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Flashcards in Please be the last set: Ob/Gyn Deck (57)
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1
Q

adrenarche

A

6-8 yrs to 13-15 yrs

regeneration of zone reticularis: increased DHEA, DHEAS, androstenedione

2
Q

gonadarche

A

begins around 8 years
pulsatile GnRh leads to LH and FSH production
initially just in sleep, eventually leads to estrogen production in ovary
stimulates: thelarche, pubarche, growth spurt, menarche

3
Q

thelarche

A

estrogen stimulates; first stage around 10
first sign of puberty
breast development

4
Q

pubarche

A

estrogen stimulates; around 11 (lags thelarche by 6 mo)

development of pubic and axillary hair

5
Q

menarche

A

12-13 yrs (2.5 years after development of breast buds)
estrogen stimulates
onset of menstruation
for first 2 years: most cycles anovulatory

6
Q

peak growth velocity

A

due to increased GH and IGF (stimulated by E)
starts around 9 or 10 and peaks around 12 (9cm/yr)
reached before tanner stage 3 in breast development and stage 2 of pubic hair development

7
Q

female tanner stages

A

I: preadolescent; elevation of papillae only
II: sparse, pigmented downy hair along labia; elevation of breast and areolar enlargement
III: darker, courser and curlier hair, further enlargement of breast and areola
IV: hair distribution is adult in type (but not full quantity); projection of areolae and papillae to from secondary mount
V: hair in adult distribution and quantity ; projection of papillae only as areolae recess to beast contour

8
Q

age considered precocious puberty in

  1. white girls
  2. AA girls
  3. risks
    4: Dx
A

breast or pubic hair development

  1. 7 years
  2. 6 years
  3. female, AA, obese, exposure to sex hormones, McCune Albright syndrome, congenital adrenal hyperplasia
  4. breast/pubic hair, growth spurt, skeletal maturity greater than age; estradiol greater than 5 pg/mL
9
Q

causes of gonadotropin dependent precocious puberty

A

most: IDIOPATHIC
CNS: tumor, lesion, primary hypothyroidism

10
Q

hamartoma

A

most frequent type of CNS tumors to cause precocious puberty

contain GnRH neurons (ectopic hypothalamic tissue)

11
Q

causes of gonadotropin independent precocious puberty

A
  1. ovarian cysts or tumors
  2. exogenous E
  3. androgen secreting tumor, CAH
  4. McCune-Albright
12
Q

McCune Albright syndrome

A

precocious puberty
cafe-au-alit skin
fibrous dysplasia
present with premature vaginal bleeding (before breast development)

13
Q

incomplete precocious puberty

A

variant of normal puberty (early development of sexual characteristics)
check bone age: normal, no further testing
monitor closely

14
Q

types of incomplete precocious puberty

  1. premature thelarche
  2. premature adrenache/pubarche
A
  1. isolated growth development; normal growth rate, girls younger than 3 usually
  2. pubic hair without signs of puberty in children younger that 7-8 years; risk of PCOS
15
Q

precocious puberty

  1. Hx
  2. PE
A
  1. age, rate of puberty, growth velocity, CNS path (headache, visual impairment, seizure), sex steroid exposure, family Hx
  2. growth curve, neurological exam, thyroid, skin, pubic hair breast, genitalia, palpation for pelvic/abdominal mass
16
Q

precocious puberty: labs

A
  1. bone age: skeletal 2 years greater than age
  2. LH, FSH levels in pubertal ranges
  3. estradiol greater than 5
  4. GnRH stimulation
17
Q

additional testing for precocious puberty

  1. Gn dependent
  2. Gn independent
A
  1. thyroid testing, brain MRI

2. additional blood tests, pelvic US, bone scan

18
Q

Tx of precocious puberty

  1. Gn dependent
  2. Gn independent
A
  1. GnRH antagonist therapy: leuprolide

2. Tx underlying condition

19
Q

delayed puberty

A
  1. absence of sexual maturation by 13 years
  2. no evidence of monarch by 15-16 years
  3. when menses have not begun 5 years after thelarche
20
Q

causes of delayed puberty

  1. hypogonadotropic hypogonadism
  2. hypergonadotropic hypergonadism
  3. Eugonadism
A

hypogonadism

  1. pituitary tumor, GnRH insufficiency, hyper-prolactinemia, constitutional delay, chronic disease, CNS disorder, trauma
  2. ovarian failure, gonadal dysgenesis, iatrogenic (CA, Sx)
  3. mullerian agenesis, outlet obstruction (imperforate hymen, transvaginal septum), androgen insensitivity
21
Q

Kallman syndrome

A

hypogonadotropic hypogonadism, anosmia

22
Q

delayed puberty

  1. PE
  2. labs
  3. Tx
A
  1. tanner staging, vaginal patency, estrogen effect, pelvic masses, signs of Turners
  2. pelvic USG, FSH, TSH, PRL, karyotype, MRI of brain
  3. address cause, induce puberty with estrogen, monitor
23
Q

stages of coming out

  1. identity confusion
  2. identity comparison
  3. identity tolerance
  4. identity acceptance
  5. identity pride
  6. identity synthesis
A

can be out of order and skip steps

  1. begins to acknowledge, but find unacceptable (make excuses for behavior)
  2. accept but don’t describe self as gay (accept behavior but not identity or vice versa)
  3. accept likelihood, try on identity
  4. move from tolerance to acceptance, anger at society rather than self; choose to be around people that accept them
  5. marches, pride and anger, us against them
  6. begin to understand that not all heterosexuals are homophobic, relax, re-integrate into society
24
Q

important to remember as a doctor when patient is in identity pride stage

A
  1. safe sex

2. don’t Dx with personality disorder, sex addiction, etc.

25
Q

What triggers awareness of homosexuality and what age?

1. male

A
  1. by 13 years; romantic feeling

2. by 19 years; sexual feelings

26
Q

problems with hormone therapy for transgender

  1. testosterone
  2. estrogen
  3. anti-androgens
A
  1. liver damage
  2. clotting, increase in BP and blood glucose
  3. lower BP, disturb electrolytes, dehydration
27
Q

PLISSIT

A
to talk about sex and sexuality
P: permission
LI: limited information
SS: specific suggestions
IT: intensive therapy
28
Q

DOUPE

A
permission 1st
D: description of problem
O: onset
U: understanding cause
P: past attempts at solution or treatment
E: expectations for treatment
29
Q

recruitment of egg

  1. first recruitment
  2. second recruitment
A

selection and growth of dominant follicle

  1. paracrine control: AMH
  2. endocrine (FSH): AMH, inhibin B and estrogen
30
Q

how can you determine if a women is ovulating?

A

day 21 of cycle:

progesterone is over 5

31
Q

AMH role in ovarian cycle

A

paracrine at first, endocrine (FSH driven) at end

primordial to primary oocyte to secondary oocyte to small antrum development

32
Q

Inhibin B role in ovarian cycle

A

FSH driven

small antrum to dominant follicle

33
Q

estradiol role in ovarian cycle

A

FSH driven

small antrum to dominant follicle and ovulation

34
Q

When and where do you implant embryo in IVF

A

uterus: upper posterior

day 3: morula or day 5: blastocyst

35
Q

infertility

A

1 year of unprotected sex without conception

6 mo if over 35 yrs

36
Q
male factor
semen analysis
1. volume
2. conc.
3. motility
4. morphology
5. pH
6. round cells
7. possible reasons for male infertility 
8. other factors to evaluate
A

sperm ascend through Cx, Ut, tubes and capacity to fertilize oocyte

  1. 1.5-5 ml
  2. greater than 20 mil/ ml
  3. greater than 40%
  4. greater than 14%
  5. greater than 7.2
  6. less than 1 mil/ml
  7. retrograde ejaculation, duct obstruction, hypogonadism, CBAVD
  8. karyotype, Y chromosome microdeletions, FSH, LH, PRL, Testosterone
37
Q

cervical factor

  1. reasons for infertility
  2. tests
A

Cx filters and nurtures sperm into Ut and tubes

  1. anatomical changes, infection, change in mucus
  2. culture, post-coital test (see if sperm are moving in cervical mucus)
38
Q

ovarian factor

  1. reasons for infertility
  2. tests
A

ovulation of mature oocyte

  1. anovulation, luteal phase deficiency
  2. menstrual Hx, basal body temp, serum progesteron, urinary LH excretion, basal FSH/clomiphene challenge, oligo-amenorrhea test
39
Q

tubal/peritoneal factor

  1. reasons for infertility
  2. evaluation
A

tubes capture oocyte and transport sperm and embryo

  1. anatomical changes (congenital, BTL, adhesions, endometriosis)
  2. hysterosalpingography, GOLD STANDARD: laparoscopy with chromopertubation, sonohysterography
40
Q

uterine factor

  1. reasons of infertility
  2. tests
A

Ut receptive to implantation and support pregnancy

  1. anatomical changes (congenital, fibroids, adhesions), functional abnormalities (endometritis)
  2. US, sonohysterography, hysterosalphingography, hysteroscopy, occasionally endometrial biopsy
41
Q

Tx of male infertility factor

A

endocrine Tx

IUI, TDI, ART

42
Q

Tx of infertility female

A

correct anatomical defects
Rx for infection
restore regular ovulatory cycles
induce ovulation: clomiphene citrate, aromatase inhibitors, gonadotropins

43
Q

assisted reproduction techniques (ART)

  1. IUI
  2. IVF-ET
  3. ICSI
A
  1. intrauterine sperm injection
  2. in vitro fertilization and embryo transfer
  3. intra-cytoplasmic sperm injection
44
Q

chronic HTN preconception management

A
  1. avoid ACE inhibitors, ARBs
  2. teach BP self monitoring
  3. diminish diuretic use
45
Q

chronic HTN antepartum evaluation

A
  1. 24 hour urine: total protein and creatinine clearance
  2. baseline lab data (CBC, CMP, serum creatinine, LFTs, LDH, uric acid
  3. EKG, echocardiogram, ophthalmologic exam
  4. if proteinuria disproportionate to HTN: SLE and renal disease workup
  5. severe range BP less than 20weeks: hyperaldosteronism, molar pregnancy workup
46
Q

When should you start anti-hypertensives antepartum?

A

BP greater than 150/100

weight loss should NOT be encouraged

47
Q

anti-HTN options in pregnancy

A
  1. methyldopa
  2. labetalol
  3. nifedipine
  4. thiazide diuretics
  5. hydralizine
    reduces hospitalization and maternal stroke
    does NOT improve fetal condition or prevent preeclampsia
48
Q

methyldopa

A

alpha agonist
tx: first line for HTN in pregnancy
AE: hepatitis, hemolytic anemia

49
Q

labetalol

A

beta blocker with alpha blocking activity
Tx: second line for HTN in pregnancy
does NOT cause IUGR like other beta blocker

50
Q

nifedipine

A

Ca channel blocker

AE: headache, tachycardia, orthostatic hypotension

51
Q

delivery recommendation for chronic HTN

A

39 weeks

indications for earlier delivery: preeclampsia, eclampsia, sever HTN beyond 37 wks, fetal compromise

52
Q

DM in pregnancy evaluation

A
  1. urine creatinine, total protein
  2. Hemoglobin A1C
  3. thyroid function tests
  4. urinalysis and urine culture
  5. BP and EKG
53
Q

Blood glucose value goals

  1. fasting
  2. pre-prandial
  3. 1 hour post prandial
  4. 2 hour post
A
  1. 95 mg/dL
  2. 100 or less
  3. 140 or less
  4. 120 or less
54
Q

DM Tx in pregnancy

A

BEST: insulin only
glyburide
metformin
increase insulin needs as pregnancy progresses

55
Q

what should be checked in DM pregnancy

  1. 20 wks
  2. 15-21 wks
  3. starting at 32 weeks
A
  1. fetal echocardiogram
  2. alpha fetoprotein; neural tube defects
  3. serial growth ultrasounds
56
Q

During labor: DM management

  1. latent labor
  2. active
  3. if glucose exceeds 110
A

insulin night before, hold morning dose since not eating

  1. IV saline, monitor blood glucose
  2. add 5% dextrose, maintain glucose level of 100, may continue infusion of insulin pump
  3. short acting insulin
57
Q

postpartum DM management

A

maintain glucose below 150 when not eating

HALF antepartum regimen