Hormonal Effects THE ENDOCRINE SYSTEM

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widespread diverse most body cells control and integrate

Karen Marshall, Associate Professor Montgomery College Takoma Park Campus

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Endocrine System (ES)

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Hormonal Effects
major processes
reproduction growth & development body defenses mobilization blood electrolytes, H2O, nutrient balance maintainence cellular metabolism regulation energy balance

interacts with nervous system (NS) to coordinate and integrate body cell activity endocrinology
scientific study of hormones and endocrine organs

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Control of Body Functioning

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Glands
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NS regulate activity of muscles and glands

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ES regulate cell activity via hormones

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endocrine~ductless
lack ducts release hormones into surrounding tissue rich vascular and lymphatic drainage

exocrine
have ducts more numerous secrete products onto skin or into body cavities examples
mucous, sweat, oil, salivary, liver

via electrochemical imupulses via neurons

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chemical messengers released in blood and transported in body

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organ response time

ms

tissue and organ response time

lag period (s or days) more prolonged

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Major Endocrine Glands

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Hormone Chemical Groups

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pituitary thyroid parathyroid hypothalamus (neuroendocrine) adrenal pineal thymus pancreas gonads
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amino acid-based
majority of hormones molecule size varies
simple to long polymers

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Major Endocrine Glands (fig 17.4)

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Hormone Chemical Groups

steroids
synthesized from cholesterol examples
only gonadal and adrenocortical hormones

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Hormone Chemical Groups

? ? ? two group classification amino acid-based steroids ?

Target Cell
cell capable of responding to a hormone because it bears receptors to which a hormone can bind

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Mechanisms of Hormone Action

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Mechanisms of Hormone Receptor Binding

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alter cell activity cellular processes

increase or decrease in rate

amino acid-based hormones

G proteins (regulatory molecules)

response
dependent on target cell type

second messenger systems

steroids with gene activation

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Target Cells
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Target Cell Specificity Response ~ Hormone-Receptor Binding

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respond to a hormone bear receptors changed by a hormone via stimulus five ways

protein receptors
specific location
target cell PM interior response hormone binding
performance preprogrammed function

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*hormones ~molecular triggers

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Target Cells
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Target Cell Activation

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five ways
change in MP or electrical state enzyme synthesis enzyme activation or inhibition secretory activity gene 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

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Half-Life
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up-regulation
formation of additional receptors blood hormonal levels greater target cell response to stimulation

persistence of hormone (blood) brief

a fraction of a minute ~ 30 min

down-regulation
prolonged [high hormone] desensitization loss of hormonal receptors less target cell response to stimulation

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Target Cell Phenomena

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Time and Hormonal Effects

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# and affinity of other receptors

respond to other hormones example
progesterone
induces estrogen receptor loss (uterus) antagonizes estrogen effects s

target cell reponse varies almost immediately hours to days (steroids)

inactive form (pro-hormone)
secreted activated by target cell example
testosterone

estrogen
cause progesterone receptor production (same cells) enhances response to progesterone

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Hormonal Inactivation and Removal

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Duration of Hormone Action

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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

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

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Feedback Mechanisms (fig 1.4)

regulated by negative feedback system internal or external stimulus

triggers hormone secretion

hormone levels target organ effects hormone release

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Negative vs. Positive Feedback Mechanisms

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Negative Feedback (fig 1.5)

negative feedback
original stimulus contributes to homeostasis ex. glucose blood levels

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Negative vs. Positive Feedback Mechanisms

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Positive Feedback (fig 1.6)

positive feedback
initial stimulus enhances hormonal response rarely contributes to homeostasis ex. blood clotting

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Control (Regulation) of Hormone Release

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Hormonal Stimuli
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hormonal release
response to hormones produced by other endocrine organs

three major types of stimuli

humoral neural hormonal result in:
endocrine organ activation hormonal manufacture and release
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example
ant pit
regulated by hypothalamus hormones stimulate other endocrine organs to release hormones blood hormonal levels inhibition pit hormones and final target hormone release

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hypothalamic-pituitary-target endocrine organ feedback loop

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Humoral Stimuli
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Hypothalamic-Pituitary-Target Endocrine Organ Feedback Loop

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hormonal secretion
direct response to changing blood levels
ions, nutrients

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simplest control system examples

insulin production (pancreas) aldosterone production (adrenal cortex)

promotes rhythmic hormone release ing and ing hormone blood levels some endocrine organs respond to multiple stimuli

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Neural Stimuli
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Hypothalamic-Pituitary-Target Endocrine Organ Relationship (fig 17.5)

hormonal release
response to nerve fiber stimulation

examples
oxytocin release (hypothalamus) ADH release (hypothalamus) SNS stimulation
epi and nor release (adrenal medulla)
stress

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Endocrine Gland Stimuli (fig 17.3)

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Posterior Lobe
aka neurohypophysis consists of lobe and infundibulum composed of pituicytes (glia-like supporting cells) and nerve fibers releases neurohormones produced in hypothalamus hormone storage area
not true endocrine gland

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Hormones
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Anterior Lobe
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~ 14 required description producing organ primary body effect secretion regulation other hormonal influences source of regulating hormones
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aka adenohypophysis composed of glandular tissue manufactures and releases

a number of hormones

master endocrine gland regulates activity of other endocrine glands 6 distinct hormones known
specific physiological actions proteins

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Major Endocrine Organ - Pituitary Gland (Hypophysis)

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Tropic Hormone (Tropins)

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secretes ~ 9 major hormones size and shape of pea pea on a stalk

funnel-shaped infundibulum
connection to hypothalamus superiorly

regulate secretory action of other endocrine glands example

four of the six adenophyophyseal hormones
thyroid stimulating hormone (TSH) adrenocorticotrophic hormone (ACTH) follicle-stimulating hormone (FSH) lutenizing hormone (LH)

two major lobes

anterior (glandular tissue) posterior (neural tissue)

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Growth Hormone (GH)

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Adenohypophyseal Hormones

acts directly or indirectly via insulin-like growth factors (IGF or somatomeidins s) regulation
GHRH and GHIH (hypothalamus) low levels GH 2o triggers
estrogen hypoglycemia a.a. (blood) f.a. exercise other stressors

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Adenohypophyseal Hormones
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Metabolic Actions of GH (fig 17.6)

GH LH FSH PRL

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Growth Hormone (GH)

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Hyposecretion of GH
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action
stimulates most body cells to size and divide

major target organs

bones and skeletal muscle
bones - stimulate epiphyseal plate bone growth muscles mass long

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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

anabolic hormone
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Hypersecretion of GH
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Gonadotropins
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homeostatic imbalance gigantism (children) abnormally tall - 8 ft 1 o cause

adenohypophyseal tumor

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

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trt - surgical removal excessive secretion post-epiphyseal plate closure

acromegaly

enlarged extremeties overgrowth of bony areas (hands, feet, face) still 49 2/10/2003 responsive to GH

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Gonadotropins
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Gonadotropin Regulation
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glycoproteins regulate function of gonads

ovaries & testes

FSH
in both sexes stimulates gamete (egg or sperm) production

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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LH

in both sexes promotes production of gonadal hormones50 2/10/2003

Lutenizing Hormone (LH)

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Homeostatic Imbalances
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females
works w/ FSH
maturation of egg-containing ovarian follicle triggers expulsion egg from follicle (ovulation) promotes synthesis & release of ovarian hormones
estrogen & progesterone

hyposecretion
failure of sexual maturation

hypersecretion
no important effects

males
stimulates testosterone production
testesinterstitial cells

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Prolactin (PRL)
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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

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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
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oxytocin ADH (vasopressin)

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Oxytocin & Antidiuretic Hormone

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ADH Regulation
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inhibition
drinking alcohol
urine output morning afterdry mouth dehydration

stored in neurohypophysis synthesized & forwarded by hypo neurons

(osmoreceptors)

released demandby hypo neurons on

(osmoreceptors)

composed of nine a.a. differ only in two a.a. different physiological effects on target organs
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drinking H2O diuretic drugs

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ADH
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ADH Effects
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action
influence body H2O balance
prevents dehydration prevents H 2O overload

pressor effect
high [blood] vasoconstriction
primarily visceral b.v.

inhibit or prevent urine formation

?

target organ
kidneys
tubule cells reabsorb more H2O from urine return H2O to bloodstream urine and BV [solute] ADH release

severe blood loss

ADH release systemic BP

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ADH Regulation
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Homeostatic Imbalance
?

osmoreceptors monitor [solute] and thus [H 2O] in blood stimulation

blood osomolarity or blood volume stimulation hypo neurons pain receptors some drugs
nicotine, morphine, barbituates

diabetes insipidus (DI)

polyuria ( urine production) thirst 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

low BP
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Oxytocin
?

action
strong stimulant of uterine contractions hormonal trigger for milk ejection in women actively producing milk (in response to PRL)
positive feedback
suckling event

role in sexual arousal and orgasm (2o)

feeling of sexual satisfaction responsible for nurturing & affectionate behavior known as cuddle hormone
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Oxytocin
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Thyroid Gland (fig. 17.8)

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childbirth and nursing

amts released

butterfly-shaped gland location

anterior neck on trachea inferior to larynx

near end of pregnancy

# oxytocin receptors peaks uterine smooth muscle becomes more and more sensitive stretching of uterus & cervix sends impulses to hypo oxytocin release (post pit) oxytocin birth contractions childbirth
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largest pure endocrine gland in body unique

stores hormone extracellularly in large quantities

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TH Calcitonin
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Natural & Synthetic Oxytocic Drugs

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Thyroid Hormone
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induce labor or hasten normal labor that is slow ex. pitocin

major metabolic hormone affects virtually every cell in body

exceptions
adult brain, spleen, testes, uterus, thyroid gland

two active iodine-containing hormones

T 4 (thyroxine)
major hormone secreted

T 3 (triiodothyronine) *more active form (10 x s)

most made at target organs by conversion of T 4
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Thyroid Hormone
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Thyroid Hormone Regulation

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actions
BMR O 2 consumption body heat production maintains BP
# of adrenergic receptors in BV

TSH
thyroid-stimulating hormone adenohypophyseal hormone regulates TH secretion

TRH
thyrotropin-releasing hormone secreted by hypothalamus triggers TSH release *can overcome negative feedback controls

*regulator of tissue growth & development

primarily skeletal & nervous system, reproduction
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Biosynthesis of Thyroid Hormones

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TRH Regulation
Stimulus for TRH release

pregnancy prolonged cold

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(low levels of T4 )

body energy requirements

Inhibition of TRH release (high levels of T4 ) somatostatin (GHIH)

levels of glucocorticoids levels of sex hormones
estrogen testosterone

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blood [iodine]

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Thyroid Hormone Transport

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Hypothyroid Disorders
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1. most released T4 and T 3 bind to transport proteins

T4 - main hormonal product secreted some T4 converted to T3 before secretion

2. T4 and T 3 bind to target tissue receptors 3. T3 binds more avidly and is more active
conversion of T4 to T3 most T3 generated in target organs by enzymatic action
removal of one iodine group

homeostatic imbalance thyroid defect thyroidectomy dietary iodine secondarily

TSH or TRH release

adults
myxedema

- children
- cretinism
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Myxedema
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Cretinism
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low MR chills constipation thick, dry skin puffy eyes edema lethargic mental sluggishness

severe hypothyroidism short, disproportionate body thick tongue and neck mentally retarded genetic deficiency of thyroid gland lack of dietary iodine (maternal)

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Myxedema
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Cretinism
?

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

tx
preventable by TH replacement therapy
before developmental abnormalities and mental retardation

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Myxedema
?

Grave Disease s
? ? ? ? ? ? ? ?

tx
iodine supplements hormone replacement therapy surgery

goiter belt
parts of US
iodine poor soil no access to iodine-rich shellfish

hyperthyroid pathology autoimmune ds MR sweating rapid, irregular heartbeat nervousness weight loss (despite food intake) serum contains abnormal AB
mimic TSH TH release
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Grave Disease s
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Calcitonin Regulation
?

protrusion of eyeballs
exophthalmos

stimulus
humoral Ca 2+ blood levels
~20% above normal

tx
surgical removal thyroid gland
?

inhibition
Ca 2+ blood levels
inhibit C cell secretory activity

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Calcitonin
? ?

polypeptide hormone thyroid gland

parafollicular (C) cells

Calcitonin Regulation of Blood Ca2+ Levels

? ? ?

action
lower blood Ca 2+ levels direct antagonist of PTH weak hypocalcemic agent

short-lived rapid important only in childhood

skeleton grows quickly bones changing
mass size shape

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Calcitonin
?

Parathyroid Gland (fig 17.10)

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target organ
skeleton (bone sparing effects)
1. inhibits osteoclast activity
bone resorption release of ionic Ca2+ (bony matrix)

tiny, yellow-brown gland posterior aspect of thyroid gland

can be located in other neck regions or throat

2. stimulates Ca 2+ uptake
incorporation into bony matrix ?

usually 4 glands
number varies

?
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chief cells
secrete PTH
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Parathyroid Hormone (PTH)

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PTH Regulation
?

aka parathormone protein hormone action

single most important Ca2+ controller
Ca2+ balance (blood)

stimulus
Ca 2+ blood levels Ca 2+ blood levels
hypocalcemia

inhibition

target organs
skeleton (bone) kidneys intestines

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PTH Effects on Target Organs

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Vitamin D
? ? ? ? ?

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 Ca 2+ reabsorption

required for absorption of Ca2+ ingestion of food produced in skin inactive form converted in kidneys to active vitamin D form
calcitrol stimulated by PTH

intestines
promotes activation of vitamin D Ca 2+ absorption
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PTH Effects on Target Organs (fig 17.11)

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Adrenal (Suprarenal) Glands (fig 17.12)

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paired pyramid shaped organs perched on top kidneys (caps) enclosed in a fibrous capsule & cushion of fat two endocrine organs
structurally & functionally

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Adrenal Cortex
?

Mineralocorticoids
?

over two dozen steroid hormones

corticosteroids (collectively)

regulation of [electrolyte] in ECF

primarily Na2+ and K+
Na 2+ most abundant cation in ECF
vital to homeostasis Na 2+ intake and retention HBP

synthesized from cholesterol by adrenal cortex large, lipid cortical cells arranged in three layers (zones)
corticosteroids produced
zona glomerulosa (outer) zona fasciculata (middle) zona reticularis (inner)

aldosterone
most potent of all mineralocorticoids accounts for over 95% of mineralocorticoids produced

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Adrenal (Suprarenal) Glands (fig 17.12)

?

Aldosterone
?

zona glomerulosa
secrete primarily mineralocorticoids
control electrolyte balance in ECF
primarily Na and K ions

action
maintain Na 2+ balance
reduces excretion of Na from the body enhances Na reabsorption
perspiration, saliva and gastric juice

regulation of other ions

coupled w/ Na 2+ regulation K+, H+, HCO 3-, Cl- ,

zona fasciculata
arranged in linear cords secrete glucocorticoids
?

significance
Na 2+ regulation crucial to overall body homeostasis
where Na 2+ goes, H2O follows BV & BP changes in
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metabolic hormone resist stressors

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Adrenal (Suprarenal) Glands (fig 17.12)

?

Aldosterone
?

target organ
distal part of kidney tubules
stimulates reabsorption of Na 2+ from forming urine
return of Na2+ to bloodstream

zona reticularis
produce small amts of gonadocorticoids
sex hormones

**division of labor in corticosteroid production all corticosteroids are produced in all 3 layers

causes Na 2+ & H 2O retention accompanied by K+ elimination

occasionally alterations in acid-base balance of blood by H + excretion

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Aldosterone
?

Regulation of Aldosterone Secretion

?

stimulus
rising blood levels of K + low blood levels of Na, BV and BP

3) adrenocorticotropic hormone (ACTH)

ant pit hormone minor influence under normal circumstances major influence under stress
hypo secretes more CRH* ACTH secretion of aldosterone (zona glomerulosa) 2+ and H O absorption of Na BP and BV 2
ensures adequate delivery of nutrients and respiratory gases during stress

inhibition
rev erse conditions low blood levels of K + high blood levels of Na, BV and BP

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? *corticotropin 2/10/2003

releasing hormone

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Aldosterone
?

Regulation of Aldosterone Secretion (fig 17.15)

regulatory effects are brief

lasts approximately 20 min plasma electrolyte balance precisely controlled and modified

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Regulation of Aldosterone Secretion

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Regulation of Aldosterone Secretion

?

1) renin-angiotensin system
major regulator of aldosterone release
kidney cells release renin BP

4) atrial natriuretic peptide (ANP)

hormone secreted by the heart
response to BP

2) plasma [Na 2+] and [K+]

fluctuating blood levels directly influence zona glomerulosa cells
K+ and Na 2+ are stimulatory K+ and Na 2+ are inhibitory

fine-tune BP fine-tune Na 2+ -H 2O balance in body

inhibits the renin-angiotensin effect
BP by Na and H 2O in urine

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Summary of Aldosterone Regulation (fig 17.13)

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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

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Glucocorticoids
?

Cortisol
?

hormones
cortisol (hydrocortisone)
secreted in significant amts

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

cortisone corticosterone
?

absolutely essential for life

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Cortisol
?

Cortisol Regulation
?

action
influence the metabolism of most body cells help resistance of stressors help body adapt to intermittent food intake
maintain constant blood sugar levels

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

maintain BV
prevent shifts of H2O into tissue cells

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Cortisol Regulation
?

Excessive Glucocorticoid Levels

? ?

cortisol secretory bursts

driv en 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

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
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interruption in normal rhythm

acute stress
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Stress
?

Pathology of Cortisone Excess

? ?

SNS overrides the usually inhibitory effects of elevated cortisol levels

triggers CRH ACTH blood levels cortisol from the adrenal cortex
blood levels
glucose f.a. a.a

Cushing Ds s causes
ACTH releasing tumor of pit ACTH releasing malignancy of lungs, pancreas, or kidneys tumor of adrenal cortex clinical administration of glucocorticoid meds

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Regulation of Cortisol Secretion (fig 17.15)

?

Pathology of Cortisone Excess

persistent hyperglycemia
aka steriod diabetes
?

dramatic losses in muscle & bone protein water and salt retention
HTN, edema

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Cushing-oid Signs
? ?

Gonadocorticoids
?

swollen moon-face redistribution of fat

abdomen posterior neck (buffalo hump)

action
not fully understood adrenal androgen levels rise continuously between ages of 7 and 13
boys and girls

? ?

tendency to bruise poor wound healing

contribute to onset of puberty and the appearance of axillary and pubic hair

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Pathology of Cortisone Excess

? ?

Gonadocorticoids
action
responsible for sex drive
adult women

enhanced anti-inflammatory effects

infections
overwhelming severe before producing recognizable symptoms

converted to estrogens after menopause

when ovarian estrogens are no longer produced

trt (only)
removal of the cause
surgery drug discontinuation

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Gonadocorticoids
?

Gonadocorticoids
?

androgens primarily secreted

male sex hormones
most importanly testosterone

amt sex hormones produced

adrenal cortex
insignificant in comparison to amts produced by the gonads
during late puberty and adulthood

? ?

small amts estrogen also secreted stimulus

ACTH (appears)

inhibition
mechanism not understood
ACTH does not exert feedback control

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Hypersecretion of Gonadocorticoids
? ? ?

Adrenal Medulla
?

homeostatic imbalance results in masculinization or virilization adult males

testicular testosterone has already produced virilization

location
ctr of the adrenal gland
surrounded by the adrenal cortex

formed from nervous tissue

releases NT as its hormones s

secretes catecholamines into the blood

epinephrine (adrenaline) norepinephrine
secretion controlled by ANS in response to stress

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Hypersecretion of Gonadocorticoids
?

Adrenal Medulla
?

prepubertal males
dramatic effects maturation of reproductive organs and appearance of secondary sex characteristics occur rapidly

unequal amts two hormones released

approx 80% is epinephrine

exert same effects

few exceptions
epinephrine
more potent stimulator of heart & metabolic activities clinically heart stimulator bronchiole dilator

massive onslaughtof sex drive

norepinephrine
greater influence on peripheral vasoconstriction & bp
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Hypersecretion of Gonadocorticoids
? ?

Catecholamine Regulation
stimulus
body fight-or-flight status by short-term s stressor or emergency
SNS is mobilized
blood sugar bv consriction heart beat bp blood diversion from nonessential organs to brain, heart, skeletal muscles

females
androgenital syndrome (virilization of females)
~adrenogenital syndrome beard development masculine pattern of body hair distribution clitoris grows to resemble a small penis

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Stress and Catecholamines (fig 17.15)

?

Pancreas (fig 17.4)

location
partially behind stomach in the abdomen
?

mixed gland
composed of endocrine and exocrine gland cells

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Stress and the Adrenal Gland

? ? Medulla hypo activates medulla via SNS impulses mediates short-term responses secretion of catecholamines ? ? Cortex hypo activates cortex via hormonal signals ACTH ? ?

Pancreatic Cells
?

pancreatic acinar cells

form bulk of gland exocrine fnc produce enzyme-rich product
ducted into small intestine
digestion

mediates long-term responses secretion of steroid hormones

mineralocorticoids
aldosterone

pancreatic islets (islets of Langerhans)

tiny cell clusters
produce pancreatic hormones
glucagon insulin

epi and norepi

glucocorticoids
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cortisol

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Stress and Adrenal Gland

?

Pancreatic Islet Cells

?

catecholamines
cause fairly brief responses to stress

two major pop of hormone-producing cells

alpha cells
glucagon producing cells

adrenocortical hormones
promote long-lasting responses to stress

beta cells
insulin producing cells more numerous

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138

23

Pancreatic Islets
? ?

Glucagon Regulation
stimulus
humoral

?

act as tiny fuel sensors

secrete glucagon and insulin
independently
during fasting and feeding states fluctuations in blood glucose

blood sugar levels amino acid levels

after a protein rich meal

opposite effects
glucagon hyperglycemic hormone insulin hypoglycemic hormone

inhibition
blood sugar levels somatostatin

?
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* believed that hypoglycemics are deficient in glucagon

142

2/10/2003

Glucagon
? ?

Glucagon Regulation (fig 25.20)

polypeptide extremely potent hyperglycemic agent 1 molecule release of 100 mil molecules of glucose in blood

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143

Glucagon
?

target organ
liver
glycogenolysis
breakdown of glycogen to glucose

Insulin
? ?

gluconeogenesis
synthesis of glucose lactic acid noncarbohydrate molecules (fats, a.a)

small protein initally synthesized as part of larger polypeptide

proinsulin

release of glucose to blood by liver

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blood sugar blood [a.a.]

141 2/10/2003 144

2O effect

24

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

Insulin Regulation
?

inhibition
sugar plasma levels somatostatin (indirect)

does not accelerate glucose entry into liver, kidney and brain tissue
easy access to blood glucose regardless of insulin levels

blood sugar levels

represent a balance of humoral and hormonal control

sweeps glucose out of blood

used for energy or converted to other forms (glycogen, fats)

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148

Insulin
?

Insulin Regulation (fig 25.18)

target organ
liver
other effects
influence protein & fat metabolism
promotes protein synthesis & fat storage

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149

Insulin Regulation
?

Regulation of Blood Sugar (fig 17.17)

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

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150

25

Diabetes Mellitus (DM)

? ?

Metabolic Rate
?

homeostatic imbalance hyposecretion or hypoactivity of insulin

insulin deficient or absent
blood sugar levels remain high after a meal

calorimetry measurement
direct method of measuring MR person enters a chamber (calorimeter) heat liberated by body is absorbed by water circulating around the chamber rise in water temp is directly related to heat produced by the person body s

abnormal insulin receptors

glucose unavailable to most body cells
? ?

blood glucose levels amts glucose excreted in urine

151

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154

Diabetes Mellitus (DM)

? ? ?

Metabolic Rate
?

metabolic acidosis protein wasting weight loss

amts fat & tissue proteins used for energy

respirometry measurement
indirect method of measuring MR
O 2 use and heat liberation directly proportional
during food oxidation

avg amt of O 2 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 O 2 the body produces ~4.8 kcal of
heat

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155

Metabolic Rate
?

Metabolic Rate
?

body rate of energy output s

usually expressed per hr

measured under standard conditions

postabsorptive state
not eaten for at least 12 hrs

total heat produced by all chemical rxns and mechanical work of the body measured
calorimeter (directly)
heat liberated by the body

reclining position mentally & physically relaxed temperature is 20-25 degrees Celsius measurements obtained
basal metabolic rate (BMR)

respirometer (indirectly)
O 2 consumption
directly proportional to heat production
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156

26

Basal Metabolic Rate (BMR)

?

Factors Influencing BMR

?

reported in kcal/m2 of body surface/hr

kcal/m2 /h

young person
higher BMR
require large amts of energy for growth

energy body needs to drive only the resting body processes

most essential activities
breathing, maintaining resting organ fnc levels

old age
decrease BMR
skeletal muscle atropy
w/out caloric intake wt

not lowest metabolic state

lowest occurs during sleep
skeletal muscles are completely relaxed

males
higher BMR
more muscle, more active

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160

Factors Influencing BMR

? ? ? ? ? ? ? ?

Factors Influencing BMR

?

age sex size stress body surface area thyroxine levels food effects muscular activity
158

females
fatty tissue in greater relative amts
metabolically sluggish

body temperature
rises and falls w/ MR fev ers MR

stress
higher MR
mobilizes the SNS
epi and nor MR stimulate fat catabolism

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161

Calculation of BMR
?

Factors Influencing BMR

?

avg 70 kg (154 lb) adult

BMR ~ 60-72 kcal/h

thyroxine
most important hormonal factor in determining BMR AKA metabolic hormone

quick approximation of one BMR s

wt (kg) X factor = BMR
2.2 lbs = 1 kg male factor = 1 female factor = 0.9

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162

27

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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28