Download Document

Copyright © 2010 Pearson Education, Inc.
Figure 16.8
Thyroid follicle cells
Colloid
1 Thyroglobulin is synthesized and
discharged into the follicle lumen.
Capillary
Tyrosines (part of thyroglobulin
molecule)
Golgi
apparatus
Rough
ER
Colloid in
lumen of
follicle
Copyright © 2010 Pearson Education, Inc.
Figure 16.9, step 1
Thyroid follicle cells
Colloid
1 Thyroglobulin is synthesized and
discharged into the follicle lumen.
Capillary
Tyrosines (part of thyroglobulin
molecule)
Golgi
apparatus
Rough
ER
Iodide (I–)
2 Iodide (I–) is trapped
(actively transported in).
Colloid in
lumen of
follicle
Copyright © 2010 Pearson Education, Inc.
Figure 16.9, step 2
Thyroid follicle cells
Colloid
1 Thyroglobulin is synthesized and
discharged into the follicle lumen.
Capillary
Tyrosines (part of thyroglobulin
molecule)
Golgi
apparatus
Rough
ER
Iodide (I–)
Iodine
3 Iodide
is oxidized
to iodine.
2 Iodide (I–) is trapped
(actively transported in).
Colloid in
lumen of
follicle
Copyright © 2010 Pearson Education, Inc.
Figure 16.9, step 3
Thyroid follicle cells
Colloid
1 Thyroglobulin is synthesized and
discharged into the follicle lumen.
Capillary
Tyrosines (part of thyroglobulin
molecule)
4 Iodine is attached to tyrosine
in colloid, forming DIT and MIT.
Golgi
apparatus
Rough
ER
Iodide (I–)
Iodine
3 Iodide
is oxidized
to iodine.
DIT (T2) MIT (T1)
Thyroglobulin
colloid
2 Iodide (I–) is trapped
(actively transported in).
Colloid in
lumen of
follicle
Copyright © 2010 Pearson Education, Inc.
Figure 16.9, step 4
Thyroid follicle 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
Iodide (I–)
2 Iodide (I–) is trapped
(actively transported in).
Iodine
3 Iodide
is oxidized
to iodine.
T4
T3
DIT (T2) MIT (T1)
Thyroglobulin
colloid
5 Iodinated tyrosines are
linked together to form T 3
and T4.
Colloid in
lumen of
follicle
Copyright © 2010 Pearson Education, Inc.
Figure 16.9, step 5
Thyroid follicle 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
Iodide (I–)
Iodine
3 Iodide
is oxidized
to iodine.
2 Iodide (I–) is trapped
(actively transported in).
Lysosome
T4
T3
6 Thyroglobulin colloid is
endocytosed and combined
with a lysosome.
Copyright © 2010 Pearson Education, Inc.
DIT (T2) MIT (T1)
Thyroglobulin
colloid
5 Iodinated tyrosines are
linked together to form T 3
and T4.
Colloid in
lumen of
follicle
Figure 16.9, step 6
Thyroid follicle 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–)
Lysosome
T4
T3
DIT (T2) MIT (T1)
Thyroglobulin
colloid
5 Iodinated tyrosines are
linked together to form T 3
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
colloid and hormones diffuse
into bloodstream.
Colloid in
lumen of
follicle
To peripheral tissues
Copyright © 2010 Pearson Education, Inc.
Figure 16.9, step 7
Hypothalamus
TRH
Anterior pituitary
TSH
Thyroid gland
Thyroid
hormones
Target cells
Copyright © 2010 Pearson Education, Inc.
Stimulates
Inhibits
Figure 16.7
Homeostatic Imbalances of TH
• Hyposecretion in adults—myxedema;
endemic goiter if due to lack of iodine
• Hyposecretion in infants—cretinism
• Hypersecretion—Graves’ disease
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Figure 16.10
Pharynx
(posterior
aspect)
Thyroid
gland
Parathyroid
glands
Chief
cells
(secrete
parathyroid
hormone)
Oxyphil
cells
Esophagus
Trachea
(a)
Copyright © 2010 Pearson Education, Inc.
Capillary
(b)
Figure 16.11
Hypocalcemia (low blood Ca2+) stimulates
parathyroid glands to release PTH.
Rising Ca2+ in
blood inhibits
PTH release.
Bone
1 PTH activates
osteoclasts: Ca2+
and PO43S released
into blood.
Kidney
2 PTH increases
2+
Ca reabsorption
in kidney
tubules.
3 PTH promotes
kidney’s activation of vitamin D,
which increases Ca2+ absorption
from food.
Intestine
Ca2+ ions
PTH Molecules
Copyright © 2010 Pearson Education, Inc.
Bloodstream
Figure 16.12
Capsule
Zona
glomerulosa
• Medulla
• Cortex
Cortex
Adrenal gland
Zona
fasciculata
Zona
reticularis
Medulla
Kidney
Adrenal
medulla
(a) Drawing of the histology of the
adrenal cortex and a portion of
the adrenal medulla
Copyright © 2010 Pearson Education, Inc.
Figure 16.13a
Mechanisms of Aldosterone Secretion
1. Renin-angiotensin mechanism: decreased blood
pressure stimulates kidneys to release renin,
triggers formation of angiotensin II, a potent
stimulator of aldosterone release
2. Plasma concentration of K+: Increased K+ directly
influences the zona glomerulosa cells to release
aldosterone
3. ACTH: causes small increases of aldosterone
during stress
4. Atrial natriuretic peptide (ANP): blocks renin and
aldosterone secretion, to decrease blood pressure
Copyright © 2010 Pearson Education, Inc.
Primary regulators
Blood volume
and/or blood
pressure
Other factors
K+ in blood
Stress
Blood pressure
and/or blood
volume
Hypothalamus
Kidney
Heart
CRH
Renin
Initiates
cascade
that
produces
Direct
stimulating
effect
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
Blood volume
and/or blood pressure
Copyright © 2010 Pearson Education, Inc.
Figure 16.14
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
Copyright © 2010 Pearson Education, Inc.
Homeostatic Imbalances of Glucocorticoids
• Hypersecretion—Cushing’s syndrome
• Depresses cartilage and bone formation
• Inhibits inflammation
• Depresses the immune system
• Promotes changes in 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
Copyright © 2010 Pearson Education, Inc.
Copyright © 2010 Pearson Education, Inc.
Figure 16.15
Short-term stress
More prolonged stress
Stress
Nerve impulses
Hypothalamus
CRH (corticotropinreleasing hormone)
Spinal cord
Corticotroph cells
of anterior pituitary
To target in blood
Preganglionic
sympathetic
fibers
Adrenal medulla
(secretes amino acidbased hormones)
Catecholamines
(epinephrine and
norepinephrine)
Short-term stress response
1. Increased heart rate
2. Increased blood pressure
3. Liver converts glycogen to glucose and releases
glucose to blood
4. Dilation of bronchioles
5. Changes in blood flow patterns leading to decreased
digestive system activity and reduced urine output
6. Increased metabolic rate
Copyright © 2010 Pearson Education, Inc.
Adrenal cortex
(secretes steroid
hormones)
ACTH
Mineralocorticoids
Glucocorticoids
Long-term stress response
1. Retention of sodium
and water by kidneys
2. Increased blood volume
and blood pressure
1. Proteins and fats converted
to glucose or broken down
for energy
2. Increased blood glucose
3. Suppression of immune
system
Figure 16.16
Glucagon
• Major target liver promotes
• Glycogenolysis—breakdown glycogen to
glucose
• Gluconeogenesis—synthesis of glucose from
lactic acid and noncarbohydrates
• Release of glucose to the blood
Copyright © 2010 Pearson Education, Inc.
Insulin
• Effects of insulin
• Lowers blood glucose levels
• Enhances membrane transport of glucose into
fat and muscle cells
• Participates in neuronal development and
learning and memory
• Inhibits glycogenolysis and gluconeogenesis
Copyright © 2010 Pearson Education, Inc.
Insulin Action on Cells
• Activates a tyrosine kinase enzyme receptor
• Cascade leads to increased glucose uptake
and enzymatic activities that
• Catalyze the oxidation of glucose for ATP
production
• Polymerize glucose to form glycogen
• Convert glucose to fat (particularly in adipose
tissue)
Copyright © 2010 Pearson Education, Inc.
Stimulates glucose uptake by cells
Tissue cells
Insulin
Pancreas
Stimulates
glycogen
formation Glucose Glycogen
Blood
glucose
falls to
normal
range.
Liver
Stimulus
Blood
glucose level
Stimulus
Blood
glucose level
Blood
glucose
rises to
normal
range.
Pancreas
Liver
Glucose Glycogen
Stimulates
glycogen Glucagon
breakdown
Copyright © 2010 Pearson Education, Inc.
Figure 16.18
Copyright © 2010 Pearson Education, Inc.
Table 16.4
Other Hormone-Producing Structures
• Kidneys
• Erythropoietin signals production of red blood cells
• Renin initiates the renin-angiotensin mechanism
• Skin
• Cholecalciferol, the precursor of vitamin D
• Adipose tissue
• Leptin is involved in appetite control, and stimulates
increased energy expenditure
Copyright © 2010 Pearson Education, Inc.
Other Hormone-Producing Structures
• Skeleton (osteoblasts)
• Osteocalcin prods pancreatic beta cells to
divide and secrete more insulin, improving
glucose handling and reducing body fat
• Thymus
• Thymulin, thymopoietins, and thymosins are
involved in normal the development of the T
lymphocytes in the immune response
Copyright © 2010 Pearson Education, Inc.
Developmental Aspects
• 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
Copyright © 2010 Pearson Education, Inc.
Developmental Aspects
• Ovaries undergo significant changes with age
and become unresponsive to gonadotropins;
problems associated with estrogen deficiency
begin to occur
• Testosterone also diminishes with age, but
effect is not usually seen until very old age
Copyright © 2010 Pearson Education, Inc.
Developmental Aspects
• GH levels decline with age and this 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 bone-demineralizing
effects of PTH
Copyright © 2010 Pearson Education, Inc.