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pharmacology 4810 > Sex Steroids (Final Exam) > Flashcards

Sex Steroids (Final Exam) Flashcards

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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
true or false: estrogen therapy is not readily absorbed through the skin and mucous membrane
false: it is readily absorbed b/c lipophilic!
26
true or false: both natural and synthetic forms of estrogen are rapidly metabolized in the liver
false: natural estrogens are rapidly metabolized by the liver. synthetic estrogens have slower hepatic metabolism
27
true or false: estrogens are plasma bound to albumin only
false: albumin AND sex-hormone binding globulin (SHBG)
28
what are some side effects of estrogens
- 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)
29
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
selective estrogen receptor modulators (SERMs)
30
tamoxifen produces anti-estrogenic effects on these tissues
mammary gland (GOOD) & uterus (BAD)
31
tamoxifen produces pro-estrogenic effects on these tissues
plasma lipids (GOOD), bone (GOOD) and coagulation factors (BAD)
32
true or false: tamoxifen-receptor complex does not readily dissociate, which interferes which receptor recycling
true
33
what are some adverse effects of tamoxifen
- increased risk of blood clots - "menopause-like" symptoms - hot flashes, breast tenderness, etc
34
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)
anti-estrogens
35
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!)
clomiphene
36
what is the MOA of clomiphene?
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
what is the MOA of letrozole?
- inhibits aromatase activity, blocking estrogen biosynthesis from precursors - inhibits peripheral conversion of other sex steroids to estrogen
38
the main use of Letrozole is in the treatment of hormones-responsive breast cancer in POST-MENOPAUSAL women, why?
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
what are the two main classes of oral contraceptives
1. estrogen and progesterone combined oral contraceptives (COC's) 2. progestin-only pills (POP's)
40
what is the mechanism if combination oral contraceptives (COCs) *what I use!!!!*
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
why is progestins administered in combination with estrogen if estrogen is what inhibits ovulation?
estrogen alone promotes endometrial growth and may increase the risk of cancer. therefore, progestins are administered to limit endometrial growth
42
_______ generally have cross-over activity on androgen receptors and therefore can cause androgenic side effects such as weight gain, acne, hair thinning, etc,
progestins
43
these two progestins have high androgenic activity
Norgestrel & Levonorgestrel
44
this progestin has lower androgenic activity that Norgestrel & Levonogrestrel
Norethindrone
45
these two progestins have the lowest androgenic activity. however, these agents have been linked to an increased risk of DVT
norgestimate and desogestrel
46
what is the typical regimen for COCs
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
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
extended cycle
48
what are the 3 formulations of COCs
monophasic, biphasic and triphasic
49
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
biphasic
50
this formulation of COC has a constant dose of estrogen and progestins for 21 days
monophonic
51
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)
triphasic
52
what is the main advantage of biphasic/triphasic preparations
the total amount of progestin administered is reduced therefore there is a decreased crossover for androgenic side effects
53
what are some potential risks/side effects of COCs
- increased risks of clots (usually in women >35 y/o who smoke) - nausea, mood disturbances, bloating headache
54
what are some benefits of COCs
- 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
does emergency contraception (Plan B) contain estrogen or progesterone?
progesterone - double the dose used in normal contraception pills
56
what is the MOA of Plan B
exact MOA is unknown - interferes with ovulation and/or transport of fertilized egg to the uterus
57
what is the timeline that Plan B should be taken within in order to get 75-80% efficacy
taken 72 hours within intercourse
58
what are some side effects of Plan B
nausea, menstrual disturbances
59
what type of progestin do progesterone only pills (POPs) usually contain
Norethindrone
60
what is the MOA of progestin only pills (POPs)
ovulation is prevented due to the alteration of GnRH pulsing and responsiveness of pituitary to GnRH
61
does this explain COCs or POPs
96-98% effective in preventing pregnancy when taken correctly (within a 3 hour window everyday)
62
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
Mifepristone
63
Mifepristone is often given in combination with __________ which stimulates uterine contractions, relaxes the cervix and stimulates birth/expulsion
misoprostol
64
what are some side effects related to the combination of Mifepristone (single dose) and Misoprostol
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
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
Misoprostol
66
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)
oxytocin
67
where is oxytocin released from
posterior pituitary
68
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)
gonadotropin receptor hormone agonists/analoges
69
what is the different in the MOA's of GnRH agonist and GnRH antagonists
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
what are some side effects of GnRH analogues
hot flashes, osteoporosis, sexual dysfunction
71
this is a agent that alters gonadotropin expression. it is a humanized choriogonadotropic alpha (hCG) and is used for ovulation induction (fertility treatment)
Ovidrel
72
what is the MOA of Ovidrel
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
what is the main natural androgen
testosterone
74
where is testosterone synthesized in the body
it is synthesized by interstitial cells of the testes and in lower amounts by the ovaries and adrenal cortex
75
what is the function of testosterone during puberty
- 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
what happens if testosterone is given to a male pre-puberty
individuals do not reach full height due to premature closure of the epiphyses of the ling bones
77
what happens if testosterone is given to someone who was assigned female at birth
causes masculinization
78
what's the difference between a male with low testosterone and a male with high testosterone
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
true or false: in most tissues testosterone is converted to an inactive metabolite, dihydrotestosterone (DHT) by the enzyme 5-alpha reductase
false: DHT is the active metabolite
80
what is the best way for administration of testosterone based on metabolism
usually injected because if given orally it is rapidly metabolized in the lover
81
true or false: almost all of testosterone is bound to plasma proteins (SHBG)
true
82
does testosterone have a short or long half life
short - 10 to 20 mins
83
what are some side effects of testosterone in biologic males
impotence, decreased spermatogenesis, gynemocastia, liver abnormalities and potential psychotic episodes
84
what are some side effects of testosterone in biologic females
acne, growth of facial hair, depending of the voice, muscle development
85
this class of medications are used to treat BPH by inhibiting the conversion of testosterone to DHT] e.g. finasteride, duasteride
Anti-androgens
86
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
Flutamine & cyproterone acetate
87
this are androgen receptor antagonists that is used to treat PCOS
spironolcatone (Aldactone)

pharmacology 4810 (12 decks)

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