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