Transcript Chapter 18: The Endocrine System

Chapter 18:
The Endocrine System
Primary sources for figures and content:
Marieb, E. N. Human Anatomy & Physiology. 6th ed. San Francisco: Pearson Benjamin Cummings, 2004.
Martini, F. H. Fundamentals of Anatomy & Physiology. 6 th ed. San Francisco: Pearson Benjamin Cummings,
2004.
Endocrine System
• Regulates long-term processes:
– growth
– development
– reproduction
Intercellular Communication
1. Direct Communication
– Occurs between two cells of the same type through
gap junctions via ions or small solutes
2. Paracrine Communication
– Uses chemical messengers to transfer signals
between cells in a single tissue
– Messenger = cytokines or local hormones
Intercellular Communication
3. Endocrine Communication
– Uses hormones to coordinate cellular activities in
distant portions of the body
– Hormones = chemical messengers released from one
tissue and transported in blood to reach target cells in
other tissues
– Gradual, coordinated but not immediate
4. Synaptic Communication
– Involves neurons releasing neurotransmitter at a
synapse close to target
– Immediate but short lived
Mechanisms of
Intercellular Communication
Table 18–1
The Endocrine System
• Consists of glands and glandular tissue involved
in paracrine and endocrine communication
• Endocrine cells produce secretions  released
into extracellular fluid  enters blood  bodywide distribution to find target
– Target cell = specific cells that possess receptors
needed to bind and “read” hormonal messages
Endocrine
System
Endocrine
Cells located
In:
Figure 18–1
Hormones
• Can be divided into 3 groups:
– amino acid derivatives
– peptide hormones
– lipid derivatives
Hormones
• Structure
1. Amino Acid Derivatives
• Structurally similar to or based on amino
acids
• E.g. catecholamines (epinephrine,
norepinephrine, dopamine), thyroid
hormones, melatonin
Hormones
• Structure
2. Peptide Hormones
• Chains of amino acids
A. Peptides
– <200 amino acids
– E.g. ADH, oxytocin, GH
B. Glycoproteins
– >200 amino acids with carbohydrate side
chain
– E.g. TSH
Hormones
• Structure
3. Lipid Derivatives
A. Steroid Hormones
– Structurally similar to/based on cholesterol
– E.g. Androgens, Estrogens, Calcitriol
B. Eicosanoids
– Derived from arachidonic acid
– Not circulating: autocrine or paracrine only
– E.g. Leukotrienes: from leukocytes 
coordinate inflammation
– E.g. Prostaglandins: from mast cells 
coordinate local activities (smooth muscle
contractions, clotting, etc.)
Classes of
Hormones
Figure 18–2
Mechanism of Action
• Hormones circulate in blood  contact all cells
• Only cause effects in cells with receptors for
hormone  called target cells
• Receptors present on a cell determines the cell’s
hormonal sensitivity
Hormone stimulus effects in
target cells
1. Alter plasma membrane permeability or
transmembrane potential by opening/closing ion
channels
2. Stimulate synthesis of  structural proteins,
receptors, regulatory enzymes within cell
3. Activate or deactivate enzymes
4. Induce secretory activity
5. Stimulate mitosis
Hormone Receptors
• Located on plasma membrane or inside
target
1. Cell membrane hormone receptors
2. Intracellular hormone receptors
Hormone Receptors
1. Cell membrane hormone receptors
– Catecholamines, peptide hormones, glycoprotein
hormones, eicosanoids
– Bind receptors on cell surface
– Indirectly trigger events inside cell via second
messengers (cAMP, Ca++)
– 2nd messenger acts as activator, inhibitor, or cofactor
for intracellular enzymes
• Enzymes catalyze reactions for cell changes
– Receptor linked to 2nd messenger by G protein
(regulatory enzyme complex)
Hormone Receptors
1. Cell membrane hormone receptors
– 2nd messenger mechanism results in amplification of
hormone signals
• One hormone molecule binds one receptor but can result
in millions of final products
G Proteins and Hormone Activity
cAMP Mechanism
1. Hormone binds
receptor
2. G-protein activated
3. Adenylate cyclase
activated
4. ATP  cAMP
5. Kinases activated
6. Proteins (enzymes)
phosphorylated
7. Enzymes
activated/deactivated
Figure 18–3
G Proteins and Hormone Activity
PIP-Calcium Mechanism
1. Hormone binds receptor
2. G-protein activated
3. Phospholipase C (PLC)
activated
4. Phospholipids (PIP2)
cleaved into
diacyglycerol (DAG) and
inositol triphosphate
(IP3)
5. DAG opens Ca++ channels
on membrane
6. IP3 releases Ca++ from ER
7. Calcium binds calmodulin
8. Enzymes Activated
Figure 18–3
Hormone Receptors
2. Intracellular hormone receptors
– Steroid hormones, thyroid hormones
– Result in direct gene activation by hormone
– Hormone diffuses across membrane, binds
receptors in cytoplasm or nucleus
– Hormone + receptor bind DNA  transcription
 translation = protein production  metabolic
enzymes, structural proteins, secretions
Steroid Hormones
Figure 18–4a
Thyroid Hormones
Figure 18–4b
Target cell activation depends on
1. Blood level of hormone
2. Relative number of receptors
3. Affinity of bond between hormone and
receptor
• If hormone levels are excessively high for too
long  cells can reduce receptor number or
affinity and become  non-responsive to a
hormone
Distribution and Duration of Hormones
• Circulating hormones either free or bound to
carrier/transport proteins
• Free hormones last seconds to minutes
– Rapidly broken down by liver, kidney, or plasma
enzymes in blood
• Bound hormones last hours to days in blood
• Effect at target cell can take seconds to days
depending on mechanism and final effect, but
hormone once bound to receptor is broken down
quickly
Interaction of Hormones at Target Cells
• Target cells have receptors for multiple hormones
• Effects of one hormone can be different depending
on presence or absence of other hormones
• Hormone Interactions
1. Antagonistic = hormones oppose each other
2. Synergistic = hormones have additive effects
3. Permissive = one hormone is needed for the
other to cause its effect
Control of Endocrine Activity
• Synthesis and release of most
hormones regulated by negative
feedback
Control of Endocrine Activity
• 3 Major Stimuli for Hormone Release
1. Hormonal stimuli
• Ion and nutrient levels in blood trigger release
• E.g. PTH released when blood Ca++ is low
2. Neural stimuli (autonomic nervous system)
• Nerve fibers directly stimulate release
• E.g. sympathetic  adrenal medulla = epinephrine
release
Control of Endocrine Activity
• 3 Major Stimuli for Hormone Release
3. Hormonal stimuli
• Hormones stimulate the release of other
hormones
• E.g. Releasing hormones of hypothalamus cause
release of hormones from anterior pituitary
– Hormone release turned on by stimuli and off by
negative feedback but can be modified by nervous
system
KEY CONCEPT
• Hormones coordinate cell, tissue, and
organ activities
• Circulate in extracellular fluid and bind
to specific receptors
• Hormones modify cellular activities by:
– altering membrane permeability
– activating or inactivating key enzymes
– changing genetic activity
How could you distinguish between a
neural response and an endocrine
response on the basis of response time
and duration?
A. Neural responses are quicker and longer
lasting.
B. Neural responses are slower and longer
lasting.
C. Neural responses are quicker and shorter in
duration.
D. Neural responses are slower and shorter in
duration.
How would the presence of a molecule that
blocks adenylate cyclase affect the activity of
a hormone that produces its cellular effects by
way of the second messenger cAMP?
A.
B.
C.
D.
It would block the action of the hormone.
It would enhance the action of the hormone.
It would increase sensitivity to the hormone.
It would decrease speed of hormonal
changes.
What primary factor determines each
cell’s hormonal sensitivities?
A. pH of intracellular fluid
B. life cycle phase of cell
C. presence/absence of necessary
receptor complex
D. tissue where cell is found
Endocrine Organs
1. Hypothalamus
Figure 18–5
1. Hypothalamus
•
•
•
•
Located at base of 3rd ventricle
Master regulatory organ
Integrates nervous and endocrine systems
Three mechanisms of control
1. Secrete regulatory hormones to control secretion from
anterior pituitary
- Hormones from anterior pituitary control other
endocrine organs
2. Act as endocrine organ  Produce ADH and oxytocin
3. Has autonomic centers of neural control or adrenal
medulla  Neuroendocrine reflex
2. Pituitary Gland
Figure 18–6
2. Pituitary Gland (Hypophysis)
• Hangs inferior to hypothalamus via infundibulum
• In sella turcica of sphenoid
• Anterior lobe secretes 7 hormones
– Function via cAMP 2nd messenger
• Posterior lobe secretes 2 hormones
– Function via cAMP 2nd messenger
2. Pituitary Gland
Figure 18–7
2. Pituitary Gland
A. Anterior lobe (Adenohypophysis)
– Glandular tissue
– Anterior pituitary hormones are all tropic
hormones
• Turn on secretion or support function of other
organs
– Secretion of the hormones controlled by
releasing and inhibiting hormones from the
hypothalamus
2. Pituitary Gland
A. Anterior lobe (Adenohypophysis)
– Hormones of the Anterior Lobe
2. Pituitary Gland
A. Anterior lobe (Adenohypophysis)
– Disease of Growth Hormone
• Excess
– Usually due to pituitary tumor
– Before epiphyseal closure = gigantism
– After = acromegaly, excessive growth of
hands, feet, face, internal organs
• Deficiency
– Pituitary dwarfism: failure to thrive
2. Pituitary Gland
B. Posterior lobe (Neurohypophysis)
– Neural tissue
– Contains axons of hypothalamus
• Release hormones to posterior lobe for storage
– Hormones release by Posterior Lobe
The Hormones of the Pituitary Gland
Figure 18–9
Hypothalamas and Anterior Lobe
• Rate of
secretion is
controlled by
negative
feedback
• Hormones
“turn on”
endocrine
glands or
support other
organs
Figure 18–8a
Prolactin (PRL)
Figure 18–8b
Hormones
• Releasing Hormones (RH)
– Stimulate synthesis and secretion of 1 or
more hormones at anterior lobe
• Inhibiting Hormones (IH)
– Prevent synthesis and secretion of
hormones from anterior lobe
KEY CONCEPT
• Hypothalamus produces regulatory factors that
adjust activities of anterior lobe of pituitary gland,
which produces 7 hormones
• Most hormones control other endocrine organs,
including thyroid gland, adrenal gland, and
gonads
KEY CONCEPT
• Anterior lobe produces growth hormone, which
stimulates cell growth and protein synthesis
• Posterior lobe of pituitary gland releases 2
hormones produced in hypothalamus:
– ADH restricts water loss and promotes thirst
– oxytocin stimulates smooth muscle
contractions in:
• mammary glands
• uterus
• prostate gland
If a person were dehydrated, how would
the level of ADH released by the
posterior lobe change?
A.
B.
C.
D.
More ADH is released.
Less ADH is released.
It would not change at all.
Initially ADH would decrease, then
increase until hydration is restored.
A blood sample shows elevated levels of
somatomedins. Which pituitary
hormone would you expect to be
elevated as well?
A.
B.
C.
D.
thyroid stimulating hormone
growth hormone
oxytocin
adrenocorticotropic hormone
What effect would elevated circulating
levels of cortisol, a steroid hormone from
the adrenal cortex, have on the pituitary
secretion of ACTH?
A.
B.
C.
D.
ACTH levels would slowly rise.
ACTH levels would increase rapidly.
ACTH levels would decrease.
ACTH levels would remain the
same.
3. Thyroid Gland
Figure 18–10a, b
3. Thyroid Gland
•
•
•
•
Inferior to larynx
Left and right lobes connected by isthmus
Largest pure endocrine organ
Tissue
1. Follicles  Spheres or simple cuboidal epithelium
2. Parafollicular cells/C cells between follicles
• Follicles filled with colloid  thyroglobulin
• Thyroglobulin protein constantly synthesized by follicle
cells and exocytosed into follicle for storage
• Upon stimulation by TSH, thyroglobulin is processed into
thyroid hormones (T3/T4)
Formation and Release of Thyroid Hormones
Thyroid Follicles
Figure 18–11a, b
3. Thyroid Gland
• Receptors for thyroid hormones located in all
cells except
– Adult brain, spleen, testes, uterus, thyroid
• 3 receptors in target cells
1. Cytoplasm: hold hormone in reserve
2. Mitochondria: increase cellular respiration
3. Nucleus: activate genes for enzymes involved
in energy transformation and utilization
3. Thyroid Gland
• Overall effect of thyroid hormones
– Increase metabolic rate and body heat production
– Regulate tissue growth and development
1. Hypothyroidism  lack of T3/T4
A. Myxedema (adults)
• Low body temp, muscle weakness, slow reflexes,
cognitive dysfunction and goiters  swollen thyroid
– Produce thyroglobulin but fail to endocytose
B. Cretinism (infants) = Genetic defect
• Causes lack of skeletal and nervous system
development
3. Thyroid Gland
2. Hyperthyroidism  excessive T3/T4
– High metabolic rate, high heart rate, restlessness,
fatigue
3. Graves Disease
– Autoimmune disorder
– Produce antibodies that mimic TSH causing
overproduction of thyroid hormones
3. Thyroid Gland
• Parafollicular cells/C cells
– in basement membrane of follicles
– Produce Calcitonin
• Calcitonin stimulates decrease in blood calcium
levels
– Inhibits osteoclasts
– Promotes Ca++ loss at kidneys
– Parafollicular cells respond directly to blood calcium
levels, not controlled by hypothalamus
– Ca++ 20% above normal = calcitonin release
3. Thyroid Gland
Figure 18–10c
Rate of Thyroid
Hormone Release
• Major factor:
– TSH concentration in
circulating blood
Figure 18–11b
Thyroid Gland
Table 18–3
Iodide Ions
• Are actively transported into thyroid
follicle cells:
– stimulated by TSH
• Reserves in thyroid follicles
• Excess removed from blood at kidneys
• Deficiency limits rate of thyroid
hormone production
5. Parathyroid Glands
• Four glands embedded in posterior surface of
thyroid gland
Figure 18–12
5. Parathyroid Gland
• Two cell types
– Oxyphiles: few, functions unknown
– Chief Cells: majority
• Produce Parathyroid hormone (PTH)/Parathormone
– Most important regulator of blood calcium
– Secreted when blood calcium is low
– Acts to raise blood calcium levels by acting on various
tissues
1. Bone  stimulates osteoclasts and inhibits
osteoblasts
2. Kidney  enhances reabsorption of Ca++
3. Intestines  promotes conversion of Vit. D to
calcitriol in kidney to enhance Ca++ and PO43absorption in small intestine
4 Effects of PTH
3. It enhances reabsorption of Ca2+ at
kidneys, reducing urinary loss
4. It stimulates formation and secretion
of calcitriol at kidneys
Parathyroid Glands
• Primary regulators
of blood calcium I
levels in adults
Figure 18–13
Parathyroid Glands
Table 18–4
KEY CONCEPT
• Thyroid gland produces:
– hormones that adjust tissue metabolic
rates
– a hormone that usually plays minor role in
calcium ion homeostasis by opposing
action of parathyroid hormone
What symptoms would you expect to see
in an individual whose diet lacks iodine?
A.
B.
C.
D.
increased rate of metabolism
increased body temperature
rapid response to physiological stress
goiter
When a person’s thyroid gland is removed,
signs of decreased thyroid hormone
concentration do not appear until about one
week later. Why?
A. Thyroid hormone is produced by
other endocrine glands.
B. Thyroid hormone remains in
circulation for 14 days.
C. Thyroid-binding globulins provide
thryoxine reservoirs.
D. Thyroid hormone is used slowly.
The removal of the parathyroid glands
would result in a decrease in the blood
concentration of which important
mineral?
A.
B.
C.
D.
calcium ions
phosphate ions
sodium ions
potassium ions
What effect would elevated cortisol
levels have on the level of glucose in
the blood?
A. increased glucose
B. decreased glucose
C. modulated glucose around
homeostatic optimum
D. dramatic increase of glucose, then a
crash
6. Adrenal Glands
Figure 18–14
6. Adrenal Gland
•
•
•
•
2 glands, in renal fascia, superior to kidney
Glandular adrenal cortex
Medulla mostly nervous tissue
In general  adrenal hormones are used to cope
with stressors
6. Adrenal Glands
A. Adrenal Cortex
– Produces 24+ corticosteriods
• In target alter gene transcription to affect
metabolism
– Glandular
– 3 layers
1. zona glomerulosa
2. zona fasciculate
3. zona reticularis
6. Adrenal Glands
A. Adrenal Cortex
1. Zona glomerulosa  Mineralcorticoids
- Control water and electrolyte balance
- 95% Aldosterone
- Stimulates Na+ retention and K+ loss
- Released in response to
- Low Na+ or high K+
- Angiotension mechanism
- Low blood pressure or volume
- Excessive ACTH
6. Adrenal Glands
A. Adrenal Cortex
2.
Zona fasciculate  glucocorticoids
Metabolic hormones
Control glucose metabolism
Most common = cortisol, hydrocortisone
Secretion controlled by ACTH
Effects 
gluconeogenesis in liver
release of fatty acid from adipose
triggers protein hydrolysis to release free amino acids
from skeletal muscle
triggers body cells to utilize fatty acids and amino acids
instead of glucose
Excess  anti-inflammatory, inhibit immune response and
healing
6. Adrenal Glands
A. Adrenal Cortex
3. Zona reticularis  gonadocorticoids
- Mostly androgens, may aid onset of puberty
- Excess = androgenital syndrome
Adrenal Cortex
Table 18–5
6. Adrenal Glands
A. Adrenal Cortex – Disease’s that affect the cortex:
1. Cushing’s Syndrome
- Excessive corticosteroids 
- increase ACTH from pituitary tumor
- Results in 
- hyperglycemia, decr. Muscle and bone mass,
hypertension, edema, poor healing, chronic
infections
2. Addison’s Disease
- Deficient in corticosteroids
- Results in 
- Weight loss, hyopglycemia, decr. Na+, incr. K+ in
plasma, dehydration, hypotension
6. Adrenal Glands
B. Adrenal Medulla
- Neural, produces catecholamines to enhance effects of other
adrenal hormones
- Modified ganglionic sympathetic neurons called chromaffin
cells release  epinephrine (80%) and norepinephrine (20%)
in response to sympathetic stimulation
- Epinephrine effects:
- Stimulate heart
- Stimulate metabolic activities 
- Skeletal muscle – mobilize glucogen reserves,
accelerate ATP production
- Adipose – promote release of fatty acids
- Liver – promotes release of glucose
KEY CONCEPT
• Adrenal glands produce hormones that
adjust metabolic activities at specific
sites
• Affects either pattern of nutrient
utilization, mineral ion balance, or
rate of energy consumption by active
tissues
6. Pancreas
Figure 18–15
6. Pancreas
• Inferior and posterior to stomach
• Mostly exocrine cells  pancreatic acini
– Secrete digestive enzymes
• 1% endocrine  pancreatic islets
6. Pancreas
• Pancreatic Islets cell types
1. Alpha cells  glucagon  increase blood glucose
2. Beta cells  insulin  decrease blood glucose
3. Delta cells  somatostatin 
• Suppresses glucagon and insulin release
• Slows enzyme release into intestines
4. F cells  pancreatic polypeptide 
• Regulates production of pancreatic enzymes
6. Pancreas
• Insulin
– Secreted in response to high blood glucose or ANS
• Parasympathetic = incr. insulin
• Sympathetic = decr. Insulin
– Effect only on insulin dependent cells (have
receptors)
– Brain, kidney, GI mucosa, and RBCs
• ALL INSULIN DEPENDENT
5 Effects of Insulin
1. Accelerates glucose uptake
2. Accelerates glucose utilization and
enhanced ATP production
3. Stimulates glycogen formation
4. Stimulates amino acid absorption and
protein synthesis
5. Stimulates triglyceride formation in
adipose tissue
6. Pancreas
• Diabetes mellitus  too much glucose in blood
(hyperglycemia)
– Type I  failure to produce insulin
– Type II  insulin resistance, sometimes insulin
deficiency
– Cells can not utilize glucose  ketone bodies
produced  too many ketone bodies lead to
ketoacidosis
• Glucagon
– Secreted in response to low blood glucose or
sympathetic stimulation
3 Effects of Glucagons
1. Stimulates breakdown of glycogen in
skeletal muscle and liver cells
2. Stimulates breakdown of triglycerides
in adipose tissue
3. Stimulates production of glucose in
liver
Insulin and Glucagon Effects
Figure 18–16
Pancreatic Islets
Table 18–6
KEY CONCEPT
• Pancreatic islets release insulin and glucagons
• Insulin is released when blood glucose levels rise
• Stimulates glucose transport into, and utilization
by, peripheral tissues
• Glucagon released when blood glucose levels
decline
• Stimulates glycogen breakdown, glucose
synthesis, and fatty acid release
7. Pineal Gland
• Posterior of third ventricle
• Pinealocytes
– Synthesize melatonin from serotonin
• Secretion on diurnal cycle
– High at night, low during dayligh
• Melatonin functions
1. Play role in timing of sexual maturation
2. Antioxidant  free radical protection
3. Sets circadian rhythms
Why does a person with Type 1 or Type 2
diabetes urinate frequently and have a
pronounced thirst?
A. Glucose in the blood inhibits ADH release.
B. Sugar in the urine prevents kidneys from
reabsorbing water.
C. High blood sugar dehydrates the tissues of
the mouth.
D. Blood sugar elevates blood volume,
increasing urine output.
What effect would increased levels of
glucagon have on the amount of
glycogen stored in the liver?
A.
B.
C.
D.
increased glycogen
decreased glycogen
no effect
rapid increase of glycogen, with a
slow return to homeostasis
Increased amounts of light would
inhibit the production of which
hormone?
A.
B.
C.
D.
prolactin
melanocyte stimulating hormone
aldosterone
melatonin
Hormones Produced
by Specific Organs
Table 18–7
8. Gastrointestinal Tract
• Enteroendorine cells in GI mucosa secrete many
hormones  coordinate digestive activity
• Mostly paracrine communication
– Cholecystokinin
– Enterocrinin
– Gastric inhibitory peptide
– Gastrin
– Secretin
– Vasoactive intestinal peptide
9. Kidneys
• Various endocrine cells
• Three products
1. Calcitrol  Steroid hormone
• Stimulate Ca++, PO43- absorption in GI
• Stimulate osteoclast activity
• Stimulate Ca++ retention in kidney
• Suppress PTH production
2. Erythropoeitin  Peptide hormone
• Released in response to low O2 in kidney
3. Renin  Enzyme
9. Kidneys
• Three products
3. Renin  Enzyme
• Released in response to sympathetic stimulation or decline in
renal blood flow
• Converts angiotensin in blood into Angiotensin II (hormone)
• Angiotensin II effects
– Stimulate secretion of aldosterone  adrenal
– Stimulate secretion of ADH  pituitary
– Stimulate thirst
– Elevate BP
» Both aldosterone and ADH  restrict Na+ and H2O
loss at kidney
Calcitriol
• Stimulates
calcium and
phosphate ion
absorption along
digestive tract
Figure 18–17a
The Renin–Angiotensin System
Figure 18–17b
10. Heart
• Some cells of atrial walls secrete Atrial Natriuretic
Peptide in response to stretch
• ANP promotes Na+ and water loss at kidney
– Inhibits release of renin, ADH, and aldosterone
 reduce BP and volume
11. Thymus
• Located deep to sternum
• Cell produces thymosin hormones:
– Promote development and maturation of T
lymphocytes and the immune response
12. Gonads
A. Testes  male
– Interstitial cells produce androgens in response
to LH
– Testosterone, most common
• Produces male secondary sex characteristics
• Promotes sperm production
• Maintains secretory glands
12. Gonads
B. Ovaries  Female
– Follicle cells produce estrogens in response to FSH and
LH
– Estradiol, most important
• Produce female secondary sex characteristics
• Support maturation of oocytes
• Stimulate growth of uterine lining
– Surge in LH causes
• Ovulation
• Follicle reorganizes to form corpus luteum
– Produces estrogens and progestins, especially
progesterone
12. Gonads
B. Ovaries  Female
– Progesterone, most important
• Prepares uterus for embryo growth
• Accelerates movement of oocyte/embryo to uterus
• Enlargement of mammary glands
13. Adipose
1. Leptin secretion
– in response to absorption of glucose and lipids
– Triggers satiation in appetite center of
hypothalamus
– controls normal levels of GnRH, gonadotropin
synthesis
2. Resistin secretion
– Reduces insulin sensitivity
Hormones interact
to produce coordinated
physiological responses.
Hormone Interactions
1. Antagonistic (opposing) effects
2. Synergistic (additive) effects
3. Permissive effects:
–
1 hormone is necessary for another to
produce effect
4. Integrative effects:
–
hormones produce different and
complementary results
Hormones Important to Growth
1.
2.
3.
4.
5.
6.
GH
Thyroid hormones
Insulin
PTH
Calcitriol
Reproductive hormones
Growth Hormone (GH)
• In children:
– supports muscular and skeletal
development
• In adults:
– maintains normal blood glucose
concentrations
– mobilizes lipid reserves
Thyroid Hormones
• If absent during fetal development or
for first year:
– nervous system fails to develop normally
– mental retardation results
• If T4 concentrations decline before
puberty:
– normal skeletal development will not
continue
Insulin
• Allows passage of glucose and amino
acids across cell membranes
Parathyroid Hormone
(PTH) and Calcitriol
• Promote absorption of calcium salts for
deposition in bone
• Inadequate levels causes weak and
flexible bones
Reproductive Hormones
• Androgens in males, estrogens in
females
• Stimulate cell growth and
differentiation in target tissues
• Produce gender-related differences in:
– skeletal proportions
– secondary sex characteristics
Insulin lowers the level of glucose in the
blood, and then glucagon causes glucose
levels to rise. What is this type of
hormonal interaction called?
A.
B.
C.
D.
additive
antagonism
permissive
integrative
The lack of which hormones would
inhibit skeletal formation?
A. GH, thyroid hormone, PTH, gonadal
hormones
B. prolactin, FSH, LH, GH
C. thyroid hormone, melatonin, PTH,
calcitonin
D. GH, TSH, ACTH, FSH
Why do levels of GH-RH and CRH rise
during the resistance phase of the general
adaptation syndrome?
A. to bolster immune response
B. to decrease excess blood volume
C. to increase needed supplies of blood
glucose
D. to heighten sensory perceptions
General
adaptation syndrome.
General Adaptation
Syndrome (GAS)
• Also called stress
response
• How bodies respond to
stress-causing factors
Figure 18–18
General Adaptation
Syndrome (GAS)
• Is divided into 3 phases:
1. alarm phase
2. resistance phase
3. exhaustion phase
Alarm Phase
•
•
•
•
•
Is an immediate response to stress
Is directed by ANS
Energy reserves mobilized (glucose)
“Fight or flight” responses
Dominant hormone is epinephrine
7 Characteristics of Alarm Phase
1.
2.
3.
4.
Increased mental alertness
Increased energy consumption
Mobilization of energy reserves (glycogen and lipids)
Circulation changes:
– increased blood flow to skeletal muscles
– decreased blood flow to skin, kidneys, and digestive organs
5. Drastic reduction in digestion and urine production
6. Increased sweat gland secretion
7. Increases in blood pressure, heart rate, and respiratory rate
Resistance Phase
• Entered if stress lasts longer than few
hours
• Dominant hormones are glucocorticoids
• Energy demands remain high
• Glycogen reserves nearly exhausted
after several hours of stress
Effects of Resistance Phase
1. Mobilize remaining lipid and protein
reserves
2. Conserve glucose for neural tissues
3. Elevate and stabilize blood glucose
concentrations
4. Conserve salts, water, and loss of K+, H+
Exhaustion Phase
• Begins when homeostatic regulation
breaks down
• Failure of 1 or more organ systems will
prove fatal
• Mineral imbalance
Aging Related Changes
• Very little change in most hormone levels
• Adverse effects due to changes in target tissue
– Prevent reception or response to hormone
• Gonads decrease in size and hormone production
Review: Endocrine System
• Provides long-term regulation and
adjustments of homeostatic mechanisms:
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fluid and electrolyte balance
cell and tissue metabolism
growth and development
reproductive functions
assists nervous system response to stressful
stimuli through general adaptation syndrome
SUMMARY
• Paracrine communication
• Endocrine communication
• Classes of hormones:
– amino acid derivatives
– peptide hormones
– lipid derivatives, including steroid hormones and
eicosanoids
• Secretion and distribution of hormones
• Endocrine reflexes
• Hypothalamus regulation of the endocrine system
• The pituitary gland:
– the anterior lobe
– the posterior lobe
SUMMARY
• Releasing hormones
• Inhibiting hormones
• The thyroid gland:
– thyroid follicles
– thyroid hormones
• The parathyroid glands
• The adrenal glands:
– the adrenal cortex and adrenal medulla
• The pineal gland
• The pancreas:
– the pancreatic islets
– insulin and glucagons
SUMMARY
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Endocrine tissues in other systems
Hormonal interaction
Role of hormones in growth
Hormonal response to stress
Effects of hormones on behavior
Effects of aging on hormone production