Endo/Repro Flashcards
5 cell types of the anterior pituitary
acidophils
somatotrope- GH
lactotrope- prolactin
basophils
gonadotrope- LH/FSH
corticotrope- ACTH
thyrotrope- TSH
list 4 steroid hormones, where they act
GCs, androgens, estrogens, vit D
nuclear receptors, slow effects
what does cortisol stimulate
- gluconeogenesis, lipolysis, proteolysis
- inhibits NFkappaB by binding to Ikappab promoter, forming complexes with it outside cell
4 layers of the adrenal gland and what it produces
glomerulosa- aldosterone, MRs
fasiculata- GRs
reticulata- weak androgens
common effects of adrenal cortex enzyme deficiencies
- no CORT
- adrenal hyperplasia due to excess ACTH
ACTH receptor
MC2R
21 hydroxylase deficiency
- no cortisol or aldosterone, increased androgens
- hypotension, hyperkalemia
- high renin
- masculinization
11-hydroxylase deficiency
- no cortisol, low aldosterone, high MR activity (11-DOC), increased androgens
- hypertension, hypokalemia
- masculinization
17 hydroxylase deficiency
- no cortisol , low aldosterone, high 11-DOC
- hypertension, hypokalemia
- feminization
cushing’s syndrome vs cushing’s disease; symptoms
- when ACTH comes from the pituitary, it’s cushing’s disease
- hypertension (cort stimulating alpha adrenergics) , central obesity, thinning of skin, hyperglycemia, insulin resistance
what is required for the NE to E conversion in the adrenal medulla?
cortisol
excess VMA in the urine, what do you suspect
pheochromocytoma, excess degradation of NE/E
thyroid hormone synthesis; what all steps are dependent upon
trap, transport, (oxidize iodide- TPO) iodinate (organification-TPO), conjugate (TPO), endocytose, proteolysis, secrete; everything dependent on TSH
T3 vs T4
T3- MIT-DIT
T4- DIT-DIT
type 1, 2, 3 deiodinase
1) outer and inner rings, makes T3/RT3, liver, kidney, thyroid, skeletal muscle
2) outer- pituitary, brain, heart, placenta
3) inner- brain, skin, placenta
actions of T3
increases BMR, increases brain maturation, increase beta adrenergic receptors
what stimulates prolactin; what inhibits it
stimulates- TRH, GH
inhibits- dopamine
lactation inhibited by estrogen and progesterone
where do the incretins come from?
glucagon gene, GLP1 & GLP2 activated in the intestines in response to low glucose
transcription factor which increase glucokinase?
SREPB1 in WAT
PPAR gamma increases adipocytes
targets of PTH
kidney- increases Ca reabsorption, Pi excretion
bone- releases Ca
targets of vitamin d
chief cells- inhibits PTH
bone- mobilizes Ca
gut- increases Ca and Pi absorption
estrogens effects of Ca2+ regulation
increases 1alphahydroxylase activity, stimulates OPG, decreases bone loss
endocrine disrupters
PCBs compete with TBG
DES synthetic estrogen
what does the product of epsilon cells in the stomach do?
ghrelin- inhibits insulin release by reducing the amount of intracellular Ca2+
which gene in linked with type 2 diabetes?
TCF72
what happens if, while genital ducts are maturing they encounter testosterone? antimullerian hormone?
what produces each?
w/ testosterone from leydig cells (normally from testes), keep wolffian ducts
w/ antimullerian hormone from sertoli cells- degrade mullarian ducts
what does 5 alpha reductase do?
converts testosterone to more potent DHT, which is important for male genitalia development via androgen receptors
where does spermatogenesis occur?
seminiferous tubules
what do coelomic epithelium cells become?
sertoli cells in male, granulosa cells in female (nurse cells)
what do mesenchymal cells become?
leydig cells in males, theca cells in females (hormone cells)
what converts testosterone to estadiol?
aromatase
what does testosterone do during fetal development?
epididymis
vas deferens
seminal vesicles
what does DHT do during fetal development?
penis/urethera
scrotum
prostate
what does testosterone do during puberty?
penis seminal vesicles musculature voice skeleton spermatogenesis
what does DHT do during puberty?
scrotum prostate male pattern baldness happy trail beards sebaceous glands
where does GnRH come from? what is it inhibited/stimulated by?
- arcuate nucleus and preoptic area of hypothalamus;
- inhibitors: dopamine, endorphins, CRH
stimulator: NE
hormone actions during follicular phase
1) GnRH causing FSH/LH release (pulsatile)
2) increasing FSH/LH stimulate ovary to develop follicle
3) follicle secretes E2 (estradiole)
4) E2 has positive feedback on follicle BUT
5) E2 has negative feedback (with inhibin) on pituitary/hypothalamus on FSH cells - keeps volume down as capacity builds (LH rising)
hormone actions during ovulatory phase
1) E2 gets past a certain threshold for a sustained period of time, switches to positive feedback (timing determined by ovary)
1b) increase GnRH receptors on gonadotrophs
2) get LH surge - reinforcing self and E2
3) causes rupture of follicle
4) everything dips because it’s all disorganized
hormone actions during luteal phase
1) corpus luteum becomes dominant- makes E2 (not as high as surge) and progesterone (off the charts)
2) switch back to inhibition, get little LH/FSH/GnRH
3) no LH causes corpus luteum to degrade
4) once CL degrades, lose E2 and progesterone, FSH levels recover
5) lose functional endometrial layer
what are the actions of estradiol secreted by the dominant follicle?
- inhibits growth of other follicles
- makes mucus thin
- prepares fallopian tubes
- potentiates action of progesterone so uterus goes into secretory mode
- primes GnRH action on LH surge to get more LH
how does high insulin impact ovaries? what do you treat with?
stimulates androgen production, causing impaired follicle development and no ovulation; follicles degrade into cysts and ovaries double in size
- treat with metformin
two exocytotic events during the fertilization process
1) Exocytosis of spermatozoan internal membrane contents- allows sperm to attach to zona pellucida
2) Exocytosis of oocyte’s internal vesicles- harden the rest of the zona pellucida (Ca2+ mediated- also triggers second meiotic division after metaphase II)
what happens during adhesion?
- zona pellucida dissolves
- Il-1 increases integrins in endometrial cells
- osteopontin (bridging molecules) binds integrins together
- trophopblasts develop
what happens during penetration?
- stromal cells of endometrium enlarge to form the decidua (progesterone-promoted) and secrete nutrients (source until placenta)
- cells preform some endocrine functions (e.g. prolactin)
what happens during invasion?
- find balance between decidual cells and trophoblast migration
- trophoblasts differentiate into syncytiotrophoblasts (like pituitary- most endocrine functions, makes hCG/hCL) and cytotrophoblasts (like hypothalamus- CRH, TRH, somatostatins)
what is hPL?
HCS aka human placental lactogen (HPL)
- similar to growth hormone
- stimulates lipolysis and has anti-insulin effects on maternal metabolism
- leads to increase in plasma glucose and FFA for fetus
- cause of gestational diabetes
how is estriol produced?
mom’s cholesterol (LDL)- pregnenolone in placenta- converted by fetal adrenal to DHEA-S- converted by fetal liver to oh-DHEA-S- sulfer removed by placenta- placenta makes estriol
T/F Maternal oxytocin initiates labor
FALSE- released in bursts once labor beings, has positive feedback loop, stimulating prostaglandin release
- stimulus is distention of the cervix: Ferguson reflex
