Hormone Study
Superior Endocrine Organs
Inferior Endocrine Organs
Growth Hormone
Promotes
protein
Hormonal;
Most
Gigantism
Pituitary
cells,
in
Click
on the but
synthesis
and
Peptide
increased
by
header button
to
especially
dwarfism
children,
encourages
use of fats
view that GHRH
hypothalmic
for
fuel;
elevates
acromegaly
bone
and
in
information.
and
decreased
by
blood
glucose (antiskeletal
muscle
insulinadults
effects
of
GH)
Hypothalmic
GHIH
(somatostatin)
Prolactin
Milk
production
in
Hormonal;
released
Overproduction
Mammary
Underproduction
lactiferous
glands
Peptide
in
response
to of
of
glands
breast
of
milk
the
the
breast
of breast
milk
hypothalmic
breast
prolactin
releasing
hormone (PRH)
stimulated by
suckling
Follicle Stimulating Hormone
(FSH)
Hormonal; released
Ovaries
and
Peptide
Stimulation
of
in response to
Infertility
Infertility
gamete
(eggGnRH
or
hypothalamic
Testes
duringproduction
and after
sperm)
puberty. Suppressed
by neg. feedback of
gonadal hormones.
Luteinizing Hormone
(LH)
Hormonal; released
Promotes
Ovaries
and
in
response
to
Polycystic
ovarian
production
of
Peptide
Infertility
hypothalamic
GnRH
Testes
disease
gonadal
hormones
during and after
like testosterone
puberty.
Suppressed
by and
neg.estrogen
feedback of
gonadal hormones.
Thyroid Stimulating
Hormone (TSH)
Causes follicular
Hormonal;
released in
cells
of
the
thyroid
response
to
Follicular
cells
Peptide
Hyperthyroidism
hypothalamic
thyroid
Hypothyroidism
to produce
(Grave’s
disease)
of
the
thyroid
releasing
hormone
precursors
(TRH). Inhibited
by
(predecessor
molecules)
risingtoblood
T3 &levels
T4 of
thyroid hormones T3 &
T4
Adrenocorticotropic
Hormone (ACTH)
Causes
release
of
Hormonal;
triggered
Pituitary
Cushing’s
Disease
Addison’s disease
(cortisol)
–glucocorticoids
“Moon
face”,
“buffalo
by
hypothalamic
(hypocortisolism) –
and gonadocorticoids
hump”,
hyperhidrosis,
corticotropin-releasing
fatigue, weight loss, skin
(androgens
or
precursors
baldness,
hypertension,
hormone
(CRH)
in
a
darkening,
hypotension
to testosterone
&
depression
of
immune
daily rhythm; also by
estrogen)
in the zona
system
fever, hypoglycemia,
fasciculata & zona
and
stressors.
reticularis of the adrenal
cortex
Cortex
of
the
Peptide
adrenal glands
Oxytocin
Stimulates
uterine
Stronger
labor
Labor
Uterine
that
is
smooth
slow of
to
Neural; Stretching
contractions
during
contractions
(possibly
uterus,
sexual
arousal,
muscle;
progress;
breast,
childbirth; triggers milk
Peptide
leading
to
fetal
hearing
baby’s
cry
&
ejection
(“letdown”
reflex)
insufficient
amygdala
of
milk
the
distress),
hyperactive
insuckling;
women producing
milk;
enhanced
“letdown”;
brain
less
sexual
arousal;
increases
milk
“letdown”;
more
release by positive
level
of
trust
between
trust
diencephalon
&
bonding
trust
&
bonding
feedback; stimulus
males & females, mate
removal
bonding, &inhibits
motherrelease
newborn
bonding
Antidiuretic Hormone
(ADH)
“Syndrome
of
Neural;
Released
Inhibitsinsipidus;
diuresis
Diabetes
Inappropriate
ADH
under
high
blood
Tubules
of
the
dehydration
from
(urine
production)
Peptide
Secretion”
(SIADH),
solute
kidneys
excessive
urine
common
in CHS
injury
and
increases
concentrations,
patientsintense
trauma, thirst
some
output;
blood
pressure
inhibited
by low.
cancers; causes
hyponatremia
Alcohol
inhibits ADH
release.
Thyroid hormones
(T3 & T4)
Hormonal;
released
in
Increases
metabolic
rate
Grave’s
disease;
fatigue,
In
adults, hypothyroidism
response
to
TRH
from
the
Skeletal
and
and
heat
production
goiter, pituitary.
weight
loss,
(myxedema)
& endemic
anterior
Rising
(calorigenic
effect);
hypertension,
muscle
tissue
goiter
if
iodine
deficient;
in
TH levels provide negative
indirectly
involved
in
BP,
children,
Can
exopthalmos,
breasts
in
feedback.cretinism.
Hypothalamic
tissue
growth,
skeletal
arise
from
autoimmune
or&
TRH
can
overcome
the
men,
nervousness,
Hashimoto’s
hypothyroidism;
nervous
development,
negative
feedback
restlessness during
fatigue,
cold
pregnancy
or sensitivity,
exposure to
reproduction
depression,
puffy face,
cold.
weight gain
Peptide
Calcitonin
Humoral; released by
Decreases blood
thryroid
parafollicular
C
Possible
hypercalcemia
calcium
levels
by
cells Possible
when blood Ca+2 is
but
thyroid
removal
causing
bone
calcium
high; inhibited when
hypocalcemia
deposition;
inhibits
doesn’t
Ca+2
blood effect
Ca+2 is
low.
osteoclasts,
homeostasis.
Regulated
bystimulates
negative
osteoblasts.
feedback
mechanism.
Antagonist
to parathyroid
Hypocalcemic
effect.
hormone.
Bone
Tissue
Peptide
Parathyroid Hormone
Humoral;osteoclasts
released to
if
Stimulates
Hyperparathyroidism;
Hypoparathyroidism
remove
calcium
from
blood Ca
+2 is low;
softening
of
bones,
bone.
Stimulates
the
leads
to
muscle
rising
calcium
levels
Bone
tissue
kidneys
and
intestine
to
depressed
nervous
spasms,
respiratory
inhibit
release.
absorb
more
calcium.
system,
blurred
vision
paralysis,
death
Antagonist
to
Increases Ca+2 absorption
calcitonin.
by
intestines.
Hypercalcemic effect.
Peptide
Aldosterone
Hormonal; decreased
BPof
Aldosteronism
usually
Stimulates
tubules
stimulates kidneys renin and
from
adrenal
tumors;
the
kidney
to
Aldosterone
Steroid,
thus
angiotensin reabsorb
II release
causes
hypertension
&
stimulating
aldosterone
(save)
Na+
and
retain
insufficiency causes
edima
due
to
excessive
Tubules
of
the
release.
Also
released
by
mineralocorticoid
water;
increases
blood
sodium
loss,
humoral
hyponatremia/
Na+ & excretion of K+
pressure;
causes
kidneys
hyperkalemia
ACTH
causes
hyperkalemia,
acidosis
leading to abnormal
release during
stress.
secreation
of
K+
in
the
function of
neurons
&
Aldosterone
release
inhibited
urine
by heartmuscle
atrial natururetic
peptide (ANP).
Cortisol
Maintains
blood
pressure by
Cushing’s
disease:
Hormonal;
released
Addison’s
disease
increasing
the
action of&
depression
of
cartilage
(adrenalcortico
in
response
to
vasoconstrictors;
promotes
bone
formation,
reduction
insufficiency):
coupled
with
increased
bloodand
normal
cell
metabolism
ofdeficits
inflammatory
response,
in aldosterone,
rise
in blood
glucose
levels
of
ACTH;
depression
of immune
decrease
in
glucose
&
Na+
(hyperglycemia hormone).
patterns
of
eating
&
system;
“moon
face”,
levels,
weight
loss,
severe
Decreases edema & pain“buffalo
hump”
activity,
stress
dehydration,
&
producing
prostaglandins.
Steroid,
Nearly all cells
glucocorticoid
hypotension; skin
pigmentation.
Adrenal Androgen
(Precursors to testosterone & estrogen)
Hormonal;
Contributes
to(rapid
the onset
Virilization
sex of
Often
associated
withof
puberty,
appearance
development);
inby
children:
Stimulated
ACTH
Addison’s
disease
secondary
sex characteristics,
pubic hair, acne, body odor,
thethat
(adrenalcortico
sex from
drive. insufficiency)
Note
muscle
&
skeletal
growth,
testosterone
made
fromcortex
testes
since
the
whole
adrenal
hypothalamus;
precocious
puberty;
in
or
estrogen
from
ovaries
is far
makes insufficient hormones
adults:
cessation
of
inhibition
more
abundant
than androgens
menstruation,
excessive
hair,
from the adrenals,
and plays
mechanism
unknown
themasculination
largest role in sex
determination, etc.
Urogenital tissue,
hair
follicles,
Steroid,
muscle and bone
gonadocorticoid
tissue
Epinephrine
and Norepinephrine
Neural;
Released
in
Epinephrine
stimulates
Adrenergic
metabolic
activities,
response
to
Prolonged
fight-orEffects
relatively
bronchial dilation,
&
blood
receptors
on
many
Catecholamines
sympathetic
flight
response,
unimportant
flow to skeletal muscles &
different
organs
stimulation;
hypertension
the heart.
Norepinephrine
influences
peripheral
and tissues
inhibited
by
lack of
vasoconstriction & blood
stimulus
pressure
Insulin
Humoral;
synthesized
Lowers
blood
glucose
levels
Diabetes
mellitus
(DM)
caused
by
Hyperinsulinism:
beta
cells
hyposecretion
(Type
I:
by
enhancing
membrane
in
islet
beta
cells
and
excessive
insulin
juvenile)
or
insulin
resistance
transport
of
glucose
into
fat
released
in
response
(Type
II: late cells.
onset
orInhibits
adult)
secretion;
results
in
& muscle
to
high
blood
glucose
associated
with polyuria,
hypoglycemia,
glycogen
breakdown &
polydipsia
(thirst), polyphagia
(hyperglycemia).
reconstruction
of
glucose
disorientation,
(hunger); acetone breath,
from
lactic breathing),
acid.
A
Antagonist
to
hyperpnea
(heavy
unconsciousness
hypoglycemic
hormone.
ketonuria
in urine,
blood
glucagon.
ketoacidosis
All cells but
especially
liver,
Peptide
adipose tissue,
muscles
Glucagon
Glycogenolysis
(breakdown
Humoral;
Synthesized
Overproduction
of
glycogen
to
glucose),
in & released
by
islet
develops
when
insulin
gluconeogenesis
(synthesis
Hypoglycemia
alpha
cells
in
response
levels
are
too
low;
of glucose from lactic
acid
to
blood
causes
weightglucose
loss,
& low
non-carbohydrates),
release
of glucose
to the
(hypoglycemia).
wasting,
diabetes
blood. A hyperglycemic
Antagonist
to insulin.
mellitus, anemia
hormone
Peptide
The
liver