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Pharmacology III > Exam 2- Repro > Flashcards

Exam 2- Repro Flashcards

1
Q

In the developing bi-potential gonad, a complex series of events are triggered by the _____

A
  • sex chromosomes
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2
Q

Outside the gonads, male and female is mainly dependent upon _________

A
  • levels of androgen hormones
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3
Q

Bi-potential organ precursors develop into ________

A
  • male-specific (testosterone high)

- female-specific (testosterone low)

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4
Q

What day in the developing embryo is the first surge of hormones?

A
  • day 40
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5
Q

Presence of the Y chromosome triggers male gonadal development how?

A
  • SRY gene triggers leydig cells to secrete testosterone
  • testosterone triggers sertoli cells to secrete anti-mullerian hormone which leads to regression of the mullerian ducts
  • the testosterone also leads to development of male repro organs
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6
Q

Testosterone and its metabolites trigger _________

A
  • male-specific development in and outside the gonads
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7
Q

female development is considered the default pathway and female hormones are not required until when?

A
  • puberty
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8
Q

Female anatomical devel occurs when?

A
  • the absence of androgens

- no ledig cells and no sertoli cells lead to formation of mullerian ducts and degeneration of the wolffian ducts

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9
Q

Male anatomical devel depends on what?

A
  • androgen, testosterone, and its metabolites (DHT)
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10
Q

Testis

A
  • site of repro cells and male sex steroid production
  • seminiferous tubules
  • interstitial space
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11
Q

seminiferous tubules

A
  • found in the testes

- consists of sertoli cells and spermatogonia

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12
Q

interstitial space

A
  • found in the testes

- consists of leydig cells which secrete testosterone

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13
Q

Ovaries

A
  • site of repro cells and female sex steroid development

- consists of granulosa and thecal cells

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14
Q

In what stage of follicle development does the follicle develop a thecal cell layer

A
  • secondary follicles
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15
Q

Are there different stages of follicles in the ovary?

A
  • yes
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16
Q

in a tertiary follicle which layer is the inner layer?

A
  • granulosa is the inner layer, theca is the outer
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17
Q

What all activates the progesterone receptor?

A
  • Progesterone and a number of therapeutically synthetically altered progesterone derivs
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18
Q

What all activates the androgen receptor?

A
  • Androgens, DHEA, androstenedione, testosterone, DHT, others
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19
Q

What all activates the estrogen receptor?

A
  • Estrogens (alpha and beta), 17b- estradiol is most potent, estrone and estriol (less potent), others like environ estrogens (endocrine disrupters)
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20
Q

Progestogens- what it do

A
  • generally exert anti-proliferative effects on the female uterus: endometrium
  • promote endometrial lining secretion rather than proliferation
  • required for maintenance of pregnancy
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21
Q

Androgens- what it do

A
  • have masculinizing properties
  • T is considered the classic circulating androgen
  • DHT is the classic INTRACELLULAR androgen
  • required for conversion to a male phenotype during development
  • required for male sexual maturation
  • required for male repro function
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22
Q

Synth of androgens

A
  • DHEA is a precursor to testosterone
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23
Q

Testosterone

A
  • major form of androgen in circulation

- must be converted into DHT in peripheral target tissues

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24
Q

Testosterone action at the receptor

A
  • T can bind the androgen receptor but only modest affinity and modest androgenic activity
  • T is converted in target tissues to more active DHT
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25
Q

Pseudovaginal perineoscrotal hypospadias, what chromosome?

A
  • XY chromosome
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26
Q

Estrogens- what it do

A
  • share a common feminizing activity
  • estrogens are derived from aromatization of precursor androgens
  • adipose tissue is the main source of estrogen in postmenopausal women and men
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27
Q

Aromatase

A
  • enzyme that converts precursor androgens to estrogens
  • most active in the placenta and ovaries
  • adipose, hypothalamic neurons, and muscle synthesizes aromatase
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28
Q

Aromatase can convert ____ to estradiol?

A
  • testosterone
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29
Q

Testosterone to DHT to ______ to _______

A
  • 3B-A-diol which can stim ERb receptor
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30
Q

Because the receptors of hormones are all very similar, what can happen?

A
  • can have cross talk (different hormones binding the receptor they weren’t supposed to and still activating a cascade)
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31
Q

Examples of superfamily nuclear hormone receptors

A
  • progestogens, androgens, estrogens
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32
Q

Carrier proteins for hormone transport (2)

A
  • sex-hormone binding globulin (SHBG)
  • high affinity, low levels
  • Albumin
  • low affinity, high levels
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33
Q

when the hormone ligand (plus carrier protein) binds to the receptor and dimerizes, what happens next?

A
  • recruits co-activators/co-repressors
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34
Q

Progesterone Receptor

A
  • most progestins have significant cross-reactivity with androgen receptors
  • prolonged progestin administration produces an androgenic effect
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35
Q

Synthetic progestins and receptors

A
  • most synthetic progestins used as drugs are modified to minimize their androgenic effects
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36
Q

Androgen receptor: does whole complex translocate to the nucleus?

A
  • yes
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37
Q

Estrogen receptor

A
  • two types:
  • classical/genomic: ERa and ERb
  • membrane/non-genomic: GPR30/ERa36
  • many actions of estrogens involve association of the receptor with other transcriptional cofactors
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38
Q

One way estrogens receptors increase their specificity?

A
  • specific transcription co-factors are tissue- and ligand-dependent
  • AR and PR likely share these complexities
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39
Q

Antagonists of the estrogen receptor result in what?

A
  • selective gene transcription

- usually results in lack of a particular gene or set of genes

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40
Q

HPG Axis overview

A
  • hypo secretes GnRH
  • travels via the hypothalamic-pituitary portal system
  • stims gonadotroph cells of the anterior pituitary
  • pulsatile secretion of GnRH stims gonadotropin (LH, FSH) release
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41
Q

continuous application of GnRH does what?

A
  • suppresses gonadotroph activity

- important pharmacological consequences in the admin of EXOGENOUS GnRH (chemical castration)

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42
Q

LH - males

A
  • stims Leydig cells to synthesize testosterone
  • T then diffuses into neighboring sertoli cells and bloodstream
  • stims production of other proteins necessary for sperm maturation
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43
Q

FSH - males

A
  • stims Sertoli cells which increases synth of androgen binding protein (ABP)
  • ABP maintains high testicular [ ] of testosterone
  • necessary for spermatogenesis
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44
Q

Ovaries (Pre-ovulation) - FSH

A
  • Stims granulosa cells and increases estrogen production
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45
Q

Ovaries (Pre-ovulation) - LH

A
  • Stims theca cells which increases production of androgens

- androgens diffuse into neighboring granulosa cells

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46
Q

Both FSH and LH required for formation of

A
  • estradiol
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47
Q

Ovaries (post-ovulation)

A
  • makes estrogens and progesterone
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48
Q

HPG: feedback in males

A
  • T produced in Leydig cell acts as a negative regulator of pituitary gland and hypo
  • sertoli cells synth and secrete inhibin which works back on FSH to inhibit
  • Sertoli cells also synth and secrete activin
  • stims FSH release, does not affect LH release
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49
Q

HPG: feedback in females

A
  • granulosa production of inhibins and activins
  • estrogen more complex than T in men
  • can involve either pos or neg feedback (depending on follicle stage)
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50
Q

Combination of estradiol and progesterone on HPG

A
  • synergistically suppress GnRH, LH, and FSH secretion

- actions at both the hypo and pituitary gland

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51
Q

Menstrual cycle normal range

A
  • 24-35 days

- “28” day model

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52
Q

Portion of menstrual cycle before ovulation (2 names)

A
  • Follicular or proliferative phase
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53
Q

E2 (comes from where and does what)

A
  • comes from the developing ovarian follicle

- stims cellular prolif of the endometrium

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54
Q

Portion of menstrual cycle after ovulation (2 names)

A
  • secretory or luteal phase
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55
Q

Corpus luteum produces which hormone and induces what in the endometrium?

A
  • progesterone, induces endometrium to become secretory rather than proliferative
56
Q

Ovulation: what is happening?

A
  • estrogen levels peak at the end of the proliferative phase
  • this leads to surge in LH and FSH
  • results in eruption of follicle which releases the oocyte
  • remaining follicle changes to lutein cells
57
Q

Corpus luteum (what it does and processes it stimulates)

A
  • cellular remains of the ruptured ovarian follicle
  • secretes estrogen and progesterone
  • endometrium begins synthesizing proteins for implantation of a fertilized egg
  • blood supply to the endometrium also increases
58
Q

First trimester of pregnancy and the endometrial glands

A
  • secretions are very important for the fetus in first trimester
59
Q

Uterus: proliferative phase

A
  • follicles grow
  • estrogens increase
  • leads to proliferation
60
Q

Uterus: secretory (luteal) phase

A
  • corpus luteum produces progest and estrogen
  • leads to decreased proliferation and increased secretion
  • uterine secretions important for embryo
61
Q

If fertilization and implantation do not occur within ____ days, what happens?

A
  • within 14 days
  • corpus luteum ceases production of estrogen and progesterone
  • corpus luteum regresses to corpus albicans
62
Q

Absence of estrogen and progesterone

A
  • endometrial lining sheds and menstruation begins
  • pituitary inhibition removed, FSH and LH increase
  • stims the development of new ovarian follicles and another cycle
63
Q

Fertilization and Pregnancy

A
  • embryo secretes hCG
  • corpus luteum remains viable and secretes progesterone
  • production of hCG decreases after 10 to 12 weeks
  • placenta begins to secrete progesterone autonomously
64
Q

General Mechs of Repro Tract disorders for which pharmacologic agents are currently used (3)

A
  • disruption of HPG axis
  • inappropriate growth of hormone-dependent tissue
  • decreased estrogen or androgen secretion
65
Q

Disruption of HPG axis diseases (2)

A
  • Polycystic ovarian syndrome (PCOS)

- Prolactinoma

66
Q

Inappropriate growth of hormone-dependent tissue (5)

A
  • Breast cancer
  • prostatic hyperplasia, prostate cancer
  • endometriosis, endometrial
  • hyperplasia
  • leiomyomas (uterine fibroids)
67
Q

Decreased estrogen or androgen secretion (2)

A
  • hypogonadism

- menopause

68
Q

PCOS

A
  • characterized by anovulation and increased levels of plasma ANDROGENS
  • 3-5% of women of repro age
  • diagnosis typically clinical (find hirsutism and anovulation)
  • Multiple etiologies are likely responsible
69
Q

LH hypoth of PCOS devel

A
  • increase in GnRH, which increases freq and amplitude of pituitary LH pulses (90% of women with PCOS have increased circulating LH)
  • Increased LH activity effects (stims thecal cells to synth increased amounts of androgens)
  • increased LH and androgen levels prevent normal follicle growth
  • patients with PCOS menstruate irregularly and usually very heavy
70
Q

Insulin theory of PCOS devel

A
  • observation that many women with PCOS are obese, insulin resistant, and secrete increased insulin
  • increased insulin: decreased production of SHBG
  • results in higher concentration of free testosterone
  • greater androgenic effects on peripheral tissues
  • insulin directly synergizes with LH to increase androgen production of thecal cells
71
Q

Ovarian hypoth of PCOS devel

A
  • dysreg of sex steroid synth at the level of the thecal cell
  • abnormal increase in activity of oxidative enzymes for androgen synth
  • greater thecal cell production of androgens in response to any given stim
72
Q

PCOS common treatments

A
  • Target HPG
  • Target AR
  • Target associated pathways
73
Q

Target HPG for PCOS

A
  • estrogen-progestin contraceptive to suppress LH and therefore prevent ovarian production of testosterone
  • adverse: clotting, weight gain
74
Q

Target AR for PCOS

A
  • Spironolactone as an anti-androgen to block the masculinzing effects of T
75
Q

Target associated pathways for PCOS

A
  • metformin, decreases hepatic gluconeogenesis leading to decrease in insulin
  • regular ovulatory menses and normalization of T levels
76
Q

Hyperprolactinemia

A
  • common cause of infertility among women of repro age
  • clonal, benign tumors of lactotrophs in the anterior pituitary (prolactinoma)
  • prolactin-secreting tumors remain responsive to inhibitory effect of dopamine agonists
77
Q

High prolactin levels like in hyperprolactinemia results in what

A
  • suppress GnRH release

- causes reduction in circulating levels of LH, FSH, and estrogens

78
Q

3 ways you can treat breast carcinoma expressing ERs

A
  • modify hormone signalling by:
  • pure antagonist
  • SERM
  • Aromatase Inhibitor
79
Q

Inappropriate growth: prostate

A
  • normal growth and maintenance requires androgens
  • requires local conversion of T to DHT (stromal and basal cells of prostate)
  • Treatment of BPH and metastatic prostate cancer includes androgen blockade
80
Q

Androgen blockade for inappropriate prostate growth (3)

A
  • 5alpha-reductase inhibitors
  • receptor antagonism
  • GnRH AGONIST
81
Q

Inappropriate growth: endometriosis

A
  • growth of endometrial tissue outside uterus
  • usually found in areas surrounding fallopian tubes
  • endometriosis tissues respond to estrogen stim
  • grows and regresses with menstrual cycle which results in severe pain, abnormal bleeding, adhesion formation in peritoneal cavity
82
Q

Hypoth of endometriosis origin (4)

A
  • result from retrograde migration of endometrial tissue during menstruation
  • result of metaplastic tissue growth from the peritoneum
  • result of spread of endometrial cells to extra-uterine sites via lymphatic ducts
  • result of increased aromatase activity in endometrial tissues
83
Q

Endometriosis treatment

A
  • usually estrogen dependent
  • estrogen-progestin oral contraceptives
  • long half-life GnRH AGONISTS
84
Q

Hypogonadism

A
  • impaired production of sex hormones before adolescence
  • patients do not undergo sexual maturation
  • hormone replacement can allow the devel of secondary sex characteristics
85
Q

Decreased estrogen secretion: menopause

A
  • normal physiologic response to exhaustion of the ovarian follicles
  • menstrual cycles cease when all follicles are depleted from ovaries
  • leads to relative lack of estrogen
86
Q

Effects of follicle depletion in menopause

A
  • decreased estrogen and inhibins
  • results in increased LH adn FSH
  • androstenedione continues to be converted to estrone
87
Q

Effects of relative lack of estrogen in menopause

A
  • hot flashes
  • vaginal dryness
  • decreased libido
  • dermal atrophy
  • osteoporosis
88
Q

Post menopause: where does most estrogen come from?

A
  • adipose tissue
89
Q

Decreased androgen secretion: age dependent changes in men

A
  • androgen secretion declines gradually with age
  • androgen therapy in normal elderly men is controversial
  • androgen replacement therapy is indicated in men with adult hypogonadism
90
Q

as testosterone levels decrease what happens?

A
  • muscle goes to fat… fat has more estrogen secretion

- shift in ratios

91
Q

Can target two major things for drugs

A
  • HPG axis target

- Ligand/Rc targets

92
Q

GnRH AGONISTS

A
  • suppress HPG axis (no longer as sensitive to GnRH in pituitary
  • treats prostate cancer, some breast cancers, uterine fibroids, endometriosis, premature puberty
  • prevents premature ovulation (IVF), and delays puberty for transgender
  • symptoms: menopause sympt, me –> castration symptoms
  • initial spike before suppression, often also given a receptor antagonist at first
93
Q

GnRH ANTAGONISTS

A
  • block release of FSH and LH

- immediate action without stimulation first

94
Q

Contraception: Combined Est and Progestin –> What does it do? (primary and secondary mechanisms)

A
  • suppress GnRH, LH, and FSH secretion and follicular development
  • Primary mech: inhibit ovulation
  • most potent known way to suppress GnRH, LH, and FSH secretion
  • secondary mechs: inhibit proper transport of both egg and sperm, alterations in tubal peristalsis, alterations in endometrial receptivity, alterations in cervical mucus secretions
95
Q

Combined Est and Progestin: Rationale and Progestin actions

A
  • Rationale: use of just estrogens causes endometrial growth which increases risk of endo cancer.. progestin administered to limit endo growth
  • progestin actions: progestin receptor AGONISTS, can have some androgenic cross reactivity
96
Q

Vaginal Ring

A
  • cylinder packed with ethinyl estradiol and etonogestrel
  • steroids released with zero-order kinetics (elim is linear)
  • ring placed in vagina for 21 days, out for 7
97
Q

Transdermal Patch

A
  • continuous release of ethinyl estradiol and norelgestromin
  • changed weekly for 3 weeks, off for 1 week
98
Q

Oral Tablets: 21 days on, 7 days off

A

7 day placebo period simulates physiologic involution of corpus luteum

  • causes endo to slough off leading to menstruation
  • progestin inhibits endometrium proliferative growth (lighter menstruation)
  • menstrual cycles often become more regular
99
Q

Oral Tablets: 84 days on, 7 days off

A
  • ethinyl estradiol and levonorgestrel

- same efficacy as 21 days on, 7 days off

100
Q

Oral Tablets: 24 days on, 4 days off

A
  • advantage: ovulation won’t occur if patient forgets to start back up after placebo
101
Q

Formulations of the Pill

A
  • Monophasic/constant dose (most common): same dose of estrogen and progestin for 21 days
  • Biphasic: constant estrogen throughout cycle, progestin initially low and then increases during second half of cycle
  • Triphasic: levels change every 7 days, increased progestin latter half of cycle, midcycle increase in estrogen dose to prevent breakthrough bleeding
  • Quadphasic: Dienogest/Estradiol
102
Q

Advantage of Biphasic or Triphasic formulation- oral contraceptives

A
  • total amt of progestin administered over each month is reduced
  • trend has been to decrease administered estrogen and progestin amounts
103
Q

Disadvantage of multi-phase pills compared to monophasic pills

A
  • trickier to take

- if next pack is started late: increased risk of pregnancy

104
Q

Any differences in adverse effects from the different phasic oral contraceptives?

A
  • no clearly established differences

- lowest ethinyl estradiol dose is preferred to reduce deep vein thrombosis

105
Q

Adverse effects combined oral contraceptives

A
  • deep vein thrombosis and pulmonary embolism
  • no demonstrated increase or decrease in breast cancer
  • increase in gallbladder disease (formation of gallstones)
  • over 35 who smoke should not take (increased thrombotic cardiovascular events
106
Q

Why does combined est and progest oral contraceptives increase gallbladder disease?

A
  • estrogens can increase biliary concentration of cholesterol in bile salts
  • causes increased formation of gall stones
107
Q

Benefits of combined est and progestin oral contraceptives?

A
  • reduces risk of endometrial cancer

- reduces risk of ovarian cancer (lowering circulating levels of gonadotropins)

108
Q

Progestin-Only contraception

A
  • continuous low-dose oral progestins “mini pill”
  • two progestin only contraceptives available in US
  • prevents ovulation 70-80% of the time
  • b/c progestins alter freq of GnRH pulsing; decrease pituitary responsiveness to GnRH
  • 96-98% effective
  • 2ndary mechs like alterations in cervical mucus, endometrial receptivity, tubal peristalsis
  • inhibits endo prolif and promotes endo secretion
  • patients taking these drugs do not typically menstruate
  • breakthrough spotting and irregular, light periods common in first year
109
Q

Progestin only contraceptive preparations (3, just list)

A
  • Injectables
  • Implants
  • IUDs
110
Q

Progestin-only contraceptives: injectables

A
  • medroxyprogesterone acetate
  • given every 3 months
  • good for women who have difficulty remembering to take a pill or change a patch
111
Q

Progestin-only contraceptives: silastic implant

A
  • releases etonogesterel
  • effective for 3 years
  • implant typically inserted into dorsal side of forearm
112
Q

Progestin-only contraceptives: IUD

A
  • levonorgestrel
  • liletta (3), skyla (3 yrs), mirena (5)
  • only small amt of localized hormone reaches bloodstream
  • inserted by physician
  • Liletta contains same amt of progestin as Mirena and release rate about the same but only approved for 3 years
113
Q

What kind of Birth control do breast-feeding women usually take?

A
  • progestin-only, allows for production of breast milk
114
Q

Emergency Contraception

A
  • used because of failure of barrier contraceptive, recent unprotected intercourse
  • Oral Levonorgestrel
  • blocks LH surge disrupting normal ovulation
  • produces endometrial change that prevents implantation
  • dose given as soon as possible after exposure and repeated in 12 hours
  • more efficacious than the ones with estrogen and progestin: fewer side effects
115
Q

Male Contraception

A
  • goal is to suppress endogenous production of sperm reversibly
  • produce azoospermia (no sperm in ejaculate)
  • difficult because even suppressing 99% leaves enough for pregnancy
  • no suppression of libido or sexual functioning
  • initial studies of male contraception used androgens
  • admin of testosterone enanthate
  • T significantly suppresses gonadotropin release
  • reduced levels of LH and FSH are unable to stim sertoli cell function
116
Q

Male contraception clinical trials

A
  • suppression of spermatogenesis: combined androgen and progestin more completely suppresses gonadotropin release than just androgen alone
  • Testosterone enanthate + daily oral levonorgestrel
  • Testosterone undecanoate + Medroxyprogesterone acetate
  • large population variability in degree of spermatogenesis inhibition
  • on average, 60% of men because azoospermic
  • significant adverse effects: acne, weight gain, potential increase in prostate size
117
Q

Hormone Replacement Therapy: women

A
  • perimenopausal and postmenopausal
  • indications: suppress hot flashes, treat urogenital tissue atrophy (vaginal dryness)
  • current recommendation: use only to treat vasomotor symptoms (hot flashes, night sweats) or vaginal dryness; use lowest possible dose for shortest amt of time
  • delivery systems: Oral tablets, transdermal patches, vaginal rings
118
Q

Women’s Health Initiative: Estrogen Treatment and continuous est-progest treatment findings

A
  • Estrogen Treatment: no increased risk of coronary heart disease or BC, decreased risk osteoporotic fracture, increased risk stroke/thromboembolism
  • continuous est-progest treatment: increased risk cardiovascular, BC, and stroke, decreased osteoporotic fracture
119
Q

Hormone Replacement: Men (Injected)

A
  • Androgens are effective therapy for hypogonadism
  • needs to be injected b/c oral is metabolized by liver in first pass
  • testosterone enanthate and testosterone cyprionate
  • increase plasma T to normal physiological levels
  • injected IM every 2-4 weeks
120
Q

Hormone Replacement: Men (Transdermal Patches)

A
  • plasma testosterone remains relatively constant
  • first-pass hepatic metabolism is bypassed
  • adverse: skin irritation
121
Q

Hormone Replacement: Men (Topical Gel)

A
  • 1x/day
  • plasma levels gradually increase to physiologic levels over 1 month
  • can be risk of exposure if others come into contact with gel
122
Q

Hormone Replacement: Men (Tablet)

A
  • adheres to buccal mucosa
  • results in rapid systemic absorption
  • problem of compliance
123
Q

Hormone Replacement: Men –> types of applications

A
  • IM Injection
  • Transdermal Patches
  • Topical Gel
  • Tablet
124
Q

Hypogonadism in aging Men (Symptoms and recent guidelines for replacement therapy)

A
  • Symptoms: decreased energy, libido, muscle mass, facial hair growth, gynecomastia
  • recent guidelines: consistent signs and symptoms w/ low plasma T (<3 ng/ml)
  • T should not be administered to men with prostate cancer
125
Q

Abuse of androgenic/anabolic steroids

A
  • schedule III controlled substances, illegal to use/distribute without a prescription or license
  • abuse comes from ability to increase muscle mass and fat-free mass
  • almost every type of androgen has been abused
  • new designer androgens are harder to detect because they are metabolized quicker
126
Q

Side effects of anabolic steroids

A
  • CV problems including increased LDL/HDL ratio and hypertension
  • Liver damage
  • cancer risk increased
  • male infertility
  • acne
  • increase in plasma estrogen resulting in gynecomastia
  • mood/behavior changes
  • erythrocytosis and derangements in lipid metabolism
  • likely causes early mortality
127
Q

ED causes

A
  • hypertension
  • diabetes
  • CV disease
  • End-stage renal disease
  • nerve disorder
  • psychological factors
  • drugs (B-blockers, anti-androgens, estrogens)
128
Q

What percent of men with ED suffer from low T levels?

A
  • 8-10%
129
Q

What is the driving force behind male sexual response?

A
  • smooth muscle of the helicine arteries is the driving force
130
Q

Regulation of Erection

A
  • Norep through a-adrenergic receptor increases intracellular calcium and inhibits K channels (smooth muscle contraction)
  • Prostaglandin E1 (PGE1) stims K channels and decreases intracellular Ca)
  • NO stims synth of cGMP which stims K channels and decreases intracellular Ca ( smooth muscle relaxation)
131
Q

Drugs for ED

A
  • PDE5 inhibitors
  • male sexual response is down-regulated by process that includes destruction of cGMP by PDE5
  • promote penial erection by blocking destruction of cGMP in the helicine arteries
132
Q

Female Sexual Dysfunction

A
  • associated w/ a variety of diseases or conditions (esp est deficiency) and psychological factors
  • depression
  • stress
  • anxiety
  • hormone deficiency
  • vaginal atrophy
  • diminished vaginal/clitoral blood flow
133
Q

Treatment of female sexual dysfunction w/ estrogens

A
  • Systemic treatment (high doses est/progest)
  • benefits not limited to sexual function (relief hot flashes, bone loss, improved sleep)
  • risks include venous thrombosis, stroke, breast cancer
  • Local/topical treatment
  • vaginal estrogen cream
  • vaginal estrogen ring
  • vaginal tablets
134
Q

Treatment of female sexual dysfunction with “female viagra”

A
  • Flibanserin
  • agonist at serotonin receptors, partial agonist at dopamine receptors (gets into CNS)
  • FDA approved drug originally developed as anti-depressant
  • treatment of premenopausal with hypoactive sexual desire disorder
  • risk of serious hypotension and syncope esp in patients with hepatic dysfunction or on CYP3A4 inhibitors
135
Q

Other approaches to treat female sexual dysfunction

A
  • Testosterone (not FDA approved): many side effects

- Sildenafil also not FDA approved in women

Pharmacology III (18 decks)

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