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Pharmacology > GYN/Final: contraceptives, HRT, etc > Flashcards

GYN/Final: contraceptives, HRT, etc Flashcards

1
Q

Estrogen’s effect on

  • women
  • men
A

WOMEN

  • developmental effects
  • neuroendocrine actions on ovulation
  • preparation of reproductive tract for fertilization and implantation
  • mineral, CHO, protein and lipid metabolism

MEN:

  • effects on bone
  • spermatogenesis
  • behavior
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2
Q

list the three clinically significant estrogens

A
  1. 17-b estradiol
  2. estrone
  3. estriol
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3
Q

which estrogen is most potent

A

estradiol

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4
Q

Estradiol

  • natural or synthetic
  • priimary circulating estrogen in who
A

natural–>secr by ovary

primary circulatng estrogen in PRE-menopausal

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5
Q

what is the primary estrogen circulating in pre-menopausal women

A

estradiol

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6
Q

Estriol

  • more or less potent than estradiol
  • secreted and synthesized?
A

less potent—its a metabolite of estradiol

synthesized and secretd by placenta during pregnancy

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7
Q

estrone

  • potent?
  • circulates predominanly in who
A

metabolite of estradiol
1/3 potent as estradiol

primary circulating estrogen in post-menopausal women

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8
Q

what is the primary circulating estrogen in post-menop women

A

estrone

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9
Q

do we use synthetic or natural estrogens in contraceptives and HRT?

A

synthetic

mainly ethinyl estradiol

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10
Q

MOA of estrogen

A
  • protein bound
  • diffuses acrross CM to bind with receptor proteins
  • causes RNA synthesis of proteins specific to target tissues
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11
Q

list the 3 main clinical uses of estrogen

A
  1. HRT
  2. contraception
  3. stimulation of sexual chacteristics
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12
Q

benefits of estrogen in HRT (2)

A
  • in PM women— rid of vasomotor challeneges of menopause
  • hot flahses
  • rid of genitourinary s/s too
  • vaginal atrophy
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13
Q

risk of estrogen in HRT (5)

A
  1. decrrs bone resoprtion— incrs risk of bone fx
  2. 3-10x incr risk of endometrial CA (esp with unopposed estrogen)
  3. 2.5x incr risk of VTE (transdermal patches asoc with decr risk)
  4. incr risk of BCA
  5. incr risk of gallstones
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14
Q

in women with intact uterus—- what are they at risk of with unopposed estrogen tx

-how can this risk be reduced?

A

endometrial CA

risk can be reduced by adding progestin with estrogen

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15
Q

what patient would it be indicated to give estrogen tx alone for HRT?

A

s/p hysterectomy

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16
Q

what is very imp to do before HRT

A
  • **evaluate risks vs benefits

* **each woman is diff and therefore tx will be individualized

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17
Q

estrogen preparations

A

oral
transdermal
topical

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18
Q

oral preps of estrogen

indications?

A

OCPs and HRT

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19
Q

transdermal estrogen

  • which estrogen is used
  • inds
A

estradiol

INDS

  • both PM osteoporosis and menopausal symptoms
  • contraception
  • control ovulation in preparation for assisted reproductive therapy
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20
Q

topical preps of estrogen are used for

A

vaginal atrophy

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21
Q

Kinetics for natural estrogens (estradiol)

  • abs
  • met
A

well abs– orally, skin, and mucous mems

partially met by first pass effect, metabolites still effective

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22
Q

synthetic estrogens

-list them

A

ethinyl estradiol and estradiol valerate

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23
Q

kinetics for synthetic estrogens

  • ___ soluble
  • stored where
  • released how
  • more or less potent than natural
  • DOA
A 
fat solube 
stored in adipose tissue 
released slowly 
more potent than natural 
longer acting
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24
Q

SE of estrogen (7)

A
  • nausea
  • HA
  • breast tenderness
  • thromboembolic events
  • MI
  • incr risk of BCA
  • incr risk of endo CA (estrogen unopposed)
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25
Q

define progestogens

A

compounds with bioligc activities similar to progesterone

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26
Q

progestin

A

synthetic progesterone

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27
Q

MC progestogen

A

progesterone

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28
Q

what secreted progesterone

-secreted in resp to?

A

in the ovary— by corpus luteum

in response to LH in 2nd phase of menstrual cycle

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29
Q

imp functions of progesterone

A
  1. development of secretory endometrium—allows implantation
  2. maintain endometrium after implantation
  3. decline in progesterone stimulates menstruation— shedding the basilar layer of endometrium
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30
Q

decline in progesterone levels causes

A

menstruation

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31
Q

list the physiologic functions of progesterone (7)

A
  1. develops secretory endometirum
  2. affects endocerivcal glands–leading to changes decreasing sperm penetration into cervix
  3. maintains pregnancy by suppressing menstruation and uterine contractility
  4. invovled in preparing mammary glands for lactation
  5. slightly elevates body temp during menstruation
  6. incr ventilatino in lueteal phase and pregnancy–>reducing CO2
  7. incrs basil insulin levels and enhances fat deoposition
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32
Q

wht is the primary hormone hat maintains pregnancy

A

progesterone

33
Q

routes of admin/uses for Medroxyprogesterone

A

PO for HRT

injectable for contraception

34
Q

clinical uses for progesterone (6)

A
  1. contracption (with estrogen)
  2. HRT (with estrogen)
  3. DUB
  4. tx of dysmenorrhea
  5. management of endometriosis
  6. interfitlity
35
Q

kinetics of progestogens

  • met
  • bioavail
  • half lives
A 
rapidly met (t 1/2 is 5 min) 
-first pass affect-->gives it poor bioavail
36
Q

kinetics for progestins

  • t 1/2
  • stability vs progestogens
A

more stable to first pass effect

half life=7-30 hours

37
Q

Medroxyprogesterone

  • synthetic or natural
  • routes and their diff metabolisms and half lives
  • uses
A

synthetic

PO with a short half life– of hours—due to extensive hepatic metabolism

IM injection half life for 40-50 days

uses;
*IM for prolonged contraception (3 MO)

38
Q

Norethidrone, Norethidrone acetate, Norgestrel and Levonorgestrel

  • natural or synthetic
  • MOA
  • SEs
A

androgenic activity bc their structures are similar to testosterone

SEs= acne and hirsutism

39
Q

Norgestimate and Drospirenone

  • good for PT with what?
  • uses
A

good for PTs with acne

*found in combined oral contraceptives

40
Q

SE of progestins

A

HA
Depression
Wt gain
Libido changes

41
Q

Mifepristone RU-486

  • drug class
  • MOA
  • uses
  • route
  • se
A

Anti-progestin

MOA
*Progesterone antagonist–resulting in inability to maintain pregnacy

INDS= termination of preg
*combined with prostaglandin analog (Misoprostol)– which causes uterine contractions

PO

SE

  • uterine cramps
  • bleeding
  • abd pain
  • incomplete abortion
42
Q

list the non-hormonal contraceptives

A

diaphgram
contraceptive sponge
copper IUD

43
Q

in combined OCPs, name the MOA for

  • estrogen
  • progestin
A

ESTROGEN MOA
*prevents (-) feedback to PG–>prevents released of FSH–>preventing selection of dominant follicle

PROGESTIN MOA
*inhibits LH secretion—>preventing ovulation

44
Q

for the biphasic or triphasic COCs, what hormone is varying doses

A

progestin

45
Q

places to put the transdermal patch

A
  • abdomen
  • upper torso
  • buttock
  • upper outer arm
46
Q

which contraception has greatest estrogen exposure

A

transdermal patch (vs PO)

47
Q

who is NOT a good candidate for transdermal patch

A

PT over 200 pounds

48
Q

who is GOOD candidate for transdermal patch

A

woman who is non-compliant with taking a pill everyday

49
Q

major SE with transdermal patch

A

higher breakthrough bleeding, spotting

  • breast tenderness in the first two cycles
  • *rash/site rxn
50
Q

with the vaginal ring, when do you need to use backup protection

A

for the first 7 days

if ring has been out for >3 hours

51
Q

main SE with vaginal ring

A

breakthrough bleeding

incr vaginal secretions

52
Q

progestin only pills “mini-pills”

  • who gets them
  • MOA
  • cons
  • pros
A

BREASTFEEDING moms (never give then estrogen OCPs in PP phase) or any woman who has a contra to estrogen

MOA

  • suppress ovulation
  • thicken cervical mucus
  • alter endometrium
  • inhibit tubal transport

CONS

  • less effective
  • more room for error–has to be taken SAME EXACT TIME every day
  • breakthrough bleeding

PROS
*no incr risk of thromboembolic evvents

53
Q

list the 3 long acting forms of contraception and how long each lasts

A
  1. depo shot– 3 MO
  2. IUD
    * progestin ones: 3-5 yrs
    * copper: 10 yrs
  3. Implants–3 yrs
54
Q

Injectable contraception

  • what hormone is in it
  • how is it administered
  • effectiveness
  • SE
  • not recc for?
A

only progestin—Medroxyprogesterone

given IM or SC every 3 MO

effectiveness= as close as sterilization

SE

  • wt gain
  • menstrual irregularity

NOT recc for
* treatment > 2 years bc it can decr bone density

55
Q

Implants

  • what hormone
  • MOA
  • pros
  • cons/se
A

progestin only–>etonogestrol

LARC– long acting reversible contraceptive

MOA

  • inhibs ovulation
  • thickens cervical mucous

PROS

  • good for compliance
  • good for effectiveness
  • not assoc with decr bone density or thromboembolic events

SE/CONS
*irregular menses and HA

56
Q

IUDS

  • what hormone is released
  • duraton
A

Progestin IUDS
LARCs

also have copper only ones– no hormones

Release Levonorgestrel for 3-5 years

MOA
*prostaglandin release–>alters urterine and tubual activity–>drectly toxic to sperm–>

PROS

  • effective
  • little systemic SE
  • helps with heavy menses (copper)
57
Q

which contraceptive is one of the most effective with least systemic SEs

A

IUDS

58
Q

most effective method for EC?

A

copper IUD

59
Q

Plan B, Next step

  • hormones
  • how to take
  • effecetivenss
A

Progestin ONLY– levonorgestrel

take 1 or 2 doses wihtin 72 hrs

75-89% effective

60
Q

Ella/Ulipristal

  • hormones
  • MOA
  • directions to take
A

Progesterone agonist/antagonists

MOA: delays or inhibis ovulation

take within 5 days

61
Q

Yuzpe Method

-hormones

A

COC–estrogen and progestin

one dose— then 2nd dose 12 hrs later
-decrs pregnancy by 75%

62
Q

copper IUD insertion for EC

  • timing of insertion
  • contra
A

inserted within 5 days

CONTRA

  • PT with STDs
  • risk of ectopic pregnancy
63
Q

list the four EC

A
  1. progestin only pills
  2. Progestin antagonist/agonist pills
  3. COCs
  4. Copper IUD
64
Q

SE of contraceptives depends on?

A

[ ] of estrogen and progestin in individual formulations

65
Q

list the serious SE of combined hormonal contraceptives

-esp in women who——

A

ESP IN WOMEN WHO ARE >35 and SMOKERS ::

  • incr BP
  • migraines with aura
  • thromboemobism
  • MI
  • Stroke
  • incr risk of cerivcal CA

BUT decr risk of endometrial and ovarian CA

AKA— ACHES

Abominal pain 
Chest pain 
Headaches 
Eye problems 
Severe leg pain
66
Q

COCs

  • incr risk of what CA
  • decr risk of waht CA
A

INCR risk of cervical CA

DECR risk of ovarian and endometrial CA

67
Q

red flags for OCPs/contras

A 
>35 
smokerrs 
hx of: thromboembolic dz, MI, stroke 
HTN 
migranes with aura
68
Q

SERMS?

  • moa
  • list the drug
A

selective estrogen receptor modulators

**class of estrogen-related drugs that display selective agonism or antiagonism on estrogen receptors dep on target tissue

DRUGS

  • Tamoxifen
  • Raloxifen
  • Clomiphene
69
Q 
Tamoxifen 
-MOA
-kinetics--routes, met, 
-uses 
-SE 
-
A

MOA
*estrogen receptor modulator—competes with estrogen for binding in breast tissue

KINETICS

  • PO
  • extensively met by CYP450— so drug-drug interactions can reduce efficacy

USES

  • BC that is estrogen rec receptive
  • endometrial CA
  • prophylaxis in high-risk PT after they finish tx
SE 
*flushing 
*periphereal edema 
*HTN 
*N/V/D 
*irreg menses 
*endometrial hyperplasia
BBW******* stroke, thromboembolic events--PE, uterine malignancies
70
Q

post-menopausal osteoporosis

A

Raloxifene

71
Q

Climiphene

  • MOA
  • Kinetics–how to adminsiter, rtoue
  • uses
  • SE
  • incr risk of?
A

MOA:
*estrogen agonist interfering with negative feedback of estrogens on the hypothal—- incrs secretion of GnRH–leading to ovarian stimualtion and ovulaiton

KINETICS

  • PO
  • given on or about 5th day of cycle with a 5- day course of medication

USES
*anovulation— stimualtes ovulation in infertility

SE

  • Hyperstimulation of ovary
  • ovary enlargement
  • HA
  • ****Very high risk of multiple gestation
72
Q

what is the most imp androgen in huans

A

testosterone

73
Q

what organs synthesize testosterone

A

ovaires
testes
adrenal gland

74
Q

clinical uses of testosterone

A
  1. primary hypogonadism or secondary
  2. wasting due to CA or HIV
  3. controlled substances to incr lean body mass– muscles stregnth, endurance—UNAPPROVED USE
75
Q

is testosterone active if taken PO

A

no—– highly effected by first pass metabolism

76
Q

two uses for anti-androgens

A

Prostate CA

BPH

77
Q

Flutamide
-use
0moa

A

prostate ca

MOA: inhibits androgens at target cell

78
Q

Finasteride use and MOA

A

BPH

*inhibits 5-alpha reductase–which converts testosterone to DHT– which can bind to receptors

Pharmacology (28 decks)

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