Hormone Study Superior Endocrine Organs Inferior Endocrine Organs.

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Hormone Study Superior Endocrine Organs Inferior Endocrine Organs

Transcript of Hormone Study Superior Endocrine Organs Inferior Endocrine Organs.

Page 1: Hormone Study Superior Endocrine Organs Inferior Endocrine Organs.

Hormone StudySuperior Endocrine

OrgansInferior Endocrine Organs

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Page 3: Hormone Study Superior Endocrine Organs Inferior 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

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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

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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

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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

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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

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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

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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

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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

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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

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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.

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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

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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

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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.

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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

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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

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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

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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