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POWERPOINT® LECTURE SLIDE PRESENTATION
by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin
Additional material by J Padilla for Physiology 31 at ECC
UNIT 4
23
Endocrine Control
of Growth
and Metabolism
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
DEE UNGLAUB SILVERTHORN
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FOURTH EDITION
About this Chapter
 Adrenal glucocorticoids
 Thyroid hormones
 Growth hormone
 Tissue and bone growth
 Calcium balance
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Adrenal Glucocorticoids
Structure and function of the
adrenal gland
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Figure 23-1a
Cortisol
The HPA pathway for the
control of cortisol secretion
CRH- Corticotrophic
Releasing Hormone
ACTH- Adrenocorticotrophic
hormone
Cortisol- lipophilic hormone
that enters the nucleus and
althers gene expression,
transcription, and
translation
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Figure 23-3
Cortisol
Cortisol receptors are
found in every tissue in
the body and release
varies throughout the day.
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Cortisol
 Promotes gluconeogenesis- stimulates the liver to increase
blood glucose levels
 Causes breakdown of skeletal muscle proteins – releases
amino acids to act as substrates for gluconeogenesis
 Enhances lipolysis- releases glycerol for gluconeogenesis and
fatty acids for cellular respiration
 Suppresses the immune system- reduces inflammation and
other immune system functions. When used as a medication
(ibuprofen) it need to be taper off once not needed.
 Causes negative calcium balance - reduces absorption and
increases bone matrix breakdown
 Influences brain function – affect mood, memory, and
learning.
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Cortisol: Therapeutic Drug
 Suppresses the immune system – prevents cytokine
& antibody production, helps prevent organ rejection,
 Inhibits the inflammatory response – reduced the
mobility of leukocytes
 Used to treat:
 Bee stings, poison ivy, and pollen allergies
 Prevents rejection of transplanted organs
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Hypercortisolism
Adrenal tumor that autonomously secretes cortisol- primary
hypercortisolism
Pituitary tumor that autonomously secretes ACTH
(adrenocorticotropic hormone)- secondary hypercortisolism
Cushing’s disease- hyperglycemia, muscle breakdown, lipolysis, extra
fat in trunk and face,
Iatrogenic hypercortisolism- resulting from cortisol therapy (exogenous
cause)
Individual with
Cushing’s
Syndrome
cause by
adrenal or
pituitary tumor
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Figure 23-5
Hypocortisolism
 Less common than Cushing’s syndrome
 Addison’s disease- hereditary defects in enzymes
needed to make the steroid hormones
 Hyposecretion of all adrenal steroid hormones
 Autoimmune destruction of adrenal cortex
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CRH Family
 CRH (corticotropin-releasing hormone) – is involved
in the following:
 Inflammation and immune response
 Decreases food intake
 Signals that mark onset of labor
 Linked to anxiety, depression, and other mood
disorders
 Urocortin: brain neuropeptide related to CRH
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ACTH and Melanocortins
 ACTH- secretion stimulated by CRH
 Synthesized from POMC (pro-opiomelanocortin)
 POMC products include -endorphin- an opiate
that blocks pain
 Processed in tissue outside the pituitary- produces
different molecules
 Additional processing creates -MSH- it inhibits
food intake in brain and acts on melanocytes in skin
 Melanocortins
 Family name for the MSH (melanocyte-stimulating
hormone) hormones and ACTH
**there are five melanocortin receptors in the adrenal
gland and skin cells (melanocytes)
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Thyroid: Structure
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Figure 23-7a
Thyroid
Thyroid hormones are made from iodine and
tyrosine- they are thermogenic so they increase O2 for
oxydative phosphorylation. Thyroid hormones synthesis takes
place in the colloid of the thyroid follicle
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Figure 23-8
Pathway of Thyroid Hormone Control
Negative feedback
mediated by
thyroid hormones
reaches the
hypothalamus to
stop production at
the pituitary.
In thyroid
disorders negative
feedback is
removed
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Figure 23-12
Hyperthyroidism
 Affects: metabolism, the nervous system, & the heart
 Increases oxygen consumption and metabolic heat
production – patients have a high metabolism and
since they generate a lot of heat they don’t tolerate
hot environments well.
 Increase protein catabolism and may cause muscle
weakness – the body breaks down the protein in
muscle cells which also causes weight loss.
 Hyperexcitable reflexes and psychological
disturbances – may affect the nervous tissue
structure and receptors.
 Influence -adrenergic receptors in the heart increases heart rate and contraction force
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Thyroid
Exophthalmus, caused by hypertrophy of tissues in the
eye socket, is a sign of hyperthyroidism
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Figure 23-15
Hypothyroidism
 Slow metabolic rate and oxygen consumption –
less tolerant to cold because they don’t generate
much internal heat due to lower metabolic rate.
 Decreases protein synthesis – causing brittle nails,
thinning hair, dry thin skin, and myxedema. In
children it retards growth.
 Slowed reflexes, slow speech and thought
processes, and feelings of fatigue – nervous
response is slower or less efficient
 Cretinism in infants- decreased mental capacity
 Bradycardia – slower heart rate
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Thyroid
A man with goiter
due to excessive
TSH stimulation –
immunoglobulins
released in
hyperthyroidism
mimic TSH and
stimulate thyroid
enlargement
(Grave’s Disease)
may also be caused by
excess thyroidstimulation in
hypothyroidism
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Figure 23-13
Thyroid
Goiter can occur in both hyperthyroidism and hypothyroidism
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Figure 23-14a
Normal Growth
 Growth hormone and other hormones - GH,
thyroid hormones, insulin, and sex hormones at
puberty are important for normal growth and
development.
 An adequate diet – sufficient calories, protein,
vitamins and minerals provide the building blocks for
proper growth.
 Absence of stress – stressful environments cause
children to release cortisol which stunts growth
 Genetics – height potential is inherited
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Pathway of Growth Hormone Control
Growth hormone
promotes
anabolism of
proteins. It is
released by
anterior pituitary
and IGF provides
negative feedback
cycles. GH is
bound to a binding
protein to keep it
from being
excreted in urine
and to increase its
lifetime.
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Figure 23-16
Growth Hormone
In adults, pulses
of GH are
released during
the first two
hours of sleep.
The greatest
amount of GH
release occurs
during puberty.
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Growth Hormone
 Severe GH deficiency leads to dwarfism
 Oversecretion of GH in children leads to giantism
 Oversecretion of GH in adults leads to acromegaly
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Tissue and Bone Growth
 Growth is determined by increase in soft tissue
(weight) and bone length (height)
 Tissue growth requires hormones and paracrines
 GH and IGFs required for protein and cell division for
hypertrophy and hyperplasia
 Thyroid hormone plays permissive role- directly
affects nervous system development
 Insulin supports tissue growth- stimulates protein
synthesis and provides energy, has a permissive role
 Bone growth requires adequate dietary calcium
 Hydroxyapatite- most common form of calcium
**review parts of a long bone as covered in anatomy
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Bone Growth
Compact and trabecular bone
Bone length
increases at
the
epiphyseal
plate and
diameter with
matrix
deposits
around
surface
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Figure 23-18
Bone growth
Linear growth of long bones takes place at the epiphyseal platessex hormones eventually inactivate epilhyseal plates.
Epiphysis
is the end
of a long
bone.
Bone growth
Epiphyseal plate is the
site of bone growth.
Dividing
chondrocytes
add length
to bone.
Chondrocytes
produce
cartilage.
Old
chondrocytes
disintegrate.
Diaphysis
Compact
bone
Chondrocyte
Cartilage
Direction of growth
Diaphysis
is the
shaft of a
long bone.
Osteoblasts lay
down bone on
top of cartilage.
Newly calcified Osteoblast
bone
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Figure 23-19
Calcium
 Important signal molecule – increased Ca 2+
concentrations allows for cell responses like
exocytosis and muscle contraction. Active transport is
needed to decrease cytosolic Ca 2+ concentration.
 Part of intercellular cement that holds cells
together at tight junction – integrated component of
the cell junction protein structure
 Cofactor in the coagulation cascade – The body
will always have enough calcium to mediate
coagulation
 Affects the excitability of neurons – hypocalcemia
causes the NS to become hyperexcitable, thus
increasing muscle contraction. Hypercalcemia cause
NS to be hypoexcitable causing depressed
neuromuscular activity.
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Calcium Balance in the Body
Calcium in the
ECF is either
bound to proteins
or free to diffuse.
ECF
[Ca2+]
2.5 mM
Electrochemical
gradient
Active
transport
Cells
[free Ca2+]
0.001 mM
Calcium in ICF is
stored in
mitochondria, or
ER, or free in
cytosol
KEY
PTH = parathyroid
hormone
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Figure 23-20 (2 of 5)
Calcium Balance in the Body
ECF
Bone
Ca2+
Calcitonin
[Ca2+]
PTH
Calcitriol
Cortisol
2.5 mM
Electrochemical
gradient
Active
transport
Cells
[free Ca2+]
0.001 mM
Bone is largest
calcium
reservoir. It is
stored as
hydroxyapartite
crystals.
Calcium is
released to
maintain plasma
levels
KEY
PTH = parathyroid
hormone
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Figure 23-20 (3 of 5)
Calcium Balance in the Body
Small intestine
Dietary
calcium
Ca2+
Calcitrol
(PTH, prolactin)
ECF
Bone
Ca2+
Calcitonin
[Ca2+]
PTH
Calcitriol
Cortisol
2.5 mM
Electrochemical
gradient
Active
transport
Cells
[free Ca2+]
0.001 mM
Only 1/3 of the
calcium ingested is
absorbed.
Absorption is
regulated by a
hormone. A healthy
diet needs to be
high in calcium in
order to match the
amount excreted
KEY
PTH = parathyroid
hormone
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Figure 23-20 (4 of 5)
Calcium Balance in the Body
Small intestine
Dietary
calcium
Calcitrol
(PTH, prolactin)
Some calcium is secreted
into the small intestine.
ECF
Bone
Ca2+
Calcium
in feces
Ca2+
Kidney
Calcitonin
[Ca2+]
PTH
Calcitriol
Cortisol
2.5 mM
Electrochemical
gradient
Passive
filtration
PTH
Calcitonin
Ca2+ in
kidney
tubules
Active
transport
Calcium is mostly
excreted by the
kidneys through urine
and a small amount is
lost in feces. Calcium
reabsorption at the
kidneys is regulated
by hormones or
transport proteins
Cells
[free Ca2+]
0.001 mM
KEY
Ca2+
in urine
PTH = parathyroid
hormone
Total body calcium = intake  output
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Figure 23-20 (5 of 5)
Calcium Balance
Osteoclasts are responsible for bone resorption – a low pH
environment and proteases are needed to dissolve bone matrix.
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Figure 23-21
Calcium Balance
 Parathyroid hormone: increases plasma Ca.
concentration by stimulating its release/reabsorption
from bone, kidney, and intestine.
 Mobilizes calcium from bone- does not bind
osteoclast but promotes release of paracrines the
increse its activity
 Enhances renal reabsorption- prevents excessive
build up of calcium in urine
 Indirectly increases intestinal absorption- used
calcitrol to increase absorption
 Calcitriol – vitamin D3, most important in adults,
acts bone, liver, intestine
 Calcitonin- targets osteoclasts and reduces bone
resorption, thus dropping blood ]Ca 2+ ]
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Calcium Balance: Parathyroid Glands
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Figure 23-22
Calcium Balance
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Endocrine Control of Calcium Balance
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Figure 23-23
Calcium Balance
 Calcium and phosphate homeostasis are linkedmost phosphate in the body is found in bone, it is
processed similarly in the same three organs that
process calcium by the same hormones.
 Phosphate is key ingredient of hydroxyapatite
 Phosphate has other roles
 Energy transfer and storage
 Activation and deactivation of enzymes, transports,
and ion channels
 Part of DNA and RNA backbone
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Osteoporosis
Normal bone (left) and bone loss in osteoporosis (right)
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Figure 23-24