endocrine syetem
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THE ENDOCRINE SYSTEM
Karen Marshall, Associate Professor
Montgomery College
Takoma Park Campus
2/10/2003 2
Endocrine System (ES)
? interacts with nervous system (NS) tocoordinate and integrate body cellactivity
? endocrinology
scientific study of hormones and endocrine
organs
2/10/2003 3
Control of Body Functioning
? NS
? regulate activity of
muscles and glands
via electrochemical
imupulses vianeurons
? organ response time
ms
? ES
? regulate cell activity
via hormones
chemical messengers
released in blood andtransported in body
? tissue and organ
response time
lag period (s or days)
more prolonged
2/10/2003 4
Hormonal Effects
?widespread? diverse
?most body cells
? control and integrate
2/10/2003 5
Hormonal Effects
?major processes
reproduction
growth & development
body defenses mobilization
blood electrolytes, H2O, nutrient balance
maintainence
cellular metabolism regulation
energy balance
2/10/2003 6
Glands
? endocrine~ductless
lack ducts
release hormonesinto surroundingtissue
rich vascular andlymphatic drainage
? exocrine
have ducts
more numerous
secrete productsonto skin or into
body cavities examples
mucous, sweat, oil,salivary, liver
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Major Endocrine Glands
? pituitary
? thyroid
? parathyroid
? hypothalamus (neuroendocrine)
? adrenal
? pineal
? thymus
? pancreas
? gonads
2/10/2003 8
Major Endocrine Glands (fig 17.4)
2/10/2003 9
Hormone Chemical Groups
? two group classification
? amino acid-based
? steroids
2/10/2003 10
Hormone Chemical Groups
?
amino acid-based majority of hormones
molecule size varies
simple to long polymers
2/10/2003 11
Hormone Chemical Groups
? steroids
synthesized from cholesterol
examples
only gonadal and adrenocortical hormones
2/10/2003 12
Target Cell
? cell capable of responding to a hormonebecause it bears receptors to which ahormone can bind
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Mechanisms of Hormone Action
? alter cell activity? cellular processes
increase or decrease in rate
? response
dependent on target cell type
2/10/2003 14
Target Cells
? respond to a hormone
? bear receptors
? changed by a hormone via stimulus
? five ways
2/10/2003 15
Target Cells
? five ways
change in MP or electrical state
enzyme synthesis
enzyme activation or inhibition
secretory activity gene activation
2/10/2003 16
Mechanisms of Hormone Receptor
Binding
? amino acid-based hormones
G proteins (regulatory molecules)
? second messenger systems
steroids with gene activation
2/10/2003 17
Target Cell Specificity Response ~
Hormone-Receptor Binding
? protein receptors
specific
location
target cell PM
interior
response
hormone binding
performance
preprogrammed function
?
*hormones ~molecular triggers
2/10/2003 18
Target Cell Activation
? three dependent factors (=)
blood levels (hormonal)
# of receptors (hormone)
affinity (strength) of H-R bond
? crucial 1st step
H-R binding
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Target Cell Phenomena
?
up-regulation formation of additional receptors
blood hormonal levels
greater target cell response to stimulation
? down-regulation
prolonged [high hormone] desensitization
loss of hormonal receptors
less target cell response to stimulation
2/10/2003 20
Target Cell Phenomena
? # and affinity of other receptors
respond to other hormones
example
progesterone
induces estrogen receptor loss (uterus)
antagonizes estrogens effects
estrogen
cause progesterone receptor production (same cells)
enhances response to progesterone
2/10/2003 21
Hormonal Inactivation and Removal
? effects exerted at low [hormonal]
indicative
rate of release
speed of inactivation and removal
rapid enzymatic degradation target cells
some hormones
kidney & liver enzyme removal
product excretion [urine (primarily) or feces]
most hormones
2/10/2003 22
Half-Life
? persistence of hormone (blood)? brief
a fraction of a minute ~ 30 min
2/10/2003 23
Time and Hormonal Effects
? target cell reponse varies
? almost immediately
? hours to days (steroids)
inactive form (pro-hormone)
secreted
activated by target cell
example
testosterone
2/10/2003 24
Duration of Hormone Action
? limited
20 min to several hours
? effects
disappear rapidly
with decreasing blood levels
persist for hours
after low levels reached
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Hormone Synthesis and Release
? regulated by negative feedback system? internal or external stimulus
triggers hormone secretion
? hormone levels target organeffects hormone release
2/10/2003 26
Negative vs. Positive
Feedback Mechanisms
? negative feedback
original stimulus
contributes to homeostasis
ex. glucose blood levels
2/10/2003 27
Negative vs. Positive
Feedback Mechanisms
? positive feedback
initial stimulus
enhances hormonal response
rarely contributes to homeostasis ex. blood clotting
2/10/2003 28
Feedback Mechanisms (fig 1.4)
2/10/2003 29
Negative Feedback (fig 1.5)
2/10/2003 30
Positive Feedback (fig 1.6)
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2/10/2003 31
Control (Regulation) of Hormone
Release
? three major types of stimuli humoral
neural
hormonal
result in:
endocrine organ activation
hormonal manufacture and release
2/10/2003 32
Humoral Stimuli
? hormonal secretion
direct response to changing blood levels
ions, nutrients
? simplest control system
? examples
insulin production (pancreas)
aldosterone production (adrenal cortex)
2/10/2003 33
Neural Stimuli
? hormonal release
response to nerve fiber stimulation
? examples
oxytocin release (hypothalamus)
ADH release (hypothalamus)
SNS stimulation
epi and nor release (adrenal medulla)
stress
2/10/2003 34
Hormonal Stimuli
? hormonal release
response to hormones produced by other
endocrine organs
? example
ant pit
regulated by hypothalamus
hormones stimulate other endocrine organs torelease hormones
blood hormonal levels inhibition pithormones and final target hormone release
hypothalamic-pituitary-target endocrine organ
feedback loop
2/10/2003 35
Hypothalamic-Pituitary-Target Endocrine Organ
Feedback Loop
? promotes rhythmic hormone release
? ing and ing hormone blood levels
? some endocrine organs respond tomultiple stimuli
2/10/2003 36
Hypothalamic-Pituitary-Target Endocrine Organ
Relationship (fig 17.5)
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2/10/2003 37
Endocrine Gland Stimuli (fig 17.3)
2/10/2003 38
Hormones
? ~ 14 required
? description
? producing organ
? primary body effect
? secretion regulation
? other hormonal influences
? source of regulating hormones
2/10/2003 39
Major Endocrine Organ - Pituitary Gland
(Hypophysis)
? secretes ~ 9 major hormones
? size and shape of pea
? pea on a stalk
funnel-shaped infundibulum connection to hypothalamus superiorly
? two major lobes
anterior (glandular tissue)
posterior (neural tissue)
2/10/2003 40
Posterior Lobe
?
aka neurohypophysis consists of lobe and infundibulum
? composed of pituicytes (glia-like supporting cells)and nerve fibers
? releases neurohormones produced inhypothalamus
? hormone storage area
not true endocrine gland
2/10/2003 41
Anterior Lobe
? aka adenohypophysis
? composed of glandular tissue
?manufactures and releases a number of hormones
?master endocr ine gland
? regulates activity of other endocrineglands
? 6 distinc t hormones known specific physiological actions
proteins
2/10/2003 42
Tropic Hormone (Tropins)
? regulate secretory action of otherendocrine glands
? example
four of the six adenophyophysealhormones
thyroid stimulating hormone (TSH)
adrenocorticotrophic hormone (ACTH)
follicle-stimulating hormone (FSH)
lutenizing hormone (LH)
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Adenohypophyseal Hormones
2/10/2003 44
Adenohypophyseal Hormones
?GH
? LH
? FSH
? PRL
2/10/2003 45
Growth Hormone (GH)
? action
stimulates most body cells to size anddivide
?major target organs
bones and skeletal muscle bones - stimulate epiphyseal plate long
bone growth
muscles - mass
? anabolic hormone
2/10/2003 46
Growth Hormone (GH)? acts directly or indirectly via insulin-like
growth factors (IGFs) or somatomeidins? regulation
GHRH and GHIH (hypothalamus)
low levels GH
2o triggers estrogen
hypoglycemia
a.a. (blood)
f.a.
exercise
other stressors
2/10/2003 47
Metabolic Actions of GH (fig 17.6)
2/10/2003 48
Hyposecretion of GH
? homeostatic imbalance
? causes pituitary dwarfism (children)
? slowed long bone growth
?max ht - 4 ft
? usually no problems - adults
? rare cases
severe deficit progeria
premature aging and atrophy of body tissues
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Hypersecretion of GH? homeostatic imbalance
? gigantism (children)? abnormally tall - 8 ft
? 1o cause
adenohypophyseal tumor
? trt - surgical removal
? excessive secretion post-epiphyseal plateclosure
acromegaly enlarged extremeties
overgrowth of bony areas (hands, feet, face) stillresponsive to GH
2/10/2003 50
Gonadotropins
? glycoproteins
? regulate function of gonads
ovaries & testes
? FSH
in both sexes
stimulates gamete (egg or sperm)production
? LH
in both sexes
promotes production of gonadal hormones
2/10/2003 51
Lutenizing Hormone (LH)
? females
works w/ FSH
maturation of egg-containing ovarian follicle
triggers expulsion egg from follicle (ovulation)
promotes synthesis & release of ovarianhormones
estrogen & progesterone
?males stimulates testosterone production
testes interstitial cells
2/10/2003 52
Gonadotropins
? prepuberty
virtually absent
blood of prepubertal boys & girls
? puberty
gonadotrope cells (ant pit) are activated
gonadotropin levels begin to rise
cause gonads to mature to adult state
2/10/2003 53
Gonadotropin Regulation
? release by ant pit
? prompted by GnRH (produced by hypo)
? hormonal suppression
FSH
estrogen (females)
testosterone & inhibin (males)
LH
estrogen (females)
testosterone (males)
2/10/2003 54
Homeostatic Imbalances
? hyposecretion
failure of sexual maturation
? hypersecretion
no important effects
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2/10/2003 55
Prolactin (PRL)
? protein hormone
? similar to GH? stimulates milk production (breast)
? enhances testosterone production (male)
? brief rise in levels prior to menstration
breast swelling & tenderness (some)
no milk production
? dramatic rise at end of pregnancy (pregnant women)
? infant suckling stimulates release (afterbirth)
2/10/2003 56
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Neurohypophyseal Hormones
2/10/2003 60
Neurohypophyseal Hormones
? oxytocin
?ADH (vasopressin)
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2/10/2003 61
Oxytocin & Antidiuretic Hormone
? stored in neurohypophysis? synthesized & forwarded by hypo neurons
(osmoreceptors)
? released on demand by hypo neurons(osmoreceptors)
? composed of nine a.a.
? differ only in two a.a.
? different physiological effects on targetorgans
2/10/2003 62
ADH? action
influence body H2O balance prevents dehydration
prevents H2O overload
inhibit or prevent urine formation
? target organ kidneys
tubule cells
reabsorb more H2O from urine
return H2O to bloodstream urine andBV [solute] ADH release
2/10/2003 63
ADH Regulation
? osmoreceptors monitor [solute] andthus [H2O] in blood
? stimulation blood osomolarity or blood volume
stimulation hypo neurons
pain receptors
some drugs nicotine, morphine, barbituates
low BP
2/10/2003 64
ADH Regulation
? inhibition
drinking alcohol urine output
morning after dry mouth
dehydration
drinking H2O
diuretic drugs
2/10/2003 65
ADH Effects
? pressor effect
high [blood] vasoconstriction
primarily visceral b.v.
? severe blood loss
ADH release systemic BP
2/10/2003 66
Homeostatic Imbalance
? diabetes insipidus (DI)
polyuria ( urine production)
thi rst
caused by blow to head
damage to hypo or post pit ADH release
not serious condition
remedied by drinking more H2O
exception
unconscious or comatose patients
life-threatening
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2/10/2003 67
Oxytocin
? action
strong stimulant of uterine contractions
hormonal trigger for milk ejection in womenactively producing milk (in response to PRL)
positive feedback
suckling event
role in sexual arousal and orgasm (2o)
feeling of sexual satisfaction
responsible for nurturing & affectionatebehavior
known as cuddle hormone
2/10/2003 68
Oxytocin
? childbirth and nursing
amts released
? near end of pregnancy
# oxytocin receptors peaks
uterine smooth muscle becomes more andmore sensitive
stretching of uterus & cervix sends
impulses to hypo oxytocin release(post pit) oxytocin birth
contractions childbirth
2/10/2003 69
Natural & Synthetic Oxytocic Drugs
? induce labor or hasten normal labor thatis slow
? ex. pitocin
2/10/2003 70
2/10/2003 71
Thyroid Gland (fig. 17.8)
? butterfly-shaped gland
? location
anterior neck on trachea
inferior to larynx
? largest pure endocrinegland in body
? unique
stores hormoneextracellularly in large
quantities
? TH
? Calcitonin
2/10/2003 72
Thyroid Hormone
?major metabolic hormone
? affects virtually every cell in body
exceptions
adult brain, spleen, testes, uterus, thyroid gland
?
two active iodine-containing hormones T4 (thyroxine)
major hormone secreted
T3 (triiodothyronine)
*more active form (10 xs)
most made at target organs by conversion of T4
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2/10/2003 73
Thyroid Hormone
?
actions BMR
O2 consumption
body heat production
maintains BP
# of adrenergic receptors in BV
*regulator of tissue growth & development
primarily skeletal & nervous system,reproduction
2/10/2003 74
Biosynthesis of Thyroid Hormones
2/10/2003 75
Thyroid Hormone Transport
? 1. most released T4 and T3 bind totransport proteins T4- main hormonal product secreted
some T4converted to T3before secretion
? 2. T4
and T3
bind to target tissuereceptors
? 3. T3 binds more avidly and is moreactive conversion of T4 to T3 most T3generated in target organs by enzymatic action
removal of one iodine group
2/10/2003 76
Thyroid Hormone Regulation
?
TSH thyroid-stimulating hormone
adenohypophyseal hormone
regulates TH secretion
? TRH
thyrotropin-releasing hormone
secreted by hypothalamus
triggers TSH release
*can overcome negative feedback controls
2/10/2003 77
TRH Regulation
?Stimulus for TRH release (low levels of T4)
body energy requirements
pregnancy
prolonged cold
? Inhibi tion of TRH release (high levels of T4)somatostatin (GHIH)
levels of glucocorticoids
levels of sex hormones
estrogen
testosterone
blood [ iodine]
2/10/2003 78
Hypothyroid Disorders
? homeostatic imbalance
? thyroid defect
? thyroidectomy
? dietary iodine
? secondarily TSH or TRH release
? adults - children
myxedema - cretinism
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Myxedema
? low MR
? chills
? constipation
? thick, dry skin
? puffy eyes
? edema
? lethargic
? mental sluggishness
2/10/2003 80
Myxedema
? if result of lack of iodine
thyroid gland enlargement
AKA endemic (colloidal) goiter
follicle cells cannot take up iodine or
make functional hormone
pituitary secretes TSH TH
2/10/2003 81
Myxedema
? tx
iodine supplements
hormone replacement therapy
surgery
? goiter belt parts of US
iodine poor soil
no access to iodine-rich shellfish
2/10/2003 82
Cretinism
? severe hypothyroidism? short, disproportionate body
? thick tongue and neck
?mentally retarded
? genetic defic iency of thyroid gland
? lack of dietary iodine (maternal)
2/10/2003 83
Cretinism
? tx
preventable by TH replacement therapy
before developmental abnormalities andmental retardation
2/10/2003 84
Graves Disease
? hyperthyroid pathology
? autoimmune ds
? MR
? sweating
? rapid, i rregular heartbeat
? nervousness
?weight loss (despite food intake)
? serum contains abnormal AB
mimic TSH TH release
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2/10/2003 85
Graves Disease
? protrusion of eyeballs exophthalmos
? tx
surgical removal thyroid gland
2/10/2003 86
Calcitonin
? polypeptide hormone
? thyroid gland
parafollicular (C) cells
? action
lower blood Ca2+ levels
direct antagonist of PTH
weak hypocalcemic agent
2/10/2003 87
Calcitonin
? target organ
skeleton (bone sparing effects)
1. inhibits osteoclast activity
bone resorption
release of ionic Ca2+ (bony matrix)
2. stimulates Ca2+ uptake
incorporation into bony matrix
2/10/2003 88
Calcitonin Regulation
? stimulus
humoral
Ca2+ blood levels
~20% above normal
? inhibition
Ca2+ blood levels
inhibit C cell secretory activity
2/10/2003 89
Calcitonin Regulation of Blood
Ca2+ Levels
? short-lived
? rapid
? important only in childhood
skeleton grows quickly
bones changing
mass
size
shape
2/10/2003 90
Parathyroid Gland (fig 17.10)
? tiny, yellow-brown
gland
? posterior aspect ofthyroid gland
can be located inother neck regions orthroat
? usually 4 glands
number varies
? chief cells
secrete PTH
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Parathyroid Hormone (PTH)
? aka parathormone
? protein hormone
? action
single most important Ca2+ controller
Ca2+ balance (blood)
? target organs
skeleton (bone)
kidneys
intestines
2/10/2003 92
PTH Effects on Target Organs? skeleton (bone)
activates osteoclasts (bone resorption~removal)
dig pits or grooves (resorption bays)
break down the bone matrix
release of calcium & phosphate ions (blood)
? kidneys
promotes activation of vitamin D
Ca2+ reabsorption
? intestines
promotes activation of vitamin D
Ca2+ absorption
2/10/2003 93
PTH Effects on Target Organs
(fig 17.11)
2/10/2003 94
PTH Regulation
? stimulus
Ca2+ blood levels
? inhibition
Ca2+ blood levels
hypocalcemia
2/10/2003 95
Vitamin D
? required for absorption of Ca2+
? ingestion of food
? produced in skin
? inactive form
? converted in kidneys to active vitamin Dform
calcitrol
stimulated by PTH
2/10/2003 96
Adrenal (Suprarenal) Glands
(fig 17.12)
? paired pyramidshaped organs
? perched on topkidneys (caps)
?
enclosed in a fibrouscapsule & cushion of
fat
? two endocrine organs
structurally &functionally
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Adrenal Cortex
? over two dozen steroid hormones
corticosteroids (collectively)? synthesized from cholesterol by adrenal
cortex
? large, lipid cortical cells arranged inthree layers (zones)
corticosteroids produced
zona glomerulosa (outer)
zona fasciculata (middle)
zona reticularis (inner)
2/10/2003 98
Adrenal (Suprarenal) Glands
(fig 17.12)
? zona glomerulosa
secrete primarilymineralocorticoids
control electrolytebalance in ECF
primarily Na and Kions
? zona fasciculata
arranged in linearcords
secreteglucocorticoids
metabolic hormone
resist stressors
2/10/2003 99
Adrenal (Suprarenal) Glands
(fig 17.12)
? zona reticularis
produce small amtsof gonadocorticoids
sex hormones
? **division of labor incorticosteroidproduction
all corticosteroids areproduced in all 3layers
2/10/2003 100
Mineralocorticoids
? regulation of [electrolyte] in ECF primarily Na2+ and K+
Na2+ most abundant cation in ECF
vital to homeostasis
Na2+ intake and retention HBP
? aldosterone
most potent of all mineralocorticoids
accounts for over 95% of
mineralocorticoids produced
2/10/2003 101
Aldosterone
? action maintain Na2+ balance
reduces excretion of Na from the body
enhances Na reabsorption perspiration, saliva and gastric juice
regulation of other ions coupled w/ Na2+ regulation
K+, H+, HCO3-, Cl- ,
? significance Na2+ regulation crucial to overall body
homeostasis where Na2+ goes, H
2O follows changes in
BV & BP
2/10/2003 102
Aldosterone
? target organ
distal part of kidney tubules
stimulates reabsorption of Na2+ from formingurine
return of Na2+ to bloodstream
causes Na2+ & H2O retention accompanied byK+ elimination
occasionally
alterations in acid-base balance of blood by H+
excretion
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2/10/2003 103
Aldosterone
? stimulus
rising blood levels of K+
low blood levels of Na, BV and BP
? inhibition
reverse conditions
low blood levels of K+
high blood levels of Na, BV and BP
2/10/2003 104
Aldosterone
? regulatory effects are brief
lasts approximately 20 min
plasma electrolyte balance prec isely
controlled and modified
2/10/2003 105
Regulation of Aldosterone Secretion
? 1) renin-angiotensin system
major regulator of aldosterone release
kidney cells release renin BP
? 2) plasma [Na2+] and [K+]
fluctuating blood levels directly influencezona glomerulosa cells
K+ and Na2+ are stimulatory
K+ and Na2+ are inhibitory
2/10/2003 106
Regulation of Aldosterone Secretion
? 3) adrenocorticotropic hormone (ACTH)
ant pit hormone
minor influence under normalcircumstances
major influence under stress
hypo secretes more CRH* ACTHsecretion of aldosterone (zona glomerulosa)
absorption of Na2+ and H2O BP and BV
ensures adequate delivery of nutrients and
respiratory gases during stress
? *corticotropin releasing hormone
2/10/2003 107
Regulation of Aldosterone Secretion
(fig 17.15)
2/10/2003 108
Regulation of Aldosterone Secretion
? 4) atrial natriuretic peptide (ANP)
hormone secreted by the heart
response to BP
fine-tune BP
fine-tune Na 2+-H2O balance in body inhibits the renin-angiotensin effect
BP by Na and H2O in urine
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2/10/2003 109
Summary of Aldosterone Regulation
(fig 17.13)
2/10/2003 110
Glucocorticoids
? hormones
cortisol (hydrocortisone)
secreted in significant amts
cortisone
corticosterone
? absolutely essential for life
2/10/2003 111
Cortisol
? action
influence the metabolism of most body cells
help resistance of stressors
help body adapt to intermittent food intake
maintain constant blood sugar levels maintain BV
prevent shifts of H2O into tissue cells
2/10/2003 112
Cortisol
? target organs
body cells promote gluconeogenesis prime metabolic effect
formation of glucose from noncarbohydrate molecules
fats
proteins
promote hyperglycemia mobilization of fats for energy metabolism
2/10/2003 113
Cortisol
? target organs body cells
stimulate protein catabolism
assist body resist stressors
enhances vasoconstrictive effects of epi BP and circulation
ensure adequate nutrient distribution to cells
2/10/2003 114
Cortisol Regulation
? stimulation
promoted by ACTH (ant pit)
triggered by CRH (hypo)
? inhibition
cortisol levels feedback to hypo and ant pit shut off CRH release
ACTH and cortisol secretion
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2/10/2003 115
Cortisol Regulation
? cortisol secretory bursts
driven by patterns of eating and activity definite pattern throughout the day and night
blood levels
peak
shortly after rising (morning)
lowest
evening
just before and shortly after sleep ensues
interruption in normal rhythm
acute stress
2/10/2003 116
Stress
? SNS overrides the usually inhibitoryeffec ts of elevated cortisol levels
triggers CRH ACTH blood levels
cortisol from the adrenal cortex
blood levels
glucose
f.a.
a.a
2/10/2003 117
Regulation of Cortisol Secretion
(fig 17.15)
2/10/2003 118
Excessive Glucocorticoid Levels
?Undesirable Effects
? 1) depress cartilage and bone formation? 2) inhibit inflammation and prevent
vasodilation
? 3) depress the immune system
? 4) promote changes in cardiovascular,neural and GI fnc
? *ideal amts promote normal fnc
2/10/2003 119
Pathology of Cortisone Excess
?Cushings Ds
? causes
ACTH releasing tumor of pit
ACTH releasing malignancy of lungs,
pancreas, or kidneys
tumor of adrenal cortex
clinical administration of glucocorticoidmeds
2/10/2003 120
Pathology of Cortisone Excess
? persistent hyperglycemia
aka steriod diabetes
? dramatic losses in muscle & boneprotein
?water and salt retention HTN, edema
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2/10/2003 121
Cushing-oid Signs
? swollen moon-face
? redistribution of fat
abdomen
posterior neck (buffalo hump)
? tendency to bruise
? poor wound healing
2/10/2003 122
Pathology of Cortisone Excess
? enhanced anti-inflammatory effects
infections
overwhelming severe before producingrecognizable symptoms
? trt (only)
removal of the cause
surgery
drug discontinuation
2/10/2003 123
Gonadocorticoids
? androgens primarily secreted
male sex hormones
most importanly testosterone
? small amts estrogen also secreted
? stimulus ACTH (appears)
? inhibition
mechanism not understood
ACTH does not exert feedback control
2/10/2003 124
Gonadocorticoids
? action not fully understood
adrenal androgen levels rise continuouslybetween ages of 7 and 13
boys and girls
contribute to onset of puberty and theappearance of axillary and pubic hair
2/10/2003 125
Gonadocorticoids
? action
responsible for sex drive adult women
converted to estrogens after menopause when ovarian estrogens are no longer
produced
2/10/2003 126
Gonadocorticoids
? amt sex hormones produced
adrenal cortex
insignificant
in comparison to amts produced by the gonads during late puberty and adulthood
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2/10/2003 127
Hypersecretion of Gonadocorticoids
? homeostatic imbalance
?
results in masculinization or virilization? adult males
testicular testosterone has already producedvirilization
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Hypersecretion of Gonadocorticoids
? prepubertal males
dramatic effects
maturation of reproductive organs and
appearance of secondary sex characteristicsoccur rapidly
massive onslaught of sex drive
2/10/2003 129
Hypersecretion of Gonadocorticoids
? females
androgenital syndrome (virilization of females)
~adrenogenital syndrome
beard development
masculine pattern of body hair distribution
clitoris grows to resemble a small penis
2/10/2003 130
Adrenal Medulla
? location
ctr of the adrenal gland surrounded by the adrenal cortex
? formed from nervous tissue
releases NTs as its hormones
? secretes catecholamines into the blood
epinephrine (adrenaline)
norepinephrine
secretion controlled by ANS in response tostress
2/10/2003 131
Adrenal Medulla
? unequal amts two hormones released
approx 80% is epinephrine
? exert same effec ts
few exceptions
epinephrine
more potent stimulator of heart & metabolic acti vities
clinically
heart stimulator
bronchiole dilator
norepinephrine
greater influence on peripheral vasoconstriction & bp
2/10/2003 132
Catecholamine Regulation
? stimulus
bodys fight-or-flight status by short-term
stressor or emergency
SNS is mobilized
blood sugar
bv consriction
heart beat
bp
blood diversion fr om nonessential organs tobrain, heart, skeletal muscles
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2/10/2003 133
Stress and Catecholamines
(fig 17.15)
2/10/2003 134
Stress and the Adrenal Gland
? Medulla
? hypo activates
medulla via SNSimpulses
? mediates short-termresponses
? secretion ofcatecholamines
epi and norepi
? Cortex
? hypo activatescortex via hormonalsignals
A CTH
? mediates long-termresponses
? secretion of steroidhormones mineralocorticoids
aldosterone
glucocorticoids cortisol
2/10/2003 135
Stress and Adrenal Gland
? catecholamines
cause fairly brief responses to stress
? adrenocortical hormones
promote long-lasting responses to stress
2/10/2003 136
Pancreas (fig 17.4)
? location partially behind
stomach in theabdomen
? mixed gland
composed ofendocrine andexocrine gland cells
2/10/2003 137
Pancreatic Cells
? pancreatic acinar cells
form bulk of gland
exocrine fnc
produce enzyme-rich product
ducted into small intestine
digestion
? pancreatic islets (islets of Langerhans)
tiny cell clusters
produce pancreatic hormones
glucagon
insulin
2/10/2003 138
Pancreatic Islet Cells
? two major pop of hormone-producingcells
alpha cells
glucagon producing cells
beta cells insulin producing cells
more numerous
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Pancreatic Islets
? act as tiny fuel sensors secrete glucagon and insulin
independently
during fasting and feeding states
fluctuations in blood glucose
opposite effects
glucagon
hyperglycemic hormone
insulin
hypoglycemic hormone
2/10/2003 140
Glucagon
? polypeptide
? extremely potent hyperglycemic agent
1 molecule release of 100 milmolecules of glucose in blood
2/10/2003 141
Glucagon? target organ
liver
glycogenolysis
breakdown of glycogen to glucose
gluconeogenesis
synthesis of glucose
lactic acid
noncarbohydrate molecules (fats, a.a)
release of glucose to blood by liver
blood sugar
2O effect
b lood [a.a. ]
2/10/2003 142
Glucagon Regulation
? stimulus
humoral blood sugar levels
amino acid levels
after a protein rich meal
? inhibition
blood sugar levels
somatostatin
? * believed that hypoglycemics are deficient in glucagon
2/10/2003 143
Glucagon Regulation (fig 25.20)
2/10/2003 144
Insulin
? small protein
? initally synthesized as part of largerpolypeptide
proinsulin
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2/10/2003 145
Insulin? target organ
liver
blood sugar levels (main effect) enhances membrane transport of glucose and other
simple sugars into body cells
especially muscle & fat cells
does not accelerate glucose entry into liver, kidney
and brain tissue
easy access to blood glucose regardless of insulin
levels
sweeps glucose out of blood
used for energy or converted to other forms(glycogen, fats)
2/10/2003 146
Insulin
? target organ
liver
other effects
influence protein & fat metabolism
promotes protein synthesis & fat storage
2/10/2003 147
Insulin Regulation
? stimulation
blood glucose levels (primary)
plasma levels of a.a, f.a. (secondary)
other direct or indirect effects
hyperglycemic hormones glucagon
epinephrine
GH
thyroxine
glucocorticoids
2/10/2003 148
Insulin Regulation
? inhibition sugar plasma levels
somatostatin (indirect)
? blood sugar levels
represent a balance of humoral and
hormonal control
2/10/2003 149
Insulin Regulation (fig 25.18)
2/10/2003 150
Regulation of Blood Sugar
(fig 17.17)
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2/10/2003 151
Diabetes Mellitus (DM)
? homeostatic imbalance
? hyposecretion or hypoactivity of insulin
insulin deficient or absent
blood sugar levels remain high after a meal
abnormal insulin receptors
glucose unavailable to most body cells
? blood glucose levels
? amts glucose excreted in urine
2/10/2003 152
Diabetes Mellitus (DM)
?metabolic acidosis
? protein wasting
?weight loss
amts fat & tissue proteins used for
energy
2/10/2003 153
Metabolic Rate
? bodys rate of energy output
usually expressed per hr
? total heat produced by all chemical rxnsand mechanical work of the body
?measured calorimeter (directly)
heat liberated by the body
respirometer (indirectly)
O2 consumption
directly proportional to heat production
2/10/2003 154
Metabolic Rate
? calorimetry measurement
direct method of measuring MR
person enters a chamber (calorimeter)
heat liberated by body is absorbed bywater circulating around the chamber
rise in water temp is directly related to heat
produced by the persons body
2/10/2003 155
Metabolic Rate
? respirometry measurement
indirec t method of measuring MR
O2 use and heat liberation directly proportional
during food oxidation
avg amt of O2 consumed/hr (L/h) is x by 4.83
person breathes into a respirometer
the total amt of oxygen consumed during
testing is measured
for each L of O2 the body produces ~4.8 kcal ofheat
2/10/2003 156
Metabolic Rate
?measured under standard conditions
postabsorptive state
not eaten for at least 12 hrs
reclining position
mentally & physically relaxed temperature is 20-25 degrees Celsius
measurements obtained
basal metabolic rate (BMR)
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Basal Metabolic Rate (BMR)
? reported in kcal/m2 of body surface/hr
kcal/m2/h
? energy body needs to drive only theresting body processes
most essential activities
breathing, maintaining resting organ fnc levels
? not lowest metabolic state
lowest occurs during sleep
skeletal muscles are completely relaxed
2/10/2003 158
Factors Influencing BMR
? age
? sex
? size
? stress
? body surface area
? thyroxine levels
? food effects
?muscular activity
2/10/2003 159
Calculation of BMR
? avg 70 kg (154 lb) adult
BMR ~ 60-72 kcal/h
? quick approximation of ones BMR
wt (kg) X factor = BMR
2.2 lbs = 1 kg
male factor = 1
female factor = 0.9
2/10/2003 160
Factors Influencing BMR
? young person
higher BMR require large amts of energy for growth
? old age
decrease BMR
skeletal muscle atropy
w/out caloric intake wt
?males
higher BMR
more muscle, more active
2/10/2003 161
Factors Influencing BMR
? females
fatty tissue in greater relative amts
metabolically sluggish
? body temperature
rises and falls w/ MR
fevers MR
? stress
higher MR
mobilizes the SNS
epi and nor MR
stimulate fat catabolism
2/10/2003 162
Factors Influencing BMR
? thyroxine
most important hormonal factor indetermining BMR
AKA metabolic hormone
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Factors Influencing BMR
? thyroxine
direct effects
on most body cells (exception: brain cells)
increase oxygen consumption
increase use of ATP to operate Na-K pump
decrease in ATP reserves
acceleration in ATP cellular respiration
more thyroxine produced
higher BMR
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