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Flashcards in REPRO Deck (169)
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1
Q

juvenile pause

A

18 months to 4 yyears

when GABA, melatonin, DA, and 5HT inhibit hypothalamus

2
Q

what is true in constitutional pubertal delay

A

pubertal age aligns with bone age

3
Q

kallman syndrome

A

doesnt make GnRH

cant smell

4
Q

PROP 1 defect only ___ is conserved

A

ACTH

5
Q

four types of inherited hypogonadotropic hypergonadism

A

Prop 1 defect
CAH
leptin R def
kallman syndrome

6
Q

main issue with klinefelters

A

leydig cells dont respond to LH to make testosterone

7
Q

what is the most potent estrogen

A

estradiol (e2)

8
Q

what is primarily secreted from the ovary

A

estradiol

9
Q

definition of precocious puberty

A

females before age 8 and males before age 9

10
Q

causes of complete precocious puberty

A

idiopathic
central-glioma, hamartoma (secreting GNRH)
primary severe hypothyroidism (excess TSH mimics FSH)

11
Q

MC of incomplete precocious puberty in females

A

autonomous small ovarian c ysts with estrogen secretion by granulosa cells

tx-progestin

12
Q

four causes of incomplete precocious puberty

A

McCune Albrihgt
auto E producing follicular cysts
ovarian neoplasm
peutz jeghers

13
Q

4 stages of sexual differentiation

A

genetic sex
formation fo gonad
formation of ductal system
differentiatin of eternal genetalia

14
Q

indifferent gonads

A

at six weeks
mesenchymal- theca/leydig
epithelial-granulosa/sertoili

15
Q

wolfian goes with

A

mesonephric

16
Q

mullerian goes with

A

paramesonephric

17
Q

what produces MIF

A

sertoli cells

18
Q

what 2 things does fetal testosterone cause

A

wolfian completion

DHT–>masculinization

19
Q

four requirements of masculinization

A

testicular determining gene action
bilateral gonadal elaboration mIF
5 alpha reductase
androgen R at target organ

20
Q

what does wolfian duct become

A

vas deferns
epidiymis
seminal vesicle

21
Q

gardner’s duct

A

between ovary and human which can have cysts –if wolfian doesnt regress all the way

22
Q

what does mullerian duct become

A

fallopain tube
upper 1/3 vag
uterus

23
Q

genital tubecle in men and women

A

men- penis

wo-glans–>clit

24
Q

urogenital slit

A

bpy-prostate

girl- lower 2/3 vagina and anterior uretra

25
Q

labioscotcal sweelings

A

boy scrotum

girl- labia majora

26
Q

urethral folds

A

labia mino

27
Q

undifferentiated primordial germ cell arises from

A

endodermal lining of yolk sac

28
Q

androgen insensitivity aka

A

pseudohemathro

29
Q

four most necessary things for graffian follicle

A

highest mitotic index
most optimal FSH response
high E and inhibin B synthesis
optimal aromatase activity to convert androgens–>E

30
Q

what prevents E from stimulating another LH surge

A

progesterone

31
Q

what is fixed at 14 days

A

luteal phase

32
Q

clomiphene

A

E antagonist; given in luteal phase to increase circulating FSH levels–> follicular recruitment for next cycle

33
Q

what three things does the menstraul phase involve

A

hormonlly-regulated matrix degrading proteases
lysosomes
endothelians

34
Q

pathway of menstrural phase

A

decrease P–>decrease hydroxyP dehydrogenase–>increase PGF2a–> myometrial and vascular contractions (along with txa2) –>endotheial ischemia and sloughing

35
Q

mennorhagia

A

blood loss greater than 80 ml and regular cycles

36
Q

metrorrhagia

A

irregular frequent bleeding

37
Q

menorrhagia

A

irregular menses with prolonged or excessive blood loss; break through bleeding: unexpected bleeding that occurs while a women is on exogenous hormone mes

38
Q

definition of delayed puverty

A

after 16 in boys

or after 13 in girls

39
Q

main s/sx polycystic ovarian syndrome

A

insuin resistance
hyperandrogenism
chronic anovulation

40
Q

athway PCOS

A

insulin R–>hhyperinsulinemia–>decrease sHBG–>increased androgens

–>ovarian and adrenal hyperandrogenism

–>hypeothalamic effect-increase pulse GnRH

41
Q

ultrasound criteria of PCOS

A

12 or more follicles in one or both ovaries, 2-9mm

ovarian volume >10cm

42
Q

major cx PCOS

A

endometrial hyperpalsia–>endometrial carcinoma

43
Q

tx for PCOS not try to get pregs

A

lifestyle mod
combination hormonal contraceptives or progestin
anti-androgen (spirnolactone) if desired
insulin-sens agents

44
Q

tx if trying to get preg

A

clomiphene

but if clomiphene fails, gonadotropin tx but much higher likelihood of multifetal pregn

45
Q

4 reasons for chronic anov

A

1) hypothalalmus fails to secrete GnRH
2) pit fails to respond to GnRH
3) failure of HPO axis + feedback needed for LH surge
4) inteference with gonadal steroid feedback by other endocrine systems

46
Q

end organ abnormalities in primary amen

A

inability of organs to respond to normal cyclic ovarian steroid production adn produce bleed

47
Q

explanations for primary amen

A

kallman

transverse vaginal septa

48
Q

definition of primary amenorrhea

A

failure to menstruate by age 16 with normal secondary sex chracteristics OR
age 14 without signs of normal sex maturatin

49
Q

secondary amen

A

absence of three menstraul cycles or absence of menstraul bkleeding for 6 months

first step-check hcg

50
Q

reasons for secondary amenorrhea

A
PCOS
premature ovarian failure
asherman syndrome
hyperprolactinemia
hypothyroidism
CAH, cushing, obseity
pituitray disorder
51
Q

asherman syndrome

A

occlusion of uterine cavity by adhesions secondayr to postpartum cutterage or some bad uterine procedure (D&C)

52
Q

biggest decline in fertility between ages

A

25-29

53
Q

fecundability

A

probability of conception in a single menstraul cycle

54
Q

aneuploid comes from

A

errors in meiosis 2

55
Q

definitions of abnormal fetility

A

under 35: failure to conceive after 1 year unprotected six

>35: after 6 months

56
Q

blastocyst hatches into

A

trophoectodermal cells–>trophoblast cells–>anchor to endometrium

endometrium–>decidualization

57
Q

on implantation..

A

embryo invades maternal tissue and trophoblast cells differentiate into cytotrophonlast and syncutitrophoblst

58
Q

3 processes implantation

A

apposition- blasto sits next to endo metrium (LIF, PGs)
adhesiob- ligands on surface of trophoblast bind R on endometrial site of implantation (hep & hep sulfate proteoglycans)
invasion- regional change expressed surface molecules and secretion of proteases by embryo to digest cells of decidua

59
Q

job of cytotrophoblast

A

invade endometrium and connect to spiral arterioles

60
Q

syncytiotrophoblast secretes

A

hcg

61
Q

TGFB

A

tgfB–>increase in syncytioblast formation, block trophoblast invasiofa

62
Q

factors that help with implantation

A
Leukemia inhib factor
integrins
TGF B
EPGF
ILIB
63
Q

when does placenta take over producing progesterone

A

9 weeks

64
Q

hcg serum level correlates with

A

cytotrophoblast cell mass

65
Q

three jobs hcg

A

rescue CL
gonadal and adrenal hormone production
immune sup so can tolerate fetus

66
Q

variation in hcg level

A

higher than normal- multiple gestations

failure to rise on subsequent hcg levels- nonviable or ectopic

67
Q

HPL

A

keeps mothers blood glucose stable, similar to GH

product of placenta

68
Q

CRH, POMC (ACTH PRECURSOR)

A

preduced in last month, timing partuition

69
Q

2 sides of placenta

A

uterine side: millions of villi

fetal side: smooth membrane (amnion)–umbilival cord inserts here

70
Q

increased placental E leads to

A

increased hepatic production TBG–>decrease free thyroid hormone so increase trh and tsh, increase in total t3 t4

also increase in pit to double its lacototrophs and therefore prolactin secretion–>puts placenta at risk for ischemic damage

71
Q

four jobs of prostaglandins

A

myometrium contraction
cervical ripening (PGE2)
inhibit PDA closure in ductus
induce labor or term preg

72
Q

alpha fetoprotein is high and low in

A

high in spina bifida (decreased by taking folate but doesnt decrease already elevated levels of alpha FP)

derease in trisomy 21

73
Q

where does afp come from

A

fetal liver

74
Q

estrogen fx in preg

A

increase uterine flow

comes from E3 in preg

75
Q

progesterone jobs

A

increase decidual rxn to allow implantation
decrease myometrial contract
increased stretchiness of uterine muscle
breast dev

76
Q

main cause of ectopic pregnancy

A

PID with chronic salpingitis

77
Q

dx ectopic preg

A

US or bcg (either serial or one over 1500)

78
Q

if unclear whether ectopic yet (empty uterus, Bhcg

A

wait

79
Q

tx of ectopic

A

surgery and mtx

80
Q

hcg indications of getstaional trophoblastic disease

A

plateau of hcg x 3 weks or hcg inc x 2 weeks

81
Q

what do moles look liek

A

edematous tissue with highly edematous villi

82
Q

complete hydafiform mole

A

always 2n
only trophoblastic tissue
mets 20% of time

83
Q

tx of complete hydatiform mole

A

evac of molar tissue, serial hcg, avoid preg for 6 months and take hcg for six months

84
Q

partial hydaliform mole

A

fetal + trophoblast tissue

persists or mets less ffre

85
Q

placentazl site trophoblastic tumor

A

rare intermediate trophoblast cells
deeply microinvASIVE and non respon to chemo
hpl and hcg lo

86
Q

MC maternal death in US

A

HTNisve disorder due to CNS hem

87
Q

placenta previa increases risk for

A

placenta acretia

88
Q

pain in placneta previa

A

painless

89
Q

CAUSE OF ABRUPT PLACENTA

A

dissecting hematoma into decidus basalis due to trauma, inherent weakness of spiral aa (pre-eclampsia)

90
Q

pre-eclamp/eclamp is an imbalance between

A
angiogenic factors (decrease VEGF, PIGF)
antangiogenic (inccreased SFLT1)
91
Q

endometriosis is common after preg because

A

normally protective vaginal acidity neutralized by alkaline amniotic fluid–>overgrowth of bacteria

92
Q

what does the mother/fetus need in preg

A

volume support/perfusion
nutrition/oxygenation
waste/toxin clearance
mother surviving potential hemorrhage (increase coag)

93
Q

factors that increase CO

A

increased exertion

labor (pain, catec)

94
Q

arterials and venous

A

arterial- decrease PVR

venous- increase elasticity adn capacity

95
Q

supine hypotensionsyndrome

A

aka inferior vena cava syndrome
compression of inf vena canva–>diminished venous certurn–>decrease CO
aorta compression–>decreased blood flow to uterus, bradycardia, hypotension, syncope, fetal heart changes

96
Q

physiological anemia of preg

A

plasma expands more than RBC making hematocrit and hemoglobin appear to fall

97
Q

hematological changse

A

incressed Fe absorption in gut
increased bolume
increase RBC volume

98
Q

placenta does not express

A

MHC I or MHC II

99
Q

liver chemistry in rpeg

A

generally unchanged, except increased alk phos due to placental isoenzyme

100
Q

progesterone and physiological dyspnea

A

progesterone induces increase sensitivity of central Co2 chemo R

101
Q

start of labor

A

placental CRH+ Acth increase–>increase fetal adrenal rpoduction–> fetal DHEAs converted to E by placenta–>develop gap jx in myometrium so contract

–>fetal cortisol (pos FB on CRH)–> develops surfactant and phospholipids–>increase fetal lung maturation –>increase Pgs–>cervical ripening

102
Q

3 phases of parturition casade

A

phase 0= pregnancy- functional quiescence
phase 2= primring- relase of inhib–>gap jx
phase 3- stimulation–>pushing, increase pge2, p2a, oxytocin

103
Q

walking in labor

A

true labor- makes worse

false labor- makes less

104
Q

effects of contraction (4)

A

cervical effacement-obliteration of cancal
cervical dilation-enlarge cervical opening
fetal descent
pain

105
Q

3 ps labor

A

power

passage passenger

106
Q

4 passage components

A

lie
presenting part/presentation
position
attitude (flexed, military, extended)

107
Q

4 stages labor

A

prodrome- prelabor changes
stage 1- 10 hrs; begin labor->full cervical dilation (10cm)
stge 2- 30 mins: full dilation–>delivery of fetus
stage 3-5 mins: delivery of fetus–> delivery of placenta

108
Q

pain is due to

A

cervical idlation (visceral aff to t10, 11,12)
hypoxia
nerve compression
peritoneal stretch

109
Q

stage 2 pain

A

distention of plevic floor, vagina, perineum

sensory branch purdenal (s2,3,4)

110
Q

4 changes hwen going into labor

A

cervical ripening
lightening (dropping - mom feels like she can breathe better, but increase urination)
passing out mucus plug
braxton-hicks contraction

111
Q

what happens in cervical ripening

A

collagen chains fracture
more hydrophilic glycosaminoglycans
increase h20–softer, thnned out

112
Q

monozygotic pregnancies occur

A

72 hours post fertilization

113
Q

monoamniotic monochronic

A

13-16 days
same streak, yolk sac
conjoined twins

114
Q

damc

A

mc monozygotic twins

3-8 days

115
Q

diamniotic dichornoc

A

fused placenta–divison before inner mas forms

116
Q

dizygotic pregnancy is the main cause of

A

spontaenous mutlifetal pregnancies

117
Q

main cause of multifetal pregnancy

A

increase in GNrh–>more follicles mature

118
Q

manual vaccum aspiration

A

5-10 weeks
simplest, safetst
no need cervical dilation

119
Q

D&C

A

upper limit 12-13 weeks

vacuum/mechanical means-requires cervical dilation

120
Q

medical

A

mifepristone-progestin R antagon
5 weeks or less 85% success rate
given day 1, misoprostol on day 3 and deliver within 3 hrs

121
Q

how does progestin work in OC

A

increase cervical mucosa–>block LH surge–>decrease estrogen Receptors

122
Q

how do OCps work

A

gonadotropin secretion inhibited
LH surge suppressed by progestin
follciular maturaiton and selection of dominant follicle blocked by estrogen

123
Q

aboslute risks of ocp

A
thromboembolic disorders
impaired LFTs
abnroaml vaginal bleed
pregnancy
smokers >35 with suspect brst cancer
migraines with aura
focal seizures
124
Q

injectables patches

A

depo- weight gain, not good if plannign preg in year

transdermal patches- weekly app, less effective in obese

125
Q

IUD Cooper does NOT

A

block ovulation

126
Q

mechanism of IUD

A

blocks interaction of oocyte and sperm

127
Q

conceptive rod

A

prog only
3 years
irreg bleeding for first few months
CI in breast cancer

128
Q

vaginal ring

A

doesnt decrease bleeding

129
Q

thelarche

A

estrogen stimulates lactiferous duct growth
fat accumulates between lobes
duct branching and elongating
terminal buds

130
Q

luteal phase and boobs

A

increase proliferation of duct system
slight aloveolar lubualr devlepment
increase vascularity
edema and tenderness

131
Q

1st trimester-early 2nd breasts

A

hyperplasia/hypertrophy
stromal decreases
increase vascularity

132
Q

mid prg–>onward

A

less mitosis as alveolar cells differentiate and begin to secrete–pricen by progesterone

133
Q

pre-reqs for brast feeding

A

fully developed mammary glands

withdrawal a and p to show prolactin binding sites

134
Q

lactopoesis (stage 3)

A

prolactin (increases casein protein)

oxytocin->contract myoepi cells–>milk let down

135
Q

preadolescent

A

gender identity, gender roles

136
Q

early adolescent

A

early puberty, sexual fantasys, mast

137
Q

middle adolescent

A

physical maturty, sexual exploration

138
Q

late adoelscent

A

adult

intimate sharing

139
Q

oxytocin pathways

A
nipple stim
anterolateral columns
brainstem
medialf orebrain bundle
paraventricular nucleus
post-pituitary-->increase oxygen relase
140
Q

purple boobs on H

A

glandular lumina
benign microcalc
fat necrosis

141
Q

benign breast tumors

A

fibroadenoma

hamartma

142
Q

apocrine metaplasia in fibrocystic change

A

does not incerase risk carcinoma

143
Q

2x risk for carcinoma

A

ducta hyperplasia and sclerosing adenosis

144
Q

5x risk of breast cancer

A

atypical hyperplasia

145
Q

MC of bloody nipple discharge

A

intraductal papilloma!–benign but can have cancer in it

146
Q

not risk factors of braest cancer

A

smoking
breast size
fibrocystic change

147
Q

conervative lumpectomy and chemo contraindicated in

A

large tumors
highly invasive
female where XRT is contraindicated

148
Q

neoadjuvant therapy given before surgery to

A

decrease tunor size or effects

149
Q

estrone in menopause

A

dominant androgen

does not protect or change bone density except in obese people because increase in aromatase–>increase in estrone

150
Q

changes in menopause

A

1) shorter cycles (due to increase fsh)
2) luteal insufficency (decrease progesterone)
3) annovulation

151
Q

bleeding occurs due to

A

estrogen withdrawal

152
Q

what continues after menopause

A

androgens

153
Q

hot glash mech

A

decrease E–>decrease endorphins in hypothal–>increase NE–>inapp heat lsos

5ht involved so ssris help

154
Q

how does estrogen work on osteoporosis

A

blocks it by blocking PTH stimulation of Ca mobilation (impedes osteoclast activity)

155
Q

tx lichen schelrosis

A

steroids

156
Q

.leiomyoma

A

premaeno women, enlarge with estrogen

157
Q

serous neoplasms often

A

bilateral

158
Q

Ca125

A

serous ovaraian neoplasm

159
Q

kra mutation

A

mucinous carcinoma

160
Q

seminoma chrom

A

12p

161
Q

treatment of spermatocytic sepminma

A

none unless transform- chemo and rad

162
Q

teratoma and chemo

A

destroys malignant potential but leaves cartilage can grow and undergo malignant transformation

163
Q

peyronie’s disease

A

penis bleeds when erect

164
Q

HGPIN

A

high grade prostatic intraepithelial neoplasm

repeat 2-3 years

165
Q

atypical small acinar proliferation

A

repeat by 3 months

166
Q

1st lne tx prostate cnacer

A

castration

or leuprolide

167
Q

2nd line prostate cancer

A

docetazel- apoptosis through blocking of microtubule depol

bispohphates and vitd/ca

168
Q

mechanism of erection

A

release NT–>smooth muscle relax in sinusoids–>arterial dilation–>increase BF–>sinusoids expand and compress emissary vein–>trap blood–>increase intracavernosal pressure

169
Q

three jobs of granulosa cells

A

1) make inhibin
2) aromatize androgens to estrogen
3) follicular growth