Download 4 Lec 2 Endocrine System 2 V9

Human Anatomy & Physiology
Ninth Edition
CHAPTER
16
The Endocrine
System: Part 2
© Annie Leibovitz/Contact Press Images
© 2013 Pearson Education, Inc.
Figure 16.9 The thyroid gland.
Hyoid bone
Epiglottis
Thyroid cartilage
Colloid-filled
follicles
Follicular cells
Superior thyroid
artery
Common carotid
artery
Inferior thyroid
artery
Isthmus of
thyroid gland
Trachea
Left subclavian
artery
Left lateral
lobe of thyroid
gland
Aorta
Parafollicular cells
Gross anatomy of the thyroid gland, anterior view
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Photomicrograph of thyroid gland
follicles (145x)
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Thyroid Hormone (TH)
• Actually two related compounds
– T4 (thyroxine); has 2 tyrosine molecules + 4
bound iodine atoms
– T3 (triiodothyronine); has 2 tyrosines + 3
bound iodine atoms
• Affects virtually every cell in body
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Thyroid Hormone
• Major metabolic hormone
• Increases metabolic rate and heat
production (calorigenic effect)
• Regulation of tissue growth and
development
– Development of skeletal and nervous systems
– Reproductive capabilities
• Maintenance of blood pressure
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Figure 16.10 Synthesis of thyroid hormone.
Slide 1
Thyroid follicular cells
Colloid
1 Thyroglobulin is synthesized and
discharged into the follicle lumen.
Tyrosines (part of thyroglobulin
molecule)
Capillary
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus
Rough
ER
Iodine
3 Iodide
is oxidized
to iodine.
2 Iodide (I–) is trapped
(actively transported in).
Iodide (I−)
T4
T3
Lysosome
DIT
MIT
Thyroglobulin
colloid
5 Iodinated tyrosines are
linked together to form T3
and T4.
T4
T3
T4
T3
6 Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
7 Lysosomal enzymes
cleave T4 and T3 from
thyroglobulin and hormones
diffuse into bloodstream.
Colloid in
lumen of
follicle
To peripheral tissues
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Transport and Regulation of TH
• T4 and T3 transported by thyroxine-binding
globulins (TBGs)
• Both bind to target receptors, but T3 is ten
times more active than T4
• Peripheral tissues convert T4 to T3
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Transport and Regulation of TH
• Negative feedback regulation of TH
release
– Rising TH levels provide negative feedback
inhibition on release of TSH
– Hypothalamic thyrotropin-releasing hormone
(TRH) can overcome negative feedback
during pregnancy or exposure to cold
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Homeostatic Imbalances of TH
• Hyposecretion in adults—myxedema;
goiter if due to lack of iodine
• Hyposecretion in infants—cretinism
• Hypersecretion—Graves' disease
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Figure 16.11 Thyroid disorders.
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Parathyroid Glands
• Four to eight tiny glands embedded in
posterior aspect of thyroid
• Contain oxyphil cells (function unknown)
and parathyroid cells that secrete
parathyroid hormone (PTH) or
parathormone
• PTH—most important hormone in Ca2+
homeostasis
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Figure 16.12 The parathyroid glands.
Pharynx
(posterior
aspect)
Capillary
Thyroid
gland
Parathyroid
glands
Esophagus
Oxyphil
cells
Trachea
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Parathyroid
cells
(secrete
parathyroid
hormone)
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Figure 16.13 Effects of parathyroid hormone on bone, the kidneys, and the intestine.
Hypocalcemia
(low blood Ca2+)
PTH release from
parathyroid gland
Osteoclast activity
in bone causes Ca2+
and PO43- release
into blood
Ca2+ reabsorption
in kidney tubule
Activation of
vitamin D by kidney
Ca2+ absorption
from food in small
intestine
Ca2+ in blood
Initial stimulus
Physiological response
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Result
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Homeostatic Imbalances of PTH
• Hyperparathyroidism due to tumor
– Bones soften and deform
– Elevated Ca2+ depresses nervous system and
contributes to formation of kidney stones
• Hypoparathyroidism following gland
trauma or removal or dietary magnesium
deficiency
– Results in tetany, respiratory paralysis, and
death
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Adrenal (Suprarenal) Glands
• Paired, pyramid-shaped organs atop
kidneys
• Structurally and functionally are two
glands in one
– Adrenal medulla—nervous tissue; part of
sympathetic nervous system
– Adrenal cortex—three layers of glandular
tissue that synthesize and secrete
corticosteroids
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Adrenal Cortex
• Three layers and the corticosteroids
produced
– Zona glomerulosa—mineralocorticoids
(chiefly aldosterone
– Zona fasciculata—glucocorticoids (chiefly
cortisol)
– Zona reticularis—sex hormones, or
gonadocorticoids (chiefly androgens)
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Figure 16.14 Microscopic structure of the adrenal gland.
Hormones
secreted
Zona
glomerulosa
Aldosterone
Zona
fasciculata
Cortex
Adrenal gland
• Medulla
• Cortex
Capsule
Cortisol
and
androgens
Kidney
Medulla
Zona
reticularis
Adrenal
medulla
Drawing of the histology of the
adrenal cortex and a portion of
the adrenal medulla
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Epinephrine
and
norepinephrine
Photomicrograph (115x)
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Mineralocorticoids
• Regulate electrolytes (primarily Na+ and K+)
in ECF
– Importance of Na+: affects ECF volume, blood
volume, blood pressure, levels of other ions
– Importance of K+: sets RMP of cells
• Aldosterone most potent mineralocorticoid
– Stimulates Na+ reabsorption and water
retention by kidneys; elimination of K+
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Mechanisms of Aldosterone Secretion
• Renin-angiotensin-aldosterone mechanism:
decreased blood pressure stimulates kidneys to
release renin  triggers formation of angiotensin
II, a potent stimulator of aldosterone release
• Plasma concentration of K+: increased K+
directly influences zona glomerulosa cells to
release aldosterone
• ACTH: causes small increases of aldosterone
during stress
• Atrial natriuretic peptide (ANP): blocks renin and
aldosterone secretion to decrease blood
pressure
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Figure 16.15 Major mechanisms controlling aldosterone release from the adrenal cortex.
Primary regulators
Blood volume
and/or blood
pressure
K+ in blood
Other factors
Stress
Blood pressure
and/or blood
volume
Hypothalamus
Kidney
Heart
CRH
Renin
Direct
stimulating
effect
Initiates
cascade
that
produces
Anterior
pituitary
Atrial natriuretic
peptide (ANP)
ACTH
Angiotensin II
Inhibitory
effect
Zona glomerulosa
of adrenal cortex
Enhanced
secretion
of aldosterone
Targets
kidney tubules
Absorption of Na+ and
water; increased K+ excretion
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Blood volume
and/or blood pressure
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Homeostatic Imbalances of Aldosterone
• Aldosteronism—hypersecretion due to
adrenal tumors
– Hypertension and edema due to excessive Na+
– Excretion of K+ leading to abnormal function of
neurons and muscle
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Glucocorticoids
• Keep blood glucose levels relatively
constant
• Maintain blood pressure by increasing
action of vasoconstrictors
• Cortisol (hydrocortisone)
– Only one in significant amounts in humans
• Cortisone
• Corticosterone
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Glucocorticoids: Cortisol
• Released in response to ACTH, patterns of
eating and activity, and stress
• Prime metabolic effect is gluconeogenesis—
formation of glucose from fats and proteins
– Promotes rises in blood glucose, fatty acids, and
amino acids
• "Saves" glucose for brain
• Enhances vasoconstriction  rise in blood
pressure to quickly distribute nutrients to cells
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Homeostatic Imbalances of Glucocorticoids
• Hypersecretion—Cushing's
syndrome/disease
– Depresses cartilage and bone formation
– Inhibits inflammation
– Depresses immune system
– Disrupts cardiovascular, neural, and
gastrointestinal function
• Hyposecretion—Addison's disease
– Also involves deficits in mineralocorticoids
• Decrease in glucose and Na+ levels
• Weight loss, severe dehydration, and hypotension
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Figure 16.16 The effects of excess glucocorticoid.
Patient before onset.
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Same patient with Cushing’s
syndrome. The white arrow shows
the characteristic “buffalo hump” of
fat on the upper back.
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Gonadocorticoids (Sex Hormones)
• Most weak androgens (male sex
hormones) converted to testosterone in
tissue cells, some to estrogens
• May contribute to
– Onset of puberty
– Appearance of secondary sex characteristics
– Sex drive in women
– Estrogens in postmenopausal women
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Gonadocorticoids
• Hypersecretion
– Adrenogenital syndrome (masculinization)
– Not noticeable in adult males
– Females and prepubertal males
• Boys – reproductive organs mature; secondary sex
characteristics emerge early
• Females – beard, masculine pattern of body hair;
clitoris resembles small penis
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Adrenal Medulla
• Medullary chromaffin cells synthesize
epinephrine (80%) and norepinephrine
(20%)
• Effects
– Vasoconstriction
– Increased heart rate
– Increased blood glucose levels
– Blood diverted to brain, heart, and skeletal
muscle
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Adrenal Medulla
• Responses brief
• Epinephrine stimulates metabolic
activities, bronchial dilation, and blood flow
to skeletal muscles and heart
• Norepinephrine influences peripheral
vasoconstriction and blood pressure
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Adrenal Medulla
• Hypersecretion
– Hyperglycemia, increased metabolic rate,
rapid heartbeat and palpitations,
hypertension, intense nervousness, sweating
• Hyposecretion
– Not problematic
– Adrenal catecholamines not essential to life
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Figure 16.17 Stress and the adrenal gland.
Short-term stress
Prolonged stress
Stress
Nerve impulses
Hypothalamus
CRH (corticotropinreleasing hormone)
Spinal cord
Corticotropic cells
of anterior pituitary
To target in blood
Preganglionic
sympathetic
fibers
Adrenal medulla
(secretes amino acid–
based hormones)
Catecholamines
(epinephrine and
norepinephrine)
Short-term stress response
• Heart rate increases
• Blood pressure increases
• Bronchioles dilate
• Liver converts glycogen to glucose and releases
glucose to blood
• Blood flow changes, reducing digestive system activity
and urine output
• Metabolic rate increases
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ACTH
Mineralocorticoids
Adrenal cortex
(secretes steroid
hormones)
Glucocorticoids
Long-term stress response
• Kidneys retain
• Proteins and fats converted
sodium and water
to glucose or broken down
for energy
• Blood volume and
• Blood glucose increases
blood pressure
• Immune system
rise
supressed
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Pineal Gland
• Small gland hanging from roof of third ventricle
• Pinealocytes secrete melatonin, derived from
serotonin
• Melatonin may affect
– Timing of sexual maturation and puberty
– Day/night cycles
– Physiological processes that show rhythmic variations
(body temperature, sleep, appetite)
– Production of antioxidant and detoxification molecules
in cells
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Pancreas
• Triangular gland partially behind stomach
• Has both exocrine and endocrine cells
– Acinar cells (exocrine) produce enzyme-rich
juice for digestion
– Pancreatic islets (islets of Langerhans)
contain endocrine cells
• Alpha () cells produce glucagon (hyperglycemic
hormone)
• Beta () cells produce insulin (hypoglycemic
hormone)
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Figure 16.18 Photomicrograph of differentially stained pancreatic tissue.
Pancreatic islet
•  (Glucagonproducing)
cells
•  (Insulinproducing)
cells
Pancreatic acinar
cells (exocrine)
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Glucagon
• Major target—liver
• Causes increased blood glucose levels
• Effects
– Glycogenolysis—breakdown of glycogen to
glucose
– Gluconeogenesis—synthesis of glucose
from lactic acid and noncarbohydrates
– Release of glucose to blood
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Insulin
• Effects of insulin
– Lowers blood glucose levels
– Enhances membrane transport of glucose into
fat and muscle cells
– Inhibits glycogenolysis and gluconeogenesis
– Participates in neuronal development and
learning and memory
• Not needed for glucose uptake in liver,
kidney or brain
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Figure 16.19 Insulin and glucagon from the pancreas regulate blood glucose levels.
Stimulates glucose
uptake by cells
Tissue cells
Insulin
Stimulates
glycogen
formationw
Pancreas
Glucose
Glycogen
Blood
glucose
falls to
normal
range.
Liver
Stimulus
Blood
glucose level
Stimulus
Blood
glucose level
Blood
glucose
rises to
normal
range.
Pancreas
Glucose
Glycogen
Liver
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Stimulates
glycogen
breakdown
Glucagon
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Homeostatic Imbalances of Insulin
• Diabetes mellitus (DM)
– Due to hyposecretion (type 1) or hypoactivity (type 2)
of insulin
• Three cardinal signs of DM
– Polyuria—huge urine output
• Glucose acts as osmotic diuretic
– Polydipsia—excessive thirst
• From water loss due to polyuria
– Polyphagia—excessive hunger and food
consumption
• Cells cannot take up glucose; are "starving"
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Type 1 - IDDM
•
•
•
•
•
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10% of DM cases
Early onset
No insulin produced
Treatment – testing and insulin injections
Long term problems
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Type II - NIDDM
•
•
•
•
90% of DM cases
Develops after age 40
Causes
Produce insulin but receptors are reduced
or non-responsive
• Symptoms
• Consequences
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Homeostatic Imbalances of Insulin
• Hyperinsulinism:
– Excessive insulin secretion
– Causes hypoglycemia
• Low blood glucose levels
• Anxiety, nervousness, disorientation,
unconsciousness, even death
– Treated by sugar ingestion
• Gestational Diabetes
– Elevated levels of estrogen and progesterone
make target cells resistant to insulin
– Placenta releases insulinase – breakdown of
insulin
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What if????
• Type I – IDDM and you eat a lot of carbs
but do not take insulin
• Type I – Give insulin shot but do not eat.
• Type II – NIDDM – eat a big Thanksgiving
meal
• Tumor affecting posterior pituitary –
inhibits secretion of ?
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Other Hormone-producing Structures
• Adipose tissue
– Leptin – appetite control; stimulates
increased energy expenditure
– Resistin – insulin antagonist
– Adiponectin – enhances sensitivity to insulin
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Other Hormone-producing Structures
• Enteroendocrine cells of gastrointestinal
tract
– Gastrin stimulates release of HCl
– Secretin stimulates liver and pancreas
– Cholecystokinin stimulates pancreas,
gallbladder, and hepatopancreatic sphincter
– Serotonin acts as paracrine
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Other Hormone-producing Structures
• Heart
– Atrial natriuretic peptide (ANP) decreases
blood Na+ concentration, therefore blood
pressure and blood volume
• Kidneys
– Erythropoietin signals production of red
blood cells
– Renin initiates the renin-angiotensinaldosterone mechanism
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Other Hormone-producing Structures
• Skeleton (osteoblasts)
– Osteocalcin
• Prods pancreas to secrete more insulin; restricts
fat storage; improves glucose handling; reduces
body fat
• Activated by insulin
• Low levels of osteocalcin in type 2 diabetes –
perhaps increasing levels may be new treatment
• Skin
– Cholecalciferol, precursor of vitamin D
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Other Hormone-producing Structures
• Thymus
– Large in infants and children; shrinks as age
– Thymulin, thymopoietins, and thymosins
• May be involved in normal development of T
lymphocytes in immune response
• Classified as hormones; act as paracrines
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Developmental Aspects
• Hormone-producing glands arise from all three
germ layers
• Most endocrine organs operate well until old age
• Exposure to pesticides, industrial chemicals,
arsenic, dioxin, and soil and water pollutants
disrupts hormone function
• Sex hormones, thyroid hormone, and
glucocorticoids are vulnerable to the effects of
pollutants
• Interference with glucocorticoids may help
explain high cancer rates in certain areas
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Developmental Aspects
• Ovaries undergo significant changes with
age and become unresponsive to
gonadotropins; problems associated with
estrogen deficiency occur
• Testosterone also diminishes with age, but
effect is not usually seen until very old age
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Developmental Aspects
• GH levels decline with age - accounts for
muscle atrophy with age
• TH declines with age, contributing to lower
basal metabolic rates
• PTH levels remain fairly constant with age,
but lack of estrogen in older women
makes them more vulnerable to bonedemineralizing effects of PTH
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