Lecture 7 Endocrine Part 2 Flashcards
4 hormone structural classification groups
amines, polypeptides, glycoproteins, and steroids
which 2 amines are hormones made from
tyrosine and tryptophan
list the 4 steroid hormones and what they are made from
cholestrol –> estrogen, progesterone, testosterone, and cortisol
hydrophobic hormones - which are they, what type of mechanism and why
steroids and T3/T4, genomic mechanism, they are lipophilic/hydrophobic and can enter the cell plasma membrane and bind to receptors in the cytoplasm/nucleus
hydrophilic hormones - which are they and what mechanism and why
- all other hormones except steroid and T3/T4
- bind to surface receptors and use secondary messengers
- hydrophilic aka lipophobic and cannot pass through plasma membrane
series of events of genomic effect of a hormone
hormone dissociates from carrier protein –> enters cell –> binds to cytoplasmic/nuclear receptor –> hormone receptor complex binds to promoter regions and acts as a transcription factor –> transcription / gene expression turned on
how is progesterone produced and what function does it have
FSH –> follicle matures and ovulation releases egg –> follicle becomes corpus luteum –> progresteroen released –> causes vascularization and thickening of endometrium in preparation for implantation
how is testosterone produced
LH –> interstitial cells of Lyedig –> produce testosterone
how is estrogen produced
FSH –> follicle matures and releases estrogen
explain what could happen when hormone levels are at pharmacological doses
pharmacological concentration –> hormone binds to other receptors and causes side effects
prohormone vs prehormones and example
- prohormone = precursor to a hormone ex: proinsulin
- prehormone = precursor to a prohormone ex preproinsulin
synergistic hormones and example
- 2 hormone with similar effect together have effect that is greater than their sum - ex: glucagon and cortisol to raise blood glucose
- glucagon and epi to raise blood glucose
permissive hormone and example if permissive hormone not present
- permissive = necessary for other hormones to function, allows other hormones to function
- ex: testosterone and estrogen may be present in boy and girl but if not thyroid hormone development will not occur
antagonistic hormone and example
- hormones have opposite effect
- glucagon and insulin
- calcitonin and parathyroid hormone
half life meaning
- amount of time for the concentration to decrease by half
priming effect aka upregulation
hormone causes cell to increase receptors for itself
densenitization and down regulation - how does this relate to diabetes and insulin secretion
- hormone causes cells to decrease receptors for itself
- diabetes: constant insulin –> downregulation of insulin receptors –>. insulin resistance
- can be reversed by exercise
- insulin secretion is supposed to be pulsatile
3 characteristics of hormone receptors
- high affinity to the hormone
- specificity to the hormone
- low capacity = not a lot of hormone is needed
time for genomic action vs non genomic action
- genomic = slow, 30 minutes because transcription and translation
- nongenomic = fast, a few minutes
albumin
most abundant blood protein, a carrier protein
amount of free vs bond hormones
- free hormones are very low, 99% are bound to carrier proteins
- amount of free hormone depends on interaction between receptor and hormone and concentration of hromone
nuclear hormone receptor and 2 domains
- receptor for hormone located inside cell, travels into nucleus
- ligand binding and DNA binding domain
another name for promoter region
hormone response element
explain dimerization and how it differs for steroid vs T3/T4
steroid = homodimerziation T3/T4 = heterodimerzation with cis retinoic acid from vitamin A
list 3 nongenomic hormone mechanisms
adenylate cyclase, phospholipase C, and tyrosine kinase
adenylate cyclase cAMP workflow
hormone binds to receptor –> G protein activation –> adenylate cyclase activated and converts ATP to cAMP –> cAMP activates kinases –> activates other enzymes and protein kinases
phospholipase C work flow
hormone binds to receptor –> G protein activated –> binds to phospholipase C which uses phospholipid from membrane to make DAG and IP3 –> Ca2+ released from ER –> Ca2+ calmodulin complex –> complex phosphorylates protein kinases –> activation of other enzymes and protein kinases
tyrosine kinase work flow
dimerization –> insulin or IGF binds –> autophosphorylation on tyrosine amino acids –> activation of protein kinases and other enzymes
liver cell as an example of having 2 receptors
- alpha adrenergic uses phosphlipase C
- beta adrenergic uses adenylate cyclase
- both result in activation of protein kinases ultimately causing glycogen break down
3 zones of adrenal gland what they produce and general effect of products
- GFR
- glomerolsa = aldosterone and mineralcorticoid, Na+ and water reabsorption and K+ excretion
- fasiculata = glucocorticoid, stress steroid hormones which increase blood glucose - cortisol and corticosterone
- reticularis - androgens which are masculinizing
congenital adrenal hyperplasia cause and effect on hormone levels
- cause is lack of any enzyme that plays a role in conversion of cholestrol to cortisol
- low cortisol –> high CRH and ACTH
- intermediates build up and result in lots of androgens
symptoms for onset iin utero/infants
- female = ambiguous genitalia
- male = large and hairy penis
symptoms for childhood onset
- male = early puberty
- female = infertility
symptoms for adult onset
- salt wasting in male and female
- female = hirsutism
- male = salt wasting
hirsutism
- facial hair, acne
salt wasting
- cortisol is a weak mineralcorticoid so without cortisol Na+ and water are NOT reabsorbed and K+ is not excreted –> lots of urine and low sodium leading to chronic hypotension and hyperkalemia
thyroid follicles
make up the thyroid - single layer of follicle cells with hollow inside filled with protein solution of thyroglobulin
colloid
= solution where solute is a protein - in this case thyroglobulin
process of T3/T4 production
iodide enters follicle cells –> follicle cells release iodide and thyroglobulin into inside of follicle –> iodide converted to iodine –> iodine binds to tyrosine amino acids on thyroglobulin forming DIT and MIT –> MIT and DIT bind together to form T3/T4
process of T3/T4 release
TSH –> receptors on thyroid follicle cells –> follicle cells bring in T3/T4 still connected to thyroglobulin –> T3/T4 cleaved from thryoglobulin and released into blood after attaching to carrier protein and thyroglobulin is recycled
endemic goiter and cause
enlarged thyroid caused by hypothyroidism
- low T3/T4 –> lots of TRH and TSH –> thryoid swells
graves disease and cause
autoimmune disease - autoantibodies that mimic TSH accidentally created (thyroid stimulating immunoglobulin TSI) –> bind to thyroid –> lots of T3/T4 –> low TSH and TRH
expohtalmos
clear sign of graves = protruding of eyes
hypothyroidism symptoms
fatigure, lethargy, lack of appetite, weight gain, depression and moodiness, low pulse rate, always cold
MYXEDEMA
hyperthyroidism symptoms
insomnia, excited, weight loss, always hot, nervous, sweating constantly high heart rate
myxedema
- advanced hyPOthryoidism
puffiness of face, hands, and feet
parathyroid hormone effects - 3
increases blood calcium by increasing reabsorption of calcium in kidneys, increasing resorption of bone (bone break down) and activation
pancreas - acinar cell function
- most cells are acinar cells that secrete pancreatic juices into duodenum of small intestine
islet of langherhans 2 types of cells and differing functions
- beta cells, adenylate cyclase release insulin
- alpha cells use phospholipase C and release glucagon
autocrine vs paracrine signaling
- autocrine = hormones go to the same cell type
- paracrine = molecules go ot a different cell type
- both are local
cytokines
- regulate immune system
growth factors
- cause cell growth and division
insulin like growth factors
- tyrosine kinase, release by cartilage and liver causing cell growth and division
NO
- paracrine, made in epithelial cells but effect smooth vascular muscle to cause vasodilation
interluekins
- cytokines between WBC
prostaglandin production
- omega 3/6 –> COX or LOX –> prostaglandins
NSAID effect and side effect
- inhibits COX1 and COX2
- COX1 used by stomach and kidney to produce protective proteins
- COX2 causes inflammation
- binding is non specific
tylenol / acetaminophen effect
- COX3 inhibition, reduces fever and pain but not inflammation
