1. The Endocrine System: Part B

2. Two lateral lobes connected by median mass called isthmus
Thyroid Gland
Two lateral lobes connected by median mass called isthmus
Composed of follicles that produce glycoprotein thyroglobulin
Parafollicular cells produce the hormone calcitonin
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3. Figure 16.9 The thyroid gland.
Hyoid bone
Colloid-filled
follicles
Thyroid cartilage
Epiglottis
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
Photomicrograph of thyroid gland
follicles (145x)
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4. Actually two related compounds
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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5. Major metabolic hormone
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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6. Synthesis of Thyroid Hormone
Thyroid gland stores hormone extracellularly
Thyroglobulin synthesized and discharged into follicle lumen
Iodides (I–) actively taken into cell and released into lumen
Iodide oxidized to iodine (I2),
Iodine attaches to tyrosine, mediated by peroxidase enzymes
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7. Figure 16.10 Synthesis of thyroid hormone.
Slide 1
Thyroid follicular cells
Colloid
Thyroglobulin is synthesized and discharged into the follicle lumen. 1
Tyrosines (part of thyroglobulin
molecule)
Capillary
Iodine is attached to tyrosine in colloid, forming DIT and MIT. 4
Golgi
apparatus
Rough ER
Thyro-
globulin
colloid
Iodine
Iodide is oxidized to iodine. 3
DIT
MIT
Iodide (I−)
Iodide (I–) is trapped (actively transported in). 2 T4
Iodinated tyrosines are linked together to form T3 and T4. 5 T3
Lysosome T4
Thyroglobulin colloid is endocytosed and combined with a lysosome. 6 T3
Lysosomal enzymes cleave T4 and T3 from thyroglobulin and hormones diffuse into bloodstream. 7 T4
Colloid in
lumen of
follicle T3
To peripheral tissues
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8. 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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9. Hypothalamus TRH Anterior pituitary TSH Thyroid gland
Figure Regulation of thyroid hormone secretion.
Hypothalamus
TRH
Anterior pituitary
TSH
Thyroid gland
Thyroid
hormones
Stimulates
Target cells
Inhibits
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10. 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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11. Figure 16.11 Thyroid disorders.
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12. Produced by parafollicular (C) cells
Calcitonin
Produced by parafollicular (C) cells
No known physiological role in humans
Antagonist to parathyroid hormone (PTH)
At higher than normal doses
Inhibits osteoclast activity and release of Ca2+ from bone matrix
Stimulates Ca2+ uptake and incorporation into bone matrix
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13. Four to eight tiny glands embedded in posterior aspect of thyroid
Parathyroid Glands
Four to eight tiny glands embedded in posterior aspect of thyroid
Contain parathyroid cells that secrete parathyroid hormone (PTH) or parathormone
PTH—most important hormone in Ca2+ homeostasis
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14. Capillary Parathyroid cells (secrete parathyroid hormone) Oxyphil
Figure The parathyroid glands.
Pharynx
(posterior
aspect)
Capillary
Parathyroid
cells
(secrete
parathyroid
hormone)
Thyroid
gland
Parathyroid
glands
Esophagus
Oxyphil
cells
Trachea
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15. Negative feedback control: rising Ca2+ in blood inhibits PTH release
Parathyroid Hormone
Functions
Stimulates osteoclasts to digest bone matrix and release Ca2+ to blood
Enhances reabsorption of Ca2+ and secretion of phosphate by kidneys
Promotes activation of vitamin D (by kidneys); increases absorption of Ca2+ by intestinal mucosa
Negative feedback control: rising Ca2+ in blood inhibits PTH release
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16. 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
Result
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17. 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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18. 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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19. Three layers of cortex produce the different corticosteroids
Adrenal Cortex
Three layers of cortex produce the different corticosteroids
Zona glomerulosa—mineralocorticoids
Zona fasciculata—glucocorticoids
Zona reticularis—gonadocorticoids
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20. Figure 16.14 Microscopic structure of the adrenal gland.
Hormones
secreted
Capsule
Zona
glomerulosa
Aldosterone
Zona
fasciculata
Adrenal gland
• Medulla
Cortex
• Cortex
Cortisol
and
androgens
Kidney
Zona
reticularis
Medulla
Adrenal
medulla
Epinephrine
and
norepinephrine
Drawing of the histology of the
adrenal cortex and a portion of
the adrenal medulla
Photomicrograph (115x)
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21. Regulate electrolytes (primarily Na+ and K+) in ECF
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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22. Aldosterone Release triggered by
Decreasing blood volume and blood pressure
Rising blood levels of K+
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23. water; increased K+ excretion
Figure Major mechanisms controlling aldosterone release from the adrenal cortex.
Primary regulators
Other factors
Blood volume
and/or blood
pressure
K+ in blood
Stress
Blood pressure
and/or blood
volume
Hypo-
thalamus
Heart
Kidney
CRH
Direct
stimulating
effect
Anterior
pituitary
Renin
Initiates
cascade
that
produces
ACTH
Atrial natriuretic
peptide (ANP)
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
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24. 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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25. Keep blood glucose levels relatively constant
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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26. 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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27. 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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28. Same patient with Cushing’s syndrome. The white arrow shows
Figure The effects of excess glucocorticoid.
Patient before onset.
Same patient with Cushing’s
syndrome. The white arrow shows
the characteristic “buffalo hump” of
fat on the upper back.
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29. 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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30. 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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31. 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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32. 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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33. Adrenal Medulla Hypersecretion Hyposecretion
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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34. Figure 16.17 Stress and the adrenal gland.
Short-term stress
Prolonged stress
Stress
Nerve impulses
Hypothalamus
CRH (corticotropin-
releasing hormone)
Spinal cord
Corticotropic cells
of anterior pituitary
Preganglionic
sympathetic
fibers
To target in blood
Adrenal cortex
(secretes steroid
hormones)
Adrenal medulla
(secretes amino acid–
based hormones)
ACTH
Catecholamines
(epinephrine and
norepinephrine)
Mineralocorticoids
Glucocorticoids
Short-term stress response
Long-term stress response
• Heart rate increases
• Kidneys retain
sodium and water
• Proteins and fats converted
to glucose or broken down
for energy
• Blood pressure increases
• Bronchioles dilate
• Blood volume and
blood pressure
rise
• Liver converts glycogen to glucose and releases
glucose to blood
• Blood glucose increases
• Immune system
supressed
• Blood flow changes, reducing digestive system activity
and urine output
• Metabolic rate increases
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35. 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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36. Triangular gland partially behind stomach
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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37. Pancreatic islet •  (Glucagon- producing) cells •  (Insulin-
Figure Photomicrograph of differentially stained pancreatic tissue.
Pancreatic islet
•  (Glucagon-
producing)
cells
•  (Insulin-
producing)
cells
Pancreatic acinar
cells (exocrine)
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38. Causes increased blood glucose levels Effects
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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39. Not needed for glucose uptake in liver, kidney or brain
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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40. Insulin Action on Cells
Activates tyrosine kinase enzyme receptor
Cascade  increased glucose uptake
Triggers enzymes to
Catalyze oxidation of glucose for ATP production – first priority
Polymerize glucose to form glycogen
Convert glucose to fat (particularly in adipose tissue)
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41. BALANCE: Normal blood glucose level (about 90 mg/100 ml)
Figure Insulin and glucagon from the pancreas regulate blood glucose levels.
Stimulates glucose
uptake by cells
Insulin
Tissue cells
Stimulates
glycogen
formationw
Pancreas
Glucose
Glycogen
Blood
glucose
falls to
normal
range.
Liver
IMBALANCE
Stimulus
Blood
glucose level
BALANCE: Normal blood glucose level (about 90 mg/100 ml)
Stimulus
Blood
glucose level
IMBALANCE
Blood
glucose
rises to
normal
range.
Pancreas
Glucose
Glycogen
Liver
Stimulates
glycogen
breakdown
Glucagon
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42. Factors That Influence Insulin Release
Elevated blood glucose levels – primary stimulus
Rising blood levels of amino acids and fatty acids
Release of acetylcholine by parasympathetic nerve fibers
Hormones glucagon, epinephrine, growth hormone, thyroxine, glucocorticoids
Somatostatin; sympathetic nervous system
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43. Homeostatic Imbalances of Insulin
Diabetes mellitus (DM)
Due to hyposecretion (type 1) or hypoactivity (type 2) of insulin
Blood glucose levels remain high  nausea  higher blood glucose levels (fight or flight response)
Glycosuria – glucose spilled into urine
Fats used for cellular fuel  lipidemia; if severe  ketones (ketone bodies) from fatty acid metabolism  ketonuria and ketoacidosis
Untreated ketoacidosis  hyperpnea; disrupted heart activity and O2 transport; depression of nervous system  coma and death possible
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44. Diabetes Mellitus: Signs
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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45. Homeostatic Imbalances of Insulin
Hyperinsulinism:
Excessive insulin secretion
Causes hypoglycemia
Low blood glucose levels
Anxiety, nervousness, disorientation, unconsciousness, even death
Treated by sugar ingestion
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46. Table 16.4 Symptoms of Insulin Deficit (Diabetes Mellitus)
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47. Ovaries and Placenta Gonads produce steroid sex hormones
Same as those of adrenal cortex
Ovaries produce estrogens and progesterone
Estrogen
Maturation of reproductive organs
Appearance of secondary sexual characteristics
With progesterone, causes breast development and cyclic changes in uterine mucosa
Placenta secretes estrogens, progesterone, and human chorionic gonadotropin (hCG)
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48. Testes produce testosterone
Initiates maturation of male reproductive organs
Causes appearance of male secondary sexual characteristics and sex drive
Necessary for normal sperm production
Maintains reproductive organs in functional state
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49. 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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50. 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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51. 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-angiotensin-aldosterone mechanism
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52. 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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53. 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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54. 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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55. 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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56. 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 bone-demineralizing effects of PTH
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