endocrine syetem

8/3/2019 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


?

amino acid-based majority of hormones

molecule size varies

simple to long polymers

2/10/2003 11


? 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

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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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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

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Hypothalamic-Pituitary-Target Endocrine Organ

Relationship (fig 17.5)


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2/10/2003 37

Endocrine Gland Stimuli (fig 17.3)

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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

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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)

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Homeostatic Imbalances

? hyposecretion

failure of sexual maturation

? hypersecretion

no important effects


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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)

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Neurohypophyseal Hormones

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Neurohypophyseal Hormones

? oxytocin

?ADH (vasopressin)


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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

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ADH Regulation

? inhibition

drinking alcohol urine output

morning after dry mouth

dehydration

drinking H2O

diuretic drugs

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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

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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


? 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

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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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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

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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

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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


(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


(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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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


? 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


(fig 17.15)

2/10/2003 108


? 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


? 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


? 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


?

results in masculinization or virilization? adult males

testicular testosterone has already producedvirilization

2/10/2003 128


? prepubertal males

dramatic effects

maturation of reproductive organs and

appearance of secondary sex characteristicsoccur rapidly

massive onslaught of sex drive

2/10/2003 129


? 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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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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Diabetes Mellitus (DM)


? 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


? 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


? 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


? thyroxine

most important hormonal factor indetermining BMR

AKA metabolic hormone


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2/10/2003 163


? 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

endocrine syetem

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