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16 Cards in this Set

  • Front
  • Back
Thyrotropin; thyroid stimulating hormone (TSH)
- produced by anterior pituitary
- glycoprotein with α and
ß subunits, 28 kD
- Stimulates growth of thyroid gland, TH production and release
- stiumlates iodine uptake, iodination, pinocytosis of colloid
Follicle stimulating hormone (FSH)
- produced by anterior pituitary
- glycoprotein with α and
ß subunits, 29 kD
- Stimulates ovarian follicle development / spermatogenesis
- gets sertoli cells (do spermogenesis)
- gets granulosa cells to convert androgens to estrogens
- inhibin inhibits (via AP)
Luteinizing hormone
(LH)
- produced by anterior pituitary
- glycoprotein with α and
ß subunits, 29 kD
- Causes ovulation and production corpus luteum / sex steroid synthesis
- gets leydig cells to make testosterone (testosterone inhibits via GnRH)
- gets thecal cells which make androgens
Growth hormone (GH),
somatotropin
- produced by anterior pituitary
- 191 amino acids, 22 kD
- Stimulates body growth, organ growth and regulates metabolism
- via stiumlating IGF-1 in liver and lipolysis, decresing glucose use
- GHRH increases, SS decreases
- IGF-1 increases SS and decreases GHRH
Gonadotropin releasing hormone (GnRH)
- 10 aa
- acts on gonadotrophs (LH and FSH)
- stimulatory
- pulsular (1 pulse/hr)
- works more on LH b/c FSH has other controling factors
- more as you mature
Leydig cells
- abundant in newborn's and post-pubertal and scattered in CT
- make testosterone via LH stimulation of cAMP -> cholestrol estrase -> testosterone
- testosterone receptors in sertoli cells and T->estradiol to do something in the s cells
Sertoli Cells
- surround semineferous tubules - do proliferation bustst in newborn and just before puberty
- FSH induces p450 acromatase activity to increase proliferation and binding protein production (to store androgens) - sperm count increases inhibin and decreases FSH
follicular stages
primordial - inactive
1o - single granulosa layer
2o - multiple granulosa layers and thecal cells
3o - more granuulosa and thecal
Preovulatory - full of follicular fluid
atretic -
ovarian cycle
- after 1o need Gn
- 3 wks to 2o
- to 3o right after menses
- advance stages need more LH and less FSH
- late stage - LH maintenance combined w/ granulosa making P causes high estrogens and + feedback -> FSH and LH surge -> ovulation
- luteal phase - CL increases 17-OH P which decreases FH and LSH
endometrial cycle
- start prolif on day 5 (secretory galnds, vacularization, cervix mucus)
- E causes P receptors in uterus
- when CL does 17-OH P, secretory phase (more vasc, less mucous)
- menstruation when E, P, FSH, LH decrease and spiral arteries constrict and BV rupture
Thyroid Hormone
- T3 and T4
- stimuate GH expression in somatotrophs and AP
- brain development timing
- reulate ox. phos.
- do (-) feedback on TSH by decreaseing TRH sensitvity and gene expressing of a and b for TSH
- 70% bound to liver glycoprotein, the rest bound to albumin
- 5' deoidinase does t4 -> T3
parathyroid hormone
- increase Ca and decrease Ph
- increases kidney resoption
- increases D3 sythesis
- increases osteocasts and inhibits osteoblasts
- increases GI uptake
important D3 formation
- D3 to 25-OH-D3 in liver
- 25-OH-D3 to 1,25(OH)2-D3 in kidney (active)
- it increase Ca binding protein in GI epi
hCS
- lactogen, incresas until term
- decrases maternal glucose consumption, increases fat metab
- helps w/ mammary cells
DHEA-S
- made in fetal andrenal gland
- converted to estradol and strone by sufatase in placenta
- converted to estriol (most imp) in fetal liver
maternal changes in pregnancy
- Increase E -> increase prolactin
- increase pitutary
- decreased LH and FSH
- total Ca decreases, but ionized increase b/c of PTH
- TH increases
- P increases fat along w/ GH, prolacin and hCS (decrease glucsoe, increase GN)