Endocrine System Flashcards
common function of the ES and NS
maintain homeostasis
NS sends messages by:
nerve fibers along neural pathways
ES sens messages by:
hormones in the blood
NS characteristics different from ES
Initiates responses rapidly,
short-duration responses, acts via action potentials and neurotransmitters, acts at specific locations determined by axon pathways, and neurotransmitters act over very short distances
ES characteristics different from NS
Initiates responses slowly, long-duration responses, acts via hormones released into the blood, acts at diffuse locations-targets can be anywhere blood reaches, and hormones act over long distances
endocrine functions
cell differentiation (in utero), growth and development, reproductive systems, homeostasis, and emergency responses
pure endocrine glands
pineal, pituitary, thyroid, and adrenal glands
mixed glands
hypothalamus and pancreas
negative feedback system
change in one direction produces change in the opposite direction; response will reverse or cause the opposite effect of the og stimulus.
positive feedback system
change in one direction produces change in the same direction (rare)
2 classes of hormones
amino acid based (amino acid derivatives, peptides, and proteins) and steriod (from cholesterol)
Are all cells affected by hormones?
no, only cells with receptors are effected
ways hormones produce changes:
alter plasma membrane permeability or membrane potential or both by opening or closing ion channels, stimulates synthesis of enzymes and other proteins within the cell, activates or deactivates enzymes, induces secretory activity, or stimulates mitosis
water-soluble hormones
all amino acid based hormones except thyroid hormone; acrt on plasma membrane receptors; second messenger systems with G-proteins; DOES NOT ENTER THE CELL ALONE
lipid-soluble hormones
steriod and thyroid hormone; act on intracellular receptors that directly activate genes; can enter the cell
humoral stimuli
changes blood levels of ions and nutrients directly stimulates secretion of hormones
neural stimuli
nerve fibers stimulate hormone release
hormonal stimuli
hormones stimulate targets to release their hormones
hypothalamic-pituitary-target organ feedback loop
hypothalamic hormones stimulate release of most anterior pituitary hormones, anterior pituitary hormones stimulate target to secrete more hormones; hormones from the final target organs inhibit release of anterior pituitary hormones
can NS adjust hormone levels?
yes
how can hormones be removed from the blood
degrading enzymes, liver, kidney
half life
time required for level of hormone in blood level to decrease by half
up regulation
target cells form more receptors in response to low hormone levels
down regulation
target cells lose receptors in response to high hormone levels; desensitizes the cell to prevent overreactions
alcohol and ADH
kidneys release water-dehydrated
anterior pituitary hormones
growth hormone (GH), thyroid stimulating hormone (TSH), adrenocorticotropic hormone (ACTH)
posterior pituiatary hormones
oxytocin and antidiuretic horomones
posterior pituitary
neural
anterior pituitary
hormonal
growth hormone (GH)
triggered by low blood levels of GH, sleep, hypoglycemia, increased amino acids, and low fatty acids; inhibited by growth inhibiting hormone or decreased growth releasing hormone; target organs are liver, muscle and bone; increase: giantism or acromegaly; decrease: dwarfism
thyroid stimulating hormone (TSH)
stimulated by releasing hormones or cold temp in infants; stimulates thyroid gland; inhibited by rising blood levels of thyroid hormones that act on pituitary and hypothalamus;
is antidiuretic hormone produced or stored in the posterior pituitary?
stored; it’s produced in the hypothalamus
antidiuretic hormone inhibition
good hydration and alcohol
what hormone affects most of the systems of the body?
thyroid hormone
2 forms of thyroid hormone
T3 (triiodothyronine) and T4 (thyroxine-must be converted to T3 at tissue level)
goiter
enlarged thyroid from lack of iodine (not seen often in the US); less iodine=decreased TH=increased TSH to synthesize more=enlarged thryoid
calorigenic effect
increased basal metabolic rate and heat production
graves disease
hypersecretion of TH; autoimmune disease where body makes abnormal antibodies directed against thyroid follicular cells, the antibodies mimic TSH, stimulating TH release; s/s:elevated metabolic rate, sweating, rapid and irregular heartbeats, nervousness, and weight loss despite adequate food, exophthalmos (protruding eyes)
graves disease treatments
surgical removal the thyroid or radioactive iodine to destroy active thyroid cells
parathyroid glands
secrete parathyroid hormone which is important in calcium; triggered by low calcium levels; inhibited by too much calcium; target organs: bones, kidneys, small intestines; KIDNEY IS INVOLVED IN RELEASE OF CALCIUM!!!!
what vitamin helps with calcium absorption?
vitamin D
adrenal glands
atop kidneys
adrenal cortex (outer)
3 layers of glandular tissues that secrete aldosterone and cortisol; this area produces 24 hormone collectively called corticosteriods (mineralcorticoids, glucocorticoids, and gonadocorticoids)
mineralcorticoids
primarily aldosterone; regulates sodium ion reabsorption and potassium ion excretion;
release of aldosterone
renin-angiotensin-aldosterone mechanism
glucocorticoids
primarily cortisol; helps body resist stressors by increasing blood glucose, fatty acid and amino acid levels, and BP; high levels depress the immune system
adrenal medulla (inner)
nervous tissue that is a part of the SNS; produces catecholamines (epinephrine and norepinephrine) in response to SNS stimulation
epinephrine
stimulator of metabolic activities
norepinephrine
influence on periferal vasoconstriction and BP
effects of catecholemines
vasoconstriction, increased heart rate, increased blood glucose levels, and blood diverted to the brain, heart, and skeletal muscle
short-term stress
1st action potential triggers hypothalamus activitating SNS, adrenal medulla release norepinephrine/epinephrine (fight or flight), respiratory/cardiac affects
long-term stress
stimulates anterior and posterior pituitary, anterior pituitary releases adrenocorticotropin hormones to adrenal cortex causing metabolic and renal effects
hyposecretion of epinephrine and norepinephrine
not essential to life, so no effects
hypersecretion of epinephrine and norepinephrine
symptoms of uncontrolled SNS: hyperglycemia, increased metabolic rate, rapid heartbeat, palpitations, hypertension, intense nervousness, sweating
aldosterone
steroid hormone; mineralcorticoid; increased blood volume by promoting reabsorption of sodium and water while increasing excretion of potassium
renin-angiotensin-aldosterone mechanism
- low blood volume stimulates release of angiotensin 2; angiotensin 2 stimulates adrenal cortex to produce aldosterone; aldosterone causes sodium reabsorption, water reabsorption, potassium excretion, and net increase in blood volume; increased blood volume inhibits the production of angiotensin 2 via negative feedback loop
- renin makes angiotensin to angiotensin 1, lungs make angiotensin 2, stimulates cortex, aldosterone release, salt retention, higher BP; stimulated by low BP
where is angiotensin produced?
in the liver
med for high BP
ACE inhibitor
where is ACE made?
in the lungs
cortisol
released in response to ACTH which is released in response to CRH which is released in response to low cortisol levels; increased cortisol levels inhibit ACTH and CRH through negative feedback loop; governed by patterns of eating and activity; CNS can override inhibition of cortisol
cortisol actions
increase in blood levels of glucose, fatty acids, and amino acids; fight or flight; prime metabolic effect is gluconeogenesis (new glucose formation); enhance vasoconstriction (causes rise in BP);
excessive cortisol
Depress cartilage and bone formation, inhibit inflammation by decreasing the release of inflammatory chemicals, depress immune system, and disrupt normal cardiovascular, neural, and gastrointestinal functions
corticosteriod hypersecretion (Cushings)
Depresses cartilage/bone formation and immune system; inhibits inflammation; disrupts neural, cardiovascular, and gastrointestinal function.
Causes: tumor on pituitary, lungs, pancreas, kidney, or adrenal cortex; overuse of corticosteroids.
Moon face and buffalo hump.
Treatments: removal of tumor or discontinuation of drug
corticosteriod hyposecretion (Addisons)
Usually involves deficits in both glucocorticoids and mineralocorticoids
Decrease in plasma glucose and Na+ levels
Weight loss, severe dehydration, and hypotension are common
Treatment: corticosteroid replacement therapy
Early sign is characteristic bronzing of skin due to high levels of ACTH, which triggers melanin production in melanocytes
pineal gland
small gland hanging from the roof of the 3rd ventricle; melatonin
pancreas
exocrine and endocrine cells; insulin levels
acinar cells (exocrine)
produce enzyme rich juice for digestion
pancreatic islets (islets of Langerhans) (endocrine)
alpha cells (hyperglycemic hormone) produce glucagon; beta cells (hypoglycemic hormone) produce insulin (secreted when blood glucose levels increase)
insulin lowers glucose levels in 3 ways:
Enhances membrane transport of glucose into fat and muscle cells
Inhibits breakdown of glycogen to glucose
Inhibits conversion of amino acids or fats to glucose
glucagon
potent hyperglycemic agent; triggerd by decreased blood glucose levels, rising amino acid levels, or SNS
raises blood glucose levels by targeting liver to:
- break down glycogen into glucose (glycogenolysis)
- synthesize glucose from lactic acid and other noncarbohydrates (gluconeogenesis)
- release glucose into the blood
hormone secretion by other organs
adipose tissue, GI tract, skin, heart, kidneys (renin-initiates renin-angiotensis-aldosterone mechanism), and skeleton
where is glycogen stored?
in the liver
