GYN/Final: contraceptives, HRT, etc Flashcards
(78 cards)
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
2
Q
list the three clinically significant estrogens
A
- 17-b estradiol
- estrone
- estriol
3
Q
which estrogen is most potent
A
estradiol
4
Q
Estradiol
- natural or synthetic
- priimary circulating estrogen in who
A
natural–>secr by ovary
primary circulatng estrogen in PRE-menopausal
5
Q
what is the primary estrogen circulating in pre-menopausal women
A
estradiol
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
7
Q
estrone
- potent?
- circulates predominanly in who
A
metabolite of estradiol
1/3 potent as estradiol
primary circulating estrogen in post-menopausal women
8
Q
what is the primary circulating estrogen in post-menop women
A
estrone
9
Q
do we use synthetic or natural estrogens in contraceptives and HRT?
A
synthetic
mainly ethinyl estradiol
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
11
Q
list the 3 main clinical uses of estrogen
A
- HRT
- contraception
- stimulation of sexual chacteristics
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
13
Q
risk of estrogen in HRT (5)
A
- decrrs bone resoprtion— incrs risk of bone fx
- 3-10x incr risk of endometrial CA (esp with unopposed estrogen)
- 2.5x incr risk of VTE (transdermal patches asoc with decr risk)
- incr risk of BCA
- incr risk of gallstones
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
15
Q
what patient would it be indicated to give estrogen tx alone for HRT?
A
s/p hysterectomy
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
17
Q
estrogen preparations
A
oral
transdermal
topical
18
Q
oral preps of estrogen
indications?
A
OCPs and HRT
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
20
Q
topical preps of estrogen are used for
A
vaginal atrophy
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
22
Q
synthetic estrogens
-list them
A
ethinyl estradiol and estradiol valerate
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
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)
25
define progestogens
compounds with bioligc activities similar to progesterone
26
progestin
synthetic progesterone
27
MC progestogen
progesterone
28
what secreted progesterone
| -secreted in resp to?
in the ovary--- by corpus luteum
in response to LH in 2nd phase of menstrual cycle
29
imp functions of progesterone
1. development of secretory endometrium---allows implantation
2. maintain endometrium after implantation
3. decline in progesterone stimulates menstruation--- shedding the basilar layer of endometrium
30
decline in progesterone levels causes
menstruation
31
list the physiologic functions of progesterone (7)
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
32
wht is the primary hormone hat maintains pregnancy
progesterone
33
routes of admin/uses for Medroxyprogesterone
PO for HRT
injectable for contraception
34
clinical uses for progesterone (6)
1. contracption (with estrogen)
2. HRT (with estrogen)
3. DUB
4. tx of dysmenorrhea
5. management of endometriosis
6. interfitlity
35
kinetics of progestogens
- met
- bioavail
- half lives
```
rapidly met (t 1/2 is 5 min)
-first pass affect-->gives it poor bioavail
```
36
kinetics for progestins
- t 1/2
- stability vs progestogens
more stable to first pass effect
half life=7-30 hours
37
Medroxyprogesterone
- synthetic or natural
- routes and their diff metabolisms and half lives
- uses
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
Norethidrone, Norethidrone acetate, Norgestrel and Levonorgestrel
- natural or synthetic
- MOA
- SEs
androgenic activity bc their structures are similar to testosterone
SEs= acne and hirsutism
39
Norgestimate and Drospirenone
- good for PT with what?
- uses
good for PTs with acne
| *found in combined oral contraceptives
40
SE of progestins
HA
Depression
Wt gain
Libido changes
41
Mifepristone RU-486
- drug class
- MOA
- uses
- route
- se
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
list the non-hormonal contraceptives
diaphgram
contraceptive sponge
copper IUD
43
in combined OCPs, name the MOA for
- estrogen
- progestin
ESTROGEN MOA
*prevents (-) feedback to PG-->prevents released of FSH-->preventing selection of dominant follicle
PROGESTIN MOA
*inhibits LH secretion--->preventing ovulation
44
for the biphasic or triphasic COCs, what hormone is varying doses
progestin
45
places to put the transdermal patch
- abdomen
- upper torso
- buttock
- upper outer arm
46
which contraception has greatest estrogen exposure
transdermal patch (vs PO)
47
who is NOT a good candidate for transdermal patch
PT over 200 pounds
48
who is GOOD candidate for transdermal patch
woman who is non-compliant with taking a pill everyday
49
major SE with transdermal patch
higher breakthrough bleeding, spotting
- breast tenderness in the first two cycles
* *rash/site rxn
50
with the vaginal ring, when do you need to use backup protection
for the first 7 days
if ring has been out for >3 hours
51
main SE with vaginal ring
breakthrough bleeding
| incr vaginal secretions
52
progestin only pills "mini-pills"
- who gets them
- MOA
- cons
- pros
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
list the 3 long acting forms of contraception and how long each lasts
1. depo shot-- 3 MO
2. IUD
* progestin ones: 3-5 yrs
* copper: 10 yrs
3. Implants--3 yrs
54
Injectable contraception
- what hormone is in it
- how is it administered
- effectiveness
- SE
- not recc for?
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
Implants
- what hormone
- MOA
- pros
- cons/se
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
IUDS
- what hormone is released
- duraton
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
which contraceptive is one of the most effective with least systemic SEs
IUDS
58
most effective method for EC?
copper IUD
59
Plan B, Next step
- hormones
- how to take
- effecetivenss
Progestin ONLY-- levonorgestrel
take 1 or 2 doses wihtin 72 hrs
75-89% effective
60
Ella/Ulipristal
- hormones
- MOA
- directions to take
Progesterone agonist/antagonists
MOA: delays or inhibis ovulation
take within 5 days
61
Yuzpe Method
| -hormones
COC--estrogen and progestin
one dose--- then 2nd dose 12 hrs later
-decrs pregnancy by 75%
62
copper IUD insertion for EC
- timing of insertion
- contra
inserted within 5 days
CONTRA
* PT with STDs
* risk of ectopic pregnancy
63
list the four EC
1. progestin only pills
2. Progestin antagonist/agonist pills
3. COCs
4. Copper IUD
64
SE of contraceptives depends on?
[ ] of estrogen and progestin in individual formulations
65
list the serious SE of combined hormonal contraceptives
-esp in women who------
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
COCs
- incr risk of what CA
- decr risk of waht CA
INCR risk of cervical CA
| DECR risk of ovarian and endometrial CA
67
red flags for OCPs/contras
```
>35
smokerrs
hx of: thromboembolic dz, MI, stroke
HTN
migranes with aura
```
68
SERMS?
- moa
- list the drug
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
```
Tamoxifen
-MOA
-kinetics--routes, met,
-uses
-SE
-
```
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
post-menopausal osteoporosis
Raloxifene
71
Climiphene
- MOA
- Kinetics--how to adminsiter, rtoue
- uses
- SE
- incr risk of?
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
what is the most imp androgen in huans
testosterone
73
what organs synthesize testosterone
ovaires
testes
adrenal gland
74
clinical uses of testosterone
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
is testosterone active if taken PO
no----- highly effected by first pass metabolism
76
two uses for anti-androgens
Prostate CA
| BPH
77
Flutamide
-use
0moa
prostate ca
| MOA: inhibits androgens at target cell
78
Finasteride use and MOA
BPH
| *inhibits 5-alpha reductase--which converts testosterone to DHT-- which can bind to receptors
