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pharmacology 4810 > Sex Steroids (Final Exam) > Flashcards

Sex Steroids (Final Exam) Flashcards

1
Q

What is the function of FSH in FEMALES

A

Stimulates growth and development of ovarian follicles and promotes secretion of estrogen by ovaries

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2
Q

What is the function of FSH in MALES

A

Production of sperm

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3
Q

What is the function of LH in FEMALES

A

Ovulation, formation of corpus luteum, and regulation of release of sex hormones from ovary

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4
Q

What is the function of LH in MALES

A

Stimulates cells in testis to secrete testosterone

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5
Q

What are the three main endogenous estrogens produced and where are they produced in the body

A

Estradiol (most potent), estriol and estrone. Produced in the ovary and placenta (small amounts produced in testis and adrenal cortex)

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6
Q

This exerts anti-proliferative effects on the female endometrium (by promoting the endometrial lining to secrete rather than proliferate). Also required for maintenance of pregnancy. It is a plasma bound protein (to albumin and steroid hormone binding globulin [SHBG])

A

Progesterone

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7
Q

what do glucocorticoids, mineralocorticoids and gonadocorticoids all originate from?

A

cholesterol

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8
Q

these two sex steroids can switch back and forth in the blood stream in order to maintain homeostasis

A

estrogen and testosterone

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9
Q

how does neurohormonal control of estrogens change from before puberty to the onset of puberty

A

before puberty, the hypothalamus lacks GnRH pulse generator (so gonadotropin secretion is absent)

when puberty begins, the pulse generator is activated -> increase in release of hypothalamic and anterior pituitary hormones -> increase in release of estrogenic sex hormones -> maturation of reproductive organs and secondary sex characteristics

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10
Q

what causes FSH and LH to be released

A

GnRH binds to GnRH receptor -> G-coupled protein activation -> increase IP3 and DAG -> increased intracellular Ca++ -> LH and FSH release

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11
Q

what is the pharmacological action of estrogen in the female body?

A

induces synthesis of progesterone receptors in the uterus, vagina, anterior pituitary and hypothalamus

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12
Q

what is the pharmacological action of progesterone in the female body?

A

decreases estrogen receptor expression in the reproductive tract (e.g. decreases receptor synthesis)

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13
Q

what is the pharmacological action of prolactin in the female body?

A

increases estrogen receptor expression in the mammary gland

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14
Q

true or false: the effects of exogenous estrogens are dependant on the state of sexual maturity

A

true

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15
Q

how does exogenous estrogen work during primary hypogonadism (e.g. puberty)

A

estrogen stimulate the development of secondary sex characteristics and accelerates growth

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16
Q

how does exogenous estrogen work in adults with primary amenorrhea?

A

estrogen supplementation induces an artificial menstrual cycle

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17
Q

how does exogenous estrogen work in sexually mature females?

A

estrogen (+ progesterone) is a contraceptive

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18
Q

how does exogenous estrogen work near or after menopause

A

estrogen replacement prevents menopausal symptoms and bone loss

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19
Q

what are some metabolic effects of estrogen?

A

effects on lipid metabolism: increases plasma triglycerides levels (BAD), but also can increase HDL (GOOD) and decrease LDL (GOOD)

effects on blood coagulation: can decrease anticoagulation factors therefore an increased risk of thromboembolism formation (clot) & smoking can increase this risk

effect on bone: causes fusion of epiphyses near end of puberty. inhibits osteoclasts and stimulates osteoblasts

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20
Q

what are the two distinct receptors estrogen can bind to and where in the body are they located?

A

ER-alpha: uterus, vagina, ovary, mammary glands, hypothalamus, endothelial cells, vascular smooth muscle

ER-beta: prostate, ovaries, lung, brain and vasculature

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21
Q

what is the MOA of estrogen

A

estrogen enters the cells (as it is lipophilic) and binds to intracellular receptors -> this leads to a conformational change & dimerization -> this receptor complex binds to estrogen receptor elements (EREs) which leads to gene transcription or repression

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22
Q

list some therapeutic uses of estrogens

A
  • replacement therapy for:
    primary ovarian failure (histerectomy)
    secondary ovarian failure (menopause)
  • contraception
  • treatment of osteoporosis/prevention of CVD
  • potential neuroprotective effects??????
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23
Q

true or false: estrogen therapy is available in many different dosage forms

A

true: oral, topical cream/patch, vaginal cream/tablet/ring

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24
Q

true or false: both natural and synthetic forms of estrogen are well absorbed in the GI tract

A

true

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25
Q

true or false: estrogen therapy is not readily absorbed through the skin and mucous membrane

A

false: it is readily absorbed b/c lipophilic!

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26
Q

true or false: both natural and synthetic forms of estrogen are rapidly metabolized in the liver

A

false: natural estrogens are rapidly metabolized by the liver. synthetic estrogens have slower hepatic metabolism

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27
Q

true or false: estrogens are plasma bound to albumin only

A

false: albumin AND sex-hormone binding globulin (SHBG)

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28
Q

what are some side effects of estrogens

A
  • nausea
  • loss of appetite
  • breast tenderness
  • clots
  • salt and water retention
  • gallbladder stones
  • increased vaginal lubrication in post-menopausal women
  • feminization (in individuals assigned male at birth)
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29
Q

this class of synthetic estrogens have estrogenic actions that are tissue selective - this preserves estrogenic activity for tissues where this is beneficial (CV and bone) while reducing/preventing acvtivity in tissues that may potentiate and undesirable effect on the body (breasts/uterus). e.g. tamoxifen & raloxifene

A

selective estrogen receptor modulators (SERMs)

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30
Q

tamoxifen produces anti-estrogenic effects on these tissues

A

mammary gland (GOOD) & uterus (BAD)

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31
Q

tamoxifen produces pro-estrogenic effects on these tissues

A

plasma lipids (GOOD), bone (GOOD) and coagulation factors (BAD)

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32
Q

true or false: tamoxifen-receptor complex does not readily dissociate, which interferes which receptor recycling

A

true

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33
Q

what are some adverse effects of tamoxifen

A
  • increased risk of blood clots
  • “menopause-like” symptoms - hot flashes, breast tenderness, etc
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34
Q

this class of drugs compete with natural estrogens for receptors in target tissues (uterus, vagina, breasts, anterior pituitary, hypothalamus). they are PURE ANTAGONISTS in most tissues.
e.g. clomiphene (estrogen receptor blocker) and letrozole (aromatase inhibitor - decreases estrogen production)

A

anti-estrogens

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35
Q

the main use of this anti-estrogen is for female infertility as there is a paradoxical increase in estrogen by administering an anti-estrogen (affects the negative feedback loop!)

A

clomiphene

36
Q

what is the MOA of clomiphene?

A

inhibits estrogen binding in the anterior pituitary which affects the normal negative feedback loop:
- decreased estrogen causes increased secretion of GnRH and gonadotropins
- stimulation and enlargement of the ovaries
- increased estrogen secretion
- induction of ovulation (therefore used to infertility)

37
Q

what is the MOA of letrozole?

A
  • inhibits aromatase activity, blocking estrogen biosynthesis from precursors
  • inhibits peripheral conversion of other sex steroids to estrogen
38
Q

the main use of Letrozole is in the treatment of hormones-responsive breast cancer in POST-MENOPAUSAL women, why?

A

in post-menopausal women, the only source of estrogen is through peripheral conversion. therefore, if peripheral conversion is blocked there will be a decrease in estrogen therefore treat the breast cancer

39
Q

what are the two main classes of oral contraceptives

A
  1. estrogen and progesterone combined oral contraceptives (COC’s)
  2. progestin-only pills (POP’s)
40
Q

what is the mechanism if combination oral contraceptives (COCs) what I use!!!!

A

exogenous estrogen inhibits the release of FSH and LH, which prevents the normal mid cycle LH surge and therefore ovulation does not occur

the combination of estrogen and progestin may also alter tubal peristalsis and cervical mucous secretion which alters the transport of eggs and sperm even if ovulation does tend to occur

41
Q

why is progestins administered in combination with estrogen if estrogen is what inhibits ovulation?

A

estrogen alone promotes endometrial growth and may increase the risk of cancer. therefore, progestins are administered to limit endometrial growth

42
Q

_______ generally have cross-over activity on androgen receptors and therefore can cause androgenic side effects such as weight gain, acne, hair thinning, etc,

A

progestins

43
Q

these two progestins have high androgenic activity

A

Norgestrel & Levonorgestrel

44
Q

this progestin has lower androgenic activity that Norgestrel & Levonogrestrel

A

Norethindrone

45
Q

these two progestins have the lowest androgenic activity. however, these agents have been linked to an increased risk of DVT

A

norgestimate and desogestrel

46
Q

what is the typical regimen for COCs

A

21 days of drugs followed by 7 days of the placebo
(7 days placebo removes exogenous hormone influence which allows for shedding of the uterine lining that occurs at the end of a normal menstrual cycle - menses)

47
Q

this type of regimen with COCs has the drug combination given for 84 days followed by a 7 days placebo. the number of menstrual cycles is reduced to 4 per year, and may be useful in heavy menses, endometriosis and dysmenorrhea

A

extended cycle

48
Q

what are the 3 formulations of COCs

A

monophasic, biphasic and triphasic

49
Q

this formulation of COC has a constant dose of estrogen, but progestin dose is initially low and then increases during the second half of cycle

A

biphasic

50
Q

this formulation of COC has a constant dose of estrogen and progestins for 21 days

A

monophonic

51
Q

this formulation of COC has an increased progestin dose in the second half of the cycle and a mid cycle increase in estrogen dose (which prevents breakthrough bleeding)

A

triphasic

52
Q

what is the main advantage of biphasic/triphasic preparations

A

the total amount of progestin administered is reduced therefore there is a decreased crossover for androgenic side effects

53
Q

what are some potential risks/side effects of COCs

A
  • increased risks of clots (usually in women >35 y/o who smoke)
  • nausea, mood disturbances, bloating headache
54
Q

what are some benefits of COCs

A
  • prevention of pregnancy
  • can cause period to be less, heavy, less painful, on a more regular schedule
  • benefit in acne (low progestin)
  • decreased incidence of endometrial and ovarian cancer
55
Q

does emergency contraception (Plan B) contain estrogen or progesterone?

A

progesterone - double the dose used in normal contraception pills

56
Q

what is the MOA of Plan B

A

exact MOA is unknown - interferes with ovulation and/or transport of fertilized egg to the uterus

57
Q

what is the timeline that Plan B should be taken within in order to get 75-80% efficacy

A

taken 72 hours within intercourse

58
Q

what are some side effects of Plan B

A

nausea, menstrual disturbances

59
Q

what type of progestin do progesterone only pills (POPs) usually contain

A

Norethindrone

60
Q

what is the MOA of progestin only pills (POPs)

A

ovulation is prevented due to the alteration of GnRH pulsing and responsiveness of pituitary to GnRH

61
Q

does this explain COCs or POPs

A

96-98% effective in preventing pregnancy when taken correctly (within a 3 hour window everyday)

62
Q

this medication is used to induce first trimester abortion. it is a competitive antagonist at progesterone receptors bc progesterone is needed for maintenance of the endometrium during pregnancy. the PR bloackade causes the blastocyst to die and detach from the uterus

A

Mifepristone

63
Q

Mifepristone is often given in combination with __________ which stimulates uterine contractions, relaxes the cervix and stimulates birth/expulsion

A

misoprostol

64
Q

what are some side effects related to the combination of Mifepristone (single dose) and Misoprostol

A

side effects to Mifepristone are rare because only single dose, but will get some vaginal bleeding which is a part of the medical absorption

misoprostol can cause N/D

65
Q

this is a myometrial stimulant (PGE1 analog) that activates EP3 receptors to cause contraction of the uterus and relaxation of the cervix; can cause abortion in early and middle pregnancy

A

Misoprostol

66
Q

this is a myometrial stimulant that is used to induce or augment existing labour when uterine muscles are not functioning adequately (contracts uterus and relaxes/dilates cervix)

A

oxytocin

67
Q

where is oxytocin released from

A

posterior pituitary

68
Q

this class of medications are “hormone blockers” as they inhibit the beginning of the hormone producing pathway. they are used in prostate cancer, endometriosis, adolescent gender-transition and infertility.
e.g. Goserelin (Zoladex) & Leuprolide (Lupron, Eligard)

A

gonadotropin receptor hormone agonists/analoges

69
Q

what is the different in the MOA’s of GnRH agonist and GnRH antagonists

A

GnRH agonist: causes an initial overstimulation og GnRH receptors which leads to an increase in LH and testosterone. chronic administration eventually leads to suppression of LH and testosterone due to negative feedback loop.

GnRH antagonist: have an immediate affection of preventing gonadotropin release through receptor blockade, which leads to suppression of LH and testosterone.

therefore, they both suppress LH and testosterone eventually, they just have different MOA’s on how they do it and their onset of action is different based on the difference in MOA

70
Q

what are some side effects of GnRH analogues

A

hot flashes, osteoporosis, sexual dysfunction

71
Q

this is a agent that alters gonadotropin expression. it is a humanized choriogonadotropic alpha (hCG) and is used for ovulation induction (fertility treatment)

A

Ovidrel

72
Q

what is the MOA of Ovidrel

A

it binds to the LH/hCG receptor in the ovary to cause release of egg (in the absence of an endogenous LH surge)
OVidrel = OVulation

73
Q

what is the main natural androgen

A

testosterone

74
Q

where is testosterone synthesized in the body

A

it is synthesized by interstitial cells of the testes and in lower amounts by the ovaries and adrenal cortex

75
Q

what is the function of testosterone during puberty

A
  • rapid development of secondary sexual characteristics
  • maturation of reproductive organs
  • increase in muscular strength
  • skin thickens and darkens
  • sebaceous glands become more active (often resulting in acne)
  • growth of facial and pubic hair
  • hypertrophy of vocal cords
  • increase in physical visor, feelings of euphoria and potential increase in libido
76
Q

what happens if testosterone is given to a male pre-puberty

A

individuals do not reach full height due to premature closure of the epiphyses of the ling bones

77
Q

what happens if testosterone is given to someone who was assigned female at birth

A

causes masculinization

78
Q

what’s the difference between a male with low testosterone and a male with high testosterone

A

low testosterone
- mental fogginess
- always tired
-depression
- big belly
- low sex drive/ED
- risk of osteoporosis

high testosterone
- clear thinking
- deepened voice + hair growth
- increased muscle mass
- reduced sperm
- strong bones
- helps erection but may reduce ejaculation volume
- improved mood but increased aggression

79
Q

true or false: in most tissues testosterone is converted to an inactive metabolite, dihydrotestosterone (DHT) by the enzyme 5-alpha reductase

A

false: DHT is the active metabolite

80
Q

what is the best way for administration of testosterone based on metabolism

A

usually injected because if given orally it is rapidly metabolized in the lover

81
Q

true or false: almost all of testosterone is bound to plasma proteins (SHBG)

A

true

82
Q

does testosterone have a short or long half life

A

short - 10 to 20 mins

83
Q

what are some side effects of testosterone in biologic males

A

impotence, decreased spermatogenesis, gynemocastia, liver abnormalities and potential psychotic episodes

84
Q

what are some side effects of testosterone in biologic females

A

acne, growth of facial hair, depending of the voice, muscle development

85
Q

this class of medications are used to treat BPH by inhibiting the conversion of testosterone to DHT]
e.g. finasteride, duasteride

A

Anti-androgens

86
Q

these are androgen receptor antagonists that are used to treat prostate cancer by inhibiting binding for DHT to its receptors. s/e: gynecomastia, liver dysfunction

A

Flutamine & cyproterone acetate

87
Q

this are androgen receptor antagonists that is used to treat PCOS

A

spironolcatone (Aldactone)

pharmacology 4810 (12 decks)

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