Download Thyroid gland

• Chapter 19
The Peripheral Endocrine Glands
Peripheral Endocrine Glands
• Thyroid gland controls basal metabolic rate.
• Adrenal glands maintain salt balance,
involved in nutrient metabolism and stress
adaptation.
• Endocrine pancreas important in nutrient
metabolism and glucose homeostasis.
• Parathyroid glands important in Ca2+
metabolism.
Thyroid Gland
• Contains two types of endocrine secretory cells:
•
•
follicular cells produce
tetraiodothyronine (T4 or thyroxine) and tri-iodothyronine
(T3)
C cells produce Ca2+-regulating hormone calcitonin.
Thyroid Hormone Synthesis
•
Basic ingredients:
• amino acid tyrosine synthesized in sufficient amounts by
body
• iodine obtained from dietary intake
•
Thyroid hormone is synthesized and stored on the
thyroglobulin molecule.
•
•
Thyroid hormones remain in colloid until they are split off
and secreted.
Usually enough thyroid hormone stored to supply body’s
needs for several months.
Thyroid
follicular cell
Blood
Colloid
Golgi
complex
Endoplasmic
reticulum
2
Na+
9b
MIT
DIT 8
MIT
DIT
4b
Tg
MIT
5a
3
Na+ (Iodinase
action)
Lysosome
K+
K+
Tg
4a
1
4
MIT
DIT
7
I–
6a
1 MIT + 1 DIT
5b
DIT
6b
2 DITs
9a
Thyroid
follicle
Tyrosine-containing thyroglobulin is exported
from follicular cells into colloid by exocytosis.
–
–
Iodine from blood pumped into colloid.
Within colloid iodine attaches to tyrosine.
Process forms MIT and DIT.
Coupling of MIT and DIT forms thyroid
hormones.
MIT coupled to DIT produces T3
DIT coupled to DIT produces T4
Fig. 19-2, p. 688
Stress
Cold in infants
•
Regulated negative-feedback
between hypothalamic TRH,
anterior pituitary TSH, and
thyroid gland T3 and T4.
•
Main determinant of basal
metabolic rate.
Influences synthesis and
degradation of carbohydrate,
fat, and protein.
Increases responsiveness to
catecholamines.
Increases heart rate and force
of contraction.
Essential for normal growth.
Plays crucial role in normal
development of nervous
system.
Hypothalamus
Thyrotropin-releasing
hormone (TRH)
•
Anterior pituitary
•
Thyroid-stimulating
hormone (TSH)
Thyroid gland
•
•
•
Thyroid hormone
(T3 and T4)
Metabolic rate and heat production;
enhancement of growth and CNS development;
enhancement of sympathetic activity
Fig. 19-3, p. 689
Hypothyroidism
•
Causes:
•
•
•
•
•
primary due to failure of thyroid gland
secondary due to deficiency of TRH, TSH
inadequate dietary supply of iodine
Treatment:
•
taking replacement thyroid hormone
•
providing dietary iodine for deficiency
Symptoms:
– reduced BMR, poor cold tolerance, excessive weight gain, fatigue, decreased cardiac
output, slow reflexes and slow mental responsiveness
– myxedema from accumulation of water-retaining carbohydrate molecules
– in infants causes cretinism characterized by dwarfism and mental retardation
Hyperthyroidism
Causes:
•
•
•
Grave’s Disease when body
produces thyroid-stimulating
immunoglobulins (TSI)
secondary to excess TRH or TSH
Treatment:
•
removal of over-secreting thyroid
lobes
•
administration of radioactive iodine
•
use of antithyroid drugs
Symptoms:
–
increased BMR, poor heat
tolerance, excessive weight loss,
skeletal muscle loss, increased
cardiac output, excessive degree of
mental alertness leading to
agitation/anxiousness
–
Exophthalmos (bulging) eyes
–
Goiter: enlarged thyroid gland
develops when the thyroid gland is
overstimulated
Adrenal Glands
•
•
Located above each kidney
Composed of two endocrine organs:
–
•
adrenal cortex
• outer portion
• secretes steroid hormones
–
adrenal medulla
• inner portion
secretes catecholamines
Consists of three layers:
•
•
•
•
zona glomerulosa, outer layer
zona fasciculata, middle layer
zona reticularis, inner layer
Secretes hormones called “corticoids”
•
•
•
mineralocorticoids
glucocorticoids
sex hormones
Capsule
Zona
glomerulosa
Zona
fasciculata
Adrenal
medulla
Adrenal
cortex
Adrenal Mineralocorticoids
gland
(aldosterone)
Glucocorticoids
(cortisol)
and
sex hormones
(dehydroepiandrosterone)
Catecholamines
(epinephrine and
norepinephrine)
(a) Location and gross structure of adrenal glands
Cortex
Zona
reticularis
Medulla
Connective tissue
capsule
Zona
glomerulosa
Zona
fasciculata
Cortex
Zona
reticularis
Medulla
(b) Layers of adrenal cortex
Fig. 19-7, p. 693
Cholesterol
Pregnenolone
17-Hydroxypregnenolone
Progesterone
17-Hydroxyprogesterone
Dehydroepiandrosterone
(adrenal cortex hormone)
Androstenedione
Estrone
Testosterone
Estradiol
(female sex hormone)
11-Deoxycorticosterone
Deoxycortisol
Androgens
(male sex hormones)
Corticosterone
Cortisol
Aldosterone
Glucocorticoid
(adrenal cortex hormone)
Estriol
Estrogens
(female sex hormones)
Mineralocorticoid
adrenal cortex hormone)
Fig. 19-8, p. 694
Adrenal Cortex
•
Glucocorticoids:
–
–
–
–
–
–
•
produced primarily in
zona fasciculata
major hormone is
cortisol
plays role in nutrient
metabolism
increase levels of
blood glucose by
gluconeogenesis
involved in stress
resistance
exerts antiinflammatory and
immunosuppressive
effects
Mineralocorticoids:
•
•
•
•
•
•
produced by zona
glomerulosa
primarily aldosterone
increase Na+ reabsorption
and K+ secretion
help maintain blood
pressure homeostasis
mineralocorticoids are
essential for life
Sex hormones:
•
•
•
•
•
produced in inner two
layers
similar to testosterone
no effects in males
most important is
dehydroepiandosterone
(DHEA)
regulates sex drive and
growth of axillary and
pubertal hair in females
Stress
Diurnal rhythm
Hypothalamus
Corticotropin-releasing
hormone (CRH)
Anterior pituitary
Adrenocorticotropic
hormone (ACTH)
Adrenal cortex
Cortisol
Metabolic fuels
and building blocks
available to help
resist stress
Blood glucose
(by stimulating
gluconeogenesis
and inhibiting glucose uptake)
Blood amino acids
(by stimulating protein
degradation)
Blood fatty acids
(by stimulating lipolysis)
Fig. 19-9, p. 696
Cortisol Hyper/hyposecretion
•
•
Cushing’s syndrome
Causes:
•
•
•
overstimulation of adrenal cortex
adrenal tumors secrete excess cortisol
Signs and symptoms:
•
•
hyperglycemia and glucosuria (adrenal
diabetes)
abnormal fat distributions “buffalo hump”
and “moon face”
Primary adrenocortical insufficiency
known as Addison’s disease:
–all three layers under-produce
hormones
–changes in blood pressure, nutrient
metabolism
Adrenal Medulla
•
•
•
Contains modified sympathetic postganglionic neurons.
Primary stimulus for secretion is sympathetic nervous
system.
Releases epinephrine and norepinephrine:
•
•
•
Epinephrine 80%
Norepinephrine 20% of secretion
Epinephrine:
•
•
•
reinforces sympathetic system in mounting general systemic “fightor-flight” responses
maintenance of arterial blood pressure
increases blood glucose and blood fatty acids
Endocrine Control of Fuel Metabolism
• Metabolism
• all the chemical reactions that occur within the
cells of the body
• Intermediary metabolism or fuel
metabolism
• includes reactions involving degradation,
synthesis, and transformation of proteins,
carbohydrates, and fats
Tissues in Metabolism
• Liver:
•
•
primary role in maintaining normal blood glucose levels
principal site for metabolic interconversions
• Adipose tissue:
•
•
primary energy storage site
important in regulating blood fatty acid levels
• Muscle:
•
•
primary site of amino acid storage
major energy user
• Brain:
•
•
•
normally uses only glucose for energy
does not store glycogen
blood glucose levels must be maintained to supply energy
source to brain
Food intake
Dietary
carbohydrate
Dietary protein
D
Absorbable units
Amino
acids
E
S
T
Glucose
A
= Anabolism
= Catabolism
I G
Storage, structural,
and functional
macromolecules
in cells
Body proteins
(structural or
secretory
products)
Glycogen storage
in liver and muscle
Triglycerides
in adipose tissue
stores (fat)
B
S
O
R
Dietary
triglyceride fat
I
O
N
Fatty acids Monoglycerides
P
Metabolic
pool in body
T
I O
N
Urea
Urinary
excretion (elimination
from body)
Amino
acids
Glucose
Use as metabolic fuel
in cells:
Oxidation to
CO2+H2O+ATP
(energy)
Fatty
acids
Expired
(elimination from
body)
F
Table 19-3 p704
Stressor
Stress is
generalized
nonspecifc
response of the
body to any factor
that overwhelms,
or threatens to
overwhelm, the
body’s
compensatory
ability to maintain
homeostasis.
Stressor is any
stimulus that
causes stress
response.
All actions
coordinated by
the
hypothalamus.
Hypothalamus
CRH
Sympathetic
nervous system
Posterior
Pituitary
Anterior
pituitary
Vasopressin
ACTH
Conserve salt and
H2O to expand the
plasma volume;
help sustain blood
pressure when
acute loss of
plasma volume
occurs
Vasopressin and
angiotensin II
cause arteriolar
vasoconstriction
to increase blood
pressure
Adrenal cortex
Adrenal medulla
Epinephrine
Cortisol
Prepare body for
“fight or flight”
Arteriolar
smooth muscle
Mobilize energy
stores and
metabolic
building blocks
for use as needed
Glucagon-secreting cells
Insulin-secreting cells
Endocrine
pancreas
Vasoconstriction
Blood flow
through kidneys
Glucagon
Renin
Angiotensin
Aldosterone
Insulin
Fig. 1
Table 19-2 p702
Factors that increase blood glucose
Factors that decrease blood glucose
Transport of glucose into cells:
––For utilization for energy production
––For storage
• as glycogen through glycogenesis
• as triglycerides
Glucose absorption from digestive tract
Blood
glucose
Hepatic glucose production:
––Through glycogenolysis
of stored glycogen
––Through gluconeogenesis
Urinary excretion of glucose (occurs
only abnormally, when blood glucose
level becomes so high it exceeds the
reabsorptive capacity of kidney tubules
during urine formation)
KEY
= Factors subject to hormonal control to maintain blood
glucose level
Fig. 19-16, p. 710
Insulin and glucagon
Insulin
Anabolic hormone
• Lowers blood concentration
of glucose, fatty acids, and
amino acids by promoting
cellular uptake.
• Enhances their conversion
into glycogen, triglycerides,
and proteins.
• Secretion is increased
during absorptive state.
• Primary stimulus for
secretion is increase in
blood glucose
concentration.
Glucagon
• Catabolic hormone
• Secreted during postabsorptive state in
response to a fall in blood glucose.
• Mobilizes energy-rich molecules from
their stores.
• Increases blood glucose levels.
• In general opposes the actions of
insulin.
Gastrointestinal
hormones (incretins)
Blood amino acid
concentration
Blood amino acid
concentration
Major control
Food intake
Parasympathetic
stimulation
Islet  cells
Sympathetic stimulation
(and epinephrine)
Insulin secretion
Blood glucose
Blood fatty acids
Blood amino acids
Protein synthesis
Fuel storage
Fig. 19-18, p. 713
Diabetes Mellitus
• Most common of all endocrine disorders.
• Results in elevated blood glucose levels.
• Two major types:
• type I diabetes characterized by lack of insulin
secretion.
• type II diabetes characterized by reduced
sensitivity of insulin’s target cells.
Endocrine Control of Calcium Metabolism
• Plasma Ca2+ must be closely regulated to prevent
changes in neuromuscular excitability.
• Role in other essential activities:
•
•
•
•
excitation-contraction coupling in cardiac and smooth muscle
stimulus-secretion coupling
maintenance of tight junctions
clotting of blood
• Three hormones regulate plasma concentration of Ca2+
(and PO43-)
•
•
•
parathyroid hormone (PTH)
calcitonin
vitamin D
PTH/Vitamin D/Calcitonin
PTH
•
•
•
Vitamin D
Secreted by parathyroid
•
glands.
Primary regulator of
Ca2+
•
Actions:
• promotes Ca2+
movement from
bone fluid into the •
plasma
• enhances Ca2+
reabsorption by
•
kidneys
• facilitates activation
of vitamin D
Stimulates Ca2+ and PO43absorption from intestine.
Calcitonin
• Produced by the C cells
of the thyroid gland.
• Secreted in response to
Can be synthesized from
an increase in plasma
cholesterol derivative
Ca2+
when exposed to sunlight. • Lowers plasma Ca2+ by
inhibiting activity of
Supplemented by dietary
bone osteoclasts.
intake.
• Calcitonin is
Must be activated first by
unimportant except
liver and then by kidneys
during the rare
before it can affect the
condition of
intestines.
hypercalcemia.
Plasma Ca2+
Plasma Ca2+
Parathyroid glands
Thyroid C cells
PTH
Plasma Ca2+
Calcitonin
Plasma Ca2+
Fig. 19-26, p. 729
Precursor in skin
(7-dehydrocholesterol)
Dietary vitamin D
Sunlight
Vitamin D3
Hydroxyl group (OH)
Liver enzymes
25-OH-vitamin D3
Hydroxyl group
PTH
Plasma Ca2+
Kidney enzymes
Plasma PO43−
1,25-(OH)2-vitamin D3
(active vitamin D)
Promotes intestinal
absorption of Ca2+ and
PO43−
Fig. 19-27, p. 730