1. around longer (longer residence time/half life): increased chance of receptor-ligand binding

2. systemic delivery: unforseen side effects

3. bioactive products of chemical breakdown: chemical modification makes hormones sometimes bind to other receptors

-has epithelial orgin (like adrenal cortex)

-secretes trophic hormones

glucocorticoid stimulated by release of ACTH from anterior pituitary

causes gluconeogenesis, lypolysis, elevated blood glucose, controls immunity

hypersecretion of corticosteroids

causes hypertension, hyperglycemia, weakness, puffyness

hyposecretion of glucocorticoids and mineralcorticoids

caused by changes in electrolyte balance/hydration

hypertension, dehydration, rapid weight loss, weakness

CRH --> ACTH --> cortisol

back to anterior pituitary and hypothalamus

line sacs of thyroid

synthesize thyroxine (T4)

matrix inside thyroid sacs

contain thyroglobin

-synthesize I- from colloid and attach to tyrosine (MIT and DIT)

-remains attached to T3/T4 cells until hydrolyzed by follicular cells and secreted in free form

-99.6% bound to plasma proteins for stabilization, remainder is available for uptake

-maintain BMR

1. T3/T4 enter cell, convert T4 to T3

2. translocation to nucleus through series of binding proteins

3. T3 enters nucleus, binds to nuclear receptor

4. r-h complex responds to DNA response element

5. heterodimerizes with vitamin A (9-cis-retnoic acid)

6. activates transcription of specific genes

1. alters gene transcription

2. stimulate protein synthesis

3. increase cell respiration

4. elevate BMR

lack of iodine, so no T3/T4 production

TSH still secreted to thyroid, but no negative feedback from T3/T4

-associated with hyperthyroidism

toxic goiter, inherited autoimmune

-thyroid-stimulating antibody produced, causing thyroid to release a lot of hormone uncontrolled

-endocrine and exocrine

-alpha(glucagon) and beta(insulin) cells

-released with decline in blood sugar/fasting

-glycogenolysis in liver (also ketone production, which decreases blood pH)

-lipolysis in adipose tissue (produces free fatty acids)

-increased blood glucose is negative feedback to pancreas

-fasting hyperglycemia

type I: lack insulin, destruction of beta cells

type II: reduced sensitivity of tissue insulin receptors

-inhibit GnRH secretion (seasonal development of repoduction)

-SAD: excess melatonin, jet lag

-antioxidant, anti-aging

-metabolites of arachidonic acid (20-C f.a.'s with 4 double bonds)

-released by PLA2 action (blocked by release of glucocorticoids)

-leukotrienes & prostaglandins: ligands for specific g-coupled receptors

-potent, short lived, local

action of lipoxygenases (eicosaniods)

-inflammation, bronchoconstriction, vasoconstriction, capillary permeability

-medical inhibition: montelukast inhibits lipoxygenase, and zafirlukast inhibits leukotrienes

eicosanoids synthesized from action of COX enzymes

-medical inhibition of cyclooxygenase by ibuprophen, celecoxib, rofeconib, aspirin

"good" prostaglandins of inflammatory tract (gastric mucosa)

-protect blood vessel endothelial cells

-encourages TXA2 activity: clotting (heart attack prevention with aspirin)

-can cause excessive prostaglandin production (vasoconstriction, atherosclerosis, respiratory disease, gynecological disorders, asthma, arthritis)

inhibit COX 1/2

-side effects: gastric mucosa bleeding, kidney problems, blood clotting time alteration, bronchoconstriction

-new generation to inhibit COX 2 only = celecoxib, rofecoxib

epimysum around muscle > perimysum around fasicle > endomysum arounf sarcolemma, which contains nerve, muscle fiber, adn myofibrils

-prevents pulling apart of muscles when they contract