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Pharmacology Exam III

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waveurflag's version from 2018-03-29 00:56

Section

Question Answer
GHRH releasesGH
TRH releasesTSH
CRH releasesACTH
GnRH releasesLH & FSH
Follicular phase – day 1-14 (follicular maturation)Estrogen dominant
Luteal phase – day 15-28Progesterone dominant
Step 1: Menstrual CycleGnRH gets released from the hypothalamus
Step 2GnRH reaches pituitary gland to secrete FSH that will travel through the blood to mature the follicle. This process takes about 5 days. o There is a competitive follicular maturation going on. Many follicles are trying to mature but only the best one will become fully mature.
Step 3Mature follicle starts producing estrogen. This estrogen travels back to the pituitary has two effects: o Directly shuts down level of FSH (negative feedback to stop FSH because the follicle is already mature) o Will begin an LH burst from the pituitary. Will directly cause ovulation and to have follicle release egg. (this is why LH levels are detected when determining ovulation)
Step 4LH causes ovulation, release of egg from follicle.
Step 5Corpus luteum (envelope remnant of follicle after release of egg) begins releasing progesterone hormone. o Progesterone prepares uterus for embryonic implantation – progesterone receptors are present in the uterus. Uterus becomes bigger and bigger o Progesterone goes back to pituitary and hits progesterone receptors in pituitary to slow release of LH. Prevents over-ovulation.
Step 6No fertilization o Corpus luteum degenerates  no more progesterone being produced o Huge drop in progesterone o Progesterone receptors in uterine lining have no more signals  lining is shed  menstruation o Also estrogen level will decrease
Step 7Cycle starts over again
Why FSH Comes First and not LH?• FSH and LH are completely dependent on GnRH levels • GnRH levels start low (by default) o FSH is high while LH is low
High estrogen =High GnRH
GPCR Involvement of GnRHo GPCR (alpha)  PLC  hydrolyze PIP2  DAG and IP3  inc intracellular Ca++ o DAG  PKC  genetic production that helps LH and FSH release
Estrogen activates hypothalamus through positive feedback
shuts down FSH production in case it did not work through the hypothalamusnegative feedback
The death of the corpus luteum results in falling levels of progesterone and estrogen • These falling levels of ovarian hormones cause increased levels of FSH, which begins recruiting follicles for the next cycle
Corpus Luteumlike a 2nd placenta which the baby feeds on before the developed placenta appears
Thecal CellMakes androgens via 17 B HSD
Granulosa CellTurns androgens into estradiol via P450 aromatase
Order of potencyE2>E1>E3
How do contraceptives work? They trick the body into believing it is already pregnant
Estrone --> Ethinyl Estradiol is a change in which carbonC17
ProgesteroneDismantles the lining of the uterus, – creates a less-than-ideal environment for sperm and have less sperm able to travel to the oocyte
4th Generation ProgestinsHigher side effects. Drospirenone induces more blood clots that other progestins
1st generationNorethindrone acetate is a progestin of low progestational activity and slight estrogenic affects. It tends to be less androgenic than the second-generation progestins, but more androgenic than newer progestins, like desogestrel.
2nd generationLevonorgestrel has high progestational and androgenic effects. Levonorgestrel birth control has also been FDA approved for emergency contraception
3rd generationDesogestrel has high progestational selectivity, minimizing androgenic effects and estrogenic activity. It shows less negative impact on metabolism, weight gain, acne, and other side effects typical of older progestins. It shows positive effects on lipoproteins as seen by a slight rise of HDL cholesterol. Clinical trials show a possibly higher risk of non-fatal venous thrombosis with desogestrel pills versus those with levonorgestrel.
Kariva3rd generation (desogestrel), Estrogen suppresses production of FSH. Levels of both LH and FSH will be low.
Estrogen Genomic MOAInduces dimerization of estrogen receptor. Will cause conformational changes which will attract coactivators
Women who use third generation desogestrel oral contraceptives should be strongly advised not to smoke due to the increased risk of cardiovascular side effects and BLOOD CLOTTING
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