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Reproduction Pharmacology > Fertility, Contraception, Gonadal Hormones & Inhibitors > Flashcards

Fertility, Contraception, Gonadal Hormones & Inhibitors Flashcards

1
Q

Oxytocics Drugs:

A

Oxytocin

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2
Q

Prostaglandins Drugs:

A

Dinoprostone, PGE2
Misoprostol, PGE1
Carboprost tromethamine, 15methylPGF2α

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3
Q

Tocolytics Drugs:

A

Magnesium sulfate

Indomethacin

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4
Q

OTC Drugs:

A

Caster Oil, Blue Cohosh, Black Cohosh, Oil of

Evening Primrose, etc.

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5
Q

The myometrium is?

A

smooth muscle controlled by Calcium.

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6
Q

During pregnancy- high concentrations of what hormone predominate?

A

progesterone predominates

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7
Q

Progesterone causes?

A

– Hyperpolarizes uterine smooth muscle membrane
– Makes muscle non-excitable
– Prevents release of arachidonic acid aPrecursor for prostaglandins

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8
Q

As parturition approaches three thinks occur?

A

– increase in estrogen to progesterone ratio.
– Increase in number of gap junctions that electrically couple myometrial muscle cells
– Increase in receptors for contractile agonists

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9
Q

Clinical Use of Oxytocics

A

• Induction or augmentation of labor in case of:
• Control of postpartum uterine hemorrhage
• Induction of uterine contraction after C-section
or during uterine surgery
• Induction of therapeutic abortion

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10
Q

Four reasons for Induction or augmentation of labor:

A

– Premature rupture of membranes
– Fetal growth restriction
– Uteroplacental insufficiency
– Pre-eclampsia/eclampsia

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11
Q

Clinical Use of Tocolytic Agents”

A
  • Delay or prevent premature parturition
  • Slow or arrest delivery for brief periods for therapeutic measures including glucocorticoid therapy to increase pulmonary surfactants
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12
Q

Magnesium Sulfate

Mechanism of action when given Orally :

A

laxative effect

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13
Q

Magnesium Sulfate

Mechanism of action when given Parenterally

A

• As anticonvulsant - depresses the CNS and blocks peripheral neuromuscular transmissio
• To treat hypomagnesemia
• To prevent or control preeclampsia & eclampsia
– Toxemia of late pregnancy characterized by hypertension, edema and proteinuria. w/ convulsions and coma = eclampsia

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14
Q

Magnesium Sulfate Pharmacokinetics:

Administered:

A

– IV administration gives immediate effect lasting 30 min

– IM administration- onset occurs in 1 hour & the duration is about 4 hours

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15
Q

Magnesium Sulfate Pharmacokinetics:

Excretion:

A

Renal excretion

Mg++ reabsorbed

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16
Q

Magnesium Sulfate effect on fetus & infant?

A

Crosses placenta & excreted into breast milk. No reported problems.

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17
Q

The gonadotropic hormones are?

A

LH, FSH and CG because of their actions on the gonads.

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18
Q

GnRH regulates systhesis & secretion of?

A

LH & FSH.

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19
Q

In men, LH acts on the testicular

A

Leydig cells to stimulate synthesis of androgens, primarily testosterone, necessary for spermatogenesis.

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20
Q

Dysfunction in Gonadotropic Hormones?

A

Can lead to infertility in males or females.

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21
Q

Commercial pregnancy diagnostic kits depend on?

A

Qualitative detection of CG in urine of pregnant women (based on the use of antibodies specific for the unique β subunit).

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22
Q

Ovulation occurs 36 hours after the onset of the?

A

LH surge, so urinary concentrations of LH (measured using LH-specific antibodies) can be used to predict the time of ovulation

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23
Q

Degarelix is approved for men with?

A

advanced prostate cancer & works as GnRH Receptor Antagonists

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24
Q

Goserelin, triptorelin, & leuprolide (Lupron®) are agonists of GnRH used in treatment of & work by?

A

Prostate cancer. Initially increases LH production, then decreases LH & testosterone dramatically due to receptor down regulation.

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25
Q

Histrelin nonapeptide analog of GnRH also down regulates & is used for?

A

Receptors. Used in treatment of precocious puberty in boys & girls.

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26
Q

Estrogen Drugs:

A 
Estrogen (The natural hormones are rapidly metabolized.)
ethinyl estradiol 
mestranol (ethinyl estradiol 3-methylether )
conjugated esters of estrogens
esters of estradiol
estropipate crystalline estrone sulfate
diethylstilbesterol
clorotrianisene
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27
Q

Progestins drugs:

A
  1. norethindrone
  2. norgestrel
  3. levonorgestrel
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28
Q

Selective Estrogen Receptor Modulators Drugs:

A
  1. tamoxifen
  2. raloxifene
  3. toremifene
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29
Q

Antiestrogens Drugs:

A
  1. clomiphene

2. fulvestrant

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30
Q

Antiprogestins Drugs:

A
  1. mifepristone - RU 486

2. onapristone

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31
Q

Aromatase inhibitors Drugs:

A
  1. anastrozole

2. letrozole

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32
Q

Androgens Drugs:

A

The natural hormones is rapidly metabolized.

  1. testosterone
  2. testosterone transdermal patches
  3. testosterone derivatives
  4. methyltestosterone
  5. testosterone propionate
  6. testosterone cypionate
  7. testosterone enanthate
  8. fluoxymesterone
  9. danazol
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33
Q

Androgen receptor antagonistsDrugs:

A
  1. cyproterone acetate
  2. flutamide
  3. bicalutamide
  4. nicalutamide
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34
Q

Inhibitors of 5α-Reductase Drugs:

A

finasteride

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35
Q

Estrogens most potent to least:

A
  • Estradiol (the most potent & principal ovarian steroid)
  • Estrone
  • Estriol (least potent, principal placental steroid) also made by conversion of estradiol & estrone in liver & adipose tissue.
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36
Q

Estrogens & Androgens are bound to?

A

70 % bound to Sex Hormone Binding Globulin (SHBG).

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37
Q

Administration of estrogen increases?

A

SHBG, so free androgen level will decrease

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38
Q

Progesterone is transported?

A

Bound to transcortin (which also binds corticosteroids)

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39
Q

Estrogen acts through

A

nuclear receptors

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40
Q

Two types of estrogen receptors are? Where are they located?

A

ERα and ERβ
– ERα is located in the female reproductive tract (uterus, vagina and ovary) as well as many other tissues.
– ERβ is located primarily in the prostate gland & ovary.

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41
Q

Receptor/ligand complexes bind to specific regions of?

A

DNA & affect the rate of transcription of genes at
variable distance from the HRE (hormone response
element = DNA sequence).

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42
Q

Many steroid hormones weakly?

A

Cross-react with receptors for other steroid hormones.

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43
Q

Progesterone may have weak?

A

Androgenic & glucocorticoid effects.

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44
Q

Most steroid hormones affect the synthesis?

A

Of their own receptors.

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45
Q

Antihormone action is achieved by?

A

Competitive binding of ligands (antagonists) to the receptor. Such a ligand-receptor complex may still bind to the DNA, but exert no effect.

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46
Q

Actions of Estrogens Coordinate the systemic responses?

A

During the menstrual cycle
– Reproductive tract
– Pituitary gland
– Breasts and other tissues

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47
Q

Actions of Estrogens in the body?

A

• Increases HDL and lowers LDL cholesterol.
• Breast development
• Hastens bone maturation & closure of epiphyseal
plates of long bones.
• Antagonizes bone resorption
• Shapes pelvis (larger opening for birth)
• Increases muscle content of the myometrium
• Increases libido
• Increases synthesis of several hepatic proteins: TBG, transcortin, SHBG & clotting factors.

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48
Q

The major effect of estrogen on bone is to?

A

Decrease the numbers and activity of osteoclasts.

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49
Q

Progesterone is a precursor to?

A

Estrogens, androgens & adrenocortical steroids

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50
Q

Progesterone is synthesized in the?

A

Ovary, adrenal gland & testis. Released in large amounts by the placenta during pregnancy.

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51
Q

Actions of Progesterone:

A

• Responsible for the alveolobular development
of the secretory apparatus in the breast
• Modulates estrogen action on the uterus
• Aids in the maintenance of pregnancy
• Inhibits uterine contraction

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52
Q

Actions of Progesterones on metabolism:

A

• Alters carbohydrate metabolism (increases
basal insulin levels, promotes glycogen
storage)
• Decreases HDL levels and stimulates LDL
production
• Stimulates lipoprotein lipase (fat transfer from
lipoproteins to tissues)
• Responsible for body temperature increase at
ovulation
• May have depressant and hypnotic effects on
the brain.

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53
Q

Native estrogens are rapidly degraded by & making them not useful for?

A

The liver (high first-pass effect). Not effective given orally in treament or replacement therapy.

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54
Q

Synthetic estrogens such as?

Have ethinyl groups (triple bonds) which greatly?

A

ethinyl estradiol & mestranol

decrease hepatic metabolism.

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55
Q

Ethinyl estradiol & mestranol are often used?

A

In oral contraceptives. Similar alterations are also effective in progestin preparations.

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56
Q

Synthetic nonsteroidal estrogens such as DES
(diethylstilbesterol) & clorotrianisene have also been
used in?

A

Prostate cancer therapy & birth control.

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57
Q

Nonsteroidal estrogens such as DES (diethylstilbesterol) & clorotrianisene (replaced once or twice weekly) have been used to avoid?

A

The first pass effect.

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58
Q

Intramuscular injections of sulfate esters of estrone from equine sources or esters of estradiol dissolved in oil are absorbed over several weeks time and also avoid?

A

The first pass effect.

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59
Q

Sulfate esters of estrone from equine sources or esters of estradiol used to treat?

A

Symptoms of menopause in women with hysterectomy (also HRT).

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60
Q

SERMS ( Selective Estrogen Receptor Modulators ) are drugs whose estrogenic activities are?

A

tissue selective.

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61
Q

SERMS produce estrogenic activities in tissues some tissues & no activity in others?

A

They are beneficial (bone, brain and liver), but have no activity or antagonistic activity in breast or
endometrium.

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62
Q

SERMS Examples are?

A

tamoxifen, raloxifene, and

torimifene.

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63
Q

Tamoxifen has been reclassified?

A

no longer considered an antiestrogen.

64
Q

SERMs are used in?

A

breast cancer treatment because they block estrogen stimulation of the cancer growth, but have normal effects elsewhere.

65
Q

The true antiestrogen is?

A

clomiphene are pure antagonists in all tissues. It is used as an ovulation inducing agent.

66
Q

Therapeutics - Estrogen and Progesterone

Fertility control:

A

– Combination of estrogen & progestin for contraception
– Progestin only pill for contraception
– Postcoital contraception (morning after pill)
– Contragestation (antiprogestin - mifepristone - RU 486)

67
Q

Therapeutics - Estrogen and Progesterone

Hormone Replacement Therapy

A

– Menopause (mostly estrogens)
– Osteoperosis in menopause or in young women after ovariectomy (estrogens)
– Ovarian failure (estrogens & progestins)

68
Q

Therapeutics - Estrogen and Progesterone

Dysfunctional uterine bleeding:

A

Irregular menstrual cycle (progestins, estrogens)

69
Q

Ovulation induction for infertility in an ovulatory

women what drugs used?

A

clomiphene & fulvestrant

70
Q

Clomiphene & fulvestrant are antiestrogens, pure

antagonists in?

A

All tissues, bind to both ERα and ERβ.

71
Q

Clomiphene & fulvestrantact on the ER in the hypothalamu to/

A

Block feedback inhibition of natural estrogens, & stimulate release of GnRH which stimulates the pituitary to increase LH and FSH secretion leading to ovulation. (This results in increased estrogen levels, also.)

72
Q

Aromatase inhibitors are used for?
2. Progestins and antiestrogens used in treatment of
Endometrial cancer.
3. Estrogens used in treatment of prostate cancer.

A

breast cancer (anastrozole & letrozole) used after tamoxifen failure.

73
Q

Aanastrozole & letrozole decrease?

A

Estrogen to extremely low levels after estrogen levels are lowered by hysterectomy. Inhibit conversion of adrenal androgens to estrogens.

74
Q

Long known (1936) that administration of estrogen to several mammalian species will?

A

Produce tumors of breast, uterus, testis, bone, kidney and other tissues (high dose).

75
Q

Developmental exposure to some estrogens (especially DES) causes?

A

tumors in the fetus.

76
Q

Some risk of endometrial cancer with estrogen alone used for?

A

HRT in menopause.

77
Q

Recent studies indicate that the progestin component may play a role in?

A

cancer risk in HRT.

78
Q

Difficult to assess the problem because of high incidence of?

A

breast cancer in women without known risk factors. 50% of women who develop breast cancer have no known risk factors other than gender & age.

79
Q

Cardiovascular problems with Estrogens & Progestins:

A

• Estrogens decrease risk of CHD, progestins raise
the risk.
• Estrogens increase the risk of stroke by increasing the chance of venous thromboembolism.
• Even more elevated risk for women who smoke.

80
Q

Additional clinical problems with estrogens include:

A
  • GI disturbances
  • menstrual disorders
  • breast discomfort
  • hypertension
  • endometrial cancer
  • decreased lactation
  • adverse effects on the fetus (DES)
81
Q

Additional clinical problems with progestins include:

A
  • GI disturbances
  • menstrual disorders
  • adverse changes in lipoprotein levels
82
Q

Contraception most effective:

A

IUDs, progestin implants & sterilization are most effective.

83
Q

Contraception least effective:

A

Barrier and fertility-based methods (calendar) are least effective.

84
Q

Contraception most popular:

A

Hormonal contraceptive are most popular

85
Q

Birth Control Combination of Estrogen/Progestin Mechanism?

A

Prevents LH & FSH release by feedback inhibition

86
Q

Birth Control Combination of Estrogen/Progestin Component drugs?

A

• Estrogen component is ethinyl estradiol or mestranol
• Synthetic progestin component is norethindrone,
norgestrel or levonorgestrel

87
Q

Birth Control Combination of Estrogen/Progestin Component side effects?

A

• Estrogen component is responsible for breast enlargement, increased excitability
• Progestin component is responsible for acne & weight gain
• Formulations of various combinations are available
to minimize side effects.

88
Q

Contraindications for Combination Oral Contraceptives Include?

A
  • Thromboembolic disease
  • Cerebral vascular disease
  • Myocardial infarction
  • Coronary artery disease
  • Congenital hyperlipidemia
  • Known or suspected breast cancer
  • Endometrial cancer
89
Q

Single component type Contraceptives such as low dose of progestin success rate?

A

Blocks ovulation in only 60 to 80 % of cycles. Impairs sperm transport by thickening the
cervical mucus, decreases motility of ovules in
the oviduct & alters endometrium to impair
implantation. Minipill has a slightly higher failure rate than the combination pill.

90
Q

ORAL CONTRACEPTIVES have decreased over the

years?

A

Hormone content. Lower dose formulations (<20 mcg of ethinyl estradiol) are effective, but have higher risk of failure and changes in bleeding patterns (irregular, frequent or prolonged)

91
Q

Monophasic oral contraceptives have?

A

Fixed doses of estrogen & progestin in each

active pill

92
Q

Multiphasic oral contraceptives vary the?

A

Dose of one or both hormones (but no evidence of decreased adverse effects)

93
Q

Most oral contraceptive packaged as/

A

21/7 cycle (21 active/7 placebo)

–Results in 13 bleeding episodes per year

94
Q

Some newer oral contraceptive regimens have?

A

2-4 placebo tablets per 28 days

95
Q

One new oral contraceptive regimen has

A

No placebo tablets (28 identical active pills)

96
Q

Women taking combination oral contraceptives

have reduced risk of?

A

Ovarian & endometrial cancer (after 1 yr & continues)

97
Q

Non-Contraceptive Benefits reduced dysfunctional?

A

Uterine bleeding & dysmenorrhea

98
Q

Non-Contraceptive Benefits Menstrual regularity leads to?

A

Increased hemoglobin.

99
Q

Non-Contraceptive Benefits Combination pills raise?

A

SHBG, decrease androgens, so less hirsuitism & acne

100
Q

Combination Contraceptive pills used “off-label” to treat?

A

poly cystic ovary syndrome

101
Q

Adverse Effects of Oral Contraceptives Include:

A

• Estrogens cause nausea, breast tenderness,
breast enlargement
• Lower dose of ethinyl estradiol have more breakthrough bleeding
• Unexpected bleeding common with extended cycle (24/4) or continuous regimen (no placebo)
• Older formulations with >50 mcg of ethinyl estradiol caused more MI and stroke
• Venous thromboembolism with combination pills, especially in smokers

102
Q

Progesterone-only “Mini-pill” taken?

A
  • Taken daily and continuously. No placebo.

* Take pills at the same time each day

103
Q

Progesterone-only “Mini-pill” best for?

A
  • Best for women who are breast-feeding

* For women >35 years old who smoke

104
Q

Contraceptive failure reported in women

taking?

A

Antibiotics, including penicillins & tetracyclines (cause not established)

105
Q

Rifampin, some anti-HIV agents, anticonvulsants, and St. John’s wort effect on Oral Contraceptives?

A

Increase hormone metabolism & decrease

effectiveness

106
Q

Hormonal Contraceptives: Transdermal Patch Delivers & administered?

A

• Delivers ethinyl estradiol and progestin.
• New patch each week for 3 weeks, then
patch-free for one week.

107
Q

Hormonal Contraceptives: Transdermal Patch Effectiveness & AE?

A
  • The Patch is less effective in women >90 kg (198 lb) because of adipose tissue
  • Break-through bleeding more common in first 2 cycles
  • Skin irritation may be a problem
108
Q

Vaginal Contraceptive Ring- (Not IUD) Administered?

A
  • Inserted intravaginally by the patient

* In place 3 weeks, one “ring-free” week

109
Q

Vaginal Contraceptive Ring- (Not IUD) delivers & effectiveness?

A
  • Delivers ethinyl estradiol and progestin
  • Ring should not be removed for more than 3 hr
  • Not effective until in place for 7 days
110
Q

Vaginal Contraceptive Ring- (Not IUD) advantage & adverse effects?

A

• Rapid return to fertility after removal
• Discomfort, headaches and vaginal discharge are
adverse effects

111
Q

Hormonal Contraceptives: Injectable Contraceptives

Progesterone only is?

A

Usually medroxyprogesterone

112
Q

Hormonal Contraceptives: Injectable Contraceptives: Given how often?

A
  • Intramuscular and Subcutaneous preparations

* Injected every 3 months

113
Q

Hormonal Contraceptives: Injectable Contraceptives:

Adverse effects & disadvantages?

A
  • Amenorrhea common, irregular bleeding can occur
  • Adverse effects – weight gain, headache, decreased bone density
  • Discontinue after 2 years unless no alternative
  • Delayed return to fertility (6-12 months)
114
Q

Hormonal Contraceptives: Implant

Progesterone only is?

A

Usually etonogestrel.

115
Q

Hormonal Contraceptives: Implant administered & adverse effects?

A
  • Single rod implanted under the skin (upper arm)
  • Effective for 3 years
  • Adverse effects – same as all progestins
116
Q

INTRAUTERINE CONTRACEPTIVE DEVICES (IUDs) Two types of IUD :

A
  • Copper containing (copper is spermacidal). Effective 15-20 years (FDA recommends 10 yr)
  • Progestin releasing (20 mcg/day levonorgestrel) Release rate decreases with time (FDA – 5yr limit).
117
Q

INTRAUTERINE CONTRACEPTIVE DEVICES (IUDs) Advantages & Disadvantages?

A
  • Fertility quickly restored after removal
  • Less blood loss – FDA approved for dysmenorrhea
  • Adverse effects: copper may cause cramping; progestin-irregular bleeding (6-12 mo)
  • High initial cost. Very low overall cost.
118
Q

BARRIER CONTRACEPTIVE DEVICES Types & functions?

A

• Male and female condoms
– Protect against HIV and STDs
• Diaphragms and cervical caps
– With spermicide (in place 6 hr before and after)
– Protection against HIV and STDs unclear

119
Q

BARRIER CONTRACEPTIVE DEVICES Adverse effects:

A

Less effective than hormone contraceptives or IUDs.

120
Q

SPERMICIDES Most common is?

A

Nonoxynol-9, a surfactant. Available in foams, gels, creams & suppositories, also used as lubricant for condoms, diaphragms

121
Q

Nonoxynol-9 dose effectiveness & adverse effects?

A

• 100 to 150 mg dose is best
• Effective for only 1 hr, reapplication necessary
• Must be in contact with the cervix
• Adverse effects: less effective, irritation of vaginal
mucosa, toxic shock syndrome

122
Q

SPONGE: mechanism, effectiveness, & adverse effects?

A
  • Barrier containing Nonoxynol-9
  • Moisten in water, place over cervix
  • Effective immediately and for up to 24 hr
  • Must remain in place 6 hr after intercourse
  • Adverse effects: inferior to diaphragms
123
Q

FERTILITY AWARENESS METHODS examples & effectiveness?

A

• “Calendar method” based on calculated time of
ovulation
• Ovulation detected by increased body temperature
• Avoid intercourse on presumed fertile days
• Relatively high failure rates

124
Q

EMERGENCY CONTRACEPTION mechanism?

A

Prevent or delay ovulation

125
Q

EMERGENCY CONTRACEPTION Progestins (levonorgestrel) dose effectiveness?

A

• Progestins (levonorgestrel) 2 doses 12 hr apart
• Can prevent 50-80% of pregnancies
• Best if taken within 24 to 72 hr of intercourse
• Usually available without prescription for women
17 years or older

126
Q

EMERGENCY CONTRACEPTION Ethics?

A

• Ethics questions for physicians & pharmacists?
• Contraception has always been controversial
ethically and/or legally! In 1960’s birth control pills were only available to married women!

127
Q

EMERGENCY CONTRACEPTION Other Alternatives & adverse effects?

A

• Many oral contraceptives can be used. Different
doses (1.5 mg levonorgestrel). Not recommended
• Vomiting within 1 hr suggests repeated dose
• Copper IUD inserted within 5 days
• None are as effective as two dose progestin
• Adverse effects: Nausea and vomiting with
ethinyl estradiol, headache, breast tenderness,
and abdominal pain.

128
Q 
Postcoital Contraception (Morning after pill) there are now two FDA approved preparations that
consist of two doses of?
A

Levonorgestrel separated by 12 hours (first dose within 72 hours of intercourse). Now over-the-counter with some state control regarding age, etc.

129
Q

Antiprogestins or Contragestation drugs:

A
  • Mifepristone

* Onapristone

130
Q

Mifepristone (the first antiprogestin, RU 486) is now

approved by the FDA for the?

A

termination of pregnancy (49 days or less into
pregnancy). [State laws regulate dispensing!] Mifepristone blocks binding of progesterone to its
receptor.

131
Q

Onapristone more pure

A

antagonist of progesterone.

132
Q

Binding of testosterone to androgen receptor which binds to DNA response element causes?

A

Tissue specific transcription coactivators & corepressors allow different effects in different tissues.

133
Q

Conversion of testosterone in some tissues (in prostate, but not in muscle or kidney) to?

A

5α-dihydrotestosterone (DHT) which binds to the androgen receptor.

134
Q

DHT more potent than?

A

testosterone, binds 10x tighter.

135
Q

testosterone conversion to estradiol by?

A

Aromatases

136
Q

Primary Uses of Androgens Men & Women?

A
  • Androgen-deficient men (replacement) for development or maintenance of male sex characteristics. IM injection most effective
  • Treatment of Endometriosis & PMS (danazol) = advantageous because weakly androgenic
137
Q

Use as anabolic agents (anabolic steroids)

A
  • some androgens are less androgenic than testosterone but have significant anabolic effects
  • abused by athletes
  • side effects are serious: lower testosterone levels, decreased libido, decreased spermatogenesis, increased hepatotoxicity, development of CHD
  • may be useful in children to promote linear growth
138
Q

Absorption, Metabolism, Excretion Testosterone:

A
  • Administered by injection or by mouth both result in rapid metabolism
  • Other routes of administration are better (transdermal patches)
  • Testosterone esters are more lipid soluble, have longer duration of action.
  • Alkylation at the 17-α position allows testosterone administration by mouth because it decreases hepatic metabolism.
139
Q

Administration Duration

methyltestosterone

A

oral

short

140
Q

Administration Duration

testosterone propionate

A

IM

short

141
Q

Administration Duration

testosterone cypionate

A

IM

long

142
Q

Administration Duration

testosterone enanthate

A

IM

long

143
Q

Administration Duration

fluoxymesterone

A

oral

short

144
Q

Administration Duration

danazol

A

IM

long

145
Q

Androgen supplements are currently used in?

A

Elderly men (primarily testosterone) to maintain muscle mass.

146
Q

Although transdermal patches are available?

A

Most men prefer injections because of tearing of skin when patch is removed.

147
Q

Androgen Supplements Side Effects:

A
  • Dose related
  • Virilizing effects when used in females (facial hair, voice changes)
  • Feminizing effects when used in males due to testosterone conversion to estradiol
  • Suppression of LH & FSH secretion leading to decreased size of testis, decreased spermatogenesis, decreased endogenous testosterone synthesis. NOT useful as male contraceptives because zero sperm count cannot be achieved.
  • Decreased HDL & increased LDL levels increasing risk of CHD.
148
Q

Androgen Receptor Antagonists Drugs?

A

Cyproterone acetate
Flutamide
Bicalutamide
Nicalutamide

149
Q

Cyproterone acetate competes with?

A

DHT for the androgen receptor, prevents translocation into the nucleus.

150
Q

Cyproterone acetate used in treatment of?

A

Acne, baldness, hirsutism, virilizing syndrome, inhibits libido in sex deviant males.

151
Q

Flutamide, bicalutamide, & nicalutamide used in treatment of?

A

prostate cancer

152
Q

Nicalutamide replacing flutamide because of?

A

Lower hepatic toxicity & once a day administration (vs. 3x)

153
Q

Inhibitors of 5α-Reductase cause?

A

inhibition of DHT production

154
Q

Inhibitors of 5α-Reductase drug?

A

Finasteride

155
Q

Antagonists of 5α-reductase, blocks?

A

Testosterone conversion to DHT

156
Q

Finasteride treatment for?

A
  • treatment for benign prostatic hyperplasia

- now approved for treatment of male pattern baldness

157
Q

Finasteride adverse effects?

A

Should not be touched by pregnant women, absorbed through skin & can cause birth defect in male fetus. Men should not donate blood.

Reproduction Pharmacology (9 decks)

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