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Chapter 18: The Endocrine System

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Title: Chapter 18: The Endocrine System


1
Chapter 18 The Endocrine System
Primary sources for figures and content Marieb,
E. N. Human Anatomy Physiology. 6th ed. San
Francisco Pearson Benjamin Cummings,
2004. Martini, F. H. Fundamentals of Anatomy
Physiology. 6th ed. San Francisco Pearson
Benjamin Cummings, 2004.
2
Endocrine System
  • Regulates long-term processes
  • growth
  • development
  • reproduction

3
Intercellular Communication
  • 1. Direct Communication
  • Occurs between two cells of the same type through
    gap junctions via ions or small solutes
  • 2. Paracrine Communication
  • Uses chemical messengers to transfer signals
    between cells in a single tissue
  • Messenger cytokines or local hormones

4
Intercellular Communication
  • 3. Endocrine Communication
  • Uses hormones to coordinate cellular activities
    in distant portions of the body
  • Hormones chemical messengers released from one
    tissue and transported in blood to reach target
    cells in other tissues
  • Gradual, coordinated but not immediate
  • 4. Synaptic Communication
  • Involves neurons releasing neurotransmitter at a
    synapse close to target
  • Immediate but short lived

5
Mechanisms of Intercellular Communication
Table 181
6
The Endocrine System
  • Consists of glands and glandular tissue involved
    in paracrine and endocrine communication
  • Endocrine cells produce secretions ? released
    into extracellular fluid ? enters blood ?
    body-wide distribution to find target
  • Target cell specific cells that possess
    receptors needed to bind and read hormonal
    messages

7
Endocrine System
Endocrine Cells located In
Figure 181
8
Hormones
  • Can be divided into 3 groups
  • amino acid derivatives
  • peptide hormones
  • lipid derivatives

9
Hormones
  • Structure
  • 1. Amino Acid Derivatives
  • Structurally similar to or based on amino acids
  • E.g. catecholamines (epinephrine, norepinephrine,
    dopamine), thyroid hormones, melatonin

10
Hormones
  • Structure
  • 2. Peptide Hormones
  • Chains of amino acids
  • A. Peptides
  • lt200 amino acids
  • E.g. ADH, oxytocin, GH
  • B. Glycoproteins
  • gt200 amino acids with carbohydrate side chain
  • E.g. TSH

11
Hormones
  • Structure
  • 3. Lipid Derivatives
  • A. Steroid Hormones
  • Structurally similar to/based on cholesterol
  • E.g. Androgens, Estrogens, Calcitriol
  • B. Eicosanoids
  • Derived from arachidonic acid
  • Not circulating autocrine or paracrine only
  • E.g. Leukotrienes from leukocytes ? coordinate
    inflammation
  • E.g. Prostaglandins from mast cells ? coordinate
    local activities (smooth muscle contractions,
    clotting, etc.)

12
Classes of Hormones
Figure 182
13
Mechanism of Action
  • Hormones circulate in blood ? contact all cells
  • Only cause effects in cells with receptors for
    hormone ? called target cells
  • Receptors present on a cell determines the cells
    hormonal sensitivity

14
Hormone stimulus effects in target cells
  1. Alter plasma membrane permeability or
    transmembrane potential by opening/closing ion
    channels
  2. Stimulate synthesis of ? structural proteins,
    receptors, regulatory enzymes within cell
  3. Activate or deactivate enzymes
  4. Induce secretory activity
  5. Stimulate mitosis

15
Hormone Receptors
  • Located on plasma membrane or inside target
  • Cell membrane hormone receptors
  • Intracellular hormone receptors

16
Hormone Receptors
  • 1. Cell membrane hormone receptors
  • Catecholamines, peptide hormones, glycoprotein
    hormones, eicosanoids
  • Bind receptors on cell surface
  • Indirectly trigger events inside cell via second
    messengers (cAMP, Ca)
  • 2nd messenger acts as activator, inhibitor, or
    cofactor for intracellular enzymes
  • Enzymes catalyze reactions for cell changes
  • Receptor linked to 2nd messenger by G protein
    (regulatory enzyme complex)

17
Hormone Receptors
  • 1. Cell membrane hormone receptors
  • 2nd messenger mechanism results in amplification
    of hormone signals
  • One hormone molecule binds one receptor but can
    result in millions of final products

18
G Proteins and Hormone Activity
  • cAMP Mechanism
  • Hormone binds receptor
  • G-protein activated
  • Adenylate cyclase activated
  • ATP ? cAMP
  • Kinases activated
  • Proteins (enzymes) phosphorylated
  • Enzymes activated/deactivated

Figure 183
19
G Proteins and Hormone Activity
  • PIP-Calcium Mechanism
  • Hormone binds receptor
  • G-protein activated
  • Phospholipase C (PLC) activated
  • Phospholipids (PIP2) cleaved into diacyglycerol
    (DAG) and inositol triphosphate (IP3)
  • DAG opens Ca channels on membrane
  • IP3 releases Ca from ER
  • Calcium binds calmodulin
  • Enzymes Activated

Figure 183
20
Hormone Receptors
  • 2. Intracellular hormone receptors
  • Steroid hormones, thyroid hormones
  • Result in direct gene activation by hormone
  • Hormone diffuses across membrane, binds receptors
    in cytoplasm or nucleus
  • Hormone receptor bind DNA ? transcription ?
    translation protein production ? metabolic
    enzymes, structural proteins, secretions

21
Steroid Hormones
Thyroid Hormones
Figure 184a
Figure 184b
22
Target cell activation depends on
  • 1. Blood level of hormone
  • 2. Relative number of receptors
  • 3. Affinity of bond between hormone and receptor
  • If hormone levels are excessively high for too
    long ? cells can reduce receptor number or
    affinity and become ? non-responsive to a hormone

23
Distribution and Duration of Hormones
  • Circulating hormones either free or bound to
    carrier/transport proteins
  • Free hormones last seconds to minutes
  • Rapidly broken down by liver, kidney, or plasma
    enzymes in blood
  • Bound hormones last hours to days in blood
  • Effect at target cell can take seconds to days
    depending on mechanism and final effect, but
    hormone once bound to receptor is broken down
    quickly

24
Interaction of Hormones at Target Cells
  • Target cells have receptors for multiple hormones
  • Effects of one hormone can be different depending
    on presence or absence of other hormones
  • Hormone Interactions
  • Antagonistic hormones oppose each other
  • Synergistic hormones have additive effects
  • Permissive one hormone is needed for the other
    to cause its effect

25
Control of Endocrine Activity
  • Synthesis and release of most hormones regulated
    by negative feedback

26
Control of Endocrine Activity
  • 3 Major Stimuli for Hormone Release
  • 1. Hormonal stimuli
  • Ion and nutrient levels in blood trigger release
  • E.g. PTH released when blood Ca is low
  • 2. Neural stimuli (autonomic nervous system)
  • Nerve fibers directly stimulate release
  • E.g. sympathetic ? adrenal medulla epinephrine
    release

27
Control of Endocrine Activity
  • 3 Major Stimuli for Hormone Release
  • 3. Hormonal stimuli
  • Hormones stimulate the release of other hormones
  • E.g. Releasing hormones of hypothalamus cause
    release of hormones from anterior pituitary
  • Hormone release turned on by stimuli and off by
    negative feedback but can be modified by nervous
    system

28
KEY CONCEPT
  • Hormones coordinate cell, tissue, and organ
    activities
  • Circulate in extracellular fluid and bind to
    specific receptors
  • Hormones modify cellular activities by
  • altering membrane permeability
  • activating or inactivating key enzymes
  • changing genetic activity

29
How could you distinguish between a neural
response and an endocrine response on the basis
of response time and duration?
  1. Neural responses are quicker and longer lasting.
  2. Neural responses are slower and longer lasting.
  3. Neural responses are quicker and shorter in
    duration.
  4. Neural responses are slower and shorter in
    duration.

30
How would the presence of a molecule that blocks
adenylate cyclase affect the activity of a
hormone that produces its cellular effects by way
of the second messenger cAMP?
  1. It would block the action of the hormone.
  2. It would enhance the action of the hormone.
  3. It would increase sensitivity to the hormone.
  4. It would decrease speed of hormonal changes.

31
What primary factor determines each cells
hormonal sensitivities?
  1. pH of intracellular fluid
  2. life cycle phase of cell
  3. presence/absence of necessary receptor complex
  4. tissue where cell is found

32
Endocrine Organs
33
1. Hypothalamus
Figure 185
34
1. Hypothalamus
  • Located at base of 3rd ventricle
  • Master regulatory organ
  • Integrates nervous and endocrine systems
  • Three mechanisms of control
  • Secrete regulatory hormones to control secretion
    from anterior pituitary
  • - Hormones from anterior pituitary control other
    endocrine organs
  • Act as endocrine organ ? Produce ADH and oxytocin
  • Has autonomic centers of neural control or
    adrenal medulla ? Neuroendocrine reflex

35
2. Pituitary Gland
Figure 186
36
2. Pituitary Gland (Hypophysis)
  • Hangs inferior to hypothalamus via infundibulum
  • In sella turcica of sphenoid
  • Anterior lobe secretes 7 hormones
  • Function via cAMP 2nd messenger
  • Posterior lobe secretes 2 hormones
  • Function via cAMP 2nd messenger

37
2. Pituitary Gland
Figure 187
38
2. Pituitary Gland
  • A. Anterior lobe (Adenohypophysis)
  • Glandular tissue
  • Anterior pituitary hormones are all tropic
    hormones
  • Turn on secretion or support function of other
    organs
  • Secretion of the hormones controlled by releasing
    and inhibiting hormones from the hypothalamus

39
2. Pituitary Gland
  • A. Anterior lobe (Adenohypophysis)
  • Hormones of the Anterior Lobe

40
2. Pituitary Gland
  • A. Anterior lobe (Adenohypophysis)
  • Disease of Growth Hormone
  • Excess
  • Usually due to pituitary tumor
  • Before epiphyseal closure gigantism
  • After acromegaly, excessive growth of hands,
    feet, face, internal organs
  • Deficiency
  • Pituitary dwarfism failure to thrive

41
2. Pituitary Gland
  • B. Posterior lobe (Neurohypophysis)
  • Neural tissue
  • Contains axons of hypothalamus
  • Release hormones to posterior lobe for storage
  • Hormones release by Posterior Lobe

42
The Hormones of the Pituitary Gland
Figure 189
43
Hypothalamas and Anterior Lobe
  • Rate of secretion is controlled by negative
    feedback
  • Hormones turn on endocrine glands or support
    other organs

Figure 188a
44
Prolactin (PRL)
Figure 188b
45
Hormones
  • Releasing Hormones (RH)
  • Stimulate synthesis and secretion of 1 or more
    hormones at anterior lobe
  • Inhibiting Hormones (IH)
  • Prevent synthesis and secretion of hormones from
    anterior lobe

46
KEY CONCEPT
  • Hypothalamus produces regulatory factors that
    adjust activities of anterior lobe of pituitary
    gland, which produces 7 hormones
  • Most hormones control other endocrine organs,
    including thyroid gland, adrenal gland, and
    gonads

47
KEY CONCEPT
  • Anterior lobe produces growth hormone, which
    stimulates cell growth and protein synthesis
  • Posterior lobe of pituitary gland releases 2
    hormones produced in hypothalamus
  • ADH restricts water loss and promotes thirst
  • oxytocin stimulates smooth muscle contractions
    in
  • mammary glands
  • uterus
  • prostate gland

48
If a person were dehydrated, how would the level
of ADH released by the posterior lobe change?
  1. More ADH is released.
  2. Less ADH is released.
  3. It would not change at all.
  4. Initially ADH would decrease, then increase until
    hydration is restored.

49
A blood sample shows elevated levels of
somatomedins. Which pituitary hormone would you
expect to be elevated as well?
  1. thyroid stimulating hormone
  2. growth hormone
  3. oxytocin
  4. adrenocorticotropic hormone

50
What effect would elevated circulating levels of
cortisol, a steroid hormone from the adrenal
cortex, have on the pituitary secretion of ACTH?
  1. ACTH levels would slowly rise.
  2. ACTH levels would increase rapidly.
  3. ACTH levels would decrease.
  4. ACTH levels would remain the same.

51
3. Thyroid Gland
Figure 1810a, b
52
3. Thyroid Gland
  • Inferior to larynx
  • Left and right lobes connected by isthmus
  • Largest pure endocrine organ
  • Tissue
  • 1. Follicles ? Spheres or simple cuboidal
    epithelium
  • 2. Parafollicular cells/C cells between follicles
  • Follicles filled with colloid ? thyroglobulin
  • Thyroglobulin protein constantly synthesized by
    follicle cells and exocytosed into follicle for
    storage
  • Upon stimulation by TSH, thyroglobulin is
    processed into thyroid hormones (T3/T4)

53
Formation and Release of Thyroid Hormones
54
Thyroid Follicles
Figure 1811a, b
55
3. Thyroid Gland
  • Receptors for thyroid hormones located in all
    cells except
  • Adult brain, spleen, testes, uterus, thyroid
  • 3 receptors in target cells
  • Cytoplasm hold hormone in reserve
  • Mitochondria increase cellular respiration
  • Nucleus activate genes for enzymes involved in
    energy transformation and utilization

56
3. Thyroid Gland
  • Overall effect of thyroid hormones
  • Increase metabolic rate and body heat production
  • Regulate tissue growth and development
  • 1. Hypothyroidism ? lack of T3/T4
  • A. Myxedema (adults)
  • Low body temp, muscle weakness, slow reflexes,
    cognitive dysfunction and goiters ? swollen
    thyroid
  • Produce thyroglobulin but fail to endocytose
  • B. Cretinism (infants) Genetic defect
  • Causes lack of skeletal and nervous system
    development

57
3. Thyroid Gland
  • 2. Hyperthyroidism ? excessive T3/T4
  • High metabolic rate, high heart rate,
    restlessness, fatigue
  • 3. Graves Disease
  • Autoimmune disorder
  • Produce antibodies that mimic TSH causing
    overproduction of thyroid hormones

58
3. Thyroid Gland
  • Parafollicular cells/C cells
  • in basement membrane of follicles
  • Produce Calcitonin
  • Calcitonin stimulates decrease in blood calcium
    levels
  • Inhibits osteoclasts
  • Promotes Ca loss at kidneys
  • Parafollicular cells respond directly to blood
    calcium levels, not controlled by hypothalamus
  • Ca 20 above normal calcitonin release

59
3. Thyroid Gland
Figure 1810c
60
Rate of Thyroid Hormone Release
  • Major factor
  • TSH concentration in circulating blood

Figure 1811b
61
Thyroid Gland
Table 183
62
Iodide Ions
  • Are actively transported into thyroid follicle
    cells
  • stimulated by TSH
  • Reserves in thyroid follicles
  • Excess removed from blood at kidneys
  • Deficiency limits rate of thyroid hormone
    production

63
5. Parathyroid Glands
  • Four glands embedded in posterior surface of
    thyroid gland

Figure 1812
64
5. Parathyroid Gland
  • Two cell types
  • Oxyphiles few, functions unknown
  • Chief Cells majority
  • Produce Parathyroid hormone (PTH)/Parathormone
  • Most important regulator of blood calcium
  • Secreted when blood calcium is low
  • Acts to raise blood calcium levels by acting on
    various tissues
  • 1. Bone ? stimulates osteoclasts and inhibits
    osteoblasts
  • 2. Kidney ? enhances reabsorption of Ca
  • 3. Intestines ? promotes conversion of Vit. D to
    calcitriol in kidney to enhance Ca and PO43-
    absorption in small intestine

65
4 Effects of PTH
  1. It enhances reabsorption of Ca2 at kidneys,
    reducing urinary loss
  2. It stimulates formation and secretion of
    calcitriol at kidneys

66
Parathyroid Glands
  • Primary regulators of blood calcium I levels in
    adults

Figure 1813
67
Parathyroid Glands
Table 184
68
KEY CONCEPT
  • Thyroid gland produces
  • hormones that adjust tissue metabolic rates
  • a hormone that usually plays minor role in
    calcium ion homeostasis by opposing action of
    parathyroid hormone

69
What symptoms would you expect to see in an
individual whose diet lacks iodine?
  1. increased rate of metabolism
  2. increased body temperature
  3. rapid response to physiological stress
  4. goiter

70
When a persons thyroid gland is removed, signs
of decreased thyroid hormone concentration do not
appear until about one week later. Why?
  1. Thyroid hormone is produced by other endocrine
    glands.
  2. Thyroid hormone remains in circulation for 14
    days.
  3. Thyroid-binding globulins provide thryoxine
    reservoirs.
  4. Thyroid hormone is used slowly.

71
The removal of the parathyroid glands would
result in a decrease in the blood concentration
of which important mineral?
  1. calcium ions
  2. phosphate ions
  3. sodium ions
  4. potassium ions

72
What effect would elevated cortisol levels have
on the level of glucose in the blood?
  1. increased glucose
  2. decreased glucose
  3. modulated glucose around homeostatic optimum
  4. dramatic increase of glucose, then a crash

73
6. Adrenal Glands
Figure 1814
74
6. Adrenal Gland
  • 2 glands, in renal fascia, superior to kidney
  • Glandular adrenal cortex
  • Medulla mostly nervous tissue
  • In general ? adrenal hormones are used to cope
    with stressors

75
6. Adrenal Glands
  • A. Adrenal Cortex
  • Produces 24 corticosteriods
  • In target alter gene transcription to affect
    metabolism
  • Glandular
  • 3 layers
  • zona glomerulosa
  • zona fasciculate
  • zona reticularis

76
6. Adrenal Glands
  • Adrenal Cortex
  • Zona glomerulosa ? Mineralcorticoids
  • Control water and electrolyte balance
  • 95 Aldosterone
  • Stimulates Na retention and K loss
  • Released in response to
  • Low Na or high K
  • Angiotension mechanism
  • Low blood pressure or volume
  • Excessive ACTH

77
6. Adrenal Glands
  • Adrenal Cortex
  • Zona fasciculate ? glucocorticoids
  • Metabolic hormones
  • Control glucose metabolism
  • Most common cortisol, hydrocortisone
  • Secretion controlled by ACTH
  • Effects ?
  • gluconeogenesis in liver
  • release of fatty acid from adipose
  • triggers protein hydrolysis to release free amino
    acids from skeletal muscle
  • triggers body cells to utilize fatty acids and
    amino acids instead of glucose
  • Excess ? anti-inflammatory, inhibit immune
    response and healing

78
6. Adrenal Glands
  • Adrenal Cortex
  • 3. Zona reticularis ? gonadocorticoids
  • Mostly androgens, may aid onset of puberty
  • Excess androgenital syndrome

79
Adrenal Cortex
Table 185
80
6. Adrenal Glands
  • Adrenal Cortex Diseases that affect the
    cortex
  • 1. Cushings Syndrome
  • Excessive corticosteroids ?
  • increase ACTH from pituitary tumor
  • Results in ?
  • hyperglycemia, decr. Muscle and bone mass,
    hypertension, edema, poor healing, chronic
    infections
  • 2. Addisons Disease
  • Deficient in corticosteroids
  • Results in ?
  • Weight loss, hyopglycemia, decr. Na, incr. K in
    plasma, dehydration, hypotension

81
6. Adrenal Glands
  • B. Adrenal Medulla
  • Neural, produces catecholamines to enhance
    effects of other adrenal hormones
  • Modified ganglionic sympathetic neurons called
    chromaffin cells release ? epinephrine (80) and
    norepinephrine (20) in response to sympathetic
    stimulation
  • Epinephrine effects
  • Stimulate heart
  • Stimulate metabolic activities ?
  • Skeletal muscle mobilize glucogen reserves,
    accelerate ATP production
  • Adipose promote release of fatty acids
  • Liver promotes release of glucose

82
KEY CONCEPT
  • Adrenal glands produce hormones that adjust
    metabolic activities at specific sites
  • Affects either pattern of nutrient utilization,
    mineral ion balance, or rate of energy
    consumption by active tissues

83
6. Pancreas
Figure 1815
84
6. Pancreas
  • Inferior and posterior to stomach
  • Mostly exocrine cells ? pancreatic acini
  • Secrete digestive enzymes
  • 1 endocrine ? pancreatic islets

85
6. Pancreas
  • Pancreatic Islets cell types
  • 1. Alpha cells ? glucagon ? increase blood
    glucose
  • 2. Beta cells ? insulin ? decrease blood glucose
  • 3. Delta cells ? somatostatin ?
  • Suppresses glucagon and insulin release
  • Slows enzyme release into intestines
  • 4. F cells ? pancreatic polypeptide ?
  • Regulates production of pancreatic enzymes

86
6. Pancreas
  • Insulin
  • Secreted in response to high blood glucose or ANS
  • Parasympathetic incr. insulin
  • Sympathetic decr. Insulin
  • Effect only on insulin dependent cells (have
    receptors)
  • Brain, kidney, GI mucosa, and RBCs
  • ALL INSULIN DEPENDENT

87
5 Effects of Insulin
  1. Accelerates glucose uptake
  2. Accelerates glucose utilization and enhanced ATP
    production
  3. Stimulates glycogen formation
  4. Stimulates amino acid absorption and protein
    synthesis
  5. Stimulates triglyceride formation in adipose
    tissue

88
6. Pancreas
  • Diabetes mellitus ? too much glucose in blood
    (hyperglycemia)
  • Type I ? failure to produce insulin
  • Type II ? insulin resistance, sometimes insulin
    deficiency
  • Cells can not utilize glucose ? ketone bodies
    produced ? too many ketone bodies lead to
    ketoacidosis
  • Glucagon
  • Secreted in response to low blood glucose or
    sympathetic stimulation

89
3 Effects of Glucagons
  1. Stimulates breakdown of glycogen in skeletal
    muscle and liver cells
  2. Stimulates breakdown of triglycerides in adipose
    tissue
  3. Stimulates production of glucose in liver

90
Insulin and Glucagon Effects
Figure 1816
91
Pancreatic Islets
Table 186
92
KEY CONCEPT
  • Pancreatic islets release insulin and glucagons
  • Insulin is released when blood glucose levels
    rise
  • Stimulates glucose transport into, and
    utilization by, peripheral tissues
  • Glucagon released when blood glucose levels
    decline
  • Stimulates glycogen breakdown, glucose synthesis,
    and fatty acid release

93
7. Pineal Gland
  • Posterior of third ventricle
  • Pinealocytes
  • Synthesize melatonin from serotonin
  • Secretion on diurnal cycle
  • High at night, low during dayligh
  • Melatonin functions
  • 1. Play role in timing of sexual maturation
  • 2. Antioxidant ? free radical protection
  • 3. Sets circadian rhythms

94
Why does a person with Type 1 or Type 2 diabetes
urinate frequently and have a pronounced thirst?
  1. Glucose in the blood inhibits ADH release.
  2. Sugar in the urine prevents kidneys from
    reabsorbing water.
  3. High blood sugar dehydrates the tissues of the
    mouth.
  4. Blood sugar elevates blood volume, increasing
    urine output.

95
What effect would increased levels of glucagon
have on the amount of glycogen stored in the
liver?
  1. increased glycogen
  2. decreased glycogen
  3. no effect
  4. rapid increase of glycogen, with a slow return to
    homeostasis

96
Increased amounts of light would inhibit the
production of which hormone?
  1. prolactin
  2. melanocyte stimulating hormone
  3. aldosterone
  4. melatonin

97
Hormones Produced by Specific Organs
Table 187
98
8. Gastrointestinal Tract
  • Enteroendorine cells in GI mucosa secrete many
    hormones ? coordinate digestive activity
  • Mostly paracrine communication
  • Cholecystokinin
  • Enterocrinin
  • Gastric inhibitory peptide
  • Gastrin
  • Secretin
  • Vasoactive intestinal peptide

99
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100
9. Kidneys
  • Various endocrine cells
  • Three products
  • 1. Calcitrol ? Steroid hormone
  • Stimulate Ca, PO43- absorption in GI
  • Stimulate osteoclast activity
  • Stimulate Ca retention in kidney
  • Suppress PTH production
  • 2. Erythropoeitin ? Peptide hormone
  • Released in response to low O2 in kidney
  • 3. Renin ? Enzyme

101
9. Kidneys
  • Three products
  • 3. Renin ? Enzyme
  • Released in response to sympathetic stimulation
    or decline in renal blood flow
  • Converts angiotensin in blood into Angiotensin II
    (hormone)
  • Angiotensin II effects
  • Stimulate secretion of aldosterone ? adrenal
  • Stimulate secretion of ADH ? pituitary
  • Stimulate thirst
  • Elevate BP
  • Both aldosterone and ADH ? restrict Na and H2O
    loss at kidney

102
Calcitriol
  • Stimulates calcium and phosphate ion absorption
    along digestive tract

Figure 1817a
103
The ReninAngiotensin System
Figure 1817b
104
10. Heart
  • Some cells of atrial walls secrete Atrial
    Natriuretic Peptide in response to stretch
  • ANP promotes Na and water loss at kidney
  • Inhibits release of renin, ADH, and aldosterone ?
    reduce BP and volume

105
11. Thymus
  • Located deep to sternum
  • Cell produces thymosin hormones
  • Promote development and maturation of T
    lymphocytes and the immune response

106
12. Gonads
  • A. Testes ? male
  • Interstitial cells produce androgens in response
    to LH
  • Testosterone, most common
  • Produces male secondary sex characteristics
  • Promotes sperm production
  • Maintains secretory glands

107
12. Gonads
  • B. Ovaries ? Female
  • Follicle cells produce estrogens in response to
    FSH and LH
  • Estradiol, most important
  • Produce female secondary sex characteristics
  • Support maturation of oocytes
  • Stimulate growth of uterine lining
  • Surge in LH causes
  • Ovulation
  • Follicle reorganizes to form corpus luteum
  • Produces estrogens and progestins, especially
    progesterone

108
12. Gonads
  • B. Ovaries ? Female
  • Progesterone, most important
  • Prepares uterus for embryo growth
  • Accelerates movement of oocyte/embryo to uterus
  • Enlargement of mammary glands

109
13. Adipose
  • 1. Leptin secretion
  • in response to absorption of glucose and lipids
  • Triggers satiation in appetite center of
    hypothalamus
  • controls normal levels of GnRH, gonadotropin
    synthesis
  • 2. Resistin secretion
  • Reduces insulin sensitivity

110
Hormones interact to produce coordinated
physiological responses.
111
Hormone Interactions
  • Antagonistic (opposing) effects
  • Synergistic (additive) effects
  • Permissive effects
  • 1 hormone is necessary for another to produce
    effect
  • Integrative effects
  • hormones produce different and complementary
    results

112
Hormones Important to Growth
  1. GH
  2. Thyroid hormones
  3. Insulin
  4. PTH
  5. Calcitriol
  6. Reproductive hormones

113
Growth Hormone (GH)
  • In children
  • supports muscular and skeletal development
  • In adults
  • maintains normal blood glucose concentrations
  • mobilizes lipid reserves

114
Thyroid Hormones
  • If absent during fetal development or for first
    year
  • nervous system fails to develop normally
  • mental retardation results
  • If T4 concentrations decline before puberty
  • normal skeletal development will not continue

115
Insulin
  • Allows passage of glucose and amino acids across
    cell membranes

116
Parathyroid Hormone (PTH) and Calcitriol
  • Promote absorption of calcium salts for
    deposition in bone
  • Inadequate levels causes weak and flexible bones

117
Reproductive Hormones
  • Androgens in males, estrogens in females
  • Stimulate cell growth and differentiation in
    target tissues
  • Produce gender-related differences in
  • skeletal proportions
  • secondary sex characteristics

118
Insulin lowers the level of glucose in the blood,
and then glucagon causes glucose levels to rise.
What is this type of hormonal interaction called?
  1. additive
  2. antagonism
  3. permissive
  4. integrative

119
The lack of which hormones would inhibit skeletal
formation?
  1. GH, thyroid hormone, PTH, gonadal hormones
  2. prolactin, FSH, LH, GH
  3. thyroid hormone, melatonin, PTH, calcitonin
  4. GH, TSH, ACTH, FSH

120
Why do levels of GH-RH and CRH rise during the
resistance phase of the general adaptation
syndrome?
  1. to bolster immune response
  2. to decrease excess blood volume
  3. to increase needed supplies of blood glucose
  4. to heighten sensory perceptions

121
Generaladaptation syndrome.
122
General Adaptation Syndrome (GAS)
  • Also called stress response
  • How bodies respond to stress-causing factors

Figure 1818
123
General Adaptation Syndrome (GAS)
  • Is divided into 3 phases
  • alarm phase
  • resistance phase
  • exhaustion phase

124
Alarm Phase
  • Is an immediate response to stress
  • Is directed by ANS
  • Energy reserves mobilized (glucose)
  • Fight or flight responses
  • Dominant hormone is epinephrine

125
7 Characteristics of Alarm Phase
  • Increased mental alertness
  • Increased energy consumption
  • Mobilization of energy reserves (glycogen and
    lipids)
  • Circulation changes
  • increased blood flow to skeletal muscles
  • decreased blood flow to skin, kidneys, and
    digestive organs
  • Drastic reduction in digestion and urine
    production
  • Increased sweat gland secretion
  • Increases in blood pressure, heart rate, and
    respiratory rate

126
Resistance Phase
  • Entered if stress lasts longer than few hours
  • Dominant hormones are glucocorticoids
  • Energy demands remain high
  • Glycogen reserves nearly exhausted after several
    hours of stress

127
Effects of Resistance Phase
  1. Mobilize remaining lipid and protein reserves
  2. Conserve glucose for neural tissues
  3. Elevate and stabilize blood glucose
    concentrations
  4. Conserve salts, water, and loss of K, H

128
Exhaustion Phase
  • Begins when homeostatic regulation breaks down
  • Failure of 1 or more organ systems will prove
    fatal
  • Mineral imbalance

129
Aging Related Changes
  • Very little change in most hormone levels
  • Adverse effects due to changes in target tissue
  • Prevent reception or response to hormone
  • Gonads decrease in size and hormone production

130
Review Endocrine System
  • Provides long-term regulation and adjustments of
    homeostatic mechanisms
  • fluid and electrolyte balance
  • cell and tissue metabolism
  • growth and development
  • reproductive functions
  • assists nervous system response to stressful
    stimuli through general adaptation syndrome

131
SUMMARY
  • Paracrine communication
  • Endocrine communication
  • Classes of hormones
  • amino acid derivatives
  • peptide hormones
  • lipid derivatives, including steroid hormones and
    eicosanoids
  • Secretion and distribution of hormones
  • Endocrine reflexes
  • Hypothalamus regulation of the endocrine system
  • The pituitary gland
  • the anterior lobe
  • the posterior lobe

132
SUMMARY
  • Releasing hormones
  • Inhibiting hormones
  • The thyroid gland
  • thyroid follicles
  • thyroid hormones
  • The parathyroid glands
  • The adrenal glands
  • the adrenal cortex and adrenal medulla
  • The pineal gland
  • The pancreas
  • the pancreatic islets
  • insulin and glucagons

133
SUMMARY
  • Endocrine tissues in other systems
  • Hormonal interaction
  • Role of hormones in growth
  • Hormonal response to stress
  • Effects of hormones on behavior
  • Effects of aging on hormone production
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