name the glucocorticoids:

Cortisol(natural in body)

Hydrocortisone

prednisone

dexamethasone

what are the three types

of stimuli for hormonal release?

Humoral stimuli: secretion of hormones in direct response to changing blood levels of ions and nutrients.

Neural stimuli:      nerve fibers stimulate hormone release(i.e. preganglionic s.n.s. fibers stim. adrenal medulla-secrete epiniphrine).

Hormonal stimuli:            hormonal release in response to hormones produced by other endocrine glands(i.e. hypothalamus hormones stim. ant. pit. to stim. targets to secrete still more hormones.)

Describe the antagonistic

relationship between PTH and Calcitonin:

PTH(produced-parathyroid gland):stim for release=Low blood Ca²⁺ levels:increases osteoclast activity(tears down bone matrix & releases more Ca2+ : increase intestinal absorption of Ca2+/increase Kidney tubules reabsob Ca2+.

Calcitonin(produced in thyroid gland):stim for release=high blood calcium levels: causes increased osteoblast activity: decreased kidney reabsorb/increased kidney excretion of calcium.

How is menopause confirmed?

what are the hormones

produced in the anterior pituitary?

where is GH produced?

What is it's stim for release?

What does it affect?

What type of hormone is it?

what does it promote(think metabolic process)?

--produced(&released) in Anterior pituitary

--stimulation for release = GHRH

--Affects skeletal muscle & bone

--is an anabolic hormone(promotes protein synthesis)

--GH directly encourages use of fats(lipolysis)

--produces "somatomedins"(promote sulfur uptake)(in amino acid-cystine & hyaline cartilage)

Where is PRL produced?

what is its target?

what is its effect?

what other hormone has a direct&indirect effect on PRL?

What is the inhibitor for PRL?

-produced in anterior pituitary

--targets are mammary glands

--effect=milk production

--Estrogen has both direct & indirect effect on PRL: high estrogen=high PRL;  Low estrogen=low PRL)

PIH(prolactin inhibiting hormone) inhibits

Oxytocin:

produced where?

stim. for release?

regulated how?

what are its effects?

how does it travel to post. pit?

--produced in paraventricular nucleus of hypothalamus

--stim for release=pressure/birth canal or uterus

--regulated by positive feedback loop

--causes sm. muscle contraction of uterus/mam. glands

--also causes milk let-down (stim. suckling)

--travels from hypothal. to post pit. via hypophyseal tract

ADH: antidiuretic hormone

where produced?

Where released?

how does it get there?

Stim for release?

target organ?

--produced in supraoptic nucleus of hypothalamus

--released in posterior pituitary

--travels via hypophyseal tract to post. pit

--stim for release=angiotensin 2,high solute conc. by macula densa cells monitoring for osmolarity. (ADH helps prevent water overload)

--targets:kidney tubules and distal convuluted tubules-to reabsorb more water

(Alcohol directly intereferes with ADH so that body cannot reabsorb/consume water)

Is the largest gland  & located on the anterior of neck.  Is highly vascularized and close to the carotid arteries.

consists of follicular and parafollicular cells which are composed of simple cuboidal epithelium

composition of T₃, T₄?

relevance?

T3= tyrosine plus 3 iodines

T4=tyrosine plus 4 iodines

tyrosine is an amino acid but with binding of iodine, it acts like a steroid hormone.

these are hormones that regulates metabolism

1)amino acid based hormones will be taken out of blood circulation quickly while steroid hormones stay in the blood much longer.

2)Steroid hormone cell receptors are inside the cell (in cytosol, nucleus, or mitochondria) while the amino acid based hormone receptors are typically on the plasma membrane.

3)Steroid(intracellular)hormones directly activate genes while plb receptors(a.a.'s) are coupled via regulatory molecule(g proteins) to one or more 2nd messengers that cause response

Androgens(testosterone)

Progesterones

Estrogens

Glococorticoids(coritsol)

Mineralocorticoids(aldosterone)

Thyroid Gland: T₃, T₄

(both essential for bone, muscle, nerv. system)

target tissue?

Stimulus?

periperal tissue preference?

Inhibition?

target tissues=ALL; stimulus for release=TSH

thyroid hormone concerned w/ glucose oxidation,ATP:the higher the metabolic rate, the higher the heat production.

TH plays a role in *regulating tissue growth*developing sk.muscle & CNS*maturation & reproductive capabilities

--peripheral tissues prefer T3, so T₄ gets converted to T_3.

inhibition=negative feedback or GHIH

Hyperthyroidism: TH sensitizes Beta receptors in heart/take very little sympathetic stimulation to increase contractility/heart enlarges

Hypothyroidism:  impedes neurological system;top cause of depression, slowdown of metabolic rate;2nd most common endocrine disorder in humans.

Problem converting T₄ to T₃ in peripheral tissues

it takes a hormone and a receptor for system to work.  if a pt has been hypothyroidal for long time, they have developed too many receptors. they need to eliminate some of those receptors.

That is why dose alterations in thyroid medication need to be done in a stepwise function.

define up regulation

define down regulation

Up-regulation=when target cells develop more receptors in response to a hormone or in the absence of a hormone.

Down-regulation=when target cells lose receptors to a hormone either via a loss of the stimulating hormone or the presence of another hormone causes a decrease in receptors

Calcitonin(produced by parafollicular cells in thyroid)

stim for release=high blood calcium levels

causes decreased osteoclast activity/decrease in osteoclast activity;increase in excretion by kidney tubules;lower reabsorption rate by kidney tubules;

PTH(follicular cells/chief cells)

4 glands

stim for release=low blood calcium levels

result=high blood calcium levels because:

PTH stimulates osteoclast activity to digest bone matrix-intestinal cells to absorb calcium-distal convuluted tubules to reabsorb calcium.

is a negative feedback loop

Zonaglomerulosa:outelayerer/locorticoid/aldosterone:secreted from outer layer in response to Na⁺ deprivation)

zonafasciculata:middlelayer/glucocorticoid/cortisol/stimulated by ACTH.

Zona Reticularis:  innerlayer/gonadocorticoids/testosterone

zona glomerulosa:outer layer

zona fasciculata: middle layer

zona reticularis: inner layer

What does ACTH stimulate?

where produded?

target organ?

Ihibition of release?

ACTH stimulates zona fasciculata to produce cortisol

--in the adrenal cortex, fasciculata layer

--target organ(s): Liver {effects=gluconeogenesis}

Adipose tissue{effects=mobilize fatty acids}

Muscle{mobilize use of amino acids}

Immune system: {anti-inflammatory suppression}

inhibition of release=negative feedback

why are corticosteroid drugs not

indicated for long term use?

these types of meds suppress the immune system;

collagen formation is impeded by cortisol; it inhibits any connective tissue longterm; it causes longterm damage to endothelial tissue in the cardiovascular system

Cortisol has a __________________

effect and causes ___________________.

Aldosterone(a mineralocorticoid)

stimulation for release=1) angiotensin2;  2)low Na⁺ levels 3)high blood levels of K^+; 4) ACTH

ANP wants to decrease Na⁺ (blood volume)

works opposite to Aldosterone(antagonistic to)

An ____________ of blood glucose causes

insulin to be released

1) to augment response

2) to allow for variable response

All protein hormones work by

__________  _____________

The 2nd messenger system, a.k.a the ___________

or the __________________ system, allows for

multiple responses in multiple cells.  But can also have different responses in the same cells.

in the cAMP 2nd messenger system, the 1st messenger causes the _______ to _____ __________;

the 2nd messnger _______________ will be augmented

and will then _____________________________.

hormone; change shape;

cAMP; cause other responses

--thru a series of proteins changing shape

-then produces a 2nd messenger

--that 2nd messenger then initiates responses

--there will be more of the responses and they will last longer

The second messenger system is  process of

_________________________.  a small number of hormone molecules bind to membrane receptors, which leads to 1000's of 2nd messengers in cell.  this magnifies the effect of hormone on target cell.

Hormones binding to intracellular receptor prompts ______

_____________ to produce __________.   The _____ is

translated into proteins, which bring about a cellular effect & directly affect metabolic activity and structure of target cell: includes steroid and __________ hormones.

Target cell activation depends on 3 factors:

___________________________

______________________________

______________________________

--blood levels of the hormone

--relative number of receptors on the target cell

--the affinity of those receptors for the hormone

concentrations of circulating hormone reflect:

________________________

____________________________________________.

Hormones are removed from the blood by:

______________________,  ____________________

and _______________________.

Free hormones:

--remain functional for __________________.

they can leave the bloodstream in the following 3 ways:

1) _____________________________

2) _____________________________

3) _____________________________

diffuse out of bloodstream (binds to receptors on target cells);

gets broken down & absorbed by liver or kidney;

gets broken down by enzyme in plasma or I.F.

bound hormones: are primarily

_______________ and ______________.  they remain in circulation much longer.  when they enter the boodstream, more than 99% become attached to special transport proteins.  the bloodstream contains substantial reserve of bound hormones.