Aug29 M3-Pituitary_Repro Flashcards
(EXAM) HP axis of the diff hormones from the anterior pituitary (all controlled by post H nuclei)
- thyrotropin releasing hormone (TRH) (H) leads to TSH release by pit
- CRH (corticotropin RH) of H leads to ACTH and MSH release by pit
- GnRH of H leads to LH and FSH release by ant pit
- GHRH from H and ghrelin (stomach) lead to GH release. somatostatin (from everywhere in body but mostly from H) inhibits release of GH from ant pit
- dopamine BLOCKS release of prolactin by ant pit. PRH stims it (oxytocin in blood also, coming from post pit and breast)
embryo origin of the anterior pituitary
outgrowth of the pharynx. later glued itself to the pituitary. neurous of post hypothalamus attached vessels there
(IMP) H and P anterior vs posterior relation
- anterior nuclei of the H control post pit
- post nuclei of the H control ant pit
(EXAM) hormones of the posterior pituitary
- AVP (arginine vasopressin) (controls water balance and BP)
- oxytocin (suckling and birth)
(EXAM) why posterior pituitary hormones not really in HP axis
- neurons of ant H travel to post pit and release oxytocin and AVP there.
- no portal venous system with releasing hormones
(imp) oxytocin functions
- stimulates delivery (uterine contractions) by shutting down vessels to the uterus
- contracts ducts in the breasts to allow milk to go down
(EXAM) HP axis + other glycoprotein hormones
- LH
- FSH
- TSH
- HCG (remember is LH like)
(EXAM) LH, FSH, TSH and HCG similarities + diff
- same alpha chain + all heavily glycosylated
- diff beta chains
(EXAM) 4 factors regulating when the HP gonads axis is active in humans and most important one
age nutrition light social factors (stress) *MOST IMP IS NUTRITION*
(EXAM) hormones and ntrs related to age and affecting HP gonad axis
- right age for reprod + HPG axis working = kisspeptin activating it
- wrong age for reprod + HPG axis not working = MKRN3 inhibiting it
(EXAM) hormones and ntrs related to nutrition and affecting HP gonad axis
- proper nutrition for long term HPG axis working = leptin activating it
- proper nutrition for short-term HPG axis working = insulin activating it
(EXAM) hormones and ntrs related to light and affecting HP gonad axis
melatonin and pineal input (from the pineal gland)
pulsatile hormones in the pituitary
- FSH and LH (pulsatile GnRH) (even though FSH more constant in men because long half life)
- GH (GHRH)
- ACTH (CRH)
- prolactin (dopamine)
pulsatile hormones affecting the release of sex steroids ultimately
sex steroids integrate the cycles of
- leptin
- insulin
- kisspeptin
- etc
most common cause of amenorrhea in the developing world
underweight
most common cause of amenorrhea in the developed world (us)
overweight
(imp) most common cause of amenorrhea worldwide, overall
underweight
factors influencing HP function in general (so not only related to HPG axis)
- age (kisspeptin and MKRN3)
- fat mass (leptin)
- food supply (insulin)
- stress
pulses of GnRH and FSH, LH in follicular vs luteal phase
slower in luteal
kisspeptin charact and fct
- gene Kiss 1, many H nuclei
- is regulated epigenetically. is acetylated
- causes neuronal depolarization
- creates the GnRH pulse
estrogen effect on brain during feedback on hypothalamus
acts on two diff nuclei to affect kisspeptin cycle in 2 diff ways leading to
- suppression of FSH
- stimulation of LH (leading to ovulation)
why does underweight cause infertility in women
- in women, fat is essential for reproduction
- insulin is needed for GnRH secretion (no GnRH secretion = no LH and FSH secretion)
tx of infertility due to underweight
gonadotropins (LH and FSH)
problem assoc with abnormal MKRN3
precocious puberty
hormones signaling the fat mass of the body to the H and P
leptin and estrone
hormones that inhibits FSH
- inhibin
- estrogen
how lactation induces contraception
causes infertility by causing an increase in prolactin (high prolactin) which prevents pulsatility
what mediates the LH surge
kisspeptin. estrogen stimulates the kisspeptin neurons of the H to activate and release GnRH in an increased frequency
consequences of prolactin excess (due to lactation for ex)
-amenorrhea
-hypogonadism
(via suppression of GnRH pulses)
so prolactin controlled by dopamine but ends up affecting GnRH
estradiol and estrone effects
help feminize the body pre and post puberty
GH and gonadotropins link during puberty
mutually increased, so their resulting tissue hormones IGF1 and sex steroids rise together
(EXAM) testo effect in the body other than making its functions
- inhibits LH by slowing the GnRH pulse
- becomes estrogen by aromatisation
(EXAM) progesterone effect in the body other than its fcts
inhibits LH by slowing the GnRH pulse
why women get more autoimmune disease than men
have less testo and testo inhibits B and T cells activity so their immune cells are more active
3 possible mechanisms of gonadal underactivity
- hypogonadotropic hypogonadism (HP failure)
- hypergonadotropic hypogonadism (gonadal failure)
- end organ resistance to gonadal steroids (sex steroids made but target organs resist to them)
* MOST COMMON CAUSE OF GONADAL UNDERACTIVITY IS NO PULSE (prolactin excess, low weight)*
(imp) hypogonadotropic hypogonadism lab signs
- low sex steroids
- low LH and FSH
causes of hypogonadotropic hypogonadism
- congenital
- hypothalamic (low weight, prolactin excess: slow GnRH pulses)
- pituitary damage
(IMP) gonadal failure lab signs
HIGH gonadotropin and LOW steroids
causes of gonadal failure
- chromosomal (Turner)
- menopause
- autoimmune
- surgical, chemo
(imp?) reproductive investigation checks for what
- androgen level (testo, DHEA)
- estrogen level (estradiol)
- FSH, LH, prolactin level
- fasting insulin level
- screen for diabetes if overweight
- scan pituitary if suspected lesion
