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! Thyroid gland
! Parathyroid glands
! Adrenal glands
! Pancreas
! Gonads
! Pineal Gland
! Location
! Anatomy/Histology
! Regulation
!Hormonal, humoral,
nervous
! Hormones
! Functions
!Target cell & actions
on target cells
! Diseases
(homeostatic imbalances)
49
Characterize the
hypothalamus gland:
! Master
endocrine gland
(along w/
pituitary)
! Location
! Functions
! Hypophyseal
portal system
50
Hypothalamus:
Master Controller
of Endocrine
System
! Hypothalamus secretes regulatory (releasing) hormones
that travel through the hypothalamo-hypophyseal portal
system to the anterior pituitary and release
Anterior pituitary
Posterior pituitary
Muscle
TSH
Thyroid-stimulating hormone
(TSH) stimulates thyroid gland
to release thyroid hormone.
GH
Thyroid
Bone
PRL
Adipose
connective tissue
Mammary gland
Adrenal cortex
Prolactin (PRL) acts on mammary
glands to stimulate milk production.
ACTH
Adrenocorticotropic hormone (ACTH)
acts on the adrenal cortex to cause
release of corticosteroids
(e.g., cortisol).
FSH and LH
Adrenal gland
Ovary
53
! 2 Lobes/3 Sections:
! Anterior pituitary
(adenohypophysis)
! Posterior pituitary
(neurohypophysis)
! Intermedia
54
55
-TSH
Hormone
Function
-PRL
-FSH
-LH
-ACTH
-GH
-MSH
56
Mnemonic Device
Page 672
61
62
Describe the
regulation of GH:
! Antagonistic hypothalamic
HM regulate GH
! GHRH stimulates GH
release
! GIH (aka GHIH) inhibits GH
release
! Hypoglycemia stimulates
release of GHRH from
hypothalamus
! Hyperglycemia & high levels
of GH/IGFs
! Inhibit GHRH & GH release
! Stimulate GIH release
What
Stimulates
GHRH
Secretion?
Growth hormone
Stimulation
Inhibition
STIMULUS
1 Variables that influence the release
of GHRH from the hypothalamus:
Age
Time of day
Nutrient levels in the blood
Stress and exercise
Good
Summary:
Fig. 17.15
on p. 674
Hypothalamus
1
2
RECEPTOR
GH
8 Increased levels of both GH
and IGF inhibit the release
of GHRH from the
hypothalamus; Increased
levels of GH also inhibits
the release of GH from the
anterior pituitary.
3
GHRH
IGF
GH
CONTROL CENTER
2 The hypothalamus
responds to various
stimuli.
4 GH
GH
NET EFFECT
7
Liver
Hepatocytes
IGF
Glycerol
Fatty acids
Glucose
Amino acids
GH
Bone
Muscle
IGF
Increased growth
Increased amino acid uptake which results in protein synthesis
Stimulated mitosis
Liver tissue
Adipose connective
tissue
Increased glycogenolysis
and gluconeogenesis
Increased lipolysis
Decreased glycogenesis
Decreased lipogenesis
Cell differentiation
66
Clinical
Applications:
! Hyposecretion hGH
! childhood = Hypopituitary
dwarfism
! Hypersecretion hGH
! childhood = giantism
! adult = acromegaly
67
http://www.chauvet-translation.com/figures/Figure027.jpg
INTEGRATE
CLINICAL VIEW
Disorders of Growth Hormone Secretion
Pituitary dwarfism
Pituitary dwarfism is a
condition that exists at birth
as a result of inadequate
growth hormone production
due to a hypothalamic or
pituitary problem. Growth
retardation is typically not
evident until a child reaches
1 year of age, because the
influence of growth hormone
(GH) is minimal during the
first 6 to 12 months of life. In
addition to short stature,
children
with
pituitary
dwarfism often have periodic
low
blood
sugar
(hypoglycemia). Injections of
growth hormone over a
period of many years can
bring about improvement,
but not a normal
state.
Too much growth
hormone causes excessive
growth
and
leads
to
increased levels of blood
sugar.
Oversecretion
of
growth
hormone
in
childhood causes pituitary
gigantism.
Beyond
extraordinary
height
(sometimes up to 8 feet),
these people have enormous
internal organs, a large and
protruding
tongue,
and
significant problems with
blood glucose management.
If untreated, a pituitary giant
dies at a comparatively early
age,
often
from
complications of diabetes
Age 9
Age 16
Age 33
Age 52
or heart failure.
Gigantism
Acromegaly
! No hormone
synthesis
! Stores/releases
ADH & oxytocin
69
Characterize
oxytocin:
! Two target tissues:
! Both involved in
neuroendocrine reflexes
70
! decrease sweating
! increase BP
71
Describe the
regulation of
ADH:
! ADH released when
blood osmotic pressure
is high (dehydration or
blood loss)
Clinical Application:
! Central or pituitary diabetes insipidus
! kidneys are unable to conserve water
74
! Functions
75
Describe the
histology of
thyroid gland:
! Consists of follicles
! Follicular cells
! Thyroglobulin
! T3 & T4
! Parafollicular cells
! Calcitonin
76
Functions of T3 & T4
! Increase BMR (basal
!
!
!
!
metabolic rate)
Stimulate protein
synthesis
Increase use of glucose &
fatty acids for ATP
production
Heat production
Regulating tissue growth
# Developing skeletal &
nervous systems
Functions Calcitonin
! Parafollicular cells or C cells produce calcitonin
! peptide HM
Mechanism of
Thyroid
Hormone
Production
1 Low blood levels of T3
T3 & T4 Secretion
Regulation
! Hypothalamus secretes
TRH in response to
blood levels of T3 & T4
Hypothalamus
TRH
TRH, carried
by hypophyseal
portal veins to
anterior pituitary,
stimulates
release of TSH
by thyrotrophs
5 Elevated
T3inhibits
release of
TRH and
TSH
(negative
feedback)
TSH
Anterior
pituitary
4
Thyroid
follicle
T3 and T4
released into
blood by
follicular cells
! TSH stimulates
synthesis/secretion of
T3 & T4
80
Enhance some actions of catecholamines
Regulate development and growth of nervous tissue and bones
Good
Summary
Figure
17.19
Clinical Application:
Thyroid Gland Disorders
! Hypothyroidism
! Congential # Cretinism
! Adult # Myxedema
82
Clinical Application:
Thyroid Gland Disorders
! Hyperthyroidism
(Graves disease)
! Goiter = enlarged
thyroid (dietary)
83
Page 678
85
(PTH) or parathormone
! Major regulator of Ca+2,
86
87
Parathyroid Hormones
Clinical Application:
Hyperparathyroidism
! Parathyroid adenoma #1 cause
! Serum calcium imbalance
90