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Endo/Repro Block2 > Female Pharm [last years material...do paper notecards too!] > Flashcards

Female Pharm [last years material...do paper notecards too!] Flashcards

1
Q

What should we use to promote folliculogenesis in women with hypothalamic anovulatory [dys]fxn?

A

daily injxn of both FSH & LH

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2
Q

What should we use to promote superovulatory folliculogenesis in women with hypothalamic anovulatory [dys]fxn?

A

inject **FSH & LH **on day 2-3 of menstrual cycle

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3
Q

What should we use to promote folliculogenesis in women with endogenous estrogen activity & normal hypopit-ovarian fxn?

A

clomiphene citrate: estrogen antagonist that induces FSH secretion

  • MC used
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4
Q

What are menotropins and urofolitropin?

A

urinary derived human gonadotropins [FSH & LH] pooled from postmeopausal women, concentr8d and purified

menotropins: injected, w/ FSH & LH activity (Pergonal)

  • pergonal & hCG given in sequence for ovulation in anovulatory women & for prodxn of multiple follicles

Urofolitropin: injected, w/ FSH activity ONLY (Metrodin)

  • metrodin & hCG given in sequence to induce ovulation in PCOS
    • in pt’s w/ high FSH/LH & IF clomiphene Tx FAILED
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5
Q

What are recombinant human gonadotropins?

what are they used for?

A

available immediately & are consistent

follitropin** a (Gonal-f; FSH) & follitropin b **(Follistim; FSH)

  • a & b are synthesized the same, making identical dimeric a-FSH & B-FSH subunits that differ in glycosylation & purification
  • induce follicle development
  • w/ hCG = induce ovulation
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6
Q

Which has a better rate of pregnancy?

Mixed gonadotropins or FSH [recombinants] only dosing?

A

neither; they have similar pregnancy rates

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7
Q

What are the side effects of the folliculogenesis inducing drugs and recombinant gonadotropins?

A

Hyperstimulation

Multiple Fetuses

Ovarian hyperstimulation syndrome

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8
Q

What is ovarian hyperstimulation syndrome?

A

shift of vascular fluids to abdominal & thoracic cavities

-usually mild Sx’s, occassionally severe

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9
Q

Clomiphene citrate!

A

Its the one to know!!! See paper notecard

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10
Q

What is/are 2 Step Ovulation Induxn?

A
  1. follicular stimulation using combined FSH +/- LH or clomiphene followed by:
  2. hCG to stimulate LH surge
    • induces follicular maturation
    • follicle aspiration or ovulation if desired
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11
Q

What is the role of hCG?

A
  • binds LH/CG-R so has LH-like indxn of ovulation
  • stimulates estrogen primed follicle to induce meiotic resumption of oocytes
  • used following follicle stimulation by clomiphene or gonadotropins
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12
Q

What is a synthetic GnRH agonist?

A

Leuprolide [See paper NC]

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13
Q

What are Cetrorelix and Ganirelix?

A

GnRH Antagonists

  • competitive antagonists–> suppress gonadotropin release
  • Use: fertility, prevents endogenous LH surge while promoting folliculogenesis w/ exogenous gonadotropins
    • in prostate & breast cancer Tx to inhibit steroid prdxn
    • in benign uterine disease [fibroids]

***DO NOT see transient increase in FSH & LH as w/ GnTH agonists

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14
Q

Describe the formation of natural estrogens

A
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15
Q

What do estrogens do?

Fxns?

A
  • development, growth, & maintenance of sex accessory tissues
  • skeletal growth & body shape development
  • key regulator in HPO axis & thus; in maintenance of mense cycle
  • metabolic: Na+ & H2O retention, ^^HDL & decrease LDL
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16
Q

What are the 3 major uses for estrogen?

A
  1. oral contraceptives
    • usually in combo w/ progestin
    • interfere w/ LH surge & ovulation
  2. H replacement therapy
    • usually with progesterone
  3. Dysmenorrhea
17
Q

Which is the principal/primary form of natural estrogen?

what biochemical addition can be made to it?

A

Estradiol 17b

  • readily absorbed in tissues
  • 1st pass metabolism limits oral effectiveness
  • Addition at C-17 reduces metabolism & makes orally active
18
Q

What are some pharmokinetics of estrogens in general?

What does esterification do to estrogens?

A
  • 1st pass metabolism limits oral efectiveness [add C-17 decreases this problem]
  • esterification decreases abdorption rate from parenteral site
  • use: patch, gel, vaginal ring = BC
  • metabolism: LIVER
    • metabolites conjugated
    • conjugates excreted in K or bile
  • circulating estradiol is bound to steroid hormone binding globulin {SHBG]
    • estrogens increase synthesis of SHBG
    • androgens decrease synthesis of SHBG
19
Q

What are examples of a SERM?

A

Tamoxifen [selective estrogen R modulator]

Raloxifene & Toremifene

[see paper NC]

20
Q

What is Fulvestrant?

MOA?

Use?

SE’s?

A

SERD: selective estrogen R Down Regulator

  • PURE estrogen antagonist [blox R binding & down regulates R in al tissues]
  • Use: also ER+ breast cancer Tx
    • IM injxn [1 month?]
  • oxidized & conjugated, excreted in feces
  • SE’s: GI disturbances, hot flashes, thromboembolism
21
Q

What are the axns/fxns of progesterone?

what gene is involved?

A
  • develop & maintain secretory endometrium
  • promote uterine relaxation in prego
  • w/drawal during late prego ids part of parturition
  • preps breast for lactation
  • 2 R’s: PR-a & PR-b on one gene
22
Q

What are the 5 major uses for synthetic Progestins?

A
  1. oral contraceptive
    • alone or w/ estrogens
  2. Emergency contraception =/- estrogens
  3. H Replacement Therapy
    • alone or w/ estrogens
  4. Dysmenorrhea
  5. Luteal support for implantation & pregnancy
23
Q

What is the main form of Progestin?

How is it synthesized?

A

Progesterone, C21 Steroid

Synthesis:

  • corpus luteum makes it during 2nd half of menstrual cycle
  • Placenta makes it in 2nd & 3rd trimester
  • Other tissues: Testes & adrenal…anytime/always?
24
Q

What is a synthetic form of:

C21 Progestin/Pregnanes?

19-nor-testosterones/Estrane?

19-nor-testosterone/Gonane?

A

C21/Pregnane= Medroxyprogesterone acetate

19NT/Estrane= Norethindrone

19NT/Gonane= Levonorgestrel

  • more potent & used at lower doses than others
25
Q

What are the PK’s of progestins?

What do they bind?

A

note: similar to estrogens

  • absorbed readily, but significant 1st pass metabolism
  • esterification retaeds absorption
  • 17C substitutions decrease 1st pass metabolism
  • metabolized, conjugated, excreted by kidney 7 in bile

BIND

  • prgesterone binds to Cortisol Binding globulin
  • 19-nor-progestins bind Steroid H Binding Globulin
26
Q

What are the advantages of contraception using estrogens & progestins?

A
  • reliable contraception
  • decrease endometrial & ovarian cancer risk
  • decrease incidence of ectopic prego
  • menses regulation
27
Q

What are some disadvantages of contraception w/ estrogens & progestins?

A
  • daily admin [compliance]
  • no STD protexn
  • ^^^breast cancer risk w/ triphasic oral E& P
    • risk nullified after 10 yr cessation
  • some SE’s:
    • depression, w8 gain, N, HTN
    • DVT due to hypercoag
28
Q

What is Ulipristal acetate [Ella]

A

emergency contraception

  • interferes w/ or delays ovulation
  • alters endometrium –> may contribute to efficacy
  • efficacy up to 5 days after intercourse

Endo/Repro Block2 (11 decks)

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