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repro Flashcards

1
Q

Kartagener Syndrome

A

absence of dynein –> immotile sperm –> infertility for males

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2
Q

TEXT-14

A

Testis-expressed gene 14: essential for cytoplasmic bridges in mice

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3
Q

sperm - longer in meiosis I or II?

A

meiosis I takes much longer - which is wh yyou see many more primary spermatocytes

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4
Q

Tunica Albiginea

A

fibrous capsule of connective tissue around testes. Divides testes into lobules

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5
Q

haploid/diploid for primary/secondary spermatocyte

A

primary = diploid // secondary = haploid

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6
Q

menstrual cycle length

A

24-35

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7
Q

GnRH pulsatility for LH

A

HIGH amplitude, low frequency

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8
Q

how many oocytes do you have?

A

@ 5 months gestation: 6 million –> 2 million @ birth –> 300k @ puberty –> 0 @ menopause

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9
Q

follicles start to be recruited to mature starting at…

A

5 months in utero until menopause

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10
Q

follicles become dependent on FSH at the….

A

secondary follicle stage (defined by formation of the antrum)

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11
Q

hormones at the end of the menstrual cycle

A

decrease in E and P leads to an increase in FSH, which recruits next round of follicles

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12
Q

actions of FSH on follice

A

stimulates granulosa cell prolif. stimulates aromatase activity, increases FSH AND LH receptors

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13
Q

3 actions of p on uterus

A

limit growth, make glands more tortuous, coiling of b.v.

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14
Q

LH surge (3 things)

A

resume meiosis II and extrude first polar body, ovulation occurs 36 hours after, switches hormone production: E –> E + P

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15
Q

Corpus luteam makes E and P for…

A

8-10 weeks (Then placenta takes over)

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16
Q

most common contraceptives

A

OCPs&raquo_space; tubal sterilization&raquo_space; male condom&raquo_space; vasectomy

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17
Q

timing of copper IUD

A

insert before 7 days after sex, good for 12 years

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18
Q

medroxyprogesterone acete

A

progesterone only depot injection. Take every 3 months. Ver effect, but people quite because of irregular bleeding

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19
Q

effect of combination pills on androgens

A

they decrease free T by 1. increasing the binding protein (SHBG), and 2. via (-) feedback –> lower LH and FSH

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20
Q

Patch - contraceptive

A

like OCP (combined) - similar efficacy. MOA: no ovulation. Replaced weekly

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21
Q

vaginal ring

A

like OCP: combined, similar efficacy to OCP. change every 3 weeks. MOA: stops ovulation

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22
Q

IUD

A

P only –> thickens cervical mucosa (woman still ovulates) Works for 5 years.

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23
Q

Implanon

A

P only. Placed under arm. Works for 3 years. Rapid return to fertility (period within 3 months)

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24
Q

Implanon

A

progesterone only LARC. Placed under arm - effect for 3 years

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25
Q

Do OCPs increase risk of venous embolisms?

A

YES, but not to the extent of pregnancy

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26
Q

Do OCP increase CV risk?

A

only in smokers

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27
Q

How many pregnancies a year?

A

6 million pregnancies a year, 1/2 are unplanned, of the unplanned, 1/3 will abort

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28
Q

% of women who have had induced abortions

A

40%

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29
Q

strongest risk factor for abortion-related mortality

A

gestational age

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30
Q

can use medical abortion..

A

up to 9 weeks (used in 1/4 of eligible abortions)

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31
Q

mifepristone

A

blocks the P receptor –> decidual necrosis, increased prostaglandin receptors, cervical ripening

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32
Q

misoprostal

A

prostaglandin E1 analog –> contractions and cervical ripening. Used with mifepristone, methotrexate, and by itself

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33
Q

side effects of misoprostol

A

** responsible for most side effects of abortion. GI (nausea, vomiting, diarrhea), and systemic (fever/chills, HA)

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34
Q

methotrexate

A

blocks cells division. Takes longer (3-45 days), used off label with misoprostal

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35
Q

signs of perimenopause/menopause transition

A

irregular menses (fewer follicles to make E), and Sx (e.g., hot flashes)

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36
Q

timing of perimenopause

A

median age is around 45 - 47.5 (MWHS), duration is 4-5 years (can last 2-8 years)

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37
Q

What defines the onset of menopause?

A

follicular cohort + rate of atresia –> DECREASED ESTROGEN

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38
Q

biochem profile of menopause

A

decreased estrogen –> increased and LH and FSH

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39
Q

MOA of CVD and OP in post-menopausal women

A

lower estrogen leads to increased cholesterol & LDL levels, and increased bone lose

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40
Q

smoking and estrogen

A

smoking increases the metabolism of estrogen –> faster onset of menopause

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41
Q

sstreak gonads seen with

A

Turner’s syndrome. Need both X’s for normal ovarian function –> accelerated atresia, streak gonads , ovarian failiure

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42
Q

HCG mimcs

A

LH

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43
Q

endometrial receptivity window

A

Determined by progesterone. Day 20-24

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44
Q

timing of implantation

A

at 7 days post-ovulation (blastocyst stage)

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45
Q

when is embryo fully embedded in endometrial stroma?

A

7 days post-implantation (14 days post-ovulation)

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46
Q

where does embryo implant?

A

usually mid-posterior of uterus.

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47
Q

functions of syncytiotrophoblasts

A
  1. direct contact with maternal blood; 2. secrets hormones (HCG, P4, E2)
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48
Q

most common endocrine disorder in young, reproductive aged women

A

PCOS

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49
Q

describe the hyperandrogenism in PCOS

A

chronic, low-grade elevation in androgens coming from ovaries (not adrenal glands, HEAD levels moderately elevated in 10-15% patients)

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50
Q

Dx for PCOS

A
  1. hyperandorgenism //2. anovulation or oligo-ovulation (<6-9/yr) // ultrasound - 12 follicles/ovary
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51
Q

anti-Mullerian hormone in PCOS?

A

it’s elevated = new marker? in PCOS, the granulosa cells are more sensitive to FSH - greater AMH production

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52
Q

long term effects of PCOS

A

lifetime metabolic disorder, higher risk of endometrial cancer (lack of periods), increase risk of psych disorders

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53
Q

E and P in PCOS

A

women will have normal E levels, but lower P levels (won’t make P in the 2nd half of cycle) –> chronic relatively unopposed estrogen –> can see thickened endometrial stripe on ultrasound

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54
Q

effect of estrogen on bone

A

decreases osteoclasts and determines the closure of the epiphyseal plates

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55
Q

estrogen - CV effects

A

increases blood coagulability (BAD) but improves cholesterol profile: increases HDL, and decreases LDL (Good)

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56
Q

Metabolic effects of estrogen

A

increases leptin (involved in fat redistribution also), and increases protein synthesis in liver –> including TBG!!!

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57
Q

two roles of P

A
  1. prepares uterus for implantation; 2. render uterus refractory to oxytocin until labr
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58
Q

type 3-4 antagonist

A

mixed agonist/antagonist - binding of receptor to HRE can recruit co-activator or co-repressor

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59
Q

type 2 antagonist

A

pure antagonist - binding of receptor to HRE recruits co-repressor

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60
Q

Type 1 antagonist

A

pure antagonist - does not allow the receptor to bind the HRE

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61
Q

exogenous estrogens and cancer risk

A

INCREASES endometrial and ovarian (E only) and breast (E+P) but DECREASES colon cancer (E+P)

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62
Q

RU486

A

Progesterone receptor Type 2 antagonist

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63
Q

hormone independent breast cancer

A

1/3 of cases –> do mastectomy then chemo + rad

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64
Q

hormone dependent breast cancer

A

2/3 cases - can do adrenalectomy, aromatase inhibitors (part of chemo) or SERM (prophylactic Rx)

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65
Q

SERM

A

selective estrogen receptor modulators. Are tumoristatic, can be used for prophylaxis Rx after treatment for breast cancer

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66
Q

aromatase inhibitors

A

used as chemo for ER-positive tumors

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67
Q

Tamoxefin

A

Type 4 SERM: ANTAGONIST: breast // AGONIST: bone, uterus (bad), maybe CV

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68
Q

Raloxifene

A

type 3 SERM: ANTAGONIST in breast and uterus, AGONIST in bone and CV

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69
Q

sperm can stay in the cervix for

A

80 hours.

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70
Q

sperm capacitation

A

secretions for woman trigger sperm maturation (so it can fertilize egg). characterized by increased motility of sperm

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71
Q

sperm penetrating the cumulus cells

A

assisted by sperm motility and enzymes (PH20 - hyaluronidase)

72
Q

What happens in the acrosome reaction?

A

the sperm adheres to ZP. ZP3 receptor on sperm is activated. Ca entry via T type Ca channels. Activates PLC and IP3. The sustained Ca triggers fusion of outer acrosome membrane with sperm plasma membrane

73
Q

hallmark of egg activation

A

Ca oscillations - lead to exocytosis of cortical granules and blocks polyspermy

74
Q

timing of egg activation

A

occurs AFTER fertilization. Egg finishes 2nd meiosis –> mitosis –> embryonic dev.

75
Q

globozoospermia

A

round headed sperm that don’t have acrosome reaction - can’t move past ZP. Can use ICSI, but success rate is low

76
Q

PESA and TESE

A

look at notes

77
Q

describe fertilization

A

penetrate cumulus –> penetrate ZP –> merge with egg plasma membrane –> fertilization (2 pro nu) –> egg activation –> block polyspermy

78
Q

drugs that can cause impotence

A

beta blockers, exogenous androgens

79
Q

initiating erection

A

CNS –> limbic system activates paraS system, which increases cGMP and causes vasodilation. Local reflex supports this

80
Q

MOA phosphodiesterase 5 inhibitrs

A

they inhibit phosphodiesterase 5, increase cGMP, MAINTAIN erection (still need the limbic system to initiate erection and get cGMP production)

81
Q

metabolism of sildenafil

A

metabolized in liver by CYP3A4 to active metabolite (20% activity). Excreted via kidneys

82
Q

can’t use PD5 inhibitors with….

A

nitrates (anti-hypertensives) because both cause vasodilation (dizziness, hypotension, fatal events)

83
Q

Timing of adrenarche

A

usually 2 years before secondary sex char (usually thelarche, then pubarche)

84
Q

timing of thelarche

A

usually between 8-13

85
Q

timing of menarche

A

average age =13 (after gonadarche, takes about 2 years to build up estrogen secretion and increase endometrial lining)

86
Q

estrogen and height

A

low levels == bone growth; high levels = close epiphyseal plates

87
Q

hormone levels in neonates

A

release from maternal E&P inhibition –> high LH and FSH –> high fetal E and P

88
Q

sign of puberty

A

LH pulses at night (represent GnRH pulses because LH has a short half-life)

89
Q

what initiates pubertal changes?

A

the hypoT (arcuate nucleus) is released from inhibition –> starts GnRH pulses (This is NOT controlled by the gonads)

90
Q

signals that inhibit GnRH pulsatility (delay puberty)

A

GABA (in girls) and Neuropeptide Y (in boys)

91
Q

Leptin and puberty

A

leptin promotes puberty (and decreases NPY). It is NECESSARY for gonadarche, but doesn’t prompt the start of GnRH pulsatility

92
Q

Kisspeptin receptor

A

GPR54

93
Q

Kisspeptin

A

simulates GnRH neurons (in the arcuate nu of the hypoT) -sudden appearance o kisspeptin fibers surround GnRH neuron just before onset of puberty

94
Q

why is the ureter vulnerable to injury during pelvic surgery? 1

A
  1. in a hysterectomy, the uterine artery crosses the ureter ~2” over the ischial spines; 2. the LEFT ureter comes close to the lateral cervix 3. the ureter lies close to the ovarian vessels
95
Q

what procedure is commonly performed through the rectouterine pouch?

A

oocyte retreival

96
Q

what ligaments support the uterus and vagina?

A

uterosacral and cardinal ligaments

97
Q

what is the major cause of infertility in females and how to Dx?

A

tubal obstruction. Dx with hysterosalpingography (radiography)

98
Q

perineal body

A

fibromusclar mass anterior to retum. Can tear during labor to enlarge vaginal orfice. Increases chance of vaginal prolapse

99
Q

when do you start to dev gonads?

A

6 weeks gestation (from last menses)

100
Q

prev of mullerian abnormalities in the general pop

A

4%

101
Q

most common mullerian abnormality

A

septated uterus

102
Q

inhibin

A

produced by granulosa and Sertoli cells. Decrease pituitary GnRH receptors –> decrease FSH secretion. Increase LH receptors on thecal cells

103
Q

Klinefelter Syndrome

A

47XXY. bilateral atrophic testes. Congenital cause of primary hypogonadism

104
Q

Kallman Syndrome

A

GnRH precursor doesn’t migrate from nose to hypoT. no LH/FSH (need supplementation), and altered smell

105
Q

males and infertility

A

15% couples are infertile. males account for 30% of blame (females - 50%; combined 20%)

106
Q

5 alpha reductase

A

turns testosterone into DHT (external virilization and sexual maturation at puberty)

107
Q

most common location for BPH

A

around the proximal urethra (transitional zone)

108
Q

definition of BPH

A

nodular prostate enlargement due to proliferation of glands, stroma, or both, that LEADS TO lower urinary tract Sx

109
Q

PCA epidemiology in the US

A

most common malignancy in men, 2nd most deadly after lung cancer

110
Q

PCA epidemiology in the word

A

6th MOST COMMON cancer

111
Q

high serum PSA levels signal

A

that the PCA has broken through the basement membrane

112
Q

The Sx you see with PCA

A

** most often asymptomatic. Sx = obstructive bladder Sx, pelvic pain, bone pain

113
Q

origin of PCA

A

75-80% from peripheral zone / 15-25% from transitional zone. Central zone can be secondarily involved

114
Q

Chlamydia vs. Gonorrhea

A

Chlamydia is an IC org –> fewer Sx –> more common than G

115
Q

Dx for PID

A
  1. lower abdominal pain 2. adnexal tenderness, 3. cervical motion tenderness.
116
Q

ectopic pregnancies are most common in,.

A

the ampulla

117
Q

what makes the vagina resistant to micro-org?

A

Vagina has lactobacilli which make H2O2 –> acidic environment = resistant to many STIs

118
Q

dysfunctional uterine bleeding

A

LACK OF OVULATION - means no progesterone & secretory endometrium. Estrogen causes proliferation - outgrows blood supply - breakdown/bleeding

119
Q

Endometrial atrophy

A

Lack of estrogen causes endometrium to break down –> common cause of abnormal uterine bleeding in post-M women

120
Q

three things to know about polyps

A

they arise from Basalis layer // they are benign (but have different morphology - thick-walled arteries and enlarged glands) // they are focal (sessile or pedunculated)

121
Q

most frequent tumor in female genital tract

A

leiomyoma

122
Q

leiomyoma and hormones

A

we know hormones have an effect - tumors increase in preg and decrease after menopause. They are sensitive to estrogen (Tamoxifen)

123
Q

endometriosis

A

endometrial tissue (glands & stroma) outside of uterus - usually in ovaries or peritoneal cavity

124
Q

Adenomyosis

A

endometrial tissue in uterine wall (myometrium)

125
Q

most common malignant tumor of female genital tract

A

endometrial carcinoma

126
Q

Estrogen dependent endometrial carcinoma

A

during pre-menopause, perimenopause / myometrial invasion is variable, us/minimal, low tumor grade, indolent behavior, genes: PTEN, K-ras

127
Q

features of endometrial carcinoma, not hyperplasia,

A

invasion into myometrium, desmoplastic response, cribriform glands, extensive papillary pattern

128
Q

mutation found in Type 2 endometrial carcinoma

A

non-estrogen dependent. p53 mutation (can statin for it)

129
Q

is type 1 or type 2 more common for endometrial carcinoma?

A

Type 1 = 80-85% // type 2 = 15-20%

130
Q

in a post-menopausal women with bleeding, consider….

A

endometrial hyperplasia (most common) or endometrial carcinoma - type 2 (most concerning)

131
Q

endometroid endometrial carcinoma

A

type 1 - it was similar to complex atypical hyperplasia. Saw cribriform plates

132
Q

Serous endometrial carcinoma

A

type 2 form (can be mixed with clear cell form). Saw complex papillae structure. Can see calcification (psammoma bodies)

133
Q

staging of endometrial cacner

A

look at notes

134
Q

prognosis for ovarian cancer

A

5 year survival is 30-50%. Staging is the most impt prognostic factor

135
Q

most common malignant ovarian tumor (overall)

A

serous carcinoma

136
Q

genetics seen in serous carcinoma

A

LOW GRADE: K-ras or BRAF // HIGH GRADE: BRCA1 or BRCA2 –> usually due to +p53

137
Q

endometroid ovarian carcinoma

A

genetics: PTEN, K-ras, microsatellite instability (think type 1 endometroid carcinoma). 15-20% accompanied by endometriosis

138
Q

Origin of germ cell tumors

A

the oocyte (in the follicle)

139
Q

malignant transformation of dermoid cyst

A

can turn into any kind of cancer. Common = squamous cell carcinoma

140
Q

Dysgerminoma makes up a sig. % of malignant tumors in…

A

during pregnancy (20-30%), and before age 30 (80%)

141
Q

prognosis for dysgerminoma

A

excellent prognosis - 80-90% survival for high-stage disease

142
Q

cystadenoma

A

benign form of surface epithelial carcinoma. See a cyst lined by one layer of cells, filled with fluid. Smooth, thin cyst wall.

143
Q

Call-Exner bodies

A

seen in adult granulosa - sex-cord stroma tumors. The granulosa tumor cells are trying to form follices!

144
Q

what kind of ovarian carcinoma can make estrogem?

A

adult granulosa (sex-cord stroma) –> endometrial hyperplasia and carcinoma (type 1)

145
Q

4 side effects of PD5 inhibitors

A
  1. vasodilation (don’t use with nitrates) 2. CV - hypotension, tachycardis, decreased platelets; 3. GI - heartburn and indigestion 4. eyes - see blue/green
146
Q

site of 1st lesions - cervical cancer

A

squamo-columnar junction (transition zone). As you get older, the transition zone moves higher into the cervical canal

147
Q

high risk HPV strains

A

16 & 18

148
Q

Reflex HPV testing

A

take the residual liquid from the Pap smear, do high risk-HPV testing. (+) = colposcopy , (-) = Pap smear in 1 year

149
Q

Co-Test

A

cytology (papsmear) + high risk HPV testing simultaneously. Used in women >30. (-) = come back in 5 years.

150
Q

cervical cancer subtypes

A

squamous cell (80%+), adenocarcinoma (glandular - 15%), other (5%)

151
Q

biggest factor in cervical cancer deaths

A

never been screened (50% cervical cancer cases)

152
Q

worst - HPV 16 or 18?

A

HPV 16 = more carcinogenic (60% all cervical cancers). HPV 18 = 15% - more in adenocarcinomas

153
Q

how many cases of cervical cancer a year?

A

15K in the US - 450K in the world

154
Q

principle age for HPV vaccine

A

12-Nov

155
Q

most common cause of abnormal pap dx

A

ASC-US –> do reflex testing (if women is 25+)

156
Q

Timing of testing for cervical cancer

A

START screening at 21. Can do reflex testing at 24. Can to co-test at 30. You don’t want to start earlier because younger women have higher levels of HPV but lower levels of CIN 3

157
Q

Cases: LSIL on papsmear, no high risk testing

A

answer: colposcopy (assume the high risk testing could be positive)

158
Q

Clue: cyclic bleeding

A

suggest that ovaries/hormones are in tact (even if duration of cycle if abnormal)

159
Q

19-year old presenting with malignant cancer

A

think: dysgeminoma

160
Q

breast changes during puberty

A

ductal elongation, driven by estrogen. mitotic rate of glandular epithelial cells is greatest in luteal phase (E+P)

161
Q

what stimulates the differentiation of breast glands

A

progesterone and prolactin - prepare glands to lactate

162
Q

what suppresses the lactogenic action of prolactin?

A

Estrogen and progesterone

163
Q

supernumerary nipples (polymastia)

A

secondary to incomplete regression of milk streak

164
Q

2 etiologies of galactorrhea

A
  1. increased prolactin (amenorrhea) 2. increases sensitivity of breasts to prolactin (regular prolactin levels & regular menses)
165
Q

Sheehan’s syndrome

A

infarction of pituitary during labor/delivery –> no lactation, etc.

166
Q

Gynecomastia - causes

A

due to imbalance between E and androgens. See it transiently in newborns (mother’s E), transiently during puberty (E production before androgens), in elderly - taking drug that decreases androgens

167
Q

seminal vesicles add…

A

fructose

168
Q

alkylation at 17 alpha

A

makes androgens with more ANAbolic properties - JUICING

169
Q

Esterification @ 17-beta

A

makes regular androgens (similar in potency to T and DHT)

170
Q

what’s a common OTC male hormone supplement?

A

DHEA

171
Q

the adrogen potencies

A

DHEA and androstenedione=weak // testosterone = moderate.// DHT = very potent (but you make very little)

172
Q

ARA70

A

it’s a coactivator for AR-testosterone and AR-DHT

173
Q

which androgen increases prostate size?

A

DHT

174
Q

flutamide

A

its a receptor antagonist. It prevents the binding of the receptor complex to ARA70

175
Q

Finasteride

A

blocks 5-alpha reductase TYPE 2 - can decreased BPH and male pattern baldness (both are caused by 5-DHT)

Patho flash cards (33 decks)

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