Endocrine System Flashcards
examples of steroid hormones
testosterone, estrogen, progesterone, cortisol
examples of peptide hormones
insulin, glucagon, oxytocin, luteinizing hormone
example of hydrophobic and hydrophilic amine hormone
pho-thyroxine
phi-epinephrine
steroid hormone precursor, solubility, transportation through blood, location of receptor, action time
-cholesterol
-hydrophobic
-carrier protein
-inside cell
-slow action
peptide hormone precursor, solubility, transportation through blood, location of receptor, action time
amino acid
-hydrophilic
-dissolves in blood
-on cell membrane
-fast action
hydrophobic amine hormone precursor, transportation through blood, location of receptor, action time
-amino acid > tyrosine
-hydrophobic
-carrier protein
-inside cell
-slow action
hydrophilic amine hormone precursor, transportation through blood, location of receptor, action time
amino acid > tyrosine
-hydrophilic
-dissolves in blood
-on cell membrane
-fast action
steroid hormone response
-hormone goes through cell membrane and binds to receptor
-then receptor and hormone go to nucleus, works with DNA, transcription to make mRNA
(for inhibitory, stops transcription)
-slow
Protein hormone response
bind to receptor on cell membrane to trigger signaling events
-molecules in cell are already made, signal sends them out
-quick
PRH
prolactin releasing hormone
-released after birth from anterior pituitary to stimulate breast tissue to make milk
-released by hypothalamus
prolactin inhibiting hormone PIH
-inhibits the release of prolactin from anterior pituitary to stop making milk
-released by hypothalamus
TRH
thyrotropin releasing hormone
causes the release of thyrotropin stimulating hormone at anterior pituitary
-released by hypothalamus
CRH
corticotropin releasing hormone CRH
stimulates anterior pituitary to release adrenocorticotropic (ACTH) and then release cortisol
-released by hypothalamus
GHRH
growth hormone releasing hormones
-stimulate anterior pituitary to release growth hormone
-released by hypothalamus
growth hormone inhibiting hormone (GHIH)
-slight inhibiting effect on growth hormone
-released by hypothalamus
gonadotropin releasing hormone (GnRH)
stimulate anterior pituitary to release hormones that affect gonads
-released by hypothalamus
hypothalamic-hypophyseal portal system
communicates with anterior pituitary and hypothalamus using hormones
-small blood vessels directly connect them together
hypothalamic-hypophyseal tract
communicate with posterior pituitary
axons from cell bodies in hypothalamus
-these neurons produce neurohormone and then travels to posterior pituitary
anterior pituitary
controls bodily functions by releasing GH, TSH, ACTH, LH and FSH
posterior pituitary
-release oxytocin and ADH (neurohormones)
-doesn’t produce its own hormones but is hypothalamus
oxytocin
stimulates uterine contractions and promotes milk release during breast feeding
-released when hugging
adrenal gland
on top of each kidney
-receives blood from superior, middle and inferior adrenal arteries
-produce cortisol, aldosterone, (no)epinephrine
zona glomerulosa
outermost layer of adrenal cortex
-produces aldosterone
-crucial for electrolyte and h2o balance
aldosterone
regulates mineral balance by increase Na reabsorbed and K excretion
-maintains BP and fluid balance
zona fasciculata
-thickest layer of cortex
-between zona glomerulosa and reticularis
produces glucocorticoids like cortisol
-responses to ACTH
zona reticularis
innermost layer of adrenal cortex
-produces androgens (DHEA)
-produces less androgens compared to gonads
androgens
-develops secondary sexual characteristics during puberty
-in females, can be converted to estrogen
adrenal medulla
-center of adrenal gland
produces catecholamines ((nor)epinephrine)
-part of SNS
-activated by physical activity or stress
cortisol
-release energy stores during periods of stress
produced by zona fasciculata
-effects metabolism and immune system
-stress response
-controlled by hypothalamic-pituitary-adrenal (HPA) axis
cortisol glucose metabolism
increase blood glucose by stimulating gluconeogenesis (NRG from non carbs)
cortisol fat metabolism
promotes lipolysis (breaks down fat) releasing glycerol and fatty acids for NRG production
cortisol protein catabolism
breaks down proteins in muscle to provide amino acids for gluconeogenesis
Steps in the HPA axis
1) stress activation hypothalamus to release CRH
2) CRH travels to anterior pituitary and anterior pit. release ACTH
3) ATCH stimulates and binds to adrenal cortex to secrete cortisol
4) cortisol increase blood glucose, suppresses immune response, affects mood, mobilizes NRG
5) too much cortisol inhibits secretion of CRH and ACTH
Cushing’s disease
-high levels of cortisol
-common cause is a tumor in pituitary
epinephrine
-adrenaline
-produced by adrenal medulla
-fight or flight
increase glucagon, decrease insulin
-not negative feedback by stimulated by SNS
pancreas
-produce and secrete hormones to regulate blood glucose
-release digestive enzymes and substance into digestive tract
-has endocrine and exocrine tissues
endocrine tissue in pancreas
has 2 million pancreatic islets which each contacts 3 principal cells’
alpha cells (secrete glucagon) beta (secrete insulin and amylin) delta (secrete somatostatin)
glucagon
-responses to low blood glucose
increase blood glucose by signaling liver to release store glucose into blood stream
-secrete by alpha cells
insulin
-responses to high blood glucose
-decreases blood glucose by uptake of glucose into cells so it can be used for energy (cellular resp.) or stored as glycogen
-released by beta cells
type I diabetes mellitus
damage to beta cells
-pancreas can’t produce insulin
type II diabetes mellitus
-caused by diet, lifestyle, genetics
-target cells don’t respond to insulin
polyuria
high frequency in urination
-not all glucose is reabsorbed which causes less h2o to be reabsorbed
diabetic ketoacidosis
metabolic acidosis
-since body can’t use glucose properly, it uses fat >losses weight
-breaks down fat leads to ketones in blood, more acidic
thyroid
in neck
-has 4 small glands called parathyroid
thyroid hormone production and regulation
-regulated by hypothalamic -pituitary- thyroid (HPT) axis
-metabolism, growth and energy balance
-2 hormones, thyroxine and triiodothyronine
thyroxine
t4
inactive form
-converts into triiodothyronine when needed
triiodothyronine
T3
active form that regulates metabolism
steps of HPT axis
1) hypothalamus detect low thyroid hormone and releases TRH
2)TRH goes to anterior pituitary, and stimulates the release of TSH
3) TSH goes to thyroid and thyroid absorbs iodine and combines it with tyrosine > T4 and a bit of T3
4)T4 and T3 regulates metabolism by T3 binding to receptors to increase o2 use and energy production, increase Cardiac output, generates heat
5) high t3 and t4, reduces TRH and TSH
thyroid hormone function
*increase breakdown and release of energy stores
BMR: increase metabolism by affecting mitochondria
-increase cardiac output and HR
-dilates vasculature in skin to muscles
-stimulates o2 delivery by making more hemoglobin
colloid in thyroid
site where T3 and T4 is stored
epithelial cells in thyroid
site of T3 and T4 synthesis
parafollicular cell/ C cell
-in thyroid gland, outside thyroid follicles
-produces and release calcitonin to regulate Ca
-trigger is high Ca
primary effects of hypothyroidism
(low t3 and t4)
- low BMR
-sensitive to cold
-increase fat storage
-low BP
-slow reflexes
-depressions
ex. Hashimoto’s thyroiditis
primary effects of hyperthyroidism
-high BMR
-sensitive to warm
-decrease fat storage
-rapid HR
-hyperactive
ex. Graves’ disease
calcitonin
hormone to decrease Ca
steps to regulate Ca
1) parafollicular cells detect increase levels of Ca and secrete calcitonin
2) calcitonin lowers blood Ca by acting on 3 target cells (bone-inhibits osteoclast/ prevent breakdown, kidney- increase excretion intestine-lowers absorption from food)
3)back to normal/ - feed back
parathyroid hormone
-increases Ca
target cells
bones: stimulate osteoclasts to break down bone
Kidneys: reduces Ca excretion and increase calcitriol production
intestine: enhances Ca absorption from food via calcitriol
somatostatin effects
inhibitory effect on insulin
precursors to thyroid
thyroglobulin
