Endocrine Flashcards
why are the kidneys considered endocrine glands?
release erythropoetin for RBC maintenance
how is the pancreas endocrine?
alpha cells- glucagon
beta cells- insulin
delta cells- somatostatin
somatostatin aka
growth hormone
four hormones produce in anterior pituitary
luteinizing hormone, follicle-stim hormone, somatotropin (growth hormone), corticotropin
what 2 hormones does the posterior pituitary release
anti-diuretic hormone (ADH)- vasopressin and Oxytocin (OT)
vasopressin
anti-diuretic; posterior pituitary
why does insulin have to be injected
its not a steroid its a protein, would be destroyed by stomach acid
4 “not steroid” hormones
amines, proteins, and peptides (amino acids), and glycoprotein (protein and carb)
what are steroids formed from
cholesterol
4 examples of steroids
estrogens, testosterone, aldosterone, cortisol
sequence of steroid hormone action
endocrine secrete steroid hormone –> diffuse through target cell membrane to NUCLEUS –> receptor molecule –> bind to DNA make RNA –> RNA into cytoplasm, protein synthesis –> new protein direct hormone effects
sequence of non steroid hormone
endocrine secretes non steroid –> body fluid carries to target –> binds to receptor site on MEMBRANE activating G protein –> activates adenylate cyclase molecules in membrane –> converts ATP into cyclic AMP –> AMP activates protein kinases –> these activate protein substrates in cell that change metabolic process –> cell changes produce hormone effects
difference btwn receptor site in steroid vs non steroid
steroid receptor on nucleus
non steroid receptor on cell membrane
AMP
Adenine MONOphosphate (only one phosphate bc two have detached by ADENYLATE CYCLASE); activates protein kinases
Which phosphate in ATP has most energy
terminal (3rd) phosphate
adenylate cyclase
in non steroid hormone, coverts ATP to AMP
protein kinases
breakdown substrates that have already been broken down; a kinase enzyme that modifies other proteins by chemically adding phosphate groups to them (phosphorylation); activated by AMP in non steroid hormone
How is ATP similar to DNA
both nucleotides (sugar, phosphate, base)
can nervous system stim. glands in endocrine
yes
hormone levels
fluctuate** make waves because of negative feedback
what kind of hormones from hypothalamus
releasing hormone
what kind of hormones from anterior pituitary
stimulating hormones
TRH
Hypothalamus (thyrotropin releasing hormone)–> Anterior pituitary: TSH (thyroid stimulating hormone) –> thyroid
PRF and PIH
Hypothalamus: prolactin releasing factor and prolactin release inhibiting hormone –> PRL (prolactin in pituitary) –> Mammary glands
PRL and target
prolactin to mammary glands
TSH and target
Thyroid stim. hormone to thyroid
CRH
Hypothalamus: cortico-tropin releasing hormone–> ACTH in pituitary (adrenocorticotropin hormone) –> adrenal cortex
ACTH and target
adrenocorticotropin hormone to adrenal cortex
GNRH
Hypothalamus: Gonadotropin releasing hormone –> LH and FSH (leteinizing and follicle stim. hormones in pituitary) –> ovary (FSH) and testes (FSH)
LH and target
luteinizing hormone to ovaries
FSH and target
follicle stimulating hormone to testes
GHRH and SS
Hypothalamus: Growth hormone releasing hormone and somatostatin –> GH (growth hormone in pituitary) –> bone, muscle, adipose
GH and target
growth hormone to bone, muscle, adipose
what does thyroid make and why
thyroxin to regulate rate of metabolism
stalk of pituitary
infundibulum
how many lobes does pituitary gland have
2
does pituitary have many BV and why
YES, very bloody w/ capillaries and such bc hormones travel through blood
where in skull doest the pituitary sit
in the sella turcica in the sphenoid bone
system of BV that connect pituitary with hypothalamus
hypophyseal veins/arteries
hypophyseal veins/arteries
connect pituitary and hypothalamus
growth below or under brain
Hypophesis or Pituitary physis
what lobe (s) in pituitary have blood supply
BOTH
hypothalamic control
of peripheral endocrine glands may utilize as many as 3 types of hormones; multiple negative feedback controls
GH actions
stim size and rate of division of body cells, growth of long bones, enhance amino acids through membranes
PRL actions
secretes milk production after birth; increases effect of LH in males
TSH actions
controls secretion of hormones from thyroid
ACTH actions
controls secretion of hormones from adrenal cortex; STRESS HORMONES
FSH actions
development of egg containing follicles in ovaries; stim follicle cells to secrete estrogen; stim sperm production in males
LH (ICSH in males) actions
promotes secretion of sex hormones; release egg cells in female
ADH actions
Anti-diuretic hormone- causes kidneys to reduce water excretion, in high concentration, raises blood pressure
OT actions
Oxytocin- contracts muscles in uterine wall and those associated with milk secreting glands
location of thyroid gland
below larynx
where are follicular cells located
in the thyroid gland
calcitonin
reservoir for calcium; lowers amount of calcium in blood by inhibiting release of calcium from bones and increasing rate calcium is deposited in bone (TON- tone it down)
what controls calcitonin
elevated blood calcium ion concentration, digestive hormones
what helps calcitonin to inhibit release of calcium from bone increase rate calcium is deposited in bone
osteoblasts bc building bone
what controls if theres too little calcium in blood
parathyroid; raises calcium level
what helps chop down skeletal system to increase calcium in blood
osteoclasts
Grave’s disease
autoantibodies against self bind to TSH receptors mimicking TSH actions, overstim thyroid gland (hyperthyroidism); exothalmic goiter
hashimoto disease
autoantibodies against self attack thyroid cells producing hypothyroidism
cretinism
stunted growth, abnormal bone formation, MR, low body temp, sluggishness (hypothyroidism)
how many are there and where are the parathyroid glands
4, embedded in thyroid gland
what hormone do parathyroid glands produce
PTH- parathyroid hormone
main function of parathyroid glands
calcium regulation
what does PTH do
promotes calcium absorption in small intestine; tells kidney to hold onto calcium and keeps it out of urine
what makes vitamin D and how
liver with presence of kidney and PTH; vitamin D absorbs calcium in intestines *study slide 23
3 actions of PTH
stim bone release of Ca (osteoclasts), stim kidneys to conserve Ca, stim intestines to absorb Ca
hyperparathyroidism cause and symptoms
tumor; fatigue, muscle weakness, depression, increase PTH–> more osteoclasts
hypoparathyroidism cause and symptoms
injury; muscle cramps and seizures, decrease PTH secretion inhibit osteoclasts and decrease calcium concentration
where are the adrenal glands
on top of kidneys
process kidney regulates low bp
low bp–> renin –> angiotensinogen –> angiotensin –> angiotensin II= VASOCONSTRICTOR –> aldosterone= Na retaining hormone
Aldosterone
STEROID; Na retaining hormone to higher bp in kidney; where Na goes, water follows
what releases aldosterone
adrenal gland
cortisol
STEROID from adrenal gland; make more sugar and lay off protein synthesis (stress hormones); decreases protein syn., increase fatty acid release, stim. glucose syn. from noncarbs;
adrenal androgens
supplement sex hormones from gonads; may be converted to estrogens
what molecular structures have “house” at end
steroids; every Cholesterol module
cortisol and aldosterone molecular structures
VERY SIMILAR
making proteins from non-carbs
neoglucogenesis (fats or protein–> glucose)
epinephrine/norepinephrine in heart
rate/force of contraction increase
what in pancreas secrete hormones
islet of langerhans–> alpha cells- glucagon
beta cells- insulin
delta cells- somatostatin
glucagon
from alpha cells in pancreas; stim liver to break down glycogen and convert non-carbs to glucose
somatostatin
delta cells in pancreas; regulate carbs
where is glycogen stored
liver
what does pancreas secrete if blood glucose level is too high
insulin
what does pancreas secrete is blood glucose level is too low
glucagon
sympathetic NS
automatic; don’t control
what can cause release of epinephrine and norepinephrine
STRESS –> hypothalamus –> sympathetic impulses –> adrenal medulla –> fight or flight
what happens during short term fight or flight from eli/norepinepherine
pupils dilate, bp/heart rate increase, blood glucose increase, increase breathing rate
long term adjustment or resistance stage caused from?
stress –> hypothalamus CRH –> pituitary ACTH –> adrenal cortex cortisol
long term adjustment or resistance stage
from cortisol: increased blood concentration of amino acids, increase release fatty acids, increased glucose formed from non-carbs
why do you produce more glucose in fight or flight?
need more energy
