
acids

c. Amino acid–based hormones act through


III. HORMONES
second messengers. Steroid hormones can
a. chemical messengers that are secreted into
directly influence the target cell’s DNA or act
the bloodstream and stimulate physiological
via second messenger.
responses in distant organs.
b. regulate the metabolic activity of other cells
d. Direct Gene Activation
in the body.
c. Hormones can:
i. once inside, the steroid hormone enters b. Humoral Stimuli - changing blood levels of
the nucleus, certain ions and nutrients may also stimulate
ii. and binds to a specific hormone receptor, hormone release.
iii. the hormone-receptor complex then binds c. Neural Stimuli - in isolated cases, nerve fibers
to specific sites on the cell’s DNA, stimulate hormone release, and the
iv. activating certain genes to transcribe endocrine cells are said to respond to neural
messenger RNA (mRNA) stimuli.
v. the mRNA is translated in the cytoplasm,
vi. resulting in the synthesis of new proteins.
Alternatively, the steroid hormone may
bind to receptors in the cytoplasm, and VI. CHEMICAL REGULATORS AND THEIR
then the complex moves into the nucleus FUNCTIONS

to activate certain genes. a. Hypothalamus


i. It regulates primitive functions of the body
e. Second-Messenger System ranging from water balance to sex drive.
i. the hormone (first messenger) binds to ii. Many of its functions are carried out by
the receptor protein on the membrane, the pituitary gland.
ii. and the activated receptor sets off a series iii. The hypothalamus produces nine
of reactions (a cascade) that activates an hormones of importance. Seven of them
enzyme, travel through the portal system and
iii. the enzyme, in turn, catalyzes reactions regulates the activities of the anterior
that produce second-messenger pituitary.
molecules,
iv. (in this case, cyclic AMP, also known as b. Pituitary Gland
cAMP, or cyclic adenosine i. It hangs from the hypothalamus of the
monophosphate) that oversee additional brain by a stalk and is enclosed by bone. It
intracellular changes that promote the is approximately the size of a pea.
typical response of the target cell to the ii. It has two functional lobes - the anterior
hormone. pituitary (glandular tissue) and the
posterior pituitary (nervous tissue).
V. STIMULI FOR CONTROL OF HORMONE RELEASE
a. Hormonal Stimuli - which endocrine organs
are prodded into action by other hormones.
2. Prolactin (PRL): Stimulates production
of breast milk.
3. Adrenocorticotropic hormone (ACTH):
Stimulates the adrenal cortex to release
its hormones, mainly glucocorticoids.
4. Thyroid-stimulating hormone (TSH):
Stimulates the thyroid gland to release
thyroid hormone.
5. Gonadotropic hormones
a. Follicle-stimulating hormone
(FSH): Beginning at puberty,
stimulates follicle development and
estrogen production by the female
ovaries; promotes sperm
production in the testes.
iii. Anterior Pituitary - It synthesizes and b. Luteinizing hormone (LH):
secretes six principal hormones. The Beginning at puberty, stimulates
release of each of its hormones is ovulation, causes the ruptured
controlled by releasing hormones and ovarian follicle to produce
inhibiting hormones produced by the progesterone; stimulates testes to
hypothalamus. produce testosterone

1. Growth hormone (GH): An anabolic and iv. Posterior Pituitary - It does not make the
protein-conserving hormone that peptide hormones it releases. It acts as a
promotes total body growth. Its most

important effect is on skeletal muscles storage are for hormones made by


and bones. Untreated hyposecretion hypothalamic neurons.
during childhood results in pituitary 1. Oxytocin (OT): Stimulates powerful
dwarfism; hypersecretion produces uterine contractions and causes milk
gigantism (in childhood) and ejection in nursing women.
acromegaly (in adulthood).
2. Antidiuretic hormone (ADH): Causes 2. Calcitonin is released by parafollicular
kidney tubule cells to reabsorb and cells surrounding the thyroid follicles in
conserve body water and increases response to a high blood level of
blood pressure by constricting blood calcium ions. It causes calcium to be
vessels. Hyposecretion leads to deposited in bones.
diabetes insipidus.
e. Parathyroid Gland
i. Tiny masses of glandular tissue often
c. Pineal Gland found on the posterior surface of the
i. A pine cone-shaped growth attached to thyroid gland.
the roof of the third ventricle, beneath the ii. Typically, there are two parathyroid glands
posterior end of the corpus callosum. on each thyroid lobe = a total of four
ii. Although many chemical substances have parathyroids.
been identified in the pineal gland, only iii. But about 5% if people have more than
the hormone melatonin appears to be four and can be found in other regions of
secreted in substantial amounts. the neck.
iv. A low blood level of calcium stimulates the
d. Thyroid Gland parathyroid glands to release parathyroid
i. It is located at the base of the throat, just hormone (PTH). It causes liberation of
inferior to the Adam’s apple, where it is calcium from bone to blood.
easily palpated during a physical Hyposecretion of PTH results in tetany;
examination. hypersecretion leads to extreme bone
ii. A fairly large gland consisting of two lobes wasting and fractures.
joined by a central mass, or isthmus.
iii. It makes two hormones: thyroid hormone,
and calcitonin (produced by the f. Thymus
parafollicular cells). i. It is located in the upper thorax, posterior
1. Thyroid hormone, which has two forms to the sternum.
(thyroxine [T4] and triiodothyronine ii. It is large in infants and children, but
[T3]), is released from the thyroid decreases in size throughout adulthood.
follicles when the blood level of TSH iii. It produces thymosin and other hormones
rises. Thyroid hormone is the body’s that are essential for the normal
major metabolic hormone. It increases development of a special group of white
the rate at which cells oxidize glucose blood cells and the immune response.
and is necessary for normal growth and
development. Lack of iodine leads to g. Adrenal Glands
goiter. Hyposecretion of thyroxine i. A pair of glands perched on the kidneys
results in cretinism in children and that are triangular in shape.
myxedema in adults. Hypersecretion ii. The adrenal gland is formed by the merger
results from Graves’ disease or other of two fetal glands with different origins
forms of hyperthyroidism. and functions.
iii. Adrenal medulla is 10% - 20% of the gland. ii. They also produce sex hormones that are
It is surrounded by a much thicker adrenal identical to those produced by adrenal
cortex. cortex cells.
iv. Adrenal cortex hormones include the iii. Their endocrine products are gonadal
following: hormones, most of which are steroid.
1. Mineralocorticoids, primarily iv. Female Gonads = Ovaries
aldosterone, regulate sodium ion (Na+ ) 1. slightly larger than other almond-sized
reabsorption and potassium ion (K+ ) organs located in the pelvic cavity
secretion by the kidneys. Their release v. Male Gonads = Testes
is stimulated primarily by low Na+ 1. suspended in a sac, the scrotum,
and/or high K+ levels in blood. outside of the pelvic cavity.
2. Glucocorticoids enable the body to
resist long-term stress by increasing the
blood glucose level and depressing the
inflammatory response.
3. Sex hormones (mainly androgens) are
produced in small amounts throughout
life.
v. The adrenal medulla produces
catecholamines (epinephrine and
norepinephrine) in response to
sympathetic nervous system stimulation.
Its catecholamines enhance and prolong
the effects of the “fight-or-flight”
(sympathetic nervous system) response to
short-term stress. Hypersecretion leads to
symptoms typical of sympathetic nervous
system overactivity.

h. Pancreatic Islets (Pancreas)


i. The pancreas, located close to the
stomach in the abdominal cavity, is a
mixed gland.
ii. The pancreatic islets (islets of Langerhans)
are little masses of endocrine
(hormone-producing) tissue scattered
among the exocrine (enzyme-producing)
tissue of the pancreas.

i. Gonads
i. The female and male gonads produce sex
cells (an exocrine function).
VII. OTHER HORMONE-PRODUCING TISSUES
AND ORGANS
a. Several organs that are generally
nonendocrine in overall function, such as the
stomach, small intestine, kidneys, and heart,
have cells that secrete hormones.
b. The placenta is a temporary organ formed in
the uterus of pregnant women. Its primary
endocrine role is to produce estrogen and
progesterone, which maintain pregnancy and
ready the breasts for lactation.

VIII. DEVELOPMENTAL ASPECTS OF THE


ENDOCRINE SYSTEM
a. Decreasing function of female ovaries at
menopause leads to such symptoms as
osteoporosis, increased chance of
arteriosclerosis, and possible mood changes.
b. Efficiency of all endocrine glands gradually
decreases with aging, which leads to a
generalized increase in incidence of diabetes
mellitus, immune system depression, lower
metabolic rate, and, in some areas, cancer
rates.

IX. ENDOCRINE PHYSIOLOGICAL PROCESSES


a. Human physiological processes that are made
possible due to hormones are:
i. Homeostasis
ii. Metabolism
iii. Development
iv. Reproduction

b. Hormonal Regulation of the Excretory


System
i. Osmoreceptors – monitors the water
concentration in the hypothalamus, which
detects the concentration of electrolytes
in the extracellular fluid.
ii. The concentration of electrolytes in the
blood rises when there is water loss
caused by excessive perspiration,
inadequate water intake, or low blood which stimulates the production and release
volume due to blood loss. of follicle-stimulating hormone (FSH) and
iii. Antidiuretic Hormone (ADH) luteinizing hormone (LH) from the anterior
(vasopressin) pituitary gland.
1. Polypeptide hormone produced by
hypothalamus. d. Hormonal Regulation of the Male
2. Regulate the amount of water excreted Reproductive System
by the kidneys (water reabsorption). i. FSH stimulates the maturation of sperm
iv. Aldosterone (mineralocorticoid) cells. Its production is inhibited by the
1. Produced by adrenal cortex. hormone inhibin, released by the testes.
2. Maintains proper water balance by ii. LH stimulates the production of the sex
enhancing Na+ reabsorption and K+ hormones (androgens) called the interstitial
secretion from the extracellular fluid of cell-stimulating hormone.
the cells in kidney tubules. iii. Testosterone promotes the production of
v. Aldosterone production can be stimulated sperm and masculine characteristics
by low blood pressure, which triggers a iv. Steroids: artificial hormones enhancing
muscle performance and build muscle mass
1. Anabolic steroids: most widely known
performance-enhancing drugs
2. Erythropoietin: triggers production of
red blood cells and human growth
hormone

e. Hormonal Regulation of the Female


Reproductive System
sequence of chemical release, as i. FSH stimulates the development of egg
illustrated in the figure. When blood cells (ova), which develop in structures
pressure drops, the called follicles, producing inhibin.
renin-angiotensin-aldosterone system ii. LH also plays a role in the development of
(RAAS) is activated to increase blood ova, induction of ovulation, and
pressure. stimulation of estradiol and progesterone
production by the ovaries.
c. Hormonal Regulation of the Reproductive 1. Estradiol: produces secondary sex
System characteristics
i. Regulation of the reproductive system is a 2. Estradiol & progesterone: regulate the
process that requires the action of hormones menstrual cycle
from the iii. Anterior pituitary
1. Pituitary gland, 1. Prolactin: production of milk by the
2. Adrenal cortex, mammary glands following childbirth
3. and the gonads iv. Posterior pituitary
ii. During puberty in both males and females, 1. Oxytocin: stimulates uterine
the hypothalamus produces contractions during childbirth.
gonadotropin-releasing hormone (GnRH),
f. Hormonal Regulation of Metabolism viii. Hormonal Regulation of Metabolism:
i. Blood glucose levels vary widely over the Blood Glucose Levels by Thyroid
course of a day as periods of food Hormones
consumption alternate with periods of 1. The basal metabolic rate, which is the
fasting. number of calories required by the
ii. Insulin and glucagon are the two body at rest, is determined by two
hormones primarily responsible for hormones produced by the thyroid
maintaining homeostasis of blood glucose gland:
levels. a. Thyroxine (tetraiodothyronine or T4)
iii. Additional regulation is mediated by the b. Triiodothyronine (T3)
thyroid hormones. ix. They are transported across the plasma
membrane of target cells and bind to
iv. Hormonal Regulation of Metabolism: receptors on the mitochondria resulting in
Blood Glucose Levels by Insulin & increased ATP production. In the nucleus,
Glucagon T3 and T4 activate genes involved in
energy production and glucose oxidation.
v. Insulin This results in increased rates of
1. Produced by the beta cells of the metabolism and body heat production,
pancreas which is known as the hormone’s
2. Lowers blood glucose levels calorigenic effect.
3. Stimulates the liver to convert glucose x. Thyroid-stimulating hormone (TSH)
to glycogen 1. Produced by the anterior pituitary
4. Increases glucose transport into certain 2. Stimulates the T3 and T4 release
cells (e.g., muscle cells and the liver) xi. TSH binding at the receptors of the follicle
vi. Glucagon of the thyroid triggers the production of T3
1. Released from the alpha cells of the and T4 from a glycoprotein called
pancreas when blood glucose levels thyroglobulin.
decline
2. Raises blood glucose levels g. Hormonal Control of Blood Calcium Levels
vii. Gluconeogenesis i. Regulation of blood calcium
1. process of glucose synthesis concentrations is important for generation
2. stimulates adipose cells to release fatty of muscle contractions and nerve
acids into the blood impulses, which are electrically stimulated.
ii. If calcium levels get too high, membrane
permeability to sodium decreases.
iii. If calcium levels get too low, membrane
permeability to sodium increases.

iv. Parathyroid hormone (PTH)


1. Release in response to low blood Ca2+ 3. Growth hormone-releasing hormone
levels, increasing them by targeting the (GHRH): stimulation
skeleton, the kidneys, and the intestine. 4. Hormone-inhibiting hormone (GHIH)
2. Skeleton: PTH stimulates osteoblasts (somatostatin): inhibition
and inhibits osteoclasts
3. Kidneys: PTH stimulates reabsorption of ii. Glucose-sparing effect (direct)
the Ca2+ 1. GH stimulates triglyceride breakdown
4. Intestines: increases dietary Ca2+ (lipolysis) and release into the blood by
absorption adipocytes, resulting in a switch by
5. Triggers the formation of calcitriol an most tissues from utilizing glucose as an
active form of vitamin D, which acts on energy source to utilizing fatty acids
the intestines to increase absorption of 2.
dietary calcium and decreases blood iii. Diabetogenic effect (direct)
calcium levels 1. GH stimulates glycogen breakdown in
v. Calcitonin the liver, which is then released into the
1. decreases blood calcium levels by blood as glucose, thus blood glucose
inhibiting osteoclasts, stimulating levels increase as most tissues are
osteoblasts, and stimulating calcium utilizing fatty acids instead of glucose
excretion by the kidneys. for their energy needs.
iv. The indirect mechanism of GH action is
mediated by insulin-like growth factors
(IGFs) or somatomedins, which are a
family of growth-promoting proteins
produced by the liver, which stimulates
tissue growth.

h. Hormonal Regulation of Growth


i. Growth hormone (GH)
1. Produced by the anterior pituitary
2. Accelerates the rate of protein
synthesis, particularly in skeletal muscle
and bones i. Hormonal Regulation of Stress
i. Alarm Phase
1. The sympathetic nervous system 5. prioritize body function by increasing
stimulates an increase in energy levels blood supply to essential organs.
through increased blood glucose levels.
2. This prepares the body for physical iv. From the anterior pituitary gland, the
activity that may be required to hypothalamus triggers the release of
respond to stress: to either fight for ACTH, which stimulates the release of
survival or to flee from danger steroid hormones called corticosteroids.
3. Glycogen reserves, which provide v. Corticosteroids:
energy in the short-term response to 1. turn on transcription of certain genes in
stress, are exhausted after several the nuclei of target cells
hours and cannot meet long-term 2. change enzyme concentrations in the
energy needs. cytoplasm and affect cellular
4. The glucocorticoids mobilize lipid and metabolism
protein reserves, stimulate 3. Glucocorticoids (e.g., cortisol):
gluconeogenesis, conserve glucose for primarily affect glucose metabolism by
use by neural tissue, and stimulate the stimulating glucose synthesis
conservation of salts and water. 4. Mineralocorticoids (e.g., aldosterone):
regulate ion and water balance of the
ii. The sympathetic nervous system regulates body
the stress response via the hypothalamus.
Stressful stimuli cause the hypothalamus
to signal the adrenal medulla (which
mediates short-term stress responses) via
nerve impulses, and the adrenal cortex
(which mediates long-term stress
responses) via the hormone
adrenocorticotropic hormone (ACTH),
which is produced by the anterior
pituitary.

iii. Epinephrine (adrenaline) and


norepinephrine (noradrenaline)
1. Catecholamines
2. released by the adrenal medulla X. Common Problems/Ailments of the Endocrine
3. increase blood glucose levels by System
stimulating the liver and skeletal a. DIABETES MELLITUS
muscles to break down glycogen and by i. A chronic condition characterized by
stimulating glucose release by liver elevated blood sugar levels.
cells. ii. Occurs when pancreas does not produce
4. increase oxygen availability to cells by enough insulin or when the body cannot
increasing the heart rate and dilating effectively use the insulin it produces.
the bronchioles iii. TYPE 1 DIABETES
1. Cause: by autoimmune reaction when blood test. Adjustment to the medication
the body’s immune system mistakenly dosage may be made based on these
attacks and destroys insulin-producing periodic assessments.
Beta cell in the pancreas.
2. Onset: typically occurs in childhood or c. HYPERTHYROIDISM
adolescence, but it can develop at any i. A condition characterized by an overactive
age. thyroid gland, leading to excessive
3. Treatment: requires life-long insulin production of thyroid
replacement therapy. hormones—primarily thyroxine (T4) and
triiodothyronine (T3).
ii. Excessive production of thyroid hormones,
iv. TYPE 2 DIABETES resulting in symptoms such as weight loss,
1. Cause: results from insulin resistance, rapid heart rate, and heat intolerance.
where the body’s cells don’t respond iii. Diagnosis: typically involves blood tests to
properly to insulin. Pancreas may not measure levels of thyroid hormones (T3
produce enough insulin to overcome and T4) and thyroid-stimulating hormone
this resistance. (TSH). In hyperthyroidism, T3 and T4 levels
2. Onset: often develops in adulthood, but are usually elevated, and TSH levels are
it can occur at any age, including in decreased.
children. iv. Treatment:
3. Treatment: lifestyle modifications (e.g., 1. Antithyroid Medications
diet and exercise). Medications or 2. Radioactive Iodine Therapy
insulin therapy may be necessary as the 3. Beta-Blockers
condition progresses. 4. Thyroidectomy
v. Monitoring and Management: regular
b. HYPOTHYROIDISM follow-up and monitoring of thyroid
i. A medical condition characterized by an function are essential to assess the
underactive thyroid gland, meaning that effectiveness of treatment and make any
the thyroid gland does not produce necessary adjustments.
enough thyroid hormones to meet the
body's needs. d. POLYCYSTIC OVARY SYNDROME (PCOS)
ii. The thyroid gland produces insufficient i. A hormonal disorder that affects people
thyroid hormones, leading to symptoms with ovaries, causing irregular periods,
like fatigue, weight gain, and cold infertility, and the development of small
intolerance. cysts on the ovaries.
iii. Diagnosis: A blood test measuring levels of ii. Diagnosis: A hormonal disorder that
thyroid-stimulating hormone, and T3 is affects people with ovaries, causing
typically used to diagnose hypothyroidism. irregular periods, infertility, and the
iv. Treatment: usually treated with thyroid development of small cysts on the ovaries.
hormone replacement therapy. iii. Diagnostic Criteria:
v. Monitoring & Management: regular 1. Irregular Menstrual Cycles
monitoring of thyroid function through 2. Signs of Hyperandrogenism
3. Appearance of Polycystic Ovaries on
Ultrasound
iv. Management and Treatment:
v. Lifestyle Modifications
vi. Medications
vii. Fertility Treatment

e. ADDISON’S DISEASE
i. A rare but serious disorder that occurs
when the adrenal glands do not produce
enough of the hormone’s cortisol and, in
some cases, aldosterone.
ii. Insufficient production of adrenal
hormones, causing fatigue, weight loss,
and low blood pressure.

iii. KEY FEAUTURES OF ADDISON’S DISEASE


1. Insufficient Cortisol Production
2. Insufficient Aldosterone Production

iv. Diagnosis: involves a combination of


clinical evaluation and laboratory tests.
Blood tests are conducted to measure
cortisol and aldosterone levels, and an
adrenocorticotropic hormone (ACTH)
stimulation test is often performed to
assess the adrenal glands' ability to
respond to stimulation.
v. Treatment: the primary treatment for
Addison's disease involves hormone
replacement therapy to replace the
deficient hormones.

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