repro Flashcards
(175 cards)
1
Q
Kartagener Syndrome
A
absence of dynein –> immotile sperm –> infertility for males
2
Q
TEXT-14
A
Testis-expressed gene 14: essential for cytoplasmic bridges in mice
3
Q
sperm - longer in meiosis I or II?
A
meiosis I takes much longer - which is wh yyou see many more primary spermatocytes
4
Q
Tunica Albiginea
A
fibrous capsule of connective tissue around testes. Divides testes into lobules
5
Q
haploid/diploid for primary/secondary spermatocyte
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primary = diploid // secondary = haploid
6
Q
menstrual cycle length
A
24-35
7
Q
GnRH pulsatility for LH
A
HIGH amplitude, low frequency
8
Q
how many oocytes do you have?
A
@ 5 months gestation: 6 million –> 2 million @ birth –> 300k @ puberty –> 0 @ menopause
9
Q
follicles start to be recruited to mature starting at…
A
5 months in utero until menopause
10
Q
follicles become dependent on FSH at the….
A
secondary follicle stage (defined by formation of the antrum)
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
12
Q
actions of FSH on follice
A
stimulates granulosa cell prolif. stimulates aromatase activity, increases FSH AND LH receptors
13
Q
3 actions of p on uterus
A
limit growth, make glands more tortuous, coiling of b.v.
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
15
Q
Corpus luteam makes E and P for…
A
8-10 weeks (Then placenta takes over)
16
Q
most common contraceptives
A
OCPs»_space; tubal sterilization»_space; male condom»_space; vasectomy
17
Q
timing of copper IUD
A
insert before 7 days after sex, good for 12 years
18
Q
medroxyprogesterone acete
A
progesterone only depot injection. Take every 3 months. Ver effect, but people quite because of irregular bleeding
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
20
Q
Patch - contraceptive
A
like OCP (combined) - similar efficacy. MOA: no ovulation. Replaced weekly
21
Q
vaginal ring
A
like OCP: combined, similar efficacy to OCP. change every 3 weeks. MOA: stops ovulation
22
Q
IUD
A
P only –> thickens cervical mucosa (woman still ovulates) Works for 5 years.
23
Q
Implanon
A
P only. Placed under arm. Works for 3 years. Rapid return to fertility (period within 3 months)
24
Q
Implanon
A
progesterone only LARC. Placed under arm - effect for 3 years
25
Do OCPs increase risk of venous embolisms?
YES, but not to the extent of pregnancy
26
Do OCP increase CV risk?
only in smokers
27
How many pregnancies a year?
6 million pregnancies a year, 1/2 are unplanned, of the unplanned, 1/3 will abort
28
% of women who have had induced abortions
40%
29
strongest risk factor for abortion-related mortality
gestational age
30
can use medical abortion..
up to 9 weeks (used in 1/4 of eligible abortions)
31
mifepristone
blocks the P receptor --> decidual necrosis, increased prostaglandin receptors, cervical ripening
32
misoprostal
prostaglandin E1 analog --> contractions and cervical ripening. Used with mifepristone, methotrexate, and by itself
33
side effects of misoprostol
** responsible for most side effects of abortion. GI (nausea, vomiting, diarrhea), and systemic (fever/chills, HA)
34
methotrexate
blocks cells division. Takes longer (3-45 days), used off label with misoprostal
35
signs of perimenopause/menopause transition
irregular menses (fewer follicles to make E), and Sx (e.g., hot flashes)
36
timing of perimenopause
median age is around 45 - 47.5 (MWHS), duration is 4-5 years (can last 2-8 years)
37
What defines the onset of menopause?
follicular cohort + rate of atresia --> DECREASED ESTROGEN
38
biochem profile of menopause
decreased estrogen --> increased and LH and FSH
39
MOA of CVD and OP in post-menopausal women
lower estrogen leads to increased cholesterol & LDL levels, and increased bone lose
40
smoking and estrogen
smoking increases the metabolism of estrogen --> faster onset of menopause
41
sstreak gonads seen with
Turner's syndrome. Need both X's for normal ovarian function --> accelerated atresia, streak gonads , ovarian failiure
42
HCG mimcs
LH
43
endometrial receptivity window
Determined by progesterone. Day 20-24
44
timing of implantation
at 7 days post-ovulation (blastocyst stage)
45
when is embryo fully embedded in endometrial stroma?
7 days post-implantation (14 days post-ovulation)
46
where does embryo implant?
usually mid-posterior of uterus.
47
functions of syncytiotrophoblasts
1. direct contact with maternal blood; 2. secrets hormones (HCG, P4, E2)
48
most common endocrine disorder in young, reproductive aged women
PCOS
49
describe the hyperandrogenism in PCOS
chronic, low-grade elevation in androgens coming from ovaries (not adrenal glands, HEAD levels moderately elevated in 10-15% patients)
50
Dx for PCOS
1. hyperandorgenism //2. anovulation or oligo-ovulation (<6-9/yr) // ultrasound - 12 follicles/ovary
51
anti-Mullerian hormone in PCOS?
it's elevated = new marker? in PCOS, the granulosa cells are more sensitive to FSH - greater AMH production
52
long term effects of PCOS
lifetime metabolic disorder, higher risk of endometrial cancer (lack of periods), increase risk of psych disorders
53
E and P in PCOS
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
54
effect of estrogen on bone
decreases osteoclasts and determines the closure of the epiphyseal plates
55
estrogen - CV effects
increases blood coagulability (BAD) but improves cholesterol profile: increases HDL, and decreases LDL (Good)
56
Metabolic effects of estrogen
increases leptin (involved in fat redistribution also), and increases protein synthesis in liver --> including TBG!!!
57
two roles of P
1. prepares uterus for implantation; 2. render uterus refractory to oxytocin until labr
58
type 3-4 antagonist
mixed agonist/antagonist - binding of receptor to HRE can recruit co-activator or co-repressor
59
type 2 antagonist
pure antagonist - binding of receptor to HRE recruits co-repressor
60
Type 1 antagonist
pure antagonist - does not allow the receptor to bind the HRE
61
exogenous estrogens and cancer risk
INCREASES endometrial and ovarian (E only) and breast (E+P) but DECREASES colon cancer (E+P)
62
RU486
Progesterone receptor Type 2 antagonist
63
hormone independent breast cancer
1/3 of cases --> do mastectomy then chemo + rad
64
hormone dependent breast cancer
2/3 cases - can do adrenalectomy, aromatase inhibitors (part of chemo) or SERM (prophylactic Rx)
65
SERM
selective estrogen receptor modulators. Are tumoristatic, can be used for prophylaxis Rx after treatment for breast cancer
66
aromatase inhibitors
used as chemo for ER-positive tumors
67
Tamoxefin
Type 4 SERM: ANTAGONIST: breast // AGONIST: bone, uterus (bad), maybe CV
68
Raloxifene
type 3 SERM: ANTAGONIST in breast and uterus, AGONIST in bone and CV
69
sperm can stay in the cervix for
80 hours.
70
sperm capacitation
secretions for woman trigger sperm maturation (so it can fertilize egg). characterized by increased motility of sperm
71
sperm penetrating the cumulus cells
assisted by sperm motility and enzymes (PH20 - hyaluronidase)
72
What happens in the acrosome reaction?
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
hallmark of egg activation
Ca oscillations - lead to exocytosis of cortical granules and blocks polyspermy
74
timing of egg activation
occurs AFTER fertilization. Egg finishes 2nd meiosis --> mitosis --> embryonic dev.
75
globozoospermia
round headed sperm that don't have acrosome reaction - can't move past ZP. Can use ICSI, but success rate is low
76
PESA and TESE
look at notes
77
describe fertilization
penetrate cumulus --> penetrate ZP --> merge with egg plasma membrane --> fertilization (2 pro nu) --> egg activation --> block polyspermy
78
drugs that can cause impotence
beta blockers, exogenous androgens
79
initiating erection
CNS --> limbic system activates paraS system, which increases cGMP and causes vasodilation. Local reflex supports this
80
MOA phosphodiesterase 5 inhibitrs
they inhibit phosphodiesterase 5, increase cGMP, MAINTAIN erection (still need the limbic system to initiate erection and get cGMP production)
81
metabolism of sildenafil
metabolized in liver by CYP3A4 to active metabolite (20% activity). Excreted via kidneys
82
can't use PD5 inhibitors with....
nitrates (anti-hypertensives) because both cause vasodilation (dizziness, hypotension, fatal events)
83
Timing of adrenarche
usually 2 years before secondary sex char (usually thelarche, then pubarche)
84
timing of thelarche
usually between 8-13
85
timing of menarche
average age =13 (after gonadarche, takes about 2 years to build up estrogen secretion and increase endometrial lining)
86
estrogen and height
low levels == bone growth; high levels = close epiphyseal plates
87
hormone levels in neonates
release from maternal E&P inhibition --> high LH and FSH --> high fetal E and P
88
sign of puberty
LH pulses at night (represent GnRH pulses because LH has a short half-life)
89
what initiates pubertal changes?
the hypoT (arcuate nucleus) is released from inhibition --> starts GnRH pulses (This is NOT controlled by the gonads)
90
signals that inhibit GnRH pulsatility (delay puberty)
GABA (in girls) and Neuropeptide Y (in boys)
91
Leptin and puberty
leptin promotes puberty (and decreases NPY). It is NECESSARY for gonadarche, but doesn't prompt the start of GnRH pulsatility
92
Kisspeptin receptor
GPR54
93
Kisspeptin
simulates GnRH neurons (in the arcuate nu of the hypoT) -sudden appearance o kisspeptin fibers surround GnRH neuron just before onset of puberty
94
why is the ureter vulnerable to injury during pelvic surgery? 1
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
what procedure is commonly performed through the rectouterine pouch?
oocyte retreival
96
what ligaments support the uterus and vagina?
uterosacral and cardinal ligaments
97
what is the major cause of infertility in females and how to Dx?
tubal obstruction. Dx with hysterosalpingography (radiography)
98
perineal body
fibromusclar mass anterior to retum. Can tear during labor to enlarge vaginal orfice. Increases chance of vaginal prolapse
99
when do you start to dev gonads?
6 weeks gestation (from last menses)
100
prev of mullerian abnormalities in the general pop
4%
101
most common mullerian abnormality
septated uterus
102
inhibin
produced by granulosa and Sertoli cells. Decrease pituitary GnRH receptors --> decrease FSH secretion. Increase LH receptors on thecal cells
103
Klinefelter Syndrome
47XXY. bilateral atrophic testes. Congenital cause of primary hypogonadism
104
Kallman Syndrome
GnRH precursor doesn't migrate from nose to hypoT. no LH/FSH (need supplementation), and altered smell
105
males and infertility
15% couples are infertile. males account for 30% of blame (females - 50%; combined 20%)
106
5 alpha reductase
turns testosterone into DHT (external virilization and sexual maturation at puberty)
107
most common location for BPH
around the proximal urethra (transitional zone)
108
definition of BPH
nodular prostate enlargement due to proliferation of glands, stroma, or both, that LEADS TO lower urinary tract Sx
109
PCA epidemiology in the US
most common malignancy in men, 2nd most deadly after lung cancer
110
PCA epidemiology in the word
6th MOST COMMON cancer
111
high serum PSA levels signal
that the PCA has broken through the basement membrane
112
The Sx you see with PCA
** most often asymptomatic. Sx = obstructive bladder Sx, pelvic pain, bone pain
113
origin of PCA
75-80% from peripheral zone / 15-25% from transitional zone. Central zone can be secondarily involved
114
Chlamydia vs. Gonorrhea
Chlamydia is an IC org --> fewer Sx --> more common than G
115
Dx for PID
1. lower abdominal pain 2. adnexal tenderness, 3. cervical motion tenderness.
116
ectopic pregnancies are most common in,.
the ampulla
117
what makes the vagina resistant to micro-org?
Vagina has lactobacilli which make H2O2 --> acidic environment = resistant to many STIs
118
dysfunctional uterine bleeding
LACK OF OVULATION - means no progesterone & secretory endometrium. Estrogen causes proliferation - outgrows blood supply - breakdown/bleeding
119
Endometrial atrophy
Lack of estrogen causes endometrium to break down --> common cause of abnormal uterine bleeding in post-M women
120
three things to know about polyps
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
most frequent tumor in female genital tract
leiomyoma
122
leiomyoma and hormones
we know hormones have an effect - tumors increase in preg and decrease after menopause. They are sensitive to estrogen (Tamoxifen)
123
endometriosis
endometrial tissue (glands & stroma) outside of uterus - usually in ovaries or peritoneal cavity
124
Adenomyosis
endometrial tissue in uterine wall (myometrium)
125
most common malignant tumor of female genital tract
endometrial carcinoma
126
Estrogen dependent endometrial carcinoma
during pre-menopause, perimenopause / myometrial invasion is variable, us/minimal, low tumor grade, indolent behavior, genes: PTEN, K-ras
127
features of endometrial carcinoma, not hyperplasia,
invasion into myometrium, desmoplastic response, cribriform glands, extensive papillary pattern
128
mutation found in Type 2 endometrial carcinoma
non-estrogen dependent. p53 mutation (can statin for it)
129
is type 1 or type 2 more common for endometrial carcinoma?
Type 1 = 80-85% // type 2 = 15-20%
130
in a post-menopausal women with bleeding, consider....
endometrial hyperplasia (most common) or endometrial carcinoma - type 2 (most concerning)
131
endometroid endometrial carcinoma
type 1 - it was similar to complex atypical hyperplasia. Saw cribriform plates
132
Serous endometrial carcinoma
type 2 form (can be mixed with clear cell form). Saw complex papillae structure. Can see calcification (psammoma bodies)
133
staging of endometrial cacner
look at notes
134
prognosis for ovarian cancer
5 year survival is 30-50%. Staging is the most impt prognostic factor
135
most common malignant ovarian tumor (overall)
serous carcinoma
136
genetics seen in serous carcinoma
LOW GRADE: K-ras or BRAF // HIGH GRADE: BRCA1 or BRCA2 --> usually due to +p53
137
endometroid ovarian carcinoma
genetics: PTEN, K-ras, microsatellite instability (think type 1 endometroid carcinoma). 15-20% accompanied by endometriosis
138
Origin of germ cell tumors
the oocyte (in the follicle)
139
malignant transformation of dermoid cyst
can turn into any kind of cancer. Common = squamous cell carcinoma
140
Dysgerminoma makes up a sig. % of malignant tumors in...
during pregnancy (20-30%), and before age 30 (80%)
141
prognosis for dysgerminoma
excellent prognosis - 80-90% survival for high-stage disease
142
cystadenoma
benign form of surface epithelial carcinoma. See a cyst lined by one layer of cells, filled with fluid. Smooth, thin cyst wall.
143
Call-Exner bodies
seen in adult granulosa - sex-cord stroma tumors. The granulosa tumor cells are trying to form follices!
144
what kind of ovarian carcinoma can make estrogem?
adult granulosa (sex-cord stroma) --> endometrial hyperplasia and carcinoma (type 1)
145
4 side effects of PD5 inhibitors
1. vasodilation (don't use with nitrates) 2. CV - hypotension, tachycardis, decreased platelets; 3. GI - heartburn and indigestion 4. eyes - see blue/green
146
site of 1st lesions - cervical cancer
squamo-columnar junction (transition zone). As you get older, the transition zone moves higher into the cervical canal
147
high risk HPV strains
16 & 18
148
Reflex HPV testing
take the residual liquid from the Pap smear, do high risk-HPV testing. (+) = colposcopy , (-) = Pap smear in 1 year
149
Co-Test
cytology (papsmear) + high risk HPV testing simultaneously. Used in women >30. (-) = come back in 5 years.
150
cervical cancer subtypes
squamous cell (80%+), adenocarcinoma (glandular - 15%), other (5%)
151
biggest factor in cervical cancer deaths
never been screened (50% cervical cancer cases)
152
worst - HPV 16 or 18?
HPV 16 = more carcinogenic (60% all cervical cancers). HPV 18 = 15% - more in adenocarcinomas
153
how many cases of cervical cancer a year?
15K in the US - 450K in the world
154
principle age for HPV vaccine
12-Nov
155
most common cause of abnormal pap dx
ASC-US --> do reflex testing (if women is 25+)
156
Timing of testing for cervical cancer
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
Cases: LSIL on papsmear, no high risk testing
answer: colposcopy (assume the high risk testing could be positive)
158
Clue: cyclic bleeding
suggest that ovaries/hormones are in tact (even if duration of cycle if abnormal)
159
19-year old presenting with malignant cancer
think: dysgeminoma
160
breast changes during puberty
ductal elongation, driven by estrogen. mitotic rate of glandular epithelial cells is greatest in luteal phase (E+P)
161
what stimulates the differentiation of breast glands
progesterone and prolactin - prepare glands to lactate
162
what suppresses the lactogenic action of prolactin?
Estrogen and progesterone
163
supernumerary nipples (polymastia)
secondary to incomplete regression of milk streak
164
2 etiologies of galactorrhea
1. increased prolactin (amenorrhea) 2. increases sensitivity of breasts to prolactin (regular prolactin levels & regular menses)
165
Sheehan's syndrome
infarction of pituitary during labor/delivery --> no lactation, etc.
166
Gynecomastia - causes
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
seminal vesicles add...
fructose
168
alkylation at 17 alpha
makes androgens with more ANAbolic properties - JUICING
169
Esterification @ 17-beta
makes regular androgens (similar in potency to T and DHT)
170
what's a common OTC male hormone supplement?
DHEA
171
the adrogen potencies
DHEA and androstenedione=weak // testosterone = moderate.// DHT = very potent (but you make very little)
172
ARA70
it's a coactivator for AR-testosterone and AR-DHT
173
which androgen increases prostate size?
DHT
174
flutamide
its a receptor antagonist. It prevents the binding of the receptor complex to ARA70
175
Finasteride
blocks 5-alpha reductase TYPE 2 - can decreased BPH and male pattern baldness (both are caused by 5-DHT)
