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Block 10 Week 3 > Burkin > Estrogens & Progestins > Flashcards

Burkin > Estrogens & Progestins Flashcards

1
Q

what is a combined oral contraceptive?

A

hormonal contraceptive administered orally that contains estrogen & a progestin

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2
Q

what is HRT?

A

hormone replacement therapy

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3
Q

what is MHT?

A

menopausal hormone therapy

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4
Q

what is a SERM?

A

selective estrogen receptor modulator

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5
Q

what tissues does estrogen affect (7)?

A 
heart & liver
brain
bone
breast
ovary
uterus
vagina
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6
Q

what are estrogen’s effects on the brain (3)?

A
  1. maintain body temp
  2. delay memory loss
  3. prep for sexual & repro dvlpmnt
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7
Q

what are estrogen’s effects on the heart & liver?

A

regulate cholesterol production > dec plaques in coronary arteries

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8
Q

what are estrogen’s effects on the ovary?

A
  1. stimulate maturation

2. stimulate start of menstrual cycle

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9
Q

what are estrogen’s effects on the vagina?

A
  1. stimulate maturation

2. maintain lubricated & thick vaginal lining

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10
Q

what are estrogen’s effects on the breast?

A
  1. stimulate development at puberty

2. prep glands for future milk pdtion

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11
Q

what are estrogen’s effects on the uterus?

A
  1. stimulate maturation

2. prep the uterus for a fetus

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12
Q

what are estrogen’s effects on the bone?

A

preserve bone density

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13
Q

what are the 2 broad therapeutic indications for estrogens?

A
  1. contraception

2. hormone replacement regimens

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14
Q

what are 4 instances where hormone replacement regimens may be appropriate?

A
  1. menopause
  2. hypogonadism
  3. dysfxnal uterine bleeding
  4. combo w/ androgens to promote growth
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15
Q

what are 2 clinical applications of antiestrogens?

A
  1. infertility

2. breast cancer

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16
Q

what does 3-b-hydroxysteroid dehydrogenase do?

A

converts pregnenolone to progesterone

pregnenolone has 3 ns

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17
Q

what does 17-b-hydroxysteroid dehydrogenase do?

A

converts estrone to estradiol
&
converts androstenedione to testosterone

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18
Q

what does aromatase do?

A

converts androgens to estrogens

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19
Q

what are the 3 classes of estrogens available for therapeutic use?

A
  1. natural
  2. synthetic steroidal
  3. synthetic non-steroidal
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20
Q

what are the 3 natural estrogen preparations?

A

estradiol
estrone
estriol

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21
Q

what is essential about the natural estrogen preps?

A

phenolic A ring

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22
Q

how does aromatase convert androgens to estrogens?

A

catalyzes aromatic hydroxylation of the A ring of C19 androgens to form estrogens

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23
Q

what can convert estradiol & estrone into estriol?

A

16α-hydroxylase in the liver

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24
Q

are natural estrogen preps orally active?

A

nope

extensive 1st pass metabolism

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25
Q

what is ESTRADERM?

A

transdermal estradiol patch that provides slow sustained release

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26
Q

why would you use transdermal estradiol?

A

lower hepatic exposure, less metabolism

you can reach therapeutic levels of estradiol at lower circulating levels of estrone & estriol

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27
Q

what are the 3 classes of synthetic steroidal estrogens?

A
  1. estradiol esters
  2. conjugated estrogens
  3. alkyl estrogens
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28
Q

which synthetic steroidal estrogens are the most potent?

A

alkyl estrogens

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29
Q

name the 2 estradiol esters

A

estradiol valerate

estradiol cypionate

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30
Q

what is notable about the structure of estradiol esters?

A

have short chain fatty acids at C17

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31
Q

how do you give estradiol esters?

A

dissolve it in oil & inject it IM

*poor oral bioavailability

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32
Q

how long does the effect of estradiol esters last?

A

several weeks

takes a while to kick in though

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33
Q

name 2 conjugated estrogens

A
  1. estrone sulfate

2. equilin sulfate

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34
Q

what routes can you use for conjugated estrogens?

A
  1. oral
  2. parenteral
  3. topical
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35
Q

what happens to conjugated esters in the intestine?

A

they are hydrolyzed to remove sulfate groups & allow absorption

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36
Q

when would you use an oral conjugated estrogen?

A

for menopausal HRT

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37
Q

when would you use an IV conjugated estrogen?

A

for emergency treatment of dysfxnal uterine bleeding

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38
Q

what are the 2 alkyl estrogens?

A
  1. mestranol

2. ethinyl estradiol

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39
Q

what are the most potent steroidal estrogens & why?

A 
alkyl estrogens (mestranol)
d/t increased affinity for ER
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40
Q

why is first pass metabolism of alkyl estrogens inhibited?

A

ethinyl substitution at C17

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41
Q

mestranol is a pro-drug of what?

A

ethinyl estradiol

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42
Q

how is mestranol activated?

A

removing the C3 methyl group

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43
Q

when do you use alkyl estrogens?

A

oral contraception

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44
Q

which class of estrogens is no longer used clinically?

A

synthetic non-steroidal estrogens

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45
Q

name the synthetic non-steroidal estrogens (3)

A
  1. Diethylstilbestrol
  2. chlorotrianisene
  3. methallenestril
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46
Q

why is diethylstilbestrol important?

A

it was a cheap, oral estrogen used for endocrine therapies when natural pdts were unavailable

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47
Q

what types of synthetic agents have estrogenic or antiestrogenic properties?

A

polycyclic compounds w/ phenolic rings resembling the steroid A ring

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48
Q

what are 3 examples of synthetic agents that have estrogenic or antiestrogenic properties?

A
  1. pesticides
  2. plasticizers (bisphenol A)
  3. industrial chemicals (polychlorinated biphenyls)
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49
Q

what are the 2 natural progestins?

A
  1. P4

2. 17α-hydroxyprogesterone

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50
Q

what structure is favored by the progesterone receptor & recognized by other steroid receptors?

A

C21 structure

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51
Q

how is P4 administered?

A

IM as an oil soln

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52
Q

what is the main side effect of P4 administration?

A

injection site has local irritation

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53
Q

what are the 2 structures of synthetic progestins?

A
  1. C21

2. C19

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54
Q

what can you do to a C21 synthetic progestin to reduce hepatic metabolism?

A

substitute an ester at C17

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55
Q

which synthetic progestin is more selective for PR: C21 or C19?

A

C21

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56
Q

which synthetic C21 progestin can you administer IM?

A

hydroxyprogesterone caproate

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57
Q

which synthetic C21 progestin can you administer orally?

A

MPA > medroxyprogesterone acetate

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58
Q

what are synthetic C19 progestins derived from?

A

C19 nor-testosterone

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59
Q

which synthetic progestin has more androgenic activity: C19 or C21?

A

C19

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60
Q

what are the uses for synthetic C19 progestins?

A

oral & implantable contraception

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61
Q

what are the 2 MAJOR uses of progestins?

A
  1. contraceptives (alone)

2. HRT (in combo w/ estrogen)

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62
Q

what are the 4 MINOR uses of progestins?

A
  1. dysmenorrhea
  2. endometriosis
  3. hirsutism
  4. uterine bleeding
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63
Q

what is menopause?

A

permanent end of menstruation & fertility

12 months after LMP

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64
Q

what is the average age of menopause in the US?

A

51 yo

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65
Q

what is the average age of perimenopause?

A

47 yo

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66
Q

how long before menopause do you get perimenopause?

A

2-8 years

avg = 4 yrs

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67
Q

how much does smoking accelerate the transition from perimenopause to menopause?

A

2 years

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68
Q

how do the symptoms of perimenopause work?

A

may begin at mid-level intensity

may come & go unpredictably for months or years

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69
Q

what are the sx of perimenopause (there are a lot)

A 
fatigue
weight gain
loss of libido
depression
hot flashes
night sweats
mood swings
vaginal dryness
irritability
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70
Q

what are estradiol levels of perimenopausal women like?

A

can be higher conc than in women under 35 yo

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71
Q

what are the early physiological changes of perimenopause (hormonal)?

A

DEC inhibin > INC FSH > INC ovarian follicular response > INC estrogen

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72
Q

what is the most common cause of erratic bleeding?

A

anovulation

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73
Q

what % of pts have irregular menses?

A

> 50%

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74
Q

make sure you look at that picture of the menstrual cycle

A

okay

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75
Q

when can you discontinue contraception in ALL women?

A

at 55 yo

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76
Q

if a woman has abn uterine bleeding, what should you suspect?

A

endometrial cancer

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77
Q

what is the overall incidence of endometrial cancer?

A

0.1%

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78
Q

what is the risk of endometrial cancer if a woman has abn uterine bleeding?

A

10%

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79
Q

how long do hot flashes last?

A

1-5 minutes

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80
Q

how many women are affected by hot flashes?

A

up to 60%

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81
Q

why does skin temp rise in a hot flash?

A

peripheral vasodilation

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82
Q

what are the sx of a hot flash (other than hot skin)

A 
inc systolic BP
inc HR
palpitations
anxiety
irritability
panic
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83
Q

what can happen if you withdraw or rapidly fluctuate estrogen levels?

A

NT levels &/or fxn are affected

beta endorphins

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84
Q

what receptors do estrogens modulate?

A

adrenergic (specifically NE)

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85
Q

what happens to the temp set point during menopausal transition?

A

DEC estrogen > unstable set point > altered response to external stimuli
over time, the set point becomes stable again (or you can use exogenous hormones to help)

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86
Q

what receptor is out of whack during menopausal transition?

A

hypothalamic serotonin 5-HT2A receptor

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87
Q

what are the risk factors for hot flashes & menopause side FX?

A

surgical menopause
race/ethnicity
smoking
body mass

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88
Q

what happens to follicles & ovulation during late menopausal transition?

A

impaired folliculogenesis

INC anovulation

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89
Q

why is there impaired folliculogenesis in late menopause?

A

FSH levels rise > ovarian follicles undergo accelerated rate of loss until all the follicles are depleted > FSH levels keep rising

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90
Q

WHY do FSH levels rise in late menopause?

A

aging follicles can’t secrete inhibin > INC FSH levels

d/t no estrogen

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91
Q

how long is a woman considered post-menopausal?

A

from the moment menopause occurs until she DIES

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92
Q

T/F: all the sx assoc w/ menopause disappear once post-menopause begins

A

FALSE

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93
Q

what are the sx of post-menopause?

A 
BONE LOSS
vaginal dryness
weight gain
stress incontinence
UTIs
insomnia
occasional hot flashes
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94
Q

what is osteoporosis?

A

a skeletal disorder that compromises bone strength d/t progressive reduction in bone mass

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95
Q

what is the precursor to osteoporosis?

A

osteopenia

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96
Q

what is a major indicator for HRT?

A

osteoporosis

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97
Q

what hormone prevents bone loss?

A

estrogen

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98
Q

which cells control bone formation?

A

osteoblasts

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99
Q

which cells control bone resorption?

A

osteoclasts

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100
Q

why is osteoclast formation limited in premenopausal women?

A

E1 limits RANKL expression from osteoblasts > limits osteoclast formation

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101
Q

why do postmenopausal women have increased osteoclast numbers, activity, & life span?

A

DEC E2 > INC RANKL expression > INC osteoclasts

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102
Q

what imbalance is involved in bone loss?

A

formation vs resorption

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103
Q

what is the leading cause of death in women?

A

CVD

104
Q

what can help maintain favorable lipid profiles in women?

A

estrogen

105
Q

where is fat deposited that leads to weight gain in postmenopausal women?

A

abdomen

106
Q

what does INC abdominal fat lead to in women?

A

HIGHER total cholesterol, triglys, & LDL

LOWER HDL

107
Q

what are the 3 management options for menopause?

A
  1. HRT
  2. lifestyle changes
  3. alternative remedies
108
Q

what particular sx, not related to osteoporosis, may respond to estrogen treatment?

A

atrophic vaginitis
irritability
anxiety
fatigue

109
Q

what do HRT regimens usu include?

A

low dose estrogen + progestin

in women w/ a uterus

110
Q

what do you give (HRT) for perimenopause?

A

oral contraception: static doses of estrogen & progestin (i.e. ethinyl estradiol + norethindrone acetate)

111
Q

what FX are you looking to achieve w/ HRT in perimenopause?

A
  1. eliminate vasomotor sx
  2. restore regular cyclicity
  3. protect against ovarian & endometrial cancer
  4. inc bone density
  5. contraception
112
Q

what are the contraindications of HRT in perimenopause?

A 
cigarette smoking
liver dz
hx of thromboembolism or CVS dz
breast cancer
unexplained vaginal bleeding
113
Q

which one requires lower doses of estrogen & progestin: perimenopause or postmenopause?

A

post

114
Q

what makes a woman more likely to choose HRT?

A

if they are healthy
have better access to medical care
are more compliant
maintain a more health-promoting lifestyle

115
Q

what was the turning point for HRT?

A

the 2002 WHI study of Prempro that showed inc risk of CVS events, inc risk of dementia, & inc risk of ovarian cancer

116
Q

how does HRT affect breast cancer? (2002 WHI study showed)

A

increases risk

makes it harder to detect

117
Q

what are the CURRENT GUIDELINES for MHT/HRT?

A

prescribe hormone therapy to treat sx for the shortest period of time possible

118
Q

why shouldn’t you give estrogen by itself?

A

it can lead to uncontrolled endometrial proliferation

119
Q

what 2 things do you actually DECREASE your risk for if you take HRT?

A

colorectal cancer & hip fx

120
Q

what test results confirm that a woman is postmenopausal?

A

high FSH
high LH
low estrogen

121
Q

what are the estrogen receptors?

A

ER alpha

ER beta

122
Q

what theory evolved to help explain why estrogen has effects on numerous organs?

A

hormone selectivity theory

123
Q

where is ER alpha (what tissues)?

A

uterus & ovary
testes & epididymis
pituitary
adrenal gland & kidney

124
Q

where is ER beta (what tissues)?

A 
testes & prostate
uterus & ovary
lung
bladder
brain
125
Q

what do SERMs do?

A

cause estrogenic effects where you want them, and non-estrogenic activity in cells where you don’t want them

126
Q

what does SERM stand for?

A

selective estrogen receptor modulators

127
Q

what is the prototypical & BEST SERM?

A

Raloxifene

Raloxifene rox

128
Q

what receptors does raloxifene bind?

A

ERalpha & ERbeta

129
Q

what does raloxifene do in bone & CVS?

A

agonist

130
Q

what are raloxifene’s actions on bone?

A

INC bone density

DEC fx

131
Q

what are raloxifene’s actions on cholesterol?

A

DEC total cholesterol

132
Q

what does raloxifene do in the uterus & breast?

A

it’s an antagonist

133
Q

how does raloxifene impact overall cancer incidence?

A

50%+ decrease in cancer incidence

134
Q

what about raloxifene makes it as good as estrogen for bone density & lipoprotein profiles, but w/o the side FX that estrogen has?

A

the unique agonist/antagonist activity

135
Q

why is raloxifene better than estrogen?

A

raloxifene doesn’t have the adverse FX on endometrial & breast tissue & doesn’t inc risk of breast or uterine cancer

136
Q

what are the 3 side FX of raloxifene?

A

hot flashes
leg cramps
blood clots

137
Q

what are the 4 contraindications for raloxifene?

A

pregnant/breastfeeding women
premenopausal women
hx of thromboembolic events/stroke
smoking

138
Q

what is ospemifene used for?

A

dyspareunia (painful sex)

139
Q

what is ospemifene?

A

SERM w/ estrogenic effects on vaginal epithelium

140
Q

what would the IDEAL SERM do?

A
  1. prevent fx
  2. reduce menopausal sx
  3. treat vaginal atrophy
  4. be neutral or protective on the uterus, breast, & CVS
141
Q

is there an ideal SERM?

A

nope, not yet

142
Q

T/F: conventional hormone therapy is preferred over compounded

A

TRUE

143
Q

is there evidence that bioidentical hormones are superior?

A

nope

144
Q

what are 2 alternative therapies for menopause?

A
  1. phytoestrogens

2. black cohosh

145
Q

what does black cohosh maybe help w/?

A

short term treatment of hot flashes & vaginal dryness

146
Q

what are phytoestrogens?

A

substances found in plant-based foods that have weak estrogenic effects

147
Q

what do phytoestrogens maybe help w/?

A

lowering cholesterol

relieving hot flashes

148
Q

what is genistein?

A

a natural phytoestrogen

149
Q

what receptor does genistein work at?

A

higher affinity for ERbeta

150
Q

what does genistein do (what are its physiological FX)?

A
  1. stimulate bone formation
  2. inhibit bone resorption
  3. prevent bone loss
  4. lower LDL & triglys
  5. help relieve hot flashes
151
Q

what is genistein’s effect on cancer?

A

LOW DOSE: inhibit prostate, cervical, brain, colon, & breast cx
HIGH DOSE: inc rate of growth of some ER-dependent breast cx

152
Q

how does genistein interact w/ tamoxifen & aromatase inhibitors?

A

reduces efficacy

153
Q

what does genistein do to the thyroid?

A

depress fxn > infertility (who cares if you are already in menopause though?)

154
Q

what are the lifestyle factors you can do to help w/ menopause?

A
  1. get good sleep
  2. exercise
  3. decrease stress & maintain a schedule
  4. limit booze, drugs, cigs
  5. eat well
  6. sun, vitamin D, Ca
  7. drink enough water in the early part of the day
155
Q

what is the action of antiestrogens?

A

competitive antagonists
precisely: partial agonists
of the estrogen receptor
inhibit estrogen synthesis

156
Q

why does clomiphene citrate have a long half life of 5-7 days?

A

plasma protein binding
hepatic recycling
accumulation in fatty tissue

157
Q

where is clomiphene citrate less active as an antiestrogen?

A

in the periphery

158
Q

what is the treatment of choice for postmenopausal women w/ breast cancer?

A

tamoxifen

usu in combo w/ surgery & chemo

159
Q

where is tamoxifen less active as an antiestrogen?

A

at the pituitary

160
Q

in premenopausal women, what is used to decrease ovarian estrogen synthesis?

A

oophorectomy
or
tx w/ GnRH analogs (leuprolide)

161
Q

what is the preferred adjuvant tx for postmenopausal women w/ localized or metastatic ER+ breast cancer?

A

anastrozole

162
Q

what should you combine exemestane w/?

A

Everolimus (Afinitor) which is an mTOR inhibitor

163
Q

what are the 6 hormonal birth control methods?

A
  1. pills
  2. injections
  3. skin patches
  4. subdermal implants
  5. vaginal rings
  6. IUDs
164
Q

what is the PRACTICAL efficacy of oral contraceptives?

A

97-98%

165
Q

T/F: OCs are available as mono, bi, or tri phasic

A

true

166
Q

if you have a combination hormonal contraceptive, what’s in it?

A

an estrogen & a progestin

167
Q

what are the 2 types of OC?

A

combination
AND
progestin only

168
Q

what is the primary MOA of combination OC pills?

A

suppress FSH & LH secretion via negative feedback

i.e. suppress ovulation

169
Q

what does progestin stimulate in the cervix?

A

thick viscous mucus > reduces sperm penetration

170
Q

what do combo OCs do to the endometrium?

A

make it not receptive to implantation

171
Q

what do monophasic combo pills have?

A

fixed amts of hormones

21 days on, 7 days off

172
Q

what do biphasic & triphasic combo pills do?

A

DEC total amt of steroids administered

more closely approximate the menstrual cycle

173
Q

what is special about extended cycle pills?

A

they let women have fewer periods

174
Q

T/F: women who take OCs don’t have “true” periods

A

TRUE

175
Q

what is the point of having a period if you are on OCs?

A

reassure a woman that she isn’t pregnant

no medical fxn

176
Q

if you take Seasonale or Seasonique, how many periods a year do you have?

A

4

177
Q

if you take Lybrel, how many periods a year do you have?

A

NONE! amazing!

178
Q

what drugs can interrupt enterohepatic cycling & diminish OC efficacy?

A

ABX!

179
Q

what happens to estrogens in the liver?

A

they undergo either sulphation or glucuronidation

180
Q

how do estrogen conjugates get to the small intestine from the liver?

A

bile duct

181
Q

what happens to estrogen conjugates once they get to the small intestine?

A

intestinal bacteria break the conjugates down > release free, active estrogenic hormone

182
Q

what is responsible for plasma estrogen levels necessary for contraception?

A

enterohepatic cycling

183
Q

how often do you apply the patch?

A

weekly

184
Q

where do you put the patch?

A

upper outer arm, butt, abs, or thigh

185
Q

what hormones are in the patch?

A

combo

ethinyl estradiol & norelgestromin

186
Q

why do combo pills reduce the incidence of endometrial cancer?

A

bc progestin is anti-proliferative

187
Q

what are the 2 potential benefits of contraceptives?

A

dec incidence of endometrial & ovarian cancers

188
Q

T/F: combo contraceptives are assoc w/ inc breast cancer rates

A

FALSE

189
Q

what are the contraindications of combo contraceptives?

A

hepatic dz
suspected pregnancy
undx vaginal bleeding
smokers >35 yo

190
Q

what is NuvaRing?

A

flexible plastic ring that releases a low dose of ethinyl estradiol & progestin (etonogestrel) over 3 wks

191
Q

what reduces the efficacy of NuvaRing?

A

if the ring is removed or accidentally expelled for 3+ hours

192
Q

what was drosperinone approved for?

A

moderate acne & premenstrual dysmorphic disorder

193
Q

why was drosperinone withdrawn?

A

inc thrombo 6-7x

risk of hyperkalemia

194
Q

what is a mini-pill?

A

progestin-only low dose contraceptives

195
Q

how do mini-pills affect natural estrogen levels?

A

they don’t!

196
Q

T/F: the FDA recommends mini-pills during breastfeeding

A

FALSE

they CAN be taken during breastfeeding, but the FDA doesn’t recommend ANY hormonal contraception during breastfeeding

197
Q

why are mini-pills effective?

A

thickening of cervical mucus

198
Q

are mini-pills affected by abx?

A

nope

not dependent on gut bacteria for absorption

199
Q

what are the side FX of mini-pills?

A

can affect lipid profile

thrombo

200
Q

what does a mini-pill cause in a dog but not in a person?

A

breast tumors

201
Q

why is medroxyprogesterone acetate effective?

A

thickening of cervical mucus

202
Q

how fast does a depo shot (medroxyprogesterone) provide protection?

A

instantly

203
Q

how long can you use depo (medroxyprogesterone)?

A

2 years

concerns over bone loss

204
Q

what is norplant?

A

implanted silicone capsules filled w/ levonorgestrel

205
Q

what drug do IUDs use?

A

levonorgestrel

206
Q

how long do IUDs work?

A

5 years

207
Q

T/F: IUDs are irreversible

A

FALSE

208
Q

what do IUDs decrease the risk of?

A

cervical cancer

209
Q

when is the critical period for exposure to contraceptives in utero?

A

2-9 weeks post-fertilization

210
Q

what is the guideline on contraceptives during pregnancy?

A

stop OC use as soon as a pregnancy is detected

but teratogenic risk is prob low

211
Q

when should you use a post-coital contraceptive?

A

when other means of contraception have failed

212
Q

what is in post-coital contraceptives?

A

either high dose estrogen or high dose progestin or both

213
Q

how effective are post-coital contraceptives?

A

99% in 1st 72 hours

214
Q

define “infertility”

A

the inability to conceive after 1 year of unprotected intercourse

215
Q

how many couples (%) are affected by infertility?

A

10-15%

216
Q

most couples are considered to be (__?__) instead of infertile

A

subfertile

217
Q

what is primary infertility?

A

no prior pregnancies

218
Q

what is secondary infertility?

A

infertility following at least one prior conception

219
Q

which is worse to have a baby: overweight or underweight

A

underweight

220
Q

can you overcome assisted reproductive technologies if your pt smokes?

A

nope

221
Q

what 3 lifestyle factors can cause infertility?

A

smoking
booze/caffeine
weight

222
Q

what is your first question for infertile females?

A

are your menstrual periods regular or not

223
Q

what is the pattern of menses of a woman who is most likely ovulating?

A

cyclic menses at an interval of 25-35 days w/ duration of bleeding 3-7 days

224
Q

what is the best predictor of regular ovulation?

A

regular menstrual pattern

225
Q

what are 4 tests you can use to assess ovulation?

A
  1. basal body temp
  2. sonography
  3. ovulation prediction kit
  4. midluteal serum progesterone levels
226
Q

if you do sonography to assess ovulation, what do you look for?

A

follicle development

227
Q

if you do a midluteal serum progesterone level, what level suggests ovulation?

A

~10 ng/mL or higher, 7 days after ovulation

228
Q

abnormalities WHERE can perturb ovulation?

A

w/i the hypothalamus, ant pituitary, or ovaries

229
Q

what are 2 types of inherited female anatomical disorders that can cause infertility?

A
  1. distal outflow tract obstruction

2. mullerian defects

230
Q

what are 3 types of distal outflow tract obstruction?

A
  1. imperforate hymen
  2. transverse vaginal septum
  3. isolated vaginal atresia
231
Q

what are 4 congenital uterine abnormalities?

A
  1. uterine septum
  2. bicornuate uterus
  3. unicornuate uterus
  4. uterine didelphys.
232
Q

what birth defect is diethylstilbestrol linked to?

A

malformations of uterine development > small T shaped uterus

plus inc risk for vaginal adenosis

233
Q

what are 3 acquired uterine abnormalities?

A
  1. intrauterine polyps
  2. Leiomyomas
  3. asherman syndrome
234
Q

what are leiomyomas?

A

benign smooth muscle tumors

235
Q

what is asherman syndrome?

A

intrauterine adhesions

236
Q

what happens in hypergonadotropic hypogonadism?

A

loss of oocytes & the surrounding support cells before 40 yo
(dec or absent ovarian fxn)
(thus the hypogonadism)

237
Q

what happens to FSH in hypergonadotropic hypogonadism?

A

they are HIGH

thus the “hypergonadotropic

238
Q

where is the primary dysfxn in hypergonadotropic hypogonadism?

A

ovary

239
Q

what is another name for hypergonadotropic hypogonadism?

A

premature ovarian failure (POF)

240
Q

what else, besides hypergonadotropic hypogonadism, can cause premature ovarian failure?

A

heavy smoking
ovarian surgery
chemo
pelvic irradiation

241
Q

how can you predict that medical therapy will be of little benefit for a hypergonadotropic hypogonadism pt?

A

basal (day 2 or 3) FSH level above 15 IU/L

242
Q

where is the primary abnormality in hypOgonadotropic hypogonadism?

A

hypothalamic-pituitary axis

243
Q

what happens to FSH & LH in hypOgonadotropic hypogonadism?

A

low or even undetectable

244
Q

is hypOgonadotropic hypogonadism inherited or acquired?

A

can be either

245
Q

what is Kallmann syndrome?

A

a subset of pts w/ idiopathic hypOgonadotropic hypogonadism that have assoc ANOSMIA

246
Q

what type of neurons are affected in hypOgonadotropic hypogonadism?

A

GnRH (?)

247
Q

what is the mechanism in women that prevents pregnancy when resources are suboptimal?

A

hypothalamic amenorrhea or acquired hypothalamic dysfxn

248
Q

what 5 things can bring on acquired hypothalamic dysfxn?

A
  1. eating disorders
  2. exercise induced
  3. stress
  4. hypothalamic tumors, trauma, radiation
  5. pseudocyesis
249
Q

what is Sheehan syndrome?

A

follows massive postpartum hemorrhage & assoc hypotension > leads to pituitary ischemia & necrosis

250
Q

what is eugonadotropic amenorrhea?

A

chronic sex-steroid secretion interferes w/ normal feedback btwn the ovary & the hypothalamic-pituitary axis

251
Q

what are 4 causes of eugonadotropic amenorrhea?

A
  1. PCOS
  2. adult-onset congenital adrenal hyperplasia
  3. ovarian tumor
  4. hyperprolactinemia & hypothyroidism
252
Q

what causes adult-onset congenital adrenal hyperplasia?

A

21-hydroxylase gene mutation

unable to convert enough P4 to cortisol so it all gets shunted to the androgen pathway

253
Q

what does adult-onset congenital adrenal hyperplasia mimic?

A

PCOS

254
Q

how can you correct hyperprolactinemia?

A
  1. dopamine agonist

2. surgery if resistant

255
Q

how can you treat hypothyroidism?

A
  1. thyroxine
256
Q

how do you induce ovulation in hyperprolactinemia or hypothyroidism?

A

clomiphene citrate

Block 10 Week 3 (7 decks)

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